Focal Septic Arthritis Elicits Age and TLR2-Dependent Periarticular Bone Loss.

Introduction: Septic arthritis, primarily caused by (), is a severe joint infection that leads to joint and bone damage. lipoproteins (LPPs) bind to Toll-like Receptor 2 (TLR2), inducing arthritis and localized bone loss. Aging affects TLR2 immune response to pathogens.

Combination Dornase and Alteplase for Intra-abdominal Drain, Abscess, and Hematoma Clearance: A Retrospective Case Series.

Background: Since the advent of the MIST2 trial, the combined instillation of dornase and alteplase has become an effective nonsurgical treatment option for empyema and pleural fluid collection. Percutaneous drainage of abdominal abscesses and fluid collections, rather than open surgical treatment, also has become commonplace. The are several case reports and studies on the use of fibrinolytics to drain abdominal fluid collections but no literature reporting use of both alteplase and dornase for abdominal administration.

Bacterial Lipoproteins Shift Cellular Metabolism to Glycolysis in Macrophages Causing Bone Erosion.

Belonging to a group of membrane proteins, bacterial lipoproteins (LPPs) are defined by a unique lipid structure at their -terminus providing the anchor in the bacterial cell membrane. In Gram-positive bacteria, LPPs play a key role in host immune activation triggered through a Toll-like receptor 2 (TLR2)-mediated action resulting in macrophage stimulation and subsequent tissue damage demonstrated in experimental models. Yet the physiologic links between LPP activation, cytokine release, and any underlying switches in cellular metabolism remain unclear.

Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis.

Phenol-soluble modulin α (PSMα) is identified as potent virulence factors in Staphylococcus aureus (S. aureus) infections. Very little is known about the role of PSMβ which belongs to the same toxin family.

Saving Money and Reducing Waste With a Tailored Hand Surgery Kit.

Background And Objectives: There is growing interest in containing cost and decreasing waste in the operating room. As part of a quality improvement initiative, we redesigned the supply kit used for 2 common surgical procedures (carpal tunnel release and trigger finger release) performed under local anesthesia.

Methods: A hand surgeon, a medical student, and an operating room nurse examined each item that would be necessary for performing carpal tunnel release and trigger finger release.

Lipoproteins Cause Bone Resorption in a Mouse Model of Septic Arthritis.

Septic arthritis, most often caused by , is a rapidly progressive and destructive joint disease with substantial mortality and morbidity. lipoproteins (Lpps) are known to induce arthritis and bone destruction. Here, we aimed to investigate the bone resorptive effect of Lpps in a murine arthritis model by intra-articular injection of purified Lpps, synthetic lipopeptides, and live strains.

Ex vivo Vitamin D supplementation improves viscoelastic profiles in prostate cancer patients.

Background: Increased risk of thromboembolic events is associated with prostate cancer, specifically linked to activation of tissue factor. Vitamin D has potential anticoagulant effects by the downregulation of tissue factor expression.

Objectives: To evaluate the effects on clot formation, the morphological and viscoelastic profiles of prostate cancer patients, before and after ex vivo supplementation of Vitamin D was studied.

Fetal Alcohol Spectrum Disorder-Issues of Misdiagnosis and Missed Diagnosis in Black Youth: A Case Report.

Fetal alcohol spectrum disorder (FASD) is an umbrella term used to describe the set of conditions that result from prenatal alcohol exposure (PAE) that lead to cognitive impairment, neurodevelopmental delays, socioemotional and behavioral problems, medical complications, and/or secondary disabilities. In addition, various internalizing and externalizing disorders share similar symptoms with FASD, resulting in misdiagnoses and/or missed diagnosis of FASD. This is amplified for Black youths due to the later onset of referral for assessment and lower frequency of referral to specialty clinics.

Omega-3 Fatty Acids Prevent Early Pancreatic Carcinogenesis via Repression of the AKT Pathway.

