To investigate the pharmacokinetic characteristics and absolute bioavailability of ginkgolide A (GA), ginkgolide B (GB) and bilobalide (BB) in rats. In this experiment, a high-performance liquid chromatography-tandem mass spectrometry (LC-MS/ MS) method was established to determine the plasma concentrations of GA, GB and BB in rats after rats were administrated with the three drugs through ig and iv respectively. The main pharmacokinetic parameters and absolute bioavailability of three ginkgolide compounds were obtained by using pharmacokinetic software DAS 2. 0. After the inject of GA, GB and BB, the results showed Cmax at (513.9 ± 116.9), (701.3 ± 76.0), (5,255.6 ± 476.8) µg · L(-1) and AUC0.24h of (960.9 ± 268.5), (779.5 ± 140.6), (7,409.3 ± 1,181.1) µg · h · L(-1), respectively; after the oral administration, the results showed Cmax at (522.9 ± 39.9), (146.8 ± 31.6), (2,711.9 ± 588.9) µg · L(-1) and AUC0-24 h of (1,760.4 ± 300.7), (636.6 ± 180.3), (16,651.4 ± 1,306.5) µg · h · L(-1), respectively. The absolute bioavailability of GA, GB and BB in rats was (61.1 ± 10.4)%, (27.2 ± 7.7)%, (56.2 ± 4.4)%, respectively. The method established in this experiment has a good specificity and sensitivity and so can be used to study the pharmacokinetics and absolute bioavailability of GA, GB and BB in rats.
Animals ; Biological Availability ; Chromatography, High Pressure Liquid ; Cyclopentanes ; pharmacokinetics ; Furans ; pharmacokinetics ; Ginkgolides ; pharmacokinetics ; Lactones ; pharmacokinetics ; Male ; Rats ; Rats, Sprague-Dawley ; Tandem Mass Spectrometry

0.05). Conclusions Biofeedback and pelvic electric stimulation could be used to treat stress incontinence. Menopause status,BMI and severity of stress incontinence can not obvious affect the outcomes of biofeedback and pelvic electric stimulation.

OBJECTIVETo study the mechanism of spontaneous rupture of hepatocellular carcinoma (HCC).

METHODSThe specimens of 30 patients with ruptured HCC and 30 patients with non-ruptured HCC were collected. Immunofluorescence, immunohistochemical and flow cytometry techniques were used to detect the phagocytosis of macrophages and the deposition of immune complex (IC) on vascular wall.

RESULTSIn this study, the poor function of macrophage phagocytosis was found in patients with ruptured HCC, which could results in the cumulating of IC and deposition on vascular wall. The IC, which composed of hepatitis B virus e1 antigen (HBeAg/1), complement C1q and immunoglobulins, was found deposited in the elastic membrane of arteries. Likely as a result of IC deposition, vascular injury occurs mainly in the small arteries where the deposition of IC was present. As the small arteries were the blood vessels with predominant injury, they would likely to be the ones to split and cause hemorrhage and rupture of HCC during vascular load increase.

CONCLUSIONSWe would conclude that the poor function of macrophage phagocytosis, which lead to the IC deposition and vascular injury may be the factors involved in the pathogenesis of ruptured HCC.

Adult ; Antigen-Antibody Complex ; metabolism ; Carcinoma, Hepatocellular ; immunology ; pathology ; Complement C1q ; metabolism ; Female ; Flow Cytometry ; Hepatitis B e Antigens ; metabolism ; Humans ; Immunoglobulins ; metabolism ; Immunohistochemistry ; Liver Neoplasms ; immunology ; pathology ; Macrophages ; immunology ; Male ; Middle Aged ; Rupture, Spontaneous ; immunology

OBJECTIVETo study the effect of arsenic trioxide (As2O3) and all-trans retinoic acid (ATRA) on human cervical carcinoma HeLa cell line.

METHODSHeLa cells were treated with As2O3 and ATRA. The cell proliferation was evaluated by MTT assay. The expressions of NDRG-1 protein and mRNA were determined by Western blot and RT-PCR analysis.

RESULTSMTT assay showed that As2O3 and ATRA inhibited the growth of human cervical carcinoma HeLa cells in vitro in a dose- and time-dependent manner. Western blot and RT-PCR techniques showed that As2O3 and ATRA down-regulated the expressions of NDRG-1 protein and mRNA (P < 0.05).

CONCLUSIONAs2O3 and ATRA can significantly inhibit the growth and proliferation of HeLa cells. The reason of these changes may be related with the down-regulation of expression of NDRG-1.

