Abstract Objective To investigate the effects of atorvastatin calcium on pulmonary vascular remodeling, the authors explored the regulatory mechanism of Histone Deacetylation Enzyme-2 (HDAC2) in rats with Chronic Obstructive Pulmonary Disease (COPD), and provided a new direction for drug treatment in the progression of vascular remodeling. Methods Eighteen female SD rats were randomly divided into control (Group S1), COPD (Group S2), and atorvastatin calcium + COPD (Group S3) groups. A COPD rat model was established by passive smoking and intratracheal injection of Lipopolysaccharide (LPS). Haematoxylin and eosin staining and Victoria Blue + Van Gibson staining were used to observe pathological changes in the lung tissue. The pulmonary vascular inflammation score was calculated, and the degree of pulmonary vascular remodeling was evaluated. The ratio of Muscular Arteries in lung tissue (MA%), the ratio of the vessel Wall Area to the vessel total area (WA%), and the ratio of the vessel Wall Thickness to the vascular outer diameter (WT%) were measured using imaging software. The expression of HDAC2 was measured using western blotting, ELISA (Enzyme-Linked Immunosorbent Assay), and qPCR (Real-time PCR). Results Compared with the control group, the degree of pulmonary vascular inflammation and pulmonary vascular remodeling increased in rats with COPD. The WT%, WA%, and lung inflammation scores increased significantly; the expression of HDAC2 and HDAC2mRNA in the serum and lung tissue decreased, and the level of Vascular Endothelial Growth Factor (VEGF) in the lung tissues increased (p< 0.05). Compared with the COPD group, the lung tissues from rats in the atorvastatin group had fewer inflammatory cells, and the vascular pathological changes were significantly relieved. The WT%, WA%, and lung inflammation scores decreased significantly; the expression of HDAC2 and HDAC2mRNA in the serum and lung tissues increased, and the level of VEGF in the lung tissues decreased (p< 0.05). Conclusion The present study revealed that atorvastatin calcium could regulate the contents and expression of HDAC2 in serum and lung tissues and inhibit the production of VEGF, thereby regulating pulmonary vascular remodeling in a rat model with COPD. Enzyme2 Enzyme 2 Enzyme- HDAC (HDAC2 COPD, , (COPD) Group S1, S1 S S1) S2, S2 S2) S3 groups LPS. LPS . (LPS) calculated evaluated MA%, MA MA% (MA%) WA WA% (WA%) WT% WT (WT% software blotting EnzymeLinked Linked Assay, Assay Assay) Realtime Real time PCR. PCR PCR) HDACmRNA mRNA (VEGF p< p (p 0.05. 005 0.05 0 05 0.05) cells relieved (HDAC (COPD (LPS (MA% (WA% (WT 00 0.0 (MA (WA 0.

ABSTRACT Purpose: To investigate the role of cyanidin-3-O-glucoside (C3G) in renal ischemia/reperfusion (I/R) injury and the potential mechanisms. Methods: Mouse models were established by clamping the left renal vessels, and in vitro cellular models were established by hypoxic reoxygenation. Results: Renal dysfunction and tissue structural damage were significantly higher in the I/R group. After treatment with different concentrations of C3G, the levels of renal dysfunction and tissue structural damage decreased at different levels. And its protective effect was most pronounced at 200 mg/kg. The use of C3G reduced apoptosis as well as the expression of endoplasmic reticulum stress (ERS)-related proteins. Hypoxia/reoxygenation (H/R)-induced apoptosis and ERS are dependent on oxidative stress in vitro. In addition, both AG490 and C3G inhibited the activation of JAK/STAT pathway and attenuated oxidative stress, ischemia-induced apoptosis and ERS. Conclusions: The results demonstrated that C3G blocked renal apoptosis and ERS protein expression by preventing reactive oxygen species (ROS) production after I/R via the JAK/STAT pathway, suggesting that C3G may be a potential therapeutic agent for renal I/R injury. Purpose cyanidin3Oglucoside cyanidinOglucoside cyanidin 3 O glucoside CG C G (C3G ischemiareperfusion ischemia reperfusion IR I R (I/R mechanisms Methods vessels reoxygenation Results group 20 mgkg mg kg mg/kg ERSrelated related proteins Hypoxiareoxygenation Hypoxia H/Rinduced HRinduced H/R induced H addition AG AG49 JAKSTAT JAK STAT ischemiainduced Conclusions ROS (ROS Oglucoside 2 Rinduced HR AG4

