tbuckley/cabot-search huggingface dataset:
Drug points: Diabetes inspidus induced by ofloxacin
Authors: A. Bharani, H. Kumar
Journal: BMJ (2001)

Nephrogenic diabetes insipidus occurs with agents such as lithium, methoxyfluorane, vitamin D, and demeclocycline. 1 2 We report a case of diabetes insipidus induced by ofloxacin (Tarivid; Hoescht Marion Roussel).

A 25 year old man was admitted with fever, a dry cough, and dyspnoea of three days' duration. He had had an influenza-like illness in the preceding week, and his doctor had prescribed ampicillin 2 g daily for three days. On examination he was febrile, toxic, dyspnoeic, and had poor oral hygiene. His pulse was 130 beats/min, blood pressure 110/70 mm Hg, and respiration 35 breaths/min. A chest …
THE MECHANICS OF DEFORMITIES OF THE HANDS IN ATROPHIC ARTHRITIS, AND A DISCUSSION OF THEIR PREVENTION AND CORRECTION
Authors: J C SMALL
Journal: Annals of Internal Medicine (1950)

Article1 June 1950THE MECHANICS OF DEFORMITIES OF THE HANDS IN ATROPHIC ARTHRITIS, AND A DISCUSSION OF THEIR PREVENTION AND CORRECTIONJAMES C. SMALL, M.D., F.A.C.P.JAMES C. SMALL, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-32-6-1087 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptOne of the earliest deformities in atrophic arthritis occurs in the hands. Characteristically, it develops into an ulnar deviation of the fingers with contractures at the metacarpophalangeal joints. This so greatly reduces the ability to use the hands that it may be regarded as one of the most distressing deformities of the disease. The morale of patients usually suffers less from their inability to walk than it does from inability to use the hands in some time-consuming occupation which might tend to shorten the long waking hours. Since more than 90 per cent of patients with this disease are women,...Bibliography1. GRAY H: Anatomy of the human body, 24th Ed., Lea & Febiger, Philadelphia. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Philadelphia, Pennsylvania*Received for publication May 7, 1949.Figures 1, 2, 3 and 4 are from Gray's Anatomy1 and are presented by permission of the publishers, Lea & Febiger, Philadelphia. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRHEUMATISM AND ARTHRITIS REVIEW OF AMERICAN AND ENGLISH LITERATURE OF RECENT YEARS (TENTH RHEUMATISM REVIEW)* Part IIWILLIAM D. ROBINSON, M.D., F.A.C.P., EDWARD W. BOLAND, M.D., F.A.C.P., JOSEPH J. BUNIM, M.D., F.A.C.P., DARRELL C. CRAIN, M.D., F.A.C.P., EPHRAIM P. ENGLEMAN, M.D., F.A.C.P., WALLACE GRAHAM, M.D., F.R.C.P. (C), L. MAXWELL LOCKIE, M.D., F.A.C.P., MAX M. MONTGOMERY, M.D., F.A.C.P., CHARLES RAGAN, M.D., F.A.C.P., MARIAN W. ROPES, M.D., F.A.C.P., EDWARD F. ROSENBERG, M.D., F.A.C.P., CHARLEY J. SMYTH, M.D. 1 June 1950Volume 32, Issue 6Page: 1087-1094KeywordsArthritis ePublished: 1 December 2008 Issue Published: 1 June 1950 PDF downloadLoading ...
The Abuse of Digitalis
Authors: Walter A. Bloedorn
Journal: Annals of Internal Medicine (1928)

Article1 September 1928The Abuse of DigitalisWALTER A. BLOEDORN, A.M., M.D.WALTER A. BLOEDORN, A.M., M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-2-3-261 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThere is no member of the pharmacopeia more fascinating and intriguing than digitalis. The history of this drug is almost a medical epic. Its botanical name, Digitalis purpurea, was given to it by Fuchsius in 1542 because of the resemblance of its flowers to a finger or thimble and because of its purple color. Boerhaave regarded digitalis as a poison but other writers held that it was one of the native plants of England which should be considered a medicine of considerable virtue.To that sterling old English physician, William Withering, the world owes a tremendous debt for his careful... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Washington, D.C. Medical Corps United States Navy Howard University School of Medicine George Washington University School of Medicine U. S. Naval Medical School Washington, D. C.*Read before District of Columbia Medical Society, April 18, 1928. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1928Volume 2, Issue 3Page: 261-268KeywordsDrugs ePublished: 1 December 2008 Issue Published: 1 September 1928 PDF downloadLoading ...
Abstract 79: Deletion of STAT3 in a mouse model for metastatic melanoma
Authors: Alexander Swoboda, Isabel J. Sobieszek, Michaela Schlederer, Safia Zahma, Jelena Marjanovic, Valeria Poli, Lukas Kenner, Markus Hengstschläger, Mario Mikula, Richard Moriggl
Journal: Cancer Research (2014)

