ABSTRACT Low light levels during rice (Oryza sativa L.) growing seasons may lead to significant reductions in grain yield and quality. The effect of shading stress on remobilization of nonstructural carbohydrates (NSC) from the stem plus sheath (SPS) to the grain, a process crucial to rice grain formation, was investigated. Field shading experiments were conducted in Hanyuan and Wenjiang, China, using two rice varieties (Huanghuazhan and Guichao II) subjected to shading stress after heading. Stored NSC of 60.00-159.15 g m-2 were remobilized from SPS after heading, contributing 9.63%-23.63% to grain dry weight at maturity. Shading stress resulted in the 23.99%-50.30% and 31.65%-61.33% reduction in NSC content of SPS at 20 d after heading (DAH20) and maturity stages, respectively. This contributed to the 13.80%-89.00% increase in the remobilization of stored NSC from SPS to the grain (RASN) and 15.86%-73.30% increase in remobilization percentage of removed NSC from SPS to the grain (RPRN). The effect of shading stress on remobilization differed between sites and varieties. Owing to a greater sink capacity, shading stress led to a higher RASN and RPRN from heading to DAH20 for ‘Huanghuazhan’ in Hanyuan. To compensate for photosynthate deficiency under shading stress, rice is adapted to remobilize stored NSC during early grain filling stages. Consequently, grain yield loss caused by shading could be reduced by increasing the SPS remobilization ability (especially in low light areas). Increasing NSC accumulation in SPS before heading for later remobilization may be a feasible way to alleviate rice yield loss under adverse light conditions.

OBJECTIVES: Diagnosis and management of essential hypertension (EH) or type 2 diabetes mellitus (T2DM) by combining comprehensive treatment and classificatory diagnosis have been continuously improved. However, understanding the pathogenesis of EH patients with concomitant T2DM and subsequent treatment remain the major challenges owing to the lack of non-invasive biomarkers and information regarding the underlying mechanisms. METHODS: Herein, we collected 200 serum samples from EH and/or T2DM patients and healthy donors (N). Gene-expression profiling was conducted to identify candidate microRNAs with clinical significance. Then, a larger cohort of the aforementioned patients and 50 N were used to identify the correlation between the tumor suppressor miR-195-5p and EH and/or T2DM. The dual-luciferase reporter assay was used to explore the target genes of miR-195-5p. The suppressive effects of miR-195-5p on the 3′-UTR of the dopamine receptor D1 (DRD1) transcript in EH patients with concomitant T2DM were verified as well. RESULTS: Compared with that in other groups, serum miR-195-5p was highly downregulated in EH patients with concomitant T2DM. miR-195-5p overexpression efficiently suppressed DRD1 expression by binding to the two 3′-UTRs. Additionally, two single nucleotide polymorphisms, including 231T-A and 233C-G, in the miR-195-5p binding sites of the DRD1 3′-UTR were further identified. Collectively, we identified the potential clinical significance of DRD1 regulation by miR-195-5p in EH patients with concomitant T2DM. CONCLUSIONS: Our data suggested that miR-195-5p circulating in the peripheral blood served as a novel biomarker and therapeutic target for EH and T2DM, which could eventually help address major challenges during the diagnosis and treatment of EH and T2DM.

Abstract Objective: To modify the chronic atrial fibrillation of atrial tachycardia pacing in beagles with a homemade pacemaker placed outside the body and to evaluate connective tissue growth factor and fibrosis of atrial tissue in our modified atrial tachycardia pacing beagle model. Methods: Twelve adult beagles of either sex were randomly divided into an atrial tachycardia pacing group and a control group (n=6 in each group). We performed the temporary pacemaker implantation at the right atrial appendage and put the pacemaker into the pocket of dog clothing in the atrial tachycardia pacing group. After eight weeks of atrial tachycardia pacing, the electrocardiography, transthoracic echocardiography, hematoxylin-eosin staining, and Masson’s staining of the right atrial appendages were performed along with the immunohistochemistry, quantitative real-time polymerase chain reaction, and Western blot analysis of connective tissue growth factor, collagen I, and collagen III. Results: In the atrial tachycardia pacing group, atrial fibrillation was induced in five beagles (83.3%); the left atrium enlarged significantly; more canines had mitral regurgitation; and the Masson’s staining, quantitative real-time polymerase chain reaction, and Western blot results demonstrated more obvious fibrosis of the left atrium. Conclusion: The modified beagle model of atrial fibrillation using a right atrium pacemaker outside the body was effective, increased connective tissue growth factor and collagen I messenger ribonucleic acid overexpression, and induced atrial fibrosis.

