tbuckley/cabot-search huggingface dataset:
Irrational Beliefs and Psychological Distress: A Meta-Analysis
Authors: Andreea Vîslă, Christoph Flückiger, Martin grosse Holtforth, Daniel David
Journal: Psychotherapy and Psychosomatics (2015)

&lt;b&gt;&lt;i&gt;Background:&lt;/i&gt;&lt;/b&gt; Since the cognitive revolution of the early 1950s, cognitions have been discussed as central components in the understanding and treatment of mental illnesses. Even though there is an extensive literature on the association between therapy-related cognitions such as irrational beliefs and psychological distress over the past 60 years, there is little meta-analytical knowledge about the nature of this association. &lt;b&gt;&lt;i&gt;Methods:&lt;/i&gt;&lt;/b&gt; The relationship between irrational beliefs and distress was examined based on a systematic review that included 100 independent samples, gathered in 83 primary studies, using a random-effect model. The overall effects as well as potential moderators were examined: (a) distress measure, (b) irrational belief measure, (c) irrational belief type, (d) method of assessment of distress, (e) nature of irrational beliefs, (f) time lag between irrational beliefs and distress assessment, (g) nature of stressful events, (h) sample characteristics (i.e. age, gender, income, and educational, marital, occupational and clinical status), (i) developer/validator status of the author(s), and (k) publication year and country. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; Overall, irrational beliefs were positively associated with various types of distress, such as general distress, anxiety, depression, anger, and guilt (omnibus: r = 0.38). The following variables were significant moderators of the relationship between the intensity of irrational beliefs and the level of distress: irrational belief measure and type, stressful event, age, educational and clinical status, and developer/validator status of the author. &lt;b&gt;&lt;i&gt;Conclusions:&lt;/i&gt;&lt;/b&gt; Irrational beliefs and distress are moderately connected to each other; this relationship remains significant even after controlling for several potential covariates.
Author of retracted BMJ paper is ordered to pay $C1.6m to Canadian broadcaster
Authors: C. White
Journal: BMJ (2015)

Ranjit Kumar Chandra, the doctor accused of fraud and financial deception by the Canadian Broadcasting Corporation (CBC), has been ordered to pay the broadcaster just over $C1.6m (£0.8m; €1.1m; $US1.2m) in costs after losing the court case he brought against it this summer.1

Chandra, who has been awarded a slew of prestigious honours, including the Order of Canada, sued CBC for $C137m for defamation and invasion of privacy after it …
Membrane-anchored Serine Protease Matriptase Is a Trigger of Pulmonary Fibrogenesis
Authors: Olivier Bardou, Awen Menou, Charlène François, Jan Willem Duitman, Jan H. von der Thüsen, Raphaël Borie, Katiuchia Uzzun Sales, Kathrin Mutze, Yves Castier, Edouard Sage, Ligong Liu, Thomas H. Bugge, David P. Fairlie, Mélanie Königshoff, Bruno Crestani, Keren S. Borensztajn
Journal: American Journal of Respiratory and Critical Care Medicine (2015)

Idiopathic pulmonary fibrosis (IPF) is a devastating disease that remains refractory to current therapies.To characterize the expression and activity of the membrane-anchored serine protease matriptase in IPF in humans and unravel its potential role in human and experimental pulmonary fibrogenesis.Matriptase expression was assessed in tissue specimens from patients with IPF versus control subjects using quantitative reverse transcriptase-polymerase chain reaction, immunohistochemistry, and Western blotting, while matriptase activity was monitored by fluorogenic substrate cleavage. Matriptase-induced fibroproliferative responses and the receptor involved were characterized in human primary pulmonary fibroblasts by Western blot, viability, and migration assays. In the murine model of bleomycin-induced pulmonary fibrosis, the consequences of matriptase depletion, either by using the pharmacological inhibitor camostat mesilate (CM), or by genetic down-regulation using matriptase hypomorphic mice, were characterized by quantification of secreted collagen and immunostainings.Matriptase expression and activity were up-regulated in IPF and bleomycin-induced pulmonary fibrosis. In cultured human pulmonary fibroblasts, matriptase expression was significantly induced by transforming growth factor-β. Furthermore, matriptase elicited signaling via protease-activated receptor-2 (PAR-2), and promoted fibroblast activation, proliferation, and migration. In the experimental bleomycin model, matriptase depletion, by the pharmacological inhibitor CM or by genetic down-regulation, diminished lung injury, collagen production, and transforming growth factor-β expression and signaling.These results implicate increased matriptase expression and activity in the pathogenesis of pulmonary fibrosis in human IPF and in an experimental mouse model. Overall, targeting matriptase, or treatment by CM, which is already in clinical use for other diseases, may represent potential therapies for IPF.
High-dose cisplatin and vinblastine infusion with or without radiation therapy in patients with advanced non-small-cell lung cancer.
Authors: M S Blumenreich, T M Woodcock, P S Gentile, G R Barnes, B Jose, E J Sherrill, S P Richman, B E Epremian, T T Kubota, J C Allegra
Journal: Journal of Clinical Oncology (1987)

