tbuckley/cabot-search huggingface dataset:
Postoperative starvation after gastrointestinal surgery
Authors: F Bozzetti
Journal: BMJ (2002)

Editor—We appreciated Lewis et al's wise conclusions in their study: “there seems to be no clear advantage to keeping patients nil by mouth after elective gastrointestinal resection.”1 The subtitle of the accompanying editorial sounded less prudent: “early feeding is beneficial.”2 This positive statement stimulates readers to raise several questions that cannot be answered from the study. Which diet is beneficial? By which route? And compared with which intravenous feeding?

From table 1 we note that four types of diet were used in the 11 studies (standard, elemental, oral, and immune enhancing), through four different routes (oral, nasoduodenal, nasojejunal, and jejunostomy), giving rise to seven different combinations. No indication is given of the quality and quantity of the intravenous nutrition in the control groups. This is because the original studies were more concerned with feasibility, safety, and tolerance of enteral feeding than with its effect on postoperative outcome. The control diet was consequently defined only as conventional or traditional treatment or routine intravenous crystalloid solutions or hypocaloric fluids. Moreover, in one study the control group was not nil by mouth, as a placebo was given through a nasoduodenal feeding tube.3

This issue is not an academic one. In a randomised clinical trial Lobo et al showed in postoperative patients that salt and water restriction (water ⩽2 l and sodium ⩽77 mmol/day) was significantly better than standard management (water roughly 3 l and sodium roughly 154 mmol/day) in reducing postoperative gastric emptying times, time to passage of flatus and stools, and postoperative stay.4

In the absence of clear information on the composition of the intravenous support in the control arm we can speculate that the advantage of early feeding, as reported in this meta-analysis, reflects not a true benefit but simply the lack of detriment due to the intravenous standard treatment.

Finally, we agree with Lewis et al that the role of early enteral feeding should be assessed in a randomised clinical trial. Such a trial, sponsored by the Italian Society of Parenteral and Enteral Nutrition, was recently done in 317 malnourished patients with cancer who were candidates for elective gastrointestinal surgery. They were randomised to two postoperative isoenergetic and isoprotein nutritional regimens given enterally or parenterally; the results have just been reported.5
CSIG-12CLK2 IS A KEY REGULATOR OF THE CELL CYCLE THROUGH FOXO3a/p27 IN GLIOMA MODELS
Authors: Soon Young Park, Yuji Piao, Craig R. Thomas, Fuller Greg, John F. de Groot
Journal: Neuro-Oncology (2015)

