tbuckley/cabot-search huggingface dataset:
Pitfalls in the Measurement of the Nocturnal Blood Pressure Dip in Adolescents with Type 1 Diabetes
Authors: Angela Delaney, Margaret Pellizzari, Phyllis W. Speiser, Graeme R. Frank
Journal: Diabetes Care (2008)

The purpose of this study was to screen adolescents with type 1 diabetes using ambulatory blood pressure monitoring (ABPM) to 1) test the hypothesis that using a preset sleep time results in an overdiagnosis of abnormal nocturnal dipping in systolic blood pressure and 2) assess the reproducibility of an abnormal nocturnal systolic blood pressure dip.For aim 1, ABPM from 53 adolescent patients with type 1 diabetes was reviewed. Nocturnal dips in systolic blood pressure calculated by actual sleep time were compared with those from a preset sleep time. For aim 2, blood pressure monitoring from 98 patients using actual reported sleep time was reviewed. Reproducibility of the nocturnal dip in systolic blood pressure was assessed in a subset of "nondippers."For aim 1, the actual mean +/- SE decline in nocturnal systolic blood pressure was 11.6 +/- 4.7%, whereas the mean decline in nocturnal systolic blood pressure calculated using the preset sleep time was 8.8 +/- 4.9% (P < 0.0001). For aim 2, 64% of patients had a normal nocturnal decline in systolic blood pressure (14.9 +/- 3.1% mmHg), whereas 36% had an abnormal dip (5.7 +/- 2.8% mmHg). Repeat ABPM performed in 22 of the 35 nondippers revealed that only 36% had abnormal systolic dipping confirmed on the repeat ABPM.The use of actual reported sleep time is required to accurately determine the nocturnal dip in systolic blood pressure. Repeating ABPM in nondippers is essential to confirm this abnormality.
In vivo altered unfolded protein response and apoptosis in livers from lipopolysaccharide-challenged cirrhotic rats
Authors: Khalid A. Tazi, Ivan Bièche, Valérie Paradis, Cécile Guichard, Ingrid Laurendeau, Delphine Dargère, Agnès Legrand, Michèle Fay, Eric Pedruzzi, Marie-Anne Robin, Dominique Cazals-Hatem, Zéra Tellier, Dominique Bernuau, Gérard Feldmann, Michel Vidaud, Didier Lebrec, Eric Ogier-Denis, Richard Moreau
Journal: Journal of Hepatology (2007)
HUMAN THROMBIN AS VEHICLE OF INFECTION IN HOMOLOGOUS SERUM HEPATITIS
Authors: Joseph E. Porter
Journal: JAMA (1953)

The increasingly wide use of blood and blood products in medical practice has carried with it an increasing risk of homologous serum hepatitis (viral hepatitis B) among recipients of these materials. With the development, by Cohn and co-workers, 1 of techniques for the fractionation of the plasma proteins and with the widespread clinical use of the blood fractions thus produced, the question of whether these fractions might transmit homologous serum hepatitis has become a pressing one. The gamma globulin fraction, as prepared by ethyl alcohol (ethanol) precipitation, appears to be free of the agent of homologous serum hepatitis, 2 despite the fact that individual lots of gamma globulin may represent the pooled plasmas of thousands of donors. 3 It would appear that, in the preparation of this fraction by ethyl alcohol, the virus is inactivated, eliminated, or neutralized. 3 The albumin fraction prepared in this way has not been shown
Follow up of an immunocompromised contact group of a case of open pulmonary tuberculosis on a renal unit.
Authors: F A Drobniewski, J Ferguson, K Barritt, R M Higgins, M Higgon, D Neave, A H Uttley, D O'Sullivan, A Hay
Journal: Thorax (1995)

The organisation, management, outcome and cost of follow up of a large group of mainly immunocompromised patients and healthcare workers who were exposed to a staff member of a London renal unit with smear positive pulmonary tuberculosis are described.Following British Thoracic Society (BTS) guidelines, 576 close contacts were identified and divided into three groups: (1) 303 renal patients including 61 with renal transplants; (2) 90 surgical patients; and (3) 183 staff members. Screened contacts were interviewed, completed a symptoms questionnaire, and were offered a chest radiograph and Heaf or Mantoux test if appropriate with referral to a chest physician if required.Overall, 524 (85%) living contacts have been screened: 243 (97%) renal (first screening), 63 (70%) surgical, and 135 (74%) staff contacts. Thirty one transplant patients were prescribed isoniazid chemoprophylaxis. Fifty two renal patients had died before screening and 11 deaths occurred after first interview. One case of tuberculosis epidemiologically related to the index case was diagnosed on clinical criteria. A review of the case records and/or death certificates and entries on to tuberculosis registers indicated no further cases. The cost of the investigation was estimated to be approximately franc25 000, or franc44 per contact screened, with staff costs comprising 79% of the total.Undiagnosed tuberculosis in healthcare workers working with immunosuppressed patients can lead to large and expensive follow up studies. The applicability of the 1990 and 1994 BTS guidelines to the investigation of tuberculosis in an immunocompromised nosocomial group, and the role of the infection control doctor and the consultant in Communicable Disease Control in overlapping nosocomial and community incidents, are discussed.
Hypertrophic cardiomyopathy with unusual locations of left ventricular hypertrophy undetectable by M-mode echocardiography. Identification by wide-angle two-dimensional echocardiography.
Authors: B J Maron, J S Gottdiener, R O Bonow, S E Epstein
Journal: Circulation (1981)

