tbuckley/cabot-search huggingface dataset:
Life as a physician in general internal medicine
Authors: Jacqui Wise
Journal: BMJ (2020)

Life as a physician in general internal medicine Jacqui WiseLondon, UK General internal medicine is mainly a hospital inpatient specialty, with some outpatient work in rapid access clinics and for patient follow-up.Work is usually based in an acute medical unit, medical admissions unit, or on the wards.Doctors specialising in general internal medicine are part of the acute medical care workforce which includes those who practise acute medicine, cardiology, diabetology, gastroenterology, geriatrics, renal medicine, respiratory medicine, and rheumatology.Most doctors who practise general internal medicine are also trained in another specialty or subspecialty.Some may also combine general internal medicine with academic research or a non-clinical role.
Anti-Androgen Therapy for the Patients with Recurrent and/or Metastatic Salivary Duct Carcinoma Expressing Androgen Receptors: A Retrospective Study
Authors: Y. Yajima, S. Fujii, T. Kobayashi, H. Ishiki, R. Hayashi, M. Tahara
Journal: Annals of Oncology (2012)
Mental Health of Refugee Children and Youth: Epidemiology, Interventions, and Future Directions
Authors: Rochelle L. Frounfelker, Diana Miconi, Jordan Farrar, Mohamad Adam Brooks, Cécile Rousseau, Theresa S. Betancourt
Journal: Annual Review of Public Health (2020)

The number of refugee youth worldwide receives international attention and is a top priority in both academic and political agendas. This article adopts a critical eye in summarizing current epidemiological knowledge of refugee youth mental health as well as interventions aimed to prevent or reduce mental health problems among children and adolescents in both high- and low-to-middle-income countries. We highlight current challenges and limitations of extant literature and present potential opportunities and recommendations in refugee child psychiatric epidemiology and mental health services research for moving forward. In light of the mounting xenophobic sentiments we are presently witnessing across societies, we argue that, as a first step, all epidemiological and intervention research should advocate for social justice to guarantee the safety of and respect for the basic human rights of all refugee populations during their journey and resettlement. A constructive dialogue between scholars and policy makers is warranted.
Efficacy and Safety of Temsirolimus in Patients with Metastatic Renal Cell Carcinoma: Results from the Spanish Experience
Authors: L. Ruiz, E. Esteban, L. León, A. Pinto, C. Suarez, I. Duran, N. Lainez, A. Lopez, A. Viqueira, P. Maroto
Journal: Annals of Oncology (2012)
Is Adjuvant Chemotherapy (CT) Beneficial to Stage II Colon Cancer (CC) with Elastic Laminanl Invasion (ELI)?
Authors: M. Yokota, M. Kojima, S. Nomura, A. Koyama, M. Sugito, M. Ito, A. Kobayashi, Y. Nishizawa, A. Ochiai, N. Saito
Journal: Annals of Oncology (2012)
ER + /HER2+ and ER-/Her2+ Breast Cancers are Molecularly Distinct but Immune Gene Signatures are Prognostic and Predictive in Both Groups
Authors: T. Iwamoto, L. Pusztai, J. Matsuoka, M. Callari, C.M. Kelly, Y. Qi, T. Motoki, N. Taira, L. Santarpia, H. Doihara, L. Gianni, G. Bianchini
Journal: Annals of Oncology (2012)
3-O-Acetyl-11-keto- -boswellic acid ameliorated aberrant metabolic landscape and inhibited autophagy in glioblastoma
Authors: Wan Li, Liwen Ren, Xiangjin Zheng, Jinyi Liu, Jinhua Wang, Tengfei Ji, Guanhua Du
Journal: Acta Pharmaceutica Sinica B (2020)

Glioblastoma is the most common and aggressive primary tumor in the central nervous system, accounting for 12%–15% of all brain tumors. 3-O-Acetyl-11-keto-β-boswellic acid (AKBA), one of the most active ingredients of gum resin from Boswellia carteri Birdw., was reported to inhibit the growth of glioblastoma cells and subcutaneous glioblastoma. However, whether AKBA has antitumor effects on orthotopic glioblastoma and the underlying mechanisms are still unclear. An orthotopic mouse model was used to evaluate the anti-glioblastoma effects of AKBA. The effects of AKBA on tumor growth were evaluated using MRI. The effects on the alteration of metabolic landscape were detected by MALDI-MSI. The underlying mechanisms of autophagy reducing by AKBA treatment were determined by immunoblotting and immunofluorescence, respectively. Transmission electron microscope was used to check morphology of cells treated by AKBA. Our results showed that AKBA (100 mg/kg) significantly inhibited the growth of orthotopic U87-MG gliomas. Results from MALDI-MSI showed that AKBA improved the metabolic profile of mice with glioblastoma, while immunoblot assays revealed that AKBA suppressed the expression of ATG5, p62, LC3B, p-ERK/ERK, and P53, and increased the ratio of p-mTOR/mTOR. Taken together, these results suggested that the antitumor effects of AKBA were related to the normalization of aberrant metabolism in the glioblastoma and the inhibition of autophagy. AKBA could be a promising chemotherapy drug for glioblastoma.
