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BackgroundAs a sensitive diagnostic marker for myocardial infarction (MI) in people with normal renal function, elevated high sensitivity cardiac troponin T (hs-cTnT) was often found in chronic kidney disease (CKD) patients requiring dialysis. However, the accuracy of baseline hs-cTnT in the diagnosis of MI (including Type 1 MI (T1MI) and Type 2 MI (T2MI)) in dialysis patients is still controversial. The aim of this study was to retrospectively explore whether there were any clinical indices that could increase the predictive value of hs-cTnT on admission for MI occurrence in dialysis patients.MethodsHere, 136 patients with uremia who underwent regular dialysis with coronary angiography in the First Affiliated Hospital of Nanjing Medical University from August 2017 to October 2021 were enrolled. According to the coronary angiography results and the presence of clinical symptoms, the patients were divided into: (1). AMI group (n = 69; angiography positive) and Control group (n = 67; angiography negative); (2). T1MI group (n = 69; angiography positive), T2MI group (n = 7; angiography negative & symptomatic), and Control group (n = 60; angiography negative & asymptomatic).ResultsHere, we found the mean hs-cTnT on admission in the Control group was much lower than that in the AMI group. Hs-cTnT alone had a mediocre predictive performance, with an AUROC of 0.7958 (95% CI: 0.7220, 0.8696). Moreover, the ROC curve of hs-cTnT combined with the Triglyceride (TG), Time of dialysis, and Albumin (Alb) showed a higher sensitivity area [0.9343 (95% CI: 0.8901, 0.9786)] than that of single hs-cTnT. Next, hs-cTnT combined with the TG, Time of dialysis, and Alb also presented a better performance in predicting T1MI [0.9150 (95% CI: 0.8678, 0.9621)] or T2MI (0.9167 [0.9167 (95% CI: 0.8427, 0.9906)] occurrences. Last, these combined variables could better distinguish patient between T1MI and T2MI group than hs-cTnT alone.ConclusionsOn admission, a combination of hs-cTnT, TG, Time of dialysis, and Alb presented a higher sensitivity than hs-cTnT alone in predicting MI occurrence in dialysis patients, suggesting a better diagnostic approach for future clinical applications.

BACKGROUND: Unraveling gene–environment interaction can provide a novel insight into early disease prevention. Nevertheless, current understanding of the interplay between genetic predisposition and air pollution in relation to myocardial infarction (MI) risk remains limited. Furthermore, the potential long-term influence of air pollutants on MI incidence risk warrants more conclusive evidence in a community population. OBJECTIVE: We investigated interactions between genetic predisposition and exposure to air pollutants on MI incidence. METHODS: This study incorporated a sample of 456,354 UK Biobank participants and annual mean air pollution (PM2.5, PM10, NO2, and NOx) from the UK Department for Environment, Food and Rural Affairs (2006–2021). The Cox proportional hazards model was employed to explore MI incidence after chronic air pollutants exposure. By quantifying genetic risk through the calculation of polygenic risk score (PRS), this study further examined the interactions between genetic risk and exposure to air pollutants in the development of MI on both additive and multiplicative scales. RESULTS: Among 456,354 participants, 9,114 incident MI events were observed during a median follow-up of 12.08 y. Chronic exposure to air pollutants was linked with an increased risk of MI occurrence. Specifically, the hazard ratios (per interquartile range) were 1.12 (95% CI: 1.10, 1.13) for PM2.5, 1.20 (95% CI: 1.19, 1.22) for PM10, 1.13 (95% CI: 1.12, 1.15) for NO², and 1.12 (95% CI: 1.11, 1.13) for NOx. In terms of the joint effects, participants with high PRS and high level of air pollution exposure exhibited the greatest risk of MI among all study participants (∼255% to 324%). Remarkably, both multiplicative and additive interactions were detected in the ambient air pollutants exposure and genetic risk on the incidence of MI. DISCUSSION: There were interactions between exposure to ambient air pollutants and genetic susceptibility on the risk of MI onset. Moreover, the joint effects of these two exposures were greater than the effect of each factor alone. [ABSTRACT FROM AUTHOR]

Lipoprotein(a) (Lp[a]) is associated with an increased risk of myocardial infarction (MI). However, the mechanism underlying this association has yet to be fully elucidated. This multicenter study aimed to investigate whether association between Lp(a) and MI risk is reinforced by the presence of low-attenuation plaque (LAP) identified by coronary computed tomography angiography (CCTA). In a derivation cohort, a total of 5,607 patients with stable chest pain suspected of coronary artery disease who underwent CCTA and Lp(a) measurement were prospectively enrolled. In validation cohort, 1,122 patients were retrospectively collected during the same period. High Lp(a) was defined as Lp(a) ≥50 mg/dL. The primary endpoint was a composite of time to fatal or nonfatal MI. Associations were estimated using multivariable Cox proportional hazard models. During a median follow-up of 8.2 years (Q1-Q3: 7.2-9.3 years), the elevated Lp(a) levels were associated with MI risk (adjusted HR [aHR]: 1.91; 95% CI: 1.46-2.49; P < 0.001). There was a significant interaction between Lp(a) and LAP (P interaction <0.001) in relation to MI risk. When stratified by the presence or absence of LAP, Lp(a) was associated with MI in patients with LAP (aHR: 3.03; 95% CI: 1.92-4.76; P < 0.001). Mediation analysis revealed that LAP mediated 73.3% (P < 0.001) for the relationship between Lp(a) and MI. The principal findings remained unchanged in the validation cohort. Elevated Lp(a) augmented the risk of MI during 8 years of follow-up, especially in patients with LAP identified by CCTA. The presence of LAP could reinforce the relationship between Lp(a) and future MI occurrence. [Display omitted] [ABSTRACT FROM AUTHOR]

Monsoon Inversion (MI) plays a key role and is one of the semi-permanent features of Asian Summer Monsoon. MI is defined as a sustained temperature inversion (TI) that is observed in the lower troposphere, during summer monsoon (June to September) over the Western AS (WAS) with its peak between July and August. A comprehensive analysis of formation, evolution, and dissipation of MI is made using long-term observations from satellites and ERA-5 reanalysis of 15 years (2008–2022). The climatological day-to-day and monthly variations of MI over the Arabian Sea are studied. The occurrence of inversion (TI) during pre-monsoon, i.e., during April and May, is at a lower altitude and is strengthened by subsidence. The MI is found to occur strongly over the WAS, while it is seen occasionally with lesser strength over the Eastern Arabian Sea (EAS) during July–August. The advection is nearly five times stronger than subsidence. The reasons for the existence and strength of MI are investigated using the data of dust from the CALIPSO. There is a ~ 15% difference in the occurrence of dust over WAS compared to EAS. Also, MI occurrence has shown significant differences in temperature profiles during dust and non-dust cases. The analysis of MI reveals that strong MI is due to more advection of warm dry and dust laden air from desert regions (west, north and northwest directions). The present study has significance to the understanding of interannual monsoon variability. [ABSTRACT FROM AUTHOR]

