tbuckley/cabot-search huggingface dataset:
Flexibility and development of mirroring mechanisms
Authors: Matthew R. Longo, Bennett I. Bertenthal
Journal: Behavioral and Brain Sciences (2008)

Abstract The empirical support for the shared circuits model (SCM) is mixed. We review recent results from our own lab and others supporting a central claim of SCM that mirroring occurs at multiple levels of representation. By contrast, the model is silent as to why human infants are capable of showing imitative behaviours mediated by a mirror system. This limitation is a problem with formal models that address neither the neural correlates nor the behavioural evidence directly.
Does sustained ERP activity in posterior lexico-semantic processing areas during short-term memory tasks only reflect activated long-term memory?
Authors: Steve Majerus, Martial Van der Linden, Fabienne Collette, Eric Salmon
Journal: Behavioral and Brain Sciences (2003)

We challenge Ruchkin et al.'s claim in reducing short-term memory (STM) to the active part of long-term memory (LTM), by showing that their data cannot rule out the possibility that activation of posterior brain regions could also reflect the contribution of a verbal STM buffer.
Transplantation of parthenogenetic embryonic stem cells ameliorates cardiac dysfunction and remodelling after myocardial infarction
Authors: Yi Liu, Xiaoying Ye, Lina Mao, Zhaokang Cheng, Xinpeng Yao, Xiaohua Jia, Duo Mao, Lailiang Ou, Zongjin Li, Yongzhe Che, Na Liu, Gustav Steinhoff, Lin Liu, Deling Kong
Journal: Cardiovascular Research (2012)

Parthenogenetic embryonic stem cells (pESCs) derived from artificially activated oocytes without fertilization presumably raise minimal ethical concerns and may serve as attractive candidates for regenerative medicine. Here we investigated whether pESCs could repair myocardial infarction (MI), in comparison to embryonic stem cells (ESCs). A total of 89 mice that survived coronary artery ligation randomly received an intramyocardial injection of undifferentiated pESCs, ESCs, or saline. Sham-operated mice (n = 21) that received no treatment served as control animals. After 7 days, transplantation of pESCs increased expression of pro-angiogenic factors and reduced leucocyte infiltration. By 14 and 30 days post-MI, similar to treatment with ESCs, treatment with pESCs efficiently prevented cardiac remodelling and enhanced angiogenesis, in contrast to saline-treated hearts. Improved heart contractile function was also notable 30 days following transplantation of pESCs. Immunofluorescence staining revealed that tissues regenerated from pESCs in the infarcted myocardium were positive for markers of cardiomyocytes, endothelial cells, and smooth muscle cells. Unlike ESC-treated mice, which exhibited a high incidence of teratoma (6 of 34), the pESC-treated mice showed no teratomas (0 of 30) 30 days following transplantation. Transplantation of pESCs could attenuate cardiac dysfunction and adverse ventricular remodelling post-MI, suggesting that pESCs may provide promising therapeutic sources for MI in females.
The Biphasic Role of NF-κB in Progression and Chemoresistance of Ovarian Cancer
Authors: Gong Yang, Xue Xiao, Daniel G. Rosen, Xi Cheng, Xiaohua Wu, Bin Chang, Guangzhi Liu, Fengxia Xue, Imelda Mercado-Uribe, Paul Chiao, Xiang Du, Jinsong Liu
Journal: Clinical Cancer Research (2011)

NF-κB is a transcription factor known to promote tumorigenesis. However, NF-κB is also known to be proapoptotic and may potentially function as a tumor suppressor, although such a functional role has not been extensively investigated in human cancer.A dominant-negative mutant of IκBα with mutations at S32A and S36A was used to inhibit the function of NF-κB in ovarian cancer cell lines. The transcription ability, tumorigenesis, apoptosis, and drug sensitivity were examined in derivative cell lines in comparison with parental cells. We also analyzed the association of nuclear expression of NF-κB p65 with patient survival in an ovarian cancer tissue array.We show that NF-κB functions as a tumor suppressor in four ovarian cancer cell lines, but it functions as an oncogene in their aggressive chemoresistant isogenic variants. NF-κB can exert its proapoptotic or antiapoptotic effect by activating or repressing mitogen-activated protein kinase (MAPK) phosphorylation in parental or aggressive chemoresistant variant cell lines. We also show that the nuclear accumulation of p65 in epithelial cancer tissue is associated with a good response to chemotherapy and can predict longer overall survival for patients with ovarian cancer.Our data provide strong evidence that NF-κB can function as a biphasic regulator, either suppressing or enhancing ovarian cancer growth through the regulation of MAPK and cellular apoptosis.
Tumor Growth Inhibition by Interferon-α using PEGylated Protein or Adenovirus Gene Transfer with Constitutive or Regulated Expression
Authors: G.William Demers, Duane E. Johnson, Todd Machemer, L.David Looper, Amy Batinica, Josefina C. Beltran, Barry J. Sugarman, John A. Howe
Journal: Molecular Therapy (2002)

