tbuckley/cabot-search huggingface dataset:
Long-Term Surgical Results in Children
Authors: John G. Raffensperger
Journal: JAMA (1977)

Pediatric surgery has progressed to the point where children with birth defects who are fortunate enough to be treated at a major center enjoy a nearly 100% opportunity for survival. With this achievement, pediatric surgeons are now concerned about their long-term results and the quality of life enjoyed by patients following correction of congenital anomalies. Volume 10 of<i>Progress in Pediatric Surgery</i>is a collection of papers presented at the 1975 meeting of the German Society of Pediatric Surgery on the long-term surgical results in children. The contributors, most of whom represent European clinics, went to great length to follow up patients who had been operated on at least ten years previously. There was one 60-year follow-up on the first patient to survive an operation for duodenal atresia. The problems discussed included cleft palate, esophageal atresia, pyloric stenosis, biliary atresia, genitourinary anomalies, and many other problems in pediatric surgery. It
Aspirin and Colon Cancer — Targeting Prevention?
Authors: Sanford D Markowitz
Journal: New England Journal of Medicine (2007)

The compelling evidence that chronic use of aspirin or certain nonsteroidal antiinflammatory drugs (NSAIDs) can substantially lower the risk of colon cancer has important implications, especially because colon cancer is the second leading cause of cancer death. Aspirin and nonselective NSAIDs each inhibit the generation of prostaglandins by inhibiting the two cyclooxygenase (COX) enzymes that initiate prostaglandin synthesis, COX-1 and COX-2. NSAIDs that are selective for COX-2 also inhibit the generation of prostaglandins. COX-1 is constitutively expressed in the colon, but COX-2 is inducible and markedly up-regulated in many colon cancers. Interventional trials have shown a decreased risk of the . . .
Antibiotic Prophylaxis for Digestive Endoscopy
Authors: M. Barthet, B. Napoleon, G. Gay, T. Ponchon, D. Sautereau, J. P. Arpurt, C. Boustiere, J. Boyer, J. M. Canard, P. A. Dalbies, J. Escourrou, M. Greff, J. Lapuelle, R. Laugier, J. C. Letard, B. Marchetti, L. Palazzo, B. Vedrenne
Journal: Endoscopy (2004)

The aim in antibiotic prophylaxis is to prevent general and local infectious complications related to a medical procedure. General complications are rare in digestive endoscopy (five cases of endocarditis have been reported in the English-language literature [1]), but the rate of local complications can reach 1 % for certain procedures (such as endoscopic retrograde cholangiopancreatography, ERCP).
Recent developments in understanding the pathogenesis of aplastic anemia
Authors: John H. Fitchen, Martin J. Cline
Journal: American Journal of Hematology (1978)

Abstract Bone marrow failure in aplastic anemia (AA) could result from abnormalities of hematopoietic stem cells, abnormal control of hematopoiesis, or abnormalities of the hematopoietic environment. Bone marrow transplantation, in vitro marrow culture techniques, and studies in animal models of marrow failure have provided insights on the possible pathogenetic mechanisms underlying AA. Studies in man and in murine models suggest that most often AA results from injuries to hematopoietic stem cells. Despite the intriguing report of abnormal regulatory cells in congenitally anemic mice, instances of marrow failure due to defective humoral or cellular control of hematopoiesis have not been identified in man. In vitro studies employing allogeneic marrow targets have suggested that immune suppression of hematopoiesis may occasionally mediate AA in man. Marrow failure due to abnormalities of the hematopoietic microenvironment has been suggested by experience with bone marrow transplantation, but no direct study of this possibility has been reported. Based on available evidence, it seems likely that AA will prove to be many diseases that share common clinical and morphologic features.
Occult aortic stenosis as cause of intractable heart failure
Authors: D J R Morgan, R J C Hall
Journal: BMJ (1979)

