Objective To compare the effectiveness of medicated γintrauterine device (IUD) and medicated genefix IUD inserted immediately after abortion. Methods A multicenter clinical trail was performed for the study from Mar. 2012 to Jan. 2013. Totally 840 women who volunteered to participate were randomly allocated to γ-group (medicated γ IUD) or genefix-group (medicated genefix IUD) immediately after abortion. While 464 abortion women who had not used IUD or steroids contraceptive methods were chosen as control group. The effectiveness of the IUD were followed up for 1 year. All women were required to record the number of vaginal bleeding days and blood volume of vaginal bleeding within 3 months after abortion. Results At the 12th month, the expulsion was the most common reason for termination. The expulsion rates of genefix-group and γ-group were 2.48/100 women years and 3.12/100 women years, respectively (P>0.05). For the expulsion reasons, IUD moving down could account for more than seventy percent. The removal rate for IUD usage of two IUD groups were almost equal (3.91/100 women years verus 4.35/100 women years), the differences were not statistically significant (P>0.05). At the 90th day after abortion, comparing with control group, the bleeding and (or) spotting days of genefix-group and γ-group extended by 3.9 and 2.6 days respectively, the differences had statistical significance between the three groups (P<0.05). Among the bleeding and (or) spotting days, spotting days prolonged significantly. At the 12th month, spotting days of genefix-group andγ-group were (9.2±5.9) days and (8.5±4.6) days respectively, more than (5.2 ± 4.0) days of control group. The differences had statistical significance between IUD with control group (P<0.05), and had not between the two kinds of IUD (P>0.05). Conclusion The insertion of medicated genefix IUD and medicated γ IUD immediately after abortion is safe, feasible, has slight side effects and could be effective contraception.

[Summary] The aim of this study was to examine the association between obstructive sleep apnea-hypopnea syndrome ( OSAHS ) and microalbuminuria in type 2 diabetes mellitus patients. We found that severe OSAHS significantly increases the risk of early renal damage in type 2 diabetes mellitus patients with HbA1C<7% ( lowest oxygen saturation:OR=2. 41, 95% CI 1. 19-8. 08; apnea hyponea index: OR=2. 91, 95% CI 1. 50-9. 11), suggesting that OSAHS may increase the risk for early renal damage in type 2 diabetes mellitus, especially in those with successful control of glucose.

Objective The study was to evaluate the behavioral differences in learning and memory abilities among three ani -mal models of Alzheimer′s disease. Methods Three SD rat models(n=20) were used in this study.The first SD rat model was es-tablished by intracerebral injection of Aβ25-35 into the bilateral hippocampus , the second mouse model was induced by intraperitoneal in-jection of scopolamine and the third was a senescence accelerated mouse model .Morris Water maze test was performed to investigate behavioral differences by comparison to corresponding blank control groups ( sham operation group , blank group and P8 group ) . Results The learning and memory abilities of senescence accelerated rats and scopolamine -treated rats were worse than those of the corresponding control groups, especially the scopolamine-treated rat ([35.47 ±3.78]s vs [50.61 ±3.94]s, P<0.01).There was no significant difference between Aβrats and sham-operated rats(P>0.05). Conclusion The model of Alzheimer′s disease in-duced by intraperitoneal injection of scopolamine represents more distinct changes in learning and memory abilities .Morris water maze test can be used to well evaluate whether the scopolamine-induced model is successfully established or not .

