Redescription of Lasioseius floridensis Berlese, 1916 (Acari: Mesostigmata: Blattisociidae), with notes on closely related species

A redescription of Lasioseius floridensis Berlese, 1916 is presented based on examination with descriptive notes of primary type material in the Berlese Collection and on a study of specimens collected from gerbera leaves in Mogi das Cruzes, State of Sao Paulo, Brazil representing all postembryonic stages. This species was originally described from Lake City, Florida, USA, where it was collected from moss; it is considered a senior synonym of Lasioseius arboreus Chant, 1963 (new synonymy) and Lasioseius fimetorum Karg, 1971 (new synonymy), based on examination of primary type material of the latter two species. Examination of other primary type material also indicated that Lasioseius sugawarai Ehara, 1964 is a senior synonym of Lasioseius tridentatus Baker, Delfinado & Abbatiello, 1976 (new synonymy). Placement of L. floridensis among other of the ca 150 species of Lasioseius, based on available keys, and the need for more detailed descriptions of species of genera such as Lasioseius, confirmed by examination of their primary type material, are discussed.

ADA-deficient SCID is associated with a specific microenvironment and bone phenotype characterized by RANKL/OPG imbalance and osteoblast insufficiency

Adenosine deaminase (ADA) deficiency is a disorder of the purine metabolism leading to combined immunodeficiency and systemic alterations, including skeletal abnormalities. We report that ADA deficiency in mice causes a specific bone phenotype characterized by alterations of structural properties and impaired mechanical competence. These alterations are the combined result of an imbalanced receptor activator of nuclear factor-kappa B ligand (RANKL)/osteoprotegerin axis, causing decreased osteoclastogenesis and an intrinsic defect of osteoblast function with subsequent low bone formation. In vitro, osteoblasts lacking ADA displayed an altered transcriptional profile and growth reduction. Furthermore, the bone marrow microenvironment of ADA-deficient mice showed a reduced capacity to support in vitro and in vivo hematopoiesis. Treatment of ADA-deficient neonatal mice with enzyme replacement therapy, bone marrow transplantation, or gene therapy resulted in full recovery of the altered bone parameters. Remarkably, untreated ADA-severe combined immunodeficiency patients showed a similar imbalance in RANKL/osteoprotegerin levels alongside severe growth retardation. Gene therapy with ADA-transduced hematopoietic stem cells increased serum RANKL levels and children`s growth. Our results indicate that the ADA metabolism represents a crucial modulatory factor of bone cell activities and remodeling. The trials were registered at www.clinicaltrials.gov as #NCT00598481 and #NCT00599781. (Blood. 2009; 114: 3216-3226)