tbuckley/cabot-search huggingface dataset:
Native beta-adrenergic support for left ventricular dysfunction in experimental mitral regurgitation normalizes indexes of pump and contractile function.
Authors: M Nagatsu, M R Zile, H Tsutsui, P G Schmid, G DeFreyte, G Cooper, B A Carabello
Journal: Circulation (1994)

BACKGROUND It is generally accepted that the adrenergic nervous system provides inotropic support for the failing heart. However, the magnitude of this support has never been studied extensively. The present study was performed to test the hypothesis that the adrenergic nervous system is capable of maintaining indexes of pump and contractile function in the normal range despite significant innate myocardial depression. METHODS AND RESULTS We used our model of experimental canine mitral regurgitation, which produces left ventricular dysfunction after 3 months of volume overload. We studied indexes of contractile function on and off beta-blockade at baseline and again on and off beta-blockade 3 months after chronic mitral regurgitation had induced significant contractile dysfunction. At baseline, acute beta-blockade caused insignificant reductions in the mass-corrected slope of the end-ejection stress-volume relation (EESVR), the end-systolic stiffness constant, and the ejection fraction-end-systolic stress and the mean velocity of circumferential fiber shortening (VCF)-end-systolic stress relations. After 3 months of chronic mitral regurgitation, all indexes of contractile function were normal in the unblocked state except for the VCF-stress relation, which was mildly reduced. However, after acute beta-blockade after 3 months of chronic mitral regurgitation, the EESVR fell to 303 +/- 27 versus 443 +/- 24 during acute beta-blockade before mitral regurgitation was created (P &lt; .05), and the end-systolic stiffness constant was reduced to 2.54 +/- 0.15 versus 3.27 +/- 0.11 (P &lt; .05). Only after beta-blockade was the ejection fraction-stress relation significantly reduced for dogs with chronic mitral regurgitation. The VCF-stress relation became markedly more abnormal. The viscosity-velocity relation of myocytes isolated from the ventricles of the dogs with mitral regurgitation confirmed that substantial innate contractile depression was present. CONCLUSIONS After 3 months of chronic mitral regurgitation, the adrenergic nervous system was able to maintain most indexes of contractile function in the normal range despite significant depression in innate contractile function. Thus, in the absence of beta-blockade, significant innate contractile depression may be obscured by adrenergic support.
On the Physical Death of Jesus Christ
Authors: Amnon Ben-Tor
Journal: JAMA (1986)

<h3>To the Editor.—</h3> As an archaeologist and a historian of biblical times, we must warn your readers that the purported historical and archaeological "facts" presented in the recent<i>JAMA</i>article, "On the Physical Death of Jesus Christ,"<sup>1</sup>are in sharp variance with the consensus among academic scholars of the New Testament and Jewish and Roman legal and political procedures in New Testament times, as we shall shortly detail. These errors on the part of the article's writers are not merely accidental oversights. The repeated claims to historical accuracy barely disguise theological, we dare say fundamentalist, biases of serious and unfortunate consequence. Curiously, not only are historians and archaeologists not represented among the "interdisciplinary" writers, but the standard scholarly historical treatments of the trial and execution of Jesus are absent from the references. To begin with an obvious example of such pseudoscholarship, it may well be, as the authors affirm,
Left ventricular diastolic pressure-segment length relations and end-diastolic distensibility in dogs with coronary stenoses. An angina physiology model.
Authors: S Momomura, A B Bradley, W Grossman
Journal: Circulation Research (1984)

