tbuckley/cabot-search huggingface dataset:
Childhood Cardiovascular Risk Factors and Carotid Vascular Changes in Adulthood
Authors: Shengxu Li, Wei Chen, Sathanur R. Srinivasan, M. Gene Bond, Rong Tang, Elaine M. Urbina, Gerald S. Berenson
Journal: JAMA (2003)

<h3>Context</h3> Carotid artery intima-media thickness (IMT) is associated with cardiovascular risk factors and is recognized as an important predictive measure of clinical coronary atherosclerosis events in middle-aged and elderly populations. However, information on the association of carotid IMT in young adults with different risk factors measured in childhood, adulthood, or as a cumulative burden of each of the risk factors measured serially from childhood to adulthood is limited. <h3>Objective</h3> To examine the association between carotid IMT in young adults and traditional cardiovascular risk factors measured since childhood. <h3>Design, Setting, and Participants</h3> A cohort study of 486 adults aged 25 to 37 years from a semirural black and white community in Bogalusa, La (71% white, 39% men), who had at least 3 measurements of traditional risk factors since childhood, conducted between September 1973 and December 1996. <h3>Main Outcome Measure</h3> Association of carotid IMT with risk factors, including systolic blood pressure, lipoprotein levels, and body mass index. <h3>Results</h3> Male vs female (0.757 mm vs 0.719 mm) and black vs white (0.760 mm vs 0.723 mm) participants had increased carotid IMT (<i>P</i>&lt;.001 for both). In multivariable analyses, significant predictors for being in top vs lower 3 quartiles of carotid IMT in young adults were childhood measures of low-density lipoprotein cholesterol (LDL-C) level (odds ratio [OR], 1.42, corresponding to 1-SD change specific for age, race, and sex; 95% confidence interval [CI], 1.14-1.78) and body mass index (BMI; OR, 1.25; 95% CI, 1.01-1.54); adulthood measures of LDL-C level (OR, 1.46; 95% CI, 1.16-1.82), high-density lipoprotein cholesterol (HDL-C) level (OR, 0.67; 95% CI, 0.51-0.88), and systolic blood pressure (OR, 1.36; 95% CI, 1.08-1.72); and long-term cumulative burden of LDL-C (OR, 1.58; 95% CI, 1.24-2.01) and HDL-C (OR, 0.75; 95% CI, 0.58-0.97) levels measured serially from childhood to adulthood. An increasing trend in carotid IMT across quartiles of LDL-C level measured in childhood was observed, with a mean value of 0.761 mm (95% CI, 0.743-0.780 mm) for those at the top quartile vs 0.724 mm (95% CI, 0.715-0.734 mm) for those in the lower 3 quartiles (<i>P</i>&lt;.001). <h3>Conclusions</h3> Childhood measures of LDL-C level and BMI predict carotid IMT in young adults. The prevention implications of these findings remains to be explored.
Bullous Amyloidosis vs Epidermolysis Bullosa Acquisita
Authors: John Fredrick Bluhm
Journal: JAMA (1981)

To the Editor.—  In the article by Trump et al (1980;243:1461), the case was referred to as epidermolysis bullosa acquisita rather than bullous amyloidosis; the distinction is more than semantic and should be clarified. Although both are subepidermal bullous diseases, the bullae in epidermolysis bullosa acquisita form through the anchoring fibril region just below the basal lamina unrelated to cutaneous amyloid deposits, 1-4 whereas bullous amyloidosis shows separation through the fragile amyloid-laden dermis as demonstrated nicely by Trump et al in their case report.  Of those cases referenced by Trump et al, the reports by Sams and Smith and Brauner et al 5 are epidermolysis bullosa acquisita associated with visceral amyloidosis in contrast to those of Northover et al and Muller et al that show bullae through cutaneous amyloid deposits and should be called bullous amyloidosis. The distinction was recognized by Brauner et al 5 and has been clarified further
Abstract 2199: Associations of genetic polymorphisms in <i>VEGFR1</i> with progression-free and overall survival in patients with neuroendocrine tumors treated with the VEGFA inhibitor bevacizumab.
Authors: Monica Ter-Minassian, ZhiRong R. Qian, Jennifer A. Chan, Susanne M. Hooshmand, Lauren K. Brais, Rachel Heafield, Xihong Lin, Geoffrey Liu, David C. Christiani, Matthew H. Kulke
Journal: Cancer Research (2013)

