tbuckley/cabot-search huggingface dataset:
Encouraging news on temporary coverings for burn wounds
Authors: William A. Check
Journal: JAMA (1980)

Successful temporary protection of burns by two very different materials was described at the recent meeting of the American College of Surgeons in Atlanta. One covering, human amniotic membrane, has been used for this purpose, although sparingly, since 1913. However, a group of physicians from Allentown, Pa, has now developed a way of collecting and storing the membrane that makes it much easier to use. The other substance, called Biobrane, is a newly developed semisynthetic membrane composed of nylon, Silastic, and a collagen derivative. The new processing method for human amnion was reported by Andrew B. Walker, MD, a pediatric surgeon, Tamar Earnest, MD, and Alan Schragger, MD. Amniotic membrane has been known for some years to have desirable permeability properties, keeping wounds from drying out and preventing exogenous bacterial infection. But the usual method of preparing it entailed stripping the membrane from the placenta immediately after delivery. This
Abstract 739: Small molecule inhibitor, PZ39C8, promotes BCRP degradation via binding to TM5-loop-TM6
Authors: Jing Qi, Wei Mo, Zizheng Dong, Hui Peng, Jian-Ting Zhang
Journal: Cancer Research (2011)

Abstract Multidrug resistance (MDR) and existing cancer stem cells (CSCs) are two major problems in successful treatment of cancers. Expression of breast cancer resistance protein (BCRP) is known to associate with both MDR and CSCs, suggesting that BCRP is an interesting and ideal target for development of chemosensitizing agents for better treatment of drug resistant cancers and elimination of CSCs. Recently, we identified a novel BCRP inhibitor PZ39 and its analogue compound PZ39C8 which are capable of inhibiting BCRP function and inducing BCRP degradation in lysosome. In the present study, we (1) investigated the mechanism of inhibitor-induced BCRP degradation using a stable cell line expressing GFP-BCRP in combination with pharmacological agents of endocytosis and trafficking and (2) determined the inhibitor binding site in BCRP using compound-conjugated Sepharose 4B beads and pull-down assay. We found that (1) the lysosomal inhibitor Bafilomycin A but not the proteosome inhibitor MG132 abolished PZ39C8-induced BCRP degradation; (2) dynasore, a potent endocytosis inhibitor, and 3-Methyladenine, a autophagy inhibitor, both efficiently blocked the PZ39C8-induced BCRP degradation from plasma and internal membranes; (3) following co-treatment with PZ-39C8 and endocytosis, trafficking, and lysosome inhibitors, BCRP co-localized with the LAMP-1, LC3II and Clathrin, EEA1, the markers of Lysosome, autophagy and endocytic pathways, respectively; and (4) PZ39C8 directly binds BCRP and the binding site/s appears to locate in the domain including TM5-loop-TM6. Taken together, we conclude that PZ39C8 binds to TM5-ECL3-TM6 of BCRP and induces BCRP degradation in lysosome via endocytic and autophagic dependent pathways. Thus, PZ39C8 is potentially a valuable probe for structure-function studies of BCRP and a lead compound for developing therapeutics targeting BCRP-mediated MDR in combinational cancer chemotherapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 739. doi:10.1158/1538-7445.AM2011-739
"Scalloping" of the Ureter
Authors: Leonard Berlin, Irving Waldman
Journal: JAMA (1964)

THE RECENT ADVENT of newer radiologic techniques and diagnostic methods such as renal angiography and radioisotope renography have brought forth a resurgence of interest in the entity of renovascular hypertension. While these procedures have achieved a high degree of accuracy and have gained considerable popularity, it is the feeling of many that intravenous urography is, and shall remain, a basic tool in the diagnosis of renal artery disease. It is the purpose of this report to emphasize a new, little-known urographic sign of this disease, "scalloping" of the ureter. <h3>Report of a Case</h3> A 31-year-old white male airman was admitted to US Air Force Hospital Wright-Patterson on June 20, 1963, for evaluation of hypertension. Hypertension was first discovered in May, 1963, when his blood pressure went as high as 220/150 mm Hg. At this time the patient was given chlorthalidone (Hygroton) and guanethidine sulfate (Ismelin), but no significant depression of
Enhanced Y1-receptor-mediated vasoconstrictive action of neuropeptide Y (NPY) in superior mesenteric arteries in portal hypertension
Authors: Reiner Wiest, Lars Jurzik, Lukas Moleda, Matthias Froh, Bernd Schnabl, Stephan von Hörsten, Juergen Schölmerich, Rainer H. Straub
Journal: Journal of Hepatology (2005)
Genetics of Common Diseases
Authors: A. Read
Journal: BMJ (1998)

