tbuckley/cabot-search huggingface dataset:
Oral misoprostol in preventing postpartum haemorrhage in resource-poor communities: a randomised controlled trial
Authors: Richard J Derman, Bhalchandra S Kodkany, Shivaprasad S Goudar, Stacie E Geller, Vijaya A Naik, MB Bellad, Shobhana S Patted, Ashlesha Patel, Stanley A Edlavitch, Tyler Hartwell, Hrishikesh Chakraborty, Nancy Moss
Journal: The Lancet (2006)
Detection and characterization of high affinity plasma membrane receptors for human interleukin 1.
Authors: S K Dower, S R Kronheim, C J March, P J Conlon, T P Hopp, S Gillis, D L Urdal
Journal: The Journal of Experimental Medicine (1985)

Interleukin 1 (IL-1) is a polypeptide hormone that acts as a central mediator of inflammation. Since IL-1 action is presumably mediated by specific cell surface receptor(s), we have characterized the binding of this hormone to cells. Purified human IL-1 was labeled to high specific activity with 125I, using Bolton-Hunter reagent. The labeled protein binds specifically to LBRM-33-1A5 (a murine T lymphoma line previously shown to produce IL-2 in response to phytohemagglutinin and IL-1) with an affinity of approximately 0.2-2 X 10(10)/M and, at saturation, to approximately 500 receptors per cell, on intact cells at 8 degrees C in the presence of sodium azide. The affinity of unmodified IL-1 for the murine plasma membrane receptor is 0.9-2 X 10(10)/M, as measured by the inhibition of 125I-IL-1 binding. The murine receptor specificity has been confirmed by demonstrating that, among a series of 12 polypeptide hormones, only IL-1 inhibits 125I-IL-1 binding to LBRM-33-1A5 cells. Treatment of surface-bound 125I-IL-1 with bivalent water-soluble crosslinkers identified a membrane polypeptide of Mr 79,500 to which IL-1 is crosslinked. A variety of cell types have been surveyed for the capacity to bind 125I-IL-1 specifically. The presence of specific binding correlates with the capacity of the cells tested to respond to IL-1. Our results indicate that the biological effects of the polypeptide hormone IL-1 are mediated by high affinity plasma membrane receptors. The identification of these receptors should provide valuable insight into the apparently diverse biological activities of IL-1.
Fetus and Neonate: Physiology and Clinical Applications. Volume 1. The Circulation.
Authors: M. ARTMAN
Journal: Cardiovascular Research (1993)

Fetus and Neonate: Physiology and Clinical Applications. Volume 1. The Circulation. Get access MICHAEL ARTMAN MICHAEL ARTMAN University of South Alabama Mobile, Alabama, USA Edited by Mark A Hanson, John A D Spencer, and Charles H Rodeck. (Pp 454; £24.95.) Cambridge: Cambridge University Press, 1993. ISBN 0521-423-279. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 27, Issue 9, September 1993, Page 1698, https://doi.org/10.1093/cvr/27.9.1698a Published: 01 September 1993
Methylation of Stat1 Promoter Can Contribute to Squamous Cell Carcinogenesis
Authors: Heehyoung Lee, Hua Yu
Journal: JNCI Journal of the National Cancer Institute (2006)

