Antes de integrar dispositivos com restrições de recursos computacionais em domínios de IoT, deve-se garantir que possuam ferramental criptográfico suficiente para estabelecer mecanismos de segurança essenciais. Neste contexto, as Assinaturas baseadas em Atributos (ABS) mostramse uma opção elegante na implementação de um esquema de autenticação e autorização. Neste trabalho discutimos diferentes abordagens para a aceleração de (ABS) considerando-se como plataforma alvo os dispositivos com restrições de recursos computacionais em domínios de IoT.
Abstract Data continue to accumulate indicating that many systematic reviews are methodologically flawed, biased, redundant, or uninformative. Some improvements have occurred in recent years based on empirical methods research and standardization of appraisal tools; however, many authors do not routinely or consistently apply these updated methods. In addition, guideline developers, peer reviewers, and journal editors often disregard current methodological standards. Although extensively acknowledged and explored in the methodological literature, most clinicians seem unaware of these issues and may automatically accept evidence syntheses (and clinical practice guidelines based on their conclusions) as trustworthy. A plethora of methods and tools are recommended for the development and evaluation of evidence syntheses. It is important to understand what these are intended to do (and cannot do) and how they can be utilized. Our objective is to distill this sprawling information into a format that is understandable and readily accessible to authors, peer reviewers, and editors. In doing so, we aim to promote appreciation and understanding of the demanding science of evidence synthesis among stakeholders. We focus on well-documented deficiencies in key components of evidence syntheses to elucidate the rationale for current standards. The constructs underlying the tools developed to assess reporting, risk of bias, and methodological quality of evidence syntheses are distinguished from those involved in determining overall certainty of a body of evidence. Another important distinction is made between those tools used by authors to develop their syntheses as opposed to those used to ultimately judge their work. Exemplar methods and research practices are described, complemented by novel pragmatic strategies to improve evidence syntheses. The latter include preferred terminology and a scheme to characterize types of research evidence. We organize best practice resources in a Concise Guide that can be widely adopted and adapted for routine implementation by authors and journals. Appropriate, informed use of these is encouraged, but we caution against their superficial application and emphasize their endorsement does not substitute for in-depth methodological training. By highlighting best practices with their rationale, we hope this guidance will inspire further evolution of methods and tools that can advance the field.
Excess deaths provide total impact estimates of major crises, such as the COVID-19 pandemic. We evaluated excess death trajectories across countries with accurate death registration and population age structure data and assessed relationships with vulnerability indicators. Using the Human Mortality Database on 34 countries, excess deaths were calculated for 2020–2023 (to week 29, 2023) using 2017–2019 as reference, with adjustment for 5 age strata. Countries were divided into less and more vulnerable; the latter had per capita nominal GDP < $30,000, Gini > 0.35 for income inequality and/or at least ≥2.5% of their population living in poverty. Excess deaths (as proportion of expected deaths, p%) were inversely correlated with per capita GDP ( r = −0.60), correlated with proportion living in poverty ( r = 0.66), and modestly correlated with income inequality ( r = 0.45). Incidence rate ratio for deaths was 1.062 (95% CI, 1.038–1.087) in more versus less vulnerable countries. Excess deaths started deviating in the two groups after the first wave. Between-country heterogeneity diminished gradually within each group. Less vulnerable countries had mean p% = −0.8% and 0.4% in 0–64 and >65-y-old strata. More vulnerable countries had mean p% = 7.0% and 7.2%, respectively. Lower death rates were seen in children of age 0–14 y during 2020–2023 versus prepandemic years. While the pandemic hit some countries earlier than others, country vulnerability dominated eventually the cumulative impact. Half the analyzed countries witnessed no substantial excess deaths versus prepandemic levels, while the others suffered major death tolls.