Non-small-cell lung cancer (NSCLC) patients with locally advanced or metastatic measurable disease were given a combination of cisplatin, 200 mg/m2 divided in five daily doses, and simultaneously, vinblastine, 7.5 mg/m2 as a continuous intravenous (IV) infusion over five days. Five courses of chemotherapy were planned. Afterwards or on progression, patients were randomized to receive maximally tolerated radiation to all sites of disease v observation only. Forty males and seven females were entered. Median age was 60 years (range, 37 to 74), median Karnofsky performance status was 70 (range, 30 to 90). Five patients had previous brain radiation therapy for metastatic disease, all others were previously untreated. Side effects in the 87 courses of chemotherapy administered included leukopenia (WBC less than 1,000/microL following nine courses) and thrombocytopenia (platelets less than 20,000/microL following four courses). Ten patients became septic, nine of them while leukopenic. Elevations of serum creatinine followed eight courses; in all cases the level was less than 3.0 mg/dL. Nausea and vomiting were mild to moderate. Five patients experienced mild hypoacusis and six had sensory polyneuropathy. The deaths of three patients were considered drug-related. The response rate was 28%. The median survival for the group was 22 weeks, 63.2 weeks for responders and 17.9 weeks for nonresponders. Twenty-six patients received radiation therapy, 16 randomized to this arm as planned, ten to palliate symptoms. Median survival of all irradiated patients was 24.8 weeks. Seven responders to chemotherapy were randomized to receive radiotherapy; their median survival was 25 weeks. In six responders randomized not to receive radiation, the median survival was 77.8 weeks (P greater than .3). Among nonresponding patients, the median survival of those radiated was 22.2 weeks, while that of nonradiated patients was 11 weeks. This regimen is cumbersome and toxic. It has offered no major survival benefits, or improvement in response rates, therefore, we do not recommend it for the standard treatment of NSCLC.
Envenomation by the spiders Chiracanthium inclusum and Argiope aurantia. Observations on arachnidism in the United States
Authors: J. R. Gorham
Journal: JAMA (1968)

Two cases of arachnidism were caused by<i>Chiracanthium inclusum</i>and<i>Argiope aurantia</i>, both common spiders in the domestic environment. Other spiders capable of producing dermal or systemic reactions may be recognized. The hypersensitivity phenomenon makes any spider bite potentially dangerous. Epidemiologic study of arachnidism and the evaluation of its role as a public health problem are frustrated because most cases are unrecognized or unreported. The study of arachnidism and other forms of envenomation would be facilitated by a national repository of information on spider bites and venomous spiders.
Molecular Pathways: Increased Susceptibility to Infection Is a Complication of mTOR Inhibitor Use in Cancer Therapy
Authors: Adrian M. Eiden, Shuling Zhang, Joy M. Gary, John K. Simmons, Beverly A. Mock
Journal: Clinical Cancer Research (2015)

As one of the earliest examples of "chemical biology," the M: echanistic T: arget of R: apamycin (mTOR) protein and its chemical inhibitors have been extensively studied across a spectrum of physiologic and pathologic processes at the molecular, organismal, and patient population levels. There are several FDA-approved mTOR inhibitors (sirolimus, everolimus, and temsirolimus) with indications for cancer treatment and for prevention of solid organ rejection. Dozens of mTOR inhibitors are currently being evaluated in hundreds of ongoing clinical trials across a spectrum of diseases, including numerous cancer indications, autoimmune diseases, and a number of congenital disorders. As many of the approved and investigational indications for mTOR inhibitors require long-term treatment, the magnitude and incidence of particular side effects differ from those observed in shorter-term treatments. Here, we focus on the increased risk of infections in patients being treated with mTOR inhibitors. While increased infection rates might be expected from a class of drugs approved as posttransplant immunosuppressants, we review reports from clinical, mechanistic, and genetically engineered mouse model studies detailing a much more nuanced view of mTOR inhibitor drug action and target biology.
Maternally Transmitted Antigen of Mice: A Model Transplantation Antigen
Authors: K F Lindahl, E Hermel, B E Loveland, C R Wang
Journal: Annual Review of Immunology (1991)

