scholarly journals Dietary, Cultural and Pathogens-related Selective Pressures Shaped Differential Adaptive Evolution Among Native Mexican Populations

2021 ◽  
Author(s):  
Claudia Ojeda-Granados ◽  
Paolo Abondio ◽  
Alice Setti ◽  
Stefania Sarno ◽  
Guido Alberto Gnecchi-Ruscone ◽  
...  
Keyword(s):  
Native American ◽  
Adaptive Evolution ◽  
Disease Risk ◽  
Biological Traits ◽  
Network Analyses ◽  
Selective Pressures ◽  
Genomic Signatures ◽  
Genetic Components ◽  
Increased Risk ◽  
Mexican Populations

Native American genetic ancestry has been remarkably implicated with increased risk of diverse health issues in several Mexican populations, especially in relation to the dramatic changes in environmental, dietary and cultural settings they have recently undergone. In particular, the effects of these ecological transitions and Westernization of lifestyles have been investigated so far predominantly on Admixed individuals. Nevertheless, indigenous groups, rather than admixed Mexicans, have plausibly retained the highest proportions of genetic components shaped by natural selection in response to the ancient milieu experienced by Mexican ancestors during their pre-Columbian evolutionary history. These formerly adaptive alleles/haplotypes have the potential to represent the genetic determinants of some biological traits peculiar to the Mexican people and a reservoir of loci with potential biomedical relevance. To test such a hypothesis, we used high-resolution genomic data to infer the unique adaptive evolution of 15 Native Mexican groups selected as reasonable descendants of the main pre-Columbian Mexican civilizations. A combination of haplotype-based and gene-network analyses enabled us to detect genomic signatures ascribable to polygenic adaptive traits evolved by the main genetic clusters of indigenous Mexican populations to cope with local environmental and/or cultural conditions. Some of them were also found to play a role in modulating the susceptibility/resistance of these groups to certain pathological conditions, thus providing new evidence for diverse selective pressures having contributed to shape current biological and disease-risk patterns in present-day Native and Mestizo Mexican populations.

Family Environment and Its Correlation with Anxiety and Depression: A Study on Heart Patients

2016 ◽  
Vol 3 (2) ◽  
Author(s):  
Dr. Meena Jain ◽  
Saloni Chandalia
Keyword(s):  
Heart Disease ◽  
Family Environment ◽  
Heart Attack ◽  
Psychiatric Symptoms ◽  
Disease Risk ◽  
Positive Association ◽  
Anxiety And Depression ◽  
Depression And Anxiety ◽  
Increased Risk ◽  
Artery Disease

This research paper deals with the Family Environment and its Correlation with Anxiety and Depression level among persons with Heart Disease. There had been a number of researches that investigated that ischemic heart disease patients who suffer significant anxiety have close to a 5-fold increased risk of experiencing frequent angina and those with depression have more than a 3-fold increased risk for these episodes. This observed link between psychiatric symptoms and angina underlines the importance of treating anxiety and depression in cardiac patients, according to study co author Dr Mark D Sullivan (University of Washington School of Medicine, Seattle). To gather the needed data, Hamilton Anxiety Scale and Becks Depression Inventory were used. As stated from literatures, for people with heart dysfunction, depression and anxiety can increase the risk of an adverse cardiac event such as a heart attack or blood clots. For people who do not have heart disease, depression and anxiety can also increase the risk of a heart attack and development of coronary artery disease. Researchers have also emphasized on the role of family psychosocial environment and its positive association with the Coronary Heart Disease risk.

Cardiovascular Complications of Sleep Disorders: A Better Night’s Sleep for a Healthier Heart / From Bench to Bedside

2020 ◽  
Vol 19 (2) ◽  
pp. 210-232 ◽  
Author(s):  
Theodora A. Manolis ◽  
Antonis A. Manolis ◽  
Evdoxia J. Apostolopoulos ◽  
Helen Melita ◽  
Antonis S. Manolis
Keyword(s):  
Sleep Disorders ◽  
Disease Risk ◽  
Behavioral Therapy ◽  
Benzodiazepine Receptor ◽  
Cardiovascular Complications ◽  
Gamma Aminobutyric Acid ◽  
Acid Type ◽  
Increased Risk ◽  
Cv Disease ◽  
Meta Analyses

