tbuckley/cabot-search huggingface dataset:
Cytokine Gene Expression After Myocardial Infarction in Rat Hearts
Authors: Koh Ono, Akira Matsumori, Tetsuo Shioi, Yutaka Furukawa, Shigetake Sasayama
Journal: Circulation (1998)

A large transmural myocardial infarction may initiate structural and geometric changes in the left ventricle that are commonly referred to as remodeling. Progressive, adverse remodeling of the myocardium may lead to ventricular dilatation and congestive heart failure. Recent studies have highlighted the effects of some cytokines on immune-mediated myocyte injury, postischemic myocardial inflammation, and cardiac function. However, studies of the involvement of cytokines in remodeling of the heart are few.In a rat model of myocardial infarction, progressive dilatation of the left ventricular cavity and lack of appropriate hypertrophy of the surviving myocardium were confirmed by transthoracic echocardiography. The relative expression of mRNA for tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 in the infarcted and noninfarcted myocardium of these rats, as well as in a group of sham-operated animals, was assessed by the technique of quantitative polymerase chain reaction amplification. In the infarcted region, TNF-alpha, IL-1beta, and IL-6 gene expression peaked at 1 week after infarction and decreased rapidly thereafter. In contrast, at 20 weeks after infarction, the gene expression levels of these cytokines remained significantly higher in the noninfarcted than in the infarcted zone or in the myocardium of sham-operated animals. Furthermore, the levels of these cytokines in the noninfarcted region correlated with the left ventricular end-diastolic diameter measured at 8 and 20 weeks after infarction. Among these cytokines, IL-1beta expression was highest, and its level correlated well with collagen deposition in the noninfarcted myocardium at 8 and 20 weeks after surgery. At 20 weeks after infarction, immunohistochemical analysis revealed the presence of IL-1beta in macrophages, endothelial cells, and vascular smooth muscle cells in the noninfarcted region, whereas no such immunoreactivity was found in the myocardium of sham-operated animals.These findings suggest the possible involvement of cytokines during the remodeling process of the noninfarcted left ventricular myocardium.
Glomerular and tubular adaptive responses to acute nephron loss in the rat. Effect of prostaglandin synthesis inhibition.
Authors: J C Pelayo, P F Shanley
Journal: Journal of Clinical Investigation (1990)

These studies, using in vivo micropuncture techniques in the Munich-Wistar rat, document the magnitude of changes in glomerular and tubular function and structure 24 h after approximately 75% nephron loss (Nx) and compared these results with those obtained in sham-operated rats. The contribution of either nephron hypertrophy or renal prostaglandin to these adjustments in nephron function was also explored. After acute Nx, single nephron GFR (SNGFR) was increased, on average by approximately 30%, due primarily to glomerular hyperperfusion and hypertension. The approximately 45% reduction in preglomerular and the constancy in postglomerular vascular resistances was entirely responsible for these adaptations. Although increases in fluid reabsorption in proximal convoluted tubules correlated closely with increase in SNGFR, the fractional fluid reabsorption between late proximal and early distal tubular segments was depressed. Nephron hypertrophy could not be substantiated based on either measurements of protein content in renal tissue homogenates or morphometric analysis of proximal convoluted tubules. However, acute Nx was associated with increased urinary excretory rates per functional nephron for 6-keto-PGF1 alpha and TXB2. Prostaglandin synthesis inhibition did not affect function in control nephrons, but this maneuver was associated with normalization of glomerular and tubular function in remnant nephrons. The results suggest that enhanced synthesis of cyclooxygenase-dependent products is one of the earliest responses to Nx, and even before hypertrophy the pathophysiologic effects of prostaglandin may be important contributors to the adaptations in remnant nephron function.
One-Month Diesel Exhaust Inhalation Produces Hypertensive Gene Expression Pattern in Healthy Rats
Authors: Reddy R. Gottipolu, J. Grace Wallenborn, Edward D. Karoly, Mette C. Schladweiler, Allen D. Ledbetter, Todd Krantz, William P. Linak, Abraham Nyska, Jo Anne Johnson, Ronald Thomas, Judy E. Richards, Richard H. Jaskot, Urmila P. Kodavanti
Journal: Environmental Health Perspectives (2008)

