[Abnormal experience reaction with psychotic symptoms].
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
H Ota
Publications and source records attributed to H Ota.
A new triple stain for Helicobacter pylori suitable for the autostainer: carbol fuchsin/Alcian blue/hematoxylin-eosin.
OBJECTIVE: To develop an inexpensive stain to simultaneously visualize gastric morphology and Helicobacter pylori. METHODS: Gastric biopsies were stained with Genta stain using manual methods, and with carbol fuchsin/Alcian blue/hematoxylin-eosin using an automatic slide stainer (Sakura DRS-601). Slides were then coded and interpreted by 2 pathologists. Helicobacter pylori was scored using a visual scale (0 [none] to 5 [maximum]). RESULTS: One hundred slides were scored; H pylori was present in 64%. Carbol fuchsin/Alcian blue/hematoxylin-eosin stain gave excellent demonstration of gastric morphology. All positive cases (score > or =2) were correctly interpreted. Thirty-six slides had a score of 1 (< or =2 bacteria per entire slide). Of these, 10 were scored negative by Genta stain and 12 were scored negative by the carbol fuchsin/Alcian blue/hematoxylin-eosin stain (P = not significant). Hematoxylin-eosin was significantly less accurate than either of the other 2 stains (P < .02). CONCLUSION: The carbol fuchsin/Alcian blue/hematoxylin-eosin (El-Zimaity) stain is an economical stain suitable for simultaneous visualization of H pylori infection and gastric morphology.
Alcian Blue↗
Mature cystic teratoma of the uterine corpus.
Explore the source record for details and available documents.
Adnexa Uteri↗
[Case of myocarditis and congestive heart failure as main symptoms of systemic erythematosus].
Explore the source record for details and available documents.
Adult↗
Cocaine-induced liver injury in mice is mediated by nitric oxide and reactive oxygen species.
The modulating effects of nitric oxide (NO) and reactive oxygen species on cocaine-induced hepatotoxicity were examined by measuring plasma alanine aminotransferase activity and by carrying out histological studies. Liver injury was induced by a single injection of cocaine in adult male ICR mice. Pretreatment with aminoguanidine (an inhibitor of NO synthase), N-methyl-D-glucamine dithiocarbamate complex with iron ion (II) (Fe2+(MGD)2, a trapping reagent of NO) or deferoxamine complex with iron ion (III) (Fe3+-deferoxamine, a scavenger of NO) produced a marked inhibition of the hepatotoxicity induced by cocaine. In addition, pretreatment with allopurinol (an inhibitor of xanthine oxidase) and 1,3-dimethylthiourea (a scavenger of hydroxyl radical) also produced a potent inhibition. These findings suggest that a hydroxyl radical produced by the reaction of NO and superoxide anion (O2-) via peroxynitrite may be involved in the pathogenesis of cocaine hepatotoxicity.
Allopurinol↗
Involvement of annexin V in antiproliferative effects of gonadotropin-releasing hormone agonists on human endometrial cancer cell line.
We studied the involvement of annexin V in the antiproliferative effects of gonadotropin-releasing hormone (GnRH) agonists on human endometrial cancer cell line HHUA. HHUA cell line expressed mRNA for GnRH receptors as assessed by reverse transcriptase-PCR with oligonucleotide primers. In the presence of buserelin, the proliferation of this cell line was significantly (P < 0.01) reduced to 60% of control after 72 hr. Peak intracellular concentrations of annexin V, equivalent to about twice the control value, were obtained after 48 hr exposure to buserelin. Intracellular annexin V concentration was increased not only by buserelin, but also by protein kinase C (PKC) activator. However, there was no increase in intracellular annexin V concentration when cells were incubated with PKC inhibitor before the addition of buserelin. The results suggest that GnRH agonists inhibit cell proliferation by increasing intracellular concentrations of annexin V, an effect mediated by the activation of PKC.
Annexin A5↗
Distribution of heat shock proteins in eutopic and ectopic endometrium in endometriosis and adenomyosis.
