A rapid deployment valve option for failing Medtronic Freestyle full root: a single centre experience.

Background: There are several high-risk treatment options for valve failure of a biological full root replacement. When tailoring the best treatment option for the patient, implantation of a rapid deployment valve (RDV) should be considered.

Case Presentation: Six patients presented with aortic regurgitation in a full root Freestyle bioprosthesis.

Cardiac Involvement in Systemic and Local Vasculitides: The Value of Noninvasive Multimodality Imaging.

Despite significant advances in managing systemic vasculitides, cardiovascular morbidity, and mortality are still of primary concern. Advances in noninvasive imaging have broadened our understanding of the clinical heterogeneity of cardiac involvement in vasculitides. Common cardiovascular complications in primary or secondary vasculitides are; coronary artery aneurysms, acute coronary syndromes, myocarditis, pericarditis, endocarditis, and valvular dysfunction.

The Impact of Aging and Toll-like Receptor 2 Deficiency on the Clinical Outcomes of Staphylococcus aureus Bacteremia.

Staphylococcus aureus (S. aureus) causes a broad range of infections. Toll-like receptor (TLR) 2 senses the S.

An Unexpected Cause of Severe Hypertension and Bradycardia: The Role of Hemodynamic Assessment by Echocardiography.

Severe hypertension has numerous etiologies. When accompanied by bradycardia, the spectrum of differential diagnoses is greatly narrowed and is commonly seen in patients with increased intracranial pressure. However, other etiologies such as bradycardia-induced hypertension are rarely mentioned.

lipoproteins in infectious diseases.

Infections with the Gram-positive bacterial pathogen remain a major challenge for the healthcare system and demand new treatment options. The increasing antibiotic resistance of poses additional challenges, consequently inflicting a huge strain in the society due to enormous healthcare costs. expresses multiple molecules, including bacterial lipoproteins (Lpps), which play a role not only in immune response but also in disease pathogenesis.

Commensal Bacteria Augment septic Arthritis in a Dose-Dependent Manner.

Background: Septic arthritis is considered one of the most dangerous joints diseases and is mainly caused by the Gram-positive bacterium (). Human skin commensals are known to augment infections. The aim of this study was to investigate if human commensals could augment -induced septic arthritis.

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.

Staphylococcus aureus lipoproteins promote abscess formation in mice, shielding bacteria from immune killing.

Despite being a major bacterial factor in alerting the human immune system, the role of Staphylococcus aureus (S. aureus) lipoproteins (Lpp) in skin infections remains largely unknown. Here, we demonstrated that subcutaneous injection of S.

Bacteria and Host Interplay in Septic Arthritis and Sepsis.

() infections are a major healthcare challenge and new treatment alternatives are needed. septic arthritis, a debilitating joint disease, causes permanent joint dysfunction in almost 50% of the patients. bacteremia is associated with higher mortalities than bacteremia caused by most other microbes and can develop to severe sepsis and death.

The Expression of von Willebrand Factor-Binding Protein Determines Joint-Invading Capacity of Staphylococcus aureus, a Core Mechanism of Septic Arthritis.

Septic arthritis, one of the most dangerous joint diseases, is predominantly caused by In contrast, coagulase-negative staphylococci are rarely found in septic arthritis. We hypothesize that coagulases released by , including coagulase (Coa) and von Willebrand factor-binding protein (vWbp), play potent roles in the induction of septic arthritis. Four isogenic strains differing in expression of coagulases (wild-type [WT] Newman, Δ, Δ, and Δ Δ) were used to induce septic arthritis in both wild-type and von Willebrand factor (vWF)-deficient mice.

Tofacitinib treatment aggravates Staphylococcus aureus septic arthritis, but attenuates sepsis and enterotoxin induced shock in mice.

Tofacitinib, a janus kinase inhibitor, is a novel immunosuppressive drug for treatment of rheumatoid arthritis (RA). Septic arthritis (SA) and sepsis caused by Staphylococcus aureus (S. aureus), for which RA patients are at risk, are infections with high mortality.

The role of Staphylococcus aureus lipoproteins in hematogenous septic arthritis.

Permanent joint dysfunction is a devastating complication in patients with septic arthritis. Staphylococcus aureus (S. aureus) lipoproteins (Lpp), the predominant ligands for TLR2, are known to be arthritogenic and induce bone destruction when introduced directly into the joint.

Pre-treatment with IL2 gene therapy alleviates Staphylococcus aureus arthritis in mice.

Background: Staphylococcus aureus (S. aureus) arthritis is one of the most detrimental joint diseases known and leads to severe joint destruction within days. We hypothesized that the provision of auxiliary immunoregulation via an expanded compartment of T regulatory cells (Tregs) could dampen detrimental aspects of the host immune response whilst preserving its protective nature.

