tbuckley/cabot-search huggingface dataset:
The genetics of obstructive lung disease: big is beautiful
Authors: I. P. Hall, D. A. Lomas
Journal: Thorax (2010)

Chronic obstructive pulmonary disease (COPD) is defined as airflow obstruction that is not fully reversible.It results from abnormal inflammation following exposure to noxious particles or gases. 1 This is typically exposure to cigarette smoke but may also include exposure to biomass fuels and some industrial dusts.COPD clusters within families, suggesting that heritable factors play a role in the pathogenesis of this disease. 2 3The only genetic factor that is widely accepted to be associated with COPD is severe deficiency of a 1 -antitrypsin. 4This depletes an
Pleural disease and acquired immune deficiency syndrome
Authors: RW Light, H Hamm
Journal: European Respiratory Journal (1997)

Patients with acquired immune deficiency syndrome (AIDS) do not frequently have pleural complications. However, pneumothorax is a troublesome complication of patients with AIDS. At some medical centres, more than 50% of patients with spontaneous pneumothorax have AIDS. Most patients with spontaneous pneumothorax and AIDS have Pneumocystis carinii infection and necrotic subpleural blebs. The pneumothoraces in these patients usually cannot be managed with tube thoracostomy alone. Patients who do not respond to tube thoracostomy are best managed with a Heimlich valve or with thoracostomy with stapling of blebs and pleural abrasion. Approximately 2% of human immunodeficiency virus (HIV)-positive individuals will have a pleural effusion. Parapneumonic effusions or empyema, tuberculosis and Kaposi's sarcoma are the three leading causes. P. carinii infection is frequently responsible for pulmonary infections, but is only occasionally responsible for a pleural effusion. Pleural effusions may also develop from non-Hodgkin's lymphoma (NHL). There is one relatively rare NHL that is associated with the Kaposi's sarcoma associated virus that produces a lymphoma confined to the body cavity.
CDH5 is specifically activated in glioblastoma stemlike cells and contributes to vasculogenic mimicry induced by hypoxia
Authors: X.-g. Mao, X.-y. Xue, L. Wang, X. Zhang, M. Yan, Y.-y. Tu, W. Lin, X.-f. Jiang, H.-g. Ren, W. Zhang, S.-j. Song
Journal: Neuro-Oncology (2013)

A proportion of glioblastoma stemlike cells (GSCs) expressing endothelial cell marker CDH5 (vascular-endothelial–cadherin or CD144) can transdifferentiate into endothelial cells and form blood vessels. However, the implications of CDH5 expression in gliomas and how it is regulated in GSCs remain to be clarified. The mRNA and protein levels of CDH5 were detected in glioma samples and cultured cell lines, and the prognostic value of the CDH5 expression level for GBM patients was evaluated. Bioinformatics analysis was performed to reveal the potential functional roles of CDH5 in glioblastoma multiforme. Gene knockdown induced by short hairpin RNA, chromatin immunoprecipitation analysis, and a vasculogenic tube formation assay were performed to investigate the relationships among hypoxia, CDH5 expression level, and angiogenesis. CDH5 was overexpressed in gliomas, correlated with tumor grades, and was an independent adverse prognostic predictor for glioblastoma multiforme patients. CDH5 was specifically activated in GSCs but not in non-GSCs or neural stem cells, and CDH5+ cells could produce xenografts in immunocompromised mice. Bioinformatics analysis demonstrated that CDH5 might interact directly with hypoxia-inducible factor (HIF)2α. CDH5 expression was significantly upregulated in GSCs, but not in non-GSCs or normal neural stem cells, under a 1% O2 condition. Both HIF1α and HIF2α positively regulated CDH5 level in GSCs and could bind to the promoter of CDH5. Furthermore, CDH5 contributed to the vasculogenic mimicry of GSCs, especially under hypoxic conditions. The specific expression of CDH5 in GSCs may contribute to GSC-derived neovasculogenesis in glioblastoma multiforme, especially under hypoxic conditions, revealing novel tumorigenic mechanisms contributed by GSCs.
Helical computed tomographic cholangiography versus endosonography for suspected bile duct stones: a prospective blinded study in non-jaundiced patients
Authors: M Polkowski, J Palucki, J Regula, A Tilszer, E Butruk
Journal: Gut (1999)

