tbuckley/cabot-search huggingface dataset:
The society of genes: networks of functional links between genes from comparative genomics
Authors: Itai Yanai, Charles DeLisi
Journal: Genome biology (2002)

Comparative genomics provides at least three methods beyond traditional sequence similarity for identifying functional links between genes: the examination of common phylogenetic distributions, the analysis of conserved proximity along the chromosomes of multiple genomes, and observations of fusions of genes into a multidomain gene in another organism. We have previously generated the links according to each of these methods individually for 43 known microbial genomes. Here we combine these results to construct networks of functional associations. We show that the functional networks obtained by applying these methods have different topologies and that the information they provide is largely additive. In particular, the combined networks of functional links contain an average of 57% of an organism's complete genetic complement, uncover substantial portions of known pathways, and suggest the function of previously unannotated genes. In addition, the combined networks are qualitatively different from the networks obtained using individual methods. They have a dominant cluster that contains approximately 80%-90% of the genes, independent of genome size, and the dominant clusters show the small world behavior expected of a biological system, with global connectivity that is nearly random, and local properties that are highly ordered. When the information on functional linkage provided by three emerging computational methods is combined, the integrated network uncovers large numbers of conserved pathways and identifies clusters of functionally related genes. It therefore shows considerable utility and promise as a tool for understanding genomic structure, and for guiding high throughput experimental investigations.
Brief Report: Involvement of <i>TNFRSF11A</i> Molecular Defects in Autoinflammatory Disorders
Authors: Isabelle Jéru, Emmanuelle Cochet, Philippe Duquesnoy, Véronique Hentgen, Bruno Copin, Maria Teresa Mitjavila‐Garcia, Shayan Sheykholeslami, Gaëlle Le Borgne, Florence Dastot‐Le Moal, Valérie Malan, Sonia Karabina, Mathieu Mahevas, Sandra Chantot‐Bastaraud, Jean‐Claude Lecron, Laurence Faivre, Serge Amselem
Journal: Arthritis & Rheumatology (2014)

Autoinflammatory disorders are caused by a primary dysfunction of the innate immune system. Among these disorders are hereditary recurrent fevers, which are characterized by recurrent episodes of fever and inflammatory manifestations affecting multiple tissues. Hereditary recurrent fevers often lack objective diagnostic criteria, thereby hampering the identification of disease-causing genes. This study was undertaken to identify a gene responsible for hereditary recurrent fevers.Copy number variations and point mutations were sought by array-comparative genomic hybridization and polymerase chain reaction sequencing, respectively. Serum cytokine levels were measured using Luminex technology. The effect of TNFRSF11A molecular defects on NF-κB signaling in cells expressing wild-type and mutated forms of the receptor was evaluated by luciferase assay.A patient with multiple congenital anomalies and hereditary recurrent fever was found to carry a de novo heterozygous complex chromosomal rearrangement encompassing a duplication of TNFRSF11A, a gene known to regulate fever in rodents. We also identified a heterozygous frameshift mutation (p.Met416Cysfs*110) in TNFRSF11A in a mother and daughter with isolated hereditary recurrent fever. This mutation was associated with increased secretion of several inflammatory cytokines (tumor necrosis factor α [TNFα], interleukin-18 [IL-18], IL-1 receptor antagonist, interferon-γ) and altered the biologic effects of the receptor on NF-κB signaling. The disease in the patients described herein exhibits striking clinical similarities to TNF receptor-associated periodic syndrome, another hereditary recurrent fever involving a gene of the same family (TNFRSF1A).The involvement of TNFRSF11A in hereditary recurrent fever highlights the key role of this receptor in innate immunity. The present results also suggest that TNFRSF11A screening could serve as a new diagnostic test for autoinflammatory disorders.
Radiolabeled Antitumor Antibodies. II. Quantitative Analysis of Moloney Tumor Antigens on Moloney Lymphoma Cells (LSTRA)2
Authors: S. Nord, I.L. Weissman
Journal: JNCI Journal of the National Cancer Institute (1974)

Radiolabeled anti-Moloney antiserum in a paired radiolabel technique detected ≈ 5 X 10 4 Moloney antigen-specific sites/LSTRA Moloney lymphoma cell. The calculated average association constant (KA ) for this radiolabeled antibody on LSTRA cells was 7.8–20 X 107 liters/mole.
De-escalation therapy in ventilator acquired pneumonia (VAP)
Authors: Abdalla Khoury, Houda Al-Nasser, Fawaz Al-Hamad, Hivin Hannan
Journal: European Respiratory Journal (2011)