Objective To clarify the intravenous thrombolysis utilization of acute ischemic stroke patients in Huashan hospital,and to analyze the factors affecting thrombolytic therapy compliance.Methods The data from a prospective cohort were analyzed.Consecutive acute stroke and transient ischemic attack patients from Huashan Hospital emergency room were recruited in 2014.Eligible ischemic stroke patients were divided into two groups according to intravenous thrombolysis or not.Results Totally 220 patients from emergency room were assessed in 2014.Among eligible patients,43 patients refused intravenous thrombolysis,whereas 59 patients chose this therapy.After multiple analysis,age,baseline NIHSS score,limb weakness,hemiplegic paralysis,facial paralysis or speech symptoms were significantly different between the two groups (U =936.000,P =0.024;U =284.500,P ＜ 0.01;x2 =8.824,P =0.003;x2 =7.732,P=0.005;x2 =5.169,P=0.038;x2 =5.040,P=0.025).Patients with NIHSS score ＜7 tended to refuse thrombolysis therapy in the receiver operating characteristic curve analysis (sensitivity 0.93,specificity 0.71).From 2008 to 2014,244 cases were analyzed in the thrombolysis database.Compared with patients with higher baseline NIHSS score,intracranial hemorrhage rate (2.6％ vs 19.4％;x2 =12.466,P ＜0.01),7-day mortality rate (1.3％ vs 16.9％;x2 =12.308,P ＜0.01) and 3-month mortality rate (3.8％ vs 21.1％;x2 =11.993,P ＜0.01) were lower in patients whose baseline NIHSS score ＜ 7 (minor group).A higher rate of excellent outcome (3-month modified Rankin Scale score ≤ 1)was observed in minor group (78.2％ vs 38.0％;x2 =34.403,P ＜ 0.01).Conclusions Intravenous thrombolysis was performed in 54.6％ of eligible ischemic stroke patients.Age,baseline NIHSS score,limb weakness,hemiplegic paralysis,facial paralysis or speech symptoms were associated with patients' decision of thrombolysis.The effectiveness and safety of intravenous thrombolysis were promising for patients with mild stroke.

AIMTo compare the effects of the non-mitogenetic human acidic fibroblast growth factor (nmhaFGF) and the human acidic fibroblast growth factor (haFGF) on the proliferation and MAPK signal transduction pathway of the malignant tumor cell and to study the clinical safety of nmhaFGF.

METHODSThe mammary tumor cells (MCF-7) were treated with haFGF and nmhaFGF separately. The mitogenic activities of both haFGF and nmhaFGF were detected by MTT method and the cell cycle was analyzed by flow cytometer (FCM). The expression levels of the signal proteins, Grb2 (growth factor receptor bound 2) and ERK1/2 (extracellular signal-regulated kinase 1/2), were detected by semi-quantitative Western blotting method.

RESULTSThe mitogenic activity of nmhaFGF was obviously lower than that of haFGF. The activity of nmhaFGF was weaker than that of the haFGF. The ratio of G1/G0, G2/M of haFGF was markedly lower than that of nmhaFGF and control group, and was reverse in S phase. The expression levels of both Grb2 and ERK1/2 of the nmhaFGF treated group were lower than that of the haFGF treated group and approaching the control group.

CONCLUSIONThe mitogenic activity of the nmhaFGF decreased remarkably. Its mechanism probably via down-regulation of the expression of the signal moleculars, MAPK-ERK1/2 and Grb2.

Breast Neoplasms ; metabolism ; pathology ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Down-Regulation ; Female ; Fibroblast Growth Factor 1 ; genetics ; pharmacology ; GRB2 Adaptor Protein ; metabolism ; Humans ; Mitogen-Activated Protein Kinase 1 ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Mitosis ; drug effects ; Mutation

OBJECTIVETo investigate whether the effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on transforming growth factor beta (TGF-beta1) and connective tissues growth factor (CTGF) was involved in AcSDKP's antifibrotic effect on the rats with silicosis.

METHODSRats were divided into 6 groups randomly, 10 rats in each group: Control of silicotic model: 1.0 ml normal sodium and was killed after 4 or 8 weeks; Silicotic model 1: 50 mg/ml silica suspension and was killed after 4 weeks; Silicotic model 2: 50 mg/ml silica suspension and was killed after 8 weeks; Anti-fibrosis treatment of AcSDKP: after each rat was intratracheally instilled with 50 mg/ml silica suspension for 4 weeks, AcSDKP 800 microg/(kg x d) was administered into every rat and rats were killed at the 8 weeks; Preventing fibrosis treatment of AcSDKP: after AcSDKP [800 microg/(kg x d)] was administered into every rat for 48 hours, each rat was intratracheally instilled with 50 mg/ml silica suspension and rats were killed at the 8 weeks. Lung fibrosis in morphology was observed by HE staining. The expressions of TGF-beta1 and CTGF in lung were observed by immunohistochemistry. The mRNA expressions of TGF-beta1 and CTGF in lung were observed by real-time PCR.

