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Physical interaction can enhance motor learning, but it remains unclear what type of interaction is best suited to increasing the active effort put into a task, which should support learning. Here, we used the same interactive tracking task with different instructions to induce three training conditions: competition, collaboration, and self-improvement, where partners improve their own performance while interacting haptically with each other. The effort was gauged by measuring the total normalized muscle activity. Feedback of task performance and the haptic dynamics were identical in all three training conditions, so the effort needed to complete the task was the same. Only the instructions to ‘compete with the partner’, ‘improve your and your partner's accuracy’ and ‘improve your accuracy’ were different among the competition, collaboration, and self-improvement conditions, respectively. Despite having the same goal of maximizing self-performance during competition and self-improvement, participants exerted significantly more effort during competition, and their tracking accuracy was highest during competitive practice. Least effort was put into collaboration but tracking accuracy during collaboration was comparable to self-improvement. Our results suggest that interactive haptic competition can induce higher active drive or effort than either collaborative training or self-focused practice.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1067/mob.2000.104804 Byline: Atsushi Imai, Atsushi Takagi, Teruhiko Tamaya Keywords: Endometriosis; apoptosis; endometrium; gonadotropin-releasing hormone analog Abstract: Objective: Impaired sensitivity of endometrial tissue to spontaneous apoptosis in women with endometriosis contributes to the abnormal implantation and growth of endometrium at ectopic sites. Our purpose was to examine the effect of gonadotropin-releasing hormone analog, widely used in the treatment of endometriosis, on the reduced rate of endometrial apoptosis in endometriosis. Study Design: Paired ectopic and eutopic endometrial tissue specimens were obtained from 13 patients with endometriosis, and control samples were taken from 8 patients with uterine myoma. Apoptotic cell death was assessed biochemically and morphologically with an enzyme-linked immunoassay and Hoechst No. 33342 staining of deoxyribonucleic acid fragment, respectively. Results: Spontaneous apoptosis was significantly lower in ectopic and eutopic endometrial tissue from patients with endometriosis (0.22 [+ or -] 0.082 in absorbance) than in endometrial tissue from control subjects (0.52 [+ or -] 0.483)(P < 0.001). Incubation with a gonadotropin-releasing hormone analog (1 [mu]mol/L) increased the apoptotic rate of endometrial cells from patients with endometriosis to 0.56 [+ or -] 0.501 (P < .001). The effect of this gonadotropin-releasing hormone revealed a dose dependency; a half-maximal effect occurred with 10 nmol/L; however, the control endometrium was not affected. Conclusion: Exposure to gonadotropin-releasing hormone results in changes of the sensitivity of endometriotic endometrium to spontaneous apoptosis; these changes in sensitivity may, in turn, release endometrial cells from resistance to apoptosis and result in reduced survival and growth. This phenomenon could, at least in part, account for the therapeutic action of gonadotropin-releasing hormone analog on endometriosis. (Am J Obstet Gynecol 2000;182:1142-6.) Author Affiliation: Department of Obstetrics and Gynecology, Gifu University School of Medicine. Gifu, Japan Article History: Received 16 April 1999; Revised 18 October 1999; Accepted 3 December 1999 Article Note: (footnote) [star] Reprint requests: Atsushi Imai, MD, Department of Obstetrics and Gynecology, Gifu University School of Medicine, Tsukasamachi, Gifu 500-8705 Japan.

