Objective To study the expression and cellular localization of STAT3 and SOCS-3 in the motor neurons of normal rat spinal cord. Methods Immunocytochemistry and morphometry methods were used in the present study. Results STAT3 immunocytochemical staining was mainly distributed in the cytoplasm of the motor neurons of the ventral horns, SOCS-3 immunoreactive products were extensively distributed in the neurons of the ventral and dorsal horns, glia and fibers of the spinal cord. In the ventral horn, SOCS-3 immunoreactivity was found in the nuclei and/or cytoplasm of the motor neurons.Conclusions STAT3 and SOCS-3 are extensively distributed in the normal adult rat spinal cord and SOCS-3 is existence in the forms of nuclear or cytoplasmic protein.

High mobility group box-1(HMGB1)distributed widely.It exists in many organs.HMGB1 locates in nuclei and cytoplasm in normal condition.It involves in many activity of life(i.e.,duplication of DNA,cellular differentiation,gene expression).The immunocytes(i.e.,mononuclear macrophage and dendritic cells)secrete HMGB1 into the extracellular milieu when stimulated with LPS and cytokines.It acts as proinflammatory cytokines,activates inflammatory and immunological responses.As a late mediators of inflammation and last long,HMGB1 plays an important role in sepsis,so it may be a convenient and practical index in evaluating severity of sepsis and may be an important and new therapeutic target in sepsis.It has been initially proved in experimental and clinical study.

Objective To study the basic expression and cellular localization of SOCS-3 in normal rat retina. Methods Neuro-immunocytochemistry techniques were used. Results SOCS-3 positive cells were widely distributed in the ganglion cell layer (GCL) and inner nuclear layer (INL) in the retina. In the GCL, SOCS-3 immunoreactivity was mainly in the neuclei of the ganglion cells.Some of the SOCS-3 positive cells in INL were M?ller cells.Conclusion Basal expression of SOCS-3 is widely present in the neurons and glia in normal adult rat retina and mainly in the form of nuclear protein.

Following the requirements for libraries in the Implementing Rules for Evaluation Standards of Tertiary Hospitals in Guangdong Province and taking municipal or above occupational disease prevention and control institutions as objects,the paper analyzes the construction situations,current collections and operating modes of libraries and discusses the setting of the occupational health information service function from 6 aspects of information sources,service objects and function setting,book retrieval,inter-library loan,service feedback and occupational health information service for labor.

Objective To evaluate the value of international normalized ratio (INR) in predicting and diagnosing hemorrhagic events in patients with nonvalvular atrial fibrillation (NVAF)receiving wafarin, to determine the optimal cut-off value of INR for predicting hemorrhagic events by receiver operator characteristic (ROC) curve. Methods The data of 231 patients with NVAF receiving wafarin were retrospectively analyzed, including 93 patients with hemorrhagic events and 138cases without hemorrhagic events as control group. The PT and INR were detected by Sysmex CA-500 with Medcalc software plotting ROC curve. Results The area under the ROC curve for INR was 0. 822 (95%CI: 0. 717-0. 900), the analysis of ROC curve revealed the optimal cut-off value of INR was 2.71, which presented a sensitivity of 77.40% and a specificity of 78.30%. Conclusions Through evaluation by ROC curve, the new cut-off value provides substantial improvement in sensitivity, with an acceptable loss of specificity. The value on predicting hemorrhagic events is better, the discriminative power of INR between hemorrhagic events and nonhemorrhagic events is satisfactory. The cut-off value of INR can guide the clinical physicians to predict the risks of hemorrhagic and promote proper use of clinical medications.

