tbuckley/cabot-search huggingface dataset:
Maternal exposure to fish oil primes offspring to harbor intestinal pathobionts associated with altered immune cell balance
Authors: DL Gibson, SK Gill, K Brown, N Tasnim, S Ghosh, S Innis, K Jacobson
Journal: Gut Microbes (2015)

Our previous studies revealed that offspring from rat dams fed fish oil (at 8% and 18% energy), developed impaired intestinal barriers sensitizing the colon to exacerbated injury later in life. To discern the mechanism, we hypothesized that in utero exposure to fish oil, rich in n-3 polyunsaturated fatty acid (PUFA), caused abnormal intestinal reparative responses to mucosal injury through differences in intestinal microbiota and the presence of naïve immune cells. To identify such mechanisms, gut microbes and naïve immune cells were compared between rat pups born to dams fed either n-6 PUFA, n-3 PUFA or breeder chow. Maternal exposure to either of the PUFA rich diets altered the development of the intestinal microbiota with an overall reduction in microbial density. Using qPCR, we found that each type of PUFA differentially altered the major gut phyla; fish oil increased Bacteroidetes and safflower oil increased Firmicutes. Both PUFA diets reduced microbes known to dominate the infant gut like Enterobacteriaceae and Bifidobacteria spp. when compared to the chow group. Uniquely, maternal fish oil diets resulted in offspring showing blooms of opportunistic pathogens like Bilophila wadsworthia, Enterococcus faecium and Bacteroides fragilis in their gut microbiota. As well, fish oil groups showed a reduction in colonic CD8+ T cells, CD4+ Foxp3+ T cells and arginase+ M2 macrophages. In conclusion, fish oil supplementation in pharmacological excess, at 18% by energy as shown in this study, provides an example where excess dosing in utero can prime offspring to harbor intestinal pathobionts and alter immune cell homeostasis.
Abstract 421: Differences of DNA methylation patterns according to histologic subtypes of early gastric carcinomas
Authors: Khalilullah Mia-Jan, Hoon Ryu, Mi-Ra Lee, Sun-Young Ji, Mee-Yon Cho
Journal: Cancer Research (2014)

Abstract Background: The DNA methylation change is known to play a crucial role in early gastric carcinogenesis. However, its association with the histologic subtypes of EGCs has not been fully elucidated. In this study, we aim to know whether the subtypes of early gastric carcinomas (EGCs) are related to the differences of DNA methylation or not using genome wide methylation assay. Materials and Method: The comprehensive methylation analysis was performed by Illumina Infinium methylation assay (IIMA, 450K BeadChip kit) covering 450,000 sites on 12 tumors and 12 matched non-tumor mucosa from 12 patients with EGC. Hisytologically, the EGCs were devided into intestinal type (group A, n=6) and non-intestinal type (group B, diffuse=4 and mixed=2). The CpG sites in 450K microarray chip are classified into CpG islands, shores (2kb), shelves (2kb∼4kb) and open sea (&amp;gt;4kb) by CpG content and neighborhood context. According to the functional genomic distribution they are classified into promoter, body, 3′UTR and intergenic. To determine DMRs, average β-values were computed with β-values in signal intensity of over 3000. The Δβ-value was a result substracted average β-value of one from the other. When Δβ is over 0.2 or below -0.2, it was considered to be meaningful and refered to differentially methylated regions (DMRs) . Results: There were 484 DMRs in group A tumor and 208 DMRs in group B. The pattern of DMRs were different between two groups. In group A tumor, most of DMRs (97.73%) were hypermethylated and 75.26% were in CpG island. On the other hand, the group B tumors showed that 63.94% of DMRs were hypermethylated and only less than half of them (48.87%) were in CpG island. In terms of functional genomic distribution of DMRs, promoter (38.66%) was the most common site in group A while body (54.14%) was in group B. On Hierarchical clustering analysis, the clear grouping was made by 208 DMRs in three cases, two of them being mixed-type, by both correlation and Euclidean methods. However, no distinct grouping was found with DMRs in group A. Hierarchical clustering analysis of non-tumor mucosa showed a distinct separation between group A and B. Conclusions: DNA methylation pattern was distinctively different between the histologic subtype of EGCs. In the intestinal type of EGCs, the DNA methylation seems to be started in non-tumor mucosa. Citation Format: Khalilullah Mia-Jan, Hoon Ryu, Mi-Ra Lee, Sun-Young Ji, Mee-Yon Cho. Differences of DNA methylation patterns according to histologic subtypes of early gastric carcinomas. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 421. doi:10.1158/1538-7445.AM2014-421
Abstract 16442: Unusually High Incidence of Dressler’s Syndrome After Hybrid Ablation for Atrial Fibrillation
Authors: Tina C Sichrovsky, David F Rivera, Suneet Mittal, Aysha Arshad, Mark Preminger, Dan Musat, Jonathan S Steinberg
Journal: Circulation (2014)

