tbuckley/cabot-search huggingface dataset:
Molecular Switch Triggers Fats’ Harm
Authors: Tracy Hampton
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
Abstract 2372: Validity of the MEDFICTS Dietary Assessment Questionnaire in a Diverse Population
Authors: Heidi Mochari, Qian Gao, Lori Mosca
Journal: Circulation (2007)

Background: The National Cholesterol Education Program (NCEP) recommends MEDFICTS, a rapid dietary fat screening instrument, for assessment of adherence to the Adult Treatment Panel (ATP) III Therapeutic Lifestyle Change (TLC) diet (Score &lt; 40 points = &lt; 7% of calories from saturated fat, &lt;30% of calories from total fat, and &lt;200mg dietary cholesterol/day). MEDFICTS has only been validated in small, select populations and its utility in diverse clinical settings is unknown. The purpose of this study was to evaluate the ability of MEDFICTS to identify individuals non-adherent to a TLC diet against a gold standard in an ethnically diverse population. Methods: MEDFICTS was administered concurrently with the Gladys Block Food Frequency Questionnaire to participants (n=470; 35% non-white; 66% female; mean age 48.1 ± 13.6y) in the NHLBI F amily I ntervention T rial for Heart Health ( F.I.T. Heart ) at the baseline screening visit. Correlation, agreement, sensitivity and specificity analyses were conducted overall and by sex, age, and race/ethnicity. Results: MEDFICTS score correlated significantly with % calories from saturated fat (r=.51, p&lt;.0001), % calories from total fat (r=.30, p&lt;.0001), and mg/day dietary cholesterol (r=.53, p=&lt;.0001). Categorical agreement between MEDFICTS score &lt;40 and Gladys Block on TLC diet adherence was poor overall (κ = 0.07) and for individual TLC components: &lt;7% calories from saturated fat (κ=.12), &lt;30% calories from total fat (κ=.16), &lt;200mg dietary cholesterol per day (κ=.34). Sensitivity of MEDFICTS to correctly identify TLC diet adherence was 84% and did not differ significantly by sex, age, or race/ethnicity. Specificity of MEDFICTS to correctly identify non-adherence to TLC diet was low (57%) and was significantly worse for females than males (48% vs. 74%; p&lt;.0001), but did not differ significantly in older vs. younger participants or among whites and non-whites. Conclusion: The NCEP ATP III MEDFICTS dietary assessment questionnaire performed poorly as a screening tool to correctly identify patients non-adherent to a TLC diet. Our data suggest a re-calibration of the instrument to improve specificity may increase its clinical utility.
Rab and SNARE isoform expression in cytotoxic T-cells (CTL)*1Potential players in regulated release of granzyme-B (GrB)
Authors: D.L. Garofoli, S.O. Odemuyiwa, M.R. Logan, K. Lo, R.C. Bleackley, R. Moqbel
Journal: Journal of Allergy and Clinical Immunology (2004)
Rocks of Central Park
Authors: Harriet O. Kelley
Journal: JAMA (2002)

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
Checkpoint responses and repair of broken yeast chromosome.
Authors: James E. Haber, Jung-Ae Kim, Jacob Harrison
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

