Objective:To explore the effect of group cognitive behavior therapy (GCBT) on anxiety, depression and quality of life in patients with chronic obstructive pulmonary disease (COPD) in community.Methods:From August to November 2019, patients with moderate COPD in 18 communities in Xuzhou City were randomly divided into the intervention group ( n=240) and the control group ( n=223). The control group received routine management and the intervention group received group cognitive behavioral therapy intervention for 8 weeks on the basis of routine management.Before and after the intervention, FEV 1% predicted value and FEV 1/FVC were measured by pulmonary function tester.Hospital Anxiety and Depression Scale (HADS) was used to evaluate the anxiety and depression of patients.St.George's respiratory questionnaire (SGRQ), COPD assessment test (CAT) and modified medical research council dyspnea (mMRC) were used to evaluate the quality of life of patients.SPSS 20.0 software was used for analysis.The χ 2 test, independent sample t-test, paired sample t-test were used for statistical analysis. Results:After 8 weeks of intervention, the anxiety and depression scores of the intervention group were lower than those of the control group (anxiety: (8.23±4.02) vs (10.71±3.60); depression: (7.87±3.73) vs (10.20±3.72)( t=6.415, 6.185, both P<0.01). After the intervention, there was no significant difference in FEV 1%((51.7±12.3)% vs (52.0±12.6)%) predicted value and FEV 1/FVC((57.3±10.8)% vs (56.9±10.7)%) between the two groups( t=-0.259, 0.400, both P>0.05). The scores of CAT, mMRC and SGRQ in the intervention group were lower than those in the control group((17.35±5.78) vs (20.90±8.00), (1.55±0.82) vs (2.30±1.21), (41.78±21.56) vs (57.08±24.46))( t=-5.061, -7.227, -6.580, all P<0.01). Conclusion:Group cognitive behavioral therapy can relieve the anxiety and depression and improve the quality of life of patients with COPD.

Objective:To investigate the prevalence and risk factors of stroke in Xuzhou city.Methods:A total of 41 932 residents aged 18 years and above were selected using the multi-stage stratified cluster sampling method. A questionnaire survey was conducted to investigate the rate of stroke, and a physical examination was performed to investigate height, weight, blood pressure, etc. Univariate analyses of stroke were performed using the Chi square test and trend chi-square test. Logistic regression analysis was performed for multi-factor analysis.Results:A total of 39 854 participants (19 222 males, 10 323 from urban areas) from 41 932 eligible participants were included in the statistical analysis, and their average age was (52.1±16.8). In this study, 885 stroke patients (464 males, 302 from urban areas) were found among 39 854 participants. The prevalence of stroke was 2 220.61/100 000, which was separately 2 413.90/100 000 and 2 040.52/100 000 among males and females. The difference between males and females was significant (χ2=6.22, P=0.013). The prevalence of stroke in urban areas (2 925.51/100 000) was higher than in rural areas (1 974.20/100 000) (χ2 =31.45, P<0.001). The results of univariate analysis revealed that the risk factors for stroke were [ OR(95% CI)] smoking [1.82(1.53-2.08)], drinking [1.22(1.08-1.81)], sleep quality [1.42(1.13-1.96)], physical activities [1.44(1.11-2.14)], hypertension [3.53(2.44-6.02)], heart disease [1.23(1.11-1.75)], diabetes [1.42(1.31-2.05)], family history of hypertension [1.43(1.30-2.37)], family history of diabetes [1.22(1.10-1.65)], and family history of stroke [1.57(1.46-2.06)]. Logistic regression analysis showed that age [3.02(2.14-4.96)], smoking [1.59(1.12-3.85)], poor sleep quality [1.15(1.03-3.23)], lack of physical activity [1.22(1.08-3.38)], hypertension [4.53(3.07-7.36)], diabetes [1.08(1.02-3.23)], and family history of stroke [1.15(1.08-3.31)] were related to stroke. Conclusion:The epidemic of stroke in Xuzhou city was relatively high, and prevention and control measures of stroke should be taken according to the risk factors of stroke in the population distribution.

