Patient Reidentification from Chest Radiographs: An Interpretable Deep Metric Learning Approach and Its Applications.

Purpose: To train an explainable deep learning model for patient reidentification in chest radiograph datasets and assess changes in model-perceived patient identity as a marker for emerging radiologic abnormalities in longitudinal image sets.

Materials And Methods: This retrospective study used a set of 1 094 537 frontal chest radiographs and free-text reports from 259 152 patients obtained from six hospitals between 2006 and 2019, with validation on the public ChestX-ray14, CheXpert, and MIMIC-CXR datasets. A deep learning model was trained for patient reidentification and assessed on patient identity confirmation, retrieval of patient images from a database based on a query image, and radiologic abnormality prediction in longitudinal image sets.

Development and validation of open-source deep neural networks for comprehensive chest x-ray reading: a retrospective, multicentre study.

Background: Artificial intelligence (AI) systems for automated chest x-ray interpretation hold promise for standardising reporting and reducing delays in health systems with shortages of trained radiologists. Yet, there are few freely accessible AI systems trained on large datasets for practitioners to use with their own data with a view to accelerating clinical deployment of AI systems in radiology. We aimed to contribute an AI system for comprehensive chest x-ray abnormality detection.

A descriptive analysis of wheelchair repair registry data.

Wheeled mobility and seating (WMS) devices allow users to achieve greater mobility independence. Previous studies determined that 53% of wheelchair users required one or more repairs over a 6-month period; however, there are a limited number of studies that have evaluated types of repairs. The purpose of this study was to describe the types of manual wheelchair, power wheelchair, and scooter repairs within the Wheelchair Repair Registry (WRR) and examine the association between WMS devices and the frequency of repairs.

The β2 integrin-kindlin-3 interaction is essential for T-cell homing but dispensable for T-cell activation in vivo.

Kindlin-3 is mutated in the rare genetic disorder, leukocyte adhesion deficiency type III, which is characterized by deficient integrin-mediated adhesion of leukocytes and platelets. However, the specific roles of kindlin-3-β2-integrin interactions in T-cell adhesion and homing and immune responses in vivo remain unclear. Here, we show that the TTT motif in β2 integrins controls kindlin-3 binding.

Characterization of the SNAG and SLUG domains of Snail2 in the repression of E-cadherin and EMT induction: modulation by serine 4 phosphorylation.

Snail1 and Snail2, two highly related members of the Snail superfamily, are direct transcriptional repressors of E-cadherin and EMT inducers. Previous comparative gene profiling analyses have revealed important differences in the gene expression pattern regulated by Snail1 and Snail2, indicating functional differences between both factors. The molecular mechanism of Snail1-mediated repression has been elucidated to some extent, but very little is presently known on the repression mediated by Snail2.

A systemic lupus erythematosus-associated R77H substitution in the CD11b chain of the Mac-1 integrin compromises leukocyte adhesion and phagocytosis.

The Mac-1 integrin is expressed mainly on myeloid cells and binds several ligands, including members of the ICAM family and the complement factor iC3b. It is involved in essential immunological processes, such as leukocyte extravasation and phagocytosis. In addition, Mac-1 has been described to negatively regulate immune cell signaling.

Phosphorylation of serine 11 and serine 92 as new positive regulators of human Snail1 function: potential involvement of casein kinase-2 and the cAMP-activated kinase protein kinase A.

Snail1 is a major factor for epithelial-mesenchymal transition (EMT), an important event in tumor metastasis and in other pathologies. Snail1 is tightly regulated at transcriptional and posttranscriptional levels. Control of Snail1 protein stability and nuclear export by GSK3beta phosphorylation is important for Snail1 functionality.

Transient receptor potential-like channels are essential for calcium signaling and fluid transport in a Drosophila epithelium.

Calcium signaling is an important mediator of neuropeptide-stimulated fluid transport by Drosophila Malpighian (renal) tubules. We demonstrate the first epithelial role, in vivo, for members of the TRP family of calcium channels. RT-PCR revealed expression of trp, trpl, and trpgamma in tubules.

The dg2 (for) gene confers a renal phenotype in Drosophila by modulation of cGMP-specific phosphodiesterase.

Fluid transport in Drosophila melanogaster tubules is regulated by guanosine 3',5'-cyclic monophosphate (cGMP) signalling. Here we compare the functional effects on tubules of different alleles of the dg2 (foraging or for) gene encoding a cGMP-dependent protein kinase (cGK), and show that the fors allele confers an epithelial phenotype. This manifests itself as hypersensitivity of epithelial fluid transport to the nitridergic neuropeptide, capa-1, which acts through nitric oxide and cGMP.

Analysis of Drosophila cGMP-dependent protein kinases and assessment of their in vivo roles by targeted expression in a renal transporting epithelium.

cGMP-dependent protein kinase (cGK) forms encoded by the dg2 (for) gene are implicated in behavior and epithelial transport in Drosophila melanogaster. Here, we provide the first biochemical characterization and cellular localization of cGKs encoded by the major transcripts of dg2: dg2P1 and dg2P2. cGMP stimulates kinase activity of DG2P1 (EC(50): 0.

Interactions between epithelial nitric oxide signaling and phosphodiesterase activity in Drosophila.

Signaling by nitric oxide (NO) and guanosine 3',5'-cyclic monophosphate (cGMP) modulates fluid transport in Drosophila melanogaster. Expression of an inducible transgene encoding Drosophila NO synthase (dNOS) increases both NOS activity in Malpighian (renal) tubules and DNOS protein in both type I (principal) and type II (stellate) cells. However, cGMP content is increased only in principal cells.