tbuckley/cabot-search huggingface dataset:
Education and debate: Consent, confidentiality, and the threat to public health surveillance * Commentary: Don't waive consent lightly---involve the public
Authors: C. Verity
Journal: BMJ (2002)

# Consent, confidentiality, and the threat to public health surveillance {#article-title-2}

Effective protection of public health requires direction from the information provided by disease surveillance1—for example, in the cases of AIDS and variant Creutzfeldt-Jakob disease surveillance data led to action that protected health. 2 3 Health surveillance relies entirely on prompt and accurate reporting of the occurrence of disease by doctors and other health professionals.1 Recently there has been increased concern in the United Kingdom about the need to maintain the confidentiality of information arising from consultations between doctor and patient. Documents have been issued regulating or advising on transfer of patient data. Some have argued that, unless needed for direct patient care, data should not be transferred to third parties without patients' explicit consent, or, alternatively, that all identifying information must first be removed.4 The difficulty in countering these arguments arises partly from the fact that health surveillance, including that for communicable diseases, has been neglected in official guidance on confidentiality.5 We and our colleagues are concerned that if some interpretations of this guidance were enforced they would impair or stop important surveillance activities and thus seriously prejudice public health.

#### Summary points

In the light of recent guidelines some doctors have been advised not to share health data that could potentially identify patients without either obtaining the patients'explicit consent or totally anonymising the data

These interpretations, if widely held and enforced, would compromise many surveillance activities essential for protection of the health of individuals and the public overall

The public should be made aware of the important ways in which information about individual patients is used to protect health

Those responsible for framing guidelines on the handling of clinical data and for advising doctors should consider issues related to health surveillance so that public health is not put at risk

Data derived from patient consultations, investigations, and …
Comparison of methods for intestinal histamine application: histamine in enterosoluble capsules or via a duodeno‐jenunal tube
Authors: S. Vind, I. Søndergaard, L. Kergaard Poulsen, U. Gerner Svendsen, B. Weeke
Journal: Allergy (1991)

The study was conducted to investigate whether introduction of histamine in enterosoluble capsules produced the same amount of urinary histamine metabolites as that found after application of histamine through a duodeno‐jejunal tube. Secondly, to examine whether a histamine‐restrictive or a fast diet affected the amount of urinary metabolites. Fifteen healthy subjects were challenged four times with 100 nig of histamine. Results were monitored by the urinary recovery of 1,4‐methylimidazole acetic acid (MIAA) from 24 h before to 72 h after challenge. Urine was collected in 24 h samples except on the first day after challenge when separation into 0–2 h‐, 2–4 h‐ and 4–24 h‐fractions was made. MIAA was measured by high performance liquid chromatography (HPLC). The results showed that during the first 2 h after challenge the recovery of MIAA was higher with tubes than with capsules. Measurements from all other intervals did not differ significantly between the two challenge regimens. Fast (water only) and histamine‐restrictive diet versus non‐restrictive diet did not affect the urinary MIAA. MIAA was significantly higher overall during the first 24 h after challenge than in any other fraction. We conclude that oral administration of enterosoluble capsules is an easy and appropriate method for intestinal histamine challenge. Fast and histamine‐restrictive diets are not necessary, but subjects should record unexpected responses in a food and symptom diary.
Uluslararası Bir Çalıştay Raporu: Kronik Hepatit B için Ağız Yoluyla Tedavi Uygulanan Hastaların Yönetiminde Yol Haritası
Authors: Emmet B. Keeffe, Stefan Zeuzem, Raymond S. Koff, Douglas T. Dieterich, ║ Rafael Esteban-Mur, Edward J. Gane, Ira M. Jacobson, Seng G. Lim, Nikolai Naoumov, Patrick Marcellin, Teerha Piratvisuth, Stanford, Frankfurt, Farmington, Connecticut, Barcelona, Spain, Auckland, New Zealand, Singapore, London, United Kingdom, Hôpital Beaujon, Clichy, Hat Yai, Thailand, Hospices Civils de Lyon, Hôtel Dieu
Journal: Clinical Gastroenterology and Hepatology (2007)
Abstract 5517: Coronary Microvessel Spasm is a Frequent Cause of Myocardial Ischemia in Women With Angina-like Chest Pain
Authors: Keisuke Ohba, Seigo Sugiyama, Koichi Sugamura, Toshimitsu Nozaki, Yasushi Matsuzawa, Junichi Matsubara, Masaaki Konishi, Eiichi Akiyama, Hitoshi Sumida, Koichi Kaikita, Sunao Kojima, Yasuhiro Nagayoshi, Megumi Yamamuro, Yasuhiro Izumiya, Kenji Sakamoto, Seiji Hokimoto, Hiroshige Yamabe, Hisao Ogawa
Journal: Circulation (2009)

