PubMed Health⌕ Search

Biomedical subjects

Y Taguchi

Publications and source records attributed to Y Taguchi.

At least 127 records · Page 7Linked to original sources

[Prediction of outcome after acute exacerbation of idiopathic interstitial pneumonia].

Some patients with chronic idiopathic interstitial pneumonia (IIP) experience acute exacerbations (AE). Because the precise mechanisms of AE in patients with IIP remain unclear, the treatment for AE is not established and the efficacy of steroids is controversial. Consequently, it is difficult to predict outcomes in patients with AE of IIP. We therefore studied the relationship between clinical findings, efficacy of treatment, and clinical outcome in patients with AE of IIP. Thirty-two patients were enrolled, and were divided into two groups: 10 who were alive more than one year after the onset of the AE survivors, 8 men and 2 women, and 22 who died within one year of the AE (non-survivors, 17 men and 5 women). Survivors were significantly younger than non-survivors (59.7 +/- 9.9 vs 67.5 +/- 8.2 years, respectively, p < 0.05). The values of PaCO2 measured before the AE were higher in survivors than in non-survivors (43.0 +/- 3.7 vs 38.4 +/- 4.0 torr, respectively, p < 0.05). At the onset of the AE the levels of C-reactive protein in serum were higher in survivors than in non-survivors (13.9 +/- 7.9 vs 7.3 +/- 5.8 mg/dl, respectively, p < 0.05). Chest X-ray films showed progression of ground-glass shadows in both groups when the AE occurred; the radiographic findings did not differ markedly between groups. Of the 22 non-survivors, 7 had received medication before the AE; none of the survivors had received medication before the AE. At the time of the AE all patients were treated with steroid pulse therapy, and the dose of methylprednisolone used, did not differ significantly between groups. These data suggest that three factors are closely related to responsiveness to steroid therapy and to clinical outcomes after AE in patients with IIP: 1) age at the onset on IIP, 2) respiratory status before the AE, and 3) disease activity as reflected by inflammatory reactions.

Age Factors↗

[Skew deviation].

Explore the source record for details and available documents.

Brain Diseases↗

[Venous angioma].

Explore the source record for details and available documents.

Brain Neoplasms↗

[Creutzfeldt-Jakob disease with a widespread presence of kuru-type plaques after cadaveric dural graft replacement. An autopsy case].

A case of Creutzfeldt-Jakob disease (CJD) is reported in a 48-year-old woman who had received a cadaveric dural graft after a clipping procedure of a cerebral artery aneurysm in September 1985. In November 1994, she noticed unsteady gait and blurred vision at first. She successively developed ataxic gait, dementia and myoclonus, and became mute. Serial CT scans revealed no abnormal findings, and serial EEGs showed diffuse slow activity without periodic discharge. The patient died in March 1996, 17 months after the initial symptoms. A brain autopsy demonstrated extensive spongiform degeneration in the cerebral neocortex, thalamus, striatum, and cerebellum especially in the granular layer, with associated astrocytosis and marked neuronal loss. Immunohistochemically, PrP plaques, so called kuru-type plaques, were extensively distributed throughout the cerebrum and cerebellum. Moreover, some of these plaques resembled "florid" plaques, which were surrounded by a zone of spongiform change. The PrP gene analysis of her blood and brain tissue revealed no mutations with homozygosity, Met/Met, at codon 129. The unusual features of this case, that is the absence of PSD on EEG and the widespread presence of kuru-type plaques including "florid" plaques, may be similar to the features of "new variant" CJD.

Cadaver↗

Aureobasidin A, an antifungal cyclic depsipeptide antibiotic, is a substrate for both human MDR1 and MDR2/P-glycoproteins.

The human MDR1 gene encodes the multidrug transporter P-glycoprotein (Pgp). Although the MDR2/Pgp shares about 80% identity at the amino acid level with the MDR1/Pgp, the MDR2/Pgp cannot act as a multidrug transporter. We examined the drug sensitivity of Saccharomyces cerevisiae expressing either the human MDR1/Pgp or MDR2/ Pgp. The human MDR1/Pgp conferred about 4-fold resistance to aureobasidin A, a cyclic depsipeptide antifungal antibiotic, on the drug-sensitive yeast strains. Interestingly the human MDR2/Pgp also conferred about 2.5-fold resistance to aureobasidin A. The resistance to aureobasidin A conferred by the MDR2/Pgp as well as by the MDR1/Pgp was overcome by vinblastine, verapamil, and cyclosporin A, depending on their concentrations, but not by colchicine. Aureobasidin A probably interacts directly with Pgps, because it overcame multidrug resistance of human cells and inhibited azidopine photoaffinity labeling of MDR1/Pgp in human cell membranes. These results suggest the possibility that the human MDR1 and MDR2/Pgps have conserved domain(s) for drug recognition.

