Search

Aims: Conventional patient-reported surveys, used for patients undergoing total hip arthroplasty (THA), are limited by subjectivity and recall bias. Objective functional evaluation, such as gait analysis, to delineate a patient's functional capacity and customize surgical interventions, may address these shortcomings. This systematic review endeavours to investigate the application of objective functional assessments in appraising individuals undergoing THA., Methods: The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were applied. Eligible studies of THA patients that conducted at least one type of objective functional assessment both pre- and postoperatively were identified through Embase, Medline/PubMed, and Cochrane Central database-searching from inception to 15 September 2023. The assessments included were subgrouped for analysis: gait analysis, motion analysis, wearables, and strength tests., Results: A total of 130 studies using 15 distinct objective functional assessment methods (FAMs) were identified. The most frequently used method was instrumented gait/motion analysis, followed by the Timed-Up-and-Go test (TUG), 6 minute walk test, timed stair climbing test, and various strength tests. These assessments were characterized by their diagnostic precision and applicability to daily activities. Wearables were frequently used, offering cost-effectiveness and remote monitoring benefits. However, their accuracy and potential discomfort for patients must be considered., Conclusion: The integration of objective functional assessments in THA presents promise as a progress-tracking modality for improving patient outcomes. Gait analysis and the TUG, along with advancing wearable sensor technology, have the potential to enhance patient care, surgical planning, and rehabilitation., Competing Interests: M. P. Ast reports royalties or licenses from OrthAlign, consulting fees from BD Biosciences, Bioventus, Confirmis, OrthAlign, Convatec, Smith & Nephew, Stryker, and Surgical Care Affiliates, payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from BD Biosciences, OrthAlign, Smith & Nephew, and Stryker, stock or stock options from ConveyMED, HS2, OrthAlign, Ospitek, Osso VS, and Parvizi Surgical Innovations, all of which are unrelated to this study. J. M. Vigdorchik reports royalties or licenses from Corin and DePuy Synthes, consulting fees from DePuy Synthes, Stryker, and Intellijoint Surgical, stock or stock options from Aware, Corin, Intellijoint Surgical, Motion Insights, Ortho AI, and Polaris, and is a member of the editorial board of The Bone & Joint Journal, all of which are unrelated to this study. E. M. Debbi reports royalties or licenses from Ortho Development, consulting fees from DePuy Synthes, payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Ortho Development, and stock or stock options in Think Surgical, all of which are unrelated to this study., (© 2024 The British Editorial Society of Bone & Joint Surgery.)

The biomedical research community addresses reproducibility challenges in animal studies through standardized nomenclature, improved experimental design, transparent reporting, data sharing, and centralized repositories. The ARRIVE guidelines outline documentation standards for laboratory animals in experiments, but genetic information is often incomplete. To remedy this, we propose the Laboratory Animal Genetic Reporting (LAG-R) framework. LAG-R aims to document animals' genetic makeup in scientific publications, providing essential details for replication and appropriate model use. While verifying complete genetic compositions may be impractical, better reporting and validation efforts enhance reliability of research. LAG-R standardization will bolster reproducibility, peer review, and overall scientific rigor., (© 2024. The Author(s).)

Background: The purpose of this study was to evaluate postoperative outcomes at minimum 5-year follow-up in patients following unicompartmental knee arthroplasty (UKA) compared to a matched cohort of total knee arthroplasty (TKA) patients., Methods: Patients who had primarily medial compartment osteoarthritis (OA) who met criteria for medial UKA underwent TKA or medial UKA between 2014 and 2015 at a single institution, matched for age, sex, and body mass index. There were 127 UKAs in 120 patients and 118 TKAs in 116 patients included with minimum 5-year follow-up (range, 6 to 8). Mean age was 69 years (range, 59 to 79) and 71 years (range, 62 to 80) in the UKA and TKA groups, respectively (P = .049)., Results: Patients who underwent UKA had significantly higher mean (±SD) Forgotten Joint Scores (87 ± 20 versus 59 ± 34, P < .001); higher Knee Society Scores (88 ± 14 versus 75 ± 21, P < .001); and lower Numeric Pain Rating Scores (0.8 ± 1.6 versus 1.9 ± 2.2, P < .001). Survivorship free from all-cause revision was 96% (95% CI = 93%-99%) and 99% (95% CI = 97%-100%) at 5 years for TKA and UKA, respectively (P = .52). There were 8 both component revisions in the TKA group within 5 years from the date of surgery and 2 UKA conversions to TKA after 5-year follow-up., Conclusion: Patients who have medial compartment OA and underwent UKA had significantly lower joint awareness, decreased pain, improved function, and higher satisfaction compared to matched TKA patients at minimum 5-year follow-up while maintaining excellent survivorship., (Copyright © 2023 Elsevier Inc. All rights reserved.)

