tbuckley/cabot-search huggingface dataset:
HDL protein composition alters from proatherogenic into less atherogenic and proinflammatory in rheumatoid arthritis patients responding to rituximab
Authors: Hennie G Raterman, Han Levels, Alexandre E Voskuyl, Willem F Lems, Ben A Dijkmans, Michael T Nurmohamed
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Objective</h3> An atherogenic lipid profile is an established risk factor for cardiovascular (CV) diseases. Interestingly, high inflammatory states as present in rheumatoid arthritis (RA) are associated with unfavourable lipid profile. Data about effects of novel immunomodulating agents as rituximab (RTX) on lipid profile are limited. Therefore, changes in lipids in RTX treated RA patients were evaluated. <h3>Methods</h3> In 49 consecutive RTX treated RA patients, serum and EDTA plasma samples were collected at baseline, 1, 3 and 6 months. In these samples, lipid and levels were assessed to determine changes in time. Surface-enhanced laser desorption/ionisation time-of-flight (SELDI-TOF) MS analysis was performed in six good and six non-responding RA patients to study functional high density lipoprotein (HDL) protein composition changes in time. <h3>Results</h3> In the total group (n=49), the atherogenic index decreased from 4.3 to 3.9 (∼9%) after 6 months. Testing for effect modification revealed a difference in the effect on lipid levels between responders and non-responders upon RTX (p&lt;0.001). ApoB to ApoA-I ratios decreased significantly (∼9%) in good responding (n=32) patients. SELDI-TOF MS analysis revealed a significant decrease in density of mass charge (m/z) marker 11743, representing a decrease in serum amyloid A, in good responding patients. <h3>Conclusion</h3> This study indicates beneficial effects on cholesterol profile upon RTX treatment along with improvement of disease activity. Proteomic analysis of the HDL particle reveals composition changes from proatherogenic to a less proatherogenic composition during 6 months RTX treatment. Whether these HDL particle alterations during immunotherapies result in a lower CV event rate remains to be established.
Primary and Transplantable Adenocarcinomas of the A × C Rat Ventral Prostate Gland: Morphologic Characterization and Examination of C&lt;sub&gt;19&lt;/sub&gt;-Steroid Metabolism by Early-Passage Tumors&lt;xref ref-type="fn" rid="fn2"&gt;2&lt;/xref&gt;
Authors: S A Shain, B McCullough, W M Nitchuk
Journal: JNCI Journal of the National Cancer Institute (1979)

Spontaneous adenocarcinomas of the ventral prostate gland were observed with a frequency of 70% in a population of 33 aged (30- to 46-month-old), virgin male A × C rats. Some of these adenocarcinomas involved multiple acini, and in 6 rats the lesions were bilateral. Atypical hyperplasia of ventral prostate acinar epithelium was also observed. It consisted of thickened epithelium in which various numbers of epithelial cells had swollen, foamy, periodic acid-Schiff-positive cytoplasm and condensed, eccentric nuclei. The atypical hyperplasia was found in association with both atrophic and neoplastic epithelium. Treatment with exogenous testosterone caused the development of columnar epithelium in many of the ventral prostate acini, increased the frequency of detected adenocarcinoma, and amplified the anaplastic characteristics of neoplastic cells. The malignant character of these spontaneous prostate adenocarcinomas was demonstrated by their transplantability to male A × C rats. The transplantable prostate adenocarcinomas were composed of neoplastic epithelial cells that were arranged in cribriform patterns and supported by a delicate connective tissue stroma. In addition, highly anaplastic epithelial cells growing in sheets were also present. When compared to nonneoplastic ventral prostate glands of senescent A × C rats, testosterone metabolism by the transplantable adenocarcinomas was distinguished by a shift to more prominent elaboration of 17-ketosteroids, principally 4androstenedione, and a concomitant decreased production of 5αreduced 17β-hydroxysteroids. Most acid phosphatase activity of the transplantable adenocarcinomas was tartrate-inhibitable. The data suggested that these early-passage tumors retain biochemical properties characteristic of differentiated prostate acinar epithelium.
Developmental Aspects of Long QT Syndrome Type 3 and Brugada Syndrome on the Basis of a Single SCN5AMutation in Childhood
Authors: Gertie C.M. Beaufort-Krol, Maarten P. van den Berg, Arthur A.M. Wilde, J. Peter van Tintelen, Jan Willem Viersma, Connie R. Bezzina, Margreet Th.E. Bink-Boelkens
Journal: Journal of the American College of Cardiology (2005)
Time required for disappearance of urate crystals from synovial fluid after successful hypouricaemic treatment relates to the duration of gout
Authors: E. Pascual, F. Sivera
Journal: Annals of the Rheumatic Diseases (2007)