Background: Angina without coronary stenosis is frequent in women, indicating that non-obstructive coronary artery disease (NOCAD) including coronary spasm should be clinically examined. Coronary microvessel spasm (CMVS) as well as epicardial coronary artery spastic angina (eCSA) can cause NOCAD, however clinical significance and diagnostic criteria of CMVS have not been established. Methods and Results: 239 consecutive patients suspected NOCAD (135 women and 104 men, age 64±11) were investigated by the intra-coronary acetylcholine-provocation test (ACh-test) with simultaneous measurement of cardiac lactic acid production (CLAP) and coronary blood flow volume (CBFV) calculated from average peak velocity using Doppler FloWire and coronary diameter by quantitative coronary angiography. eCSA was predominantly provoked in men [women 66 (48.9%) vs. men 75 (72.2%), p&lt;0.001]. We diagnosed CMVS by our following criteria; occurrence of chest pain with ischemic electrocardiographic change, decrease in CBFV, and positive CLAP without epicardial spasm. CMVS was significantly frequent in women [women 30 (22.2%) vs. men 2 (1.9%), p&lt;0.001]. 51 patients (21.3%) exhibited no evidence of myocardial ischemia by ACh-test [control; women 26 (19.3%) vs. men 25 (24.0%), p=0.37] and remaining 15 patients (6.3%) showed equivocal results. At baseline condition, CMVS patients showed significantly lower coronary flow values of diastolic to systolic velocity ratio compared to control (1.5±0.2 vs. 1.9±0.4, p&lt;0.001). Women with CMVS exhibited significant decrease in CBFV (−50.7±24.0%, p&lt;0.001) and increase in CLAP (31.8±30.7%, p&lt;0.001) as compatible as eCSA by ACh-test (eCSA: CBFV; −45.2±40.7%, p=0.58, CLAP; 29.1±44.7%, p=0.74). We treated both patients with CMVS and eCSA by calcium-channel blockers. During 39 months follow-up, four cardiovascular events were documented in patients with eCSA, however, none in patients with CMVS. Conclusion: CMVS is the frequent cause of myocardial ischemia (22%) in women with chest pain and the medical treatment with calcium-channel blockers is effective. CMVS could be clinically identified as NOCAD by the diagnostic ACh-test with simultaneous measurement of CLAP and CBFV to provide optimal care for improving prognosis.
Usefulness and limitations of contractile reserve evaluation in patients with low-flow, low-gradient aortic stenosis eligible for cardiac resynchronization therapy
Authors: Fabien Garnier, Jean‐Christophe Eicher, Saed Jazayeri, Géraldine Bertaux, Olivier Bouchot, Ludwig‐Serge Aho, Jean‐Eric Wolf, Gabriel Laurent
Journal: European Journal of Heart Failure (2014)
981. Gene Therapy Clinical Trials Worldwide 1989-2003: An Overview
Authors: Michael L. Edelstein, Mohammad R. Abedi, Jo Wixon, Richard M. Edelstein
Journal: Molecular Therapy (2004)

In 1989, Rosenberg et al. performed the first human gene therapy trial when they used a retrovirus to introduce the gene coding for resistance to neomycin into human tumor-infiltrating lymphocytes before infusing them into five patients with advanced melanoma (N Engl J Med. 1990, 323(9): 570-8). This study demonstrated the feasibility of using retroviral gene transduction in humans and set the stage for further studies. Since then, over 900 clinical trials have been completed, are ongoing or have been approved worldwide. These trials have been designed to establish feasibility and safety, to demonstrate the reality of expression of therapeutic protein(s) in vivo by the genes transferred and, in some cases, to show therapeutic benefit. In 1990, 2 trials were initiated. The number then climbed rapidly as hopes for early therapeutic success prompted an ever-increasing number of trials. The peak was reached in 1999 with 113 trials initiated. With the realisation that numerous obstacles needed to be overcome, and the occurrence of some untoward effects, the pace slowed somewhat with 53 trials approved in 2003.
Abstract 12230: Estimation of Acute Onset Global Longitudinal Strain by 3D Speckle Tracking After ST-Elevation Myocardial Infarction is Useful for Predicting Left Ventricular Remodeling
Authors: Noriaki Iwahashi, Masaomi Gohbara, Eiichi Akiyama, Nobuhiko maejima, Kengo Tsukahara, Kiyoshi Hibi, Masami Kosuge, Toshiaki Ebina, Satoshi Umemura, Kazuo Kimura
Journal: Circulation (2014)

