tbuckley/cabot-search huggingface dataset:
L-Selectin Facilitation of Metastasis Involves Temporal Induction of<i>Fut7</i>-Dependent Ligands at Sites of Tumor Cell Arrest
Authors: Heinz Läubli, Jennifer L. Stevenson, Ajit Varki, Nissi M. Varki, Lubor Borsig
Journal: Cancer Research (2006)

Abstract Hematogenous carcinoma metastasis is supported by aggregated platelets and leukocytes, forming tumor cell emboli. Early tumor cell-platelet interactions can be mediated by P-selectin binding to tumor cell surface ligands and this process is blocked by heparin. We previously showed that L-selectin deficiency also attenuates experimental metastasis. However, the mechanisms and timing of L-selectin action remained unknown. Here, we study how L-selectin facilitates establishment of pulmonary metastatic foci in syngeneic mice by using experimental metastasis to time events following entry of tumor cells into the bloodstream. Although L-selectin deficiency did not affect platelet aggregation or initial tumor cell embolization, the association of leukocytes with tumor cells was reduced and tumor cell survival was diminished 24 hours later. Temporal inhibition of L-selectin by a function-blocking antibody reduced metastasis. Moreover, although selectin blockade by heparin 6 to 18 hours after tumor cell injection was synergistic with P-selectin deficiency in reducing metastasis, there was no further effect in L-selectin-deficient animals. Thus, heparin apparently works at these time points primarily by blocking L-selectin. Endogenous L-selectin ligands were concomitantly induced adjacent to established intravascular tumor cell emboli in a similar time window when leukocytes were also present. Metastasis was attenuated in mice missing these induced endogenous L-selectin ligands due to fucosyltransferase-7 deficiency. Thus, L-selectin facilitation of metastasis progression involves leukocyte-endothelial interactions at sites of intravascular arrest supported by local induction of L-selectin ligands via fucosyltransferase-7. These data provide the first explanation for how leukocyte L-selectin facilitates tumor metastasis. (Cancer Res 2006; 66(3): 1536-42)
Glucocorticoids inhibit activation-induced cell death (AICD) via direct DNA-dependent repression of the CD95 ligand gene by a glucocorticoid receptor dimer
Authors: Sven Baumann, Anja Dostert, Natalia Novac, Anton Bauer, Wolfgang Schmid, Stefanie C. Fas, Andreas Krueger, Thorsten Heinzel, Sabine Kirchhoff, Günther Schütz, Peter H. Krammer
Journal: Blood (2005)
Identification and characterization of specific receptors for monocyte-derived neutrophil chemotactic factor (MDNCF) on human neutrophils.
Authors: A K Samanta, J J Oppenheim, K Matsushima
Journal: The Journal of Experimental Medicine (1989)

Specific receptors for a recently purified and cloned monocyte-derived neutrophil chemotactic factor (MDNCF) have been identified on the surface of normal human peripheral blood neutrophils using 125I-labeled recombinant human MDNCF (125I-MDNCF). Competitive binding of 125I-MDNCF to human neutrophils reached a maximal level at 1-3 h at 4 degrees C. The Scatchard analysis showed that there are approximately 20,000 receptors per cell with a single type of high affinity binding (Kd, 8 x 10(-10) M). The receptors for MDNCF are clearly distinct from the receptors for other cytokines and chemotactic agents, e.g., IL-1 alpha, TNF-alpha, and FMLP, C5a, leukotriene B4, and platelet activating factor. Based on the SDS-PAGE analysis of chemically crosslinked 125I-MDNCF receptor complex, there are two polypeptides that bind MDNCF; the molecular weight of these two MDNCF receptors were estimated to be 67,000 and 59,000. Treatment of a promyelocytic cell line, HL60, with 1.25% DMSO for 5 d in vitro increased the number of receptors up to 7,000 receptors/cell with a Kd of 1.2 x 10(-9) M.
Atopic asthma caused by <i>Candida albicans</i> acid protease: case reports
Authors: K. Akiyama, T. Shida, H. Yasueda, H. Mita, T. Yamamoto, H. Yamaguchi
Journal: Allergy (1994)