Isovolumic relaxation abnormalities have been noted in the ischemic left ventricle, but altered end-diastolic distensibility, as well as the role of right ventricular distention, is debated. Accordingly, left ventricular end-diastolic pressure and myocardial segment length were studied in the open-chest dogs with critical (90% diameter reduction) stenoses on both left anterior descending and circumflex coronary arteries. Regional segment length was measured with ultrasonic crystals placed subendocardially, and ischemia was induced by pacing tachycardia for 3 minutes. Transient vena caval occlusion was done to unload the right ventricle and to produce a series of left ventricular end-diastolic pressure and left ventricular end-diastolic segment length points before and after pacing tachycardia. After pacing tachycardia, left ventricular end-diastolic pressure (9.3 +/- 0.9 to 16.9 +/- 1.5 mm Hg, P less than 0.001) and time constant T of left ventricular isovolumic pressure decline (46 +/- 3 to 60 +/- 5 msec, P less than 0.01) increased, with an increase in left ventricular end-systolic segment length (9.8 +/- 0.3 to 10.5 +/- 0.3 mm, P less than 0.001), and a decrease in fractional shortening (17.6 +/- 1.7 to 14.5 +/- 1.3%, P less than 0.01) in the ischemic region, although right ventricular end-diastolic pressure was unchanged. With vena caval occlusion, right ventricular diastolic pressure fell promptly to near zero, followed by decrease in left ventricular pressure and segment length. In each dog, the left ventricular end-diastolic pressure-end-diastolic segment length relation shifted upward after pacing tachycardia. Pacing tachycardia was performed again in six dogs without stenoses. In this group, fractional shortening was preserved after pacing tachycardia (15.7 +/- 2.3 to 15.3 +/- 2.3%, NS), and left ventricular end-diastolic pressure (9.4 +/- 1.8 to 9.8 +/- 1.8 mm Hg, NS) was unchanged. The left ventricular end-diastolic pressure-segment length relation did not shift upward after pacing tachycardia. These data indicate that extrinsic compression of left ventricle by right ventricle is unlikely to be responsible for the upward shift in this model, and the upward shift in end-diastolic left ventricular pressure-segment length relations, as well as dynamic left ventricular diastolic pressure-segment length, supports the concept that persistent myosin-actin interaction throughout diastole plays an important role in the diastolic abnormalities in this angina physiology model.
Scintigraphic quantification of myocardial necrosis in patients after intravenous injection of myosin-specific antibody.
Authors: B A Khaw, H K Gold, T Yasuda, R C Leinbach, M Kanke, J T Fallon, M Barlai-Kovach, H W Strauss, F Sheehan, E Haber
Journal: Circulation (1986)

The Fab fragments of antimyosin antibodies, labeled with 99mTc, were used in the scintigraphic examination of 30 patients with myocardial infarction. The ability to detect necrosis and determine its extent from the antimyosin scan were compared with the results of quantitative regional wall motion analysis by contrast ventriculography at 10 to 14 days and 99mTc-pyrophosphate imaging. Antimyosin images recorded by planar and single photon-emission computed tomography (SPECT) delineated areas of myocardial necrosis in 27 of 30 patients (90%) compared with a 91% sensitivity of pyrophosphate in 21 of 23 patients. Infarct size was determined by both antimyosin and pyrophosphate SPECT images. Results by both techniques showed a significant correlation with computer-derived hypokinetic segment length (r = .79 for both, p = .002) and peak creatine kinase (r = .9 for both, p less than .01). Although sensitivity for and correlations with markers of necrosis were similar with both techniques, infarct size by pyrophosphate SPECT was 1.7 times larger than infarct size by antimyosin SPECT (p less than .01). Certain zones in the infarct area were differentially labeled; the nature and irreversibility of injury within these zones remains to be clarified.
Distribution of interleukin 1 receptor antagonist protein (IRAP), interleukin 1 receptor, and interleukin 1α in normal and psoriatic skin. Decreased expression of IRAP in psoriatic lesional epidermis
Authors: M. KRISTENSEN, B. DELEURAN, D.J. EEDY, M.F. LDMANN, S.M. BREATHNACH, F.M. BRENNAN
Journal: British Journal of Dermatology (1992)

