tbuckley/cabot-search huggingface dataset:
Platelet Glycoprotein IIb/IIIa Receptor Blockade Improves Vascular Nitric Oxide Bioavailability in Patients With Coronary Artery Disease
Authors: Thomas Heitzer, Isabel Ollmann, Katharina Köke, Thomas Meinertz, Thomas Munzel
Journal: Circulation (2003)

Platelet glycoprotein IIb/IIIa receptor blockade not only enhances epicardial flow but also improves microvascular perfusion. Inhibition of abnormal platelet-endothelial interactions may contribute to this beneficial effect. The present study was designed to determine whether glycoprotein IIb/IIIa receptor blockade influences endothelial vasomotor function and NO bioactivity in patients with coronary artery disease.Forty patients with symptomatic coronary artery stenosis were studied before planned percutaneous coronary intervention. By using venous occlusion plethysmography, endothelium-dependent and -independent vasodilation was determined by measuring forearm blood flow responses to acetylcholine with and without NG-monomethyl-L-arginine (L-NMMA) and sodium nitroprusside. Vascular function tests were repeated during glycoprotein IIb/IIIa receptor blockade by tirofiban in 27 patients and by eptifibatide in 13 patients. A subgroup of 10 patients was retested 6 hours after stopping infusion of tirofiban. Glycoprotein IIb/IIIa receptor blockade by both substances improved acetylcholine-induced vasodilation and L-NMMA responses. Six hours after withdrawal of tirofiban infusion, the beneficial effects were not evident. Sodium nitroprusside-induced vasodilation was not changed by glycoprotein IIb/IIIa receptor blockade.These findings support the concept that abnormal platelet-endothelial interactions contribute to endothelial dysfunction and impaired NO bioactivity in patients with symptomatic coronary artery disease.
Identification of Clostridium difficile as a cause of pseudomembranous colitis.
Authors: R H George, J M Symonds, F Dimock, J D Brown, Y Arabi, N Shinagawa, M R Keighley, J Alexander-Williams, D W Burdon
Journal: BMJ (1978)

rest was instituted and the temperature resolved in 24 hours, while all signs and symptoms disappeared in five days.Subsequent investigations showed no evidence of streptococcal infection (a throat swab grew no pathogens and the antistreptolysin titre was < 125 units/ml both one day after admission and six weeks later).The antibody titre for psittacosis LGV was > 1/1000 on admission and six weeks later was still raised at 1/128.Inquiry later showed that before his illness he had visited regularly a neighbouring house in which a healthy, psittacine bird was kept. DiscussionIn this case there are two major and three minor criteria of rheumatic fever present, but without evidence of a recent streptococcal infection.On the contrary, the presence of a cough and constitutional disturbance associated with patchy shadowing on the chest x-ray film and a signific- ant and changing antibody titre all support a diagnosis of psittacosis.The rashes described in association with this disease include "rose spots,"2 erythema nodosum,2 and a macular scaly rash.3We could find no reports of an exanthem resembling erythema marginatum.Arthritis, which may be migratory,4 is a rare complication of psittacosis in man, though in sheep and cattle polyarthritis it is well recognised.5This case shows that psittacosis may present with minimal respira- tory disturbance and with a clinical picture resembling rheumatic fever with erythema marginatum and polyarthritis.
860-1 The success of surgical pulmonary vein isolation for atrial fibrillation is not influenced by omission of the mitral annular connecting lesion
Authors: Deon W Vigilance, Brian Kim, Mauricio Garrido, Mathew Williams, Joy Peacock, Ann Zeidner, Aftab R Kherani, Jeffery A Morgan, Satish Kesava, Mehmet C Oz, Michael Argenziano
Journal: Journal of the American College of Cardiology (2004)
Effects of propranolol and metoprolol on the peripheral circulation.
Authors: P D McSorley, D J Warren
Journal: BMJ (1978)

The effects of single doses of propranolol and metoprolol on skin temperature and skin and muscle blood flow were compared in 10 normal subjects and four patients with essential hypertension. In normal subjects the mean skin temperature fell by 1.30 +/- 0.62 degrees C 90 minutes after 80 mg propranolol and 0.15 +/- 0.05 degrees C after 100 mg metoprolol. Skin blood flow and resting muscle blood flow were not affected by metoprolol but fell significantly after propranolol. Both drugs reduced post-exercise muscle hyperaemia, propranolol by more than metoprolol. Similar changes were seen in the hypertensive patients. Propranolol should be used with care in patients with known vascular disease.
Teaching of Anatomy to the Medical Student
Authors: T. P. McMurray
Journal: BMJ (1949)

