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PURPOSE OF REVIEW: To review the most recent clinical trials and data regarding epidemiology, pathophysiology, diagnosis, and treatment of heart failure with preserved ejection fraction with an emphasis on the recent trends in cardiometabolic interventions. RECENT FINDINGS: Heart failure with preserved ejection fraction makes up approximately half of overall heart failure and is associated with significant morbidity, mortality, and overall burden on the healthcare system. It is a complex, heterogenous syndrome and clinical trials, to this point, have not revealed quite as many effective treatment options when compared to heart failure with reduced ejection fraction. Nevertheless, there is an expanding amount of data insight into the pathogenesis of this disease and the potential for newer therapies and management strategies. Heart failure with preserved ejection fraction pathology has been found to be linked to abnormal energetics, myocyte hypertrophy, cell signaling, inflammation, ischemia, and fibrosis. These mechanisms also intricately overlap with the significant comorbidities often associated with heart failure with preserved ejection fraction including, but not limited to, atrial fibrillation, chronic kidney disease, hypertension, obesity and coronary artery disease. Treatment of this disease, therefore, should focus on the management and strict regulation of these comorbidities by pharmacologic and nonpharmacologic means. In this review, a clinical update is provided reviewing the most recent clinical trials and data regarding epidemiology, pathophysiology, diagnosis, and treatment of heart failure with preserved ejection fraction with an emphasis on the recent trend in cardiometabolic interventions.

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INTRODUCTION: Industry 4.0 has brought new paradigms to businesses based on high levels of automation and interconnectivity and the use of technologies. This new context has an impact on the work environment and workers. Nevertheless, these impacts are still inconclusive and controversial, requiring new investigative perspectives. This study aimed to investigate the requirements sought, the risk factors identified, and the adverse effects on workers caused by the characteristics of I4.0. METHOD: The methodology was based on a systematic literature review utilizing the PRISMA protocol, and 30 articles were found eligible. A descriptive and bibliometric analysis of these studies was performed. RESULTS: The results identified the main topics that emerged and have implications for workers' Occupational Health and Safety (OHS) and divided them into categories. The requirements are related mainly to cognitive, organizational, and technological demands. The most significant risk factors generated were associated with the psychosocial ones, but organizational, technological, and occupational factors were also identified. The adverse effects cited were categorized as psychic, cognitive, physical, and organizational; stress was the most cited effect. An explanatory theoretical model of interaction was proposed to represent the pathway of causal relations between the requirements and risk factors for the effects caused by I4.0. CONCLUSIONS AND PRACTICAL APPLICATIONS: This review has found just how complex the relationships between the principles of Industry 4.0 are (e.g., requirements, risk factors, and effects) and the human factors. It also suggests a pathway for how these relationships occur, bridging the gap left by the limited studies focused on connecting these topics. These results can help organizational managers understand the impacts of I4.0 on workers' safety and health.

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Ferroelectric tunnel junctions (FTJs) are a class of memristor which promise low-power, scalable, field-driven analog operation. In order to harness their full potential, operation with identical pulses is targeted. In this paper, several weight update schemes for FTJs are investigated, using either nonidentical or identical pulses, and with time delays between the pulses ranging from 1 µs to 10 s. Experimentally, a method for achieving nonlinear weight update with identical pulses at long programming delays is demonstrated by limiting the switching current via a series resistor. Simulations show that this concept can be expanded to achieve weight update in a 1T1C cell by limiting the switching current through a transistor operating in subthreshold or saturation mode. This leads to a maximum linearity in the weight update of 86% for a dynamic range (maximum switched polarization) of 30 µC/cm2. It is further demonstrated via simulation that engineering the device to achieve a narrower switching peak increases the linearity in scaled devices to >93% for the same range.