ATP Binding Cassette Transporter, Subfamily B↗

Advance directives and withdrawal of dialysis in the United States, Germany, and Japan.

OBJECTIVE: To determine the role of advance directives in decisions to withdraw chronic dialysis in the United States, Germany, and Japan. DESIGN: Survey by questionnaire. PARTICIPANTS: Seventy-two American, 87 German, and 73 Japanese nephrologists. MAIN OUTCOME MEASURES: Each nephrologist's total number of (1) dialysis patients, (2) cases of withdrawal of dialysis, (3) patients with advance directives, and (4) uses of such directives. Nephrologists also stated whether they would continue or stop dialysis in 8 hypothetical cases. RESULTS: American, German, and Japanese nephrologists reported withdrawing dialysis for 5.1%, 1.6%, and 0.7% of their patients in the last year, respectively. Thirty percent of American patients had advance directives, and such directives were used in decision making for 3.2% of all patients. Only 0.3% of German and Japanese patients had advance directives, and such directives were used in decision making for 0.09% of patients. When asked about a hypothetical mentally incompetent patient whose family requests withdrawal of dialysis, American nephrologists were much more likely to stop dialysis in the absence of an advance directive than German or Japanese nephrologists. However, almost all nephrologists from the 3 countries would stop dialysis when a family request to withdraw was supported by a patient advance directive. CONCLUSIONS: There is a high prevalence of advance directives among American dialysis patients, and such directives frequently play a role in decision making. German and Japanese nephrologists appear willing to follow advance directives, but the low prevalence of such directives limits the frequency of their use.

Advance Directive Adherence↗

A dnaA box can functionally substitute for the priming signals in the oriV of the broad host-range plasmid RSF1010.

The initiation of replication from oriV RSF1010, the replication origin of the broad host-range plasmid RSF1010, depends on RepA (helicase), RepB' (primase), and RepC (initiator protein), encoded by RSF1010 itself, while this initiation event in E. coli is independent of dnaA, dnaB, dnaC, and dnaG [Scherzinger et al. (1984) Proc. Natl. Acad. Sci. USA 81, 654-658; Scholz et al. (1985) in: Plasmids in Bacteria, pp. 243-259, Plenum, New York; Haring and Scherzinger (1989) in: Promiscuous Plasmids of Gram-negative Bacteria, pp. 95-124, Academic Press, London; Scherzinger et al. (1991) Nucl. Acids Res. 19, 1203-1211]. We showed in this work that a newly constructed origin consisting of an oriV RSF1010 and a DnaA protein binding site, the dnaA box, inserted near oriV RSF1010 (oriV RSF1010-dnaA box) could function without RepB' primase, but required RepA and RepC. This oriV RsF1010-dnaA box could not replicate in a dnaA46 strain in which only RepA and RepC were supplied, even at a permissive temperature. These results indicate that an inserted dnaA box can functionally substitute for the RSF1010-specific ssi signals, the RepB' dependent priming signals in oriV RSF1010, and can direct a priming pathway different from the RSF1010-specific one, but related to DnaA protein.

Bacterial Proteins↗

Helicobacter pylori infection in patients with gastric carcinoma in biopsy and surgical resection specimens.

BACKGROUND: The discrepancy between the high seropositivity for Helicobacter pylori (H. pylori) and the low diagnostic yield of H. pylori organism in gastric biopsies of patients with gastric carcinoma has yet to be clarified. The present study attempted to clarify this controversial point by performing a comparative evaluation between the detection rate of H. pylori in biopsy and in surgical specimens. METHODS: The presence of H. pylori in biopsy samples from 50 patients with gastric carcinoma and 50 age-matched controls was evaluated histologically. Six histologic sections were obtained from gastric noncancerous areas and the presence of H. pylori was evaluated in those H. pylori negative patients who underwent gastrectomy. RESULTS: H. pylori was positive in 35 of 50 controls (70%). In biopsy samples, H. pylori was detected in 29 of 37 patients (78.4%) with early gastric carcinoma, 7 of 13 (53.8%) with advanced carcinoma, 16 of 23 (69.6%) with intestinal type of gastric carcinoma, and 20 of 27 (74.1%) with diffuse type of carcinoma. Studies carried out in gastrectomy specimens increased the diagnostic yield of H. pylori to 33 (89.2%), 12 (92.3%), 19 (82.6%), and 26 (96.3%) in patients with early, advanced intestinal, and diffuse types of gastric carcinoma, respectively. Overall, H. pylori was positive in 36 biopsy specimens (72%) and 45 gastrectomy specimens (90%). Namely, the detection of H. pylori infection was significantly higher in patients with gastric carcinoma using gastrectomy specimens than in patients with gastric carcinoma using biopsy specimens only (P < 0.05). CONCLUSIONS: These results indicate that the actual prevalence of H. pylori in patients with gastric carcinoma is considerably higher than that previously reported.

