ELECTRON MICROSCOPIC STUDY ON BENZENE INTOXICATED RAT BONE MARROW, WITH SPECIAL REFERENCE TO ITS RETICULOENDOTHELIAL STRUCTURE

Subcutaneous injection of benzene, 2 ml/kg daily is per formed for 21 days on male Wister rats. Cellular changes of the bone marrow are studied serially in the light and electron microscopic levels. As signs of cellular injury, swelling of the mitochondria, severe dilatation of the membrane system such as rough surfaced endoplasmic reticulum (rER), smooth surfaced endoplasmic reticulum (sER) and Golgi complexes, expansion of outer nuclear membrane, and swelling of the specific granules with clear content are revealed. Existence of membrane free ribosomes even in the mature leukocytes is also seen, and which phenomenon is considered as the maturation dissociation. Severely desintegrated haematopoietic cells are observed mostly caught within the phagocytic reticular cells. The mechanism through which bone marrow are injured by benzene is discussed. Reticulo-endothelial structure of the bone marrow in normal and benzene intoxicated animals is also studied. Reticulo-endothelial cells of the bone marrow are classified in to three types, among which special attention is paid to the subsinusoidally lying reticular cells. This particular cells show lower phagocytic activity, and often transform into the fat cells

MULTIPLE MYCOTIC ANEURYSMS OF INTERNAL CAROTID ARTERIES CAUSED BY OSTEOMYELITIS OF SKULL Report of a case

We presented a case with multiple mycotic aneurysms of the internal carotid arteries, which were located in the carotid canals and on the base of the skull and considered to be caused by osteomyelitis of the skull, namely extravascular in origin. Carotid angiography showed seven saccular aneurysms with an irregular contour, which were stalked or sessile, one in the right and two in the left at the cavernous portion and two at the canal portion on both sides. No literature was found on the study on the multiple mycotic aneurysms of extravascular origin, located at these portions. Based on the clinical course, the location and multiplicity of the aneurysms, we concluded that thrombophlebitis of the diploic veins and cavernous sinuses occurred secondary to the osteomyelitis of the skull and the microorganisms were transferred into the venous plexuses of the carotid canals by way of the venous system bilaterally, developing the aneurysms of extravascular origin

Mannitol infusion immediately after reperfusion suppresses the development of focal cortical infarction after temporary cerebral ischemia in gerbils

Previously we found that, after temporary cerebral ischemia, microvasculogenic secondary focal cerebral cortical ischemia occurred, caused by microvascular obstruction due to compression by swollen astrocytic end‐feet, resulting in focal infarction. Herein, we examined whether mannitol infusion immediately after restoration of blood flow could protect the cerebral cortex against the development of such an infarction. If so, the infusion of mannitol might improve the results of vascular reperfusion therapy. We selected stroke‐positive animals during the first 10 min after left carotid occlusion performed twice with a 5‐h interval, and allocated them into four groups: sham‐operated control, no‐treatment, mannitol‐infusion, and saline‐infusion groups. Light‐ and electron‐microscopic studies were performed on cerebral cortices of coronal sections prepared at the chiasmatic level, where the focal infarction develops abruptly in the area where disseminated selective neuronal necrosis is maturing. Measurements were performed to determine the following: (A) infarct size in HE‐stained specimens from all groups at 72 and 120 h after return of blood flow; (B) number of carbon‐black‐suspension‐perfused microvessels in the control and at 0.5, 3, 5, 8, 12 and 24 h in the no‐treatment and mannitol‐infusion groups; (C) area of astrocytic end‐feet; and (D) number of mitochondria in the astrocytic end‐feet in electron microscopic pictures taken at 5 h. The average decimal fraction area ratio of infarct size in the mannitol group was significantly reduced at 72 and 120 h, associated with an increased decimal fraction number ratio of carbon‐black‐suspension‐perfused microvessels at 3, 5 and 8 h, and a marked reduction in the size of the end‐feet at 5 h. Mannitol infusion performed immediately after restitution of blood flow following temporary cerebral ischemia remarkably reduced the size of the cerebral cortical focal infarction by decreasing the swelling of the end‐feet, thus preventing the microvascular compression and stasis and thereby microvasculogenic secondary focal cerebral ischemia.ArticleNEUROPATHOLOGY.34(4):360-369(2014)journal articl

Temporary focal cerebral ischemia results in swollen astrocytic end-feet that compress microvessels and lead to focal cortical infarction

We examined the mechanisms underlying the abrupt onset of the focal infarction in disseminated selective neuronal necrosis (DSNN) after temporary ischemia. Stroke-positive animals were selected according to their stroke-index score during the first 10 minutes after left carotid occlusion performed twice at a 5-hour interval. The animals were euthanized at various times after the second ischemia. Light- and electron-microscopical studies were performed chronologically on the coronal-cut surface of the cerebral cortex at the chiasmatic level, where focal infarction evolved in the maturing DSNN. We counted the number of neurons, astrocytes, and astrocytic processes (APs); measured the areas of end-feet and astrocytes; and counted the numbers of obstructed microvessels and carbon-black-suspension-perfused microvessels (CBSPm). Between 0.5 and 5 hours after ischemia, DSNN matured, with the numbers of degenerated and dead neurons increasing, and those of APs cut-ends decreasing; whereas the area of the end-feet and the numbers of obstructed microvessels increased and those of CBSPm decreased. At 12 and 24 hours after ischemia, the infarction evolved, with the area of end-feet and astrocytic number decreased; whereas the numbers of obstructed microvessels decreased and the CBSPm number increased. The focal infarction evolved by temporary microvascular obstruction because of compression by swollen end-feet