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Biomedical subjects

T Murase

Publications and source records attributed to T Murase.

At least 127 records · Page 7Linked to original sources
PubMed1998

Lymphoepithelial cyst and epidermoid cyst of the accessory spleen in the pancreas.

We report here two rare cystic lesions, a lymphoepithelial cyst (LEC) and an epidermoid cyst of the accessory spleen (ECAS) occurring in the pancreas. Histologically, the LEC was lined by stratified squamous epithelium and surrounded by a layer of lymphoid tissue with germinal centers. The ECAS showed similar histologic features with scattered lymphoid tissue, but splenic pulp tissue was present in the wall. In both cysts, some small pancreatic islets and ducts were seen in the fibrous tissue surrounding the lymphoid layer or the splenic pulp, respectively. The lining epithelia of the LEC and the ECAS, as well as those of retention cysts of the pancreas and epidermoid cysts of the spleen used for comparison, were similarly positive with AE1/3, CAM5.2, CK7, CK13, and carcinoembryonic antigen. CA19-9 was also detected in the epithelial cells of the LEC, the ECAS, and the retention cyst of the pancreas, but not in those of the splenic epidermoid or branchial cleft cysts used for comparison. These findings indicate that LECs and ECASs might develop from the pancreatic ducts protruding into a lymph node or accessory spleen located in the pancreas, respectively. Some of both cysts might cause elevated levels of serum carcinoembryonic antigen and/or CA19-9 and should be distinguished from malignant cystic tumors.

Aged↗
PubMed1997

Role of renal aquaporins in escape from vasopressin-induced antidiuresis in rat.

The purpose of this study was to investigate whether escape from vasopressin-induced antidiuresis is associated with altered regulation of any of the known aquaporin water channels. After 4-d pretreatment with 1-deamino-[8-D-arginine]-vasopressin (dDAVP) by osmotic mini-pump, rats were divided into two groups: control (continued dDAVP) and water-loaded (continued dDAVP plus a daily oral water load). A significant increase in urine volume in the water-loaded rats was observed by the second day of water loading, indicating onset of vasopressin escape. The onset of escape coincided temporally with a marked decrease in renal aquaporin-2 protein (measured by semiquantitative immunoblotting), which began at day 2 and fell to 17% of control levels by day 3. In contrast, there was no decrease in the renal expression of aquaporins 1, 3, or 4. The marked suppression of whole kidney aquaporin-2 protein was accompanied by a concomitant suppression of whole kidney aquaporin-2 mRNA levels. Immunocytochemical localization and differential centrifugation studies demonstrated that trafficking of aquaporin-2 to the plasma membrane remained intact during vasopressin escape. The results suggest that escape from vasopressin-induced antidiuresis is attributable, at least in part, to a vasopressin-independent decrease in aquaporin-2 water channel expression in the renal collecting duct.

Animals↗
PubMed1997

Multivariate evaluation of prognostic determinants for renal cell carcinomas which are metastatic at initial diagnosis.

To clarify the relative importance of clinicopathological factors potentially affecting the survival of individuals initially diagnosed as having metastatic renal cell carcinoma (RCC), univariate and multivariate analyses using Cox's proportional hazards model were performed for 111 RCC patients who were admitted to four hospitals in Nagoya, Japan, between 1978 and 1993. Survival time was calculated from the date of diagnosis to the date of death or the end of May, 1995. Nineteen factors (17 clinically applicable before treatment and 2 histological in nature) were included for assessment. Univariate analysis revealed that 10 of the total 19 factors were significantly associated with patient survival. Multivariate analysis found 7 factors to be statistically significant determinants. Survival was further evaluated by categorizing the patients into three groups according to the number of the 7 factors. These groups showed clearly different survivals (log-rank test, p < 0.0001), confirming the importance of the 7 factors as definite determinants. They should therefore prove to be of advantage for classifying metastatic RCC patients when designing clinical prospective studies of immunotherapy and chemotherapy.

Adult↗
PubMed1997

Intravesical bacillus Calmette-Guérin (Tokyo 172 strain) therapy for carcinoma in situ of the bladder.