P-0253 The Addition of a Third Active Drug Increases R0 Resection Rate in Metastatic Colorectal Cancer: Meta-Analysis of Randomized Trials
Authors: Lucjan Wyrwicz, Agnieszka Byszek, Agnieszka Domurad, Joanna Chodzyn´ska, Maciej Krzakowski
Journal: Annals of Oncology (2012)
De novo mutations identified by exome sequencing implicate rare missense variants in SLC6A1 in schizophrenia
Authors: Elliott Rees, Jun Han, Joanne Morgan, Noa Carrera, Valentina Escott-Price, Andrew J. Pocklington, Madeleine Duffield, Lynsey S. Hall, Sophie E. Legge, Antonio F. Pardiñas, Alexander L. Richards, Julian Roth, Tatyana Lezheiko, Nikolay Kondratyev, Vasilii Kaleda, Vera Golimbet, Mara Parellada, Javier González-Peñas, Celso Arango, Micha Gawlik, George Kirov, James T. R. Walters, Peter Holmans, Michael C. O’Donovan, Michael J. Owen
Journal: Nature Neuroscience (2020)
ONO-7475, a Novel AXL Inhibitor, Suppresses the Adaptive Resistance to Initial EGFR-TKI Treatment in<i>EGFR</i>-Mutated Non–Small Cell Lung Cancer
Authors: Naoko Okura, Naoya Nishioka, Tadaaki Yamada, Hirokazu Taniguchi, Keiko Tanimura, Yuki Katayama, Akihiro Yoshimura, Satoshi Watanabe, Toshiaki Kikuchi, Shinsuke Shiotsu, Takeshi Kitazaki, Akihiro Nishiyama, Masahiro Iwasaku, Yoshiko Kaneko, Junji Uchino, Hisanori Uehara, Mano Horinaka, Toshiyuki Sakai, Kohei Tanaka, Ryohei Kozaki, Seiji Yano, Koichi Takayama
Journal: Clinical Cancer Research (2020)

Abstract Purpose: Currently, an optimal therapeutic strategy comprising molecularly targeted agents for treating EGFR-mutated non–small cell lung cancer (NSCLC) patients with acquired resistance to osimertinib is not available. Therefore, the initial therapeutic intervention is crucial for the prolonged survival of these patients. The activation of anexelekto (AXL) signaling is known to be associated with intrinsic and acquired resistance to EGFR tyrosine kinase inhibitors (EGFR-TKIs). In this study, we investigated the best therapeutic strategy to combat AXL-induced tolerance to EGFR-TKIs using the novel AXL inhibitor ONO-7475. Experimental Design: We examined the efficacy of ONO-7475 in combination with EGFR-TKIs in EGFR-mutated NSCLC cells using in vitro and in vivo experiments. We investigated the correlation between AXL expression in tumors and clinical outcomes with osimertinib for EGFR-mutated NSCLC patients with acquired resistance to initial EGFR-TKIs. Results: ONO-7475 sensitized AXL-overexpressing EGFR-mutant NSCLC cells to the EGFR-TKIs osimertinib and dacomitinib. In addition, ONO-7475 suppressed the emergence and maintenance of EGFR-TKI–tolerant cells. In the cell line–derived xenograft models of AXL-overexpressing EGFR-mutated lung cancer treated with osimertinib, initial combination therapy of ONO-7475 and osimertinib markedly regressed tumors and delayed tumor regrowth compared with osimertinib alone or the combination after acquired resistance to osimertinib. AXL expression in EGFR-TKI refractory tumors did not correlate with the sensitivity of osimertinib. Conclusions: These results demonstrate that ONO-7475 suppresses the emergence and maintenance of tolerant cells to the initial EGFR-TKIs, osimertinib or dacomitinib, in AXL-overexpressing EGFR-mutated NSCLC cells, suggesting that ONO-7475 and osimertinib is a highly potent combination for initial treatment.
