tbuckley/cabot-search huggingface dataset:
Quality of life assessed 6 months after hospitalisation for acute heart failure: an analysis from <scp>REPORT‐HF</scp> (international REgistry to assess <scp>medical</scp> Practice with <scp>lOngitudinal obseRvation</scp> for Treatment of Heart Failure)
Authors: Candace D. McNaughton, Alex McConnachie, John G. Cleland, John A. Spertus, Christiane E. Angermann, Patrycja Duklas, Jasper Tromp, Carolyn S.P. Lam, Gerasimos Filippatos, Ulf Dahlstrom, Kenneth Dickstein, Anja Schweizer, Sergio V. Perrone, Mahmoud Hassanein, Georg Ertl, Achim Obergfell, Mathieu Ghadanfar, Sean P. Collins
Journal: European Journal of Heart Failure (2022)
Attention2majority: Weak multiple instance learning for regenerative kidney grading on whole slide images
Authors: Ziyu Su, Thomas E. Tavolara, Gabriel Carreno-Galeano, Sang Jin Lee, Metin N. Gurcan, M.K.K. Niazi
Journal: Medical Image Analysis (2022)

Deep learning consistently demonstrates high performance in classifying and segmenting medical images like CT, PET, and MRI. However, compared to these kinds of images, whole slide images (WSIs) of stained tissue sections are huge and thus much less efficient to process, especially for deep learning algorithms. To overcome these challenges, we present attention2majority, a weak multiple instance learning model to automatically and efficiently process WSIs for classification. Our method initially assigns exhaustively sampled label-free patches with the label of the respective WSIs and trains a convolutional neural network to perform patch-wise classification. Then, an intelligent sampling method is performed in which patches with high confidence are collected to form weak representations of WSIs. Lastly, we apply a multi-head attention-based multiple instance learning model to do slide-level classification based on high-confidence patches (intelligently sampled patches). Attention2majority was trained and tested on classifying the quality of 127 WSIs (of regenerated kidney sections) into three categories. On average, attention2majority resulted in 97.4%±2.4 AUC for the four-fold cross-validation. We demonstrate that the intelligent sampling module within attention2majority is superior to the current state-of-the-art random sampling method. Furthermore, we show that the replacement of random sampling with intelligent sampling in attention2majority results in its performance boost (from 94.9%±3.1 to 97.4%±2.4 average AUC for the four-fold cross-validation). We also tested a variation of attention2majority on the famous Camelyon16 dataset, which resulted in 89.1%±0.8 AUC1. When compared to random sampling, the attention2majority demonstrated excellent slide-level interpretability. It also provided an efficient framework to arrive at a multi-class slide-level prediction.
CSF2-dependent monocyte education in the pathogenesis of ANCA-induced glomerulonephritis
Authors: Anthony Rousselle, Janis Sonnemann, Kerstin Amann, Alexander Mildner, Dörte Lodka, Lovis Kling, Markus Bieringer, Udo Schneider, Achim Leutz, Philipp Enghard, Ralph Kettritz, Adrian Schreiber
Journal: Annals of the Rheumatic Diseases (2022)

Objectives Myeloid cell activation by antineutrophil cytoplasmic antibody (ANCA) is pivotal for necrotising vasculitis, including necrotising crescentic glomerulonephritis (NCGN). In contrast to neutrophils, the contribution of classical monocyte (CM) and non-classical monocyte (NCM) remains poorly defined. We tested the hypothesis that CMs contribute to antineutrophil cytoplasmic antibody-associated vasculitis (AAV) and that colony-stimulating factor-2 (CSF2, granulocyte-macrophage colony-stimulating factor (GM-CSF)) is an important monocyte-directed disease modifier. Methods Myeloperoxidase (MPO)-immunised MPO −/− mice were transplanted with haematopoietic cells from wild-type (WT) mice, C–C chemokine receptor 2 (CCR2) −/− mice to abrogate CM, or transcription factor CCAAT–enhancer-binding protein beta (C/EBPβ) −/− mice to reduce NCM, respectively. Monocytes were stimulated with CSF2, and CSF2 receptor subunit beta (CSF2rb)-deficient mice were used. Urinary monocytes and CSF2 were quantified and kidney Csf2 expression was analysed. CSF2-blocking antibody was used in the nephrotoxic nephritis (NTN) model. Results Compared with WT mice, CCR2 −/− chimeric mice showed reduced circulating CM and were protected from NCGN. C/EBPβ −/− chimeric mice lacked NCM but developed NCGN similar to WT chimeric mice. Kidney and urinary CSF2 were upregulated in AAV mice. CSF2 increased the ability of ANCA-stimulated monocytes to generate interleukin-1β and to promote T H 17 effector cell polarisation. CSF2rb −/− chimeric mice harboured reduced numbers of kidney T H 17 cells and were protected from NCGN. CSF2 neutralisation reduced renal damage in the NTN model. Finally, patients with active AAV displayed increased urinary CM numbers, CSF2 levels and expression of GM-CSF in infiltrating renal cells. Conclusions CMs but not NCMs are important for inducing kidney damage in AAV. CSF2 is a crucial pathological factor by modulating monocyte proinflammatory functions and thereby T H 17 cell polarisation.
Expansion of Cancer Risk Profile for <i>BRCA1</i> and <i>BRCA2</i> Pathogenic Variants
Authors: Yukihide Momozawa, Rumi Sasai, Yoshiaki Usui, Kouya Shiraishi, Yusuke Iwasaki, Yukari Taniyama, Michael T. Parsons, Keijiro Mizukami, Yuya Sekine, Makoto Hirata, Yoichiro Kamatani, Mikiko Endo, Chihiro Inai, Sadaaki Takata, Hidemi Ito, Takashi Kohno, Koichi Matsuda, Seigo Nakamura, Kokichi Sugano, Teruhiko Yoshida, Hidewaki Nakagawa, Keitaro Matsuo, Yoshinori Murakami, Amanda B. Spurdle, Michiaki Kubo
Journal: JAMA Oncology (2022)

