tbuckley/cabot-search huggingface dataset:
Sharing emergency department data with police could reduce violence
Authors: Owen Dyer
Journal: BMJ (2006)

Emergency departments should collect information on assaults and share it with police and local authorities in an effort to control violence, the Academy of Medical Sciences said last week.

The call came at a meeting in London on the science of violence, after members heard research findings from Jonathan Shepherd of Cardiff University showing that hospitals record many attacks that are never reported to police.

“About three quarters of the violence related injuries treated in emergency departments come from assaults that were never reported to the police,” Professor Shepherd told the BMJ . “Pooling …
Dangers of cardiopulmonary bypass operations
Authors: R P. Alston
Journal: BMJ (1989)

significance.In a recent study urinary tract abnormalities were found in 47% of children investigated as a result of this finding.'Dr Smyth and her colleagues ask for an agreed common approach to the investigation and management of urinary tract infection in children.Until studies of the different investigation protocols are completed, and in view of the variable facilities available, an approach is unlikely to be agreed.It is paramount, however, that recurrent or persistent infection should be promptly detected and appropriately acted upon.I have recently attempted to set out protocols, both for general practitioners and for paediatricians, which, provided that good microbiological facilities are available, may be used to determine pathways of investigation and management appropriate to the individual child.4
The Psychiatric Interview in Clinical Practice, Second Editionby Roger A. MacKinnon, M.D., Robert Michels, M.D., and Peter J. Buckley, M.D. Arlington, Va, American Psychiatric Publishing, 2006, 679 pp., $65.00.
Authors: RICHARD M. WAUGAMAN, JOANNA LHULIER
Journal: American Journal of Psychiatry (2008)
Involvement of Bone Marrow Cells and Neuroinflammation in Hypertension
Authors: Monica M. Santisteban, Niousha Ahmari, Jessica Marulanda Carvajal, Michael B. Zingler, Yanfei Qi, Seungbum Kim, Jessica Joseph, Fernando Garcia-Pereira, Richard D. Johnson, Vinayak Shenoy, Mohan K. Raizada, Jasenka Zubcevic
Journal: Circulation Research (2015)

Microglial activation in autonomic brain regions is a hallmark of neuroinflammation in neurogenic hypertension. Despite evidence that an impaired sympathetic nerve activity supplying the bone marrow (BM) increases inflammatory cells and decreases angiogenic cells, little is known about the reciprocal impact of BM-derived inflammatory cells on neuroinflammation in hypertension.To test the hypothesis that proinflammatory BM cells from hypertensive animals contribute to neuroinflammation and hypertension via a brain-BM interaction.After BM ablation in spontaneously hypertensive rats, and reconstitution with normotensive Wistar Kyoto rat BM, the resultant chimeric spontaneously hypertensive rats displayed significant reduction in mean arterial pressure associated with attenuation of both central and peripheral inflammation. In contrast, an elevated mean arterial pressure along with increased central and peripheral inflammation was observed in chimeric Wistar-Kyoto rats reconstituted with spontaneously hypertensive rat BM. Oral treatment with minocycline, an inhibitor of microglial activation, attenuated hypertension in both the spontaneously hypertensive rats and the chronic angiotensin II-infused rats. This was accompanied by decreased sympathetic drive and inflammation. Furthermore, in chronic angiotensin II-infused rats, minocycline prevented extravasation of BM-derived cells to the hypothalamic paraventricular nucleus, presumably via a mechanism of decreased C-C chemokine ligand 2 levels in the cerebrospinal fluid.The BM contributes to hypertension by increasing peripheral inflammatory cells and their extravasation into the brain. Minocycline is an effective therapy to modify neurogenic components of hypertension. These observations support the hypothesis that BM-derived cells are involved in neuroinflammation, and targeting them may be an innovative strategy for neurogenic resistant hypertension therapy.
Intestinal Absorption and Malabsorption of Folates
Authors: C H Halsted
Journal: Annual Review of Medicine (1980)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
Secondary bacterial infections in children with proved Mycoplasma pneumoniae.
Authors: R Staugas, A J Martin
Journal: Thorax (1985)

