tbuckley/cabot-search huggingface dataset:
Continuous replication of Friend virus complex (spleen focus-forming virus-lymphatic leukemia-inducing virus) in mouse embryo fibroblasts. Retention of leukemogenicity and loss of immunosuppressive properties.
Authors: R J Eckner
Journal: The Journal of Experimental Medicine (1975)

Exposure of NIH Swiss mouse embryo fibroblasts (MEF) to infectious Friend virus (FV) complex [containing defective spleen focus-forming virus (SFFV) and endogenous NB-tropic leukemia-inducing helper virus (LLV-F)] resulted in the productive infection of these cells by both SFFV and LLV-F. Stocks of SFFV derived after extensive growth in this Swiss MEF cell culture system are fully leukemogenic in adult mice for the induction of erythroleukemia and spleen foci. In addition, in vitro-derived LLV-F, when isolated free of SFFV, is fully leukemogenic for the induction of lymphatic leukemia when inoculated into susceptible newborn BALB/c mice. The host range of in vitro-derived FV complex (i.e., FV-TC) for focus formation in vivo is NB-tropic. Unlike in vivo-derived FV complex, FV-TC does not suppress the responsiveness of murine thymocytes to concanavalin A (Con A) in vitro. Rather, FV-TC acts as a mitogen to nonspecifically stimulate the proliferation of BALB/c thymocytes. The mitogenicity of in vitro-derived FV complex is directly associated with the presence of type-C virus particles, is a heat-labile and UV-sensitive property of the virus, and may be primarily due to LLV since equivalent amounts of LLV with or without SFFV present are equally mitogenic. One in vivo passage of FV-TC resulted in the total loss of this mitogenic property with the reappearance of full immunosuppressive properties. This result demonstrates a clear association between in vivo growth of FV and its ability to suppress mouse thymocytes, and suggests that FV complex (SFFV-LLV) is not inherently immunosuppressive for these cells. While the mechanism of this interconversion between immunostimulatory and fully suppressive virus is unknown, both virus markers appear to be dependent upon the presence of infectious FV.
Nitric oxide attenuates normal and sickle red blood cell adherence to pulmonary endothelium
Authors: Sharon L. Space, Peter A. Lane, Cheryl K. Pickett, John V. Weil
Journal: American Journal of Hematology (2000)

Increased adherence of sickle red blood cells (RBC) to endothelium is implicated as an initiating event of vaso-occlusion in sickle cell disease. Although much is known about the humoral influences of this interaction, there has been little investigation regarding endothelial contributions. Endothelial derived nitric oxide (NO) inhibits adhesion of platelets and leukocytes to endothelium and decreases expression of VCAM-1, an endothelial adhesion site implicated in sickle RBC/endothelial adherence. However, whether NO inhibits RBC adherence to endothelium is unexplored. We tested this hypothesis with endothelial monolayers exposed to RBC from normal (Hb AA) and sickle cell (Hb SS) volunteers in a parallel plate flow chamber. To decrease NO production, endothelial monolayers were exposed to 100 μM nitro-L-arginine (NLA), an inhibitor of nitric oxide synthase, resulting in an 87% increase in normal RBC adherence (P = 0.002). Because adherence of normal RBC to endothelium was low, the effect of DETA-NO, an NO donor, was tested after activation of endothelium with TNF-α increased adherence by 130% (P < 0.001). Subsequent addition of 2 mM DETA-NO produced a 75% decrease in adherence of normal RBC to endothelium (P = 0.03). At baseline, sickle RBC were significantly more adherent than normal RBC (P < 0.001) and DETA-NO decreased sickle RBC adherence by 54% (P = 0.04). Thus, NO inhibits both normal and sickle RBC adherence to endothelium. Strategies that enhance NO activity may be therapeutic in sickle cell disease. Am. J. Hematol. 63:200–204, 2000. © 2000 Wiley-Liss, Inc.
First trimester topical tretinoin and congenital disorders
Authors: S.S. Jick, B.Z. Terris, H. Jick
Journal: The Lancet (1993)

