tbuckley/cabot-search huggingface dataset:
Desamidation of Glutamine and Asparagine in Normal and Neoplastic Hepatic Tissues
Authors: Maurice Errera, Jesse P. Greenstein
Journal: JNCI Journal of the National Cancer Institute (1947)

Journal Article Desamidation of Glutamine and Asparagine in Normal and Neoplastic Hepatic Tissues Get access Maurice Errera, Maurice Errera research fellow National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar Jesse P. Greenstein Jesse P. Greenstein principal biochemist National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 7, Issue 4, February 1947, Pages 285–288, https://doi.org/10.1093/jnci/7.4.285 Published: 01 February 1947 Article history Received: 20 January 1947 Published: 01 February 1947
Age and the dexamethasone suppression test in depression
Authors: K L Davis, B M Davis, A A Mathé, R C Mohs, A B Rothpearl, M I Levy, L K Gorman, P Berger
Journal: American Journal of Psychiatry (1984)

The authors examined the effects of age on plasma cortisol concentrations of 81 depressed men after dexamethasone administration. Dexamethasone nonsuppression was significantly more frequent in patients older than age 55 than those younger. Similarly, older patients had significantly higher postdexamethasone cortisol concentrations than younger patients at all time points sampled. These differences could not be attributed to severity or to the prevalence of psychosis in older and younger depressed patients.
PWE-056 Five year prospective study of the use of tacrolimus in patients with refractory subacute ulcerative colitis: final report
Authors: L Macken, A Dhillon, A Harris
Journal: Gut (2015)

<h3>Introduction</h3> The management of moderately active ulcerative colitis (UC) refractory to standard medical treatment remains a challenge. NICE<sup>2</sup>recommends tacrolimus as one of the treatment options in refractory disease. Previously we reported our experience of tacrolimus in the first 17 patients, 7 of whom remained well. Here we provide our latest results. <h3>Method</h3> Prospective data was collected from January 2010–January 2015 on all patients with UC who were refractory to, or intolerant of, standard therapy and were started on oral tacrolimus (Prograf). Initial dosing was 0.1 mg/kg/day in 2 divided doses; monitoring was undertaken following a local policy with blood testing and tacrolimus trough levels at week 2, 4 and at 3 monthly intervals thereafter. A target trough level between 5–20 ng/ml was maintained, with dosing adjusted accordingly. Clinical response was assessed by one consultant gastroenterologist (AWH) in clinic. <h3>Results</h3> A total of 34 patients were treated with oral tacrolimus over the 5 year period. Of these, 17 (50%) demonstrated a clinical response, however only 10 (29%) of these tolerated the drug. Of the 10 patients who continued on tacrolimus the median duration of treatment was 7 months (range 2–60 months). Reasons for intolerance included renal impairment (n = 4), hypertension (n = 2), nausea and headache, which resulted in cessation of treatment. Therefore at the end of the 5 year period only 10 of 34 (29%) patients continued on treatment with tacrolimus. Of the 24 who were either non-responders or intolerant, 15 (63%) underwent colectomy and 9 received treatment with methotrexate, a biological agent or alicaforsen. <h3>Conclusion</h3> This 5 year prospective audit using tacrolimus in patients with refractory UC in a general hospital outpatient setting has shown that with careful monitoring the drug may be used safely with a clinical response in about a third of patients for up to 60 months. Our findings are similar to those from tertiary centres where clinical remissions of 44%<sup>4</sup>and 20%<sup>5</sup>were reported. No long term adverse events to date have been reported in this group however close monitoring is essential. <h3>Disclosure of interest</h3> None Declared. <h3>References</h3> Dhillon AS, Harris AW. Gut. 2014;<b>63</b>(Suppl 1):A63 NICE. 2013 UC:CG166 Ogata H, <i>et al</i>. <i>Gut</i>. 2006;55(9):1255-62 Landy J, <i>et al</i>. <i>JCC</i>. 2013;(7):e516-e521 Lena W, <i>et al</i>. IBD. 2013;19:1490–1498
Germline<i>CDKN2A</i>Mutation Status and Survival in Familial Melanoma Cases
Authors: Hildur Helgadottir, Veronica Höiom, Rainer Tuominen, Kari Nielsen, Göran Jönsson, Håkan Olsson, Johan Hansson
Journal: JNCI Journal of the National Cancer Institute (2016)

