0.05).ICP increased rapidly to the maximum 1min after SAH(P

Although the treatment of aneurysmal subarachnoid hemorrhage (SAH) has made considerable progress in recent years,its mortality and disability have not been effectively controlled.Ischemic brain injury after SAH is considered to be an important reason for the poor prognosis of patients; however,its mechanism is still not fully understood.Studies have shown that the cerebral microcirculation disturbance after SAH is closely associated with ischemic brain injury.This article reviews the advances in research on cerebral microcirculation disturbance and ischemic brain injury after SAH.

Objective To explore the dynamic changes of blood brain barrier(BBB)permeability after experimental subarachnoid hemorrhage(SAH)in rats.Methods Eighty female SD rats were divided into normal saline control group(n=10)and SAH group(n=70).The SAH model was induced by injecting 300 ?l of autologous arterial blood into the subarachnoid space near the circle of Willis via a cannula in an artificial hole between the olfactory bulb and frontal lobe.BBB permeability in cerebral cortex of SAH and normal saline rats was assessed at 6,12,24,36,48,60,and 72 h after SAH establishment by fluorescence spectrophotometer and fluorescence microscopy for Evans Blue(EB)extravasation.The ultrastructural changes in BBB were observed with transmission electron microscope.Results Compared with the control group,the changes of Evans Blue content and extravasation in cerebral cortex of SAH group peaked at 36 h(P0.05).The severe ultrastructural abnormality was found at 36 h after SAH.Conclusion The changes of BBB permeability develop at the acute stage of SAH,resulting from multiple factors together.The BBB after SAH possesses a self-repairable property.

Objective To evaluate the surgical methods and clinical effects of the reconstruction of soft tissue defect in distal thumbwith dorsal thumb neurocutaneous vascular flap.Methods From January,2014 to December,2016,32 patients with soft tissue defects of distal thumb were repaired with dorsal thumb neurocutaneous vascular flaps,including left thumbs in 11 cases and right thumbs in 21 cases.They were including 7 cases of nail bed defects,9 cases of pulp defects under nails,16 cases ofthe defects of tips or stump of fingers;skin and soft tissue defects range of 1.5 cm×1.0 cm-3.5 cm×3.2 cm;Flap cutting areas range of 2.0 cm×l.5 cm-4.0 cm×3.5 cm.If the donor areas could be sutured directly,be sutured;if they could not,be covered with intermediate split thickness skin grafts.All patients were followed up when they were reviewed in outpatient department,and to be evaluated the shape,texture,sensation,flexion and extension function,and donor site of the flaps.Results One case of flaps blood circulation disordereddue to tight suture,and eased after the removal of part of the sutures;One case of flaps atrophied,and the phalangette was exposed after 3 months,so we removed the end part of bone and the wound was closed;other flaps were survived,with primary wound healing.In the total 32 patients,they were followed up range of 3 to 36 months,with an average of 12 months.Eighteen cases were followed up at least 6 months,which were 4 of the 7 cases of nail bed defects,5 of the 9 cases of pulp defects under nail and 9 of the 16 cases of the defects of tip or stump of fingers.The appearances and textures of flaps were good,protective sensations were restored,and skin flap two-point discriminationswere 8-10 mm.According to the Trial Standard for Evaluation of Upper Limb Function of Chinese Society of Hand Surgery,it was excellent in 11 cases,good in 17 cases and moderate in 4 cases,with the excellent and good rate of 87.5％.Conclusion It has advantages of simple operation,low risk,high success rate and satisfactory curative effects of the use of dorsal thumb neurocutaneous vascular flap for repair of distal thumb defect of skin and soft tissue.It is not only suitable for the hospital with good technical and equipment,but also suitable for the primary hospital.

RBC membrane shear elastic modulus and membrane viscosity are two important indexes reflecting RBC membrane viscoelasticity. Their variation was investigated in this study after rabbits were radiated with l60Co. With a new ektacytometer, we measured the small deformation index (DId) and the half-time of deformation relaxation (t0.5) of RBC in flow field then we calculated RBC membrane shear elastic modulus and membrane viscosity. We found that the value of RBC membrane shear elastic modulus and membrane viscosity continuously increased from 0 to 16th day then continuously decreased and tended to be stable on 60th day or so. The reason may lie in the variation of proportion of new and old RBC in blood and variation of microconformation of RBC membrane after rabbits were radiated with　60Co.