Abstract Background: Neuroendocrine tumors (NET) have been shown to be responsive to treatment with VEGF pathway inhibitors. We hypothesized that genetic variation in VEGFA, VEGFR1 or VEGFR2 is associated with progression free survival (PFS) and/or overall survival (OS) in patients with metastatic NET treated with bevacizumab, a monoclonal antibody targeting VEGFA. Methods: We selected 61 functional and tagging SNPs with a minor allele frequency of 5% or greater, with full gene coverage of VEGFA, VEGFR1 and VEGFR2. We pooled data from two genotyped datasets, selecting 82 patients with metastatic NET who received bevacizumab administered either as a single agent or as part of a combination regimen. Using a Cox proportional hazards regression analysis, and an additive genetic model, we tested the SNPs’ associations with PFS and OS adjusting for age and stage at diagnosis, gender, tumor origin, grade of differentiation, and genotyping dataset. Results: We found that 4 intronic tagging SNPs in VEGFR1, rs7987649, rs9508021, rs9513095 and rs2104330 were associated with PFS at p&amp;lt;0.05. The association between rs7987649 and PFS (multivariate Hazard Ratio 0.55 (0.38, 0.81) p=0.002) remained significant after adjusting for multiple testing. One of the four SNPs associated with PFS, rs7987649, as well as another SNP in VEGFR1, rs3794339, were associated with OS at p&amp;lt;0.05 although these associations did not remain significant after multiple testing adjustment. No SNPs in either VEGFR2 or VEGFA were associated with PFS or OS. Conclusions: In patients with neuroendocrine tumors treated with bevacizumab, the VEGFR1 SNP rs7987649 appears to be associated with progression-free survival. We note that three SNPs identified in our analysis, rs9508021, rs9513095 and rs2104330, are in strong linkage disequilibrium with SNPs rs7993418 and rs9582036, which have been associated with increased VEGFR1 expression and with PFS and OS in pancreatic adenocarcinoma (Lambrechts, 2012). Further study of loci within this region of VEGFR1 is warranted to discover potential causal variants affecting NET survival. Citation Format: Monica Ter-Minassian, ZhiRong R. Qian, Jennifer A. Chan, Susanne M. Hooshmand, Lauren K. Brais, Rachel Heafield, Xihong Lin, Geoffrey Liu, David C. Christiani, Matthew H. Kulke. Associations of genetic polymorphisms in VEGFR1 with progression-free and overall survival in patients with neuroendocrine tumors treated with the VEGFA inhibitor bevacizumab. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2199. doi:10.1158/1538-7445.AM2013-2199
Blood compatibility of amorphous titanium oxide films synthesized by ion beam enhanced deposition
Authors: Huang Nan, Yang Ping, Cheng Xuan, Leng Yongxang, Zheng Xiaolan, Cai Guangjun, Zhen Zihong, Zhang Feng, Chen Yuanru, Liu Xianghuai, Xi Tingfei
Journal: Biomaterials (1998)
Airborne Endotoxin Concentrations in Homes Burning Biomass Fuel
Authors: Sean Semple, Delan Devakumar, Duncan G. Fullerton, Peter S. Thorne, Nervana Metwali, Anthony Costello, Stephen B. Gordon, Dharma S. Manandhar, Jon G. Ayres
Journal: Environmental Health Perspectives (2010)

