Unusually high incidence of appendicitis cases at Dohad Town in Panch Mahals District in Bombay State.
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Appendicitis↗
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Etiology of an outbreak of appendicitis in Dohad town of Panchmahals District, Bombay State.
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Appendicitis↗
The effect of low birth weight as an intrauterine exposure on the early onset of sarcopenia through possible molecular pathways.
Sarcopenia, a musculoskeletal disease characterized by the progressive loss of skeletal muscle mass, strength, and physical performance, presents significant challenges to global public health due to its adverse effects on mobility, morbidity, mortality, and healthcare costs. This comprehensive review explores the intricate connections between sarcopenia and low birth weight (LBW), emphasizing the developmental origins of health and disease (DOHaD) hypothesis, inflammatory processes (inflammaging), mitochondrial dysfunction, circadian rhythm disruptions, epigenetic mechanisms, and genetic variations revealed through genome-wide studies (GWAS). A systematic search strategy was developed using PubMed to identify relevant English-language publications on sarcopenia, LBW, DOHaD, inflammaging, mitochondrial dysfunction, circadian disruption, epigenetic mechanisms, and GWAS. The publications consist of 46.2% reviews, 21.2% cohort studies, 4.8% systematic reviews, 1.9% cross-sectional studies, 13.4% animal studies, 4.8% genome-wide studies, 5.8% epigenome-wide studies, and 1.9% book chapters. The review identified key factors contributing to sarcopenia development, including the DOHaD hypothesis, LBW impact on muscle mass, inflammaging, mitochondrial dysfunction, the influence of clock genes, the role of epigenetic mechanisms, and genetic variations revealed through GWAS. The DOHaD theory suggests that LBW induces epigenetic alterations during foetal development, impacting long-term health outcomes, including the early onset of sarcopenia. LBW correlates with reduced muscle mass, grip strength, and lean body mass in adulthood, increasing the risk of sarcopenia. Chronic inflammation (inflammaging) and mitochondrial dysfunction contribute to sarcopenia, with LBW linked to increased oxidative stress and dysfunction. Disrupted circadian rhythms, regulated by genes such as BMAL1 and CLOCK, are associated with both LBW and sarcopenia, impacting lipid metabolism, muscle mass, and the ageing process. Early-life exposures, including LBW, induce epigenetic modifications like DNA methylation (DNAm) and histone changes, playing a pivotal role in sarcopenia development. Genome-wide studies have identified candidate genes and variants associated with lean body mass, muscle weakness, and sarcopenia, providing insights into genetic factors contributing to the disorder. LBW emerges as a potential early predictor of sarcopenia development, reflecting the impact of intrauterine exposures on long-term health outcomes. Understanding the complex interplay between LBW with inflammaging, mitochondrial dysfunction, circadian disruption, and epigenetic factors is essential for elucidating the pathogenesis of sarcopenia and developing targeted interventions. Future research on GWAS and the underlying mechanisms of LBW-associated sarcopenia is warranted to inform preventive strategies and improve public health outcomes.
Humans↗
Early life events and their consequences for later disease: a life history and evolutionary perspective.
Biomedical science has little considered the relevance of life history theory and evolutionary and ecological developmental biology to clinical medicine. However, the observations that early life influences can alter later disease risk--the "developmental origins of health and disease" (DOHaD) paradigm--have led to a recognition that these perspectives can inform our understanding of human biology. We propose that the DOHaD phenomenon can be considered as a subset of the broader processes of developmental plasticity by which organisms adapt to their environment during their life course. Such adaptive processes allow genotypic variation to be preserved through transient environmental changes. Cues for plasticity operate particularly during early development; they may affect a single organ or system, but generally they induce integrated adjustments in the mature phenotype, a process underpinned by epigenetic mechanisms and influenced by prediction of the mature environment. In mammals, an adverse intrauterine environment results in an integrated suite of responses, suggesting the involvement of a few key regulatory genes, that resets the developmental trajectory in expectation of poor postnatal conditions. Mismatch between the anticipated and the actual mature environment exposes the organism to risk of adverse consequences-the greater the mismatch, the greater the risk. For humans, prediction is inaccurate for many individuals because of changes in the postnatal environment toward energy-dense nutrition and low energy expenditure, contributing to the epidemic of chronic noncommunicable disease. This view of human disease from the perspectives of life history biology and evolutionary theory offers new approaches to prevention, diagnosis and intervention.
