tbuckley/cabot-search huggingface dataset:
We are jungles
Authors: Therese Woodring
Journal: Annals of Internal Medicine (2018)

Ad Libitum4 December 2018We are junglesTherese WoodringTherese WoodringUniversity of Illinois College of Medicine, Peoria, Illinois (T.W.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/M18-1354 Audio Reading - “We are jungles” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "We are jungles," by T. Woodring. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail We are jungles—howling, stormy schemesof bacilli like lightning bolts within,of creeping hyphae, and of feral genesthat leap like monkeys through our chromatin.Float back to the first quiet laid uponthe cell that birthed four billion years of life:your native microbes know what's come and gone;your reading mind did only just arrive.Sense now the vastness of the unexplored.What grows inside our guts, across our skin?We are of one, but this sterilized wardbelies the omnipresence of our kin—their wildness that beckons expeditionthrough thickets of our nonhuman condition. Author, Article, and Disclosure InformationAffiliations: University of Illinois College of Medicine, Peoria, Illinois (T.W.)Current Author Address: Therese Woodring; e-mail, [email protected]edu. PreviousarticleNextarticle Advertisement Audio Reading - “We are jungles” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "We are jungles," by T. Woodring. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ FiguresReferencesRelatedDetails Metrics 4 December 2018Volume 169, Issue 11Page: 816KeywordsChromatin ePublished: 4 December 2018 Issue Published: 4 December 2018 Copyright & PermissionsCopyright © 2018 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Elevated Circadian Period 2: A Missing Beneficial Factor in Sickle Cell Disease By Lowering Pulmonary Inflammation, Iron Overload and Mortality
Authors: Morayo Adebiyi, Zhaoyang Zhao, Jeanne Manalo, Cheng Chi Lee, Wa Xian, Ye Youqiong, Frank McKeon, Rachel Culp-Hill, Angelo D'Alessandro, Rodney Kellems, Seung-Hee Yoo, Leng Han, Yang Xia
Journal: Blood (2018)
Circ_Lrp6, a Circular RNA Enriched in Vascular Smooth Muscle Cells, Acts as a Sponge Regulating miRNA-145 Function
Authors: Ignacio Fernando Hall, Montserrat Climent, Manuela Quintavalle, Floriana Maria Farina, Tilo Schorn, Stefania Zani, Pierluigi Carullo, Paolo Kunderfranco, Efrem Civilini, Gianluigi Condorelli, Leonardo Elia
Journal: Circulation Research (2019)

microRNAs (miRNAs) modulate gene expression by repressing translation of targeted genes. Previous work has established a role for miRNAs in regulating vascular smooth muscle cell (VSMC) activity. Whether circular RNAs are involved in the modulation of miRNA activity in VSMCs is unknown.We aimed to identify circular RNAs interacting with miRNAs enriched in VSMCs and modulating the cells' activity.RNA sequencing and bioinformatics identified several circular RNAs enriched in VSMCs; however, only one, possessing multiple putative binding sites for miR-145, was highly conserved between mouse and man. This circular RNA gemmed from alternative splicing of Lrp6 (lipoprotein receptor 6), a gene highly expressed in vessels and implicated in vascular pathologies and was thus named circ_Lrp6. Its role as a miR-145 sponge was confirmed by determining reciprocal interaction through RNA immunoprecipitation, stimulated emission depletion microscopy, and competitive luciferase assays; functional inhibition of miR-145 was assessed by measuring expression of the target genes ITGβ8 (integrin-β8), FASCIN (fascin actin-bundling protein 1), KLF4 (Kruppel-like factor 4), Yes1 (YES proto-oncogene 1), and Lox (lysyl oxidase). The interaction was preferentially localized to P-bodies, sites of mRNA degradation. Using loss- and gain-of-function approaches, we found that circ_Lrp6 hindered miR-145-mediated regulation of VSMC migration, proliferation, and differentiation. Differential expression of miR-145 and circ_Lrp6 in murine and human vascular diseases suggests that the ratio of circ_Lrp6 bound to miR-145 versus unbound could play a role in vascular pathogenesis. Viral delivery of circ_Lrp6 shRNA prevented intimal hyperplasia in mouse carotids.circ_Lrp6 is an intracellular modulator and a natural sponge for miR-145, counterbalancing the functions of the miRNA in VSMCs.
Effects of tumor metabolic microenvironment on regulatory T cells
Authors: Yi-an Wang, Xiao-Ling Li, Yong-Zhen Mo, Chun-Mei Fan, Le Tang, Fang Xiong, Can Guo, Bo Xiang, Ming Zhou, Jian Ma, Xi Huang, Xu Wu, Yong Li, Gui-Yuan Li, Zhao-yang Zeng, Wei Xiong
Journal: Molecular Cancer (2018)

