Discoveries And Inventions In Fundamental Sciences History Essay

Discoveries And Inventions In Fundamental Sciences History Essay There is a general concept that the sciences are exclusively the products of Western minds. Review of any standard book or encyclopedias regarding the history of science makes evident that the only contributors are Europeans and/or Americans. The most oft-mentioned names are Kepler, Galileo, Copernicus, Bacon, Da Vinci, Franklin, Newton, Benjamin etc. Thus it is made unavoidable to conclude the major contributions to the development of the modern sciences by other cultures are minimal. The advancements made by ancient Chinese, Indian or particularly, Muslim scholars are hardly mentioned in most standard books and literature. Although Western civilization has made many invaluable contributions to the development of the sciences however, so have numerous other cultures. Unfortunately, Westerners have long been credited with discoveries that were made by muslims scientists many centuries before. Thus, many of the basic sciences were invented by non-Europeans. For instance, George Sarton states that modern Western medicine did not originate from Europe and that it actually arose from the (Islamic) orient. inShare91 515 points on reddit Major Inventions of Muslim Scientists: A number of inventions and discoveries were made by the Muslim scientists throughout the history. Muslim geographers and navigators learned the use of magnetic needle, from the Chinese, and were the first to use magnetic needles in navigation. Muslims invented the compass and its use in navigation, which was later on passed to the West. European navigators relied on Muslim pilots and their instruments while exploring the unknown territories. Gustav Le Bon claims that the magnetic needle and compass were the inventions of Muslims. The Chinese, probably learned of it from Muslim traders. It is noteworthy that after the interaction with the Muslims during the 8th century the Chinese improved their navigational expertise. Ibn Firnas a Muslim scientist of Islamic Spain invented, constructed and tested a flying machine in the 800s A.D. Roger Bacon learned of flying machines from Arabic references to Ibn Firnas machine. According to Will Durant, Ibn Firnas of Islamic Spain, invented a watch-like device in 9th century, which kept accurate time. The Muslims also constructed a variety of highly accurate astronomical clocks for use in their observatories. As early as the 9th century A.D Muslim mathematicians, the inventors of algebra, introduced the concept of using letters for unknown variables in equations. They solved a variety of complex equations through this system, including quadratic and cubic equations. They used symbols to develop and perfect the binomial theorem. Thabit bin Qurrah was among the first Mathematicians of the Islamic Empire who accomplished this precisely this as early as the 9th century A.D, and he was followed by Abul Wafa, whose 10th century book utilized algebra to advance geometry into an exact and simplified science. In the 9th century Muslim astronomers made numerous improvements upon Ptolemys findings. They were the first astronomers to dispute his archaic ideas. They produced hundreds of highly accurate astronomical tables and star charts. Many of their calculations are so precise that they are regarded as contemporary. Copies of works on astronomy the Alphonsine Tables was transmitted to Europe via Islamic Spain, i.e. the Toledo Tables. In their critic of the Greeks, Muslims synthesized proof that the sun is the center of the solar system and that the orbits of other planets and the earth might be elliptical. During the 9th century the Muslim physician originated the science of pharmacology and was developed into a highly refined and exact science. Muslim chemists, pharmacists and physicians produced thousands of drugs and/or crude herbal extracts one thousand years prior to the supposed birth of pharmacology. During the 9th century, eyeglasses were invented by Ibn Firnas of Islamic Spain and they were manufactured and sold throughout Spain for over two centuries. Any mention of eyeglasses by Roger Bacon was simply a regurgitation of the work of al-Haytham (d. 1039), whose research Bacon frequently referred to. During the 8th through 15th centuries, Muslim geographers produced untold volumes of books on the geography of Africa, Asia, India, China and the Indies. These writings included the worlds first geographical encyclopedias, almanacs and road maps. The 14th century masterpieces of Ibn Battutah provide a detailed view of the geography of the ancient world. The science of ethnography was invented by the Muslim scholars of the 9th through 14th centuries. A number of Muslim geographers classified the races, writing detailed explanations of their physical appearances and unique cultural habits. Blumenbachs works were insignificant in comparison. Muslim physicians used a variety of specific substances to destroy microbes. They applied sulfur topically specifically to kill the scabies