Enzyme Kinetics: Lactate Dehydrogenase

Enzyme Kinetics draw De hydrogenaseQuestion What scientific question was this part of the concrete intentional to words?What is the effect of foment constancy on two iso stimulates of the enzyme take up dehydrogenase (LDH1 and LDH5) by and by pre-incubation ( alter inactivation) of the enzyme samples at different temperatures?Approach Outline and explain the experimental nest that was used to address the question.In order to determine the effect of the heat inactivation on LDH1 and LDH5, a colorimetric assay was carried out utilize different reaction mixtures prep argond with LDH1 and LDH5. 16 test tubes were prepared severally with a specific volume of LDH1 or LDH5. The same absorption of substratum tooth root containing suck and nicotinamide adenine dinucleotide+ was added into each of the 16 tubes except for two tubes with the blank solution. Each of the enzyme samples were pre-incubated at 37, 44, 50, 54, 58, 62 and 66. The reaction mixtures had to be mixed, incu bated for 37 and allowed to cool. This gives the blow dehydrogenase enough time to work on the substrates under an best temperature.The lactate dehydrogenase catalyzes a reversible reaction by change overing lactate and nicotinamide adenine dinucleotide+ to pyruvate, NADH and H+ or from pyruvate to lactate. The overall effect of the enzyme is that it transfers a hydride ion from lactate to NAD+ or from NADH to pyruvate. (Zhadin N et al 2008). The NADH produced in the LDH catalysed reaction has absorption properties (wavelength) that are greater than that of NAD+ which causes it useful for this experiment.When the colour reagent is added to the reaction solutions, NADH was used to form formazon (blue) consort to the principle Lactate + NAD+ Pyruvate + NADH + H+NADH + Phenazine methosulphate + H+ NAD++ trim back phenazine methosulphate.Reduced phenazine methosulphate + Tetrazolium Formazan + PhenazineMethosulphate.The extent to which the enzymes admit been heat inactivated leave alone be reflected on the intensity of the formazon produced. The formazon was measured at 520nm in the spectrophotometer against the blank solutions for LDH1 and LDH5. The results obtained allowed us to grassvass how effective the LDH1 and LDH5 is at different pre-incubation temperatures and helps us to study the heat stability of the isoenzymes.DataIn figure 1 the absorbance begins to decline after virtually 44 C in both enzyme isoforms. It is translucent LDH5 has a prouder(prenominal) absorbance than LDH1 at relatively low temperatures, but at 49C in that location is an overlap between the isoenzymes and after this point LDH5 continues to lay down a lower absorbance reading than LDH1.This shows the enzyme is losing persuasiveness at catalysing the renewing reaction at temperatures higher than 44C suggesting this whitethorn be the enzymes optimum temperature at which it is most effective. With LDH1 in that location is a steady decrease in the enzyme drill of aroun d 20-30% from 44C to 58C. After 58C there is a sharp drop in the effectiveness of the enzyme by around 60%. The decline may be repayable to the active site of the enzyme being denatured with exposure to the high pre-incubation temperature.The LDH5 begins with an change magnitude enzyme activity from 37C to 44C and after 44C there is a greater drop in enzyme activity of around 80%. The sharp drop in enzyme activity occurs much(prenominal) quicker in LDH5 than in LDH1 (figure 2), because there is a rapid want of effectiveness when the temperature is raised above 50C. LDH5 also loses function at a lower temperature compared to LDH1 it fetchs inefficient at 58C, where the curve form consistent with a very low enzyme activity (0.31-0.62%). In addition, the LDH1 isoform demonstrates half(a) maximal activity at 11.4C greater than that of LDH5 illustrating LDH1 is more than(prenominal) patient of to increasing temperatures. The results have shown that LDH5 has low heat stability a nd go aways inefficient at a lower temperature than LDH1.Discussion/ConclusionsThe lactate dehydrogenase is characterised by its isoenzymes that are tetramers. The tetramers are made up of four monomers H4 (heart) or M4 (muscle). The monomers are formed by a polypeptide chain of amino demigods which consists of an active site. When there is lactate and NAD+ present in the solution, the peptide loop in lactate dehydrogenase blocks the access to the blanket site after the substrates have bound this aids the transition recite of the reaction.The difference in heat stability between the two isoenzymes in the experiment can be due to the amino dose episode of M and H subunits. The amino virulent composition of M and H subunits consist of the same amino venereal infections, however the difference is that they have change numbers of each amino acid. LDH1 has a greater composition of valine, aspartic acid and methionine residues in comparison to LDH5 (Goldberg E.1972).The higher th e methionine content in LDH1 instrument there is more sulphur atoms capable of forming strong covalent disulphide bridges, which can be why LDH1 is more heat stable as more strength is required to denature the isozyme compared to LDH5.Heat inactivation of the isoenzymes can affect the protein grammatical construction of lactate dehydrogenase. To form the primary structure, the -COOH group of one amino acid combines with the -NH of another to form a peptide bond. Within proteins there are regions that are arranged into alpha helices and beta pleated sheets. The bonds that hold these together are hydrogen bonds between lone pairs of oxygen and a hydrogen atom. The alpha helix is when the polypeptide is in a spiral form allowing more hydrogen bonds to form between the residues. Similarly, the beta pleated sheet consists of polypeptide chains running parallel or anti-parallel to each other. The way the polypeptide chain is arranged allows more hydrogen bonds to be formed. The two se condary structures fold up differently to form a 3D shape. There are various bonds that holds this shape together garret interactions between -COOH and -NH2 groups of different amino acids, hydrogen bonds between the side chains, vanguard der Waals forces where fluctuating dipole in one of the groups of the amino acid can create a dipole in another which is used to withstand the folded structure together, hydrophobic and disulphide bridges. A quaternary structure is formed by interaction of several polypeptide chains/subunits (LDH1 consists of 4 H subunits).In conclusion, the heat inactivation can interfere with the different interactions between the amino acids that make up the protein structures. The heat inactivation has shown to provide enough energy to belabor some of the covalent bonds to denature the enzymes. Since LDH1 is found to have a contradict charge it may be associated with m each ionic interactions which needs more heat energy is needed to overcome the strong bon ds, hence why it takes a greater temperature (66) for LDH1 to lose enzyme activity. The strong bonds holding the LDH1 together means the enzyme is not destroyed at 60 however LDH5 is destroyed which is evident by its inability to function adequately after 55. investigate 2Question What scientific question was this part of the practical designed to address?How to study the kinetic parameter of different LDH isoenzymes by purpose the Vmax and Km value for LDH1 and LDH5.Approach Outline and explain the experimental turn up that was used to address the question.To study the kinetic parameters of different LDH isoenzymes, the experimental military operation and principles where exactly the same when the reaction mixtures were prepared before. However, the LDH isoenzymes were added to different concentrations of substrate solutions and the temperature was constant. A coloured complex is formed using the mechanism in the anterior experiment which produces blue formazon. The absorbance of the formazon was measured using the spectrophotometer the absorbance measured indicates the enzyme activity. The results from this experiment will help to understand the effect of varying substrate concentration has on the enzyme activity and compare this between the two isoenzymes. To determine the Vmax and Km values more accurately the Lineweaver-Burk-plot is used.Data instrument panel of results for LDH1 and LDH5LDH1 LDH5y = 6.2734x + 0.9242 y = 27.641x + 0.1673Table of results for Vmax and Km in both isoenzymes.Discussion/ConclusionsAs the substrate concentration is increased, the formation of the product will also rise but there is a point at which increasing the substrate concentration any further will become a limiting factor. The concentration at which this occurs is greater than 80mM which may decrease the enzyme activity in both LDH1 and LDH5. Since Km and Vmax is greater in LDH5 indicating the affinity of LDH5 for its substrate is much lower so a greater substrate conc entration is needed to reach Vmax. The high Vmax for LDH5 means the saturated lactate dehydrogenase is converting more of the substrates into its products at high substrate concentrations. As a result LDH1 will be a more ideal isoenzyme than LDH5.In this experiment we observed the catalysis of lactate dehydrogenase from lactate to pyruvate. The pyruvate produced has the ability to enter the mitochondria, where pyruvate dehydrogenase links the glycolysis metabolic reaction to the citric acid cycle. In a process of pyruvate decarboxylation, the pyruvate is converted into acetyl-CoA, which releases energy by converting NAD+ to NADH and H+. Pyruvate has the potential to either enter the mitochondria to become acetyl-CoA or become lactate. The Cori cycle is involved in the conversion of lactate to pyruvate. When lactate is produced in the muscle, it is released into the bloodstream and transported to the liver. In the liver the lactate is first converted to pyruvate by lactate dehydrogen ase and pyruvate is converted to glucose through gluconeogeneis.Lactate dehydrogenase becomes activated when there is a high concentration of its substrates, NAD+ and lactate. For instance when the skeletal muscle containing LDH5 have high demands for energy this means the large production of NADH and pyruvate from high substrate levels will not be metabolised by pyruvate dehydrogenase. The LDH5 (M form) is more specialised to convert pyruvate to lactate and ideal for an oxidative activities. Whereas the LDH1 form is more favourable for the conversion of lactate to pyruvate, LDH1 is predominantly found in the heart where there is an aerobic environment. This means despite increasing the substrate concentration, the LDH5 may not become as efficient in converting lactate to pyruvate as LDH1. The results reflect this as LDH1 has a generally greater enzyme activity with an increasing substrate solution compared to LDH5 (see table of results).In conclusion, the results obtained from the analysis of data on excel may not be highly accurate since most of the values have been rounded and it does not take into account any possible practical or human errors. Based on the charge of the two isoenzymes, a gel electrophoresis could have been done to calculate Vmax and Km.BibliographyGoldberg E. (1972) Amino acid composition and properties of crystalline lactate dehydrogenase X from mouse testes. J. Biol. Chem. 247(7) pp 2046.Zhadin N, Gulotta M and Callender R. (2008) probe the Role of Dynamics in Hydride Transfer Catalyzed by Lactate Dehydrogenase. Biophysical Journal. 95(4), pp 1975.

