In Utero and Childhood/Adolescence Exposure to Tobacco Smoke, Genetic Risk, and Lung Cancer Incidence and Mortality in Adulthood.

Rationale: The individual effects of early-life tobacco smoke exposure and its interactions with genetic factors on lung cancer in adulthood remain unclear. Objectives: To investigate the associations of early-life tobacco exposures as well as their interactions with polygenic risk scores (PRSs) with lung cancer incidence and mortality. Methods: A total of 432,831 participants from the UK Biobank study were included. We estimated the associations of in utero exposure to tobacco smoke, the age of smoking initiation and their interactions with PRSs with lung cancer incidence and mortality in adulthood using Cox proportional hazard models. Measurements and Main Results: Lung cancer incidence (hazard ratio [HR]: 1.59, 95% confidence interval [CI], 1.44-1.76) increased among participants with in utero tobacco exposure. Multivariable-adjusted HRs (with 95% CIs) of lung cancer incidence for smoking initiation in adulthood, adolescence, and childhood (versus never-smokers) were 6.10 (5.25-7.09), 9.56 (8.31-11.00), and 15.15 (12.90-17.79) (Ptrend < 0.001). Similar findings were observed in lung cancer mortality. Participants with high PRSs and in utero tobacco exposure (versus low PRSs participants without in utero exposure) had an HR of 2.35 for lung cancer incidence (95% CI, 1.97-2.80, Pinteraction = 0.089) and 2.43 for mortality (95% CI, 2.05-2.88, Pinteraction = 0.032). High PRSs with smoking initiation in childhood (versus never-smokers with low PRSs) had HRs of 18.71 for incidence (95% CI, 14.21-24.63, Pinteraction = 0.004) and 19.74 for mortality (95% CI, 14.98-26.01, Pinteraction = 0.033). Conclusions: In utero and childhood/adolescence exposure to tobacco smoke and its interaction with genetic factors may substantially increase the risks of lung cancer incidence and mortality in adulthood.

Construction of Phenanthridinone Skeletons through Palladium-Catalyzed Annulation.

Herein, a straightforward synthetic approach for the construction of phenanthridin-6(5H)-one skeletons is disclosed. The developed protocol relies on palladium catalysis, providing controlled access to a range of functionalized phenanthridin-6(5H)-ones in 59-88% yields. Furthermore, plausible reaction pathways are proposed based on mechanistic experiments.

Synthesis of pyrimidine-fused skeletons through copper-catalyzed consecutive Sonogashira coupling and aminocyclization.

A copper-catalyzed sequence involving a Sonogashira coupling reaction and 5-exo-dig aminocyclization between a terminal alkyne and a 2-(2-bromophenyl)pyrimidine analog based on six-membered rings is presented. This protocol provides a controlled and modular approach to access a variety of synthetically useful pyrimidine-fused skeletons with high efficiency, broad substrate scope, and excellent functional group compatibility. Under acidic conditions, the (Z)-configuration of products spontaneously converts into (E)-9-benzylidene-1,9-dihydro-11H-pyrazolo[4',3':4,5]pyrimido[2,1-a]isoindol-11-ones.

Short-term impacts of air pollution on the platelet-lymphocyte ratio and neutrophil-lymphocyte ratio among urban adults in China.

