Mouse models of aggression have traditionally compared strains, most notably BALB/cJ and c57BL/6. However, these strains were not designed to study aggression despite differences in aggression-related traits and disti...
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Mouse models of aggression have traditionally compared strains, most notably BALB/cJ and c57BL/6. However, these strains were not designed to study aggression despite differences in aggression-related traits and distinct reactivity to stress. This study evaluated expression of genes differentially regulated in a stress (behavioral) mouse model of aggression with those from a recent genetic mouse model aggression. The study used a discovery-replication design using two independent mRNA studies from mouse brain tissue. The discovery study identified strain (BALB/cJ and c57BL/6J) x stress (chronic mild stress or control) interactions. Probe sets differentially regulated in the discovery set were intersected with those uncovered in the replication study, which evaluated differences between high and low aggressive animals from three strains specifically bred to study aggression. Network analysis was conducted on overlapping genes uncovered across both studies. A significant overlap was found with the genetic mouse study sharing 1,916 probe sets with the stress model. Fifty-one probe sets were found to be strongly dysregulated across both studies mapping to 50 known genes. Network analysis revealed two plausible pathways including one centered on the UBc gene hub which encodes ubiquitin, a protein well-known for protein degradation, and another on P38 MAPK. Findings from this study support the stress model of aggression, which showed remarkable molecular overlap with a genetic model. The study uncovered a set of candidate genes including the Erg2 gene, which has previously been implicated in different psychopathologies. The gene networks uncovered points at a Redox pathway as potentially being implicated in aggressive related behaviors. (c) 2016 Wiley Periodicals, Inc.
community-acquired pneumonia is caused by intra- and extracellular bacteria, with some of these bacteria also being linked to the pathogenesis of chronic lung diseases, including asthma and chronic obstructive pulmona...
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community-acquired pneumonia is caused by intra- and extracellular bacteria, with some of these bacteria also being linked to the pathogenesis of chronic lung diseases, including asthma and chronic obstructive pulmonary disease. chlamydiapneumoniae is an obligate intracellular pathogen that is highly sensitive to micro-environmental conditions controlling both pathogen growth and host immune responses. The availability of nutrients, as well as changes in oxygen, pH and interferon- levels, have been shown to directly influence the chlamydial life cycle and clearance. Although the lung has been traditionally regarded as a sterile environment, sequencing approaches have enabled the identification of a large number of bacteria in healthy and diseased lungs. The influence of the lung microbiota on respiratory infections has not been extensively studied so far and data on chlamydial infections are currently unavailable. In the present study, we speculate on how lung microbiota might interfere with acute and chronic infections by focusing exemplarily on the obligate intracellular ***. Furthermore, we consider changes in the gut microbiota as an additional player in the control of lung infections, especially in view the increasing evidence suggesting the involvement of the gut microbiota in various immunological processes throughout the human body.
AIM To assess the etiology of chronic liver diseases(cLD) from 1998 to 2014 at the outpatient clinic of Gastroenterology of the main hospital in Northwest of Italy among those dedicated to *** A random sample of chart...
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AIM To assess the etiology of chronic liver diseases(cLD) from 1998 to 2014 at the outpatient clinic of Gastroenterology of the main hospital in Northwest of Italy among those dedicated to *** A random sample of charts of patients referred to for increased liver enzymes between January 1998 and December 2006, and between January 2012 and December 2014 were reviewed. Etiology search included testing for hepatitis B virus(HBV), hepatitis c virus(HcV), autoimmune hepatitis, primary biliary cirrhosis, Wilson's disease and hereditary hemocromatosis. A risky alcohol consumption was also considered. Nonalcoholic fatty liver disease(NAFLD) was diagnosed in patients with histological and/or ultrasound evidence of steatosis/steatohepatitis, and without other causes of *** The number of patients included was 1163. Of them, 528(45%) had positivity for HcV and 85(7%) for HBV. Among the virus-free patients, 417(36%) had metabolic disorders whereas the remaining had history of alcohol abuse, less prevalent causes of cLD or concomitant conditions. In comparison to 1998-2000(41%), a reduction of HcV alone-related cases was detected during the periods 2001-2003(35%, OR = 0.75, 95%cI: 0.53-1.06), 2004-2006(33%, OR = 0.70, 95%cI: 0.50-0.97) and 2012-2014(31%, OR = 0.64, 95%cI: 0.46-0.91). On the contrary, in comparison to 1998-2000(31%), metabolic-alone disorders increased in the period 2004-2006(39%, OR = 1.37, 95%cI: 0.99-1.91) and 2012-2014(41%, OR = 1.53, 95%cI: 1.09-2.16). The other etiologies remained stable. The increase of incidence of metabolic-alone etiology during the period 2004-2006 and 2012-2014 tended to be higher in older patients(≥ 50 years) compared to younger(P = 0.058).cONcLUSION In the Northwest of Italy, during this study period, the prevalence of HcV infection decreased notably whereas that of NAFLD increased.
