98 research outputs found
Family Quality of Life from the Perspective of Parents of Children with Intellectual Disabilities
Aim: The quality of life of families with children with intellectual disabilities has been frequently analysed in recent research. There are numerous factors that influence the quality of life of families. The aim of the study was to determine the quality of life of families of children with intellectual disabilities who are cared for by the Sloboština Rehabilitation Centre.
Methods: The study used the Beach Center Family Quality of Life Scale questionnaire, which was completed online by the parents. 51 parents of children and adolescents with intellectual disabilities took part in the study.
Results: The results of the study show that the overall quality of life is satisfactory. However, parents of children with intellectual disabilities are least satisfied with emotional well-being and disability-related support. They are not satisfied with the time they have to pursue their interests or with outside help for all family members. They also consider the support a child with disabilities receives at school to be mediocre. No statistically significant differences in quality of life were found in relation to the age and gender of parents and children, except for the family interaction subscale, where families with girls had a better quality of life.
Conclusion: The results of the study show that although the overall quality of life is satisfactory, families of children with intellectual disabilities need external support that provides them with some free time but also aims to support all family members
Expression of CD11c Is Associated with Unconventional Activated T Cell Subsets with High Migratory Potential
Ajudes rebudes: Marie Curie Career Integration Grant; Dexeus Foundation for Women's Health Research; i Contratos Ramón y CajalCD11c is an α integrin classically employed to define myeloid dendritic cells. Although there is little information about CD11c expression on human T cells, mouse models have shown an association of CD11c expression with functionally relevant T cell subsets. In the context of genital tract infection, we have previously observed increased expression of CD11c in circulating T cells from mice and women. Microarray analyses of activated effector T cells expressing CD11c derived from naïve mice demonstrated enrichment for natural killer (NK) associated genes. Here we find that murine CD11c+ T cells analyzed by flow cytometry display markers associated with non-conventional T cell subsets, including γδ T cells and invariant natural killer T (iNKT) cells. However, in women, only γδ T cells and CD8+ T cells were enriched within the CD11c fraction of blood and cervical tissue. These CD11c+ cells were highly activated and had greater interferon (IFN)-γ secretory capacity than CD11c- T cells. Furthermore, circulating CD11c+ T cells were associated with the expression of multiple adhesion molecules in women, suggesting that these cells have high tissue homing potential. These data suggest that CD11c expression distinguishes a population of circulating T cells during bacterial infection with innate capacity and mucosal homing potential
Effect of acute kidney injury on mortality and hospital stay in patient with severe acute pancreatitis
AimSevere acute pancreatitis (SAP) is believed to be a major risk factor leading to acute kidney injury (AKI) among critically ill patients, but little is known about SAP‐induced AKI. We study the incidence of AKI defined by the Acute Kidney Injury Network (AKIN) criteria and the risk factors associated with outcomes among SAP‐induced AKI patients.MethodWe conducted a multicenter retrospective study of critically ill SAP‐induced AKI patients during the period August 2009 to June 2013. Data on enrolled patients were retrieved from electronic records. Univariate and multiple regression analyses were performed.ResultsAmong a total of 414 SAP patients admitted to intensive care units(ICU), 287 (69.3%) developed AKI during their ICU stay, with 16.7%, 18.4%, and 34.3% classified as AKI stage I,II, and III, respectively. SAP‐induced AKI patients experienced a significantly higher ICU mortality than those without AKI. The risk factors associated with ICU mortality among SAP‐induced AKI patients included ACS (odds ratio (OR) 10.58), RRT (OR 3.31), sepsis (OR 2.46), CTSI (OR 3.01), APACHE II score (OR 1.82), AKI III (OR 1.38), ICU‐length‐of‐stay (OR 1.04), and multi‐organ failure.ConclusionsThe paper represents the first attempt to investigate the etiology and epidemiology of AKI following SAP under the AKIN criteria among critically ill patients. Several independent risk factors were found to be associated with ICU mortality for AKI patients. The findings may pinpoint crucial therapeutic measures for preventing AKI among a vulnerable population and for more effective management of SAP‐induced AKI to improve the quality of intensive care.Summary at a GlanceIn this retrospective study of AKI following acute pancreatitis, the authors identify risk factors associated with mortality. These findings provide a basis for focussing on high risk patients for future trials of therapeutic interventions.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/111910/1/nep12439.pd