A Phase 2 Trial of the Multitargeted Kinase Inhibitor Lenvatinib (E7080) in Patients (PTS) with Recurrent Glioblastoma (GBM) And Disease Progression Following Prior Bevacizumab Treatment
Authors: D.A. Reardon, E. Pan, J. Fan, J. Mink, D.P. Barboriak, J.J. Vredenburgh, A. Desjardins, K. Peters, J.P. O'Brien, P.Y. Wen
Journal: Annals of Oncology (2012)
Polycystins 1 and 2 as Novel Prognostic Markers in Colorectal Cancer
Authors: A.N. Gargalionis, G. Dalagiorgou, P. Korkolopoulou, C. Piperi, G. Levidou, C. Adamopoulos, A. Zizi-Sermpetzoglou, N. Tsavaris, E.K. Basdra, A.G. Papavassiliou
Journal: Annals of Oncology (2012)
A small-molecule c-Myc inhibitor triggers mitochondria-mediated apoptosis and induces monocytic differentiation of human acute myeloid leukemia
Authors: Ming-Jer Huang, Yuenchi Cheng, Shufan Lin, Zhilone Chen, Techeng Su, Gi-Ming Lai, Hsingjin E. Liu
Journal: Cancer Research (2005)

5901  The proto-oncogene c-Myc plays an important role in the control of cell proliferation, apoptosis and differentiation, and its aberrant expression is a common molecular defect in human cancers, including acute myeloid leukemia (AML). The heterodimeric formation of Myc with Max transactivates the multiple downstream genes responsible for leukemogenesis. Recently several small-molecule inhibitors that block the interaction between Myc and Max have shown promise in the treatment of solid tumors. Here we studied whether inhibition of Myc/Max interactions might be useful for AML. We first used MTT assays to screen the sensitivity to a small molecule c-Myc inhibitor (MYCi), 10058-F4, in various leukemic cell lines: KG1a, HL-60, K562, and NB4, and found that HL-60 cells were particularly sensitive to c-Myc inhibition. MYCi arrested HL-60 cells at G0/G1 phase (from 50.9% to 85.0% of cells in G0/G1phase, 48.4% to 11.6% in S phase), and induced apoptosis over prolonged exposure. The MYCi-induced apoptosis was mediated via mitochondrial pathway, by activating caspase 9, caspase 3 and caspase 7 but caspase 6, and caspase 8 were not affected. The expression of CD95 was also not affected by MYCi. MYCi downregulated anti-apoptotic Bcl-2 expression and upregulated pro-apoptotic bax, p21 and p27 expression. But the expression of cyclin D1, cyclin D3, cyclin E and cyclin B was not affected by MYCi. We further examined the effects of MYCi on the differentiation of AML cells. MYCi induced monocytic but not neutrophilic differentiation by upregulating CD11c, and CD14 but not CD11b. We also used real-time PCR to show that MYCi upregulated the expression of c-Jun, Jun-B, C/EBPalpha, EGR-1 and PU.1 but not ICSBP. Therefore, our data suggest that small-molecule c-Myc inhibitors could be useful in myelomonocytic leukemia by inducing cell cycle arrest, apoptosis and monocytic differentiation of through specific pathways. This inhibitor might also provide an alternative approach to identify c-Myc downstream target genes, and to elucidate the role of c-Myc on monocytic differentiation.
Patient Dignity Inventory (PDI) Questionnaire: The Validation Study in Italian Patients with Solid and Haematological Cancers on Active Oncological Treatments
Authors: C.I. Ripamonti, L. Buonaccorso, A. Maruelli, E. Bandieri, M.A. Pessi, S. Boldini, C. Primi, G. Miccinesi
Journal: Annals of Oncology (2012)
Neuronal Epac1 mediates retinal neurodegeneration in mouse models of ocular hypertension
Authors: Wei Liu, Yonju Ha, Fan Xia, Shuang Zhu, Yi Li, Shuizhen Shi, Fang C. Mei, Kevin Merkley, Gianmarco Vizzeri, Massoud Motamedi, Xiaodong Cheng, Hua Liu, Wenbo Zhang
Journal: The Journal of Experimental Medicine (2020)

Progressive loss of retinal ganglion cells (RGCs) leads to irreversible visual deficits in glaucoma. Here, we found that the level of cyclic AMP and the activity and expression of its mediator Epac1 were increased in retinas of two mouse models of ocular hypertension. Genetic depletion of Epac1 significantly attenuated ocular hypertension–induced detrimental effects in the retina, including vascular inflammation, neuronal apoptosis and necroptosis, thinning of ganglion cell complex layer, RGC loss, and retinal neuronal dysfunction. With bone marrow transplantation and various Epac1 conditional knockout mice, we further demonstrated that Epac1 in retinal neuronal cells (especially RGCs) was responsible for their death. Consistently, pharmacologic inhibition of Epac activity prevented RGC loss. Moreover, in vitro study on primary RGCs showed that Epac1 activation was sufficient to induce RGC death, which was mechanistically mediated by CaMKII activation. Taken together, these findings indicate that neuronal Epac1 plays a critical role in retinal neurodegeneration and suggest that Epac1 could be considered a target for neuroprotection in glaucoma.
