Preventing bad behavior in academia.

We gave young scientists this prompt: Describe one change to scientific policy or culture that would substantially decrease incidents of scientific misconduct or other unethical behavior.

Hepatitis E virus superinfection impairs long-term outcome in hospitalized patients with hepatitis B virus-related decompensated liver cirrhosis.

INTRODUCTION AND OBJECTIVES: Hepatitis E virus (HEV) superinfection is a common excerbating event in patients with chronic hepatitis B, but the impact on the long-term prognosis is not clear. This study investigates the specific role of HEV superinfection in the long-term outcome of hepatitis B virus (HBV) patients with liver cirrhosis. PATIENTS AND METHODS: A retrospective, observational cohort study was conducted using clinical, laboratory, and survival data collected from patients suffering from hepatitis B cirrhosis with or without HEV superinfection. Disease progression and mortality rates were analyzed. RESULTS: After a two-year follow-up, HEV superinfection was identified in 27 of 811 patients. The transplantation-free mortality was significantly increased (51.9% vs. 14.3%, p< 0.001) in HEV superinfection compared to that in hepatitis B cirrhosis patients without HEV superinfection. Logistic regression analysis demonstrated that elderly people were independent host risk factors for hepatitis B cirrhosis patients with HEV superinfection before and after propensity score matching (PSM). Moreover, HEV superinfection was a risk factor for patients with hepatitis B cirrhosis with new acute decompensation (AD) and acute-on-chronic liver failure (ACLF) during hospitalization. A multivariate Cox proportional hazards regression model demonstrated that acute HEV co-infection is associated with two-year mortality (hazard ratio [HR]: 2.49; 95% CI: 1.40-4.43; p= 0.002; and HR: 5.79; 95% CI: 1.87-17.87; p= 0.002) in patients with hepatitis B cirrhosis before and after PSM. CONCLUSIONS: Elder patients with hepatitis B cirrhosis are susceptible to HEV superinfection, accelerating disease progression and increasing long-term mortality in hospitalized patients with HBV-related decompensated liver cirrhosis.

Population genomics of Zea species identifies selection signatures during maize domestication and adaptation.

BACKGROUND: Maize (Zea mays L. ssp. mays) was domesticated from teosinte (Zea mays ssp. parviglumis) about 9000 years ago in southwestern Mexico and adapted to a range of environments worldwide. Researchers have depicted the maize domestication and adaptation processes over the past two decades, but efforts have been limited either in sample size or genetic diversity. To better understand these processes, we conducted a genome-wide survey of 982 maize inbred lines and 190 teosinte accessions using over 40,000 single-nucleotide polymorphism markers. RESULTS: Population structure, principal component analysis, and phylogenetic trees all confirmed the evolutionary relationship between maize and teosinte, and determined the evolutionary lineage of all species within teosinte. Shared haplotype analysis showed similar levels of ancestral alleles from Zea mays ssp. parviglumis and Zea mays ssp. mexicana in maize. Scans for selection signatures identified 394 domestication sweeps by comparing wild and cultivated maize and 360 adaptation sweeps by comparing tropical and temperate maize. Permutation tests revealed that the public association signals for flowering time were highly enriched in the domestication and adaptation sweeps. Genome-wide association study identified 125 loci significantly associated with flowering-time traits, ten of which identified candidate genes that have undergone selection during maize adaptation. CONCLUSIONS: In this study, we characterized the history of maize domestication and adaptation at the population genomic level and identified hundreds of domestication and adaptation sweeps. This study extends the molecular mechanism of maize domestication and adaptation, and provides resources for basic research and genetic improvement in maize.

Modulation of CO2 adsorption in novel pillar-layered MOFs based on carboxylate-pyrazole flexible linker.

