Imaging and diagnosis of postpartum complications: sonography and other imaging modalities.

Postpartum complications can be broadly divided into 4 categories: postpartum hemorrhage, obstetrical trauma, thromboembolic complications, and puerperal infections. Postpartum hemorrhage is most commonly caused by uterine atony, abnormal placentation, or genital tract trauma. Secondary causes of hemorrhage include retained products of conception and, rarely, subinvolution of the placental implantation site.

Imaging of hepatic infections.

Hepatic infections include pyogenic and amebic abscesses and fungal and parasitic diseases. Entry of the infectious organisms into the liver can occur by hematogenous spread via the portal vein or hepatic artery, ascension of the infection from the biliary tract, or from trauma. Worldwide, liver abscess is most often caused by Entamoeba histolytica, but in the developed world, pyogenic liver abscess is more common.

Office visit copayments: patient knowledge, response, and communication with providers.

Background: There is limited information on patients' knowledge about their cost-sharing requirements and how that influenced their care-seeking behavior.

Objective: To examine patients' knowledge of their office visit copayments, their self-reported responses to perceived and actual copayments, and discussions with physicians about costs.

Research Design: Cross-sectional telephone interview study with a 71% response rate.

A neutralizing anti-Nogo66 receptor monoclonal antibody reverses inhibition of neurite outgrowth by central nervous system myelin.

The Nogo66 receptor (NgR1) is a neuronal, leucine-rich repeat (LRR) protein that binds three central nervous system (CNS) myelin proteins, Nogo, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein, and mediates their inhibitory effects on neurite growth. Although the LRR domains on NgR1 are necessary for binding to the myelin proteins, the exact epitope(s) involved in ligand binding is unclear. Here we report the generation and detailed characterization of an anti-NgR1 monoclonal antibody, 7E11.

Alpha 7 nicotinic acetylcholine receptors mediate beta-amyloid peptide-induced tau protein phosphorylation.

The Alzheimer's disease pathogenic peptide, beta-amyloid42 (A beta 42), induces tau protein phosphorylation. Because hyperphosphorylated tau is a consistent component of neurofibrillary tangles, a pathological hallmark of Alzheimer's disease, we investigated the signaling molecules involved in A beta 42-induced tau phosphorylation. We show that A beta 42 elicited rapid and reversible tau protein phosphorylation on three proline-directed sites (Ser-202, Thr-181, and Thr-231) in systems enriched in alpha 7 nicotinic acetylcholine receptors (alpha 7nAChR) including serum-deprived human SK-N-MC neuroblastoma cells and hippocampal synaptosomes.