Biomedical subjects

J A Xu

Publications and source records attributed to J A Xu.

5 recordsLinked to original sources

PubMed1994

Quantitative analysis of masticatory muscles using computed tomography.

Quantitative information on the normal size range of the masticatory muscles needed for successful treatment of facial asymmetry is sparse. Our purpose in this study was to define morphological indicators for the volume of the masticatory muscles on CT. Cross-sectional areas and volumes of the masseter and medial pterygoid muscles were measured from CT scans of 65 patients. The muscles were scanned from origin to insertion and the maximum cross-sectional area (MCSA) and its location together with the total volume were determined. The mandibular foramen was used as a landmark to determine the location of MCSA. The location of MCSA of masseter muscle was centred 8 mm above the mandibular foramen, and that of medial pterygoid muscle at the foramen. The MCSA of both muscles was highly correlated with volume suggesting that this parameter might serve as an indicator of their volume. Knowledge of the location of the MCSA would facilitate its measurement and so reduce radiation exposure. There was a positive correlation between the two muscles for both volume and MCSA. This finding could be relevant for future studies of the relationship between the morphology, biomechanics and pathology of the masticatory muscles.

Adult↗

PubMed1991

Role of xanthine dehydrogenase and oxidase in focal cerebral ischemic injury to rat.

The role of xanthine dehydrogenase and oxidase as a source of free radicals contributing to focal cerebral ischemic injury was evaluated in Long-Evans rats after the middle cerebral artery was permanently occluded and both carotid arteries were clamped for 90 min. The fraction of xanthine dehydrogenase present as the free radical producing oxidase increased slightly from 22% in control cortex to 30% in the ischemic right cortex during the first 3 h of reperfusion and then remained relatively unchanged over the next 24 h. This increase may in part be due to entrapped plasma, which contained 4.5 +/- 0.8 nmol.min-1.ml-1 xanthine oxidase entirely in the free radical-producing form. Infarct volume was unaffected by pretreatment with 50 mg allopurinol/kg per day over 3 days before surgery but was decreased by 8% with 100 mg/kg and 24% with 150 mg/kg of allopurinol (P less than 0.05). However, inhibition of xanthine oxidase by dietary depletion of the essential molybdenum cofactor increased infarct volume by 19%, suggesting that protection by allopurinol at higher dosages was independent of xanthine oxidase inhibition. Neither xanthine oxidase present in rat brain nor circulating in plasma appears to be the primary source of oxygen radicals that contributes to infarction in focal cerebral ischemia.

Allopurinol↗

PubMed1990

Leukotriene B4 release and polymorphonuclear cell infiltration in spinal cord injury.

Activation of arachidonic acid occurs after spinal cord injury. Leukotriene B4 is a lipoxygenase metabolite of arachidonic acid. In a rat model of experimental spinal cord injury, we found that the leukotriene B4 content was less than the sensitivity of our assay (8 pg/mg of protein) in non-traumatized spinal cord. Leukotriene B4 was detectable in traumatized cord (mean +/- SE, 25 +/- 5 pg/mg of protein; n = 3). Release of leukotriene B4 from spinal cord slices into the incubation medium was also noted after trauma (9 +/- 1 pg/mg of protein; n = 12) and was enhanced by exposure of traumatized spinal cord slices to the calcium ionophore A23187 (375 +/- 43 pg/mg of protein; n = 12). The amount of leukotriene B4 released corresponded to the extent of post-traumatic polymorphonuclear cell infiltration determined by a myeloperoxidase assay. Results from this study suggest that the source of leukotriene B4 in spinal cord injury is infiltrating polymorphonuclear cells.

Animals↗

PubMed1985

Exposure to light accelerates the formation of dopamine from exogenous L-dopa in the rat retina.

Dopaminergic neurons of retina are activated when rats are placed in a lighted environment. L-DOPA, the precursor of dopamine, was administered to rats that were housed either in the light or the dark. In the light more dopamine and its metabolite 3,4-dihydroxyphenylacetic acid were formed from L-DOPA when compared with animals given the same dose of L-DOPA, but kept in the dark. Our results suggest that the in vivo decarboxylation of DOPA may be modulated by neuronal activity in the rat retina.

Animals↗

PubMedDate not supplied

O-acetyl sialomucin and differentiation of stomach cancer: a histochemical study.

In one hundred surgical specimens with stomach cancer, 78 cases contained intestinal metaplasia (IM) in the outer margin mucosa nearby carcinoma focus, while the remaining 22 had no IM. IM was histochemically classified into small intestinal type, sulphomucin colonic type (S), O-acetyl sialo-sulphomucin colonic type (OS) and O-acetyl sialomucin colonic type (O). The incidence of OS and O in well differentiated carcinoma (WCa) (22/27) was obviously higher than in poorly and undifferentiated carcinomas (PUCa) (17/51) (X2 = 14.5011, P less than 0.001). This suggests that O-acetyl sialomucin in IM may be correlated with the differentiation of gastric cancer, that is, OS may often be transformed into WCa if malignant change of IM occurs.

Cell Transformation, Neoplastic↗