tbuckley/cabot-search huggingface dataset:
Correlation of Electrocardiographic Studies and Arteriographic Findings with Angina Pectoris
Authors: GOTTLIEB C. FRIESINGER, RAPHAEL F. SMITH
Journal: Circulation (1972)

The relationships among angina pectoris, stress tests, and arteriography are complex. The majority of patients with angina pectoris can be adequately diagnosed by a careful history. Considerable attention to detail and repeated questioning is often necessary before the pain syndrome can be accurately classified. The resting electrocardiogram is of limited value in the diagnosis despite the fact that there is a high positive correlation between abnormal ST-T changes on the electrogram and significant obstructive lesions on coronary arteriograms. The value of the electrocardiogram is enhanced, and its specifiicity and sensitivity increased, when used in combination with exercise stress. The lowest error percentage is achieved by utilizing rate-standardized exercise tests and multiple leads with loads that produce heart rate responses of 80-90% of the expected maximum. Coronary arteriography gives the most specific anatomic information in patients with ischemic cardiac pain but will not directly disclose the cause of the pain. This fact assumes considerable importance when the pain has atypical features or when the patient is in the age group that has a high prevalence of coronary atherosclerosis. Similarly, the presence of past myocardial infarction is likely to be associated with obstructive disease, regardless of the cause of the patient's current symptoms. The exact role of lipid and other metabolic abnormalities in producing coronary arteriographic changes in the absence of symptoms needs further clarification, although the available data suggest that marked elevations in lipid fractions are frequently associated with atherosclerotic change, regardless of symptoms. Finally, the data imply that the anatomic abnormalities and functional consequences of the coronary atherosclerotic process are more important predictors of the patient's course than any specific symptomatic expression such as angina pectoris.
S102 Lipoxin A4 Improves Efferocytosis Via Inhibition Of The Hmgb1 In Human Alveolar Macrophages
Authors: Q. Wang, D. Parekh, V. D'Souza, R. Dancer, J. Patel, D. Bartis, F. Gao, Q. Lian, S. Jin, D. Thickett
Journal: Thorax (2014)

<h3>Introduction</h3> Effective clearance of apoptotic cells by macrophages, termed efferocytosis, is a pre-requisite for successful resolution of inflammation. High mobility group box protein 1 (HMGB1), is an alarmin that may promote inflammation as well as suppress phagocytosis. Lipoxin A<sub>4</sub>, represents one of a unique class of lipid mediators that possess a wide spectrum of anti-inflammatory and pro-resolution actions. We hypothesised that lipoxin A<sub>4</sub> may promote both apoptosis in neutrophils, and stimulate macrophage efferocytosis, acting as an antagonist to HMGB-1. <h3>Methods</h3> Neutrophils were obtained from healthy volunteers and cultured for 24 h with or without lipoxin A<sub>4.</sub> Apoptosis of neutrophils was determined with Annexin V/SyTox staining by flow cytometry. HMGB-1 levels in Acute Respiratory Distress Syndrome (ARDS) bronchoalveolar lavage fluid (BALF) was measured by ELISA. The effects of HMGB-1 and lipoxin A<sub>4</sub> upon alveolar macrophage efferocytosis was assessed by measuring the ingestion of CMFDA labelled apoptotic neutrophils by flow cytometry. The PI3K (P85) protein expression was measured by western blotting. <h3>Results</h3> Treatment of lipoxin A4 (100 nM) increased the apoptosis of neutrophils (p = 0.0244), and reduced the dead (p = 0.0238) and necrotic neutrophils (p = 0.0358) compared to control (n = 8). BALF from patients with ARDS suppressed efferocytosis of apoptotic neutrophils. The effects of BALF correlated with HMGB-1 levels in the BALF fluid. HMGB-1 decreased efferocytosis (p &lt; 0.05) in a dose dependent manner, and reached a significant effect at 150 ng/ml (p = 0.008). Lipoxin A4 increased the efferocytosis (p &lt; 0.05) of alveolar macrophages in a dose dependent manner, and reached the maximal effect at 100 nM (p = 0.008). Moreover, lipoxin A4 (100 nM) blocked the decreased efferocytosis response to HMGB-1 (150 ng/ml) (p = 0.005, n = 8). The lipoxin A4 beneficial effects were abrogated by ALX antagonist, BOC-2 (p &lt; 0.05) and PI3K inhibitor (p &lt; 0.05). <h3>Conclusions</h3> Lipxin A<sub>4</sub><i>in vitro</i> promotes the apoptosis but not necrosis of neutrophils. In tandem it stimulates efferocytosis of alveolar macrophages. Elevated HMGB-1 in ARDS BALF suppresses efferocytosis. Lipoxin A<sub>4</sub> can block these effects of HMGB-1. The effect of lipoxin A4 increasing efferocytosis was through ALX–PI3K signalling pathways. Lipoxin A<sub>4</sub> may therefore have potential as a therapeutic agent to promote the resolution of neutrophilic inflammation in ARDS.
Mobilized Human Hematopoietic Stem/Progenitor Cells Promote Kidney Repair After Ischemia/Reperfusion Injury
Authors: Bing Li, Amy Cohen, Thomas E. Hudson, Delara Motlagh, David L. Amrani, Jeremy S. Duffield
Journal: Circulation (2010)

