Conversion total hip arthroplasty following proximal femur fracture: A retrospective analysis.

Background: The incidence of conversion total hip arthroplasty (cTHA) following reduction and fixation for proximal femur fractures will increase in parallel to the aging population worldwide.

Objective: The goal of this study is to report the frequency of bacterial detection and the outcome of cTHA at the authors' institution and to analyze preoperative factors that correlate with higher rates of bacterial growth and septic revision.

Methods: 48 patients who had been converted to THA after osteosynthesis of a proximal femur fracture either by a one- or two-stage procedure were included.

Distinct Phenotypic Consequences of Pathogenic Mutants Associated with Late-Onset Retinal Degeneration.

A pathologic feature of late-onset retinal degeneration caused by the S163R mutation in C1q-tumor necrosis factor-5 (C1QTNF5) is the presence of unusually thick deposits between the retinal pigmented epithelium (RPE) and the vascular choroid, considered a hallmark of this disease. Following its specific expression in mouse RPE, the S163R mutant exhibits a reversed polarized distribution relative to the apically secreted wild-type C1QTNF5, and forms widespread, prominent deposits that gradually increase in size with aging. The current study shows that S163R deposits expand to a considerable thickness through a progressive increase in the basolateral RPE membrane, substantially raising the total RPE height, and enabling their clear imaging as a distinct hyporeflective layer by noninvasive optical coherence tomography in advanced age animals.

Mass-Encoded Reporters Reporting Proteolytic Activity from within the Extracellular Matrix.

Reporting matrix metalloproteinase (MMP) activity directly from the extracellular matrix (ECM) may provide critical insights to better characterize 2D and 3D cell culture model systems of inflammatory diseases and potentially leverage in vivo diagnosis. In this proof-of-concept study, we designed MMP-sensors, which were covalently linked onto the ECM by co-administration of the activated transglutaminase factor XIIIa (FXIIIa). Elements of the featured MMP-sensors are the D-domain of insulin-like growth factor I (IGF-I) through which co-administered FXIIIa covalently links the sensor to the ECM followed by an MMP sensitive peptide sequence and locally reporting on MMP activity, an isotopically labeled mass tag encoding for protease activity, and an affinity tag facilitating purification from fluids.

An arrestin-1 surface opposite of its interface with photoactivated rhodopsin engages with enolase-1.

Arrestin-1 is the arrestin family member responsible for inactivation of the G protein-coupled receptor rhodopsin in photoreceptors. Arrestin-1 is also well-known to interact with additional protein partners and to affect other signaling cascades beyond phototransduction. In this study, we investigated one of these alternative arrestin-1 binding partners, the glycolysis enzyme enolase-1, to map the molecular contact sites between these two proteins and investigate how the binding of arrestin-1 affects the catalytic activity of enolase-1.

Revision of unicompartmental knee arthroplasty using the in situ referencing technique.

Objective: Revision of unicompartmental knee arthroplasty (UKA) to total knee arthroplasty (TKA) with the in situ referencing technique aiming to preserve as much ligament function and epi-metaphyseal bone stock as possible.

Indications: Aseptic loosening, progression of osteoarthritis, periprosthetic fracture, periprosthetic infection, arthrofibrosis, polyethylene wear, malalignment, instability, femoro-tibial impingement.

Contraindications: Unexplained pain, localized or systemic active infection (anywhere).

Systemic Delivery of Genes to Retina Using Adeno-Associated Viruses.

Mutations in more than 80 genes lead to photoreceptor degeneration. Although subretinal delivery of genes to photoreceptor neurons using AAV vectors has proven itself as an efficient therapeutic and investigative tool in various mouse models, the surgical procedure itself could lead to loss of retinal function even in healthy animals, complicating the interpretation of experimental studies and requiring thoroughly designed controls. A noninvasive approach, such as a systemic delivery of genes with AAV through the bloodstream, may serve as a promising direction in tool development.

Clarin-1 expression in adult mouse and human retina highlights a role of Müller glia in Usher syndrome.

Usher syndrome type 3 (USH3) is an autosomal recessively inherited disorder caused by mutations in the gene clarin-1 (CLRN1), leading to combined progressive hearing loss and retinal degeneration. The cellular distribution of CLRN1 in the retina remains uncertain, either because its expression levels are low or because its epitopes are masked. Indeed, in the adult mouse retina, Clrn1 mRNA is developmentally downregulated, detectable only by RT-PCR.

Extensor hallucis longus-transfer for tibialis anterior tendon rupture repair.

