Medical School Characteristics Associated with Matched Otolaryngology Residency Applicants.

OBJECTIVE: Identify which medical schools produce the most otolaryngology residents, and associated characteristics which may contribute to this productivity. DESIGN: The medical school and residency program of each otolaryngology-matched student was identified. Various characteristics for each medical school and residency were compared in univariate and multivariate analysis after adjusting for class size. Percentage of matched students relative to class size was identified and compared for each geographic region. SETTING: Cross-sectional study of publicly available match data from otomatch.com and otolaryngology residency program websites from 2020-2023. PARTICIPANTS: 1411 students from 174 medical schools matched into 126 otolaryngology residencies were identified. RESULTS: Private medical schools (ß = 0.50, p = 0.03), larger otolaryngology departments (ß = 0.01, p = 0.04), and higher U.S. News and World Report (USNWR) ranking (ß = -0.01, p = 0.02) was associated with a greater percentage of otolaryngology-matched students while schools in the Mountain region were associated with a lower percentage of matched students (ß = -1.08, p = 0.02). A difference in percentage of matched students was observed when comparing across all regions (p < 0.01) but no significant differences were observed between any individual regions. The East North Central Region and the Middle Atlantic regions were more likely to match students from their respective regions compared to the Mountain region (OR: 4.98, 95% CI: 1.18, 21.01; OR: 8.20, 95% CI: 1.92, 34.99, respectively). Additionally, the Mountain region was less likely to match students from their own region compared to the Pacific (OR: 0.21, 95% CI: 0.05, 0.90), South Atlantic (OR: 0.20, 95% CI: 0.05, 0.85), and West South Central (OR: 0.15, 95% CI: 0.03, 0.67) regions. CONCLUSIONS: Medical school characteristics such as private vs public status, size of otolaryngology department, higher USNWR ranking, and geographic region impact the number of otolaryngology-matched students. Applicants should consider the impact of their geographic region when allocating signals during the residency application process.

Identification of immune- and oxidative stress-related signature genes as potential targets for mRNA vaccines for pancreatic cancer patients.

Adenocarcinoma of the pancreas (PAAD) is one of the deadliest malignant tumors, and messenger ribonucleic acid vaccines, which constitute the latest generation of vaccine technology, are expected to lead to new ideas for the treatment of pancreatic cancer. The Cancer Genome Atlas-PAAD and Genotype-Tissue Expression data were merged and analyzed. Weighted gene coexpression network analysis was used to identify gene modules associated with tumor mutational burden among the genes related to both immunity and oxidative stress. Differentially expressed immune-related oxidative stress genes were screened via univariate Cox regression analysis, and these genes were analyzed via nonnegative matrix factorization. After immune infiltration analysis, least absolute shrinkage and selection operator regression combined with Cox regression was used to construct the model, and the usefulness of the model was predicted based on the receiver operating characteristic curve and decision curve analysis curves after model construction. Finally, metabolic pathway enrichment was analyzed using gene set enrichment analysis combined with Kyoto Encyclopedia of Genes and Genomes and gene ontology biological process analyses. This model consisting of the ERAP2, mesenchymal-epithelial transition factor (MET), CXCL9, and angiotensinogen (AGT) genes can be used to help predict the prognosis of pancreatic cancer patients more accurately than existing models. ERAP2 is involved in immune activation and is important in cancer immune evasion. MET binds to hepatocyte growth factor, leading to the dimerization and phosphorylation of c-MET. This activates various signaling pathways, including MAPK and PI3K, to regulate the proliferation, invasion, and migration of cancer cells. CXCL9 overexpression is associated with a poor patient prognosis and reduces the number of CD8 + cytotoxic T lymphocytes in the PAAD tumor microenvironment. AGT is cleaved by the renin enzyme to produce angiotensin 1, and AGT-converting enzyme cleaves angiotensin 1 to produce angiotensin 2. Exposure to AGT-converting enzyme inhibitors after pancreatic cancer diagnosis is associated with improved survival. The 4 genes identified in the present study - ERAP2, MET, CXCL9, and AGT - are expected to serve as targets for messenger ribonucleic acid vaccine development and need to be further investigated in depth.

Attention spotlight in V1-based cortico-cortical interactions in human visual hierarchy.

