tbuckley/cabot-search huggingface dataset:
Immunohistochemical identification of interleukin 1α and β in human eccrine sweat-gland apparatus
Authors: S. REITAMO, HELI S.I. ANTTILA, LILIANE DIDIERJEAN, J-H. SAURAT
Journal: British Journal of Dermatology (1990)

Journal Article Immunohistochemical identification of interleukin 1α and β in human eccrine sweat‐gland apparatus Get access S. REITAMO, S. REITAMO Department of Dermatology, Helsinki University Central Hospital, Helsinki, Finland Dr S.Reitamo, Department of Dermatology, Helsinki Utiiversity Central Hospital, Snellmanin‐katu 14, 00170 Helsinki, Finland. Search for other works by this author on: Oxford Academic Google Scholar HELI S.I. ANTTILA, HELI S.I. ANTTILA Department of Dermatology, Helsinki University Central Hospital, Helsinki, Finland Search for other works by this author on: Oxford Academic Google Scholar LILIANE DIDIERJEAN, LILIANE DIDIERJEAN Department of Dermatology, Hôspital Cantonal Universitaire, Geneva, Switzerland Search for other works by this author on: Oxford Academic Google Scholar J‐H. SAURAT J‐H. SAURAT Department of Dermatology, Hôspital Cantonal Universitaire, Geneva, Switzerland Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 122, Issue 3, 1 March 1990, Pages 315–323, https://doi.org/10.1111/j.1365-2133.1990.tb08279.x Published: 01 March 1990
Mode of action of parathyroid hormone and cyclic adenosine 3′,5′-monophosphate on renal tubular phosphate reabsorption in the dog
Authors: Zalman S. Agus, Jules B. Puschett, Dorothy Senesky, Martin Goldberg
Journal: Journal of Clinical Investigation (1971)

To evaluate the effects of parathyroid hormone and cyclic adenosine monophosphate on proximal tubular sodium and phosphate reabsorption, micropuncture studies were performed on dogs that received a highly purified preparation of parathyroid hormone (PTH), dibutyryl cyclic 3',5'-adenosine monophosphate (cyclic AMP), 5'-AMP, and saline. PTH resulted in a 30-40% inhibition of sodium and phosphate reabsorption in the proximal tubule unassociated with a rise in either total kidney or single nephron glomerular filtration rate (GFR). The bulk of the phosphate rejected proximally was excreted in the final urine while sodium excretion rose minimally despite the marked proximal inhibition, consistent with the presence of reabsorptive sites in the distal nephron for sodium but not phosphate. The infusion of dibutyryl cyclic AMP either systemically or directly into the renal artery inhibited proximal sodium and phosphate reabsorption in the absence of changes in either total kidney or single nephron GFR, resembling the effects of PTH quantitatively and qualitatively. In contrast, another adenine nucleotide, 5'-AMP, did not inhibit the reabsorption of either sodium or phosphate. These observations support the thesis that renal effects of PTH are mediated via stimulation of renal cortical adenyl cyclase. The infusion of a moderate saline load, 25 ml/kg, also produced a similar inhibition of proximal tubular fractional sodium and phosphate reabsorption with a marked phosphaturia but only minimal natriuresis. Thus, changes in sodium and phosphate reabsorption occur in parallel in the proximal tubule when sodium reabsorption is inhibited either with volume expansion or with administration of "specific" phosphaturic agents such as PTH or cyclic AMP. These data are consistent with the thesis that phosphate reabsorption is dependent upon proximal tubular sodium reabsorption wherein the phosphaturic effect of PTH might be the result of a primary inhibition of proximal tubular sodium reabsorption mediated by adenyl cyclase stimulation.
Specific IgG4 responses during chronic and transient antigen exposure in aspergillosis.
Authors: J F Tomee, A E Dubois, G H Koëter, F Beaumont, T S van der Werf, H F Kauffman
Journal: American Journal of Respiratory and Critical Care Medicine (1996)