Twenty-one patients without evidence of hypertrophy by M-mode echocardiography were studied by wide-angle two-dimensional echocardiography to determine if they had a form of hypertrophic cardiomyopathy that could not be detected by conventional M-mode echocardiography. Each patient was suspected clinically of having hypertrophic cardiomyopathy because of a distinctly abnormal ECG and either a family history of hypertrophic cardiomyopathy or cardiac symptoms. Patients were 5-49 years old (mean 16 years) and 16 of the 21 had no functional limitation. The most common electrocardiographic abnormalities were deep Q waves, T-wave inversion and right ventricular hypertrophy. Using wide-angle two-dimensional echocardiography to reconstruct the geometry of the left ventricular wall, 16 of the 21 patients (76%) were shown to have prominent but unusually located regions of left ventricular wall hypertrophy. In each instance, the hypertrophy involved regions of the left ventricular wall through which the M-mode ultrasound beam does not usually pass, i.e., posterior ventricular septum (seven patients), anterior or lateral left ventricular free wall (seven patients) and ventricular septum near the apex (two patients). There was no echocardiographic or hemodynamic evidence of left ventricular outflow tract obstruction in any patient. Hence, some patients with hypertrophic cardiomyopathy may have substantial hypertrophy present in unusual locations of the left ventricular wall. Although electrocardiographic abnormalities suggested the presence of myocardial disease, conventional M-mode echocardiography (performed from standard parasternal positions) did not reliably identify such sites of hypertrophy, which were limited to regions of the left ventricle not accessible to the M-mode beam. Only wide-angle two-dimensional echocardiography permits definitive identification of these unusually located regions of cardiac hypertrophy and confirmation of the diagnosis of hypertrophic cardiomyopathy.
Pathways for degradation of connexins and gap junctions
Authors: V Berthoud
Journal: Cardiovascular Research (2004)

Gap junctional proteins, connexins, and gap junctional plaques are short-lived. Three pathways for their degradation have been proposed: (1) misfolded/abnormally oligomerized connexins are retrogradely translocated and degraded by the proteasome through endoplasmic reticulum-associated degradation; (2) connexins (as monomers or oligomers) may traffic directly from an early secretory compartment to the lysosome for degradation without reaching the plasma membrane; (3) connexins within gap junction plaques are degraded by the lysosome after endocytotic internalization. Degradation of gap junction plaques is proteasome-dependent in some cell types. Degradation may be regulated by ubiquitinylation, phosphorylation, or polypeptide domains that act as sorting signals.
PPARα deficiency reduces insulin resistance and atherosclerosis in apoE-null mice
Authors: Karen Tordjman, Carlos Bernal-Mizrachi, Laura Zemany, Sherry Weng, Chu Feng, Fengjuan Zhang, Teresa C. Leone, Trey Coleman, Daniel P. Kelly, Clay F. Semenkovich
Journal: Journal of Clinical Investigation (2001)