CSIG-12. CLK2 IS A KEY REGULATOR OF THE CELL CYCLE THROUGH FOXO3a/p27 IN GLIOMA MODELS Soon Young Park, Yuji Piao, Craig R. Thomas, Fuller Greg, and John F. de Groot; UT MD Anderson Cancer Center, Houston, TX, USA TheCdc2-likekinases (CLKs)phosphorylateSR(serineandarginine-rich)proteins, which regulate RNA splicing. Inhibitors of CLK protein kinases suppress cell growth and induce apoptosis. The Cdc2-like kinases 2 (CLK2) haspreviously been reported to regulate various physiological processes. Phosphorylation of CLK2 at serine 34 and threonine 127 by Akt controls cells survival after ionizing radiation. The function of CLK2 in glioblastoma has not been previously described. We investigated the regulation of CLK2 in glioma stem cells (GSCs) and the impact of CLK2 expression on tumor proliferation in vitro and in vivo. CLK2 expression in two GSCs was stably knocked down using infection with a specific shRNA-containing lentivirus. We compared RPPA (Reverse phase protein array) to identify CLK2-associated proteins. The results indicate that CLK2 knockdown influenced the expression of survival, proliferation and cell cycle related proteins. These results were validated using Western blot and FACS analysis. We found that knockdown of CLK2 induced G1/S-phase check point arrest in several GSCs. Depletion of CLK2 regulates dephosphorylation of Akt whereas phosphorylation of ERK and p38 MAPK were not changed in GSC7-2, GSC8-11 and GSC17 or increased in GSC272. Knock down of CLK2 decreased phosphorylation of FOXO3a, which translocated to the nucleus. FOXO3a in nucleus increased p27 expression and arrest G1 phase cell cycle. These results were confirmed in two orthotopic xenograft models of glioma. The survival of mice orthotopically implanted with GSC272 CLK2 knockdown cells was significantly prolonged compared to mice implanted with GSC272-shRNA control cells. In addition, tumor volumes were significantly decreased in the CLK2 knockdown groups compared to controls. Knockdown of CLK2 reduced the phosphorylation of FOXO3a and Ki67 in the two in vivo studies. Our findings suggest that CLK2 may play a role in the control of cell cycle and survival of glioblastoma through FOXO3a/p27. Neuro-Oncology 17:v66–v68, 2015. doi:10.1093/neuonc/nov210.12 Published by Oxford University Press on behalf of the Society for Neuro-Oncology 2015.
LIM Kinase Inhibitor Pyr1 Reduces the Growth and Metastatic Load of Breast Cancers
Authors: Chloé Prunier, Véronique Josserand, Julien Vollaire, Evelyne Beerling, Christos Petropoulos, Olivier Destaing, Christopher Montemagno, Amandine Hurbin, Renaud Prudent, Leanne de Koning, Reuben Kapur, Pascale A. Cohen, Corinne Albiges-Rizo, Jean-Luc Coll, Jacco van Rheenen, Marc Billaud, Laurence Lafanechère
Journal: Cancer Research (2016)

Abstract LIM kinases (LIMK) are emerging targets for cancer therapy, and they function as network hubs to coordinate actin and microtubule dynamics. When LIMKs are inhibited, actin microfilaments are disorganized and microtubules are stabilized. Owing to their stabilizing effect on microtubules, LIMK inhibitors may provide a therapeutic strategy to treat taxane-resistant cancers. In this study, we investigated the effect of LIMK inhibition on breast tumor development and on paclitaxel-resistant tumors, using a novel selective LIMK inhibitor termed Pyr1. Treatment of breast cancer cells, including paclitaxel-resistant cells, blocked their invasion and proliferation in vitro and their growth in vivo in tumor xenograft assays. The tumor-invasive properties of Pyr1 were investigated in vivo by intravital microscopy of tumor xenografts. A striking change of cell morphology was observed with a rounded phenotype arising in a subpopulation of cells, while other cells remained elongated. Notably, although Pyr1 decreased the motility of elongated cells, it increased the motility of rounded cells in the tumor. Pyr1 administration prevented the growth of metastasis but not their spread. Overall, our results provided a preclinical proof of concept concerning how a small-molecule inhibitor of LIMK may offer a strategy to treat taxane-resistant breast tumors and metastases. Cancer Res; 76(12); 3541–52. ©2016 AACR.
SP0080 Autoantibodies in Dermatomyositis
Authors: N. McHugh
Journal: Annals of the Rheumatic Diseases (2015)

There are an increasing number of myositis-related autoantibodies found in adult and juvenile dermatomyositis (JDM) that identify distinct clinical profiles of disease, and may facilitate diagnosis and disease management. In JDM autoantibodies to MDA5, NXP2 and TIF1γ account for approximately 50% of cases and identify different profiles of disease (e.g. anti-NXP2 and calcinosis). In adult-onset disease there are important additional risks such as between anti-TIF1γ and cancer and between anti-MDA5 and lung disease, and others such as anti-Mi2 are more common. The potential for using autoantibody levels to monitor disease activity and adjust therapy needs more exploration which will be possible when quantitative assays are more widely available. <h3>Disclosure of Interest</h3> None declared
Global survey of the omega-3 fatty acids, docosahexaenoic acid and eicosapentaenoic acid in the blood stream of healthy adults
Authors: Ken D. Stark, Mary E. Van Elswyk, M. Roberta Higgins, Charli A. Weatherford, Norman Salem
Journal: Progress in Lipid Research (2016)

