tbuckley/cabot-search huggingface dataset:
Book Review Bloopers
Authors: CHARLES WELLER
Journal: Annals of Internal Medicine (1970)

Letters and Comments1 February 1970Book Review BloopersCHARLES WELLER, M.D.CHARLES WELLER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-72-2-289_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The October issue of ANNALS OF INTERNAL MEDICINE carried a review of my most recent book, The New Management of Stable Diabetes, and I point out two errors in the review: My name is spelled incorrectly; the price of the book is $6.75, and not $16.75.One other point needs clarification; Dr. Boshell's otherwise excellent review cites "unnecessary repetition." Some repetition, to allow for freedom of expression and emphasis, is intrinsic in a book that comprises the efforts of many contributors working independently.... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: 17 North Chatsworth Ave. Larchmont, N. Y. 10538 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1970Volume 72, Issue 2Page: 289-289KeywordsType 2 diabetes Issue Published: 1 February 1970 PDF downloadLoading ...
A3.24 Distinct profile of cytokine production by th17 cells in systemic sclerosis
Authors: Mariana Galante Santiago, Mariana Raposo, Tiago Carvalheiro, Ângela Andrade, Maria João Salvador, José António Pereira da Silva, Artur Paiva
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> The pathogenesis of systemic sclerosis (SSc) is largely unknown, although proinflammatory cytokines are considered to play an important role. <h3>Aims</h3> Investigate the pattern of expression of proinflammatory cytokines by peripheral blood (PB) Th17 cell and IL-2 and IL-17 relative gene expression in SSc and to explore their clinical associations. <h3>Methods</h3> This study included 41 SSc patients and 20 age- and sex-matched healthy controls (HC). SSc patients were classified according to LeRoy et al. as having limited cutaneous SSc (lSSc, n = 29) or diffuse cutaneous SSc (dSSc, n = 12). A further subdivision was made based upon clinical parameters of disease duration and clinical manifestations. Intracellular expression of IL-17, IL-2, TNF-α and IFN-γ in Th17 cells was assessed by flow cytometry. A detailed functional activity characterisation of Th17 cells was performed in a single multicolour data file obtained after merging the original six-colour-staining (eight-parameter) data files from each sample using the Infinicyt (Cytogonos) software. Relative gene expression of IL-2 and IL-17 in total PB cells was determined by qRT-PCR <h3>Results</h3> No differences were observed concerning the frequency of Th17 cells or Tc17 cells between SSc patients and HC. Th17 cells from both diffuse and limited SSc showed a higher expression of IL-2 (particularly in dSSc) than Th17 cells from HC. Similar observations were made for TNF-α expression but it only reached statistical significance in lSSc. Likewise, an increased frequency of Tc17 cells expressing IL-2 in lSSc was also observed. Eight distinct Th17 cell subpopulations according to their pattern of cytokine expression (IL-17, IL-2, TNF-α and IFN-γ) were identify after merging data files. A higher frequency of Th17 cells simultaneously producing simultaneously IL17, IL-2 and TNF-α was observed in lSSc. On the other hand a significantly lower frequency of Th17 cells simultaneously producing IL-17, TNF-α and IFN-γ was also observed in the same group. The percentage of Th17 cells producing only TNF-α or IFN-γ was significantly decreased in SSc patients compared to HC group. Moreover a higher IL-17 mRNA expression in total PB cells was observed in SSc patients and no differences were found concerning IL-2 mRNA levels. <h3>Conclusions</h3> These results suggest that Th17 cells are functionally altered in SSc patients, exhibiting a higher ability to simultaneously produce IL-17, IL-2 and TNF-α. We also observed in SSc patients increased levels of IL-17 mRNA expression in total PB cells. These data suggest that Th17 cells may be involved in pathophysiology and/or disease progression of SSc.
Effect of Alcohol on Serum Folate Level
Authors: Edward R. Eichner, Robert S. Hillman
Journal: Journal of Clinical Investigation (1973)