MEDIBARLJOHRNAL_seeks to disclose this orderliness, this regularity, and to explain it; to exercise the student in the methods of science-the logical methods of reasoning, inductive and deductive, and the techni- cal or technological methods of manipulation and measurement (including the elements of statistics); to exercise the student's curiosity in the stream of natural events that flows past him; to encourage his capacity for imaginfative speculation (and his capacity to hold this in check); by every possible means to interest the student in the higher values of science-e.g., the aesthetic quality in scientific thinking, fairness in judgment, openness of mind, scepticism, intellectual honesty, dispassionate observation, critical discrimination; to contrast the relative values of reward in the form of wealth, security, social eleva- tion, popular acclaim on the one hand and on the other the calm delight that comes from the contemplation of the har- monies of science and the exaltation that follows upon scientific
Earlier expression of the transcription factor HFH-11B diminishes induction of p21CIP1/WAF1 levels and accelerates mouse hepatocyte entry into S-phase following carbon tetrachloride liver injury
Authors: Xinhe Wang, Nai-Jung Hung, Robert H. Costa
Journal: Hepatology (2001)

Partial hepatectomy (PH) or toxic liver injury induces the proliferation of terminally differentiated hepatic cells to regenerate the original size of the adult liver. Previous PH liver regeneration studies showed that premature transgenic expression of the Forkhead Box M1b (FoxM1b, HFH–11B) transcription factor accelerated hepatocyte entry into DNA replication (S–phase). In this study, we used carbon tetrachloride (CCl 4 ) liver injury to induce a different type of mouse liver regeneration and show that premature hepatic HFH–11B levels also accelerate the onset of hepatocyte S–phase in this injury model. Unlike PH liver regeneration, earlier hepatocyte proliferation after CCl 4 liver injury is correlated with diminished transgenic hepatic levels of p21 CIP1/WAF1 at the G1/S transition of the cell cycle. Differential hybridization of cDNA arrays and RNase protection studies determined that CCl 4 regenerating liver of transgenic mice displayed early stimulated expression of the S–phase promoting cyclin D1 and cyclin E and sustained levels of Cdc25a phosphatase genes. Compared with previous PH liver regeneration studies, our data suggest that premature expression of HFH–11B activates distinct S–phase promotion pathways in the CCl 4 liver injury model. Although proliferating transgenic hepatocytes induced by either PH or CCl 4 liver injury displayed early expression of identical M–phase cyclin genes (cyclin B1, B2, A2, and F), only CCl 4 regenerating transgenic liver exhibited earlier expression of the M–phase promoting Cdc25b. These studies suggest that CCl 4 injury of transgenic liver not only uses the same mechanisms as PH to mediate accelerated hepatocyte entry into mitosis, but also promotes M–phase entry by stimulating Cdc25b expression.
Pancreatic Fibrosis with Islet Cell Pseudoneoplastic Proliferation as a Cause of Hypoglycemia
Authors: Omar Sangueza, John Wei, Carlos M. Isales
Journal: Annals of Internal Medicine (1997)

