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Dexterous object manipulation remains an open problem in robotics, despite the rapid progress in machine learning during the past decade. We argue that a hindrance is the high cost of experimentation on real systems, in terms of both time and money. We address this problem by proposing an open-source robotic platform which can safely operate without human supervision. The hardware is inexpensive (about \SI{5000}[\$]{}) yet highly dynamic, robust, and capable of complex interaction with external objects. The software operates at 1-kilohertz and performs safety checks to prevent the hardware from breaking. The easy-to-use front-end (in C++ and Python) is suitable for real-time control as well as deep reinforcement learning. In addition, the software framework is largely robot-agnostic and can hence be used independently of the hardware proposed herein. Finally, we illustrate the potential of the proposed platform through a number of experiments, including real-time optimal control, deep reinforcement learning from scratch, throwing, and writing.

Assessment of right ventricular (RV) function in rodents is a challenge due to the complex RV anatomy and structure. Subsequently, the best characterization of RV function is achieved by accurate cardiovascular phenotyping, involving a combination of non-invasive imaging and intra-cardiac pressure-volume measurements. We sought to investigate the feasibility of two complementary phenotyping techniques for the evaluation of RV function in an experimental mouse model of sustained RV pressure overload. Mice underwent either Sham surgery (n = 5) or pulmonary artery banding (PAB) (n = 8) to induce isolated RV pressure overload. After three weeks indices of RV function were assessed by echocardiography (Vevo2100) and closed chest-derived invasive pressure-volume measurements (PVR-1030). PAB resulted in RV hypertrophy and dilatation accompanied by systolic and diastolic dysfunction. Invasive RV hemodynamic measurements demonstrate an increased end-systolic as well as arterial elastance after PAB as compared to sham, resulting in ventricular-arterial decoupling. Regression analysis revealed that TAPSE is rather correlated with ventricular-arterial coupling (r² = 0.77, P = 0.002) than RV contractility (r² = -0.61, P = 0.07). Furthermore, IVRT/RR and E/E' correlate well with RV end-diastolic pressure (r² = 0.87, P = 0.0001 and r² = 0.82, P = 0.0009; respectively). Commonly used indices of systolic RV function are associated with RV-arterial coupling rather than contractility, while diastolic indices are interrelated with end-diastolic pressure where there is maintained pressure overload. This article is protected by copyright. All rights reserved.

Auszug Das Lungenemphysem ist pathologisch-anatomisch definiert. Man versteht darunter eine irreversible abnorme Erweiterung der lufthaltigen Räume distal der Bronchioli terminales, die mit einer Destruktion der Alveolarsepten einhergeht. Neben der chronischen Bronchitis und der Bronchiolitis ist das Lungenemphysem eine der morphologischen Komponenten der chronisch-obstruktiven Lungenkrankheit (COPD). Bei fortgeschrittenen Formen der COPD besteht mit Regelmäßiigkeit ein erhebliches Lungenemphysem.

Auszug Das Lungenödem ist charakterisiert durch eine vermehrte interstitielle und/oder alveoläre Flüssigkeitseinlagerung. Zugrunde liegt entweder eine Erhöhung des kapillären Filtrationsdrucks, die zumeist kardial verursacht ist, oder eine erhöhte Durchlässigkeit der pulmonalen Gefäßschranke (⊡ Tab. 9.1).

Riociguat, a soluble guanylate cyclase stimulator, has been shown in a phase 2 trial to be beneficial in the treatment of pulmonary arterial hypertension. METHODS: In this phase 3, double-blind study, we randomly assigned 443 patients with symptomatic pulmonary arterial hypertension to receive placebo, riociguat in individually adjusted doses of up to 2.5 mg three times daily (2.5 mg-maximum group), or riociguat in individually adjusted doses that were capped at 1.5 mg three times daily (1.5 mg-maximum group). The 1.5 mg-maximum group was included for exploratory purposes, and the data from that group were analyzed descriptively. Patients who were receiving no other treatment for pulmonary arterial hypertension and patients who were receiving endothelin-receptor antagonists or (nonintravenous) prostanoids were eligible. The primary end point was the change from baseline to the end of week 12 in the distance walked in 6 minutes. Secondary end points included the change in pulmonary vascular resistance, N-terminal pro-brain natriuretic peptide (NT-proBNP) levels, World Health Organization (WHO) functional class, time to clinical worsening, score on the Borg dyspnea scale, quality-of-life variables, and safety. RESULTS: By week 12, the 6-minute walk distance had increased by a mean of 30 m in the 2.5 mg-maximum group and had decreased by a mean of 6 m in the placebo group (least-squares mean difference, 36 m; 95% confidence interval, 20 to 52; P

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and fatal lung disease with no known etiology and treatment options. The hallmarks of the histopathology, which is characteristic of usual interstitial pneumonia (UIP) pattern, include interstitial fibrosis, honeycomb changes and fibroblast foci that develop owing to fibroblast proliferation and excessive matrix deposition. Although the complete pathomechanism is not yet understood, several molecular culprits, including transforming growth factor (TGF)-ß, Angiotensin (Ang) II, endothelin (ET)-1, matrix metalloproteinases (MMPs) and cytokines have been identified. IPF is increasingly believed to be an epithelial-driven disease; however, the literature does support an implication of altered immune response and inflammatory processes in the onset or progression of the disease. Mast cells (MCs) are multifunctional tissue resident cells involved in the inflammatory and immune response. An increasing body of evidence suggests a role of MCs and their mediator chymase in the pathology of IPF. With regard to the underlying mechanisms, it is conceivable that MC chymase may function via activation or processing of factors such as proteases, cytokines and growth factors. In this review, we will discuss how MC chymase is linked to and can potentially contribute to the development of IPF. Moreover, the findings from animal model studies will be discussed to highlight the chymase inhibitors as a promising strategy for the treatment of pulmonary fibrosis.