Attention is often viewed as a mental spotlight, which can be scaled like a zoom lens at specific spatial locations and features a center-surround gradient. Here, we demonstrate a neural signature of attention spotlight in signal transmission along the visual hierarchy. fMRI background connectivity analysis was performed between retinotopic V1 and downstream areas to characterize the spatial distribution of inter-areal interaction under two attentional states. We found that, compared to diffused attention, focal attention sharpened the spatial gradient in the strength of the background connectivity. Dynamic causal modeling analysis further revealed the effect of attention in both the feedback and feedforward connectivity between V1 and extrastriate cortex. In a context which induced a strong effect of crowding, the effect of attention in the background connectivity profile diminished. Our findings reveal a context-dependent attention prioritization in information transmission via modulating the recurrent processing across the early stages in human visual cortex.

The impact of neck circumference on hypoglossal nerve stimulator therapy outcomes.

STUDY OBJECTIVES: Hypoglossal nerve stimulation (HGNS) therapy has historically had strict eligibility requirements including a body mass index (BMI) < 32 kg/m2. However, recent Food and Drug Administration approval expanded indications to a BMI < 40 kg/m2. There is a wide variability in body fat distribution. This study sought to determine if neck circumference is a better surrogate predictive variable for HGNS outcomes than BMI. METHODS: A retrospective chart review was conducted at a tertiary care center on adults who underwent HGNS implantation by a single surgeon from March 2017 to October 2021. Baseline demographic data including neck circumference, diagnostic sleep studies and post-implantation HGNS titration studies were collected. Linear regression and Spearman's Correlation Coefficient (SCC) analysis were utilized to compare neck circumference (NC), percentage of predicted neck circumference (PPNC) and BMI with the apnea-hypopnea index at effective voltage (AHI-v). RESULTS: This study included 43 patients who were middle aged (61.1 years), predominantly male (76.7%), with severe obstructive sleep apnea (median AHI 35) and mean neck circumference of 15.3 inches. Utilizing the NC and PPNC, positive correlations with AHI-v were observed (p = 0.0033, SCC = .438, and p = 0.0029, SCC = .444). While controlling for BMI, a 1-inch increase in neck circumference was associated with a 35% increase in AHI-v (p = 0.0411). CONCLUSIONS: A larger neck circumference was independently associated with worse HGNS outcomes. Further research is needed to support and confirm these findings, particularly across sexes.

Inhibiting mitochondrial citrate shuttling induces hepatic triglyceride deposition in Nile tilapia (Oreochromis niloticus) through lipid anabolic remodeling.

The solute carrier family 25 member 1 (Slc25a1)-dependent mitochondrial citrate shuttle is responsible for exporting citrate from the mitochondria to the cytoplasm for supporting lipid biosynthesis and protein acetylation. Previous studies on Slc25a1 concentrated on pathological models. However, the importance of Slc25a1 in maintaining metabolic homeostasis under normal nutritional conditions remains poorly understood. Here, we investigated the mechanism of mitochondrial citrate shuttle in maintaining lipid metabolism homeostasis in male Nile tilapia (Oreochromis niloticus). To achieve the objective, we blocked the mitochondrial citrate shuttle by inhibiting Slc25a1 under normal nutritional conditions. Slc25a1 inhibition was established by feeding Nile tilapia with 250 mg/kg 1,2,3-benzenetricarboxylic acid hydrate for 6 weeks or intraperitoneal injecting them with dsRNA to knockdown slc25a1b for 7 days. The Nile tilapia with Slc25a1 inhibition exhibited an obesity-like phenotype accompanied by fat deposition, liver damage and hyperglycemia. Moreover, Slc25a1 inhibition decreased hepatic citrate-derived acetyl-CoA, but increased hepatic triglyceride levels. Furthermore, Slc25a1 inhibition replenished cytoplasmic acetyl-CoA through enhanced acetate pathway, which led to hepatic triglycerides accumulation. However, acetate-derived acetyl-CoA caused by hepatic Slc25a1 inhibition did not activate de novo lipogenesis, but rather modified protein acetylation. In addition, hepatic Slc25a1 inhibition enhanced fatty acids esterification through acetate-derived acetyl-CoA, which increased Lipin1 acetylation and its protein stability. Collectively, our results illustrate that inhibiting mitochondrial citrate shuttle triggers lipid anabolic remodeling and results in lipid accumulation, indicating the importance of mitochondrial citrate shuttle in maintaining lipid metabolism homeostasis.

