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S Matsuo

Publications and source records attributed to S Matsuo.

At least 145 records · Page 8Linked to original sources
PubMed1997

Neuronal apoptosis and necrosis following spinal cord ischemia in the rat.

We examined the characteristics of neuronal death induced by ischemia in the spinal cord. Spinal cord ischemia was induced in Long-Evans rats by occlusion of the descending aorta with a 2F Fogarty catheter for 20 min (model 1) or more limited aortic occlusion (15 min) coupled with blood volume reduction (model 2); rats were sacrificed 6 h-7 days later. The animals developed variable paraparesis in model 1 and reliable paraplegia in model 2. The extent of histopathological spinal cord damage, being maximal in the lumbar cord, correlated well with the severity of paraparesis. Two distinct types of spinal cord neuronal death were observed, consistent with necrosis and apoptosis. Neuronal necrosis was seen in gray matter laminae 3-7, characterized by the rapid (6 h) onset of eosinophilia on hematoxylin/eosin-stained sections, and gradual (1-7 days) development of eosinophilic ghosting. Although TUNEL positivity was present, disintegration of membranes and cytoplasmic organelles was seen under electron microscopy. Neuronal apoptosis was seen after 1-2 days in dorsal horn laminae 1-3, characterized by both TUNEL positivity and electron microscopic appearance of nuclear chromatin aggregation and the formation of apoptotic bodies. DNA extracted from the ischemic lumbar cord showed internucleosomal fragmentation (laddering) on gel electrophoresis. These data suggest that distinct spinal cord neuronal populations may undergo necrosis and apoptosis following transient ischemic insults.

Animals↗
PubMed1997

Protection of rat spinal cord from ischemia with dextrorphan and cycloheximide: effects on necrosis and apoptosis.

OBJECTIVE: We examined the characteristics of neuronal cell death after transient spinal cord ischemia in the rat and the effects of an N-methyl-D-aspartate antagonist, dextrorphan, and a protein synthesis inhibitor, cycloheximide. METHODS: Spinal cord ischemia was induced for 15 minutes in Long-Evans rats with use of a 2F Fogarty catheter, which was passed through the left carotid artery and occluded the descending aorta, combined with a blood volume reduction distal to the occlusion. The rats were killed after 1, 2, and 7 days. Other groups of rats were pretreated with dextrorphan (30 mg/kg, intraperitoneally, n = 7), cycloheximide (30 mg, intrathecally, n = 7), or vehicle (saline solution, n = 12) and killed after 2 days. RESULTS: This model reliably produced paraplegia and histopathologically distinct morphologic changes consistent with necrosis or apoptosis by light and electron microscopic criteria in different neuronal populations in the lumbar cord. Scattered necrotic neurons were seen in the intermediate gray matter (laminae 3 to 7) after 1, 2, and 7 days, whereas apoptotic neurons were seen in the dorsal horn laminae 1 to 3 after 1 and 2 days. Deoxyribonucleic acid extracted from lumbar cord showed internucleosomal fragmentation (laddering) on gel electrophoresis indicative of apoptosis. The severity of paraplegia in the rats treated with dextrorphan and cycloheximide was attenuated 1 day and 2 days after ischemia. The numbers of both necrotic and apoptotic neurons were markedly reduced in both dextrorphan- and cycloheximide-treated rats. CONCLUSIONS: The results suggest that both N-methyl-D-aspartate receptor-mediated excitotoxicity and apoptosis contribute to spinal cord neuronal death after ischemia and that pharmacologic treatments directed at blocking both of these processes may have therapeutic utility in reducing spinal cord ischemic injury.

Animals↗
PubMed1997

A case of a dialysis patient with sclerosing peritonitis successfully treated with corticosteroid therapy alone.

Sclerosing peritonitis (SCP) is a rare complication of peritoneal dialysis. Most of the patients with this serious complication have been treated in a symptomatic and conservative manner. Other patients have undergone risky surgical interventions. Recently it was reported that immunosuppressive therapy after renal transplantation was effective for this complication. A 56-year-old man developed sclerosing peritonitis 5 months after switching from peritoneal dialysis to hemodialysis because of ultrafiltration failure. The patient had ongoing inflammatory signs and symptoms, and corticosteroid therapy was commenced. His condition was dramatically improved within 1 week, and he is now well on an outpatient basis with the maintenance dosage of corticosteroid. This is the first report of a patient with peritoneal dialysis-related SCP who responded favorably to corticosteroid therapy alone.