Ed INM Day, SE Humphries

Bios Scientific Publishers, £65, pp 344

ISBN

Everybody agrees that the major impact of genetics on health is through genes that influence susceptibility to heart attacks, diabetes, schizophrenia, and other common diseases. Until recently, attempts to identify these genes failed. In retrospect we can see that the tools available were inadequate for the task. The methods that had led so successfully to understanding simply inherited diseases (such as cystic fibrosis and Huntington's chorea) broke down when applied to diseases to which susceptibility depends on several (possibly many) genes together with environmental factors. Now new laboratory and statistical tools have been developed for fresh assaults on these …
The Convenience Revolution for Treatment of Low-Acuity Conditions
Authors: Ateev Mehrotra
Journal: JAMA (2013)

Approximately fifty million times annually, patients visit physicians for low-acuity conditions such as bronchitis and urinary tract infections.1 Many more would likely visit their primary care physician if there were shorter appointment delays at primary care offices – such delays will likely worsen with the Affordable Care Act as millions gain insurance and seek primary care.
Results of Long-Term Treatment with Orthophosphate and Pyridoxine in Patients with Primary Hyperoxaluria
Authors: Dawn S. Milliner, Jeffrey T. Eickholt, Erik J. Bergstralh, David M. Wilson, Lynwood H. Smith
Journal: New England Journal of Medicine (1994)

The prognosis for patients with primary hyperoxaluria has been ominous, with the expectation of renal failure, poor results with transplantation, and early death.
Adult Respiratory-Distress Syndrome
Authors: Jean E. Rinaldo, Robert M. Rogers
Journal: New England Journal of Medicine (1982)

THE adult respiratory-distress syndrome (ARDS) — acute respiratory failure due to noncardiogenic pulmonary edema — is a complex sequela of shock, systemic sepsis, battlefield or highway trauma, viral respiratory infections, and many other insults. This disorder is particularly tragic because it often afflicts patients who are young and were previously healthy.Recognized only 14 years ago, the syndrome has since been found to be both common and lethal, affecting an estimated 150,000 persons each year and killing at least half of them despite current supportive therapy.1 2 3 We will briefly summarize this extraordinary history and focus on recent progress in understanding . . .
Canadian universities' links to tobacco industry shown
Authors: David Spurgeon
Journal: BMJ (2002)

The first national study of links between Canada's universities and medical schools and the tobacco industry shows that such institutions receive research grants and donations from the industry and that many tobacco industry officials hold senior university governance appointments.

Dr Fernand Turcotte, of Laval University's Department of Social and Preventive Medicine, revealed the results of the study recently at the first international francophone conference on tobacco control in Montreal. The study's authors, from the universities of Toronto and Laval, were supported by the National Cancer Institute of Canada and received funding from the Canadian Cancer Society. …
STK33 Kinase Is Not Essential in KRAS-Dependent Cells–Letter
Authors: Stefan Fröhling, Claudia Scholl
Journal: Cancer Research (2011)

Babij and colleagues report that STK33 is dispensable for KRASmut-dependent cancer cells ([1][1]), a finding in contrast to previous investigations ([2–4][2]). We believe the data do not support this conclusion and wish to bring selected methodologic issues to the authors' attention. Because of
The expression pattern of interferon-inducible proteins reflects the characteristic histological distribution of infiltrating immune cells in different cutaneous lupus erythematosus subsets
Authors: J. Wenzel, S. Zahn, S. Mikus, A. Wiechert, T. Bieber, T. Tüting
Journal: British Journal of Dermatology (2007)

