The relationship between body roundness index and depression: A cross-sectional study using data from the National Health and Nutrition Examination Survey (NHANES) 2011-2018.

BACKGROUND: Depression is linked to obesity. The body roundness index (BRI) provides a more accurate assessment of body and visceral fat levels than the body mass index or waist circumference. However, the association between BRI and depression is unclear. Therefore, we investigated this relationship using the National Health and Nutrition Examination Survey (NHANES) database. METHODS: In this population-based cross-sectional study, data from 18,654 adults aged ≥20 years from the NHANES 2011-2018 were analyzed. Covariates, including age, gender, race/ethnicity, education level, marital status, poverty-income ratio, alcohol status, smoking status, hypertension, diabetes mellitus, cardiovascular disease, energy intake, physical activity, total cholesterol, and triglycerides were adjusted in multivariable logistic regression models. In addition, smooth curve fitting, subgroup analysis, and interaction testing were conducted. RESULTS: After adjusting for covariates, BRI was positively correlated with depression. For each one-unit increase in BRI, the prevalence of depression increased by 8 % (odds ratio = 1.08, 95 % confidence interval = 1.05-1.10, P < 0.001). LIMITATIONS: As this was a cross-sectional study, we could not determine a causal relationship between BRI and depression. Patients with depression in this study were not clinically diagnosed with major depressive disorder. CONCLUSION: BRI levels were positively related to an increased prevalence of depression in American adults. BRI may serve as a simple anthropometric index to predict depression.

Association between dietary sugar intake and depression in US adults: a cross-sectional study using data from the National Health and Nutrition Examination Survey 2011-2018.

BACKGROUND: Studies examining whether diet sugar intake increases the risk of depression have produced inconsistent results. Therefore, we investigated this relationship, using the US' National Health and Nutrition Examination Survey (NHANES) database. METHODS: This cross-sectional study included 18,439 adults (aged ≥ 20 years) from NHANES (2011-2018). Depressive symptoms were assessed using the nine-item version of the Patient Health Questionnaire (PHQ-9). Covariates, including age, sex, race/ethnicity, poverty-income ratio, education, marital status, hypertension, diabetes mellitus, cardiovascular disease, alcohol intake, smoking status, physical activity, and dietary energy intake, were adjusted in multivariate logistic regression models. Subgroup and threshold saturation effect analyses were performed. RESULTS: After adjusting for potential confounders, we found that a 100 g/day increase in dietary sugar intake correlated with a 28% higher prevalence of depression (odds ratio = 1.28, 95% confidence interval = 1.17-1.40, P < 0.001). CONCLUSION: Dietary sugar intake is positively associated with depression in US adults.

Upregulation of Wheat Heat Shock Transcription Factor TaHsfC3-4 by ABA Contributes to Drought Tolerance.

Drought stress can seriously affect the yield and quality of wheat (Triticum aestivum). So far, although few wheat heat shock transcription factors (Hsfs) have been found to be involved in the stress response, the biological functions of them, especially the members of the HsfC (heat shock transcription factor C) subclass, remain largely unknown. Here, we identified a class C encoding gene, TaHsfC3-4, based on our previous omics data and analyzed its biological function in transgenic plants. TaHsfC3-4 encodes a protein containing 274 amino acids and shows the basic characteristics of the HsfC class. Gene expression profiles revealed that TaHsfC3-4 was constitutively expressed in many tissues of wheat and was induced during seed maturation. TaHsfC3-4 could be upregulated by PEG and abscisic acid (ABA), suggesting that this Hsf may be involved in the regulation pathway depending on ABA in drought resistance. Further results represented that TaHsfC3-4 was localized in the nucleus but had no transcriptional activation activity. Notably, overexpression of TaHsfC3-4 in Arabidopsis thaliana pyr1pyl1pyl2pyl4 (pyr1pyl124) quadruple mutant plants complemented the ABA-hyposensitive phenotypes of the quadruple mutant including cotyledon greening, root elongation, seedling growth, and increased tolerance to drought, indicating positive roles of TaHsfC3-4 in the ABA signaling pathway and drought tolerance. Furthermore, we identified TaHsfA2-11 as a TaHsfC3-4-interacting protein by yeast two-hybrid (Y2H) screening. The experimental data show that TaHsfC3-4 can indeed interact with TaHsfA2-11 in vitro and in vivo. Moreover, transgenic Arabidopsis TaHsfA2-11 overexpression lines exhibited enhanced drought tolerance, too. In summary, our study confirmed the role of TaHsfC3-4 in response to drought stress and provided a target locus for marker-assisted selection breeding to improve drought tolerance in wheat.