Germline mutations in CDKN2A have been associated with increased risk of melanoma and tobacco-related cancers in respiratory and upper digestive tissues. In CDKN2A wild-type (wt) melanoma families, other known high-risk, melanoma-predisposing mutations are rare, and no increased risk has been observed for nonskin cancers in this group. This study is the first to compare survival in germline CDKN2A mutated (mut) and nonmutated melanoma cases.Melanoma-prone families participating in this study were identified through a nationwide predictive program starting in 1987. Information on cancer diagnoses (types, stages, and dates) and deaths (causes and dates) were obtained through the Swedish Cancer Registry and Cause of Death Registry. Kaplan Meier and Cox proportional hazards regression models were used to assess survival in CDKN2A(mut) (n = 96) and CDKN2A(wt) (n = 377) familial melanoma cases and in matched sporadic melanoma cases (n = 1042). All statistical tests were two-sided.When comparing CDKN2A(mut) and CDKN2A(wt) melanoma cases, after adjusting for age, sex, and T classification, CDKN2A(mut) had worse survival than melanoma (hazard ratio [HR] = 2.50, 95% confidence interval [CI] = 1.49 to 4.21) and than nonmelanoma cancers (HR = 7.77, 95% CI = 3.65 to 16.51). Compared with matched sporadic cases, CDKN2A(mut) cases had statistically significantly worse survival from both melanoma and nonmelanoma cancers while no differences in survival were seen in CDKN2A(wt) compared with sporadic cases.CDKN2A(mut) cases had statistically significantly worse survival than nonmelanoma cancers and, intriguingly, also from melanoma, compared with melanoma cases with no CDKN2A mutations. Further studies are required to elucidate possible mechanisms behind increased carcinogen susceptibility and the more aggressive melanoma phenotype in CDKN2A mutation carriers.
Anxiety and depressive disorders in attention deficit disorder with hyperactivity: new findings
Authors: P S Jensen, R E Shervette, S N Xenakis, J Richters
Journal: American Journal of Psychiatry (1993)

The authors examined the discriminant validity of the diagnosis of attention deficit disorder with hyperactivity.They used standardized rating scales of life stresses and child and family functioning to assess psychosocial and family risk factors in 47 children who had the diagnosis of attention deficit disorder with hyperactivity, a matched group of 47 children in the community, and a matched group of 47 children seen in a psychiatric clinic.Children who had the diagnosis of attention deficit disorder and children in the psychiatric clinic reported significantly more depression and anxiety than did the children in the community; furthermore, children diagnosed as having attention deficit disorder with hyperactivity had more externalizing symptoms than did children in the psychiatric clinic. Children diagnosed as having attention deficit disorder with hyperactivity plus a comorbid anxiety or depressive disorder had higher levels of coexisting life stresses and parental symptoms than did children who had the single diagnosis of attention deficit disorder with hyperactivity.These results underscore the need for future studies to carefully assess children diagnosed as having attention deficit disorder with hyperactivity for concurrent psychiatric disorders as well as family and psychosocial stressors that may contribute to childhood symptoms. Such information is essential because different subtypes of attention deficit disorder with comorbid disorders may arise from different etiologic pathways, may require varying treatment options, and may foreshadow different eventual outcomes.
Quality-of-care standards and professional norms
Authors: H C Schulberg
Journal: American Journal of Psychiatry (1976)

Incursions upon professional prerogatives are increasing with the advent of new requirements for accoutability; this has stemmed in part from the government's enlarged role in paying for mental health services. The author discusses the effect of professional norms on the assessment of quality of care, including the concepts of risk and autonomy, observability and privacy, the perspective of time, and the appropriateness of the penalty. He offers some suggestions for the design and implementation of quality-of-care standards that he believes will benefit both professionals and administrators, as well as protect the patient.
RISK STRATIFICATION SCORING PREDICTS STROKE IN DIALYSIS PATIENTS WITH ATRIAL FIBRILLATION
Authors: Jose Cuellar-Silva, Jennifer Waller, Avirup Guha, Matthew Diamond, Robert Sorrentino, Michele Murphy, Sheldon Litwin, Stan Nahman, Mufaddal Kheda, William Maddox
Journal: Journal of the American College of Cardiology (2014)
Real-time measurement of luminal compliance during transoral incisionless fundoplication
Authors: Sheba Vohra, Vincent Kuo, Bahar Madani, Reem Sharaiha, Michel Kahaleh, Paul Tarnasky, Prashant Kedia
Journal: Endoscopy (2015)