PPARalpha is a ligand-dependent transcription factor expressed at high levels in the liver. Its activation by the drug gemfibrozil reduces clinical events in humans with established atherosclerosis, but the underlying mechanisms are incompletely defined. To clarify the role of PPARalpha in vascular disease, we crossed PPARalpha-null mice with apoE-null mice to determine if the genetic absence of PPARalpha affects vascular disease in a robust atherosclerosis model. On a high-fat diet, concentrations of atherogenic lipoproteins were higher in PPARalpha(-/-)apoE(-/-) than in PPARalpha(+/+)apoE(-/-) mice, due to increased VLDL production. However, en face atherosclerotic lesion areas at the aortic arch, thoracic aorta, and abdominal aorta were less in PPARalpha-null animals of both sexes after 6 and 10 weeks of high-fat feeding. Despite gaining as much or more weight than their PPARalpha(+/+)apoE(-/-) littermates, PPARalpha(-/-)apoE(-/-) mice had lower fasting levels of glucose and insulin. PPARalpha-null animals had greater suppression of endogenous glucose production in hyperinsulinemic clamp experiments, reflecting less insulin resistance in the absence of PPARalpha. PPARalpha(-/-)apoE(-/-) mice also had lower blood pressures than their PPARalpha(+/+)apoE(-/-) littermates after high-fat feeding. These results suggest that PPARalpha may participate in the pathogenesis of diet-induced insulin resistance and atherosclerosis.
Treatment-Related Risk Factors for Transformation to Acute Myeloid Leukemia and Myelodysplastic Syndromes in Myeloproliferative Neoplasms
Authors: Magnus Björkholm, Åsa R. Derolf, Malin Hultcrantz, Sigurdur Y. Kristinsson, Charlotta Ekstrand, Lynn R. Goldin, Björn Andreasson, Gunnar Birgegård, Olle Linder, Claes Malm, Berit Markevärn, Lars Nilsson, Jan Samuelsson, Fredrik Granath, Ola Landgren
Journal: Journal of Clinical Oncology (2011)

Purpose Patients with myeloproliferative neoplasms (MPNs), including polycythemia vera, essential thrombocythemia, and primary myelofibrosis, have a propensity to develop acute myeloid leukemia (AML) and myelodysplastic syndromes (MDSs). Using population-based data from Sweden, we assessed the role of MPN treatment and subsequent AML/MDS risk with special focus on the leukemogenic potential of hydroxyurea (HU). Methods On the basis of a nationwide MPN cohort (N = 11,039), we conducted a nested case-control study, including 162 patients (153 and nine with subsequent AML and MDS diagnosis, respectively) and 242 matched controls. We obtained clinical and MPN treatment data for all patients. Using logistic regression, we calculated odds ratios (ORs) as measures of AML/MDS risk. Results Forty-one (25%) of 162 patients with MPNs with AML/MDS development were never exposed to alkylating agents, radioactive phosphorous (P 32 ), or HU. Compared with patients with who were not exposed to HU, the ORs for 1 to 499 g, 500 to 999 g, more than 1,000 g of HU were 1.5 (95% CI, 0.6 to 2.4), 1.4 (95% CI, 0.6 to 3.4), and 1.3 (95% CI, 0.5 to 3.3), respectively, for AML/MDS development (not significant). Patients with MPNs who received P 32 greater than 1,000 MBq and alkylators greater than 1 g had a 4.6-fold (95% CI, 2.1 to 9.8; P = .002) and 3.4-fold (95% CI, 1.1 to 10.6; P = .015) increased risk of AML/MDS, respectively. Patients receiving two or more cytoreductive treatments had a 2.9-fold (95% CI, 1.4 to 5.9) increased risk of transformation. Conclusion The risk of AML/MDS development after MPN diagnosis was significantly associated with high exposures of P 32 and alkylators but not with HU treatment. Twenty-five percent of patients with MPNs who developed AML/MDS were not exposed to cytotoxic therapy, supporting a major role for nontreatment-related factors.
The hypoxia-induced miR-130 increases proliferation of pulmonary arterial smooth muscle cells by targeting the tumour suppressor CDKN1A (p21)
Authors: Matthias Brock, Max Gassmann, Rudolf Speich, Silvia Ulrich, Lars Huber
Journal: European Respiratory Journal (2013)

Background. Vascular remodelling is one of the hallmark features in the pathogenesis of pulmonary hypertension (PH) and is mainly driven by overshooting proliferation of pulmonary arterial smooth muscle cells (PASMCs). We have shown previously that the microRNA (miRNA) family miR-130 (i.e. miR-130a and miR-301a) is upregulated in the murine model of hypoxia-induced PH. Here we addressed the effects of miR-130 on the proliferation of PASMCs in vitro and identified novel targets of miR-130.  Methods. For inhibition of the miR-130 family LNA-modified seed blockers were designed. BrdU proliferation assay was employed in PASMCs transfected with miRNA precursor molecules or LNA seed blockers. Expression of cyclin-dependent kinase inhibitor (CDKN)1A was measured on RNA and on protein level. Reporter gene assay was used to proof direct miRNA-target interaction.  Results. Proliferation of PASMCs was significantly increased by overexpression of miR-130a and miR-301a (by 37.9% and 62.4%, respectively) and decreased by transfection of seed blockers (reduction of 65.4%). Inhibition of the miR-130 family increased the expression of the tumour suppressor CDKN1a (by 55.7% on mRNA level, and by 72.2% on protein level). Reporter gene assays showed that miR-130 family directly targets CDKN1A.  Conclusion. Our results show that the miR-130 family triggers proliferation of PASMCs probably mediated through repression of CDKN1A. Since levels of the miR-130 family are induced by hypoxia in vivo, these data emphasize the potential role of miR-130 in the process of vascular remodelling in PH.
Serum ferritin is derived primarily from macrophages through a nonclassical secretory pathway
Authors: Lyora A. Cohen, Lucia Gutierrez, Avital Weiss, Yael Leichtmann-Bardoogo, De-liang Zhang, Daniel R. Crooks, Rachid Sougrat, Avigail Morgenstern, Bruno Galy, Matthias W. Hentze, Francisco J. Lazaro, Tracey A. Rouault, Esther G. Meyron-Holtz
Journal: Blood (2010)
Health-Related Quality of Life and Treatment Satisfaction in Dutch Patients With Type 2 Diabetes
Authors: W. Ken Redekop, Marc A. Koopmanschap, Ronald P. Stolk, Guy E.H.M. Rutten, Bruce H.R. Wolffenbuttel, Louis W. Niessen
Journal: Diabetes Care (2002)