mite. Ar-Razi (10th century) used mercurial compounds as topical antiseptics. During the 9th and 10th centuries, the Venetians learned of the art of fine glass production from Syrian artisans. Glass mirrors were in use in Islamic Spain as early as the 11th century. Ibn Yunus al-Masri discovered the pendulum in the 10th century, and was the first to study and document its oscillatory motion. Its value for use in clocks was introduced by Muslim physicists during the 15th century. Muslim mathematicians as early as the 10th century solved numerous equations of even higher degrees with ease. Binomial theorem was utilized and perfected for its use in the systematic solution of algebraic problems by hundreds of the Muslim mathematicians. In the 10th century numerous Muslim chemists produced medicinal-grade alcohol through the process of distillation and manufactured the first distillation devices on a large scale for use in chemistry. They used alcohol as a solvent and antiseptic. The prophet Muhammad wisely warned against entering or leaving a region suffering from plague thus introducing the concept of quarantine for the very first time in the 7th century A.D. later in the 10th century, Muslim physicians innovated the use of isolation wards for individuals suffering with communicable diseases. As early as the 10th century, Muslim physicians and surgeons of 10th century used to apply purified alcohol to wounds as an antiseptic agent. In Islamic Spain surgeons utilized special methods for maintaining antisepsis prior to and during surgery. The origin of specific protocols for maintaining hygiene during the post-operative period raised the success rate so high that dignitaries throughout Europe came to Cordova, Spain, to be treated at what was comparably the Mayo Clinic of the Middle Ages. Islams ar-Razi wrote an in-depth treatise on the venous system, accurately describing the function of the veins and their valves in the 10th century. Timeline of Muslim Scientists from 700 900 AD: 8th century: 700s [petroleum; civil engineering] In Baghdad the streets were constructed and paved with tar, coming from the petroleum that oozed in natural oil fields in the region.   700s 800s [cosmetics] In Spain a beauty institute was started by Ziryab (Blackbird). 740 828 Al-Amai, Zoology, Botany, Animal husbandry.   770 840 [mathematics] The Calculus of resolution and juxtaposition (hisab al-jabr wal-muqabala), more briefly referred to as al-jabr, or algebra, was developed by Kharazmi, Algebra was a unifying theory which allowed rational numbers, irrational numbers, geometrical magnitudes, etc., to all be treated as algebraic objects. It gave mathematics a whole new development path so much broader in concept to that which had existed before, and provided a vehicle for future development of the subject. Another important aspect of the introduction of algebraic ideas was that it allowed mathematics to be applied to itself in a way which had not happened before.   Al-Khwarizmis successors undertook a systematic application of arithmetic to algebra, algebra to arithmetic, both to trigonometry, algebra to the Euclidean theory of numbers, algebra to geometry, and geometry to algebra. This was how the creation of polynomial algebra, combinatorial analysis, numerical analysis, the numerical solution of equations, the new elementary theory of numbers, and the geometric construction of equations arose.   Late 700s 800 [musical science] Mansour Zalzal of Kufa was a musician (luth) and composer of the Abbasid era. Contributed musical scales that were later named after him (the Mansouri scale) and introduced positions (intervals) within scales such as the wasati-zalzal that was equidistant from the alwasati alqadima and wasati al-fors who made improvements on the design of the luth instrument and designed the Luth. In 715 800 [chemistry] The Muslim chemist, Geber (Jabir ibn Hayyan), is considered the father of chemistry, for introducing the experimental scientific method for chemistry, such as alembic, still, retort, pure distillation, liquefaction, crystallisation, purification, oxidisation, evaporation, and filtration. He was the first chemist known to produce sulfuric acid, as well as many other laboratory instruments and chemical substances. His works include The elaboration of the Grand Elixir, The chest of wisdom in which he writes on nitric acid, Kitab al-Istitmam (translated to Latin later as Summa Perfectionis), and many others.   715 800 [alchemy] Geber, introduced the first theories on the transmutation of metals, the philosophers stone, and the artificial creation of life in the laboratory.   715 800 [glass] Geber added colour to glass by introducing small quantities of metallic oxides to the glass, such as manganese dioxide (magnesia). This was a new advancement in the glass industry unknown in antiquity.   