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The setting of Thai Jones's wonderful book will be all too familiar to those involved in direct action politics: a liberal urban administration, a radical protest movement, disparities of wealth deepened by economic crisis. There are some obvious points of interest for historians of American, urban, and Progressive Era history, and also some illuminations that are less obvious, and perhaps beyond the author's intent.\\n Anyone who has worked hard to organize social movement mobilization, only to see the movement either founder or explode based on incidents outside of collective control, will recognize the importance of this point.

Pimpare reviews Hell's Kitchen and the Battle for Urban Class Struggle and Progressive Reform in New York City, 1894-1914 by Joseph J. Varga.

Objectives To assess the impact of scan modes and reconstruction kernels using a novel dual-source photon-counting detector CT (PCD-CT) on lumen visibility and sharpness of different stent sizes. Methods A phantom containing six balloon-expandable stents (2.5 to 9 mm diameter) in silicone tubing was scanned on a PCD-CT with standard (0.6 mm and 0.4 mm thicknesses) and ultra-high-resolution (0.2 mm thickness) modes. With the use of increasing contrast medium concentrations, densities of 0, 200, 400, and 600 HU were achieved. Standard-resolution scans were reconstructed using increasing sharpness kernels, using both polyenergetic quantitative soft tissue “conventional” ((Qr40 c (0.6 mm), Qr40 c (0.4 mm), Qr72 c (0.2 mm)) and vascular (Bv) virtual monoenergetic reconstructions (Bv44 m (0.4 mm), Bv60 m (0.4 mm)) at 70 keV. In-stent lumen visibility, sharpness (max. ΔHU of the stent measured in profile plots), and in-stent noise (standard deviation of HU) were measured. Results In-stent lumen visibility was highest for Qr72 c (0.2 mm) (86.5 ± 2.8% to 88.3 ± 2.6%) and in Bv60 m (0.4 mm) reconstructions (77.3 ± 2.9 to 82.7 ± 2.5%). Lumen visibility was lowest in the smallest stent (2.5 mm) ranging from 54.1% in Qr40 c (0.6 mm) to 74.1% in Qr72 c (0.2 mm) and highest in the largest stent (9 mm) ranging from 93.8% in Qr40c(0.6 mm) to 99.1% in the Qr72 c (0.2 mm) series. Lumen visibility decreased by 2.1% for every 200-HU increase in lumen attenuation. Max. ΔHU between stents and stent lumen was highest in Qr72 c (0.2 mm) (ΔHU 892 ± 504 to 1526 ± 517) and Bv60 m (0.4 mm) series (ΔHU 480 ± 357 to 1030 ± 344). Improvement of lumen visibility and sharpness in UHR and Bv60 m (0.4 mm) series was strongest in smaller stent sizes. Conclusion UHR acquisition mode and sharp reconstruction kernels on a novel PCD-CT system significantly improve in-stent lumen visibility and sharpness—especially for smaller stent sizes. Key Points • In-stent lumen visibility and sharpness of stents significantly improve using sharp reconstruction kernels (Bv60) and ultra-high-resolution mode in photon-counting detector computed tomography. • The observed improvement of stent-lumen visibility was highest in smaller stent sizes.

Systemic sclerosis (SSc) is a devastating autoimmune disease characterized by excessive production and accumulation of extracellular matrix, leading to fibrosis of skin and other internal organs. However, the main cellular participants in SSc skin fibrosis remain incompletely understood. Here using differentiation trajectories at a single cell level, we demonstrate a dual source of extracellular matrix deposition in SSc skin from both myofibroblasts and endothelial-to-mesenchymal-transitioning cells (EndoMT). We further define a central role of Hippo pathway effectors in differentiation and homeostasis of myofibroblast and EndoMT, respectively, and show that myofibroblasts and EndoMTs function as central communication hubs that drive key pro-fibrotic signaling pathways in SSc. Together, our data help characterize myofibroblast differentiation and EndoMT phenotypes in SSc skin, and hint that modulation of the Hippo pathway may contribute in reversing the pro-fibrotic phenotypes in myofibroblasts and EndoMTs. Systemic sclerosis (SSc) is an autoimmune disease causing skin fibrosis and organ inflammation. Here the authors generate and analyze SSc skin single cell RNA sequencing data to propose contributions from both myofibroblasts and endothelial-to-mesenchymal -transitioning cells (EndoMT) to skin fibrosis, and to implicate the involvement of Hippo signaling pathways.

Objectives To analyze trends of in-hospital treatment of patients admitted due to peripheral artery disease (PAD) from 2009 to 2018 with special focus on comorbidities, revascularization procedures, resulting costs, and outcome. Methods Using data from the research data center of the German Federal Statistical Office, we included all hospitalizations due to PAD Fontaine stage IIb or higher from 2009 to 2018. To analyze comorbidities, Elixhauser diagnostic groups and linear van Walraven score (vWS) were assessed. Results A total of 1.8 million hospitalizations resulting in €10.3 billion in reimbursement costs were included. From 2009 to 2018, the absolute number of hospitalizations due to PAD increased by 13.3% (163,547 to 185,352). The average cost per hospitalization increased by 20.8% from €5,261 to €6,356. The overall in-hospital mortality decreased from 3.1 to 2.6%. Median vWS of all PAD cases increased by 3 points (2 to 5). The number of percutaneous transluminal angioplasties (PTA) increased by 43.9% while some surgical procedures such as bypasses and embolectomies decreased by 30.8% and 6.8%, respectively. Many revascularization procedures showed a disproportionate increase of those performed in vessels below the knee for example in PTA (+ 68.5%) or in endarterectomies (+ 38.8%). Conclusions This decade-long nationwide analysis shows a rising number of hospitalizations due to PAD with more comorbid patients resulting in increasing reimbursement costs. Interventions are shifting from surgical to endovascular approaches with a notable trend towards interventions in smaller vessels below the knee. Key Points • The number of hospitalizations due to peripheral artery disease is rising and it is associated with increasing reimbursement costs. • Admitted patients are older and show an increasing number of comorbidities while overall in-hospital mortality is decreasing. • Revascularization procedures are shifting from surgical to endovascular approaches and show a trend towards intervention in smaller vessels below the knee. • Major amputations are decreasing while the number of minor amputations is increasing.

