tbuckley/cabot-search huggingface dataset:
Deprivation, low birth weight, and children's height: a comparison between rural and urban areas.
Authors: R Reading, S Raybould, S Jarvis
Journal: BMJ (1993)

OBJECTIVE--To compare proportions of low birthweight babies and mean heights of schoolchildren between rural and urban areas at different levels of social deprivation. DESIGN--Cross sectional population based study classifying cases by Townsend material deprivation index of enumeration district of residence and by rural areas, small towns, and large towns. SETTING--Northumberland Health District. SUBJECTS--18,930 singleton infants delivered alive during January 1985 to September 1990 and resident in Northumberland in October 1990; 9055 children aged 5 to 8 1/2 years attending Northumberland schools in the winter of 1989-90. MAIN OUTCOME MEASURES--Odds ratios for birth weight less than 2800 g; difference in mean height measured by standard deviation (SD) score. RESULTS--Between the most deprived and most affluent 20% of enumeration districts the odds ratio for low birth weight adjusted for rural or urban setting was 1.71 (95% confidence interval 1.51 to 1.93) and the difference in mean height -0.232 SD score (-0.290 to -0.174). Between large towns and rural areas the odds ratio for low birth weight adjusted for deprivation was 1.37 (1.23 to 1.53) and the difference in mean height -0.162 SD score (-0.214 to -0.110). Results for small towns were intermediate between large towns and rural areas. CONCLUSIONS--Inequalities in birth weight and height exist in all rural and urban settings between deprived and affluent areas. In addition, there is substantial disadvantage to living in urban areas compared with rural areas which results from social or environmental factors unrelated to current levels of deprivation.
Severe combined immunodeficiency caused by deficiency in either the δ or the ε subunit of CD3
Authors: Geneviève de Saint Basile, Frédéric Geissmann, Elisabeth Flori, Béatrice Uring-Lambert, Claire Soudais, Marina Cavazzana-Calvo, Anne Durandy, Nada Jabado, Alain Fischer, Françoise Le Deist
Journal: Journal of Clinical Investigation (2004)

We investigated the molecular mechanism underlying a severe combined immunodeficiency characterized by the selective and complete absence of T cells. The condition was found in 5 patients and 2 fetuses from 3 consanguineous families. Linkage analysis performed on the 3 families revealed that the patients were carrying homozygous haplotypes within the 11q23 region, in which the genes encoding the γ, δ, and ε subunits of CD3 are located. Patients and affected fetuses from 2 families were homozygous for a mutation in the CD3D gene, and patients from the third family were homozygous for a mutation in the CD3E gene. The thymus from a CD3δ-deficient fetus was analyzed and revealed that T cell differentiation was blocked at entry into the double positive (CD4+CD8+) stage with the accumulation of intermediate CD4–single positive cells. This indicates that CD3δ plays an essential role in promoting progression of early thymocytes toward double-positive stage. Altogether, these findings extend the known molecular mechanisms underlying severe combined immunodeficiency to a new deficiency, i.e., CD3ε deficiency, and emphasize the essential roles played by the CD3ε and CD3δ subunits in human thymocyte development, since these subunits associate with both the pre-TCR and the TCR.
NHS must reimburse patients treated abroad because of delays at home
Authors: Clare Dyer
Journal: BMJ (2006)

The NHS must reimburse UK patients who travel to another European Union member state for treatment when they face “undue delay” at home, the European Court of Justice in Luxembourg ruled this week.

The ruling came in a case brought by Yvonne Watts, aged 75, who had a £4000 €5900; $7500) hip operation in France, but she was told that Bedford Primary Care Trust would not pay for it.

The judgment will have significant implications for the NHS, although waiting times have come down substantially since Mrs Watts opted to have her operation in France. The Department of Health said that the wait for a hip operation was now down to six months.

