tbuckley/cabot-search huggingface dataset:
A piece of my mind. Sudden death
Authors: M. C. Greengold
Journal: JAMA (1995)

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
Paradoxical Hypotension after Volume Expansion with Plasma Protein Fraction
Authors: Robert W. Colman
Journal: New England Journal of Medicine (1978)

The enormous growth of knowledge of the kallikrein-kinin system has resulted from advances in the detailed protein chemistry of these proteolytic enzymes, cofactors and substrates. Equally important in the development of this understanding have been careful investigation of the three congenital disorders of the system (deficiencies of Hageman factor, prekallikrein and high-molecular-weight kininogen) and delineation of the role of the kinins in a wide variety of diseases. The formation of bradykinin is initiated in plasma by conversion of Hageman factor (molecular weight of 85,000) from its precursor form to an activated molecule (factor XIIa) that triggers the intrinsic coagulation cascade. . . .
Mental Health and the Army—Reply
Authors: Ronald C. Kessler, Matthew K. Nock, Michael Schoenbaum
Journal: JAMA Psychiatry (2014)

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 Psychiatry HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Psychiatry journal
Reply to E.M. Gilles
Authors: Geoffrey R. Oxnard, Lawrence H. Schwartz, Gregory J. Riely
Journal: Journal of Clinical Oncology (2011)

We appreciate the perspectives provided by Gilles 1 in response to our recent article. 2 Gilles 1 appropriately notes that it is difficult to identify the "correct" size of a tumor that has been measured by multiple radiologists.It is for this reason that we compared each measurement to the paired measurement made by the same radiologist of the same tumor but on the other scan of the patient, which allowed us to calculate the measurement change.We did not compare measurements between radiologists, which eliminated any contribution of inter-reader variability to our results.An average tumor measurement was calculated to provide an approximate method for the classification of tumors of different sizes.Indeed, the correct tumor size has little role in clinical decision making for patients with advanced cancer; it is the presence or absence of a change in size that is the biomarker of primary clinical interest.Gilles 1 is correct in describing our interest in studying "procedurerelated variability."However, the procedure in our study was not just the computed tomography (CT) scan but rather the entire modern measurement process, which includes obtaining the CT scan, formatting the images, and measuring the tumor by using a computer interface.The same procedure was used for both scans for each patient, and thus, calculation of the change between the two measurements made by each radiologist allowed us to quantify the variability in the entire measurement process because it was performed in the clinical research and routine-care settings.We agree that there is uncertainty regarding how much of the variability we identified should be attributed to actual changes on the CT scan or perceived changes by the radiologist, but this distinction is not as clinically important as the fact that tumor diameter changes of up to 10% are not uncommon from variability alone.We disagree with the suggestion that the reason for the variability seen in our study may lie in the lack of "reliable readers." 1 The readers who participated in our study were each experienced radiologists working at an academic cancer center, and each of them have extensive personal experience in serial tumor measurement for clinical trials.Indeed, it is their reliability that made the variability we identified even more striking.Even tumor measurements made by the best radiologists can have unexpected variability because there are multiple factors that influence the measurement process, and we must consider this as we interpret the clinical meaning of small changes.Techniques for the reduction of measurement variability to allow a more accurate assessment of tumor response, including the reconstruction of scans with a smaller slice thickness and semiautomated measurement of entire tumor volumes, are actively being investigated.
In vivo cytokine profiles in patients with kala-azar. Marked elevation of both interleukin-10 and interferon-gamma.
Authors: C L Karp, S H el-Safi, T A Wynn, M M Satti, A M Kordofani, F A Hashim, M Hag-Ali, F A Neva, T B Nutman, D L Sacks
Journal: Journal of Clinical Investigation (1993)

