Ambient air pollution, lifestyle, and genetic predisposition on all-cause and cause-specific mortality: A prospective cohort study.

BACKGROUND: Although it is widely acknowledged that long-term exposure to ambient air pollution is closely related to the risk of mortality, there were inconsistencies in terms of cause-specific mortality and it is still unknown whether lifestyle and genetic susceptibility could modify the association. METHODS: This population-based prospective cohort study involved 461,112 participants from the UK Biobank. The land-use regression model was used to estimate the concentrations of particulate matter (PM2.5, PMcoarse, PM10), and nitrogen oxides (NO2 and NOx). The association between air pollution and mortality was evaluated using Cox proportional hazard models. Furthermore, a lifestyle score incorporated with smoking status, physical activity, alcohol consumption, and diet behaviors, and polygenic risk score using 12 genetic variants, were developed to assess the modifying effect of air pollution on mortality outcomes. RESULTS: During a median follow-up of 14.0 years, 33,903 deaths were recorded, including 17,083 (2835; 14,248), 6970, 2429, and 1287 deaths due to cancer (lung cancer, non-lung cancer), cardiovascular disease (CVD), respiratory and digestive disease, respectively. Each interquartile range (IQR) increase in PM2.5, NO2 and NOx was associated with 7 %, 6 % and 5 % higher risk of all-cause mortality, respectively. Specifically, for cause-specific mortality, each IQR increase in PM2.5, NO2 and NOx was also linked to mortality due to cancer (lung cancer and non-lung cancer), CVD, respiratory and digestive disease. Furthermore, additive and multiplicative interactions were identified between high ambient air pollution and unhealthy lifestyle on mortality. In addition, associations between air pollution and mortality were modified by lifestyle behaviors. CONCLUSION: Long-term exposure to air pollutants increased the risk of all-cause and cause-specific mortality, which was modified by lifestyle behaviors. In addition, we also revealed a synergistically detrimental effect between air pollution and an unhealthy lifestyle, suggesting the significance of joint air pollution management and adherence to a healthy lifestyle on public health.

Associations Between Sex-Specific Reproductive Factors and Risk of New-Onset Lung Cancer Among Female Patients.

BACKGROUND: Several characteristics distinguish lung cancer in female patients from that in male patients, with adenocarcinoma being more prevalent in female patients and occurring more frequently in female patients who do not smoke. Uncertainty surrounds the relationship between female-specific reproductive factors and lung cancer risk. RESEARCH QUESTION: Are sex-specific reproductive factors associated with risk of lung cancer in different genetic risk groups and histologic types? STUDY DESIGN AND METHODS: A Cox proportional hazard model was used to evaluate the association between multiple reproductive factors and the risk of lung cancer developing in a prospective cohort study involving 273,190 female individuals from the UK Biobank. Subgroup analyses stratified by age, smoking status, BMI, genetic risk, and histologic subtype were conducted to emphasize the modification effects further. RESULTS: A total of 1,182 cases of lung cancer in female patients were recorded over a median follow-up period of 12.0 years in the cohort study. In multivariable-adjusted models, early menarche (age ≤ 11 years: hazard ratio [HR], 1.22; 95% CI, 1.03-1.46), early menopause (age ≤ 46 years: HR, 1.49; 95% CI, 1.19-1.86), a shorter reproductive span (≤ 32 years: HR, 1.42; 95% CI, 1.18-1.71; and 33-35 years: HR, 1.24; 95% CI, 1.00-1.53), and early age at first birth (age ≤ 20 years: HR, 1.63; 95% CI, 1.33-2.01) were associated with a higher risk of lung cancer. Stratified analysis revealed that several reproductive factors, including early age at menopause, shortened reproductive span, and early age at first birth, showed a substantially stronger relationship with an elevated risk of lung cancer, particularly of lung adenocarcinoma, in populations with high genetic risk and more detrimental behaviors. INTERPRETATION: Early age at menopause, a shortened reproductive life span, and early age at first birth were associated with higher risks of lung cancer, particularly of lung adenocarcinoma, in a subpopulation with higher genetic susceptibility and detrimental behaviors. The evidence provided by this study emphasizes the significance of screening for multiple reproductive factors to prevent lung cancer among female individuals.

