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Biomedical subjects

S Watanabe

Publications and source records attributed to S Watanabe.

At least 199 records · Page 11Linked to original sources

Immunohistochemical analysis of human milk fat globulin 1 and cytokeratin expression in median raphe cyst of the penis.

Because median raphe cyst of the penis shares histological findings with apocrine cystadenoma, some cases were thought to be erroneously reported as apocrine cystadenoma of the penis. Further, there is some controversy as to whether the entity, apocrine cystadenoma of the penis, exists or not. Nine cases of median raphe cyst which were clinically unequivocal from their location on the ventral aspects of the penis, were analysed immunohistochemically by using an antibody against human milk fat globulin 1 (HMFG) and a panel of monoclonal anti-cytokeratin antibodies. HMFG expression was not observed in eight out of nine cases of median raphe cyst of the penis, and the remaining case showed a faint expression of HMFG focally in its luminal surface, while conventional apocrine cystadenoma in extra-genital area expressed HMFG definitively in our previous study. Our results suggest a possibility that apocrine cystadenoma of the penis is very rare or not present. Therefore, we thought that HMFG expression should be examined in the cases in which apocrine cystadenoma on the penis is reported.

Adolescent↗

Immunohistochemical analysis of human milk fat globulin expression in extramammary Paget's disease.

Primary extramammary Paget's disease is thought to be an intraepidermal carcinoma indicating apocrine secretory differentiation. In addition to expression in breast tissue, human milk fat globulin (HMFG) is expressed in the normal apocrine glands and tumours with apocrine differentiation. In this study HMFG expression in extramammary Paget's disease was analysed immunohistochemically in 18 cases of primary extramammary Paget's disease and two cases of secondary extramammary Paget's disease. The proportion and staining pattern of positive tumour cells with the anti-HMFG antibody was variable in each case. Cytoplasmic staining was observed frequently in dermal invasion and metastasis of Paget cells. The variabilities were thought to be due to modulation of the cellular localization of the cell surface component, HMFG, according to changes in cellular differentiation or malignant potency.

Adenocarcinoma↗

Identification and expression of a novel gene in odour-taste associative learning in the terrestrial slug.

Odour-taste associative learning in the terrestrial slug offers a useful model for long-term memory formation and retention. The genes which are expressed over 2 h after a learning event are thought to include those related to memory formation and/or consolidation. It is very important to examine what kinds of genes are expressed following associative learning. We identified a novel slug gene, the expression of which was regulated by associative learning and mostly restricted to the procerebrum (PC), a place that olfactory information is believed to be processed in slug. This gene encodes a 121 amino acid, 18 kDa secretory protein which we term LAPS18. Expression of the LAPS18 gene was induced in somata and the protein spread to neurites in the PC of slugs subjected to paired conditioning. Recombinant LAPS18 promoted the aggregation and movement of PC neurones in culture and they were blocked by the anti-LAPS18 antibody. Beads coupled with LAPS18 protein attached to PC neurones and the beads aggregated through PC cells but not by themselves, suggesting that LAPS18 may require a counterpart molecule for PC neurone aggregation. An increased expression and translocation of LAPS18 protein after paired conditioning may be needed for long-term memory formation and retention in the slug. Since genes homologous to LAPS18 genes in the land slug Limax are found from vertebrates including human, analysing the expression and function of LAPS18 may be important in understanding the molecular mechanism of memory formation and retention.

Amino Acid Sequence↗

Comparison of maximum bite force and dentate status between healthy and frail elderly persons.

The purpose of the present study was to (1) determine the standard value of maximum bite force and to (2) compare the maximum bite force of the elderly between healthy and frail subjects. Subjects included 349 healthy elderly individuals (149 males, 200 females) and 24 frail elderly individuals (seven males, 17 females) ranging from 65 to 74 years of age. Maximum bite force was evaluated using a Dental Prescale system. The maximum bite force of the healthy subjects was significantly higher than that of the frail subjects in both males (P=0.020) and females (P=0.015). However, no significant difference was observed in the number of present teeth between the healthy and frail subjects. Median of maximum bite force in healthy males was 408.0 N, and that of the healthy females was 243.5 N. These results suggest that the frail elderly have latent bite force problems.

Aged↗

Nicotianamine synthase gene expression differs in barley and rice under Fe-deficient conditions.

