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BrCF2CN for photocatalytic cyanodifluoromethylation

40th Anniversary of the TIMI Study Group

Exploring the physiological, biochemical, and enzymatic responses of Vigna mungo varieties to Mungbean Yellow Mosaic India Virus (MYMIV) infection

Mitotic block and epigenetic repression underlie neurodevelopmental defects and neurobehavioral deficits in congenital heart disease

Spotlight on YAP: Unlocking New Insights to Overcome the Barriers to Heart Regeneration

Multi-level clustering and Prediction based energy efficient routing protocol to eliminate Hotspot problem in Wireless Sensor Networks.

AbstractConserving energy of sensor nodes and ensuring balanced workloads among them are fundamental concerns in Wireless Sensor Network (WSN) design. Clustering strategies offer a promising avenue to minimize node energy consumption, thereby prolonging network lifespan. Nevertheless, numerous multi-hop routing protocols using clustering technique face the challenge of nodes nearer to the Base Station (BS) depleting their energy faster due to forwarding data from the entire network leading to premature node failure and network partitioning known as ‘hotspot problem’. The paper introduces an Energy-Efficient Mega-Cluster-Based Routing (EEMCR) protocol specially designed for expansive coverage area. The primary principle behind designing this protocol is to eliminate the hotspot problem and restrict the transmission range of nodes to the threshold distance defined by the radio energy model, thereby enhancing the overall network lifespan. The protocol adopts a centralized approach employing fixed clustering wherein the BS partitions the network into square-shaped clusters. The cluster size is determined by the threshold transmission range of the sensor radio energy model, guaranteeing that all network communication stays within this threshold distance. Four such clusters form a mega-cluster with a Mega-Cluster-Head (MCH) elected among the four Cluster Heads (CHs). The MCH role is evenly distributed among nodes of all four clusters in subsequent rounds for uniform distribution of its overhead. Implementing data aggregation at two levels (CH level as well as MCH level) leads to reduced data traffic and energy consumption throughout the network. Moreover, data collection by two data mules based on odd–even round number ensures balanced data traffic and energy distribution across the network. Analysis indicates that the proposed protocol effectively mitigates the hot-spot problem and reduces data transmission overhead of sensor nodes. In simulation, the proposed protocol on an average improves network life by 34.5%, 23.5%, 14.5% and 5.5% as compared to existing protocols FCEEC, DBSCAN, LPGCR and FBECS respectively for deployment of nodes between 600 to 1200. Also, approximately 46%, 32%, 21% and 14% of lesser sensor nodes are dead for proposed protocol in respective rounds as compared to existing protocols FCEEC, DBSCAN, LPGCR and FBECS respectively. Comparative evaluations demonstrate improved network lifetime when compared to equivalent recent routing protocols.

Stable antivortices in multiferroic ε-Fe2O3 with the coalescence of misaligned grains

AbstractAntivortices have potential applications in future nano-functional devices, yet the formation of isolated antivortices traditionally requires nanoscale dimensions and near-zero magnetocrystalline anisotropy, limiting their broader application. Here, we propose an approach to forming antivortices in multiferroic ε-Fe2O3 with the coalescence of misaligned grains. By leveraging misaligned crystal domains, the large magnetocrystalline anisotropy energy is counterbalanced, thereby stabilizing the ground state of the antivortex. This method overcomes the traditional difficulty of observing isolated antivortices in micron-sized samples. Stable isolated antivortices were observed in truncated triangular multiferroic ε-Fe2O3 polycrystals ranging from 2.9 to 16.7 µm. Furthermore, the unpredictability of the polarity of the core was utilized as a source of entropy for designing physically unclonable functions. Our findings expand the range of antivortex materials into the multiferroic perovskite oxides and provide a potential opportunity for ferroelectric polarization control of antivortices.