Two cases of atopic asthma caused by acid protease produced by Candida albicans are reported. Both patients had high levels of serum IgE antibodies against the acid protease and showed positive conjunctival and immediate bronchial responses when challenged with the protease. Significant histamine release was detected in both patients when their peripheral leukocytes were challenged with the protease antigen. These findings clearly showed that C. albicans acid protease is the causative allergen of atopic asthma.
Demonstration of 26-hydroxylation of C27-steroids in human skin fibroblasts, and a deficiency of this activity in cerebrotendinous xanthomatosis.
Authors: S Skrede, I Björkhem, E A Kvittingen, M S Buchmann, S O Lie, C East, S Grundy
Journal: Journal of Clinical Investigation (1986)

26-Hydroxylation of 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha-triol and other C27-steroids was demonstrated in cultured skin fibroblasts from healthy individuals. Activities in skin fibroblasts were approximately 5-10% of those previously found in human liver homogenates, and were inhibited by CO. The apparent Km was lowest for 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha-triol (1.3 mumol/liter) and highest for 5-cholestene-3 beta, 7 alpha-diol (12 mumol/liter). The rate of 26-hydroxylation was highest with 7 alpha-hydroxy-4-cholesten-3-one. These characteristics are similar to those of hepatic mitochondrial C27-steroid 26-hydroxylase. In skin fibroblasts from three patients with cerebrotendinous xanthomatosis (CTX), 26-hydroxylation of C27-steroids proceeded at a rate of only 0.2-2.5% of healthy controls. No accumulation of endogenous 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha-triol could be demonstrated in these cells, and the lowered formation of radioactive, 26-hydroxylated products could not be explained by dilution of the labeled exogenous substrate. The present results add strong evidence to the concept that the primary metabolic defect in CTX is a deficiency of C27-steroid 26-hydroxylase.
Part 15: Neonatal Resuscitation
Authors: John Kattwinkel, Jeffrey M. Perlman, Khalid Aziz, Christopher Colby, Karen Fairchild, John Gallagher, Mary Fran Hazinski, Louis P. Halamek, Praveen Kumar, George Little, Jane E. McGowan, Barbara Nightengale, Mildred M. Ramirez, Steven Ringer, Wendy M. Simon, Gary M. Weiner, Myra Wyckoff, Jeanette Zaichkin
Journal: Circulation (2010)

Anticipation of Resuscitation NeedAnticipation, adequate preparation, accurate evaluation, and prompt initiation of support are critical for successful neonatal resuscitation.At every delivery there should be at least 1 person whose primary
Oxidative stress inhibits axonal transport: implications for neurodegenerative diseases
Authors: Cheng Fang, Dennis Bourdette, Gary Banker
Journal: Molecular Neurodegeneration (2012)

Reactive oxygen species (ROS) released by microglia and other inflammatory cells can cause axonal degeneration. A reduction in axonal transport has also been implicated as a cause of axonal dystrophies and neurodegeneration, but there is a paucity of experimental data concerning the effects of ROS on axonal transport. We used live cell imaging to examine the effects of hydrogen peroxide on the axonal transport of mitochondria and Golgi-derived vesicles in cultured rat hippocampal neurons.Hydrogen peroxide rapidly inhibited axonal transport, hours before any detectable changes in mitochondrial morphology or signs of axonal degeneration. Mitochondrial transport was affected earlier and was more severely inhibited than the transport of Golgi-derived vesicles. Anterograde vesicle transport was more susceptible to peroxide inhibition than retrograde transport. Axonal transport partially recovered following removal of hydrogen peroxide and local application of hydrogen peroxide inhibited transport, suggesting that the effects were not simply a result of nerve cell death. Sodium azide, an ATP synthesis blocker, had similar effects on axonal transport, suggesting that ATP depletion may contribute to the transport inhibition due to hydrogen peroxide.These results indicate that inhibition of axonal transport is an early consequence of exposure to ROS and may contribute to subsequent axonal degeneration.
Effect of TNF inhibitors on lipid profile in rheumatoid arthritis: a systematic review with meta-analysis
Authors: Claire Immediato Daïen, Yohan Duny, Thomas Barnetche, Jean-Pierre Daurès, Bernard Combe, Jacques Morel
Journal: Annals of the Rheumatic Diseases (2012)