Association of telomere length with risk of lung cancer: A large prospective cohort study from the UK Biobank.

OBJECTIVES: Leukocyte telomere length (LTL) is associated with a wide variety of diseases, including cancer. However, findings regarding the association between LTL and the risk for lung cancer have been inconclusive and inconsistent across previous observational studies. METHODS: This prospective cohort study included data from 425,146 participants 37-73 years of age housed in the UK Biobank. Quantitative polymerase chain reaction (qPCR) was used to measure LTL in baseline DNA samples. A multivariate Cox proportional hazards model was used to evaluate the relationship between LTL and the risk for lung cancer. RESULTS: An increase in LTL per interquartile range (IQR) was associated with a 9% increase in the risk for lung cancer (hazard ratio [HR] 1.09 [95% confidence interval (CI) 1.03-1.16]). Participants in the highest LTL quintile exhibited an approximately 25% elevated risk for developing lung cancer (HR 1.25 [95% CI 1.09-1.45]) compared with those in the lowest quintile. The relationship between per IQR increase in LTL and elevated risk for lung cancer was greater in the histological subtype of adenocarcinoma (HR 1.30 [95% CI 1.18-1.43]), female sex (HR 1.16 [95% CI 1.06-1.26]), non-smokers (HR 1.45 [95% CI 1.23-1.71]), and individuals with high genetic risk for lung cancer (HR 1.18 [95% CI 1.03-1.34]), respectively. Surprisingly, a per IQR increase in LTL was associated with increased risks for both lung adenocarcinoma (HR 1.56 [95% CI 1.24-1.96]) and squamous cell carcinoma (HR 2.01 [95% CI 1.13-3.56]) in never smokers. CONCLUSIONS: Longer LTL was associated with an elevated risk for lung cancer, particularly for adenocarcinoma and squamous cell carcinoma in never smokers. The results suggest the potential of telomeres as non-invasive biomarkers for the early screening of lung cancer, particularly in non-smokers, who are typically overlooked.

Vitamin D status, sleep patterns, genetic susceptibility, and the risk of incident adult-onset asthma: a large prospective cohort study.

Introduction: Vitamin D has been known to be associated with asthma, particularly in children, while the evidence among adults is limited and inconclusive. This study aimed to investigate the association between serum, vitamin D concentrations, and the incidence of adult-onset asthma and also the modified effect caused by sleep patterns and genetic risks. Methods: A prospective cohort study with 307,872 participants aged between 37 and 73 years was conducted based on the UK Biobank, with a median follow-up of 12 years. The Cox proportional hazard model was applied to evaluate the association between vitamin D status and incident adult-onset asthma, and the modified effect was investigated by conducting stratified analysis according to sleep pattern score and genetic risk score, and subgroup analyses were performed by sex, age, BMI, and smoking status as well. Results: Individuals with optimal vitamin D concentration were associated with 11.1% reduced risk of incident asthma compared to those participants with deficient vitamin D (HR = 0.889; 95% CI: 0.820-0.964; p = 0.005). Moreover, stratification analysis demonstrated that the protective effect of vitamin D on asthma risk was modified by sleep patterns or genetic susceptibility, with the strongest protective effect being observed in the subpopulation with a moderate sleep pattern (HR = 0.883; 95% CI: 0.797-0.977; p = 0.016) and a moderate genetic risk (HR = 0.817; 95% CI: 0.711-0.938; p = 0.004). In subgroup analyses, the protective effect of optimal vitamin D levels was only significant among men, individuals younger than 60 years of age, overweight individuals, and current or previous smokers. Conclusion: Increased serum vitamin D levels were associated with a lower risk of incident adult-onset asthma, and this association was modified by sleep patterns and genetic predisposition to some extent.

Association of genetic risk and lifestyle with incident adult-onset asthma in the UK Biobank cohort.