We used information from the Group Health Cooperative of Puget Sound, Washington, USA, to evaluate the risk of birth defects in mothers exposed to topical tretinoin—a retinoid preparation used to treat acne—in the first trimester of pregnancy. We identified 215 women who delivered live or stillborn infants at Group Health Cooperative hospitals and who were exposed to topical tretinoin early in pregnancy, and 430 age-matched nonexposed women who delivered live or stillborn infants at the same hospitals. The prevalence of major anomalies among babies born to the exposed women was 1·9% and among babies born to the nonexposed women was 2·6%. The relative risk estimate for having a baby with a major congenital anomaly for exposed versus nonexposed women was 0·7 (95% Cl 0·2-2·3). We conclude that topical tretinoin is not associated with an increased risk for major congenital disorders.
On a Portable Pneumatic Apparatus for the Mechanical Treatment of Diseases of the Lungs and Heart
Authors: L. Waldenburg
Journal: BMJ (1874)

For inspiration of rarefied air, I employ a mtich smaller force, usually one- three-hundredth to one-hundredth of an atmosphere.* This agrees with the theory long advanced by me and others concerning the Ctiology of phthisis, according to which the insufficient fulness of blood in the lungs
STUDIES ON THE CHEMOTHERAPY OF THE HUMAN MALARIAS. IV. THE METABOLISM OF CINCHONINE IN RELATION TO ITS ANTIMALARIAL ACTIVITY 123
Authors: David P. Earle, William J. Welch, James A. Shannon
Journal: Journal of Clinical Investigation (1948)

The study of the host metabolism of a chemical agent has both theoretical and practical interest in any consideration of chemotherapeutic action.Metabolic change can modify chemotherapeutic effect through a conversion of an active to an inactive agent or through a conversion of an inac- tive to an active agent.Or activity itself may in some way be associated with the process of metabolism.The cinchona alkaloids were selected for special study since it appeared that they offered a good opportunity to obtain information which might bear on these generalizations.The cinchona alkaloids are extensively metabolized by the tissues of man and certain animals (1, 2, 3), their fate being primarily determined by the rate of their metabolic alteration (4).A number of metabolic products formed in man from quinine, quinidine, cinchonine and cinchoni- dine have been isolated (3) and some, character- ized (3, 5).When administered to human subjects, cinchonine is metabolized much more rapidly than any of the other cinchona alkaloids, with 1 The work described in this paper was done under a contract, recommended by the
Survival after aortic dissection in giant cell arteritis.
Authors: M P Richardson, A M Lever, A M Fink, A K Dixon, B L Hazleman
Journal: Annals of the Rheumatic Diseases (1996)

Letters to the editor pressure or hypotensive episodes were recorded during the trial.Among the side effects, mild flushing (35%) and headache (24%) were the most frequent in isradipine recipients.This study has demonstrated the favour- able effects of isradipine on patients with Raynaud's phenomenon; moreover, it is the first to demonstrate a significant reduction in plasma concentrations of ET-1 during calcium antagonist treatment.The most usual manifestations of Raynaud's phenomenon are pain and numbness in the fingers, which in some subjects can be complicated by skin ulcers5 requiring prompt inter- vention.3 4 In the present study, isradipine was able to reduce the frequency, severity, and disabling nature of acute attacks of Raynaud's phenomenon; this result agrees with previous experience of the use of calcium antagonists in patients with Raynaud's phenomenon,' 3 4 and reflects an appropriate selection of patients to receive the treatment.In addition, the clinicosero- logical manifestations and changes in capillaroscopic findings in this series of patients, including those with type I and type II Raynaud's phenomenon, were relatively homogeneous.The clinical improvement of our patients with Raynaud's phenomenon in response to isradipine was reflected in a reduction in plasma concentrations ofET-1.Although the pathophysiological ftmction of ET-1 remains unknown,"3 a number of vascular disorders are characterised by increased concentrations of this vasoactive peptide." How isradipine may influence the titres of ET-1 is difficult to explain but, because ET-l is released in response to ischaemic stimuli," we hypothe- sise that isradipine is able to induce a change in ET-l concentrations indirectly, by improv- ing tissue perfusion.The findings of this preliminary investigation merit further in- vestigation in larger series of patients with Raynaud's phenomenon.
Sarcoidosis and Lymphoma
Authors: S. MARSH WILLIS
Journal: Annals of Internal Medicine (1984)

