Adenoma, Pleomorphic ; pathology ; Adult ; Ear Neoplasms ; pathology ; Humans ; Male

Objective To investigate the possible mechanism of the gap junctional influence on the change in permeability of the blood-brain barrier(BBB)after reperfusion subsequent to cerebral ischemia.Methods In the test laser scanning confocal microscope(LSCM)was used to investigate the change of Cx43 levels and distribution.The MCAO/R model was induced using intraluminal suture technique first described by Longa with a little modification.A total of 60 Wistar rats were divided into 4 groups:the sham-operation group,control group,octanol-treatment group and DMSO vehicle control group. Control group were further divided into seven subgroups at different time points of reperfusion after middle cerebral artery occlusion.To observe the change in permeability of BBB,Evans blue(EB)in the brain tissue was surveyed by the means of EB fluorescent quantitation.Octanol-treatment group and DMSO vehicle control group were done at the point of the peak of permeability of BBB.Octanol,the specific blocker for gap junctions(GJ)was used in an intervention study.To compare the amount of EB with the same point of groups,the influence of octanol on BBB permeability was investigated.Results At 3 h of reperfusion after cerebral ischemia for 2 h,the permeability of BBB began to increase,reached the peak at 24 h of reperfusion and was still elevated at 72 h.The Cx43 expression formed into bigger plague and remained linear disposition in the penumbra after reperfusion subsequent to cerebral ischemia.Octanol group was done at 24 h of reperfusion after cerebral ischemia.The amount of EB of octanol group((4.924?0.296)?g/g)was significantly lower than that of corresponding operation control group(5.543?0.506)?g/g.Conclusions (1)Cx43 expression is concentrated around vessels in brain.The Cx43 forms into bigger plague and the function maybe strengthens after reperfusion.Gap junction might aggravate the disruption of BBB.(2) Octanol,the specific blocker of gap junctions,could effectively prevent the permeability of BBB from increasing and has a protective effect on BBB.

OBJECTIVE: To investigate the protective effect and possible mechanism of Rhizoma Coptis(RC) on lipopolysaccharide(LPS)-induced inflammatory injury in rat hepatocytes(BRL). METHODS: LPS-induced BRL cells injury model was established in vitro, then the damaged cells were given different interventions and treatment with 0.175, 0.1 mg• mL-1 RC aqueous extract as the test drug, and dexamethasone(Dex) as positive control drug. The optimal test doses of LPS and RC aqueous extract were selected and determined by cell counting kit-8(CCK-8), the cellular apoptosis rate was determined by flow cytometry, TLR4/NF-κB and TLR4/IRF3 signaling pathways and the mRNA level of related inflammatory mediators(TNF-α, IL-1β, IL-6) were detected by RT-PCR, the NF-κB p65 protein expression was analysed by Western blot and immunofluorescence techniques. RESULTS: ①Compared with normal control group, 0.1 mg•mL-1 LPS affected on BRL cells for 24 h, the cell survival rate was decreased significantly(P<0.01), the apoptotic rate increased significantly(P<0.01), the mRNA level of TLR4, NF-κB, IRF3, TNF-α, IL-1β, IL-6 were significantly increased(P<0.01), and the NF-κB p65 protein expression was increased. ②Compared with the model group, 0.1 and 0.175 mg•mL-1 RC affected on LPS-induced BRL cells for 24 h, the survival rate of BRL cells was increased significantly(P<0.05), the apoptotic rate decreased significantly(P<0.01), the mRNA level of TLR4, NF-κB, IRF3, TNF-α, IL-1β, IL-6 and the NF-κB p65 protein expression were decreased significantly(P<0.01). CONCLUSION: Rhizoma Coptis has obviously protective effect on LPS-induced inflammatory injury in rat hepatocytes(BRL), the mechanism of which may be related with inhibiting apoptosis, reducing the release of inflammatory factors such as TNF-α, IL-1β and IL-6, blocking NF-κB p65 protein nuclear translocation, interfering the R4/NF-κB and TLR4/IRF3 signaling pathway.

