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In the realm of topology, various constraints are frequently imposed on the types of topological spaces under examination and these constraints are defined by what are known as separation axioms. Also, the separation axioms can be seen as additional conditions that may be incorporated into the definition of topological spaces. Separation axioms serve various purposes in lattice theory. They provide tools for classifying and comparing different lattices, revealing their structural and topological properties. While traditional separation axioms like T0, T1, T2, etc., still play a role, their interpretation and implications differ in the context of soft sets and lattice structures. This paper introduces the separation axioms, soft lattice -space (for i = 4, 5, 6), within the context of a soft lattice topological space and investigates several of their associated properties. Studying lattices through these axioms can reveal connections between their order-theoretic properties and their topological features. This work goes beyond simply applying separation axioms to soft lattice topological spaces. It ventures into unveiling soft lattice invariant properties. Additionally, the study explores soft lattice invariant properties that are derived from these soft lattice -space concepts, specifically, soft lattice hereditary and soft lattice topological properties. In conclusion, the study's exploration of soft lattice invariant properties pushes the boundaries of understanding soft lattice topological spaces. By delving into the essence of these structures and their local and global characteristics, the study opens doors to exciting theoretical possibilities and potential applications in diverse fields.

The objective of the study is to analyze the multifaceted crises affecting global development, such as the Covid-19 pandemic, climate change, and increasing inequality. It critiques the traditional gross domestic product (GDP) driven development model and suggests an alternative framework based on the principles of equity and sustainability. This approach aligns with the Lifestyle for Environment (LiFE) initiative and seeks to integrate human development with ecological sustainability. The research emphasizes the importance of global leadership, particularly through the Group of Twenty (G20), in fostering international cooperation to facilitate a just transition through policy reforms and behavioral changes.

Abstract A comprehensive atlas of cis-regulatory elements and their dynamic activity is necessary to understand the transcriptional basis of cellular structure maintenance, metabolism, and responses to the environment. Here we show, using matched single-nucleus chromatin accessibility and RNA-sequencing from juvenile male C57BL6 mice, an atlas of accessible chromatin regions in both normal and denervated skeletal muscles. We identified cell-type-specific cis-regulatory networks, highlighting the dynamic regulatory circuits mediating transitions between myonuclear types. Through comparison of normal and perturbed muscle, we delineated the reprogramming of cis-regulatory networks in response to denervation, described the interplay of promoters/enhancers and target genes. We further unveil a hierarchical structure of transcription factors that delineate a regulatory network in atrophic muscle, identifying ELK4 as a key atrophy-related transcription factor that instigates muscle atrophy through TGF-β1 regulation. This study furnishes a rich genomic resource, essential for decoding the regulatory dynamics of skeletal muscle in both physiological and pathological states.

Chronic kidney disease (CKD) is associated with a higher risk of atrial fibrillation (AF). The mechanistic link between CKD and AF remains elusive. IL-1β, a main effector of NLR family pyrin domain–containing 3 (NLRP3) inflammasome activation, is a key modulator of conditions associated with inflammation, such as AF and CKD. Circulating IL-1β levels were elevated in patients with CKD who had AF (versus patients with CKD in sinus rhythm). Moreover, NLRP3 activity was enhanced in atria of patients with CKD. To elucidate the role of NLRP3/IL-1β signaling in the pathogenesis of CKD-induced AF, Nlrp3–/– and WT mice were subjected to a 2-stage subtotal nephrectomy protocol to induce CKD. Four weeks after surgery, IL-1β levels in serum and atrial tissue were increased in WT CKD (WT-CKD) mice versus sham-operated WT (WT-sham) mice. The increased susceptibility to pacing-induced AF and the longer AF duration in WT-CKD mice were associated with an abbreviated atrial effective refractory period, enlarged atria, and atrial fibrosis. Genetic inhibition of NLRP3 in Nlrp3–/– mice or neutralizing anti–IL-1β antibodies effectively reduced IL-1β levels, normalized left atrial dimensions, and reduced fibrosis and the incidence of AF. These data suggest that CKD creates a substrate for AF development by activating the NLRP3 inflammasome in atria, which is associated with structural and electrical remodeling. Neutralizing IL-1β antibodies may be beneficial in preventing CKD-induced AF.

