Система показателей социальной диагностики состояния общества в условиях демократических преобразований в Украине

В статье предпринята попытка проанализировать различные подходы к показателям социальной диагностики состояния современного общества. Предложена методика социальной диагностики состояния современного общества с позиций объективных показателей развития.У статті зроблена спроба проаналізувати різні підходи до показників соціальної діагностики стану сучасного суспільства. Запропонована методика соціальної діагностики стану сучасного суспільства з позицій об'єктивних показників розвитку.An attempt to analyze different approaches to the indexes of social diagnostics of the state of modern society is undertaken in the article. The method of social diagnostics of the state of modern society is offered from positions of objective indexes of development

Внутренние источники финансирования инвестиционной деятельности в Украине

В статье рассмотрены 4 основных источника финансирования инвестиционной деятельности, и проблемы связанные с их формированием и использованием. Учитывая непосредственное влияние внутренних источников инвестиций на экономический рост, и их минимальное использование в Украине, тема становится актуальной, требующей детальной проработки.У статті розглянуті 4 основні джерела фінансування інвестиційної діяльності та проблеми, пов'язані з їх формуванням та використанням. З огляду на безпосередній вплив внутрішніх джерел інвестицій на економічний зріст, та їх мінімальне використання в Україні, тема стає актуальною, потребуючою детального опрацювання.Four basic sources of financing investment activity as well as problems related to their forming and use are considered in the article. This theme is essential and needs detailed development under circumstances of direct impact of the internal sources of investment on economical growth and still minimum use in Ukraine

Combined effects of smoking and alcohol on metabolic syndrome:The LifeLines cohort study

INTRODUCTION: The development of metabolic syndrome (MetS) is influenced by environmental factors such as smoking and alcohol consumption. We determined the combined effects of smoking and alcohol on MetS and its individual components. METHODS: 64,046 participants aged 18-80 years from the LifeLines Cohort study were categorized into three body mass index (BMI) classes (BMI<25, normal weight; BMI 25-30, overweight; BMI≥30 kg/m2, obese). MetS was defined according to the revised criteria of the National Cholesterol Education Program's Adult Treatment Panel III (NCEP ATP III). Within each BMI class and smoking subgroup (non-smoker, former smoker, <20 and ≥20 g tobacco/day), the cross-sectional association between alcohol and individual MetS components was tested using regression analysis. RESULTS: Prevalence of MetS varied greatly between the different smoking-alcohol subgroups (1.7-71.1%). HDL cholesterol levels in all alcohol drinkers were higher than in non-drinkers (0.02 to 0.29 mmol/L, P values<0.001). HDL cholesterol levels were lower when they were also a former or current smoker (<20 and ≥20 g tobacco/day). Consumption of ≤1 drink/day indicated a trend towards lower triglyceride levels (non-significant). Concurrent use alcohol (>1 drink/day) and tobacco showed higher triglycerides levels. Up to 2 drinks/day was associated with a smaller waist circumference in overweight and obese individuals. Consumption of >2 drinks/day increased blood pressure, with the strongest associations found for heavy smokers. The overall metabolic profile of wine drinkers was better than that of non-drinkers or drinkers of beer or spirits/mixed drinks. CONCLUSION: Light alcohol consumption may moderate the negative associations of smoking with MetS. Our results suggest that the lifestyle advice that emphasizes smoking cessation and the restriction of alcohol consumption to a maximum of 1 drink/day, is a good approach to reduce the prevalence of MetS

Body mass index and annual increase of body mass index in long-term childhood cancer survivors; relationship to treatment

Evaluation of body mass index (BMI) at final height (FH) and annual BMI increase in adult childhood cancer survivors (CCS) after treatment with anthracyclines, platinum, and/or radiotherapy. BMI (weight/heightA(2)) was calculated retrospectively from diagnosis until FH. The prevalence of underweight (BMI < 18.5 kg/m(2)) and overweight (BMI a parts per thousand yenaEuro parts per thousand 25 kg/m(2))/obesity (BMI a parts per thousand yenaEuro parts per thousand 30 kg/m(2)) at FH was compared with age-matched controls. The association between underweight/overweight at FH and treatment was assessed by multivariate logistic regression. Annual BMI increase after treatment was assessed by multilevel analysis. Analyses were adjusted for age and underweight/overweight at diagnosis, and age at FH. At FH the prevalence of overweight had not increased, while CCS experienced more underweight as compared to controls (14% vs. 4%, P < 0.001). Overweight at FH was associated with cranial/craniospinal radiotherapy (CRT; OR, 2.23; 95% CI, 1.17-4.26) and underweight at FH with anthracyclines > 300 mg/m(2) (OR, 2.84; 95% CI, 1.33-6.06). Annual BMI increase was +0.47 (0.34-0.60) kg/m(2)/year. In CCS, the annual BMI increase was greater in those with CRT a parts per thousand yenaEuro parts per thousand 30 Gy as compared with those with less or no CRT (+0.15 kg/m(2)/year [0.04-0.25 kg/m(2)/year], P = 0.008) and smaller in those with a higher cumulative anthracycline dose (-0.03 kg/m(2)/year [-0.05 to -0.0005 kg/m(2)/year] per 100 mg/m(2), P = 0.046). After treatment with anthracyclines, platinum, and/or radiotherapy, CRT-treated survivors have more overweight at FH, and a greater annual BMI increase, while anthracycline-treated survivors have more underweight at FH and a lower annual BMI increase

