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Biomedical subjects

R Hirata

Publications and source records attributed to R Hirata.

At least 37 records · Page 2Linked to original sources
PubMed1997

[Activation of skin cells by inorganic compounds].

It has been known that the stimulation of skin cells by physiologically active substances is accompanied by the quantitative and qualitative alterations of the glycosaminoglycans (GAGs) in skin. This phenomenon make it possible to evaluate the activity of test substances for the stimulation of skin cells. The purpose of our study is to elucidate the effectiveness of inorganic compounds for the stimulation of skin cells. (1) The cultured skin cells including keratinocytes and fibroblasts, (2) the cultured model skin constituted of collagen gel, fibroblasts and keratinocytes, and (3) the mouse damaged skin were used in the present study. The results obtained from these studies demonstrate that inorganic substances commonly have a possibility to activate cyclic AMP-dependent protein kinase (A-kinase), and the A-kinase activation results in an increase in GAGs. These findings brought the scientific basis for the effectiveness of the Japanese traditional balneotherapy for damaged skin.

Animals↗
PubMed1997

[Retinoic acid-induced cell growth inhibition and differentiation in testicular carcinoma cells in culture].

Testicular germ tumor cells could be differentiated spontaneously or by some chemotherapeutic compounds. However, the mechanism by which the cells are differentiating from the stem cell remains unclear. The KU-MT cells, which were newly established from lung metastasis of testicular carcinoma, have been continuously producing alpha fetoprotein (AFP). Retinoic acids are well-known to induce cellular differentiation in culture and have already been applied for a clinical usage against leukemia. In the present study, all-trans-retionic acid (ATRA) elevated the level of AFP and inhibited the growth of KU-MT cells in vitro. ATRA also arrested the cell cycle in G1 and reduced the percentage of the S phase cell in terms of wild type p53, leading to apoptosis in part. Retinoids, especially retinoic acid receptor (RAR)-alpha specific agonists induced laminin production, a marker of endodermal differentiation; whereas arotinoid, a retinoid not bound to RAR-alpha, did not affect laminin expression. In summary, retinoic acids could mediate cell growth and differentiation of testicular tumor through RAR-alpha.

Antineoplastic Agents↗
PubMed1996

Reducing activity level of alliin.

Alliin has been reported to have antioxidative activity. We tried to reexamine the antioxidative activity of alliin with a purified alliin preparation, and found that it has no antioxidative activity in a linoleic acid oxidation system. The reducing activity of alliin tested by the ECD method was also weak in showing antioxidative activity.

Antioxidants↗
PubMed1995

HLA-DR8 and acute anterior uveitis in ankylosing spondylitis.

OBJECTIVE: To identify possible factors in the development of acute anterior uveitis (AUU) in patients with ankylosing spondylitis (AS). METHODS: We investigated HLA antigens serologically, and HLA-DRB1*08 alleles by polymerase chain reaction-restriction fragment length polymorphism, in 42 Japanese AS patients with and without AAU. RESULTS: Thirty-six of the AS patients (85.7%) had HLA-B27. Thirteen (65%) of the 20 patients with AAU had HLA-DR8, whereas only 1 (4.5%) of the 22 patients without AAU had DR8. The difference was statistically significant (Pcorr < 0.001). CONCLUSION: Our data suggest that HLA-B27 is strongly associated with AS in Japanese patients and that HLA-DR8 is important for the development of AAU in Japanese patients with AS.

Acute Disease↗
PubMed1995

Administration of phosphatidylcholine increases brain acetylcholine concentration and improves memory in mice with dementia.

