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.

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 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.

AIM To investigate the patterns of potassium channel gene Kv 1 5 mRNA expression in the developing rat brain by using RNase protection assay. METHODS (1) RNA was extracted from brain tissues by one step method, (2) The preparation of DNA template, (3) Synthesis of RNA probe in vitro transcription, (4) RNA:RNA. RESULTS Kv 1 5 was absent in embryo tissue, but significantly increased at postnatal day 25 with adult rat, the mRNA expression did not show any change. CONCLUSION there is close relationship between Kv 1 5 mRNA expression is pertinent to the development and function differentiation of rat brain.

Microglia are immunocells in the brain and play key roles in the chronic inflammation of Alzheimers disease. Potassium channels are the important pathway for the microglia response to thechanges of microcircumtance in the brain. And the changes of potassium channels are the important marker of the activated microglia. The potassium channels are involved in the normal and pathological functions of microglia such as maintaining the membrane potential, proliferation, ramification, and the respiratory burst.

Small conductance Ca 2+ activated potassium channels ( SK channels) are potassium selective , voltage independent, and Ca 2+ high sensitivity. SK channels are widely distributed in neurons. SK underlie the slow afterhyperpolarization , which regulate the fire of neurons by spike frequency adaptation. Three mammalian SK channels (SK 1, SK 2, SK 3) have been cloned . Ca 2+ , CaM and neurotransimitters involve in the gating of these channels. The changes of these channels may result in memory, neuromuscular disorder and schizophrenia.

There is an evidence that mitochondrial cytochrome C has dual functions in controlling both cellular energetic metabolism and apoptosis. Once released, cytochrome C, in interaction with apoptotic protease activating factors (Apaf 1), initiates the activation of the execution caspases that lead to the subsequent apoptosis. Release of cytochrome C is the result of a perturbation of mitochondrial membrane permeability. Anti apoptotic Bcl 2 family proteins function as gatekeepers to prevent the release of cytochrome C. In addition to cytochrome C, mitochondria release other apoptogenic proteins including apoptosis inducing factor (AIF) during apoptosis. These two pathways may work together to induce complete apoptosis. After transient cerebral ischemia, the release of cytochrome C occurs from mitochondria, preceding DNA fragmentation.