Prevalence and severity of atherosclerosis in different arterial territories and its relation with obesity

BackgroundThere is uneven association between obesity, traditional risk factors, and cardiovascular events. We aimed to analyze the relation between cardiovascular risk factors, including obesity, with the severity of atherosclerosis in different arterial territories.MethodsArteries from five territories (circle of Willis, carotids, coronaries, aorta, and renal) were taken from 185 persons, newborn to 90 years undergoing autopsy in the Forensic Medical Service in Mexico City, to determine atherosclerotic lesions by histopathological study. Lesions were classified according to the American Heart Association grading system as early (types I–III) and advanced (types IV–VI). The degree of atherosclerosis was correlated with arterial territories and risk factors.ResultsFrequencies of advanced lesions according to arterial territories were as follows: circle of Willis, 28%; right carotid, 36%; left carotid, 25%; right coronary, 71%; left coronary, 85%; right renal, 26%; left renal, 29%; and aorta, 52%; P=.0001, for all analyses. There was a higher risk for advanced lesions with increasing body mass index (BMI) (P=.004). However, after adjusting for age, gender, smoking status, hypertension, and diabetes mellitus, BMI was not independently associated with advanced lesions.ConclusionsCoronary arteries are significantly more affected than other arterial territories regardless of risk factors, showing the effect of local and systemic factors in the severity of atherosclerosis. We did not find an independent association between advanced atherosclerotic lesions and obesity.     

Brushing associated with oral irrigation in maintaining implants and overdentures hygiene – a randomized clinical trial

Odontology - Evaluate, through a randomized clinical trial, the efficacy of brushing associated with oral irrigation in maintaining implant and overdenture hygiene. Thirty-eight participants, who...     

Specialized pro‐resolving lipid mediators in experimental periodontitis: A systematic review

Recently, several studies demonstrated the potential of using specialized pro‐resolving lipid mediators (SPMs), as a novel approach, in treating periodontitis in pre‐clinical models. This review aimed to systematically evaluate the biological actions of SPMs on periodontal tissues in animals with experimentally induced periodontitis. This systematic review was performed by following the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) guidelines. Studies were searched in three databases. Meta‐analysis was not performed because of the data heterogeneity. Study quality was assessed using Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE) Risk of Bias tool. Six studies using an experimental periodontitis model to test the efficacy of SPMs were selected. Resolvin E1 and lipoxins were topically applied to treat experimental periodontitis. Alveolar bone loss could be significantly prevented and regenerated by applying SPMs, when compared to the control group. The dosages of SPMs and the periods of disease induction varied based on the pre‐clinical model employed. Two studies further demonstrated the positive shift in microbial composition, in line with positive shift in inflammatory status, that are regulated by SPMs. Clinical studies are needed to optimize the application of SPMs in treating periodontal diseases in humans.     

The psychological impact of cryptic chromosomal abnormalities diagnosis announcement

This qualitative study aims to describe the psychological impact of the diagnosis announcement of pathogenic Copy Number Variations (pCNVs). We performed semi-structured interviews of 60 parents of 41 affected children and 5 geneticists who announced the diagnoses. The diagnosis of the best characterized microdeletion syndromes, often defined by patronymic names (e.g. Williams syndrome), is generally made on a clinical basis by geneticists and confirmed by fluorescence in situ hybridization analysis. Chromosomal microarray, on the contrary, can allow the disclosure of rare pCNVs named after cytogenetic formulas, with poorly known clinical consequences: this makes doctors feel less confident with these diagnosis announcements. The disclosure of pCNVs named after cytogenetic formulas does not facilitate the parental mental representation of the disease, leading some parents to call into question the genotype-phenotype correlation or the very notion of a diagnosis. The announcement of inherited pCNVs can increase the feeling of parental guilt; the disclosure of de novo pCNVs can induce a feeling of “breakage” in the mental representation of the parent-child vertical transmission. In conclusion, our study shows that the disclosure of pCNVs has a significant psychological impact: a multidisciplinary approach to the diagnosis announcement, including a psychological support, should be systematically warranted.     