Studies on the effect of phosphatidylcholine administration on memory are limited. We administered egg phosphatidylcholine to mice with dementia and to normal mice and compared the differences in memory and serum choline concentration, and choline and acetylcholine concentrations and choline acetyltransferase activities of three forebrain regions (cortex, hippocampus and the remaining forebrain). Mice with dementia were produced by mating sibling mice who had impaired memory for > 20 generations. These mice had poor memory and low brain acetylcholine concentration. We administered 100 mg of egg phosphatidylcholine (phosphatidylcholine group) or water (control group) by gavage to each mouse daily for about 45 d. Control mice with dementia had poorer memory in passive avoidance performance and lower brain choline (cortex and hippocampus) and acetylcholine (hippocampus and forebrain excluding cortex and hippocampus) concentrations and lower cortex choline acetyltransferase activity than the control normal mice (P < 0.05). The administration of phosphatidylcholine to mice with dementia improved memory and generally increased brain choline and acetylcholine concentrations to or above the levels of the control normal mice. In normal mice, phosphatidylcholine treatment did not affect memory or acetylcholine concentrations in spite of the great increase in choline concentrations in the three brain regions. Serum choline concentration in mice treated with phosphatidylcholine increased to a similar level in both strains of mice, indicating that the absorption of phosphatidylcholine was not impaired in mice with dementia. The results suggest that administration of egg phosphatidylcholine to mice with dementia increases brain acetylcholine concentration and improves memory.

Acetylcholine↗
PubMed1995

Isolation of Porphyromonas gingivalis strain from tubal-ovarian abscess.

An unusual case of involvement of Porphyromonas gingivalis is described. Two anaerobic isolates, identified as Fusobacterium nucleatum and P. gingivalis, were recovered from the pus of a tubal-ovarian abscess in a 35-year-old woman. Identification of the P. gingivalis isolate was confirmed by randomly amplified polymorphic DNA fingerprinting.

Abscess↗
PubMed1995

[HLA-DR2 alleles and uveitis in leprosy].

In order to investigate the role of immunogenetic factors in the pathogenesis of uveitis in leprosy, HLA antigens were analyzed between the leprotics with and without uveitis. Sixty-five Japanese leprosy patients comprised 32 with uveitis and 33 without uveitis. Controls consisted of 138 healthy subjects. A lymphocyte cytotoxicity test was used for typing HLA-A, -B, -C, -DR and -DQ antigens. HLA-DR2 genotyping was performed by the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and PCR-restriction fragment length polymorphism (RFLP) methods. The frequency of HLA-DR2 antigen was significantly increased in the patients with uveitis as compared with the control subjects (Pc < 0.0005), whereas HLA-DR53 antigen was significantly decreased (Pc < 0.05). At the genomic level the frequency of HLA-DRB1*1501 was significantly increased in the patients with uveitis and without uveitis as compared with that in the controls. The association with DRB1*1501 was even stronger in patients with uveitis (odds ratio = 7.1, Pc < 0.000005) than in the patients without uveitis (odds ratio = 4.1, Pc < 0.005). Our results suggest that HLA-DRB1*1501 contribute to the susceptibility to uveitis in the Japanese with leprosy.

Alleles↗
PubMed1995

[HLA and uveitis in leprosy].

In order to investigate the role of immunogenetic factors in the pathogenesis of uveitis in leprosy, human leukocyte antigens (HLA) were analyzed among leprotics with and without uveitis. The subjects were 85 Japanese leprosy patients, 44 with uveitis and 41 without uveitis. Controls were 138 healthy subjects. A modified two-stage complement dependent microcytotoxicity test was used for typing HLA-A, -B, -C, -DR and -DQ antigens. The occurrence of HLA-DR2 antigen was significantly increased in patients as a whole (69.4%), and in the patients with uveitis (79.5%) as compared with the control subjects (35.5%). The association with DR2 was even stronger in the patients with uveitis (odds ratio = 7.1, Pc < 0.000005) than in the patients as a whole (odds ratio = 4.1, Pc < 0.0001). On the other hand, HLA-DR53 antigen was significantly decreased in the patients as a whole (43.5%) and in the patients with uveitis (36.4%) as compared with the control subjects (69.6%). No significant difference in the distribution of HLA antigens was observed in the patients without uveitis. Our results suggest that HLA-DR2 contributes to the susceptibility to uveitis in Japanese leprosy patients.