Reports of important pulmonary complications, including bronchiectasis, have been reported after Mycoplasma pneumoniae infection.'-4Two reports56 have noted more subtle pulmonary function abnormalities, several years after mycoplasma infection, in children.Haemophilus influenzae has been implicated as a secon- dary invader following initial Mycoplasma pneumoniae infection in two reports."The complications so far recorded may therefore be manifestations of secondary infection.This report describes five children with proved Mycoplasma pneumoniae infection whose illness was pro- longed and in whom secondary bacterial infection was possible.Case reports
Multicenter Case-Control Study of Exposure to Environmental Tobacco Smoke and Lung Cancer in Europe
Authors: P Boffetta, A Agudo, W Ahrens, E Benhamou, S Benhamou, S C Darby, G Ferro, C Fortes, C A Gonzalez, K H Jöckel, M Krauss, L Kreienbrock, M Kreuzer, A Mendes, F Merletti, F Nyberg, G Pershagen, H Pohlabeln, E Riboli, G Schmid, L Simonato, J Trédaniel, E Whitley, H E Wichmann, C Winck, P Zambon, R Saracci
Journal: JNCI Journal of the National Cancer Institute (1998)

Background: An association between exposure to environmental tobacco smoke (ETS) and lung cancer risk has been suggested. To evaluate this possible association better, researchers need more precise estimates of risk, the relative contribution of different sources of ETS, and the effect of ETS exposure on different histologic types of lung cancer. To address these issues, we have conducted a case-control study of lung cancer and exposure to ETS in 12 centers from seven European countries. Methods: A total of 650 patients with lung cancer and 1542 control subjects up to 74 years of age were interviewed about exposure to ETS. Neither case subjects nor control subjects had smoked more than 400 cigarettes in their lifetime. Results: ETS exposure during childhood was not associated with an increased risk of lung cancer (odds ratio [OR] for ever exposure = 0.78; 95% confidence interval [CI] = 0.64-0.96). The OR for ever exposure to spousal ETS was 1.16 (95% CI = 0.93-1.44). No clear dose-response relationship could be demonstrated for cumulative spousal ETS exposure. The OR for ever exposure to workplace ETS was 1.17 (95% CI = 0.94-1.45), with possible evidence of increasing risk for increasing duration of exposure. No increase in risk was detected in subjects whose exposure to spousal or workplace ETS ended more than 15 years earlier. Ever exposure to ETS from other sources was not associated with lung cancer risk. Risks from combined exposure to spousal and workplace ETS were higher for squamous cell carcinoma and small-cell carcinoma than for adenocarcinoma, but the differences were not statistically significant. Conclusions: Our results indicate no association between childhood exposure to ETS and lung cancer risk. We did find weak evidence of a dose-response relationship between risk of lung cancer and exposure to spousal and workplace ETS. There was no detectable risk after cessation of exposure. [J Natl Cancer Inst 1998;90:1440-50]
Outcomes of Treatment for Hepatitis C Virus Infection by Primary Care Providers
Authors: Sanjeev Arora, Karla Thornton, Glen Murata, Paulina Deming, Summers Kalishman, Denise Dion, Brooke Parish, Thomas Burke, Wesley Pak, Jeffrey Dunkelberg, Martin Kistin, John Brown, Steven Jenkusky, Miriam Komaromy, Clifford Qualls
Journal: New England Journal of Medicine (2011)

The Extension for Community Healthcare Outcomes (ECHO) model was developed to improve access to care for underserved populations with complex health problems such as hepatitis C virus (HCV) infection. With the use of video-conferencing technology, the ECHO program trains primary care providers to treat complex diseases.We conducted a prospective cohort study comparing treatment for HCV infection at the University of New Mexico (UNM) HCV clinic with treatment by primary care clinicians at 21 ECHO sites in rural areas and prisons in New Mexico. A total of 407 patients with chronic HCV infection who had received no previous treatment for the infection were enrolled. The primary end point was a sustained virologic response.A total of 57.5% of the patients treated at the UNM HCV clinic (84 of 146 patients) and 58.2% of those treated at ECHO sites (152 of 261 patients) had a sustained viral response (difference in rates between sites, 0.7 percentage points; 95% confidence interval, -9.2 to 10.7; P=0.89). Among patients with HCV genotype 1 infection, the rate of sustained viral response was 45.8% (38 of 83 patients) at the UNM HCV clinic and 49.7% (73 of 147 patients) at ECHO sites (P=0.57). Serious adverse events occurred in 13.7% of the patients at the UNM HCV clinic and in 6.9% of the patients at ECHO sites.The results of this study show that the ECHO model is an effective way to treat HCV infection in underserved communities. Implementation of this model would allow other states and nations to treat a greater number of patients infected with HCV than they are currently able to treat. (Funded by the Agency for Healthcare Research and Quality and others.).
Multifunctional dendrimer-entrapped gold nanoparticles for dual mode CT/MR imaging applications
Authors: Shihui Wen, Kangan Li, Hongdong Cai, Qian Chen, Mingwu Shen, Yunpeng Huang, Chen Peng, Wenxiu Hou, Meifang Zhu, Guixiang Zhang, Xiangyang Shi
Journal: Biomaterials (2012)
ATP directly affects junctional conductance between paired ventricular myocytes isolated from guinea pig heart.
Authors: H Sugiura, J Toyama, N Tsuboi, K Kamiya, I Kodama
Journal: Circulation Research (1990)