Objective:  To evaluate the new strategy (De-Escalation therapy) for patients with VAP.   Methods:  We studied patients who were admitted to the ICU in a tertiary university Hospital. The study ran for 2009 full year, with a total 602 patients admission, 337 of them required mechanical ventilation, according to the daily assessment by CPIS below 6, 235 patients developed VAP (69,73%), Bacterial evaluation was achieved for 78 patients with BAL during guided Fibroscopy. We divided ours patients randomly into two groups:  Group A: 32 of the patients were treated in the traditional manner using Broad spectrum antibiotics for two weeks.  Group B: 46 of the patients were treated according to the new strategy (De-Escalation of Antibiotics) for eight days. All patients were followed up and assessed clinically and by CPIS (Clinical Pulmonary Infection Score), at starting therapy and the days (three, eight, and fourteen)   Results:  The proportions of patients with late and early VAP in Group A were 56.25%, 43,75% and Group B were 54.34%, 45.65%. The mortality rate was significantly higher in late and early VAP in both groups. In Group B the CPIS and clinical improvement was noticed and statistically significant in day eight, comparing to Group A (39.13%, 28.12% respectively). We studied the type of bacteria and its resistance to antibiotics, the proportion of Gram-negative almost consists two thirds in both groups with no difference in distribution of germ. The mortality rate in Group A and Group B was (65.62%, 56.52% Respectively) the difference was statistically significant.   Conclusion:  The (De-Escalation of antibiotics) was possible and safe with diminution of mortality, the amounts of antibiotics used and a shorter stay in the ICU.
Exposure to Commonly Prescribed Drugs and the Etiology of Cryptogenic Fibrosing Alveolitis
Authors: RICHARD HUBBARD, ANDREA VENN, CHRIS SMITH, MARIE COOPER, IAN JOHNSTON, JOHN BRITTON
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

Cryptogenic fibrosing alveolitis is an interstitial lung disease of unknown etiology. Since pulmonary fibrosis is a recognized, if rare, complication of certain drug exposures, including antidepressants, betablockers, antibiotics, anticonvulsants, and nonsteroidal antiinflammatory drugs (NSAIDs), we tested the hypothesis that exposure to these drugs might contribute to the etiology of cryptogenic fibrosing alveolitis. Lifetime drug exposure data were collected from general practitioner records for 141 cases of cryptogenic fibrosing alveolitis and 246 age-, sex-, and community-matched control subjects from the Trent region of England. Additional data on lifetime smoking habits were obtained by postal questionnaire. The odds of disease in relation to ever exposure to antidepressants, betablockers, antibiotics, anticonvulsants, and NSAIDs were calculated by conditional logistic regression. For drug groups significantly associated with cryptogenic fibrosing alveolitis, subset analyses were performed to investigate the effects of individual drugs. Cryptogenic fibrosing alveolitis was associated with exposure to antidepressants (odds ratio [OR] 1.79 [95% CI 1.09–2.95], p = 0.022) and specifically to imipramine (OR 4.79 [1.50–15.3], p = 0.01), dothiepin (OR 2.37 [0.99–5.69], p = 0.05), and mianserin (OR 3.27 [1.11–9.61], p = 0.03). The magnitude of the overall effect of antidepressants was not changed by excluding all drug exposures within the 5 yr preceding the diagnosis of cryptogenic fibrosing alveolitis (OR 1.62 [0.94–2.77], p = 0.081), nor were the strong individual effects of imipramine (OR 5.72 [1.54–21.2], p = 0.009) and dothiepin (OR 5.58 [1.12–27.8], p = 0.036). These estimates were not appreciably affected by controlling for smoking history. The attributable risk for antidepressant exposure was in the region of 9–14%. No significant association was noted between cryptogenic fibrosing alveolitis and the four other drug groups in the primary hypothesis. The results of this study suggest that some antidepressant drugs can cause cryptogenic fibrosing alveolitis.
Pancytopenia in CBA Mice After Rauscher Virus Infection&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: H.-J. Seidel
Journal: JNCI Journal of the National Cancer Institute (1972)