Abstract Objective: The relationship between lipid metabolism and pneumonia in under-five children remains unclear. The aim of the study was to explore the association of several lipids, lipoproteins and apolipoproteins with the risk of childhood pneumonia, and to initially reveal the mechanisms involved. Methods: There were 1000 children with confirmed severe pneumonia and 1000 healthy controls (18-59 months old) in the study. Serum levels of several lipids, lipoproteins and apolipoproteins were measured. The occurrence of hypoxaemia and serum level of C-reactive protein were recorded. Multivariate logistic regression and spearman correlation analysis were adopted to assess the correlation between these variables to achieve the research objective. Results: First, higher triglycerides, total cholesterol, LDL cholesterol, VLDL cholesterol and apolipoprotein B levels were associated with the elevated risk of severe pneumonia (OR: 1.407, 95%CI: 1.336~1.480; OR: 1.947, 95%CI: 1.741~2.175; OR: 1.153, 95%CI: 1.116~1.189; OR: 1.310, 95%CI: 1.222~1.404; OR: 1.075, 95%CI: 1.003~1.151). Higher HDL cholesterol and apolipoprotein A1 levels were associated with a decreased risk of the disease (OR: 0.903, 95%CI: 0.873~0.933; OR: 0.921, 95%CI: 0.891~0.952). Second, higher triglycerides level was associated with an increased risk of hypoxemia in these children (OR: 1.142, 95%CI: 1.072~1.215). Third, serum HDL cholesterol level was linearly associated with C-reactive protein level in these children (p = -0.343, P < 0.001). Conclusion: Abnormal levels of several lipids, lipoproteins and apolipoproteins were related to severe childhood pneumonia. The findings that triglycerides and HDL cholesterol were respectively implicated in hypoxaemia and inflammation might partly explain the mechanisms linking lipid metabolism to severe pneumonia. Objective underfive under five unclear lipids involved Methods 100 1859 18 59 (18-5 old measured Creactive C reactive recorded objective Results First OR (OR 1407 1 407 1.407 95%CI 95CI CI 95 1.336~1.480 13361480 336 480 1947 947 1.947 1.741~2.175 17412175 741 2 175 1153 153 1.153 1.116~1.189 11161189 116 189 1310 310 1.310 1.222~1.404 12221404 222 404 1075 075 1.075 1.003~1.151. 10031151 1.003~1.151 . 003 151 1.003~1.151) A 0903 0 903 0.903 0.873~0.933 08730933 873 933 0921 921 0.921 0.891~0.952. 08910952 0.891~0.952 891 952 0.891~0.952) Second 1142 142 1.142 1.072~1.215. 10721215 1.072~1.215 072 215 1.072~1.215) Third p 0.343, 0343 343 -0.343 0.001. 0001 0.001 001 0.001) Conclusion 10 185 5 (18- 140 40 1.40 9 1.336~1.48 1336148 33 48 194 94 1.94 1.741~2.17 1741217 74 17 115 15 1.15 1.116~1.18 1116118 11 131 31 1.31 1.222~1.40 1222140 22 107 07 1.07 1003115 1.003~1.15 00 090 90 0.90 0.873~0.93 0873093 87 93 092 92 0.92 0891095 0.891~0.95 89 114 14 1.14 1072121 1.072~1.21 21 0.343 034 34 -0.34 000 0.00 (18 4 1.4 1.336~1.4 133614 3 19 1.9 1.741~2.1 174121 7 1.1 1.116~1.1 111611 13 1.3 1.222~1.4 122214 1.0 100311 1.003~1.1 09 0.9 0.873~0.9 087309 8 089109 0.891~0.9 107212 1.072~1.2 0.34 03 -0.3 0.0 (1 1. 1.336~1. 13361 1.741~2. 17412 1.116~1. 11161 1.222~1. 12221 10031 1.003~1. 0. 0.873~0. 08730 08910 0.891~0. 10721 1.072~1. 0.3 -0. ( 1.336~1 1336 1.741~2 1741 1.116~1 1116 1.222~1 1222 1003 1.003~1 0.873~0 0873 0891 0.891~0 1072 1.072~1 -0 1.336~ 133 1.741~ 174 1.116~ 111 1.222~ 122 1.003~ 0.873~ 087 089 0.891~ 1.072~ - 1.336 1.741 1.116 1.222 12 1.003 0.873 08 0.891 1.072 1.33 1.74 1.11 1.22 1.00 0.87 0.89 1.7 1.2 0.8