A 71-year-old woman who had a family history of esophageal cancer presented with symptoms of chronic heartburn. The patient expressed interest in definitive treatment, declining long-term medical therapy and opting to undergo transoral incisionless fundoplication (TIF) ([Fig. 1]). This was accomplished by using the EsophyX Device (EndoGastric Solutions, San Mateo, California, USA). Before and after the TIF procedure, an EndoFLIP Endolumenal Functional Lumen Imaging Probe (Crospon, Carlsbad, California, USA) was used to measure the luminal compliance and high pressure zone of the gastroesophageal junction. EndoFLIP utilizes impedance planimetry technology to measure the geometry and physical properties of hollow lumina. The patient was observed for 24 hours after the procedure and was discharged in a stable condition.
Differentiation of Early Pregnancy from Functional Amenorrhea
Authors: F W BONE, E B MENDEL, S HABERMAN
Journal: JAMA (1963)

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Tumor Resistance to Therapy: A Genetic or Kinetic Problem?
Authors: R E Durand, S L Vanderbyl
Journal: Cancer Communications (1989)

Chinese hamster V79 spheroids exposed to cisplatin for 2 hr daily for 3 weeks responded very similarly to tumors undergoing chemotherapy. Initially, the number of viable cells per spheroid decreased in a dose-dependent fashion but, after several treatments, the apparent effectiveness of the cisplatin decreased. At low doses, spheroid regrowth eventually occurred despite continued therapy. A detailed examination of the cellular basis for this response showed that the so-called acquired resistance was not due to a change in cellular responsiveness to cisplatin but, rather, was the result of a marked increase in the cellular growth fraction in the treated spheroids.
Growth hormone response to edrophonium in patients with Alzheimer's disease and normal control subjects
Authors: M Davidson, B M Davis, L Bastiaens, J Macaluso, M Aryan, T Ryan, K L Davis
Journal: American Journal of Psychiatry (1988)

The authors found that growth hormone (GH) response to edrophonium was no different in 12 Alzheimer's disease patients than in eight healthy elderly subjects. Previously reported differences could be due to differences in gender or baseline GH concentrations between patients and control subjects.
SAT0535 Usefulness of FDG-PET Imaging and Serological Biomarkers in Lymphadenopathy of IgG4-Related Disease
Authors: H. Ozaki, R. Wakiya, H. Shimada, S. Nakashima, Y. Takeuchi, M. Izumikawa, T. Kameda, H. Dobashi
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Background</h3> IgG4-related disease (IgG4-RD) is not rare and clinically important disease. It is very difficult to confirm the diagnosis because IgG4 positive lymphocyte infiltrates various organs such as pancreas, salivary glands, retroperitoneum, and kidney. Especially, lymphadenopathy is a common symptom in IgG4-RD patients. In addition, some cases have only lymphadenopathy in IgG4-RD. On the other hand, we presented that FDG-PET/CT was useful to improve a diagnosis rate in our facility. However, it is difficult for the rheumatologist to distinguish lymphadenopathy from other benign disorders such as viral infection and sarcoidosis using FDG-PET/CT only. <h3>Objectives</h3> We examine the tool to distinguish for the case of lymphadenopathy suspected IgG4-RD. <h3>Methods</h3> We enrolled 26 cases with suspected IgG4-RD in our facility between Jan. 2008 and Dec. 2014. Furthermore, we classified these 26 cases into IgG4-RD (IgG4- RD group) and other benign disorders (non IgG4-RD group). The diagnosis for IgG4-RD was based on comprehensive diagnostic criteria for IgG4-RD. We investigated the serum IgG4 levels, sIL2-R levels and maximum standardized uptake value (SUVmax) of abnormal lymph node accumulation by FDG-PET/CT. We retrospectively examined the relations of these three values. <h3>Results</h3> Lymphadenopathy were detected in 19 of 26 cases (IgG4-RD definite: 8, IgG4-RD possible: 5, IgG4-RD probable: 1, infectious disease: 2, SLE: 1, EGPA: 1, Castleman disease: 1). In IgG4-RD group, serum IgG4 level elevated and serum sIL-2R levels decreased in comparison with non IgG4-RD group respectively. There is no difference between two groups in SUVmax. <h3>Conclusions</h3> In our study, we examined the differentiation of lymphadenopathy. We proved that it was difficult to distinguish IgG4-RD from other benign disorders for lymphadenopathy only by FDG-PET/CT. We suggested that combination of serum IgG4 and sIL-2R levels is useful for diagnosis of IgG4-RD with lymphadenopathy. <h3>References</h3> Umehara H, Okazaki K, Masaki Y, et al. Comprehensive diagnostic criteria for IgG4-related disease (IgG4-RD), 2011. Mod Rheumatol. 2012 Feb;22(1):21-30. Nakatani K. Utility of FDG PET/CT in IgG4-related systemic disease Clin Radiol. 2012 Apr;67(4):297-305. <h3>Disclosure of Interest</h3> None declared
Reply
Authors: Matthias Hardtke-Wolenski, Michel P. Manns, Elmar Jäckel
Journal: Hepatology (2013)