Byline: Atsushi Imai, Shinji Horibe, Atsushi Takagi, Teruhiko Tamaya Keywords: guanosine triphosphate binding protein; endometrial cancer; protein dephosphorylation; gonadotropin-releasing hormone receptor; gonadotropin-releasing hormone analog Abstract: OBJECTIVE: Gonadotropin-releasing hormone receptor is demonstrated in uterine endometrial carcinomas. This study was performed to determine gonadotropin-releasing hormone receptor-mediated membrane events and to identify the guanosine triphosphate binding protein (G protein) subtypes linked to gonadotropin-releasing hormone receptor in the tumors. STUDY DESIGN: Endometrial carcinomas surgically removed had been screened for gonadotropin-releasing hormone receptor expression before plasma membrane isolation. The phosphoprotein level was observed in the phosphorus 32-labeled incorporation from [[gamma]-.sup.32P]adenosine triphosphate into the isolated plasma membranes. The G.sub.i ([alpha] subunit) protein was detected by immunoblotting and pertussis toxin-catalyzed adenosine diphosphate ribosylation. RESULTS: Incubation of phosphorus 32-labeled membranes with a gonadotropin-releasing hormone analog in the presence of guanosine thiotriphosphate caused a remarkable loss of phosphoprotein from 35 kd protein. This dephosphorylation action was dose dependent of the gonadotropin-releasing hormone analog, and the maximal effect (90% loss) occurred at 100 nmol/L. Pertussis toxin brought about adenosine diphosphate ribosylation of an immunodetected G[alpha].sub.i. Gonadotropin-releasing hormone analog alone or guanosine thiotriphosphate alone had no effect. Pretreatment of the membrane with the pertussis toxin completely inhibited gonadotropin-releasing hormone-mediated dephosphorylation of the 35 kd protein. CONCLUSION: These data demonstrate the coupling of gonadotropin-releasing hormone receptor to protein dephosphorylation through G.sub.i, raising the possibility that the antimitogenic action of gonadotropin-releasing hormone may occur by release of the action of protein phosphorylation to promote cell growth.(Am J Obstet Gynecol 1997;176:371-6.) Author Affiliation: Gifu, Japan Article History: Received 19 April 1996; Revised 22 August 1996; Accepted 29 September 1996 Article Note: (footnote) [star] From the Department of Obstetrics and Gynecology, Gifu University School of Medicine., [star][star] Supported by research grant No. 07457383 from the Ministry of Education, Culture, and Science, Japan., a Reprint requests: Atsushi Imai, MD, Department of Obstetrics and Gynecology, Gifu University School of Medicine, Tsukasamachi, Gifu 500 Japan., aa 6/1/77896

Odontomas are generally encountered in permanent dentition and rarely seen in primary dentition. These lesions are regarded as essentially benign, though they often cause disturbances in eruption of the associated tooth. We present clinical findings and management of 3 cases of odontomas that occurred in primary dentition, including a 3-year-old girl referred for examination of an unerupted left upper primary canine, a 6-year-old boy with an unerupted left lower second primary molar, and a 5-year-old girl who was presented with an unerupted right upper second primary molar. In all cases, periapical and panoramic radiography revealed a radio-opaque mass surrounded by a narrow radiolucent space located above the crown of the unerupted tooth. Each was diagnosed as a compound odontoma interfering with eruption of a primary tooth and surgical removal was performed under general anesthesia for all patients, with the final diagnosis based on histological findings. Following surgery, the primary canine in Case 1 spontaneously erupted, while a space maintenance appliance was applied in Case 2 and 3. It is important to recognize that an odontoma can appear in primary dentition, though the incidence is quite low. Early detection and removal of an odontoma associated with an impacted primary tooth is necessary for optimal dentition.

We report 3 cases (all men, age: 69–81 years) of acute exacerbation of interstitial pneumonia (AEIP) that were successfully treated with a high-flow nasal cannula (HFNC), which delivers heated, humidified gas at a fraction of inspired oxygen (FIO2) up to 1.0 (100%). Oxygenation was insufficient under non-rebreathing face masks; however, the introduction of HFNC with an FIO2of 0.7–1.0 (flow rate: 40L/min) improved oxygenation and was well-tolerated until the partial pressure of oxygen in blood/FIO2ratio increased (between 21 and 26 days). Thus, HFNC might be an effective and well-tolerated therapeutic addition to the management of AEIP.

Epidermal hyperplasia is a histological hallmark observed in both atopic dermatitis (AD) and psoriasis, although the clinical features and the underlying immunological disorders of these diseases are different. We previously showed that periostin, a matricellular protein, plays a critical role in epidermal hyperplasia in AD, using a mouse model and a 3-dimensional organotypic coculture system. In this study, we explore the hypothesis that periostin is involved in epidermal hyperplasia in psoriasis.

IMPORTANCE: Pemphigus vulgaris (PV) is a disease that features blistering of the skin and mucous membranes caused by autoantibodies directed against desmoglein 3 (Dsg3) and/or desmoglein 1 (Dsg1). Indirect immunofluorescence (IIF) and enzyme-linked immunosorbent assay (ELISA) are 2 methods that are widely used to measure Dsg3 or Dsg1 antibody titers in PV. Although the titers of these autoantibodies are generally correlated with disease activity, some patients with a high ELISA index do not have severe symptoms. We encountered a patient with PV in remission, who had a high anti-Dsg3 antibody ELISA index while the IIF result was negative. OBSERVATIONS: The anti-Dsg3 antibodies of our patient mainly recognized Ca2+-dependent conformational epitopes and targeted mature Dsg3 protein. We report this case focusing on the discrepancy between ELISA and IIF findings, as well as on the specific characteristics of the patient’s autoantibodies evaluated by newly developed methods. CONCLUSIONS AND RELEVANCE: This case emphasizes that a discrepancy between disease activity, the ELISA index for Dsg3, and/or IIF findings can occur in PV. Further research on similar patients will be required to elucidate the pathogenic mechanisms in patients with PV who have nonpathogenic antibodies and show a discrepancy between ELISA and IIF.

