Objective To study the clinical efficacy and safety of improved thrombolytic regimen combined with systemic anticoagulation therapy for cerebral venous sinus thrombosis (CVST).Methods Fifty-seven patients with CVST were divided into anticoagulation group (34 cases) and combined thrombolysis group (23 cases) according to different treatment.On the basis of conventional therapy,patients in anticoagulation group were given low molecular weight heparin anticoagulant therapy; while patients in combined thrombolysis group were given improved thrombolytic interventional treatment program.Neurological deficit scores,the degree of disabihty,the recanalization rate and adverse reaction rate after treatment of two groups were compared.Results Cases in combined thrombolysis group received thrombolytic therapy for 2-8 d,and urokinase total application was 26 million-384 million U.Nerve function in combined thrombolysis group improved significantly compared with that in anticoagulatian group after treatment (Z =-1.725,P =0.048).The degree of disability after treatment was assessed by menopause rating scale (mRS) scores.The number of fully restored,partially restored,disability and death in anticoagulation group was 19,6,6 and 3 cases,respectively,while in combined thrombolysis group was 20,2,1 and 0 case.The degree of disability in combined thrombolysis group after treatment was significantly lower than that in anticoagulation group (Z =-1.894,P =0.043).Sixteen patients in combined thrombolysis group underwent angiography after treament,among whom complete recanalization occurred in 7 cases,and partial recanalization in 9 cases.Magnetic resonance imaging on veins review was done in 19 cases in anticoagulation group,among whom complete recanalization occurred in 3 cases,partial recanalization in 15 patients,and no significant change in 1 case.Thrombus recanalization rate in combined thrombolysis group was significantly higher than that in anticoagulantion group (Z=-2.126,P=0.024).Incidence of adverse reactions was higher than that in anticoagulation group [30.4％(7/23) vs.5.9％(2/34)](x2 =17.432,P＜0.01).The incidence of intracranial hemorrhage of the two groups had no significant difference (Z =-0.766,P =0.157).Conclusion The improved thrombolytic therapy program is more suitable for patients of a relatively short duration,especially with acute onset of CVST,which can effectively improve neurological function in patients and improve clinical outcomes.

Objective To observe the morphological changes by different electron beam radiation methods and different triamcinolone acetonide treatments on the role of hypertrophic scar of rabbit ear,and to explore the optimal treatment for the rabbit ear scar.Methods The ventral rabbit ear hypertrophic scar model was established,and intervention began at 28 days after surgery.The animals were randomly divided into control group (group A),saline group (group B),surgery plus saline group (group C),triamcinolone acetonide group (group D),surgery plus triamcinolone group (group E),and electron beam group (group F),2 days after surgical electron beam group (group G),and 7 days after surgical electron beam group (group H).HE stain,VG stain,toluidine blue stain,CD34 and Alpha-SMA immunohistochemical staining were performed,and comparied on histomorphology of each group.Results Collagen fibers observed showed that there was no statistically significance between groups A and B,groups D and G and groups F and H (P＞0.05),and the difference was statistically significant between other groups (P＜0.05).Mast cells were not typical by toluidine blue staining.The microvascular observation showed there was no statistically significance between groups A and B,groups F and H,and groups G and H (P＞0.05),and the difference was statistically significant between other groups (P＜0.05).Myofibroblasts showed no statistically significance between the groups A and B (P＞0.05),but the difference was statistically significant between other groups (P＜0.05).Conclusions Compared with electron beam radiation methods,triamcinolone acetonide injection is a better treatment.Early postoperative radiotherapy is better than late.Triamcinolone acetonide or electron beam radiation combined with surgery is better than simple treatment.

Hypcrlipidemia is one of etiological factors of pancreatitis,of which the genesis has somewhat speci ficity.This article reviews hyperlipidemia related pancreatitis about its conception,etiology,classification,pathogene sis.specific clinical manifestation as well as diagnosis and treatment.

AIM　To study the effects and mechanisms of cromakal im, an ATP-sensitive K+(KATP) channel opener, on rat vascular smooth mu scl e. METHODS　Isometric tension recording of aorta rings. RESULT S　Vasorelaxant effects to cromakalim which contracted by phenylephrine we re markedly reduced in the old rats. Endothelium removal or treatment either wit h the NO synthesis inhibitor L-NAME or the guanylate cyclase inhibitor meth ylene blue reduced the effects, however with the change of age, the IC50 v alues and maximal relaxation responses to cromakalim had little difference. Ach and SNP, which are the endogenous and exogenous donors of NO respectively, induc ed a lesser vasodilator effect in aortic segments from old compared with the oth er groups of rats. CONCLUSIONS　The vasodilator responses to cromaka lim decreased in old rats, its mechanism may be involved the lower release of NO or the lower sensitivity of vascular smooth muscle to NO.

