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Biomedical subjects

K Fujii

Publications and source records attributed to K Fujii.

At least 451 records · Page 25Linked to original sources
PubMed1995

Inhibitory effect of cold stress on lung tumours induced by 7,12-dimethylbenz[a]anthracene in mice.

The effect of cold stress on lung tumours induced by 7,12-dimethylbenz[a]anthracene (DMBA) was investigated in ICR male and female mice. When mice were exposed to cold stress at 0 +/- 1 degree C for 2 h, three times per week (every other day) for 3 months, the rectal temperatures and hepatic glutathione levels were significantly decreased. On the other hand, when DMBA (10 mg/kg) was subcutaneously injected into neonatal mice, lung tumours were observed in 81.8% of non-stressed mice of both sexes 4 months after injection. However, when mice treated with the same dose of DMBA were exposed to cold stress under the same conditions, lung tumours were observed in 53.3% and 30.3% of the male and female mice 4 months after DMBA injection. In addition, although DMBA (1 mg/kg) caused lung tumours in 20% or 40% of the treated male or female mice 4 months after injection, it did not cause lung tumours in all of the male and female mice exposed to cold stress. These results suggest that cold stress may inhibit lung tumours induced by chemicals.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1995

Glycine-to-arginine substitution at codon 145 of HBsAg in two infants born to hepatitis B e antigen-positive carrier.

Two daughters born to an HBeAg-positive carrier became hepatitis B virus carriers despite immunoprophylaxis with hepatitis B immune globulin or hepatitis B vaccine. The elder daughter received hepatitis B immune globulin alone and the younger daughter received both hepatitis B immune globulin and hepatitis B vaccine. They acquired anti-HBs passively immediately after birth, and the younger daughter did not respond to active immunization. The nucleotide sequence of the S gene of hepatitis B virus DNA from the four carriers in the family was determined. A 531-bp fragment within the S gene, which includes a region encoding both the common a and type-specific d/y or r/w determinants, was amplified by polymerase chain reaction and sequenced. Antigenic subtypes of HBV were identified as adr in the father and adw in both the mother and two daughters. Amino acid residues 122-160 of HBsAg were identical between the daughters and their mother except for a glycine-to-arginine substitution at codon 145. A possibility that this escape mutant had selective advantage over wild-type hepatitis B virus under immune pressure is discussed.

Amino Acid Sequence↗
PubMed1995

"Rebound" phenomenon of hepatitis C viremia after interferon therapy in "relapsed" patients with chronic hepatitis C.

The correlation between serum hepatitis C virus (HCV)-RNA and aminotransferase levels following completion of interferon therapy was evaluated in eight relapsed patients with chronic hepatitis C. Both HCV-RNA and aminotransferase levels were significantly increased in the relapsed patients 1 month after completion of therapy, compared to pretreatment values, despite aminotransferase levels being normal and HCV-RNA being undetectable by reverse transcription polymerase chain reaction assay at the end of therapy. The serum levels of HCV-RNA and aminotransferase were significantly elevated 1 and 2 months post-treatment. They then decreased to pretreatment values 3-5 months after the completion of therapy. Thus, in relapsed patients after the completion of therapy, the changes in HCV-RNA levels preceded the elevation in aminotransferase levels. These findings suggest a correlation between serum HCV-RNA levels and aminotransferase levels in relapsed patients with chronic hepatitis C after the completion of interferon therapy.

Adult↗
PubMed1995

Venous tumor thrombosis and cavernous transformation of the portal vein in a patient with gastric carcinoma.

A case of extensive extra- and intrahepatic portal tumor thrombosis, with no metastatic foci in liver parenchyma, secondary to advanced gastric carcinoma in a 69-year-old man is reported. The portal tumor thrombosis was characterized by enlargement of the thrombosed segment of the vein, decreased density mass without intraluminal enhancement of the involved vein, nonvisualization of the portal venous branch in the involved lobe, and the so-called cavernous transformation of the portal vein. The surgically resected gastric specimen showed Borrmann type 3 advanced papillary adenocarcinoma. The portal tumor thrombus is presumed to have arisen from vascular invasion in the primary foci of gastric carcinoma, and then to have permeated the portal vein without invasion of liver parenchyma.

