tbuckley/cabot-search huggingface dataset:
Endobronchial Metastasis From the Uterine Cervix
Authors: Talmadge E. King
Journal: JAMA (1979)

METASTASIS to a central airway occurs in only 2% to 5% of patients dying of solid tumors of extrathoracic origin.<sup>1,2</sup>That these tumor metastases can produce clinical and roentgenographic features indistinguishable from those of primary lung cancer is not widely appreciated. Renal and colorectal carcinomas are the most common extrathoracic tumors that metastasize to the bronchus, but other reported cases of tumors with endobronchial metastases include those of the pancreas, adrenal gland, testis, thyroid, ovary, uterus, and breast, and malignant melanoma, fibrosarcoma, and osteogenic sarcoma. A patient with cervical uterine cancer experienced the first manifestation of a cancer recurrence as the symptomatic and roentgenographic appearance of endobronchial obstruction of a major central airway. These chest examination findings mimicked a primary lung cancer. <h3>Report of a Case</h3> A 28-year-old, gravida 4, para 4 woman complained in May 1977 of a persistent, dry, hacking cough of six weeks' duration and the
Comparison of the PBC-40 and PBC-27 tools for quality of life assessment in english speaking primary biliary cirrhosis patients
Authors: D. Jones, I. Patanwala, J. Newton
Journal: Gut (2011)

<h3>Introduction</h3> The PBC-40 is a patient-derived, disease-specific, quality of life (QOL) measure for Primary Biliary Cirrhosis (PBC). It is the only QOL measure developed using optimal methods in liver disease, that has proven to be of real value in the study of the pathogenesis of important symptoms in PBC, in increasing our understanding of patient experience and as an outcome measure in clinical trials. Derived in an English speaking population it had not, until a recent validation study in Italian and Japanese language groups, been validated in other languages. This study re-examined domain structure using the original PBC-40 items, and proposed an abbreviated form consisting of 27 of the original 40 items with a modification in the domain structure. <h3>Methods</h3> To evaluate the English version of the PBC-27 in comparison with the original PBC-40 in a randomly selected group of PBC patients (n=40) and utilising novel versions of both measures developed as experimental tools for use in age and sex matched normal subjects (n=40). <h3>Results</h3> The experimental normal subject versions of the PBC-40 and PBC-27 both proved psychometrically robust and were acceptable to control subjects. Unsurprisingly both measures were highly discriminatory between PBC patients and controls for all symptom domains, confirming the utility of both measures for the assessment of QOL in PBC patients. When comparing the discriminatory ability of the two measures between the PBC and control populations, the PBC-40 outperformed the PBC 27 with regards to fatigue (auc 0.8 (0.69–0.91), p&lt;0.0001 vs 0.78 (0.66–0.9), p&lt;0.0001) and cognition assessment (0.74 (0.63–0.86), p=0.0001 vs 0.70 (0.57–0.84), p&lt;0.005) as well as other symptoms domain compared with the combined symptoms and dryness domains of the PBC-27. In contrast, both measures performed equally in discriminating between patients and controls with regard to the social and emotional domains (although in the former instance the PBC-27 was unduly reliant on a single item relating to holiday). In this population there was no difference in completion rates and acceptability between the shorter and the longer measures. <h3>Conclusion</h3> The PBC-27 is valid for use in English-speaking populations and is highly effective at quantifying symptoms in English-speaking PBC patients. Any advantages associated with compliance and usability for a shorter measure are, however, outweighed by lowered sensitivity for cognitive and fatigue symptom severity (the two domains with the greatest impact). When compared to the PBC-40 the optimum measure may be a hybrid containing the fatigue and cognitive domains of the PBC 40 and the shortened social domain of the PBC 27.
Chekhov's Doctors 8. Tsvyetkov
Authors: Jack Coulehan
Journal: JAMA (1997)

