GB virus C/hepatitis G virus infection in autoimmune liver diseases.
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Aged↗
Biomedical subjects
H Okamoto
Publications and source records attributed to H Okamoto.
Bowel perforation caused by silicone drains: a report of two cases.
We recently encountered two patients who suffered bowel perforation due to pressure necrosis caused by an open silicone drain placed in the abdominal cavity during surgery. These perforations healed spontaneously after removal of the drains from the site of perforation. Silicone drains are frequently placed in the abdominal cavity to prevent the collection of fluid or blood following surgery; however, a risk of this complication must be borne in mind. Our review of the English literature revealed eight cases of bowel perforations occurring due to a drainage system; six to closed suction drains, and two to open drainage tubes. Seven of these eight patients underwent repeat laparotomy for peritonitis, while the remaining one, who had a closed suction drain, was managed conservatively following discontinuation of the vacuum. Our experience and the literature review suggest that conservative management may be possible in patients without any signs of generalized peritonitis, although repeat laparotomy is required for those with generalized peritonitis. In conclusion, drains should be placed carefully in the abdominal cavity and removed early after the drainage has decreased.
Aged↗
High-dose (9 MU) long-term (60 weeks) alfa-interferon therapy for chronic hepatitis patients infected with HCV genotype 1b.
Efficacy of standard regimens (e.g., 3-6 MU for 24 weeks) of alfa-IFN therapy for chronic hepatitis C has been limited, particularly in patients with HCV/1b. To see if higher-dose longer term treatment is more effective, we tried a 9 MU 60-week regimen. HCV/1b-infected chronic hepatitis patients received 9 MU IFN alpha 2a everyday but Sunday for 2 weeks and thrice a week for next 10 weeks, and 76 patients became HCV RNA-negative while 81 remained positive. The RNA-negative patients were then randomized to receive 3 MU (group I, n = 37) or 9 MU (group II, n = 39) for 48 weeks. Of the RNA-positive patients, only those with normal ALT received another 9 MU 48-week treatment (group III, n = 45). Sustained responders (SR) were defined as those with negative RNA and normal ALT 6 months after the therapy. SR rates based on intent-to-treat principle did not differ significantly between groups I and II (30% vs 41%), but those based on the protocol-compatible cases showed a significantly lower than those in group II. Adverse effects of IFN, developed more frequently in groups II and III than in group I, were mostly reversible. In conclusion, our results encourage 9 MU 60-week IFN alpha treatment in HCV/1b-infected patients with careful attention to adverse effects, and suggest that the treatment should be discontinued if HCV RNA does not disappear within 12 weeks.
Genotype↗
Regenerating gene protein may mediate gastric mucosal proliferation induced by hypergastrinemia in rats.
BACKGROUND & AIMS: Regenerating gene (Reg) has been isolated from rat regenerating pancreatic islets, and Reg protein is mitogenic to islet cells. We have recently shown that Reg gene and Reg protein are expressed in gastric enterochromaffin-like (ECL) cells. This study aimed to clarify whether gastrin enhances Reg protein production in ECL cells and whether Reg protein is mitogenic to gastric mucosal cells. METHODS: Reg gene expression in response to acute and chronic hypergastrinemia was investigated in rats. Immunohistochemical studies, Northern blotting, and in situ hybridization were performed to investigate the expression of Reg protein and Reg gene. The direct effect of gastrin on Reg gene expression was investigated using isolated ECL cells, and the trophic effect of Reg protein on cultured gastric epithelial cells was assessed by [3H]thymidine uptake. RESULTS: Both chronic hypergastrinemia and short-term gastrin administration stimulated Reg gene expression and Reg protein production in fundic mucosa. Reg gene expression was also augmented in isolated ECL cells after incubation with rat gastrin. Reg protein was mitogenic to cultured rat gastric epithelial cells. CONCLUSIONS: Gastrin stimulates the production of Reg protein in gastric ECL cells, which may be involved in the gastrin-induced gastric mucosal cell growth.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Antihypertensive effect of a proteasome inhibitor in DOCA-salt hypertensive rats.
