tbuckley/cabot-search huggingface dataset:
Vascular and Cardiac Impairments in Rats Inhaling Ozone and Diesel Exhaust Particles
Authors: Urmila P. Kodavanti, Ronald Thomas, Allen D. Ledbetter, Mette C. Schladweiler, Jonathan H. Shannahan, J. Grace Wallenborn, Amie K. Lund, Matthew J. Campen, Elizabeth O. Butler, Reddy R. Gottipolu, Abraham Nyska, Judy E. Richards, Deborah Andrews, Richard H. Jaskot, John McKee, Sainath R. Kotha, Rishi B. Patel, Narasimham L. Parinandi
Journal: Environmental Health Perspectives (2010)

Mechanisms of cardiovascular injuries from exposure to gas and particulate air pollutants are unknown.We sought to determine whether episodic exposure of rats to ozone or diesel exhaust particles (DEP) causes differential cardiovascular impairments that are exacerbated by ozone plus DEP.Male Wistar Kyoto rats (10-12 weeks of age) were exposed to air, ozone (0.4 ppm), DEP (2.1 mg/m(3)), or ozone (0.38 ppm) + DEP (2.2 mg/m(3)) for 5 hr/day, 1 day/week for 16 weeks, or to air, ozone (0.51 or 1.0 ppm), or DEP (1.9 mg/m(3)) for 5 hr/day for 2 days. At the end of each exposure period, we examined pulmonary and cardiovascular biomarkers of injury. In the 16-week study, we observed mild pulmonary pathology in the ozone, DEP, and ozone + DEP exposure groups, a slight decrease in circulating lymphocytes in the ozone and DEP groups, and decreased platelets in the DEP group. After 16 weeks of exposure, mRNA biomarkers of oxidative stress (hemeoxygenase-1), thrombosis (tissue factor, plasminogen activator inhibitor-1, tissue plasminogen activator, and von Willebrand factor), vasoconstriction (endothelin-1, endothelin receptors A and B, endothelial NO synthase) and proteolysis [matrix metalloprotease (MMP)-2, MMP-3, and tissue inhibitor of matrix metalloprotease-2] were increased by DEP and/or ozone in the aorta, but not in the heart. Aortic LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1) mRNA and protein increased after ozone exposure, and LOX-1 protein increased after exposure to ozone + DEP. RAGE (receptor for advanced glycation end products) mRNA increased in the ozone + DEP group. Exposure to ozone or DEP depleted cardiac mitochondrial phospholipid fatty acids (DEP > ozone). The combined effect of ozone and DEP exposure was less pronounced than exposure to either pollutant alone. Exposure to ozone or DEP for 2 days (acute) caused mild changes in the aorta.In animals exposed to ozone or DEP alone for 16 weeks, we observed elevated biomarkers of vascular impairments in the aorta, with the loss of phospholipid fatty acids in myocardial mitochondria. We conclude that there is a possible role of oxidized lipids and protein through LOX-1 and/or RAGE signaling.
Neurology in Pediatrics
Authors: Henry W. Baird
Journal: JAMA (1970)

This text will undoubtedly become widely used and respected by the busy house officers and practicing physicians. Bray has divided his presentation into two parts. The first is organized according to symptoms, signs, and laboratory abnormalities, the way in which the patient commonly presents himself. In part two the categories of disease are discussed in a more traditional fashion with chapters on congenital malformations, trauma, tumors, metabolic disease, etc. One of the most helpful chapters in part one gives clear succinct information on indications for laboratory tests and how to interpret them. The tables and outlines in the various chapters are well done and contribute significantly to the usefulness of the text. In several places Dr. Bray takes a dogmatic approach to diagnosis and treatment. However, ocularmotor apraxia has been reported in girls. Subacute sclerosing panencephalitis (leukoencephalitis in the text) is not always fatal. His view that daily anticonvulsant medication
AUTOPLASTIC OVARIAN TRANSPLANTATION
Authors: J. H. Nattrass
Journal: BMJ (1923)

A1JTOPLASTIC TRANSPT~~ANTATIONL MEDICAL.J0UNWAl I15 27 cases in thirteen years at the London Hospital.In a series of 9 cases at the Massachusetts General Hospital from 1893 to 1907 the mortality was 100 per cent.Richardson' records 16 cases (8 affecting the large intes- tine) operated on at the same hospital between 1908 and 1917, with a mortality of only 25 per cent.
Checklists can reduce errors in intraoperative emergencies by 75%, says expert
Authors: K. Chinthapalli
Journal: BMJ (2013)

