Pathology quiz case 2. Leukemia cutis.
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Biomedical subjects
Publications and source records attributed to S Baker.
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1. We investigated the role of calcium and albumin on the perfusate flow in isolated perfused rat kidneys. The initial perfusion medium was Krebs-Henseleit bicarbonate solution with 1.82 mm-calcium without albumin. Perfusate flow autoregulation occurred above 100 mmHg.2. Raising albumin concentration to 20 and 60 g/l. abolished autoregulation and increased perfusate flow.3. Keeping ionized calcium at 1.82 mm restored autoregulation in medium containing 20 and 60 g albumin/l. However, in 60 g albumin/l. autoregulation occurred at a significantly higher flow.4. 1.82 mm-ionized calcium appears to be a critical level for autoregulation of flow in these experiments, for autoregulation was not obtained in 60 g albumin/l. medium containing 1.80 mm-ionized calcium. On the other hand, autoregulation occurred in medium containing 1.83 mm-ionized calcium, but at a lower perfusate flow.5. Raising albumin concentration to 120 g/l. increased perfusate flow from 14.6+/-0.8 to 20.8+/-0.7 ml./min.g (n = 5, P < 0.01) in the presence of 1.82 mm-total calcium, and from 11.6+/-1.0 to 15.8+/-0.7 ml./min.g (n = 5, P < 0.01) in 1.82 mm-ionized calcium. The effect of raising albumin concentration was reversible.6. Removing the capsule from the kidneys abolished the increased flow in response to raising albumin concentration.7. We conclude that (a) the mechanism for the autoregulation of renal perfusate flow in isolated perfused kidneys is critically dependent on an extremely narrow range of ionized calcium concentration in the perfusion medium, below this range, autoregulation is not achieved; above it, however, autoregulation is achieved, but during intense vasoconstriction; (b) raising albumin concentration in the perfusion medium increases perfusate flow and abolishes autoregulation by lowering extracellular ionized calcium and by raising intrarenal tissue pressure.
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Alcohol is a well-recognised cause of fasting hypoglycaemia but may also provoked reactive hypoglycaemia when drunk together with a carbohydratee mixer. In this study the ability of sorghum beer (an 'in-built' alcohol-starch beverage widely enjoyed in Southern Africa) to induce reactive hypoglycaemia was compared with "gin and tonic' in eight non-obese health African men. After an overnight fast, each subject drank, in random sequence on their different occasions, 2 litres of sorghum beer (carbohydrat content approximately 5% and alcohol concentration 2.24 g/dl-2.8% v/v), the same volume of a control solution providing a similar carbohydrate load, or a gin and standard tonic water mixture. No evidence of reactive hypoglycaemia was apparent during the 5 hours after the beginning of the sorghum beer tolerance tests, despite a mean peak blood alcohol level reaching 80 mg/dl. both the peak and total plasma insulin responses were significantly reduced (p less than or equal to 0.05) when compared to the brisk responses elicited by the carbohydrate solution alone and the gin and tonic drinks, with consequent hypoglycaemia. These data suggest that African home-brews are not potent causes of reactive hypoglycaemia, although they may be implicated in the development of ethanol-induced hypoglycaemia in the fasting state.
The hemostatic properties and effect on osteogenesis of gelatin foam paste and bone wax were compared on surgical bone lesions in experimental animals. Thirty rabbits each received four trephine craniotomies and four lumbar laminectomies. Alternate bone incisions in each animal were treated with either gelatin foam paste or bone wax. Blood loss was measured by absorbing the blood into dry surgical cottonoids weighed before and after use. Bone healing sites of three rabbits were examined histologically to assess the effect of each agent on osteogenesis. The trephination sites of eight rabbits were subjected to fracture force testing at 6 weeks postoperatively to compare the effect ot the two agents on bone healing. No significant difference was found between gelatin foam paste and bone wax in either effectiveness of hemostasis or effect on osteogenesis.
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Different strains of Saccharomyces cerevisiae exhibit alternative patterns of trehalose accumulation during growth on a glucose medium. The active pattern is designated as TAC(+) phenotype and the alternative, low-activity pattern as tac(-) phenotype. The tac(-) phenotype is expressed only during growth, since tac(-) strains actively accumulate trehalose during incubation in a glucose medium lacking a nitrogen source. The tac(-) phenotype appears to be determined by a single, recessive gene tac1. The quantitative expression of the dominant, alternative allele TAC1 is subject to wide variation. A highly active pattern of trehalose accumulation requires TAC1 and an amplification factor, TAM, which consists of one or more dominant gene(s). TAM does not appear to alter significantly the expression of tac1. Highly amplified TAC(+) strains may contain a labile factor not present in a TAC(+) strain which accumulates intermediate levels of trehalose.