Letters and Corrections1 March 1984Sarcoidosis and LymphomaS. MARSH WILLIS, M.D.S. MARSH WILLIS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-100-3-464_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The case reported by Rosenfelt and colleagues (1) is interesting, but whether this case represents progression of sarcoidosis to malignant lymphoma is debatable. The coexistence of sarcoidosis and malignant lymphoma cannot be excluded, but another, more likely possibility is that the patient had a steroid-responsive lymphoma, even from the onset of his disease.The nonnecrotizing granuloma of sarcoidosis has been studied extensively (2). This pathologic finding is distinctive but highly nonspecific. It can be seen in various clinical situations, including infectious and inflammatory conditions; drug and chemical-induced states; other granulomatoses; and in association with malignancy. Many cases...References1. ROSENFELT F, YOUNG W, LONKEY S, and ROSENBLOOM B. Sarcoidosis progressing to lymphoma [Letter]. Ann Intern Med. 1983;99:878. LinkGoogle Scholar2. MITCHELL D, SCADDING J, and HEARD B. Sarcoidosis: histopathologic definition and clinical diagnosis. J Clin Pathol. 1977;30:395-400. CrossrefMedlineGoogle Scholar3. ROMER F. Sarcoidosis in cancer—a critical view. In: WILLIAMS WJ, DAVIES, BH, eds. Eighth International Conference on Sarcoidosis and Other Granulomatous Diseases. London: Alpha Omega Publishing, Limited; 1980:567-71. Google Scholar4. BRINCKER H. Sarcoid reactions and sarcoidosis in Hodgkin's disease and other malignant lymphomata. Br J Cancer. 1972;26:120-8. CrossrefMedlineGoogle Scholar5. PICK A, DUER D, and KESSLER H. Delayed hypersensitivity and lymphocytic transformation in patients with Hodgkin's disease and granulomas. Cancer. 1978;41:2192-6. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: S. MARSH WILLIS, M.D.Affiliations: Fitzsimons Army Medical Center Aurora, CO, 80045 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 March 1984Volume 100, Issue 3Page: 464-464KeywordsDrugsGranulomasLymphomaSarcoidosis ePublished: 1 December 2008 Issue Published: 1 March 1984 PDF downloadLoading ...
Switch from Mnt-Max to Myc-Max induces p53 and cyclin D1 expression and apoptosis during cholestasis in mouse and human hepatocytes
Authors: Heping Yang, Tony W. H. Li, Kwang Suk Ko, Meng Xia, Shelly C. Lu
Journal: Hepatology (2008)

Toxic bile acids induce hepatocyte apoptosis, for which p53 and cyclin D1 have been implicated as underlying mediators. Both p53 and cyclin D1 are targets of c-Myc, which is also up-regulated in cholestasis. Myc and Mnt use Max as a cofactor for DNA binding. Myc-Max typically activates transcription via E-box binding. Mnt-Max also binds the E-box sequence but serves as a repressor and inhibits the enhancer activity of Myc-Max. The current work tested the hypothesis that the switch from Mnt-Max to Myc-Max is responsible for p53 and cyclin D1 up-regulation and apoptosis during cholestasis. Following common bile duct ligation or left hepatic bile duct ligation, the expression of p53, c-Myc, and cyclin D1 increased markedly, whereas Mnt expression decreased. Nuclear binding activity of Myc to the E-box element of p53 and cyclin D1 increased, whereas that of Mnt decreased in a time-dependent fashion. Lithocholic acid (LCA) treatment of primary human hepatocytes and HuH-7 cells induced a similar switch from Mnt to Myc and increased p53 and cyclin D1 promoter activity and endogenous p53 and cyclin D1 expression and apoptosis. Blocking c-Myc induction in HuH-7 cells prevented the LCA-mediated increase in p53 and cyclin D1 expression and reduced apoptosis. Lowering Mnt expression further enhanced LCA's inductive effect on p53 and cyclin D1. Bile duct–ligated mice treated with a lentivirus harboring c-myc small interfering RNA were protected from hepatic induction of p53 and cyclin D1, a switch from Mnt to Myc nuclear binding to E-box, and hepatocyte apoptosis. Conclusion: The switch from Mnt to Myc during bile duct ligation and in hepatocytes treated with LCA is responsible for the induction in p53 and cyclin D1 expression and contributes to apoptosis. (HEPATOLOGY 2008.)
Quinine-induced granulomatous hepatitis.
Authors: B Katz, M Weetch, S Chopra
Journal: BMJ (1983)

