Aristolochic Acids ; adverse effects ; Humans ; Kidney Diseases ; chemically induced

Objective:To establish a method for the simultaneous determination of fluoxertine and olanzapine in capsules by re-versed-phase high performance liquid chromatography ( RP-HPLC) . Methods:The successful separation of fluoxertine and olanzapine was achieved on a Phenomenex C18 column (250 mm × 4. 6 mm, 5 μm) with 10 mmol·L-1 potassium dihydrogen phosphate buffer (pH 4. 0)-acetonitrile-methanol (55 ∶40 ∶5, v/v/v) as the mobile phase. The flow rate was 1. 0 ml·min-1, the detection wave-length was 227 nm, the column temperature was 30℃, and the injection volume was 20 μl. Results:Fluoxertine could be well separa-ted from olanzapine under the chromatographic conditions. The linearity between the peak areas and the concentrations was observed within the range of 5. 0-80. 0 mg·L-1(r=0. 999 9) for fluoxertine and 1. 2-19. 2 mg·L-1(r=0. 999 9) for olanzapine. The mean recovery of fluoxertine and olanzapine was 99. 9%(RSD=0. 94%, n=9) and 100. 2%(RSD=2. 08%, n=9), respectively. Con-clusion:The method is simple, sensitive and accurate, and it can be applied in the content determination of fluoxertine and olanzapine in capsules.

Objective:To compare the similarity of dissolution curves of domestic ibuprofen suspension and the imported prepara-tion to provide the basis for the comprehensive quality evaluation of ibuprofen suspension. Methods: The in vitro dissolution of the products from four different manufacturers was investigated in pH 7. 2 phosphate buffer solution. The similarity of dissolution behavior was compared with that of the imported preparation in pH 1. 2 hydrochloric acid solution, pH 4. 5 acetate buffer solution, pH 6. 8 phos-phate buffer solution, pH 7. 2 phosphate buffer solution and water, respectively. Results:The dissolution rate of ibuprofen suspension from the four different manufacturers reached above 80% in 60 min. The dissolution profiles of ibuprofen suspension from two different manufacturers were similar with that of the imported preparation. Conclusion: The dissolution behavior of ibuprofen suspension from different manufacturers is significantly different.

Objective To observe the effect of propofol target-controlled infusion on stress response during nasoscopic procedures.Methods Totally 40 patients with ASA gradesⅠ-Ⅱ scheduled for the nasoscopic operation ware randomly divided into two groups:Group A(propofol continuously injection,2.5 mg?kg-1,n=20)and Group B(propofol target-controlled infusion,4 ?g?ml-1,n=20).The operations were all performed under general anesthesia.Venous blood samples were taken to measure cortisol and blood glucose at three time points:before operation,at 30 min after the operation started,and 60 min after the endotracheal catheter was withdrawn.Meanwhile,HR and MAP of the patients were recorded.Results At both 30 min after the operation started and and 60 min after the endotracheal catheter was withdrawn,Group A showed significantly higher MAP and serum levels of glucose and cortisol than Group B.At 30 min after the operation started:HR:(73?8)/min vs(65?13)/min,t=2.344,P=0.024;MAP:(74?7)mm Hg vs(68?7)mm Hg,t=2.711,P=0.010;blood glucose:(6.28?0.11)mmol/ml vs(5.31?0.15)mmol/ml,t=23.321,P=0.000;cortisol:(125.3?11.5)ng/ml vs(89.6?9.9)ng/ml,t=10.521,P=0.000.At 60 min after the endotracheal catheter was withdrawn:MAP:(79?6)mm Hg vs(73?8)mm Hg,t=2.683,P=0.011;blood glucose:(6.18?0.09)mmol/ml vs(5.62?0.16)mmol/ml,t=10.082,P=0.000;cortisol:(169.1?16.3)ng/ml vs(149.5?15.3)ng/ml,t=3.921,P=0.000.Conclusion Propofol target-controlled infusion can inhibit the stress response caused by nasoscopic operation.

Cell Culture Techniques ; Endothelial Cells ; cytology ; Humans ; Lymphangiogenesis ; physiology ; Lymphatic Metastasis ; Lymphatic Vessels ; pathology ; Neoplasms ; blood supply ; metabolism ; physiopathology ; Vascular Endothelial Growth Factor C ; metabolism ; physiology ; Vascular Endothelial Growth Factor Receptor-3 ; metabolism

