tbuckley/cabot-search huggingface dataset:
Suprascapular nerve block in chronic shoulder pain: are the radiologists better?
Authors: E M Shanahan
Journal: Annals of the Rheumatic Diseases (2004)

<b>Background:</b> Suprascapular nerve block is a safe and effective treatment for chronic shoulder pain in arthritis, which can be performed either by direct imaging (CT guided) or in the clinic using anatomical landmarks to determine needle placement. <b>Objective:</b> To compare a CT guided versus an anatomical landmark approach in a randomised, single blind trial examining the efficacy of suprascapular nerve block for shoulder pain in patients with degenerative joint/rotator cuff disease. <b>Methods:</b> 67 patients with chronic shoulder pain from degenerative disease participated in the trial. 77 shoulders were randomised. The group randomised to receive the block through the anatomical landmark approach received a single suprascapular nerve block. Those in the CT guided group received an injection of methylprednisolone acetate and a smaller volume of bupivacaine around the suprascapular nerve. The patients were followed up for 12 weeks by a "blinded" observer and reviewed at weeks 1, 4, and 12 after the injection. <b>Results:</b> Significant improvements were seen in all pain scores and disability in the shoulders receiving both types of nerve block, with no significant differences in the improvement in pain and disability between the two approaches at any time. Improvements in pain and disability scores were clinically and statistically significant. No significant adverse effects occurred in either group. Patient satisfaction scores for pain relief using either approach were high. <b>Conclusion:</b> The CT guided control and landmark approaches to performing suprascapular nerve blocks result in similar significant and prolonged pain and disability reductions; both approaches are safe.
Human Epidermal Growth Factor Receptor 2 Status and Interval Breast Cancer in a Population-Based Cancer Registry Study
Authors: Antonino Musolino, Maria Michiara, Giovanni Maria Conti, Daniela Boggiani, Marella Zatelli, Dario Palleschi, Maria Angela Bella, Paolo Sgargi, Beatrice Di Blasio, Andrea Ardizzoni
Journal: Journal of Clinical Oncology (2012)

To determine whether human epidermal growth factor receptor 2 (HER2) -positive status is associated with risk of breast cancer diagnosis in the interval between mammographic screening, we estimated the distribution of features of aggressive tumor behavior in a general population with newly diagnosed breast cancer and known screening status.We evaluated all invasive breast cancers (N = 641) that were systematically collected by the Parma Province Cancer Registry and diagnosed in women age 50 to 69 years from 2004 to 2007. From this population, 292 screen-detected cancers and 48 interval cases with negative screening mammograms on expert rereading (true interval cancers) were selected for study purposes. Unconditional logistic regression adjusted for age and tumor size was used to determine whether interval cancers were associated with selected clinicobiologic characteristics.Tumors with a high histologic grade (odds ratio [OR], 1.8; 95% CI, 1.2 to 3.8), high proliferative rate (OR, 2.4; 95% CI, 1.2 to 4.5), negative estrogen receptor status (OR, 1.6; 95% CI, 1.1 to 3.1), or HER2-positive status (OR, 3.4; 95% CI, 1.7 to 7.1) were more likely to be diagnosed in the interval between screening. Women age less than 60 years with HER2-positive breast cancer were four times more likely to be diagnosed in the interval between screening compared with only a two-fold increased risk for older women.This population-based cancer registry study demonstrated that HER2-positive tumors account for a substantial proportion of mammographic screening failure. The distribution of biologic characteristics in screen-detected cancers differs from that observed in interval cancers and may account in part for the more aggressive behavior of interval-detected cases.
Neonatal MRI scan could predict cognitive outcome in preterm children
Authors: Jacqui Wise
Journal: BMJ (2015)

Neonatal magnetic resonance imaging (MRI) could be a useful tool to identify premature babies at risk of cognitive impairment, a study reported in the journal Brain has shown.1 Researchers said that such children could then be offered early intervention and monitoring.

