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Waste management in winery and distillery industries faces numerous disposal challenges as large volumes of both liquid and solid waste by-products are generated yearly during cellar practices. Composting has been suggested as a feasible option to beneficiate solid organic waste. This incentivized the quest for efficient composting protocols to be put in place. The objective of this study was to experiment with different composting strategies for spent winery solid waste. Compost materials consisting of chopped pruning grape stalks, skins, seed and spent wine filter material consisting of a mixture of organic and inorganic expend ingredients were mixed in compost heaps. The filter material component varied (in percentage) among five treatments: T1 (40%) lined, T2 (20%) lined, T3 (0%) lined, T4 (40%) ground material, lined and T5 (40%) unlined. Composting was allowed to proceed under open field conditions over 12months, from autumn to summer. Indicators such as temperature, moisture, enzyme activities, microbial counts, pH, and C/N ratio, were recorded. Generally, season (df=3, 16, P<0.05) had significant effects (df=1, 3, P<0.05) on heap temperature and moisture in all treatments. Similarly, microorganisms (actinobacteria and heterotrophs) varied significantly in all treatments in response to seasonal change (df=3, 16; P<0.05). Enzyme activities fluctuated in accordance with seasonal factors and compost maturity stages, with phosphatases, esterases, amino-peptidases, proteases and glycosyl-hydrolases being most prominent. Compared to treatments T2 and T3, compost treatments with higher percentage waste filter materials (T1, T4 and T5) had higher N (16,100-21,300mg/kg), P (1500-2300mg/kg), K (19,800-28,200mg/kg), neutral pH, and lower C/N ratios (13:1-10:1), which were also comparable with commercially produced composts. Filter materials therefore, appears to be a vital ingredient for composting of winery solid waste.

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BACKGROUND: Clinicians involved in medical errors can experience significant distress. This study aims to examine (1) how medical errors impact anaesthesiologists in key work and life domains; (2) anaesthesiologists' attitudes regarding support after errors; (3) and which anaesthesiologists are most affected by errors. METHODS: This study is a mailed cross-sectional survey completed by 281 of the 542 clinically active anaesthesiologists (52% response rate) working at Switzerland's five university hospitals between July 2012 and April 2013. RESULTS: Respondents reported that errors had negatively affected anxiety about future errors (51%), confidence in their ability as a doctor (45%), ability to sleep (36%), job satisfaction (32%), and professional reputation (9%). Respondents' lives were more likely to be affected as error severity increased. Ninety per cent of respondents disagreed that hospitals adequately support them in coping with the stress associated with medical errors. Nearly all of the respondents (92%) reported being interested in psychological counselling after a serious error, but many identified barriers to seeking counselling. However, there were significant differences between departments regarding error-related stress levels and attitudes about error-related support. Respondents were more likely to experience certain distress if they were female, older, had previously been involved in a serious error, and were dissatisfied with their last error disclosure. CONCLUSION: Medical errors, even minor errors and near misses, can have a serious effect on clinicians. Health-care organisations need to do more to support clinicians in coping with the stress associated with medical errors.

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Transformation of follicular lymphoma (FL) into aggressive disease and relapse of de novo diffuse large B cell lymphoma (DLBCL) are considered highly unfavourable events. However, most published data were acquired when rituximab was not routinely used. We retrospectively analysed 50 patients with transformed FL (tFL) in a multicenter study and compared them to 50 individuals with relapsed DLBCL (rDLBCL) who all obtained rituximab for the treatment of their disease. Our goal was to identify factors that predict a more favourable prognosis. After a median follow-up of 5.4 years from diagnosis, there was no significant difference in median overall survival (OS) from the date of transformation (tFL) or date of the first relapse (rDLBCL) (1.9 versus 3.9 years, P = .542). Of note, 5-year OS of patients with tFL was 46 %. Follicular lymphoma patients, treatment naïve prior to transformation, fared significantly better than pretreated patients (median not reached versus 1.4 years, P = .014). Regarding rDLBCL, female gender (13.9 versus 1.8 years, P = .019) and absence of rituximab prior to the first relapse (14.0 versus 1.8 years, P = .035) were favourable prognostic factors in a uni- and multivariate analysis. Only a proportion of patients received high-dose chemotherapy with autologous stem cell transplantation (HDT-ASCT), i.e. 38 and 52 % of patients with tFL and rDLBCL, respectively. Our data indicate that a favourable prognosis is conferred by treatment naivety in tFL and by rituximab naivety in rDLBCL. In contrast, we did not find a prognostic impact of HDT-ASCT in our series.