Pharmacological ascorbate (i.e., intravenous infusions of vitamin C reaching ~ 20 mM in plasma) is under active investigation as an adjuvant to standard of care anti-cancer treatments due to its dual redox roles as an antioxidant in normal tissues and as a prooxidant in malignant tissues. Immune checkpoint inhibitors (ICIs) are highly promising therapies for many cancer patients but face several challenges including low response rates, primary or acquired resistance, and toxicity. Ascorbate modulates both innate and adaptive immune functions and plays a key role in maintaining the balance between pro and anti-inflammatory states. Furthermore, the success of pharmacological ascorbate as a radiosensitizer and a chemosensitizer in pre-clinical studies and early phase clinical trials suggests that it may also enhance the efficacy and expand the benefits of ICIs.

Wnt/β-catenin signaling has been implicated in lung fibrosis, but how this occurs and whether expression changes in Wnt pathway components predict disease progression is unknown. To determine whether the Wnt coreceptor Lrp5 drives pulmonary fibrosis in mice and is predictive of disease severity in humans. We examined mice with impaired Wnt signaling caused by loss of the Wnt coreceptor Lrp5 in models of lung fibrosis induced by bleomycin or an adenovirus encoding an active form of transforming growth factor (TGF)-β. We also analyzed gene expression in peripheral blood mononuclear cells (PBMC) from patients with idiopathic pulmonary fibrosis (IPF). In patients with IPF, analysis of peripheral blood mononuclear cells revealed that elevation of positive regulators, Lrp5 and 6, was independently associated with disease progression. LRP5 was also associated with disease severity at presentation in an additional cohort of patients with IPF. Lrp5 null mice were protected against bleomycin-induced pulmonary fibrosis, an effect that was phenocopied by direct inhibition of β-catenin signaling by the small molecular inhibitor of β-catenin responsive transcription. Transplantation of Lrp5 null bone marrow cells into wild-type mice did not limit fibrosis. Instead, Lrp5 loss was associated with reduced TGF-β production by alveolar type 2 cells and leukocytes. Consistent with a role of Lrp5 in the activation of TGF-β, Lrp5 null mice were not protected against lung fibrosis induced by TGF-β. We show that the Wnt coreceptor, Lrp5, is a genetic driver of lung fibrosis in mice and a marker of disease progression and severity in humans with IPF. Evidence that TGF-β signaling can override a loss in Lrp5 has implications for patient selection and timing of Wnt pathway inhibitors in lung fibrosis.

Background: The World Health Organization (WHO) introduced the International Classification of Functioning, Disability, and Health (ICF) as a scientific method of disability data collection comprised of >1,200 categories describing the spectrum of impairment types (functional, symptoms-based and anatomical) under the bio-psycho-social model with consideration of environmental and personal factors (pf). ICF Core Sets and ICF Checklists are streamlined disease-specific resources for clinical use, service provision, and for use in health economics and health policy. ICF can disclose strengths and weaknesses across multiple patient-reported outcome measures (PROMs) and help consolidate best-fitting question-items from multiple PROMs. Interstitial lung diseases (ILDs), are generally progressive, with restrictive physiology sometimes occurring in the context of multi-organ autoimmunity/inflammatory conditions such as connective tissue diseases (CTDs). In spite of significant associated morbidity and potential disability, ILD has yet to be linked to the ICF. Methods: Each instrument and their question-items within the consensus-recommended core sets for clinical trials in ILD were deconstructed to single concept units, and then linked per updated ICF linkage rules. Inter-linker agreement was established. Three additional subsequently validated measures were also included. Results: One-hundred-eleven ICF categories were identified for ten PROMs and three traditional objective measures that were amenable to ICF linkage. The proportion of agreement ranged from 0.79 (95% CI: 0.62, 0.91) to 0.93 (0.76, 0.99) with the overall proportion of inter-linker agreement being very high 0.86 (0.82, 0.89) for the initial instruments, with 94–100% for the three additional PROMs. Thirty-four new ‘Personal Factors’ emerged to capture disease-specific qualities not elsewhere described in ICF, e.g. ‘pf_embarrassed by cough’ or ‘pf_panic/afraid when can’t get a breath’. Conclusion: This first known effort in ICF linkage of ILD has provided important revelations on the current utility of the ICF in lung disease. Results have indicated areas for meaningful assessment of ICF descriptors for lung impairment. The mapping across PROMs provides insight into possibilities of developing more streamline and precise instrumentation. Finally, familiarity with the ICF in ILD may enable clinicians to experience a smoother transition with the imminent harmonization of ICD and ICF, ICD-11.