Progesterone metabolism in vitro by ovaries from androgen-sterilized rats of different ages.
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Biomedical subjects
Publications and source records attributed to S Fukuda.
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There are many cAUSES OF ALTERED AMINO ACID AND PROTEIN METABOLISM IN UREMIA WHICH MAY Lead to impaired growth, wasting, malnutrition, and other aspects of the uremic syndrome. These causes have complex interrelationships that are not well understood. The factors include altered nutrition due to poor intake, losses of nutrients during dialysis, and abnormal metabolism of many nutrients. Uremic toxins, superimposed catabolic illnesses, elevated or reduced serum hormone levels, reduced capacity of the kidney to synthesize certain amino acids and to degrade other amino acids, peptides, and small proteins, and decreased excretion of certain amino acids and peptides may also contribute to altered amino acid and protein metabolism. The response of certain plasma amino acids to protein restriction appears to differ in uremic patients as compared to normal subjects. Increased plasma levels of many products of amino acids and proteins in renal failure are due primarily to decreased urinary clearance by the kidney. However, for some metabolites, increased synthesis or decreased degradation may also contribute to elevated levels. These latter compounds include guanidinosuccinic acid, methylguanidine, certain middle molecules, and in some patients, phenylpyruvic acid.
The formation of cowpox virus-specific cell surface antigen (CPV S-ag) was significantly enhanced by double infection with HVJ (Sendai virus). Simultaneous double infection, superinfection with HVJ and superinfection with CPV of cells persistently infected with HVJ similarly enhanced the formation of CPV S-ag, while pre-infection with HVJ was ineffective. To be effective, cells must be infected at a m.o.i. of greater than or equal to 1.0 and HVJ gene functions had to be expressed. The HVJ-infected cell extracts had an ability to accelerate uncoating (or degradation) of CPV, causing an early increase and a subsequent decrease in the infectivity of CPV. This activity reached a maximum 4--6 hr after HVJ infection, the increase paralleling enhancement of the total activity of several cellular enzymes. Addition of puromycin abolished the increase of these activities and the formation of CPV S-ag. Thus, the double infection with HVJ of CPV-infected cells induces an enhancement of CPV S-ag formation presumably as a consequence of activation of cellular enzymes which in turn accelerates uncoating of CPV.
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The development of so-called long bones in the extremity has been studied roentgenographically in forty-seven males and fifty-one females cynomolgus monkeys bred and reared at the National Institute of Health. The age of the females ranged from five months to eight years and nine months, and that of the males was from four months to seven years. In addition, the fetuses of six to twenty weeks of gestation age were examined for the time of appearance of ossification centers. As the biological parameters concerning body growth, the body weight and the bone length were measured and the secondary ossification centers were scrutinized and assessed the maturity process on the basis of the criteria that divided the state into eleven stages. Also the allometric analyses of body weight against bone length was conducted. Most of the secondary ossification centers except the proximal fibulal epiphysis appeared during the period from the prenatal stage (15-20 weeks of gestationage) to the postnatal one (several months of age). From four to five months of age, many ossification centers had developed to some extent. But, the appearance of proximal fibulal epiphysis was delayed and often lacking until 10 months of age in female and one year and three months of age in male. The earliest epiphyseal fusion was observed at the distal humeral epiphysis in both sexes. The latest epiphyseal fusion was observed at the distal ulnal epiphysis in both sexes and at the distal ulnal and radial epiphyses in female. From this study, the time of fusion was at five and three guarters years of age in females and at six and a half years of age in males. As a result, it is suggested that the estimation of animal's age might be put to practical use by introducing the assessing method that the score was given from the observation of the secondary ossification center.
