55 research outputs found

    Propensity score matched comparison of transcatheter aortic valve implantation versus conventional surgery in intermediate and low risk aortic stenosis patients: A hint of real-world

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    Background: Recently, the use of transcatheter aortic valve implantation (TAVI) in inter­mediate-low risk patients has been evaluated in the PARTNER II randomized trial. However, in the last years, this therapy has been employed in this scenario with underreported results, as compared to surgical aortic valve replacement (SAVR). Methods: We enrolled 362 consecutive patients with severe symptomatic aortic stenosis and intermediate-low surgical risk (logEuroSCORE < 20%), treated in our center with TAVI (103 patients) or single SAVR (259 patients) between 2009 and 2014. Patients were matched according to age, gender, logEuroSCORE, and use of bioprosthesis. Results: Mean age of the patients was 73 ± 10.4 years, and 40.3% were women. LogEuroSCORE and Society Thoracic Surgeons score were 7.0 ± 4.4% and 4.2 ± 2.5%, respectively, with mean left ventricular ejection fraction of 52 ± 9%. There were no differences regarding other comorbidities. The length-of-hospitalization was 11 ± 5 days after TAVI vs. 17 ± 9 days after SAVR (p = 0.003). After matched comparison, no differences in terms of in-hospital mortality (5.7% after TAVI vs. 2.9% after SAVR, p = 0.687) and 1-year mortality (11.4% vs. 7.1%, p = 0.381) were found. The combined endpoint of stroke and mortality at 1-year was also similar between both groups (15.7% in TAVI patients vs. 14.4% after SAVR, p = 0.136). Multivariate analysis determined that aortic regurgitation (AR) was an independent predictor of mortality (OR = 3.623, 95% CI: 1.267–10.358, p = 0.016). Although the rate of AR was higher after TAVI, none of the patients treated with the newest generation devices (10.7%) presented more than a mild degree of AR. Conclusions: TAVI is feasible and shows comparable results to surgery in terms of early, 1-year mortality, as well as cerebrovascular events in patients with severe aortic stenosis and intermediate-low operative risk. Better transvalvular gradients, yet higher rates of AR were found, however, newer devices presented comparable rate of AR.

    Transient carnitine transport defect with cholestatic jaundice: report of one case in a premature baby

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    Carnitine (β-hydroxy-γ-trimethylaminobutyric acid) is involved in the transport of long-chain fatty acids into the mitochondrial matrix and the removal of potentially toxic acylcarnitine esters. Transient carnitine transport defect is a rare condition in newborns reported in 1/90,000 live births. In this paper, we describe a case of transient carnitine transport defect found in a premature baby who had prolonged cholestatic jaundice and poor weight gain, and who responded dramatically to oral carnitine supplementation

    Chromosome 10q26-driven age-related macular degeneration is associated with reduced levels of HTRA1 in human retinal pigment epithelium

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    Genome-wide association studies have identified the chromosome 10q26 (Chr10) locus, which contains the age-related maculopathy susceptibility 2 (ARMS2) and high temperature requirement A serine peptidase 1 (HTRA1) genes, as the strongest genetic risk factor for age-related macular degeneration (AMD) [L.G. Fritsche et al., Annu. Rev. Genomics Hum. Genet. 15, 151–171, (2014)]. To date, it has been difficult to assign causality to any specific single nucleotide polymorphism (SNP), haplotype, or gene within this region because of high linkage disequilibrium among the disease-associated variants [J. Jakobsdottir et al. Am. J. Hum. Genet. 77, 389–407 (2005); A. Rivera et al. Hum. Mol. Genet. 14, 3227–3236 (2005)]. Here, we show that HTRA1 messenger RNA (mRNA) is reduced in retinal pigment epithelium (RPE) but not in neural retina or choroid tissues derived from human donors with homozygous risk at the 10q26 locus. This tissue-specific decrease is mediated by the presence of a noncoding, cis-regulatory element overlapping the ARMS2 intron, which contains a potential Lhx2 transcription factor binding site that is disrupted by risk variant rs36212733. HtrA1 protein increases with age in the RPE–Bruch’s membrane (BM) interface in Chr10 nonrisk donors but fails to increase in donors with homozygous risk at the 10q26 locus. We propose that HtrA1, an extracellular chaperone and serine protease, functions to maintain the optimal integrity of the RPE–BM interface during the aging process and that reduced expression of HTRA1 mRNA and protein in Chr10 risk donors impairs this protective function, leading to increased risk of AMD pathogenesis. HtrA1 augmentation, not inhibition, in high-risk patients should be considered as a potential therapy for AMD