Letters1 December 1997Pancreatic Fibrosis with Islet Cell Pseudoneoplastic Proliferation as a Cause of HypoglycemiaOmar Sangueza, MD, John Wei, MD, and Carlos M. Isales, MDOmar Sangueza, MDMedical College of Georgia; Atlanta, GA 30912Search for more papers by this author, John Wei, MDMedical College of Georgia; Atlanta, GA 30912Search for more papers by this author, and Carlos M. Isales, MDMedical College of Georgia; Atlanta, GA 30912Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-127-11-199712010-00029 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Islet cell tumors (insulinomas) or islet hypertrophy (nesidioblastosis) are well-described causes of fasting hypoglycemia. The older medical literature, however, also lists exocrine pancreatic involvement as a cause of hypoglycemia [1]. In animal models, ligation of the pancreatic duct leads to atrophy of the exocrine pancreas with secondary hypertrophy of the endocrine portion of the pancreas (Herxheimer-Mansfield phenomenon) [1, 2]. In humans, this islet hypertrophic reaction to pancreatic fibrosis has been termed “pseudoneoplastic proliferation” [3] and can be seen in patients with pancreatic carcinoma, mucoviscidosis associated with cystic fibrosis [4], and chronic pancreatitis [5]. We describe a patient ...References1. Friedlander EO. Hyperinsulinism secondary to disease of the pancreas and organs adjacent to the pancreas: a review of the world literature. Ann Intern Med. 1960; 52:838-48. Google Scholar2. Traverso LW, Bockman DE, Pleis SK, Dail DH. Nesidioblastosis as a mechanism to prevent fibrosis-induced diabetes after pancreatic duct obstruction. Pancreas. 1993; 8:325-9. Google Scholar3. Bartow SA, Mukai K, Rosai J. Pseudoneoplastic proliferation of endocrine cells in pancreatic fibrosis. Cancer. 1981; 47:2627-33. Google Scholar4. Brown RE, Madge GE. Cystic fibrosis and nesidioblastosis. Arch Pathol. 1971; 92:53-7. Google Scholar5. Kloppel G, Bommer G, Commandeur G, Heitz P. The endocrine pancreas in chronic pancreatitis. Virchows Arch. 1978; 377:157-74. Google Scholar Author, Article, and Disclosure InformationAffiliations: Medical College of Georgia; Atlanta, GA 30912 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByTrefoil Factor Family Peptides in Normal and Diseased Human PancreasPancreatitis, Other Inflammatory Lesions, and Pancreatic Pseudotumors 1 December 1997Volume 127, Issue 11Page: 1042-1043KeywordsAtrophyBloodCell proliferationCystic fibrosisFibrosisGlucoseHypoglycemiaInsulinPancreasSurgery Issue Published: 1 December 1997 CopyrightCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Resectable pancreatic cancer needs surgery, then chemotherapy
Authors: Scott Gottlieb
Journal: BMJ (2004)

Adjuvant chemotherapy has a significant survival benefit in patients with resected pancreatic cancer, whereas treatment with chemoradiotherapy has a negative effect on survival, the results of a new study, in the New England Journal of Medicine , show. The negative effect of chemoradiotherapy was thought to be due to the fact that it delayed the administration of chemotherapy.

Pancreatic cancer, with an overall five year survival rate ranging from 0.4% to 4%, has a poor prognosis and is one of the top 10 causes of death from cancer in the Western world. Previous studies have shown that surgical …
P27. Alemtuzumab (anti-CD52 monoclonal antibody) as single-agent therapy in patients with relapsed/refractory chronic lymphocytic leukaemia (CLL) – a single region experience on consecutive patients
Authors: S Eketorp Sylvan, J Lundin, M Ipek, M Palma, C Karlsson, L Hansson
Journal: Journal for ImmunoTherapy of Cancer (2014)

Meeting abstracts Alemtuzumab, a humanised CD52 monoclonal antibody, is routinely used as treatment for patients with refractory chronic lymphocytic leukaemia (CLL). Although alemtuzumab has been evaluated in numerous prospective clinical trials, little is known about its safety and efficacy in the
Mounting ECG Leads
Authors: Richard W. Watts
Journal: JAMA (1967)

<h3>To the Editor:—</h3> If one may comment on the comments of another correspondent, Joseph Schuster, Jr. (<b>200</b>:728, 1967), in his fourth paragraph refers to the fact that the present method of mounting electrocardiogram leads is without reference to the hexaxial reference system and therefore makes computation of the vectors more difficult. Being aware of this deficiency, we at Fairview General Hospital in Cleveland have been mounting the ECG leads as shown in the Figure. The long strip of lead I helps in analysis of rhythm (as does the longer strip of V<sub>1</sub>) and gives a balanced appearance to the folder, although admittedly it should only be on the right half of that side of the folder to conform to the reference system. An Instrument Company has prepared these folders for our use but probably any printer could do the same for other institutions interested in mounting the frontal
Initial alkylating agent chemotherapy in a leukemic hairy cell patient
Authors: Ellen Gaynor, Harvey M. Golomb, Jason McClellan
Journal: American Journal of Hematology (1984)