OBJECTIVE: To evaluate the pathophysiologic role of heat shock proteins and to examine the effect of danazol on these proteins in patients with endometriosis and adenomyosis. DESIGN: Immunohistochemical identification of human heat shock proteins 27, 60, and 70 in endometrial glandular cells identified using monoclonal antibodies. SETTING: Department of obstetrics and gynecology in a university hospital. PATIENT(S): Subjects were 119 women with documented endometriosis or adenomyosis. The subjects were divided into three groups: fertile control (n = 38), with 14 in the proliferative phase and 24 in the secretory phase; endometriosis (n = 38); and adenomyosis (n = 43), including 33 who underwent hysterectomy and 10 treated with danazol. MAIN OUTCOME MEASURE(S): Staining of glandular cells by semiquantitative immunostaining (evaluation nomogram) score. RESULT(S): Significantly increased expression of heat shock protein 27 was noted in eutopic endometrium from patients with endometriosis and adenomyosis as compared with controls, regardless of the menstrual phase. The scores for heat shock protein 27 and heat shock protein 70 in the ectopic endometrium of patients with endometriosis were low compared with those in eutopic endometrium, whereas in adenomyosis, the scores were similar to those of eutopic endometrium. After treatment with danazol, the expression of heat shock proteins returned to control levels. CONCLUSION(S): We suggest that abnormally increased expression of heat shock proteins plays a role in the pathophysiology of endometriosis and adenomyosis.
Adult↗
Mast cell involvement in gastritis with or without Helicobacter pylori infection.
BACKGROUND & AIMS: Mast cells are initiators and regulators of inflammation, but their role in the human stomach remains unclear. Therefore, the extent and distribution of mast cell involvement in gastritis with or without Helicobacter pylori infection was investigated. METHODS: Mapped biopsy specimens from 17 H. pylori-positive and 20 H. pylori-negative subjects were examined. Sections were assessed for infection and inflammation and stained with anti-human mast cell tryptase to count mucosal and epithelial mast cells. Density of mast cells in different gastric compartments, their response to infection treatment, and their relationship with other inflammatory cells were evaluated. Mast cell degranulation was evaluated by electron microscopy. RESULTS: Mast cell density was significantly greater in the mucosa with gastritis, with or without H. pylori infection, than in the mucosa of noninfected normal subjects. In the antrum, density was much greater in H. pylori-infected peptic ulcer subjects than in the other gastritis groups. It also correlated significantly with the intensity of inflammation. Mast cell degranulation was demonstrated by electron microscopy in H. pylori-infected mucosa. Mast cell density in ulcer patients decreased significantly after cure of H. pylori infection. CONCLUSIONS: Mast cells may be important effector cells in the pathogenesis of gastritis, especially in H. pylori-associated peptic ulcer.
Adult↗
Helicobacter pylori induces proinflammatory cytokines and major histocompatibility complex class II antigen in mouse gastric epithelial cells.
Although Helicobacter pylori has been reported to stimulate the release of various cytokines from gastric tissue, it remains unknown whether normal and nontumorous gastric epithelial cells produce these cytokines. Therefore, in this study, we used a normal mouse gastric surface mucous cell line (GSM06) to determine whether gastric epithelial cells produce proinflammatory cytokines in response to H. pylori. The expression of MHC class II antigen was also examined, to investigate whether gastric epithelial cells participate in the immune response to H. pylori. In the study, GSM06 cells were incubated with H. pylori or its lipopolysaccharide (LPS). Proinflammatory cytokines were detected by Northern and Western blot analysis. The expression of MHC class II antigen was examined by fluorescence activated cell sorter (FACS) analysis. Genetic expression of proinflammatory cytokines such as interleukin-1alpha, tumor necrosis factor-alpha, and cytokine-induced neutrophil chemoattractant-2beta was enhanced by both intact and sonicated H. pylori, but not by H. pylori LPS. The expression of MHC class II antigen was induced by H. pylori more strongly than by interferon-gamma. We conclude that H. pylori induces the expression of proinflammatory cytokines and MHC class II antigen in gastric epithelial cells. Gastric epithelial cells may act as antigen-presenting cells and participate in the immune response to H. pylori infection.
Animals↗
Clarithromycin, amoxycillin and H2-receptor antagonist therapy for Helicobacter pylori peptic ulcer disease in Korea.
BACKGROUND: Effective anti-Helicobacter pylori therapies with few side-effects are needed. We previously showed that the regimen of amoxycillin, clarithromycin and an H2-receptor antagonist was effective in the United States. The current study tested whether this therapy would also be successful in Korea. METHODS: Patients with gastric or duodenal ulcers received amoxycillin (750 mg t.d.s.) plus clarithromycin (500 mg t.d.s.) for 2 weeks and nizatidine 300 mg at bedtime for 6 weeks. Endoscopic examinations were performed before treatment and 4 or more weeks after ending antimicrobial therapy. H. pylori status was confirmed by rapid urease testing and histological examination of gastric antrum and corpus biopsies using the Genta stain. Antibiotic resistance was tested using the E-test method. Cure was defined as no evidence of H. pylori infection 4 or more weeks after ending therapy. RESULTS: Seventy-two patients (59 males and 13 females; mean age 46 years), including 35 with duodenal ulcers, 30 with gastric ulcers and seven with both, were studied. H. pylori infection was cured in 95.8% (69/72 patients; 95% CI = 88.3-99.1%). Two of the treatment failures had culture data and one had pre-treatment resistance to clarithromycin. Smoking did not have an adverse effect on therapy. Ten patients (15%) developed side-effects during treatment, but all were mild and did not require treatment interruption. No case of reinfection was noted during follow-up. CONCLUSION: The combination of amoxycillin, clarithromycin and an H2-receptor antagonist is effective in Korean patients with H. pylori infection.
