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Biomedical subjects

H Mine

Publications and source records attributed to H Mine.

At least 19 recordsLinked to original sources

Epidemiology of blood donors in Japan, positive for hepatitis B virus and hepatitis C virus by nucleic acid amplification testing.

BACKGROUND AND OBJECTIVES: The Japanese Red Cross screens seronegative blood donors by nucleic acid amplification testing (NAT) for hepatitis B, hepatitis C and human immunodeficiency virus-1 markers. NAT-positive donors thus identified seemed to have a different infectious background from serologically positive donors. The purpose of our study was to characterize this background in the hepatitis B virus (HBV) and hepatitis C virus (HCV) NAT-positive donors. MATERIALS AND METHODS: Some 328 HBV DNA-positive and 44 HCV RNA-positive donors were detected by NAT testing of seronegative blood donors. These were characterized regarding age, gender and genotype of HBV and HCV. RESULTS: Those who were HBV NAT-positive were mainly young, in particular teenage girls. In Japan, genotypes C and B have previously been dominant, but recently genotype A has increased, and genotype H was recently detected. In HBV NAT-positive donors, the rate of genotype A was high (12.2%) compared with patients in hospital (1.7-2%). Donors who were HCV NAT-positive were also young, but mostly men in their twenties. The ratio of genotype 1b to 2a or 1b to 2b in HCV NAT-positive donors differed from that of hospitalized patients in Japan. We did not find genotype 1a, which is dominant in the USA. CONCLUSIONS: The high-risk donors detected by NAT were mainly young, with a different distribution of genotypes from that of hospitalized patients, regarding both HBV and HCV. The rare HBV genotype H has been found for the first time in Japan. The findings reflect the present spread of hepatitis viruses B and C.

Adolescent↗

Status of NAT screening for HCV, HIV and HBV: experience in Japan.

The first nationwide nucleic acid amplification testing (NAT) for hepatitis B virus (HBV), hepatitis C virus (HCV), and human immunodeficiency virus type 1 (HIV-1) of voluntarily donated blood after serological pre-screening and before release of cellular components and plasma for fractionation was implemented by the Japanese Red Cross Blood Transfusion Services. The NAT screening assay using multiplex reagent is time-saving, cost effective, and labour-saving procedure for all blood and blood products including short-shelf life platelets. During the 50-mini-pool NAT screening of serologically negative donations (February 1, 2001-April 30, 2001), we were able to screen out 112 HBV-positive, 25 HCV-positive, and 4 HIV-1 positive units from blood and blood components.

Blood↗

The first large-scale nucleic acid amplification testing (NAT) of donated blood using multiplex reagent for simultaneous detection of HBV, HCV, and HIV-1 and significance of NAT for HBV.

The first nationwide nucleic acid amplification testing (NAT) for hepatitis B virus (HBV), hepatitis C virus (HCV), and human immunodeficiency virus type 1 (HIV-1) of voluntarily donated blood after serological pre-screening and before release of cellular components and plasma for fractionation was implemented by the Japanese Red Cross Blood Transfusion Services. From February 1, 2000 to April 30, 2001, specimens from 6,805,010 units of serologically negative donation were screened in minipools of 50 samples within 24 hr after blood donation by NAT using multiplex HBV/HCV/HIV-1 reagent for blood transfusion including short shelf-life platelets. Among them, 112 HBV DNA-positives, 25 HCV RNA positives and 4 HIV-1 RNA positives were screened out and we could prevent transfusion of these NAT positive units. Subtypes/genotypes of HBV DNA, adr/C, adw/A, adw/B, adw/C, ayr/C and ayw/D were found and adr/C was predominant. A total of 61.6 % of them (69/112) were negative by overnight EIA. Sixth three of HBV NAT-positive samples carried virus loads less than 10(4) copies/mL and 92.1 % of them (58/63) were negative by overnight EIA. The virus growth curves of HBV in 6 cases obtained by retrospective and prospective follow-up study showed exponential straight lines in the early stage of serological window periods and the log times of HBV growth (10 fold increase) in serological window period were between 4.6 and 7.6 days. NAT screening with highly sensitive reagents in pool of specimens is useful to exclude blood units with low level of HBV and HBV mutants from blood transfusion.

Blood Donors↗

Multiple sclerosis with caudate lesions on MRI.

