tbuckley/cabot-search huggingface dataset:
NSRG-09. AN INTERNATIONAL WORKSHOP TO DEVELOP A PRE-OPERATIVE SCORING SYSTEM FOR PREDICTING RISK OF POST-OPERATIVE PAEDIATRIC CEREBELLAR MUTISM SYNDROME (CMS) IN CHILDREN AND YOUNG PEOPLE
Journal: Neuro-Oncology (2018)

Cerebellar mutism syndrome (CMS) complicates posterior fossa surgery in up to 30% of cases leading to prolonged rehabilitation and most often incomplete recovery and life long disability. This project seeks to develop and validate predictive scoring system based upon imaging characteristics from pre-operative scans to inform the surgical consent procedure. International workshop involving neuroradiologists, neurosurgeons and neuro-oncologists from 11 European and North American centres. During the workshop, experts reviewed pre-operative scans blinded to mutism status. Imaging data were recoded in to binary variables to test a previous preliminary risk assessment tool which based on data from two UK centres. The cohort consists of 245 posterior fossa tumour cases (mean age 8.23 ± 4.45 years) of whom 40 developed post-operative CMS (latency 0-8 days, duration 1 day-3 months). Inter-rater agreement of imaging predictors ranged from moderate (primary location k=0.6, dentate nucleus invasion k=0.41) to fair (cerebellar hemisphere invasion k=0.38, middle cerebellar peduncle invasion and/or compression k=0.20). The preliminary model demonstrated the ability to identify low risk patients (CMS rate 1%, 1/83). Further mathematical modelling to identify patients with higher risks is in process based upon prediction accuracy, inter-rater reliability of predictors and usefulness in clinical setting. This is the largest multi-centre cohort to be studied in this way. We identified low risk cases from all participating centres, accounting for 83/245 (34%) cases. We propose extending access to this scoring system to additional centres via a web based module offering training and scoring validation for each centre.
This Week in &lt;EMPH&gt;JAMA&lt;/EMPH&gt;
Journal: JAMA (2007)

A Piece of My Mind"He is primed for autonomic overload, the anxiety that won't subside, the depression that is too heavy to bear, the nightmare that won't go away."From "Stress, Redeployed." SEE PAGE 18 Medical News & PerspectivesStudies of the mechanisms underlying migraine and rare pain disorders are providing insights that may help efforts to develop treatments that selectively target sources of pain.
Abstract 64: Regulation and functional role of the cell-cell junction-associated RNAi machinery in colon cancer
Authors: Amanda C. Daulagala, Catherine Bridges, Lauren Rutledge, Joyce Nair-Menon, Micheal Yost, Antonis Kourtidis
Journal: Cancer Research (2019)

Abstract Colon cancer is the third most common and the second deadliest type of cancer in the United States. A typical characteristic of colon tumors is the compromised integrity of the colonic epithelial monolayer. The Adherens Junction (AJ) is a cell-cell adhesion complex essential for the maintenance of the epithelial integrity, composed of E-cadherin and the catenin family of proteins. We have recently shown that the E-cadherin-p120 catenin partner PLEKHA7 is critical for epithelial monolayer integrity. We have also revealed that PLEKHA7 recruits the core components of the RNA interference (RNAi) machinery, such as Ago2, DROSHA and DGCR8, as well as miRNAs at the mature apical adherens junctions, to suppress expression of pro-tumorigenic markers, through miRNA-mediated silencing. However, we still haven’t examined the extend of the contribution of this mechanism to colon tumorigenesis and its modes of regulation. We hypothesize that the adherens junction-RNAi mechanism acts as an epithelial sensor that tethers monolayer integrity to cell behavior. To examine this, we generated 3D cultures of well-differentiated Caco2 colon epithelial cells on Matrigel to examine the distribution of RNAi proteins. Indeed, co-localization of PLEKHA7 with RNAi proteins occurs specifically at the apical surface of these spheroids, whereas PLEKHA7 depletion results in loss of junctional localization of RNAi proteins and in enlarged, multilayered structures. Corroborating these results, PLEKHA7 and RNAi components co-localize specifically at the apical surface of normal colon crypts, whereas extensive disruption or loss of this co-localization was observed in colon tumor patient samples. Fibrosis and extensive deposition of extracellular matrix (ECM) due to chronic inflammation is a precursor to colon cancer. ECM can affect adherens junctions integrity, through integrin-Src signaling. Indeed, we have found that Src activity disrupts localization of PLEKHA7 and RNAi proteins to the junctions. To investigate the potential role of ECM in the regulation of the junctional RNAi mechanism, we are now examining Caco2 cells grown on different ECM substrates, as well as under different conditions of mechanical strain, since fibrosis poses mechanical stress on cells. In summary, our data point towards a novel putative tumor suppressor mechanism, of which we are investigating its modes of regulation and its involvement in colon tumorigenesis. Citation Format: Amanda C. Daulagala, Catherine Bridges, Lauren Rutledge, Joyce Nair-Menon, Micheal Yost, Antonis Kourtidis. Regulation and functional role of the cell-cell junction-associated RNAi machinery in colon cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 64.
Abstract 5307: Androgen Receptor promotes localization of E-cadherin to cell-cell junctions through Abi1 signaling
Authors: Baylee Porter, Disharee Nath, Susan A. Krum, Gennady Bratslavsky, Vladimir A. Kuznetsov, Leszek Kotula
Journal: Cancer Research (2019)