Many adverse reactions to quinine have been reported. A 65 year old woman taking quinine sulphate for nocturnal leg cramps presented for investigation of episodes of malaise, fever, nausea, vomiting, and polyarthralgia. Granulomatous hepatitis was diagnosed, for which no common cause was found. She was challenged with quinine sulphate; within hours her temperature had risen and her symptoms returned; transaminase activities rose within 48 hours, as did erythrocyte sedimentation rate. After withdrawal of the drug symptoms abated and transaminase activities returned to normal. The biochemical response to challenge with quinine implicates the drug as the cause of the liver disturbances. Quinine should be added to the list of drugs known to cause granulomatous hepatitis and should be considered in cases where symptoms are episodic or where no other cause is apparent.
Increased Sebum Excretion in Patients with Breast Cancer
Authors: J. L. Burton, W. J. Cunliffe, S. Shuster
Journal: BMJ (1970)

The rate of sebum excretion from the forehead skin of patients with early breast cancer was found to be just significantly higher than in age-matched control women. This may indicate that some breast cancer patients have an increase in circulating or tissue-bound sebotrophic hormones, or a decrease in their inhibitors.
Unsuspected Thyroid Metastases From Renal Cell Cancer Detected on In-111-Octreotide With No Uptake in Primary Renal Cancer
Authors: Gad Abikhzer, Anthony Ciarralo, Marc Hickeson
Journal: Clinical Nuclear Medicine (2011)

A patient with a remote history of a left radical nephrectomy for renal cell carcinoma (RCC) underwent a CT scan for abdominal pain. A 2-cm enhancing solid lesion in the right kidney was seen as well as an incidental hypervascular 1.3-cm pancreatic lesion. An In-111-octreotide scan showed no uptake in the pancreatic lesion. There was, however, increased uptake in the neck, which on SPECT/CT localized to the thyroid. Pathology findings of a right partial nephrectomy were consistent with clear-cell RCC. A thyroid biopsy was consistent with metastatic clear-cell RCC and a total thyroidectomy was performed.
New thoughts on essential hypertension.
Authors: F S Golby, L J Beilin
Journal: BMJ (1972)

The authors report a case of a 30-year-old nulliparous woman with a prior medical history of asthma who developed intrapartum pneumomediastinum with surgical emphysema during the second stage of labour. She was managed conservatively with supportive care and there was complete resolution of symptoms within 4 days. Clinical and radiological findings were consistent with Hamman’s syndrome (spontaneous pneumomediastinum). This case reiterates the possibility of childhood asthma or a family history of asthma as being an associated risk factor for Hamman’s syndrome and reminds us of the need to distinguish such clinical findings from more important and potentially life-threatening conditions such as oesophageal rupture, pulmonary embolism and aortic dissection that can present with similar findings.
HRS/ACCF Expert Consensus Statement on Pacemaker Device and Mode Selection
Authors: Anne M. Gillis, Andrea M. Russo, Kenneth A. Ellenbogen, Charles D. Swerdlow, Brian Olshansky, Sana M. Al-Khatib, John F. Beshai, Janet M. McComb, Jens Cosedis Nielsen, Jonathan M. Philpott, Win-Kuang Shen
Journal: Journal of the American College of Cardiology (2012)
APPRAISAL OF TOPICAL USE OF ANTIHISTAMINES
Authors: Francis A. Ellis
Journal: JAMA (1952)

The era of antihistaminic therapy was instituted in 1933 when Fourneau and Bovet1demonstrated that certain phenolic ethers had the property of counteracting the action of histamine in vivo and in vitro. Their most effective compound, 929 F, as well as compound 1571 F, studied by Staub,2were so toxic to humans as to preclude their therapeutic usage. In 1942 Halpern3reported his studies with compound 2339 RP (antergan® [dimethylamino-ethyl-benzylamine]), which proved to be well tolerated. Since then numerous antihistamines have been synthesized, studied, and made available for oral, parenteral, and topical use.  The rapid succession of new and better antihistamines made appraisal of their value difficult and prompted a report by the Council on Pharmacy and Chemistry of the American Medical Association entitled Too Many Drugs?4Reports relating to the chemistry and pharmacology of the antihistamines and to the results of oral administration are
Sirolimus-Eluting Stent Implantation Aggravates Endothelial Vasomotor Dysfunction in the Infarct-Related Coronary Artery in Patients With Acute Myocardial Infarction
Authors: Jyun-ei Obata, Yoshinobu Kitta, Hajime Takano, Yasushi Kodama, Takamitsu Nakamura, Akira Mende, Ken-ichi Kawabata, Yukio Saitoh, Daisuke Fujioka, Tsuyoshi Kobayashi, Toshiaki Yano, Kiyotaka Kugiyama
Journal: Journal of the American College of Cardiology (2007)
Dapsone, Trimethoprim-Sulfamethoxazole, and the Acquired Immunodeficiency Syndrome
Authors: Paul J. Edelson, Craig E. Metroka, Alvin Friedman-Kien
Journal: Annals of Internal Medicine (1985)