    Effect of Carnitine and herbal mixture extract on obesity induced by high fat diet in rats

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    <p>Abstract</p> <p>Background</p> <p>Obesity-associated type 2 diabetes is rapidly increasing throughout the world. It is generally recognized that natural products with a long history of safety can modulate obesity.</p> <p>Aim</p> <p>To investigate the development of obesity in response to a high fat diet (HFD) and to estimate the effect of L-carnitine and an Egyptian Herbal mixture formulation (HMF) (consisting of T. chebula, Senae, rhubarb, black cumin, aniseed, fennel and licorice) on bodyweight, food intake, lipid profiles, renal, hepatic, cardiac function markers, lipid Peroxidation, and the glucose and insulin levels in blood and liver tissue in rats.</p> <p>Method</p> <p>White male albino rats weighing 80-90 gm, 60 days old. 10 rats were fed a normal basal diet (Cr), 30 rats fed a high-fat diet (HFD) for 14 weeks during the entire study. Rats of the HFD group were equally divided into 3 subgroups each one include 10 rats. The first group received HFD with no supplement (HFD), the 2<sup>nd </sup>group HFD+L-carnitine and the third group received HFD+HMF. Carnitine and HMF were administered at 10<sup>th </sup>week (start time for treatments) for 4 weeks.</p> <p>Body weight, lipid profile & renal function (urea, uric acid creatinine) ALT & AST activities, cardiac markers, (LDH, C.K-NAC and MB) the oxidative stress marker reduced glutathione (GSH), and Malondialdehyde (MDA) catalase activity, in addition to glucose, insulin, and insulin resistance in serum & tissues were analyzed.</p> <p>Results</p> <p>Data showed that feeding HFD diet significantly increased final body weight, triglycerides (TG), total cholesterol, & LDL concentration compared with controls, while significantly decreasing HDL; meanwhile treatment with L-carnitine, or HMF significantly normalized the lipid profile.</p> <p>Serum ALT, urea, uric acid, creatinine, LDH, CK-NAC, CK-MB were significantly higher in the high fat group compared with normal controls; and administration of L-carnitine or herbal extract significantly lessened the effect of the HFD. Hyperglycemia, hyperinsulinemia, and high insulin resistance (IR) significantly increased in HFD in comparison with the control group. The treatment with L-carnitine or HMF improved the condition. HFD elevated hepatic MDA and lipid peroxidation associated with reduction in hepatic GSH and catalase activity; whereas administration of L-carnitine or herbal extract significantly ameliorated these hepatic alterations.</p> <p>Conclusion</p> <p>HFD induced obesity associated with a disturbed lipid profile, defective antioxidant stability, and high values of IR parameters; this may have implications for the progress of obesity related problems. Treatment with L-carnitine, or HMF extract improved obesity and its associated metabolic problems in different degrees. Also HMF has antioxidant, hypolipidaemic insulin sensitizing effects. Moreover HMF might be a safe combination on the organs whose functions were examined, as a way to surmount the obesity state; and it has a distinct anti-obesity effect.</p

    Del commercio e della navigazione dell'isola di Sardegna nei secoli XIV e XV : con alcuni documenti inediti o rari /

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    Also covers the role of the Jewish community in Sardinian trade and commerce.Contains documents in Latin and Spanish.Facsimile reprint. Originally published: Cagliari : Timon, 1865.Includes bibliographical references.Mode of access: Internet
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