This study aimed to investigate the prevalence, clinical characteristics, and prognostic impact of 1p32.3 deletion in patients with newly diagnosed multiple myeloma (MM). A retrospective analysis was conducted on 411 patients with newly diagnosed MM; among which, 270 received bortezomib-based therapies, and 141 received thalidomide-based therapies. Fluorescence in situ hybridization (FISH) was performed to detect six cytogenetic abnormalities, namely, del(1p32.3), gain(1q21), del(17p13), del(13q14), t(4;14), and t(11;14). Results showed that 8.3% of patients with MM were detected with del(1p32.3) and had significantly more bone marrow plasma cells (P = 0.025), higher β2-microglobulin levels (P = 0.036), and higher lactate dehydrogenase levels (P = 0.042) than those without del(1p32.3). Univariate analysis showed that patients with del(1p32.3) under thalidomide-based therapies (median PFS 11.6 vs. 31.2 months, P = 0.002; median OS 16.8 vs. 45.9 months, P < 0.001) were strongly associated with short progression-free survival (PFS) (P = 0.002) and overall survival (OS) (P < 0.001). Multivariate analysis revealed that del(1p32.3) remained a powerful independent factor with worse PFS (P = 0.006) and OS (P = 0.016) for patients under thalidomide-based treatments. Patients with del(1p32.3) under bortezomib-based treatments tended to have short PFS and OS. In conclusion, del(1p32.3) is associated with short PFS and OS in patients with MM who received thalidomide- or bortezomib-based treatments.

Objective: To screen and verify the differential expression profiles of long non-coding RNAs(LncRNAs) in peripheral blood of patients with type 2 diabetes mellitus(T2DM), to identify the potential molecular specific markers of early T2DM. Methods: The blood samples of 4 type 2 diabetic patients and 4 normal control subjects were collected for microarray analysis. Then six candidate markers of LncRNAs screened from the differential expression profile were tested by qRT-PCR among the subjects (80 cases in the T2DM group and 50 cases in the control group). The possibility of these LncRNAs as molecular diagnostic markers was analyzed, and finally two of them were carried out by receiver operating characteristic (ROC) analysis. Results: Compared with control subjects, there were differentially expressed 133 LncRNAs in type 2 diabetic patients, among which 5 were up-regulated with the maximum up-regulated fold 3.29 and 128 were down-regulated with the maximum down-regulated fold 8.99. Six down-regulated LncRNAs were selected for validation and revealed a similar result to that of microarray.The expressions of two LncRNAs(NONHSAT160746 and NONHSAT140069) in peripheral blood of diabetic patients were significantly lower than those of control subjects (P<0.01). The areas under the ROC curve of the two LncRNAs were 0.734 and 0.703, respectively(P<0.01). Conclusion LncRNAs NONHSAT160746 and LncRNAs NONHSAT140069 are the potential molecular specific markers for the diagnosis of diabetes mellitus.

Objective To explore the interaction of smoking and diabetes on stroke.Methods In this case-control study,a face to face questionnaire survey was conducted.Logistic regression models were used to analyze the relationship between smoking or diabetes and stroke.The indicators of interaction were calculated according to the Bootstrap method in this study.Results A total of 918 cases and 918 healthy controls,who participated in the chronic disease risk factor survey in Xuzhou in 2013,were included in this study.Logistic regression analysis found that cigarette smoking was associated with stroke (OR=1.63,95％ CI:1.33-2.00),and diabetes was also associated with stroke (OR=2.75,95％CI:2.03-3.73) after adjusting confounders.Compared with those without diabetes and smoking habit,the odds ratio of stroke in those with diabetes and smoking habits was 8.94 (95％CI:3.77-21.19).Diabetes and smoking combined interaction index was 3.65 (95％CI:1.68-7.94),the relative excess risk was 5.77 (95％ CI:0.49-11.04),the attributable proportion was 0.65 (95％ CI:0.42-0.87).Conclusion The results suggest that there are additive interactions between smoking and diabetes on stroke.

