[The clinical classification of tuberculosis of the penis: report of 2 cases].
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Biomedical subjects
Publications and source records attributed to S Y Lu.
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Since January 1981, we have used the Exacon thermometer to monitor skin temperature of 180 completely amputated digits during and after replantation surgery. When skin temperature on the first day after surgery was above 32 degrees, 153 of 154 replanted digits survived. In contrast, when skin temperature was 32 degrees or lower, 22 of 26 replanted digits failed. Data were analyzed by the Probit model, which indicated that skin temperature monitoring with 32 degrees as critical temperature is significant at P = 0.01. Also, critical temperature was tested in the range of 31.0 degrees to 33 degrees at intervals of 0.1 degree. We found the probability of predicting the viability for replanted digits is highest when skin temperature is 32 degrees or higher.
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Numerous studies have examined receptor expression in neural transplants and their possible role in transplant-induced functional recovery from lesion-induced deficits. Herein we attempt to summarize the results of these studies, especially those from studies involving striatal transplants. Autoradiographic studies indicate that dopamine D1 and D2, muscarinic, cholinergic, 5-HT2, opiate mu, beta adrenergic and cholecystokinin (CCK) receptors are present in striatal transplants. Many of these receptors are present regardless of the transplant location and surrounding environment. This suggests that the expression of these receptors is determined by intrinsic properties of transplanted tissue, and is independent of transplant location and environment. Some transplant receptors, such as dopamine D1 and D2 and muscarinic receptors in striatal transplants, or 5-HT2 receptors in cortical transplants, display a patchy distribution which is dissimilar to that in the corresponding adult host tissue. This manuscript discusses this "abnormal" receptor distribution and possible explanations. Electrophysiological studies have indicated that some of the transplant receptors respond to physiological and pharmacological stimulation, suggesting that they are functional. However, the association of receptor expression with behavioral recovery is uncertain. The expression of neurotransmitter receptors in neural transplants may not be essential for the functional recovery associated with trophic mechanisms. However, neurotransmitter receptors may play an important role when functional recovery requires neuroanatomical integration between the host brain and the transplanted tissue.
Studies have suggested that neurotrophic mechanisms may underlie transplant-induced functional recovery. Astrocytes have been reported to be a source of neurotrophic factors. The present study examined the possible role of cultured astrocytes in promoting recovery of apomorphine-induced rotation behavior in rats with unilateral kainic acid (KA) lesions of the striatum. Five weeks after the lesions, one group of rats received fetal striatal tissue (E17) transplants, another group received transplants of cultured astrocyte suspension, and the remaining rats received sham transplants and served as controls. Apomorphine-induced rotation behavior was tested 4 weeks after the KA lesions, and 5 and 10 weeks following the transplantation. The KA-induced rotation behavior was reduced by the striatal transplants but not by the cultured astrocyte transplants 5 and 10 weeks following the transplantation. Histochemical analysis indicated that the striatal transplants had survived and grown and contained neurons and glia with similar morphology to those in the host brain. Immunocytochemical analysis of the astrocyte transplant sites revealed heavy glial fibrillary acidic protein and OX-42 staining in the transplant areas, suggesting that the transplanted astrocytes may have survived in the host brain. Although fetal striatal transplants can ameliorate apomorphine-induced rotation behavior, transplants of astrocytes alone may not be sufficient to reverse the functional deficits produced by KA lesions.