The clinical importance of genetic testing of BRCA1 and BRCA2 in breast, ovarian, prostate, and pancreatic cancers is widely recognized. However, there is insufficient evidence to include other cancer types that are potentially associated with BRCA1 and BRCA2 in clinical management guidelines.To evaluate the association of BRCA1 and BRCA2 pathogenic variants with additional cancer types and their clinical characteristics in 100 914 individuals across 14 cancer types.This case-control analysis to identify cancer types and clinical characteristics associated with pathogenic variants in BRCA1 and BRCA2 included DNA samples and clinical information from 63 828 patients with 14 common cancer types and 37 086 controls that were sourced from a multi-institutional hospital-based registry, BioBank Japan, between April 2003 and March 2018. The data were analyzed between August 2019 and October 2021.Germline pathogenic variants in coding regions and 2 bp flanking intronic sequences in BRCA1 and BRCA2 were identified by a multiplex polymerase chain reaction-based target sequence method. Associations of (likely) pathogenic variants with each cancer type were assessed by comparing pathogenic variant carrier frequency between patients in each cancer type and controls.A total of 65 108 patients (mean [SD] age at diagnosis, 64.1 [11.6] years; 27 531 [42.3%] female) and 38 153 controls (mean [SD] age at registration, 61.8 [14.6] years; 17 911 [46.9%] female) were included in this study. A total of 315 unique pathogenic variants were identified. Pathogenic variants were associated with P < 1 × 10-4 with an odds ratio (OR) of greater than 4.0 in biliary tract cancer (OR, 17.4; 95% CI, 5.8-51.9) in BRCA1, esophageal cancer (OR, 5.6; 95% CI, 2.9-11.0) in BRCA2, and gastric cancer (OR, 5.2; 95% CI, 2.6-10.5) in BRCA1, and (OR, 4.7; 95% CI, 3.1-7.1) in BRCA2 in addition to the 4 established cancer types. We also observed an association with 2 and 4 other cancer types in BRCA1 and BRCA2, respectively. Biliary tract, female breast, ovarian, and prostate cancers showed enrichment of carrier patients according to the increased number of reported cancer types in relatives.The results of this large-scale registry-based case-control study suggest that pathogenic variants in BRCA1 and BRCA2 were associated with the risk of 7 cancer types. These results indicate broader clinical relevance of BRCA1 and BRCA2 genetic testing.
Open for connections: HiCAR reveals the interactions of accessible DNA
Authors: Benoit Moindrot, Daan Noordermeer
Journal: Cell Genomics (2022)

Hi-C is a powerful technology for exploring 3D genome organization on a genome-wide scale, yet it can be financially and computationally challenging. In a recent issue of Molecular Cell, Wei et al.1 introduce HiCAR, which simplifies Hi-C by targeting the 3D interactions of accessible regions only.
Tripartite motif‐containing protein 31 confers protection against nonalcoholic steatohepatitis by deactivating mitogen‐activated protein kinase kinase kinase 7
Authors: Min‐Xuan Xu, Jun Tan, Chen‐Xu Ge, Wei Dong, Li‐Ting Zhang, Lian‐Cai Zhu, Jun‐Jie Zhao, Long‐Yan Wang, Jin Liu, Hao Wei, Yan Sun, Xian‐Ling Dai, Qin Kuang, Yan‐Liang Li, Han Li, Jun‐Yan Liu, Lei Zou, Ran‐Ran Liang, Chu‐Feng Zhang, Juan Xu, Bo‐Chu Wang
Journal: Hepatology (2022)

