bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rural and Urban Primary Care Physician Professional Beliefs and Quality Improvement Behaviors
Authors: Kirchhoff Anne C. , Hart Gary , Campbell Eric G. 
Published: February 2014

AbstractPurposeWe evaluated whether primary care physicians (PCPs) from urban and rural practices differ on attitudes and behaviors related to quality improvement (QI) activities, patient relationships, and professionalism/self‐regulation.MethodsData from a national survey that assessed physician attitudes and behaviors based on the Physician Charter on Medical Professionalism were used. Of the 1,891 survey respondents, N = 840 were PCPs (n = 274 family medicine (response rate = 67.5%); n = 257 general internal medicine (60.8%); and n = 309 pediatricians (72.7%)). Using Rural‐Urban Commuting Area (RUCA) codes, PCPs were classified as urban and rural according to their practice ZIP code.FindingsA total of n = 691 physicians were urban and n = 127 rural. Attitudes regarding participating in QI did not differ by practice location; however, rural PCPs were more likely to have reviewed an other physician's records for QI than urban PCPs (65.6% vs 48.0%, P < .001). Rural physicians were more likely to agree that physicians should talk with their patients about the cost of care than urban PCPs (40.5% vs 29.2%, P = .02). While all PCPs endorsed attitudes regarding the importance of professional behaviors (eg, reporting impaired/incompetent colleagues, disclosing medical errors) at generally similar levels, their behaviors differed. More rural physicians had a personal knowledge of an impaired/incompetent physician than urban physicians (20.7% vs 12.7%, P = .02).ConclusionsPCPs from rural and urban areas share similar attitudes regarding the importance of participating in QI and fulfilling professional responsibilities. However, certain behaviors (eg, knowledge of impaired colleagues) do differ. These results should be confirmed in larger studies of rural PCPs.
Associations Between Premature Ejaculation, Lower Urinary Tract Symptoms, and Erectile Dysfunction in Middle-Aged Korean Policemen
Authors: Lee Jun Ho 
Published: February 2014

Abstract

Introduction
There is controversy concerning the relationship between premature ejaculation (PE) and erectile dysfunction (ED), as well as the scan data regarding the association between PE and lower urinary tract symptoms (LUTS).

Aims
We performed this study to evaluate the association between PE and ED or LUTS.

Methods
A total of 2,591 policemen aged 40–59 years who had participated in a health examination were included in this study. PE, LUTS, and ED were evaluated using the premature ejaculatory diagnostic tool (PEDT), the International Prostate Symptoms Score (IPSS), and the International Index of Erectile Function questionnaire-5 (IIEF), respectively. Spearman's correlation test, the multiple linear regression test, and logistic regression analyses were used to evaluate the relationship between PE and ED or LUTS.

Main Outcome Measures
Associations between PEDT, IPSS, and IIEF.

Results
The middle age of the study group was 49.1 years, and the middle PEDT, IIEF, and IPSS was 7.5, 17.0, and 10.7, respectively. By univariate analysis, PEDT showed a significant correlation with IPSS (r = 0.310, P &lt; 0.001) and IIEF (r = −0.413, P &lt; 0.001). After adjusting for age, components of metabolic syndrome, testosterone, and IIEF, PEDT was significantly correlated with IPSS (Beta = 0.166, P &lt; 0.001). PEDT was also significantly correlated with IIEF after adjusting for age, components of metabolic syndrome, testosterone, and IPSS (Beta = −0.274, P &lt; 0.001). Additionally, the severity of LUTS or ED was associated with the PE positive ratio (P trend &lt; 0.001). The odds ratio (OR) for PE also increased with the severity of LUTS or ED after adjusting for potential confounding factors.

Conclusions
ED and LUTS were significantly and independently correlated with PE.
Work productivity among treatment‐naïve patients with genotype 1 chronic hepatitis C infection receiving telaprevir combination treatment
Authors: Aggarwal J. , Vera‐Llonch M. , Donepudi M. , Suthoff E. , Younossi Z. , Goss T. F. 
Published: February 2014

