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Biomedical subjects

K Nakata

Publications and source records attributed to K Nakata.

At least 289 records · Page 16Linked to original sources
PubMed1995

Second-look arthroscopy after meniscal repair. Review of 132 menisci repaired by an arthroscopic inside-out technique.

From 1986 to 1993, we repaired 278 torn menisci in 264 patients using an arthroscopically assisted inside-out technique. A total of 132 meniscal repairs in 122 patients were evaluated by second-look arthroscopy. At review, only nine patients had meniscal symptoms, such as locking, swelling or pain. Ninety-seven menisci (73%) had healed completely at the repair site, but there were new tears in different areas of 21 menisci, some of which had complete healing at the repair site. Incomplete healing, seen in 23 menisci (17%), was frequently near the popliteus tendon, most commonly where there had been an associated anterior-cruciate-ligament injury. Arthroscopically-assisted meniscal repair seems to be a reliable procedure, but some clinically successful cases had incomplete healing at the repair site or a newly-formed tear in the meniscal body or both. These lesions may cause meniscal symptoms to appear at a later date.

Adolescent↗
PubMed1995

[Successful treatment of acute myelomonocytic leukemia developed from MDS with cytarabine ocfosfate (SPAC)].

A 65-year-old female with acute myelomonocytic leukemia (AMMoL) developed from myelodysplastic syndrome (MDS), successfully treated with cytarabine ocfosfate (SPAC) is reported. Ubenimex, calcitriol and corticosteroid had a minor effect on her MDS. Since she had severe anemia and congestive heart failure on developing leukemia, she was treated with oral administration of SPAC, a cytidine deaminase resistant derivative of Ara-C. After the second course of SPAC (200 mg/day, for 14-28 days), marked erythroid bursts were found and she entered complete remission. The samplings of SPAC and its metabolites of SPAC were investigated in 2 cases including this case, but there seemed to be no relation between their content and effects. In AML patients, especially in cases developed from MDS, SPAC might be useful because it can be given orally even in an outpatient.

Aged↗
PubMed1995

Low copy number and limited variability of proviral DNA in alveolar macrophages from HIV-1-infected patients: evidence for genetic differences in HIV-1 between lung and blood macrophage populations.

BACKGROUND: We investigated the human immunodeficiency virus (HIV) proviral DNA sequence and copy number in alveolar macrophages (AM) and peripheral blood monocytes (PBM) from 10 HIV-positive patients without any active concurrent pulmonary disease to understand the nature of HIV-1 infection in vivo in the lung microenvironment. MATERIALS AND METHODS: The 10 seropositive patients without active pulmonary disease were selected based on chest roentegenography and pathological/cytological test of bronchoalveolar (BAL) fluid. In order to determine accurate proviral copy numbers, AM and PBM were isolated to 99 and 94% purity, respectively, and quantitative polymerase chain reaction (PCR), with a sensitivity to detect three copies of HIV proviral DNA per 10(5) cells, was applied. For analysis of genetic variation in HIV-1, PCR-amplified HIV-1 DNA from AM and PBM of five patients were subcloned and 2-12 clones from each sample underwent DNA sequence analysis of HIV-1 gp120 V3-V5. Heteroduplex mobility assays were performed to confirm the results of the sequence analysis. RESULTS: The proviral copy number in AM or PBM were less than 20 copies/10(5) cells in all patients, and five patients had less than the detection limit. There was no significant difference in HIV copy number between AM and PBM. No correlation was found between PBM/AM HIV copy number and CD4+ lymphocyte count in the peripheral blood. Sequence analysis revealed that the mean intrapatient genetic similarity in AM was 97.5 +/- 0.18% (n = 107), which was significantly higher than that in PBM (96.2 +/- 0.26% (n = 94), p < 0.001), suggesting that variability of HIV-1 DNA in AM was relatively limited. Divergence occurred when AM derived HIV-1 sequence was compared with PBM derived sequence from the same patient (95.8 +/- 0.17% (n = 223) p < 0.001). Phylogenetic analysis of DNA sequence demonstrated complete separation of HIV lineages from lung and blood in four of five patients. CONCLUSIONS: The results suggest the HIV-1 infection in AM is restricted in vivo with low viral burden and homogenous genotype. We propose that the pulmonary microenvironment may limit the extent of HIV-1 infection.

Adult↗
PubMed1994

Risk of hepatocellular carcinoma in patients with cirrhosis in Japan. Analysis of infectious hepatitis viruses.