Adolescent↗
Integrin adhesion molecules in the endometrial glandular epithelium in patients with endometriosis or adenomyosis.
OBJECTIVE: To assess the role of beta 1-integrin and E-cadherin molecules in the eutopic glandular epithelium in patients with endometriosis or adenomyosis. STUDY DESIGN: Twenty-four patients with endometriosis, and 22 patients with adenomyosis diagnosed histologically were selected as subjects. The controls consisted of 29 fertile women. Eutopic endometria were obtained by curettage or immediately after the operation. The samples were immunohistochemically examined for the expression of very late activation antigen-2 (VLA-2), VLA-3, VLA-4, VLA-5, VLA-6, and E-cadherin. RESULTS: The expression of each VLA molecule and E-cadherin except VLA-4, VLA-5, and VLA-6 was significantly increased throughout the menstrual cycle in endometria in both the endometriosis and adenomyosis groups. In contrast, the expression of VLA-4 in the adenomyosis group was significantly reduced in the secretory phase. CONCLUSION: Altered expression of beta 1-integrins and E-cadherin was observed throughout the menstrual cycle in patients with endometriosis and adenomyosis, suggesting the defective microenvironment of the endometrium.
Adult↗
Histochemistry of the surface mucous gel layer of the human colon.
BACKGROUND AND AIMS: Histochemical analysis of the surface mucous gel layer of the human colon is difficult, as it dissolves in fixatives. This study was undertaken to explore the surface mucous gel layer on the normal mucosa and neoplastic tissues of the large intestine. In addition, the distribution of different mucins secreted from goblet cells was studied with a series of histochemical stains for mucins. METHODS: Twenty four surgically resected specimens were fixed in Carnoy's solution and embedded in paraffin. In four cases, the surface mucous gel layer was also studied in frozen sections. Serial sections were stained by a battery of histochemical techniques characterising mucins. RESULTS AND CONCLUSION: The surface mucous gel layer consisted of the inner and outer layers. The first covered the luminal surface of the mucosa, consisted of mucins, and showed a vertical striped pattern. The second overlaid the first, showed a lateral striped pattern, and was contaminated with bacteria and other substances. Their thickness in paraffin sections varied considerably among the sites in the large intestine, but was the thickest in the rectum and measured 12.7 (SEM 6.0) microns and 88.8 (SEM 80.1) microns respectively. Mucins forming the inner layer were obviously derived from goblet cells underlying it.
Acetic Acid↗
[Clonal deletion and clonal anergy as the mechanism of self-tolerance induction].
In the immune system, it is most important to discriminate self from nonself and to acquire and maintain the unresponsiveness to self antigens, self-tolerance. Recently, the transgenic animals provides the evidence of the mechanism of self-tolerance induction. Self-tolerance is established mainly by elimination, clonal deletion, and functional inactivation, clonal energy, of the autoreactive T cells and B cells. Clonal deletion and clonal anergy are involved not only in the central tolerance, in thymus or bone marrow, but also in the peripheral tolerance. The failure of self-tolerance involves the induction of auto-immune disease.
Animals↗
[An imbalance between Th1 and Th2-like cytokines in patients with autoimmune diseases--differential diagnosis between Th1 dominant autoimmune diseases and Th2 dominant autoimmune diseases].
An imbalance between T helper cell (Th)1 and Th2-like cytokines has been described in several autoimmune diseases. Organ specific autoimmune diseases such as multiple sclerosis (MS) and inflammatory bowel diseases (IBD) are caused by Th1 dominant immune responses. On the contrary, systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and Sjögren's syndrome(SS) are characterized by Th2 dominant imbalance of cytokine production. It might be useful for differential diagnosis among patients with various autoimmune diseases such as SLE, SS, IBD, and MS to measure the serum levels of cytokines such as IL-10, IFN gamma, and TNF alpha using ultrasensitive enzyme-linked immunosorbent assay system.
Animals↗
Peripheral alpha-linked N-acetylglucosamine on the carbohydrate moiety of mucin derived from mammalian gastric gland mucous cells: epitope recognized by a newly characterized monoclonal antibody.