<h3>BACKGROUND</h3> Helical computed tomography performed after intravenous administration of a cholangiographic contrast material (HCT-cholangiography) may be useful for detecting bile duct stones in non-jaundiced patients. However, this method has never been compared with other non-invasive biliary imaging tests. <h3>AIMS</h3> To compare prospectively HCT-cholangiography and endosonography (EUS) in a group of non-jaundiced patients with suspected bile duct stones. <h3>METHODS</h3> Fifty two subjects underwent both HCT-cholangiography and EUS. Endoscopic retrograde cholangiography (ERCP), with or without instrumental bile duct exploration, served as a reference method, and was successful in all but two patients. <h3>RESULTS</h3> Thirty four patients (68%) were found to have choledocholithiasis at ERCP. The sensitivity for HCT-cholangiography in stone detection was 85%, specificity 88%, and accuracy 86%. For EUS the sensitivity was 91%, specificity 100%, and accuracy 94%. The differences were not significant. No serious complications occurred with either method. <h3>CONCLUSIONS</h3> HCT-cholangiography and EUS are safe and comparably accurate methods for detecting bile duct stones in non-jaundiced patients.
DC-SIGN Is the Major <i>Mycobacterium tuberculosis</i> Receptor on Human Dendritic Cells
Authors: Ludovic Tailleux, Olivier Schwartz, Jean-Louis Herrmann, Elisabeth Pivert, Mary Jackson, Ali Amara, Luc Legres, Donatus Dreher, Laurent P. Nicod, Jean Claude Gluckman, Philippe H. Lagrange, Brigitte Gicquel, Olivier Neyrolles
Journal: The Journal of Experimental Medicine (2002)

Early interactions between lung dendritic cells (LDCs) and Mycobacterium tuberculosis, the etiological agent of tuberculosis, are thought to be critical for mounting a protective anti-mycobacterial immune response and for determining the outcome of infection. However, these interactions are poorly understood, at least at the molecular level. Here we show that M. tuberculosis enters human monocyte-derived DCs after binding to the recently identified lectin DC-specific intercellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN). By contrast, complement receptor (CR)3 and mannose receptor (MR), which are the main M. tuberculosis receptors on macrophages (Mϕs), appeared to play a minor role, if any, in mycobacterial binding to DCs. The mycobacteria-specific lipoglycan lipoarabinomannan (LAM) was identified as a key ligand of DC-SIGN. Freshly isolated human LDCs were found to express DC-SIGN, and M. tuberculosis–derived material was detected in CD14−HLA-DR+DC-SIGN+ cells in lymph nodes (LNs) from patients with tuberculosis. Thus, as for human immunodeficiency virus (HIV), which is captured by the same receptor, DC-SIGN–mediated entry of M. tuberculosis in DCs in vivo is likely to influence bacterial persistence and host immunity.
Cutaneous ultrastructural diagnosis of ceroid-lipofuscinosis
Authors: MASAMITSU ISHII, KUNIAKI TAKAHASHI, TOSHIO HAMADA, AKEMI TANAKA, SHINOBU HIGAMI
Journal: British Journal of Dermatology (1981)

Journal Article Cutaneous ultrastructural diagnosis of ceroid‐lipofuscinosis Get access MASAMITSU ISHII, MASAMITSU ISHII The Department of Dermatology, Osaka City University Medical School, Osaka, Japan Masamitsu Ishii, Department of Dermatology, Osaka City University Medical School, Abenoku Osaka 545, Japan. Search for other works by this author on: Oxford Academic Google Scholar KUNIAKI TAKAHASHI, KUNIAKI TAKAHASHI The Department of Dermatology, Osaka City University Medical School, Osaka, Japan Search for other works by this author on: Oxford Academic Google Scholar TOSHIO HAMADA, TOSHIO HAMADA The Department of Dermatology, Osaka City University Medical School, Osaka, Japan Search for other works by this author on: Oxford Academic Google Scholar AKEMI TANAKA, AKEMI TANAKA The Department of Pediatrics, Osaka City University Medical School, Osaka, Japan Search for other works by this author on: Oxford Academic Google Scholar SHINOBU HIGAMI SHINOBU HIGAMI The Department of Pediatrics, Osaka City University Medical School, Osaka, Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 104, Issue 5, 1 May 1981, Page 581, https://doi.org/10.1111/j.1365-2133.1981.tb08176.x Published: 01 May 1981 Article history Accepted: 17 June 1980 Published: 01 May 1981
Leukocyte Reduction of Red Blood Cell Transfusions Does not Decrease Allosensitization Rates in Potential Kidney Transplant Candidates
Authors: Martin Karpinski, Denise Pochinco, Iga Dembinski, Willie Laidlaw, James Zacharias, Peter Nickerson
Journal: Journal of the American Society of Nephrology (2004)