Introduction:The clinical manifestation of acute myocarditis (AM) is highly variable, and the mechanisms of this diversity have not been fully elucidated. Hence, it is hard to precisely predict their prognosis, and some cases with AM rapidly progress into cardiogenic shock, resulting in the increased in-hospital mortality.Hypothesis:There are some parameters in the initial presentations to predict the prognosis of patients with AM.Methods:This is a multicenter observational study including hospitalized AM patients between 2007 and 2019. We set the primary endpoint of this study as a composite of in-hospital death from any cause and implantation of ventricular assist devices during the index hospitalization.Results:Of 76 enrolled patients [average age: 42 years; male: 79%; mean left ventricular ejection fraction (LVEF): 41%], 13 patients (17%) developed the composite endpoint, and 8 (11%) died within 10 days after the admission. Patients who experienced the composite endpoint were more likely to be older, and have diabetes, anemia, impaired renal functions, higher creatine kinase-MB, lower LVEF, and longer QRS duration on ECG at admission. In the multivariable logistic regression analysis, QRS duration on ECG at admission was independently associated with the composite endpoint, even after adjusting for confounding factors such as age, sex, and LVEF at admission [OR: 1.31, 95% CI: 1.01-1.72]. The ROC curves for the primary endpoint revealed that the cut-off value of QRS duration at admission were 140 msec (sensitivity: 100%, specificity: 90%, AUC: 0.97). Kaplan-Meier analysis showed that patients with baseline QRS duration > for >140 msec had a significantly higher rate of the primary endpoint than those with QRS duration <140 msec (p<0.001, Figure).Conclusions:Prolonged QRS duration at admission could predict in-hospital prognosis in patients with AM. We should consider the intensive care and close observation in such a high-risk population with AM.

We estimated the food sources of macroinvertebrates using carbon, nitrogen, and sulfur stable isotopes in a headwater stream. Stream food webs, including macroinvertebrates, rely on production from autochthonous and allochthonous photosynthesis. We found that a freshwater grazer, the snail Semisulcospira libertina, may assimilate different food sources, based on stable carbon and nitrogen isotope evidence from snail muscle and the much lighter sulfur isotope signature than those of other associated macroinvertebrates. Previous studies have shown the importance of methanotrophic and sulfur bacteria in reductive environments (clay and organic-rich sediments) as food sources for macroinvertebrates. Our results show that the production by chemoautotrophic bacteria contributes to the food sources of a snail in a stream. Thus, the chemoautotrophic bacteria are important in the freshwater food webs, even in mostly aerobic habitats. (© 2006 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)

This paper presents the construction of a pneumatic active suspension system for a one-wheel car model using fuzzy reasoning and a disturbance observer. The one-wheel car model can be approximately described as a nonlinear two degrees of freedom system subject to excitation from a road profile. The active control is composed of fuzzy and disturbance controls, and the active control force is constructed by actuating a pneumatic actuator. A phase lead-lag compensator is inserted to counter the performance degradation due to the delay of the pneumatic actuator. The experimental result indicates that the proposed active suspension improves much the vibration suppression of the car model.

Bacteroides, a predominant commensal bacteria in the gut, are thought to be responsible for the development of inflammatory bowel disease (IBD). In the present study, we examined whether or not bifidobacteria suppress B. vulgatus, a representative pathogenic Bacteroidesspecies, in both the coculture system and the gnotobiotic murine model. As a result, Bifidobacterium infantis1222 highly inhibited the growth of B. vulgatusin the coculture and also significantly suppressed the systemic antibody response raised by B. vulgatuscolonizing the gut in gnotobiotic mice. Colonization of the mice by B. vulgatusincreased the number of Peyer's patch (PP) cells bearing PNA (peanut agglutinin)+/anti‐κ+phenotype, which represents plasma cell‐like B cells. Moreover, treatment of those B. vulgatus‐implanted mice with B. infantis1222 abrogated such increase in the number of PNA+/anti‐κ+cells. These results thus suggested that B. infantis1222 protected the gut epithelial layer including the PP from being invaded by Bacteroides, thereby suppressing the systemic antibody response raised by Bacteroides.