Glucocorticoids↗
PubMed1997

Involucrin and SPRR are synthesized sequentially in differentiating cultured epidermal cells.

Epidermal keratinocytes form cornified cell envelopes during terminal differentiation. These envelopes are composed of several cross-linked molecules, including involucrin, loricrin, and SPRR. We have previously reported that involucrin is synthesized earlier in terminal differentiation than loricrin. To further elucidate the mechanisms of terminal differentiation, we have now examined the expression of the two differentiation markers, involucrin and SPRR, in cultured human epidermal keratinocytes. In confluent nonstratified cultures, many involucrin-immunoreactive cells were detected, but few SPRR1/3-positive cells. Double staining demonstrated that cells containing SPRR1/3 almost always contained involucrin, but involucrin was present in many cells that did not contain SPRR. Light and electron microscopic immunohistochemistry of a stratified culture demonstrated that lower cells (close to the basal layer) were occasionally involucrin-positive, but lacked SPRR1/3, whereas more superficial cells contained both involucrin and SPRR. We conclude that involucrin and SPRR are sequentially induced in this order during keratinocyte differentiation.

Adult↗
PubMed1997

[Rapid detection of Escherichia coli 0157:H7 in feces by latex agglutination and immunochromatographic assay].

The rapid detection method of Escherichia coli O157 in feces by using the latex agglutination test kit (Prolex; Pro Lab Diagnostics) and the immunochromatic assay kit (NOW EH. E. coli; Binax) was studied. 176 fecal samples obtained from 154 healthy men and 22 patients who had diarrhea by E. coli O157 were examined. Tellurite cefixim sorbitol MacConkey (TC-SMAC), Prolex and NOW were used for studies and also these were done after the enriched culture by tellurite cefixime vancomycin toriptic soy broth (TCV-TSB). In the direct inoculation, 5 (23%) of 22 samples, 7 (32%) and 9 (41%), and after the enriched culture, 7 (32%), 10 (46%) and 11 (50%) were positive by culture, Prolex and NOW, respectively. On the other hand, 154 samples from healthy men were all negative in the direct inoculation, but in the enriched culture, 7 of 40 (18%) were positive by NOW. These samples were negative by boiled (100 degrees C, 15 minutes). Our results indicated that Prolex and NOW were useful for accurate and rapid diagnosis of E. coli O157 enteritis, and more sensitivity results were obtained with the enrichment broth.

Chromatography↗
PubMed1997

[Rapid detection of Shiga-like toxin gene in feces with rapid-cycle polymerase chain reaction].

A rapid detection for Shiga-like toxin in feces was developed with the nucleic acid extraction method by silicondioxide-guanidine thiothianate and rapid-cycle polymerase chain reaction by RapidCycler (model 1002; Idaho Technology, RC-PCR here after). Twenty-two fecal samples that were collected from patients with diarrhoea caused by E. coli O157:H7 and frozen for 6 months were examined directly by RC-PCR, conventional PCR assay using by ThermalCycler 9600-R (Roche, TC-PCR here after) and by the culture method using tellurite-cefixime sorbitol MacConkey (direct method). These examinations were done also after being injected into TCV-TSB and incutated at 35 degrees C overnight (indirect method). The sensitivity of RC-PCR and TC-PCR using a diluted suspension of broth enriched at 35 degrees C overnight were 4.1 pg and 410 fg, respectively. Positive results in the direct method were obtained in 7 for RC-PCR, 10 for TC-PCR and 5 for culture. Positive results on indirect assay were obtained in 9 for RC-PCR, 9 for TC-PCR and 7 for culture. It was demonstrated that the RC-PCR assay was able to detect Shiga-like toxin gene in feces in less than 90 minutes after being received at the laboratory.

Bacterial Toxins↗
PubMed1997

[Significance of Aspergillus fumigatus rDNA detected by polymerase chain reaction in diagnosis of pulmonary aspergillosis].

