RANGKUMAN TINJAUAN PUSTAKA Nurprimadita R Bovine ephemeral fever virus has been classified as the type species of the

genus Ephemerovirus in the Rhabdoviridae (1). (2). BEFV is a single stranded, negative sense RNA virus. The complete virus particle is bullet shaped, enveloped and consists of helical nucleocapsid. Specific fluorescence indicating the presence of BEF viral antigen could be detected at the time of peak clinical response in individual cells in the lungs, spleen and lymph nodes as well as neutrophils. Before and after the peak fever some fluorescence was seen in cells which appeared to be reticular cells in the lymph nodes. Viral isolation in mice could be made from blood, lungs, spleen and lymph nodes over a period of no more than 3 days. It is postulated that viral growth takes place mainly in the reticuloendothelial cells in the lungs, spleen and lymph nodes and not in vascular endothelium or lymphoid cells. (Studies on Bovine Ephemeral Fever virus Abuelyazeed A. EL-Sheikh, Department of Virology, Faculty of Veterinary Medicine Zagazig University) Transmission The disease can be reproduced experimentally in cattle only by the intravenous inoculation of BEF virus. Subcutaneous or intramuscular injection is ineffective. Epizootiological evidence indicates that BEF virus is spread in nature only by an insect bite. The disease will not spread from cow to cow by close contact, droplet infection, bodily excretions, or by the transfer or injection of exudates (10). There is experimental evidence that BEF virus is not spread by semen. Meat does not represent even a theoretical risk for transmission because the virus is rapidly inactivated at pH levels below 5 (7). Such acidic levels are attained rapidly in bovine muscle after death. Disinfection plays no part whatsoever in control of spread. Incubation Period The incubation period following experimental intravenous inoculation of BEF virus varies between 2 and 4 days, and 9 days is the rare extreme. The time is probably influenced by the strain and dose used. The natural incubation period can only be inferred but is probably similar. An index case or cases occur under epizootic conditions approximately 1 week ahead of the main wave of cases in a herd. The peak of viremia occurs 24 hours before the onset of fever (10). Clinical Signs The name ephemeral fever was applied very early in the disease's recorded history. The disease is not ephemeral in the sense of being hard to see. The clinical signs are very obvious and can be quite severe (2). The fever of ephemeral fever is generally biphasic, sometimes triphasic, with peaks of 40-41.5 C (104- 107 F) spaced 12-18 hours apart. Thus, the actual height of the rectal temperature measured

during an initial examination varies with the stage of the febrile cycle. The physical signs during the first febrile phase tend to be mild except for the dramatic fall in milk production of lactating cows. The characteristic signs associated with BEF are those of the second febrile phase (5,10,18,22). These signs include accelerated heart and respiratory rates, anorexia, ruminal atony, depression, serous or mucoid nasal and ocular discharges, salivation, muscle twitching or waves of shivering, a generalized stiffness or a shifting lameness. There may be submandibular edema or patchy edema elsewhere on the head. Many animals become recumbent for 12-24 hours but are able to rise if sufficiently stimulated. Others are completely unable to rise and remain in sternal recumbency for hours or days with the head turned to the flank, or in lateral recumbency with or without loss of most reflexes. Recovery begins 1-2 days after the overt clinical signs are first noticed and is usually complete and without sequelae in a further 1- 2 days after the overt clinical signs are first noticed. The early signs of improvement develop in a few hours after fever disappears in most cattle. Most cases, especially those in young cattle, are mild to moderately severe, and recovery is well advanced by the third day after clinical signs are first observed. Lactating cows, bulls in good condition, and fat steers are the worst affected, and their recovery may take up to a week even without complications. A range of complications can occur in a minority of cases. Death can occur suddenly in the febrile or in the recovery phase. Paralysis of the limbs may persist for days, weeks, or permanently. Recovery from the longer-term paralysis can be complete, or some disablement of gait may remain. A temporary infertility may occur in bulls that show structural defects in spermatozoa persisting for up to 6 months, but infertility may be a nonspecific effect of the inflammatory nature of the illness. The loss of fertility of bulls can be minimized with nursing care treatment. Field Diagnosis Single cases are difficult to diagnose, but with a herd outbreak, when cattle at various stages of disease can be examined, diagnosis is made from clinical observations and the history of the outbreak. Differential Diagnosis Various diseases may be confused with ephemeral fever when a diagnosis in the field has to be made on a single animal (for example, early Rift Valley fever, heartwater, bluetongue, botulism, babesiosis, or blackleg). The salivation may suggest foot-and-mouth disease; however, there is no vesicular lesion in the mouth or on the feet. It is very simple to have a blood smear stained and examined at any veterinary or human laboratory to check for the characteristic neutrophilia and to obtain supporting, though not definitive, evidence to exclude most other viral diseases. When many cattle are involved, different stages of the disease will be observed some with the characteristicly rapid resolution of severe clinical signs. Treatment Ephemeral fever is one of the rare virus diseases for which treatment is effective (21). The inflammatory nature of the disease process means it is responsive to anti-inflammatory drugs. These drugs must be