Objective: Restore the function of the tibialis anterior muscle, which is responsible for dorsiflexion and inversion of the foot.

Indications: Spontaneous or traumatic rupture of the tibialis anterior tendon.

Contraindications: Patients with multimorbidity or lack of functional demands.

A Splice Variant of Bardet-Biedl Syndrome 5 (BBS5) Protein that Is Selectively Expressed in Retina.

Purpose: Bardet-Biedl syndrome is a complex ciliopathy that usually manifests with some form of retinal degeneration, amongst other ciliary-related deficiencies. One of the genetic causes of this syndrome results from a defect in Bardet-Biedl Syndrome 5 (BBS5) protein. BBS5 is one component of the BBSome, a complex of proteins that regulates the protein composition in cilia.

Activation of phospholipase C mimics the phase shifting effects of light on melatonin rhythms in retinal photoreceptors.

Many aspects of retinal photoreceptor function and physiology are regulated by the circadian clocks in these cells. It is well established that light is the primary stimulus that entrains these clocks; yet, the biochemical cascade(s) mediating light's effects on these clocks remains unknown. This deficiency represents a significant gap in our fundamental understanding of photoreceptor signaling cascades and their functions.

Light-dependent phosphorylation of Bardet-Biedl syndrome 5 in photoreceptor cells modulates its interaction with arrestin1.

Arrestins are dynamic proteins that move between cell compartments triggered by stimulation of G-protein-coupled receptors. Even more dynamically in vertebrate photoreceptors, arrestin1 (Arr1) moves between the inner and outer segments according to the light conditions. Previous studies have shown that the light-driven translocation of Arr1 in rod photoreceptors is initiated by rhodopsin through a phospholipase C/protein kinase C (PKC) signaling cascade.

A checklist for streamlining organ donation after cardiac death.

There is currently a shortage of organ donors to meet the demands of transplantation waiting lists. In recent years there has been renewed interest in donation after cardiac death in order to increase the pool of potential donors. The Organ and Tissue Authority has recently developed a national policy for donation after cardiac death.

Interaction of arrestin with enolase1 in photoreceptors.

Purpose: Arrestin is in disequilibrium in photoreceptors, translocating between inner and outer segments in response to light. The purpose of this project was to identify the cellular component with which arrestin associates in the dark-adapted retina.

Methods: Retinas were cross-linked with 2.

Light-dependent translocation of arrestin in rod photoreceptors is signaled through a phospholipase C cascade and requires ATP.

Partitioning of cellular components is a critical mechanism by which cells can regulate their activity. In rod photoreceptors, light induces a large-scale translocation of arrestin from the inner segments to the outer segments. The purpose of this project is to elucidate the signaling pathway necessary to initiate arrestin translocation to the outer segments and the mechanism for arrestin translocation.

Localization, annotation, and comparison of the Escherichia coli K-12 proteome under two states of growth.

Here we describe a proteomic analysis of Escherichia coli in which 3,199 protein forms were detected, and of those 2,160 were annotated and assigned to the cytosol, periplasm, inner membrane, and outer membrane by biochemical fractionation followed by two-dimensional gel electrophoresis and tandem mass spectrometry. Represented within this inventory were unique and modified forms corresponding to 575 different ORFs that included 151 proteins whose existence had been predicted from hypothetical ORFs, 76 proteins of completely unknown function, and 222 proteins currently without location assignments in the Swiss-Prot Database. Of the 575 unique proteins identified, 42% were found to exist in multiple forms.

Synergistic interactions between two skeletal mutations in mice: individual and combined effects of the semidominants cleidocranial dysplasia (Ccd) and short digits (Dsh).

Heterozygotes for cleidocranial dysplasia (Ccd) and short digits (Dsh) were crossed to test whether synergistic interactions occur between different dominant mutations whose individual pleiotropic phenotypic effects exhibit a common feature. These unlinked mutations are homozygous lethal, and they are congenic on the C57BL/10 background. Each mutation caused more than 10 different anomalies and showed variable expressivity.

A comparison of stem cell populations and hemoglobin switching in normal versus beta-thalassemic mice.

The hematopoietic stem cell concentrations in tissues of homozygous beta-thalassemic and non-thalassemic fetuses and neonates were compared by using the spleen colony-forming units (CFU-S) assay. The relative quantities of embryonic and adult hemoglobins were also determined for fetuses. Beta-thalassemic fetuses had a reduced incidence of CFU-S in the liver throughout gestation, but after birth the beta-thalassemic neonates maintained a greater number of CFU-S in the liver for an extended period.