tbuckley/cabot-search huggingface dataset:
Can stereotactic ablative radiotherapy for oligometastatic pancreatic cancer help avoid perpetual chemotherapy and improve outcomes?
Authors: Ahmed Elamir, John D Karalis, Nina Niu Sanford, Patricio Polanco, Matthew R. Porembka, Robert D. Timmerman, Matteo Ligorio, Muhammad Shaalan Beg, Todd Anthony Aguilera
Journal: Journal of Clinical Oncology (2022)

571 Background: The oligometastatic state is increasing recognized and improved outcomes after local regional therapies have been observed in many malignancies, however there is a paucity of data on outcomes of patients with limited extent pancreatic ductal adenocarcinoma (PDAC). We hypothesize oligometastatic pancreatic cancer (OPanc) with 1-5 metastases would benefit from stereotactic ablative radiotherapy (SABR) to all active sites of disease, can improve outcome, and offer time off chemotherapy. Here in, we report our institutional experience of treating OPanc with SABR to evaluate the outcome and feasibility of the approach and compare outcomes with other institutional cohorts. Methods: A retrospective review was conducted on patients with stage IV PDAC who received SABR after noted to have OPanc. Patients with a histological diagnosis of PDAC, number of metastases ranging between 1-5, and who received SABR to all active disease at time of treatment were included. We identified a comparable group of 16 patients with similar metastatic burden but did not receive SABR. Overall survival and time off chemotherapy were evaluated in addition to assessment of each patients’ disease course. Results: Fourteen patients met the inclusion criteria. Five patients had metastases confined to lung only and nine to the liver only. Median baseline CA 19-9 was 105 U/mL (range &lt; 1, 921 U/mL). Eight patients had metachronous OPanc diagnosis. SABR was delivered to 22 metastatic tumors. Median progression free and overall survivals were 25 and 12.8 months, and 46 and 14.5 months for the SABR treated and the chemotherapy cohorts respectively. A total of 85.7% of patients that received SABR had a chemotherapy treatment break of greater than 6 months. Conclusions: Management of OPanc (1-5 lesions) with SABR as local regional therapy could improve outcomes in this selected population and warrants prospective evaluation.
Pegylated arginine deiminase drives arginine turnover and systemic autophagy to dictate energy metabolism
Authors: Yiming Zhang, Cassandra B. Higgins, Brian A. Van Tine, John S. Bomalaski, Brian J. DeBosch
Journal: Cell Reports Medicine (2022)

Obesity is a multi-systemic disorder of energy balance. Despite intense investigation, the determinants of energy homeostasis remain incompletely understood, and efficacious treatments against obesity and its complications are lacking. Here, we demonstrate that conferred arginine iminohydrolysis by the bacterial virulence factor and arginine deiminase, arcA, promotes mammalian energy expenditure and insulin sensitivity and reverses dyslipidemia, hepatic steatosis, and inflammation in obese mice. Extending this, pharmacological arginine catabolism via pegylated arginine deiminase (ADI-PEG 20) recapitulates these metabolic effects in dietary and genetically obese models. These effects require hepatic and whole-body expression of the autophagy complex protein BECN1 and hepatocyte-specific FGF21 secretion. Single-cell ATAC sequencing further reveals BECN1-dependent hepatocyte chromatin accessibility changes in response to ADI-PEG 20. The data thus reveal an unexpected therapeutic utility for arginine catabolism in modulating energy metabolism by activating systemic autophagy, which is now exploitable through readily available pharmacotherapy.
Measurement of lipoprotein subclasses by nuclear magnetic resonance spectroscopy may identify high risk individuals with borderline hyperlipidemia Roger S. Blumenthal, Diane M. Becker, Taryn F. Moy, Lisa R. Yanek, Raphael M. Yook, Lewis C. Becker. Johns Hopkins Medical Institutions, Baltimore, MD
Journal: Journal of the American College of Cardiology (2001)
Child Psychiatrist
Authors: Bhuvana Chandra
Journal: JAMA (1998)

