tbuckley/cabot-search huggingface dataset:
Characteristics Associated With Differences in Survival Among Black and White Women With Breast Cancer
Authors: Jeffrey H. Silber, Paul R. Rosenbaum, Amy S. Clark, Bruce J. Giantonio, Richard N. Ross, Yun Teng, Min Wang, Bijan A. Niknam, Justin M. Ludwig, Wei Wang, Orit Even-Shoshan, Kevin R. Fox
Journal: JAMA (2013)

<h3>Importance</h3> Difference in breast cancer survival by race is a recognized problem among Medicare beneficiaries. <h3>Objective</h3> To determine if racial disparity in breast cancer survival is primarily attributable to differences in presentation characteristics at diagnosis or subsequent treatment. <h3>Design, Setting, and Patients</h3> Comparison of 7375 black women 65 years and older diagnosed between 1991 to 2005 and 3 sets of 7375 matched white control patients selected from 99 898 white potential controls, using data for 16 US Surveillance, Epidemiology and End Results (SEER) sites in the SEER-Medicare database. All patients received follow-up through December 31, 2009, and the black case patients were matched to 3 white control populations on demographics (age, year of diagnosis, and SEER site), presentation (demographics variables plus patient comorbid conditions and tumor characteristics such as stage, size, grade, and estrogen receptor status), and treatment (presentation variables plus details of surgery, radiation therapy, and chemotherapy). <h3>Main Outcomes and Measures</h3> 5-Year survival. <h3>Results</h3> The absolute difference in 5-year survival (blacks, 55.9%; whites, 68.8%) was 12.9% (95% CI, 11.5%-14.5%;<i>P</i> &lt; .001) in the demographics match. This difference remained unchanged between 1991 and 2005. After matching on presentation characteristics, the absolute difference in 5-year survival was 4.4% (95% CI, 2.8%-5.8%;<i>P</i> &lt; .001) and was 3.6% (95% CI, 2.3%-4.9%;<i>P</i> &lt; .001) lower for blacks than for whites matched also on treatment. In the presentation match, fewer blacks received treatment (87.4% vs 91.8%;<i>P</i> &lt; .001), time from diagnosis to treatment was longer (29.2 vs 22.8 days;<i>P</i> &lt; .001), use of anthracyclines and taxols was lower (3.7% vs 5.0%;<i>P</i> &lt; .001), and breast-conserving surgery without other treatment was more frequent (8.2% vs 7.3%;<i>P</i> = .04). Nevertheless, differences in survival associated with treatment differences accounted for only 0.81% of the 12.9% survival difference. <h3>Conclusions and Relevance</h3> In the SEER-Medicare database, differences in breast cancer survival between black and white women did not substantially change among women diagnosed between 1991 and 2005. These differences in survival appear primarily related to presentation characteristics at diagnosis rather than treatment differences.
Remodeling of Resistance Arteries in Renal Failure
Authors: KERSTIN AMANN, GABRIEL MIL TENBERGER-MIL TENYI, AURELIA SIMONOVICIENE, ANDREAS KOCH, STEPHAN ORTH, EBERHARD RITZ
Journal: Journal of the American Society of Nephrology (2001)

