Objective To determine the effects of ?-lipoic acid on bone metabolism in lead-poisoned rats.Methods Totally 31 SD rats were randomly divided into two groups,8 rats in blank control group and 23 in lead group that received gastric lavage with lead acetate(230 mg/L).After 40 days,3 rats from each group were taken for the measurement of lead in the blood and bone.The rats in lead group were then randomly divided into four groups: lead control group and three lead groups with different concentrations of ?-lipoic acid [30,60 and 100 mg/(kg?d)],with 5 rats in each.At the end of the experiment(80 d),the rats were killed and the samples of whole blood,serum and bone were collected to detect osteocalcin content with radioimmunoassay and alkaline phosphatase expression with immunohistochemistry staining.Results ① Blood and bone lead contents in each ?-lipoic treatment group were significantly lower than those in lead control group(P

Objective The purpose of this study was to investigate the correlation of high sensitivity C-reactive protein (hsCRP) and fibrinogen with carotid artery arteriosclerosis of patients with cerebral infarction. Methods One hundred and thirteen patients with cerebral infarction were assigned as study group, and 102 healthy persons as control group. The levels of serum hsCRP and Fib in the two groups were measured. The carotid artery arteriosclerosis and carotid intimal-medial thickness (IMT) were examined by color Doppler and B-ultrasound. Results The value of IMT between study group and control group was statistically significant. The positive rates of carotid artery arteriosclerosis plaque and vulnerable plaque in study group were significantly higher than those in control group (all<0.05) . The level of serum hsCRP was significantly higher in study group than that of control ( <0.05) . The level of serum Fib between study group and control group was not statistically significant ( >0.05) . Conclusion The level of hsCRP was closely related to the degree of carotid artery arteriosclerosis and the occurrence and development of cerebral infarction. But the level of Fib was not closely related to the degree of carotid artery arteriosclerosis.

To promote bilingual teaching reform and explore a proper bilingual teaching mode in China,we studied the bilingual teaching of the course “Biochemistry on special subjects”.The present paper mainly designs and discusses the object of the course,teaching materials,contents and methods as well as the building of feedback and evaluation system of the course.

Objective To synthesize a derivative of 5-fluorouracil (5-FU) modified by D-glucosamine(Glc) and preliminarily investigate the biodistribution profile of the derivative in mice.Methods 5-FU-D-Glc was synthesized by conjugating 5-fluorouracil and D-glucosamine via an amide bond.The quantitative measurement of 5-FU and its derivative was established by HPLC in vitro and in vivo.Stabilities of 5-FU-D-Glc were investigated in phosphate buffer (pH7.4),freshly prepared mouse plasma and kidney homogenates,respectively.Tissue distributions of 5-FU and 5-FU-D-Glc were monitored by HPLC after drugs were intravenously administrated to mice.Results The chemical structures of target compound was confirmed by 1H-NMR,13C-NMR and LC-MS.The 5-FU-D-Glc showed a good stability under all given conditions with no substantial hydrolysis(＜ 10％).After intravenous administration to mice by caudal vein,the AUC0-t of 5-FU-D-Glc achieved in kidney was (9680.07 ± 330.20) μg · g-1 · min,which was enhanced by 20.3 fold compared with that of 5-FU.Meanwhile,the relative uptake efficiency (RE) and concentration efficiency (CE) were 21.27 and 10.45 respectively.Moreover,remarkably enhanced drug distribution and prolonged blood circulation time in plasma were found in 5-FU-D-Glc.Conclusion 5-fluorouracil-D-glucosamine derivative showed a good stability profile in vitro.The in vivo results highlighted a significant improvement of the kidney -tageted delivery of 5-FU by linked with D-glucosamine.

Inflammation has been implicated as a secondary mechanism underlying neuronal injury induced by ischemia. A variety of experimental models, including thromboembolic stroke, focal and global ischemia, have been used to evaluate contributions of inflammation to neuronal damage. The vasculature endothelium promotes inflammation through upregulation of adhesion molecules such as intercellular adhesion molecule (ICAM), E-selectin, and P-selectin that bind to circulating leukocytes and facilitate migration of leukocytes into the central nervous system (CNS). Once being in the CNS, leukocytes produce cytotoxic molecules that promote cell death. The response of macrophages and microglia to injury may either be beneficial by scavenging necrotic debris or be detrimental by facilitating cell death of neurons that would otherwise recover. While many studies have tested these hypotheses, the significance of inflammation in stroke models is inconclusive. This review summarizes data regarding roles of cell adhesion molecules, astrocytes, microglia and leukocytes in stroke.

