[Objective] To establish a method for rapid identification of Fructus Citri Sarcodactylis (FCS) from different production areas. [Methods] Fourier transform infrared (FTIR) spectroscopy was adopted to identify FCS. The height and position of the characteristic absorption peaks, and I value (a quantitative parameter of peak height ratio) were compared in FCS from different production areas. [Results] Each kind of FCS had their fixed range in peak height ratio I: 0.7-0.9 in FCS from Guangdong, 1.3-1.6 in FCS from Sichuan, 0.9-1.1 in FCS from Zhejiang, indicating that I value can be used to identify FCS from different areas . [Conclusion] For the identification of FCS from different production areas, FTIR spectroscopy is an effective method, in which there is no need for isolation, purification and chemical treatment.

Hepatic nodules in patients with Budd-Chiari syndrome (B-CS) are identified in clinical work and the differentiating diagnosis is very important for making the treatment strategy.Most B-CS patients with hepatic nodules have nonspecific clinical manifestations.Ultrasonography,computed tomography and magnetic resonance imaging are often used for differentiating diagnosis.According to the results of retrospective study on clinical and imaging data of 51 B-CS patients with hepatic nodules,we draw a conclusion that the differentiating diagnosis of hepatic nodules in patients with B-CS depends on imaging characteristics.Different treatment strategies are adopted according to the comprehensive analysis of these imaging data and satisfactory results can be achieved.

Objective To develop a HPLC method for the determination of oridonin in the leaves and stems of Rabdosia nervosa.Methods All of reference substances and samples were separated with the mobile phase of methanol:water (45 ∶55) under isocratic elution for 20 min on a Kromasil C18 reversed-phase column(250 mm?4.0 mm,5 ?m),the flow rate was 1.0 mL?min-1,the detection wavelength was 235 nm,and the column temperature was 30 ℃.Results The content of oridonin was 0.047 mg/g in stems and 0.791 mg/g in leaves,the content in stems being about one seventeenth of that in leaves.The average recovery of oridonin was 98.33 %.Conclusion This method is simple,sensitive,accurate and suitable for quantitative determination of oridonin in Rabdosia nervosa.

Objective To establish the HPLC fingerprints(HPLC-FPS)of Fructus Citri Sarcodactylis(FCS)from Guangdong for reflecting the internal chemical information,evaluating its internal quality of FCS and identifying them from different cultural areas.Methods The HPLC-FPS of 12 FCS samples were obtained.The HPLC separation was performed on a Kromasil C18 analytical column by gradient eluting with acetonitrile-0.5% acetic acid at the flow rate of 1.0 mL/min.The column temperature was 30 ℃,the UV detection wavelength was 290 nm,and the collection time was 75 min.Results The mutual mode of HPLC fingerprints was set up and the similar degrees to the crude drugs from different cultural areas were compared.Conclusion The method is stable,reliable,and with full information which can be used as a quality control item for FCS from Guangdong.

AIM: To investigate the role and signal mechanism of PPAR-α in the pathogenesis of cardiac hypertrophy. METHODS: Small interfering RNA (siRNA) was applied to efficiently silence the gene expression of PPAR-α in cardiac myocytes. [~3H] leucine incorporation assay was performed to measure protein synthesis. Reverse transcription-polymerase chain reaction (RT-PCR) was used to analyze the mRNA level of atrial natriuretic factor (ANF) and PPAR-α. Western blotting analysis was performed to investigate the levels of phosphorylation of protein kinase B (PKB/Akt) and glycogen synthase kinase 3β (GSK3β). Immunofluorescence analysis was used to examine the cellular localization of NFATc4. RESULTS: (1)RSS304168 was the most efficient stealth RNAi duplex to specifically inhibit PPAR-α expression. (2)RSS304168 significantly potentiated the ET-1-induced cardiomyocyte hypertrophy and enhanced ET-1-induced protein synthesis and ANF mRNA expression in cardiomyocytes. Moreover, RSS304168 completely reversed the inhibitory effects of fenofibrate on ET-1-induced protein synthesis and ANF mRNA expression. (3)RSS304168 enhanced ET-1-induced phosphorylation of Akt at Ser473 and GSK3β at Ser9. The effects of ET-1 or ET-1 combined with RSS304168 on phosphorylation of Akt/GSK3β were completely blocked by LY294002, a PI3K specific inhibitor. Fenofibrate markedly inhibited ET-1-induced phosphorylation of Akt/GSK3β while RSS304168 abolished these effects of fenofibrate. (4)Fenofibrate prevented the nuclear translocation of NFATc4 induced by ET-1 while RSS304168 abolished this effect of fenofibrate. CONCLUSION: Activation of PPAR-α inhibits ET-1-induced cardiomyocyte hypertrophy through blocking Akt/GSK3β-NFATc4 signaling pathways.