SummaryWork productivity is impacted in hepatitis C virus (HCV)‐infected patients and has been linked to treatment. In two Phase 3 trials, ADVANCE and ILLUMINATE, treatment‐naïve genotype 1 chronic HCV‐infected patients received 12‐week telaprevir (T) with 24 (T12PR24)‐ or 48 (T12PR48)‐week peginterferon alfa‐2a/ribavirin. The objective of this analysis was to examine the impact of chronic HCV infection and its treatment with combination therapy on work productivity. The 5‐item, self‐reported work productivity questionnaire (WPQ) was administered in Phase 3 trials to assess unemployment status, days unable to work due to HCV/treatment, reduced hours worked and impact on productivity in prior 4 weeks. Descriptive statistics and multivariate regression analyses were employed in analyses of pooled trial data. About 1147 patients were included; 22% (n = 255) were unemployed at baseline, with 8% being unemployed due to health reasons. At week 12, there were no differences by treatment regimen in the number of days unable to work. At week 48, improvements were observed earlier among patients receiving the shorter duration of T combination treatment. Mean (95% CI) change from baseline in days unable to work was −0.48 (−0.85, −0.11) days for T12PR24, 1.43 (0.63, 2.24) days for T12PR48 and 1.24 (0.18, 2.30) days for PR48 with placebo. Predictors of days unable to work were identified and include demographic characteristics, pretreatment and on‐treatment levels of fatigue, as well regional variation. In post hoc analyses of the ADVANCE and ILLUMINATE trials, work productivity decreased during the initial 12 weeks regardless of treatment group.
Impact of nucleos(t)ide analogues on the estimated glomerular filtration rate in patients with chronic hepatitis B: a prospective cohort study in China
Authors: Qi X. , Wang J.‐Y , Mao R.‐C , Zhang J.‐M 
Published: February 2014

SummaryChronic hepatitis B therapy with nucleos(t)ide analogues, particularly tenofovir or adefovir, may affect renal function. To date, there has not been a head‐to‐head controlled study to assess estimated glomerular filtration rate (eGFR) fluctuations in nucleos(t)ide‐treated CHB patients. We aimed to evaluate the long‐term effects of nucleos(t)ide on eGFR in Chinese patients with chronic hepatitis B. This prospective cohort study included 275 patients. Patient subgroups included those treated with lamivudine (n = 50), adefovir (n = 60), telbivudine (n = 68) and entecavir (n = 61); untreated patients (n = 36) served as control. After an average follow‐up duration of 23 months, eGFR calculated by Cockcroft–Gault and Modification of Diet in Renal Disease formulas increased by 18.35 mL/min and 19.34 mL/min (P < 0.0001) in the telbivudine group, respectively, and decreased by 10.95 mL/min and 12.17 mL/min (P = 0.0001) in the adefovir group, respectively. Even if renal function was normal or mildly impaired at baseline, eGFR increased significantly more in the telbivudine group than in the other groups (P < 0.001). More patients in the adefovir group (23%) had a ≥20% decrease in eGFR than the other groups (P < 0.0001). More patients in the telbivudine group (31%) had a ≥20% increase in eGFR than the other groups (P < 0.0001). In conclusion, prolonged telbivudine therapy resulted in improved eGFR, while adefovir therapy was associated with decreased eGFR. Lamivudine and entecavir therapy did not significantly influence eGFR.
Atlantic rain forest recovery: successional drivers of floristic and structural patterns of secondary forest in Southern Brazil
Authors: Zanini K. J. , Bergamin R. S. , Machado R. E. , Pillar V. D. , Müller S. C. 
Published: February 2014

AbstractQuestionsThe growing importance of secondary forests has stimulated research on the patterns of structure, biomass, species diversity and species composition of successional tropical forests. Despite current knowledge, the future of tropical forests and their ability to recover from human impacts are still a challenge for researchers. The Atlantic Forest is one of the most endangered ecosystems on Earth, yet has been reduced in size and distribution due to human disturbance such that most of the remaining fragments are secondary forest at different successional stages. How do these forests recover structure and species composition during succession? What are the main drivers of community assembly during succession?LocationSubtropical Atlantic rain forest, South Brazil (29°42′S, 50°11′W).MethodUsing four replicate chronosequences, we described floristic and structural successional patterns of subtropical Atlantic Forest in Brazil, and investigated causal relationships with environmental, spatial and temporal variables in structuring tree species composition. The chronosequences were described by four successional stages, according to floristic (species composition and richness) and structural (density, basal cover and height of trees) characteristics, tested using ANOVA with randomization tests. Time since abandonment and environmental conditions of topsoil, relief and spatial components were considered as possible successional drivers. Hypotheses about causal relationships in the successional process were tested using path analysis, considering the influence of those variables on the successional forest communities.ResultsWe found that forest stands of 26–45 yr old displayed structural characteristics similar to those of old‐growth stands, but that species composition of successional forest was somewhat different from reference areas (old‐growth forests). In our study, time since abandonment overcame the influence of environmental and spatial variables on forest assembly patterns in the chronosequences.ConclusionsOur study is the first one describing floristic and structural successional patterns of the Atlantic rain forest in a subtropical context and proposing causal relationships between recovery age, environment and community composition of secondary successional forests. We conclude that the dynamic of forest succession is autogenic and not entirely predictable from local environmental conditions of soil, space and relief.
Job Quality and Employment of Older People in Europe
Authors: Schnalzenberger Mario , Schneeweis Nicole , Winter‐Ebmer Rudolf , Zweimüller Martina 
Published: February 2014