Abstract According to American Cancer Society, prostate cancer is a slow progressing disease that affects nearly 50 percent of males over the age of 60. Every year, 165,000 new cases are diagnosed and 30,000 deaths are reported. Current therapies such as Androgen Depravation Therapy (ADT) and Anti-Androgen treatments such as Enzalutamide increase quality of life and extend survival but do not provide a definitive treatment and are ineffective in highly metastatic prostate cancer. Castrate Resistant Prostate Cancer (CRPC) is an untreatable highly metastatic form of prostate cancer and once diagnosed the survival rate is 1-2 years. Hence, the understanding of molecular mechanisms of CRPC is of critical importance. We previously linked prostate cancer to Abi1 gene. Abl interactor 1 (Abi1) is a scaffolding protein and an integral member of the WAVE Regulatory Complex (WRC). WRC is actin nucleation promoting factor that acts upstream of Arp2/3 to enhance the speed of actin polymerization and is critical for various cellular functions including cell-cell junction formation. Our previous research using a prostate cancer mouse models shows that loss of Abi1 expression leads to down-regulation of cellular adhesion proteins such as E-cadherin. Studies using our CRISPR KO RWPE cell line indicate that loss of Abi1 disrupts cell-cell junction formation via decreased levels of E-cadherin. Analysis of patient data demonstrated loss of Abi1 in a subset of CRPC patients. Castrate resistant tumor growth is androgen independent therefore anti-androgen therapy is ineffective. In search of a link between the androgen signaling and the role of Abi1 in prostate cancer we found that Abi1 gene contains androgen receptor (AR) binding sites. Consistent with the idea that Abi1 is an AR responsive gene, expression levels of Abi1 are increased following AR stimulation with the synthetic androgen, R1881, of the hormone sensitive cell line LNCaP. We also observed increased levels of E-cadherin at the cell-cell junctions. In contrast, cells lacking Abi1 do not form proper cell junctions neither respond to AR stimulation in the same way as wild type cells. We propose that Abi1 is a critical part of androgen signaling by promoting cell-cell junctions and tissue integrity. Supported by NCI R01 CA161018 (LK). Citation Format: Baylee Porter, Disharee Nath, Susan A. Krum, Gennady Bratslavsky, Vladimir A. Kuznetsov, Leszek Kotula. Androgen Receptor promotes localization of E-cadherin to cell-cell junctions through Abi1 signaling [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 5307.
Optimization of a synthetic $beta;-catenin-dependent promoter for tumor-specific cancer gene therapy
Authors: K LIPINSKI
Journal: Molecular Therapy (2004)

We recently published the construction and evaluation of a β-catenin-dependent, highly active promoter, CTP1, and its possible application for the treatment of colorectal cancer using gene-directed enzyme prodrug therapy with adenoviral (Ad) vectors. Alternative Ad-based approaches such as tumor-specific, replication-competent vectors and/or exploiting therapeutic gene products with intrinsic toxic activity, such as gibbon ape leukemia virus fusogenic membrane glycoprotein, diphtheria toxin A (DTA), and ricin, would demand a very tightly regulated promoter to avoid breakthrough replication and toxicity in nontumor tissue and Ad producer cell lines. In this study we optimized the activity/specificity profile of the synthetic β-catenin-dependent promoter by varying its basal promoter, the number of Tcf binding sites, and the distance between these and the basal promoter. The optimal promoter, CTP4, showed virtually undetectable expression in cells with normal β-catenin regulation but high level expression in cells deregulated for β-catenin. Using CTP4 we were able to generate, for the first time to our knowledge, an Ad vector expressing fully active wild-type DTA without the need for time-consuming and cumbersome production systems. CTP4 should be the promoter of choice for Ad-based gene therapies of tumors deregulated for β-catenin. We provide preliminary evidence that these may include prostate and ovarian as well as colorectal cancer.
Cherchez la chienne. Erythropoietic hypoplasia after exposure to gamma-benzene hexachloride
Authors: H. Vodopick
Journal: JAMA (1975)

