Job satisfaction in Japanese nurses

This study investigated job satisfaction among nurses in Japan The instrument for measuring occupational satisfaction of hospital nurses developed by Stamps and her associates was used Initial items were reviewed by content experts who were familiar with measurement of work satisfaction among health professionals and nursing practice in Japan Based on the item analysis in the cultural context, several items were reworded or eliminated from the original version Twenty-five items were retained and translated into English by bilingual professionals The questionnaire was administered to 613 nurses Practising in a large, acute-care hospital in a southern part of Japan The results from testing psychometric properties of the translated version of the instrument were satisfactory It may be concluded that nurses in the study were not satisfied but not dissatisfied either On all items, they showed relatively strong commitment to their work However, extrinsic factors such as having little opportunities for promotion or less favourable working conditions appeared to negatively influence job satisfaction in the study The findings support the dual factor theory of Herzberg and also Maslow's theory Considering the lowest scored item, little opportunities for promotion, which reflects the employment system in Japan, administrators, who are usually male medical practitioners, should be made aware of a need for creating clinical ladder opportunities for nurses who would be promoted based on a merit system, instead of the current practice of a seniority system     

Mapping of gene encoding mouse placental alkaline phosphatase to chromosome 4

The gene encoding the mouse placental alkaline phosphatase (ALP; orthophosphoric-monoester phosphohydrolase, alkaline optimum, EC 3.1.3.1) is mapped to chromosome 4, based on Southern blot hybridization of the mouse cDNA with DNAs from mouse-Chinese hamster somatic cell hybrids. This assignment is consistent with the genetic analysis of theAkp-2 locus, which is responsible for the genetic variation of alkaline phosphatase enzyme in placenta as well as in liver, kidney, and bone.     

Leukocyte cytotoxicity in a persistent virus infection: presence of direct cytotoxicity but absence of antibody-dependent cellular cytotoxicity in horses infected with equine infectious anemia virus.

Antibody-dependent cellular cytotoxicity and direct cytotoxicity assays were performed with equine infectious anemia virus-infected target cells, equine leukocytes, and equine anti-equine infectious anemia virus antibody to determine whether these mechanisms play a role in controlling viral replication in equine infectious anemia. Direct cytotoxicity was observed by using peripheral blood mononuclear cells from 7 of 10 infected horses. Antibody-dependent cellular cytotoxicity was not observed. The antibody-dependent cellular cytotoxicity reaction in horses was then studied by using sheep erythrocytes and trinitrophenylated sheep erythrocytes as target cells. Lysis of these target cells was mediated by neutrophils, monocytes, and lymphocytes. The reaction was activated by antibody of the immunoglobulin G class but not by immunoglobulin G(T). Furthermore, immunoglobulin G(T) efficiently inhibited immunoglobulin G in this function.     

Intracerebroventricular administration of NPY stimulates resistin gene expression in mice

Resistin is thought to cause insulin resistance and link obesity to type 2 diabetes mellitus. However, little is known about the effects of neuropeptide Y (NPY) on resistin gene expression in white adipose tissue (WAT). Resistin gene expression was determined by northern blot analysis in food-deprived mice after NPY administration. Administered NPY (1 nmol/mouse) significantly increased resistin mRNA expression in WAT by 72% compared with artificial cerebrospinal fluid treated controls. These observations indicate that NPY might have a role in regulating resistin gene expression in WAT and that the novel brain-fat axis might be involved in the pathogenesis of obesity and related diseases.     

Ghrelin Induces Fasted Motor Activity of the Gastrointestinal Tract in Conscious Fed Rats

Ghrelin is a newly discovered orexigenic peptide originating from the stomach. However, its action in regulating the fed and fasted motor activity of the digestive tract is not fully understood. In the present study, we examined the effects of intracerebroventricular ( i.c.v. ) and intravenous ( i.v. ) injection of ghrelin on the physiological fed and fasted motor activities in the stomach and duodenum of freely moving conscious rats. i.c.v. and i.v. injection of ghrelin induced fasted motor activity in the duodenum in normal fed rats, while i.v. injection of ghrelin induced fasted motor activity in both the stomach and duodenum in vagotomized rats. The effects of i.c.v. and i.v. injected ghrelin were blocked by growth hormone secretagogue receptor (GHS-R) antagonist given by the same route and also blocked by immunoneutralization of neuropeptide Y (NPY) in the brain. The effects of i.v. injected ghrelin were not altered by i.c.v. injection of GHS-R antagonist in vagotomized rats. Injection of GHS-R antagonist blocked the fasted motor activity in both the stomach and duodenum in vagotomized rats but did not affect the fasted motor activity in normal rats. Low intragastric pH inhibited the effect of ghrelin. The present results indicate that ghrelin is involved in regulation of fasted motor activity in the stomach and duodenum. Peripheral ghrelin may induce the fasted motor activity by activating the NPY neurons in the brain, probably through ghrelin receptors on vagal afferent neurons. Once the brain mechanism is eliminated by truncal vagotomy, ghrelin might be primarily involved in the regulation of fasted motor activity through ghrelin receptors on the stomach and duodenum. The action of ghrelin to induce fasted motor activity is strongly affected by intragastric pH; low pH inhibits the action.     

