tbuckley/cabot-search huggingface dataset:
Inhaled Corticosteroids and the Beneficial Effect of Deep Inspiration in Asthma
Authors: Nicola Scichilone, Solbert Permutt, Vincenzo Bellia, Alkis Togias
Journal: American Journal of Respiratory and Critical Care Medicine (2005)

Deep inspiration-induced bronchoprotection and bronchodilation are impaired in asthma. We evaluated the effect of inhaled glucocorticosteroids on these phenomena. Two groups of subjects with asthma, 9 with moderate/severe hyperresponsiveness to methacholine, and 12 with mild/borderline hyperresponsiveness to methacholine, received inhaled fluticasone (880 microg daily) for 12 weeks. Serial bronchoprovocations were performed at Weeks 0, 6, and 12. The impact of deep inspirations on the airway response to methacholine was evaluated on the basis of inspiratory vital capacity and FEV(1). Fluticasone produced a wide spectrum of changes in the beneficial effects of deep inspiration, but the mean changes were not significant. The magnitude of the steroid-induced changes in bronchoprotection by deep inspiration correlated with baseline log PC(20) (the provocative concentration of methacholine causing a 20% fall in FEV(1); higher log PC(20) predicted improvement of the deep inspiration effect). The steroid-induced changes led to the emergence of strong positive correlations between the effects of deep inspiration and the methacholine log PC(20) that did not exist at baseline. We conclude that deep inspiration-induced bronchoprotection can be restored by inhaled glucocorticosteroids only in individuals with mild hyperresponsiveness. After steroid treatment, the beneficial effects of deep inspiration become significant determinants of the magnitude of airway hyperresponsiveness.
Impacts of Climate Change on Public Health in India: Future Research Directions
Authors: Kathleen F. Bush, George Luber, S. Rani Kotha, R.S. Dhaliwal, Vikas Kapil, Mercedes Pascual, Daniel G. Brown, Howard Frumkin, R.C. Dhiman, Jeremy Hess, Mark L. Wilson, Kalpana Balakrishnan, Joseph Eisenberg, Tanvir Kaur, Richard Rood, Stuart Batterman, Aley Joseph, Carina J. Gronlund, Arun Agrawal, Howard Hu
Journal: Environmental Health Perspectives (2011)

BackgroundClimate change and associated increases in climate variability will likely further exacerbate global health disparities. More research is needed, particularly in developing countries, to accurately predict the anticipated impacts and inform effective interventions.ObjectivesBuilding on the information presented at the 2009 Joint Indo–U.S. Workshop on Climate Change and Health in Goa, India, we reviewed relevant literature and data, addressed gaps in knowledge, and identified priorities and strategies for future research in India.DiscussionThe scope of the problem in India is enormous, based on the potential for climate change and variability to exacerbate endemic malaria, dengue, yellow fever, cholera, and chikungunya, as well as chronic diseases, particularly among the millions of people who already experience poor sanitation, pollution, malnutrition, and a shortage of drinking water. Ongoing efforts to study these risks were discussed but remain scant. A universal theme of the recommendations developed was the importance of improving the surveillance, monitoring, and integration of meteorological, environmental, geospatial, and health data while working in parallel to implement adaptation strategies.ConclusionsIt will be critical for India to invest in improvements in information infrastructure that are innovative and that promote interdisciplinary collaborations while embarking on adaptation strategies. This will require unprecedented levels of collaboration across diverse institutions in India and abroad. The data can be used in research on the likely impacts of climate change on health that reflect India's diverse climates and populations. Local human and technical capacities for risk communication and promoting adaptive behavior must also be enhanced.
The Columbo Phenomenon
Authors: Joseph P. Frolkis
Journal: JAMA (2013)

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
SURGICAL INDICATIONS IN "SILENT" AND FULMINANT CHOLECYSTOLITHIASIS
Authors: B. O. C. Pribram
Journal: JAMA (1952)

