tbuckley/cabot-search huggingface dataset:
Surveillance of influenza in Iceland during the 2009 pandemic
Authors: G Sigmundsdottir, T Gudnason, Ö Ólafsson, G E Baldvinsdóttir, A Atladottir, A Löve, L Danon, H Briem
Journal: Eurosurveillance (2010)

In a pandemic setting, surveillance is essential to monitor the spread of the disease and assess its impact. Appropriate mitigation and healthcare preparedness strategies depend on fast and accurate epidemic surveillance data. During the 2009 influenza A(H1N1) pandemic, rapid improvements in influenza surveillance were made in Iceland. Here, we describe the improvements made in influenza surveillance during the pandemic , which could also be of great value in outbreaks caused by other pathogens. Following the raised level of pandemic influenza alert in April 2009, influenza surveillance was intensified. A comprehensive automatic surveillance system for influenza-like illness was developed, surveillance of influenza-related deaths was established and laboratory surveillance for influenza was strengthened. School absenteeism reports were also collected and compared with results from the automatic surveillance system. The first case of 2009 pandemic influenza A(H1N1) was diagnosed in Iceland in May 2009, but sustained community transmission was not confirmed until mid-August. The pandemic virus circulated during the summer and early autumn before an abrupt increase in the number of cases was observed in October. There were large outbreaks in elementary schools for children aged 6–15 years throughout the country that peaked in late October. School absenteeism reports from all elementary schools in Iceland gave a similar epidemiological curve as that from data from the healthcare system. Estimates of the proportion of the population infected with the pandemic virus ranged from 10% to 22%. This study shows how the sudden need for improved surveillance in the pandemic led to rapid improvements in data collection in Iceland. This reporting system will be improved upon and expanded to include other notifiable diseases, to ensure accurate and timely collection of epidemiological data.
Completeness and diagnostic validity of recording acute myocardial infarction events in primary care, hospital care, disease registry, and national mortality records: cohort study
Authors: E. Herrett, A. D. Shah, R. Boggon, S. Denaxas, L. Smeeth, T. van Staa, A. Timmis, H. Hemingway
Journal: BMJ (2013)

<b>Objective</b> To determine the completeness and diagnostic validity of myocardial infarction recording across four national health record sources in primary care, hospital care, a disease registry, and mortality register. <b>Design</b> Cohort study. <b>Participants</b> 21 482 patients with acute myocardial infarction in England between January 2003 and March 2009, identified in four prospectively collected, linked electronic health record sources: Clinical Practice Research Datalink (primary care data), Hospital Episode Statistics (hospital admissions), the disease registry MINAP (Myocardial Ischaemia National Audit Project), and the Office for National Statistics mortality register (cause specific mortality data). <b>Setting</b> One country (England) with one health system (the National Health Service). <b>Main outcome measures</b> Recording of acute myocardial infarction, incidence, all cause mortality within one year of acute myocardial infarction, and diagnostic validity of acute myocardial infarction compared with electrocardiographic and troponin findings in the disease registry (gold standard). <b>Results</b> Risk factors and non-cardiovascular coexisting conditions were similar across patients identified in primary care, hospital admission, and registry sources. Immediate all cause mortality was highest among patients with acute myocardial infarction recorded in primary care, which (unlike hospital admission and disease registry sources) included patients who did not reach hospital, but at one year mortality rates in cohorts from each source were similar. 5561 (31.0%) patients with non-fatal acute myocardial infarction were recorded in all three sources and 11 482 (63.9%) in at least two sources. The crude incidence of acute myocardial infarction was underestimated by 25-50% using one source compared with using all three sources. Compared with acute myocardial infarction defined in the disease registry, the positive predictive value of acute myocardial infarction recorded in primary care was 92.2% (95% confidence interval 91.6% to 92.8%) and in hospital admissions was 91.5% (90.8% to 92.1%). <b>Conclusion</b> Each data source missed a substantial proportion (25-50%) of myocardial infarction events. Failure to use linked electronic health records from primary care, hospital care, disease registry, and death certificates may lead to biased estimates of the incidence and outcome of myocardial infarction. <b>Trial registration </b>NCT01569139 clinicaltrials.gov.
Macrophage Inhibitory Cytokine-1: Possible Bridge Molecule of Inflammation and Prostate Cancer
Authors: Dev Karan, Jeffrey Holzbeierlein, J. Brantley Thrasher
Journal: Cancer Research (2008)

