0.05). - 40 mV activated threshold potential and - 30 mV peak potential for control group respectively droppedto - 60 mV and - 40 mV after irradiating 7 min. The half-activation voltage and the slope factor of the activationcurves of Na+ channel were also changed by the laser's exposure. The former changed from (- 42.091 ?1.537) mVto (54.971 ?1.846) mV (n= 8, P

Objective: To study the biotransformation of Poria cocos by Ganoderma lucidum and the changes of total polysaccharide and total triterpenes contents of the biotransformation products. Method: The experiment uses the microwave method to extract and sulfuric acid-phenol method to measure total polysaccharide content. And the ultrasonic wave method was used to extract total triterpenes and the content was measured by vanillin-perchloric method. Result: After treatment by G. lucidum, the total polysaccharide and triterpenes content of the biotransformation products were significantly higher than the non-conversed P. cocos (P<0.01), showing that the original performance of P. cocos was changed by way of biotransformation of G. lucidum; P. cocos had a promotion effect on the growth of G. lucidum. Conclusion: Biotransformation of P. cocos for Increasing the total polysaccharide and triterpenes contents by using G. lucidum has advantages of simple, low cost and so on. This method has a certain application value in modernization of Chinese traditional medicine.

AIM: To establish the quality standard for Gubiling Capsules (Penis Et Testis Canis, Radix Noto ginseng, Radix Achyranthis Bidentatae, Herba Epimedii, Radix Aucklandiae, etc.). METHODS: Radix Achyranthis Bidentatae, Herba Epimedii, Radix Aucklandiae were identified by TLC, and the ginsenoside Rg 1 content was determined by HPLC. RESULTS: Ginsenoside Rg 1 showed a good linear relationship in the range of 1.2-6.0 ?g ( r = 1.00 0 ) and average recovery was 96.9%. RSD was 0.4%. CONCLUSION: These methods are simple, accurate and specific and can be used for the quality control for Gubiling Capsules.

Objective To investigate the correlation between diabetes and brainstem infarction. Methods The diagnozed patients with acute cerebral infarction were recruited in the study. Firstly, they were divided into brainstem infarction group and non-brainstem infarction group, and then they were redivided into brainstem infarction with diabetes, brainstem infarction without diabetes, non-brainstem infarction with diabetes and non-brainstem infarction without diabetes groups according to whether they had diabetes or not. Carotid artery intima-media thickness (IMT) and carotid atherosclerosis were detected and identified with Doppler ultrasound; brain stem infarction and its location were identified with diffusion-weighted imaging; basilar artery atherosclerosis was detected with magnetic resonance angiography (MRA). A multivariate logistic regression analysis was used to screen the different risk factors impacting brainstem infarction. Neurological deficit was evaluated with the modified Rankin Scale (mRS)scores. Results A total of 286 patients with acute cerebral infarction were recruited: brain stem infarction in 63, and 34 of them with diabetes; non-brain stem infarction in 223, and 77 of them with diabetes. The proportions of diabetes (54. 0％ vs. 34. 5%, x2 = 7. 816, P = 0. 005),previous cerebral infarction (38. 1％ vs. 24. 2％ ,x2 =4. 771, P =0. 029), basilar artery atherosclerosis (73.0％ vs. 57. 4％,x2 =5. 028, P =0. 025), as wall as the levels of hemoglobin A1C (HbA1c) (7. 30 ± 2. 42％ vs. 6. 46 ± 1.82％, t = - 2. 531, P = 0. 011 ) and apolipoprotein B (ApoB) (0. 97 ± 0. 33 mmol/L vs. 0. 90 ± 0. 34 mmol/L, t =-2. 180, P = 0. 029) in the brainstem infarction group were significantly higher than those in the non-brainstem infarction group. Multivariate logistic regression analysis showed that diabetes (odds ratio [ OR] 2. 150, 95％confidence interval [ CI] 1. 214-3. 808; P =0. 009) and previous cerebral infarction (OR 1. 835, 95％ CI 1.004-3. 352, P = 0. 048) were the independent risk factors for brainstem infarction. There were significant differences in the levels of HbA1c (P ＜ 0. 001 ), fasting blood glucose (FBG) (P ＜0. 001), ApoB (P =0. 007) and high-density lipoprotein cholesterol (P =0. 018) as well as the proportion of basilar artery atherosclerosis (P = 0. 001 ) among the brainstem infarction with diabetes, without diabetes, non-brainstem infarction with diabetes and without diabetes groups. The levels of HbA1c (8. 81 ±2. 36％), FBG (8. 23 ±3. 12 mmol/L andApoB (1.04 ± 0. 41 mmol/L) as well as the proportion of basilar artery atherosclerosis (85. 3％ )were the highest in the brainstem infarction with diabetes group. Conclusions Diabetes is closely associated with brainstem infarction. Diabetes is more likely to result in pontine infarction.