Adenocarcinoma, Papillary↗
PubMed1995

Effect of angina pectoris on myocardial protection in patients with reperfused anterior wall myocardial infarction: retrospective clinical evidence of "preconditioning".

OBJECTIVES: We examined whether angina pectoris occurring shortly before the onset of acute myocardial infarction can actually preserve postischemic left ventricular function in humans. BACKGROUND: Experimental studies indicate that brief, transient episodes of ischemia render the heart very resistant to infarction from a subsequent sustained ischemic insult, an effect termed ischemic preconditioning. However, no clinical data are available concerning the implications of angina pectoris shortly before the onset of infarction in humans. METHODS: We studied 84 patients with an acute anterior myocardial infarction. All patients had total occlusion of the proximal or medial portion of the left anterior descending coronary artery and achieved reflow within 6 h of onset. Patients were classified into three groups on the basis of duration of antecedent angina pectoris: group 1 = no angina (37 patients); group 2 = new angina pectoris occurring < or = 7 days of onset of infarction (22 patients); group 3 = angina pectoris beginning > 7 days before onset of infarction (25 patients). All patients underwent left ventriculography on the day of, and 28 days after, onset of infarction to determine ejection fraction and regional wall motion in the territory of the left anterior descending coronary artery by the centerline method. RESULTS: Angiographic collateral flow grade was higher in group 3 than in groups 1 and 2 ([mean +/- SD] group 1 = 0.08 +/- 0.7, group 2 = 0.7 +/- 0.7, group 3 = 1.5 +/- 0.8). Although there were no differences in baseline ejection fraction and regional wall motion among the three groups, the degree of improvement was significantly greater in groups 2 and 3 than in group 1 (late minus baseline ejection fraction: group 1 = 0 +/- 8%, group 2 = 7 +/- 10% group 3 = 6 +/- 10% [p < 0.05 group 1 vs. groups 2 and 3]; late minus baseline regional wall motion: group 1 = 0.2 +/- 0.4, group 2 = 0.6 +/- 0.5, group 3 = 0.5 +/- 0.6 SD/chord [p < 0.05, group 1 vs. group 2]). When the study was limited to those patients with no or poor collateral flow (31 in group 1, 19 in group 2, 10 in group 3), only group 2 patients had a significant improvement in wall motion. Angina pectoris within 24 h before onset of infarction was more frequent in group 2 (82%) than group 3 (28%, p < 0.05). CONCLUSIONS: Episodes of angina pectoris occurring shortly before the onset of infarction may preserve myocardial contractile function in reperfused myocardial infarction despite less support from collateral flow channels, although these are suggestive results in a limited number of patients.

Angina Pectoris↗
PubMed1995

Optic neuritis with silent cerebral lesions: availability of FLAIR sequences.

A 10-year-old male suffering from acute optic neuritis is reported with multiple silent cerebral lesions, which remained visible only with fluid-attenuated inversion recovery sequences at 3-week intervals. Conventional sequences with magnetic resonance imaging did not visualize the lesions. Fluid-attenuated inversion recovery sequences are highly sensitive for the detection of silent lesions in acute optic neuritis.

Brain↗
PubMed1995

Reduction of unscheduled DNA synthesis and plasminogen activator activity in Hutchinson-Gilford fibroblasts during passaging in vitro: partial correction by interferon-beta.

Two fibroblast cell lines (PG3KT and PG1NA) derived from Hutchinson-Gilford syndrome (progeria) cases were characterized, at various population doubling levels (PDL), with respect to the capacity of ultraviolet light (UV, mainly 254 nm wavelength)-induced unscheduled DNA synthesis (UDS) and plasminogen activator-like protease activity (PA). The UDS levels in PG3KT and PG1NA cells at PDL 2-3 were only slightly less than those in normal fibroblasts. With increasing PDL, both progeria cell lines exhibited reduction of the UDS levels and undetectable ones at PDL 9-11. Prompt and transient induction of PA was also detectable at less than PDL 5, whereas it was undectable at higher PDL. However, the levels of UDS and PA induction were increased about 3-7 times after pretreatment with 100 IU/ml human interferon (HuIFN)-beta preparations for more than 24 h prior to UV irradiation, although UDS and PA were undetectable at more than PDL 10. These results suggest that cytokines such as HuIFN-beta transiently compensate for the decreases in UDS and PA inducibility in progeria cells with aging.