Association between plasma proteome and pulmonary heart disease: A two-stage Mendelian randomization analysis.

Pulmonary heart disease (PHD) involves altered structure and function of the right ventricle caused by an abnormal respiratory system that causes pulmonary hypertension. However, the association between changes in plasma proteomics and PHD remains unclear. Hence, we aimed to identify causal associations between genetically predicted plasma protein levels and PHD. Mendelian randomization was performed to test the target proteins associated with PHD. Summary statistics for the human plasma proteome and pulmonary heart disease were acquired from the UK Biobank (6038 cases and 426 977 controls) and the FinnGen study (6753 cases and 302 401 controls). Publicly available pQTLs datasets for human plasma proteins were obtained from a largescale genome-wide association study in the INTERVAL study. The results were validated using a case-control cohort. We first enrolled 3622 plasma proteins with conditionally independent genetic variants; three proteins (histo-blood group ABO system transferase, activating signal cointegration 1 complex subunit 1, and calcium/calmodulin-dependent protein kinase I [CAMK1]) were significantly associated with the risk of pulmonary heart disease in the UK Biobank cohort. Only CAMK1 was successfully replicated (odds ratio: 1.1056, 95% confidence interval: 1.019-1.095, p = 0.0029) in the FinnGen population. In addition, the level of CAMK1 in 40 patients with PHD was significantly higher (p = 0.023) than that in the control group. This work proposes that CAMK1 is associated with PHD, underscoring the importance of the calcium signaling pathway in the pathophysiology to improve therapies for PHD.

SiPM joint likelihood reception for mobile LED-optical communication under pointing errors.

Light-emitting diode (LED)-optical communication is a novel spectrum communication with wide field of view (FOV), light weight, and long-distance free-space capabilities. Due to atmospheric turbulence attenuation and pointing errors caused by long-distance communication, this Letter proposes a multi-pixel channel joint maximum likelihood (JML) reception method using a highly sensitive silicon photomultiplier (SiPM). To evaluate the performance of the SiPM under mobile terminal jittering communication, we analyze the effect of optical transmitting power, pointing errors, and signal-to-noise ratio (SNR) gain on optical communication by comparing JML with signal channel using the maximum likelihood (ML) algorithm. Both simulation analysis and experimental results demonstrate that the proposed JML algorithm to process signals received from SiPM multi-pixel channels can effectively mitigate the impact of pointing errors on the bit error rate (BER) of optical communications by two orders of magnitude at large jitter radians and SNR.

Syringic acid attenuates acute lung injury by modulating macrophage polarization in LPS-induced mice.

