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Natural processes and human interference can lead to undesirable sedimentation of a magnitude difficult to deal with in an economical, ecological and societally acceptable manner. Showcasing various examples throughout the world, criteria to choose an adequate river remediation technology will be discussed, in three distinct scenarios: (1) the case of natural processes leading to a build-up of contaminated sediments; (2) the case of industrial activity leading to contamination; and finally (3) the case of disaster management. For the first time we will discuss the approach taken in Portugal to clean the Tago river at Vila Velha do Rodão where a layer of sediment with high cellulose levels covering the bottom on both sides of the Porta de Rodão at the heart of the Natura 2000 Site and UNESCO World Heritage listed natural park had to be removed and dewatered. Other cases of river remediation projects will be presented as well, such as the case of Fox river (USA) and Zutphen (the Netherlands), where contaminated sediments were used to rebuild the entrance of a river port. We will also touch upon the potential for tube dewatering technology as a response during disaster management and the hurdles encountered in the actions around two red mud disasters. The first dating from 2010 in Hungary at Ajka where a dam breach in a containment facility released 1.1 Mm3 of red sludge into a widespread area, polluting agricultural land and water ways. The second at the Rio Doce at Vale Samarco in Brazil in 2015, where dewatering bags were used to build a dam using the red mud spilled into the river.

Reaction Forces zijn gespecialiseerde militaire eenheden die als belangrijkste eigenschap hebben dat zij - vooruitlopend op de beslissing tot inzet van een grote(re) vredesmacht - zeer snel in een bepaald crisisgebied kunnen worden ontplooid. De laatste tijd wordt er veel aandacht besteed aan dit onderwerp, vooral vanwege een aantal recente voorstellen tot oprichting van een snelle reactiemacht speciaal voor VN-vredesoperaties. Dit artikel geeft een overzicht van de ontwikkelingen op bet gebied van Reaction Forces en heeft mede ten doel om de bestaande spraakverwarring over dit onderwerp weg te nemen.

PurposeHaematopoietic stem cell transplantation (HSCT) is potentially lifesaving. However, it comes with negative consequences such as impaired physical functioning, fatigue and poor quality of life. The aim of this systematic review and meta-analysis is to determine the effect of exercise and nutrition interventions to counteract negative consequences of treatment and improve physical functioning in patients receiving HSCT.MethodsThis systematic review and meta-analysis included randomised controlled trials from three electronic databases between 2009 and 2020. The trials included adult patients receiving HSCT and an exercise or nutrition intervention. Study selection, bias assessment and data extraction were independently performed by two reviewers. Physical functioning outcomes were meta-analysed with a random-effects model.ResultsThirteen studies were included using exercise interventions (n = 11) and nutrition interventions (n = 2); no study used a combined intervention. Meta-analysis of the trials using exercise intervention showed statistically significant effects on 6-min walking distance (standardised mean difference (SMD) 0.41, 95% CI: 0.14–0.68), lower extremity strength (SMD 0.37, 95% CI 0.12–0.62) and global quality of life (SMD 0.27, 95% CI: 0.08–0.46).ConclusionOur physical functioning outcomes indicate positive effects of exercise interventions for patients receiving HSCT. Heterogeneity of the exercise interventions and absence of high-quality nutrition studies call for new studies comparing different types of exercise studies and high quality studies on nutrition in patients with HSCT.