Objective To analyze the relationship between diabetics and the onset, clinical outcomes and prognosis of brainstem infarction, and to evaluate the impact of diabetes on brainstem infarction. Method Compare 172 cases of acute brainstem infarction in patients with or without diabetes.Analyze the associated risk factors of patients with brain-stem infarction in diabetics by multi-variate logistic regression analysis. Compare the National Institutes of Health Stroke Scale (NIHSS) and Modified Rankin scale (mRS) Score, pathogenetic condition and the outcome of the two groups in different times. Results The systolic blood pressure ( SBP ), TG, LDL-C, apolipoprotein B ( Apo B ), glutamyl transpeptidase (γ-GT), fibrinogen(Fb), fasting blood glucose (FPG) and glycosylated hemoglobin( HbA1c)in diabetic group were higher than those in non-diabetic group , which was statistically significant ( P ＜ 0. 05 ). From multi-variate logistic regression analysis, γ-GT, Apo B and FPG were the risk predictors of diabetes with brainstem infarction( OR = 1. 017, 4. 667 and 3. 173, respectively), while HDL-C was protective( OR =0. 288). HbA1c was a risk predictor of severity for acute brainstem infarction( OR = 1. 299), while Apo A was beneficial( OR =0. 212). Compared with brain-stem infarction in non-diabetic group, NIHSS score and intensive care therapy of diabetic groups on the admission had no statistically significance, while the NIHSS score on discharge and the outcome at 6 months' of follow-up were statistically significant. Conclusions Diabetes is closely associated with brainstem infarction. Brainstem infarction with diabetes cause more rapid progression, poorer prognosis, higher rates of mortality as well as disability and higher recurrence rate of cerebral infarction.

Objective To investigate the effects of unaggregated amyloid ? protein(A?25～35) on transient outward potassium channel(IA) in Rat Hippocampal CA3 Pyramidal Neurons.Methods Patch-clamp technique with whole cell recording was used.Results Unaggregated A?25～35 inhibited IA in neonatal rat hippocampal CA3 pyramidal neurons and displayed a time-,concentration- and voltage-dependent manner;the dynamic characteristics of IA were influenced:shifted the steady-state activation and inactivation curves to left significantly.Conclusion These results suggest that the inhibition of unaggregated A?25-35 on transient outward potassium channel in acutely isolated hippocampal CA3 pyramidal neurons may be an important mechanism of its toxicity,which participates in pathological changes of AD.

Objective To investigate the effects of β-Elemene on the apoptosis of human pancreatic cancer Panc-1 cells; To discuss its mechanism of action. Methods β-Elemene (10, 20, 40, 80, 160 μg/mL) were incubated to the Panc-1 cells in vitro cultured for 24 h, 48 h and 72h, and trypan blue refusal method was used to detect cell inhibition rate;Apoptosis rate was measured by TUNEL; Hoechst33258 fluorescent staining was used to observe the changes of the nucleus. The activity of Caspase-3, 8 and 9 were detected by ELISA. Western blot was used to detect the expressions of Fas, FasL and Cyt c and AIF. Results The activity of Panc-1 cells was obviously inhibited time/concentration dependent inhibition (P<0.05, P<0.01), and the apoptosis rate increased after incubated with β-Elemene (P<0.01, P<0.001) after incubated with β-Elemene for 24 h, 48 h and 72 h; After giving β-Elemene 72 h, Panc-1 cells nucleus were broken obviously, and chromatin condensed and showed strong blue fluorescence, along with of apoptotic bodies; After incubated with β-Elemene for 48 h, Caspase-3, 8 and 9 activity significantly increased (P<0.05, P<0.01); protein expressions of Fas, FasL, Cyt c and AIF were significantly enhanced (P<0.05, P<0.01, P<0.001). Conclusion β-Elemene can inhibit Panc-1 cell proliferation, induce apoptosis, and the mechanism may be related to activating cell death receptor pathway and mitochondrial apoptosis pathway to play anti-tumor effects.