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The fundamental pathophysiological mechanism in the progression of chronic heart failure following acute myocardial infarction (AMI) is ventricular remodeling, in which innate and adaptive immunity both play critical roles. Myeloid-derived suppressor cells (MDSCs) have been demonstrated to function in a range of pathological conditions, such as infections, inflammation, autoimmune diseases, and tumors. However, it is unclear how MDSCs contribute to cardiac remodeling following AMI. This study aimed to identify the function and underlying mechanism of MDSCs in controlling cardiac remodeling following AMI. Following AMI in mice, MDSCs frequencies changed dynamically, considerably increased on day 7 in blood, spleens, lymph nodes and hearts, and decreased afterwards. Consistently, mice with AMI displayed enhanced cardiac function on day 14 post-AMI, reduced infract size and higher survival rates on day 28 post-AMI following the adoptive transfer of MDSCs. Furthermore, MDSCs inhibited the inflammatory response by decreasing pro-inflammatory cytokine (TNF-α, IL-17, Cxcl-1, and Cxcl-2) expression, up-regulating anti-inflammatory cytokine (TGF-ß1, IL-10, IL-4, and IL-13) expression, reducing CD3+ T cell infiltration in the infarcted heart and enhancing M2 macrophage polarization. Mechanistically, MDSCs improved the release of anti-inflammatory factors (TGF-ß1 and IL-10) and decreased the injury of LPS-induced cardiomyocytes in vitro in a manner dependent on cell-cell contact. Importantly, blockade of IL-10 partially abolished the cardioprotective role of MDSCs. This study found that MDSCs contributed to the restoration of cardiac function and alleviation of adverse cardiac remodeling after AMI possibly by inhibiting inflammation.

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The Internet of Things (IoT) is a significant technological advancement that allows for seamless device integration and data flow. The development of the IoT has led to the emergence of several solutions in various sectors. However, rapid popularization also has its challenges, and one of the most serious challenges is the security of the IoT. Security is a major concern, particularly routing attacks in the core network, which may cause severe damage due to information loss. Routing Protocol for Low-Power and Lossy Networks (RPL), a routing protocol used for IoT devices, is faced with selective forwarding attacks. In this paper, we present a federated learning-based detection technique for detecting selective forwarding attacks, termed FL-DSFA. A lightweight model involving the IoT Routing Attack Dataset (IRAD), which comprises Hello Flood (HF), Decreased Rank (DR), and Version Number (VN), is used in this technique to increase the detection efficiency. The attacks on IoT threaten the security of the IoT system since they mainly focus on essential elements of RPL. The components include control messages, routing topologies, repair procedures, and resources within sensor networks. Binary classification approaches have been used to assess the training efficiency of the proposed model. The training step includes the implementation of machine learning algorithms, including logistic regression (LR), K-nearest neighbors (KNN), support vector machine (SVM), and naive Bayes (NB). The comparative analysis illustrates that this study, with SVM and KNN classifiers, exhibits the highest accuracy during training and achieves the most efficient runtime performance. The proposed system demonstrates exceptional performance, achieving a prediction precision of 97.50%, an accuracy of 95%, a recall rate of 98.33%, and an F1 score of 97.01%. It outperforms the current leading research in this field, with its classification results, scalability, and enhanced privacy.