Alzheimer disease(AD) is the most common cau se of dementia today. Th e characteristic histopathologic changes include neurofibrillary tangles, neurit ic plaques, neuronal loss, and amyloid angiopathy. The noted Alzheimer symptom is the dysfunction of learning a nd memory. Potassium channels play a key role in it. A 113-pS tetraethylammoniu m-sensitive potassium channel was consistently absent from AD fibroblasts and o lfactory neuroblasts. Cp20, a memory-associated protein, amyloid precuror prote in and presenilin which are all tightly associated with genetic Alzheimer diseas e can regulate the activities of potassium channels. The changes of potassium ch annels subtype need further study. Potassium channels are maybe the important dr ug targets in the treatment of Alzheimer disease.

Objective To investigate clinical effect of collagen dressing in treatment of facial hormone dependent dermatitis.Methods 107 patients were divided randomly into treatment group and control group.53 cases of control group were given citrate desloratadine,ompound glycyrrhizin tablets, 0.3% tacrolimus ointment, cod liver oil ointment for 4 weeks.54 cases of treatment group were given collagen dressing 25 minutesper night, based on control group.After 4 weeks of drug treatment,treatment group continued to be given collagen dressing once every other night, control group were given cod liver oil ointment twice a day, morning and night.Both groups continued to observe for 12 weeks, at the same time, 0.3% tacrolimus ointment was given once every other day.Compared effect of two groups in the short-term and long-term.Results There were no significant differences in symptom scores between the two groups pre-treatment; compared with pre-treatment,the symptom scores were decreased(P<0.05).Compared with control group, the symptoms of treatment group were lower than that of treatment group(P<0.05).Compared with control group, the clinical total effective rate was higher than treatment group ( P<0.05 ) .Conclusion The collagen dressing can improve the facial treatment of hormone-dependent dermatitis.

Object To study the effects of SINI TANG (SNT) on the rat aortic rings pre-contracted by high K + and phenylephrine (Phe). Methods The effects of SNT on the aortic rings in the presence of 60 mmol/L KCl and Phe (1?10 -9 -1?10 -4 mmol/L) were observed and t heir me chanisms were studied after treatment with Propranolol (Pro, 3?10 -6 mmol/ L) and Bay K8644 (BK, 1?10 -5 mmol/L) as tool drugs. Results SNT inhibited the contraction induced by cumulative Phe and decreased the maximum tension (T max ); Pro couldn't influe nce the effects of SNT. SNT attenuated the amplitude of contractile effect of hi gh K +; BK couldn't reverse the effects of SNT. Conclusion SNT can shift the dose-response curve to the right and decrease the T max . It shows that SNT is a kind of noncompe titive antagonism. SNT decreases the effect of high K + against contraction of the artery. BK, a L-type Ca 2+ channels activator, couldn't recover the inhibition induced by SNT. The results suggest that SNT inhibit ? 1 recep tor, while calcium channel may not be involved in attenuating the effect of SNT on high K +-induced contraction.

Potassium channels which are targets of antiarrhythmic drugs (class III) play an important role in cardiomyocyte membrane. Recently, with the application of molecular biology techniques , development of cloned potassium channels, successful isolation of human cardiomyocytes and research of single channel, scientists have learnedmore characteristics of kinetics, electrophysiology and pharmacology of potassium channels. All these help them to develop and study new antiarrhythmic drugs.

KCNQ channels are an important sub-family in potassium channels. They are divided into five subtypes, including KCNQ1, KCNQ2, KCNQ3, KCNQ4, KCNQ5. KCNQ channels have a wide range of physiological and pathophysiologi-cal correlates. KCNQ1 (KvLTQ1) forms cardiac-delayed rectifier-like K+ current in the heart with other subunits. Mutations in this channel can cause one form of inherited long QT syndrome (LQT1). KCNQ2 and KCNQ3 heteromultimers are thought to underlie the M-current; mutations in these genes may cause an inherited form of juvenile epilepsy. The KCNQ4 gene is thought to encode the molecular correlate of the 7K.n in outer hair cells of the cochlea mutations whose mutation leads to a form of inherited deafness. KCNQ5 co-assemble with KCNQ3 in brain, and may also play a role in the M-current heterogeneity.

Tau is a multifunctional protein that are originally identified as a microtubule-associated protein. Tau is mainly expressed in neurons. There is a protein phosphorylation/dephosphorylation imbalance and tau is abnormally hyperphosphorylatied in the brain of patients with AD and in this form it is the major protein subunit of paired helical filaments/neurofibrillary tangles(PHF/NFT). The modulation of the activities of phosphatase(PP)-2A, PP1 and tau kinase, such as GSK-3, cdk5 and MAPK effect tau protein hyperphosphorylation. It is unclear about the relation between tau and A? in AD, increased or altered A? production may be an initiating event in the pathogenic process in AD; but aberrant alternations in tau function are likely necessary for the subsequent neuronal dysfunction and death. Therefore, clearly defining the metabolism and function of tau in both normal and disease states is necessary for our understanding of AD and the development of appropriate therapeutic interventions.