The short-term impacts of urban air pollution on the platelet-lymphocyte ratio (PLR) and neutrophil-lymphocyte ratio (NLR) remain obscure. In this study, we included 3487 urban adults from the Wuhan-Zhuhai cohort. Individual inhalation exposure to air pollutants was estimated by combining participants' daily breath volume and ambient concentrations of six air pollutants (including fine particulate matter (PM2.5), inhalable particulate matter (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO) and ozone (O3)). The cumulative impacts were assessed by applying lag structures of up to 7 days before the survey date. Associations of air pollutants with PLR and NLR were assessed using a linear mixed model and Bayesian kernel machine regression (BKMR) model. We found that PLR was negatively related to PM2.5 (lag02-lag06), PM10 (lag02-lag07), NO2 (lag02-lag07), and SO2 (lag03-lag05) and NLR was negatively related to PM10 (lag05 and lag07). In the BKMR model, a negative joint association between the six-air-pollutant mixture and PLR and NLR was observed, whereas PM10 and NO2 appeared to be more important than the other pollutants in the mixture. The negative impact of air pollutants was stronger in males, participants with lower body mass index (< 24 kg/m2), those cooking meals at home, drinkers, and non-exercisers. In conclusion, short-term exposure to air pollutants is significantly related to PLR and NLR in peripheral blood. PLR and NLR may provide new insight into the molecular mechanism underlying the adverse health impact of air pollutants.

Ectonucleoside triphosphate diphosphohydrolase-1 (CD39) impacts TGF-ß1 responses: insights into cardiac fibrosis and function following myocardial infarction.

Extracellular purine nucleotides and nucleosides released from activated or injured cells influence multiple aspects of cardiac physiology and pathophysiology. Ectonucleoside triphosphate diphosphohydrolase-1 (ENTPD1; CD39) hydrolyzes released nucleotides and thereby regulates the magnitude and duration of purinergic signaling. However, the impact of CD39 activity on post-myocardial infarction (MI) remodeling is incompletely understood. We measured the levels and activity of ectonucleotidases in human left ventricular samples from control and ischemic cardiomyopathy (ICM) hearts and examined the impact of ablation of Cd39 expression on post-myocardial infarction remodeling in mice. We found that human CD39 levels and activity are significantly decreased in ICM hearts (n = 5) compared with control hearts (n = 5). In mice null for Cd39, cardiac function and remodeling are significantly compromised in Cd39-/- mice following myocardial infarction. Fibrotic markers including plasminogen activator inhibitor-1 (PAI-1) expression, fibrin deposition, α-smooth muscle actin (αSMA), and collagen expression are increased in Cd39-/- hearts. Importantly, we found that transforming growth factor ß1 (TGF-ß1) stimulates ATP release and induces Cd39 expression and activity on cardiac fibroblasts, constituting an autocrine regulatory pathway not previously appreciated. Absence of CD39 activity on cardiac fibroblasts exacerbates TGF-ß1 profibrotic responses. Treatment with exogenous ectonucleotidase rescues this profibrotic response in Cd39-/- fibroblasts. Together, these data demonstrate that CD39 has important interactions with TGF-ß1-stimulated autocrine purinergic signaling in cardiac fibroblasts and dictates outcomes of cardiac remodeling following myocardial infarction. Our results reveal that ENTPD1 (CD39) regulates TGF-ß1-mediated fibroblast activation and limits adverse cardiac remodeling following myocardial infarction.NEW & NOTEWORTHY We show that CD39 is a critical modulator of TGF-ß1-mediated fibroblast activation and cardiac remodeling following myocardial infarction via modulation of nucleotide signaling. TGF-ß1-induced CD39 expression generates a negative feedback loop that attenuates cardiac fibroblast activation. In the absence of CD39 activity, collagen deposition is increased, elastin expression is decreased, and diastolic dysfunction is worsened. Treatment with ecto-apyrase attenuates the TGF-ß1-induced profibrotic cardiac fibroblast phenotype, revealing a novel approach to combat post-myocardial infarction cardiac fibrosis.

Synthesis of the Red-Emitting (Ba, Ca)2ScAlO5:Eu3+ Phosphors with Photoluminescence Properties.

