tbuckley/cabot-search huggingface dataset:
Characterization of gene expression changes associated with MNNG, arsenic, or metal mixture treatment in human keratinocytes: application of cDNA microarray technology.
Authors: Dong-Soon Bae, William H Hanneman, Raymond S H Yang, Julie A Campain
Journal: Environmental Health Perspectives (2002)

The identification of molecular markers related to critical biological processes during carcinogenesis may aid in the evaluation of carcinogenic potentials of chemicals and chemical mixtures. Work from our laboratory demonstrated that a single treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) enhanced spontaneous malignant transformation of the human keratinocyte cell line RHEK-1. In contrast, chronic low-level exposure of cells to arsenic alone or in a mixture containing arsenic, cadmium, chromium, and lead inhibited malignant conversion. To identify changes in gene expression that influence these different outcomes, cDNA microarray technology was used. Analysis of multiple human arrays in MNNG-transformed RHEK-1 cells, designated OM3, and those treated with arsenic or the arsenic-containing metal mixture showed unique patterns of gene expression. Genes that were overexpressed in OM3 included oncogenes, cell cycle regulators, and those involved in signal transduction, whereas genes for DNA repair enzymes and inhibitors of transformation and metastasis were suppressed. In arsenic-treated cells, multiple DNA repair proteins were overexpressed. Mixture-treated cells showed increased expression of a variety of genes including metallothioneins and integrin 4. These cells showed decreased expression of oncogenes, DNA repair proteins, and genes involved in the mitogen-activated protein kinase pathway. For comparison we are currently analyzing gene expression changes in RHEK-1 cells transformed by other means. The goal of these studies is to identify common batteries of genes affected by chemical modulators of the carcinogenic process. Mechanistic studies may allow us to correlate alterations in their expression with sequential stages in the carcinogenic process and may aid in the risk assessment of other xenobiotics.
Arthur Dudley Payne
Authors: Helen Payne
Journal: BMJ (2006)

Former general practitioner Hythe, Kent (b 1916; q Cambridge/St Bartholomew's Hospital, London, 1940; SBStJ), d 2 August 2006.

Arthur Dudley Payne (Dudley) qualified in time to join the surgical staff of St Bartholomew's Hospital for the 90 day London Blitz in 1940. He joined the Royal Army Medical Corps, becoming regimental medical officer to the Royal Norfolk Regiment, seeing the fall of Caen and being mentioned in despatches. He was then regimental medical officer of the “Desert Rats,” the 7th Armoured Division, the only British troops entering Berlin in May 1944. Dudley returned to civilian life as a singlehanded general practitioner in Hythe, Kent, later being joined by Peter Ford until his retirement in 1966. He enjoyed a long and happy retirement. He leaves a wife, Helen; two children; and three grandchildren.
Disability in Adult Survivors of Childhood Cancer: A Swedish National Cohort Study
Authors: Anders Hjern, Frank Lindblad, Krister K. Boman
Journal: Journal of Clinical Oncology (2007)

We studied the effects of childhood or adolescent cancer and cancer treatment on disability as indicated by persistent aid needs in adult life.A group of 2,503 survivors of childhood cancer diagnosed before their 16th birthday were studied with data from registers in a national cohort of 1.91 million Swedish residents. Disability indicators were created from information in national registers about income (sickness pension, handicap allowance), personal assistance, and family situation in 2002. Multivariate logistic regression on the log scale was used to estimate relative risk (RR) ratios.A total of 7.6% of survivors received handicap allowance indicating permanent disability, including brain tumors (14.0%), other solid tumors (6.3), and leukemias/lymphomas (2.9%), compared with 0.6% in the general population. Twenty-six percent of survivors of CNS tumor and 10% of survivors of solid tumors had at least one indication of a disability. Younger age at diagnosis suggested a higher risk for disability. CNS tumor survivors had an RR of 10.7 (95% CI, 9.3 to 12.8) for having at least one disability indication compared with the noncancer population, whereas leukemia and lymphoma survivors had an RR of 3.0, and survivors of other cancers had an RR of 3.8. Survivors of CNS tumor only had an increased RR for living in the parental household (RR = 1.6; 95% CI, 1.4 to 1.9).Childhood cancer survivors more often have persistent needs of supportive measures provided by community and/or the parental household. The survivors of CNS tumors were at particular risk, indicating a need of safer treatment protocols, and tailored follow-up, prevention, and rehabilitation to address this persistent social disability.
Demonstration of Regional Sympathetic Denervation of the Heart in Diabetes: Comparison between patients with NIDDM and IDDM
Authors: Anu K Turpeinen, Esko Vanninen, Jyrki T Kuikka, Matti IJ Uusitupa
Journal: Diabetes Care (1996)