Recent studies have shown that on one hand, tumors need to obtain a sufficient energy supply, and on the other hand they must evade the body's immune surveillance. Because of their metabolic reprogramming characteristics, tumors can modify the physicochemical properties of the microenvironment, which in turn affects the biological characteristics of the cells infiltrating them. Regulatory T cells (Tregs) are a subset of T cells that regulate immune responses in the body. They exist in large quantities in the tumor microenvironment and exert immunosuppressive effects. The main effect of tumor microenvironment on Tregs is to promote their differentiation, proliferation, secretion of immunosuppressive factors, and chemotactic recruitment to play a role in immunosuppression in tumor tissues. This review focuses on cell metabolism reprogramming and the most significant features of the tumor microenvironment relative to the functional effects on Tregs, highlighting our understanding of the mechanisms of tumor immune evasion and providing new directions for tumor immunotherapy.
Acupuncture for Aromatase Inhibitor–Related Joint Pain Among Breast Cancer Patients
Authors: Dawn L. Hershman, Joseph M. Unger, Katherine Crew
Journal: JAMA (2018)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Islet α-cell Inflammation Induced By NF-κB inducing kinase (NIK) Leads to Hypoglycemia, Pancreatitis, Growth Retardation, and Postnatal Death in Mice
Authors: Xinzhi Li, Linna Jia, Xiaoyue Chen, Ying Dong, Xiaomeng Ren, Yuefan Dong, Ying Chen, Liwei Xie, Ming Liu, Chiyo Shiota, George K. Gittes, Liangyou Rui, Zheng Chen
Journal: Theranostics (2018)

Islet α-cell dysfunction has been shown to contribute to type 2 diabetes; however, whether islet α-cell inflammation is involved in the occurrence of pancreatitis is largely unknown.The aims of this study were to investigate how NF-κB inducing kinase (NIK) regulates pancreatic α-cell function, both in vitro and in vivo, and to assess how islet α-cell inflammation induced by NIK affects the development of pancreatitis.Methods: We utilized adenovirus-mediated NIK overexpression, ELISA, qPCR, RNA-seq, and Western blot analyses to study the role of NIK in islet α cells in vitro.Islet α-cell-specific NIK overexpressing (α-NIK-OE) mice were generated, and pancreatic α/β-cell function and the occurrence of pancreatitis in these mice were assessed via ELISA, qPCR, and immunohistochemical analyses. Results:The LTβR/noncanonical NF-κB signaling pathway is present in islet α cells.Overexpression of NIK in αTC1-6 cells induces inflammation and cell death, contributing to a decrease in the expression and secretion of glucagon.Additionally, α-cell specific overexpression of NIK (α-NIK-OE) results in α-cell death, lower serum glucagon levels, and hypoglycemia in mice.Strikingly, α-NIK-OE mice also display a reduced β-cell mass, growth retardation, pancreatitis, and postnatal death.Conclusions: Islet α-cell specific overexpression of NIK results in islet α-cell dysfunction and causes islet β-cell death and pancreatitis, which are most likely due to paracrine secretion of cytokines and chemokines from islet α cells, thus leading to hypoglycemia, growth retardation, and postnatal death in mice.
Combination of BCR-ABL1 Tyrosine Kinase Inhibitors with a Small Molecule LIM kinase1/2 Inhibitor in BCR-ABL1 Positive Acute Lymphoblastic Leukemia (ALL)
Authors: Thorsten Braun, Jeannig Berrou, Renaud Prudent, Hanane Djamai, Melanie Dupont, Anna Kaci, Emilie Adiceam, Fabrice Paublant, Andre Baruchel, Jacques Ghysdael, Claude Gardin, Herve Dombret
Journal: Blood (2018)
Establishing a denominator for palliative care quality metrics for patients with advanced cancer.
Authors: Sidharth Anand, John A. Glaspy, Lily Roh, Vilay Khandelwal, Neil Wenger, Christine Ritchie, Anne Margaret Walling
Journal: Journal of Clinical Oncology (2018)