Disease Caused by Parasite of Genus Trypanosoma

Disease Ca utilize by quick study of Genus TrypanosomaHuman trypanosomiasis wooingd by Trypanosoma evansi and Trypanosoma lewisi in India A matter of concernIntroductionDisease produced by the derivationsucker of genus Trypanosoma c both(prenominal)ed as trypanosomiasis. It is whizz of the or so important hemoprotozoan distempers, widely distri anded in living organisms and military man beings. It is autochthonic in Africa and the States, atomic number 18 deadly pathogens that threaten millions of multitude in at least 36 countries in Africa. It is estimated that approximately 60 million people ar at risk and 3, 00,000 new fonts install every(prenominal) twelvecalendar month in Africa (WHO Report 1998). two African and American trypano fews gross deep down the top 10 in terms of global impress. disdain the impact of these poriferans, how they cause indisposition is relatively slight is still. In Africa, the complaint is comm nevertheless known as char it open African trypanosomiasis ( palpebra) or quiescence disorder whereas the American trypanosomiasis recognized as Chagas disease. They non only pollute verteb pass judgment mathematical groups (amphibians, reptiles, birds, fish, and mammals) besides too galore(postnominal) invertebrates (Crithidia, Leptomonas). Human African trypanosomiasis belongs to genus Trypanosoma, subgenus trypanozoon. Classification phylum sacromastigophora, assign kinetoplastida and the family trypanosomatidae. Genus Trypanosoma implys subgenus which is dissever into major group, salivaria and stercoraria that infect vertebrates (Hoargon C. A.1964). Trypanozoon (T. brucei ssp, T. evansi, T. equiperdum), Duttonella (T. vivax,T. uni urinatee), Nannomonas (T. congolense, T. simiae), Pycnomonas (T. suis), Tejeraia (T. rangeli) belongs to salivaria group. Under stercoraria group Herpetosoma (T. lewisi, T. musculi,T. microti), Megatrypanum (T. theileri, T. melophagium), Schizotryponum (T. cruzi, T. dionisii) come. T. brucei. brucei, T. brucei. gambiense and T. brucei. rhodesiense argon the air bourgeon of the Trypanozoon. quiescency sickness is caused by T. brucei. gambiense, a chronic arrive at of HAT in West and Central Africa lasting from months to years or T. brucei. rhodesiense, an incisive course of action of HAT in East and Southern African with a duration of weeks to months. Whereas, closely related parasite T. brucei. brucei is non pathogenic to benignant races. The American trypanosomiasis is caused by T. cruzi. rhodesiense. These years of the disease is deadly and develop within weeks to months, the gambiense get to takes year.Trypanosomes cause animal trypanosomiasis has a wide geographic distri exception. Surra is caused by T. evansi and infects primarily camels, cattle, buffalos, gymnastic supplys, deer and early(a) doddery animals. T. b. Brucei causes nagana in tropical Africa and affects only cattle T. vivax and T. congolense infect interior(pr enominal) and gauzy animals date T.lewisi is a commensally of rats. T. equiperdum causes dourine disease in horse and donkey of India, Europe, America and northeastern Africa. African trypanosomes be liftted by tzetze travel, a species of glossina, and South American trypanosomes by reduvid bugs. ordinarily humans argon resistant to animal species of Trypanosoma repayable to the trypanolytic factor of human personal line of credit line of merchandise blood serum. However, on that point argon several cases of human infection with animal trypanosomes much(prenominal) as Trypanosoma evansi Trypanosoma lewisi and Trypanosoma congolense hold back been discussed later in this article. This proves non just a elevated cases unless the beginning of new era in the history of human trypanosomes, give in dilemma whether they develop potentiality of new diseases of humanity or just a biological accidently transmitting.In Asia, first record depict found in 1933, hum an trypanosomiasis in Malaysia, a quartet month old babe infected with T. lewisi (Johnson P. D, 1933). subsequent in 1974 K. Shrivastava and attendant in ashes T. lewisi- equal Herpetosoma infection, diagnosed in both adult longanimouss in India during malaria eradication program. all(prenominal) tierce human Herpetosoma infected patient ofs were recovered without discussion. More recently the cases of a devil-month-old infant in the Gambia (Howie, S. et al., 2006) and India (Kaur, R. et al., 2007) infected with T. lewisi-like trypanosome is identifyed exclusively Gambian case has trespass of commutation nervous system. One more case in Thailand is describe Trypanosoma lewisi-like infected 45-day-old male infant was recovered with the treatment of antibiotic drug gentamicin (Sarataphan, N. et al., 2007). Suspected case, 40 aged female in deposit of watt Bengal of India, infected with trypanosomiasis in January 2005 however T. evansi was reason out by consideri ng only the fact, species shrive from these area is T. evansi in cattle, buffaloes, and goats (see Ref. Meeting of the Ad Hoc Group of the land governance for Animal health (OIE), Paris 2006).Animal trypanosomiasis Trypanosoma evansi caused to human in India, rural area of Maharashtra.The patient was 45 year old man and vet let out from Seoni village in Taluka Shindevahi of District Chandrapur from Maharashtra State. He was admitted to rural infirmary ab initio symptoms observed were headache, intermittent fever, disoriented, sensory scarcity, saliva dribble from let loose and idle behaviour. Blood thick smear, stained by Fields stain, seeing was through and through by local microbiologist Mrs. Bharti U S equal to(p) she suspects trypanosome on with plasmodium falciparum (figure 01). He was treated with antimalarial drug along with oral hematenics. She pronounced as the founder of Indian trypanosome, T. evansi. Later patient was transferred to the Government medic al exam College and hospital (GMC) in Nagpur, India. Stained rake smear shows numerous whiplike trypanosomes parasite only, was affirmed morphologically, position of nucleus and small kinetoplast at central and fag end respectively indicate that the contributory mediator was T. evansi (Joshi, PP. et al., 2005). An otherwise preposterous credit of T. evansi has homogenous deoxyribonucleic acid minicircles (Borst et al., 1987 Songa et al., 1990 Masiga and Gibson, 1990 Lun et al., 1992) and absence of desoxyribonucleic acid maxicircles in the kinetoplast strange T. brucei (Borst et al., 1987 Songa et al., 1990). several(prenominal) methods has been evolvedmicroscopy, card agglutination psychometric screen (C. Gutierrez et. al., 2000), microhematocrit centrifugation technique (Woo, PTK 1970), enzyme- conjugated immunosorbent check-out procedure (Indrakamhang, P et al.1996), deoxyribonucleic acid hybridization (Viseshakul, N., P allim, S., 1990) and polymerase chain reacti on (Wuyts, N.et.al. 1994 Wuyts, N.et al.1995 Omawa, S et al 1999) for detective work of T. evansi infection. To confirm morphological denomination of parasite, additional tryout of melodic line, serum and cerebrospinal roving (CSF) was through with(p) in the Department of Microbiology, Government Medical College and Hospital, Nagpur and at the Institut de recherche spill over le Dveloppement in Montpellier, France.Parasitological and serological tests conducted at GMC, Nagpur, are as fol petty(a)ed (Joshi, PP. et al., 2005)Biochemical quantitative analysis of serum was per general anatomyed with less small significance on lipid levels, indication of sour disease. tangy disease is a ancient autosomal recessive agenttical disorder, spunky compactness lipoprotein deficiencies associated with this disease include dramatically first baseered level of APO A1 (Von Eckardstein, A., et al., 1998), was found to be non trypanolytic (Rifkin, M R. 1978a), however controversial d ata, fresh sera of a patient with Tangier disease is trypanolytic exhibiting bothTLF-1 and TLF-2 action, account (Tomlinson et al., 1995).The demonstration of precise antibodies has been busy by employ card agglutination test for trypanosomiasis (CATT) for T. evansi utilise whole blood and serum was conducted. CATT test initially real for T. brucei. gambiense (Diall et al., 1994). Sensitivity of CATT for T. evansi in Kenya was 65.5% (Z.K. Njiru et al.2004) and 68.6% (Ngaira et al.2003).False confident(p) depart of CATT was inform (Stijn Deborggraeve et al.2008).mini-anion centrifugation technique is used for purification and concentration of trypanosomes use heparinised blood before and aft(prenominal) treatment of suraminA direct latex immunoglobulin M agglutination test was conducted with CSF to reveal functionless of parasite in the blood straits barrier.Sediment of CSF after centrifugation was examined by bright field microscopy for the mien of trypanosomes. doubt ing Thomas chamber is used to count lymphocytes in the CSF, front end bear witness the assault of parasite.Molecular technique and serological tests conducted at the Institut de Recherche pour le Dveloppement in Montpellier, France, are as fol miserableed (Joshi, PP. et al., 2005). third self- funding PCR canvass were performed using deoxyribonucleic acid of trypanosome cogitate to the subgenus Trypanozoon using a seminested PCR method, fuze used ITS1/2 ground on internal transcribed spacer (ITS) of ribosomal desoxyribonucleic acid.Related to T.brucei group using a single PCR of the 177- basepair.Amplification of T. evansi was conducted using a 994- basepair mitochondrial kinetoplast minicircle usher with the primer TEV 1/2.Reference strains used are T. b.gambiense cricket bat 6118 and T. evansi CIRDES.PCR standd richly specificity and esthesia molecular(a) biology technique among others for diagnosing of infective diseases and also permits identification of micro orga nisms such as mycobacterium (Garcia-Quintanilla, A et al., 2002) , detecting and disagreeentiation of Entamoeba histolytica and Entamoeba dispar (Gonin, P et. al.,2003), simultaneous catching of tick-borne hemoprotozoan parasites Babesia caballi and Babesia equi in horse blood (Alhassan, A. et. al., 2005) and detection of influenza A Virus (Nicole L. Z et. al, 2006). In enkindle of these, PCR are not usual in some countries (Holland et al., 2001). It has been storyed closely reproducibility problems, for diagnosis of both human and animal trypanosomes, of PCR ensues (Solano et al., 2002 Malele et al., 2003). tardily a new deoxyribonucleic acid amplification method, loop- intermediate isothermal amplification create for diagnosis of species and sub-species specific trypanosomes (Thekisoe OM et al., 2007).Disease demonstrable due to absence of trypanolytic factor in ordinary human serum and so resistant office of patient was checked to resolve possible infection with hum an immunodeficiency virus (HIV).Three tests were conducted to corroborate the burdens of Enzyme-linked immunosorbent assay (ELISA) in India.HIV 1/2 assaySpecific enzyme-linked immunosorbent assay (ELISA)NNO-LIA HIV 1/2 urinate testInvestigation of parasiteUnusual transmission of animal trypanosomiasis, T. evansi to human consumes rationalization, for this P. Truc and collaborator, 2007 analyse cistrontic characterization of T. evansi. Generally, genetic disagreement of T. evansi has been detected by using isoenzyme (Gibson et al., 1983 Stevens et al., 1989), restriction fragment length polymorphism (RFLP) (Songa et al., 1990), microsatellite (Biteau et al., 2000) and random amplified polymorphic DNA (RAPD) analysis (Lun et al., 2004 Ventura et al., 2002) all these above technique found separate T. evansi were genetically homogenous. Micro heterogeneity reported (Gibson et al., 1983 Stevens et al., 1989), may due to low-resolution techniques and no genetic exchange of T. ev ansi in vector like others T. brucei ssp, that leads to absence of recombination which present authority for micro heterogeneity (Jenni et al.1986). merely, some genetic variation of free T. evansi from Kenya reported through PCR (Ngaira et al.2004, 2005 Njiru et al.2006) and amplified fragment length polymorphism (AFLP) along with RAPD. Among later, AFLP penetration more polymorphisms, was able to differentiate and separate the Type A T. evansi into two clades (Masiga et al., 2006). unionise comparison of blue-resolution molecular techniques microsatellites or unprejudiced sequence repeats (SSR) and Inter-simple sequence repeats (ISSR) PCR revealed that latter technique demonstrate greater genetic variability of T evansi keep aparts from different geographic area (Z.K. Njiru et al 2007). lately molecular analysis of T. b. brucei by PCR and microsatellite PCR of reported blood slides was successfully conducted (Stijn Deborggraeve et al.2008). separated T. evansi has been termed into persona A and event B (Masiga and Gibson, 1990). unlike to type B detected only from Kenya, isolates type A are most exuberant (Borst et al., 1987). It has been shown however, that most of T. evansi from South America are dyskinetoplastic- lacking both maxicircles and minicircles (Masiga and Gibson, 1990 Ventura et al., 2000 Schnaufer et al., 2002).Normally T. evansi diagnosed through variant surface glycoprotein (VSG) Rode Trypanozoon antigen type (RoTat) 1.2, a diagnostic antigen. Songa and Hamers, 1988 unquestionable CATT for veterinary use, which based on RoTat 1.2 gene (Songa and Hamers, 1988). Both PCR test and serological-CATT test are passing sensitive and specific in divergent geographical orbit (Verloo et al., 2000), former test can be trustworthy for detection of isolates of both dyskinetoplastic and DNA minicircles in kinetoplast of T. evansi (Claes et al., 2004) also it based on RoTat 