Short-term effect of particulate matter on lung function and impulse oscillometry system (IOS) parameters of chronic obstructive pulmonary disease (COPD) in Beijing, China.

OBJECTIVE: This study aimed to evaluate the associations between particulate matter (PM), lung function and Impulse Oscillometry System (IOS) parameters in chronic obstructive pulmonary disease (COPD) patients and identity effects between different regions in Beijing, China. METHODS: In this retrospective study, we recruited 1348 outpatients who visited hospitals between January 2016 and December 2019. Ambient air pollutant data were obtained from the central monitoring stations nearest the participants' residential addresses. We analyzed the effect of particulate matter with aerodynamic diameter ≤ 2.5 µm (PM2.5) exposure on lung function and IOS parameters using a multiple linear regression model, adjusting for sex, smoking history, education level, age, body mass index (BMI), mean temperature, and relative humidity . RESULTS: The results showed a relationship between PM2.5, lung function and IOS parameters. An increase of 10 µg/m3 in PM2.5 was associated with a decline of 2.083% (95% CI: -3.047 to - 1.103) in forced expiratory volume in one second /predict (FEV1%pred), a decline of 193 ml/s (95% CI: -258 to - 43) in peak expiratory flow (PEF), a decline of 0.932% (95% CI: -1.518 to - 0.342) in maximal mid-expiratory flow (MMEF); an increase of 0.732 Hz (95% CI: 0.313 to 1.148) in resonant frequency (Fres), an increase of 36 kpa/(ml/s) (95% CI: 14 to 57) in impedance at 5 Hz (Z5) and an increase of 31 kpa/(ml/s) (95% CI: 2 to 54) in respiratory impedance at 5 Hz (R5). Compared to patients in the central district, those in the southern district had lower FEV1/FVC, FEV1%pred, PEF, FEF75%, MMEF, X5, and higher Fres, Z5 and R5 (p < 0.05). CONCLUSION: Short-term exposure to PM2.5 was associated with reductions in lung function indices and an increase in IOS results in patients with COPD. The heavier the PM2.5, the more severe of COPD.

Moderate coffee or tea consumption decreased the risk of cognitive disorders: an updated dose-response meta-analysis.

CONTEXT: Although several epidemiological studies have examined the association between coffee or tea intake and the risk of cognitive disorders, the results to date are inconsistent. OBJECTIVE: An updated systematic review and dose-response meta-analysis was conducted to confirm the association between coffee, tea, and caffeine consumption and the risk of cognitive disorders. DATA SOURCES: PubMed, Embase, and Web of Science were searched from inception to January 2022 for relevant studies, including dementia, Alzheimer disease (AD), and cognitive impairment or decline. DATA EXTRACTION: Two reviewers independently performed data extraction and assessed the study quality. DATA ANALYSIS: Restricted cubic splines were used to conduct the dose-response meta-analysis for coffee and tea intake. RESULTS: Twenty-two prospective studies and 11 case-control studies involving 389 505 participants were eligible for this meta-analysis. Coffee and tea consumption was linked to a lower risk of cognitive disorders, with an overall relative risk (RR) of 0.73 (95% CI: 0.60-0.86) and 0.68 (95% CI: 0.56-0.80), respectively. The subgroup analysis revealed that ethnicity, sex, and outcomes had significant effects on this association. Protection was stronger for men than that for women in both coffee and tea consumption. A nonlinear relationship was found between coffee consumption and AD risk, and the strength of protection peaked at approximately 2.5 cups/day (RR: 0.74; 95% CI: 0.59-0.93). A linear relationship was found between tea consumption and cognitive disorders, and the risk decreased by 11% for every 1-cup/day increment. CONCLUSION: This meta-analysis demonstrated that the consumption of 2.5 cups coffee/day minimizes the risk of AD, and 1 cup/day of tea intake leads to an 11% reduction in cognitive deficits. Effective interventions involving coffee and tea intake might prevent the occurrence of dementia.