Remodeling of vessels is a known feature of renal failure, but it is unclear whether this represents an appropriate or inappropriate response to the known changes in blood flow, shear stress, and wall tension. To investigate remodeling in response to variations in blood flow, first-order mesenteric arteries were exposed to high- and low-flow conditions via the ligation of second-order branches, according to the technique described by Pour-ageaud and De Mey. The resulting changes in vessel geometric features, relative proportions of intima and media, submicroscopic structure, and immunostaining for proliferating cell nuclear antigen (PCNA), endothelin-1 (ET-1), and ETA receptors were assessed in first-order mesenteric arteries under low-flow and high-flow conditions. Subtotally nephrectomized (SNX) animals were compared with sham-operated rats. Animals either were left untreated or were treated with the ETA receptor antagonist (ET-RA) LU-135252, because of suggestions in the literature that ET is involved in vascular remodeling in uremia. A highly significant increase in intimal thickness was noted in low-flow arteries (4.21 ± 1.39 μm) of SNX animals, compared with normal-flow arteries (2.06 ± 0.61 μm), but this increase was not observed in sham-operated rats (1.38 ± 0.77 in low-flow arteries versus 2.40 ± 0.35 μm in normal-flow arteries). The increase in intimal thickness in low-flow arteries was abrogated by ET-RA. The medial thickness was increased in untreated SNX animals (19.5 ± 3.61 μm), compared with sham-operated rats, and this increase was also prevented by ET-RA. The medial thickness was not affected by low flow in either sham-operated or SNX animals. In parallel, the number of PCNA-positive intimal cells was higher in low-flow, but not high-flow, arteries of SNX rats, compared with sham-operated rats. No significant change was observed in sham-operated animals. In the media, the number of PCNA-positive cells was higher in untreated SNX animals than in sham-operated rats. The number was even more markedly increased in high-flow, but not low-flow, vessels. This increase was abrogated by ET-RA. It is concluded that, in uremic animals, the response of the intima to low flow and the response of the media to high flow are exaggerated. Both responses are apparently mediated by ET.
Myocardial Infarction Triggers Chronic Cardiac Autoimmunity in Type 1 Diabetes
Authors: Raju V. S. R. K. Gottumukkala, HuiJuan Lv, Lizbeth Cornivelli, Amy J. Wagers, Raymond Y. Kwong, Roderick Bronson, Garrick C. Stewart, P. Christian Schulze, William Chutkow, Howard A. Wolpert, Richard T. Lee, Myra A. Lipes
Journal: Science Translational Medicine (2012)

Acute myocardial infarction triggers an autoimmune attack on the heart in a mouse model of type 1 diabetes and in human type 1 diabetic patients.
Changes in the Activities of Lysosomal Enzymes in Infarcted Canine Heart Muscle
Authors: KURT G. RAVENS, S. GUDBJARNASON
Journal: Circulation Research (1969)

Experimental myocardial infarction was produced in 32 mongrel dogs. The changes in activity of four lysosomal enzymes (acid phosphatase, glucuronidase, deoxyribonuclease, and γ-glutamyl-transpeptidase) were examined in the soluble and the particle-bound fraction. The pattern of changes in free and particle-bound enzyme activity observed was similar for all four enzymes. During the first 48 hours after coronary occlusion, the particle-bound enzyme activity was decreased, while the free activity was moderately increased, reflecting the autolytic phase of cell and tissue destruction. Between the second and the sixth day, the soluble hydrolytic enzyme activity was maximal and the particle-bound activity was slowly increasing. During this period, the main part of tissue degradation and removal of cell debris takes place. Ten days after myocardial infarction the free hydrolytic activity had returned to control values, but the particle-bound enzyme activity was four to ten times higher in the infarcted tissue than in the control muscle.
A Randomized Trial of Icatibant in ACE-Inhibitor–Induced Angioedema
Authors: Murat Baş, Jens Greve, Klaus Stelter, Miriam Havel, Ulrich Strassen, Nicole Rotter, Johannes Veit, Beate Schossow, Alexander Hapfelmeier, Victoria Kehl, Georg Kojda, Thomas K. Hoffmann
Journal: New England Journal of Medicine (2015)

Angioedema induced by treatment with angiotensin-converting–enzyme (ACE) inhibitors accounts for one third of angioedema cases in the emergency room; it is usually manifested in the upper airway and the head and neck region. There is no approved treatment for this potentially life-threatening condition.
The quest for genetic risk factors for Crohn's disease in the post-GWAS era
Authors: Karin Fransen, Mitja Mitrovic, Cleo C van Diemen, Rinse K Weersma
Journal: Genome Medicine (2011)

