tbuckley/cabot-search huggingface dataset:
P174 Severity of Bronchiectasis on High Resolution CT Scanning and Its Relationship to Chronic Bacterial Colonisation
Authors: RJ Stretton, KE Leighton, S Marshall, S Schembri, T Fardon, JD Chalmers
Journal: Thorax (2012)

<h3>Introduction</h3> Bacterial colonisation and particularly colonisation with <i>Pseudomonas aeruginosa</i> is associated with a more severe clinical course in bronchiectasis. It is often presumed that patients with more extensive radiological bronchiectasis are at higher risk of chronic bacterial colonisation, but data on this is lacking. The aim of this study was to determine if severity of bronchiectasis on HRCT predicts chronic bacterial colonisation. <h3>Methods</h3> Data was collected from a specialist bronchiectasis clinic from April 2011 to April 2012. A total of 88 patients were diagnosed with bronchiectasis following assessment by a respiratory physician and a high resolution CT scan. Sputum cultures from the previous 2 years were used to determine colonisation status. The severity of disease on CT scanning was determined for each patient using a modified Reiff scoring system. This attributed to every lobe a score dependant on the type of Bronchiectasis seen and the number of lobes involved – Cylindrical=1, Varicose=2, Cystic=3. The minimum score is 1 and the maximum score is 18. <h3>Results</h3> 88 patients had bronchiectasis confirmed on HRCT by a clinical radiologist. For each set of patients colonised with a particular organism the average Reiff score was calculated. 11 patients had <i>P. aeruginosa</i> (Reiff mean 5.6, SD 4.8). This score was significantly higher than those patients colonised with other pathogenic microorganisms (Reiff mean 3.4, SD 2.9) (p=0.03), and for patients not colonised with microorganisms (Reiff mean 3.0, SD 2.2) (p=0.005).- figure 1. Among the other organisms isolated 29 patients had <i>Haemophilus influenzae</i> (Reiff Mean 3.7, SD 3.5). This mean Reiff score was significantly lower than for <i>P. aeruginosa</i>,(p=0.03) – figure 1. <i>Streptococcus pneumoniae</i> (Reiff Mean 3.4), <i>Moraxella catarrhalis</i> (Reiff Mean 3.7) and <i>Staphylococcus aureus</i> (Reiff Mean 3.2), were also isolated in lesser numbers and a further 28 patients had a mix of other colonising organisms (Reiff Mean 3.5). <h3>Conclusion</h3> More severe radiological bronchiectasis is associated with the presence of bacterial colonisation and particularly colonisation with <i>Pseudomonas aeruginosa</i>. This simple assessment of radiological severity may be a useful clinical tool in non-CF bronchiectasis.
Stromal Cell–Derived Factor-1α and CXCR4 Expression in Hemangioblastoma and Clear Cell-Renal Cell Carcinoma: von Hippel-Lindau Loss-of-Function Induces Expression of a Ligand and Its Receptor
Authors: David Zagzag, Balaji Krishnamachary, Herman Yee, Hiroaki Okuyama, Luis Chiriboga, M. Aktar Ali, Jonathan Melamed, Gregg L. Semenza
Journal: Cancer Research (2005)

Abstract The genetic hallmark of hemangioblastomas and clear cell-renal cell carcinomas (CC-RCCs) is loss-of-function of the von Hippel-Lindau (VHL) tumor suppressor protein. VHL is required for oxygen-dependent degradation of hypoxia-inducible factor-1α (HIF-1α). In hemangioblastomas and CC-RCCs, HIF-1α is constitutively overexpressed leading to increased transcription of HIF-1–regulated genes, including vascular endothelial growth factor (VEGF). Because loss of VHL function is associated with increased expression of the chemokine receptor CXCR4 in CC-RCCs, we investigated the expression of HIF-1α, CXCR4, and its ligand stromal cell–derived factor-1α (SDF-1α) in hemangioblastomas and CC-RCCs. Immunohistochemistry revealed overexpression of both CXCR4 and SDF-1α within tumor cells and endothelial cells of hemangioblastomas and CC-RCCs. HIF-1α was detected in tumor cell nuclei of both hemangioblastomas and CC-RCCs. A specific ELISA showed that hemangioblastomas and CC-RCCs expressed SDF-1α protein at levels that were significantly higher than those found in normal tissue. Analysis of the VHL-null RCC line 786-0 revealed that SDF-1α mRNA levels were 100-fold higher than in a subclone transfected with the wild-type VHL gene. Expression of CXCR4 and SDF-1α mRNA was significantly decreased in HIF-1α-null compared with wild-type mouse embryo fibroblasts (MEFs). ELISA and Western blot studies for SDF-1α and CXCR4 protein expression confirmed the RNA findings in RCC lines and MEFs. These results suggest that loss-of-function of a single tumor suppressor gene can up-regulate the expression of both a ligand and its receptor, which may establish an autocrine signaling pathway with important roles in the pathogenesis of hemangioblastoma and CC-RCC.
Effects of anti-rheumatic herbal medicines on cellular adhesion molecules
Authors: D.-M. Chang, S.-Y. Kuo, J.-H. Lai, M.-L. Chang
Journal: Annals of the Rheumatic Diseases (1999)