Long-term effects of air pollution on hospital admissions and mortality for chronic obstructive pulmonary disease in Beijing, China.

OBJECTIVE: We aimed to clarify the association between air pollution and hospital admissions for chronic obstructive pulmonary disease (COPD) and mortality in Beijing, China. METHODS: In this retrospective study, we recruited 510 COPD patients from 1 January 2006 to 31 December 2009. The patient data were obtained from the electronic medical records of Peking University Third Hospital in Beijing. Air pollution and meteorological data were obtained from the Institute of Atmospheric Physics of the Chinese Academy of Sciences. Monthly COPD hospital admissions, mortality and air pollution data were analysed using Poisson regression in generalised additive models adjusted for mean temperature, pressure and relative humidity. RESULTS: There were positive correlations between sulfur dioxide (SO2 ), particulate matter with an aerodynamic diameter ≤ 10 µm (PM10 ) and COPD hospital admissions in the single-pollutant model. An increase of 10 µg/m3 in SO2 and PM10 were associated with an increase of 4.053% (95% CI: 1.470-5.179%) and 1.401% (95%CI: 0.6656-1.850%) in COPD hospital admissions. In the multiple-pollutant model [SO2 and nitrogen dioxide (NO2 ) combinations], there was only a positive correlation between SO2 and COPD hospital admissions. An increase of 10 µg/m3 in SO2 were associated with an increase of 1.916% (95% CI: 1.118-4.286%) in COPD hospital admissions. There was no correlation between three pollutant combinations and COPD hospital admissions. We did not find correlations between air pollution and COPD mortality in either single- or multiple-pollutant models. CONCLUSIONS: SO2 and PM10 may be important factors for the increase in COPD hospital admissions in Beijing, China.

The relationship between frailty and community-acquired pneumonia in older patients.

PURPOSES: To explore the relationship between frailty and community-acquired pneumonia (CAP) in older patients. METHODS: A prospective observational study included 109 older patients(≥ 65 years) hospitalized with CAP in respiratory department of Fuxing hospital, Capital Medical University from June 2018 to December 2020. Frailty scores(Frail Scale, range 0-5) and pneumonia severity CURB-65 scale(mild = 1, modest = 2, and severe ≥ 3) were measured. We extracted clinical variables including white blood cell(WBC), neutrophil-to-lymphocyte ratio (NLR), C-reactive protein(CRP), hemoglobin, and albumin. Charlson Comorbidity Index(CCI) was calculated as well. The correlations between the variables and frailty scores were investigated, respectively. After adjusting for covariates, binomial logistic regression analysis was used to assess independent effect of frailty scores on the outcome(discharge or death/progression) in older CAP patients. RESULTS: The subjects had a median age 87(interquartile range,8.5) years, 60.6% male, 45.9% pre-frail, and 32.1% frail. There were positive correlations between frailty scores and CURB-65 scale (p = 0.000, r = 0.542), CCI(p = 0.000, r = 0.359) and NLR(p = 0.005, r = 0.268). Negative correlations were observed between frailty scores and hemoglobin (p = 0.002, r = - 0.298), albumin (p = 0.000, r = - 0.465). In multivariable logistic regression analysis, the factors associated with discharge or death/progression of CAP were frailty scores (OR = 1.623, p = 0.037), NLR (OR = 1.086, p = 0.008) and albumin (OR = 0.869, p = 0.034). CONCLUSIONS: Frailty is correlated with CURB-65 scale, CCI and hemoglobin, and albumin in older patients with CAP. Frailty is also a correlate of increased risk for death or progression in these older people.

Relationship Between Particulate Matter (PM2.5) and Hospitalizations and Mortality of Chronic Obstructive Pulmonary Disease Patients: A Meta-Analysis.