BACKGROUND: Acute lung injury (ALI) is a continuum of lung changes caused by multiple lung injuries, characterized by a syndrome of uncontrolled systemic inflammation that often leads to significant morbidity and death. Anti-inflammatory is one of its treatment methods, but there is no safe and available drug therapy. Syringic acid (SA) is a natural organic compound commonly found in a variety of plants, especially in certain woody plants and fruits. In modern pharmacological studies, SA has anti-inflammatory effects and therefore may be a potentially safe and available compound for the treatment of acute lung injury. PURPOSE: This study attempts to reveal the protective mechanism of SA against ALI by affecting the polarization of macrophages and the activation of NF-κB signaling pathway. Trying to find a safer and more effective drug therapy for clinical use. METHODS: We constructed the ALI model using C57BL/6 mice by intratracheal instillation of LPS (10 mg/kg). Histological analysis was performed with hematoxylin and eosin (H&E). The wet-dry ratio of the whole lung was measured to evaluate pulmonary edema. The effect of SA on macrophage M1-type was detected by flow cytometry. BCA protein quantification method was used to determine the total protein concentration in bronchoalveolar lavage fluid (BALF). The levels of Interleukin (IL)-6, IL-1ß, and tumor necrosis factor (TNF)-α in BALF were determined by the ELISA kits, and RT-qPCR was used to detect the expression levels of IL-6, IL-1ß and TNF-α mRNA of lung tissue. Western blot was used to detect the expression levels of iNOS and COX-2 and the phosphorylation of p65 and IκBα in the NF-κB pathway in lung tissue. In vitro experiments were conducted with RAW267.4 cell inflammation model induced by 100 ng/ml LPS and A549 cell inflammation model induced by 10 µg/ml LPS. The effects of SA on M1-type and M2-type macrophages of RAW267.4 macrophages induced by LPS were detected by flow cytometry. The toxicity of compound SA to A549 cells was detected by MTT method which to determine the safe dose of SA. The expressions of COX-2 and the phosphorylation of p65 and IκBα protein in NF-κB pathway were detected by Western blot. RESULTS: We found that the pre-treatment of SA significantly reduced the degree of lung injury, and the infiltration of neutrophils in the lung interstitium and alveolar space of the lung. The formation of transparent membrane in lung tissue and thickening of alveolar septum were significantly reduced compared with the model group, and the wet-dry ratio of the lung was also reduced. ELISA and RT-qPCR results showed that SA could significantly inhibit the production of IL-6, IL-1ß, TNF-α. At the same time, SA could significantly inhibit the expression of iNOS and COX-2 proteins, and could inhibit the phosphorylation of p65 and IκBα proteins. in a dose-dependent manner. In vitro experiments, we found that flow cytometry showed that SA could significantly inhibit the polarization of macrophages from M0 type macrophages to M1-type macrophages, while SA could promote the polarization of M1-type macrophages to M2-type macrophages. The results of MTT assay showed that SA had no obvious cytotoxicity to A549 cells when the concentration was not higher than 80 µM, while LPS could promote the proliferation of A549 cells. In the study of anti-inflammatory effect, SA can significantly inhibit the expression of COX-2 and the phosphorylation of p65 and IκBα proteins in LPS-induced A549 cells. CONCLUSION: SA has possessed a crucial anti-ALI role in LPS-induced mice. The mechanism was elucidated, suggesting that the inhibition of macrophage polarization to M1-type and the promotion of macrophage polarization to M2-type, as well as the inhibition of NF-κB pathway by SA may be the reasons for its anti-ALI. This finding provides important molecular evidence for the further application of SA in the clinical treatment of ALI.

Rational design of PspAlgL to improve its thermostability and anti-biofilm activity against Pseudomonas aeruginosa.

Pseudomonas aeruginosa biofilm enhances tolerance to antimicrobials and immune system defenses. Alginate is an important component of biofilm and a virulence factor of P. aeruginosa. The degradation of alginate by alginate lyases has come to serve as an adjunctive therapeutic strategy against P. aeruginosa biofilm, but poor stability of the enzyme limited this application. Thus, PspAlgL, an alginate lyase, can degrade acetylated alginate but has poor thermostability. The 3D structure of PspAlgL was predicted, and the thermostability of PspAlgL was rationally designed by GRAPE strategy, resulting in two variants with better stability. These variants, PspAlgLS270F/E311P and PspAlgLG291S/E311P, effectively degraded the alginate in biofilm. In addition, compared with PspAlgL, these variants were more efficient in inhibiting biofilm formation and degrading the established biofilm of P. aeruginosa PAO1, and they were also able to destroy the biofilm attached to catheters and to increase the sensitivity of P. aeruginosa to the antibiotic amikacin. This study provides one potential anti-biofilm agent for P. aeruginosa infection.

Mobile recognition and positioning for multiple visible light communication cells using a convolutional neural network: publisher's note.

This publisher's note contains a correction to Opt. Lett.48, 6468 (2024)10.1364/OL.503007.

Extracellular vesicle encapsulated Homer1a as novel nanotherapeutics against intracerebral hemorrhage in a mouse model.

Homer1a and A2 astrocytes are involved in the regulation of inflammation induced by intracerebral hemorrhage (ICH). However, there is no anticipated treatment strategy based on the anti-inflammatory effect of Homer1a and A2 astrocytes. Here, we successfully induced A2 astrocytes in vitro, and then we report an efficient method to prepare Homer1a+ EVs derived from A2 astrocytes which making it more stable, safe, and targetable to injured neurons. Homer1a+ EVs promotes the conversion of A1 to A2 astrocytes in ICH mice. Homer1a+ EVs inhibits activation and nuclear translocation of NF-κB, thereby regulating transcription of IL-17A in neurons. Homer1a+ EVs inhibits the RAGE/NF-κB/IL-17 signaling pathway and the binding ability of IL-17A: IL17-AR and RAGE: DIAPH1. In addition, Homer1a+ EVs ameliorates the pathology, behavior, and survival rate in GFAPCreHomer1fl/-Homer1a± and NestinCreRAGEfl/fl ICH mice. Our study provides a novel insight and potential for the clinical translation of Homer1a+ EVs in the treatment of ICH.

