The morbidity and mortality of cardiovascular diseases(CVD)are still high in our country,they severely threaten peopleS health and quality of life.A dysregulated or reduced autophagy is associated with ischemic heart disease,cardiac hypertrophy,heart failure and arrhythmia.Autophagy is a key regulator in CVD development,and is essential for maintenance of heart function and improvement of prognosis.Thus,modulating autophagy represents an attractive future therapeutic target for treating cardiovascular disease.This article reviewed the research progression about effects of autophagy on ischemic heart disease,cardiac hypertrophy,heart failure and arrhythmia.

This article introduced the biological characteristics of N-methyl-D-aspartate (NMDA), and reviewed the relationship be-tween NMDA receptor and neurological disease, including cerebral trauma, cerebral ischemia, epilepsy, neuropathic pain, depression and Al-zheimer disease.

Objective To investigate the expression of H1 protein in the prefrontal cortex of comatose rats which have suffered traumatic brain injury (TBI) after electrical stimulation of the median nerve (MNS).Methods Seventy-two Sprague-Dawley rats (weighing 250 to 300 g) were randomly divided into a stimulated group (MNS+ TBI),an antagonist group (MNS+TBI+OXR1 antagonist),a model group (TBI) and a control group,with 18 rats in each group.Traumatic brain injury was modeled in all of the rats except those of the control group.After the modeling,the stimulated group was given MNS,the antagonist group was provided with MNS and an OXR1 injection,and the model group was given MNS with a current intensity of 0.One hour after the experiment,the consciousness of each rat was evaluated using a double-blind method.Animals were sacrificed at 6,12 and 24 hours after the intervention and brain tissue was removed.H1 protein expression was examined using immunohistochemistry.Results One hour after the experiment,significant differences were observed in the consciousness of the 4 groups,with the 18 rats of the control group on consciousness level one.Thirteen rats in the stimulated group exhibited a righting reflex,compared with 9 in the antagonist group and 5 in the model group.Immunohistochemistry showed that H1 expression was strongest in the stimulated group,followed by the antagonist,control and model groups.The H1 expression was highest at 24 hours after the experiment,followed by that at 6 h and 12 h,but those differences were not statistically significant.Conclusion Median nerve electrical stimulation might modulate wakefulness after traumatic brain injury by promoting H1 expression via orexin-A in the prefrontal contex.

blood stasis vessel obstruction syndrome among all cases,occupying 40.91%,31.31% and 13.89% respectively;the groups of damp-heat of liver and gall and stagnation of the liver Qi and deficiency of the spleen have very active replication of virus;however,insufficiency of both the spleen and the kidney are in lower-lever replication.[Conclusion]There is significant correlation between damp-heat of liver and gall and stagnation of the liver Qi and deficiency of the spleen and activity replication of HBV.In Chronic Hepatitis B,the dampness has a close relation with HBV.

Objective:To investigate the expression of 5-HT 2A receptor in the prefrontal cortex of traumatic brain injuryinduced coma rats after median nerve electrical stimulation.Method:A total of 72 SD rats (weighing 250-300g) were randomly divided into 4 groups:a stimulationgroup,an antagonist group,a sham-stimulation group and a control group.This traumatic brain injury model was established by a weight-drop head injury,and we evaluated the change of behavior through the six classical levels of consciousness.The animals were sacrificed and their brain tissues were removed at 6,12,and 24 hours after injury.5-HT 2A protein expression was examined by immunohistochemistry.Result:Thirteen rats exhibited righting reflex in the stimulation group.In the antagonist group,9 rats exhibited righting reflex.5 rats in the sham-stimulation group had the same response.The mean rank of consciousness degree were degree 9.50 in the control group,degree 52.75 in the sham-stimulation group,degree 37.61 in the stimulation group,degree 46.14 in the antagonist group.Comparison among groups presented an increasing consciousness degree:control group＜stimulation group＜antagonist group＜sham-stimulation group(P＜0.01).Resuits from immunohistochemistry showed that significant differences in the 5-HT 2A expression among the four groups (sham-stimulation＜control＜antagonist＜stimulation))(P＜0.05),and a within-group comparison showed that the 5-HT 2A expression level was as follows:6 hours＜24 hours ＜12 hours(P＜0.05).Conclusion:Median nerve electrical stimulation might modulate wakefulness by promoting the 5-HT 2A expression via orexin-A in the prefrontal cortex of rats with traumatic brain injury-induced coma.