Alcohol was given orally and intravenously to normal and chronic alcoholic volunteers to study its effect on folate metabolism. Oral alcohol, given to nine subjects on a low folate diet, caused a greater fall in serum Lactobacillus casei folate levels than that seen in eight subjects on a low folate diet alone. This alcohol-induced fall in serum folate level occurred largely during the 1st day of the protocol. Although brief infusions of intravenous ethanol had no effect on serum folate level, a 13 h infusion caused a striking fall in serum folate level between the 8th and 10th h. When ethanol was stopped, the serum folate level returned rapidly to normal. Two chronic alcoholic subjects with different basal levels of serum folate were studied for several weeks on a low folate diet plus alcohol. The serum folate level fell promptly in each subject, rose when alcohol was temporarily stopped, and fell when alcohol was resumed. Folate-deficient megaloblastic anemia developed in 3 wk in the subject with initially marginal serum folate levels, but failed to develop in almost 7 wk in the subject with normal folate stores, as reflected by initially high serum folate levels. Thus, the alcohol-induced fall in serum folate level was apparently not a result of depletion of folate stores. In vitro experiments ruled out an assay artifact as an explanation for the alcohol-induced fall in serum L. casei folate level. It seems likely that alcohol interferes with the delivery of n-5-methyltetrahydrofolic acid from storage areas.
897 Homozygous deletion on chromosome 1P36.2 and hypermethylation of RIZ1 gene in hepatocellular carcinoma
Authors: H LI, C LIEW, C ZHANG, L YAU, P SANLAI, L HIN, K SUEN, J WANYEELAU, H LI
Journal: Hepatology (2003)

Hesperidin (HES) has been reported to exhibit anti-invasive and antimetastatic activities by suppressing the enzymatic activity of matrix metalloproteinase-9 (MMP-9). However, the underlying mechanism of anti-invasive activity remains unclear so far. First, we suggest that the expression of MMP-9 by TPA involves phosphorylation of IKK, p38, and PKC in hepG2. We also demonstrate that hesperidin reduced 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cell invasion and inhibited the secreted and cytosolic MMP-9 forms in HepG2 cells. Hesperidin significantly suppressed the TPA-induced the mRNA level of MMP-9. Hesperidin suppressed MMP-9 transcription by inhibiting nuclear factor-kappaB (NF-kappaB) and Activator protein 1 (AP-1) activity. Hesperidin suppressed TPA-stimulated NF-κB translocation into the nucleus through IκB inhibitory signaling pathways and also inhibited TPA-induced AP-1 activity by the inhibitory phosphorylation of p38 kinase and c-Jun N-terminal kinase (JNK) signaling pathways. In conclusion, Hesperidin might be a potent antiinvasive agent that suppresses the MMP-9 enzymatic activity via NF-kappaB an AP-1 signaling pathway.
Correction of the sickle cell disease mutation in human hematopoietic stem/progenitor cells
Authors: Megan D. Hoban, Gregory J. Cost, Matthew C. Mendel, Zulema Romero, Michael L. Kaufman, Alok V. Joglekar, Michelle Ho, Dianne Lumaquin, David Gray, Georgia R. Lill, Aaron R. Cooper, Fabrizia Urbinati, Shantha Senadheera, Allen Zhu, Pei-Qi Liu, David E. Paschon, Lei Zhang, Edward J. Rebar, Andrew Wilber, Xiaoyan Wang, Philip D. Gregory, Michael C. Holmes, Andreas Reik, Roger P. Hollis, Donald B. Kohn
Journal: Blood (2015)
The Image Tetrahedron in Man Determined by Reciprocal Stimulation of a Tridimensional Esophageal Electrode
Authors: JACOB I. HIRSCH, STANLEY A. BRILLER, CHARLES E. KOSSMANN, Nathan Marchand
Journal: Circulation Research (1956)