RESULTSIn anti-fibrosis treatment of AcSDKP group, protein expression of TGF-beta1 and CTGF were (0.244 +/- 0.016) and (0.241 +/- 0.017) respectively, and significantly lower that those in the silicotic model 1 and 2 groups; mRNA expressions of TGF-beta1 and CTGF decreased, mRNA expressions of CTGF were significantly lower that those in the silicotic model 1 and 2 groups (P < 0.05); In preventing fibrosis treatment of AcSDKP group, protein expression and mRNA expression of TGF-beta1 were significantly lower that those in the silicotic model 2 group (P < 0.05).

CONCLUSIONAcSDKP can decrease the expressions of TGF-beta1 and CTGF in lung tissues of the rats with experimentally induced pulmonary fibrosis.

Animals ; Connective Tissue Growth Factor ; metabolism ; Disease Models, Animal ; Lung ; drug effects ; metabolism ; Male ; Oligopeptides ; pharmacology ; Pulmonary Fibrosis ; metabolism ; Rats ; Rats, Sprague-Dawley ; Silicosis ; metabolism ; Transforming Growth Factor beta ; metabolism

OBJECTIVETo investigate the role of extracellular signal-regulated kinase 1/2 on the inhibition of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on the proliferation and collagen synthesis of cultured rat pulmonary fibroblasts induced by platelet-derived growth factor (PDGF).

METHODSPulmonary fibroblasts were prepared from lungs of neonatal Wistar rats as described previously. Cells were divided into 4 groups: (1) control group (0.4% FBS group); (2) PDGF (10 ng/ml) stimulated group; (3) PD98059+PDGF group (25 micromol/L PD98059+10 ng/ml PDGF); (4) AcSDKP+PDGF group (10(-8) mol/L AcSDKP+10 ng/ml PDGF). All experiments were performed in the fourth passages. Metabolic activity of fibroblasts was observed by MTT, and expressions of type I and type III collagen were measured by immunocytochemistry and western blot. Expressions of phospho-ERK1/2 and ERK1/2 were detected by western blot.

RESULTSCompared with control group, exposure of pulmonary fibroblasts to 10 ng/ml PDGF increased cell metabolic activity, expression of type I and type III collagen and phosphorylation of ERK1/2. 25 micromol/L PD98059 and AcSDKP both could inhibit the metabolic activity of pulmonary fibroblasts, type I and type III collagen synthesis and phosphorylation of ERK1/ 2 induced by PDGF, with significant differences (P < 0.05). AcSDKP+PDGF group compared with PDGF stimulated group, metabolic activity of pulmonary fibroblasts decreased to 77.4%. Immunocytochemistry result showed that in AcSDKP+PDGF group, expressions of type I and type III collagen decreased to 69.3% and 67.2% compared with those of PDGF stimulated group. Western blot result showed that in AcSDKP+PDGF group, expressions of type I and type III collagen decreased to 92.4% and 78.0%, phospho-ERK1/2 decreased to 83.5% compared with those of PDGF stimulated group, with significant differences (P < 0.05).

CONCLUSIONERK1/2 plays an important role in the inhibition of AcSDKP on the proliferation and collagen synthesis of cultured rat pulmonary fibroblasts induced by PDGF.

Animals ; Cell Proliferation ; drug effects ; Cells, Cultured ; Collagen ; biosynthesis ; Fibroblasts ; drug effects ; metabolism ; physiology ; MAP Kinase Signaling System ; physiology ; Oligopeptides ; pharmacology ; Platelet-Derived Growth Factor ; pharmacology ; Rats ; Rats, Wistar

OBJECTIVETo explore the efficacy of homemade hemostatics of injected gelatin matrix (HIGM) for immediately treating blunt hepatic trauma in canine model without additional pressure.

METHODSA total of 27 commercial hybrid dogs underwent celiotomy to establish hepatic trauma model after general anesthesia. The dogs were prospectively randomized into 3 groups: the treatment group (n=9, with the direct application of homemade hemostat), the positive control group (n=9, with thrombin solution), and the negative control group (n=9, with 0.9% normal saline). Time to hemostasis and intra-abdominal blood loss were recorded, and heart rate (HR), mean arterial pressure (MAP), and hematological parameters were compared among these three groups. Gross examinations were performed 30 minutes after surgery.

RESULTSSignificantly shorter time to hemostasis [(1.20±0.33) min] and less blood loss [(47.22±8.61) ml] were observed in the treatment group than in control groups (P 0.05). No cases of bleeding occurred in any animals in the treatment group, and no signs of infection and adhesion formation were evident due to exposure to HIGM. Two cases in the positive control group (22.22%) were found to have rebleeding. All animals in the negative control group experienced visible bleeding.