Comparison of total parathyroidectomy without autotransplantation and without thymectomy versus total parathyroidectomy with autotransplantation and with thymectomy for secondary hyperparathyroidism: TOPAR PILOT-Trial
<p>Abstract</p> <p>Background</p> <p>Secondary hyperparathyroidism (sHPT) is common in patients with chronic renal failure. Despite the initiation of new therapeutic agents, several patients will require parathyroidectomy (PTX). Total PTX with autotransplantation of parathyroid tissue (TPTX+AT) and subtotal parathyroidectomy (SPTX) are currently considered as standard surgical procedures in the treatment of sHPT. Recurrencerates after TPTX+AT or SPTX are between 10% and 12% (median follow up: 36 months).</p> <p>Recent retrospective studies demonstrated a lower rate of recurrent sHPT of 0–4% after PTX without autotransplantation and thymectomy (TPTX) with no higher morbidity when compared to the standard procedures. The observed superiority of TPTX is flawed due to different definitions of outcomes, varying follow up periods and different surgical treatment strategies (with and without thymectomy).</p> <p>Methods/Design</p> <p>Patients with sHPT (intact parathyroid hormone > 10 times above the upper limit of normal) on long term dialysis (>12 months) will be randomized either to TPTX or TPTX+AT and followed for 36 months. Outcome parameters are recurrence rates of sHPT, frequencies of reoperations due to refractory hypoparathyroidism or recurrent/persistent hyperparathyroidism, postoperative morbidity and mortality and quality of life. 50 patients per group will be randomized in order to obtain relevant frequencies of outcome parameters that will form the basis for a large scale confirmatory multicentred randomized controlled trial.</p> <p>Discussion</p> <p>sHPT is a disease with a high incidence in patients with chronic renal failure. Even a small difference in outcomes will be of clinical relevance. To assess sufficient data about the rate of recurrent sHPT after both methods, a multicentred, randomized controlled trial (MRCT) under standardized conditions is mandatory.</p> <p>Due to the existing uncertainties the calculated number of patients necessary in each treatment arm (n > 4000) makes it impossible to perform this study as a confirmatory trial. Therefore estimates of different outcomes are performed using a pilot MRCT comparing 50 versus 50 randomized patients in order to establish a hypothesis that can be tested thereafter.</p> <p>If TPTX proves to have a lower rate of recurrent sHPT, no relevant disadvantages and no higher morbidity than TPTX+AT, current surgical practice may be changed.</p> <p>Trial registration</p> <p>International Standard Randomized Controlled Trial Number Registration (ISRCTN86202793)</p
Novel role for the Streptococcus pneumoniae toxin pneumolysin in the assembly of biofilms
Streptococcus pneumoniae is an important commensal and pathogen responsible for almost a million deaths annually in children under five. The formation of biofilms by S. pneumoniae is important in nasopharyngeal colonization, pneumonia, and otitis media. Pneumolysin (Ply) is a toxin that contributes significantly to the virulence of S. pneumoniae and is an important candidate as a serotype-independent vaccine target. Having previously demonstrated that a luxS knockout mutant was unable to form early biofilms and expressed less ply mRNA than the wild type, we conducted a study to investigate the role of Ply in biofilm formation. We found that Ply was expressed in early phases of biofilm development and localized to cellular aggregates as early as 4 h postinoculation. S. pneumoniae ply knockout mutants in D39 and TIGR4 backgrounds produced significantly less biofilm biomass than wild-type strains at early time points, both on polystyrene and on human respiratory epithelial cells, cultured under static or continuous-flow conditions. Ply’s role in biofilm formation appears to be independent of its hemolytic activity, as S. pneumoniae serotype 1 strains, which produce a nonhemolytic variant of Ply, were still able to form biofilms. Transmission electron microscopy of biofilms grown on A549 lung cells using immunogold demonstrated that Ply was located both on the surfaces of pneumococcal cells and in the extracellular biofilm matrix. Altogether, our studies demonstrate a novel role for pneumolysin in the assembly of S. pneumoniae biofilms that is likely important during both carriage and disease and therefore significant for pneumolysin-targeting vaccines under development. IMPORTANCE The bacterium Streptococcus pneumoniae (commonly known as the pneumococcus) is commonly carried in the human nasopharynx and can spread to other body sites to cause disease. In the nasopharynx, middle