Hematology of female CBA mice was studied 5–30 days affer Rauscher virus infection. After 10 days pancytopenia was observed; this included reticulocytes, neutrophils, and thrombocytes. Bone marrow cellularity had decreased. Later there was a partial regeneration in some animals, but most remained anemic and thrombopenic. Spleen tumors developed weighing up to 2.5 g. In the bone marrow, a defect in cellular differentiation in the granulopoietic series with a maturation block was noted; erythropoiesis seemed normal. A leukemic blast cell population was not seen. From these results it is concluded that the underlying mechanism in Rauscher disease is a common disorder in hematopoietic cell differentiation, probably caused by the action of the virus on a common precursor cell. This could be a useful model for aplastic anemia, preleukemia, or both.
<i>In vivo</i>detection of peripheral clefting in melanocytic lesions
Authors: E. Benati, I. Zalaudek, S. Piana, G. Argenziano, E. Moscarella, A. Lallas, G. Pellacani, C. Longo
Journal: British Journal of Dermatology (2015)

Journal Article In vivo detection of peripheral clefting in melanocytic lesions Get access E. Benati, E. Benati Department of Dermatology University of Modena and Reggio Emilia Via del Pozzo 71 Modena Italy Search for other works by this author on: Oxford Academic Google Scholar I. Zalaudek, I. Zalaudek Department of Dermatology and Venereology Medical University of Graz Graz Austria Search for other works by this author on: Oxford Academic Google Scholar S. Piana, S. Piana Pathology Unit Arcispedale Santa Maria Nuova Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Reggio Emilia Italy Search for other works by this author on: Oxford Academic Google Scholar G. Argenziano, G. Argenziano Skin Cancer Unit Arcispedale Santa Maria Nuova Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Reggio Emilia Italy Search for other works by this author on: Oxford Academic Google Scholar E. Moscarella, E. Moscarella Skin Cancer Unit Arcispedale Santa Maria Nuova Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Reggio Emilia Italy Search for other works by this author on: Oxford Academic Google Scholar A. Lallas, A. Lallas Skin Cancer Unit Arcispedale Santa Maria Nuova Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Reggio Emilia Italy Search for other works by this author on: Oxford Academic Google Scholar G. Pellacani, G. Pellacani Department of Dermatology University of Modena and Reggio Emilia Via del Pozzo 71 Modena Italy Search for other works by this author on: Oxford Academic Google Scholar C. Longo C. Longo Skin Cancer Unit Arcispedale Santa Maria Nuova Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Reggio Emilia Italy Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 173, Issue 6, 1 December 2015, Pages 1525–1526, https://doi.org/10.1111/bjd.13959 Published: 01 December 2015
Treatment of advanced stages of Philadelphia chromosome-positive chronic myelogenous leukemia with interferon-alpha and low-dose cytarabine.
Authors: H M Kantarjian, M J Keating, E H Estey, S O'Brien, S Pierce, M Beran, C Koller, E Feldman, M Talpaz
Journal: Journal of Clinical Oncology (1992)

PURPOSE To evaluate the efficacy of interferon-alpha (IFN-A) and low-dose cytarabine (ara-C) combination chemotherapy in patients with chronic myelogenous leukemia (CML). PATIENTS AND METHODS Sixty patients with advanced phases of Philadelphia chromosome (Ph)-positive CML received combination therapy with IFN-A 5 x 10(6) U/m2 daily, and low-dose ara-C 15 mg/m2 daily for 2 weeks every 4 weeks until remission, then for 1 week every month as maintenance. Forty patients were in late chronic-phase CML, and 20 were in accelerated-phase CML (16 with clonal evolution only, four with other criteria). Their outcome was compared with 58 patients (39 late chronic-phase CML and 19 accelerated-phase CML) who had been previously treated with IFN-A alone in the same dose schedule. RESULTS In late chronic-phase CML, patients receiving IFN-A plus ara-C had a better complete hematologic response (CHR) rate compared with those treated with IFN-A alone (55% v 28%; P = .02), a trend for better Ph suppression (15% v 5%; P = .13), and a longer survival (3-year survival rate 75% v 48%; P less than .01). These differences do not seem to be caused by imbalances in prognostic factors between the two treatment groups. In accelerated-phase CML, the addition of ara-C to IFN-A did not improve the response rate of treated patients, and the difference in survival was accounted for by different patient characteristics. Suppression of clonal evolution was observed in five patients (25%). Patients with clonal evolution as the only criterion for disease acceleration had a longer survival than those with other or additional accelerated-phase criteria (3-year survival rate 67% v 22%; P less than .01). CONCLUSION The results with the combination of IFN-A plus ara-C in late chronic-phase CML are encouraging, and suggest the need for its evaluation in early chronic-phase CML.
Characterization of Immune Responses to Spontaneous Hamster Lymphomas2
Authors: Kathy A. Vasa-Thomas, Kathleen R. Ambrose, Bruce B. Bellomy, Joseph H. Coggin
Journal: JNCI Journal of the National Cancer Institute (1977)

