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The gaps in evidence are also highlighted, especially the lack of randomized clinical trials with new generation drug eluting stents versus coronary artery bypass grafting or those regarding the best revascularization strategy for an acute coronary syndrome when unprotected left main coronary disease is involved. © 2020 Macovei et al. Published by IMR press.Cardiovascular disease is still the main cause of morbidity and mortality worldwide. Currently, the frontier of research into cardiovascular disease is the field of non-coding RNA. In this review, information was collected on the use of micro-RNAs as non-invasive biomarkers and their role in pathophysiological processes and therapeutic applications. In the case of microRNA-1 and microRNA-133, the roles and regulatory mechanisms of them are reviewed for arrhythmia, myocardial infarction, diabetic cardiomyopathy, myocardial hypertrophy, cardiomyocyte differentiation, and cell reprogramming. It was observed that microRNA-1 and microRNA-133 do not exist independently, but are two co-transcriptional and cooperative regulatory factors. They have diagnostic value as biomarkers, but also have the potential as therapeutic targets such as for antiarrhythmia and cardiac reprogramming. © 2020 Song et al. Published by IMR press.The curve that describes the relationship between glomerular filtration rate (GFR) and cardiovascular risk is U-shaped, indicating that both reduced GFR (kidney failure) and elevated GFR (glomerular hyperfiltration) are equivalent cardiovascular risk factors. The elevated cardiovascular risk associated with abnormal GFR is not explained by standard cardiovascular risk factors. The relationship between GFR and all-cause mortality follows a similar pattern, so that altered GFR (either low or high) increases the risk for overall mortality. Glomerular hyperfiltration is an adaptive process that arises under conditions that demand improved kidney excretory capacity, such as animal protein ingestion and kidney failure. Unlike vegetable protein, animal protein consumption increases dietary acid load and requires an elevation of the GFR to restore acid-base balance. The loss of functioning nephrons in diseased kidneys requires a compensatory increase of the GFR in the nephrons that remain working to enhance whole-kidney GFR. A major factor that raises GFR is the pancreatic hormone glucagon. Glucagon infusion and endogenous glucagon release increase GFR in healthy subjects and patients with kidney failure. In addition to its kidney hemodynamic effect, glucagon causes insulin resistance. Like hyperglucagonemia, insulin resistance develops across the entire spectrum of abnormal GFR, from glomerular hyperfiltration to advanced kidney disease. Insulin resistance is associated with subclinical vascular injury in the general population and patients with diabetes and kidney failure, being a strong cardiovascular risk factor in these population groups. Animal protein consumption activates glucagon secretion and promotes insulin resistance, having a detrimental effect on cardiovascular disease and renal outcomes. © 2020 Adeva-Andany et al. Published by IMR press.End-stage kidney disease (ESKD) and heart failure (HF) often coexist and must be managed simultaneously. Multidisciplinary collaboration between nephrology and cardiology is critical when treating patients with such complicated physiology. There is no "one-size-fits-all" approach to the evaluation of patients with new left ventricular systolic dysfunction, and diagnostic testing should be adapted to an individual's risk factors. Guideline-directed medical therapy (GDMT) for systolic heart failure should be employed in these patients. While limited randomized data exist, observational data and post hoc analyses suggest that GDMT, including renin angiotensin aldosterone system inhibitors, is associated with improved cardiovascular outcomes and can be safely initiated at low doses with close monitoring of kidney function in this population. Volume status is typically managed through ultrafiltration, so close communication between cardiology and nephrology is necessary to achieve a patient's optimal dry weight and mitigate intradialytic hypotension. Patient education and engagement regarding sodium and fluid restriction is crucial, and symptom burden should be reassessed following changes to the dialysis regimen. © 2020 Joseph et al. Published by IMR press.Low serum sodium concentration has long been recognized as an established marker of short- and long-term morbidity and mortality in patients with heart failure (HF), and is commonly included in various risk prediction models. Mechanisms leading to hyponatremia (e.g. maladaptive neurohormonal activation) could also lead to concurrent decline in serum chloride levels. Besides, chloride has distinct biological roles (e.g. modulation of renal tubular sodium transporters) that are relevant to the pathophysiology and therapy of HF, making it a potent cardiorenal connector. Several clinical studies have recently reported on a potentially overlooked link between low serum chloride levels and adverse outcomes in patients with a wide variety of HF syndromes, which could indeed be stronger than that of sodium. While evidence on predictive value of chloride is accumulating in various patient populations and settings, the limited available interventional studies have so far yielded conflicting results. It remains to be elucidated whether hypochloremia represents a marker of disease severity and prognosis, or it is an actual pathogenetic mechanism, hence being a potential novel target of therapy. Current ongoing studies are designed to better understand the mechanistic aspects of the role of hypochloremia in HF and shed light on its clinical applicability. © 2020 Kazory and Costanzo Published by IMR press.Contrast-induced acute kidney injury (CI-AKI) is a serious complication that can affect outcome and prognosis of patients undergoing percutaneous diagnostic and interventional procedures in catheterization laboratories. There have been