Pulsatilla decoction alleviates colitis by enhancing autophagy and regulating PI3K­Akt­mTORC1 signaling pathway.

The aim of the present study was to investigate the therapeutic effect of Pulsatilla decoction (PD) on ulcerative colitis (UC) and to elucidate its potential molecular mechanisms. C57BL/6 mice expressing natural killer (NK)1.1 were used as experimental animals in the present study and a model of oxazolone­induced colitis was established. Mice were randomly divided into the following five groups: i) PD group; ii) oxazolone­induced colitis group; iii) IL­13 intervention group; iv) 5­aminosalicylic acid positive control group; and v) negative control group (equal volume saline gavage). A total of 10 animals were used in each group. The effects of PD on UC and the association between this regimen and the PI3K­Akt­mTORC1 signaling pathway were evaluated by disease activity index (DAI), hematoxylin and eosin staining, reverse transcription­quantitative PCR (RT­qPCR), immunofluorescence assay, ELISA and western blotting. The UC models were successfully established by injecting oxazolone gavage solution. Clinical colitis evaluation and histological examination revealed that PD reduced the DAI values in oxazolone­induced colitis in mice and the degree of infiltration in NK1.1 cells. PD significantly reduced the secretion of IL­13, as determined using an ELISA. In addition, western blotting and RT­qPCR analyses demonstrated that Beclin1 and LC3II/I expression levels were downregulated following treatment of the mice with PD. In addition, PD not only partially restored alterations in the expression of tight junction proteins in the colon tissues, but also suppressed the activation of the PI3K­Akt­mTORC1 signaling pathway. The data indicated that this regimen could alleviate oxazolone­induced UC in mice, which could significantly reduce tissue inflammation and autophagy. The mechanism of action was associated with the PI3K­Akt­mTORC1 signaling pathway.

Complete Genome Sequence of a Bluetongue Virus Serotype 15 Strain Isolated from China in 1996.

The full-genome sequence of bluetongue virus serotype 15 (BTV-15) strain B105/YN/1996 isolated in China was determined for the first time. The virus was isolated from sentinel cattle in Yunnan Province, China, in 1996. The total size of the BTV-15 strain B105/YN/1996 genome is 19,161 bp in length. Phylogenetic analyses demonstrate that it belongs to the major eastern BTV topotype. This work is the first to document the complete genomic sequence of a BTV-15 strain from China. The sequence information will help determine the geographic origin of Chinese BTV-15 and provide data to facilitate future analyses of the genetic diversity and phylogenetic relationships of BTV strains.

Full-Genome Sequence of Bluetongue Virus Serotype 1 (BTV-1) Strain Y863, the First BTV-1 Isolate of Eastern Origin Found in China.

The full-genome sequence of the bluetongue virus serotype 1 (BTV-1) strain Y863, the first BTV-1 isolate of Eastern origin found in China, was determined. The virus was isolated from sheep during a severe outbreak of bluetongue in Shizhong County, Yunnan Province, southwest China, in 1979. The total size of the BTV-1 strain Y863 genome is 19,170 bp. Phylogenetic analyses demonstrate that it belongs to the major "Eastern" BTV topotype. The sequence information provided here will help in understanding the geographical origin and spread of this Chinese isolate of BTV-1, as well as aid in its comparison with global isolates of BTV-1 from sheep, cattle, and other host species origins.

Full genome sequence of bluetongue virus serotype 4 from China.

The complete genomic sequence of a bluetongue virus serotype 4 (BTV-4) strain (strain YTS-4), isolated from sentinel cattle in Yunnan Province, China, is reported here. This work is the first to document the complete genomic sequence of a BTV-4 strain from China. The sequence information will help determine the geographic origin of Chinese BTV-4 and provide data to facilitate future analyses of the genetic diversity and phylogenetic relationships of BTV strains.

Guanethidine treatment does not block the ability of central leptin administration to decrease blood glucose concentrations in streptozotocin-induced diabetic rats.

Leptin, administered either into the ventricles of the brain or systemically, has been shown to normalize blood glucose concentrations in streptozotocin (STZ)-induced diabetic rats. We hypothesized that an intact sympathetic nervous system is necessary for centrally administered leptin to normalize or attenuate high blood glucose concentrations in STZ-induced diabetic rats. Young male Wistar rats (approximately 50 g) were treated every other day with either s.c. guanethidine (100 mg/kg) or vehicle for 2 weeks. Rats were then implanted with an intracerebroventricular cannula directed to the lateral ventricle and made diabetic with an i.v. injection of STZ (50 mg/kg). Half of the animals in each group were given daily injections of leptin (10 microl), while the remaining animals received vehicle injections. Blood glucose concentrations were measured daily and tissue norepinephrine content was determined by high performance liquid chromatography at the end of the study. Guanethidine pretreatment did not block the ability of centrally administered leptin to decrease blood glucose concentrations in diabetic rats. This suggests that the sympathetic nervous system does not mediate the leptin-induced attenuation of high blood glucose concentrations observed in diabetic rats.