The immunological mechanisms underlying the susceptibility to disseminated visceral parasitism of mononuclear phagocytes in patients with kala-azar remain undefined.Resistance and susceptibility are correlated with distinct patterns of cytokine production in murine models of disseminated leishmanial dis- ease.To assess lesional cytokine profiles in patients with kala- azar, bone marrow aspirates were analyzed using a quantitative reverse transcriptase PCR technique to amplify specific mRNA sequences of multiple Thl-, Th2-, and/or macrophage-asso- ciated cytokines.Transcript levels of IL-10 as well as IFN-y were significantly elevated in patients with active visceral leish- maniasis; IL-10 levels decreased markedly with resolution of disease.These findings suggest that IL-10, a potent, pleiotropic suppressor of all known microbicidal effector functions of macrophages, may contribute to the pathogenesis of kala-azar by inhibiting the cytokine-mediated activation of host macro- phages that is necessary for the control of leishmanial infection.(
Autoimmunity after Alpha-Interferon Therapy for Malignant Carcinoid Tumors
Authors: Lars E. Rönnblom, Gunnar V. Alm, Kjell E. Öberg
Journal: Annals of Internal Medicine (1991)

To determine the incidence of autoantibodies and autoimmune disease and their influence on therapeutic results during alpha-interferon treatment in patients with malignant midgut carcinoid tumors.Consecutive sample of patients.University hospital.One hundred thirty-five patients (70 women, 65 men; median age, 59 years) with biopsy-proven tumors, liver metastases, and no autoimmune disease.Leukocyte alpha-interferon (n = 88) or alpha-interferon 2b (n = 47) three times a week.Signs and symptoms of autoimmune disease or development of autoantibodies to thyroid antigens, nuclear antigens, or gastric parietal cells. Tumor responses were determined by reduced liver metastases or reduced urinary 5-hydroxyindole acetic acid excretion, or both.Twenty-five patients (19%) developed the following autoimmune disorders after a median of 9 months of therapy: thyroid disease (n = 18), systemic lupus erythematosus (n = 1), pernicious anemia (n = 4), and vasculitis (n = 2). Antibodies to microsomal thyroid antigen or thyroglobulin were detected in 16 patients before therapy and in another 11 patients during therapy. Antinuclear antibodies were detected in 16 patients before and in another 19 patients during therapy. Clinical thyroid disease developed in more than 60% of patients who had or developed thyroid antibodies but in only 7% of initially autoantibody-negative patients. Autoimmunity did not correlate with objective tumor response.Patients with malignant carcinoid tumors may develop autoimmune disease during alpha-interferon therapy, especially when autoantibodies are present. They should therefore be monitored for autoimmunity, which does not appear, however, to influence tumor responses.
David Lockhart Cowan
Authors: A I G Kerr
Journal: BMJ (2009)

David Lockhart Cowan was the son of James Cowan, a respected general practitioner in Penicuik, and his wife, Merryl. He attended school at George Watson’s College in Edinburgh before going to Glenalmond, where he completed his education. He qualified as a doctor in Edinburgh in 1965 and progressed to FRCSEd in 1969. He was appointed a consultant in ear, nose, and throat surgery in 1974 and pursued a successful career in Edinburgh, working mostly at the Royal Hospital for Sick Children but also at the City Hospital and Western General Hospital. After a long and fruitful career he retired in 2006.

His interest in otolaryngology began early in his career, and his aptitude in that subject led him to be appointed …
Synthesis and antiviral activity of a series of novel N-phenylbenzamide and N-phenylacetophenone compounds as anti-HCV and anti-EV71 agents
Authors: Zhi Jiang, Huiqiang Wang, Yanping Li, Zonggen Peng, Yuhuan Li, Zhuorong Li
Journal: Acta Pharmaceutica Sinica B (2015)