Background—The identification and stratification of patients at risk of fatal outcomes after myocardial infarction (MI) is of considerable interest to guide secondary prevention therapies. Currently, no accurate biomarkers are available to identify subjects who are at risk of suffering acute manifestations of coronary heart disease as well as to predict adverse events after MI. Non-coding circulating microRNAs (miRNAs) have been proposed as novel diagnostic and prognostic biomarkers in cardiovascular diseases. The aims of the study were to investigate the clinical value of a panel of circulating miRNAs as accurate biomarkers associated with MI and mortality risk prediction in patients with documented MI. Methods and Results—seven circulating plasma miRNAs were analyzed in 67 MI patients and 80 control subjects at a high cardiovascular risk but without known coronary diseases. Multivariate logistic regression analyses demonstrated that six miRNAs were independently associated with MI occurrence. Among them, miR-223 and miR-186 reliably predicted long-term mortality in MI patients, in particular miR-223 (HR 1.57 per one-unit increase, p = 0.02), after left ventricular ejection fraction (LVEF) adjustment. Kaplan–Meier survival analyses provided a predictive threshold value of miR-223 expression (p = 0.028) for long-term mortality. Conclusions—Circulating miR-223 and miR-186 are promising predictive biomarkers for long-term mortality after MI. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) is one of the leading causes of death in Europe. It is known that atherosclerosis is the primary risk factor of CAD development. MMP-9 is involved in all stages of atherosclerosis and thus may contribute to CAD emergence. To investigate the influence of MMP-9 on the (CAD) development 25 patients with intact coronary arteries (CA), 40 patients with acute coronary syndrome (ACS), and 63 patients with chronic coronary syndrome (CCS) were enrolled in the study. Real-time PCR was carried out for genotyping on the rs17567-polymorphic locus, and ELISA study was performed to measure the MMP-9 plasma concentration. It was found the lower risk of MI occurrence for AG-carriers ( P a = 0.023 ; ORa = 0.299, 95% CI = 0.106–0.848) in Ukrainian population. [ABSTRACT FROM AUTHOR]

Nontuberculous mycobacterium (NTM) infections are increasing in the USA and have a high cost burden associated with treatment. Thus, it is necessary to understand what changes could be contributing to this increase in NTM disease rate. Water samples from 40 sites were collected from around the USA. They represented three water types: groundwater disinfected with chlorine and surface water disinfected with chlorine or monochloramine. Two methods, culture and qPCR, were used to measure M. avium and M. intracellulare. Heterotrophic bacteria and NTM counts were also measured. M. avium and M. intracellulare were molecularly detected in 25% (73/292) and 35% (102/292) of samples. The mean concentrations of M. avium and M. intracellulare were 2.8 × 103 and 4.0 × 103 genomic units (GU) L−1. The Northeast sites had the highest sample positively rate for both M. avium and M. intracellulare. The highest NTM counts and M. avium concentrations were observed in the surface water treated with chloramine. Geographic location and source water/disinfectant type were observed to significantly influence M. avium and M. intracellulare occurrence rates. These studies can help improve public health risk management by balancing disinfectant treatments and diverse microbial loads in drinking water. Key points: • M. avium (MA) culture rate increased significantly: 1% (1999) to 13%. • Culture versus qPCR method: 13% vs 31% for MA and 6% vs 35% for MI. • The results of each method type tell two different stories of MA and MI occurrence. [ABSTRACT FROM AUTHOR]

Background: Myocardial infarction (MI) is one of the most common presentations of coronary artery diseases that the age of its prevalence is decreasing. Survivors of MI are at an increased risk of the recurrence of the disease. This study aimed to determine the frequency of recurrent MI and its ppredictive factors in patients with MI. Methods: This descriptive cross-sectional study was conducted on 398 patients with MI referred to Dr. Heshmat hospital in Rasht, the exclusive heart center in Guilan province (north of Iran). Convenience sampling method was used and a valid six-part questionnaire including demographic information, patient's desire to improve knowledge, adherence to the Mediterranean diet, patients' awareness of factors predisposing to re-MI, depression status, and adherence to the therapeutic regimen was employed to collect data. The data were analyzed using descriptive statistics and analytical statistics in SPSS21 at the significance level of P≤ 0.05. Results: The results of the Logistic regression analysis performed by LR method indicated illness duration (OR=0.97, 95% CI=0.95-0.99), history of receiving education (OR=0.1, 95% CI=0.02–0.7), MI type (OR=0.04, 95% CI=0.01–0.34 and OR=0.006, 95% CI=0.001–0.1, respectively for Ant-MI and Post-MI than non-ST-elevation MI) and level of patients' awareness of predisposing factors to MI occurrence (OR=7.31, 95% CI=1.17–45.71, moderate level than good level) as predictors of re-MI. Conclusion: The findings of this study urges policymakers and planners to consider the necessity of applying educational programs related to factors affecting the recurrence of MI. [ABSTRACT FROM AUTHOR]

Introduction Myocardial infarction (MI), a potentially fatal cardiovascular condition, develops when the blood flow through the coronary arteries is diminished due to various factors, leading to inadequate oxygen supply to [...], BACKGROUND: Unraveling gene--environment interaction can provide a novel insight into early disease prevention. Nevertheless, current understanding of the interplay between genetic predisposition and air pollution in relation to myocardial infarction (MI) risk remains limited. Furthermore, the potential long-term influence of air pollutants on MI incidence risk warrants more conclusive evidence in a community population. OBJECTIVE: We investigated interactions between genetic predisposition and exposure to air pollutants on MI incidence. METHODS: This study incorporated a sample of 456,354 UK Biobank participants and annual mean air pollution ([PM.sub.2.5], [PM.sub.10], [NO.sub.2], and [NO.sub.x]) from the UK Department for Environment, Food and Rural Affairs (2006-2021). The Cox proportional hazards model was employed to explore MI incidence after chronic air pollutants exposure. By quantifying genetic risk through the calculation of polygenic risk score (PRS), this study further examined the interactions between genetic risk and exposure to air pollutants in the development of MI on both additive and multiplicative scales. RESULTS: Among 456,354 participants, 9,114 incident MI events were observed during a median follow-up of 12.08 y. Chronic exposure to air pollutants was linked with an increased risk of MI occurrence. Specifically, the hazard ratios (per interquartile range) were 1.12 (95% CI: 1.10, 1.13) for [PM.sub.2.5], 1.20 (95% CI: 1.19, 1.22) for [PM.sub.10], 1.13 (95% CI: 1.12, 1.15) for [NO.sub.2], and 1.12 (95% CI: 1.11, 1.13) for [NO.sub.x]. In terms of the joint effects, participants with high PRS and high level of air pollution exposure exhibited the greatest risk of MI among all study participants ( ~ 255% to 324%). Remarkably, both multiplicative and additive interactions were detected in the ambient air pollutants exposure and genetic risk on the incidence of MI. DISCUSSION: There were interactions between exposure to ambient air pollutants and genetic susceptibility on the risk of MI onset. Moreover, the joint effects of these two exposures were greater than the effect of each factor alone. https://doi.org/10.1289/EHP14291