Background: Both genetic and lifestyle factors contribute to the development of asthma, but whether unfavourable lifestyle is associated with similar increases in risk of developing asthma among individuals with varying genetic risk levels remains unknown. Methods: A healthy lifestyle score was constructed using body mass index, smoking status, physical activities and dietary pattern to further categorise into ideal, intermediate and poor groups. Genetic risk of asthma was also categorised as three groups based on the tertiles of polygenic risk score established using 212 reported and verified single-nucleotide polymorphisms of European ancestry in the UK Biobank study. We examined the risk of incident asthma related with each lifestyle level in each genetic risk group by Cox regression models. Results: Finally, 327 124 participants without baseline asthma were included, and 157 320 (48.1%) were male. During follow-up, 6238 participants (1.9%) developed asthma. Compared to ideal lifestyle in a low genetic risk group, poor lifestyle was associated with a hazard ratio of up to 3.87 (95% CI, 2.98-5.02) for developing asthma in a high genetic risk group. There was interaction between genetic risk and lifestyle, and the population-attributable fraction of lifestyle and genetic risk were 30.2% and 30.0% respectively. Conclusion: In this large contemporary population, lifestyle and genetic factors jointly play critical roles in the development of asthma, and the effect values of lifestyle on incident adult-onset asthma were greater than that of genetic risk. Our findings highlighted the necessity of a comprehensive intervention for the prevention of asthma despite the genetic risk.

Association of air pollution, genetic risk, and lifestyle with incident adult-onset asthma: A prospective cohort study.

BACKGROUND: Numerous studies have explored the association of air pollution with asthma but have yielded conflicting results. The exact role of air pollution in the incidence of adult-onset asthma and whether this effect is modified by genetic risk, lifestyle, or their interaction remain uncertain. METHODS: We conducted a prospective cohort study on 298,738 participants (aged 37-73 years) registered in the UK Biobank. Cox proportional hazard models were used to evaluate the association of air pollution, including particulate matter (PM2.5, PMcoarse, and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOx), with asthma incidence. We constructed genetic risk and lifestyle scores, assessed whether the impact of air pollution on adult-onset asthma risk was modified by genetic susceptibility or lifestyle factors, and evaluated the identified interactions. RESULTS: We found that each interquartile range increase in annual concentrations of PM2.5, NO2, and NOx was related to 1.04 (95% confidence interval [CI]: 1.01, 1.08), 1.04 (95% CI: 1.00, 1.08), and 1.03 (95% CI: 1.00, 1.06) times the risk of adult-onset asthma, respectively. The size of the effect of air pollution was greater among subpopulations with low genetic risk or unfavorable lifestyles. We also identified an additive interaction effect of air pollution with lifestyle factors, but not with genetic risk, on the risk of adult-onset asthma. CONCLUSION: Our analyses show that air pollution increases the risk of adult-onset asthma, but that the size of the effect is modified by lifestyle and genetic risk. These findings emphasize the need for integrated interventions for environmental pollution by the government as well as adherence to healthy lifestyles to prevent adult-onset asthma.

Associations Between Reproductive Factors and the Risk of Adult-Onset Asthma: A Prospective Cohort Study of European Ancestry.