Application of artificial intelligence in ultrasound imaging for predicting lymph node metastasis in breast cancer: A meta-analysis.

BACKGROUND: This study aims to comprehensively evaluate the accuracy and effectiveness of ultrasound imaging based on artificial intelligence algorithms in predicting lymph node metastasis in breast cancer patients through a meta-analysis. METHODS: We systematically searched PubMed, Embase, and Cochrane Library for literature published up to May 2023. The search terms included artificial intelligence, ultrasound, breast cancer, and lymph node. Studies meeting the inclusion criteria were selected, and data were extracted for analysis. The main evaluation indicators included sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and area under the curve (AUC). The heterogeneity was assessed using the Cochrane Q test combined with the I^2 statistic expressing the percentage of total effect variation that can be attributed to the effect variation between studies, as recommended by the Cochrane Handbook for heterogeneity quantification. A threshold p-value of 0.10 was considered to compensate for the low power of the Q test. Sensitivity analysis was performed to assess the stability of individual studies, and publication bias was determined with funnel plots. Additionally, fagan plots were used to assess clinical utility. RESULTS: Ten studies involving 4726 breast cancer patients were included in the meta-analysis. The results showed that ultrasound imaging based on artificial intelligence algorithms had high accuracy and effectiveness in predicting lymph node metastasis in breast cancer patients. The pooled sensitivity was 0.88 (95% CI: 0.81-0.93; P < 0.001; I2 = 84.68), specificity was 0.75 (95% CI: 0.66-0.83; P < 0.001; I2 = 91.11), and AUC was 0.89 (95% CI: 0.86-0.91). The positive likelihood ratio was 3.5 (95% CI: 2.6-4.8), negative likelihood ratio was 0.16 (95% CI: 0.10-0.26), and diagnostic odds ratio was 23 (95% CI: 13-40). However, the combined sensitivity of ultrasound imaging based on non-AI algorithms for predicting lymph node metastasis in breast cancer patients was 0.78 (95%CI: 0.63-0.88), the specificity was 0.76 (95%CI: 0.63-0.86), and the AUC was 0.84 (95%CI: 0.80-0.87). The positive likelihood ratio was 3.3 (95% CI: 1.9-5.6), the negative likelihood ratio was 0.29 (95% CI: 0.15-0.54), and the diagnostic odds ratio was 11 (95% CI: 4-33). Due to limited sample size (n = 2), meta-analysis was not conducted for the outcome of predicting lymph node metastasis burden. CONCLUSION: Ultrasound imaging based on artificial intelligence algorithms holds promise in predicting lymph node metastasis in breast cancer patients, demonstrating high accuracy and effectiveness. The application of this technology helps in the diagnosis and treatment decisions for breast cancer patients and is expected to become an important tool in future clinical practice.

Elevated pulse pressure correlated with reduced retinal peripapillary capillary in thyroid-associated ophthalmology with visual field defect.

Purpose: To quantify the retinal vessel density in thyroid-associated ophthalmology (TAO) patients with visual field (VF) defect and examine its associations with mechanical and system vascular risk factors for underlying pathogenesis of VF defect in TAO. Methods: The cohort was composed of 62 TAO eyes (39 with VF defect and 23 without VF defect). The pulse pressure (PP), intraocular pressure (IOP), ophthalmic rectus muscular index (MI), superficial retinal capillary plexus (SRCP), radial peripapillary capillary (RPC) density, and other related parameters were measured. The associations among these factors and VF mean deviation (MD) were analyzed. Results: In TAO patients with VF defect, reduced RPC density, higher PP, and larger horizontal and vertical MI were found (all P < 0.03) when compared to TAO patients without VF defect. The RPC density was correlated with VF MD value (r = 0.242, P = 0.029), while SRCP density was not (P = 0.419). In univariable general estimating equation (GEE) analysis with RPC density as the outcome, PP and its fluctuation showed a significant association (both P < 0.04). In the final RPC model with multivariable GEE analysis, only PP (ß = -0.082, P = 0.029) showed significance while PP fluctuation (P = 0.080) did not. Conclusions: The elevated PP was correlated with reduced retinal peripapillary perfusion in TAO resulting in VF defect. These data suggested that the system vascular factor may be important in the pathogenesis of reduced retinal perfusion resulting in visual impairment in TAO.