Exposure to diesel exhaust (DE) is linked to vasoconstriction, endothelial dysfunction, and myocardial ischemia in compromised individuals.We hypothesized that DE inhalation would cause greater inflammation, hematologic alterations, and cardiac molecular impairment in spontaneously hypertensive (SH) rats than in healthy Wistar Kyoto (WKY) rats.Male rats (12-14 weeks of age) were exposed to air or DE from a 30-kW Deutz engine at 500 or 2,000 microg/m3, 4 hr/day, 5 days/week for 4 weeks. Neutrophilic influx was noted in the lung lavage fluid of both strains, but injury markers were minimally changed. Particle-laden macrophages were apparent histologically in DE-exposed rats. Lower baseline cardiac anti-oxidant enzyme activities were present in SH than in WKY rats; however, no DE effects were noted. Cardiac mitochondrial aconitase activity decreased after DE exposure in both strains. Electron microscopy indicated abnormalities in cardiac mitochondria of control SH but no DE effects. Gene expression profiling demonstrated alterations in 377 genes by DE in WKY but none in SH rats. The direction of DE-induced changes in WKY mimicked expression pattern of control SH rats without DE. Most genes affected by DE were down-regulated in WKY. The same genes were down-regulated in SH without DE producing a hypertensive-like expression pattern. The down-regulated genes included those that regulate compensatory response, matrix metabolism, mitochondrial function, and oxidative stress response. No up-regulation of inflammatory genes was noted.We provide the evidence that DE inhalation produces a hypertensive-like cardiac gene expression pattern associated with mitochondrial oxidative stress in healthy rats.
Multiple Sclerosis and Hysteria
Authors: Charles D. Aring
Journal: JAMA (1981)

<h3>To the Editor.—</h3> In their article on "Multiple Sclerosis [MS] and Hysteria: Lessons Learned From Their Association," Caplan and Nadelson (1980;243:2418) note a modicum of confusion with something I wrote on the subject in 1965.<sup>1</sup> I liked the speculation of Langworthy<sup>2</sup>that the hysteria and MS in those patients with whom he worked might represent branches off of the same trunk. I saw nothing to be gained in the discussion of organic vs functional dichotomy, which at the time was absorbing so much energy, time, and talent to the detriment of the patient. This is in accord with the dynamic approach advocated by Caplan and Nadelson. As then, and in considering the present state of the art, I see nothing to be gained in separating clinically what Wilson<sup>3</sup>termed the predisseminated type of MS from conversion hysteria, where the symptoms are compatible in the patient. There is
Abstract 8128: Clinical Implications of ST-Segment Elevation in Leads V5-6 in Patients with Reperfused Inferior Wall Acute Myocardial Infarction
Authors: Masami Kosuge, Toshiaki Ebina, Kiyoshi Hibi, Mitsuaki Endo, Nobuhiko Maejima, Noriaki Iwahashi, Satoshi Morita, Kazuaki Uchino, Toshiyuki Ishikawa, Satoshi Umemura, Kazuo Kimura
Journal: Circulation (2011)

Background: During inferior wall acute myocardial infarction (IWMI), ST-segment elevation (ST↑) often occurs in leads V5-6, but its clinical implications remain unclear. Methods: We examined admission ECG in 357 patients with a first IWMI who had TIMI 3 flow of the right coronary artery (RCA) or left circumflex artery (LCX) within 6 h after symptom onset. Patients were divided according to the presence (n=76) or absence (n=281) of ST↑ of &gt;2 mm in leads V5-6. Patients in the former group were divided into the 2 subgroups according to the degrees of ST↑ in leads III and V6: ST↑ III&gt;V6 (n=53) and ST↑ III&lt;V6 (n=23). The perfusion territory of the culprit artery was assessed on the basis of the angiographic distribution score, and mega-artery was defined as a score of &gt;0.7. Results: Both ST↑ in leads V5-6 with ST↑ III&gt;V6 and that with ST↑ III&lt;V6 were associated with mega-artery occlusion, impaired myocardial reperfusion as defined by myocardial blush grade 0/1 on the final angiogram, and a larger infarct size. RCA occlusion was most common in the former, whereas LCX occlusion, especially proximal LCX occlusion, was most common in the latter. Multivariate analysis showed that both ST↑ in leads V5-6 with ST↑ III&gt;V6 (odds ratio 4.81, 95%CI 2.10-11.0, p&lt;0.001) and that with ST↑ III&lt;V6 (odds ratio 5.96, 95%CI 3.28-27.6, p&lt;0.001) were independent predictors of impaired myocardial reperfusion; but ST↑ in leads II, III, and aVF was not. Conclusions: In patients with reperfused IWMI, ST↑ in leads V5-6 on admission ECG was associated with mega-artery occlusion with a larger infarct size; furthermore, it was a strong predictor of impaired myocardial reperfusion. In addition, by comparing the degree of ST↑ in lead V6 with that in lead III, we could differentiate between RCA occlusion and LCX occlusion.
Pain Threshold and Arthritis
Authors: E. C. Huskisson, F. D. Hart
Journal: BMJ (1972)