BackgroundAbout half of the world's population is exposed to smoke from burning biomass fuels at home. The high airborne particulate levels in these homes and the health burden of exposure to this smoke are well described. Burning unprocessed biological material such as wood and dried animal dung may also produce high indoor endotoxin concentrations.ObjectiveIn this study we measured airborne endotoxin levels in homes burning different biomass fuels.MethodsAir sampling was carried out in homes burning wood or dried animal dung in Nepal (n = 31) and wood, charcoal, or crop residues in Malawi (n = 38). Filters were analyzed for endotoxin content expressed as airborne endotoxin concentration and endotoxin per mass of airborne particulate.ResultsAirborne endotoxin concentrations were high. Averaged over 24 hr in Malawian homes, median concentrations of total inhalable endotoxin were 24 endotoxin units (EU)/m3 in charcoal-burning homes and 40 EU/m3 in wood-burning homes. Short cooking-time samples collected in Nepal produced median values of 43 EU/m3 in wood-burning homes and 365 EU/m3 in dung-burning homes, suggesting increasing endotoxin levels with decreasing energy levels in unprocessed solid fuels.ConclusionsAirborne endotoxin concentrations in homes burning biomass fuels are orders of magnitude higher than those found in homes in developed countries where endotoxin exposure has been linked to respiratory illness in children. There is a need for work to identify the determinants of these high concentrations, interventions to reduce exposure, and health studies to examine the effects of these sustained, near-occupational levels of exposure experienced from early life.
In vitro metabolism of the phosphorothioate radioprotectors WR-2721 and WR-3689
Authors: John C. Livesey, Janet S. Rasey, Sarah Vertrees, Lynne M. Freeman, Sara Magee, Norma J. Nelson, Lay Chin, Zdenka Grunbaum, Kenneth A. Krohn
Journal: Pharmacology & Therapeutics (1988)
Landmines: A Deadly Legacy
Authors: I Doucet
Journal: BMJ (1994)

Arms Project of Human Rights Watch/Physicians for Human Rights, £20, pp 528 ISBN 1-56432-113-4

“We may be leaving, but your land will go on fighting you for many generations to come.” That possibly apocryphal statement by a soldier during the Soviet withdrawal from Afghanistan conveys the moral and legal objections to landmines: they cannot distinguish between the footfall of a soldier and of a civilian and they remain hidden, and dangerous, for decades after the war's end. Landmines: A Deadly Legacy is an acutely appropriate title, which this book elaborates in convincing detail.

In …
Kenneth Newton Lloyd
Authors: J. Jessop, G. Nuki
Journal: BMJ (2012)

Kenneth Newton Lloyd (“Ken”) was a champion of physical medicine and rheumatology in Wales. Combining vision, forceful personality, and political skills, he created, more than 60 years ago, the first department in Wales to specialise in the treatment of rheumatic diseases. It was an NHS facility, designed to respond to not only the huge clinical demands from the population of Cardiff, with a heritage of heavy industries and physical injuries, but also to referrals of patients with chronic rheumatic diseases from across south Wales. This formed the nucleus for what later became the first teaching centre in Wales for trainees in rheumatology.

Kenneth Newton Lloyd was born in London, the second of five sons of Grace and Ernest Lloyd, an Inner Temple barrister at law. He boarded at Mill Hill School, and then entered the London Hospital Medical College in 1932. He completed house jobs at the London Hospital before further medical training was interrupted by the second world war.

The defeat at Dunkirk prompted Ken to volunteer for service in the Royal Air Force. He was appointed as a medical officer at RAF Tangmere in West Sussex, the home of two Hurricane fighter squadrons, where he remained throughout the Battle of Britain. After marriage to Phyllis in 1941, he was posted to north Africa at the time of Rommel’s north African …
Abstract 574: α-santalol induces caspase-dependent apoptosis and G2/M phase cell cycle arrest in human breast cancer cells
Authors: Sreevidya Santha, Ajay Bommareddy, Brittny Rule, Ruth Guillermo, Radhey S. Kaushik, Alan Young, Chandradhar Dwivedi
Journal: Cancer Research (2012)

