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Background and Objectives: Metabolic syndrome (MS) represents several diseases encompassing a heterogeneous group of biochemical and physiological abnormalities characterized by structural and functional alterations in the myocardium, including the endothelium of the coronary arteries. MS also affects a substantial portion of the global population. Understanding the risk factors, the development and treatment associated with MS are of paramount importance for early identification, treatment and prevention. This study was designed to evaluate the role of the supplementation of omega-3 polyunsaturated fatty acids (n-3 PUFAs) on endothelial function in patients with MS. Materials and Methods: A total of 80 patients with MS were enrolled in two groups. The study evaluated endothelial function (EF) in subjects before and after a three-month treatment with n-3 PUFAs in a dose of 2.4 g daily (800 mg, three times a day) vs. placebo, using an Endo-PAT2000 device (Itamar Medical Ltd., Caesarea, Israel) measuring the reactive hyperemia index (a parameter of EF) and augmentation index (a parameter of arterial stiffness). Plasmatic levels of glutathione peroxidase, homocysteine, apolipoprotein B and lipoprotein were also evaluated for comparison. Results: The results showed that the average value of reactive hyperemia index before the treatment with n-3 PUFAs was 1.62 ± 0.42, compared to 1.96 ± 0.62 at the end of the study (p < 0.005). The augmentation index changed from 14.66 ± 19.55 to 9.21 ± 15.64 after the treatment (p = 0.003) with n-3 PUFA. The results also revealed a statistically significant decrease in apolipoprotein B (0.94 ± 0.36 vs. 1.13 ± 0.35, p = 0.001) and homocysteine (19.31 ± 5.29 vs. 13.78 ± 3.05, p = 0.001) and an increase in glutathione peroxidase plasma levels (41.65 ± 8.90 vs. 45.20 ± 8.01), p = 0.001. Conclusions: The results of this prospective study showed a significant improvement in EF in subjects with MS treated with n-3 PUFAs in a dose of 2.4 g daily.

The underlying mechanism for clinical and biochemical manifestations of chronic heart failure (HF) may be due in part to neurohumoral adaptations, such as activation of the renin-angiotensin-aldosterone and sympathetic nervous systems in the periphery and the brain. Internet search and discussion with colleagues are the methods for this study. Since chronic HF is associated with autonomic imbalance with increased sympathetic nerve activity and a withdrawal of parasympathetic activity, it may be considered a brain disease. This phenomenon may be the result of an increased systemic and cerebral angiotensin II signaling because plasma angiotensin II is increased in humans and animals with chronic HF. The increase in angiotensin II signaling enhances sympathetic nerve activity through actions on both central and peripheral sites during chronic HF. Activation of angiotensin II signaling in different brain sites such as the paraventricular nucleus (PVN), rostral ventrolateral medulla (RVLM), and area postrema (AP) may increase the release of norepinephrine, oxidative stress, and inflammation leading to increased cardiac contractility. It is possible that blocking angiotensin II type 1 receptors decreases sympathetic nerve activity and cardiac sympathetic afferent reflex when therapy is administered to the PVN. The administration of an angiotensin receptor blocker by injection into the AP activates the sympatho-inhibitory baroreflex indicating that receptor blockers act by increasing parasympathetic activity. In chronic HF, in peripheral regions, angiotensin II elevates both norepinephrine release and synthesis and inhibits norepinephrine uptake at nerve endings, which may contribute to the increase in sympathetic nerve activity. Increased circulating angiotensin II during chronic HF may enhance the sympatho-excitatory chemoreflex and inhibit the sympatho-inhibitory baroreflex resulting in worsening of HF. Increased circulating angiotensin II signaling can directly act on the central nervous system via the subfornical organ and the AP to increase sympathetic outflow resulting in to neurohumoral dysfunction, resulting in to heart failure.

Background/Objectives: This study aimed to investigate the association between right ventricular (RV) structure and function and established markers of alcohol septal ablation (ASA) efficacy in patients with hypertrophic cardiomyopathy (HCM). We hypothesized that RV characteristics may serve as predictors of left ventricular outflow tract gradient (LVOTG) in the early period following ASA. Methods: A retrospective analysis was performed in 50 HCM patients who underwent ASA. Correlations between echocardiographic RV parameters and standard indicators of ASA success were assessed at 3 months, 1 year, 3 years, and 5 years post-procedure. Results: Echocardiographic measurements of RV wall thickness (RVWT) at 3 months and 1 year after ASA showed significant correlations with maximum LVOTG (p < 0.001), NYHA functional class, and left ventricular end-diastolic dimension (LVD) (both p < 0.01). At 3 and 5 years, these correlations were no longer statistically significant (p = ns). No associations were observed for other parameters. Conclusions: Echocardiographic assessment of RVWT may serve as an early predictor of subsequent LVOTG development as soon as 3 months after ASA. RVWT could therefore provide an estimate of long-term treatment effects. Further studies are needed to confirm these findings.