Cell Division↗
PubMed1995

Clinical information on serum IGFBP-3 levels and IGFBP-3 proteolytic activity in childhood.

In this review paper, three pieces of clinical information in childhood are presented: (1) IGFBP-3 may replace GH provocation tests in the diagnosis of GH deficiency (GHD); (2) IGFBP-3 levels are regulated by IGF-I levels in a short period, and (3) ratio of free IGF-I to total IGF-I is high in serum of early infancy, similarly to serum of pregnancy, only partially owing to the presence of IGFBP-3 proteolytic activity. Each paper will be published soon.

Adolescent↗
PubMed1995

Inhibition of acetylcholinesterase modulates the autoregulation of cerebral blood flow and attenuates ischemic brain metabolism in hypertensive rats.

We designed the present study to examine whether or not the inhibition of acetylcholinesterase modulates cerebral microcirculation in hypotension and improves brain metabolism in ischemia induced by bilateral carotid artery occlusion in hypertensive rats. Blood flow to the parietal cortex was determined by the H2 clearance method. Lactate, pyruvate, and ATP were estimated by enzymatic methods. Acetylcholinesterase inhibitor (AChEI, ENA-713), at 0.05, 0.1, or 0.5 mg/kg, was intravenously injected 10 min before either hemorrhagic hypotension or cerebral ischemia. The levels of acetylcholine in the control were 29.3 +/- 8.1 (mean +/- SD) and 39.5 +/- 8.1 pmol/mg in the cortex and hippocampus, respectively, and they were significantly decreased by 15-19% after 60 min of ischemia in the vehicle-treated rats. AChEI preserved the levels to 93-98% of the control (p < 0.05 versus vehicle). The lower limit of autoregulation was 74 +/- 9% of the resting values. The administration of AChEI helped preserve blood flow and lowered the limit to 64 +/- 6% (p < 0.05 versus control). After 60 min of ischemia, lactate increased 6.5-fold and ATP decreased to 64% of the control value. The administration of AChEI dose-dependently reduced the lactate level 1.9- to 3.9-fold and well preserved the ATP level to 94-97% of the control. The inhibition of acetylcholinesterase activity may preserve cerebral autoregulation during hypotension and protect cerebral metabolism against ischemic insult.

Acetylcholine↗
PubMed1995

Isolation and characterization of a cDNA that encodes maize glutamate dehydrogenase.

A full-length cDNA clone, pMGDH1, encoding maize NADH-glutamate dehydrogenase (NADH-GDH) was isolated from a maize root cDNA library. The identity of the cDNA was established by the coincidence of the structure of the purified protein with that inferred from the nucleotide sequence of the cDNA. pMGDH1 had a cDNA insert of 1,638 bp and the open reading frame encoded 411 amino acid residues. The deduced amino acid sequence was similar to putative partial sequences of GDHs from higher plants and to the sequences of GDHs from organisms as diverse as mammals and bacteria. The NH2-terminal sequence deduced from the open reading frame had a typical structure that is associated with the import of proteins into the mitochondrial matrix. The cDNA hybridized to an RNA of about 1.6 kb. This transcript was more abundant in roots than in leaves and was localized in the bundle sheath cells in leaf tissues. Analysis of genomic DNA by Southern hybridization suggested the existence of gene(s) for another NADH-GDH subunit(s).

Amino Acid Sequence↗
PubMed1995

A case of autoimmune bullous dermatosis with features of pemphigus vulgaris and bullous pemphigoid.

Pleomorphic blisters, including tense bullae and annularly arranged vesicles around the erythema as well as erosive eruptions in the oral cavity, appeared on a 61-year-old woman 5 years after surgery for cholangiocellular carcinoma. A biopsy specimen from the oral cavity showed intraepidermal blisters, and those from skin lesions showed subepidermal blisters with infiltrates of eosinophils and neutrophils. The early-stage vesicles showed infiltrates along the epidermal-dermal junction, where electron microscopy disclosed disruption of the lamina densa, basal cells remaining on the dermis, and acantholytic keratinocytes among the infiltrates, but there was no cleavage of the epidermal-dermal junction at the lamina lucida. Direct immunofluorescence studies showed immune deposition at the intercellular space (ICS) and along the basement membrane zone (BMZ). Indirect immunofluorescence studies confirmed coexistence of IgG class anti-ICS and anti-BMZ antibodies. Although this case showed immunohistochemical features of bullous pemphigoid, the presence of suprabasal cleavage in the oral mucosa, acantholytic cells in the blister cavity, the deposition of IgG at the ICS of the perilesional epidermis, and circulating anti-ICS antibodies strongly suggested that this case was primarily pemphigus. The strong inflammation along the epidermal-dermal junction due to unknown factors may have modified the clinical appearance and the histopathology.