Molecular identification proved Mta, the maternally transmitted antigen of mice, to be a model minor histocompatibility (H) antigen. It consists of a peptide, MTF, that is presented on the cell surface by an H-2 class-I molecule, HMT. MTF is derived from ND1, a mitochondrially encoded protein, and the amino-terminal N-formyl-methionine is essential for binding to HMT; conservative substitutions at the sixth residue causes MTF to be a minor H antigen. HMT is encoded by the M3 gene at the telomeric end of the H-2 complex. The peptide-binding site of HMT is hydrophobic, and allelic forms of the mature protein differ by only three amino acids. Homologues and analogues of the mouse Mta system have recently been identified in rats.
Associations between Deceased-Donor Urine Injury Biomarkers and Kidney Transplant Outcomes
Authors: Peter P. Reese, Isaac E. Hall, Francis L. Weng, Bernd Schröppel, Mona D. Doshi, Rick D. Hasz, Heather Thiessen-Philbrook, Joseph Ficek, Veena Rao, Patrick Murray, Haiqun Lin, Chirag R. Parikh
Journal: Journal of the American Society of Nephrology (2015)

Assessment of deceased-donor organ quality is integral to transplant allocation practices, but tools to more precisely measure donor kidney injury and better predict outcomes are needed. In this study, we assessed associations between injury biomarkers in deceased-donor urine and the following outcomes: donor AKI (stage 2 or greater), recipient delayed graft function (defined as dialysis in first week post-transplant), and recipient 6-month eGFR. We measured urinary concentrations of microalbumin, neutrophil gelatinase–associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), IL-18, and liver-type fatty acid binding protein (L-FABP) from 1304 deceased donors at organ procurement, among whom 112 (9%) had AKI. Each biomarker strongly associated with AKI in adjusted analyses. Among 2441 kidney transplant recipients, 31% experienced delayed graft function, and mean±SD 6-month eGFR was 55.7±23.5 ml/min per 1.73 m 2 . In analyses adjusted for donor and recipient characteristics, higher donor urinary NGAL concentrations associated with recipient delayed graft function (highest versus lowest NGAL tertile relative risk, 1.21; 95% confidence interval, 1.02 to 1.43). Linear regression analyses of 6-month recipient renal function demonstrated that higher urinary NGAL and L-FABP concentrations associated with slightly lower 6-month eGFR only among recipients without delayed graft function. In summary, donor urine injury biomarkers strongly associate with donor AKI but provide limited value in predicting delayed graft function or early allograft function after transplant.
Abstract 4218: Phenotypic selection screening reveals cancer stem cell therapeutic targets
Authors: Elaine M. Hurt, Matt Flynn, Suneetha Thomas, Lilian van Vlerken-Ysla, Alan Sandercock, Steven Rust, Minter Ralph, Robert Hollingsworth
Journal: Cancer Research (2015)

Abstract Cancer stem cells (CSCs) represent an important subpopulation of tumor cells that are untouched and perhaps even expanded after chemotherapy and radiation. This population has been shown in murine models of cancer to be solely responsible for the regrowth of tumors following chemotherapy, underscoring the importance of therapeutically targeting this population. Therefore, we sought to find novel targets against CSCs using a phenotypic selection screen. Using a designed ankyrin repeat (DARpin) library, we panned cells disaggregated from tumor spheres from three patient-derived xenograft models of late stage pancreatic cancer to enrich for DARPins that bind CSCs. Once released from the cells, the DARPins were further analyzed for binding to both normal, pancreatic cancer total tumor cells and pancreatic CSCs in order to choose targets that showed either pancreatic cancer-specific or pancreatic CSC-specific binding. These DARPins were then tested in a sphere formation assay, an EZH2-based high content imaging screen, and a standard proliferation assay. Those DARPins showing good cancer-specific binding profiles were also tested for internalization and killing using a saporin-conjugated secondary antibody. Using this approach, we identified 30 DARPins of interest for either direct inhibitory antibody approaches or for potential antibody drug conjugate or nanoparticle delivery approaches. Identification of the proteins bound by each of the DARPins was done using either immunopreciptation followed by liquid chromatography tandem-mass spectrometry or through Retrogenix's cell expression microarray technology. Identified targets included known CSC antigens such as integrin alpha6 (CD49f) as well as other potentially novel targets. These results highlight the possibilities of finding therapeutic targets for CSCs and opens up an exciting possibility for novel therapies. Citation Format: Elaine M. Hurt, Matt Flynn, Suneetha Thomas, Lilian van Vlerken-Ysla, Alan Sandercock, Steven Rust, Minter Ralph, Robert Hollingsworth. Phenotypic selection screening reveals cancer stem cell therapeutic targets. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4218. doi:10.1158/1538-7445.AM2015-4218
Stage I to IIB Hodgkin's disease: the combined experience at Stanford University and the Joint Center for Radiation Therapy.
Authors: M J Crnkovich, K Leopold, R T Hoppe, P M Mauch
Journal: Journal of Clinical Oncology (1987)