Effects of ATP on junctional conductance (gj) were investigated in paired ventricular myocytes isolated from guinea pig hearts. One cell of the pair was voltage-clamped with a single-patch pipette, and gj was measured after the perforation of the nonjunctional membrane of the partner cell. The current-voltage relation of gj was linear between -30 and +30 mV. The control gj at 5.0 mM ATP in 88 pairs of cells ranged from 100 to 1,055 nS (average, 268 nS). ATP within the range from 0.1 to 5.0 mM increased gj in a dose-dependent manner. The Hill coefficient was 2.6, and the half-maximum effective concentration of ATP was 0.68 mM. Adenylylimidodiphosphate (2 mM) caused a transient increase in gj in the presence of 0.5 mM ATP, but forskolin (30 microM), cyclic AMP (50 microM), catalytic subunit of cyclic AMP-dependent protein kinase (1 microM), and ADP (10 mM) had no significant effect on gj. The temperature coefficient of gj in the presence of 5.0 mM ATP was 1.29. These findings suggest that gj in paired ventricular myocytes is directly regulated by ATP probably through a specific ligand-receptor interaction between ATP and gap junctional channel protein.
Bone morphogenetic protein-7 in focus: A member of the transforming growth factor-β superfamily is implicated in the maintenance of liver health
Authors: Ralf Weiskirchen, Steffen K. Meurer, Kris Kowdley, Geoffrey McCaughan, Christian Trautwein
Journal: Hepatology (2007)

Bone morphogenic protein-7 (BMP-7) is a key protein involved in liver organogenesis and development. The physiological circulating concentration of BMP-7 is between 100 and 300 pg/ml. BMP-7 expression is absent in the liver, but the receptors for BMP-7 are present on adult hepatocytes. Therefore, we hypothesized that BMP-7 might function as an endogenous regulator of adult hepatocyte proliferation and liver homeostasis. Here, we demonstrate that neutralization of circulating endogenous BMP-7 results in significantly impaired regeneration of the liver after partial hepatectomy. Therapeutic administration of recombinant human BMP-7 (rhBMP-7) significantly enhances liver regeneration associated with accelerated improvement of liver function. Collectively, our results argue for the role of BMP-7 as a kidney- and bone-produced endogenous regulator of hepatocyte health.
Inhibition of p-STAT3 Enhances IFN-α Efficacy against Metastatic Melanoma in a Murine Model
Authors: Ling-Yuan Kong, Alexander Gelbard, Jun Wei, Chantal Reina-Ortiz, Yongtao Wang, Eric C. Yang, Yared Hailemichael, Izabela Fokt, Arumugam Jayakumar, Wei Qiao, Gregory N. Fuller, Willem W. Overwijk, Waldemar Priebe, Amy B. Heimberger
Journal: Clinical Cancer Research (2010)

Melanoma is a common and deadly tumor that upon metastasis to the central nervous system has a median survival duration of <6 months. Activation of the signal transducer and activator of transcription 3 (STAT3) has been identified as a key mediator that drives the fundamental components of melanoma malignancy, including immune suppression in melanoma patients. We hypothesized that WP1193, a novel inhibitor of STAT3 signaling, would enhance the antitumor activity of IFN-alpha against metastatic melanoma.Combinational therapy of STAT3 blockade agents with IFN-alpha was investigated in a metastatic and an established syngeneic intracerebral murine tumor model of melanoma. The immunologic in vivo mechanisms of efficacy were investigated by T-cell and natural killer (NK) cell cytotoxic assays.IFN-alpha immunotherapy was synergistic with WP1193 showing marked in vivo efficacy against metastatic and established intracerebral melanoma. At autopsy, it was noted that there was a decreased trend in mice with melanoma developing leptomeningeal disease treated with combinational therapy. The combinational approach enhanced both NK-mediated and T-cell-mediated antitumor cytotoxicity.The immune modulatory effects of STAT3 blockade can enhance the therapeutic efficacy of IFN-alpha immunotherapy by enhancing both innate and adaptive cytotoxic T-cell activities. This combination therapy has the potential in the treatment of metastatic melanoma that is typically refractory to this type of immune therapeutic approach.
Protein tyrosine phosphatase–σ regulates hematopoietic stem cell–repopulating capacity
Authors: Mamle Quarmyne, Phuong L. Doan, Heather A. Himburg, Xiao Yan, Mai Nakamura, Liman Zhao, Nelson J. Chao, John P. Chute
Journal: Journal of Clinical Investigation (2014)

