Interaction of eta mesons with nuclei.

Back in the mid-1980s, a new branch of investigation related to the interaction of eta mesons with nuclei came into existence. It started with the theoretical prediction of possible exotic states of eta mesons and nuclei bound by the strong interaction and later developed into an extensive experimental program to search for such unstable states as well as understand the underlying interaction via eta-meson producing reactions. The vast literature of experimental as well as theoretical works that studied various aspects of eta-producing reactions such as the π(+)n → ηp, pd → (3)Heη, p (6)Li → (7)Be η and γ (3)He → η X, to name a few, had but one objective in mind: to understand the eta-nucleon (ηN) and hence the η-nucleus interaction which could explain the production data and confirm the existence of some η-mesic nuclei. In spite of these efforts, there remain uncertainties in the knowledge of the ηN and hence the η-nucleus interaction. Therefore, this review is an attempt to bind together the findings in these works and draw some global and specific conclusions which can be useful for future explorations.The ηN scattering length (which represents the strength of the η-nucleon interaction) using different theoretical models and analyzing the data on η production in pion, photon and proton induced reactions was found to be spread out in a wide range, namely, 0.18 ≤ Re aηN ≤ 1.03 fm and 0.16 ≤ Rm aηN ≤ 0.49 fm. Theoretical searches of heavy η-mesic nuclei based on η-nucleus optical potentials and lighter ones based on Faddeev type few-body approaches predict the existence of several quasibound and resonant states. Although some hints of η-mesic states such as (3)(η)He and (25)(η)Mg do exist from previous experiments, the promise of clearer signals for the existence of η-mesic nuclei lies in the experiments to be performed at the J-PARC, MAMI and COSY facilities in the near future. This review is aimed at giving an overall status of these efforts.

Quantum reflection and dwell times of metastable states.

The concept of phase and dwell times used in tunneling is extended to quantum collisions to derive a relation between the phase and dwell time delays in scattering. This relation can be used to remove the near threshold s-wave singularities in the Wigner-Eisenbud delay times and amounts to an extension of the concept of quantum reflection to strong interactions. Dwell time delay emerges as the quantity which gives the correct behavior of the density of states of a metastable state at all energies. This fact is demonstrated by investigating some recently found metastable states of mesic nuclei.

Requirement of the JIP1 scaffold protein for stress-induced JNK activation.

The c-Jun N-terminal kinase (JNK) signal transduction pathway is activated in response to the exposure of cells to environmental stress. Components of the JNK signaling pathway interact with the JIP1 scaffold protein. JIP1 is located in the neurites of primary hippocampal neurons. However, in response to stress, JIP1 accumulates in the soma together with activated JNK and phosphorylated c-Jun. Disruption of the Jip1 gene in mice by homologous recombination prevented JNK activation caused by exposure to excitotoxic stress and anoxic stress in vivo and in vitro. These data show that the JIP1 scaffold protein is a critical component of a MAP-kinase signal transduction pathway.

Interaction of a mitogen-activated protein kinase signaling module with the neuronal protein JIP3.

The c-Jun NH(2)-terminal kinase (JNK) group of mitogen-activated protein kinases (MAPKs) is activated in response to the treatment of cells with inflammatory cytokines and by exposure to environmental stress. JNK activation is mediated by a protein kinase cascade composed of a MAPK kinase and a MAPK kinase kinase. Here we describe the molecular cloning of a putative molecular scaffold protein, JIP3, that binds the protein kinase components of a JNK signaling module and facilitates JNK activation in cultured cells. JIP3 is expressed in the brain and at lower levels in the heart and other tissues. Immunofluorescence analysis demonstrated that JIP3 was present in the cytoplasm and accumulated in the growth cones of developing neurites. JIP3 is a member of a novel class of putative MAPK scaffold proteins that may regulate signal transduction by the JNK pathway.

Dose computation for irregular fields in cobalt-60 beam.

Dose computation in large irregular fields used for treating certain malignant tumors cannot be done by equivalent field methods. The present methods available for such dose computations are accurate but complicated and tedious and are amenable to only computers. This paper describes an algorithm (a semiempirical formula) of dose computation in an irregular field. Attempt is also made to estimate the dose outside the field border and in the shielded region. The dose values computed with this method at different depths in mantle and inverted Y-field in a cobalt-60 beam are compared with the experimentally measured values. The method proves to be simple and accurate. The calculations can be done even manually with a calculator and a statistical table in the absence of computer facility. It also successfully estimates the dose in the shielded region and in the penumbra.

A simple computational approach to irregular field dosimetry.

Treatment of certain malignant tumors requires very large and irregular fields. The dose computations in such field configurations are quite complicated and tedious and hence accessible to computer methods only. This paper describes an easy method for estimating dose to any point in such irregular fields except those which are in the shielded region. For radiotherapy centres which do not have access to a computer, this paper presents an algorithm that can be used with a desk calculator for dose computation at any point. The dose values calculated using this algorithm at different points and at different depths in the mantle and inverted Y-fields agree within +/- 3% with the values computed using detailed sector integration method of Clarkson.

A simple formula for depth dose calculation for Co-60 teletherapy beam dosimetry.

Knowledge of dose at all the points of interest, in the plane of tumour, is essential for treatment planning. A very simple formula for scatter dose calculation along the central axis of a Co-60 beam has been derived. This formula uses primary dose at depth d, scatter air ratio at the depth of maximum ionisation and the effective depth of the volume, irradiating the medium. The method for calculation of percentage depth dose at any point in the principal plane has been explained in detail. The simple form of the formulation will help in improving the treatment plans for treatments of lesions using Co-60 teletherapy machines.