BACKGROUND: The development of hepatocellular carcinoma (HCC) is associated closely with cirrhosis. In the present study, the cumulative risk of HCC in patients with cirrhosis was investigated. METHODS: A total of 401 patients were registered from April 1977 and followed for a mean of 4.4 years. Of 401 patients, 255 (64%) were tested for hepatitis B surface antigen (HBsAg) and antibody (anti-) to the hepatitis C virus (HCV); 87 (34%) patients were positive for HBsAg but were negative for anti-HCV (hepatitis B virus [HBV] group), 126 (49%) were negative for HBsAg but were positive for anti-HCV (HCV group), 10 (4%) were positive for both and 32 (13%) were negative for both (non-B non-C group). RESULTS: By the end of March 1993, HCC was diagnosed in 127 (31.6%) patients. The cumulative risk of HCC in the HCV group was slightly higher than that in HBV group (P = 0.3, 5-year risk: 36.9 versus 21.2%). In contrast, the rate was significantly lower in the non-B non-C group than in the HBV or HCV groups (P < 0.05 and P < 0.01, respectively, 5 year risk: 12.4%). CONCLUSIONS: These results suggest that not only HBV infection but also HCV infection increase the risk for HCC in patients with cirrhosis.

Adult↗
PubMed1994

Treatment of hepatocellular carcinoma with transcatheter arterial embolization. Analysis of prognostic factors.

BACKGROUND: Transcatheter arterial embolization (TAE) is a useful treatment modality for hepatocellular carcinoma (HCC). To study the prognostic factors, survival time of patients with HCC after TAE was analyzed retrospectively using clinical manifestations of coexisting liver cirrhosis and clinical features of HCC. METHODS: Eighty-seven patients with HCC were treated with TAE between 1984 and 1991 and observed at Nagasaki University Hospital. All the patients also had liver cirrhosis. RESULTS: The survival time of the 87 patients after TAE ranged from 2 months to 8.1 years (mean +/- standard deviation, 2.7 +/- 0.3 years). Survival curves after TAE did not differ between men and women (P > 0.5) or between hepatitis B and C viral infection (P > 0.8), but they depended on clinical stages of coexisting liver cirrhosis (P < 0.01). The cumulative survival after TAE was significantly longer in patients with uninodular tumors than in patients with multinodular tumors (P < 0.0001) (3-year survival, 53.3% vs. 13.3%; 5-year survival, 32.2% vs. 3.3%, respectively). In contrast, patients' survival time was not associated with the size of the tumor detected at the time of treatment with TAE (P > 0.1). CONCLUSIONS: Treatment of HCC with TAE is well indicated regardless of tumor size for patients with nonadvanced liver cirrhosis and uninodular tumors. Alternatively, treatment of HCC with TAE alone is still insufficient in patients with multinodular tumors. Other treatment modalities in combination with TAE should be considered to achieve a more favorable prognosis of these patients.

Adult↗
PubMed1994

Serial change of sliding in intertrochanteric femoral fractures treated with sliding screw system.

We investigated the serial change of the extent of sliding of the compression screw in 42 intertrochanteric femoral fractures fixed with a sliding screw system. Neither age, gender, bone density, fracture type nor quality of fracture reduction could accurately predict healing time. There was a significant correlation between the extent of sliding at union and healing time (correlation coefficient r = 0.505). The average healing time in group B (the extent of sliding at union of 8 mm or greater) was 13.8 weeks postoperatively, and that in group A (the extent of sliding at union of less than 8 mm) was 8.9 weeks. There was a significant difference in the average healing time between groups A and B (P = 0.0004). The extent of sliding at union had a influence on the healing time. The phenomenon of sliding progressed mainly during the first 2 weeks postoperatively. There was a significant positive correlation between the extent of sliding at union and the extent of sliding at 2 weeks postoperatively (r = 0.977). An assessment using the extent of sliding at 2 weeks postoperatively can accurately predict the extent of sliding at union and the healing time. It is important to examine the phenomenon of sliding during the early postoperative course, especially until 2 weeks postoperatively, in order to predict fracture repair.

Age Factors↗
PubMed1994

Phosphorus-31 nuclear magnetic resonance in vivo spectroscopy of human liver during hepatitis A virus infection.

To evaluate the changes in hepatocellular phospholipid metabolism during hepatitis virus infection, 26 patients with acute viral hepatitis A were studied by means of phosphorus-31 nuclear magnetic resonance (31P-NMR) spectroscopy. The spectroscopy of liver showed six signal components in all patients as well as in the normal volunteers. During the early phase of illness, the phosphomonoester (PME)-phosphodiester (PDE) ratios in the patients became markedly greater than the ratios in the controls (P < 0.001). Within six weeks after the onset, the PME/PDE ratios returned to the level of controls. The time course analysis indicated an inverse correlation between the PME/PDE ratio and the period of time after onset (r = 0.738, P < 0.001). The spectral changes of human liver observed in acute viral hepatitis A are similar to those in the regenerating rat liver, indicating that 31P-NMR spectroscopy allows a noninvasive study of cell turnover in human liver disease associated with acute virus infection.