OBJECTIVE— To estimate the health-related quality of life (HRQOL) and treatment satisfaction for patients with type 2 diabetes in the Netherlands and to examine which patient characteristics are associated with quality of life and treatment satisfaction. RESEARCH DESIGN AND METHODS—For a sample of 1,348 type 2 diabetes patients, recruited by 29 general practitioners, we collected data regarding HRQOL. This study was performed as part of a larger European study (Cost of Diabetes in Europe - Type 2 [CODE-2]). We used a generic instrument (Euroqol 5D) to measure HRQOL. Treatment satisfaction was assessed using the Diabetes Treatment Satisfaction Questionnaire. RESULTS—Patients without complications had an HRQOL (0.74) only slightly lower than similarly aged persons in the general population. Insulin therapy, obesity, and complications were associated with a lower HRQOL, independent of age and sex. Although higher fasting blood glucose and HbA1c levels were negatively associated with HRQOL, these factors were not significant after adjustment for other factors using multivariate analysis. Overall treatment satisfaction was very high. Younger patients, patients using insulin, and patients with higher HbA1c levels were less satisfied with the treatment than other patients. CONCLUSIONS—Obesity and the presence of complications are important determinants of HRQOL in patients with type 2 diabetes.
The EEG<i>data</i>indicate stochastic nonlinearity
Authors: Walter S. Pritchard
Journal: Behavioral and Brain Sciences (1996)

Abstract Wright &amp; Liley contrast their theory that the global dynamics of the EEG are linear with that of Freeman, who hypothesizes an EEG governed by (nonlinear) deterministic-chaotic dynamics. A “call for further discussion” on the part of the authors is made as to how either theory fits with experimental findings indicating that EEG dynamics are non-linear but stochastic.
A variant near MTNR1B is associated with increased fasting plasma glucose levels and type 2 diabetes risk
Authors: Nabila Bouatia-Naji, Amélie Bonnefond, Christine Cavalcanti-Proença, Thomas Sparsø, Johan Holmkvist, Marion Marchand, Jérôme Delplanque, Stéphane Lobbens, Ghislain Rocheleau, Emmanuelle Durand, Franck De Graeve, Jean-Claude Chèvre, Knut Borch-Johnsen, Anna-Liisa Hartikainen, Aimo Ruokonen, Jean Tichet, Michel Marre, Jacques Weill, Barbara Heude, Maithé Tauber, Katleen Lemaire, Frans Schuit, Paul Elliott, Torben Jørgensen, Guillaume Charpentier, Samy Hadjadj, Stéphane Cauchi, Martine Vaxillaire, Robert Sladek, Sophie Visvikis-Siest, Beverley Balkau, Claire Lévy-Marchal, François Pattou, David Meyre, Alexandra I F Blakemore, Marjo-Riita Jarvelin, Andrew J Walley, Torben Hansen, Christian Dina, Oluf Pedersen, Philippe Froguel
Journal: Nature Genetics (2008)
Artemis C-terminal region facilitates V(D)J recombination through its interactions with DNA Ligase IV and DNA-PKcs
Authors: Shruti Malu, Pablo De Ioannes, Mikhail Kozlov, Marsha Greene, Dailia Francis, Mary Hanna, Jesse Pena, Carlos R. Escalante, Aya Kurosawa, Hediye Erdjument-Bromage, Paul Tempst, Noritaka Adachi, Paolo Vezzoni, Anna Villa, Aneel K. Aggarwal, Patricia Cortes
Journal: The Journal of Experimental Medicine (2012)

