Shusei Fujimori

Induction and intracellular localization of a 72-kDa heat shock protein in rat gastric mucosa after water-immersion stress

We investigated the expression and changes in the intracellular localization of a 72-kDa heat shock protein (HSP72) in rat gastric pyloric and fundic mucosa before and after water-immersion stress. Severe mucosal damage was found in the fundic mucosal area of the stomach after this stress. However, no mucosal lesion developed in the pyloric mucosal area. HSP72 in both the soluble and insoluble fractions of the pyloric and the fundic mucosal areas was significantly increased after water-immersion stress, peaking 6 h after the initiation of the stress. The increase in HSP72 was more significant in the pyloric mucosal area than in the fundic mucosal area under both normal and stress conditions. The increase of HSP72 in the pyloric mucosal cells occurred prior to the formation of the mucosal lesions, whereas the increase of HSP72 in the fundic mucosal cells was observed after ulcer formation. An immunohistochemical study showed that HSP72 was constitutively expressed in the cytoplasm of the gastric mucosal cells, and that the intranuclear induction of HSP72 was remarkably intense in the pyloric mucosal cells, especially in the proliferative zone, compared with the fundic mucosal cells. Our results may suggest that HSP72 has an important cytoprotective function in gastric mucosal cells and that there is a “biophysical” difference between pyloric and the fundic mucosal cells.

Induction of a 72-kDa Heat Shock Protein and Cytoprotection Against Thioacetamide-Induced Liver Injury in Rats

Heat shock proteins are ubiquitous intracellularproteins induced by various physiological stress-relatedevents. A 72-kDa heat shock protein (HSP72) has beenreported to be an endogenous cytoprotectant in variety of cells in vitro . In order tostudy the cytoprotective function of HSP72 in the liver,the effect of preinduction of HSP72 in rat liver bysystemic hyperthermia on thioacetamide-induced hepatic injury was investigated in this study.Expression of HSP72 in the liver was investigated byimmunoblot and densitometric analysis. Rats wereinjected with thioacetamide (100 mg/kg, subcutaneously)with or without preinduction of HSP72 byhyperthermia. Serum AST and ALT concentrations weremeasured before and after thioacetamide injection inboth group. Histologic alteration of the liver wasevaluated also. Systemic hyperthermia (42.5°C, 20min) significantly induced HSP72 in the liver.Thioacetamide-induced hepatic injury was clearlyprevented by preinduction of HSP72 by hyperthermia.Prevention of hepatocyte damage was more clear in the areaaround central veins where HSP72 induction was apparent.Our findings might suggest that HSP72 has an importantfunction in the liver with respect to cytoprotection. These results might be important forunderstanding the mechanism of “adaptivecytoprotection” in the liver mediated by thefunction of heat shock proteins as “molecularchaperons” as reported in vitro.

Regulation of 60-kDa heat shock protein expression by systemic stress and 5-hydroxytryptamine in rat colonic mucosa

Bowel dysfunction such as irritable bowel syndrome caused by stress is well described. Previous reports suggest that 5-hydroxytryptamine (5-HT) mediates alteration of bowel motility. In this study, the effects of water-immersion stress and the administration of 5-HT on the expression of a 60-kDa heat shock protein (HSP60) in rat colonic mucosa were investigated. The effect of YM-060, a 5-hydroxytryptamine 3 (5-HT3) receptor antagonist, on the expression of this protein was also studied. Water-immersion stress and the administration of 5-HT induced synthesis of HSP60 in rat colonic mucosa. The induction of HSP60 and the number of defecations were clearly inhibited by the oral administration of YM-060. Our results suggest that the induction of HSP60 in rat colonic mucosa by water-immersion stress may be associated with gastrointestinal motility mediated by 5-HT, especially via 5-HT3 receptors.

