20ng/ml.The total three-year survival rate is 87%(33/35).Conclusion The effect and prognosis of ?-knife on prostate cancer treatment can be evaluated by the value of PSA before and after the treatment.

AIM:As a factor that can improve cell growth,there are few studies about the effect of insulin-like growth factor Ⅰ(IGF-Ⅰ) on the apoptosis of endothelial cell.The study investigated the inhibition and mechanism of IGF-Ⅰ on the apoptosis of human umbilical vein endothelial cells(HUVEC) induced by oxidized low density lipoprotein(ox-LDL).METHODS:The experiment was performed in the Institute of Cardiovascular Disease,Union Hospital of Huazhong University of Science and Technology from December 2006 to July 2007.①Fresh human umbilical cord was obtained(the informed consent) to isolate and culture HUVECs.The cells were divided into four groups.Except the control group,HUVEC cells were cultured with IGF-Ⅰ(1?10-9mmol/L),ox-LDL(200 mg/L)+IGF-Ⅰ(1?10-9mmol/L),and ox-LDL(200 mg/L),respectively after cultured for 24 hours.②Cell viability was determined by MTT assay,morphology and apoptosis by DAPI fluorescence staining,and expressions of caspase-3 were analyzed.RESULTS:①Ox-LDL could significantly inhibit HUVEC cell proliferation.After treated with both IGF-Ⅰand ox-LDL,the cell proliferation increased obviously compared with the cells treated with ox-LDL(P

This study examined the change of p16(INK4a) and PNCA protein expression in myocardium after injection of hIGF-1 gene modified skeletal myoblasts into post-infarction rats. HIGF-1 gene modified skeletal myoblasts (hIGF-1-myoblasts) were injected into hind limb muscles of 18 post-infraction rats (experimental group). Primary-myoblasts were injected into 18 post-infraction rats (control group) and 12 non-infarction rats (sham group). Expression of p16(INK4a) and PCNA protein in myocardiums were separately detected immunocytochemically 1, 2 and 4 weeks after the inuection. The level of hIGF-1 and rIGF-1 protein in serum and myocardium were detected by enzyme-linked immunosorbent assay (ELISA). Compared with the sham group, the percentage of p16(INK4a) and PCNA positive cells reached a peak after 1 week in the control group and the experimental group (P<0.01). Moreover, the percentage of p16(INK4a)-positive cells in the experimental group was lower than in control group whereas the percentage of PCNA-positive cells was lower in the control group than in the experimental group (P<0.01). The percentage of p16(INK4a)-positive cells in the experimental group and the percentage of PCNA-positive cells in the control group were close to that in the sham group from the 2nd week (P>0.05). ELISA analysis disclosed that the myocardium level of rIGF-1 protein increased gradually in the controls and especially in the experimental group (P<0.01). The serum level of rIGF-1 decreased significantly in post-infraction rats, but these conditions were improved in the experimental group (P<0.01). The hIGF-1 protein in serum and myocardium were detected from the 1st week to the 4th week in the experimental group. Statistical analysis revealed significant associations of myocardium level of hIGF-1 protein with expression of p16(INK4a) and PCNA protein (r=-0.323, P<0.05; r=0.647, P<0.01). It is concluded that genetically hIGF-1-myoblast provides a means for constant synthesis and release of hIGF-1. It could not only improve the expression of rIGF-1 and PCNA protein in myocardium, but also suppress the expression of p16(INK4a) protein for 30 days in post-infraction rats. Myoblasts-mediated IGF-1 gene therapy may provide a new alternative for the clinical treatment of heart failure.