BACKGROUND: Multiple studies showed sex discrepancies in the prevalence, incidence, and disease control of asthma. The relationships between different reproductive factors and the risk of asthma in females remain uncertain. DESIGN: A prospective cohort study recruited 239,701 female participants from the UK Biobank. The Cox proportional hazard model and multiple adjusted restricted cubic splines were used to evaluate the association between each reproductive factor and the risk of adult-onset asthma. KEY RESULTS: We observed that the association of age at menarche and age of menopause with adult-onset asthma risk presented as U-shaped, with multiple adjusted HRs for age at menarche being 1.129 (95% CI, 1.038-1.228) for ≤ 11 years old and 1.157 (95% CI, 1.058-1.265) for ≥ 15 years old referenced to 13 years old, and for age at menopause being 1.368 (1.237-1.512) for ≤ 46 years old and 1.152 (1.026-1.294) for ≥ 55 years old referenced to 50-52 years old. Early age at first live birth (≤ 20 years old), a greater number of miscarriages (≥ 2) or stillbirths (≥ 2), more children (≥ 4), and shorter reproductive years (≤ 32 years) were associated with elevated risk of asthma. In addition, history of hysterectomy or oophorectomy was associated with increased risk of adult-onset asthma, particularly in those with simultaneous hysterectomy and oophorectomy (HR, 1.239; 95% CI, 1.063-1.445). For exogenous sex hormones, hormone replacement therapy (HR, 1.482; 95% CI, 1.394-1.574) was identified to be associated with elevated risk of adult-onset asthma. CONCLUSIONS: This study not only demonstrated significant associations between multiple reproductive factors and the risk of adult-onset asthma in a female's later life, but also found that history of hysterectomy or oophorectomy, as well as hormone replacement therapy, was linked to an elevated incidence of adult-onset asthma. Our findings highlighted the significance of reproductive factors in the development of asthma in female populations.

Association of outdoor air pollution, lifestyle, genetic factors with the risk of lung cancer: A prospective cohort study.

OBJECTIVES: The effect of air pollution exposure on incident lung cancer remains uncertain, and the modifying role of lifestyle and genetic susceptibility in association between air pollution and lung cancer is ambiguous. METHODS: A total of 367,623 participants from UK biobank cohort were enrolled in the analysis. The concentrations of particle matter (PM2.5, PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOx), were evaluated by land-use regression model. Cox proportional hazard model was applied to assess the associations between air pollution and incident lung cancer. A lifestyle risk score and a polygenic risk score were established to investigate whether lifestyle and heritable risk could modify the effect of air pollution on lung cancer risk. RESULTS: Per interquartile range (IQR) increment in annual concentrations of PM2.5 (HR = 1.22, 95% CI, 1.15∼1.30), NO2 (HR = 1.19, 95% CI, 1.10∼1.27), and NOx (HR = 1.14, 95% CI, 1.09∼1.20) were associated with increased risk of lung cancer. We observed an additive interaction between air pollution including PM2.5 and NOx and lifestyle or genetic risk. Individuals with high air pollution exposure, poor lifestyle and high genetic risk had the highest risk of incident lung cancer. CONCLUSION: Long-term exposures to air pollution is associated with increased risk of lung cancer, and this effect was modified by lifestyle or genetic risk. Integrated interventions for environmental pollution by government and adherence to healthy lifestyle by individuals are advocated for lung cancer prevention.

Clinical characteristics and prognosis of patient with leptospirosis: A multicenter retrospective analysis in south of China.

Purpose: Leptospirosis is a zoonotic disease caused by pathogenic spirochetes of the genus Leptospira. However, there is currently no consensual definition or diagnostic criteria for severe and different forms of leptospirosis. Therefore, more insight on clinical manifestations, risk factors, and outcomes of leptospirosis is warranted. The identification of leptospirosis with distinct clinical manifestations and prognosis in our population. Methods: Multiple correspondence analysis and hierarchical classification on principal components were presented to identify different clinical types of leptospirosis. The outcomes were clinical phenotypes, laboratory and imaging findings, and prognosis. Results: The 95 enrolled patients had median values of 54.0 years (39.0-65.0) for age, 9.0 (7.0-14.0) for total hospital stay lengths, of whom 86.3% was male and 40.0% was transferred to ICU. Three clinical types were distinguished: mild leptospirosis (n=43, 45.3%) with less organ dysfunction and shorter hospital stays; respiratory leptospirosis (n=28, 29.5%) with hemoptysis, and respiratory and circulatory failure; and hepato-renal leptospirosis (n=24, 25.3%) with worst liver and kidney dysfunction. Total hospital mortality was 15.8% and was associated with dyspnea and high levels of neutrophil counts. Conclusions: The identification of leptospirosis with distinct clinical manifestations and prognosis in our population may assist clinicians to distinguish leptospirosis-like disease. Moreover, dyspnea and neutrophil count were found to be independent risk factors for severe leptospirosis progression.

