Purpose:To evaluate the effect of biological response modifiers for Ⅲ stage non-small-cell lung cancer.Methods:Fifty-nine patients were randomized into two groups.Twenty-nine patients were put into radiotherapy and chemotherapy(R+C) groups,thirty patients were into Biological response modifiers and radiotherapy chemotherapy(BRMS+R+C) groups.All patients received routine radiotherapy 2.0 Gy per day,5times a week to a total dose of 60-65 Gy,in 42-45 days.Radiation fields just covered clinical tumors.Chemotherapy consisted of cisplatin 25-30 mg/m 2 ,etoposide 50-70 mg/m 2 on days 1?2and 3 every 4 week,for squamous cell carcinoma.For adenocarcinoma,it was mitemycin 4-6 mg/m 2 on day1 and vindesine 3 mg on day1 and8,and cisplatin25-30 mg/m 2 on day1?2 and 3,every 4 weeks interferon-?(IFN-?)and interleukin-2(IL-2)were used in(BRMS+R+C)groups after the second chemotherapy was over. IFN-? was given on days 1?2?3 and IL-2 on days 2?4?6 to a total of forty-eight day.Results:The overall response rate was 51.7% and 76.6% in(R+C) and(BMRS+R+C) groups.The one.two year survival rates were 62.1% 17 3% and 83 3%,43 3% in (R+C) and (BMRS+R+C) groups respectively.Conclusions:The preliminary results from our study has shown that biological response modifiers combined with radiotherapy and chemotherapy for non -small cell lung cancer has better early response rate and survival rate.

OBJECTIVE To re-evaluate systematic review/meta-analysis of escitalopram in the treatment of depression， and to provide reference for clinical use of escitalopram. METHODS Retrieved from CNKI， Wanfang database， VIP， SinoMed， PubMed and the Cochrane Library， etc.， systematic review/meta-analysis of escitalopram in the treatment of depression were collected from the construction of the database to May 17， 2022. The literatures were screened according to the inclusion and exclusion criteria， the basic information of the included literatures was extracted， and the methodological quality， reporting quality and evidence quality of the included literatures were evaluated by using AMSTAR 2 scale， PRISMA statement， and GRADE system， respectively. RESULTS A total of 16 systematic reviews/meta-analyses were included. The results of efficacy comparison showed that escitalopram in the treatment of depression was superior to sertraline in improving the total effective rate， and was comparable to paroxetine， duloxetine and fluoxetine in improving cure rate. The results of safety comparison showed that the safety of escitalopram was higher than that of paroxetine and venlafaxine. The overall methodological quality evaluation of AMSTAR 2 scale was low， and all of them were rated as extremely low； main reason was the lack of many key items. PRISMA score was between 12 and 23 points. Among them， there were 5 literatures with scores ＞21 points， and the reports were relatively complete， 10 literatures with scores between 15 and 21 points， and the reports had certain defects， and 1 literature with scores ≤15 points， with serious information missing. The results of the grading of GRADE evidence showed that， of the 160 included outcome indicators， 69 were moderate evidence， 64 were low-level evidence， and 27 were very low-level evidence. CONCLUSIONS The total effective rate of escitalopram in improving depressive patients is not inferior to that of sertraline； compared with paroxetine， escitalopram is safer. However， the evidence level of the above conclusions is low.

Objective To study the expression of S100A8 and the relationship between S100A8 and Toll-like receptor 4 (TLR4) in focal cerebral ischemia reperfusion (I/R) injury.Methods C3H/HeJ mice with TLR4 gene mutation (n =30) and C3H/HeN with normal TLR4 gene mice (n =30) were divided into 4 groups at random (random number),namely C3H/HeJ model group (n =18),C3H/HeJ control group (n =12),and C3H/HeN model group (n =18).C3H/HeN control group (n =12).Middle cerebral artery was occluded to make I/R model in mice by using thread embolism method.Brain tissues were collected after ischemia for one hour and reperfusion for 12 hours.Stroke outcome was evaluated by determination of infarct volume of brain tissue and assessment of neurological scores.And brain injury after cerebral I/R was observed by optical microscope after TTC and HE staining.The immunofluorescence technique and RT-PCR were used to determine the protein level and expression of S100A8 mRNA in damaged brain tissues.Results Compared with C3H/HeN model mice,TLR4-deficient model mice (C3H/ He J) had lower infarct volumes and better outcomes of neurological function after resuscitation for 12 hours.Compared with control groups,the expression of S100A8 mRNA and level of S100A8 protein increased greatly in damaged brain tissues of model mice after I/R injury.In addition,model mice with lacked TLR4 (C3H/HeJ) had lower expression of I/R-induced S100A8 mRNA than C3H/HeN mice in model group,indicating that the close relationship between the levels of S100A8 and TLR4.Conclusions S100A8 interaction with TLR4 might be involved in brain damage and in inflammation triggered by I/R injury.

