Adolescent ; Adult ; Aged ; Female ; Humans ; Janus Kinase 2 ; genetics ; Karyotyping ; Male ; Middle Aged ; Mutation ; Myelodysplastic Syndromes ; genetics ; Nuclear Proteins ; genetics ; Proto-Oncogene Proteins c-kit ; genetics ; Young Adult ; fms-Like Tyrosine Kinase 3 ; genetics

Acanthoma ; metabolism ; pathology ; surgery ; Adenoma ; metabolism ; pathology ; Adult ; Aged ; Diagnosis, Differential ; Female ; Humans ; Keratin-14 ; metabolism ; Keratin-5 ; metabolism ; Keratin-6 ; metabolism ; Keratosis ; metabolism ; pathology ; surgery ; Male ; Poroma ; classification ; metabolism ; pathology ; surgery ; Sweat Gland Neoplasms ; classification ; metabolism ; pathology ; surgery

Objective To explore the influence of electrical stimulation on prefrontal cortical neurons and synaptic ultramicrostructure of hypoxic-ischemic brain damage(HIBD)in neonatal rats.Methods The sixty 7-day-old newborn healthy SD rats were randomly divided into hypoxic-ischemic group(model group),electrical stimulation(intervention)group and sham operation group(control group),which 20 for each group.The models of perinatal HIBD rats were prepared by ligation of left common carotid artery with a temporary systemic hypoxia for 2 hours.Intervention group was subject to electric stimulation for 30 minutes,once everyday after surgery.Control group and model group were not subject to electric stimulation but caught to fix in corresponding period.Fastigial nucleus electric stimulations were performed for 3 d,14 d and 21 d.Five rats were killed in each group after the application of electron microscope to observe the brain cortex neurons and synaptic ultrastructure changes.Results In model group,the neuronal shrinkage,the amount of organelles dacrease,ob-vious edema of cytoplasm,obvious swellen mitochondria,and synapse quantity decrease,synaptic space fusion,obvious synaptic vesicle were observed.Intervention group different times,mitochondria hydrops gradually alleviated,synaptic space gradually cleared,synaptic vesicle increased,pathological changes obviously lessened compared to model group at the same time,and there was no apparent abnormality compared with control group on the 21st d.Conclusion Electric stimulation can promote the ultramicrostructures recovery of HIBD rats.

Objective To investigate the effects of electrical stimulation on vascular endothelial growth factor(VEGF) and its receptor expressions of neonatal rat brain with hypoxic-ischemic brain damage(HIBD).Methods Seventy-five 7-day-old newborn health SD rats were randomly divided into sham operation group(control group,n=25),hypoxia-ischemia group(model group,n=25) and the electrical sti-mulation group(intervention group,n=25).To bulid HIBD animal model of neonatal rats,the left common carotid artery was ligated and nitrogen-oxygen gas mixture was inhaled 2 hours.Fastigial nucleus stimulation was given 12 hours after the operation in intervention group,30 min?time-1,1 time?d-1,the time length was 1 d,3 d,7 d,14 d or 21 d,respectively.There was no electrical stimulation in model group and control group.The rats in these groups were captured at the corresponding time.Five rats in each group were killed at the corresponding pe-riods after electrical stimulation,the expression of VEGF and its receptor fam-like tyrosine kinase receptor(flt-1 / VEGFR1),fetal liver kinase receptor(flk-1/KDR/VEGFR2) in hippocampus were observed by immunohistochemistry.SPSS 15.0 software was used to analyze the data.Results The expression of VEGF,VEGFR1,VEGFR2 at every time point in electrical stimulation group were higher significantly than those in model group and control group(Pa0.05).Conclusion Electrical stimulation can promote the expression of VEGF and its receptors VEGFR1,VEGFR2.

Non-small-cell lung carcinoma (NSCLC) is one of the most frequently diagnosed malignancies worldwide.Previous studies have shown that microRNA-449b (miR-449b) functions as a tumor suppressor in many cancers.However,the role of miR-449b in NSCLC is still unknown.In the present study,miR-449b was significantly downregulated in NSCLC samples and cell lines.Bioinformatics analysis revealed that 3'-UTR region of leucine rich repeat containing G protein-coupled receptor 4 (LGR4) mRNA had putative complementary sequences to miR-449b,which was further confirmed by the luciferase assay.Western blotting showed that restoration of miR-449b in NSCLC cells decreased the expression of LGR4.Interestingly,over-expression of miR-449b inhibited growth and invasion of NSCLC cells in vitro.Furthermore,ectopic expression of LGR4 reversed miR-449b-suppressed proliferation and invasion of NSCLC cells.Therefore,the data of the present study demonstrate that miR-449b inhibits tumor cell growth and invasion by targeting LGR4 in NSCLC.