Cardiovascular diseases (CVDs) constitute the first cause of death among the population of developing and developed countries. Atherosclerosis, which is a disorder with multifactorial etiopathogenesis, underlies most CVDs. The available literature includes ample research studies on the influence of classic cardiovascular (CV) risk factors. However, environmental exposure to heavy metals, among other substances, is still an unappreciated risk factor of CVDs. This study aimed to assess the concentration of some heavy metals (copper (Cu), zinc (Zn), manganese (Mn), cobalt (Co), and iron (Fe)) in the blood serum of postmyocardial infarction (post-MI) patients and patients free from myocardial infarction (MI) as well as estimate the relationship between the occurrence of MI and increased concentration of heavy metals. The concentration of heavy metals (Cu, Zn, Mn, Co, and Fe) was assessed using the inductively coupled plasma mass spectrometry technique in a group of 146 respondents divided into two groups: post-MI group (study group (SG), n = 74) and group without cardiovascular event (CVE) having a low CV risk (control group (CG), n = 72). The concentration of the analyzed heavy metals was higher in SG. All the heavy metals showed a significant diagnostic value p < 0.001 . The highest value of area under the curve (AUC) was observed for manganese (Mn) (0.955; 95% confidence interval (CI) = 0.922–0.988), while the lowest value was found for zinc (Zn) (0.691; 95% CI = 0.599–0.782). In one-dimensional models, high concentrations of each of the analyzed heavy metals significantly increased the chances of having MI from 7-fold (Cu) to 128-fold (Mn). All the models containing a particular metal showed a significant and high discrimination value for MI occurrence (AUC 0.72–0.92). Higher concentrations of Cu, Zn, Mn, Co, and Fe were found to considerably increase the chances of having MI. Considering the increasingly higher environmental exposure to heavy metals in recent times, their concentrations can be distinguished as a potential risk factor of CVDs. [ABSTRACT FROM AUTHOR]

We hypothesized that tumor necrosis factor receptor 1 (TNFR1) levels are associated with long-term trajectories of functional status independently of vascular risk factors and the occurrence of stroke and myocardial infarction (MI) during follow-up. In the Northern Manhattan Study, stroke-free persons aged ≥40 years in northern Manhattan (New York, New York) had annual assessments with the Barthel index (BI) for a median of 13 years (1993-2015). Assessment of baseline demographic factors, risk factors, and laboratory studies included measurement of TNFR1 (n = 1,863). Generalized estimating equations models were used to estimate standardized associations between TNFR1 and 1) baseline functional status and 2) change in function over time, adjusting for demographic factors, vascular risk factors, social variables, cognition, and depression, as well as stroke and MI occurrence during follow-up. The mean age of participants was 70 (standard deviation (SD), 10) years; 66% were women, and 55% were Hispanic. The mean TNFR1 level was 2.57 mg/L. TNFR1 was associated with baseline BI (-0.93 BI points per SD increment in TNFR1; 95% confidence interval: -1.59, -0.26) and change over time (-0.36 BI points per year per SD increment in TNFR1; 95% confidence interval: -0.69, -0.03). In this large population-based study, higher TNFR1 levels were associated with greater baseline disability and disability over time, even with adjustment for baseline covariates and stroke and MI occurrence during follow-up. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Major adverse cardiovascular events occurrences of patients with different cardiac troponin-I (cTnI) levels following percutaneous coronary intervention (PCI) remained controversial. The prognostic relevance and risk factors of PCI-related myocardial infarction (MI) were not very clear as well. PATIENTS AND METHODS: Our study included 249 coronary artery disease patients without preoperative cTnI elevation who successfully accepted PCI from 2013 to 2014. A three-year follow-up was conducted for each patient. The patients were divided into PCI-related MI group and non-PCI-related MI group. Risk factors of PCI-related MI were first explored. The occurrence of MACE was recorded. The prognostic relevance between PCI-related MI (PMI) group and non-PCI-related MI group, as well as different postoperative cTnI levels, were compared. RESULTS: Low-density lipoprotein cholesterol (LDL-C), age, Gensini Score, total stent length, and intra-operative complication were found positively correlated with PCI-related MI occurrence, while hemoglobin and prior PCI history were negatively correlated. After 3-year follow-up, the Kaplan-Meier survival curve showed MACE occurrence was significantly increased in PCI-related MI group. Comparing to patients with normal postoperative cTnI, MACE occurrence was increased in patients with a 10xupper limit of normal (ULN)≤cTnI<70xULN and cTnI≥ 70xULN, while there was no difference in patients with 1xULN≤cTnI<5xULN and 5xULN≤cTnI< 10xULN. Cox proportional hazard regression analysis revealed PMI, NT-proBNP, and left ventricular ejection function (LVEF)<50% were positively correlated with MACE occurrence, while maximum inflation pressure and apoA-I were negatively correlated. CONCLUSIONS: Prognosis of PCI-related MI was poor, as well as in patients with postoperative cTnI≥10xULN. Among the risk factors of PMI, LDL-C, age, Gensini Score, total stent length, and intra-operative complication were positively correlated with PCI-related MI occurrence, while hemoglobin and prior PCI history were negatively correlated. [ABSTRACT FROM AUTHOR]

The rapid rise of cyanotoxins production poses a serious threat to global freshwater ecosystems and has become an important issue of global public health. In Africa, a continent facing serious environmental problems, including poisoning by cyanotoxins, knowledge of the presence and distribution of these toxins remains limited. The primary objective of our review is to assess the occurrence and distribution of cyanotoxins, particularly microcystins (MCs), in African freshwater ecosystems. We aim to analyze the limited but existing literature on this subject, focusing specifically on studies published between 2001 and 2023. Recognizing the scarcity of research on this topic in Africa, we strive to elucidate the emerging patterns of toxin variants and their correlation with environmental variables, such as water temperature and nutrient concentrations. Our investigation reveals MCs as the predominant cyanobacterial secondary metabolites detected across the majority of African freshwater environments where cyanotoxins have been documented. Furthermore, their concentrations have exceeded the World Health Organization's (WHO) provisional guideline for lifetime human exposure through drinking water, which is set at 1 µg L−1, as indicated by data in Table 1. Highly significant positive relationships were found between toxin-producing cyanobacteria and environmental factors, in particular water temperature and nutrient concentrations. Given the associated exposure risks in Africa, we recommend frequent monitoring of water quality, the development of guidelines based on international best practice, toxicity tests, and epidemiological investigations to understand the health risks and impacts of cyanotoxin exposure. These measures are essential to both protect the well-being of humans and to ensure the sustainability of African aquatic ecosystems. [ABSTRACT FROM AUTHOR]

Aim: Although a growing number of studies have shown that elevated uric acid (UA) levels are associated with multiple cardiovascular risk factors and progression of coronary artery disease, the causal relationship between UA and the occurrence of myocardial infarction (MI) remains uncertain. The aim of this study was to investigate the relationship between UA and the risk of MI. Methods: We screened 23,080 patients in the National Health and Nutrition Examination Survey (NHANES) database for 2009-2018 and explored the association between UA and MI risk using multivariate logistic regression model. In addition, a two-way two-sample Mendelian randomization (TSMR) analysis was performed to examine the causal relationship of UA on MI, and inverse variance-weighted (IVW) results were used as the primary outcome in this study. Sensitivity analysis and horizontal multiple validity test were also performed to verify the reliability of the results. Results: After multivariable adjustment, individuals with the severe elevation of UA levels have a significantly increased risk of MI (OR=2.843, 95%CI: 1.296-6.237, P=0.010). In TSMR analysis, the IVW method demonstrated a significant association between UA and increased risk of MI (OR=1.333, 95%CI: 1.079- 1.647, P=0.008). Results from the MR-Egger intercept test, Cochran’s Q test, and MR-PRESSO test all suggest the reliability of the IVW analysis. Reverse TSMR analysis did not indicate a causal relationship between genetic susceptibility to MI and UA levels (IVW: OR=1.001, 95%CI: 0.989-1.012, P=0.922). Conclusion: Based on cross-sectional study and Mendelian randomization analysis, it has been demonstrated that UA is an independent risk factor for MI. Elevated levels of UA increase the risk of MI, particularly in cases of severe elevation. [ABSTRACT FROM AUTHOR]