To search for a possible role for vascular proteasome in hypertension, we examined changes in proteasome level in aorta of deoxycorticosterone acetate (DOCA)-salt hypertensive rats and evaluated the antihypertensive effect of a proteasome inhibitor, N-benzyloxycarbonyl-Ile-Glu(O-t-Bu)-Ala-leucinal (PSI). Two weeks after the start of DOCA-salt treatment, the rats, with systolic blood pressure being 154 +/- 5 mmHg, were randomly divided into two groups and were given PSI or its vehicle for 2 weeks. Vehicle-treated DOCA-salt rats developed marked hypertension after 4 weeks (198 +/- 9 mmHg), with increases in aortic proteasome activity and content. The systolic blood pressure was positively correlated with both the content and activity of aortic proteasome. The administration of PSI to DOCA-salt hypertensive rats suppressed the elevation of systolic blood pressure (144 +/- 4 mmHg), accompanied by decreases in aortic proteasome activity and content. These results suggest that proteasome production in vascular tissues is increased in DOCA-salt hypertensive rats, and that PSI exhibits antihypertensive effect in this experimental hypertensive model. Thus, the findings indicate the pathophysiological importance of increased vascular proteasome in the development of DOCA-salt hypertension.
Animals↗
A randomized controlled trial of sulfamethoxazole/trimethoprim plus norfloxacin versus sulfamethoxazole/trimethoprim alone for the prophylaxis of bacteria infection during chemotherapy for lung cancer.
The efficacy of the prophylactic administration of sulfamethoxazole/trimethoprim (ST) plus norfloxacin (NFLX) versus ST alone to prevent the development of bacterial infection during chemotherapy-induced leukopenia was compared in patients with lung cancer. Patients who underwent systemic chemotherapy were randomized into one of the prophylactic regimens when grade 3 or 4 leukopenia occurred. Prophylactic treatment was performed on 133 courses of leukopenia in 75 patients and the efficacy was evaluated on 127 of those courses after excluding those patients who demonstrated a fever within 24 h from the start of the prophylaxis. The number of patients who had leukopenia associated fever was two out of 63 (3.2%) with the ST plus NFLX regimen and 10 out of 64 (15.6%) with ST alone; the difference was statistically significant. The prophylactic use of ST plus NFLX was thus found to be more useful than ST alone for the treatment of chemotherapy-induced leukopenia in patients with lung cancer.
Adult↗
Down-regulation of focal adhesion kinase, pp125FAK, in endothelial cell retraction during tumor cell invasion.
Although endothelial cell retraction is required before tumor cell invasion, its molecular mechanism still remains obscure. We previously demonstrated that conditioned medium (CM) derived from a human pancreatic cancer cell line, PSN-1, induced endothelial cell retraction and facilitated tumor cell invasion. To investigate the molecular change of events in the transduction of extracellular signals during endothelial cell retraction, we examined the effect of the CM derived from PSN-1 cells on the tyrosine phosphorylation in endothelial cells. Immunoblot analyses revealed that the PSN-1 CM decreased tyrosine phosphorylation of a 120-130 kD protein, and induced the concomitant down-regulation of focal adhesion kinase, pp125FAK, during endothelial cell retraction in time- and dose-dependent fashions. These changes preceded endothelial cell retraction and were reversible after removal of the CM. Further quantitative densitometric analyses demonstrated that the extent of decrease in tyrosine phosphorylated 120-130 kD protein during the endothelial cell retraction was likely to be proportional to that of the down-regulation of pp125FAK. A tyrosine phosphorylated 120-130 kD protein immunoprecipitated by anti-phosphotyrosine antibody immunoreacted with anti-pp125FAK antibody. These results suggested that decreased amount of a tyrosine phosphorylated 120-130 kD protein probably due to the down-regulation of pp125FAK might be associated with the signal transduction pathway in the endothelial cells during their retraction. Furthermore, these findings were also observed in the CM from another four human cancer cell lines, suggesting the down-regulation of pp125FAK in endothelial cells during tumor cell invasion.
Animals↗
Increased mRNA expression of cardiac renin-angiotensin system and collagen synthesis in spontaneously hypertensive rats.