Nicotianamine (NA) is an intermediate in the biosynthetic pathway of the mugineic acid family phytosiderophores (MAs), which are crucial components of the iron acquisition apparatus of graminaceous plants. In non-graminaceous plants, NA is thought to be an essential chelator for metal cation homeostasis. Thus NA plays a key role in Fe metabolism and homeostasis in all higher plants. Nicotianamine synthase (NAS, EC 2.5.1.43) catalyzes the trimerization of S-adenosylmethionine to form one molecule of NA. Barley, a plant that is resistant to Fe deficiency, secretes large amounts of MAs, whereas rice, a plant that is susceptible to Fe deficiency, secretes only small amounts. In this study we isolated a genomic fragment containing HvNAS1 from barley and three rice cDNA clones, osnas1, osnas2 and osnas3, from Fe-deficient rice roots. We also isolated a genomic fragment containing both OsNAS1 and OsNAS2. In contrast to barley, in which Fe deficiency induces the expression of NAS genes only in roots, Fe deficiency in rice induced NAS gene expression in both roots and chlorotic leaves. The amounts of endogenous NA in both the roots and leaves were higher than in barley. We introduced barley genomic DNA fragments containing HvNAS1 with either 9 or 2 kb of the 5'-flanking region into rice, using Agrobacterium-mediated transformation. Fe deficiency induced HvNAS1 expression in both roots and leaves of the transgenic rice, as occurs with rice NAS genes. Barley and rice NAS genes are compared in a discussion of alteration of the NAS genes during adaptation to Fe deficiency.

Alkyl and Aryl Transferases↗

Case report. First isolation of Trichosporon domesticum from a cat.

The present study deals with the first isolation of Trichosporon domesticum from the urine of a cat with chronic cystitis. A 5-year-old domestic short hair cat weighing 5.6 kg was referred to an animal hospital with the chief complaint of haematuria having persisted for 3 weeks. The isolate was identified as T. domesticum, confirming the result of mycological examination by molecular analysis.

Animals↗

Clinical significance of TT virus in chronic hepatitis C.

BACKGROUND AND AIMS: Much is still unknown about the clinical significance of TT virus (TTV), which has been reported as a candidate for non A-G hepatitis virus. The aim of this study was to clarify the clinical significance of TTV in patients coinfected with TTV and hepatitis C virus (HCV). METHODS: The 95 subjects studied had chronic hepatitis C (CHC), and underwent interferon (IFN) therapy. TT Virus DNA was detected by using polymerase chain reaction. The nucleotide sequences were determined by using a dideoxy chain termination method. A phylogenetic tree was drawn up by using the neighbor-joining method. RESULTS: TT Virus DNA was detected in 37.9% of patients with the use of an open reading frame 1 (ORF1) primer, and in 88.4% of patients by using a 5' untranslated region (5' UTR) primer. Using both sets of primers, no differences were found between TTV-DNA-positive and -negative subjects with CHC in the clinical findings. Serum TTV DNA was eradicated in 30.6% of patients with the ORF1 primer, and in 19.1% of patients with the 5' UTR primer at 6 months after the cessation of IFN therapy. The levels of TTV DNA before IFN therapy were significantly lower in the viral eradication group than in non-eradication group. The changes in alanine aminotransferase (ALT) concentrations were significantly correlated with changes in HCV-RNA in CHC patients with TTV. Moreover, there was no correlation between the changes in TTV DNA and the course of ALT. CONCLUSION: Hepatocellular injury in patients with chronic hepatitis who are coinfected with HCV and TTV appears to primarily be caused by HCV and is less attributable to TTV.

Adult↗

Role of UGT1A1 mutation in fasting hyperbilirubinemia.

BACKGROUND AND AIM: Low-grade fasting hyperbilirubinemia is a common observation in healthy subjects (HS), whereas high-grade fasting hyperbilirubinemia is believed to be a characteristic finding of Gilbert's syndrome. This study was undertaken to assess the role of mutation in bilirubin UDP- glycosyltransferase gene (UGT1A1) on fasting hyperbilirubinemia. METHODS: Analysis of UGT1A1 and a caloric restriction test (400 kcal for 24 h) were performed in 56 healthy subjects (25 males, 31 females), and 28 patients with Gilbert's syndrome (18 males, 10 females). There were 29 healthy subjects with no mutation in UGT1A1, and 27 healthy subjects and 26 Gilbert's syndrome patients with mutations in the coding and/or promoter (TATA box) regions of UGT1A1. RESULTS: The mean increment of serum bilirubin (DeltaSB) was 7.6 micromol/L [corrected] (males) and 4.1 micromol/L (females) in subjects with no UGT1A1 mutation. Subjects with mutation in UGT1A1 showed higher levels of DeltaSB than individuals without mutation. Among healthy subjects, gender difference in DeltaSB values was observed only in individuals with the wild type of UGT1A1, but not in those with mutations in this gene. CONCLUSION: The results of the present study suggest that UGT1A1 mutation has a role in the development of high-grade fasting hyperbilirubinemia after caloric restriction.

