tbuckley/cabot-search huggingface dataset:
Atopic dermatitis and cancer risk
Authors: H. Wang, T.L. Diepgen
Journal: British Journal of Dermatology (2005)

Epidemiological studies have provided growing evidence of a link between atopy and cancer risk.To review the evidence from case-control studies and cohort studies on a possible association between atopic dermatitis (AD) and cancer risk, with particular attention to the case definition of AD.Studies with quantitative data on the association between AD (eczematous disease) and cancer risk were obtained from MEDLINE in combination with a review of cited references.In 23 publications, AD was implicated in the risk of haematological [childhood leukaemia (n = 3), adult leukaemia (n = 3), non-Hodgkin lymphoma (NHL; n = 4) and different haematological cancers (n = 1)], pancreatic (n = 5), skin (n = 2) and brain malignancies (n = 5). The overall picture of the results of these studies shows that a history of AD may be associated with a decreased risk of pancreatic cancer, brain tumour and childhood leukaemia, although in most instances the findings were not statistically significant. No consistent associations were observed for skin cancer or NHL. The definition of AD had varying quality, and was imprecise in the majority of publications.The findings of the epidemiological studies tend to support a lower risk of cancer among persons with a history of AD. Although a more careful definition of AD is needed, these epidemiological studies could provide an estimate of the background cancer risk in patients with AD when the long-term effects of treatments for AD are assessed.
COMPARISON OF PERCUTANEOUS CORONARY INTERVENTION AND CORONARY ARTERY BYPASS GRAFTING FOR REVASCULARIZATION OF PATIENTS WITH DIABETES MELLITUS
Authors: Dion Stub, William Chan, Nick Andrianopoulos, Michelle Butler, David J. Clark, Andrew E. Ajani, Angela Brennan, Andrew E. Newcomb, Julian A. Smith, Pratyusha Naidu, Anthony M. Dart, Diem T. Dinh, Stephen J. Duffy
Journal: Journal of the American College of Cardiology (2011)
Detection of Incident Field Loss Using the Glaucoma Henaifield Test
Authors: Joanne Katz, Harry A. Quigley, Alfred Sommer
Journal: Ophthalmology (1996)

To examine different definitions of incident visual field loss among patients with elevated intraocular pressure and varying numbers of abnormal glaucoma hemifield test results over an average of 6 years of follow-up.A cohort of patients with annual C-30-2 Humphrey visual fields were followed for a minimum of 5 years. Three different definitions of field loss were compared: 1, 2, or 3 consecutive annual abnormal glaucoma hemifield test results.Of 253 subjects, 506 eyes were followed for 5 to 9 years. If incident field loss was defined as one or more normal fields followed by one abnormal glaucoma hemifield test result, the incidence of field loss was 63.6 per 1000 person-years of follow-up. For two or three consecutive abnormal glaucoma hemifield test results, the rates were 27.6 and 19.2 per 1000 person-years of follow-up, respectively. Among patients with field loss in one eye at the start of the study, the incidence of field loss in the fellow eye using 1, 2, or 3 consecutive abnormal fields as the definition of incident field loss was 60.9, 55.5, and 25.5 per 1000 person-years of follow-up, respectively. Three years after incident field loss, 31.9% (1 abnormal test result), 76.5% (2 abnormal test results), and 88.5% (3 abnormal test results) of eyes with incident field loss had an abnormal hemifield test result. For eyes with one, two, and three consecutive abnormal glaucoma hemifield test results at the start of the study, 59.2%, 83.6%, and 89.1%, respectively, had an abnormal field 3 years later.One abnormal glaucoma hemifield test result is not a consistent criterion for defining incident field loss. The use of two or three consecutive abnormal fields to define incident field loss makes it more likely that subsequent test results will be abnormal.
The Combined Effects of Xeroderma Pigmentosum C Deficiency and Mutagens on Mutation Rates in the Mouse Germ Line
Authors: Laurent Miccoli, Karen L-A. Burr, Peter Hickenbotham, Errol C. Friedberg, Jaime F. Angulo, Yuri E. Dubrova
Journal: Cancer Research (2007)

