Cerebral vasospasm is one of the most severe complications of subarachnoid hemorrhage. Its incidence is as high as 30-90%. It often causes severe regional cerebral ischemia or delayed ischemic brain damage, even resulting in cerebral infarction, and it thus becomes the primary cause of mortality and disability. In recent years, with the development of studies, people have realized that the oxyhemoglobin, inflammatory reaction, accumulation of vasoconstrictive substances, apoptosis, blood hypercoagulability and blood vessel cell proliferation play important roles in the development of cerebral vasospasm. Although its mechanism remains unclear, better effects have been achieved by using related treatment methods according to the available pathogenesis.

OBJECTIVE: To evaluate the effect and causes of failure of vitreoretinal(VR) surgery in rbegmatogenous retinal detachments associated with choroidal detachment. METHOD: Reviewing the operative effects of the vitreoretinal surgeries in 61 patients(61 eyes) with rhegmatogenous retinal detachment associated with choroidal detachment and PVR in this hospital. Vitrectomy, peeling of preretinal membranes, fluid/air echange and inert gas, silicone oil tamponade were used in these patients according to need. RESULTS: On discharge from the hospital, the postoperative effect obtained in 40 case(65.57%), and out of 35 eyes receiving the inert gas tamponade 26(74.3%)got ef fective pesults. Fourteen cases were followed up for 3 months(averge 9.5 months)and 10(7.4%)of them revealed stable. The factors of influencing VR surgery seemed to be the range of the choroidal detachments, number of opreative times, the inert gas tamponede and the time of corticosteroid application. The causes of failure of opreation might relate to severe and anterior PVR, and giant tears. CONCLUSIONS: The VR surgery was thought to be profitable in treating rhegmatogenous retinal detachment associated with choroidal detachment and PVR.

Objective To discuss the ultrastructural pathological characteristics and dynamic changes of brain vessel after subarachnoid hemorrhage(SAH),and the mechanism of these changes in delayed cerebral vasospasm.Methods SAH model was made by infusing blood twice into the cistern magna of Japanese rabbits.The animals were divided randomly into SAH group,saline group,puncture group and blank group,at 1 h,3 d,5 d,7 d and 10 d after the first infusion the animals were perfused and basilar artery was harvested.Ultrastructural changes were observed under light microscope and electron microscope.Results Under the light microscope,the vessel wall became thick,the vessel cavity became narrow,the endothelia cells became swollen,vacuoles could be found in the chromatin,inner elastic membrane became reductus and broke.Under the electron microscope,the close connection between the endothelial cells disappeared,the membrane of the cells fell off,and the mitochondria became swollen,vacuoles could be seen,the chromatin became concentrated,heterochromatin could be seen,smooth muscle became deformed,chromatin became uneven, myofilament had derangement and fragmentation and dissolved,vacuolus could be seen in the kytoplasm,mitochondrion became swollen.The structural change of basilar artery under the light microscope got similar to that under the electron microscope;slight change was observed right after 1 h of SAH,significant change was observed at 3 d,and most obvious change was observed between 5 d and 7 d.Conclusion Ultrastructural changes were observed in the basilar artery after SAH,and significant dynamic changes were observed in the progress.The damage of endothelia cells may be the important factors which cause delayed cerebral vasospasm.

Objective To design a new experimental facility to induce rat diffuse axonal injury model. Methods Rat diffuse axonal injury was induced by a new experimental facility,which was developed to let the rat head spin 90 degree at the moment to cause shearing injury.Vital sign and behavior of rat were measured simultaneously.The rats were sacrificed at 2 h,6 h,12 h,24 h,36 h,72 h and 10 d after injury,respectively,and the brain tissues were removed to prepare paraffin section.Then silver staining and HE staining were conducted to investigate changes of axonal fibers. Results There were unconsciousness,respiratory rhythm disturbance and hyporeflexia of pupil light reflex immediately after injury,and reactiveness decrease and activity retardation still existed even after resuming consciousness.At anatomical scene,subarachnoid hemorrhage or cerebroventricular haemorrhage were widespread.At an early stage,there were swelling,collapse,and axonal retraction ball formation at cortico-medulla junction,callosum,brainstem,and cerebellar white matter under microscope.But at the later stage,gitter cell proliferation and nest-like aggregation were major pathophysiological changes at focal brain tissue. Conclusion The new experimental facility is suit able to be used to induce rat diffuse axonal injury,since it is convenient,controlable,and precise.

