Neutron and proton spectra from the decay of Λ\Lambda hypernuclei

We have determined the spectra of neutrons and protons following the decay of $\Lambda$ hypernuclei through the one- and two-nucleon induced mechanisms. The momentum distributions of the primary nucleons are calculated and a Monte Carlo simulation is used to account for final state interactions. From the spectra we calculate the number of neutrons ($N_n$) and protons ($N_p$) per $\Lambda$ decay and show how the measurement of these quantities, particularly $N_p$, can lead to a determination of $\Gamma_n / \Gamma_p$, the ratio of neutron to proton induced $\Lambda$ decay. We also show that the consideration of the two-nucleon induced channel has a repercussion in the results, widening the band of allowed values of $\Gamma_n / \Gamma_p$ with respect to what is obtained neglecting this channel.Comment: 30 pages, 12 Postscript figures, uuencoded file, ReVTeX, epsf.st

“Where, O Death, Is Thy Sting?” A Brief Review of Apoptosis Biology

Apoptosis was a term introduced in 1972 to distinguish a mode of cell death with characteristic morphology and apparently regulated, endogenously driven mechanisms. The effector processes responsible for apoptosis are now mostly well known, involving activation of caspases and Bcl2 family members in response to a wide variety of physiological and injury-induced signals. The factors that lead of the decision to activate apoptosis as opposed to adaptive responses to such signals (e.g. autophagy, cycle arrest, protein synthesis shutoff) are less well understood, but the intranuclear Promyelocytic Leukaemia Body (PML body) may create a local microenvironment in which the audit of DNA damage may occur, informed by the extent of the damage, the adequacy of its repair and other aspects of cell status

Two nucleon induced Lambda decay and the proton to neutron induced ratio

We reanalyze the decay mode of Lambda hypernuclei induced by two nucleons modifying previous numerical results and the interpretation of the process. The repercussions of this channel in the ratio of neutron to proton induced Lambda decay is studied in detail in connection with the present experimental data. This leads to ratios that are in greater contradiction with usual one pion exchange models than those deduced before

The TSC1 Tumour Suppressor Hamartin Regulates Cell Adhesion Through ERM Proteins and The GTPase Rho.

Loss of the tumour-suppressor gene TSC1 is responsible for hamartoma development in tuberous sclerosis complex (TSC), which renders several organs susceptible to benign tumours. Hamartin, the protein encoded by TSC1, contains a coiled-coil domain and is expressed in most adult tissues, although its function is unknown. Here we show that hamartin interacts with the ezrin-radixin-moesin (ERM) family of actin-binding proteins. Inhibition of hamartin function in cells containing focal adhesions results in loss of adhesion to the cell substrate, whereas overexpression of hamartin in cells lacking focal adhesions results in activation of the small GTP-binding protein Rho, assembly of actin stress fibres and formation of focal adhesions. Interaction of endogenous hamartin with ERM-family proteins is required for activation of Rho by serum or by lysophosphatidic acid (LPA). Our data indicate that disruption of adhesion to the cell matrix through loss of hamartin may initiate the development of TSC hamartomas and that a Rho-mediated signalling pathway regulating cell adhesion may constitute a rate-limiting step in tumour formation

Relationship between Financial Stress and Workplace Absenteeism of Credit Counseling Clients

Credit counseling, Financial education, Financial stress, Personal finance, Work absenteeism,