Self-organized Critical Model Of Biological Evolution

A punctuated equilibrium model of biological evolution with relative fitness between different species being the fundamental driving force of evolution is introduced. Mutation is modeled as a fitness updating cellular automaton process where the change in fitness after mutation follows a Gaussian distribution with mean $x>0$ and standard deviation $\sigma$. Scaling behaviors are observed in our numerical simulation, indicating that the model is self-organized critical. Besides, the numerical experiment suggests that models with different $x$ and $\sigma$ belong to the same universality class. PACS numbers: 87.10.+e, 05.40.+jComment: 8 pages in REVTEX 3.0 with 4 figures (Figures available on request by sending e-mail to [email protected]

Association between nonspecific bronchial hyperreactivity and superoxide anion production by polymorphonuclear leukocytes in chronic airflow obstruction

Inflammatory reactions are believed to be important in nonspecific bronchial hyperreactivity (BHR). To investigate the potential role for oxidant-mediated modulation of BHR, we investigated oxidative metabolism of polymorphonuclear leukocytes (PMN) from the peripheral blood in 28 nonallergic patients with chronic airflow obstruction (CAO). No difference in O −2 generation was found between 14 smokers and 14 ex-smokers with CAO. A significant correlation was found between the degree of BHR and O −2 generation of PMN after stimulation with 20 ng/ml phorbol myristate acetate, both in smokers (r=0.59,p<0.01) and in ex-smokers (r=0.79,p<0.01). The results suggest that oxygen radicals in a direct or indirect way may modulate BHR. Thus, in nonallergic patients with CAO, BHR and inflammation may be linked in a similar way as in allergic patients with asthm

Characterization of (-)-[3H]dihydroalprenolol binding to intact and broken cell preparations of human peripheral blood lymphocytes

In this study we compared characteristics of (-)-[3H]dihydroalprenolol ([3H]DHA) binding sites in crude membrane preparations of human peripheral blood lymphocytes with those of intact, viable cells. A valid determination of specific β-adrenergic receptor binding in both preparations was obtained by defining non-specific [3H]DHA binding with 10−6 M l- or dl-propranolol or 10−3 M l-isoproterenol. Higher concentrations of propranolol were used in prior reports on lymphocyte membranes. We showed that these concentrations may inhibit non-specific binding, causing non-saturability and inhomogeneity of the estimated ‘specific’ binding. In the intact cell preparations, inclusion of 10−4 M phentolamine was necessary to reduce the high degree of non-specific binding. By contrast, phentolamine (10−4 M) showed no effect on the [3H]DHA binding to membrane preparations. At 37°C the [3H]DHA binding to β-adrenergic receptor sites in both intact and broken cell preparations was rapid and reversible. The sites were stereoselective, as l-propranolol was about two orders of magnitude more potent to inhibit [3H]DHA binding than was the d-isomer. In both preparations, agonists competed for specific binding with a rank order of potency isoproterenol > epinephrine > norepinephrine, which indicated a β2-type of adrenergic receptor. The specific [3H]DHA binding was saturable and Scatchard analysis revealed comparable numbers of homogenous, non-cooperative binding sites (approximately 1250 receptors/cell in the membrane preparations and 1700 receptors/cell in the intact cells). In spite of these similarities the membrane sites showed a lower affinity for the antagonists [3H]DHA and propranolol than did the intact cell sites, whereas their affinity for the agonists was increased. These differences indicate that the membrane system might be less suited to provide physiologically significant information about the β-adrenergic receptor system

Resistance of quiescent and proliferating airway epithelial cells to H2O2 challenge

Alveolar epithelial cell injury and recovery are important in the pathogenesis of oxidant-induced lung damage. The alveolar cell line A549 was used to study responses of proliferating and quiescent cells in culture to time- and dose-dependent hydrogen peroxide (H2O2) challenges. Recovery was monitored after 24 h of incubation in fresh medium with 10% serum. The adherent cells were counted and the resistance and recovery of the attached cells was assessed by appearance, by measuring the number of viable, apoptotic and necrotic cells using fluorescent-activated cell sorting, and by determining the intracellular free thiol content. A549 cells recovered from a 1-h challenge with up to 1 mM H2O2 but could not sustain a more prolonged challenge (6 or 24 h) with 0.5 mM or 1.0 mM H2O2. These more severe conditions resulted in: loss of cells by detachment from the plate surface; reduced numbers of viable cells primarily due to necrosis; and a strong reduction of the intracellular free thiol content. Quiescent cells proved to be more sensitive to oxidative stress than proliferating cells. Intracellular free thiol levels apparently play a decisive role in cell survival, preferentially protecting proliferating cells