PHYSICIANS are called on with increasing frequency to be sleuths. With the wide distribution of proprietary medicines and numerous chemical compounds, the ability to pinpoint any one of these as a cause of organ dysfunction or failure becomes a formidable task for the busy physician. The number of patients found to have aplastic anemia has apparently increased, presumably because of greater exposure to many toxic agents. Physicians caring for such patients know how difficult it is to determine which agent is the offender. Exposure to proved toxins may be overlooked because they appear in forms that mask their identity. To draw attention to one such agent that may cause marrow suppression is the purpose of this report. <h3>Report of a Case</h3> Because of an accidental fall down a flight of stairs, a 2-year-old boy, who had been in good health, was taken to a pediatrician. On physical examination, the patient
THE LATEST CANCER PARASITE
Journal: JAMA (1925)

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
Precursor lesions in familial melanoma. A new genetic preneoplastic syndrome
Authors: R. R. Reimer
Journal: JAMA (1978)

In seven consecutive melanoma-prone families, pigmented lesions with distinctive clinical and histologic characteristics occurred in 18 of 20 melanoma patients (90%) and 24 of 43 first-degree relatives (56%). Recognition of these lesions led to the detection of early-stage melanoma in six family members. This syndrome appears to represent an autosomal dominant trait and may serve as a cutaneous marker to identify persons at high risk for melanoma. (<i>JAMA</i>239:744-746, 1978)
A Treasure Trove of Hypothalamic Neurocircuitries Governing Body Weight Homeostasis
Authors: Claudia R. Vianna, Roberto Coppari
Journal: Endocrine Reviews (2010)

Changes in physical activities and feeding habits have transformed the historically rare disease of obesity into a modern metabolic pandemic. Obesity occurs when energy intake exceeds energy expenditure over time. This energy imbalance significantly increases the risk for cardiovascular disease and type 2 diabetes mellitus and as such represents an enormous socioeconomic burden and health threat. To combat obesity, a better understanding of the molecular mechanisms and neurocircuitries underlying normal body weight homeostasis is required. In the 1940s, pioneering lesion experiments unveiled the importance of medial and lateral hypothalamic structures. In the 1980s and 1990s, several neuropeptides and peripheral hormones critical for appropriate feeding behavior, energy expenditure, and hence body weight homeostasis were identified. In the 2000s, results from metabolic analyses of genetically engineered mice bearing mutations only in selected neuronal groups greatly advanced our knowledge of the peripheral/brain feedback-loop modalities by which central neurons control energy balance. In this review, we will summarize these recent progresses with particular emphasis on the biochemical identities of hypothalamic neurons and molecular components underlying normal appetite, energy expenditure, and body weight homeostasis. We will also parse which of those neurons and molecules are critical components of homeostatic adaptive pathways against obesity induced by hypercaloric feeding.
Safe transfer of civilian burn casualties
Authors: J. M. Stein
Journal: JAMA (1977)

The advisability of transporting severely burned civilian patients to a definitive burn-care facility during the first hours following injury is discussed and methods providing safe transport for 353 civilian burn patients are described. Feasibility of and methods for transporting patients over various distances are outlined and the problems of jet transportation presented. Adequate communication between referring and receiving physicians is imperative, as are adequate preparation before evacuation and maintenance of intravenous fluid resuscitation, intake and output records, and sterile technique during transport. (<i>JAMA</i>238:489-492, 1977)
Beneficial effects of colestipol-niacin on coronary atherosclerosis. A 4-year follow-up
Authors: L Cashin-Hemphill, W J Mack, J M Pogoda, M E Sanmarco, S P Azen, D H Blankenhorn
Journal: JAMA (1990)