Antineoplastic Agents ; administration & dosage ; pharmacology ; Arsenicals ; administration & dosage ; pharmacology ; Blotting, Western ; Cell Cycle Proteins ; genetics ; metabolism ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins ; genetics ; metabolism ; Oxides ; administration & dosage ; pharmacology ; RNA, Messenger ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Tretinoin ; administration & dosage ; pharmacology

China ; epidemiology ; Female ; Humans ; Liver Diseases, Alcoholic ; epidemiology ; etiology ; Male ; Obesity ; complications ; Risk Factors ; Sex Factors

Objective To explore the association between polymorphisms of adiponectin gene and the risk of ischemic stroke in Han population from the Northern parts of China.Methods TaqMan probe of RT-PCR was applied to detect the genotype frequency of single nucleotide polymorphism(SNPs)(rs266729 and rs2241766)of adiponectin gene in 357 ischemic stroke cases who developed the episode at first time and with 345 healthy controls.Logistic regression analysis was used to evaluate the relationship of each genotype of SNPs and ischemic stroke.Results Mutation of rs2241766(T＞G)increased the risk of ischemic stroke among all the samples(0R=1.55,P=0.01)and it was still the risk factor of ischemic stroke when analyzed by multi-factors logistic regression after each factor was adjusted(OR=1.55,P=0.00).The polymorphism of rs266729 was not related to the risk of ischemic stroke among all the samples(OR=1.13,P=0.57).However,the genotype GG of rs266729 increased the risk of ischemic stroke among female population(OR=3.25,P=0.04).Conclusion The variance of rs2241766 in adiponectin gene was related to the risk of ischemic stroke in Han population from the Northern parts of China and the genotype GG of rs266729 could possibly increase the risk of ischemic stroke in women of Han population from the Northern parts of the country.

OBJECTIVEThis study is aimed to observe the natural draining state of maxillary sinus, to search for the key draining location (KDL) in the natural ostium, to investigate the relation between maxillary sinus draining and sinus inflammation, and to guide the treatment of maxillary sinus opening in endoscopic sinus surgery (ESS).

METHODSMethylene blue was used as tracer agent in this study. Fifteen cases with or without light maxillary sinus inflammation (without any treatment) were selected to observe the natural draining state and the key draining location in maxillary sinus fontanel. Eighty-nine cases with chronic rhinosinusitis, but without nasal polyp, were selected, of which the maxillary sinus mucosa restored well 6 months after ESS, to observe the draining state and modes in maxillary sinus. All patients were followed up for 12 months to evaluate the inflammation state of mucosa, and to analyze the relations between the draining mode and mucosa inflammation.

RESULTSThe KDL for maxillary sinus was located in the posterior-inferior portion of the natural ostium, close to the attachment of caudal end of the uncinate process. The draining flowed along it from maxillary sinus to nasopharynx. After conventional transnasal endoscopic operation, 15 cases showed relatively normal drainage, others displayed abnormal state and mode,including reverse draining (maxillary sinus-ethmoid sinus) , multiphase draining (outflow from front, back and lower wall of natural ostium), draining failure (with cilia transporting function of maxillary epithelium mucosae), cistern like change (maxillary sinus and ethmoid sinus formed one operation cavity, secretion accumulated in maxillary sinus) and mucosa disfunction (loss of cilia transporting function of maxillary epithelium mucosae). Inflammation was observed in 33.7% of the patients 12 months after ESS, especially in those with mucosa disfunction, draining failure and reverse draining.

CONCLUSIONSThe KDL for maxillary sinus may be located in the posterior-inferior portion of the natural ostium, close to the attachment of caudal end of the uncinate process, and the drainage mode is not affected by gravity and posture. The KDL lesion after ESS results in abnormal draining of maxillary sinus, and excessively large maxillary sinus opening may aggravate mucosa inflammation of maxillary sinus. The abnormal draining state and mode may be related with the incidence of mucosa inflammation after operation. Preserving caudal end of uncinate process and avoiding injury of KDL would be beneficial to the restoration of mucosa and lessen the incidence of inflammation recurrence.

Adolescent ; Adult ; Aged ; Endoscopy ; adverse effects ; Female ; Humans ; Inflammation ; Male ; Maxillary Sinusitis ; etiology ; Middle Aged ; Nasal Mucosa ; pathology ; Otorhinolaryngologic Surgical Procedures ; adverse effects ; Young Adult

OBJECTIVETo study mechanism of the apoptosis of rat pancreas islet β cell strain (INS-1 cells) induced by sodium arsenite.