ObjectiveTo explore the effects of recombinant human growth hormone(rhGH)on myocardial inflammatory cytokine expression and heart function in rats with acute myocardial infarction (AMI). MethodsRats with AMI induced by left anterior descending coronary branch ligation were randomized to rhGH and control groups compared with sham-operated group. The effects of 4 weeks of therapy with GH starting 24 hours after myocardial infarction on myocardial cytokines expression and heart function were studied. Myocardial inflammation was examined by analyzing the myocardial cytokine production including the pro-inflammatory cytokines: interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α and the anti-inflammatory cytokine: IL-10. Echocardiography was used to evaluate heart function. ResultsThe levels of TNF-α, IL-1β, IL-6 and IL-10 in the infarcted and non-infarcted region of control group were markedly elevated compared to sham-operated group (all P＜0.05). After 4 weeks therapy, rhGH reduced the expression of TNF -α, IL-1β, IL-6 and increased IL-10 expression in the infarcted and non-infarcted region of rhGH group compared to control group (all P＜0. 05 ). Echocardiography showed that rhGH markedly improved left heart function (P＜0. 05 ). ConclusionsEarly rhGH treatment can improve heart function and myocardial inflammatory cytokine expression after AMI. One of immunopharmacologic mechanisms underlying the beneficial effects of rhGH on heart function improvement may involve the attenuation of pro-inflammatory cytokines and the increase of anti-inflammatory cytokine levels in cardiac myocytes.

Objective To evaluate bone marrow mesenchymal stem cells combined with VEGF gene in the treatment of limb ischemia in rabbits.Methods The right hind limb ischemia model of New Zealand rabbit was established by superficial femoral artery excision and deep femoral artery ligation.Rabbits then were divided randomly into 4 groups: empty plasmid control group(EP group),bone marrow mesenchymal stem cells group(BMSC group),VEGF gene therapy group(VEGF group),combination bone mesenchymal stem cells and VEGF gene therapy group(BV group).There were 8 rabbits in each group.Angiogenesis was detected by arteriography on day 28 after treatment and expression of VEGF was detected by immunohistochemical staining on day 30 after treatment.Results There were no differences of collateral vessel count between the EP group,BMSC group and VEGF group.The collateral vessel count in BV group was higher than that of the other three groups.Immunohistochemistry of VEGF showed that the integrated optical density(IOD)in BMSC and VEGF groups increased significantly compared with the EP group; the IOD in BV group was the highest compared with the other three groups.Conclusions Combination bone marrow mesenchymal stem cells and VEGF gene in the treatment of limb ischemia in rabbits can obtain stable and effective expression of VEGF along with significant improvement of limb ischemia.

The efficacy of decompressive craniectomy (DC) in reducing traumatic brain injury mortality has been affirmed,but there are also many serious complications.Syndrome of the trephined (ST) and paradoxical herniation (PH) are rare complications.ST is characterized by a series of neurological deterioration due to skin flaps subsidence from weeks to months after DC.These neurological impairments are closely related to the subsequent repair of skull defects.PH shows progressive decrease in consciousness on the basis of ST,changes in pupils on the side of skull defects,low touch pressure at the defect window,and obvious midline shift and brain stem compression on CT.ST and PH have common inducements in pathophysiology,including cerebrospinal fluid dynamics,atmospheric pressure,cerebral blood flow and brain material metabolism.There is no consensus on the diagnosis of ST and PH,and early cranioplasty is suggested in terms of treatment.This article reviews the clinical manifestations,pathophysiological changes,diagnosis and treatment of ST and PH after DC operation,so as to provide references for clinicians to further understand ST and PH.