Chronic kidney disease (CKD) is associated with a higher risk of atrial fibrillation (AF). The mechanistic link between CKD and AF remains elusive. IL-1[beta], a main effector of NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation, is a key modulator of conditions associated with inflammation, such as AF and CKD. Circulating IL-1[beta] levels were elevated patients with CKD who had AF (versus patients with CKD in sinus rhythm). Moreover, NLRP3 activity was enhanced in atria of patients with CKD. To elucidate the role of NLRP3/IL- 1[beta] signaling in the pathogenesis of CKD-induced AF, [Nlrp3.sup.-/-] and WT mice were subjected to a 2-stage subtotal nephrectomy protocol to induce CKD. Four weeks after surgery, IL-1[beta] levels in serum and atrial tissue were increased in WT CKD (WT-CKD) mice versus sham-operated WT (WT-sham) mice. The increased susceptibility to pacing-induced AF and the longer AF duration in WT-CKD mice were associated with an abbreviated atrial effective refractory period, enlarged atria, and atrial fibrosis. Genetic inhibition of NLRP3 in [Nlrp3.sup.-/-] mice or neutralizing anti-IL- 1[beta] antibodies effectively reduced IL- 1[beta] levels, normalized left atrial dimensions, and reduced fibrosis and the incidence of AF. These data suggest that CKD creates a substrate for AF development by activating the NLRP3 inflammasome in atria, which is associated with structural and electrical remodeling. Neutralizing IL-1[beta] antibodies may be beneficial in preventing CKD-induced AF., Introduction Atrial fibrillation (AF) is the most commonly diagnosed cardiac arrhythmia, with a high prevalence worldwide (1, 2). AF significantly affects the quality of life, as it is associated with [...]

Evolutionarily conserved genes often play critical roles in organismal physiology. Here, we describe multiple roles of a previously uncharacterized Class III metallophosphodiesterase in Drosophila, an ortholog of the MPPED1 and MPPED2 proteins expressed in the mammalian brain. dMpped, the product of CG16717, hydrolyzed phosphodiester substrates including cAMP and cGMP in a metal-dependent manner. dMpped is expressed during development and in the adult fly. RNA-seq analysis of dMppedKO flies revealed misregulation of innate immune pathways. dMppedKO flies showed a reduced lifespan, which could be restored in Dredd hypomorphs, indicating that excessive production of antimicrobial peptides contributed to reduced longevity. Elevated levels of cAMP and cGMP in the brain of dMppedKO flies was restored on neuronal expression of dMpped, with a concomitant reduction in levels of antimicrobial peptides and restoration of normal life span. We observed that dMpped is expressed in the antennal lobe in the fly brain. dMppedKO flies showed defective specific attractant perception and desiccation sensitivity, correlated with the overexpression of Obp28 and Obp59 in knock-out flies. Importantly, neuronal expression of mammalian MPPED2 restored lifespan in dMppedKO flies. This is the first description of the pleiotropic roles of an evolutionarily conserved metallophosphodiesterase that may moonlight in diverse signaling pathways in an organism.