Adult↗

FR167653, a potent suppressant of interleukin-1 and tumor necrosis factor-alpha production, ameliorates colonic lesions in experimentally induced acute colitis.

BACKGROUND: Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are believed to play a significant role in the pathogenesis of inflammatory bowel disease (IBD). Interleukin-1 and TNF-alpha possess overlapping and synergetic activities inducing the production in cascade of other cytokines, adhesion molecules, arachidonic acid metabolites, as well as activating immune and non-immune cells. FR167653 (C24H18FN5O2-H2SO4-H2O) is a newly synthesized organic compound with a potent inhibitory effect on IL-1beta and TNF-alpha production. We hypothesized that the suppression of IL-1 and TNF-alpha induced by FR167653 could effectively attenuate experimentally induced colonic damage. METHODS: Colonic lesions were induced in male Sprague-Dawley rats (250-300 g) by intrarectal instillation of 4% acetic acid. The effect of FR167653 administration at 1.0, 1.5, 2.5 mg/kg per 6 h subcutaneously on acetic acid-induced colonic damage was assessed. The lesion area, microscopic findings, colonic and serum levels of TNF-alpha and IL-1beta were also evaluated. RESULTS: Treatment with FR167653 at 1.5 and 2.5 mg/kg per 6 h was able to ameliorate the gross macroscopic appearance of colonic lesions significantly, as well as ameliorate the lesion area induced by acetic acid. Colonic mucosal TNF-alpha and IL-1beta levels of rats treated with FR167653 showed significant decrease in a dose-dependent fashion compared with the control group. In the same manner, serum TNF-alpha of rats treated with FR167653 was significantly lower than that of respective controls. CONCLUSIONS: Subcutaneous administration of FR167653 was able to ameliorate the acute changes induced by acetic acid instillation in a dose-dependent manner. This is the first report to evaluate the dual inhibition of the production of IL-1 and TNF-alpha, offered by FR167653, in acute experimental colitis. Further studies are necessary to evaluate FR167653's efficacy and safety on long-term conditions.

Acetic Acid↗

Intracellular 3',5'-adenosine cyclic monophosphate level regulates house dust mite-induced interleukin-13 production by T cells from mite-sensitive patients with atopic dermatitis.

We studied the relationship between cAMP and house dust mite-induced cytokine production in T cells from mite-sensitive patients with atopic dermatitis. T cells from atopic dermatitis patients secreted high level of interleukin-13 (mean 851.1 pg per ml) when cultured with autologous monocytes pulsed with Dermatophagoides pteronyssinus extract. Dermato- phagoides pteronyssinus-induced interleukin-13 secretion was not detected in normal subjects. Adenylate cyclase inhibitor MDL 12,330A and cyclic nucleotide phosphodiesterase type 4 inhibitor rolipram blocked Dermatophagoides pteronyssinus-induced interleukin-13 secretion in atopic dermatitis T cells. In atopic dermatitis T cells, cAMP level rose at 5 min after Dermatophagoides pteronyssinus stimulus then decreased to the basal level at 1 h. MDL 12,330A blocked the Dermatophagoides pteronyssinus-induced cAMP elevation while rolipram blocked its reversal. In atopic dermatitis T cells, adenylate cyclase activity increased at 5 min after Dermatophagoides pteronyssinus stimulus, followed by the increase of cyclic nucleotide phosphodiesterase activity at 15 min. In atopic dermatitis T cells, phospholipase C inhibitor ET-18-OCH3 blocked Dermatophagoides pteronyssinus-induced activation of adenylate cyclase, while rolipram, protein kinase A inhibitor H-89, and MDL 12,330A blocked the activation of cyclic nucleotide phosphodiesterase. These results suggest that Dermatophagoides pteronyssinus may first increase cAMP in atopic dermatitis T cells by activating adenylate cyclase via phospholipase C, and next decrease cAMP by activating cyclic nucleotide phosphodiesterase 4 via protein kinase A, which may be activated by adenylate cyclase-generated cAMP signal. These events are required for interleukin-13 response Dermatophagoides pteronyssinus.

