Brown-Sequard Syndrome ; etiology ; Cervical Vertebrae ; Humans ; Intervertebral Disc Displacement ; complications ; surgery ; Male ; Middle Aged

Objective To evaluate the effect of cell-penetrating peptide (protein transduction domain 4,PTD4) mediated copper-zinc superoxide dismutase (Cu/Zn SOD) on hypoxia/reoxygenation injury (HRI) in rat myocardial cells.Methods Rat myocardial cell H9C2 HRI model was prepared by using the anaerobic incubator (85% N2,10% H2,5% CO2).The HRI group (without adding any treating factor in HRI cell culture fluid),HRI+Cu/Zn SOD group (adding 10 μmol/L Cu/Zn SOD) and HRI+PTD4-Cu/Zn SOD group (10 μmol/L PTD4-Cu/Zn SOD) were set up.In addition,normally cultured myocardial cells served as the normal control group.After incubating for 30 min,the ultra microstructure of mitochondria was observed under transmission electron microscope.The mitochondrial membrane potential was detected by JC-1 kit.The myocardial cell apoptosis was detected by TdT mediated dUTP nick end labeling TUNEL technique.Results The mitochondria injury degree after 30 min incubation in the PTD4-Cu/Zn SOD group was significantly improved compared with the HRI group.Compared with the normal control group,the mitochondrial membrane potential in the HRI group was significantly decreased,while the mitochondrial membrane potential in the PTD4-Cu/Zn SOD group was lower than that in the normal control group,but compared with the HRI group,which was obviously recovered.The cardiomyocyte apoptosis in the HRI+PTD4-Cu/Zn SOD group was (10.20±2.77)%,which was significantly decreased compared with (28.40±2.41)% in the HRI group,the difference was statistically significant (P<0.05).Conclusion PTD4 mediated Cu/Zn SOD can attenuate HRI in rat myocardial cells.

Animals ; Apoptosis ; physiology ; Carcinoma, Squamous Cell ; drug therapy ; physiopathology ; prevention & control ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors ; therapeutic use ; Head and Neck Neoplasms ; drug therapy ; physiopathology ; prevention & control ; Humans ; Membrane Proteins ; Neoplasm Invasiveness ; Neoplasm Metastasis ; drug therapy ; Neovascularization, Pathologic ; drug therapy ; metabolism ; Prostaglandin-Endoperoxide Synthases ; metabolism

Objective To explore the effect of lysophosphatidic acid(LPA)on blood-brain barrier(BBB) permeability and its possible mechanism.Methods LPA or LPA+suramin(L+S)were stereotaxically injected into the right eaudate nucleus in SD rats in vivo.Evans blue(EB)was used to quantitatively measure the permeability of BBB at different time points.The expression of matrix metalloproteinase-9 was detected by immunohistochemistry technique.The pathological ultrastruetural changes of BBB were assessed by transmission electron microscopy.Results The BBB permeability began to increase after LPA administered into ipsilateral eaudate nucleus,and reached the peak at 24h.Then the permeability of BBB gradually lowered after 48h.In comparison with the same time points of control group,there were quite significant differences(P＜0.01).After L+S was injected,the change of BBB permeability had differences in comparison with those of LPA group in the same time points,(P＜0.05).MMP-9 positive cells were mainly vascular endothelial cells.The numbers of MMP-9 positive blood vessels grew at 6h in LPA group,and the expression of it reached maximum at 24h,then the number of it decreased at 48h,showing significant statistical differences in comparison with the L+S group(P＜0.01),It was observed microscopically that ultrastrueture of BBB of the LPA group was changed sharply,such as basement membrane roughed and fragmented,astroeyte end-feet swolled markedly and perivaseular space enlarged obviously.But there were no remarkable changes in BBB in L+S group.Conclusion LPA can induce increase of BBB permeability and its possible mechanism is the strong expression of MMP-9 protein produeted by endothelial cells through the mediation of LPA receptor,leading to degradation of basement membrane.