The distribution of interleukin 1 alpha (IL-1 alpha), type 1 interleukin 1 receptor (IL-1R), and the interleukin 1 receptor antagonist protein (IRAP), was investigated in biopsies of normal skin, and in uninvolved and lesional skin of patients with psoriasis, using specific monoclonal antibodies. We report the novel finding that IRAP is distributed throughout the living layers of the epidermis in normal skin, and is also associated with sebaceous glands and eccrine sweat glands. Our finding that the inhibitor protein IRAP is present in areas where the pro-inflammatory cytokine IL-1 alpha is distributed provides strong evidence in favour of a cytokine regulatory system in normal skin. We further document for the first time that IL-1R in normal skin is localized to the living layers of the epidermis, sebaceous and eccrine glands, as well as to a prominent network of dermal dendritic cells, and upper dermal blood vessels. There was a consistent reduction in the level of IRAP expression in lesional compared with uninvolved skin in biopsies from six out of seven psoriasis patients. Decreased IRAP expression in lesions of psoriasis indicates that alterations in the level of this inhibitor protein may be important in the pathogenesis of inflammatory skin conditions.
Bank Vole a Novel Model of Prion Transmission
Authors: Tracy Hampton
Journal: JAMA (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 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
Evaluating memory clinics
Authors: Steve Iliffe, Jill Manthorpe
Journal: Journal of the Royal Society of Medicine (2010)

Melis and colleagues1 argue for rigorous evaluation of memory clinics but at the same time admit that the need for service development is urgent, given the ageing of the population and the expected rise in the prevalence of dementia syndrome. This dilemma is a common one, and leads to the use of ‘best available’ evidence to inform policy, rather than ‘best quality’.

The National Dementia Strategy proposes a public education campaign about the early signs of dementia and asserts that general practice lacks the skills and confidence to undertake memory assessment. This risks weakening the gatekeeper function of general practitioners (GPs) and an unevaluated expansion of specialist services. The evaluation of such services that Melis and colleagues rightly desire cannot, in such circumstances, be about their effectiveness, since they are needed to manage the demand created by new policies. It could be an evaluation of their costs, and possibly their cost effectiveness.

Since one-quarter of the population aged 65 years and over have sufficient subjective memory impairment to cause them some concern,2 GPs could become very busy referring people with memory lapses to clinics that will in turn become increasingly crowded. Unfortunately subjective memory impairment correlates poorly with objective impairment, and is only a weak predictor of dementia; it is associated more strongly with depression. If those admitting to memory impairment are followed through with psychological testing, only one in five of those who subsequently develop dementia will be identified.3 The memory clinics could quickly fill up with the depressed. There is much that can be done for older people with depression, of course, but this would again require a re-engineering of a memory clinic model. Melis and colleagues have drawn an important issue to our attention.
Four year follow up of fatigue in a geographically defined primary biliary cirrhosis patient cohort
Authors: D E J Jones
Journal: Gut (2005)

Fatigue is the commonest symptom described by patients in most populations with the autoimmune liver disease primary biliary cirrhosis (PBC), and appears to be unrelated to liver disease severity. At present, it is unclear how the fatigue experienced by patients (only characterised to date in cross sectional studies) evolves over time. In this study, we set out to address how fatigue had changed over four years of follow up in a geographically defined cohort of PBC patients who participated in an earlier cross sectional study of fatigue impact.
Predictive value of longitudinal whole-body magnetic resonance imaging in patients with smoldering multiple myeloma
Authors: M Merz, T Hielscher, B Wagner, S Sauer, S Shah, M S Raab, A Jauch, K Neben, D Hose, G Egerer, M-A Weber, S Delorme, H Goldschmidt, J Hillengass
Journal: Leukemia (2014)
<i>In Silico</i> Proteome-Wide Amino aCid and Elemental Composition (PACE) Analysis of Expression Proteomics Data Provides A Fingerprint of Dominant Metabolic Processes
Authors: David M. Good, Anwer Mamdoh, Harshavardhan Budamgunta, Roman A. Zubarev
Journal: Genomics Proteomics & Bioinformatics (2013)

