tbuckley/cabot-search huggingface dataset:
Accuracy of Laryngeal Examination during Upper Gastrointestinal Endoscopy for Premalignancy Screening: Prospective Study in Patients with and without Reflux Symptoms
Authors: G. Cammarota, J. Galli, S. Agostino, E. De Corso, M. Rigante, R. Cianci, P. Cesaro, E. Nista, M. Candelli, A. Gasbarrini, G. Gasbarrini
Journal: Endoscopy (2006)

Background and Study Aims: Gastroesophageal reflux disease may be associated with laryngeal damage caused by reflux material. The aim of this study was to investigate the accuracy of laryngeal examinations during routine upper gastrointestinal endoscopy as a method of screening for major laryngeal injury in a series of patients with reflux symptoms. Patients and Methods: A total of 100 consecutive patients with reflux symptoms and 100 control individuals underwent upper gastrointestinal endoscopy with standard or high-resolution magnifying video endoscopes. Any laryngeal abnormalities were initially identified by the gastroenterologist before the scope was inserted into the esophagus. All of the examinations were recorded on video and subsequently reevaluated by an otorhinolaryngologist. All of the patients underwent standard laryngoscopy as a reference procedure.Results: All of the patients completed the study. The sensitivity, specificity, negative predictive value, and positive predictive value of the preliminary laryngeal exploration for detecting laryngeal abnormalities (such as laryngitis and vocal leukoplakia) were 90 %, 90 %, 92 %, and 89 %, respectively. High-resolution magnifying endoscopy had a higher sensitivity and specificity than standard endoscopy for detecting laryngeal pathology. Two patients were found to have laryngeal leukoplakia. Conclusions: This study shows that preliminary diagnosis of laryngeal disorders can be accurately carried out by the gastroenterologist when patients are undergoing upper endoscopy for reflux symptoms. This approach could also be helpful for the timely diagnosis of major reflux-related laryngeal disease.
Brain Single Photon Emission Computed Tomography With Tc-99m MIBI or Tc-99m ECD in Comparison to MRI in Multiple Sclerosis
Authors: Majid Assadi, Hooman Salimipour, Mohammad Seyedabadi, Jamshid Saberifard, Hamid Javadi, Iraj Nabipour, Reza Nemati
Journal: Clinical Nuclear Medicine (2010)

To evaluate whether or not brain single photon emission computed tomography (SPECT) with Tc-99m MIBI or Tc-99m ECD (ethyl cysteinate dimer) can detect any abnormality in patients with definite multiple sclerosis (MS). We then compared these values with the results of T1, T2, and fluid-attenuated inversion recovery in magnetic resonance imaging (MRI).A total of 16 patients with proved MS were enrolled in the study, and the MRI with and without gadolinium contrast and also brain SPECT with Tc-99m MIBI (8 cases) or Tc-99m ECD (8 other cases) were performed.MRI studies was performed in 16 patients (13 women and 3 men, aged 16-38 years) and an average of 10.47, 3.7, 5.3, 1.7, and 0.9 lesions was found in respect in periventricular white matter, juxtacortical white matter, corpus callosum, cerebellar peduncles, and brainstem, whereas brain SPECT with Tc-99m MIBI or Tc-99m ECD detected no abnormality. In addition, 6 cases had some degree of contrast enhancement.It seems that brain SPECT with Tc-99m MIBI or Tc-99m ECD would not improve this insufficiency. The small sizes of some plaques, particularly in chronic atrophic form of lesions, and the possibility of deeper anatomic positions of plaques can explain to some extent why the MS lesions were impossible to delineate on brain scan, although additional studies are needed.
Identification of adverse reactions to new drugs. III: Alerting processes and early warning systems.
Authors: G R Venning
Journal: BMJ (1983)

The process of discovery for 18 important adverse drug reactions was analysed in terms of study designs and other features which determined whether published reports of suspected adverse reactions were convincing or provided valid evidence of causality. First alerts were almost always anecdotal reports. For earlier alerting during clinical trials event recording is needed, associated with dose-response data and the use of patients as their own controls.
Allele Loss at the Retinoblastoma Locus in Human Ovarian Cancer
Authors: S.-b. Li, P. E. Schwartz, W.-H. Lee, T. L. Yang-Feng
Journal: JNCI Journal of the National Cancer Institute (1991)