Objective: To investigate the clinical practicability and prognostic value of Helsinki CT score in patients with traumatic brain injury (TBI). Methods: A retrospective case series study was conducted to analyze the clinical data of 124 TBI patients admitted to First Affiliated Hospital of Xinjiang Medical University from September 2016 to October 2018. There were 91 males and 33 females, aged 14-84 years, with an average age of 49 years. Glasgow coma score (GCS) at admission ranged from 3-8 points in 45 patients, 9-12 points in 42 patients, and 13-15 points in 37 patients. According to Glasgow outcome scale (GOS) at 6 months after injury, 26 patients were classified into the poor prognosis group with GOS of 1-3 points and 98 patients were in the good prognosis group with GOS of 4-5 points. The prognosis-related risk factors were analyzed, and the role of Helsinki CT score to predict the adverse prognosis and mortality of TBI patients in the two groups was investigated. The sensitivity and specificity of Helsinki CT Score for 6-month poor prognosis were evaluated by receiver operation characteristic (ROC) curve and area under the curve (AUC). Results: Univariate analysis suggested that there were significant differences in terms of subdural hematoma, intracranial hematoma, extradural hematoma, hematoma volume >25 cm^3, intraventricular hemorrhage and suprasellar cistern pressure between the poor prognosis group and good prognosis group (P<0.05). Multivariate logistic regression analysis showed that the mortality and bad prognosis were related to the hemorrhage of ventricles, the pressure of suprasellar cistern and the disappearance of suprasellar cistern in the poor prognosis group and the good prognosis group (P<0.05), while intracranial hematoma and hematoma volume showed no association with mortality and poor prognosis (P>0.05). The Helsinki CT score could independently predict the adverse prognosis and mortality of TBI patients at 6 months (multivariate logistic regression: OR_death=1.21, OR_{adverse prognosis}=1.14). Helsinki CT score had a better predictive ability of 6-month mortality (AUC=0.85) than that of 6-month adverse prognosis (AUC=0.76), and had a predictive value for 6-month mortality and adverse prognosis. Conclusions Subdural hematoma, extradural hematoma, intraventricular hemorrhage and suprasellar cistern state (compression or disappearance) are the risk factors for the poor prognosis of TBI patients. Intraventricular hemorrhage and suprasellar cistern state are the main risk factors for predicting the mortality of 6 months. Helsinki CT score can independently predict the adverse prognosis and mortality of TBI patients at 6 months, and has relatively better value in predicting the mortality.

Abstract: Olfactory receptors (ORs) are transmembrane proteins mainly distributed in olfactory sensory neurons of the nasal epithelium, mediating the transmission of real-time sensory signals to the brain to produce smell. Recent studies have reported that ORs can also be expressed in tissues or organs outside the nasal cavity, and are closely related to a variety of biological processes, such as sperm chemotaxis, wound healing, glycolipid metabolism and intestinal secretion. In addition, ORs are closely related to a variety of malignant tumors such as prostate cancer, breast cancer and colorectal cancer, and may affect the occurrence and development of tumors by regulating cell proliferation, apoptosis, migration and invasion. This review provides an overview of the effects of ectopic ORs on the function of various human tissues and organs and assesses their potential value as drug targets for the treatment of human diseases.