Abstract The incidence of metastatic melanoma, a very aggressive type of human skin cancer, has steadily increased over the last years and is associated with high mortality. Activating mutations in the N-Ras proto-oncogene are characteristic for cutaneous melanoma. The most frequent mutation found in N-Ras is a lysine substitution of glutamine at codon 61 (Q61K) constitutively activating the protein. Together with other mutations, especially inactivation of the CDKN2A locus, it is sufficient for spontaneous melanoma formation and subsequent metastasis formation in mice. STAT3 proteins are highly phosphorylated in melanoma. We identified strong STAT3 expression and activation in 70% of patients that show melanoma brain metastases. Here, we investigated whether deletion of this transcription factor in a mouse model expressing mutant N-RasQ61K transgene under the control of the tyrosinase promoter in combination with a homozygous CDKN2A deletion, leads to modified melanoma formation. Interestingly, we found decreased survival in male mice that do not express STAT3 in melanoma cells. We analyzed primary tumor development, metastasis, and survival using histo-pathological examination between groups of STAT3 positive and negative mice. To further assess whether the enhanced tumor progression upon loss of STAT3 is a cell autonomous effect we established melanoma cell lines derived from mouse tumors with or without STAT3. These novel cell lines will be used to analyze growth and survival properties. We will also test the influence of a functional immune system to question immunoediting by xenotransplantation experiments. Citation Format: Alexander Swoboda, Isabel J. Sobieszek, Michaela Schlederer, Safia Zahma, Jelena Marjanovic, Valeria Poli, Lukas Kenner, Markus Hengstschläger, Mario Mikula, Richard Moriggl. Deletion of STAT3 in a mouse model for metastatic melanoma. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 79. doi:10.1158/1538-7445.AM2014-79
Abstract 3802: Withacnistin blocks binding of STAT3 and STAT5 to growth factor and cytokine receptors and induces regression of breast tumors in vivo
Authors: Xiaolei Zhang, Michelle A. Blaskovich, Kara D. Forinash, Said M. Sebti
Journal: Cancer Research (2014)

Abstract The binding of STAT3 and STAT5 to growth factor and cytokine receptors such as EGFR and the IL-6 receptor gp130 is critical to their activation and ability to contribute to malignant transformation. Therefore, interfering with these biochemical processes could lead to the discovery of novel anti-cancer agents. In this manuscript, we show that the natural product, Withacnistin (Wit) blocks EGF- and IL-6-stimulated binding of STAT3 and STAT5 to EGFR and gp130. Furthermore, Wit inhibits EGF-, PDGF-, IL-6-, IFNβ- and GM-CSF-stimulation of tyrosine phosphorylation of STAT3 and STAT5 but not of EGFR or PDGFR. The inhibition of P-STAT3 and P-STAT5 occurred very rapidly, within minutes of Wit treatment and growth factor stimulation. Wit also inhibits STAT3 nuclear translocation, DNA binding, promoter transcriptional activation, and it suppresses the expression levels of STAT3 target genes such as Bcl-xL and Mcl-1. Finally, Wit induces apoptosis, inhibits anchorage-independent growth and invasion, and causes breast tumor regression in an ErbB2-driven transgenic mouse model. These data warrant further development of Wit as a novel anti-cancer drug for targeting tumors that harbor hyperactivated STAT3 and STAT5. Citation Format: Xiaolei Zhang, Michelle A. Blaskovich, Kara D. Forinash, Said M. Sebti. Withacnistin blocks binding of STAT3 and STAT5 to growth factor and cytokine receptors and induces regression of breast tumors in vivo. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3802. doi:10.1158/1538-7445.AM2014-3802
Abstract 1933: Novel roles of receptor tyrosine kinase AXL in the control of stem cell pluripotency and reprogramming
Authors: Yee Sook Cho, Mi-Young Son, Binna Seol
Journal: Cancer Research (2014)