Objective To discuss the changes of the S100B protein concentration in serum and cerebral spinal fluid(CSF) after subarachnoid hemorrhage(SAH) in rabbit model and their significance.Methods Rabbit SAH model was induced by the cisterna magna puncture and injection two times of autogeneic blood into the cisterna magna.The animals were divided randomly into SAH group,saline group,puncture group and blank group.The serum and CSF were taken in blank group after 3 days' breeding.At 1 h,3 d,5 d,7 d and 10 d after the first infusion,the serum and CSF of the other groups were taken.ELISA method was used to detect S100B protein concentration in serum and CSF.The result data was analyzed by software SPSS13.0.Results S100B protein concentration in serum and CSF of SAH group was much higher than that in the other three groups(P=0).S100B protein concentration in serum ascended from 1 h after SAH,reached the peak at 3～5 d after SAH,and then descended slowly.S100B protein concentration in CSF ascended from 1 h after SAH,then slightly descended,ascended and reached the peak at 5～7 d after SAH,and then descended slowly.S100B protein concentration in serum and CSF of saline group was higher than that in puncture group and blank group from 1 h after model establishment(P

Objective To investigate the mechanism of unbalanced expressions of endothelin receptors (ETA/ETB )in cerebral vasospasm (CVS)after subarachnoid hemorrhage (SAH).Methods The rat CVS models were established by injecting autologous blood into the cisterna magna the second time.Basilar artery morphology was observed under light microscope and immunofluorescence staining was conducted to dynamically detect ETA/ETB receptor expression.Results The cross-sectional area of the basilar artery in the SAH model group decreased at 2 d to 3 d,and then gradually returned to normal.ETA receptor expression in endothelial cells of the basilar artery increased at 2 d after SAH,peaked at 3 d and remained increased till 14 d.ETB receptor expression increased significantly in endothelial cells at 3 d,peaked at 7 d and remained the same level till 14 d.Conclusion The results suggest that ETA/ETB receptors play an important role in cerebral vasospasm after SAH.The specific expression differences of ETB receptor subtypes in the brain vascular layers need further study.

Objective To study the dynamic expression and distribution of high mobility group box 1 (HMGB-1)in diffuse axonal injury (DAI)in rats and to clarify its involvement in the inflammatory reaction after DAI in rats,in order to provide new targets for the clinical treatment of DAI.Methods A DAI model was established using a coronal rotation device and evaluated by HE,Glees-Marsland silver staining,and Mallory phosphotungstic acid hematoxylin staining.Immunohistochemistry,Western blot and RT-PCR were used to detect the expression and distribution of HMGB-1 in the cortex of DAI rats at 6 h,1 d,3 d and 7 d.And TUNEL was used to examine the apoptosis of neurons in DAI rats.Results Immunohistochemical results showed that at 6 h and 1 d after DAI,the number of HMGB-1-positive cells decreased,but at 3 and 7 d it began to increase.Western blot also showed that during the early stage after DAI (6 h and 1 d),the level of HMGB-1 protein in the cortex was significantly lower than that in the control group,but at the late stage (3 and 7 d)after DAI it significantly increased compared with that in the control group until 7 d.RT-PCR showed that at 6 h after DAI there was no significant increase in the level of HMGB-1mRNA,but at 1 d there was a slight increase compared with the control group;at 3 and 7 d,it showed an obvious significance.TUNEL staining indicated that the significant neuronal apoptosis appeared as early as 6 h after DAI,and reached the peak at 3 d;it started to decrease at 7 d but still remained at a relatively high level.Conclusion The dynamic expression and distribution of HMGB-1 showed significant changes with the time course after DAI in rats.They decreased at the early stage but increased at the late stage.At the early stage, HMGB-1 is mainly passively released by the necrotic neurons,and at the late stage it may be actively secreted by the active inflammatory cells.HMGB-1 may mediate the post-DAI neural cell apoptosis by inducing the inflammatory reaction.