The factors that lead to increased production of specific IgG subclasses are still largely unknown. Recent studies suggest that increased IgG4 responses may be related to prolonged antigen exposure. We present data showing that increased IgG4 responses are found under conditions of chronic exposure to Aspergillus fumigatus (Af) antigen. IgG(total), IgG subclass, and IgE responses were studied using ELISA, CAP-FEIA, and immunoblotting techniques in patients with pulmonary aspergilloma (PA), which is a model for chronic antigen exposure, and allergic bronchopulmonary aspergillosis (ABPA), characterized by transient antigen exposure. Af-IgG1 was increased in patients with PA compared with those with ABPA. Patients with PA and IgE responses to Af and/or other inhalant allergens showed significantly higher Af-IgG4 responses than did patients with PA and negative IgE responses or patients with ABPA. Surveillance studies over time in individual patients showed concordance in Af-IgG1 and Af-IgG4 responses. Both Af-IgG1 and Af-IgG4 levels followed the course of disease progression and treatment. Immunoblotting revealed correlations between Af-IgG1 and Af-IgG4 binding to most, but not all, antigenic Af components. This study documents for the first time increased IgG4 levels under conditions of chronic exposure to fungal antigen in PA. Furthermore, a significantly higher IgG4 response was found in those patients with PA who produced IgE. The transient exposure to Af antigen during exacerbation of ABPA gives rise to transient elevations in IgG4 levels.
Ursodeoxycholic acid as adjunctive therapy for problematic type 1 autoimmune hepatitis: A randomized placebo-controlled treatment trial
Authors: Albert J. Czaja, Herschel A. Carpenter, Keith D. Lindor
Journal: Hepatology (1999)

To evaluate the efficacy of ursodeoxycholic acid as adjunctive therapy in type 1 autoimmune hepatitis, 37 patients who had experienced treatment failure, repeated relapse, or incomplete response were randomized to ursodeoxycholic acid (13-15 mg/kg daily) or placebo for 6 months in addition to their usual corticosteroid schedule. Serum aspartate transaminase (70% vs.31%, P = .04) and alkaline phosphatase (47% vs. 7%, P = .02) levels improved more commonly in the 21 patients randomized to ursodeoxycholic acid. Mean serum levels, however, were similar before and after the treatment period. The frequency of dose reduction or corticosteroid withdrawal was comparable in both groups (29% versus 31%, P &gt;.9), and clinical improvement (48% vs. 44%, P &gt;.9)orits absence (52% vs. 56%, P &gt; .9) occurred as commonly in patients receiving ursodeoxycholic acid or placebo.The modifed histological activity score (3.5 ± 0.8 vs. 3.5 ± 0.9)and the modified fibrosis score (2.4 ± 0.4 vs. 2.4 ± 0.4)were similar before and after treatment with ursodeoxycholic acid and no different than after placebo therapy.We conclude that ursodeoxycholic acid can improve certain laboratory tests in problematic patients with type 1 autoimmune hepatitis when administered adjunctively for 6 months. Short-term therapy, however, does not facilitate reduction in the dose of corticosteroids or its withdrawal, affect clinical outcome, or reduce histological activity.
Macrophage enrichment from induced sputum
Authors: Liv I B Sikkeland, Johny Kongerud, Astrid M Stangeland, Terje Haug, Neil E Alexis
Journal: Thorax (2007)

Since induced sputum has become a widely used non-invasive method of recovering cells from the surfaces of the bronchial airways, isolating specific cell populations will be necessary in order to learn more about their specific role in innate immunity and inflammation in the airways. Several studies have demonstrated the ability to conduct ex vivo analyses on sputum cells such as phagocytosis and surface marker measurements, but these have not been performed on isolated cell types.1–3 This study demonstrates the capability to isolate sputum macrophages from human volunteers in order to advance our understanding of macrophage biology in the airways. To this end, techniques that can enrich and isolate cells without significant activation would prove extremely useful. We compared two common methods for isolating and enriching macrophages in sputum: (1) magnetic bead separation; and (2) Percoll gel density gradient centrifugation. Cell purity and markers of cell activation (mRNA tumour necrosis factor α (TNFα)) …
AML1-ETO Inhibits Maturation of Multiple Lymphohematopoietic Lineages and Induces Myeloblast Transformation in Synergy with ICSBP Deficiency
Authors: Maike Schwieger, Jürgen Löhler, Jutta Friel, Marina Scheller, Ivan Horak, Carol Stocking
Journal: The Journal of Experimental Medicine (2002)