Objective To explore the relationship between poor sleep quality and stoke.Methods A total of 738 stroke patients in Xuzhou city in 2013 were selected as the case group and age-and sex-matched healthy non-stroke subjects (n =738)as control group.The writer-designed general situation questionnaire and the Pittsburgh Sleep Quality Index(PSQI)analyses were conducted for a face-to-face investigation.Results No significant difference in mean age(66.1±10.9 and 65.8 ± 10.6,t =0.60,P =0.58)and in sex (50％ vs.50 ％) was found between two groups.There were statistically significant differences between case and control groups in baseline values of BMI(t=2.40,P =0.02),histories of hypertension(x2 =174.30,P =0.00),diabetes mellitus (x2 =27.20,P =0.00),coronary heart disease(x2 =115.60,P =0.00),smoking(x2 =6.10,P =0.01),drinking (x2 =7.30,P =0.01)and living stress(x2 =11.40,P =0.01).The PSQI sub-scores and PSQI total scores were higher in case group than in control group.The rate of poor sleep quality was higher in case group(279 cases,37.8 ％) than in control group(136 cases,18.4 ％) (x2 =6.10,P =0.01).Multivariate logistic analysis showed that,after adjusting for confounding factors of BMI,histories of hypertension,diabetes,coronary heart disease.smoking,drinking and living stress,the poor sleep quality in total male plus female was independent predictor variables for stroke[odds ratio(95 ％ CI) of 2.3 (1.8-3.0)],no matter their sex,with odds ratio (95 ％ CI) in male (2.5,1.7-3.7) or in female (2.2,1.5-3.2),respectively,but there was no significance difference in the odds ratio between male and female in case group(x2 =0.04,P=0.85).The risk stroke was 2.3 folds higher in poor sleep quality versus control in male plus female,with pure male or female of 2.5 or 2.2 folds.There was no significance difference between male and female in case group versus.the control(x2 =0.04,P=0.85).Conclusions Poor sleep quality is associated with the occurrence of stroke and may be a risk factor for stroke.

Objective: To analyze the epidemiological characteristics and trend of ischemic heart disease and cerebrovascular disease mortality among Xuzhou residents from 2011 to 2015. Methods: The mortality data of the ischemic heart disease and cerebrovascular disease were obtained from the registration disease surveillance system covering the residents of the city from 2011 to 2015. Ischemic heart disease and cerebrovascular disease were identified according to the international classification of diseases (ICD-10), Ischemic heart diseases include I20 to I25 (angina pectoris, acute myocardial infarction, certain current complications following acute myocardial infarction, other acute ischemic heart diseases chronic ischemic heart disease); cerebrovascular diseases include I60 to I69 (subarachnoid hemorrhage, intracerebral hemorrhage, other non-traumatic hemorrhage, cerebral infarction, stroke not specified as hemorrhage or infarction, other cerebrovascular diseases, sequelae of cerebrovascular disease). Results: (1)From 2011 to 2015, the chronic ischemia Cardio-Cerebrovascular disease mortality of residents in Xuzhou was 261.2 per one hundred thousand (129 950/49 748 321), 269.9 per one hundred thousand(69 562/25 775 930)for male residents, 252.0 per one hundred thousand(60 388/23 972 391)for female residents, the mortality rate in men was significantly higher than that in women (P<0.05). The chronic ischemic Cardio-Cerebrovascular disease mortality rate of urban residents was 243.8 per one hundred thousand(17 049/6 993 787), which was lower than the rate of rural residents (264.0 per one hundred thousand(112 901/42 754 534), P<0.05). (2)From 2011 to 2015, the mortality rate of ischemic heart disease in Xuzhou city remained unchanged: 117.1 per one hundred thousand(11 416/9 747 768), 126.8 per one hundred thousand(12 177/9 600 745), 112.0 per one hundred thousand(11 184/9 986 877), 115.2 per one hundred thousand(11 697/10 151 842), 117.1 per one hundred thousand(12 019/10 261 089, P>0.05). The mortality rate of cerebrovascular disease were 154.0 per one hundred thousand(15 014/9 747 768), 155.9 per one hundred thousand(14 964/9 600 745), 143.5 per one hundred thousand(14 330/9 986 877), 135.5 per one hundred thousand(13 752/10 151 842), 130.6 per one hundred thousand(13 397/10 261 089)respectively, presented with a downward trend(P<0.05). The mortality rate of ischemic cerebrovascular disease were 62.7 per one hundred thousand(6 108/9 747 768), 74.7 per one hundred thousand(7 176/9 600 745), 72.3 per one hundred thousand(7 221/9 986 877), 70.9 per one hundred thousand(7 200/10 151 842)and 72.4 per one hundred thousand(7 431/10 261 089)respectively(P>0.05). The mortality rate of hemorrhagic cerebrovascular disease were 77.6 per one hundred thousand(7 562/9 747 768), 71.6 per one hundred thousand(6 873/9 600 745), 61.2 per one hundred thousand(6 115/9 986 877), 55.3 per one hundred thousand(5 613/10 151 842)and 46.4 per one hundred thousand(4 763/10 261 089)respectively, presented with a downward trend(P<0.05). (3)The average death age due to ischemic heart diseases of all residents was (77.0±13.1)years old, (76.4±13.2) years old among urban residents, (77.1±7.1 )years old among rural residents, (74.3±13.5)years old for male residents, (80.0±12.0) years old for female residents. The average death age due to ischemic cerebrovascular diseases of all residents was (76.4±11.9)years old, (76.5±12.3) years old among urban residents, (76.4±11.9 )years old among rural residents, (74.3±12.2)years old among male residents, (79.0±11.1) years old among female residents. From 2011 to 2015, the death age due to ischemic heart diseases were (76.3±13.5), (77.2±13.0), (76.6±13.3), (77.1±12.9)and(77.8±12.9)years old respectively; the death age due to cerebrovascular disease were (75.8±12.1), (76.3±11.8), (76.6±11.8), (76.6±12.0)and(77.1±11.9)years old respectively. The Spearman rank correlation analysis showed that the death age due to ischemic heart disease and cerebrovascular disease increased year by year in the past 5 years. (r value was 0.033 and 0.038, respectively, all P<0.01). Conclusion From 2011 to 2015, the mortality of hemorrhagic cerebrovascular disease decreased, while the mortality of ischemic cardiovascular and cerebrovascular diseases remained unchanged among Xuzhou residents.