Plasmacytoid dendritic cells and type I interferons (IFNs) are supposed to play a central proinflammatory role in the pathogenesis of cutaneous lupus erythematosus (LE). The IFN-inducible chemokines CXCL9 and CXCL10 are involved in recruiting CXCR3+ effector lymphocytes from the peripheral blood into skin lesions of LE. We hypothesized that the expression pattern of IFN-inducible proteins reflects the characteristic distribution of the inflammatory infiltrate in different subsets of cutaneous LE.To test this hypothesis in patients with LE.Lesional skin biopsies taken from patients with different subsets of LE [chronic discoid LE (CDLE), n = 12; subacute cutaneous LE (SCLE), n = 5; LE tumidus (LET), n = 4; LE profundus (LEP), n = 6] were investigated by immunohistochemistry using monoclonal antibodies to the lymphocyte surface markers CD3, CD4, CD8, CD20 and CD68, the cytotoxic proteins Tia1 and granzyme B, the chemokine receptor CXCR3, the specifically type I IFN-inducible protein myxovirus protein A (MxA) and the chemokines CXCL9 and CXCL10.The expression pattern of MxA followed the distribution of the inflammatory infiltrate typically seen in the investigated cutaneous LE subsets. In CDLE and SCLE, expression was focused in the epidermis and upper dermis, while in LET a perivascular and in LEP a subcutaneous pattern was found. Similar findings were obtained for CXCL9 and CXCL10.Our results demonstrate a close morphological association between the expression pattern of IFN-inducible proteins and the distribution of CXCR3+ CD3+ lymphocytes in all investigated subsets of cutaneous LE. This supports the importance of an IFN-driven inflammation in this condition. Infiltrating lymphocytes carrying CXCL10 in their granules might amplify the lesional inflammation and be responsible for the chronic course of this disease.
European centre warns of need for better surveillance of C difficile
Authors: M. Day
Journal: BMJ (2008)

Europe must urgently boost its methods of infection surveillance with the emergence of deadly new strains of the hospital acquired infection Clostridium difficile , the European Centre for Disease Prevention and Control says.

The warning comes after a new study showing that the virulent polymerase chain reaction (PCR) ribotype 027 strain of C difficile has now struck healthcare facilities in 16 European countries, with serious outbreaks in Belgium, Germany, Finland, France, Ireland, Luxembourg, the Netherlands, Switzerland, and the United Kingdom ( Euro Surveillance www.eurosurveillance.org/ViewArticle.aspx?Articleid=18942).

The 027 strain caused many of the cases in two outbreaks at Stoke Mandeville Hospital, in Aylesbury, Buckinghamshire, in 2004 …
Mortality and Cancer Frequency Among Military Nuclear Test (Smoky) Participants
Authors: Murray M. Finkelstein
Journal: JAMA (1984)

<h3>To the Editor.—</h3> In analyzing their data concerning follow-up of nuclear test participants and in drawing their conclusions, Caldwell et al<sup>1</sup>have failed to take account of current knowledge of the epidemiology of human radiation exposure. It is known that the bone marrow has a high relative sensitivity to the induction of cancer and that leukemias may appear within five years of radiation exposure; solid tumors, however, generally appear later, and excess risk may not become apparent earlier than 15 to 20 years from exposure.<sup>1</sup>Since the reason for undertaking this study was the report of leukemia in one participant and because leukemia is known, a priori, to be caused by exposure to ionizing radiation, it seems reasonable that the null hypothesis for this study should be that leukemia rates among test participants are the same as in the US population; this hypothesis is convincingly rejected by the
Climate change and human health in Europe
Authors: R S. Kovats, A. Haines, R. Stanwell-Smith, P. Martens, B. Menne, R. Bertollini
Journal: BMJ (1999)

Editorials by Brundtland and Pershagen Evidence that our world is warming has become stronger in recent years. Scientists have now confirmed that these changes are due to human activities.1 This century the average annual temperature in most of Europe has increased by about 0.8°C.2 Warming has been particularly great during the past two decades and in the middle to high latitudes (fig 1). In the Alps, temperature increases have exceeded 1°C above the long term mean. Northern Europe has become wetter, but a region encompassing the Mediterranean and central Europe has become significantly drier.2 Scientists of the Intergovernmental Panel on Climate Change forecast a 1°C-3.5°C increase in average global temperature by 2100.1 Although there is considerable uncertainty in forecasting regional and local changes in climate in Europe, it is likely that these observed trends will continue.2 The potential impact of a global climate change on human health has been identified as a priority for research and action in the next century, and this will be debated at a forthcoming ministerial conference on the environment and health. Our paper reviews the state of current knowledge for the WHO European region. Climate change will not affect human health in isolation, but will do so simultaneously with other ecological and demographic changes. It should be noted that effects on other regions surrounding Europe (Africa and Asia) may be of considerable importance for the European region as well. ### Summary points
Airway epithelial damage and inflammation in children with recurrent bronchitis.
Authors: D Gaillard, J B Jouet, L Egreteau, L Plotkowski, J M Zahm, R Benali, D Pierrot, E Puchelle
Journal: American Journal of Respiratory and Critical Care Medicine (1994)

