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Dynamic brain activity requires timely communications between the brain parenchyma and circulating blood. Brain–blood communication is facilitated by intricate networks of brain vasculature, which display striking heterogeneity in structure and function. This vascular cell heterogeneity in the brain is fundamental to mediating diverse brain functions and has long been recognized. However, the molecular basis of this biological phenomenon has only recently begun to be elucidated. Over the past century, various animal species and in vitro systems have contributed to the accumulation of our fundamental and phylogenetic knowledge about brain vasculature, collectively advancing this research field. Historically, dye tracer and microscopic observations have provided valuable insights into the anatomical and functional properties of vasculature across the brain, and these techniques remain an important approach. Additionally, recent advances in molecular genetics and omics technologies have revealed significant molecular heterogeneity within brain endothelial and perivascular cell types. The combination of these conventional and modern approaches has enabled us to identify phenotypic differences between healthy and abnormal conditions at the single-cell level. Accordingly, our understanding of brain vascular cell states during physiological, pathological, and aging processes has rapidly expanded. In this review, we summarize major historical advances and current knowledge on blood endothelial cell heterogeneity in the brain, and discuss important unsolved questions in the field. [ABSTRACT FROM AUTHOR]

The presence of arterial media calcification, a highly complex and multifactorial disease, puts patients at high risk for developing serious cardiovascular consequences and mortality. Despite the numerous insights into the mechanisms underlying this pathological mineralization process, there is still a lack of effective treatment therapies interfering with the calcification process in the vessel wall. Current anti-calcifying therapeutics may induce detrimental side effects at the level of the bone, as arterial media calcification is regulated in a molecular and cellular similar way as physiological bone mineralization. This especially is a complication in patients with chronic kidney disease and diabetes, who are the prime targets of this pathology, as they already suffer from a disturbed mineral and bone metabolism. This review outlines recent treatment strategies tackling arterial calcification, underlining their potential to influence the bone mineralization process, including targeting vascular cell transdifferentiation, calcification inhibitors and stimulators, vascular smooth muscle cell (VSMC) death and oxidative stress: are they a friend or foe? Furthermore, this review highlights nutritional additives and a targeted, local approach as alternative strategies to combat arterial media calcification. Paving a way for the development of effective and more precise therapeutic approaches without inducing osseous side effects is crucial for this highly prevalent and mortal disease. [ABSTRACT FROM AUTHOR]

Introduction: Hypertension is a condition which represents one of the main risk factors for the development of cardiovascular diseases. High sodium intake contributes to occurrence of hypertension, increasing the volume of extracellular fluid. Therefore, World Health Organization (WHO) and other associations involved with hypertension research advise to decrease intake of sodium. Effervescent dosage forms usually contain high levels of sodium which could lead to above mentioned health issues. Aim: The aim of this study was to evaluate the levels of sodium in the effervescent dosage forms available in the Serbian drug market. Methods: Data about sodium levels, and excipients was obtained from Summary of Product Characteristics from website of Medicines and Medical Devices Agency of Serbia (ALIMS). Maximum daily doses recommended by the manufacturer and approved by ALIMS were observed. Exposure to sodium through consumption of maximum daily doses was calculated as percentages of the adequate daily intake given by Food and Nutrition Board (Institute of Medicine, National Academies, Washington D.C., USA), and also as percentage of recommended daily intake of sodium given by WHO. Results: There are five formulations with exposure to sodium through consumption of maximum daily doses higher than 100% of the adequate daily intake (2 g), all of which are effervescent tablet formulations. The highest exposure to sodium was found in effervescent tablets containing acetylsalycic acid (500 mg) as active pharmaceutical ingredient: 250.62 % for people aged 51 to 70 years; 271.50 % for people aged 70 and older. Conclusion: In effervescent dosage forms available on Serbian market, level of sodium can be very high, even up to 271.50% of adequate daily intake when maximum daily doses are consumed. Major cause for concern is for vascular patients who use effervescents for chronic therapy. This data should be considered during prescribing and dispensing this category of medicines as well as during analyzing pharmacovigilance.