OBJECTIVE:To explore the effect of dabigatran etexilate on coagulation indexes and safety of elderly patients with persistent atrial fibrillation. METHODS:52 elderly patients with persistent atrial fibrillation were randomly divided into obser-vation group and control group by random number table,26 cases in each group. Creatinine clearance rate in observation group was higher than 30 ml/min,110 mg Dabigatran etexilate capsule was orally given,bid;when 15-30 ml/min,55 mg capsule was orally given,bid. Control group orally received Warfarin sodium tablet with initial dose of 2.5 mg,qd,according to international normal-ized ratio (INR) after 3-5 days till maintained in 2.0-3.0. After 3 months,coagulation indexes [prothrombin time (PT),activated partial thromboplastin time (APTT),thrombin time (TT),INR,platelet count (PLT),fibrinogen (FIB)] before and after treat-ment,incidences of clinical events (cerebral embolism,cerebral hemorrhage,fatal bleeding,the remaining parts of embolism, death)and adverse reactions in 2 groups were compared. RESULTS:There was no significant difference in PT,APTT,TT,PLT and FIB between 2 groups before treatment(P>0.05);after treatment,PT and INR in 2 groups significantly increased,and obser-vation group was obviously better than control group,the difference was statistically significant(P<0.05). No cerebral hemorrhage or fatal hemorrhage occurred in the two groups. There was no significant difference in the incidence of cerebral embolism between 2 groups (P>0.05);the incidence of remaining parts of embolism,death in observation group significantly lower than control group,the difference was statistically significant(P<0.05). The incidence of adverse reactions in observation group was significant-ly lower than control group,the difference was statistically significant (P<0.05). CONCLUSIONS:Dabigatran etexilate shows good coagulation effect on elderly patients with persistent atrial fibrillation,which can effectively improve PT and INR levels and reduce the incidences of clinical events,with good safety.

