tbuckley/cabot-search huggingface dataset:
Respiratory mechanics I
Authors: J. Mancebo, I. Vallverdú, E. Bak, G. Domínguez, M. Subirana, S. Benito, A. Net, V. M. Ranieri, R. Giuliani, F. Bruno, J. Milic-Emili, S. Nava, F. Rubini, E. Zanotti, C. Fracchia, C. Rampulla, M. Leon, J. Räsänen, D. Gommers, K. L. So, C. Vilstrup, B. Lachmann, M. Olivei, G. Iotti, J. X. Brunner, A. Palo, S. Mencherini, C. Galbusera, Pallavicini F. Bobbio, A. Braschi
Journal: Intensive Care Medicine (1992)
THE PREVENTION OF COMPLICATIONS IN THYROID SURGERY
Authors: ARNOLD S. JACKSON
Journal: JAMA (1933)

The prevention of complications, both immediate and remote, following thyroidectomy is a subject of extreme importance to those interested in thyroid surgery. The statistical study of operative records reveals the number of patients who were successfully operated on, but it tells nothing of the patients whose lives perhaps hung in the balance for hours or days. An error in judgment either at the operating table or later may be responsible for the development of complications that greatly alter mortality statistics. Although such a mistake may not result in the death of the patient, it may change his whole future health and welfare. In perhaps no field of surgery are complications more prone to develop than following operations on the thyroid. This is so true that there are few surgeons who have not experienced most of the unfortunate sequelae at some time during their careers. It has been my misfortune to
1163-116 Neurohormones but not adrenomedullin correlate with left ventricular structure in patients with heart failure: Results from an EARTH substudy
Authors: Jens P Hellermann, Tatsuo Shimosawa, Frank Ruschitzka, Kurt Quitzau, Inder Anand, Thomas F Luescher
Journal: Journal of the American College of Cardiology (2004)
Anomalies of the Gastrointestinal Tract
Authors: R. Bretney Miller, Aubrey O. Hampton
Journal: New England Journal of Medicine (1950)

MAJOR congenital anomalies of the alimentary tract that produce symptoms are seen almost entirely in infancy and childhood. They are seldom reported in adults. Some of these, such as atresia of the esophagus or other portions of the digestive tract, are inconsistent with continued life. Attempts to remedy these situations pose difficult if not impossible surgical problems. Other anomalies, such as imperforate anus, duplications of portions of the gastrointestinal tract, "congenital bands" and errors of rotation with volvulus, are amenable to successful surgical correction. Still other anomalies are compatible with normal growth and development, do not produce symptoms and may . . .
Persistent Pain: Modern Methods of Treatment
Authors: Oscar Sugar
Journal: JAMA (1978)

This is the first in a series of five or six consecutive volumes (to appear at intervals) intended to cover the subject of pain. No attempt was made to standardize the 11 presentations. Overlap is apparent, especially in chapters on drug therapy by Williams and on psychiatric therapy by Mersky. The latter is particularly lucid and worthwhile in contrast to the unsatisfying chapter on acupuncture by Mann. I would mention the informative and useful chapter by Mumford that clarifies some of the mysteries of dental and oral pain, ignored by most physicians except when they themselves are the sufferers. Maher and Mehta give detailed instructions on the use of alcohol and phenol as neurolytic agents in producing spinal and extradural analgesia. Peripheral nerve (and sympathetic) blocking is well illustrated by Swerdlow. Treatment of pain by percutaneous cordotomy is expounded by the two American authors, Ganz and Mullan. Although the chapters
Distribution of choline acetyltransferase in cerebral and extracerebral cranial arteries of the cat. Its relationship to neurogenic atropine-sensitive dilation.
Authors: J A Bevan, G M Buga, V M Florence, A Gonsalves, A Snowden
Journal: Circulation Research (1982)

Choline-acetyltransferase (ChAT) activity was surveyed in segments of cranial arteries--both cerebral and extracerebral--from the cat. High levels were found in pial arteries, both cerebral and cerebellar, and in the arteries to salivary glands, tongue, and nose. Intermediate levels were found in the external and internal maxillary arteries and many of their branches. Enzyme levels in the arteries supplying the head--common carotid, vertebral, and in several systemic arteries and veins and also the lingual vein--were probably not significant. Only those vessels that have higher ChAT contents show capacity for neurogenic vasodilation. The dilation of segments of a number of these arteries, the basilar, middle cerebral, lingual, and internal maxillary, is reduced significantly by atropine (5 X 10(-7) M). ChAT activity did not correlate with vessel norepinephrine content. The data may be interpreted as defining a functional vasodilator system to the head encompassing both cerebral and extracerebral arteries that depends in part on a functional cholinergic link involving a muscarinic receptor. It is separate from the adrenergic outflow. The tissues supplied by vasculature receiving this type of innervation are of ectodermal origin.
UV-Targeted Dinucleotides Are Not Depleted in Light-Exposed Prokaryotic Genomes
Authors: L. Palmeira
Journal: Molecular Biology and Evolution (2006)