Patients with rheumatoid arthritis (RA) are at increased risk of cardiovascular disease. Lipid changes related to inflammation have been described in RA. Tumour necrosis factor α (TNFα) inhibitor (TNFi) treatment is effective in controlling inflammation and decreasing the number of cardiovascular events.To assess the change in lipid levels with TNFi treatment in patients with RA by systematic review and meta-analysis.A Medline search was performed for articles published up to March 2011. Reports describing values for total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides (TGs), atherogenic index (AI) and apolipoprotein B/A (apoB/A) collected before and after TNFi initiation were included. Data were analysed according to short-, mid- and long-term treatment. Statistical analysis of pre-post data was performed by comprehensive meta-analysis. A random effects model was used when there was evidence of heterogeneity.The search retrieved 32 articles, of which 13 prospective before/after studies were analysed. Long-term TNFi treatment was associated with increased levels of HDL (+0.27 mmol/l, p<0.0001) and TC (+0.27 mmol/l, p=0.03), whereas LDL levels and AI remained unchanged. After long-term treatment, TG levels increased (+0.28 mmol/l, p<0.001) and apoB/A decreased (-0.3, p<0.0001).The presumed cardioprotective effects of TNFi in RA do not seem to be explained by quantitative lipid changes since long-term treatment has no effect on LDL levels or on AI. Increased HDL levels could have some beneficial effects, but this needs to be confirmed by prospective studies with long-term follow-up.
Respiratory performance and grip strength tests in Indian school bodys of different socio-economic status.
Authors: A. K. De, P. K. Debnath, N. K. Dey, J. Nagchaudhuri
Journal: British Journal of Sports Medicine (1980)

Physical efficiency tests were performed on urban school boys drawn from high socio-economic status in comparison to rural school boys. The height and weight records of the subjects indicating growing process showed that the rural boys attained less physical growth than their urban counterparts. The Vital Capacity and Peak Expiratory Flow Rate data expressed either per unit of height or body surface area were significantly lower in rual boys. these findings indicated a poor development of the thorax in the rural group. However, the determined grip strengths for both the group were similar. The grip test might reflect improvement of muscle mass in case of rural boys as a result of regular physical activity employing the arm muscles.
Diagnosis of Pheochromocytoma by Assay of Catecholamine Metabolites
Authors: STANLEY E. GITLOW, MILTON MENDLOWITZ, ELIZABETH KRUK, SARAH KHASSIS
Journal: Circulation Research (1961)

Methods for the determination of urinary vanillylmandelic acid (VMA) have been reviewed and variations in VMA excretion in different disease states summarized. The determination of VMA excretion is believed to represent a reliable method for the detection of a pheochromocytoma. Colorimetric screening tests for the detection of elevated VMA excretion have been reviewed and evaluated as laboratory aids in the diagnosis of pheochromocytoma.
Corrigendum to: Targeting atrioventricular differences in ion channel properties for terminating acute atrial fibrillation in pigs
Authors: S. V. Pandit, S. Zlochiver, D. Filgueiras-Rama, S. Mironov, M. Yamazaki, S. R. Ennis, S. F. Noujaim, A. J. Workman, O. Berenfeld, J. Kalifa, J. Jalife
Journal: Cardiovascular Research (2011)

[Cardiovascular Research, Volume 89, Issue 4, 1 March 2011, Pages 843–851; doi:10.1093/cvr/cvq359.]