Studies reporting blood levels of the omega-3 polyunsaturated fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), were systematically identified in order to create a global map identifying countries and regions with different blood levels. Included studies were those of healthy adults, published in 1980 or later. A total of 298 studies met all inclusion criteria. Studies reported fatty acids in various blood fractions including plasma total lipids (33%), plasma phospholipid (32%), erythrocytes (32%) and whole blood (3.0%). Fatty acid data from each blood fraction were converted to relative weight percentages (wt.%) and then assigned to one of four discrete ranges (high, moderate, low, very low) corresponding to wt.% EPA+DHA in erythrocyte equivalents. Regions with high EPA+DHA blood levels (>8%) included the Sea of Japan, Scandinavia, and areas with indigenous populations or populations not fully adapted to Westernized food habits. Very low blood levels (≤4%) were observed in North America, Central and South America, Europe, the Middle East, Southeast Asia, and Africa. The present review reveals considerable variability in blood levels of EPA+DHA and the very low to low range of blood EPA+DHA for most of the world may increase global risk for chronic disease.
Abstract P2-05-13: A novel mutagenesis screen identifies <i>SHARPIN</i> as a breast cancer metastasis gene that predicts survival of breast cancer patients
Authors: VM Bii, DT Rae, GD Trobridge
Journal: Cancer Research (2016)

Abstract Breast cancer (BC) is a heterogeneous disease and the second leading cause of malignancy among women in the U.S.. Metastasis of the primary tumor results in poor prognosis and increased mortality and the molecular mechanisms by which metastatic tumors occur are not well understood. Identifying the genes that drive the metastatic process could provide targets for improved therapy and biomarkers to improve outcomes for BC patients. Here, we utilized a replication-incompetent gammaretroviral vector (γRV) to perform a forward insertional mutagenesis screen to identify genes involved in BC metastasis. In this approach, BC cells mutagenized with a γRV were xenotransplanted into the mammary fat pad of immunodeficient mice, and primary tumors and metastases were allowed to develop. Metastatic lesions were collected and analyzed for proviral integration sites to identify vector integration sites and nearby candidate metastasis genes. The γRV has a bacterial origin of replication and kanamycin resistance gene that allows for rescue in bacteria and rapid identification of vector integration sites. Using this approach, we identified the previously described metastasis gene WWTR1, and several other novel candidate metastasis genes including SHARPIN. SHARPIN was then independently validated as a BC metastasis gene in vivo using RNAi. Analysis of patient data showed that SHARPIN expression predicts metastasis-free survival after adjuvant chemotherapy (p &amp;lt; 0.005, Concordance Index = 55.3, Risk Groups Hazard Ratio = 1.87). Our replication-incompetent γRV approach is efficient and has broad potential to identify genes involved in oncogenic processes for BC and other cancers. Keywords Insertional mutagenesis screen, Gammaretroviral vector (γRV), Metastasis, Inducible shRNA, Prognostic biomarker. Citation Format: Bii VM, Rae DT, Trobridge GD. A novel mutagenesis screen identifies SHARPIN as a breast cancer metastasis gene that predicts survival of breast cancer patients. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P2-05-13.
Psychopathology in individuals with sexual dysfunction
Authors: L R Derogatis, J K Meyer, K M King
Journal: American Journal of Psychiatry (1981)