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BACKGROUND: Paced QRS morphology may vary during left bundle branch area pacing (LBBAP) as per the pacing location. It remains unclear whether electrocardiographic changes observed during LBBAP can predict clinical outcomes. OBJECTIVE: To assess correlation between characteristics of paced QRS on electrocardiogram and clinical outcomes in heart failure (HF) patients with non-ischemic cardiomyopathy. METHODS: Of 79 consecutive HF patients receiving LBBAP, 59 patients were included in this prospective study after exclusions. LBBAP was performed using Medtronic 3830 lead. Patients were categorized into various groups based on paced QRS morphology in lead V1 (qR and Qr), QRS axis (normal, left or right) and V6 R wave peak time (RWPT, ≤80 or >80 ms) to compare echocardiographic outcomes. RESULTS: RWPT was significantly shorter (75.7±17.5 vs 85.3±11.3 ms, P=0.014), transition during threshold test more commonly observed (81.5% vs 53%, P=0.02) and improvement in left ventricular ejection fraction (LVEF) was significantly greater in qR group (21.4±6.4 vs 16.4±8.3%, P=0.013) compared to Qr group. RWPT or LVEF did not differ in patients with different paced QRS axis (P>0.05). While qR morphology and presence of transition during threshold test independently predicted LVEF improvement, RWPT lacked predictive value. Non-responders had greater incidence of loss of 'R' prime (P=0.009) and prolonged RWPT (P=0.003) on follow up compared to average and super-responders. CONCLUSIONS: Paced qR morphology and transition during threshold test predicted greater improvement in LVEF while RWPT lacked predictive value. Loss of terminal 'R' in lead V1 and prolongation of RWPT on follow up prognosticated non-response to LBBAP.

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BACKGROUND: Heart failure (HF) is the leading cause of morbidity and mortality worldwide. Stemness refers to the self-renewal and differentiation ability of cells. However, little is known about the heart's stemness properties. Thus, the current study aims to identify putative stemness-related biomarkers to construct a viable prediction model of HF and characterize the immune infiltration features of HF. METHODS: HF datasets from the Gene Expression Omnibus (GEO) database were adopted as the training and validation cohorts while stemness-related genes were obtained from GeneCards and previously published papers. Feature selection was performed using two machine learning algorithms. Nomogram models were then constructed to predict HF risk based on the selected key genes. Moreover, the biological functions of the key genes were evaluated using Gene Ontology (GO) and Kyoto Encyclopedia of Genes Genomes (KEGG) pathway analyses, and gene set variation analysis (GSVA) and enrichment analysis (GSEA) were performed between the high- and low-risk groups. The immune infiltration landscape in HF was investigated, and the interaction network of key genes was analysed to predict potential targets and molecular mechanisms. RESULTS: Seven key genes, namely SMOC2, LUM, FNDC1, SCUBE2, CD163, BLM and S1PR3, were included in the proposed nomogram. This nomogram showed good predictive performance for HF diagnosis in the training and validation sets. GO and KEGG analyses revealed that the key genes were primarily associated with ageing, inflammatory processes and DNA oxidation. GSEA and GSVA identified various inflammatory and immune signalling pathways that were enriched between the high- and low-risk groups. The infiltration of 15 immune cell subsets suggests that adaptive immunity has an important role in HF. CONCLUSIONS: Our study identified a clinically significant stemness-related signature for predicting HF risk, with the potential to improve early disease diagnosis, optimize risk stratification and provide new strategies for treating patients with HF.

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BACKGROUND AND AIM: Remnant cholesterol (RC) is substantially related to negative outcomes in cardiac patients. Patients with coexisting hypertension and heart failure (HF) often develop left ventricular hypertrophy (LVH) and have poor prognoses. This study investigated baseline RC levels and LV remodelling and patients' prognoses. METHODS AND RESULTS: Six hundred thirty consecutive individuals with hypertension and HF participated in this prospective trial from October 2018 to August 2020. Based on left ventricular mass index (LVMI), 560 those eligible were separated into LVH and non-LVH groups. Multiple linear regression and receiver operating characteristic (ROC) curves examined the RC and LV relationship. A Cox regression analysis was conducted to examine the predictive value of RC for clinical outcomes. The LVH group presented significantly elevated values of RC, triglyceride, and cholesterol and decreased high-density lipoprotein cholesterol (HDLC). The optimal cutoff value for RC to predict LV remodelling was 0.49. The subjects were observed for a median of 58 months, and 104 participants met the primary endpoint. The risk models involving the two Cox models were adjusted to incorporate confounding factors, which revealed that those with elevated baseline levels of RC were more susceptible to cardiovascular mortality, as shown by an increased hazard ratio. (HR: 1.91, 95% CI: 1.62-2.26 vs. HR: 1.75, 95% CI: 1.43-2.16, P < 0.001). CONCLUSIONS: RC is linked to LV remodelling in patients with hypertensive HF, with LVH having greater RC values. Moreover, patients with hypertensive HF who had a higher RC suffered from an increased risk of cardiovascular mortality. TRIAL REGISTRATION: NCT03727828, 21 Oct 2018.