Objective To explore the sensitivity of HER-2-positive BT474 breast cancer cells to trastuzumab after knockdown or overexpression of RNA binding protein 38 ( RNPC1 ) .Methods The expressions of RNPC1 and HER-2 mRNA were detected by qRT-PCR, and the expressions of RNPC1, HER-2 and PI3K/AKT proteins were detected by Western blot after transfected with RNPC1 lentiviral vector, respectively.The experimental groups were treated with different concentration of trastuzumab, and cell apoptosis rate was analyzed by 7-AAD/APC double staining flow cytometry, and cell growth inhibition rate was tested by cell counting kit 8 ( CCK-8) .The expression of apoptosis-related proteins was detected by Western blot assay.Results The results of qRT-PCR showed that overexpression of RNPC1 increased the expressions of RNPC1 and HER-2 mRNA, and the expressions of RNPC1 and HER-2 were decreased after RNPC1 knockdown.The knockdown of RNPC1 decreased the expressions of RNPC1 and HER-2.Moreover, overexpression of RNPC1 decreased and knockdown of RNPC1 increased the levels of p-PI3K and p-AKT while the total protein expressions of both were marginally changed.The results of analysis using a cell counting CCK-8 kit showed that the RNPC1 overexpressed group had a higher growth inhibition rate [(20.33± 1.25)%,(35.38±2.05)%,(50.43±2.12)%,(65 .35±2.08)%and(76.00±2.16)%, respectively] than that of the control group [(13.67±1.24)%,(27.86±2.05)%,( 39.72±1.69)%,(53.33±1.70)%and(62.68± 2.07)%] when treated with different concentrations of trastuzumab (5, 10, 15, 20 and 25 μg/ml).The cell apoptosis rates in the RNPC1-overexpressed group [ ( 19.46 ±1.06 )%, ( 30.87 ±0.98 )%, ( 50.45 ± 1.1)3%, respectively] were also increased compared with that in the control group [(14.38±0 .64)%,(21.65± 1.24)%,(38.03±0.85)%] when treated with different concentrations of trastuzumab (0, 10, 20 and 30μg/ml) ( P<0.05 for all).Reverse results were observed in the RNPC1 knockdown experiments [ experimental groups:(9.67±1.18)%, ( 21.67 ±1.23)%, ( 30.33 ±1.25)%, ( 40.33 ±1.69)%, and ( 53.00 ± 1.63)%] compared with those of control groups:[(14.00±0.82)%, (27.67±1.25)%, (39.67±1.79)%, (53.67±1.50)%, and (63.33±1.52)%];and experimental groups:[(11.64±0.68)%, (16.60±1.01)%, and (25.14±3.12)%] compared with those of the control groups: [(14.71±0.61)%, (22.65±0.96)%, and (39.03±0.85)%].The overexpression of RNPC1 increased the expression levels of Bim and Bad and decreased the level of Bcl-xl, and reverse result was observed after knockdown of RNPC1.Conclusion RNPC1 may promote the sensitivity of breast cancer cells to trastuzumab through the increased expression of HER-2 in the BT474 breast cancer cells.

Objective To investigate the regulatory mechanism of RNA binding motif protein 38 (RNPC1) on the expression of progesterone receptor (PR) in breast cancer cell line ZR?75?1. Methods Lentiviral vector was used to induce overexpression of RNPC1 in ZR?75?1 cells. qRT?PCR and Western blot were used to assess the regulatory effect of RNPC1 on PR expression. Actinomycin was used to detect the regulatory mechanism involved. Immunohistochemical ( IHC) staining was used to determine the protein expression of RNPC1 and PR in 80 breast cancer tissues. Results IHC staining showed that the expression of RNPC1 was significantly higher in the PR positive breast cancer tissues than that in the PR negative breast cancer tissues ( P<0.05) . The qRT?PCR results showed that overexpression of RNPC1 in ZR?75?1 cells significantly upregulated the mRNA level of PR (1.764±0.028 vs. 1.001±0.037, P<0.01), whereas knockdown of RNPC1 did the opposite (0.579± 0.007 vs. 1.000±0.002, P<0.01).The Western blot results also showed that overexpression of RNPC1 up?regulated PR levels, while knockdown of RNPC1 resulted in down?regulation of PR levels in the ZR?75?1 cells. The actinomycin assay showed that overexpression of RNPC1 increased the mRNA stability of PR. The half?life of PR mRNA was increased from 4. 0 h to 6. 5 h. Knockdown of RNPC1 decreased the mRNA stability of PR and the half?life of PR transcript was decreased from 4.1 h to 3.0 h. Conclusion RNPC1 plays a crucial role in regulating the expression of PR in breast cancer ZR?75?1 cells.