RESUMO
E896 has measured Lambda production in 11.6A GeV/c Au-Au collisions over virtually the whole rapidity phase space. The midrapidity p(t) distributions have been measured for the first time at this energy and appear to indicate that the Lambda hyperons have different freeze-out conditions than protons. A comparison with the relativistic quantum molecular dynamics model shows that while there is good shape agreement at high rapidity the model predicts significantly different slopes of the m(t) spectra at midrapidity. The data, where overlap occurs, are consistent with previously reported measurements.
RESUMO
Mice lacking the POU domain-containing transcription factor Brn-3a have several neuronal deficits. In the present paper, we show that Brn-3a plays two distinct roles during development of the trigeminal ganglion. In this ganglion, neurons expressing the neurotrophin receptors, TrkB and TrkC, are born between E9.5 and E11.5. In the absence of Brn-3a, very few neurons ever express TrkC, but TrkB-expressing neurons are present at E12.5 in elevated numbers, suggesting that Brn-3a may be a constituent of a regulatory circuit determining which Trk receptor is expressed by these early-born neurons. Most neurons expressing the neurotrophin receptor TrkA are generated between E11.5 and E13.5 in this ganglion and their initial generation is not prevented by absence of Brn-3a. However, after E12. 5, absence of Brn-3a results in a progressive loss in neuronal TrkA and TrkB expression, which leads to a massive wave of apoptosis that peaks at E15.5. Despite complete absence of the Trk receptors at E17. 5 and P0, approximately 30% of the normal complement of neurons survive to birth in Brn-3a mutants. Approximately 70% of these express the GDNF receptor subunit, c-ret; many can be sustained by GDNF, but not by NGF in culture. Thus, the vast majority of surviving neurons are probably sustained in vivo by trophic factor(s) whose receptors are not regulated by Brn-3a. In conclusion, our data indicate the specific functions of Brn-3a in controlling the survival and differentiation of trigeminal neurons by regulating expression of each of the three Trk receptors.
Assuntos
Proteínas de Ligação a DNA/metabolismo , Proteínas de Drosophila , Fatores de Crescimento Neural , Receptores Proteína Tirosina Quinases/genética , Receptores de Fator de Crescimento Neural/genética , Fatores de Transcrição/metabolismo , Gânglio Trigeminal/embriologia , Animais , Apoptose , Contagem de Células , Diferenciação Celular , Sobrevivência Celular , Células Cultivadas , Regulação da Expressão Gênica no Desenvolvimento , Fator Neurotrófico Derivado de Linhagem de Célula Glial , Receptores de Fator Neurotrófico Derivado de Linhagem de Célula Glial , Imuno-Histoquímica , Camundongos , Camundongos Knockout , Proteínas do Tecido Nervoso/genética , Neurônios/metabolismo , Parvalbuminas/genética , Proteínas Proto-Oncogênicas/genética , Proteínas Proto-Oncogênicas c-ret , Receptor do Fator Neutrófico Ciliar , Receptor de Fator de Crescimento Neural , Receptor trkA/genética , Receptor trkC , Fator de Transcrição Brn-3 , Fator de Transcrição Brn-3ARESUMO
Correct and early diagnosis, along with appropriate therapy, should limit mortality. In the pediatric population, signs and symptoms may be subtle. PE should be on the differential diagnosis in patients that present with dyspnea in association with significant risk factors, chest pain, or hemoptysis. PE may be missed if a high index of suspicion is not maintained. In a patient with a PE, an appropriate hypercoagulable workup (Table 1) needs to be considered prior to initiation of anticoagulation therapy. This case highlights the need for further awareness.
