267 research outputs found

    Exercise improves endothelial dysfunction in young women with metabolic syndrome

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    Recent studies have reported that regular exercise reduces pro-inflammatory biomarkers in women with metabolic syndrome. However, to date little information is available on the influence of exercise on endothelial dysfunction, despite its important role during the development of atherosclerotic plaque. Accordingly, this study was designed to determine the influence of exercise on soluble vascular cell adhesion molecule (VCAM-1) in women with metabolic syndrome. Sixty adult women with metabolic syndrome according to the criteria reported by the National Cholesterol Education Program Adult Treatment Panel III volunteered for this study. Fourty-five were randomly included in experimental group to perform a 12-weeks aerobic training program, 3 days/week, consisting of warm up (10-min), main part (20-35-min [increasing 5 minutes each 3 weeks]) at a work intensity of 60-75% of peak heart rate (increasing 5% each 3 weeks) and cool-down (10-min). Control group included 15 age, sex and BMI-matched women with metabolic syndrome who did not perform any program. Written informed consent was obtained. Further the protocol was approved by an institutional ethic committee. Serum soluble VCAM-1 concentration was measured by ELISA, using a commercially available kit (Parameter, R&D Systems) twice: 72-hours before starting the program (pre-test) and after its ending (post-test). When compared to baseline soluble VCAM-1 concentration was significantly decreased after the 6-week protocol (448.3±26.7 vs 372.2±24.7 ng/ml; p\u3c0.05). No changes were reported in controls. A 12-weeks training program decreased soluble VCAM-1 concentration in women with metabolic syndrome. Further studies on this topic are required

    Plasmatic E-selectin levels were decreased in young women with metabolic syndrome after exercise training

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    Cellular adhesion molecules (CAMs) such as E-selectin are involved in the rolling, adhesion and extravasation of monocytes into the atherosclerotic plaque. Fortunately regular exercise may improve pro-inflammatory status in individuals with metabolic syndrome. Accordingly, this study was designed to determine the influence of exercise on soluble plasmatic E-selectin levels in women with metabolic syndrome. Sixty adult women with metabolic syndrome according to the criteria reported by the National Cholesterol Education Program Adult Treatment Panel III volunteered for this study. Fourty-five were randomly included in experimental group to perform a 12-weeks aerobic training program, 3 days/week, consisting of warm up (10-min), main part (20-35-min [increasing 5 minutes each 3 weeks]) at a work intensity of 60-75% of peak heart rate (increasing 5% each 3 weeks) and cool-down(10-min). Control group included 15 age, sex and BMI-matched women with metabolic syndrome that will not perform any program. Written informed consent was obtained. Further the protocol was approved by an institutional ethic committee. Plasmatic E-Selectin levels was measured by ELISA, using a commercially available kit (Parameter, R&D Systems) twice: 72-hours before starting the program (pre-test) and after its ending (post-test).Results: When compared to baseline soluble E-Selectin concentration was significantly decreased after the 6-weeks protocol (76.4±7.2 vs 57.1±6.4 ng/ml; p\u3c0.05). No changes were reported in controls. A 12-weeks aerobic training program decreased plasmatic E-Selectin concentration in women with metabolic syndrome

    Extreme High-Field Superconductivity in Thin Re Films

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    We report the high-field superconducting properties of thin, disordered Re films via magneto-transport and tunneling density of states measurements. Films with thicknesses in the range of 9 nm to 3 nm had normal state sheet resistances of \sim0.2 kΩ\Omega to \sim1 kΩ\Omega and corresponding transition temperatures in the range of 6 K to 3 K. Tunneling spectra were consistent with those of a moderate coupling BCS superconductor. Notwithstanding these unremarkable superconducting properties, the films exhibited an extraordinarily high upper critical field. We estimate their zero-temperature Hc2H_{c2} to be more than twice the Pauli limit. Indeed, in 6 nm samples the estimated reduced critical field Hc2/TcH_{c2}/T_c\sim 5.6 T/K is among the highest reported for any elemental superconductor. Although the sheet resistances of the films were well below the quantum resistance RQ=h/4e2R_Q=h/4e^2, their Hc2H_{c2}'s approached the theoretical upper limit of a strongly disordered superconductor for which kF1k_F\ell\sim1.Comment: 12 pages, 10 figure