: Sleep is essential to and an integral part of life and when lacking or disrupted, a multitude of mental and physical pathologies ensue, including cardiovascular (CV) disease, which increases health care costs. Several prospective studies and meta-analyses show that insomnia, short (<7h) or long (>9h) sleep and other sleep disorders are associated with an increased risk of hypertension, metabolic syndrome, myocardial infarction, heart failure, arrhythmias, CV disease risk and/or mortality. The mechanisms by which insomnia and other sleep disorders lead to increased CV risk may encompass inflammatory, immunological, neuro-autonomic, endocrinological, genetic and microbiome perturbations. Guidelines are emerging that recommend a target of >7 h of sleep for all adults >18 years for optimal CV health. Treatment of sleep disorders includes cognitive-behavioral therapy considered the mainstay of non-pharmacologic management of chronic insomnia, and drug treatment with benzodiazepine receptor agonists binding to gamma aminobutyric acid type A (benzodiazepine and non-benzodiazepine agents) and some antidepressants. However, observational studies and meta-analyses indicate an increased mortality risk of anxiolytics and hypnotics, although bias may be involved due to confounding and high heterogeneity in these studies. Nevertheless, it seems that the risk incurred by the non-benzodiazepine hypnotic agents (Z drugs) may be relatively less than the risk of anxiolytics, with evidence indicating that at least one of these agents, zolpidem, may even confer a lower risk of mortality in adjusted models. All these issues are herein reviewed.

scholarly journals Long term alterations of growth after antenatal steroids in preterm twin pregnancies

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Thorsten Braun ◽  
Vivien Filleböck ◽  
Boris Metze ◽  
Christoph Bührer ◽  
Andreas Plagemann ◽  
...  
Keyword(s):  
Early Childhood ◽  
Disease Risk ◽  
Later Life ◽  
Ponderal Index ◽  
Childhood Growth ◽  
Antenatal Steroids ◽  
Increased Risk ◽  
Infancy And Early Childhood ◽  
Twin Pregnancies

AbstractObjectivesTo compare the long-term effects of antenatal betamethasone (ANS, ≤16 mg, =24 mg and >24 mg) in twins on infant and childhood growth.MethodsA retrospective cohort follow up study among 198 twins after ANS including three time points: U1 first neonatal examination after birth and in the neonatal period; U7 examination from the 21st to the 24th month of life and U9 examination from the 60th to the 64th month of life using data from copies of the children’s examination booklets. Inclusion criteria are twin pregnancies with preterm labor, cervical shortening, preterm premature rupture of membranes, or vaginal bleeding, and exposure to ANS between 23+5 and 33+6 weeks. Outcome measures are dosage-dependent and sex-specific effects of ANS on growth (body weight, body length, head circumference, body mass index and ponderal index) up to 5.3 years.ResultsOverall, 99 live-born twin pairs were included. Negative effects of ANS on fetal growth persisted beyond birth, altered infant and childhood growth, independent of possible confounding factors. Overall weight percentile significantly decreased between infancy and early childhood by 18.8%. Birth weight percentiles significantly changed in a dose dependent and sex specific manner, most obviously in female-female and mixed pairs. The ponderal index significantly decreased up to 42.9%, BMI index increased by up to 33.8%.ConclusionsANS results in long-term alterations in infant and childhood growth. Changes between infancy and early childhood in ponderal mass index and BMI, independent of dose or twin pair structure, might indicate an ANS associated increased risk for later life disease.SynopsisFirst-time report on long-term ANS administration growth effects in twin pregnancies, showing persisting alterations beyond birth in infant and childhood growth up to 5.3 years as potential indicator of later life disease risk.

scholarly journals An artificial neural network approach integrating plasma proteomics and genetic data identifies PLXNA4 as a new susceptibility locus for pulmonary embolism

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Misbah Razzaq ◽  
Maria Jesus Iglesias ◽  
Manal Ibrahim-Kosta ◽  
Louisa Goumidi ◽  
Omar Soukarieh ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Genome Wide Association Study ◽  
Susceptibility Gene ◽  
Biological Traits ◽  
Nucleotide Polymorphisms ◽  
Ann Model ◽  
Neural Network Approach ◽  
A Genome ◽  
Increased Risk ◽  
Artificial Neural