BACKGROUND: Numerous studies have reported associations between particulate matter with aerodynamic diameters of ≤2.5 µm (PM2.5) and chronic obstructive pulmonary disease (COPD) hospitalizations and mortality in cities worldwide. Nonetheless, the evidence of an association remains varied and limited. METHODS: Systematic searches were conducted in 6 common English and Chinese electronic databases (i.e., PubMed, Web of Science, EMBASE, Ovid, Google Scholar, and China National Knowledge Infrastructure [CNKI]). A meta-analysis was performed to estimate the odds ratio (OR) to evaluate the relationship between PM2.5 and COPD hospitalizations and mortality. Publication bias and heterogeneity of samples were tested using a funnel plot and the Egger's test. Studies were analyzed using either a random-effect model or a fixed-effect model. RESULTS: The search yielded 18 studies suitable for meta-analysis during the period from Jan 1, 2010 to Dec 31, 2018. A 10-µg/m³ increase in PM2.5 was associated with a 2.5% (95% confidence interval [CI]: 1.8-3.2%) increase in COPD hospitalizations, with an OR of 1.025 (95% CI: 1.018-1.032), and a 1.5% (95% CI: 0.9-2.2%) increase in COPD mortality, with an OR of 1.015 (95% CI: 1.009-1.022). Comparing different age groups, elderly people were more sensitive to the adverse effects. The estimated risk was higher in European countries than Asian countries, and in warm compared cold seasons. Various additional confounding factors also led to different results. CONCLUSIONS: PM2.5 is associated with COPD hospitalizations and mortality. Controlling ambient air pollution would provide benefits to COPD patients.

Downregulation of AATK mediates microRNA-558-induced resistance of A549 cells to radiotherapy.

The deregulation of microRNAs (miRNAs) is often implicated in the control of sensitivity to radiotherapy. The objective of the present study was to identify the association between miR­558 and apoptosis­associated tyrosine kinase (AATK), and their importance in regulating the development of resistance to radiotherapy. The current study demonstrated that AATK, a radiosensitization-associated gene, is a target of miR­558 in lung cancer cells, using in silico analysis and a luciferase reporter system. Furthermore, it was determined that transfection of 30 or 50 nM miR­558 mimics and AATK specific siRNA markedly suppressed the mRNA and protein expression of AATK. To determine whether miR­558 was required for lung cancer cell radioresistance, A549 cells were treated with different doses of ionizing radiation, from 0 to 10 Gy, following transfection with miR­558 mimics or AATK specific siRNA. It was determined that the administration of miR­558 mimics or AATK specific siRNA alone did not significantly alter the survival rate of the cells. By contrast, in the cells exposed to 4, 6 or 8 Gy, the administration of miR­558 mimics or AATK specific siRNA significantly promoted cell survival rate and overexpression of AATK reversed this effect. In conclusion, these data demonstrate that the miR­558/AATK cascade is important for the radiosensitization of lung cancer cells and may be a potential radiotherapy target.

Association of MTHFR C677T with total homocysteine plasma levels and susceptibility to Parkinson's disease: a meta-analysis.

The C677T single-nucleotide polymorphism in the methylenetetrahydrofolate reductase gene (MTHFR) may elevate homocysteine (Hcy) levels and increase the risk of Parkinson's disease (PD); however, results are conflicting. Our aim was to resolve contradictions in the literature and to determine whether MTHFR C677T has a significant role in regulating Hcy levels and/or is a significant risk factor for PD. MEDLINE, EMBASE, the Cochrane Library, China Biological Medicine Database and Google Scholar were searched until May 2014. Strict selection and exclusion criteria were determined, and odds ratios (ORs)/weighted mean differences (WMDs) with 95 % confidence intervals (CIs) were used to assess the strength of associations. Statistical analyses were performed using STATA 12.0. Fifteen studies that together assessed 2690 PD cases and 8465 controls were included. Meta-analysis showed that no significant difference in the distribution of MTHFR C677T between PD cases and controls was found. While stratifying for ethnicity, significant association was revealed in Europeans (T vs. C, OR = 1.17, 95 % CIs 1.04-1.31) but not in Asians. Significant association between the T allele and increased Hcy levels was found in PD cases and controls; Hcy levels were higher in PD cases and controls carrying the MTHFR T677 allele than in non-carriers (TT vs. CC, PD WMD = 6.50, 95 % CIs 6.20-6.80; controls WMD = 4.52, 95 % CIs 4.24-4.80). Other within-group comparisons showed similar results. This meta-analysis suggests that MTHFR C667T may confer PD susceptibility in Europeans. The T allele may be an independent risk factor for elevated Hcy levels in PD patients.