In the first article of this series, we reviewed the basic genetics concepts necessary to understand genetic association studies. In this second article, we enumerate the major issues in judging the validity of these studies, framed as critical appraisal questions. Was the disease phenotype properly defined and accurately recorded by someone blind to the genetic information? Have any potential differences between disease and nondisease groups, particularly ethnicity, been properly addressed? In genetic studies, one potential cause of spurious associations is differences between cases and controls in ethnicity, a situation termed population stratification. Was measurement of the genetic variants unbiased and accurate? Methods for determining DNA sequence variation are not perfect and may have some measurement error. Do the genotype proportions observe Hardy-Weinberg equilibrium? This simple mathematic rule about the distribution of genetic groups may be one way to check for errors in reading DNA information. Have the investigators adjusted their inferences for multiple comparisons? Given the thousands of genetic markers tested in genome-wide association studies, the potential for false-positive and false-negative results is much higher than in traditional medical studies, and it is particularly important to look for replication of results.
Several polymorphisms in the 5α-reductase type 2 ( SRD5A2 ) gene have been implicated as risk factors for prostate cancer. We performed a meta-analysis of 9 studies (12 comparisons) with V89L genotyping (2558 prostate cancer cases and 3349 controls), 7 studies (8 comparisons) with A49T genotyping (1594 cases and 2137 controls), and 4 studies with TA repeat genotyping (1109 cases and 1378 controls). The random effects odds ratio (OR) for the L versus V allele was 1.02 [95% confidence interval (CI), 0.94–1.11]. There was no suggestion of an overall effect either in recessive or dominant modeling, and comparison of L/L versus V/V also showed no differential prostate cancer susceptibility (OR, 1.03; 95% CI, 0.83–1.28). The random effects OR for the T versus A allele was 1.56 (95% CI, 0.93–2.62). However, excluding the first published study there was no evidence for any effect (OR, 1.08; 95% CI, 0.72–1.61). Moreover, the T allele had a low prevalence (0%, 1%, and 2% in Asian, African and European controls, respectively). The random effects OR for longer versus short TA alleles was 0.88 (95% CI, 0.74–1.05). Longer TA allele homozygotes were nonsignificantly under-represented among prostate cancer cases (OR, 0.53; 95% CI, 0.26–1.06). We exclude a role for the V89L polymorphism in conferring susceptibility to prostate cancer. The A49T and TA repeat polymorphisms may have a modest effect on prostate cancer susceptibility, but bias and chance findings cannot be excluded; any genuine genetic effects would account only for a small proportion of prostate cancer in the population.
Abstract Objective: We studied the independent and joint effects of the genes encoding alpha‐synuclein ( SNCA ) and microtubule‐associated protein tau ( MAPT ) in Parkinson disease (PD) as part of a large meta‐analysis of individual data from case–control studies participating in the Genetic Epidemiology of Parkinson's Disease (GEO‐PD) consortium. Methods: Participants of Caucasian ancestry were genotyped for a total of 4 SNCA (rs2583988, rs181489, rs356219, rs11931074) and 2 MAPT (rs1052553, rs242557) single nucleotide polymorphism (SNPs). Individual and joint effects of SNCA and MAPT SNPs were investigated using fixed‐ and random‐effects logistic regression models. Interactions were studied on both a multiplicative and an additive scale, and using a case–control and case‐only approach. Results: Fifteen GEO‐PD sites contributed a total of 5,302 cases and 4,161 controls. All 4 SNCA SNPs and the MAPT H1‐haplotype–defining SNP (rs1052553) displayed a highly significant marginal association with PD at the significance level adjusted for multiple comparisons. For SNCA , the strongest associations were observed for SNPs located at the 3′ end of the gene. There was no evidence of statistical interaction between any of the 4 SNCA SNPs and rs1052553 or rs242557, neither on the multiplicative nor on the additive scale. Interpretation: This study confirms the association between PD and both SNCA SNPs and the H1 MAPT haplotype. It shows, based on a variety of approaches, that the joint action of variants in these 2 loci is consistent with independent effects of the genes without additional interacting effects. ANN NEUROL 2011