9th century: 800 868 [biology, zoology, linguistics, language,] Amr ibn Bahr al-Jahiz wrote a number of works on zoology, lexicography, rhetoric, and Arabic grammar. In his most famous book the Book of Animals, he was the first to discuss food chains, and environmental determinism by arguing that the environment can determine the physical characteristics of the inhabitants in a certain community he also stated that the origins of different colors of human skin is the result of the environment. The struggle for existence and the theory of evolution by natural selection was first discussed by him. 800 873 Ibn Ishaq Al-Kindi (Latinized, Alkindus.) was an expert in Optics, Metallurgy, Cryptography, Medicine, Mathematics, Physics and Philosophy. He worked at the House of Wisdom which was set up in 810. He introduces quantification into medicine in his book De Gradibus.   In 810 the works of Greek and Indian scientists on astronomy and mathematics were translated into Arabic in Bayt al-Hikma (House of Wisdom) which was set up in Baghdad. 820 [mathematics] Mahani (full name Abu Abdollah Muhammad ibn Isa Mahani in Arabic Al-Mahani). Conceived the idea of reducing geometrical problems such as duplicating the cube to algebraic problems.   836 901 [anatomy; astronomy; mathematics; mechanics] Born Thabit Ibn Qurra (Latinized, Thebit.) made considerable contributions in mathematics particularly in number theory and geometry while studying at Baghdads House of Wisdom under the Banu Musa brothers. He discovered the theorem by which pairs of amicable numbers can be found; i.e., two numbers such that each is the sum of the proper divisors of the other. Later, al-Baghdadi (b. 980) and al-Haytham (born 965) developed variants of the theorem.   838 870 Tabari (full name: Ali ibn Sahl Rabban Al-Tabari) made many contributions in Calligraphy, Mathematics, Literature, and Medicine.   In mid 800s [chemistry] Al-Kindi gave 107 recipes for making perfumes and also wrote on the distillation of wine as that of rose water, in his book Kitab Kimia al-`otoor wa al-tas`eedat (book of the chemistry of perfumes and distillations).   850 930 [mathematics] Abu Kamil of Egypt (full name, Abu Kamil Shuja ibn Aslam ibn Muhammad ibn Shuja) made an important link in the development of algebra between al-Khwarizmi and al-Karajis time not using the symbols, but writing powers of x in words, he had begun to understand what should be written in symbols. 852 [aviation, flight] Abbas Ibn Firnas (Armen Firman) made the first successful parachute fall near CÃÆ' ³rdoba, Spain using a huge wing-like cloak. 858 929 [astronomy mathematics] Al-Battani (Albategnius) made valuable works on astronomy, trigonometry etc.   860 Al-Farghani (Al-Fraganus) was master in Civil engineering and Astronomy. 864 930 [chemistry; medicine] Al-Razi (Rhazes) studied Astronomy, Chemistry, Medicine, Ophthalmology and Smallpox. He wrote on Naft (naphta or petroleum) and its distillates in his book Kitab sirr al-asrar (book of the secret of secrets). When choosing a site to build Baghdads hospital, he hung pieces of fresh meat in different parts of the city and selected the location where the meat took the longest to rot, for building the hospital. He also suggested that patients must not be told about their real condition so that fear or despair may not affect the healing process. His notable works were on soap, alkali, caustic soda, and glycerine. He also gave the descriptions of equipment, processes and methods for their preparation in his book Kitab al-Asrar (book of secrets) in 925.   870 950 Al-Farabi (Al-Pharabius) wrote on early Islamic philosophy, logic in Islamic philosophy, Muslim sociology, musical science and political science. In   875 [aviation, flight] Abbas Ibn Firnas made the first flight in a hang glider with artificial wings, but his landing was unsuccessful. He also worked on mechanics of Flight, Planetarium, and Artificial Crystals. Ibn Firnas was the first to investigate the means of flight.   800s [chemistry; petroleum] Oilfields in Baku, Azerbaijan, generated commercial activities and industry. These oilfields, were wells dug to get the Naft (or naphta, or crude petroleum) these were described by geographer Masudi in the 10th century and by Marco Polo in the 13th century, who described the output of those wells as hundreds of shiploads.   10th century: 900s [mathematics; accounting] By this century, three systems of counting were used in the Arab world. First was the Finger-reckoning arithmetic, in this system the numerals were written entirely in words this system was used by the business community. Second was the sexagesimal system, originated by the Babylonians, in this system the numerals were denoted by letters of the arabic alphabet it was used by Arab mathematicians in astronomical work. The third was the Hindu-Arabic numeral system, which was used with various sets of symbols. Arithmetic of this system required the use of a dust board (a sort of handheld blackboard) because the methods required moving of numbers in the calculation and rubbing some out as the calculation proceeded. Later these methods were modified by Al-Uqlidisi (born 920) for pen and paper use. Eventually the advances enabled the decimal system to be used throughout the world in its standard form.  