Abstract The extensive molecular characterization of human pluripotent stem cells (hPSCs), human embryonic stem cells (hESCs), and human induced pluripotent stem cells (hiPSCs) is required Binnbefore they can be applied in the future for personalized medicine and drug discovery. Despite the efforts that have been made with kinome analyses, we still lack in-depth insights into the molecular signatures of receptor tyrosine kinases (RTKs) that are related to pluripotency. Here, we present the first detailed and distinct repertoire of RTKs characteristic for hPSC pluripotency by determining both the expression and phosphorylation profiles of RTKs in hESCs and hiPSCs using RT-PCR with degenerate primers that target conserved tyrosine kinase domains and phospho-RTK array, respectively. Among the RTKs tested, the up-regulation of EPHA1, ERBB2, FGFR4, and VEGFR2 and the down-regulation of AXL, EPHA4, PDGFRB, and TYRO3 in terms of both their expression and phosphorylation levels were predominantly related to the maintenance of hPSC pluripotency. Notably, the specific inhibition of AXL was significantly advantageous in maintaining undifferentiated hESCs and hiPSCs and for the overall efficiency and kinetics of hiPSC generation. Additionally, a global phosphoproteomic analysis showed that approximately 30% of the proteins (293 of 970 phosphoproteins) showed differential phosphorylation upon AXL inhibition in undifferentiated hPSCs, revealing the potential contribution of AXL-mediated phosphorylation dynamics to pluripotency-related signaling networks. Our findings provide a novel molecular signature of AXL in pluripotency control that will complement existing pluripotency-kinome networks. Citation Format: Yee Sook Cho, Mi-Young Son, Binna Seol. Novel roles of receptor tyrosine kinase AXL in the control of stem cell pluripotency and reprogramming. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1933. doi:10.1158/1538-7445.AM2014-1933
Neutrophilic eccrine hidradenitis secondary to infection with Serratia marcescens
Authors: P. Combemale, M. Faisant, C. Azoulay-Petit, M. Dupin, J. Kanitakis
Journal: British Journal of Dermatology (2000)

Neutrophilic eccrine hidradenitis (NEH) is a rare dermatosis which usually develops after administration of chemotherapeutic treatments. An infective origin is exceptional. We report a patient, previously operated on for ependymoma, who presented with an eruption typical of NEH even though he had not received chemotherapy. Culture of a skin biopsy revealed Serratia marcescens. The dermatosis improved after antibiotic therapy but recurred twice and culture again isolated S. marcescens; electron microscopy revealed cytoplasmic inclusions within neutrophils, suggestive of bacteria. The disease improved every time with appropriate antibiotic therapy. An infective aetiology for NEH is rare: three such cases have been reported, of which one was due to S. marcescens. The originality of our case is the recurrence of the disease on three occasions with the same bacterium isolated on each occasion, with disease remission after antibiotic therapy. This case confirms that infections may be a possible cause of NEH and underlines the necessity to search for infective agents, especially in patients immunocompromised by haematopoietic malignancies and/or chemotherapeutic treatments.
Abstract 75: Electronic Integrated Monitoring of Medical Emergency Team Calls to a Step Down Unit
Authors: Marilyn Hravnak, Leslie Edwards, Molly Foster-Heasley, Amy Clontz, Cynthia Valenta, Michael DeVita, Michael Pinsky
Journal: Circulation (2007)