METHODSINS-1 cells were exposed to sodium arsenite at the different concentrations. MTT assay was used to detect the viability of INS-1 cells. The potentials on mitochondrial membrane and lysosome membrane of INS-1 cells were determined with the fluorescence spectrophotometer. The apoptotic levels of INS-1 cells exposed to sodium arsenite were observed by a fluorescence microscope and flow cytometry.

RESULTSAfter exposure to sodium arsenite, the viability of INS-1 cells significantly decreased with the doses of sodium arsenite. At 24 h after exposure, the OD values of the mitochondrial membrane potentials declined observably with the doses of sodium arsenite (P < 0.01). At 48 h after exposure, the OD values of the lysosome membrane potentials significantly increased with the doses of sodium arsenite (P < 0.01). At 72 h after exposure, the apoptotic cells were observed under a fluorescence microscope and enhanced with the doses of sodium arsenite. The apoptosis cells with light blue, karyopyknosis, karyorrhexis, apoptotic body and chromatin concentration appeared. The results detected with flow cytometry indicated that after exposure, the apoptotic INS-1E cells significantly increased with the doses of sodium arsenite.

CONCLUSIONSThe sodium arsenite can induce the apoptosis of INS-1 cells through the mitochondria-lysosome pathway.

Animals ; Apoptosis ; drug effects ; Arsenites ; toxicity ; Cells, Cultured ; Insulin-Secreting Cells ; drug effects ; Lysosomes ; metabolism ; Membrane Potentials ; drug effects ; Mitochondria ; metabolism ; Rats ; Sodium Compounds ; toxicity

OBJECTIVETo investigate the ultrastructure of small artery wall in patients with spontaneous rupture of hepatocellular carcinoma (HCC).

METHODSTransmission electron microscopy was used to study 11 specimens from ruptured HCC and 11 cases with non-ruptured HCC.

RESULTSThe phenomenon of activated phagocytosis in macrophage could be found in 3 cases with ruptured HCC and 10 cases with non-ruptured HCC, respectively (P < 0.05). In 9 specimens with ruptured HCC, the evidence of vascular injury characterized as less cell junctions and larger fenestrae in endothelial cells, broken elastic lamina, proliferated and fragmented elastin and damaged structure of collagen was found in small arteries. The phenomenon of electron-dense deposit in the elastic lamina, and signs of more protein synthesis in endothelial cells were also present in these specimens. In the patients with non-ruptured HCC, the evidence of vascular injury can be found only in 2 cases (P < 0.01). Less cell junctions and larger fenestrae could increase the permeability of vascular wall. The electron-dense deposition in elastic lamina may represent the deposition of antigen-antibody complex in elastic membrane which had been found in our previous study. The vascular injury was postulated to be caused by the deposition of antigen-antibody complex in vascular wall which was identified by our previous study. The vascular wall in the patient with ruptured HCC could become stiff and weak due to the proliferated fragment elastin and damaged collagen which would make the blood vessels more prone to splitting and result in hemorrhage and the rupture of HCC.

CONCLUSIONSThe vascular injury caused by antigen-antibody complex deposition might related to the spontaneous rupture of HCC.

Carcinoma, Hepatocellular ; pathology ; ultrastructure ; Humans ; Liver Neoplasms ; pathology ; ultrastructure ; Macrophages ; immunology ; Microscopy, Electron ; Rupture, Spontaneous ; pathology

Migraine is a complex and heterogeneous disorder. Although several genetic models has been proposed including autosomal-dominant/autosomal recessive, sex-linked, sex-limited, mitochondrial, and multi-gene, none of these models can well-explain the transmission of the disease. We hypothesied that migraine is a sex-conditioned inherited disorder (autosomal dominant in females and autosomal recessive in males). This hypothesis is supported by the evidence such as the locations of genes associated with familial hemiplegic migraine, possibly "typical" migraine as well (dominantly on chromosome 19p, 1q, and 2q), male:female ratio of prevalence (1:2-1:4), the mostly youth-onset, the provocation by the contraceptives, the induction by menstruation, and the self-limitation after menopause. Female sex-hormones appear to be the key contributor to a higher prevalence of migraine in female. Socio-environmental factors may also play an important role.
Age of Onset ; China ; epidemiology ; Female ; Genes, Dominant ; genetics ; Genetic Predisposition to Disease ; epidemiology ; genetics ; Gonadal Steroid Hormones ; metabolism ; Humans ; Inheritance Patterns ; genetics ; Male ; Menstrual Cycle ; genetics ; Migraine Disorders ; epidemiology ; genetics ; Sex Factors