tbuckley/cabot-search huggingface dataset:
Abstract 4243: Assessment Of Physiologic And Pathologic Cardiac Hypertrophy By Two-dimensional Strain And Torsion Analysis
Authors: Antonio Vitarelli, Mauro Bernardi, Giuseppe Placanica, Ysabel Conde, Simona D’Orazio, Simona Stellato, Daniela Battaglia, Fiorella Caranci, Giovanna Continanza, Olga Dettori, Attilio Placanica, Massimo Vitarelli, Lidia Capotosto
Journal: Circulation (2008)

PURPOSE . We sought to determine whether speckle tracking imaging (STI) could distinguish between subjects with athletic LVH and those with pathological LVH, such as occurs in hypertensive heart disease, hypertrophic cardiomyopathy (HCM), or aortic stenosis. METHODS . A total of 127 participants were studied, comprising competitive athletes (30), hypertensive heart disease (30), HCM (12), aortic stenosis (25), and healthy volunteers (30). Left ventricular mass index, ejection fraction, diastolic wall thickness, wall thickness ratio and diastolic and systolic wall-to-volume ratios were determined. LV longitudinal peak systolic strain (L-ϵ), peak systolic strain rate (SR-S), peak early diastolic strain rate (SR-E), and peak late diastolic strain rate (SR-A) values were measured by STI in the basal, mid and apical segments in apical 4-chamber view. LV radial strain (R-ϵ) in parasternal short-axis view was determined by STI. Averaged LV rotation and rotational velocities from the base and apex were also obtained (EchoPac, General Electric), and used for calculation of LV torsion (LVtor). RESULTS . Left ventricular (LV) mass indices were similar for all forms of LVH (p&gt;.05), which were higher than those obtained in healthy volunteers (p&lt;.05). Athletes had no significant differences in L-ϵ, SR-E and R-ϵ compared with control subjects (p = .21, .85, and .67, respectively). Patients with pathologic LVH had significantly decreased L-ϵ, SR-E, and R-ϵ (average septum: −15.9 ± 3.4%, 1.71 ± 0.35 s −1 , and 24.5 ± 11.6%, respectively) compared with control subjects (−22.4 ± 3.3%, 2.51 ± 0.49 s −1 , and 37.6 ± 15.2%, respectively; all p&lt;.0005). LVtor increased significantly in pathologic LVH and in athletes compared to normals (p&lt;.005 and .0001, respectively). In pathologic LVH LVtor increased mainly as a result of reduced basal rotation (−3.6±1.2 vs −6.4±1.5 degrees, p=.03). In athletes the LVtor increase was the result of an increase in both basal and apical rotation (basal rotation, −6.2±1.4 vs −9.1±1.6 degrees, p=.05; apical rotation, 16.9±3.1 vs 26.5±4.2 degrees, p=.08). CONCLUSIONS . Pathologic LVH has significant strain and SR-E reduction versus controls and a different pattern of LV torsion compared to athletes.
Textbook of Benign Prostatic Hyperplasia
Authors: J L H R Bosch, F H Schrodder
Journal: BMJ (1996)

Ed Roger Kirby, John D McConnell, John M Fitzpatrick, Claus G Roehrborn, Peter Boyle Isis Medical Media, £99.50, pp 566 ISBN 1 899066 24 1

It is some time since the last edition of Hinman's Benign Prostatic Hypertrophy was published, and Kirby and his colleagues identified the need for a modern textbook on benign prostatic hyperplasia. The result is a beautifully produced, well illustrated, and for the most part easily readable book.