<b>Objectives:</b> To determine whether hypouricaemic treatment results in the disappearance of urate crystals from gouty joints and to define the time required. <b>Methods:</b> In 18 patients with monosodium urate (MSU) crystal proven gout, and after the initiation of successful serum uric acid (SUA)-lowering treatment, an arthrocentesis of the asymptomatic signal joint (11 knees, 7 first metatarsophalangeal joints) was performed every 3 months to obtain a synovial fluid (SF) sample. The sample was then analysed for the presence of MSU crystals, and the number of crystals/400× field was noted. SUA levels and the duration of gout were also noted. <b>Results:</b> MSU crystals disappeared from the SF of all 18 joints after reduction of SUA to normal levels. The time required for disappearance ranged from 3 to 33 months; disappearance time correlated with the duration of gout (<i>r</i><sub>s</sub> = 0.71; p&lt;0.01). The median number of MSU crystals in the SF samples before urate-lowering treatment was 7.5 (2.5–11) crystals/400× field, reducing to 3 (1–6.5) crystals/400× field (p&lt;0.05) at 3 months. Crystal counts continued to decrease after 3 months. <b>Conclusions:</b> In gout, reduction of SUA to normal levels results in disappearance of urate crystals from SF, requiring a longer time in those patients with gout of longer duration. This indicates that urate crystal deposition in joints is reversible. Normalisation of SUA levels results in a decrease in the concentration of MSU crystals in SF in the asymptomatic gouty joints. This may partially explain the reduced frequency of gouty attacks when a patient has been treated with SUA-lowering drugs.
Abstract 3766: Development of a model using genetics and PSA to reduce unnecessary prostate biopsies
Authors: Deanna S. Cross, Catherine McCarty, Douglas J. Reding
Journal: Cancer Research (2010)

Abstract Background: Prostate cancer screening with PSA has decreased the average age of prostate cancer detection and increased the number of men who undergo prostate biopsies. Currently two thirds of the prostate biopsies performed due to a high PSA test are negative for prostate cancer leading to unnecessary expense and distress for the individual. One way to decrease the unnecessary procedures associated with PSA screening would be to identify individuals who are at higher or lower risk of prostate cancer using newly discovered genetic and environmental risk factors. Aims: Using the males in the Personalized Medicine Research Project (PMRP) population that have had a PSA test, determine if genetic and environmental factors can be incorporated into the PSA screening model to better discriminate individuals who will have a diagnosis of prostate cancer from those with negative biopsies. Methods: All men in PMRP who have had a PSA test (N=4659) were genotyped for 12 polymorphisms that have been associated with prostate cancer in GWAS studies and an additional 52 polymorphisms that were associated with a number of diseases. We also included dietary history, particularly dairy intake if available for the individual. Results: A total of 935 of the 4659 men in the study have had a prostate biopsy with a positive biopsy rate of 34%. Using a panel of 12 previously identified polymorphisms; seven were significantly associated with prostate cancer in our population. Another three polymorphisms were found to be associated in our population (LPL rs328, NOS3 rs1799983, and PON2 rs7493). None of the tested polymorphisms were associated with the biopsy procedure. Individuals with 4 or fewer of the 10 associated risk alleles (17.33% of the population) were more likely to have a negative biopsy (OR 1.87 p=0.0017) while those individuals who have 8 or more associated risk alleles (11% of the population) were more likely to have a positive biopsy (OR 2.68). Conclusions: The PMRP population that has experienced at least one PSA screen is a viable population for testing new screening algorithms that incorporate genetic and environmental factors for better identification of prostate cancer risk. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3766.
ON THE SIGNIFICANCE OF CERTAIN NERVE CELL CHANGES, PROBABLY TOXIC, IN RELATION TO CLINICAL DIAGNOSIS
Authors: Otis F. Kelly
Journal: American Journal of Psychiatry (1924)