A 31-year-old woman displayed sleepiness and impairment of recent memory. T2-weighted MRI revealed high signal intensity lesions in the bilateral basal ganglia, thalamus, and brainstem. Although remission was achieved with corticosteroid therapy, she again displayed memory dysfunction and emotional disturbance one year later, at which time MRI disclosed new lesions in the right caudate nucleus and left frontal white matter. Corticosteroid therapy lead to improvement, and she suffered no recurrence on maintenance steroid therapy. These findings suggest that caudate lesions do occur in multiple sclerosis, the manifestations of which can be abulia and memory dysfunction, as in the present case.

Adrenal Cortex Hormones↗

Tumor necrosis factor, tumor necrosis factor receptors type 1 and 2, lymphotoxin-alpha, and HLA-DRB1 gene polymorphisms in human T-cell lymphotropic virus type I associated myelopathy.

We studied tumor necrosis factor (TNF), lymphotoxin-alpha (LT-alpha), and TNF receptors type 1 (TNFR-1) and type 2 (TNFR-2) gene polymorphisms as well as HLA class II DRB1 alleles in Japanese patients with human T-cell lymphotropic virus type I (HTLV-I) associated myelopathy (HAM) (n = 51), patients with adult T-cell leukemia/lymphoma (ATL) (n = 48), asymptomatic HTLV-I carriers (n = 50), and HTLV-I seronegative, normal controls (n = 112). There were significant differences between HAM patients and normal controls in the distributions of TNF promoter region polymophism at position --857, the LT-alpha gene NcoI polymorphism, and the T-G substitution in exon 6 of the TNFR-2 gene. The distribution of the NcoI polymorphism of the LT-alpha gene was also significantly different between HAM patients and asymptomatic HTLV-I carriers. In contrast, we failed to detect any difference in the frequency of DRB1, TNF promoter at position --1031, --863, or the TNFR-1 promoter --383 polymorphism. The results suggest that the TNF/LT-alpha gene region within the HLA class III of chromosome 6 and the TNFR-2 gene region located on chromosome 1p36 might contribute to susceptibility to HAM, and that aberrant expression or function of these cytokines and the receptor could be involved in the development of HAM.

Alleles↗

Watershed infarction associated with dementia and cerebral atrophy.

A 63-year-old man was admitted with progressive left hemiparesis and left homonymous hemianopsia of 1 month's duration. During the 2 months before admission, he had suffered from slowly progressive dementia. The diagnosis of right-sided watershed (WS) infarction was made. He exhibited slow progression of dementia and cerebral atrophy during the period of observation after discharge. There was a positive relationship between cerebral atrophy and the degree of dementia. In the present case, WS infarction caused by right internal carotid artery occlusion might be related to dementia and cerebral atrophy.

Atrophy↗

Neuroblastoma cell lines showing smooth muscle cell phenotypes.

Neuroblastoma is a tumor that is derived from the neural crest. Recent studies demonstrated that several human neuroblastoma cell lines exhibit at least three morphologic types: neuroblastic (N)-type, substrate-adhesive (S)-type and intermediate (I)-type cells. However, the origin of the S-type cells has not been clearly identified. In this study, the expressions of smooth muscle-specific proteins (desmin, alpha-smooth muscle actin, basic calponin and the smooth muscle myosin heavy-chain isoforms of SM1 and SM2) in three parent and four cloned neuroblastoma cell lines, composed of S-type cells, were examined by indirect immunofluorescence, Western blot and/or by reverse transcription-polymerase chain reaction (RT-PCR). Desmin was found in two of the seven cell lines, and alpha-smooth muscle actin and basic calponin were detected in all of seven of the cell lines. In three parent cell lines and one cloned cell line composed of N-type cells, none of three smooth muscle-specific proteins were detected. In smooth muscle myosin heavy-chain isoforms, SM1 was detected in two parent cell lines composed of S-type cells (MP-N-MS and KP-N-YS) by immunofluorescence, Western blot and/or by RT-PCR, whereas the SM2 isoform was detected in one parent cell line (MP-N-MS) by RT-PCR. These findings indicate that S-type cells have either the immature or mature smooth muscle cell phenotype, and neural crest cells very likely have the ability of to differentiate into smooth muscle cells in the human system.