Biological Evolution↗
Modelling the developmental origins of health and disease in the early embryo.
The concept that certain adult diseases, such as hypertension, type 2 diabetes and dyslipidaemia can originate from events occurring in utero arose from epidemiological studies in humans but has since been supported by numerous animal-based studies. Referred to as the "developmental origins of health and disease" or "DOHaD" hypothesis, nutritional studies to date have largely focused on two experimental paradigms involving either calorie or protein restriction for varying intervals during pregnancy, where the favoured animal models have been the sheep and rat. In recent times, attention has been directed towards the earliest stages of gestation, where there is emerging evidence to indicate that the pre-implantation embryo may be particularly sensitive to environmentally induced perturbations leading to impaired health in adulthood. In this article, we make the case for hESCs as a model of the human pre-implantation embryo. Working with comparatively large populations of embryonic cells from the species of clinical interest, the scope exists to investigate the effects of specific genetic manipulations or combinations of metabolites against contrasting genetic backgrounds, where the consequences can be evaluated in downstream tissue specific progenitor and/or terminally differentiated cells. In order to fully realize these potentials, however, both derivation and culture conditions need to be harmonized and refined so as to preclude the requirement for feeder cells and serum.
Animals↗
Pilot prospective evaluation of counterpulsation with different intra-aortic balloon volumes on cardiac performance in humans.
UNLABELLED: Smaller intra-aortic balloons (IAB) may minimize peripheral vascular complications. To determine the influence of different IAB volumes on cardiac performance, we studied 20 hemodynamically stable patients on IAB counterpulsation. Variables were measured with either a 40cc or 32cc IAB displacement, at an assist ratio of 1:1 or 1:8: Heart rate, Ao and PA pressures, and Fick cardiac output. By echo-Doppler, the velocity time integral (VTI) across the LV outflow tract, a measure of stroke volume was also calculated. The mean age was 60 yr (range 18-77), height 5'6" (5'2"-5'11"), and body surface area 1.9M2 (1.5-2.3). Results presented as mean values were: [table: see text] *P < 0.005 1:1 vs 1:8 for both 40 and 32cc IAB. CONCLUSION: IAB pumping at 1:1 with either 40 cc or 32 cc volume displacement yields similar degrees of improvement in cardiac performance. A larger cohort is required to determine if smaller balloons may decrease complications without compromising efficacy.
Adolescent↗
Drug-eluting stenting is superior to bare metal stenting in saphenous vein grafts.
This study compared the outcomes of percutaneous coronary intervention (PCI) of saphenous vein grafts (SVGs) with drug-eluting stents (DES) with bare metal stents (BMS). PCI of degenerated SVG is associated with worse outcomes and high incidence of in-stent restenosis compared with PCI of native coronary arteries. There is a paucity of data on the outcomes of PCI of SVG with DES. Data from 223 consecutive patients who underwent PCI of SVG were imputed into a dedicated clinical database. We assessed the clinical outcomes at a mean follow-up of 9.1+/-2.1 months. A total of 139 patients underwent PCI of SVG with DES and 84 patients with BMS. The mean age of the SVG was 7.6+/-3.8 years in the DES group and 7.7+/-2.8 years in the BMS group (P=0.38). Procedural success was achieved in all patients except for one patient in the BMS group who underwent emergent coronary artery bypass graft surgery for SVG dissection. There were no other in-hospital cardiac events in both groups. There was one cardiac death in the DES group and three deaths in the BMS group (P=0.03). When compared to the BMS, PCI of SVG with DES was associated with a lower incidence of myocardial infarction (4.3% vs. 20.2%; P=0.04) and target vessel revascularization (10.1% vs. 36.9%; P=0.035). When compared with BMS, PCI of SVG with DES was associated with a lower incidence of death, myocardial infarction, and target vessel revascularization.
Aged↗
Comparison of stress-induced myocardial ischemia in patients with and without coronary arterial collaterals.