The active vitamin D metabolites 1 alpha, 25-dihydroxycholecalciferol (Rocaltrol) and the analogue 1 alpha-hydroxycholecalciferol (One-Alpha) are adequately absorbed after oral administration in the preterm infant. The absorption pattern is similar to that seen in adults.
Bottlenose dolphins understand relationships between concepts
Authors: Louis M. Herman, Robert K. Uyeyama, Adam A. Pack
Journal: Behavioral and Brain Sciences (2008)

Abstract We dispute Penn et al.'s claim of the sharp functional discontinuity between humans and nonhumans with evidence in bottlenose dolphins (Tursiops truncatus) of higher-order generalizations: spontaneous integration of previously learned rules and concepts in response to novel stimuli. We propose that species-general explanations that are “bottom-up” in approach are more plausible than Penn et al.'s innatist approach of a genetically prespecified supermodule.
SAFETY AND EFFICACY OF TRANSRADIAL VERSUS TRANSFEMORAL CORONARY INTERVENTION IN ACUTE MYOCARDIAL INFARCTION: A META-ANALYSIS OF RANDOMIZED TRIALS
Authors: Param P. Singh, Updesh S. Bedi, Mukesh Singh, Sasikanth Adigopula, Vamsi Kodumuri, Amol Bahekar, Ankur Sethi, Janos Molnar, Rohit Arora, Sandeep Khosla
Journal: Journal of the American College of Cardiology (2010)
Nutritional survey data are inaccurate
Authors: J. T. Winkler
Journal: BMJ (2014)

Micha and colleagues’ paper is the latest of many articles attempting to investigate the diets of nations.1 Its extended description of data analysis techniques may bemuse many readers. Surely authors of such statistical sophistication know what they are talking about?

But this research suffers from the same fundamental flaw as all such studies—the poor quality of the primary data on individual food …
Exchange of IgM and albumin between plasma and synovial fluid in rheumatoid arthritis.
Authors: D L Brown, A G Cooper, R Bluestone
Journal: Annals of the Rheumatic Diseases (1969)

Most of the plasma proteins have been identified in normal synovial fluid (Schur and Sandson, 1963; Ropes and Bauer, 1953) but they are usually present in lower concentrations than those found in the plasma (Ropes and Bauer, 1953; Pekin and Zvaifler, 1964; Sundblad, Jonsson, and Nettelbladt, 1961).The higher molecular weight proteins, such as IgM macroglobulins, a2-macroglobulin, and fibrinogen, may not always be detectable.This synovial fluid protein pattern is altered in rheuma- toid arthritis so that relatively greater concentrations of the high molecular weight components are present and quantitatively the constituent proteins more closely resemble plasma (Wilkinson and Jones, 1964;
Soothing baby's skin
Authors: Amy Maxmen
Journal: The Journal of Experimental Medicine (2009)

Learning to tolerate ourselvesOn < a d d a r t t y p e = " r e l " d o i = " 1 0 . 1 0 8 4 / j e m . 2 0 0 8 0 6 1 1 " > page 139, Duty et al. find self-reactive B cells in healthy adults that might harm their own body if given the chance.Checkpoints during B cell development ensure that immune cells won't confuse the self for an intruder.At birth, many B cells express self-reactive receptors.Most of these potentially harmful cells are either set straight by rearranging new receptors or are eliminated before leaving the bone marrow.Yet a minority manages to escape, slipping into the periphery as mature B cells with a propensity for self-attack.In healthy mice, autoimmunity is avoided because most self-reactive escapees, which classically express high levels of IgD and reduced IgM, are arrested in an anergic state.But until now, a similar population of anergic, autoreactive B cells hadn't been found in humans.Duty et al. have now spotted these cells in the blood of healthy adults, where they accounted for 2.5% of peripheral B cells.These cells turned out to be mature and autoreactive, bearing no signs of antigen encounter in vivo.The cells were also anergic, as they had faulty signaling in response to BCR ligation.These defects were overcome, however, when the authors gave cells a strong enough signal.Autoreactive B cells are common in patients with autoimmune diseases, such as lupus or rheumatoid arthritis (RA).And the authors suspect that the new population may contain the precursors of these troublemaking cells.Lapses in early steps of self-tolerance have been shown to contribute to disease in patients with lupus or RA.Alternatively, suggests author Patrick Wilson, anergy may fail in these patients, allowing self-sabotaging cells to run free.Why the body silences these potentially mutinous cells after they escape rather than putting them to death is unclear.Perhaps, suggests Wilson, a limited amount of autoimmunity isn't such a bad thing, as long as it's not chronic.For example, anergic cells might help attack pathogens disguised as self-antigens.
Ghrelin-Producing Well-Differentiated Neuroendocrine Tumor (Carcinoid) of Tailgut Cyst. Morphological, Immunohistochemical, Ultrastructural, and RT-PCR Study of a Case and Review of the Literature
Authors: Stefano La Rosa, Luigi Boni, Giovanna Finzi, Davide Vigetti, Nikolaos Papanikolaou, Silvia Maria Tenconi, Gianlorenzo Dionigi, Moira Clerici, Silvana Garancini, Carlo Capella
Journal: Endocrine Pathology (2010)
Anesthesia and Uncommon Diseases
Authors: Alexander W. Gotta
Journal: JAMA (1990)