Potential biomarkers of DNA replication stress in cancer.

Oncogene activation is an established driver of tumorigenesis. An apparently inevitable consequence of oncogene activation is the generation of DNA replication stress (RS), a feature common to most cancer cells. RS, in turn, is a causal factor in the development of chromosome instability (CIN), a near universal feature of solid tumors. It is likely that CIN and RS are mutually reinforcing drivers that not only accelerate tumorigenesis, but also permit cancer cells to adapt to diverse and hostile environments. This article reviews the genetic changes present in cancer cells that influence oncogene-induced RS and CIN, with a particular emphasis on regions of the human genome that show enhanced sensitivity to the destabilizing effects of RS, such as common fragile sites. Because RS exists in a wide range of cancer types, we propose that the proteins involved counteracting this stress are potential biomarkers for indicating the degree of RS in cancer specimens. To test this hypothesis, we conducted a pilot study to validate whether some of proteins that are known from in vitro studies to play an essential role in the RS pathway could be suitable as a biomarker. Our results indicated that this is possible. With this review and pilot study, we aim to accelerate the development of a biomarker for analysis of RS in tumor biopsy specimens, which could ultimately help to stratify patients for different forms of therapy such as the RS inhibitors already undergoing clinical trials.

Synthesis, crystal structure and hydrolysis activity of a novel heterobinuclear cobalt(ІІІ) sodium(І) Schiff base complex.

A novel heterobinuclear complex [CoNa(C15H10NO4F)2(CH3OH)]2 with Schiff base (C15H10NO4F: 2-amino-4-fluorobenzoic acid-3-methoxysalicylaldehyde) was synthesized and characterized by IR and 1H NMR spectroscopy, elemental analysis and single crystal X-ray diffraction. X-ray crystallography reveals that the cobalt atom is six-coordinated by two nitrogen atoms from -CN-, two carboxylate oxygen atoms and two hydroxyl oxygen atoms in different ligands, while the sodium atom is seven-coordinated by two methoxy oxygen atoms, two hydroxyl oxygen atoms in different ligands, two oxygen atoms in the same carboxylate and one oxygen atom of solvent methanol. The reaction results of the complex with the p-nitrophenylphosphate (pNPP) and the adenosine monophosphate (AMP) reveal that the complex can hydrolyze phosphoester bonds. Then the DNA-hydrolysis activity is studied experimentally and theoretically, indicating that the complex can effectively hydrolyze the pBR322 supercoiled plasmid DNA. The molecular docking technology predicts the best binding site and binding affinity between the complex and DNA, and then the catalytic mechanism of hydrolysis is supposed. The study results suggest that the Schiff base metal complex, as a potent artificial enzyme, may find its applications in catalytic hydrolysis and biotechnological areas.

Improvement of soybean transformation via Agrobacterium tumefaciens methods involving α-aminooxyacetic acid and sonication treatments enlightened by gene expression profile analysis.