Inducible synthesis and secretion of therapeutic proteins following gene transfer could be a viable strategy to deliver biopharmaceuticals that currently require parenteral administration. Evaluating the protein pharmacokinetics and biological responses generated by different delivery modalities will provide a better understanding of the advantages and disadvantages of each strategy. The interferon-alpha (IFN-alpha) family of proteins, used clinically for infectious and malignant diseases, has a short half-life, and IFN-alpha therapy requires frequent administration of the drug by injection. Subcutaneous xenograft tumors were inhibited by weekly administration of polyethylene glycol modified (PEGylated) IFN-alpha protein or by a single administration of an adenovirus constitutively expressing IFN-alpha (IACB). Both treatment modalities inhibited tumor growth in a dose-dependent manner, suggesting that increasing exposure to IFN-alpha could result in effective tumor control. A single adenovirus that encodes the components necessary for tetracycline induction (IADR) expressed IFN-alpha in a ligand-dependent manner. Adding doxycycline to the drinking water of mice treated intravenously with the inducible adenovirus IADR inhibited tumor growth by 85% compared with mice that were not given doxycycline. The correlation between serum IFN-alpha concentration and the degree of tumor growth inhibition did not depend on the delivery technology used. It is likely that it will be feasible to control expression of IFN-alpha by oral administration of small molecule drugs after gene delivery to induce therapeutic concentrations of proteins.
An Official ATS Clinical Practice Guideline: Interpretation of Exhaled Nitric Oxide Levels (F<scp>e</scp><sub>NO</sub>) for Clinical Applications
Authors: Raed A. Dweik, Peter B. Boggs, Serpil C. Erzurum, Charles G. Irvin, Margaret W. Leigh, Jon O. Lundberg, Anna-Carin Olin, Alan L. Plummer, D. Robin Taylor
Journal: American Journal of Respiratory and Critical Care Medicine (2011)

Section:ChooseTop of pageAbstract <<ContentsExecutive SummaryEvidence Quality and Reco...IntroductionMethodsReferencesCITING ARTICLES
Pharmacology of Cannabinoid Receptors
Authors: A C Howlett
Journal: The Annual Review of Pharmacology and Toxicology (1995)

Two subtypes of cannabinoid receptors, CB1 and CB2, have been described to date, although future investigations may elucidate other receptors. The actions of cannabimimetic agents via CB1 receptors in brain are mediated by GI/O to inhibit adenylate cyclase and Ca2+ channels. Little is known about signal transduction mechanisms utilized by CB2 receptors. Three classes of agonist ligands regulate cannabinoid receptors: cannabinoid, aminoalkyl-indole, and eicosanoid derivatives. Cannabinoid receptors produce analgesia and modify cognition, memory, locomotor activity, and endocrine functions in mammals.
Cumulative Incidence in Competing Risks Data and Competing Risks Regression Analysis
Authors: Haesook T. Kim
Journal: Clinical Cancer Research (2007)

Abstract Competing risks occur commonly in medical research. For example, both treatment-related mortality and disease recurrence are important outcomes of interest and well-known competing risks in cancer research. In the analysis of competing risks data, methods of standard survival analysis such as the Kaplan-Meier method for estimation of cumulative incidence, the log-rank test for comparison of cumulative incidence curves, and the standard Cox model for the assessment of covariates lead to incorrect and biased results. In this article, we discuss competing risks data analysis which includes methods to calculate the cumulative incidence of an event of interest in the presence of competing risks, to compare cumulative incidence curves in the presence of competing risks, and to perform competing risks regression analysis. A hypothetical numeric example and real data are used to compare those three methods in the competing risks data analysis to their respective counterparts in the standard survival analysis. The source and magnitude of bias from the Kaplan-Meier estimate is also detailed.
Exogenous Pathogen and Plant 15-Lipoxygenase Initiate Endogenous Lipoxin A4 Biosynthesis
Authors: Gerard L. Bannenberg, Julio Aliberti, Song Hong, Alan Sher, Charles Serhan
Journal: The Journal of Experimental Medicine (2004)