Objective: A growing body of research suggests a link between varicocele and male infertility (MI). However, current evidence is mainly based on retrospective studies, which are prone to interference from confounding factors and cannot establish causal relationships. Mendelian randomization (MR) studies on the causal relationship between varicocele and MI are very limited. Therefore, this study conducted a two-sample MR study to elucidate the causal effect between the two. Methods: Download the data set GSE216907 from the GEO database, and use R software to screen differential genes in normal and varicocele tissue samples. The drug targets of Bu Shen Huo Xue Prescription (BSHXP) were derived from the Herb database. All genetic datasets were obtained using publicly available summary statistics based on individuals of European ancestry from the IEU GWAS database. MR analysis was performed using MR Egger, weighted median (WM) and inverse variance weighted (IVW) methods to assess the causal relationship between exposure and outcome and to validate the findings by comprehensively evaluating the effects of pleiotropic effects and outliers. The renal vein constriction method was used to establish a pathological model of varicocele infertility. The drug was administered continuously for 60 days and the relevant indicators of the rats were observed. Results: Obtain two therapeutic targets for varicocele through intersection analysis: MEGF9 and MLLT11, and were verified by molecular docking. MR analysis showed that MEGF9 was positively associated with MI (MR Egger, OR: 1.639, 95% CI: 1.124-2.391, P = 0.024; WM, OR: 1.235, 95% CI: 1.003-1.521, P = 0.047). MEGF9 is also positively associated with MI (IVW, OR: 1.35, 95% CI: 1.069- 1.705, P = 0.012). Sensitivity analysis showed no heterogeneity and horizontal pleiotropy. The expression of MEGF9 and MLLT11 increased in the varicocele model group, while the expression decreased after treatment with low, medium, and high doses of BSHXP. In addition, the sperm number, motility, morphology, and fertility of rats in the model group were significantly lower than those in the control group (P<0.05). After BSHXP treatment, all indicators were significantly better than those of the model group (P<0.05). Conclusion: In conclusion, this study indirectly supports that varicocele causes MI. BSHXP inhibiting MEGF9 and MLLT11 may become a potential therapeutic target for alleviating varicocele and MI. [ABSTRACT FROM AUTHOR]

Background: Cohort studies have increasingly shown associations between inflammatory markers and myocardial infarction (MI); however, the specific causal relationships between inflammatory markers and the development of MI remain unclear. Methods and results: By utilizing publicly accessible genome-wide association studies, we performed a two-sample Mendelian randomization (MR) analysis to explore the causal associations between inflammatory markers and myocardial infarction (MI). A random-effects inverse-variance weighted method was used to calculate effect estimates. The study included a total of 395,795 European participants for MI analysis and various sample sizes for inflammatory factors, ranging from 3,301 to 563,946 participants.Neutrophil count was found to increase the risk of MI (odds ratio [OR] = 1.08; 95% confidence interval [CI], 1.00–1.17; p = 0.04). C-reactive protein levels correlated positively with MI. No associations were observed with IL-1 beta, IL-6, IL-18, procalcitonin, TNF-α, total white cell count, or neutrophil percentage of white cells. Neutrophil count and C-reactive protein were inversely associated with lactate dehydrogenase: neutrophil cell count (OR 0.95; 95% CI, 0.93–0.98; p < 0.01) and C-reactive protein (OR 0.96; 95% CI, 0.92–1.00; p = 0.02). No associations of MI with myoglobin, troponin I, and creatine kinase-MB levels were found. Conclusions: This two-sample MR analysis revealed a causal positive association of MI with neutrophil count, C-reactive protein level, and the myocardial injury marker lactate dehydrogenase. These results indicate that monitoring C-reactive protein and neutrophil counts may be useful in management of MI patients. [ABSTRACT FROM AUTHOR]

The study aimed to explore the clinical diagnostic significance of lipoprotein(a) [Lp(a)] and neck circumference (NC) in patients with coronary heart disease (CHD). Methods: This cross-sectional study was conducted at Chengde Central Hospital from September 2021 to June 2023, enrolling 791 patients with suspected CHD who underwent selective coronary angiography (CAG). Patients were categorized into CHD and non-CHD groups based on the severity of arterial narrowing. Subsequently, the diagnostic value of Lp(a) combined with NC in patients with CHD was assessed using receiver operating characteristic (ROC) curves. Based on the results of multivariate logistic regression, a nomogram was constructed, and its clinical applicability was validated using decision curve analysis (DCA) and clinical impact curve (CIC). Results: Multivariate logistic regression proved that high Lp(a) and high NC are risk factors for CHD, with OR of 1.836 (95% CI: 1.282– 2.630) and 1.383 (1.0.978– 1.955), respectively. Patients in the high NC or Lp(a) group exhibited a higher prevalence of multi-vessel disease. The area under the ROC curve (AUC) of the predictive model combining high Lp(a) and high NC was 0.710 (95% CI: 0.670– 0.751) and also demonstrated good calibration (Hosmer-Lemeshow goodness-of-fit test P value=0.494). The DCA and CIC confirmed the clinical utility of the nomogram developed to predict CHD based on the combination of high Lp(a) and high NC. Conclusion: The levels of Lp(a) and NC exhibit a significant correlation with the presence of CHD, and their combined assessment holds specific clinical value in the diagnosis of CHD. [ABSTRACT FROM AUTHOR]

Background: Pathological cardiac hypertrophy is linked to immune-inflammatory injury, and regulatory T cells (Tregs) play a crucial role in suppressing immune-inflammatory responses. However, the precise role of Tregs in pathological cardiac hypertrophy remains unclear. Objective: To summarize the current knowledge on the role and mechanisms of Tregs in pathological cardiac hypertrophy and explore their perspectives and challenges as a new therapeutic approach. Results: Treg cells may play an important protective role in pressure overload (hypertension, aortic stenosis), myocardial infarction, metabolic disorders (diabetes, obesity), acute myocarditis, cardiomyopathy (hypertrophic cardiomyopathy, storage diseases), and chronic obstructive pulmonary disease–related pathological cardiac hypertrophy. Although some challenges remain, the safety and efficacy of Treg-based therapies have been confirmed in some clinical trials, and engineered antigen-specific Treg cells may have better clinical application prospects due to stronger immunosuppressive function and stability. Conclusion: Targeting the immune-inflammatory response via Treg-based therapies might provide a promising and novel future approach to the prevention and treatment of pathological cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

