Unfolding the downloads of datasets: A multifaceted exploration of influencing factors.

Scientific data are essential to advancing scientific knowledge and are increasingly valued as scholarly output. Understanding what drives dataset downloads is crucial for their effective dissemination and reuse. Our study, analysing 55,473 datasets from 69 data repositories, identifies key factors driving dataset downloads, focusing on interpretability, reliability, and accessibility. We find that while lengthy descriptive texts can deter users due to complexity and time requirements, readability boosts a dataset's appeal. Reliability, evidenced by factors like institutional reputation and citation counts of related papers, also significantly increases a dataset's attractiveness and usage. Additionally, our research shows that open access to datasets increases their downloads and amplifies the importance of interpretability and reliability. This indicates that easy access enhances the overall attractiveness and usage of datasets in the scholarly community. By emphasizing interpretability, reliability, and accessibility, this study offers a comprehensive framework for future research and guides data management practices toward ensuring clarity, credibility, and open access to maximize the impact of scientific datasets.

Downregulation of enhancer RNA AC003092.1 is associated with poor prognosis in kidney renal clear cell carcinoma.

Kidney renal clear cell carcinoma (KIRC) is the most common histological type of renal cancer, enhancer RNA plays a significant role in tumor growth, however, it has been less studied in renal cancer. The aim of this study was to investigate the role of eRNA AC003092.1 in KIRC. Clinical and RNA expression data were downloaded from a TCGA database, and performed bioinformatics analysis, including expression level analysis, survival analysis, clinical correlation analysis, immune correlation analysis. We further confirmed the expression level of AC003092.1 between normal and tumor cell, predicted the biological role of AC003092.1 in KIRC, and performed cell proliferation and wound healing assays, followed by GSEA enrichment analysis and western blot to detect the proteins of the enriched pathway. Bioinformatics results showed that AC003092.1 expression was elevated in tumor tissues, and knockdown of AC003092.1 expression inhibited cell proliferation and migration. GSEA and western blot results showed that knockdown AC003092.1 expression alleviated the extracellular matrix (ECM) process in KIRC cell lines. Our study provides evidence that AC003092.1 play an important role in KIRC, and AC003092.1 may promote tumor cell progression by affecting the ECM process during tumor development.

Efficient Energy Transfer for Near-Perfect Quantum Efficiency and Thermal Stability.

The pursuit of high-quality phosphors exhibiting swift response to near-ultraviolet (n-UV) excitation, elevated quantum efficiency (QE), superior thermal stability, and impeccable light quality has been a focal point of investigation. In this research, we synthesized a novel K2La2B2O7:Ce3+,Tb3+ (KLBO:Ce3+,Tb3+) color-tunable phosphor that meets these requirements. KLBO:Ce3+ can be stimulated efficiently by the n-UV light and shows an intense blue emission centered at 437 nm. Notably, KLBO:0.04Ce3+ exhibits exceptional internal QE (IQE = 94%) and outstanding thermal stability (I423 K/I303 K = 88%). Optimization of doping compositions enables efficient Ce3+ → Tb3+ energy transfer, resulting in substantial enhancements in QE and thermal stability. Specifically, KLBO:0.04Ce3+,0.28Tb3+ achieves an IQE of 98% and a thermal stability of 97%, higher than those of most phosphors of the same type. White light-emitting diodes fabricated using phosphor samples emit warm white light characterized by high Ra (Ra = 96.6 and 93.4) and low CCT (CCT = 4886 and 4400 K). This study underscores the feasibility of enhancing phosphor QE and thermal stability through energy transfer mechanisms.

Modulation of ER-mitochondria tethering complex VAPB-PTPIP51: Novel therapeutic targets for aging-associated diseases.