Background: Left ventricular (LV) global strain estimated immediately after ST elevation AMI (STEMI) was reported as a predictor of LV remodeling. However, strain analysis ideally should be assessed by 3D speckle tracking, in order to avoid through plane motion. We explored the usefulness of global strain estimated by 3D speckle tracking in patients with a first STEMI in comparison with infarct size estimated by Tc99m-sestamibi. Methods: 239 consecutive patients (194 men, age 65 years, peak CPK=3132±3817 IU/l) presenting with a first ST-elevation AMI (STEMI) who underwent primary PCI within 12 hours of onset were enrolled. Within 24 h of PCI, echocardiography were performed by E33. 3D speckle tracking was analyzed by 4D LV-Analysis (TOM-TEC, Germany). Global longitudinal strain (GLS) was calculated; 3D (3D-GLS). Final infarct size was defined using Tc99m-sestamibi as the total area of <50%uptake area at 2 weeks. Echocardiography was repeated 12 months later and LV remodeling was defined as an absolute inc...
Safety-Belt Use Among Drivers Involved in Alcohol-Related Fatal Motor-Vehicle Crashes—United States, 1982-1989
Authors: M E Vegega, T M Klein
Journal: JAMA (1991)

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Abstract 2677: Lysyl Oxidase a therapeutic target in pancreatic cancer
Authors: Grazia Saturno, Filipa Lopes, Amaya Viros, Jennifer Morton, Owen Sansom, Caroline Springer, Richard Marais
Journal: Cancer Research (2014)

Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, with a 5-year survival rate of only 6%. Despite advances in conventional therapies and targeted therapies, survival has not improved in the past three decades. We found that high expression of LOX (Lysyl Oxidase) is a poor prognostic marker in PDAC, suggesting a role in this disease. LOX is an amine oxidase that catalyzes the cross-linking of collagens and elastin in the extracellular matrix (ECM) thus regulating extracellular stiffness and contributing to desmoplasia (abundant fibrotic stroma). LOX inhibition has been associated with decreased phosphorylation of SRC (Proto-oncogene tyrosine-protein kinase Src) and FAK (Focal Adhesion Kinase) as a result of decreased interaction of integrins with the ECM. To further investigate the role of LOX in pancreatic cancer, we obtained PDAC cells derived from a transgenic mouse model that faithfully recapitulates the human disease. We found that LOX was upregulated in tumor cells from Pdx1-Cre KrasG12D/+ Trp53R172H/+ (KPC) mice compared to Pdx1-Cre KrasG12D/+ (KC) mice. Using a genetic approach we developed LOX-relevant models by silencing LOX in KPC cells via shRNA and overexpressing LOX in KC cells. We characterized these cells for their invasion ability and growth in a 3D environment. We then confirmed these in vitro results in allograft models in mice. Collectively, our results validate LOX as a therapeutic target in PDAC and suggest that its inhibition represents a new therapeutic strategy for PDAC patients. Citation Format: Grazia Saturno, Filipa Lopes, Amaya Viros, Jennifer Morton, Owen Sansom, Caroline Springer, Richard Marais. Lysyl Oxidase a therapeutic target in 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 2677. doi:10.1158/1538-7445.AM2014-2677
Gene-Induced Chondrogenesis of Primary Mesenchymal Stem Cells in vitro
Authors: Glyn D. Palmer, Andre Steinert, Arnulf Pascher, Elvire Gouze, Jean-Noel Gouze, Oliver Betz, Brian Johnstone, Christopher H. Evans, Steven C. Ghivizzani
Journal: Molecular Therapy (2005)