SY06-01 

Using a galactose-inducible HO endonuclease to create a site-specific double strand break (DSB) on one chromosome of budding yeast, it is possible to analyze both the mechanisms of DSB repair and also the ways that cells turn on and later turn off the DNA damage checkpoint. A single double-strand break, if not repaired, is sufficient to cause cells to arrest prior to mitotic anaphase for as long as 6 generation times, after which cells adapt and resume cell cycle progression even though still suffering DNA damage. The activation of this checkpoint, which can be monitored by hyperphosphorylation of the ATR-dependent Rad53 (Chk2) kinase, is delicately balanced; repair by homologous recombination (gene conversion) using an intrachromosomal donor does not trigger the checkpoint, but the longer time required to accomplish repair from an interchromosomal donor is sufficient to trigger arrest. a more rapid response, is the ATM- or ATR-dependent phosphorylation of histone H2AX (virtually of yeast histone H2A is of the “X” type, able to be phosphorylated at a C-terminal SQE sequence (termed ∈3-H2AX). In yeast, about 50 kb of chromatin around the DSB site is phosphorylated; however heterochromatic sequences are unmodified. Unlike in mammals, ∈3-H2AX modification has little effect on DSB repair, except in the case of sister-chromatid repair, when the recruitment of cohesin to the region covered by ∈3-H2AX markedly facilitates repair. Recently we have focused our attention on several phosphatases that are important in regulating the checkpoint kinases and their downstream targets. The PP2C phosphatases Ptc2 and Ptc3 are required to turn off the DNA damage checkpoint after DSB repair has been accomplished; when they are absent cells fail to recover and remain permanently arrested. Several other genes required for recovery will also be discussed. When the DSB is repaired, ∈3-H2AX is rapidly lost from chromatin; however it is not dephosphorylated “in place”; rather dephosphorylation occurs when ∈3-H2AX, presumably in the form of ∈3-H2AX-H2B dimers are displaced from chromatin. Dephosphorylation of ∈3-H2AX requires the PP4C phosphatases, Pph3, which is found as part of a 3-protein complex that is evolutionarily conserved. The roles of various chromatin remodeling complexes in displacing ∈3-H2AX will be discussed.
Abstract 4429: Loss of function Cbl-c mutations in solid tumors
Authors: Stephen C. Kales, Philip E. Ryan, Marion M. Nau, Jeffrey E. Green, Stanley Lipkowitz
Journal: Cancer Research (2014)

Abstract Receptor Tyrosine Kinase (RTK) signaling is essential for normal biological processes and disruption of this regulation can lead to tumor initiation and progression. Cbl proteins are a family of RING finger ubiquitin ligases that negatively regulate a variety of RTKs, including EGFR, MET, RET and components of the TCR pathway. Recent studies have identified a growing number of Cbl mutations associated with human myeloid neoplasias and epithelial tumors. Cbl-c is the most recently identified human Cbl protein and is expressed exclusively in epithelial cells. Recently, a novel cDNA has been isolated from the ductal carcinoma of a mouse mammary cancer model. This mutant has a deletion in the catalytic domain of Cbl-c, thereby resembling known Cbl family mutations associated with myeoloid neoplasias. Genomic analysis of both parental and transgenic lines shows no evidence of germline mutation indicating that this mutation is likely a somatic mutation. In overexpression studies, this mutant cDNA fails to mediate ubiquitination and degradation of activated EGFR and, acting as a dominant negative, enhances cell transformation. Furthermore, data mining reveals several Cbl family mutations associated with solid tumors in humans. Subsequent cell-based analysis demonstrates a similar loss of E3 function in some of these human mutations. Through subsequent analysis of transforming capacity and signal pathway regulation, we are assessing interacting partners of Cbl-c and the potential role of these mutations in tumorigenesis. Citation Format: Stephen C. Kales, Philip E. Ryan, Marion M. Nau, Jeffrey E. Green, Stanley Lipkowitz. Loss of function Cbl-c mutations in solid tumors. [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 4429. doi:10.1158/1538-7445.AM2014-4429
Arterial Tortuosity Syndrome
Authors: Pamela Moceri, Juliette Albuisson, Marie Saint-Faust, Florence Casagrande, Fabienne Giuliano, Caroline Devos, Philippe Benoit, Nicolas Hugues, Dorothée Ducreux, Pierre Cerboni, Christian Dageville, Xavier Jeunemaitre
Journal: Journal of the American College of Cardiology (2013)
A Workman That Needeth Not to Be Ashamed
Authors: Frank Bateman Stanger
Journal: New England Journal of Medicine (1959)