OBJECTIVE Global myocardial uptake of 123I-metaiodobenzylguanidine (MIBG) has been shown to be decreased in diabetic patients with autonomic neuropathy, indicating cardiac sympathetic dysfunction. However, possible differences in myocardial MIBG distribution between NIDDM and IDDM diabetic patients are not known. RESEARCH DESIGN AND METHODS Regional myocardial distribution of 123I-MIBG was studied in seven male IDDM patients (age 45 ± 2 years, duration of diabetes 30 ± 3 years, means ± SE) and 13 NIDDM patients (8 men, 5 women, age 59 ± 2 years, duration of diabetes 10 ± 1 years). A dual-tracer single-photon emission tomography was carried out with 123I-MIBG and 99mTc-methoxyisobutylisonitrrile to asses simultaneously myocardial sympathetic innervation and perfusion at rest. Conventional autonomic nervous function tests, power spectral analysis of heart rate variability, and echocardiography were performed for assessments of autonomic function and cardiac dimensions and function. RESULTS Autonomic nervous function tests and echocardiography showed similar results in IDDM and NIDDM patients. Despite this, global myocardial MIBG uptake (0.43 ± 0.04 vs. 0.59 ± 0.06, P = 0.03) and MIBG heart-to-liver ratio (0.59 ± 0.03 vs. 0.68 = 0.03, P = 0.05) were lower in NIDDM compared with IDDM patients. Regional distribution of MIBG uptake and regional MIBG/perfusion ratio revealed significantly reduced uptake in NIDDM patients especially in the inferoposterior segments of the left ventricle compared with IDDM patients. Difference in age between NIDDM and IDDM patients did not explain the results. CONCLUSIONS Reduced myocardial MIBG uptake was found in NIDDM patients compared withthe uptake in IDDM patients, particularly involving inferoposterior segments.Regional sympathetic damage not detectable with conventional autonomic function tests is relatively common in NIDDM.
The child whisperer
Authors: J A M Wright
Journal: BMJ (2002)

Over the past four years, since retirement from active practice, I have conducted an experiment that has only anecdotal evidence. None the less, our son, also a doctor, has carried out a similar test with the same results. Neither of us can explain these results nor can we find it mentioned in any reference book, but perhaps we have not looked in the right places.

And what …
A new urethral catheter
Authors: J C Brocklehurst, D S Hickey, I Davies, A P Kennedy, J A Morris
Journal: BMJ (1988)

A new balloon catheter for women with a flexible urethral portion that conforms to the shape of the closed urethra was tested. In sheep control catheters caused epithelial destruction, which was absent with the conformable catheter. A 12 week crossover trial compared control catheters in 52 long stay geriatric patients. Eighty two out of 91 conformable catheters were rated as comfortable compared with 68 of 87 control (p=0·006). The average length of time in situ was 15·9 days for the conformable catheter compared with 12·9 days for the control (p=0·001). The average number of bypasses a week with the conformable catheter was 1·1 compared with 1·3 for the control; this difference was not significant. Examination of 249 used catheters showed significantly fewer with intraluminal obstruction with struvite among the conformable than control catheters (1 (0·8%) versus 15 (11·5%); p&lt;0·001). This new catheter for women is a substantial improvement over the Foley catheter and (except in urethral stricture) is suitable for all forms of drainage.
Nonsurgical Closure of Large Arteriovenous Fistulas
Authors: Wilfrido R. Castaneda-Zuniga
Journal: JAMA (1976)

We report a nonsurgical closure of large postnephrectomy arteriovenous fistulas in two patients. To our knowledge, this method has not previously been attempted because of the large size of the communication and the risk of pulmonary embolization. However, the development of new embolization techniques makes a nonsurgical approach feasible and safe. (<i>JAMA</i>236:2649-2650, 1976)
Schwannoma of the brachial plexus with intrathoracic extension.
Authors: A Gyhra, J Israel, C Santander, D Acuna
Journal: Thorax (1980)