Metal-organic frameworks (MOFs) have attracted significant attention as sorbents due to their high surface area, tunable pore volume and pore size, coordinatively unsaturated metal sites, and ability to install desired functional groups by post-synthetic modification. Herein, we report three new MOFs with pillar-paddlewheel structures that have been synthesized solvothermally from the mixture of the carboxylate-pyrazole flexible linker (H2L), 4,4-bipyridine (BPY)/triethylenediamine (DABCO), and Zn(ii)/Cu(ii) ions. The MOFs obtained, namely [ZnII(L)BPY], [CuII(L)BPY], and [CuII(L)DABCO], exhibit two-fold interpenetration and dinuclear paddle-wheel nodes. The Zn(ii)/Cu(ii) cations are coordinated by two equatorial L linkers that result in two-dimensional sheets which in turn are pillared by BPY or DABCO in the perpendicular direction to obtain a neutral three-dimensional framework that shows one-dimensional square channels. The three pillar-layered MOFs were characterized as microporous materials showing high crystalline stability after activation at 120 °C and CO2 adsorption. All MOFs contain uncoordinated Lewis basic pyrazole nitrogen atoms in the framework which have an affinity toward CO2 and hence could potentially serve as CO2 adsorption material. The CO2 uptake capacity was initially enhanced by replacing Zn with Cu and then replacing the pillar, going from BPY to DABCO. Overall, all the MOFs exhibit low isosteric heat (Qst) of adsorption which signifies an advantage due to the energy required for the adsorption and regeneration processes.

Knockout of Adamts7, a novel coronary artery disease locus in humans, reduces atherosclerosis in mice.

BACKGROUND: Genome-wide association studies have established ADAMTS7 as a locus for coronary artery disease in humans. However, these studies fail to provide directionality for the association between ADAMTS7 and coronary artery disease. Previous reports have implicated ADAMTS7 in the regulation of vascular smooth muscle cell migration, but a role for and the direction of impact of this gene in atherogenesis have not been shown in relevant model systems. METHODS AND RESULTS: We bred an Adamts7 whole-body knockout mouse onto both the Ldlr and Apoe knockout hyperlipidemic mouse models. Adamts7(-/-)/Ldlr(-/-) and Adamts7(-/-)/Apoe(-/-) mice displayed significant reductions in lesion formation in aortas and aortic roots compared with controls. Adamts7 knockout mice also showed reduced neointimal formation after femoral wire injury. Adamts7 expression was induced in response to injury and hyperlipidemia but was absent at later time points, and primary Adamts7 knockout vascular smooth muscle cells showed reduced migration in the setting of tumor necrosis factor-α stimulation. ADAMTS7 localized to cells positive for smooth muscle cell markers in human coronary artery disease lesions, and subcellular localization studies in cultured vascular smooth muscle cells placed ADAMTS7 at the cytoplasm and cell membrane, where it colocalized with markers of podosomes. CONCLUSIONS: These data represent the first in vivo experimental validation of the association of Adamts7 with atherogenesis, likely through modulation of vascular cell migration and matrix in atherosclerotic lesions. These results demonstrate that Adamts7 is proatherogenic, lending directionality to the original genetic association and supporting the concept that pharmacological inhibition of ADAMTS7 should be atheroprotective in humans, making it an attractive target for novel therapeutic interventions.

Clinical findings of 40 patients with nocardiosis: A retrospective analysis in a tertiary hospital.

To the best of our knowledge, no Chinese case studies concerning Nocardia infection have been published to date. Therefore, the present study aimed to retrospectively evaluate the risk factors, clinical features, imaging results, laboratory abnormalities, treatments and outcomes of nocardiosis in a Chinese tertiary hospital. Data collected from patients with laboratory-confirmed nocardiosis were retrospectively analyzed. A total of 40 patients who had a positive culture of Nocardia were included. The median time between the onset of symptoms and diagnosis was 42 days. Underlying diseases were identified in 72.5% of the patients of which diabetes was the most common (32.5%). The most important risk factor was corticosteroid administration. Fever and cough were common clinical symptoms. The pleuropulmonary (85%) were the most frequently involved sites and the disseminated disease rate was 30.0%. Frequent chest computed tomography scans revealed the presence of airspace opacities, nodules and masses, in addition to cavitary lesions that were particularly common among the study group. Brain images revealed lesions associated with abscesses. The majority of the patients (71.1%) were treated with trimethoprim sulfamethoxazole alone or in combination with other drugs. The in-hospital mortality rate was 15.0%. Disseminated disease, immunocompromised patients, an older age, brain involvement and concomitant infections were associated with a poor prognosis. Nocardiosis is an uncommon but emerging disease. The present study reports the first case series on nocardiosis from China and provides important information on the clinical features and risk factors of nocardiosis. Early recognition of the disease and the initiation of appropriate treatment are essential for a good prognosis.