Association of Coffee and Tea Consumption with the Risk of Asthma: A Prospective Cohort Study from the UK Biobank.

Background: Previous observational studies investigated the relationship between coffee and tea intake and the risk of asthma, however, the conclusions were inconsistent. Further, the combined effect of coffee and tea consumption on asthma has rarely been studied. Methods: We examined associations between the self-reported intake of tea and coffee and the risk of incident asthma in a total of 424,725 participants aged from 39 to 73 years old from the UK Biobank. Cox proportional hazards models were used to estimate the associations between coffee/tea consumption and incident adult-onset asthma, adjusting for age, sex, race, smoking status, body mass index (BMI), education, and Townsend deprivation index. Results: Cox models with penalized splines showed J-shaped associations of coffee, tea, caffeinated coffee, and caffeine intake from coffee and tea with the risk of adult-onset asthma (p for nonlinear <0.01). Coffee intake of 2 to 3 cups/d (hazard ratio [HR] 0.877, 95% confidence interval [CI] 0.826−0.931) or tea intake of 0.5 to 1 cups/d (HR 0.889, 95% CI 0.816−0.968) or caffeinated coffee intake of 2 to 3 cups/d (HR 0.858, 95% CI 0.806−0.915) or combination caffeine intake from tea and coffee of 160.0 to 235.0 mg per day (HR 0.899, 95% CI 0.842−0.961) were linked with the lowest hazard ratio of incident asthma after adjustment for age, sex, race, smoking status, BMI, qualification, and Townsend deprivation index. Conclusions: Collectively, the study showed light-to-moderate coffee and tea consumption was associated with a reduced risk of adult-onset asthma and controlling total caffeine intake from coffee and tea for a moderate caffeine dose of 160.0 to 305.0 mg/day may be protective against adult-onset asthma. Further investigation on the possible preventive role of caffeine in asthma is warranted.

Vitamin D status and asthma, lung function, and hospitalization among British adults.

Background: Vitamin D has been known to be associated with asthma. However, the association between vitamin D status and asthma, lung function as well as hospitalization among adults remains unclear. Objective: To investigate the role of serum vitamin D in asthma prevalence, lung function, and asthma control in adults. Methods: Multivariable logistic regression was applied to assess the relationship between serum vitamin D and asthma prevalence, lung function (FEV1, FVC, and FEV1/FVC), current wheeze, and asthma-linked hospitalizations in a cross-sectional study of 435,040 adults aged 37-73 years old from the UK Biobank. Results: Compared to vitamin D deficiency, the odds of asthma were decreased by 6.4% [adjusted odds ratio (aOR) = 0.936; 95% CI: 0.911-0.962; p < 0.001] and 9.8% (aOR = 0. 0.902; 95% CI: 0.877-0. 0.927; p < 0.001) in individuals with insufficient and optimal vitamin D concentration, respectively, in the fully adjusted model. In total asthmatic patients, serum vitamin D was obviously and positively related with FEV1 (ß = 1.328 ml, 95% CI = 0.575-2.080), FVC (ß = 2.018 ml, 95% CI = 1.127-2.908), and FEV1/FVC (ß = 0.006%, 95% CI = 0.002-0.010). Asthmatic patients whose vitamin D level was in the deficient category had 9.3-19.9% higher odds of current wheeze than insufficient categories (aOR = 0.907; 95% CI: 0.861-0.957; p < 0.001) and optimal categories (aOR = 0.801; 95% CI: 0.759-0.845; p < 0.001), but the relationship between vitamin D and asthma hospitalization was not significant. Conclusion: Vitamin D deficiency was related to higher odds of asthma and current wheeze, and lower lung function in a large sample size study of British adults. Our results indicate a potential positive impact of serum vitamin D on asthma occurrence and disease control in adults.

MiR-29a-3p Improves Acute Lung Injury by Reducing Alveolar Epithelial Cell PANoptosis.