ObjectiveTo study the quality of life of patients with hepatolenticular degeneration (HLD)and analyze the influencing factors.Methods287 patients with HLD and 51 health people were investigated by World Health Organization quality of life assessment instrument brief version (WHOQOL-BREF),Symptom Checklist 90 (SCL-90),Life Satisfaction Index A (LSIA) and variance analysis,t-test and multiple linear regression analysis were analyzed the influencing factors.Results①Scores of WHOQOL-BREF:physical domain(54.64 ± 17.11 ),psychological domain ( 52.09 ± 15.83 ) in patients with HLD were lower than those in the health people (67.30 ± 12.66,58.90 ± 12.75 ) with statistically significant difference (P ＜ 0.01 ) ; social domain ( 51.35± 17.18),the domain of environment(53.54 ± 16.67) in patients with HLD were lower than those in the health people (57.53 ± 14.99,58.42 ± 10.55 ) with statistically significant difference (P ＜ 0.05 ).②The quality of life of the patients with HLD was influenced by LSIA,total score of SCL-90,the attitude toward the doctors,economic status,the attitude toward the disease,residence with statistically significant difference (P ＜ 0.0l ).ConclusionThe quality of life in patients with HLD is lower than that in health people and much factors influence it,so it is necessary to take multi-facet interventions to improve their quality of life.

From air bacteria capable of decomposing creatinine, three single independent strains K9510、K9511 and K9512 have been isolated. The highest creatinine amidohydrolase (EC 3.5.2.10; creatininase) producing strain K9510 was screened out. The strain K9510 was identified as Pseudomonas sp. The results of culture condition for creatininase formation by strain K9510 were obtained as follows: creatinine and creatine were found to be the effective inducers for enzyme formation; the solution of mixed metallic salts could stimulate cell growth and enzyme formation. The suitable medium for creatininase formation was consisted of 0.9% creatinine、 0. 15% yeast extract、 0. 09% malt extract、0.05% NH4C1 and some amount of the solution of mixed metallic salts at pH5. 5. When the bacterium was grown in 250mL conic flask containing 50mL of the medium mentioned above on the rotary shaker(250r/min) at 35℃ for 33 h, about 50 u creatininase was obtained.

Objective To investigate the role of insulin resistance index (HOMA-IR) in premonishing hepatogenous diabetes subsequent to chronic liver disease related to hepatitis B virus. Methods Fasting plasma glucose (FPG) and fasting serum insulin (FINS) were measured in 176 patients, including 80 patients with chronic hepatitis B (CHB), 66 patients with liver cirrhosis (LC) and 30 patients with chronic severe hepatitis B (CSHB). In addition 30 healthy subjects served as control (group HC). None of the subjects in the study had a history of diabetes. FPG and FINS were measured in all the subjects to exclude impaired glucose tolerance and diabetes. Then HOMA-IR was calculated. Results Among the HC and CHB, LC and CSHB patients, both FINS and HOMA-IR levels gradually elevated. FINS and HOMA-IR in CHB patients (10.58?6.48, 2.35?1.55) were significantly higher than those in group HC (8.06?2.14,1.68?1.53), while lower than those in LC (12.73?5.88, 2.91?1.41) and CSHB (18.30?14.17, 4.35?3.17) patients (P0.05), while the values of FINS and HOMA-IR were significantly higher in severe patients than those in moderate patients (P0.05), while the values of FPG were significantly higher in LC and CSHB patients than those in group HC (P

Objective To invetigate the feature of Th 17 cells in chronically HBV-infected patients whole responsed to pegylated interferon α-2a treatment.Methods Serum and PBMCs were obtained from enrolled CHB patients and health controls and monitored for ALT , HBV DNA, HBV Markers as well as the frequency of IL-17 +T cells.Results The frequency of IL-17 +,IL-17 +IFN-γ+and IL-17 +IFN-γ-T cells increased in whole response time point and decreased in followed 6 month ;and lower than that of health controls at any group .Conclusion Tteatment with pegylated interferon α-2a minght effect the fre-quency and composition of Th 17 cells, which effect the immune regulation in the disease .

