Biomedical subjects
Publications and source records attributed to X M Xu.
In this study the content of cantharidin in Mylabris was analyzed quantitatively by UV. Analytical results thus obtained agree well with those by the neutralization method set forth in ChP. The average recovery of cantharidin is 99.98% and the coefficient of variation is 0.719%.
Based on the pathological observation of 100 cases of severe deep stromal herpetic keratitis, the author suggested the classification of the disease, according to the nature and progression of the chronic inflammation, into 2 categories of the acute active stage (40%) and chronic progressive stage (60%), which were in agreement with the clinical manifestations and also satisfactorily explained the pathogenetic basis of the clinical types. Inflammatory granuloma appeared in 21% of the cases, indicating that the corneal lesions were still in progress.
Using axonal tracing techniques we have shown that rubral axons are capable of growing around lesions of the rubrospinal tract during early stages of development in the North American opossum and that a critical period for such growth exists. The opossum was employed for study because it is born in a very immature state 12-13 days after conception and the entire development of its rubrospinal tract occurs postnatally.
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By using X-ray cinemographic techniques and biomechanical methods, the open-closing movement of the human temporomandibular joint was investigated in 14 living subjects. The theory of the instantaneous center of rotation (IRC) of the mandibular movement is strongly recommended and the position and the tendency of the IRC are also roughly determined. Moreover, a two-step model of the joint is put forward.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
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Alterations in thyroid hormone level or responsivity to thyroid hormone have significant neurologic sequelae throughout the life cycle. During fetal and early neonatal periods, disorders of thyroid hormone may lead to the development of motor and cognitive disorders. During childhood and adult life, thyroid hormone is required for neuronal maintenance as well as normal metabolic function. Those with an underlying disorder of thyroid hormone homeostasis or mitochondrial function may be at greater risk for developing cognitive, motor, or metabolic dysfunction upon exposure to substances which alter thyroid hormone economy. Polychlorinated biphenyls (PCBs) and dioxins have been argued to interfere with thyroid hormone action and thus may affect the developing and mature brain. Animal models provide useful tools for studying the effects of thyroid hormone disorders and the effects of environmental endocrine disruptors. The congenitally hypothyroid, hyt/hyt, mouse exhibits abnormalities in both the cognitive and motor systems. In this mouse and other animal models of thyroid hormone disorders, delayed somatic and reflexive development are noted, as are permanent deficits in hearing and locomotor and adaptive motor behavior. This animal's behavioral abnormalities are predicated on anatomic abnormalities in the nervous system. In turn, these abnormalities are correlated with differences in neuronal structural proteins. In normal mice, the expression of mRNAs coding for these proteins occurs temporally with the onset of autonomous thyroid hormone production. The hyt/hyt mouse has a mutation in the thyroid stimulating hormone receptor (TSHr) gene which renders it incapable of transducing the TSH signal in the thyrocyte to produce thyroid hormone. Some behavioral and possibly some biochemical abnormalities in mice exposed to PCBs are similar to those seen in the hyt/hyt mouse. In addition to direct effects on brain development and neuronal maintenance, thyroid hormone is necessary for maintaining metabolic functioning through its influence on mitochondria. Because the brain is particularly sensitive to inadequate energy generation, disorders of thyroid hormone economy also indirectly impair brain functioning. Alterations in thyroid hormone level result in differing expression of mitochondrial genes. Mutations in these mitochondrial genes lead to well-recognized syndromes of encephalomyopathy, myopathy, and multisystem disorder. Hence, PCBs and dioxins, by possibly altering the thyroid hormone milieu, may alter the functioning of mitochondria in the generation of adenosine triphosphate (ATP). The use of animal models of thyroid hormone deficiency for behavioral, anatomic, histologic, and molecular comparison will help elucidate the mechanisms of action of these putative endocrine-disrupting compounds. The study of thyroid hormone disorders provides a template for relating thyroid hormone mediated effects on the brain to these compounds.