This is an account of observations on a condition of the cortical ganglion cells believed by the writer to be caused probably by the action of severe toxic or retained metabolic substances, the observations having been made in the course of routine study of state hospital autopsy material. It has been reported by Mott as occurring in dementia præcox, and by Dunlap as occurring in control cases. Comparison of histological findings in certain cases of acute mania- cal near delirious states thought to be manic depressive psychoses with similar findings in uremic and severely toxic conditions of more or less chronicity, aside from its purely histological interest, also affords an example of one way in which coöperation between the state hospital laboratory (the decline of which is alluded to in the body of this paper) and the state hospital clinical staff, can be valuable without being spectacular.
Adverse Events Associated With Stopping Clopidogrel After Acute Coronary Syndrome—Reply
Authors: P. Michael Ho
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
Plasma glutamate–modulated interaction of A2AR and mGluR5 on BMDCs aggravates traumatic brain injury–induced acute lung injury
Authors: Shuang-Shuang Dai, Hao Wang, Nan Yang, Jian-Hong An, Wei Li, Ya-Lei Ning, Pei-Fang Zhu, Jiang-Fan Chen, Yuan-Guo Zhou
Journal: The Journal of Experimental Medicine (2013)

The bone marrow-derived cell (BMDC)-associated inflammatory response plays a key role in the development of acute lung injury (ALI). Activation of adenosine A2A receptor (A2AR) is generally considered to be antiinflammatory, inhibiting BMDC activities to protect against ALI. However, in the present study, we found that in a mouse model of neurogenic ALI induced by severe traumatic brain injury (TBI), BMDC A2AR exerted a proinflammatory effect, aggravating lung damage. This is in contrast to the antiinflammatory effect observed in the mouse oleic acid-induced ALI model (a nonneurogenic ALI model.) Moreover, the A2AR agonist CGS21680 aggravated, whereas the antagonist ZM241385 attenuated, the severe TBI-induced lung inflammatory damage in mice. Further investigation of white blood cells isolated from patients or mouse TBI models and of cultured human or mouse neutrophils demonstrated that elevated plasma glutamate after severe TBI induced interaction between A2AR and the metabotropic glutamate receptor 5 (mGluR5) to increase phospholipase C-protein kinase C signaling, which mediated the proinflammatory effect of A2AR. These results are in striking contrast to the well-known antiinflammatory and protective role of A2AR in nonneurogenic ALI and indicate different therapeutic strategies should be used for nonneurogenic and neurogenic ALI treatment when targeting A2AR.
FORMATION AND MODE OF ACTION OF FLAVOPROTEINS
Authors: A. H. Merrill, J. D. Lambeth, D. E. Edmondson, D. B. McCormick
Journal: Annual Review of Nutrition (1981)

INTRODUCTION     281 NATURALLY OCCURRING FLAVINS     282 Modifications Found on the Ribityl Sidechain   282 Modifications Found on the Flavin Ring   283 Chemical and. Biological Degradation Products •...... 286 TRANSPORT AND METABOLISM   287 Uptake and E�cretion   287 Association with Binding (Caier) Proteins   288 Conversion to Coenzymatic Forms     290 COENZYME BINDING BY APOFLA VOPROTEINS   ....... 292 INFLUENCE OF NUTRITIONAL STATUS ON FLAVOPROTEINS ..   ...... 294 FLAVOPROTEIN REACTIONS AND MECHANISMS   296 Survey of F/avoenzymes     296 One-Electron Trans/erases   300 Dehydrogenases   301 Pyridine nuc/eotide-dependent dehydrogenases ...   ......... ........   301 Non-pyridine nucleotide-dependent dehydrogenases   302 Complex jlavoproteins       303 Pyridine nucleotide-disulftde oxidoreductases   304 Dehydrogenase/O�ygen Reductase Enzymes   305
Appropriate Use of Cervical Cancer Vaccine
Authors: Gregory D. Zimet, Marcia L. Shew, Jessica A. Kahn
Journal: Annual Review of Medicine (2008)

