Influence of taxonomic resolution on mutualistic network properties.

Ecologists are increasingly interested in plant-pollinator networks that synthesize in a single object the species and the interactions linking them within their ecological context. Numerous indices have been developed to describe the structural properties and resilience of these networks, but currently, these indices are calculated for a network resolved to the species level, thus preventing the full exploitation of numerous datasets with a lower taxonomic resolution. Here, we used datasets from the literature to study whether taxonomic resolution has an impact on the properties of plant-pollinator networks.For a set of 41 plant-pollinator networks from the literature, we calculated nine network index values at three different taxonomic resolutions: species, genus, and family. We used nine common indices assessing the structural properties or resilience of networks: nestedness (estimated using the nestedness index based on overlap and decreasing fill [NODF], weighted NODF, discrepancy [BR], and spectral radius [SR]), connectance, modularity, robustness to species loss, motifs frequencies, and normalized degree.We observed that modifying the taxonomic resolution of these networks significantly changes the absolute values of the indices that describe their properties, except for the spectral radius and robustness. After the standardization of indices measuring nestedness with the Z-score, three indices-NODF, BR, and SR for binary matrices-are not significantly different at different taxonomic resolutions. Finally, the relative values of all indices are strongly conserved at different taxonomic resolutions.We conclude that it is possible to meaningfully estimate the properties of plant-pollinator interaction networks with a taxonomic resolution lower than the species level. We would advise using either the SR or robustness on untransformed data, or the NODF, discrepancy, or SR (for weighted networks only) on Z-scores. Additionally, connectance and modularity can be compared between low taxonomic resolution networks using the rank instead of the absolute values.

Human septic myopathy: induction of cyclooxygenase, heme oxygenase and activation of the ubiquitin proteolytic pathway.

BACKGROUND: Skeletal muscle failure and wasting are manifestations of sepsis in humans that leads to serious and prolonged complications. The authors investigated the role of the major proinflammatory and antiinflammatory pathways, namely the inducible isoforms cyclooxygenase (COX-2) and heme oxygenase (HO-1), and the ubiquitin proteolytic pathway in skeletal muscle of septic patients. METHODS: Protein expression was detected by Western blot techniques. Muscle biopsies were taken from two muscle groups, rectus abdominis and vastus lateralis, of septic and control patients. RESULTS: The study showed an increase in COX-2 and HO-1 proteins expression and an activation of the proteolytic ubiquitin pathway with a parallel increase in free ubiquitin and ubiquitinated proteins in skeletal muscle of septic but not of control patients. In addition, those patients who would die from septic shock expressed more COX-2 and HO-1 proteins in muscle biopsies than did those patients who would survive. CONCLUSIONS: This study showed a marked involvement of local proinflammatory and antiinflammatory pathways and, more importantly, demonstrated the existence of an active ubiquitin proteolytic pathway in skeletal muscle of septic patients. Activation of ubiquitin pathway could be involved in sepsis-related muscle catabolism and wasting.

Acute right ventricular failure--from pathophysiology to new treatments.

The right ventricle (RV) provides sustained low-pressure perfusion of the pulmonary vasculature, but is sensitive to changes in loading conditions and intrinsic contractility. Factors that affect right ventricular preload, afterload or left ventricular function can adversely influence the functioning of the RV, causing ischaemia and right ventricular failure (RVF). As RVF progresses, a pronounced tricuspid regurgitation further decreases cardiac output and worsens organ congestion. This can degenerate into an irreversible vicious cycle. The effective diagnosis of RVF is optimally performed by a combination of techniques including echocardiography and catheterisation, which can also be used to monitor treatment efficacy. Treatment of RVF focuses on alleviating congestion, improving right ventricular contractility and right coronary artery perfusion and reducing right ventricular afterload. As part of the treatment, inhaled nitric oxide or prostacyclin effectively reduces afterload by vasodilating the pulmonary vasculature. Traditional positive inotropic drugs enhance contractility by increasing the intracellular calcium concentration and oxygen consumption of cardiac myocytes, while vasopressors such as norepinephrine increase arterial blood pressure, which improves cardiac perfusion but increases afterload. A new treatment, the calcium sensitiser, levosimendan, increases cardiac contractility without increasing myocardial oxygen demand, while preserving myocardial relaxation. Furthermore, it increases coronary perfusion and decreases afterload. Conversely, traditional treatments of circulatory failure, such as mechanical ventilation and volume loading, could be harmful in the case of RVF. This review outlines the pathophysiology, diagnosis and treatment of RVF, illustrated with clinical case studies.

Paresis acquired in the intensive care unit: a prospective multicenter study.

CONTEXT: Although electrophysiologic and histologic neuromuscular abnormalities are common in intensive care unit (ICU) patients, the clinical incidence of ICU-acquired neuromuscular disorders in patients recovering from severe illness remains unknown. OBJECTIVES: To assess the clinical incidence, risk factors, and outcomes of ICU-acquired paresis (ICUAP) during recovery from critical illness in the ICU and to determine the electrophysiologic and histologic patterns in patients with ICUAP. DESIGN: Prospective cohort study conducted from March 1999 to June 2000. SETTING: Three medical and 2 surgical ICUs in 4 hospitals in France. PARTICIPANTS: All consecutive ICU patients without preexisting neuromuscular disease who underwent mechanical ventilation for 7 or more days were screened daily for awakening. The first day a patient was considered awake was day 1. Patients with severe muscle weakness on day 7 were considered to have ICUAP. MAIN OUTCOME MEASURES: Incidence and duration of ICUAP, risk factors for ICUAP, and comparative duration of mechanical ventilation between ICUAP and control patients. RESULTS: Among the 95 patients who achieved satisfactory awakening, the incidence of ICUAP was 25.3% (95% confidence interval [CI], 16.9%-35.2%). All ICUAP patients had a sensorimotor axonopathy, and all patients who underwent a muscle biopsy had specific muscle involvement not related to nerve involvement. The median duration of ICUAP after day 1 was 21 days. Mean (SD) duration of mechanical ventilation after day 1 was significantly longer in patients with ICUAP compared with those without (18.2 [36.3] vs 7.6 [19.2] days; P =.03). Independent predictors of ICUAP were female sex (odds ratio [OR], 4.66; 95% CI, 1.19-18.30), the number of days with dysfunction of 2 or more organs (OR, 1.28; 95% CI, 1.11-1.49), duration of mechanical ventilation (OR, 1.10; 95% CI, 1.00-1.22), and administration of corticosteroids (OR, 14.90; 95% CI, 3.20-69.80) before day 1. CONCLUSIONS: Identified using simple bedside clinical criteria, ICUAP was frequent during recovery from critical illness and was associated with a prolonged duration of mechanical ventilation. Our findings suggest an important role of corticosteroids in the development of ICUAP.