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Biomedical subjects

K Nosaka

Publications and source records attributed to K Nosaka.

At least 37 records · Page 2Linked to original sources
PubMed2001

Effect of elbow joint angle on the magnitude of muscle damage to the elbow flexors.

PURPOSE: It has been shown that eccentric actions at a long muscle length result in a larger decrease in force and more muscle tenderness compared with those at a short muscle length. To further investigate the effect of elbow joint angle on the development of muscle damage, this study compared two maximal eccentric exercise regimens in which the starting position of the action was different, but the range of movement was the same. METHODS: One arm of 10 male students performed 24 maximal eccentric actions of the elbow flexors at the elbow joint angle from 0.87 to 2.27 rad (50-130 degrees: S condition) and the other arm at the elbow joint angle from 1.74 to 3.14 rad (100-180 degrees: L condition). Maximal isometric force, range of motion, muscle soreness, plasma creatine kinase activity, upper arm circumference, and B-mode ultrasound pictures of the elbow flexors (US) were measured before and for 5 d postexercise in both conditions. Magnetic resonance imaging (MRI) of the transverse scans of the upper arm was taken at 4 d after exercise. RESULTS: All measures changed significantly (P < 0.01) after exercise for both conditions; however, significantly (P < 0.01) larger changes in the measures were found in the L condition compared with the S condition. MRI and US displayed that only the brachialis was damaged for the S condition but the biceps brachii was also damaged for the L condition. CONCLUSION: The greater development of muscle damage in the L condition compared with the S condition is likely to be associated with the elbow flexors muscles affected by the exercise.

Adult↗
PubMed2001

How long does the protective effect on eccentric exercise-induced muscle damage last?

PURPOSE: One bout of eccentric exercise produces an adaptation that reduces muscle damage in subsequent bouts. Because it is not known how long this adaptation lasts, the present study investigated the maximal length of the attenuated changes in muscle damage indicators after high-force eccentric exercise. METHODS: Male students (N = 35) were placed into three groups and performed two bouts of eccentric exercise of the nondominant elbow flexors separated by either 6 (N = 14), 9 (N = 11), or 12 (N = 10) months. Maximal isometric force (MIF), range of motion (ROM), upper arm circumference (CIR), muscle soreness (SOR), and plasma creatine kinase activity (CK) were measured before and for 5 d after exercise. Magnetic resonance (MR) images of the transverse and longitudinal scans of the upper arm were taken 4 d after exercise. Changes in the criterion measures were compared between the first and second bouts and between groups by a two-way repeated measures ANOVA. RESULTS: A faster recovery in MIF was evident after a second bout performed at 6 or 9 months, and reduced SOR as well as smaller increases in CIR, CK, and T2 relaxation time of MR images also occurred after the second exercise bout at 6 months compared with initial responses. No significant differences between the bouts were found for ROM, and the 12-month group did not show any repeated bout effect. CONCLUSION: These results show that the repeated bout effect for most of the criterion measures lasts at least 6 months but is lost between 9 and 12 months.

Adolescent↗
PubMed2000

Increasing methylation of the CDKN2A gene is associated with the progression of adult T-cell leukemia.

In this study, we examined the methylation status of the CDKN2A gene in patients with different forms of adult T-cell leukemia (ATL) using Southern blot analysis, methylation-specific PCR (MSPCR), and nucleotide sequencing. We found that the CDKN2A gene was more frequently methylated in fresh tumor cells isolated from patients with acute ATL (47%) or lymphoma-type ATL (73%) than in those with less malignant chronic (17%) and smoldering (17%) ATL. In addition, deletions of the CDKN2A gene were found in 24% of acute ATL patients; thus, abnormalities of the CDKN2A gene totaled 71% in acute ATL patients. In contrast, no CDKN2A gene methylation was found in asymptomatic carriers or uninfected individuals. Methylation of the p15 gene was not found in any samples from 36 ATL patients. Direct sequencing of the CDKN2A gene after sodium bisulfite treatment of genomic DNA revealed that the methylation of CpG sites had occurred in 24 of 32 ATL cases (75%) including chronic and smoldering ATL, even when MSPCR and the Southern blot had failed to detect CDKN2A gene methylation. Among fresh ATL samples with methylation, methylation was detected in the promoter region and exon in 17 of 24 cases, and methylation in the exon without promoter region was detected in 7 of 24 cases. In one case, the pattern of methylation proved to be different between peripheral blood cells and lymph node cells, suggesting the presence of multiple subclones with regard to methylation patterns, despite the same HTLV-I integration site. Quantitative PCR showed a marked decrease in CDKN2A mRNA expression in the cells with a methylated CDKN2A gene, especially if the promoter region was methylated. These findings suggest that CpG methylation decreases CDKN2A expression and represents a critical factor in the disease progression of ATL.