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
Mimicking Native Heart Tissue Physiology and Pathology in Silk Fibroin Constructs through a Perfusion‐Based Dynamic Mechanical Stimulation Microdevice
Authors: Shreya Mehrotra, Bruna Alice Gomes de Melo, Mario Miscuglio, Kiavash Kiaee, Su Ryon Shin, Biman B. Mandal
Journal: Advanced Healthcare Materials (2021)

In vitro cardiomyocyte (CM) maturation is an imperative step to replicate native heart tissue-like structures as cardiac tissue grafts or as drug screening platforms. CMs are known to interpret biophysical cues such as stiffness, topography, external mechanical stimulation or dynamic perfusion load through mechanotransduction and change their behavior, organization, and maturation. In this regard, a silk-based cardiac tissue (CT) coupled with a dynamic perfusion-based mechanical stimulation platform (DMM) for achieving maturation and functionality in vitro is tried to be delivered. Silk fibroin (SF) is used to fabricate lamellar scaffolds to provide native tissue-like anisotropic architecture and is found to be nonimmunogenic and biocompatible allowing cardiomyocyte attachment and growth in vitro. Further, the scaffolds display excellent mechanical properties by their ability to undergo cyclic compressions without any deformation when places in the DMM. Gradient compression strains (5% to 20%), mimicking the native physiological and pathological conditions, are applied to the cardiomyocyte culture seeded on lamellar silk scaffolds in the DMM. A strain-dependent difference in cardiomyocyte maturation, gene expression, sarcomere elongation, and extracellular matrix formation is observed. These silk-based CTs matured in the DMM can open up several avenues toward the development of host-specific grafts and in vitro models for drug screening.
Keyword Index – Volumes 73+74
Journal: Cardiovascular Research (2007)

Keyword Index -Volumes 73+74 Abdominal aortic aneurysm (73) 227 ACE (73) 463 ACE2 (73) 463 Acetyl-CoA carboxylase (73) 278 Acidosis (73) 172, (73) 648 Activation (74) 416 Activin-like kinase receptor 1 (74) 279 Acute myocardial infarction (74) 343 Adeno-associated virus (74) 235 Adiponectin (74) 471 Adrenergic agonist (73) 92 h-adrenergic receptor (74) 445 Aggregated LDL (73) 208 Agiotensin II (73) 153 Ahnak (73) 19 Akt (73) 153 Alkaline phosphatase (73) 504 AMP-activated protein kinase (73) 278 Angiogenesis (73) 453, (73) 481, (73) 783, (73) 823 Angioplasty (74) 169 Angiotensin (74) 196 Angiotensin (1-7) (73) 463 Angiotensin II (73) 463, (74) 388 Angiotensin-receptor blockade (73) 539 Animal model (73) 217, (74) 29 Antiarrhythmic agents (73) 395, (73) 761, (74) 75, (74) 104 Antihypertensive agents (73) 395 Antimicrobial peptides (73) 26 Antioxidants (73) 414, (73) 806 Apelin (74) 388 APJ receptor (74) 388 Apoptosis (73) 48, (73) 172, (73) 470, (73) 481, (73) 689, (73) 794, (73) 806 l-arginine (73) 359 l-arginine supplementation (73) 359 l-arginine-nitric oxide signalling pathway (73) 359 Arhythmia (mechanisms) (74) 96 Arrhythmia (73) 37, (73) 310, (73) 539, (74) 104 Arrhythmia (mechanism) (73) 316 Arrhythmia (mechanisms) (73) 82, (74) 75 Arrhythmias (73) 531, (73) 657 Arrhythmias (mechanisms) (73) 386 Arteries (73) 424, (74) 169 Arteriosclerosis (73) 504 Artery (73) 368 Atherosclerosis (73) 181, (73) 198, (73) 310, (73) 341, (73) 348, (73) 368, (73) 470, (73) 597, (73) 833, (73) 841, (74) 19, (74) 537 ATP (74) 487 ATP-sensitive potassium channel opener (73) 497 Atrial function (73) 37 Atrial natriuretic peptide (73) 678, (73) 729 Atrium (74) 426 Atrophy (74) 133 Autoimmunity (74) 213 Autonomic nervous system (73) 750, (74) 438 AZT (73) 432Basic science research (74) 19 Beta subunit (73) 19 Blood flow (74) 515 Blood pressure (73) 190 Blood vessel (74) 213 BMP signaling (74) 244 Bone morphogenetic protein (74) 279 Ca 2+ pump (74) 39 Cachexia (73) 298 Calcium (73) 101, (73) 568, (73) 631, (73) 641, (74) 39 Calcium (cellular) (73) 164, (73) 316 Calcium channel (73) 19, (73) 641 Calcium cycling (73) 678 Calcium signaling (73) 111 Calmodulin (73) 631, (73) 641 Calmodulin kinase II (73) 657 CaM kinase (73) 631, (73) 667 CaMKII (73) 641, (73) 648, (73) 678, (73) 689 Capillaries (73) 575 Capillary permeability (73) 575 Cardiac function (73) 144 Cardiac myocytes (73) 111 Cardiac myofibroblasts (74) 140 Cardiomyocyte (73) 19 Cardiomyocytes (74) 256, (74) 304 Cardiomyopathy (73) 549, (74) 290 Cardiovascular (73) 348 Cardiovascular development (74) 244 Cardiovascular disease (73) 227, (73) 326 Cardiovascular surgery (74) 366 Carnitine palmitoyltransferase 1 (73) 278 Caspase-12 (73) 172 Catabolism (73) 298 Catechins (73) 348 Caveolae (73) 190 CDK2 (74) 304 Cell culture/isolation (73) 341 Cellular calcium (73) 376 CeO 2 nanoparticles (73) 549 cGMP (74) 377 Chamber formation (74) 244 Channel proteins (73) 512 Cholesterol (73) 66 Cholesterol accumulation (74) 526 Chromatin (73)
Evaluating the technical feasibility of novel salvage endoscopic submucosal dissection after chemoradiotherapy for locally advanced rectal adenocarcinoma.
Authors: Galen Leung, Makoto Nishimura, Neha Hingorani, I-Hsin Lin, Mark Schattner
Journal: Journal of Clinical Oncology (2022)