Genome-wide association studies identify CHRNA5/3 and HTR4 in the development of airflow obstruction

RATIONALE: Genome-wide association studies (GWAS) have identified loci influencing lung function, but fewer genes influencing chronic obstructive pulmonary disease (COPD) are known.OBJECTIVES: Perform meta-analyses of GWAS for airflow obstruction, a key pathophysiologic characteristic of COPD assessed by spirometry, in population-based cohorts examining all participants, ever smokers, never smokers, asthma-free participants, and more severe cases.METHODS: Fifteen cohorts were studied for discovery (3,368 affected; 29,507 unaffected), and a population-based family study and a meta-analysis of case-control studies were used for replication and regional follow-up (3,837 cases; 4,479 control subjects). Airflow obstruction was defined as FEV(1) and its ratio to FVC (FEV(1)/FVC) both less than their respective lower limits of normal as determined by published reference equations.MEASUREMENTS AND MAIN RESULTS: The discovery meta-analyses identified one region on chromosome 15q25.1 meeting genome-wide significance in ever smokers that includes AGPHD1, IREB2, and CHRNA5/CHRNA3 genes. The region was also modestly associated among never smokers. Gene expression studies confirmed the presence of CHRNA5/3 in lung, airway smooth muscle, and bronchial epithelial cells. A single-nucleotide polymorphism in HTR4, a gene previously related to FEV(1)/FVC, achieved genome-wide statistical significance in combined meta-analysis. Top single-nucleotide polymorphisms in ADAM19, RARB, PPAP2B, and ADAMTS19 were nominally replicated in the COPD meta-analysis.CONCLUSIONS: These results suggest an important role for the CHRNA5/3 region as a genetic risk factor for airflow obstruction that may be independent of smoking and implicate the HTR4 gene in the etiology of airflow obstruction.</p

NFE2L2 polymorphisms, mortality, and metabolism in the general population

The nuclear factor (erythroid-derived 2)-like 2 (NFE2L2 or NRF2) gene regulates transcription of enzymes involved in cellular detoxification and lipids homeostasis. NFE2L2 is associated with pathophysiology of atherosclerosis and chronic obstructive pulmonary disease (COPD). Therefore we studied the relation between NFE2L2 and all-cause, cardiovascular, and COPD mortality and its associations with triglyceride and cholesterol levels. We genotyped five tagging single nucleotide polymorphisms (SNPs) (rs4243387, rs2364723, rs13001694, rs1806649, and rs6726395) in NFE2L2 in 1,390 subjects from the Vlagtwedde-Vlaardingen cohort. Participants were examined in 1989/1990 and followed up till the vital status evaluation on December 31st, 2008. Associations between SNPs and mortality were estimated by Cox proportional hazards regression, and associations between SNPs and triglyceride and cholesterol levels were tested with linear regression. After 18 yr, 284 (20.4%) subjects had died, 107 from cardiovascular disease and 20 from COPD. Minor allele carriers of rs13001694 had a significantly reduced risk of all-cause mortality compared with wild types: hazard ratio (HR) 0.8 [95% confidence interval (CI) 0.6 to 1.0]. Minor allele carriers of rs2364723 had significantly reduced risk of cardiovascular mortality: HR = 0.5 (95% CI: 0.3-0.7). This result was consistent in stratified analyses: females 0.4 (0.2-0.7), males 0.6 (0.3-0.9), never smokers 0.5 (0.2-1.1), ever smokers 0.5 (0.3-0.8). Minor allele carriers of rs1806649 had a markedly reduced COPD mortality: HR = 0.3 (95% CI: 0.1-0.9). Rs2364723 was associated with lower triglyceride levels. None of the SNPs was associated with cholesterol levels. This study shows for the first time that NFE2L2 is associated with reduced risk of all-cause, cardiovascular and COPD mortality in humans

Gender differences in asthma development and remission during transition through puberty:The TRacking Adolescents' Individual Lives Survey (TRAILS) study