AbstractVenous thromboembolism is the third common cardiovascular disease and is composed of two entities, deep vein thrombosis (DVT) and its potential fatal form, pulmonary embolism (PE). While PE is observed in ~ 40% of patients with documented DVT, there is limited biomarkers that can help identifying patients at high PE risk. To fill this need, we implemented a two hidden-layers artificial neural networks (ANN) on 376 antibodies and 19 biological traits measured in the plasma of 1388 DVT patients, with or without PE, of the MARTHA study. We used the LIME algorithm to obtain a linear approximate of the resulting ANN prediction model. As MARTHA patients were typed for genotyping DNA arrays, a genome wide association study (GWAS) was conducted on the LIME estimate. Detected single nucleotide polymorphisms (SNPs) were tested for association with PE risk in MARTHA. Main findings were replicated in the EOVT study composed of 143 PE patients and 196 DVT only patients. The derived ANN model for PE achieved an accuracy of 0.89 and 0.79 in our training and testing sets, respectively. A GWAS on the LIME approximate identified a strong statistical association peak (rs1424597: p = 5.3 × 10–7) at the PLXNA4 locus. Homozygote carriers for the rs1424597-A allele were then more frequently observed in PE than in DVT patients from the MARTHA (2% vs. 0.4%, p = 0.005) and the EOVT (3% vs. 0%, p = 0.013) studies. In a sample of 112 COVID-19 patients known to have endotheliopathy leading to acute lung injury and an increased risk of PE, decreased PLXNA4 levels were associated (p = 0.025) with worsened respiratory function. Using an original integrated proteomics and genetics strategy, we identified PLXNA4 as a new susceptibility gene for PE whose exact role now needs to be further elucidated.

scholarly journals Assessing evidence for adaptive evolution in two hearing-related genes important for high-frequency hearing in echolocating mammals

2021 ◽  
Author(s):  
Hui Wang ◽  
Hanbo Zhao ◽  
Yujia Chu ◽  
Jiang Feng ◽  
Keping Sun
Keyword(s):  
Adaptive Evolution ◽  
Hair Cells ◽  
High Frequency ◽  
Phylogenetic Trees ◽  
Outer Hair Cells ◽  
Functional Domain ◽  
Coding Region ◽  
Selective Pressures ◽  
Wide Range ◽  
Different Parts

Abstract High-frequency hearing is particularly important for echolocating bats and toothed whales. Previously, studies of the hearing-related genes Prestin, KCNQ4, and TMC1 documented that adaptive evolution of high-frequency hearing has taken place in echolocating bats and toothed whales. In this study, we present two additional candidate hearing-related genes, Shh and SK2, that may also have contributed to the evolution of echolocation in mammals. Shh is a member of the vertebrate Hedgehog gene family and is required in the specification of the mammalian cochlea. SK2 is expressed in both inner and outer hair cells, and it plays an important role in the auditory system. The coding region sequences of Shh and SK2 were obtained from a wide range of mammals with and without echolocating ability. The topologies of phylogenetic trees constructed using Shh and SK2 were different; however, multiple molecular evolutionary analyses showed that those two genes experienced different selective pressures in echolocating bats and toothed whales compared to non-echolocating mammals. In addition, several nominally significant positively selected sites were detected in the non-functional domain of the SK2 gene, indicating that different selective pressures were acting on different parts of the SK2 gene. This study has expanded our knowledge of the adaptive evolution of high-frequency hearing in echolocating mammals.

scholarly journals C-Reactive Protein and All-Cause Mortality in a Large Hospital-Based Cohort

2008 ◽  
Vol 54 (2) ◽  
pp. 343-349 ◽  
Author(s):  
Claudia Marsik ◽  
Lili Kazemi-Shirazi ◽  
Thomas Schickbauer ◽  
Stefan Winkler ◽  
Christian Joukhadar ◽  
...  
Keyword(s):  
Hospital Admission ◽  
Acute Phase ◽  
Cox Regression ◽  
Disease Risk ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Increased Risk ◽  
All Cause Mortality ◽  
Low Sensitivity

Abstract Background: C-reactive protein (CRP), an acute-phase protein, is a sensitive systemic marker of inflammation and acute-phase reactions. Testing CRP concentrations at hospital admission may provide information about disease risk and overall survival. Methods: All first-ever transmittals to the department of medical and chemical laboratory diagnostics for determination of low-sensitivity CRP (n = 274 515, 44.5% male, median age 51 years) between January 1991 and July 2003 were included [median follow-up time: 4.4 years (interquartile range, 2.3–7.4 years)]. The primary endpoint was all-cause mortality. Multivariate Cox regression adjusted for sex and age was applied for analysis. Results: Compared to individuals within the reference category (CRP &lt;5 mg/L), hazard ratios (HR) for all-cause mortality increased from 1.4 (5–10 mg/L category) to 3.3 in the highest category (&gt;80 mg/L, all P &lt;0.001). CRP was associated with various causes of death. The relation of CRP to cancer death was stronger than to vascular death. Younger patients with increased CRP had relatively far worse outcome than older patients (maximal HR: ≤30 years: 6.7 vs &gt;60 years: 1.7–3.7). Interestingly, both short- and long-term mortality were associated with increasing CRP concentrations (&gt;80 mg/L: HR 22.8 vs 1.4). Conclusion: Measurement of low-sensitivity CRP at hospital admission allowed for the identification of patients at increased risk of unfavorable outcome. Our findings indicate that close attention should be paid to hospitalized patients with high CRP not only because of very substantial short-term risk, but also long-term excess risk, the basis for which needs to be determined.