Hematopoietic stem cell (HSC) function is regulated by activation of receptor tyrosine kinases (RTKs). Receptor protein tyrosine phosphatases (PTPs) counterbalance RTK signaling; however, the functions of receptor PTPs in HSCs remain incompletely understood. We found that a receptor PTP, PTPσ, was substantially overexpressed in mouse and human HSCs compared with more mature hematopoietic cells. Competitive transplantation of bone marrow cells from PTPσ-deficient mice revealed that the loss of PTPσ substantially increased long-term HSC-repopulating capacity compared with BM cells from control mice. While HSCs from PTPσ-deficient mice had no apparent alterations in cell-cycle status, apoptosis, or homing capacity, these HSCs exhibited increased levels of activated RAC1, a RhoGTPase that regulates HSC engraftment capacity. shRNA-mediated silencing of PTPσ also increased activated RAC1 levels in wild-type HSCs. Functionally, PTPσ-deficient BM cells displayed increased cobblestone area-forming cell (CAFC) capacity and augmented transendothelial migration capacity, which was abrogated by RAC inhibition. Specific selection of human cord blood CD34⁺CD38⁻CD45RA⁻lin⁻ PTPσ⁻ cells substantially increased the repopulating capacity of human HSCs compared with CD34⁺CD38⁻CD45RA⁻lin⁻ cells and CD34⁺CD38⁻CD45RA⁻lin⁻PTPσ⁺ cells. Our results demonstrate that PTPσ regulates HSC functional capacity via RAC1 inhibition and suggest that selecting for PTPσ-negative human HSCs may be an effective strategy for enriching human HSCs for transplantation.
The Average Cumulative Risks of Breast and Ovarian Cancer for Carriers of Mutations in <i>BRCA1</i> and <i>BRCA2</i> Attending Genetic Counseling Units in Spain
Authors: Roger L. Milne, Ana Osorio, Teresa Ramón y Cajal, Ana Vega, Gemma Llort, Miguel de la Hoya, Orland Díez, M. Carmen Alonso, Conxi Lazaro, Ignacio Blanco, Ana Sánchez-de-Abajo, Trinidad Caldés, Ana Blanco, Begoña Graña, Mercedes Durán, Eladio Velasco, Isabel Chirivella, Eva Esteban Cardeñosa, María-Isabel Tejada, Elena Beristain, María-Dolores Miramar, María-Teresa Calvo, Eduardo Martínez, Carmen Guillén, Raquel Salazar, Carlos San Román, Antonis C. Antoniou, Miguel Urioste, Javier Benítez
Journal: Clinical Cancer Research (2008)

Abstract Purpose: It is not clear that the published estimates of the breast and ovarian cancer penetrances of mutations in BRCA1 and BRCA2 can be used in genetic counseling in countries such as Spain, where the incidence of breast cancer in the general population is considerably lower, the prevalence of BRCA2 mutations seems to be higher, and a distinct spectrum of recurrent mutations exists for both genes. We aimed to estimate these penetrances for women attending genetic counseling units in Spain. Experimental Design: We collected phenotype and genotype data on 155 BRCA1 and 164 BRCA2 mutation carrier families from 12 centers across the country. Average age-specific cumulative risks of breast cancer and ovarian cancer were estimated using a modified segregation analysis method. Results: The estimated average cumulative risk of breast cancer to age 70 years was estimated to be 52% [95% confidence interval (95% CI), 26-69%] for BRCA1 mutation carriers and 47% (95% CI, 29-60%) for BRCA2 mutation carriers. The corresponding estimates for ovarian cancer were 22% (95% CI, 0-40%) and 18% (95% CI, 0-35%), respectively. There was some evidence (two-sided P = 0.09) that 330A&amp;gt;G (R71G) in BRCA1 may have lower breast cancer penetrance. Conclusions: These results are consistent with those from a recent meta-analysis of practically all previous penetrance studies, suggesting that women with BRCA1 and BRCA2 mutations attending genetic counseling services in Spain have similar risks of breast and ovarian cancer to those published for other Caucasian populations. Carriers should be fully informed of their mutation- and age-specific risks to make appropriate decisions regarding prophylactic interventions such as oophorectomy.
Stem Cell Gene Therapy for Fanconi Anemia: Report from the 1st International Fanconi Anemia Gene Therapy Working Group Meeting
Authors: Jakub Tolar, Jennifer E Adair, Michael Antoniou, Cynthia C Bartholomae, Pamela S Becker, Bruce R Blazar, Juan Bueren, Thomas Carroll, Marina Cavazzana-Calvo, D Wade Clapp, Robert Dalgleish, Anne Galy, H Bobby Gaspar, Helmut Hanenberg, Christof Von Kalle, Hans-Peter Kiem, Dirk Lindeman, Luigi Naldini, Susana Navarro, Raffaele Renella, Paula Rio, Julián Sevilla, Manfred Schmidt, Els Verhoeyen, John E Wagner, David A Williams, Adrian J Thrasher
Journal: Molecular Therapy (2011)