Human papillomavirus (HPV) is a necessary, though not sufficient, cause of cervical cancer. Two vaccines have been developed that prevent two HPV types associated with 70% of cervical cancers. One of the vaccines (a quadrivalent vaccine) also prevents two HPV types associated with 90% of genital warts. Both HPV vaccines have shown very good efficacy and safety. This review summarizes the guidelines for use of the quadrivalent vaccine published by the Advisory Committee on Immunization Practices, presents data on vaccine efficacy and safety, and gives an overview of the findings of cost-effectiveness studies. In addition, we summarize the research on the attitudes of parents and health care providers toward HPV vaccine and critically evaluate controversial and challenging issues surrounding HPV vaccination, including concerns about sexual disinhibition and potential obstacles to vaccine distribution and uptake.
The ratio of ELR+ to ELR? CXC chemokines affects the lung and liver injury following hepatic ischemia/reperfusion in the rat
Authors: Lisa M. Colletti, Maranne E. Green, Marie D. Burdick, Robert M. Strieter
Journal: Hepatology (2000)

Hepatic ischemia/reperfusion (I/R) results in a neutrophil-dependent lung and liver injury. The process of neutrophil recruitment and activation in this injury is at least partially dependent on the presence of the ELR+ CXC chemokines. Other investigations have shown that ELR− CXC chemokines can block ELR+ CXC chemokine neutrophil recruitment and activation in vitro . To begin to investigate the role of the balance between these 2 types of molecules in vivo in neutrophil recruitment and activation following hepatic I/R, we used our rat model of lobar hepatic I/R and pretreated animals with pharmacologic doses of gamma-interferon (γ-IFN). γ-IFN is known to upregulate some of the ELR− CXC chemokines, including γ-IFN-inducible protein (IP-10) and monokine-induced by γ-IFN (MIG), as well as down-regulate ELR+ CXC chemokine production. Following hepatic I/R or sham laparotomy, hepatic and pulmonary levels of the ELR− chemokines, IP-10 and MIG, and the ELR+ chemokines, rat cytokine-induced neutrophil chemoattractant (KC), macrophage inflammatory protein-2 (MIP-2), and epithelial neutrophil activating protein (ENA-78) were determined by ELISA, and lung and liver injury were assessed. In response to γ-IFN, hepatic and pulmonary levels of the ELR− chemokines were increased and the levels of the ELR+ chemokines were decreased. Immunohistochemical staining confirmed the hepatocyte as the source of these molecules, as well as the changes in chemokine levels in response to γ-IFN. There was an associated significant decrease in liver and lung injury, although there was no significant decrease in neutrophil influx in either tissue. This suggests that the alteration in the balance of ELR+ to ELR− CXC chemokines results in a decrease in tissue injury through a mechanism other than through an alteration in tissue neutrophil levels.
OSTEOIMMUNOLOGY: Interplay Between the Immune System and Bone Metabolism
Authors: Matthew C. Walsh, Nacksung Kim, Yuho Kadono, Jaerang Rho, Soo Young Lee, Joseph Lorenzo, Yongwon Choi
Journal: Annual Review of Immunology (2005)

Studies of bone and the immune system have converged in recent years under the banner of osteoimmunology. The immune system is spawned in the bone marrow reservoir, and investigators now recognize that important niches also exist there for memory lymphocytes. At the same time, various factors produced during immune responses are capable of profoundly affecting regulation of bone. Mechanisms have evolved to prevent excessive interference by the immune system with bone homeostasis, yet pathologic bone loss is a common sequela associated with autoimmunity and cancer. There are also developmental links, or parallels, between bone and the immune system. Cells that regulate bone turnover share a common precursor with inflammatory immune cells and may restrict themselves anatomically, in part by utilizing a signaling network analogous to lymphocyte costimulation. Efforts are currently under way to further characterize how these two organ systems overlap and to develop therapeutic strategies that benefit from this understanding.
Inhibition of eNOS phosphorylation mediates endothelial dysfunction in renal failure: new effect of asymmetric dimethylarginine
Authors: Hidemi Kajimoto, Hisashi Kai, Hiroki Aoki, Suguru Yasuoka, Takahiro Anegawa, Yuji Aoki, Seiji Ueda, Seiya Okuda, Tsutomu Imaizumi
Journal: Kidney International (2012)
Hospital Quality
Authors: Laurent G. Glance, Andrew W. Dick, Turner M. Osler, Arthur L. Kellermann
Journal: JAMA Surgery (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 Surgery 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 Surgery journal
Molecular cloning and epitope analysis of the peanut allergen Ara h 3
Authors: Pat Rabjohn, Erica M. Helm, J. Steven Stanley, C. Michael West, Hugh A. Sampson, A. Wesley Burks, Gary A. Bannon
Journal: Journal of Clinical Investigation (1999)

