Objective: To prepare voriconazole (VCZ) sulfonated butyl ether-β-cyclodextrin (SBE-β-CD) inclusion compound and study the properties in vitro.Methods: VCZ SBE-β-CD inclusion compound was prepared respectively by a stirring method, an ultrasonic method and a grinding method, and the one with the highest inclusion rate and inclusion compound yield was chosen as the final preparation method.The formula and preparation process were optimized by an orthogonal design.The inclusion compound was identified by differential scanning calorimetry and solubility determination, and the in vitro dissolution was determined as well.Results: The stirring method had the highest inclusion rate and inclusion compound yield, and the optimal preparation and formula conditions were as follows: the inclusion temperature was 25℃, the stirring time was 4 h and the amount ratio of VCZ to SBE-β-CD was 1∶1.After the optimization, the inclusion rate was (86.14 ± 0.69)%, and the yield of inclusion compound was (97.11 ± 0.31)%.After the inclusion, the characteristic peak of VCZ disappeared and the solubility of VCZ increased significantly.Compared with those of VCZ, the dissolution rate and amount of VCZ inclusion compound both increased notably.Conclusion: VCZ SBE-β-CD inclusion compound can be prepared by the stirring method, which lays foundation for the further studies on VCZ eye drop.

OBJECTIVE To analyze the cleaning efficiency of using Ruhof multi-enzyme detergent to clean endoscopies. METHODS Take 80 sets of used endoscopies as samples and clean them with multi-enzyme detergent in "four-trough" way as instructed by the Ministry of Health.After cleaning,the changes in bio-burden residual on the endoscope′s surface and jet obstruction were observed. RESULTS After cleaning the endoscopes with Ruhof multi-enzyme detergent,the bio-burden residual on the endoscope′s surface as well as jet obstruction,and the surface cleanness evaluation value had decreased enormously.The difference value before and after cleaning was significant(P

IEEE Std 1708-2014 breaks through the traditional standards of cuff based blood pressure measuring devices and establishes a normative definition of wearable cuffless blood pressure measuring devices and the objective performance evaluation of this kind of devices. This study firstly introduces the background of the new standard. Then, the standard details will be described, and the impact of cuffless blood pressure measuring devices with the new standard on manufacturers and end users will be addressed.
Blood Pressure ; Blood Pressure Monitors ; standards ; Humans ; Reference Standards ; Telemedicine

The changes of the hemorheology, plasma cholesterol and albumin and clinicaleffects in 36 children with refractory nephrosis after treatment with polysaccharide sulfate (PSS) were observed. The results showed that the indices of hemorheology and the plasma cholesterol decreased obviously and the albumin increased obviously than the control group ( P

nses (P<0.01).Standardized management is favorable in community management of patients with coronary heart disease.

Objective:To establish an HPLC method for the determination of isomeric impurity in fasudil hydrochloride. Meth-ods:The chromatographic method was carried out on a Kromasil 100-5 Phenyl C18 column with phenyl bonded silica as the filler (250 mm × 4. 6 mm, 5 μm), and phosphate buffer (10 mmol· L-1 ammonium dihydrogen phosphate, adjusting pH to 4. 0 with 1% phos-phoric acid) -acetonitrile (80∶ 20) was used as the mobile phase. The detection wavelength was 275nm and the column temperature was 40℃. The flow rate was 1. 0 ml· min-1 , and the injection volume was 10 μl. Results:Fasudil hydrochloride and its derivative was linear within the range of 0. 148-2. 960 μg·ml-1(r=1. 0000) and 0. 101-2. 014μg·ml-1(r=0. 999 9), respectively. The av-erage recovery of isomer impurity in fasudil hydrochloride was 101. 9% with RSD of 0. 98%(n=9). Conclusion:The method is sim-ple,accurate and reproducible,which can be used for the quality control of fasudil hydrochloride and its isomer.