We have investigated the hypothesis that pyrimidine dinucleotides are avoided in light-exposed genomes as the result of selective pressure due to high ultraviolet (UV) exposure. The main damage to DNA produced by UV radiation is known to be the formation of pyrimidine photoproducts: it is estimated that about 10 dimers per minute are formed in an Escherichia coli chromosome exposed to the UV light in direct overhead sunlight at sea level. It is also known that on an E. coli chromosome exposed to UVb wavelengths (290–320 nm), pyrimidine photoproducts are formed in the following proportions: 59% TpT, 7% CpC, and 34% CpT plus TpC. We have analyzed all available complete prokaryotic genomes and the model organism Prochlorococcus marinus and have found that pyrimidine dinucleotides are not systematically avoided. This suggests that prokaryotes must have sufficiently effective protection and repair systems for UV exposure to not affect their dinucleotide composition.
Hammerhead ribozyme-mediated destruction of nuclear foci in myotonic dystrophy myoblasts
Authors: Marc-André Langlois, Nan Sook Lee, John J Rossi, Jack Puymirat
Journal: Molecular Therapy (2003)

Myotonic dystrophy type 1 (DM1) is caused by an unstable CTG expansion in the 3′ untranslated region (3′UTR) of the myotonic dystrophy protein kinase gene (DMPK). Transcripts from this altered gene harbor large CUG expansions that are retained in the nucleus of DM1 cells and form foci. It is believed that the formation of these foci is closely linked to DM1 muscle pathogenesis. Here we investigated the possibility of using a nuclear-retained hammerhead ribozyme expressed from a modified tRNAmeti promoter to target and cleave mutant transcripts of DMPK. Accessible ribozyme target sites were identified in the 3′UTR of the DMPK mRNA and a hammerhead ribozyme was designed to cut the most accessible site. Utilizing this system, we have achieved 50 and 63% reductions, respectively, of the normal and CUG expanded repeat-containing transcripts. We also observed a significant reduction in the number of DMPK mRNA-containing nuclear foci in human DM1 myoblasts. Reduction of mutant DMPK mRNA and nuclear foci also corroborates with partial restoration of insulin receptor isoform B expression in DM1 myoblasts. These studies demonstrate for the first time intracellular ribozyme-mediated cleavage of nuclear-retained mutant DMPK mRNAs, providing a potential gene therapy agent for the treatment of myotonic dystrophy.
CHIR-124, a Novel Potent Inhibitor of Chk1, Potentiates the Cytotoxicity of Topoisomerase I Poisons <i>In vitro</i> and <i>In vivo</i>
Authors: Archie N. Tse, Katherine G. Rendahl, Tahir Sheikh, Haider Cheema, Kim Aardalen, Millicent Embry, Sylvia Ma, Edward J. Moler, Zhi Jie Ni, Daniel E. Lopes de Menezes, Barbara Hibner, Thomas G. Gesner, Gary K. Schwartz
Journal: Clinical Cancer Research (2007)

Abstract Purpose: Chk1 kinase is a critical regulator of both S and G2-M phase cell cycle checkpoints in response to DNA damage. This study aimed to evaluate the biochemical, cellular, and antitumor effects of a novel Chk1 inhibitor, CHIR124. Experimental Design: CHIR-124 was evaluated for its ability to abrogate cell cycle checkpoints, to potentiate cytotoxicity, and to inhibit Chk1-mediated signaling induced by topoisomerase I poisons in human tumor cell line and xenograft models. Results: CHIR-124 is a quinolone-based small molecule that is structurally unrelated to other known inhibitors of Chk1. It potently and selectively inhibits Chk1 in vitro (IC50 = 0.0003 μmol/L). CHIR-124 interacts synergistically with topoisomerase poisons (e.g., camptothecin or SN-38) in causing growth inhibition in several p53-mutant solid tumor cell lines as determined by isobologram or response surface analysis. CHIR-124 abrogates the SN-38–induced S and G2-M checkpoints and potentiates apoptosis in MDA-MD-435 breast cancer cells. The abrogation of the G2-M checkpoint and induction of apoptosis by CHIR-124 are enhanced by the loss of p53. We have also shown that CHIR-124 treatment can restore the level of cdc25A protein, which is normally targeted by Chk1 for degradation following DNA damage, indicating that Chk1 signaling is suppressed in the presence of CHIR-124. Finally, in an orthotopic breast cancer xenograft model, CHIR-124 potentiates the growth inhibitory effects of irinotecan by abrogating the G2-M checkpoint and increasing tumor apoptosis. Conclusions: CHIR-124 is a novel and potent Chk1 inhibitor with promising antitumor activities when used in combination with topoisomerase I poisons.
Genomic scanning for expressed sequences in Xp21 identifies the glycerol kinase gene
Authors: Weiwen Guo, Kim Worley, Volker Adams, Jestina Mason, Desirée Sylvester-Jackson, Yao-Hua Zhang, Jeffrey A. Towbin, Donna D. Fogt, Stella Madu, David A. Wheeler, Edward R.B. McCabe
Journal: Nature Genetics (1993)
Exfoliative dermatitis due to nifedipine
Authors: N.J. REYNOLDS, S.K. JONES, J. CROSSLEY, R.R.M. HARMAN
Journal: British Journal of Dermatology (1989)