To gain a broad spectrum on allelic loss of specific loci in ovarian tumors, we initially examined DNA from 23 pairs of ovarian tumors and matched peripheral blood lymphocyte samples from the same patients, using 27 polymorphic DNA markers distributed on 13 chromosomes. Significant high frequency of allelic deletion (22%-44%) at chromosome 13 loci (D13S31, D13S32, D13S33, and D13S34) at bands q12-q34 was observed in tumor tissues. These results led us to investigate the loss of heterozygosity at the retinoblastoma (RB) locus in ovarian tumors, because the RB gene is a tumor-suppressor gene located at 13q14. Analysis of the variable number of tandem repeat sequence polymorphism in intron 20 in the RB gene revealed that 6 (30%) of 20 patients with informative samples showed allelic loss at the RB locus in their tumor tissues. This loss, of relatively high frequency, suggests that the RB gene, or a closely linked gene, seems to be involved in the development of ovarian cancer.
Engineered measles virus as a novel oncolytic viral therapy system for hepatocellular carcinoma
Authors: Boris Blechacz, Patrick L. Splinter, Suzanne Greiner, Rae Myers, Kah-Whye Peng, Mark J. Federspiel, Stephen J. Russell, Nicholas F. LaRusso
Journal: Hepatology (2006)

The oncolytic measles virus Edmonston strain (MV-Edm), a nonpathogenic virus targeting cells expressing abundant CD46, selectively destroys neoplastic tissue. Clinical development of MV-Edm would benefit from noninvasive monitoring strategies to determine the speed and extent of the spread of the virus in treated patients and the location of virus-infected cells. We evaluated recombinant MV-Edm expressing carcinoembryonic antigen (CEA) or the human sodium iodide symporter (hNIS) for oncolytic potential in hepatocellular carcinoma (HCC) and efficiency in tracking viruses in vivo by noninvasive monitoring. CD46 expression in human HCC and primary hepatocytes was assessed by flow cytometry and immunohistochemistry. Infectivity, syncytium formation, and cytotoxicity of recombinant MV-Edm in HCC cell lines were evaluated by fluorescence microscopy, crystal violet staining, and the MTS assay. Transgene expression in HCC cell lines after infection with recombinant MV-Edm in vitro and in vivo was assessed by CEA concentration, 125I-uptake, and 123I-imaging studies. Toxicology studies were performed in IfnarKO×CD46 transgenic mice. The CD46 receptor was highly expressed in HCC compared to nonmalignant hepatic tissue. Recombinant MV-Edm efficiently infected HCC cell lines, resulting in extensive syncytium formation followed by cell death. Transduction of HCC cell lines and subcutaneous HCC xenografts with recombinant MV-Edm resulted in high-level expression of transgenes in vitro and in vivo. MV-Edm was nontoxic in susceptible mice. Intratumoral and intravenous therapy with recombinant MV-Edm resulted in inhibition of tumor growth and prolongation of survival with complete tumor regression in up to one third of animals. In conclusion, engineered MV-Edm may be a potent and novel cancer gene therapy system for HCC. MV-Edm expressing CEA or hNIS elicited oncolytic effects in human HCC cell lines in vitro and in vivo, enabling the spread of the virus to be monitored in a noninvasive manner. (HEPATOLOGY 2006;44:1465–1477.)
Increased vascular permeability in C1 inhibitor–deficient mice mediated by the bradykinin type 2 receptor
Authors: Eun D. Han, Ryan C. MacFarlane, Aideen N. Mulligan, Jennifer Scafidi, Alvin E. Davis
Journal: Journal of Clinical Investigation (2002)

Heterozygosity for C1 inhibitor (C1INH) deficiency results in hereditary angioedema. Disruption of the C1INH gene by gene trapping enabled the generation of homozygous- and heterozygous-deficient mice. Mating of heterozygous-deficient mice resulted in the expected 1:2:1 ratio of wild-type, heterozygous, and homozygous-deficient offspring. C1INH-deficient mice showed no obvious phenotypic abnormality. However, following injection with Evans blue dye, both homozygous and heterozygous C1INH-deficient mice revealed increased vascular permeability in comparison with wild-type littermates. This increased vascular permeability was reversed by treatment with intravenous human C1INH, with a Kunitz domain plasma kallikrein inhibitor (DX88), and with a bradykinin type 2 receptor (Bk2R) antagonist (Hoe140). In addition, treatment of the C1INH-deficient mice with an angiotensin-converting enzyme inhibitor (captopril) increased the vascular permeability. Mice with deficiency of both C1INH and Bk2R demonstrated diminished vascular permeability in comparison with C1INH-deficient, Bk2R-sufficient mice. These data support the hypothesis that angioedema is mediated by bradykinin via Bk2R.
Schizophrenia and neurosis.
Authors: M Livingston
Journal: BMJ (1978)