Multiple genome-wide association studies (GWASs) and two large scale meta-analyses have been performed for Crohn's disease and have identified 71 susceptibility loci. These findings have contributed greatly to our current understanding of the disease pathogenesis. Yet, these loci only explain approximately 23% of the disease heritability. One of the future challenges in this post-GWAS era is to identify potential sources of the remaining heritability. Such sources may include common variants with limited effect size, rare variants with higher effect sizes, structural variations, or even more complicated mechanisms such as epistatic, gene-environment and epigenetic interactions. Here, we outline potential sources of this hidden heritability, focusing on Crohn's disease and the currently available data. We also discuss future strategies to determine more about the heritability; these strategies include expanding current GWAS, fine-mapping, whole genome sequencing or exome sequencing, and using family-based approaches. Despite the current limitations, such strategies may help to transfer research achievements into clinical practice and guide the improvement of preventive and therapeutic measures.
Innate and adaptive immune responses in chronic hepatitis B virus infections: towards restoration of immune control of viral infection
Authors: Antonio Bertoletti, Carlo Ferrari
Journal: Gut (2011)

Knowledge of the immunological events necessary to control hepatitis B virus (HBV) infection has accelerated in recent years, but their translation towards therapeutic strategies able to achieve a durable HBV suppression has been challenging. The scenario of how HBV deals with the host immunity is presented and used to discuss how the immune response can be harnessed to potentially achieve infection control.
Signatures of the Preagricultural Peopling Processes in Sub-Saharan Africa as Revealed by the Phylogeography of Early Y Chromosome Lineages
Authors: C. Batini, G. Ferri, G. Destro-Bisol, F. Brisighelli, D. Luiselli, P. Sanchez-Diz, J. Rocha, T. Simonson, A. Brehm, V. Montano, N. E. Elwali, G. Spedini, M. E. D'Amato, N. Myres, P. Ebbesen, D. Comas, C. Capelli
Journal: Molecular Biology and Evolution (2011)

The study of Y chromosome variation has helped reconstruct demographic events associated with the spread of languages, agriculture, and pastoralism in sub-Saharan Africa, but little attention has been given to the early history of the continent. In order to overcome this lack of knowledge, we carried out a phylogeographic analysis of haplogroups A and B in a broad data set of sub-Saharan populations. These two lineages are particularly suitable for this objective because they are the two most deeply rooted branches of the Y chromosome genealogy. Their distribution is almost exclusively restricted to sub-Saharan Africa where their frequency peaks at 65% in groups of foragers. The combined high-resolution single nucleotide polymorphism analysis with short tandem repeats variation of their subclades reveals strong geographic and population structure for both haplogroups. This has allowed us to identify specific lineages related to regional preagricultural dynamics in different areas of sub-Saharan Africa. In addition, we observed signatures of relatively recent contact, both among Pygmies and between them and Khoisan speaker groups from southern Africa, thus contributing to the understanding of the complex evolutionary relationships among African hunter-gatherers. Finally, by revising the phylogeography of the very early human Y chromosome lineages, we have obtained support for the role of southern Africa as a sink, rather than a source, of the first migrations of modern humans from eastern and central parts of the continent. These results open new perspectives on the early history of Homo sapiens in Africa, with particular attention to areas of the continent where human fossil remains and archaeological data are scant.
Silicon Micro‐ and Nanofabrication for Medicine
Authors: Daniel Fine, Alessandro Grattoni, Randy Goodall, Shyam S. Bansal, Ciro Chiappini, Sharath Hosali, Anne L. van de Ven, Srimeenkashi Srinivasan, Xuewu Liu, Biana Godin, Louis Brousseau, Iman K. Yazdi, Joseph Fernandez‐Moure, Ennio Tasciotti, Hung‐Jen Wu, Ye Hu, Steve Klemm, Mauro Ferrari
Journal: Advanced Healthcare Materials (2013)

