Increase Of Average Multiplicity Research Articles

Systematic study of rapidity dispersion parameter in high energy nucleus–nucleus interactions

A systematic study of rapidity dispersion parameter as a quantitative measure of clustering of particles has been carried out in the interactions of 16 O , 28 Si and 32 S projectiles at 4.5 A GeV/c with heavy ( AgBr ) and light (CNO) groups of targets present in the nuclear emulsion. For all the interactions, the total ensemble of events has been divided into four overlapping multiplicity classes depending on the number of shower particles. For all the interactions and for each multiplicity class, the rapidity dispersion parameter values indicate the occurrence of clusterization during the multiparticle production at Dubna energy. The measured rapidity dispersion parameter values are found to decrease with the increase of average multiplicity for all the interactions. The dependence of rapidity dispersion parameter on the average multiplicity can be successfully described by a relation D(η) = a + b〈ns〉 + c〈ns〉2. The experimental results have been compared with the results obtained from the analysis of Monte Carlo simulated (MC-RAND) events. MC-RAND events show weaker clusterization among the pions in comparison to the experimental data.

Void analysis of pions and its multiplicity dependence at Dubna and SPS energies

This paper investigates the multiplicity dependence of void probability scaling of fluctuation of pions (i.e. classifying fluctuation patterns of pions on the basis of their number, ns) for a wide range of projectile energy from 4.5 to 200 A GeV. The study reveals that void probability scaling is dependent on pion multiplicity at all energies. At comparatively lower projectile energy the scaling becomes poor with increase in average multiplicity, however at high energy the scaling is found to be independent of multiplicity.

The Gap Junction Protein Connexin32 Is a Mouse Lung Tumor Suppressor

Although loss of connexin expression and/or gap junction intercellular communication correlates with decreased growth control and increased neoplastic potential, there is limited evidence directly linking gap junction intercellular communication function with tumor suppression in situ. Here, we show for the first time that a gap junction protein, connexin32 (Cx32), acts as a lung tumor suppressor in a mouse model. Cx32-deficient nontumorous lung tissue exhibited an increased proliferative index (P < 0.001), and, after exposure to the carcinogen diethylnitrosamine, Cx32-deficient mice exhibited a highly statistically significant (P < 0.001) increase in bronchioloalveolar lung tumor incidence (28 of 45, 62%) and a 45% increase in average multiplicity compared with wild-type mice (7 of 29, 24%). Tumors from Cx32-deficient mice also showed increased activation of mitogen-activated protein kinase (P < 0.001) compared with wild-type tumors, implicating this signaling pathway in Cx32/gap junction intercellular communication-associated lung tumorigenesis.