To evaluate the clinical response to intravesical instillation therapy with bacillus Calmette-Guérin (BCG) Tokyo 172 strain for carcinoma in situ (CIS) of the bladder and subsequent patient prognosis, we reviewed data for 30 patients treated between 1985 and 1994. Median follow-up was 56 months. The CIS cases comprised two groups: primary (19 patients) and subsequent to development of a gross neoplasm (11 patients). Either 40 mg (n = 20) or 80 mg (n = 10) doses of BCG were instilled weekly for 8 weeks. This intravesical therapy resulted in apparent eradication of tumour cells in 25 of the 30 patients for a complete response (CR) rate of 83%, with no difference found between primary and secondary groups. Tumours later recurred in 6 of the 25 patients (24%) and disease progression was found in only 3 (12%). In contrast, progression occurred in 3 of 5 patients (60%) for which a complete response was not achieved with intravesical BCG therapy. The difference between these two groups was significant (p = 0.04). Total cystectomy was performed in 2 of 25 CR patients (8%) first and in 4 of the 5 unresponsive (80%), the statistical difference being highly significant (p = 0.003). The 5-year survival rate was 96% for the study subjects as a whole. In conclusion, CIS unresponsive to BCG therapy should be treated with immediate total cystectomy while cases demonstrating a complete response should be followed up for a long period.

Administration, Intravesical↗
PubMed1997

A G+1 to C mutation in a donor splice site of intron 2 in the apolipoprotein (apo) C-II gene in a patient with apo C-II deficiency. A possible interaction between apo C-II deficiency and apo E4 in a severely hypertriglyceridemic patient.

Familial apolipoprotein C-II (apo C-II) deficiency is an autosomal recessive genetic disorder characterized by fasting hypertriglyceridemia and accumulation of chylomicrons in the plasma. To elucidate the genetic defect, the apo C-II gene of a neonatal Japanese patient (C-IITokyo) was analyzed. Nucleotide sequence analysis showed a G+1 to C transversion at the donor splice site of intron 2 (INT2 G+1 to C). Restriction fragment length polymorphism analyses of the patient's family members with Hph I showed that the patient was homozygous and the parents were heterozygous for the INT2 G+1 to C mutation. Although consanguinity could not be demonstrated, haplotype analysis of the C-II gene revealed the identity of the patient's alleles on the mutation, suggesting that the parents had a common Japanese ancestor. Sequence analysis of the patient's cDNA isolated from peripheral blood lymphocytes revealed that the INT2 G+1 to C mutation causes skipping of exon 2, which encodes the initiation codon, and results in deficiency of apo C-II proteins. The outstanding feature of our patient was that he showed severe hypertriglyceridemia beginning in the neonatal period, a feature not reported in a case of apo C-II deficiency (C-IIHamburg) with the same mutation as our patient. A previous report of another case of apo C-II deficiency (C-IIToronto) suggested that the apo E4 isoform is associated with higher levels of plasma triglycerides in subjects heterozygous for the apo C-II mutation. Determination of the apo E isoform of our patient revealed that apo E4 was coinherited with the INT2 G+1 to C mutation, whereas the apo E isoform has been reported to be E2/3 in C-IIHamburg. We speculate that apo E4/4 aggravated the hypertriglyceridemia in our patient with apo C-II deficiency.

Apolipoprotein C-II↗
PubMed1997

The novel compound NO-1886 elevates plasma high-density lipoprotein cholesterol levels in hamsters and rabbits by increasing lipoprotein lipase without any effect on cholesteryl ester transfer protein activity.

Lipoprotein lipase (LPL) and cholesteryl ester transfer protein (CETP) are determinants of high-density lipoprotein (HDL) cholesterol concentrations in plasma. We have previously reported that NO-1886, by increasing LPL activity, causes elevation of HDL cholesterol levels in rats. In the present study, we studied the effect of NO-1886 on CETP activity in experimental animals. Since previous reports suggest that rats may lack CETP, we examined hamsters and rabbits, as well as rats. We found that NO-1886 increased LPL activity, resulting in elevation of plasma HDL cholesterol in all three animals. We confirmed that rats lack CETP and that both hamsters and rabbits have high CETP activity. NO-1886 had no effect on CETP activity in hamsters and rabbits. These results demonstrate that the compound NO-1886 elevates HDL cholesterol in experimental animals by selectively increasing LPL activity without any effect on CETP. Animals with low CETP and high LPL activities appear to be more sensitive to NO-1886 than those with high CETP and low LPL activities.