A series of novel N-phenylbenzamide and N-phenylacetophenone compounds were synthesized and evaluated for their antiviral activity against HCV and EV71 (strain SZ-98). The biological results showed that three compounds (23, 25 and 41) exhibited considerable anti-HCV activity (IC50=0.57–7.12 μmol/L) and several compounds (23, 28, 29, 30, 31 and 42) displayed potent activity against EV71 with the IC50 values lower than 5.00 μmol/L. The potency of compound 23 (IC50=0.57 μmol/L) was superior to that of reported compounds IMB-1f (IC50=1.90 μmol/L) and IMB-1g (IC50=1.00 μmol/L) as anti-HCV agents, and compound 29 possessed the highest anti-EV71 activity, comparable to the comparator drug pirodavir. The efficacy in vivo and antiviral mechanism of these compounds warrant further investigations.
Abstract 4488: Everolimus (RAD001) activity in renal and hepatocellular carcinoma cells resistant to sunitinib and sorafenib
Authors: Maria Serova, Maria Eugenia Riveiro, Safi Dokmak, Sandrine Faivre, Eric Raymond
Journal: Cancer Research (2011)

Abstract Background. Acquired resistance to multikinase inhibitors stands as a major clinical challenge. The aim of present study was to evaluate the effects of everolimus in cancer cells that developed resistance to sunitinib and sorafenib. Materials and Methods: SK-HEP1 (hepatocarcinoma), CAKI1 and 786-0 (renal carcinoma) cells were exposed to stepwise increasing doses of sunitinib or sorafenib for &amp;gt;6 months. Antiproliferative effects of RAD001 were assessed using MTT assay. mRNA levels of selected genes were evaluated using q-RT-PCR. Protein phoshorylation (p) was assessed by western-blot analysis. Results. CAKI-suni, 786-suni cells and SK-suni were 2-fold more resistant to sunitinib than parental cells. CAKI-sora, 786-sora, and SK-sora were also 2-fold more resistant than parental counterparts. Several changes in gene expressions were detected in cell acquiring resistance to sunitinib. For instance, protracted exposure to sunitinib led to a &amp;gt;3-fold increase mRNA expression of CXCR4, CXCL12, MIF, PDGFRα, RET, IGF1R, VEGFR3, CDH1 in SK-suni as compared to parental SK-HEP1 cells. In hepatocarcinoma models, we showed that the CXCL12/CXCR4 axis was over expressed and functional in resistant tumor. Resistance to sunitinib and/or sorafenib was frequently associated with AKT activation. Interestingly, no cross-resistance between sunitinib (or sorafenib) and everolimus was observed at everolimus concentrations ranging 1-20µM in our models. At concentrations ranging 0.1-10µM everolimus still inhibited 20-70% cell proliferation in sunitinib- and sorafenib-resistant cells. Everolimus (0.1µM) also reduced migration of SK-suni cells. Consistent with mTOR inhibition, 0.05-0.1µM everolimus completely inhibited p-S6 activation in sensitive and sunitinib-resistant 786-suni, CAKI-suni, and SK-suni cells. Interestingly, protracted exposure to everolimus also reduced p-AKT(Ser473) activation and in a lower extent p-PKCα, an antiapoptotic factor downstream to AKT, in resistant cancer cells. Mouse experiments assessing the effects of everolimus and TKIs using those resistant models are ongoing. Conclusions. Everolimus retains potent antiproliferative effects in hepato- and/or renal carcinoma cells developing resistance to sunitinib/sorafenib. The activated AKT/mTOR signalling observed in sunitinib/sorafenib-resistant models was inhibited by everolimus at clinically relevant concentrations. Altogether, our data suggest that everolimus is an attractive drug to counteract acquired resistance to sunitinib and sorafenib in renal and hepatocellular carcinomas. 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 4488. doi:10.1158/1538-7445.AM2011-4488
Therapeutics targeting tumor immune escape: Towards the development of new generation anticancer vaccines
Authors: Simone Mocellin, Donato Nitti
Journal: Medicinal Research Reviews (2007)