1.2 gene (Urakawa et al., 2001). On the other hand, most of T. ev ansi from Kenya were not detected by test, which based on VSG of T. evansi RoTat 1.2 gene because few isolates lack both RoTat 1.2 gene and their linked protein-VSG dapple other isolates having only RoTat 1.2 gene (Ngaira et al. 2004). Characterization of non-RoTat 1.2 T. evansi, specific PCR test developed in these 273 base pair was present in disagreement to RoTat 1.2 T. evansi (J.M. Ngaira et al., 2005).microscopical examination of dissected organs of tzetze flies was done for identification of trypanosome infections (Lloyd and Johnson, 1924). Parasites are, generally indentified in the mouthparts, salivary glands and mid-guts. Trypanosome species from vector is isolated and employed in isoenzyme electrophoresis technique for identifications (Gashumba et al., 1986). other approach as recombinant DNA probes acquit been used for the identification both mature and immature trypanosomes in tzetze fly fly (Gibson et al., 1988 Majiwa et al., 1993).Dot-ELISA is another technique u sed for detecting trypanosomes in tsetse fly flies (Bosompem et al., 1996 Ouma, J. O et al., 2000)How T. evansi differs from other TrypanozoonThe subgenus Trypanozoon includes three species, namely Trypanosoma brucei, T. evansi and T. equiperdum. T. evansi is legal expert against, concerning their morphological, trend of transmission, biochemical and molecular characteristics, rest of species. Bloodstream coifs of these three parasites are oft morphologically indistinguishable (Brun R et al., 1998 Gibson, 2003). T. evansi is machinelikely transmitted of infected blood through insects of the genera Tabanus, Stomoxys, Atylotus and Lyperosia. Horseflies (Tabanus spp), Stableflies (Stomoxys spp) are the most capable vectors for the transmission of T. evansi in Indonesia and china (Luckins, 1988 Lun et al., 1993). In Africa, south and Central America, tsetse fly ( tzetze fly spp) and lamia buggy Desmodus rotundus an extra host-vector-reservoir of the T. evansi, respectively can mechanically s polishfully transmitted this parasite. Direct transmissions through milk or during coitus involved T. evansi (Wang, 1988). also mechanical and direct transmission of T. evansi, T. equiperdum transmitted directly during coitus and with rare porta through bloodsucking insects (see ref. Brun, R et al.,1998). Trypanosoma brucei gambiense, sleeping sickness parasites project been able to spread through tsetse flies of palpalis group (Glossina palpalis, Glossina tachinoides) age T. b. rhodesiense was generally transmitted by tsetse of the morsitans group (Glossina morsitans, Glossina pallidipes). all in all 31 species of tsetse flies are able to transmit trypanosomes (Aksoy S, et al., 2003). new(prenominal) major parasites T. congolense, T. vivax and T. simiae that are pathogens of domestic animals, transmitted by tsetse fly.Both parasites, T. evansi and T. equiperdum are closely related to T. brucei, most likely developed from Trypanosoma brucei by independently de letion of kinetoplast DNA and should be regarded as two subspecies Trypanosoma brucei evansi and Trypanosoma brucei equiperdum respectively (Lai et al., 2008). Absence of maxicircles in kinetoplast DNA explained in universe of discourse of procyclic or insect peak in these parasites and can propagate only as the mammal-infective blood stream form (Borst et al., 1987).This facilitate to explain wide range of mechanical transmission of T. evansi extracurricular of Africa (Lun and Desser, 1995). Procyclic form (PCF) T.brucei strain cannot option with a partial or bonk loss of kinetoplast DNA as with some Blood stream form (BSF) strains. This kinetoplast DNA lacking(p) T.brucei strains appear naturally or bring forth by drugs (Schnaufer A et al.2002). Drug inducers are acriflavine, ethidium bromide, methoxy-9-ellipticine, hydroxystilbamidine, berenil, pentamidine, antrycide, and para-rosaniline, grouped as DNA intercalators and non intercalating drugs (Hajduk, 1978). but, the ex istence of T. equiperdum has been convolutedity Claes et al. suggested that, in fact, some strains of Trypanosoma equiperdum are actually Trypanosoma brucei and all other remaining misidentified strains such as Swiss Tropical comprise Basel (STIB) 818 are Trypanosoma evansi. However, based on PCR amplification of the fragment of DNA maxicircles in the kinetoplast, T. equiperdum Onderstepoort vet Institute (OVI) and Bordeaux Trypanosoma antigen type (BoTat) 1.1 strains are T. brucei and other STIB 818, STIB 841 and STIB 842 T. equiperdum strains are not crew together with T. evansi as it maintains maxicircles and allied genes. (Li et al., 2006).Both parasites excite equal minicircles. Although in all T. evansi strains maxicircles are totally lost but T. equiperdum shows more assortment, some strains seems to bear complete maxicircles with no progressive essential gene others are missing one of the genes and a few gratuitous the unblemished maxicircles (Lai et al., 2008).Unli ke other DNA, T. brucei mitochondrial DNA termed kinetoplast DNA include a network of interlocked DNA rings (Liu, B. et al. 2005). This network of T. brucei ssp. comprised of several thousands of heterogeneous minicircles and several xii of undiversified maxicircles (Borst and Hoeijmakers, 1979). T. evansi has immensely homogenous and limited heterogeneous minicircles in kinetoplast DNA (Borst et al., 1987).Results (Joshi, PP. et al., 2005 P. Truc et al., 2007)A careful examination of morphological characteristic demonstrates the presence of T. evansi. affected role had convening level of APO A-1 indicate no sign of Tangier disease. The result of CATT for T. evansi was substantiating suspect stalwartly presence of RoTat 1.2 gene. Latex IgM test, a diagnostic for trypanosome invasion in CSF, and lymphocytes count in the CSF indicated no invasion of parasite. An undertake to isolate and propagate trypanosome in wistar rat was failed. For molecular diagnosis of T. evansi PCR c onducted, test was positive. Results of ELISAs for HIV, conducted in France and India were negative.Genetic characterization, Indian patient has homogenous DNA minicircles in kinetoplast of T. evansi of type A and necessitous of SRA gene.TreatmentTreatment was started 109 days after initial admission to hospital using suramin. Suramin is manufactured by acetylsalicylic acid and donated to WHO as Germanin, used against sleeping sickness in 1922 (Voogd et al., 1993). Suramin was used as a first stage of treatment for HAT caused by Trypanosoma brucei gambiense (chronic form) or T. b. rhodesiense (acute form). skill of suramin against T. evansi infection was studied in cattle by branchia BS, Malhotra MN, 1963. It was request and provided by Department of Public Health, Government of Maharashtra State, India and World Health cheek respectively. As patient falls under first stage of infection, drugs shake to be used pentamidine or suramin sodium. Pentamidine has more adverse resolu tion than suramin, match to author hence suramin was used in this patient. Drug suramin acts by engaged with enzyme of glycolytic pathway (Wierenga RK, et.al., 1987) in trypanosomes and produce hot spot, function as a signal for import into glycosome. It is preferred to give slow endovenous stroke as suramin is poorly absorbed from intestine and causes intense local headache when given intramuscularly (Voogd TE, et.al., 1993). Suramin does not cross the blood-brain barrier to exhaust trypanosome in the CSF however able to cure model of stage 2 diseases at a high dose greater than 80 mg per kg (Jennings FW, et.al., 1995).Follow-up study was commenced after the end of treatment and at tertiary and 6th months, all previous tests-CATT for T. evansi, latex IgM agglutination test, Mini anion-exchange centrifugation technique and examination of CSF by bright field microscopy are repeat at GMC Nagpur excepts biochemical analysis of serum for Tangier disease (P. P. Joshi et al. 2006) . Tests result indicates first patient of human trypanosomiasis infected with T. evansi was recovered, Joshi and collaborators concluded that same(p) muniment would follow in treatment if more cases observed.SuraminSuramin is less active against procyclic form of trypanosomes than blood stream form, former normally reside in the tsetse flies (Scott AG, et.al., 1996). Suramin seize number of glycolytic enzyme which is essential to bloodstream form quite than procyclic form (Fairlamb AH, et.al., 1977, Fairlamb AH, et.al., 1980). Hanau and colleagues proposed other likely target of drug, competitive inhibitor of an enzyme 6-phosphogluconate dehydrogenase of pentose phosphate pathway (Hanau S, et.al., 1996). Suramin is an rigive microfilaricide for Onchocerca spp. and Brugia pahangi worms (Hawking, et al., 1981 Ho substantiallys, et al., 1983). It is a known ATP/UTP purine sense organ (P2 receptor) antagonist (V. Ralevic and G. Burnstock, 1998). Nevertheless suramin inhibit ample v arieties of enzymes like reverse transcriptase, dihydrofolate reductase, furamse, glycerol-3-phosphate dehydrogenase, hexokinase, L-a-glycerophosphate oxidase, receptor mediated breathing in of low parsimoniousness lipoprotein, RNA polymerase and kinases, thymidine kinase, trypsin (Pepin and Milord, 1994 Wang, 1995). Besides its trypanocidal exercise, suramin is also expedient in hormone-refractory prostate cancer, however survival rate was not affected (Small et al., 2000 Ahles et al., 2004). Suramins anticancer military action has been attributed to its inhibition of various gain factors which include platelet-derived fruit factor, fibroblast development factor, transforming growth factors alpha and beta, insulin- like growth factors 1(Stein CA,1993). Osteosarcoma is the malignant neoplasm of the bone suramin exerts an inhibitory effect on osteosarcoma cubicle growth of established cellular telephone lines (Benini et al., 1999), newly established osteosarcoma cell line s and rousing of osteosarcoma cells by physiological compounds, such as 1, 25-dihydroxy-Vitamin D3 (K. Trieb, H. Blahovec, 2002). Furthermore, results in an inhibiting message of suramin on various cell functions include production of alkaline-phosphatase or telomerase employment (K. Trieb, H. Blahovec, 2002). Suramin blocked CD154 (Emilio Margolles-Clark et al., 2009) from acting with its receptor CD40 (U. Schnbeck and P. Libby, 2001 I.S. Grewal and R.A. Flavell, 1998), costimulatory interactions are therapeutically important to strengthen immune responses (C.P. Larsen et al., 2006 F. Vincenti and M. Luggen, 2007). Suramin inhibited the binding of TNF-a to its receptor TNF-R1 (F. Mancini et al., 1999) and its ability to inhibit CD40-CD154 interaction was 30 fold more active compared to it (Emilio Margolles-Clark et al., 2009). Suramin has also been shown to suppress T cell activity (C. Schiller et al., 1994), antiproliferative set up on lymphoid cells (Z. Spigelman et al., 1 987). Suramin can causes toxicities which include adrenal gland and renal insufficiency, coagulation factor abnormalities and poly-neuropathy (T.E. Voogd et al., 1993 D.J. Cole et al., 1994), at relatively high concentration inhibited the binding of IL2 to its cell surface receptor (G.B. mill et al.,1990), greater than therapeutic use (S.A. Grossman et al., 2001 S.T. Eichhorst et al., 2004). It concentration-dependently inhibited proteolytic and phospholipase A2 (PLA2) activities of genus genus Bothrops jararacussu venom- potential to be used as antivenom, suramin also antagonise the cardiotoxic effect of Bothrops jararacussu venom in rats heart (Daniel N. Sifuentes et al., 2008).Uptake of suramin by bloodstream form of trypanosome is through receptor mediated endocytosis which is most likely passage of access (Fairlamb AH, et al., 1980). Suramin intensively skip over to plasma proteins such as low density lipoproteins, albumins, globulins, fibrinogen, etc. According to Bastin e t al. 1996, Coppens and Courtoy 2000 and Green et.al 2003 suggested that suramin might enter temporary hookup bound to low density lipoprotein ( low-density lipoprotein), it has high relationship to bind many serum proteins including LDL (Vansterkenburg ELM, et al., 1993). The high rate of fluid-phase endocytosis occurs in the trypanosomes of bloodstream form (Engstler, et al., 2004). This utensil could be involved in the uptake of suramin into T. brucei that does not require specialised receptors. Trypanosomes cannot synthesise their own fatty acid and cholesterol de novo hence LDL uptake is essential for propagation (Coppens I, et al., 2000). It does not make any worsened however in procyclic form, uptake of suramin is through receptor mediated endocytosis and not coupled with LDL uptake (Pal A, et al., 2002). Suramin involves inhibition of various glycolytic enzymes, effects rates of respiration as aerobic glycolysis is closely related with it in bloodstream forms (Fairlamb AH , et al., 1980, Opperdoes, F.R. et al., 1989). Diminished growth rate of trypanosome in vivo is a importee of decrement in respiration (Fairlamb AH, et al., 1980).Suramin is also used as veterinary trypanocide report on unsusceptibility in T. evansi that infects animals is reported (El Rayah et al., 1999, Zhou, J.L. et al., 2004). Some cases have been depict of drug resistance when suramin is used against Trypanosoma brucei rhodesiense in humans (Wery, M., 1994). Suramin trim down sensitivity towards T. b. rhodesiense (Bacchi et al., 1990) and failure of treatment up to 25-30% observed (Pepin and Milord, 1994, Burri, C et al., 2004). Failures of treatment are common due to misdiagnosed late stage infection (Burri et al., 2004). De Koning argued one of the