Comparison of yolk fatty acid content, blood and egg cholesterol of hens fed diets containing palm olein oil and kilka fish oil

The purpose of this study was to compare the effects of dietary palm olein oil (POO) and Kilka fish oil (KFO) on yolk fatty acid content, ratio of fatty acids (FAs), antibody titre, and blood and yolk cholesterol of laying hens. One hundred White Hy-Line 26-wk-old (W-36) hens were allotted to 6 dietary treatments containing 0, 1.5, 3 and 4.5% POO or 2 and 4% KFO. The FAs and cholesterol content of yolk were measured at the end of three consecutive days of each period. Results reveal that the oleic acid increased and palmitic acid decreased (P<0.05) when hens were fed diets containing POO. The KFO diets reduced the blood cholesterol, yolk linoleic acid and yolk ω-6 FA (P<0.05), whereas the blood cholesterol increased by the supplementation of POO to dietary treatments. The yolk long chain polyunsaturated ω-3 FAs [Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] increased as KFO was increased in diets (P<0.001). The diets supplementation of KFO and POO thus, showed a decrease and an increase in the ratio of ω-6/ ω-3 FAs (P<0.05), respectively. It is concluded that supplementation of KFO to the dietary treatment may improve deposition of ω-3 FAs; however, the POO supplementation may improve deposition of ω-9 FAs without alteration of yolk cholesterol.Key words: Palm olein oil (POO), Kilka fish oil (KFO), hens, egg omega-9 and omega-3 fatty acid

B3GALNT2 mutations associated with non-syndromic autosomal recessive intellectual disability reveal a lack of genotype-phenotype associations in the muscular dystrophy-dystroglycanopathies.

BACKGROUND: The phenotypic severity of congenital muscular dystrophy-dystroglycanopathy (MDDG) syndromes associated with aberrant glycosylation of α-dystroglycan ranges from the severe Walker-Warburg syndrome or muscle-eye-brain disease to mild, late-onset, isolated limb-girdle muscular dystrophy without neural involvement. However, muscular dystrophy is invariably found across the spectrum of MDDG patients. METHODS: Using linkage mapping and whole-exome sequencing in two families with an unexplained neurodevelopmental disorder, we have identified homozygous and compound heterozygous mutations in B3GALNT2. RESULTS: The first family comprises two brothers of Dutch non-consanguineous parents presenting with mild ID and behavioral problems. Immunohistochemical analysis of muscle biopsy revealed no significant aberrations, in line with the absence of a muscular phenotype in the affected siblings. The second family includes five affected individuals from an Iranian consanguineous kindred with mild-to-moderate intellectual disability (ID) and epilepsy without any notable neuroimaging, muscle, or eye abnormalities. Complementation assays of the compound heterozygous mutations identified in the two brothers had a comparable effect on the O-glycosylation of α-dystroglycan as previously reported mutations that are associated with severe muscular phenotypes. CONCLUSIONS: In conclusion, we show that mutations in B3GALNT2 can give rise to a novel MDDG syndrome presentation, characterized by ID associated variably with seizure, but without any apparent muscular involvement. Importantly, B3GALNT2 activity does not fully correlate with the severity of the phenotype as assessed by the complementation assay

A cyclin-binding motif in human papillomavirus type 18 (HPV18) E1^E4 is necessary for association with CDK–cyclin complexes and G2/M cell cycle arrest of keratinocytes, but is not required for differentiation-dependent viral genome amplification or L1 capsid protein expression

Investigation into the effects the HPV E4 protein has in viral life cycleThe G2/M arrest function of human papillomavirus (HPV) E4 proteins is hypothesized to be necessary for viral genome amplification. Full-length HPV18 E1^E4 protein is essential for efficient viral genome amplification. Here we identify key determinants within a CDK-bipartite consensus recognition motif in HPV18 E1^E4 that are critical for association with active CDK–cyclin complexes and in vitro phosphorylation at the predicted CDK phosphorylation site (threonine 23). The optimal cyclin-binding sequence (43RRLL46) within this E4 motif is required for G2/M arrest of primary keratinocytes and correlates with cytoplasmic retention of cyclin B1, but not cyclin A. Disruption of this motif in the E4 ORF of HPV18 genomes, and the subsequent generation of stable cell lines in primary keratinocytes revealed that this motif was not essential for viral genome amplification or L1 capsid protein induction. We conclude that the HPV18 E4 G2/M arrest function does not play a role in early vegetative events

Diagnostic Accuracy of Age and Alarm Symptoms for Upper GI Malignancy in Patients with Dyspepsia in a GI Clinic: A 7-Year Cross-Sectional Study