We report a rare case of cytomegalovirus (CMV) enterocolitis in a healthy 57-year-old woman. In March 1999, she developed hematochezia, diarrhea, and abdominal pain. Total colonoscopy on March 17th showed multiple aphthoid lesions and friable mucosa from the terminal ileum to the rectum and a shallow ulcer on the ileocecal valve. Repeat total colonoscopy on April 19th showed faded aphthoid lesions in the terminal ileum, and biopsy specimen revealed CMV inclusion bodies. Symptoms and endoscopic findings improved without any specific medication. In previous reports, the definition of “immunocompetent individual” varied. Here, we define immunocompetent individual as one who has no associated diseases, is not under immunosuppressive therapy, has no recent history of operation, is negative for human immunodeficiency virus antibody, is not pregnant, has no obvious infectious course, and is less than 70 years of age. This is the ninth report of CMV enterocolitis in an immunocompetent individual in the world literature.

ABSTRACTTo clarify what bacterial species of commensal intestinal microbes are recognized as the antigens that induce a serum antibody response in patients with inflammatory bowel disease (IBD), 72 subjects consisting of 12 Crohn’s disease patients, 30 ulcerative colitis patients, and 30 healthy volunteers were examined for their titers of serum antibody to these intestinal bacteria. In IBD patients, as a result, significant elevations of both the immunoglobulin G (IgG) and IgA titers to Bacteroides ovatuswere found. Immunoblotting showed that a definite 19.5-kDa band of B. ovatuswas bound to the serum antibody raised in IBD patients. It was thus concluded that B. ovatuscauses serum antibody responses in IBD patients, and a 19.5-kDa molecule of this bacterium appears to be the responsible antigen, although the role of this event in pathogenesis remains unclear.

To clarify what bacterial species of commensal intestinal microbes are recognized as the antigens that induce a serum antibody response in patients with inflammatory bowel disease (IBD), 72 subjects consisting of 12 Crohn's disease patients, 30 ulcerative colitis patients, and 30 healthy volunteers were examined for their titers of serum antibody to these intestinal bacteria. In IBD patients, as a result, significant elevations of both the immunoglobulin G (IgG) and IgA titers to Bacteroides ovatus were found. Immunoblotting showed that a definite 19.5-kDa band of B. ovatus was bound to the serum antibody raised in IBD patients. It was thus concluded that B. ovatus causes serum antibody responses in IBD patients, and a 19.5-kDa molecule of this bacterium appears to be the responsible antigen, although the role of this event in pathogenesis remains unclear.

γ-Glutamylcysteine synthetase (γ-GCS) is a key enzyme in glutathione (GSH) synthesis, and is thought to play a significant role in intracellular detoxification, especially of anticancer drugs. Increased levels of GSH are commonly found in the drug-resistant human cancer cells. We designed a hammerhead ribozyme against γ-GCS mRNA (anti-γ-GCS Rz), which specifically down-regulated γ-GCS gene expression in the HCT-8 human colon cancer cell line. The aim of this study was to reverse the cisplatin and multidrug resistance for anticancer drugs. The cisplatin-resistant HCT-8 cells (HCT-8DDP cells) overexpressed MRP and MDR1 genes, and showed resistance to not only cisplatin (CDDP), but also doxorubicin (DOX) and etoposide (VP-16). We transfected a vector expressing anti-γ-GCS Rz into the HCT-8DDP cells (HCT-8DDP/Rz). The anti-γ-GCS Rz significantly suppressed MRP and MDR, and altered anticancer drug resistance. The HCT-8DDP/Rz cells were more sensitive to CDDP, DOX and VP-16 by 1.8-, 4.9-, and 1.5-fold, respectively, compared to HCT-8DDP cells. The anti-γ-GCS Rz significantly down-regulated γ-GCS gene expression as well as MRP/MDR1 expression, and reversed resistance to CDDP, DOX and VP-16. These results suggested that γ-GCS plays an important role in both cisplatin and multidrug resistance in human cancer cells.