The published version of this paper contained an error in the Funding section. The second grant number provided should have read PO1-HL087226, rather than PO1-HL070074.
Ability of Mature Dendritic Cells to Interact with Regulatory T Cells Is Imprinted during Maturation
Authors: Ravikumar Muthuswamy, Julie Urban, Je-Jung Lee, Todd A. Reinhart, David Bartlett, Pawel Kalinski
Journal: Cancer Research (2008)

Abstract Preferential activation of regulatory T (Treg) cells limits autoimmune tissue damage during chronic immune responses but can also facilitate tumor growth. Here, we show that tissue-produced inflammatory mediators prime maturing dendritic cells (DC) for the differential ability of attracting anti-inflammatory Treg cells. Our data show that prostaglandin E2 (PGE2), a factor overproduced in chronic inflammation and cancer, induces stable Treg-attracting properties in maturing DC, mediated by CCL22. The elevated production of CCL22 by PGE2-matured DC persists after the removal of PGE2 and is further elevated after secondary stimulation of DC in a neutral environment. This PGE2-induced overproduction of CCL22 and the resulting attraction of FOXP3+ Tregs are counteracted by IFNα, a mediator of acute inflammation, which also restores the ability of the PGE2-exposed DC to secrete the Th1-attracting chemokines: CXCL9, CXCL10, CXCL11, and CCL5. In accordance with these observations, different DCs clinically used as cancer vaccines show different Treg-recruiting abilities, with PGE2-matured DC, but not type 1–polarized DC, generated in the presence of type I and type II IFNs, showing high Treg-attracting activity. The current data, showing that the ability of mature DC to interact with Treg cells is predetermined at the stage of DC maturation, pave the way to preferentially target the regulatory versus proinflammatory T cells in autoimmunity and transplantation, as opposed to intracellular infections and cancer. [Cancer Res 2008;68(14):5972–8]
Chlorpromazine‐induced anticardiolipin antibodies and lupus anticoagulant: Absence of thrombosis
Authors: Rosa T. Canoso, Ricardo M. De Oliveira
Journal: American Journal of Hematology (1988)

Abstract Anticardiolipin antibodies were determined in 96 psychiatric patients treated chronically with chlorpromazine by an enzyme‐linked Immunosorbent assay using anti‐IgM and anti‐IgG (fab'2 fragment) as the second antibody. Fifty‐four of these patients had an IgM‐lupus anticoagulant, and the remaining 42 were followed as controls. Elevated IgM‐anticardiolipin antibodies (ACA) levels were detected in 31 patients with the lupus anticoagulant and in 5 controls (p&lt;0.001). During a median followup of 5 years, single episodes of deep vein thrombosis or pulmonary embolism occurred in three patients; one had the lupus anticoagulant and the other two had low‐level ACA. Contrary to the reported experience in systemic lupus erythematosus and related autoimmune disorders, chlorpromazine‐induced lupus anticoagulant and anticardiolipin antibodies levels appear not to be associated with an increased incidence of thrombosis.
Atrial Fibrillation and Congestive Heart Failure
Authors: Melvin M. Scheinman
Journal: Circulation (1998)

trial fibrillation is the most common sustained cardiac arrhythmia, and congestive heart failure is an increasingly frequent diagnosis as our population tends to age.Appropriate management of these patients has engaged clinicians for many years.It was long appreciated that atrial fibrillation, per se, without associated cardiac disease could result in congestive heart failure and that prompt treatment resulting in either restoration of sinus rhythm or rate control could obviate the signs and symptoms of congestive heart failure. 1-
Selenoproteins and the Metabolic Features of the Archaeal Ancestor of Eukaryotes
Authors: Charles B. Foster
Journal: Molecular Biology and Evolution (2004)

In all three branches of life, some organisms incorporate the rare amino acid selenocysteine. Selenoproteins are relevant to the controversy over the metabolic features of the archaeal ancestor of eukaryotes because among archaea, several known selenoproteins are involved in methanogenesis and autotrophic growth. Although the eukaryotic selenocysteine-specific translation apparatus and at least one selenoprotein appear to be of archaeal origin, selenoproteins have not been identified among sulfur-metabolizing crenarchaeotes. In this regard, both the phylogeny and function of archaeal selenoproteins are consistent with the argument that the archaeal ancestor was a methanogen. Selenium, however, is abundant in sulfur-rich environments, and some anaerobic bacteria reduce sulfur and have selenoproteins similar to those in archaea. As additional archaeal sequence data becomes available, it will be important to determine whether selenoproteins are present in nonmethanogenic archaea, especially the sulfur-metabolizing crenarchaeotes.
Pregnancies, Breast-Feeding, and Breast Cancer Risk in the International BRCA1/2 Carrier Cohort Study (IBCCS)
Authors: Nadine Andrieu, David E. Goldgar, Douglas F. Easton, Matti Rookus, Richard Brohet, Antonis C. Antoniou, Susan Peock, Gareth Evans, Diana Eccles, Fiona Douglas, Catherine Noguès, Marion Gauthier-Villars, Agnès Chompret, Flora E. Van Leeuwen, Irma Kluijt, Javier Benitez, Brita Arver, Edith Olah, Jenny Chang-Claude
Journal: JNCI Journal of the National Cancer Institute (2006)