During a three-year period 10 patients with critical aortic stenosis were referred to a cardiac referral centre with symptoms and signs of intractable cardiac failure and low cardiac output. In nine patients the correct diagnosis was not suspected at the referring hospital, and in the remaining patient the true severity of the aortic stenosis was not appreciated and cardiomyopathy was suggested as an additional diagnosis. The most common referral diagnoses were severe mitral regurgitation (four patients), congestive cardiomyopathy (two patients), or both (three patients). Only two patients had soft ejection systolic murmurs at the base of the heart radiating into the neck, and such a murmur appeared in a third patient during medical treatment. The carotid pulses were of small volume but the characteristic slow-rising, anacrotic nature of the pulse could not be appreciated clinically. The diagnosis was suspected in nine patients because of aortic valve calcification detected by lateral chest <i>x</i>-ray examination in seven patients and by <i>x</i>-ray screening of the heart in two, and because of abnormal aortic valve echoes in the echocardiogram of all five patients in whom the aortic valve could be seen. Eight patients underwent aortic valve replacement despite seemingly poor preoperative left ventricular function. Three patients died, of whom two had severe coexistent coronary artery disease. The five survivors all returned to normal lives and needed little or no medication. Critical aortic stenosis should be actively sought in patients with severe heart failure of unknown cause since surgery may enable them to resume their normal lives.
A case of familial cold autoinflammatory syndrome confirmed by the presence of a CIAS1 mutation
Authors: R.L. Shpall, E.W.B. Jeffes, H.M. Hoffman
Journal: British Journal of Dermatology (2004)

Sir, Familial cold autoinflammatory syndrome (FCAS) or familial cold urticaria, is a rare autosomal dominant disease characterized by a recurrent atypical urticarial rash that occurs after generalized exposure to cold. More than 20 pedigrees have been reported, primarily from North America and Europe. Recently, diagnostic criteria were proposed based on the analysis of several families,1 and mutations were identified in the gene that causes FCAS, cold‐induced autoinflammatory syndrome‐1 (CIAS1).2 We report a new case of FCAS with classic symptoms and pathology, 12 affected relatives, and a CIAS1 mutation to illustrate recent advances in understanding this dermatological disease. A 66‐year‐old male was seen for a rash that developed following exposure to cold. Since birth the patient has developed a pruritic rash approximately 2 h following prolonged generalized cold exposure. The rash lasts about 6 h and resolves with warming and sleep. Approximately once a week, the patient experiences severe bed‐confining episodes associated with diffuse rash, arthralgias and fever followed by chills and profuse sweating. The patient's mother, three of his six siblings, five of his seven children, and three of his grandchildren experience similar recurrent symptoms (Fig. 1).
THE RECENT ADVANCES OF SANITARY SCIENCETHE RELATIONS OF MICRO-ORGANISMS TO DISEASE.
Authors: HENRY O. MARCY
Journal: JAMA (1883)

(Illustrated by photo-micrographs projected upon the screen.) Address of the President of American Academy of Medicine. The unexpected honor which one year ago your kind suffrages conferred upon me in electing me to preside over your councils, I hold to be equally shared by a thoughtful discharge of the duties of the office. The profession at large may be congratulated that the American Academy of Medicine owes its origin and existence to a wide-spread spontaneity of feeling that the times were ripe for, and demanded some organized effort to aid as a controling power in elevating the standard of medicine in our country. How well thus far we have succeeded must be left not to our own prejudiced views, but rather to the unsparing criticisms of all interested in a higher medical education. Since, by our position, we have invited it; let it arouse each one of us to yet
THE AMINO ACID COMPOSITION OF HYPERTENSIN II AND ITS BIOCHEMICAL RELATIONSHIP TO HYPERTENSIN I
Authors: Kenneth E. Lentz, Leonard T. Skeggs, Kenneth R. Woods, Joseph R. Kahn, Norman P. Shumway
Journal: The Journal of Experimental Medicine (1956)

