Radiological case of the month. Denouement and discussion: synovial chondromatosis.
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Biomedical subjects
Publications and source records attributed to A Deitch.
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OBJECTIVE: The purpose of the study was to compare the body mass and fat compositions of menopausal women who were taking conventional doses of hormone replacement therapy (HRT) with that of menopausal women who were not taking any hormones. DESIGN: The body fat composition of 169 healthy postmenopausal women was measured using a noninvasive handheld machine, the Electrolipograph (BioAnalogics ELG, Beaverton, OR, USA). Impedance to electrical flow in tissues is lower with increasing water content of the tissue. Information on HRT, lifestyle, diet, smoking, and alcohol was obtained from the medical record and by a telephone interview before women were invited to participate. HRT and non-HRT groups were compared. Multivariate linear regression, which included age, years since menopause, type of menopause, and use of HRT, was performed for each of the two major outcomes: body mass index (BMI) and percentage of body fat. RESULTS: Comparisons between subgroups showed a large number of significant differences reflecting differences in age since menopause, baseline BMIs, and baseline waist to hip ratios. In the regression model, however, the only factor significantly associated with lower fat and BMI was the use of HRT. Women who were taking HRT had significantly lower percentages of body fat (-4.8%; p < 0.001) and BMI (-2.6 kg/m2; p < 0.001) compared with nonusers. Age and duration and type of menopause were not significant predictors of weight and BMI in this group of postmenopausal women. CONCLUSIONS: In this study, HRT seems to be associated with a significant reduction in postmenopausal weight and fat mass gains. This may be an important mechanism by which HRT exerts its beneficial long-term effects on cardiovascular health.
The pathophysiology of the abnormal spermatogenesis seen in the presence of the varicocele has not been elucidated in spite of extensive study. Furthermore, no satisfactory explanation exists for the bilateral abnormal spermatogenesis seen in a process which is felt to be unilateral in the majority of cases. The present study was designed to determine if a surgically produced unilateral varicocele would lead to ipsilateral testicular changes prior to the onset of contralateral testicular alterations. Utilizing the rat model and microsurgical techniques, the effects of the varicocele on ipsilateral and contralateral spermatogenesis was studied at intervals over 49 days. Mean seminiferous tubular diameter measurements and flow cytometric analysis of testicular tissue were utilized to assess spermatogenesis. A statistically significant decrease in mean seminiferous tubular diameter was seen between day 1 and day 49 in the left testicle. The right testicle tended to demonstrate similar changes but these were not significant by the method of analysis used. Flow cytometric analysis of testis DNA content also revealed a statistically significant difference in the percentage of haploid, diploid and tetraploid cells in the left testis on day 1 as compared to day 49. The right testis again tended to demonstrate similar but not significant changes. Though primarily a unilateral process, bilateral spermatic vein abnormalities were also visualized in some animals. This observation may contribute to the bilateral effect observed. These studies demonstrate that a surgically created left varicocele will result in bilateral testicular alterations. Within the time frame of the study, the ipsilateral alterations progressed to a greater degree.
The effect of the purine antagonist acivicin (AT-125) on the metabolism and cytotoxicity of 6-thioguanine was examined in the murine leukemia L1210. Cells exposed to 5 X 10(-6) M acivicin for 18 hr followed by 10(-5) M [14C]-6-thioguanine for 2 hr accumulated 2.90 +/- 0.17 nmoles 6-thioguanine/10(6) cells compared to 0.69 +/- 0.07 nmoles 6-thioguanine/10(6) cells in untreated controls. Intracellular accumulation of 6-thioguanine monophosphate, a lethal 6-thioguanine metabolite, increased from 0.27 +/- 0.05 to 1.08 +/- 0.13 nmoles 6-thioguanine monophosphate/10(6) cells following the same acivicin exposure. A similar increment was observed for the formation of 6-thioguanine triphosphate. These alterations in 6-thioguanine metabolism were associated with an increase in the intracellular level of 5-phosphoribosyl-1-pyrophosphate, an obligatory substrate in 6-thioguanine activation (57.9 +/- 7.6 vs 13.4 +/- 2.3 ng 5-phosphoribosyl-1-pyrophosphate/10(6) cells). In contrast, there was a 50% reduction in the amount of 6-thioguanine incorporated into RNA and DNA following acivicin pretreatment. Cytofluorometric analysis revealed that an 18-hr exposure to 5 X 10(6) M acivicin increased the population 5-phase cells, which are more sensitive to the actions of 6-thioguanine, by 50% relative to untreated controls. In both suspension culture growth and soft agar studies, the sequential administration of acivicin followed by 6-thioguanine resulted in substantial growth inhibitory activity; in contrast, the effects of the reverse sequence were subadditive. Pretreatment of L1210 cells with acivicin potentiates the action of subsequently administered 6-thioguanine, and the mechanism may involve both biochemical as well as cytokinetic factors. In vivo studies involving the sequential administration of these agents appear warranted.