Serum miR-152, miR-148a, miR-148b, and miR-21 as novel biomarkers in non-small cell lung cancer screening.

Lung cancer, predominantly by non-small cell lung cancer (NSCLC), is the leading cause of cancer-related deaths over the world. Late diagnosis is one of important reasons for high mortality rate in lung cancer. Current diagnostic approaches have disadvantages such as low accuracy, high cost, invasive procedure, etc. MicroRNAs were previously proposed as promising novel biomarkers in cancer screening. In this study, we evaluated the predictive power of four candidate miRNAs in NSCLC detection. Our study involved 152 NSCLC patients and 300 healthy controls. Blood samples were obtained from the total 452 subjects. After miRNA extraction from serum, the expression of miRNAs in cases and controls were quantified by qRT-PCR and normalized to the level of U6 small RNA. Statistical analyses were performed to compare miRNA levels between cases and controls. Stratified analyses were employed to compare miRNA levels in NSCLC patients with different clinical characteristics. Serum miR-148a, miR-148b, and miR-152 were significantly downregulated in NSCLC patients. However, overexpression of serum miR-21 was observed in NSCLC patients. The combination of four candidate miRNAs exhibited the highest predictive accuracy in NSCLC screening compared with individual miRNAs (AUC = 0.97). Low level of miRNA-148/152 members may associate with advanced stage, large tumor size, malignant cell differentiation, and metastasis. High expression of miR-21 was possibly correlated with large size tumor and advanced cancer stage. Our results showed the dysregulation of miR-148/152 family and miR-21 in NSCLC patients. Hence, the four candidate miRNAs have great potential to serve as promising novel biomarkers in NSCLC screening. Further large-scale studies are needed to validate our results.

Association of LOX-1 gene polymorphisms with cerebral infarction in northern Chinese Han population.

BACKGROUND: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays an important role in the pathophysiology of atherosclerosis and thrombosis. This study is aimed at evaluating the potential association of 3'-UTR-C188T and G501C in LOX-1 gene with cerebral infarction. METHODS: A total of 386 patients with cerebral infarction and 386 healthy controls were included in the study, which were unrelated Chinese Han population in the Liaoning Province of northern China. The single nucleotide polymorphisms, 3'-UTR-C188T and G501C, were analyzed by polymerase chain reaction-ligation detection reaction method. RESULTS: The frequencies of CC + GC genotype, GC genotype and C allele of G501C in the patients with cerebral infarction were significantly higher than those in the controls (P < 0.01, P < 0.01, P = 0.04, respectively). The correlation still remained after adjusting for confounding risk factors of cerebral infarction. In addition, no significant association was observed between 3'-UTR-C188T and cerebral infarction. CONCLUSIONS: The study indicated that the G501C variant in LOX-1 gene may be associated with susceptibility to cerebral infarction, independent of other common risk factors, in northern Chinese Han population.

Association of PLA2G7 gene polymorphisms with ischemic stroke in northern Chinese Han population.