One of the most recently recognized signaling pathways that regulate tumor cell proliferation and survival involves signal transducers and activators of transcription (STAT) proteins. The STAT family of proteins has seven known members: Stat1, 2, 3, 4, 5A, 5B, and 6. Interestingly, it has become evident that dif ferent STAT proteins can serve either tumor suppressing or oncogenic roles. Stat1, for example, functions as a tumor suppressor in several capacities ( 1 – 5 ) , whereas Stat3 and to a lesser extent, Stat5, play a critical role in malignant progression at multiple levels ( 6 – 9 ) . Although it has been demonstrated that interferon-induced Stat1 activity can cause growth arrest and can induce apoptosis, it is not clear whether a lack of Stat1 in human cancer directly contributes to cancer cell proliferation and survival. If so, what keeps Stat1 from functioning in this manner in tumor cells also remains largely unknown. The article by Xi et al. ( 10 ) in this issue of the Journal presents evidence that Stat1 expression in squamous cell carcinoma of the head and neck (SCCHN) is lower than that of normal tissues from individuals without cancer. Restoring Stat1 expression in the tumor cells leads to growth inhibition in vitro and in xenograft tumors, which is accompanied by an increase in p21 expression. Their work further demonstrates that the low expression of Stat1 in SCCHN tumors is associated with Stat1 promoter methylation and that treatment with a methylation inhibitor increases STAT1 and p21 expression and sensitizes SCCHN tumor cells to cisplatin. These fi ndings are novel in several respects. Many independent studies, which involve mainly mouse tumor models or cell lines, have suggested that Stat1 can function as a tumor suppressor ( 1 – 5 ) . How does Stat1 function as a tumor suppressor? Stat1’s ability to mediate host immune defenses against tumors has been elegantly demonstrated in mice ( 2 ) . Increasing Stat1 activity by interferon treatment also leads to cell growth inhibition, which can be explained by Stat1’s capacity to induce p21waf and caspase expression ( 1 , 5 ) . Moreover, Stat1defi cient cells have defects both in S-phase and G 2 – M checkpoints in response to DNA damage ( 11 ) . Also, Stat1and p53-null mice show more frequent and rapid tumor development than wild-type mice. The basal expression level of the p53 inhibitor Mdm2 is higher in Stat1 − / − cells than in wild-type cells, suggesting that Stat1 is a negative regulator of Mdm2 expression ( 12 ) . The fi ndings by Xi et al. provide direct evidence supporting the
EbolaTracks: an automated SMS system for monitoring persons potentially exposed to Ebola virus disease
Authors: L E Tracey, A K Regan, P K Armstrong, G K Dowse, P V Effler
Journal: Eurosurveillance (2015)

We report development and implementation of a short message service (SMS)-based system to facilitate active monitoring of persons potentially exposed to Ebola virus disease (EVD), whether returning from EVD-affected countries, or contacts of local cases, should they occur. The system solicits information on symptoms and temperature twice daily. We demonstrated proof-of-concept; however this system would likely be even more useful where there are many local contacts to confirmed EVD cases or travellers from EVD-affected countries.
A New Approach to Simultaneously Quantify Both TCR α- and β-Chain Diversity after Adoptive Immunotherapy
Authors: Minying Zhang, Sourindra Maiti, Chantale Bernatchez, Helen Huls, Brian Rabinovich, Richard E. Champlin, Luis M. Vence, Patrick Hwu, Laszlo Radvanyi, Laurence J.N. Cooper
Journal: Clinical Cancer Research (2012)

Abstract Purpose: T-cell receptor (TCR) variable Vα and Vβ gene diversity is a surrogate biomarker for the therapeutic potential of adoptive immunotherapy and cellular immunity. Therefore, creating a straightforward, rapid, sensitive, and reliable method to view the global changes of both TCRVα and Vβ transcripts in heterogeneous populations of T cells is appealing. Experimental Design: We designed a “direct TCR expression assay” (DTEA) using a panel of customized bar-coded probes that simultaneously detects and quantifies 45 Vα and 46 Vβ transcripts in a nonenzymatic digital multiplexed assay from a small number of cells (104 cells) or as little as 100 ng of total RNA. Results: We evaluated DTEA on total RNA samples of tumor-infiltrating lymphocytes and peripheral blood obtained from patients with melanoma after adoptive T-cell therapy. DTEA detected a similar spectrum of the dominant patterns of TCRVβ gene usage as sequencing cloned TCRVβ CDR3 regions. However, DTEA was rapid, achieved a level of sensitivity to identify rare T-cell populations, and simultaneously tracked the full array of Vα and Vβ transcripts. Conclusions: DTEA can rapidly and sensitively track changes in TCRVα and Vβ gene usages in T-cell pools following immune interventions, such as adoptive T-cell transfer, and may also be used to assess impact of vaccination or reconstitution of T-cell compartment after hematopoietic stem cell transplantation. Clin Cancer Res; 18(17); 4733–42. ©2012 AACR.
Human recombinant interleukin 4 induces Fc epsilon receptors (CD23) on normal human B lymphocytes.
Authors: T Defrance, J P Aubry, F Rousset, B Vanbervliet, J Y Bonnefoy, N Arai, Y Takebe, T Yokota, F Lee, K Arai
Journal: The Journal of Experimental Medicine (1987)

