Brownian movement analyzed from psychophysiological measures associated with ischemic heart disease and Alzheimer’s disease

There are several coronary diseases that human beings can suffer from, which in themselves generate health deterioration and can lead to the development of other diseases that diminish the quality of life. Ischemic diseases are unique in that they are evidenced by blockages generated by the accumulation of fat that impedes circulation, triggering heart and brain-related problems. By means of fractional Brownian motion in relation to Hurst’s parameter, an analysis of a data of 137 patients aged between 30 and 71 years, who present some type of ischemic disease such as mixed, restricted, effort angina and angina pectoris, is performed. The data used was European, which is found in the PhysioNet open-access medical research data repository, managed by the Massachusetts Institute of Technology Computational Physiology Laboratory. This data shows the Hurst coefficient calculations associated with each type of ischemic heart disease.

Research Trends, Hot Spots, and Prospects for Traditional Chinese Medicine in the Field of Ischemia-Reperfusion Injury

Ischemia-reperfusion (I/R) injury is one of the most common phenomena in ischemic disease or processes that causes progressive disability or even death. It has a major impact on global public health. Traditional Chinese medicine (TCM) has a long history of application in ischemic diseases and has significant clinical effect. Numerous studies have shown that the formulas or single herbs in TCM have specific roles in regulating oxidative stress, anti-inflammatory, inhibiting cell apoptosis, etc., in I/R injury. We used bibliometrics to quantitatively analyze the global output of publications on TCM in the field of I/R injury published in the period 2001–2021 to identify research hotspots and prospects. We included 446 related documents published in the Web of Science during 2001–2021. Visualization analysis revealed that the number of publications related to TCM in the field of I/R injury has increased year by year, reaching a peak in 2020. China is the country with the largest number of publications. Keywords and literature analyses demonstrated that neuroregeneration is likely one of the research hotspots and future directions of research in the field. Taken together, our findings suggest that although the inherent limitations of bibliometrics may affect the accuracy of the literature-based prediction of research hotspots, the results obtained from the included publications can provide a reference for the study of TCM in the field of I/R injury.

Placental Ischemia Says “NO” to Proper NOS-Mediated Control of Vascular Tone and Blood Pressure in Preeclampsia

In this review, we first provide a brief overview of the nitric oxide synthase (NOS) isoforms and biochemistry. This is followed by describing what is known about NOS-mediated blood pressure control during normal pregnancy. Circulating nitric oxide (NO) bioavailability has been assessed by measuring its metabolites, nitrite (NO2) and/or nitrate (NO3), and shown to rise throughout normal pregnancy in humans and rats and decline postpartum. In contrast, placental malperfusion/ischemia leads to systemic reductions in NO bioavailability leading to maternal endothelial and vascular dysfunction with subsequent development of hypertension in PE. We end this article by describing emergent risk factors for placental malperfusion and ischemic disease and discussing strategies to target the NOS system therapeutically to increase NO bioavailability in preeclamptic patients. Throughout this discussion, we highlight the critical importance that experimental animal studies have played in our current understanding of NOS biology in normal pregnancy and their use in finding novel ways to preserve this signaling pathway to prevent the development, treat symptoms, or reduce the severity of PE.

Regulation of STAT3 and its role in cardioprotection by conditioning: focus on non-genomic roles targeting mitochondrial function

