Clebsch-Gordan Coefficients for the Extended Quantum-Mechanical Poincar\'e Group and Angular Correlations of Decay Products

This paper describes Clebsch-Gordan coefficients (CGCs) for unitary irreducible representations (UIRs) of the extended quantum mechanical Poincar\'e group \pt. `Extended' refers to the extension of the 10 parameter Lie group that is the Poincar\'e group by the discrete symmetries $C$, $P$, and $T$; `quantum mechanical' refers to the fact that we consider projective representations of the group. The particular set of CGCs presented here are applicable to the problem of the reduction of the direct product of two massive, unitary irreducible representations (UIRs) of \pt with positive energy to irreducible components. Of the sixteen inequivalent representations of the discrete symmetries, the two standard representations with $U_C U_P = \pm 1$ are considered. Also included in the analysis are additive internal quantum numbers specifying the superselection sector. As an example, these CGCs are applied to the decay process of the $\Upsilon(4S)$ meson.Comment: 26 pages, double spaced. Version 2: typos corrected, introduction change

Emoções, “stress”, ansiedade e “coping": estudo qualitativo com treinadores de nível internacional

A influência dos fatores e processos psicológicos no desempenho desportivo dos atletas está, de uma forma geral, amplamente demonstrada; todavia, poucas investigações procuraram estudar esta relação nos treinadores. Neste sentido, empregando uma entrevista semi-estruturada, a presente investigação procurou, junto de seis treinadores de elite com idades compreendidas entre os 55 e os 63 anos (M = 59 ± 3,03) de diversas modalidades, identificar as características/competências psicológicas mais importantes para o sucesso desportivo, as principais fontes de “stress” e ansiedade experienciadas e as estratégias de “coping” a que recorriam em situações estressantes e/ou problemáticas, adicionalmente, pretendeu explorar o papel de outras emoções no seu desempenho. Os resultados revelaram que: 1) a motivação era uma das competências/características psicológicas percepcionadas pelos treinadores como mais importantes para o sucesso; 2) as principais fontes de “stress” estavam relacionadas com preocupações com o desempenho dos atletas, sendo comuns a diferentes modalidades; 3) os treinadores recorriam a diversas estratégias de “coping” em simultâneo, geralmente adaptativas; e 4) para além da ansiedade, outras emoções, positivas e negativas, pareciam influenciar o desempenho dos treinadores.Fundação para a Ciência e Tecnologia (FCT

On the Mass and Width of the Z-boson and Other Relativistic Quasistable Particles

The ambiguity in the definition for the mass and width of relativistic resonances is discussed, in particular for the case of the Z-boson. This ambiguity can be removed by requiring that a resonance's width $\Gamma$ (defined by a Breit-Wigner lineshape) and lifetime $\tau$ (defined by the exponential law) always and exactly fulfill the relation $\Gamma = \hbar/\tau$. To justify this one needs relativistic Gamow vectors which in turn define the resonance's mass M_R as the real part of the square root $\rm{Re}\sqrt{s_R}$ of the S-matrix pole position s_R. For the Z-boson this means that $M_R \approx M_Z - 26{MeV}$ and $\Gamma_R \approx \Gamma_Z-1.2{MeV}$ where M_Z and $\Gamma_Z$ are the values reported in the particle data tables.Comment: 23 page

Epstein-Barr virus: clinical and epidemiological revisits and genetic basis of oncogenesis

Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancie

A genome-wide gene-environment interaction study of breast cancer risk for women of European ancestry

