371 research outputs found
Comparative study of six pear cultivars in terms of their phenolic and vitamin C contents and antioxidant capacity
The main phenolic compounds in six pear cultivars were identified and quantified using high-performance liquid chromatography/diode array detection (HPLC/DAD) and HPLC/electrospray
ionisation mass spectrometry (HPLC/ESIMS). Major quantitative differences were found in the phenolic profiles. The peel contained higher concentrations of chlorogenic acid, flavonols and arbutin than the flesh, where only chlorogenic acid was detected. Total phenolics ranged from 1235 to 2005mgkg−1 in the peel and from 28 to 81mg k g−1 in the flesh. Ascorbic acid and dehydroascorbic acid were detected in the peel, whereas only dehydroascorbic acid was present in the flesh. The ranges of vitamin C content
were from 116 to 228mg kg−1 in the peel and from 28 to 53mg kg−1 in the flesh. The antioxidant capacity was correlated with the content of chlorogenic acid (r = 0.46), while ascorbic acid made only a small
contribution to the total antioxidant capacity of the fruit
Introducing medical parasitology at the University of Makeni, Sierra Leone
The file attached to this record is the author's final peer reviewed version.Capacity building in Sierra Leone (West Africa) is critical to prevent potential future outbreaks similar to
the 2013-16 Ebola outbreak that had devastating effects for the country and its poorly developed
healthcare system. De Montfort University (DMU) in the United Kingdom (UK), in collaboration with
parasitologists from the Spanish Universities of San Pablo CEU and Miguel Hernández de Elche, is
leading a project to build the teaching and research capabilities of medical parasitology at the University
of Makeni (UniMak, Sierra Leone). This project has two objectives: a) to introduce and enhance the
teaching of medical parasitology, both theoretical and practical; and b) to implement and develop
parasitology research related to important emerging human parasites such as Cryptosporidium spp. due
to their public health significance. Two UniMak academics, hired to help initiate and implement the
research part of the project, shared their culturally sensitive public health expertise to broker parasitology
research in communities and perform a comprehensive environmental monitoring study for the detection
of different emerging human parasites. The presence of targeted parasites are being studied
microscopically using different staining techniques, which in turn have allowed UniMak’s academics to
learn these techniques to develop new practicals in parasitology. To train UniMak’s academics and
develop both parts of our project, a DMU researcher visited UniMak for two weeks in April 2019 and
provided a voluntary short training course in basic parasitology, which is currently not taught in any of
their programmes, and was attended by 31 students. These sessions covered basic introduction to
medical parasitology and life-cycle, pathogenesis, detection, treatment and prevention of: a) coccidian
parasites (Cryptosporidium, Cyclospora and Cystoisospora); b) Giardia intestinalis, Entamoeba and
free-living amoebas; c) malaria and d) microsporidia. A theoretical session on common staining
techniques was also provided. To facilitate the teaching and learning of these parasites, the novel
resource DMU e-Parasitology was used, a package developed by the above participating universities
and biomedical scientists from the UK National Health Service (NHS): http://parasitology.dmu.ac.uk/
index.htm. Following the two weeks of training, UniMak’s academics performed different curriculum
modifications to the undergraduate programme ‘Public Health: Medical Laboratory Sciences’, which
includes the introduction of new practicals in parasitology and changes to enhance the content of
medical parasitology that will be subjected to examination. Thus, a new voluntary practical on Kinyoun
stain for the detection of coccidian parasites was introduced in the final year module of ‘Medical
Bacteriology and Parasitology’; eighteen students in pairs processed faecal samples from pigs provided
by the Department of Agriculture and Food Security from a nearby farm. Academics at UniMak used the
Kinyoun staining unit (available at http://parasitology.dmu.ac.uk/learn/lab/Kinyoun/story_html5.html; [1])
to deliver this practical. Although our project is at a preliminary stage, it has been shown to be effective