Preparations of hypertensin II, obtained from the treatment of hypertensin I by the action of the hypertensin converting enzyme of plasma and purified by countercurrent distribution, were quantitatively analyzed for their amino acid content. Chromatography on ion exchange columns showed the presence of equimolar amounts of aspartic acid, proline, valine, isoleucine, tyrosine, phenylalanine, histidine, and arginine. Hypertensin I was found to contain one mole of leucine and one mole of histidine in addition to the amino acids of hypertensin II. These two amino acids were isolated from the conversion products of hypertensin I and identified as the peptide histidylleucine. Carboxypeptidase digestion of hypertensin I showed the carboxyl terminal sequence of amino acids to be residue-phenylalanyl-histidylleucine. Similar studies of hypertensin II demonstrated residue-phenylalanine. It was concluded that the conversion of hypertensin I by the plasma hypertensin converting enzyme involved hydrolysis of the phenylalanyl-histidine bond to form hypertensin II and histidylleucine. The further removal by carboxypeptidase of phenylalanine from hypertensin II destroyed all of the vasoconstrictor activity.
Care Management for Low-Risk Patients with Heart Failure
Authors: Robert Frank DeBusk, Nancy Houston Miller, Kathleen Marie Parker, Albert Bandura, Helena Chmura Kraemer, Daniel Joseph Cher, Jeffrey Alan West, Michael Bruce Fowler, George Greenwald
Journal: Annals of Internal Medicine (2004)

Background: Nurse care management programs for patients with chronic illness have been shown to be safe and effective. Objective: To determine whether a telephone-mediated nurse care management program for heart failure reduced the rate of rehospitalization for heart failure and for all causes over a 1-year period. Design: Randomized, controlled trial of usual care with nurse management versus usual care alone in patients hospitalized for heart failure from May 1998 through October 2001. Setting: 5 northern California hospitals in a large health maintenance organization. Patients: Of 2786 patients screened, 462 met clinical criteria for heart failure and were randomly assigned (228 to intervention and 234 to usual care). Intervention: Nurse care management provided structured telephone surveillance and treatment for heart failure and coordination of patients' care with primary care physicians. Measurements: Time to first rehospitalization for heart failure or for any cause and time to a combined end point of first rehospitalization, emergency department visit, or death. Results: At 1 year, half of the patients had been rehospitalized at least once and 11% had died. Only one third of rehospitalizations were for heart failure. The rate of first rehospitalization for heart failure was similar in both groups (proportional hazard, 0.85 [95% CI, 0.46 to 1.57]). The rate of all-cause rehospitalization was similar (proportional hazard, 0.98 [CI, 0.76 to 1.27]). Limitations: The findings of this study, conducted in a single health care system, may not be generalizable to other health care systems. The overall effect of the intervention was minor. Conclusions: Among patients with heart failure at low risk on the basis of sociodemographic and medical attributes, nurse care management did not statistically significantly reduce rehospitalizations for heart failure or for any cause. Such programs may be less effective for patients at low risk than those at high risk.
Calicheamicin-conjugated humanized anti-CD33 monoclonal antibody (gemtuzumab zogamicin, CMA-676) shows cytocidal effect on CD33-positive leukemia cell lines, but is inactive on P-glycoprotein-expressing sublines
Authors: K Naito, A Takeshita, K Shigeno, S Nakamura, S Fujisawa, K Shinjo, H Yoshida, K Ohnishi, M Mori, S Terakawa, R Ohno
Journal: Leukemia (2000)
Lymph Node Biopsy in Thrombotic Thrombocytopenic Purpura
Authors: WILLIAM M. MILLER
Journal: Annals of Internal Medicine (1979)