Reduced coupling between global signal and cerebrospinal fluid inflow in patients with depressive disorder: A resting state functional MRI study.

BACKGROUND: Depressed patients often suffer from sleep disturbance, which has been recognized to be responsible for glymphatic dysfunction. The purpose of this study was to investigate the coupling strength of global blood­oxygen-level-dependent (gBOLD) signals and cerebrospinal fluid (CSF) inflow dynamics, which is a biomarker for glymphatic function, in depressed patients and to explore its potential relationship with sleep disturbance by using resting-state functional MRI. METHODS: A total of 138 depressed patients (112 females, age: 34.70 ± 13.11 years) and 84 healthy controls (29 females, age: 36.6 ± 11.75 years) participated in this study. The gBOLD-CSF coupling strength was calculated to evaluate glymphatic function. Sleep disturbance was evaluated using the insomnia items (item 4 for insomnia-early, item 5 for insomnia-middle, and item 6 for insomnia-late) of The 17-item Hamilton Depression Rating Scale for depressed patients, which was correlated with the gBOLD-CSF coupling strength. RESULTS: The depressed patients exhibited weaker gBOLD-CSF coupling relative to healthy controls (p = 0.022), possibly due to impairment of the glymphatic system. Moreover, the gBOLD-CSF coupling strength correlated with insomnia-middle (r = 0.097, p = 0.008) in depressed patients. Limitations This study is a cross-sectional study. CONCLUSION: Our findings shed light on the pathophysiology of depression, indicating that cerebral waste clearance system deficits are correlated with poor sleep quality in depressed patients.

Pparα activation stimulates autophagic flux through lipid catabolism-independent route.

Autophagy is a cellular process that involves the fusion of autophagosomes and lysosomes to degrade damaged proteins or organelles. Triglycerides are hydrolyzed by autophagy, releasing fatty acids for energy through mitochondrial fatty acid oxidation (FAO). Inhibited mitochondrial FAO induces autophagy, establishing a crosstalk between lipid catabolism and autophagy. Peroxisome proliferator-activated receptor α (PPARα), a transcription factor, stimulates lipid catabolism genes, including fatty acid transport and mitochondrial FAO, while also inducing autophagy through transcriptional regulation of transcription factor EB (TFEB). Therefore, the study explores whether PPARα regulates autophagy through TFEB transcriptional control or mitochondrial FAO. In aquaculture, addressing liver lipid accumulation in fish is crucial. Investigating the link between lipid catabolism and autophagy is significant for devising lipid-lowering strategies and maintaining fish health. The present study investigated the impact of dietary fenofibrate and L-carnitine on autophagy by activating Pparα and enhancing FAO in Nile tilapia (Oreochromis niloticus), respectively. The dietary fenofibrate and L-carnitine reduced liver lipid content and enhanced ATP production, particularly fenofibrate. FAO enhancement by L-carnitine showed no changes in autophagic protein levels and autophagic flux. Moreover, fenofibrate-activated Pparα promoted the expression and nuclear translocation of Tfeb, upregulating autophagic initiation and lysosomal biogenesis genes. Pparα activation exhibited an increasing trend of LC3II protein at the basal autophagy and cumulative p62 protein trends after autophagy inhibition in zebrafish liver cells. These data show that Pparα activation-induced autophagic flux should be independent of lipid catabolism.

Activated carbon fiber as an efficient co-catalyst toward accelerating Fe2+/Fe3+ cycling for improved removal of antibiotic cefaclor via electro-Fenton process using a gas diffusion electrode.

