Sorghum is a food and feed cereal crop adapted to heat and drought and a staple for 500 million of the world’s poorest people. Its small diploid genome and phenotypic diversity make it an ideal C4 grass model as a complement to C3 rice. Here we present high coverage (16–45 × ) resequenced genomes of 44 sorghum lines representing the primary gene pool and spanning dimensions of geographic origin, end-use and taxonomic group. We also report the first resequenced genome of S. propinquum, identifying 8 M high-quality SNPs, 1.9 M indels and specific gene loss and gain events in S. bicolor. We observe strong racial structure and a complex domestication history involving at least two distinct domestication events. These assembled genomes enable the leveraging of existing cereal functional genomics data against the novel diversity available in sorghum, providing an unmatched resource for the genetic improvement of sorghum and other grass species.

Background— Hospital readmission is an important clinical outcome of patients with heart failure. Its relation to length of stay for the initial hospitalization is not clear. Methods and Results— We used hierarchical modeling of data from a clinical trial to examine variations in length of stay across countries and across hospitals in the United States and its association with readmission within 30 days of randomization. Main outcomes included associations between country-level length of stay and readmission rates, after adjustment for patient-level case mix; and associations between length of stay and readmission rates across sites in the United States. Across 27 countries with 389 sites and 6848 patients, mean length of stay ranged from 4.9 to 14.6 days (6.1 days in the United States). Rates of all-cause readmission ranged from 2.5% to 25.0% (17.8% in the United States). There was an inverse correlation between country-level mean length of stay and readmission ( r =–0.52; P <0.01). After multivariable adjustment, each additional inpatient day across countries was associated with significantly lower risk of all-cause readmission (odds ratio, 0.86; 95% confidence interval, 0.75–0.98; P =0.02) and heart failure readmission (odds ratio, 0.79; 95% confidence interval, 0.69–0.99; P =0.03). Similar trends were observed across US study sites concerning readmission for any cause (odds ratio, 0.92; 95% confidence interval, 0.85–1.00; P =0.06) and readmission for heart failure (odds ratio, 0.90; 95% confidence interval, 0.80–1.01; P =0.07). Across countries and across US sites, longer median length of stay was independently associated with lower risk of readmission. Conclusions— Countries with longer length of stay for heart failure hospitalizations had significantly lower rates of readmission within 30 days of randomization. These findings may have implications for developing strategies to prevent readmission, defining quality measures, and designing clinical trials in acute heart failure. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00475852.

A key step leading to influenza viral infection is the highly specific binding of a viral spike protein, hemagglutinin (HA), with an extracellular glycan receptor of a host cell. Detailed and timely characterization of virus-receptor binding profiles may be used to evaluate and track the pandemic potential of an influenza virus strain. We demonstrate a label-free glycan microarray assay platform for acquiring influenza virus binding profiles against a wide variety of glycan receptors. By immobilizing biotinylated receptors on a streptavidin-functionalized solid surface, we measured binding curves of five influenza A virus strains with 24 glycans of diverse structures and used the apparent equilibrium dissociation constants (avidity constants, 10–100 pM) as characterizing parameters of viral receptor profiles. Furthermore by measuring binding kinetic constants of solution-phase glycans to immobilized viruses, we confirmed that the glycan-HA affinity constant is in the range of 10 mM and the reaction is enthalpy-driven.

Background: Adrenocortical tumors (ACTs) are rare in children. Because of the rarity and various manifestations of ACTs, patients of ACTs are not easily diagnosed. Some patients were misdiagnosed before surgery. Objective: Identify the clinical, laboratorial, imaging and histopathological characteristics of adrenocortical tumors in children. Compare adrenalcortical adenoma with carcinoma. Methods: A retrospective review of 34 identifi ed patients who were younger than 15 years old with histologic confi rmation of adrenocortical carcinoma (ACC) or adenomas from 1991 to 2010. Results: In these 34 patients, 19 were adrenocortical adenoma (ACA) and 15 were ACC. The median age at diagnosis was 3.33 years (range, 0 -16 years), and 70.6 % of the patients were younger than fi ve years. Girls slightly predominated over boys (1.4:1). For endocrine abnormality, 14 patients had isolated precocious puberty, fi ve patients had isolated Cushing syndrome, 10 patients had precocious puberty plus Cushing syndrome, and fi ve patients did not have any symptoms. The most frequent fi ndings in laboratory tests were disturbance of the normal circadian rhythm of cortisol secretion (93.8 % ), followed by elevated serum level of testosterone (89.7 % ). Only 3.8 % of ultrasound diagnosis and 12.1 % of computed tomography (CT) diagnosis were consistent with pathologic diagnosis. Conclusion: Different from those in adult, the most frequent presentation in children with ACTs is peripheral precocious puberty with or without Cushing syndrome, and isolated Cushing syndrome. Few present with non-functional local mass. Laboratory tests usually reveal the discordantly elevated serum levels of sexual corticosteroid hormones, change of diurnal rhythm of cortisol or increase of morning cortisol. The differentiation of malignant from benign tumor cannot merely depend on imaging. Final diagnosis relies on comprehensive evaluation of clinical manifestations, laboratory data, imaging and pathology.