Animals↗
PubMed1997

Extensor tendon rupture due to Kienböck's disease.

Extensor tendon rupture as a complication of Kienbock's disease is rare. We report a case of attritional rupture of the extensor tendon to the index finger by a comminuted dorsal fragment of the lunate after Kienböck's disease in an elderly woman. Excision of the fragment and extensor reconstruction with tendon graft led to a favourable result.

Female↗
PubMed1997

Malignant histiocytosis-like B-cell lymphoma, a distinct pathologic variant of intravascular lymphomatosis: a report of five cases and review of the literature.

Malignant histiocytosis (MH)-like B-cell lymphoma (BCL) is a neoplastic proliferation of large B cells clinically characterized by fever, hepatosplenomegaly, haemophagocytosis and abnormal laboratory data, without lymphadenopathy or skin lesions. Interestingly, most cases have been reported in Asian patients, and it is unclear whether MH-like BCL is biologically distinct from conventional large B-cell lymphomas. We report five Japanese patients with MH-like BCL. Biopsied specimens of bone marrow, liver and/or spleen showed infiltration of neoplastic B cells accompanied by haemophagocytosing histiocytes. Lymphoma cells were positive for CD19, CD20 and HLA-DR surface antigens, and negative for CD5 and CD10. In four cases elevated serum levels of interleukin (IL)-6 and the soluble IL-2 receptor isoform were noted, but not IL-1beta, IL-2 or tumour necrosis factor-alpha. Autopsies of two cases were pathologically diagnosed as intravascular lymphomatosis (IVL). Based on these observations, the current and nine previous cases reported as MH-like BCL in Japan were re-evaluated. They appear to form a peculiar variant of IVL, characterized by bone marrow involvement at presentation, haemophagocytic syndrome, and a rapidly aggressive clinical course, but rarely neurological complications or skin lesions. This variant may merit separate consideration because of the problems posed in the initial diagnosis and therapeutic approaches.

Aged↗
PubMed1997

Recovery of pancreatic beta-cell function in hemochromatosis: combined treatment with recombinant human erythropoietin and phlebotomy.

A patient with diabetes mellitus caused by secondary hemochromatosis was treated using recombinant human erythropoietin and phlebotomy. A total of 12 g of iron had been infused in the patient because of iron deficiency anemia. Blood glucose level was 17.3 mmol/L, and hemoglobin A1c level was 9.0% at admission. He was treated using phlebotomy (400 mL per week), along with subcutaneous injection of 3,000 U of recombinant human erythropoietin three times a week. After approximately 100 days, a total of 5,500 mL of blood (2.75 g iron) could be removed. Serum ferritin level decreased from 10,000 micrograms/L to 4,807 micrograms/L. Fasting and maximum serum C-peptide immunoreactivity values during 100-g oral glucose tolerance tests were improved from 0.14 nmol/L to 0.42 nmol/L and from 1.84 nmol/L to 2.61 nmol/L, respectively. This case suggests that pancreatic beta-cell recovers in diabetes caused by hemochromatosis by reducing iron overload during a short period.

Aged↗
PubMed1997

Identification of a point mutation (G727T) in the glucose-6-phosphatase gene in Japanese patients with glycogen storage disease type 1a, and carrier screening in healthy volunteers.

Glycogen storage disease type 1a (GSD 1a) is an autosomal recessive metabolic disorder caused by a deficiency in glucose-6-phosphatase (G6Pase). We analyzed the G6Pase gene of two unrelated Japanese families with GSD 1a. DNA sequencing of all five exons and exon-intron junctions revealed a G-to-T transversion at nucleotide 727 (G727T) in exon 5, which has been previously reported to cause abnormal splicing. Family studies using mismatch PCR showed that three patients were homozygous for the G727T mutation, while the parents were heterozygous. To investigate allele frequencies, we screened 216 Japanese healthy volunteers and found one asymptomatic carrier. Our findings suggest that the G727T mutation may be prevalent in Japan.