Letters1 February 1979Lymph Node Biopsy in Thrombotic Thrombocytopenic PurpuraWILLIAM M. MILLER, M.D., SANFORD A. STASS, M.D., HAROLD R. SCHUMACHER, M.D.WILLIAM M. MILLER, M.D.Search for more papers by this author, SANFORD A. STASS, M.D.Search for more papers by this author, HAROLD R. SCHUMACHER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-90-2-278_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In the article by Goodman and colleagues (1) on the use of gingival biopsy in the diagnosis of thrombotic thrombocytopenic purpura, the authors mention the use of lymph node biopsy in passing but make no further reference.The article by Amorosi and Ultmann (2) references five reports in which lymph node biopsy was used in making the diagnosis of thrombotic thrombocytopenic purpura during life. Four of the five cases had positive lymph node biopsies. Although this is a small sampling, it does represent a positive biopsy rate of 80%.In addition to a positive lymph node biopsy...References1. GOODMANRAMOSPETRELLIHIRSCHBUKOWSKIHARRIS ARMSRJ: Gingival biopsy in thrombotic thrombocytopenic purpura. Ann Intern Med 89:501-504, 1978 LinkGoogle Scholar2. AMOROSIULTMANN EJ: Thrombotic thrombocytopenic purpura: report of 16 cases and review of the literature. Medicine (Baltimore) 45:139-159, 1966 CrossrefGoogle Scholar3. SHARNOFF J: Thrombotic thrombocytopenic purpura. Am J Med 23:740-747, 1957 CrossrefMedlineGoogle Scholar4. ADELSONHEITZMANFENNESSEY EEJ: Thrombohemolytic thrombocytopenic purpura. Arch Intern Med 94:42-60, 1954 CrossrefGoogle Scholar5. MOREYWHITEDAILY DJW: Thrombotic thrombocytopenic purpura diagnosed by random lymph node biopsy. Arch Intern Med 98:821-823, 1956 CrossrefGoogle Scholar1. ADELSONHEITZMANFENNESSEY EEJ: Thrombohemolytic thrombocytopenic purpura. Arch Intern Med 94:42-60, 1954 CrossrefGoogle Scholar2. SYMMERSST WC: Thrombotic microangiopathy: histologic diagnosis during life. Lancet 1:592-596, 1956 CrossrefGoogle Scholar3. AMOROSIULTMANN EJ: Thrombotic thrombocytopenic purpura: report of 16 cases and review of the literature. Medicine (Baltimore) 45:139-159, 1966 CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Division of Hematopathology Department of Laboratory Medicine National Naval Medical Center Bethesda, MD 20014 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1979Volume 90, Issue 2Page: 278-279KeywordsBiopsyLymph nodesThrombotic thrombocytopenic purpura Issue Published: 1 February 1979 PDF DownloadLoading ...
Epidemic of AIDS related virus infection among intravenous drug abusers.
Authors: G Webb, B Wells, J R Morgan, T J McManus
Journal: BMJ (1986)

priority is to re-establish circulation.Achievement of that objective will often render respiratory attention unnecessary.The best chance of defibrillating the heart and restoring cardiac output is within the first minute.Two or three praecordial thumps are well worth a try while the defibrillator is being prepared (or if none is available), but the potentially life (and brain) saving direct current shock should not be otherwise delayed, particularly by slavish ad- herence to the simplistic ABC routine.In practice the priorities are usually self evident and their management not mutually exclusive.
919 ENTECAVIR (ETV) THERAPY IN CHRONIC HEPATITIS B PATIENTS PREVIOUSLY TREATED WITH ADEFOVIR (ADV) WITH INCOMPLETE RESPONSE ON-TREATMENT OR RELAPSE OFF-TREATMENT
Authors: C.L. Lai, R. Elion, M. Sherman, H.W. Hann, D.L. Tyrell, C.W. Hsu, C.K. Tan, C.Y. Peng, N. Leung, K. Mercarni, H. Zhang, U.H. Iloeje, B. Kreter
Journal: Journal of Hepatology (2009)
Gold induced nephropathy in rheumatoid arthritis and HLA class II genes.
Authors: L I Sakkas, I C Chikanza, R W Vaughan, K I Welsh, G S Panayi
Journal: Annals of the Rheumatic Diseases (1993)

To elucidate the role of HLA-DRB, -DQA, and -DQB genes in patients with rheumatoid arthritis (RA) who developed gold induced nephropathy.Southern blot analysis of HLA-DRB, -DQA, and -DQB genes was performed on DNA from 27 patients with RA with gold induced nephropathy, 37 patients with RA who were treated with gold but did not develop nephropathy, and 122 ethnically matched normal subjects.The 4.7 kb DQA1/Taq I band associated with DQA1*0501 and DR3 and DR5 was found in 16 (59%) patients with gold induced nephropathy compared with five (14%) patients without gold induced nephropathy.It is concluded that HLA-DQA region genes may be an important susceptibility factor for the development of gold induced nephropathy in patients with RA.
Platelet aggregation. Adult-onset diabetes mellitus and coronary artery disease
Authors: J. W. Davis
Journal: JAMA (1978)