Recent discussions of surgical indications for so-called silent as well for acute and fulminant lithiasis reveal that the opinions of both physicians and surgeons are still widely divergent. The existence of a silent stone has been denied by many surgeons. W. Mayo called it a myth. Other surgeons, while admitting its existence, usually fail to give an explanation. However, the complete absence of clinical signs and symptoms despite the presence of stones in an organ of known sensitivity is not so mysterious as it may seem. Indeed, there is a pathologic basis providing an entirely satisfactory explanation. The following observations in a clinical experiment may serve to illustrate this statement. <h3>THE SILENT ZONE IN THE GALLBLADDER</h3> In a patient with a cholecystostomy the following experiment was made. A flexible probe was introduced through the opening, and the mucosa was scratched in all parts of the fundus of the gallbladder without
Case Reports of Six Children from Birmingham.
Authors: M. Ganpule
Journal: British Journal of Dermatology (1967)

Journal Article Case Reports of Six Children from Birmingham. Get access M. Ganpule, M.B., B.S., Poona. M. Ganpule, M.B., B.S., Poona. Formerly Registrar, Skin Hospital, Birmingham Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 79, Issue 4, 1 April 1967, Pages 221–228, https://doi.org/10.1111/j.1365-2133.1967.tb11478.x Published: 01 April 1967
Trends in Emergency Department Visits for Ambulatory Care Sensitive Conditions by Elderly Nursing Home Residents, 2001 to 2010
Authors: Julia Brownell, Joseph Wang, Alexander Smith, Caroline Stephens, Renee Y. Hsia
Journal: JAMA Internal Medicine (2013)

Author(s): Brownell, Julia; Wang, Joseph; Smith, Alexander; Stephens, Caroline; Hsia, Renee Y
EFFECT OF PASSAGE THROUGH GLOSSINA on the RESISTANCE OF A TRYPARSAMIDE-FAST TRYPANOSOME
Authors: W. Yorke, F. Murgatroyd, F. Hawking
Journal: BMJ (1933)

DRUG RESISTANCE OF TRYPANOSOMES MTHEBAJITISR200 and 300 yards.The patient is very worn and tired from severe rest-pain.On the right side there is a feeble pulse to apex of Scarpa's triangle, but the femoral artery is felt as a solid cord below this point.On the left side all pulses present, but very weak.Operation: trans- peritoneal excision right and left lumbar cords, July 4th, 1932.Temperature rose on right 0.60 C. and on left 50 C.This man walks well and is free from pain, excepting a slight cramp of the right calf if he hurries.His general condition i, greatly improved.Result classified as " good."15.E. W., aged 31 years, chemist.History eight months.Began with claudication of left calf and thrombo-phlebitis of internal saphenous vein.All pulses in each leg are so feeble as to be doubtful, excepting the common femoral, which is strong on both sides.Operation: transperitoneal excision right and left lumbar cords, December 12th, 1931.Temperature rose on right 1.8°C.and on left 0.8°C.He is now free from pain, "can walk miles," and is playing cricket.He has, three months after the operation, developed Raynaud's disease of both hands.Result classified as " gocd."16.J. W., aged 55 years, taxi-owner.History of sixteen years.Began with pain in left calf.Has got steadily worse and now has claudication at 200 yards.Has had onychia of first toe of left foot for two years.A callous ulcer has been present the whole of this time.There is much rest-pain.All pulses were perceptible in right leg, but no pulse was felt in left leg, excepting good common femoral.Operation: extraperitoneal excision of left lumbar cord, August 8th, 1932.Temperature rose on right 40 C. and on left 2.80 C.There was immediate improvement in the condi- tion of the left foot.The ulcer healed quickly.Result classified as " good.
OBSERVATIONS ON USE OF INSULIN IN DIABETES MELLITUS
Authors: W. H. OLMSTED
Journal: JAMA (1923)

The discoverers of insulin have made fundamental observations 1 on its clinical application to the treatment of diabetes. The observations may be thus summarized:   Blood sugar is reduced and glycosuria disappears.  Glycogen is stored in diabetic animals, and the respiratory quotients are raised, showing the burning of sugar.  Ketonuria rapidly disappears, and patients in coma may be successfully restored to consciousness and life.  An overdose of insulin in animals produces violent symptoms of a convulsive nature, followed by coma and death. The antidote for this state is glucose.   Of the mass of invaluable physiologic data presented by the Toronto workers, these are the main facts of direct clinical bearing.  Through the courtesy of Professor Shaffer of the department of biologic chemistry, insulin 2 produced by his laboratory became available for clinical use, Oct. 1, 1922. The observations here recorded have been made from work on more than forty patients. Effort
Hepatocellular uptake of organic cations by the organic anion transporting polypeptides (Oatp1, Oatp2 and OATP-A) and the organic cation transporters (rOCT1 and hOCT1)
Authors: J.E. van Montfoort, B. Stieger, H. Koepsell, M. Müller, G.M.M. Groothuis, D.K.F. Meijer, P.J. Meier
Journal: Journal of Hepatology (2000)
ABC of clinical genetics. Genetics of cancer.
Authors: H. M. Kingston
Journal: BMJ (1989)