Objective To investigate the virus-carrying rate of non-polio enteroviruses ( NPEV) in patients with acute flaccid paralysis ( AFP) in Yunnan province of China in 2015 and to analyze the genetic characteristics of enterovirus 71 (EV71) strains. Methods A total of 213 cases under 15 years old with AFP were reported by Center for Disease Control and Prevention ( CDC) of Yunnan Province of China. Virus isolation was conducted for all samples and the serotypes of isolated NPEV strains were identified by VP1 se-quencing. The isolation rates of NPEV in the past consecutive 5 years were analyzed by SPSS22. 0 software. Phylogenetic trees of NPEV and EV71 strains were constructed by MEGA6. 06 software based on neighbor-joining algorithm and Kimura 2-parameter substitution model and the reliability of the phylogenetic trees was determined by bootstrap analysis with 100 pseudo replicate datasets. Results Altogether, 23 NPEV strains were isolated from 213 AFP cases. Among the 23 strains, 7 strains belonged to EV-A group (2 serotypes, 6 strains of which were EV71 ) , 14 strains belonged to EV-B group ( 8 serotypes ) and the other 2 strains belonged to EV-C group. No NPEV strains of EV-D group were identified. Statistical analysis showed that no significant differences in the isolation rates were observed in the past 5 years ( P=0. 101 ) . Conclusion The isolation rate of NPEV in patients with AFP in Yunnan province in 2015 was similar to that of the previ-ous years. The EV71 strains of C4 subgenotype were the predominant strains circulating in Yunnan province.

Objective To investigate the effect of splenectomy on infarct volume in middle cerebral artery occlusion in focal cerebral ischemia rats and its possible mechanisms.Methods Eighteen male Sprague-Dawley rats were randomly divided into spleneetomy,sham splenectomy,and control groups (n =6 in each group).A model of middle cerebral artery occlusion (MCAO) was induced by the intraluminal suture method 2 weeks after spleneetomy.The rats were decapitated and their brains were removed after 24 hours.The infarct volume was measured with Nissl body staining The number of macrophages in ischemic cortex was detected with immunofluorescence staining Results The infarct volume in the splenectomy group (34.93％ + 3.23％ )was significantly smaller than that in the sham splenectomy group (74.33％ + 2.36％ ; q =39.399,P ＜ 0.001 ) and the control group (77.30％ + 2.62％ ; q =42.369,P ＜ 0.001 ).However,there was no significant difference between the sham splenectomy group and the control group (q =2.970,P =0.082).The number of macrophages of the ischemic cortex in the splenectomy group (3.4 ± 1.07/per high power field) was significantly less than that in the sham splenectomy group (20.7±4.37/per high power field; q =17.300,P＜0.001) and the control group (18.87 ±4.17/per high power field; q =15.467,P ＜0.001).However,there was no significant difference between the sham splenectomy group and the control goup (q =1.833,P =0.384).Conclusions Splenectomy may reduce the infarct volume by reducing the number of macrophages in ischemic corticalregion.

Objective To find an ideal animal model of acute respiratory distress syndrome (ARDS) through investigating the characteristics of three two-hit animal models of ARDS.Methods Forty-eight SD rats were randomly divided into 4 groups: Control group [2.5 mL/kg normal saline (NS) i.v.given at 0 min and 30 min];OA+OA group [0.5 mL/kg oleic acid (OA) i.v.given at 0 min and 30 min];LPS+LPS group [2.5 mg/kg lipopolysaccharide (LPS) i.v.given at 0 min and 30 min];and OA+LPS group [0.5 mL/kg OA i.v.given at 0 min and 2.5 mg/kg LPS,i.v.given at 30 min].The samples were collected at 5 h after the second drug injection.White blood cells count (WBC),polymorphonuclear leukocyte ratio (PMN%),total protein concentration,tumor necrosis factor α (TNF-α) level in bronchoalveolar lavage fluid (BALF),arterial blood gas analysis and lung wet-dry weight ratio (W/D) were measured,respectively.Pathological changes in the lung tissues were observed and histological scores were evaluated.Results Compared with those in the control group,PaCO2,WBC,PMN%,total protein concentration and TNF-α levels in BALF were significantly increased,while PaO2 was dramatically decreased (P<0.01) in the OA+OA,LPS+LPS and OA+LPS groups.The levels of protein concentration in BALF and lung W/D ratio in the OA+LPS group were significantly higher than these in the LPS+LPS group (P<0.05 for all),but had no statistically significant difference compared with these in the OA+OA group.The levels of WBC,PMN% and TNF-α in BALF in the OA+LPS group were significantly higher than those in the OA+OA group (P<0.05),but not significantly different from those in the LPS+LPS group.The most typical pathological changes and the highest pathological scores were found in the OA+LPS group.Conclusions All the three different methods including OA+OA,LPS+LPS,and OA+LPS can be used to establish “two-hit” animal models of acute respiratory distress syndrome.The “two-hit” animal model of acute respiratory distress syndrome induced by OA+LPS is more closer to clinical ARDS and is useful for studies on the pathophysiology of ARDS,and is an ideal “two-hit” animal model of ARDS.