Disease Caused by Parasite of Genus Trypanosoma

Disease Caused by Parasite of Genus Trypanosoma Human trypanosomiasis caused by Trypanosoma evansi and Trypanosoma lewisi in India : A matter of concern Introduction Disease 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 Report 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 commonly 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 Trypanoso ma, 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. 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 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 relate d 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 causes 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 month 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, specie s isolated from these area is T. evansi in cattle, buffaloes, and goats (see Ref. Meeting of the 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). Anoth er 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 Medical College and Hospital, Nagpur and at the Institut de Recherche pour le Dà ©veloppement 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. 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 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 suramin A 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 Dà ©veloppement in Montpellier, France, are as followed (Joshi, PP. et al., 2005). Three independent PCR assay were performed using DNA of trypanosome Related to the subgenus Trypanozoon using a seminested 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 reported 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 assay Specific enzyme-linked immunosorbent assay (ELISA) NNO-LIA HIV 1/2 Score test Investigation of parasite Unusual 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 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 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 e t 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-resolution 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 minicir cles (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 veterinary 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. evans i (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 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). 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 Trypanozoon The 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 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 (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 tran smission 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 pallidipes). 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) strains. 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, an trycide, 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. Treatment Treatment 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, Malhotra 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. Suramin Suramin 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 effective 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 (P ´epin 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(Stein 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 activi ty (K. Trieb, H. Blahovec, 2002). Suramin blocked CD154 (Emilio Margolles-Clark et al., 2009) from interacting with its receptor CD40 (U. Schà ¶nbeck 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 recept or (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 likely 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 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 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 (W ´ery, M., 1994). Suramin reduced sensitivity towards T. b. rhodesiense (Bacchi et al., 1990) and failure of treatment up to 25-30% observed (P ´epin 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 membrane transporter takes up. Role of apolipoprotein L-1 and haptoglobin-related protein T. 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). HDL 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). Apolipop rotein 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 forming domain as well as a region for the membrane insertion of it (Pà ©rez -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 ((Pà ©rez-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., 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 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 activity 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 Disease Caused by Parasite of Genus Trypanosoma Disease Caused by Parasite of Genus Trypanosoma Human trypanosomiasis caused by Trypanosoma evansi and Trypanosoma lewisi in India : A matter of concern Introduction Disease 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 Report 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 commonly 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 Trypanoso ma, 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. 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 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 relate d 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 causes 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 month 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, specie s isolated from these area is T. evansi in cattle, buffaloes, and goats (see Ref. Meeting of the 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). Anoth er 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 Medical College and Hospital, Nagpur and at the Institut de Recherche pour le Dà ©veloppement 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. 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 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 suramin A 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 Dà ©veloppement in Montpellier, France, are as followed (Joshi, PP. et al., 2005). Three independent PCR assay were performed using DNA of trypanosome Related to the subgenus Trypanozoon using a seminested 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 reported 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 assay Specific enzyme-linked immunosorbent assay (ELISA) NNO-LIA HIV 1/2 Score test Investigation of parasite Unusual 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 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 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 e t 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-resolution 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 minicir cles (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 veterinary 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. evans i (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 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). 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 Trypanozoon The 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 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 (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 tran smission 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 pallidipes). 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) strains. 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, an trycide, 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. Treatment Treatment 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, Malhotra 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. Suramin Suramin 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 effective 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 (P ´epin 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(Stein 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 activi ty (K. Trieb, H. Blahovec, 2002). Suramin blocked CD154 (Emilio Margolles-Clark et al., 2009) from interacting with its receptor CD40 (U. Schà ¶nbeck 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 recept or (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 likely 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 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 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 (W ´ery, M., 1994). Suramin reduced sensitivity towards T. b. rhodesiense (Bacchi et al., 1990) and failure of treatment up to 25-30% observed (P ´epin 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 membrane transporter takes up. Role of apolipoprotein L-1 and haptoglobin-related protein T. 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). HDL 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). Apolipop rotein 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 forming domain as well as a region for the membrane insertion of it (Pà ©rez -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 ((Pà ©rez-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., 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 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 activity 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