The treatment records of 180 patients with pathological stage (PS) IB to IIB Hodgkin's disease treated at Stanford University Medical Center (SUMC) or the Joint Center for Radiation Therapy (JCRT) were reviewed. Pretreatment characteristics were analyzed to assess their influence on survival and freedom from relapse (FFR). The two most important disease characteristics predictive of relapse were the number and type of B symptoms present and the mediastinal mass ratio (MMR). Patients with both fevers and weight loss had a 7-year survival and FFR of only 57% and 48%, respectively. The poor prognosis in this group was apparent for treatment with either radiation (XRT) alone or combined modality therapy (CMT). Patients with night sweats only had no adverse effect of B symptoms on outcome. Patients with a MMR greater than 1/3 had a 7-year FFR of only 58% after XRT, but 79% after CMT (P = .12). The 7-year survivals for these patients were 85% and 88%, respectively. CMT improved the FFR of the entire group of 180 patients when compared with XRT (7-year FFR 86% and 74%, respectively, P = .02); however, survival in the two treatment groups was similar (88% and 89%). Among patients treated with radiation alone, there was a similar survival and FFR irrespective of whether pelvic irradiation was included in the initial treatment fields.
Unique and redundant functions of NKp46+ ILC3s in models of intestinal inflammation
Authors: Christina Song, Jacob S. Lee, Susan Gilfillan, Michelle L. Robinette, Rodney D. Newberry, Thaddeus S. Stappenbeck, Matthias Mack, Marina Cella, Marco Colonna
Journal: The Journal of Experimental Medicine (2015)

Group 3 ILCs (ILC3s) are innate sources of IL-22 and IL-17 and include lymphoid tissue-inducer (LTi)-like and NKp46(+) subsets. Both depend on RORγt and aryl hydrocarbon receptor, but NKp46(+)ILC3s also require Notch and T-bet for their development and are transcriptionally distinct. The extent to which these subsets have unique functions, especially in the context of T cell- and B cell-sufficient mice, remains largely unclear. To investigate the specific function of NKp46(+)ILC3s among other ILC3 subsets and T cells, we generated mice selectively lacking NKp46(+)ILC3s or all ILC3s and crossed them to T cell-deficient mice, thus maintaining B cells in all mice. In mice lacking T cells, NKp46(+)ILC3s were sufficient to promote inflammatory monocyte accumulation in the anti-CD40 innate colitis model through marked production of GM-CSF. In T cell-competent mice, lack of NKp46(+)ILCs had no impact on control of intestinal C. rodentium infection, whereas lack of all ILC3s partially impaired bacterial control. Thus, NKp46(+)ILC3s have a unique capacity to promote inflammation through GM-CSF-induced accumulation of inflammatory monocytes, but are superseded by LTi-like ILC3s and T cells in controlling intestinal bacterial infection.
Surgically documented response to intraperitoneal cisplatin, cytarabine, and bleomycin after intravenous cisplatin-based chemotherapy in advanced ovarian adenocarcinoma.
Authors: M S Piver, S B Lele, D L Marchetti, T R Baker, L J Emrich, A B Hartman
Journal: Journal of Clinical Oncology (1988)