Colonic polyps in familial polyposis.Pigmentation of lips in Peutz-Jeghers syndrome.Development of cancer is related to both environmental carcinogens and genetic predisposition.Though the risk of a common cancer occurring in relatives of an affected person is generally low, familial aggregations that cannot be explained by environmental factors alone exist in some O neoplasms, such as breast and ovarian cancers and melanomas.In occasional families a predisposition to a combination of common cancers is -O inherited as an incompletely penetrant autosomal dominant trait.Several 0 mendelian syndromes are also associated with a high risk of malignancy, -0 although these are generally rare disorders.Chromosomal rearrangements -o may be markers for or the cause of certain neoplasias, and various oncogenes may be implicated.There is evidence that two mutational events are required for the development of some malignancies, one of which is inherited in familial cancers.* Affected females ( Females at 50% risk having undergone prophylactic oophorectomy St,a
Reduction of leukotriene B4-induced intraepidermal accumulation of polymorphonuclear leukocytes by methotrexate in psoriasis
Authors: A. M. LAMMERS, P. C. M. KERKHOF, P. D. MIER
Journal: British Journal of Dermatology (1987)

The leukotriene B4 (LTB4)-induced intraepidermal accumulation of polymorphonuclear leukocytes (PMN) was quantified, using an elastase assay, in psoriatic patients receiving methotrexate and in untreated psoriatic patients. Methotrexate in therapeutic dosages inhibited PMN infiltration in six patients who had improved considerably on treatment with the drug, a gradual increase being seen during the days on which no methotrexate was taken. Two patients were in relapse, despite methotrexate treatment, and both failed to show any change in LTB4-induced accumulation of PMN.
32 A PHASE 1, MULTI-CENTER, RANDOMIZED, PLACEBO-CONTROLLED, DOSE-ESCALATION STUDY OF IMO-2125, A TLR9 AGONIST, IN HEPATITIS C-NONRESPONDERS
Authors: A. Muir, R. Ghalib, E. Lawitz, K. Patel, M. Rodriguez-Torres, A. Sheikh, S. Sapp, R. Taylor, A. Bexon, T. Sullivan, A. Dovholuk, J. Mc Hutchison
Journal: Journal of Hepatology (2010)
Peroxisome Proliferator-Activated Receptor-γ Contributes to the Inhibitory Effects of Embelin on Colon Carcinogenesis
Authors: Yun Dai, Liang Qiao, Kwok Wah Chan, Mo Yang, Jieyu Ye, Juan Ma, Bing Zou, Qing Gu, Jide Wang, Roberta Pang, H.Y. Lan, Benjamin C.Y. Wong
Journal: Cancer Research (2009)