<h3>OBJECTIVE</h3> To test the hypothesis whether herbal medicines ameliorate inflammatory diseases via the modulation of cellular adhesion molecules (CAMs). <h3>METHODS</h3> Human neutrophils, synovial fibroblasts, and endothelial cells were incubated with different concentrations of Tripterygium Wilfordii Hook-f (TWH-f) or Tetrandrine in the presence or absence of interleukin 1 (IL1). The amount of soluble E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1 (VCAM-1) secreted by cells were determined by ELISA. The cell surface expression of these three CAMs was detected by flow cytometry. <h3>RESULTS</h3> TWH-f at high concentration (50 ng/ml) has a significant (p&lt;0.05) inhibitory effect on both the secretion and the expression of the cellular adhesion molecules. However, Tetrandrine did not demonstrate the same effects. <h3>CONCLUSIONS</h3> The cellular adhesion molecules of the endothelium and leucocytes may constitute excellent targets for the development of new anti-inflammation medicines. These results indicate that TWH could be a potential therapeutic agent in the treatment of inflammatory diseases.
Legal considerations of clinical guidelines: will NICE make a difference?
Authors: A. Samanta, J. Samanta, M. Gunn
Journal: Journal of the Royal Society of Medicine (2003)

Clinical guidelines are statements that have been systematically developed and which aim to assist clinicians in making decisions about treatment for specific conditions1. They are linked to evidence and are meant to facilitate good medical practice. The National Institute for Clinical Excellence (NICE) is part of the Government's agenda for healthcare. One of its main functions is to develop, issue and encourage the use of objective guidelines, thus promoting ‘best practice’. A key issue that follows is how lawyers and the courts might use such guidelines in medical litigation.

At the heart of clinical negligence lies the question of whether or not the practice of a defendant doctor has fallen below the required standard of care. Under common law in the UK, the minimal acceptable standard of care is measured against responsible medical practice, and not against guidelines2. In law, therefore, it is expert medical evidence that primarily assists the court in determining what the standard of care should be, and until now clinical guidelines have played a subsidiary role.

This paper discusses the role of guidelines within the context of the tort of negligence, with reference to their use currently and the possible medicolegal implications of guidelines from NICE in the future.
Effects of carvedilol on LV function and remodeling in patients with dilated cardiomyopathy with persistent LV dysfunction despite optimal conventional therapy
Authors: A. Di Lenarda, L. Salvatore, D. Gregori, G. Sinagra, G. Sabbadini, F. Longaro, E. Bemobich, S. Klugmann, F. Camerini
Journal: Journal of the American College of Cardiology (1998)
Exposing Poverty and Inspiring Medical Humanitarianism
Authors: Howard Markel, Lawrence O Gostin
Journal: JAMA (2008)

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BMA urges better awareness of use of child labour in NHS supplies
Authors: A. O'Dowd
Journal: BMJ (2010)

