Editorial Commentary: Testosterone Replacement Therapy and Anterior Cruciate Ligament Injury Risk: Insights and Cautions for Clinical Application.

The relation between testosterone replacement therapy (TRT) and anterior cruciate ligament injury risk has garnered attention in recent orthopaedic research. With TRT's popularity on the rise, understanding its potential musculoskeletal risks is important for orthopaedic and sports medicine providers. Whereas some studies suggest an association, confounding variables such as activity level, number of hours of sports participation, dosing variations, physiological versus supraphysiological levels of testosterone, and individual patient characteristics may influence outcomes.

Reduced protein kinase C delta in a high molecular weight complex in mitochondria and elevated creatine uptake into Barth syndrome B lymphoblasts.

Aim: Barth syndrome (BTHS) is a rare X-linked genetic disease in which mitochondrial oxidative phosphorylation is impaired due to a mutation in the gene. The protein kinase C delta (PKCδ) signalosome exists as a high molecular weight complex in mitochondria and controls mitochondrial oxidative phosphorylation.

Method: Here, we examined PKCδ levels in mitochondria of aged-matched control and BTHS patient B lymphoblasts and its association with a higher molecular weight complex in mitochondria.

Multiligament knee injury (MLKI): an expert consensus statement on nomenclature, diagnosis, treatment and rehabilitation.

Multiligament knee injuries (MLKIs) represent a broad spectrum of pathology with potentially devastating consequences. Currently, disagreement in the terminology, diagnosis and treatment of these injuries limits clinical care and research. This study aimed to develop consensus on the nomenclature, diagnosis, treatment and rehabilitation strategies for patients with MLKI, while identifying important research priorities for further study.

Anomalous peroxidase activity of cytochrome c is the primary pathogenic target in Barth syndrome.

Barth syndrome (BTHS) is a life-threatening genetic disorder with unknown pathogenicity caused by mutations in TAFAZZIN (TAZ) that affect remodeling of mitochondrial cardiolipin (CL). TAZ deficiency leads to accumulation of mono-lyso-CL (MLCL), which forms a peroxidase complex with cytochrome c (cyt c) capable of oxidizing polyunsaturated fatty acid-containing lipids. We hypothesized that accumulation of MLCL facilitates formation of anomalous MLCL-cyt c peroxidase complexes and peroxidation of polyunsaturated fatty acid phospholipids as the primary BTHS pathogenic mechanism.

Exercise improves cognitive dysfunction and neuroinflammation in mice through Histone H3 lactylation in microglia.

Background: Exercise is postulated to be a promising non-pharmacological intervention for the improvement of neurodegenerative disease pathology. However, the mechanism of beneficial effects of exercise on the brain remains to be further explored. In this study, we investigated the effect of an exercise-induced metabolite, lactate, on the microglia phenotype and its association with learning and memory.

Outcomes of multiligament knee injury treated with versus without internal brace suture augmentation.

Purpose: To compare the postoperative outcomes between Internal Brace (IB) and non-IB patients who underwent surgical management of multiple-ligament knee injuries (MLKI).

Methods: Patients who underwent surgical management of MLKI at two institutions between 2010 and 2020 were identified and offered participation in the study via the collection of postoperative functional outcomes for MLKI; Lysholm Knee score, Multiligament Quality of Life (ML-QOL), Patient-Reported Outcomes Measurement Information System (PROMIS) computer adaptive testing (CAT), Pain Interference (PI), Physical Function (PF), and Mobility instruments (MI). The postoperative outcomes and reoperation rates were compared between the IB group and non-IB group.

Reduction in mRNA Expression of the Neutrophil Chemoattract Factor CXCL1 in Treated Barth Syndrome B Lymphoblasts.

Barth Syndrome (BTHS) is a rare X-linked genetic disease caused by a mutation in the gene, which codes for the protein tafazzin involved in cardiolipin remodeling. Approximately 70% of patients with BTHS exhibit severe infections due to neutropenia. However, neutrophils from BTHS patients have been shown to exhibit normal phagocytosis and killing activity.

Nitric oxide augments signaling for contraction in hypoxic pulmonary arterial smooth muscle-Implications for hypoxic pulmonary hypertension.

Hypoxic persistent pulmonary hypertension in the newborn (PPHN) is usually treated with oxygen and inhaled nitric oxide (NO), both pulmonary arterial relaxants. But treatment failure with NO occurs in 25% of cases. We previously demonstrated that 72 h exposure to hypoxia, modeling PPHN, sensitized pulmonary artery smooth muscle cells (PASMC) to the contractile agonist thromboxane and inhibited relaxant adenylyl cyclase (AC) activity.

Evaluation of Amoxicillin and Amoxicillin-Clavulanate (Augmentin) for Antimicrobial Postexposure Prophylaxis Following Bacillus anthracis Inhalational Exposure in Cynomolgus Macaques.

Amoxicillin is a broad-spectrum antibiotic used to treat a variety of gram-positive and gram-negative infections, such as infections of the ear, nose, and throat, genitourinary tract, skin, and lower respiratory tract; gonorrhea; and Helicobacter pylori. The prophylactic benefit of both amoxicillin and Augmentin (amoxicillin-clavulanate for use against β-lactamase-expressing bacteria) was evaluated for inhalation anthrax in cynomolgus macaques in 2 studies. A pilot study on amoxicillin-clavulanate that used a portion of the study animals demonstrated empirically that dosing twice a day was efficacious.

Tafazzin deficiency attenuates anti-cluster of differentiation 40 and interleukin-4 activation of mouse B lymphocytes.