BACKGROUND: During puberty, a gender shift in asthma prevalence occurs, with a preponderance of boys before puberty. The mechanisms underlying this gender shift are unclear. OBJECTIVES: We assessed associations of pubertal stages and transition through puberty with (1) the prevalence, incidence, and remission of asthma in male and female subjects; (2) total IgE levels; and (3) peak expiratory flow (PEF) fall during a shuttle run test (SRT). METHODS: In the TRacking Adolescents' Individual Lives Survey study (n = 2,230; 51% female subjects), associations between pubertal stages and the prevalence, incidence, and remission of asthma were tested by using logistic regression and generalized estimating equations at a mean age of 11.1 (SD, 0.6), 13.6 (SD, 0.5), and 16.3 (SD, 0.7) years. Multiple linear regression analyses were used to study log-transformed total IgE levels and PEF fall during a SRT dependent on early versus late pubertal stages at a mean age of 16.3 years. RESULTS: The prevalence of asthma was similar in boys (7.7%) and girls (7.4%) at a mean age of 11.1 years. The prevalence of asthma was significantly higher in female (6.2%) than male (4.3%) subjects at 16.3 years of age. There were no significant associations between transition of pubertal stages and the presence of asthma, either cross-sectionally or longitudinally. Pubertal stages and log-transformed total IgE levels or PEF fall during a SRT at age 16.3 years were not correlated. CONCLUSIONS: A shift in the prevalence of asthma occurs between 11.1 and 16.3 years, which is due to both an increased incidence and decreased remission of asthma in female compared with male subjects. Pubertal stages could not be proved to explain the gender shift in asthma prevalence

A disintegrin and metalloprotease 33 polymorphisms and lung function decline in the general population

ADAM33 (A Disintegrin and Metalloprotease 33) has been identified as a susceptibility gene for asthma and single nucleotide polymorphisms (SNPs) in this gene have been associated with excess decline of lung function in asthmatics. To assess whether SNPs in ADAM33 are associated with accelerated lung function loss in the general population and with chronic obstructive pulmonary disease (COPD). We have collected DNA from subjects of the Vlagtwedde/Vlaardingen cohort participating in the last survey in 1989/1990 after a follow up of 25 years. Information was collected every 3 years, including lung function measurements. We defined COPD as GOLD stage 2 or higher at the last survey. 1390 subjects from the cohort were genotyped for the following SNPs in ADAM33: F+1, Q–1, S_1, S_2, T_1, T_2, V_4, ST+5. Differences in prevalence of SNPs were analyzed with chi-square tests. Linear mixed effects models were used to analyze FEV1 decline according to genotype. In the whole population mean adjusted decline was 18.7 and 12.7 ml·y–1 in females and males respectively. Individuals homozygous for minor alleles of SNPs S_2 and Q–1 and heterozygous for SNP S_1 had a significantly accelerated decline in FEV1 of respectively 4.9, 9.6 and 3.6 ml·y–1 compared with wild type. We found a significantly higher prevalence of SNPs F+1, S_1, S_2 and T_2 in subjects with COPD. We demonstrated that SNPs in ADAM33 are associated with accelerated lung function decline in the general population. These SNPs are also risk factors for COPD

Genetic variation associates with susceptibility for cigarette smoke-induced neutrophilia in mice

Neutrophilic airway inflammation is one of the major hallmarks of chronic obstructive pulmonary disease and is also seen in steroid resistant asthma. Neutrophilic airway inflammation can be induced by different stimuli including cigarette smoke (CS). Short-term exposure to CS induces neutrophilic airway inflammation in both mice and humans. Since not all individuals develop extensive neutrophilic airway inflammation upon smoking, we hypothesized that this CS-induced innate inflammation has a genetic component. This hypothesis was addressed by exposing 30 different inbred mouse strains to CS or control air for 5 consecutive days, followed by analysis of neutrophilic lung inflammation. By genomewide haplotype association mapping, we identified four susceptibility genes with a significant association to lung tissue levels of the neutrophil marker myeloperoxidase under basal conditions and an additional five genes specifically associated with CS-induced tissue MPO levels. Analysis of the expression levels of the susceptibility genes by quantitative RT-PCR revealed that three of the four genes associated with CS-induced tissue MPO levels had CS-induced changes in gene expression levels that correlate with CS-induced airway inflammation. Most notably, CS exposure induces an increased expression of the coiled-coil domain containing gene, Ccdc93, in mouse strains susceptible for CS-induced airway inflammation whereas Ccdc93 expression was decreased upon CS exposure in nonsusceptible mouse strains. In conclusion, this study shows that CS-induced neutrophilic airway inflammation has a genetic component and that several genes contribute to the susceptibility for this response