Objective Vascular dementia(VD)is a common cognitive dysfunction associated with cerebrovascular disease.This study is aimed at investigating the therapeutic effect of anisodine hydromide(AH)on VD and the potential antioxidative stress mechanisms involved.Methods A VD model was established in Sprague-Dawley(SD)rats through permanent bilateral common carotid artery occlusion.The rats were divided into a sham group,a VD model group,and AH treatment groups receiving AH at low,medium,or high doses(n=4).The neurological function of the rats in each group was evaluated using the Bederson scale,and limb coordination ability was assessed using the pole climbing test.Superoxide dismutase(SOD)and malondialdehyde(MDA)levels in the serum and brain were measured by enzyme-linked immunosorbent assay(ELISA)to assess the level of oxidative stress.In addition,apoptosis was assessed by TUNEL assay,and reactive oxygen species(ROS)levels in neuronal cells were determined using dichloro-dihydro-fluorescein diacetate(DCFH-DA)probe.The potential mechanism of action of AH on M receptors was investigated using M1-M5 inhibitors.Results Compared with the sham group,the nerve function and limb coordination of rats in the VD model group were significantly impaired(P＜0.01),and the SOD levels were significantly decreased in the serum([100.70±18.95]U/mL vs.[44.22±7.11]U/mL,P＜0.001)and the brain([131.77±8.34]U/mg vs.[84.39±4.10]U/mg,P＜0.01),MDA levels were significantly increased in the serum([12.03±1.01]nmol/mL vs.[17.74±1.00]nmol/mL,P＜0.001)and the brain([4.41±0.30]nmol/mg vs.[6.17±0.70]nmol/mg,P＜0.05).AH treatment significantly improved the neurological function and limb coordination ability of VD rats.In comparison with the VD group,the high-dose AH treatment group,in particular,exhibited the most significant increase in SOD levels in the serum([44.22±7.11]U/mL vs.[98.67±0.86]U/mL,P＜0.001)and the brain([84.39±4.10]U/mg vs.[162.83±17.36]U/mg,P＜0.001),and the most significant decrease in MDA levels in the serum([17.74±1.00]nmol/mL vs.[6.68±0.06]nmol/mL,P＜0.001)and the brain([6.17±0.70]nmol/mg vs.[3.96±0.77]nmol/mg,P＜0.01).AH also reduced the number of TUNEL positive cells(P＜0.01)in a dose-dependent manner.The percentage of apoptotic cells was(36.10±9.07)％,(9.60±5.63)％,and(3.43±0.92)％,respectively,for AH treatment at low,medium,and high concentrations,indicating that AH had an inhibitory effect on apoptosis.According to findings from the in vitro experiments,AH treatment reduced the MDA content(P＜0.01),increased the SOD activity(P＜0.01),and decreased the ROS levels of HT22 and NSC-34 cells in a dose-dependent manner.M2 receptor inhibitors could reduce the ROS level in oxidative stress injury,suggesting that AH,as an M receptor antagonist,might exert its effect by inhibiting the M2 receptor.Conclusion AH modulates SOD and MDA levels and reduces oxidative stress injury,thereby improving neurological function and limb coordination and showing potential therapeutic effects in VD.The neuroprotective effects of AH may be related to its antioxidative stress and antiapoptotic mechanisms,and the M2 receptor may be a potential target of its actions.These findings provide an important theoretical basis for the development of new therapeutic strategies for VD.

Objective To disuss the clinic characteristics,the etiologies and the misdiagnosis cause of hyperthyroidism featuring in vomit mainly.Methods The clinic data of 35 hyperthyroids featuring in vomit mainly were reviewed and analyzed.Results The hyperthyroids in this group were middle-aged female mainly whose symptoms showd that they vomit frequently with abdominal distention,thin,inappetence,chest congestion,palpitation;tachycardia;hypohepatia and electrolyte disturbance.Furthermore,their thyroid gland function assay is in concordance with the hyperthyroidism diagnosis.Treatment for antihyperthyroidism can get remarkable effects.Conclusion The patient showing vomit of unknown origin may be taken into account as hyperthyroid.The key points to prevent misdiagnosis are to detect thyroid gland function in time and to improve the understanding for un-typical hyperthyroidism.

Aim To assess the effect of heat shock factor-1(HSF1)and heat shock protein 70(HSP70)to tachyphylaxis by bradykinin in the opening blood-tumor barrier(BTB).Methods The C6 rat intracerebral glioma model was constructed by stereotactic implantation technique.Using western blotting method to continue monitoring the protein expression of HSF1 and HSP70 in tumor tissue after bradykinin acted on animals.The expression of occludin in tumor tissue were detected by immunohistochemistry method.Using Evans blue and electron microscope,respectively,detected the permeability and pathology of BTB after intracarotid infusion of bradykinin in C6 rats.Results Bradykinin increased the tight junction opening and the permeability of BTB in C6 animals,and the relative increments of EB were 5.19 ?g?g-1(0 min),5.06 ?g?g-1(5 min),11.35 ?g?g-1(10 min,P