Adenomatous Polyposis Syndromes: Familial Adenomatous Polyposis and MutYH -Associated Polyposis

Abstract

The purpose of this review is to provide an overview of the etiology, diagnosis, and clinical management of the two most common polyposis; change adenomatous to polyposis hereditary colorectal cancer syndromes, familial adenomatous polyposis (FAP) and MUTYH-associated polyposis (MAP). The syndromes are caused by inherited genetic variants in the APC and MutYH genes, respectively. Both syndromes carry significant increased risk of colorectal and extracolonic cancers. Intense surveillance is required to reduce this risk, and colectomy or proctocolectomy is frequently the ultimate form of colorectal cancer risk reduction. The colorectal phenotype and extracolonic manifestations continue to evolve as more is learned about the natural history of the diseases, particularly MAP.

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Robust feature extraction algorithm suitable for real-time embedded applications

Abstract

Smart cameras integrate processing close to the image sensor, so they can deliver high-level information to a host computer or high-level decision process. One of the most common processing is the visual features extraction since many vision-based use-cases are based on such algorithm. Unfortunately, in most of cases, features detection algorithms are not robust or do not reach real-time processing. Based on these limitations, a feature detection algorithm that is robust enough to deliver robust features under any type of indoor/outdoor scenarios is proposed. This was achieved by applying a non-textured corner filter combined to a subpixel refinement. Furthermore, an FPGA architecture is proposed. This architecture allows compact system design, real-time processing for Full HD images (it can process up to 44 frames/91.238.400 pixels per second for Full HD images), and high efficiency for smart camera implementations (similar hardware resources than previous formulations without subpixel refinement and without non-textured corner filter). For accuracy/robustness, experimental results for several real-world scenes are encouraging and show the feasibility of our algorithmic approach.

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Inflammation – Cause or Consequence of Heart Failure or Both?

Abstract

Purpose of Review

With the intention to summarize the currently available evidence on the pathophysiological relevance of inflammation in heart failure, this review addresses the question whether inflammation is a cause or consequence of heart failure, or both.

Recent Findings

This review discusses the diversity (sterile, para-inflammation, chronic inflammation) and sources of inflammation and gives an overview of how inflammation (local versus systemic) can trigger heart failure. On the other hand, the review is outlined how heart failure-associated wall stress and signals released by stressed, malfunctioning, or dead cells (DAMPs: e.g., mitochondrial DNA, ATP, S100A8, matricellular proteins) induce cardiac sterile inflammation and how heart failure provokes inflammation in various peripheral tissues in a direct (inflammatory) and indirect (hemodynamic) manner. The crosstalk between the heart and peripheral organs (bone marrow, spleen, gut, adipose tissue) is outlined and the importance of neurohormonal mechanisms including the renin angiotensin aldosteron system and the ß-adrenergic nervous system in inflammation and heart failure is discussed.

Summary

Inflammation and heart failure are strongly interconnected and mutually reinforce each other. This indicates the difficulty to counteract inflammation and heart failure once this chronic vicious circle has started and points out the need to control the inflammatory process at an early stage avoiding chronic inflammation and heart failure. The diversity of inflammation further addresses the need for a tailored characterization of inflammation enabling differentiation of inflammation and subsequent target-specific strategies. It is expected that the characterization of the systemic and/or cardiac immune profile will be part of precision medicine in the future of cardiology.

http://ift.tt/2t7PuuZ

SGLT-2 Inhibitors in Heart Failure: Implications for the Kidneys

Abstract

Purpose of Review

This review aims to summarize the renal effects of sodium-glucose transporter-2 (SGLT-2) inhibitors and their potential implications in heart failure pathophysiology.

Recent Findings

In patients with diabetes and established atherosclerosis, the SGLT-2 inhibitor empagliflozin versus placebo significantly reduced the rate of heart failure admissions with 35%. Moreover, empagliflozin slowed kidney disease progression and reduced the need for renal replacement therapy.