Biopsy↗

Multiple myeloma-associated systemic vasculopathy due to crystalglobulin or polyarteritis nodosa.

Systemic vasculopathy is a rare complication of multiple myeloma (MM). We describe a patient diagnosed with MM who developed clinical features of systemic vasculopathy including gangrene, livedo reticularis, hypertension, renal failure, and perforation of the small intestine. Histopathologic examination of the small intestine revealed necrotizing vasculitis in the small arteries, along with crystalline deposits in the small vessels. To our knowledge, previously reported cases of systemic vasculopathy associated with MM include at least 9 cases due to crystalglobulin deposition in vessels and 2 due to polyarteritis nodosa. Deposits of crystalglobulin may have induced systemic necrotizing vasculitis in our patient.

Adult↗

Pravastatin prevents the progression of accelerated coronary artery disease after heart transplantation in a rabbit model.

This study was designed to investigate the effects of pravastatin (Pr) on accelerated coronary arteriosclerosis in transplanted hearts. The rabbit hearts were transplanted to the recipients' neck heterotopically, and received FK506. The rabbits in group 1 were fed a normal diet (ND), and cholesterol-rich diet (CD) in group 2 and 3. Pr (10 mg/kg) was given to group 3. They were sacrificed at 4 weeks and the severity of myocardial rejection and arterio-sclerosis was assessed and scored histologically. The serum lipid levels were significantly elevated by a CD. However, addition of Pr had no effect on the levels of LDL and total cholesterol (TC). There was no significant difference in myocardial rejection in each group. Transplanted hearts in group 2 showed more severe arteriosclerotic lesions than those in group 1. Pr treatment in group 3 diminished the severity of coronary arteriosclerosis. Pr may prevent the accelerated coronary arteriosclerosis after heart transplantation without significant changes in TC and LDL.

Animals↗

Weak expression of blood type B antigen in kidney tissue and successful B-incompatible kidney transplantation without special treatments.

Much attention has been paid to only natural antibody titer of the recipients in ABO-incompatible kidney transplantation. In this study, we looked at the distribution of blood type antigens in the kidney tissue. Thirty-seven biopsy specimens from patients with nephritis or transplanted kidneys were recruited. Fifteen were type A, 14 were type B, and 8 were type AB. Kidney tissues were stained with anti-A or anti-B antibody using immunohistological staining. The stained dots in each section were regarded as the area and were measured by image analyzer. B antigen was expressed very weakly both in the glomeruli and in interstitium as compared with A antigen. In type AB, B antigen was less expressed than A antigen. Based on these results, we performed B-incompatible kidney transplantation. No rejection was seen without preoperative depletion of natural antibody and splenectomy. These results may suggest that type B-incompatible kidney transplantation might possibly be performed without preoperative depletion of natural antibodies.

ABO Blood-Group System↗

High acid secretion may protect the gastric mucosa from injury caused by ammonia produced by Helicobacter pylori in duodenal ulcer patients.

The aim of the present study was to investigate the mechanism by which gastric atrophy does not tend to occur in patients with duodenal ulcer despite frequent Helicobacter pylori infection. This investigation was performed in 60 patients with duodenal ulcer and 63 age-matched gastritis patients. Endoscopic findings in the antrum and corpus were classified as normal, atrophic and superficial changes. Biopsy specimens were taken from the antrum and corpus. Ninety per cent of patients with duodenal ulcer and 63.5% of patients with gastritis had H. pylori infection (P < 0.01). The incidence of normal findings in duodenal patients was 30% in antral regions and 50% in the corpus (P < 0.05). Atrophic change was observed in 21.7% of patients in the antrum and 3.3% of patients in the corpus (P < 0.01). The grade of inflammation in duodenal ulcer specimens was significantly higher in the antrum than in the corpus (P < 0.01). H. pylori density was significantly higher in the antrum than in the corpus in ulcer patients (P < 0.01). No significant difference in endoscopic findings, H. pylori density or the grade of inflammation was found between the antrum and corpus in patients with gastritis. The mean intragastric ammonia concentration was 10.3 mg/dL in duodenal ulcer patients and 6.2 mg/dL in gastritis patients (P < 0.01). The mean pH was 3.5 and 4.6 in ulcer and gastritis specimens, respectively (P < 0.01). Our data suggest that gastric mucosa injury is less frequently associated with duodenal ulcers than with gastritis due to the low H. pylori density in the corpus and to the higher acid output that neutralizes the ammonia produced by H. pylori.

Adult↗

Continuous measurement of 13C16O2 production from [13C]pyruvate by intact liver mitochondria: effect of HCO3-.