Aged↗
PubMed1994

Protozyme: emerging evidence in nature.

The VMA1 locus in Saccharomyces cerevisiae contains a nested genetic element, the VDE gene, and expresses two functional proteins. A single VMA1 translational product seems to catalyze a self protein splicing in which an internal domain is excised out to produce a site-specific DNA endonuclease and the N- and C-domains are ligated by a transpeptidation reaction to yield a catalytic subunit of the vacuolar ATPase. Accumulating evidence in the past few years suggests that the VMA1 locus encodes a protozyme (for protos en zyme) which has dual roles in life as a protean catalyst for self protein splicing and for self gene homing. Four protozymes that share a common mechanism in protein splicing have been found in four organisms covering three major phylogenic trees.

Amino Acid Sequence↗
PubMed1994

HLA class II genes in Vogt-Koyanagi-Harada disease.

PURPOSE: Vogt-Koyanagi-Harada disease (VKH) is an autoimmune disorder causing a bilateral diffuse granulomatous uveitis, often with several associated extraocular manifestations. Strong association of human leukocyte antigens (HLA) antigens with the disease has been documented. The details of all HLA class II genotypes were investigated in Japanese patients with VKH to demonstrate the immunogenetic background of the disease. METHODS: Human leukocyte antigen tissue typing was performed in 57 Japanese patients with VKH by the modified two-stage complement-dependent microcytotoxicity method. DNA analyses were done by polymerase chain reaction (PCR)-single-strand conformation polymorphism and PCR-restriction fragment-length polymorphism methods. RESULTS: The frequencies of HLA-DR4 and HLA-DQ4 were 93% and 83% among the patients with VKH, compared with 43% and 32% among the controls, respectively (relative risks, 17.4 and 9.9; Pc < 1.0 x 10(-10)). At the genomic level, all patients had the HLA-DQA1*0301 genotype, which was present in only 67% of the normal controls (relative risk, 56.5; Pc < 1.0 x 10(-5)). With allelic combinations, -DQA1*0301/-DR4 showed the greatest relative risk ratio. Conversely, DQB1*0604 genotype was not detected among the patients. CONCLUSION: It can be postulated that VKH is a disease of combined allelic predisposition in which DQA1*0301 acts as the primary and HLA-DR4 acts as an additive factor in the development of the disease. Based on the negative association of DQB1*0604, we propose that DQB1*0604 provides considerable protection, possibly by altering other factors in the pathogenesis of VKH in the Japanese.

Base Sequence↗
PubMed1994

A prospective study on hepatocellular carcinoma in liver cirrhosis: respective roles of alcohol and hepatitis C virus infection.

To assess the interaction of alcohol and HCV infection in hepatocarcinogenesis, we prospectively studied 447 patients with liver cirrhosis (LC) who presented to our out-patient clinics in a month; 163 patients with habitual drinking (AL-LC) who had taken more than 72 g alcohol per day (HCV positive 79 cases: HCV+AL; HCV negative 84 cases: AL); 176 with HCV infection but without alcohol intake; 39 with HB infection; and 82 with liver disease from other etiologies such as primary biliary cirrhosis (PBC). In the HCV group, HCC developed in 15 patients in the first year and 10 in the second year; the cumulative appearance rate was 11% and 16%, respectively. There was no difference in the HCC appearance rate between the two groups. In the AL group, the cumulative HCC occurrence rate was only 2% in the first year, and 2% in the second year. The appearance rate was significantly lower in the AL group compared with the HCV and the HCV+AL groups. One-hundred and fourteen patients (94 with HCV, 20 with HCV+AL) who had a history of blood transfusion more than 10 years ago were selected. A year-adjusted disease occurrence rate calculated by the Kaplan-Meier method showed that the HCV+AL group had a significantly higher disease occurrence rate than the HCV group. Theses results suggest that although alcohol alone does not become an independent risk factor for HCC from LC, it may accelerate the development of HCC caused by HCV, at least in the group with a history of blood transfusion.

