Child, Preschool ; Diagnosis, Differential ; Female ; Gonadotropin-Releasing Hormone ; therapeutic use ; Humans ; Hysteroscopy ; Pediatrics ; Puberty, Precocious ; diagnosis ; therapy ; Uterine Hemorrhage ; diagnosis ; etiology ; therapy ; Vaginal Diseases ; diagnosis ; etiology ; therapy

Child ; Child, Preschool ; Epilepsy ; complications ; diagnosis ; surgery ; Female ; Humans ; Male ; Sleep Apnea, Obstructive ; complications ; diagnosis ; surgery

Objective To observed the immigration and proliferation of Schwann cells in acellular xe- no-nerve graft in rats.Methods The sciatic nerves on the right side of the rats were exposc.d and 0.8cm long segments of the nerves were removed from the mid-thigh level and replaced by 1.0cm long rabbit nerves made acellular through chemical extraction.After 4 months,the immigration and proliferation of Schwann cells in the graft were revealed by HE staining,S-100 immunohistochemieal staining and transmission electromicro- scope.Results In the rats repaired by acellular nerves,regenerated axons upgrow into the graft,and a- round regenerated axons there were abundant cells aligned,the cytoplasm of which were S-100 immunoreac- tive.Electromicroscope observing showed that regenerated axons were surrounded by myelin formed by the mi- grated cells reoccupied the acellular segments.Conclusion The host Schwann cells can immigrate into rab- bit nerve grafts made acellular through chemical extraction and form myelin enwrapping regenerated axons in rats.

The prevalence of inflammatory bowel disease (IBD) in China is increasing year by year, however, the efficacy and safety of commonly used therapeutic methods are limited.Granulocyte and monocyte adsorptive apheresis (GMA) is one of the effective methods for treatment of IBD used abroad, however, there is still lacking of such research in China.Aims: To investigate the efficacy and safety of GMA in IBD patients.Methods: A retrospective study was conducted in 21 cases of IBD patients [13 cases with ulcerative colitis (UC) and 8 with Crohn's disease (CD)] who accepted GMA treatment from May 2013 to July 2014 at the Shanghai Rui Jin Hospital.All the cases were poor responders to 5-aminosalycylic acid (5-ASA) or steroid-refractory.The clinical data were collected, and the clinical activity index (CAI), endoscopic activity index (EAI), laboratory parameters including serum albumin (Alb), hemoglobin (Hb), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), leukocyte count and percentage of neutrophils, as well as the adverse effects before and two weeks after the end of GMA treatment were analyzed.Results: After GMA treatment, both CAI and EAI were decreased significantly in UC and CD groups as compared with those before treatment (P all <0.05).Among laboratory parameters, Alb was increased in UC group and CRP was decreased in both UC and CD groups after treatment (P all <0.05).No significant differences were found in other laboratory parameters in both UC and CD groups before and after treatment (P all >0.05).The treatment was well tolerated with no severe adverse effects.Conclusions: GMA is safe and effective for ameliorating clinical symptoms, attenuating intestinal mucosal injury and controlling active inflammation in IBD patient that has not responded to 5-ASA or steroid treatment.Prospective clinical studies with large samples are needed to confirm these findings.

This study is to investigate the effect and mechanism of puerarin on DNA damage of HaCaT cells induced by UVB. Puerarin pre-treated cells were irradiated with UVB at 30 mJ x cm(-2). Twenty four hours after irradiation, DNA damage was detected by comet assay, ceramide was measured by thin layer chromatography and gas chromatography, intracellular free calcium ion was analyzed by flow cytometry, the phosphorylation level of p38 protein was examined by Western blotting method. Levels of DNA damage, ceramide, free calcium ion and p-p38 protein were elevated in UVB model cells. Contrary to the model group, all indicators above were reduced in all groups pre-treated by puerarin. Puerarin restrains the ceramide accumulation to block downstream p38 MAPK pathway and calcium ion rising, therefore reduces DNA damage in HaCaT cells induced by UVB.
Calcium ; metabolism ; Cell Line ; Ceramides ; metabolism ; DNA Damage ; drug effects ; radiation effects ; Down-Regulation ; Humans ; Isoflavones ; pharmacology ; Keratinocytes ; cytology ; metabolism ; Phosphorylation ; Signal Transduction ; drug effects ; Ultraviolet Rays ; adverse effects ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVETo investigate the association of SOX9 expression and clinicopathologic factors and prognosis of gastric cancer.

METHODSA retrospective cohort study including 112 gastric cancer patients admitted to the Zhejiang Provincial People's Hospital from 2004 to 2006 was performed. Immunohistochemical analysis was used to evaluate the expression of SOX9 in the 112 specimens of gastric cancer tissues and 70 non-cancerous tissues adjacent to the tumor.