The translocation (8;21), generating the AML1-ETO fusion protein, is one of the most frequent chromosomal abnormalities associated with acute myelogenous leukemia (AML). To elucidate its role in oncogenesis, bone marrow (BM) cells were infected with a retroviral vector carrying AML1-ETO and transplanted into mice. In contrast to previous transgenic mouse models, we show that AML1-ETO directly stimulates granulopoiesis, suppresses erythropoiesis, and impairs the maturation of myeloid, B, and T lymphoid cells in vivo. To determine the significance of earlier findings that expression of the tumor suppressor ICSBP is often downregulated in AML myeloblasts, AML1-ETO was introduced into BM cells derived from mice lacking the interferon regulatory factor ICSBP. Our findings demonstrate that AML1-ETO synergizes with an ICSBP deficiency to induce myeloblastic transformation in the BM, reminiscent of AML.
Effect of caffeine on expression of cardiac myosin heavy chain gene in adult hypothyroid and fetal rats.
Authors: S Imamura, M Kimura, E Hiratsuka, A Takao, R Matsuoka
Journal: Circulation Research (1992)

Changes in cardiac myosin heavy chain (MHC) gene expression and isozyme transitions have been shown to be caused by developmental changes, hemodynamic overload, or the activity of various hormones. In this study, to examine whether caffeine, which has teratogenic effects on the fetal cardiovascular system, causes the distribution of cardiac MHC phenotype and, if so, to evaluate the mechanisms of the distribution of cardiac MHC phenotype by caffeine, we examined the effects of caffeine, theophylline, and cAMP on the cardiac MHC isoform transitions at the gene and protein levels using hypothyroid adult rats. Furthermore, we examined the expression of alpha- and beta-MHC gene in cardiac muscles of fetuses whose dams had received caffeine. The results showed that caffeine, theophylline, and cAMP caused accumulations of alpha-MHC mRNA and MHC isozyme V1. Furthermore, in the fetal hearts, it was recognized that caffeine induced an accumulation of alpha-MHC gene expression, as was also seen in the dams. However, this effect of caffeine on the heart was stronger in the fetus than in the dam. Intracellular cAMP concentration was increased by the administration of caffeine, theophylline, or cAMP, and the levels showed a positive correlation with those of alpha-MHC mRNA. These results suggest that the induction of alpha-MHC mRNA expression by the administration of caffeine may be induced by an increase in intracellular cAMP concentration.
Effect of intracoronary nitroglycerin administration on phasic pattern and transmural distribution of flow during coronary artery stenosis.
Authors: M Goto, A E Flynn, J W Doucette, A Kimura, O Hiramatsu, T Yamamoto, Y Ogasawara, K Tsujioka, J I Hoffman, F Kajiya
Journal: Circulation (1992)

BACKGROUND Nitroglycerin is effective in relieving myocardial ischemia; however, intracoronary nitroglycerin often fails to relieve angina and has been reported to have deleterious effects on subendocardial blood flow. To understand the mechanisms involved, we evaluated the direct effect of nitroglycerin on coronary circulation of the ischemic hearts. METHODS AND RESULTS We measured the phasic pattern of intramyocardial coronary arterial flow with an 80-channel, 20-MHz pulsed Doppler ultrasound flowmeter under moderate to severe coronary artery stenosis (distal perfusion pressure approximately 45 mm Hg group 1, n = 6) and transmyocardial blood flow distribution using radioactive microspheres while maintaining coronary pressure at a low constant level (40 mm Hg, group 2, n = 6). In anesthetized open-chest dogs, the left main coronary artery was perfused directly from the right carotid or femoral artery. In this bypass circuit, pressure was controlled with an occluder or a reservoir was connected to the circuit. In group 1, the systolic and diastolic pressures distal to the stenosis decreased significantly after intracoronary administration of nitroglycerin at maximal coronary flow from 66.5 +/- 18.5 to 56.5 +/- 13.8 mm Hg (p less than 0.01) and from 36.6 +/- 14.4 to 27.5 +/- 8.9 mm Hg (p less than 0.01), respectively. The phasic pattern of the septal artery flow was predominantly diastolic and was characterized by systolic reverse flow even in the absence of stenosis. Coronary stenosis increased systolic reverse flow. Nitroglycerin increased diastolic forward flow (p less than 0.05) but augmented systolic reverse flow markedly (p less than 0.001). In group 2, nitroglycerin increased subepicardial flow (p less than 0.05) but failed to increase subendocardial flow. With the administration of nitroglycerin, the subendocardial-to-subepicardial flow ratio decreased significantly from 0.73 +/- 0.19 to 0.32 +/- 0.14 (p less than 0.01). CONCLUSIONS The increased systolic reverse flow after intracoronary administration of nitroglycerin may be closely related to failure of subendocardial blood flow to increase with increase subepicardial flow.
Genome-wide analysis identifies a functional association of Tet1 and Polycomb repressive complex 2 in mouse embryonic stem cells
Authors: Francesco Neri, Danny Incarnato, Anna Krepelova, Stefania Rapelli, Andrea Pagnani, Riccardo Zecchina, Caterina Parlato, Salvatore Oliviero
Journal: Genome biology (2013)