We report the case of a 63-year-old Caucasian female, with reno-vascular hypertension, who developed a generalized skin eruption with lichenoid histological features, induced by nifedipine. A repeat challenge with nifedipine confirmed that it was the causative agent.
Survival of mechanically ventilated patients admitted to a specialised weaning centre
Authors: B. Schönhofer, S. Euteneuer, S. Nava, S. Suchi, D. Köhler
Journal: Intensive Care Medicine (2002)

Hospital mortality and survival rates of long-term ventilated patients.DESIGN. Retrospective cohort study.Specialised national weaning centre.Protocol-directed liberation from ventilator.Four hundred three of 640 patients with prolonged mechanical ventilation (MV) who were admitted to our respiratory intensive care unit (RICU) were studied. MV lasted longer than 2 weeks and patients had failed more than two weaning trials in the referring ICUs. The majority of patients (59.3%) had chronic obstructive pulmonary disease (COPD).After a mean duration of 41 days of MV prior to transfer, 68% of patients were liberated from the ventilator. In total, 98 of 403 patients (24.3%) died during the stay in our hospital, 305 patients (75.7%) were discharged. Compared to the non-survivors, the survivors were characterised by younger age, longer length of stay in our RICU, lower severity of illness scores at admission, fewer cardiac illnesses and a higher rate of weaning success. In 31.5% of the discharged patients non-invasive MV (NIV) was initiated during the stay at our unit. We gathered follow-up data on 293 patients (96.1%). Post-discharge survival rates were 67.6% at 3 months, 49.4% at 1 year and 38.1% at 3 years. Length of survival was significantly dependent on age, weaning success and main diagnosis (i.e., prognosis in COPD is worse compared to thoracic restriction, neuromuscular disease and others) in the multivariate analysis.Difficult-to-wean patients have a high hospital mortality rate and poor long-term prognosis. Age, main diagnosis, severity of illness, weaning success and institution of NIV predict survival.
Three–Dimensional Reconstruction of Parenchymal Units in the Liver of the Rat
Authors: Harald F. Teutsch, Dirk Schuerfeld, Elke Groezinger
Journal: Hepatology (1999)

To investigate the parenchymal units in the liver of the rat three-dimensionally, 15 micrometer cryosections were used for the demonstration of glucose-6-phosphatase (G6Pase) activity to visualize the borders of the individual units. Together with the supplying and draining vessels, they were traced through a sequence of 146 sections and reconstructed. A cone-shaped secondary unit with a height of 2.1 mm and a volume of 3.3 mm3 was reconstructed. It was "covered" by a continuous vascular surface, consisting of portal tracts and vascular septa, connecting the portal venular branches. The secondary unit was subdivided by portal tracts and vascular septa, and by branches of a draining central venular tree into 14 primary units. Most of them were tri- to heptahedral in shape. The height varied between 330 and 840 micrometer, and the volume varied between 0.094 and 0.621 mm3. The branches of the portal venular tree, with diameters from 28 +/- 5 micrometer to 61 +/- 14 micrometer, were oriented preferentially along the vertical axis of the units. Most of the primary units were drained by single branches of the central venular tree, located in the center and oriented along the vertical axis of the units. Vessel diameters ranged from 62 +/- 14 micrometer to 216 +/- 9 micrometer. The average length of the sinusoids was 355 +/- 3 micrometer. From the results of this reconstruction study, it was concluded that the concept of the liver acinus cannot be applied to the liver of the rat.
Immunopharmacology of the Heart (The Handbook of Immunopharmacology)
Authors: F Williams
Journal: Cardiovascular Research (1994)