The light-emitting diodes (LED) are regarded as one of the most promising devices for inexpensive and widely used illumination; in particular, they are highly dependent on the development of red-emitting phosphors. Herein, we developed two types of red-emitting (Ba, Ca)2ScAlO5:Eu3+ multiple excitations phosphors (λex = 255-465 nm) via freeze-drying followed by calcination. Powder X-ray diffraction and NMR results point out that they have hexagonal space group P63/mmc (194), and the structural framework is composed of multi-coordinated Al3+-O2- polyhedron and Sc3+-O2- polyhedron. In addition, the valence state of europium (Eu3+) is confirmed by X-ray photoelectron spectroscopy characterization. Investigation on the photoluminescence properties showed that the photoluminescence process of (Ba, Ca)2ScAlO5:Eu3+ is attributable to the charge transfer band of Eu-O and abundant spectral terms of Eu3+. The α-(Ba, Ca)2ScAlO5:Eu3+ and ß-(Ba, Ca)2ScAlO5:Eu3+ exhibited red emission under 465 and 395 nm excitation, respectively. The PL spectra and decay curves explain the intrinsic photoluminescence mechanism. The strongest emission peaks of the red-emitting α-(Ba, Ca)2ScAlO5:Eu3+ and ß-(Ba, Ca)2ScAlO5:Eu3+ phosphors are at 615 and 619 nm, respectively, exhibiting a high fluorescence of 64 and 67% under the temperature of 423 K (150 °C). Further exploration of the red-emitting phosphors would provide a variety of choices for the design of red LEDs and white LEDs for the solid-state lighting system.

Hepatocellular carcinoma risk variant modulates lncRNA HLA-DQB1-AS1 expression via a long-range enhancer-promoter interaction.

Substantial evidence highlighted the critical role of long non-coding RNAs (lncRNA) in driving hepatocarcinogenesis. We hypothesized that functional variants in genome-wide association studies (GWASs) associated loci might alter the expression levels of lncRNAs and contribute to the development of hepatocellular carcinoma (HCC). Here, we prioritized potentially cis-expression quantitative trait loci-based single nucleotide polymorphism (SNP)-lncRNA association together with the physical interaction by the analyses from Hi-C data in GWAS loci of chronic hepatitis B and HCC. Subsequently, by leveraging two-stage case-control study (1738 hepatitis B [HBV]) related HCC cases and 1988 HBV persistent carriers) and biological assays, we identified that rs2647046 was significantly associated with HCC risk (odds ratio = 1.26, 95% CI = 1.11 to 1.43, P = 4.14 × 10-4). Luciferase reporter assays and electrophoretic mobility shift assays showed that rs2647046 A allele significantly increased transcriptional activity via influencing transcript factor binding affinity. Allele-specific chromosome conformation capture assays revealed that enhancer with rs2647046 interacted with the HLA-DQB1-AS1 promoter to allele-specifically influence its expression by CTCF-mediated long-range loop. Cell proliferation assays indicated that HLA-DQB1-AS1 is a potential oncogene in HCC. Our study showed HLA-DQB1-AS1 regulated by a causal SNP in a long-range interaction manner conferred the susceptibility to HCC, suggesting an important mechanism of modulating lncRNA expression for risk-associated SNPs in the etiology of HCC.

Effect of public health interventions on COVID-19 cases: an observational study.

BACKGROUND: As the epidemic of COVID-19 is gradually controlled in China, a summary of epidemiological characteristics and interventions may help control its global spread. METHODS: Data for COVID-19 cases in Hubei Province (capital, Wuhan) was extracted until 7 March 2020. The spatiotemporal distribution of the epidemic in four periods (before 10 January, 10-22 January, 23 January-6 February and 7 February-7 March) was evaluated, and the impacts of interventions were observed. RESULTS: Among 67 706 COVID-19 cases, 52 111 (76.97%) were aged 30-69 years old, and 34 680 (51.22%) were women. The average daily attack rates (95% CI) were 0.5 (0.3 to 0.7), 14.2 (13.2 to 15.1), 45.7 (44.0 to 47.5) and 8.6 (7.8 to 9.3) cases per 106 people in four periods, and the harmonic means (95% CI) of doubling times were 4.28 (4.01 to 4.55), 3.87 (3.78 to 3.98), 5.40 (4.83 to 6.05) and 45.56 (39.70 to 52.80) days. Compared with the first period, daily attack rates rose rapidly in the second period. In the third period, 14 days after 23 January, the daily average attack rate in and outside Wuhan declined by 33.8% and 48.0%; the doubling times increased by 95.0% and 133.2%. In the four periods, 14 days after 7 February, the daily average attack rate in and outside Wuhan decreased by 79.1% and 95.2%; the doubling times increased by 79.2% and 152.0%. CONCLUSIONS: The public health interventions were associated with a reduction in COVID-19 cases in Hubei Province, especially in districts outside of Wuhan.