Thirty-one evaluable patients with stages III and IV invasive ovarian adenocarcinoma were treated on a phase II protocol of second-line intraperitoneal cisplatin, cytarabine, and bleomycin. All 31 patients received first-line intravenous (IV) cisplatin-based chemotherapy; the size of the residual cancer was documented surgically before intraperitoneal chemotherapy in all patients. Response to intraperitoneal chemotherapy was documented by a third-look laparotomy in all patients not evidencing progression of disease clinically. There were eight responses (26%): five surgical complete responses and three surgical partial responses. Responders were patients with stage III ovarian cancer, small residual disease of less than or equal to 1 cm (primarily less than or equal to 5 mm), and patients who previously had responded to cisplatin-based IV chemotherapy. Of the 15 patients with stage III ovarian cancer, residual disease less than or equal to 1 cm, and those who had responded to first-line IV cisplatin-based chemotherapy, 53% (eight) responded to second-line intraperitoneal chemotherapy. Intraperitoneal chemotherapy as used in this phase II protocol would appear to be an effective second-line treatment in advanced ovarian cancer in this specific subset of patients.
Heritability of naevus patterns in an adult twin cohort from the Brisbane Twin Registry: a cross-sectional study
Authors: S. Lee, D.L. Duffy, P. McClenahan, K.J. Lee, E. McEniery, B. Burke, K. Jagirdar, N.G. Martin, R.A. Sturm, H.P. Soyer, H. Schaider
Journal: British Journal of Dermatology (2015)

Heritability of naevi counts is widely acknowledged as a potential surveillance parameter for prevention purposes. The contribution of heritability to the changes seen in naevus number and morphology over time and their corresponding dermoscopic characteristics is unknown, but is important to understand in order to account for adequate prevention measures. To identify naevus characteristics that are strongly influenced by heritability. This cross‐sectional study included 220 individuals [76 monozygotic (MZ), 144 dizygotic (DZ)], recruited from the Brisbane Twin Naevus Study. Participants received full body imaging and dermoscopy of naevi ≥ 5 mm in diameter. Dermoscopic type, total naevus count (TNC), change in TNC with age, and naevus distribution, size, colour and profile were compared between MZ and DZ twins. Heritability of these traits was assessed via Falconer's estimate. Significant differences were found in comparing MZ and DZ twins for TNC, numbers of naevi 5·0–7·9 mm in diameter, counts of light‐brown naevi, naevi on the back and sun‐protected sites, and naevi with the 'nonspecific' dermoscopic pattern. This study strongly supports a heritable component to TNC, as well as changes in TNC, and the number of medium‐sized naevi, light‐brown naevi, specific sites and certain dermoscopic features in adults. These characteristics should be taken into account by naevus surveillance programmes and further studied to identify candidate gene associations for clinical and dermoscopic patterns in conjunction with melanoma risk stratification.
Inhibition of STAT3 using shRNA inhibits Thymidine Kinase (TK) mediated glioma cell death in vitro and abrogates Flt3L and TK dependent tumor regression in vivo.
Authors: James Curtin, Mary Clark, Tamer Fakhouri, Kurt Kroeger, Chunyan Liu, Leda Raptis, Rui Wu, Zuoshang Xu, Pedro Lowenstein, Maria Castro
Journal: Cancer Research (2008)

4991   STAT3 signaling plays important roles in tumor progression and immune mechanisms. It is required for survival and proliferation of tumor cells and also mediates the function of tumor immune cells. Recently, preclinical models have investigated whether STAT3 antagonists can be used in combination with immunotherapy to induce tumor cell death and enhance immune responses against GBM antigens. Owing to the multiple roles of STAT3 in both tumor cells and immune cells, we wished to investigate whether inhibition of STAT3 using adenoviral vectors expressing STAT3 specific shRNA would augment or inhibit T cell dependent tumor regression. We have previously demonstrated that intratumoral delivery of Flt3L and TK using adenoviral vectors drives T cell dependent tumor regression. Here, we demonstrate that expression of STAT3 shRNA from U6 promoter can specifically silence STAT3 expression and activity by more than 95% (p
Diagnosing pelvic osteomyelitis beneath pressure ulcers in spinal cord injured patients: a prospective study
Authors: A.-S. Brunel, B. Lamy, C. Cyteval, H. Perrochia, L. Téot, R. Masson, H. Bertet, A. Bourdon, D. Morquin, J. Reynes, V. Le Moing, Isabelle Alméras, Aurélie Du Thanh, Anthony Gélis, Claire Reynaud, Hélène Rouays, Chloé Trial, Sergio Fliueraru, Christian Herlin, Jean-Philippe Lavigne, Christophe Delfour, Marie-Pierre Baron, Pierre Viala, Thibaut Mura, Philippe Géraud
Journal: Clinical Microbiology and Infection (2015)