Adult↗
PubMed1997

[Isolation of enterohemorrhagic Escherichia coli (O157:H7) by an immunomagnetic separation method].

Three sporadic cases of enterohemorrhagic Escherichia coli (EHEC) O157 infection which occurred in Kanagawa in 1996 were investigated. In an attempt to determine sources of the infection, a novel method of immunomagnetic separation (IMS) was employed to isolate the bacterium from feces, foods, and other associated items. In the first case, strains of EHEC O157:H7 producing Vero toxin (VT) 2 were isolated from both feces of the patient and suspected food (cattle liver) kept at a restaurant, and the strains were found to be genotypically identical through an analysis of pulsed-field gel electrophoresis (PFGE). Subsequent investigation in the meat processing store, from which the above cattle liver had been retailed to the restaurants revealed that the store was contaminated with EHEC O157:H7 producing both VT1 and VT2. In the second case, a strain isolated from the patient was EHEC O157:H7 producing both VT1 and VT2 while strains isolated from the patient's family (without apparent symptom) and the suspected facility were O137:NM producing VT2. PFGE analysis indicated that the latter two strains were genotypically identical, suggesting that the facility thus contaminated with EHEC O157 caused the infection in question. In the third case, EHEC O157:NM producing VT2 was isolated from 4 out of 7 family members including the patient, and these strains were found to be genotypically identical by subsequent PFGE analysis. Source of the infection was, however, not determined due to lack of suspected food items. In this context, four slaughterhouses in Kanagawa Prefecture were investigated for presence of EHEC O157. As a result, strains of EHEC O157:H7 producing VT1 and VT2 were isolated from the contents of cattle's distal colon and surface of the skinned carcasses. Additional attempt was also made to determine a possibility of river water being contaminated with EHEC O157. The bacterium was, however, not isolated from water samples collected from 4 major rivers in the prefecture (at 10 collecting sites). Experiments were undertaken in order to evaluate the use of IMS in isolation of EHEC O157 from food items, with different pre-enrichment media and conditions. The results indicated that pre-enrichment by trypticase soy broth at 36 degrees C for 6 h followed by inoculating onto sorbitol MacConkey agar plate containing cefixime and tellurite was most appropriate to isolate EHEC O157 strains.

Adolescent↗
PubMed1997

[Studies of Vibrio cholerae O140 (serogroup Hakata) isolated from river water].

Strains of Vibrio cholerae O140, which were isolated from river (Hikichi River) water in Kanagawa, Japan, were studied for their biochemical characteristics and toxin genes, and analyzed by an amplified polymorphic DNA method in comparison with both clinical and environmental isolates of V. cholerae O140. Biochemical characteristics of 4 river isolates studied were found to be unanimous by conventional tests and a commercially available identification kit (Api 50 CH). The strains were also found to react positively with both cholera Inaba factor (C) and V. cholerae O140 specific factor (F). A total of 34 V. cholerae O140 strains including the 4 stains, a reference strains (487-95), 25 strains isolated from samples of river or sea water in Japan, 4 strains isolated from a patient and imported foods, was investigated by the PCR method for presence of ctx, zot, hlyA, and NAG-ST genes. It was found that all strains carried the hlyA gene but none of them carried either ctx, zot, or NAG-ST genes. V. cholerae O140 shared a common antigenic structure with pathogenic V. cholerae strains but its pathogenicity seems to be comparable to that of V. cholerae non-O1 non-O139. Subsequent RAPD analysis indicated that the strains can be divided into 9 groups. Four strains from the Hikichi River showed the same RAPD pattern. The results suggest that the analysis can be a useful epidemiological tool for V. cholerae O140, and that V. cholerae O140 persists in the Hikichi River throughout years.

Japan↗
PubMed1997

Effects of apolipoprotein E phenotype on serum cholesterol level and cholesterol response to diet therapy in patients with hypercholesterolemia.

