tbuckley/cabot-search huggingface dataset:
Abstract 11: Fructosamine and Glycated albumin with Risk of Coronary Heart Disease and Death
Authors: Elizabeth Selvin, Andreea M Rawlings, Pamela L Lutsey, James S Pankow, Linda Kao, Michael W Steffes, Josef Coresh
Journal: Circulation (2014)

Background: HbA1c is the standard measure to monitor glucose control and is now used for diagnosis of diabetes. Fructosamine and glycated albumin are markers of short-term glycemic control that may add complementary information to HbA1c. However, the associations of fructosamine and glycated albumin with cardiovascular outcomes are uncharacterized. Methods: We measured glycated albumin and fructosamine in 11104 adult participants (792 with a history of diabetes) of the community-based ARIC Study without cardiovascular disease at baseline (1990-1992). We evaluated the associations of fructosamine and glycated albumin with incident coronary heart disease and total mortality. We compared these associations to those for HbA1c. Results: Baseline HbA1c was highly correlated with fructosamine (Pearson’s r =0.82) and glycated albumin (Pearson’s r=0.86). During over two decades of follow-up there were 1,032 new cases of coronary heart disease and 2,594 deaths. In Cox proportional hazards models adjusted for traditional cardiovascular risk factors, elevated baseline levels of fructosamine and glycated albumin were significantly associated with coronary heart disease and total mortality ( Figure ). After additional adjustment for HbA1c, the associations were attenuated but remained significant, particularly at diabetic levels of fructosamine and glycated albumin. The associations with death were J-shaped, with an elevation of risk also apparent at the lowest levels of each biomarker, as has been previously observed for HbA1c. Conclusions: The acceptance of new measures of hyperglycemia is partly dependent on establishing their association with long-term outcomes. We found that fructosamine and glycated albumin were associated with coronary heart disease and mortality and that these associations were similar to those observed for HbA1c. The elevated risk of death at very low levels of fructosamine, glycated albumin, and HbA1c deserves further examination.
Abstract 4363: Macrophage migration inhibitory factor (MIF) and miR-301b interactively enhance disease aggressiveness by targeting NR3C2 in human pancreatic cancer
Authors: Shouhui Yang, Peijun He, Jian Wang, Aaron Schetter, Naotake Funamizu, Katsuhiko Yanaga, Jochen Gaedcke, B. Michael Ghadimi, Matthias M. Gaida, Thomas Ried, Nader Hanna, H. Richard Alexander, S. Perwez Hussain
Journal: Cancer Research (2014)

Abstract MIF is a pleiotropic cytokine, which plays a role in inflammatory and immune responses and is implicated in tumorigenesis. Our previous study showed that MIF enhances tumor aggressiveness and predicts outcome in patients with pancreatic ductal adenocarcinoma (PDAC). Aberrant microRNA (miRNA) expression is a common feature in cancer and cytokine responsive miRNAs are recently described as critical effectors in tumor progression. We have investigated MIF-associated miRNAs and their interactive roles in the progression of human pancreatic cancer. Global analysis of miRNA expression revealed 38 differentially expressed miRNAs in MIF-high as compared with MIF-low cases of PDAC based on the median value. Kaplan-Meier survival analysis showed that a higher expression of miR-301b in tumors was associated with poorer survival (p=0.008, N=37), which was further validated in an independent cohort of PDAC patients (p=0.021, N=42). Additionally, MIF expression positively correlated with miR-301b and mediated its expression in several human pancreatic cancer cells. Mechanistic analysis revealed that miR-301b promotes pancreatic cancer cell migration and invasion. Furthermore, nuclear receptor subfamily group c member 2 (NR3C2) was identified as a functional target of miR-301b. NR3C2 inhibited tumor migration and invasion and a higher expression of NR3C2 predicted better survival in pancreatic cancer patients. Further in vivo studies showed a significant decrease in NR3C2 in MIF-overexpressing orthotopic xenograft as compared to control. Taken together, our results demonstrate that MIF and miR-301b interactively contribute to pancreatic cancer progression by targeting NR3C2. This novel MIF-miR-301b-NR3C2 axis may provide potential targets for improving disease outcome in pancreatic cancer. Citation Format: Shouhui Yang, Peijun He, Jian Wang, Aaron Schetter, Naotake Funamizu, Katsuhiko Yanaga, Jochen Gaedcke, B. Michael Ghadimi, Matthias M. Gaida, Thomas Ried, Nader Hanna, H. Richard Alexander, S. Perwez Hussain. Macrophage migration inhibitory factor (MIF) and miR-301b interactively enhance disease aggressiveness by targeting NR3C2 in human pancreatic cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4363. doi:10.1158/1538-7445.AM2014-4363
REPORT OF A CASE OF XANTHOMA TUBEROSUM TREATED WITH LIPOCAIC
Authors: B. D. Rosenak
Journal: Annals of Internal Medicine (1943)