<h3>Abstract</h3> <h3>Objective</h3> To address common “what if” questions that arise relating to the long-term clinical follow-up and management of patients receiving the new oral anticoagulants (NOACs). <h3>Sources of information</h3> For this narrative review, we searched the PubMed database for recent (January 2008 to week 32 of 2013) clinical studies relating to NOAC use for stroke prevention in atrial fibrillation and for the treatment of acute venous thromboembolism. We used this evidence base to address prespecified questions relating to NOAC use in primary care settings. <h3>Main message</h3> Dabigatran and rivaroxaban should be taken with meals to decrease dyspepsia and increase absorption, respectively. There are no dietary restrictions with any of the NOACs, beyond moderating alcohol intake, and rivaroxaban and apixaban can be crushed if required. The use of acid suppressive therapies does not appear to affect the efficacy of the NOACs. As with warfarin, patients taking NOACs should avoid long-term use of nonsteroidal anti-inflammatory and antiplatelet drugs. For patients requiring surgery, generally NOACs should be stopped 2 to 5 days before the procedure, depending on bleeding risk, and the NOAC should usually be resumed at least 24 hours after surgery. Preoperative coagulation testing is generally unnecessary. In patients who develop bleeding, minor bleeding typically does not require laboratory testing or discontinuation of NOACs; with major bleeding, the focus should be on local measures to control the bleeding and supportive care, and coagulation testing should be performed. There are currently no antidotes to reverse NOACs. The NOACs should not be used in patients with valvular heart disease, prosthetic heart valves, cancer-associated deep vein thrombosis, or superficial thrombophlebitis. <h3>Conclusion</h3> Management of “what if” scenarios for patients taking NOACs have been proposed, but additional study is needed to address these issues, especially periprocedural management and bleeding.
Orthopedist is pioneer in prosthetic design
Authors: J. Elliott
Journal: JAMA (1979)

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
Averting a malaria disaster
Authors: NJ White, F Nosten, S Looareesuwan, WM Watkins, K Marsh, RW Snow, G Kokwaro, J Ouma, TT Hien, ME Molyneux, TE Taylor, CI Newbold, TK Ruebush, M Danis, BM Greenwood, RM Anderson, P Olliaro
Journal: The Lancet (1999)
Leptin Gene Epigenetic Adaptation to Impaired Glucose Metabolism During Pregnancy
Authors: Luigi Bouchard, Stéphanie Thibault, Simon-Pierre Guay, Marta Santure, Alexandre Monpetit, Julie St-Pierre, Patrice Perron, Diane Brisson
Journal: Diabetes Care (2010)

OBJECTIVE To verify whether the leptin gene epigenetic (DNA methylation) profile is altered in the offspring of mothers with gestational impaired glucose tolerance (IGT). RESEARCH DESIGN AND METHODS Placental tissues and maternal and cord blood samples were obtained from 48 women at term including 23 subjects with gestational IGT. Leptin DNA methylation, gene expression levels, and circulating concentration were measured using the Sequenom EpiTYPER system, quantitative real-time RT-PCR, and enzyme-linked immunosorbent assay, respectively. IGT was assessed after a 75-g oral glucose tolerance test (OGTT) at 24–28 weeks of gestation. RESULTS We have shown that placental leptin gene DNA methylation levels were correlated with glucose levels (2-h post-OGTT) in women with IGT (fetal side: ρ = −0.44, P ≤ 0.05; maternal side: ρ = 0.53, P ≤ 0.01) and with decreased leptin gene expression (n = 48; ρ ≥ −0.30, P ≤ 0.05) in the whole cohort. Placental leptin mRNA levels accounted for 16% of the variance in maternal circulating leptin concentration (P &amp;lt; 0.05). CONCLUSIONS IGT during pregnancy was associated with leptin gene DNA methylation adaptations with potential functional impacts. These epigenetic changes provide novel mechanisms that could contribute to explaining the detrimental health effects associated with fetal programming, such as long-term increased risk of developing obesity and type 2 diabetes.
Calmodulin modulation of single sarcoplasmic reticulum Ca2+-release channels from cardiac and skeletal muscle.
Authors: J S Smith, E Rousseau, G Meissner
Journal: Circulation Research (1989)

Sarcoplasmic reticulum (SR) contains a Ca2+-conducting channel that is believed to play a central role in excitation-contraction coupling by releasing the Ca2+ necessary for muscle contraction. The effects of calmodulin on single cardiac and skeletal muscle SR Ca2+-release channels were studied using the planar lipid bilayer-vesicle fusion technique. Calmodulin inhibited Ca2+-release channel opening by reducing the mean duration of single-channel open events without having an effect on single-channel conductance. Inhibition by calmodulin was dependent on Ca2+ concentration and occurred in the absence of ATP. The effects of calmodulin were reversed by mastoparan, a calmodulin-binding peptide. Two other calmodulin antagonists [calmidazolium and N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide] modified the gating behavior of the channel in the absence of exogenous calmodulin in a concentration- and Ca2+-dependent manner. Our results suggest that calmodulin can modulate excitation-contraction coupling by directly interacting with the SR Ca2+-release channel of cardiac and skeletal muscle.
REGENERATION OF THE HEART BY CONTROLLED RELEASE OF ANTAGOMIR-92A USING GELATIN HYDROGEL MICROSPHERES INCORPORATED PATCH IN RATS WITH MYOCARDIAL INFARCTION
Authors: Masanori Fujita, Hajime Otani, Takayuki Shimazu, Kei Yoshioka, Toru Okazaki, Daisuke Sato, Masayoshi Iwasaki, Toshiji Iwasaka, Yasuhiko Tabata
Journal: Journal of the American College of Cardiology (2011)
Life’s Hourglass
Authors: Linda DeMello
Journal: JAMA (2012)

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
Patients can't stop their data being put onto NHS “spine,” department says
Authors: Owen Dyer
Journal: BMJ (2006)

The government's chief medical officer for England, Liam Donaldson, has written to GPs urging them to pass on to the Department of Health letters from patients who do not want their medical records uploaded to a national computerised database. 