103 Background: According to the National Comprehensive Cancer Network guideline, locally advanced rectal cancer is treated with chemotherapy with or without radiation, followed by transabdominal resection. However, there has been an emerging role for nonoperative management after chemoradiotherapy, and there is significant morbidity and risks associated with surgical resection. Endoscopic submucosal dissection (ESD) after chemoradiotherapy (CRT) for rectal cancer, which is termed “salvage ESD,” may be a viable option for patients, in terms of evaluating pathological response and providing potential curative resection. We aim to evaluate the feasibility and safety of salvage ESD. Methods: Retrospective chart review of cases of salvage ESD after CRT for locally advanced rectal cancer (salvage group) and standard ESD cases for rectal tumors without prior CRT (standard group) from July 2018 to August 2020 at our institution was performed. Clinical factors, imaging, procedural, and pathology results were collected and compared between the two groups. Results: 12 salvage ESD cases were compared to 27 standard ESD cases. 83.3% of the lesions in the salvage ESD group were initially staged as T3 prior to CRT. 100% of the lesions in the salvage ESD group were scarred down, compared to 33.3% in the standard ESD group (p &lt;0.01). Technical outcomes are shown in the table. The en bloc resection rates were 92.7% and 91.7% (p=1.00) and R0 resection rates were 66.7% and 75.0% (p=0.55) for the standard and salvage groups, respectively. In the salvage ESD group, no adverse events were observed. 66.7% of the adenocarcinomas in the salvage ESD group had morphologically changed to hyperplasia or adenoma after CRT and there were no identifiable lesions greater than T1 staging. Conclusions: Salvage ESD after CRT for locally advanced rectal cancer is technically feasible and with comparable low complication rates. There may be a diagnostic role in salvage ESD in assessing pathological response to CRT, as well as a possibly therapeutic role in resection of residual lesions with the potential to avoid surgery. Further studies are underway comparing the clinical outcomes of salvage ESD with standard surgical resection after CRT for locally advanced rectal cancer.[Table: see text]
JOURNALS ABSTRACTED IN THE CURRENT MEDICAL LITERATURE DEPARTMENT, MAY—AUGUST 1949
Journal: JAMA (1949)