Peanut allergy is a significant IgE-mediated health problem because of the increased prevalence, potential severity, and chronicity of the reaction. Following our characterization of the two peanut allergens Ara h 1 and Ara h 2, we have isolated a cDNA clone encoding a third peanut allergen, Ara h 3. The deduced amino acid sequence of Ara h 3 shows homology to 11S seed-storage proteins. The recombinant form of this protein was expressed in a bacterial system and was recognized by serum IgE from ∼45% of our peanut-allergic patient population. Serum IgE from these patients and overlapping, synthetic peptides were used to map the linear, IgE-binding epitopes of Ara h 3. Four epitopes, between 10 and 15 amino acids in length, were found within the primary sequence, with no obvious sequence motif shared by the peptides. One epitope is recognized by all Ara h 3–allergic patients. Mutational analysis of the epitopes revealed that single amino acid changes within these peptides could lead to a reduction or loss of IgE binding. By determining which amino acids are critical for IgE binding, it might be possible to alter the Ara h 3 cDNA to encode a protein with a reduced IgE-binding capacity. These results will enable the design of improved diagnostic and therapeutic approaches for food-hypersensitivity reactions.
Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma
Authors: S. S. An, T. R. Bai, J. H. T. Bates, J. L. Black, R. H. Brown, V. Brusasco, P. Chitano, L. Deng, M. Dowell, D. H. Eidelman, B. Fabry, N. J. Fairbank, L. E. Ford, J. J. Fredberg, W. T. Gerthoffer, S. H. Gilbert, R. Gosens, S. J. Gunst, A. J. Halayko, R. H. Ingram, C. G. Irvin, A. L. James, L. J. Janssen, G. G. King, D. A. Knight, A. M. Lauzon, O. J. Lakser, M. S. Ludwig, K. R. Lutchen, G. N. Maksym, J. G. Martin, T. Mauad, B. E. McParland, S. M. Mijailovich, H. W. Mitchell, R. W. Mitchell, W. Mitzner, T. M. Murphy, P. D. Paré, R. Pellegrino, M. J. Sanderson, R. R. Schellenberg, C. Y. Seow, P. S. P. Silveira, P. G. Smith, J. Solway, N. L. Stephens, P. J. Sterk, A. G. Stewart, D. D. Tang, R. S. Tepper, T. Tran, L. Wang
Journal: European Respiratory Journal (2007)

Excessive airway obstruction is the cause of symptoms and abnormal lung function in asthma. As airway smooth muscle (ASM) is the effecter controlling airway calibre, it is suspected that dysfunction of ASM contributes to the pathophysiology of asthma. However, the precise role of ASM in the series of events leading to asthmatic symptoms is not clear. It is not certain whether, in asthma, there is a change in the intrinsic properties of ASM, a change in the structure and mechanical properties of the noncontractile components of the airway wall, or a change in the interdependence of the airway wall with the surrounding lung parenchyma. All these potential changes could result from acute or chronic airway inflammation and associated tissue repair and remodelling. Anti-inflammatory therapy, however, does not “cure” asthma, and airway hyperresponsiveness can persist in asthmatics, even in the absence of airway inflammation. This is perhaps because the therapy does not directly address a fundamental abnormality of asthma, that of exaggerated airway narrowing due to excessive shortening of ASM. In the present study, a central role for airway smooth muscle in the pathogenesis of airway hyperresponsiveness in asthma is explored.