Nuclear factor erythroid-related factor 2 (Nrf2) has been implicated in several detoxifying and antioxidant defense processes. Nrf2-mediated heme oxygenase-1 (HO-1) expression was demonstrated to play a key role against oxidative stress. Gastrodin (GSTD) is a well-known active compound isolated from the roots of Rhizoma gastrodiae, a plant used in ancient Chinese traditional medicine. The aim of this work was to investigate whether GSTD could alleviate H2O2-induced oxidative stress in mouse liver sinusoidal endothelial cells (LSECs). In LSECs exposed to 1 mM H2O2, treatment with GSTD (1, 10, or 50 µM) resulted in higher cell viability than the untreated control. Treated cells maintained a higher Bcl2/Bax ratio and suppressed caspase-9 expression compared with untreated cells, reducing cell apoptosis. GSTD was protective for H2O2-induced oxidative injury by reducing the generation of intracellular reactive oxygen species and malondialdehyde. HO-1 and Nrf2 expressions were synergistically upregulated by GSTD. Inhibition of HO-1 by 10 µM zinc protoporphyrin resulted in less protective effects on cell viability and malondialdehyde reduction by GSTD treatment in H2O2-exposed LSECs. Additionally, phosphorylated p38 in LSECs exposed to H2O2 was elevated by GSTD. Inhibition of p38 phosphorylation by SB203580 did not induce Nrf2 and HO-1 expression after 1 or 10 µM GSTD treatment and the protective effect on cell viability and malondialdehyde reduction in H2O2-exposed LSECs was reduced. The data conclusively demonstrated that GSTD-induced HO-1 and Nrf2 expression is involved in protection of LSECs from H2O2-induced oxidative injury, which may be regulated by p38 phosphorylation.

Gene networks have been broadly used to predict gene functions based on guilt by association (GBA) principle. Thus, in order to better understand the molecular mechanisms of esophageal squamous cell carcinoma (ESCC), our study was designed to use a network-based GBA method to identify the optimal gene functions for ESCC. To identify genomic bio-signatures for ESCC, microarray data of GSE20347 were first downloaded from a public functional genomics data repository of Gene Expression Omnibus database. Then, differentially expressed genes (DEGs) between ESCC patients and controls were identified using the LIMMA method. Afterwards, construction of differential co-expression network (DCN) was performed relying on DEGs, followed by gene ontology (GO) enrichment analysis based on a known confirmed database and DEGs. Eventually, the optimal gene functions were predicted using GBA algorithm based on the area under the curve (AUC) for each GO term. Overall, 43 DEGs and 67 GO terms were gained for subsequent analysis. GBA predictions demonstrated that 13 GO functions with AUC>0.7 had a good classification ability. Significantly, 6 out of 13 GO terms yielded AUC>0.8, which were determined as the optimal gene functions. Interestingly, there were two GO categories with AUC>0.9, which included cell cycle checkpoint (AUC=0.91648), and mitotic sister chromatid segregation (AUC=0.91597). Our findings highlight the clinical implications of cell cycle checkpoint and mitotic sister chromatid segregation in ESCC progression and provide the molecular foundation for developing therapeutic targets.