Tumor resistance could be induced against the transplantation of cell lines derived from spontaneous lymphomas that occurred in the third of three lymphoma epizootics in a hamster colony. Immunization of normal hamsters with irradiated lymphoma cells promoted resistance to homologous lymphoma challenge and prevented the development of spontaneous lymphomas when immunized hamsters were exposed to the contaminated colony. This immunity could be transferred in an adoptive transfer assay. Resistance to direct challenge was not extended to simian virus 40 (SV40)-induced sarcomas carrying SV40 tumor-specific transplantation antigen nor to herpesvirus-Induced carcinoma cells, indicating specificity. The nature of the antigen(s) involved was discussed.
Promoting physical activity in general practice: should prescribed exercise be free?
Authors: Sharon See Tai, Mairi Gould, Paul Smith, Steve Iliffe
Journal: Journal of the Royal Society of Medicine (1999)

In the UK there are numerous schemes whereby general practitioners can prescribe exercise programmes, usually based in leisure centres. Of the factors that discourage adherence to such programmes in the USA, cost has proved important. We collected demographic and questionnaire data from 152 inner-London patients (108 women, 44 men) before they started an exercise programme on a National Health Service prescription, and analysed the results according to whether they dropped out of the programme (78%) or not. Use of logistic regression revealed only one previous barrier to exercise, ‘not knowing about local exercise facilities’, as a significant positive determinant of adherence (adjusted odds ratio 3.51,95% confidence interval, 1.04 to 11.86). For ‘lack of money' patients were more likely to drop out of the programme (adjusted odds ratio 0.25, 95% CI 0.07–0.85). The very low cost of participation in this scheme, did not encourage adherence, particularly by those who had cited ‘lack of money' as a previous barrier. The case of making prescribed exercise free or even low-cost remains unproven.
Assessing the diagnostic validity of a structured psychiatric interview in a first‐admission hospital sample
Authors: JULIE NORDGAARD, RASMUS REVSBECH, DITTE SÆBYE, JOSEF PARNAS
Journal: World Psychiatry (2012)

The use of structured psychiatric interviews performed by non-clinicians is frequent for research purposes and is becoming increasingly common in clini-cal practice. The validity of such interviews has rarely been evaluated empirically. In this study of a sample of 100 diagnostically heterogeneous, first-admitted inpatients, the results of an assessment with the Structured Clinical Interview for DSM-IV (SCID), yielding a DSM-IV diagnosis and performed by a trained non-clinician, were compared with a consensus lifetime best diagnostic estimate (DSM-IV) by two experienced research clinicians, based on multiple sources of information, which included videotaped comprehensive semi-structured narrative interviews. The overall kappa agreement was 0.18. The sensitivity and specificity for the diagnosis of schizophrenia by SCID were 19% and 100%, respectively. It is concluded that structured interviews performed by non-clinicians are not recommendable for clinical work and should only be used in research with certain precautions. It is suggested that a revival of systematic theoretical and practical training in psychopathology is an obvious way forward in order to improve the validity and therapeutic utility of psychiatric diagnosis.
Comparison of inspiratory effort in sniff-like aspiration reflex, gasping and normal breathing in cats
Authors: Z Tomori, V Donic, M Kurpas
Journal: European Respiratory Journal (1993)

The changes in airway occlusion pressure and airflow, occurring during two spasmodic breathing patterns, were studied and compared with normal breathing pattern in 12 anaesthetized cats. The inspiratory effort developed during the sniff-like aspiration reflex elicited by mechanical stimulation of the nasopharynx under control conditions proved to be very similar in character and intensity to the activity observed during gasping which occurred on resuscitation, of the same cats, from hypoxic apnoea. The starting (P50) and maximum (Pmax) airway occlusion pressure developed in these two spasmodic breathing patterns were very high. Extremely rapid rates of contraction and relaxation were detected by computer-assisted measurements of dynamic changes in both the pressure values and the slopes of pressure curves. The results suggest common effector mechanisms, reflecting similar forceful inspiratory drives, for the aspiration reflex and gasping. These two spasmodic processes differ substantially from normal breathing. Nevertheless, the aspiration reflex differs from gasping in that it can be elicited by activation of upper airway afferents during eupnea. Moreover, as yet, there is no definitive evidence that the brainstem mechanisms responsible for generating the aspiration reflex are the same as those of the gasp. The main benefits of this reflex are its rather easy elicitability under various conditions and its capability to induce important cardiorespiratory effects (e.g.) reversal of central apnoea) owing to its powerful activity.
Chromosomal Alteration and Development of Tumors. XIX. Chromosome Constitution of Tumor Cells in 16 Plasma Cell Neoplasms of BALB/c Mice&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: Tosihide H. Yosida, Hirotami T. Imai, Michael Potter
Journal: JNCI Journal of the National Cancer Institute (1968)