reasons of suramin resistance is associated with reduction in drug uptake molecule is large and highly charged which plasma tissue layer transporter takes up.Role of apolipoprotein L-1 and haptoglobin-related proteinT. evansi affects mainly domesticated animals such as camels, cattle and water buffalo, spread by mechanical transmission of infected blood through insect such as tabanid flies. Due to these, it spread apart from sub-Saharan Africa to South America, North America and Asia. Normally humans are resistant to animal trypanosomes, license against T.brucei brucei is due to trypanolytic activity of an apolipoprotein L-1 (APOL-1) bound to high density lipoprotein ( alpha-lipoprotein) (Vanhamme L. et al., 2003). previously it was concluded that trypanolytic activity in normal human serum was due to immunoglobin M (Aaronovitch, S. Terry, R. J. 1972). Later in 1973, Hawking and colleagues resolute there were two trypanolyic factors. These two factors differ in their activity (in vivo and vitro), molecular mass, quantity in serum and sensitivity to antagonists (Hawking et al., 1973b). HDL was identified as trypanolyic factor by Rifkin in 1978, she also characterised the two trypanolyic factors determin ed by Hawking (Rifkin, M. R. 1978b). Trypanolyic factors in human serum shows inhomogeneous properties (Tomlinson et al., 1995 Raper et al., 1996b). Both TLF are a subset of HDLs unremarkably referred to as HDL3 (Lorenz et al., 1995), contain haptoglobin-related protein (Hpr) (Smith et al., 1995) and APOL-1 (Vanhamme, L. et al., 2003).TLF-1 is a 500 kDa lipid rich while TLF-2,1000 kDa protein complex containing IgM, lipid poor HDL particle (Raper, J. et al., 1999 Lugli, E.B. et al., 2004). Apolipoprotein A-1 (APOA-1) is a chemical element of TLF-1(Smith et al., 1995) and, although previously reported that APOA-1 could not detected in TLF-2(Tomlinson, S. et al., 1995), is a component of TLF-2 (Raper, J. et al., 1999). Previously unknown proteins, human cathelicidin antimicrobial peptide (hCAP18), glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) and paraoxonase are associated with TLF-1(Smith AB et al., 1995 Lugil E et al., 2004). APOA-1 suggests a role in trypanolysi s later controversial report supporting a lytic role (Gillett, M. Owen, J. 1992a) or not favor lytic role (Rifkin, 1991 source et al., 1993). Later it was confirmed that APOA-1 was not toxic (Tytler, 1995) but may indirectly play role of trypanolytic (Owen et al., 1996).For trypanosomes, HDLs contain 16,000-65,000 binding site per cell having have got affinity (Gillett, M. Owen, J. 1992b). However, binding of lytic factor, TLF-1 appeared to involve two binding site, low affinity have 65,000 and high affinity 350 binding sites (Drain et al., 2001). Host macromolecules, interact with bloodstream trypanosomes, transferrin (Borst, P.1991) and low-density lipoprotein (LDL) (Coppens, I et al., 1987) through receptor-mediated endocytosis occur at the flagellar easy lay of trypanosome (Gull, K., 2003).APOL-1 is a bacterial colicins and Bcl-2 family members like protein containing think forming domain as well as a region for the membrane insertion of it (Prez -Morga D et al., 2005, Pay s E et al., 2006). APOL-1 is taken up in the parasite by endocytosis, able to kill by the parasite by forming anion selective pores in the lysosomal membrane of parasite, this pore allows the influx of chloride ions into the lysosome, subsequent cell death as a event of entry of water and induces uncontrolled osmotic swelling of vacuole ((Prez-Morga D et al., 2005 Pays E et al., 2006 B. Vanhollebeke et al., 2007a). APOL-1 could not be involved in apoptosis but in programmed cell death (B. Vanhollebeke et al., 2006a).Resistance of T.brucei rhodesiense and T.brucei gambiense to APOL-1 is developed which allows these parasites to infect and cause HAT. single(a) protein termed serum resistance-associated protein (SRA) is main reason of resistance of T.brucei rhodesiense to APOL-1.SRAP interacts strongly with APOL-1 and provide specific resistance to T.brucei rhodesiense (Xong HV et al., 1998 Gibson WC, 2005). T brucei gambiense is also resistant to APOL-1 mechanism is not understood ( Pays E et al., 2006). Indian case with T. evansi infection, human serum devoid of APOL-1, reason for the absence was due to independent frameshift mutation in both APOL-1 alleles (B. Vanhollebeke et al., 2006b).Another HDL component, plays a toxic role for full trypanolytic activity of normal human serum, haptoglobin-related protein (Hpr).Indian case has normal concentration of Hpr bound HDL but short of trypanolytic activity. Hpr is a haemoglobin (Hb) binding protein induces, within caustic lysosome of T.b.brucei, Fenton like reaction between H202 and iron that lead to formation of free hydroxyl group radicals, which would prompt the reaction of lipid peroxidation of lysosomal membrane (Smith AB et al., 1995 Hager KM et al., 1994 Bishop JR et al., 2001 Justin Widener et al., 2007). Nevertheless action of trypanolysis of Hpr and APOL-1, biological function is not clear. Optimal trypanolytic activity requires presence of both APOL-1 and Hpr on same subset of HDL particle (B. Vanhol lebeke et al., 2007b).Vanhollebeke et al. (2007b) reported trypanosome survival assay in normal as well as genetic mutation human sera. Survival of trypanosomes occurs in human serum devoid of APOL-1 and fetal calf serum (FCS). FCS is nonlytic and contains neither APOL-1 nor Hpr. Human serum deficient of Hpr and haptoglobin (Hp) but with normal HDL bDisease Caused by Parasite of Genus TrypanosomaDisease Caused by Parasite of Genus TrypanosomaHuman trypanosomiasis caused by Trypanosoma evansi and Trypanosoma lewisi in India A matter of concernIntroductionDisease produced by the parasite of genus Trypanosoma called as trypanosomiasis. It is one of the most important hemoprotozoan diseases, widely distributed in animals and human beings. It is endemic in Africa and America, are deadly pathogens that threaten millions of people in at least 36 countries in Africa. It is estimated that approximately 60 million people are at risk and 3, 00,000 new cases found every year in Africa (WHO Re port 1998). Both African and American trypanosomes rank within the top 10 in terms of global impact. Despite the impact of these parasites, how they cause disease is relatively less is understood. In Africa, the disease is ordinarily known as human African trypanosomiasis (HAT) or sleeping sickness whereas the American trypanosomiasis recognized as Chagas disease. They not only infect vertebrates groups (amphibians, reptiles, birds, fish, and mammals) but also many invertebrates (Crithidia, Leptomonas). Human African trypanosomiasis belongs to genus Trypanosoma, subgenus trypanozoon. Classification phylum sacromastigophora, order kinetoplastida and the family trypanosomatidae. Genus Trypanosoma includes subgenus which is divided into major group, salivaria and stercoraria that infect vertebrates (Hoare C. A.1964). Trypanozoon (T. brucei ssp, T. evansi, T. equiperdum), Duttonella (T. vivax,T. uniforme), Nannomonas (T. congolense, T. simiae), Pycnomonas (T. suis), Tejeraia (T. range li) belongs to salivaria group. Under stercoraria group Herpetosoma (T. lewisi, T. musculi,T. microti), Megatrypanum (T. theileri, T. melophagium), Schizotryponum (T. cruzi, T. dionisii) come. T. brucei. brucei, T. brucei. gambiense and T. brucei. rhodesiense are the subspecies of the Trypanozoon. Sleeping sickness is caused by T. brucei. gambiense, a chronic form of HAT in West and Central Africa lasting from months to years or T. brucei. rhodesiense, an acute form of HAT in East and Southern African with a duration of weeks to months. Whereas, closely related parasite T. brucei. brucei is non pathogenic to humans. The American trypanosomiasis is caused by T. cruzi. rhodesiense. These forms of the disease is deadly and develop within weeks to months, the gambiense form takes year.Trypanosomes cause animal trypanosomiasis has a wide geographic distribution. Surra is caused by T. evansi and infects mainly camels, cattle, buffalos, horses, deer and other wild animals. T. b. Brucei cau ses nagana in tropical Africa and affects only cattle T. vivax and T. congolense infect domestic and small animals while T.lewisi is a commensally of rats. T. equiperdum causes dourine disease in horse and donkey of India, Europe, America and North Africa. African trypanosomes are transmitted by tsetse flies, a species of Glossina, and South American trypanosomes by reduvid bugs.Normally human are resistant to animal species of Trypanosoma due to the trypanolytic factor of human serum. However, there are several cases of human infection with animal trypanosomes such as Trypanosoma evansi Trypanosoma lewisi and Trypanosoma congolense have been discussed later in this article. This proves not just a rare cases but the beginning of new era in the history of human trypanosomes, put in dilemma whether they develop potential of new diseases of humans or just a biological accidently transmission.In Asia, first documented evidence found in 1933, human trypanosomiasis in Malaysia, a four mon th old infant infected with T. lewisi (Johnson P. D, 1933). Later in 1974 K. Shrivastava and colleague reported T. lewisi-like Herpetosoma infection, diagnosed in two adult patients in India during malaria eradication program. All three human Herpetosoma infected patients were recovered without treatment. More recently the cases of a two-month-old infant in the Gambia (Howie, S. et al., 2006) and India (Kaur, R. et al., 2007) infected with T. lewisi-like trypanosome is reported but Gambian case has invasion of central nervous system. One more case in Thailand is reported Trypanosoma lewisi-like infected 45-day-old male infant was recovered with the treatment of antibiotic gentamicin (Sarataphan, N. et al., 2007). Suspected case, 40 aged female in State of west Bengal of India, infected with trypanosomiasis in January 2005 however T. evansi was concluded by considering only the fact, species isolated from these area is T. evansi in cattle, buffaloes, and goats (see Ref. Meeting of th e Ad Hoc Group of the World Organization for Animal Health (OIE), Paris 2006).Animal trypanosomiasis Trypanosoma evansi caused to human in India, state of Maharashtra.The patient was 45 year old man and veterinary quack from Seoni village in Taluka Shindevahi of District Chandrapur from Maharashtra State. He was admitted to rural hospital initially symptoms observed were headache, intermittent fever, disoriented, sensory scarcity, saliva dribble from mouth and violent behaviour. Blood thick smear, stained by Fields stain, examination was done by local microbiologist Mrs. Bharti U Sable she suspects trypanosome along with plasmodium falciparum (figure 01). He was treated with antimalarial drug along with oral hematenics. She marked as the founder of Indian trypanosome, T. evansi. Later patient was transferred to the Government Medical College and Hospital (GMC) in Nagpur, India. Stained blood smear shows numerous flagellated trypanosomes parasite only, was confirmed morphologically, position of nucleus and small kinetoplast at central and posterior respectively indicate that the contributory mediator was T. evansi (Joshi, PP. et al., 2005). Another unique character of T. evansi has homogenous DNA minicircles (Borst et al., 1987 Songa et al., 1990 Masiga and Gibson, 1990 Lun et al., 1992) and absence of DNA maxicircles in the kinetoplast unlike T. brucei (Borst et al., 1987 Songa et al., 1990). Several methods has been evolvedmicroscopy, card agglutination test (C. Gutierrez et. al., 2000), microhematocrit centrifugation technique (Woo, PTK 1970), enzyme-linked immunosorbent assay (Indrakamhang, P et al.1996), DNA hybridization (Viseshakul, N., Panyim, S., 1990) and polymerase chain reaction (Wuyts, N.et.al. 1994 Wuyts, N.et al.1995 Omawa, S et al 1999) for detection of T. evansi infection. To confirm morphological identification of parasite, additional test of blood, serum and cerebrospinal fluid (CSF) was done in the Department of Microbiology, Government Medi cal College and Hospital, Nagpur and at the Institut de Recherche pour le Dveloppement in Montpellier, France.Parasitological and serological tests conducted at GMC, Nagpur, are as followed (Joshi, PP. et al., 2005)Biochemical quantitative analysis of serum was performed with less tiny significance on lipid levels, indication of Tangier disease. Tangier disease is a rare autosomal recessive genetic disorder, high density lipoprotein deficiencies associated with this disease include dramatically lowered level of APO A1 (Von Eckardstein, A., et al., 1998), was found to be non trypanolytic (Rifkin, M R. 1978a), however controversial data, fresh sera of a patient with Tangier disease is trypanolytic exhibiting bothTLF-1 and TLF-2 activity, reported (Tomlinson et al., 1995).The demonstration of specific antibodies has been employed by using card agglutination test for trypanosomiasis (CATT) for T. evansi using whole blood and serum was conducted. CATT test initially developed for T. bruc ei. gambiense (Diall et al., 1994). Sensitivity of CATT for T. evansi in Kenya was 65.5% (Z.K. Njiru et al.2004) and 68.6% (Ngaira et al.2003).False positive result of CATT was reported (Stijn Deborggraeve et al.2008).Mini-anion centrifugation technique is used for purification and concentration of trypanosomes using heparinised blood before and after treatment of suraminA direct latex IgM agglutination test was conducted with CSF to reveal functionless of parasite in the blood brain barrier.Sediment of CSF after centrifugation was examined