Background: There have been 20.5 million deaths due to cardiovascular diseases (CVDs), including atherosclerotic coronary artery disease (CAD) and stroke, so far in 2025. Atherosclerosis, which begins in newborns, may be influenced by preconception factors and continues to develop in adults, requiring a proper assessment of the burden of atherosclerotic plaque, as it is the direct cause of CAD. This review aims to emphasize the role of a staging system proposed by the Lancet Commission for the quantification of atherosclerotic coronary artery disease (ACAD) with an emphasis on preconception risk factors and protective factors, based on coronary computed tomography angiography (CCTA). Methods: It is suggested that the use of CCTA scanning makes it possible to quantify the atherosclerotic plaque burden into four stages. Results: CCTA enables us to see how much plaque has built up, as well as the type of plaque, but not the biochemistry of the plaque, to determine its vulnerability. However, if the plaque is a non-calcified fatty plaque, it is considered to be a strong predictor of the risk of myocardial infarction (MI), whereas a more stable calcified plaque is known to be protective against MI. There are several risk factors and protective factors which may influence the process of the rupture or vulnerability of the plaque. A randomized trial revealed that, after a median follow-up of 10·0 years, deaths due to CAD or non-fatal MI were less frequent in the CCTA group compared with a control group. Conclusions: Despite a few gaps in knowledge about the value of a staging system of ACAD, the available evidence indicates that it is helpful in decreasing morbidity and mortality with available therapies.

The concept of fasting as a potential cancer treatment has garnered increasing interest, particularly in light of emerging evidence linking dietary interventions to cancer progression and therapy outcomes. This article explores whether fasting, either intermittent or prolonged, can be a viable standalone treatment for cancer or if its therapeutic potential lies in its adjunctive role. Current research suggests that fasting induces a metabolic shift, which may inhibit cancer cell proliferation by depriving them of essential nutrients. Additionally, fasting has been shown to enhance the body's stress resistance, promote autophagy, and possibly make cancer cells more vulnerable to standard treatments such as chemotherapy and radiotherapy. However, the application of fasting as a sole treatment for cancer remains controversial and lacks substantial clinical validation. While animal models and in vitro studies indicate promising results, the translation to human trials is complex, with various types of cancer responding differently to dietary interventions. Moreover, concerns about malnutrition, loss of muscle mass, and the overall health of cancer patients undergoing fasting without supervision must be addressed. The paper critically examines the myth and reality surrounding fasting as a cancer treatment, reviewing key studies and clinical trials to provide a comprehensive understanding of its efficacy and safety. While fasting may hold promise as a supportive therapy, particularly in combination with traditional treatments, there is currently insufficient evidence to support its use as a primary treatment modality. Further research is needed to establish the parameters in which fasting might be beneficial, such as specific cancer types, patient populations, and optimal fasting regimens. Thus, while the idea of fasting as a cancer breakthrough is compelling, it remains a complementary approach rather than a standalone solution in oncology.

Purpose Fibromyalgia syndrome (FMS) presents a chronic pain condition affecting muscles and joints. Investigating circadian rhythms' disruption, integral to physiological responses, this study delves into the potential impact of  gene polymorphism (rs57875989) on FMS pathogenesis. Methods In this study, we investigated gene polymorphism in 100 FMS patients and an equal number of control individuals. The genotyping of the gene polymorphism was conducted using polymerase chain reaction (PCR) methodology. Subsequently, we evaluated the association between   gene polymorphism and FMS susceptibility using odds ratios (ORs) and 95% confidence intervals (CIs) by comparing the genotype and allele frequencies of the  gene polymorphism between FMS patients and controls. Results The  gene revealed three genotypes: 4/4, 4/5, and 5/5, with allele frequencies showing significant associations between FMS patients and controls (p<0.05). Notably,   gene polymorphism was linked to FMS development, particularly the 4/4 genotype versus the combined 4/5 and 5/5 genotypes (OR=2.85; 95% CI, 1.35-6.0; p=0.008). These findings suggest a potential role of  gene variation as a genetic risk factor for FMS. Conclusion These findings reported a potential association between   gene polymorphism and FMS, illuminating novel pathways for comprehending and addressing this complex condition. This study holds promise for advancing our understanding of FMS etiology and may inform the development of innovative management strategies tailored to individual genetic profiles, potentially leading to more effective treatments and improved outcomes for patients grappling with FMS.

Despite increased availability of effective drug therapy for treatment of heart failure (HF), the morbidity and mortality in chronic heart failure (CHF) are unacceptably high. Therefore, there is an urgent need to ascertain new imaging techniques to identify early sub-clinical forms of cardiac dysfunctions, to guide early relevant treatment. It seems that all the behavioral risk factors—such as tobacco, alcoholism, Western-type diet, sedentary behavior and obesity, emotional disorders, and sleep disorder are associated with early cardiac dysfunction, which may be identified by speckle-tracking echocardiography (STE). Cardiac remodeling can also occur chronologically in association with biological risk factors of CHF, such as diabetes mellitus (DM), hypertension, cardiomyopathy, valvular heart disease, and coronary artery disease (CAD). In these conditions, twisting and untwisting of the heart, cardiac fibrosis, and hypertrophy can be identified early and accurately with 2-Dimentional (2D) and 3D echocardiography (2D echo and 3D echo) with tissue Doppler imaging (TDI), strain imaging via STE, and cardiac magnetic resonance imaging (CMR). Both 2D and 3D echo with STE are also useful in the identification of myocardial damage during chemotherapy and in the presence of risk factors. It is possible that global longitudinal systolic strain (GLS) obtained by STE may be an accurate marker for early identification of the severity of CAD in patients with non-ST segment elevation MI. Left ventricular ejection fraction (LVEF) is not the constant indicator of HF and it is normal in early cardiac dysfunction. In conclusion, this review suggests that GLS can be a useful early diagnostic marker of early or pre-cardiac dysfunction which may be treated by suitable drug therapy of HF along with the causes of HF and adhere to prevention strategies for recurrence. In addition, STE may be a superior clinical tool in the identification of cardiac dysfunction in its early stages compared to ejection fraction (EF) based on conventional echocardiography. Therefore, it is suggested that the chances of either stalling or reversing HF are far better for patients who are identified at an early stage of the disease.