OBJECTIVE: To investigate the potential risk factors and management of excessive epistaxis after endoscopic endonasal surgery (EES). METHOD: Six hundred and forty-one patients who underwent EES in our hospital from December 2011 to December 2012 were reviewed retrospectively. Factors which potentially affect the incidence of excessive epistaxis after EES were analyzed with univariate and multivariate logistic regression model. RESULT: The incidence rate of excessive epistaxis after EES was 8.4% in our study. Multivariate logistic regression analysis revealed that history of previous EES, along with other four factors, correlated significantly with the occurrence of excessive epistaxis after EES. CONCLUSIONS Previous EES, along with other three factors, may increase the chance of excessive epistaxis after EES, while pre-operative corticosteroid therapy may reduce the risk to some extent.
Adolescent ; Adult ; Aged ; Child ; Endoscopy ; adverse effects ; Epistaxis ; etiology ; Female ; Humans ; Logistic Models ; Male ; Middle Aged ; Multivariate Analysis ; Nasal Surgical Procedures ; adverse effects ; Nose ; surgery ; Postoperative Complications ; etiology ; Retrospective Studies ; Risk Factors ; Young Adult

OBJECTIVE: to investigate the origin characters of snore in simple snorers and provide the basis for its treatment. METHOD: Thirty-two simple snorers diagnosed by polysomnography were induced to sleep by propofol and dexmedetomidine, then we observed the vibration sites, pattern and concomitant collapse of soft tissue in pharyngeal cavity by nasendoscopy. RESULT: Thirteen cases showed palatal fluttering only, and 1 case showed vibration of epiglottis only. Six cases showed palatal fluttering with vibration of epiglottis, and 2 cases showed palatal fluttering with vibration of epiglottis and tongue base. Five cases showed palatal fluttering with vibration of pharyngeal lateral wall, and 5 cases showed palatal fluttering with vibration of lateral wall, epiglottis and tongue base together. Palate and pharyngeal lateral wall vibrated strongly and always collapsed with vibrating, but epiglottis and tongue base usually vibrated slightly and seldom collapsed. CONCLUSION The palatal fluttering is the main source of snoring sounds for most simple snorers, then followed by vibration of palatal and pharyngeal lateral wall together. The site of collapse in pharyngeal cavity is consistent with the main site of vibration.
Endoscopy ; Epiglottis ; physiopathology ; Humans ; Palate ; physiopathology ; Pharynx ; physiopathology ; Polysomnography ; Propofol ; Sleep ; Sleep Apnea, Obstructive ; Snoring ; diagnosis ; Tongue ; physiopathology