104 Background: Measurement and feedback of palliative care quality metrics for patients with advanced cancer is an important aspect of supporting a shared mental model for the early integration of palliative care within the oncology clinic. Accurately identifying the subset of advanced cancer patients within a population of cancer patients is critical to the development of quality improvement activities; however, there is not a methodology of identifying these patients in real time. Methods: We evaluated two main approaches to identifying patients with advanced cancer among active cancer patients defined as patients who were seen by an oncologist at least twice in the last 6 months and who had received chemotherapy or radiation at least once in the last two years. These approaches included: 1) Pattern matching of words indicating advanced cancer (e.g. metastatic, advanced) in oncology notes, radiology imaging and problem lists and 2) ICD-10 codes. To determine the final set of ICD-10 codes for the second approach, we used a conceptual model of the meaning of advanced cancer (evidence of distant metastasis and/or poor prognostic cancer with &gt; 50% mortality rate at 5 years) and iterative chart review. In order to test our final definitions, we randomly selected 588 charts of patients with active cancer who see one of 64 oncologists in our health system. These charts were abstracted by an oncologist to establish a gold standard for advanced cancer. We evaluated the sensitivity and specificity of our approaches to identify advanced cancer patients compared to this gold standard. Results: We found that the methods used to identify patients using pattern matching had a specificity of 76% and a sensitivity of 80%. Using our final ICD-10 algorithm we achieved a specificity of 93% and a sensitivity of 68%. We improved our sensitivity to 74% while maintaining our specificity at 92% when we excluded oncologists who predominantly see hematological malignancies. Conclusions: We achieved high specificity and reasonable sensitivity for an advanced cancer quality metric denominator using an ICD-10 algorithm within an academic oncology practice. This will help inform quality improvement efforts locally and beyond.
Sepsis Bundles and Mortality Among Pediatric Patients
Authors: Halden F. Scott, Fran Balamuth, Raina M. Paul
Journal: JAMA (2018)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Systemic Inflammation and Cardio-Renal Organ Damage Biomarkers in Middle Age Are Associated With Physical Capability Up to 9 Years Later
Authors: Diana Kuh, Rachel Cooper, Naveed Sattar, Paul Welsh, Rebecca Hardy, Yoav Ben-Shlomo
Journal: Circulation (2019)