<h3>Abstract</h3> Human NKR-P1 (CD161, <i>KLRB1</i>) and its ligand LLT1 (<i>CLEC2D</i>) are a prototypical inhibitory C-type lectin-like receptor:ligand pair of NK cells with a critical role in homing lymphocytes to immune-privileged sites, particularly in multiple sclerosis, rheumatoid arthritis, and Crohn's disease. Furthermore, NKR-P1:LLT1 inhibitory signaling is associated with glioblastoma, non-Hodgkin's lymphoma, breast, and prostate cancer. However, the lack of structural data on the formation of the NKR-P1:LLT1 complex limits our understanding of this signaling. We thus solved the crystal structures of NKR-P1 and the NKR-P1:LLT1 complex. NKR-P1 forms a homodimer with an unexpected arrangement that enables LLT1 binding in two modes, bridging two LLT1 molecules, thereby forming interaction clusters suggestive of an inhibitory immune synapse. Moreover, observing the formation of these clusters by SEC-SAXS analysis in solution and by dSTORM super-resolution microscopy on the cell surface, and following their role in receptor signaling using <i>in vitro</i> cytotoxicity assay with freshly isolated NK cells, we show how NKR-P1:LLT1 clustering allows these proteins to overcome the weak affinity of C-type lectin-like receptors to their ligands. Furthermore, only the ligation of both primary and secondary LLT1 binding interfaces leads to effective NKR-P1 inhibitory signaling. Therefore, our findings show how inhibitory receptor cross-linking and clustering work together to trigger signal transduction upon cellular contact in the immune synapse.
Toxic effects of local anesthetics
Authors: R. H. de Jong
Journal: JAMA (1978)

LOCAL anesthetics are among the most widely used drugs in medical and dental practice; systemic toxic reactions thus may be expected on occasion. As these drugs have found some new applications of late, their toxic effects warrant review—all the more because improved methods of preventing and treating unwanted side effects have become available. This communication describes why a locally injected drug can produce reactions in distant organ systems and what the common symptoms are; it shows ways to minimize the incidence of side effects and, finally, suggests how to treat reactions.  Until recent years, local anesthetics were used primarily to numb circumscribed parts of the body by injecting the drug close to spinal roots or peripheral nerve, or by infiltrating it near cutaneous nerve endings. Though some of the drug reaches its intended neural target (there to block impulse conduction), much of the perineurally injected anesthetic falls short of the
An Antagonist of Dishevelled Protein-Protein Interaction Suppresses β-Catenin–Dependent Tumor Cell Growth
Authors: Naoaki Fujii, Liang You, Zhidong Xu, Kazutsugu Uematsu, Jufang Shan, Biao He, Iwao Mikami, Lillian R. Edmondson, Geoffrey Neale, Jie Zheng, R. Kiplin Guy, David M. Jablons
Journal: Cancer Research (2007)

Abstract Recent progress in the development of inhibitors of protein-protein interactions has opened the door for developing drugs that act by novel and selective mechanisms. Building on that work, we designed a small-molecule inhibitor of the Wnt signaling pathway, which is aberrantly activated across a wide range of human tumors. The compound, named FJ9, disrupts the interaction between the Frizzed-7 Wnt receptor and the PDZ domain of Dishevelled, down-regulating canonical Wnt signaling and suppressing tumor cell growth. The antitumorigenic effects of FJ9 were pronounced, including induction of apoptosis in human cancer cell lines and tumor growth inhibition in a mouse xenograft model. FJ9 is thus among the first non-peptide inhibitors to show therapeutic efficacy through disruption of PDZ protein-protein interactions. [Cancer Res 2007;67(2):573–9]
Creeping fat in Crohn's disease: travelling in a creeper lane of research?
Authors: A Schäffler, H Herfarth
Journal: Gut (2005)