Acute Disease↗
PubMed1994

Reciprocal regulation of alpha-fetoprotein and albumin gene expression by butyrate in human hepatoma cells.

BACKGROUND/AIMS: Butyrate, a product of colonic bacterial flora, functions as an antiproliferative agent and induces cell differentiation in a variety of cell types. In the present study, the effects of butyrate on cell growth and expression of alpha-fetoprotein (AFP) and albumin genes in HuH-7 human hepatoma cells were investigated. METHODS: The HuH-7 cells were treated with sodium butyrate (0-1 mmol/L), and numbers of viable cells were counted at 24, 48, and 72 hours after treatment. To elucidate the effects of sodium butyrate on AFP and albumin gene expression, Northern blotting and transient chloramphenicol acetyltransferase plasmid transfection experiments were performed. RESULTS: Cell growth was dose dependently inhibited by sodium butyrate. By Northern blot analysis, the level of AFP messenger RNA was reduced by treatment with sodium butyrate, whereas the level of albumin messenger RNA was elevated by this treatment. In transient chloramphenicol acetyltransferase plasmid transfection experiments, sodium butyrate repressed the AFP promoter activity but did not change the AFP enhancer or silencer activities. In contrast, the albumin promoter activity was stimulated by sodium butyrate. CONCLUSIONS: These results suggest that butyrate leads to the reciprocal differentiating regulation of AFP and albumin gene expression at the transcriptional level in human hepatoma cells.

Albumins↗
PubMed1994

Changes in the prevalence of HBeAg-negative mutant hepatitis B virus during the course of chronic hepatitis B.

Hepatitis B virus with a G-to-A point mutation at nucleotide 83 in the precore region (mutant hepatitis B virus 83), which cannot produce HBeAg, is commonly found in HBe antibody-positive hepatitis B virus carriers. We analyzed the consecutive changes in the prevalence of mutant hepatitis B virus 83 during the course of chronic hepatitis B virus infection. Forty-five patients with chronic hepatitis B who were followed up for more than 2 yr in our hospital were studied by polymerase chain reaction in combination with a restriction fragment length polymorphism assay. Mutant hepatitis B virus 83 was found in 14 of 18 (78%) HBe antibody-positive patients and in 8 of 27 (30%) HBeAg-positive patients at baseline. Eighteen of the 22 patients who had mutant hepatitis B virus 83 (82%) showed mixed viral populations of wild-type hepatitis B virus and mutant hepatitis B virus 83, whereas 4 (18%) had only mutant hepatitis B virus 83 and were positive for HBe antibody. During a 2 yr follow-up period, mutant hepatitis B virus 83 was newly detected in 9 of 23 (39%) patients who had wild-type hepatitis B virus alone at baseline. The proportion of mutant hepatitis B virus 83 to whole hepatitis B virus in the serum of 18 patients with mixed viral populations at baseline fluctuated during follow-up. In contrast, wild-type hepatitis B virus was never detected throughout the study in all four patients who had only mutant hepatitis B virus 83 at baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Failure of protection against endotoxin hepatotoxicity by selenium.

The present study was undertaken in rats to test the ability of selenium to prevent endotoxin hepatotoxicity. There were no significant morphological changes in the liver and no abnormalities of liver function in rats given 0, 6.25 or 12.5 mumol of selenium. Endotoxin administration to these rats induced focal hepatocellular coagulative necrosis and increased serum transaminase activities. However, endotoxin hepatotoxicity and mortality of the rats given endotoxin after treatment with 6.25 or 12.5 mumol of selenium were not significantly lower than in those given endotoxin alone. These facts suggest that selenium does not prevent endotoxin hepatotoxicity.

Animals↗
PubMed1994

Role of activated macrophages in augmentation of endotoxin hepatotoxicity.

In this study, to clarify the role of activated macrophages in the augmentation of endotoxin hepatoxicity, rats were pretreated with zymosan, an activator of macrophages, before the induction of endotoxin hepatotoxicity, and some were given pentoxifylline, an inhibitor of tumour necrosis factor production. The intravenous injection of zymosan induced many granulomas composed of macrophages in the lungs and the liver, while the intraperitoneal injection caused granulomas in the greater omentum. Endotoxin hepatotoxicity. as shown by focal and random hepatocellular coagulative necrosis and elevation of serum transaminase activities, was more intense in the rats pretreated with zymosan than in those which were not injected with zymosan. This augmented endotoxin hepatotoxicity was significantly inhibited by pentoxifylline treatment. These findings indicate that endotoxin hepatotoxicity may be augmented in the presence of activated macrophages which produce chemical mediators, particularly tumour necrosis factor.

Animals↗
PubMed1994

Protective effects of sparfloxacin in experimental pneumonia caused by Chlamydia pneumoniae in leukopenic mice.