A spokesman said that the government would be issuing updated guidance to the NHS shortly, adding, “We do not expect this judgment …
Bubble Continuous Positive Airway Pressure Enhances Lung Volume and Gas Exchange in Preterm Lambs
Authors: J. Jane Pillow, Noah Hillman, Timothy J. M. Moss, Graeme Polglase, Geoff Bold, Chris Beaumont, Machiko Ikegami, Alan H. Jobe
Journal: American Journal of Respiratory and Critical Care Medicine (2007)

Rationale: The technique used to provide continuous positive airway pressure (CPAP) to the newborn may influence lung function and breathing efficiency.Objectives: To compare differences in gas exchange physiology and lung injury resulting from treatment of respiratory distress with either bubble or constant pressure CPAP and to determine if the applied flow influences short-term outcomes.Methods: Lambs (133 d gestation; term is 150 d) born via cesarean section were weighed, intubated, and treated with CPAP for 3 hours. Two groups were treated with 8 L/minute applied flow using the bubble (n = 12) or the constant pressure (n = 12) technique. A third group (n = 10) received the bubble method with 12 L/minute bias flow. Measurements at study completion included arterial blood gases, oxygraphy, capnography, tidal flow, multiple breath washout, lung mechanics, static pressure–volume curves, and bronchoalveolar lavage fluid protein.Measurements and Main Results: Birth weight and arterial gas variables at 15 minutes were comparable. Flow (8 or 12 L/min) did not influence the 3-hour outcomes in the bubble group. Bubble technique was associated with a higher pH, PaO2, oxygen uptake, and area under the flow–volume curve, and a decreased alveolar protein, respiratory quotient, PaCO2, and ventilation inhomogeneity compared with the constant pressure group.Conclusions: Compared with constant pressure technique, bubble CPAP promotes enhanced airway patency during treatment of acute postnatal respiratory disease in preterm lambs and may offer protection against lung injury.
Frequent Inactivation of <i>Cysteine Dioxygenase Type 1</i> Contributes to Survival of Breast Cancer Cells and Resistance to Anthracyclines
Authors: Jana Jeschke, Heather M. O'Hagan, Wei Zhang, Rajita Vatapalli, Marilia Freitas Calmon, Ludmila Danilova, Claudia Nelkenbrecher, Leander Van Neste, Ingrid T.G.W. Bijsmans, Manon Van Engeland, Edward Gabrielson, Kornel E. Schuebel, Andreas Winterpacht, Stephen B. Baylin, James G. Herman, Nita Ahuja
Journal: Clinical Cancer Research (2013)

Genome-wide DNA methylation analyses have identified hundreds of candidate DNA-hypermethylated genes in cancer. Comprehensive functional analyses provide an understanding of the biologic significance of this vast amount of DNA methylation data that may allow the determination of key epigenetic events associated with tumorigenesis.To study mechanisms of cysteine dioxygenase type 1 (CDO1) inactivation and its functional significance in breast cancer in a comprehensive manner, we screened for DNA methylation and gene mutations in primary breast cancers and analyzed growth, survival, and reactive oxygen species (ROS) production in breast cancer cells with restored CDO1 function in the context of anthracycline treatment.DNA methylation-associated silencing of CDO1 in breast cancer is frequent (60%), cancer specific, and correlates with disease progression and outcome. CDO1 function can alternatively be silenced by repressive chromatin, and we describe protein-damaging missense mutations in 7% of tumors without DNA methylation. Restoration of CDO1 function in breast cancer cells increases levels of ROS and leads to reduced viability and growth, as well as sensitization to anthracycline treatment. Priming with 5-azacytidine of breast cancer cells with epigenetically silenced CDO1 resulted in restored expression and increased sensitivity to anthracyclines.We report that silencing of CDO1 is a critical epigenetic event that contributes to the survival of oxidative-stressed breast cancer cells through increased detoxification of ROS and thus leads to the resistance to ROS-generating chemotherapeutics including anthracyclines. Our study shows the importance of CDO1 inactivation in breast cancer and its clinical potential as a biomarker and therapeutic target to overcome resistance to anthracyclines.
Potassium depletion downregulates chloride-absorbing transporters in rat kidney.
Authors: H Amlal, Z Wang, M Soleimani
Journal: Journal of Clinical Investigation (1998)