3',5'-Cyclic-AMP Phosphodiesterases↗

The effects of Malassezia yeasts on cytokine production by human keratinocytes.

Yeasts of Malassezia, members of the microbiologic flora of the skin, cause pityriasis versicolor and have also been implicated in the pathogenesis of other superficial dermatoses; the most important ones are seborrheic dermatitis, folliculitis, and atopic dermatitis. The mechanisms by which the yeasts cause these dermatoseş however, are not yet clear, and there have been no studies on the interaction between fungi and keratinocytes, especially the effects of fungi on the production of cytokines by human keratinocytes. Recently, the genus Malassezia has been expanded to seven species based on molecular data. In this study, we estimated the effects of Malassezia yeasts on cytokine (interleukins 1beta, 6, and 8, monocyte chemotactic protein-1, and tumor necrosis factor-alpha) production by human keratinocytes in order to examine whether the pathogenicity of the respective Malassezia yeasts is different from each other and to elucidate the mechanism by which Malassezia yeasts cause the dermatoses with different clinical and pathologic manifestations. Variable levels of interleukin 6 and 8, and tumor necrosis factor-alpha in the supernatants in response to Malassezia yeasts (except M. furfur) increased from 1 to 24 h co-culture, but the monocyte chemotactic protein-1 was undetectable. Furthermore, cytokine levels in the supernatants were undetectable 1-24 h after the keratinocytes were harvested with only supernatants of Malassezia. These results indicate that Malassezia stimulates cytokine production by keratinocytes, the cytokine production needs the presence of Malassezia, and there are differences in ability to induce cytokine production by human keratinocytes among Malassezia yeasts. These differences may reflect the different inflammatory responses in Malassezia-associated dermatoses, resulting in different clinical and pathologic manifestations.

Cell Survival↗

17beta-estradiol, progesterone, and dihydrotestosterone suppress the growth of human melanoma by inhibiting interleukin-8 production.

We studied the effects of 17beta-estradiol, progesterone, and dihydrotestosterone on in vitro growth of human metastatic melanoma. Each sex hormone inhibited the growth of melanoma receptor-dependently; 17beta-estradiol inhibited 3H-thymidine uptake of estrogen receptor-positive WM266-4 and NM26, but not that of the receptor-negative HS15. Progesterone inhibited 3H-thymidine uptake of progesterone receptor-positive WM266-4 and HS15, but not that of the receptor-negative NM26. Dihydrotestosterone inhibited 3H-thymidine uptake of androgen receptor-positive HS15 and NM26, but not that of the receptor-negative WM266-4. The growth inhibition by each hormone was counteracted by the respective hormone receptor antagonist. The combination of more than two hormones neither gave additive nor synergistic growth inhibition. The growth inhibition by each sex hormone was counteracted by interleukin-8 but not by the other growth factors. Each sex hormone reduced the constitutive interleukin-8 secretion and mRNA levels in the respective receptor-positive melanoma but not in the receptor-negative melanoma. Transient transfection showed that each sex hormone inhibited the constitutive chloramphenicol acetyltransferase expression driven by interleukin-8 promoter in the respective receptor-positive melanoma but not in the receptor-negative melanoma. Transfection with a series of 5'-deleted interleukin-8 promoter/chloramphenicol acetyltransferase reporter constructs demonstrated that the sequences between -98 and -63 bp on interleukin-8 promoter may be involved in the transcriptional repression. These data suggest that 17beta-estradiol, progesterone, and dihydrotestosterone suppress the growth of melanoma by inhibiting interleukin-8 production in a receptor-dependent manner.

Antibodies↗

EUS-guided one-step drainage of pancreatic pseudocysts: experience in 3 patients.