Lipoxin A4 (LXA4) is a potent endogenous lipoxygenase-derived eicosanoid with antiinflammatory and proresolving properties. Supraphysiological levels of LXA4 are generated during infection by Toxoplasma gondii, which in turn reduces interleukin (IL) 12 production by dendritic cells, thus dampening Th1-type cell-mediated immune responses and host immunopathology. In the present work, we sought evidence for the structural basis of T. gondii's ability to activate LXA4 biosynthesis. Proteomic analysis of T. gondii extract (soluble tachyzoite antigen [STAg]), which preserves the immunosuppressive and antiinflammatory activity of the parasite, yielded several peptide matches to known plant lipoxygenases. Hence, we incubated STAg itself with arachidonic acid and found using LC-UV-MS-MS-based lipidomics that STAg produced both 15-HETE and 5,15-diHETE, indicating that T. gondii carries 15-lipoxygenase activity. In addition, T. gondii tachyzoites (the rapidly multiplying and invasive stage of the parasite) generated LXA4 when provided with arachidonic acid. Local administration of a plant (soybean) lipoxygenase itself reduced neutrophilic infiltration in murine peritonitis, demonstrating that 15-lipoxygenase possesses antiinflammatory properties. Administration of plant 15-lipoxygenase generated endogenous LXA4 and mimicked the suppression of IL-12 production by splenic dendritic cells observed after T. gondii infection or STAg administration. Together, these results indicate that 15-lipoxygenase expressed by a pathogen as well as exogenously administered 15-lipoxygenase can interact with host biosynthetic circuits for endogenous "stop signals" that divert the host immune response and limit acute inflammation.
Continuity and change in sporting and leisure time physical activities during adolescence.
Authors: S M Dovey, A I Reeder, D J Chalmers
Journal: British Journal of Sports Medicine (1998)

OBJECTIVES: To map the pattern of involvement in physical activities by adolescents at ages 15 and 18 years. METHODS: Data from a longitudinal cohort study were used. Participants in the Dunedin Multidisciplinary Health and Development Study provided information about their sporting and similar physical activities during the 12 months before study assessments at ages 15 and 18 years. RESULTS: Total participation time at age 18 was 63% of that reported at age 15. Mean participation time for girls decreased from 7.5 hours a week to 4.3 hours a week (p&lt;0.001) whereas for boys it decreased from 11.7 hours a week to 7.8 hours a week (p&lt;0.001). At both ages, boys spent significantly more time in physical activity than girls. More time in physical activity at age 18 was reported by participants who judged their fitness higher than their peers (odds ratio (OR) 1.7: 1.2, 2.5), those who played sport for their school (OR 1.8: 1.3, 2.4), and those reporting very good self assessed health (OR 1.4: 1.0, 1.8) at age 15. The overall median number of activities decreased from seven at age 15 to three at 18. Boys were involved in more activities at age 15 but there was no sex difference at age 18 in the number of different activities reported. CONCLUSION: Although involvement in school sporting activities and high levels of fitness in mid-adolescence may protect against marked reductions in physical activity in late adolescence, social and organisational factors are also likely to be important. There is a need for innovative approaches to health promotion which will encourage adolescents to maintain higher levels of physical activity after they leave school.
Prevalence and factors associated with hidradenitis suppurativa: Results from two case-control studies
Authors: Jean E. Revuz, Florence Canoui-Poitrine, Pierre Wolkenstein, Cedric Viallette, Germaine Gabison, Florence Pouget, Florence Poli, Ousmane Faye, Jean Claude Roujeau, Genevieve Bonnelye, Jean Jacques Grob, Sylvie Bastuji-Garin
Journal: Journal of the American Academy of Dermatology (2008)
Effect of Soymilk Consumption on Serum Estrogen Concentrations in Premenopausal Japanese Women
Authors: C. Nagata, N. Takatsuka, S. Inaba, N. Kawakami, H. Shimizu
Journal: JNCI Journal of the National Cancer Institute (1998)