Case Reports1 September 1943REPORT OF A CASE OF XANTHOMA TUBEROSUM TREATED WITH LIPOCAICB. D. ROSENAK, M.D. F.A.C.P.B. D. ROSENAK, M.D. F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-19-3-514 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptSevere disorders of fat metabolism are not extremely rare and the following case report is not submitted because of the rarity of the condition, but rather to relate the results of certain therapeutic efforts in this disease.CASE REPORTThe patient was a white woman 49 years old at the time of examination in May 1939. She then complained of bright orange colored nodules on the palms of her hands, on the elbows, feet, knees and other areas of the skin which were frequently irritated by friction. This condition was of about four years' duration and was becoming more extensive....Bibliography1. THANNHAUSER SJ: Lipidoses: disease of the cellular lipid metabolism, Oxford Medicine, 1940, Oxford Univ. Press, New York, Vol. IV, part I, page 214. Google Scholar2. DRAGSTEDT LR: Lipocaic, Northwest Med., 1938, xxxvii, 33-36. Google Scholar3. COMFORTSHEPARD MWVD: Xanthomatous biliary cirrhosis: report of a case, Proc. Staff Meet. Mayo Clin., 1941, xvi, 374-377. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication October 29, 1941. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1943Volume 19, Issue 3Page: 514-518KeywordsElbowFatsKnees ePublished: 1 December 2008 Issue Published: 1 September 1943 PDF downloadLoading ...
Ranolazine protects from doxorubicin‐induced oxidative stress and cardiac dysfunction
Authors: Carlo G. Tocchetti, Andrea Carpi, Carmela Coppola, Cristina Quintavalle, Domenica Rea, Marika Campesan, Antonella Arcari, Giovanna Piscopo, Clemente Cipresso, Maria Gaia Monti, Claudia De Lorenzo, Claudio Arra, Gerolama Condorelli, Fabio Di Lisa, Nicola Maurea
Journal: European Journal of Heart Failure (2014)
Treatment of Hyperkalemia
Authors: Wolfgang C. Winkelmayer
Journal: JAMA (2015)

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
MicroRNA-195 Suppresses Angiogenesis and Metastasis of Hepatocellular Carcinoma by Inhibiting the Expression of VEGF, VAV2, and CDC42
Authors: Ruizhi Wang, Na Zhao, Siwen Li, Jian-Hong Fang, Mei-Xian Chen, Jine Yang, Wei-Hua Jia, Yunfei Yuan, Shi-Mei Zhuang
Journal: Hepatology (2013)