BACKGROUND: Recently,liver transplantation technique has been developed rapidly,and prevention of ischemia/reperfusion injury and protection of liver regeneration have become a research focus.Ischemic preconditioning(IPC)is an effective method for protecting liver ischemic injury.However,the mechanism remains controversial.OBJECTIVE: To investigate the mechanism of IPC on hepatic injury and regeneration after reduced-size rat liver transplantation.METHODS: Animals were randomly divided into 3 groups.Rat reduced-size liver transplantation model was established in liver transplantation group.IPC+liver transplantation group underwent first porta hepatis blocking for 10 minutes before liver graft reperfusion,followed by reperfusion for 15 minutes.The ligament around the liver was dissociated in the sham-surgery group.The samples were collected 0.5,2,6 and 24 hours post-operation.The hepatic injury was examined by the serum alanine aminotransferase(ALT)and hepatic tissue histopathology analysis of grafts.Semi-quantitative immunohistochemistry and westernblotting were used to examine the redox factor-1(Ref-1)protein expression.The hepatic regeneration of the grafts was examined by the expression of proliferating cell nuclear antigen(PCNA)in hepatic cells.RESULTS AND CONCLUSION: Compared with liver transplantation group,the ALT values at 6 and 24 hours after operation in IPC group decreased significantly(P < 0.05; P < 0.01).Pathological analysis indicated that there were lots of inflammation cells around the portal veins,the serious sinus hepaticus dilation and damage of hepatic tissue in liver transplantation group.However,the tissue injury observed in IPC group was comparatively slight.Semi-quantitative immunohistochemistry revealed that Ref-1 protein was more abundant in IPC grafts tissue compared to liver transplantation group.These observations were supported by westernblotting studies where Ref-1 protein was shown to be over-expressed in IPC specimens at 24 hours after reduced-size liver transplantation(P < 0.05).In addition,the number of PCNA-positive cells in IPC group was more than liver transplantation group at 2,6 and 24 hours after operation(P < 0.05).IPC improves hepatic regeneration and relieves grafts injury in earlier period after reduced-size rat liver transplantation,which is associated with the over-expression of Ref-1protein.

Objective Beta platelet-derived growth factor receptor ( PDGFR-β)-mediated signaling plays a key role in mor-phine tolerance , but its molecular mechanisms are not yet completely understood .The present study aims to investigate whether the ex-tracellular signal-regulated kinase ( ERK) and cyclic AMP response element binding protein ( REB) signaling pathways are involved in the development of PDGFR-βactivation-induced morphine tolerance in rats . Methods Thirty-six adult male SD rats were randomly divided into six groups of equal number:normal saline (20μL), morphine (15μg), morphine +imatinib (morphine 15μg +ima-tinib 10μg), morphine +PDGF-BB (morphine 15μg +PDGF-BB 10 ng), imatinib (10μg), and PDGF-BB (10 ng), all treated intrathecally at 20μL once daily for 7 consecutive days .Paw withdrawal latency ( PWL ) was measured 1 d before and 30 min after medication at 1, 3, 5, and 7 days, respectively, followed by calculation of the maximal possible effect of analgesia (MPE).On the 8th day, PWL was again obtained from all the rats at 30 min after intrathecal injection of morphine (15μg).Then, all the animals were sacrificed and the L4-5 segment of the spinal cord was isolated for determination of the expressions of ERK , phosphorylated ERK ( p-ERK) , CREB, and phosphorylated CREB ( p-CREB) by Western blot. Results At 5 and 7 days after medication, MPE was significant decreased in the morphine group ([52.90 ±8.20] and [15.12 ±3.80] %) and the morphine +PDGF-BB group ([43.51 ±5.42] and [14.81 ±3.60] %) as compared with (100.00 ± 0.00) %in both groups at 1 day (P<0.05), but had no significant changes in the morphine +imatinib group at 1, 3, 5, and 7 days.After intrathecal injection of morphine on the 8th day, MPE was (16.22 ±2.51) %in the morphine group, (15.22 ±3.50) %in the morphine +PDGF-BB group, and (35.21 ±4.51) %in the PDGF-BB group, all remarkably lower than (100.00 ±0.00) %in the control group (P<0.05).There were no significant differences in the expression levels of ERK and CREB among the six groups.The expressions of spinal p-ERK and p-CREB were markedly increased in the morphine , morphine +PDGF-BB, and PDGF-BB groups as compared with the control group (P<0.05), but significantly decreased in the morphine +imatinib group in compari-son with the morphine group, (P<0.05). Conclusion The PDGFR-βsignaling pathway plays an important role in the develop-ment of tolerance to morphine-induced analgesia and its underlying mechanisms may be associated with the activation of the ERK and CREB pathways .