Letters and Corrections1 December 1985Dapsone, Trimethoprim-Sulfamethoxazole, and the Acquired Immunodeficiency SyndromePAUL J. EDELSON, M.D., CRAIG E. METROKA, M.D., Ph.D., ALVIN FRIEDMAN-KIEN, M.D.PAUL J. EDELSON, M.D.Search for more papers by this author, CRAIG E. METROKA, M.D., Ph.D.Search for more papers by this author, ALVIN FRIEDMAN-KIEN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-103-6-963 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Pneumocystis pneumonia occurs in about 60% of patients with the acquired immunodeficiency syndrome (AIDS) (1), and in many may recur. However, therapy with either trimethoprim-sulfamethoxazole or pentamidine carries substantial risks of severe side effects (2). Because dapsone (4,4′-diaminodiphenylsulfone) has been effective in a rat model of pneumocystis infection (3), we studied its safety in patients with AIDS who have previously had severe reactions to trimethoprim-sulfamethoxazole.Four patients were closely monitored while they received 25 to 200 mg of drug daily for up to 1 year. All were initially screened for glucose-6-phosphate dehydrogenase deficiency. Patients were begun on...References1. . Acquired immunodeficiency syndrome (AIDS) update—United States. MMWR. 1983;32:309-11. MedlineGoogle Scholar2. GORDINSIMONWOFSYMILLS FGCJ. Adverse reactions to trimethoprim-sulfamethoxazole in patients with the acquired immunodeficiency syndrome. Ann Intern Med. 1984;100:495-9. LinkGoogle Scholar3. HUGHESSMITH WB. Efficacy of diaminodiphenylsulfone and other drugs in murine Pneumocystis carinii pneumonitis. Antimicrob Agents Chemother. 1984;26:436-40. CrossrefMedlineGoogle Scholar4. DEGOWIN R. A review of therapeutic and hemolytic effects of dapsone. Arch Intern Med. 1967;120:242-8. CrossrefMedlineGoogle Scholar5. USPDI: Drug Information for the Health Care Provider. Rockville, Maryland: United States Pharmacopeial Convention; 1982:317-9. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySafety of dapsone as Pneumocystis carinii pneumonia prophylaxis in human immunodeficiency virus-infected patients with allergy to trimethoprim/sulfamethoxazoleAerosolized Pentamidine ProphylaxisPneumocystis carinii, an opportunist in immunocompromised patientsDapsone in low doses prevents Pneumocystis carinii pneumonia in the rat modelComparison of dosages, intervals, and drugs in the prevention of Pneumocystis carinii pneumonia 1 December 1985Volume 103, Issue 6_Part_1Page: 963-963KeywordsAIDSDrugsGlucose-6-phosphate dehydrogenase deficiencyPneumocystisPneumoniaRat modelsSafety Issue Published: 1 December 1985 PDF downloadLoading ...
Structure of avian flu virus confirmed
Authors: J. Wise
Journal: BMJ (1998)

Researchers have confirmed the molecular structure of the avian influenza virus that has so far killed six people in Hong Kong. The structure offers clues about why the strain is so deadly in both birds and people.

A team led by Kanta Subbarao of the Centers for Disease Control and Prevention in Atlanta isolated an avian H5N1 influenza virus from a 3 year old boy who is thought to have died from the …
Delivery after caesarean section
Authors: C. Fitzpatrick
Journal: BMJ (1987)

The exchange-traded fund industry has seen tremendous growth in the past years. Experts still see high potential for a future increase in assets and trading. When things go so well, it isn’t usually the time to think about how to improve strategic marketing. Strategic marketing includes strategies to efficiently reach clearly defined target groups with an optimized mix of products, price, message, brand, and products. The other side of the coin of the remarkable growth of the industry is that the ETF industry is still a dwarf when it comes to absolute figures. Few investors are savvy about ETFs—less than 5% of European ETF assets belong to private investors, according to estimates by the largest providers. Relatively well-educated institutional investors hold the rest of the assets in larger lots. ETFs are definitely not yet a mass market phenomenon. To get there, we need smart, strategic marketing. Although many investors could take advantage of ETFs, there is no budget for broad marketing and lots of competition. The article analyzes the current situation in Europe, provides insight into the mechanics, and makes suggestions on how to cope with these restrictions to make ETFs more accepted.