Risk-stratified treatment strategies have the potential to increase survival and lower toxicity in relapsed/refractory classical Hodgkin lymphoma (R/R cHL) patients. This study investigated the prognostic value of serum (s)TARC, vitamin D and lactate dehydrogenase (LDH), TARC immunohistochemistry and quantitative PET parameters in 65 R/R cHL patients who were treated with brentuximab vedotin (BV) and DHAP followed by autologous stem-cell transplantation (ASCT) within the Transplant BRaVE study (NCT02280993). At a median follow-up of 40 months, the 3-year progression free survival (PFS) was 77% (95% CI: 67–88%) and the overall survival was 95% (90–100%). Significant adverse prognostic markers for progression were weak/negative TARC staining of Hodgkin Reed-Sternberg cells in the baseline biopsy, and a high standard uptake value (SUV)mean or SUVpeak on the baseline PET scan. After one cycle of BV-DHAP, sTARC levels were strongly associated with the risk of progression using a cutoff of 500 pg/ml. On the pre-ASCT PET scan, SUVpeak was highly prognostic for progression post-ASCT. Vitamin D, LDH and metabolic tumor volume had low prognostic value. In conclusion, we established the prognostic impact of sTARC, TARC staining, and quantitative PET parameters for R/R cHL, allowing the use of these parameters in prospective risk-stratified clinical trials. Trial registration: NCT02280993.

Background Diaphragm weakness frequently develops in critically ill patients and is explained by a combination of atrophy and myofiber dysfunction. Myofibers are large syncytial cells maintained by a population of myonuclei, which provide gene transcripts to a finite fiber volume, termed the myonuclear domain. Myonuclear number is a determinant of transcriptional capacity and therefore critical for diaphragm and peripheral muscle regeneration after critical illness. Changes in myonuclear number in myofibers undergoing atrophy have not been investigated in mechanically ventilated ICU patients, but they are of potential clinical importance. Our objective was to investigate if and how myonuclear number changes in the diaphragm of mechanically ventilated ICU patients and whether changes are associated with myofiber atrophy and clinical parameters. Methods We used a combination of transcriptomics, immunohistochemistry and confocal microscopy to study myonuclear alterations in the diaphragm and quadriceps biopsies from mechanically ventilated ICU patients (n = 24) and non‐critically ill patients (n = 10). Results Compared to control patients, myonuclear number and myonuclear domain were reduced in critically ill patients with diaphragm myofiber atrophy (n = 14) (myonuclear number per mm of 133 [92–183] vs. 92 [83–105], p = 0.03 (slow myofibers) and 149 [118–189] vs. 88 [69–109], p = 0.004 (fast myofibers); myonuclear domain size was 44 [34–51] vs. 29 pL, p = 0.004 (slow myofibers) and 41 [39–48] vs. 27 pL, p = 0.001 (fast myofibers) of control patients and ICU patients with atrophy, respectively). Increased intrinsic apoptotic pathway activation was identified as a mechanism underlying myonuclear removal (percentage of apoptotic myonuclei of 0.64 [0.60–0.84] and 0.95 [0.84–1.2], p = 0.015 and increased percentage of activated caspase‐3 positive myonuclei of 2,5 [1.6–3.3] vs. 5.7 [4.3–11], p = 0.001 in control patients and ICU patients with atrophy, respectively). Total transcriptional activity in myofibers decreased with myonuclear loss (RNA‐Pol‐2 Ser5 fluorescence intensity per fibre of 2.6 [2.2–3.3] vs. 5.8 [3.1–6.7] AU, p = 0.036 in control patients and ICU patients with atrophy, respectively). Furthermore, muscle stem cell number was reduced in the patients with diaphragm atrophy (PAX7 positive nuclei per myofiber of 0.10 [0.09–0.11] vs. 0.05 [0.04–0.07], p = 0.002 in control patients and ICU patients with atrophy, respectively). No correlation was found between myonuclear loss and duration or mode of mechanical ventilation. Conclusions We identified myonuclear loss due to intrinsic apoptotic pathway activation as a potential mechanism underlying diaphragm atrophy in mechanically ventilated patients. The loss of myonuclei may contribute to impaired regeneration of myofibers after critical illness. Duration and mode of mechanical ventilation are not the major drivers of these modifications.