Abstract Despite the evidence that immune effectors can play a significant role in controlling tumor growth under natural conditions or in response to therapeutic manipulation, it is clear that malignant cells evade immune surveillance in most cases. Considering that anticancer vaccination has reached a plateau of results and currently no vaccination regimen is indicated as a standard anticancer therapy, the dissection of the molecular events underlying tumor immune escape is the necessary condition to make anticancer vaccines a therapeutic weapon effective enough to be implemented in the routine clinical setting. Recent years have witnessed significant advances in our understanding of the molecular mechanisms underlying tumor immune escape. These mechanistic insights are fostering the development of rationally designed therapeutics aimed at reverting the immunosuppressive circuits that undermine an effective antitumor immune response. In this review, the best characterized mechanisms that allow cancer cells to evade immune surveillance are overviewed and the most debated controversies constellating this complex field are highlighted. In addition, the latest therapeutic strategies devised to overcome tumor immune escape are described, with special regard to those entering clinical phase investigation. © 2007 Wiley Periodicals, Inc. Med Res Rev, 28, No. 3, 413–444, 2008
Hypoxaemic reperfusion ameliorates the histopathological changes in the pig brain after a severe global cerebral ischaemic insult
Authors: Emmanuel E. Douzinas, Efstratios Patsouris, Epaminondas M. Kypriades, Dimitrios J. Makris, Ilias Andrianakis, Penelope Korkolopoulou, Vasilios Boursinos, Apostolos Papalois, Christina Sotiropoulou, Panagiotis Davaris, Charis Roussos
Journal: Intensive Care Medicine (2001)
Response of Human Tongue Protrudor and Retractors to Hypoxia and Hypercapnia
Authors: JASON H. MATEIKA, DANIEL L. MILLROOD, JAEHEE KIM, HECTOR P. RODRIGUEZ, GHASSAN J. SAMARA
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

It is well established that the genioglossus muscle (tongue protrudor) has a role in protecting or enhancing upper airway patency in individuals with obstructive sleep apnea. However, no investigation completed to date has addressed the role of the styloglossus and hyoglossus muscles (tongue retractors) in maintaining upper airway patency in humans. As a first step toward this goal, the present investigation was designed to examine the response of human tongue protrudor and retractor muscles during a breathhold maneuver and in steady-state hypoxic hypercapnia. The results showed that the protrudor and retractor muscles were coactivated under both conditions. Measurements of onset time of electromyographic activity during steady-state hypoxic hypercapnia revealed that phasic protrudor and retractor activity was initiated immediately before or during the early part of inspiration. We conclude that the tongue protrudor and retractor muscles are coactivated in response to hypoxia and hypercapnia, and that the tongue retractors may have a significant role in protecting upper airway patency during both apnea and hyperpnea. Mateika JH, Millrood DL, Kim J, Rodriguez HP, Samara GJ. Response of human tongue protrudor and retractors to hypoxia and hypercapnia.
Prolonged Peritoneal Insulin Infusion in a Diabetic Man
Authors: David S Schade, R Philip Eaton, Neal M Friedman, William Spencer
Journal: Diabetes Care (1980)

This study examines the feasibility of prolonged (5-day) peritoneal insulin administration in an insulindependent diabetic subject. Regular insulin was delivered through a 22-gauge polyethylene catheter into the peritoneal space by a portable, rotary solenoid pump at a concentration of 60 ∪/ml. The protocol permitted normal daily activities and attendance at work. At night, the diabetic subject slept in the Clinical Research Center, which allowed frequent monitoring of plasma glucose concentration. Blood samples were obtained every 2 h throughout the 5-day period for glucose, insulin, and C-peptide assay. The results of this study were compared with a control, subcutaneous insulin injection study completed during an additional 5-day period. The results suggest that 5-day intraperitoneal insulin infusion is superior to a comparative 5-day period of subcutaneous insulin injection. Not only were large swings in plasma glucose concentration prevented by intraperitoneal insulin delivery but also mean blood glucose concentration was reduced significantly. Furthermore, intraperitoneal insulin administration resulted in acute meal-related increases in plasma free insulin concentration, suggestive of a normal plasma insulin profile. Thus, intraperitoneal insulin may be a rational insulin delivery site for long-term insulin delivery by a mechanical insulin delivery device.
Daily mortality and air pollution in Santa Clara County, California: 1989-1996.
Authors: D Fairley
Journal: Environmental Health Perspectives (1999)