Objective To investigate the correlation of blood-brain barrier (BBB) damage and depression in patients with cerebral small vessel disease (CSVD).Methods Consecutive patients with CSVD admitted to hospital were enrolled prospectively.The patients completed head MRI and cerebrospinal fluid (CSF) examination after admission.The BBB damage degree was evaluated by using albumin CSF/serum ratio (Q-Alb).At 3 months after onset,the depression was assessed according to the Hamilton depression scale (HAMD) and the American Diagnostic and Statistical Manual of mental disorders,4th edition (DSM-Ⅳ).The correlation between the BBB damage and depression in patients with CSVD was analyzed,Results A total of 130 consecutive patients with CSVD were enrolled,including 58 (44.62％) had depression within 3 months.There were significant differences in the proportions of patients with lacunar infarction (43.10％ vs.26.39％;x2 =4.008,P =0.045),leukoaraiosis (75.86％ vs.58.33％;x2 =4.408,P =0.036),and cerebral microbleed (27.59％ vs.12.50％;x2 =4.707,P =0.030),and baseline National Institutes of Health Stroke Scale (NIHSS) scores (5.02 ± 2.51 vs.3.60 ± 2.43;t =3.256,P =0.001),Fazekas scales of deep white matter (2.35 ± 1.00 vs.1.56 ± 1.05;t =4.358,P ＜0.001) and the proportion of Q-AIb category (x2 =6.852,P =0.033) between the depression group and the non-depression group.Multivariate logistic regression analysis showed that the baseline NIHSS scores (odds ratio [OR] 1.248,95％ confidence interval [CI] 1.027-1.517;P =0.026),leukoaraiosis (OR 14.786,95％ CI 1.776-123.111;P=0.013),Fazekas scales of deep white matter (OR 1.847,95％ CI 1.210-2.819;P=0.004),and Q-Alb (OR 30.417,95％ CI 3.662-252.643;P =0.004) had significant independent correlation with depression.Conclusions The BBB damage is independently associated with depression in patients with CSVD.

This study is to investigate the effect of ethyl gallate on invasion capabilities and its mechanism of breast cancer MDA-MB-231 cells. Using cell adhesion and transwell assay, separately, the effects of ethyl gallate on the invasion of MDA-MB-231 cells were measured. The Akt-NF-κB signal pathway protein expressions were analyzed with Western blot. Also, the mRNA levels of MMP-9 and MMP-2 were analyzed by RT-PCR. Ethyl gallate inhibited the abilities of motility, adhesion and invasion of breast cancer MDA-MB-231 cells in vitro (P<0.05), inhibited the mRNA levels of MMP-9, MMP-2, phosphorylation of AKt and protein expression of NF-κB. It is concluded that ethyl gallate can inhibit the abilities of invasion of breast cancer in vitro by inhibiting the mRNA levels of MMP-9/MMP-2, phosphorylation of Akt and protein expression of NF-κB.
Breast Neoplasms ; pathology ; Cell Adhesion ; drug effects ; Cell Line, Tumor ; Cell Movement ; drug effects ; Gallic Acid ; analogs & derivatives ; pharmacology ; Humans ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; NF-kappa B ; metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; metabolism ; RNA, Messenger ; Signal Transduction

ObjectiveTo explore the character of cognitive potential P300 in major depressive disorder ( MDD ) patients between with and without family history and compare the cognitive function between them.MethodsSixty-seven MDD patients with family history and sixty-seven MDD patients without family history were assigned to research group,sixty-seven healthy volunteers were assigned to control group,and ERP P300 detections were conducted in all subjects.Results①To compare with control group ( ( 189.33 ± 51.13 ) ms) and MDD without family history group( ( 193.55 ± 40.01 )ms),the N2 latency was prolonged more significantly in MDD with family history group ( ( 208.40 ± 33.05 ) ms ) (P ＜ 0.05 ).②Compared with control group ( ( 3.38 ± 5.52 ) μV ),the N2 amplitude was decreased more significantly in MDD without ( ( 2.47 ± 1.87 ) μV ) and with family history ( ( 2.36 ± 2.10) μV ),(P ＜ 0.05 ).ConclusionThere is an obvious cognitive function damaged in the MDD patients with and without family history and the MDD patients with family history are more serious.

Heart rate variability (HRV) is a reliable, innocuous and sensitive new index to measure cardiac autonomic nervous function. Anxiety disorder is often accompanied by autonomic nerve dysfunction and its main sign is abnormal HRV. Acupuncture can affect HRV indices, correct abnormal HRV and improve cardiac autonomic nerve dysfunction to relieve anxiety. This article sorts out and analyzes recent years’ studies on abnormal HRV in anxiety disorder, the effect of acupuncture on HRV and acupuncture regulation of abnormal HRV in anxiety disorder to provide a therapeutic basis for clinical acupuncture intervention in abnormal HRV in anxiety disorder.

Objective To investigate the expressions and significances of Bcl-2 and Bax in basal-like breast carcinoma (BLBC).Methods The expressions of Bcl-2 and Bax were detected in 43 cases of BLBC, 57 cases of non-BLBC and 60 cases of normal breast tissues by immunohistochemistry,and their relationships with physiological and pathological characteristics of patients were analysized.Results The positive rate of Bcl-2 in BLBC was 69.77%,higher than 43.86% in non-BLBC (χ2 =6.647,P =0.01 0)and 21 .67% in normal breast tissues (χ2 =23.831 ,P =0.001 ).The positive rate of Bax in BLBC was 20.93%,lower than 45.61 % in non-BLBC (χ2 =6.564,P =0.01 0)and 76.67% in normal breast tissues (χ2 =31 .270,P =0.001 ).The expressions of Bcl-2 and Bax were correlated with lymphnode metastasis (χ2 =6.927,P =0.008;χ2 =6.203,P =0.01 3)and pTNMstaging of BLBC (χ2 =6.331 ,P =0.01 2;χ2 =5.972,P =0.01 5).There was negative correlation between the expression of Bcl-2 and Bax in BLBC (r = -0.408,P <0.01 0). Conclusion High expression of Bcl-2 and low expression of Bax interact with each other leading to unbalance of cell deferation and apoptosis,resulting in promoting genesis and progress of BLBC.