Background Dyslipidemia is one of the major causes of age-related macular degeneration (AMD).At present,the study of the preventive and treating methods of A MD is still a hot spot.Objective The purpose of this study was to observe the effect of tonifying the spleen and promoting blood circulation on the retina and Bruch membrane in apolipoprotein E-deficient (ApoE-/-) mice with dyslipidemia.Methods Thirty-six ApoE-/-mice aged 2 months were randomly divided into the normal diet group,high fat diet group and medicine group.A diet with a higher content of fat was given for 5 consecutive months to the mice of the high fat diet group and medicine group,and in the last month,a concoction that tonifies the spleen and promotes blood circulation was gavagely administered in the medicine group,and an equivalent volumes of normal saline solution was administered in the same way in the normal diet group and high fat diet group.Total plasma cholesterol (TC),low density lipoprotein (LDL)and triglyceride (TG) were detected by (ELISA? Name of assay?) using the 7170 Hitachi automatic biochemical analyzer,and morphological changes of the retina and Bruch membrane were examined by light microscopy and transmission electron microscopy.The number of outer nuclear layer (ONL) cells,retinal pigment epithelial (RPE) cells and the thickness of the Bruch membrane were examined by semi-quantitative histopathology with the Mias 2000 Imaging Analyzer System.Results The concentrations of TC,LDL and TG were (6.47 ±0.49) mmol/L,(1.46 ±0.10)mmol/L and (0.62 ±0.21) mmol/L,respectively,in 7-month-old mice of the medicine group,showing a significant reduction in comparison with (10.53 ±0.30) mmol/L,(1.90±0.13) mmol/L,(1.15±0.29) mmol/L of the high fat diet group,and (9.63 ± 0.18) mmol/L,(1.12 ± 0.15) mmol/L,(0.88 ± 0.21) mmol/L in the normal diet group (P＜0.05-0.01).The disorder and atrophy of ONL and RPE cells,divergence of fiber of the Bruch membranes were found in both the high fat diet group and normal diet control group under the light microscope,and drusen formed in some of the mice in the high fat diet group.However,ONL and RPE were well organized in the medicine group.The cell numbers in the ONL and RPE layer in the 7-month-old mice were (23 124.00±755.18) and (10.75±0.59),respectively,in the medicine group,(19 107.00 ± 1436.82) and (8.55 ± 1.11),respectively,in the high fat diet group,(21 663.00± 1073.27) and (9.75 ±0.58),respectively,in the normal diet group,with significant differences among them (P＜0.05-0.001).Thickness of the Bruch membrane in the medicine group extensively reduced in high fat diet group and normal diet control group (P＜0.01).The ultrastructures of the RPE and Bruch membrane were much more improved in the mdedicine group.Conclusions Tonifying the spleen and promoting blood circulation can attenuate hyperlipemia in ApoE-/-mouse;furthermore,it lessens the pathological abnormalities in the ONL,RPE and Bruch membrane.

Objective To study the anti-tumor activity of quercetin in NB4 leukemia cells and the roles of PI3K/Akt,bcl-2,and Bax on the quercetin-induced apoptosis,and to investigate the potential underlying mechanism.Methods MTT assay was used to monitor cell proliferation,Hoechst 33258 fluorescent staining and flow cytometry were employed to detect apoptosis in NB4 cells.Western blot was used to detect the expression changes of related proteins in quercetin treated NB4 cells.Confocal laser microscopy was used to test the distributional variation of Akt between cytoplasm and nucleus.Results Quercetin significantly inhibited the NB4 cell proliferation in a dose-and time-dependent manner (20-160 μ mol/L).In addition,treated by 20,40 80 μmol/L quercetin,the rates of apoptosis were (9.25±0.11) ％,(20.83±2.10) ％and (41.43±2.90) ％,there were statistical difference compared with blank cells (t were 4.14,6.56 and 7.02,all P ＜ 0.05).This was concentration dependent and accompanied by morphological changes characteristic of apoptosis.Further,quercetin induced a G~M arrest,which might account for its cytotoxic effects.Quercetin decreased PI3k/Akt expression and caused an inhibition of the anti-apoptotic protein bcl-2,while increasing the expression of Bax.Quercetin had no effects on total Akt,but it promoted Akt translocation from cell nucleus to the cytoplasm (F =15.12,P ＜ 0.05).Conclusion Quercetin induces the leukemia NB4 cell apoptosis by affecting multiple signal pathways and plays a strong anti-leukemia effect.In addition,our results suggest that PI3K/Akt pathway could be a novel target for the leukemia chemotherapy.

