tbuckley/cabot-search huggingface dataset:
The DD Genotype of the Angiotensin Converting Enzyme Gene Is Negatively Associated with Right Ventricular Hypertrophy In Male Patients with Chronic Obstructive Pulmonary Disease
Authors: ROBERT J. van SUYLEN, EMIEL F. WOUTERS, HERMAN J. PENNINGS, EMILE C. CHERIEX, PETRA E. van POL, ANTON W. AMBERGEN, ANNE-MARIE VERMELIS, MAT J. DAEMEN
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

The renin angiotensin system plays an important role in the development of pulmonary artery remodeling and right ventricular hypertrophy in hypoxia-induced pulmonary hypertension as may occur in patients with COPD. Several polymorphisms of genes encoding for components of the renin angiotensin system such as the M235T polymorphism in the angiotensinogen gene, the 287-base-pair insertion (I)/deletion (D) polymorphism at intron 16 of the ACE gene, and the A1166C polymorphism in the angiotensin II type 1 receptor gene have been associated with an increased risk of cardiovascular diseases. With respect to the pulmonary circulation, only limited data exist on possible associations between polymorphisms of these genes and pulmonary hypertension and/or right ventricular hypertrophy. The objective of the present study was to investigate a possible relationship between polymorphisms of the renin angiotensin system and electrocardiographic evidence of right ventricular hypertrophy in patients with COPD. We therefore determined the angiotensinogen (M235T), angiotensin converting enzyme (I/D), and angiotensin II type 1 receptor (A1166C) genotypes in 87 patients with severe COPD and correlated these data with electrocardiographic parameters of right ventricular hypertrophy. Thirty-one patients (36%) of 87 patients with COPD showed electrocardiographic evidence of right ventricular hypertrophy. In the male, but not in the female, subgroup, the angiotensin-converting enzyme DD genotype was negatively associated with electrocardiographic evidence of right ventricular hypertrophy (male: chi2 = 3.8, p = 0.05; female: chi2 = 0.05, p = 0.82). We found no associations between the investigated polymorphisms in the angiotensinogen and angiotensin II type 1 receptor genes and electrocardiographic evidence of right ventricular hypertrophy.
Distribution and conservation of sequences homologous to the 1731 retrotransposon in Drosophila.
Authors: C Montchamp-Moreau, S Ronsseray, M Jacques, M Lehmann, D Anxolabéhère
Journal: Molecular Biology and Evolution (1993)

The distribution of 1731 retrotransposon-hybridizing sequences in the family Drosophilidae has been studied using a 1731 probe from Drosophila melanogaster. Squash blot and Southern blot analyses of 42 species reveal that the 1731 sequences are widespread within both the Sophophora and Drosophila subgenera and are also present in the genera Scaptomyza and Zaprionus. Hence the 1731 retrotransposon family appears to have a long evolutionary history in the Drosophilidae genome. Differences of hybridization signal intensity suggested that the 1731 sequence is well conserved only in the three species most closely related to D. melanogaster (D. simulans, D. mauritiana, and D. sechellia). A survey of insertion sites in numerous different populations of the previous four species by in situ hybridization to polytene chromosomes has shown in all cases both chromocentric hybridizations and a low number of sites (0-5) on the chromosomal arms. This number of sites is among the lowest observed in D. melanogaster and D. simulans when 1731 is compared with other retrotransposon families. In addition, we have observed species-specific patterns of the chromocentric hybridization signal, suggesting rapid modifications of the beta-heterochromatin components since the radiation of the melanogaster subgroup.
Serum Free Light Chain Analysis and Urine Immunofixation Electrophoresis in Patients with Multiple Myeloma
Authors: Mohammad R. Nowrousian, Dieter Brandhorst, Christiane Sammet, Michaela Kellert, Rainer Daniels, Philipp Schuett, Miriam Poser, Siemke Mueller, Peter Ebeling, Anja Welt, Arthur R. Bradwell, Ulrike Buttkereit, Bertram Opalka, Michael Flasshove, Thomas Moritz, Siegfried Seeber
Journal: Clinical Cancer Research (2005)