Background &amp; Aims: As a global health threat, NASH has been confirmed to be a chronic progressive liver disease that is strongly associated with obesity. However, no approved drugs or efficient therapeutic strategies are valid, mainly because its complicated pathological processes is underestimated. Approach &amp; Results: We identified the RING‐type E3 ubiquitin transferase‐tripartite motif‐containing protein 31 (TRIM31), a member of the E3 ubiquitin ligases family, as an efficient endogenous inhibitor of transforming growth factor‐beta‐activated kinase 1 (mitogen‐activated protein kinase kinase kinase 7; MAP3K7), and we further confirmed that TRIM31 is an MAP3K7‐interacting protein and promotes MAP3K7 degradation by enhancing ubiquitination of K48 linkage in hepatocytes. Hepatocyte‐specific Trim31 deletion blocks hepatic metabolism homeostasis, concomitant with glucose metabolic syndrome, lipid accumulation, up‐regulated inflammation, and dramatically facilitates NASH progression. Inversely, transgenic overexpression, lentivirus, or adeno‐associated virus‐mediated Trim31 gene therapy restrain NASH in three dietary mice models. Mechanistically, in response to metabolic insults, TRIM31 interacts with MAP3K7 and conjugates K48‐linked ubiquitination chains to promote MAP3K7 degradation, thus blocking MAP3K7 abundance and its downstream signaling cascade activation in hepatocytes. Conclusions: TRIM31 may serve as a promising therapeutic target for NASH treatment and associated metabolic disorders.
Radiotherapy combined with nivolumab or temozolomide for newly diagnosed glioblastoma with unmethylated <i>MGMT</i> promoter: An international randomized phase III trial
Authors: Antonio Omuro, Alba A Brandes, Antoine F Carpentier, Ahmed Idbaih, David A Reardon, Timothy Cloughesy, Ashley Sumrall, Joachim Baehring, Martin van den Bent, Oliver Bähr, Giuseppe Lombardi, Paul Mulholland, Ghazaleh Tabatabai, Ulrik Lassen, Juan Manuel Sepulveda, Mustafa Khasraw, Elodie Vauleon, Yoshihiro Muragaki, Anna Maria Di Giacomo, Nicholas Butowski, Patrick Roth, Xiaozhong Qian, Alex Z Fu, Yanfang Liu, Von Potter, Alexandros-Georgios Chalamandaris, Kay Tatsuoka, Michael Lim, Michael Weller
Journal: Neuro-Oncology (2022)

Addition of temozolomide (TMZ) to radiotherapy (RT) improves overall survival (OS) in patients with glioblastoma (GBM), but previous studies suggest that patients with tumors harboring an unmethylated MGMT promoter derive minimal benefit. The aim of this open-label, phase III CheckMate 498 study was to evaluate the efficacy of nivolumab (NIVO) + RT compared with TMZ + RT in newly diagnosed GBM with unmethylated MGMT promoter.Patients were randomized 1:1 to standard RT (60 Gy) + NIVO (240 mg every 2 weeks for eight cycles, then 480 mg every 4 weeks) or RT + TMZ (75 mg/m2 daily during RT and 150-200 mg/m2/day 5/28 days during maintenance). The primary endpoint was OS.A total of 560 patients were randomized, 280 to each arm. Median OS (mOS) was 13.4 months (95% CI, 12.6 to 14.3) with NIVO + RT and 14.9 months (95% CI, 13.3 to 16.1) with TMZ + RT (hazard ratio [HR], 1.31; 95% CI, 1.09 to 1.58; P = .0037). Median progression-free survival was 6.0 months (95% CI, 5.7 to 6.2) with NIVO + RT and 6.2 months (95% CI, 5.9 to 6.7) with TMZ + RT (HR, 1.38; 95% CI, 1.15 to 1.65). Response rates were 7.8% (9/116) with NIVO + RT and 7.2% (8/111) with TMZ + RT; grade 3/4 treatment-related adverse event (TRAE) rates were 21.9% and 25.1%, and any-grade serious TRAE rates were 17.3% and 7.6%, respectively.The study did not meet the primary endpoint of improved OS; TMZ + RT demonstrated a longer mOS than NIVO + RT. No new safety signals were detected with NIVO in this study. The difference between the study treatment arms is consistent with the use of TMZ + RT as the standard of care for GBM.ClinicalTrials.gov NCT02617589.
COVID-19 Mortality and Vaccine Coverage — Hong Kong Special Administrative Region, China, January 6, 2022–March 21, 2022
Authors: Dallas J. Smith, Avi J. Hakim, Gabriel M. Leung, Wenbo Xu, W. William Schluter, Ryan T. Novak, Barbara Marston, Bradley S. Hersh
Journal: MMWR Morbidity and Mortality Weekly Report (2022)

