Limb-shaking transient ischemic attack (TIA), a rare manifestation, is commonly caused by severe stenosis or occlusion of an extracranial internal carotid artery. Such patients are usually treated with surgical revascularization or anti-platelet therapy. We present a 56-year-old woman with 6 months’ episodic attacks starting with mouth skewed to the right and a sensation of ‘weakness’ involving predominantly her left arm, and at times, also involved the left leg. This was immediately followed by rhythmic jerky movements of the left arm and at times, also involved the left leg. Magnetic resonance angiography revealed severe stenosis of M1 segment of the right middle cerebral artery. The patient’s symptoms were signifi cantly improved by treatment with anti-platelet drugs and nimodipine.

Objective To study the differentially expressed genes and analyze its functional pathways of retinopathy of prematurity(ROP),in order to discover the pathogenesis and provide the theoretical basis for the prevention and treatment of ROP.Methods Fetal eyeballs of induced labor were obtained and retinal microvascular endothelial cells were isolated and cultured.The endothelial cells were divided into 7 groups according to the medium of cobalt chloride (CoC12) concentration (0 μ mol/L,100 μ mol/L,150 pμmol/L,200 μmol/L,250 pμmol/L,300 μmol/L,350 μmol/L),and 150 μmol/L CoCl2 was finally used to induce ROP model in vitro.Retinal microvascular endothelial cells were verified by adopting Ⅷ factor and CD31 antibody fluorescence staining.RNA purification,gene chip hybridization and signi-ficant analysis of microarrays were performed to screen differentially expressed genes.Genes functional pathways were studied by using gene ontology analysis software.Results (1) The proliferation activity of vascular endothelial cells decreased when CoCl2 ≥ 150 μmol/L(F =21,P ＜ 0.05).(2) In 150 μmol/L CoC]2 group,blue nucleus and green cytoplasm were visible in the second and the third generation vascular endothelial cells stained by factor Ⅷ antibody,and red fluorescence could also be observed in the cytoplasm by means of CD31 monoclonal antibody staining.However,only blue nucleus was detected in the group without CoCl2.(3)There were 326 genes differently expressed in retinal micro vascular endothelial cells induced by CoCl2 in vitro,among whom,198 genes were up-regulated and 128 genes were down-regulated.Up-regulated expression genes were 1.5 times more than those of the down-regulated genes.(4)Ten biological pathways including cell hypoxia,angiogenesis suppression and iron ion transport etc.may play important roles in ROP pathogenesis.Conclusions Hypoxic retinal microvascular endothelial cells induced by CoCl2 can successfully be used to induce cell model of ROP in vitro.Differentially expressed genes may play an important role in ROP development.Functional pathway such as hypoxic cells,inhibition of angiogenesis,iron ion transport may be associated with ROP pathogenesis.

[Summary] The aim of this study was to detect the levels of serum miR-130b expression in patients with type 2 diabetes mellitus and to analyze their correlation with diabetic renal damage. 243 patients with type 2 diabetes mellitus were divided into three groups according to urinary albumin/creatinine ratio ( UACR ): normoalbuminuria group (UACR<30 mg/g, n=103), microalbuminuria group (UACR 30-300 mg/g, n=86), and macroalbuminuria group(UACR>300 mg/g, n=54). The levels of serum miR-130b were validated by realtime polymerase chain reaction. Serum transforming growth factor-β1 (TGF-β1) and tumor necrosis factor-α(TNF-α) were determined by enzyme-linked immunosorbent assay ( ELISA) in all patients and 59 healthy volunteers. Compared with control group, the level of serum miR-130b in the type 2 diabetes mellitus group were significantly decreased, gradually with the increases of UACR. The level of serum miR-130b was inversely correlated with blood urea nitrogen ( r=-0. 295, P<0.05), serum creatinine(r=-0. 316, P<0. 05), UACR(r=-0. 463, P<0. 05), but positively related to the estimated glomerular filtration rate(r=0. 367, P<0. 01). The level of serum miR-130b was also negatively correlated to homeostasis model assessment for insulin resistance, triglyceride, low density lipoprotein-cholesterol, TNF-α, and TGF-β1 (r=-0. 257,-0. 345,-0. 242,-0. 562,-0. 622, all P<0. 01). The present study indicates that serum miR-130b might be a potential new biomarker for early diagnosis of diabetic nephropathy. Serum miR-130b might be involved in the pathogenesis of diabetic nephropathy.