in promoting the introduction and establishment of medical parasitology at UniMak and could be viewed
as a case-study for other universities in low-income countries to promote the United Nations (UN)
Sustainable Development Goals (SDGs) and improve public health understanding of infectious
diseases
Predictive accuracy of semi-quantitative scoring to screen for unfavorable ejection fraction and infarct size
Oxidative Stress Induced by Excess of Adiposity Is Related to a Downregulation of Hepatic SIRT6 Expression in Obese Individuals
Sirt6 is a member of the sirtuin family involved in physiological and pathological processes including aging, cancer, obesity, diabetes, and energy metabolism. This study is aimed at evaluating the relationship between liver SIRT6 gene expression and the oxidative stress network depending on adiposity levels in Zucker rats, an animal model of metabolic syndrome. We observed that liver-specific SIRT6 expression is reduced in an in vivo model of spontaneous obesity and metabolic syndrome. We also observed that SIRT6 expression in the liver is positively associated with SIRT1 and GST-M2 expressions, two proteins involved in antioxidant protection pathways and inversely related to body weight and plasmatic oxidative status. Interestingly, the SIRT6 expression is upregulated after energy restriction-induced weight loss concomitantly with an improvement in oxidative stress markers. These results suggest that SIRT6 may be a potential therapeutic target for the treatment of obesity and associated metabolic disorders, such as liver disease.Centro de Investigacion Biomedica en Red de Fisiopatologia de la Obesidad y Nutricion (CIBERobn)Instituto de Salud Carlos IIIEuropean Regional Development Fund (FEDER
Concurrent Training Followed by Detraining: Does the Resistance Training Intensity Matter?
The aim of this study was to analyze the training and detraining (DT) effects of concurrent aerobic training and resistance training against 3 different external loads on strength and aerobic variables. Thirty-two men were randomly assigned to 4 groups: low-load (LLG, n = 9), moderate-load (MLG, n = 9), high-load (HLG, n = 8), and control group (CG, n = 6). Resistance training consisted of full squat (FS) with a low load (40-55% 1 repetition maximum [1RM]), a moderate load (55-70% 1RM), or a high load (70-85% 1RM) combined with jump and sprint exercises. Aerobic training was performed at 75% of the maximal aerobic speed for 15-20 minutes. The training period lasted for 8-week, followed by 4-week DT. Pretraining, post-training, and post-DT evaluations included 20-m running sprints (0-10 m: T10; 0-20 m: T20), shuttle run test, countermovement vertical jump (CMJ) test, and loading test (1RM) in FS. All the experimental groups showed improvements (p ≤ 0.05) in all the parameters assessed, except the LLG for T10 and the HLG for T20. The LLG, MLG, and HLG showed great changes in 1RM and V[Combining Dot Above]O2max compared with the CG (p ≤ 0.05), whereas the HLG and MLG showed a greater percentage change than the CG in T10 (p < 0.001) and CMJ (p ≤ 0.05). The 4-week DT period resulted in detrimental effects in all variables analyzed for all 3 experimental groups. In conclusion, our results suggest that strength training programs with low, moderate, or high external loads combined with low-intensity aerobic training could be effective for producing significant gains in strength and aerobic capacities. Moreover, the higher loads used increased gains in explosive efforts.info:eu-repo/semantics/publishedVersio
Prevalence of myocardial viability in dysfunctional areas by cardiovascular magnetic resonance in patients with coronary artery disease
The infectious synapse formed between mature dendritic cells and CD4 + T cells is independent of the presence of the HIV-1 envelope glycoprotein