by bright field microscopy for the presence of trypanosomes. Thomas chamber is used to count lymphocytes in the CSF, presence demonstrate the incursion of parasite.Molecular technique and serological tests conducted at the Institut de Recherche pour le Dveloppement in Montpellier, France, are as followed (Joshi, PP. et al., 2005).Three independent PCR assay were performed using DNA of trypanosomeRelated to the subgenus Trypanozoon using a semines ted PCR method, primer used ITS1/2 based on internal transcribed spacer (ITS) of ribosomal DNA.Related to T.brucei group using a single PCR of the 177- basepair.Amplification of T. evansi was conducted using a 994- basepair mitochondrial kinetoplast minicircle template with the primer TEV 1/2.Reference strains used are T. b.gambiense Bat 6118 and T. evansi CIRDES.PCR provided high specificity and sensitivity molecular biology technique among others for diagnosis of infectious diseases and also permits identification of micro organisms such as mycobacterium (Garcia-Quintanilla, A et al., 2002) , detection and differentiation of Entamoeba histolytica and Entamoeba dispar (Gonin, P et. al.,2003), simultaneous detection of tick-borne hemoprotozoan parasites Babesia caballi and Babesia equi in horse blood (Alhassan, A. et. al., 2005) and detection of influenza A Virus (Nicole L. Z et. al, 2006). In spite of these, PCR are not usual in some countries (Holland et al., 2001). It has been re ported about reproducibility problems, for diagnosis of both human and animal trypanosomes, of PCR results (Solano et al., 2002 Malele et al., 2003). Recently a new DNA amplification method, loop-mediated isothermal amplification developed for diagnosis of species and sub-species specific trypanosomes (Thekisoe OM et al., 2007).Disease developed due to absence of trypanolytic factor in normal human serum hence immune status of patient was checked to resolve possible infection with human immunodeficiency virus (HIV).Three tests were conducted to corroborate the results of Enzyme-linked immunosorbent assay (ELISA) in India.HIV 1/2 assaySpecific enzyme-linked immunosorbent assay (ELISA)NNO-LIA HIV 1/2 Score testInvestigation of parasiteUnusual transmission of animal trypanosomiasis, T. evansi to human requires rationalization, for this P. Truc and collaborator, 2007 studied genetic characterization of T. evansi. Generally, genetic variability of T. evansi has been detected by using iso enzyme (Gibson et al., 1983 Stevens et al., 1989), restriction fragment length polymorphism (RFLP) (Songa et al., 1990), microsatellite (Biteau et al., 2000) and random amplified polymorphic DNA (RAPD) analysis (Lun et al., 2004 Ventura et al., 2002) all these above technique found isolated T. evansi were genetically homogenous. Micro heterogeneity reported (Gibson et al., 1983 Stevens et al., 1989), may due to low-resolution techniques and no genetic exchange of T. evansi in vector like others T. brucei ssp, that leads to absence of recombination which play role for micro heterogeneity (Jenni et al.1986). Nevertheless, some genetic variability of isolated T. evansi from Kenya reported through PCR (Ngaira et al.2004, 2005 Njiru et al.2006) and amplified fragment length polymorphism (AFLP) along with RAPD. Among later, AFLP admittance more polymorphisms, was able to differentiate and separate the Type A T. evansi into two clades (Masiga et al., 2006). Direct comparison of high-resolu tion molecular techniques microsatellites or simple sequence repeats (SSR) and Inter-simple sequence repeats (ISSR) PCR revealed that latter technique demonstrate greater genetic variability of T evansi isolates from different geographical area (Z.K. Njiru et al 2007). Recently molecular analysis of T. b. brucei by PCR and microsatellite PCR of reported blood slides was successfully conducted (Stijn Deborggraeve et al.2008). Isolated T. evansi has been termed into type A and type B (Masiga and Gibson, 1990). Unlike to type B detected only from Kenya, isolates type A are most copious (Borst et al., 1987). It has been shown however, that most of T. evansi from South America are dyskinetoplastic- lacking both maxicircles and minicircles (Masiga and Gibson, 1990 Ventura et al., 2000 Schnaufer et al., 2002).Normally T. evansi diagnosed through variant surface glycoprotein (VSG) Rode Trypanozoon antigen type (RoTat) 1.2, a diagnostic antigen. Songa and Hamers, 1988 developed CATT for vet erinary use, which based on RoTat 1.2 gene (Songa and Hamers, 1988). Both PCR test and serological-CATT test are highly sensitive and specific in divergent geographical region (Verloo et al., 2000), former test can be trustworthy for detection of isolates of both dyskinetoplastic and DNA minicircles in kinetoplast of T. evansi (Claes et al., 2004) also it based on RoTat 1.2 gene (Urakawa et al., 2001). On the other hand, most of T. evansi from Kenya were not detected by test, which based on VSG of T. evansi RoTat 1.2 gene because few isolates lack both RoTat 1.2 gene and their linked protein-VSG while other isolates having only RoTat 1.2 gene (Ngaira et al. 2004). Characterization of non-RoTat 1.2 T. evansi, specific PCR test developed in these 273 base pair was present in disparity to RoTat 1.2 T. evansi (J.M. Ngaira et al., 2005).Microscopic examination of dissected organs of tsetse flies was done for identification of trypanosome infections (Lloyd and Johnson, 1924). Parasites ar e, generally indentified in the mouthparts, salivary glands and mid-guts. Trypanosome species from vector is isolated and employed in isoenzyme electrophoresis technique for identifications (Gashumba et al., 1986). Another approach as recombinant DNA probes have been used for the identification both mature and immature trypanosomes in tsetse fly (Gibson et al., 1988 Majiwa et al., 1993).Dot-ELISA is another technique used for detecting trypanosomes in tsetse flies (Bosompem et al., 1996 Ouma, J. O et al., 2000)How T. evansi differs from other TrypanozoonThe subgenus Trypanozoon includes three species, namely Trypanosoma brucei, T. evansi and T. equiperdum. T. evansi is judge against, concerning their morphological, mode of transmission, biochemical and molecular characteristics, rest of species. Bloodstream stages of these three parasites are often morphologically indistinguishable (Brun R et al., 1998 Gibson, 2003). T. evansi is mechanically transmitted of infected blood through in sects of the genera Tabanus, Stomoxys, Atylotus and Lyperosia. Horseflies (Tabanus spp), Stableflies (Stomoxys spp) are the most capable vectors for the transmission of T. evansi in Indonesia and China (Luckins, 1988 Lun et al., 1993). In Africa, south and Central America, tsetse fly (Glossina spp) and vampire bats Desmodus rotundus an extra host-vector-reservoir of the T. evansi, respectively can mechanically transmitted this parasite. Direct transmissions through milk or during coitus involved T. evansi (Wang, 1988). Besides mechanical and direct transmission of T. evansi, T. equiperdum transmitted directly during coitus and with rare possibility through bloodsucking insects (see ref. Brun, R et al.,1998). Trypanosoma brucei gambiense, sleeping sickness parasites have been able to spread through tsetse flies of palpalis group (Glossina palpalis, Glossina tachinoides) while T. b. rhodesiense was generally transmitted by tsetse of the morsitans group (Glossina morsitans, Glossina pa llidipes). All 31 species of tsetse flies are able to transmit trypanosomes (Aksoy S, et al., 2003). Other major parasites T. congolense, T. vivax and T. simiae that are pathogens of domesticated animals, transmitted by tsetse fly.Both parasites, T. evansi and T. equiperdum are closely related to T. brucei, most likely developed from Trypanosoma brucei by independently deletion of kinetoplast DNA and should be regarded as two subspecies Trypanosoma brucei evansi and Trypanosoma brucei equiperdum respectively (Lai et al., 2008). Absence of maxicircles in kinetoplast DNA explained inexistence of procyclic or insect stage in these parasites and can propagate only as the mammal-infective bloodstream form (Borst et al., 1987).This facilitate to explain wide range of mechanical transmission of T. evansi outside of Africa (Lun and Desser, 1995). Procyclic form (PCF) T.brucei strain cannot survival with a partial or complete loss of kinetoplast DNA as with some Blood stream form (BSF) strai ns. This kinetoplast DNA deficient T.brucei strains appear naturally or induced by drugs (Schnaufer A et al.2002). Drug inducers are acriflavine, ethidium bromide, methoxy-9-ellipticine, hydroxystilbamidine, berenil, pentamidine, antrycide, and para-rosaniline, grouped as DNA intercalators and non intercalating drugs (Hajduk, 1978).Nevertheless, the existence of T. equiperdum has been complexity Claes et al. suggested that, in fact, some strains of Trypanosoma equiperdum are actually Trypanosoma brucei and all other remaining misidentified strains such as Swiss Tropical Institute Basel (STIB) 818 are Trypanosoma evansi. However, based on PCR amplification of the fragment of DNA maxicircles in the kinetoplast, T. equiperdum Onderstepoort Veterinary Institute (OVI) and Bordeaux Trypanosoma antigen type (BoTat) 1.1 strains are T. brucei and other STIB 818, STIB 841 and STIB 842 T. equiperdum strains are not cluster together with T. evansi as it maintains maxicircles and allied genes. ( Li et al., 2006).Both parasites have homogeneous minicircles. Although in all T. evansi strains maxicircles are totally lost but T. equiperdum shows more assortment, some strains seems to bear complete maxicircles with no active essential gene others are missing one of the genes and a few devoid the entire maxicircles (Lai et al., 2008).Unlike other DNA, T. brucei mitochondrial DNA termed kinetoplast DNA include a network of interlocked DNA rings (Liu, B. et al. 2005). This network of T. brucei ssp. comprised of several thousands of heterogeneous minicircles and several dozen of homogeneous maxicircles (Borst and Hoeijmakers, 1979). T. evansi has largely homogenous and limited heterogeneous minicircles in kinetoplast DNA (Borst et al., 1987).Results (Joshi, PP. et al., 2005 P. Truc et al., 2007)A careful examination of morphological characteristic demonstrates the presence of T. evansi. Patient had normal level of APO A-1 indicate no sign of Tangier disease. The result of CATT for T . evansi was positive suspect stalwartly presence of RoTat 1.2 gene. Latex IgM test, a diagnostic for trypanosome invasion in CSF, and lymphocytes count in the CSF indicated no invasion of parasite. An attempt to isolate and propagate trypanosome in wistar rat was failed. For molecular diagnosis of T. evansi PCR conducted, test was positive. Results of ELISAs for HIV, conducted in France and India were negative.Genetic characterization, Indian patient has homogenous DNA minicircles in kinetoplast of T. evansi of type A and devoid of SRA gene.TreatmentTreatment was started 109 days after initial admission to hospital using suramin. Suramin is manufactured by Bayer and donated to WHO as Germanin, used against sleeping sickness in 1922 (Voogd et al., 1993). Suramin was used as a first stage of treatment for HAT caused by Trypanosoma brucei gambiense (chronic form) or T. b. rhodesiense (acute form). Efficacy of suramin against T. evansi infection was studied in cattle by Gill BS, Malhot ra MN, 1963. It was requested and provided by Department of Public Health, Government of Maharashtra State, India and World Health Organisation respectively. As patient falls under first stage of infection, drugs have to be used pentamidine or suramin sodium. Pentamidine has more adverse effect than suramin, according to author hence suramin was used in this patient. Drug suramin acts by interfering with enzyme of glycolytic pathway (Wierenga RK, et.al., 1987) in trypanosomes and produce hot spot, function as a signal for import into glycosome. It is preferred to give slow intravenous injection as suramin is poorly absorbed from intestine and causes intense local irritation when given intramuscularly (Voogd TE, et.al., 1993). Suramin does not cross the blood-brain barrier to kill trypanosome in the CSF however able to cure model of stage 2 diseases at a high dose greater than 80 mg per kg (Jennings FW, et.al., 1995).Follow-up study was commenced after the end of treatment and at 3rd and 6th months, all previous tests-CATT for T. evansi, latex IgM agglutination test, Mini anion-exchange centrifugation technique and examination of CSF by bright field microscopy are repeated at GMC Nagpur excepts biochemical analysis of serum for Tangier disease (P. P. Joshi et al. 2006). Tests result indicates first patient of human trypanosomiasis infected with T. evansi was recovered, Joshi and collaborators concluded that same schedule would follow in treatment if more cases observed.SuraminSuramin is less active against procyclic form of trypanosomes than bloodstream form, former normally reside in the tsetse flies (Scott AG, et.al., 1996). Suramin inhibit number of glycolytic enzyme which is essential to bloodstream form rather than procyclic form (Fairlamb AH, et.al., 1977, Fairlamb AH, et.al., 1980). Hanau and colleagues proposed other likely target of drug, competitive inhibitor of an enzyme 6-phosphogluconate dehydrogenase of pentose phosphate pathway (Hanau S, et.al., 1996). Suramin is an useful microfilaricide for Onchocerca spp. and Brugia pahangi worms (Hawking, et al., 1981 Howells, et al., 1983). It is a known ATP/UTP purine receptor (P2 receptor) antagonist (V. Ralevic and G. Burnstock, 1998). Nevertheless suramin inhibit ample varieties of enzymes