Introduction:  Dressler’s syndrome (DS), often difficult to diagnose, occurs after open-heart surgery or myocardial infarction but rarely after catheter ablation (abl). With the emergence of minimally invasive hybrid abl (HA) strategies for atrial fibrillation (AF), combining more extensive epicardial abl with standard pulmonary vein isolation (PVI), we became concerned regarding an increased incidence of DS. The purpose of this report is to review incidence, risk factors and treatment for DS after HA.   Methods:  HA used videoscopic-guided epicardial abl of the posterior left atrium (LA) (“Convergent” procedure) with radiofrequency (RF) followed by endocardial PVI with RF or cryoballoon in the same procedure. Pts received NSAID during hospital stay. All pts had drug-refractory symptomatic long-standing persistent AF and/or failed prior abls.   Results:  Thirty-seven pts (age 62±8yrs, 71% male) were followed after HA and 6 developed DS (16%) at 28±21 days post HA. This incidence was much greater than the 0.2% in a control group of the last 1000 pts with standard PVI (p   Conclusions:  DS was a much more common complication after HA compared to standard abl for AF. The extensive abl of the posterior LA may cause significant myolysis enhancing the possibility of an immune response. More studies will be needed to identify risk factors that may allow early intervention to prevent DS, which adds substantial morbidity and cost to this otherwise well tolerated and highly successful treatment for difficult to treat pts with AF.
Abstract 430: Identification of novel methylation-silenced genes in oral squamous cell carcinomas
Authors: Masanobu Abe, Satoshi Yamashita, Yoshiyuki Mori, Takahiro Abe, Hideto Saijo, Toshikazu Ushijima, Tsuyoshi Takato
Journal: Cancer Research (2014)

Abstract To identify novel methylation-silenced genes in oral squamous cell carcinomas (OSCCs), we took a combined approach of methylated DNA immunoprecipitation (MeDIP)-CpG island (CGI) microarray analysis and expression microarray analysis after treatment with a demethylating agent. MeDIP-CGI microarray revealed that promoter CGIs of 324 genes were methylated in two OSCC cell lines (Ca9-22, HSC-2). By treatment of the cell lines with 5-aza-2′-deoxycytidine, 125 of the 324 genes were up-regulated in at least one of the two cell lines. For 23 of the 125 genes that have not been focused on in the field of oral malignancy, we analyzed their promoter methylation statuses in 16 normal oral tissues, five OSCC cell lines, 26 OSCC tissues and 24 oral leukoplakia tissues. Ten promoter CGIs were methylated not only in OSCC cell lines but also OSCC tissues. The methylation profile indicated the presence of the CpG island methylator phenotype (CIMP) in OSCC tissues. Furthermore, the CIMP was observed in three of the 13 oral dysplastic leukoplakia tissues. The CIMP was considered as one of early molecular events in malignant transformation from oral premalignant lesions to OSCCs. Citation Format: Masanobu Abe, Satoshi Yamashita, Yoshiyuki Mori, Takahiro Abe, Hideto Saijo, Toshikazu Ushijima, Tsuyoshi Takato. Identification of novel methylation-silenced genes in oral squamous cell carcinomas. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 430. doi:10.1158/1538-7445.AM2014-430
The Garden of Eden
Authors: M Therese Southgate
Journal: JAMA (2005)