Human rIL-4 is able to induce the expression of low-affinity receptors for IgE (Fc epsilon RL/CD23) on resting B lymphocytes, as determined by the binding of either the anti Fc epsilon RL/CD23-specific mAb 25 or IgE. Stimulation of B cells with insolubilized anti-IgM antibody increases the number of cells expressing Fc epsilon RL/CD23 upon culturing with IL-4 and enhances the level of Fc epsilon RL/CD23 expression on these cells. Fc epsilon RL/CD23 induction is specific for IL-4 since IL-1 alpha, IL-2, IFN-gamma, B cell-derived B cell growth factor (BCGF), and a low-molecular-weight BCGF were ineffective. IFN-gamma strongly inhibited the induction of Fc epsilon RL/CD23 by IL-4.
Increased radiosensitivity of granulocyte macrophage colony-forming units and skin fibroblasts in human autosomal recessive severe combined immunodeficiency.
Authors: M Cavazzana-Calvo, F Le Deist, G De Saint Basile, D Papadopoulo, J P De Villartay, A Fischer
Journal: Journal of Clinical Investigation (1993)

We studied the radiosensitivity of granulocyte macrophage colony-forming units (GM-CFU) in patients with a severe combined immunodeficiency (SCID). Three patients lacking both mature T and B cells showed a twofold higher GM-CFU radiosensitivity calculated as the DO value (dose required to reduce survival to 37%), and an identical observation was made with fibroblasts from one of these patients. A patient with an SCID with hypereosinophilia, i.e., Omenn's syndrome characterized by extremely restricted T cell heterogeneity and a lack of B cells, also showed abnormal GM-CFU radiosensitivity. In contrast, GM-CFU from a patient lacking only T cells (X-linked form of SCID) showed normal GM-CFU radiosensitivity. These data further support the similarity between human T(-) B(-) SCID and the murine acid mutation characterized by a defect in T cell receptor and immunoglobulin gene rearrangement, and by an abnormal double-strand DNA break repair function. In addition, they strongly suggest that the Omenn's immunodeficiency syndrome may be a leaky T(-)B(-) SCID phenotype as previously indicated by the coexistence of the two phenotypes in siblings.
Topical photodynamic therapy is immunosuppressive in humans
Authors: Y.J. Matthews, D.L. Damian
Journal: British Journal of Dermatology (2009)

Background Visible light irradiation after application of a photosensitizer (topical photodynamic therapy; PDT) is increasingly used to treat nonmelanoma skin cancers and premalignant actinic keratoses. PDT can provide a cosmetically superior alternative to surgery, but carries failure rates of 10–40%. While some murine studies have suggested immune enhancement by PDT, others reported immunosuppressive effects, which may indicate impaired antitumour immunity and thus compromised tumour clearance. Objectives This study aimed to determine the in vivo immune effects of PDT in humans. Methods Using healthy, Mantoux‐positive volunteers, we irradiated discrete areas of the back with narrowband red light (630 nm; 37 J cm−2), with and without prior application of 5‐aminolaevulinic acid (ALA) or methyl aminolaevulinate (MAL). Adjacent, untreated areas served as immunologically intact control sites. Delayed‐type hypersensitivity responses to tuberculin purified protein derivative (Mantoux reactions) were then elicited in each of the irradiated, unirradiated and control sites, and the intensity of the reactions was quantitated with an erythema meter and by measurement of Mantoux diameter. By comparing Mantoux intensity at treated and control sites, immunosuppression was determined in each volunteer for each intervention. Results We found that both MAL‐PDT and ALA‐PDT significantly suppressed Mantoux erythema (by 30% and 50%, respectively) and diameter (41% and 38%). Red light alone significantly suppressed diameter (22%) but not erythema (13%). Conclusions Topical PDT induced significant immune suppression, which could impair local antitumour immune responses and may thus contribute to treatment failure.
Vasoactive intestinal peptide in cirrhotic rats: Hemodynamic effects and mesenteric arterial receptor characteristics
Authors: S S Lee, M Huang, Z Ma, O Rorstad
Journal: Hepatology (1996)