Background— Understanding the mechanisms of repair and regeneration of the kidney after injury is of great interest because there are currently no therapies that promote repair, and kidneys frequently do not repair adequately. We studied the capacity of human CD34 + hematopoietic stem/progenitor cells (HSPCs) to promote kidney repair and regeneration using an established ischemia/reperfusion injury model in mice, with particular focus on the microvasculature. Methods and Results— Human HSPCs administered systemically 24 hours after kidney injury were selectively recruited to injured kidneys of immunodeficient mice (Jackson Labs, Bar Harbor, Me) and localized prominently in and around vasculature. This recruitment was associated with enhanced repair of the kidney microvasculature, tubule epithelial cells, enhanced functional recovery, and increased survival. HSPCs recruited to kidney expressed markers consistent with circulating endothelial progenitors and synthesized high levels of proangiogenic cytokines, which promoted proliferation of both endothelial and epithelial cells. Although purified HSPCs acquired endothelial progenitor markers once recruited to the kidney, engraftment of human endothelial cells in the mouse capillary walls was an extremely rare event, indicating that human stem cell mediated renal repair is by paracrine mechanisms rather than replacement of vasculature. Conclusions— These studies advance human HSPCs as a promising therapeutic strategy for promoting renal repair after injury.
Hepatitis Associated with Coxsackie Virus Group A, Type 4
Authors: J. A. Morris, B. L. Elisberg, W. L. Pond, P. A. Webb
Journal: New England Journal of Medicine (1962)

HERPANGINA is generally associated in man with infection with Group A Coxsackie viruses.1 Less frequently, Coxsackie viruses occur with encephalitis,1 aseptic meningitis2 and ill defined febrile illnesses that are sometimes associated with rash.3 On rare occasions Coxsackie viruses have been recovered from patients with clinical hepatitis4 5 6; in at least 1 of these patients there was an associated rash.6 In 1956 an organism subsequently identified as Coxsackie virus Group A, Type 4, was recovered by one of us (W.L.P.) from the blood of a one-and-a-half-year-old child with clinical hepatitis associated with jaundice and rash. During convalescence at least a sixteenfold . . .
Sequence of Authors' Names In Articles
Authors: Jack Lieberman
Journal: JAMA (1970)

<h3>To the Editor.—</h3> The editorial by Frank Hinman, Jr., MD, (<b>212</b>:618, 1970) offers a practical sequence of authors' names in association with scientific articles. The suggestion made by Dr. Hinman would be practical and useful had not a recent change been made in the manner of listing references in most scientific journals. References currently list the first three authors by name and then include the remaining authors by an "et al." This format for listing references, therefore, eliminates the last-named individual who, according to Dr. Hinman's recommendation, would be the secondmost important contributor to the article. In order to repair this miscarriage of accreditation, I suggest that the authors be listed in decreasing order of their contribution to the paper, so that the second name would be that of the secondmost important contributor. An alternative would be to change the manner of listing authors in the references so that
How to Avoid Mistakes in a Physician's Office Laboratory
Authors: Stebbins B. Chandor
Journal: JAMA (1990)