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
The DNA-repair protein AlkB, EGL-9, and leprecan define new families of 2-oxoglutarate- and iron-dependent dioxygenases
Authors: L Aravind, Eugene V Koonin
Journal: Genome biology (2001)

Protein fold recognition using sequence profile searches frequently allows prediction of the structure and biochemical mechanisms of proteins with an important biological function but unknown biochemical activity. Here we describe such predictions resulting from an analysis of the 2-oxoglutarate (2OG) and Fe(II)-dependent oxygenases, a class of enzymes that are widespread in eukaryotes and bacteria and catalyze a variety of reactions typically involving the oxidation of an organic substrate using a dioxygen molecule.We employ sequence profile analysis to show that the DNA repair protein AlkB, the extracellular matrix protein leprecan, the disease-resistance-related protein EGL-9 and several uncharacterized proteins define novel families of enzymes of the 2OG-Fe(II) oxygenase superfamily. The identification of AlkB as a member of the 2OG-Fe(II) oxygenase superfamily suggests that this protein catalyzes oxidative detoxification of alkylated bases. More distant homologs of AlkB were detected in eukaryotes and in plant RNA viruses, leading to the hypothesis that these proteins might be involved in RNA demethylation. The EGL-9 protein from Caenorhabditis elegans is necessary for normal muscle function and its inactivation results in resistance against paralysis induced by the Pseudomonas aeruginosa toxin. EGL-9 and leprecan are predicted to be novel protein hydroxylases that might be involved in the generation of substrates for protein glycosylation.Here, using sequence profile searches, we show that several previously undetected protein families contain 2OG-Fe(II) oxygenase fold. This allows us to predict the catalytic activity for a wide range of biologically important, but biochemically uncharacterized proteins from eukaryotes and bacteria.
Duty to Warn About Hereditary Disease Risks
Authors: Daniel P. Sulmasy
Journal: JAMA (2005)

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
Anecortave acetate as monotherapy for treatment of subfoveal neovascularization in age-related macular degeneration
Authors: Donald J D'Amico, Morton F Goldberg, Henry Hudson, Janice A Jerdan, D Scott Krueger, Susan P Luna, Stella M Robertson, Stephen Russell, Lawrence Singerman, Jason S Slakter, Lawrence Yannuzzi, Patricia Zilliox
Journal: Ophthalmology (2003)
Abstract 20665: Cardiac Arterial Spin Labeling MRI as a Novel Approach for in vivo Quantification of the Area-At-Risk
Authors: Rachel Dongworth, Adrienne E Campbell-Washburn, Thomas Roberts, Derek M Yellon, Mark Lythgoe, Derek J Hausenloy
Journal: Circulation (2014)