Estrogens have been implicated in the development of breast cancer. Preliminary evidence suggests that consumption of soy products, which contain isoflavones (phytoestrogens), can reduce serum estrogen levels. Our purpose was to determine the effect of soy consumption on serum estrogen levels in premenopausal women by use of a dietary intervention approach.Premenopausal Japanese women were randomly assigned to receive either a soymilk-supplemented diet (n = 31) or a normal (control) diet (n = 29). The women in the soymilk-supplemented group were asked to consume about 400 mL of soymilk (containing about 109 mg of isoflavones) daily during a study period that involved three consecutive menstrual cycles. Follicular-phase blood samples were to be obtained in the menstrual cycles preceding (cycle 1) and following (cycle 3) the 2-month dietary intervention. All statistical tests were two-sided.At the end of the study period, estrone and estradiol levels were decreased by 23% and 27%, respectively, in the soymilk-supplemented group and were increased by 0.6% and 4%, respectively, in the control group. The changes for each hormone between the two groups were not statistically significantly different. In the soymilk-supplemented group, menstrual cycle length was increased by nearly 2 days, and, in the control group, it was decreased by approximately 1 day, a difference that was not statistically significant. A subgroup analysis restricted to subjects who provided follicular-phase blood samples on the same day or 1 day apart in menstrual cycles 1 and 3 showed a reduction in serum estrone levels in the soymilk-supplemented group that was of borderline statistical significance (P = .07 for change in serum estrone level in soymilk-supplemented group versus control group).Much larger studies will be required to confirm the ability of soy products to reduce serum estrogen levels.
Cocal-pseudotyped Lentiviral Vectors Resist Inactivation by Human Serum and Efficiently Transduce Primate Hematopoietic Repopulating Cells
Authors: Grant D Trobridge, Robert A Wu, Michael Hansen, Christina Ironside, Korashon L Watts, Philip Olsen, Brian C Beard, Hans-Peter Kiem
Journal: Molecular Therapy (2009)

Lentiviral vectors are established as efficient and convenient vehicles for gene transfer. They are almost always pseudotyped with the envelope glycoprotein of vesicular stomatitis virus (VSV-G) due to the high titers that can be achieved, their stability, and broad tropism. We generated a novel cocal vesiculovirus envelope glycoprotein plasmid and compared the properties of lentiviral vectors pseudotyped with cocal, VSV-G, and a modified feline endogenous retrovirus envelope glycoprotein (RD114/TR). Cocal-pseudotyped lentiviral vectors can be produced at titers as high as with VSV-G, have a broad tropism, and are stable, allowing for efficient concentration by centrifugation. Additionally, cocal vectors are more resistant to inactivation by human serum than VSV-G-pseudotyped vectors, and efficiently transduce human CD34+ nonobese diabetic/severe combined immunodeficient (NOD/SCID) mouse–repopulating cells (SRCs), and long-term primate hematopoietic repopulating cells. These studies establish the potential of cocal-pseudotyped lentiviral vectors for a variety of scientific and therapeutic gene transfer applications, including in vivo gene delivery and hematopoietic stem cell (HSC) gene therapy. Lentiviral vectors are established as efficient and convenient vehicles for gene transfer. They are almost always pseudotyped with the envelope glycoprotein of vesicular stomatitis virus (VSV-G) due to the high titers that can be achieved, their stability, and broad tropism. We generated a novel cocal vesiculovirus envelope glycoprotein plasmid and compared the properties of lentiviral vectors pseudotyped with cocal, VSV-G, and a modified feline endogenous retrovirus envelope glycoprotein (RD114/TR). Cocal-pseudotyped lentiviral vectors can be produced at titers as high as with VSV-G, have a broad tropism, and are stable, allowing for efficient concentration by centrifugation. Additionally, cocal vectors are more resistant to inactivation by human serum than VSV-G-pseudotyped vectors, and efficiently transduce human CD34+ nonobese diabetic/severe combined immunodeficient (NOD/SCID) mouse–repopulating cells (SRCs), and long-term primate hematopoietic repopulating cells. These studies establish the potential of cocal-pseudotyped lentiviral vectors for a variety of scientific and therapeutic gene transfer applications, including in vivo gene delivery and hematopoietic stem cell (HSC) gene therapy.
Intravenous Ancrod for Treatment of Acute Ischemic Stroke
Authors: David G. Sherman, Richard P. Atkinson, Thomas Chippendale, Kenneth A. Levin, Ken Ng, Nancy Futrell, Chung Y. Hsu, David E. Levy, None for the STAT Participants
Journal: JAMA (2000)