The anatomic apices of a tetrahedron were located on the image surface of living man by reciprocal stimulation of an electrode placed in the esophagus at the assumed electric center of the heart. The rectilinear components of the three-dimensional electrode were not oriented with respect to the axes of the body. Therefore, it was possible to determine the shape of the image tetrahedron but not its orientation in the body. The method is applicable to living man with the electrode placed at any assumed electric center of the heart.
Hyperthermia Sensitizes Breast Cancer Stem Cells to Radiation Therapy.
Authors: R. Atkinson, M. Zhang, P. Diagaradjane, S. Krishnan, J. Rosen, J. Rosen, J. Chang, J. Chang
Journal: Cancer Research (2009)

Abstract Background In cancer, metastatic disease and recurrence are hypothesized to result, at least in part, from the residual cancer stem cells (CSCs), also referred to as tumor-initiating cells(TICs), which evade initial treatment. In several genetically engineered mouse models that resemble human breast cancer, the tumor subpopulation CD29+/CD24+/lin- has been shown to be more tumorigenic as compared to other subpopulations by in vitro and in vivo assays. We and others have demonstrated that the tumorigenic CD29+/CD24+/lin- subpopulation repairs radiation-induced DNA strand breaks more efficiently than the other subpopulations. Therefore, we hypothesized that hyperthermia, a documented means of inhibiting DNA repair, may radiosensitize CSCs to radiation therapy(RT) by delaying and inhibiting the repair of DNA strand breaks. Methods To test this hypothesis, we assayed for tumorigenic CD29+/CD24+/lin- cells in p53null mouse mammary tumor model with and without radiation, and in combination with hyperthermia (42°C) administered as optically-activated gold nanoparticles. We then determined if there was a decrease in functional CSCs by FACS analysis and limiting dilution transplantation assays. Results These studies confirmed that CD29+/CD24+/lin- cells were more radiation resistant and that their relative proportion was increased after RT, as compared to the other cell populations. However, the addition of hyperthermia increased the sensitivity of the CD29+/CD24+/lin- subpopulation to radiation. Radiation treatment alone in vivo resulted in a decrease in tumor size, but the percentage of tumorigenic cells increased as compared to untreated controls. In contrast, following post-treatment with 20 minutes of local hyperthermia, using intravenously administered optically activated gold nanoparticles, a larger regression in tumor size was observed, without a concomitant increase in the percentage of CD29+/CD24+/lin- tumorigenic cells. Using the functional limiting dilution transplantation assay to assay for CSCs, we showed that 48 hours after treatment cells derived from tumors treated with RT exhibited an increased frequency of TICs as compared to untreated controls, and tumors treated with radiation and hyperthermia. In addition, clonogenic survival assays of this tumorigenic subpopulation had consistent results with the in vivo data. Conclusion These results suggest that localized hyperthermia serves as a simple strategy to selectively sensitize the radioresistant subpopulation of CSCs to enhance their response to radiation therapy. The mechanisms responsible for these effects of hyperthermia are currently under investigation. Supported by grant NCI R01 CA112305 and CA16303. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 506.
Zur Psychodynamik der Ess-und Stehlsucht (Hyperorexie und Kleptomanie)
Authors: H.U. Ziolko
Journal: Psychotherapy and Psychosomatics (1966)