Microsporidia are eukaryotic, obligate intracellular, spore-forming parasites. The resistant spores, which harbor a rigid cell wall, are critical for their host-to-host transmission and persistence in the environment. The spore wall comprises two major layers: the exospore and the endospore. In Nosema bombycis, two spore wall proteins have been characterized--an endosporal protein, SWP30, and an exosporal protein, SWP32. Here, we report the identification of the third spore wall protein of N. bombycis, SWP25, the gene of which has no known homologue. SWP25 is predicted to posses a signal peptide and a heparin-binding motif. Immunoelectron microscopy analysis showed that this protein is localized to the endospore. This characterization of a new spore wall protein of N. bombycis may facilitate our investigation of the relationship between N. bombycis and its host, Bombyx mori.

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Background: In Inner Mongolia, China, more than 300 ,000 people are chronically exposed to arsenic via their drinking water. We have previously reported that the prevalence of arsenical dermatosis was as high as 40% in the Hetao Plain area. However , the association between exposure to arsenic in drinking water and adverse health effects has not been fully examined. The purpose of this study was to examine the association between exposure to arsenic and prevalence of subjective symptoms .Methods: A cross-sectional study was carried out in 431 residents of an arsenic-affected village and 189 residents of an arsenic-free village in 1996. Health-related interviews and physical examinations were conducted. The odds ratio for each subjective symptom was estimated , comparing residents of arsenic-free and affected villages.Results: An arsenic level of 50+ jig/L was found in 90.6% of wells in the arsenic-affected village . Adjusted odds ratios of subjective symptoms, including coughs (odds ratio [OR]=12.8, 95% confidence interval [CI]: 6.4-25.6), stomachaches (OR=5.8, 95% CI: 3.6-9.4), palpitations (OR=3.6, 95% CI: 1.5-8.2), urination problems (OR=14.7, 95% Cl: 3.3-65.5) and spontaneous abortions (OR=2.7, 95% CI: 0.8-8.4), were markedly higher amongst residents of the arsenic-affected village, including those without arsenic dermatosis.Conclusions: The present study shows a high prevalence of subjective symptoms amongst residents of an arsenic-affected village. Symptoms occurred in people with and without arsenic dermatosis. Our findings suggest that symptoms other than dermatosis should be considered when a clinical diagnosis of arsenic toxicosis is made. J Epidemiol 2003;13:211-215.

Objective: Long noncoding RNAs (lncRNAs) have already been proposed to function in Parkinson's disease (PD). However, the role of lncRNA BACE1-AS in PD has never been discussed. This study aims to examine the mechanism of BACE1-AS on oxidative stress injury of dopaminergic neurons in PD rats. Methods: Rat models of PD were established through the injection of 6-hydroxydopamine. The rotation of rats was induced by intraperitoneal injection of apomorphine, and number of rotations per minute was detected. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px), glutamic acid (Glu), dopamine (DA), tyrosine hydroxylase (TH), αsynuclein and inducible nitric oxide synthase (iNOS) in the substantia nigra of rats in each group were detected. Apoptosis and pathological changes in the substantia nigra were also observed. BACE1-AS, miR-34b-5p, BACE1, Bax and Bcl-2 expression in the substantia nigra were detected. The binding of BACE1-AS and miR-34b-5p and the targeting relationship of miR-34b-5p and BACE1 were further determined. Results: Downregulated BACE1-AS reduced iNOS, α-synuclein and Glu levels and elevated DA and TH levels in the substantia nigra of PD rats. Downregulated BACE1-AS repressed apoptosis and oxidative stress injury in the substantia nigra neurons of PD rats. BACE1-AS specifically bound to miR-34b-5p. BACE1 was a direct target gene of miR-34b-5p. Conclusion: Collectively, our study reveals that downregulation of lncRNA BACE1-AS inhibits iNOS activation in the substantial nigra and improve oxidative stress injury in PD rats by upregulating miR-34b-5p and downregulating BACE1.