Blotting, Western↗

[A family with DRPLA and chronic renal failure].

We reported a family with dentato-rubro-pallido-luysian atrophy (DRPLA) and chronic renal failure. The proband was a 66-year-old woman who developed gait disturbance, limb ataxia, pyramidal tract signs, and dementia since age 54. T2-weighted brain MR images revealed symmetric high-signal lesions in the cerebral white matter, in addition to cerebellar, brainstem, and cerebral cortical atrophy. She suffered from renal failure and became dialysis-dependent at the age of 59, four years after the onset of chronic nephritic syndrome. At the age of 66, she was admitted to our hospital because of hyperthermia and disturbance of consciousness, and died of DIC. Her CAG repeats in the DRPLA gene were 58 and 12. An autopsy was performed. The brain weighed 910 g. Histological findings confirmed the diagnosis of DRPLA. Her mother died of chronic renal failure. All three siblings had cerebellar ataxia, and two siblings had chronic nephritic syndrome. Among them, only her younger brother was diagnosed as non-IgA glomerulonephritis based on kidney biopsy findings at the age of 48. Though the nature of the association between DRPLA and renal dysfunction remains obscure, the DRPLA gene abnormality may be correlated with chronic renal failure in this family.

Aged↗

Malignant rhabdoid-tumor cell line showing neural and smooth-muscle-cell phenotypes.

Malignant rhabdoid tumor (MRT) is a rare and extremely aggressive malignant tumor in childhood. In this study, an MRT cell line, designated KP-MRT-NS, was established from the ascitic fluid taken from an 11-month-old girl, whose tumor had originated from the left kidney. Ultrastructural findings demonstrated the typical aggregation of whorls of intermediate filaments. Chromosome constitution was described as 46, XX, add (10)(q26)[17]/46, idem, dis (1;2)(q22;q31)[3] based on ISCN (1995) and a del (22)(q11.2) was not found in this cell line. The origin of MRT is controversial, various cellular origins having been proposed because of the phenotypic diversity of MRT. Therefore, in this study, to clarify the origin of MRT, the expressions of cytoplasmic proteins including smooth-muscle-specific proteins (alpha-smooth-muscle actin, basic calponin, smooth-muscle-myosin-heavy-chain isoforms of SM1 and SM2) in the primary-MRT tissue and cell line were analyzed. In the primary-tumor tissue, the expressions of neurofilament, vimentin and alpha-smooth-muscle actin were demonstrated by indirect immunofluorescence. In the KP-MRT-NS cell line, the expression of neurofilament, alpha-smooth-muscle actin, basic calponin and smooth-muscle-myosin heavy chain of SM1 and SM2 isoforms was revealed by immunofluorescence, Western blot and/or reverse transcriptase-polymerase chain reaction (RT-PCR). MyoD1 mRNA, determined as a skeletal-muscle-cell lineage marker, was not expressed in the primary-tumor tissue or in the KP-MRT-NS cell line. According to our findings, the MRT cells are of both neural and smooth-muscle cell phenotypes, and support the neural-crest origin of MRT.

Blotting, Western↗

HLA-DRB1 and tumor necrosis factor gene polymorphisms in Japanese patients with multiple sclerosis.

We studied genetic polymorphisms in the tumor necrosis factor (TNF) region as well as HLA-DRB1 of 42 patients with Western-type multiple sclerosis (MS) and 38 with Asian-type MS in Japan. The sex ratio (Female:Male) was significantly higher in Asian than in Western type MS (3.8 vs. 1.3, P = 0.038). The frequency of HLA-DRB1 * 1501 allele in the Western-type MS group increased significantly compared with the control group, while Asian-type MS and control groups showed similar distribution in the frequencies of HLA-DRB1 alleles. No significant differences existed in the TNF region, however, including TNF-a microsatellite alleles. The results suggest that MS in Asians may present two different clinical and immunogenetic manifestations.

Adult↗

Genetic contribution of the tumor necrosis factor region in Guillain-Barré syndrome.

We studied genetic polymorphisms in the tumor necrosis factor (TNF) region in 81 Japanese patients with Guillain-Barré syndrome (GBS) and 85 controls. A significantly higher frequency of the 100-base pair (bp) (TNFa2) allele of the TNFa microsatellite marker, which is associated with high TNF alpha production, existed in Campylobacter jejuni-positive (Cj+) GBS patients than in controls, suggesting the involvement of a genetic predisposition to high TNF alpha secretion in the development of C. jejuni-related GBS.