We investigated the association of the apolipoprotein (apo) E isoform phenotype with the basal serum cholesterol level and cholesterol response to diet therapy in outpatients with primary hypercholesterolemia. The basal levels of serum cholesterol, triglyceride and HDL-cholesterol in the 132 subjects were 286 +/- 26 mg/dl, 154 +/- 83 mg/dl and 54 +/- 14 mg/dl, respectively. The frequencies of apo E 3/2, 3/3, 4/2, 4/3 and 4/4 were 1, 104, 2, 24 and 1, respectively. There were no differences in serum lipids between subjects with the two most common apo E phenotypes, i.e., apoE 3/3 (n = 104) and apoE 4/3 (n = 24). The serum cholesterol response to diet therapy was evaluated by measuring the serum lipids of 52 participants before and 2-3 months after diet therapy. After dietary counselling, serum cholesterol values were reduced significantly from 293 +/- 27 to 256 +/- 36 mg/dl (P < 0.01) in the total group of study subjects. There was no significant difference in serum cholesterol reduction in response to diet therapy between subjects with apoE4 (E4/2, E4/3 and E4/4, n = 12) and without apoE4 (E3/3 and E3/2, n = 40). Following dietary counselling, patients who lost a large amount of body weight (BM I > or = 1.0) exhibited a greater reduction in serum cholesterol than those who showed less weight loss. In conclusion, the results of our study demonstrated the primary importance of diet therapy in the treatment of hypercholesterolemia, although other investigators have suggested that apo E phenotypes influence the response of serum cholesterol to dietary changes.

Adult↗
PubMed1997

In situ characterization of islets in diabetes with a mitochondrial DNA mutation at nucleotide position 3243.

Changes in the pancreas of diabetic patients with the A-to-G mitochondrial DNA (mtDNA) mutation at nucleotide position 3243 base pair (bp) have not previously been described. The clinical phenotypes of diabetes associated with the mtDNA 3243 mutation range from NIDDM to IDDM. We sought the presence of the mutation and studied volume of beta-, alpha-, and delta-cells, mitochondrial enzyme activity, and presence of apoptosis in diabetic pancreases obtained at autopsy. Pancreases were obtained from 16 patients with IDDM, from 18 patients with NIDDM, and from 11 nondiabetic patients. Mitochondrial enzyme activity was determined for cytochrome c oxidase (COX), the subunits of which are partially encoded by mtDNA, and for succinate dehydrogenase (SDH), the subunits of which are solely encoded by nuclear DNA. The volumes of islet beta-, alpha-, and delta-cells were estimated by computerized morphometry. Pancreatic cells were examined for apoptosis by an in situ end-labeling procedure. The mtDNA 3243 mutation was detected in 1 of 16 (6%) pancreases from the IDDM patients; none of the pancreases from 18 NIDDM patients and 11 nondiabetic patients had the mutation. The single patient with the mtDNA 3243 mutation was a 56-year-old woman with IDDM, aged 39 years at diabetes onset, whose mother was diagnosed with NIDDM. The patient had a history of secondary failure of oral hypoglycemic agents and had a marked decrease in the number of beta-cells. The islet beta-cells and non-beta-cells of the patient showed extremely decreased COX enzyme activity. The islet cells in the patient showed a high activity when examined for SDH. Some pancreatic exocrine cells also showed decreased COX activity with high SDH activity. In IDDM, NIDDM, and nondiabetic patients without the mtDNA 3243 mutation, only weak staining for SDH of the islet cells showed. The percentage of heteroplasmy of the mtDNA 3243 mutation in pancreatic micropunched islet specimens was 63 +/- 5% (mean +/- SD) in the islets, 32 +/- 3% in the exocrine pancreas, and 8 +/- 1% in peripheral polymorphonuclear cells. Apoptotic cells were not observed in the IDDM pancreas in the patient with the mtDNA 3243 mutation. The fact that higher levels of mutated mtDNA at 3243 bp were found in affected islets rather than in other tissue suggests that the distribution of the mutant may determine the effect on islet function. A characteristic decrease in the mitochondrial enzyme with COX activity and accelerated SDH activity of the affected islets may provide new insights into the pathogenesis of mitochondrial diabetes.

Adult↗