We have measured continuously the production of mass 45 CO2(13C16O2) from 13C-labeled pyruvate in a guinea pig liver mitochondrial suspension and simultaneously the O2 consumption at 37 degrees C and pH 7.4. The reactions took place in a closed 3-ml volume, stirred, thermoregulated chamber separated from the ion source of a mass spectrometer by a gas-permeable membrane that permitted recording the mass peaks of any gas dissolved in the reaction mixture with a response time as fast as 3 s. If the pyruvate was labeled on C-2, no 13C16O2 was formed, even after 1 h, indicating that C-2 and C-3 were not metabolized in the citric acid cycle. We found that production of 13C16O2 was five times greater in the presence of 25 mM HCO3- than in its absence. A probable mechanism of this CO2/HCO3- effect is carboxylation of pyruvate to oxaloacetate, which would react with acetyl CoA to form citrate and with NADH to form malate, thus removing two major inhibitors of pyruvate dehydrogenase. We conclude that CO2/HCO3- has a potent and hitherto unappreciated regulatory effect on liver pyruvate dehydrogenase.

Animals↗

Osteoclast function is activated by osteoblastic cells through a mechanism involving cell-to-cell contact.

We have established a method for obtaining an enriched preparation of functionally active osteoclast-like multinucleated cells (enriched OCLs) from co-cultures of mouse primary osteoblasts and bone marrow cells. Using these enriched OCLs, the effect of osteoblastic cells on osteoclast function was examined in two assays: a pit formation assay and an assay for actin ring formation. The enriched OCLs cultured for 24 h on dentine slices formed only a few resorption pits. When various numbers of primary osteoblasts were added to the enriched OCLs, the areas of the resorption pits increased proportionally to the number of osteoblasts added. Like primary osteoblasts, the established cell lines of osteoblastic cells (MC3T3-E1 and KS-4) and bone marrow-derived stromal cells (MC3T3-G2/PA6 and ST2) potentiated the pit formation caused by enriched OCLs. In contrast, the fibroblastic cell lines NIH3T3 and C3H10T1/2) and the myoblastic cell line (C2C12) failed to activate OCL function. When cell-to-cell contact between MC3T3-E1 cells and enriched OCLs was prevented, only a few resorption pits were formed. Pit formation by enriched rat osteoclasts placed on dentine slices was also stimulated by adding MC3T3-E1 cells. Actin ring formation and pit forming activity were well correlated in either culture of enriched mouse OCLs or authentic rat osteoclasts on dentine slices. These results indicate that osteoclast function is activated by osteoblastic cells through a mechanism involving cell-to-cell and/or cell-to matrix contact.

3T3 Cells↗

Osteoclast function is activated by osteoblastic cells through a mechanism involving cell-to-cell contact.

We have established a method for obtaining an enriched preparation of functionally active osteoclast-like multinucleated cells (enriched OCLs) from co-cultures of mouse primary osteoblasts and bone marrow cells. Using these enriched OCLs, the effect of osteoblastic cells on osteoclast function was examined in two assays: a pit formation assay and an assay for actin ring formation. The enriched OCLs cultured for 24 h on dentine slices formed only a few resorption pits. When various numbers of primary osteoblasts were added to the enriched OCLs, the areas of the resorption pits increased proportionally to the number of osteoblasts added. Like primary osteoblasts, the established cell lines of osteoblastic cell (MC3T3-E1 and KS-4) and bone marrow-derived stromal cells (MC3T3-G2/PA6 and ST2) potentiated the pit formation caused by enriched OCLs. In contrast, the fibroblastic cell lines (NIH3T3 and C3H10T1/2) and the myoblastic cell line (C2C12) failed to activate OCL function. When cell-to-cell contact between MC3T3-E1 cells and enriched OCLs was prevented, only a few resorption pits were formed. Pit formation by enriched rat osteoclasts placed on dentine slices was also stimulated by adding MC3T3-E1 cells. Actin ring formation and pit forming activity were well correlated in either culture of enriched mouse OCLs or authentic rat osteoclasts on dentine slices. These results indicate that osteoclast function is activated by osteoblastic cells-through a mechanism involving cell-to-cell and/or cell-to-matrix contact.

Animals↗

Is Baker's cyst a risk factor for pulmonary embolism?

We encountered a 73-year-old man with acute pulmonary embolism (PE) and Baker's cyst. Venography revealed that the right popliteal vein was compressed by Baker's cyst and deep venous thrombosis (DVT) had developed. DVT associated with Baker's cyst is rather common and these two conditions are thought to be causally related. Baker's cyst is the most frequent mass lesion in the popliteal region. We suggest that Baker's cyst is a risk factor for PE as well as surgery and trauma.

Acute Disease↗