The literature contains contradictory reports on the psychiatric status of individuals with sexual dysfunction. As a step toward resolving the controversy the authors administered the SCL-90-R to a large series of patients who sought treatment for sexual disorders (N = 325). Psychiatric evaluations were also done for each patient. Results showed disproportionate levels of psychological distress, reflected in SCL-90-R symptom profiles; approximately one-third of the 199 men and one-half of the 126 women in the series were also assigned psychiatric diagnoses. Findings provided evidence suggesting that the various sexual dysfunctions have characteristic symptom profiles; however, interpretation should be cautious because the cause-and-effect relationship between psychological distress and sexual dysfunctions remains complex and uncharted.
In Vivo PET Imaging of HDL in Multiple Atherosclerosis Models
Authors: Carlos Pérez-Medina, Tina Binderup, Mark E. Lobatto, Jun Tang, Claudia Calcagno, Luuk Giesen, Chang Ho Wessel, Julia Witjes, Seigo Ishino, Samantha Baxter, Yiming Zhao, Sarayu Ramachandran, Mootaz Eldib, Brenda L. Sánchez-Gaytán, Philip M. Robson, Jason Bini, Juan F. Granada, Kenneth M. Fish, Erik S.G. Stroes, Raphaël Duivenvoorden, Sotirios Tsimikas, Jason S. Lewis, Thomas Reiner, Valentín Fuster, Andreas Kjær, Edward A. Fisher, Zahi A. Fayad, Willem J.M. Mulder
Journal: JACC. Cardiovascular imaging (2016)
Routine Chromoendoscopy for Gastrointestinal Diseases: Indications Revised
Authors: M.  Kida, K.  Kobayashi, K.  Saigenji
Journal: Endoscopy (2003)

Can we be sure that we have identified every lesion after an endoscopic examination? We may believe we have seen all of the sites that need to be examined - but what percentage of the cancers diagnosed are early ones? In our department, some 50-60 % of lesions identified are early gastric cancers, but this still means that 40-50 % of lesions found represent advanced gastric cancer. Of course, the principal reason for late diagnosis is late presentation; however, a proportion of cases are likely to be due to lesions being overlooked during endoscopy.
Updosing nonsedating antihistamines in patients with chronic spontaneous urticaria: a systematic review and meta-analysis
Authors: S. Guillén-Aguinaga, I. Jáuregui Presa, E. Aguinaga-Ontoso, F. Guillén-Grima, M. Ferrer
Journal: British Journal of Dermatology (2016)

There is a lack of large, randomized, double-blind studies that address antihistamine updosing for chronic spontaneous urticaria (CSU). The objective of this systematic review is to explore and analyse available data to provide clinical evidence for the efficacy of antihistamine updosing. We searched the literature in Medline, Scopus, Google Scholar, Embase, Web of Science and Cochrane databases using the keywords 'chronic, urticaria, antihistamines' to identify studies published between January 1990 and November 2014. We assessed quality using the Jadad score that evaluates quality of randomization, double-blinding and losses to follow-up. We identified 1042 articles and 15 articles were included in the final evaluation. We performed two meta-analyses, one that included studies that analysed treatment response among groups receiving different antihistamine dosages vs. placebo, and another that analysed antihistamine updosing in those patients who did not respond to standard dosages. Only five articles obtained a high quality level score. We did not find significant differences in response rates or number of weals in those patients who received a standard dosage vs. a high dosage. We found a significant improvement only in the pruritus variable of the Urticaria Activity Score scale. The estimated relative risk for improvement by increasing the antihistamine dosage was 2·27 [95% confidence interval (CI) 1·68-3·06]; however, there was significant heterogeneity. The proportion of nonrespondent patients with CSU who responded to antihistamine updosing was 63·2% (95% CI 57-69·6). We found that updosing antihistamines significantly improved control of pruritus but not weal number. However, the relative weakness of the studies and the significant heterogeneity among them made it difficult to reach a final conclusion.
Aldolase in the Serum and Tissues of Tumor-Bearing Animals&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;
Authors: John A. Sibley, Albert L. Lehninger
Journal: JNCI Journal of the National Cancer Institute (1949)