Potassium depletion (KD) causes renal chloride wasting, suggesting defect(s) in Cl- reabsorption in renal tubules. To determine whether alterations in expression of the major Cl- transporter genes might contribute to the chloride wasting, we analyzed their expression in renal cortex and medulla of animals placed on KD diet. Feeding KD diet to rats resulted in significant hypokalemia at 14 d but not at 6 d. Northern hybridization revealed that mRNA levels for the apical Na-K-2Cl cotransporter in the medulla decreased by 56 and 51% at 6 and 14 d of KD diet, respectively. Functional studies in tubular suspensions from medullary thick ascending limb demonstrated that the Na-K-2Cl cotransporter activity decreased by approximately 45 and approximately 37% at 6 and 14 d of KD diet, respectively. mRNA levels for the thiazide-sensitive Na-Cl cotransporter decreased by 57 and 64% at 6 and 14 d of KD diet. Decreased expression of the apical Na-Cl and the Na-K-2Cl cotransporters became evident at 48 and 72 h of KD, respectively. Urinary chloride excretion increased at 48 h and further increased at 72 h of KD, correlating with suppression of the Na-Cl and the Na-K-2Cl transporters. Our results indicate that increased urinary chloride loss in KD results from suppression of the chloride-absorbing transporters. Downregulation of chloride transporters in KD is an early event and can lead to hypochloremia and subsequently hypovolemia and decreased glomerular filtration rate.
Abstract 1181: The Apoptosis repressor with a CARD domain (ARC) is a direct HIF1 target gene and promotes survival and proliferation of VHL deficient renal cancer cells
Authors: Olga V. Razorenova, Laura Castellini, Renata Colavitti, Laura E. Edgington, Monica Nicolau, Xin Huang, Barbara Bedogni, Edward M. Mills, Matthew Bogyo, Amato J. Giaccia
Journal: Cancer Research (2014)

Abstract The induction of hypoxia inducible factors (HIFs) is essential for the adaptation of tumor cells to a low oxygen environment. We found that the expression of the apoptosis inhibitor ARC was induced by hypoxia in a variety of cancer cell types and its induction is primarily HIF1 dependent. Chromatin immunoprecipitation (ChIP) and reporter assays also indicate that the ARC gene is regulated by direct binding of HIF1 to a hypoxia response element (HRE) located at -190 bp upstream of the transcription start site. HIFs play an essential role in the pathogenesis of renal cell carcinoma (RCC) under normoxic conditions, through the loss of the Von Hippel Lindau (VHL) gene. Accordingly, our results show that ARC is not expressed in normal renal tissue, but is highly expressed in 65% of RCC tumors, which also express high levels of Carbonic Anhydrase IX (CAIX), a HIF1-dependent gene. Compared to controls, ARC-deficient RCCs exhibited decreased colony formation and increased apoptosis in vitro. In addition, loss of ARC resulted in a dramatic reduction of RCC tumor growth in SCID mice in vivo. Thus, HIF-mediated increased expression of ARC in RCC can explain how loss of VHL can promote survival early in tumor formation. Citation Format: Olga V. Razorenova, Laura Castellini, Renata Colavitti, Laura E. Edgington, Monica Nicolau, Xin Huang, Barbara Bedogni, Edward M. Mills, Matthew Bogyo, Amato J. Giaccia. The Apoptosis repressor with a CARD domain (ARC) is a direct HIF1 target gene and promotes survival and proliferation of VHL deficient renal cancer cells. [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 1181. doi:10.1158/1538-7445.AM2014-1181
Fluoridation and the Occurrence of Down's Syndrome
Authors: Howard L. Needleman, Siegfried M. Pueschel, Kenneth J. Rothman
Journal: New England Journal of Medicine (1974)

The prevalence rates of Down's syndrome at birth were compared for Massachusetts residents ingesting fluoridated and non-fluoridated water. The observations included nearly all children born alive with Down's syndrome in Massachusetts during the 17-year period 1950–1966. A rate of 1.5 cases per 1000 births was found both for fluoride-related births and appropriate comparison groups; the upper bound of a one-sided 95 per cent confidence interval for the ratio of fluoride to non-fluoride rates was 1.2. Thus, the data provide strong evidence that fluoridation does not cause any important elevation in risk for Down's syndrome, at least not for several years after its introduction. (N Engl J Med 291:821–823, 1974)
Deciphering Cholesterol Treatment Guidelines
Authors: Om P. Ganda
Journal: JAMA (2015)

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
ONCOSCINTIGRAPY OF NEUROENDOCRINE AND NONNEUROENDOCRINE TUMORS WITH A NOVEL SSR BINDING PEPTIDE-TECHNETIUM TC-99M P829-PRELIMINARY EXPERIENCE IN 39 PATIENTS
Authors: H. Handmaker, K. T. Mohler, R. W. Dann, J. Lister-James, Y. M. Baran
Journal: Clinical Nuclear Medicine (1997)