Research Articles| February 11 2010 Zur Psychodynamik der Ess-und Stehlsucht (Hyperorexie und Kleptomanie) Subject Area: Psychiatry and Psychology H.U. Ziolko H.U. Ziolko Psychotherapeutische Abteilung der Psychiatrischen und Neurologischen Klinik der Freien Universität Berlin (Direktor: Prof. Dr. H. Selbach) Search for other works by this author on: This Site PubMed Google Scholar Psychother Psychosom (1966) 14 (3): 226–236. https://doi.org/10.1159/000285827 Article history Published Online: February 11 2010 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation H.U. Ziolko; Zur Psychodynamik der Ess-und Stehlsucht (Hyperorexie und Kleptomanie). Psychother Psychosom 1 March 1966; 14 (3): 226–236. https://doi.org/10.1159/000285827 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsPsychotherapy and Psychosomatics Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1966Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
Abstract LB-126: ARID1B is a specific vulnerability in ARID1A-mutant cancers
Authors: Katherine Helming, Xiaofeng Wang, Boris Wilson, Francisca Vazquez, Jeffrey Haswell, Haley Manchester, Youngha Kim, Gregory V. Kryukov, Mahmoud Ghandi, Andrew J. Aguirre, Zainab Jagani, Zhong Wang, Levi Garraway, William Hahn, Charles Roberts
Journal: Cancer Research (2014)

Abstract Cancer genome sequencing efforts have revealed that ARID1A is frequently mutated in many types of cancer. Inactivating mutations occur in 45% of ovarian clear cell and endometrioid carcinomas, 19% of gastric cancers, 19% of bladder cancers, 14% of hepatocellular cancers, 12% of melanomas, and less frequently in colorectal, lung, breast and pancreatic cancers. ARID1A has also been validated as having bona fide tumor suppressor properties. Consequently, identification of specific vulnerabilities conferred by ARID1A mutation would have major relevance for human cancer. We therefore performed a systematic search for genetic vulnerabilities created by ARID1A mutation. Out of 9000+ genes screened, ARID1B, a related but mutually exclusive homolog of ARID1A in the SWI/SNF chromatin remodeling complex, was the number one gene preferentially required in ARID1A-mutant cancer cells. In validation studies, we find that knockdown of ARID1B indeed specifically impairs the proliferation of ARID1A-mutant cancer cell lines. Mechanistically, we show that loss of ARID1B in ARID1A-mutant cancer cell lines destabilizes the SWI/SNF complex and results in dissociation of the catalytic ATPase subunit SMARCA4. We further show that this finding also holds true in primary murine fibroblasts genetically engineered conditional for ARID1A. Our findings demonstrate that cancer cell lines harboring mutations in ARID1A are specifically dependent upon ARID1B and provide insight into the structural role of ARID1A/B in the SWI/SNF complex. Intriguingly, we also find that ARID1A and ARID1B are frequently co-mutated in cancer, but that all ARID1A-deficient cancers retain at least one ARID1B allele. These results suggest that loss of ARID1A and ARID1B alleles cooperatively promotes cancer formation but also results in a unique functional dependence. These results also indicate that ARID1B could be considered a potential therapeutic target for the wide variety of ARID1A-mutant human cancers. [K.H. and X.W contributed equally to this work.] Citation Format: Katherine Helming, Xiaofeng Wang, Boris Wilson, Francisca Vazquez, Jeffrey Haswell, Haley Manchester, Youngha Kim, Gregory V. Kryukov, Mahmoud Ghandi, Andrew J. Aguirre, Zainab Jagani, Zhong Wang, Levi Garraway, William Hahn, Charles Roberts. ARID1B is a specific vulnerability in ARID1A-mutant cancers. [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 LB-126. doi:10.1158/1538-7445.AM2014-LB-126
Inhibition of Interleukin-6 with CNTO328, an Anti-Interleukin-6 Monoclonal Antibody, Inhibits Conversion of Androgen-Dependent Prostate Cancer to an Androgen-Independent Phenotype in Orchiectomized Mice
Authors: Lauren Wallner, Jinlu Dai, June Escara-Wilke, Jian Zhang, Zhi Yao, Yi Lu, Mohit Trikha, Jeffrey A. Nemeth, Mohamed H. Zaki, Evan T. Keller
Journal: Cancer Research (2006)