scholarly journals Vital exhaustion and sudden cardiac death in the Atherosclerosis Risk in Communities Study

Heart ◽  
2017 ◽  
Vol 104 (5) ◽  
pp. 423-429 ◽  
Author(s):  
Brittany M Bogle ◽  
Nona Sotoodehnia ◽  
Anna M Kucharska-Newton ◽  
Wayne D Rosamond
Keyword(s):  
Risk Factors ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Disease Risk ◽  
Ventricular Tachyarrhythmia ◽  
Atherosclerosis Risk In Communities ◽  
Vital Exhaustion ◽  
Increased Risk ◽  
Atherosclerosis Risk ◽  
Aric Study

ObjectiveVital exhaustion (VE), a construct defined as lack of energy, increased fatigue and irritability, and feelings of demoralisation, has been associated with cardiovascular events. We sought to examine the relation between VE and sudden cardiac death (SCD) in the Atherosclerosis Risk in Communities (ARIC) Study.MethodsThe ARIC Study is a predominately biracial cohort of men and women, aged 45–64 at baseline, initiated in 1987 through random sampling in four US communities. VE was measured using the Maastricht questionnaire between 1990 and 1992 among 13 923 individuals. Cox proportional hazards models were used to examine the hazard of out-of-hospital SCD across tertiles of VE scores.ResultsThrough 2012, 457 SCD cases, defined as a sudden pulseless condition presumed due to a ventricular tachyarrhythmia in a previously stable individual, were identified in ARIC by physician record review. Adjusting for age, sex and race/centre, participants in the highest VE tertile had an increased risk of SCD (HR 1.48, 95% CI 1.17 to 1.87), but these findings did not remain significant after adjustment for established cardiovascular disease risk factors (HR 0.94, 95% CI 0.73 to 1.20).ConclusionsAmong participants of the ARIC study, VE was not associated with an increased risk for SCD after adjustment for cardiovascular risk factors.

Abstract 228: National Prevalence of Substance Use Disorders Among Hospitalized Heart Failure Patients

2018 ◽  
Vol 11 (suppl_1) ◽  
Author(s):  
Sarah C Snow ◽  
Gregg C Fonarow ◽  
Joseph A Ladapo ◽  
Donna L Washington ◽  
Katherine Hoggatt ◽  
...  
Keyword(s):  
Heart Failure ◽  
Substance Use ◽  
Native American ◽  
Drug Use ◽  
Substance Use Disorders ◽  
Age Groups ◽  
Opioid Use ◽  
Drug Use Disorders ◽  
Increased Risk ◽  
Drug Use Disorder

Background: Several cardiotoxic substances contribute to the development of heart failure (HF). The burden of comorbid substance use disorders (SUD) among patients with HF is under-characterized. Objectives: To describe the national burden of comorbid SUD (tobacco, alcohol, or drug use disorders) among hospitalized HF patients in the U.S. Methods: We used data from the 2014 National Inpatient Sample to calculate the proportion of hospitalizations for a primary HF admission with tobacco, alcohol, or drug use disorder diagnoses, accounting for demographic factors. Drug use disorder analysis was further sub-divided into specific illicit substance categories. Results: There were a total of 989,080 HF hospitalizations of which 35.3% (n=348,995) had a documented SUD. Tobacco use disorder (TUD) was most common (n= 327,220, 33.1%) followed by drug use disorder (DUD) (n=34,600, 3.5%) and alcohol use disorder (AUD) (n=34,285, 3.5%). Female sex was associated with less TUD (OR 0.59; 95% CI, 0.58-0.60), AUD (OR 0.23; 95% CI, 0.22-0.25) or DUD (OR 0.58; 95% CI 0.55-0.62). Tobacco, alcohol, cocaine, and opioid use disorders were highest among HF patients age 45 to 55, while cannabis and amphetamine use was highest in those <45 years. Native American race (versus White) was associated with increased risk of AUD (OR 1.67; 95% CI 1.27-2.20). Black race was associated with increased risk of AUD (OR 1.09; 95% CI 1.02-1.16) or DUD (OR 1.63; 95% CI 1.53-1.74). Medicaid insurance (versus Medicare) was associated with greater TUD (OR 1.27; 95% CI 1.23-1.32), AUD (OR 1.74; 95% CI 1.62-1.87), and DUD (OR 2.15; 95% CI 2.01-2.30). Decreasing quartiles of median household income were associated with increasing SUD. Conclusions: Comorbid SUD disproportionately affects certain HF populations, including men, younger age groups, lower SES patients, and race/ethnic minorities. Further research on interventions to improve prevention and treatment of SUD among hospitalized HF patients are needed given the high rates of SUD in this population. Systematically screening hospitalized HF patients for SUD may reveal opportunities for treatment and secondary prevention.