Aging is a gradual and irreversible natural process. With aging, the body experiences a functional decline, and the effects amplify the vulnerability to a range of age-related diseases, including neurodegenerative, cardiovascular, and metabolic diseases. Within the aging process, the morphology and function of mitochondria and the endoplasmic reticulum (ER) undergo alterations, particularly in the structure connecting these organelles known as mitochondria-associated membranes (MAMs). MAMs serve as vital intracellular signaling hubs, facilitating communication between the ER and mitochondria when regulating various cellular events, including calcium homeostasis, lipid metabolism, mitochondrial function, and apoptosis. The formation of MAMs is partly dependent on the interaction between the vesicle-associated membrane protein-associated protein-B (VAPB) and protein tyrosine phosphatase-interacting protein-51 (PTPIP51). Accumulating evidence has begun to elucidate the pivotal role of the VAPB-PTPIP51 tether in the initiation and progression of age-related diseases. In this study, we delineate the intricate structure and multifunctional role of the VAPB-PTPIP51 tether and discuss its profound implications in aging-associated diseases. Moreover, we provide a comprehensive overview of potential therapeutic interventions and pharmacological agents targeting the VAPB-PTPIP51-mediated MAMs, thereby offering a glimmer of hope in mitigating aging processes and treating age-related disorders.

The role of STAT3/VAV3 in glucolipid metabolism during the development of HFD-induced MAFLD.

Metabolic-associated fatty liver disease (MAFLD) is a globally prevalent chronic hepatic disease. Previous studies have indicated that the activation of the signal transducer and activator of transcription3 (STAT3) plays a vital role in MAFLD progression at the very beginning. However, the specific association between STAT3 and abnormal hepatic metabolism remains unclear. In this study, activated inflammation was observed to induce abnormal glucolipid metabolic disorders in the hepatic tissues of high-fat diet (HFD)-fed ApoE-/- mice. Furthermore, we found that the activation of STAT3 induced by HFD might function as a transcriptional factor to suppress the expression of VAV3, which might participate in intracellular glucolipid metabolism and the regulation of glucose transporter 4 (GLUT4) storage vesicle traffic in the development of MAFLD both in vitro and in vivo. We verified that VAV3 deficiency could retard the GLUT4 membrane translocation and impair the glucose homeostasis. Additionally, VAV3 participates in cholesterol metabolism in hepatocytes, eventually resulting in the accumulation of intracellular cholesterol. Moreover, rAAV8-TBG-VAV3 was conducted to restore the expression of VAV3 in HFD-fed ApoE-/- mice. VAV3 overexpression was observed to improve glucose homeostasis as well as attenuate hepatic cholesterol accumulation in vivo. In conclusion, the STAT3/VAV3 signaling pathway might play a significant role in MAFLD by regulating glucose and cholesterol metabolism, and VAV3 might be a potential therapeutic strategy which could consequently ameliorate MAFLD.

Enhancing salt tolerance and crop growth in agricultural systems: the impact of magnetized-ionized water irrigation on soil properties, microbial communities, and cotton growth.

BACKGROUND: The development of agricultural practices requires an understanding of the improvement of salt tolerance and crop growth in agricultural systems through magnetized-ionized water irrigation. METHOD: This study examined the impacts of fresh water (F), brackish water (B), magnetized-ionized fresh water (MIF), and magnetized-ionized brackish water (MIB) on soil properties and the growth of cotton seedlings through microbial analysis during the cotton seedling period. RESULTS: The results revealed that magnetized-ionized water irrigation improved soil water retention and promoted salt leaching. In comparison with F irrigation, plant height, leaf area index (LAI), dry matter accumulation (DM), and chlorophyll content (SPAD) levels increased by 3.61%, 4.07%, 5.76%, and 1.33%, respectively, under MIF irrigation. Similarly, when compared with B irrigation, LAI, DM, and SPAD increased by 5.13%, 6.12%, and 3.12% under MIB irrigation. Magnetized-ionized water irrigation also led to a notable rise in the relative abundance of beneficial soil bacterial communities, particularly Pseudomonas and Azoarcus, as well as fungal communities like Trichoderma, while reducing the prevalence of pathogenic fungi, such as Lasionectria, Gibberella, and Alternaria. Notably, this irrigation approach induced alterations in soil properties, and partial least squares path modeling revealed significant links between soil properties and both cotton growth and fungal community structure (with path coefficients of -0.884 and 0.693, respectively). CONCLUSION: This study elucidated the distinct effects of soil properties and growth indices on cotton yield during the seedling period, providing a crucial scientific foundation for enhancing future agricultural production through the use of magnetized-ionized water irrigation. © 2024 Society of Chemical Industry.

Ferroptosis in age-related vascular diseases: Molecular mechanisms and innovative therapeutic strategies.