Adult mesenchymal stem cells (MSCs) have the capacity to differentiate into various connective tissues such as cartilage and bone following stimulation with certain growth factors. However, less is known about the capacity of these cells to undergo chondrogenesis when these proteins are delivered via gene transfer. In this study, we investigated chondrogenesis of primary, bone marrow-derived MSCs in aggregate cultures following genetic modification with adenoviral vectors encoding chondrogenic growth factors. We found that adenoviral-mediated expression of TGF-β1 and BMP-2, but not IGF-1, induced chondrogenesis of MSCs as evidenced by toluidine blue metachromasia and immunohistochemical detection of type II collagen. Chondrogenesis correlated with the level and duration of expressed protein and was strongest in aggregates expressing 10–100 ng/ml transgene product. Transgene expression in all aggregates was highly transient, showing a marked decrease after 7 days. Chondrogenesis was inhibited in aggregates modified to express >100 ng/ml TGF-β1 or BMP-2; however, this was found to be partly due to the inhibitory effect of exposure to high adenoviral loads. Our findings indicate that parameters such as these are important functional considerations for adapting gene transfer technologies to induce chondrogenesis of MSCs.
Abstract 10958: Circulating CD14++CD16+ Monocyte Subsets as a Surrogate Marker of Inflammatory Activity in Patients With Cardiac Sarcoidosis
Authors: Makoto Orii, Toshio Imanishi, Mao Yokoyama, Ikuko Teraguchi, Tsuyoshi Nishiguchi, Yasutsugu Shiono, Kunihiro Shimamura, Takashi Yamano, Takashi Tanimoto, Yoshiki Matsuo, Yasushi Ino, Tomoyuki Yamaguchi, Takashi Kubo, Kumiko Hirata, Atsushi Tanaka, Takashi Akasaka
Journal: Circulation (2014)

Aims: The aim of this study was to evaluate whether specific monocyte subsets could serve as surrogate markers of disease activity in cardiac sarcoidosis (CS) evaluated by 18F-fluoro-2-deoxyglucose positron emission tomography (18F-FDG PET).

Methods and Results: Twenty-five patients with CS (8 men, 17 women; mean age, 60 ± 9 years) diagnosed according to consensus criteria were enrolled in this study. We divided CS patients into two groups, known CS receiving corticosteroid therapy (Rx (+); n = 13) and new-onset CS (Rx (-); n = 12), and analyzed 3 distinct monocyte subsets (CD14+CD16–, CD14++CD16+, and CD14+–CD16+). Monocyte subsets were also analyzed in 7 Rx (-) patients before and 12 weeks after starting corticosteroid therapy. Inflammatory activity was quantified by 18F-FDG PET using the coefficient of variation (COV) of the standardized uptake value (SUV). The proportion of CD14++CD16+ monocytes in Rx (+) patients (10.8 \[0.2 to 23.5] %) was significantly lower than those in Rx (-) patients (25.2 [17.7 to 38.4] %, P = 0.001). After corticosteroid therapy, the COV of the SUV was significantly improved from 0.32 [0.14 to 0.46] to 0.14 [0.10 to 0.22\] (P = 0.011). The proportion of CD 14++16+ monocytes showed a significant decrease from 25.8 [17.7 to 38.4] % to 9.7 [2.5 to 16.8] % (P = 0.002). The decrease in the proportion of CD 14++16+ monocytes was significantly correlated with the decrease in the COV of the SUV (r = 0.693, P = 0.006).

Conclusion: CD 14++16+ monocytes are a possible surrogate marker of inflammatory activity in CS.

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921. Biopump: A Novel Approach to Gene-Mediated Protein Production and Delivery with Application for Erythropoietin Treatment of Anemia
Authors: Einat Brill-Almon, Andrew Pearlman, Baruch Stern, Noga Langer, Daniel Afik, Menachem Shavit, Yitzhak Lippin, Amos Panet, Eithan Galun, Eduardo Mitrani, Noam Shani
Journal: Molecular Therapy (2004)

We have developed the Biopump: a new approach to therapeutic protein production and delivery using the patient's own skin.
Abstract B24: Attenuated expression of a novel mitochondrial and metabolic gene contributes to acquired gefitinib resistance in lung tumors
Authors: Imoh S. Okon, Kathleen A. Coughlan, Ming-Hui Zou
Journal: Clinical Cancer Research (2015)