Ten-Eleven Translocation (TETs)proteins mediate the oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). Tet1 is expressed at high levels in mouse embryonic stem cells (ESCs), where it mediates the induction of 5hmC decoration on gene-regulatory elements. While the function of Tet1 is known, the mechanisms of its specificity remain unclear.We perform a genome-wide comparative analysis of 5hmC in pluripotent ESCs, as well as in differentiated embryonic and adult cells. We find that 5hmC co-localization with Polycomb repressive complex 2 (PRC2) is specific to ESCs and is absent in differentiated cells. Tet1 in ESCs is distributed on bivalent genes in two independent pools: one with Sin3a centered at non-hydroxymethylated transcription start sites and another centered downstream from these sites. This latter pool of Tet1 co-localizes with 5hmC and PRC2. Through co-immunoprecipitation experiments, we show that Tet1 forms a complex with PRC2 specifically in ESCs. Genome-wide analysis of 5hmC profiles in ESCs following knockdown of the PRC2 subunit Suz12 shows a reduction of 5hmC within promoter sequences, specifically at H3K27me3-positive regions of bivalent promoters.In ESCs, PRC2 recruits Tet1 to chromatin at H3K27me3 positive regions of the genome, with 5hmC enriched in a broad peak centered 455 bp after the transcription start site and dependent on the PRC2 component Suz12. These results suggest that PRC2-dependent recruitment of Tet1 contributes to epigenetic plasticity throughout cell differentiation.
Cardiovascular disease assessment in rheumatoid arthritis: a guide to translating knowledge of cardiovascular risk into clinical practice
Authors: Anne Grete Semb, Silvia Rollefstad, Piet van Riel, George D Kitas, Eric L Matteson, Sherine E Gabriel
Journal: Annals of the Rheumatic Diseases (2014)

As physicians we like to have evidence for making decisions about interventions to improve health. The evidence vacuum in the field of cardiovascular disease (CVD) prevention and clinical outcome in patients with rheumatoid arthritis (RA) has received vigorous attention in the recent literature. There is broad agreement that a patient with RA fulfilling the criteria established for the general population on CVD risk reduction should receive proven interventions, including smoking cessation, weight reduction, blood pressure control and lipid-lowering therapy. In accordance with these recommendations, and despite all the uncertainties about CVD treatment threshold, targets and outcome results in RA, we firmly advocate that CVD risk should be assessed and acted on in patients with RA as recommended for the general population, even while educational CVD-preventive programmes are being developed and hard CVD end point studies are undertaken in this patient population. The initial strategies for implementing CVD risk evaluation will necessarily be modest at first. There are several possible strategies for collection of data that can be incorporated into the daily routine during rheumatology consultations at outpatient clinics. We recommend starting with these simple procedures: 1. CVD risk factor recording and evaluation using risk calculators available for the general population 2. Referral of patients with high CVD risk to a primary care physician or a cardiologist skilled in this subject for follow-up 3. Providing information about excess CVD risk and how to modify it to the patients as major stakeholders.
Orexin Synthesis and Response in the Gut
Authors: Annette L Kirchgessner, Min-tsai Liu
Journal: Neuron (1999)

Orexin (hypocretin) appears to play a role in the regulation of energy balances. Previous reports have indicated that orexin-containing neurons are found only in the lateral hypothalamic (LH) area. We show that a subset of neurons in the gut which also express leptin receptors display orexin-like immunoreactivity and express functional orexin receptors. Orexin excites secretomotor neurons in the guinea pig submucosal plexus and increases motility. Moreover, fasting upregulates the phosphorylated form of cAMP response element–binding protein (pCREB) in orexin-immunoreactive neurons, indicating a functional response to food status in these cells. Together, these data suggest that orexin in the gut may play an even more intimate role in regulating energy homeostasis than it does in the CNS.
Alterations in γ-Actin and Tubulin-Targeted Drug Resistance in Childhood Leukemia
Authors: Nicole M. Verrills, Sela T. Po'uha, Marjorie L. M. Liu, Tracy Y. E. Liaw, Martin R. Larsen, Michael T. Ivery, Glenn M. Marshall, Peter W. Gunning, Maria Kavallaris
Journal: JNCI Journal of the National Cancer Institute (2006)