given for the expected course of the clinical disease. During fever, the paresis or paralysis responds to injected calcium borogluconate in the same manner as parturient paresis (milk fever) (15). http://www.vet.uga.edu/vpp/gray_book/Handheld/bef.htm (2 of 11)3/5/2004 4:12:31 AM Transmission Bovine ephemeral fever appears to be transmitted by arthropods. The vector or vectors are not known, but BEFV has been isolated from a mixed pool of Culicine and Anopheline mosquitoes, as well as Anopheles bancroftii, in Australia, and from Culicoides (biting midges) in both Africa and Australia. Mosquitoes are suspected to be the most important biological vectors. The disease can also be spread by intravenous inoculation of small amounts of blood. Bovine ephemeral fever is not transmitted by close contact, body secretions, or aerosol droplets. The virus does not seem to be transmitted in semen and it is rapidly inactivated in meat. Carriers are not known to occur. Incubation Period In experimental infections, the incubation period is 1 to 10 days, with most cases developing between three and five days after exposure. The natural incubation period is probably similar. Clinical Signs Bovine ephemeral can be either mild or severe in cattle, with the most severe cases occurring in bulls and high-producing cows. Subclinical infections are also seen. The symptoms vary in individual animals, but the classic course begins with a fever, which is often biphasic, triphasic or polyphasic. The temperature peaks typically occur 12 to 18 hours apart. During the first fever spike, milk production in lactating cows often drops dramatically, but other clinical signs tend to be mild. Some animals may be depressed, stiff or reluctant to move. On the second day of illness, which may coincide with a second elevation in temperature, the symptoms are more severe. Animals usually become inappetent and depressed, with an increased heart rate, tachypnea, and serous or mucoid discharges from the nose. Profuse salivation, muscle twitching, waves of shivering or a watery ocular discharge may also be seen. Some animals develop submandibular or periorbital edema, or patchy edema on the head. Shifting lameness, stiffness and joint pain are common; the joints may or may not be swollen. The lameness can be severe enough tomimic a fracture or dislocation. Pulmonary emphysema and rales may be found in severe cases. Many animals, particularly cows in good condition and bulls, become recumbent for eight hours to days. Most animals lie in sternal recumbency, but in severe cases, animals may become laterally recumbent. Some animals temporarily lose their reflexes and are unable to rise. Recumbent animals may be bloated, have ruminal stasis, or lose their swallowing reflex. These clinical signs can be exacerbated by severe environmental stress or forced exercise. Most animals begin to improve a day or two after the first symptoms appear, and recover completely within another one to two days. Lactating cows and animals in good condition are usually affected more