Handmaker, H.; Mohler, K. T.; Dann, R. W.; Lister-James, J.; Baran, Y. M. Author Information
Dental Anxiety and Illness Behaviour
Authors: Klaus Portmann, Bogdan P. Radanov
Journal: Psychotherapy and Psychosomatics (1997)

To analyse the relationship between dental anxiety and illness behaviour.Dental anxiety was assessed in 165 patients from private practice using the Dental Anxiety Scale (DAS), aspects of illness behaviour were evaluated by the Illness Attitude Scale (IAS), and aspects of general anxiety were analysed by the State Trait Anxiety Inventory (STAI). Dental status was documented using the DMFS index and Bleeding-on-Probing index (BOP).Multiple regression analysis (explained proportion of variance = 32%) showed that dental anxiety was significantly correlated with female gender (t = 3.109, p < 0.002) and IAS health habits (t = -2.210, p < 0.03). In addition, a correlation trend was found between dental anxiety and BOP index (t = -1.789, p < 0.08).Dental anxiety appears to be a gender-specific phenomenon. Results indicate a tendency towards abnormal illness behaviour (i.e. denial of dental anxiety) in a considerable proportion of subjects and as a consequence display of poor health habits (i.e. counterphobic behaviour). The latter may lead to an increased tendency to develop gingivitis as indicated by the correlation trend between dental anxiety and BOP index.
Dynamic Airway Narrowing
Authors: Hajime Kurosawa, Masahiro Kohzuki
Journal: New England Journal of Medicine (2004)

A 61-year-old man who reported progressive exertional dyspnea of 12 years' duration received a diagnosis of chronic obstructive pulmonary disease on the basis of a 150-pack-year history of smoking, emphysema on radiographic evaluation, and a forced expiratory volume in one second of 0.72 liter (28.8 percent of the predicted value). An upper thoracic high-speed electron-beam computed tomographic scan showed small airways (approximately 3 mm in diameter) that were open during inspiration (Panel A, arrows) but extremely narrow during expiration (Panel B, arrows). Dynamic narrowing of the airways is common in patients with chronic obstructive pulmonary disease and is caused by . . .
A developmental perspective on action and social cognition
Authors: Sheila Krogh-Jespersen, Courtney Filippi, Amanda L. Woodward
Journal: Behavioral and Brain Sciences (2014)

Abstract The target article argues that developmental processes are key to understanding the mirror neuron system, yet neglects several bodies of developmental research that are informative for doing so. Infants' actions and action understanding are structured by goals, and the former lends structure to the latter. Evaluating the origins and functions of mirror neurons depends on integrating investigations of neural, social-cognitive and motor development.
Radioactive Nuclides in Medicine and Biology
Authors: E. James Potchen
Journal: JAMA (1969)

The clinical application of radionuclides to medical care has burgeoned in the past decade. Some 15 years ago, the first edition of Quimby, Fidelberg, and Silver entitled<i>Radioactive Isotopes in Medicine</i>was widely received as an authoritative book and was a forerunner of modern texts in nuclear medicine. As with the second edition, Dr. Silver now encompasses the medical aspects of radioactive nuclides in one volume. The companion text on physics and instrumentation has not yet been published. Although Dr. Silver makes an attempt to cover the entire field of nuclear medicine, a single-authored text in such a multidisciplined area will undoubtedly be limited by the interest of the author. There is, therefore, considerable emphasis on the thyroid gland and iodine metabolism and adequate coverage of static clinical scintiscanning, but only limited discussion of new radiopharmaceuticals, kinetic analysis, or tracer-method theory. The book contains an exhaustive review of the literature,
Pharmacokinetics of Cetuximab After Administration of Escalating Single Dosing and Weekly Fixed Dosing in Patients with Solid Tumors
Authors: Antoinette R. Tan, Dirk F. Moore, Manuel Hidalgo, James H. Doroshow, Elizabeth A. Poplin, Susan Goodin, David Mauro, Eric H. Rubin
Journal: Clinical Cancer Research (2006)