Castration-resistant prostate cancer is a fatal disease with rapid progress. This malignancy usually presents with metastasis and poor prognosis. This type of disease also often causes 100%mortality, of which the median survival time is less than 20 months. Thus, treatment of castration-resistant prostate cancer remains challenging, and the underlying mechanisms of this cancer have yet to be identified. Several new therapies for castration-resistant prostate cancer have been proposed, such as androgen receptor antago-nists, immunotherapeutic drugs, taxanes, antiangiogenic agents, radionuclides, and bone-targeting drugs. These therapies can im-prove the survival time of patients. The advances in the treatment of castration-resistant prostate cancer are briefly reviewed in this ar-ticle.

Genetic Engineering ; Humans ; Rabies ; virology ; Rabies virus ; genetics ; pathogenicity ; Viral Proteins ; genetics ; Virulence

Objective To investigate the effect and mechanism of epigallocatechin-3-gallate(EGCG) on intestine ischemia reperfusion injury(IRI) in rats. Methods Forty SD rats were randomly and equally divided into 4 groups:sham group(Sham),intestinal ischemia reperfusion injury group(IRI),EGCG pretreatment group(EGCG) and HLY78 group (Wnt-Ag).The IRI,EGCG and WNT-AG groups were performed the superior mesenteric artery(SMA) ligation for 45 min by non-injury vascular clamp to construct the IRI model.EGCG (50 mg/kg) was administrated by intraperitoneal injection at 45 min before ischemia in EGCG group.The Wnt-Ag group was administrated by intraperitoneal injection of EGCG(50 mg/kg) plus Wnt-Ag (5 mg/kg) at 45 min before ischemia.The IRI group and Sham group were administrated by same dosage of normal saline.The pathological morphology of intestinal tissue was observed by staining at 4 h after reperfusion.The cellular apoptosis was detected by immunohistochemistry.The expressions of tumor necrosis factor-α(TNF-α),interleukin-1(IL-1),interleukin-6(IL-6) in the serum and intestinal tract were examined by ELISA and RT-PCR.The expressions of Wnt,β-catenin,p53,Bax and BCL-2 were measured by Western blot.Results Compared with the Sham group,the expression of IL-6,IL-1,TNF-α,Wnt,β-catenin,Bax,cell apoptosis and pathological change of intestinal tract in the IRI group were significantly increased,while the expression of BCL-2 was significantly decreased.Compared with the IRI group,the expression of IL-6,IL-1,TNF-α,Wnt,β-catenin,p53,Bax,cell apoptosis and the pathological change of intestinal tracrt in the EGCG group were significantly decreased,while the expression of BCL-2 was significantly increased.Compared with the EGCG group,the expression of IL-6,IL-1,TNF-α,Wnt,β-catenin,Bax,cell apoptosis and pathological change of intestinal tract in the Wnt-Ag group were increased,while the expression of BCL-2 was significantly decreased.Conclusion EGCG can alleviate intestine ischemia-reperfusion injury by suppressing inflammation and apoptosis,this protective effect may be mediated by suppressing Wnt/β-catenin signal pathway.

Objective To investigate the wake-promoting action of median nerve electrical stimulation(MNES) in coma rats induced by traumatic brain injury(TBI) and its influence on the expression of α1-adrenergic receptor(α1 R) in the prefrontal contex (PFC).Methods Seventy-two healthy Sprague Dawley(SD) rats were randomly divided into the control group,sham-stimulated group(TBI),stimulated group (TBI+ MNES) and antagonist group(TBI+ OX1R antagonist +MNES).The control group had no any treatment.The TBI coma rat models were prepared in the other 3 groups.The sham stimulated group had no treatment.The antagonist group was injected with orexin receptor-l(OX1R) antagonist SB334867 into lateral ventricle,and both the antagonist group and stimulated group received MNES treatment.Then the behavior changes of rats in each group were observed and the α1 R expression level in PFC was detected by using the immunohistochemistry technique.Results Thirteen rats in the stimulated group and 8 rats in the antagonist group revived,while only 4 rats in the TBI group.The α1R levels from low to high were the blank control group,sham-stimulated group,antagonist group and stimulated group,showing the increasing trend,and the difference was statistically significant(P＜0.05).Conclusion MNES can improve the rat consciousness level after TBI coma,and its mechanism may be related with up-regulating the α1 R expression level in PFC area,moreover Orexin-A participates in this regulation process.

Child, Preschool ; Coronary Aneurysm ; diagnosis ; etiology ; prevention & control ; Diagnosis, Differential ; Early Diagnosis ; Humans ; Immunoglobulins, Intravenous ; administration & dosage ; therapeutic use ; Immunologic Factors ; administration & dosage ; therapeutic use ; Infant ; Mucocutaneous Lymph Node Syndrome ; classification ; complications ; diagnosis ; drug therapy ; Prognosis