Pancreatic cancer remains a daunting foe despite a vast number of accumulating molecular analyses regarding the mutation and expression status of a variety of genes. Indeed, most pancreatic cancer cases uniformly present with a mutation in the allele leading to enhanced RAS activation. Yet our understanding of the many epigenetic/environmental factors contributing to disease incidence and progression is waning.

Thioredoxin system-mediated regulation of mutant Kras associated pancreatic neoplasia and cancer.

Peroxiredoxin-1 (Prdx1), a member of the thioredoxin (Txn) system, is overexpressed and correlates with poor prognosis in pancreatic cancer patients and can suppress Kras signaling through redox-mediated inhibition of ERK and AKT in lung and breast cancer. Its redox function is maintained by Txn and sulfiredoxin (Srxn), and its tumor promoting functions are activated by post-translational modification. We studied the role of the Txn system in pancreatic neoplasia and cancer by determining how it regulates the phosphorylation of Kras effectors and by determining its association with patient survival.

Ablation of 5-lipoxygenase mitigates pancreatic lesion development.

Background: Pancreatic ductal adenocarcinoma (PDAC), which continues to have a dismal prognosis, is associated with a pronounced fibroinflammatory response. Inflammation in vivo can be mediated by 5-lipoxygenase (5LO), an enzyme that converts omega-6 fatty acids (FA) to eicosanoids, including leukotriene B4 (LTB4). We have previously shown that diets rich in omega-6 FA increase pancreatic lesions and mast cell infiltration in EL-Kras mice.

Nrf1 and Nrf2 transcription factors regulate androgen receptor transactivation in prostate cancer cells.

Despite androgen deprivation therapy (ADT), persistent androgen receptor (AR) signaling enables outgrowth of castration resistant prostate cancer (CRPC). In prostate cancer (PCa) cells, ADT may enhance AR activity through induction of oxidative stress. Herein, we investigated the roles of Nrf1 and Nrf2, transcription factors that regulate antioxidant gene expression, on hormone-mediated AR transactivation using a syngeneic in vitro model of androgen dependent (LNCaP) and castration resistant (C4-2B) PCa cells.

Loss of Nrf2 accelerates ionizing radiation-induced bone loss by upregulating RANKL.

Radiation therapy is an integral part of treatment for cancer patients; however, major side effects of this modality include aberrant bone remodeling and bone loss. Ionizing radiation (IR) is a major external factor that contributes to a significant increase in oxidative stress such as reactive oxygen species (ROS), has been implicated in osteoporotic phenotypes, and has been implicated in osteoporotic phenotypes, bone loss, and fracture risk. One of the major cellular defenses against heightened oxidative stress is mediated by nuclear factor (erythroid-derived 2)-like 2 (Nrf2), a master transcription factor that regulates induction of antioxidant gene expression and phase II antioxidant enzymes.

Studies on molecular mechanisms of growth inhibitory effects of thymoquinone against prostate cancer cells: role of reactive oxygen species.

Thymoquinone (TQ), an active ingredient of black seed oil (Nigella Sativa), has been shown to possess antineoplastic activity against a variety of experimental tumors. However, the precise mechanism of action of TQ is not known. We investigated the mechanism of action of TQ in androgen receptor (AR)-independent (C4-2B) and AR naïve (PC-3) prostate cancer cells, as models of aggressive prostate cancers.

The nrf1 and nrf2 balance in oxidative stress regulation and androgen signaling in prostate cancer cells.

Reactive oxygen species (ROS) signaling has recently sparked a surge of interest as being the molecular underpinning for cancer cell survival, but the precise mechanisms involved have not been completely elucidated. This review covers the possible roles of two ROS-induced transcription factors, Nrf1 and Nrf2, and the antioxidant proteins peroxiredoxin-1 (Prx-1) and Thioredoxin-1 (Txn-1) in modulating AR expression and signaling in aggressive prostate cancer (PCa) cells. In androgen independent (AI) C4-2B cells, in comparison to the parental androgen dependent (AD) LNCaP cells, we present evidence of high Nrf1 and Prx-1 expression and low Nrf2 expression in these aggressive PCa cells.