Identification of genetic variants in m6A modification genes associated with pancreatic cancer risk in the Chinese population.

N6-Methyladenosine (m6A) is the most prevalent modification of RNA in eukaryotes, and is associated with many cellular processes and even the development of cancers. We hypothesized that single-nucleotide polymorphisms (SNPs) in m6A modification genes, including its "writers", "erasers" and "readers", might affect the m6A functions and associate with the susceptibility to pancreatic ductal adenocarcinoma (PDAC). We first conducted a two-stage case-control study in Chinese population to interrogate all SNPs in 22 m6A modification genes. In the discovery stage, a total of 2735 SNPs were genotyped in 980 patients and 1991 controls. Then, the promising SNP was replicated in another independent population consisting of 858 cases and 2084 controls. As a result, we found the rs7495 in 3'UTR of hnRNPC was significantly associated with increased risk of PDAC in both stages (combined odds ratio = 1.22, 95% confidence interval = 1.12-1.32, P = 2.39 × 10-6). To further reveal the biological function of rs7495 and hnRNPC, we performed a series of biochemical experiments. Luciferase reporter assays indicated that rs7495G allele promoted hnRNPC expression through disrupting a putative binding site for has-miR-183-3p. Cell viability assay demonstrated that knockdown of hnRNPC suppressed the proliferation of PDAC cells. RNA-seq analysis suggested that as an m6A "reader", hnRNPC played an important role in RNA biological processes. In conclusion, our findings elucidated that rs7495G could confer higher risk of PDAC via promoting the expression of hnRNPC through a miRNA-mediated manner. These results provided a novel insight into the critical role of m6A modification in tumorigenesis.

The air quality changes and related mortality benefits during the coronavirus disease 2019 pandemic in China: Results from a nationwide forecasting study.

Air quality changes during the coronavirus disease 2019 (COVID-19) pandemic in China has attracted increasing attention. However, more details in the changes, future air quality trends, and related death benefits on a national scale are still unclear. In this study, a total of 352 Chinese cities were included. We collected air pollutants (including fine particulate matter [PM2.5], inhalable particulate matter [PM10], nitrogen dioxide [NO2], and ozone [O3]) data for each city from January 2015 to July 2020. Convolutional neural network-quantile regression (CNN-QR) forecasting model was used to predict pollutants concentrations from February 2020 to January 2021 and the changes in air pollutants were compared. The relationships between the socioeconomic factors and the changes and the avoided mortality due to the changes were further estimated. We found sharp declines in all air pollutants from February 2020 to January 2021. Specifically, PM2.5, PM10, NO2, and O3 would drop by 3.86 µg/m3 (10.81%), 4.84 µg/m3 (7.65%), 0.55 µg/m3 (2.18%), and 3.14 µg/m3 (3.36%), respectively. The air quality changes were significantly related to many of the socioeconomic factors, including the size of built-up area, gross regional product, population density, gross regional product per capita, and secondary industry share. And the improved air quality would avoid a total of 7237 p.m.2.5-related deaths (95% confidence intervals [CI]: 4935, 9209), 9484 p.m.10-related deaths (95%CI: 5362, 13604), 4249 NO2-related deaths (95%CI: 3305, 5193), and 6424 O3-related deaths (95%CI: 3480, 9367), respectively. Our study shows that the interventions to control COVID-19 would improve air quality, which had significant relationships with some socioeconomic factors. Additionally, improved air quality would reduce the number of non-accidental deaths.