Hypertensive cardiac hypertrophy is associated with the accumulation of collagen in the myocardial interstitium. Previous studies have demonstrated that this myocardial fibrosis accounts for impaired myocardial stiffness and ventricular dysfunction. Although cardiac fibroblasts are responsible for the synthesis of fibrillar collagen, the factors that regulate collagen synthesis in cardiac fibroblasts are not fully understood. We investigated the effects of angiotensin II on cardiac collagen synthesis in cardiac fibroblasts. Cardiac fibroblasts of 10 week old spontaneously hypertensive rats and age-matched Wistar-Kyoto rats were prepared and maintained in culture medium supplemented with 10% fetal calf serum. The expression of mRNA of the renin-angiotensin system (renin, angiotensinogen, angiotensin converting enzyme) was determined by using a ribonuclease protection assay. Basal collagen synthesis in cardiac fibroblasts from spontaneously hypertensive rats was 1.6 fold greater than that in the cell of Wistar-Kyoto rats. Angiotensin II stimulated collagen synthesis in cardiac fibroblasts in a dose-dependent manner. The responsiveness of collagen production to angiotensin II was significantly enhanced in cardiac fibroblasts from spontaneously hypertensive rats (100 nM angiotensin II resulted in 185 +/- 18% increase above basal levels, 185 +/- 18 versus 128 +/- 19% in Wistar-Kyoto rats p < 0.01). This effect was receptor-specific, because it was blocked by the competitive inhibitor saralasin and MK 954. These results indicate that collagen production was enhanced in cardiac fibroblasts from spontaneously hypertensive rats, that angiotensin II had a stimulatory effect on collagen synthesis in cardiac fibroblasts, and that cardiac fibroblasts from spontaneously hypertensive rats were hyper-responsive to stimulation by angiotensin II. Level of angiotensin and renin mRNA expressed in ventricles, and angiotensinogen mRNA expressed in fibroblasts from SHR were higher than those from WKY. These findings suggest that the cardiac renin-angiotensin system may play an important role in collagen accumulation in hypertensive cardiac hypertrophy.
Angiotensin II↗
Incidence and influence of GB virus C and hepatitis C virus infection in patients undergoing bone marrow transplantation.
Markers of GB virus C (GBV-C) and hepatitis C virus (HCV) were sought in 80 patients before and after they underwent BMT in a metropolitan hospital in Tokyo between 1990 and 1996. RNA of GBV-C was detected in 14 (18%) patients before BMT. Of the 55 patients who had been transfused, 14 (25%) possessed GBV-C RNA at a frequency significantly higher than in the 25 untransfused patients who were all negative (P < 0.01). HCV RNA was detected in three of the 55 (5%) transfused patients, but in none of the 25 untransfused patients. Sera at 3 months after BMT were available for 57 patients. GBV-C RNA persisted in all 10 patients who were infected before BMT, while it was detected in five of the remaining 47 (11%) patients who were not. However, persistent and/or ongoing GBV-C infection had no appreciable influence on patient morbidity or mortality. Two of the 57 patients were positive for HCV RNA before BMT and this persisted after BMT in both. HCV RNA became positive in eight of the remaining 55 (15%) patients who were negative before BMT. Of the 14 patients who received transfusions screened by the first-generation test at BMT, seven (50%) became positive for HCV RNA, a rate significantly higher than the one of 41 (2%) patients who received transfusions screened by the second-generation test (P < 0.001). These results indicate that BMT patients are at increased risk of GBV-C infection transmitted by transfusions received before and at the time of BMT, and that the risk of HCV infection has decreased after the implementation of the second-generation anti-HCV test.
Adolescent↗
The "T-shaped" thoracotomy for pericardiectomy after midline crossed IMA grafting.
In the presence of an internal mammary artery graft crossing the mid-sternal line, a median sternotomy may jeopardize the graft and consequently bring a hemodynamic compromise. We describe a case of successful radical pericardiectomy for postoperative constrictive pericarditis using a "T-shaped" thoracotomy in a 68-year-old male patient who had a right IMA graft to the left anterior descending coronary artery.
Aged↗
Results of omental flap transposition for deep sternal wound infection after cardiovascular surgery.
OBJECTIVE: Our experience with omental flap transposition in the treatment of deep sternal wound infections is reviewed here with an emphasis on efficacy, risk factors for in-hospital mortality rates, and long-term results. SUMMARY BACKGROUND DATA: Even with improvements in muscle and omental flap transposition, the timing of closure and the surgical strategy are controversial. METHODS: Forty-four consecutive patients with deep sternal wound infections were treated using the omental flap transposition from 1985 through 1994. The strategies included debridement with delayed omental flap transposition or single-stage management, which consisted of debridement of the sternal wound and omental flap transposition. Methicillin-resistant Staphylococcus aureus was cultured from more than 50% of the wounds. A logistic regression analysis was used to identify the predictors of in-hospital death after omental flap transposition. RESULTS: There were seven (16%) in-hospital deaths. Univariate analysis demonstrated that hemodialysis and ventilatory support at the time of omental flap transposition were significantly associated with in-hospital mortality rates (p = 0.0023 and p = 0.0075, respectively). Thirty-seven patients whose wounds healed well were discharged from the hospital. Two patients with cultures positive for methicillin-resistant Staphylococcus aureus had recurrent sternal infections. Patients without positive methicillin-resistant Staphylococcus aureus cultures had good long-term results after reconstructive surgery. CONCLUSIONS: Transposition of an omental flap is a reliable option in the treatment of deep sternal wound infections, unless the patients require ventilatory support or hemodialysis at the time of transposition.