Hepatocellular carcinoma (HCC) is characterized by active angiogenesis and metastasis, which account for rapid recurrence and poor survival. There is frequent down-regulation of miR-195 expression in HCC tissues. In this study, the role of miR-195 in HCC angiogenesis and metastasis was investigated with in vitro capillary tube formation and transwell assays, in vivo orthotopic xenograft mouse models, and human HCC specimens. Reduction of miR-195 in HCC tissues was significantly associated with increased angiogenesis, metastasis, and worse recurrence-free survival. Both gain-of-function and loss-of-function studies of in vitro models revealed that miR-195 not only suppressed the ability of HCC cells to promote the migration and capillary tube formation of endothelial cells but also directly repressed the abilities of HCC cells to migrate and invade extracellular matrix gel. Based on mouse models, we found that the induced expression of miR-195 dramatically reduced microvessel densities in xenograft tumors and repressed both intrahepatic and pulmonary metastasis. Subsequent investigations disclosed that miR-195 directly inhibited the expression of the proangiogenic factor vascular endothelial growth factor (VEGF) and the prometastatic factors VAV2 and CDC42. Knockdown of these target molecules of miR-195 phenocopied the effects of miR-195 restoration, whereas overexpression of these targets antagonized the function of miR-195. Furthermore, we revealed that miR-195 down-regulation resulted in enhanced VEGF levels in the tumor microenvironment, which subsequently activated VEGF receptor 2 signaling in endothelial cells and thereby promoted angiogenesis. Additionally, miR-195 down-regulation led to increases in VAV2 and CDC42 expression, which stimulated VAV2/Rac1/CDC42 signaling and lamellipodia formation and thereby facilitated the metastasis of HCC cells. Conclusion : miR-195 deregulation contributes to angiogenesis and metastasis in HCC. The restoration of miR-195 expression may be a promising strategy for HCC therapy. (Hepatology 2013;58:642-653)
The relationships of ΔFVC and PC20 on the dose-response curve to methacholine with peak expiratory flow variability in children with mild asthma
Authors: Young Yull Koh, Dong In Suh
Journal: European Respiratory Journal (2014)

Background : In asthmatic subjects, not only airway sensitivity but maximal airway response are increased on the dose-response curve to methacholine. The percentage decrease in forced vital capacity (ΔFVC) at the methacholine PC20 (provocative concentration causing a 20% fall in FEV1) has been proposed as a surrogate marker of maximal airway response. Another hallmark of asthma is increased spontaneous variation in airway caliber, which is commonly measured by peak expiratory flow (PEF) variability.

Aims : The aim of this study was to compare airway sensitivity and ΔFVC with regard to their relationships with PEF variability in children with mild asthma.

Methods : Fifty-five children with mild asthma underwent methacholine challenge testing, and ΔFVC and PC20 were measured. Subjects recorded PEF each morning and each evening for 14 consecutive days. PEF variability was expressed as amplitude percentage mean (amp%mean), averaged over 14 days, and as the lowest percentage highest (low%high), recorded over the period.

Results : Methacholine PC20 did not correlate with both indices of PEF variability (amp%mean r=-0.220, P=0.106 ; low%high r=0.189, P=0.166). However, there was a significant and strong correlation between ΔFVC and both amp%mean (r=0.444, P=0.001) and low%high (r=-0.352, P=0.008).

Conclusions : The close relationship between PEF variability and ΔFVC, but not methacholine PC20, suggests that PEF variability may be better refracted by maximal airway response than by airway hypersensitivity.
Abstract 15217: Prevalence of Abnormal Cardiovascular Findings in Preparticipation Cardiovascular Screening by Focused Echocardiography in Collegiate Athletes
Authors: Sheila Hegde, Daniel Modaff, Dennis Helwig, Nancy Bell, Peter Rahko
Journal: Circulation (2014)

Background: Sudden cardiac arrest in a young healthy athlete is a rare but catastrophic event. Current American Heart Association preparticipation screening (AHA PPS) guidelines recommend a focused history and physical without routine imaging or ECG screening. We propose that a focused echocardiogram is a useful modality to identify structural abnormalities that may lead to sudden cardiac arrest or other cardiovascular events in athletes. Methods: We performed a focused 5 minute echocardiogram on all incoming varsity Division I collegiate athletes at the University of Wisconsin from 2005 to 2013. The echocardiograms were performed on the same day as their routine AHA-based PPS exam. Abnormal findings on a focused echocardiogram prompted further testing for confirmation. In this investigation, we report the prevalence of abnormal findings in these athletes. Results: Of the 2898 athletes screened, 1484 (51.2%) were female. The average age was 18.8 years. The majority (98.3%) of athletes had normal screens. ...
mir-126 contribute to angiogenesis defect in pulmonary arterial hypertension right ventricle failure
Authors: Francois Potus, Roxane Paulin, Evangelos Michelakis, Steeve Provencher, Sébastien Bonnet
Journal: European Respiratory Journal (2014)