In the preface to this book is the bold statement, "The third edition represents the best compilation of basic science and clinical data available. Many chapters will become recognized as the definitive treatise for the subject matter presented.... We believe that the resulting text is a meaningful and exciting addition to the literature." In fact, the book struggles mightily, striking out several times, before getting a scratch hit here and there and a few notable home runs. Practicing anesthesiologists, desperately in need of a concise presentation of anticipated problems and projected solutions for unexpected clinical situations on the surgical list, will find some chapters suiting their needs. The section on infectious diseases is particularly well done, although the treatment of the acquired immunodeficiency syndrome suffers from data that can never be current in a rapidly evolving epidemic. The author is particularly adept at tying together implications of the pathophysiology of
AN EXPERIMENTAL STUDY OF DIATHERMY
Authors: Carl A. L. Binger, Ronald V. Christie
Journal: The Journal of Experimental Medicine (1927)

1. A method of measuring intravascular temperatures in anesthetized dogs has been described. 2. The temperature in the abdominal aorta is uniform throughout, and varies only with the systemic temperature. 3. The temperature in the inferior vena cava rises as the thermo-couple approaches the heart, reaching its maximum at about the level of the hepatic veins. Between the hepatic veins and the right chambers of the heart there is no further elevation in venous temperature. 4. The temperature of the right heart blood normally exceeds that of the left heart blood by 0.05-0.2 degrees C. 5. During the application of high frequency currents to the thorax, this relationship is reversed. 6. This indicates that the lungs are being heated but that the blood passing through the pulmonary vessels is removing the heat at approximately the rate of production.
Differential Diagnosis between Endogenous and Exogenous Insulin-Induced Refractory Hypoglycemia in a Nondiabetic Patient
Authors: William A. Bauman, Rosalyn S. Yalow
Journal: New England Journal of Medicine (1980)

THIS report describes a nondiabetic patient who had rectal adenocarcinoma and who suffered an episode of acute hypoglycemia while receiving intravenous fluids containing glucose. Workup of the case required determination of whether the hypoglycemia was associated with the malignant disease or with hyperinsulinism. If hyperinsulinism had been the causative factor, it could have been a consequence of augmented endogenous insulin secretion or accidental injection of insulin. Laboratory studies distinguished directly and definitively among these possibilities. We concluded that NPH insulin had been inadvertently injected.Case ReportThe patient was a 67-year-old man with adenocarcinoma of the rectum. After radiotherapy, he . . .
Acute epithelial injury in the rat small intestine in vivo is associated with expanded expression of transforming growth factor alpha and beta.
Authors: A U Dignass, J L Stow, M W Babyatsky
Journal: Gut (1996)

BACKGROUND--Previous studies have shown the importance of transforming growth factors alpha and beta (TGF alpha and TGF beta) in modulating epithelial cell restitution after injury in vitro. AIM--To investigate the role of the growth factors TGF alpha and TGF beta after acute epithelial injury in vivo. METHODS--An in vivo model of phytohaemagglutinin (PHA) induced acute epithelial injury in rat small intestine was used. Epithelial cell turnover was assessed by autoradiography and liquid scintillation counting of thymidine uptake. Expression of TGF alpha and TGF beta was assessed by immunohistochemistry. RESULTS--An expansion of the proliferative compartment and increased turnover of intestinal epithelial cells was seen in rats with PHA induced intestinal epithelial injury. Expression of TGF alpha and TGF beta peptides was shown in both the epithelial cell and lamina propria compartment. Different patterns of TGF alpha and TGF beta expression were seen, however, within the epithelium of rats with acute intestinal injury compared with untreated controls, while the expression of these peptides within the lamina propria was not changed. CONCLUSIONS--These findings suggest that acute intestinal epithelial cell injury in vivo is associated with compensatory changes in expression of TGF alpha and TGF beta in the epithelial cell compartment, while the lamina propria does not seem to be significantly affected.
A Genetic Defect in the Binding of Protein 4.1 to Spectrin in a Kindred with Hereditary Spherocytosis
Authors: Lawrence C. Wolfe, Kathryn M. John, John C. Falcone, Ann M. Byrne, Samuel E. Lux
Journal: New England Journal of Medicine (1982)

