Characteristics of vascular lesions in patients with posterior circulation infarction according to age and region of infarct

Patients with posterior circulation infarction underwent CT angiography and magnetic resonance angiography. Intracranial and extracranial vasculopathy was evaluated according to age group and location of stroke. Patients aged 〉 60 years and 〈 60 years had similar rates of vertebral artery dominance and vertebrobasilar artery developmental or origin anomalies. Vertebrobasilar artery stenosis or occlusion and tortuosity occurred more frequently in patients aged 〉 60 years than 〈 60 years. The rates of vertebrobasilar artery anomalies and tortuosity were high in patients with posterior circulation infarction. Vertebrobasilar artery tortuosity occurred more frequently in patients aged 〉 60 years, whereas vertebrobasilar artery developmental anomalies occurred with similar frequency in patients aged 〈 60 years and 〉 60 years. Patients with infarction of the brainstem or cerebellum were more ~ikely to have vertebral artery stenosis or occlusion, basi^ar artery stenosis or occlusion, vertebral artery dominance or tortuosity, and basilar artery tortuosity, and patients with infarction of the thalamus, medial temporal, or occipital lobes were more likely to have stenosis or occlusion of the vertebral or basilar arteries. Vertebrobasilar artery tortuosity, vertebral artery dominance （hypoplasia）, and congenital variations of the vertebrobasilar system may lead to posterior circulation infarction at different locations in different age groups.

ClC-3 chloride channel in hippocampal neuronal apoptosis

Over-production of nitric oxide is pathogenic for neuronal apoptosis around the ischemic area fol- lowing ischemic brain injury. In this study, an apoptotic model in rat hippocampal neurons was es- tablished by 0.5 mmol/L 3-morpholinosyndnomine （SIN-l）, a nitric oxide donor. The models were then cultured with 0.1 mmol/L of 4,4＇-diisothiocyanostilbene-2,2＇-disulfonic acid （DIDS; the chloride channel blocker）for 18 hours. Neuronal survival was detected using the 3-（4,5-dimethylthiazol- 2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay, and apoptosis was assayed by Hoechst 33342-labeled neuronal DNA fluorescence staining. Western blot analysis and immunochemilumi- nescence staining were applied to determine the changes of activated caspase-3 and CIC-3 channel proteins. Real-time PCR was used to detect the mRNA expression of CIC-3. The results showed that SIN-1 reduced the neuronal survival rate, induced neuronal apoptosis, and promoted CIC-3 chloride channel protein and mRNA expression in the apoptotic neurons. DIDS reversed the effect of SIN-I. Our findings indicate that the increased activities of the CIC-3 chloride channel may be involved in hippocampal neuronal apoptosis induced by nitric oxide.

Chloride channel blocker 4,4-diisothiocyanatostilbene-2,2'-disulfonic acid inhibits nitric oxide-induced apoptosis in cultured rat hippocampal neurons

Apoptosis in cultured rat hippocampal neurons was induced using the nitric oxide donor 3-morpholinosydnonimine, and cells were treated with the chloride channel blocker, 4,4- diisothiocyanatostilbene-2,2＇-disulfonic acid. Results showed that the survival rate of neurons was significantly increased after treatment with 4,4-diisothiocyanatostilbene-2,2＇-disulfonic acid, and the rate of apoptosis decreased. In addition, the expression of the apoptosis-related proteins poly（adenosine diphosphate-ribose）polymerase-1 and apoptosis-inducing factor were significantly reduced. Our experimental findings indicate that the chloride channel blocker 4,4- diisothiocyanatostilbene-2,2＇-disulfonic acid can antagonize apoptotic cell death of hippocampal neurons by inhibiting the expression of the apoptosis-related proteins poly（adenosine diphosphate-ribose）polymerase-1 and apoptosis-inducing factor.

Effects of calcium channel on 3-morpholinosydnonimine-induced rat hippocampal neuronal apoptosis

Previous studies have demonstrated that increased chloride channel activity plays a role in nitric oxide-induced neuronal apoptosis in the rat hippocampus. The present study investigated the effects of the broad-spectrum calcium channel blocker CdCI2 on survival rate, percentage of apoptosis, and morphological changes in hippocampal neurons cultured in vitro, as well as the effects of calcium channels on neuronal apoptosis. The chloride channel blockers 4-acetamido-4＇-isothiocyanatostilbene-2, 2＇-disulfonic acid （SITS） or 4, 4＇-diisethiocyanostilbene-2, 2＇-disulfonic acid （DIDS） increased the survival rate of 3-morpholinosydnonimine （SIN-1）-treated neurons and suppressed SIN-l-induced neuronal apoptosis. The calcium channel blocker CdCI2 did not increase the survival rate of neurons and did not affect SIN-l-induced apoptosis or SITS- or DIDS-suppressed neuronal apoptosis. Results demonstrated that calcium channels did not significantly affect neuronal apoptosis.