Risk Assessment of Small Fishing Vessel Trap Net Operations

1995 ◽  
Vol 32 (03) ◽  
pp. 231-243
Author(s):  
Todd Schauer ◽  
Barry Romberg ◽  
Changben Jiang ◽  
Armin W. Troesch
Keyword(s):  
Native American ◽  
Nonlinear Dynamic System ◽  
Line Tension ◽  
Operating Conditions ◽  
Fishing Vessel ◽  
Moment Curve ◽  
Upper Great Lakes ◽  
Small Vessels ◽  
Increased Risk ◽  
Nonlinear Rolling

This paper describes a means by which the capsize risk associated with various fishing vessel operating conditions can be evaluated. Rather than relying on the static restoring moment curve as the primary criteria for vessel safety, modern nonlinear systems analysis is applied to the problem of extreme nonlinear rolling in random beam sea. While the method is quite general and not limited to small vessels, it is illustrated with a specific application involving Native American trap net fishing on the upper Great Lakes. General trap net operations, as practiced by Native American fishermen and women in the Grand Traverse Bay region, are presented in detail. The most significant characteristic of trap net operations is the heel induced during net deployment and net lifting. The increased risk to the vessel, in terms of the increased probability of capsize is quantified for various heel angles and various sea states. A significant advantage of the capsize analysis method presented here is its ability to investigate quickly the effects of many parameters (e.g., trap net line tension, wave height, and/or wave period) on a nonlinear dynamic system without having to resort to extensive simulation studies.

Abstract 288: Novel Mechanisms of Non-coding Genomic Regulation Identified in Cardiac Disease-in-a-dish Models

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Aditya Kumar ◽  
Stephanie Thomas ◽  
Kirsten Wong ◽  
Kevin Tenerelli ◽  
Valentina Lo Sardo ◽  
...  
Keyword(s):  
Heart Attack ◽  
Connexin 43 ◽  
Disease Risk ◽  
Association Studies ◽  
Correlation Coefficients ◽  
Induced Pluripotent Stem Cell ◽  
Genome Wide Association Studies ◽  
Isogenic Line ◽  
Nucleotide Polymorphisms ◽  
Increased Risk

Genome-wide association studies have identified single nucleotide polymorphisms (SNPs) at gene loci that affect cardiovascular function, and while mechanisms in protein-coding loci are obvious, those in non-coding loci are difficult to determine. 9p21 is a recently identified locus associated with increased risk of coronary artery disease (CAD) and myocardial infarction. Associations have implicated SNPs in altering smooth muscle and endothelial cell properties but have not identified adverse effects in cardiomyocytes (CMs) despite enhanced disease risk. Using induced pluripotent stem cell-derived CMs from patients that are homozygous risk/risk (R/R) and non-risk/non-risk (N/N) for 9p21 SNPs and either CAD positive or negative, we assessed CM function when cultured on hydrogels capable of mimicking the fibrotic stiffening associated with disease post-heart attack, i.e. “heart attack-in-a-dish” stiffening from 11 kiloPascals (kPa) to 50 kPa. While all CMs independent of genotype and disease beat synchronously on soft matrices, R/R CMs cultured on dynamically stiffened hydrogels exhibited asynchronous contractions and had significantly lower correlation coefficients versus N/N CMs in the same conditions. Dynamic stiffening reduced connexin 43 expression and gap junction assembly in R/R CMs but not N/N CMs. To eliminate patient-to-patient variability, we created an isogenic line by deleting the 9p21 gene locus from a R/R patient using TALEN-mediated gene editing, i.e. R/R KO. Deletion of the 9p21 locus restored synchronous contractility and organized connexin 43 junctions. As a non-coding locus, 9p21 appears to repress connexin transcription, leading to the phenotypes we observe, but only when the niche is stiffened as in disease. These data are the first to demonstrate that disease-specific niche remodeling, e.g. a “heart attack-in-a-dish” model, can differentially affect CM function depending on SNPs within a non-coding locus.

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