Artemis is an endonuclease that opens coding hairpin ends during V(D)J recombination and has critical roles in postirradiation cell survival. A direct role for the C-terminal region of Artemis in V(D)J recombination has not been defined, despite the presence of immunodeficiency and lymphoma development in patients with deletions in this region. Here, we report that the Artemis C-terminal region directly interacts with the DNA-binding domain of Ligase IV, a DNA Ligase which plays essential roles in DNA repair and V(D)J recombination. The Artemis–Ligase IV interaction is specific and occurs independently of the presence of DNA and DNA–protein kinase catalytic subunit (DNA-PKcs), another protein known to interact with the Artemis C-terminal region. Point mutations in Artemis that disrupt its interaction with Ligase IV or DNA-PKcs reduce V(D)J recombination, and Artemis mutations that affect interactions with Ligase IV and DNA-PKcs show additive detrimental effects on coding joint formation. Signal joint formation remains unaffected. Our data reveal that the C-terminal region of Artemis influences V(D)J recombination through its interaction with both Ligase IV and DNA-PKcs.
NI-15 * USE OF VOLUMETRIC MR SPECTROSCOPIC IMAGING AND 5-ALA FLUORESCENCE-GUIDED SURGERY FOR RESECTION OF GLIOBLASTOMA
Authors: J. S. Cordova, Z. Liang, C. A. Holder, C. Appin, E. Schreibmann, X. Bian, D. Brat, H.-K. Shu, J. Olson, A. Maudsley, H. Shim, C. Hadjipanayis
Journal: Neuro-Oncology (2014)

RATIONALE: Glioblastoma (GBM) resection based on neuronavigation with contrast-enhanced MRI (CE-MRI) results in a high rate of local recurrence as infiltrating tumor cells extend beyond areas of contrast enhancement. Integrating metabolic maps from magnetic resonance spectroscopic imaging (MRSI) into neuronavigation may identify high-risk tumor infiltration zones outside of CE-MRI for surgery. Coupling MRSI with fluorescence-guided surgery (FGS) using 5-aminolevulinic acid (5-ALA) may provide a means to further enhance the degree of tumor resection. METHODS: In a new Phase II trial for new and recurrent GBM patients, 3D-echo planar spectroscopic imaging was performed and processed to give full-brain metabolite volumes for import into a neuronavigation station. Patients were administered 5-ALA orally 3-5 h before surgery. To minimize error due to shift, needle biopsies were collected from tumor regions with elevated choline/NAA values within T1CE and/or T2/FLAIR hyperintense regions before tumor resection. Fluorescence intensity of fresh tissue was quantified ex vivo using a hand-held spectroscopic device. Samples were then fixed/stained with H&E and analyzed for tumor cell density and tissue infiltration using automated image analysis techniques. Quantitative tumor segmentation was used to evaluate extent of tumor resection. RESULTS: Choline/NAA values show a positive linear trend with the number of tumor nuclei per high power field and the degree of tumor infiltration. Real-time intraoperative tumor fluorescence was also confirmed ex vivo and shows a similar positive linear trend with choline/NAA ratios. CONCLUSIONS: The linear trend that Cho/NAA values exhibit with histopathology and quantitative intraoperative fluorescence of tumor tissue outside of CE-MRI regions supports its use for identifying regions of tumor infiltration. This is the first time that 5-ALA induced tumor fluorescence has been shown to correlate with MRSI-derived metabolic markers in GBM tumors. We believe the continued combination of MRSI-neuronavigation with 5-ALA FGS in this trial will result in more complete GBM resections.
Simple atrophic gastritis and gastric carcinoma
Authors: I. R. Walker, R. G. Strickland, B. Ungar, I. R. Mackay
Journal: Gut (1971)

Gastric carcinoma was detected nine, 10, 18, and 21 years after the biopsy diagnosis of atrophic gastritis in four patients of a group of 40. The gastritis was presumed to be of the simple type. Tests of vitamin B(12) absorption in three patients gave normal results, no gastric autoantibodies were detected in the two patients tested, in all patients histological examination of the gastrectomy specimens revealed a multifocal gastritis differing from the diffuse gastritis of pernicious anaemia and in three patients the gastritis affected the antrum, which is unusual in pernicious anaemia. The 10% incidence of gastric carcinoma in 40 patients with simple atrophic gastritis followed for a mean period of 15 years is equivalent to that previously described in pernicious anaemia. However, in view of the relative incidence of atrophic gastritis with and without pernicious anaemia in the general adult population, it emerges that atrophic gastritis without pernicious anaemia is numerically the more important precursor of gastric carcinoma.