Abstract Alpha-santalol, an active component of sandalwood oil, has been shown to have chemopreventive effects on skin cancer both in vitro and in vivo. However, effects of alpha-santalol on other types of cancer have not been studied. In this study, we examine the effects and mechanisms of action of alpha-santalol on human breast cancer cells using estrogen receptor (ER)- positive (MCF-7) and estrogen receptor- negative (MDA-MB-231) breast cancer cell lines. MTT and BrdU cell proliferation ELISA results showed inhibition of cell viability and proliferation in a time and dose-dependent manner in both cell lines. Alpha-santalol at 25-150 µM concentration decreased cell viability after 12h treatment. In addition, TUNEL assay and flow cytometry results revealed that alpha-santalol significantly induced apoptosis in MCF-7 and MDA-MB-231 cells. Further, immunoblotting and caspase activity assays showed involvement of caspase-3, caspase-8 and caspase-9 in apoptotic cell death. Induction of apoptosis by alpha-santalol was further confirmed by detecting the cleavage of Poly (ADP-ribose) Polymerase (PARP) through western blotting. Cell cycle distribution of alpha-santalol treated MFC-7 and MDA-MB-231 cells were analyzed by fluorescence- activated cell sorting (FACS) analysis of propidium iodide staining. We observed that alpha-santalol treatment arrests cell cycle at G2/M phase at 25µM −75µM concentration in both cell lines. Taken together, our studies reveal a potential mechanism for the chemopreventive effect of alpha-santalol on ER- positive and ER- negative breast cancer cells through induction of apoptosis and cell cycle arrest at G2/M phase. Alpha-santalol could be effective for the prevention and treatment of breast cancer. (Supported by Translational Cancer Research Center funded by South Dakota, Governors Office of Economic Development) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 574. doi:1538-7445.AM2012-574
Risk of Human Immunodeficiency Virus Transmission From Heterosexual Adults With Transfusion-Associated Infections
Authors: Thomas A. Peterman
Journal: JAMA (1988)

The risk of human immunodeficiency virus (HIV) transmission was studied by interviewing and testing the serum of heterosexual contacts and casual family contacts of adults with transfusion-associated HIV infections. Two (8%) of 25 husbands and ten (18%) of 55 wives who had had sexual contact with infected spouses were seropositive for HIV. Compared with seronegative wives, the seropositive wives were older (median ages, 54 and 62 years; P = .08) and actually reported somewhat fewer sexual contacts with their infected husbands (means, 156 and 82; P greater than .1). There was no difference in the types of sexual contact or methods of contraception of the seropositive and seronegative spouses. There was no evidence of HIV transmission to the 63 other family members. Although most husbands and wives remained uninfected despite repeated sexual contact without protection, some acquired infection after only a few contacts. This is consistent with an as yet unexplained biologic variation in transmissibility or susceptibility.
Interim Policy to Prevent Coronary Heart Disease
Authors: James J. Nora
Journal: JAMA (1976)

While neither Williams and Wynder in this issue (p 2196) nor we are in a position to set national policy to prevent coronary heart disease, it is useful to discuss, with the goal of defining, what could reasonably be included in such a policy at the present stage of our knowledge. Williams and Wynder begin with the currently popular assumption, not yet proved, that the frequency rate of heart attacks in adults may be decreased by instituting preventive programs in childhood. This assumption arose in part from the realization that preventive measures started in middle-adult life did little to decrease heart attacks.<sup>1</sup>It is also known that atherosclerotic lesions begin in childhood and can be fairly advanced by the age of 20 years. Therefore, a way to prevent heart attacks is to begin a "moderate intervention program" in childhood. The questions we raise are (1) is the intervention suggested
Results of triple valve replacement in 91 patients: perioperative mortality and long-term follow-up.
Authors: B J Gersh, H V Schaff, P J Vatterott, G K Danielson, T A Orszulak, J M Piehler, F J Puga, J R Pluth, D C McGoon
Journal: Circulation (1985)

Between 1961 and 1984, 91 patients underwent simultaneous triple valve replacement at the Mayo Clinic. Of the 273 prosthetic valves used, 77% were Starr-Edwards. Perioperative (30 day) mortality was 24% to 27% between 1962 and 1974 and 7% between 1975 and 1983 (p = .17). In patients with NYHA class IV symptoms, perioperative mortality was 44%, and in those with milder symptoms, it was 8% (p less than .0001). The median follow-up was 7.5 years (range, 6 weeks to 20 years). Cumulative survival, which was calculated taking into consideration perioperative mortality, was 64% at 1 year, 55% at 5 years, 40% at 10 years, and 25% at 15 years. Multivariate analysis identified preoperative functional class and age as predictors of late survival. Among causes of late mortality were sudden death in 32.5%, congestive heart failure in 15%, thromboembolism in 12.5%, prosthetic valve dysfunction in 7.5%, and infective endocarditis in 5%. Late complications included systemic emboli in 42% (embolic rate, 12.3 events per 100 patient-years), bleeding in 22%, myocardial infarction in 16%, and infective endocarditis in 6%. Eight patients required reoperation for prosthetic valve dysfunction, and 12 patients had permanent pacemakers. Of the 29 patients still alive, 79% are in NYHA class I or II. In summary, perioperative mortality after triple valve replacement appears to be declining; long-term survival in 30 day survivors is similar to that after single valve replacement and excellent symptomatic improvement can be obtained, although morbidity is high.
The Role of Endoplasmic Reticulum Stress in the Progression of Atherosclerosis
Authors: Ira Tabas
Journal: Circulation Research (2010)