AbstractWe study the relationship between job quality and retirement using data from the Survey of Health, Ageing and Retirement in Europe, a longitudinal survey covering individuals aged 50+ in several European countries. Although most previous studies looked at the impact of bad working conditions on retirement intentions, we can use the panel dimension to study actual retirement as well as other pathways out of a job. As indicators for job quality we use three different approaches: overall job satisfaction, over‐ and undereducation for a particular job as well as effort–reward imbalance, which measures the imbalance between a worker's effort and the rewards he or she receives in turn. The analysis gives some evidence that poor job quality decreases retirement age, in particular for women.
Characterisation of temporal microglia and astrocyte immune responses in bile duct‐ligated rat models of cirrhosis
Authors: Wright Gavin A. K. , Sharifi Yalda , Newman Tracy A. , Davies Nathan , Vairappan Balasubramaniyam , Perry Hugh V. , Jalan Rajiv 
Published: February 2014

AbstractBackground & AimsMicroglia and astrocyte related pro‐inflammatory responses are thought to underpin cerebral sequelae of acute liver failure. Conversely, despite background pro‐inflammatory responses in cirrhosis, overt brain swelling and coma associated with acute‐on‐chronic liver failure, is infrequent unless precipitated (e.g. sepsis). Moreover in other chronic neurodegenerative disorders and sepsis, the brain is protected from recurrent microbial insults by compensatory microglial‐associated immune responses. To characterise longitudinal cerebral immune responses in a bile duct‐ligated (BDL) rat model of cirrhosis.MethodRats underwent BDL or sham operation before sacrifice at either 1‐day, 1, 2 and 4 weeks post‐surgery. We analysed consciousness, brain water, biochemistry and immunohistochemistry to assess activation of microglia (ED‐1, OX6 and Iba‐1), astrocytes (Glial fibrillary acidic protein ‐ GFAP), cellular stress (Heat shock protein ‐ Hsp 25) and pro‐inflammatory mediator expression (inducible nitric oxide synthase (iNOS), interleukin‐1beta (IL‐1β) and tumour growth factor‐beta (TGF‐β)).ResultsBDL significantly increased ammonia and bilirubin (P < 0.01 respectively). The classical microglial markers OX6, ED1 and Iba‐1 and pro‐inflammatory IL‐1β and iNOS were not significantly increased. However, the alternative microglial marker and regulatory cytokine TGF‐β was elevated from day 1 to 4 weeks post‐BDL. GFAP expression was significantly increased in corpus callosum in all groups. In BDL rats, Hsp 25 was also increased in the corpus callosum, peaking at 2 weeks.ConclusionBDL triggers early alternative, but not classical, microglial activation. There was a correlation between astrocyte activation and cellular stress. These findings indicate early cerebral immune responses, which may be associated with immune tolerance to further challenge.
Reversible non‐ischaemic cardiomyopathy and left ventricular dysfunction after liver transplantation: a single‐centre experience
Authors: Yataco Maria L. , Difato Thomas , Bargehr Johannes , Rosser Barry G. , Patel Tushar , Trejo‐Gutierrez Jorge F. , Pungpapong Surakit , Taner C. Burcin , Aranda‐Michel Jaime 
Published: February 2014