Background Genome-wide studies of gene–environment interactions (G×E) may identify variants associated with disease risk in conjunction with lifestyle/environmental exposures. We conducted a genome-wide G×E analysis of ~ 7.6 million common variants and seven lifestyle/environmental risk factors for breast cancer risk overall and for estrogen receptor positive (ER +) breast cancer. Methods Analyses were conducted using 72,285 breast cancer cases and 80,354 controls of European ancestry from the Breast Cancer Association Consortium. Gene–environment interactions were evaluated using standard unconditional logistic regression models and likelihood ratio tests for breast cancer risk overall and for ER + breast cancer. Bayesian False Discovery Probability was employed to assess the noteworthiness of each SNP-risk factor pairs. Results Assuming a 1 × 10–5 prior probability of a true association for each SNP-risk factor pairs and a Bayesian False Discovery Probability < 15%, we identified two independent SNP-risk factor pairs: rs80018847(9p13)-LINGO2 and adult height in association with overall breast cancer risk (ORint = 0.94, 95% CI 0.92–0.96), and rs4770552(13q12)-SPATA13 and age at menarche for ER + breast cancer risk (ORint = 0.91, 95% CI 0.88–0.94). Conclusions Overall, the contribution of G×E interactions to the heritability of breast cancer is very small. At the population level, multiplicative G×E interactions do not make an important contribution to risk prediction in breast cancer

Homeobox gene Dlx3 is regulated by p63 during ectoderm development: relevance in the pathogenesis of ectodermal dysplasias

Ectodermal dysplasias (EDs) are a group of human pathological conditions characterized by anomalies in organs derived from epithelial-mesenchymal interactions during development. Dlx3 and p63 act as part of the transcriptional regulatory pathways relevant in ectoderm derivatives, and autosomal mutations in either of these genes are associated with human EDs. However, the functional relationship between both proteins is unknown. Here, we demonstrate that Dlx3 is a downstream target of p63. Moreover, we show that transcription of Dlx3 is abrogated by mutations in the sterile alpha-motif (SAM) domain of p63 that are associated with ankyloblepharon-ectodermal dysplasia-clefting (AEC) dysplasias, but not by mutations found in ectrodactylyectodermal dysplasia-cleft lip/palate ( EEC), Limb-mammary syndrome (LMS) and split hand-foot malformation (SHFM) dysplasias. Our results unravel aspects of the transcriptional cascade of events that contribute to ectoderm development and pathogenesis associated with p63 mutations

Neoantigen-specific immunity in low mutation burden colorectal cancers of the consensus molecular subtype 4

Background: The efficacy of checkpoint blockade immunotherapies in colorectal cancer is currently restricted to a minority of patients diagnosed with mismatch repair-deficient tumors having high mutation burden. However, this observation does not exclude the existence of neoantigen-specific T cells in colorectal cancers with low mutation burden and the exploitation of their anti-cancer potential for immunotherapy. Therefore, we investigated whether autologous neoantigen-specific T cell responses could also be observed in patients diagnosed with mismatch repair-proficient colorectal cancers.Methods: Whole-exome and transcriptome sequencing were performed on cancer and normal tissues from seven colorectal cancer patients diagnosed with mismatch repair-proficient tumors to detect putative neoantigens. Corresponding neo-epitopes were synthesized and tested for recognition by in vitro expanded T cells that were isolated from tumor tissues (tumor-infiltrating lymphocytes) and from peripheral mononuclear blood cells stimulated with tumor material.Results: Neoantigen-specific T cell reactivity was detected to several neo-epitopes in the tumor-infiltrating lymphocytes of three patients while their respective cancers expressed 15, 21, and 30 non-synonymous variants. Cell sorting of tumor-infiltrating lymphocytes based on the co-expression of CD39 and CD103 pinpointed the presence of neoantigen-specific T cells in the CD39(+)CD103(+) T cell subset. Strikingly, the tumors containing neoantigen-reactive TIL were classified as consensus molecular subtype 4 (CMS4), which is associated with TGF-beta pathway activation and worse clinical outcome.Conclusions: We have detected neoantigen-targeted reactivity by autologous T cells in mismatch repair-proficient colorectal cancers of the CMS4 subtype. These findings warrant the development of specific immunotherapeutic strategies that selectively boost the activity of neoantigen-specific T cells and target the TGF-beta pathway to reinforce T cell reactivity in this patient group.Surgical oncolog