Effect of pre-induction of heat shock proteins on indomethacin-induced small-intestinal lesion in rats

Systemic hyperthermia induces the synthesis of heat shock proteins (HSPs) in several organs. However, the mechanism of induction and the functions of HSPs in the small-intestinal mucosa have not been established. We examined the expression of HSPs in the small-intestinal mucosa after systemic hyperthermia, and evaluated the cytoprotective function of preinduced HSPs on experimentally induced mucosal damage. HSP expression was investigated by Western blot and densitometric analysis before and after hyperthermia (42.5°C; 20min). Expression of a 72-kDa heat shock protein (HSP72) and a 73-kDa heat shock protein (HSP73), both of which are endogenous cytoprotectants in vitro significantly increased, peaking 6–9h after hyperthermia, without any pathologic alterations, whereas the expression of a 60-kDa heat shock protein (HSP60) did not increase. To investigate the influence of pre-induction of HSPs on small-intestinal damage, rats received indomethacin (10mg/kg; orally) with or without pre-treatment with hyperthermia. Small-intestinal damage caused by indomethacin was not influenced by pre-induction of HSP72 and HSP73. We demonstrated that systemic hyperthermia induced HSP72 and HSP73, although pre-induction of these proteins did not have a cytoprotective function in the smallintestinal damage caused by indomethacin.

Intussusception in Peutz-Jeghers syndrome: sonographic findings

An intussusception can easily occur in patients with Peutz-Jeghers syndrome (PJS), and its early detection is crucial. We present a PJS patient in whom sonography (US) helped in detecting intussusception at a time when there was only a very vague symptom and provided successful conservative treatment. Close clinical and US follow-up of PJS patients should improve management of this condition.

Induction of a 60-kDa heat shock protein in rat gastric mucosa by restraint and water-immersion stress

Many studies have shown the importance of heat shock proteins (HSPs) for the survival of cells under stressed conditions. A 70-kDa heat shock protein (HSP70) has recently been induced in cultured gastric mucosal cells by heat stress, and this protein has been shown to have a cytoprotective function in vitro. However, little is known about the expression and function of a 60-kDa heat shock protein (HSP60) in the gastric mucosa under stressed conditions, particularly in vivo. In this study, the influence of waterimmersion stress on the expression of HSP60 in rat gastric mucosa was investigated.

Novel colorectal adenocarcinoma-associated 40- and 47-kDa protein antigens recognized by anti-60-kda heat shock protein antibody

Expression of 40- and 47-kDa proteins recognized by anti-60-kDa heat shock protein antibody was investigated in colorectal adenocarcinoma tissue. In all cases of colorectal adenocarcinoma tissue (n = 9), 40- and 47-kDa proteins were detected by immunoblot analysis. However, expression of these two proteins was extremely low or was not expressed in control tissue. There was no correlation between the quantity of these two bands and histologic type or the location of the tumors. Our results first demonstrate the accumulation of structurally altered 60-kDa heat shock protein-associated antigens in carcinoma tissue and suggest that these two proteins could be a possible candidate for tumor-specific 60-kDa heat shock protein-related protein antigens.

Malignant triton tumor in a patient with neurofibromatosis type 1

We report a case of neurofibromatosis type 1 (NF1) complicated by a malignant triton tumor (MTT), with an emphasis on B-mode sonographic (US) and contrast-enhanced US (CEUS) findings. To the best of our knowledge, this is the first report describing CEUS findings of MTT. The mass was poorly demarcated and composed of an internal echogenic area and an outer hypoechoic zone. CEUS findings showed the outer zone to be strongly enhanced, and the internal area was very poor in blood flow because of necrotic tissues.

Rupture of liver metastasis: report of a case with an emphasis on contrast-enhanced US

We present a case of liver metastasis from an uterine leiomyosarcoma in which contrast-enhanced ultrasonography (CEUS) helped determine the bleeding point and prevented a delay in devising diagnostic and therapeutic strategies. CEUS allowed us to differentiate active from nonactive bleeding on the basis of presence or absence of contrast extravasation in the ascites. CEUS is the first examination performed when liver tumor rupture is suspected. Reference to the preangiographic CEUS results is expected to provide a road map for angiography.

Mobile echoes in liver cysts: a form of range-ambiguity artifact.

Faint moving echoes are occasionally encountered in large hepatic cysts, as an example of range‐ambiguity artifacts. The aim of this article is to describe the pattern of these intracystic mobile echoes, to analyze the mechanism of their formation, and to discuss options to clear them.