The electro-Fenton (EF) based on gas-diffusion electrodes (GDEs) reveals promising application prospective towards recalcitrant organics degradation because such GDEs often yields superior H2O2 generation efficiency and selectivity. However, the low efficiency of Fe2+/Fe3+ cycle with GDEs is always considered to be the limiting step for the EF process. In this study, activated carbon fiber (ACF) was firstly employed as co-catalyst to facilitate the performance of antibiotic cefaclor (CEC) decomposition in EF process. It was found that the addition of ACF co-catalyst achieved a rapid Fe2+/Fe3+ cycling, which significantly enhanced Fenton's reaction and hydroxyl radicals (•OH) generation. X-ray photoelectron spectroscopy (XPS) results indicated that the functional groups on ACF surface are related to the conversion of Fe3+ into Fe2+. Moreover, DMSO probing experiment confirmed the enhanced •OH production in EF + ACF system compared to conventional EF system. When inactive BDD and Ti4O7/Ti anodes were paired to EF system, the addition of ACF could significantly improve mineralization degree. However, a large amount of toxic byproducts, including chlorate (ClO3-) and perchlorate (ClO4-), were generated in these EF processes, especially for BDD anode, due to their robust oxidation capacity. Higher mineralization efficiency and less toxic ClO4- generation were obtained in the EF + ACF process with Ti4O7/Ti anode. This presents a novel alternative for efficient chloride-containing organic removal during wastewater remediation.

Insights into the efficient mineralization of antibiotic trimethoprim in aqueous media by Fe2+ catalytically enhanced vacuum-UV irradiation: Kinetics, mechanisms, and toxicity evaluation.

The widespread existence of antibiotics in the environment has attracted growing concerns regarding the potential adverse effects on aquatic organisms, ecosystems, and human health even at low concentrations. Extensive efforts have been devoted to developing new methods for effective elimination of antibiotics from wastewater. Herein, a novel process of Fe2+ catalytically enhanced vacuum ultraviolet (VUV) irradiation was proposed as a promising approach for the removal of antibiotic trimethoprim (TMP) in water. Compared with UVC photolysis, VUV photolysis, and UVC/Fe2+, VUV/Fe2+ could increase the pseudo-first-order reaction rate constant of TMP removal by 6.6-38.4 times and the mineralization rate by 36.5%-59.9%. The excellent performance might originate from the synergistic effect of VUV and Fe2+, i.e., VUV irradiation could effectively split water and largely accelerate the Fe3+/Fe2+ cycle to generate more reactive oxygen species (ROS). EPR results indicated that •OH and O2•- were identified as the main ROS in the UVC/Fe2+ and VUV/Fe2+ processes, while •OH, O2•-, and 1O2 were involved in the VUV process. The operating parameters, such as Fe2+ dosage and initial TMP contents, were evaluated and optimized. Up to 8 aromatic intermediates derived from hydroxylation, demethylation, carbonylation, and methylene group cleavage were identified by UPLC-QTOF-MS/MS technique, the possible pathways of TMP degradation were proposed. Finally, the acute and chronic toxicity of intermediates formed during TMP degradation in the VUV/Fe2+ process were also evaluated.

Healthy lifestyles, systemic inflammation and breast cancer risk: a mediation analysis.

BACKGROUND: Despite the known association between healthy lifestyles and reduced risk of breast cancer, it remains unclear whether systemic inflammation, as a consequence of unhealthy lifestyles, may mediate the association. METHODS: A cohort study of 259,435 female participants in the UK Biobank was conducted to estimate hazard ratio (HR) for breast cancer according to 9 inflammation markers using Cox regression models. We further estimated the percentage of total association between healthy lifestyle index (HLI) and breast cancer that is mediated by these inflammation markers. RESULTS: During 2,738,705 person-years of follow-up, 8,889 cases of breast cancer were diagnosed among 259,435 women in the UK Biobank cohort. Higher level of C-reactive protein (CRP), systemic immune-inflammation index (SII), CRP-to-albumin Ratio (CAR), CRP-to-lymphocyte Ratio (CLR), monocyte-to-HDL-c ratio (MHR), and neutrophil-to-HDL-c ratio (NHR) were associated with increased breast cancer risk, while a higher lymphocyte-to-monocyte ratio (LMR) was associated with a lower risk. The inverse association between HLI and breast cancer was weakly mediated by CRP (8.5%), SII (1.71%), CAR (8.66%), CLR (6.91%), MHR (6.27%), and NHR (7.33%). When considering individual lifestyle factors, CRP and CAR each mediated 16.58% and 17.20%, respectively, of the associations between diet score and breast cancer risk, while the proportion mediated for physical activity and breast cancer were 12.13% and 11.48%, respectively. Furthermore, MHR was found to mediate 13.84% and 12.01% of the associations between BMI, waist circumference, and breast cancer. CONCLUSION: The association of HLI and breast cancer is weakly mediated by the level of inflammation, particularly by CRP and CAR. Systemic inflammatory status may be an intermediate in the biological pathway of breast cancer development.