Hills Like White Elephants Essay -- Hills Like White Elephants Essays

  Ã‚  Ã‚  Ã‚  Ã‚  The story â€Å"Hills Like White Elephants† is about a couple who discuss an abortion. The American in the story addresses it as a â€Å"simple operation,† (487) while Jig seems to feel it is the wrong choice. I feel the man is encouraging her to have the abortion done in his own selfish way.   Ã‚  Ã‚  Ã‚  Ã‚  I feel the American is being very selfish and thinking what a simple operation it would be. He tells Jig, â€Å"It’s really an awfully simple operation, Jig.† (487)†It’s not really an operation at all.† (487)How easy it would be for the American to have an opinion like this since he would never have to experience the pain. He doesn’t have to deal with any of the physical or emotional scares. He just keeps reassuring her that it will be a simple operation. He says, â€Å"I know you wouldn’t mind it, Jig. It’s really not anything. It’s just to let the air in.† Is this what other men have told him? Has he ever taken the time to talk with women who have had the â€Å"simple operation?† As a man it would be very easy to think it’s a simple operation, but is this the reassurance that women want and need from men when they are faced with this decision? The American says, â€Å"I’ll go with you and stay with you all the time. They just let the air in and then it’s all perfectly natural.† (487)   Ã‚  Ã‚  Ã‚  Ã‚  Jig shows signs of regret as though the American is forcing her into this decision. I don’t feel that it is something that she wants to do. Ji...

Basics of Quantum Computing Essay -- Physics Computers Science

Fundamental Differences of Quantum Computers In the standard architecture of computer storage, values are arranged as a series of bits, each of which is either true or false(0 or 1). This fundamental restriction of two states is the most basic difference when working with quantum states. Rather than allowing just the two singles states, a superposition of the two states is also possible, forming a state that is neither 0 nor 1, but something in between with a probability of either state. Further, in the standard organization, it is possible to attach various bits together to force correlations between their values. This is also possible within the superposition of the states represented in a quantum bit. (Qubit) The correlation between these superpositions in the two qubits is referred to as Entanglement. With proper tying it is possible to evaluate the qubit as both one and zero at the same time, and do so across the entirety of the set of qubits at the same time, allowing for massively parallel evaluations of all possible sequences at the same time. Of course in the end there can only be a single full set for the stable state, but information can be gathered from each of the possibilities by its influence upon the whole system during each step of the evaluation. History of Quantum Computers Initially the famous physicist Robert Feynman breached the subject of using quantum effects for computation in 1982, though his primary interest was in using the effects of one quantum effect to simulate another. Three years later in 1985 David Deutsch of the University of Oxford published a paper detailing the workings of a universal quantum computer, detailing the functionality of the theoretical process, but not... ...e technological barrier has not progressed so far as to allow convenient usage. At every stage of production the quantum computer has a great deal of work that needs to be done, and each step must be painstakingly analyzed and protected from the harsh environment that surrounds the extremely delicate system. Even once such systems can be produced for small experiments to confirm the effects we seek, it will be quite some time before the production techniques and applications are so well refined as to allow for mass production or even a working prototype. More importantly, there does not seem to be any choice but to move to these systems. As our computers become more and more compact, the effects of quantum events are going to make themselves first known and then become overwhelming. The solutions appear to be evolution or stagnation.

