Masaharu Uemoto

Teachers' knowledge, beliefs and attitudes concerning schizophrenia- a cross-cultural approach in Japan and Taiwan.

Abstract.Background:Mental health literacy of the general public is essential for the effective promotion of society’s mental health. However, there has been no investigation of the general public’s mental health literacy with Japanese and Taiwanese socio-cultural backgrounds.Methods:A total of 129 Japanese and 150 Taiwanese elementary school teachers were surveyed about knowledge, beliefs and attitudes concerning schizophrenia by means of a questionnaire with a vignette describing a case of the disease. Identification of the case, cause of the disease, coping behavior for the case, and perception of stigmatizing and supporting attitudes by parents and neighbors of the case were investigated.Results:As a common finding with the studies in Western countries, only small percentages of the Japanese and Taiwanese respondents were able to make a correct identification. A further common finding was the emphasis on psychosocial factors as a cause of schizophrenia, as was the rejection of psychotropic medication, although future study is required to determine to what extent the respondents know about therapeutic procedures utilized by psychiatrists. Significantly stronger stigma perception was shown in the Japanese respondents than in the Taiwanese, which may be attributable to the high institutionalization rate in Japan.Conclusions:Japanese and Taiwanese teachers’ knowledge, beliefs and attitudes regarding schizophrenia were similar to those found in the general public in Western societies. Although the present study is limited in sampling and the components of the mental health literacy investigated, several working hypotheses have been extracted from it to be tested in future investigations on the Japanese and Taiwanese and other Asian general public’s mental health literacy.

Ob/ob mice as a model of delayed gastric emptying.

Diabetic gastroparesis is a well-recognized delay of gastric emptying in diabetic patients. We assessed the gastric emptying rate in ob/ob mice, a genetic model of obesity and diabetes. The basal gastric emptying rate in 22- to 27-week-old ob/ob mice was significantly lower than that in 10- to 11-week-old ob/ob mice (P<.01). Our results indicate that the ob/ob mice are a useful model not only of glucose intolerance but also of delayed gastric emptying as a diabetic complication.

Stimulation of the rat dorsal raphe in vivo releases labeled serotonin from the parietal cortex.

In vivo release of labeled serotonin ([3H]5-HT) from the parietal cortex was investigated by cortical cup technique and electrical stimulation of midbrain raphe in rats anesthetized with pentobarbital sodium. The spontaneous efflux of tritium from the parietal cortex preload with [3H]5-HT followed a multiphasic exponential course. After 120 min, the rate of efflux appeared to fit the single exponential function (slow phase). Imipramine (10(-6)-10(-3) M) produced a dose-dependent increase in the spontaneous release. When pargyline in concentrations ranging from 10(-4) to 10(-3) M were added to the medium in the cup, the unchanged [3H]5-HT significantly increased in a dose-dependent manner and the slow declining coefficient of tritium efflux significantly decreased in the presence of 10(-4) pargyline. Stimulation of the rostral two-thirds of the dorsal raphe and the lateral 5-HT bundle originating from the dorsal raphe significantly increased the release of [3H]5-HT and its metabolites while stimulation of the caudal one-third of the dorsal raphe did not produce a significant increase in the release of [3H]5-HT and its metabolites. Stimulation of the medium raphe produced no or only a slight increase in the release of [3H]5-HT and its metabolites. These findings are a direct demonstration of the in vivo release of [3H]5-HT from the parietal cortex with stimulation of the dorsal raphe, particularly the rostral two-thirds of the nucleus and provide the neurochemical evidence for the dorsal raphe-cortical 5-HT pathway via the lateral 5-HT bundle.

Peptide YY3‐36 and pancreatic polypeptide suppress food intake

To the Editor , Here, we show that peptide YY (PYY) 3–36 and pancreatic polypeptide (PP) suppress food intake in both lean mice and ob/ob obese mice. Pancreatic polypeptide and PYY are 36 amino acid peptides that belong to a family of peptides including neuropeptide Y (NPY). Since the discovery of leptin and ghrelin, much progress has been made in the study of controlling energy homeostasis. Until now, various peptides, including NPY, ghrelin, agoutirelated protein (AGRP), orexin, melanin-concentrating hormone (MCH), leptin, α -melanocyte-stimulating hormone (MSH), cocaineand amphetamine-regulated transcript (CART), cholecystokinin (CCK), corticotropin-releasing factor (CRF) and urocortin, have been shown to be involved in the regulation of food intake. Tschop et al . reported that gut hormone PYY3-36 does not suppress food intake in rodents and they cannot replicate the anorexigenic effects of PYY3-36 reported by Batterham et al . 1–3

Kobe Earthquake and the Patients on Hemodialysis

Kobe Earthquake and the Patients on Hemodialysis A. Akio Inui H. Hideaki Inoue M. Masaharu Uemoto M. Masato Kasuga H. Hiroshi Taniguchi Study Group of Kansai Society of Behavioral Medicine, Second Department of Internal Medicine, Department of Metabolism and Community Health Science, Kobe University School of Medicine, Inoue Clinic, and Department of Psychiatry, NishiKobe Medical Center, Kobe, Japan

METABOLIC ALKALOSIS AND CHRONIC RENAL FAILURE IN A BULIMIC PATIENT

Dr. Akio Inui, 2nd Department of Internal Medicine, Kobe University School of Medicine, Kusunoki-cho, Chuo-ku, Kobe 650 (Japan) Dear Sir, Metabolic acidosis is a characteristic of chronic renal failure that is mostly due to inability of the damaged kidney to excrete hydrogen ion. We recently treated a bulimic patient who developed metabolic alkalosis when chronic renal failure was advanced. A 25-year-old woman was transferred to our institution because of elevation of serum creatinine (736 μmol/l) and blood urea nitrogen (18.0 mmol/l) levels. She had a 10-year history of bulimia nervosa and anorexia ner-vosa (body mass index 13.6) with frequent episodes of binging and vomiting. High fever preceded the onset of her symptoms such as nausea. Arterial blood gas analysis revealed metabolic alkalosis (pH 7.52, bicarbonate 55.8 mmol/l) with marked retention of CC1⁄8 (pC < 3⁄4 9.1 kPa). Serum potassium and chloride levels were decreased (3.5 and 72 mmol/l, respectively), but the urinary chloride concentration was initially increased (50 mmol/l). Water and electrolyte deficits were carefully replaced, and reduction of self-induced vomiting was achieved. The blood pH was restored, and the ventilation was improved. Metabolic alkalosis associated with chronic renal failure is extremely rare. Severe loss of acid gastric juice appears to be a cause of this condition. Care should be taken in the management of chronic renal failure combined with bulimia nervosa.