Alleles↗

HLA and T-cell receptor gene polymorphisms in Guillain-Barré syndrome.

OBJECTIVE: We examined a possible involvement of genetic factors influencing the development of Guillain-Barré syndrome (GBS). METHODS: We studied T-cell receptor (TCR), alpha-chain constant (AC), and beta-chain variable (BV) gene polymorphisms using microsatellite markers and serologic HLA class I antigens, HLA-DRB1, and HLA-DQB1 alleles in 81 Japanese patients with GBS and 87 controls. RESULTS: There were no significant differences in these genetic markers between GBS patients and controls. Subgrouping of GBS patients according to recent Campylobacter jejuni infection, the presence of anti-GM1 antibody in the sera, or their combinations also failed to reveal significant associations with these genetic markers. There was, however, a tendency for an increased frequency of HLA-DRB1*0803 in the C. jejuni + GM1 + GBS group, when compared with controls. CONCLUSIONS: The data suggest that the roles of TCRAC, T-cell receptor beta-chain variable (TCRBV), HLA class I or class II in the development of GBS are not critical, and further research is necessary to clarify other genes encoded within the HLA region for genetic susceptibility to GBS.

Campylobacter Infections↗

[Basic calponin expressing human neuroblastoma cell line of KP-N-YS].

Recent studies have demonstrated that human neuroblastoma (NB) cell lines have at least two morphological appearance of neuroblastic (N-type) and substrate-adhesive (S-type) cells. Our previous study revealed that S-type cells expressed alpha-smooth muscle actin and/or desmin, suggesting the smooth muscle cell characteristics of S-type cells. In the present study, a new human NB cell line, KP-N-YS, was established from bone marrow metastasis of a four-year-old boy with advanced NB, originating from the left adrenal gland. Subsequently N-type cell clone (YS1n) and S-type cell clone (YS2s) was isolated from the parent cell line. Parent and clones cell lines were identified as NB by surface membrane antigen and cytoskeletal protein analysis, and these cell lines were demonstrated as common progenitors by chromosomal analysis. Furthermore the presence of basic calponin were determined by indirect immunofluorescence, Western blot, as well as by RT-PCR (reverse transcriptase-polymerase chain reaction). Our demonstration of basic calponin not in N-type cells, but in S-type cells supports the plausible smooth muscle cell characteristics of this NB cell line.

Antigens, Surface↗

Cardiac dysfunction in patients with chronic progressive external ophthalmoplegia.

BACKGROUND: Chronic progressive external ophthalmoplegia (CPEO), which includes Kearns-Sayre syndrome, is a mitochondrial disorder with large deletions of mitochondrial DNA. Recently, mtDNA deletions in cardiac muscle cells were thought to be a cause of dilated cardiomyopathy. However, the cardiac involvement in patients with CPEO is generally considered to be limited to the cardiac conduction system. HYPOTHESIS: The purpose of this study was to evaluate left ventricular function in patients with CPEO. METHODS: We evaluated the cardiac function of five patients with CPEO by means of carotid pulse recording and Doppler echocardiography. RESULTS: The ratio of the pre-ejection period to ejection time was increased to 0.67 in one patient and to 0.50 in another. Echocardiography showed left ventricular dilatation and diffuse hypokinetic wall motion in both cases. Left ventricular fractional shortening was decreased to 5 and 19%, respectively, and the mean rate of circumferential shortening was decreased to 0.12 and 0.63 circ/s, respectively. One of the two patient died of congestive heart failure 2 months after the study. The Doppler pattern of left ventricular filling in the three remaining patients showed a decrease in the ratio of peak flow velocity in early diastole to that in late diastole, with an increase in deceleration time. CONCLUSION: Although cardiac involvement in patients with CPEO is generally considered to be limited to the cardiac conduction system, left ventricular dysfunction may be present and should receive more attention in the management of patients with CPEO.

Adult↗

An HLA-B null allele (B*1526N) with a stop codon in exon 3 generated by a point mutation.