We have studied the clinical significance of Aspergillus fumigatus rDNA detected by polymerase chain reaction (PCR) for diagnosing aspergillosis. For this purpose, a specific and sensitive PCR assay was developed to amplify the 26S rDNA/intergenic spacer region of A. fumigatus. Control experiments showed that the set of primers used was capable of amplifying A. fumigatus DNA specifically and that the DNA amount of detection limit was 1 pg. Eighteen samples from 13 patients with aspergillosis and 36 samples from 24 patients without aspergillosis were tested by means of PCR, culture, latex agglutination test for galactomannan antigen and double gel diffusion assay for precipitation of antibodies to A. fumigatus. PCR showed positive test in 8 among 13 patients with pulmonary aspergillosis. On the other hand, culture of samples detected A. fumigatus in 6 patients. Galactomannan antigen and antibodies specific to A. fumigatus were positive in 2 and 6 patients respectively. These results indicated that PCR is the most sensitive among these 4 methods. Five patients showed negative PCR test despite of having pulmonary aspergillosis. Two of these patients were proved to have aspergillosis caused by A. flavus and A. niger. On the other hand, galactomannan antigen and A. fumigatus antibody were positive in one and 2 patients, respectively. PCR was positive in 2 out of 24 patients diagnosed as not having aspergillosis: one patient had diagnosis of acute bronchitis, but she showed positive culture of A. fumigatus. The other patient had diagnosis of lobar pneumonia, because any pathogens were not detected before PCR assay. The PCR assay we developed is a useful method for diagnosing aspergillosis caused by A. fumigatus as compared with other conventional methods.

Aspergillosis↗
PubMed1997

The role of complement in the pathogenesis of tubulointerstitial lesions in rat mesangial proliferative glomerulonephritis.

Persistent proteinuria and tubulointerstitial lesions are important signs of progressive renal disease. The purpose of this study was to assess the role of complement in the development of tubulointerstitial lesions in rats with proteinuria due to primary glomerulonephritis. Mesangial proliferative glomerulonephritis was induced in mononephrectomized rats by intravenous injection of monoclonal antibody (mAb) 1-22-3 (Clin Exp Immunol 102: 181-185, 1995). As early as 24 h after the injection, proteinuria became evident, persisted throughout the observation period, and was associated with mesangial cell proliferation and tubulointerstitial lesions when examined at 7 and 14 d after mAb administration. Deposition of rat C3 and C5b-9 was observed at the luminal surface of proximal tubules and in cellular debris present in the tubular lumen (group I). Rats injected with mAb 1-22-3 and depleted of complement by injections of cobra venom factor starting at day 3 developed glomerulonephritis and proteinuria comparable to rats of group I, but complement deposition in the tubules and the tubulointerstitial lesions were markedly reduced (group II). Rats in group III were injected with mAb and, from day 3, with soluble complement receptor type 1, which became detectable at the luminal surface of proximal tubules and in the urine. Deposition of C5b-9 in tubular cells was not detectable, and the severity of tubulointerstitial lesions was reduced compared with rats in group I. These results indicate that, in this model of primary mesangial proliferative glomerulonephritis with proteinuria, the development of tubulointerstitial lesions is associated with activation of serum complement at the level of tubular brush border, and tubulointerstitial lesions can be reduced by inhibition of complement activity.

Animals↗
PubMed1997

Venous hemangioma. An immunohistochemical and ultrastructural study.

We present a case of (arterio) venous hemangioma of 15 years' duration, which arose in a 43-year-old Japanese man on his right infraorbital area. Elastic stain and electron microscopy did not show any evidence for arterial components. Some thick-walled vessels showed mucin deposition and wide intercellular spaces between smooth muscle cells. Several glomoid cells were encountered among these cells. Although the histogenesis of (arterio) venous hemangioma is controversial, the presence of glomoid cells and the mucin deposition, which is occasionally detected in glomus tumors, suggest the relation of this tumor to the Suquet-Hoyer canal.

Actins↗
PubMed1997

Compound heterozygosity for a nonsense mutation and a splice site mutation in the type VII collagen gene (COL7A1) in recessive dystrophic epidermolysis bullosa.