Purpose: Early discharge from intensive care units (ICU) to lower acuity monitoring units (step-down units or SDU) is increasing to improve care throughput. However, the ability of minimally invasive monitoring via electronic integrated monitoring systems (IMS) in SDUs to identify cardiopulmonary deterioration in order to activate Medical Emergency Team (MET) response is unknown. We evaluated the ability of an IMS index value to detect clinically significant events which might trigger activation of the MET earlier than called. Methods: Patients were monitored on a 24 bed trauma SDU according to prevailing policy and bedside decision making. An IMS (BioSign TM ) was inserted into the monitoring system and IMS data were collected in a blinded fashion for 8 weeks from all patients. The IMS uses 4 parameters (heart rate [HR], respiratory rate [RR], blood pressure [BP], peripheral oxygen saturation [SpO 2 ]) to develop a single neural networked signal known as the BioSign Index (BSI). Data were analyzed for patient deterioration according to both BSI trigger value and local MET criteria (DeVita, Qual Safety Health Care 2004). Results: Data from 333 patient admissions were evaluated reflecting 18,692 hours of continuous monitoring. SpO 2 monitoring data were absent in 38.5% of monitored hours, despite being mandatory. Most patients were stable throughout their SDU stay. MET activation occurred on 10 occasions (4 respiratory cause [2 SpO 2 , 2 SpO 2 +RR], 2 cardiac (BP), 1 mixed respiratory + cardiac, and 3 other (1 chest pain, 2 acute mental status change). All 7 MET events of respiratory and/or cardiac cause were detected by BSI in advance (mean advanced detection time prior to MET activation was 6.33 hours). Cardiopulmonary deterioration was generally characterized by progressive increases in BSI over time, not step increases. Conclusion : In this population, cardiopulmonary deterioration requiring MET activation was uncommon but always preceded by IMS index elevations which would have alerted the nursing staff in advance. Continuous monitoring of physiological variables may be augmented by integrating information from multiple parameters to create a new variable. The new index parameter may detect patient deterioration earlier than single parameter monitoring.
Poisons centre will monitor cases
Authors: H. Wheeler, V. Murray
Journal: BMJ (1995)

Treating CS gas injuries to the eye Exposure at close range is particularly dangerous EDr1OR,-Jean-Paul Yih's editorial on injuries to the eye caused by O-chlorobenzylidene malono- nitrile (CS) gas, or tear gas, draws attention to the short term effects of the gas on the eye and suggests that such injuries may well be a future problem as individual police officers in Britain will soon be carrying pocket aerosols of CS gas.' Yih implies that the ocular toxicity of CS gas is rapidly reversible; however, the ocular irritation from 1-chloroacetophenone (another tear gas agent) typically lasts only 15 minutes but may persist for up to three days.2The problems are particularly pronounced when the charge of tear gas is fired at close range: powder infiltration of the conjunctiva, cornea, and sclera will occur.The forces are so great that conjunctival tearing may occur.Corneal stromal oedema and later deep vascularisation may ensue, and a multitude of complications have been reported, including symblepharon, pseudopterygium, infective keratitis, trophic ketatopathy, posterior synechia, secondary glaucoma, cataracts, hyphaema, vitreous haemor- rhage, and traumatic optic neuropathy.' Thus
Medical negligence awards set to rise
Authors: Clare Dyer
Journal: BMJ (1998)

The biggest compensation awards for medical negligence are set to rise by an average of about 30% after a judgment last week by Britain's highest court,the House of Lords.

The ruling, which affects all cases of catastrophic injuries, means much larger payments to compensate for loss of earnings and the cost of future care. In the field of medical negligence, the cases most affected will be those of brain damaged babies, in which the victim will need to be looked after for a lifetime.

The law lords were asked to decide …
Abstract 11618: Low Antithrombin Level Correlates With Failing Fontan Circulation and Predicts the Mortality
Authors: Nobuyuki Tsujii, Hideo Ohuchi, Yosuke Hayama, Jun Negishi, Kanae Noritake, Osamu Sasaki, Aya Miyazaki, Osamu Yamada
Journal: Circulation (2014)

Background:  Antithrombin is one of natural anticoagulants produced by the liver and the activity (AT) decreases as a result of liver dysfunction. Fontan pathophysiology includes heart failure-related hepatopathy that accompanies coagulation abnormality.   Purpose:  To clarify clinical significance of AT in Fontan patients.   Methods and Results:  We prospectively measured AT in consecutive 303 Fontan patients (17±9 years) and compared with the clinical variables, including hemodynamics, peak oxygen uptake (PVO2), liver function, plasma brain natriuretic peptide (BNP), and unscheduled hospitalization (USH), including all-cause mortality. The AT was 109±14 (%, normal range: 80-120%) and it correlated inversely with age, central venous pressure (CVP), and plasma levels of BNP and creatinine, and positively with arterial oxygen saturation (Sat) and PVO2 (p    Conclusions:  Low AT was an ominous clinical manifestation that closely associated with failing Fontan circulation in adults, especially those with HS, and predicted the morbidity and morbidity.
Cultivating the Child's Appetite.
Authors: E. A. Morgan
Journal: JAMA (1933)