Physical capability, a key component of healthy aging, is associated with cardiovascular and other risk factors across life. We investigated whether midlife biomarkers of heart and kidney damage capturing the cumulative impact of long-term adverse exposures were associated with the level and decline in physical capability over 9 years of follow-up, taking account of systemic inflammatory biomarkers and conventional cardiovascular risk factors.We used data on 1736 men and women from the oldest British birth cohort study with walking speed, chair rise speed, balance time, and grip strength assessed at ages 60 to 64 and 69 years. We tested associations between logged and standardized measures of cystatin C, NT-proBNP (N-terminal pro-B-type natriuretic peptide), interleukin (IL)-6, and E-selectin at age 60 to 64 years with performance at age 69 years, adjusting for sex, height, and body mass index; then for performance at age 60 to 64 years. These biomarkers were mutually adjusted, and additionally adjusted for cardiovascular risk factors (pulse pressure, total/high density lipoprotein cholesterol, glycosylated hemoglobin), diabetes mellitus, cardiovascular and kidney disease, smoking status, and lifetime socioeconomic position.Cystatin C, NT-proBNP, and IL-6 (but not E-selectin) were inversely associated with all outcomes, adjusted for sex, height, and body mass index. For example, a 1-SD increase in logged NT-proBNP was associated with weaker grip (-0.63 kg, 95% CI, -0.99 to -0.28); the equivalent association for cystatin C was -0.60 kg (95% CI, -0.94 to -0.25) and for IL-6 was -0.76 kg (95% CI, -1.11 to -0.41). Most associations remained, albeit attenuated, after adjustment for previous performance and mutual adjustment of the biomarkers. NT-proBNP and IL-6 (but not cystatin C) were more strongly associated with the outcomes than many of the conventional risk factors after mutual adjustment.Higher levels of NT-proBNP may identify those in midlife at risk of accelerated physical decline. Before considering the use of NT-proBNP for risk stratification, further research should untangle whether these associations exist because the biomarker is an integrated measure of cumulative exposures to relevant stressors across life, or whether it is marking additional risk pathways. Randomized trials to reduce the rate of decline in physical capability or delay incident disability could benefit from including middle-aged adults and adding NT-proBNP and IL-6 as intermediate outcomes.
Abstract 24035: Human iPSC-Derived Endothelial Cells Predict Predilection to Atherogenesis by Endothelial Proinflammatory Activation
Authors: David T Paik, Youngkyun Kim, June-Wha Rhee, Hyoju Yi, Ridhima Mishra, Joseph C Wu
Journal: Circulation (2017)

Introduction: Coronary artery disease (CAD), the direct outcome of atherosclerosis, is the leading cause of death in the United States. Previous studies demonstrated that impaired function of aldehyde dehydrogenase 2 (ALDH2), a key enzyme for alcohol metabolism, is linked to increased susceptibility to CAD. A single-nucleotide polymorphism that generates E487K mutation (ALDH2*2) reduces enzymatic activity of ALDH2 to less than 40% of the wild type (WT) and is present in ~560 million people. However, it remains unclear how ALDH2 regulates atherosclerotic progression. Hypothesis: Recent studies suggest a critical role of ALDH2 in plaque development and endothelial activation. Therefore, we hypothesize that endothelial cells of ALDH2*2 carriers possess greater susceptibility to proinflammatory activation, whereby endothelial cells recruit immune cells, leading to increased risk of atherogenesis. Methods: To study the patient-specific effects of ALDH2*2 mutation on endothelial proinflammatory activation, we generated and characterized iPSC-derived endothelial cells (iPSC-ECs) from 5 WT subjects and 5 ALDH2*2 carriers. We exposed the iPSC-ECs to pro-inflammatory conditions and assessed the level of endothelial proinflammatory activation by gene expression analysis and monocyte adhesion assay. Results: Our preliminary data show ALDH2*2-iPSC-ECs exhibit impaired ALDH2 function resulting in metabolic dysregulation compared to WT. Presence of ALDH2*2 mutation resulted in enhanced inflammatory response in the iPSC-ECs when treated with proinflammatory cytokines such as TNFα and IL-1β, as evidenced by up-regulation of cell adhesion molecules and augmented adherence to monocytes. The ALDH2*2-iPSC-ECs also exhibited an increased basal expression of vascular endothelial growth factor receptor 1 (FLT1) gene, which was further augmented upon inflammatory stimulation. FLT1 is a receptor for vascular endothelial growth factor ligands, playing a critical role in endothelial homeostasis and biology. Conclusion: Taken together, we elucidate the effects of impaired ALDH2 function on increased susceptibility to atherogenesis by endothelial proinflammatory activation using patient-derived iPSC-ECs.
Multimodal Cancer Theranosis Using Hyaluronate‐Conjugated Molybdenum Disulfide
Authors: Myeong‐Hwan Shin, Eun‐Yeong Park, Seulgi Han, Ho Sang Jung, Do Hee Keum, Geon‐Hui Lee, Taeyeon Kim, Chulhong Kim, Ki Su Kim, Seok Hyun Yun, Sei Kwang Hahn
Journal: Advanced Healthcare Materials (2018)