Ischemia–reperfusion injury (IRI) is one of the biggest challenges for cardiovascular researchers given the huge death toll caused by myocardial ischemic disease. Cardioprotective conditioning strategies, namely pre- and post-conditioning maneuvers, represent the most important strategies for stimulating pro-survival pathways essential to preserve cardiac health. Conditioning maneuvers have proved to be fundamental for the knowledge of the molecular basis of both IRI and cardioprotection. Among this evidence, the importance of signal transducer and activator of transcription 3 (STAT3) emerged. STAT3 is not only a transcription factor but also exhibits non-genomic pro-survival functions preserving mitochondrial function from IRI. Indeed, STAT3 is emerging as an influencer of mitochondrial function to explain the cardioprotection phenomena. Studying cardioprotection, STAT3 proved to be crucial as an element of the survivor activating factor enhancement (SAFE) pathway, which converges on mitochondria and influences their function by cross-talking with other cardioprotective pathways. Clearly there are still some functional properties of STAT3 to be discovered. Therefore, in this review, we highlight the evidence that places STAT3 as a promoter of the metabolic network. In particular, we focus on the possible interactions of STAT3 with processes aimed at maintaining mitochondrial functions, including the regulation of the electron transport chain, the production of reactive oxygen species, the homeostasis of Ca2+ and the inhibition of opening of mitochondrial permeability transition pore. Then we consider the role of STAT3 and the parallels between STA3/STAT5 in cardioprotection by conditioning, giving emphasis to the human heart and confounders.

Mendelian Randomization Focused Analysis of Vitamin D on the Secondary Prevention of Ischemic Stroke

Background and Purpose: Experimental studies showed vitamin D (Vit-D) could promote vascular regeneration and repair. Prior randomized studies had focused mainly on primary prevention. Whether Vit-D protects against ischemic stroke and myocardial infarction recurrence among subjects with prior ischemic insults was unknown. Here, we dissected through Mendelian randomization any effect of Vit-D on the secondary prevention of recurrent ischemic stroke and myocardial infarction. Methods: Based on a genetic risk score for Vit-D constructed from a derivation cohort sample (n=5331, 45% Vit-D deficient, 89% genotyped) via high-throughput exome-chip screening of 12 prior genome-wide association study–identified genetic variants of Vit-D mechanistic pathways ( rs2060793 , rs4588 , and rs7041 ; F statistic, 73; P <0.001), we performed a focused analysis on prospective recurrence of myocardial infarction (MI) and ischemic stroke in an independent subsample with established ischemic disease (n=441, all with prior first ischemic event; follow-up duration, 41.6±14.3 years) under a 2-sample, individual-data, prospective Mendelian randomization approach. Results: In the ischemic disease subsample, 11.1% (n=49/441) had developed recurrent ischemic stroke or MI and 13.3% (n=58/441) had developed recurrent or de novo ischemic stroke/MI. Kaplan-Meier analyses showed that genetic risk score predicted improved event-free survival from recurrent ischemic stroke or MI (log-rank, 13.0; P =0.001). Cox regression revealed that genetic risk score independently predicted reduced risk of recurrent ischemic stroke or MI combined (hazards ratio, 0.62 [95% CI, 0.48–0.81]; P <0.001), after adjusted for potential confounders. Mendelian randomization supported that Vit-D is causally protective against the primary end points of recurrent ischemic stroke or MI (Wald estimate: odds ratio, 0.55 [95% CI, 0.35–0.81]) and any recurrent or de novo ischemic stroke/MI (odds ratio, 0.64 [95% CI, 0.42–0.91]) and recurrent MI alone (odds ratio, 0.52 [95% CI, 0.30–0.81]). Conclusions: Genetically predicted lowering in Vit-D level is causal for the recurrence of ischemic vascular events in persons with prior ischemic stroke or MI.

Abstract P493: Histone Reader PHF7 Cooperates With The SWI/SNF Complex At Cardiac Super Enhancers To Promote Direct Reprogramming