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To determine the fate of macrophages within the afferent lymph stream, the popliteal lymph nodes at various times (3 h to 6 months) after subcutaneous injection of india ink into the footpads of guinea pigs were examined. Two types of cells which had phagocytized india ink were observed in the germinal centers. A small number of type I phagocytes (engulfing india ink as small particles which were often found together with tingible bodies in their cytoplasm) were scattered through the germinal center. A large number of type II phagocytes (packed full of india ink) presented preferentially in the medullary portion of the germinal center, together with many pyroninophil lymphoblastoid cells. In the second experiment, the afferent lymphatics of the popliteal lymph node were ligated 15-20 min after india ink injection. Although the type I phagocytes were distributed as in the first experiment, the type II phagocytes were scanty. In the third experiment, the afferent lymphatics of the popliteal lymph node were ligated 7 days after india ink injection. The type II phagocytes disappeared rapidly from the germinal center, whereas the type I phagocytes remained and were not affected by ligature. These results suggest that the type I phagocytes are the fixed macrophages or tingible body macrophages in the germinal center, and that the type II phagocytes are the macrophages migrating from the peripheral tissues. It was also shown that many macrophages reaching the regional node via afferent lymphatics entered the germinal center through the medullary pole where the cap of small lymphocytes became thinner or disappeared.
Comparative studies are needed on the bilogical stage of the bone growth in experimental animals and human to extrapolate the data from animals to for estimating the risk of bone seeking redionuclides in man. The growth of bone length and the appearance and fusion of the secondary ossification centers of seven long bones were compared between both species. The stage of ossification was determined radiographically. The results showed that the ossifying process of the secondary ossification centers could be divided into the following three categories in mice; (1) acute ossification type, (2) remaining metastable stage type which is specific in mice and generally at the proximal end of bone, and (3) delayed ossification type. Compared with the average life span, differences in ossification between both species were that the appearance of secondary ossification centers was observed within concentrated period in mice and not in man, and that the fusion of these was observed with long duration in mice and not in man. From 17 weeks of age, the metastable status of the bone appeared in mice without complete fusion even at 27 weeks of age, for the experiment with bone seeking radionuclides, mice of age 17 weeks or more should be used consequently.
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Antitumor activity of 1-(gamma-chloropropyl)-2-chloromethylpiperidine hydrobromide (CAP-2) was studied in vivo and in vitro, using various rat ascites hepatoma cell lines. Among eight ascites hepatoma cell lines, AH-13 was extremely sensitive both to in vivo antitumor and to in vitro lethal action of the agent, whereas AH-44 was resistant in both cases. The sensitivity of ascites hepatoma cell lines to CAP-2, nitrogen mustard N-oxide, 4-nitroquinoline 1-oxide, and ultraviolet ray in vitro was widely different but their relative sensitivities were very similar against these agents. For all the agents, AH-13 was inactivated very rapidly and AH-109A moderately, whereas AH-44 was relatively resistant. These results indicate that the sensitivity of the cells to CAP-2 may be closely related to their repair-capability of damaged DNA. Similar experiments using various DNA repair-deficient mutants of Escherichia coli B strain demonstrated that the repair-deficient mutants were several times more sensitive to CAP-2 than the wild type strain. From these results, it may be concluded that CAP-2 induces DNA lesions repairable by the same repair mechanisms that work on pyrimidine dimers.
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In Experiment I, the rat was given 15 mg/kg of chlordiazepoxide (CDP) and trained on a black-white discrimination task, motivated by electric shocks; the same animal, when given saline, was treated similarly with the reversed cue relationship on different and usually alternate sessions. Training was continued until a learning criterion under both drug and saline states and then tested with only one of five testing CDP doses (2.5, 5, 10, 20 and 25 mg/kg). During training, the rat made more errors under drug than under saline but there were little differences in starting and running times at least during the last sessions. In the transfer test, choice responses showed a bi-directional gradient around the training dose as in stimulus generalization gradient. Experiment II was identical to Experiment I, except that the same drug was tested at all five transfer doses and the resulting transfer gradient was a simple monotonic increasing function of dose levels. Discrepancy between the two experiments was discussed.
Rats were trained to escape electric shock by running into one arm of a T-maze on 10-trial daily sessions with pentobarbital (10 mg/kg), and to the opposite arm of the maze on other sessions with saline, the drug and saline sessions being alternated. This drug-learning dissociation or state-dependent learning was achieved by rats with medial septal lesions, abolishing hippocampal theta activity, as efficiently as rats with cortical lesions and intact rats. The suggested relationship between drug-learning dissociation and the suppression of hippocampal theta waves, produced by the drug, was not evidenced.