Resumo Justificativa e objetivos Dexmedetomidina (DEX) demonstrou ter efeito pré-condicionante e também efeitos protetores contra lesão organizada. Neste estudo, com células A549 (células epiteliais alveolares humanas), investigamos se o pré-condicionamento com DEX proporcionaria proteção contra lesão pulmonar aguda (LPA) in vitro. Métodos Células A549 foram aleatoriamente distribuídas em quatro grupos (n = 5): controle, DEX, lipopolissacarídeos (LPS) e D-LPS (DEX + LPS). Administramos solução de PBS (tampão fosfato-alcalino) ou DEX. Após 2 h de pré-condicionamento, o meio foi renovado e as células desafiadas com LPS por 24 h nos grupos LPS e D-LPS. Em seguida, malondialdeído (MDA), superóxido dismutase (SOD), Bcl-2, Bax, caspase-3 e em A549 foram testados. Apoptose também foi avaliada nas células. Resultados Em comparação com o grupo LPS, o pré-condicionamento com DEX reduziu a apoptose (26,43% ± 1,05% vs. 33,58% ± 1,16%, p < 0,05) em células A549, o que está correlacionado com a diminuição de MDA (12,84 ± 1,05 vs. 19,16 ± 1,89 nmol.mg-1 de proteína, p < 0,05) e aumento da atividade de SOD (30,28 ± 2,38 vs. 20,86 ± 2,19 U.mg-1 de proteína, p < 0,05). O pré-condicionamento com DEX também aumentou o nível de Bcl-2 (0,53 ± 0,03 vs. 0,32 ± 0,04, p < 0,05) e diminuiu o nível de Bax (0,49 ± 0,04 vs. 0,65 ± 0,04, p < 0,05), caspase-3 (0,54 ± 0,04 vs. 0,76 ± 0,04, p < 0,05) e citocromo c. Conclusão O pré-condicionamento com DEX tem efeito protetor contra LPA in vitro. Os potenciais mecanismos envolvidos são inibição da morte celular e melhoria da antioxidação.

Abstract Background and objectives Dexmedetomidine (DEX) has demonstrated the preconditioning effect and shown protective effects against organize injury. In this study, using A549 (human alveolar epithelial cell) cell lines, we investigated whether DEX preconditioning protected against acute lung injury (ALI) in vitro. Methods A549 were randomly divided into four groups (n = 5): control group, DEX group, lipopolysaccharides (LPS) group, and D-LPS (DEX + LPS) group. Phosphate buffer saline (PBS) or DEX were administered. After 2 h preconditioning, the medium was refreshed and the cells were challenged with LPS for 24 h on the LPS and D-LPS group. Then the malondialdehyde (MDA), superoxide dismutase (SOD), Bcl-2, Bax, caspase-3 and the cytochrome c in the A549 were tested. The apoptosis was also evaluated in the cells. Results Compare with LPS group, DEX preconditioning reduced the apoptosis (26.43% ± 1.05% vs. 33.58% ± 1.16%, p < 0.05) in the A549, which is correlated with decreased MDA (12.84 ± 1.05 vs. 19.16 ± 1.89 nmoL.mg-1 protein, p < 0.05) and increased SOD activity (30.28 ± 2.38 vs. 20.86 ± 2.19 U.mg-1 protein, p < 0.05). DEX preconditioning also increased the Bcl-2 level (0.53 ± 0.03 vs. 0.32 ± 0.04, p < 0.05) and decreased the level of Bax (0.49 ± 0.04 vs. 0.65 ± 0.04, p < 0.05), caspase-3 (0.54 ± 0.04 vs. 0.76 ± 0.04, p < 0.05) and cytochrome c. Conclusion DEX preconditioning has a protective effect against ALI in vitro. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation.

The morphology of Chinese fire-bellied newt liver consists of 5 lobes, with exception of a few individual differences present, which are composed by a number of hepatic lobules. Passing through the center of the lobules, a central vein radiates and is arranged in orderly row from one to several layers. The interval of the hepatic cords or masses are irregular and variable sinusoid. The hepatic sinusoidal wall consists of one layer endothelial cells or Macrophagocytus stellatus (Kupffer cells), which have protrusions and elongations. The intervals of the hepatic cells have perisinusoidal space (space of Disse). The hepatic cell is polygonal in shape with uniform, round or oval nucleus, 17.812.4µm in diameter, mean 14.2 µm 2-6 nucleoli, nuclear-cytoplasmic volume ratio was 0.24:1. There is a lot of pigmentation in the hepatic parenchyma.