ear, and lungs, the pneumococcus forms multicellular surface-associated structures called biofilms. Pneumolysin is an important toxin produced by almost all S. pneumoniae strains, extensively studied for its ability to cause damage to human tissue. In this paper, we demonstrate that pneumolysin has a previously unrecognized role in biofilm formation by showing that strains without pneumolysin are unable to form the same amount of biofilm on plastic and human cell substrates. Furthermore, we show that the role of pneumolysin in biofilm formation is separate from the hemolytic activity responsible for tissue damage during pneumococcal diseases. This novel role for pneumolysin suggests that pneumococcal vaccines directed against this protein should be investigated for their potential impact on biofilms formed during carriage and disease.Joshua R. Shak, Herbert P. Ludewick, Kristen E. Howery, Fuminori Sakai, Hong Yi, Richard M. Harvey, James C. Paton, Keith P. Klugman, Jorge E. Vida
The role of arterial hypertension in the progression of non-diabetic glomerular diseases
PERSPEKTIVE KREDIBILNOG PROŠIRENJA EVROPSKE UNIJE NA ZAPADNI BALKAN: POJAČANO ANGAŽOVANJE EU U SFERI REGULATIVE I PRAKSE SUZBIJANJA PRANJA NOVCA
Predmet analize ovog rada je ocena usaglašenosti pravne i prateće regulative zemalja regiona Zapadnog Balkana u sferi suzbijanja pranja novca i finansiranja terorizma sa srodnim normativnim aktima Evropske unije. Pretnje međunarodnog terorizma rastu, nastaju novi rizici poreske utaje, korupcije, transnacionalnog organizovanog kriminala, sajber ‒ kriminala i dr. Jedan od ključnih kriterijuma priključenja zemalja Zapadnog Balkana EU postali su ostvareni efekti suprotstavljanja pranju novca. Glavne teškoće sa kojima se suočavaju ove zemlje jeste uvreženo viđenje EU i međunarodnih regulatornih tela da nacionalni regulatorni sistemi ne čine dovoljno na praktičnom planu ostvarenja efekata stvarnog suzbijanja pranja novca. Brzina, obim i snaga regulatornih promena EU su dinamični te time predstavlja preveliki teret za nacionalne regulatorne sisteme, koji su objektivno u procesu izgradnje, uz inerciju istorijskih problema i nasleđa. Ocena je da će zahtevi međunarodne zajednice a još više EU rasti, biti sve stroži, tako da je period „kreni ‒ stani“ završen. Sledi faza Olimpijskog gesla brže ‒ dalje – snažnije. Terorizam uzrokuje rastuće troškove za društva, stoga je značajan izazov za sve civilizovane zemlje. U tom svetlu je suprotstavljanje finansiranju terorizma kroz suzbijanje pranja novca ključna polazna, centralna i završna karika. Korišćene metode u analizi ove teme su istorijskopravna metoda, pozitivnopravna metoda i uporednopravna metoda.</jats:p
Characterization of lineage-specific expression and signaling function of mouse NKR-P1 (CD161)
Furthermore, although it is known that the NK1.1 marker is encoded by the Nkrp1c gene, its transcriptional regulation has not been elucidated. The results presented in this thesis define the molecular basis of Nkrp1c expression in NK lineage cells. In particular, the location of the Nkrp1c transcriptional initiation site, a novel 5' untranslated exon, and the minimal functional core promoter have been identified. Furthermore, we describe the detection and analysis of a DNaseI hypersensitive site (HS1), located 9 kb upstream of the transcriptional initiation site, which exhibits NK cell-specific enhancer-like activity. Taken together, our findings identify the minimal elements necessary for conferring NK cell lineage-specific expression of the Nkrp1c gene. These findings set the stage for the further characterization of the DNA-binding factors responsible for the expression of this and other NK-specific genes, shedding light on our understanding of how NK cell functions are regulated. For over fifteen years, surface expression of the NK1.1 marker has been used to identify all cells belonging to a specific subset of lymphocytes, defining them as natural killer (NK) cells. NK1.1 epitope is shared by two closely related, but functionally opposing NK cell receptors, the stimulatory NKR-P1C and inhibitory NKR-P1B gene products. Thus, the molecular basis of NKR-P1B/C signaling in NK cells was investigated. In particular, the tyrosine kinase, Lck, was identified as the initiator of signaling for both the stimulatory and inhibitory NKR-P1 receptors. Furthermore, the amino acid motif (CxCP) was shown to mediate Lck association to the receptors, as well as the inhibitory motif (LxYxxL) responsible for their divergent functions. Most strikingly, the Lck tyrosine kinase is required for NKR-P1 activation, as NK cells from Lck-deficient mice cannot mediate NKR-P1-directed killing. Importantly, this discovery represents the first NK cell defect reported in these mice. These findings provide the foundation for a sequential model to explain the opposing functional outcomes induced by these two NKR-P1 receptors, shedding light on our understanding of how NK cell functions are regulated.Ph.D
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