The prospective cohort study included 224 premature babies born at a gestational age of less than 30 weeks and 46 …
Virus-specific and anticellular antibodies in molluscum contagiosum
Authors: P.V. SHIRODARIA, R.S. MATTHEWS, MEMY SAMUEL
Journal: British Journal of Dermatology (1979)

Journal Article Virus‐specific and anticellular antibodies in molluscum contagiosum Get access P.V. SHIRODARIA, P.V. SHIRODARIA Department of Microbiology and Immunobiology, The Queen's University of Belfast and Department of Dermatology, Royal Victoria Hospital, Belfast Dr P.V. Shirodaria, Department of Microbiology and Immunobiology, Queen's University, Grosvenor Road, Belfast BT12 6BN. Search for other works by this author on: Oxford Academic Google Scholar R.S. MATTHEWS, R.S. MATTHEWS Department of Microbiology and Immunobiology, The Queen's University of Belfast and Department of Dermatology, Royal Victoria Hospital, Belfast Search for other works by this author on: Oxford Academic Google Scholar MEMY SAMUEL MEMY SAMUEL Department of Microbiology and Immunobiology, The Queen's University of Belfast and Department of Dermatology, Royal Victoria Hospital, Belfast Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 101, Issue 2, 1 August 1979, Pages 133–140, https://doi.org/10.1111/j.1365-2133.1979.tb05597.x Published: 01 August 1979
Involvement of Rel/Nuclear Factor-κB Transcription Factors in Keratinocyte Senescence
Authors: David Bernard, Karo Gosselin, Didier Monte, Chantal Vercamer, Fatima Bouali, Albin Pourtier, Bernard Vandenbunder, Corinne Abbadie
Journal: Cancer Research (2004)

Abstract After a finite doubling number, normal cells become senescent, i.e., nonproliferating and apoptosis resistant. Because Rel/nuclear factor (NF)-κB transcription factors regulate both proliferation and apoptosis, we have investigated their involvement in senescence. cRel overexpression in young normal keratinocytes results in premature senescence, as defined by proliferation blockage, apoptosis resistance, enlargement, and appearance of senescence-associated β-galactosidase (SA-β-Gal) activity. Normal senescent keratinocytes display a greater endogenous Rel/NF-κB DNA binding activity than young cells; inhibiting this activity in presenescent cells decreases the number of cells expressing the SA-β-Gal marker. Normal senescent keratinocytes and cRel-induced premature senescent keratinocytes overexpressed manganese superoxide dismutase (MnSOD), a redox enzyme encoded by a Rel/NF-κB target gene. MnSOD transforms the toxic O2 into H2O2, whereas catalase and glutathione peroxidase convert H2O2 into H2O. Neither catalase nor glutathione peroxidase is up-regulated during cRel-induced premature senescence or during normal senescence, suggesting that H2O2 accumulates. Quenching H2O2 by catalase delays the occurrence of both normal and premature cRel-induced senescence. Conversely, adding a nontoxic dose of H2O2 to the culture medium of young normal keratinocytes induces a premature senescence-like state. All these results indicate that Rel/NF-κB factors could take part in the occurrence of senescence by generating an oxidative stress via the induction of MnSOD.
PREVENTION OF PNEUMOCYSTIS CARINII PNEUMONIA RELAPSE BY PENTAMIDINE AEROSOL IN ZIDOVUDINE-TREATED AIDS PATIENTS
Authors: Pierre-Marie Girard, Claude Gaudebout, Philippe Lottin, PierreDe Truchis, Françoise Camus, Claudie Marche, Roland Landman, Annie Lepretre, Christophe Michon, Sophie Matheron, Robert Farinotti, Jean-Pierre Coulaud, AdrienGérard Saimot
Journal: The Lancet (1989)
Inhibition of TRPC6 Channel Activity Contributes to the Antihypertrophic Effects of Natriuretic Peptides-Guanylyl Cyclase-A Signaling in the Heart
Authors: Hideyuki Kinoshita, Koichiro Kuwahara, Motohiro Nishida, Zhong Jian, Xianglu Rong, Shigeki Kiyonaka, Yoshihiro Kuwabara, Hitoshi Kurose, Ryuji Inoue, Yasuo Mori, Yuhao Li, Yasuaki Nakagawa, Satoru Usami, Masataka Fujiwara, Yuko Yamada, Takeya Minami, Kenji Ueshima, Kazuwa Nakao
Journal: Circulation Research (2010)