Civic Virtue: The Right Thing for Our Society Essay -- society

Introduction Perhaps, the American society is the most divergent, the most accommodating and the most culturally diverse among all societies across the globe. Interestingly, most Americans reflect similar elements of behavior in many respects which are distinct to our American society. There are a number conscious and unconscious core values which are expected to guide every American character. Most of the American culture has to some extent embedded western civilization: A civilization that accommodates different cultures, merges multiple ideas, and values the freedom of choice. Still, a number of challenges in the direction of promoting our general wellbeing have been arising; thus, leading to questions on the direction that our society should direct for our common wellbeing. Here, I will be discussing approaches that can be designed in addressing the issues of wealth distribution, and the relationship between politics and community beliefs so as to have an even happier society. Inequality, Cohesiveness and Civic Virtue One among the challenges that face our society today is the widening rift between the rich and the poor. Although our politics has evaded the reality of a widening society, several philosophers have given their opinions on the challenge of wealth distribution. Our politics has become so distant from the challenge of widening social gaps that president Obama’s proposal to review tax laws in the direction of burdening the wealthy with more taxes has received heavy criticism from the republican political quarter. Apart from philosophical ideologies on the topic of wealth distribution, there is a more important challenge which requires the attention of our political leaders: Civic Virtue. Getting a picture of ... ...place in our schools and other institutions. Instead of focusing on the teaching of various religious and moral beliefs, students should be allowed to openly present their opinions on various religious matters. Such a direction must be done under an environment that respects the right of people to choose various religious and moral beliefs which are available in our society. Conclusion As I have discussed, I agree with Sandel’s opinions on the two issues (the distribution of wealth, and an open engagement between religion and politics) that I have discussed above. Wealth distribution is especially useful in guarding our democracy, promoting, cohesiveness, and improving the welfare of the poor. On the other hand, an engagement between politics and religion will be useful in promoting unity, tolerance and knowledge within our society.

Ellen Goodman Columnist Essay

Ellen Goodman, a Pulitzer prize winning columnist, author, speaker, and commentator who refuses to call herself a pundit. Ellen has long been a chronicler of social change in America, especially the women’s movement and effects on our public, private lives, and has spent most of her life chronicling social change and its impact on American life. As a Pulitzer Prize winning columnist she was one of the first women to open up the pages to women’s voices and became, according to Media Watch, the most widely syndicated progressive columnist in the country.Proof of her strong passion for impacts on an average American life, her column titled â€Å"Dispensing Morality† shows just that. In her column, she expresses how those in professions and careers should reserve the right to distribute drugs or anything that has the ability to harm someone, even if it’s intentions is to aid, if the decision on handing it out conflicts with their ethics, morals, and values. Sh e uses scenarios of situation like those and rhetorical questions to prove a point based on ethos with a tad bit of pathos; while she uses statistics of a considerable amount of claims, facts, expert opinions to appeal to the reader’s logos.She ends of this column saying: â€Å".. last time I looked, the pharmacist's license did not include the right to dispense morality. † Matching the last word with exact title of her column gives it a serious conclusion displaying how serious she is about the subject. In another column of Goodman’s, â€Å"Those Poor College Conservatives† she boldly evinces how politics does not only have a monumental spotlight as the nation as its theatre, but it also has a college level arena where students can take the initial stand of having grand debates as would senators and other officials perform when running for office of any kind.Here she uses statistics of how much Democrats there is for one Republican in the universities of Stanford and Berkeley to indicate how much national politics is effected by students who, as we know, are the next generation – the future. She also uses ExxonMobil; The Independent Women's Forum; and a quote of Harvey Mansfield, a Harvard conservative, to add on to her use logos in addition with her statistics. However, as much as logical this column may be, she uses her strong opinions to include pathos to approve to reader’s emotions, morals, and beliefs.This column demonstrates how much of a determination Goodman has toward the inclusiveness of American lives. One column of hers clearly exhibits her drive for righting wrongs of America. In Goodman’s column, â€Å"Will Her Voice Ever Be Heard? † she stands up for foreign writers to be able to have published books in the United States. This column mainly surrounds Iranian writer, Shirin Ebadi, who was the first Iranian woman to become a judge and the first to receive a Nobel Prize, who’s been es chewed by the government because she’s Iranian and the American government will not allow people who the country fears and is currently in war with.Goodman uses the background and story of Ebadi to convey the difficulties she has had in order to have her books published, those trails are an example of pathos because it is attempting to attract the reader’s emotional state. The author also uses facts revealing discrimination, such as: â€Å"A law written in 1917 allows the president to bar transactions during times of war or national emergency. It was amended twice to exempt publishers.Nevertheless, the Treasury Department in its wisdom has ruled that it's illegal even to enhance the value of anything created in Iran without permission. † To appeal to the audience’s logos state. The purpose of this article is to strike up people’s ethos so they will also stand up for those like Ebadi and hopefully let them have a share of this â€Å"country of free dom. † Ellen Goodman, currently does not write columns, however, as stated earlier, she is considered one of the most advanced columnist in the country.Her passionate columns of justifying the unjust in America truly exemplifies her love for this nation and how much she wants to make it an ideal land for not only its citizens but for those seeking liberty and freedom. Through her use of pathos, ethos, and logos she desires to please everyone’s emotions, value, and intellectual mind-sets, thus spreading her drive and motivation toward others. Her goal for composing such column makes her an astounding writer – not for money, not for fame, not for glory, but to touch reader’s hearts for good.