    Development of DFSI using Fuzzy Logic to Analyze Risk Levels of Driving Activity

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    The objective of this study is to develop a Driving Fatigue Strain Index using fuzzy logic to analyze the risk levels of driving activity among road users. Driving fatigue is always related to the driving activity and has been identified as one of the vital contributors to the road accidents and fatalities in Malaysia. Therefore, the present paper introduces the use of fuzzy logic for the development of strain index to provide the systematic analysis and propose an appropriate solution in minimizing the number of road accidents and fatalities. The development of strain index is based on the six risk factors associated with driving fatigue; muscle activity, heart rate, hand grip pressure force, seat pressure distribution, whole-body vibration, and driving duration. The data is collected for all the risk factors and consequently, the three conditions or risk levels are defined as “safe”, “slightly unsafe”, and “unsafe”. A membership function is defined for each fuzzy conditions. IF-THEN rules were used to define the input and output variables which correspond to physical measures. This index is a reliable advisory tool for providing analysis and solutions to driving fatigue problem, which constitutes the first effort toward the minimization of road accidents and fatalities

    SDF1 in the dorsal corticospinal tract promotes CXCR4+ cell migration after spinal cord injury

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    <p>Abstract</p> <p>Background</p> <p>Stromal cell-derived factor-1 (SDF1) and its major signaling receptor, CXCR4, were initially described in the immune system; however, they are also expressed in the nervous system, including the spinal cord. After spinal cord injury, the blood brain barrier is compromised, opening the way for chemokine signaling between these two systems. These experiments clarified prior contradictory findings on normal expression of SDF1 and CXCR4 as well as examined the resulting spinal cord responses resulting from this signaling.</p> <p>Methods</p> <p>These experiments examined the expression and function of SDF1 and CXCR4 in the normal and injured adult mouse spinal cord primarily using CXCR4-EGFP and SDF1-EGFP transgenic reporter mice.</p> <p>Results</p> <p>In the uninjured spinal cord, SDF1 was expressed in the dorsal corticospinal tract (dCST) as well as the meninges, whereas CXCR4 was found only in ependymal cells surrounding the central canal. After spinal cord injury (SCI), the pattern of SDF1 expression did not change rostral to the lesion but it disappeared from the degenerating dCST caudally. By contrast, CXCR4 expression changed dramatically after SCI. In addition to the CXCR4+ cells in the ependymal layer, numerous CXCR4+ cells appeared in the peripheral white matter and in the dorsal white matter localized between the dorsal corticospinal tract and the gray matter rostral to the lesion site. The non-ependymal CXCR4+ cells were found to be NG2+ and CD11b+ macrophages that presumably infiltrated through the broken blood-brain barrier. One population of macrophages appeared to be migrating towards the dCST that contains SDF1 rostral to the injury but not towards the caudal dCST in which SDF1 is no longer present. A second population of the CXCR4+ macrophages was present near the SDF1-expressing meningeal cells.</p> <p>Conclusions</p> <p>These observations suggest that attraction of CXCR4+ macrophages is part of a programmed response to injury and that modulation of the SDF1 signaling system may be important for regulating the inflammatory response after SCI.</p

    Antiretroviral activity of 5-azacytidine during treatment of a HTLV-1 positive myelodysplastic syndrome with autoimmune manifestations