RESULTSLow expression of SOX9 was seen in 5(7.1%) tissues out of 70 non-cancerous tissues adjacent to the tumor. A total of 94(83.9%) patients had varying expression of SOX9, of whom 51(45.4%) had overexpression. Univariate analysis demonstrated that the expression of SOX9 was significantly associated with Lauren classification (P<0.05), tumor invasion(P<0.01), lymph node metastasis(P<0.05), distant metastasis(P<0.05) and tumor stage(P<0.05), however there was no significant association between SOX9 expression and sex, age, histological type, histology differentiation or tumor size. Kaplan-Meier analysis showed that the 5-year survival rate of patients with SOX9 over-expression was significantly lower than that of patients with low expression(29.4% vs. 49.2%, P=0.031). Multivariate Cox regression analysis showed that histology differentiation(P=0.046), tumor invasion(P=0.001), and distant metastasis(P<0.01) were independent prognostic factors for gastric cancer, however the over-expression of SOX9 was not significant(P=0.948).

CONCLUSIONSThe expression SOX9 is associated with the growth, invasion, and metastasis of gastric cancer, as well as the prognosis. However, SOX9 expression is not an independent factor for the prognosis in patients with gastric cancer.

Adult ; Aged ; Aged, 80 and over ; Female ; Humans ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Prognosis ; Retrospective Studies ; SOX9 Transcription Factor ; metabolism ; Stomach Neoplasms ; metabolism ; pathology

AIM To explore the effects of ligustrazine on blood rheology,aldose reductase (AR) and renal function in diabetic nephropathy (DN) rats.METHODS The DN rat model was established by intraperitoneal injection of streptozotoein (55 mg/kg),rats were randomly divided into five groups,model group,irbesartan [50 mg/(kg · d)] group,high-,middle-and low-dose of ligustrazine [200,100,50 mg/(kg · d)] groups,together with normal control group.All the rats received daily garage for eight successive weeks.At the end of experiment,blood rheology,blood glucose,aldose reductase in erythrocyte and kidney tissue,24 h urinary protein,blood urea nitrogen,creatinine,creatinine clearance and renal function were observed.RESULTS Compared with the model group,blood rheology,blood glucose and renal function in various treatment groups were effectively improved,and aldose reductase activity was significantly decreased (P ＜ 0.05).HE staining and PAS staining showed that the pathological changes in kidney were significantly alleviated.CONCLUSION Ligustrazine can protect kidney of DN rats by ameliorating blood rheology,decreasing blood glucose and inhibiting aldose reductase activity.

BACKGROUND/OBJECTIVES: The objectives of this study were to investigate the effects of lycopene on the migration, adhesion, tube formation capacity, and p38 mitogen-activated protein kinase (p38 MAPK) activity of endothelial progenitor cells (EPCs) cultivated with high glucose (HG) and as well as explore the mechanism behind the protective effects of lycopene on peripheral blood EPCs. MATERIALS/METHODS: Mononuclear cells were isolated from human peripheral blood by Ficoll density gradient centrifugation. EPCs were identified after induction of cellular differentiation. Third generation EPCs were incubated with HG (33 mmol/L) or 10, 30, and 50 microg/mL of lycopene plus HG. MTT assay and flow cytometry were performed to assess proliferation and apoptosis of EPCs. EPC migration was assessed by MTT assay with a modified boyden chamber. Adhesion assay was performed by replating EPCs on fibronectin-coated dishes, after which adherent cells were counted. In vitro vasculogenesis activity was assayed by Madrigal network formation assay. Western blotting was performed to analyze protein expression of both phosphorylated and non-phosphorylated p38 MAPK. RESULTS: The proliferation, migration, adhesion, and in vitro vasculogenesis capacity of EPCs treated with 10, 30, and 50 microg/mL of lycopene plus HG were all significantly higher comapred to the HG group (P < 0.05). Rates of apoptosis were also significantly lower than that of the HG group. Moreover, lycopene blocked phosphorylation of p38 MAPK in EPCs (P < 0.05). To confirm the causal relationship between MAPK inhibition and the protective effects of lycopene against HG-induced cellular injury, we treated cells with SB203580, a phosphorylation inhibitor. The inhibitor significantly inhibited HG-induced EPC injury. CONCLUSIONS: Lycopene promotes proliferation, migration, adhesion, and in vitro vasculogenesis capacity as well as reduces apoptosis of EPCs. Further, the underlying molecular mechanism of the protective effects of lycopene against HG-induced EPC injury may involve the p38 MAPK signal transduction pathway. Specifically, lycopene was shown to inhibit HG-induced EPC injury by inhibiting p38 MAPKs.
Apoptosis ; Blotting, Western ; Centrifugation, Density Gradient ; Ficoll ; Flow Cytometry ; Glucose* ; Humans ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein Kinases ; Signal Transduction ; Stem Cells*