Atrial and brain natriuretic peptides (ANP and BNP, respectively) exert antihypertrophic effects in the heart via their common receptor, guanylyl cyclase (GC)-A, which catalyzes the synthesis of cGMP, leading to activation of protein kinase (PK)G. Still, much of the network of molecular mediators via which ANP/BNP-GC-A signaling inhibit cardiac hypertrophy remains to be characterized.We investigated the effect of ANP-GC-A signaling on transient receptor potential subfamily C (TRPC)6, a receptor-operated Ca(2+) channel known to positively regulate prohypertrophic calcineurin-nuclear factor of activated T cells (NFAT) signaling.In cardiac myocytes, ANP induced phosphorylation of TRPC6 at threonine 69, the PKG phosphorylation site, and significantly inhibited agonist-evoked NFAT activation and Ca(2+) influx, whereas in HEK293 cells, it dramatically inhibited agonist-evoked TRPC6 channel activity. These inhibitory effects of ANP were abolished in the presence of specific PKG inhibitors or by substituting an alanine for threonine 69 in TRPC6. In model mice lacking GC-A, the calcineurin-NFAT pathway is constitutively activated, and BTP2, a selective TRPC channel blocker, significantly attenuated the cardiac hypertrophy otherwise seen. Conversely, overexpression of TRPC6 in mice lacking GC-A exacerbated cardiac hypertrophy. BTP2 also significantly inhibited angiotensin II-induced cardiac hypertrophy in mice.Collectively, these findings suggest that TRPC6 is a critical target of antihypertrophic effects elicited via the cardiac ANP/BNP-GC-A pathway and suggest TRPC6 blockade could be an effective therapeutic strategy for preventing pathological cardiac remodeling.
Macrophage fusion
Authors: Agnès Vignery
Journal: The Journal of Experimental Medicine (2005)

The fusion of cells is a fundamental biological event that is essential for a variety of developmental and homeostatic processes. Fusion is required for the formation of multinucleated osteoclasts and giant cells, although the mechanisms that govern these processes are poorly understood. A new study now reveals an unexpected role for the receptor, dendritic cell–specific transmembrane protein (DC-STAMP), in this process. The potential mechanism by which DC-STAMP governs fusion and the implications of this finding will be discussed.
Effects of oral magnesium sulphate on colonic motility in patients with the irritable bowel syndrome
Authors: R. F. Harvey, A. E. Read
Journal: Gut (1973)

Magnesium sulphate, a substance known to cause release of cholecystokinin (CCK) from the small intestinal mucosa, was given by mouth (dose 0.1g/kg in 150 ml water) to 20 patients with the irritable bowel syndrome. A rapid increase in colonic segmental motor activity (onset within two to six minutes in most cases) was seen (percentage activity increased from 16.2 to 23.7 p<0.05; mean wave amplitude from 7.1 to 9.1 cm H(2)O, NS; motility index from 144 to 259, p<0.01). This increase was most marked in 10 patients who complained of attacks of abdominal pain after food (16.1 to 29.8%, p<0.01; 6.8 to 9.6 cm H(2)O, p<0.05; 135 to 350, p<0.05), and after the magnesium sulphate three of these patients experienced an attack of their usual pain. These findings provide further evidence that ;functional' abdominal pain after food may in some cases be related to an exaggerated intestinal motor response to cholecystokinin.
Fuel Metabolism in Starvation
Authors: George F. Cahill
Journal: Annual Review of Nutrition (2006)

This article, which is partly biographical and partly scientific, summarizes a life in academic medicine. It relates my progress from benchside to bedside and then to academic and research administration, and concludes with the teaching of human biology to college undergraduates. My experience as an intern (anno 1953) treating a youngster in diabetic ketoacidosis underscored our ignorance of the controls in human fuel metabolism. Circulating free fatty acids were then unknown, insulin could not be measured in biologic fluids, and beta-hydroxybutyric acid, which was difficult to measure, was considered by many a metabolic poison. The central role of insulin and the metabolism of free fatty acids, glycerol, glucose, lactate, and pyruvate, combined with indirect calorimetry, needed characterization in a near-steady state, namely prolonged starvation. This is the main topic of this chapter. Due to its use by brain, D-beta-hydroxybutyric acid not only has permitted man to survive prolonged starvation, but also may have therapeutic potential owing to its greater efficiency in providing cellular energy in ischemic states such as stroke, myocardial insufficiency, neonatal stress, genetic mitochondrial problems, and physical fatigue.
Pneumomediastinum in dermatomyositis: association with cutaneous vasculopathy
Authors: H. Kono
Journal: Annals of the Rheumatic Diseases (2000)