Craniosynostosis (Cruzon's, Pfeiffer's and Apert's Syndrome, etc.) can cause forehead deformities that frequently need reconstruction. In general, osteotomies and/or bone grafting are the preferred methods for obtaining proper orbital protection from above and a good aesthetic appearance. In certain cases however, osteotomies and/or bone grafting are not possible or a patient may refuse to have such an extensive procedure. Preformed methylmethacrylate prostheses have in such cases been implanted in patients with significant skull deformities with only minimal morbidity. The ease of this technique coupled with the shortened operative time, minimal hospitalization, and few, minor complications offer the reconstructive surgeon another and relatively simple method for treatment of extensive forehead and supraorbital deformities.
The effect of protein binding upon the penetration of six-beta-lactam (three penicillins and three cephalosporins) antibiotics into tissue fluid was studied in humans. A cantharides blister technique was used. It was found that there was a linear relationship between the percentage of protein binding and the penetration into the blister fluid of the antibiotic as measured by the area under the curve of the protein-free fraction. This finding is further evidence that protein binding may have important influence upon the likely efficacy of an antimicrobial agent.
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The pharmacokinetics of cefotaxime and moxalactam were compared in six healthy male volunteers aftr the administration of 1-g doses intravenously. Penetration of the compounds into tissue fluid was studied in cantharides-induced blisters. Both serum and tissue fluid levels of moxalactam were higher than those of cefotaxime. The elimination half-life of cefotaxime was 1.2 h, and that of moxalactam was 2.85 h. On the average, 50.5% of cefotaxime and 87.5% of moxalactam were recovered in the urine in 24 h.
Five dihydrodiols derived from benz[a]anthracene (BA) and 4 dihydrodiols derived from 7,12-dimethylbenz[a]anthracene (DMBA) have been tested, together with the parent hydrocarbons, for their abilities to induce mutations to 8-azaguanine resistance in V79 (Chinese hamster cells and malignant transformation in M2 mouse fibroblasts. The syn- and anti-isomers of benz[a]anthracene 8,9-diol 10,11-oxide were also tested for biological activity in these two systems. The non-K-region 1,2- and 3,4-dihydrodiols of BA induced mutations but the non-K-region 8,9-dihydrodiol and the K-region 5,6-dihydrodiol were inactive as mutagens; none of these BA diols transformed M2 mouse fibroblasts. The 3,4- and the 8,9-dihydrodiols derived from 7,12-dimethylbenz[a]anthracene induced mutations in V79 cells and malignant transformation in M2 mouse fibroblasts and both were more active than the hydrocarbon itself. The K-region 5,6-dihydrodiol and the non-K-region 10,11-dihydrodiol of DMBA were inactive in both test systems. The results are not inconsistent with other data suggesting that the metabolic activation of both BA and DMBA occurs through conversion of the respective 3,4-dihydrodiols into the related vicinal diol-epoxides, although other dihydrodiols may also be involved in vivo. Both the BA diol-epoxides tested were mutagenic, but although the anti-isomer transformed M2 fibroblasts, the syn-isomer was inactive.
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This is a case report of a Black baby girl who presented at the age of 7 days with incontinentia pigmenti. While the classic 3 phases of inflammation, hyperkeratosis, and irregular pigmentation are the rule, this patient demonstrates an accepted variation, presenting with irregular pigmentation without having gone through the other phases. Ninety-five per cent of the described cases have been in females. A negative family history, as in this case, is not unusual.
A 21-year-old woman developed persistent polyarthritis indistinguishable from rheumatoid arthritis after rubella. The arthritis persisted for approximately 30 months and was associated with high levels of antibody to rubella virus and with rheumatoid factor. The antibody titres declined pari passu with clinical improvement which progressed to complete resolution. Fractionation of serial serum specimens showed a substantial and persistent IgM antibody response to rubella virus. Rubella antigen was not demonstrated in the synovial exudate.
Four different dihydrodiols derived from 7-methylbenz(a)anthracene have been tested, together with the parent hydrocarbon, for their ability to induce the in vitro malignant transformation of mouse M2 fibroblasts and mutations in V79 Chinese hamster cells. In the transformation tests withe the non-K-region dihydrodiols, the 3,4-diol was the most active dihydrodiol tested and the 8,9-diol was also more active than 7-methylbenz(a)anthracene itself; the 1,2-diol showed only slight activity. The K-region dihydrodiol, the 5,6-diol, which cannot be directly metabolized to a vicinal diol-epoxide, was inactive. These differences in biological activity were similar to those apparent in the results from the mutagenicity tests. The data support the general hypothesis that non-I-region dihydrodiols, which can be metabolized to vicinal diol-epoxides, are important in the metabolic activation of the carcinogenic polycyclic hydrocarbons and, when taken together with other results, indicate that 3,4-dihydro-3,4-dihydroxy-7-methylbenz(a)anthracene is most probably involved in the metabolic activation of 7-methylbenz(a)anthracene presumably following conversion into the related diol-epoxide, 3,4-dihydro-3,4-dihydroxy-7-methylbenz(a)anthracene 1,2,-oxide.
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