Carcinoma ; diagnosis ; pathology ; Humans ; Laryngeal Neoplasms ; diagnosis ; pathology ; Larynx ; pathology

OBJECTIVETo investigate the expression of motilin-immunoreactive neurons in the hypothalamus and the effect of central administration of erythromycin (EM) on the regulation of gastric motility in diabetic rats.

METHODSThe motilin immunoreactive neurons in the hypothalamus and the hippocampus were detected by immunohistochemistry with rabbit anti-motilin polyclonal antibody. To measure the gastric motility, force transducers were surgically affixed to the gastric serosa. A microinjection syringe was connected via a plastic tube to an injection cannula, which was connected with a stainless steel guide cannula. The syringe was inserted into the right lateral cerebral ventricle for microinjecting the chemicals.

RESULTSDiabetic mellitus was successfully induced in cohorts of rats. Motilin-immunoreactive neurons significantly increased in the paraventricular (PVN) and supraoptic nuclei (SON) of the hypothalamus in the diabetic rats. Intracerebroventricular (i.c.v.) administration of EM, a motilin receptor agonist, stimulated the gastric motility of diabetic rats. EM (91.56 nmol, i.c.v.) dose-dependently increased the amplitude by (174.82 +/- 48.62)% (P<0.05), and increased the frequency by (70.43 +/- 27.11)% (P < 0.05) in 5 min. The stimulatory effect lasted more than 15 min to the end of the measurement, and can be blocked partially by the prior treatment of motilin receptor antagonist GM-109.

CONCLUSIONMotilin-immunoreactive neurons are increased in the PVN and SON of the hypothalamus in diabetic rats. Centrally administered EM may regulate gastric motility by binding to the central motilin receptors, and central motilin might be involved in regulation of gastric motility in diabetic rats.

Animals ; Diabetes Mellitus, Experimental ; metabolism ; Dose-Response Relationship, Drug ; Erythromycin ; administration & dosage ; pharmacology ; Gastrointestinal Agents ; administration & dosage ; pharmacology ; Gastrointestinal Motility ; drug effects ; physiology ; Hippocampus ; cytology ; metabolism ; Injections, Intraventricular ; Male ; Microinjections ; Motilin ; agonists ; metabolism ; Neurons ; cytology ; metabolism ; Paraventricular Hypothalamic Nucleus ; cytology ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Gastrointestinal Hormone ; agonists ; Receptors, Neuropeptide ; agonists ; Statistics, Nonparametric ; Supraoptic Nucleus ; cytology ; metabolism

Objective To investigate expression of Human papillomavirus (HPV) 11 type E7 protein antigen in prokaryotic cells and its potential use for the serodiagnosis of condyloma acuminatum (CA).Methods The full-length gene encoding for HPV11 E7 protein was amplified by PCR,and cloned into vector pET32a(+) to form recombinant pET32a(+)/HPVll E7 plasmid.The fusion His-E7 protein was expressed and analyzed by using SDS-PAGE and Western blotting.Using ELISA assay,HPV11 E7 fusion protein were also used to screen human serum IgG antibody from 93 patients with CA,43 patients with cervix cancer and 58 healthy control subjects.Results Highly expressed fusion His-E7 protein was obtained,and purified protein served as a special diagnostic antigen to screen human serum antibody for CA serodiagnosis.It showed that CA group,cervix cancer group and healthy control human serum IgG antibody average value were 1.545?0.131,0.586?0.155 and 0.674?0.150 respectively,positive rate were 76.3% (71/93),11.6% (5/43) and 5.2% (3/58).There was significantly difference between the CA group to compare cervix cancer group and healthy control (P

