Clinical rearfoot and knee static alignment measurements are not associated with patellofemoral pain syndrome Medidas clínicas estáticas do retropé e joelho não estão associadas à síndrome da dor patelofemoral

The aim of the present study was to investigate the association between the patellofemoral pain syndrome and the clinical static measurements: the rearfoot and the Q angles. The design was a cross-sectional, observational, case-control study. We evaluated 77 adults (both genders), 30 participants with patellofemoral pain syndrome, and 47 controls. We measured the rearfoot and Q angles by photogrammetry. Independent t-tests were used to compare outcome continuous measures between groups. Outcome continuous data were also transformed into categorical clinical classifications, in order to verify their statistical association with the dysfunction, and &#967;2 tests for multiple responses were used. There were no differences between groups for rearfoot angle [mean differences: 0.2º (95%CI -1.4-1.8)] and Q angle [mean differences: -0.3º (95%CI -3.0-2.4). No associations were found between increased rearfoot valgus [Odds Ratio: 1.29 (95%CI 0.51-3.25)], as well as increased Q angle [Odds Ratio: 0.77 (95%CI 0.31-1.93)] and the patellofemoral pain syndrome occurrence. Although widely used in clinical practice and theoretically thought, it cannot be affirmed that increased rearfoot valgus and increased Q angle, when statically measured in relaxed stance, are associated with patellofemoral pain syndrome (PFPS). These measures may have limited applicability in screening of the PFPS development.<br>O objetivo deste estudo foi investigar se existe associação entre a síndrome da dor patelofemoral e as medidas clínicas estáticas: os ângulos do retropé e Q. Foi realizado um estudo observacional, transversal, caso-controle, no qual foram avaliados 77 adultos (ambos os sexos), 30 participantes com síndrome da dor patelofemoral e 47 controles. Foram medidos os ângulos do retropé e Q, por meio da fotogrametria. Testes t para amostras independentes foram usados para comparações dos resultados das variáveis contínuas entre os grupos. Os resultados das variáveis contínuas foram transformados em classificações clínicas categóricas, para verificar a associação estatística com a disfunção, e o teste do &#967;2 para respostas múltiplas também foi utilizado. Não houve diferença entre os grupos para o ângulo do retropé [média da diferença: 0,2º (IC95% -1,4-1,8)] e ângulo Q [média da diferença: -0,3º (IC95%-3,0-2,4). Não houve associação entre o ângulo do retropé [Odds Ratio: 1,29 (IC95% 0,51-3,25)], assim como entre o ângulo Q [Odds Ratio: 0.77 (IC95% 0,31-1,93)] e a ocorrência da síndrome da dor patelofemoral. Apesar de serem teoricamente justificadas e amplamente utilizadas na prática clínica fisioterapêutica, não pode-se afirmar que as medidas dos ângulos do retropé e Q, quando mensuradas em posição ortostática, estão associadas com a ocorrência da síndrome da dor patelofemoral. Essas medidas podem ter aplicabilidade limitada na triagem desta disfunção

E2F-1 regulation by an unusual DNA damage-responsive DP partner subunit

E2F activity is negatively regulated by retinoblastoma protein (pRb) through binding to the E2F-1 subunit. Within the E2F heterodimer, DP proteins are E2F partner subunits that allow proper cell cycle progression. In contrast to the other DP proteins, the newest member of the family, DP-4, downregulates E2F activity. In this study we report an unexpected role for DP-4 in regulating E2F-1 activity during the DNA damage response. Specifically, DP-4 is induced in DNA-damaged cells, upon which it binds to E2F-1 as a non-DNA-binding E2F-1/DP-4 complex. Consequently, depleting DP-4 in cells re-instates E2F-1 activity that coincides with increased levels of chromatin-bound E2F-1, E2F-1 target gene expression and associated apoptosis. Mutational analysis of DP-4 highlighted a C-terminal region, outside the DNA-binding domain, required for the negative control of E2F-1 activity. Our results define a new pathway, which acts independently of pRb and through a biochemically distinct mechanism, involved in negative regulation of E2F-1 activity