The power of diversity over large solution spaces

We consider a team of agents with limited problem-solving ability facing a disjunctive task over a large solution space. We provide sufficient conditions for the following four statements. First, two heads are better than one: a team of two agents will solve the problem even if neither agent alone would be able to. Second, teaming up does not guarantee success: if the agents are not sufficiently creative, even a team of arbitrary size may fail to solve the problem. Third, "defend it numerous": when the agent's problem-solving ability is adversely affected by the complexity of the solution space, the solution of the problem requires only a mild increase in the size of the team. Fourth, groupthink impairs the power of diversity: if agents' abilities are positively correlated, a larger team is necessary to solve the problem

MAGNETIZATION OF VERY DILUTE PdMn AND PdFe ALLOYS : RE-ENTRANT BEHAVIOUR ?

The static magnetization of three very dilute Pd-based alloys containing 700 ppm Fe, 700 ppm Mn and 1 000 ppm Mn has been measured in low applied fields up to 10 Oe as a function of temperature between 50 mK and 1.0 K. The zero field cooled magnetization possesses features which can be replicated by a mean field effective-field model for bond disordered systems with arbitrary spin S, suggesting that these alloys may be in the re-entrant regime of the magnetic phase diagram. Measurements of the time dependence of the thermoremanent magnetization yield essentially logarithmic behaviour over a wide range of temperatures

Adenosine Deaminase (ADA)-Deficient Severe Combined Immune Deficiency (SCID): Molecular Pathogenesis and Clinical Manifestations

Deficiency of adenosine deaminase (ADA, EC3.5.4.4), a housekeeping enzyme of purine metabolism encoded by the Ada gene, is a cause of human severe combined immune deficiency (SCID). Numerous deleterious mutations occurring in the ADA gene have been found in patients with profound lymphopenia (T(-) B(-) NK(-)), thus underscoring the importance of functional purine metabolism for the development of the immune defense. While untreated ADA SCID is a fatal disorder, there are multiple life-saving therapeutic modalities to restore ADA activity and reconstitute protective immunity, including enzyme replacement therapy (ERT), allogeneic hematopoietic stem cell transplantation (HSCT) and gene therapy (GT) with autologous gene-corrected hematopoietic stem cells (HSC). We review the pathogenic mechanisms and clinical manifestations of ADA SCID