We appreciate the comments by by Lapierre et al. on our article on experimental murine autoimmune hepatitis (emAIH),1 because the group is known for their expertise on autoimmune hepatitis (AIH). The major advantage of our model is the genetic background predisposing to (1) a more rapid development of AIH and (2) a disease phenotype closely resembling the human disease. As discussed in the article, nonobese diabetic (NOD) mice share genetic predispositions also relevant in human AIH (e.g., major histocompatibility complex and cytotoxic T-lymphocyte antigen 4), whereas such associations are not known for C57Bl/6 and FVB/N mice. However, even after follow-up for 30 weeks, we did not see signs of AIH in the latter two strains. Our model offers the additional advantage that mechanisms leading to a break of tolerance and therapeutic interventions could be studied. Besides this, the more severe course of the disease enabled us to study disease end-points such as fibrosis. Fibrosis was verified by a pathologist in a blinded way with a standard staining used in clinical routine. Others' models did not see any fibrosis2, 3 or unphysiological subcapsular fibrosis just after intraperitoneal virus injection.4 Other researchers have also described the need for strong “danger signals” to break tolerance against liver antigens3-5; however, we could show that the mere overexpression of the autoantigen is not sufficient to cause AIH. This is well in line with the experience of Lapierre et al. employing a repeated prime boost protocol with DNA vaccination with a plasmid encoding for a secreted chimeric antigen of cytochrome P4502D6 (CYP2D6) and formiminotransferase cyclodeaminase (FTCD), with the addition interleukin (IL)-122 or expression with an adenovirus.3 Of note, we have also tested intramuscular DNA injection with cytomegalovirus-promoter-driven FTCD and IL-12, but did not see meaningful AIH within 6 months in NOD mice (see Fig. 1). The important publication by Bowen et al.6 did not use danger signals, but rather induced a self-limited hepatitis, followed by immune tolerance, thereby, rather supporting our statement. Regarding the nature of the inducing autoantigen, we could show that similar antigens can induce AIH as well as identical antigens. However, we did not try CYP2D6 as an orthologous autoantigen. The amount of virus could be excluded as a variable, because we tried 1 × 109 to 1 × 1010 plaque-forming units of our adenovirus, as reported by Holdener et al.4 As recently discussed,7 we think that all the mentioned models are important and can be used to explain various aspects of AIH and hepatic immune tolerance. Matthias Hardtke-Wolenski, Ph.D. Michel P. Manns, M.D. Elmar Jäckel, M.D. Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Hannover, Germany
Structural Determinants of Sleeping Beauty Transposase Activity
Authors: György Abrusán, Stephen R Yant, András Szilágyi, Joseph A Marsh, Lajos Mátés, Zsuzsanna Izsvák, Orsolya Barabás, Zoltán Ivics
Journal: Molecular Therapy (2016)