<h3>Background</h3> Metformin is one of the most commonly used medications for the treatment of type 2 diabetes mellitus. Potential side effects of metformin include diarrhea, lactic acidosis, and, less commonly reported, vitamin B<sub>12</sub> deficiency. We report a case of vitamin B<sub>12</sub> deficiency in a patient on metformin. <h3>Case Presentation</h3> A 54-year-old male with type 2 diabetes mellitus for 15 years was referred to our diabetes center for evaluation of peripheral neuropathy. He was taking glipizide 10 mg bid and metformin 1,000 mg bid. He was nonvegetarian and regularly consumed red meat. His symptoms began approximately 9 months previously with tingling and numbness in the feet, ascending slowly to knees and hands. His gait was unsteady, with several falls. He also had an 80-pack-year history of smoking. His examination was significant for extremity tremor and absent sensation below the knees. Vibration and proprioception were impaired. Motor strength was normal. He also had bilateral extensor plantar reflexes. Laboratory tests showed a macrocytic anemia (hematocrit 31.6%, hemoglobin 10.4 g/dL, mean corpuscular volume 107 fL). Vitamin B<sub>12</sub> level was low (284 pg/mL), folic acid level was normal (2.8 ng/mL), and methylmalonic acid and homocysteine were elevated (10.8 μmol/L and 41 μmol/L, respectively). Anti-intrinsic factor antibody was negative. EMG/nerve conduction study showed a pure sensory axonal polyneuropathy. Evaluations for infection, paraneoplastic syndromes, heavy metal toxicity, autoimmune diseases, and vasculitis were all negative. Bone marrow biopsy showed hypercellular marrow consistent with nutritional deficiency. Although he was treated with oral vitamin B<sub>12</sub> 1,000 μg/day (refused IM injections), his functional status continued to decline over the next 2 months. Metformin was discontinued with improvement in B<sub>12</sub> levels and symptoms over the following 3 months. <h3>Discussion</h3> Vitamin B<sub>12</sub> deficiency has been reported to occur in patients taking metformin. The underlying mechanism of metformin-related vitamin B<sub>12</sub> deficiency is unclear, but proposed unproven mechanisms include (1) alterations in intestinal motility; (2) bacterial overgrowth; (3) decreased intestinal absorption; and (4) altered intestinal calcium metabolism leading to decreased B<sub>12</sub> intrinsic factor uptake by the ileal cell surface. A recent study suggested that metformin-induced malabsorption may be reversible with oral calcium intake, but larger studies are needed. Monitoring vitamin B<sub>12</sub> levels in patients on metformin is not currently recommended. As neuropathy is a common finding in patients with diabetes, the potential contribution of vitamin B<sub>12</sub> deficiency should also be considered.
Systemic lupus erythematosus complicated by tricuspid stenosis and regurgitation: successful treatment by valve transplantation.
Authors: D E Ames, R A Asherson, J D Coltart, V Vassilikos, J K Jones, G R Hughes
Journal: Annals of the Rheumatic Diseases (1992)

Clinical tricuspid stenosis has not previously been reported in patients with systemic lupus erythematosus (SLE). A 25 year old woman with active SLE presented with signs of severe right ventricular failure. Cardiac catheterisation confirmed the diagnosis of tricuspid stenosis and regurgitation together with mitral regurgitation. This patient underwent successful tricuspid and mitral valve replacement.
Non-steroidal anti-inflammatory drugs as a risk factor for acute diarrhoea: a case crossover study
Authors: I Etienney
Journal: Gut (2003)

Several cases of acute colitis induced by non-steroidal anti-inflammatory drugs (NSAIDs) have been reported but the general role of recent NSAID intake as a risk factor for acute diarrhoea has not been studied to date. The aim of our study was to determine whether the risk of acute diarrhoea is increased by NSAIDs in a prospective series of acute diarrhoea cases which were seen by general practitioners in France and were serious enough to require a stool culture. Patients, physicians, and methods: A total of 285 consecutive patients with acute diarrhoea, seen by Sentinel general practitioners (GPs) between December 1998 and July 1999, were enrolled in a case crossover study in which each case served as his/her own control. GPs collected information on exposure to NSAIDs during the four month period preceding the onset of diarrhoea. The relative risk of NSAID related acute diarrhoea was estimated by comparing exposure to NSAIDs during a risk period preceding the onset of diarrhoea with exposure during the first part of the four month observation period. Three risk periods lasting for one, three, and six days before the onset of diarrhoea were considered.
Bacterial and fungal infection in children with fulminant hepatic failure: possible role of opsonisation and complement deficiency.
Authors: V F Larcher, R J Wyke, A P Mowat, R Williams
Journal: Gut (1982)