Proteome-wide Amino aCid and Elemental composition (PACE) analysis is a novel and informative way of interrogating the proteome. The PACE approach consists of in silico decomposition of proteins detected and quantified in a proteomics experiment into 20 amino acids and five elements (C, H, N, O and S), with protein abundances converted to relative abundances of amino acids and elements. The method is robust and very sensitive; it provides statistically reliable differentiation between very similar proteomes. In addition, PACE provides novel insights into proteome-wide metabolic processes, occurring, e.g., during cell starvation. For instance, both Escherichia coli and Synechocystis down-regulate sulfur-rich proteins upon sulfur deprivation, but E. coli preferentially down-regulates cysteine-rich proteins while Synechocystis mainly down-regulates methionine-rich proteins. Due to its relative simplicity, flexibility, generality and wide applicability, PACE analysis has the potential of becoming a standard analytical tool in proteomics.
Transient Cardiac Apical Ballooning Syndrome: Prevalence and Clinical Implications of Right Ventricular Involvement
Authors: Ahmad A. Elesber, Abhiram Prasad, Kevin A. Bybee, Uma Valeti, Arashk Motiei, Amir Lerman, Krishnaswamy Chandrasekaran, Charanjit S. Rihal
Journal: Journal of the American College of Cardiology (2006)
Mucosal memory CD8+ T cells are selected in the periphery by an MHC class I molecule
Authors: Yujun Huang, Yunji Park, Yiran Wang-Zhu, Alexandre Larange, Ramon Arens, Iván Bernardo, Danyvid Olivares-Villagómez, Dietmar Herndler-Brandstetter, Ninan Abraham, Beatrix Grubeck-Loebenstein, Stephen P Schoenberger, Luc Van Kaer, Mitchell Kronenberg, Michael A Teitell, Hilde Cheroutre
Journal: Nature Immunology (2011)
A sinister cause of back pain in a young man
Authors: A. B. O'Keeffe, J. Terris, P. Hormbrey
Journal: BMJ (2012)

A 16 year old man presented to the emergency department with a two week history of back pain in the left lower lumbar region. The pain came on suddenly while he was bending over and persisted as a dull ache. The pain was associated with him waking up at night feeling sweaty and feverish. His general practitioner had suspected a urinary tract infection after a urine dipstick tested positive for blood and protein. A course of nitrofurantoin did not improve his symptoms. He presented to the emergency department with difficulty bearing weight on his left leg. He kept his left hip and knee flexed at 45° when lying supine. Systems review was unremarkable. The only positive finding on examination was tenderness over the left paraspinal region at the level of L4-L5, with no associated skin changes.

He had a heart rate of 70 beats/min, respiratory rate of 14 breaths/min, blood pressure of 116/86 mm Hg, and temperature of 36.9oC. Blood (++) and protein (+) were seen on urinalysis, but no nitrites or leucocytes. Routine blood results were normal except for a C reactive protein >160 mg/L (normal range 0.0-5.0), neutrophils 8.4×109/L (2.0-7.5), and monocytes 1.48×109/L (0.2-1.0). Magnetic resonance imaging (MRI) was performed (fig 1 ⇓).





### 1 What does magnetic resonance imaging show?

#### Short answer

This STIR (short T1 inversion recovery) MRI scan shows high signal in the L5 vertebral body, with a large paraspinal high signal area that displaces the body of the left psoas muscle laterally (fig 2⇓). There is no abnormality of the intervertebral discs. The most likely diagnosis …
Attenuation of the Glucocorticoid Response during Ad5IL-12 Adenovirus Vector Treatment Enhances Natural Killer Cell–Mediated Killing of MHC Class I–Negative LNCaP Prostate Tumors
Authors: Claudia Raja Gabaglia, Yaiza Diaz de Durana, Frank L. Graham, Jack Gauldie, Eli E. Sercarz, Todd A. Braciak
Journal: Cancer Research (2007)