Aging, an inevitable aspect of human existence, serves as one of the predominant risk factors for vascular diseases. Delving into the mystery of vascular disease's pathophysiology, the profound involvement of programmed cell death (PCD) has been extensively demonstrated. PCD is a fundamental biological process that plays a crucial role in both normal physiology and pathology, including a recently discovered form, ferroptosis. Ferroptosis is characterized by its reliance on iron and lipid peroxidation, and its significant involvement in vascular disease pathophysiology has been increasingly acknowledged. This phenomenon not only offers a promising therapeutic target but also deepens our understanding of the complex relationship between ferroptosis and age-related vascular diseases. Consequently, this article aims to thoroughly review the mechanisms that enable the effective control and inhibition of ferroptosis. It focuses on genetic and pharmacological interventions, with the goal of developing innovative therapeutic strategies to combat age-related vascular diseases.

Effects of solution chemistry on dielectric barrier atmospheric non-thermal plasma for operative degradation of antiretroviral drug nevirapine.

The global prevalence of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) has been an environmental menace. Tons of drug wastes from antiretroviral therapy are released into the environment annually. We, for the first time, employed the novel dielectric barrier atmospheric non-thermal plasma (DBANP) discharge, to mitigate the inadvertent pollution arising from the antiretroviral therapy. A 40-min treatment of nevirapine achieved >94 % (0.075 min-1) removal efficiency at discharge power of 63.5 W and plasma working gas of atmospheric air. Chemical probes confirmed •OH, ONOO- and eaq- as the dominant reactive species whilst further revealing the reaction acceleration role of NaNO3 and CCl4 which are known reaction terminators. The commonly coexisting inorganic anions potentiated nevirapine removal with over 98 % efficiency, achieving the highest rate constant of 0.148 min-1 in this study. Moreover, the initial solution pH (1.5-11.1) was no limiting factor either. The insensitivity of the DBANP discharge to actual water matrices was an eminent inference of its potential applicability in practical conditions. With reference to data obtained from the liquid chromatography-mass spectrometer analysis, nevirapine degradation pathway was proposed. A nucleophilic attack by ONOO- at the cyclopropyl group and •OH attack at the carbonyl carbon of the amide group, respectively, initiated nevirapine degradation process. It is anticipated that the findings herein, will provide new insights into antiretroviral drug waste management in environmental waters using the innovative and green non-thermal plasma process.

Terazosin attenuates abdominal aortic aneurysm formation by downregulating Peg3 expression to inhibit vascular smooth muscle cell apoptosis and senescence.

Abdominal aortic aneurysm (AAA), a vascular degenerative disease, is a potentially life-threatening condition characterised by the loss of vascular smooth muscle cells (VSMCs), degradation of extracellular matrix (ECM), inflammation, and oxidative stress. Despite the severity of AAA, effective drugs for treatment are scarce. At low doses, terazosin (TZ) exerts antiapoptotic and anti-inflammatory effects in several diseases, but its potential to protect against AAA remains unexplored. Herein, we investigated the effects of TZ in two AAA animal models: Angiotensin II (Ang II) infusion in Apoe-/- mice and calcium chloride application in C57BL/6J mice. Mice were orally administered with TZ (100 or 1000 µg/kg/day). The in vivo results indicated that low-dose TZ alleviated AAA formation in both models. Low-dose TZ significantly reduced aortic pulse wave velocity without exerting an apparent antihypertensive effect in the Ang II-induced AAA model. Paternally expressed gene 3 (Peg3) was identified via RNA sequencing as a novel TZ target. PEG3 expression was significantly elevated in both mouse and human AAA tissues. TZ suppressed PEG3 expression and reduced the abundance of matrix metalloproteinases (MMP2/MMP9) in the tunica media. Functional experiments and molecular analyses revealed that TZ (10 nM) treatment and Peg3 knockdown effectively prevented Ang II-induced VSMC senescence and apoptosis in vitro. Thus, Peg3, a novel target of TZ, mediates inflammation-induced VSMC apoptosis and senescence. Low-dose TZ downregulates Peg3 expression to attenuate AAA formation and ECM degradation, suggesting a promising therapeutic strategy for AAA.