PERSEVERE Biomarkers Predict Severe Acute Kidney Injury and Renal Recovery in Pediatric Septic Shock
Authors: Natalja L. Stanski, Erin K. Stenson, Natalie Z. Cvijanovich, Scott L. Weiss, Julie C. Fitzgerald, Michael T. Bigham, Parag N. Jain, Adam Schwarz, Riad Lutfi, Jeffrey Nowak, Geoffrey L. Allen, Neal J. Thomas, Jocelyn R. Grunwell, Torrey Baines, Michael Quasney, Bereketeab Haileselassie, Hector R. Wong
Journal: American Journal of Respiratory and Critical Care Medicine (2020)

Rationale: Acute kidney injury (AKI), a common complication of sepsis, is associated with substantial morbidity and mortality and lacks definitive disease-modifying therapy. Early, reliable identification of at-risk patients is important for targeted implementation of renal protective measures. The updated Pediatric Sepsis Biomarker Risk Model (PERSEVERE-II) is a validated, multibiomarker prognostic enrichment strategy to estimate baseline mortality risk in pediatric septic shock.Objectives: To assess the association between PERSEVERE-II mortality probability and the development of severe, sepsis-associated AKI on Day 3 (D3 SA-AKI) in pediatric septic shock.Methods: We performed secondary analysis of a prospective observational study of children with septic shock in whom the PERSEVERE biomarkers were measured to assign a PERSEVERE-II baseline mortality risk.Measurements and Main Results: Among 379 patients, 65 (17%) developed severe D3 SA-AKI. The proportion of patients developing severe D3 SA-AKI increased directly with increasing PERSEVERE-II risk category, and increasing PERSEVERE-II mortality probability was independently associated with increased odds of severe D3 SA-AKI after adjustment for age and illness severity (odds ratio, 1.4; 95% confidence interval, 1.2–1.7; P < 0.001). Similar associations were found between increasing PERSEVERE-II mortality probability and the need for renal replacement therapy. Lower PERSEVERE-II mortality probability was independently associated with increased odds of renal recovery among patients with early AKI. A newly derived model incorporating the PERSEVERE biomarkers and Day 1 AKI status predicted severe D3 SA-AKI with an area under the received operating characteristic curve of 0.95 (95% confidence interval, 0.92–0.98).Conclusions: Among children with septic shock, the PERSEVERE biomarkers predict severe D3 SA-AKI and identify patients with early AKI who are likely to recover.