like reverse transcriptase, dihydrofolate reductase, furamse, glycerol-3-phosphate dehydrogenase, hexokinase, L-a-glycerophosphate oxidase, receptor mediated uptake of low density lipoprotein, RNA polymerase and kinases, thymidine kinase, trypsin (Pepin and Milord, 1994 Wang, 1995). Besides its trypanocidal activity, suramin is also useful in hormone-refractory prostate cancer, however survival rate was not affected (Small et al., 2000 Ahles et al., 2004). Suramins antitumor activity has been attributed to its inhibition of various growth factors which include platelet-derived growth factor, fibroblast growth factor, transforming growth factors alpha and beta, insulin- like growth factors 1(Stei n CA,1993). Osteosarcoma is the malignant tumor of the bone suramin exerts an inhibitory effect on osteosarcoma cell growth of established cell lines (Benini et al., 1999), newly established osteosarcoma cell lines and stimulation of osteosarcoma cells by physiological compounds, such as 1, 25-dihydroxy-Vitamin D3 (K. Trieb, H. Blahovec, 2002). Furthermore, results in an inhibiting capacity of suramin on various cell functions include production of alkaline-phosphatase or telomerase activity (K. Trieb, H. Blahovec, 2002). Suramin blocked CD154 (Emilio Margolles-Clark et al., 2009) from interacting with its receptor CD40 (U. Schnbeck and P. Libby, 2001 I.S. Grewal and R.A. Flavell, 1998), costimulatory interactions are therapeutically important to modulate immune responses (C.P. Larsen et al., 2006 F. Vincenti and M. Luggen, 2007). Suramin inhibited the binding of TNF-a to its receptor TNF-R1 (F. Mancini et al., 1999) and its ability to inhibit CD40-CD154 interaction was 30 fold more active compared to it (Emilio Margolles-Clark et al., 2009). Suramin has also been shown to suppress T cell activity (C. Schiller et al., 1994), antiproliferative effects on lymphoid cells (Z. Spigelman et al., 1987). Suramin can causes toxicities which include adrenal and renal insufficiency, coagulation factor abnormalities and poly-neuropathy (T.E. Voogd et al., 1993 D.J. Cole et al., 1994), at relatively high concentration inhibited the binding of IL2 to its cell surface receptor (G.B. Mills et al.,1990), greater than therapeutic use (S.A. Grossman et al., 2001 S.T. Eichhorst et al., 2004). It concentration-dependently inhibited proteolytic and phospholipase A2 (PLA2) activities of Bothrops jararacussu venom- potential to be used as antivenom, suramin also antagonise the cardiotoxic effect of Bothrops jararacussu venom in rats heart (Daniel N. Sifuentes et al., 2008).Uptake of suramin by bloodstream form of trypanosome is through receptor mediated endocytosis which is most like ly route of entry (Fairlamb AH, et al., 1980). Suramin intensively bound to plasma proteins such as low density lipoproteins, albumins, globulins, fibrinogen, etc. According to Bastin et al. 1996, Coppens and Courtoy 2000 and Green et.al 2003 suggested that suramin might enter while bound to low density lipoprotein (LDL), it has high affinity to bind many serum proteins including LDL (Vansterkenburg ELM, et al., 1993). The high rate of fluid-phase endocytosis occurs in the trypanosomes of bloodstream form (Engstler, et al., 2004). This mechanism could be involved in the uptake of suramin into T. brucei that does not require specialized receptors. Trypanosomes cannot synthesise their own fatty acid and cholesterol de novo hence LDL uptake is essential for propagation (Coppens I, et al., 2000). It does not make any worse however in procyclic form, uptake of suramin is through receptor mediated endocytosis and not coupled with LDL uptake (Pal A, et al., 2002). Suramin involves inhibiti on of various glycolytic enzymes, effects rates of respiration as aerobic glycolysis is closely related with it in bloodstream forms (Fairlamb AH, et al., 1980, Opperdoes, F.R. et al., 1989). Diminished growth rate of trypanosome in vivo is a consequence of decrease in respiration (Fairlamb AH, et al., 1980).Suramin is also used as veterinary trypanocide report on resistance in T. evansi that infects animals is reported (El Rayah et al., 1999, Zhou, J.L. et al., 2004). Some cases have been described of drug resistance when suramin is used against Trypanosoma brucei rhodesiense in humans (Wery, M., 1994). Suramin reduced sensitivity towards T. b. rhodesiense (Bacchi et al., 1990) and failure of treatment up to 25-30% observed (Pepin and Milord, 1994, Burri, C et al., 2004). Failures of treatment are common due to misdiagnosed late stage infection (Burri et al., 2004). De Koning argued one of the reasons of suramin resistance is associated with reduction in drug uptake molecule is lar ge and highly charged which plasma membrane transporter takes up.Role of apolipoprotein L-1 and haptoglobin-related proteinT. evansi affects mainly domesticated animals such as camels, cattle and water buffalo, spread by mechanical transmission of infected blood through insect such as tabanid flies. Due to these, it spread apart from sub-Saharan Africa to South America, North America and Asia. Normally humans are resistant to animal trypanosomes, immunity against T.brucei brucei is due to trypanolytic activity of an apolipoprotein L-1 (APOL-1) bound to high density lipoprotein (HDL) (Vanhamme L. et al., 2003).Previously it was concluded that trypanolytic activity in normal human serum was due to immunoglobin M (Aaronovitch, S. Terry, R. J. 1972). Later in 1973, Hawking and colleagues resolute there were two trypanolyic factors. These two factors differ in their activity (in vivo and vitro), molecular mass, quantity in serum and sensitivity to antagonists (Hawking et al., 1973b). HD L was identified as trypanolyic factor by Rifkin in 1978, she also characterised the two trypanolyic factors determined by Hawking (Rifkin, M. R. 1978b). Trypanolyic factors in human serum shows inhomogeneous properties (Tomlinson et al., 1995 Raper et al., 1996b). Both TLF are a subset of HDLs commonly referred to as HDL3 (Lorenz et al., 1995), contain haptoglobin-related protein (Hpr) (Smith et al., 1995) and APOL-1 (Vanhamme, L. et al., 2003).TLF-1 is a 500 kDa lipid rich while TLF-2,1000 kDa protein complex containing IgM, lipid poor HDL particle (Raper, J. et al., 1999 Lugli, E.B. et al., 2004). Apolipoprotein A-1 (APOA-1) is a component of TLF-1(Smith et al., 1995) and, although previously reported that APOA-1 could not detected in TLF-2(Tomlinson, S. et al., 1995), is a component of TLF-2 (Raper, J. et al., 1999). Previously unknown proteins, human cathelicidin antimicrobial peptide (hCAP18), glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) and paraoxonase are associated with TLF-1(Smith AB et al., 1995 Lugil E et al., 2004). APOA-1 suggests a role in trypanolysis later controversial report supporting a lytic role (Gillett, M. Owen, J. 1992a) or not favor lytic role (Rifkin, 1991 Seed et al., 1993). Later it was confirmed that APOA-1 was not toxic (Tytler, 1995) but may indirectly play role of trypanolytic (Owen et al., 1996).For trypanosomes, HDLs contain 16,000-65,000 binding site per cell having moderate affinity (Gillett, M. Owen, J. 1992b). However, binding of lytic factor, TLF-1 appeared to involve two binding site, low affinity have 65,000 and high affinity 350 binding sites (Drain et al., 2001). Host macromolecules, interact with bloodstream trypanosomes, transferrin (Borst, P.1991) and low-density lipoprotein (LDL) (Coppens, I et al., 1987) through receptor-mediated endocytosis occur at the flagellar pocket of trypanosome (Gull, K., 2003).APOL-1 is a bacterial colicins and Bcl-2 family members like protein containing pore formi ng domain as well as a region for the membrane insertion of it (Prez -Morga D et al., 2005, Pays E et al., 2006). APOL-1 is taken up in the parasite by endocytosis, able to kill by the parasite by forming anion selective pores in the lysosomal membrane of parasite, this pore allows the influx of chloride ions into the lysosome, subsequent cell death as a consequence of entry of water and induces uncontrolled osmotic swelling of vacuole ((Prez-Morga D et al., 2005 Pays E et al., 2006 B. Vanhollebeke et al., 2007a). APOL-1 could not be involved in apoptosis but in programmed cell death (B. Vanhollebeke et al., 2006a).Resistance of T.brucei rhodesiense and T.brucei gambiense to APOL-1 is developed which allows these parasites to infect and cause HAT. Single protein termed serum resistance-associated protein (SRA) is main reason of resistance of T.brucei rhodesiense to APOL-1.SRAP interacts strongly with APOL-1 and provide specific resistance to T.brucei rhodesiense (Xong HV et al., 199 8 Gibson WC, 2005). T brucei gambiense is also resistant to APOL-1 mechanism is not understood (Pays E et al., 2006). Indian case with T. evansi infection, human serum devoid of APOL-1, reason for the absence was due to independent frameshift mutation in both APOL-1 alleles (B. Vanhollebeke et al., 2006b).Another HDL component, plays a toxic role for full trypanolytic activity of normal human serum, haptoglobin-related protein (Hpr).Indian case has normal concentration of Hpr bound HDL but short of trypanolytic activity. Hpr is a haemoglobin (Hb) binding protein induces, within acidic lysosome of T.b.brucei, Fenton like reaction between H202 and iron that lead to formation of free hydroxyl radicals, which would prompt the reaction of lipid peroxidation of lysosomal membrane (Smith AB et al., 1995 Hager KM et al., 1994 Bishop JR et al., 2001 Justin Widener et al., 2007). Nevertheless action of trypanolysis of Hpr and APOL-1, biological function is not clear. Optimal trypanolytic acti vity requires presence of both APOL-1 and Hpr on same subset of HDL particle (B. Vanhollebeke et al., 2007b).Vanhollebeke et al. (2007b) reported trypanosome survival assay in normal as well as mutant human sera. Survival of trypanosomes occurs in human serum devoid of APOL-1 and fetal calf serum (FCS). FCS is nonlytic and contains neither APOL-1 nor Hpr. Human serum deficient of Hpr and haptoglobin (Hp) but with normal HDL b

Overview of Pediatrics Malignancies

Overview of Pediatrics MalignanciesMuhammad Tahir SaleemI am rotated in the paediatric hematology and oncology ward for clinical practicum as go bad of the Masters of Nursing (MSc.N) program. hematology is the branch of medicine that deals with the diseases and link up to blood and its functional pervertedities including anemia, polycythemia and hemophilia and every bleeding disorders (Brunner and Suddarths, 2010). Oncology is the branch of medicine that deals with the diagnosis and discussion of the pubic louse in the body (Brunner and Suddarths, 2010). Since serviceman body is composed of cadres so the pubic louse kickof expandes from abnorm on the wholey occurring cells in the body (Porth Matfin, 2009). T present ar many definition of the give-and-take sterncer in medicine, only whatever the way of defining genus Cancer is adopted, the definition should incorporate two properties uncontrollable appendage of cells originating from normal winds, and plaza of kil ling of host by means of using components of border weaves or by spreading to other(a) organs (metastases) to other organ and constitutions of the human body (Itano Taoka, 2005). nigh experts dress crabmeat as the autonomous sourth of the body cells that is unresponsive to the physiological issue-control mechanism of the body which is responsible for self-colored emergence of all body organs normally. Other hand define cancer as a condition in which normally increase cells lose their structure, look and functioning (shoib book). The cells as well as lose their self-destructive office (apoptosis) to die after certain period of time as they do normally (e.g. red blood cells die after 120 days) and the cells die hard to live longer and at times become immortal and discommode the functions of other normal cells.There ar certain terminologies that be frequently referred to the set of events occurred during the pathogenesis of cancer. These terminologies atomic num ber 18 dysplasia, metaplasia and anaplasia. Dysplasia is a disruption in the size of it, appearance, and arrangement of cells and winds (Porth Matfin, 2009). Dysplasia is abnormal wander ascendment but non yet malignant. Dysp finishic changes frequently occur in the mucosal lining of the mouth, nose, intestine and cervix where the cells keep an eye on on going under cellular multiplication, differentiation, organization and replacement of stark naked-made cells (Porth Matfin, 2009). The epithelial lining of elementary canal (mouth to anus) completely changes in triad days. So it is the frequent site of villoma formation as a result of dysplastic changes. The epithelial lining of the mouth of cervix also changes as a result of dysplastic changes ascribable to human papillary tumour virus (Porth Matfin, 2009). Dysplasia is also present in chronic inflammatory and proliferative lesions, and it is recognised as part of a developmental phase of many cancers. Metaplasia is the exchange of one cell sign with another cell type, for physical exertion in smokers ciliated columnar bronchial epithelium is replaced by non-ciliated squamous epithelium due to the constant exposure of smoke to the bronchus (Porth Matfin, 2009). Metaplasia is also considered as the developmental phase in many neoplasms. Anaplasia is the structural change and cellular appearance and inability to perform the normal functions of a cell. This stage of cellular changes is cognise as cancerous (Porth Matfin, 2009). Anaplastic cells resemble the undifferentiated unenlightened cells that have not developed specialized structure