Abstract Tumor cells can evolve to evade immune responses by down-modulating surface MHC class I expression and become refractory to T cell–directed immunotherapy. We employed a strategy to bypass this escape mechanism using a recombinant adenovirus vector expressing interleukin-12 (Ad5IL-12) to target natural killer (NK) cell–mediated killing of human prostate tumors in NOD.scid mice. Fluorescence-activated cell sorting analysis revealed that LNCaP tumor cells bear negligible levels of MHC class I molecules; yet, they express MICA/B molecules, ligands for the NKG2D receptors found on NK cells. Transduction of LNCaP cells with the Ad5IL-12 vector prevented tumor formation in NOD.scid mice, indicating that NK cells alone can conduct tumor immunosurveillance and mediate protection. Intratumor injection of the Ad5IL-12 vector to established LNCaP tumors in NOD.scid mice resulted in a significant delay of tumor growth mediated by NK cell killing activity. The dependency of NK cells in this protective response was shown by the complete loss of Ad5IL-12 therapeutic efficacy on LNCaP tumors established in NOD.Cg-Rag1tm1MomPrf1tm1Sdz congenic mice, which are devoid of NK cell activity. More pronounced attenuation of tumor growth and enhanced NK killing activity was observed when pharmacologic adrenalectomy with mitotane was done in combination with Ad5IL-12 vector treatment. The Ad5IL-12 vector treatment also induced killing of MICA/B-negative MHC class I–positive PC3 tumors formed in NOD.scid mice. Together, these results indicate that a targeted NK cell response could provide a generic approach for cancer immunotherapy, and that enhancing the NK cell response via control of cortisol levels may provide an additional therapeutic avenue in cancer. [Cancer Res 2007;67(5):2290–7]
SYPHILIS OF THE LIVER.
Authors: CHARLES G. STOCKTON
Journal: JAMA (1902)

Two notable contributions on the morbid anatomy of hepatic syphilis, the one by Adami<sup>1</sup>the other by Flexner,<sup>2</sup>render superfluous any review which I might make of this part of the question. Although the chief pathologic changes induced by syphilis of the liver appear to have been carefully studied and classified, the clinician occasionally meets with instances of undoubted syphilis in which there develop hepatic manifestations that so puzzle him as to the precise character of the morbid change that classification has to be abandoned. There is abundant literature of the classical expressions of the disease with which all recognized students substantially agree, and there are to be found many scattered reports of individual cases that are sufficiently rare to warrant description; but these are so commonly benefited by treatment that they either escape autopsy altogether or else are delayed until the specific effects of mercury or iodid
Anaphylatoxin-induced histamine release with human leukocytes: studies of C3a leukocyte binding and histamine release.
Authors: M M Glovsky, T E Hugli, T Ishizaka, L M Lichtenstein, B W Erickson
Journal: Journal of Clinical Investigation (1979)

Purified human C3a and synthetic COOH-terminal peptides of C3a, i.e., a pentapeptide, Leu-Gly-Leu-Ala-Arg (5R), and an octapeptide, Ala-Ala-Ala-Leu-Gly-Leu-Ala-Arg (8R) induced histamine release from human basophil granulocytes. On a molar basis, 5R was one-tenth and 8R was one-fifth as active as C3a in causing histamine release. It was found that 125I-C3a binds to whole leukocytes, interacting with both mononuclear cells and neutrophils and the binding was inhibited by preincubation of cells with unlabeled C3a, but not by C5a. 5R and 8R also inhibited the binding of 125I-C3a to the cells. However, on a molar basis, 2,000 times more 8R or 6,000 times more 5R is required for 50% inhibition of 125I-C3a binding as compared with native C3a. Autoradiography of cells using 125I-C3a and 125I-C5a showed preferential binding of 125I-C3a to eosinophils and basophils, whereas 125I-C5a binds primarily to neutrophils and eosinophils and to a lesser extent to basophils. The preferential binding of C3a and C5a to different cell types may herald significance related to their physiological functions.
Incidence of primary cutaneous T-cell lymphoma in Norway
Authors: M. Saunes, T.I. Lund Nilsen, T.B. Johannesen
Journal: British Journal of Dermatology (2008)

Journal Article Incidence of primary cutaneous T‐cell lymphoma in Norway Get access M. Saunes, M. Saunes Department of Dermatology, St Olavs Hospital, Trondheim University Hospital, and Department of Cancer Research & Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway Correspondence: Marit Saunes. E‐mail: marit.saunes@ntnu.no Search for other works by this author on: Oxford Academic Google Scholar T.I. Lund Nilsen, T.I. Lund Nilsen Human Movement Science Programme, Norwegian University of Science and Technology, Trondheim, Norway Search for other works by this author on: Oxford Academic Google Scholar T.B. Johannesen T.B. Johannesen Cancer Registry of Norway, Institute of Population‐Based Cancer Research, Oslo, Norway Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 160, Issue 2, 1 February 2009, Pages 376–379, https://doi.org/10.1111/j.1365-2133.2008.08852.x Published: 01 February 2009