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BACKGROUND: The PARALLEL-HF trial showed that treatment with sacubitril/valsartan resulted in more symptomatic hypotension versus enalapril in Japanese patients with heart failure (HF) and reduced ejection fraction, similar to PARADIGM-HF. Use of sacubitril/valsartan in these patients may be limited by concerns regarding hypotension. METHODS: This post-hoc analysis characterized hypotension-related adverse events (AEs) and their effects on efficacy using data from PARALLEL-HF, in which patients received sacubitril/valsartan 200 mg twice daily or enalapril 10 mg twice daily. RESULTS: Of 223 patients, 28.2 % experienced hypotension-related AEs and incidence was higher with sacubitril/valsartan versus enalapril (hazard ratio, 2.2; 95 % CI, 1.3-3.8; p = 0.0027). However, reduction in mean systolic blood pressure from baseline to study end did not significantly differ (sacubitril/valsartan: -2.2 mmHg vs enalapril: -1.3 mmHg; p = 0.6895). Patients who experienced hypotension-related AEs had lower mean body mass index, higher median N-terminal pro-brain natriuretic peptide at randomization, and more frequent history of stroke. Hypotension-related AEs leading to treatment discontinuation were not significantly different for sacubitril/valsartan versus enalapril (3.4 % vs 6.9 %, p = 0.5957). Reduction in risk of cardiovascular death or HF hospitalization was similar with sacubitril/valsartan versus enalapril in patients with or without hypotension-related AEs. CONCLUSIONS: Incidence of hypotension-related AEs was higher in the sacubitril/valsartan versus enalapril group but did not affect risk of cardiovascular death or HF hospitalization, which was similar between treatment groups.

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In end-stage heart failure, which is characterized by persistent or progressive ventricular dysfunction despite optimal medical therapy, a left ventricular assist device (LVAD) can be beneficial. Congestive heart failure provokes inflammatory and prothrombotic activation. The aim of this study was to evaluate the serum concentration of citrullinated histone 3 (CH3) representing neutrophil extracellular trap (NET) formation in patients referred for LVAD implantation. There were 10 patients with a median age of 61 (57-65) years enrolled in a prospective single-center analysis who underwent LVAD implantation. The CH3 plasma concentration was measured preoperatively and on the 1st and 7th postoperative days, followed by control measurements on the median (Q1-3) 88th (49-143) day. The preoperative CH3 concentration strongly correlated with brain natriuretic peptide (r = 0.879, p < 0.001). Significant differences in CH3 serum concentration were observed between pre- and postoperative measurements, including an increase on the first postoperative day (p < 0.001), as well as a decrease on the seventh day (p = 0.016) and in follow-up (p < 0.001). CH3 concentration, as a marker of NET formation, decreases after LVAD implantation.