La morfología del hígado del tritón de vientre de fuego chino está constituida por 5 lóbulos, excepto unos pocos que presentan diferencias individuales, los cuales se componen de una gran cantidad de lóbulos hepáticos. Pasando por el centro de los lóbulos, se encuentra una vena central radial y los organiza en cordones o placas hepáticas. La vena central es delgada de 61,6-30,2 µm de diámetro, con una media 42 de µm. Los hepatocitos alrededor de la vena central están organizados en filas ordenadas por una a varias capas. El intervalo de los cordones hepáticos o masas es irregular y sinusoidal variable. La pared del sinusoide hepático está formada por una capa de células endoteliales o macrófagos hepáticos (células de Kupffer) que tienen protuberancias y elongaciones. El intervalo de las células hepáticas tienen el espacio perisinusoidal (de Disse). La célula hepática es de forma poligonal con un núcleo redondo u oval uniforme de 17,8-12,4 µm de diámetro, con una media 14,2µm. 2 a 6 nucléolos, con un radio de volumen nuclear-citoplasmático de 0,24:1. Hay una gran cantidad de pigmentación en el parénquima hepático.

Despite great strides in schistosomiasis control over the past several decades in Sichuan Province, China the disease has re-emerged in areas where it was previously controlled. We reviewed historical records and found that schistosomiasis had reemerged in eight counties by the end of 2004 - seven of 21 counties with transmission control and one of 25 with transmission interruption as reported in 2001 were confirmed to have local disease transmission. The average "return time" (from control to re-emergence) was about eight years. The onset of re-emergence was commonly signalled by the occurrence of acute infections. Our survey results suggest that environmental and sociopolitical factors play an important role in re-emergence. The main challenge would be to consolidate and maintain effective control in the longer term until "real" eradication is achieved. This would be possible only by the formulation of a sustainable surveillance and control system.

A pesar de los grandes avances registrados en materia de control de la esquistosomiasis en los últimos decenios en la provincia de Sichuan, China, la enfermedad ha reaparecido en zonas donde ya había sido controlada. Examinando los registros históricos descubrimos que la esquistosomiasis había reaparecido en ocho cantones al final de 2004: se confirmó que siete de 21 cantones con control de la transmisión y uno de 25 con interrupción de la misma, según datos de 2001, presentaban transmisión local de la enfermedad. El «tiempo de retorno» medio (el transcurrido entre el control y la reaparición) era de aproximadamente ocho años. Los resultados de nuestro estudio llevan a pensar que hay factores ambientales y sociopolíticos que tienen un papel importante en la reaparición de la enfermedad. El reto principal sería consolidar y mantener un control efectivo a más largo plazo hasta lograr la erradicación «real». Esto sólo será posible si se concibe un sistema de vigilancia y control sostenible.

Malgré les grands progrès réalisés dans la lutte contre la schistosomiase au cours des dernières décennies dans la province du Sichuan, en Chine, cette maladie a réapparu dans des régions où elle était auparavant sous contrôle. Après analyse des dossiers, on a constaté une réémergence de la schistosomiase dans huit paysà la fin de l'année 2004 : l'existence d'une transmission locale de la maladie a été confirmée dans sept des 21 pays dans lesquels la maladie était endiguée et dans l'un des 25 dans lesquels la transmission était interrompue d'après les notifications de 2001. Le « temps de retour » moyen (de l'endiguement à la réémergence) était d'environ huit ans. L'apparition de la réémergence se manifestait habituellement par la survenue d'infections aiguës. Les résultats de l'enquête laissent à penser que des facteurs environnementaux et sociopolitiques jouent un rôle important dans le retour de la maladie. Le principal défi serait de consolider et de maintenir une lutte efficace à long terme jusqu'à obtenir une éradication « véritable ». Cet objectif ne serait réalisable qu'en organisant un système durable de surveillance et de lutte.