Abstract Purpose: Previous studies of cetuximab pharmacokinetics did not fully characterize its elimination phase. The purpose of this trial was to evaluate the pharmacokinetics of cetuximab given as a single dose followed by weekly fixed repeated dosing in patients with solid tumors. Experimental Design: Patients were randomly assigned to treatment with a single 2-hour infusion of cetuximab at doses of 50, 100, 250, 400, or 500 mg/m2 followed 3 weeks later by weekly 1-hour infusions of cetuximab at a fixed dose of 250 mg/m2. Extended pharmacokinetic sampling was collected through 504 hours after the first drug administration. Trough samples were obtained before each fixed weekly dose. Single and multidose pharmacokinetic variables were correlated with clinical outcomes. Results: Forty patients were enrolled. Pharmacokinetic analysis confirmed previous reports of nonlinear pharmacokinetics for cetuximab. Modeling studies predicted a 90% saturation of clearance at a dose of 260 mg/m2. Analyses of weekly trough concentrations indicated a slight accumulation of drug concentrations following repeated weekly dosing. Correlative studies indicated a significant association between cetuximab clearance and both body surface area (P = 0.002) and weight (P = 0.002). The occurrence of rash was significantly associated with disease stability (P &amp;lt; 0.002) but not with cetuximab pharmacokinetic variables. Conclusions: Pharmacokinetic results support using body surface area or weight in calculating individual cetuximab doses. A weekly dose of 250 mg/m2 is predicted to nearly fully saturate cetuximab clearance and, by inference, epidermal growth factor receptors. The association between rash and disease stability supports further prospective studies of this relationship.
NO more muscle fatigue
Authors: Ahlke Heydemann, Elizabeth McNally
Journal: Journal of Clinical Investigation (2009)

NOS is a key enzyme in the production of NO, a molecule that directly regulates vasorelaxation and blood supply. Diverse forms of muscle disease have been clinically associated with unusual fatigue after exercise. The localization of neuronal NOS (nNOS) at the plasma membrane of muscle has recently been shown to prevent muscle fatigue after exercise. In this issue of the JCI, Lai et al. show that dystrophin--the structural protein missing in individuals with Duchenne muscular dystrophy--anchors nNOS to the sarcolemma through a direct interaction with dystrophin spectrin-like repeats 16 and 17 (see the related article, doi:10.1172/JCI36612). Furthermore, in another recently reported study of mouse models of muscular dystrophy, phosphodiesterase 5A inhibitors were used to treat the downstream ischemia that is associated with nNOS mislocalization. Collectively, these findings significantly advance our understanding of exercise-induced muscle fatigue and its role in muscle disease.
Receptor for activated C kinase 1 promotes hepatocellular carcinoma growth by enhancing mitogen-activated protein kinase kinase 7 activity
Authors: Yuanyuan Guo, Wendie Wang, Jing Wang, Jiannan Feng, Qingyang Wang, Jianfeng Jin, Ming Lv, Xinying Li, Yan Li, Yuanfang Ma, Beifen Shen, Jiyan Zhang
Journal: Hepatology (2012)

c-Jun N-terminal protein kinase (JNK) is a member of the mitogen-activated protein kinase (MAPK) superfamily. The activation of JNK is mediated by sequential protein phosphorylation through a MAPK module, namely, MAPK kinase kinase (MAP3K or MEKK) → MAPK kinase (MAP2K or MKK) → MAPK. Elevated levels of JNK activity have been frequently observed in hepatocellular carcinoma (HCC) and have been demonstrated to contribute to HCC growth by promoting HCC cell proliferation and resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)- or Fas-mediated apoptosis. Chronic inflammation contributes to the up-regulation of JNK activity in HCC. However, it remains unknown whether aberrant JNK activity also results from some cell intrinsic defect(s). Here, we show that receptor for activated C kinase 1 (RACK1), an adaptor protein implicated in the regulation of multiple signaling pathways, could engage in a direct interaction with MKK7, the JNK-specific MAP2K, in human HCC cells. Levels of RACK1 protein show correlation with the activity of the JNK pathway in human HCC tissues and cell lines. RACK1 loss-of-function or gain-of-function analyses indicate that RACK1 enhances MKK7/JNK activity in human HCC cells. Further exploration reveals that the interaction of RACK1 with MKK7 is required for the enhancement of MKK7/JNK activity by RACK1. RACK1/MKK7 interaction facilitates the association of MKK7 with MAP3Ks, thereby enhancing MKK7 activity and promoting in vitro HCC cell proliferation and resistance to TRAIL- or Fas-mediated apoptosis as well as in vivo tumor growth.Overexpressed RACK1 augments JNK activity and thereby promotes HCC growth through directly binding to MKK7 and enhancing MKK7 activity.