Biomedical subjects
Publications and source records attributed to S Taniguchi.
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We report a 19-year-old woman with the associated disorders of generalized pruritus, hypertrichosis and anorexia nervosa, all of which had been present for approximately 4 months. Psychotherapy induced both weight gain and resolution of the pruritus. We propose that anorexia-associated pruritus be considered one of the important cutaneous signs in anorexia nervosa.
We measured serum concentrations of nitrite/nitrate (NOX), type II phospholipase A2 (PLA2), leukotriene B4 (LTB4), and platelet-activating factor (PAF) in patients with sepsis. These findings were compared between patients with and without septic shock. Serum concentrations of NOX, type II PLA2, LTB4, and PAF acetylhydrolase (PAF-AH) were significantly higher in the group with septic shock (P < 0.0001; P = 0.0060; P = 0.0052; P = 0.0052), indicating the severity of the disease. There were significant correlations between the serum NOX level and serum levels of type II PLA2, LTB4, and PAF-AH (r = 0.6890, P < 0.0001; r = 0.3755, P = 0.0409; r = 0.5095, P = 0.0040, respectively). It is speculated that LTB4 and PAF, both produced with type II PLA2, interact with each other and are involved in the deterioration of pathologic features associated with sepsis. Furthermore, nitric oxide (NO) and eicosanoids interact to play an important role in vascular dilatation during septic shock.
We assessed the plasma levels of nitrite/nitrate (NOx) and soluble Fas antigen (sFas) in patients with multiple organ failure (MOF). The NOx levels showed high levels in MOF patients with sepsis and without infection. A significant difference was not seen between the MOF patients complicated by sepsis and uncomplicated by infection, although the NOx levels in the former group tended to be higher. There was a significant correlation between NOx levels and sFas levels in MOF patients. Both sFas and NOx levels were high during MOF, and rapidly decreased when MOF was relieved. These findings suggest that sFas and NOx contribute to the development of MOF.
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To investigate the involvement of nitrite/nitrate oxide (NOx) in septic shock, and to evaluate the relationships between NOx and cytokines in patients with this disorder, we evaluated 11 patients with septic shock and 12 patients with sepsis unassociated with shock. NOx were measured with an automated system based on the Griess reaction. The plasma concentrations of various cytokines were determined by enzyme-linked immunosorbent assay. Endotoxin was determined by a specific assay after the plasma samples were processed by a perchloric acid method. The mean plasma levels of NOx in the group with shock significantly exceeded those in the group without shock. Significant correlations were observed between the plasma levels of NOx and those of endotoxin, tumor necrosis factor-alpha, and interleukin 8 in both groups. NOx appeared to be involved in the development of septic shock in humans. Endotoxin and cytokines appeared to be involved in the production of NOx.
We assessed the blood interleukin 11 (IL-11) levels in patients with disseminated intravascular coagulation (DIC). The IL-11 level exceeded the detection limit, i.e., IL-11 was positive, in 14 of the 21 patients in the group with DIC complicated by sepsis, with a mean value of 20.4 pg/ml. In the group with DIC uncomplicated by infection, IL-11 levels were above the detection limit in 8 of the 17 patients, and the average level was 10.6 pg/ml. The difference between the IL-11-positive rate in the two groups was not significant. Although IL-11 levels tended to be higher in the group with sepsis as a complication, the difference was not significant. The elevated IL-11 levels observed in patients with DIC, with or without complication by infection, seem quite appropriate as a biological response to increased platelets.
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The present study was conducted to determine whether a plasma interleukin-1 receptor antagonist (IL-1ra) would reflect the severity of burn injury and to examine the relation between IL-1ra and the cytokines. We studied 24 burn patients in whom the total burn surface area (TBSA) accounted for at least 20% of the body surface, and in whom serial blood samples could be obtained beginning immediately after the burn injury. Plasma levels of IL-1ra were determined by enzyme-linked immunosorbent assay (ELISA). Plasma levels of tumor necrosis factor-alpha (TNF-alpha), IL-6, and IL-8 were also determined by ELISA. Endotoxin was measured by an endotoxin-specific synthetic substrate method. There was a significant correlation between the plasma levels of IL-1ra and TBSA during the first week following burn injury. The IL-1ra level was the highest immediately after the burn injury. The level decreased markedly thereafter, and again rose when infection occurred. The IL-1ra level was extraordinarily elevated in patients who developed concomitant sepsis, septic shock or the septic multiple organ dysfunction syndrome. The IL-1ra level on admission and the maximum IL-1ra level during the observation period were significantly higher in the patients who eventually died than in the survivors. There was a significant correlation between the level of IL-1ra and that of TNF-alpha, IL-6 or IL-8 during the observation period. No correlation was found between IL-1ra and endotoxin. The plasma IL-1ra level was closely correlated with the severity of inflammation and the clinical status of the burn patients, regardless of the infection. Results suggest that IL-1ra can serve as an index of the systemic inflammatory response syndrome (SIRS).
We have succeeded in the establishment of a human endothelial cell line derived from a human angiosarcoma. These cells grew as monolayers with a "cobble stone" morphology. The cells produced endothelin and showed Weibel-Palade bodies in their cytoplasm. These findings show that the cells have specific differenciated functions, and might be useful for both fundamental endothelial cell biology and biological investigation of angiosarcoma.