INTRODUCTION: Right Ventricular Failure (RVF) is the most important predictor of both morbidity and mortality in pulmonary arterial hypertension (PAH). In PAH patients, hypertrophied RV is relatively ischemic, potentially because of suppressed angiogenesis that lead to an imbalance between O2 demand and delivery. MicroRNAs (miRNAs) have emerged as important determinants of angiogenesis especially angio-miR-126, which by inhibiting SPRED-1, triggers VEGF pathway and thus promotes angiogenesis. We hypothesized that specific miR-126 downregulation will promote RV ischemia and the transition from compensated (CRV) to a decompensated (DRV) RV. METHODS/RESULTS: We studied free RV wall tissue from humans with normal RV functions, CRV and PAH (DRV). We used qRT-PCR to study the expression of miR-126 and CD31 immunofluorescence to measure heart microcirculation. As expected, compared to both control and CRV, DRV has decreased miR-126 and microvessels density creating an imbalance between O2 demand and delivery. Interestingly, under the same conditions, miR-126 expression did not fall in LV. miR-126 downregulation in DRV increases SPRED-1, decreasing RAF (P-RAF/RAF) and MAP kinase (P-MAP/MAP) thus decreasing VEGF pathway. Finally, in endothelial cells isolated from human RV, miR-126 up-regulation increased angiogenesis in a PAH model while downregulation of miR-126 in control or CRV mimicked PAH phenotype by decreasing angiogenesis CONCLUSION: We demonstrated for the first time that: 1) specific RV downregulation of miR-126 contributes to ischemic status of the DRV. Targeting miR-126 represents a new avenue of investigation in preventing and reversing failing RV.
Evidence for both oxygen and non-oxygen dependent mechanisms of antibody sensitized target cell lysis by human monocytes
Authors: DK Klassen, AL Jr Sagone
Journal: Blood (1980)

Abstract Recent studies suggest that the generation of reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) or superoxide (O2-) may play a role in monocyte antibody-dependent cytotoxicity (ADCC). We studied ADCC by normal human monocytes, and monocytes from chronic granulomatous disease (CGD) patients, cells unable to generate ROS, toward anti-D sensitized human red cells (RBC) and an antibody sensitized lymphoblastoid cell line (CEM) by 51Cr release. The effects of hypoxia, scavengers of ROS, and the activity of the hexose monophosphate shunt pathway (HMPS) were examined. We found that monocyte HMPS activity increased two to threefold during ADCC toward RBC but was unchanged during ADCC toward CEM cells. Hypoxia decreased lysis of RBC targets by 80% but did not affect lysis of CEM cells even though hypoxia markedly decreased monocyte HMPS activity. Monocytes from CGD patients had impaired lysis of RBC but lysed CEM cells normally. We could not, however, demonstrate protection by scavengers of ROS. We conclude that monocyte ADCC involves two independent mechanisms: a nonoxidative mechanism active in the lysis of CEM cells, and an oxidative mechanism that may involve an unidentified ROS activated during ADCC toward RBC. The activation and possible interaction of these two mechanisms is determined by the nature of the target cell and sensitizing antibody.
Interstitial Granulomatous Dermatitis as the Initial Manifestation of Myeloma
Authors: Lauren Thompson, Sabra Abner, Janine Malone, Jeffrey P. Callen
Journal: JAMA Dermatology (2015)

Interstitial granulomatous dermatitis (IGD) has been associated with pharmacotherapy, various autoimmune conditions, and hematologic malignant conditions. Herein, we report a patient in whom IGD was the initial manifestation of a previously undiagnosed myeloma.
Fumarate hydratase deficiency and tumorigenesis: hypoxia-response is independent of fumarate levels
Authors: Nuno Raimundo, Jouni Ahtinen, Risto Renkonen, Risto Lapatto, Anu Suomalainen
Journal: Cancer Research (2007)