Summary The adult respiratory distress syndrome (ARDS) is characterized by extended inflammatory processes in the lung microvascular, interstitial, and alveolar compartments, resulting in vasomotor disturbances, plasma leakage, cell injury, and complex gas exchange disturbances. Abnormalities in the alveolar surfactant system have long been implicated in the pathogenetic sequelae of this life-threatening syndrome. This hypothesis is supported by similarities in pulmonary failure between patients with ARDS and preterm babies with infant respiratory distress syndrome, known to be triggered primarily by lack of surfactant material. Mechanisms of surfactant alterations in ARDS include: (a) lack of surface-active compounds (phospholipids, apoproteins) due to reduced generation/release by diseased pneumocytes or to increased loss of material (this feature includes changes in the relative composition of the surfactant phospholipid and/or apoprotein profiles); (b) inhibition of surfactant function by plasma protein leakage (inhibitory potencies of different plasma proteins have been defined); (c) “incorporation” of surfactant phospholipids and apoproteins into polymerizing fibrin upon hyaline membrane formation; and (d) damage/inhibition of surfactant compounds by inflammatory mediators (proteases, oxidants, nonsurfactant lipids). Alterations in alveolar surfactant function may well contribute to a variety of pathophysiological key events encountered in ARDS. These include decrease in compliance, ventilation-perfusion mismatch including shunt flow due to altered gas flow distribution (atelectasis, partial alveolar collapse, small airway collapse), and lung edema formation. Moreover, more speculative at the present time, surfactant abnormalities may add to a reduction in alveolar host defense competence and an upregulation of inflammatory events under conditions of ARDS. Persistent atelectasis of surfactant-deficient and in particular fibrin-loaded alveoli may represent a key event to trigger fibroblast proliferation and fibrosis in late ARDS (“collapse induration”). Overall, the presently available data on surfactant abnormalities in ARDS lend credit to therapeutic trials with transbronchial surfactant administration. In addition to the classical goals of replacement therapy defined for preterm infants (rapid improvement in lung compliance and gas exchange), this approach will have to consider its impact on host defense competence and inflammatory and proliferative processes when applied in adults with respiratory failure.

The Communications Center's portfolio covers areas such as marketing, contacts, distribution of information, sales activities and collection of bills by telephone (encashment). A special emphasis is Customer Care Management (Customer Relationship Management) to the patient and his caregivers (relatives), the customers, especially the physicians who send their patients to the hospital and the hospital doctor. By providing communication centers, the hospital would be able to improve the communication with the G.P.s, and identify the wishes and requirements more accurately and easily from the beginning. Dealing effectively with information and communication is already also of special importance for hospital doctors today. One can assume that the demands on doctors in this respect will become even more complex in the future. Doctors who are involved in scientific research are of course fully aware of the growing importance of the Internet with its new information and communication channels. Therefore analysing the current situation, the demands on a future information management system can be formulated: A system that will help doctors to avoid dealing with little goal-oriented information and thus setting up effective communication channels; an information system which is multi-media oriented towards the interests and needs of the patients and patient's relatives and which is further developed continually and directly by those involved.

Background— By its inhibitory effect on platelet-derived growth factor signaling, imatinib could be efficacious in treating patients with pulmonary arterial hypertension (PAH). Methods and Results— Imatinib in Pulmonary Arterial Hypertension, a Randomized, Efficacy Study (IMPRES), a randomized, double-blind, placebo-controlled 24-week trial, evaluated imatinib in patients with pulmonary vascular resistance ≥800 dyne·s·cm −5 symptomatic on ≥2 PAH therapies. The primary outcome was change in 6-minute walk distance. Secondary outcomes included changes in hemodynamics, functional class, serum levels of N-terminal brain natriuretic peptide, and time to clinical worsening. After completion of the core study, patients could enter an open-label long-term extension study. Of 202 patients enrolled, 41% patients received 3 PAH therapies, with the remainder on 2 therapies. After 24 weeks, the mean placebo-corrected treatment effect on 6-minute walk distance was 32 m (95% confidence interval, 12–52; P =0.002), an effect maintained in the extension study in patients remaining on imatinib. Pulmonary vascular resistance decreased by 379 dyne·s·cm −5 (95% confidence interval, −502 to − 255; P Conclusions— Imatinib improved exercise capacity and hemodynamics in patients with advanced PAH, but serious adverse events and study drug discontinuations were common. Further studies are needed to investigate the long-term safety and efficacy of imatinib in patients with PAH. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00902174 (core study); NCT01392495 (extension).