Abstract Background: Non-canonical Wnt pathways play important roles in liver fibrosis. Notum is a newly discovered inhibitor to Wnt proteins. This study was to investigate anti-fibrotic effects of Notum. Methods: 53 patients with hepatitis B virus (HBV) infection as well as a cell co-culture system of LX-2 and Hep AD38 cells were engaged in this study. Clinical, biological and virological data of each patient were analyzed. Cell viability was detected at different time points. mRNA and protein levels of NFATc1 (Nuclear factor of activated T-cells), Jnk, α-SMA, Col1A1 and TIMP-1 were detected both in LX-2 and liver tissue. Protein levels of NFATc1 and Jnk in liver tissue and their correlations with fibrosis score were analyzed. Results: Hepatitis B virus replication up-regulated Wnt5a induced NFATc1 and Jnk activity in Hep AD38. Notum suppressed NFATc1, Jnk and fibrosis genes expression, reduced cell viability in co-cultured LX-2 cells induced by HBV. Interestingly, Patients with HBV DNA > 5log copies/ml had higher mRNA levels of NFATc1 and fibrosis genes than patients with HBV DNA < 5log copies/ml. Most importantly, protein expressions of NFATc1 and pJnk have positive correlations with liver fibrosis scores in HBV-infected patients. Conclusions: Our data showed that Notum inhibited HBV-induced liver fibrosis through down-regulating Wnt 5a mediated non-canonical pathways. This study shed light on anti-fibrotic treatment.

ABSTRACT Picris japonica Thunb., Asteraceae, is an herbal medicine used to dispel heat, reduce swelling and alleviate pain in traditional Mongolian medicine. Its dried whole plant is mainly used to treat flu and mammary abscesses. Given the potential applications of such an herb, detailed pharmacognostic research on P. japonica is needed. This study attempted to fill this need by producing permanent and semi-permanent slides of different organs (root, stem, leaf, pollen grain, fruit and powder of the whole plant) using safranine staining, safranine-fast green double staining and common methods. Furthermore, several featured microscopic structures of P. japonica are described herein. The results obtained provide us with valuable information for botanical quality control and species identification and enable us to detect adulterations in commercial samples of Picris or in laboratory samples.