ovary 5 59 stage III 45 Carcinoma ovary 6 16 stage IV 61 Carcinoma ovary 7 76 stage IV 92 Carcinoma ovary 8 62 stage IV 59 Carcinoma endometrium 9 65 stage I 34 Carcinoma endometrium 10 64 stage I 39 Carcinoma 11 57 cervix stage I 25
Reserpine in the Diseased Heart.
Authors: J. William Fewell
Journal: Annals of Internal Medicine (1967)

s1 May 1967Reserpine in the Diseased Heart.J. William Fewell, M.D., Felix M. Cortes, M.D., Howard N. Baier, M.D.J. William Fewell, M.D.Search for more papers by this author, Felix M. Cortes, M.D.Search for more papers by this author, Howard N. Baier, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-66-5-1036_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThis study was devised to investigate the effects of reserpine on the normal and the diseased heart. The results of 5 of 15 patients are presented in this pilot study. The following parameters were measured at rest and during standardized exercise: mean arterial pressure, heart rate, ejection time, cardiac index, stroke index, and mean stroke ejection rate. The patient was given 1.0 mg of reserpine daily for 4 weeks, and the studies were repeated.The normal patients demonstrated the following changes at rest while on reserpine: heart rate, -9%; ejection time, 0%; cardiac index, -63%; stroke index, -58%; and mean... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: J. William Fewell, M.D.; Felix M. Cortes, M.D.; Howard N. Baier, M.D.Affiliations: Philadelphia, Pennsylvania PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1967Volume 66, Issue 5Page: 1036-1036KeywordsExerciseHeartHeart rateLongitudinal studiesMean arterial pressurePilot studiesReserpineStroke ePublished: 1 December 2008 Issue Published: 1 May 1967 PDF downloadLoading ...
CARDIAC REHABILITATION PARTICIPATION REDUCES 90-DAY HOSPITAL READMISSIONS AFTER ACUTE MYOCARDIAL INFARCTION OR PERCUTANEOUS CORONARY INTERVENTION
Authors: Daniel W. Mudrick, Lynn Shaffer, Michelle Lalonde, Anirudh Ruhil, Greg Lam, Jesse Hickerson, Teresa Caulin-Glaser, Richard Snow
Journal: Journal of the American College of Cardiology (2013)
Kupffer cells from carbon tetrachloride-injured rat livers produce chemotactic factors for fibroblasts and monocytes: The role of tumor necrosis factor-α
Authors: Juan Armendariz-Borunda, Jerome M. Seyer, Arnold E. Postlethwaite, Andrew H. Kang
Journal: Hepatology (1991)

Conditioned media from cultured Kupffer and mononuclear macrophagic cells obtained 48 hr after CCl4 administration to rats contains chemotactic factors for human skin fibroblasts and human monocytes. The chemotactic mediator for fibroblasts was approximately 17 kD and was more prominent at early stages of culture. It induced a dose-dependent chemotactic response in fibroblasts. Although the conditioned medium from cultured Kupffer cells of normal rats also contained detectable biological activity, it was significantly less than that in conditioned medium from cultured Kupffer cells from CCl4-treated rats. The activity obtained after purification by high-performance liquid chromatography was completely ablated by incubation with tumor necrosis factor-alpha antibody. Transforming growth factor-beta antibody diminished biological activity by 20%. Human recombinant tumor necrosis factor-alpha and transforming growth factor-beta used in the assay as control showed significant chemotactic activity. The chemotactic activity present in whole normal conditioned medium was only present after 24 and 48 hr of culture. Furthermore, this activity was not neutralized by human recombinant tumor necrosis factor-alpha or transforming growth factor-beta antibodies. Incubation of whole 6-hr conditioned medium with human recombinant tumor necrosis factor-alpha and transforming growth factor-beta antibodies demonstrated and confirmed that tumor necrosis factor-alpha plays a major role in inducing the chemotactic response. On acidification of this supernatant, we found a notable increase in the biological response that could be neutralized by transforming growth factor-beta antibody. Thus tumor necrosis factor-alpha and transforming growth factor-beta may sequentially provide important signals for fibroblast and monocyte recruitment in vivo at initial stages of liver injury.
Case 13-1981
Authors: Richard C. Cabot, Robert E. Scully, James J. Galdabini, Betty U. McNeely, W. Hallowell Churchill, Nancy L. Harris
Journal: New England Journal of Medicine (1981)