Pain threshold was measured in 106 patients with rheumatoid arthritis, 50 with ankylosing spondylitis, and 50 normal controls using Keele9s algometer. In rheumatoid arthritis patients with a low pain threshold had more severe pain for a greater part of the day and required more tablets for pain relief. In ankylosing spondylitis the pain threshold was higher and was not related to pain or analgesic requirements. There was no evidence that pain threshold affected the course or outcome of rheumatoid arthritis in any way.
Comparison of IgE‐binding antigens in horse dander and a mixture of horse hair and skin scrapings
Authors: B. E. Fjeldsgaard, B. Smestad Paulsen
Journal: Allergy (1993)

Extracts of horse dander (HD) and horse hair and skin scrapings (HHSS) have been compared with respect to their content of proteins and carbohydrates. The protein content of HD is more than double that of HHSS, while the carbohydrate content is of the same order. SDS‐PAGE and IEE, both combined with immunoblotting, and CIE/CRIE showed the IgE‐binding ability of the proteins/glycoproteins present in the two extracts. SDS‐PAGE/immunoblotting showed the presence of mainly the same IgE‐binding bands in the two extracts. Nine were detected in HD, and seven in HHSS. Four of these were glycoproteins. The most important allergen was a glycoprotein with molecular mass of 27 kDa showing IgE‐binding ability to the 16 patient sera available. Another important allergen with molecular mass of 67 kDa is probably horse albumin, IEF/immunoblotting showed the presence of a glycoprotein with IgE‐binding ability at pH 3.2 in both extracts. Tandem CRIE showed that both extracts contained the same four allergens as major allergens. In addition, as we observed when analyzing both extracts in CRIE against 16 different patient sera, each extract contained allergens not present in the other extract. We may conclude from this investigation that commercial allergen extracts to be used in diagnosis and immunotherapy should include both horse dander and horse hair and skin scrapings in the starting material for the preparation of extracts. If not, allergens which may be of importance for some patients will be missing.
Sex Differences in Hospital Mortality in Adults With Congenital Heart Disease
Authors: A. Carla Zomer, Raluca Ionescu-Ittu, Ilonca Vaartjes, Louise Pilote, Andrew S. Mackie, Judith Therrien, Maurice M. Langemeijer, Diederick E. Grobbee, Barbara J.M. Mulder, Ariane J. Marelli
Journal: Journal of the American College of Cardiology (2013)
A Framework for Widespread Replication of a Highly Spatially Resolved Childhood Lead Exposure Risk Model
Authors: Dohyeong Kim, M. Alicia Overstreet Galeano, Andrew Hull, Marie Lynn Miranda
Journal: Environmental Health Perspectives (2008)

Preventive approaches to childhood lead poisoning are critical for addressing this longstanding environmental health concern. Moreover, increasing evidence of cognitive effects of blood lead levels < 10 microg/dL highlights the need for improved exposure prevention interventions.Geographic information system-based childhood lead exposure risk models, especially if executed at highly resolved spatial scales, can help identify children most at risk of lead exposure, as well as prioritize and direct housing and health-protective intervention programs. However, developing highly resolved spatial data requires labor-and time-intensive geocoding and analytical processes. In this study we evaluated the benefit of increased effort spent geocoding in terms of improved performance of lead exposure risk models.We constructed three childhood lead exposure risk models based on established methods but using different levels of geocoded data from blood lead surveillance, county tax assessors, and the 2000 U.S. Census for 18 counties in North Carolina. We used the results to predict lead exposure risk levels mapped at the individual tax parcel unit.The models performed well enough to identify high-risk areas for targeted intervention, even with a relatively low level of effort on geocoding.This study demonstrates the feasibility of widespread replication of highly spatially resolved childhood lead exposure risk models. The models guide resource-constrained local health and housing departments and community-based organizations on how best to expend their efforts in preventing and mitigating lead exposure risk in their communities.
Interferon in Human Infections with St. Louis Encephalitis Virus
Authors: JAMES P. LUBY
Journal: Annals of Internal Medicine (1969)

