Objective To observe the effect of digestive load from senna on the adaptive thermogenesis in hypothyroid rats.Methods After being born(d1),rats were given the intraperitoneal injection with a series ratio of 131Ⅰ at neutral temperature 28℃ and a graded developmental hypothyrosis was resulted in.Since d56,they were fed with higher lipid 24 h then fasted 24 h interval to make them sensitive to digestive load.Since d70,senno sides were given intragastrical administration for 14 d to resulted in the digestive load with its empting function of the bowels.Pre-(d67-69)and post-(d85-86)administration of senna under the neutral environmental temperature,all changes of rat temperature,included peaks(℃)and areas under curve(℃?h),were measured and recorded with physiography,during 180 min after being injected with 106 ?g?kg-1 isoprenaline intravenously.The correlation between the effect and the logarithmic dose of 131Ⅰ(nCi?g-1)was analyzed.As well as EC50,the decreased thermogenesis induced by 131Ⅰ,was calculated with peaks and areas under curve respectively.The correlative analysis between the digestive load and the adaptive thermogenesis was performed especially with senna.Results Before and after administrated senna,it was negative correlation between rat temperature change(peaks and areas under curve)induced with isoprenaline and the degree of hypothyrodism(P

A total of 100 HIN1 flu real-time-PCR positive throat swabs collected from fever patients in Zhejiang,Hubei and Guangdong between June and November 2009,were provided by local CDC laboratories.After MDCK cell culture,57 Influenza A Pandemic (H1N1) viruses were isolated and submitted for whole genome sequencing.A total of 39 HA sequences,52 NA sequences,36 PB2 sequences,31 PB1 sequences,40 PA sequences,48 NP sequences,51 MP sequences and 36 NS sequences were obtained,including 20 whole genome sequences.Sequence comparison revealed they shared a high degree of homology (96％～99％) with known epidemic strains (A/Califomia/04/2009(H1N1).Phylogenetic analysis showed that although the sequences were highly conserved,they clustered into a small number of groups with only a few distinct strains.Site analysis revealed three substitutions at loop 220 (221-228) of the HA receptor binding site in the 39 HA sequences:A/Hubei/86/2009 PKVRDQEG→PKVRDQEA,A/Zhejiang/08/2009 PKVRDQEG→PKVRDQER,A/Hubei/75/2009PKVRDQEG→PKVRDQGG,the A/Hubei/75/2009 was isolated from an acute case,while the other two were from patients with mild symptoms.Other key sites such as 119,274,292 and 294 amino acids of NA protein,627 of PB2 protein were conserved.Meanwhile,all the M2 protein sequences possessed the Ser32Asn mutation,suggesting that these viruses were resistant to adamantanes.Comparison of these sequences with other H1N1 viruses collected from the NCBI database provides insight into H1N1 transmission and circulation patterns.

Objective To investigate the clinical significance of combined heart and lung ultrasound in patients with severe left heart failure and pulmonary hypertension. Methods From March 2016 to June 2017, 75 patients with grade Ⅲ and Ⅳ heart failure and dyspnea were enrolled in Qingdao Municipal Hospital Affiliated to Qingdao University. Thirty-three patients had normal pulmonary artery pressure (normal pulmonary arterial pressure group), 25 patients had mild pulmonary hypertension (mild pulmonary hypertension group), and 17 patients had moderate to severe pulmonary hypertension (moderate to severe pulmonary hypertension group). The patient′s plasma B-type natriuretic peptide (BNP) was measured. Left ventricular diameter (LVD), right ventricular diameter (RVD), and left ventricular ejection fraction (LVEF) were measured by echocardiography. The patient′s lungs were observed by lung ultrasonography, and its number was recorded. One-way analysis of variance was used to compare the differences of LVD, RVD, and LVEF in three groups of patients with severe left heart failure. Further comparison between groups was performed using LSD-t test. Kruskal-wallis H test was used to compare the plasma BNP concentration and B-line number in three groups of patients with severe left heart failure. The Mann-Whitney U test was used to further compare the groups. The receiver operating characteristic (ROC) curve of pulmonary hypertension diagnosed by plasma BNP concentration and B line number in patients with severe left heart failure were drwan. Results The concentrations of BNP in patients with normal pulmonary arterial pressure, mild pulmonary hypertension, and moderate to severe pulmonary hypertension were 890 (614, 1516), 1460 (1245, 1950), and 2660 (1670, 3279) ng/L, respectively. The number of B line was 12 (9, 16), 17 (14, 18), 26 (20, 28), and the RVD was (22.1±1.7), (24.9±2.0), (26.3±2.8) mm, respectively. The number of B-line and RVD in the moderate-severe pulmonary hypertension group were both lager than those in the mild pulmonary hypertension group, and the number of B-line and RVD in the mild pulmonary hypertension group were both lager than those in the normal pulmonary artery pressure group. There was significant difference between any two groups (BNP concentration: U=210.500, P < 0.05; U=47.000, 73.000, both P < 0.001;B line number:U=189.000,P < 0.05;U=38.5000,64.000,both P < 0.001;RVD:t=0.553, 0.623, both P<0.001; t=0.656, P<0.05). There was no significant difference in LVD and LVEF between the three groups of patients. The ROC curve showed that the optimal threshold for the diagnosis of pulmonary hypertension in patients with severe left heart failure with BNP concentration was 1225 ng/L. The sensitivity was 85.7%,the specificity was 69.7%,the area under the curve was 0.814,and the 95% CI was 0.717 to 0.911. The optimal threshold for diagnosis of pulmonary hypertension in patients with severe left heart failure was B line number 14, the sensitivity was 88.1%, specificity was 66.7%, the area under the curve was 0.836, and 95%CI was 0.747 to 0.925.Conclusion Patients with severe left heart failure at different pulmonary artery pressure levels have different B-line findings, and the number of B-line increases with the severity of pulmonary hypertension, which warrants further study and application.