Objective To observe the changes in concentrations of pulmonary surfactant SP-A/B in lung tissue during acute lung injury (ALI) /acute respiratory distress syndrome (ARDS) induced by acute paraquat poisoning (PQP) after the treatment with metabolic antioxidant,lipoic acid,and to explore the potential involvement of TNF-α in ALI/ARDS as well as to discuss the assumed protective mechanisms of lipoic acid against acute lung injury.Methods Sixty-six male Sprage-Dawley rats were randomly (random number) divided into 3 groups,namely control group (NS,n =6),paraquat poisoning group (PQ,n =30),paraquat + lipoic acid treatment group (LA,n =30).Then both group PQ and group LA were further divided separately into five subgroups,namely 3,6,12,24 and 48 h subgroups (n =6 in each subgroup).After rats sacrificed,the lung tissues were selected,and after HE staining,histological changes were observed under light microscope.Histopathological changes were inflammation and fibrosis in models successfully established.The lung tissues were also taken for tests of SOD and MDA levels.Specimens of whole blood 0.8 mL without anticoagulant were taken from tail vein of rats for determining the TNF-α level.The expressions of SP-A mRNA and SP-B mRNA were measured with RT-PCR from total RNA of the lung tissue.Results ① HE staining showed that the histopathological changes were milder in LA group than that in PQ group.② There were significant differences in MDA and SOD levels between different intervals both in intergroups and intragroup except the groups of 3 hours (P ＜ 0.01).③ Likewise,the significant differences in the levels of TNF-α were also present between three groups and between different intervals (P＜0.01).④ The significant differences in SP-A mRNA and SP-B mRNA amplification ratio existed between three groups at the same interval (P ＜ 0.01),but those differences between different intervals in group PQ were of statistical significance (P ＜ 0.05).And those differences between diffirent intervals in group LA were statistically significant (P ＜0.01).Conclusions Lipoic acid in acute paraquat poisoning could lessen lung tissue damage,which might be directly dominated by the levels of tumor necrosis factor,and in turn indirectly affect the content of pulmonary surfactant,thereby reducing pulmonary edema and improving lung compliance,then protecting the lung tissues.

Purpose To observe the impact of sleep deprivation (SD) for 24 hours on human brain regional homogeneity (ReHo) by using functional magnetic resonance imaging (fMRI),and briefly discuss the intervening effect of transcranial direct current stimulation (tDCS) on ReHo after SD.Material and Methods Sixteen healthy individuals were enrolled,and self-controlled study were adopted.Resting-state fMRI scans were performed in wakefulness,after SD,and after tDCS (true or placebo stimuli).The ReHo analysis approach was employed to calculate the ReHo values of whole brain in different states.The differences between before and after SD,and between true and false tDCS after SD,were analyzed.Results Compared with wakefulness,SD mainly enhanced ReHo in brain regions of left precentral gyrus,right precentral gyrus,bilateral temporal lobe and thalamus,but decreased ReHo in brain regions of right precuneus,left superior occipital gyrus,limbic lobe and bilateral angular gyrus,superior frontal gyrus,middle frontal gyrus.Compared with placebo stimuli,the true tDCS enhanced ReHo in brain regions of bilateral precuneus,angular gyrus and right forehead,superior middle gyrus,but decreased ReHo in brain regions of the medial side of left frontal lobe,right precentral gyrus,parahippocampal gyrus,substantia nigra and bilateral temporal lobe,pons and so on.Conclusion SD can cause ReHo change in a large number of brain regions.The tDCS on the prefrontal cortex improves the brain regions with ReHo reduction caused by SD.The improved brain regions mainly include bilateral precuneus/posterior cingulate cortex.Therefore,tDCS on the prefrontal cortex can improve brain dysfunction caused by SD.

Objective To explore the mechanism of azithromycin (AZM) for inhibiting the proliferation of rat airway smooth muscle cells (ASMCs).Methods Thirty Sprague-Dawley (SD) rats were divided into the control group,asthma model group and AZM group.The rat model of asthma was established by ovalbumin (OVA) sensitization and stimulation in vitro.The airway related parameters of rat lung tissue were determined by using the medical image analysis system.Primary passage ASMCs were isolated and cultured using the tissue-sticking method,and the vascular endothelial growth factor (VEGF) overexpression vector or tumor necrosis factor receptor-associated factor 6 (TRAF6) overexpression vector was transfected into ASMCs in the AZM group.The protein levels of VEGF,NF-κB p65 and TRAF6 were detected by Western blotting,and the proliferation of ASMCs was evaluated by CCK-8 kit.Results AZM significantly inhibited the increase of thickness of total airway wall,thickness of inner airway wall and thickness of airway smooth muscle layer in asthma rats (P<0.05),also significantly inhibited the proliferation of ASMCs in the asthma model group (P<0.05).AZM significantly inhibited the protein expression of VEGF and NF-κB p65 induced by asthma (P<0.05),and the overexpression of VEGF significantly reduced the inhibiting effects of AZM on proliferation of ASMCs (P<0.05).AZM significantly inhibited the high expression of TRAF6 induced by asthma (P<0.05),and the overexpression of TRAF6 significantly reduced the inhibiting effects of AZM on expression of VEGF and NF-κB p65 as well as proliferation of ASMCs (P<0.05).Conclusion AZM can suppress the proliferation of ASMCs,its partial mechanism may be realized through inhibiting TRAF6/NF-κB/VEGF signaling pathway.