Coronary artery collaterals may have a protective role against myocardial ischemia at rest. However, their role during stress is controversial and poorly defined. We evaluated 212 consecutive patients (57 +/- 16 years; 70% men) who underwent coronary angiography and stress echocardiography within a 3-month period. This cohort of patients (all had significant epicardial coronary artery disease) was divided into 3 groups based on the presence and type of collaterals: group A, no collaterals; group B, collaterals supplied by vessels without flow-limiting stenosis; and group C, collaterals supplied by vessels with flow-limiting stenosis. In all patients, angiographic jeopardy score, ejection fraction, and regional and cumulative wall motion score indexes (WMSIs) at rest and during stress were evaluated. Angiographic jeopardy scores were 2.9, 3.5, and 7.3 for groups A, B, and C, respectively. Baseline ejection fraction was similar between groups A and B (48% vs 46%, p = NS) but lower in group C (31%, p <0.01). During stress echocardiography, all groups demonstrated a significant increase in WMSI from baseline (WMSI at rest vs that during stress 1.72 +/- 0.06 vs 1.79 +/- 0.04 for group A, 1.97 +/- 0.06 vs 2.09 +/- 0.03 for group B, 2.35 +/- 0.11 vs 2.41 +/- 0.07 for group C; p <0.01 for all groups). In addition, the number of ischemic segments increased significantly in all groups (2.96 +/- 0.07 in group A vs 4.52 +/- 0.11 in group B vs 5.61 +/- 0.13 in group C, p <0.01). Coronary artery collaterals do not offer protection against stress-induced myocardial ischemia. Moreover, the presence of jeopardized angiographic coronary collaterals (group C) is associated with a higher angiographic jeopardy score, higher baseline WMSI, and decreased ejection fraction.
Collateral Circulation↗
Comparison of coronary artery bypass surgery with percutaneous coronary intervention with drug-eluting stents for unprotected left main coronary artery disease.
OBJECTIVES: This study evaluated the clinical outcomes of consecutive, selected patients treated with coronary artery bypass graft (CABG) surgery or percutaneous coronary intervention (PCI) with drug-eluting stents (DES) for unprotected left main coronary artery (ULMCA) disease. BACKGROUND: Although recent data suggest that PCI with DES provides better clinical outcomes compared to bare-metal stenting for ULMCA disease, there is a paucity of data comparing PCI with DES to CABG. METHODS: Since April 2003, when DES first became available at our institution, 123 patients underwent CABG, and 50 patients underwent PCI with DES for ULMCA disease. RESULTS: High-risk patients (Parsonnet score >15) comprised 46% of the CABG group and 64% of the PCI group (p = 0.04). The 30-day major adverse cardiac and cerebrovascular event (MACCE) rate for CABG and PCI was 17% and 2% (p < 0.01), respectively. The mean follow-up was 6.7 +/- 6.2 months in the CABG group and 5.6 +/- 3.9 months in the PCI group (p = 0.26). The estimated MACCE-free survival at six months and one year was 83% and 75% in the CABG group versus 89% and 83% in the PCI group (p = 0.20). By multivariable Cox regression, Parsonnet score, diabetes, and CABG were independent predictors of MACCE. CONCLUSIONS: Despite a higher percentage of high-risk patients, PCI with DES for ULMCA disease was not associated with an increase in immediate or medium-term complications compared with CABG. Our data suggest that a randomized comparison between the two revascularization strategies for ULMCA may be warranted.
Aged↗
Perinatal Lead (Pb) Exposure Increases Mouse Embryonic Weight and Alters Neuronal Gene Expression.
Acute and chronic exposure to lead (Pb) during pregnancy is linked to adverse health outcomes, including delayed neurodevelopment in offspring. However, the pathways by which Pb exposure influences long-term health remain poorly understood. To address this, we measured the effects of perinatal Pb exposure on gene expression including imprinted genes, X-linked genes, and sexually dimorphic genes. Female mice were given control or Pb acetate dosed (32 ppm) drinking water two weeks prior to timed mating until embryonic day (E)10-12, upon which whole embryos were collected, weighed, and sexed at E13-15. From a subset of embryo heads (n≥9 per sex per group), we extracted and sequenced RNA. We used linear regression to assess Pb impacts on embryonic weight and gene expression across all mice and stratified by sex. Among the differentially expressed genes, we identified significantly enriched pathways. Pb-exposed embryos weighed more than controls (p=0.007), across both sexes. Collectively, we identified 2,920 differentially expressed genes (FDR<0.05), including 31 imprinted genes and 120 X-linked genes upon Pb exposure. Pb exposure altered expression in gene pathways related to neuronal structure and function as well as sexually dimorphic genes (44 for females; 76 for males). These findings highlight perinatal Pb-linked alterations that may drive later-life health outcomes.
DOHaD↗