Associations of Combined Exposure to Metabolic and Inflammatory Indicators with Thyroid Nodules in Adults: A Nested Case-Control Study.

Objective: To explore associations of combined exposure to metabolic/inflammatory indicators with thyroid nodules. Methods: We reviewed personal data for health screenings from 2020 to 2021. A propensity score matching method was used to match 931 adults recently diagnosed with thyroid nodules in a 1 : 4 ratio based on age and gender. Conditional logistic regression and Bayesian kernel machine regression (BKMR) were used to explore the associations of single metabolic/inflammatory indicators and the mixture with thyroid nodules, respectively. Results: In the adjusted models, five indicators (ORQ4 vs. Q1: 1.30, 95% CI: 1.07-1.58 for fasting blood glucose; ORQ4 vs. Q1: 1.30, 95% CI: 1.08-1.57 for systolic blood pressure; ORQ4 vs. Q1: 1.26, 95% CI: 1.04-1.53 for diastolic blood pressure; ORQ4 vs. Q1: 1.23, 95% CI: 1.02-1.48 for white blood cell; ORQ4 vs. Q1: 1.28, 95% CI: 1.07-1.55 for neutrophil) were positively associated with the risk of thyroid nodules, while high-density lipoproteins (ORQ3 vs. Q1: 0.75, 95% CI: 0.61-0.91) were negatively associated with the risk of thyroid nodules. Univariate exposure-response functions from BKMR models showed similar results. Moreover, the metabolic and inflammatory mixture exhibited a significant positive association with thyroid nodules in a dose-response pattern, with systolic blood pressure being the greatest contributor within the mixture (conditional posterior inclusion probability of 0.82). No interaction effects were found among the five indicators. These associations were more prominent in males, participants with higher age (≥40 years old), and individuals with abnormal body mass index status. Conclusions: Levels of the metabolic and inflammatory mixture have a linear dose-response relationship with the risk of developing thyroid nodules, with systolic blood pressure levels being the most important contributor.

Short-term effects of heatwaves on clinical and subclinical cardiovascular indicators in Chinese adults: A distributed lag analysis.

AIMS: Previous studies have related heat waves to morbidity and mortality of cardiovascular diseases; however, potential mechanisms remained limited. Our aims were to investigate the short-term effects of heat waves on a series of clinical/subclinical indicators associated with cardiovascular health. METHODS: Our study used 80,574 health examination records from the Health Management Center of Nanjing Zhongda Hospital during the warm seasons of 2019-2021, including 62,128 participants. A total of 11 recognized indicators of cardiovascular risk or injury were assessed. Air pollution and meteorological data were obtained from the Nanjing Ecological Environment Bureau and the China Meteorological Data Network, respectively. Heat waves were defined as a daily average temperature over the 95th percentile for three or more consecutive days from May to September. We used a combination of linear mixed effects models and distributed lag nonlinear models to assess the lagged effects of heat waves on clinical and subclinical cardiovascular indicators. Stratified analyses based on individuals' characteristics, including gender, age, body mass index (BMI), diabetes, and hypertension, were also performed. RESULTS: Heat waves were related to significant changes in most indicators, with the magnitude of effects generally peaking at a lag of 0 to 3 days. Moreover, the cumulative percentage changes over lag 0-7 days were -0.82 % to -2.55 % in blood pressure, 1.32 % in heart rate, 0.20 % to 2.66 % in systemic inflammation markers, 0.36 % in a blood viscosity parameter, 9.36 % in homocysteine, and 1.35 % to 3.25 % in injuring myocardial enzymes. Interestingly, females and males showed distinct susceptibilities in different indicators. Stronger effects were also found in participants aged 50 years or over, individuals with abnormal BMI status, and patients with diabetes. CONCLUSION: Short-term exposure to heat waves could significantly alter clinical/subclinical cardiovascular indicator profiles, including blood pressure changes, increased heart rate, acute systemic inflammation, elevated blood viscosity, and myocardial injury.

Association between ambient air pollutants and lipid profile: A systematic review and meta-analysis.

BACKGROUND: Studies of the effects of atmospheric pollutants on lipid profiles remain inconsistent and controversial. AIM: The study was aimed to investigate the relationship between the exposure to ambient air pollutants and variations in the blood lipid profiles in the population. METHODS: A comprehensive search of three different databases (PubMed, Web of Science, and the Cochrane Library) until December 17, 2022, yielded 17 origional studies fulfilling the inclusion criteria for a meta-analysis. Aggregate effect measures and 95% confidence intervals (95% CI) for the relevant ambient air pollutants were deduced employing random effects models. RESULTS: The collective meta-analysis indicated that long-term exposure to PM1, PM2.5, PM10 and CO showed a substantial correlation with TC (PM1: ß = 2.04, 95%CI = 0.15-3.94; PM2.5: ß = 1.11, 95%CI = 0.39-1.84; PM10: ß = 1.70, 95%CI = 0.67-2.73; CO: ß = 0.08, 95%CI = 0.06-0.10), PM10 exhibited a significant association with TG (ß = 0. 537,95% CI = 0.09-0.97), whereas HDL-C demonstrated notable relationships with PM1, PM10, SO2 and CO (PM1: ß = -2.38, 95%CI = -4.00 to -2.76; PM10: ß = -0.77, 95%CI = -1.33 to -0.21; SO2: ß = -0.91, 95%CI = -1.73 to -0.10; CO: ß = -0.03, 95%CI = -0.05 to 0.00). PM2.5, PM10 also showed significant associations with LDL-C (PM2.5: ß = 1.44 95%CI = 0.48-2.40; PM10: ß = 1.62 95%CI = 0.90-2.34). Subgroup analysis revealed significant or stronger correlations predominantly in cohort study designs, with higher male comparisons, and in regions exhibiting elevated contaminant levels. CONCLUSION: In summary, the analysis substantiates that ambient air pollutants can be recognized as potent contributors to alterations in lipid profiles, particularly particulate pollutants which exert more obvious effects on lipid profiles.