Mutations in the type VII collagen gene (COL7A1) have recently been established as the molecular basis of the inherited blistering skin disorder, dystrophic epidermolysis bullosa. We report a novel combination of COL7A1 mutations in a Japanese patient with an autosomal recessive form of dystrophic epidermolysis bullosa. Clinically, the patient had suffered from generalized trauma-induced blistering since the first week of life loss of most finger- and toenails, esophageal stenosis and partial fusion of the fingers and toes. Immunofluorescence microscopy of the dermal-epidermal junction in the patient's skin revealed reduced intensity of staining with an anti-type VII collagen antibody. Transmission electron microscopy showed only a few thin, poorly formed anchoring fibrils. The patient was a compound heterozygote for a nonsense mutation on one COL7A1 allele and a donor splice site mutation on the other allele. The mutations were identified by PCR amplification of genomic DNA, heteroduplex analysis, and nucleotide sequencing, and verified by restriction endonuclease digestion. Reverse transcriptase-PCR and sequencing of cDNA from the patient's cultured keratinocyte mRNA showed evidence of aberrant splicing resulting from the donor splice site mutation, due to activation of a cryptic intronic splice site that leads to a frameshift and a downstream premature termination codon. Knowledge of the genetic lesions in this patient is helpful in elucidating the molecular consequences of COL7A1 mutations in dystrophic epidermolysis bullosa and in providing information about the fundamental mechanisms involved in maintaining adhesion between the epidermis and the dermis.

Adult↗
PubMed1997

Loss of heterozygosity at the N-ras locus in 7,12-dimethylbenz[a] anthracene-induced rat leukemia.

The 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat leukemia model enables scientists to analyze cells altered by carcinogens at various stages of leukemogenesis. We have reported that a consistent type of point mutation. A-->T transversion at the second base in codon 61 of the N-ras gene, was present in this leukemia and that this mutation appeared in bone marrow cells as early as 48 h after a single dose of DMBA. In addition, two leukemia cell lines with the N-ras mutation had no wild-type N-ras allele. Therefore, we examined whether these alterations were essential to the DMBA-induced leukemias. In the study reported here, we confirmed the occurrence of this N-ras mutation in 18 (86%) of 21 primary leukemias and loss of the N-ras wild-type allele in 12 (67%) of 18 leukemias with the mutated N-ras. By using microsatellite markers on chromosome 2, loss of heterozygosity (LOH) at the N-ras locus was observed in eight leukemias, all of which were shown to have lost the wild-type N-ras allele by mutant-allele-specific amplification. These results suggest that LOH related to loss of the wild-type N-ras allele reproducibly occurs in leukemias with the N-ras mutation. Considering the timing of the N-ras mutation and LOH, it is likely that the N-ras mutation is induced early, and cells that have lost the wild-type N-ras allele seem to develop into leukemia. We believe that this system provides a suitable model for studying a series of genetic alterations from the earliest stage of carcinogenesis that cannot be approached in human malignancies.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

The specific N-ras mutation in rat 7,12-dimethylbenz[a]anthracene (DMBA)-induced leukemia.

Intravenous injections of 7,12-dimethylbenz[a]anthracene (DMBA) induce erythroblastic leukemia (erythroleukemia) with #2 trisomy and Long #2 in Long-Evans rats. Recently, a consistent type of mutation, A to T transversion in codon 61 of N-ras gene, was found in all of 6 cultured leukemia cell lines and 13 primary leukemias induced by DMBA using polymerase chain reaction (PCR) and direct sequencing. On the contrary, no mutation was observed in Ha- and Ki-ras genes in these leukemias. The consistent occurrence of the above N-ras mutation in DMBA-induced leukemias indicates that N-ras gene plays an important role in DMBA-leukemogenesis. Mutations in ras genes generally takes place during the initiation stage of carcinogenesis because they often appear in the premalignant stage of tumors. In order to detect the N-ras mutation in an early stage of leukemogenesis, we designed the mutant-allele-specific amplification (MASA) method to detect the mutation in bone marrow (BM) cells of DMBA-treated rats. The MASA method was sensitive enough to detect one mutant cell mixed in 10(6) normal cells. Using this method, the N-ras mutation was found in BM cells 2 days after single DMBA injection and thereafter throughout the preleukemic stage. These results suggest that the N-ras mutation is an earliest event in DMBA-induced leukemogenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

Role of complement in acute tubulointerstitial injury of rats with aminonucleoside nephrosis.