FRAT1 positively regulates the WNT signaling pathway by stabilizing β-catenin through the association with glycogen synthase kinase-3β. Here, we have cloned FRAT2 cDNAs, spanning the complete coding sequence, from a human fetal lung cDNA library. FRAT2 encoded 233 amino-acid protein, which showed 77.3% total amino-acid identity with FRAT1. FRAT2 and FRAT1 were more homologous in the acidic domain (96% identity), the proline-rich domain (92% identity), and the GSK-3β binding domain (100% identity). The FRAT2 gene was mapped to human chromosome 10q24.1. The FRAT2 mRNA of 2.4-kb in size was relatively highly expressed in MKN45 (gastric cancer), HeLa S3 (cervical cancer), and K-562 (chronic myelogenous leukemia). Xenopus axis duplication assay revealed that the wild-type FRAT2 mRNA, but not the mutant FRAT2 mRNA lacking the acidic domain and the proline-rich domain, has the capacity to induce the secondary axis. These results indicate that FRAT2, just like FRAT1, functions as a positive regulator of the WNT signaling pathway. Thus, up-regulation of FRAT2 in human cancer might be implicated in carcinogenesis through activation of the WNT signaling pathway.

ABSTRACTThe mechanism by which Helicobacter pyloriinduces apoptosis remains unclear. In a previous study using biopsy samples, we found a significant correlation between the urease activity of anH. pyloristrain and the apoptosis level induced by this strain. Therefore, in this study, we investigated whether urease and/or the ammonia generated by urease can induce apoptosis. Human gastric epithelial cell lines were cocultured with H. pylori, and the levels of apoptosis and ammonia production were measured. The medium was supplemented (or not supplemented) with urea and cytokines. While a large amount of ammonia (>30 mM) accumulated in the coculture containing urease-positive H. pyloriand urea, no significant degree of apoptosis occurred. In the presence of tumor necrosis factor alpha (TNF-α), however, a marked acceleration of apoptosis was found in this coculture. Such enhancement of apoptosis was also induced by the addition of 4 to 8 mM ammonia to the cell culture without either H. pylorior urea but containing TNF-α. These results suggested that ammonia accelerates cytokine-induced apoptosis in gastric epithelial cells, while ammonia or urease molecules alone are unable to induce a significant degree of apoptosis.

β-Catenin, IκBα, and HIV Vpu are recruited to the ubiquitin–proteasome degradation pathway by βTRCP, one of the components of the ubiquitin ligase complex. βTRCP2, a related gene of βTRCP, was cloned and characterized. Three isoforms, βTRCP2A, βTRCP2B, and βTRCP2C, were identified. All of these βTRCP2 isoforms consist of an F-box and seven WD repeats. Human βTRCP2A shows 86% total amino acid identity with human βTRCP. βTRCP2 mRNA of 4.5 kb in size was detected almost ubiquitously. Sequence analyses on βTRCP2 genomic clones revealed that the βTRCP2 gene consists of at least 14 exons. Exons 1 and 4–14 are shared among all βTRCP2 isoforms. βTRCP2A of 508 amino acids lacks exons 2 and 3, βTRCP2B of 529 amino acids contains exon 3, and βTRCP2C of 542 amino acids contains exon 2. These results indicate that three βTRCP2 isoforms are transcribed due to alternative splicing. The βTRCP2 gene has been mapped to human chromosome 5q35.1 by fluorescence in situ hybridization.

The Frizzledgenes encode WNT receptors. Frizzled-10(FZD10), a novel member of the Frizzledgene family, has been cloned and characterized. Nucleotide sequence analysis showed that human FZD10gene encodes a seven-transmembrane-receptor of 581 amino acids, with the N-terminal cysteine-rich domain and the C-terminal Ser/Thr–Xxx–Val motif. Larger amounts of FZD10mRNA, 4.0 kb in size, were detected in the placenta and fetal kidney, followed by fetal lung and brain. In adult brain, FZD10mRNA was abundant in the cerebellum. Among cancer cell lines, FZD10was highly expressed in a cervical cancer cell line, HeLa S3, and moderately in a colon cancer cell line, SW480. The FZD10 gene was mapped to human chromosome 12q24.33. FZD10 shares 65.7% amino-acid identity with Frizzled-9 (FZD9). FZD10and FZD9constitute a subfamily among the Frizzledgenes.

Abstract: To determine the pathological role of interleukin‐8 (IL‐8) which has been implicated in the gastric mucosal injury caused by Helicobacter pylori (H. pylori)infection, the gastric mucosal IL‐8 level and IL‐8 mRNA expression rate were studied in patients with peptic ulcers and chronic gastritis. The IL‐8 levels in biopsy homogenates were determined by Enzyme‐linked immunosorbent assay (ELISA). Expression of IL‐8 mRNA was studied by the reverse transcriptase polymerase chain reaction (RT‐PCR) method. The gastric mucosal IL‐8 levels were significantly higher in patients with peptic ulcers than in those with normal mucosa. The IL‐8 level correlated with urease activity. Eradication therapy for H. pyloridecreased both the IL‐8 level and IL‐8 mRNA expression. Treatment with omeprazole also decreased the IL‐8 level without eradication of H. pylori.Our findings suggest that IL‐8 plays an important role in the pathogenesis of peptic ulcers.