Autoantibodies↗
PubMed1995

Periventricular haemosiderin deposition in patients with congenital hemiplegia.

Two patients with congenital hemiplegia without obvious prenatal, perinatal or neonatal difficulties showed linear low signal intensity lesions along the wall of the dilated lateral ventricles without any parenchymal lesions on T2- and proton density weighted MRI. Haemosiderin deposition secondary to intra-uterine subependymal haemorrhage with intraventricular haemorrhage was considered most likely from the signal intensity, distribution and clinical histories. MRI, which is the only means of detecting haemosiderin deposition, could be beneficial for evaluating the pathogenetic cause of congenital hemiplegia.

Cerebral Ventricles↗
PubMed1995

Mechanism of action of antimycobacterial activity of the new benzoxazinorifamycin KRM-1648.

The mechanism of antimicrobial activity of KRM-1648 (KRM), a new rifamycin derivative with potent antimycobacterial activity, was studied. Both KRM and rifampin (RMP) inhibited RNA polymerases from Escherichia coli and Mycobacterium avium at low concentrations: the 50% inhibitory concentrations (IC50s) of KRM and RMP for E. coli RNA polymerase were 0.13 and 0.10 micrograms/ml, respectively, while the IC50s for M. avium RNA polymerase were 0.20 and 0.07 microgram/ml. Both KRM and RMP exerted weak inhibitory activity against Mycobacterium fortuitum RNA polymerase, rabbit thymus RNA polymerases, E. coli DNA polymerase I, and two types of reverse transcriptases. Uptake of 14C-KRM by M. avium reached 18,000 dpm/mg (dry weight) 1.5 h after incubation, while uptake by E. coli cells was slight. KRM was much more effective in inhibiting uptake of 14C-uracil than was RMP (IC50 of KRM, 0.04 microgram/ml; IC50 of RMP, 0.12 microgram/ml). These findings suggest, first, that the potent antimycobacterial activity of KRM is due to inhibition of bacterial RNA polymerase and, second, that the activity of KRM against target organisms depends on target cell wall permeability.

Antibiotics, Antitubercular↗
PubMed1995

Evidence that PGF2 alpha-induced contraction of isolated guinea pig bronchi is mediated in part by release of tachykinins.

To investigate whether prostaglandin F2 alpha (PGF2 alpha) stimulates the release of tachykinins and whether the tachykinins play a role in the PGF2 alpha-induced bronchial contraction, we examined the contractile response to PGF2 alpha in the presence or absence of a neutral endopeptidase (NEP) inhibitor phosphoramidon in the guinea pig main bronchus in vitro. Because NEP effectively cleaves tachykinins, we hypothesized that the inhibition of NEP would enhance a PGF2 alpha-induced bronchial contraction if PGF2 alpha stimulates the release of tachykinins. Phosphoramidon significantly enhanced the concentration-response curve to PGF2 alpha. And it also significantly enhanced 10(-5) M PGF2 alpha-induced contraction. The enhancement was significantly attenuated in tissues where the tachykinins had been depleted by treatment with capsaicin. Furthermore, the enhancement of contraction was also significantly attenuated in the presence of tachykinin antagonist FK-224 (10(-5) M). Tetrodotoxin, a sodium-channel blocker that blocks nerve conduction, did not affect the enhancement. From these results we conclude that 1) PGF2 alpha causes the release of tachykinin-like substances, 2) these substances play a role in bronchial contraction in tissues where NEP activity is inhibited, and 3) nerve conduction is not necessary for the release of these substances in the guinea pig bronchus.

Animals↗
PubMed1995

Enhanced predictability of myocardial infarction in Japanese by combined genotype analysis.