The production of I-131 for use in medicine can be accomplished by the neutron irradiation of tellurium, typically in the form of TeO 2 . Unfortunately, the literature contains conflicting data concerning the I-131 yield as a function of neutron fluence, target mass, irradiation time and post-irradiation decay. In this work, the activity of the I-131 was determined using calculations and experimental verifications based on the interplay of these variables., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Over the past 25 years, genetically engineered mouse models have become an integral and invaluable research tool to develop our understanding of mammalian physiology and pathology. This unit describes methods for generating transgenic mice, focusing on reporter animals relevant to chemokine receptor and ligand expression. Specifically, we describe the use of bacterial artificial chromosome (BAC) engineering and embryonic stem cell manipulation to generate "knock in" and transgenic mice.

Knockout of caspase-8, a cysteine protease that participates in the signaling for cell death by receptors of the TNF/nerve growth factor family, is lethal to mice in utero. To explore tissue-specific roles of this enzyme, we established its conditional knockout using the Cre/loxP recombination system. Consistent with its role in cell death induction, deletion of caspase-8 in hepatocytes protected them from Fas-induced caspase activation and death. However, application of the conditional knockout approach to investigate the cause of death of caspase-8 knockout embryos revealed that this enzyme also serves cellular functions that are nonapoptotic. Its deletion in endothelial cells resulted in degeneration of the yolk sac vasculature and embryonal death due to circulatory failure. Caspase-8 deletion in bone-marrow cells resulted in arrest of hemopoietic progenitor functioning, and in cells of the myelomonocytic lineage, its deletion led to arrest of differentiation into macrophages and to cell death. Thus, besides participating in cell death induction by receptors of the TNF/nerve growth factor family, caspase-8, apparently independently of these receptors, also mediates nonapoptotic and perhaps even antiapoptotic activities.

The p53 tumor suppressor protein is a sequence-specific transcriptional activator of target genes. Exposure of cells to DNA damage results in accumulation of biochemically active p53, with consequent activation of p53-responsive promoters. In order to study how the transcriptional activity of the p53 protein is regulated in vivo, a transgenic mouse strain was generated. These mice harbor the p53-dependent promoter of the mdm2 gene, fused to a lacZ reporter gene. Induction of lacZ activity by DNA damage (ionizing radiation) was monitored in embryos of different p53 genotypes. The transgenic promoter was substantially activated in vivo following irradiation; activation required functional p53. The activation pattern became more restricted with increasing embryo age, as well as with the state of differentiation of a given tissue. Generally, maximal p53 activation occurred in rapidly proliferating, relatively less differentiated cells. A striking extent of haploinsufficiency was revealed-induction of promoter activity was far less efficient in mice carrying only one wild-type p53 allele. This suggests that normal levels of cellular p53 are limiting, and any further reduction already compromises the p53 response significantly. Thus, the activation potential of p53 is tightly controlled in vivo, both spatially and temporally, and an important element in this control is the presence of limiting basal levels of activatable p53.

Previously we reported that neu differentiation factor (NDF)/heregulin (HRG) elevates tyrosine phosphorylation of its receptors erbB-3, erbB-4, and erbB-2 (through heterodimer formation). We also showed that both NDF/HRG and antibodies to erbB-2 can arrest growth and induce differentiation in breast cancer cells. In this study, we report on the mechanism of NDF/HRG-induced cellular effects. We show that NDF/HRG and antibodies to erbB-2 receptors up-regulate expression of p53 by stabilizing the protein. This is accompanied by up-regulation of the p53 inducible gene, p21CIP1/WAF1, in a variety of cell lines: MCF7 and their derivatives (MCF7/HER2, MN1 and MCF-7-puro), ZR75T and LnCap cells. The induction of p21 is further enhanced when cells are treated with both NDF/HRG and DNA-damaging chemotherapeutic agents (i.e. doxorubicin). The NDF/HRG mediated induction of p21 is dependent on wildtype p53, as it fails to occur in cells expressing dominant negative p53 (MDD2). Furthermore, p21 induction is capable of inactivating cdk2 complexes as measured by Histone H1 phosphorylation assays. Finally, we show that in primary cultures of breast and other cancers, p21 is significantly induced in response to NDF/HRG treatment. Collectively, these observations suggest that the mechanism of breast cancer cell growth inhibition and differentiation via erbB receptors activation is through a p53-mediated pathway.