Palliative care workshop primarily aimed for physicians and nurses in order to improve the care of the end-of- life homecare patient

Since 2008, we held a palliative care workshop primarily aimed for physicians, who engaged in clinical practice for cancer treatment. In order to improve the end-of-life stage patient care at home, we made all sorts of efforts not only for physicians, but we also made a workshop available for healthcare professionals to participate. There were more than 60 people participated the workshop: our 20% of physicians and 24% of nurses, 13% of nearby hospital and clinic physicians, 12% of pharmacists and 17% of nurses. According to our questionnaire survey, more than 90% of the participants were satisfied with the workshop. Only 8% of the participants expressed that the workshop was rather difficult. From our analysis of the results, it was clear that we attained a high level of participants' satisfaction.     

Identification of 7α-hydroxypregnenolone, a novel bioactive amphibian neurosteroid stimulating locomotor activity, and its physiological roles in the regulation of locomotion

We now know that steroids can be synthesized de novo by the brain and the peripheral nervous system. Such steroids are called neurosteroids and de novo neurosteroidogenesis from cholesterol is a conserved property of vertebrate brains. Our studies over the past decade have demonstrated that the brain expresses several kinds of steroidogenic enzymes and produces a variety of neurosteroids in sub-mammalian species. However, neurosteroid biosynthetic pathways in amphibians, as well as other vertebrates may still not be fully mapped. We first found that the newt brain actively produces 7α-hydroxypregnenolone, a previously undescribed amphibian neurosteroid. We then demonstrated that 7α-hydroxypregnenolone acts as a novel bioactive neurosteroid to stimulate locomotor activity of newt by means of the dopaminergic system. Subsequently, we analyzed the physiological roles of 7α-hydroxypregnenolone in the regulation of locomotor activity of newt. This paper summarizes the advances made in our understanding of 7α-hydroxypregnenolone, a newly discovered bioactive amphibian neurosteroid stimulating locomotor activity, and its physiological roles in the regulation of locomotion in newt.     

Adiponectin deficiency enhanced the severity of cerulein-induced chronic pancreatitis in mice

Background

Adiponectin is recognized as an antiinflammatory and antifibrotic protein derived from adipocytes, and low serum adiponectin levels are present in obesity. Recent studies have highlighted the relationship between obesity and pancreatic diseases. However, the role of adiponectin in chronic pancreatitis remains uncertain. The aim of this study was to determine the effects of adiponectin in chronic pancreatitis.

Methods

We investigated the effects of adiponectin in experimental chronic pancreatitis by using adiponectin-knockout (APN-KO) mice. Chronic pancreatitis was induced by repeated hourly (6 times) intraperitoneal injections of 50 µg/kg cerulein three times per week for 4 weeks in wild-type (WT) and APN-KO mice. We evaluated the severity of chronic pancreatitis biochemically and morphologically.

Results

In cerulein-treated mice, macroscopically and histologically, severe pancreatic damage was observed in APN-KO mice compared with findings in WT mice. The histological scores for chronic pancreatitis, including glandular atrophy, pseudotubular complex, fibrosis, and total scores, were significantly higher in APN-KO mice than in WT mice. Activated pancreatic stellate cells and F4/80-positive pancreatic macrophages accumulated in the pancreas of APN-KO mice but not in WT mice. Overexpression of the mRNAs of transforming growth factor-β1, CD68, and monocyte chemoattractant protein-1 was noted in APN-KO mice but not in WT mice. The gene expression level of collagen1 (α1) tended to be higher in APN-KO mice than in WT mice, albeit insignificantly.

Conclusions

Adiponectin deficiency enhanced the severity of cerulein-induced chronic pancreatitis in mice. Hypoadiponectinemia could enhance the severity of chronic pancreatitis.     

Rapid detection of trisomy 21 by gene dosage analysis using quantitative real-time polymerase chain reaction

AIM: Rapid detection of fetal aneuploidy helps inform a mother's choice about the course of her pregnancy. Obtaining results by fluorescent in situ hybridization (FISH) requires more than 24 h, and thus a more rapid method is needed. METHODS: Conventional G-banding and FISH for chromosome 21 were performed for cultured amniocytes. Genomic DNA was extracted from uncultured amniocytes obtained from 23 patients. TaqMan polymerase chain reaction (PCR) primers were designed to amplify the potassium voltage gated channel gene on chromosome 21q22.12 and the ribosomal phosphoprotein gene on 18q21.1. Quantitative real-time PCR was performed for these two gene fragments and the differences of the threshold cycle (Ct) of the two genes (Ct 18-Ct 21) were calculated for each sample. RESULTS: G-banding revealed that 19 patients had a normal karyotype and four had trisomy 21. FISH resulted in one case of a false positive. The Delta Ct values (Ct 18-Ct 21) of trisomy 21 patients were significantly higher than the values of individuals with normal karyotypes (P < 0.001) and there was no overlapping. CONCLUSIONS: Fetal trisomy 21 is rapidly detectable by gene dosage analysis from amniocytes using quantitative real-time PCR.