AIM:To evaluate the clinical significance of cystatin c and renal resistive index for the determination of renal function in patients with liver ***:We conducted a study of 63 patients with liver cirrhosis.A control g...
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AIM:To evaluate the clinical significance of cystatin c and renal resistive index for the determination of renal function in patients with liver ***:We conducted a study of 63 patients with liver cirrhosis.A control group comprised of 30 age and gender-matched healthy *** cystatin c was determined in all study subjects and renal Doppler ultrasonography was *** glomerular filtration rate from serum creatinine(GFRcr)and cystatin c(GFRcys)was ***:We confirmed significant differences in val-ues of cystatin c between patients with different stages of liver cirrhosis according to child-Pugh(P=0.01),and a significant correlation with model of end stage liver disease(MELD)score(rs=0.527,P<0.001).More patients with decreased glomerular filtration rate were identified based on GFRcys than on GFRcr(P<0.001).Significantly higher renal resistive index was noted in child-Pugh c than in A(P<0.001)and B stage(P=0.001).Also,a significant correlation between renal resistive index and MELD score was observed(rs=0.607,P<0.001).Renal resistive index correlated significantly with cystatin c(rs=0.283,P=0.028)and showed a negative correlation with GFRcys(rs=-0.31,P=0.016).cONcLUSION:cystatin c may be a more reliable marker for assessment of liver ***,cystatin c and renal resistive index represent sensitive indicators of renal dysfunction in patients with liver cirrhosis.
Metazoan introns contain a polypyrimidine tract immediately upstream of the AG dinucleotide that defines the 3 splice site. In the nematode caenorhabditis elegans, 3 splice sites are characterized by a highly conserve...
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Metazoan introns contain a polypyrimidine tract immediately upstream of the AG dinucleotide that defines the 3 splice site. In the nematode caenorhabditis elegans, 3 splice sites are characterized by a highly conserved UUUUcAG/R octamer motif. While the conservation of pyrimidines in this motif is strongly suggestive of their importance in pre-mRNA splicing, in vivo evidence in support of this is lacking. In an N-ethyl-N-nitrosourea (ENU) mutagenesis screen in caenorhabditis elegans, we have isolated a strain containing a point mutation in the octamer motif of a 3 splice site in the daf-12 gene. This mutation, a single base T-to-G transversion at the -5 position relative to the splice site, causes a strong daf-12 loss-of-function phenotype by abrogating splicing. The resulting transcript is predicted to encode a truncated DAF-12 protein generated by translation into the retained intron, which contains an in-frame stop codon. Other than the perfectly conserved AG dinucleotide at the site of splicing, G at the -5 position of the octamer motif is the most uncommon base in c. elegans 3 splice sites, occurring at closely paired sites where the better match to the splicing consensus is a few bases downstream. Our results highlight both the biological importance of the highly conserved -5 uridine residue in the c. elegans 3 splice site octamer motif as well as the utility of using ENU as a mutagen to study the function of polypyrimidine tracts and other AU- or AT-rich motifs in vivo.
In response to stressful conditions, eukaryoticcells launch an arsenal of regulatory programs to protect the proteome. One major protective response involves the arrest of protein translation and the formation of str...
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In response to stressful conditions, eukaryoticcells launch an arsenal of regulatory programs to protect the proteome. One major protective response involves the arrest of protein translation and the formation of stress granules, cytoplasmic ribonucleoprotein complexes containing the conserved RNA-binding proteins TIA-1 and TIAR. The stress granule response is thought to preserve mRNA for translation when conditions improve. For cells of the germlinethe immortal cell lineage required for sexual reproductionprotection from stress is critically important for perpetuation of the species, yet how stress granule regulatory mechanisms are deployed in animal reproduction is incompletely understood. Here, we show that the stress granule protein TIAR-1 protects the caenorhabditis elegans germline from the adverse effects of heat shock. Animals containing strong loss-of-function mutations in tiar-1 exhibit significantly reduced fertility compared to the wild type following heat shock. Analysis of a heat-shock protein promoter indicates that tiar-1 mutants display an impaired heat-shock response. We observed that TIAR-1 was associated with granules in the gonad core and oocytes during several stressful conditions. Both gonad core and oocyte granules are dynamic structures that depend on translation;protein synthesis inhibitors altered their formation. Nonetheless, tiar-1 was required for the formation of gonad core granules only. Interestingly, the gonad core granules did not seem to be needed for the germ cells to develop viable embryos after heat shock. This suggests that TIAR-1 is able to protect the germline from heat stress independently of these structures.
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