Vasoactive intestinal peptide (VIP) blood levels in cirrhosis are elevated, but its hemodynamic and receptor characteristics remain unclarified. We aimed to quantify VIP receptor characteristics in mesenteric arteries, plasma VIP concentration by radioimmunoassay (RIA), and the hemodynamic effects of VIP infusion in bile duct-ligated (BDL) cirrhotic and sham-operated control rats. Mesenteric arterial membranes were prepared by ultracentrifugation, and receptor characteristics were studied using 125 I-labeled VIP as a radioligand. For the hemodynamic study, there were four groups: cirrhotic and sham-operated rats were infused with either VIP (50 ng/kg/min for 15 minutes) or equivolumic isotonic saline. Regional blood flows were measured in conscious rats with radioactive microspheres. Receptor studies showed high-and low-affinity binding sites for VIP, which had similar equilibrium dissociation constants (binding affinities) and receptor densities for both the cirrhotic and control rats. Plasma VIP concentrations were significantly elevated in the cirrhotic rats. In both cirrhotic and sham-operated rats, VIP infusion produced plasma levels approximately twofold to threefold increased over the basal levels observed in cirrhotic rats. In cirrhotic rats, VIP infusion did not affect any hemodynamic parameter, whereas in the sham-operated rats VIP infusion significantly increased the mesenteric visceral blood flow. These results show that the hyporesponsiveness to VIP in cirrhotic rats is not attributable to receptor downregulation, implying postreceptor alterations. This suggests that VIP may not play a major role in the maintenance of splanchnic hyperemia in cirrhosis.
Re: Population-Based Study of BRCA1 and BRCA2 Mutations in 1035 Unselected Finnish Breast Cancer Patients
Authors: P. O. Chappuis, N. Hamel, A.-J. Paradis, J. Deschenes, P. N. Tonin, P. Ghadirian, W. D. Foulkes
Journal: JNCI Journal of the National Cancer Institute (2001)
Human infection with a novel tick-borne Anaplasma species in China: a surveillance study
Authors: Hao Li, Yuan-Chun Zheng, Lan Ma, Na Jia, Bao-Gui Jiang, Rui-Ruo Jiang, Qiu-Bo Huo, Ya-Wei Wang, Hong-Bo Liu, Yan-Li Chu, Yu-Dong Song, Nan-Nan Yao, Tie Sun, Fan-Yi Zeng, J Stephen Dumler, Jia-Fu Jiang, Wu-Chun Cao
Journal: The Lancet Infectious Diseases (2015)
Multigenerational epigenetic adaptation of the hepatic wound-healing response
Authors: Müjdat Zeybel, Timothy Hardy, Yi K Wong, John C Mathers, Christopher R Fox, Agata Gackowska, Fiona Oakley, Alastair D Burt, Caroline L Wilson, Quentin M Anstee, Matt J Barter, Steven Masson, Ahmed M Elsharkawy, Derek A Mann, Jelena Mann
Journal: Nature Medicine (2012)
Laser angioplasty of restenosed coronary stents: results of a multicenter surveillance trial
Authors: Ralf Köster, Christian W Hamm, Ricardo Seabra-Gomes, Gunhild Herrmann, Horst Sievert, Carlos Macaya, Eckart Fleck, Klaus Fischer, Johannes J.R.M Bonnier, Jean Fajadet, Jürgen Waigand, Karl-Heinz Kuck, Michel Henry, Marie Claude Morice, Luciano Pizzulli, Michael M Webb-Peploe, Arnd B Buchwald, Lars Ekström, Eberhard Grube, Saad Al Kasab, Antonio Colombo, Archimedes Sanati, Sjef M.P.G Ernst, Michael Haude, Martin B Leon, Charles Ilsley, Rafael Beyar, Yvo Taeymans, Uwe Gladbach, Karl Wegscheider, Patrick W Serruys
Journal: Journal of the American College of Cardiology (1999)
Control of Total Systemic Vascular Capacity by the Carotid Sinus Baroreceptor Reflex
Authors: ARTIN A. SHOUKAS, KIICHI SAGAWA
Journal: Circulation Research (1973)

