Objective To explore the effects of wogonin on hyperlipidemia in mice and clarify the molecule mechanism. Methods Thirty mice were evenly divided into three group normal control group,model control group and treatment group. The normal control group was given normal diet,the model control group received high-fat diet,the treatment group received high-fat diet with wogonin (500 mg·kg-1 ). Results The mice developed hyperlipidemia 12 weeks after starting the high-fat diet. The body weight,visceral fat and fat index were increased (P<0. 05). After treatment,these indices were reduced ( P < 0. 01). Wogonin significantly reduced the total cholesterol ( TC),low density lipoprotein ( LDL),high density lipoprotein (HDL),except the triglyceride (TG). Compared to the model control group,the hepatic lipase(HL) and lipoprotein lipase(LPL) activity in the treatment group were recovered (P<0. 05),but HMG-CoA reductase activity was inhibited ( P<0. 01). Mechanistic study suggested that the lipid-lowering effect might be related to the lipid synthesis genes (SREBP-1c,FAS, PPARγ) and the lipid metabolism genes (PPARα,CPT-1). Conclusion Wogonin can prevent hyperlipidemia,which might be related to the regulation of enzyme activity and the changes of lipid synthesis and oxidative metabolism.

Objective: To study the effect of ghrelin on L-type calcium channel current (ICa-L) of ventricular myocytes in experimental rats. Methods: The single ventricular myocyte in experimental rats were obtained by enzymolysis method, and the whole-cell patch-clamp technique was used to investigate the effect of ghrelin on ICa-L of ventricular myocytes at different doses of 10 nmol/L, 100 nmol/L and 1μmol/L respectively. Results: Ghrelin at 10 nmol/L, 100 nmol/L and 1μmol/L may inhibit ICa-L at (8.95 ± 2.13) %, (31.18 ± 4.78) % and (64.63 ± 8.57)% respectively,P<0.05, and the current-voltage curve was shifted upwards. The channel half inactivation curve decreased from (-1.34 ± 1.9) mV to (-8.04 ± 1.32 ) mV, (9.76 ± 1.17) mV and (-11.81 ± 0.73) mV respectively,P<0.05, and the recovery time after inactivation was prolonged as τ value from (63.23 ± 9.32) to (98.95 ± 10.74), (109.56 ± 13.42) and (127.39 ± 16.13) respectively,P<0.05. Conclusion: Ghrelin may accelerate ICa-L inactivation and prolong the recovery time after inactivation. Ghrelin inhibits ICa-L in a dose-dependent manner.

OBJECTIVE To observe the effect of baicalin on Aβ25-35 induced learning and memory deficits and changes in autophagy-related genes in mice so as to explore the related mechanisms of Alzheimer disease (AD) treatment . METHODS C57 mice were administered with 3μL Aβ25-35 3 mmol·L-1 by intracerebroventricular injection to establish an AD model. Baicalin was given by intracerebroventricular injection at the dose of 25, 50 and 100 mg · kg-1 for 15 d, respectively. The total distance and the central grid residence time were measured in the open-field test. The escape latency and the time to reach the platform were monitored in the Morris water maze trial. The autophagic vacuoles in the hippocampus of the mice were observed by transmission electron microscopy before the protein expressions of microtu?bule-associated protein 1 light chain 3 (LC3) and Beclin1 in brain tissue were analyzed by Western blot?ting assay. RESULTS Intracerebroventricular injection of Aβ25-35 could reduce the total distance from (3984±321)cm to (2790±306)cm and extend central grid residence time from (3.6±1.2)s to (8.8±2.9)s in the open-field test. The escape latency of water maze also increased from (22.0 ± 1.9)s to (38.8 ± 2.2)s. Autophagic vacuoles or late autophagic vacuoles and increased Beclin1 and LC3 and protein level were observed in the hippocampus after Aβ25-35 injection. Intraperitoneal injection of Baicalin 50 and 100 mg · kg-1 for fifteen consecutive days extended the total distance in open-field test to (3705 ± 337)cm and (3968 ± 448)cm, respectively, while the central grid residence time was reduced to (5.6 ± 1.8)s and (3.9±1.5)s, respectively. The total time taken to reach the platform in water maze test was reduced to (28.6± 1.9)s, (22.9 ± 1.7)s. Mitochondrial swelling, vacuolar membrane structure or autophagic vacuoles were visible in the hippocampus. LC3 and Beclin1 protein expression was significantly up-regulated(P<0.01). CONCLUSION Baicalin shows protective effect against Aβ25-35 induced learning and memory deficits, and this effect may be related to the activation of autophagy in the mouse hippocampus.

Autologous platelet-rich plasma (PRP) is plasma with high concentration of platelet extracted from autologous blood. After activation, growth factors involved in wound healing are released from PRP. Current clinical investigations have demonstrated that the application of PRP seems to enhance the clinical outcome of plastic surgery, oral implantology, maxillofacial region and bone repair, and cardio-thoracic surgery. PRP can stimulate angiogenesis and promote fibroblast proliferation, therefore the application of PRP has shown good results in wound healing. However, up to date there is few current clinical researches on application of PRP on wound healing in burn patients. The application of PRP is not currently standardized, and the effects in burn wounds are poorly understood. This review is to determine if the application of PRP can enhance the clinical outcome of burns and scar formation.

A 54 years old male patient with chronic leg ulcers was admitted in our hospital in November 2017. He was diagnosed as pyoderma gangrenosum by the pathological examination. Then the wound was treated with simple vacuum sealing drainage combined with irrigation of oxygen loaded fluid. This therapy overcame the shortage of hypoxia in the Tibetan Plateau on wound healing, resulting in a better wound healing. The patient was eventually cured and discharged from hospital.

BACKGROUNDNovel influenza A viruses of avian-origin may be the precursors of pandemic strains. This descriptive study aims to introduce a novel avian-origin influenza A (H10N8) virus which can infect humans and cause severe diseases.

METHODSCollecting clinical data of three cases of human infection with a novel reassortment avian influenza A (H10N8) virus in Nanchang, Jiangxi Province, China.

RESULTSThree cases of human infection with a new reassortment avian influenza A(H10N8) virus were described, of which two were fatal cases, and one was severe case. These cases presented with severe pneumonia that progressed to acute respiratory distress syndrome (ARDS) and intractable respiratory failure.

CONCLUSIONThis novel reassortment avian influenza A (H10N8) virus in China resulted in fatal human infections, and should be added to concerns in clinical practice.

Aged ; Antiviral Agents ; therapeutic use ; Female ; Fluoroquinolones ; therapeutic use ; Humans ; Imipenem ; therapeutic use ; Influenza A Virus, H10N8 Subtype ; drug effects ; pathogenicity ; Influenza, Human ; complications ; diagnosis ; drug therapy ; Male ; Middle Aged ; Oseltamivir ; therapeutic use