Abstract Spontaneous and induced mutation rates at two expanded simple tandem repeat (ESTR) loci were studied in the germ line of xeroderma pigmentosum group C (Xpc) knockout mice defective in global genome nucleotide excision repair. Spontaneous and radiation-induced mutation rates in homozygous Xpc−/− males were significantly higher than those in isogenic wild-type (Xpc+/+) and heterozygous (Xpc+/−) mice. In contrast, exposure to the monofunctional alkylating agent ethylnitrosourea resulted in similar increases in ESTR mutation rates across all genotypes. ESTR mutation spectra in the germ line of Xpc−/−, Xpc+/− and Xpc+/+ did not differ. Considering these data and the results of other publications, we propose that the Xpc-deficient mice possess a mutator phenotype in their germ line and somatic tissues that may significantly enhance carcinogenesis across multiple tissues. [Cancer Res 2007;67(10):4695–9]
Abstract 5299: Separate functions of caspase-3 in cell migration and apoptosis
Authors: Erika Libby, Shannon Eble, Martin Adelson, Eli Mordechai, Jason Trama
Journal: Cancer Research (2010)

Abstract The cysteine protease function of caspase-3 in the execution phase of apoptosis is well known. However, even though subverting apoptosis is beneficial for tumor development and survival, some tumors maintain high expression levels of caspase-3 in positive correlation with malignancy. Here we show that caspase-3 expression is positively correlated with tumor cell migration and invasion. Furthermore, the enhanced migration and invasion is protease-independent and is specifically conferred by the inactive precursor form of caspase-3. Ectopic expression of caspase-3 in the MCF7 cell line, which is caspase-3 deficient and showed low migration ability, enhanced wound healing and chemotaxis. In contrast, shRNA reducing the expression of caspase-3 in the 5637 cell line, which expressed a high level of caspase-3 and high migration ability, hampered wound healing, chemotaxis, and matrigel invasion. Use of a caspase cysteine protease inhibitor or site directed mutagenesis of caspase-3 either rendering the ectopically expressed precursor form non-processable or inactivating the cysteine protease site did not diminish the caspase-3-dependent increase of cell migration. In addition, only reconstitution of the MCF7 cell line with the wild-type or non-processable precursor form of caspase-3 enhanced cell migration. Ectopic expression of the p17 or p12 fragment alone, the cysteine protease active p17 and p12 fragments together, or the cysteine protease inactive p17 fragment and p12 fragment together did not enhance cell migration. Fluorescence microscopy showed the enrichment of the non-processable mutant of caspase-3 in the leading edge of cells under experimental conditions of wound healing. In summary, the precursor form of caspase-3 induces cell migration by a protease-independent mechanism. This indentifies a new role for caspase-3 in tumor metastasis and represents a novel target for cancer therapeutics. Since the current evidence indicates that the role of caspase-3 in apoptosis and the role in migration are functionally separate, it is conceivable to design a molecule that disrupts the metastasis-inducing function of caspsase-3 while preserving the apoptosis-inducing function. We are currently investigating proteins that associate with caspase-3 under experimental conditions of caspase-3-dependent migration. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5299.
Challenges relating to solid tumour brain metastases in clinical trials, part 2: neurocognitive, neurological, and quality-of-life outcomes. A report from the RANO group
Authors: Nancy U Lin, Jeffrey S Wefel, Eudocia Q Lee, David Schiff, Martin J van den Bent, Riccardo Soffietti, John H Suh, Michael A Vogelbaum, Minesh P Mehta, Janet Dancey, Mark E Linskey, D Ross Camidge, Hidefumi Aoyama, Paul D Brown, Susan M Chang, Steven N Kalkanis, Igor J Barani, Brigitta G Baumert, Laurie E Gaspar, F Stephen Hodi, David R Macdonald, Patrick Y Wen
Journal: The Lancet Oncology (2013)
Faith and Health: Religion, Science, and Public Policy
Authors: Pat Fosarelli
Journal: JAMA (2010)

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
Isolation of genes identified in mouse renal proximal tubule by comparing different gene expression profiles
Authors: Masaru Takenaka, Enyu Imai, Tetsuya Kaneko, Takahito Ito, Toshiki Moriyama, Atsushi Yamauchi, Masatsugu Hori, Shoko Kawamoto, Kousaku Okubo
Journal: Kidney International (1998)
Kidney Development and Disease in the Zebrafish
Authors: Iain A. Drummond
Journal: Journal of the American Society of Nephrology (2005)