Objective: To observe the influence of electroacupuncture with different frequencies on rats swimming endurance and sift out the optimal frequency parameter.Methods: Wistar rats were randomly allocated to control group, non-acupoint group and electroacupuncture with low frequency group (EA with 2 Hz group), electroacupuncture with medium frequency group (EA with 15 Hz group), and electroacupuncture with high frequency group (EA with 100 Hz group), acupoints Zusanli (ST 36) and Taichong (LR 3) were punctured and rats load swimming time was used as an index, and the change of swimming endurance time before and after acupuncture was observed. Results: After electro-acupuncture, swimming time was increased in 15 Hz and 100 Hz groups respectively, with the significant differences between before and after acupuncture (P＜0.05). There was also a significant difference in the percentage of increase in swimming time between 15 Hz group and other groups (P＜0.05).Conclusion: It is suggested that electroacupuncture at acupoints Zusanli (ST 36) and Taichong (LR 3) with a frequency of 15 Hz could enhance rats's swimming endurance, and 15 Hz might be an optimal frequency parameter during the electrical stimulation.

Adolescent ; Adult ; Child ; Child, Preschool ; Electrocoagulation ; methods ; Female ; Humans ; Hypothermia, Induced ; Male ; Middle Aged ; Prospective Studies ; Tonsillectomy ; methods ; Young Adult

Objective To assess which of topical tacrolimus and topical highly potent steroids,is more effective and safer in the treatment of pediatric vitiligo.Methods The PubMed,Cochrane library,Scopus and CINAHL plus databases were retrieved.The search was confined to English language articles.The randomized controlled trial(RCT) articles were included in our study.The quality of the identified articles was examined by using the CASP Randomised Controlled Trials Checklist.Results As a result,there were only a few studies related to the comparison.However,there were only two RCTs regarding a comparison of topical tacrolimus 0.1％ and clobetasol propionate 0.05 ％ in childhood vitiligo.Conclusion When the body surface area (BSA) involved in the child is ＜20 ％,and the disease is not rapidly spreading,topical therapy is the first choice.Topical tacrolimus may be considered as an alternative therapy for childhood vitiligo,especially for acrofacial and segmental types,before considering other modalities,but still need to observe long-term side effects.

Objective To investigate the differences of expression and activation of natural killer (NK) cell G2D (NKG2D) in patients with different immune status of chronic hepatitis B virus (HBV) infection, and to explore the significance of NKG2D-mediated immune injury in HBV infection.Methods Fifteen chronic HBV carriers (immune tolerance),15 chronic hepatitis B (CHB, immune activation) patients, 15 HBV-related acute/subacute-on-chronic liver failure (HBV-ACLF, immune over-activation) patients were enro1led in this study from January 2010 to December 2011 in the Third Hospital of Hebei Medical University.The frequencies of NK cells and NKG2D+ NK cells in peripheral blood mononuclear cells (PBMC) were detected by flow cytometry.The NKG2D mRNA expressions were measured by real-time fluorescent quantitative polymerase chain reaction.Localization and hemi-quantitative analysis of NKG2D+ cells in liver tissue were performed by immunohistochemistry staining.Concentrations of serum interferon(IFN)-γ, tumor necrosis factor(TNF)-α, perforin and granzyme B were quantified by enzyme 1inked immunosorbent assay (ELISA).Normally distributed continuous variables were analyzed using one-way analysis of variance (ANOVA), followed by Student-Newman-Keuls q test for evaluating variances between each two groups.For non-normally distributed data or heterogeneity of variance, differences between groups were analyzed using nonparametric Kruskal-Wallis H test, followed by Nemenyi test for pairwise comparisons.Pearson chi-square test was used to analyze categorical variables.Results The percentages of NK cells in PBMC were (13.58±3.24)% in healthy controls, (5.42±2.18)% in chronic HBV carriers, (7.92±2.85)% in HBV-ACLF group and (8.43±2.92)% in CHB group.The percentage of NK cells in PBMCs was lower in each chronic HBV-infected group compared with healthy controls (F=22.04, P<0.05).The frequency of NKG2D+ NK cells in HBV-ACLF group (18.92±5.85)% was the highest, followed by CHB group (12.85±3.39)%, healthy controls (8.45±2.86)%, and chronic HBV carriers (3.36±1.05%), with the statistically significant differences between each two groups (H=46.09, P<0.01).Intrahepatic NKG2D mRNA expression and NKG2D+ cells density were highest in HBV-ACLF group (6.58±1.86 and 30.69±6.67, respectively), followed by CHB group (3.25±0.95 and 17.36±4.13, respectively) and chronic HBV carriers (0.69±0.20 and 3.16±1.24, respectively), with the statistically significant differences between each two groups (H=52.10 and 52.73 respectively, both P<0.01).The similar patterns were observed in serum IFN-γ, TNF-α, perforin and granzyme B concentrations.Conclusions NKG2D expresses variously in patients with different immune status of chronic HBV infection.Activation of NKG2D may take part in the immune pathogenesis of chronic HBV infection.