<b>Physician's Office Laboratory Guidelines</b>, vol 9, No. 4, by David M. Jeffers, Betty V. Addison, Paul M. Free, et al (NCCLS document POL-1-T), various pagination, loose-leaf binder, $85, ISBN 0-273-3099;<b>Physician's Office Laboratory Procedure Manual</b>, vol 9, No. 5, Villanova, Pa, National Committee for Clinical Laboratory Standards, 1989. <i>How to Avoid Mistakes in a Physician's Office Laboratory</i>is an instructional text in the form of a loose-leaf notebook with 71 pages in 11 sections, an accompanying set of Kodachromes, a viewer, and a cassette tape. It is presented as a guide for those working in a physician's office laboratory, based on the authors' experience giving seminars. On page 1 they point out that the book deals with "simple and seemingly unimportant" steps that actually are very important in the laboratory, a theme that is carried throughout. The first three pages set the tone by reviewing the topics: protecting oneself from
Adaptation in the env Gene of HIV-1 and Evolutionary Theories of Disease Progression
Authors: S. Williamson
Journal: Molecular Biology and Evolution (2003)

The exact mechanisms by which HIV overwhelms the immune system remain poorly understood. Among the several explanations of HIV disease progression, most include adaptation of the viral genome to the host environment as a causal factor. Therefore, quantifying the rate and pattern of adaptive evolution within infected patients is critical to understanding the development of AIDS. Using sequence data from infected individuals sampled at multiple time points, I estimate the within-host adaptation rate of the HIV-1 env gene for viral populations from 50 different patients. I find that, averaging across patients, one adaptive substitution occurs every 3.3 months. Also, one adaptive mutation is driven to a high frequency (>50% but <100%) every 2.5 months. Taken together, such adaptive events occur once every 25 viral generations, which is the fastest adaptation rate ever recorded for a single protein-coding gene. Within the entire env gene, I estimate that a majority ( approximately 55%) of both nonsynonymous substitutions and high-frequency polymorphisms are adaptive. Further, in the C2-V5 region of env, I find that patients with longer asymptomatic periods have virus populations with higher adaptation rates, corroborating the notion that a broad, strong immune response against epitopes in the env gene product leads to longer asymptomatic periods. I conclude by discussing the distribution of nonsynonymous changes over the env gene.
Report calls for strategies to reduce medication errors
Authors: S. Mayor
Journal: BMJ (2004)

Comprehensive strategies—rather than piecemeal efforts—and measures that focus on the entire process of medication rather than on individual mistakes are needed to reduce the incidence of serious errors, said a UK report published last week.

The report, Building a safer NHS for patients. Improving medication safety , reviewed the causes and frequency of medication error and identified models of good practice to improve medication safety.

It found that the causes of errors were complex, involving human lapses and mistakes. Attention was usually focused on the actions of individuals who were considered to be the cause of error, the report warned. However, it found that systems weaknesses that predisposed to human error were important and recommended checks and error …
Phylogenetic Dating and Characterization of Gene Duplications in Vertebrates: The Cartilaginous Fish Reference
Authors: Marc Robinson-Rechavi, Bastien Boussau, Vincent Laudet
Journal: Molecular Biology and Evolution (2004)

Vertebrates originated in the lower Cambrian. Their diversification and morphological innovations have been attributed to large-scale gene or genome duplications at the origin of the group. These duplications are predicted to have occurred in two rounds, the "2R" hypothesis, or they may have occurred in one genome duplication plus many segmental duplications, although these hypotheses are disputed. Under such models, most genes that are duplicated in all vertebrates should have originated during the same period. Previous work has shown that indeed duplications started after the speciation between vertebrates and the closest invertebrate, amphioxus, but have not set a clear ending. Consideration of chordate phylogeny immediately shows the key position of cartilaginous vertebrates (Chondrichthyes) to answer this question. Did gene duplications occur as frequently during the 45 Myr between the cartilaginous/bony vertebrate split and the fish/tetrapode split as in the previous approximately 100 Myr? Although the time interval is relatively short, it is crucial to understanding the events at the origin of vertebrates. By a systematic appraisal of gene phylogenies, we show that significantly more duplications occurred before than after the cartilaginous/bony vertebrate split. Our results support rounds of gene or genome duplications during a limited period of early vertebrate evolution and allow a better characterization of these events.
Cholestyramine and Gallstones
Authors: THOMAS M. MALM
Journal: Annals of Internal Medicine (1974)