Unraveling the molecular pathogenesis of human disease presents many experimental challenges, not the least of which is that experiments on humans are generally frowned upon. Model organisms, including the zebrafish, allow for experimental analysis of gene function and the detailed characterization of disease processes. Zebrafish have matured as a vertebrate model organism now that genetic tools for targeted "knockdowns" and unbiased mutagenesis approaches are in hand. The fish larval pronephros is a relevant kidney in which to pursue many aspects of human kidney development and disease. This short review outlines recent progress in applying the zebrafish pronephros to issues of human health and development.
Arrhythmogenic Brugada syndrome substrate: a proof of principle
Authors: J. R. Ehrlich
Journal: Cardiovascular Research (2008)

The Brugada syndrome is an inherited, arrhythmogenic entity affecting predominantly young men without structural heart disease.1 It is associated with a specific ECG pattern of coved-type ST-segment elevation in right precordial leads ( Figure 1 ). Patients are at increased risk for sudden cardiac death often triggered by vagal influence and many times occurring at rest. After its description as a distinct entity in 1992, a first genetic link was identified in 1998.2 The Brugada syndrome has a complex electrophysiological substrate, and several aspects are important for understanding its pathology. Many lines of evidence suggest a central role of I to in the genesis of the Brugada syndrome. First, the balance of de- and repolarizing forces during the cardiac action potential is disturbed, leading to a loss of dome in epicardial action potentials and to increased dispersion of refractoriness. Reduced depolarizing (sodium current, I Na, or calcium current, I Ca) or increased repolarizing ion currents (transient outward … 

*Corresponding author. Tel: +49 69 6301 83661, fax: +49 69 6301 4037. E-mail address: j.ehrlich{at}em.uni-frankfurt.de
Surprising Activity of Flutamide Withdrawal, When Combined With Aminoglutethimide, in Treatment of "Hormone-Refractory" Prostate Cancer
Authors: O. Sartor, M. Cooper, M. Weinberger, D. Headlee, A. Thibault, A. Tompkins, S. Steinberg, W. D. Figg, W. M. Linehan, C. E. Myers
Journal: JNCI Journal of the National Cancer Institute (1994)

The best treatment for patients with "hormone-refractory" metastatic prostate cancer is unclear, particularly in patients for whom suramin and hydrocortisone have failed.We investigated a combination of flutamide withdrawal and aminoglutethimide in suramin- and hydrocortisone-pretreated patients with "hormone-refractory" prostate cancer.Twenty-nine patients with metastatic prostate cancer were treated with simultaneous flutamide withdrawal and aminoglutethimide (250 mg given orally four times daily). All patients were taking flutamide at the time of entry, and previous treatments with medical or surgical castration, flutamide, suramin, and hydrocortisone had failed in all of these patients. Because of suramin-induced adrenal insufficiency, all patients had previously received, and continued to receive, physiological doses of hydrocortisone. Treatment of all non-surgically castrated patients had previously failed; however, these patients continued to receive depot leuprolide.In 14 (48%) of 29 patients, the prostate-specific antigen (PSA) decreased by more than 80% for 4 or more weeks. Improvements in anemia, thrombocytopenia, soft-tissue masses, bone scans, and symptoms were also noted. Factors associated with response included prolonged flutamide pretreatment, a markedly elevated pretreatment PSA, and the absence of soft-tissue disease.Flutamide withdrawal, when combined with the simultaneous administration of aminoglutethimide, is a therapeutically active approach in patients with "hormone-refractory" prostate cancer.On the basis of these and additional data, we hypothesize that prolonged exposure to flutamide results in the selective proliferation of cancer cells containing a mutant androgen receptor that aberrantly recognizes flutamide metabolites and nonandrogenic steroids as androgenic stimuli.
Requirement for hexose, unrelated to energy provision, in T-cell-mediated cytolysis at the lethal hit stage.
Authors: I C MacLennan, P Golstein
Journal: The Journal of Experimental Medicine (1978)