Identification of a distinct secretion pattern of adipocytokines from creeping fat in Crohn’s disease and from mesenteric adipose tissue in chronic inflammatory bowel diseases (IBD) or mesenteric diseases can be considered as work in progress. Characterisation of visceral adipose tissue by its highly active secretory products may lead to the discovery of specific discrimination and activity markers in IBD and may provide future targets for drug therapy. In addition, the cellular compartment of macrophages residing within the mesenteric adipose tissue is becoming recognised as bearing pathophysiological relevance.

The connective and adipose tissue changes observed in patients with Crohn’s disease (CD) have received only little attention from pathologists, although fat hypertrophy, fat wrapping (fat creeping upon the bowel), and creeping fat have long been recognised by surgeons as a phenomenon suitable for delineating the extent of active disease. Dr Burril B Crohn himself, who gave his name to this chronic inflammatory bowel disease, initially described the changes in the appearance of the mesenteric adipose tissue as a characteristic symptom of the disease.1 Sheehan and colleagues2 and others3 defined fat wrapping as present if more than 50% of the intestinal surface is covered by adipose tissue. Fat encroachment of the antimesenteric surface of the bowel displays a characteristic feature of CD, leading to complete enveloping of the antimesenteric surface and obliteration of the bowel-mesentery angle.3

To date, the pathophysiology of creeping fat has been investigated only sporadically2–5 and it seems to have fallen into oblivion.6

Adipose tissue has long been regarded as a passive type of connective tissue that stores energy as triglycerides and releases energy as free fatty acids. However, due to the wide variety of hormones, proteins, peptides, complement factors, cytokines, enzymes, and receptors expressed in and secreted by adipocytes, the total adipose …
Dietary Patterns and Survival After Breast Cancer Diagnosis
Authors: Candyce H. Kroenke, Teresa T. Fung, Frank B. Hu, Michelle D. Holmes
Journal: Journal of Clinical Oncology (2005)

Purpose There is little prior study of major dietary patterns and breast cancer survival. Methods Patients included 2,619 Nurses' Health Study participants who were diagnosed with invasive breast cancer between 1982 and 1998 and completed a dietary questionnaire more than 1 year after diagnosis. Participants were followed through 2002 (median = 9 years). During follow-up, 414 patients died of any cause, 242 patients died of breast cancer, and 172 patients died from causes other than breast cancer. Women with in situ or metastatic disease at diagnosis were excluded. We used Cox proportional hazards models to evaluate prospective associations of prudent and Western dietary patterns assessed both before and after diagnosis with time to event after diagnosis. Results In multivariate-adjusted analyses assessed after diagnosis, the Western and prudent dietary patterns were unrelated to all-cause or breast cancer mortality. However, compared with women with the lowest intake of the prudent dietary pattern, the relative risks (and 95% CIs) of death from causes other than breast cancer were 0.85 (95% CI, 0.53 to 1.35), 0.74 (95% CI, 0.45 to 1.21), 0.70 (95% CI, 0.42 to 1.17), and 0.54 (95% CI, 0.31 to 0.95; P = .03, from lowest to highest quintile of intake). In contrast, the Western dietary pattern was positively associated with this outcome (P = .04). Results for the assessment of dietary patterns before diagnosis were similar, except the prudent dietary pattern was unrelated to mortality. Conclusion A higher intake of the prudent pattern and a lower intake of the Western pattern may protect against mortality from causes unrelated to breast cancer.
Physical work environment risk factors for long term sickness absence: prospective findings among a cohort of 5357 employees in Denmark
Authors: Thomas Lund, Merete Labriola, Karl Bang Christensen, Ute Bültmann, Ebbe Villadsen
Journal: BMJ (2006)

