infection.

Objective To describe survival of patients with aneurysm subarachnoid hemorrhage (aSAH) and its related factors. Methods Data of 88 patients with aSAH were analyzed retrospectively, including their age, gender, past medical history, therapeutic measures, complications and prognosis, and so on. Their survival and its related factors were identified by Kaplan-Meier method and COX proportional hazard regression model. Results Eighty-eight patients were followed-up for a total of 141. 9 person-year,with an average of (1.6 ?.0) years, and the longest of 5. 6 years. Survival was 78 percent, 73 percentand 68 percent in the first month, first year and 2. 5 - 5. 6 years after onset, respectively. Administration ofnimodipine (RR = 0. 981, 95 % CI = 0. 965 - 0. 997, P = 0. 023) was potential protective factor for deaths caused by aSAH. Compared with conservative medical treatment, both surgical occlusion (RR =0. 147, 95% CI = 0. 041 - 0. 532, P = 0. 003) and intervention embolotherapy (RR = 0. 221, 95% CI = 0. 060-0. 823, P= 0.024) were also protective factors. However, complications such as hyponatremia, pulmonary infection, alimentary tract hemorrhage (RR = 1. 965, 95% CI - 1. 404 - 2. 748, P ＜ 0. 05) and cerebral vasospasm (RR = 2. 951, 95% CI = 1. 473 - 5. 911, P = 0. 002) were independent risk factors for aSAH.Conclusions Prognosis in patients with hyponatremia, pulmonary infection, alimentary tract hemorrhage and cerebral vasospasm is unfavorable, and aneurysm occlusion by surgical operation, embolotherapy andadministration of nimodipine all can decrease fatality caused by aSAH.

Objective To investigate the risk factors related to cerebral vsospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH).Metrods The risk factors related to cerebral vasospasm in 88 patients with aSAH were identified through the multivariate logistic regression analysis and Cox analysis, including demographic factors, healthy habits, past mescal history, acute stress factors, acute complications, acute evaluation indexes, treatment time, therapeutic measures, and hemorrhage involving brain regions. Results Drinking history (OR=1.077,95%CI 1.015-1.142;P=0.014)was an independent risk factor for cerebral vasospasm before admission. Histories of smoking(RR=1.031,95%CI 1.001-1.063:P=0.042),diabetes mellitus(RR=1.333,95%CI 1.100-1.614;P=0.003)and hypertension (RR=1.066,95%CI 1.008-1.127;P=-0.024)were the independent risk factors for cerebral vasospasm during hospitalization. The increased leukocyte count(RR=1.117,95%CI 1.039-1.200;P=0.003)was a predictive factor for cerebral vasospasm; the administration of Nimotop(RR=0.990,95%CI 0.979-1.001;P=0.088)significantly decreased the risk of cerebral vasospasm;the blood glucose lexels in acute stage were not associated with the occurrence of cerebral vasospasm(RR=1.076,95%CI 0.968-1.196;P=0.175);there was no significant difference between endovascular embolization group and surgical clipping group in the risk of cerebral vasospasm(RR=0.792,95%CI 0.322-1.950;P=0.612).Conclusions The risk of cerebral vasospasm increased significantly in patients with aSAH who have the histories of long-term drinking, smoking, diabetes mellitus, hypertension as well as increased leukocyte count. The administration of Nimotop may significantly decrease the risk of cerebral vasospasm

Objective To observe influence of atorvastatin combining with berberine on blood cholesterol level and carotid atherosclerotic plaques in patients with acute artery atherosclerosis cerebral infarction disease. Methods Fif-ty-five cases of acute cerebral infarction patients were randomized into 3 groups: group A (n=28), group B (n=11) and group C (n=16). Group A, B or C received atorvastatin 20 mg (qn), atorvastatin 40 mg (qn) or atorvastatin 20 mg (qn) +berberine 0.4 g (tid), respectively. All groups were then followed up for 3 months. The total cholesterol(TC), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C),high-density lipoprotein-cholesterol(HDL-C and the changes of carotid atherosclerotic plaques including total plaque area (TPA), crouse score,carotid intima-media thickness (IMT) and the stability of carotid plaques as well as the serum levels of creatinine(Scr), alanine aminotransferase(ALT), aspartate aminotransferase(AST), were compared among three groups. Results After 3 months, the TC, TG and LDL-C were de-creased in all three groups. There were statistically significant differences in the TC and LDL-C among these three groups (P=0.011,P=0.033) after treatment. The compliance rate of group C (75.0%) was significantly higher than group A ( 32.1% ) and group B (45.5%) in LDL-C (P=0.026). Both berberine combining with atorvastatin and atorvastatin monotherapy(20mg could significantly reduce crouse score. Conclusions Berberine can significantly enhance the benefi-cial effects of atorvastatin on LDL-C and the crouse score in patients with acute artery atherosclerosis cerebral infarction patients.

