[Z-line alteration in plasmocid-induced myopathy].
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Biomedical subjects
Publications and source records attributed to H Nakase.
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Acute muscle necrosis was induced in rats by intramuscular injection of plasmocid, a known myotoxic agent. A single injection of 5 mg/ml plasmocid produced massive fiber necrosis with extensive phagocytosis. Plasmocid administration led to a preferential decrease of alpha-actinin with preservation of other structural proteins within 3 h after injection, and large increases (2-7-fold) in the activities of acid hydrolases, cathepsins B and L, cathepsin D and alpha-galactosidase within 48 h after injection. The plasmocid-induced stimulation of alpha-actinin loss seen at 3 h, when no increases of acid hydrolases occurred, could be inhibited by a cysteine protease inhibitor, Ep-475 (E-64-c), and EGTA. On the other hand, increased lysosomal enzyme activity seemed to have a close correlation with the appearance of invading mononuclear cells, probably macrophages, and not muscle lysosomes. These observations suggest that a two step mechanism of protein degradation (nonlysosomal and lysosomal processes) possibly occurs in plasmocid-induced muscle degradation and macrophages can serve as a main endogenous reservoir of proteases in pathological states.
A single direct injection of a local anesthetic, 0.5% bupivacaine hydrochloride (BPVC) (Marcaine), into rat soleus and extensor digitorum longus (EDL) muscles produced massive fiber necrosis with extensive phagocytosis followed by rapid regeneration, predominantly in the soleus. Since the sarcoplasmic reticulum (SR) was functionally disturbed by BPVC administration as confirmed by an in vitro study, the sarcolemmal lysis seen in the early phase of degeneration was not assumed to simply result from direct damage to the plasma membrane caused by BPVC. The extracellular fluid containing a high concentration of calcium (Ca) ions then permeated into the sarcoplasm through the defective membrane resulting in hyper-contracted myofibrils. Selective damage to the Z-line, an early sign of muscle degeneration, was shown by electron microscopy and SDS gel electrophoresis (preferential loss of alpha-actinin). Administration of leupeptin, a thiol protease inhibitor, proved to be ineffective in inhibiting the necrotic process, because the BPVC induced muscle fiber breakdown was probably too acute and fulminant to demonstrate the inhibitory effect upon the degenerative process. Well preserved satellite cells, peripheral nerves, and acetylcholinesterase activity, and the absence of fibrous tissue proliferation in this system may be responsible for the extremely rapid regeneration with complete muscle fiber type differentiation. Since the sequence of fiber breakdown induced by BPVC administration was similar to that of progressive muscular dystrophy, this chemical will be one of the most useful tools for studying the pathophysiology of fiber necrosis and regeneration in diseased muscle.
Experimental acute degenerative changes in skeletal muscle accompanied by a drastic increase in cathepsins B&L were induced in rats by intramuscular injection of a local anesthetic, bupivacaine. Cathepsins B&L have been implicated in the rapid disappearance of muscle fibers. Degenerating muscle showed a spotty fluorescence when stained with antibodies against cathepsin B, indicating that the increased cathepsin B did not originate from the muscle itself, but from invading phagocytes. We report here results showing that cathepsin B of nonmuscle cell origin is involved in the breakdown of myofibrillar proteins in acute bupivacaine-induced muscle degeneration.
Progressive multifocal leukoencephalopathy developed in a 70-year-old man with hepatoma treated with oncostatica. The brain showed multiple demyelinated lesions in the upper half of the cerebral white matter. The lesions consisted of proliferation of hypertrophied astrocytes and glial cells with abnormally large nuclei. These nuclei were shown to be filled with DNA by DAPI staining and reacted specifically with anti-JC antibody by immunofluorescence. Papova-like virions were confirmed on both the sections and negatively-stained brain extract under electron microscopy. The sixteen cases so far reported in Japan were reviewed.
Most ependymal cysts occur intracerebrally, with a few cases situated in the subarachnoid space. The cerebellopontine angle is a common site for arachnoid cysts, but a very rare site for ependymal cysts. A case is described here of a large ependymal cyst in the cerebellopontine angle. A 12-year-old girl with left hearing disturbance was admitted. CT and MRI revealed a cystic tumor in the left cerebellopontine angle. At operation, we obtained a discrete thin-walled cyst which had arisen from a continuation of the choroid plexus of the lateral foramen of Luschka, which had no connection with the arachnoid. The cyst proved to be an ependymal cyst.
Germ cell tumors originating in the posterior fossa are very rare. Described herein is a case of primary germ cell tumor (yolk sac tumor) found in the cerebellar vermis. A 5-year-old boy who complained of headache was admitted. CT and MRI revealed a tumor with diffuse enhancement by contrast medium in the right cerebellar vermis. Total removal was performed and a diagnosis of medulloblastoma or ependymoma was suspected. However, the tumor proved to be a yolk sac tumor with embryonal carcinomatous components from histological findings. Abnormally high levels of alpha-fetoprotein were found in blood and cerebrospinal fluid. Extensive examination indicated that the intracranial lesion had not metastasized from a primary extracranial tumor.