The in vivo antichlamydial activities of sparfloxacin and reference drugs were examined in a experimental model of pneumonia caused by Chlamydia pneumoniae in leukopenic mice; their in vitro activities were also examined. The most potent agents in vitro were sparfloxacin (MICs for C. pneumoniae Kajaani and IOL 207, (0.031 and 0.031 micrograms/ml, respectively), clarithromycin (0.031 and 0.031 micrograms/ml, respectively), and minocycline (0.031 and 0.031 micrograms/ml, respectively); these were followed by tosufloxacin (0.063 and 0.125 micrograms/ml, respectively) and ofloxacin (0.5 and 0.5 micrograms/ml, respectively). The MBCs of sparfloxacin, tosufloxacin, ofloxacin, clarithromycin, and minocycline for these two strains were 0.063 and 0.063 micrograms/ml, 0.125 and 0.25 micrograms/ml, 1.0 and 1.0 micrograms/ml, 0.125 and 0.125 micrograms/ml, and 0.25 and 0.25 micrograms/ml, respectively. Fatal pneumonia was induced by intranasal inoculation of cyclophosphamide-treated leukopenic mice with C. pneumoniae IOL 207; infiltration of neutrophils and lymphocytes was observed in the lungs of these mice by histopathological examination. The 50% effective dose of sparfloxacin (oral dose of 0.97 mg/kg of body weight) against the pneumonia was the lowest among the drugs tested; this was followed by those of minocycline (2.22 mg/kg), tosufloxacin (3.47 mg/kg), clarithromycin (4.66 mg/kg), and ofloxacin (16.6 mg/kg). The results indicate that it may be worthwhile to use sparfloxacin against C. pneumoniae infections in humans.

Animals↗
PubMed1994

Gamma-delta T cells in sarcoidosis. Correlation with clinical features.

This study investigated the relationship between the clinical features of sarcoidosis and the level of peripheral blood gamma-delta (gamma delta) T cells. Both the mean percentage of T cells and the mean cell number of gamma delta T cells in the peripheral blood were significantly higher in patients with clinically active sarcoidosis than in patients with inactive sarcoidosis or active tuberculosis and in normal subjects (active sarcoidosis: 18.9 +/- 17.2%, 142 +/- 130.4 cells/microliters, n = 29; inactive sarcoidosis: 7.0 +/- 3.7%, 48.7 +/- 35.0 cells/microliters, n = 16; active tuberculosis: 4.3 +/- 3.2%, 47.9 +/- 36.6 cells/microliters, n = 19; control subjects: 5.0 +/- 1.9%, 77.6 +/- 37.7 cells/microliters, n = 12). gamma delta T cells were significantly elevated in patients with sarcoidosis for 2 yr or more or those with Stage III radiographs. The level of gamma delta T cells, however, showed no correlation to the serum angiotensin-converting enzyme, a marker of active granuloma formation. gamma delta T cells were scarcely seen in bronchoalveolar lavages and in biopsy specimens, suggesting that these cells did not increase at the sites of inflammation. These findings suggest that increased levels of gamma delta T cells in the peripheral blood occur in active, long-term sarcoidosis, but that they are not directly related to granuloma formation.

Adult↗
PubMed1994

Exacerbation of thyroid autoimmunity by interferon alpha treatment in patients with chronic viral hepatitis: our studies and review of the literature.

In the present studies, the long term effects of IFN alpha on thyroid function and thyroid autoantibodies were evaluated in 42 patients with chronic viral hepatitis type C treated with IFN alpha for at least 4 months. Before IFN treatment, 41 patients tested were all euthyroid. Five (12%) out of 24 patients tested had positive tests for thyroid autoantibodies. MCHA/TPOAb was detected in all 5 and TGHA/TGAb in 3 out of these 5 patients. Six to 10 x 10(6) units (U) of recombinant or natural IFN alpha were given intramuscularly daily for the first 2 to 4 weeks, followed by 3 to 10 x 10(6) U thrice weekly for the subsequent 14 to 22 weeks. Thyroid dysfunction and/or rises in titers of thyroid autoantibodies were observed in 6 patients during IFN alpha treatment; clinically overt thyroid dysfunctions, destructive thyroiditis and thyrotoxicosis of unidentified etiology, developed in 2 patients 4 to 5 months after start of IFN treatment, subclinical hypothyroidism with a slight increase in serum TSH concentrations but no serum thyroid hormone alternations was observed in 2 patients, and increases in titers of thyroid autoantibodies without thyroid dysfunction were found in 2 patients. Thus, IFN alpha exacerbated thyroid autoimmunity exclusively in all patients with positive tests for thyroid autoantibodies prior to treatment, but did not induce thyroid autoimmunity in thyroid autoantibody-negative patients. These data suggest that the prolonged IFN alpha therapy can lead to exacerbation of thyroid autoimmunity in susceptible (thyroid autoantibody-positive) patients.

Adult↗