The function of vascular endothelial cells is to adjust blood vessel tonus, which contributes to maintaining homeostasis within blood vessels. However, inflammatory cytokines are produced in response to invasion by stimulating vascular endothelial cells and sometimes lead to shock or multiple organ failure. In the present study, we assessed cytokines in sepsis and septic shock, and various factors that are said to have a damaging effect on vascular endothelium. Endotoxin was measured by endotoxin-specific methods. Tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and interleukin 8 (IL-8) were measured by enzyme-linked immunosorbent assay (ELISA). Endothelin-I was measured by radioimmunoassay (RIA). Nitric oxide was measured as metabolites of nitrite and nitrate oxides (NOx) by a method based on the Griess method. Thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (PGF 1 alpha) were both measured by RIA. All of the factors except endotoxin were significantly higher in the septic shock group than in the non-shock group and significantly higher in the non-survivor group than in the survivor group. Significant correlations were also found between endothelin-1 and NOx and between TXB2 and PG1 alpha. Significant correlations were also found between TNF-alpha and IL-6, endothelin-1, NOx and TXB2, but no significant correlations were detected between any of them and endotoxin. In serious diseases such as septic shock, the vascular endothelial constricting factors, endothelin and TXB2, and the blood vessel relaxing factors NOx and PGF1 alpha increase almost simultaneously. This suggests that the body's regulating mechanisms are disrupted in these serious conditions. The results of this study also suggest that inflammatory cytokines may be involved in stimulating the production of these factors.
The beta 1-6 structure of N-linked oligosaccharides, formed by beta-1,6-N-acetylglucosaminyltransferase (GnT-V), is associated with metastatic potential. We established a highly metastatic subclone, B16-hm, from low metastatic B16-F1 murine melanoma cells. The gene encoding beta-1,4-N-acetylglucosaminyltransferase (GnT-III) was introduced into the B16-hm cells, and three clones that stably expressed high GnT-III activity were obtained. In these transfectants, the affinity to leukoagglutinating phytohemagglutinin was reduced, whereas the binding to erythroagglutinating phytohemagglutinin was increased, indicating that the level of beta 1-6 structure was decreased due to competition for substrate between intrinsic GnT-V and ectopically expressed GnT-III. Lung metastasis after intravenous injection of the transfectants into syngeneic and nude mice was significantly suppressed, suggesting that the decrease in beta 1-6 structure suppressed metastasis via a mechanism independent of the murine system. These transfectants also displayed decreased invasiveness into Matrigel and inhibited cell attachment to collagen and laminin. Cell growth was not affected. Our results demonstrate a causative role for beta 1-6 branches in invasion and cell attachment in the extravasation stage of metastasis.
It remains uncertain whether xenotransplantation can sensitize the recipient to alloantigens, rendering subsequent allotransplantation unsuccessful. This is of considerable importance if a xenograft is to be used as a "bridge" to support the patient until a suitable allograft becomes available. When sera from 9 baboons that had received pig or African green monkey heart or liver xenografts were tested against a panel of lymphocytes from 5 or 6 potential donor baboons, positivity was seen in only 1 baboon (and then to only 2 of the potential 5 donors). In 4 baboons that had undergone previous xenotransplants (1 from this series of 9 baboons and 3 others), subsequent organ allografting was not followed by hyperacute, antibody-mediated, or accelerated cellular rejection. We conclude that organ xenotransplantation using discordant or concordant donor species does not prohibit subsequent allotransplantation.
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A new gene, nel, was isolated from a 9-day-old chick embryonic cDNA library. The gene encodes a protein of 835 amino acids (93,407 M(r)) consisting of two hydrophobic domains presumed to be the signal and transmembrane sequences, a histidine rich domain, two repeats of a cysteine rich structure similar to the C-terminal domain of von Willebrand factor, five EGF-like repeats, and again two repeats of the cysteine rich sequence similar to the C-terminal domain of von Willebrand factor in the presumed cytoplasmic domain. The expression of the nel gene was studied by Northern blot and in situ hybridization analyses of chick embryos. The mRNA of the gene was found in all tissues of 10- and 17-day-old embryos by Northern blot hybridization. Among the tissues examined, the level in the brain was highest and increased with age. After hatching, gene expression was retained in the brain at about the same level found in old embryos, increased in the retina, and disappeared from the other tissues. In situ hybridization with a nel gene probe revealed that the gene was strongly expressed in neural tissues such as brain, spinal cord, and dorsal root ganglia of early embryos. Gene expression was observed in the mantle layer of the neurepithelium of the brain and of the spinal cord. Gene expression in early embryos was not restricted to the neural tissues, but was also detected in the cells around cartilage, myocardium, lung mesenchymal cells, and in the liver, etc. One band of about 4.5 Kb mRNA was detected in all tissues and stages by Northern blot hybridization analysis. The possible function of the gene is discussed.
Although antiobesity effect of dehydroepiandrosterone (DHEA) has been reported in rats, it remains unclear whether the effect is brought about by itself or mediated by sex steroids converted from DHEA in gonads. In the present study, to clarify this point, the effect of DHEA on growth in obese Zucker male rats was reevaluated under two conditions: with or without castration. Castration did not affect the pattern of growth curve of obese Zucker male rats. Three-months treatment of castrated Zucker rats with 0.3% DHEA in the diet resulted in dramatic decrease of body weight gain in comparison to DHEA-untreated and castrated rats. The degree of antiobesity effect of DHEA in castrated rats was almost same as that observed in non-castrated rats. These results suggest that DHEA exerted its antiobesity effect by itself rather than through conversion to testosterone in testis.