1,721,009 research outputs found

    Vascular actions of insulin with implications for endothelial dysfunction

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    Hemodynamic actions of insulin depend largely on the hormone’s ability to stimulate synthesis and release of endothelial mediators, whose balanced activity ensures dynamic control of vascular function. Nitric oxide (NO), endothelin-1 (ET-1), and reactive oxygen species (ROS) are important examples of endothelial mediators with opposing properties on vascular tone, hemostatic processes, and vascular permeability. Reduced NO bioavailability, resulting from either insufficient production or increased degradation of NO, characterizes endothelial dysfunction. In turn, endothelial dysfunction predicts vascular complications of metabolic and hemodynamic disorders. In the cardiovascular system, insulin stimulates the production and release of NO, ET-1, and ROS via activation of distinct intracellular signaling pathways. Under insulin-resistant conditions, increased insulin concentrations and/or impaired insulin-signaling pathways in the vasculature may contribute to imbalance in secretion of endothelial mediators that promote pathogenesis of vascular abnormalities. This short review describes signaling pathways involved in insulin-stimulated release of NO, ROS, and ET-1 and suggests possible molecular mechanisms by which abnormal insulin signaling may contribute to endothelial dysfunction

    Mitochondria and Reactive Oxygen Species

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    Fascination by the mitochondria, “the colonial posterity of migrant prokaryocytes, probably primitive bacteria that swam into ancestral precursors of our eukaryotic cells and stayed there,”1 stems from the above-mentioned nebulous endosymbiotic theory of their origin, as well as from the growing realization of a very special role that they play in the pathogenesis of diverse diseases. These organelles generate energy primarily in the form of the electrochemical proton gradient (H), which fuels ATP production, ion transport, and metabolism.2 Generation of this universal energy currency, H, occurs through the series of oxidative reactions conducted by the respiratory chain complexes at the ion-impermeable, almost cholesterolfree inner membrane. Reduced nicotinamide adenine dinucleotide represents the entry point to the complex I (reduced nicotinamide adenine dinucleotide:ubiquinone reductase), whereas the reduced ubiquinol enters the respiratory chain in the complex III (ubiquinol:cytochrome c [cyt-c] reductase) to reduce cyt-c, the electron carrier to the complex IV, cyt-c oxidase. Each of these steps generates H by electrogenic pumping of protons from the mitochondrial matrix to the intermembrane space and is coupled to electron flow, thus generating the electric membrane potential of 180 to 220 mV and a pH gradient of 0.4 to 0.6 U across the inner mitochondrial membrane resulting in the negatively charged matrix side of the membrane and alkaline matrix. Ultimately, accumulated H is converted into the influx of protons into the matrix driving ATP synthesis or protein transport. In addition, these end points are necessary for the execution of 2 major enzymatic metabolic pathways within the mitochondrial matrix: the tricarboxylic acid (TCA) oxidation cycle and the fatty acid -oxidation pathway. This intricate system fueling cellular functions is as elegant as it is vulnerable: practically every component of the system, from the electron transport chain complexes to the permeability properties of the membranes, is a target for various noxious stimuli, some of which can be generated within mitochondria themselves. The list of these noxious stimuli is too long to be recounted here, and the interested reader may refer to a recent excellent review.3 These ancestral oxygen-using proteobacterial invaders carried with them into eukaryotic cells not only evolutionary benefits but also potential side reactions, most dangerous of which are “exothermic oxygen combustion and free radical emission.” This review is focused on one component of the noxious mitochondrial pathway: reactive oxygen species (ROS) from a mitochondrial perspective, which has previously been extensively reviewed.4 Therefore, we shall present the most recent findings but periodically offer historical perspective

    Piezoelectric device vs. conventional rotative instruments in impacted third molar surgery: relationships between surgical difficulty and postoperative pain with histological evaluations

