Biomedical subjects

T Koide

Publications and source records attributed to T Koide.

490 records · Page 28Linked to original sources

PubMedDate not supplied

Cystic lymphangioma of the gall-bladder: a case report.

Intra-abdominal cystic lymphangiomas are rare lesions that can be difficult to diagnose. We present a report of a patient with a giant multilocular cystic lesion in the abdomen. Ultrasonography and computed tomography scans of the abdomen revealed that the cyst had originated in the gall-bladder fossa. There was some calcification and thickening of the cyst wall. Endoscopic retrograde cholangiopancreatography demonstrated a medially deviated common bile duct, an elongated cystic duct and an inferior compressed gallbladder. There was no apparent communication between the cyst and the biliary tract; however, an abdominal angiogram revealed that the lesion was supplied by a branch of the cystic artery. Histological findings obtained intra-operatively were consistent with a cystic lymphangioma. Its characteristic histology was observed in the subserous layer of the gall-bladder. This case is a rare instance of a cystic lymphangioma originating in the gall-bladder.

Adult↗

PubMedDate not supplied

Ischemic brain edema following occlusion of the middle cerebral artery in the rat. I: The time courses of the brain water, sodium and potassium contents and blood-brain barrier permeability to 125I-albumin.

The present study was undertaken to analyze the roles of brain cations and of the blood-brain barrier (BBB) to albumin in the development of ischemic brain edema. Using the rat middle cerebral artery (MCA) occlusion model, changes in the brain water, sodium, and potassium contents were followed for a period of seven days. The permeability of the BBB to proteins was also followed by 125I-albumin transfer from the blood into the brain. A significant edema developed as early as three hours after MCA occlusion. This progressed rapidly to reach a maximum on the third day, gradually regressing thereafter. The increase in the brain water contents showed a parallel time course to the increase in the sodium and decrease in the potassium contents. A significant increase in the BBB permeability to albumin occurred 72 hours after MCA occlusion. However, there was no correlation between the brain water content and BBB permeability to albumin in the hemispheres studied 72 hours after MCA occlusion. The correlation between the brain water and sodium contents was not clear during the first six hours, but became highly significant thereafter. The data suggest that an increase in the BBB permeability to sodium occurred 12-48 hours after MCA occlusion, which, together with an antecedent intracellular shift of sodium, resulted in a massive influx of water and sodium into the brain. The BBB permeability change to sodium, not to proteins, seems to play a predominant role in the pathogenesis underlying ischemic brain edema.

Animals↗

PubMedDate not supplied

Ischemic brain edema following occlusion of the middle cerebral artery in the rat. II: Alteration of the eicosanoid synthesis profile of brain microvessels.

Using the rat middle cerebral artery occlusion model, alterations in the eicosanoid synthetic capacity of brain microvessels following ischemia were studied by radiochromatography. Brain microvessels of normal rats predominantly produced hydroxyacids with relatively small amounts of PGD2 and PGE2 from exogenous arachidonic acid. Confirmation that hydroxyacids and prostaglandins were products respectively of lipoxygenase(s) and cyclooxygenase was obtained by experiments using indomethacin and eicosatetraynoic acid. The eicosanoid synthetic capacity of the brain microvessel, especially of hydroxyacids, was significantly enhanced 24 and 72 hours after the onset of ischemia. Because this is the phase of maximum edema in the present model, enhanced eicosanoid production in the brain microvessel may be involved in the mechanisms that underly ischemic brain edema.

Animals↗

PubMedDate not supplied

Quality control of protein C: protein C synthesized in the presence of warfarin is selectively degraded in the endoplasmic reticulum.

Warfarin is known to disrupt the microsomal vitamin K cycle, which results in a decrease of the plasma level of protein C, an anticoagulant factor, as well as some other vitamin K-dependent coagulation factors. We examined the effect of warfarin on secretion of recombinant protein C expressed in human kidney 293 or BHK cells. In transient expression, warfarin caused a two- to four-fold decrease in the quantity of protein C secreted, compared to findings with vitamin K-treated cells. Pulse-chase experiments using stable cells showed that, although recombinant protein C was secreted in the presence of vitamin K, the decrease in total amount of the radioactivity in the warfarin-treated cells suggested intracellular degradation. This degradation depended on the concentration of warfarin and was not inhibited by an endoplasmic reticulum (ER)-Golgi transport inhibitor or by lysosomotropic inhibitors. Thus, protein C synthesized in the presence of warfarin is selectively degraded and the degradation occurs in a pre-Golgi, nonlysosomal compartment. Among the protease inhibitors tested, N-acetyl-Leu-Leu-methioninal and N-acetyl-Leu-Leu-norleucinal blocked the degradation of protein C synthesized in the presence of warfarin and the protein C accumulated intracellularly, in a dose-dependent manner. Both inhibitors, however, did not disturb the secretion of protein C in the vitamin K-treated cells. Thus, a cysteine protease(s) appeared to be responsible for the degradation. These results suggest that protein C synthesized in the presence of warfarin was selectively degraded by a cysteine protease(g) in the ER through a "quality control" mechanism.

Biodegradation, Environmental↗