Biomedical subjects
Publications and source records attributed to Y Maeda.
A case with primary torsion of the greater omentum is reported. This pathological condition is an uncommon cause of acute abdominal emergency and it is very difficult even for general surgeons to differentiate this from other acute abdomen. The etiology remains unknown and the treatment of choice is resection of the affected organ.
Expression of low-affinity Fc receptor for IgE (Fc epsilon RII), which is identical to the lymphocyte differentiation antigen CD23, is associated with activation of lymphoid cells. The mechanism of signal transduction through Fc epsilon RII/CD23 was dissected by transfection of cDNA coding for Fc epsilon RII to the YT human natural killer-like cell line, activation of which was easily detected by the induction of interleukin 2 receptor/p55(Tac). Cross-linking of Fc epsilon RII/CD23 with H107 anti-Fc epsilon RII monoclonal antibody markedly enhanced interleukin 2 receptor/p55 expression on the YT cells transfected with Fc epsilon RII cDNA (YTSER cells). Similar induction of interleukin 2 receptor/p55 by the cross-linking of Fc epsilon RII was observed on an Epstein-Barr virus-transformed B-cell line, 3B6, and fresh leukemic cells isolated from a patient with B-cell chronic lymphoblastic leukemia. Thus Fc epsilon RII/CD23 provides activation signals not only in YTSER cells but also in activated B cells. A possible involvement of protein-tyrosine kinase in the Fc epsilon RII-mediated signal transduction was studied. Fc epsilon RII was physically associated with a src family tyrosine kinase p59fyn and not with p56lck, which was also found in YT cells. Recently it was reported that p59fyn was associated with T-cell antigen receptor. Our results collectively suggest the multiple functions of p59fyn that may be implicated in Fc epsilon RII-mediated activation signal in YT cells.
The prevalence of hepatitis C virus infection in hemodialysis patients in Japan was examined using sera from 418 patients from six dialysis units in 1989. The authors made use of an enzyme-linked immunosorbent assay (Ortho Diagnostics). Antibody to hepatitis C virus (anti-HCV) was detected in 127 patients (30.4%), the frequency varying from 20.0% to 34.9% in different units. The mean prevalence of anti-HCV was 20 times higher than that in blood donors. Anti-HCV positivity was not associated with antibody to hepatitis B core antigen, which was not a surrogate marker for non-A, non-B hepatitis agents in this study. Another striking finding of this study was that 84.3% of the anti-HCV-positive patients had normal liver function. Anti-HCV positivity correlated positively with the number of blood transfusions and increased with the duration of hemodialysis; however, it was 22.1% even in 113 patients never given blood transfusion. Acquisition of hepatitis C virus by dialysis patients is, therefore, not only through blood transfusions but also because of hepatitis C virus present within the unit itself. Liver dysfunction in the anti-HCV-positive patients was rare.
The gene and protein structure of the mouse UBF (mUBF), a transcription factor for mouse ribosomal RNA gene, have been determined by cDNA and genomic clones. The unique mUBF gene consists of 21 exons spanning over 13 kb. Two mRNAs coding for mUBF1 and mUBF2 having 765 a.a. and 728 a.a., respectively, are produced by an alternative splicing of exon 8. It specifies 37 amino acids constituting a part of the regions homologous to high mobility group proteins (HMG box 2). A human UBF (hUBF) cDNA obtained by polymerase chain reaction also indicates the presence of two kinds of mRNAs, the shorter form lacking the same region as mUBF2. Comparison of the cDNAs from hUBF and mUBF revealed an unusual conservation of nucleotide sequence in the 3'-terminal non-coding region. We examined the relative amounts of expression of mUBF1 and mUBF2. The eight tissues studied contained both molecular species, although mUBF2 was the predominant form of UBF. The mRNA of mUBF1 was expressed one half of the mUBF2 in quiescent mouse fibroblasts but reached the same amount in growing state.
Using the peptides from amino acids 100-130 of the HTLV-I gag protein, 175-199 of the HTLV-I env protein and the corresponding peptides of HTLV-II (amino acids 106 to 135 of the gag protein and 171 to 196 of the env protein), we tested for reactivity against antibodies by enzyme immunoassay in sera from HTLV-I and HTLV-II carriers. The peptides derived from the env proteins have high specificity for antibody binding. The peptide based on amino acids 175-199 of HTLV-I reacted with antibodies in sera from all HTLV-I carriers, and the peptide composed of amino acids 171-196 of HTLV-II reacted with antibodies in sera from all HTLV-II carriers. For the peptides derived from the gag proteins, we observed some cross-reactivity in sera from persons with anti-HTLV-I and anti-HTLV-II, due to antibody binding to the peptide corresponding to 12 amino acids from the C-terminal end of the gag protein. Separate enzyme immunoassays that used the four synthetic peptides as antigens clearly distinguished between serum with antibodies to HTLV-I or HTLV-II in various individuals and excluded false positive results using the particle agglutination assay that used a whole-virus lysate of HTLV-I as antigen.