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    Myelodysplastic syndromes (MDS) are often accompanied by autoimmune phenomena. The underlying mechanisms for these associations remain uncertain, although T cell activation seems to be important. Human T-lymphotropic virus (HTLV-1) has been detected in patients with myelodysplastic syndromes, mostly in regions of the world which are endemic for the virus, and where association of HTLV-1 with rheumatological manifestation is not rare. We present here the case of a 58 year old man who presented with cytopenias, leukocytoclastic vasculitis of the skin and glomerulopathy, and was diagnosed as MDS (refractory anemia with excess blasts - RAEB 1). The patient also tested positive for HTLV-1 by PCR. After 8 monthly cycles of 5-azacytidine he achieved a complete hematologic remission. Following treatment, a second PCR for HTLV-1 was carried out and found to be negative. This is the first report in the literature of a HTLV-1-positive MDS with severe autoimmune manifestations, which was treated with the hypomethylating factor 5-azacitidine, achieving cytogenetic remission with concomitant resolution of the autoimmune manifestations, as well as HTLV-1-PCR negativity. HTLV-1-PCR negativity may be due to either immune mediated clearance of the virus, or a potential antiretroviral effect of 5-azacytidine. 5-azacytidine is known for its antiretroviral effects, although there is no proof of its activity against HTLV-1 infection in vivo

    Chondroitinase and Growth Factors Enhance Activation and Oligodendrocyte Differentiation of Endogenous Neural Precursor Cells after Spinal Cord Injury

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    The adult spinal cord harbours a population of multipotent neural precursor cells (NPCs) with the ability to replace oligodendrocytes. However, despite this capacity, proliferation and endogenous remyelination is severely limited after spinal cord injury (SCI). In the post-traumatic microenvironment following SCI, endogenous spinal NPCs mainly differentiate into astrocytes which could contribute to astrogliosis that exacerbate the outcomes of SCI. These findings emphasize a key role for the post-SCI niche in modulating the behaviour of spinal NPCs after SCI. We recently reported that chondroitin sulphate proteoglycans (CSPGs) in the glial scar restrict the outcomes of NPC transplantation in SCI by reducing the survival, migration and integration of engrafted NPCs within the injured spinal cord. These inhibitory effects were attenuated by administration of chondroitinase (ChABC) prior to NPC transplantation. Here, in a rat model of compressive SCI, we show that perturbing CSPGs by ChABC in combination with sustained infusion of growth factors (EGF, bFGF and PDGF-AA) optimize the activation and oligodendroglial differentiation of spinal NPCs after injury. Four days following SCI, we intrathecally delivered ChABC and/or GFs for seven days. We performed BrdU incorporation to label proliferating cells during the treatment period after SCI. This strategy increased the proliferation of spinal NPCs, reduced the generation of new astrocytes and promoted their differentiation along an oligodendroglial lineage, a prerequisite for remyelination. Furthermore, ChABC and GF treatments enhanced the response of non-neural cells by increasing the generation of new vascular endothelial cells and decreasing the number of proliferating macrophages/microglia after SCI. In conclusions, our data strongly suggest that optimization of the behaviour of endogenous spinal NPCs after SCI is critical not only to promote endogenous oligodendrocyte replacement, but also to reverse the otherwise detrimental effects of their activation into astrocytes which could negatively influence the repair process after SCI

    Antimicrobial stewardship effectiveness on rationalizing the use of last line of antibiotics in a short period with limited human resources: A single centre cohort study

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    Objective: Antibiotics reserve (ARs) are given as a last line of treatment when other antibiotics are no longer effective. Rising threat of antimicrobial resistance makes growing use of ARs a real problem to patient safety. A single centre interventional cohort study was conducted in order to measure impact on clinical outcomes of A-team programme with limited human resources in a short period. A-team programme started on 01. September 2017. Results: In 3 months preintervention and 3 months intervention period, from 3038 and 3156 hospitalized adult patients, 249 (59% of them were male, median age = 69 years) and 96 (51% of them were male, median age = 70 years) received parenteral ARs. Total duration of hospitalization of patients on AR was reduced from 28 to 17 days of hospitalization on 100 patient-days (OR = 1.92; 95% CI 1.83-2.01; p < 0.001) with no statistical significant difference in rehospitalisation due to infection of patients that were treated with ARs within 2 months after discharge. Despite short period of time and limited human resources, A-team restrictive interventions rationalised parenteral AR use and led to positive impact on clinical outcomes. These results could help our and other A-teams in similar situation in continuing with the programme to bring more evidence
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