Glioblastoma multiforme (GBM) is the most malignant primary brain tumor and is characterized by vascular hyperplasia, necrosis, and high cell proliferation. Despite current standard therapies, including surgical resection and chemoradiotherapy, GBM patients survive for only about 15 months after diagnosis. Recently, the U.S. Food and Drug Administration (FDA) has approved an antiangiogenesis medication for recurrent GBM-bevacizumab-which has improved progression-free survival in GBM patients. Although bevacizumab has resulted in significant early clinical benefit, it inescapably predisposes tumor to relapse that can be represented as an infiltrative phenotype. Fundamentally, bevacizumab antagonizes the vascular endothelial growth factor A (VEGFA), which is consistently released on both endothelial cells (ECs) and GBM cells. Actually, VEGFA inhibition on the ECs leads to the suppression of vascular progression, permeability, and the vasogenic edema. However, the consequence of the VEGFA pathway blockage on the GBM cells remains controversial. Nevertheless, a piece of evidence supports the relationship between bevacizumab application and compensatory activation of kinase signaling within GBM cells, leading to a tumor cell invasion known as the main mechanism of bevacizumab-induced tumor resistance. A complete understanding of kinase responses associated with tumor invasion in bevacizumab-resistant GBMs offers new therapeutic opportunities. Thus, this study aimed at presenting a brief overview of preclinical and clinical data of the tumor invasion and resistance induced by bevacizumab administration in GBMs, with a focus on the kinase responses during treatment. The novel therapeutic strategies to overcome this resistance by targeting protein kinases have also been summarized. [ABSTRACT FROM AUTHOR]

Recently there has been a great evolution of new diagnostic and therapeutic methods of cardiovascular diseases. However, they still remain the most common death cause in the Western countries. Despite the fact that new methods of dealing with cardiovascular diseases like for example percutaneous coronary interventions or coronary artery bypass grafting are constantly being improved, there is still a group of patients that can not undergo the routine treatment. It is a good stimulus for searching different ways of dealing with cardiovascular diseases. New vascular methods based on interfering in processes of vessels' creation and regression, seem to be an interesting direction of current studies. This article reviews the basis of vasculogenesis, angiogenesis and arteriogenesis and angiogenic therapies, learned from the latest trials. Vascular therapies offer a promise as a novel treatment for ischemic heart disease, particularly for patients who are not candidates for current methods of revascularization.

Background: Early cardiovascular disease starts in the endothelium leading to functional changes in the vasculature. These changes can be depicted by assessment of arterial stiffness or elasticity. There are several techniques to assess arterial stiffness. Increased arterial stiffness or decreased arterial elasticity has been associated with cardiovascular risk factors. There is now evidence that small artery elasticity is a strong predictor for arterial hypertension. Moreover arterial elasticity provides extra prognostic information beyond arterial blood pressure measurement. Arterial stiffness attenuation may reflect the true reduction of arterial wall damage. Results: ACE-inhibitors, angiotensin II receptor blockers, aldosterone antagonists and calcium antagonists have favorable effects in improving arterial elasticity, while beta-blockers have an inverse effect. Diuretics have not been evaluated. Lipid lowering therapy, some antidiabetic therapy have shown to reduce arterial stiffness. Inflammatory and infectious diseases have been associated with vascular inflammation and consequently increase in arterial stiffness. The effect of anti-inflammatory agents and antiretroviral therapy on arterial stiffness is under investigation. Conclusions: Measurement of arterial stiffness will not only be helpful in the detection of early vascular disease but also as a tool in the selection and follow-up monitoring of therapeutic strategies aimed at preventing or delaying progression of vascular disease. [ABSTRACT FROM AUTHOR]

Marfan syndrome is a congenital disorder of the connective tissue with a long history of clinical and basic science breakthroughs that have forged our understanding of vascular-disease pathogenesis. The biomedical importance of Marfan syndrome was recently underscored by the discovery that the underlying genetic lesion impairs both tissue integrity and transforming growth factor-β regulation of cell behavior. This discovery has led to the successful implementation of the first pharmacological intervention in a connective-tissue disorder otherwise incurable by either gene-based or stem cell–based therapeutic strategies. More generally, information gathered from the study of Marfan syndrome pathogenesis has the potential to improve the clinical management of common acquired disorders of connective-tissue degeneration. Mt Sinai J Med 77:366–373, 2010. © 2010 Mount Sinai School of Medicine [ABSTRACT FROM AUTHOR]

Endoscopic ultrasound (EUS) is an imaging technique that has consolidated its role as an important tool for diagnosis and therapeutics. In recent years we have seen a dramatic increase in the number of EUS-guided therapeutic indications (celiac plexus neurolysis/block, pseudocyst drainage, etc). Preliminary reports have suggested EUS may also be used to guide vascular access for both imaging and treating different vascular diseases. This review aims to objectively describe the existing evidence in the field.