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Background: Mechanical circulatory support (MCS), temporary or durable, is essential in patients with acute heart failure presenting in cardiogenic shock (CS). MCS is fundamental in patients with advanced heart failure when used as a bridge to decision, transplant or left ventricular recovery. Limited data on acute-on-chronic heart failure (HF) patients exists in the era of axillary mechanical circulatory support with the Impella 5.5. We describe a case of chronic ischemic cardiomyopathy, HF-CS, in a patient who underwent Impella placement, medical optimization, and explant, now with sustained normalization in ejection fraction. Case summary: A Caucasian female in her 50 s was referred to our center for evaluation for advanced therapies, including transplantation or durable left ventricular assist device placement. Her initial ejection fraction was 30% with comorbidities including multivessel coronary artery disease revascularized with 3 vessel bypass grafting ten years prior, type 2 diabetes (A1c 8.6%), and peripheral vascular disease. During her evaluation, she had acute decompensation leading to cardiogenic shock and required hospitalization with inotrope initiation, which was unable to be weaned. She was approved for organ transplant and listed; however, she required escalation of support and eventual placement of right axillary Impella 5.5. While on Impella support, her vasoactive needs reduced, and she was found to have left ventricular recovery and tolerated the initiation of guideline medical therapy. After three weeks of support, the Impella was weaned and explanted, and the patient was discharged. She remains stable with a sustained ejection fraction of greater than 50% with NYHA class 1 functional status at follow-up. One year later, the patient showed sustained myocardial recovery with guideline-directed medical therapy (GDMT). Conclusion: Our case highlights a unique approach in patients with long-standing (>5 years) heart failure who may benefit from early consideration for axillary support and concomitant optimization with guideline-directed medical therapy to assess for explant and native heart recovery.

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Background: Heart failure (HF) remains one of the most common events in the progression of hypertension. Magnoflorine (MNF) has been shown beneficial effects on the cardiovascular system. However, the action of MNF on angiotensin (Ang) II-induced cardiac remodeling and its underlying mechanisms have not yet been characterised. Here, we assessed the action of MNF in the development of hypertension-related HF. Methods: C57BL/6 male mice were subjected to Ang II through a micro-osmotic pump infusion continuously for 4 weeks to induce hypertensive HF. MNF (10 and 20 mg/kg) was administered in the final 2 weeks. Ang II content was measured by enzyme-linked immunosorbent assay (ELISA) kit. Values of ejection fraction (EF) and fractional shortening (FS) were detected using an ultrasound diagnostic instrument. The mRNA levels of hypertrophic and fibrotic genes were determined by real-time quantitative polymerase chain reaction (RT-qPCR). Haematoxylin and eosin (H&E), wheat germ agglutinin (WGA), Masson trichrome, and Sirius Red staining were used to analyse pathologic changes in heart tissues. The expression levels of phosphorylated AMP-activated protein kinase (AMPK), light chain 3 microtubule associated protein II (LC3 II) to LC3 I, and p62 were detected by western blot assay. Results: MNF significantly improved cardiac dysfunction and the content of creatine kinase-MB without altering blood pressure in Ang II-challenged mice. MNF obviously corrected the phenotypes of cardiac hypertrophy and fibrosis, including the high mRNA levels of atrial natriuretic peptide (Anp), brain natriuretic peptide (Bnp), collagen1a (Col1a1), transforming growth factor beta (Tgfb1), enlarged myocardial areas, and increased positive areas of Masson trichrome and Sirius Red staining. In addition, MNF alleviated oxidative injury, reflected by the upregulation of glutathione and the downregulation of reactive oxygen species and malondialdehyde. The activation of AMPK was elevated accompanied by an increased level of autophagy by MNF in hypertensive heart tissues. The therapeutic action of MNF was confirmed in Ang II-challenged H9c2 cells. Specifically, the AMPK inhibitor could eliminate the autophagy pathway in which MNF is involved. Conclusions: MNF has benefits in hypertension-induced cardiac remodeling, which was partially associated with the improvement of oxidative stress via the mediation of the AMPK/autophagy axis.