On January 6, 2022, a cluster of COVID-19 cases* caused by the Omicron variant of SARS-CoV-2, the virus that causes COVID-19, was detected in Hong Kong Special Administrative Region, China (Hong Kong), resulting in the territory's fifth wave of COVID-19 cases (1). This wave peaked on March 4, 2022, with 8,764 COVID-19 cases per million population (2), resulting in a total of 1,049,959 cases and 5,906 COVID-19-associated deaths reported to the Hong Kong Department of Health during January 6-March 21, 2022.
Development of a TNF-α-mediated Trojan Horse for bacteria-based cancer therapy
Authors: Che-Wei Hu, You-Chiun Chang, Cheng-Hao Liu, Yao-An Yu, Kurt Yun Mou
Journal: Molecular Therapy (2022)

Tumor necrosis factor α (TNF-α) is upregulated in a chronic inflammatory environment, including tumors, and has been recognized as a pro-tumor factor in many cancers. Applying the traditional TNF-α antibodies that neutralize TNF-α activity, however, only exerts modest anti-tumor efficacy in clinical studies. Here, we develop an innovative approach to target TNF-α that is distinct from the neutralization mechanism. We employed phage display and yeast display to select non-neutralizing antibodies that can piggyback on TNF-α and co-internalize into cells through receptor ligation. When conjugating with toxins, the antibody exhibited cytotoxicity to cancer cells in a TNF-α-dependent manner. We further implemented the immunotoxin to an E. coli vehicle specially engineered for a high secretion level. In a syngeneic murine melanoma model, the bacteria stimulated TNF-α expression that synergized with the secreted immunotoxin and greatly inhibited tumor growth. The treatment also dramatically remodeled the tumor microenvironment in favor of several anti-tumor immune cells, including N1 neutrophils, M1 macrophages, and activated CD4+ and CD8+ lymphocytes. We anticipate that our new piggyback strategy is generalizable to targeting other soluble ligands and/or conjugates with different drugs for managing a diverse set of diseases. Tumor necrosis factor α (TNF-α) is upregulated in a chronic inflammatory environment, including tumors, and has been recognized as a pro-tumor factor in many cancers. Applying the traditional TNF-α antibodies that neutralize TNF-α activity, however, only exerts modest anti-tumor efficacy in clinical studies. Here, we develop an innovative approach to target TNF-α that is distinct from the neutralization mechanism. We employed phage display and yeast display to select non-neutralizing antibodies that can piggyback on TNF-α and co-internalize into cells through receptor ligation. When conjugating with toxins, the antibody exhibited cytotoxicity to cancer cells in a TNF-α-dependent manner. We further implemented the immunotoxin to an E. coli vehicle specially engineered for a high secretion level. In a syngeneic murine melanoma model, the bacteria stimulated TNF-α expression that synergized with the secreted immunotoxin and greatly inhibited tumor growth. The treatment also dramatically remodeled the tumor microenvironment in favor of several anti-tumor immune cells, including N1 neutrophils, M1 macrophages, and activated CD4+ and CD8+ lymphocytes. We anticipate that our new piggyback strategy is generalizable to targeting other soluble ligands and/or conjugates with different drugs for managing a diverse set of diseases.
An allosteric inhibitor against the therapy-resistant mutant forms of EGFR in non-small cell lung cancer
Authors: Ciric To, Tyler S. Beyett, Jaebong Jang, William W. Feng, Magda Bahcall, Heidi M. Haikala, Bo H. Shin, David E. Heppner, Jaimin K. Rana, Brittaney A. Leeper, Kara M. Soroko, Michael J. Poitras, Prafulla C. Gokhale, Yoshihisa Kobayashi, Kamal Wahid, Kari J. Kurppa, Thomas W. Gero, Michael D. Cameron, Atsuko Ogino, Mierzhati Mushajiang, Chunxiao Xu, Yanxi Zhang, David A. Scott, Michael J. Eck, Nathanael S. Gray, Pasi A. Jänne
Journal: Nature Cancer (2022)
Mediterranean Diet or Mindfulness-Based Stress Reduction and Prevention of Small-for-Gestational-Age Birth Weights in Newborns
Authors: Shu-Tsen Liu, Chieh-Chung Lin, James Cheng-Chung Wei
Journal: JAMA (2022)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
<scp>Pseudo‐Pelger‐Huët</scp> neutrophil morphology due to sodium valproate toxicity
Authors: Alison Laing, Kirsteen Harper, Mike Leach, Barbara J. Bain
Journal: American Journal of Hematology (2022)