Pancreatic Islet Vasculature Adapts to Insulin Resistance Through Dilation and Not Angiogenesis

Pancreatic islets adapt to insulin resistance through a complex set of changes, including β-cell hyperplasia and hypertrophy. To determine if islet vascularization changes in response to insulin resistance, we investigated three independent models of insulin resistance: ob/ob, GLUT4^+/−, and mice with high-fat diet–induced obesity. Intravital blood vessel labeling and immunocytochemistry revealed a vascular plasticity in which islet vessel area was significantly increased, but intraislet vessel density was decreased as the result of insulin resistance. These vascular changes were independent of islet size and were only observed within the β-cell core but not in the islet periphery. Intraislet endothelial cell fenestration, proliferation, and islet angiogenic factor/receptor expression were unchanged in insulin-resistant compared with control mice, indicating that islet capillary expansion is mediated by dilation of preexisting vessels and not by angiogenesis. We propose that the islet capillary dilation is modulated by endothelial nitric oxide synthase via complementary signals derived from β-cells, parasympathetic nerves, and increased islet blood flow. These compensatory changes in islet vascularization may influence whether β-cells can adequately respond to insulin resistance and prevent the development of diabetes.Pancreatic islets are highly vascularized, and this feature is critical for β-cells to rapidly sense the blood glucose and secrete insulin into the systemic circulation (1,2). Islet vascularization begins early in pancreas development and is maintained in adulthood as a consequence of islet cell production of angiogenic factors such as vascular endothelial growth factor-A (VEGF-A) and angiopoietin-1 (Ang-1) (3–6). These factors recruit endothelial cells (ECs), stimulate blood vessel growth and maturation, and in the case of VEGF-A, promote formation of EC fenestrations (5,6). In addition, ECs adjacent to pancreatic epithelium reciprocally influence islet cell differentiation and development (7,8).β-Cells have a remarkable ability to respond to changes in an organism’s metabolic state, such as changes in the blood glucose or increased insulin requirements. For example, when insulin resistance develops, β-cells of the pancreatic islet can dramatically increase insulin production and secretion with an increase of β-cell mass, thus maintaining normoglycemia (9,10). In this way, mouse models with marked insulin resistance and humans with obesity-related insulin resistance are hyperinsulinemic but not hyperglycemic. The mechanisms underlying this β-cell adaptation to insulin resistance and their subsequent failure in some individuals who develop type 2 diabetes are incompletely understood.Because of the highly vascularized state of pancreatic islets and the marked changes in β-cell size and number in the setting of insulin resistance, we hypothesized that the islet vasculature must adapt to these changes in β-cell mass and insulin requirements. We envisioned that a hyperplastic islet, like a growing tumor mass, would increase production of angiogenic factors to increase its vascular supply with expanding β-cell mass (11). To test this hypothesis, we examined islet vascularization in three mouse models of insulin resistance and found, unexpectedly, that islet vessel density was decreased, not increased, and that the intraislet vasculature became markedly dilated whereas vessels in the exocrine tissue were unchanged. The dilation of intraislet capillaries was independent of islet size, suggesting the vascular adaptation may primarily support increased β-cell insulin secretory demand rather than β-cell mass expansion. Moreover, these vascular changes were accompanied by an increase in islet parasympathetic innervation. Our results indicate that the metabolic state influences islet angioarchitecture and innervation, suggesting that islet neurovascular remodeling may influence whether β-cells can adequately respond to insulin resistance and maintain normoglycemia.     

Muscle strength and ankle mobility for the gait parameters in diabetic neuropathies

AimsTo evaluate the spatio-temporal variables of gait and the isometric muscle strength component of the ankle in patients with peripheral diabetic neuropathy. Also, verify the relationship between these variables and gait parameters.MethodsThis study involved 25 diabetic peripheral neuropathy (DPN) participants (62.4 ± 8.36 years) and 27 age-matched healthy control individuals (64.48 ± 6.21 years). The assessment of the spatio-temporal parameters of gait was performed using an electronic baropodometry treadmill. Prior to the collection data, each participant was instructed to walk on the treadmill in her/his habitual self-selected speed.ResultsDiabetic neuropathy group showed impairment of gait, with a smaller stride and length speed of the cycle, and increased duration of support time. Restricted dorsiflexion mobility and increased plantarflexion mobility were found, with a decrease in muscle strength of the dorsiflexors and plantiflexors. There was a significant relationship between plantiflexor muscle strength and the length and speed of the gait cycle. Also the muscle strengths of the plantiflexors and dorsiflexors, and the range of motion of dorsiflexion were predictors of gait performance.ConclusionsThe ankle, muscle strength and ankle mobility variables could explain changes in gait speed and range of motion in patients with DPN, allowing for the application of preventive strategies.