The Outcome Comparison of Neoadjuvnat and Adjuvant Gemcitabine–Cisplatin Chemotherapy for Muscle-Invasive Bladder Cancer
Authors: N. Matsubara, H. Mukai, Y. Naito, T. Yamaguchi, M. Sasaki, M. Nezu, K. Itoh
Journal: Annals of Oncology (2012)
Fulvestrant 500 Mg as First-Line Treatment in Hormone-Positive (HR+) Metastatic Breast Cancer (MBC) Patients (PTS): Prospective Evaluation of Activity, Safety, Quality of Life (QOL) and Tumour Markers Changes
Authors: R. Palumbo, G. Bernardo, A. Riccardi, F. Sottotetti, B. Tagliaferri, E. Pozzi, C.M. Teragni, A. Bernardo
Journal: Annals of Oncology (2012)
Pemetrexed and Whole-Brain Radiation Therapy for Treatment of Brain Metastases from Non Small-Cell Lung Adenocarcinoma: A Single Instituton Analysis
Authors: C. Chargari, Y. Moussaid, C. Helissey, J. Jacob, O. Bauduceau, B. Ceccaldi, L. Védrine, S. Le Moulec
Journal: Annals of Oncology (2012)
Inhibiting the coregulator CoREST impairs Foxp3+ Treg function and promotes antitumor immunity
Authors: Yan Xiong, Liqing Wang, Eros Di Giorgio, Tatiana Akimova, Ulf H. Beier, Rongxiang Han, Matteo Trevisanut, Jay H. Kalin, Philip A. Cole, Wayne W. Hancock
Journal: Journal of Clinical Investigation (2020)

Foxp3+ Tregs are key to immune homeostasis, but the contributions of various large, multiprotein complexes that regulate gene expression remain unexplored. We analyzed the role in Tregs of the evolutionarily conserved CoREST complex, consisting of a scaffolding protein, Rcor1 or Rcor2, plus Hdac1 or Hdac2 and Lsd1 enzymes. Rcor1, Rcor2, and Lsd1 were physically associated with Foxp3, and mice with conditional deletion of Rcor1 in Foxp3+ Tregs had decreased proportions of Tregs in peripheral lymphoid tissues and increased Treg expression of IL-2 and IFN-γ compared with what was found in WT cells. Mice with conditional deletion of the gene encoding Rcor1 in their Tregs had reduced suppression of homeostatic proliferation, inability to maintain long-term allograft survival despite costimulation blockade, and enhanced antitumor immunity in syngeneic models. Comparable findings were seen in WT mice treated with CoREST complex bivalent inhibitors, which also altered the phenotype of human Tregs and impaired their suppressive function. Our data point to the potential for therapeutic modulation of Treg functions by pharmacologic targeting of enzymatic components of the CoREST complex and contribute to an understanding of the biochemical and molecular mechanisms by which Foxp3 represses large gene sets and maintains the unique properties of this key immune cell.
A Phase II Study of Pemetrexed in Chemotherapy-Naive Elderly Patients with Advanced Non-Squamous Non-Small-Cell Lung Cancer: Hanshin Oncology Group 003
Authors: Y. Namba, Y. Hattori, M. Edagawa, H. Yoshioka, M. Iwasaku, T. Shimada, M. Satouchi, N. Katagami, S. Fujita, M. Mori, F. Imamura, Y. Kotani, T. Nishimura, S. Morita, S. Negoro
Journal: Annals of Oncology (2012)
Gasdermin E–mediated target cell pyroptosis by CAR T cells triggers cytokine release syndrome
Authors: Yuying Liu, Yiliang Fang, Xinfeng Chen, Zhenfeng Wang, Xiaoyu Liang, Tianzhen Zhang, Mengyu Liu, Nannan Zhou, Jiadi Lv, Ke Tang, Jing Xie, Yunfeng Gao, Feiran Cheng, Yabo Zhou, Zhen Zhang, Yu Hu, Xiaohui Zhang, Quanli Gao, Yi Zhang, Bo Huang
Journal: Science Immunology (2020)

Cytokine release syndrome (CRS) counteracts the effectiveness of chimeric antigen receptor (CAR) T cell therapy in cancer patients, but the mechanism underlying CRS remains unclear. Here, we show that tumor cell pyroptosis triggers CRS during CAR T cell therapy. We find that CAR T cells rapidly activate caspase 3 in target cells through release of granzyme B. The latter cleaves gasdermin E (GSDME), a pore-forming protein highly expressed in B leukemic and other target cells, which results in extensive pyroptosis. Consequently, pyroptosis-released factors activate caspase 1 for GSDMD cleavage in macrophages, which results in the release of cytokines and subsequent CRS. Knocking out GSDME, depleting macrophages, or inhibiting caspase 1 eliminates CRS occurrence in mouse models. In patients, GSDME and lactate dehydrogenase levels are correlated with the severity of CRS. Notably, we find that the quantity of perforin/granzyme B used by CAR T cells rather than existing CD8+ T cells is critical for CAR T cells to induce target cell pyroptosis.