Many new medical and minimally invasive treatments for benign prostatic hyperplasia have become available in recent years. Patients are generally treated earlier, and attempts are made to identify the condition in …
Abstract 14916: Combined Assessment of Urinary Neutrophil Gelatinase-Associated Lipocalin and Albumin to Creatinine Ratio on Admission Improves the Prediction of Acute Kidney Injury in Patients Hospitalized to Coronary Care Units
Authors: Ryunosuke Okuyama, Junnichi Ishii, Hideki Kawai, Takashi Muramatsu, Hiroyuki Naruse, Sadako Motoyama, Shigeru Matsui, Hideo Izawa, Yukio Ozaki
Journal: Circulation (2014)

Background: The early and accurate prediction of acute kidney injury (AKI) by current clinical and laboratory methods remains inadequate. We prospectively investigated the incremental predictive value of a combination of urinary markers such as neutrophil gelatinase-associated lipocalin (NGAL), albumin to creatinine ratio (UAC), and liver-type fatty-acid binding protein (LFABP) for AKI which develops after admission to coronary care units (CCUs).

Methods: We studied 896 consecutive patients (median,74 yrs) who admitted to CCUs. Baseline urinary samples for measurements of NGAL, UAC, and LFABP were obtained on admission. Among these patients, heart failure was present in 52%, and acute coronary syndrome in 41%. AKI was defined as a greater than 25% increase in creatinine from the baseline or an absolute increase of ≥ 0.5 mg/dl within 48h after admission.

Results: NGAL levels significantly (P < 0.0001) correlated with UAC (r = 0.34) and LFABP (r = 0.52) levels. AKI occurred in 126 (14%) patients. Patients with AKI were older (76 vs. 73 yrs, p = 0.006) , had a higher prevalence of heart failure (76 vs. 54 %, p = 0.0004), higher serum levels of NT-proBNP (2585 vs. 1530 pg/ml, p =0.0002) and high-sensitive C-reactive protein (4.0 vs. 2.0 mg/l, p = 0.003), had higher urinary levels of NGAL (76 vs. 19 μg/gCr, p < 0.0001), UAC (127 vs. 46 mg/gCr, p < 0.0001), and LFABP (34 vs. 15 μg/gCr, p < 0.0001), and had lower estimated GFR values compared with those without AKI. Patients with AKI had a higher risk for in-hospital mortality (18 vs. 4%, P < 0.0001) compared with those without AKI. In stepwise multivariate logistic analysis including 13 clinical variables, tertiles of NGAL (P = 0.008) and UAC (P = 0.007), but not LFABP, were independently associated with the development of AKI. The combination of NGAL and UAC tertiles were associated with increased AKI rates ( Figure ).

Conclusions: The combined assessment of NGAL and UAC on admission can improve the prediction of AKI in patients hospitalized to CCUs.

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Comparison of the epidermal growth factor receptor gene mutation in matched primary tumor and lymph node metastasis of non-small cell lung cancer
Authors: S. Park, B. Park, I. Hwang, S. Lee, E. Cho, W. Kang, J. Ahn, M. Ahn, K. Park
Journal: Journal of Clinical Oncology (2007)

7614 Background: Mutations in epidermal growth factor receptor (EGFR) are considered as a strong predictive marker to EGFR tyrosine kinase inhibitors (TKIs) in non-small-cell lung cancer (NSCLC). Recent studies suggested EGFR status may change between primary NSCLC and corresponding metastatic site. However, it has not fully been evaluated whether EGFR mutation differs in metastases compared to primary NSCLC. Methods: In total, 128 tumor samples from 64 NSCLC patients were investigated comparing matched 64 primary tumors, and 64 lymph node metastases. The epidermal growth factor receptor mutation status was analyzed by a direct sequencing method (exons 18–21 in EGFR) on tumor samples of primary NSCLC and corresponding lymph node metastasis. Results: In 17.2% of patents (11/64), EGFR mutation was identified in either primary NSCLC or metastasis by DNA sequencing. Six (54.5%) out of eleven cases showed discordance of EGFR mutation in the primary tumor/metastasis site. Two cases showed EGFR mutation in the metastasis but not in the primary tumor, while, in four cases, EGFR mutation was detected in the primary tumor but not in the metastasis site. The majority of discordance of EGFR mutations was identified in exon 19 (83.3%, 5/6). The median overall survival (OS) was 17.7 months (95% confidence interval, 9.4–20.0). Median OS was not varied by the discordance of EGFR mutation status between primary NSCLC and corresponding metastatic site. Conclusions: The status of EGFR mutation in primary NSCLC and that in corresponding metastasis site varied in considerable cases by DNA sequencing. Whether the status of EGFR mutation changes during the process of metastasis remains to be evaluated. Future study to evaluate the correlation of tumour response to TKIs and the discordance of the EGFR mutation status is warranted. No significant financial relationships to disclose.
Determinants of eczema: population-based cross-sectional study in Germany
Authors: C. J. Apfelbacher, T. L. Diepgen, J. Schmitt
Journal: Allergy (2010)