severely and may take up to a week to recover. Generally, animals lose condition rapidly during the illness, and regain their weight only slowly. Complications are uncommon but can include temporary or (rarely) permanent paralysis, as well as gait impairment, aspiration pneumonia, emphysema, mastitis, and the subcutaneous accumulation of air along the back. Many of these complications may be the result of trauma or complications of recumbency. Temporary infertility (up to 6 months) can develop in bulls, and abortions can occur in cows. Permanent infertility is rare. In recovered animals, milk production is decreased by 10-15% for the rest of the lactation, but usually returns to normal after subsequent pregnancies. Cows that become ill late in lactation may not return to production. Death is uncommon, but may occur during either the febrile or the convalescent stage. Deaths are usually the result of secondary complications such as pneumonia or trauma. Water buffalo have similar symptoms, but the disease is usually milder. Experimentally infected sheep remain asymptomatic. Differential Diagnosis Bovine ephemeral fever in a single animal can be confused with early Rift Valley fever, heartwater, bluetongue, botulism, babesiosis or blackleg. The salivation may also resemble foot-and-mouth disease, but no vesicles are found. Control Because illness and viremia are both transient, and the incubation period is short, import restrictions are usually effective unless the country shares a border with an endemic region. The vectors for BEFV are unknown, and successful eradication has not been reported once this disease becomes endemic. If an outbreak occurs among imported animals in a limited area, placing them in an insect-proof area and treating the area with insecticides has a chance of success. Sodium hypochlorite and other disinfectants effectively destroy BEFV; however, disinfection is relatively unimportant in preventing the spread of this virus. BEFV is not spread by casual contact or in secretions, and it is rapidly inactivated in carcasses after death. Treatment is often unnecessary in non-lactating cows, but bulls or high-producing, lactating animals are often treated, particularly when they have become recumbent. Anti-inflammatory drugs and calcium borogluconate injections are effective. Good nursing can also aid recovery. Recumbent animals should be provided with water, food and shelter if necessary, but animals should not be forced to stand or move. Force-feeding is not advisable due to the risk of aspiration pneumonia. Laterally recumbent animals may be rolled periodically to prevent loss of circulation and muscle damage. Public Health There is no evidence that humans can be infected by the ephemeral fever virus. (the center for food security and public health (CFSPH) iowa state university tahun 2008)

Tentang antibodi BEF After primary infection of cattle with BEF virus, an antibody response is first detected 2-3 days after recovery (St George 1980; Young and Spradbrow 1990). Neutralising antibody titres reach their maximum levels 4-5 weeks after infection and high titres of antibody are still present 422 days after 71 inoculation of the virus (Snowdon 1970). Cattle which fail to react clinically also develop neutralising antibody (Snowdon 1970; Young and Spradbrow 1990). In Australia the serological diagnosis of ephemeral fever is complicated by the existence of a number of antigenically related viruses in the BEFVgroup. These viruses may play a role in sensitising cattle, so that an accelerated antibody response follows infection with BEF virus (Cybinski & Zakrzewski 1983; St George et al. 1984). The role of these or similar viruses in southern Africa has not yet been investigated. Differential Diagnosis The clinical signs of ephemeral fever are not pathognomonic and could easily be confused with other diseases, for example, post-parturient hypocalcaemia or milk fever. Hypocalcaemia in cases of ephemeral fever is probably related to clinical signs such as anorexia, reduced movements or stasis of the gastrointestinal tract, muscle tremors or shivering and recumbency (St George et al. 1984; Uren and Murphy 1985). J .A. W. Coetzer Department of Infectious Diseases, Faculty of Veterinary Science, University of Pretoria, Onderstepoort 0110, South Africa RADANG Mediator dan substansi radang Kerusakan sel akibat adanya noksi akan membebaskan berbagai mediator atau substansi radang antara lain histamin, bradikinin, kalidin, serotonin, prostaglandin, leukotrien dan sebagainya. Histamin terdapat pada semua jaringan juga pada leukosit basofil. Di dalam jaringan, histamin disimpan dalam sel mast dan dibebaskan sebagai hasil interaksi antigen dengan antibodi IgE pada permukaan sel mast, berperanan pada reaksi hipersensitif dan alergi. Substans tersebut merupakan mediator utusan pertama dari sedemikian banyak mediator lain, segera muncul dalam beberapa detik. Reseptor-reseptor histamin adalah H1 dan H2. Stimulasi pada kedua reseptor ini menyebabkan vasodilatasi pada arterial dan pembuluh darah koronaria, merendahkan resistensi kapiler dan menurunkan tekanan darah sistemik. Pada reaksi radang permeabilitas kapiler meningkat karena dibebaskannya histamin (Mutschler, 1991; Garrison, 1991). Volume darah yang membawa leukosit ke daerah radang bertambah, dengan gejala klinis di sekitar jaringan berupa rasa panas dan warna kemerah-merahan (PGE2 dan PGI2). Aliran darah menjadi lebih lambat, leukosit beragregasi di sepanjang dinding pembuluh darah menyebabkan pembuluh darah kehilangan tekstur. Peningkatan permeabilitas kapiler disebabkan kontraksi sel-sel endotel sehingga