Presentation of CaseA 91-year-old woman was admitted to the hospital because of collapse.She was well until 21 years earlier, when hypertension was found and medication was prescribed. For several years before admission she received hydrochlorothiazide. One month before entry she observed purpuric spots on the lower extremities. The hematocrit was 31 per cent, and the platelet count 100,000. A physician advised discontinuance of hydrochlorothiazide. During the two weeks before entry purpuric lesions appeared on the arms. On the day of admission she was found lying on the floor of her apartment, alert but unable to arise.The patient . . .
SI Unit Implementation—the Next Step
Authors: George D. Lundberg
Journal: JAMA (1988)

In recognition of the need to participate fully in the global medical community, the AMA has been planning a method of implementing certain of the Systéme International (SI) units for more than a decade. In December 1984, the House of Delegates (HOD) of the AMA adopted a report of the Council on Scientific Affairs<sup>1</sup>entitled "SI Units for Clinical Laboratory Data." That report set a date of 1987 for a change in medical laboratory data reporting in the United States. By adopting that report, the HOD reaffirmed earlier policy on SI units that dated to 1978, when Council on Scientific Affairs Report E<sup>2</sup>—which stated, "For a year or more prior to the transition date, new units would be used parenthetically with the comparable old units in all AMA and other cooperating publications. For at least one year after the transition date, the old units will be used
Successful Nonoperative Management of the Most Severe Blunt Renal Injuries
Authors: Gwendolyn M. van der Wilden, George C. Velmahos, D'Andrea K. Joseph, Lenworth Jacobs, M. George DeBusk, Charles A. Adams, Ronald Gross, Barbara Burkott, Suresh Agarwal, Adrian A. Maung, Dirk C. Johnson, Jonathan Gates, Edward Kelly, Yvonne Michaud, William E. Charash, Robert J. Winchell, Steven E. Desjardins, Michael S. Rosenblatt, Sanjay Gupta, Miguel Gaeta, Yuchiao Chang, Marc A. de Moya
Journal: JAMA Surgery (2013)

Severe renal injuries after blunt trauma cause diagnostic and therapeutic challenges for the treating clinicians. The need for an operative vs a nonoperative approach is debated.To determine the rate, causes, predictors, and consequences of failure of nonoperative management (NOM) in grade IV and grade V blunt renal injuries (BRIs).Retrospective case series.Twelve level I and II trauma centers in New England.A total of 206 adult patients with a grade IV or V BRI who were admitted between January 1, 2000, and December 31, 2011.Failure of NOM, defined as the need for a delayed operation or death due to renal-related complications during NOM.Of 206 patients, 52 (25.2%) were operated on immediately, and 154 (74.8%) were managed nonoperatively (with the assistance of angiographic embolization for 25 patients). Nonoperative management failed for 12 of the 154 patients (7.8%) and was related to kidney injury in 10 (6.5%). None of these 10 patients had complications because of the delay in BRI management. The mean (SD) time from admission to failure was 17.6 (27.4) hours (median time, 7.5 hours; range, 4.5-102 hours), and the cause was hemodynamic instability in 10 of the 12 patients (83.3%). Multivariate analysis identified 2 independent predictors of NOM failure: older than 55 years of age and a road traffic crash as the mechanism of injury. When both risk factors were present, NOM failure occurred for 27.3% of the patients; when both were absent, there were no NOM failures. Of the 142 patients successfully managed nonoperatively, 46 (32.4%) developed renal-related complications, including hematuria (24 patients), urinoma (15 patients), urinary tract infection (8 patients), renal failure (7 patients), and abscess (2 patients). These patients were managed successfully with no loss of renal units (ie, kidneys). The renal salvage rate was 76.2% for the entire population and 90.3% among patients selected for NOM.Hemodynamically stable patients with a grade IV or V BRI were safely managed nonoperatively. Nonoperative management failed for only 6.5% of patients owing to renal-related injuries, and three-fourths of the entire population retained their kidneys.
Evidence of a genetic contribution to lung function decline in asthma
Authors: Gerard H. Koppelman, Ian Sayers
Journal: Journal of Allergy and Clinical Immunology (2011)