Objective To explore the effect of electroacupuncture on CD 34 +VEGFR2 +endothelial progenitor cell (EPC)-derived vessels and stromal cell-derived factor-1α(SDF-1α)/CXCR4, and study its mechanism of promoting an-giogenesis in hippocampus after focal cerebral ischemia /reperfusion .Methods A total of 180 healthy male adult Sprague Dawley (SD) rats were randomly divided into sham operation (sham) group, model (I/R) group, electroacupuncture (I/RE) group, I/RE plus AMD3100 (A specific antagonist of CXCR4) group (I/REA) and AMD3100 (I/RA) group. The rats received filament occlusion of the right middle cerebral artery for 2 hours followed by reperfusion .Electroacupunc-ture was applied to “Baihui” (GV20)/“Siguan” (Hegu LI 4/Taichong LR 3) acupoints for 30 min, once a day.The mR-NA expression of SDF-1αand CXCR4 were detected by reverse transcription-polymerase chain reaction ( RT-PCR) .Double immunofluorescence was used to stain CD 34 +VEGFR2 +EPC-derived vessels.Results Compared with the sham group, the mRNA expressions of SDF-1αand CXCR4 were significantly upregulated in I/R and I/RE group ( P<0.05 ) , but that in I/RE group was more significantly increased than I/R group(P<0.05).In addition, the mRNA expression of SDF-1αand CXCR4 were highly increased on day 1 in the I/REA group than that of I/RE group, but decreased than that of I/RE group on day 7 after reperfusion (P<0.01).CD34 +VEGFR2 +EPCs-derived vessels were obviously increased on 3d and 7d in the I/RE group compared with that of the I/R group, and significantly decreased on 7d in the I/REA group compared with that of the I/RE group ( P<0.01) .Conclusions Electroacupuncture can effectively promote an-giogenesis through upregulating the expression of SDF-1αand CXCR4 in rat ischemic hippocampus after focal cerebral is-chemia/reperfusion.

Objective to investigate the level of platelet leukocyte aggregates in patients with acute cerebral infarction and their short term prognosis.Methods 105 patients with acute cerebral infarction onset within 24 hours were selected continuously,then platelet leukocyte aggregates including neutrophil aggregates (PNA) and platelet monocyte aggregates (PMA) and platelet lymphocyte aggregates (PlyA) were detected by flow cytometry within 24 hours of admission and the incidence of 14 days.modified Rankin Scale(mRS) was performed at 14 days of onset,as a prognostic indicator,and the mRS score was good at 3.The score >3 mRS was divided into poor prognosis.The level of platelet leukocyte aggregates was detected in 50 healthy subjects.Results (1) The platelet leukocyte aggregates in patients with acute cerebral infarction group were significantly higher than that of the healthy group,which was statistically significant (P<0.05).(2)MRs score <3 group and mRS score >3 score comparison,the difference of white blood cell aggregates was statistically significant(P<0.05).Conclusion leukocyte aggregates could be used as an index of short-term prognosis in patients with acute cerebral infarction.

Background and purpose:Drug resistance is a major cause of failure in lung cancer chemotherapy. This study aimed to investigate the effect of YAP on doxorubicin resistance in lung cancer and its underlying mechanism. Methods:Doxorubicin resistant lung cancer cell clones were established from parental sensitive cancer PC9 cell line via in vitroinduction, and the expression of YAP was analyzed. YAP was down-regulated via shRNA to different levels. MTS assay was employed to determine cell proliferation and drug sensitivity. Flow cytometry was used to determine cell cycle distribution, apoptosis and uptake of Rh-123. Western blot and quantitative real-time polymerase chain reaction (QRT-PCR) assay were used to determine the expression of ABCB1, ABCC1, p53, Runx2, ITGB2 and ErbB4. The phosphory-lation of serine/threonine kinase (AKT) was determined as well.Results:Doxorubicin resistant PC9/Adr cell clone was obtained with over-expressed YAP. Expression of YAP in PC9/Adr cells was down-regulated to different levels via shR-NA. After YAP silencing, cell proliferation was reduced, while sensitivity to doxorubicin was increased. The cell cycle was significantly halted by G0/G1 phase. Doxorubicin induced-apoptotic rate and cellular uptake of Rh-123 were increased,with positive correlation to YAP silencing level. Western blot and QRT-PCR results showed that after YAP silencing, ABCB1, ABCC1, Runx2, ITGB2, and ErbB4 proteins were down-regulated, while the expression of p53 was up-regulated. Phosphorylation of AKT was inhibited as well.Conclusion:Over-expression of YAP is involved in doxorubicin resistance in PC9/Adr cell line. Silencing of YAP could restore doxorubicin sensitivity. The mechanism involves regulation of drug resistance-related genes and promotion of apoptosis.