Summary

SGLT-2 inhibitors inhibit proximal tubular sodium and chloride reabsorption, leading to increased nephron flux throughout the distal renal tubules, most notably at the level of the macula densa. Afferent arteriolar vasoconstriction is promoted through tubulo-glomerular feedback and reduces glomerular capillary hydrostatic pressure, relieving podocyte stress and explaining renal preservation. Further, plasma volume is contracted and natriuresis promoted without inducing neurohumoral activation. Finally, SGLT-2 inhibitors may improve endothelial function and energy metabolism efficiency. Together, these promising features place them as a potential novel treatment for heart failure.

http://ift.tt/2sn989b

Lysophosphatidic Acid Protects Against Endotoxin-Induced Acute Kidney Injury

Abstract

Septic shock is the most common cause of acute kidney injury (AKI), but the underlying mechanisms remain unclear and no targeted therapies exist. Lysophosphatidic acid (LPA) is a bioactive lipid which in vivo administration was reported to mitigate inflammation and injuries caused by bacterial endotoxemia in the liver and lung. The objective of the present study was to determine whether LPA can protect against sepsis-associated AKI. C57BL/6 mice were treated with LPA 18:1 (5 mg/kg, i.p.) 1 h before being injected with the endotoxin lipopolysaccharide (LPS), and AKI was evaluated after 24 h. LPA significantly decreased the elevation of plasma urea and creatinine caused by LPS. In the kidney, LPA pretreatment significantly reduced the upregulation of inflammatory cytokines (IL-6, TNFα, monocyte chemoattractant protein-1 (MCP-1)), and completely prevented downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha and upregulation of heme oxygenase-1 caused by LPS. LPA also prevented LPS-mediated alterations of the renal mitochondrial ultrastructure. In vitro pretreatment with LPA 18:1 significantly attenuated LPS-induced upregulation of the inflammatory cytokines (TNFα and MCP-1) in RAW264 macrophages. Moreover, in vivo LPS treatment lowered urinary LPA concentration and reduced LPA anabolic enzymes (autotaxin and acylglycerol kinase), and increased the LPA catalytic enzyme (lipid phosphate phosphatase 2) expression in the kidney cortex. In conclusion, exogenous LPA exerted a protective action against renal inflammation and injuries caused by bacterial endotoxemia. Moreover, LPS reduces the renal production of LPA suggesting that sepsis-associated AKI could be mediated, at least in part, by alleviation of the protective action of endogenous LPA.

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Antipyretic Effects of Citral and Possible Mechanisms of Action

Abstract

Citral is a mixture of the two monoterpenoid isomers (neral and geranial) widely used as a health-promoting food additive safe for human and animal (approved by the US Food and Drug Administration). In vitro studies have reported on the capability of citral to reduce inflammation. Here, we report antipyretic effects of citral in vivo using the most well-accepted model of sickness syndrome, i.e., systemic administration of lipopolysaccharide (LPS) to rats. Citral given by gavage caused no change in control euthermic rats (treated with saline) but blunted most of the assessed parameters related to the sickness syndrome [fever (hallmark of infection), plasma cytokines (IL-1β, IL-6, and TNF-α) release, and prostaglandin E₂ (PGE₂) synthesis (both peripherally and hypothalamic)]. Moreover, LPS caused a sharp increase in plasma corticosterone levels that was unaltered by citral. These data are consistent with the notion that citral has a corticosterone-independent potent antipyretic effect, acting on the peripheral febrigenic signaling (plasma levels of IL-1β, IL-6, TNF-α, and PGE₂), eventually down-modulating hypothalamic PGE₂ production.

http://ift.tt/2s8bHHM

Biomarkers in Sleep Apnea and Heart Failure

Abstract

Purpose of Review

Sleep-disordered breathing (SDB) is highly prevalent in heart failure (HF) and may confer significant stress to the cardiovascular system and increases the risk for future cardiovascular events. The present review will provide updates on the current understanding of the relationship of SDB and common HF biomarkers and the effect of positive airway pressure therapy on these biomarkers, with particular emphasis in patients with coexisting SDB and HF.

Recent Findings

Prior studies have examined the relationship between HF biomarkers and SDB, and the effect of SDB treatment on these biomarkers, with less data available in the context of coexisting SDB and HF. Overall, however, the association of SDB and circulating biomarkers has been inconsistent.

Summary

Further research is needed to elucidate the relationship between biomarkers and SDB in HF, to evaluate the clinical utility of biomarkers over standard methods in large, prospective studies and also to assess the impact of treatment of SDB on these biomarkers in HF via interventional studies.

http://ift.tt/2s8j9m8