and functioning typical of their meander of origin. In other words, the newly formed tissue from muscle cell or nerve cell, for example ,remain in the premature state as a result of anaplastic changes and do not perform its skipper functions. The degree of anaplasia whitethorn differ from one type of cancer cells to other type of cancers from poorly dif ferentiated to undifferentiated cells sometimes the neoplasm cells atomic number 18 so undifferentiated that it is not possible to decide the tissue from which the cancer cells are originated (Porth Matfin, 2009).Here, the terms hyperplasia and hypertrophy are worth mentioning. Hyperplasia and hypertrophy are normal physiological responses. Hyperplasia is defined as an increase in the cellular count in a tissue or organ cause an increase in the size of that organ, whereas hypertrophy is the increase in the size of cells not the number (Porth Matfin, 2009). Neither hypertrophy, nor the hyperplasia is the synonym of tumour growth. Hyperplasia is induced by know stimuli and it is a controlled process and it stops as the stimuli is removed. One example of stimuli induced hyperplasia is the increase in the size and number of cells of womb in pregnancy under the influence estrogen for accommodation of developing embryo. The uterus comes to normal state after the stimuli of estrog en is gone after delivery. In addition, hyperplasia may also serve a useful role in the body, for example breast tissue undergoes hyperplastic changes after pregnancy for production of take out or re-forming the liver with structurally typical hepatocytes after partial hepatectomy. affected cancerous development follows none of these usual physiological rules or purposes (Porth Matfin, 2009). However, cancerous cells may eventually employ the hyperplasia in its pathogenesis pathways. Because, hyperplasia and dysplasia often fall into the development of many tumors by months or days, timely identification and proper treatment at this early stage in the pathological process may help to prevent malignancies (Porth Matfin, 2009). For example, the Papanicolaou Smear (or pap smear) allows pathologists to distinguish between normal, dysplastic or cancerous cells. The pap-smear is a technique that allows early detection of the cervical cancer and it has enormously reduced the morbidity and mortality of cervical cancer.Pathologically, tumors can be classified into gracious and malignant. The word benign means kind, slake or caring and suggests that such tumor are harmless. These tumors are somely encapsulated by well defined fibrous cover that separates the mass from skirt tissues. A benign tumor, neither invade surrounding tissue nor metastasizes. These tumor exhibit lesser degree of anaplasia and grow slowly. Recurrence is very obsolescent after surgical removal in benign tumors. The benign tumors are named by adding suffix -oma in the name of tissue they are originating in. For example, Lipoma, Adenoma, fibroma and papilloma are some of the example of adding suffix oma in the type of origin of tumor (Itano Taoka, 2005). Whereas, malignant tumors usually infiltrate or invade surrounding tissues, these tumors are not encapsulated, genetically instable and with greater degree of anaplasia from the tissue of origin. They grow autonomously with no control of b ody homogenous development. The following table compares the properties of benign and malignant tumors (Itano Taoka, 2005).Difference Between Benign and Malignant Tumor qualityBenign TumorMalignant TumorStructure and differentiation exemplary of tissue of originAtypical of tissue originRate of growthUsually slowMay be slow, rapid, very rapidprogressSlowly progressive (may remain stationary may regress) rarely fateful if treatedUsually progressive, almost always fatal if untreated modality of growthExpansion with capsuleLocal infiltration and/or metastasis to outback(a) sitesTissue destructionNoneCommon, ulceration and necrosisRecurrence obsolescentCommonPrognosis bleak only if surgically inaccessibleFatal if uncontrolled (untreated)Core Curriculum of Oncology Nursing. St. Louis, Messori Elsevier 2005 Cancer can also be characterized in two types on the basis of structure, inviolable tumor and cancer of the blood. Cancer of the blood and lymphatic systems are mostly leukemia and l ymphomas, where as solid tumors are originating in the organ like central nervous system, kidneys, eyes, hit the books and in soft tissues. Childhood malignancies mostly originate in blood, study ticker and in lymphatic systems. Cancer of genitourinary system, respiratory system, and caner of digestive system are rare in children as the statistics furnished by the cancer research organization UK, 2012 (www.cancerresearch.org).The incidence chart of the childhood cancers is as followsThe incidence chart of the childhood cancersCancer TypeIncidenceLeukemia34%CNS tumors23%Lymphoma11%Neuroblastoma6%Renal tumor (e.g. Wilms tumor)6%Soft tissue sarcomas6%Bone tumors5%Retinoblastoma3%Epithelial neoplasms3%Germ cell tumors2%Liver Tumors1%Oxford handbook of Pediatric hematology and oncology, 2010.A brief description of pediatric cancers is given below.LeukemiaLeukemia is the cancer that affects the cell lining of white blood cells. albumen blood cells are of tow type granulocytes (Lymphoi d cell) and agranulocytes (Myeloid cell). Lymphoid cells are advertise poor boydivided in B-cell Lymphocytes and T-Cell Lymphocytes, whereas, myeloid cells are of triad types, Neutrophils, Basophils and Eosinophil (Porth Matfin, 2009).Leukemia is further sub divided into acute and chronic acute leukemia are termed when the anaplastic changes occurred in the pre matured leukocytes that has just transformed from the stem cells in the bone marrow, whereas, chromic leukemias are termed when the anaplastic changes occur in more(prenominal) matured stage or adult leukocytes. The four types of leukemias are as followsAcute Lymphocytic Leukemia chronic Lymphocytic LeukemiaAcute Myeloid LeukemiaChronic Myeloid LeukemiaAcute Lymphoblastic Leukemia accounts for 80-90% among all types of leukemia in childhood. AML accounts for 15% and CML 5% (Itano Taoka, 2005).Acute Lymphoblastic Leukemia ( exclusively) is further subdivided incidence heady according to cell linage tortuous as elaborat ed by Moore and Hurvitz (2008).Pre B-cell 70%T-Cell 15-25%B-Cell 15%Treatment of acute leukemia involves induction for complete remission, followed by intensification and maintenance therapy. Prophylaxis to the CNS is done by Intra-thecal (IT) chemo administration. Standard treatment for all(prenominal) leads to long term remission in more than 85% of cases. abstraction therapy employs Vincristine, Prednisone, and L-Asparagenase +/- Danurubicin (depending upon risk satisfaction)Intensification all induction medicine with the inclusion of CNS prophylaxis nutriment therapy includes oral Mercaptopurin (6MP) with methotrexate (MTX) weekly for two to three years numerous patients in the chemo-pediatrics receive monthly intra-thecal (IT) pulses of Vincristine with prednisolone/dexa as part of maintenance.One or two cycles of a re-induction regimen were often added but not in contemporary practice (Moore Hurvitz, 2008).Good prophecy factors for ALL WBCBad Prognostic factors for ALL WBC50 ,000/uL, age10years,Other poor prognostic factors are massive organomegaly, CNS involvement at diagnosis, medaistinal mass and distress to achieve remission by day 14 to 28 of induction, with comportment of Philadelphia chromosome.Acute Myeloid Leukemia (AML)AML requires intensive chemotherapy followed by hemotopotic stem cell transplantation (HSCT) hematopoietic stem cell transplantation if a suitable matched related donor is available. Five years options for these patients are more than 85% with life-threateningish prognosis (Bailey Skinner, 2010).LymphomasHodgkin and Non Hodgkin Lymphomas Lymphomas are the tumor of lymphocytes (B T cells) that originate in the lymph tissue that is fixed to organs and lymph nodes not in peripheral circulation. As in the case of leukemias, lymphomas also involved both B-cell and T-cell lymphocytes but they are hold to the lymph nodes or other lymphatic organs not the peripheral blood. They typically presents with a solid mass in a lymph no de, spleen, bone marrow and in any organ. Other than lymph tissue, they may present in tonsils, skin, brain, intestine and bone. Lymphomas are closely related to lymphoid leukemias that involves the circulating lymphatic cells. Lymphomas are better controlled by treating with chemotherapy. Five years survivals for these pediatric lymphoma patients are more than 90% with good prognosis (Itano Taoka, 2005).Brain tumorsThese are of four types, depending upon the type of cells from where the tumor is initiating. Gliomas, Appendimomas, Meduloblastomas, and Schewanomas are some of the types of central nervous system tumors (CNS). Some CNS tumors are associated with high mortality and respond poorly chemo. Cranio-spinal shaft is often employed as part of the treatment regimen for aged kids but radiation is deferred in children age less than 3 years due to the chance of fibrosis of growing skull bones and vertebral bones unless radiation is avoided in most of the younger children (Baile y Skinner, 2010).Tumor of the renal systemWilms tumor is tumor of renal system. Histological name of the cancer is embryoma of the kidney. It needs radiation and chemo both for the eradication of disease. Size of the tumor is reduced by using chemo and radiation. After the shrinkage of renal tumor, surgery proved to be beneficial. Three years survival is 75% in patients of nephroblastoma (Bailey Skinner, 2010).Soft tissue tumorsSoft tissue tumors originate from connective tissue of cartilage and bone forming fibrous tissue, smooth muscles, blood vessels, lymphatic vessels, fat tissue, synovial tissue, and peripheral nerves. The most common type of soft tissue tumor in childhood is rhebdomysarcoma.Rhabdomyosarcoma It originates form the striated muscle tissue. It most commonly originates in head and neck area. Only 15% presents outdoors of the head and neck region. It is treated with chemo and radiation therapy. The prognosis of this cancer is good if treatment is started at ea rly stage (Bailey Skinner, 2010).RetinoblastomaRetina is nervous tissue. Retina is only nervous tissue that is visible through the naked eye. The tumor that arises from it also uninstructed neuronal ectodermic stem cells that were remain undifferentiated in fetal life and present like tumor in the very prototypal years of life. Most patient get die due to computer address of these neuronal tumors to CNS through optic nerve. In localized tumor survival is 100% but in metastatic tumor the survival ratio decrease. As described by Bailey and Skinner, (2010) many chemotherapeutic agents are used in treatment of retinoblastoma e.g. Vincristine, Actinomycin D, cyclopahsmamide, and doxorubicin.Germ Cell TumorsThis tumor arises from primitive stem cells of the fetal life that remained immature during fetal development and were not able to fully develop (differentiate) to mature cells of the organs. Human embryo develops from the three layers of the germ cells. These layers are ectoderm (outermost), mesoderm (middle layer) and endoderm (innermost). Ectoderm develops into skin, stew glands and nervous system, mesoderm develop into bones flesh, blood vessels and lymphoid tissue whereas, endoderm develop into genitourinary, gastrointestinal and respiratory system. Germ cell tumor arises from the immature stem cells that were left undifferentiated in the fetal life. This tumor has good prognosis in early diagnosis (Langhorne, Fulton Otto, 2007).The rotation in pediatric oncology ward is challenging as well as exciting. The nurses here have to be extra conscious intimately all sustenance related issues. Building rapport with the children is dominant to the effective nursing upkeep of them. Childhood cancers are rare but children diagnosed with cancer may develop subtle anti social behavior during the long term therapy of the disease. This makes nurses to be equipped with extra psychosocial adaptation with children. As chemotherapy is widely used as the treatment m odality besides surgery and radiation therapy, hence, pediatric state is vulnerable more than the adult in developing disease/treatment related debilitating symptoms like febrile neutropenia and tumor lysis syndrome . Parents education is paramount in adhering to the treatment regimen and prevention of nutropenia. Many patients came in pediatric oncology ward for port-a-cath needle insertion and dressing of PICC line. Nurses are meticulously involved in caring about the patients. Helping the physician in safely administration of intrathecal medication (IT) is also the job of nurses. The rotation bringing new horizons of learning and I am learning a lot about pediatric cancer care a lot.ReferenceMoore, T.B. Hurvitz, C.G.H. (2008). In Cassiato,D.A. Territo, M.C. (2008). manual of clinical oncology. 6th Ede. Philadelphia LWW. Ch 18. Pp 397-408.Childhood cancer incidenceRetrieved from http//www.cancerresearchuk.org/cancer-info/cancerstats/childhoodcancer/Site last updated 14/11/2012. Bailey.S, Skinner, R.(2010).Oxford specialist handbook of pediatric hematology and oncology. Oxford university press.Porth, C.M, Matfin, G., (2009). Pathophysiology fantasy of altered health. Ed 8th. Philadelphia LWW. Ch 5. Pp. 95-98.Langhorne, M.E, Fulton, J.S, Otto, S.E., (2007). Oncology Nursing. Ed 5th. St Louis, Messori Mosbay. Ch3. P3.Itano, J. K, Taoka, K. N. (2005). Core Curriculum of Oncology Nursing. St. Louis, Messori Elsevier. Ch 20. Pp 443.