There has been great progress in identifying new asthma susceptibility genes. In asthmatic subjects there is variable airway remodeling that includes features such as smooth muscle hypertrophy/hyperplasia, basement membrane thickening, and increased extracellular matrix deposition. Does airway remodeling have a genetic contribution in asthma? Data from different murine strains suggest there is a genetic contribution to the development and progression of airway remodeling. In human subjects it is important to consider what surrogate markers of remodeling have been used in genetic studies. Baseline FEV1 and airway hyperresponsiveness are determined by a complex interplay of factors, including nonremodeling mechanisms; however, we consider a decline in FEV1 as a robust marker of remodeling. To date, single nucleotide polymorphisms spanning ADAM33, ESR1, PLAUR, and VEGF have been associated with an excess decline in lung function in asthmatic subjects carrying the rare alleles (FEV1, −13.0 to 55.2 mL/y excess). Interestingly these genes have overlapping functions in proteolytic pathways in the airways. There is accumulating evidence that genetic factors are important in the development of airway remodeling in asthmatic subjects, and further longitudinal studies with additional remodeling phenotypes and genome-wide association studies will identify novel susceptibility genes, leading to new approaches to target remodeling in asthmatic subjects.
The United States Preventive Services Task Force Recommendation Statement on Screening for Peripheral Arterial Disease
Authors: Joshua A. Beckman, Michael R. Jaff, Mark A. Creager
Journal: Circulation (2006)

Under the auspices of the Agency for Healthcare Research and Quality, the United States Preventive Services Task Force (USPSTF) recently released an update to its 1996 Peripheral Arterial Disease (PAD) Screening Recommendation Statement. The USPSTF recommended against PAD screening, giving the practice a "D" level recommendation. This level suggests that little or no benefit could accrue from PAD screening and that screening-associated harm could occur. The present commentary disputes the Task Force's recommendation. The USPSTF statement omitted important peer-reviewed data on the prevalence, screening efficacy, and short-term adverse prognosis of patients with PAD and failed to consider the beneficial outcomes that probably would result from timely diagnosis and treatment of this important manifestation of atherosclerosis. The Task Force implied that screening may lead to unnecessary tests, including increased risk associated with use of contrast angiographic studies. However, most patients with PAD have neither classic symptoms of leg claudication nor threatened limbs but have an extraordinarily high rate of adverse cardiovascular events, such as myocardial infarction, stroke, and death--events that should serve as a key rationale for screening. Medical therapy, including risk factor modification and antiplatelet medications, is known to reduce cardiovascular morbidity and mortality rates in these patients. The Task Force's recommendation against PAD detection may itself adversely result in inadequate recognition and treatment of PAD, with adverse public health consequences. We encourage the USPSTF to reevaluate the extant data, add vascular specialty expertise to its review group, and reconsider its recommendation.
Diagnosis of Bernard-Soulier syndrome and Glanzmann's thrombasthenia with a monoclonal assay on whole blood.
Authors: R R Montgomery, T J Kunicki, C Taves, D Pidard, M Corcoran
Journal: Journal of Clinical Investigation (1983)

Two hereditary platelet disorders, Bernard-Soulier syndrome and Glanzmann's thrombasthenia, are characterized by selective deficiencies of platelet membrane glycoproteins. Murine monoclonal antibodies were developed against platelet membrane glycoprotein Ib and against the glycoprotein IIb/IIIa complex. A rapid whole blood assay for the deficiency of these glycoproteins was developed and used to study whole blood samples from six patients with Glanzmann's thrombasthenia and three patients with Bernard-Soulier syndrome. Patients with type I and type II Glanzmann's thrombasthenia were easily detectable with this assay. This permits the diagnosis of these disorders on 200 microliters of whole blood within 2 h of blood sampling.