Adult↗
Chronic effects of enalapril and amlodipine on cardiac remodeling in cardiomyopathic hamster hearts.
This study examined the effects of long-term treatments with the angiotensin-converting enzyme inhibitor, enalapril, and the calcium antagonist, amlodipine, on the morphologic changes, progressive left ventricular dysfunction, and gene expression of the ryanodine receptor (RyR) and phospholamban (PLN) in dilated cardiomyopathy. From the ages of 5 through 20 weeks, dilated cardiomyopathic hamsters, BIO53.58 (BIO), and control hamsters, F1b, orally received either enalapril or amlodipine. Cardiac function was assessed by echocardiography. At the age of 20 weeks, the collagen volume fractions were analyzed by the stereologic method. RyR and PLN messenger RNAs (mRNAs) were examined by Northern blot in the amlodipine group. In BIO, the reduction of left ventricular percentage of fractional shortening was attenuated in the enalapril group (p < 0.05) and amlodipine group (p < 0.001), and the increase in the collagen volume fraction and the loss of myocytes were suppressed in the amlodipine group compared with the untreated group. RyR mRNA level decreased in BIO (p < 0.01) compared with F1b, but PLN mRNA level was unchanged. RyR and PLN mRNA levels were unaffected by the treatment with amlodipine. Enalapril and amlodipine prevent progressive remodeling and reduce cardiac dysfunction in BIO. Amlodipine prevents fibrosis and cell death without modifying RyR and PLN mRNA levels in BIO.
Amlodipine↗
The entire nucleotide sequences of three hepatitis C virus isolates in genetic groups 7-9 and comparison with those in the other eight genetic groups.
We have proposed that hepatitis C virus should be classified into eleven genetic groups (types) which further divide into more than 80 genotypes (subtypes). However, only eight genetic groups (1-6, 10 and 11) have been defined on the basis of the full-length sequence. Hence, the entire nucleotide sequences of three HCV isolates in genetic groups 7-9 have now been determined. Phylogenetic analysis over the full-length sequences of these three isolates, along with 30 more in the other eight genetic groups, indicated that genetic groups 6-9 and 11 have bifurcated from a common branch and groups 3 and 10 from another. In the former branch groups 7 and 11, and groups 8 and 9, are closely related. Consequently, HCV can be classified into either eleven (1-11) or six groups (1; 2; 3 and 10; 4; 5; 6-9 and 11), allowing a clear separation of group and genotype similarity within the NS5b region or a subregion of 1093 nt. When pairwise comparison of 1093 nt in the NS5b sequence was performed on 106 HCV isolates of 36 genotypes in eleven genetic groups, they were classified into either eleven (1-11) or six (1; 2; 3 and 10; 4; 5; 6-9 and 11) genetic groups. However, group and genotype similarities were not clearly separable in either classification. The overlapping range was smaller using the classification into eleven genetic groups as compared to six genetic groups (2.7 vs 4-7%). These results indicate that HCV might not have evolved in the two-tiered fashion, at least in a strict sense.
Base Sequence↗
A possible increase in plasma norepinephrine by removal of the liver.
BACKGROUND: It has recently been suggested that the human liver plays an important role in clearing plasma norepinephrine, especially in restricting most of the norepinephrine to reach the systemic circulation from the gut. METHODS: We examined the changes in plasma catecholamine levels in a patient undergoing extracorporeal hepatic resection and 4 patients undergoing living-related orthotopic liver transplantation. RESULTS: While the changes in plasma epinephrine levels were not necessarily consistent with the proposal that plasma catecholamine levels increase during the anhepatic period, plasma norepinephrine did show a transient increase in accordance with the anhepatic period in all cases. Although we could not rule out the increase in the inflow rate of norepinephrine into plasma, the interrupted hepatic elimination of norepinephrine, especially released from the gut, seemed to be partly responsible for the anhepatic period-associated increase in plasma norepinephrine. CONCLUSION: The present finding might have the potential to improve perioperative management of patients undergoing extracorporeal hepatic resection and orthotopic liver transplantation.
Adrenergic Agonists↗
Antisense oligonucleotides targeting c-fos mRNA inhibit rheumatoid synovial fibroblast proliferation.