AbstractBackground & AimsNon‐ischaemic cardiomyopathy (NIC) is an early complication of liver transplantation (LT). Our aims were to define the prevalence, associated clinical factors, and prognosis of this condition.MethodsA retrospective study was performed on patients undergoing LT at our institution from January 2005 to December 2012. Patients who developed NIC were identified. Data collected included demographic and clinical data.ResultsA total 1460 transplants were performed in this period and seventeen patients developed NIC. Pretransplant median QTc interval was 459 (range, 405–530), and median E/A ratio was 1 (range, 0.71–1.67). Fourteen patients (82%) were severely malnourished and required nutritional support. Thirteen patients (76%) had renal insufficiency. Median time to onset was 2 days post‐transplant (range, 0–20). Echocardiograms showed global left ventricular hypokinesis and a decrease in ejection fraction (EF) from a median of 65% (range, 50–81) pretransplant to a median of 21% (range, 15–32). Median raw model for end‐stage liver disease (MELD) score was 29 in patients with NIC vs. 18 in patients without cardiomyopathy (P = 0.01). There was no significant difference between recipients with NIC vs. recipients without cardiomyopathy regarding donor age, donor risk index, and cold and warm ischaemia time. Recovery of cardiac function occurred in 16 patients, with a median EF of 44% (range, 25–65%) at the time of discharge. The last echocardiogram available showed a median EF of 59% (range, 49–73%). One‐year survival of NIC patients was 94.1%.ConclusionNon‐ischaemic cardiomyopathy is a rare complication after LT. Patients with NIC are critically ill, with high MELD score, and severe malnutrition.
Prognostic factors of hepatic decompensation and hepatocellular carcinoma in patients with transfusion‐acquired HCV infection
Authors: Zavaglia Claudio , Silini Enrico , Mangia Alessandra , Airoldi Aldo , Piazzolla Valeria , Vangeli Marcello , Stigliano Rosa , Foschi Antonella , Mazzarelli Chiara , Tinelli Carmine 
Published: February 2014

AbstractAimsAim of this study was to assess if host (immunogenetic traits, age, sex), exogenous (alcohol) or viral factors (viral type, past HBV infection) might affect the progression of chronic hepatitis C to liver decompensation or the development of HCC in a cohort of patients exposed to a single blood transfusion prior to the introduction of anti‐HCV screening.MethodsTwo hundred and forty‐eight patients with a history of a single exposure to blood or blood products prior to 1990 were retrospectively considered. Patients were devoid of other risk factors of liver disease or immunosuppression and naïve to antiviral therapies. Eight baseline variables were assessed: age at transfusion, sex, HBV core antibody, immunogenetic profile (DRB1*11, DRB1*1104, DRB1*07), HCV genotype and alcohol consumption.ResultsThe follow‐up was 22 (SD: 11) years. Sixty‐eight patients (27%) progressed to hepatic decompensation over a median period of 22.5 years (IQR: 14–30) and 41 patients (16%) developed HCC over a median period of 31 years (IQR: 24–38). The cumulative incidence of liver failure was 0.4% (95% CI: 0.1–3.1), 4.9% (95% CI: 2.6–9.3) and 16.2% (95% CI: 10.4–24.7) at 10, 20 and 30 years after blood transfusion respectively. By univariate analysis, only age at transfusion was correlated with the risk of decompensation. Stratifying the age of transfusion by tertiles, the incidence of hepatic decompensation was 0.7% per year in patients transfused at ≤24 years of age as compared to 1.2% and 1.9% per year in those transfused at 25–35 and >36 years of age respectively (HR: 5.5, 95% CI: 2.78–10.7, P < 0.001). The risk of HCC development was correlated by univariate analysis with age at transfusion (as continuous variable, HR: 1.12, 95% CI: 1.08–1.16 per year of age, P < 0.001, >36 compared to ≤24 years, HR: 10.3, 95% CI: 3.9–26.9, P < 0.001) and male sex (HR: 4.2, 95% CI: 1.7–10, P = 0.001). Multivariate analysis confirmed age at transfusion and male sex as independent predictors of HCC development [HR: 1.12 per year (95% CI: 1.08–1.16), P < 0.001 and HR: 5.4 (95% CI: 2.2–13.2), P < 0.001 respectively].ConclusionsIn patients with transfusion‐acquired HCV infection, age at transfusion affects the risk for hepatic decompensation. Age at transfusion and male sex are independent risk factors for HCC development.
CHD5 a tumour suppressor is epigenetically silenced in hepatocellular carcinoma
Authors: Zhao Rui , Wang Nisha , Huang Haili , Ma Wenli , Yan Qitao 
Published: February 2014