Abstract There is emerging evidence that inflammation may lead to prostate cancer development. Although inflammation is an essential response to injury or infection, chronic inflammation is harmful and causes tissue damage. Increasing evidence suggests that inflammation leads to the development of epithelial cancers; however, studies on inflammation-targeted genes that might contribute to the development of cancer are at the beginning stage. Here, we describe macrophage inhibitory cytokine-1, which provides a potential link between inflammation and prostate cancer. Understanding the regulation of macrophage inhibitory cytokine-1 in response to inflammation may have potential for novel therapeutic strategies. [Cancer Res 2009;69(1):2–5]
Effects On Quality Of Life Evaluated With Rhinasthma Of Mometasone Furoate Nasal Spray In Moderate-severe Persistent Allergic Rhinitis And Intermittent Asthma
Authors: I. Baiardini, G. Passalacqua, E. Villa, A. Rogkakou, S. Pellegrini, M. Bacic, E. Compalati, F. Braido, None W G
Journal: Journal of Allergy and Clinical Immunology (2010)
Liposome-Mediated Gene Transfection of Endothelial Nitric Oxide Synthase Reduces Endothelial Activation and Leukocyte Infiltration in Transplanted Hearts
Authors: Akiko Iwata, Sadahiro Sai, Yoshio Nitta, Megan Chen, Ricarda de Fries-Hallstrand, Joy Dalesandro, Robert Thomas, Margaret D. Allen
Journal: Circulation (2001)

Background —During cardiac ischemia-reperfusion injury, neutrophilic infiltration of the myocardium is mediated by adhesion molecule expression on activated coronary endothelium. Nitric oxide inhibits neutrophil adhesion to endothelium in vitro by blocking the nuclear factor (NF)-κB–dependent transcription of adhesion molecules. We investigated whether intraoperative gene delivery of endothelial nitric oxide synthase (eNOS) into donor hearts before transplantation would have a similar effect on an entire organ. Methods and Results —In an allogeneic rabbit heart transplant model, liposomes complexed to the gene encoding eNOS were infused into the donor coronary circulation before transplantation. By 24 hours after transplantation, calcium-dependent nitrite production was significantly higher in eNOS-transfected donor hearts than in the 3 control groups: donor hearts transfected with empty plasmids alone, donor hearts treated with diluent only, and untransplanted native hearts. Intramyocardial neutrophil and T-lymphocyte populations were halved in eNOS-transfected hearts compared with control donor hearts ( P &lt;0.05). Moreover, the prevalence of NF-κB activation in microvascular endothelial cells and surrounding cardiac myocytes as well as endothelial vascular cell adhesion molecule-1 and intracellular adhesion molecule-1 expression were all significantly reduced in eNOS-transfected hearts compared with control donor hearts ( P &lt;0.01). Without immunosuppression, eNOS-transfected hearts survived longer than controls. Conclusions —Intraoperative liposome-mediated gene delivery of eNOS to donor hearts can result in early gene expression sufficient to reduce ischemia-reperfusion injury by inhibiting NF-κB activation, adhesion molecule expression, and the early infiltration of leukocytes, all of which may improve graft survival.
Effects of Photoacoustic Imaging and Photothermal Ablation Therapy Mediated by Targeted Hollow Gold Nanospheres in an Orthotopic Mouse Xenograft Model of Glioma
Authors: Wei Lu, Marites P. Melancon, Chiyi Xiong, Qian Huang, Andrew Elliott, Shaoli Song, Rui Zhang, Leo G. Flores, Juri G. Gelovani, Lihong V. Wang, Geng Ku, R. Jason Stafford, Chun Li
Journal: Cancer Research (2011)

Advancements in nanotechnology have made it possible to create multifunctional nanostructures that can be used simultaneously to image and treat cancers. For example, hollow gold nanospheres (HAuNS) have been shown to generate intense photoacoustic signals and induce efficient photothermal ablation (PTA) therapy. In this study, we used photoacoustic tomography, a hybrid imaging modality, to assess the intravenous delivery of HAuNS targeted to integrins that are overexpressed in both glioma and angiogenic blood vessels in a mouse model of glioma. Mice were then treated with near-infrared laser, which elevated tumor temperature by 20.7°C. We found that PTA treatment significantly prolonged the survival of tumor-bearing mice. Taken together, these results show the feasibility of using a single nanostructure for image-guided local tumor PTA therapy with photoacoustic molecular imaging.
Reduced Response to Activated Protein C Is Associated with Increased Risk for Cerebrovascular Disease
Authors: Johanna G. van der Bom
Journal: Annals of Internal Medicine (1996)