PS-MPs promotes the progression of inflammation and fibrosis in diabetic nephropathy through NLRP3/Caspase-1 and TGF-ß1/Smad2/3 signaling pathways.

BACKGROUND: Diabetic nephropathy (DN) is a prevalent chronic microvascular complication of diabetes and the leading cause of end-stage renal disease (ESRD). Understanding the progressive etiology of DN is critical for the development of effective health policies and interventions. Recent research indicated that polystyrene microplastics (PS-MPs) contaminate our diets and accumulate in various organs, including the liver, kidneys, and muscles. METHODS: In this study, ten-week-old db/db mice and db/m mice were fed. Besides, db/db mice were divided into two groups: PS-MPs group (oral administration of 0.5 µm PS-MPs) and an H2O group, and they were fed for three months. A type II diabetes model was established using db/db mice to investigate the effects of PS-MPs on body weight, blood glucose level, renal function, and renal fibrosis. RESULTS: The results demonstrated that PS-MPs significantly exacerbated various biochemical indicators of renal tissue damage, including fasting blood glucose, serum creatinine, blood urea nitrogen, and blood uric acid. Additionally, PS-MPs worsened the pathological alterations and degree of fibrosis in renal tissue. An increased oxidative stress state and elevated levels of inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and monocyte chemoattractant protein-1 (MCP-1) were identified. Furthermore, PS-MPs significantly enhanced renal fibrosis by inhibiting the transition from epithelial cells to mesenchymal cells, specifically through the inhibition of the TGF-ß/Smad signaling pathway. The expression levels of NOD-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), Caspase-1, and cleaved Caspase-1, which are inflammasome proteins, were significantly elevated in the PS-MPs group. CONCLUSION: The findings suggested that PS-MPs could aggravate kidney injury and renal fibrosis in db/db mice by promoting NLRP3/Caspase-1 and TGF-ß1/Smads signaling pathways. These findings had implications for elucidating the role of PS-MPs in DN progression, underscoring the necessity for additional research and public health interventions.

Remote Control and Noninvasive Detection Enabled by a High-performance NIR pc-LED.

In an increasing manner, near-infrared phosphor-converted light-emitting diodes (NIR pc-LEDs) are considered to be exemplary light sources owing to their notable attributes of elevated output power, economical nature, and exceptional portability. NIR phosphors are critical components of NIR pc-LEDs. Herein, we report a novel blue light excitable NIR phosphor CaLu2ZrScAl3O12:Cr3+ (CLZSA:Cr3+) as a crucial and efficient broadband NIR emitter. The CLZSA:Cr3+ phosphor displays an intense NIR broadband emission peaking at 776 nm and with a full width at half-maximum (fwhm) of 140 nm. The designed material also exhibits superior resistance to thermal quenching, as the intensity of emission at 423 K remains at 80% of that at room temperature. The constructed NIR pc-LED device based on CLZSA:Cr3+ demonstrates a high total output power of 68.4 mW at a drive current of 100 mA, along with a high photoelectric conversion efficiency of 23.0%. Impressively, the high-power NIR pc-LEDs are utilized as light sources for remote control and non-invasive detection, resulting in the excellent performance and remarkable achievement.

Counteracting Age-Related Netrin-1 Signaling Insufficiency Ameliorates Endothelial Cell Senescence and Angiogenesis Impairment.

Senescent cells that accumulate are regarded as promising therapeutic targets. However, senolytic therapy failed to achieve satisfactory results. We previously discovered that young human plasma improved vascular endothelial cell senescence, and UNC5B might be a novel intervention target. Netrin-1, as a natural ligand of UNC5B, plays roles in multiple age-related vascular disorders, but its involvement in aging is still unclear. Here, we observed a significant decrease in plasma Netrin-1 levels in old healthy subjects compared to the young. In vivo, adeno-associated-virus-mediated delivery of Netrin-1 into aged mice significantly improved functional recovery in a model of hindlimb ischemia, promoted angiogenesis in ischemic tissues, and activated the endothelial nitric oxide synthase. Furthermore, we revealed that low-dose Netrin-1 recombinant protein significantly reduced senescence-associated-ß-galactosidase-positive cells, inhibited the P53 pathway, promoted cell migration, increased tubule formation, and elevated nitric oxide production in senescent endothelial cells. However, UNC5B inhibition blocked the pro-angiogenesis effect of low-dose Netrin-1 on senescent cells or aortic rings. In summary, this study depicts that modulating Netrin-1 signaling can result in improved vascular health and Netrin-1 may have therapeutic potential for age-related ischemic diseases.