To cite this article: Apfelbacher CJ, Diepgen TL, Schmitt J. Determinants of eczema: population-based cross-sectional study in Germany. Allergy 2011; 66: 206–213. Abstract Background: Eczema is a chronic inflammatory skin disease and is among the most frequent chronic conditions in childhood and adolescence. It is the aim of this study to investigate determinants of eczema in German children and adolescents. Methods: Data were drawn from the public use files of the German Interview and Examination Survey for Children and Adolescents (KIGGS), a nationwide cross-sectional representative survey conducted between 2003 and 2006, including 17 641 children aged 0–17 (response rate: 66.6%). We investigated the association of a broad set of environmental and lifestyle exposures with ever physician-diagnosed eczema by means of univariable analyses and multivariable logistic regression modelling. Results: The weighted prevalence of ever physician-diagnosed eczema was 13.2% [95% confidence interval (CI) 12.5–13.9%]. In multivariable analysis, significant positive associations of parental allergies (OR 1.94, 95% CI 1.72–2.19), parent-reported infection after birth (OR 1.45, 95% CI 1.05–2.00) and parent-reported jaundice after birth (OR 1.27, 95% CI 1.04–1.54) were revealed. Being a migrant (OR 0.63, 95% CI 0.49–0.80) and keeping a dog (OR 0.78, 95% CI 0.64–0.96) showed significant inverse associations with eczema. Other lifestyle (alcohol consumption during pregnancy) and environmental factors (mould on the walls, pets, origin from East/West Germany) were not significantly related to eczema. Conclusions: This study suggests that a family history of allergies is the strongest determinant of eczema. Perinatal health problems were associated with eczema, pointing to the importance of early life factors in the manifestation of eczema.
Abstract 4335: A p53/HIF-1alpha-mediated metabolic response to stress
Authors: Suthakar Ganapathy, Zhi-Min Yuan
Journal: Cancer Research (2014)

Abstract p53 is a key player in the cellular stress response. Apart from its canonical role in cell checkpoint functions, p53 also regulates cellular metabolism by blocking glycolysis and promoting oxidative phosphorylation. The hypoxia-inducible factor 1(HIF-1), on the other hand, is a master transcription factor promoting glycolysis. We describe a previously unrecognized metabolic response to low levels of stress, including low doses of ionizing radiation or arsenic. By using an integrated approach, we demonstrate that low-level stress induces a metabolic shift from oxidative phosphorylation to aerobic glycolysis leading to increased stress tolerance in both cell and animal models. Low-level stress-induced metabolic changes are mediated by a functional cooperation between p53 and HIF-1α. Our work provides a novel metabolic mechanism of the stress response. Citation Format: Suthakar Ganapathy, Zhi-Min Yuan. A p53/HIF-1alpha-mediated metabolic response to stress. [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 4335. doi:10.1158/1538-7445.AM2014-4335
Abstract 11864: Examining Rare and Low-Frequency Genetic Variants Previously Associated With Lone or Familial Forms of Atrial Fibrillation in an Electronic Medical Record System: A Cautionary Note
Authors: Peter Weeke, Joshua C Denny, Lisa Basterache, Christian Shaffer, Erica Bowton, Christiana Ingram, Dawood Darbar, Dan M Roden
Journal: Circulation (2014)