A Rare Noncoding Enhancer Variant in <i>SCN5A</i> Contributes to the High Prevalence of Brugada Syndrome in Thailand

BACKGROUND: Brugada syndrome (BrS) is a cardiac arrhythmia disorder that causes sudden death in young adults. Rare genetic variants in the SCN5A gene encoding the Na v 1.5 sodium channel and common noncoding variants at this locus are robustly associated with the condition. BrS is particularly prevalent in Southeast Asia but the underlying ancestry-specific factors remain largely unknown. METHODS: Genome sequencing of BrS probands and population-matched controls from Thailand was performed to identify rare noncoding variants at the SCN5A-SCN10A locus that were enriched in patients with BrS. A likely causal variant was prioritized by computational methods and introduced into human induced pluripotent stem cell (hiPSC) lines using CRISPR-Cas9. The effect of the variant on SCN5A expression and Na v 1.5 sodium channel current was then assessed in hiPSC-derived cardiomyocytes (hiPSC-CMs). RESULTS: A rare noncoding variant in an SCN5A intronic enhancer region was highly enriched in patients with BrS (detected in 3.9% of cases with a case-control odds ratio of 45.2). The variant affects a nucleotide conserved across all mammalian species and predicted to disrupt a Mef2 transcription factor binding site. Heterozygous introduction of the enhancer variant in hiPSC-CMs caused significantly reduced SCN5A expression from the variant-containing allele and a 30% reduction in Na v 1.5-mediated sodium current density compared with isogenic controls, confirming its pathogenicity. Patients with the variant had severe phenotypes, with 89% experiencing cardiac arrest. CONCLUSIONS: This is the first example of a functionally validated rare noncoding variant at the SCN5A locus and highlights how genome sequencing in understudied populations can identify novel disease mechanisms. The variant partly explains the increased prevalence of BrS in this region and enables the identification of at-risk variant carriers to reduce the burden of sudden cardiac death in Thailand.

Agrivoltaics shading enhanced the microclimate, photosynthesis, growth and yields of vigna radiata genotypes in tropical Nigeria

Precisely designing asymmetrical selenium-based dual-atom sites for efficient oxygen reduction

Impact of Smokeless Oral Nicotine Products on Cardiovascular Disease: Implications for Policy, Prevention, and Treatment: A Policy Statement From the American Heart Association

Smokeless oral nicotine products are addictive, and their use has potential adverse effects on some but not all biomarkers of cardiovascular risk. The use of some types of these products, for instance, is associated with an increased mortality risk in those with ischemic heart or cerebrovascular disease. Similarly, smokeless tobacco has the potential to increase the risk of oral cancer, but the risks depend on the chemical composition of the product. The market of smokeless oral nicotine products has transformed since the last American Heart Association smokeless tobacco policy statement. Several varieties of tobacco-free oral nicotine products—including oral nicotine pouches; nontherapeutic nicotine gums, lozenges, and tablets; and nicotine gummies—have rapidly proliferated. The sales of oral nicotine pouches, in particular, have increased substantially; however, no data are available on their cardiovascular or health risks. In addition, synthetic (compared with tobacco-derived) nicotine has been used in some brands of oral nicotine products, but its cardiovascular and health effects have been inadequately studied. Robust public policy levers are identified to support ending addiction to all commercial tobacco products. Critical components and policy initiatives include clinicians emphasizing the prevention of tobacco product initiation and supporting cessation with established pharmacological and behavioral tobacco dependence treatment therapies as primary goals for achieving an end to commercial tobacco and nicotine addiction.

Evolutionary game of international trade network based on trade policy differences

Exciton-polariton ring Josephson junction

<i>Circulation</i> Editors and Editorial Board

Mechanistic insights into gut microbe derived siderophores and PHD2 interactions with implications for HIF-1α stabilization

Geographic Disparities in Availability of Hospital-Based Cardiac Services Across the United States

Research on detection and treatment of loose zones in weak fracture zone tunnel

YAP Overcomes Mechanical Barriers to Induce Mitotic Rounding and Adult Cardiomyocyte Division