Barth syndrome (BTHS) is a rare X-linked genetic disease caused by mutations in TAFAZZIN. The tafazzin (Taz) protein is a cardiolipin remodeling enzyme required for maintaining mitochondrial function. Patients with BTHS exhibit impaired mitochondrial respiratory chain and metabolic function and are susceptible to serious infections.

Tafazzin deficiency in mouse mesenchymal stem cells promote reprogramming of activated B lymphocytes toward immunosuppressive phenotypes.

Barth Syndrome (BTHS) is a rare X-linked genetic disorder caused by mutation in the TAFAZZIN gene. Tafazzin (Taz) deficiency in BTHS patients results in an increased risk of infections. Mesenchymal stem cells (MSCs) are well known for their immune-inhibitory function.

Impaired surface marker expression in stimulated Epstein-Barr virus transformed lymphoblasts from Barth Syndrome patients.

Primary B lymphocytes rapidly respond to lipopolysaccharide (LPS) and cytosine linked to a guanine by a phosphate bond deoxyribonucleic acid (CpG DNA) stimulation to promote adaptive immune function through increased surface marker expression. Here we examined expression of surface markers in LPS and CpG DNA stimulated Epstein-Barr virus transformed B lymphoblasts from control and BTHS patients with different mutations. The percentage of cluster of differentiation (CD) positive cells including CD38 + , CD138 + , CD80 + surface expression and programmed cell death protein 1 (PD1 +) surface expression was similar between control and BTHS lymphoblasts incubated plus or minus LPS.

Interobserver and Intraobserver Reliability of the Sirveaux Classification of Scapular Notching After Reverse Total Shoulder Arthroplasty.

The Sirveaux classification characterizes the severity of scapular notching after reverse total shoulder arthroplasty (rTSA). However, its reliability has not been validated. The goal of the current study was to determine the interobserver and intraobserver reliability of the Sirveaux classification.

Altered cardiolipin metabolism is associated with cardiac mitochondrial dysfunction in pulmonary vascular remodeled perinatal rat pups.

Pulmonary vascular remodeling (PVR) in utero results in the development of heart failure. The alterations that occur in cardiac lipid and mitochondrial bioenergetics during the development of in utero PVR was unknown. In this study, PVR was induced in pups in utero by exposure of pregnant dams to indomethacin and hypoxia and cardiac lipids, echocardiographic function and cardiomyocyte mitochondrial function were subsequently examined.

Adiponectin deficiency induces hepatic steatosis during pregnancy and gestational diabetes in mice.

Aims/hypothesis: Obesity and hepatic steatosis are risk factors for gestational diabetes mellitus (GDM), a common complication of pregnancy. Adiponectin is a fat-derived hormone that improves hepatic steatosis and insulin sensitivity. Low levels of circulating adiponectin are associated with GDM development.

Incidence of injuries among lacrosse athletes: a systematic review and meta-analysis.

Objectives: The purpose of this systematic review was to determine the incidence of injuries among lacrosse athletes and the differences in rates of injury by location and gender.

Methods: The PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines were implemented to conduct this systematic review.[1] The following variables were extracted from each of the included articles: location of injury, gender of patient, and incidence of injury among study population.

Development of a Hamster Natural Transmission Model of SARS-CoV-2 Infection.

The global pandemic of coronavirus disease (COVID-19) caused by infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has led to an international thrust to study pathogenesis and evaluate interventions. Experimental infection of hamsters and the resulting respiratory disease is one of the preferred animal models since clinical signs of disease and virus shedding are similar to more severe cases of human COVID-19. The main route of challenge has been direct inoculation of the virus via the intranasal route.

Misoprostol treatment prevents hypoxia-induced cardiac dysfunction through a 14-3-3 and PKA regulatory motif on Bnip3.

Systemic hypoxia is a common element in most perinatal emergencies and is a known driver of Bnip3 expression in the neonatal heart. Bnip3 plays a prominent role in the evolution of necrotic cell death, disrupting ER calcium homeostasis and initiating mitochondrial permeability transition (MPT). Emerging evidence suggests a cardioprotective role for the prostaglandin E1 analog misoprostol during periods of hypoxia, but the mechanisms for this protection are not completely understood.

Tafazzin deficiency impairs mitochondrial metabolism and function of lipopolysaccharide activated B lymphocytes in mice.

B lymphocytes are responsible for humoral immunity and play a key role in the immune response. Optimal mitochondrial function is required to support B cell activity during activation. We examined how deficiency of tafazzin, a cardiolipin remodeling enzyme required for mitochondrial function, alters the metabolic activity of B cells and their response to activation by lipopolysaccharide in mice.

Tafazzin deficiency in mouse mesenchymal stem cells potentiates their immunosuppression and impairs activated B lymphocyte immune function.

Barth Syndrome (BTHS) is a rare X-linked genetic disorder caused by mutation in the TAFAZZIN gene which encodes the cardiolipin (CL) transacylase tafazzin (Taz). Taz deficiency in BTHS patients results in reduced CL in their tissues and a neutropenia which contributes to the risk of infections. However, the impact of Taz deficiency in other cells of the immune system is poorly understood.

Increased Sociability in Mice Lacking Intergenic Enhancers.

The homeodomain transcription factors play important roles in the differentiation and migration of GABAergic interneuron precursors. The mouse and human genomes each have six genes organized into three convergently transcribed bigene clusters (, , and ) with -regulatory elements (CREs) located in the intergenic region of each cluster. Amongst these, the I56i and I12b enhancers from the and locus, respectively, are active in the developing forebrain.