The requirement for D-glucose in T-cell-mediated cytolysis was studied using mouse spleen cells sensitized against alloantigens in vitro. Glucose was required for cytolysis: (a) cytolysis proceeded in a simple buffered salt solution containing Ca++ and Mg++ (low phosphate-buffered saline, LPBS) in the presence but not in the absence of added glucose; (b) 2-deoxy-D-glucose blocked cytolysis. The block by this agent was overcome by excess glucose added as late as 40 min after the inhibitor. This block was not due to inhibition of NADP reduction, since 2-deoxy-D-glucose failed to interfere with the rate of CO2 production by the pentose cycle which we found to be of significant activity in sensitized spleen cells; (c) dialyzed fetal bovine serum (DFBS) in LPBS supported cytolysis in the absence of added glucose. However, 2-deoxy-D-glucose was also inhibitory under these conditions, suggesting that carbohydrate was required here as well. Further results supported the conclusion that DFBS was not acting as a direct source of the required carbohydrate. The relationship between cytolysis, glucose requirement, and provision of energy was studied. As little as 0.1 mM D-glucose in LPBS supported cytolysis. At this glucose concentration, there was no measurable accumulation of lactate in sensitized spleen cells, but Krebs cycle activity was detectable. In 3 mM glucose or above, the range covered by standard tissue culture media, anaerobic glycolysis became a major source of energy in sensitized spleen cells. Consequently, it appears that in standard tissue culture medium, effector cells can generate sufficient energy for cytolysis either by aerobic or anaerobic metabolism. However, the addition of an energy source alone in the absence of glucose was insufficient to support cytolysis in LPBS. Pyruvate in LPBS did not support cytolysis but was shown to be a good substrate for aerobic metabolism in sensitized spleen cells. Glycogenic amino acids and glycerol also failed to support cytolysis. The stage of cytolysis at which glucose is required was investigated. Glucose was necessary for the calcium-dependent lethal hit phase, but not for the cytochalasin A-blockable recognition stage, nor for 51Cr release from injured target cells. Models for the lethal hit process are discussed, which are compatible with the observed requirement for certain hexoses unrelated to their capacity to serve as sources of energy.
Protecting the Medical Commons: Who Is Responsible?
Authors: Howard H. Hiatt
Journal: New England Journal of Medicine (1975)

The resources for medical care are clearly finite, but demands on those resources are growing rapidly. Of particular concern are the demands on those resources for medical practices of three kinds: those that pose conflicts between the interests of the individual and those of society; those of no value or of undetermined value; and those for potentially preventable conditions. Such practices must be evaluated in terms of social and medical priorities, and this requirement will become more urgent with the establishment of national health insurance. Who will make decisions is less clear, but it is not likely to be physicians alone. It is imperative that physicians and other health providers work closely with professionals from many fields, and with consumers, to ensure the availability and dissemination of information that will permit decisions that are in the best interests of society.
New clinics for HIV testing. Improve public access.
Authors: N J Beeching, F N Nye, M Prior, C Morrison, S M Ruben, K J Mutton
Journal: BMJ (1993)

does not seem to warrant interferon being withheld if active hepatitis C has been diagnosed.Even if chronic hepatitis C is responsible for precipitating autoimmune liver injury-which remains to be shown-treatment of the primary disease may improve both, as in a recent report of successful treatment with interferon of membranous glomerulonephritis associated with chronic hepatitis C.5Liver biopsy may be helpful in determining whether autoimmune disease or hepatitis C predominates in individual patients with markers of both.When diagnostic doubt persists despite serological examination and biopsy we agree with the authors of the editorial that steroids are a reasonable first choice.Given the possibility of lasting eradication of hepatitis C virus and prevention of the long term sequelae of chronic hepatitis C, however, we think that patients with a firm diagnosis of chronic hepatitis C should generally receive interferon first and be closely observed in the early stages of treatment.
Taste loss associated with captopril treatment.
Authors: J J McNeil, A Anderson, N Christophidis, B Jarrott, W J Louis
Journal: BMJ (1979)