Just War Essay

Current events all over the globe raise questions with respect to the propriety and ethics of waging by one country to another. For example, there are some events that force people to think, rationalize, and make a distinction between war in its traditional concept and a war against terrorism, which makes it crucial for a state to obtain information from captured terrorists in a short period of time (Moseley). There are international standards and agreements that set the rules with respect to the waging of war, specifically applied in determining whether the war waged is just or not (Williams, Jr.and Caldwell). For one, there is the Geneva Convention, which deals with the noble objective of protecting Prisoners of War (POW) from various abuses (Moseley). The most popular theory dealing with the ethics, morality, or propriety of waging war is the â€Å"just war† theory (Moseley; Williams, Jr. and Caldwell). This theory refers to justice in war, or moral support for war (Moseley). Just war theory has two aspects: the theoretical and the historical tradition (Moseley; Williams, Jr. and Caldwell). In the former, the justification and reasons behind war are discussed; while in the latter, the focus of attention revolves around the body of rules and agreements entered into by international bodies that are supposed to be applied in times of war (Moseley). The former is also known as jus ad bellum, while the latter is also known as jus in bello (Moseley). Both concepts are not mutually exclusive, and both deal with the morality of conduct and the decision to go into war (Moseley). These concepts have a long history of tradition that built the rules of conduct to be observed during war (Moseley). The concept of jus in bello had been formulated due to decades, or even centuries of experience (Moseley). Thus, it must be deemed applicable, even to modern types of war experienced by the world today, like the war against terrorism. Indeed, the war against terrorism is of a different kind from the other kinds of wars that humankind had seen (Schwartz). However, the differences, such as the alleged pressing need for information, are not enough to abandon standards that are designed to protect the dignity of the human person (Schwartz). One of the criteria of jus in bello is strict proportion of the conduct with the objective desired (Moseley). Applying this criterion to any proposal to wage war against a country or group of people, there would ultimately be the question of whether the use of force, that would necessarily end in the loss of thousands, if not millions of lives, would justify the achievement of various goals, such as freedom, economic independence, or national security (Schwartz). Works Cited Moseley, Alexander. â€Å"Just War Theory. † 2006. 10 Oct. 2007. . Schwartz, Joseph M. â€Å"Misreading Islamist Terrorism: The â€Å"War Against Terrorism† and Just-War Theory. † Metaphilosophy 35(2004): 273-302. Williams, Jr. , Robert E. and Dan Caldwell. â€Å"Jus Post Bellum: Just War Theory and the Principles of Just Peace. † International Studies Perspectives 7(2006): 309-320