Aldolase in the Serum and Tissues of Tumor-Bearing Animals Get access John A. Sibley, John A. Sibley Search for other works by this author on: Oxford Academic PubMed Google Scholar Albert L. Lehninger Albert L. Lehninger Department of Surgery, University of Chicago Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 9, Issue 4, February 1949, Pages 303–309, https://doi.org/10.1093/jnci/9.4.303 Published: 01 February 1949 Article history Received: 19 August 1948 Published: 01 February 1949
Anniversary reactions masquerading as manic-depressive illness
Authors: J O Cavenar, J L Nash, A A Maltbie
Journal: American Journal of Psychiatry (1977)

The authors suggest that many patients diagnosed as having manic-depressive illness, depressed type, may in fact be experiencing anniversary reactions--time-specific psychological and physiological reactions to a past trauma. They report three cases of cyclic depressive disorder, two of which were first diagnosed as manic-depressive illness, depressed type. Careful, complete interviewing and attention to temporal sequence led to the correct diagnosis of anniversary reaction.
Prevalence of traumatic early life events in 31 agoraphobic patients with panic attacks
Authors: C Faravelli, T Webb, A Ambonetti, F Fonnesu, A Sessarego
Journal: American Journal of Psychiatry (1985)

The rate of traumatic early life events in 31 agoraphobic subjects with panic attacks was significantly higher than that in matched control subjects. Experience of maternal separation, parental divorce, and events occurring after the age of 4 years was significantly more common.
Atlas of Minimally Invasive Surgery
Journal: JAMA (2006)

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
Childhood Cancer and Nuclear Installations
Authors: A M Stewart
Journal: BMJ (1994)

Ed Valerie Beral, Eve Roman, Martin Bobrow BMJ, pounds sterling 27.95, pp 453 ISBN 0-7279-0815-4

The late Martin Gardner, to whom this book is dedicated, remains a central figure in the current debate about childhood leukaemia in the vicinity of nuclear installations. Most of his papers can be found in the BMJ or the Lancet. There are, however, arguments that take one further afield, such as whether childhood leukaemia can be caused by small leakages of radioactivity from nuclear power plants, or by fathers following occupations that increase the risk of sperm cell mutations, or by unusual patterns of migration increasing the risk of meeting with a rare leukaemia virus. These arguments are of great interest to lay people as well as doctors. So Beral, Roman, and Bobrow have done a public service by providing easy access to more than 50 papers, abstracts, letters, editorials, and reports published since 1984 and …
Abstract B43: Dose and context-dependent roles for Arid1a in liver tumorigenesis
Authors: Xuxu Sun, Sam Wang, Liem Nguyen, Hao Zhu
Journal: Cancer Research (2016)

Abstract Frequent Arid1a loss-of-function mutations suggest tumor suppressive roles, but the functional impact of Arid1a and SWI/SNF chromatin-remodeling aberrations in human cancer are not clear. Liver-specific Arid1a knockout mice do not develop cancer after 15 months and surprisingly, homozygous mice are potently protected from diethylnitrosamine (DEN) + carbon tetrachloride induced hepatocellular carcinoma (HCC). This is likely due to the fact that Arid1a deficient livers are resistant to chemical damage in a Cytochrome P450 dependent fashion. To determine if genetic drivers of cancer might reveal additional roles for Arid1a, we showed that Arid1a loss results in increased survival in a MYC driven liver cancer model. Given the physical interactions between MYC and Arid1a and a global reduction in mRNA levels, we hypothesize that MYC's transcriptional activities are constrained by the lack of normal SWI/SNF chromatin remodeling. Interestingly, in vivo anti-Arid1a siRNA delivery to mice overexpressing MYC also prolonged survival, demonstrating that mutation timing does not explain the lack of tumor suppressor activity. Our models build the case that Arid1a is not a bona fide tumor suppressor gene in many important contexts. Citation Format: Xuxu Sun, Sam Wang, Liem Nguyen, Hao Zhu. Dose and context-dependent roles for Arid1a in liver tumorigenesis. [abstract]. In: Proceedings of the AACR Special Conference on Chromatin and Epigenetics in Cancer; Sep 24-27, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2016;76(2 Suppl):Abstract nr B43.