Indirect evidence suggests that the genetic defect in hereditary spherocytosis lies in the erythrocyte membrane skeleton, a submembranous meshwork of proteins (principally spectrin, actin, and protein 4.1) responsible for membrane shape and structural stability. To test this premise we systematically assayed the interactions of spectrin, the major skeletal protein, in six kindreds with autosomal dominant hereditary spherocytosis. In one of these kindreds, enhancement of spectrin-actin binding by protein 4.1 was reduced, owing to a 39±4 per cent decrease (mean ±S.D.) in the binding of normal protein 4.1 by spectrin, in all of four members with the disorder. The defective spectrin was separated into two populations by affinity chromatography on immobilized normal protein 4.1. One population (41±2 per cent) lacked the ability to bind 4.1, but the other functioned normally. Presumably, the nonfunctional spectrin was the product of the autosomal dominant gene responsible for the hereditary spherocytosis in this kindred. (N Engl J Med. 1982; 307:1367–74.)
TIP30 Mutant Derived from Hepatocellular Carcinoma Specimens Promotes Growth of HepG2 Cells through Up-Regulation of N-cadherin
Authors: Chao Jiang, Jill Pecha, Isamu Hoshino, David Ankrapp, Hua Xiao
Journal: Cancer Research (2007)

Abstract TIP30 is a tumor suppressor whose expression is altered in human liver, prostate, lung, colon, and breast cancers. Mice lacking TIP30 spontaneously developed hepatocellular carcinomas (HCC) and other tumors at a higher incidence than wild-type mice. Somatic missense mutations in the TIP30 gene were identified in human HCC tissue specimens, which resulted in instability or abnormal cellular distribution of TIP30 protein in cells. Here, we show that TIP30 mutants are able to promote cell growth and invasion and inhibit cisplatin-induced apoptosis in the HCC cell line HepG2 negative for endogenous TIP30. Moreover, one of the TIP30 mutants can dramatically accelerate tumor formation in immunodeficient mice. Analysis of gene expression in HepG2 cells, ectopically expressing either wild-type TIP30 or mutant TIP30, by Affymetrix GeneChip array, real-time quantitative PCR, and Western blotting assays reveals that TIP30 mutants can alter expression of genes involved in the regulation of tumorigenesis. This includes up-regulation of expression of N-cadherin and c-MYC and down-regulation of expression of p53 and E-cadherin. N-cadherin knockdown with small interfering RNA in HepG2 cells expressing mutant TIP30 resulted in a profound reduction in cell viability. Taken together, our data indicate that somatic mutations in the TIP30 gene may abolish its native tumor-suppressor activity and gain oncogenic activities partially through up-regulation of N-cadherin, thereby potentiating the pathogenesis of HCC in patients. [Cancer Res 2007;67(8):1–9]
Homeostasis Model Assessment of Insulin Resistance in Relation to the Incidence of Cardiovascular Disease
Authors: Anthony J.G. Hanley, Ken Williams, Michael P. Stern, Steven M. Haffner
Journal: Diabetes Care (2002)

The prospective association between insulin levels and risk of cardiovascular disease (CVD) is controversial. The objective of the present study was to investigate the relationship of the homeostasis model assessment of insulin resistance (HOMA-IR), as well as insulin levels, with risk of nonfatal and fatal CVD over the 8-year follow-up of the San Antonio Heart Study.Between 1984 and 1988, randomly selected Mexican-American and non-Hispanic white residents of San Antonio participated in baseline examinations that included fasting blood samples for glucose, insulin, and lipids, a glucose tolerance test, anthropometric measurements, and a lifestyle questionnaire. Between 1991 and 1996, 2,569 subjects who were free of diabetes at baseline were reexamined using the same protocol.Over the follow-up period, 187 subjects experienced an incident cardiovascular event (heart attack, stroke, heart surgery, angina, or CVD death). Logistic regression analysis indicated that risk of a CVD event increased across quintiles of HOMA-IR after adjustment for age, sex, and ethnicity (P for trend <0.0001; quintile 5 vs. quintile 1, odds ratio [OR] 2.52, 95% CI 1.46-4.36). Additional adjustment for LDL, triglyceride, HDL, systolic blood pressure, smoking, alcohol consumption, exercise, and waist circumference only modestly reduced the magnitude of these associations (P for trend 0.02; quintile 5 vs. quintile 1, OR 1.94, 95% CI 1.05-3.59). Furthermore, there were no significant interactions between HOMA-IR and ethnicity, sex, hypertension, dyslipidemia, glucose tolerance (impaired glucose tolerance versus normal glucose tolerance), or obesity. The magnitude and direction of the relationship between insulin concentration and incident CVD were similar.We found a significant association between HOMA-IR and risk of CVD after adjustment for multiple covariates. The topic remains controversial, however, and additional studies are required, particularly among women and minority populations.
Cimetidine in Intensive Care Units
Authors: DANIEL P. SCHUSTER
Journal: Annals of Internal Medicine (1985)

