Grade 0 plasma leakage on days 4-6, respectively). Conclusions We present the first human in vivo evidence of glycocalyx disruption in dengue, with worse visual glycocalyx damage and higher plasma degradation products associated with more severe plasma leak.Introduction Palmoplantar pustular psoriasis (PPPP) is a debilitating inflammatory skin disorder of the palms and soles that poses a high burden on affected patients. Satisfactory treatment response is rarely achieved using current treatment options, little is known about the potential benefit of the PDE4 inhibitor apremilast in the treatment of refractory PPPP patients. We aimed to evaluate the use of apremilast in PPPP patients. Patients and Methods Six patients, four with severe physician global assessment (PGA) = 3 on a scale of 0-4 and two with very severe (PGA = 4) treatment-refractory PPPP [mean age (years ± SD) 56.2 ± 15.6], were included in this study. Five patients had concomitant psoriatic arthritis (PsA). Prior to apremilast administration, topical corticosteroids, psoralen-UVA and multiple systemic oral and biologic anti-inflammatory treatments were insufficient to improve their skin condition or had to be discontinued due to adverse events. Apremilast (titrated to a maintenance dose of 30 mg 2x/d) was commenced in all patients with clinical follow-up over 18 months. Results Within the first 4 weeks of treatment, each patient’s symptoms improved as assessed by PGA score. At 3 months, four patients had a mild PGA score and two were cleared from PPPP. After 18 months of follow-up, three patients improved from PGA = 3 to PGA = 1 and one patient from PGA = 4 to PGA = 1. Two patients discontinued treatment, one due to a lack of efficacy against PsA and the other to a desire to have a child. However, both patients recorded improvements before discontinuing treatment. Conclusion Apremilast may be a promising treatment option for refractory and severely affected PPPP patients. Our observation, however, requires further validation.Background Prosthetic hip infection (PHI) is a disastrous scenario after an arthroplasty. International guidelines contraindicate one-stage exchange arthroplasty for fistulizing chronic prosthetic hip infection (FCPHI), nevertheless few surgical teams, mostly from Europe, support one stage procedure for this indication. Questions/Purposes Analysis of infection recurrence and implant failure of a series of FCPHIs treated with one stage arthroplasty. Patients and Methods Sixty-six FCPHIs treated with one-stage exchange arthroplasty were prospectively followed up at least 2 years. Clinical, radiological and bacteriological signs suggestive of reinfection were sought, as well as implant failures and PHI related deaths. Results Thirty-four females and thirty-two males with median age of 69.5 years [61-77] and BMI of 26 kg/m2 [22-31] were included. Fistulae were productive in 50 patients (76%). Staphylococcus was responsible for 45% of PHI and 21% were polymicrobial. Twenty-nine patients (44%) received preoperative antibiotic therapy. After a median 60-month follow-up [35-82], 3 patients (4.5%) presented reinfection (two new infections, one relapse) and 3 patients experienced implant failure (1 femoral fracture, 1 stem breakage, 1 recurrent dislocation). One death was related to PHI. After a minimum of 2 years, the infection control rate was of 95.3% (±0.02). Conclusion One-stage exchange arthroplasty for FCPHIs showed a good infection control rate similar to that of non-fistulizing PHI. Systematic preoperative microbiological documentation with joint aspiration and, in some specific cases, the use of preoperative antibiotic therapy are among the optimizations accounting for the success of the one-stage arthroplasty. In light of these results, and those of other studies, international recommendations could evolve. Level of Evidence Descriptive therapeutic prospective cohort study. Olaparib in vivo Level of evidence IV.Background Sarcoidosis and tuberculosis share similarities in clinical manifestations and histopathological features. We aimed to identify the microRNA (miRNA) profiles of the lymph nodes of individuals with sarcoidosis and of those with tuberculous lymphadenitis to investigate the value of miRNAs in the differential diagnosis of sarcoidosis and tuberculous lymphadenitis. Methods The miRNA profiles of the lymph nodes of individuals with sarcoidosis, those with tuberculous lymphadenitis (TBLN) and controls were detected by miRNA microarray analysis in the age- and sex-matched development group of the controls (n = 3), patients with TBLN (n = 3) and patients with sarcoidosis (n = 3), and the results were validated by quantitative real-time polymerase chain reaction in the validation group of the controls (n = 30), TBLN (n = 30) and patients with sarcoidosis (n = 31). The relationship between miRNA expression and the clinical parameters of sarcoidosis was analyzed. Results miR-145, miR-185-5p, miR-301, miR-425-5een individuals with sarcoidosis and those with tuberculous lymphadenitis, which were experimentally selected. miR-185-5p in the lymph nodes can be used as an auxiliary marker for the differential diagnosis of sarcoidosis and tuberculous lymphadenitis.The T-cell coreceptors CD4 and CD8 have well-characterized and essential roles in thymic development, but how they contribute to immune responses in the periphery is unclear. Coreceptors strengthen T-cell responses by many orders of magnitude – beyond a million-fold according to some estimates – but the mechanisms underlying these effects are still debated. T-cell receptor (TCR) triggering is initiated by the binding of the TCR to peptide-loaded major histocompatibility complex (pMHC) molecules on the surfaces of other cells. CD4 and CD8 are the only T-cell proteins that bind to the same pMHC ligand as the TCR, and can directly associate with the TCR-phosphorylating kinase Lck. At least three mechanisms have been proposed to explain how coreceptors so profoundly amplify TCR signaling (1) the Lck recruitment model and (2) the pseudodimer model, both invoked to explain receptor triggering per se, and (3) two-step coreceptor recruitment to partially triggered TCRs leading to signal amplification. More recently it has been suggested that, in addition to initiating or augmenting TCR signaling, coreceptors effect antigen discrimination.