<div><h3>Objectives</h3><p>We investigated whether using demographic characteristics and alarm symptoms can accurately predict cancer in patients with dyspepsia in Iran, where upper GI cancers and <em>H. pylori</em> infection are common.</p> <h3>Methods</h3><p>All consecutive patients referred to a tertiary gastroenterology clinic in Tehran, Iran, from 2002 to 2009 were invited to participate in this study. Each patient completed a standard questionnaire and underwent upper gastrointestinal endoscopy. Alarm symptoms included in the questionnaire were weight loss, dysphagia, GI bleeding, and persistent vomiting. We used logistic regression models to estimate the diagnostic value of each variable in combination with other ones, and to develop a risk-prediction model.</p> <h3>Results</h3><p>A total of 2,847 patients with dyspepsia participated in this study, of whom 87 (3.1%) had upper GI malignancy. Patients reporting at least one of the alarm symptoms constituted 66.7% of cancer patients compared to 38.9% in patients without cancer (p<0.001). Esophageal or gastric cancers in patients with dyspepsia was associated with older age, being male, and symptoms of weight loss and vomiting. Each single predictor had low sensitivity and specificity. Using a combination of age, alarm symptoms, and smoking, we built a risk-prediction model that distinguished between high-risk and low-risk individuals with an area under the ROC curve of 0.85 and acceptable calibration.</p> <h3>Conclusions</h3><p>None of the predictors demonstrated high diagnostic accuracy. While our risk-prediction model had reasonable accuracy, some cancer cases would have remained undiagnosed. Therefore, where available, low cost endoscopy may be preferable for dyspeptic older patient or those with history of weight loss.</p> </div

Investigation into the immuno-therapeutic potential of melanocortin peptides on activated chondrocytes

Melanocortin peptides are endogenously produced peptides originating from the posttranslational processing of the pro-opiomelanocortin hormone (POMC), exerting their effect by binding to class A G-protein-coupled 7 transmembrane domain receptors, positively coupled to adenylate cyclase. To date five melanocortin receptors have been identified and termed MC1 to MC5. MC1 and MC3 have previously been proposed to exert anti-inflammatory effects by modulating the host inflammatory response. The expression and the functional activity of both receptors was identified and confirmed in the C-20/A4 chondrocyte cell-line, isolated primary bovine and in situ bovine articular chondrocytes. Pro-inflammatory cytokines including IL-1β, IL-6, IL-8, TNF-α, produced by activated articular chondrocytes significantly up-regulate matrix metalloproteinases (MMPs) gene expression, and inhibit the chondrocyte’s compensatory synthesis pathways required to restore the integrity of the degraded extracellular matrix (ECM). Human C-20/A4 and primary bovine articular chondrocytes were found to produce CC and CXC chemokines, which induced the release of matrix degrading enzymes and activated cell apoptotic pathways. TNF-α significantly up-regulated the expression of pro-inflammatory cytokines and chemokines IL-1β, IL-6, IL-8, MCP-1 and MMP1 and 13 from C-20/A4 cell line and freshly isolated primary bovine articular chondrocytes. An effect attenuated in the presence of α-MSH and D[TRP]8-γ-MSH. The MC3/4 antagonist SHU9119 blocked the effects of D[TRP]8-γ-MSH but not α-MSH. TNF-α (60.0 pg/ml) stimulation caused ~30% cell death and was partially, but significantly inhibited by treatment of the cells with the melanocortin peptides. The antiinflammatory and chondroprotective effect of melanocortin peptides were then tested on in situ bovine articular chondrocytes, injured by a single blunt impact delivered by a drop tower. The mechanical injury caused significant cell death and up-regulation of the proinflammatory cytokines IL-6 and IL-8, which were significantly reduced on pre-treatment of cartilage explants with melanocortin peptides. Modulation of pro-inflammatory pathways and inflammation-modulated cartilage destruction with subsequent chondrocyte apoptosis appears to be logical development in the potential medical therapy of OA. The small molecular weight of melanocortin peptides should facilitate the absorption from the GI tract and the movement to the cartilage matrix, which together with creative drug delivery methods might potentially prove to be potent therapeutic agents in the future

A population-based survey of the epidemiology of symptom-defined gastroesophageal reflux disease: the Systematic Investigation of Gastrointestinal Diseases in China