Background As a common form of gastric cancer migration,lymph node metastasis largely affects the surgical treatment and prognosis of gastric cancer.Surgery is the fundamental curative option for gastric cancer that varies depending on different stages.The study aimed to compare the clinicopathological characteristics and lymph node metastatic patterns in patients of proximal gastric cancer with different T stages and investigate a reasonable radical gastrectomy approach in terms of the range of lymphadenectomy for proximal gastric cancer.Methods In our retrospective study,the data of 328 patients of proximal gastric cancer with different T stages were analyzed.By comparing the differences of lymph node metastatic rate and ratio,we investigated the clinicopathological characteristics and metastatic patterns of lymph nodes.Also,we were especially interested in the differences in survival rates between patients with and without No.5 and 6 group metastasis with the same TNM stage.Results The overall lymph node metastatic rate and ratio of advanced proximal gastric cancer were 73.4％ and 23.3％,respectively.The tumors of different T stages were statistically significant in size and differentiation degree (P ＜0.05),multivariate analysis showed that the depth of tumor invasion was an independent risk factor for lymph node metastasis in proximal gastric cancer (RR,12.025; 95％ CI,2.326 to 62.157; P=0.003).The overall survival rate of patients with No.5,6 group lymph node metastasis and those without was significantly different,but the differences in survival rates between patients with and without No.5 and 6 group metastasis with the same TNM stage were not statistically significant.Conclusions Different T stages in proximal gastric cancer showed different patterns and characteristics of lymph node metastasis.D2 lymphadenectomy in patients with early gastric cancer had little survival benefit because metastasis to level 2 nodes was rare.Therefore the range of the lymph node dissection in radical gastrectomy for earty gastric cancer was considered reasonable.Moreover,to meet the requirements of the lymph node dissection,total gastrectomy plus D2 lymphadenectomy or more are supposed to be applied for the advanced proximal gastric cancer patients.Precise T staging larqely determines the range of gastrectomy and lymphadenectomy.

Objective To investigate the role of JAK2/STAT3 signaling pathway in regulating the expression and nuclear-cytoplasm translocation of high mobility group box 1 (HMGB1) in early brain injury (EBI) after subarachnoid hemorrhage (SAH).Methods Ninety SD rats were divided into a sham group (15 rats),an SAH group (altogether 45 rats,with 15 ones for each time point of 6 h,1 d,and 3 d),an SAH+AG490 (JAK2/STAT3 inhibitor) group (15 rats) and an SAH+dimethyl sulfoxide (DMSO)group (15 rats).The SAH models in the later 3 groups were established by endovascular perforation;the blood vessels were not perforated in the sham group but the other operations were the same as in the SAH groups.(1) Western blotting was used to detect the expression of HMGB1 and phosphorylated JAK2/STAT3 (p-JAK2/p-STAT3) in the 4 groups (at different time points in the SAH group) and compared the expression changes between the 4 groups after AG490 intervention.(2)Immunofluorescence confocal microscopy was used to detect HMGB1 nuclear translocation in the 4 groups.(3) TUNEL staining was used to detect apoptosis in the 4 groups.(4) Brain water contents and neurobehavioral scores in the 4 groups were measured.Results (1) Western blotting showed that the expression levels ofp-JAK2 and p-STAT3 were significantly increased at 6 h,1 d,and 3 d after SAH,and there were significant differences between the sham group and the SAH group (P＜0.05).HMGB1 total protein,cytoplasmic HMGB1 and nucleus HMGB1 also increased significantly at different time points after SAH,and statistically significant differences existed between the sham group and the SAH group (P＜0.05).The expression levels ofp-JAK2/p-STAT3,HMGB1 and cytoplasm and nucleus HMGB1 in the SAH+AG490 group were significantly lower than in the SAH group and SAH+DMSO group(P＜0.05).(2) The immunofluorescence staining showed that HMGB1 staining was positive in the SAH group while the positive staining of HMGB1 was present mainly in the nucleus but not in the cytoplasm in the sham and SAH+AG490 groups,suggesting that AG490 might inhibit the nucleus-cytoplasm transposition of HMGB1.(3) Compared with the SAH and SAH+DMSO groups,the TUNEL staining positive cells in the SAH+AG490 group were significantly decreased (P＜0.05).(4) Compared with the SAH and SAH+DMSO groups,the brain water contents in the SAH+AG490 group decreased significantly and the neurobehavioral scores increased significantly (P＜0.05).Conclusions JAK2/STAT3 signaling pathway is involved in the pathological process of early brain injury after SAH,and its mechanism may be related to the regulation of HMGB1 expression and nuclear-cytoplasm transposition.The regulation of JAK2/STAT3 may contribute to the neuroprotection dependent of HMGB 1.