LRCH1 suppresses migration of CD4+ T cells and refers to disease activity in ulcerative colitis.

Background: Ulcerative colitis (UC) is a chronically remittent and progressive inflammatory disorder. LRCH1 is reported to be involved in the immune-regulation of several diseases. However, the exact roles of LRCH1 in UC are still obscure. Materials and Methods: LRCH1 expression was analyzed in the inflamed mucosa and peripheral blood mononuclear cells (PBMCs) from patients with UC by quantitative RT-PCR and immunohistochemistry. Peripheral blood CD4+ T cells were transfected with lentivirus-expressing LRCH1 (LV-LRCH1) or LV-sh-LRCH1, and cytokine expression was determined by using flow cytometry, quantitative RT-PCR and ELISA. Transfected CD4+ T cells were harvested to examine the capacity of chemotaxis using Transwell plate. Results: LRCH1 expression was highly decreased in colonic mucosa and PBMCs from patients with A-UC, and negatively correlated with disease activity. Up or down regulation of LRCH1 did not affect the differentiation of CD4+ T cells, and the related cytokines expression. Moreover, LRCH1 inhibited migratory capacity of CD4+ T cells toward CXCL12 by PKCα. Conclusion: LRCH1 plays an important role in the pathogenesis of UC, possibly through modulating the migration of CD4+ T cells. Therefore, targeting LRCH1 might serve as a novel therapeutic approach in the management of UC.

Multilocus Mitochondrial Mutations Do Not Directly Affect the Efficacy of Gene Therapy for Leber Hereditary Optic Neuropathy.

PURPOSE: Clinical trials of gene therapy for Leber hereditary optic neuropathy (LHON) were conducted in 9 volunteers with the mitochondrial mutation, G11778A in ND4. The purpose of this study was to investigate whether multilocus mitochondrial mutations directly influence the efficacy of gene therapy for LHON. METHODS: Nine volunteers with LHON participated in a clinical trial with intravitreal injection of an adenoviral vector expressing wild-type ND4. Patients were subsequently divided into 2 groups: according to the differences in therapy efficacy and based on improvements in visual acuity. Full mitochondrial DNA sequences of the 2 groups of patients were generated and compared using PubMed, PolyPhen, and PROVEAN. Furthermore, the association between the detected mutations and clinical effects of gene therapy was analyzed. RESULTS: Best-corrected visual acuity (BCVA) significantly improved (≥0.3 log of minimum angle of resolution [logMAR]) in 7 patients 6 months after gene therapy, whereas there was no significant change in BCVA (<0.3 logMAR) of the remaining 2 patients. All 9 patients carried the G1178A mutation in addition to other nonsynonymous mutations. Among these mutations, some were predicted to be neutral and deleterious. Meanwhile, different mitochondrial mutations in the group in which treatment was ineffective, compared with those in responders, were at nucleotide positions 6569 (CO1; Patient 3), 9641 (CO3; Patient 3), and 4491 (ND2; Patient 5). CONCLUSIONS: Detection of the 3 primary mitochondrial mutations causing LHON is sufficient for screening before gene therapy; sequencing of the entire mitochondrial genome is unnecessary before treatment. Patients with LHON can respond to targeted gene therapy irrespective of additional multilocus mitochondrial mutations.

Shift work and ischaemic heart disease: meta-analysis and dose-response relationship.