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
Text-Book of Anatomy.
Journal: JAMA (1902)

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
Immunodeficiency diseases
Authors: R. H. Buckley
Journal: JAMA (1987)

UNTIL the acquired immunodeficiency syndrome (AIDS) emerged six years ago,<sup>1</sup>defects in immunity were considered rare. It is important to realize, however, that it was from patients with genetic abnormalities of the immune system<sup>2-5</sup>that the functions and components of the normal immune system were elucidated, information that was later applied to the delineation of the immunologic abnormalities in AIDS.<sup>1</sup>Immunodeficiency diseases may involve any of the components of the immune system, including lymphocytes, phagocytic cells, and complement proteins.<sup>2-4</sup>Despite considerable advances in understanding of the cellular and molecular abnormalities present in the various known primary immune defects,<sup>5</sup>it is clear that the fundamental biologic errors for most of them remain unknown.<sup>2-4</sup>Exceptions include two accompanied by purine salvage pathway enzyme deficiencies—adenosine deaminase (ADA) in some cases of autosomal recessive severe combined immunodeficiency (SCID) and purine nucleoside phosphorylase (PNP) in some patients with Nezelof's
Tumor microbiome variation in young versus average onset colorectal cancer.
Authors: Shimoli V Barot, Naseer Sangwan, Kanika G. Nair, Stephanie Schmit, Shao Xiang, Suneel Deepak Kamath, David Liska, Alok A. Khorana
Journal: Journal of Clinical Oncology (2022)

144 Background: The incidence of young onset colorectal cancer (yoCRC) is rising at alarming rates. The gut microbiome may be a factor accounting for the increase. We analyzed differences in the intratumoral microbiome of yoCRC vs average onset CRC (aoCRC) and its clinical impact. Methods: We identified 314 histologically confirmed cases of stage I-IV CRC that underwent surgical resection at our institution from 2000-2020, diagnosed &lt;50 years of age for yoCRC and &gt;60 years for aoCRC, who consented to a prospective biorepository. 36 cases were excluded due to nonmalignant, non-adenocarcinoma or metastatic site specimens. Fresh frozen tissue from the primary tumor with paired adjacent nonmalignant tissue specimens were analyzed. 16S rDNA was isolated and sequence reads were assigned to genus level amplicon sequence variants in DADA2 and analyzed for alpha and beta diversity using Phyloseq. Statistical tests included analysis of variance (ANOVA), permutational multivariate analysis (PERMANOVA), linear regression, and Wilcoxon test. Differential abundance and correlation analysis were adjusted for sex and ethnicity as confounding factors. Correlation analysis was adjusted with Benjamini Hochberg correction. Clinical differences were analyzed using Fisher's exact test. Results: Of the cohort of 278 patients, 137 had yoCRC (median age 43 years, range 16-49) and 141 had aoCRC (median age 73 years, range 61-95). yoCRC patients were more likely to have stage III or IV disease at presentation (29% vs 14%, p =0.002; 29% vs 18%, p =0.024 respectively), left sided tumors (74% vs 58%, p =0.003) and receive neoadjuvant therapy (29% vs 15%, p =0.004). yoCRC had significantly higher tumor microbial alpha diversity than aoCRC ( p &lt;2.22e−16, Wilcoxon rank-sum test). Beta diversity analysis demonstrated significantly different diversity of genera between the groups (R2=0.12, p =0.001, PERMANOVA). The prevalent taxa identified in both groups were Lactobacillus, Bacillus and Listeria. Differential abundance analysis (ANOVA, p &lt;0.05) revealed a significant variation of intratumoral microbiome (Table). Correlation analysis revealed an association of longer overall survival (OS) with the presence of Akkermansia in yoCRC (R2 =0.36, p &lt;0.001), but not in aoCRC. Conclusions: We found significant differences between the intratumoral microbiome of yoCRC and aoCRC. In particular, Akkermansia, considered a healthy gut microbe, was found in greater relative abundance in yoCRC and correlated with improved OS. Further studies are warranted to understand the nature of association of these microbes with the development of and outcomes in yoCRC. [Table: see text]
Error in Author Degrees
Journal: JAMA Network Open (2021)