The government's plan to centralise the medical records of 50 million patients in England in a national database known as the national care record, or simply as the “spine,” is meeting increasing opposition. 

A poll conducted by ICM Research two weeks ago found that 53% of NHS patients who responded opposed the plan. A Medix poll of GPs found that 52% would refuse to upload data without a patient's specific consent. 

The Department of Health now says that patients do not …
Embryotoxic effects of brief maternal insulin-hypoglycemia during organogenesis in the rat.
Authors: T A Buchanan, J K Schemmer, N Freinkel
Journal: Journal of Clinical Investigation (1986)

To test whether maternal hypoglycemia can impair organogenesis, we induced brief glucopenia with insulin in conscious pregnant rats during either the headfold stage or the early neural tube closure stage of embryogenesis. At each time, 10 pairs of animals received identical insulin infusions for 1 h. Half the animals were maintained at euglycemia during the infusions, while the others were allowed to become hypoglycemic. Euglycemia was maintained or restored in all animals immediately after the insulin was stopped. Spontaneous activity was diminished during the hypoglycemia but consciousness was preserved. Embryos were removed from mothers and examined 2 d later. This examination revealed that embryos from the hypoglycemic mothers were growth-retarded and displayed a small but significant incidence of gross developmental anomalies compared with embryos from the insulin-infused euglycemic mothers. Thus, brief, mild maternal hypoglycemia during early organogenesis can disrupt normal embryo development in the rat. The effect is due to the hypoglycemia per se rather than to the insulin employed for its induction.
Abstract LB-218: Role of ERBB family negative regulator Mig6 in estimating erlotinib responsiveness.
Authors: Eugene Izumchenko, Xiofei Chang, David Sidransky
Journal: Cancer Research (2013)

Abstract The sensitivity of some tumors to anti-epidermal growth factor receptor EGFR tyrosine kinase inhibitors (TKIs) can be explained by the presence of EGFR tyrosine kinase (TK) domain mutations. However, such mutations are rare and the clinical benefit of a subset of patients with wild-type EGFR may be underestimated due to the lack of appropriate predictive markers to stratify them from larger number of patients who do not response. In this study we sought to elucidate mechanisms of resistance to EGFR-targeted therapies in tumors that harbor no TK sensitizing mutations in order to identify markers capable of guiding the decision to incorporate these drugs into chemotherapeutic regimens. Here we show that mitogen-inducible gene 6 (Mig6), a negative regulator of EGFR, was selectively upregulated by the PI3K-AKT pathway during the evolution of resistance to the EGFR tyrosine kinase inhibitor erlotinib, resulting in decreased EGFR phosporylation. Moreover, we found that high Mig6/EGFR ratio was highly correlated with erlotinib sensitivity, AKT activity, loss of PTEN and epithelial-mesenchymal transition (EMT) status in the panel of 20 lung and head and neck cancer cell lines. Since depletion of Mig6 in erlotinib resistant cell lines didn't render significant increase in drug sensitivity and did not affect AKT activity, we tested whether in resistant cells, activation of kinases other then ERBB family can sustain high level of AKT activation thus suspending erlotinib sensitivity in Mig6-depleted cells. Surprisingly, we found that despite significant deactivation of EGFR, HER2 and HER3 kinases in erlotinib resistant cell lines, activation of PDGFR, FGFR, VEGFR, IGFR or FAK kinases was upregulated in these cells. Here we show that combined treatment with erlotinib and regorafinib (a novel multi-target inhibitor for VEGFR, PDGFR, FGFR, Kit, RET and Raf-1) markedly enhances erlotinib-induced growth inhibition in erlotinib-resistant cells. Collectively, our data highlights the importance of Mig6 in estimating erlotinib responsiveness. Furthermore, our data suggests that by inhibiting EGFR activity in sensitive neoplastic cells, elevated expression of Mig6 triggers acquisition of alternative growth factor pathways that can sustain high level of AKT activity, thus further promoting erlotinib resistance. Citation Format: Eugene Izumchenko, Xiofei Chang, David Sidransky. Role of ERBB family negative regulator Mig6 in estimating erlotinib responsiveness. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-218. doi:10.1158/1538-7445.AM2013-LB-218