Comments1 January 1974Cholestyramine and GallstonesTHOMAS M. MALM, M.D.THOMAS M. MALM, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-80-1-120_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Reading the article, "Cholestyramine in Type II Hyperlipoproteinemia," by Levy and associates (Ann Intern Med79:51-88, 1973), reminded me of the recent paper from the Mayo Clinic (THISTLEJL, SCHOENFIELDLJ, Induced alterations in composition of bile of persons having cholelithiasis.Gastroenterology61:488-496, 1971), describing the treatment of gallstones with cholic acids. Grossly simplified, the contention of the authors is that alteration of the cholesterol/cholic acid ratio was intimately related to stone formation and that a decrease in cholic acid led to super saturation of cholesterol and hence cholesterol stone formation. The treatment of choice, then, was...Reference1. NEIDERHISER D and ROTH H: Cholesterol solubilization by solutions of bile salts and bile salts plus lecithin. Proc Soc Exp Biol Med 128:221-225, 1968 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: THOMAS M. MALM, M.D. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1974Volume 80, Issue 1Page: 120-120KeywordsAcidsBileCholelithiasisCholesterol ePublished: 1 December 2008 Issue Published: 1 January 1974 PDF downloadLoading ...
Compliance with CPAP therapy in patients with the sleep apnoea/hypopnoea syndrome.
Authors: H M Engleman, S E Martin, N J Douglas
Journal: Thorax (1994)

BACKGROUND--Continuous positive airway pressure (CPAP) therapy is the treatment of choice for the sleep apnoea/hypopnoea syndrome. Compliance with this relatively obtrusive therapy has not been well studied. METHODS--Usage of CPAP was investigated in 54 patients with sleep apnoea/hypopnoea syndrome (median 36 (range 7-129) apnoeas + hypopnoeas/hour slept) over the first 1-3 months after starting CPAP therapy. In all cases CPAP usage was monitored by hidden time clocks that indicated for how long the machines were switched on--that is, the CPAP run time. In 32 patients the time at which the CPAP mask pressure was at the therapeutic level of CPAP pressure set for that patient--that is, the mask time--was also monitored. In all patients objective daytime sleepiness was assessed by multiple sleep latency before and after CPAP therapy. RESULTS--The mean (SE) nightly CPAP run time was 4.7 (0.4) hours. There was no correlation between run time and severity of the sleep apnoea/hypopnoea syndrome as assessed by apnoea + hypopnoea frequency or multiple sleep latency, and no correlation between CPAP usage and improvement in multiple sleep latency. Thirty two patients in whom mask time was recorded had therapeutic CPAP pressures for 89% (3%) of their CPAP run times. Patients who experienced side effects from CPAP used their CPAP machines significantly less than those who did not. CONCLUSIONS--Patients with sleep apnoea/hypopnoea syndrome used CPAP for less than five hours/night on average with no correlation between severity of sleep apnoea/hypopnoea syndrome and CPAP usage. Patients who complained of side effects used their CPAP therapy less. It is recommended that, as a minimum, CPAP run time should be regularly recorded in all patients receiving CPAP therapy.
584 TOLL LIKE RECEPTOR MEDIATED SUPPRESSION OF WOODCHUCK HEPATITIS VIRUS REPLICATION IN PRIMARY WOODCHUCK HEPATOCYTES
Authors: X.Y. Zhang, Z.J. Meng, S. Qiu, Y. Xu, J. Wu, J. Schlaak, M. Roggendorf, M.J. Lu
Journal: Journal of Hepatology (2008)
882. Non-Viral Ocular Gene Transfer for Hereditary Retinal Degeneration
Authors: Muna I. Naash, Ron M. Ballard, Jeff Skaggs, Zack Nash, Alexander B. Quiambao, Mark J. Cooper, Rafal Farjo
Journal: Molecular Therapy (2006)