Abstract Therapeutic benefits provided by tyrosine kinase inhibitors (TKIs), such as Gefitinib (Iressa) and Erlotinib (Tarceva) have been limited by resistance which contributes to treatment failure and cancer-related mortality. Dysregulated metabolism (Warburg effect), a property of cancer cells has been linked to drug resistance, but the mechanisms remain unknown. In this study, MRC-9 (normal “non-cancer” cells), as well as A549, H1650, H1792 and H1975 lung adenocarcinoma cell lines (from ATCC; Manassas, VA) were used in order to examine those process(es) involved in the development of gefitinib resistance. Gefitinib is a specific, targeted agent against the epidermal growth factor receptor (EGFR) that competes for ATP-binding sites in the tyrosine activation domain of the receptor. Gefitinib-resistant H1650G cells were generated by subjecting parental H1650 cells to chronic gefitinib exposure for 12-16 weeks, and continuous culture under gefitinib selection. Consistent with existing literature, micro-array analysis of gefitinib-resistant H1650G cells confirmed differential expression of epithelial-mesenchymal transition (EMT) genes, such as vimentin, fascin1 and keratin19 compared to parental H1650 cells. Importantly, we uncovered the loss of a mitochondrial/metabolic gene intimately involved with glycolysis as a contributor to acquired gefitinib resistance in lung cancer cell lines and clinical specimens. Loss of expression of the novel target correlated with decreased ATP generation, and concomitant up-regulation of autophagy marker (LC3II), consistent with a compensatory mechanism of energy generation. Depletion (siRNA) of EGFR in parental H1650 cells was employed to mimic attenuated expression of the receptor due to sustained gefitinib treatment in H1650G cells, and correlated with decreased expression of the mitochondrial/metabolic target. This observation connects the EGFR signaling pathway with a novel mitochondrial/metabolic gene, and provides new insight into the development of acquired gefitinib resistance and adaptations by resistant cancer cells. The findings identify a novel potential target for therapeutic intervention, or biomarker functions that would enable informed patient selection with respect to gefitinib resistance. Citation Format: Imoh S. Okon, Kathleen A. Coughlan, Ming-Hui Zou. Attenuated expression of a novel mitochondrial and metabolic gene contributes to acquired gefitinib resistance in lung tumors. [abstract]. In: Proceedings of the AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; Jun 18-21, 2014; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(4 Suppl): Abstract nr B24.
Topical calcitriol restores the impairment of epidermal permeability and antimicrobial barriers induced by corticosteroids
Authors: S.P. Hong, Y. Oh, M. Jung, S. Lee, H. Jeon, M-Y. Cho, S.H. Lee, E.H. Choi
Journal: British Journal of Dermatology (2010)

Background The active form of vitamin D3, calcitriol, is widely used for the treatment of psoriasis, with or without topical corticosteroids. Topical corticosteroids are known to disrupt permeability and antimicrobial barriers, even with short-term use. Yet, the effect of topical calcitriol on epidermal permeability and antimicrobial barriers disrupted by topical corticosteroids has not been determined. Objectives To examine the effect of calcitriol on epidermal permeability and antimicrobial barrier function that has been impaired by corticosteroids, as well as to elucidate the mechanism of improvement. Material and methods Topical calcitriol or the control vehicle was applied to each flank of hairless mice 20 min after treatment with topical clobetasol propionate and repeated every 12 h for 3·5 days. Barrier function assessment, Nile red staining, electron microscopy, immunohistochemistry, Western blotting, and real-time reverse transcriptase–polymerase chain reaction studies were performed 24 h after the last application. Results Epidermis co-treated with topical calcitriol showed an improvement of stratum corneum integrity and barrier recovery, more intense fluorescence staining with Nile red, and an increase in lamellar body (LB) maturation and density, as well as upregulation of major epidermal lipid synthesis-related enzymes (3-hydroxy-3-methylglutaryl-CoA, serine-palmitoyl transferase and fatty acid synthase), mouse beta-defensin 3, cathelin-related antimicrobial peptide and vitamin D receptor. Conclusions We found that topical calcitriol restored both the epidermal permeability and antimicrobial barrier that had been impaired by corticosteroids. This restoration was mediated by both an activation of the cutaneous vitamin D pathway and an increase of epidermal lipids and antimicrobial peptides, promoted by the formation of the LB and the activity of epidermal lipid synthesis-related enzymes.