The growing interest in vitamin D deficiency as a potential contributor to coronary artery disease (CAD) has prompted increased scrutiny. Nevertheless, its status as a confirmed risk factor remains unestablished. This study seeks to explore the connection between serum vitamin D levels and CAD. Employing a cross-sectional approach, 205 patients eligible for coronary computed tomography angiography (CCTA) were chosen. Serum vitamin D levels were assessed and juxtaposed with the outcomes of CCTA, which encompassed the coronary artery calcium score (CACS), as well as the presence and severity of coronary artery involvement attributed to atherosclerotic plaques. The average age of the participants was 61.4 ±10.8 years, and the mean serum vitamin D level was 19.6 ±10.3 ng/dl (ranging from 4.7 to 39.7 ng/dl). In total, 52.1% of the participants ( = 107) exhibited vitamin D deficiency, while 47.9% ( = 98) had no deficient levels of vitamin D. The mean serum vitamin D level was notably lower in patients with severe coronary artery disease (CAD) ( < 0.0001). According to the Spearman test, a significant negative correlation (-0.48) was identified between the serum vitamin D level and CACS ( < 0.0001). Conversely, the mean CACS in the vitamin D deficient group was significantly higher than in the insufficient and non-insufficient vitamin D groups ( < 0.0001 for both comparisons). There was a correlation between vitamin D deficiency and both CACS and the severity of coronary artery stenosis.

Digital pathology has emerged as a revolutionary field, transforming traditional diagnostic practices by integrating advanced imaging technologies, computational tools, and artificial intelligence (AI). Adopting digital slides over conventional glass slides enables high-resolution imaging, facilitating remote consultations, second opinions, and telepathology. The digitalization of pathology laboratories enhances workflow efficiency and allows for large-scale data storage, retrieval, and analysis, paving the way for developing robust diagnostic algorithms. One of the most transformative aspects of digital pathology is its synergy with AI and machine learning (ML). These technologies have enabled the automation of repetitive processes, including diseased feature detection, biomarker quantification, and tissue segmentation. This has decreased inter-observer variability and increased diagnostic accuracy. AI-driven algorithms are particularly beneficial in complex cases, assisting pathologists in detecting subtle patterns that might be missed through manual examination. Furthermore, digital pathology plays a critical role in personalized medicine by enabling the precise characterization of tumors, which leads to targeted therapy decisions. Integrating digital pathology with genomics and other omics data holds promise for a more holistic understanding of diseases, driving innovation in diagnostics and treatment. However, the transition to digital pathology is challenging. Issues such as data standardization, regulatory compliance, and the need for robust IT infrastructure must be addressed to realize its full potential. This review provides a detailed examination of these advances, their clinical applications, and the challenges faced in the widespread adoption of digital pathology. As the field continues to evolve, it is poised to play a pivotal role in shaping the future of diagnostics, offering new possibilities for improving patient outcomes. This comprehensive review explores the significant advances in digital pathology, highlighting its impact on diagnostics, research, and patient care.

Background: Recently, chronic lung diseases have been found to be associated with marked inflammation and oxidative stress, which leads to fibrosis in the lungs and chronic respiratory failure. This study aims to determine if hydrogen-rich water (HRW) can enhance oxygen saturation among patients with chronic lung diseases. Methods: Ten patients with chronic lung diseases due to COPD (n = 7), bronchial asthma (n = 2), and tuberculosis of the lung (n = 1) with oxygen saturation of 90–95% were provided high-concentration (>5 mM) HRW using H2-producing tablets for 4 weeks. Oxygen saturation was measured via oximeter and blood pressure via digital automatic BP recorder. Results: HRW administration was associated with a significant increase in oxygen saturation (SpO2) and decrease in TBARS, MDA, and diene conjugates, with an increase in vitamin E and nitrite levels, compared to baseline levels. Physical training carried out after HRW therapy appeared to increase exercise tolerance and decrease hypoxia, as well as delay the need for oxygen therapy. Conclusion: Treatment with HRW in patients with hypoxia from chronic lung diseases may decrease oxidative stress and improve oxygen saturation in some patients. HRW therapy may also provide increased exercise tolerance in patients with chronic hypoxia, but further research is needed.