Inflammation and epithelial damage of the bronchial mucosa are frequently identified in children with bronchial diseases. Nevertheless, until now the quantitative assessment of the epithelial damage has never been studied in relation to clinical or respiratory function or mucus abnormalities. Bronchial biopsies and brushings were performed in 31 children with recurrent bronchitis and without atopia. The quantitative histologic data were compared with clinical results, the endoscopic appearance of the mucosa, ciliary beating frequency, mucus transport capacity, leukocyte count, and protein concentration in mucus samples. Most of the biopsies (87%) collected in this group of children without recent acute infections showed extensive epithelial damage. A significant correlation was observed between the degree of shedding and edema (p < 0.01). Bronchial epithelial edema was associated with a significantly decreased (p < 0.01) mucus transport rate. Inflammation of the submucosa was significantly correlated with lymphocyte epithelial infiltration (p < 0.01), total mucus protein content (p < 0.01), and local airway inflammation estimated by bronchoscopy. These results demonstrate that children with recurrent bronchitis develop a severe bronchial inflammation associated with an increased mucus protein content and a reduction in the mucociliary function.
Eotaxin-2 and IL-5 cooperate in the lung to regulate IL-13 production and airway eosinophilia and hyperreactivity
Authors: Ming Yang, Simon P Hogan, Surendran Mahalingam, Sam M Pope, Nives Zimmermann, Patricia Fulkerson, Lindsay A Dent, Ian G Young, Klaus I Matthaei, Marc E Rothenberg, Paul S Foster
Journal: Journal of Allergy and Clinical Immunology (2003)
Treatment of unresectable hepatocellular carcinoma with lipiodol chemoembolization: a multicenter randomized trial
Authors: Gilles Pelletier, Michel Ducreux, France Gay, Monique Luboinski, Herve Hagège, Dao Thong, Werner Van Steenbergen, Catherine Buffet, Philippe Rougier, Michael Adler, Jean-Pierre Pignon, Alain Roche
Journal: Journal of Hepatology (1998)
Physical Fitness in United States and Austrian Military Personnel
Authors: Kenneth H. Cooper
Journal: JAMA (1971)

A difference between the United States and Austria in number of deaths from heart attacks among men 35 to 44 years of age aroused considerable interest with respect to the role of physical activity. The purpose of the present study was to evaluate the level of physical fitness of younger men, ie, 18 to 29 years of age, in the US Air Force and the Austrian Army. A marked difference in endurance performance was observed on a 12-minute field test of performance irrespective of the stage of training or the age, even though the Austrian soldiers weighed more and a comparable percentage of them smoked cigarettes. The results indicate that the 12-minute field test is a good substitute for the laboratory-determined maximal oxygen consumption if the subjects are well motivated.
Abstract 3787: ERK and AKT signaling cooperate to translationally regulate survivin expression for promotion of cell motility and metastasis in colorectal cancer.
Authors: Qing Ye, Weijia Cai, Yongbin Zheng, B. Mark Evers, Qing-Bai She
Journal: Cancer Research (2013)

Abstract The MEK/ERK and PI3K/AKT pathways are often concurrently activated by separate genetic alterations in colorectal cancer (CRC), which is associated with CRC progression and poor survival. However, how activating both pathways is required for CRC metastatic progression remains unclear. Our recent study showed that both ERK and AKT signaling are required to activate eIF4E-initiated cap-dependent translation via convergent regulation of the translational repressor 4E-BP1 for maintaining CRC transformation. Here, we identified that the activation of cap-dependent translation by cooperative ERK and AKT signaling is critical for promotion of CRC motility and metastasis. In CRC cells with coexistent mutational activation of ERK and AKT pathways, inhibition of either MEK or AKT alone showed limited activity in inhibiting cell migration and invasion, but combined inhibition resulted in profound effects. Genetic blockade of the translation initiation complex by eIF4E knockdown or expression of a dominant active 4E-BP1 mutant effectively inhibited migration, invasion and metastasis of CRC cells, whereas overexpression of eIF4E or knockdown of 4E-BP1 had the opposite effect and markedly reduced their dependence on ERK and AKT signaling for cell motility. Mechanistically, we found that these effects were largely dependent on the increase in mTORC1-mediated survivin translation by ERK and AKT signaling. Despite the modest effect of survivin knockdown on tumor growth, reduction of the translationally-regulated survivin profoundly inhibited motility and metastasis of CRC. These findings reveal a critical mechanism underlying the translational regulation of CRC metastatic progression, and suggest that targeting cap-dependent translation may provide a promising treatment strategy for advanced CRC. Citation Format: Qing Ye, Weijia Cai, Yongbin Zheng, B. Mark Evers, Qing-Bai She. ERK and AKT signaling cooperate to translationally regulate survivin expression for promotion of cell motility and metastasis in colorectal cancer. [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 3787. doi:10.1158/1538-7445.AM2013-3787
Exposure of remote maritime populations to coplanar PCBs.
Authors: E Dewailly, J J Ryan, C Laliberté, S Bruneau, J P Weber, S Gingras, G Carrier
Journal: Environmental Health Perspectives (1994)