Objective:To investigate the risk factors for refracture after percutaneous kyphoplasty (PKP) in patients with osteoporotic vertebral compression fracture (OVCF).Methods:A retrospective cohort study was conducted on the clinical data of 149 OVCF patients who were admitted to the First Affiliated Hospital of Soochow University from June 2019 to June 2022, including 21 males and 128 females, aged 56-97 years [(73.2±8.7)years]. Initial surgical segments included T 7 in 1 patient, T 8 in 10, T 9 in 6, T 10 in 6, T 11 in 19, T 12 in 28, L 1 in 38, L 2 in 18, L 3 in 11, L 4 in 7 and L 5 in 5. Patients were divided into refracture group ( n=32) and non-refracture group ( n=117) according to whether they had postoperative refracture after PKP. Refractured surgical segments included T 8 in 2 patients, T 9 in 2, T 11 in 4, T 12 in 5, L 1 in 7, L 2 in 4, L 3 in 6, and L 5 in 2. The age, gender, underlying diseases (hypertension, diabetes), body mass index (BMI), preoperative bone mineral density (BMD), smoking history, drinking history, follow-up time, preoperative visual analogue scale (VAS), and preoperative Oswestry dysfunction index (ODI) of the two groups were recorded. Preoperative paravertebral muscle-related parameters of the two groups were calculated including cross-sectional area of bilateral psoas, bilateral erector spinae, bilateral multifidus, and vertebral bodies, paravertebral muscle mass, and vertebral bone quality (VBQ) score. Univariate analysis was performed to evaluate the correlation between the fore-mentioned indicators and postoperative refracture after PKP in OVCF patients. Multivariate logistic regression analysis was employed to identify the independent risk factors for postoperative refracture after PKP in OVCF patients. Results:Univariate analysis revealed that there was certain correlation of BMI, preoperative BMD, cross-sectional area of bilateral psoas, bilateral erector spinae, bilateral multifidus, paravertebral muscle mass and VBQ score with postoperative refracture after PKP in OVCF patients ( P<0.01), while no correlation was found between age, gender, hypertension, diabetes, smoking history, drinking history, follow-up time, preoperative VAS, preoperative ODI, or cross-sectional area of vertebral bodies and postoperative refracture after PKP in OVCF patients ( P>0.05). Multivariate logistic regression analysis showed that preoperative BMD ≤-3.4 SD ( OR=0.27, 95% CI 0.09, 0.80, P<0.05), paravertebral muscle mass ≤281.2% ( OR=0.98, 95% CI 0.97, 0.99, P<0.01) and VBQ score ≥4.8 points ( OR=4.41, 95% CI 1.18, 16.44, P<0.05) were significantly correlated with postoperative refracture after PKP in OVCF patients. Conclusion:Preoperative BMD ≤-3.4 SD, paravertebral muscle mass ≤281.2%, and VBQ score ≥4.8 points are the independent risk factors for refracture after PKP in OVCF patients.