Abstract Among various 2D nanomaterials, molybdenum disulfide (MoS 2 ) exhibits unique visible photoluminescence with high absorption at the near‐infrared (NIR) range. Despite these optical properties, the efforts to use MoS 2 nanomaterials for optical imaging and photothermal therapy are hampered by their instability and low intracellular delivery efficiency. Multifunctional MoS 2 conjugated with hyaluronate (HA) for cancer theranosis is reported herein. HA facilitates the delivery of MoS 2 to tumor cells by the HA‐receptor mediated endocytosis. In BALB/c nude mice inoculated with a colorectal cancer cell line of HCT116, HA‐MoS 2 conjugates appear to be accumulated in the primary tumor at a content more than that in the liver and kidney. The disulfide bonding between MoS 2 and thiolated HA seems to degrade in the cytoplasm, releasing MoS 2 sheets in stacks and enhancing luminescence efficiency. The HA‐MoS 2 conjugates are readily detected via photoacoustic imaging as well as upconversion and downconversion fluorescence imaging. With NIR light illumination, HA‐MoS 2 conjugates enable highly effective photothermal tumor ablation. All these results confirm the promising potential of HA‐MoS 2 conjugates for cancer theranosis.
When One Data Set Is Insufficient—Things to Consider When Linking Secondary Data
Authors: Lee Squitieri, Tara A. Russell, Clifford Y. Ko
Journal: JAMA Surgery (2018)

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 Surgery HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Surgery journal
Radiation-responsive scintillating nanotheranostics for reduced hypoxic radioresistance under ROS/NO-mediated tumor microenvironment regulation
Authors: Yan Dou, Yajuan Liu, Fangshi Zhao, Yanyan Guo, Xue Li, Menglin Wu, Jin Chang, Chunshui Yu
Journal: Theranostics (2018)

Hypoxia-induced radioresistance is the primary reason for failure of tumor radiotherapy (RT). Changes within the irradiated tumor microenvironment (TME) including oxygen, reactive oxygen species (ROS) and nitric oxide (NO) are closely related to radioresistance. Therefore, there is an urgent need to develop new approaches for overcoming hypoxic radioresistance by incorporating TME regulation into current radiotherapeutic strategies.Herein, we explored a radiation-responsive nanotheranostic system to enhance RT effects on hypoxic tumors by multi-way therapeutic effects. This system was developed by loading S-nitrosothiol groups (SNO, a NO donor) and indocyanine green (ICG, a photosensitizer) onto mesoporous silica shells of Eu3+-doped NaGdF4 scintillating nanocrystals (NSC).Under X-ray radiation, this system can increase the local dosage by high-Z elements, promote ROS generation by X-ray-induced photodynamic therapy, and produce high levels of NO to enhance tumor-killing effects and improve hypoxia via NO-induced vasodilation. In vitro and in vivo studies revealed that this combined strategy can greatly reinforce DNA damage and apoptosis of hypoxic tumor cells, while significantly suppressing tumor growth, improving tumor hypoxia and promoting p53 up-regulation and HIF1α down-regulation. In addition, this system showed pronounced tumor contrast performance in T1-weighted magnetic resonance imaging and computed tomography.This work demonstrates the great potential of scintillating nanotheranostics for multimodal imaging-guided X-ray radiation-triggered tumor combined therapy to overcome radioresistance.