Background: Resistance to activated protein C (APC), which results from various factors, including a mutation in the gene for coagulant factor V, has been associated with increased risk for venous thrombosis. However, its relation to arterial disease is still not well defined. Objective: To investigate the association of both response to APC and the factor V Leiden mutation with arterial disease. Design: Population-based case–control study. Setting: A district of Rotterdam, the Netherlands. Participants: 115 patients with a history of myocardial infarction; 112 patients with a history of stroke, transient ischemic attack, or both; and 222 age-matched controls without arterial disease chosen from among 7983 persons in the Rotterdam Study cohort. Patients using anticoagulant drugs were excluded. Measurements: Response to APC was determined in double-centrifuged platelet-poor plasma. Patients were genotyped for the Arg 506 to Gln mutation in the gene for coagulant factor V. Results: The prevalence of cerebrovascular disease increased gradually and corresponded to a decreasing response to APC (odds ratio per 1-unit decrease of response to APC, 1.43 [95% CI, 1.12 to 1.81], adjusted for age and sex). Adjustment for the factor V mutation did not change the findings. We found no association between response to APC and myocardial infarction or between factor V mutation and cerebrovascular disease or myocardial infarction. Conclusions: Low response to APC is associated with an increased risk for cerebrovascular disease but not with an increased risk for myocardial infarction, independent of the factor V Leiden mutation. The association between the factor V Leiden mutation and cerebrovascular disease or myocardial infarction remains to be determined.
Maternal Anti-Ro and Anti-La Antibody–Associated Endocardial Fibroelastosis
Authors: Lynne E. Nield, Earl D. Silverman, Glenn P. Taylor, Jeffrey F. Smallhorn, J. Brendan M. Mullen, Norman H. Silverman, John P. Finley, Yuk M. Law, Derek G. Human, P. Gareth Seaward, Robert M. Hamilton, Lisa K. Hornberger
Journal: Circulation (2002)

Background — Maternal anti-Ro and anti-La antibodies are associated with congenital heart block (CHB). Although endocardial fibroelastosis (EFE) has been described in isolated cases of autoantibody-mediated CHB, the natural history and pathogenesis of this disease are poorly understood. Methods and Results — We retrospectively reviewed the clinical history, echocardiography, and pathology of fetuses and children with EFE associated with CHB born to mothers positive for anti-Ro or anti-La antibodies at 5 centers. Thirteen patients were identified, 6 with a prenatal and 7 with a postnatal diagnosis. Six mothers were positive for anti-Ro and anti-La antibodies, and 7 were positive for anti-Ro antibodies only. Only 1 mother had autoimmune disease. Severe ventricular dysfunction was seen in all fetal and postnatal cases. Four fetal and 3 postnatal cases had EFE at initial presentation. However, 2 fetal and 4 postnatal cases developed EFE 6 to 12 weeks and 7 months to 5 years from CHB diagnosis, respectively, even despite ventricular pacing in 6 postnatal cases. Eleven (85%) either died (n=9) or underwent cardiac transplantation (n=2) secondary to the EFE. Pathologic assessment of the explanted heart, available in 10 cases, revealed moderate to severe EFE in 7 and mild EFE in 3 cases, predominantly involving the left ventricle. Immunohistochemistry in 4 cases (including 3 fetuses) demonstrated deposition of IgG in 4 and IgM in 3 and T-cell infiltrates in 3 cases, suggesting an immune response by the affected fetus or child. Conclusions — EFE occurs in the presence of autoantibody-mediated CHB despite adequate ventricular pacing. Autoantibody-associated EFE has a very high mortality rate, whether developing in fetal or postnatal life.
Palmar rheumatoid nodulosis associated with local pressure.
Authors: E Ben-Chetrit, C Enk, A Rubinow
Journal: Annals of the Rheumatic Diseases (1992)

Rheumatoid nodulosis is a term used to describe adult patients with rheumatoid arthritis with little or no clinical joint inflammation who have numerous subcutaneous nodules indistinguishable from those of patients with active rheumatoid arthritis. This paper reports the case of a woman with quiescent rheumatoid arthritis who developed palmar nodulosis three weeks after the strenuous activity of painting her apartment. This case illustrates the direct association between the appearance of nodulosis and physical pressure despite inactive disease.
Two components of use-dependent block of Na+ current by disopyramide and lidocaine in guinea pig ventricular myocytes.
Authors: A Sunami, Z Fan, J Nitta, M Hiraoka
Journal: Circulation Research (1991)