Aged↗
PubMed1993

VMA13 encodes a 54-kDa vacuolar H(+)-ATPase subunit required for activity but not assembly of the enzyme complex in Saccharomyces cerevisiae.

Previous purifications and characterizations of the Saccharomyces cerevisiae vacuolar proton-translocating ATPase (V-ATPase) have indicated that this enzyme is a multisubunit complex composed of at least eight subunits of 100-, 69-, 60-, 42-, 36-, 32-, 27-, and 17-kDa (Kane, P. M., Yamashiro, C. T., and Stevens, T. H. (1989) J. Biol. Chem. 264, 19236-19244). We report the cloning and characterization of an additional V-ATPase subunit, the 54-kDa subunit, which is encoded by the VMA13 gene. VMA13 was isolated by complementation of the growth phenotypes associated with the vma13 mutation, which was originally described as cls11 (Ohya, Y., Umemoto, N., Tanida, I., Ohta, A., Iida, H., and Anraku, Y. (1991) J. Biol. Chem. 266, 13971-13977). The nucleotide sequence of the VMA13 gene predicted a hydrophilic polypeptide with a calculated molecular mass of 54,415 daltons. The VMA13 54-kDa gene product resides on the vacuolar membrane and co-purified with the active V-ATPase complex. Characterization of a null vma13 mutant (delta vma13) revealed that the Vma13 polypeptide is essential for V-ATPase activity. However, the Vma13 polypeptide is not required for targeting of the other V-ATPase subunits (100-, 69-, 60-, 42-, 27-, or 17-kDa subunits) to the vacuolar membrane as shown by the association of these subunits with vacuolar membranes isolated from delta vma13 cells. The nature of the V-ATPase "complex" in delta vma13 mutant is, nevertheless, fundamentally different from the wild-type enzyme. This is evidenced by the fact that the inactive V-ATPase complex from delta vma13 cells is less stable than the wild-type enzyme. Taken together, these results indicate that VMA13 encodes the 54-kDa subunit of the V-ATPase and that this subunit is essential for activity, but not assembly, of the enzyme complex.

Amino Acid Sequence↗
PubMed1993

VMA12 is essential for assembly of the vacuolar H(+)-ATPase subunits onto the vacuolar membrane in Saccharomyces cerevisiae.

vma12 mutants of the yeast Saccharomyces cerevisiae, which were originally identified as calcium-sensitive (cls) mutants that were also respiratory deficient (Pet-), have a defect in vacuolar membrane H(+)-ATPase activity (Ohya, Y., Umemoto, N., Tanida, I., Ohta, A., Iida, H., and Anraku, Y. (1991) J. Biol. Chem. 266, 13971-13977). The VMA12 gene was cloned by complementation of the growth defects of vma12 mutants. The nucleotide sequence of the gene predicts a polypeptide of 215 amino acids (25.2 kDa) with two putative membrane-spanning domains. A null vma12 mutant, constructed by chromosomal deletion of the gene, is viable but has completely lost the vacuolar membrane H(+)-ATPase activity and exhibits the same growth defects as observed for the original vma12 mutants. Synthesis and targeting of the subunits of the H(+)-ATPase in the delta vma12 mutant cells were examined by Western blotting analyses of whole cell and vacuolar membrane protein extracts. None of the peripheral membrane subunits that we analyzed (the 69-, 60-, 42-, and 27-kDa subunits) was detected in the vacuolar membrane fractions, although the cellular levels of these polypeptides appeared to be normal. The 100- and 17-kDa integral membrane subunits of the enzyme were absent or present at a substantially reduced level in mutant vacuolar membrane fractions. Anti-Vma12p antibodies recognized a vacuolar protein with the expected molecular mass of 25 kDa. However, the Vma12 protein was not detected in the vacuolar membrane ATPase complex that had been solubilized with a zwitterionic detergent, ZW3-14, and purified by glycerol gradient centrifugation (Kane, P. M., Yamashiro, C. T., and Stevens, T. H. (1989) J. Biol. Chem. 264, 19236-19244). These results indicate that the VMA12 gene product is not a component of the active vacuolar ATPase complex and instead suggest that this protein is required during the process of assembly and/or targeting of the enzyme complex to the vacuolar membrane.