The present work was designed to elucidate the in vivo role of complement in the proteinuria-associated tubulointerstitial injury. Rats were intravenously injected with puromycin aminonucleoside, and massive proteinuria was observed within 5 days. Prominent tubulointerstitial injury characterized by proximal tubular degeneration, tubular dilatation, and leukocyte infiltration were observed 7 days after injection. C3 and C5b-9 were observed in the luminal side of proximal tubular cells. Renal function, assessed by inulin and para-aminohippurate clearance, was significantly decreased. To-assess the role of complement in this model, rats were injected with either cobra venom factor or soluble recombinant human complement receptor type 1 starting at day 3. These manipulations significantly improved tubulointerstitial pathology and para-aminohippurate clearance without affecting the degree of proteinuria. Deposition of C3 and C5b-9 was not detected in the kidney of rats depleted of complement by cobra venom factor. In rats treated with soluble complement receptor, C3 was still detected in the tubules, but deposition of C5b-9 was not observed. Soluble complement receptor was detected at the site of C3 deposition and in the urine. These data strongly suggest that complement plays a pivotal role in proteinuria-associated tubulointerstitial injury and that systemic complement depletion or inhibition of complement in the tubular lumen may diminish the tubulointerstitial damage.

Animals↗
PubMed1997

[One of the procedure for quality control].

It goes without saying that assurance of quality control in a clinical laboratory is the most essential factor which can be easily influenced by how medical support is practiced. In recent years, the appreciation of a narrow sense of quality control in analysis has become the central focus. These days, however, we are seeing that reports of examinations have been submitted to doctor with mistake which come in stages from the patient's materials for examinations to making the report. We have not only cleared up the cause but we have also checked our work on these kinds of faulty reports and thought of measures for mistake in putting them to practical use. Moreover, as we have developed the laboratory system with full-time staff in our institution, we have been able to take advantage of this kind of problem to accomplish our laboratory work. To avoid a mistake, comprehension and collaboration of MD and co-medical staff is required. To ensure this end, it is also required that we usually communicate with an MD and nurse. It is possible that our carelessness cause us to make mistake in our work such as bleeding examination after usual hours. These examinations are based on a basic line of sharing this sort of work with all staff. In future, we aim for laboratory examination to permeate not only in a laboratory but also in the whole hospital.

Humans↗
PubMed1997

Two optimal prefilter cutoff frequencies needed for SPECT images of myocardial perfusion in a one-day protocol.

OBJECTIVE: The purpose of this study was to determine if cutoff frequencies of two-dimensional Butterworth filters need to be changed, depending upon the amount of radiopharmaceutical administered in one-day protocols for reconstructing SPECT images of myocardial perfusion. METHODS: A scintilation camera and a phantom were used with 2.2 MBq and 10.6 MBq 99mTc. These activities corresponded to the approximate amounts used in our one-day myocardial perfusion imaging protocol. The projection data were collected in 30 positions spread over 180 degrees. Thirty- and 150-sec acquisitions per position were performed to obtain the study and the high-quality reference images. Thirteen cutoff frequencies of the filter were used to reconstruct the SPECT images. Optimal cutoff frequencies were determined by visual assessment and by calculating the normalized mean square error (n.m.s.e). These results were then compared. The same protocol was used to image three volunteers with no heart disease and the images were evaluated visually. RESULTS: In the phantom study, the optimal cutoff frequencies were 0.225 cycles/pixel for 2.2 MBq, and 0.275 cycles/pixel and 0.25 cycles/pixel for 10.6 MBq by visual inspection, and were 0.225 cycles/pixel and 0.275 cycles/pixel by calculating the n.m.s.e., respectively. In the patient study, the lower cutoff frequency of 0.20 cycles/pixel was optimal for the exercise study (low dose), while the higher cutoff frequencies of 0.275 cycles/pixel was optimal for the resting study (high dose). CONCLUSION: The optimal cutoff frequencies differed for the two activity levels. Cutoff frequencies should be changed according to the amounts of radiopharmaceuticals used for the first and the second examinations in one-day protocols.

Heart↗