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Many metal-organic frameworks (MOFs) incorporate nodes that are metal oxide clusters, and ligands that have been observed on these nodes include formates, acetates, water, hydroxyl groups, and others, all of which are potentially important in affecting reactivities for applications in separations, catalysis, and sensing. Formate is a common node ligand, arising from formic acid used as a modulator and from N,N-dimethylformamide used as a solvent in MOF syntheses. Yet only little work has been reported characterizing the reactivities of node formate ligands. Infrared spectra reported here show that formate bonds to two types of sites on the paired Hf6O8 nodes of hcp UiO-66, namely, defect and µ2-OH sites. Quantifying the number of formate ligands by 1H NMR spectroscopy of digested samples showed an almost equal number of formate ligands on the two sites, indicating the likelihood that they neighbor each other. These formate ligands interact with water molecules, reversibly switching their bonding from bidentate to monodentate. The formates on µ2-OH sites of hcp Hf-UiO-66 interact much more strongly with water than those on defect sites of the same node, and both interact more strongly than isolated defect sites of Hf-UiO-66. Correspondingly, the catalytic activities of hcp UiO-66 determined as turnover frequencies on each site are approximately twofold higher than those on UiO-66, bolstering the inference that methanol dehydration is catalyzed by a node defect site and a neighboring node µ2-OH site. The results show how MOFs, with their well-defined node structures, provide unprecedented opportunities to understand details of reactivities and catalysis on metal oxide clusters, in contrast to bulk metal oxide surfaces.

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Hydrofluoric Acid (HF) is considered one of the most hazardous chemicals used in industrial plants. Even small exposures to HF can have fatal consequences if not promptly and properly treated. Various research teams have presented numerous substances with the objective of capturing or detecting toxic HF gas. In this study, we explore the impact of HF gas on a single layer of SnS by employing density functional theory (DFT). The interaction nature between the gas molecule and the adsorbent is elucidated by analyzing the related adsorption energy, electronic structure properties and differential charge transfer. The findings indicate that HF is physically adsorbed on the pristine SnS with an adsorption energy value of -0.63 eV. By introducing a Sn mono vacancy defect, the modification of SnS enhances the adsorption energy to -1.26 eV, resulting in a chemisorption process. Molecular fluorine (F2) was discovered to undergo a barrierless reaction with SnS, resulting in the formation of fluorine-substituted SnS. It has been discovered that the substitution of fluorine atoms enhances the reactivity of SnS towards hydro-gen fluoride gas. The adsorption potential of the studied structures towards HF gas was determined to be in the following order: F2SnS > VSn-SnS > VS-SnS âˆ¼ SnS. The current study is anticipated to offer new molecular insights that could lead to the creation of innovative devices for detecting or eliminating HF toxic gas from a specific atmosphere.

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INTRODUCTION: Menstrual cycle characteristics are regulated hormonally and are integrated at the level of the hypothalamus. Stress can affect the hypothalamic-pituitary gonadal axis. The objective of the study was to analyse the stress levels of women and compare their autonomic tone and menstrual characteristics. METHODOLOGY: A group of 100 apparently healthy, young, female volunteers were included in this pilot cohort study. Subjects were assessed for perceived stress using the Perceived Stress Scale 14 Item (PSS-14) questionnaire, underwent a heart rate variability (HRV) test on the second, 10th, and 21st days of their menstrual cycle, and their menstrual history was recorded. The statistical analysis was done using Statistical Product and Service Solutions (SPSS, version 21.0; IBM SPSS Statistics for Windows, Armonk, NY) software. Metric data were expressed in terms of numerical value and analysed as mean ± SD. Paired Student's T-test was used to compare the HRV data of all three days of the menstrual cycle separately, and p value<0.05 was considered significant. Menstrual irregularity was complained of by 13 subjects (Group A), and the rest (87 subjects) reported regular menses (Group B). RESULT: The perceived stress scores of Group A were significantly higher than Group B (32.53±5.062 vs 28.057±7.618; p=0.044). On second day, Group A had higher median R-R interval (714.38±106 vs 656.84±73.50 ms; p=0.015) and lower average heart rate (85.85±12.07 vs 92.39±9.98 bpm; p=0.034) than Group B, suggesting parasympathetic dominance. On the 10th day, Group A had a higher standard deviation of heart rate (7.09±1.88 vs 5.97±1.71 bpm; p=0.032) and a very low-frequency band (1105.94±984.12 vs 730.49±557.41 µs2; p=0.046) than Group B, indicating parasympathetic dominance in Group A. On the 21st day, Group A had a higher standard deviation of R-R interval (58.19±20.46 vs 44.85±14.55 ms; p=0.004), root mean square standard deviation (55.71±29.84 vs 31.89±15.99 ms; p<0.001), percentage of R-R differing by 50 ms (19.20±19.58 vs 10.87±10.31%; p=0.020), total power (3,440.23±2722.29 vs 2,068.28±1,322.49 µs2; p=0.004), high-frequency band (1,247.57±1173.54 vs 539.06±HPO438.92 µs2; p<0.001), standard deviation ratio of the Poincaré plot (0.53±0.19 vs 0.39±0.16; p=0.003), normalised HF (44.0±12.9 vs 35.4±10.6; p=0.009), and a lower LF/HF ratio (1.43±0.80 vs 2.11±1.16; p=0.043) and normalised LF (53.9±14.4 vs 64.1±11.9; p=0.006) than Group B, suggesting higher parasympathetic tone of Group A than Group B. CONCLUSION: Analysing these results, it can be concluded that, in apparently healthy young women, menstrual irregularity is a physiological adaptation to combat perceived stress and maintain parasympathetic dominance.