KEY MESSAGE: Antagonists and sonication treatment relieved the structural barriers of Agrobacterium entering into cells; hindered signal perception and transmission; alleviated defense responses and increased cell susceptibility to Agrobacterium infection. Soybean gene expression analysis was performed to elucidate the general response of soybean plant to Agrobacterium at an early stage of infection. Agrobacterium infection stimulated the PAMPs-triggered immunity (BRI1, BAK1, BZR1, FLS2 and EFR) and effector-triggered immunity (RPM1, RPS2, RPS5, RIN4, and PBS1); up-regulated the transcript factors (WRKY25, WRKY29, MEKK1P, MKK4/5P and MYC2) in MAPK pathway; strengthened the biosynthesis of flavonoid and isoflavonoid in the second metabolism; finally led to a fierce defense response of soybean to Agrobacterium infection and thereby lower transformation efficiency. To overcome it, antagonist α-aminooxyacetic acid (AOA) and sonication treatment along with Agrobacterium infection were applied. This novel method dramatically decreased the expression of genes coding for F3'H, HCT, ß-glucosidase and IF7GT, etc., which are important for isoflavone biosynthesis or the interconversion of aglycones and glycon; genes coding for peroxidase, FLS2, PBS1 and transcription factor MYC2, etc., which are important components in plant-pathogen interaction; and genes coding for GPAT and α-L-fucosidase, which are important in polyesters formation in cell membrane and the degradation of fucose-containing glycoproteins and glycolipids on the external surface of cell membrane, respectively. This analysis implied that AOA and sonication treatment not only relieved the structural membrane barriers of Agrobacterium entering into cells, but also hindered the perception of 'invasion' signal on cell membrane and intercellular signal transmission, thus effectively alleviated the defense responses and increased the cell susceptibility to Agrobacterium infection. All these factors benefit the transformation process; other measures should also be further explored to improve soybean transformation.

Interleukin 7 signaling prevents apoptosis by regulating bcl-2 and bax via the p53 pathway in human non-small cell lung cancer cells.

Interleukin 7/Interleukin 7 receptor (IL-7/IL-7R) signaling induces the upregulation of cyclin D1 to promote cell proliferation in lung cancer, but its role in preventing the apoptosis of non-small cell lung cancer (NSCLC) cell lines remains unknown. To study the role of IL-7 in lung cancer cell apoptosis, normal HBE cells as well as A549 and H1299 NSCLC cells were examined using flow cytometry. The results showed that the activation of IL-7R by its specific ligand, exogenous interleukin-7, was associated with a significant decline in apoptotic cells. Western blot and real-time PCR assays indicated that the activation of IL-7/IL-7R significantly upregulated anti-apoptotic bcl-2 and downregulated pro-apoptotic bax and p53 at both protein and mRNA levels. The knockdown of IL-7R through small interfering RNAs significantly attenuated these effects of exogenous IL-7. However, there was no significant anti-apoptotic effect in H1299 (p53-) cells. Furthermore, the inhibition of p53 significantly abolished the effects of IL-7/IL-7R on lung cancer cell apoptosis. These results strongly suggest that IL-7/IL-7R prevents apoptosis by upregulating the expression of bcl-2 and by downregulating the expression of bax, potentially via the p53 pathway in A549 and HBE cells.

Overexpression of JAM-A in non-small cell lung cancer correlates with tumor progression.

The objective of the current study was to determine the clinical significance of junctional adhesion molecule A (JAM-A) in patients with non-small cell lung cancer (NSCLC) and the biological function of JAM-A in NSCLC cell lines. We showed that JAM-A is predominantly expressed in cell membranes and high expression of JAM-A occurred in 37% of lung tumor specimens compared to corresponding normal tissues. High expression of JAM-A was significantly correlated with TNM stage (P = 0.021), lymph node metastasis (P = 0.007), and decreased overall survival (P = 0.02), In addition, we observed that silencing JAM-A by small interfering RNA inhibited tumor cell proliferation and induced cell cycle arrest at the G1/S boundary. Western blotting analysis revealed that knockdown of JAM-A decreased the protein levels of cyclin D1, CDK4, 6, and P-Rb. Thus, JAM-A plays an important role in NSCLC progression.

DEK depletion negatively regulates Rho/ROCK/MLC pathway in non-small cell lung cancer.