To study the pathogenesis of pneumomediastinum in polymyositis/dermatomyositis (PM/DM).The clinical records of 48 patients with PM/DM were reviewed, focusing mainly on the presence of pneumomediastinum and cutaneous vasculopathy, and the chest radiographic changes. A patient with pneumomediastinum with a characteristic change in his bronchus is described in detail. Case reports of pneumomediastinum in PM/DM in English publications are reviewed.Among the 48 patients with PM/DM, pneumomediastinum was observed as a complication in four patients with DM and none of the patients with PM. Three of the four patients with pneumomediastinum, but only six of the 44 patients without this complication, had associated cutaneous vasculopathy. There was a significant association of pneumomediastinum with cutaneous vasculopathy (p = 0.02) and younger age (p = 0.04), but not with the prevalence of lung disease. A 30 year old man (patient 1) with DM, who had interstitial pneumonitis and skin ulceration due to vasculopathy, developed pneumomediastinum. Fibreoptic bronchoscopy showed white plaques on the bronchial mucosa, which were confirmed by microscopic examination as representing subepithelial necrosis. A literature review showed 13 cases of DM but no patient with PM with pneumomediastinum.In patient 1, bronchial necrosis due to vasculopathy was strongly suspected as being responsible for the pneumomediastinum. The results suggest that pneumomediastinum was associated not with interstitial pneumonitis but with the complication of vasculopathy appearing as skin lesions in DM.
Insulin Signaling in the Pancreatic β-Cell
Authors: Ingo B. Leibiger, Barbara Leibiger, Per-Olof Berggren
Journal: Annual Review of Nutrition (2008)

The appropriate function of insulin-producing pancreatic β-cells is crucial for the regulation of glucose homeostasis, and its impairment leads to diabetes mellitus, the most common metabolic disorder in man. In addition to glucose, the major nutrient factor, inputs from the nervous system, humoral components, and cell-cell communication within the islet of Langerhans act together to guarantee the release of appropriate amounts of insulin in response to changes in blood glucose levels. Data obtained within the past decade in several laboratories have revitalized controversy over the autocrine feedback action of secreted insulin on β-cell function. Although insulin historically has been suggested to exert a negative effect on β-cells, recent data provide evidence for a positive role of insulin in transcription, translation, ion flux, insulin secretion, proliferation, and β-cell survival. Current insights on the role of insulin on pancreatic β-cell function are discussed.
Immunomodulating cytokines in atopic dermatitis and psoriasis: production of tumour necrosis factor and lymphotoxin by mononuclear cells in vitro
Authors: A. KAPP, A. TEXTOR, J. KRUTMANN, A. MoLLER
Journal: British Journal of Dermatology (1990)

The immunomodulating cytokines, tumour necrosis factor/cachectin (TNF) and lymphotoxin (LT) are thought to play an essential role as mediators of inflammatory reactions. To evaluate the role of TNF and LT in atopic dermatitis (AD) and psoriasis, we investigated their production by mononuclear cells (MNC) in vitro. The 24-h supernatants of lipopolysaccharide (LPS)- and phytohaemagglutinin (PHA)-stimulated and unstimulated MNC from 26 patients with AD and 20 with psoriasis and from 17 non-atopic healthy controls were tested for the concentrations of TNF and LT using an ELISA technique. In patients with AD, TNF levels were significantly decreased in the supernatant of PHA-stimulated (P less than or equal to 0.005) and LPS-stimulated (P less than or equal to 0.02) MNC in comparison to controls. There was no significant difference in TNF production between psoriatic patients and the control group. Release of LT in the supernatant of PHA-stimulated MNC by patients and controls did not differ significantly. There was no significant spontaneous production of TNF and LT by MNC of patients and controls. These studies indicate that different immunomodulating mechanisms are responsible for triggering the inflammatory response in AD and psoriasis.
EGFR/Src/Akt signaling modulates Sox2 expression and self-renewal of stem-like side-population cells in non-small cell lung cancer
Authors: Sandeep Singh, Jose Trevino, Namrata Bora-Singhal, Domenico Coppola, Eric Haura, Soner Altiok, Srikumar P Chellappan
Journal: Molecular Cancer (2012)