Journal Article Immunopharmacology of the Heart (The Handbook of Immunopharmacology) Get access F Williams F Williams London UK Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 28, Issue 9, September 1994, Page 1450, https://doi.org/10.1093/cvr/28.9.1450 Published: 01 September 1994
Global Burden of Aflatoxin-Induced Hepatocellular Carcinoma: A Risk Assessment
Authors: Yan Liu, Felicia Wu
Journal: Environmental Health Perspectives (2010)

BackgroundHepatocellular carcinoma (HCC), or liver cancer, is the third leading cause of cancer deaths worldwide, with prevalence 16–32 times higher in developing countries than in developed countries. Aflatoxin, a contaminant produced by the fungi Aspergillus flavus and Aspergillus parasiticus in maize and nuts, is a known human liver carcinogen.ObjectivesWe sought to determine the global burden of HCC attributable to aflatoxin exposure.MethodsWe conducted a quantitative cancer risk assessment, for which we collected global data on food-borne aflatoxin levels, consumption of aflatoxin-contaminated foods, and hepatitis B virus (HBV) prevalence. We calculated the cancer potency of aflatoxin for HBV-postive and HBV-negative individuals, as well as the uncertainty in all variables, to estimate the global burden of aflatoxin-related HCC.ResultsOf the 550,000–600,000 new HCC cases worldwide each year, about 25,200–155,000 may be attributable to aflatoxin exposure. Most cases occur in sub-Saharan Africa, Southeast Asia, and China where populations suffer from both high HBV prevalence and largely uncontrolled aflatoxin exposure in food.ConclusionsAflatoxin may play a causative role in 4.6–28.2% of all global HCC cases.
FURTHER OBSERVATIONS ON AN EXPERIMENTALLY PRODUCED SARCOMA OF THE CHICKEN
Authors: Ernest Sturm, James B. Murphy
Journal: The Journal of Experimental Medicine (1928)

Numerous attempts have been made by us to separate from the cells of a tar sarcoma of the chicken (Chicken Tumor 9) a causative agent for the growth. Experiments with filtrates and desiccates injected as such or in combinations with embryonic tissues have all failed to give positive results. So too have injections of filtrates and desiccates into developing chick embryos failed to yield a response. The results confirm those of previous work with the tumor in this laboratory. The growth would appear to differ in a fundamental respect from all tumors of the fowl previously studied.
Abstract B73: Unraveling the role of a novel endoplasmic reticulum protein in cancer cell migration
Authors: Nikki Ann Evensen, Cem Kuscu, Antoine Dufour, Stanley Zucker, Jian Cao
Journal: Cancer Research (2013)

Abstract Although considerable progress has been made in our understanding of cancer cell invasion, much of this complex cellular process remains a mystery, ultimately hindering advancements in treatment strategies targeting metastasis. Here we report, for the first time, the vital role of a novel endoplasmic reticulum (ER) resident protein identified by a PCR-subtraction hybridization technique, designated Cancer ER Invasion Gene (CERIG), in cancer cell migration and invasion. Clinical relevance of CERIG is highlighted by upregulation of CERIG in human invasive breast cancer specimens examined by immunohistochemistry and real-time RT-PCR, as well as increased expression in various other forms of human cancer as determined by data mining. This up-regulation of CERIG correlates with poor prognosis of patients with breast cancer assessed by a DNA microarray data-mining approach from three publicly available cohorts containing a total of 696 breast cancer patients. Silencing of CERIG in metastatic MDA-MB-435 cancer cells disrupted mesenchymal morphogenesis in vitro, resulting in a mesenchymal-to-epithelial transition, and interfered with cancer metastasis in vivo. Employing both gain- and loss-of-function approaches, CERIG was found to induce cancer cell migration and invasion. Enhanced cell migration required retention of CERIG within the ER, where this protein forms a stable complex with the ER chaperone protein, GRP78/BiP. Mutagenesis studies identified a novel ER retention motif within CERIG required for its ER localization, BiP interaction, and enhanced migration. Furthermore, fusion of the ER-retention domain to a soluble matrix metalloproteinase (MMP) prevents the secretion of the MMP by retaining it in the ER. Mechanistically, overexpression of CERIG results in ER calcium leakage via the inositol trisphosphate receptor (IP3R) and a subsequent increase in cytosolic calcium, ultimately resulting in activation of PKCα and cell migration. Moreover, chelating intracellular calcium abrogates CERIG induced PKCα activation and cell migration. Taken together, our data indicate that CERIG, as a novel ER resident protein, plays an important role in cancer progression, serving as a novel cell migration-promoting gene. Citation Format: Nikki Ann Evensen, Cem Kuscu, Antoine Dufour, Stanley Zucker, Jian Cao. Unraveling the role of a novel endoplasmic reticulum protein in cancer cell migration. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr B73.
Role of Sympathectomy for Hyperhidrosis
Authors: P. Fitzgerald
Journal: BMJ (1971)