Short-term effects of cold spells on hematocrit among adults in Nanjing, China: A distributed-lagged effect analysis.

BACKGROUND: Previous studies have linked exposure to cold spells with cardiovascular diseases, however, underlying mechanisms remained to be understood. We aimed to explore the short-term effects of cold spells on hematocrit, a blood indicator associated with cardiovascular disease. METHODS: Our study was performed among 50,538 participants (68,361 health examination records) who visited the health examination centers of Zhongda Hospital in Nanjing City, China, during the cold seasons from 2019 to 2021. Data on meteorology and air pollution were obtained from the China Meteorological Data Network and the Nanjing Ecological Environment Bureau, respectively. Cold spells in this study were defined as daily mean temperatures (Tmean) <3rd or 5th percentile with two or more consecutive days. Linear mixed-effect models combined with distributed lag nonlinear models were applied to estimate associations of cold spells with hematocrit. RESULTS: Cold spells were found to be significantly correlated with increased hematocrit on lag 0 to 26 days. Moreover, the cumulative effects of cold spells on hematocrit remained significant at varying lag days. These single and cumulative effects were robust across different definitions of cold spells and conversions of hematocrit. For instance, cold spells (Tmean <3rd percentile) at lags 0, 0-1, and 0-27 days were significantly associated with 0.09 [95 % confidence interval (CI): 0.03, 0.15], 0.17 (95 % CI: 0.07, 0.28), and 3.71 (95 % CI: 3.06, 4.35) - unit (%) increases in original hematocrit, respectively. In subgroup analyses, stronger effects of cold spells on hematocrit were observed in females and participants aged 50 years or over. CONCLUSION: Cold spells have significant immediate and longer-lagged effects (up to 26 days) on hematocrit. Females and individuals aged 50 years or over are more sensitive to cold spells. These findings might provide a new perspective for exploring the effects of cold spells on adverse cardiac events.

Acute effects of electronic cigarettes on vascular endothelial function: a systematic review and meta-analysis of randomized controlled trials.

AIM: The effects of e-cigarettes on endothelial function remained controversial. The study aimed to investigate the effects of e-cigarettes on vascular endothelial function. METHODS AND RESULTS: PubMed, Web of Science, Embase, and Cochrane Library were searched up to December 2021. We only included the studies in which the control group included vaping without nicotine and tobacco. Pairwise and network meta-analyses were conducted for flow-mediated dilation (FMD), pulse wave velocity (PWV), and heart rate corrected augmentation index (AIx75). Eight studies involving 372 participants were eligible for this review. Compared with vaping without nicotine, e-cigarettes significantly increase in PWV (mean difference = 3.09; 95% confidential interval: 1.51-4.68, P < 0.001) and AIx75 (mean difference = 2.11; 95% confidential interval: 1.02-3.21, P < 0.001) indicators, but not affect FMD (mean difference = 0.78; 95% confidential interval: -0.08 to 1.64, P = 0.075). But compared with traditional tobacco, e-cigarettes did not affect FMD (mean difference = 0.28, 95% confidential interval: -0.45 to 0.59, P = 0.084). According to surface under the cumulative ranking curve (SUCRA), the e-cigarette ranked first for FMD (SUCRA = 97%), tobacco ranked first for PWV (SUCRA = 75%), and AIx75 (SUCRA = 99%). CONCLUSION: In summary, evidence from our pooled analyses indicated that acute inhalation of e-cigarettes leads to negative changes in vascular endothelial function. E-cigarettes cannot be used as an alternative to public health strategies for tobacco control and should not be considered cardiovascular safety products. More future research should be conducted to verify our findings.

Protein kinase C activation induces platelet apoptosis / 中国实验血液学杂志

Platelet apoptosis elucidated by either physical or chemical compound or platelet storage occurs wildly, which might play important roles in controlling the numbers and functions of circulated platelets, or in the development of some platelet-related diseases. However, up to now, a little is known about the regulatory mechanisms of platelet apoptosis. Protein kinase C (PKC) is highly expressed in platelets and plays central roles in regulating platelet functions. Although there is evidence indicating that PKC is involved in the regulation of apoptosis of nucleated cells, it is still unclear whether PKC plays a role in platelet apoptosis. The aim of this study was to investigate the role of PKC in platelet apoptosis. The effects of PKC on mitochondrial membrane potential (ΔΨm), phosphatidylserine (PS) exposure, and caspase-3 activation of platelets were analyzed by flow cytometry and Western blot. The results showed that the ΔΨm depolarization in platelets was induced by PKC activator in time-dependent manner, and the caspase-3 activation in platelets was induced by PKC in concentration-dependent manner. However, the platelets incubated with PKC inhibitor did not results in ΔΨm depolarization and PS exposure. It is concluded that the PKC activation induces platelet apoptosis through influencing the mitochondrial functions and activating caspase 3. The finds suggest a novel mechanism for PKC in regulating platelet numbers and functions, which has important pathophysiological implications for thrombosis and hemostasis.