BACKGROUND: Shift work is common in many industries. The potential association between shift work and ischaemic heart disease (IHD) remains controversial. AIMS: To conduct a systematic review and meta-analysis of epidemiological evidence and summarize the potential relationship between shift work and IHD. METHODS: We searched all relevant case-control and cohort studies that were published from January 1970 to October 2017 on PubMed, Web of Science and Embase. The random-effects model and the generalized least-squares trend model were, respectively, used to evaluate the pooled relative risk and dose-response relationship between shift work and IHD. Two different authors extracted data and assessed the quality of each study independently. RESULTS: Twenty-one articles with 31 independent results of 19 782 IHD cases in 320 002 participants were included. The pooled relative risk for the association between shift work and risk of IHD was 1.13 (95% CI 1.08-1.20, I2 = 53%, P < 0.001). Further evaluation of dose-response relationship indicated that each 1-year increase in shift work was associated with 0.9% (RR = 1.009; 95% CI 1.006-1.012) increase of the risk of IHD. CONCLUSIONS: This meta-analysis updated the evidence that shift work was associated with the risk of IHD and supported a positive dose-response relationship between the risk of IHD and increasing duration of shift work.

Chemical and material communication between the optic nerves in rats.

BACKGROUND: To examine interactions between optic nerves. METHODS: A total of 24 Sprague-Dawley rats received unilateral intravitreal injections. The rats were equally divided into four groups: group A was administered an adeno-associated virus (AAV) carrying an exogenous gene (ND4; rAAV-ND4); group B, AAV carrying a green fluorescent protein (GFP; rAAV-GFP); group C, fluorogold (FG) nerve tracer dye; and group D, phosphate-buffered saline (PBS) as a control. Two weeks later, GFP expression was evaluated in both retinas and optic nerves of group B rats after frozen sectioning. The presence of FG was also evaluated in group C optic nerves by fluorescent microscopy after frozen sectioning. Four weeks after injection, ND4 expression was evaluated in both eyes of groups A and D using western blotting and immunofluorescence. RESULTS: FG was observed in the optic chiasm posterior segment along the optic nerve of injected eyes. Some FG reached the anterior optic nerve of the non-injected eye. GFP fluorescence was observed only in the retina of the injected eye but not in the contralateral retina or either optic nerve. ND4 expression was significantly different between injected and non-injected eyes but not between the non-injected eyes in groups A and D. CONCLUSION: Unilaterally injected material can reach the contralateral optic nerve through axoplasmic transport. It is possible that this the only mechanism by which the optic nerves directly communicate.

Molecular phylogeny and genetic variation in the genus Lilium native to China based on the internal transcribed spacer sequences of nuclear ribosomal DNA.

We present a comprehensive phylogeny derived from nuclear ribosomal DNA (nrDNA) for 214 samples representing 98 species and five varieties, including 44 species and five varieties native to China. Our collection of 25 species and five varieties (44 samples) covering all five sections of the genus (Comber) distributed in China also were included in the internal transcribed spacer (ITS) database. This study incorporates previous research with an emphasis on Chinese species, including the controversial subsection, Sinomartagon 5c Comber. In the phylogenetic tree obtained by maximum parsimony (PAUP) and maximum likelihood (RAxML) analyses, the samples were divided into four major groups. Our results suggest that the subsection (subsect.) 5c Comber should be classified into the true subsect. 5c and the section (sect.) Lophophorum. And the latter was divided into three subsections (subsect. Lophophorum I, subsect. Lophophorum II, and subsect. Lophophorum III). Based on molecular phylogenetic analysis and fluorescence in situ hybridization, we report that L. henryi and L. rosthornii are closely related, and we propose their classification into subsect. Leucolirion 6a. Our results support Comber's subdivision of sect. Leucolirion, which was primarily based on bulb color. Chinese species were divided into five sections: sect. Martagon, sect. Archelirion, sect. Leucolirion, sect. Sinomartagon, and sect. Lophophorum. These findings contribute to our understanding of the phylogeny, origin, and classification of Lilium.

Analysis of public opinion on employment issues using a combined approach: a case study in China.

To analyze the public opinion related to the employment situation, a combined approach is proposed to study the valuable ideas from social media. Firstly, the popularity of public opinion was analyzed according to the time series from a statistical point of view. Secondly, the feature extraction was carried out on the public opinion information, and the thematic analysis of the employment environment was carried out based on the Latent Dirichlet Allocation model. Thirdly, the Bert model was used to analyze the sentiment classification and trend of the employment-related public opinion data. Finally, the employment public opinion texts in different regions were studied based on the spatial sequence popularity analysis, keyword difference analysis. A case study in China is conducted to verify the effectiveness of proposed combined approach. Results shown that the popularity of employment public opinion reached the highest level in March 2022. Public opinions towards employment situation are negative. There is a specific relationship between the popularity of employment public opinion in different provinces.