Objective To investigate the clinical efficacy and safety of bortezomib-based chemotherapy regimen [BTD chemotherapy regimen (bortezomib and thalidomide combined with dexamethasone) and BCD chemotherapy regimen (bortezomib and cyclophosphamide combined with dexamethasone)] in the treatment of new multiple myeloma (MM). Methods From May 2015 to May 2019, 80 newly diagnosed MM patients hospitalized in the Department of Hematology of Sanya Central Hospital were divided into BTD group (n=40) and BCD group (n=40). Patients in BTD group were given BTD chemotherapy regimen, and BCD group patients were given BCD chemotherapy regimen. Clinical efficacy, changes in myeloma markers [serum M protein, serum free light chain (κ-λ), immunofixation electrophoresis, β2 microglobulin, bone marrow plasma cells] and adverse reactions were evaluated in the two groups after 4 courses of treatment. Overall survival (OS) and progression-free survival (PFS) in the two groups were evaluated at follow-up period. Results The overall response rate (ORR) of the BTD group was significantly higher than that of the BCD group [95.0%(38/40) vs. 75.0%(30/40)], the difference was statistically significant (P<0.05). After treatment, the levels of M protein, serum free light chain (κ-λ), immunofixation electrophoresis, β2 microglobulin and bone marrow plasma cells in the two groups were significantly lower than those before treatment, and the BTD group was significantly lower than that of the BCD group, with statistically significant differences (P<0.05). The adverse reaction rate of BTD group was lower than that of BCD group [55.0%(22/40) vs. 97.5%(39/40)], and the difference was statistically significant (P<0.05). There was no significant difference in OS and PFS time between the two groups (P>0.05). Conclusion In the bortezomib-based chemotherapy regimen, the efficacy of BTD group is significantly better than that of BCD group, which could effectively reduce the indexes of myeloma, and the adverse reactions are lower, but there would be no significant difference in OS and PFS between the two groups.

Objective To compare the local control (LC), long-term overall survival (OS), and clinical adverse reactions in esophageal carcinoma patients receiving concurrent chemoradiotherapy at different radiotherapy doses.Methods A total of 373 esophageal carcinoma patients who received concurrent chemoradiotherapy in our hospital during 2004-2013 were included in this retrospective study.These patients were divided into<60 Gy group (n=99), 60 Gy group (n=155), and>60 Gy group (n=119) based on the dose of radiation.The Kaplan-Meier method was used to calculate LC and OS rates;the log-rank test was used for survival comparison and univariate prognostic analysis;the Cox model was used for multivariate prognostic analysis.Results The 3-, 5-, 7-, and 10-year sample sizes were 97,96,56, and 38 in the<60 Gy group, 146,141,72, and 17 in the 60 Gy group, and 118,115,56, and 20 in the>60 Gy group.The 3-, 5-, 7-, and 10-year LC rates were 55.3%, 51.4%, 48.9%, and 48.9% in the<60 Gy group, 65.1%, 60.1%, 55.1%, and 55.1% in the 60 Gy group, and 49.4%, 45.1%, 37.7%, and 37.7%(8-year) in the>60 Gy group (P=0.020).The 3-, 5-, 7-, and 10-year OS rates were 35.4%, 26.1%, 22.0%, and 22.0% in the<60 Gy group, 49.0%, 41.3%, 32.1%, and 28.9% in the 60 Gy group, and 31.1%, 25.2%, 14.5%, and 12.9%(8-year) in the>60 Gy group (P=0.000).The univariate analysis showed that for stage Ⅱ esophageal carcinoma patients with gross tumor volume (GTV) ≤44 cm3, the LC rate was higher in the 60 Gy group than in the<60 Gy group (P=0.040,0.035), and the OS rate was higher in the 60 Gy group than in the other two groups (P=0.001,0.003 and P=0.045,0.006).Similarly, for stage Ⅲ esophageal carcinoma patients with GTV>44 cm3, the LC rate was higher in the 60 Gy than in the>60 Gy group (P=0.011,0.015), and the OS rate was higher in the 60 Gy group than in the other two groups (P=0.045,0.006 and P=0.033,0.002).The incidence rates of acute radiation esophagitis and radiation pneumonia were significantly higher in the>60 Gy group than in the other two group (P=0.007,0.033).Furthermore, the multivariate analysis indicated that radiotherapy dose, T stage, and N stage were independent prognostic factors for esophageal carcinoma (P=0.004,0.008,0.037).Conclusions Concurrent chemoradiotherapy at 60 Gy is most efficacious for patients with esophageal carcinoma, and the radiotherapy dose of>60 Gy significantly increases the incidence of adverse reactions.