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BACKGROUND: Marginal zone lymphoma (MZL) is a non-Hodgkin lymphoma that occurs as extra nodal, nodal, or splenic. While MZL is generally considered an indolent disease, a substantial percentage of patients follow an unfavorable course. The objective of this retrospective analysis was to identify predictors for a reduced overall survival (OS), or conversely an increased OS. PATIENTS AND METHODS: One hundred and ninety-seven MZL patients were analyzed. Apart from assessing previously published risk factors, concomitant morbidity at diagnosis, transformation into aggressive lymphoma, and occurrence of additional malignancies were evaluated. RESULTS: Next to the known risk factors, i.e. above 60 years of age and elevated serum lactate dehydrogenase (LDH), we demonstrate that transformation into aggressive lymphoma, as well as additional malignancies, are important independent risk factors for a shortened OS in a multivariate analysis, irrespective of the MZL localization. Impressively, in the group of patients lacking LDH elevation, transformation, and/or additional malignancies, only 1 of 63 patients died during follow-up compared with 37 of 87 patients in the high-risk group (HR = 22.8; 95% confidence interval 3.1-167.0; P = 0.002). CONCLUSIONS: Our analysis proposes novel risk factors and warrants for a continuous follow-up to detect the occurrence of transformation and additional malignancies early on.

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Environmentally induced epigenetic alterations are related to mental health. We investigated quantitative DNA methylation status before and after an acute psychosocial stressor in two stress-related genes: oxytocin receptor (OXTR) and brain-derived neurotrophic factor (BDNF ). The cross sectional study took place at the Division of Theoretical and Clinical Psychobiology, University of Trier, Germany and was conducted from February to August 2009. We included 83 participants aged 61-67 years. Thereof, 76 participants completed the full study procedure consisting of blood sampling before (pre-stress), 10 min after (post-stress) and 90 min after (follow-up) the Trier social stress test. We assessed quantitative DNA methylation of whole-blood cells using Sequenom EpiTYPER. Methylation status differed between sampling times in one target sequence of OXTR (P<0.001): methylation increased from pre- to post-stress (P=0.009) and decreased from post-stress to follow-up (P<0.001). This decrease was also found in a second target sequence of OXTR (P=0.034), where it lost statistical significance when blood cell count was statistically controlled. We did not detect any time-associated differences in methylation status of the examined BDNF region. The results suggest a dynamic regulation of DNA methylation in OXTR-which may in part reflect changes in blood cell composition-but not BDNF after acute psychosocial stress. This may enhance the understanding of how psychosocial events alter DNA methylation and could provide new insights into the etiology of mental disorders.

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OBJECTIVE: To investigate whether negative mood and unbalanced nutrition style (fat rich/carbohydrate low) synergistically trigger binge eating in overweight and obese binge eating disorder (BED) patients. METHODS: Subsequently to following an unbalanced or a balanced nutrition plan for three days, participants' food intake in a taste test was measured. During the taste test, participants were either in a negative or a neutral mood that was induced through a guided imagery task. PARTICIPANTS: Sixty-nine overweight and obese women with BED (mean age: 36.7 years, mean body mass index: 32.8 kg/m2). MEASUREMENTS: Eating behavior was assessed by measuring the amount of eaten food during the taste test. Visual analog scales were used to assess negative affect, tension, urge to eat, and hunger before and after the mood induction and after the taste test. RESULTS: Negative mood and unbalanced nutrition had neither a combined synergistic effect nor separate additive effects on the amount of food intake. Negative affect and tension decreased after the taste test in the negative mood group. CONCLUSIONS: Negative mood does not invariably enhance the risk of binge-eating behavior. Fat-rich, carbohydrate-low nutrition style did not influence food intake during a taste test. This finding questions the role of this specific nutrition style as a crucial factor in promoting binge eating. If replicated, these findings are important, since they could guide development of treatment protocols.