Despite evidence for the expression of low affinity Fc receptor for IgE (Fc epsilon RII)/CD23 in T cell lines and pathologic T cells, Fc epsilon RII/CD23 in normal human T cells is still unclear. We studied the expression of Fc epsilon RII/CD23 on T cells in short-term culture of normal human PBMC stimulated with 15 micrograms/ml PHA. PHA stimulation also resulted in the release of soluble Fc epsilon RII/CD23 (IgE binding factor). Using two-dimensional flow cytometry, more than 10% of the Fc epsilon RII/CD23+ cells were found to co-express CD3 Ag. Both CD4+ and CD8+ T cells expressed Fc epsilon RII/CD23. The induction of Fc epsilon RII/CD23 on PHA-activated T cells was enhanced by IL-2 as well as IL-4. Both IL-2 and IL-4 also augmented PHA-induced production of soluble Fc epsilon RII/CD23. The enhanced expression of Fc epsilon RII/CD23 on T cells by both lymphokines was suppressed by rabbit anti-IL-4 antiserum, suggesting the involvement of an IL-4-dependent process even in the IL-2-dependent Fc epsilon RII/CD23 expression on T cells. The expression of mRNA for Fc epsilon RII/CD23 on PHA and IL-4-stimulated PBMC was examined by Northern blot analysis. Fc epsilon RII/CD23 mRNA was detected in RNA prepared from the T cell fraction depleted of B cells and macrophages (Fc epsilon RII+CD3+ = 6.2%, Fc epsilon RII+CD3- = 0.8%). The expression of the mRNA for Fc epsilon RII/CD23 on CD3+ T cells was also confirmed by in situ hybridization with Fc epsilon RII/CD23 cDNA combined with CD3 rosette formation at the single cell level.
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We conducted case-control studies of hepatocellular carcinoma (HCC) and liver cirrhosis (LC) in relation to hepatitis C virus (HCV) and hepatitis B virus infection, involving 91 patients with HCC, 75 patients with LC who had no evidence of HCC, and 410 control subjects from the Japanese population. Serum antibody to HCV (anti-HCV) was detected by both enzyme-linked immunosorbent assay and recombinant immunoblot assay in 51, 51, and 3% of HCC, LC, and controls, respectively, whereas the corresponding prevalence of serum hepatitis B surface antigen (HBsAg) was 21, 11, and 2%, respectively. The relative risks (and 95% confidence intervals) for the presence of serum anti-HCV were estimated as 52.3 (23.9-114.3) for HCC and 64.4 (27.4-151.4) for LC. These values exceeded the relative risk of HCC (15.3) and that of LC (6.1) for positive serum HBsAg. Among male patients with HCC or LC, anti-HCV rates were very high in blood recipients (about 70%), heavy drinkers (46-62%), and those who had no identifiable risk factors (65-75%), indicating possible transmission of HCV via routes other than transfusion. No significant difference in anti-HCV status was observed between the HCC and LC groups. It was notable that anti-HCV was much less prevalent among HBsAg-positive patients with HCC or LC than among HBsAg-negative ones. There was a slight to moderate increase in HCC or LC risk among blood recipients and heavy drinkers after adjustment for anti-HCV status. These results indicate that, in Japan, the possible role of HCV infection in the etiology of HCC and LC is extremely large and seems to be more important than chronic hepatitis B virus infection.