Introduction: T2-weighted cardiac magnetic resonance (CMR) imaging, which detects myocardial edema, has been used to retrospectively delineate the area-at-risk (AAR) in clinical cardioprotection studies. However, some of these cardioprotective interventions have been reported to reduce the extent of myocardial edema, thereby affecting the AAR delineated by T2-CMR. Here, we investigate arterial spin labelling (ASL)-CMR, which measures myocardial perfusion, as an alternative approach to measuring the AAR following acute ischemia-reperfusion injury (IRI). Methods: B6sv129 mice (10-14 weeks old) were subjected to an in vivo left main coronary artery ligation for 30 minutes followed by 72 hours reperfusion following which CMR was performed to determine MI size (late gadolinium enhancement) and the AAR (T2-mapping CMR and ASL CMR). These were then validated against MI size and the AAR measured by ‘gold-standard’ triphenyl tetrazolium chloride and Evan’s blue staining, respectively. Animals were subjected to a standard ischemic preconditioning (IPC) protocol comprising 5 minutes ischemia and reperfusion prior to the index ischemic insult. Results: T2-maps showed clearly defined regions of elevated T2-signal corresponding to the AAR delineated by histology (AAR/LV% in control: T2-CMR 60.4±2.4 versus histology 64.3±2.5:N=6/group;P&gt;0.05). However, in IPC-treated animals, the T2-maps significantly underestimated the AAR (AAR/LV% with IPC: T2-CMR 46.0±13.2 versus histology 59.8±7.8:N=10/group;P&lt;0.05). ASL-CMR also revealed clearly defined regions of attenuated ASL signal (indicated reduced myocardial blood flow) which appeared to correspond to the AAR delineated by histology (AAR/LV% in control: ASL-CMR 60.6±4.3 versus histology 64.3±3.9:N=6/group;P&gt;0.05). Crucially, the estimation of the AAR by ASL-CMR was not affected by IPC (AAR/LV% with IPC: ASL-CMR 53.4±7.9 versus histology 58.0±3.0:N=8/group;P&gt;0.05). Conclusions: We find that ASL-CMR has the potential to retrospectively delineate the AAR in the adult murine heart subjected to acute IRI in a similar manner to T2-mapping CMR. Crucially, unlike T2-mapping CMR however, the AAR delineated by ASL-CMR was not affected by the cardioprotective intervention, IPC.
Combined aerobic/inspiratory muscle training vs. aerobic training in patients with chronic heart failure
Authors: Stamatis Adamopoulos, Jean‐Paul Schmid, Paul Dendale, Daniel Poerschke, Dominique Hansen, Athanasios Dritsas, Alexandros Kouloubinis, Toon Alders, Aggeliki Gkouziouta, Ilse Reyckers, Vasiliki Vartela, Nikos Plessas, Costas Doulaptsis, Hugo Saner, Ioannis D. Laoutaris
Journal: European Journal of Heart Failure (2014)
Use of steroids for acute spinal cord injury must be
Authors: Deborah Short
Journal: BMJ (2000)

EDITOR—Yates and Roberts's editorial on corticosteroids in head injury caused me considerable concern in so far as it portrayed the situation for treating acute spinal cord injury.1 Intravenous high dose methylprednisolone given within eight hours of injury has been promoted since the second American national acute spinal cord …
SYPHILITIC PAN-MENINGITIS (SO-CALLED CHRONIC HYPERTROPHIC SPINAL PACHYMENINGITIS)
Authors: Gordon R. Kamman, A. B. Baker
Journal: Annals of Internal Medicine (1941)

Case Reports1 October 1941SYPHILITIC PAN-MENINGITIS (SO-CALLED CHRONIC HYPERTROPHIC SPINAL PACHYMENINGITIS)GORDON R. KAMMAN, M.D., F.A.C.P., A. B. BAKER, M.D., Ph.D.GORDON R. KAMMAN, M.D., F.A.C.P.Search for more papers by this author, A. B. BAKER, M.D., Ph.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-15-4-748 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe case about to be reported belongs to the group of disorders erroneously referred to as "chronic hypertrophic spinal pachymeningitis." We say "erroneously referred to" because in most cases reported, the leptomeninges as well as the dura were adherent and involved in the pathological process. Since the detailed histological studies in our case provide additional evidence that the pathological process is something more than a hypertrophic "pachymeningitis" and since such cases are comparatively rare, a report of the present case seems justified.Syphilis and tuberculosis have been considered the chief etiological agents in this disease, the former being by far...Bibliography HASSIN GB: Circumscribed suppurative (non-tuberculous) peripachymeningitis. Histopathologic study of a case, Arch. Neur. and Psychiat., 1928, xx, 110-129. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication September 17, 1940.From the University of Minnesota Department of Nervous and Mental Diseases ; Ancker Hospital Division, Saint Paul, Minnesota, and the Department of Neuropathology. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byIncomplete myelographic block with hypertrophic spinal pachymeningitisHypertrophic Spinal Pachymeningitis 1 October 1941Volume 15, Issue 4Page: 748-756KeywordsMeningitisNeuropathologySyphilis ePublished: 1 December 2008 Issue Published: 1 October 1941 PDF downloadLoading ...
Abstract 669: Aggressive Cholesterol Reduction with High-Dose Statins Improves Prognosis in Peripheral Arterial Disease
Authors: Harm H Feringa, Martin Dunkelgrun, Sanne Hoeks, Ron van Domburg, Radosav Vidakovic, Stefanos Karagiannis, Fahim Azizi, Gijs Welten, Thomas Lameris, Olaf Schouten, Don Poldermans
Journal: Circulation (2006)

