Towards an individualized protocol for workload increments in cardiopulmonary exercise testing in children and adolescents with cystic fibrosis

AbstractBackgroundThere is no single optimal exercise testing protocol for children and adolescents with cystic fibrosis (CF) that differs widely in age and disease status. The aim of this study was to develop a CF-specific, individualized approach to determine workload increments for a cycle ergometry testing protocol.MethodsA total of 409 assessments consisting of maximal exercise data, anthropometric parameters, and lung function measures from 160 children and adolescents with CF were examined. 90% of the database was analyzed with backward linear regression with peak workload (Wpeak) as the dependent variable. Afterwards, we [1] used the remaining 10% of the database (model validation group) to validate the model's capacity to predict Wpeak and [2] validated the protocol's ability to provide a maximal effort within a 10±2minute time frame in 14 adolescents with CF who were tested using this new protocol (protocol validation group).ResultsNo significant differences were seen in Wpeak and predicted Wpeak in the model validation group or in the protocol validation group. Eight of 14 adolescents with CF in the protocol validation group performed a maximal effort, and seven of them terminated the test within the 10±2minute time frame. Backward linear regression analysis resulted in the following equation: Wpeak (W)=−142.865+2.998×Age (years)−19.206×Sex (0=male; 1=female)+1.328×Height (cm)+23.362×FEV1 (L) (R=.89; R2=.79; SEE=21). Bland–Altman analysis showed no systematic bias between the actual and predicted Wpeak.ConclusionWe developed a CF-specific linear regression model to predict peak workload based on standard measures of anthropometry and FEV1, which could be used to calculate individualized workload increments for a cycle ergometry testing protocol

Electrochemistry: From sense to sustainability (ISE 2016). Foreword

Catalysis and Surface Chemistr

Dendritic Cells in Human Atherosclerosis: From Circulation to Atherosclerotic Plaques

Background. Atherosclerosis is a chronic inflammatory disease with atherosclerotic plaques containing inflammatory infiltrates predominantly consisting of monocytes/macrophages and activated T cells. More recent is the implication of dendritic cells (DCs) in the disease. Since DCs were demonstrated in human arteries in 1995, numerous studies in humans suggest a role for these professional antigen-presenting cells in atherosclerosis. Aim. This paper focuses on the observations made in blood and arteries of patients with atherosclerosis. In principal, flow cytometric analyses show that circulating myeloid (m) and plasmacytoid (p) DCs are diminished in coronary artery disease, while immunohistochemical studies describe increased intimal DC counts with evolving plaque stages. Moreover, mDCs and pDCs appear to behave differently in atherosclerosis. Yet, the origin of plaque DCs and their relationship with blood DCs are unknown. Therefore, several explanations for the observed changes are postulated. In addition, the technical challenges and discrepancies in the research field are discussed. Future. Future studies in humans, in combination with experimental animal studies will unravel mechanisms leading to altered blood and plaque DCs in atherosclerosis. As DCs are crucial for inducing but also dampening immune responses, understanding their life cycle, trafficking and function in atherosclerosis will determine potential use of DCs in antiatherogenic therapies

Performance of the BioIntegral Bovine Pericardial Graft in Vascular Infections:VASCular No-REact Graft Against INfection Study

Background: Vascular graft and endograft infections (VGEI) and native vessel infections (NVI) remain considerable challenges in vascular surgery, leading to high mortality and morbidity rates. Although in situ reconstruction is the preferred treatment, the material of choice is still a source of debate. Autologous veins are considered the first choice; however, xenografts may be an acceptable alternative. The performance of a biomodified bovine pericardial graft is assessed when implemented in an infected vascular area. Methods: This is a prospective multicenter cohort study. Patients who underwent reconstruction for VGEI or NVI with a biomodified bovine pericardial bifurcated or straight tube graft were included from December 2017 until June 2021. The primary outcome measure was reinfection at mid-term follow-up. Secondary outcome measures included mortality, patency, and amputation rate. Results: Thirty-four patients with vascular infections were included, of which 23 (68%) had an infected Dacron prosthesis after primary open repair and 8 (24%) had an infected endovascular graft. The remaining 3 (9%) had infected native vessels. At secondary repair, 3 (7%) patients had an in situ aortic tube reconstruction, 29 (66%) had an aortic bifurcated reconstruction, and 2 (5%) had an iliac-femoral reconstruction. At 1-year follow-up after the BioIntegral bovine pericardial graft reconstruction, the reinfection rate was 9%. The 1-year infection-related and procedure-related mortality rate was 16%. The occlusion rate was 6% and in total 3 patients underwent a lower limb amputation during the 1-year follow-up period. Conclusions: In situ reconstruction as treatment of (endo)graft and native vessel infections remains a challenge and reinfection looms as a potential consequence. In cases where time is of essence or when autologous venous repair is not feasible, a swift available solution is needed. The BioIntegral biomodified bovine pericardial graft may be an option as it shows reasonable results in terms of reinfection, in aortic tube and bifurcated grafts.</p

Feline calicivirus virulent systemic disease: Clinical epidemiology, analysis of viral isolates and in vitro efficacy of novel antivirals in australian outbreaks

Feline calicivirus (FCV) causes upper respiratory tract disease (URTD) and sporadic outbreaks of virulent systemic disease (FCV-VSD). The basis for the increased pathogenicity of FCVVSD viruses is incompletely understood, and antivirals for FCV-VSD have yet to be developed. We investigated the clinicoepidemiology and viral features of three FCV-VSD outbreaks in Australia and evaluated the in vitro efficacy of nitazoxanide (NTZ), 2′-C-methylcytidine (2CMC) and NITD008 against FCV-VSD viruses. Overall mortality among 23 cases of FCV-VSD was 39%. Metagenomic sequencing identified five genetically distinct FCV lineages within the three outbreaks, all seemingly evolving in situ in Australia. Notably, no mutations that clearly distinguished FCVURTD from FCV-VSD phenotypes were identified. One FCV-URTD strain likely originated from a recombination event. Analysis of seven amino-acid residues from the hypervariable E region of the capsid in the cultured viruses did not support the contention that properties of these residues can reliably differentiate between the two pathotypes. On plaque reduction assays, dose–response inhibition of FCV-VSD was obtained with all antivirals at low micromolar concentrations; NTZ EC50, 0.4–0.6 µM, TI = 21; 2CMC EC50, 2.7–5.3 µM, TI &gt; 18; NITD-008, 0.5 to 0.9 µM, TI &gt; 111. Investigation of these antivirals for the treatment of FCV-VSD is warranted