To explore the genes responsible for myocardial infarction and restenosis after percutaneous transluminal coronary angioplasty, we performed association studies of the polymorphisms of the angiotensinogen and angiotensin-converting enzyme (ACE) genes. In the first study, normotensive myocardial infarction patients (n = 103) and control subjects (n = 103), who were matched for established risk factors with the myocardial infarction patients, were randomly selected. The angiotensinogen-TT genotype (T indicates threonine instead of methionine at position 235) was more frequent in the myocardial infarction group than in the control group (P < .05). The ACE-DD genotype (D indicates a deletion polymorphism in intron 16) was also more frequent in the myocardial infarction group (P < .0001). The odds ratio estimated by the combined analysis of the angiotensinogen-TT and ACE-DD genotypes (11.2) was markedly increased compared with that estimated separately from the angiotensinogen-TT (1.75) or ACE-DD (4.43) genotype. In the second study, we investigated 91 consecutive patients with acute myocardial infarction who underwent successful direct angioplasty. Combined analysis showed that the angiotensinogen-TT genotype did not enhance the predictability of myocardial infarction from the ACE-DD genotype. In conclusion, the angiotensinogen-TT genotype is a predictor for myocardial infarction, as well as the ACE-DD genotype, and the combined analysis of the angiotensinogen-TT and ACE-DD genotypes further enhanced the predictability of myocardial infarction in Japanese, suggesting its future clinical usefulness.

Angioplasty, Balloon, Coronary↗
PubMed1995

Can transcranial Doppler really detect reduced cerebral perfusion states?

BACKGROUND AND PURPOSE: This study was designed to determine whether transcranial Doppler ultrasonography (TCD) may detect reduced perfusion states of the brain in patients with hypertension or diabetes mellitus with suspected cerebral atherosclerosis and arteriolosclerosis. METHODS: We determined blood flow velocity with TCD in the middle cerebral artery and cerebrovascular vasodilator responses to carbon dioxide in 22 patients with or without carotid artery occlusive disease and minor stroke; we compared the results with the measurements of cerebral blood flow and oxygen metabolism by positron emission tomography (PET). RESULTS: Blood flow velocity measured by TCD correlated with ipsilateral cerebral blood flow measured by PET in frontal, temporal, and striatal regions and throughout the entire hemisphere (P < .05 to P < .005). Relative changes in blood flow velocity and calculated cerebrovascular resistance tested by carbon dioxide inhalation both correlated closely with regional mean transit time (calculated as the ratio of cerebral blood volume divided by cerebral blood flow) in frontal, striatal, temporal, parietal, and occipital regions and also in the entire hemisphere (P < .05 to P < .0001). TCD variables did not correlate with hemispheric measurements of oxygen metabolism by PET. CONCLUSIONS: Although TCD is not useful in assessing impairments of cerebral metabolism, it is useful for detecting abnormalities of cerebral hemodynamics among patients with risk factors for cerebrovascular disease.

Adult↗
PubMed1995

Brain infarction developed in hypertensive and normotensive patients during hospitalization--hemodynamic factors.

To determine the effects of changes in blood pressure (BP) on the development of ischemic stroke, 17 patients who developed acute brain infarction during hospitalization were analyzed in relation to the vascular risk factors such as hypertension, previous stroke, diabetes mellitus, and hyperlipidemia. Their BPs were retrospectively referred to the onset of stroke. The average values of mean arterial blood pressure (MABP) on admission were 137 mmHg in hypertensive patients (HT; n = 9) and 101 mmHg in normotensives (NT; n = 8). HT patients received antihypertensive treatment after admission and MABP decreased by 22 mmHg (14%) prior to the ictus (three to sixty-five days after admission). MABP in NT patients remained constant before the attack (-1.4 mmHg, four to one hundred ten days after admission). Similarly, MABP decreased by 17 mmHg (four to ninety-three days) before the ictus in patients with previous stroke (n = 9), whereas it changed only a little in patients without history of stroke (n = 8). BP in each group elevated immediately after the stroke and gradually decreased to 90% of the resting level after two weeks. An excessive reduction of BP may induce brain infarction in HT or chronic stroke patients or cause it to recur.

Acute Disease↗