High-protein diets (HPDs) offer health benefits, such as weight management and improved metabolic profiles. The effects of HPD on cardiac arrhythmogenesis remain unclear. Atrial fibrillation (AF), the most common arrhythmia, is associated with inflammasome activation. The role of the Absent-in-Melanoma 2 (AIM2) inflammasome in AF pathogenesis remains unexplored. In this study, we discovered that HPD increased susceptibility to AF. To demonstrate the involvement of AIM2 signaling in the pathogenesis of HPD-induced AF, wildtype (WT) and Aim2−/− mice were fed normal-chow (NC) and HPD, respectively. Four weeks later, inflammasome activity was upregulated in the atria of WT-HPD mice, but not in the Aim2−/−-HPD mice. The increased AF vulnerability in WT-HPD mice was associated with abnormal sarcoplasmic reticulum (SR) Ca2+-release events in atrial myocytes. HPD increased the cytoplasmic double-strand (ds) DNA level, causing AIM2 activation. Genetic inhibition of AIM2 in Aim2−/− mice reduced susceptibility to AF, cytoplasmic dsDNA level, mitochondrial ROS production, and abnormal SR Ca2+-release in atrial myocytes. These data suggest that HPD creates a substrate conducive to AF development by activating the AIM2-inflammasome, which is associated with mitochondrial oxidative stress along with proarrhythmic SR Ca2+-release. Our data imply that targeting the AIM2 inflammasome might constitute a novel anti-AF strategy in certain patient subpopulations.

This study aims to investigate the interaction between market volatility, economic growth, and cognitive biases over the period from April 2006 to March 2024. Market volatility and economic growth are critical indicators that influence economic stability and investment behavior. Financial market volatility, defined by abrupt and erratic changes in asset values, can have a big impact on the expansion and stability of the economy. According to conventional economic theory, there should be an inverse relationship between market volatility and economic growth since high volatility can discourage investment and erode trust. Market participants' cognitive biases are a major aspect that complicates this connection. Due to our innate susceptibility to cognitive biases, including herd mentality, overconfidence, and loss aversion, humans can make poor decisions and increase market volatility. These prejudices frequently cause investors to behave erratically and irrationally, departing from reasonable expectations and causing inefficiencies in the market. Cognitive biases have the capacity to sustain feedback loops, which heighten market turbulence and may hinder economic expansion. Similarly, cognitive biases have the potential to cause investors to misread economic indicators or ignore important details, which would increase volatility. This study uses the generalized autoregressive conditional heteroskedasticity (GARCH) model on GDP growth data from the US, the UK, and India, alongside S&P 500, FTSE 100, and NIFTY 50 data sourced from Bloomberg, to examine evidence of these biases. The results show evidence of the predictive nature of market fluctuations on economic performance across the markets and highlight the substantial effects of cognitive biases on market volatility, disregarding economic fundamentals and growth, emphasizing the necessity of considering psychological factors in financial market analyses and developing strategies to mitigate their adverse effects. [ABSTRACT FROM AUTHOR]

Herein, rGO–MnO2 nanocomposite was synthesized via a hydrothermal method. The prepared rGO–MnO2 powders underwent various characterizations to examine their structural, morphological, and electrical properties. XRD was used for preliminary identification of the synthesized powders, while Raman spectroscopy confirmed bond types and functional groups. UV–visible spectroscopy provided key insights into the electronic and optical properties through linear optical studies. SEM and TEM were employed to evaluate the catalyst’s morphological structure. Electrochemical sensing properties were analyzed using cyclic voltammetry, revealing that rGO–MnO2 exhibits good sensitivity toward histamine, making it a promising candidate for real-time histamine sensing in the human body. Additionally, the rGO–MnO2 nanocomposite demonstrated remarkable photocatalytic activity, achieving a 91.7% degradation efficiency of Eriochrome Black T, significantly higher than pure MnO2 and rGO catalysts. This enhanced performance is primarily due to effective charge transfer from MnO2 nanowires’ conduction band to reduced graphene oxide. Furthermore, the stability of the nanocomposite was confirmed through repeated experiments, and the key active radicals were identified using trapping experiments. [ABSTRACT FROM AUTHOR]

Xanthogranulomatous cholecystitis (XGC) is a rare inflammatory disease of the gallbladder (GB) that is characterized by a focal or diffuse destructive inflammatory process. We present a patient with chronic liver disease with portal hypertension who had features of obstructive jaundice due to choledocholithiasis and a palpable mass in the right hypochondrium masquerading as an empyema/carcinoma of the GB. This presentation was preceded by cholestatic jaundice due to acute hepatitis E virus infection. [ABSTRACT FROM AUTHOR]