<p>Abstract</p> <p>Background</p> <p>The epidemiology of gastroesophageal reflux disease (GERD) has yet to be investigated using the symptomatic threshold criteria recommended by the Montreal Definition. This study aimed to determine the prevalence of symptom-defined GERD across five regions of China, and to investigate variables associated with GERD.</p> <p>Methods</p> <p>A representative sample of 18 000 adults (aged 18-80 years) were selected equally from rural and urban areas in each region (n = 1800). According to the Montreal Definition, GERD is present when mild symptoms of heartburn and/or regurgitation occur on ≥2 days a week, or moderate-to-severe symptoms of heartburn and/or regurgitation occur on ≥1 day a week.</p> <p>Results</p> <p>In total, 16 091 participants completed the survey (response rate: 89.4%) and 16 078 responses were suitable for analysis. Applying the Montreal criteria, the prevalence of symptom-defined GERD was 3.1% and varied significantly (<it>p </it>< 0.001) among the five regions (from 1.7% in Guangzhou to 5.1% in Wuhan) and between rural and urban populations (3.8% vs 2.4%). Factors significantly associated with GERD included living in a rural area and a family history of gastrointestinal diseases.</p> <p>Conclusions</p> <p>This population-based survey found that the prevalence of symptom-defined GERD in China was 3.1%, which is lower than that found in Western countries.</p

Epidemiology of Gastroesophageal Reflux Disease in Asia: A Systematic Review

Ethnic and geographical differences are important factors in studying disease frequencies, because they may highlight the environmental or genetic influences in the etiology. We retrieved the studies which have been published regarding the epidemiologic features of gastroesophageal reflux disease (GERD) in Asia, based on the definitions of GERD, study settings, publication years and geographical regions. From the population-based studies, the prevalence of symptom-based GERD in Eastern Asia was found to be 2.5%-4.8% before 2005 and 5.2%-8.5% from 2005 to 2010. In Southeast and Western Asia, it was 6.3%-18.3% after 2005, which was much higher than those in Eastern Asia. There were robust epidemiologic data of endoscopic reflux esophagitis in medical check-up participants. The prevalence of endoscopic reflux esophagitis in Eastern Asia increased from 3.4%-5.0% before 2000, to 4.3%-15.7% after 2005. Although there were only limited studies, the prevalence of extra-esophageal syndromes in Asia was higher in GERD group than in controls. The prevalence of Barrett's esophagus was 0.06%-0.84% in the health check-up participants, whereas it was 0.31%-2.00% in the referral hospital settings. In summary, the prevalence of symptom-based GERD and endoscopic reflux esophagitis has increased in Asian countries. However, the prevalence of Barrett's esophagus in Asia has not changed and also still rare

Exploring UK medical school differences: the MedDifs study of selection, teaching, student and F1 perceptions, postgraduate outcomes and fitness to practise

BACKGROUND: Medical schools differ, particularly in their teaching, but it is unclear whether such differences matter, although influential claims are often made. The Medical School Differences (MedDifs) study brings together a wide range of measures of UK medical schools, including postgraduate performance, fitness to practise issues, specialty choice, preparedness, satisfaction, teaching styles, entry criteria and institutional factors. METHOD: Aggregated data were collected for 50 measures across 29 UK medical schools. Data include institutional history (e.g. rate of production of hospital and GP specialists in the past), curricular influences (e.g. PBL schools, spend per student, staff-student ratio), selection measures (e.g. entry grades), teaching and assessment (e.g. traditional vs PBL, specialty teaching, self-regulated learning), student satisfaction, Foundation selection scores, Foundation satisfaction, postgraduate examination performance and fitness to practise (postgraduate progression, GMC sanctions). Six specialties (General Practice, Psychiatry, Anaesthetics, Obstetrics and Gynaecology, Internal Medicine, Surgery) were examined in more detail. RESULTS: Medical school differences are stable across time (median alpha = 0.835). The 50 measures were highly correlated, 395 (32.2%) of 1225 correlations being significant with p < 0.05, and 201 (16.4%) reached a Tukey-adjusted criterion of p < 0.0025. Problem-based learning (PBL) schools differ on many measures, including lower performance on postgraduate assessments. While these are in part explained by lower entry grades, a surprising finding is that schools such as PBL schools which reported greater student satisfaction with feedback also showed lower performance at postgraduate examinations. More medical school teaching of psychiatry, surgery and anaesthetics did not result in more specialist trainees. Schools that taught more general practice did have more graduates entering GP training, but those graduates performed less well in MRCGP examinations, the negative correlation resulting from numbers of GP trainees and exam outcomes being affected both by non-traditional teaching and by greater historical production of GPs. Postgraduate exam outcomes were also higher in schools with more self-regulated learning, but lower in larger medical schools. A path model for 29 measures found a complex causal nexus, most measures causing or being caused by other measures. Postgraduate exam performance was influenced by earlier attainment, at entry to Foundation and entry to medical school (the so-called academic backbone), and by self-regulated learning. Foundation measures of satisfaction, including preparedness, had no subsequent influence on outcomes. Fitness to practise issues were more frequent in schools producing more male graduates and more GPs. CONCLUSIONS: Medical schools differ in large numbers of ways that are causally interconnected. Differences between schools in postgraduate examination performance, training problems and GMC sanctions have important implications for the quality of patient care and patient safety