BACKGROUND: EUS-guided drainage has been recognized as a nonsurgical treatment for pancreatic pseudocysts. Bleeding at the puncture site is a known complication of this procedure. This is a report of the use of new equipment for one-step drainage without the use of an electrosurgical needle. METHODS: EUS-guided cystoenterostomy was performed in 3 patients. The mean size of the pseudocysts was 8 cm (head = 1, body = 2). A needle and drainage tube were inserted in a one-step procedure into the cyst through the accessory channel of an echoendoscope under EUS. The drainage tube was released immediately after insertion. OBSERVATIONS: All 3 patients were treated successfully without complication. A drainage tube was inserted through the duodenal bulb (n = l) and the body of the stomach (n = 2). The drain was removed after 1 month in all patients. Two of the 3 drains were obstructed by sludge. One pseudocyst recurrence was observed at a mean follow-up of 3.6 months (range 2-6 months). CONCLUSIONS: The EUS-guided one-step system is simple to use and suitable for drainage of pancreatic pseudocysts. It appears to minimize the risk of hemorrhage.

Adolescent↗

Acquisition of the monocyte/macrophage phenotype in human mesangial cells.

The function of intrinsic glomerular cells in active glomerular inflammation may be similar to that of monocytes/macrophages. Mesangial cells have phagocytic properties and release numerous mediators. In this study we examined whether human mesangial cells (hMCs) express a monocyte/macrophage phenotype in active glomerular inflammation. We report that the proto-oncogene c-fms, the macrophage colony-stimulating factor (M-CSF) receptor, which is a characteristic gene of monocytes/macrophages, is expressed in hMCs. Normal unmanipulated hMCs express weak c-fms mRNA by reverse transcriptase-polymerase chain reaction (RT-PCR), and its expression increases after stimulation with platelet-derived growth factor-BB (PDGF-BB) and epidermal growth factor (EGF). The expression of c-fms was also demonstrated by flow cytometry with a specific polyclonal antibody. By immunohistochemistry, c-fms was prominently detected in acute glomerulonephritis, IgA nephritis, and lupus nephritis. These results indicate that hMCs express c-fms in active glomerular inflammation and are consistent with mesangial cells acquiring some macrophage-like characteristics in diseased states.

Acute Disease↗

E-cadherin is essential for gastric epithelial restitution in vitro: a study using the normal rat gastric mucosal cell line RGM1.

The proliferation and migration of epithelial cells appear to have important roles in intercellular adhesion and the regeneration of gastric mucosal lesions. However, the role of E-cadherin, an important intercellular adhesion molecule, in restitution after gastric mucosal damage is unknown. This study was designed to investigate the possible role of E-cadherin in the regeneration of gastric mucosal lesions. Artificial small wounds were made in an RGM1 confluent monolayer sheet, and the healing process was monitored with or without the presence of different concentrations of anti-E-cadherin antibodies. E-cadherin mRNA and protein expression were determined by Northern blot analysis and immunostaining, respectively. Epithelial restitution in anti-E-cadherin antibody-treated monolayers was inhibited as compared with that in the controls without antibody. E-cadherin mRNA and protein expression were up-regulated transiently during the healing process. E-cadherin plays an important role during wound healing of gastric epithelial lesions and is crucial for sheet migration.

Animals↗

The adenosine triphosphate-sensitive potassium channel opener nicorandil protects the ischemic rabbit spinal cord.

OBJECTIVE: We investigated the protective effects of an adenosine triphosphate-sensitive potassium channel opener nicorandil in the rabbit model of spinal cord ischemia. METHODS: Rabbits were randomized into 4 groups (each n = 6): the nicorandil group (100 microg/kg intravenous nicorandil 10 minutes before ischemia); the glibenclamide plus nicorandil group (3 mg/kg intravenous glibenclamide, an antagonist of adenosine triphosphate-sensitive potassium channels, 10 minutes before nicorandil administration); the vehicle group (vehicle alone); and the sham operation group (without spinal cord ischemia). Spinal cord ischemia was induced by balloon occlusion of the infrarenal abdominal aorta for 15 minutes at 39 degrees C. Neurologic function was graded into Johnson's score at 8 hours, 1 day, and 2 days. Histopathologic examination was performed at 2 days, and the number of intact motor neuron cells was compared. RESULTS: Johnson scores of the glibenclamide plus nicorandil and vehicle groups were significantly lower than those of the sham operation and nicorandil groups at each time point, and no statistically significant difference was observed between the glibenclamide plus nicorandil and vehicle groups. Histopathologic examination revealed that motor neurons were almost normal in the nicorandil group, whereas about 55% of motor neurons were lost in the vehicle and glibenclamide plus nicorandil groups. CONCLUSIONS: Nicorandil has a protective effect on the ischemic rabbit spinal cord, and the beneficial effect seems mediated through the activation of adenosine triphosphate-sensitive potassium channels.

Animals↗