Abstract Down-regulation of XIAP (X-linked inhibitor of apoptosis protein) sensitizes colon cancer cells to the anticancer effect of peroxisome proliferator-activated receptor-γ (PPARγ) ligands in mice. The aims of this study were to evaluate the effect of embelin (2,5-dihydroxy-3-undecyl-1,4-benzoquinone), an antagonist of XIAP, on colon cancer, with a particular focus on whether PPARγ is required for embelin to exert its effect. A dominant-negative PPARγ was used to antagonize endogenous PPARγ in HCT116 cells. Cells were treated with or without embelin. Cell proliferation, apoptosis, and nuclear factor-κB (NF-κB) activity were measured. For in vivo studies, 1,2-dimethylhydrazine dihydrochloride (DMH) was s.c. injected to induce colon cancer in PPARγ+/+ and PPARγ+/− mice. Mice were fed embelin daily for 10 days before DMH injection, and continued for 30 more weeks. Embelin inhibited proliferation and induced apoptosis in HCT116 cells with marked up-regulation of PPARγ. In addition, embelin significantly inhibited the expressions of survivin, cyclin D1, and c-Myc. These effects were partially dependent on PPARγ. PPARγ+/− mice were more susceptible to DMH-induced colon carcinogenesis than PPARγ+/+ mice, and embelin significantly reduced the incidence of colon cancer in PPARγ+/+ mice but not in PPARγ+/− mice. Embelin inhibited NF-κB activity in PPARγ+/+ mice but marginally so in PPARγ+/− mice. Thus, reduced expression of PPARγ significantly sensitizes colonic tissues to the carcinogenic effect of DMH. Embelin inhibits chemical carcinogen-induced colon carcinogenesis, but this effect is partially dependent on the presence of functional PPARγ, indicating that PPARγ is a necessary signaling pathway involved in the antitumor activity of normal organisms. [Cancer Res 2009;69(11):4776–83]
A glycosaminoglycan inhibitor of thrombin: A new mechanism for abnormal hemostatic assays in cancer
Authors: Howard A. Liebman, Raymond Comenzo, Suzanne T. Allen, Jere M. Dilorio
Journal: American Journal of Hematology (1991)

Abstract The isolation and partial characterization of a novel anticoagulant from the plasma of a patient with metastatic prostate cancer is described. The patient had a prolonged activated partial thromboplastic time, prothrombin time and thrombin time which did not correct by mixing with normal plasma. The reptilase time was normal and the prolonged thrombin time was corrected with protamine sulfate suggesting a heparin‐like anticoagulant. A glycosaminoglycan anticoagulant (GAC) was isolated from the patient's plasma. The inhibitory activity of the GAC was destroyed by treatment with chondroitinase ABC. The GAC migrated on agarose gel electrophoresis between keratin sulfate and heparan sulfate. Purified GAC possessed only 2% (W/W) of the antithrombin III cofactor activity of porcine heparin. In assays using purified fibrinogen, the GAC was shown to directly inhibit fibrinogen proteolysis by thrombin. It is concluded that this glycosaminoglycan anticoagulant directly inhibits thrombin clotting of fibrinogen and is a new mechanism for abnormal hemostatic assays in cancer.
Genetic determinants of diastolic and pulse pressure map to different loci in Lyon hypertensive rats
Authors: Christopher Dubay, Madeleine Vincent, Nilesh J. Samani, Pascale Hilbert, Michael A. Kaiser, Jean-Paul Beressi, Yuri Kotelevtsev, Jacques S. Beckmann, Florent Soubrier, Jean Sassard, G. Mark Lathrop
Journal: Nature Genetics (1993)
Amino acid substitutions can influence the natural killer (NK)-mediated recognition of HLA-C molecules. Role of serine-77 and lysine-80 in the target cell protection from lysis mediated by "group 2" or "group 1" NK clones.
Authors: R Biassoni, M Falco, A Cambiaggi, P Costa, S Verdiani, D Pende, R Conte, C Di Donato, P Parham, L Moretta
Journal: The Journal of Experimental Medicine (1995)

Natural killer (NK) cells have been shown to express a clonally distributed ability to recognize HLA class I alleles. The previously defined NK clones belonging to "group 1" recognize HLA-C*0401 (Cw4) and other HLA-C alleles sharing Asn at position 77 and Lys at position 80. Conversely, the "group 2" NK clones recognize HLA-Cw*0302 (Cw3) and other HLA-C alleles characterized by Ser at position 77 and Asn at position 80. We assessed directly the involvement of these two residues in the capacity of NK cell clones to discriminate between the two groups of HLA-C alleles. To this end, Cw3 and Cw4 alleles were subjected to site-directed mutagenesis. Substitution of the amino acids typical of the Cw3 allele (Ser-77 and Asn-80) with those present in Cw4 (Asn-77 and Lys-80) resulted in a Cw3 mutant that was no longer recognized by group 2 NK cell clones, but that was recognized by group 1 clones. Analysis of Cw3 or Cw4 molecules containing single amino acid substitutions indicates roles for Lys-80 in recognition mediated by group 1 clones and for Ser-77 in recognition mediated by group 2 clones. These results demonstrate that NK-mediated specific recognition of HLA-C allotypes is affected by single natural amino acid substitutions at positions 77 and 80 of the heavy chain.
Radiologists' Interpretations: The Problem of Context Bias
Authors: Andrei I. Vermont
Journal: JAMA (1997)