We studied the kinetics of the use-dependent block of the Na+ current (INa) by disopyramide and lidocaine. INa was recorded from isolated guinea pig ventricular myocytes by using the whole-cell patch-clamp technique. The use-dependent block of INa by disopyramide with 20- and 200-msec depolarizing pulses developed in two exponential functions. The degree of the use-dependent block and the amplitude of the fast (Af) and slow (As) components with the short (20-msec) pulse protocol were comparable to those with the long (200-msec) pulse protocol. When pH was raised from 7.3 to 8.0, disopyramide increased Af without a change in As. At pH 6.5, INa block developed with a single exponential function revealing only the slow component. The fast and slow components of INa block by disopyramide could be explained by binding of the uncharged and charged forms, respectively, to the activated state of the channel. Development of INa block by lidocaine also was expressed by two exponentials at all pulse durations (5-200 msec). As pulse durations were prolonged or holding potentials were depolarized, the degree of the use-dependent block and Af increased. When pH was lowered to 6.5, the short pulse produced only the slow component, whereas the long pulse caused two exponentials with decreased Af and increased As. Internal application of QX-314, a permanently charged lidocaine analogue, produced a single exponential block of INa with a very slow onset rate.(ABSTRACT TRUNCATED AT 250 WORDS)
The Role of the Social Environment in Children and Adolescents with Asthma
Authors: Edith Chen, Louise S. Chim, Robert C. Strunk, Gregory E. Miller
Journal: American Journal of Respiratory and Critical Care Medicine (2007)

Rationale: Biopsychosocial models of asthma have been proposed in the literature, but few empirical tests of social factors at various levels of influence have been conducted.Objectives: To test associations of neighborhood, peer, and family factors with asthma outcomes in youth, and to determine the pathways through which these social factors operate.Methods: Observational study of youths with asthma (n = 78).Measurements and Main Results: Youths completed questionnaires about neighborhood problems, peer support, and family support. Biological (IgE, eosinophil count, production of IL-4) and behavioral (youth smoking, exposure to smoke, adherence to medications) pathways were measured. Asthma symptoms and pulmonary function were assessed in the laboratory and at home for 2 weeks. Lower levels of family support were associated with greater symptoms (β coefficients: −0.26 to −0.33, P < 0.05) and poorer pulmonary function (β: 0.30, P < 0.05) via biological pathways (Z statistics from 1.19 to 1.51, P < 0.05). Higher levels of neighborhood problems were associated with greater symptoms (β coefficients: 0.27–0.33, P < 0.05) via behavioral pathways related to smoking (Z statistics = 1.40, P < 0.05). Peer support was not associated with symptoms or pulmonary function.Conclusions: This study indicates that family factors may affect youths' asthma via physiologic changes, whereas community factors may help shape the health behaviors of youths with asthma.
Estrogen Inhibits Bone Resorption by Directly Inducing Apoptosis of the Bone-resorbing Osteoclasts
Authors: Takashi Kameda, Hiroshi Mano, Tatsuhisa Yuasa, Yoshihisa Mori, Koshi Miyazawa, Miho Shiokawa, Yukiya Nakamaru, Emi Hiroi, Kenji Hiura, Akira Kameda, Na N. Yang, Yoshiyuki Hakeda, Masayoshi Kumegawa
Journal: The Journal of Experimental Medicine (1997)