Background: Myocardial infarction (MI) induces complex transcriptional changes across diverse cardiac cell types. Single-cell RNA sequencing (scRNA-seq) provides an unparalleled ability to discern cellular diversity during infarction, yet the veracity of these discoveries necessitates confirmation. This investigation sought to elucidate MI mechanisms by integrating scRNA-seq and bulk RNA-seq data. Methods: Publicly available scRNA-seq (GSE136088) and bulk RNA-seq (GSE153485) data from mice MI models were analyzed. Cell types were annotated, and differential expression analysis conducted. Bulk RNA-seq underwent quality control, principal component analysis, and differential expression analysis. Results: In scRNA-seq data, the comparison between MI and sham groups unveiled a reduction in endothelial cell populations, but macrophages and monocytes increased. Within fibroblast subgroups, three distinct categories were discerned, with two exhibiting upregulation in MI. Notably, endothelial cells exhibited an elevated expression of genes associated with apoptosis and ferroptosis. In bulk RNA-seq analysis, distinct patterns emerged when comparing MI and sham groups. Specifically, six genes linked to endothelial ferroptosis exhibited heightened expression in MI group, thereby corroborating the scRNA-seq findings. Moreover, the examination of isolated cardiac macrophages from mice MI model revealed increased expression of Spp1, Col1a2, Col3a1, Ctsd, and Lgals3 compared to sham group, thus substantiating the dysregulation of macrophage apoptosis-related proteins following MI. Conclusion: MI altered the transcriptomic landscapes of cardiac cells with increased expression of apoptotic genes. Moreover, the upregulation of macrophage apoptosis marker was confirmed within MI models. The presence of endothelial cell depletion and ferroptosis in MI has been demonstrated. [ABSTRACT FROM AUTHOR]

Aim. To determine the relationships between serum concentrations of growth and differentiation factor 15 (GDF 15) and NTproBNP and features of heart remodeling in patients with heart failure and preserved ejection fraction (HFPEF) depending on the history of Q-myocardial infarction (MI). Materials and methods. The study was performed on the basis of the Cardiology Department of the Municipal non-profit Enterprise “City Hospital of Urgent and Emergency Medical Care” of Zaporizhzhia City Council. 72 patients (mean age 62.1 ± 1.7 years) with HFPEF after MI were enrolled. The patients were divided into two groups depending on the time of previous MI. The patients were examined using two-dimensional echocardiography on a MyLab50 device (Esaote, Italy) according to the recommendations of the American Society of Echocardiography. Serum concentrations of GDF 15 and NTproBNP were measured by enzyme immunoassay using Elabscience reagent kits (USA). Results. In the 1st and 2nd groups of patients who suffered MI within a year, a significant increase in GDF 15 has been found (by 66.1 % and 74.7 %, respectively; p < 0.05) compared to the control group. The level of GDF 15 was significantly higher (by 41.8 %, p < 0.05) in the group of patients who had MI over a one-to-two-year period as compared to those who had MI within one year. The serum concentration of NTproBNP was also significantly higher in HFPEF groups compared to the control group (by 84.7 % and 87.2 %, respectively, p < 0.05). In the 2nd group of patients with the history of MI between 1 and 2 years, a significant increase in end-systolic volume (by 11.8 %, p < 0.05), end-diastolic volume (by 22.3 %, p < 0.05), left ventricular myocardial mass index (by 19.1 %, p < 0.05) and the E/e’ ratio (by 20.9 %, p < 0.05) has been revealed as compared to the 1st patient group. A strong direct correlation has been shown between the time of MI occurrence and the concentration of GDF 15 (r = 0.58, p < 0.05), the interventricular septum thickness at diastole (r = 0.61, p < 0.05) and the left ventricular myocardial mass index (r = 0.63, p < 0.05), GDF 15 and E/e’ (r = 0.37, p < 0.05), GDF 15 and the left atrial volume index (r = 0.41, p < 0.05), GDF 15 and NTproBNP (r = 0.56, p < 0.05). Conclusions. Progression of left ventricular myocardial hypertrophy and diastolic dysfunction with dilatation of the heart chambers has been observed in HFPEF patients with a longer history of MI. The time period of MI in patients with HFPEF was associated with the serum concentration of GDF 15, the interventricular septum thickness and the mass index of the left ventricular myocardium. The serum concentration of GDF 15 was significantly correlated with the deterioration of the left ventricular diastolic function, such as an increase in the E/e’ ratio and the left atrial volume index.

Although childhood maltreatment has been reported to be associated with the incidence of cardiovascular diseases, its association with specific major cardiovascular events remains unclear. This study aimed to examine the relationship between different types of childhood maltreatment (CM) and myocardial infarction (MI) occurrence in a nationally representative sample. We used data from the National Epidemiologic Survey of Alcohol and Related Conditions, a nationally representative US sample of adults aged 20 years and older (N = 34, 653). Logistic regression models were constructed to investigate the associations between five types of CMs including physical abuse, physical neglect, emotional abuse, emotional neglect, and sexual abuse and the risk of MI adjusting for sociodemographic variables. After adjusting for sociodemographic variables, childhood sexual abuse was significantly associated with increased odds of MI occurrence (adjusted odds ratio [aOR] = 1.85, 95%CI = 1.24–2.76, p = 0.003). Additionally, childhood physical abuse was significantly associated with increased odds of MI occurrence in men (aOR = 2.45, 95%CI = 1.35–4.44, p = 0.004) but this association was not observed in women (aOR = 0.72, 95%CI = 0.32–1.66, p = 0.440). Compared to those who did not experience CM, those who experienced more than three types of CMs showed increased odds of MI occurrence (adjusted OR = 2.08–3.05, all p < 0.05). Using data from a nationally representative US sample of adults, we found significant positive associations between CM and odds of MI occurrence in adulthood. Future longitudinal prospective studies are needed to confirm our findings. • This study investigated the association between childhood maltreatment and risk of myocardial infarction in adulthood. • Sexual abuse was significantly associated with odds of MI occurrence and physical abuse was significantly associated with increased odds of MI occurrence in men. • Those who suffered more than three types of maltreatment showed increased odds of MI. • Early interventions are warranted to prevent long-term physical sequelae in those who suffer from childhood maltreatment. [ABSTRACT FROM AUTHOR]

Background: According to James Fries morbidity compression is present if morbidity rates are decreasing to a larger extent than mortality rates. Compression also occurs if age at onset is increasing at a faster pace than age at death. These two variants of the compression hypothesis were formulated as a population concept. Compression has seldom been studied with a specific disease as application. Methods: Morbidity compression was examined in terms of myocardial infarction (MI) by using German claims data covering the years 2006 to 2015. The findings are based on an annual case number of about 2 m women and men aged 18 years and older. Analyses were performed by means of proportional hazards regression and by using linear regression. Results: Decreases of morbidity rates were more pronounced than those of mortality. For men, the hazard ratio for contracting MI in 2015 as compared to 2006 was hr = 0.66 and hr = 0.71 for the female population. The respective results for mortality were hr = 0.75 in men and hr = 1.0 in women. They can be interpreted in favor of morbidity compression. For the subgroup of women and men with MI, changes of onset age revealed marked gender differences. For 2015 as compared with 2006, age at MI-occurrence in men increased by 10.5 months as compared to an increase of 10.4 months for age at death. In women changes were smaller and statistically not significant. The findings referring to women have to be interpreted against the backdrop of higher onset age and higher age at death than in men. Conclusions: Taken together, morbidity compression has occurred in terms of decreasing MI-rates as well as in terms of increased onset age in men. It can be concluded that both processes have led to an improvement of healthy lifetime. Decreasing morbidity rates in women are also pointing towards morbidity compression, a finding that is not complemented by changes of onset age. Our data are demonstrating that morbidity rates and age at onset may vary independently. From this perspective morbidity compression is a multi-faceted phenomenon. [ABSTRACT FROM AUTHOR]