Mild hypothermia effects on intercellular adhesion molecule-1 and serum interleukin-6 expression in brain tissues of a rat focal ischemia model

BACKGROUND： Previous studies have confirmed the neuroprotective effect of mild hypothermia on ischemic brain injury. OBJECTIVE： To investigate the effects of mild hypothermia on intercellular adhesion molecule-1 expression and serum interleukin-6 levels in ischemic brain tissues of focal brain ischemia rats, and to explore the neuroprotective effects of mild hypothermia on ischemic brain injury. DESIGN, TIME AND SETTING： A randomized, controlled, neurobiological experiment was performed at the Central Laboratory, First Affiliated Hospital, Xinxiang Medical College, China from February to July 2006. MATERIALS： Thirty healthy, adult, Sprague Dawley rats were used to establish middle cerebral artery occlusion models using the suture method, The immunohistochemistry （streptavidin-biotin-peroxidase complex method） kit was purchased from Boster, China. Interleukin-6 radioimmunoassay was supplied by Institute of Radioimmunity, Technology Development Center, General Hospital of Chinese PLA. METHODS： The rats were equally and randomly assigned into mild hypothermia and control groups, and middle cerebral artery occlusion models were established. The rectal temperature was maintained at （37 ±0.5）℃ in the control group. In the mild hypothermia group, the rectal temperature was maintained at （33±1）℃. MAIN OUTCOME MEASURES： At 12 hours after model establishment, the ischemic brain hemispheres were coronally sliced at the level of the optic chiasm. The number of intercellular adhesion molecule-1-positive vessels per high-power field was observed with an optical microscope. Serum interleukin-6 levels were measured by radioimmunoassay. RESULTS： Compared with the control group, intercellular adhesion molecule-1 and serum interleukin-6 expressions were significantly decreased in ischemic brain tissues of the mild hypothermia group （P 〈 0.01）. CONCLUSION： Mild hypothermia exhibits a neuroprotective effect by reducing serum interleukin-6 and intercellular adhesion molecule-1 expression following cerebral ischemia.

Business Process Dynamic Reengineering Technology Based on Mode

To ensure the efficiency and quality of complex business process design,a mode-based dynamic business process reengineering approach is proposed in this paper.Firstly,the composition of business process is divided into five levels.Business process modes from three levels of mission,content and resource are defined,and the transition relationships between modes are given.Secondly,the architecture model of business process is defined based on the architecture analysis and design language(AADL).The dynamic reengineering framework and implementation procedure are designed.Finally,the AADL architecture models are analyzed and verified to evaluate the business process performance,and a blueprint for reengineering is formulated.Under the guidance of the blueprint,the detailed design and development of attributes such as business processes,activities,resources and cost are completed.Case studies are presented to validate that the mode analysis and dynamic reengineering approach based on the AADL architecture is able to improve the efficiency,reliability and reusability of business process design.

Dendritic mesoporous silica nanoparticles for enzyme immobilization

Dendritic mesoporous silica nanoparticles(DMSNs)are a new class of solid porous materials used for enzyme immobilization support due to their intrinsic characteristics,including their unique open central-radial structures with large pore channels and their excellent biocompatibility.In this review,we review the recent progress in research on enzyme immobilization using DMSNs with different structures,namely,flower-like DMSNs and tree-branch-like DMSNs.Three DMSN synthesis methods are briefly compared,and the distinct characteristics of the two DMSN types and their effects on the catalytic performance of immobilized enzymes are comprehensively discussed.Possible directions for future research on enzyme immobilization using DMSNs are also proposed.

Effect of aerobic exercise on GRP78 and ATF6 expressions in mice with non-alcoholic fatty liver disease

Nonalcoholic fatty liver disease(NAFLD)is a prevalent medical condition with an ever-growing trend.Although multiple intracellular mechanisms are involved,endoplasmic reticulum(ER)stress has been demonstrated to play a significant role in the genesis and progression.Most of the research supports the advantages of exercise for NAFLD.However,little is known about the molecular mechanism(s)that underpin the effectiveness of exercise training in NAFLD.This study aimed to identify how aerobic exercise affected hepatic ER stress in a mouse NAFLD model.In this study,the mice were fed either a standard diet(SD)or a high-fat diet(HFD)for 17 weeks.HFD mice were trained on a treadmill during the last eight weeks.All animals were tested for serum levels of biochemical assays,protein expression,and gene expression.The hematoxylin and eosin,Oil red O,and immunohistochemistry staining were also performed.The results indicated that a high-fat diet generated NAFLD,with serum lipid disruption and hepatic function impairment,and increased GRP78 and ATF6 expressions.However,aerobic training reversed the majority of these alterations.It is concluded that NAFLD appears to be associated with hepatic ER stress response,and aerobic exercise mitigates NAFLD via lowering ER stress proteins GRP78 and ATF6.

Mouse tumor susceptibility genes identify drug combinations for multiple myeloma

Long-term genetic studies utilizing backcross and congenic strain analyses coupled with positional cloning strategies and functional studies identified Cdkn2a,Mtor,and Mndal as mouse plasmacytoma susceptibility/resistance genes.Tumor incidence data in congenic strains carrying the resistance alleles of Cdkn2a and Mtor led us to hypothesize that drug combinations affecting these pathways are likely to have an additive,if not synergistic effect in inhibiting tumor cell growth.Traditional and novel systems-level genomic approaches were used to assess combination activity,disease specificity,and clinical potential of a drug combination involving rapamycin/everolimus,an Mtor inhibitor,with entinostat,an histone deacetylase inhibitor.The combination synergistically repressed oncogenic MYC and activated the Cdkn2a tumor suppressor.The identification of MYC as a primary upstream regulator led to the identification of small molecule binders of the G-quadruplex structure that forms in the NHEIII region of the MYC promoter.These studies highlight the importance of identifying drug combinations which simultaneously upregulate tumor suppressors and downregulate oncogenes.