A novel mouse model for septic arthritis induced by Pseudomonas aeruginosa.

Septic arthritis is one of the most aggressive joint diseases. Although caused predominantly by S. aureus, Gram-negative bacteria, Pseudomonas aeruginosa among them, account for a significant percentage of the causal agents of septic arthritis.

The YIN and YANG of lipoproteins in developing and preventing infectious arthritis by Staphylococcus aureus.

Rapid bone destruction often leads to permanent joint dysfunction in patients with septic arthritis, which is mainly caused by Staphylococcus aureus (S. aureus). Staphylococcal cell wall components are known to induce joint inflammation and bone destruction.

Human skin commensals augment Staphylococcus aureus pathogenesis.

All bacterial infections occur within a polymicrobial environment, from which a pathogen population emerges to establish disease within a host. Emphasis has been placed on prevention of pathogen dominance by competing microflora acting as probiotics. Here we show that the virulence of the human pathogen Staphylococcus aureus is augmented by native, polymicrobial, commensal skin flora and individual species acting as 'proinfectious agents'.

Lack of Receptor for Advanced Glycation End Products Leads to Less Severe Staphylococcal Skin Infection but More Skin Abscesses and Prolonged Wound Healing.

Background: Lack of receptor for advanced glycation end products (RAGE) ameliorates several infections including Staphylococcus aureus pneumonia. We sought to investigate the role of RAGE in staphylococcal skin infection in mice.

Methods: Wild-type (WT) and RAGE deficient (RAGE-/-) mice were subcutaneously inoculated with S.

Galectin-3 Is a Target for Proteases Involved in the Virulence of Staphylococcus aureus.

is a major cause of skin and soft tissue infection. The bacterium expresses four major proteases that are emerging as virulence factors: aureolysin (Aur), V8 protease (SspA), staphopain A (ScpA), and staphopain B (SspB). We hypothesized that human galectin-3, a β-galactoside-binding lectin involved in immune regulation and antimicrobial defense, is a target for these proteases and that proteolysis of galectin-3 is a novel immune evasion mechanism.

Both anti-TNF and CTLA4 Ig treatments attenuate the disease severity of staphylococcal dermatitis in mice.

Background: RA patients being treated with biologics are known to have an increased risk of infections. We recently demonstrated that both CTLA4 Ig and anti-TNF treatment aggravate systemic Staphylococcus aureus (S. aureus) infection in mice, but with distinct clinical manifestations.

Radiological features of experimental staphylococcal septic arthritis by micro computed tomography scan.

Background: Permanent joint dysfunction due to bone destruction occurs in up to 50% of patients with septic arthritis. Recently, imaging technologies such as micro computed tomography (μCT) scan have been widely used for preclinical models of autoimmune joint disorders. However, the radiological features of septic arthritis in mice are still largely unknown.

RAGE Deficiency Impairs Bacterial Clearance in Murine Staphylococcal Sepsis, but Has No Significant Impact on Staphylococcal Septic Arthritis.

Background: Septic arthritis is a serious joint disease often caused by Staphylococcus aureus (S. aureus). Receptor for Advanced Glycation End products (RAGE) has an important role in several infections.

Deficiency of the Complement Component 3 but Not Factor B Aggravates Staphylococcus aureus Septic Arthritis in Mice.

The complement system plays an essential role in the innate immune response and protection against bacterial infections. However, detailed knowledge regarding the role of complement in Staphylococcus aureus septic arthritis is still largely missing. In this study, we elucidated the roles of selected complement proteins in S.

IL-1 Receptor Antagonist Treatment Aggravates Staphylococcal Septic Arthritis and Sepsis in Mice.

Background: Interleukin-1 receptor antagonist (IL-1Ra) is the primary therapy against autoinflammatory syndromes with robust efficacy in reducing systemic inflammation and associated organ injury. However, patients receiving IL-1Ra might be at increased risk of acquiring serious infections.

Aims: To study whether IL-1Ra treatment deteriorates Staphylococcus aureus (S.

CTLA4 Immunoglobulin but Not Anti-Tumor Necrosis Factor Therapy Promotes Staphylococcal Septic Arthritis in Mice.

Background: The development of biologics has greatly increased the quality of life and the life expectancy of many patients with rheumatoid arthritis. However, a large number of these patients have an increased risk of developing serious infections. The aim of this study was to examine differential effects of anti-tumor necrosis factor (TNF) treatment and CTLA4 immunoglobulin (Ig) treatment on both immunological response and host defense in a murine model of septic arthritis.