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J Sokol

Publications and source records attributed to J Sokol.

45 records · Page 3Linked to original sources
PubMed1975

[Year-round buffering of cattle feed mixture and its effect on metabolism and productivity].

Commercial feed mixture was buffered with a 2% and 3% admixture of bentonite buffer in two beef cattle herds in the course of one year. The mixtures were fed on a continuous basis. The two-per-cent buffer concentration was tested in 110 test animals with 104 control animals and the three-per-cent concentration in 50 test animals with 50 controls. Throughout the trial the over-all health condition remained unchanged, the hematocrit and hemoglobin values were balanced in both groups. The biochemical indices were better in the test groups: hypocalcemia improved (in the controls it grew worse), magnesiemia was slightly increased, the inorganic serum factor did not go beyond physiological limits, and acidosis did not occur (as distinct from the control animals). The levels of transaminases (GOT, GPT), glutamic acid dehydrogenase, total serum protein, alkaline phosphatase as well as ammonia and urea in blood serum were at physiological values with po-differences within groups. In the case of the three-per-cent buffer concentration the daily gains were higher by 0.073 kg, and in the two-per-cent concentration by 0.058 kg, in the test animals. The average annual gain was higher by 25.5 kg, and by 18.3 kg, respectively. With respect to the price of buffer and to the efficiency of the animals tested, the economic indices of feed mixture buffering are highly effective.

Alanine Transaminase↗
PubMedDate not supplied

[Infectious diseases of animals and their prevention].

Infectious diseases of animals are the subject of continuous concern. On the one hand there are some diseases which have not yet been described and on the other hand the presence of microbial agents is proved also in diseases which have been considered non-infectious. Undoubtedly, microbes and parasites take part also in the development of malignant transformation of cells. The question of possible transfer of animal oncogenic microorganisms (retroviruses in particular) to humans remains open. The study points to the changes in the incidence of orthopoxviruses which occurred after eradication of human variola and the increasing importance of bartonelloses. Disease prevention in animals is affected to an increasing extent by DNA recombinant methods. So called "Gene farming" has developed, consisting in production of narrow-profile therapeutically important proteins via animal bioreactors. We enter a period in which the resistance of animal organism begins to affect the transfer of genes encoding non-specific and specific protective mechanisms of organisms. (Tab. 7, Ref. 39.)

Animals↗
PubMedDate not supplied

[Prionoses--neurodegenerative diseases caused by prions, offectious proteinaceous molecules].

Prionoses are a group of human and animal neurodegenerative diseases caused by prions, infectious pathogens that differ from bacteria, fungi, parasites, viroids, and viruses. Despite intensive searches over the past three decades, no nucleic acid has been found within prions and considerable experimental data argue that prions are composed exclusively of proteins (glycoproteins). Normal prion protein (PrPC) is encoded by a gene present in all nuclear cells of humans and other mammals but is constitutively expressed mainly in neurons. PrPC is protease sensitive and nonpathogenic but it can be modified to the pathological and protease resistant form designated PrPSC which is essential for infectivity. Prion diseases are manifested as infectious, genetic, or sporadic disorders and are also named as transmissible spongiform encephalopathies (TSE). TSE culminate with a progressive and fatal degeneration of the CNS. The human prionoses include Creutzfeldt-Jakob disease (CJD), kuru, Gerstman-Sträussler-Scheinker syndrome (GSS), and fatal familial insomnia (FFI). In mammals, more than 15 different species have been described to suffer from prion disorders till now. Scrapie of sheep and goats is the oldest and the most studied of the prion diseases. Bovine spongiform encephalopathy (BSE) and transmissible mink encephalopathy are thought to result from the feeding of scrapie-infected animal products, whereas BSE has been identified in transmission to mice, domestic cats, two exotic species of ruminant, and monkey. More than 20 cases of clinically and pathologically atypical form of CJD, referred to as "new variant" CJD (vCJD) have been recognized in unusually young people in the United Kingdom. There is a strong evidence that the same prion strain is involved in both BSE and vCJD. It suggest the breaking of species barrier which results by spreading of BSE to humans, putatively by dietary exposure. Understanding the function of prion proteins and their modification to the pathological form may give new insight into the etiologic and pathogenic mechanisms also other diseases caused by aberrant proteins, including Alzheimer' disease, amyotrophic lateral sclerosis, and Parkinson's disease. (Tab. 4, Fig. 3, Ref. 76.)

Animals↗