Background: Proteomic investigations have revealed alterations in cytoskeletal proteins expressed in human acute lymphoblastic leukemia cells that are resistant to microtubule-disrupting agents. We characterized γ-actin expression in antimicrotubule drug–resistant leukemia and examined the effect of altered γ-actin in resistance of acute lymphoblastic leukemia to antimicrotubule agents. Methods: Two-dimensional polyacrylamide gel electrophoresis and mass spectrometry were used to identify actin proteins in human acute lymphoblastic leukemia cell lines resistant to vinblastine (CCRF-CEM/VLB100 cells) and desoxyepothilone B (CCRF-CEM/dEpoB140 cells). Fluorescence-based cycle sequencing was used to detect gene mutations. Site-directed mutagenesis was used to generate mutant γ-actin expression plasmids, which were used to transfect mouse NIH/3T3 cells. Clonogenic analysis was used for drug sensitivity studies. A small interfering RNA (siRNA) was used to block γ-actin gene expression in human neuroblastoma SH-EP cells. Expression of γ-actin (normalized to that of β 2 -microglobulin [β 2 M]) in primary leukemia cells obtained from patients at diagnosis (n = 44) and relapse (n = 25) was examined using semiquantitative reverse transcription–polymerase chain reaction. Statistical significance of changes in the ratio of γ-actin to β 2 M expression between diagnosis and relapse samples was determined by two-sided unpaired Student's t tests. Results: We identified novel mutant forms of γ-actin and the concomitant loss of wild-type γ-actin in CCRF-CEM/VLB100 cells and CCRF-CEM/dEpoB140 cells. Mouse NIH/3T3 cells that expressed the mutant γ-actin proteins were more resistant to antimicrotubule agents than cells transfected with empty plasmid. Human neuroblastoma SH-EP cells transfected with γ-actin siRNA displayed higher relative resistance to paclitaxel ( P <.001), vinblastine ( P = .04), and epothilone B ( P = .045) than mock-transfected cells. No γ-actin gene mutations were identified in 37 samples of primary leukemia cells (eight from patients at diagnosis, 29 from patients at relapse). γ-Actin gene expression was lower in acute lymphoblastic leukemia samples collected at clinical relapse (n = 25; mean γ-actin/β 2 M = 0.53) than in samples collected at diagnosis (n = 44; mean γ-actin/β 2 M = 0.68; difference = 0.15, 95% confidence interval [CI] = 0.04 to 0.27, P = .01). Conclusions: These data provide functional and associative clinical evidence of a novel form of drug resistance that involves interactions between γ-actin and microtubules.
Tuberculosis in HIV-infected persons in the context of wide availability of highly active antiretroviral therapy
Authors: E. Girardi, G. Antonucci, P. Vanacore, F. Palmieri, A. Matteelli, E. Iemoli, S. Carradori, B. Salassa, M. Bruna Pasticci, M.C. Raviglione, G. Ippolito
Journal: European Respiratory Journal (2004)

Highly active antiretroviral therapy (HAART) greatly reduces the risk of developing tuberculosis for HIV‐infected persons. Nonetheless, HIV‐associated tuberculosis continues to occur in countries where HAART is widely used. To identify the characteristics of HIV‐infected persons who develop tuberculosis in the context of the availability of HAART, the current authors analysed data taken from 271 patients diagnosed, in Italy, during 1999–2000. These patients represent 0.7% of the 40,413 HIV‐infected patients cared for in the clinical units participating in this current study. From the data it was observed that 20 patients (7.4%) had a previous episode of tuberculosis whose treatment was not completed. Eighty-one patients (29.9%) were diagnosed with HIV at tuberculosis diagnosis, 108 (39.8%) were aware of their HIV status but were not on antiretroviral treatment and 82 (30.3%) were on antiretroviral treatment. Patients on antiretroviral treatment were significantly less immunosuppressed than patients with HIV diagnosed concurrently with tuberculosis, or other patients not on antiretrovirals (median CD4 lymphocytes count: 220 cells·mm −3 versus 100 cells·mm −3 , and 109 cells·mm −3 , respectively). No significant differences in clinical presentation of tuberculosis according to antiretroviral therapy status were recorded. Failure of tuberculosis control interventions ( e.g. noncompletion of treatment) and of HIV care (delayed diagnosis of HIV infection and suboptimal uptake of therapy) may contribute to continuing occurrence of HIV‐associated tuberculosis in a country where highly active antiretroviral therapy is largely available. However, a significant proportion of cases occur in patients who are on antiretroviral treatment.