BACKGROUND AND AIM: A group of the proinflammatory and chemotactic cytokines (chemokines) has been considered as an important factor in the pathomechanism of different bacterial diseases, among them the common Helicobacter pylori infection. Experimental results obtained with gastric biopsy samples of H. pylori positive patients, and with H. pylori infected tumor originated gastric cell lines indicated that these cytokines have essential roles in the development and maintenance of the immune response and inflammation of the gastric mucosa during H. pylori infection. Although the mRNA expression was shown in these biopsy samples and cell lines, it is not yet proved that the normal gastric mucosal epithelial cells themselves express these cytokines. The establishment of a gastric surface mucous cell line with non-tumor origin (GSM06), and the usage of Helicobacter felis as a model of the classic H. pylori infection gave us the possibility to check this question. MATERIALS AND METHODS: in this study GSM06 cells were infected with different numbers (10(5), 10(6), 10(7), 10(8), 10(9) bacterium/ml medium) of H. felis for two different time periods (2, 4 h). Cells treated with medium only were used as control. Then the mRNA expression of the following cytokines was measured by RT-PCR method in the GSM06 cells: proinflammatory cytokine IL1-beta, and chemokine RANTES, eotaxin, MCP-1, MIP1-alpha and MIP1-beta. RESULTS: we found that neither mRNA of the investigated cytokines was expressed constitutively, however the GSM06 cells expressed the mRNA of each cytokine during H. felis infection. CONCLUSION: our results prove that normal gastric surface mucous epithelial cells express immunologically active peptides during H. felis infection. We may suppose that the epithelial cells of the gastric mucosa contribute to the immune response and inflammation by expressing proinflammatory (IL1-beta) and chemotactic (RANTES, eotaxin, MCP-1, MIP1-alpha and beta) cytokines during H. pylori infection in human.
The authors report 11 cases who underwent reoperations upon for recurrent aneurysms. The initial operations were performed on average 10.1 years earlier for subarachnoid hemorrhage (SAH). The patients' mean age at the first surgery was 39.7 years. The locations were 9 internal carotid (IC)-posterior communicating artery (PC) and 2 anterior communicating artery (A-com) aneurysms. A residual aneurysmal neck after the first operation was observed in 3 of 10 cases confirmed by postoperative angiography. The primitive-type PC artery was seen in 8 of 9 recurrent IC-PC aneurysms. The recurrent manifestations were SAH in 9 cases. Clipping operations were conducted in 10 and ligation of the IC artery together with extracranial-intracranial bypass in 1 large IC-PC aneurysm. The present study demonstrated two risk factors for aneurysm recurrence, namely, young age and IC-PC aneurysms with a primitive-type PC. Furthermore, direct operation for recurrent aneurysm is often embarrassing due to adhesions to the surrounding tissue as a sequela of the previous operation, hence understanding of the anatomical correlation between the old clip and the recurrent portion is important.
A major limitation of laser-Doppler (LD) flowmetry, which enables noninvasive and continuous recording of tissue perfusion, is its inability to evaluate the absolute cerebral blood flow (CBF). Using a computer-controlled micromanipulator, the LD scanning technique provides information on the brain microcirculation in many different locations, information which is not available from a single stationary probe. The purpose of the current study was to examine whether LD scanning estimates can be calibrated for the absolute CBF by comparing LD scanning with the hydrogen clearance (HC) method. In Wistar rats (n = 31) including old rats (122-123 weeks old, n = 8), the CBF was altered using the global ischemia model by bilateral carotid artery occlusion coupled with hypobaric hypotension. The CBF was determined simultaneously by the LD scanning technique and HC at each mean arterial blood pressure step, and the correlation of CBF between the two techniques was analyzed. CBF measured by LD scanning was expressed as LD units. Absolute CBF values obtained by methods were correlated (r = 0.87), and the formula to calibrate absolute CBF values from LD units was y = 1.8x - 0.6. On the other hand, in old rats the formula to calibrate the absolute values was different (y = 1.3x + 8.3, r = 0.85). The results suggest that CBF data obtained by LD scanning could be calibrated into absolute blood flow values in particular circumstances, and that LD scanning could compensate in part for the weakness of LD flowmetry.
We reported a 58-year-old man with facioscapulohumeral muscular dystrophy who had acute compression neuropathy of the sciatic nerve after prolonged sitting position. MRI and percutaneous electric stimulation studies were usefull for the diagnosis. Gd-DTPA T1-weighted MRI images showed the enhanced right sciatic nerve at the level of gluteus maximus muscle. An evoked potential study by a percutaneous electric stimulation revealed evidence of a conduction block at the same level. After methylprednisolone pulse therapy, muscle weakness and sensory disturbance improved. Acute compression neuropathy of the sciatic nerve may be seen as a complication in the advanced stage of (FSH) muscular dystrophy.
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