Abstract Initially, prostate cancer is androgen dependent. However, most cases progress to an androgen-independent state through unknown mechanisms. Interleukin-6 (IL-6) has been associated with prostate cancer progression including activation of the androgen receptor (AR). To determine if IL-6 plays a role in the conversion of prostate cancer from androgen dependent to androgen independent, we established androgen-dependent LuCaP 35 human prostate cancer xenografts in nude mice, castrated the mice, and blocked IL-6 activity using a neutralizing antibody (CNT0328) for a period of 18 weeks. IL-6 inhibition increased survival of mice and inhibited tumor growth, as reflected by decreased tumor volume and prostate-specific antigen levels, compared with that in mice receiving isotype control antibody. To test the effect of IL-6 inhibition on the conversion from androgen dependent to androgen independent, tumor cells from the treated mice were assessed for their androgen dependence both in vitro and by implanting them into sham-operated or orchiectomized mice. Tumor cells derived from the isotype-treated animals converted to androgen-independent state, whereas tumor cells from the anti-IL-6 antibody-treated mice were still androgen dependent in vitro and in vivo. Although there was no difference in AR levels between the androgen-independent and androgen-dependent tumors, IL-6 inhibition promoted both apoptosis and inhibited cell proliferation in tumors and blocked the orchiectomy-induced expression of histone acetylases, p300 and CBP, which are AR cofactors. These data show that IL-6 contributes to the development of androgen independence in prostate cancer and suggest that it mediates this effect, in part, through modulation of p300 and CBP. (Cancer Res 2006; 66(6): 3087-95)
Fast track patients more likely to beat colorectal cancer
Authors: Roger Dobson
Journal: BMJ (2001)

Early detection rates for colorectal cancer at a district general hospital in Wales have more than doubled since the setting up of a rapid access, subspecialty unit.

Emergency surgery rates have also fallen substantially, down from 29.2% to 8.2%; mortality and waiting times have reduced too.

An audit of the first three years of the unit and the …
Pathologic features of myocardial hamartomas causing childhood tachyarrhythmias.
Authors: D L Kearney, J L Titus, E P Hawkins, D A Ott, A Garson
Journal: Circulation (1987)

We have observed in 11 infants, aged 2 years or less, a distinct clinicopathologic lesion responsible for tachyarrhythmias that were fatal in 96% (25/26) of previously reported cases. Nine of the 11 patients, who underwent electrophysiologic mapping and surgical excision of the lesion, have survived, with follow-up periods ranging from 1 month to 6 years. The morphologic findings in these 11 patients and in the 26 cases cited in the literature are reviewed. Pathogenic considerations have included viral-induced lesion, cardiomyopathy, neoplasm, and developmental disorder of Purkinje cells. We believe this lesion to be a myocardial hamartoma. Supportive evidence includes prevalence in infants, tumorlike growth pattern without mitotic figures, and association of other developmental abnormalities. Through electrophysiologic mapping, this myocardial hamartoma is potentially accessible to surgical excision and long-term cure.
Better health statistics are possible
Authors: Abdallah Bchir, Zulfiqar Bhutta, Fred Binka, Robert Black, Debbie Bradshaw, Geoff Garnett, Kenji Hayashi, Prabhat Jha, Richard Peto, Cheryl Sawyer, Bernhard Schwartländer, Neff Walker, Michael Wolfson, Derek Yach, Basia Zaba
Journal: The Lancet (2006)
Integrated care results in fewer elderly people dying in hospital
Authors: M. A. H. Cohen, P. McCarthy, Y. Khan
Journal: BMJ (2012)

We agree that more integrated medical care is needed in the community.1 Many patients in residential and nursing homes lack access to appropriate medical care. This can lead to unnecessary hospital admissions and patients’ lives ending needlessly in hospital. Various models for delivering medical care in nursing homes have been proposed.2

Three …
New Bethesda Terminology and Evidence-Based Management Guidelines for Cervical Cytology Findings
Authors: Mark H. Stoler
Journal: JAMA (2002)

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