A simian virus 40 (SV40)‐transformed macrophage clone which was established from BALB/cAnN mouse bone marrow cells was used to study the effect of different cultural conditions on the expression of macrophage properties. The macrophage clone, BB‐W‐531–2 line, expressed and maintained the macrophage properties, immune phagocytosis or Fc‐ and complement receptors, under the growth‐inhibiting conditions of confluent density and of cultivation on bacteriologic dishes with reduced adhesiveness. However, the cells lost their ability to express the macrophage properties dependent upon cell density after repeated culture splits in the growing phase. These cells regained that ability when they were cocultured with cells having macrophage properties. These results suggest that there is a possible correlation between reduced multiplication and the expression of macrophage properties, and that macrophage properties which have been suppressed or blocked may be induced by diffusible factor(s) produced by macrophages.

A simian virus 40‐transformed mouse macrophage line, BB‐W‐531–2, was examined for its ability to produce interferon. BB‐W‐531–2 cells showed a phenotypic change between the macrophage and the nonmacrophage states. A viral inhibitor (interferon) was produced by the cells during the phenotypic change from the nonmacrophage to the macrophage state. Cells having macrophage properties were well capable of producing interferon when they were stimulated with ultraviolet‐inactivated vaccinia virus, lipopolysaccharide, a streptococcal preparation (OK‐432) or polyinosinate polycytidylate. In contrast, cells that had lost their macrophage properties did not produce interferon even when they were given the same treatments as the cells having macrophage properties. The results suggest that the ability of BB‐W‐531–2 cells to produce interferon is associated with the expression of several macrophage properties.

A radioimmunoassay was performed to determine the total amounts of the A, B, and E series prostaglandins (prostaglandins) in culture fluids of simian virus 40 (SV40)‐transformed mouse clonal macrophages, line 28–12, and its subline, 28–12(Ara). When the proportion of phagocytic cells in confluent 28–12 cell cultures increased, the prostaglandin levels in the culture fluids decreased. On the other hand, stably phagocytic 28–12(Ara) cells, which were derived from 28–12 cells and which had a reduced growth rate, did not release prostaglandins under the usual culture conditions; however, when they were treated with lipopolysaccharide or streptococcal preparation OK‐432, large amounts of prostaglandins were released. In contrast, nonphagocytic cell populations in the cultures of 28–12 cells were not responsive to the drug treatment. These results suggest that there is a correlation between the phenotypic change from the nonphagocytic to the phagocytic state and a decrease in prostaglandin levels in culture fluids, and indicate that phagocytic cells are responsive to prostaglandin inducers, whereas nonphagocytic cells are not.

Antiserum generated against synthetic urotensin II of the goby, Gillichthys mirabilis, was used to localize urotensin II in the caudal neurosecretory system in six species of freshwater teleosts; Cyprinus carpio, Carassius auratus, Oreochromis mossambicus, Oreochromis niloticus, Salmo gairdneri and Plecoglossus altivelis, and six species of seawater teleosts: Acanthogobius flavimanus, Pagrus major, Paapristipoma trilineatum, Trachurus japonicus, Seriola dumerili and Seriola quinqueradiata. In the carp, urotensin II-immunoreactive perikarya were classified into three groups according to their size and shape. Small cells were located in the spinal cord dorsal to the urophysis, medium-sized cells immediately anterior to the urophysis, and large cells anterior to the medium-sized cells. In each group, a small number of nonreactive cells was found. Urotensin II-immunoreactive nerve fibers extended toward the urophysis and terminated around the blood vessels. Other species of teleosts showed a similar immunoreaction to that observed in the carp. The immunoreaction of the urophysis was stronger in seawater fish than freshwater fish. Urotensin II-immunoreactive elements could not be detected in the brains of the carp, goldfish and goby.

We have developed a rendering technique to generate realistic images meeting designers' requirements by strictly analyzing various physical phenomena relevant to the appearance of actual objects.We have numerically compared the results of the calculations using this technique with colorimetry values. As a result, both values were virtually equal, so we have been able to confirm the effectiveness of the established technique.Application of this technique to car design, which has not been realized to a large extent because of severe requests for realism, will make it possible to evaluate styles and colors on a graphics display before making a clay model.