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Cardiovascular disease (CVD) stands as one of the leading causes of morbidity and mortality worldwide, and the continued search for novel therapeutics is vital for addressing this global health challenge. Over the past decade, hydrogen sulfide (H2S) has garnered significant attention in the field of medical research, as it has been proven to be a cardioprotective gaseous signaling molecule. It joins nitric oxide and carbon monoxide as endogenously produced gasotransmitters. As for its mechanism, H2S functions through the posttranslational addition of a sulfur group to cysteine residues on target proteins in a process called sulfhydration. As a result, the observed physiological effects of H2S can include vasodilation, anti-apoptosis, anti-inflammation, antioxidant effects, and regulation of ion channels. Various studies have observed the cardioprotective benefits of H2S in diseases such as myocardial infarction, ischemia-reperfusion injury, cardiac remodeling, heart failure, arrhythmia, and atherosclerosis. In this review, we discuss the mechanisms and therapeutic potential of H2S in various CVDs.

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Surface waters are vulnerable to contamination by human and animal feces, posing risks to human health due to potential exposure to enteric pathogens. This research developed a colorimetric loop-mediated isothermal amplification (cLAMP) assay to detect sewage associated Bacteroides dorei HF183/BacR287 (HF183) marker in wastewater and environmental water samples. The host sensitivity and host specificity of the assay were evaluated, and their performance was compared to the Bacteroides HF183 qPCR assay using control materials (gBlocks), environmental water samples seeded with untreated sewage, and ambient environmental water samples. In serial dilutions of control materials, qPCR produced quantifiable data across all dilutions, while cLAMP detected the marker down to 0.001 pg/µL of control materials, which was two orders of magnitude less sensitive than qPCR. All untreated sewage samples (n = 12) tested positive for HF183 by both the qPCR and cLAMP assays, demonstrating a host sensitivity value of 1.00 (maximum value of 1.00). The host specificity by analysing 70 non-human fecal nucleic acid samples revealed cLAMP's specificity value of 0.81 compared to qPCR's 0.64. When testing sewage-seeded environmental water samples, both methods detected HF183 for the lowest amount of sewage, indicating similar detection sensitivity. The application of cLAMP for tracking sewage pollution in environmental waters showed promising results, with moderate agreement between cLAMP and qPCR (κ = 0.510). However, cLAMP occasionally missed detections compared to qPCR, particularly in low-concentration samples. Overall, the cLAMP HF183 assay demonstrated promising potential as a rapid and sensitive method for detecting sewage pollution, offering a viable alternative to qPCR in certain environmental monitoring scenarios.

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