4496   Recessive defects in mitochondrial energy metabolism cause severe infantile multisystem diseases, leading to early death. Dominantly inherited fumarase (FH) defects underlie cancer predisposition in families with kidney cancer and leiomyomas, and mutations in succinate dehydrogenase cause paragangliomas and pheochromocytomas. The citric acid cycle, which integrates energy metabolism in mitochondrial matrix, seem thus to have essential roles in cell proliferation and/or differentiation control.  We used fumarase-deficient (FH-) and control primary fibroblasts to explore the role of energetic and redox metabolism in fumarase deficiency and their relation with cell proliferation. We also used primary fibroblasts with respiratory chain defects (RC-), to distinguish the general consequences of malfunctioning mitochondrial energy metabolism from those leading to tumour formation.  We analysed two FH- lines with homozygous defects, and two from compound heterozygous patients. The homozygous line had pronounced accumulation of fumarate, but neither of the compound heterozygous lines had fumarate levels differing from controls. Also in RC- cells, the fumarate levels within control range.  FH- and RC- cells had increased glycolytic energy production. This metabolic pattern is typical in addition to oxidative energy defect, also for hypoxia response, and we found nuclear accumulation of HIF-1a in both FH- and RC- cells. Furthermore, transcription of HIF-responsive genes was increased in FH- and RC- cells. Thus, both FH- and RC- activated hypoxia response, irrespective of fumarate accumulation.  To study the redox metabolism, we focused on H 2 O 2  and the major cell redox buffer, glutathione (GSH). Steady-state amounts of H 2 O 2  are similar in FH- and controls. Catalase and glutathione peroxidase (GPx) activities are lower in FH- cells, while induced in RC-. Mn-SOD expression is also decreased in FH-, suggesting a decreased generation of H 2 O 2 . GSH content is increased in FH- and unaffected in RC-. GSH synthesis is increased in FH- but not in RC-. In FH-, GSH redox cycle oxidizes GSH slower than controls and recycles it faster. In RC-, GSH is oxidized faster than in controls and recycled also faster. These results suggest that while RC- is associated with increased oxidant stimuli and the corresponding antioxidant response, FH- seem to have a more reduced redox potential, which is required to proliferative cell populations.  In conclusion, FH- and RC malfunction affect similarly the energy metabolism and hypoxia response. The reduced redox state of FH- cells may contribute to keep these cells in a more undifferentiated state, which may be a feature linking FH-deficiency to tumor predisposition.
Scabies presenting as a necrotizing vasculitis in the presence of lupus anticoagulant
Authors: None Jarrett, None Snow
Journal: British Journal of Dermatology (1998)

A 75‐year‐old man presented with a progressive eruption of 6 weeks' duration. Purpura and focal areas of cutaneous infarction were present on the legs. There were scabies burrows on the wrists and hands, and a mite was extracted. Histology of a skin biopsy showed a necrotizing leucocytoclastic vasculitis. Circulating lupus anticoagulant was detected. Treatment consisted of topical 5% permethrin cream and systemic steroids.
Hurler Syndrome: II. Outcome of HLA-Genotypically Identical Sibling and HLA-Haploidentical Related Donor Bone Marrow Transplantation in Fifty-Four Children
Authors: Charles Peters, Elsa G. Shapiro, James Anderson, P. Jean Henslee-Downey, Martin R. Klemperer, Morton J. Cowan, E. Fred Saunders, Pedro A. deAlarcon, Clare Twist, James B. Nachman, Gregory A. Hale, Richard E. Harris, Marta K. Rozans, Joanne Kurtzberg, Guy H. Grayson, Thomas E. Williams, Carl Lenarsky, John E. Wagner, William Krivit
Journal: Blood (1998)
How should we take blood pressure in clinical practice?: The wider use of home and ambulatory monitoring should be encouraged
Authors: Thomas G Pickering
Journal: BMJ (2003)

From BMJ USA 2002;October:541 

It is increasingly clear that the traditional way of measuring blood pressure in the clinic or office frequently produces numbers that grossly overestimate a patient's true blood pressure level. This is a major problem, since it is one of the most important and frequent measurements made by physicians. Two major trends have brought this issue to the forefront: first, the development of new technologies for measuring blood pressure; and second, the increasing body of evidence that even mild elevations of blood pressure are associated with increased cardiovascular risk.

The traditional gold standard for evaluating blood pressure has been clinic readings made by a physician using a mercury sphygmomanometer. It is hallowed by time, and also by the fact that it has been the standard method for evaluating the risks associated with high blood pressure and the benefits of treating it. It has been known for more than 50 years that the blood pressures recorded in …