Rat tissues were examined for gastrin-releasing peptide (GRP)-like immunoreactivity, using carboxyterminus-specific antibody made against GRP (19–27), which is thought to be the biologically active site and to be common among species. The distribution of GRP-like immunoreactivity in the rat was similar to that of bombesin-like immunoreactivity. Sephadex G 50 chromatography revealed two peaks of GRP-like reactivity in the rat stomach.

To assess the effects of endogenous GRP on vagal gastrin release and acid secretion, anti-GRP gamma-globulin was infused in anesthetized rats to bind endogenously released GRP. Anti-GRP gamma-globulin blocked the gastrin-releasing effects caused by 4 μg/kg/hr of exogenous GRP infusion and suppressed gastrin release by electrical vagal stimulation. In spite of this suppression, anti-GRP gamma-globulin did not alter basal or vagal-stimulated acid secretion.

5H-Cyclohept[a]azulen-5-one and its 11-methoxycarbonyl derivative were synthesized. The latter reacted in a novel manner with a sulfur ylide to give a new heterocyclic compound having 5-oxa-5H-dicyclohepta[cd,hi] indene skeleton.

Interleukin (IL)‐8, a potent chemoattractant and activator of neutrophils, has been implicated to have a major role in the pathogenesis of gastric mucosal injury by Helicobacter pyloriinfection. We examined the relationship between cytotoxicity and IL‐8 secretion induced by H. pylori.Furthermore, whether the vacuolating cytotoxin of H. pylorimediates IL‐8 secretion from gastric epithelial cell lines was examined. Among the inflammatory cytokines, messages for IL‐6, IL‐8 and transforming growth factor‐β1were produced by gastric cancer (MKN45) cells in response to exposure to the cytotoxic strain of H. pylori.MKN45 incubated with the viable cytotoxic strain of H. pylori.secreted IL‐8. In contrast, the supernatant of neither the cytotoxic nor the non‐cytotoxic strain induced IL‐8 secretion. There was no correlation between IL‐8 secretion and the intensity of cytotoxicity. In conclusion, these findings suggest that IL‐8 secretion from MKN45 induced by H. pyloriis mediated by factors other than cytotoxicity.

The fecal bacterial flora was examined in multiple stool specimens from 14 subjects with gastrointestinal disorders before, during and after the oral administration of bifidobacterial preparation (BBG, viableB. breveandB. bifidum, 3 × 109or 6 × 109per day) for 2 or 3 weeks. Enumerations of fecal bacterial flora showed no conspicuous alterations in total anaerobic bacterial counts during the BBG therapy, however the total number of bifidobacteria in feces increased significantly, and ofE. coliand other aerobacteria showed a tendency to decline. The administeredB. breveandB. bifidumwere recovered in the feces at a concentration of 108/g and of 107to 108/g, respectively. Both species continued to be excreted over 2 weeks after completion of the medication in the feces at concentrations of 106to 107/g and of 105to 106/g respectively, and diminished rapidly in 5 patients and continued at essentially the same level as during the medication in 6 patients. During the treatment the pH, urease activity and ammonia content in feces became lowered and showed a rerise after therapy. Symptomatic discomforts including abdominal distension and pain, anorexia, edema and fever of undetermined origin were reduced during the therapy. Urinalysis, hematological examinations and blood biochemical tests including blood ammonia level, however revealed no significant change.

The effects of gastrin releasing peptide (GRP) on gastrin release and gastric secretion were studied in anesthetized rats. Intravenous infusion of GRP (1–16 μg/kg/hr) caused a dose-dependent increase in serum gastrin level, however, it had no effect on basal gastric secretion in the lumen-perfused stomach preparation. Furthermore, GRP inhibited gastric secretion stimulated by pentagastrin or histamine dosedependently, but not by carbachol. Simultaneous infusion of GRP and a beta adrenergic blocking agent, propranolol, an inhibitor of somatostatin release, did not alter the inhibitory effect of GRP on pentagas trin-stimulated gastric secretion. These results suggest that the inhibitory effect of GRP on gastric secretion in a stimulated condition is mediated via peptide hormones coreleased by GRP, and not via betaadrenergic pathways.

To clarify the relationship between interleukin-8 (IL-8) production and virulent factors, we examined the motility and cytotoxicity of H. pylori,suggested to be a major cause of chronic gastritis and peptic ulcers. Our results demonstrated that among cytotoxic strains of H. pylori,highmotility strains induced more IL-8 than low-motility strains. There was no correlation between cytotoxicity and motility of H. pylori.Four restriction fragment length polymorphism (RFLP) patterns were observed in the flaAPCR products. There was no correlation between flaARFLP and motility. In conclusion, our findings suggest that both cytotoxicity and motility are virulent factors in the pathogenesis of gastric mucosal injury.