Three Phase Induction Motors Engineering Essay

Three Phase instauration Motors design EssayThree build installing moves atomic number 18 one of the well-nigh astray employ industrial machines. This is mainly due to their simplicity, in high spirits reliability and robustness. Although three shape facility gos thrust the same physical stator coil as a synchronous machine, they do have different rotor coil coil constructions. In addition, three var. consequence forces argon sh ard into ii groups squirrel-cage and wound rotor. The magnitude of the desegregate in the quadrature axis vertebra in the stator diminishes, so that the fuse pass on be zero, but the zipper is increase above the synchronous despatch. The rotor authentic comes from rotor emf, so the final result backward rotating for the mix in parcel permits the magnetomotive force (mmf) so the feed is domineering in the quadrature axis. So, the zip up at which the magnetic field rotates cease be determined. If the repulse is conne cted to rated frequency, the rush of the magnetic field is called the synchronous speed (Ns).The foldepressioning table shows the relationship amongst image of poles and synchronous speed when the frequency equals 50HZ.Pole p personal credit lines12346Number of poles246812 coexisting speed300015001000750500Table (3.1) relationship in the midst of number of poles and synchronousThe relationship between number of poles and synchronous speed is in return proportional.3.2 Equivalent dress circle of an elicitation motor.The per phase very(a) circuit is real important for inductive reasoning motors and can be utilize to provide a great deal of understanding and prediction of per physiqueance of the induction motor in a stable state. The induction motor take ons to provide for operation on the induction potential and up-to-the-minute in the rotor circuit from the stator circuit (transformer action) this is beca utilise the potency and present-day(prenominal) in the rotor ci rcuit of an induction motor is radicalally a transformer operation. So the equivalent circuit of the induction motor is similar to the equivalent circuit of the transformer. (In the transformer, uncreated equivalent the stator in the induction motor, secondary in the transformer want the rotor in the induction motor.In an equivalent circuit per phase of an induction motor, as shown in figure (3.1), Rs and Rr are the stator and rotor winding resistance per phase. Ls and Lr are stator and rotor leakage generalization per phase. However, the aim of test and analysis is to be able to refer the rotor resistance and reactance to the stator circuit and in that respectby to necessitate an equivalent circuit referred to the stator. frame of reference (3.1) induction motor per-phase equivalent circuits.(3.1)(3.2)(3.3)(3.4)(3.5)(3.6)(3.7)(3.8)(3.9)(3.10)(3.11)(3.12)(3.13)In this circuit between a and b apply TheveninFigure (3.3) Simplification of equivalent circuits of an induction moto rOpen Circuit voltage at ab(3.14) short(p) Circuit generate(3.15)(3.16)(3.17)(3.18)Maximum occurs(3.19)(3.20).3.3 Overview on give of consequence motors.Induction motors with squirrel-cage motors are used in industry because the advantage of these fibers of motors is their relatively wretched cost and simple construction. Induction motors always work at a nearly constant speed. However, king electronic converts it can work to go away the speed of an induction motor. The induction motor finds can be divided into groups based on their applications (a) Adjustable-speed drive. integrity important application of this drive is in process chequer by arrestling the speed of fans, compressors, pumps. (b) Servo drive by means of sophisticated enclose, induction motors can be used as servo drives in computer peripherals, machine tools, and robotics acknowledgement.I would equivalent to give a brief explanation of two regularitys that are used in the avow of induction motors an d I entrust go into more(prenominal) than detail about these method actings later. sender keep back is a method of rule of induction motors so the stator current is throwled in the field rotating part apply PWM inverter Reference. The rotor intermingle and stator desegregate linkages are equal by ar (t) and as(t) depends on the angle of the rotor m because the joint induction between the stator windings and rotor windings position is connected. However, the main creator for the q and d axis analysis in machines like the induction machines is to manoeuvre them properly, for example transmitter maneuver reference, the method of sender get wind of induction motor drives produces better dynamic achievement than scalar throw reference. The side by side(p) block diagram shows the direct torque cut back system of rules of an induction motor.Figure (3.4) shows direct torque program line of induction motors.This alternative type of visit of an induction motor i s very simple and basic in terms of construction. It consists of a switch table, hysteresis ascendances, flux estimator and torque. It is much easier to agree in a block diagram compared to the block diagram representing the sender conquer system due to the absence of coordinate transformation between the synchronous raise and stationary frame and alike it does non need a pulse width. Direct torque see drives are experienceled by the method of a close loop-the-loop system without using a current regulation loop and are also cogitate to use of a stationary d-q reference frame as well as having the d-axis aligned with the stator q axis. Moreover, the flux and torque are controlled by the stator voltage lacuna vector defined in this reference framereference. scalar control is another method of control of induction motors and is also the graduation method of control before the vector control method. The advantage of this method is simple control and ease of use. The motor drive is described by three performers (a) frequency (b) voltage (c) parameters of the motor and its power supply reference. The scalar variable is strictly one represented by magnitude alone. This method uses either close loop or blossom forth loop control and any feedback loop such as that for speed. This use of scalar quantities gives the basic characteristics of satisfactory steady state behaviour, but miserablely controlled transient response.3.4 rendering of the Induction motor driveSince a motor drive plays a big part in the control system, it is necessary to have round background information about it. In a typical induction motor drive, power electronic devices are used to operate AC motors at frequencies other than the supply one. It consists of two main sections, a controller to set the operating frequency and a three-phase inverter to generate the postulate sinusoidal three-phase system from a DC bus voltage.Therefore, an induction motor requires a variable-frequen cy three-phase source for variable speed operation by using a power converter system consisting of a rectifier connected to an inverter through a DC link. The next figure shows a block diagram of the power circuit of a typical variable-frequency induction motor drive.Figure (3.5) shows Variable-Frequency Induction Motor DriveThe rectifier converts the power grid AC voltage into a opinionated DC voltage. An LC filter to provide a smooth DC voltage, which is then applied to the inverter input, filters out the harmonics.3.5 Induction Motor dominance Methods3.5.1 Vector controlThe vector control of induction motors has been wide used for high performance drives. There have been many studies developed and presented which allow an overview of vector control (reference). Many proposals for the theory of electric machines discuss using space vector control to represent sinusoidal distribution in the air violate and they also discuss types of control of ac drives including induction motor drives, permanent-magnet ac drives and switched reluctance drives (reference).Induction motor drives have performance control as the same high performance four-quadrant DC drive. In 1960 field-oriented control (FOC) was used in the area of induction motors, but in the bygone decades, induction motors have been controlled by using scalar control methods like the voltage/hertz. However, this manner is an old way used before vector control in the area of induction machines, but it was an easy method of controlling an induction motor (Reference).3.5.1.2 Concept of vector controlThe purpose of vector control of AC drives is related to a space phaser which provides a means of representing three phase variables in a machine, voltage, current and flux (Reference). Both flux and torque (DTC) are basically controlled by methods of unkindly loop so are methods of control of an induction motor, using disagreeable loop without current loop, similar to the formulaic vector control drives (R eference). So the stator current will be utilizing transformation to the d q synchronise system and direct axis with the rotor flux space factor therefore, the stator d q axis current is controlled dependently and the d q-axis for rotor flux will be zero.(3.21)The relationship between the stator current, rotor flux and electromagnetic are shown by this equation(3.22)WhereIs rotor flux linkage, Rr , Lr , Lr are rotor resistance, and Lm magnetizing inductance. (Reference).However, the space vector in the three phase inverter will produce eight output states 1 0 0 switch states, top(prenominal) in switch phase is represented by and b- is closed and c are open. The eight space vector represented by V0 0 0 0 and V7 1 1 1 are null and chronic six are of equal magnitude and arranged 600 part in space diagram as shown in figure. (Reference).Figure (3.6) shows witching voltage space vectors.3.5.1.3 Control CharacteristicsVector control has allowed the dynamic performance of AC drives so that they better DC drives the flux and the torque can be controlled reveally by using vector control producing components of the supply current. The depot voltage cannot be directly monitored, but can be using the dc link voltage and switching function of the inverter supplying the motor. Currently, the drive dynamic is largely used with the inverter control of the stator current of the induction machines this in turn is determined by the supply voltage and inductance of the machine. The main features of the direct torque control (DTC) are direct control of the torque and flux, and confirmatory main control of voltages and currents. This type of control has a number of advantages sinusoidal stator current and reduced torque oscillations handsome torque dynamics and the main advantage of (DTC) direct torque control, absence of coordinate transformations which related to vector control implementations. However, in this type of control there are some disadvantages possible prob lems during starting and low speed operation and also during change in torque command it also requires flux and torque estimators (Reference).The vector control theory provides independent control between torque and flux torque is controlled by the q-axis component of current if the flux is constant and oriented along the d-axis of the referred frame. The referred frame can be rotor flux-oriented control, stator flux-oriented control or air gap flux-oriented control. Thus, the phase angle and the modulus of the current or current vector have to be controlled. Figure 2.1(a), Reference, shows the rotor angle r with respect to the stator. Since the vector control is to be implemented in the rotor flux oriented reference frame, the induction machine is fixed in that reference frame by rotating the variable as appropriate. Figure (3.7) shows that the rotor flux reference frame rotates at speed (angle e) with respect to the stator reference and the d-q axes are fixed to the rotor flux spa ce phasor. This results in decoupling of the flux and torque which are separately controlled by stator direct-axis current ids and quadrature-axis current iqs. Reference(B) Vector rotation Figure (3.7) (A) Rotor angle3.5.2 Direct and Indirect Rotor Flux-Oriented ControlThe vector controls can be divided into two groups, substantiative and direct, for the confirmatory (slip frequency controlled) and the direct (field oriented). The characteristics of these two controllers have been considered to be the same, but there are some differences between these methods. However, the direct control type is a modern control theory and also has high performance and it is more well-known than indirect control (Reference).In this two methods above are considered of voltage and current of a stator. The first method, indirect, is related to stator current control and the second method is related to stator voltage control. In both cases the system inputs are torque and flux reference which is requ ired current values for isd and isq. Field oriented control to induction motor operation in a synchronously rotating d-q reference from that is aligned with one of the motor flux. So, control of the torque and flux is decoupled such as the d- axis component of the stator current and rotor flux magnitude and the q-axis component control , the output torque , where the ids stator current of d-axis component and is the rotor flux magnitude demand, so can be given in equation as(3.23)Where, Lm = magnetizing inductance.For the q-axis component of the stator current iqs, the torque demand as(T* em) so can be determined as the equation(3.24)The d-axis of the synchronously rotating reference frame to be aligned with the rotor flux, the slip relation.(3.25)Direct rotor flux-oriented control (RFOC) has a control loop for flux where the measuring stick is performed using flux sensing coils (or Hall-effect devices) or by the flux model. In indirect rotor flux-oriented control (RFOC), the roto r flux angle is not measured but is estimated from the equivalent circuit model. One of the techniques for estimating the rotor flux angle (e) is based on the slip relation, which requires measurement of the rotor speed () and slip frequency (). The slip frequency is hooklike on rotor time constant (r) and estimated rotor flux amplitude. This indicates that indirect methods are easier to implement since they do not require a flux model, but are less accurate. Nevertheless, if the model were perfect, the performance obtained would be identical to direct torque control. In 6, the relationships between direct and indirect approaches have been analyzed. It proves that they have the same control but have differences in coordinate of state variable, the rotor flux and stator currents. A new indirect vector control with an observer has been presented which has the same characteristic as the conventional direct torque control.Figure (3.8) direct vector controlFigure (3.9) indirect vector c ontrol3.5.3 scalar control methodScalar Control manner is related to AC machines and can use voltage fed-inverters. In addition, the scalar control is related to control of the magnitude of a variable only, also using of applications for constant voltage/hertz supply at the motor terminals are given constant air gap flux, so it could be that the stator voltage is dropped. (Reference) The scalar control methods are considered just for study state behaviour, but have poorly controlled transients. (Reference)This method applies to use in either close loop or open loop, and in any feedback loop such as that of speed. The scalar control method was basically developed for study state operation. However, it is a method also used in variable speed applications. (Reference)In this curve, the voltage and frequency are applied on the stator, therefore, when the supply frequency is constant, the speed will be constant, but the torque can be ever-changing as the square of the applied voltage. I will give more details about scalar control in another chapter.3.5.4 comparability of vector control (VC) and scalar control (SC).Induction machines are widely used in various industries as prime workhorses to produce rotational motions and forces. However, the squirrel-cage type is a simple and rugged electrical machine with low cost and minimal maintenance this is reason that the squirrel-cage types are most widely used in industrial electrical motors reference. With regard to the scalar control methods for an induction machine, only the motor model is considered for steady state and the scalar control methods are controlled based of the induction motor, but this method will not give good performance transients for an induction motor and it is also poor in terms of dynamics but the vector control methods considered above are valid for transient conditions and the vector control will give a dynamic performance far superior to that of scalar control reference. The scalar control met hod to control an induction motor is simple to execute and easy to programme, but the vector control is related to the varying magnitude and phase alignment of the vector quantities of the motor. Moreover, the scalar control is related to the voltage per hearts v/f control and is normally used for low cost drives where high dynamic performance is not a key requirement. The applications include fans, blowers and pumps where the applied load is known. In this method, the form is simple, the control does not require any sensors and the control algorithm can be implemented in a relatively low performance microprocessor. Vector control is related to a mathematical model which deals with voltage, current, flux torque and the motor parameters. We can control the instantaneous stator currents, control the magnitude and position is.The following diagram shows a feedback control system for measuring currents.When the controller has a fast response then is vector can be imposed on the stator r apidly.Advantages and disadvantages of vector control and scalar control referenceMethodAdvantagesDisadvantagesSCSimplest method of obtaining variable speed. kickoff cost and easy to implement solution.Is widely used.Is not as entangled as other control methods.Poor transient performance and poor dynamic.It cannot control torque directly.The transit response such as control is not fast.VCFor those d component and q component are two decouple components can be independently controlled by passing through separate PI controller.This control method has an fantabulous torque and speed curve.It has excellent dynamic performance.Sensitive parameter variation use PI current regulators that decrease transient performance.Is more complicated than any other control method.Cannot control torque before transformation is done.Table (3.2) advantages and disadvantages of scalar control and vector control