CONCLUSIONFor many years, said Rev. Ralph W. Sockman of Christ Church, New York City, I have been convinced that the greatest need of the contemporary church is the strengthening of the local pulpit.There is a tragic lag between the pronouncements of general church conventions and the prac-'214.
Characterization of different foci of multifocal breast cancer using genomic, transcriptomic and epigenomic data
Authors: Christine Desmedt, Serena Nik-Zainal, Debora Fumagalli, Françoise Rothé, Sandeep Singhal, Samira Majjaj, David Norman Brown, Sarah Dedeurwaerder, Matthieu Defrance, Marion M. Maetens, Pierre-Yves Adnet
Journal: Cancer Research (2012)
Crusted scabies in a girl with epidermolysis bullosa simplex
Authors: A. Torrelo, A. Zambrano
Journal: British Journal of Dermatology (2000)

Journal Article Crusted scabies in a girl with epidermolysis bullosa simplex Get access A. Torrelo, A. Torrelo Department of Dermatology, Hospital del Niño Jesús, Menéndez Pelayo 65, 28009 Madrid, Spain Search for other works by this author on: Oxford Academic Google Scholar A. Zambrano A. Zambrano Department of Dermatology, Hospital del Niño Jesús, Menéndez Pelayo 65, 28009 Madrid, Spain Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 142, Issue 1, 1 January 2000, Pages 197–198, https://doi.org/10.1046/j.1365-2133.2000.03281.x Published: 01 January 2000
Calcitonin Gene‐Related Peptide–Expressing Sensory Neurons and Spinal Microglial Reactivity Contribute to Pain States in Collagen‐Induced Arthritis
Authors: Francisco R. Nieto, Anna K. Clark, John Grist, Victoria Chapman, Marzia Malcangio
Journal: Arthritis & Rheumatology (2015)

To evaluate the contribution of sensory neurons in ankle joints and adjacent tissue to the development of pain in collagen-induced arthritis (CIA), and to determine the relationship between pain and the appearance of clinical signs.
Abstract 18888: Less Than 2g of Dietary Sodium Intake is Associated with Shorter Event-free Survival in Patients with Compensated Heart Failure
Authors: Eun Kyeung Song, Debra K Moser, Seongkum Heo, Sandra B Dunbar, Susan J Pressler, Heather M Payne-Emerson, Terry A Lennie
Journal: Circulation (2010)

Background: Dietary sodium restriction is a standard component of heart failure (HF) management. There is a growing concern that aggressive sodium restriction is not warranted in compensated HF pat...
A novel <i>PTEN</i> mutation in a Japanese patient with Cowden disease
Authors: Y. Kubo, Y. Urano, Y. Hida, T. Ikeuchi, M. Nomoto, K. Kunitomo, S. Arase
Journal: British Journal of Dermatology (2000)

Abstract Cowden disease (CD) is an autosomal dominant syndrome characterized by multiple hamartomatous lesions and an increased risk for malignancies. Recent evidence has indicated that the PTEN gene, encoding a protein tyrosine phosphatase, is the CD susceptibility gene. However, another line of evidence has suggested that CD might be genetically heterogeneous. Clinical features of CD are variable, and there are interfamilial differences in the expression of skin lesions . Therefore, information on PTEN mutations in CD patients should be accumulated to clarify the genotype–phenotype correlation. In the present study, we found heterozygous germline mutations of PTEN in all of three Japanese patients with CD examined, indicating no genetic heterogeneity among our patients. The mutations included two non-sense mutations of R335X and R130X, and a mis-sense mutation of C136R. To the best of our knowledge, the C136R mutation has not previously been reported in CD patients. This novel mutation was located outside the core motif of the phosphatase domain of PTEN protein, where most of the missense mutations previously reported in CD patients were clustered. Mucocutaneous manifestations were far fewer in the patient with this mutation than in the patients with nonsense mutations. Whether the phenotypic difference in mucocutaneous features was due to the different mutations remains unclear.
Chlamydia pneumoniae IgG titres and coronary heart disease: prospective study and meta-analysis Commentary: Adjustment for potential confounders may have been taken too far
Authors: J. Danesh
Journal: BMJ (2000)