Transposases are important tools in genome engineering, and there is considerable interest in engineering more efficient ones. Here, we seek to understand the factors determining their activity using the Sleeping Beauty transposase. Recent work suggests that protein coevolutionary information can be used to classify groups of physically connected, coevolving residues into elements called "sectors", which have proven useful for understanding the folding, allosteric interactions, and enzymatic activity of proteins. Using extensive mutagenesis data, protein modeling and analysis of folding energies, we show that (i) The Sleeping Beauty transposase contains two sectors, which span across conserved domains, and are enriched in DNA-binding residues, indicating that the DNA binding and endonuclease functions of the transposase coevolve; (ii) Sector residues are highly sensitive to mutations, and most mutations of these residues strongly reduce transposition rate; (iii) Mutations with a strong effect on free energy of folding in the DDE domain of the transposase significantly reduce transposition rate. (iv) Mutations that influence DNA and protein-protein interactions generally reduce transposition rate, although most hyperactive mutants are also located on the protein surface, including residues with protein-protein interactions. This suggests that hyperactivity results from the modification of protein interactions, rather than the stabilization of protein fold.
FRI0459 Association of Anti-PM/SCL Antibody with Risk of Malignancy in Scleroderma: Table 1.
Authors: C. Bruni, A. Lages, H. Patel, J. Harvey, V. Ong, M. Matucci Cerinic, E. Derrett-Smith, C.P. Denton
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Background</h3> Anti-PM/Scl antibodies are heterogeneous autoantibodies in scleroderma (SSc) directed mainly against 75 kDa and 100 kDa human exosome components, associated with overlap syndromes. Published data suggest that up to 12.5% of SSc patients carry this seropositivity with associations with myositis, mild skin involvement, pulmonary fibrosis, articular involvement and calcinosis and a lower prevalence of pulmonary arterial hypertension and gastrointestinal involvement. <h3>Objectives</h3> To characterise the clinical and detailed serological phenotype of anti-PM/Scl positive SSc patients from a single centre cohort of 2200 patients and to identify a cohort within this group with increased risk of malignancy. <h3>Methods</h3> Anti-PM/Scl positive SSc patients identified by indirect immunofluorescence pattern and confirmed on counter-immunoelectrophoresis were enrolled in the study. Sera were analyzed with line immunoassay to detect antibodies to PM/Scl 75 and PM/Scl 100. Demographics and clinical data on skin, internal organ involvement and history of malignancy were recorded. <h3>Results</h3> 70 anti-PmScl positive patients were identified (3.1% of cohort), with frequent lung (57.1%), gastrointestinal (62.9%) and muscle involvement (61.4%) as described previously (table 1). 48 patients (68.6%) had antibodies targeting both PM/Scl 75 and 100; 6 (8.6%) PM/Scl 75 only and 16 (22.8%) PM/Scl 100 antibody only. There was a significant association between positivity for anti-PM/Scl 100 alone and malignancy (<i>p</i>=0.037) when compared to presence of both reactivities or reactivity to PM/Scl75 alone. 13 patients (18.6%) had developed a malignancy, 4 (30.7%) of these had onset within 36 months from SSc diagnosis and all were positive for anti-PM/Scl 100, combined with anti-PM/Scl75 in 7/13 (53.8%). The study population standardized incidence ratio (SIR) for cancer was 2.14 (CI 95%: 1.55-2.74), with higher values showed for male gender (SIR 3.10, CI 95%: 1.55-4.65) than female gender (SIR 1.95, CI 95%: 1.31-2.61). 7/13 were adenocarcinoma, mainly breast, 4/13 squamous cell and the remainder haematological malignancy. <h3>Conclusions</h3> The association of malignancy with PM/Scl reactivity in SSc is of interest in the context of recent studies describing a potential pathogenic role of anti-RNA polymerase III antibodies with malignant disease in SSc. This cohort is otherwise representative of others in terms of demographics and clinical characteristics and underlines the importance of close surveillance for concurrent malignancy in all SSc disease subphenotypes. <h3>Disclosure of Interest</h3> None declared
Selection bias in clinical trials.
Authors: S K Carter
Journal: Journal of Clinical Oncology (1986)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1986.4.1.113 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 3941329 Selection bias in clinical trials. S K CarterxS K CarterSearch for articles by this author https://doi.org/10.1200/JCO.1986.4.1.113 PDF "Selection bias in clinical trials.." Journal of Clinical Oncology, 4(1), pp. 113–114© 1986 by American Society of Clinical Oncology