Karyotypes of 16 plasma cell neoplasms induced by mineral oil or mineral oil adjuvants in BALB/c mice were |analyzed. Of these neoplasms, 13 produced specific immunoglobulins, 13 had stemlines characterized by hypotetraploid chromosome numbers, 1 (MOPC-31C) had a hyperdiploid stemline, 1 (MOPC-70E), a hypotriploid stemline, and 1 (Adj PC-6C), a hypertetraploid stemline. The stemline cells of 13 neoplasms had 1–4 marker chromosomes, whereas those of 3 neoplasms (MOPC31B, MOPC-70A, and MOPC-70E) had no detectable marker chromosomes. The wide range of chromosome numbers usually found in the early transplant generations narrowed in the later transplant generations. Three neoplasms not producing specific γ-immunogIobulins evolved from 3 neoplasms characterized by the production of γA serum, lambda chain and γF serum, and excess kappa, respectively. The karyotypes of these negative neoplasms differed significantly from those of the parental positive neoplasms.
Notes from the field: acute muscular sarcocystosis among returning travelers - Tioman Island, Malaysia, 2011.
Authors: F. von Sonnenburg, J. P. Cramer, D. O. Freedman, A. Plier, D. H. Esposito, M. J. Sotir, E. W. Lankau
Journal: MMWR Morbidity and Mortality Weekly Report (2012)
Lipopolysaccharide attenuates endothelial barrier function through a pp60Src mediated inhibition of dimethylaminohydrolase (DDAH)
Authors: Saurabh Aggarwal, Shruti Sharma, Sanjiv Kumar, Stephen Black, Yali Hou
Journal: European Respiratory Journal (2011)

Acute lung injury is a severe hypoxemic respiratory insufficiency associated with alterations in lung structure and function. Previously, we found that decreases in the activity of DDAH and increased in asymmetric dimethylarginine (ADMA) contributes to the development of ALI in mice exposed to lipopolysaccharide (LPS). In this study, we elucidated the mechanisms involved in the attenuation of DDAH2 by LPS. Utilizing an electric cell impedance sensing apparatus, we found that overexpression of DDAH2 in human lung microvascular endothelial cells (HLMVEC) prevents the LPS (1 endotoxin unit/ml) induced decrease in transendothelial resistance. Further, we found that overexpression of a dominant negative mutant of pp60 src  attenuated the LPS mediated decrease in DDAH activity and increase in ADMA levels. While, overexpression of a constitutively active mutant decreased DDAH activity and increased ADMA levels without altering DDAH2 protein levels. Further, LPS increased the interaction between DDAH2 and pp60 src  and also increased its tyrosine phosphorylation. In the LPS treated mouse lung, we found that the decrease in DDAH activity correlated with an increase in pp60 src  interaction and tyrosine phosphorylation of DDAH2. Finally, the overexpression of DDAH2 in murine lung endothelial cells, using a polyethyleneimine (PEI) derivative transfection reagent, led to an increase in DDAH activity, a decrease in ADMA levels, and the attenuation of the LPS mediated increase in the lung leak as measured by extravasation of Evans blue dye. The prevention of the pp60 src  mediated decrease in DDAH activity may have clinical utility in the prevention of LPS induced ALI.
Brief Communication : Oncofetal Protein Accompanying Irradiation-Induced Small-Bowel Adenocarcinoma in the Rat 2
Authors: R. H. Stevens, C. W. England, J. W. Osborne, H. F. Cheng, H. B. Richerson
Journal: JNCI Journal of the National Cancer Institute (1975)

A tumor-associated protein was found in tissue derived from an X-irradiation-induced adenocarcinoma in the small bowel of the rat. The protein was associated with the cell membranes of the tumor tissue. It shared common antigenic determinants both with a rat fetal protein and a perchloric acid-soluble protein isolated from the serum of the tumor-bearing rat.