BACKGROUND:Fluorouracil sustained-release agent is a commonly used anti-cancer sustained-release drug, which has a good anti-tumor effect.
OBJECTIVE:To explore the effect of fluorouracil sustained-release agent in the treatment of gastric cancer. METHODS:Literatures concerning the effect of fluorouracil sustained-release agent in the treatment of gastric cancer were retrieved and analyzed. In the paper, we investigated the preventive effect of fluorouracil sustained-release agent against tumor recurrence and metastasis after radical resection, and fol owed up the patients who underwent clinical peritoneal implantation of fluorouracil sustained-release agent. We could determine the effect of fluorouracil sustained-release agent in the treatment of advanced gastric cancer by observing the patient’s symptoms and signs, expression of tumor markers, tumor size and survival rate.
RESULTS AND CONCLUSION:After combination therapy of fluorouracil sustained-release agent and arterial infusion chemotherapy adjuvant therapy, the patient’s symptoms and tumor resection rate were significantly improved. The levels of CEA, CA19-9, CA72-4 in the serum of patients significantly reduced, while the apoptosis and necrosis of tumor cells significantly increased. Fluorouracil sustained-release agent could also reduce tumor metastasis and local recurrence, and improve patient survival.

Objective To observe the effects of nAChR antagonistα-conotoxin Eb1.6 on ther-mal pain threshold and spinal IL-1βexpression levels and astrocytes activation in rats using L5 spinal nerve transaction (SNT)model.Methods Fifty male Sprague-Dawley rats were randomly assigned into 5 groups with each group 10 rats:sham group,different doses of α-CTX Eb1.6 (0.1 5,1.5 and 1 5 nmol/kg)groups and the saline group after SNT.Saline solution or different doses of Eb1.6 were intraperitoneally injected seven days after the surgery when the model was stable and the treatment continued for seven days.Measured the TWLs of all groups of the rats 1,2,4,7,12 hours after the in-jection on 7 d and 13 d.The rats were sacrificed and L5 spinal cord tissues were collected immediately after the behavioral tests on 13 d.The expression of GFAP and IL-1βwere assessed by Western blot assay and enzyme linked immunosorbent assay (ELISA)separately.Results Groups E1,E2,E3 and C had shorter TWL before the injection on 7 d and 13 d than group N(P <0.05).The TWLs of the rats in groups E1,E2 and E3 of 1 h,2 h and 4 h after the injection on 7 d were significantly higher than that before the injection(P <0.05)with 2 h after the injection showed the most obvious change.The TWL of 1 h,2 h,4 h and 7 h after the injection of the rats in group E1,E2 and E3 and those of 12 h after the injection of the rats in group E2 and E3 on 13 d were significantly higher than that before the injection(P <0.05 )and also higher than TWL of the respective time points on 7 d(P < 0.05 ),also with 2 h after the injection showed the most obvious change.The TWLs of 2 h after the injection a-mong group E1,E2 and E3 showed significant differences both on 7 d and 13 d (P <0.05).Rats spi-nal IL-1βand GFAP expression levels of group E1,E2,E3 and C were significantly higher than those of group N(P <0.05).Rats spinal IL-1β and GFAP expression levels of groups E1,E2,E3 signifi-cantly decreased compared with group C(P <0.05).There were significant differences among the spi-nal IL-1βand GFAP expression levels of group E1,E2 and E3(P <0.05).Conclusion Eb1.6 dose-de-pendently reduced the thermal hyperalgesia induced by L5 spinal nerve transection.Repeated treat-ment of Eb1.6 could produce better analgesic effect,which might be partly attribute to the inhibition of spinal IL-βlevels and astrocytes activation.

Objective:To investigate the effect of nucleolin on cardiac cell apoptosis in Type 2 diabetic cardiomyopathy mice.Methods:Mice were fed with high-fat and high-sugar food for 20 weeks (mice were injected intraperitoneally with 60 mg/kg streptozotocin in the 5th and 6th weeks) to establish a mouse model of Type 2 diabetes.The mice were divided into 4 groups:a wild type (WT) control group,a nucleolin transgenic (TG) control group,a WT diabetic group,a TG diabetic group.Diabetesrelated indicators were detected at the end of the 8th week.At the end of the 20th week,HE staining was used to observe myocardial morphological changes;TUNEL staining and caspase-3 activity were used to detect the extent of apoptosis of cardiac myocytes.Results:The level of fasting blood glucose was significantly increased in the diabetic group than that in the control group.In WT diabetic group,myocardial disarrangement,fragmentation and dissolution were observed (determined by HE staining);cellular apoptosis (determined by TUNEL staining and caspase-3 activity) also increased markedly in the WT diabetic group.Compared with the wild mice in the diabetic group,myocardial morphological changes and cardiac myocytes apoptosis were alleviated significantly.Conclusion:Nucleolin overexpression affectes the occurrence and development of diabetic cardiomyopathy through inhibition of cardiac myocyte apoptosis.