Objective To examine neuroinflammation,oxidative damage and neuron loss in the contralateral parie-tal lobecortex of TBI model mice, and to investigate effects of berberine chloride on such secondary damage.Methods TBI model was established by a weight-drop hitting device and mice in berberine group were administered intragastrically with berberine chloride (50mg/kg.day) for 21 days.Immunofluorescence staining was used to assess activity of microglia and astrocyte.Immunohistochemistry was used to assess DNA oxidative damage, neuron loss and expression of COX-2 and iN-OS.Results Activation of microglia and astrocyte, expressions of COX-2 and iNOS and DNA oxidative damage were ob-viously increased by TBI,(19.82 ±1.88)and(16.96 ±1.69)、(13.79 ±4.32)and(8.67 ±0.96)、(27.86 ±5.38) and (16.00 ±7.59)、(31.92 ±6.57)and(24.79 ±2.78)respectively (P<0.01 or P<0.05).Activation of microglia and ex-pressions of COX-2 and iNOS were significantly suppressed by berberine ,(15.49 ±1.88)and(19.82 ±1.88)、(16.83 ± 7.89)and(27.86 ±5.38)、(26.25 ±2.41)and(31.92 ±6.57) respectively(P<0.01 or P<0.05).There was no differ-ence in neuron loss among three groups, (49.05 ±4.38),(48.56 ±3.56)and (47.75 ±4.14) respectively (P>0.05). Conclusions TBI can cause neuroinflammation and oxidative damage but not neuron loss in the contralateral parietal lobe cortex.Berberine chloride can significantly suppress neuroinflammtion in the contralateral parietal lobe cortex after TBI.

Objective To evaluate the risk factors of electrocardiographic abnormality in patients with acute cerebral infarction.Methods The clinical data of patients with acute cerebral infarction were collected,including the National Institutes of Health Stroke Scale (NIHSS),electrocardiogram (ECG),lipid,glucose,glycosylated hemoglobin,body mass index,homocysteine,high-sensitivity C-reactive protein,white blood cells,and medical history.Logistics regression was used to search the risk factors of ECG abnormality in patient with acute cerebral infarction.Results ECGs of 189 cases of patients with acute cerebral infarction were divided into normal (n =83) and abnormal (n =106).The rate of abnormal ECG was 56.09％,and abnormal ECG ST-T change was the most common.NIHSS,systolic blood pressure,total cholesterol,and white blood cells were correlated with the ECG abnormality with the one-way Logistic regression analysis.In addition,NIHSS,systolic blood pressure,and white blood cells were correlated with the ECG abnormality with the multiple Logistic regression analysis (r =1.18,P ＜0.01 ; r =1.02,P ＜0.01 ; r =1.19,P ＜ 0.05).Conclusions NIHSS,systolic blood pressure,and white blood cells were independent risk factors in patients with acute cerebral infarction.ECG monitoring should be performed especially in patients with high NIHSS,systolic blood pressure,and white blood cells count.

The most common metastatic site of breast cancer is the bone. Metastatic bone disease can alter the integrity of the bone and cause serious complications, thereby greatly reducing health-related quality of life and leading to high medical costs. Although diagnostic methods and treatments for bone metastases (BM) are improving, some patients with early breast cancer who are at high risk of BM are not diagnosed early enough, leading to delayed intervention. Moreover, whole-body scintigraphy cannot easily distinguish BM from nonmalignant bone diseases. To circumvent these issues, specific gene and protein biomarkers are being investigated for their potential to predict, diagnose, and evaluate breast cancer prognosis. In this review, we summarized the current biomarkers associated with BM in breast cancer and their role in clinical applications to assist in the diagnosis and treatment of BM in the future.

Objective To investigate the effect of berberine chloride on autophagy and β-secretase (BACE) level in mice with traumatic brain injury (TBI).Methods Eighteen female healthy C57BL/6 mice were randomly divided into three groups:control group,model group and berberine group (n=6).TBI models in the later two groups were established by a weight-drop hitting device and mice in berberine group were administered intragastricly with berberine chloride (50 mg/kg) once daily for 21 d.Immunofluorescent staining were used to assess LC3 and BACE expressions in ipsilateral cortex or thalamus,and then,their mean fluorescence intensities were calculated and compared among these three groups.Results LC3 expression in the ipsilateral cortex and thalamus and BACE expression in the ipsilateral cortex (0.02±0.01,0.06±0.02 and 0.04±0.01 in the control group,model group and berberine group) showed significant difference among the three groups (P＜0.05):LC3 expression in ipsilateral cortex and thalamus and BACE expression in the ipsilateral cortex of the model group were significantly increased as compared with those of the control group (P＜0.05);the LC3 expression in the ipsilateral cortex and thalamus and BACE expression in the ipsilateral cortex of the model group were significantly decreased as compared with those of the berberine group (P＜0.05).Conclusion Autophagy is over-activated in the ipsolateral cortex and thalamus and BACE is over-activated in the ipsolateral cortex after TBI,and these changes are significantly suppressed by berberine chloride.