High-Throughput Patch Clamp Screening in Human α6-Containing Nicotinic Acetylcholine Receptors.

Nicotine, the addictive component of tobacco products, is an agonist at nicotinic acetylcholine receptors (nAChRs) in the brain. The subtypes of nAChR are defined by their α- and β-subunit composition. The α6β2β3 nAChR subtype is expressed in terminals of dopaminergic neurons that project to the nucleus accumbens and striatum and modulate dopamine release in brain regions involved in nicotine addiction.

Electrophysiology-Based Assays to Detect Subtype-Selective Modulation of Human Nicotinic Acetylcholine Receptors.

The Family Smoking Prevention and Tobacco Control Act of 2009 (Public Law 111-31) gave the US Food and Drug Administration (FDA) the responsibility for regulating tobacco products. Nicotine is the primary addictive component of tobacco and its effects can be modulated by additional ingredients in manufactured products. Nicotine acts by mimicking the neurotransmitter acetylcholine on neuronal nicotinic acetylcholine receptors (nAChRs), which function as ion channels in cholinergic modulation of neurotransmission.

Patient Radiation Exposure During Fluoro-Assisted Direct Anterior Approach Total Hip Arthroplasty.

Background: This study sought to quantify the total patient radiation exposure during fluoro-assisted direct anterior approach (DAA) total hip arthroplasty (THA). We hypothesized that the patient radiation exposure would fall within acceptable published limits for a 1-time patient exposure.

Methods: After institutional review board approval, we performed a retrospective chart review of consecutive unilateral primary DAA THAs at 2 institutions (N = 157) between 2012 and 2014 by a single fellowship-trained arthroplasty surgeon assisted by residents and fellows.

Does Increased Coefficient of Friction of Highly Porous Metal Increase Initial Stability at the Acetabular Interface?

Background: Highly porous metal acetabular components illustrate a decreased rate of aseptic loosening in short-term follow-up compared with previous registry data. This study compared the effect of component surface roughness at the bone-implant interface and the quality of the bone on initial pressfit stability. The null hypothesis is that a standard porous coated acetabular cup would show no difference in initial stability as compared with a highly porous acetabular cup when subjected to a bending moment.

In vitro and in situ characterization of arthroscopic loop security and knot security of braided polyblend sutures: a biomechanical study.

We conducted a study to evaluate biomechanical performance during destructive testing of several different suture materials in various arthroscopic knot configurations under both in vitro and in situ conditions. Surgeons of different levels of experience tied the knots. Three different arthroscopic knots (static surgeon's, Weston, Tennessee slider) with 3 reverse half-hitches on alternating posts were tested using Fiberwire, ForceFiber, Orthocord, and Ultrabraid suture materials under both in vitro and in situ (blood plasma at 37°C) conditions.

Metaxin deficiency alters mitochondrial membrane permeability and leads to resistance to TNF-induced cell killing.

Metaxin, a mitochondrial outer membrane protein, is critical for TNF-induced cell death in L929 cells. Its deficiency, caused by retroviral insertion-mediated mutagenesis, renders L929 cells resistance to TNF killing. In this study, we further characterized metaxin deficiency-caused TNF resistance in parallel with Bcl-X(L) overexpression-mediated death resistance.

Thrombospondins use the VLDL receptor and a nonapoptotic pathway to inhibit cell division in microvascular endothelial cells.

TSPs 1 and 2 function as endogenous inhibitors of angiogenesis. Although thrombospondins (TSPs) have been shown to induce apoptosis in HMVECs, we reasoned that a homeostatic mechanism would also be needed to inhibit EC growth without causing cell death, e.g.

Thrombospondin 2 deficiency in pregnant mice results in premature softening of the uterine cervix.

The gradual disorganization of collagen fibers in the stromal connective tissue of the uterine cervix is characteristic of progressive cervical softening during pregnancy. A lack of thrombospondin (TSP) 2 has been shown to be associated with altered collagen fibril morphology of connective-tissue-rich organs such as skin and tendon. The goal of this study was to determine the role of TSP2 in cervical softening by studying a TSP2-null mouse line.

Thrombospondins 1 and 2 function as inhibitors of angiogenesis.

Thrombospondins (TSPs) 1 and 2 are matricellular proteins with the well-characterized ability to inhibit angiogenesis in vivo, and the migration and proliferation of cultured microvascular endothelial cells (ECs). Angiogenesis in developing tumors and in various models of wound healing is diminished or delayed by the presence of TSP1 or 2. Sequences within the type I repeats of TSP1 and 2 have been demonstrated to mediate the anti-migratory effects of TSPs on microvascular EC, although, paradoxically, sequences in the N- and C-terminal domains have pro-angiogenic effects.

Thrombospondin 2 inhibits microvascular endothelial cell proliferation by a caspase-independent mechanism.

The matricellular protein thrombospondin 2 (TSP2) regulates a variety of cell-matrix interactions. A prominent feature of TSP2-null mice is increased microvascular density, particularly in connective tissues synthesized after injury. We investigated the cellular basis for the regulation of angiogenesis by TSP2 in cultures of murine and human fibroblasts and endothelial cells.