No allelic association between Parkinson's disease and dopamine D2, D3, and D4 receptor gene polymorphisms

Parkinson's disease is thought to be caused by a combination of unknown environmental, genetic, and degenerative factors. Evidence from necropsy brain samples and pharmacokinetics suggests involvement of dopamine receptors in the pathogenesis or pathophysiology of Parkinson's disease. Genetic association studies between Parkinson's disease and dopamine D2, D3 and D4 receptor gene polymorphisms were conducted. The polymorphism was examined in 71 patients with Parkinson's disease and 90 controls. There were no significant differences between two groups in allele frequencies at the D2, D3, and D4 dopamine receptor loci. Our findings do not support the hypothesis that susceptibility to Parkinson's disease is associated with the dopamine receptor polymorphisms examined. © 1994 Wiley-Liss, Inc.     

Sevoflurane does not inhibit human platelet aggregation induced by thrombin

BACKGROUND: Sevoflurane reportedly inhibits adenosine diphosphate-induced platelet aggregation by suppressing thromboxane A2 formation. The increase in intracellular calcium concentration that fosters platelet aggregation, however, is also induced by other cell signaling pathways, such as activation of the production of inositol 1,4,5-triphosphate by thrombin. The current study aimed to clarify the net influence of sevoflurane on thrombin-induced platelet aggregation. METHODS: Washed platelets were stimulated by thrombin after incubation with 0.5, 1.0, or 1.5 mM sevoflurane, halothane, or isoflurane. Aggregation curves were measured by an aggregometer. Intracellular calcium concentration was measured fluorometrically using fura-2. Calcium mobilization via plasma membrane calcium channels and the dense tubular system was assessed differentially. Intracellular inositol 1,4,5-triphosphate was measured by radioimmunoassay. RESULTS: Halothane significantly suppressed aggregation ratios at 5 min compared with those in controls (89 +/- 7%) to 71 +/- 10% (1.0 mM) and 60 +/- 11% (1.5 mM) and the increase in intracellular calcium concentration (controls, 821 +/- 95 nM vs. 440 +/- 124 nM [1.0 mM] or 410 +/- 74 nM [1.5 mM]). Halothane also significantly inhibited release of calcium from the dense tubular system (controls, 220 +/- 48 nM vs. 142 +/- 31 nM [1.0 mM]). Neither sevoflurane nor isoflurane produced a net change in aggregation ratios, intracellular calcium concentration, or calcium mobilization. Halothane (1 mM) significantly suppressed inositol 1,4,5-triphosphate concentrations, whereas neither 1 mM isoflurane nor 1 mM sevoflurane had any effect. CONCLUSIONS: Although sevoflurane has been reported to inhibit human platelet aggregation induced by weak agonists such as adenosine diphosphate, it does not inhibit human platelet aggregation induced by strong agonists such as thrombin.     

Decreased food intake and body weight in pancreatic polypeptide-overexpressing mice

BACKGROUND & AIMS: Pancreatic polypeptide (PP) is a 36-amino acid hormone produced by F cells within the pancreatic islets and the exocrine pancreas. The definitive function of PP in mammalian physiology remains to be determined. This study examined the effects of chronic overexpression of PP through the development of PP transgenic mice. METHODS: PP transgenic mice were created by using mouse PP complementary DNA under the control of the cytomegalovirus immediate early enhancer-chicken beta-actin hybrid promoter (pCAGGS expression vector). RESULTS: A unique line of transgenic mice was created that overexpresses PP in the pancreatic islets with low levels of expression in other tissues including the brain. Plasma PP concentrations were more than 20 times higher than those of control littermates. However, PP overproduction led to postnatal lethality in half of the pups because of markedly decreased milk intake. The remaining PP transgenic mice gained less weight with specifically reduced food intake and fat mass compared with controls, a result that was more evident in male than in female mice. The transgenic mice exhibited a reduced rate of gastric emptying of a solid meal but had normal oxygen consumption and fasting leptin levels. Immunoneutralization with anti-PP antiserum reversed the phenotypic changes of transgenic animals. CONCLUSIONS: PP could be involved in feeding and body weight regulation partly through regulation of gastric emptying.     

Retropancreatic fascia is absent along the pancreas facing the superior mesenteric artery: a histological study using elderly donated cadavers

To determine the fascial configuration between the superior mesenteric artery and vein and the posterior aspect of the pancreas, we examined histological sections of 10 elderly donated cadavers without pathology in the abdomen. The retropancreatic fascia was absent along the pancreatic parenchyma facing the artery and vein. Abundant nerves along the artery were separated from the pancreas by loose tissue almost 10 mm in thickness. In addition, anterior renal fasciae facing the pancreatic body were not evident in these specimens, possibly due to the degeneration of the left adrenal gland with age. Thus, a definite renal fascia was restricted on the lateral and posterior sides of the left kidney. These findings suggest that interactions between a pancreatic tumor and nerves would require migration of cancer cells over a long distance. Conversely, attachment of the enlarged tumor mass to the nerves may be necessary for the invasion. The anterior renal fascia may fuse with the retropancreatic fascia.