Bidirectional Association Between Cardiovascular Disease and Lung Cancer in a Prospective Cohort Study.

INTRODUCTION: The study aimed to prospectively investigate the bidirectional association between cardiovascular disease (CVD) and lung cancer, and whether this association differs across genetic risk levels. METHODS: This study prospectively followed 455,804 participants from the United Kingdom Biobank cohort who were free of lung cancer at baseline. Cox proportional hazard models were used to estimate the hazard ratio (HR) for incident lung cancer according to CVD status. In parallel, similar approaches were used to assess the risk of incident CVD according to lung cancer status among 478,756 participants free of CVD at baseline. The bidirectional causal relations between these conditions were assessed using Mendelian randomization analysis. Besides, polygenic risk scores were estimated by integrating genome-wide association studies identified risk variants. RESULTS: During 4,007,477 person-years of follow-up, 2006 incident lung cancer cases were documented. Compared with participants without CVD, those with CVD had HRs (95% confidence interval [CI]) of 1.49 (1.30-1.71) for NSCLC, 1.80 (1.39-2.34) for lung squamous cell carcinoma (LUSC), and 1.25 (1.01-1.56) for lung adenocarcinoma (LUAD). After stratification by smoking status, significant associations of CVD with lung cancer risk were observed in former smokers (HR = 1.44, 95% CI: 1.20-1.74) and current smokers (HR = 1.38, 95% CI: 1.13-1.69), but not in never-smokers (HR = 0.98, 95% CI: 0.60-1.61). In addition, CVD was associated with lung cancer risk across each genetic risk level (pheterogeneity = 0.336). In the second analysis, 32,974 incident CVD cases were recorded. Compared with those without lung cancer, the HRs (95% CI) for CVD were 2.33 (1.29-4.21) in NSCLC, 3.66 (1.65-8.14) in LUAD, and 1.98 (0.64-6.14) in LUSC. In particular, participants with lung cancer had a high risk of incident CVD at a high genetic risk level (HR = 3.79, 95% CI: 1.57-9.13). No causal relations between these conditions were observed in Mendelian randomization analysis. CONCLUSIONS: CVD is associated with an increased risk of NSCLC including LUSC and LUAD. NSCLC, particularly LUAD, is associated with a higher CVD risk. Awareness of this bidirectional association may improve prevention and treatment strategies for both diseases. Future clinical demands will require a greater focus on cardiac oncology.

Associations of short-term ambient temperature exposure with lung function in middle-aged and elderly people: A longitudinal study in China.

The short-term associations of ambient temperature exposure with lung function in middle-aged and elderly Chinese remain obscure. The study included 19,128 participants from the Dongfeng-Tongji cohort's first (2013) and second (2018) follow-ups. The lung function for each subject was determined between April and December 2013 and re-assessed in 2018, with three parameters (forced vital capacity [FVC], forced expiratory volume in 1 s [FEV1], and peak expiratory flow [PEF]) selected. The China Meteorological Data Sharing Service Center provided temperature data during the study period. In the two follow-ups, a total of 25,511 records (average age: first, 64.57; second, 65.80) were evaluated, including 10,604 males (41.57%). The inversely J-shaped associations between moving average temperatures (lag01-lag07) and FVC, FEV1, and PEF were observed, and the optimum temperatures at lag04 were 16.5 °C, 18.7 °C, and 16.2 °C, respectively. At lag04, every 1 °C increase in temperature was associated with 14.07 mL, 9.78 mL, and 62.72 mL/s increase in FVC, FEV1, and PEF in the low-temperature zone (