Electron microscopic observation of the gunshot wounds of the truncus cerebri / 中国法医学杂志

Objective To study the ultrastructural changes of gunshot wounds at the brain stem and the cause of the death. Method A case died of the head injury and two cases died of gunshot wounds of the brain stem were studied. Brain stem tissues were taken 25 min after death. Tissue blocks from the tegmentum of the midbrain and the pons as well as the gray matter of the medulla oblongata in the deep portion of the base of the fourth ventricle were taken and were examined with ultramicroscopy and scanning electron microscopy. Results (1) The gunshot wound injuries inside the brain including burn and injuries caused by punch and pressure; (2) Although the primary gunshot wounds were located at the midbrain, the pathological changes extended to the whole brain stem; (3)The injuries of the axons and the nerve cells were more severe and extensive than those of the glia fibers. (4)The changes of the burn included condensation and degeneration of the myelin sheath and axonal cytoplasm, especially the mitochondria as well as edema of the myelin sheath and the axonal cytoplasm. The punch and pressure injuries included the torsion, deformation, fusion, compression, breach, torn and displacement of the axons with loss of cytoplasm as well as the deviation of mitochondria, micro ?neuro - fibrils and micro - tubules in the axons. Conclusion The severe and extensive injuries of the axons of nerve fibers in the brain stem might play an important role in the cause of death of gunshot.

Ultrastructural changes of fat-storing cells in experimental hepatic fibrosis / 영남의대학술지

Hepatic fibrosis was induced in Sprague-Dawley rate to evaluate the ultrastructural changes of fat-storing cells (Ito cells). For experimental induction of liver fibrosis, the rats were administered intraperitoneally with 0.5 ml of 50% Ccl4 solution per Kg body weight, twice weekly for 12 weeks. The rats were sacrificed every week. The liver tissues were examined under light and electron microscopes. And the immunohistochemical study of desmin was also performed. The results were summarized as follows: Light microscopic findings: The cellular infiltrations was inflammatory cells and Kupffer cells developed from 1 week after Ccl4 injection, and were the most severe in 4 weeks. The strong immunoreactivity for desmin was also evident in 4 weeks. The centrilobular necrosis and fibrosis developed from 2 weeks after injection, and the necrosis persisted until 8 weeks. The progress of fibrosis was accompanied by decreases in cellular infiltration and reactivity for desmin, and increased gradual nodular formation was also observed. The cirrhosis was developed after 10 weeks. Electron microscopic findings: An increase in number of fat-storing cells was observed from 1 week after injection. Transitional cells characterized by a depletion of lipid droplets and a hypertrophy of the rER appeared after 2 weeks. The number of transitional cells with abundant collagen fibers in the extracellular spaces increased in 4 weeks. With progression of fibrosis the number of fat-strong cells decreased and proliferating fibroblasts with dilated rER were observed. According to these results it was revealed that there was an apparent transition from fatstrong cells to transitional cells and to fibroblasts. These cells had a few similar characteristics and may belong to the same cell population. Thus it was suggested that fatstrong cells might play an important role in hepatic fibrosis.

Effect of Intra-and Extrahepatic Cholestasis on the Function and Morphology of the Rat Liver