Alveolar epithelial cell damage is an important determinant of the severity of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). However, the molecular mechanisms of alveolar epithelial death during the development of ALI/ARDS remain unclear. In this study, we explore the role of miR-29a-3p in ALI/ARDS and its molecular mechanism. Plasma samples were collected from healthy controls and ARDS patients. Mice were intratracheally instilled with lipopolysaccharide (LPS) to establish acute lung injury. N6-adenosine (m6A) quantification, RNA-binding protein immunoprecipitation, cell viability assay, quantitative real-time polymerase chain reaction, and western blotting were performed. We found that miR-29a-3p was down-regulated in plasma of ARDS patients and lung tissue of ALI model mice, and miR-29a-3p agomir injection down-regulated the levels of the inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6) in the lungs, reducing alveolar epithelial cell PANoptosis as evaluated by the downregulation of Z-DNA binding protein 1 (ZBP1), gasdermin D (GSDMD), caspase-3, caspase-8, and mixed lineage kinase domain-like protein (MLKL), ultimately improving lung injury in the ALI model mice. Mechanism studies demonstrated that the knockout of methyltransferase 3 (N6-adenosine-methyltransferase complex catalytic subunit) removed the m6A modification of miR-29a-3p and reduced miR-29a-3p expression. Our findings suggest that miR-29a-3p is a potential target that can be manipulated for ALI/ARDS.

Clinical Characteristics, Laboratory Findings, and Prognosis in Patients With Talaromyces marneffei Infection Across Various Immune Statuses.

Objective: Talaromyces marneffei (TM) is an opportunistic fungus that is predominantly prevalent among patients who are HIV-positive in South-East Asia. However, few studies focused on the clinical features, laboratory findings, and prognosis across varying immune states. Methods: A total of 54 patients with TM infection in Xiangya Hospital of Central South University from January 1, 2006 to October 31, 2021 were retrospectively analyzed. Clinical profiles were compared across the different immune statuses by HIV-positive (HIV group, n = 18), HIV negative but with immunocompromised conditions (Non-HIV with IC Group, n = 11), and immunocompetent patients (n = 25). Results: All the patients were diagnosed by pathogen culture or by metagenomic next-generation sequencing (mNGS). The median age was 50, and patients with HIV were much younger compared to the other two groups. The most common symptom at presentation was fever (79.6%), followed by cough (70.4%), weight loss (61.1%), and expectoration (53.7%). The patients with HIV were more likely to develop into a subtype of disseminated TM affecting multiple organs including lymph node, liver, skin, and spleen, thus, resulting in higher hospital mortality compared to the other two groups. Patients without HIV but with immunocompromised conditions presented similar hospital mortality rates compared to immunocompetent patients, while experiencing longer days of hospitalization to recover from the diseases. Additionally, in this study, the pathogen culture easily confirmed the patients with HIV. However, mNGS presented as a promising tool to confirm TM infection in those suspicious patients without HIV. Conclusions: In summary, patients with HIV were more likely to develop into disseminated TM, resulting in higher mortality compared to those patients without HIV. Additionally, mNGS presented as an important supplementary tool to confirm TM infection in patients without HIV, particularly in those with immunocompromised diseases.

Clinical characteristics of severe coronavirus disease 2019 patients with chronic obstructive pulmonary disease. / é‡åž‹æ–°åž‹å† çŠ¶ç— æ¯’è‚ºç‚Žåˆå¹¶æ ¢æ€§é˜»å¡žæ€§è‚ºç–¾ç— æ‚£è€ ä¸´åºŠç‰¹å¾.