Abstract Background Cancer stem cells are thought to be responsible for the initiation and progression of cancers. In non-small cell lung cancers (NSCLCs), Hoechst 33342 dye effluxing side population (SP) cells are shown to have stem cell like properties. The oncogenic capacity of cancer stem-like cells is in part due to their ability to self-renew; however the mechanistic correlation between oncogenic pathways and self-renewal of cancer stem-like cells has remained elusive. Here we characterized the SP cells at the molecular level and evaluated its ability to generate tumors at the orthotopic site in the lung microenvironment. Further, we investigated if the self-renewal of SP cells is dependent on EGFR mediated signaling. Results SP cells were detected and isolated from multiple NSCLC cell lines (H1650, H1975, A549), as well as primary human tumor explants grown in nude mice. SP cells demonstrated stem-like properties including ability to self-renew and grow as spheres; they were able to generate primary and metastatic tumors upon orthotopic implantation into the lung of SCID mice. In vitro study revealed elevated expression of stem cell associated markers like Oct4, Sox2 and Nanog as well as demonstrated intrinsic epithelial to mesenchymal transition features in SP cells. Further, we show that abrogation of EGFR, Src and Akt signaling through pharmacological or genetic inhibitors suppresses the self-renewal growth and expansion of SP-cells and resulted in specific downregulation of Sox2 protein expression. siRNA mediated depletion of Sox2 significantly blocked the SP phenotype as well as its self-renewal capacity; whereas other transcription factors like Oct4 and Nanog played a relatively lesser role in regulating self-renewal. Interestingly, Sox2 was elevated in metastatic foci of human NSCLC samples. Conclusions Our findings suggest that Sox2 is a novel target of EGFR-Src-Akt signaling in NSCLCs that modulates self-renewal and expansion of stem-like cells from NSCLC. Therefore, the outcome of the EGFR-Src-Akt targeted therapy may rely upon the expression and function of Sox2 within the NSCLC-CSCs.
S158 Occupational asthma; referral patterns from primary care in the UK
Authors: J. L. Hoyle, L. Hussey, R. Agius
Journal: Thorax (2010)

<h3>Introduction and Objectives</h3> Occupational asthma is the commonest reported occupational lung disease in the UK<sup>1</sup>.The British Occupational Health Research Foundation (BOHRF)<sup>2</sup> guidelines 2010 recommend that ‘all family practices be able to screen for occupational asthma, and have a plan for further management’. The standards of care for occupational asthma<sup>3</sup> recommend ‘early referrals to a specialist with an interest in occupational asthma if such a diagnosis is suspected’. This referral should take place ‘after occupational asthma is screened for before important life decisions are made’. (SIGN guidelines<sup>4</sup>). Very little is known about the proportion of cases that are referred on to clinical specialists once identified. <h3>Methods</h3> The Health &amp; Occupation Reporting network in General Practice (THOR-GP) at the University of Manchester, collects work-related ill-health data between 250 and 300 GPs trained to diploma level in occupational medicine. Cases with a diagnosis of occupational asthma reported in 2006–2009 were divided into subgroups by their causative agent. Cases referred to a hospital specialist were compared to those not referred. <h3>Results</h3> In 2006–2009, GPs reported 4902 cases of work-related ill-health, of which 115 (2%) were reports of respiratory disease. 33 were diagnosed with asthma, 6 were referred to a hospital specialist (Abstract S158 Figure 1). The cases not referred included workers exposed to a variety of known asthmagens. <h3>Conclusion</h3> Despite national recommendations, these data show that the majority of cases suspected as having occupational asthma are not referred to hospital specialists from primary care. It is not known if the lack of referral affects outcome with regards to disease prognosis, disability or employment status.
MicroRNAs - A New Generation Molecular Targets for Treating Cellular Diseases
Authors: Ramasamy Paulmurugan
Journal: Theranostics (2013)

MicroRNAs (miRNAs) are a unique class of non-coding, small RNAs, similar to mRNAs, transcribed by cells, but for entirely different reasons. While mRNAs are transcribed to code for proteins, miRNAs are produced to regulate the production of proteins from mRNAs. miRNAs are central components that tightly and temporally regulating gene expression in cells. Dysregulation of miRNAs expressions in cellular pathogenesis, including cancer, has been reported, and it clearly supports the importance of miRNAs as therapeutic targets in almost every cellular disease. This special issue compiles manuscripts from different authors in order to highlight the importance of microRNAs in cancer and other cellular diseases and how to explore them as therapeutic targets to treat patients with these genetic and metabolic disorders. This issue also covers manuscripts that highlight the obstacles associated with the delivery of therapeutic microRNAs in cells and in vivo in living animals and how to improve and noninvasively monitor the delivery in living animals through molecular imaging, including potential clinical perspectives.