Correlations between oxidative balance score and female asthma among U.S. adults.

In order to explore the association of oxidative balance score (OBS) with female asthma among U.S. adults, we applied multiple logistic regression models, restricted cubic spline, and subgroup analysis using a cross-sectional study from the National Health and Nutrition Examination Survey (NHANES). 17,582 female out of the 91,351 participants from 2001 to 2018 in NHANES were enrolled in the analysis and 2,795 female participants had asthma. In three models, the OBS was negatively associated with female asthma incidence with the odds ratios (OR) = 0.99. When comparing the ratio of Q2, Q3, and Q4 of OBS quartiles against the Q1 quartile, the adjusted OR with 95% confidence intervals (95%CI) were 0.88 (0.75-1.03), 0.84 (0.73-0.97), and 0.82 (0.70-0.96) respectively, with p < 0.01 in the all covariates adjusted models. The restricted cubic splines indicated a linear relationship between OBS and female asthma. Subgroup analysis revealed no significant interaction effects except in the smoke group (p < 0.001), and there was a significant difference in the former smoker with OR 0.97 (0.96-0.99). We observed that there is negative relationship between OBS score and female asthma incidence, which suggests OBS probably is a protective factor for female on-set asthma. According to the subgroup analysis, smoking should be recommended to reduce asthma morbidity.

The visceral adiposity index is associated with asthma, especially current asthma: A cross-sectional study of NHANES, 2003 to 2018.

To investigate the association between the visceral adiposity index (VAI) and asthma using data from National Health and Nutrition Examination Survey 2003 to 2018 by a cross-sectional study. We explored the potential relationship between the VAI and asthma incidence via a cross-sectional study of the National Health and Nutrition Examination Survey from 2003 to 2018. Multiple logistic regression analysis, restricted cubic spline analysis and subgroup analysis were performed. Among the 80,312 participants, 1984 had been told by a doctor or other health professional, and 1142 still had asthma. With all confounders controlled, the VAI was positively associated with asthma incidence (odds ratios 1.04, 95% confidence interval: 1.01, 1.08). When comparing the second, third, and fourth VAI quartiles to the lowest quartile, the adjusted odds ratios (95% confidence intervals) for asthma risk were 1.02 (0.86, 1.21), 1.14 (0.96, 1.36), and 1.18 (1, 1.39), respectively (P for trend = .02). Subgroup analysis revealed no significant interaction effect among the subgroups (P > .05). The positive association was stronger in current asthma patients (odds ratios 1.13, 95% confidence interval: 1.03, 1.24). When comparing the second, third, and fourth VAI quartiles to the lowest quartile, the adjusted odds ratios for current asthma risk were 1.15 (0.81, 1.64), 1.29 (0.91, 1.84), and 1.51 (1.01, 2.24), respectively (P for trend .04). The restricted cubic spline regression analysis did not reveal a nonlinear correlation between the VAI and asthma or current asthma. Subgroup analysis revealed a significant interaction effect between age (P for interaction = .03) and diabetes status (P for interaction = .02). Except in the age ≥60 years, Less than high school, normal body mass index subgroup, VAI, and current asthma were positively correlated. A positive relationship between the VAI and asthma incidence was observed. In particular, there was a strong positive correlation between the VAI score and current asthma. According to the subgroup analysis, more attention should be given to individuals aged 40 to 59 years who have diabetes.

FADD regulates adipose inflammation, adipogenesis, and adipocyte survival.

Adipose tissue, aside from adipocytes, comprises various abundant immune cells. The accumulation of low-grade chronic inflammation in adipose tissue serves as a primary cause and hallmark of insulin resistance. In this study, we investigate the physiological roles of FADD in adipose tissue inflammation, adipogenesis, and adipocyte survival. High levels of Fadd mRNA were observed in mitochondrial-rich organs, particularly brown adipose tissue. To explore its metabolic functions, we generated global Fadd knockout mice, resulting in embryonic lethality, while heterozygous knockout (Fadd+/-) mice did not show any significant changes in body weight or composition. However, Fadd+/- mice exhibited reduced respiratory exchange ratio (RER) and serum cholesterol levels, along with heightened global and adipose inflammatory responses. Furthermore, AT masses and expression levels of adipogenic and lipogenic genes were decreased in Fadd+/- mice. In cellular studies, Fadd inhibition disrupted adipogenic differentiation and suppressed the expression of adipogenic and lipogenic genes in cultured adipocytes. Additionally, Fadd overexpression caused adipocyte death in vitro with decreased RIPK1 and RIPK3 expression, while Fadd inhibition downregulated RIPK3 in iWAT in vivo. These findings collectively underscore the indispensable role of FADD in adipose inflammation, adipogenesis, and adipocyte survival.

Zinc finger protein 263 upregulates interleukin 33 and suppresses autophagy to accelerate the malignant progression of non-small cell lung cancer.