Introduction: Studies in individuals or small kindreds have implicated rare variants in 25 different genes in lone and familial atrial fibrillation (AF) using linkage and segregation analysis, functional characterization, and rarity in public databases. Here we used a cohort of 20,204 patients of European ancestry (EA) or African ancestry (AA) (n=18,424 and n=1,780, respectively) with electronic medical records (EMRs) and exome chip data to compare the frequency of AF among carriers and non-carriers of these rare variants. Methods and Results: The exome chip included 19/115 rare variants, in 9 genes, previously associated with lone or familial AF. Using validated algorithms querying a combination of clinical notes, structured billing codes, ECG reports, and procedure codes, we identified 1,056 AF cases (>18 years) and 19,148 non-AF controls (>50 years) with available genotype data on the Illumina HumanExome BeadChip v.1.0 in the Vanderbilt EMR-linked DNA repository, BioVU. While known correlations between...
711. Trans-Splicing Correction of CD40 Ligand Deficiency Resulting in Naturally Regulated Correction of a Murine Model of Hyper IgM X-Linked Immunodeficiency
Authors: Minoru Tahara, Robert G. Pergolizzi, Ronald G. Crystal
Journal: Molecular Therapy (2004)

X-linked immunodeficiency with hyper IgM, a human immunodeficiency disease characterized by failure of immunoglobulin isotype switching, is caused by mutations in the CD40 ligand gene (CD40L), normally expressed on CD4 + T cells in an activation-mediated, regulated fashion. The functional effect of the mutations in the CD40L gene is a deficiency of CD40L on the surface of activated CD4 + T cells, thus limiting the interaction of the CD4 + T cells with the CD40 glycoprotein on the surface of B cells, macrophages and dendritic cells. Because this interaction normally mediates immunoglobulin class switching by B cells and macrophage activation, individuals with HIGM1 suffer from recurrent bacterial infections, especially with opportunistic microorganisms such as Pneumocystis carinii (P. carinii). Other than treatment for acquired infections, the only available therapy for HIGM1 is bone marrow transplantation. Since constitutive expression of CD40L induces lymphomas, we investigated correction of the mutation while maintaining the natural regulation of CD40L expression using trans-splicing at the pre-mRNA level. A lentiviral vector trans-splicer coding for the normal exons 2 to 5 of CD40L cDNA was used for ex vivo modification of bone marrow cells harvested from CD40L-knockout (KO) mice and administered to syngenic CD40L-KO mice. Spleens from recipients 10 wk later showed corrected CD40L mRNA as evidenced by RT-PCR and sequencing, and antigen-specific IgG1 responses to keyhole limpet hemocyanin (KLH) immunization. CD40L-KO mice were able to produce antigen specific IgM against KLH, but not IgG1; however, trans-splicing-treated recipients produced both IgM and IgG1. Studies to determine whether trans-splicing functionally corrected the immunodeficiency state demonstrated that (1) regulated expression of CD40L on CD4 + T cells occurred following CD3 stimulation in 1° and 2° transplanted mice, and (2) there was marked attenuation of proliferation of P.carinii in the lung following respiratory tract challenge with the organism. Importantly, assessment of the trans-splicer corrected CD40L-KO mice over 1 yr demonstrated no evidence of lymphoproliferative disease. These studies demonstrate the feasibility of correcting endogenous CD40L in X-linked immunodeficiency with hyper IgM by trans-splicing, leading to functional correction of the genetic defect without the adverse consequences of unregulated CD40L gene expression.
Sudden Death in Childhood Cardiomyopathy
Authors: Tara Bharucha, Katherine J. Lee, Piers E.F. Daubeney, Alan W. Nugent, Christian Turner, Gary F. Sholler, Terry Robertson, Robert Justo, Jim Ramsay, John B. Carlin, Steven D. Colan, Ingrid King, Robert G. Weintraub, Andrew M. Davis
Journal: Journal of the American College of Cardiology (2015)
Tritsat' Lyet Deyatel'nosti Instituta Onkologii, 1926–1956: (“Thirty Years' Activity of the Institute of Oncology, 1926–1956”). In Russian. Edited by A. I. Serebrov, S. A. Kholdin and A. V. Chaklin. Leningrad: Acad. Med. Sc., USSR, 1956. 248 pp.
Authors: Michael B. Shimkin
Journal: Cancer Research (1958)
Report on the first PVL-positive community acquired MRSA strain in Latvia
Authors: E Miklaševics, S Hæggman, A Balode, B Sanchez, A Martinsons, B Olsson-Liljequist, U Dumpis
Journal: Eurosurveillance (2004)