Blotting, Southern↗
PubMed2000

Changes in hardness of the human elbow flexor muscles after eccentric exercise.

The purpose of this study was to investigate changes in muscle hardness after eccentric exercise of the elbow flexors muscles that produce muscle shortening and swelling. To assess muscle hardness, a pressure method was used in which the force required to deform the tissue (skin, subcutaneous tissue, muscle) was recorded. Eleven healthy male students performed 24 maximal eccentric actions of the elbow flexor muscles with their non-dominant arms. Muscle hardness, maximal isometric force (MIF), muscle soreness, plasma creatine kinase (CK) activity, relaxed elbow joint angle (RANG), upper-arm circumference (CIR) and B-mode ultrasound transverse images were measured before, immediately after, and 1-5 days after exercise. A long-lasting decrease in MIF, muscle swelling shown by increases in CIR and muscle thickness, large increases in plasma CK activity, and development of muscle soreness indicated that damage occurred to the elbow flexor muscles. The RANG had decreased by approximately 20 degrees at 1-3 days after exercise and showed a gradual recovery thereafter. The CIR increased gradually after exercise and peaked on day 5 post-exercise, the mean amount of increase in CIR being 18 mm. Muscle hardness measured at the relaxed elbow position did not change until 3 days after exercise, but increased significantly (P < 0.01) on days 4 and 5 post-exercise. On the other hand, muscle hardness measured when forcibly extending the shortened elbow joint increased significantly (P < 0.01) with time and peaked at 3 days after exercise. Muscle hardness assessed by the pressure method seems to reflect changes in muscle stiffness and swelling.

Adolescent↗
PubMed2000

Correlations between bone mineral density and circulating bone metabolic markers in diabetic patients.

Diabetic osteopenia, a known chronic complication of diabetes, has been demonstrated with alterations in the calcium-vitamin D endocrine system. In order to investigate the relationship between the decrease of bone density and the altered mineral metabolism in non-insulin-dependent diabetes mellitus (NIDDM), 104 male clinical-proven NIDDM patients were studied. All patients were examined on metacarpal bone mineral density (m-BMD) by means of computed X-ray densitometry (CXD) methods. The values of the Z-score of m-BMD were significantly lower than those of age-matched controls (P<0.01). There was a positive correlation between m-BMD and serum calcium levels (P<0.01), but a negative correlation was conversely observed between m-BMD and serum intact parathyroid hormone (PTH) (P<0.01), indicating that the negative calcium balance under diabetic conditions could cause the decrease of m-BMD in NIDDM. Interestingly, since a significantly positive correlation was found between circulating levels of calcium and parathyroid hormone-related peptide (PTHrP) (P<0.05) but not PTH, it seems likely that PTHrP plays a more compensatory role on the maintenance of calcium homeostasis than PTH under diabetic conditions. Based on these observations, the CXD method would be useful in measuring the mineral density of cortical bone, and would also be beneficial to investigate underlying pathogenetic mechanism of diabetic osteopenia.

Absorptiometry, Photon↗
PubMed2000

Circulating p53 antibody in patients with colorectal cancer: relation to clinicopathologic features and survival.

The presence of serum anti-p53 antibody has been reported to be associated with survival of patients with breast cancer, ovarian cancer, and hepatocellular carcinoma. To clarify prognostic significance of p53 antibody in colorectal cancer, serum p53 antibody was measured in patients with colorectal cancer. The 89 patients included 71 with colorectal cancer and 18 with colon polyp. An enzyme-linked immunosorbent assay was used to detect p53 antibodies in serum. Clinicopathological parameters such as age, sex, degree of differentiation of cancer, location of tumor, liver metastasis, stage classification, Dukes classification, CEA, CA19-9, and immunostaining of p53 and anti-p53 antibody were evaluated as prognostic factors of colorectal cancer. p53 antibody was positive in 18 of 71 (25%) with colorectal cancer, whereas it was positive in only 1 of 18 (6%) with colon polyp. The patients with p53 antibody had higher CEA and CA19-9 levels, higher positive rates of p53 protein expression in cancer cells, and higher liver metastasis rates. The p53 antibody positivity at stage classification I-IIIb/ Dukes classification A-C was significantly lower than that at stage classification IV/Dukes classification D. Overall survival in colorectal cancer patients with p53 antibody was significantly shorter than in those without p53 antibody. A Cox regression analysis showed that liver metastasis, stage classification, Dukes classification, CA19-9, and p53 antibody were significant prognostic factors in colorectal cancer. Serum anti-p53 antibody could serve as one of the prognostic factors in patients with colorectal cancer.