A patient with moderate splenomegaly and the leukemic phase of hairy cell leukemia presented with a white blood cell count (WBC) of 85,600/mm3 with 87% hairy cells and platelets of 125,000/mm3. Initial therapy consisted of chlorambucil alone at 4 mg each day. Within 6 months, the WBC decreased to 27,000/mm3 with 82% hairy cells, and the spleen was not palpable; platelets remained at 142,000/mm3. The patient has continued to do well for 2 years since the start of therapy, requiring no transfusions and having no problems secondary to organ infiltration. Selected hairy cell patients, those with a significant leukemic phase and with only mild thrombocytopenia, may benefit from initial chlorambucil therapy rather than immediate splenectomy.
Rescuing the Safety Net
Authors: Michael Spivey, Arthur L. Kellermann
Journal: New England Journal of Medicine (2009)

As the recession deepens, layoffs are swelling the ranks of the uninsured. Despite federal stimulus support for state Medicaid programs, some cash-strapped states have cut Medicaid payments, and others are considering such cuts. As a result, many hospitals that treat large numbers of uninsured patients are struggling to survive.In 2006, well before the recession began, U.S. hospitals provided more than $28.8 billion worth of uncompensated care1 — a burden that fell more heavily on some hospitals than on others. Hospitals that provide a large proportion of their inpatient care to the uninsured are called "safety-net" hospitals. Public safety-net hospitals . . .
ACUTE EFFECT OF ATRIAL FIBRILLATION ON LEFT VENTRICULAR LONGITUDINAL FUNCTION: SERIAL OBSERVATION BY SPECKLE TRACKING ECHOCARDIOGRAPHY
Authors: Jun Koyama, Hirohiko Motoki, Kazunori Aizawa, Megumi Koshikawa, Hiroki Kasai, Atsushi Izawa, Takeshi Tomita, Yusuke Miyashita, Setsuo Kumazaki, Uichi Ikeda
Journal: Journal of the American College of Cardiology (2010)
Serial testing of interferon-γ-release assays for the diagnosis of latent tuberculosis in hemodialysis patients
Authors: Woo Kyung Chung, Zhen Long Zheng, Hyung-Soo Kim, Jin-Woong Park, Hyun Joo Lee, Jae Hyun Chang, Ji Yong Jeong, Sejoong Kim, Hyun Hee Lee, Jaeseok Yang
Journal: Journal of Infection (2010)
Osteogenesis imperfecta in adults
Authors: Nick J. Bishop, Jennifer S. Walsh
Journal: Journal of Clinical Investigation (2014)

A 42-year-old premenopausal woman with osteogenesis imperfecta presents to the metabolic bone clinic. She has a daughter with osteogenesis imperfecta who is seen regularly in a specialist pediatric clinic, but the patient herself hasn't had a clinical consultation in years. She has pain and stiffness in her back and is worried for her future bone health. The patient asks, "Am I going to fall apart?" She had numerous fractures in childhood, including fractures of her femur and wrist; fractured her ankles several times in her late teens; and had occasional fractures in adulthood. Her last fracture was a comminuted fracture of her humerus three years ago, when she stumbled and fell forward onto her hands and knees. The woman is hyperextensible and thinks her ankles feel weak. Her bone mineral density T scores are -2.6 at the lumbar spine and -1.9 at the total hip, and spine imaging shows several vertebral endplate deformities, but overall preservation of vertebral height. What are the available pharmacological and nonpharmacological strategies to preserve her skeletal health and function?
Release of lamellar bodies from alveolar type 2 cells.
Authors: N F Johnson
Journal: Thorax (1980)

The release of lamellar bodies from rat alveolar type 2 cells has been studied during a 12hr dark/12hr light cycle. A proportion of the type 2 cell population was ultrastructurally abnormal. The cellular changes formed a spectrum raninging from mild to severe, culminating in rupture of the cell and release of its contents into the alveolar air space. The majority of aberrant cells were observed in animals killed during the dark period. A holocrine secretory mechanism is suggested for the release of lamellar bodies containing the surface active phospholipids of the alveolar lining. The release of lamellar material by a process of exocytosis was also observed, but only rarely, in spite of the numerous lamellar bodies seen in each cell cross-section.
Prospective Assessment of Continuation of Erlotinib or Gefitinib in Patients with Acquired Resistance to Erlotinib or Gefitinib Followed by the Addition of Pemetrexed
Authors: Naruo Yoshimura, Kyoichi Okishio, Shigeki Mitsuoka, Tatsuo Kimura, Tomoya Kawaguchi, Masaji Kobayashi, Tomonori Hirashima, Haruko Daga, Koji Takeda, Kazuto Hirata, Shinzoh Kudoh
Journal: Journal of Thoracic Oncology (2012)
Monocyte-endothelial adhesion in chronic rheumatoid arthritis. In situ detection of selectin and integrin-dependent interactions.
Authors: J S Grober, B L Bowen, H Ebling, B Athey, C B Thompson, D A Fox, L M Stoolman
Journal: Journal of Clinical Investigation (1993)