Infections by community-acquired methicillin resistant Staphylococcus aureus (CA-MRSA) have been reported worldwide. Here we present characterisation of the first CA-MRSA isolated in Latvia. A PVL-positive ST30-MRSA-IV strain was isolated from a nasal swab and the central venous catheter of a patient with fever and multiple organ failure. The PFGE pattern of this strain was identical to pattern SE00-3 of MRSA isolated in Sweden from 29 patients during 2000-2003. This strain is related to the South Pacific area, and its appearance in Sweden and Latvia demonstrates its global spread.
OmpA targets dendritic cells, induces their maturation and delivers antigen into the MHC class I presentation pathway
Authors: Pascale Jeannin, Toufic Renno, Liliane Goetsch, Isabelle Miconnet, Jean-Pierre Aubry, Yves Delneste, Nathalie Herbault, Thierry Baussant, Giovanni Magistrelli, Caroline Soulas, Pedro Romero, Jean-Charles Cerottini, Jean-Yves Bonnefoy
Journal: Nature Immunology (2000)
Experience With the Colloidal Silver Treatment of Cancer
Authors: William S. Stone, George T. Pack, Helen Q. Woodard
Journal: Annals of Internal Medicine (1930)

Article1 May 1930Experience With the Colloidal Silver Treatment of CancerWILLIAM S. STONE, M. D., GEORGE T. PACK, M.D., HELEN Q. WOODARD, Ph.D.WILLIAM S. STONE, M. D.Search for more papers by this author, GEORGE T. PACK, M.D.Search for more papers by this author, HELEN Q. WOODARD, Ph.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-3-11-1149 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAt the time of initiation of the lead treatment of cancer by Blair Bell it was claimed1that lead acted as a specific poison for undifferentiated tissues, whether embryonal or neoplastic. Colloidal lead was used in preference to ionic lead because of its lower toxicity, not because any beneficial action was anticipated from the colloid as such. Later work has shown that lead is deposited more freely in the liver, bones, spleen and kidneys than in the tumor;2that therapeutic doses do not necessarily induce abortion;3and that the highly embryonal chorionic epithelioma is not conspicuously lead sensitive.4The opinion...References.1 BELL (a) : Lancet, 1922, 204, 1005. (b) BELL: Lancet, 1925, 209, 1003. (c) BELL: Lancet, 1924, 206, 267. CrossrefGoogle Scholar2 WYARD : Brit. Med. Jour., 1928-1 No. 3515, 838. CrossrefMedlineGoogle Scholar3 BELL : Lancet, 1926, 211, 1236. Google Scholar4 STONECRAVER : Annals of Surgery, 1927, 86, 347. CrossrefMedlineGoogle Scholar5 CUSHNY : Pharmacology and Therapeutics, 1924, 663. Google Scholar6 STEIGER : Abs., J. A. M. A., 1917, 69, 1656. Google Scholar7 MULLER : Jour. Exp. Med., 1926, 43, 533. CrossrefMedlineGoogle Scholar8 STEWARTPARKER : Amer. Jour. Path., 1926, 2, 381. MedlineGoogle Scholar9 VOIGT (a) : Biochem. Zeit., 1915, 68, 477. (b) VOIGHT: Zeit. d. ges. exp. Med., 1926, 52, 33. Google Scholar10 WOODARD : Annals of Surgery, 1927, 86, 607. CrossrefMedlineGoogle Scholar11 ROHDENBURG : Jour. Med. Res., 1915, 31, 331. MedlineGoogle Scholar12 WEIL : J. A. M. A., 1913, 61, 1034. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Memorial Hospital New York City*This work was aided by a grant from the Littauer Fund. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1930Volume 3, Issue 11Page: 1149-1156KeywordsBoneCancer treatmentCarcinomaKidneysLiverSpleenToxicity ePublished: 1 December 2008 Issue Published: 1 May 1930 PDF downloadLoading ...
Pigmented primary carcinoma of the breast: a clinical mimic of malignant melanoma
Authors: None Saitoh, None Saga, None Okazaki, None Maeda
Journal: British Journal of Dermatology (1998)