A CONTROVERSY has existed since 1951 concerning the sites of oxidative-reductive reactions in the bacterial cell. Several investigators have demonstrated biochemically the presence of oxidative-reductive systems in particulates derived from the bacterial cytoplasmic membrane and probably also from contiguous granules. Weibull1, Mitchell and Moyle2, Storck and Wachsman3, Weibull and Bergström4, Keeler, Carr and Varner5, Cota-Robles et al.6and Weibull et al.7have presented evidence that the cytoplasmic membrane, its fragments and associated granules contain most of the cytochromes and enzymes responsible for succinate, reduced di-phosphopyridine nucleotide, DL-lactate, and α-keto-glutarate oxidation and about half the L-malate oxidative activity.

We have examined mouse peritoneal macrophages which were treated with colchicine and cytochalasin B for 6 hr from the beginning of a culture by ultra-thin sectioning in an attempt to reveal the Internal organizations with special reference to microfilaments and microtubules. In control macrophages, the cell cortex including small processes on the dorsal surface and extending pseudopodia was composed of a microfllamentous network. The colchicine treatment affected the cell cortex; thin pseudopodia extended much more and smaller processes were produced as compared with control macrophages, but the normal movements of mitochondria, lysosomes and other cytoplasmic organelles to the periphery of the cell were suppressed. Microtubules were not observed. The colchicine-induced pseudopodia and the small processes were composed of the same filamentous network as control macrophages. The cytochalasin B treatment also affected the cell cortex; however, thin pseudopodia and small processes were scarcely produced, and the filamentous network which was usually observed in the cell cortex was located in the zone beneath the surface attached to a substratum of the cell in where numerous vacuoles were gathered. Our observations suggest that the flattening of the cell body (the translocation of cytoplasmic organelles and the nucleus) is associated with the function of microtubules, and the movement and localization of the cortex composed of microfllamentous network were sensitive to cytochalasin B.

Distinctive features were observed in spreading pseudopodia on a glass substratum, when mouse peritoneal macrophages were cultured in the medium containing colchicine or cytochalasin B. Macrophages which were treated with colchicine in the medium without calf serum, spread thin pseudopodia, but flattening of the cell bodies was little. The ability to adhere to the sub stratum was suppressed by the presence of serum. On the contrary, pseudo podia of macrophages treated with cytochalasin B were thick, and in this case spreading of the pseudopodia was not marked and the adhesion to the substratum not so inhibited by serum. However, this treatment caused the diminution of the ridge-like processes and thin pseudopodia, and reduced the phagocytic activity markedly; moreover, “granular adhesive substance zone” was not recognized at the perimeter of the pseudopodia. Thus the cell cortex (including ridge-like processes, thin pseudopodia spreading on the sub stratum and the folds ingesting foreign particles) was sensitive to cytochalasin B; the inner layer (including cytoskeletal elements) was sensitive to colchi cine. The function of the cell cortex was discussed in connection with these facts.

Treatment with tannic acid and OsO4 (TA treatment) of tissue culture cells after fixation with glutaraldehyde and OsO4 resulted in good protection of the cell features against shrinkage and thermal damage caused by subsequent procedures used for specimen preparation. A difference in the degree of shrinkage between TA-treated cells and untreated cells was found, the mean diameter of the TA-treated cells being 1.4 times as large as that of untreated cells.

Mouse macrophages were cultured on formvar-coated grids and extracted with glycerination solution, and then were examined by negative staining. Both filaments of about 60 Å in diameter and amorphous entities were observed in pseudopodia of the glycerinated macrophages. The amorphous entities disappeared in the case of the glycerination with sodium pyrophos-phate. After treatment with the contraction solution containing ATP, Ca2+ and Mg2+, the filaments seemed to be covered by the amorphous entities, and were finally arranged into bundles. When macrophages were cultured with cytochalasin B, bundles of fine filaments were often seen in the cell pseudopodia. Even in the presence of cytochalasin B, the filaments seemed to be covered by the amorphous entities when the cells were glycerinated and then treated with the contraction solution. The filaments observed in the bundles which were induced with cytochalasin B appeared to be identical with about 60 Å-filaments of the glycerinated cells. Thus, it is suggested that the pseudopodia contain both about the filaments and amorphous entities (filament-associated materials) and that the arrangement of the filaments can be altered by the treatments with Ca2+-Mg2+-ATP or cytochalasin B and is mediated with the filament-associated materials.