Nonspecific lipid transfer protein (nsLTP) partially purified from human liver stimulated human microsomal cholesterol 7 alpha-hydroxylase activity. Addition of the nsLTP preparation to the reaction mixture enhanced the activity two-fold. Treatment of the nsLTP preparation with anti-rat nsLTP antiserum, which cross-reacts with human nsLTP, reduced the 7 alpha-hydroxylase-stimulating ability. These observations suggested that nsLTP plays a role in regulating the 7 alpha-hydroxylase activity in the human liver. 7 alpha-Hydroxylase activity in eight patients with cholesterol gallstones (4.7 +/- 1.6 pmol/min per mg microsomal protein) was significantly lower than that in five controls (7.9 +/- 3.4) (P less than 0.05). The amount of nsLTP in the cytosolic fraction (105,000 X g supernatant) of human liver was determined by dot-blotting immunoquantitation with the antiserum. The cytosolic level of nsLTP in the liver of the patients (716 +/- 239 cpm/3 micrograms protein) was higher than that in the controls (438 +/- 184) although the difference between the two groups was not statistically significant. This suggested that control of the cytosolic level may be affected in patients with cholesterol gallstones.
In vitro transcription of the ribosomal RNA gene (rDNA) shows a remarkable species specificity such that human and mouse rDNA cannot use heterologous extracts of each other. The region that is responsible for this specificity has been studied using human-mouse chimeric genes and characteristic structures of both core promoters are presented. When the mouse sequence is substituted by the corresponding human sequence from upstream, the promoter activity in the mouse extract begins to decline at nucleotide -32 or -30, decreasing gradually and is lost completely at -19. A similar gradual decrease was noted for the 3' side substitution, which started at nucleotide -14 and was completed when up to the nucleotide -22 mouse position was replaced by the corresponding sequence from human. Thus, in the mouse rDNA core promoter, the sequence that is involved in species specificity resides only in a stretch encompassing the non-conserved region between the distal conserved sequence (DCS) and the proximal conserved sequence (PCS), plus two altered nucleotides in the PCS. When human rDNA is transcribed with human cell extract, the mouse sequence cannot substitute for the human sequence within the region from nucleotide -43 to +17 without affecting promoter activity significantly. This asymmetry of species specificity is due to the presence of nucleotides -43, +1 and +17, which are sensitive to change in only the human core promoter. The difference in the 5' border is ascribed to the species specificity of a transcription factor TFID, which recognizes this region. But the large difference of the 3' border is apparently due to another factor, possibly RNA polymerase I itself, because this region is not recognized by TFID in either human or mouse. Mammalian rDNA core promoter appears to consist of a tandem mosaic in which three evolutionarily conserved sequences alternate with non-conserved sequences having certain functionally important nucleotides. Not only non-conserved sequences and non-conserved nucleotides in conserved sequences, but also the spacings between the three conserved regions, play a crucial role in species specificity.
A large number of patients with peripheral neuropathy and IgM paraproteinemia have IgM monoclonal antibodies which recognize a carbohydrate determinant shared by myelin-associated glycoprotein (MAG) and sulfated glucuronyl glycolipids (SGGLs). There is considerable evidence that these IgM monoclonal antibodies are responsible for demyelination in this disorder. To study the pathogenic role of SGGLs in this type of neuropathy, we sensitized Lewis rats with sulfated glucuronyl paragloboside (SGPG), a major SGGL. Fifty percent of the animals (8/16) developed neurological symptoms such as mild to moderate distal tail tone loss, with or without abnormal posture, along with development of anti-SGPG antibodies. These antibodies reacted with SGGLs, but not with rat MAG. Morphological studies showed: (1) axonal change in the lateral aspects of the dorsal columns in the spinal cord; and (2) damage to the endothelial cells in the spinal cord which suggested a breakdown of the blood-brain barrier. There was no obvious change in the peripheral nerve. Since no marked cellular infiltration was detected in these lesions, the clinicopathological findings observed could be induced by humoral mechanism, most likely anti-SGPG antibodies.
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We examined mortality from adult T-cell leukemia/lymphoma (ATL/ATLL) and other diseases alleged to be associated with human T-lymphotropic virus type I (HTLV-I) among anti-HTLV-I antibody-positive blood donors in Kyushu, Japan. During 1984-87, a total of 3,991 blood donors aged 40 years or over were followed from the date of donation to the date of death or the end of the study. Crude mortality rates from ATL (with 95 percent confidence intervals) were 68 per 100,000 (13-202) for males and 36 per 100,000 (3-132) for females. The rates were underestimated by approximately 50 percent because of self-selection and short observation periods. Neither death rates from other cancers nor death rates from all cancers were elevated.