No abstract available.
Cyclotrons*

Biomarkers, Tumor ; metabolism ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; metabolism ; pathology ; Humans ; Lung Neoplasms ; drug therapy ; metabolism ; pathology ; Oncogene Proteins, Fusion ; chemistry ; metabolism ; Protein Kinase Inhibitors ; therapeutic use ; Pyrazoles ; therapeutic use ; Pyridines ; therapeutic use ; Pyrimidines ; therapeutic use ; Smoking

Objective To investigate the effects of evodiamine on autophagy of human colon a cleno carcinoma lovo cells, and to explore the role and mechanism of autophagy which was induced by evodiamine (EVO). Methods MTT assay combined with the morphologic changes were used to observe the cell viability. Monodansylcadaverine was used to detect autophagy by fluorospectrophotometer and the confocal laser fluorescence microscopy respectively. Immunoblotting assay was used to observe the microtubule-associated protein 1 light chain 3. Finally, evodiamine combined with 3-methyladenine to detect the cell viability with MTT assay and the apoptosis with the flow cytometry, respectively.Results Evodiamine inhibited the viability of Lovo cells in dose-dependent manner ( P ＜ 0. 05 ), especially in 60 μmol/L that was obviously(60% ). Further more, the cell lysis and cell gap widened was observed by the light microscope. Evo triggered the autophagy, and after inhibition the autophagy by 3-MA, the killing capacities of the Evo was enhanced ( P ＜ 0. 01 ). However, autophagy prohibited the apoptosis pathways.Conclusions Evodiamine can trigger the autophagy, which might play a self-defense role in evodiamineinduced cell death. The cytototoxicity of evodiamine can be augmented by the autophagy inhibitors. The joint application of autophagy regulators with the chemotherapeutic agents might enhance the cell killing effects of chemotherapeutic drugs and show a potent role in cancer drug resistance.

Objective To study the macrophage colony-stimulating factor(M-CSF)expression levels of serum and synovial fluids from patients with spondyloarthropathy(SPA)and its contribution to the pathogen- esis of SpA.Methods Eleven SpA synovial tissue samples were compared to those from peripheral blood mononuclear cells(PBMC)of 10 normal subjects using a 1176 gene array.M-CSF was detected in both serum samples and synovial fluids by enzyme linked immunosorbent assay(ELISA).Two groups of AS subjects were tested.The first group consisted of 41 ankylosing spondylitis(AS)patients who had not been treated with bio- logics.The second group consisted of 13 subjects whose serum samples were collected before and 14 weeks af- ter initiation of infliximab.These were compared to serum samples from 28 normal subjects,and synovial fluid samples from 15 SpA patients.Results Expression of M-CSF could be detected in both serum samples and synovial fluids.The concentration of M-CSF in the group of 41 AS patients not treated with biologics correlated with the Bath Ankylosing Spondylitis Disease Activity Index(BASDAI)values(r=0.41,P=0.004).Treatment of infliximab in AS patients led to a significant decrease in the values of BASDAI(P=0.000 07),but no signif- icant change in the serum M-CSF values.Conclusion M-CSF is a promising candidate for research on the mechanisms of SpA and its signaling on pathway in SpA is different from tumor necrosis factor(TNF)-?,and it may provide new basis for developing new anti-biologics for SpA.

Objective To investigate the effect of insulin on D_5 dopamine receptor expression and function in renal proximal tubule (RPT).Methods Immortalized RPT cells and D_5 receptor transfected HEK293 (HEK-D_5) cells were used in the study to investigate the effect of insulin on D_5 receptor expression and function,and those effects were compared in RPT cells from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The function of D_5 receptor was determined by measurement of the Na~+-K~+-ATPase activity in HEK-D_5 cells. Results Insulin increased D_5 receptor protein expression in a concentration and time-dependent manner in WKY RPT cells,but not in SHR.The basal level of D_5 receptor expression was higher in WKY cells than that in SHR cells. Stimulation with fenoldopam(D_1-like dopamine receptor agonist) inhibited the Na~+-K~+-ATPase activity;pretreat- ment with insulin increased the inhibitory effect of fenoldopam on Na~+-K~+-ATPase activity in HEK-D_5 cells. Conclusion The abnormal regulation of insulin on D_5 receptor expression and function might be involved in the path- ogenesis of essential hypertension.