Microplastics cause hepatotoxicity in diabetic mice by disrupting glucolipid metabolism via PP2A/AMPK/HNF4A and promoting fibrosis via the Wnt/ß-catenin pathway.

In recent years, microplastics (MPs) have gained significant attention as a persistent environmental pollutant resulting from the decomposition of plastics, leading to their accumulation in the human body. The liver, particularly of individuals with type 2 diabetes mellitus (T2DM), is known to be more susceptible to the adverse effects of environmental pollutants. Therefore, to investigate the potential impact of MPs on the liver of diabetic mice and elucidate the underlying toxicological mechanisms, we exposed db/db mice to 0.5 µm MPs for 3 months. Our results revealed that MPs exposure resulted in several harmful effects, including decreased body weight, disruption of liver structure and function, elevated blood glucose levels, impaired glucose tolerance, and increased glycogen accumulation in the hepatic tissue of the mice. Furthermore, MPs exposure was found to promote hepatic gluconeogenesis by perturbing the PP2A/AMPK/HNF4A signaling pathway. In addition, MPs disrupt redox balance, leading to oxidative damage in the liver. This exposure also disrupted hepatic lipid metabolism, stimulating lipid synthesis while inhibiting catabolism, ultimately resulting in the development of fatty liver. Moreover, MPs were found to induce liver fibrosis by activating the Wnt/ß-catenin signaling pathway. Furthermore, MPs influenced adaptive thermogenesis in brown fat by modulating the expression of uncoupling protein 1 (UCP1) and genes associated with mitochondrial oxidative respiration thermogenesis in brown fat. In conclusion, our study demonstrates that MPs induce oxidative damage in the liver, disturb glucose and lipid metabolism, promote hepatic fibrosis, and influence adaptive thermogenesis in brown fat in diabetic mice. These findings underscore the potential adverse effects of MPs on liver health in individuals with T2DM and highlight the importance of further research in this area.

Toxicological effects of microplastics in renal ischemia-reperfusion injury.

The widespread presence of microplastics (MPs) in the environment poses a significant threat to biological survival and human health. However, our understanding of the toxic effects of MPs on the kidneys remains limited. This study aimed to investigate the underlying mechanism of the toxic effects of MPs on the kidneys using an ischemia-reperfusion (IR) mouse model. Four-week-old ICR mice were exposed to 0.5 µm MPs for 12 weeks prior to IR injury. The results showed that MPs exposure could aggravate the IR-induced damage to renal tubules and glomeruli. Although there were no significant changes in blood urea nitrogen and serum creatinine levels 7 days after IR, MPs treatment resulted in a slight increase in both parameters. In addition, the expression levels of inflammatory factors (MCP-1 and IL-6) at the mRNA level, as well as macrophage markers (CD68 and F4/80), were significantly higher in the MPs + IR group than in the Sham group after IR. Furthermore, MPs exposure exacerbated IR-induced renal fibrosis. Importantly, the expression of pyroptosis-related genes, including NLRP3, ASC, GSDMD, cleaved caspase-1, and IL-18, was significantly upregulated by MPs, indicating that MPs exacerbate pyroptosis in the context of renal IR. In conclusion, our findings suggest that MPs exposure can aggravate renal IR-induced pyroptosis by activating NLRP3-GSDMD signaling.

Crystal Field Engineering Yields New 3D Layered Solid Solution Phosphors (Ca/Sr)4MgAl2Si3O14:Eu2+ for White-Light-Emitting Diode Full-Spectrum Lighting.

