TRAUMA NO IDOSO

The occurrence of trauma in the elderly is growing significantly due to the increase of number of this population. Currently, the more active lifestyle of the elderly leads them to be more exposed to the risk of accidents. Besides that, physiological ageing itself contributes to such risk: reduction of sight, reduction of hearing, use of medication, associated diseases and slow locomotion. Other organic systems also present reduction of their functions: renal, pulmonary, cardiovascular, musculoskeletal and endocrine. Fall is the most frequent mechanism of trauma, followed by motor vehicle crash. After the trauma there is a decline in the quality of life of the elderly since they have difficulty to fully recover. The best method to diminish morbidity and mortality is to prevent the elderly from being exposed to risks. Minimum alteration of the physiological parameters can suggest potentially lethal injury. Therefore, the initial approach to the traumatized elderly should be with careful attention and rigorous monitoring.A ocorrência de trauma no idoso vem crescendo de forma significativa, mediante ao crescimento desta população. Atualmente, o estilo de vida mais ativa do idoso eleva a exposição ao risco de acidentes. Além desse fator, o próprio envelhecimento fisiológico contribui: diminuição da acuidade visual, diminuição da audição, uso de medicações, doenças associadas e marcha lentificada. Outros sistemas orgânicos também possuem diminuição de suas funções: renal, pulmonar, cardiovascular, osteomuscular e endócrino. A queda é o mecanismo de lesão mais freqüente, seguido por atropelamento. Após o trauma o idoso possui uma decadência na sua qualidade de vida, não conseguindo retornar plenamente ao seu estado inicial. A prevenção por meio da redução de exposição aos riscos de trauma é a melhor ferramenta para diminuir a morbidade e mortalidade. Qualquer mínima alteração dos parâmetros fisiológicos pode ser indício de uma lesão potencialmente letal. Portanto, a abordagem inicial do idoso traumatizado deve ser realizada com maior atenção e rigorosamente monitorizada

Genetic PTX3 deficiency and aspergillosis in stem-cell transplantation

BACKGROUND: The soluble pattern-recognition receptor known as long pentraxin 3 (PTX3) has a nonredundant role in antifungal immunity. The contribution of single-nucleotide polymorphisms (SNPs) in PTX3 to the development of invasive aspergillosis is unknown. METHODS: We screened an initial cohort of 268 patients undergoing hematopoietic stem-cell transplantation (HSCT) and their donors for PTX3 SNPs modifying the risk of invasive aspergillosis. The analysis was also performed in a multicenter study involving 107 patients with invasive aspergillosis and 223 matched controls. The functional consequences of PTX3 SNPs were investigated in vitro and in lung specimens from transplant recipients. RESULTS: Receipt of a transplant from a donor with a homozygous haplotype (h2/h2) in PTX3 was associated with an increased risk of infection, in both the discovery study (cumulative incidence, 37% vs. 15%; adjusted hazard ratio, 3.08; P=0.003) and the confirmation study (adjusted odds ratio, 2.78; P=0.03), as well as with defective expression of PTX3. Functionally, PTX3 deficiency in h2/h2 neutrophils, presumably due to messenger RNA instability, led to impaired phagocytosis and clearance of the fungus. CONCLUSIONS: Genetic deficiency of PTX3 affects the antifungal capacity of neutrophils and may contribute to the risk of invasive aspergillosis in patients treated (Funded by the European Society of Clinical Microbiology and Infectious Diseases and others) .with HSCT.Supported by grants from the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) (to Dr. Carvalho); the German Ministry for Education and Science (03Z2JN21, to Dr. Kurzai); the European Commission (FP7-HEALTH-2009-260338, to Dr. Romani; FP7-HEALTH-2011-280873, to Dr. Mantovani), the European Research Council (ERC-2008-AdG-233417, to Dr. Mantovani; ERC-2011-AdG-293714, to Dr. Romani), Associazione Italiana per la Ricerca sul Cancro (99629, to Dr. Mantovani); and Fundacao para a Ciencia e Tecnologia, Portugal (SFRH/BPD/46292/2008, to Dr. Carvalho; SFRH/BD/65962/2009, to Dr. Cunha; and SFRH/BPD/70783/2010, to Dr. Almeida)

Measurement of the prompt J/psi and psi(2S) polarizations in pp collisions at sqrt(s) = 7 TeV