Two remote maritime populations were evaluated for their biological exposure to organochlorines in 1989-1990. Because of their high intake of seafood, these two populations have high biological levels. One hundred nine breast milk samples from Inuit women from Arctic Québec were analyzed to determine levels of polychlorodibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and coplanar polychlorinated biphenyls (PCBs) including non-ortho, mono-ortho, and di-ortho congeners. Total 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (TEqs) for PCBs were 3.5 times higher in Inuit milk samples than in 96 Caucasian milk samples. Among the 185 fishermen from the Lower North Shore of the Gulf of the St. Lawrence River, we evaluated 10 highly exposed fishermen for their coplanar PCB blood levels. Total TEqs were 900 ng/kg for highly exposed individuals with 36 ng/kg for controls. In these two nonoccupationally exposed populations, coplanar PCBs make a larger contribution to the TEq than PCDDs and PCDFs. However, the mono-ortho penta CB No. 118 is the major contributor for the total toxicity.
Loss of amplified genes by poly(ADP-ribose) polymerase inhibitors.
Authors: M Nagao, M Nakayasu, S Aonuma, H Shima, T Sugimura
Journal: Environmental Health Perspectives (1991)

A poly(ADP-ribose) polymerase inhibitor, benzamide (BA), was found to induce flat revertants of NIH 3T3 cells that had been transformed by human Ha-ras, rat Ki-ras, rat c-raf, and human ret-II. These genes had been amplified in original transformants, but they were completely eliminated by BA. Contrary to this, endogenous activated Ha-ras in a human bladder carcinoma cell line, T24, was not eliminated by BA. The gene loss seemed to be restricted to exogenous and/or amplified sequences. BA also eliminated the amplified c-myc gene in HL-60 cells, concomitant with differentiation into granulocytes. We demonstrated that the amplified c-myc gene was not present as episomes. It is probably present as double minutes or a homogeneously staining region. Dimethylsulfoxide also induced differentiation at a concentration that did not inhibit poly(ADP-ribose) polymerase. The cell lost the c-myc gene in association with this differentiation. The amplified c-myc gene in a colon adenocarcinoma cell line, COLO 320HSR, and the amplified mdr-1 gene in an adriamycin-resistant myelogenous leukemia cell line, K562/ADM, were not eliminated by BA. Various poly(ADP-ribose) polymerase inhibitors also eliminated human Ha-ras in the NIH 3T3 transformant and the c-myc gene in HL-60 cells.
Zwilling-A and -B, Two Related Myelin Proteins of Teleosts, Which Originate from a Single Bicistronic Transcript
Authors: K. Schaefer, C. Brosamle
Journal: Molecular Biology and Evolution (2008)

Myelination, the ensheathment of axons by membranes of highly specialized glial cells, has been a crucial innovation during early vertebrate evolution. It enables high nerve signal conduction velocities, while maintaining nervous system size and energy requirements at moderate levels. Consequently, myelination has been conserved in all extant gnathostome vertebrates. In a genomewide mRNA expression screen, we identified several novel neural crest and myelin-specific transcripts in the zebrafish (Danio rerio). Here, we describe the characterization of two proteins, Zwilling-A and -B (ZwiA and ZwiB), which are exclusively expressed in myelinating glia of teleosts. They are structurally homologous and are translated from a common, bicistronic transcript. No similarities to sequences or domains of other proteins were detected. Analysis of phylogeny, genomic organization, and genomic syntenies suggests that the zwi gene has appeared soon after the teleost-specific genome duplication event and evolved under conservative selective pressure. We hypothesize that ZwiA and ZwiB serve important physiological functions in teleost myelin.