Aged↗
PubMed2000

Hoarse voice resulting from premature ageing in Werner's syndrome.

Werner's syndrome is characterized by clinical signs of premature ageing. A 42-year-old man presented with three-year history of hoarseness. Also noted were skin atrophy of the face and hands, ulcerations around the ankles, and a history of cataracts. A clinical diagnosis of Werner's syndrome was made. Laryngoscopy revealed bowed vocal folds resulting in a spindle-shaped defect with glottal incompetence during phonation. Examination also revealed decreased maximum phonation time and vocal fatigue. At surgery, atrophy of the vocalis muscle was noted. Furthermore, degeneration of muscle fibres was noted in the temporalis muscle. The atrophic changes in the vocal folds that occur with ageing and result in an increased fundamental frequency were seen in this patient. The characteristic hoarseness of Werner's syndrome appears to be the result of premature ageing of the vocal-folds.

Adult↗
PubMed1999

Molecular cloning and expression of a mouse thiamin pyrophosphokinase cDNA.

Thiamin pyrophosphokinase (EC 2.7.6.2) catalyzes the pyrophosphorylation of thiamin with adenosine 5'-triphosphate to form thiamin pyrophosphate. A mouse thiamin pyrophosphokinase cDNA clone (mTPK1) was isolated using a combination of mouse expressed sequence tag database analysis, a two-step polymerase chain reaction procedure, and functional complementation screening with a Saccharomyces cerevisiae thiamin pyrophosphokinase-deficient mutant (thi80). The predicted protein contained 243 amino acid residues with a calculated molecular weight of 27,068. When the intact mTPK1 open reading frame was expressed as a glutathione S-transferase fusion protein in Escherichia coli lacking thiamin pyrophosphokinase, marked enzyme activity was detected in the bacterial cells. The corresponding 2.5-kilobase pair mRNA was expressed in a tissue-dependent manner and was found at relatively high levels in the kidney and liver, indicating that the mode of expression of mTPK1 genes differs with cell type. The expression of mTPK1 genes in cultured mouse neuroblastoma and normal liver cells was unaffected by the thiamin concentration in the medium (10 microM versus 3.0 nM). This is the first report on identification of the primary sequence for mammalian thiamin pyrophosphokinase.

Amino Acid Sequence↗
PubMed1999

Unfolding and refolding of Escherichia coli chaperonin GroES is expressed by a three-state model.

The guanidine-hydrochloride (Gdn-HCl) induced unfolding and refolding characteristics of the co-chaperonin GroES from Escherichia coli, a homoheptamer of subunit molecular mass 10,000 Da, were studied by using intrinsic fluorescence, 1-anilino-8-naphthalene sulfonate (ANS) binding, and size-exclusion HPLC. When monitored by tyrosine fluorescence, the unfolding reaction of GroES consisted of a single transition, with a transition midpoint at around 1.0 M Gdn-HCl. Interestingly, however, ANS binding and size-exclusion HPLC experiments strongly suggested the existence of an intermediate state in the transition. In order to confirm the existence of an intermediate state between the native heptameric and unfolded monomeric states, a tryptophan residue was introduced into the interface of GroES subunits as a fluorescent probe. The unfolding reaction of GroES I48W as monitored by tryptophyl fluorescence showed a single transition curve with a transition midpoint at 0.5 M Gdn-HCl. This unfolding transition curve as well as the refolding kinetics were dependent on the concentration of GroES protein. CD spectrum and size-exclusion HPLC experiments demonstrated that the intermediates assumed a partially folded conformation at around 0.5 M Gdn-HCl. The refolding of GroES protein from 3 M Gdn-HCl was probed functionally by measuring the extent of inhibition of GroEL ATPase activity and the enhancement of lactate dehydrogenase refolding yields in the presence of GroEL and ADP. These results clearly demonstrated that the GroES heptamer first dissociated to monomers and then unfolded completely upon increasing the concentration of Gdn-HCl, and that both transitions were reversible. From the thermodynamic analysis of the dissociation reaction, it was found that the partially folded monomer was only marginally stable and that the stability of GroES protein is governed mostly by the association of the subunits.

Chaperonin 10↗
PubMed1999

Hyperostosis generalisata with striations of the bones: report of a female case and a review of the literature.

We report on a 70-year-old woman with generalized skeletal alterations, characterized by marked diaphyseal expansion of the long bones and coarse striations of the trabeculae of the tubular bones, ribs, pelvis and vertebral bodies. These findings were consistent with hyperostosis genralisata with striations of the bones, first described by Fairbank. Biopsy of the femur revealed a featureless sclerosed bone. This is the first report of a female patient with this rare sclerosing bone dysplasia.

Aged↗
PubMed1999

An operative procedure for advanced Kienböck's disease. Excision of the lunate and subsequent replacement with a tendon-ball implant.

Excision of the lunate and subsequent replacement with a tendon implant was performed in 22 patients with Kienböck's disease between 1971 and 1985. This procedure was indicated mainly for those with advanced Kienböck's disease, i.e., stage III or IV according to the Lichtman classification. After the collapsed lunate is removed, a tendon-ball implant, made of the palmaris longus and plantaris tendons is placed in the resultant space in the carpus. A forearm distractor is applied during the operation, and distraction is continued for 4 weeks postoperatively. We report the long-term results in 15 patients, whose average follow-up period was 16 years and 3 months. One patient with infection was excluded from the study because the implanted tendon was removed 2 weeks after the operation, and 6 patients were lost to follow-up. All patients were free of pain after the surgery. The flexion-extension range of the wrist increased by 14.2 degrees, on average, after the surgery. The average grip power of the operated hand was 90.2% of that in the non-operated hand. Calcification and ossification were frequent in the implanted tendons a few months postoperatively. The average carpal height ratio (defined as carpal height/length of the third metacarpal) was 0.53 before the operation and 0.49 at the time of follow-up. According to Dornan's classification of clinical results, 9 of the 15 patients were classified as having excellent results and 6 as good.

Adult↗
PubMed1999

Mutations in SLC19A2 cause thiamine-responsive megaloblastic anaemia associated with diabetes mellitus and deafness.

Thiamine-responsive megaloblastic anaemia (TRMA), also known as Rogers syndrome, is an early onset, autosomal recessive disorder defined by the occurrence of megaloblastic anaemia, diabetes mellitus and sensorineural deafness, responding in varying degrees to thiamine treatment (MIM 249270). We have previously narrowed the TRMA locus from a 16-cM to a 4-cM interval on chromosomal region 1q23.3 (refs 3,4) and this region has been further refined to a 1.4-cM interval. Previous studies have suggested that deficiency in a high-affinity thiamine transporter may cause this disorder. Here we identify the TRMA gene by positional cloning. We assembled a P1-derived artificial chromosome (PAC) contig spanning the TRMA candidate region. This clarified the order of genetic markers across the TRMA locus, provided 9 new polymorphic markers and narrowed the locus to an approximately 400-kb region. Mutations in a new gene, SLC19A2, encoding a putative transmembrane protein homologous to the reduced folate carrier proteins, were found in all affected individuals in six TRMA families, suggesting that a defective thiamine transporter protein (THTR-1) may underlie the TRMA syndrome.

Amino Acid Sequence↗
PubMed1999

Changes in plasma enzyme activity after intramuscular injection of bupivacaine into the human biceps brachii.

The purpose of this study was to examine the time course of changes in plasma creatine kinase (CK), lactate dehydrogenase (LDH), aspartate (AST) and alanine aminotransferase (ALT) activity after intramuscular injection of 0.5% bupivacaine (BPVC). A total of 10 mL BPVC was injected into the biceps brachii (two sites, 5 mL per site) of five healthy, male subjects. Blood samples were obtained from the antecubital vein before and 2, 4, 8, 12, 24, 48, 72 and 96 h after the injection. Affected muscle size was visualized using magnetic resonance imaging (MRI), which was performed 4 days after the injection. Plasma CK activity started to increase 2 h and peaked 12 h after the injection. The peak CK activity (470 +/- 62 IU L-1) was approximately four times the pre-injection value (133 +/- 24 IU L-1), and no additional increase was observed after 24 h. Plasma LDH, AST and ALT activities did not change significantly over time. Muscle around the injection sites showed increased T2 signal intensity using MRI. When smaller (2 mL) or larger (20 mL) amounts of BPVC were injected into the biceps brachii in additional experiments, the amount of increase in plasma CK activity appeared to be related to the size of the affected muscle. It was concluded that CK started to leak from damaged muscle cells shortly after the BPVC injection, and the amount of increase in plasma CK activity appeared to reflect the amount of muscle damage.

Adult↗
PubMed1999

Ubiquitous localization of leukotriene A4 hydrolase in the rat nephron.