RESUMO O objetivo primário desse estudo foi comparar a farmacocinética de florfenicol (FFL) em fluido epitelial pulmonar à farmacocinética (PK) de FFL em plasma suíno. O segundo objetivo foi avaliar o efeito de anestesia com ketamina e propofol no PK de FFL em plasma. Lavagem broncoalveolar foi utilizada para quantificar volume de fluido epitelial pulmonar (PELF) e método de diluição de uréia para determinar FFL em PELF. Injeção de FFL foi administrada intramuscular a suínos em dose única de 20mg/kg de peso corporal. Os principais parâmetros de PK em FFL em plasma e PELF foram os seguintes: a área sob a curva de concentração-tempo, concentração máxima da droga, eliminação de meia-vida e média de tempo de permanência foram 69,45±4,36 vs 85,03±9,26μg·hr/ml, 4,65±0,34 vs 5,94±0,86μg/ml, 9,87±1,70 vs 10,69±1,60hr e 12,75±0,35 vs 14,46±1,26hr, respectivamente. Não houve diferença estatisticamente significante entre os perfis de PK de FFL para os porcos anestesiados e não anestesiados. Esse estudo sugere que (i) FFL penetrou rapidamente no pulmão e concentração da droga sofre queda mais veloz em plasma que líquido pulmonar, (ii) o perfil de PK de FFL em suínos não modificou após administração de agente anestésico.

ABSTRACT The primary objective of the current study was to compare the pharmacokinetic (PK) of florfenicol (FFL) in pulmonary epithelial lining fluid and the plasma in swine. The second objectives were to evaluate the effect of anesthesia with ketamine and propofol on the PK of FFL in plasma. Bronchoaveolar lavage was utilized for quantification of PELF volume and the urea dilution method was used to determine the concentration of FFL in PELF. FFL was administered intramuscularly (IM) to swine in a single dose of 20mg/kg body weight. The main PK parameters of FFL in plasma and PELF were as follows: the area under the concentration-time curve, maximal drug concentration, elimination half-life and mean residence time were 69.45±4.36 vs 85.03±9.26μg·hr/ml, 4.65±0.34 vs 5.94±0.86μg/ml, 9.87±1.70 vs 10.69±1.60hr and 12.75±0.35 vs 14.46±1.26hr, respectively. There was no statistically significant difference between the PK profiles of FFL for the anesthetized and unanesthetized pigs. This study suggest that (i) FFL penetrated rapidly into the pulmonary and the drug concentration decay faster in plasma than in the pulmonary, (ii) the PK profile of FFL in swine was not interfered after administration of anesthetic agent.

RESUMO Na China, Peste des petits ruminants (PPR) foi relatado oficialmente em 2007. De 2010 até o surto de 2013, não houve relato de infecção por PPRV. Em Novembro de 2013, PPRV ressurgiu em Xinjiang e rapidamente se espalhou para 22 P/A/M (províncias, regiões autônomas e municípios) da China. No estudo, ovelhas com suspeita de infecção por PPRV em uma fazenda de reprodução no sul de Xinjiang form diagnosticadas em 2014 e as características da sequência completa da proteína N do gene do PPRV foi analisada. As ovelhas tinham sinais de infecção pelo PPRV, como febre, aumento de secreções oro-nasais, dispneia e diarreia, com 60% de morbidade e 21.1% de fatalidade. As lesões macroscópicas após mudanças histopatológicas foram observadas sob microscópio, incluindo estomatite, pneumonia bronco-intersticial, enterite hemorrágica catarral e inclusões eosinofílicas intracitoplasmáticas em células gigantes multinucleares no pulmão. As amostras de tecido fixadas em formalina testaram positivo para detecção de RT-PCR por extração de ácido nucleico. Os nucleotídeos da proteína N do gene da linhagem China/XJNJ/2014 apresentou extrema homologia com o China/XJYL/2013, e homologia ainda maior com a variedade PRADESH-95 da Índia. Análise filogenética baseada na sequencia completa da proteína N do gene de PPRV mostrou que as variedades China/XJNJ/2014, outra de 2013-2014 mostrada nesse estudo e as Tibetanas todas pertenciam à linhagem Ⅳ, mas as PPRV de 2013-2014 nesse estudo e as Tibetanas estavam em diferentes agrupamentos.