Letters and Corrections1 December 1985Cimetidine in Intensive Care UnitsDANIEL P. SCHUSTER, M.D., GARY R. ZUCKERMAN, D.O.DANIEL P. SCHUSTER, M.D.Search for more papers by this author, GARY R. ZUCKERMAN, D.O.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-103-6-959_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The findings recently reported by Puera and Johnson (1) may superficially appear to contradict data previously presented by us (2). Significant differences in the patient population under scrutiny are an important factor in this regard. We believe these differences should be emphasized to interpret properly the conclusions of each study.In our study, a complete accounting of all patients admitted to the intensive care unit was reported. The risk of "bleeding" (defined as guaiac positivity in nasogastric aspirate or stool specimens) was 14% in the group as a whole, but 48% in patients admitted for more than...References1. PUERA D and JOHNSON L. Cimetidine for prevention and treatment of gastroduodenal mucosal lesions in patients in an intensive care unit. Ann Intern Med. 1985;103:173-7. LinkGoogle Scholar2. SCHUSTER D, ROWLEY H, FEINSTEIN S, MCGUE M, and ZUCKERMAN G. Prospective evaluation of the risk of upper gastrointestinal bleeding after admission to a medical intensive care unit. Am J Med. 1984;76:623-30. CrossrefMedlineGoogle Scholar3. PINILLA J, OLENIUK F, REED D, MALIK B, and LAVERY W. Does antacid prophylaxis prevent upper gastrointestinal bleeding in critically ill patients? Crit Care Med. 1985;13:646-50. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: DANIEL P. SCHUSTER, M.D.; GARY R. ZUCKERMAN, D.O.Affiliations: Washington University School of Medicine St. Louis, MO 63110 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 December 1985Volume 103, Issue 6_Part_1Page: 959-960KeywordsHemorrhageIntensive care units ePublished: 1 December 2008 Issue Published: 1 December 1985 PDF downloadLoading ...
Mitral and aortic regurgitation in Behcet's syndrome.
Authors: J M Pena, J Garcia-Alegria, F Garcia-Fernandez, F Arnalich, F J Barbado, J J Vazquez
Journal: Annals of the Rheumatic Diseases (1985)

A 35-year-old man with definite Behçet9s disease developed acute mitral and aortic regurgitation. Valvular disease, we believed, was another manifestation of this disease. Cardiac involvement in Behçet9s disease and the role of prednisone therapy are discussed.
Assets for the meritocracy
Authors: T. Greenhalgh
Journal: BMJ (1999)

In Monty Python's transplant sketch, a man is sitting nonchalantly minding his own business when there is a loud knock at the door. Enter an officious, clipboard-carrying administrator, closely followed by several white coated technicians who are vigorously sharpening their scalpels.

“Mr B?”

“Yes, that's me.”

“We're from the Transplant Agency. You signed a donor card, I believe.”

“I did.”

“Well, we've come for your liver.”

“But I'm not dead yet.”

“It doesn't say anything …
Self-Administration of Tripelennamine by a Narcotic Addict
Authors: William G. O'Driscoll, Gene R. Lindley
Journal: New England Journal of Medicine (1957)

THE case reported below concerns the intravenous use of tripelennamine (Pyribenzamine) by a patient in a manner similar to that employed by morphine addicts. We have studied the literature and have found no reference to previous reports of this nature. Kells1 presented 3 cases of morphine addiction treated with tripelennamine by mouth during the withdrawal stage, the suggested mechanism of action being the neutralization of an antimorphine substance in the blood of addicts. These patients, however, were given the antihistaminic as a prescribed part of their treatment; in this and other important respects they differed from the case under discussion. . . .