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
Neurologic complications associated with intrathecal liposomal cytarabine given prophylactically in combination with high-dose methotrexate and cytarabine to patients with acute lymphocytic leukemia
Authors: Elias Jabbour, Susan O'Brien, Hagop Kantarjian, Guillermo Garcia-Manero, Alessandra Ferrajoli, Farhad Ravandi, Maria Cabanillas, Deborah A. Thomas
Journal: Blood (2007)
Extended Exhaled NO Measurement Differentiates between Alveolar and Bronchial Inflammation
Authors: LAURI LEHTIMÄKI, HANNU KANKAANRANTA, SEPPO SAARELAINEN, PAULA HAHTOLA, RITVA JÄRVENPÄÄ, TIMO KOIVULA, VÄINÖ TURJANMAA, EEVA MOILANEN
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

Lower respiratory tract inflammation can be detected by measuring exhaled nitric oxide (NO) concentration at a single exhalation flow rate, but this does not differentiate between alveolar and bronchial NO production. We assessed alveolar NO concentration and bronchial NO flux with an extended method of measuring exhaled NO at several exhalation flow rates in 40 patients with asthma, 17 patients with alveolitis, and 57 healthy control subjects. Bronchial NO flux was higher in asthma (2.5 ± 0.3 nl/s, p < 0.001) than in alveolitis (0.7 ± 0.1 nl/s) and healthy control subjects (0.7 ± 0.1 nl/s). Alveolar NO concentration was higher in alveolitis (4.1 ± 0.3 ppb, p < 0.001) than in asthma (1.1 ± 0.2 ppb) and healthy control subjects (1.1 ± 0.1 ppb). In asthma, bronchial NO flux correlated with serum level of eosinophil protein X (EPX) (r = 0.60, p < 0.001) and bronchial hyperresponsiveness (r = 0.55, p < 0.001). In alveolitis, alveolar NO concentration correlated inversely with pulmonary diffusing capacity (r = − 0.55, p = 0.022) and pulmonary restriction. Glucocorticoid treatment or allergen avoidance normalized bronchial NO flux in asthma and decreased alveolar NO concentration toward normal in alveolitis. In conclusion, extended exhaled NO measurement can be used to separately assess alveolar and bronchial inflammation and to assess disease activity/severity in asthma and alveolitis.
A MEMORIAL TABLET FOR CARLOS FINLAY
Authors: John Ruhräh
Journal: JAMA (1928)

<h3>To the Editor:</h3> —In Camagüey, the birthplace of Carlos Finlay, whose idea of the mosquito transmission of yellow fever has meant so much to the world, is not marked by any tablet. The hotel in which he was born has been torn down, but it stood on the Plaza Charles A. Dana. Would it not be a graceful thing for his American medical brethren to see that his birthplace bears a suitable tablet so that visitors would know where it is?
Intravenous methylprednisolone in minimal change nephrotic syndrome.
Authors: C Ponticelli, E Imbasciati, N Case, P Zucchelli, L Cagnoli, S Pasquali
Journal: BMJ (1980)

activity may be limited.Unwanted effects, reflecting its central and autonomic nervous system activity, include insomnia, nervousness, dry mouth, constipation, and excessive sweating.These would not induce toxicity and it seems in our case that mazindol's anorexic activity caused the intoxication.
Metabolic Determinants of Defibrillation
Authors: Bruce B. Lerman, Erica D. Engelstein
Journal: Circulation (1995)