ABSTRACT In China, Peste des petits ruminants (PPR) was officially first reported in 2007. From 2010 until the outbreak of 2013, PPRV infection was not reported. In November 2013, PPRV re-emerged in Xinjiang and rapidly spread to 22 P/A/M (provinces, autonomous regions and municipalities) of China. In the study, suspected PPRV-infected sheep in a breeding farm of South Xinjiang in 2014 were diagnosed and the characteristics of complete sequence of N protein gene of PPRV was analyzed. The sheep showed PPRV-infected signs, such as fever, orinasal secretions increase, dyspnea and diarrhea, with 60% of morbidity and 21.1% of fatality rate. The macroscopic lesions after autopsy and histopathological changes were observed under light microscope including stomatitis, broncho-interstitial pneumonia, catarrhal hemorrhagic enteritis and intracytoplasmic eosinophilic inclusions in multinucleated giantcell in lung. The formalin-fixed mixed tissues samples were positive by nucleic acid extraction and RT-PCR detection. The nucleotide of N protein gene of China/XJNJ/2014 strain was extremely high homology with the China/XJYL/2013 strain, and the highest with PRADESH_95 strain from India in exotic strains. Phylogenetic analysis based on complete sequence of N protein gene of PPRV showed that the China/XJNJ/2014 strain, other strain of 2013-2014 in this study and Tibetan strains all belonged to lineage Ⅳ, but the PPRV strains of 2013-2014 in this study and Tibetan strains were in different sub-branches.

English grain aphid (EGA, Sitobion avenae Fabricius) is an important pest in wheat (Triticum aestivum L.). To develop EGA-resistant varieties, introducing the desirable genes from related species is regarded as an efficient avenue. In this study, the F1, F2 and F3 plants derived from the cross of EGA-susceptible wheat-Psathyrostachys huashanica Keng ex Kuo amphiploid (PHW-SA, AABBDDNsNs) and EGA-resistant triticale (Zhongsi 828, AABBRR) were analyzed for EGA resistance. Consequently, PHW-SA was moderately susceptible while Zhongsi 828 and their F1 hybrids were immune, suggesting that the resistance is dominant. All the F2 plants showed high resistance or immunity over two years, indicating that EGA resistance genes are more likely carried by the rye (Secale cereale L.) chromosomes rather than the genomes A or B of Zhongsi 828. In the F3 generation, 25 of 239 lines became susceptible. Giemsa C-banding patterns revealed that these F3 lines had 38-40 chromosomes, including complete rye genome except 5R (and 2R in five lines). Genomic in situ hybridization analysis confirmed this result. During meiosis, all the chromosomes formed bivalents. Six bivalents in 20 lines and five bivalents in five lines were characterized from rye. In contrast, their F2 parental lines had 42 chromosomes (21 bivalents), containing 1R-7R of rye. No P. huashanica chromosomes were detected. Therefore, we propose that the rye chromosome 5R may be related to EGA resistance.

The efficiency of enzymatic hydrolysis of cellulose can be improved by various pretreatments of the substrate. In order to increase the efficiency of enzymatic saccharification of the wheat straw, we determined the effect of different pretreatments on the physical structure, chemical components and enzymatic saccharification of wheat straw. Our results showed that combination of grinding and sodium hydroxide (NaOH) treatment had high effect on the enzymatic hydrolysis of wheat straws. The optimal pretreatment condition was to grind the wheat straws into the sizes of 120 meshes followed by treatment with 1.0% NaOH for 1.5 h (121°C/15psi). Under this condition, the cellulose content of wheat straw was increased by 44.52%, while the content of hemicellulose and lignin was decreased by 44.15% and 42.52%, respectively. Scanning Electronic Microscopy and infrared spectrum analyses showed that significant changes occurred in the structure of wheat straws after pretreatment, which is favorable for the hydrolysis and saccharification. Cellulase produced by Penicillium waksmanii F10-2 was used to hydrolyze the pretreated wheat straw and the optimal condition was determined to be 30 h of enzymatic reaction under the temperature of 55°C, pH 5.5 and substrate concentration of 3%.