menirnbulkan celah-celah bermembran. Permeabilitas kapiler ditingkatkan oleh histamin, serotonin, bradikinin, sistim pembekuan dan komplemen dibawah pengaruh faktor Hageman dan SRS-A. Larutan mediator dapat mencapai jaringan karena meningkatnya permeabilitas kapiler dengan gejala klinis berupa udem (Korolkovas, 1988; Boyd, 1971; Robins, 1974). PIRAZOLON : menghambat pembebasan histamin, menghambat sintesis mukopolisakarida, menstabilkan membran lisosomal dan mengurangi respons terhadap enzim lisosomal (lnsel, 1991; Melmon dan Morreli, 1978). Soewarni Mansjoer Bagian Farmasi Fakultas Kedokteran Universitas Sumatera Utara Apa yang menyebab kan nyeri ? Nyeri terjadi jika organ tubuh, otot, atau kulit terluka oleh benturan, penyakit, keram, atau bengkak. Rangsangan penimbul nyeri umumnya punya kemampuan menyebabkan sel-sel melepaskan enzim proteolitik (pengurai protein) dan polipeptida yang merangsang ujung saraf yang kemudian menimbulkan impuls nyeri. Senyawa kimia dalam tubuh yang disebut prostaglandin beraksi membuat ujung saraf menjadi lebih sensitif terhadap rangsangan nyeri oleh polipeptida ini. MEKANISME KERJA NSAID (pirazolon) Telah disebutkan bahwa efek terapi naupun efek samping obat ini sebagian besar tergantung dari penghambatan biosintesis PG. penelitian lanjutan telah membuktikan bahwa PG akan dilepaskan bilamana sel mengalami kerusakan. selain itu obat AINS diketahui menghambat berbagai reaksi biokimiawi, hubungan dengan efek anlgesik, anti-piretik dan anti-inflamasinya belum jelas. selain itu obat AINS secara umum tidak menghambat biosintesis leukotrien, yang diketahui ikut berperan dalam inflamasi. golongan obat ini menghambat enzim siklooksigenase sehingga konversi asam arakidonat menjadi PGG2 terganggu. setiap obat menghambat siklo-oksigenase dengan cara yang berbeda. khusus parasetamol, hambatan biosintesis PG hanya terjadi bila lingkungannya rendah kladar peroksid seperti di hipotalamus. lokasi inflamasi biasanya mengandung banyak peroksid yang dihasilkan oleh leukosit. ini menjelaskan mengapa efek anti-inflamasi parasetamol praktis tidak ada. aaspirin sendiri menghambat dengan mengasetilasi gugus aktif serin dari enzim ini. sehingga dosis tunggal aspirin 40 mg sehari telah cukup untuk menghambat siklo-oksigenase trombosit manusia selama masa hidup trombosit, yaitu 8- 11 hari. INFLAMASI. fenomena inflamasi ini meliputi kerusakan mikrovaskuler, meningkatnya permeabilitas kapiler dan migrasi leukosit ke jaringan radang. gejala proses inflamasi yang sudah dikenal ialah kalor, rubor, dolor, tumor dan functio laesa. selam berlangsunya fenomen inflamasi banyak mediator kimiawi yang dilepaskan secara lokal antara lain histamin. 5-hidroksitriptamin (5HT), faktor kemotaktik, bradikinin,