Altres ajuts:This work was supported the Spanish AIDS Network (RD06/0006), the Catalan HIV Vaccine Development Program (HIVACAT), and the Spanish Foundation for AIDS Research and Prevention (FIPSE) project 36750/08.Since cell-mediated infection of human immunodeficiency virus type 1 (HIV-1) is more efficient than cell-free infection, cell-to-cell propagation plays a crucial role in the pathogenesis of HIV-1 infection. Transmission of HIV-1 is enabled by two types of cellular contacts, namely, virological synapses between productively infected cells and uninfected target cells and infectious synapses between uninfected dendritic cells (DC) harboring HIV-1 and uninfected target cells. While virological synapses are driven by expression of the viral envelope glycoprotein on the cell surface, little is known about the role of envelope glycoprotein during contact between DC and T cells. We explored the contribution of HIV-1 envelope glycoprotein, adhesion molecules, and antigen recognition in the formation of conjugates comprising mature DC (mDC) and CD4 + T cells in order to further evaluate their role in mDC-mediated HIV-1 transmission at the immunological synapse. Unlike virological synapse, HIV-1 did not modulate the formation of cell conjugates comprising mDC harboring HIV-1 and non-activated primary CD4 + T cells. Disruption of interactions between ICAM-1 and LFA-1, however, resulted in a 60% decrease in mDC-CD4 + T-cell conjugate formation and, consequently, in a significant reduction of mDC-mediated HIV-1 transmission to non-activated primary CD4 + T cells (p < 0.05). Antigen recognition or sustained MHC-TcR interaction did not enhance conjugate formation, but significantly boosted productive mDC-mediated transmission of HIV-1 (p < 0.05) by increasing T-cell activation and proliferation. Formation of the infectious synapse is independent of the presence of the HIV-1 envelope glycoprotein, although it does require an interaction between ICAM-1 and LFA-1. This interaction is the main driving force behind the formation of mDC-CD4 + T-cell conjugates and enables transmission of HIV-1 to CD4 + T cells. Moreover, antigen recognition boosts HIV-1 replication without affecting the frequency of cellular conjugates. Our results suggest a determinant role for immune activation driven by mDC-CD4 + T-cell contacts in viral dissemination and that this activation likely contributes to the pathogenesis of HIV-1 infection
TNF Superfamily: A Growing Saga of Kidney Injury Modulators
Members of the TNF superfamily participate in kidney disease. Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. In vivo TWEAK promotes postnephrectomy compensatory renal cell proliferation in a noninflammatory milieu. However, in the inflammatory milieu of acute kidney injury, TWEAK promotes tubular cell death and inflammation. Therapeutic targeting of TNF superfamily cytokines, including multipronged approaches targeting several cytokines should be further explored
TWEAK Activates the Non-Canonical NFκB Pathway in Murine Renal Tubular Cells: Modulation of CCL21
TWEAK is a member of the TNF superfamily of cytokines that contribute to kidney tubulointerstitial injury. It has previously been reported that TWEAK induces transient nuclear translocation of RelA and expression of RelA-dependent cytokines in renal tubular cells. Additionally, TWEAK induced long-lasting NFκB activation suggestive of engagement of the non-canonical NFκB pathway. We now explore TWEAK-induced activation of NFκB2 and RelB, as well as expression of CCL21, a T-cell chemotactic factor, in cultured murine tubular epithelial cells and in healthy kidneys in vivo. In cultured tubular cells, TWEAK and TNFα activated different DNA-binding NFκB complexes. TWEAK-induced sustained NFκB activation was associated with NFκB2 p100 processing to p52 via proteasome and nuclear translocation and DNA-binding of p52 and RelB. TWEAK, but not TNFα used as control), induced a delayed increase in CCL21a mRNA (3.5±1.22-fold over control) and CCL21 protein (2.5±0.8-fold over control), which was prevented by inhibition of the proteasome, or siRNA targeting of NIK or RelB, but not by RelA inhibition with parthenolide. A second NFκB2-dependent chemokine, CCL19, was upregulates by TWEAK, but not by TNFα. However, both cytokines promoted chemokine RANTES expression (3-fold mRNA at 24 h). In vivo, TWEAK induced nuclear NFκB2 and RelB translocation and CCL21a mRNA (1.5±0.3-fold over control) and CCL21 protein (1.6±0.5-fold over control) expression in normal kidney. Increased tubular nuclear RelB and tubular CCL21 expression in acute kidney injury were decreased by neutralization (2±0.9 vs 1.3±0.6-fold over healthy control) or deficiency of TWEAK (2±0.9 vs 0.8±0.6-fold over healthy control). Moreover, anti-TWEAK treatment prevented the recruitment of T cells to the kidney in this model (4.1±1.4 vs 1.8±1-fold over healthy control). Our results thus identify TWEAK as a regulator of non-canonical NFκB activation and CCL21 expression in tubular cells thus promoting lymphocyte recruitment to the kidney during acute injury
- …