Recombinant human A<sub>2B</sub> adenosine receptors (A<sub>2B</sub>ARs) and receptors extended on the amino terminus with hexahistidine and the FLAG epitope, DYKDDDDK (H/F-A<sub>2B</sub>) were stably overexpressed (to &gt;20,000 fmol/mg protein) in human embryonic kidney 293 cells (HEK-A<sub>2B</sub>). By Western blotting, the H/F-A<sub>2B</sub>receptor runs as a 34.8-kDa glycoprotein. Pharmacological properties of A<sub>2B</sub>ARs were characterized with<sup>125</sup>I-3-aminobenzyl-8-phenyl-(4-oxyacetic acid)-1-propylxanthine (<i>K</i><sub>D</sub>, 36 nM). In competition binding assays, the affinity of agonists is reduced by substitution on either the <i>N</i><sup>6</sup>- or the C-2 position of the adenine ring, whereas 5′-substitutions increase affinity, resulting in the potency order: 5′-<i>N</i>-ethylcarboxamidoadenosine (NECA) ≫<i>N</i><sup>6</sup>-aminobenzyl-NECA ≈2-chloroadenosine &gt; 2-[4-(2-carboxyethyl)phenethylamino]-NECA (CGS21680) &gt;<i>N</i><sup>6</sup>-aminobenzyladenosine. The A<sub>2B</sub>AR is potently blocked by the A<sub>2A</sub>-selective antagonist 4-(2-[7-amino-2-[2-furyl][1,2,4]triazolo-[2,3-<i>a</i>][1,3,5] triazin-5-yl-amino]ethyl)phenol (ZM241385; <i>K</i><sub>I</sub>, 32 nM for A<sub>2B</sub>, 1.4 nM for A<sub>2A</sub>) and the A<sub>1</sub> selective antagonist 8-cyclopentyl-1,3-dipropylxanthine (<i>K</i><sub>I</sub>, 50.5 nM for A<sub>2B</sub>; 2.5 nM for A<sub>1</sub>). The<i>K</i><sub>I</sub> values for the antiasthmatic xanthines, theophylline (7.8 μM) and enprofylline (6.4 μM), are below their therapeutic plasma concentrations (20 to 50 μM), and agree with<i>K</i><sub>I</sub> determinations for inhibition of NECA-stimulated cAMP accumulation in HEK-A<sub>2B</sub> cells. NECA or<i>N</i><sup>6</sup>-(2-iodo)benzyl-5′-<i>N</i>-methylcarboxamidodoadenosine (IB-MECA) stimulate inositol trisphosphates and calcium accumulation in HEK-A<sub>2B</sub> or HEK-A<sub>3</sub> cells, respectively, but only the A<sub>3</sub> response is prevented by pertussis toxin. In human HMC-1 mast cells, A<sub>2B</sub>AR activation stimulates calcium mobilization and cAMP accumulation. We conclude that HEK-A<sub>2B</sub> cells and HMC-1 mast cells possess A<sub>2B</sub>AR glycoproteins that are coupled to both G<sub>q/11</sub> and G<sub>s</sub>.
DETECTION OF ESCHERICHIA COLI PRODUCING HEAT-LABILE TOXIN: COMPARISION BETWEEN Y1 ADRENAL CELL ASSAY, GANGLIOSIDE-ELISA, AND BIKEN TESTS
Authors: P. De Mol, W. Hemelhof, E. Papa-Kango, J.P. Butzler, N. Bravo, T. Honda
Journal: The Lancet (1982)
Gene Therapy to Restore Hearing
Authors: Tracy Hampton
Journal: JAMA (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Congressmen demand faster publication of trial data after BMJ revealed long delays
Authors: B. Roehr
Journal: BMJ (2012)

Three members of the US House of Representatives have written to the National Institutes of Health and the Food and Drug Administration expressing concern that the results of clinical studies are not being published in a timely manner, as prescribed by law, after widespread delays to publication were highlighted in the BMJ .

“Researchers and pharmaceutical companies routinely fail to publish data from clinical drug trials in a timely fashion,” they wrote, citing a BMJ research paper that appeared earlier this year ( BMJ 2012;344:d7373, doi:10.1136/bmj.d7373). “This study raises concerns about whether the FDA is adequately enforcing the law requiring …