Abstract Purpose: Retrospective studies have shown that immunoassays measuring free light chains (FLC) in serum are useful for diagnosis and monitoring of multiple myeloma. This study prospectively evaluates the use of FLC assays and, for the first time, investigates the relationship between serum FLC concentrations and the presence and detectability of Bence Jones (BJ) proteins in the urine. Patients and Methods: Three hundred seventy-eight paired samples of serum and urine were tested from 82 patients during the course of their disease. The sensitivities of serum FLC analysis and urine immunofixation electrophoresis (IFE) in detecting monoclonal FLC were compared. Serum FLC concentrations required for producing BJ proteins detected by IFE were determined. Results: Abnormal FLC were present in 54% of serum samples compared with 25% by urine tests. In abnormal serum samples for κ or λ, the sensitivity of IFE to detect the respective BJ proteins in urine were 51% and 35% and the median serum FLC concentrations required to produce detectable BJ proteins were 113 and 278 mg/L. Renal excretions of monoclonal FLC increased with serum concentrations, but excretions significantly decreased at high serum concentrations combined with renal dysfunction. Conclusion: Serum FLC assays are significantly more sensitive for detecting monoclonal FLC than urine IFE analysis. They also have the advantage of FLC quantification and are more reliable for monitoring disease course and response to treatment.
An approach to the structure and function of the glomerular mesangium.
Authors: H Latta
Journal: Journal of the American Society of Nephrology (1992)

The mesangium of the glomerulus is a connective tissue tree arising at the vascular pole of the glomerulus and supporting the glomerular capillaries. It is partly covered by a basement membrane that follows the epithelial cells from the peripheral glomerular capillary wall over the supporting tissue. The capillary endothelium does not normally have a separate basement membrane. The endothelium has fenestrations that open directly into the mesangium and allow blood plasma and tracers to flow into the mesangium. The fenestrations partially restrict (or sieve) particles over 405 A in mean length from entry. Tracers move in intercellular channels and are filtered and concentrated by the basement membrane at the sides of the mesangium or by mesangial matrix filaments in the channels between cells. The irregular distributions of flow, matrix, and concentrations of tracers may account for irregular lobular reactions in glomerular disease. Two main pathways of flow seem to be (1) through the basement membrane and between the epithelial foot processes to form part of the glomerular filtrate and (2) into the efferent capillaries through their mesangial fenestrations. Intrinsic mesangial cells can now be regarded as myofibroblasts associated with the production of the connective tissue matrix. These cells hold the basement membrane to maintain the shape of the glomerular capillaries, they swell readily, and they can constrict like smooth muscle cells with appropriate stimulation. These reactions may enable them to control the flow of blood through the capillary network in glomerular disease. Mesangial cells can take up large amounts of foreign material within 24 h. Intrinsic mesangial cells and monocytes can increase in numbers in disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of Sucrose on Carbohydrate and Lipid Metabolism in NIDDM Patients
Authors: Clarie B Hollenbeck, Ann M Coulston, Gerald M Reaven
Journal: Diabetes Care (1989)

Recently, there has been increasing interest toward the liberalization of sucrose in the diets of individuals with non-insulin-dependent diabetes mellitus (NIDDM). However, there is evidence from several well-controlled prospective studies demonstrating that the consumption of moderate amounts of sucrose may result in hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hypercholesterolemia, and reduced high-density lipoprotein cholesterol concentrations. The fact that not all studies demonstrate these deleterious effects does not negate the positive data. The magnitude of the deleterious effects will probably vary with individual patients, baseline status, and amount of sucrose. Because these metabolic abnormalities are most disturbed in diabetes and are associated with increased risk of coronary artery disease, it would seem reasonable to continue to advise patients with NIDDM to limit sucrose consumption, at least until available data would allow us to predict in which individuals and at what level of sucrose consumption these adverse metabolic effects would not be present.
Diabetic intestinal growth adaptation and glucagon-like peptide 2 in the rat: effects of dietary fibre
Authors: J Thulesen, B Hartmann, C Nielsen, J J Holst, S S Poulsen
Journal: Gut (1999)

<h3>BACKGROUND/AIMS</h3> Dietary fibre influence growth and function of the upper gastrointestinal tract. This study investigates the importance of dietary fibre in intestinal growth in experimental diabetes, and correlates intestinal growth with plasma levels of the intestinotrophic factor, glucagon-like peptide 2 (GLP-2). <h3>METHODS</h3> Male Wistar rats were randomised to the following groups: two streptozotocin-diabetic and two control groups fed either a fibre-containing or a fibre-free diet for three weeks. Intestinal weight, length, and morphometric data (villus height, villus area, crypt depth) were measured. Blood samples were obtained after two weeks for measurement of GLP-2 and enteroglucagon (glicentin, oxyntomodulin). <h3>RESULTS</h3> The mean daily consumption of food in the two diabetic groups was 40% higher than in controls. In diabetic rats fed fibre, the increase in intestinal weight from day 0 to 20 was sixfold greater than that of the controls and small intestine weight per cm length was increased by 50%. In the diabetic rats fed a fibre-free diet, intestinal growth was 30% less than in diabetic rats fed fibre, and intestinal weight increased only threefold compared with controls. Morphometric data showed that the intestinal increase in diabetic rats fed fibre was due primarily to growth of the mucosal layer. Villus height and crypt depth increased 60% and 40% respectively, but by only 20% in fibre-free diabetic rats. The plasma levels of GLP-2 parallelled diabetic intestinal growth, whereas plasma levels of enteroglucagon increased regardless of the extent of intestinal growth. <h3>CONCLUSIONS</h3> Intestinal growth in experimental diabetes is strongly influenced by the presence of dietary fibre. The effect may be mediated by GLP-2.
LYMPHOCYTE ACTIVATION IN SUBACUTE SCLEROSING PANENCEPHALITIS VIRUS AND CYTOMEGALOVIRUS INFECTIONS
Authors: G. B. Thurman, A. Ahmed, D. M. Strong, R. C. Knudsen, W. R. Grace, K. W. Sell
Journal: The Journal of Experimental Medicine (1973)

Efforts to stimulate lymphocytes from measles seropositive and two patients with subacute sclerosing panencephalitis (SSPE) with either commercially available measles virus or virus isolated from a known case of SSPE failed to show any significant data using a microculture assay. Similar results were obtained using lymphocytes from two patients with active cytomegalovirus (CMV) infections and CMV seropositive individuals using CMV suspensions. On the other hand, lymphocytes from the patients with subacute sclerosing panencephalitis exhibited in vitro blastogenesis in culture with SSPE virus-infected HeLa cells. Similarly, lymphocytes from the CMV-infected patients demonstrated blastogenesis when cocultivated with CMV-infected WI-38 cells. This affords a new method for determining the cell-mediated immune capacity of patients with "slow" virus diseases.
Ventilator modes and settings during non-invasive ventilation: effects on respiratory events and implications for their identification
Authors: C. Rabec, D. Rodenstein, P. Leger, S. Rouault, C. Perrin, J. Gonzalez-Bermejo
Journal: Thorax (2010)

Compared with invasive ventilation, non-invasive ventilation (NIV) has two unique characteristics: the non-hermetic nature of the system and the fact that the ventilator-lung assembly cannot be considered as a single-compartment model because of the presence of variable resistance represented by the upper airway. When NIV is initiated, the ventilator settings are determined empirically based on a clinical evaluation and diurnal blood gas variations. However, NIV is predominantly applied during sleep. Consequently, to assess overnight patient–machine ‘agreement’ and efficacy of ventilation, more specific and sophisticated monitoring is needed. The effectiveness of NIV might therefore be more correctly assessed by sleep studies than by daytime assessment. The most available and simple monitoring can be done from flow and pressure curves from the mask or the ventilator circuit. Examination of these tracings can give useful information to evaluate if the settings chosen by the operator were the right ones for that patient. However, as NIV allows a large range of ventilatory parameters and settings, it is mandatory to have information about this to better understand patient–ventilator interaction. Ventilatory modality, mode of triggering, pressurisation slope, use or not of positive end expiratory pressure and type of exhalation as well as ventilator performances may all have physiological consequences. Leaks and upper airway resistance variations may, in turn, modify these patterns. This article discusses the equipment available for NIV, analyses the effect of different ventilator modes and settings and of exhalation and connecting circuits on ventilatory traces and gives the background necessary to understand their impact on nocturnal monitoring of NIV.
What's hot that the other lot got
Authors: Kathryn Prior
Journal: Thorax (2015)

By age 5 years, 50–70% of children with CF have bronchiectasis. This longitudinal study undertook a CT and BAL on 78 children diagnosed with CF on the newborn screening test aged 3 months, 1 year, 2 years and 3 years when clinically stable ( N Engl J Med 2013;368:1963–70). They showed that persistent free neutrophil elastase activity in the BAL at 3 months was predictive of persistent bronchiectasis at 12 months and at 3 years of age.

This national lung screening trial allocated smokers with a 30 pack year history to yearly screening with either low dose CT or chest radiography ( N Engl J Med 2013;368:1980–91). All nodules >4 mm in the axial plane were considered to be positive on CT and on CXR all non-calcified nodules or masses were considered to be positive. In the CT group 27.3% versus 9.2% in the CXR group had a positive screening result. In the CT group 6369 had at least one diagnostic …
Cytokine mRNA expression in intestinal tissue of interleukin-2 deficient mice with bowel inflammation
Authors: I B Autenrieth, N Bucheler, E Bohn, G Heinze, I Horak
Journal: Gut (1997)

Background —Mice deficient in interleukin-2 (IL-2) develop inflammatory bowel disease resembling ulcerative colitis in humans. Recent studies provided evidence that αβ T cells, particularly CD4 T cells, rather than B cells, are involved in the pathogenesis of bowel inflammation of IL-2 deficient mice. Aim —To analyse the pattern of expression of cytokine mRNA in intestinal tissue of normal and IL-2 deficient mice. Methods —Expression of β-actin, IL-1α, IL-1β, IL-6, IL-10, tumour necrosis factor α (TNF-α), interferon γ (IFN-γ) and transforming growth factor β1 (TGF-β1) mRNA was analysed in colon and small intestinal tissue of both IL-2 deficient (IL-2−/−) mice and normal (wild type) litter mates (IL-2+/+) at different ages by using qualitative, as well as semiquantitative, competitive reverse transcription polymerase chain reaction (RT-PCR). Results were correlated with the phase of progression of the disease, as determined by histology. Results —IL-2−/− mice had expressed low levels of IL-1α, IL-1β, IL-6, TNF-α, and IFN-γ mRNA in the colon by 1.5 weeks of age. In advance of the development of histologically and clinically detectable bowel inflammation, expression of IL-1α, IL-1β, IL-6, TNF-α, IFN-γ, and IL-10, but not TGF-β1, mRNA increased in the colon of IL-2 deficient mice. In contrast, IL-2+/+ mice expressed TGF-β1 mRNA in colon tissue at 13 and 23 weeks of age, but not IL-1α, IL-1β, IL-6, TNF-α, IL-10, or IFN-γ mRNA. Levels of expression of cytokine mRNA in tissue from the small intestine were comparable in IL-2−/− and IL-2+/+ mice. Conclusions —Bowel inflammation in IL-2 deficient mice is preceded by an increase in IL-1α, IL-1β, TNF-α, and IFN-γ mRNA expression in colon tissue. Low levels of TGF-β1, but high levels of IL-1α, IL-1β, IL-6, TNF-α, IFN-γ, and IL-10 mRNA expression correlate with the manifestation of severe colitis, and suggest that T cells and macrophages are involved in bowel inflammation of IL-2 deficient mice.
Morphologic Parameters Relevant for Visual Outcome During Anti-Angiogenic Therapy of Neovascular Age-Related Macular Degeneration
Authors: Christian Simader, Markus Ritter, Matthias Bolz, Gabor G Deák, Ulrike Mayr-Sponer, Isabelle Golbaz, Michael Kundi, Ursula M Schmidt-Erfurth
Journal: Ophthalmology (2014)
Oral rivaroxaban versus enoxaparin with vitamin K antagonist for the treatment of symptomatic venous thromboembolism in patients with cancer (EINSTEIN-DVT and EINSTEIN-PE): a pooled subgroup analysis of two randomised controlled trials
Authors: Martin H Prins, Anthonie W A Lensing, Tim A Brighton, Roger M Lyons, Jeffrey Rehm, Mila Trajanovic, Bruce L Davidson, Jan Beyer-Westendorf, Ákos F Pap, Scott D Berkowitz, Alexander T Cohen, Michael J Kovacs, Philip S Wells, Paolo Prandoni
Journal: The Lancet Haematology (2014)
Matriptase-2 Inhibits Breast Tumor Growth and Invasion and Correlates with Favorable Prognosis for Breast Cancer Patients
Authors: Christian Parr, Andrew J. Sanders, Gaynor Davies, Tracey Martin, Jane Lane, Malcolm D. Mason, Robert E. Mansel, Wen G. Jiang
Journal: Clinical Cancer Research (2007)

Abstract Purpose: The type II transmembrane serine proteases are cell surface proteolytic enzymes that mediate a diverse range of cellular functions, including tumor invasion and metastasis. Matriptase (matriptase-1) and matriptase-2 belong to the type II transmembrane serine protease family. Matriptase-1 is known to play a role in breast cancer progression, and elevated levels of matriptase-1 correlate with poor patient outcome. The role of matriptase-2 and its cellular function in cancer is unknown. This study aimed to provide new insights into the significance of matriptase-2 in cancer. Experimental Design: Matriptase-2 expression levels were assessed in a cohort of human breast cancer specimens (normal, n = 34; cancer, n = 95), in association with patient clinical variables, using both quantitative and qualitative analysis of the matriptase-2 transcript along with immunohistochemical techniques. Matriptase-2 was also experimentally overexpressed in the MDA-MB-231 human breast cancer cell line. The effects of matriptase-2 overexpression were examined through a series of in vitro and in vivo studies. Results: Here, we show that reduced matriptase-2 levels in breast cancer tissues correlate with an overall poor prognosis for the breast cancer patient. This study also reveals that matriptase-2 overexpression in breast cancer cells significantly suppressed tumorigenesis in CD1 athymic mice (P = 0.000003). Furthermore, we report that matriptase-2 overexpression dramatically reduced the invasive (P = 0.0001) and migratory properties (P = 0.01) of the breast cancer cells. Conclusions: Matriptase-2 suppresses breast tumor development in vivo, displays prognostic value for breast cancer patients, inhibits both breast cancer cell invasion and motility in vitro, and may play a contrasting role to matriptase-1 in breast cancer.
More Evidence That Unnecessary Antenatal Treatments Cause Harm
Authors: Sarah J. Stock, Matthew W. Kemp
Journal: JAMA Pediatrics (2014)

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Referral of Patients with Cancer for Participation in Randomized Clinical Trials: Ethical Considerations
Authors: R. J. Levine
Journal: CA A Cancer Journal for Clinicians (1986)

Physicians with patients with cancer may be faced with two conflicting ethical obligations. One is to contribute to the advancement of scientific knowledge. Among the ways available to respond to this duty is to refer patients for participation in RCTs. The second obligation is to serve the health interests of the individual patient. When these two duties conflict, the latter obligation to the individual takes priority. In the words of the Declaration of Helsinki, "Concern for the interests of the subject (patient) must always prevail over the interests of science and society." Quite often there is no conflict. The patient can pursue his or her health interests most effectively by enrollment in an RCT. In such cases, the referring physician can contribute to the success of the patient's participation in the RCT by explaining what the patient can expect to experience as a patient-subject. It is usually important to explain that referral does not necessarily entail severing the original doctor-patient relationship.