OBJECTIVE: To detect the expression of ERβ in laryngeal carcinoma and the its correlation with the expression of epithelial-mesenchymal transition(EMT) specific biomarkers. METHOD: Picture MT-Pv9000 was used to detect ERβ and EMT in 72 cases of human aqueous laryngeal carcinoma and 8 cases of adjacent non-neoplastic laryngeal mucosa by immunohistochemistry. RESULT: The positive rates of ERβ in tumors and adjacent non-neoplastic laryngeal mucosa were 27.78% and 25.00%, respectively. The differences were not significant (P > 0.05). The abnormal expression rates of E-cadherin and β-catenin were 61.11% and 76.39% respectively. The expression of ERβ correlated negatively with the loss of E-cadherin, nuclear translocation of β-catenin and increased TNM stage. The differences were significant (P < 0.05). CONCLUSION The positive expressions of ERβ suggest a good prognosis in the differentiation, clinical stages and lymphatic metastasis of the laryngeal carcinoma. The underlying mechanism may be related with the abnormal expressions of E-cadherin and β-catenin.
Antigens, CD ; Biomarkers, Tumor ; metabolism ; Cadherins ; metabolism ; Epithelial-Mesenchymal Transition ; Estrogen Receptor beta ; metabolism ; Humans ; Immunohistochemistry ; Laryngeal Neoplasms ; metabolism ; Lymphatic Metastasis ; beta Catenin ; metabolism

OBJECTIVETo study the overexpression of Sox9 gene on rabbit bone marrow mesenchymal stem cells for repairing articular cartilage injury in vivo.

METHODSRabbit bone marrow mesenchymal stem cells (BMSCs) were transduced with lentivirus vector containing Sox9 gene and then cartilage specific molecule was detected by RT-PCR in vitro. Total 48 knee joints of 24 mature New Zealand white rabbits were randomly divided into 3 groups according to different defect treatment. After animals anesthesia,a full-thickness cylindrical cartilage defect of 4 mm diameter and 3 mm deep was created in the patellar groove using a stainlesssteel punch. Meanwhile, the transfected cells were implanted to repair the rabbit model with full-thickness cartilage defects. Cartilage defects tissue was observed with light microscope, electron microscope, HE and immunohistochemistry staining to assess the repair of defects by the complex at 6 weeks or 12 weeks after the implantation.

RESULTSAt 3 days after the transfection, Sox9 gene expression was highest and Sox9 gene expression decreased with the increase of time. At 3 days after the transfection, the expression of collagen type II began and reached the peak at 14 days. It showed that the bone marrow mesenchymal stem cells went into chondrogenic differentiation after transfected by Sox9 gene. Histological observation showed that at 6 weeks after the operation, the defects in the experimental group was filled with hyaline like cartilage tissue, 12 weeks after operation,the defects of cartilage and subchondral bone had satisfactory healing. Both at 6 and 12 weeks postoperatively, the defects were filled with fibrous tissues in control groups. Meanwhile, immunohistochemical staining of sections with type II collagen antibodies showed the proteins in the regenerated tissue stained positive for type II collagen and stronger than the control groups. The histological scoring system indicated that the cartilage repair of experiment groups were better than the two control groups with statistical significances.

CONCLUSIONOverexpression of Sox9 gene on rabbit bone marrow mesenchymal stem cells (BMSCs) promote the repair of cartilage defect.

Animals ; Bone Marrow Cells ; metabolism ; Bone Marrow Transplantation ; Cartilage, Articular ; injuries ; metabolism ; Cell- and Tissue-Based Therapy ; Female ; Genetic Vectors ; genetics ; metabolism ; Humans ; Lentivirus ; genetics ; metabolism ; Male ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells ; metabolism ; Osteoarthritis ; genetics ; metabolism ; therapy ; Rabbits ; SOX9 Transcription Factor ; genetics ; metabolism ; Tissue Engineering

Objective To investigate the role of ?7nAChR in the pathogenesis of Alzheimer's disease(AD)through exploring the relationship between ?7nAChR and A?_(1-42) in AD brains.Methods The accumulation of ?7nAChR and the possible relationship between ?7nAChR and A?_(1-42) were observed in 3 clinically and pathologically confirmed AD brains by immunohistochemistry. 3 normal brains were set as controls.Results Respective staining of anti-?7nAChR and anti-A?_(1-42) showed that the abnormal accumulation of ?7nAChR existed in AD brains. The main location was at hippocampus and temporal cortex which was just in accordance with senile plaque consisted mainly of A?_(1-42). The major part of ?7nAChR was located extra-cellular and within senile plaque from the view of morphology. No accumulation of ?7nAChR existed in normal brains. Co-staining of anti-?7nAChR and anti-A?_(1-42) further showed that ?7nAChR and A?_(1-42) could accumulate together in senile plaque of AD brain. The average rate of positive co-staining in hippocampus, temporal lobe and frontal lobe is 57.8%, 51.0% and 21.8% respectively. The accumulation of ?7nAChR in hippocampus and temporal lobe seems much than that in the frontal lobe. Conclusion ?7nAChR may combine with A?_(1-42) in AD brains. It is suggested that the combination should destroy the ?7nAChR receptor, block the receptor or mediate the injury of cholinergic neurons with the result of recognition and memory impairment and that ?7nAChR might play an important role in the pathogenesis of Alzheimer's disease.