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
Molecular responses and chromosomal aberrations in patients with polycythemia vera treated with peg‐proline‐interferon alpha‐2b
Authors: Nicole C.C. Them, Klaudia Bagienski, Tiina Berg, Bettina Gisslinger, Martin Schalling, Doris Chen, Veronika Buxhofer‐Ausch, Josef Thaler, Ernst Schloegl, Guenther A. Gastl, Dominik Wolf, Karin Strecker, Alexander Egle, Thomas Melchardt, Sonja Burgstaller, Ella Willenbacher, Oleh Zagrijtschuk, Christoph Klade, Richard Greil, Heinz Gisslinger, Robert Kralovics
Journal: American Journal of Hematology (2014)

Fifty‐one polycythemia vera (PV) patients were enrolled in the phase I/II clinical study PEGINVERA to receive a new formulation of pegylated interferon alpha (peg‐proline‐IFNα‐2b, AOP2014/P1101). Peg‐proline‐IFNα‐2b treatment led to high response rates on both hematologic and molecular levels. Hematologic and molecular responses were achieved for 46 and 18 patients (90 and 35% of the whole cohort), respectively. Although interferon alpha (IFNα) is known to be an effective antineoplastic therapy for a long time, it is currently not well understood which genetic alterations influence therapeutic outcomes. Apart from somatic changes in specific genes, large chromosomal aberrations could impact responses to IFNα. Therefore, we evaluated the interplay of cytogenetic changes and IFNα responses in the PEGINVERA cohort. We performed high‐resolution SNP microarrays to analyze chromosomal aberrations prior and during peg‐proline‐IFNα‐2b therapy. Similar numbers and types of chromosomal aberrations in responding and non‐responding patients were observed, suggesting that peg‐proline‐IFNα‐2b responses are achieved independently of chromosomal aberrations. Furthermore, complete cytogenetic remissions were accomplished in three patients, of which two showed more than one chromosomal aberration. These results imply that peg‐proline‐IFNα‐2b therapy is an effective drug for PV patients, possibly including patients with complex cytogenetic changes. Am. J. Hematol. 90:288–294, 2015. © 2014 The Authors. American Journal of Hematology published by Wiley Periodicals, Inc.
359. Enhanced Gene Delivery by a Novel Tumor-Specific Vector Containing Peptide and Nucleic Acid Based Nuclear Translocation Signals
Authors: Stanley Saamoah-Moffatt, Sandra Wiehle, Richard J. Cristiana
Journal: Molecular Therapy (2004)

We have developed a novel formulation between Polyethylenimine (PEI) and DNA that exhibits extremely efficient gene delivery both in vitro and in vivo following an intravenous administration. In addition, this formulation can also serve as a foundation to develop targeted vectors which we have demonstrated by attaching the peptide CNGRC to the vector to further increase the resulting tumor specific delivery by targeting aminopeptidase N (CD13) expression on tumor and tumor endothelial cells. However, as is the case for most non-viral vectors, our formulation is still limited by the inability of delivered genes to efficiently translocate to the nucleus, the site of gene transcription. Previous reports have shown the ability to use nuclear localization signals and other sequence-specific targeting motifs to deliver genes to the nucleus of different cell types in vitro. When we incorporated a peptide based on the SV40 nuclear localization signal (NLS) into our CD13 targeted vector using peptide nucleic acid (PNA) coupling technology, gene expression was increased by as much as 7 times over expression in control samples based on quantitation of bgal in the human cancer cell lines H1299 (lung) and UC-3 (bladder) 24 hours after transduction. After 72 hours, gene expression increased to 16 times levels in control samples. A further increase in gene expression was also obtained by using a plasmid containing the 72bp DNA nuclear targeting sequence (DNTS) of SV40. Interestingly, the intravenous administration of the CD13 targeted PEI/DNA vector to animals bearing H1299 tumors resulted in 6 times greater expression in tumor than in lung. We also demonstrate by confocal microscopy that only the vector bearing the NLS peptide localizes in the nucleus of tumor cells. These results provide proof of principle that nuclear targeting using NLS based peptides and DNA sequences can increase the resulting gene expression obtained with our novel vector formulations, providing improved non–viral vectors for the treatment of cancer.