leukotrien dan PG. obat mirip aspirin dapat dikatakan tidak berefek terhadap mediator- mediator kimiawi tersebut kecuali PG. Secara in vitro terbukti bahwa prostaglandin E2 (PGE2) dan prostasiklin (PGI2) dalam jumlah nanogram, menimbulkan eritem, vasodilatasi dan peningkatan aliran darah lokal. histamin dan bradikinin dapat meningkatkan permeabilitas vaskular, tetapi efek vasodilatasinya tidak besar. dengan penambahan sedikit PG, efek eksudasi histamin plasma dan bradikinin menjadi lebih jelas. migrasi leukosit ke jaringan radang merupakan aspek penting dalam proses inflamasi. obat yang menghambat biosintesis PG maupun leukotrien tentu akan lebih poten menekan proses inflamasi. RASA NYERI. PG hanya berperan pada nyeri yang berkaitan dengan kerusakan jaringan atau inflamasi. penelitian telah membuktikan bahwa PG menyebabkan sensitasi reseptor nyeri terhadap stimulasi mekanik dan kimiawi. jadi PG menimbulkan keadaan hiperalgesia. kemudian mediator kimiawi seperti bradikinin dan histamin merangsangnya dan menimbulkan nyeri yang nyata. obat mirip aspirin tidak mempengaruhi hiperalgesia atau nyeri yang ditimbulkan oleh efek langsung PG. ini menunjukkan bahwa sintesis PG yang dihambat oleh golongan obat ini, dan bukannya blokade langsung. DEMAM. suhu badan diatur oleh keseimbangan antara produksi dan hilangnya panas. Alat pengatur suhu btubuh berada dihipotalamus. Pada keadaan demam keseimbangan ini terganggu tetapi dapat dikembalikan ke normal oleh obat mirip aspirin. Ada bukti bahwa peningkatan suhu tubuh pada keadaan patologik di awali pelepasan suatu zat pirogen endogen atau sitokin seperti interleukin-1 (IL-1) yang memacu pelepasan PG yang berlebihan di daerah preoptik hipotalamus. Obat mirip aspirin menekan efek zat pirogen endogen dengan menghambat sintesis PG. Tetapi demam yang timbul akibat pemberian PG tidak dipengaruhi, demikian pula peningkatan suhu oleh sebab lain seperti latihan fisik. Mosquito Life Cycle The mosquito goes through four separate and distinct stages of its life cycle and they are as follows: Egg, Larva, pupa, and adult. Each of these stages can be easily recognized by their special appearance. There are four common groups of mosquitoes living in the Bay Area. They are Aedes, Anopheles, Culex, and Culiseta. Egg : Eggs are laid one at a time and they float on the surface of the water. In the case of Culex and Culiseta species, the eggs are stuck together in rafts of a hundred or more eggs. Anopheles and Aedes species do not make egg rafts but lay their eggs separately. Culex, Culiseta, and Anopheles lay their eggs on water while Aedes lay their eggs on damp soil that will be flooded by water. Most eggs hatch into larvae within 48 hours. Larva : The larva (larvae - plural) live in the water and come to the surface to breathe. They shed their skin four times growing larger after each molting. Most larvae have siphon tubes for breathing and hang

from the water surface. Anopheles larvae do not have a siphon and they lay parallel to the water surface. The larva feed on micro-organisms and organic matter in the water. On the fourth molt the larva changes into a pupa. Pupa: The pupal stage is a resting, non-feeding stage. This is the time the mosquito turns into an adult. It takes about two days before the adult is fully developed. When development is complete, the pupal skin splits and the mosquito emerges as an adult. Adult: The newly emerged adult rests on the surface of the water for a short time to allow itself to dry and all its parts to harden. Also, the wings have to spread out and dry properly before it can fly. The egg, larvae and pupae stages depend on temperature and species characteristics as to how long it takes for development. For instance, Culex tarsalis might go through its life cycle in 14 days at 70 F and take only 10 days at 80 F. Also, some species have naturally adapted to go through their entire life cycle in as little as four days or as long as one month. The following pages show a typical mosquito egg raft, larva, pupa, and adult, and explains more about each stage. Mosquito Adult

Only female mosquitoes bite animals and drink blood. Male mosquitoes do not bite, but feed on the nectar of flowers. Aedes mosquitoes are painful and persistent biters, attacking during daylight hours (not at night). They do not enter dwellings, and they prefer to bite mammals like humans. Aedes mosquitoes are strong fliers and are known to fly many miles from their breeding sources. Culex mosquitoes are painful and persistent biters also, but prefer to attack at dusk and after dark, and readily enter dwellings for blood meals. Domestic and wild birds are preferred over man, cows, and horses. Culex tarsalis is known to transmit encephalitis (sleeping sickness) to man and horses. Culex are generally weak fliers and do not move far from home, although they have been known to fly up to two miles. Culex usually live only a few weeks during the warm summer months. Those females which emerge in late summer search for sheltered areas where they "hibernate" until spring. Warm weather brings her out in search of water on which to lay her eggs. Culiseta mosquitoes are moderately aggressive biters, attacking in the evening hours or in shade during the day. Anopheles mosquitoes are the only mosquito which transmits malaria to man.

DEMAM

Mechanism of action of NSAIDs

33

Ph h id osp olip s PhospholipaseA2 Cyclooxygenase

Blocked by

Steroids

Ara on a chid ic cid End e op roxid s e Prostaglandins PGE2 PGD2

Blocked by NSAIDs

Throm boxane A2

Prostacyclin

Namun pada patologi, demam disebabkan oleh penyetelan kembali pusat otak, pusat thermoregulasi, yang mengontrol suhu tubuh. Dengan demikian demam diakibatkan oleh gangguan terhadap thermostat itu sendiri, sedangkan pengaturan suhu nonpatologis tetgantung kepada suhu lingkungan dan jumlah panas yang dihasilkan metabolisme tubuh.

