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Understanding the pathophysiology and clinical relevance of non-neurological complications is a crucial component in the proper treatment of patients with acute stroke.Little evidence-based data is available to guide management of these complications. There is a clear need for improved surveillance and specific interventions for the prevention, early diagnosis, and proper management of non-neurological complications during the acute phase of ischaemic stroke, which should reduce morbidity and mortality.Participatory health research (PHR) is receiving increasing attention internationally as an approach for generating scientific knowledge to promote health equity for marginalized groups. A similar trend has been observed in Germany over the past several years. The primary characteristic of PHR is the direct participation of those people in the research process whose work or living conditions are the subject of the research. selleck inhibitor This article provides an overview of the origins, foundational principles, and current developments in the field of PHR. The international research literature is discussed in the form of a narrative review with a focus on previous review articles and publications from the International Collaboration for Participatory Health Research.The review indicates that a growing number of health researchers are engaged in participatory research and that a scientific discourse and various organizations have developed in many countries focused specifically on PHR. The following trends are of particular importance consolidation and networking; clarifying the question of what constitutes participation in research; evaluating the impact and added value of PHR; adapting PHR to specific areas of application; and clarifying ethical questions in PHR.Post cardiac arrest syndrome is associated with high morbidity and mortality, which is related not only to a poor neurological outcome but also to respiratory and cardiovascular dysfunctions. The control of gas exchange, and in particular oxygenation and carbon dioxide levels, is fundamental in mechanically ventilated patients after resuscitation, as arterial blood gases derangement might have important effects on the cerebral blood flow and systemic physiology.In particular, the pathophysiological role of carbon dioxide (CO2) levels is strongly underestimated, as its alterations quickly affect also the changes of intracellular pH, and consequently influence metabolic energy and oxygen demand. Hypo/hypercapnia, as well as mechanical ventilation during and after resuscitation, can affect CO2 levels and trigger a dangerous pathophysiological vicious circle related to the relationship between pH, cellular demand, and catecholamine levels. The developing hypocapnia can nullify the beneficial effects of the hypothermia. The aim of this review was to describe the pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest.According to our findings, the optimal ventilator strategies in post cardiac arrest patients are not fully understood, and oxygen and carbon dioxide targets should take in consideration a complex pattern of pathophysiological factors. Further studies are warranted to define the optimal settings of mechanical ventilation in patients after cardiac arrest.ABP 215 (MVASI™, Amgen, Thousand Oaks, CA; MVASI™, Amgen Europe B.V., Netherlands) is a biosimilar to bevacizumab (Avastin®, Genentech, South San Francisco, CA) reference product (RP), a monoclonal antibody targeting vascular endothelial growth factor A (VEGF-A). Here we provide a brief overview of the totality of evidence that supported the approval of ABP 215, along with practical considerations to ensure safe and effective administration.ABP 215 has been shown to be highly similar to the RP, with similar mechanism of action, analytical (structural and functional) characteristics, binding, and potency. The similarity of PK parameters of ABP 215 and bevacizumab RP has been confirmed in healthy volunteers.In a comparative clinical trial, patients with stage IV or recurrent non-squamous non-small cell lung cancer receiving carboplatin and paclitaxel were randomized to ABP 215 or bevacizumab RP. No clinically meaningful differences were found between ABP 215 and RP. The objective response rate (ORR) was 39% for ABP 215 and 41.7% for bevacizumab RP. The risk ratio for the ORR was 0.93 [90% confidence interval (CI), 0.80-1.09], which fell within the prespecified margin for equivalence of 0.67-1.5, indicating similar clinical efficacy.Similar to bevacizumab RP, ABP 215 is supplied as a clear to slightly opalescent, colorless to pale yellow, sterile solution in a glass vial. It should be diluted in 0.9% sodium chloride in polyvinylchloride or polyolefin bags before administering as an intravenous infusion. The ABP 215 solution should be stored at 2-8 °C (36-46°F) prior to use. Physicochemical stability studies showed that there were no meaningful changes in purity or potency and no loss of protein after storage at 2-8 °C for 35 days followed by storage at 30 °C for 48 h.

Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury.

This was a single-center prospective study investigating associations between pulmonary levels of complement activation products and two ventilator settings, tidal volume (V

) and driving pressure (ΔP), in critically ill patients under invasive ventilation. A miniature bronchoalveolar lavage (BAL) was performed for determination of pulmonary levels of C5a, C3b/c, and C4b/c. The primary endpoint was the correlation between BAL fluid (BALF) levels of C5a and V

and ΔP. Levels of complement activation products were also compared between patients with and without ARDS or with and without pneumonia.

Seventy-two patients were included. Median time from start of invasive ventilation till BAL was 27 [19 to 34] hours. Median V

and ΔP before BAL were 6.7 [IQR 6.1 plement activation products were independent of the size of VT and the level of ΔP. The associations were not different for patients with ARDS or with pneumonia. Pulmonary complement activation does not seem to play a major role in VILI, and not even in lung injury per se, in critically ill patients under invasive ventilation.