advancements in case definition and epidemiology. Additionally strategies have emerged that are positioned to have impact in the catheterization laboratory for patients undergoing cardiovascular procedures. The aim of this review is to provide the state-of-the-art of diagnosis, prevention and management of CI-AKI in interventional cardiology. © 2020 Ronco et al. Published by IMR press.Approximately 90 days of the SARS-CoV-2 (COVID-19) spreading originally from Wuhan, China, and across the globe has led to a widespread chain of events with imminent threats to the fragile relationship between community health and economic health. Despite near hourly reporting on this crisis, there has been no regular, updated, or accurate reporting of hospitalizations for COVID-19. click here It is known that many test-positive individuals may not develop symptoms or have a mild self-limited viral syndrome consisting of fever, malaise, dry cough, and constitutional symptoms. However some individuals develop a more fulminant syndrome including viral pneumonia, respiratory failure requiring oxygen, acute respiratory distress syndrome requiring mechanical ventilation, and in substantial fractions leading to death attributable to COVID-19. The pandemic is evolving in a clustered, non-inform fashion resulting in many hospitals with preparedness but few or no cases, and others that are completely overwhelmed. Thus, a considerable risk of spread when personal protection equipment becomes exhausted and a large fraction of mortality in those not offered mechanical ventilation are both attributable to a crisis due to maldistribution of resources. The pandemic is amenable to self-reporting through a mobile phone application that could obtain critical information on suspected cases and report on the results of self testing and actions taken. link2 The only method to understand the clustering and the immediate hospital resource needs is mandatory, uniform, daily reporting of hospital censuses of COVID-19 cases admitted to hospital wards and intensive care units. Current reports of hospitalizations are delayed, uncertain, and wholly inadequate. This paper urges all the relevant stakeholders to take up self-reporting and reporting of hospitalizations of COVID-19 as an urgent task in combating this devastating pandemic. © 2020 McCullough et al. Published by IMR press.A systematic review of the impact of botulinum-A toxin as a therapeutic regimen for the management of adult migraine disorders is shown to that Botulinum-A toxin provides a more significant reduction in the number of headache episodes per month relative to placebo (MD -0.61, 95% CI -1.02 to -0.19). In subgroup analysis, botulinum-A toxin significantly reduced headache episodes per month relative to placebo for chronic migraine (MD -1.68, 95% CI -3.31 to -0.06), migraine (MD -2.43, 95% CI -4.08 to -0.77), and follow-up time in 16 weeks (MD -2.19, 95% CI -3.84 to -0.53). link3 Statistical differences were not found in subgroup analyses of data relating to chronic migraine, episodic migraine, and other treatment course durations. An analysis of chronic and episodic migraine, botulinum-A toxin did not significantly differ from placebo in the proportion of patients achieving a fifty percent reduction in the number of headaches per month. In terms of patients' subjective reporting of headaches, botulinum toxin A conferred significant improvements when assessment questionnaires of migraine disability and migraine impact were analyzed. However, differences were not substantial with data from the 6-item headache impact test. This meta-analysis demonstrated that botulinum-A toxin as a therapeutic regimen improved the impact of chronic migraines after 16 weeks of therapy, although this was not the case for episodic migraine. © 2020 Shen and Wang Published by IMR press.Several epidemiological studies support low cancer rates in patients with neurodegenerative disorders, including Parkinson's disease, Huntington's disease, and Alzheimer's disease. Different mechanisms were raised as possible causes, from mutated tumor suppressor genes (PARKIN, PINK1) to small interfering RNA based on the CAG trinucleotide repeat expansions located in introns or untranslated regions. However, as every rule has an exception, some tumors have an increased incidence in these neurodegenerative diseases such as breast and skin cancer (melanoma). This mini-review aims to establish the epidemiology between these neurodegenerative disorders and cancer to determine the possible mechanisms involved and therefore set eventual therapeutic applications. According to our findings, we conclude the presence of an inverse relationship among most cancers and the aforementioned neurodegenerative disorders. However, this concept needs to be considered cautiously considering specific genetic and extra-genetic linkage factors for particular tumors. © 2020 Rojas et al. Published by IMR press.Neurological diseases in the central nervous system are mostly characterized by the failure of endogenous repair to restore tissue damage and salvage lost function. Currently, studies have shown that neural stem cell transplantation provides a good therapeutic effect on neurological diseases. For this reason, neural stem cell transplantation has been explored as a cell replacement therapy. Although transplanted cells can replace cells lost during or post central nervous system injury, many studies have shown that this mechanism is insufficient as most of these newly formed cells fail to integrate and eventually die. Although it was initially thought that neural stem cell could only replace lost cells, recent experiments have shown that transplanted neural stem cell can also play bystander roles such as neuroprotection and immune regulation, promote tissue repair by preventing tissue damage, interfere with pathogenic processes, or by rescuing endogenous nerve cells. However, compelling evidence has raised concerns about this bystander effect, which can be caused by several biologically active molecules (collectively known as the secretome) produced by neural stem cells.