AbstractBackgroundChromodomain helicase DNA binding protein 5 (CHD5) has recently been identified as a potent tumour suppressor by acting as a master regulator of a tumour‐suppressive network. Its inactivation resulted from aberrant methylation in the promoter occurs in several types of human malignancy and is associated with malignant tumour behaviour. In human hepatocellular carcinoma (HCC), CHD5 gene expression, methylation status and tumour‐suppressive function have not been elucidated.AimsIn this study, we focused on the epigenetic modification and tumour‐suppressive mechanism of CHD5 gene in HCC.MethodsCHD5 expression in nine HCC cell lines and 30 pairs of HCC specimens and adjacent non‐cancerous tissues were analysed by quantitative reverse transcription PCR and Western blotting. Methylation‐specific sequencing and methylation‐specific PCR were performed to examine DNA methylation status of the CHD5 promoter in HCC cell lines and samples. The effect of CHD5 restoration on proliferation, colony formation, senescence, apoptosis and tumourigenicity were examined.ResultsCHD5 expression was sinificantly down‐regulated in HCC cell lines and tissues examined, and the −841 to −470 region of CHD5 promoter was hypermethylated in these samples. Treatment with DNA methyltransferase inhibitor 5‐aza‐2‐deoxycytidine resulted in a striking regional demethylation of the −841 to −470 region of CHD5 promoter and an increase in CHD5 expression. The restoration of CHD5 expression inhibited tumour cell proliferation, colony formation and tumourigenicity and caused cellular senescence.ConclusionsOur findings demonstrate that CHD5 is a potential tumour suppressor gene epigenetically silenced in HCC.
Alpha‐1‐antitrypsin deficiency: from genoma to liver disease. PiZ mouse as model for the development of liver pathology in human
Authors: Giovannoni Isabella , Callea Francesco , Stefanelli Marta , Mariani Riccardo , Santorelli Filippo M. , Francalanci Paola 
Published: February 2014

AbstractBackground & AimsHomozygous individuals with alpha‐1‐antitrypsin deficiency (AATD) type PiZ have an increased risk of chronic liver disease and hepatocellular carcinoma (HCC). It is noteworthy that HCCs are composed by hepatocytes without accumulation of AAT, but the reason for this remains unclear. The aim of this study was to determine liver pathology in PiZ mice, focusing the attention on the distribution of AAT globules in normal liver, regenerative foci and neoplastic nodules.MethodsLiver of 79 PiZ mice and 18 wild type (Wt) was histologically analysed for steatosis, clear cell foci, hyperplasia and neoplasia. The expression of human‐AAT transgene and murine AAT, in non‐neoplastic liver and in hyperplastic/neoplastic nodules was tested by qPCR and qRT‐PCR. RT‐PCR was used to study expression of hepatic markers: albumin, α‐foetoprotein, transthyretin, AAT, glucose‐6‐phospate, tyrosine aminotransferase.ResultsLiver pathology was seen more frequently in PiZ (47/79) than in Wt (5/18) and its development was age related. In older PiZ mice (18–24 m), livers showed malignant tumours (HCC and angiosarcoma) (17/50), hyperplastic nodules (28/50), non‐specific changes (33/50), whereas only 9/50 were normal. Both human‐AATZ DNA and mRNA showed no differences between tumours/nodules and normal liver, while murine‐AAT mRNA was reduced in tumours/nodules.ConclusionAccumulation of AAT is associated with an increased risk of liver nodules. The presence of globule‐devoid hepatocytes and the reduced expression of murine‐AAT mRNA in hyperplastic and neoplastic nodules suggest that these hepatic lesions in AATD could originate from proliferating dedifferentiated cells, lacking AAT storage and becoming capable of AFP re‐expression.
Impact of lipid‐based nutrient supplements and corn–soy blend on energy and nutrient intake among moderately underweight 8–18‐month‐old children participating in a clinical trial
Authors: Thakwalakwa Chrissie M. , Ashorn Per , Phuka John C. , Cheung Yin Bun , Briend André , Maleta Kenneth M. 
Published: February 2014

AbstractNutrition interventions have an effect on growth, energy and nutrient intake, and development, but there are mixed reports on the effect of supplementation of energy‐dense foods on dietary intake. This substudy aimed at assessing the effect of supplementation with corn–soy blend (CSB) or lipid‐based nutrient supplement (LNS) on energy and nutrient intake in moderately underweight children participating in a clinical trial. A total of 188 children aged 8–18 months participated and received daily either 284 kcal from CSB or 220 kcal from LNS and no supplements (control). An interactive 24‐h recall method was used to estimate energy and nutrient intakes in the groups. Total mean energy intake was 548 kcal, 551 kcal and 692 kcal in the control, CSB and LNS groups, respectively (P = 0.011). The mean (95% confidence interval) intake of energy and protein were 144 (37–250; P < 0.001) and 46 (1.5–7.6; P < 0.001) larger, respectively, in the LNS group than among the controls. No significant differences were observed between the control and CSB groups. Energy intake from non‐supplement foods was significantly lower in the CSB group compared with the control group, but not in the LNS group, suggesting a lower displacement of non‐supplement foods with LNS. Both CSB and LNS supplementation resulted in higher intakes of calcium, iron, zinc and vitamin C compared with controls (all P ≤ 0.001). This study indicates that LNS might be superior to CSB to supplement underweight children as it results in higher energy intake, but this requires confirmation in other settings.