The human DEK proto-oncogene is a nuclear protein with suspected roles in human carcinogenesis. DEK appears to function in several nuclear processes, including transcriptional regulation and modulation of chromatin structure. To investigate the clinicopathological significance of DEK in patients with non-small cell lung cancer (NSCLC), we analyzed DEK immunohistochemistry in 112 NSCLC cases. The results showed that DEK was overexpressed mainly in the nuclear compartment of tumor cells. In squamous cell carcinoma, DEK-positive expression occurred in 47.9% (23/48) of cases, and in lung adenocarcinoma, DEK-positive expression occurred in 67.2% (43/64) of cases and correlated with differentiation, p-TNM stage, and nodal status. Moreover, in lung adenocarcinoma, DEK expression was significantly higher compared with DEK expression in squamous cell carcinoma. Kaplan-Meier analysis showed that patients with low DEK expression had higher overall survival compared with patients with high DEK expression. Depleting DEK expression inhibited cellular proliferation and migration. Furthermore, in DEK-depleted NSCLC cells, we found that RhoA expression was markedly reduced; in conjunction, active RhoA-GTP levels and the downstream effector phosphorylated MLC2 were also reduced. Taken together, DEK depletion inhibited cellular migration in lung cancer cell lines possibly through inactivation of the RhoA/ROCK/MLC signal transduction pathway.

CCL21/CCR7 prevents apoptosis via the ERK pathway in human non-small cell lung cancer cells.

Previously, we confirmed that C-C chemokine receptor 7 (CCR7) promotes cell proliferation via the extracellular signal-regulated kinase (ERK) pathway, but its role in apoptosis of non-small cell lung cancer (NSCLC) cell lines remains unknown. A549 and H460 cells of NSCLC were used to examine the effect of CCL21/CCR7 on apoptosis using flow cytometry. The results showed that activation of CCR7 by its specific ligand, exogenous chemokine ligand 21 (CCL21), was associated with a significant decline in the percent of apoptosis. Western blot and real-time PCR assays indicated that activation of CCR7 significantly caused upregulation of anti-apoptotic bcl-2 and downregulation of pro-apoptotic bax and caspase-3, but not p53, at both protein and mRNA levels. CCR7 small interfering RNA significantly attenuated these effects of exogenous CCL21. Besides, PD98059, a selective inhibitor of MEK that disrupts the activation of downstream ERK, significantly abolished these effects of CCL21/CCR7. Coimmunoprecipitation further confirmed that there was an interaction between p-ERK and bcl-2, bax, or caspase-3, particularly in the presence of CCL21. These results strongly suggest that CCL21/CCR7 prevents apoptosis by upregulating the expression of bcl-2 and by downregulating the expression of bax and caspase-3 potentially via the ERK pathway in A549 and H460 cells of NSCLC.

The changes of organelle ultrastructure and Ca2+ homeostasis in maize mesophyll cells during the process of drought-induced leaf senescence

The changes of cell ultra structure as well as Ca2+ homeostasis involved in the drought-induced maize leaf senescence was investigated. Meanwhile, many indicatives of leaf senescence including thiobarbituric acid reactive substance (MDA), electrolyte leakage (EL), and chlorophyll along with soluble proteins were also detected during the process. The Polyethylene glycol6000(PEG6000)-incubated detached leaves showed a slight increase in the MDA content and electrolyte leakage during the first 30 min of our detection, which was corresponded to an unobvious alteration of the cell ultrastructure. Other typical senescence parameters measured in whole leaf exhibited a moderate elevation as well. Thereafter, however, the EL and MDA rose to a large extent, which was correlated with a dramatic damage to the cell ultrastructure with concomitant sharp decrease in the chlorophyll and soluble proteins content. The deposits of calcium antimonite, being an indicator for Ca2+ localization, were observed in the vacuoles as well as intercellular spaces in the leaves grown under normal condition. Nevertheless, after PEG treatment, it was revealed a distinct increment of Ca2+ in the cytoplasm as well as chloroplasts and nuclei. Moreover, with long-lasting treatment of PEG to the detached leaves, the concentration of Ca2+ as described above showed a continuous increment which was consist with the remarked alteration of physiological parameters and severe damage to the ultrastructure of cells, all of which indicated the leaf senescence. Such drought-induced leaf senescence might result from a loss of the cell's capability to extrude Ca2+. All above findings give us a good insight into the important role of Ca2+ homeostasis in the process of leaf senescence accelerated by the drought stress.