<h3>Abstract</h3> <b>Objectives</b> To examine the effects of physical work environment on long term sickness absence and to investigate interaction between physical and psychosocial risk factors. <b>Design and setting</b> Prospective cohort study of long term sickness absence among employees in Denmark. <b>Participants</b> 5357 employees interviewed in 2000 about their physical work environment, and various covariates were followed for 18 months in a national sickness absence register. <b>Outcome measurements</b> Cox regression analysis was performed to assess risk estimates for physical risk factors in the work environment and onset of long term sickness absence, defined as receiving sickness absence compensation for eight consecutive weeks or more. <b>Results</b> 348 participants (6.9%) developed long term sickness absence during follow-up. Of these, 194 (55.7%) were women and 154 (44.3%) were men. For both female and male employees, risk of onset of long term sickness absence was increased by extreme bending or twisting of the neck or back, working mainly standing or squatting, lifting or carrying loads, and pushing or pulling loads. Significant interactions were found for three combinations of physical and psychosocial work environment risk factors among female employees (P&lt;0.05). <b>Conclusion</b> Uncomfortable working positions, lifting or carrying loads, and pushing or pulling loads increased the risk of onset of long term sickness absence. The study shows a potential for reducing long term sickness absence through modifying work postures straining the neck and back, reducing the risk of work done standing or walking, and reducing the risk associated with handling loads. Dealing with psychosocial stressors simultaneously may improve physical intervention efforts further for female employees.
Effects of Work Hour Reduction on Residents’ Lives
Authors: Kathlyn E. Fletcher, Willie Underwood, Steven Q. Davis, Rajesh S. Mangrulkar, Laurence F. McMahon, Sanjay Saint
Journal: JAMA (2005)

The Accreditation Council for Graduate Medical Education implemented mandatory work hour limitations in July 2003, partly out of concern for residents' well-being in the setting of sleep deprivation. These limitations are likely to also have an impact on other aspects of the lives of residents.To summarize the literature regarding the effect of interventions to reduce resident work hours on residents' education and quality of life.We searched the English-language literature about resident work hours from 1966 through April 2005 using MEDLINE, EMBASE, and Current Contents, supplemented with hand-search of additional journals, reference list review, and review of abstracts from national meetings.Studies were included that assessed a system change designed to counteract the effects of resident work hours, fatigue, or sleep deprivation; included an outcome directly related to residents; and were conducted in the United States.For each included study, 2 investigators independently abstracted data related to study quality, subjects, interventions, and findings using a standard data abstraction form.Fifty-four articles met inclusion criteria. The interventions used to decrease resident work hours varied but included night and day float teams, extra cross-coverage, and physician extenders. Outcomes included measures of resident education (operative experience, test scores, satisfaction) and quality of residents' lives (amount of sleep, well-being). Interventions to reduce resident work hours resulted in mixed effects on both operative experience and on perceived educational quality but generally improved residents' quality of life. Many studies had major limitations in their design or conduct.Past interventions suggest that residents' quality of life may improve with work hour limitations, but interpretation of the outcomes of these studies is hampered by suboptimal study design and the use of nonvalidated instruments. The long-term impact of reducing resident work hours on education remains unknown. Current and future interventions should be evaluated with more rigorous methods and should investigate links between residents' quality of life and quality of patient care.
URTICARIA AND ANGIO-OEDEMA.
Authors: R. H. CHAMPION, S. O. B. ROBERTS, R. G. CARPENTER, J. H. ROGER
Journal: British Journal of Dermatology (1969)

SUMMARY.— The records of 554 consecutive patients attending hospitals in the Cambridge region with urticaria have been analysed with the aid of a computer. These patients represent only a small minority of all patients with urticaria in the region. In 79%, the aetiology was unknown although in many cases aggravating factors, for example, psychological stress, aspirin, or infection, were detected. A past or family history of atopic disorders was not found more frequently in patients with urticaria than in controls and the course of the disease in patients with a background of atopy did not differ from the remainder, suggesting that an undetected allergy is not responsible for many of these undiagnosed cases. Allergy is relatively more important in acute urticaria and in patients who do not attend hospital. The frequency of attacks and total duration of the disease are different in patients with urticaria alone, angio‐oedema alone and both together but there was little difference in the aetiological factors, supporting the concept that urticaria and angio‐oedema are fundamentally similar. The prognosis is expressed in the form of life tables.