Objective To investigate the effect and underlying mechanisms of G-protein-coupled receptor 39(GPR39)activation on neuroinflammation and brain injury after experimental intracerebral hemorrhage in mice.Methods Mouse model of intracerebral hemorrhage(ICH)was established by intracerebral injection of autologous blood.A total of 176 male C57/BL6 mice were randomly divided into 8 groups:Sham group(n=42),ICH group(n=34),ICH+Vehicle group(n=32),ICH+TC-G 1008 group(n=44),ICH+GPR39 siRNA group(n=6),ICH+Scramble siRNA group(n=6),ICH+TC-G 1008+666-15 group(n=6),and ICH+TC-G 1008+Vehicle 2 group(n=6).GPR39-specific agonist TC-G 1008 was administered via oral gavage at 1 and 25 h post-ICH modeling.Additionally,GPR39 siRNA and cAMP response element binding protein(CREB)inhibitor 666-15 were intracerebroventricularly injected 24 h before induction of ICH to inhibit the expression levels of GPR39 and p-CREB.At 48 h after ICH,modified Garcia test,forelimb placement test and corner turn test were used to evaluate the short-term neurological deficits in mice.Brain water content was determined by wet/dry method.Immunofluorescence assay was performed to detect the co-localization of GPR39 in neurons and microglia in the brain tissue surrounding the hematoma,as well as the expression of NOD-like receptor thermal protein domain associated protein 3(NLRP3)in neurons.ELISA was employed to measure IL-1β,TNF-α and myeloperoxidase(MPO)levels in peri-hematoma tissue.TUNEL staining was performed to quantify apoptotic neurons around the hematoma.Nissl staining was utilized to evaluate neuronal damage.Western blotting was conducted to detect the expression of GPR39,p-CREB,CREB,NLRP3,Cleaved caspase-1(C-caspase-1),and gasdermin-D protein(GSDMD)in peri-hematoma brain tissue.Results GPR39 expression peaked at 48 h post-ICH in mice(P＜0.05),and it was expressed in both neurons and microglia.Activation of GPR39 by TC-G 1008(24 mg/kg)significantly improved the modified Garcia score,and increased success rate of left forelimb placement and the number of left turns(P＜0.05).Brain edema in the ipsilateral basal ganglia(BG)and cortex(CX)was significantly reduced(P＜0.05).The numbers of apoptotic and damaged neurons around the hematoma were obviously decreased(P＜0.05).The expression of pyroptosis-related molecules,including NLRP3,C-caspase-1 and GSDMD and the levels of inflammation-related factors,including IL-1β,TNF-α and MPO were notably decreased(P＜0.05).However,knockdown of GPR39 and downregulation of p-CREB expression significantly increased the expression of pyroptosis related molecules and inflammatory-related factors in peri-hematoma brain tissue post-ICH in mice(P＜0.05).Conclusion GPR39 activation may inhibit neuroinflammation and brain injury after ICH in mice partly through the CREB signaling pathway.Therefore,GPR39 may be a potential therapeutic target for mitigating neuroinflammation and brain damage after ICH.

Neuronal apoptosis is one of the essential mechanisms of early brain injury after subarachnoid hemorrhage (SAH). Recently, HLY78 has been shown to inhibit apoptosis in tumor cells and embryonic cells caused by carbon ion radiation through activation of the Wnt/β-catenin pathway. This study was designed to explore the anti-apoptotic role of HLY78 in experimental SAH. The results demonstrated that HLY78 attenuated neuronal apoptosis and the neurological deficits after SAH through the activation of low-density lipoprotein receptor-related protein 6 (LRP6), which subsequently increased the level of phosphorylated glycogen synthesis kinase 3 beta (p-GSK3β) (Ser9), β-catenin, and Bcl-2, accompanied by a decrease of p-β-catenin, Bax, and cleaved caspase 3. An LRP6 small-interfering ribonucleic acid reversed the effects of HLY78. In conclusion, HLY78 attenuates neuronal apoptosis and improves neurological deficits through the LRP6/GSK3β/β-catenin signaling pathway after SAH in rats. HLY78 is a promising therapeutic agent to attenuate early brain injury after SAH.