1,721,147 research outputs found
Non-dipper blood pressure pattern and glycemic alterations: does post-prandial glucose rise predict lack of nocturnal pressure drop?
Type 2 diabetes (T2DM) and non-dipping pattern of blood pressure (that is, when nocturnal systolic blood pressure falls by < 10% from the daytime systolic blood pressure values) during 24-h ambulatory blood pressure (ABPM) monitoring are two factors both increasing the risk for cardiovascular disease. Little is known about the relationship between the circadian profile of blood pressure dipping pattern and insulin glucose metabolism in patients without any known overt metabolic diseases
Valutazione del potenziale angiogenico di cellule mesenchimali staminali adulte derivate dalla polpa dentaria umana
Dental pulp has been revealed as an accessible and a rich source of mesenchymal stem cells (MSCs) and its biological potential is currently under intense investigation. MSCs from dental pulp stem cells (DPSC) have been indicated as a heterogeneous population oriented not only in repairing dentine but also in maintaining vascular and nervous homeostasis of the teeth. We sought to verify the phenotype of cells isolated from dental pulp of young donors and to investigate in vitro their role as pericyte-like cells. Specifically, we evaluated how different culture conditions can modulate expression of pericyte markers in DPSC and their capacity to stabilize endothelial tubes in vitro. DPSC cultured in standard conditions expressed MSC markers and demonstrated to contain a population expressing the pericyte marker NG2. These DPSC were associated with low sprouting capacity in extracellular (EC) Matrix and limited ability in retaining tubes formed by endothelial cells in a coculture angiogenesis model. When cultured in endothelial growth medium (EGM-2), DPSC significantly upregulated NG2. The resulting population conserved the stem marker CD73 but was negative for calponin and endothelial markers. EGM-2-conditioned DPSC showed a higher sprouting ability in EC Matrix and efficient association with human umbilical vein endothelial cells allowing the partial retention of endothelial tubes for several days. Among growth factors contained in EGM-2 we identified basic fibroblast growth factor (FGF) as mainly responsible for NG2 upregulation and long-term stabilization of endothelial tubes. According to the in vitro analysis, DPSC represent an effective source of pericytes, and the appropriate culture conditions could result in a population with a promising ability to stabilize vessels and promote vascular maturation
Aspirin, platelets, and cancer: The point of view of the internist.
Growing evidence suggests the beneficial effect of aspirin against some types of cancer, particularly of the gastrointestinal tract, and it has been provided for an effect both in cancer prevention as well as in survival improvement of cancer patients. Aspirin benefits increase with duration of treatment, especially after 10years of treatment. The inhibition of platelet activation at sites of gastrointestinal mucosal lesions could be the primary mechanism of action of low-dose aspirin. Indeed, the formation of tumor cell-induced platelet aggregates may favor immune evasion, by releasing angiogenic and growth factors, and also by promoting cancer cell dissemination. Moreover, platelets may contribute to aberrant COX-2 expression in colon carcinoma cells, thereby contributing to downregulation of oncosuppressor genes and upregulation of oncogenes, such as cyclin B1. Platelet adhesion to cancer cells leads also to an increased expression of genes involved in the EMT, such as the EMT-inducing transcription factors ZEB1 and TWIST1 and the mesenchymal marker vimentin. The aspirin-mediated inactivation of platelets may restore antitumor reactivity by blocking the release of paracrine lipid and protein mediators that induce COX-2 expression in adjacent nucleated cells at sites of mucosal injury. Thus, recent findings suggest interesting perspectives on "old" aspirin and NSAID treatment and/or "new" specific drugs to target the "evil" interactions between platelets and cancer for chemoprevention
Diabetes mellitus in the pre-school child.
Diabetes mellitus presents rarely in the pre-school child and presents specific problems because of the peculiarity of the young child physiology. Pathogenesis involves the classic immunological mechanisms, with a higher incidence of other autoimmunity and family history of diabetes. Because of the rarity of the condition in this age group, the delay of the recognition of the signs and symptoms, which are often subtle at onset, determines the increased incidence of ketoacidosis. The reasons for the lower glycaemic control in this age group include the persistence of endogenous insulin, but also a more detailed involvement by the parents in organising diabetes. For the same reason ketoacidosis is an unusual occurrence after diagnosis. As to insulin therapy, three or more injections a day should be recommended, as in the older child, while the modern devices for blood glucose monitoring have proved useful to improve glycaemic control and to decrease the frequency of nocturnal hypoglycaemia, which gives particular concern given the vulnerability of the nervous system in this age group. Management of diabetes in the pre-school child may result very difficult for both parents and health carers because of the erratic daily pattern of activity, sleep and feeding; however, with a cautious strategy which involves insulin therapy, diet and monitoring it is possible to achieve satisfactorily the following aims: physical well-being of the young child, normal growth, lack of hyperglycaemia or hypoglycaemia, acceptable value of glycosilated haemoglobin
Role of growth factors in the development of diabetic complications
The structural changes characterising diabetic microangiopathy, which may be referred to as 'abnormal growth' and 'impaired regeneration', strongly suggest a role for a number of aberrantly expressed growth factors, possibly acting in combination, in the development of these complications. This initial speculation has been supported by the detection of increased concentrations of several growth factors in the target tissues of diabetic long-term complications, and by enhanced expression of these growth factors consequent to the activation of the biochemical pathways linking hyperglycaemia to microvascular changes: the polyol pathway; non-enzymatic glycation of proteins; vasoactive hormones; oxidative stress, and hyperglycaemic pseudohypoxia. As to nephropathy, insulin-like growth factor I (IGF-I) seems to be implicated in the earlier stages of the disease, while transforming growth factor beta (TGF beta) is involved both in the early and later stages, being responsible, at least in part, for extracellular matrix (ECM) accumulation. Vascular endothelial growth factor (VEGF) plays a pivotal role both in non-proliferative and proliferative retinopathy. Finally, deficiency of several neurotrophic factors, namely nerve growth factor (NGF) and IGF-I has been related to the degeneration or impaired regeneration occurring in diabetic neuropathy. Knowledge of the involvement of growth factors in diabetic microangiopathy opens the way to new therapeutic interventions aimed at blocking the deleterious actions of several growth factors
Homocysteine, methylenetetrahydrofolate reductase, folate status and atherothrombosis: A mechanistic and clinical perspective
Observational studies consistently reported an association between plasma total homocysteine concentrations and the risk of vascular events. In contrast, data from randomized trials largely support the hypothesis that mild elevations in homocysteine level have a modest effect on cardiovascular risk.
A substantial body of evidence suggests that platelet activation is, at least in part, a transducer of the effects of high homocysteine in promoting atherothrombosis. The larger treatment effect recorded in several supplementation trials by subjects not on antiplatelet agents may support this hypothesis and justify, at least in part, the success of folate therapy in primary prevention.
Circulating folate and homocysteine levels as well as MTHFR genotype, while emerging as major predictors of the risk of vascular events and of the efficacy of folic acid therapy, have also proved to be determinants of an inter individual variability in the degree of lipid peroxidation and platelet activation, and of the extent of their down regulation by folic acid. This may justify a variability in folate requirements, to be further characterized with dose finding studies using biochemical endpoints.
The combination of low-dose aspirin and low-dose folate would appear to be ideally suited for the primary prevention of both coronary and cerebrovascular events, and additional clinical trials should assess the efficacy and safety of these agents. (C) 2015 Elsevier Inc. All rights reserved
Coagulation at the crossroads of the communicable/non-communicable disease dyad: The case of pneumonia
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