The cation-equivalent substitution strategy has the ability to manipulate the luminescence color of phosphors and enhance their overall luminescence performance. A series of novel yellow feldspar-type 3D layered phosphors (Ca1-ySry)4MgAl2Si3O14:xEu2+ were synthesized using a high-temperature solid-state reaction. The solid solution phosphors belong to a tetragonal crystal system with a space group of P4̅21m and cell parameters of a = b = 7.75407-7.91794 Å, c = 5.04299-5.22543 Å, and V = 303.166-327.602 Å3. Under near-ultraviolet (n-UV) excitation, the luminescence color of the phosphor undergoes modulation from yellow-green (530 nm) to blue (467 nm) as the Sr2+ ion substitution ratio increases. This modulation is attributed to the gradual decrease in crystal field splitting energy. Additionally, both the Stokes shift and the full width of the luminescence spectra decrease. Furthermore, there is an increase in the quantum yield (QY) from 45.50 to 60.73%. Finally, the fabricated white-light-emitting diode devices emitted warm white light and achieved high Ra (Ra = 94, 96.6, 92.7) and low correlated color temperature (CCT = 3486, 3430, 3788 K), indicating that the prepared solid solution phosphors can be used as candidate materials for WLED lighting.

The male reproductive toxicity after nanoplastics and microplastics exposure: Sperm quality and changes of different cells in testis.

Nanoplastics (NPs) and Microplastics (MPs) pollution has become a severe threat to the planet and is a growing concern. However, their effects on male reproductive toxicity remain poorly understood. In this study, a series of morphological analyses were completed to explore the influence of NPs and MPs exposure on the testis in mice. After 12-weeks exposure, although both NPs and MPs exposure can lead to reproductive toxicity, compared with NPs exposure, exposure to MPs leads to a more significant increase in reproductive toxicity dependent on some particle size. Moreover, increased reproductive toxicities, including increased spermatogenesis disorders, and sperm physiological abnormality, oxidative stress, testis inflammation was more associated with MPs group than NPs group. Ultra-pathological structure observed by transmission electron microscopy indicated that both NPs and MPs have different effects on spermatogonia, spermatocytes and Sertoli cells. Exposure to MPs resulted in decreased Sertoli cell numbers and reduced Leydig cell area, and showed no effects on differentiation of Leydig cells by the expression level of the Insulin-Like factor 3 (INSL3) in Leydig cells. Transcriptomic sequencing analysis provided valuable insights into the differential effects of NPs and MPs on cellular processes. Specifically, our findings demonstrated that NPs were predominantly involved in the regulation of steroid biosynthesis, whereas MPs primarily influenced amino acid metabolism. This study demonstrates the effect of adult-stage reproductive toxicity in mice after exposure to NPs and MPs, which will deep the understanding of the NPs and MPs induced toxicity.

Energy transfer and tunable emission in BaSrGd4O8:Bi3+,Eu3+ phosphors for warm WLED.

In this work, a series of BaSrGd4O8:xBi3+ blue phosphors was synthesized employing the high-temperature solid-state method. Phase purity of the samples was verified by X-ray diffraction and Rietveld refinement. Time-resolved photoluminescence spectra revealed the existence of two distinct Bi sites. Subsequent optimization of dopant types and doping levels in the batch led to an almost twofold increase in quantum efficiency. The introduction of Eu3+ into the phosphors facilitated the construction of an energy transfer pathway. As the concentration of Eu3+ was increased, the emission color changed from blue to purple and finally to red. In addition, the thermal stability and potential applications of the phosphors were extensively investigated. Finally, two WLED devices were successfully fabricated with color rendering indices of 96.27 and 92.18, and correlated color temperatures of 5198 and 2475 K. This underscores the prospective application of these phosphors in the field of high-quality warm WLEDs.

Basement Membrane-Associated lncRNA Risk Model Predicts Prognosis and Guides Clinical Treatment in Clear Cell Renal Cell Carcinoma.

The basement membrane (BM) affects the invasion and growth of malignant tumors. The role and mechanism of BM-associated lncRNAs in clear cell renal cell carcinoma (ccRCC) are unknown. In this study, we identified biomarkers of ccRCC and developed a risk model to assess patient prognosis. We downloaded transcripts and clinical data from the Cancer Genome Atlas (TCGA). Differential analysis, co-expression analysis, Cox regression analysis, and lasso regression were used to identify BM-associated prognostic lncRNAs and create a risk prediction model. We evaluated and validated the accuracy of the model using multiple methods and constructed a nomogram to predict the prognosis of ccRCC. GO, KEGG, and immunity analyses were used to explore differences in biological function. We constructed a risk model containing six BM-associated lncRNAs (LINC02154, IGFL2-AS1, NFE4, AC112715.1, AC092535.5, and AC105105.3). The risk model has higher diagnostic efficiency compared to clinical characteristics and can be used to forecast patient prognoses. We used renal cancer cells and tissue microarrays to verify the expression of lncRNAs in the risk model. We found that knocking down LINC02154 and AC112715.1 could inhibit the invasion ability of renal cancer cells. The risk model based on BM-associated lncRNAs can well predict ccRCC and guide clinical treatment.