The polarizations of prompt J/psi and psi(2S) mesons are measured in proton-proton collisions at sqrt(s) = 7 TeV, using a dimuon data sample collected by the CMS experiment at the LHC, corresponding to an integrated luminosity of 4.9 inverse femtobarns. The prompt J/psi and psi(2S) polarization parameters lambda[theta], lambda[phi], and lambda[theta, phi], as well as the frame-invariant quantity lambda(tilde), are measured from the dimuon decay angular distributions in three different polarization frames. The J/psi results are obtained in the transverse momentum range 14 < pt < 70 GeV, in the rapidity intervals abs(y) < 0.6 and 0.6 < abs(y) < 1.2. The corresponding psi(2S) results cover 14 < pt < 50 GeV and include a third rapidity bin, 1.2 < abs(y) < 1.5. No evidence of large transverse or longitudinal polarizations is seen in these kinematic regions, which extend much beyond those previously explored

Schadevergoeding bij overlijden: een stoel die een soort tafeltje is

In het aansprakelijkheidsrecht heeft een benadeelde in beginsel recht op volledige vergoeding van zijn schade. De gevolgen van de schadetoebrengende gebeurtenis dienen zoveel als mogelijk te worden weggenomen of te worden gecompenseerd. Daarbij wordt gekeken naar de situatie waarin de benadeelde zou hebben verkeerd indien de schadetoebrengende gebeurtenis niet zou hebben plaatsgevonden. Dat is bij overlijden per definitie problematisch. Er is iemand weggevallen, wat vele gevolgen heeft. De schade als gevolg van het overlijden komt maar beperkt voor vergoeding in aanmerking. In artikel 6:108 BW is een drietal beperkingen te vinden. Het gaat hier om beperkingen ten aanzien van de aard van de schade, de kring van gerechtigden en de omvang van de schade. Daarbij hinkt het recht op schadevergoeding bij overlijden op twee gedachten. Aan de ene kant is er het aansprakelijkheidsrecht, maar de geleden schade komt niet volledig voor vergoeding in aanmerking. Aan de andere kant is er het recht op alimentatie uit het familierecht, maar dat wordt bij overlijden niet consequent toegepast. De motieven voor de beperkingen van het recht op schadevergoeding zijn achterhaald en niet (langer) overtuigend. Het recht is niet bij de tijd, het sluit niet aan bij de maatschappelijke ontwikkelingen. De beperkingen die het recht op schadevergoeding bij overlijden in de huidige samenleving met zich meebrengt zorgen voor complexe methoden om de nabestaanden tegemoet te komen en oogsten daardoor veel kritiek. In deze bijdrage wordt die kritiek besproken. De bijdrage wordt afgesloten met enkele denkrichtingen voor nader onderzoek

Search for standard model production of four top quarks in the lepton + jets channel in pp collisions at √s = 8 TeV

Open Access, Copyright CERN, for the benefit of the CMS Collaboration. Article funded by SCOAP3.Abstract: A search is presented for standard model (SM) production of four top quarks (Formula presented.) in pp collisions in the lepton + jets channel. The data correspond to an integrated luminosity of 19.6 fb−1 recorded at a centre-of-mass energy of 8 TeV with the CMS detector at the CERN LHC. The expected cross section for SM (Formula presented.) production is (Formula presented.). A combination of kinematic reconstruction and multivariate techniques is used to distinguish between the small signal and large background. The data are consistent with expectations of the SM, and an upper limit of 32 fb is set at a 95% confidence level on the cross section for producing four top quarks in the SM, where a limit of 32 ± 17 fb is expected

Alignment of the CMS tracker with LHC and cosmic ray data

© CERN 2014 for the benefit of the CMS collaboration, published under the terms of the Creative Commons Attribution 3.0 License by IOP Publishing Ltd and Sissa Medialab srl. Any further distribution of this work must maintain attribution to the author(s) and the published article's title, journal citation and DOI.The central component of the CMS detector is the largest silicon tracker ever built. The precise alignment of this complex device is a formidable challenge, and only achievable with a significant extension of the technologies routinely used for tracking detectors in the past. This article describes the full-scale alignment procedure as it is used during LHC operations. Among the specific features of the method are the simultaneous determination of up to 200 000 alignment parameters with tracks, the measurement of individual sensor curvature parameters, the control of systematic misalignment effects, and the implementation of the whole procedure in a multi-processor environment for high execution speed. Overall, the achieved statistical accuracy on the module alignment is found to be significantly better than 10μm

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice