tbuckley/cabot-search huggingface dataset:
Lung surfactant in a cystic fibrosis animal model: increased alveolar phospholipid pool size without altered composition and surface tension function in cftrm1HGU/m1HGU mice
Authors: W. Bernhard, J. Y. Wang, T. Tschernig, B. Tummler, H. J. Hedrich, H. von der Hardt
Journal: Thorax (1997)

BACKGROUND: Progressive pulmonary dysfunction is a characteristic symptom of cystic fibrosis (CF) and is associated with functional impairment and biochemical alterations of surfactant phospholipids in the airways. However, the fundamental question of whether surfactant alterations in the CF lung are secondary to the pulmonary damage or are present before initiation of chronic infection and inflammation has yet to be resolved in patients with cystic fibrosis but can now be addressed in CF mice that exhibit the basic defect in the airways. A study was therefore undertaken to investigate the pool sizes, composition, and function of lung surfactant in the non-infected cftrm1HGU/m1HGU mouse. METHODS: The amount and composition of phospholipid classes and phosphatidylcholine molecular species were determined in bronchoalveolar lavage (BAL) fluid and lavaged lungs by high performance liquid chromatography (HPLC). Surfactant protein A (SP-A) levels in BAL fluid were determined by ELISA and surfactant for functional measurements was isolated from BAL fluid by differential ultracentrifugation. Equilibrium and minimal surface tension of surfactant was assessed by the pulsating bubble surfactometer technique. MF1, BALB/c, C57/BL6, and C3H/He mice served as controls. RESULTS: BAL fluid of cftrm1HGU/m1HGU mice contained 1.02 (95% confidence interval (CI) 0.89 to 1.16) mumol phospholipid and 259 (239 to 279) ng SP-A. BAL fluid of MF1, BALB/c, C57BL/6, and C3H/He mice contained 0.69 (0.63 to 0.75), 0.50 (0.42 to 0.57), 0.52 (0.40 to 0.64), and 0.45 (0.27 to 0.63) mumol phospholipid, respectively. After correction for the different body weights of mouse strains, phospholipid levels in BAL fluid of cftrm1HGU/m1HGU mice were increased by 64 (52 to 76)%, 60 (39 to 89)%, 72 (45 to 113)%, and 92 (49 to 163)%, respectively, compared with controls. The amount of SP-A in BAL fluid and the composition of phospholipid as well as phosphatidylcholine molecular species in BAL fluid and lung tissue was unchanged in cftrm1HGU/m1HGU mice compared with controls. The increase in phospholipids in BAL fluid of cftrm1HGU/m1HGU mice resulted from an increased fraction of large aggregates which exhibited normal surface tension function. CONCLUSION: In cftrm1HGU/m1HGU mice surfactant homeostasis is perturbed by an increased phospholipid pool in the alveolar compartment.
THE PATHOGENESIS OF EARLY OBSTRUCTIVE JAUNDICE
Authors: E. S. Guzman Barron, John H. Bumstead
Journal: The Journal of Experimental Medicine (1928)

1. After experimental ligation of the bile ducts in dogs, two distinct processes are clearly manifested: first, the accumulation of the normally circulating bilirubin in the blood with its characteristic indirect Van den Bergh reaction for a period of several hours, and second, the subsequent appearance of the bile bilirubin giving the direct Van den Bergh reaction. It is possible that the first process may be due to a temporary reflex inhibition of the function of the liver cells due to ligation of the duct and comparable to the same phenomenon which usually occurs in the kidney when the ureter is ligated. The second process begins before any rupture of the bile capillaries is visible. Liver sections made 6 to 7 hours after obstruction show these bile capillaries dilated and extending between the liver cells in small distended pouches the blind end of these lying in contact with the pericapillary spaces. It is possible that bile may diffuse from these thin walled pouches into the perivascular lymph spaces, this diffusion being favored by the mounting pressure inside the bile ducts. 2. In early obstructive jaundice bile first appears in the lymph, but exclusion of the thoracic duct from the circulation by drainage causes a delay of only a few hours in the appearance of bile bilirubin in the blood stream. We must therefore conclude that after biliary obstruction bile enters the circulation both by way of the blood capillarieś and the lymphatics, although the latter route is the more important.
The Agency for Health Care Policy and Research Smoking Cessation Clinical Practice Guideline
Authors: Michael C. Fiore
Journal: JAMA (1996)

To summarize the Smoking Cessation Clinical Practice Guideline that provides recommendations for 3 groups of professionals: primary care clinicians, smoking cessation specialists, and health care administrators, insurers, and purchasers.An independent panel of scientists, clinicians, consumers, and methodologists selected by the US Agency for Health Care Policy and Research.English-language, peer-reviewed literature published between 1975 and 1994 that addresses the assessment and treatment of tobacco dependence, nicotine addiction, and clinical practice.Four panel meetings were held over 2 years to evaluate meta-analytic and other results, to synthesize the results, and to develop recommendations. The Guideline was repeatedly reviewed and revised.The panel recommendations address 3 audiences. Major recommendations for primary care clinicians are to use officewide systems to identify smokers, treat every smoker with a cessation or motivational intervention, offer nicotine replacement except in special circumstances, and schedule follow-up contact to occur after cessation. Major recommendations to smoking cessation specialists are to use multiple individual or group counseling sessions lasting at least 20 minutes each with sessions spanning multiple weeks, offer nicotine replacement, and provide problem-solving and social support counseling. Major recommendations for health care administrators, insurers, and purchasers are that tobacco-user identification systems be used in all clinics and that smoking cessation treatment be supported through staff education and training, dedicated staff, changes in hospital policies, and the provision of reimbursement for tobacco-dependence treatment.
A computational framework for boosting confidence in high-throughput protein-protein interaction datasets
Authors: Raghavendra Hosur, Jian Peng, Arunachalam Vinayagam, Ulrich Stelzl, Jinbo Xu, Norbert Perrimon, Jadwiga Bienkowska, Bonnie Berger
Journal: Genome biology (2012)

Improving the quality and coverage of the protein interactome is of tantamount importance for biomedical research, particularly given the various sources of uncertainty in high-throughput techniques. We introduce a structure-based framework, Coev2Net, for computing a single confidence score that addresses both false-positive and false-negative rates. Coev2Net is easily applied to thousands of binary protein interactions and has superior predictive performance over existing methods. We experimentally validate selected high-confidence predictions in the human MAPK network and show that predicted interfaces are enriched for cancer -related or damaging SNPs. Coev2Net can be downloaded at http://struct2net.csail.mit.edu .
FlyMine: an integrated database for Drosophila and Anopheles genomics
Authors: Rachel Lyne, Richard Smith, Kim Rutherford, Matthew Wakeling, Andrew Varley, Francois Guillier, Hilde Janssens, Wenyan Ji, Peter Mclaren, Philip North, Debashis Rana, Tom Riley, Julie Sullivan, Xavier Watkins, Mark Woodbridge, Kathryn Lilley, Steve Russell, Michael Ashburner, Kenji Mizuguchi, Gos Micklem
Journal: Genome biology (2007)

Abstract FlyMine is a data warehouse that addresses one of the important challenges of modern biology: how to integrate and make use of the diversity and volume of current biological data. Its main focus is genomic and proteomics data for Drosophila and other insects. It provides web access to integrated data at a number of different levels, from simple browsing to construction of complex queries, which can be executed on either single items or lists.
The influence of gene-gene interaction on the development of respiratory distress syndrome in the neonates
Authors: Svetlana Kyryachenko, Natalia Gorovenko, Zoia Rossokha
Journal: European Respiratory Journal (2012)

Background: The investigation of gene-gene interaction is necessary for understanding of pathogenic mechanism in the development of respiratory distress syndrome (RDS).

The aim of this study was to evaluate the genes influence and their complex effect on the RDS development.

Methods: We conducted a case-control study of 151 neonates with RDS and 110 healthy neonates. The I/D, A1166C, G308A, C677T polymorphism of ACE, AT2R1, TNF-a, MTHFR genes were detected using PCR and RFLP analysis. Statistical analysis was performed to assess the analyzed effects (program SPSS\_17.0 and MDR\_2.0).

Results: The frequency of all investigated genotypes with mutant allele (except AC genotype of AT2R1 gene) was significantly higher among RDS cases.

![Figure][1] 



The statistical model including all investigated genotypes had high predictive value (Percentage Correct=72,8). We have found negative entropy which indicated independent effects of each gene.

![Figure][1] 



Conclusion: The investigated genes polymorphism is independent risk factor for the RDS development. The further research with including other prognostic factors may be useful for new approaches to preventive strategy.

 [1]: pending:yes
A CONTRIBUTION TO THE BACTERIOLOGY OF RHEUMATIC FEVER
Authors: James M. Beattie
Journal: The Journal of Experimental Medicine (1907)

The conclusions I would draw from this work are merely those stated in a former paper. 1. The results obtained by injections of streptococci are different from those produced by Micrococcus rheumaticus. 2. Micrococcus rheumaticus cannot be regarded as an attenuated streptococcus, nor acute rheumatism as an attenuated streptococcal pyaemia. 3. In uncomplicated cases of acute rheumatism the organism may not be found in the blood or in the joint exudates.
Haroon Rashid Chaudhry
Authors: T. A. Rana
Journal: BMJ (2010)

<h3>Background</h3> Out-of-hospital cardiac arrest (OHCA) remains the leading cause of sudden death faced by EMS personnel. Therapeutic hypothermia has been shown to improve neurological outcome and survival in certain patients after out-of-hospital cardiac arrest. The natural progression of core body temperature, particularly in the pre-hospital setting, post OHCA has yet to be established. Pre-hospital core body temperature will influence the need for possible pre-hospital cooling post OHCA. <h3>Aims</h3> To establish the natural progression of core body temperature after OHCA. <h3>Methods</h3> One year, prospective observational study across the Lothians region of Scotland. A research doctor was tasked by the Emergency Medical Dispatch Centre to attend patients in OHCA together with the attending ambulance crew. An oesophageal core body temperature probe was inserted to continuously monitor core body temperature from the earliest opportunity in the field to arrival of the patient on the Intensive Care Unit (ICU). Therapeutic hypothermia was commenced after admission to the ICU. <h3>Results</h3> 147 OHCA were included. 13 patients survived to reach hospital discharge (8.8%). After return of spontaneous circulation (ROSC) core body temperature increased until therapeutic cooling commenced. Re-warming occurred faster in survivors. There was no significant pre-hospital core body temperature difference between survivors (33.03°C) and non-survivors (33.58°C). Patients surviving to discharge had a higher core body temperature on arrival in ITU compared to non-survivors (35.44°C vs 34.25°C, p&lt;0.05). <h3>Conclusions</h3> OHCA patients in our area remain cool (&lt;35C) during the pre-hospital phase. This may suggest that pre-hospital cooling is not required for these patients. This is the first study of its kind to report on core body temperature after OHCA. Survivors rewarming faster has not yet been described and the mechanisms underlying this required further investigation. Further research is warranted into the mechanisms of action of therapeutic hypothermia, particularly the optimum timing and method of cooling.
Ubiquitous nonimmunoglobulin p-azobenzenearsonate-binding molecules from lymphoid cells.
Authors: A F Clark, J D Capra
Journal: The Journal of Experimental Medicine (1982)

A ubiquitous nonimmunoglobulin molecule that binds p-azobenzenearsonate (ABA) has been detected in the cytoplasm of several murine cell lines, including T cell hybridomas as well as in normal liver and spleen. Similar to many recently described antigen-specific T cell factors, this ABA-binding protein has a 62,000 mol wt, and, when analyzed by direct binding, the molecule reacts with several different rabbit anti-idiotypic antisera specific to the ABA system. The presence of this antigen-specific, "idiotype positive" molecule in many different cells indicates that it is not an important immunoregulatory molecule.
Early Loss of <i>Fhit</i> in the Respiratory Tract of Rodents Exposed to Environmental Cigarette Smoke
Authors: Francesco D'Agostini, Alberto Izzotti, Roumen Balansky, Nicola Zanesi, Carlo M. Croce, Silvio De Flora
Journal: Cancer Research (2006)

Abstract The Fhit gene, encompassing the most active common human chromosomal fragile region, FRA3B, has been shown to act as a tumor suppressor. Several studies have shown significant Fhit alterations or Fhit protein loss in lung cancers from smokers compared with lung cancers from nonsmokers. To evaluate the role of Fhit under controlled experimental conditions, we exposed rodents to environmental cigarette smoke (ECS) and evaluated Fhit expression or Fhit protein in the respiratory tract. After 14 days of exposure to ECS, loss of Fhit protein in the bronchial/bronchiolar epithelium affected half of the tested B6-129(F1) mice, either wild type or Fhit+/−. After 28 days, it affected the vast majority of the tested SKH-1 hairless mice and of A/J mice and all (UL53-3 x A/J)F1 mice, either wild type or P53+/−. In Sprague-Dawley rats, exposure to ECS for up to 30 days caused a time-dependent loss of Fhit in pulmonary alveolar macrophages. Moreover, ECS down-regulated Fhit expression and significantly decreased Fhit protein in the rat bronchial epithelium. The oral administration of N-acetylcysteine attenuated the ECS-related loss of Fhit, whereas oltipraz, 5,6-benzoflavone, phenethyl isothiocyanate, and indole 3-carbinol, and their combinations had no significant effect. Parallel studies evaluated a variety of molecular, biochemical, and cytogenetic alterations in the respiratory tract of the same animals. In conclusion, there is unequivocal evidence that Fhit is an early, critical target in smoke-related lung carcinogenesis in rodents, and that certain chemopreventive agents can attenuate the occurrence of this gene alteration. (Cancer Res 2006; 66(7): 3936-41)
A new technique of experimental heterotopic cardiac transplantation
Authors: H. K DASMAHAPATRA, G. J WILSON, S. L DAVID, S. KIELMANOWICZ, G. KENT, S. N GOKHALE, R. GORCZYNSKI, A. SHORE, J. G COLES
Journal: Cardiovascular Research (1988)

Heterotopic cardiac transplantation is a useful method for studying allograft rejection. In this study a new technique of cardiac transplantation was carried out, which involved retroperitoneal anastomoses of the donor ascending aorta and main pulmonary artery with the recipient abdominal aorta and inferior vena cava respectively. The procedure was simple and effective and was accomplished with minimal operative mortality and postoperative morbidity. The method allows better access to the allograft for repeated open myocardial biopsies, obviating the limitations of transvenous fluoroscopically directed endomyocardial biopsy. This technique of retroperitoneal heterotopic cardiac transplantation has important advantages compared with similar procedures performed in the neck, abdomen, or thorax.
Should All Diabetic Patients Be Treated With a Statin?
Authors: Yehuda Kamari, Rafael Bitzur, Hofit Cohen, Aviv Shaish, Dror Harats
Journal: Diabetes Care (2009)

The prevalence of diabetes for all age-groups worldwide was estimated to be 2.8% (171 million) in the year 2000, and the projected number could rise to 4.4% (366 million) in 2030 (1). This rapid rise is mainly attributable to the increase of diabetes. The continuing escalation of obesity and the metabolic syndrome contribute to the upsurge in frequency of diabetes (2,3).

Interestingly, the appreciation in the number of people >65 years of age was found to be the most important demographic change to diabetes prevalence around the world, indicating that the “diabetes epidemic” will continue even if levels of obesity remain constant. Therefore, it is likely that future diabetes preponderance is underestimated, given the growing frequency of obesity (1). Because the vast majority of diabetic patients have type 2 diabetes and almost all the studies were performed in such subjects, in this article, “type 2 diabetes” will be referred to as “diabetes.”

Cardiovascular disease (CVD) is one of the foremost causes of mortality and is a major contributor to morbidity for individuals with diabetes. In addition, diabetes is an independent risk factor for macrovascular disease, as are the common coexisting conditions (hypertension and dyslipidemia). The U.K. Prospective Diabetes Study (UKPDS) evaluated baseline risk factors for coronary artery disease in patients with newly diagnosed diabetes without evidence of vascular disease. When comparing the relative contribution of the three modifiable coexisting conditions (dyslipidemia, hypertension, and hyperglycemia) with development of future coronary heart disease (CHD), the estimated hazard ratio (HR) for the upper third, relative to the lower third, for LDL cholesterol, systolic blood pressure, and A1C were 2.26, 1.82, and 1.52, respectively (4). This finding supports the notion that dyslipidemia, and specifically LDL cholesterol, are major contributors to the increased CHD risk in patients with diabetes (4,5 …
DDX3, a potential target for cancer treatment
Authors: Guus Martinus Bol, Min Xie, Venu Raman
Journal: Molecular Cancer (2015)

RNA helicases are a large family of proteins with a distinct motif, referred to as the DEAD/H (Asp-Glu-Ala-Asp/His). The exact functions of all the human DEAD/H box proteins are unknown. However, it has been consistently demonstrated that these proteins are associated with several aspects of energy-dependent RNA metabolism, including translation, ribosome biogenesis, and pre-mRNA splicing. In addition, DEAD/H box proteins participate in nuclear-cytoplasmic transport and organellar gene expression. A member of this RNA helicase family, DDX3, has been identified in a variety of cellular biogenesis processes, including cell-cycle regulation, cellular differentiation, cell survival, and apoptosis. In cancer, DDX3 expression has been evaluated in patient samples of breast, lung, colon, oral, and liver cancer. Both tumor suppressor and oncogenic functions have been attributed to DDX3 and are discussed in this review. In general, there is concordance with in vitro evidence to support the hypothesis that DDX3 is associated with an aggressive phenotype in human malignancies. Interestingly, very few cancer types harbor mutations in DDX3, which result in altered protein function rather than a loss of function. Efficacy of drugs to curtail cancer growth is hindered by adaptive responses that promote drug resistance, eventually leading to treatment failure. One way to circumvent development of resistant disease is to develop novel drugs that target over-expressed proteins involved in this adaptive response. Moreover, if the target gene is developmentally regulated, there is less of a possibility to abruptly accumulate mutations leading to drug resistance. In this regard, DDX3 could be a druggable target for cancer treatment. We present an overview of DDX3 biology and the currently available DDX3 inhibitors for cancer treatment.
Familial aggregation of aspirin-induced urticaria and leukotriene C<sub>4</sub> synthase allelic variant
Authors: L. Mastalerz, M. Setkowicz, M. Sanak, H. Rybarczyk, A. Szczeklik
Journal: British Journal of Dermatology (2005)

Background We have reported that in patients with chronic idiopathic urticaria (CIU) who reacted adversely to aspirin, the frequency of the −444C allele of the leukotriene C4 synthase gene (LTC4S) was higher than in patients who tolerated aspirin well. Objectives To study the pattern of aspirin‐induced urticaria (AIU) in two families, with special interest on the polymorphisms of LTC4S (AA, AC, CC) and the glutathione S‐transferase M1 and P1 genes (GSTM1 and GSTP1). Methods Of 74 patients with CIU and a history of aspirin hypersensitivity studied by us, two patients (probands) gave a family history of aspirin intolerance. Oral challenge tests with aspirin were carried out in members of these families. Genomic DNA samples were obtained from peripheral blood to study the polymorphisms of LTC4S, GSTM1 and GSTP1. Results In family 1 the aspirin challenge test confirmed AIU in three of five (60%) individuals, but in family 2 only in two of seven (29%). In both families, the variant genotypes of LTC4S (AC or CC) were present in the parents, but only one of them had CIU. In family 1, with both parents healthy, the three children had AIU; in two it was associated with variant LTC4S genotype. In family 2, urticaria following aspirin ingestion was present only with variant LTC4S genotype. In patients of both families with positive aspirin challenge test, deletion of the GSTM1 gene was present. Conclusions AIU aggregates in families inheriting the LTC4S−444C allele. Segregation of aspirin sensitivity in these families does not follow a clear Mendelian pattern. A common deletion of GSTM1, one of several enzymes involved in conjugation of a wide range of electrophilic substances with glutathione, was present in all individuals ascertained to have AIU.
Psychopathology During Childhood and Adolescence Predicts Delusional-Like Experiences in Adults: A 21-Year Birth Cohort Study
Authors: James Scott, Graham Martin, Joy Welham, William Bor, Jake Najman, Michael O'Callaghan, Gail Williams, Rosemary Aird, John McGrath
Journal: American Journal of Psychiatry (2009)

Community surveys have shown that many otherwise well individuals report delusional-like experiences. The authors examined psychopathology during childhood and adolescence as a predictor of delusional-like experiences in young adulthood.The authors analyzed prospective data from the Mater-University of Queensland Study of Pregnancy, a birth cohort of 3,617 young adults born between 1981 and 1983. Psychopathology was measured at ages 5 and 14 using the Child Behavior Checklist (CBCL) and at age 14 using the Youth Self-Report (YSR). Delusional-like experiences were measured at age 21 using the Peters Delusional Inventory. The association between childhood and adolescent symptoms and later delusional-like experiences was examined using logistic regression.High CBCL scores at ages 5 and 14 predicted high levels of delusional-like experiences at age 21 (odds ratios for the highest versus the other quartiles combined were 1.25 and 1.85, respectively). Those with YSR scores in the highest quartile at age 14 were nearly four times as likely to have high levels of delusional-like experiences at age 21 (odds ratio=3.71). Adolescent-onset psychopathology and continuous psychopathology through both childhood and adolescence strongly predicted delusional-like experiences at age 21. Hallucinations at age 14 were significantly associated with delusional-like experiences at age 21. The general pattern of associations persisted when adjusted for previous drug use or the presence of nonaffective psychoses at age 21.Psychopathology during childhood and adolescence predicts adult delusional-like experiences. Understanding the biological and psychosocial factors that influence this developmental trajectory may provide clues to the pathogenesis of psychotic-like experiences.