There are various studies that have addressed the use of Cyclosporine among patients with acute myocardial infarction (AMI). However, to date there is hardly any concise and systematically structured evidence that debate on the efficacy and safety of Cyclosporine in AMI patients. The aim of this review is to systematically summarize the overall evidence from published trials, and to conduct a meta-analysis in order to determine the efficacy and safety of Cyclosporine vs. placebo or control among patients with AMI. All randomized control trial (RCT) published in English language from January 2000 to August 2017 were included for the systematic review and meta-analysis. A total of six RCTs met the inclusion and were hence included in the systematic review and meta-analysis. Based on the performed meta-analysis, no significant difference was found between Cyclosporine and placebo in terms of left ventricular ejection fraction (LVEF) improvement (mean difference 1.88; 95% CI −0.99 to 4.74; P = 0.2), mortality rate (OR 1.01; 95% Cl 0.60 to 1.67, P = 0.98) and recurrent MI occurrence (OR 0.65; 95% Cl 0.29 to 1.45, P = 0.29), with no evidence of heterogeneity, when given to patients with AMI. Cyclosporine also did not significantly lessen the rate of rehospitalisation in AMI patients when compared to placebo (OR 0.91; 95% Cl 0.58 to 1.42, P = 0.68), with moderate heterogeneity (I2 = 46%). There was also no significant improvement in heart failure events between Cyclosporine and placebo in AMI patients (OR 0.63; 95% Cl 0.31 to 1.29, P = 0.21; I2 = 80%). No serious adverse events were reported in Cyclosporine group across all studies suggesting that Cyclosporine is well tolerated when given to patients with AMI. The use of Cyclosporine in this group of patients, however, did not result in better clinical outcomes vs. placebo at improving LVEF, mortality rate, recurrent MI, rehospitalisation and heart failure event. [ABSTRACT FROM AUTHOR]

Aim: Myocardial infarction (MI) is a cardiovascular disease caused by necrosis of the myocardium, which places a heavy burden on patients. In France, the proportion of daily smokers remains high, reaching at 25.5% in 2020. We evaluated the impact of smoking reduction scenarios on the projection of MI prevalence, mean age of incident cases and number of MI prevented cases until 2035. Methods and Results: The French government has introduced smoking cessation policies that have led to an annual decrease in smoking prevalence. Based on this annual decline, we implemented three scenarios (SC) simulating an annual decrease in the proportion of smokers aged over 35 (SC1: 1%, ie, natural evolution without intervention, SC2: 2%, SC3: 9.87%) and a fourth scenario (SC4) in which there is a complete discontinuation of smoking from 2024 onwards using MI hospitalization and demographic data, estimations for the proportion of daily smokers between 35 and 95 years and multi-state models. Between 2023 and 2035, MI prevalence increased from 3.18% to 4.23% in males and from 1.00% to 1.46% in females under SC1. MI prevalence was equal to 4.21%, 4.06%, and 3.82% in males and 1.45%, 1.40%, and 1.34% in females in 2035 according to SC2, SC3, and SC4, respectively. Compared with SC1, 0.68% MI cases would be prevented with SC2, 4.52% with SC3 and 10.34% with SC4, with almost half of cases being prevented before 65 years of age. The increase in the mean age of MI incident cases ranged from 3 to 4 years among males and from 1 to 2 years among females. Conclusion: While reducing tobacco use could substantially reduce the number of MI cases prevented, its prevalence would continue to increase due to the ageing population. An integrated prevention strategy that includes the leading cardiovascular risk factors should more efficiently reduce the future burden of MI. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI), a severe outcome of cardiovascular disease, poses a serious threat to human health. Uncontrolled inflammation and excessive cardiomyocyte death, following an infarction event, significantly contribute to both the mortality rate and complications associated with MI. The protein IL-4-induced gene 1 (IL4I1 or FIG1) serves as a natural inhibitor of innate and adaptive immunity, playing a crucial role in CD4+ T cell differentiation, macrophage polarization, and ferroptosis inhibition. Previous studies have linked IL4I1 to acute MI. This review summarizes evidence from both basic and clinical research, highlighting IL4I1 as a critical immunoregulatory enzyme that not only regulates inflammatory responses, but also potentially mitigates MI-induced damage. [ABSTRACT FROM AUTHOR]

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Diabetes and its complications significantly affect individuals' quality of life. The etiology of diabetes mellitus and its associated complications is complex and not yet fully understood. There is an increasing emphasis on investigating the effects of endocrine disruptors on diabetes, as these substances can impact cellular processes, energy production, and utilization, ultimately leading to disturbances in energy homeostasis. Mitochondria play a crucial role in cellular energy generation, and any impairment in these organelles can increase susceptibility to diabetes. This review examines the most recent epidemiological and pathogenic evidence concerning the link between endocrine disruptors and diabetes, including its complications. The analysis suggests that endocrine disruptor-induced mitochondrial dysfunction--characterized by disruptions in the mitochondrial electron transport chain, dysregulation of calcium ions (Ca2+), overproduction of reactive oxygen species (ROS), and initiation of signaling pathways related to mitochondrial apoptosis--may be key mechanisms connecting endocrine disruptors to the development of diabetes and its complications. [ABSTRACT FROM AUTHOR]

Background: Adverse atherogenic lipid profile is associated with an increased risk of major adverse cardiac events in patients after acute coronary syndrome (ACS). Knowledge regarding the impact of statins on lipid profile remains limited. Methods: We retrospectively analysed multicenter, real-world data from the Chinese Cardiovascular Association Database-iHeart Project. Patients with a primary diagnosis of ACS from 2014 to 2021 during index hospitalisation and having at least one lipid panel record after discharge within 12 months were enrolled. We analysed target achievement of atherogenic lipid profile, including apolipoprotein B (< 80 mg/dL), low-density lipoprotein cholesterol (LDL-C) (< 1.8 mmol/L), lipoprotein(a) [Lp(a)] (< 30 mg/dL), triglycerides (< 1.7 mmol/L), remnant cholesterol (RC) (< 0.78 mmol/L), non-high-density lipoprotein cholesterol (< 2.6 mmol/L) at baseline and follow-up. Multivariate Cox regression models were employed to investigate the association between patient characteristics and target achievement. Results: Among 4861 patients, the mean age was 64.9 years. Only 7.8% of patients had all atherogenic lipids within the target range at follow-up. The proportion of target achievement was for LDL-C 42.7%, Lp(a) 73.3%, and RC 78.5%. Patients with female sex, younger age, myocardial infarction, hypertension, and hypercholesteremia were less likely to control LDL-C, Lp(a), and RC. An increase in the burden of comorbidities was negatively associated with LDL-C and Lp(a) achievements but not with RC. Conclusions: A substantial gap exists between lipid control and the targets recommended by contemporary guidelines. Novel therapeutics targeting the whole atherogenic lipid profile will be warranted to improve cardiovascular outcomes. What is known? 1. Long-term prognosis of ACS remains challenging, underlining the need for optimisation of secondary prevention in these patients. 2. In addition to LDL-C, the residual lipid risk attributed to other atherogenic lipids is associated with increased risk after ACS. What the study adds? 1. Only 7.8% of patients had all atherogenic lipids, including LDL-C, TG, ApoB, Lp(a), RC, and non-HDL-C, within the target range. 2. At follow-up, the proportions of the overall population and the very high-risk patients with LDL-C in the target range were 42.7% and 17.5%, respectively. 3. Patients with female sex, younger age, and comorbidities such as myocardial infarction, hypertension, and hypercholesterolemia were less likely to control their lipids. [ABSTRACT FROM AUTHOR]