<h3>Abstract</h3> <b>Objective:</b> To examine the association between coronary heart disease and serum markers of chronic <i>Chlamydia pneumoniae</i> infection. <b>Design:</b> "Nested" case-control analysis in a prospective cohort study and an updated meta-analysis of previous relevant studies. <b>Setting:</b> General practices in 18 towns in Britain. <b>Participants:</b> Of the 5661 men aged 40–59 who provided blood samples during 1978-80, 496 men who died from coronary heart disease or had non-fatal myocardial infarction and 989 men who had not developed coronary heart disease by 1996 were included. <b>Main outcome measures:</b> IgG serum antibodies to <i>C pneumoniae</i> in baseline samples; details of fatal and non-fatal coronary heart disease from medical records and death certificates. <b>Results:</b> 200 (40%) of the 496 men with coronary heart disease were in the top third of <i>C pneumoniae</i> titres compared with 329 (33%) of the 989 controls. The corresponding odds ratio for coronary heart disease was 1.66 (95% confidence interval 1.25 to 2.21), which fell to 1.22 (0.82 to 1.82) after adjustment for smoking and indicators of socioeconomic status. No strong associations were observed between <i>C pneumoniae</i> IgG titres and blood lipid concentrations, blood pressure, or plasma homocysteine concentration. In aggregate, the present study and 14 other prospective studies of <i>C pneumoniae</i> IgG titres included 3169 cases, yielding a combined odds ratio of 1.15 (0.97 to 1.36), with no significant heterogeneity among the separate studies (χ<sup>2</sup>=10.5, df=14; P&gt;0.1). <b>Conclusion:</b> This study, together with a meta-analysis of previous prospective studies, reliably excludes the existence of any strong association between <i>C pneumoniae</i> IgG titres and incident coronary heart disease. Further studies are required, however, to confirm or refute any modest association that may exist, particularly at younger ages.
Systematic Review: Why sources of heterogeneity in meta-analysis should be investigated
Authors: S G Thompson
Journal: BMJ (1994)

Although meta-analysis is now well established as a method of reviewing evidence, an uncritical use of the technique can be very misleading. One common problem is the failure to investigate appropriately the sources of heterogeneity, in particular the clinical differences between the studies included. This paper distinguishes between the concepts of clinical and statistical heterogeneity and exemplifies the importance of investigating heterogeneity by using published meta-analyses of epidemiological studies of serum cholesterol concentration and clinical trials of its reduction. Although not without some dangers of speculative conclusions, prompted by overzealous inspection of the data to hand, a sensible investigation of sources of heterogeneity should increase both the scientific and the clinical relevance of the results of meta-analyses.
Assessment of telomere length in the combined pulmonary fibrosis and emphysema syndrome
Authors: Ana Verónica Cardoso, Patrícia Caetano Mota, Aida Palmeiro, Paula Rendeiro, Natália Melo, José Miguel Pereira, Conceição Souto Moura, Oksana Sokhatska, António Morais
Journal: European Respiratory Journal (2014)

Introduction: Telomeres shortening (TS) has been associated to some patients with idiopathic pulmonary fibrosis (IPF), but the implication of this association is still unknown. Since TS is also reported in emphysema patients, there is the idea that TS should be more prevalent and significant in the combined pulmonary fibrosis and emphysema (CPFE) syndrome, but this hypothesis has never been confirmed.

Objectives: Assessment of TS in CPFE patients in comparison with IPF patients without emphysema.

Material and Methods: Extraction of DNA from peripheral blood samples of patients with IPF followed in Diffuse Lung Diseases outpatient clinic. The relative length of telomeres was performed using a quantitative polymerase chain reaction (qPCR) with SYBR® Green and it was expressed by the ratio between the number of copies of the telomeres repeat (T) and single copy gene (S) on the samples, relatively to a reference sample (T/S ratio).