The epidemic of St. Louis encephalitis in Dallas, Tex., 1966, afforded an opportunity to assess the role of interferon in human infections with this virus. Ninety-seven sera from 74 patients and 13 urine specimens from 13 patients, all with laboratory-documented St. Louis encephalitis and collected, for the most part, during the first week of illness, had no detectable interferon. Suspensions of different sections of brain, liver, kidney, and spleen from eight patients dying with St. Louis encephalitis were also assayed. Interferon was detected in suspensions of brain from three patients from whom St. Louis encephalitis virus was isolated and who died early in the course of illness. Two patients had St. Louis encephalitis virus isolated from brain but had no detectable interferon. These two patients had severe underlying illnesses: chronic lymphocytic leukemia and arteriolar nephrosclerosis with uremia. The remaining three patients died later in the course of illness, and neither virus nor interferon could be demonstrated in postmortem specimens.
THE FORMATION OF URIC ACID.
Authors: LAFAYETTE B. MENDEL
Journal: JAMA (1906)

The rôle of uric acid in physiology and pathology has long formed a theme for unrestricted discussion and controversy in scientific literature. The wealth of published contributions on this subject abounds in the most characteristic specimens of what a recent medical writer has aptly termed "truth and poetry about uric acid." Nevertheless the student of the physiology of uric acid can not fail to recognize a number of distinct epochs representing the introduction of new discoveries and consequent altered points of view in the interpretation of familiar phenomena. When the secret of each novel attitude is revealed it no longer becomes difficult to follow the march of progress in science; and, what is all-important, we are thus enabled to revise or formulate anew the problems with the solution of which advancement is coincident. This society, so happily inaugurated "for the diffusion of the knowledge of the medical sciences," will accomplish
Hypokalemic Periodic Paralysis with Arrhythmia
Authors: Lawrence P. Levitt, Leslie I. Rose, David M. Dawson
Journal: New England Journal of Medicine (1972)

IN 1963, Klein and his co-workers1 described a variant of periodic paralysis in which intermittent attacks of muscular paralysis occurred in patients who also had cardiac arrhythmia. Both their patients had normokalemic paralysis. Recently, Lisak et al.2 reported a case of hyperkalemic periodic paralysis with arrhythmia.Case ReportA.M., a 7-year-old boy, was referred to Children's Hospital in 1966 by his physician, who had obtained a history of intermittent fatigue and had noted a cardiac arrhythmia. None of 10 siblings had similar complaints. Pertinent findings included normal heart examination, hypoactive deep tendon reflexes and an electrocardiogram with normal sinus rhythm, . . .
Programme for genetic diagnosis of rare diseases proves feasible for routine clinical practice
Authors: S. Mayor
Journal: BMJ (2014)

A nationwide programme to genetically diagnose rare diseases is feasible for use in routine NHS patient care, results from the first 1000 families analysed have shown.1

Use of genomic sequencing to diagnose disease requires robust systems to track individual samples and datasets, prioritise plausible pathogenic variants, filter out benign variants, and link findings to individual clinical data for interpretation and clinical follow-up.