Disturbance of the circadian clock has been associated with increased risk of cardio-metabolic disorders. Previous studies showed that optimal timing of food intake can improve metabolic health. We hypothesized that time-restricted feeding could be a strategy to minimize long term adverse metabolic health effects of shift work and jetlag. In this study, we exposed female FVB mice to weekly alternating light-dark cycles ( i . e . 12 h shifts) combined with ad libitum feeding, dark phase feeding or feeding at a fixed clock time, in the original dark phase. In contrast to our expectations, long-term disturbance of the circadian clock had only modest effects on metabolic parameters. Mice fed at a fixed time showed a delayed adaptation compared to ad libitum fed animals, in terms of the similarity in 24 h rhythm of core body temperature, in weeks when food was only available in the light phase. This was accompanied by increased plasma triglyceride levels and decreased energy expenditure, indicating a less favorable metabolic state. On the other hand, dark phase feeding accelerated adaptation of core body temperature and activity rhythms, however, did not improve the metabolic state of animals compared to ad libitum feeding. Taken together, restricting food intake to the active dark phase enhanced adaptation to shifts in the light-dark schedule, without significantly affecting metabolic parameters.

Background Palliative care is becoming increasingly important because the number of patients with an incurable disease is growing and their survival is improving. Previous research tells us that early palliative care has the potential to improve quality of life (QoL) in patients with advanced cancer and their relatives. According to limited research on palliative care in the Netherlands, patients with advanced cancer and their relatives find current palliative care suboptimal. The aim of the eQuiPe study is to understand the experienced quality of care (QoC) and QoL of patients with advanced cancer and their relatives to further improve palliative care. Methods A prospective longitudinal observational cohort study is conducted among patients with advanced cancer and their relatives. Patients and relatives receive a questionnaire every 3 months regarding experienced QoC and QoL during the palliative trajectory. Bereaved relatives receive a final questionnaire 3 to 6 months after the patients’ death. Data from questionnaires are linked with detailed clinical data from the Netherlands Cancer Registry (NCR). By means of descriptive statistics we will examine the experienced QoC and QoL in our study population. Differences between subgroups and changes over time will be assessed while adjusting for confounding factors. Discussion This study will be the first to prospectively and longitudinally explore experienced QoC and QoL in patients with advanced cancer and their relatives simultaneously. This study will provide us with population-based information in patients with advanced cancer and their relatives including changes over time. Results from the study will inform us on how to further improve palliative care. Trial registration Trial NL6408 ( NTR6584 ). Registered in Netherlands Trial Register on June 30, 2017.

The pathogenesis of chronic joint inflammation remains unclear, although the involvement of pathogen recognition receptors has been suggested recently. In the present article, we describe the role of two members of the NACHT-LRR (NLR) family, Nod1 (nucleotide-binding oligomerization domain) and Nod2 in a model of acute joint inflammation induced by intraarticular injection of Streptococcus pyogenes cell wall fragments. Here, we show that Nod2 deficiency resulted in reduced joint inflammation and protection against early cartilage damage. In contrast, Nod1 gene-deficient mice developed enhanced joint inflammation with concomitant elevated levels of proinflammatory cytokines and cartilage damage, consistent with a model in which Nod1 controls the inflammatory reaction. To explore whether the different function of Nod1 and Nod2 occurs also in humans, we exposed peripheral blood mononuclear cells (PBMCs) carrying either Nod1ins/del or Nod2fs mutation with SCW fragments in vitro. Production of both TNFα and IL-1β was clearly impaired in PBMCs carrying the Nod2fs compared with PBMCs isolated from healthy controls. In line with results in Nod1 gene-deficient mice, PBMCs from individuals bearing a newly described Nod1 mutation produced enhanced levels of proinflammatory cytokines after 24-h stimulation with SCW fragments. These data indicate that the NLR family members Nod1 and Nod2 have different functions in controlling inflammation, and that intracellular Nod1-Nod2 interactions may determine the severity of arthritis in this experimental model. Whether a distorted balance between the function of Nod1 and/or Nod2 is involved in the pathogenesis of human autoinflammatory or autoimmune disease, such as rheumatoid arthritis, remains to be elucidated.