P-0267 Correlation Between Serum Vascular Endothelial Growth Factor (Vegf) and Vegf-1 Expression in Patients with Colorectal Cancer. Preliminary Results
Authors: Franco Lumachi, Filippo Marino, Salvatore Tumolo, Davide Santeufemia, Renato Tozzoli, Paolo Doretto, Giordano Chiara, Stefano Basso
Journal: Annals of Oncology (2012)
Lux-Lung 3: Symptom and Health-Related Quality of Life Results from a Randomized Phase III Study in 1st-Line Advanced NSCLC Patients Harbouring EGFR Mutations
Authors: L.V. Sequist, M. Schuler, N. Yamamoto, K.J. O'Byrne, V. Hirsh, T.S.K. Mok, J. Lungershausen, M. Shahidi, M. Palmer, J.C. Yang
Journal: Annals of Oncology (2012)
Neoadjuvant Addition of Bevacizumab to Chemoradiation in Rectal Cancer: Impact on Angiogenic Biomarkers
Authors: B. Laquente, J. Capdevila, M. Martínez-Villacampa, C. López, M.J. Safont, A. Gómez, J.L. Manzano, C. Grávalos, R. Salazar, E. Aranda Aguilar
Journal: Annals of Oncology (2012)
Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations
Authors: G. Curigliano, D. Lenihan, M. Fradley, S. Ganatra, A. Barac, A. Blaes, J. Herrmann, C. Porter, A.R. Lyon, P. Lancellotti, A. Patel, J. DeCara, J. Mitchell, E. Harrison, J. Moslehi, R. Witteles, M.G. Calabro, R. Orecchia, E. de Azambuja, J.L. Zamorano, R. Krone, Z. Iakobishvili, J. Carver, S. Armenian, B. Ky, D. Cardinale, C.M. Cipolla, S. Dent, K. Jordan
Journal: Annals of Oncology (2020)
シスゴルジマトリックスタンパク質GOLGA2/GM130は,抗癌遺伝子治療の新たな標的となる | 文献情報 | J-GLOBAL 科学技術総合リンクセンター
Authors: Chang Seung-Hee, Hong Seong-Ho, Jiang Hu-Lin, Minai-Tehrani Arash, YU Kyeong-Nam, Lee Jae-Ho, Kim Ji-Eun, Shin Ji-Young, Kang Bitna, Park Sungjin, Han Kiwon, Chae Chanhee, Cho Myung-Haing
Journal: Molecular Therapy (2012)
TPF Induction Chemotherapy Followed by Cisplatin-Based Concurrent Chemoradiotherapy in Patients with Stage IV Head and Neck Cancer Demonstrated no Benefit
Authors: N. Nishimura, M. Yokoyama, Y. Ohhara, E. Nara, K. Nakano, K. Ueda, Y. Mishima, S. Sakajiri, Y. Terui, S. Takahashi, K. Hatake
Journal: Annals of Oncology (2012)
Associations Between Radiographic and Ultrasound‐Detected Features in Hand Osteoarthritis and Local Pressure Pain Thresholds
Authors: Pernille Steen Pettersen, Tuhina Neogi, Karin Magnusson, Hilde Berner Hammer, Till Uhlig, Tore K. Kvien, Ida K. Haugen
Journal: Arthritis & Rheumatology (2020)

Pain sensitization contributes to the complex osteoarthritis (OA) pain experience. The relationship between imaging features of hand OA and clinically assessed pain sensitization is largely unexplored. This study was undertaken to examine the association of structural and inflammatory features of hand OA with local pressure pain thresholds (PPTs) in the Nor-Hand study.The cross-sectional relationship of severity of structural radiographic features of hand OA (measured according to the Kellgren/Lawrence scale [grade 0-4] and the absence or presence of erosive joint disease) as well as ultrasound-detected hand joint inflammation (assessed by gray-scale synovitis [grade 0-3] and the absence or presence of power Doppler activity) to the PPTs of 2 finger joints was examined by multilevel regression analyses adjusted for age, sex, and body mass index, using beta values with 95% confidence intervals (95% CIs).A total of 570 joints in 285 participants included in the Nor-Hand study were assessed. Greater structural and inflammatory severity was associated with lower PPTs, with adjusted beta values of -0.5 (95% CI -0.6, -0.4) per Kellgren/Lawrence grade increase, -1.4 (95% CI -1.8, -0.9) for erosive versus non-erosive joints, -0.7 (95% CI -0.9, -0.6) per gray-scale synovitis grade increase, and -1.5 (95% CI -1.8, -1.1) for joints with power Doppler activity on ultrasound versus those without.Greater severity of structural pathologic features and hand joint inflammation was associated with lower PPTs in the finger joints of patients with hand OA, indicating pain sensitization. Our results indicate that pain sensitization might be driven by structural and inflammatory pathology in hand OA.
Summary of the Keystone Symposium “Origins of allergic disease: Microbial, epithelial and immune interactions,” March 24-27, Tahoe City, California
Authors: Rosemarie H. DeKruyff, Wenming Zhang, Kari C. Nadeau, Donald Y.M. Leung, Marsha Wills-Karp
Journal: Journal of Allergy and Clinical Immunology (2020)