Objective To study the effects of chronic exposure to inorganic arsenic (iAs) in drinking water on bone mineral density (BMD) in mice and its underlying mechanisms.Methods Five-month-old female C57BL/6 mice were randomly divided into sham groups and ovarectomy (OVX) groups (n =19 mice each group),which were further randomly assigned into control group (distilled water) and iAs exposure groups [5 mg/L and 20 mg/L,inorganic arsenite (iAsⅢ):inorganic arsenate (iAsv) =1 ∶ 1].Following 3 months of exposure to iAs,BMD of the mice were determined by the dual energy X-ray detector.RAW 264.7 cell line and bone marrow hematopoietic stem cells (BMHSC) primarily isolated from C57BL/6 mice were used to study the in vitro effects of iAs on osteoclast differentiation and underlying mechanisms.During differentiation induced by receptor activator of nuclear factor-κ B ligand (RANKL,50 μg/L) and macrophage colony-stimulating factor (M-CSF,30 μg/L),RAW 264.7 cell line were treated with 0.00,0.25,0.50,0.75,1.00,1.50 μmol/L iAsⅢ,while BMHSC with 0.0,0.2,0.4,0.6,0.8,1.0 μmol/L iAsⅢ for 6 days.Based on the effect of iAsⅢ on the differentiation of RAW cells,RAW 264.7 cell line were treated by 0.6 μmol/L iAsⅢ combined with 0,5,10 mmol/L of N-acetyl-cysteine (NAC).Tartrate resistant acid phosphatase (TRAP)-positive red-colored cells with 3 or more nuclei were considered mature osteoclast.Results The femoral BMD of the mice [(80.04 ± 4.06) mg/cm2] that had been exposed to 20 mg/L of iAs for 3 months was substantially decreased compared to that of sham control mice [(84.44 ± 4.40) mg/cm2].As expected,the BMD of the OVX group [(76.36 ± 3.36) mg/cm2] was significant decreased compared to that of the sham control group (P ＜ 0.05).However,the BMD among the OVX groups showed no significant difference [5 mg/L:(77.74 ± 4.91) mg/cm2;20 mg/L:(75.56 ± 3.71) mg/cm2,P ＞ 0.05].In vitro studies,the iAsⅢ evidently affected the osteoclast differentiation in a concentration-dependent fashion.Low concentrations of iAs Ⅲ exposure significantly augmented osteoclast differentiation in the two cell models while high concentrations showed inhibitory effect.In RAW 264.7 cells,the number of osteoclasts in different groups was significantly different (F =1 522,P ＜ 0.05),in the 0.50 μmol/L iAs Ⅲ group the number of osteoclasts reached the peak.In the BMHSC,the nmnber of osteoclasts in different groups was also significantly different (F =1 781,P ＜ 0.05),in the 0.6 μmol/L iAsⅢ group the number of osteoclasts reached the peak.NAC pretreatment significantly abolished low-level iAsⅢ(0.6 μmol/L)-induced augmentation of osteoclast differentiation in a concentration-dependent fashion (0 mmol/L:109.33 ± 3.06;5 mmol/L:56.00 ± 2.65;10 mmol/L:22.67 ± 0.58,F =1 940,P ＜ 0.05).Conclusions The inhibitory effect of iAs on bone metabolism is dependent on the availability of ovary function,suggesting that iAs may interfere with estrogen metabolism and/or function to disturb bone metabolism.Oxidative stress induced by iAs exposure stimulates osteoclast differentiation,and the increased osteoclast differentiation may be involved in the reduction of BMD caused by chronic iAs exposure.These preliminary findings suggest that antioxidant intervention may be an effective approach to prevent osteoporosis induced by chronic iAs exposure.

Objective To investigate the effect of donepezil on subventricular zone ( SVZ) neuro-genesis related neurotrophic factors after cerebral infarction. Methods Mice were randomly assigned into three groups: vehicle-treated sham group (Sham+vehicle,n=18),vehicle-treated middle cerebral artery oc-clusion (MCAO) group (MCAO + vehicle,n=30) and donepezil-treated MCAO group (MCAO+donepezil, n=30). Middle cerebral artery occlusion( MCAO) was induced by thread-occlusion method. Nissl staining was used to measure the infarct volume and the modified neurological severity score(mNSS) was used to as-sess neurologic function and brain water content was detected to assess brain edema degree. Proliferative cells and neuroblasts were labeled with 5-bromodeoxyuridine ( BrdU) and doublecortin ( DCX). The SVZ BrdU+/DCX+cells were detected by immunofluorescence. The expression of glial cell line-derived neurotro-phic factor (GDNF),brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were detec-ted by Western blot. Results The infarct volume of MCAO + donepezil group ((13. 33±4. 55)%) was sig-nificantly lower than that of MCAO + vehicle group ((31. 33±3. 93)%,t=7. 34,P<0. 05). The neurologic deficits were significantly ameliorated after donepezil treatment,and the brain water content of MCAO + done-pezil group ((71. 82±10. 18)%)was significantly less than that of MCAO + vehicle group ((85. 93± 7. 54)%,F=13. 480,P<0. 05). All differences were statistically significant (P<0. 05). The area of BrdU+/DCX+cells within SVZ of MCAO + vehicle group ((6. 16±1. 79)%) was significantly larger than that of sham + vehicle group ((2. 25±1. 09)%),and was fewer than that of MCAO+donepezil group ((16. 19± 2. 16)%,F=102. 756,P<0. 05). MCAO significantly promoted the expression of GDNF,BDNF and NGF within SVZ compared with sham operation,and donepezil increased these protein levels(F=15. 114,27. 121, 27. 398,P<0. 05). Conclusion Donepezil regulates neurogenesis via increasesing the expression of GDNF, BDNF and NGF within SVZ after cerebral infarction.