The present study was undertaken to determine the efficacy of DNA nanotechnology as an effective therapeutic strategy for eye diseases; particularly those associated with loss-of-function mutations in the retina and retinal pigment epithelium (RPE). Since many hereditary blinding disorders have an onset from birth, we first evaluated a method of delivery to the newborn mouse eye. Subretinal injections of saline were delivered into one eye at post- natal day 2 (P2) and the contra-lateral eye was left uninjected to serve as a control. These mice were then left in normal cyclic light to develop into adults. At P21, retinal function was assessed with electroretinography (ERG) and ocular structure was examined with histology. Eyes injected at P2 demonstrated normal scotopic and photopic ERG waveforms and displayed a normal cellular organization and morphology, as compared to contra-lateral controls. As this route of delivery was safe, we then sought to determine whether this method could be used to deliver compacted DNA nanoparticles for gene transfer. The Rds+/− mouse has only one functional copy of the photoreceptor specific gene Rds, and presents with a progressive retinal degeneration which causes perturbation of retinal function and structure, eventually leading to death of photoreceptors. Rds+/− mice at P2 were injected with compacted nanoparticles of plasmid DNA carrying the wild-type Rds cDNA directed by the chicken b-actin promoter (Rds-particles), or the non-compacted naked plasmid (Rds-plasmid). Similar to experiments described above, one eye was injected, and the contra- lateral eye served as a non-injected control. At P30 and P45 these animals were subjected to ERG to assess photoreceptor viability. Eyes receiving Rds-nanoparticles showed an increased scotopic a- and b-wave, in addition to an increased photopic b-wave. However, eyes receiving naked Rds-plasmid failed to demonstrate an increase in ERG function at the timepoints examined. In contrast, Rds+/− mice that received a subretinal delivery of Rds-nanoparticles at P21 failed to show any rescue of photoreceptor function when assessed by ERG at 7, 14, and 21 days post-injection. These studies demonstrate the feasibility of newborn treatment strategies for retinal degenerative disorders and provide a rationale for future therapeutic interventions. Further studies are underway to determine the longevity of rescue in animals treated at P2 and whether nanoparticle treatment resulted in amelioration of the structural abnormalities associated with the Rds+/− retina.
Management of Candidemia
Authors: Francoise Meunier
Journal: New England Journal of Medicine (1994)

Finding the optimal treatment for patients with candidemia has been a major source of frustration for physicians during the past decade. It is a tremendous challenge, since the infection is often an obstacle to successful therapy, and the cost in terms of health resources is high. The rate of candidemia has increased by more than 400 percent since the early 1980s, and candidemia currently accounts for 10 to 15 percent of hospital-acquired infections of the bloodstream.1 There is an increased awareness of the morbidity, mortality, and economic burden associated with candidemia in various groups of patients, including those without neutropenia. . . .
Gene Expression in the Lung of <b> <i>p53</i> </b> Mutant Mice Exposed to Cigarette Smoke
Authors: Alberto Izzotti, Cristina Cartiglia, Mariagrazia Longobardi, Maria Bagnasco, Andrea Merello, Ming You, Ronald A. Lubet, Silvio De Flora
Journal: Cancer Research (2004)

Abstract We showed previously that p53 mutations play a role in cigarette smoke-related carcinogenesis not only in humans but also in A/J mice. In fact, (UL53–3 × A/J)F1 mice, carrying a dominant-negative germ-line p53 mutation, responded to exposure to environmental cigarette smoke more efficiently than their wild-type (wt) littermate controls in terms of molecular alterations, cytogenetic damage, and lung tumor yield. To clarify the mechanisms involved, we analyzed by cDNA array the expression of 1,185 cancer-related genes in the lung of the same mice. Neither environmental cigarette smoke nor the p53 status affected the expression of the p53 gene, but the p53 mutation strikingly increased the basal levels of p53 nuclear protein in the lung. Environmental cigarette smoke increased p53 protein levels in wt mice only. The p53 mutation enhanced the expression of positive cell cycle regulators in sham-exposed mice, which suggests a physiologic protective role of p53. In environmental cigarette smoke-exposed mice, the p53 mutation resulted in a lack of induction of proapoptotic genes and in overexpression of genes involved in cell proliferation, signal transduction, angiogenesis, inflammation, and immune response. Mutant mice and wt mice reacted to environmental cigarette smoke in a similar manner regarding genes involved in metabolism of xenobiotics, multidrug resistance, and protein repair. Irrespective of the p53 status, environmental cigarette smoke poorly affected the expression of oncogenes, tumor suppressor genes, and DNA repair genes. Taken together, these findings may explain the increased susceptibility of p53 mutant mice to smoke-related alterations of intermediate biomarkers and lung carcinogenesis.
CXCL13 plus interleukin 10 is highly specific for the diagnosis of CNS lymphoma
Authors: James L. Rubenstein, Valerie S. Wong, Cigall Kadoch, Hua-Xin Gao, Ramon Barajas, Lingjing Chen, S. Andrew Josephson, Brian Scott, Vanja Douglas, Mekhala Maiti, Lawrence D. Kaplan, Patrick A. Treseler, Soonmee Cha, Jimmy H. Hwang, Paola Cinque, Jason G. Cyster, Clifford Lowell
Journal: Blood (2013)