A 68-year-old man had a pigmented tumour in the breast. Although the clinical picture suggested a malignant melanoma, histology revealed that the tumour was a primary ductal carcinoma of the breast. There was no pagetoid cell proliferation in the epidermis. However, tumour nests contained numerous dendritic melanocytes that could survive in the tumour nests without the existence of epidermal keratinocytes. Further immunohistochemical study employing antibodies to melanocyte growth factors demonstrated that anti-basic fibroblast growth factor (bFGF) antibody was the only reagent to show a positive staining for tumour cells. This indicated that the breast cancer cells produced bFGF, which enabled survival of melanocytes within the tumour mass.
Caspase inhibitors improve survival in sepsis: a critical role of the lymphocyte
Authors: R. S. Hotchkiss, K. C. Chang, P. E. Swanson, K. W. Tinsley, J. J. Hui, P. Klender, S. Xanthoudakis, S. Roy, C. Black, E. Grimm, R. Aspiotis, Y. Han, D. W. Nicholson, I. E. Karl
Journal: Nature Immunology (2000)
Linkage disequilibrium of a type 1 diabetes susceptibility locus with a regulatory IL12B allele
Authors: Grant Morahan, Dexing Huang, Susie I. Ymer, Michael R. Cancilla, Katrina Stephen, Preeti Dabadghao, George Werther, Brian D. Tait, Leonard C. Harrison, Peter G. Colman
Journal: Nature Genetics (2001)
Abstract 15934: Refractory Cardiogenic Shock in a Patient With Hypertrophic Obstructive Cardiomyopathy and Mitral Regurgitation Necessitating Intra-Aortic Balloon Pump Use
Authors: Indrajeet Mahata, Michael Faulx, Snigdha kola, Sweta Singh
Journal: Circulation (2014)

Introduction: Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic disease due to a mutation in cardiac muscle protein resulting in left ventricular wall and septal hypertrophy. The presence of systolic anterior motion (SAM) of the mitral valve leads to dynamic left ventricular outflow tract (LVOT) obstruction. With increasing SAM of the anterior mitral leaflet there is resultant loss of coaptation leading to mitral regurgitation (MR). MR has been associated with HOCM but severe MR physiology causing refractory cardiogenic shock and requiring the use of afterload reduction through intra-aortic balloon pump (IABP) is rare and seems paradoxical to the conventional therapy for HOCM. Case summary: This is a case of 71year old female with HOCM, presenting with worsening shortness of breath. She had pulmonary vascular congestion on Chest X-ray and her Transthoracic Echocardiography demonstrated significant LVOT obstruction with moderate MR. She was being evaluated for myomectomy while being treated medically with beta blocker therapy for HOCM. She decompensated with acute respiratory failure from pulmonary edema, her blood pressure and oxygen saturation dropped. She was intubated. Swan- ganz catheter reading suggested wedge pressures of 22 and elevated pulmonary pressures. MvO2 was 32% and this was suggestive of cardiogenic shock. The Trans-esophageal echocardiogram (TEE) showed normal EF with severe concentric LVH and a moderate to severe (3+) MR due to restricted leaflet motion with regurgitant orifice area being 2.5cm2. At that point her MR was the dominant physiology behind her acute decompensation and cardiogenic shock and hence an IABP was placed for reducing afterload that helped in stabilizing her. Subsequently her wedge pressure and MvO2 improved, she was weaned off the IABP and extubated. The patient is being evaluated for myomectomy and mitral valve repair. Conclusion: This case illustrates complex hemodynamics and a challenging management due to competing MR and HOCM physiologies, too much central volume to offset HOCM may worsen MR and pulmonary edema while too much afterload reduction might worsen the HOCM. The use of IABP in a HOCM patient though seems paradoxical but was necessary in this setting to deal with complex physiologies.