BACKGROUND/OBJECTIVES: The objectives of this study were to investigate the effects of lycopene on the migration, adhesion, tube formation capacity, and p38 mitogen-activated protein kinase (p38 MAPK) activity of endothelial progenitor cells (EPCs) cultivated with high glucose (HG) and as well as explore the mechanism behind the protective effects of lycopene on peripheral blood EPCs. MATERIALS/METHODS: Mononuclear cells were isolated from human peripheral blood by Ficoll density gradient centrifugation. EPCs were identified after induction of cellular differentiation. Third generation EPCs were incubated with HG (33 mmol/L) or 10, 30, and 50 microg/mL of lycopene plus HG. MTT assay and flow cytometry were performed to assess proliferation and apoptosis of EPCs. EPC migration was assessed by MTT assay with a modified boyden chamber. Adhesion assay was performed by replating EPCs on fibronectin-coated dishes, after which adherent cells were counted. In vitro vasculogenesis activity was assayed by Madrigal network formation assay. Western blotting was performed to analyze protein expression of both phosphorylated and non-phosphorylated p38 MAPK. RESULTS: The proliferation, migration, adhesion, and in vitro vasculogenesis capacity of EPCs treated with 10, 30, and 50 microg/mL of lycopene plus HG were all significantly higher comapred to the HG group (P < 0.05). Rates of apoptosis were also significantly lower than that of the HG group. Moreover, lycopene blocked phosphorylation of p38 MAPK in EPCs (P < 0.05). To confirm the causal relationship between MAPK inhibition and the protective effects of lycopene against HG-induced cellular injury, we treated cells with SB203580, a phosphorylation inhibitor. The inhibitor significantly inhibited HG-induced EPC injury. CONCLUSIONS: Lycopene promotes proliferation, migration, adhesion, and in vitro vasculogenesis capacity as well as reduces apoptosis of EPCs. Further, the underlying molecular mechanism of the protective effects of lycopene against HG-induced EPC injury may involve the p38 MAPK signal transduction pathway. Specifically, lycopene was shown to inhibit HG-induced EPC injury by inhibiting p38 MAPKs.
Apoptosis ; Blotting, Western ; Centrifugation, Density Gradient ; Ficoll ; Flow Cytometry ; Glucose* ; Humans ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein Kinases ; Signal Transduction ; Stem Cells*

OBJECTIVEThe present study was designed to investigate the preventive and therapeutic effect of 3-hydroxy-3-methylglutanyl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin on the development of atherosclerosis (AS) in immature rabbits and its possible mechanism by detecting the expression level of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in the abdominal aorta.

METHODSA model of hypercholesterolemia (HC) was established by high-cholesterol diet and 24 immature rabbits were divided randomly and equally into control group, HC-diet group and fluvastatin group. At the beginning of the study and after 12 weeks, the body height (BH) and body weight (BW) of the rabbits were measured and their body mass index (BMI) was calculated. At the end of 12 weeks, serum total cholesterol (TC) and low-density lipoprotein (LDL) levels were examined. The intima-medial thickness of the abdominal aorta (aIMT) was measured by using non-invasive high-resolution (14 MHz) B-mode ultrasound imaging. Histological changes in abdominal arteries were studied by H&E-staining and histomorphometric analysis. The gene expression of LOX-1 in abdominal aorta was evaluated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and its protein expression was examined by immunohistochemistry.

RESULTSHigh cholesterol diet induced hypercholesterolemia and early AS in immature rabbits. In HC-diet group serum TC and LDL levels in rabbits elevated. B mode echocardiography showed that aIMT was thickened and pathomorphology indicated that extensive aortic intima (I) and intima and media (I + M) became thickened and the ratio of the area of intima to media (S(I)/S(M)) was increased. Aortic intimal proliferation in HC-diet group was associated with a marked increase in LOX-1 expression (protein and mRNA) in endothelium and neointima of the abdominal aorta. Treatment with fluvastatin at a dosage of 10 mg/(kg.d) deduced serum lipid, attenuated artery intimal proliferation and markedly decreased the enhanced LOX-1 expression level in endothelium and neointima in immature rabbits. There were no significant differences of BH, BW or BMI among the three groups.

CONCLUSIONSThese findings suggested that early treatment with fluvastatin not only induced a significant regression of arterial lesions of HC and early AS in immature rabbits, but also had a crucial endothelial protective effect by down-regulating LOX-1 expression level in atherosclerotic arteries in early AS.

Animals ; Aorta, Abdominal ; diagnostic imaging ; pathology ; Arteries ; metabolism ; pathology ; Atherosclerosis ; drug therapy ; metabolism ; Cholesterol, Dietary ; Cholesterol, LDL ; blood ; Echocardiography ; Fatty Acids, Monounsaturated ; pharmacology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; pharmacology ; Hypercholesterolemia ; drug therapy ; metabolism ; Indoles ; pharmacology ; Rabbits ; Scavenger Receptors, Class E ; metabolism