OBJECTIVE: Human lipoprotein-associated phospholipase A2 (Lp-PLA2), encoded by the PLA2G7 gene, plays an important role in the pathophysiology of inflammation. This study is aimed at evaluating the potential association of V279F and A379V in PLA2G7 gene with ischemic stroke where inflammatory process is involved. DESIGN AND METHODS: A total of 386 patients with ischemic stroke and 386 healthy controls were included in the study. The single nucleotide polymorphisms, V279F and A379V, were analyzed by the polymerase chain reaction-ligation detection reaction method. RESULTS: The frequencies of VV+AV genotype, AV genotype and V allele of A379V in the patients with ischemic stroke were significantly higher than those in the controls (P=0.02, P=0.03, P=0.02, respectively). These correlations still remained after adjusting for confounding risk factors of stroke. Furthermore, subgroup analysis showed that a significant association with A379V was found in large-artery atherosclerotic stroke subgroup. In addition, no significant association was observed between V279F and ischemic stroke. CONCLUSION: The study indicated that the A379V variant in PLA2G7 gene might contribute to ischemic stroke susceptibility in northern Chinese Han population.

Exhaled hydrogen sulfide in patients with chronic obstructive pulmonary disease and its correlation with exhaled nitric oxide.

BACKGROUND: Exhaled nitric oxide (NO) is a noninvasive biomarker of airway inflammation in pulmonary diseases. Hydrogen sulfide (H2S), as the third member of the gasotransmitter family, is involved in the pathophysiological process in lung diseases. H2S also exists in exhaled breath and can be sampled non-invasively. The study investigated the level of exhaled H2S in patients with chronic obstructive pulmonary disease (COPD) and its correlation with exhaled NO. METHODS: Levels of exhaled NO and H2S, lung function, and cell differential counts in induced sputum were studied in 19 patients with acute exacerbation of COPD (AECOPD), 19 patients with stable COPD and seven healthy smoke controls. RESULTS: Exhaled H2S levels were similar in patients with AECOPD (10.0 parts per billion (ppb), 8.0-13.0 ppb), stable COPD (10.0 ppb, 9.0-12.0 ppb), and healthy controls (9.0 ppb, 8.0-16.0 ppb) (P > 0.05). Exhaled NO levels were similar in patients with AECOPD (155.0 ppb, 129.0-190.0 ppb), stable COPD (154.0 ppb, 133.0-175.0 ppb) and healthy controls (165.0 ppb, 112.0-188.0 ppb) (P > 0.05). Exhaled H2S levels correlated positively with exhaled NO in all healthy controls and patients with COPD (r=0.467, P < 0.01). No significant correlation was found between the exhaled H2S level and percentage of predicted FEV1 (P > 0.05) and proportion of different cell types in induced sputum (P > 0.05). CONCLUSIONS: There is a correlation between exhaled H2S and exhaled NO. The role of exhaled H2S in airway inflammation in COPD still needs further investigation.

[Animal model of grading skeletal muscle contusion due to blunt impact in rats].

OBJECTIVE: To establish a new animal model of grading skeletal muscle contusions that could be controllable and repetitive. METHODS: The rats' gastrocnemius was injured by a new weight-dropping device designed. The force acting on gastrocnemius with a comparatively constant duration and inducing elastic deformation of the gastrocnemius was expressed with velocity (v) and deformation (DF). Instant velocity was changed to create gastrocnemius contusions. Pathological changes of gastrocnemius were graded by the gross and histological examinations of 39 rats. RESULTS: At low level of impact (v: 2 m/s, DF: 5.5 mm), mild injuries were detected in epimysium and superficial layer of gastrocnemius. At moderate level of impact (v: 2.5 m/s, DF: 6.5 mm), the injuries were observed in epimysium and whole gastrocnemius. At high level of impact (v: 3 m/s, DF: 7.5 mm), severe injuries were seen deeper to soleus with more extensive skeletal muscle damage. CONCLUSION: Grading of skeletal muscle blunt force contusion is created by parameter of velocity and muscle deformation. The model could be used for further research on skeletal muscle contusions.