<h3>To the Editor.</h3> —Drs Egglin and Feinstein<sup>1</sup>provided us with a new and commendable insight with regard to the way the diagnostic judgments of radiologists are modified by the perceptual context in which test results are presented to them. The method and arguments they presented in the article convinced me that our thought process in front of an imaging study follows Bayesian rules. The radiologists in their study appeared to use the early cases in the series they had to read as a "pilot" group: their concrete perceptions and influences were used to calibrate their readings for the rest of the cases in the series. We would like to believe that in our daily practice we also use pretest probability estimates. However, we infer the pretest probability from risk factors and the results of tests (clinical or otherwise) that are presented to us by a narrative of the clinical
Minors and contraception.
Authors: M Smith
Journal: BMJ (1974)

tion that in their experience with this drug the blood pressure, once controlled, may remain within noTmal limits for up to a month after stopping treatment.We have recently observed the same phenomenon after discontinuing therapy with indoramin in hypertensive patients,' when no¢motension may continue for considerably longer than four weeks.Indoramin -also has adrenoceptor blocking activity,23 Since prolonged normotension is seen after discontinuing other antihypertensive agents however,4 this effect may well be due to a common mechanism such as "barostat" resetting5 rather than a direct action of the drugs themselves.This phenomenon conplicates the de- sign of clinical trials, as Drs.Stokes and Weber point out.It also suggests4 that morbidity due rto antihypertensive agents could frequently be avoided by stopping or reducing the dose of these drugs afiter long periods of s,atisfactory 'blood pressure control.-Weare, etc.,
Occupation and Coronary Disease: Schooling as a Confounder-Reply
Authors: Julie E. Buring
Journal: JAMA (1988)

In Reply.  —Mr Leigh suggests that the association between occupational status and fatal coronary heart disease (CHD) observed in our study might be overstated because of a failure to control for confounding by level of schooling. For this to have accounted for the findings, schooling must have been related to occupation and, in addition, must be associated with risk of fatal CHD. Regarding the former, nobody would disagree with the statement that level of schooling is related to occupational status. With respect to the latter, however, to be a confounder, the association of schooling with CHD must be independent of the relationship with occupational status. While we agree that level of schooling, as a marker for socioeconomic status, is related to risk of CHD, we know of no evidence that schooling per se is an independent causal risk factor. Further, our study did control for a strong correlate of socioeconomic
GLUT-2 function in glucose-unresponsive beta cells of dexamethasone-induced diabetes in rats.
Authors: M Ohneda, J H Johnson, L R Inman, R H Unger
Journal: Journal of Clinical Investigation (1993)

Spontaneous and dexamethasone-induced noninsulin-dependent diabetes mellitus (NIDDM) in rats is associated with loss of glucose-stimulated insulin secretion (GSIS) and a reduction in both GLUT-2-positive beta cells and high Km glucose transport. To determine if the chronology and correlation of these abnormalities is consistent with a causal relationship, Zucker (fa/fa) rats were studied longitudinally before and during 10 d of dexamethasone-induced (0.4 mg/kg per d i.p.) NIDDM. Within 24 h of dexamethasone treatment blood glucose rose and GSIS declined, becoming paradoxically negative (-87 +/- 12 microU/ml per min) on day 10. Blood glucose was negatively correlated with GSIS (r = -0.92; P < 0.001). 3-0-methyl-D-glucose (3MG) transport was unchanged at 12 h, 23% below normal on day 1, and declined further to a nadir 59% below normal. The GLUT-2-positive beta cell area did not decline until 48 h, reaching a nadir of 35% of normal at 10 d. The area of GLUT-2-positive beta cells was correlated with GSIS (r = 0.77; P < 0.005). We conclude that the chronology and correlation between GSIS loss and hyperglycemia is consistent with a cause-effect relationship, but that the subtotal impairment in glucose transport by itself cannot explain the total loss of GSIS if one assumes that normal beta cells are functionally homogenous.