In legal medicine, the determination of post-mortem interval (PMI) is not only an important but also one of the most difficult aspects. Several methods are used to estimate PMI such as physicochemical, entomological, biochemical, metabolic, autolytic, and physical methods. These methods provide a wide range of PMI as they are affected by different factors. The approach behind the present study is to calculate an accurate PMI by using mRNA degradation and fold change expression (FCE) of cardiac-specific genes viz. N-terminal pro-B-type natriuretic peptide (NPPB) and cardiac troponin I (TNNI3). Seventeen cadaver heart tissues were analysed within a time frame of up to 12 hours from the time since death, at different time intervals at room temperature. Gene expression was determined and the data were analysed using the value of average delta Ct (ΔCt) value of the assessed gene and housekeeping gene. Delta delta Ct (ΔΔCt) method was used to calculate the FCE at the different 7-time groups. The FCE of TNNI3 was almost stable till 15 hours of PMI and then after 15 hours, expression shows a decrease up to 24 hours after death; whereas, NPPB shows that FCE was stable till 12 hours of PMI and then after 12 hours, expression shows a decrease up to 24 hours after death. The FCE of NPPB and TNNI3 was almost stable till 12 hours. Thus, the estimation of PMI by analysis of the FCE of cardiac-specific genes can be a new promising method in forensic medicine.
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http://dx.doi.org/10.4467/16891716AMSIK.22.001.18211 | DOI Listing |
Pathogens
December 2024
Departamento de Inmunología, Instituto Nacional de Cardiología Ignacio Chávez (INCICH), Mexico City 14080, Mexico.
Chronic chagasic cardiomyopathy is the most severe clinical manifestation of Chagas disease, which affects approximately seven million people worldwide. Latin American countries bear the highest burden, with the greatest morbidity and mortality rates. Currently, diagnostic methods do not provide information on the risk of progression to severe stages of the disease.
View Article and Find Full Text PDFCase Rep Genet
December 2024
Cardiovascular Research Department, Lankenau Institute for Medical Research, Lankenau Hearth Institute, Wynnewood, Pennsylvania 19096, USA.
Structural or electrophysiologic cardiac anomalies may compromise cardiac function, leading to sudden cardiac death (SCD). Genetic screening of families with severe cardiomyopathies underlines the role of genetic variations in cardiac-specific genes. The present study details the clinical and genetic characterization of a malignant dilated cardiomyopathy (DCM) case in a 1-year-old Mexican child who presented a severe left ventricular dilation and dysfunction that led to SCD.
View Article and Find Full Text PDFTurk J Biol
October 2024
Department of Genetics and Bioengineering, Faculty of Engineering, Yeditepe University, İstanbul, Turkiye.
Cardiovasc Res
December 2024
School of Cardiovascular and Metabolic Medicine & Sciences, King's College London British Heart Foundation Centre of Excellence, London, UK.
Aims: The transcription factor NRF2 is well recognized as a master regulator of antioxidant responses and cytoprotective genes. Previous studies showed that NRF2 enhances resistance of mouse hearts to chronic hemodynamic overload at least in part by reducing oxidative stress. Evidence from other tissues suggests that NRF2 may modulate glucose intermediary metabolism but whether NRF2 has such effects in the heart is unclear.
View Article and Find Full Text PDFFunction (Oxf)
December 2024
Department of Physiology and Aging, University of Florida, Gainesville FL, United States.
It has been well established that cardiovascular diseases exhibit significant differences between sexes in both preclinical models and humans. In addition, there is growing recognition that disrupted circadian rhythms can contribute to the onset and progression of cardiovascular diseases. However, little is known about sex differences between the cardiac circadian clock and circadian transcriptomes in mice.
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