An active controllable wide-angle and ultra-wideband terahertz absorber/reflector based on VO2 metamaterial.

The use of metamaterials in the design of optics is an important strategy for controlling light fields. Numerous terahertz metamaterial devices have been recently designed; however, their performance is relatively limited. Here, the thermally induced phase change characteristics of vanadium dioxide (VO2) were harnessed to design a perfect wide-angle and ultra-wideband switchable terahertz absorber/reflector with a simple structure and three layers from top to bottom (VO2, SiO2, and Au). The absorption mechanism based on the impedance matching theory and electric field distribution was investigated, and the influence of structural parameters on the absorption rate and performance of the absorber in a wide wave vector range were analyzed. The study findings showed that the device perfectly absorbed a bandwidth of over 6.0 THz (absorption >90%). The absorption (reflection) was modulated from 0.01 to 0.999 with the change of the background temperature. More importantly, the device could switch between complete ultra-wideband reflection and perfect absorption over a wide angle range. This study provides important insights into the design of terahertz functional devices.

Tumor iron homeostasis and immune regulation.

Abnormal iron metabolism has long been regarded as a key metabolic hallmark of cancer. As a critical cofactor, iron contributes to tumor progression by participating in various processes such as mitochondrial electron transport, gene regulation, and DNA synthesis or repair. Although the role of iron in tumor cells has been widely studied, recent studies have uncovered the interplay of iron metabolism between tumor cells and immune cells, which may affect both innate and adaptive immune responses. In this review, we discuss the current understanding of the regulatory networks of iron metabolism between cancer cells and immune cells and how they contribute to antitumor immunity, and we analyze potential therapeutics targeting iron metabolism. Also, we highlight several key challenges and describe potential therapeutic approaches for future investigations.

A High-Energy Aqueous All-Sulfur Battery.

Rechargeable aqueous batteries are promising energy storage devices because of their high safety and low cost. However, their energy densities are generally unsatisfactory due to the limited capacities of ion-inserted electrode materials, prohibiting their widespread applications. Herein, a high-energy aqueous all-sulfur battery was constructed via matching S/Cu2 S and S/CaSx redox couples. In such batteries, both cathodes and anodes undergo the conversion reaction between sulfur/metal sulfides redox couples, which display high specific capacities and rational electrode potential difference. Furthermore, during the charge/discharge process, the simultaneous redox of Cu2+ ion charge-carriers also takes place and contributes to a more two-electron transfer, which doubles the capacity of cathodes. As a result, the assembled aqueous all-sulfur batteries deliver a high discharge capacity of 447 mAh g-1 based on total mass of sulfur in cathode and anode at 0.1 A g-1 , contributing to an enhanced energy density of 393 Wh kg-1 . This work will widen the scope for the design of high-energy aqueous batteries.

The interaction of diet, alcohol, genetic predisposition, and the risk of breast cancer: a cohort study from the UK Biobank.

BACKGROUND: Dietary factors have consistently been associated with breast cancer risk. However, there is limited evidence regarding their associations in women with different genetic susceptibility to breast cancer, and their interaction with alcohol consumption is also not well understood. METHODS: We analyzed data from 261,853 female participants in the UK Biobank. Multivariable adjusted Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations between dietary factors and breast cancer risk. Additionally, we assessed the interaction of dietary factors with alcohol consumption and polygenic risk score (PRS) for breast cancer. RESULTS: A moderately higher risk of breast cancer was associated with the consumption of processed meat (HR = 1.10, 95% CI 1.03, 1.18, p-trend = 0.016). Higher intake of raw vegetables and fresh fruits, and adherence to a healthy dietary pattern were inversely associated with breast cancer risk [HR (95% CI):0.93 (0.88-0.99), 0.87 (0.81, 0.93) and 0.93 (0.86-1.00), p for trend: 0.025, < 0.001, and 0.041, respectively]. Furthermore, a borderline significant interaction was found between alcohol consumption and the intake of processed meat with regard to breast cancer risk (P for interaction = 0.065). No multiplicative interaction was observed between dietary factors and PRS. CONCLUSION: Processed meat was positively associated with breast cancer risk, and vegetables, fruits, and healthy dietary patterns were negatively associated with breast cancer risk. We found no strong interaction of dietary factors with alcohol consumption and genetic predisposition for risk of breast cancer.