Prolonged activation of the endoplasmic reticulum (ER) stress pathway known as the unfolded protein response (UPR) can lead to cell pathology and subsequent tissue dysfunction. There is now ample evidence that the UPR is chronically activated in atherosclerotic lesional cells, particularly advanced lesional macrophages and endothelial cells. The stressors in advanced lesions that can lead to prolonged activation of the UPR include oxidative stress, oxysterols, and high levels of intracellular cholesterol and saturated fatty acids. Importantly, these arterial wall stressors may be especially prominent in the settings of obesity, insulin resistance, and diabetes, all of which promote the clinical progression of atherosclerosis. In the case of macrophages, prolonged ER stress triggers apoptosis, which in turn leads to plaque necrosis if the apoptotic cells are not rapidly cleared. ER stress-induced endothelial cell apoptosis may also contribute to plaque progression. Another potentially important proatherogenic effect of prolonged ER stress is activation of inflammatory pathways in macrophages and, perhaps in response to atheroprone shear stress, endothelial cells. Although exciting work over the last decade has begun to shed light on the mechanisms and in vivo relevance of ER stress-driven atherosclerosis, much more work is needed to fully understand this area and to enable an informed approach to therapeutic translation.
A wiring demon meets socialized humans and calibrated photometers
Authors: Michael H. Brill
Journal: Behavioral and Brain Sciences (1999)

Ignoring consciousness, I apply Palmer's ideas to a photometer, for which calibration is analogous to socialization of humans to agree in color. Some attributes of the photometer – such as its aperture – do not need to be known because their values are transparent to calibration. But a writing demon can wreak havoc if it permutes measured values before interpolation completes calibration – as happens in Palmer's color rewirings.
Insulin Resistance, ADMA Levels, and Cardiovascular Disease
Authors: David T. Nash
Journal: JAMA (2002)

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Is coronary endothelial function impaired both at the level of resistance vessels and at that of conduit vessels in women with atypical chest pain?
Authors: Hiroki Teragawa, Keiji Matsuda, Kentaro Ueda, Masashi Kimura, Fumiharu Miura, Hidekazu Hirao, Kazuaki Chayama, Masao Yoshizumi
Journal: Journal of the American College of Cardiology (2003)
Abstract 293: Tumor cell cross-talk with tumor-associated leukocytes leads to induction of tumor exosomal fibronectin and promotes tumor progression
Authors: Huang-Ge Zhang, ZhongBin Deng
Journal: Cancer Research (2012)

Abstract Exosomes play an important role in intercellular communication. However, most data published are based on exosomes released from in vitro cultured cells that do not exhibit communication with neighboring cells located in the same microenvironment as the exosomal producing cells, and therefore in vitro culture experiments do not represent what occurs in vivo. In this study, our data show that co-culture of leukocytes isolated from breast tumor tissue leads to uptake of fibronectin on/in the tumor exosomes (Exofib+). The induction of fibronectin and exosomal uptake is tumor tissue derived, leukocyte specific, as leukocytes isolated from peripheral blood of naïve mice failed to induce fibronectin uptaken by tumor exosomes. Furthermore, depletion of both CD25+ cells and Gr-1+ cells from tumor-associated leukocytes causes a reduction of Exofib+ suggesting that tumor-associated CD25+ cells and Gr-1+ cells play a role in fibronectin production and uptake by tumor exosomes resulting in Exofib+. As a result of tumor cells taking up Exofib+ two major events are induced: FAK/Src-dependent signaling pathways are activated, and the production of proinflammatory cytokines and metalloproteinase 9 is enhanced in response to taking up exosomes and this in turn enhances tumor cell invasion in vitro as well as in vivo. Collectively, our findings provide evidence that exosomes released from freshly excised tumor tissue cells that have communicated/interacted with immune cells gain new immune evasion capacity. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 293. doi:1538-7445.AM2012-293