As the demand for power supply stability and reliability in the active distribution network (ADN) increases, the primary and secondary integrated intelligent switch (PSIIS) has become the primary choice for smart grid transformation in many weak infrastructure areas. However, the number of PSIISs that can be configured is often limited. It is necessary to comprehensively utilize the measurement data and sectional capabilities of PSIISs through the optimal configuration method to find the optimal configuration scheme. Therefore, fault observability-related indexes (FORIs) are proposed based on the functional characteristics of PSIISs. These indexes include fault type observability, fault location observability, fault current distribution characteristics observability, transition resistance observability, and weak infrastructure area observability. An optimization configuration model of PSIISs considering the comprehensive fault observability (CFO) is constructed. The adaptive genetic algorithm (AGA) is selected as the model-solving method. Subsequently, an optimal configuration method of PSIISs considering CFO is proposed. Finally, an example analysis is conducted in MATLAB to verify the effectiveness and feasibility of the proposed method. This optimal configuration method aims to maximize the use of a limited number of PSIISs by considering CFO, and the AGA proves to be an effective tool in solving the optimal configuration scheme. [ABSTRACT FROM AUTHOR]

Parasomnias are a group of sleep disorders characterized by abnormal and unpleasant motor, verbal, or behavioral events that occur during sleep or during transitions between wake and sleep states. They disrupt sleep and can have a detrimental impact on the individual experiencing them. Our goal was to identify types of parasomnias and their prevalence in the current and recent post-secondary student population and to explore their coping strategies for parasomnias they found distressing. Seventy-seven post-secondary students completed the 21-item Munich Parasomnia Screening (MUPS) frequency scale. They also rated, on a 10-point scale, how disturbing each parasomnia experienced was. Not only did 92% percent of students report at least one parasomnia, but our results also indicate that the vast majority of students experienced several parasomnias. This led us to investigate the likelihood of the co-occurrence of different parasomnias. With respect to the level of subjectively experienced distress, the most prevalent parasomnias were not always the more disturbing. Coded open-ended responses about what students do about the disturbing parasomnias indicate that grounding strategies (i.e., coping strategies that help manage distressing feelings) and physical manipulation of one's body were the most common, although most participants indicated that in spite of distress, they do nothing to cope. In conclusion, our study found a strikingly high prevalence of parasomnias in this sample of young adults and a lack of knowledge about effective means of dealing with these. Therefore, we provide some accepted ways of dealing with these. [ABSTRACT FROM AUTHOR]

Freak waves are characterized by extreme wave height, irregular wave shape, high peak energy, short duration, and formidable destructive potential, posing a significant threat to offshore structures. Therefore, analyzing dynamic responses exhibited by advanced offshore platforms such as the offshore triceratops under the influence of freak waves holds paramount importance. However, the response analysis of offshore triceratops under freak waves has not been explored so far in the literature. Hence, the present study aims to investigate the dynamics of offshore triceratops intended for ultradeep waters under the impact of freak waves. Initially, the dual superposition model was utilized to generate the freak waves, and the numerical model of the platform was developed using ANSYS AQWA. Subsequently, the dynamic response characteristics of offshore triceratops under the influence of freak waves were analyzed in the time domain. The results demonstrate the effects of freak waves on the surge, heave, and pitch responses of the deck and buoyant legs were substantial, leading to a significant increase in maximum responses and variations in mean shift and standard deviations. The innovative insights derived from this study can serve as a benchmark for validating the effective performance and design of offshore triceratops. [ABSTRACT FROM AUTHOR]

Pre-disaster protection strategies are essential for enhancing the resilience of electric power systems against natural disasters. Considering the budgets for protection strategies, the dependency of other infrastructure systems on electricity, and the uncertainty of disaster scenarios, this paper develops risk-neutral and risk management models of strategies for pre-disaster protection. The risk-neutral model is a stochastic model designed to maximize the expected value of resilience (EVR) of the integrated system. The risk management model is a multi-objective model prioritizing the minimization of risk metrics as a secondary goal alongside maximizing the EVR. A case study conducted on the energy infrastructure systems in the Greater Toronto Area (GTA) validates the effectiveness of the models. The findings reveal the following: (i) increasing the budget enhances the EVR of the integrated system; however, beyond a certain budget threshold, the incremental benefits to the EVR significantly diminish; (ii) reducing the value of the downside risk often results in an increase in the EVR, with the variation in Pareto-optimal solutions between the two objectives being non-linear; and (iii) whether for the risk-neutral or risk management protection strategies, there are reasonable budgets when considering disaster intensity and the cost of protection measures. The models can help decision-makers to select effective protection measures for natural disasters. [ABSTRACT FROM AUTHOR]

• Examined the predictors of myocardial infarction (MI) following elective spine procedures. • 436 patients had an acute MI out of 196,523 elective spine surgery patients. • MI predictors included diabetes, cardiac arrest and PVD, blood transfusion, dialysis-dependence, low preop platelet count, SSI and days from operation to discharge. • This can aid in the risk stratification of preoperative patients prior to spinal operations. Myocardial infarction (MI), and its predictive factors, has been an understudied complication following spine operations. The objective was to assess the risk factors for perioperative MI in elective spine surgery patients as a retrospective case control study. Elective spine surgery patients with a perioperative MI were isolated in the NSQIP. The relationship between MI and non-MI spine patients was assessed using chi-squared and independent samples t-tests. Univariate/multivariate analyses assessed predictive factors of MI. Logistic regression with stepwise model selection was employed to create a model to predict MI occurrence. The study included 196,523 elective spine surgery patients (57.1 yrs, 48%F, 30.4 kg/m2), and 436 patients with acute MI (Spine-MI). Incidence of MI did not change from 2010 to 2016 (0.2%–0.3%, p = 0.298). Spine-MI patients underwent more fusions than patients without MI (73.6% vs 58.4%, p < 0.001), with an average of 1.03 levels fused. Spine-MI patients also had significantly more SPO (5.0% vs 1.8%, p < 0.001) and 3CO (0.9% vs 0.2%, p < 0.001), but less decompression-only procedures (26.4% vs 41.6%, p < 0.001). Spine-MI underwent more revisions (5.3% vs 2.9%, p = 0.003), had greater invasiveness scores (3.41 vs 2.73, p < 0.001) and longer operative times (211.6 vs 147.3 min, p < 0.001). Mortality rate for Spine-MI patients was 4.6% versus 0.05% (p < 0.001). Multivariate modeling for Spine-MI predictors yielded an AUC of 83.7%, and included history of diabetes, cardiac arrest and PVD, past blood transfusion, dialysis-dependence, low preoperative platelet count, superficial SSI and days from operation to discharge. A model with good predictive capacity for MI after spine surgery now exists and can aid in risk-stratification of patients, consequently improving preoperative patient counseling and optimization in the peri-operative period. [ABSTRACT FROM AUTHOR]