Development and Validation of Robust Ferroptosis-Related Genes in Myocardial Ischemia-Reperfusion Injury.

(1) Background: Despite the evidence that ferroptosis is involved in myocardial ischemia-reperfusion (MIR), the critical regulator of ferroptosis in MIR remains unclear. (2) Methods: We included three GEO datasets and a set of ferroptosis-related genes with 259 genes. Following the identification of the differentially expressed ferroptosis-related genes (DEFRGs) and hub genes, we performed the functional annotation, protein-protein interaction network, and immune infiltration analysis. The GSE168610 dataset, a cell model, and an animal model were then used to verify key genes. (3) Results: We identified 17 DEFRGs and 9 hub genes in the MIR samples compared to the control. Heme oxygenase 1 (Hmox1), activating transcription factor 3 (Atf3), epidermal growth factor receptor (Egfr), and X-box binding protein 1 (Xbp1) were significantly upregulated in response to ischemic and hypoxic stimuli. In contrast, glutathione peroxidase 4 (Gpx4) and vascular endothelial growth factor A (Vegfa) were consistently decreased in either the oxygen and glucose deprivation/reoxygenation cell or the MIR mouse model. (4) Conclusions: This study emphasized the relevance of ferroptosis in MIR. It has been successfully demonstrated that nine ferroptosis-related genes (Hmox1, Atf3, Egfr, Gpx4, Cd44, Vegfa, asparagine synthetase (Asns), Xbp1, and bromodomain containing 4 (Brd4)) are involved in the process. Additional studies are needed to explore potential therapeutic targets for MIR.

[Seasonal Variation Characteristics and Pollution Assessment of Heavy Metals in Water and Sediment of Taipu River].

Taipu River is a river spanning two provinces and one city in a demonstration area in the Yangtze River Delta on an ecologically friendly developmentand an important water source in the upper reaches of the Huangpu River in Shanghai. To understand the multi-media distribution characteristics, pollution status, and ecological risk of heavy metals in the Taipu River, the contents of heavy metals (As, Cd, Co, Cr, Cu, Mn, Ni, Pb, Sb, and Zn) in the sediments of Taipu River were analyzed, and the pollution status and potential ecological risk were evaluated using the Nemerow comprehensive pollution index, geo-accumulation index, and potential ecological risk index methods. In addition, the health risk assessment model was used to assess the health risk of heavy metals in surface water of Taipu River. The results showed that the concentrations of Cd, Cr, Mn, and Ni in the surface water of Taipu River exceeded the class Ⅲ water limit at the upstream point in spring; the concentrations of Sb exceeded the class Ⅲ water limit at all points in winter; the average value of As exceeded the class Ⅲ water limit in overlying water during the wet season; and the average values of As and Cd exceeded the class Ⅲ water limit in pore water during the wet season. The health risk assessment of surface water implied that both adults and children had higher health risk in spring and lower health risk in other seasons. The health risk of children was significantly higher than that of adults, and it mainly came from chemical carcinogenic heavy metal elements As, Cd, and Cr. The average contents of Co, Mn, Sb, and Zn in Taipu River sediments in the four seasons all exceeded the Shanghai soil baseline; the average contents of As, Cr, and Cu in summer, autumn, and winter exceeded the Shanghai soil baseline; and the average contents of Cd, Ni, and Pb in summer and winter exceeded the Shanghai soil baseline. The evaluation results of the Nemerow comprehensive pollution index and geo-accumulation index showed that the pollution degree of the middle reaches of Taipu River was higher than that of the upper and lower reaches, and the Sb pollution was more serious. The potential ecological risk index method revealed that the Taipu River sediment was at a low risk. Cd had a high contribution in both the wet and dry seasons and could be regarded as the main heavy metal of potential ecological risk in the Taipu River sediment.