PURPOSE: Non-small cell lung cancer (NSCLC) is a complex disease that remains a major public health concern worldwide. One promising avenue for NSCLC treatment is the targeting of transcription factors that regulate key pathways involved in cancer progression. In this study, we investigated the role of the transcription factor ZNF263 in NSCLC and its impact on the regulation of IL33, apoptosis, and autophagy. METHODS: Levels of ZNF263 in tissues and cell lines were identified, after which the effects of its knockdown on cellular malignant behaviors, apoptosis and autophagy were assessed. Based on bioinformatics analysis, ZNF263 was found to bind to IL33 promoter, their mutual relationship was confirmed, as well as the role of IL33 in the regulation of ZNF263. The involvement of ZNF263 in the growth of xenograft tumors was assessed using tumor-bearing nude mouse models. RESULTS: Experimental results revealed that ZNF263 was upregulated in NSCLC tissue samples and cell lines. Its expression level is positively correlated with cellular malignant behaviors. We further demonstrated that ZNF263 upregulated IL33 expression, which, in turn, promoted the proliferation and migration, inhibited apoptosis and autophagy in NSCLC cells. Furthermore, ZNF263 knockdown reduced the growth of xenograft tumors in nude mice. CONCLUSION: This finding suggests that the inhibition of ZNF263 or IL33 may represent a novel therapeutic strategy for NSCLC. Importantly, our results highlight the crucial role of transcription factors in NSCLC and their potential as therapeutic targets.

Diagnostic and Prognostic Value of Deregulated Circulating Long Non-coding RNA TUG1 in Elderly Patients with Severe Pneumonia.

To investigate the expression pattern of long non-coding RNA TUG1 in elderly patients with severe community-acquired pneumonia (sCAP) and evaluate its diagnostic and prognostic value for sCAP. Serum TUG1 levels were detected in 130 sCAP patients and 122 healthy volunteers via qRT-PCR method. The receiver operating characteristic (ROC) curve and k-M plot were drawn for the diagnostic and prognostic value evaluation. A diminished trend of TUG1 was detected in the serum of sCAP cases, and negatively correlated with the concentration of TNF-α, CRP, suPAR and sTREM-1. Among the 130 cases, 30 cases died from sCAP within 30 days after admission. Serum TUG1 had the diagnostic value for 30-day mortality prediction with the AUC of 0.823. In the non-survival group, more cases had old age, high CURB score and PSI score. K-M plot demonstrated that cases with low TUG1 levels showed poor survival than those carrying high TUG1 levels. Serum TUG1 was an independent risk factor for death in elderly patients with sCAP within 30 days after admission. Serum TUG1 was at low expression in sCAP patients, and it had the predictive value for the clinical prognosis of elderly sCAP patients.

The effects of tocotrienol supplementation on lipid profile: A meta-analysis of randomized controlled trials.

BACKGROUND & OBJECTIVE: Tocotrienol supplementation has been emerged as a potent candidate for the treatment of dyslipidemia. In the present study, a systematic review and meta-analysis of randomized controlled trials was performed with the aim of examining the effects of tocotrienol supplementation on the lipid profile. METHODS: Four databases (Scopus, PubMed/Medline, Web of Science and Embase) were used to accomplish the literature search up to November 2019. Clinical trials encompassing the impact of tocotrienol supplementation on lipid profile were extracted regardless of clinical condition, with studies included involving only adults patients. RESULTS: A total of 15 articles with 20 arms were eligible and included in the meta-analysis to estimate the pooled effect size. Overall results showed a significant effect of tocotrienol supplementation on increasing high-density lipoprotein cholesterol (HDL-C) levels (weight mean difference (WMD): 0.146 mmol/L, I2 = 85.9%) and a non-significant influence on total cholesterol (TC) (WMD: 0.010 mmol/L, I2 = 64.5%), low-density lipoprotein cholesterol (LDL-C) (WMD: 0.095 mmol/L, I2 = 87.4%), and triglycerides (TG) (WMD: -0.112 mmol/L, I2 = 67.4%) levels. Increment in HDL-C levels was significant greater for the tocotrienol dosage ≥ 200 mg/d (WMD: 0.202 mmol/L) and ≤8 weeks (WMD: 0.278 mmol/L). Moreover, studies that investigated tocotrienol dose ≥200 mg had no heterogeneity, while showing a significant decrease in TG levels (WMD: -0.177 mmol/L). CONCLUSION: The present meta-analysis demonstrated that supplementing with tocotrienols does not decrease the concentrations of LDL-C, TC and TG. However, tocotrienol supplementation was considered a candidate for increasing HDL-C levels.

Lymphocyte-derived catecholamines induce a shift of Th1/Th2 balance toward Th2 polarization.

AIMS: Our previous work has shown that lymphocytes synthesize and secrete catecholamines (CAs), which regulate lymphocyte proliferation and apoptosis. In the present study, we explored the effect of the lymphocyte-derived CAs on differentiation and function of T helper (Th) cells. METHODS: Lymphocytes were separated from the mesenteric lymph nodes of mice and stimulated by concanavalin A (Con A). These cells were treated with alpha-methyl-p- tyrosine (α-MT), an inhibitor of tyrosine hydroxylase (TH) that is a rate-limiting enzyme for synthesis of CAs, and pargyline, an inhibitor of monoamine oxidase that degrades CAs. RESULTS: Treatment of Con A-stimulated lymphocytes with α-MT (10(-6) M) reduced CAs both in the cultured lymphocytes and in the culture supernatants. Simultaneously, α-MT upregulated expression of mRNAs and proteins of T-box expressed in T cells (T-bet) and interferon-γ (IFN-γ) but downregulated expression of mRNAs and proteins of GATA binding protein 3 (GATA-3) and interleukin-4 (IL-4) in Con A-activated lymphocytes. In contrast, pargyline (10(-6) M) increased intracellular and supernatant CA contents in Con A-activated lymphocytes. Meanwhile, the treatment with pargyline downregulated expression of T-bet and IFN-γ but upregulated expression of GATA-3 and IL-4 in these lymphocytes. CONCLUSION: CAs synthesized and secreted by lymphocytes regulate differentiation and function of Th cells, with an effect facilitating the shift of Th1/Th2 balance toward Th2 polarization.