Present study was conducted to observe effect of supplementing rumen protected methionine and choline on leukogram profile, oxidative stress, inflammatory and immunomodulatory responses during transition period in Surti buffaloes. Twenty-seven pregnant Surti buffaloes were selected and divided into three groups of nine animals each with following diet regime: Group I (Control)-basal diet, Group II (RPM)-basal diet+rumen protected methionine and Group III (RPM+RPC)-basal diet+rumen protected methionine+rumen protected choline. Supplementation of RPM @ 10 g/buffalo/day and RPC @ 50 g/buffalo/day was done from -15 d prepartum to 30 d postpartum. Blood samples were collected at start of experiment, 1st, 3rd and 6th week postpartum. At 1st and 3rd week postpartum, significantly higher level of GSH, SOD as well as TAS and lower level of LPO were observed in Group II and III as compared to control. Group III had highest SOD as well as TAS and lowest LPO levels. TNF-α and haptaglobin during postpartum period were significantly lower in Group II and III. Group III had lowest levels of TNF-α at 1st and 3rd week and haptoglobin at 1st, 3rd and 6th week postpartum. In vitro neutrophil phagocytic activity and lymphocyte proliferation were significantly higher in Group III followed by Group II and control during entire postpartum period. It was concluded that supplementation of rumen protected methionine and choline during transition phase of Surti buffaloes reduces oxidative stress as well as inflammatory tendencies and increases antioxidant status as well as immune response. Beneficial effects of supplementing both are more than supplementing rumen protected methionine alone.

Introduction: Hereditary pancreatitis (HP) is a rare debilitating disease with incompletely understood etio-pathophysiology. The reduced penetrance of genes such as PRSS1 associated with hereditary pancreatitis indicates a role for novel inherited factors.Methods: We performed whole-exome sequencing of three affected members of an Indian family (Father, Son, and Daughter) with chronic pancreatitis and compared variants with those seen in the unaffected mother.Results: We identified a novel frameshift mutation in exon 11 of TRPV6 (c.1474_1475delGT; p.V492Tfs*136), a calcium channel, in the patients. Functional characterization of this mutant TRPV6 following heterologous expression revealed that it was defective in calcium uptake. Induction of pancreatitis in mice induced Trpv6 expression, indicating that higher expression levels of the mutant protein and consequent dysregulation of calcium levels in patients with chronic pancreatitis could aggravate the disease.Discussion: We report a novel frameshift mutation in TRPV6 in an Indian family with HP that renders the mutant protein inactive. Our results emphasize the need to expand the list of genes used currently for evaluating patients with hereditary pancreatitis.

India experienced a rapid rise in COVID-19 infections from March 2021. States imposed varying levels of lockdowns and curfews to curb the spread of the disease. These restrictions severely affected the functioning of food systems. The objective of this study was to analyze how COVID-19 continues to affect agricultural production, food security and household diets of vegetable farmers. A phone-based survey was conducted with 595 vegetable farmers in the states of Andhra Pradesh, Assam, Jharkhand, Karnataka and Odisha, 60% of whom had been interviewed a year earlier. Overall, 60% of farmers experienced decreased vegetable production; over 80% reported a reduction in consumption of at least one food group; and 45% reported some level of food insecurity between May 2020 and May 2021. Farmers who reported decreased staples production, difficulty accessing seeds/seedlings, or reduced their household spending were more likely to report decreased vegetable production. Vegetable consumption was positively associated with receipt of COVID-19 relief benefits, borrowing money, or having home gardens. Farmers who received public agricultural assistance, or had reduced expenses, were more likely to have lower vegetable consumption. Greater severity of food insecurity was associated with farmers belonging to underprivileged social groups, non-Hindus, or those who experienced decrease in livestock production, weather related disruptions or received COVID-19 assistance. This is one of few studies that have conducted a longitudinal assessment of the impacts across multiple waves of COVID-19. COVID-19 is seen to be one among several shocks experienced by farm households, and exacerbated existing issues within agriculture and food security. There is a need for public policy support to strengthen both production and consumption of vegetables.