Serious bacterial infection, including eight episodes of bacteraemia, developed in seven of 15 (47%) children with fulminant hepatic failure. Those with infections had a slightly higher leucocyte response than those who did not. Serum immunoglobulin concentrations were normal or raised in all patients. Opsonisation of heat-killed baker9s yeast, functionally measured total haemolytic complement, C4, C5, total alternative pathway activity, factor B and D activity, and C3 concentrations were all significantly (p less than 0.005) reduced at presentation but returned to normal in those who survived. The severity of defects in yeast opsonisation, C4, and factor B activity at presentation were significantly correlated with the subsequent development of infection. In five patients bacteraemia occurred at a time when opsonisation and complement components were defective. Plasma infusions in vivo improved opsonisation in vitro and only one bacterial isolate was obtained within four days of such an infusion. Those patients who developed infection had received significantly (p less than 0.05) fewer plasma infusions than those who did not. Our findings suggest that both alternative and classical pathways of complement are defective in children with severe liver disease and may contribute to the susceptibility of such patients to infections. Plasma infusions might be useful in reducing the incidence of bacterial infection in such conditions.
Altered hippocampus synaptic function in selenoprotein P deficient mice
Authors: Melinda M Peters, Kristina E Hill, Raymond F Burk, Edwin J Weeber
Journal: Molecular Neurodegeneration (2006)

Abstract Selenium is an essential micronutrient that function through selenoproteins. Selenium deficiency results in lower concentrations of selenium and selenoproteins. The brain maintains it's selenium better than other tissues under low-selenium conditions. Recently, the selenium-containing protein selenoprotein P (Sepp) has been identified as a possible transporter of selenium. The targeted disruption of the selenoprotein P gene ( Sepp1 ) results in decreased brain selenium concentration and neurological dysfunction, unless selenium intake is excessive However, the effect of selenoprotein P deficiency on the processes of memory formation and synaptic plasticity is unknown. In the present studies Sepp1 (-/-) mice and wild type littermate controls ( Sepp1 (+/+)) fed a high-selenium diet (1 mg Se/kg) were used to characterize activity, motor coordination, and anxiety as well as hippocampus-dependent learning and memory. Normal associative learning, but disrupted spatial learning was observed in Sepp1 (-/-) mice. In addition, severe alterations were observed in synaptic transmission, short-term plasticity and long-term potentiation in hippocampus area CA1 synapses of Sepp1 (-/-) mice on a 1 mg Se/kg diet and Sepp1 (+/+) mice fed a selenium-deficient (0 mg Se/kg) diet. Taken together, these data suggest that selenoprotein P is required for normal synaptic function, either through presence of the protein or delivery of required selenium to the CNS.
P194 Why do lung cancer patients still die in hospital?
Authors: M. Weir, L. Magowan, M. Doherty, R. Sharkey, M. Mc Closkey, M. Kelly, J. G. Daly
Journal: Thorax (2011)

<h3>Aims</h3> The Department of Health proposes “to offer all adult patients, regardless of their diagnosis … access to high quality palliative care so that they can choose … to die at home.” We, therefore, studied those with lung cancer patients who died in our institution during 2010. <h3>Results</h3> 41 patients (33% of our annual notifications) died in hospital; 26 case records were retrieved complete (all had previously been diagnosed with lung cancer); mean age 70.6 years (53–85). 25 lived in their own dwelling (5 alone; 2 of these with only social care support) and 1 in a nursing home. 5 had been in receipt of radical treatments; 21 were in receipt of palliative interventions and the nursing home resident had no active treatment. Mean time from diagnosis to final admission was 296 (188 for those without radical treatments) days. 13 patients admitted via GP; six through A&amp;E seven from Oncology or Palliative Care outpatients. 12 had acute medical problems (eg, pneumonia, CCF); one had intestinal obstruction; 11 had progressive disease-related symptoms (eg, progressive brain metastases); two had social issues precipitating admission. No clear documentation of preferred place of death was identified at admission; during this final admission 14 indicated their preferred place of death—10 for home; four were too unwell for discharge; one had unaddressed social issues; three families couldn9t cope and two were re-admitted by their GP within 24 h of discharge. All patients were in receipt of specialist palliative care during the admission and 15 died on the Liverpool Care Pathway. <h3>Conclusion</h3> 50% of these lung cancer patients (representing 16% of our annual cases) were admitted with acute medical problems. Those identified as wishing to die at home were unable to be discharged. To prevent the remaining 50% of this population being admitted to hospital will require a significant change in practice by both primary and secondary care teams and an investment in community palliative care services. In-hospital palliative care is of a very high standard.
Functional Somatic Syndromes
Authors: Allan Clemenger
Journal: Annals of Internal Medicine (2000)