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The cerebellum maintains balance and orientation, refines motor action, stores motor memories, and contributes to the timing aspects of cognition. We generated two mouse lines for making Cre recombinase-mediated gene disruptions largely confined to adult cerebellar granule cells. For this purpose we chose the GABA(A) receptor alpha6 subunit gene, whose expression marks this cell type. Here we describe mouse lines expressing Cre recombinase generated by 1) Cre knocked into the native alpha6 subunit gene by homologous recombination in embryonic stem cells; and 2) Cre recombined into an alpha6 subunit gene carried on a bacterial artificial chromosome (BAC) genomic clone. The fidelity of Cre expression was tested by crossing the mouse lines with the ROSA26 reporter mice. The particular alpha6BAC clone we identified will be valuable for delivering other gene products to cerebellar granule cells.

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Although there is growing concern that amphibian populations are declining globally, much of the supporting evidence is either anecdotal or derived from short-term studies at small geographical scales. This raises questions not only about the difficulty of detecting temporal trends in populations which are notoriously variable, but also about the validity of inferring global trends from local or regional studies. Here we use data from 936 populations to assess large-scale temporal and spatial variations in amphibian population trends. On a global scale, our results indicate relatively rapid declines from the late 1950s/early 1960s to the late 1960s, followed by a reduced rate of decline to the present. Amphibian population trends during the 1960s were negative in western Europe (including the United Kingdom) and North America, but only the latter populations showed declines from the 1970s to the late 1990s. These results suggest that while large-scale trends show considerable geographical and temporal variability, amphibian populations are in fact declining--and that this decline has been happening for several decades.

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Amphibians are in decline in many parts of the world. Long tme-series of amphibian populations are necessary to distinguish declines from the often strong fluctuations observed in natural populations. Time-series may also help to understand the causes of these declines. We analysed 23-28-year long time-series of the frog Rana temporaria. Only one of the three studied populations showed a negative trend which was probably caused by the introduction of fish. Two populations appeared to be density regulated. Rainfall had no obvious effect on the population fluctuations. Whereas long-term studies of amphibian populations are valuable to document population declines, most are too short to reveal those factors that govern population dynamics or cause amphibian populations to decline.

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WAF1/Cip1/Sdi1 (p21) is the prototype of a family of proteins that inhibit cyclin-dependent kinases and regulate cell cycle progression in eukaryotic cells. In addition to normal cell cycle progression, p21 is involved in growth suppression mediated by p53 and transforming growth factor beta (TGFbeta), differentiation, and apoptosis. To gain insight into the possible involvement of p21 in liver cell growth, the expression and regulation of the p21 gene was evaluated in rodent models of liver regeneration and specimens of human liver diseases. Little p21 mRNA was detected in normal liver tissue. After growth stimulation in vivo by 70% partial hepatectomy (PH), the p21 transcript was upregulated in a biphasic manner, with enhanced expression during G1 phase and following S phase. The induction of p21 after PH was regulated primarily at the post-transcriptional level and was due to enhanced mRNA stability. Inhibition of protein synthesis with cycloheximide rapidly induced p21 expression, primarily by post-transcriptional stabilization of the transcript. Hepatic p21 mRNA was also induced by dietary protein deprivation in normal mice. Expression of the p21 gene after PH was similar in p53-deficient (p53 -/-) and wild-type mice, but was p53-dependent following protein deprivation. Primary hepatocytes in culture demonstrated increased p21 expression after treatment with hepatocyte growth factor, TGFbeta, and activin A. p21 mRNA was upregulated in human liver diseases, suggesting a possible role in hepatic growth regulation in pathologic states. The present study demonstrates that p21 is regulated by p53-dependent and -independent pathways in the liver, and is influenced by both mitogenic and growth inhibitory stimuli.