Abstract This manuscript constitutes a review of several innovative biomedical technologies fabricated using the precision and accuracy of silicon micro‐ and nanofabrication. The technologies to be reviewed are subcutaneous nanochannel drug delivery implants for the continuous tunable zero‐order release of therapeutics, multi‐stage logic embedded vectors for the targeted systemic distribution of both therapeutic and imaging contrast agents, silicon and porous silicon nanowires for investigating cellular interactions and processes as well as for molecular and drug delivery applications, porous silicon (pSi) as inclusions into biocomposites for tissue engineering, especially as it applies to bone repair and regrowth, and porous silica chips for proteomic profiling. In the case of the biocomposites, the specifically designed pSi inclusions not only add to the structural robustness, but can also promote tissue and bone regrowth, fight infection, and reduce pain by releasing stimulating factors and other therapeutic agents stored within their porous network. The common material thread throughout all of these constructs, silicon and its associated dielectrics (silicon dioxide, silicon nitride, etc.), can be precisely and accurately machined using the same scalable micro‐ and nanofabrication protocols that are ubiquitous within the semiconductor industry. These techniques lend themselves to the high throughput production of exquisitely defined and monodispersed nanoscale features that should eliminate architectural randomness as a source of experimental variation thereby potentially leading to more rapid clinical translation.
Acute Leukemia In Adults, 1977
Authors: M. J. Keating, E. J. Freireich, K. B. McCredie, G. P. Bodey, E. Hersh, J. P. Hester, V. Rodriguez, J. Hart
Journal: CA A Cancer Journal for Clinicians (1977)

In the last decade, considerable progress has been made in the understanding, diagnosis, classification and treatment of acute leukemia.Now known to be a malignant disorder of the blood forming organs, acute leukemia is characterized by progressive accumulation of primi tive blood cells that have lost the capac ity for normal maturation.This accumu lation impairs the production of normal blood elements by the bone marrow, re sulting in anemia, neutropenia, throm bocytopenia and, if uncontrolled by treatment, death usually from infection or hemorrhage.Formerly, the diagnosis of acute leukemia in an adult was fol lowed shortly by death.Today, modem treatment can result in complete remis sion of the disease in most adults, with some patients surviving for prolonged periods of time. IncidenceThe incidence of acute leukemia steadily increased in this century, until the 1960s, when a leveling off in the rising curve was noted.1Although much of the increase can be attributed to greater access to medical and diagnostic facili ties, a modest true increase probably oc curred.Ninety percent of patients with acute myelogenous leukemia (AML) are adults, one-third of whom are over 60 years old.However, adults account for only 20 percent of patients with acute lymphoblastic leukemia (ALL).As in other neoplastic diseases, incidence in creases with age.2 Etiology Many tantalizing clues to the cause of acute leukemia have been uncovered and are being actively pursued.Racial
Transesophageal Echocardiography
Authors: Gail E. Peterson, M. Elizabeth Brickner, Sharon C. Reimold
Journal: Circulation (2003)

A 36 year-old woman without significant past medical history was admitted with left-sided hemiparesis.Imaging studies confirmed a right middle cerebral artery (MCA) stroke with normal carotid arteries.Transesophageal echocardiogram (TEE) showed right heart enlargement and a large secundum atrial septal defect (ASD) (Figure 1).Using TEE guidance, an ASD occluder device was placed without complication (Figure 2).
Renal Denervation Prevents Immune Cell Activation and Renal Inflammation in Angiotensin II–Induced Hypertension
Authors: Liang Xiao, Annet Kirabo, Jing Wu, Mohamed A. Saleh, Linjue Zhu, Feng Wang, Takamune Takahashi, Roxana Loperena, Jason D. Foss, Raymond L. Mernaugh, Wei Chen, Jackson Roberts, John W. Osborn, Hana A. Itani, David G. Harrison
Journal: Circulation Research (2015)