The Deciphering Developmental Disorders (DDD) project has developed a UK-wide network of clinicians working across all 24 regional genetics services, to …
Group Seeks to Improve Nonmedical Aspects of Health in the United States
Authors: Tracy Hampton
Journal: JAMA (2008)

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
Provision of donors for renal transplantation 1978-80.
Authors: A D Barnes
Journal: BMJ (1981)

Regulation of myeloid-derived suppressor cells (MDSC) by ongoing inflammation following repeated chemotherapy remain elusive. In this study, we show that a multidose clinical regimen of gemcitabine (GEM) treatment enhances the immunosuppressive function of monocytic MDSC (M-MDSC), although tumor development is delayed in E0771 tumor-bearing mice. Accordingly, effector IFN-γ–producing CD4 and CD8 T cells are significantly decreased in the tumor microenvironment (TME) of GEM-treated mice. The conditioned medium of GEM-treated tumor cells enhances differentiation of mouse bone marrow cells and human PBMC into immunosuppressive M-MDSC. Cytokine profiling of GEM-treated tumor cells identifies GM-CSF as one of the most differentially expressed cytokines. Blockade or knockdown of GM-CSF can partially reduce immunosuppression of Ly6C<sup>high</sup> cells induced by GEM–conditioned medium. Knockdown of GM-CSF in tumor cells also delays tumor progression with decreased accumulation of M-MDSC in the TME. Mechanistically, enhanced production of reactive oxygen species and activation of NF-κB are observed in GEM-treated tumor cells. Treatment with the mitochondrial-targeted antioxidant and inhibitor of NF-κB signaling can abrogate GEM-induced hyperexpression of GM-CSF in E0771 cells. In addition, the phagocytic clearance of apoptotic tumor cells (efferocytosis) enhances the immunosuppressive function of bone marrow Ly6C<sup>high</sup> myeloid cells. Further, GEM treatment results in metabolic changes in residual tumor cells, leading to the resistance to T cell–mediated killing. Together, our results define an undesired effect of repeated GEM treatment promoting immunosuppression in TME via upregulation of GM-CSF and efferocytosis as well as deregulation of lipid metabolism in residual tumor cells.
Honey bee (<i>Apis mellifera</i>) venom induces <scp>AIM</scp>2 inflammasome activation in human keratinocytes
Authors: Y. Dombrowski, M. Peric, S. Koglin, N. Kaymakanov, V. Schmezer, M. Reinholz, T. Ruzicka, J. Schauber
Journal: Allergy (2012)

Abstract Background Following allergen exposure, cytokines and other pro‐inflammatory signals play an important role in the immunological cascade leading to allergic sensitization. Inflammasomes sense exogenous and endogenous danger signals and trigger IL ‐1β and IL ‐18 activation which in turn shape Th2 responses. Honey bee venom ( BV ) allergies are very common; however, the local inflammatory cascade leading to the initiation of allergic sensitization is poorly understood. In this study, the local inflammatory cascades in skin after exposure to BV were investigated. Methods The mechanisms of inflammasome activation in human skin and in cultured keratinocytes upon BV exposure were analyzed by ELISA , Western blot, flow cytometry, si RNA techniques, and immunofluorescence. Results In an ex vivo bee sting model, BV induced IL ‐1β release suggesting the activation of inflammasomes. Indeed, in cultured keratinocytes, the BV component melittin triggered IL ‐1β and IL ‐18 release via the AIM 2 inflammasome. AIM 2 is a cytosolic DNA receptor, and mitochondrial as well as genomic DNA was detected in the cytosol of melittin‐treated keratinocytes as triggers of inflammasome activation. As a mechanism, melittin mediated destruction of mitochondrial membranes leading to the leakage of mitochondrial DNA into the cytosolic compartment. Conclusion These data suggest that upon BV exposure, keratinocytes are involved in an innate immune response by the activation of the AIM 2 inflammasome and subsequent IL ‐1β and IL ‐18 release triggered by endogenous DNA . As IL ‐1β and IL ‐18 are involved in Th2‐ and IgE‐mediated immune reactions, these results could add to the understanding of the role of the tissue microenvironment to subsequent allergic responses.
Eosinophilic cellulitis—persistent cutaneous swelling with phagocytosis of eosinophilic debris
Authors: G.C. Wells, N. Smith
Journal: British Journal of Dermatology (1978)

Journal Article Eosinophilic cellulitis—persistent cutaneous swelling with phagocytosis of eosinophilic debris Get access G.C. Wells, G.C. Wells St John's Hospital for Diseases of the Skin, London WC2 Search for other works by this author on: Oxford Academic Google Scholar N. Smith N. Smith St John's Hospital for Diseases of the Skin, London WC2 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 99, Issue s16, 1 December 1978, Page 11, https://doi.org/10.1111/j.1365-2133.1978.tb15203.x Published: 01 December 1978