Tanvee Varma, BA; Joshua D. Wallach, PhD, MS; Jennifer E. Miller, PhD; Dominic Schnabel, MPH; Joshua J. Skydel, BS; Audrey D. Zhang, MD; Michaela A. Dinan, PhD; Joseph S. Ross, MD, MHS; Cary P. Gross, MD
Association of Polygenic Risk Scores With Radiographic Progression in Patients With Rheumatoid Arthritis
Authors: Suguru Honda, Katsunori Ikari, Koichiro Yano, Chikashi Terao, Eiichi Tanaka, Masayoshi Harigai, Yuta Kochi
Journal: Arthritis & Rheumatology (2022)

To investigate whether polygenic risk scores obtained using data from a genome-wide association study (GWAS) of rheumatoid arthritis (RA) susceptibility can be predictors of radiographic progression.We constructed polygenic risk scores using GWAS summary data on associations of single-nucleotide polymorphisms with RA susceptibility. The polygenic risk scores were stratified into quintiles based on levels of significance (ranging from top quintile of polygenic risk scores to bottom quintile). In addition, change in the Sharp/van der Heijde score (SHS) of radiographic progression over the first 5 years after onset of RA was assessed. The change in SHS over 5 years was stratified according to quartiles, with the top quartile of change in SHS defined as severe radiographic progression (score change of >35 points) and the remaining 3 quartiles defined as nonsevere radiographic progression. Polygenic risk scores were assessed for their ability to predict the SHS status over 5 years in a training set (n = 500 RA patients) for selection of the best model, and in a testing set (n = 740 RA patients) for validation of the data. We evaluated the performance of the polygenic risk score as a predictor of severe radiographic progression in univariable and multivariable analyses with inclusion of other factors.Polygenic risk scores constructed from 43,784 single-nucleotide polymorphisms significantly differed between patients who experienced severe radiographic progression and those with nonsevere radiographic progression in both the training set (P = 0.0064) and the testing set (P = 0.017). Patients with polygenic risk scores in the top quintile had a higher risk of severe progression compared to those with polygenic risk scores in the bottom quintile (odds ratio [OR] 1.90, P = 0.0022), and the risk of severe radiographic progression was even higher when restricted to patients who were younger at disease onset (OR 5.06, P = 0.00038). The group with polygenic risk scores in the top quintile and the anti-citrullinated protein antibody (ACPA)-positive group had significantly higher proportions of patients with severe radiographic progression (P = 0.00052 and P = 0.0022, respectively) compared to the remaining groups. Multivariable analysis showed that polygenic risk score (P = 0.00019) as well as female sex (P = 0.0033), ACPA positivity (P = 0.0023), and body mass index (P = 0.024) were independent risk factors for severe radiographic progression.A polygenic risk score that is derived from GWAS data on RA susceptibility is associated with the level of severity of radiographic progression in patients with RA.
Evaluation of left ventricular relaxation during atrial fibrillation using the color M-mode doppler propagation velocity of mitral inflow Junko Watanabe, Tomotsugu Tabata, Neil L. Greenberg, Don W. Wallick, Deborah A. Agler, Yong-jin Kim, Kent A. Mowrey, Shaowei Zhuang, Youhua Zhang, Mario J. Garcia, Todor N. Mazgalev, James D. Thomas, Richard A. Grimm. The Cleveland Clinic Foundation, Cleveland, OH
Journal: Journal of the American College of Cardiology (2001)
Pharmacodynamic interaction between the new selective cholesterol absorption inhibitor ezetimibe and atorvastatin Teddy Kosoglou, Michael Seiberling, Paul Statkevich, David L. Cutler, Bo Yang, LeShawn Anderson, Stephen E. Maxwell, Melton B. Affrime. Schering-Plough Research Institute, Kenilworth, NJ, Swiss Pharma Contract Ltd., Allschwill, Switzerland
Journal: Journal of the American College of Cardiology (2001)