To attain a quantitative understanding of carotid sinus baroreceptor reflex control of cardiac output, we studied the reflex control of total systemic vascular capacity in vagotomized dogs. In experiments measuring blood volume shifts caused by the carotid sinus reflex (series 1), venous return was diverted into a reservoir while cardiac output and central venous pressure were maintained at constant levels. The pressure in the isolated carotid sinuses (ISP) was lowered or raised in 25-mm Hg steps between 75 and 200 mm Hg. This procedure mobilized blood into or out of the reservoir, indicating a decrease or an increase in total vascular capacity, respectively. The mean maximum volume shift, 3.6 ml/kg body weight, occurred in the same ISP region, 135 ± 12.5 mm Hg, where reflex control of total peripheral resistance was strongest. The total volume shift was approximately 7.5 ml/kg for ISP changes from 75 to 200 mm Hg. When mean arterial blood pressure was maintained constant during the ISP step changes, the volume shift almost doubled. In experiments measuring the reflex effect on total systemic vascular compliance (series 2) and in experiments determining the reflex control of arterial compliance (series 3), total systemic vascular and lumped arterial compliances were measured in the same dogs that were used in series 1 experiments. The total systemic vascular and arterial compliances were approximately 2.0 ml/mm Hg kg -1 and 0.0677 ml/mm Hg kg -1 , respectively. The reflex did not affect these compliances. We concluded that the reflex controls the total systemic venous capacity to a degree that changes cardiac output potentially by 30-10% per 25-mm Hg change in ISP.
Mechanisms of Ly2 suppressor cell activity. Activation of an Ly1 I-J+ cell is required to transduce the suppressive signal.
Authors: P M Flood, D C Louie
Journal: The Journal of Experimental Medicine (1984)

A cell-free product secreted by Ly1-2+ T cells (Ly2 TsF) can suppress the in vitro response to sheep erythrocytes (SRBC) of spleen cells depleted of Ly2+ T cells. This suppressor factor expresses biological activity only when the acceptor cells share major histocompatibility complex (MHC)-linked polymorphic genes with the cells that made the Ly2 TsF. Removal of Ly1 I-J+ cells from the assay culture abrogates the ability of Ly2 TsF to suppress these cultures, but we can replace the need for the I-J+ cells in the assay culture with an I-J+ soluble factor derived from them. We investigated the cellular interactions involved in the activation of I-J+ cells by Ly2 TsF in vitro. We have been able to induce the production of an I-J+ molecule needed for Ly2 TsF activity in a 48-h intermediate culture of B cell-depleted Ly1 spleen cells, Ly2 TsF, and antigen. This molecule not only fails to bind antigen, but is also antigen nonspecific in that it can be induced by Ly2 TsF of irrelevant specificities. In order to replace the activity of the Ly1 I-J+ cell in the assay culture, the cell induced by Ly2 TsF to produce the I-J+ molecule in vitro must share genetic polymorphisms linked to the MHC with the Ly2 TsF, and genetic polymorphisms linked to the Igh-V gene complex with the target cell. In order for Ly2 TsF to induce cells of the primary culture to produce the I-J+ molecule, Ly2 TsF must share genetic polymorphisms linked to the IE region of the MHC with the Ly1 I-J+ cell producing the I-J+ molecule. These results indicate that the suppressive mechanism of Ly2 TsF involves the interaction with an Ly1 I-J+ molecule. This I-J+ molecule serves to focus the antigen-specific suppressor molecule on the target cell. The recognition event of this suppressive complex on the surface of the acceptor cell is controlled by Igh-V-linked genes restricted by the I-J+ molecule of the suppressor complex. This suppressor interaction is confined to the suppressor effector phase of the suppressor circuit since the I-J+ molecules needed for by Ly2 TsF activity do not substitute for the I-J+ molecules needed for the activity of Ly1 TsiF , a T cell factor that initiates the suppressor cell circuit.(ABSTRACT TRUNCATED AT 400 WORDS)
A systematic review of interventions to prevent lower limb soft tissue running injuries
Authors: E W Yeung, S S Yeung
Journal: British Journal of Sports Medicine (2001)