Objective:To detect the effect of microRNA-7 ( miR-7 ) knockdown on pathology in murine acute lung injury ( ALI) model,and preliminarily explore its significance.Methods:Murine ALI model was performed by intraperitoneal injection of Li-popolysaccharide (LPS) (10 mg/kg) into miR-7KD mice and wild-type (wild type,WT) mice respectively.Then,the pathologic injury of lung tissue were observed by HE staining.And total cell count of bronchoalveolarlavage(BAL) was calculated.The relative expression of related cytokines in lung tissue was analyzed by Real-time PCR assay.Furthermore,the changes on proportion of innate immune cells (γδT cell and F4/80 macrophages cell) and adaptive immune cell ( CD4+T cell and CD8+T cell) were analyzed by FACS.Meanwhile, the expression of CD62L and CD69,as well as the absolute number,in CD4+T cell were also analyzed.Results: Compared with WT mice,pathological damage in lung tissues was significantly alleviated in miR-7KD mice.Real-time PCR analysis showed that the relative expression of IL-6 was obviously reduced (P<0.01),conversely,relative expression of IL-4 and TGF-βwere obviously increased (P<0.05).Furthermore,the total cell number in BAL also reduced significantly (P<0.05).Importantly,FACS analysis showed that the proportion and the absolute number of F4/80+Mφcells obviously reduced (P<0.05);however,the proportion of γδT cells increased (P<0.05).Moreover,the proportion and the absolute number of CD4+T cells and CD8+T cells were significantly reduced (P<0.05). Finally, the proportion and the absolute number of CD62L+in CD4+T cells were upregulated vigorously,contrastly,the proportion and the absolute number of CD69+in CD4+T cells were notably up-regulated (P<0.05).Conclusion:miR-7 defeciency could significantly ameliorate the pathology of murine ALI,suggesting that it may play an important regulatory role in the development of ALI.

OBJECTIVEThis study examined the effects of PI3K inhibitor LY294002 on the differentiation of mouse preadipocytes and the expression of CCAAT enhancer binding protein α (C/EBPα) and peroxisome proliferation activated receptor γ (PPARγ), in order to study the possible roles of insulin receptor substrate (IRSs)/PI3K signal pathway in the differentiation of preadipocytes.

METHODSThe mouse 3T3-L1 cells were cultured normally and divided into experimental and control groups. 3T3-L1 cells in the experimental group were treated with PI3K inhibitor LY294002 (25 μmol/L) and those in the control group were treated with DMSO culture medium. 3-isobutyl-1-methylxanthine (IBMX) (0.5 mmol/L), dexamethasone (10-6 mol/L) and insulin (5 μg/mL) were used to induce the differentiation of 3T3-L1 preadipocytes in both groups. Before culture, and 2, 4 and 8 days after culture, the cells were collected to detect the expression of C/EBPα and PPARγ by real-time PCR and Western blot assays. The lipid droplets of 3T3-L1 preadipocytes were observed by oil-red O staining.

RESULTSPI3K inhibitor LY294002 did not affect the expression of C/EBPα and PPARγ in un-induced 3T3-L1 preadipocytes (P>0.05), but decreased the expression of C/EBPα and PPARγ during the in vitro induced differentiation of 3T3-L1 preadipocytes compared with the control group (P<0.05 or 0.01). The lipid droplets count was greatly reduced by LY294002.

CONCLUSIONSPI3K inhibitor LY294002 can inhibit the differentiation of mouse 3T3-LI preadipocytes and the expression of C/EBPα and PPARγ in the differentiation of 3T3-LI preadipoeytes, suggesting that IRSs/PI3K signal pathway may play an important role in the differentiation of 3T3-L1 preadipocytes by regulating the expression of C/EBPα and PPARγ.

3T3-L1 Cells ; Adipocytes ; cytology ; drug effects ; Animals ; CCAAT-Enhancer-Binding Protein-alpha ; analysis ; genetics ; Cell Differentiation ; drug effects ; Chromones ; pharmacology ; Gene Expression Regulation ; drug effects ; Mice ; Morpholines ; pharmacology ; PPAR gamma ; analysis ; genetics ; Phosphatidylinositol 3-Kinases ; antagonists & inhibitors ; RNA, Messenger ; analysis