The Cholesterol Lowering Atherosclerosis Study (CLAS) was a randomized, placebo-controlled, angiographic trial testing combined colestipol-niacin therapy in 162 subjects. Two-year results (CLAS-I) showed decreased atherosclerosis progression and increased regression. We now describe a subgroup of 103 subjects treated for 4 years (CLAS-II). Changes in blood lipid, lipoprotein-cholesterol, and apolipoprotein levels were maintained, and at 4 years significantly more drug-treated subjects demonstrated nonprogression (52% drug- vs 15% placebo-treated) and regression (18% drug- vs 6% placebo-treated) in native coronary artery lesions. Significantly fewer drug-treated subjects developed new lesions in native coronary arteries (14% drug- vs 40% placebo-treated) and bypass grafts (16% drug- vs 38% placebo-treated). These results confirm CLAS-I findings and indicate that regression can continue for 4 years. They reaffirm the need for early initiation of vigorous long-term lipid lowering therapy in coronary bypass subjects.
History
Journal: JAMA (1999)

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
PUBIC APOCRINE GLANDS AND ODOR
Journal: JAMA (1964)

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
Gerontologic Pharmacology
Authors: GEORGE M. STEINBERG
Journal: Annals of Internal Medicine (1982)

Letters and Corrections1 August 1982Gerontologic PharmacologyGEORGE M. STEINBERG, PH.D.GEORGE M. STEINBERG, PH.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-97-2-281_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We would like to bring to the attention of the scientific research community the recently published report of a workshop on gerontologic pharmacology (1) and a National Institute on Aging Pharmacology Program announcement (2). The elderly have a greater incidence of adverse drug reactions and of interactions between drugs than do young adults. Altered patterns of drug distribution and responsivenesss have been reported in the elderly. Because drugs are generally tested in young adults and dosage adjusted to their needs, it is not surprising that the elderly may respond differently. Much research is needed to determine where...References1. STEINBERG G and SCHNEIDER E. The National Institute on Aging's Second Workshop on Pharmacology and Aging, June 4-5, 1981. Pharmacologist. 1982;24:65-7. Google Scholar2. . Pharmacology Program. National Institutes of Health Guide for Grants and Contracts 11. 1982;5:42-4. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: GEORGE M. STEINBERG, PH.D.Affiliations: National Institute on Aging National Institutes of Health Bethesda, MD 20205 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 August 1982Volume 97, Issue 2Page: 281-281KeywordsAdverse reactionsAgingDrug distributionDrug interactionsDrugsElderlyPharmacologyYoung adults ePublished: 1 December 2008 Issue Published: 1 August 1982 PDF downloadLoading ...
THSNA 2016 Summit Abstract Proceedings
Journal: American Journal of Hematology (2016)

Abstract The above abstract from the THSNA 2016 Summit Abstract Proceedings, first published online in the American Journal of Hematology on 20 July 2016 in Wiley OnlineLibrary ( www.onlinelibrary.wiley.com ), and in Volume 91, Issue 9, p. E427, has been retracted by agreement between the authors, the journal Editor‐in‐Chief, Carlo Brugnara, and Wiley Periodicals, Inc. The retraction has been agreed due to concerns from the submitting authors that the abstract was inadvertently submitted prior to receiving approval from all authors and proper review of data analytics, thereby rendering it incomplete. Reference 2016 . Am. J. Hematol. , 91 : E427 . https://doi.org/ 10.1002/ajh.24471
Intravenous N-acetylcystine: the treatment of choice for paracetamol poisoning.
Authors: L F Prescott, R N Illingworth, J A Critchley, M J Stewart, R D Adam, A T Proudfoot
Journal: BMJ (1979)

One hundred cases of severe paracetamol poisoning were treated with intravenous N-acetylcysteine (acetyl-cysteine). There was virtually complete protection against liver damage in 40 patients treated within eight hours after ingestion (mean maximum serum alanine transaminase activity 27 IU/1). Only one out of 62 patients treated within 10 hours developed severe liver damage compared with 33 out of 57 patients (58%) studied retrospectively who received supportive treatment alone. Early treatment and acetylcysteine also prevented renal impairment and death. The critical ingestion-treatment interval for complete protection against severe liver damage was eight hours. Efficacy diminished progressively thereafter, and treatment after 15 hours was completely ineffective. Intravenous acetylcysteine was more effective than cysteamine and methionine and noticeably free of adverse effects. It is the treatment of choice for paracetamol poisoning.