Background: LDL-cholesterol lowering drugs are associated with an improved long-term outcome in patients with peripheral atherosclerotic disease (PAD). Aim: To assess the independent effect of stat...
Using area-based socioeconomic measures to study social disparities in cancer.
Authors: Nancy Krieger
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

SY09-01 

Despite longstanding US evidence of socioeconomic and racial/ethnic inequalities in health, US cancer registries lack socioeconomic data, thus precluding routine monitoring and analysis of US socioeconomic inequalities in cancer and their link to racial/ethnic disparities in the burden of cancer. Also problematic is a lack of conceptual clarity regarding the definition of cancer disparities, with the most commonly employed definitions being descriptive rather than analytic. To address these empirical and conceptual gaps, this presentation will address three topics: first, it will offer a conceptual analytic definition of cancer disparities ([1][1]), premised on ecosocial theory ([2][2]–[4][3]) and its concern with how we literally embody, biologically, social inequality, thereby producing population patterns of health, disease and well-being, including health inequities. Second, it will present the methods and results of the The Public Health Disparities Geocoding Project ([5][4]–[8][5]), which geocoded and linked public health surveillance data from Massachusetts and Rhode Island to 1990 census-derived area-based socioeconomic measures (ABSMs) to determine which ABSMs, at which geographic level (census block group, census tract, ZIP Code) could validly be used to monitor socioeconomic inequalities in health. Outcomes comprised: birth, childhood lead poisoning, sexually transmitted infections, tuberculosis, non-fatal weapons-related injuries, cancer incidence, and mortality. Key findings were that in both the total population and diverse racial/ethnic-gender groups, measures of economic deprivation proved most sensitive to expected socioeconomic gradients in health, with census tract (CT) ABSMs yielding the most consistent results and maximal geocoding across outcomes, and the CT poverty measure performing as well as more complex composite measures. These results imply that geocoding and use of the CT poverty measure permits routine monitoring of US socioeconomic inequalities in health, using a common and accessible metric. Third, to demonstrate the additional utility of geocoding and using ABSMS for etiologic investigations, selected results of analyses on socioeconomic trends in breast cancer incidence will be presented ([9][6]). The central message is that the science of health disparities requires both rigorous concepts and rigorous methods, and puts to the test our understanding of determinants of population health, including cancer.

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Genetic Factors in Exceptional Longevity—Reply
Authors: Nir Barzilai, Gil Atzmon, Clyde Schechter, Richard Lipton, Alan R. Shuldiner
Journal: JAMA (2004)

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
Subunits of the translation initiation factor eIF2B are mutant in leukoencephalopathy with vanishing white matter
Authors: Peter A.J. Leegwater, Gerre Vermeulen, Andrea A.M. Könst, Sakkubai Naidu, Joyce Mulders, Allerdien Visser, Paula Kersbergen, Dragosh Mobach, Dafna Fonds, Carola G.M. van Berkel, Richard J.L.F. Lemmers, Rune R. Frants, Cees B.M. Oudejans, Ruud B.H. Schutgens, Jan C. Pronk, Marjo S. van der Knaap
Journal: Nature Genetics (2001)