This study was designed to investigate inhibitory effects and possible mechanisms of snake venom tripeptide (pENW) on platelet adhesion in order to promote the development of a novel anti-platelet therapy. To study the inhibitory effects of pENW on platelet adhesion, washed platelets pre-incubated with pENW (116.5-466.2 μmol x L(-1)) were used to test the ability of platelet adhesion to fibrinogen. Effect of pENW on fibrin clot retraction was also tested. Effect of pENW on platelets viability was tested by MTT assay. Effect of pENW on reactive-oxygen species (ROS) levels of platelet was studied by flow cytometry assay. Calcium mobilization in Fura-2/AM-loaded platelets was monitored with a spectrofluorimeter. Cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP), thromboxane A2 (determined as its metabolite thromboxane B2) were measured using enzyme immunoassay kits. Akt, ERK and p38 phosphorylation were tested by Western blot. The results showed that pENW inhibited platelet adhesion and fibrin clot retraction in a concentration-dependent manner without cytotoxicity. Intracellular cGMP and cAMP in both resting and thrombin-activated platelets were increased by pENW. In addition, pENW attenuated intracellular Ca2+ mobilization and TXA2 production in platelets stimulated by thrombin. As shown by Western blot assay, Akt, ERK and p38 phosphorylation in thrombin-induced platelet were attenuated by pENW. However, inhibitory effects of pENW had nothing to do with ROS. Thus, pENW exhibited a significant inhibition on platelet adhesion to fibrinogen, which means pENW could block the first step of thrombosis as while as retard the more stable clot formation. The mechanisms of pENW on inhibition platelet adhesion might be related to instant regulations, such as protein kinases.
Blood Platelets ; drug effects ; Blotting, Western ; Calcium ; metabolism ; Cyclic AMP ; metabolism ; Cyclic GMP ; metabolism ; Flow Cytometry ; Phosphorylation ; Platelet Aggregation ; drug effects ; Reactive Oxygen Species ; metabolism ; Snake Venoms ; chemistry ; Thromboxane A2 ; metabolism ; Thromboxane B2 ; metabolism

Background Stickler syndrome is a genetic connective tissue disorder that affects the ocular,skeletal,orofacial and auditory systems.To determine the gene mutation loci can offer a basis for genetic diagnosis and management of Stickler syndrome.Objective The aim of this study was to research the clinical characteristics of a pedigree with Stickler syndrome and identify the disease-causing gene mutation.Methods This study was approved by Ethic Committee of Peking Union Medical College Hospital.The clinical study and pedigree analysis were performed in one family with Stickler syndrome type Ⅰ (STL Ⅰ).Nine family members were examined with informed consent.The entire coding regions of COL2A1 gene with flanking intronic regions were amplified by PCR and directly sequenced.The detected sequence change was confirmed to be mutationloci by examining whether they existed in normal control individuals.Mutant proteins were predicted with online software.Results There were 4 generations and 11 members in this family,and 2 members died,including 1 patient.Three patients were found in 9living families.Inheritance of this family complicd with an autosomal dominant inheritance mode.All affected individuals showed the consistent phenotypes with STL Ⅰ,including high myopia,membranous vitreous anomaly and surface central flat,short nose,palatoschisis,etc.Mutation screening of COL2A1 gene revealed that the first base of intron 12 was deleted(IVS12+1G del).Nucleotide sequence analysis showed that this mutation led to the functional abnormal of this gene by forming termination cordon in advance.This mutation occurred in all affected individuals,however,no mutation was observed in any unaffected member or 100 normal unrelated individuals.Conclusions This study identifies a novel splice-site mutation(IVS12+ 1G del)in COL2A1 gene in a Chinese STL Ⅰ pedigree.This is the first report on a mutation in a Chinese STL Ⅰ family.

Adult ; Aged ; Agranulocytosis ; chemically induced ; Antineoplastic Agents, Alkylating ; administration & dosage ; adverse effects ; therapeutic use ; Brain Neoplasms ; secondary ; therapy ; Carcinoma, Non-Small-Cell Lung ; pathology ; Chemoradiotherapy ; Dacarbazine ; administration & dosage ; adverse effects ; analogs & derivatives ; therapeutic use ; Disease-Free Survival ; Dose-Response Relationship, Drug ; Female ; Humans ; Lung Neoplasms ; pathology ; Male ; Middle Aged ; Remission Induction ; Survival Rate ; Vomiting ; chemically induced

Aged ; Female ; Humans ; Subclavian Vein ; abnormalities

Objective To explore the clinical and genetic characteristics of 17 cases with glucose-6-phosphate dehydrogenase(G6PD) deficiency in Guizhou,China.Methods The clinical features of 17 patients with G6PD deficiency were analyzed,DNA samples were obtained from the patients and some mothers,and the exons and flanking intronic sequences of the G6PD gene were analyzed by the polymerase chain reaction and sequencing.Results The cases had diverse phenotypes,these patients had acute haemolytic anaemia triggered by eating broad beans,infections,ingestion of specific drugs or the neonatal period and chronic nonspherocytic haemolytic anaemia.Three cases of the patients had concomitant diseases for α Mediterranean anemia,acute myeloid leukemia M2 type and neonatal anal membrane stenosis,respectively.G1376T,G1388A and A95G were the commonest G6PD variants in patients in Guizhou,China.G1376T,G1388A and A95G mutations were observed in 82.4％ cases.Two patients had only compound variants(c.1311 C ＞ T,IVS11 nt 93 T ＞ C).One case in the Rongjiang County,Guizhou Province had novel compound variants (c.G1388A,IVS10-10 T ＞ G) in the world.A patient's mother in the Guiyang City,Guizhou Province,China had compound variants (c.1376 G ＞ T,1311 C ＞ T,IVS11 nt 93 T ＞ C) as a carrier.Conclusions G6PD deficiency has a wide range of clinical heterogeneity.A novel G6PD compound variant haplotype c.G1388A,IVS10-10 T ＞ G was first found in the world,and the SNP spectrum of G6PD was enlarged.There may be a G6PD compound variant haplotype c.1376 G ＞ T,1311 C ＞ T,IVS11 nt 93 T ＞ C in Guizhou.