An HLA-B null allele was identified in a Japanese family during histocompatibility testing for bone marrow transplantation. The propositus was a healthy Japanese woman with three children, and her parents were cousins. Serological HLA typing of the family members indicated that the propositus was homozygous for the A24-Cw4-B blank (B null)-DR4.2-DQ3 haplotype. Total RNA was extracted from peripheral blood of the propositus was converted to first-strand cDNA using reverse transcriptase. The cDNA was amplified by the polymerase chain reaction (PCR) using HLA-B locus-specific primers. The PCR product showed no change in size upon polyacrylamide gel electrophoresis (PAGE) compared to that of normal controls, suggesting that HLA-B gene mRNA was normally expressed. The nucleotide sequence of the cDNA was the same as that of B*1501 except at nucleotide 369 or codon 123, where C was replaced with A; TAC encodes Tyr whereas TAA is a stop codon. This point mutation may have truncated the HLA-B molecule of the propositus, resulting in the negative results we obtained with anti-HLA-B sera.

Adult↗

Plasma levels of brain natriuretic peptide as an index for evaluation of cardiac function in female gene carriers of Duchenne muscular dystrophy.

The level of plasma brain natriuretic peptide (BNP) was elevated in 8 of 15 female gene carriers of Duchenne muscular dystrophy (DMD), and the level correlated with indices of cardiac function. In one of these carriers, whose clinical course was followed for one year, the plasma BNP level was elevated before the development of cardiac symptoms, further increased with the evolution of cardiac symptoms, and then decreased after treatment for cardiac failure. These results suggest that the plasma BNP level may be useful for the early detection of cardiac dysfunction and for evaluating the efficacy of cardiac treatment in female DMD carriers.

Adult↗

High frequencies of human T-lymphotropic virus type I (HTLV-I) infection and presence of HTLV-II proviral DNA in blood donors with anti-thyroid antibodies.

To investigate the relationship between human T-lymphotropic virus (HTLV) types I and II and the pathogenesis of autoimmune thyroid diseases, we examined serum anti-thyroid antibodies in 1019 blood donors with or without serum anti-HTLV-I antibody as well as proviral DNA for HTLV-II in leukocyte DNA by the polymerase chain reaction in 395 blood donors with or without anti-thyroid antibodies. The frequency of donors with anti-HTLV-I antibody who also showed anti-thyroid antibodies (7.9%) tended to be higher than that (6.3%) among donors who did not have the anti-HTLV-I antibody. The frequency of anti-thyroid antibodies in 125 young male donors aged 16-39 years with anti-HTLV-I antibody (4.8%) was significantly higher (P < 0.05) than that (0.6%) in 164 control donors without the antibody. In blood donors with anti-thyroid antibody, 25.0% of those with anti-HTLV-I antibody and 14.3% of those without the antibody had HTLV-II proviral DNA. In contrast, in donors without anti-thyroid antibody HTLV-II proviral DNA was detected in 2.3% of those with anti-HTLV-I antibody and in 0.6% of those without the antibody. Thus the detection rates in donors with anti-thyroid antibody were significantly higher (P < 0.001) than those in donors without the antibody, regardless of HTLV-I infection. These results suggest that HTLV-I infection and the presence of HTLV-II proviral DNA may be independently related to the pathogenesis of autoimmune thyroid diseases.

Adolescent↗

Esophageal Candida infection and adherence mechanisms in the nonimmunocompromised rabbit.

Candida infection of the esophagus has been reported not only in immunocompromised hosts but also in healthy individuals. However, its mechanisms of action in healthy individuals have not been clarified. Our previous study suggested that physical contact was an important factor for the adherence of Candida albicans. The aim of the present study was to test our hypothesis and clarify the adherence mechanisms. Suspensions of Candida albicans cells were given to rabbits in drinking water without the use of immunosuppressive drugs and/or antibiotics, and the esophagus was examined. Candidial lesions were observed in 14 of 15 rabbits given the suspensions held in water with and without 30% sucrose for 13 days. The number of Candida albicans cells adhering to the esophagus per square millimeter by subepithelial cell insertion was significantly larger than that adhering by attachment. These results indicate that adherence of Candida albicans to the esophagus occurs by sustained physical contact alone under a nonimmunosuppressive state, and that subepithelial cell insertion results in greater attachment on adherence. Our findings provide a clue that may help clarify the mechanism of Candida infection in healthy individuals.

Animals↗