Inflammation and adaptive immunity play a crucial role in the development of hypertension. Angiotensin II and probably other hypertensive stimuli activate the central nervous system and promote T-cell activation and end-organ damage in peripheral tissues.To determine if renal sympathetic nerves mediate renal inflammation and T-cell activation in hypertension.Bilateral renal denervation using phenol application to the renal arteries reduced renal norepinephrine levels and blunted angiotensin II-induced hypertension. Bilateral renal denervation also reduced inflammation, as reflected by decreased accumulation of total leukocytes, T cells, and both CD4+ and CD8+ T cells in the kidney. This was associated with a marked reduction in renal fibrosis, albuminuria, and nephrinuria. Unilateral renal denervation, which partly attenuated blood pressure, only reduced inflammation in the denervated kidney, suggesting that this effect is pressure independent. Angiotensin II also increased immunogenic isoketal-protein adducts in renal dendritic cells (DCs) and increased surface expression of costimulation markers and production of interleukin (IL)-1α, IL-1β, and IL-6 from splenic DCs. Norepinephrine also dose dependently stimulated isoketal formation in cultured DCs. Adoptive transfer of splenic DCs from angiotensin II-treated mice primed T-cell activation and hypertension in recipient mice. Renal denervation prevented these effects of hypertension on DCs. In contrast to these beneficial effects of ablating all renal nerves, renal afferent disruption with capsaicin had no effect on blood pressure or renal inflammation.Renal sympathetic nerves contribute to DC activation, subsequent T-cell infiltration and end-organ damage in the kidney in the development of hypertension.
Cancer Risks and Mortality in Heterozygous ATM Mutation Carriers
Authors: Deborah Thompson, Silvia Duedal, Jennifer Kirner, Lesley McGuffog, James Last, Anne Reiman, Philip Byrd, Malcolm Taylor, Douglas F. Easton
Journal: JNCI Journal of the National Cancer Institute (2005)

Homozygous or compound heterozygous mutations in the ATM gene are the principal cause of ataxia telangiectasia (A-T). Several studies have suggested that heterozygous carriers of ATM mutations are at increased risk of breast cancer and perhaps of other cancers, but the precise risk is uncertain.Cancer incidence and mortality information for 1160 relatives of 169 UK A-T patients (including 247 obligate carriers) was obtained through the National Health Service Central Registry. Relative risks (RRs) of cancer in carriers, allowing for genotype uncertainty, were estimated with a maximum-likelihood approach that used the EM algorithm. Maximum-likelihood estimates of cancer risks associated with three groups of mutations were calculated using the pedigree analysis program MENDEL. All statistical tests were two-sided.The overall relative risk of breast cancer in carriers was 2.23 (95% confidence interval [CI] = 1.16 to 4.28) compared with the general population but was 4.94 (95% CI = 1.90 to 12.9) in those younger than age 50 years. The relative risk for all cancers other than breast cancer was 2.05 (95% CI = 1.09 to 3.84) in female carriers and 1.23 (95% CI = 0.76 to 2.00) in male carriers. Breast cancer was the only site for which a clear risk increase was seen, although there was some evidence of excess risks of colorectal cancer (RR = 2.54, 95% CI = 1.06 to 6.09) and stomach cancer (RR = 3.39, 95% CI = 0.86 to 13.4). Carriers of mutations predicted to encode a full-length ATM protein had cancer risks similar to those of people carrying truncating mutations.These results confirm a moderate risk of breast cancer in A-T heterozygotes and give some evidence of an excess risk of other cancers but provide no support for large mutation-specific differences in risk.
Extensive annular verrucous late secondary syphilis
Authors: C.C. Pournaras, I. Masouye, P. Piletta, V. Piguet, J-H. Saurat, L.E. French
Journal: British Journal of Dermatology (2005)

We report an illustrative case of an apparently healthy 38‐year‐old man with a past history of alopecia universalis who developed extensive, slightly pruritic, infiltrated annular verrucous lesions of the scalp, perioral, lumbar, perianal and genital areas over a 6‐month period. The combination of an unusual clinical presentation, positive syphilis serology and rapid response to penicillin therapy was consistent with a diagnosis of extensive annular and verrucous late secondary syphilis. We present this case to illustrate a rare and potentially misleading clinical feature of late secondary syphilis, a disease considered to be of the past but still present in today's practice.
Targeting Vascular Risk Factors in Older Adults
Authors: Enrico Mossello
Journal: JAMA Internal Medicine (2015)

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