Approved treatment options for acute ischemic stroke in the United States and Canada are limited at present to intravenous tissue-type plasminogen activator, but bleeding complications, including intracranial hemorrhage, are a recognized complication.To evaluate the efficacy and safety of the defibrinogenating agent ancrod in patients with acute ischemic stroke.The Stroke Treatment with Ancrod Trial (STAT), a randomized, parallel-group, double-blind, placebo-controlled trial conducted between August 1993 and January 1998.Forty-eight centers, primarily community hospitals, in the United States and Canada.A total of 500 patients with an acute or progressing ischemic neurological deficit were enrolled and included in the intent-to-treat analysis.Patients were randomly assigned to receive ancrod (n=248) or placebo (n =252) as a continuous 72-hour intravenous infusion beginning within 3 hours of stroke onset, followed by infusions lasting approximately 1 hour at 96 and 120 hours. The ancrod regimen was designed to decrease plasma fibrinogen levels to 1.18 to 2.03 micromol/L.The primary efficacy end point was functional status, with favorable functional status defined as survival to day 90 with a Barthel Index of 95 or more or at least the prestroke value, compared by treatment group. Primary safety variables included symptomatic intracranial hemorrhage and mortality.Favorable functional status was achieved by more patients in the ancrod group (42.2%) than in the placebo group (34.4%; P=.04) by the prespecified covariate-adjusted analysis. Mortality was not different between treatment groups (at 90 days, 25.4% for the ancrod group and 23% for the placebo group; P=.62), and the proportion of severely disabled patients was less in the ancrod group than in the placebo group (11.8% vs 19.8%; P=.01). The favorable functional status observed with ancrod vs placebo was consistent in all subgroups defined for age, stroke severity, sex, prestroke disability, and time to treatment (< or = 3 or > 3 hours after stroke onset). There was a trend toward more symptomatic intracranial hemorrhages in the ancrod group vs placebo (5.2% vs 2.0%; P=.06), as well as a significant increase in asymptomatic intracranial hemorrhages (19.0% vs 10.7%; P=.01).In this study, ancrod had a favorable benefit-risk profile for patients with acute ischemic stroke.
Increased DC trafficking to lymph nodes and contact hypersensitivity in junctional adhesion molecule-A–deficient mice
Authors: Maria Rosaria Cera, Annalisa Del Prete, Annunciata Vecchi, Monica Corada, Ines Martin-Padura, Toshiyuki Motoike, Paolo Tonetti, Gianfranco Bazzoni, William Vermi, Francesca Gentili, Sergio Bernasconi, Thomas N. Sato, Alberto Mantovani, Elisabetta Dejana
Journal: Journal of Clinical Investigation (2004)

Junctional adhesion molecule-A (JAM-A) is a transmembrane adhesive protein expressed at endothelial junctions and in leukocytes. In the present work, we found that DCs also express JAM-A. To evaluate the biological relevance of this observation, Jam-A(-/-) mice were generated and the functional behavior of DCs in vitro and in vivo was studied. In vitro, Jam-A(-/-) DCs showed a selective increase in random motility and in the capacity to transmigrate across lymphatic endothelial cells. In vivo, Jam-A(-/-) mice showed enhanced DC migration to lymph nodes, which was not observed in mice with endothelium-restricted deficiency of the protein. Furthermore, increased DC migration to lymph nodes was associated with enhanced contact hypersensitivity (CHS). Adoptive transfer experiments showed that JAM-A-deficient DCs elicited increased CHS in Jam-A(+/+) mice, further supporting the concept of a DC-specific effect. Thus, we identified here a novel, non-redundant role of JAM-A in controlling DC motility, trafficking to lymph nodes, and activation of specific immunity.
The worldwide incidence and prevalence of primary brain tumors: a systematic review and meta-analysis
Authors: Paula de Robles, Kirsten M. Fiest, Alexandra D. Frolkis, Tamara Pringsheim, Callie Atta, Christine St. Germaine-Smith, Lundy Day, Darren Lam, Nathalie Jette
Journal: Neuro-Oncology (2014)

Primary brain tumors are a heterogeneous group of benign and malignant tumors arising from the brain parenchyma and its surrounding structures. The epidemiology of these tumors is poorly understood. The aim of our study is to systematically review the latest literature on the incidence and prevalence of primary brain tumors. The systematic review and meta-analysis were conducted according to a predetermined protocol and established guidelines. Only studies reporting on data from 1985 onward were included. Articles were included if they met the following criteria: (i) original research, (ii) population based, (iii) reported an incidence or prevalence estimate of primary brain tumors. From the 53 eligible studies overall, 38 were included in the meta-analysis. A random-effects model found the overall incidence rate of all brain tumors to be 10.82 (95% CI: 8.63–13.56) per 100 000 person-years. The incidence proportion estimates were heterogeneous, even among the same tumor subtypes, and ranged from 0.051 per 100 000 (germ cell tumors) to 25.48 per 100 000 (all brain tumors). There were insufficient data to conduct a meta-analysis of the prevalence of primary brain tumors. There is a need for more accurate and comparable incidence and prevalence estimates of primary brain tumors across the world. A standardized approach to the study of the epidemiology of these tumors is needed to better understand the burden of brain tumors and the possible geographical variations in their incidence.