FUNGSI VITAMIN Vitamin yang larut di dalam air kelompok dari vitamin B kompleks merupakan kofaktor dalam berbagai reaksi enzimatik yang terdapat di dalam tubuh kita. Vitamin B yang penting bagi nutrisi manusia adalah : -Tiamin ( vitamin B 1 ). -Riboflavin ( vitamin B2 ). -Niasin (asam nikotinat ,nikotinamida, vitamin B3 ) -Asam pantotenat ( vitamin B5 ). -Vitamin B6 ( piridoksin ,pridoksal ,piridoksamin ). -Biotin. -Vitamin B12 (kobalamin ). Karena kelarutannya dalam air ,kelebihan vitamin ini akan diekskresikan ke dalam urin dan dengan demikian jarang tertimbun dalam konsentrasi yang toksik.Penyimpanan vitamin B kompleks bersifat terbatas (kecuali kobalamin) sebagai akibatnya vitamin B kompleks harus dikomsumsi secara teratur. Vitamin B1 (Thiamin) Vitamin ini terutama berfungsi dalam metabolisme karbohidrat. Vitamin B1 bersifat labil terhadap panas dan suhu yang terlalu rendah (Papich, 2007). Thiamin yang bergabung dengan ATP akan membentuk thiamin difosfat yang sangat berperan dalam metabolisme karbohidrat, tanpa mempengaruhi kadar glukosa darah. Tidak adanya thiamin dapat mengakibatkan berkurangnya aktivitas transketolase dalam eritrosit dan meningkatnya konsentrasi asam piruvat dalam darah. Tanpa thiamin trifosfat, asam piruvat tidak dapat diubah menjadi asetil-coA, menyebabkan penurunan NADH dengan glikolisis anaerobik yang menghasilkan asam laktat. Peristiwa ini dapat mengakibatkan asidosis laktat (Plumb, 1999). Fungsi B1 adalah dalam metabolisme energi dan berperan dalam sistem saraf. Vitamin B2 (Riboflavin) Riboflavin merupakan komponen dari 2 koenzim yang berperan dalam sistem oksidatif yang memiliki fungsi dalam pelepasan energi dari karbohidrat, lemak, dan protein pada jalur-jalur biosintesis (Papich, 2007). Like thiamin, it acts as a coenzyme in the breakdown of fats, proteins, carbs, and other nutrients. Helps fatty acid reduction. CoA needs FAD to accomplish this. Assists choline catabolism. Required for neurotransmitter (such as dopamine, and others) oxidation. Necessary for catabolism of nutrients in the liver. Helps b6 (discusses shortly) in many reactions, as it is often FMN dependent. Assists eye and skin maintenance. Vitamin B3 (Niacin) Vitamin B3 berperan dalam sistem enzim oksidasi-reduksi (Papich, 2007) dan setelah diserap tubuh segera dikonversikan tubuh menjadi nicotinamid. Sediaan obat untuk niacin biasanya dalam bentuk nicotinamid karena bentuk langsung niacin dapat menyebabkan vasodilatasi (Papich, 2007). Vitamin B6 (Pyridoxine) Pyridoxine berperan dalam metabolisme asam amino, sintesis hemoglobin, dan konversi tryptophan menjadi niacin (Papich, 2007). Vitamin B12 (Cobalamin) Cobalamin mengandung mineral cobalt dan berperan dalam berbagai reaksi biokimia tubuh seperti metabolisme lemak dan karbohidrat, serta penting dalam sintesis myelin. Vitamin ini juga berperan dalam pematangan eritrosit (Papich, 2007). As discussed previously, B12 plays a large part in the conversion of homocysteine to methionine, which helps protect the heart from disease. It assists conversion of THF into any of its coenzyme forms, when deficient in B12, folate is trapped in its methyl form. Cobalamin helps oxidation of several compounds. CoA and the kreb cycle are also dependent on B12. It helps nerve cells, red blood cells, and the manufacturing/repair of DNA. It is vital for processing carbohydrates, proteins and fats, which help make all of the blood cells in our bodies. It also assists memory [7,66,41].