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    Purpose: To investigate and compare the influence of surgical difficulty on postoperative pain after treatment of impacted mandibular third molars by rotatory osteotomy or Piezoelectric surgery. Materials and methods: A prospective, randomized, split-mouth study was performed of 52 patients with bilateral and symmetrically oriented impacted mandibular third molars, who were surgically treated using a burr (Group A) on one random side of the lower jaw and a Piezoelectric device (Group B) on the contralateral side. Surgical difficulty was evaluated using a modified version of the Parant scale to cate- gorize “simple extractions” and “complex extractions”. Primary outcome parameters were the comparison of the postoperative pain evaluation rated on the Visual Analogue Scale from day 0 to day 6 postsurgery, and the assessment of differences in surgery time between the groups. Bone biopsies were taken during surgery to assess differences in bone tissue damage levels between the two different techniques. Results: In “complex extractions” lower pain evaluation and significantly shorter surgery times were recorded when rotatory instruments were used. In “simple extractions”, similar surgery times were observed for both techniques, but pain was greatest on the day of surgery when the burr was used. Bone heat osteonecrosis was observed only in the rotatory group and a high level of alkaline phosphatase was noted only in the Piezoelectric group. Conclusion: Pain after extraction of a mandibular third molar increases with increased surgical difficulty and especially in longer interventions. The integrity of the bony structure observed after the ultrasonic technique may favour the bone healing process

    Porcine-Derived Xenograft Combined with a Soft Cortical Membrane versus Extraction Alone for Implant Site Development: A Clinical Study in Humans.

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    Background: An adequate alveolar crest is essential for implant placement in terms of esthetics and function. The objective of this randomized clinical trial was to compare the preservation of the alveolar ridge dimensions following tooth extraction using porcine-derived xenograft combined with a membrane versus extraction-alone (EXT) sites. Methods: Fifteen patients who required double extraction of contralateral premolars and delayed implant placement were randomly selected to receive both ridge-preservation procedure and EXT. The test sites (alveolar ridge preservation [ARP]) included 15 sockets treated using a corticocancellous porcine bone xenograft (OsteoBiol® Gen-Os; Tecnoss srl, Giaveno, Italy) associated with a soft cortical membrane (OsteoBiol® Lamina; Tecnoss srl), while the corresponding control sites (EXT) were left without grafting for EXT. Horizontal and vertical ridge dimensions were recorded at baseline and 6 months after extractions. Results: After 6 months, the EXT sites showed a significantly greater reabsorption of the buccolingual/palatal dimension of the alveolar ridge (3.7 ± 1.2 mm) compared with the ARP sites (1.8 ± 1.3 mm). The mean vertical ridge height reduction in the control sockets was 3.1 ± 1.3 mm at the buccal sites and 2.4 ± 1.6 mm at the lingual sites compared with 0.6 ± 1.4 and 0.5 ± 1.3 mm, respectively, in the test sockets. The differences between test and control sockets were not significant for the mesial and distal measurements. Conclusions: The placement of a porcine xenograft with a membrane in an extraction socket can be used to reduce the hard tissue reabsorption after tooth extraction compared with EXT.Background: An adequate alveolar crest is essential for implant placement in terms of esthetics and function. The objective of this randomized clinical trial was to compare the preservation of the alveolar ridge dimensions following tooth extraction using porcine-derived xenograft combined with a membrane versus extraction-alone (EXT) sites. Methods: Fifteen patients who required double extraction of contralateral premolars and delayed implant placement were randomly selected to receive both ridge-preservation procedure and EXT. The test sites (alveolar ridge preservation [ARP]) included 15 sockets treated using a corticocancellous porcine bone xenograft (OsteoBiol® Gen-Os; Tecnoss srl, Giaveno, Italy) associated with a soft cortical membrane (OsteoBiol® Lamina; Tecnoss srl), while the corresponding control sites (EXT) were left without grafting for EXT. Horizontal and vertical ridge dimensions were recorded at baseline and 6 months after extractions. Results: After 6 months, the EXT sites showed a significantly greater reabsorption of the buccolingual/palatal dimension of the alveolar ridge (3.7±1.2mm) compared with the ARP sites (1.8±1.3mm). The mean vertical ridge height reduction in the control sockets was 3.1±1.3mm at the buccal sites and 2.4±1.6mm at the lingual sites compared with 0.6±1.4 and 0.5±1.3mm, respectively, in the test sockets. The differences between test and control sockets were not significant for the mesial and distal measurements. Conclusions: The placement of a porcine xenograft with a membrane in an extraction socket can be used to reduce the hard tissue reabsorption after tooth extraction compared with EXT. © 2011 Wiley Periodicals, Inc
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