Ischemic heart disease is the leading cause of death worldwide. Direct reprogramming of resident cardiac fibroblasts (CFs) to induced cardiomyocytes (iCLMs) has emerged as a potential therapeutic approach to treat heart failure and ischemic disease. Cardiac reprogramming was first achieved through forced expression of the transcription factors Gata4, Mef2c, and Tbx5 (GMT); our laboratory found that Hand2 (GHMT) and Akt1 (AGHMT) markedly enhanced reprogramming efficiency in embryonic and postnatal cell types. However, adult mouse and human fibroblasts are resistant to reprogramming due to staunch epigenetic barriers. We undertook a screen of mammalian gene regulatory factors to discover novel regulators of cardiac reprogramming in adult fibroblasts and identified the epigenetic reader PHF7 as the most potent activating factor. We validated the findings of this screen and found that PHF7 augmented reprogramming of adult fibroblasts ten-fold. Mechanistically, PHF7 localized to cardiac super enhancers in fibroblasts by reading H3K4me2 marks, and through cooperation with the SWI/SNF complex, increased chromatin accessibility and transcription factor binding at these multivalent enhancers. Further, PHF7 recruited cardiac transcription factors to activate a positive transcriptional autoregulatory circuit in reprogramming. Importantly, PHF7 achieved efficient reprogramming through these mechanisms in the absence of Gata4. Collectively, these studies highlight the underexplored necessity of cardiac epigenetic readers, such as PHF7, in harnessing chromatin remodeling and transcriptional complexes to overcome critical barriers to direct cardiac reprogramming.

Modern aspects of the application of antiplatelet and hypolipidemic therapy in ischemic heart disease after coronary artery stenting

In this article it will be discussed actual issues and modern problems of the ischemic disease of the heart, antiplatelet therapy, its effects, hypolipidemic therapy, indications, counter indications, potential side effects as well as, successful management strategies after percutaneous coronary intervention following with drug eluted stents.

Large-Area Photoreceptor Degeneration Model in Rabbits by Photocoagulation and Oxidative Stress in the Retina

Photocoagulation is used for the treatment of retinal ischemic disease. However, due to the invasive nature of photocoagulation and variety of melanin concentrations between individuals, it is challenging to avoid damaging the adjacent photoreceptors and inducing several side effects. Previous studies indicate the role of laser power, duration, and spot size on retinal lesions, but the effect of interspot distance of the laser pulses needs to be considered in panretinal photocoagulation. In this study, we examine different parameters of photocoagulation on lesions of the retina in rabbit, finding that the lesion level of the outer nuclear layer of the retina depended on the pulse duration and laser spot size, and decreasing interspot distance could completely abolish the photoreceptor layer. The degeneration of the photoreceptor by photocoagulation occurred in 24 h and was not restored afterward. We then conducted panretinal photocoagulation in rabbit and found that oxidative stress was decreased in the inner nuclear layer of the retina, and pupillary light reflex and ERG signals were impaired. Our study could provide a rabbit model to explore the mechanism of photoreceptor degeneration and therapies for the side effects after photocoagulation.

Evaluation of Ischemic Heart Disease in the Young Population of Georgia

Objective: Study of risk factors (RF) for ischemic heart disease (IHD) in young people is a significant problem in cardiology. Aims: Study and prognosis of ischemic heart disease in Georgian population under 45 years of age. Methods: The study included 107 young patients with coronary heart disease (from 18 to 44 years old), who were treated in the cardiology department of the St. John the Merciful Private Clinic. The average age was (34.68 ± 6.2) years. The control group consisted of 199 healthy volunteers without cardiovascular diseases at the age from 18 to 44 years, the average age was (35.9 ± 5.2) years. In all patients, traditional risk factors were assessed. Results: Regression analysis has shown that it increases the risk of ischemic heart disease: living in the city - OR=6.90(95%CI:1.28-37.18); sleep disturbance - OR=45.62(95%CI:3.52-590.64); obesity -OR=24.56(95%CI:4.14-145.66); hypertension - OR=40.76(95%CI:8.07-205.92); excess intake of saturated fats - OR=79.94(95%CI:10.93-584.43); night shift - OR=39.01(95%CI:3.75-405.75); early detection of ischemic disease in grade I-II relatives - OR=44.22(95%CI:8.07-242.17); decrease - female gender - OR=0.14 (95%CI:0.03-0.70) and married - OR=0.01(95%CI:0.00-0.08); Conclusion: The ability to predict the risk of developing IHD in young people on the basis of traditional RFs, most of which are modifiable, as well as the study of "new" RFs opens up new perspectives in the formation of a strategic approach to the management of young patients in the presence of high risk.