Letters15 February 2000Functional Somatic SyndromesAllan Clemenger, MDAllan Clemenger, MDPhoenix, AZ 85020 (Clemenger)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-132-4-200002150-00017 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:As a practicing physician and father of a young man who has suffered the debilitating symptoms of the chronic fatigue syndrome for 11 years, I found the article by Barsky and Borus (1) most upsetting. Why did the authors place such credence in the writings of a professor of English, Elaine Showalter, who obviously has no credentials in the field of medicine or psychiatry? Among all the authors' references, the authors were careful to avoid many substantive articles on the chronic fatigue syndrome (2, 3), even one published in Annals(4). In September 1996, the National Institutes of ...References1. Barsky AJ, Borus JF. Functional somatic syndromes. Ann Intern Med. 1999;130:910-21. LinkGoogle Scholar2. Bou-Holaigah I, Rowe PC, Kan J, Calkins H. The relationship between neurally mediated hypotension and the chronic fatigue syndrome. JAMA. 1995;274:961-7. CrossrefMedlineGoogle Scholar3. Demitrack MA, Dale JK, Straus SE, Laue L, Listwak SJ, Kruesi MJ, et al . Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome. J Clin Endocrinol Metab. 1991;73:1224-34. CrossrefMedlineGoogle Scholar4. Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A. The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Ann Intern Med. 1994;121:953-9. LinkGoogle Scholar5. CFS Information for Physicians. Bethesda, MD: National Institute of Allergy and Infections Diseases, National Institutes of Health; 1996. Google Scholar Author, Article, and Disclosure InformationAuthors: Allan Clemenger, MDAffiliations: Phoenix, AZ 85020 (Clemenger) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoFunctional Somatic Syndromes Arthur J. Barsky and Jonathan F. Borus Functional Somatic Syndromes Ellen Goudsmit Functional Somatic Syndromes Melody Heard Functional Somatic Syndromes Frank Albrecht Functional Somatic Syndromes Thomas L. English Functional Somatic Syndromes Thomas L. Kurt Functional Somatic Syndromes Arthur J. Barsky and Jonathan F. Borus Functional Somatic Syndromes Terry E. Hedrick Functional Somatic Syndromes James McSherry Functional Somatic Syndromes Kenneth Clemenger Metrics 15 February 2000Volume 132, Issue 4Page: 328KeywordsChronic fatigue syndromeHealth information technology ePublished: 15 August 2000 Issue Published: 15 February 2000 Copyright & PermissionsCopyright © 2000 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Anti-MET Targeted Therapy Has Come of Age: The First Durable Complete Response with MetMAb in Metastatic Gastric Cancer
Authors: Yan Feng, Patrick C. Ma
Journal: Cancer Discovery (2011)

The MET/hepatocyte growth factor (HGF) signaling pathway plays important roles in oncogenesis and tumor progression in a variety of human cancers. MET/HGF drives an invasive signaling program that can be dysregulated in human cancers through a number of activating mechanisms, including mutations, overexpression, amplification, alternative splicing, and HGF ligand-induced autocrine/paracrine loop signaling. As a testimony of MET-targeting therapeutics is beginning to come to clinical fruition, Catenacci and colleagues report the first case of durable complete response under an anti-MET receptor monoclonal antibody, MetMAb, in a patient with chemotherapy-refractory, advanced gastric cancer metastatic to the liver, found to have high MET gene polysomy and remarkably high serum HGF level. Serum and tissue studies also revealed predictive biomarkers for therapeutic response to MET inhibition.