Background The single most important determinant of cardiac arrest outcome is the duration of ventricular fibrillation (VF) preceding delivery of a high-energy shock, because of the adverse effect of VF duration on defibrillation threshold (DFT). Although a metabolic mechanism has been proposed, hypoxia, metabolic acidosis, or alkalosis do not adversely affect DFT. However, since (1) catecholamines and adenosine levels are markedly increased during hypoxia, (2) exogenous catecholamines decrease DFT, and (3) adenosine is a potent antagonist of the electrophysiological effects of catecholamines on ventricular myocardium, we hypothesized that release of adenosine during prolonged VF adversely affects DFT and that this effect occurs through an antiadrenergic mechanism. Methods and Results DFT was determined in dogs during infusion of adenosine (300 μg · kg −1 · min −1 ) and dipyridamole (0.25 mg/kg), an adenosine uptake blocker, a regimen that resulted in adenosine levels in the myocardial effluent equivalent to those achieved after 5 minutes of VF. Adenosine increased transthoracic DFT in each dog by 49±14% (n=21) (mean±SEM) and transmyocardial DFT in a separate group of 10 dogs by 103±16%, P =.0003. Pretreatment with the specific A 1 adenosine receptor antagonist 8-cyclopentyltheophylline (CPT) 5 mg/kg completely abolished the effects of adenosine on DFT. The effects of adenosine on DFT were also examined in the denervated state (propranolol 0.2 mg/kg plus bilateral vagotomy). In contrast to its effect in the innervated condition, adenosine had no effect on DFT in the same dogs when denervated, 49±11 versus 53±10 J ( P =NS). Conclusions Adenosine significantly increases transthoracic and transmyocardial DFT, effects that are mediated by the A 1 adenosine myocardial receptor through an antiadrenergic mechanism. These results suggest that enhanced release of adenosine during VF may have a deleterious effect on defibrillation and that intramyocardial delivery of a specific A 1 adenosine antagonist during VF may facilitate defibrillation and significantly reduce defibrillation threshold.
Vagal Cardiopulmonary Reflexes After Total Cardiac Deafferentation
Authors: Anthony J. Minisi
Journal: Circulation (1998)

Background —There are conflicting data regarding whether the primary source of afferent input for the vagal cardiopulmonary reflex emanates from receptors located in the ventricles, atria, and/or lungs. This study evaluated the effects of total cardiac deafferentation on the reflex control of efferent renal sympathetic nerve activity (RSNA) in response to a stimulus that affected all vagal receptors in the cardiopulmonary region. Methods and Results —Experiments were performed in 14 chloralose-anesthetized dogs with sinoaortic denervation. Reflex control of RSNA in response to blood volume expansion was measured before and after interruption of cardiac vagal afferents by pericardial lidocaine (PL). Reflex sensitivity (% change in RSNA/mm Hg change in left atrial pressure) was markedly attenuated after PL (pre, −10.9±2.2; post, −1.6±0.6; P =0.002). RSNA responses to intracoronary nicotine and left atrial balloon inflation were abolished after PL, confirming that cardiac afferents were interrupted. RSNA responses to lung inflation were not affected by PL, indicating that pulmonary afferents remained intact. In 8 experiments, reflex sensitivity values returned to baseline levels after the effects of PL had worn off. Conclusions —These results indicate that the heart provides the primary source of afferent input for the control of sympathetic outflow by the vagal cardiopulmonary reflex during changes in thoracic blood volumes and pressures.
Abstract P4-19-05: Breast cancer campaign tissue bank human cell culture programme: Generating new biomaterials for breast research
Authors: JJ Gomm, SG Smith, MD Allen, AS Morgan, LA Haywood, M Sarper, S Dreger, A Ironside, EJ Cortes Lopez, A Del Rio Hernandez, V Speirs, LJ Jones
Journal: Cancer Research (2013)

Abstract Background: In-vitro model systems provide an important tool in breast cancer research and, over recent years, there have been considerable advances in their construction. However, despite these advances, the majority of models still employ a narrow range of established cell lines, which frequently are not appropriate for the in-vivo cell type they are representing1. Method: As part of the Breast Cancer Campaign Tissue Bank, we have developed a cell culture programme which feeds into the main tissue collection and involves the systematic generation of materials from normal, high-risk, cancer-containing and malignant breast tissue in order to make available a breadth of material to the research community. Following informed patient consent, fresh tissue is retrieved and, using tissue digestion and magnetic bead technology2, purified cell populations are isolated, characterized and frozen down, or further processed for DNA and RNA isolation. Results: We have isolated purified populations of luminal epithelial, myoepithelial and fibroblast cells from normal breast, risk-reduction (BRCA1 and BRCA2 mutated) breast and from morphologically normal breast tissue surrounding breast cancer. We have generated matched surround and tumour-associated fibroblasts, as well as matched tumour epithelial and tumour-associated fibroblast cell isolates. These cells have been incorporated into 2- and 3-D culture models and we have demonstrated successful genetic manipulation, with siRNA gene knockdown and gene over-expression through retroviral transduction. Immortalisation of selected cell populations is currently underway. Intact organoids and tissue explants have also been generated for in-vitro experimentation. Matched frozen and FFPE samples are available, together with full clinicopathological data. The research community can access these biomaterials via a web-based search portal, with full user support. Conclusion: Through this cell culture programme we aim to make available a wider and more appropriate range of materials for breast research, which should allow more clinically relevant model systems to be developed and add value to breast cancer biobanking. References: 1. Thompson A., et al. Evaluation of the current knowledge limitations in breast cancer research: a gap analysis. Breast Cancer Research 2008; 10: R26. 2. Gomm J.J. et al. Isolation of pure populations of epithelial and myoepithelial cells from the normal human mammary gland using immunomagnetic separation with Dynabeads. Analytical Biochemistry 1995; 226: 91-99. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P4-19-05.
(34) Morphoea following radiotherapy
Authors: K.E. McKENNA, M. WALSH, C. McMILLAN
Journal: British Journal of Dermatology (1992)