Objective To discuss the optimal timing of fixation for femoral shaft fractures with concomitant head injuries. MethodsEarly and delayed complications,mortality rate,interval of ICU and duration of hospital stay were compared among 137 patients with head injuries,so as to evaluate the curative effect of early fixation of femoral shaft fracture(n=56) and delayed fixation(n=81).Results Early fixation group enjoyed advantages in the interval of ICU,duration of hospital stay,associated shock and infection rate over the delayed fixation group(P

AIM: To seek a small interfering RNA ( siRNA ) sequence targeting rat inhibitor of nuclear factor kappa Bα ( IκBα) that can specifically and effectively suppress IκBα mRNA expression of rat ciliary muscles in vivo.METHODS:Three IκBα specific double stranded siRNAs were designed and synthesized. They were transfected into rat A7r5 cells which express IκBα gene. Flow cytometry was used to assess transfected efficiency. The mRNA and protein levels of IκBα were examined by Real Time quantitative polymerase chain reaction ( Real Time-PCR ) and western blot to screen a candidate valid sequence with the highest inhibitory rate. The Cy3 labeled non-specific control siRNA or the candidate valid siRNA was then injected into rat anterior chamber. Distribution of Cy3- siRNA in rat ciliary muscles was viewed by fluorescence microscopy, and the inhibitory effect in vivo of the valid siRNA was identified via Real Time-PCR and immunofluorescence. RESULTS: The suppression effect of the siRNA targeting the CTACGATGACTGTGTGTTT of IκBα gene was most obvious by vitro screening. By anterior chamber injection, this valid siRNA could reach rat ciliary muscles and effectively suppress IκBα gene expression with the highest inhibitory rate of 59. 0% on mRNA level at 24h after RNAi, and 52. 3% on protein level at 72h after RNAi (P<0. 01).CONCLUSION: It proves that the siRNA targeting the CTACGATGACTGTGTGTTT of IκBα gene is the valid sequence to suppress rat IκBα expression of ciliary muscles by RNAi in vivo.

Appropriate selection and measurement of lead biomarkers of exposure are critically important for health care management purposes, public health decision making, and primary prevention synthesis. Lead is one of the neurotoxicants that seems to be involved in the etiology of psychologies. Biomarkers are generally classified into three groups: biomarkers of exposure, effect, and susceptibility.The main body compartments that store lead are the blood, soft tissues, and bone; the half-life of lead in these tissues is measured in weeks for blood, months for soft tissues, and years for bone. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum can lead to a variety of neurological disorders, such as brain damage, mental retardation, behavioral problems, nerve damage, and possibly Alzheimer's disease, Parkinsons disease, and schizophrenia. This paper presents an overview of biomarkers of lead exposure and discusses the neurotoxic effects of lead with regard to children and adults.
Alzheimer Disease ; chemically induced ; metabolism ; pathology ; physiopathology ; psychology ; Animals ; Behavior ; drug effects ; Biomarkers ; metabolism ; Brain ; metabolism ; pathology ; physiopathology ; Brain Diseases ; chemically induced ; pathology ; physiopathology ; Environmental Exposure ; adverse effects ; Humans ; Lead ; pharmacokinetics ; toxicity ; Lead Poisoning ; etiology ; metabolism ; pathology ; physiopathology ; psychology ; Neurotoxicity Syndromes ; etiology ; metabolism ; pathology ; physiopathology ; psychology ; Parkinson Disease, Secondary ; chemically induced ; metabolism ; pathology ; physiopathology ; psychology ; Schizophrenia ; chemically induced ; metabolism ; pathology ; physiopathology

The Uncariae Ramulus Cum Uncis is a commonly used traditional Chinese medicine. In recent years, many studies have revealed its prominent neuroprotection function. The active ingredients in Uncariae Ramulus Cum Uncis could protect the nervous system in a multi-path and multi-target manner. Uncariae Ramulus Cum Uncis shows the neuroprotective effect by resisting oxidation, scavenging free radicals, modulating neurotransmitters and their related receptors, regulating the inflammatory factors and their related pathways, attenuating neuron apoptosis, reducing intracellular Ca2+ overloads and mitigating neurodegeneration. In this paper, the authors summarized the advance in studies on neuroprotective mechanisms of Uncariae Ramulus Cum Uncis.
Animals ; Calcium ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Free Radical Scavengers ; pharmacology ; Humans ; Inflammation Mediators ; metabolism ; Neuroprotective Agents ; pharmacology ; Neurotransmitter Agents ; metabolism ; Uncaria ; chemistry