Single-needle: an effective alternative to dual-needle peripheral access in therapeutic plasma exchange.

Apheresis treatments, which involve the removal of a component of blood, generally require one access and one return line to continuously draw and return blood into the extracorporeal circuit. At our center, we prefer to use peripheral venous access to avoid central line-related complications, especially infection. Motivated by patient-centered care, the single-needle (SN) option for therapeutic plasma exchange (TPE) offered on the Spectra Optia (Terumo BCT, Lakewood, CO) was evaluated.

Hox11L1 expression by precursors of enteric smooth muscle: an alternative explanation for megacecum in HOX11L1-/- mice.

Previous studies have focused on expression of Hox11L1 in enteric neurons as the explanation for intestinal and urinary bladder dysmotility observed in mice that do not have the transcription factor. However, Hox11L1 is also expressed transiently in endo-, meso-, and ectodermal cells of the most caudal embryo during gastrulation. We sought to more fully characterize the fates of these cells because they might help explain the pathogenesis of lethal pseudo-obstruction in Hox11L1-null mice.

Malignant autosomal recessive osteopetrosis caused by spontaneous mutation of murine Rank.

Unlabelled: We report the first case of lethal autosomal recessive osteopetrosis in mice caused by a spontaneous 8-bp deletion in exon 2 of the Rank gene. The phenotype, including a block in RANKL-dependent osteoclast differentiation and lymph node agenesis, copies that of Rank(-/-) mice, which have been produced by targeted recombination.

Introduction: Commitment of osteoclast progenitors to the osteoclast lineage requires RANKL/RANK-mediated intercellular signals.

Genetic background modifies intestinal pseudo-obstruction and the expression of a reporter gene in Hox11L1-/- mice.

Background & Aims: The transcription factor Hox11L1 is expressed by enteric neurons. Two groups mutated murine Hox11L1, and reported lethal intestinal pseudo-obstruction and colonic hyperganglionosis in many, but not all, homozygous null mutants. We investigated the regulation of Hox11L1 and factors that influence the penetrance of pseudo-obstruction in Hox11L1-null mice.