Experimental cerebral vasospasm was produced in a "two-hemorrhage" canine model and examined by immunohistochemistry for leukotriene C4 (LTC4). The immunostain for LTC4 showed a strong positivity in intima and adventitia and a scattered reaction in media of normal basilar artery. The immunoreactivity after subarachnoid hemorrhage (SAH) was little changed in intima and media. Inflammatory cells which were characterized histochemically as neutrophils and macrophages, were shown to infiltrate from the adventitia of basilar artery to the periphery of blood clot after SAH and were markedly immunoreactive for LTC4. Also the neutrophils increased in number with the lapse of time after SAH. Thus, it would be reasonable to conclude that the LTC4 responsible for the development of vasospasm would most likely be produced from the infiltrating neutrophils and macrophages. In addition, neurons in hypothalamus, median eminence, and pons, as well as ependymal and arachnoid cells were immunoreactive for LTC4 both in the control and after SAH, whereas astrocytes and oligodendrocytes were not immunoreactive for LTC4 in either case.
Islet cell antibodies are usually detected in the sera of almost all Type 1 (insulin-dependent) diabetic patients within several months after onset of the disease. The antibodies then disappeared quite early during the course of the disease. The present study was undertaken to detect islet cell antibody-producing clones in peripheral blood lymphocytes of Type 1 diabetic patients whose islet cell antibodies could not be detected in sera. Epstein-Barr virus-transformed lymphocytes were employed to enhance the production of antibodies and to detect the clones from peripheral blood lymphocytes. Peripheral blood lymphocytes were obtained from 40 islet cell antibody-negative Type 1 diabetic patients, 10 antibody-positive Type 1 diabetic patients, 30 Type 2 (non-insulin-dependent) diabetic patients and 40 normal control subjects. Epstein-Barr virus-transformed lymphocytes were cultured for 4 weeks and the culture supernatants were used for assay of islet cell antibodies. Islet cell antibody assays were performed by immunohistochemical methods using peroxidase-labelled protein A for IgG antibodies, peroxidase-labelled anti-human IgM antibodies for IgM antibodies and fresh frozen human pancreatic tissue. IgG-islet cell antibodies were detected in 26 islet cell antibody-negative patients (65%), eight antibody-positive patients (80%) and one Type 2 diabetic patient (3%) in the culture supernatants. Islet cell antibodies in the supernatants could not be detected in any of the control subjects. IgM-islet cell antibodies could not be detected in any of the patients or control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
We attempted treatment with low-dose aclarubicin (ACR), a new anthracycline, in a 66-year-old man with blastic transformation of essential thrombocythemia (ET). Two courses of ACR (20 mg/day x 7 days) were given intravenously. He showed a good response to this therapy without severe side effects. He has since maintained a state of prolonged remission. These observations indicate that low-dose ACR may be beneficial for management of the blastic transformation of ET.
The specific feature of stretch activation of the indirect flight muscle of the tropical waterbug Lethocerus was used to correlate mechanical and structural aspects of muscle contraction. The time courses of the changes in intensities of the strongest equatorial reflections, the (10) and (20) and of the first meridional reflection at 14.5 nm-1 were monitored using synchrotron radiation as a high intensity X-ray source. The ratio of the intensities of the equatorial reflections, (I20/I10), which reflects the mass distribution within the filament lattice array, increases by about 10% relative to the Ca(2+)-activated level when a rapid stretch is imposed, compared with a 200% change seen when fibres change from the relaxed to the rigor state, while the spacing of the lattice planes decreases by about 1%. The intensity of the first meridional reflection at 14.5 nm-1 decreases by about 35% during stretch activation with a slightly faster time course than the delayed tension increase. The results suggest that the average structure of cycling crossbridges is different from that present in the rigor state.
The effects of water-immersion-induced stress and intraperitoneal (i.p.) administration of selected neuropeptides on the levels of thyrotropin-releasing hormone (TRH) and prostaglandin E2 (PGE2) were studied in the rat stomach. Water-immersion caused a significant decrease immunoreactive-TRH (ir-TRH) concentrations in the stomach, and a significant increase in ir-TRH concentrations in the gastric juice. The concentrations of PGE2 were significantly increased at 0.5-4 hrs, and significantly decreased at 6-8 hrs after water-immersion. In the experiment of i.p. administration of selected neuropeptides, the level of ir-TRH in the stomach was significantly decreased after VIP injection, whereas it was significantly increased after beta-endorphin injection. The concentration of PGE2 was significantly decreased in the stomach after i.p. administration of TRH and VIP. However, it did not change after beta-endorphin injection. These results indicate that some neuropeptides may participate in regulating the endogenous level of PGE2 and that these interrelations between neuropeptides and PGE2 may be important as ulcerogenic factors in stress ulcers induced by water-immersion in the rat.