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Phospholipases A2 (PLA2) form an extended class of enzymes that play an important role in signal transduction. Phospholipase A2-like (PLA2L) belongs to the secreted forms of phospholipases A2, but constitutes a new subgroup. We have assigned the gene for this enzyme to human chromosome 8q24-qter using fluorescence in situ hybridization and radiation hybrid mapping techniques.

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The effect of metabolizable (D-glucose, D-fructose) and nonmetabolizable (2-deoxy-D-glucose, L-glucose) monosaccharides on the membrane potential (Vm) of mouse hepatocytes was investigated employing a superfused liver slice technique. D-Cellobiose was used as an osmotic control. All monosaccharides tested hyperpolarized the liver cell membrane. The short-term effects of D-glucose, D-fructose and 2-deoxy-D-glucose were similar, whereas the effect of L-glucose was less pronounced. The K+ channel blocker quinine reversed the effects of glucose and 2-deoxy-D-glucose on the Vm, suggesting that opening of K+ channels is involved in the hyperpolarizing effect of monosaccharides. The bearing of these findings with regard to hepatic control of food intake is discussed. The findings argue against a role of hepatocytes as glucoreceptors sensing glucose metabolism.

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To further characterize the suppression of feeding that normally accompanies water deprivation and to test whether vasopressin contributes to this hypophagia, food intake, meal patterns and plasma vasopressin concentrations were measured during 24 h or 72 h of water deprivation in pygmy goats. The effects of exogenous vasopressin and of a V1-receptor antagonist on feeding during water deprivation were also assessed. The hypophagia during water deprivation was primarily due to decreases in meal size. The plasma vasopressin concentration increased about 2.5-fold and 10-fold after 24 and 72 h of water deprivation, respectively. Plasma osmolality also increased (measured only after 72 h of water deprivation). Intraperitoneally (ip) injected vasopressin (1.5 micrograms/kg b. wt.) that previously reduced food intake in goats with ad lib, access to water (Meyer et al., 1989), failed to affect cumulative food intake in water deprived goats, but led to a transient increase in meal size. The V1-receptor antagonist (2.5 micrograms/kg b. wt., ip) did not affect cumulative food intake or meal patterns either. These findings indicate that endogenous vasopressin is not crucially involved in the hypophagia during water deprivation. The results are in line with the hypothesis that an abnormal prandial increase in the osmolality of the ruminal fluid is a major contributor to the hypophagia during water deprivation.

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The effect of arginine vasopressin (VP) on cumulative food intake and meal pattern was tested in pygmy goats. VP injected intraperitoneally (I.P.) (0.75, 1.5 and 3.0 micrograms kg-1 body weight) appeared to reduce food intake in a dose-dependent manner by reducing the size of the first meal and by increasing the first intermeal interval (IMI). The hypophagic effect of VP was reversed by both a V1-receptor antagonist and an alpha-adrenergic antagonist. Exogenous VP (0.75 and 1.5 microgram kg-1 body weight I.P.) produced increases in plasma VP concentration which also may occur in stressful situations. VP might therefore be related to stress-induced anorexia.

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Case report of a woman who at the age of 26 underwent mammary reduction (strmbeck) for macromastia. A primary bilateral non-synchronous carcinoma of the breast was discovered 20 months and 5 years after the plastic surgery. On pathological examination lymph node metastases were not found in both instances. There was a positive family history of the occurrence of carcinoma. Mammography prior to mammary reduction is recommended.

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