Objective: Our case-control study aimed to access the potential association of insertion/deletion (I/D) ACE (angiotensin converting enzyme) gene polymorphism with myocardial infarction (MI) risk of occurrence among a sample of Moroccan patients, especially young ones. Results: Distribution of I/D ACE gene variant among cases vs controls, showed that healthy controls carried out higher frequency of wild type allele I compared to cases (23.5% vs 21.79% respectively), when cases were carrying higher frequency of mutant allele D (78.21% vs 76.5% for controls). Patients were-after this- divided into two groups of < 45 and > 55 years of age, to investigate whether or not younger patients carried out higher frequency of the mutant allele D, than older ones. As expected, < 45 years old patients carried out more DD genotype than older ones (68.9% vs 54.6% respectively), and higher frequency of mutant allele D (81.08% vs 75% respectively). Besides, a tendency to a positive association was found under the recessive genetic transmission model (OR [95% CI] = 1.85 [0.93-3.69], P = 0.08), suggesting that the I/D ACE polymorphism may be associated with MI occurrence among younger patients (< 45 years of age). [ABSTRACT FROM AUTHOR]

Today, volcanic sulfur emissions into the atmosphere are measured spectroscopically from the ground, air and space. For eruptions prior to the satellite era, two main sulfur proxies are used, the rock and ice core records, as illustrated by Peccia et al. (2023, https://doi.org/10.1029/2023gl103334). The first approach is based on calculations of the sulfur content of the magma, while the second uses traces of sulfur deposited in ice. Both approaches have their limitations. For glaciochemistry, the volcano responsible for a sulfur anomaly is often unknown and the atmospheric pathway by which the sulfur reached the ice uncertain. The petrologic method relies, too, on uncertain estimates of eruption size and a number of geochemical assumptions that are hard to verify. A deeper knowledge of processes occurring both within magma bodies prior to eruption, and within volcanic plumes in the atmosphere is needed to further our understanding of the impacts of volcanism on climate. Plain Language Summary: Volcanic emissions of sulfur gases during large eruptions can change the global climate. Today, advanced spectroscopic tools allow us to measure sulfur from the ground, air and space. But to understand the impacts of volcanic activity on climate back through history we need to estimate volcanic sulfur releases in other ways. Clues can be found in the pumice deposits found around a volcano and, perhaps more surprisingly, in the ice caps of the polar regions, which receive the eventual fallout from large eruptions. Both approaches have limitations that are addressed in a recent work by Peccia et al. (2023, https://doi.org/10.1029/2023gl103334) and that are at the focus of our commentary. Key Points: The impact of volcanic activity on climate remains difficult to quantify for eruptions prior to the instrumental eraThe petrological and glaciochemical methods each provide answers, but are still fraught with large uncertaintiesWe need to further our understanding of the physicochemical processes occurring both within magma reservoirs and volcanic plumes [ABSTRACT FROM AUTHOR]

The correct management of operations in thermoelectric plants is based on the continuous evaluation of the structural integrity of its components, among which there are elements made of stainless steel that perform water conduction functions at elevated temperatures. The working conditions generate progressive wear that must be monitored from the perspective of the microstructure of the material. When AISI 304 stainless steel is subjected to a temperature range between 450 and 850 °C, it is susceptible to intergranular corrosion. This phenomenon, known as sensitization, causes the material to lose strength and generates different patterns in its microstructure. This research analyzes three different patterns present in the microstructure of stainless steel, which manifest themselves through the following characteristics: the absence of intergranular corrosion, the presence of intergranular corrosion, and the precipitation of chromium carbides. This article shows the development of a methodology capable of recognizing the corrosion patterns generated in stainless steel with an accuracy of 98%, through the integration of a multilayer perceptron neural network and the following digital image processing methods: phase congruence and a gray-level co-occurrence matrix. In this way, an automatic procedure for the analysis of the intergranular corrosion present in AISI 304 stainless steel using artificial intelligence is proposed. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) often leads to heart failure (HF) through acute or chronic maladaptive remodeling processes. This establishes coronary artery disease (CAD) and HF as significant contributors to cardiovascular illness and death. Therefore, treatment strategies for patients with CAD primarily focus on preventing MI and lessening the impact of HF after an MI event. Myocardial fibrosis, characterized by abnormal extracellular matrix (ECM) deposition, is central to cardiac remodeling. Understanding these processes is key to identifying new treatment targets. Recent studies highlight SGLT2 inhibitors (SGLT2i) and GLP-1 receptor agonists (GLP1-RAs) as favorable options in managing type 2 diabetes due to their low hypoglycemic risk and cardiovascular benefits. This review explores inflammation's role in cardiac fibrosis and evaluates emerging anti-diabetic medications' effectiveness, such as SGLT2i, GLP1-RAs, and dipeptidyl peptidase-4 inhibitors (DPP4i), in preventing fibrosis in patients with diabetes post-acute MI. Recent studies were analyzed to identify effective medications in reducing fibrosis risk in these patients. By addressing these areas, we can advance our understanding of the potential benefits of anti-diabetic medications in reducing cardiac fibrosis post-MI and improve patient outcomes in individuals with diabetes at risk of HF. [ABSTRACT FROM AUTHOR]

Glucagon-like peptide-1 (GLP-1) is a multifunctional incretin hormone with various physiological effects beyond its well-characterized effect of stimulating glucose-dependent insulin secretion in the pancreas. An emerging role for GLP-1 and its receptor, GLP-1R, in brain neuroprotection and in the suppression of inflammation, has been documented in recent years. GLP-1R is a G protein-coupled receptor (GPCR) that couples to Gs proteins that stimulate the production of the second messenger cyclic 3',5'-adenosine monophosphate (cAMP). cAMP, acting through its two main effectors, protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac), exerts several anti-inflammatory (and some pro-inflammatory) effects in cells, depending on the cell type. The present review discusses the cAMP-dependent molecular signaling pathways elicited by the GLP-1R in cardiomyocytes, cardiac fibroblasts, central neurons, and even in adrenal chromaffin cells, with a particular focus on those that lead to anti-inflammatory effects by the GLP-1R. Fully elucidating the role cAMP plays in GLP-1R's anti-inflammatory properties can lead to new and more precise targets for drug development and/or provide the foundation for novel therapeutic combinations of the GLP-1R agonist medications currently on the market with other classes of drugs for additive anti-inflammatory effect. [ABSTRACT FROM AUTHOR]

Machine safety is not only a prerequisite for successful production but also the foundation for the sustainability and growth of any manufacturing organization. The latest approaches in this rapidly developing field integrate effective risk management tools and strategies into occupational health and safety (OHS) management systems. The study, through a real example from practice, describes the use of the analytic hierarchy process (AHP) method for machine safety improvement, considering the possible types of losses. Classification and Regression Tree Analysis (CART) was applied to assess the efficiency, cost-effectiveness, and, therefore, the overall sustainability level of the relevant safety measures. These were proposed risk reduction measures that typically raised uncertainty among managers regarding the estimation of cost-effectiveness. The advantage of the application decision tree approach is the possibility to identify and establish relatively homogeneous groups of undesirable events and their impact on the organization's objectives. A comprehensive model has been developed to support management decision making in manufacturing organizations towards implementing and improving safety measures in line with manufacturing sustainability goals. [ABSTRACT FROM AUTHOR]