OBJECTIVE: To determine whether antisense oligonucleotides targeting c-fos mRNA have the ability to inhibit the growth of interleukin 1 (IL1) stimulated fibroblast-like cells from the synovium in rheumatoid arthritis (RA). METHODS: Fibroblast-like cells established from RA synovium were stimulated by IL1 with antisense or sense oligonucleotides complementary to c-fos mRNA, and the proliferation of these cells was determined by 3H-thymidine incorporation. Effect of antisense oligonucleotides on expression of activator protein 1 (AP1) activity was evaluated using electrophoretic mobility shift assay. RESULTS: C-fos antisense oligonucleotides inhibited IL1 stimulated synovial fibroblast proliferation. The expression of AP1 activity induced by IL1 was suppressed by treatment with antisense oligonucleotides. CONCLUSION: These results suggest the feasibility of antisense strategies designed to suppress c-fos expression as therapeutic agents for RA.
Arthritis, Rheumatoid↗
Role of inducible nitric oxide synthase and cyclooxygenase-2 in endotoxin-induced cerebral hyperemia.
BACKGROUND AND PURPOSE: Bacterial lipopolysaccharide (LPS), an endotoxin, has been reported to induce the expression of inducible isoforms of both nitric oxide synthase (iNOS) and cyclooxygenase (COX-2) in various cell types. LPS is also known to dilate systemic vasculature, including cerebral vessels. This study aimed to determine to what extent LPS induces iNOS and COX-2 expression in the brain and whether NO and/or cyclooxygenase metabolites derived from iNOS and/or COX-2 contribute to the LPS-induced cerebral hyperemia. METHODS: Regional cerebral blood flow (rCBF) was measured by laser-Doppler flowmetry in halothane-anesthetized, artificially ventilated rats for 4 hours after intracerebroventricular administration of LPS. RESULTS: LPS at doses of 0.01 mg/kg to 1 mg/kg caused dose-dependent, progressive increases in rCBF at 1 to 4 hours after administration. The increase in rCBF was attenuated by systemic administration of the selective iNOS inhibitor aminoguanidine (100 mg/kg IP) or the selective COX-2 inhibitor NS-398 (5 mg/kg IP), and it was abolished by preventing induction of these isoforms with dexamethasone (4 mg/kg IP). LPS significantly increased iNOS and COX-2 mRNA, iNOS protein, and iNOS and cyclooxygenase enzyme activity. The increases in iNOS and cyclooxygenase enzyme activity were eliminated by aminoguanidine and NS-398, respectively. Dexamethasone also prevented the increase in iNOS and cyclooxygenase activity. CONCLUSIONS: These results indicate that induction of iNOS and COX-2 expression and the increased production of NO and vasodilator prostanoids in the brain contribute to the elevation in CBF after intracerebroventricular administration of LPS.
Animals↗
Studies on blood compatibility of terpolymers composed of methyl methacrylate, methoxypolyethyleneglycol methacrylate, and dimethylsiloxane methacrylate.
Terpolymers composed of methyl methacrylate (MMA), polydimethylsiloxane methacrylate (PDMSMA), and methoxypolyethyleneglycol methacrylate (MPEGMA), having different compositions were synthesized. Platelets were not adsorbed onto terpolymer surfaces composed of 50 wt% MMA, 25 wt% PDMSMA and 25 wt% MPEGMA, while on terpolymers with the other compositions, platelet adsorption and fibrin clot were observed. It was shown that PDMS segment was predominant on these terpolymer surfaces via XPS. Receding contact angles of terpolymers, on which no platelet was observed, showed intermediate values between PDMS- and MPEG-rich surfaces. It was suggested that these terpolymers had blood compatibility.
Adult↗
Effects of platelet activating factor on the tubotympanic mucosa and inner ear in the guinea pig.
The effect of platelet activating factor (PAF) was studied to elucidate its role in the pathogenesis of otitis media and sensorineural hearing loss. The PAF alone did not induce a reduction of ciliary activity of the cultured middle ear mucosa. However, a dose-dependent decrease in ciliary activity was observed in the presence of the medium containing both PAF and macrophages. Intravenous injection of PAF did not induce dysfunction of the mucociliary system or morphologic changes of epithelium in the tubotympanum, but cytoplasmic vacuolization and ballooning were observed in the inner ear within 1 hour after injection of PAF. In contrast, intratympanic injection of PAF induced mucociliary dysfunction and some pathologic changes in the tubotympanum. Intratympanic inoculation of PAF induced no pathologic findings in the inner ear. These results suggest that PAF is at least partially involved in the pathogenesis of certain middle ear diseases such as otitis media with effusion. Additionally, PAF might be involved in the pathogenesis of some types of unexplained sensorineural hearing loss.
Animals↗