The cholestasis are defined as blockade or secretory distrubance of bile and appearance of bile in hepatocytes, Kupffer cells and biliary passages, usually associated with dilated bile canaliculi. Intra-and extraheptic cholestasis were induced by 17-ethinyl estradiol, or chlorpromazine hydrochloride and by ligation of bile duct to investigate the mechanism of the hepatic injury, ultrastructural changes of liver and alterations of liver function. The results obtained were as follows. 1) Functional and histological changes of intra-and extrahepatic cholestasis differed in various experimental groups. The liver weight is increased in 17-ethinyl estradiol treated group and ligation of bile duct group (5.6+/-0.15, P<0.001, 5.3+/-0.19 gm/100 gm body weight, P<0.001). The common features of intra-and extrahepatic cholestasis were double membrane bounded amorphous vesicular material infiltrations in the cytoplasm of hepatocyte, partial loss of microvilli of bile canaliculi, anf focal thickening of pericanalicular ectoplasm on electron microscopy. 2) Intrahepatic cholestasis induced by 17-ethinyl estradiol show significantly increased serum level of alkaline phosphatase and total bile aicd (134.0+/-16.82 IU/L, 29.5+/-4.68 umol/l). Kupffer cell proliferation and focal cytoplasmic degradation with myelin figures are characteristic features on electron microscopy. Chlorpromazine hydrochloride induced intrahepatic cholestasis show increased serum level of AST, ALT, Cholesterol and bilirubin (156.9+/-11.32, 49.0+/-2.83 IU/L, 59.3+/-6.73 mg/dl, 1.8+/-.043 mg/dl). Inflammatory cell infiltration, chiefly lymphocytes and esoinophils are seen in periportal area. Prominent vesiculation and vacuolations of smooth endoplasmic reticulum are characteristic feature on electron microscopy. 3) Extrahepatic cholestasis induced by ligation of bile duct show increase serum level of AST, ALT, GGT, cholesterol, total bile acid, and bilirubin (290.2+/-50.24, 171.5+/-47.17, 159.3+/-24.54, 33.7+/-1.47 IU/L, 86.6+/-9.18 mg/dl, 246.6+/-27.34 umol/l, 13.9+/-0.83 mg/dl). Light microscopically, morphologic alterations are feathery degeneration of hepatocytes, proliferation of bile ducts, bile infarct and prominent intracytoplasmic lipid droplets. Electron microscopically, electron dense acidophilic body, bile casts and complete loss of microvilli are seen in dilated bile canaliculi. Also noted are hypertrophy of cannalicular ectoplasm. Finely granular materials are infiltrated in degenerative cytoplasm.

Ultrastructural Changes of Hair Follicles Induced by Cyclophosphamide in the Rat / 대한피부과학회지

Authors studied the effects of cyciophosphamide, a potent inhibitor of nucleoprotein synthesis, to ivestigate the morphologic evidence of destructive actions to the hair. follicles. Sprague-Dawley rats were received 4 mg/kg of eyclophosphamide for 1 to 6 weeks, intraperitoneally, and examined light and electron microscopically. Light microscopically, distortion and constriction of the hair shafts, diminished diameter of the hair bulbs, and atrophy of. the hair matri.x were developed from 1 week. which were more prominent in second weeks and they were progressed after that time. Hairs were frequently fractured due to constriction of the hair shaf ts. Electron microscopically, cells of the hair pulp were decreased in number, and cells of the hair matrix were atrophied, Degenerative changes of the cellular organelles participating in grovth. and development of the hairs were noted, such as disordered formation of tricholyaline granules, diffuse atrophy and increased electron density of the inner root sheath, and loss of the glycogen and intercellular edema of the outer root sheath, but basal cells of the matrix showed minor changes relatively. From the above results, cyclophosphamide may specifically alter the matrix cells of the hair follicles and induces anagen hair losses, which may be reversible at a small dosage when the drug is discontinued, because basal cells of the matrix ahow rninor changes.

Ultrastructural Changes in Intracranial Artery following Experimentally induced Subarachnoid Hemorrhage

Studies of the pathophysiology of intracranial artery following vasospasm remains yet incomplete. The present investigation was undertaken for the purpose of elucidating ultrastructural changes in the cerebral arterial wall sequentially from 1 hour to 24 hours following subarachnoid hemorrhage. Experimental vasospasm was induced by injecting autogenous blood into the cisterna magna of cats. The following observations were made : 1) One hour after the induction of subarachnoid hemorrhage, endothelial cells in the intima became more round and their cellular surface was markedly corrugated, these changes culminated at 7 to 24 hours with intimal thickening(due to subendothelial tissue). 2) In the media, the smooth muscle cells were most consistently and severly affected showing degeneration of mitochondria and vacuoles containing fine particles. 3) Twelve hours following SAH, some endothelial cells in the intima were displaced or seemed to have partially broken apart from the adjoining cells. On the basis of the above findings, it was concluded that the ultrastructural changes in the cerebral arterial wall was observed after the induction of SAH with normal cat's blood occurred as a consequence of vasospasm of the intracranial arteries.