Since the last revision of the national particulate standards, there has been a profusion of epidemiologic research showing associations between particulates and health effects--mortality in particular. Supported by this research, the U.S. Environmental Protection Agency promulgated a national standard for particulate matter [less than/equal to] 2.5 microm in aerodynamic diameter (PM(2.5)). Nevertheless, the San Francisco Bay Area of California may meet this new standard. This study investigates the relationship between daily mortality and air pollution in Santa Clara County (a Bay Area county) using techniques similar to those utilized in earlier epidemiologic studies. Statistically significant associations persist in the early 1990s, when the Bay Area met national air pollution standards for every criteria pollutant. Of the various pollutants, the strongest associations occur with particulates, especially ammonium nitrate and PM(2.5). The continuing presence of associations between mortality and air pollutants calls into question the adequacy of national standards for protecting public health.
Abstract 3479: Emerging Cardiovascular Risk Factors That Account For A Significant Portion Of Attributable Mortality Risk In Chronic Kidney Disease: A Precis Study.
Authors: Mehdi Shishehbor, Leonardo P. J. Oliveira, Michael Lauer, Dennis Sprecher, Kathy Wolski, Leslie Cho, Byron Hoogwerf, Stanley Hazen
Journal: Circulation (2007)

Background: Chronic kidney disease (CKD) increases cardiovascular risk and mortality. However, traditional cardiovascular risk factors do not adequately account for the substantial increase in mortality observed in CKD. Methods and Results: Prospective cohort study of 4,680 consecutive new patients from a tertiary care preventive cardiology program from 1996 to 2005. Estimated glomerular filtration rate (eGFR) was calculated by the Modification of Diet in Renal Disease (MDRD) method. Baseline levels of traditional (LDL-C, HDL-C, triglycerides, total cholesterol, fasting glucose) and emerging risk factors (apolipoprotein (apo) A1 and apoB, lipoprotein(a), fibrinogen, homocysteine, and CRP) were examined. All-cause mortality was obtained by social security death index. There were 278 deaths for a median follow up of 22 months. CKD (eGFR ≤ 60ml/min) was strongly associated with mortality after adjusting for traditional cardiovascular risk factors (Hazard ratio (HR), 2.31, 95% CI=1.77–3.11, p&lt;0.001) and with addition of propensity score (HR = 2.33, 95% CI=1.75–3.10, p&lt;0.001). Of all the traditional and emerging risk factors monitored, only addition of homocysteine and fibrinogen significantly attenuated the association between CKD and mortality (adjusted HR = 1.73, 95% CI=1.23–2.34, p&lt;0.001), explaining 38% of the attributable mortality risk from CKD. A significant interaction (p = 0.004) between homocysteine and eGFR was observed whereby annual mortality rate in CKD subjects with homocysteine &lt; 10 μmol/L (bottom tertile) was similar to those with normal renal function (1% per year), while homocysteine levels ≥ 12.5 μ mol/L (top tertile) were associated with a 7 fold higher mortality risk. Conclusion: Homocystiene and fibrinogen levels explain 38% of the attributable mortality risk from CKD.
Driving to Work
Authors: Howard F. Stein
Journal: JAMA (1987)

I have learned a lot about rural medicine from behind the wheel of my car. A behavioral science teacher of family medicine, approximately 45 Fridays a year I drive from my home outside Oklahoma City to a rural residency training program in Enid, some 80 miles northwest of "The City." Awakening at 4:15 AM, I try to arrive on time for "sit down" Grand Rounds at 7:30. Today, my 400th or so trip since beginning in 1978, anticipation is the first act upon awakening. The weather report for this early February date is for fog, light rain, and snow; the high should be in the 40s Fahrenheit. I reluctantly part the bedroom drapes; outside it looks as dismal as is forecast. But at least it is wet! The next agenda is to clear bladder and bowel for the long drive, for these roads are no interstate highway where only anonymity