According to the teaching practice in biochemistry laboratory course,we describe the characteristics of international students'teaching,teaching preparation,teaching course and so on.These experiences may provide an important source of information for teaching practice in the future.

Objective To observe the effects of turicamycin-inhibitor of N-glycosylation of proteins on expression of (?1 integrin,FAK and cyclin D1 in high glucose-induced glomerular mesangial cells (CMC), and to explore the mechanism concerned. Methods Cultured HBZY-1 rat mesangial cells were divided into 5 groups:control group;high glucose group;mannitol group;high glucose plus TM group; TM group.The expression of ?1 integrin was measured by flow cytometry, expression of FAK and cyclin D1 was measured by immunohistochemistry,and proliferation of GMCs was measured by MTT. Results There was a little expression of ?1 integrin, FAK and cyclin D1 on normal mesangial cells. High glucose induced the proliferation and increased the expression of ?1 integrin and cyclin D1.There was no significant difference in mannitol group as compared to control group.The expression of (?1 integrin FAK and cyclin D1 decreased notably by TM.TM could also decrease proliferative abilitiy of cells. All the effects of TM were dose-dependent. Conclusion Through blocking glycosylation of glycoprotein, TM can suppress cellular proliferation and expression of pi integrin induced by high glucose in a dose-dependent manners,then pi integrin affects the expression of FAK and cyclin D1.

Objective To confirm the protective effect of berberine (BBR) on cold ischemia reperfusion (I/R)-induced liver injury and to show whether the hepatic protection conferred by BBR involves the activation of phosphatidylinositol 3 kinase (PI3K) / protein kinase B (Akt)/mammalian target of rapamycin(mTOR) signal pathway.Method Adult male Sprague-Dawley rats were assigned randomly to four groups:BBR group (BBR was intragastrically administered at a dose of 100 mg·kg-1 · d-1 2 weeks before hepatic cold I/R treatment),dimethyl sulfoxide (DMSO) group (BBR was replaced by DMSO,and others were the same as BBR group),I/R group (BBR was replaced by normal saline,and others were the same as BBR group) and sham group (normal saline was administered 2 weeks before opening and closing abdomen treatment).Then the rats were sacrificed at 3,6,and 24 h after reperfusion.The liver function,oxidative stress level,apoptosis rate,and the expression of PI3K/Akt/mTOR related pathway proteins were assayed.Result As compared with sham group,the I/R-induced liver tissue displayed severe lobular distortion with widespread necrosis,high level of oxidative stress and apoptosis rate.As compared with I/R group,BBR dramatically attenuated the histopathologic damage,restored the liver function and decreased the oxidative stress level.Simultaneously,BBR significantly ameliorated the apoptosis by decreasing the apoptosis rate,increasing the Bcl-2/Bax ratio and inhibiting caspase-3 activity in rats subjected to hepatic I/R.The expression of p-Akt was effectively upregulated with the inhibited expression of p-mTOR.Conclusion Our result provides robust in vivo evidence that BBR can prevent I/R-induced oxidative stress and apoptosis.The mechanisms involved can be attributed to the activation of P]3K/Akt/mTOR signal pathway.

AIM:To observe the effect of MK-2206, an inhibitor of Akt, on the cell apoptosis and autophagy of U2OS cells.METHODS:The cell viability was detected by MTT assay .The cell apoptosis was analyzed by TdT-media-ted dUTP nick end labeling assay .The expression of LC3-II was examined by Western blotting .RESULTS:MK-2206 in-hibited the cell viability in a dose-dependent manner .MK-2206 induced the cell apoptosis via activation of caspase-3, caspase-9 and PARP.MK-2206 treatment substantially induced the U 2OS cell autophagy by increasing in the levels of LC 3-II.Blockage of autophagy using chloroquine magnified MK-2206-induced cell death in U2OS cells.CONCLUSION:The Akt inhibitor MK-2206 induces cell apoptosis and autophagy .Blocking autophagy magnifies MK-2206-induced the inhibi-tion of the viability in U2OS cells.