Survival rates after allogeneic hematopoietic cell transplantation (HCT) for Fanconi anemia (FA) have increased dramatically since 2000. However, the use of autologous stem cell gene therapy, whereby the patient's own blood stem cells are modified to express the wild-type gene product, could potentially avoid the early and late complications of allogeneic HCT. Over the last decades, gene therapy has experienced a high degree of optimism interrupted by periods of diminished expectation. Optimism stems from recent examples of successful gene correction in several congenital immunodeficiencies, whereas diminished expectations come from the realization that gene therapy will not be free of side effects. The goal of the 1st International Fanconi Anemia Gene Therapy Working Group Meeting was to determine the optimal strategy for moving stem cell gene therapy into clinical trials for individuals with FA. To this end, key investigators examined vector design, transduction method, criteria for large-scale clinical-grade vector manufacture, hematopoietic cell preparation, and eligibility criteria for FA patients most likely to benefit. The report summarizes the roadmap for the development of gene therapy for FA.
Activation of Cardiac Endothelium as a Compensatory Component in Endotoxin-Induced Cardiomyopathy
Authors: Alexandre Mebazaa, Gilles W. De Keulenaer, Xavier Paqueron, Luc J. Andries, Philippe Ratajczak, Sophie Lanone, Christian Frelin, Dan Longrois, Didier Payen, Dirk L. Brutsaert, Stanislas U. Sys
Journal: Circulation (2001)

In view of growing evidence of an important endothelial paracrine regulation of cardiac function, the present study investigated the role of cardiac endothelium-derived endothelin-1 (ET-1), prostaglandins, and nitric oxide (NO) during endotoxin-induced cardiomyopathy in rabbits.Immunohistochemical studies showed a marked transient coinduction of the inducible isoforms of NO synthase (NOS-2) and cyclooxygenase (COX-2) in endocardial endothelium and coronary arteriolar endothelium of hearts 12 hours after intravenous administration of lipopolysaccharide (LPS+12h); staining for both isoforms was much weaker 24 hours later (LPS+36h). Nitrotyrosine localization was similar to that of NOS-2, suggesting a NOS-2-related endothelial formation of peroxynitrite in septic hearts. Contractile performance of papillary muscles was depressed in both LPS-treated groups. In the LPS+12h group, however, isometric twitches were significantly prolonged (482+/-14 versus 420+/-14 ms in the saline-treated group, P<0.005). This twitch prolongation was completely reversed by simultaneous administration of BQ-123 and indomethacin to block endogenous ET-1 and prostaglandins, respectively. In addition, in the LPS+12h group, myocardial inotropic responsiveness to exogenous ET-1 was enhanced (P<0.01).Cardiac endothelial activation and myocardial sensitization to endothelium-derived mediators may be part of an adaptive response in the early (12 hours) stages of septic cardiomyopathy.
The mathematical relationship between the number of events in which people are injured and the number of people injured.
Authors: D G Uitenbroek
Journal: British Journal of Sports Medicine (1995)

In this paper the mathematical relationship between the number of times people sustained injuries and the number of people injured is discussed. The number of injury-causing events in a population will be larger than the number of people injured as people can be injured on more than one occasion. The Poisson distribution is used as a way to study the relationship between the two different sets of numbers. A practical example is given of injuries sustained while running. From this it seems that injury proneness needs to be considered in studying those who were injured on more than one occasion while running during the past year.