OBJECTIVES: Coronavirus disease 2019 (COVID-19) in elderly and patients with chronic respiratory diseases (COPD) had a poor prognosis. COPD is one of the most common chronic respiratory diseases. We explore the epidemiological characteristics of patients with severe COVID-19 with COPD patients in order to provide medical evidence for the prevention and treatment of severe COVID-19. METHODS: We retrospectively analyzed the clinical baseline characteristics, treatment strategies, disease progression and prognosis of 557 severe COVID-19 patients admitted to the West Court of Union Hospital of Huazhong University of Science and Technology from January 29, 2020 to April 8, 2020. RESULTS: A total of 465 patients with severe COVID-19 were enrolled in the study, including 248 (53.3%) males and 217 (46.7%) females. The median age of severe COVID-19 patients was 62.0 years, and 53 patients were complicated with COPD. Common symptoms at the onset included fever (78.5%), dry cough (67.1%), shortness of breath (47.3%) and fatigue (40.9%). Compared with non-COPD patients, patients with COPD had significantly lower levels of SpO2 in admission (90.0% vs 92.0%, P=0.014). In terms of laboratory examinations, patients with COPD had higher levels of C-reactive protein, interleukin-6, procalcitonin, total bilirubin, blood urea nitrogen, serum creatinine, lipoprotein (a), high-sensitivity troponin I, and D-dimer, while had lower levels of platelet counts, albumin and apolipoprotein AI. Severe COVID-19 patients with COPD had higher Sequential Organ Failure Assessment scores [3.0(2.0, 3.0) vs 2.0(2.0, 3.0), P=0.038] and CURB-65 score [1.0(1.0, 2.0) vs1.0(0.0, 1.0), P<0.001], and a higher proportion of progressing to critical illness (28.3% vs 10.0%, P<0.001) with more complications [e.g. septic shock (15.1% vs 6.1%, P=0.034)], had higher incidence rates of antibiotic therapies (90.6% vs 77.2%, P=0.025), non-invasive (11.3% vs 1.7%, P<0.001) and invasive mechanical ventilation (17.0% vs 8.3%, P=0.039), ICU admission (17.0% vs 7.5%, P=0.021) and death (15.1% vs 6.1%, P=0.016). Cox proportion hazard model was carried out, and the results showed that comorbid COPD was an independent risk factor for severe COVID-19 patients progressing to critical type, after adjusting for age and gender [adjusted hazard ratio (AHR)=2.38(1.30-4.37), P=0.005] and additionally adjusting for chronic kidney diseases, hypertension, coronary heart disease [AHR=2.63(1.45-4.77), P<0.001], or additionally adjusting for some statistically significant laboratory findings [AHR=2.10(1.13-3.89), P=0.018]. CONCLUSIONS: Severe COVID-19 patients with COPD have higher levels of disease severity, proportion of progression to critical illness and mortality rate. Individualized treatment strategies should be adopted to improve the prognosis of severe COVID-19 patients.

Identification of an Early-Middle Jurassic oxidized magmatic belt, south Gangdese, Tibet, and geological implications.

The south Gangdese region is the site of subduction of the Neo-Tethys and subsequent continental collision. Compared with widespread Cretaceous and Cenozoic magmatism, Early-Middle Jurassic magmatic rocks and related deposits are rarely reported. Our work identified a >200km long felsic rock belt associated with Cu mineralization in the south Gangdese region. We report here zircon U-Pb ages, zircon Ce4+/Ce3+ values, and mineral assemblages of two Cu mineralized intrusions within the belt. A hornblende granite and a diorite porphyry were emplaced at 177.3Ma and 166.3Ma, respectively. Geological occurrence and magmatic hematite-magnetite-chalcopyrite intergrowths suggest that Cu mineralization formed coeval with Jurassic intrusions. Mineralized intrusions have high zircon Ce4+/Ce3+ and EuN/EuN∗ ratios, and hematite-magnetite intergrowths, suggesting their parent magmas were highly oxidized. Hornblende is common and primary fluid inclusions are found in titanite and apatite, indicating their parent magmas were water-saturated and exsolved volatile phases at early stage of magmatic evolution. Those magma characters contribute to the formation of porphyry Cu deposits. Given that majority subduction-related porphyry Cu systems have been eroded following uplift and denudation, the well-preserved Early-Middle Jurassic Cu mineralized igneous rocks in south Gangdese are favorable prospecting targets for subduction-related porphyry Cu deposits.