Dietary fibre and ketone bodies: reduced urinary 3-hydroxybutyrate excretion in diabetics on guar Dietary fibre is known to modify carbohydrate absorption and metabolism in both normal and diabetic individuals.'-3Except for reports on the action of certain forms of fibre in reducing serum cholesterol concentrations,3 however, no attention has been given to other changes in lipid metabolism.Since urine testing for ketone bodies is still a major part of the clinical assessment of the diabetic, we have looked at the effect of guar gum on the output of 3-hydroxybutyric acid (3-OHB) in diabetic volunteers.If both 3-OHB and glucose outputs were reduced at the same time then this would suggest a general improvement in diabetic control rather than carbohydrate malabsorption. Patients, methods, and resultsNine diabetics (4 men, 5 women aged 42± (SE of mean) 5 years) were studied.Their blood and urinary glucose data have been reported2; two were taking oral hypoglycaemic agents and seven insulin 36 ± 6 U/day.Their mean weight was 106+ 5 % of desirable weight.Seven patients were studied in hospital on metabolically controlled diets: identical two-day rotating menus were provided over both consecutive test and control five-day periods (the order being randomised and separated in five studies by a weekend).Two were studied as outpatients and kept the same meal plans throughout.During the control period patients took between 14 and 26 slices of crispbread per day with meals, and during the test period they took guar crispbread of the same composition except that it also contained 1 g guar/slice.Serum was obtained on the last day of each period and complete 24-hour urine collections were made throughout for analysis of creatinine (Technicon, SMA 12/60).4Urinary 3-OHB, the ketone body least likely to be affected by storage, was estimated by an enzymatic technique modified for use with the Guildford 3500 enzyme analyser.5The significance of differences was calculated using Student's t test for paired data.The mean 3-OHB and glucose outputs over the last two days on guar were much lower than during the control period (see table ).Calculated as Percentage change in 24-hour urinary glucose and 3-OHB outputs for last two days on guar compared with control period Last two control days % Change on guar Case 3-OHB Glucose no (mmol/24h) (mmol/24h) 3-OHB Glucose 1 .
Endothelin-1 and Its mRNA in the Wall Layers of Human Arteries Ex Vivo
Authors: Gian Paolo Rossi, Stefania Colonna, Edoardo Pavan, Giovanna Albertin, Foscarina Della Rocca, Gino Gerosa, Dino Casarotto, Saverio Sartore, Paolo Pauletto, Achille C. Pessina
Journal: Circulation (1999)

Background —The participation of endothelin-1 (ET-1) in the control of vascular tone in humans has been questioned, on the basis of the finding of subthreshold immunoreactive (ir) ET-1 plasma levels. However, because most ET-1 is secreted abluminally, it might attain a higher concentration in the tunica media than in plasma. Furthermore, evidence indicates that vascular smooth muscle cells (VSMCs) can synthesize ET-1 on stimulation in vitro. We therefore looked for irET-1 in the different layers of the wall of human arteries, including renal, gastric, and internal thoracic artery wall, obtained ex vivo from consenting patients with coronary artery disease and/or high blood pressure undergoing surgery, as well as from young organ donors. Methods and Results —We performed immunohistochemistry with specific anti–ET-1 and anti-vWF antibodies followed by detection with an avidin-biotin complex ultrasensitive kit. The presence of preproET-1 and human endothelin-converting enzyme-1 (hECE-1) mRNA was also investigated by reverse transcription–polymerase chain reaction in homogenates of vessel wall, including preparations deprived of both endothelium and adventitia, and in isolated VSMCs. We detected irET-1 in the endothelium of all arteries and in the tunica media of internal thoracic artery from most patients with coronary artery disease. PreproET-1 and hECE-1 mRNA was also detected in VSMCs isolated from these vessels. irET-1 and irvWF staining in endothelium and tunica media was measured by use of microscope-coupled computer-assisted technology. Significant correlations between the amount of irET-1 in the tunica media and mean blood pressure ( P &lt;0.05), total serum cholesterol ( P &lt;0.05), and number of atherosclerotic sites ( P &lt;0.001) were found. Thus, in organ donors, irET-1 was detectable almost exclusively in endothelial cells, whereas in patients with coronary artery disease and/or arterial hypertension, sizable amounts of irET-1 were detectable in the tunica media of different types of arteries. In addition, VSMCs isolated from these vessels coexpressed the preproET-1 and hECE-1 genes. Conclusions —Collectively, these findings are consistent with the contention that endothelial damage occurs in most patients with atherosclerosis and/or hypertension and that ET-1 is synthesized in VSMCs of these patients.