Estrogen deficiency causes bone loss, which can be prevented by estrogen replacement therapy. Using a recently developed technique for isolation of highly purified mammalian osteoclasts, we showed that 17 β-estradiol (E2) was able to directly inhibit osteoclastic bone resorption. At concentrations effective for inhibiting bone resorption, E2 also directly induced osteoclast apoptosis in a dose- and time-dependent manner. ICI164,384 and tamoxifen, as pure and partial antagonists, respectively, completely or partially blocked the effect of E2 on both inhibition of osteoclastic bone resorption and induction of osteoclast apoptosis. These data suggest that the protective effects of estrogen against postmenopausal osteoporosis are mediated in part by the direct induction of apoptosis of the bone-resorbing osteoclasts by an estrogen receptor– mediated mechanism.
Incomplete response of inflammatory arthritis to TNFα blockade is associated with the Th17 pathway
Authors: Saba Alzabin, Sonya M Abraham, Taher E Taher, Andrew Palfreeman, Dobrina Hull, Kay McNamee, Ali Jawad, Ejaz Pathan, Anne Kinderlerer, Peter C Taylor, Richard Williams, Rizgar Mageed
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Objectives</h3> To establish if changes in Th1/Th17 cell populations previously reported in experimental arthritis occur in patients with rheumatoid arthritis (RA) treated with anti-tumour necrosis factor α (TNFα) agents, and whether the therapeutic response to anti-TNFα is compromised in patients and mice because of elevated Th17/IL-17 levels. Finally, to assess the efficacy of combined blockade of anti-TNFα and anti-IL-17 in experimental arthritis. <h3>Methods</h3> A longitudinal study of two independent cohorts (cohort 1, n=24; cohort 2, n=19) of patients with RA treated with anti-TNFα biological agents was carried out to assess their Th17/IL-17 levels before and after the start of anti-TNFα therapy. IL-12/23p40 production was assessed in plasma Peripheral blood lymphocytes (PBLs) and monocytes. Mice with collagen-induced arthritis (CIA) were treated with anti-TNFα alone, anti-IL17 alone or a combination of the two. Efficacy of treatment and response was assessed from changes in Disease Activity Score 28–erythrocyte sedimentation rate scores in patients, and in clinical scores and histological analysis in CIA. <h3>Results</h3> Significant increases in circulating Th17 cells were observed in patients after anti-TNFα therapy and this was accompanied by increased production of IL-12/23p40. There was an inverse relationship between baseline Th17 levels and the subsequent response of patients with RA to anti-TNFα therapy. In addition, PBLs from non-responder patients showed evidence of increased IL-17 production. Similarly, in anti-TNFα-treated mice, there was a strong correlation between IL-17 production and clinical score. Finally combined blockade of TNFα and IL-17 in CIA was more effective than monotherapy, particularly with respect to the duration of the therapeutic effect. <h3>Conclusions</h3> These findings, which need to be confirmed in a larger cohort, suggest that a Th17-targeted therapeutic approach may be useful for anti-TNFα non-responder patients or as an adjunct to anti-TNFα therapy, provided that safety concerns can be addressed.
Lymphoid organisation in labial salivary gland biopsies is a possible predictor for the development of malignant lymphoma in primary Sjogren's syndrome
Authors: E. Theander, L. Vasaitis, E. Baecklund, G. Nordmark, G. Warfvinge, R. Liedholm, K. Brokstad, R. Jonsson, M. V. Jonsson
Journal: Annals of the Rheumatic Diseases (2011)

<h3>Objective</h3> The development of non-Hodgkin9s lymphoma (NHL) confers a high risk of mortality in primary Sjögren9s syndrome (pSS) patients, but the sensitivity and specificity of proposed lymphoma predictors are insufficient for practical use. The performance of lymphoid organisation in the form of germinal centre (GC)-like lesions was evaluated in labial salivary gland biopsies taken at pSS diagnosis as a potential lymphoma-predicting biomarker. <h3>Methods</h3> Labial salivary gland tissue biopsies available from two Swedish pSS research cohorts (n=175) were re-evaluated by light microscopy in a blind study in order to identify GC-like structures as a sign of ectopic lymphoid tissue formation and organisation. A linkage study was performed with the Swedish Cancer Registry for lymphoma identification. The risk of developing NHL in GC-positive patients in comparison with GC-negative patients was evaluated using Kaplan–Meier statistics and log-rank test. Associations between GC-like structures and clinical and/or laboratory disease markers were also determined using χ<sup>2</sup> or Fisher9s exact tests. <h3>Results</h3> At diagnosis, 25% of pSS patients had GC-like structures in their salivary glands. Seven of the 175 patients studied (14% GC+ and 0.8% GC−) developed NHL during 1855 patient-years at risk, with a median onset of 7 years following the initial diagnostic salivary gland biopsy. Six of the seven patients had GC-like structures at diagnosis; the remaining patient was GC negative at the time of diagnosis (p=0.001). <h3>Conclusions</h3> The detection of GC-like structures by light microscopy in pSS diagnostic salivary biopsies is proposed as a highly predictive and easy-to-obtain marker for NHL development. This allows for risk stratification of patients and the possibility to initiate preventive B-cell-directed therapy.
β-Blockers and Progression of Coronary Atherosclerosis: Pooled Analysis of 4 Intravascular Ultrasonography Trials
Authors: Ilke Sipahi, E. Murat Tuzcu, Katherine E. Wolski, Stephen J. Nicholls, Paul Schoenhagen, Bo Hu, Craig Balog, Mehdi Shishehbor, William A. Magyar, Timothy D. Crowe, Samir Kapadia, Steven E. Nissen
Journal: Annals of Internal Medicine (2007)

In patients with myocardial infarction, beta-adrenergic blockers reduce recurrent myocardial infarction and total mortality rates. However, whether a direct influence of beta-blockers on coronary atherosclerosis contributes to reduced recurrent myocardial infarction and total mortality rates is not known.