BACKGROUND: Leukotriene (LT) B4 is a well-known inflammatory mediator and is implied to play some roles in glomerulonephritis. Although LTA4 hydrolase, a final-step key enzyme to produce LTB4, is located in glomerular mesangial cells, as well as in leukocytes, platelets, and endothelial cells, its precise distribution in the kidney other than in mesangial cells remains unknown. Therefore, we have investigated the localization of mRNA, protein, and enzyme activity of LTA4 hydrolase in the rat kidney. METHODS: Microdissection reverse transcriptase-polymerase chain reaction was used for the determination of LTA4 hydrolase mRNA. The enzyme protein was detected by Western blot, and immunohistochemistry was performed. Finally, LTA4 hydrolase activity and LTB4 were assayed in kidney tissues. RESULTS: LTA4 hydrolase mRNA was detectable in all microdissected nephron segments of the cortex and outer medulla. The corresponding size of approximately 70 kDa protein was shown in descending order in the inner medullary > outer medullary >/= cortical homogenates. The immunohistochemical study demonstrated the ubiquitous presence of the enzyme in all nephron segments of cortex, outer medulla, and inner collecting tubules. LTA4 hydrolase activity was detected in the inner medullary >/= outer medullary >/= cortical tissue homogenates. LTB4 was demonstrated in the inner medullary > outer medullary >/= cortical tissues during the basal condition, and was time-dependently increased by stimulation with arachidonic acid and ionomycin in the cytosolic fraction from outer medulla and in the glomerular suspension. CONCLUSIONS: These results strongly suggest that renal tubular cells as well as glomerular cells have an LTB4-forming potency, which may participate in physiological and pathophysiological roles in the kidney.

Animals↗
PubMed1998

Association of nucleoside diphosphate kinase nm23-H2 with human telomeres.

Telomeres, the ends of eukaryotic chromosomes, are essential structures formed by specific protein-DNA complexes that protect chromosomes from degradation and end-to-end fusion. TRF1, a double-stranded telomeric TTAGGG-repeat binding protein, is associated with mammalian telomeres and controls telomere length by inhibiting the action of telomerase. We identified human nucleoside diphosphate kinase nm23-H2 as a human TRF1-interacting protein by yeast two-hybrid screening. In vitro-binding assays using different recombinant nucleoside diphosphate kinases showed that TRF1 predominantly binds the nm23-H2 isoform rather than nm23-H1. Electrophoretic mobility shift analysis revealed that the recombinant nm23-H2 protein can bind the single-stranded telomeric TTAGGG-repeat while it cannot bind the double-stranded telomeric repeat. The synthetic 20 base oligoribonucleotide, which consists of the template sequence CUAACCCUAAC and the adjacent region of the RNA component of human telomerase, was also found to form the complex with the recombinant nm23-H2 protein. Furthermore, the affinity of telomerase for its substrate was increased in vitro by presence of the plentiful nm23-H2 protein. These findings indicate a close relationship between nm23-H2 and human telomeres and suggest a new biological role for nucleoside diphosphate kinase.

Cloning, Molecular↗
PubMed1998

Refined mapping of the gene for thiamine-responsive megaloblastic anemia syndrome and evidence for genetic homogeneity.

Thiamine-responsive megaloblastic anemia (TRMA, also known as Rogers syndrome, OMIM 249270) is a rare autosomal recessive disorder characterized by a triad of megaloblastic anemia, diabetes mellitus, and sensorineural deafness. Patients respond, to varying degrees, to treatment with megadoses of thiamine. We have recently shown genetic linkage of the TRMA gene to a 16-centimorgan (cM) region on 1q23.2-1q23.3 based on the analysis of four large, inbred families of Alaskan, Italian, and Israeli-Arab origin. Here we narrow the TRMA interval down to 4 cM based on genetic recombination, homozygosity mapping, and linkage disequilibrium (highest LOD score of 12.5 at D1S2799, at a recombination fraction of 0). We provide further evidence that the TRMA gene is located in this region and confirm the homogeneity of the disease. In this analysis, we genotyped seven additional families of diverse ethnic origin (Pakistani, Indian, Italian, Brazilian, and Japanese), and analyzed additional markers in two previously reported families showing evidence of linkage disequilibrium in a large area of their haplotypes. The multi-system manifestations of TRMA suggest that thiamine has a pivotal role in a multiplicity of physiological processes. Mapping the TRMA gene and understanding the molecular basis of the disease might, thus, shed light on the role of thiamine in common disorders such as deafness, anemia, and diabetes.

Anemia, Megaloblastic↗