Amino Acid Sequence↗
PubMed1993

Hepatitis C virus infection in alcoholic liver cirrhosis in Japan: its contribution to the development of hepatocellular carcinoma.

To determine risk factors for hepatocellular carcinoma (HCC) in Japan, we studied 575 patients with liver cirrhosis (LC) who presented to our out-patient clinics in a month; 217 patients with habitual drinking with or without viral infections (AL-LC), 235 with hepatitis C virus (HCV) infection, 40 with hepatitis B virus (HB) infection, and 82 with liver diseases from other aetiologies such as primary biliary cirrhosis (PBC). HCC was found in 28% of AL-LC, 27% of HCV-LC, and 18% of HB-LC. HCV antibody examined by the second-generation HCV antibody assay (HCV II) was positive in 49% of AL-LC without HCC, and 84% of AL-LC with HCC. HCV was significantly associated with the development of HCC with an odds ratio of 1.90 by multivariate analysis, whereas alcohol alone did not become a risk factor, with an odds ratio of 0.65. When both variables were combined (HCV+AL), however, the odds ratio was increased twice to 3.65. One-hundred and thirteen patients who had a history of blood transfusion more than 10 years ago were selected to assess the interaction between alcohol and HCV in hepatocarcinogenesis. A year-adjusted disease occurrence rate calculated by the Kaplan-Meyer method showed that HCV+AL had a significantly higher disease occurrence rate than HCV alone. These results suggest that although alcohol alone may not become a risk factor for HCC, it may potentiate the development of HCC caused by HCV. HCV+AL is considered to be the highest risk group; strict abstinence is necessary for these patients.

Adult↗
PubMed1993

Unique associations between HLA-B and HLA-DRB1*04 gene variants in Japanese.

HLA-DRB1*04 gene variants were determined in apparently healthy Japanese with PCR-SSCP and PCR-RFLP, and HLA-B-DRB1*04 haplotype frequencies were estimated statistically. DRB1*0405, which consisted of 60% of the Japanese DRB1*04 gene pool, was associated strongly with HLA-B54. This association was observed only for DRB1*0405, and not for any other DR4 variants. DRB1*0403 and DRB1*0406, which share the same peptide sequence except for amino acid 37, were both associated with B35 and B62. DRB1*0407 was associated exclusively with B35. DRB1*0410 was associated with B60 and B61. B60 and B61, on the other hand, were associated only with DRB1*0410 and DRB1*0405. B35 was associated with all DR4 microvariants. With this possible exception, our calculation suggests that unique B-DR associations were present even for DR4 microvariants. The knowledge of HLA-B and DRB1*04 associations would be useful in clinical settings.

Asian People↗
PubMed1992

Mutations at the putative junction sites of the yeast VMA1 protein, the catalytic subunit of the vacuolar membrane H(+)-ATPase, inhibit its processing by protein splicing.

A single gene, VMA1, encodes the 69-kDa subunit of the vacuolar membrane H(+)-ATPase in the yeast Saccharomyces cerevisiae. We have proposed that the subunit is synthesized as a precursor of 120 kDa (1,071 amino acids) and then converted to the 69-kDa form by an unusual processing reaction, which removes the internal domain of 454 amino acids (residues 284-737) and joins the N- and C-terminal domains. Cysteine to serine mutations at residues 284 and 738, the residues that bracket the internal domain, were introduced into the VMA1 gene by site-directed mutagenesis, and the mutant genes were expressed in a null vma1 mutant. Cells harboring either of the mutant vma1 genes accumulate nonfunctional fragments of the subunit. The mutation of Cys-284 inhibited the cleavage of the N-terminal junction site. Cys-738-->Ser mutation appeared to block the processing at both junction sites although the mutant gene yielded a small fraction of the functional 69-kDa subunit.

Alternative Splicing↗