Blood monocytes are the principal reservoir for tissue macro- phages in rheumatoid synovitis.Receptor-mediated adhesive interactions between circulating cells and the synovial venules initiate recruitment.These interactions have been studied pri- marily in cultured endothelial cells.Thus the functional activi- ties of specific adhesion receptors, such as the endothelial se- lectins and the leukocytic integrins, have not been evaluated directly in diseased tissues.We therefore examined monocyte- microvascular interactions in rheumatoid synovitis by modify- ing the Stamper-Woodruff frozen section binding assay ini- tially developed to study lymphocyte homing.Specific binding of monocytes to venules lined by low or high endothelium oc- curred at concentrations as low as 5 X 195 cells/ml.mAbs specific for P-selectin (CD62, GMP-140/PADGEM) blocked adhesion by > 90% in all synovitis specimens examined.In con- trast, P-selectin-mediated adhesion to the microvasculature was either lower or absent in frozen sections of normal foreskin and placenta.mAbs specific for E-selectin (ELAM-1) blocked 20-50% of monocyte attachment in several RA synovial speci- mens but had no effect in others.mAbs specific for LFA-1, Mol /Mac 1, the integrin fl2-chain, and L-selectin individually inhibited 30-40% of adhesion.An mAb specific for the integrin Bl-chain inhibited the attachment ofelutriated monocytes up to 20%.We conclude that P-selectin associated with the synovial microvasculature initiates shear-resistant adhesion of mono- cytes in the Stamper-Woodruff assay and stabilizes bonds formed by other selectins and the integrins.Thus the frozen section binding assay permits direct evaluation of leukocyte- microvascular adhesive interactions in inflamed tissues and suggests a prominent role for P-selectin in monocyte recruit- ment in vivo.(
Depression, Homocysteine Concentration, and Cardiovascular Events
Authors: Parkavi Chellappa
Journal: JAMA (2009)

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
More Precision in Diagnosing Appendicitis
Authors: Ian McColl
Journal: New England Journal of Medicine (1998)

Despite the advances in surgery over the past century, the diagnosis of acute appendicitis continues to present clinicians with problems. As Rao et al. report in this issue of the Journal, as many as 47 percent of clinical diagnoses of acute appendicitis are wrong,1 for a variety of reasons. The assessment of pain is notoriously difficult; some patients hardly seem to notice pain, and others are extremely sensitive to it. To make matters even more complicated, there are probably few patients who have not at some time in their lives simulated pain in the abdomen to avoid some obligation, such . . .
Genetic analysis of patients with chronic active hepatitis.
Authors: A R Page, H L Sharp, L J Greenberg, E J Yunis
Journal: Journal of Clinical Investigation (1975)

21 patients with chronic active hapatitis (CAH) and their families were HL-A typed. HL-A8 was significantly increased in frequency. An apparent increased frequency of HL-A1 was shown to be secondary to the increased HL-A8 due to linkage disequilibrium. Genotype analysis revealed a striking increased frequency of homozygosity for HL-A8, 6 of 21 patients (28.5%) vs. 2.8% of controls. Two patients and one normal who were homozygous for both HL-A1 and HL-A8 were found to be homozygous for a mixed lymphocyte culture (MLC) determinant 8a. Homozygous 8a cells were used as test-stimulating cells in one-way MLC reactions to determine the frequency of the expression of the 8a determinant in 17 patients and 49 controls selected for HL-A type. 8a was found to be associated with 50% of HL-A8 haplotypes and was frequent in the patient and control populations of the same HL-A types. These data suggest that susceptibility to CAH is determined by homozygosity for a gene that is in linkage disequilibrium with HL-A8 and more closely associated with the HL-A second locus then with the locus for the major MLC determinant.