Using a turbidimetric technique, we determined 1.7 μM adenosine diphosphate—induced platelet aggregation and disaggregation at 37 °C in the platelet-rich plasmas of two groups of men with coronary artery disease. Eleven men were nondiabetic and 11 had adult-onset diabetes mellitus without retinopathy. There were no significant differences (P&gt;.05) between diabetics and nondiabetics of the following variables: age, platelet count in platelet-rich plasma, first and second phases of platelet aggregation, maximum extent of aggregation, and percent disaggregation at three minutes after maximum aggregation occurred. Although the mean adenosine diphosphate—induced platelet aggregation in the platelet-rich plasmas of adult-onset diabetic men with coronary artery disease and no retinopathy was not enhanced, and the mean rate of disaggregation was not reduced, when compared with nondiabetic men with coronary artery disease or with healthy men; a slow rate of platelet disaggregation (less than 10%) occurred more frequently in the platelet-rich plasmas of men with coronary artery disease. (<i>JAMA</i>239:732-734, 1978)
Association of carcinoma yield with early papilloma development in SENCAR mice.
Authors: R J Bull, M Robinson, R D Laurie
Journal: Environmental Health Perspectives (1986)

The responsiveness of SENCAR mouse skin to 20 different chemicals with known carcinogenic properties was assessed in initiation/promotion experiments. The purpose of these experiments was to evaluate the extent of false negative responses in mouse skin initiation/promotion protocols and to determine the extent to which early papilloma development can be used to predict the eventual development of malignant tumors. The chemicals were administered as initiators by four different routes: oral, intraperitoneal, subcutaneous, and topical. Following the initiating dose of carcinogen, the animals were subjected to topical applications of 1 microgram 12-O-tetradecanoylphorbol-13-acetate (TPA) 3 times per week for a period of 20 weeks. The yield of papillomas at 24 weeks was selected as a potential predictor of carcinoma yields at 52 weeks following the start of the promotion schedule. Positive responses were observed with only eight of the compounds tested. Where positive results were observed, there was some evidence that the response could depend both qualitatively and quantitatively on the route of administration. However, no route was clearly superior, i.e., different chemicals gave greater responses by different routes. Papilloma yield at 24 weeks following the start of the promotion schedule was clearly related to the development of carcinomas at 52 weeks. No simple linear relationship existed between papilloma yield and carcinoma development, since the number of malignant tumors per papilloma decreased with increasing papilloma yields. The relationship between papilloma and carcinoma yields appeared to be independent of the carcinogen used. These data indicate that there are some limitations in using mouse skin initiation/promotion experiments as the sole basis for identifying substances with carcinogenic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Human Dendritic Cells Mediate Cellular Apoptosis via Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand (Trail)
Authors: Neil A. Fanger, Charles R. Maliszewski, Ken Schooley, Thomas S. Griffith
Journal: The Journal of Experimental Medicine (1999)

TRAIL (TNF-related apoptosis-inducing ligand) is a member of the TNF family that induces apoptosis in a variety of cancer cells. In this study, we demonstrate that human CD11c+ blood dendritic cells (DCs) express TRAIL after stimulation with either interferon (IFN)-γ or -α and acquire the ability to kill TRAIL-sensitive tumor cell targets but not TRAIL-resistant tumor cells or normal cell types. The DC-mediated apoptosis was TRAIL specific, as soluble TRAIL receptor blocked target cell death. Moreover, IFN-stimulated interleukin (IL)-3 receptor (R)α+ blood precursor (pre-)DCs displayed minimal cytotoxicity toward the same target cells, demonstrating a clear functional difference between the CD11c+ DC and IL-3Rα+ pre-DC subsets. These results indicate that TRAIL may serve as an innate effector molecule on CD11c+ DCs for the elimination of spontaneously arising tumor cells and suggest a means by which TRAIL-expressing DCs may regulate or eliminate T cells responding to antigen presented by the DCs.