Journal Article (34) Morphoea following radiotherapy Get access K.E. McKENNA, K.E. McKENNA Departments of Dermatology, The Belfast City Hospital Search for other works by this author on: Oxford Academic Google Scholar M. WALSH, M. WALSH Departments of Pathology, The Belfast City HospitalDepartments of Dermatology, The Belfast City Hospital Search for other works by this author on: Oxford Academic Google Scholar C. McMILLAN C. McMILLAN Departments of Dermatology, The Belfast City Hospital Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 127, Issue s40, 1 July 1992, Pages 70–71, https://doi.org/10.1111/j.1365-2133.1992.tb01259.x Published: 01 July 1992
Beyond NOTES: randomized controlled study of different methods of flexible endoscopic hemostasis of artificially induced hemorrhage, via NOTES access to the peritoneal cavity
Authors: A. Fritscher-Ravens, A. Ghanbari, C. Holland, F. Olagbeye, K. Hardeler, F. Seehusen, B. Jacobsen, K. Mannur
Journal: Endoscopy (2009)

See also: Commentaire de travail de A. Fritscher-Ravens et al., pp. 29Endoscopy 2009; 41(01): 95-96DOI: 10.1055/s-0032-1306724
Randomised comparison of early versus late induction of labour in post-term pregnancy.
Authors: K Augensen, P Bergsjo, T Eikeland, K Askvik, J Carlsen
Journal: BMJ (1987)

In a prospective randomised study of mothers referred for prolonged pregnancy (around the 42nd week) 214 (group 1) were submitted to attempted induction of labour and 195 (group 2) assigned to continue for a further week without intervention. Strict selection criteria were used for the certainty of term. Mothers in group 2 were given regular non-stress tests to ensure fetal wellbeing, as were those in group 1 in whom induction failed. In group 1, 48 (23%) out of 210 first attempted inductions failed. In group 2, 135 (69%) of the births started spontaneously as compared with 38 (18%) in group 1. The mean duration of labour was 7.5 hours in each group. There was no significant difference in incidence of operative delivery, use of analgesics, or signs of perinatal asphyxia. Significantly more children in group 1 needed phototherapy for hyperbilirubinaemia. There was a clustering of births in the late afternoon and evening, which was most pronounced in group 1. A policy of vigilant non-intervention up to the 44th completed week of pregnancy does not appear to jeopardize mother or fetus.
Chilaiditi's Syndrome
Authors: Timothy Melester
Journal: JAMA (1985)

PNEUMOPERITONEUM is associated with a variety of intra-abdominal pathological disorders. Interposition of the right side of the colon between the diaphragm and liver is a benign process in which the radiological appearance can be confused with more catastrophic conditions associated with pneumoperitoneum. Interposition of the right colon between the liver and the diaphragm has been described for nearly 100 years. Although the majority of cases may be merely radiological curiosities, patients may present with a variety of abdominal signs and symptoms. We present three case reports of this entity and a review of the literature. <h3>Report of Cases</h3><h3>Case 1.—</h3> A 75-year-old woman presented to the emergency room with a four-hour history of severe right upper quadrant pain with nausea and vomiting. The abdomen was mildly distended with moderate tenderness and guarding in the right upper quadrant and hyperactive bowel sounds. Roentgenograms of the chest and abdomen showed an interposed
Abstract 5552: New models for prostate and colon carcinogenesis in PhIP-treated hCYP1A mice
Authors: Guang Xun Li, Connie Cheung, Shea Loy, Anna B. Liu, Chung S. Yang
Journal: Cancer Research (2011)