BACKGROUND: Many specialized cells in adult organs acquire a state of cell cycle arrest and quiescence through unknown mechanisms. Our limited understanding of mammalian cell cycle arrest is derived primarily from cell culture models. Adult mammalian cardiomyocytes, a classic example of cell cycle arrested cells, exit the cell cycle postnatally and remain in an arrested state for the life of the organism. Cardiomyocytes can be induced to re-enter the cell cycle by YAP5SA, an active form of the Hippo signaling pathway effector YAP. METHODS: We performed clonal analyses to determine the cell cycle kinetics of YAP5SA cardiomyocytes. We also performed single-cell RNA sequencing, marker gene analysis, and functional studies to examine how YAP5SA cardiomyocytes progress through the cell cycle. RESULTS: We discovered that YAP5SA-expressing cardiomyocytes divided efficiently, with &gt;20% of YAP5SA cardiomyocyte clones containing ≥2 cardiomyocytes. YAP5SA cardiomyocytes re-entered cell cycle at the G1/S transition and had an S phase lasting ≈48 hours. Sarcomere disassembly is required for cardiomyocyte progression from S to G2 phase and the induction of mitotic rounding. Although oscillatory Cdk expression was induced in YAP5SA cardiomyocytes, these cells inefficiently progressed through G2 phase. This is improved by inhibiting P21 function, implicating checkpoint activity as an additional barrier to YAP5SA-induced cardiomyocyte division. CONCLUSIONS: Our data reveal that YAP5SA overcomes the mechanically constrained myocardial microenvironment to induce mitotic rounding with cardiomyocyte division, thus providing new insights into the in vivo mechanisms that maintain cell cycle quiescence in adult mammals.

Evaluating the effectiveness of different intervention measures for an outbreak of mycoplasma pneumoniae in hangzhou based on a dynamic model

Efficacy and Safety of Finerenone Across the Ejection Fraction Spectrum in Heart Failure With Mildly Reduced or Preserved Ejection Fraction: A Prespecified Analysis of the FINEARTS-HF Trial

BACKGROUND: The effects of treatments for heart failure (HF) may vary among patients according to left ventricular ejection fraction (LVEF). In FINEARTS-HF (Finerenone Trial to Investigate Efficacy and Safety Superior to Placebo in Patients With Heart Failure), the nonsteroidal mineralocorticoid receptor antagonist finerenone reduced the risk of cardiovascular death and total worsening HF events in patients with HF with mildly reduced or preserved ejection fraction. We examined the effect of finerenone according to LVEF in FINEARTS-HF. METHODS: FINEARTS-HF was a randomized, placebo-controlled trial examining the efficacy and safety of finerenone in patients with HF and LVEF ≥40%. The treatment effect of finerenone was examined in prespecified analyses according to LVEF categories (&lt;50%, ≥50% to &lt;60%, and ≥60%) and with LVEF as a continuous variable. The primary outcome was a composite of total (first and recurrent) worsening HF events and cardiovascular death. RESULTS: Baseline LVEF data were available for 5993 of the 6001 participants in FINEARTS-HF. Mean and median LVEF were 53±8% and 53% (interquartile range, 46%–58%), respectively. LVEF was &lt;50% in 2172 (36%), between 50% and &lt;60% in 2674 (45%), and ≥60% in 1147 (19%). Patients with higher LVEF were older, were more commonly female, were less likely to have a history of coronary artery disease, and more frequently had a history of hypertension and chronic kidney disease compared with those with a lower LVEF. Finerenone reduced the risk of cardiovascular death and total HF events consistently across LVEF categories (LVEF &lt;50% rate ratio, 0.84 [95% CI, 0.68–1.03]; LVEF ≥50% to &lt;60% rate ratio, 0.80 [0.66–0.97]; and LVEF ≥60% rate ratio, 0.94 [0.70–1.25]; P interaction =0.70). There was no modification of the benefit of finerenone across the range of LVEF when analyzed as a continuous variable ( P interaction =0.28). There was a similar consistent effect of finerenone on reducing the total number of worsening HF events (continuous P interaction =0.26). CONCLUSIONS: In patients with HF with mildly reduced or preserved ejection fraction, finerenone reduced the risk of cardiovascular death and worsening HF events, irrespective of LVEF. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04435626. URL: https://eudract.ema.europa.eu ; Unique identifier: 2020-000306-29.