Effect of increased levels of urea in the diet on ruminal protozoal counts in four ruminant species.
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Biomedical subjects
Publications and source records attributed to M A Naga.
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Growth of a mixed ruminal population taken from a sheep on a protein-free (all urea) purified diet was estimated by an in vitro fermentation technique including precipitation of microbial protein by trichloracetic acid. Volatile fatty acid production in vitro was determined, and the associated a denosine triphosphate was estimated as moles volatile fatty acids X 2.4. On this basis, the quantity of microbial protein synthesized per mole of adenosine triphosphate increased at higher microbial growth rates.
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A field survey in a village was carried out to study child health in a rural area. The vaccination scheme was found to be inadequate and the value of health education is stressed. Parasitic infestation was found to be higher than urban areas but significantly lower than 1959 and the latter is attributed to a safer water supply. Growth and development lagged behing the whole national standards particularly during the 1 - 6 years age period. Health care for the pre-school age, taking advantage of co-operation from medical faculties and local health authorities, is recommended.
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Platelet function was studied in two cases with congenital afibrinogenemia. In these two cases there was no aggregation by ADP, while, there was increased calcium-induced platelet aggregation and decreased platelet adhesiveness to glass. Platelet aggregation was corrected in vitro, by addition of fibrinogen. It can be concluded from the above findings that the fibrinogen is an important factor for platelet aggregation by ADP and for platelet adhesion to glass surfaces, while platelet aggregation by thrombin does not need fibrinogen. The increased calcium-induced aggregation can be explained by postulating that thrombin finds no substrate to act upon except the platelets.
Eleven cases of hemophilia were studied for detection of any change in the platelet function. The results showed hyperfunction in 5 cases, normal function in 4, and hypofunction in the remaining two. The hyperfunction of the platelets was shown in the case with acute hemorrhage and it might be a compensation mechanism. The normal function was shown in cases during the quiescent phase. The hypofunction of the platelets was associated with the presence of AHg inhibitor and platelet antibody. Normal function returned after Cortisone administration. It may be postulated that the inhibitor of factor VIII and the platelet antibody are one and the same thing.