To obtain a tool to study the structural characterization and the detection of mucin derived from the gastric gland mucous cells, we developed a monoclonal antibody, designated HIK1083, against mucin purified from rat gastric mucosa. In an ELISA, HIK1083 reacted strongly with the mucin purified from a deep layer of the corpus and antrum but only slightly reacted with that obtained from the surface mucosal layer. The reaction of mucin and HIK1083 was inhibited by the oligosaccharides obtained by the alkaline borohydride reduction of antigenic mucin. Two purified oligosaccharide alditols reacting with the monoclonal antibody obtained from the antigenic mucin had one and two peripheral alpha-linked N-acetylglucosamine residues, respectively, according to the evidence from NMR spectroscopy. Moreover, among the commercially available p-nitrophenyl derivatives of monosaccharides, only p-nitrophenyl-N-acetyl-alpha-D-glucosaminide inhibited the reaction of this monoclonal antibody and the antigenic mucin in a concentration-dependent manner. These results, as well as the immunohistochemical observations, indicate that alpha-linked N-acetylglucosamine residues are specifically attached to the peripheral region of the carbohydrate moiety of the mucin synthesized in and secreted from the gastric-gland-type cells, and indicate that the monoclonal antibody HIK 1083 recognizes this structure.
Acetylglucosamine↗
Establishment of monoclonal antibodies against carbohydrate moiety of gastric mucins distributed in the different sites and layers of rat gastric mucosa.
Eight monoclonal antibodies (MAbs), designated RGM21 approximately RGM42, were generated against mucin purified from the rat gastric mucosa. By applying ELISA, all of these MAbs were proved to react not only with the purified mucin, but also with the oligosaccharide mixture obtained from the antigenic mucin by alkaline borohydride treatment. Treatment of the mucin-attached ELISA well with trypsin, sodium periodate or galactose oxidase prior to the addition of the MAb was applied to characterize these MAbs. Histochemical observation indicated that all these MAbs were able to stain the formalin fixed-paraffin embedded sections of the rat gastroduodenal mucosa. Although each of these MAbs reacted with distinct mucus-producing cells localized in particular regions of the gastroduodenal mucosa, their staining specificity could generally be classified into four groups. These MAbs might be useful for estimating the physiological and pathological changes of mucins in the gastric mucosa.
Animals↗
IL-10 suppresses cell surface CD23/Fc epsilon RII expression, not by enhancing soluble CD23 release, but by reducing CD23 mRNA expression in human monocytes.
To examine a possible involvement of interleukin-10 (IL-10) in CD23/Fc epsilon RII expression in human monocytes, effects of IL-10 on the cell surface CD23 expression, soluble CD23 (sCD23) release, and CD23 type b mRNA expression were investigated. IL-10 suppressed IL-4-induced surface CD23 expression on monocytes in a dose-dependent manner, and this effect was completely neutralized by anti-IL-10 antibody. The suppressive effect of IL-10 on surface CD23 expression was not due to enhancement of sCD23 release from the cell surface because no increase in sCD23 in culture supernatant was detected after incubation with IL-10. Instead, the effect of IL-10 seemed to be exerted at the transcriptional level since IL-4-induced expression of CD23 type b mRNA was significantly reduced when IL-10 was present. Although IL-4 induced surface CD23 expression on both monocytes and B cells, the suppressive effect of IL-10 was observed only on monocytes, which underscores different regulatory mechanisms for CD23 expression between the two cell types.
B-Lymphocytes↗
Effect of danazol on the immunocompetent cells in the eutopic endometrium in patients with endometriosis: a multicenter cooperative study.
OBJECTIVE: To assess the effects of danazol on immunocompetent cells, human leukocyte antigen (HLA) expression, and adhesion molecules in the eutopic endometrium of patients with endometriosis. DESIGN: Antigens were localized immunohistochemically in the endometria, before treatment and during treatment (2 months later). PARTICIPANTS: Ten patients with laparoscopically proven endometriosis who consented to participate in this study were treated with 400 mg/d of danazol for 4 months. Forty-two infertile patients without endometriosis or adenomyosis served as controls. RESULTS: Immunohistochemical analysis revealed significantly increased expression of the T cell subsets, macrophages, adhesion molecules, and HLA antigens in eutopic endometrium in patients with endometriosis compared with the infertile group. Treatment with danazol reduced the number of cells in T cell subsets, adhesion molecules, or HLA antigen expression, especially of gamma delta T cells, to 39.5% of the pretreatment value in patients with endometriosis. CONCLUSIONS: Danazol had an immunomodulatory effect on the autoimmune response in endometrium associated with endometriosis.
Adult↗