Results: Of the 33 patients with IPF included, seventeen (51.5%) showed CPFE (58.8% of them with emphysema quantification >20%). TS (T/S ratio 20% (80%) or <20% (71.4%) (p=1.00).

Conclusions: Despite the lack of statistical significance, TS is more frequent in CPFE patients compared to IPF patients without emphysema, suggesting that this change is more significant in patients with this syndrome. However, studies with larger sample sizes are required to better determine the role of this genetic mechanism.
Mechanism of TNFerade™ suppression of lymphatic melanoma metastases
Authors: Randall S. Macgill, Dawn Hritz, Randy E. Osborn, C. Richter King
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

4026 

TNFerade™ is a second generation, replication incompetent adenovector that expresses human TNFα under the control of the chemo-radiation enhanced EGR-1 promoter. Local administration of TNFerade in conjunction with standard fractionated radiation therapy (RT) is currently in clinical development for the treatment of locally advanced solid tumors. TNFerade has been shown in both syngenic and xenograft murine tumor models to have significant local effects in conjunction with fractionated RT. In continuing preclinical studies, we have shown local treatment with TNFerade ± RT suppresses the formation of both regional and distal lymph node metastases in the syngenic B16F10 murine melanoma model. Furthermore, these distal effects were independent of both time, and primary tumor growth. The current studies were undertaken to differentiate between potential effects on the host versus potential effects on the tumor, and to determine the potential roles of both adaptive and innate immune effector cells. To differentiate whether the mechanism by which TNFerade suppresses B16F10 lymph node metastases is primarily due to effects on the host (immune stimulation, vascular effects, decreased host receptivity to metastases), or due to effects on the tumor (decreased metastatic ability), comparative local and distal efficacy studies were performed in normal and TNF receptor 1 (TNFR1) knockout mice. Of the two TNFα receptors, human TNFα only signals the TNFR1 murine receptor. The results of these studies indicated an almost exclusive role for TNFerade induced host effects in both local and metastatic efficacy. TNFerade enhanced efficacy at the locally treated primary tumor was lost in the TNFR1 knockout mice versus the RT controls. Additionally, the suppression of both regional and distal lymph node metastases was also completely lost in the TNFR1 knockout mice versus RT controls. Further comparative efficacy studies between normal and T-cell deficient nude mice suggest both the local efficacy and the impact on spontaneous metastases from TNFerade ± RT is independent of an adaptive T-cell response. This observation was further confirmed in radiation killed B16F10 cells ± TNFerade whole-cell vaccination studies which suggest TNFerade does not function through an adaptive immune response in this poorly immunogenic tumor model. Current studies are underway using various immunocompromised mouse strains to determine if innate immunity has a role in TNFerade suppression of B16F10 lymph node metastases.
Temperature measurement in intensive care patients: comparison of urinary bladder, oesophageal, rectal, axillary, and inguinal methods versus pulmonary artery core method
Authors: J.-Y. Lefrant, L. Muller, J. Emmanuel de La Coussaye, M. Benbabaali, C. Lebris, N. Zeitoun, C. Mari, G. Saïssi, J. Ripart, J.-J. Eledjam
Journal: Intensive Care Medicine (2003)
THE SYNDROME OF MULTIPLE VITAMIN DEFICIENCY
Authors: V. P. Sydenstricker
Journal: Annals of Internal Medicine (1941)

ExcerptGood nutrition depends not only on the intake of sufficient amounts of all the substances required for normal metabolic processes but also on their adequate absorption, storage and utilization. In the case of most of the vitamins it is probable that optimal intake varies with the demands of the body for energy production, repair or growth. The requirements for some members of the B group are definitely dependent on the composition of the diet and it is likely that there are interrelations or synergistic reactions between vitamins which further condition the requirements.1, 2, 3, 4The development of avitaminosis is...