Objectives —To assess the available evidence for preventive strategies for lower limb soft tissue injuries caused by running. Methods —An electronic database search was conducted using The Cochrane Musculoskeletal Injuries Group Specialised Register, The Cochrane Controlled Trials Register, Medline, Embase, Sport Discus, Heracles, Atlantes, Biosis, Cinahl, Scisearch, Current Contents, Index To Theses and Dissertation Abstracts. Any randomised or quasi-randomised trials evaluating interventions to prevent running injuries to lower limb soft tissue were included. The eligibility of trials for inclusion and the quality of the trials were independently assessed by two reviewers. Results —Exposure to a high training load (duration, frequency, or running distance) increases the risk of injury, and thus modification of the training schedule can reduce the incidence of injury. The effectiveness of stretching exercises and of insoles in the prevention of lower extremity soft tissue injuries caused by running is not known. Wearing a knee brace with a patellar support ring may be effective in the prevention of anterior knee pain caused by running. Conclusions —This review provides evidence for the effectiveness of the modification of training schedules in reducing lower limb soft tissue running injuries. More studies are required to quantify the optimal training loads and to confirm that knee braces can prevent knee pain. It is important to note that the studies included in this review had few female participants therefore the results may not be generalisable.
Genetic Markers of Suicidal Ideation Emerging During Citalopram Treatment of Major Depression
Authors: Gonzalo Laje, Silvia Paddock, Husseini Manji, A. John Rush, Alexander F. Wilson, Dennis Charney, Francis J. McMahon
Journal: American Journal of Psychiatry (2007)

Suicidal ideation is an uncommon symptom than can emerge during antidepressant treatment. The biological basis of treatment-emergent suicidal ideation is unknown. Genetic markers may shed light on the causes of treatment-emergent suicidal ideation and help identify individuals at high risk who may benefit from closer monitoring, alternative treatments, or specialty care.A clinically representative cohort of outpatients with major depressive disorder who enrolled in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial were treated with citalopram under a standard protocol for up to 14 weeks. DNA samples from 1,915 participants were genotyped for 768 single-nucleotide polymorphisms in 68 candidate genes. Allele and genotype frequencies were compared between the 120 participants who developed treatment-emergent suicidal ideation and those who did not.Two markers were significantly associated with treatment-emergent suicidal ideation in this sample (marker rs4825476, p=0.0000784, odds ratio=1.94; permutation p=0.01; marker rs2518224, p=0.0000243, odds ratio=8.23; permutation p=0.003). These markers reside within the genes GRIA3 and GRIK2, respectively, both of which encode ionotropic glutamate receptors.Markers within GRIK2 and GRIA3 were associated with treatment-emergent suicidal ideation during citalopram therapy. If replicated, these findings may shed light on the biological basis of this potentially dangerous adverse event and help identify patients at increased risk.