CONCLUSIONHIGM is effective for controlling bleeding after hepatic trauma without the additional compression, and therefore may be valuable in field surgery.

Animals ; Disease Models, Animal ; Dogs ; Gelatin ; administration & dosage ; Hemostatics ; administration & dosage ; Injections ; Liver ; injuries

OBJECTIVETo provide evidence for illustrating the molecular mechanism of nickel carcinogenesis, and to identify the differential expression of protein in crystalline NiS-induced neoplastic transformation of human bronchial epithelial cell by proteomics technology.

METHODSTwo dimensional electrophoresis (2-DE) and the ImageMaster 3.10 software were used to analyze the differential expression of protein, matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS) combined with database search was applied to identify protein peroxiredoxin 2 (PDX2) related to malignant transformation.

RESULTSThe good 2-DE pattern including resolution and reproducibility was obtained. Nearly 700 expressed proteins per 2-D gel were isolated with molecular weights (MW) ranging from 14,400 to 94,000 KD and pI 3 - 10. A protein PDX2 with MW 21,890 KD, pI 5.66, which was highly expressed in malignantly transformed cell, was identified using MALDI-TOF-MS.

CONCLUSIONPDX2 was involved in malignant transformation of human bronchial epithelial cell induced by crystalline nickel sulfide.

Bronchi ; cytology ; Cell Line ; Cell Transformation, Neoplastic ; chemically induced ; metabolism ; Epithelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Nickel ; toxicity ; Peroxiredoxins ; metabolism ; Proteome

To investigate the effects of 2-(4-methoxycarbonyl-2-tetradecyloxyphenyl)carbamoylbenzoic acid (CX09040) on protecting pancreatic β cells, the β cell dysfunction model mice were induced by injection of alloxan into the caudal vein of ICR mice, and were treated with compound CX09040. Liraglutide was used as the positive control drug. The amount and the size of islets observed in pathological sections were calculated to evaluate the β cell mass; the glucose stimulated insulin secretion (GSIS) test was applied to estimate the β cell secretary function; the oral glucose tolerance test (OGTT) was taken to observe the glucose metabolism in mice; the expressions of protein in pancreas were detected by Western blotting. The effects on the target protein tyrosine phosphatase 1B (PTP1B) were assessed by the PTP1B activities of both recombinant protein and the intracellular enzyme, and by the PTP1B expression in the pancreas of mice, separately. As the results, with the treatment of CX09040 in alloxan-induced β cell dysfunction mice, the islet amount (P<0.05) and size (P<0.05) increased significantly, the changes of serum insulin in GSIS (P<0.01) and the values of acute insulin response (AIR, P<0.01) were enhanced, compared to those in model group; the impaired glucose tolerance was also ameliorated by CX09040 with the decrease of the values of area under curve (AUC, P<0.01). The activation of the signaling pathways related to β cell proliferation was enhanced by increasing the levels of p-Akt/Akt (P<0.01), p-FoxO1/FoxOl (P<0.001) and PDX-1 (P<0.01). The effects of CX09040 on PTP1B were observed by inhibiting the recombinant hPTP1B activity with IC50 value of 2.78x 10(-7) mol.L-1, reducing the intracellular PTP1B activity of 72.8% (P<0.001), suppressing the PTP1B expression (P<0.001) and up-regulating p-IRβ/IRβ (P<0.01) in pancreas of the β cell dysfunction mice, separately. In conclusion, compound CX09040 showed significant protection effects against the dysfunction of β cell of mice by enlarging the pancreatic β cell mass and increasing the glucose-induced insulin secretion; its major mechanism may be the inhibition on target PTP1B and the succedent up-regulation of β cell proliferation.
Alloxan ; Animals ; Benzoates ; pharmacology ; Biological Assay ; Disease Models, Animal ; Glucose ; metabolism ; Glucose Tolerance Test ; Insulin ; secretion ; Insulin Resistance ; Insulin-Secreting Cells ; drug effects ; Liraglutide ; pharmacology ; Mice ; Mice, Inbred ICR ; Molecular Weight ; Pancreas ; drug effects ; enzymology ; Protein Tyrosine Phosphatase, Non-Receptor Type 1 ; antagonists & inhibitors ; Signal Transduction