Abstract The food mutagen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine(PhIP), is mainly metabolized by human CYP1A2 through N-CYP1A2 through N2-hydroxylation (activation) and by mouse Cyp1a2 through 4′-hydroxylation (detoxification). In order to mimic human PhIP carcinogenesis in mice, we treated hCYP1A mice (which express human CYP1A but not mouse Cyp1a) with PhIP by oral gavage. Following a dose of PhIP (200 mg/kg b.w.), low-grade prostate intraepithelial neoplasia (PIN) were observed after 20 weeks, high-grade PIN were observed after 30 weeks, and microinvasive carcinomas and adenocarcinomas in ventral, dorsolateral, and coagulating gland were observed after 40 and 50 weeks. Similar to human prostate carcinogenesis, higher than normal GSTP1 levels were observed in proliferative inflammatory atrophic lesions, and GSTP1 expression was lost in high-grade PIN and carcinomas. Under these experimental conditions, colon tumors were not observed. However, in mice that were treated with PhIP (200 mg/kg) and, a week later, followed by treatment with 1.5% dextran sodium sulfate (DSS) in drinking fluid for 1 week, colon tumors were observed after 6 weeks (with 85% tumor incidence and 3.75±0.70 tumors/mouse) and &amp;gt;90% of the tumors were adenocarcinomas. The tumors had overexpressed β-catenin, c-myc, cyclinD1, iNOS and COX-2. In parallel studies with wild type mice treated with PhIP, or PhIP plus DSS, only low-grade PIN, but no colon tumors, were observed. Experiments are ongoing to study the effects of high-fat diet and other dietary factors in modulating carcinogenesis. These models, when fully characterized, could be very useful experimental systems to study diet and prostate/colon cancer (supported by NIH grants CA120915 and CA120915-S2). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5552. doi:10.1158/1538-7445.AM2011-5552
Resistance to Irreversible EGF Receptor Tyrosine Kinase Inhibitors through a Multistep Mechanism Involving the IGF1R Pathway
Authors: Alexis B. Cortot, Claire E. Repellin, Takeshi Shimamura, Marzia Capelletti, Kreshnik Zejnullahu, Dalia Ercan, James G. Christensen, Kwok-Kin Wong, Nathanael S. Gray, Pasi A. Jänne
Journal: Cancer Research (2012)

The clinical efficacy of EGF receptor (EGFR) kinase inhibitors gefitinib and erlotinib is limited by the development of drug resistance. The most common mechanism of drug resistance is the secondary EGFR T790M mutation. Strategies to overcome EGFR T790M-mediated drug resistance include the use of mutant selective EGFR inhibitors, including WZ4002, or the use of high concentrations of irreversible quinazoline EGFR inhibitors such as PF299804. In the current study, we develop drug-resistant versions of the EGFR-mutant PC9 cell line, which reproducibly develops EGFR T790M as a mechanism of drug resistance to gefitinib. Neither PF299804-resistant nor WZ4002-resistant clones of PC9 harbor EGFR T790M. Instead, they have shown activated insulin-like growth factor receptor (IGF1R) signaling as a result of loss of expression of IGFBP3 with the IGF1R inhibitor, BMS 536924, restoring EGFR inhibitor sensitivity. Intriguingly, prolonged exposure to either PF299804 or WZ4002 results in the emergence of a more drug-resistant subclone that exhibits ERK activation. A MEK inhibitor, CI-1040, partially restores sensitivity to the EGFR/IGF1R inhibitor combination. Moreover, an IGF1R or MEK inhibitor used in combination with either PF299804 or WZ4002 completely prevents the emergence of drug-resistant clones in this model system. Our studies suggest that more effective means of inhibiting EGFR T790M will prevent the emergence of this common drug resistance mechanism in EGFR-mutant non-small cell lung cancer. However, multiple drug resistance mechanisms can still emerge. Preventing the emergence of drug resistance, by targeting pathways that become activated in resistant cancers, may be a more effective clinical strategy.