A 57-year-old woman was referred for investigation of chronic thrombocytopenia prior to elective hip replacement. Her blood count showed haemoglobin concentration 129 g/L, MCV 96 fL, WBC 6.5 × 109/L, neutrophils 3.9 × 109/L, lymphocytes 1.8 × 109/L, monocytes 0.7 × 109/L, and platelets 58 × 109/L. She had a history of epilepsy treated with sodium valproate 1 g twice daily. Her blood film confirmed a true thrombocytopenia and was notable for abnormal neutrophil segmentation with frequent bilobed forms and condensed nuclear chromatin, resembling the Pelger-Huët anomaly, with normal cytoplasmic granulation (images, ×100 objective). A diagnosis of a myelodysplastic syndrome was considered but it was noted that sodium valproate therapy, particularly in large doses, can cause thrombocytopenia and pseudo-Pelger-Huët neutrophil features. The sodium valproate dose was titrated down and stopped after 4 weeks being replaced by levetiracetam. The platelet count improved to 156 × 109/L and 230 × 109/L at 4 and 9 weeks, respectively, and the neutrophil morphology returned to normal. Pseudo-Pelger neutrophil morphology can result from exposure to a number of medications including mycophenolate mofetil, tacrolimus, taxols, ganciclovir, and valproate. It is important to consider this possibility, particularly in patients with associated cytopenias. The authors declare no conflicts of interest.
The Potential Clinical Benefit of Lowering Lipoprotein(a)
Authors: Brian A. Ference
Journal: JAMA (2022)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Sequentially releasing self-healing hydrogel fabricated with TGFβ3-microspheres and bFGF to facilitate rat alveolar bone defect repair
Authors: Fenglin Yu, Dezhi Geng, Zhanpeng Kuang, Shiyi Huang, Yating Cheng, Yini Chen, Fang Leng, Yu Bei, Yueping Zhao, Qingxia Tang, Yadong Huang, Qi Xiang
Journal: Asian Journal of Pharmaceutical Sciences (2022)

Resorption and loss of alveolar bone leads to oral dysfunction and loss of natural or implant teeth. Biomimetic delivery of growth factors based on stem cell recruitment and osteogenic differentiation, as the key steps in natural alveolar bone regenerative process, has been an area of intense research in recent years. A mesoporous self-healing hydrogel (DFH) with basic fibroblast growth factor (bFGF) entrapment and transforming growth factor β3 (TGFβ3) - loaded chitosan microspheres (CMs) was developed. The formulation was optimized by multiple tests of self-healing, in-bottle inversion, SEM, rheological, swelling rate and
A common framework of monocyte-derived macrophage activation
Authors: David E. Sanin, Yan Ge, Emilija Marinkovic, Agnieszka M. Kabat, Angela Castoldi, George Caputa, Katarzyna M. Grzes, Jonathan D. Curtis, Elizabeth A. Thompson, Sebastian Willenborg, Stefanie Dichtl, Susanne Reinhardt, Andreas Dahl, Erika L. Pearce, Sabine A. Eming, Alexander Gerbaulet, Axel Roers, Peter J. Murray, Edward J. Pearce
Journal: Science Immunology (2022)

Macrophages populate every organ during homeostasis and disease, displaying features of tissue imprinting and heterogeneous activation. The disconnected picture of macrophage biology that has emerged from these observations is a barrier for integration across models or with in vitro macrophage activation paradigms. We set out to contextualize macrophage heterogeneity across mouse tissues and inflammatory conditions, specifically aiming to define a common framework of macrophage activation. We built a predictive model with which we mapped the activation of macrophages across 12 tissues and 25 biological conditions, finding a notable commonality and finite number of transcriptional profiles, in particular among infiltrating macrophages, which we modeled as defined stages along four conserved activation paths. These activation paths include a "phagocytic" regulatory path, an "inflammatory" cytokine-producing path, an "oxidative stress" antimicrobial path, or a "remodeling" extracellular matrix deposition path. We verified this model with adoptive cell transfer experiments and identified transient RELMɑ expression as a feature of monocyte-derived macrophage tissue engraftment. We propose that this integrative approach of macrophage classification allows the establishment of a common predictive framework of monocyte-derived macrophage activation in inflammation and homeostasis.