Multiparity, young age at first childbirth, and breast-feeding are associated with a reduced risk of breast cancer in the general population. The breast cancer predisposition gene, BRCA1, regulates normal cell differentiation. Because mammary gland cells divide and differentiate during pregnancy, reproductive factors may influence breast cancer risk in BRCA1/2 mutation carriers differently than they do in noncarriers.We performed a retrospective cohort study of 1601 women in the International BRCA1/2 Carrier Cohort Study cohort, all of whom carried a mutation in BRCA1 or BRCA2. Information on reproductive factors was obtained from a questionnaire. At the time of interview 853 subjects were classified with breast cancer. Data were analyzed by using a weighted cohort approach. All statistical tests were two-sided.There was no statistically significant difference in the risk of breast cancer between parous and nulliparous women. Among parous women, an increasing number of full-term pregnancies was associated with a statistically significant decrease in the risk of breast cancer (Ptrend = .008); risk was reduced by 14% (95% confidence interval [CI] = 6% to 22%) for each additional birth. This association was the same for carriers of mutations in either BRCA1 or BRCA2 and was restricted to women older than 40 years. In BRCA2 mutation carriers, first childbirth at later ages was associated with an increased risk of breast cancer compared with first childbirth before age 20 years (20-24 years, hazard ratio [HR] = 2.33 [95% CI = 0.93 to 5.83]; 25-29 years, HR = 2.68 [95% CI = 1.02 to 7.07]; > or = 30 years, HR = 1.97 [95% CI = 0.67 to 5.81]), whereas in BRCA1 mutation carriers, first childbirth at age 30 years or later was associated with a reduced risk of breast cancer compared with first childbirth before age 20 years (HR = 0.58 [95% CI = 0.36 to 0.94]). Neither history of interrupted pregnancies (induced abortions or miscarriage) nor history of breast-feeding was statistically significantly associated with the risk of breast cancer.BRCA1 and BRCA2 mutation carriers older than 40 years show a similar reduction in breast cancer risk with increasing parity as non-carriers.
Expression of inducible nitric oxide synthase in human coronary atherosclerotic plaque
Authors: C Depre
Journal: Cardiovascular Research (1999)

Macrophages in atherosclerotic plaque may express the inducible isoform of NO synthase (iNOS), which produces large amounts of NO. On one hand, the production of NO can be protective by its vasodilatory, antiaggregant and antiproliferative effects. On the other hand, the formation of peroxynitrite from NO may favour vasospasm and thrombogenesis. In this study, we investigated whether iNOS is present in human coronary atherosclerotic plaque, and we correlated these data with the clinical instability of the patients.Fragments were retrieved by coronary atherectomy from 24 patients with unstable angina and 12 patients with stable angina. The presence of macrophages, and the production of TNF alpha, iNOS and nitrotyrosine were detected by immunocytochemistry.Macrophage clusters were found in 67% of stable patients and 87% of patients with unstable angina (NS). TNF alpha was expressed in about 50% of cases in both groups. iNOS was not expressed in fragments from stable patients but was found in macrophages from 58% of unstable patients (P < 0.001). The expression of iNOS was associated with the presence of nitrotyrosine residues, a marker of peroxynitrite formation. Expression of iNOS was correlated both with complaints of angina at rest (P < 0.05) and with the presence of thrombus at morphological examination (P < 0.001).The expression of iNOS may be induced in human coronary atherosclerotic plaque and is associated with different factors of instability.
Foresight, function representation, and social intelligence in the great apes
Authors: Mathias Osvath, Tomas Persson, Peter Gärdenfors
Journal: Behavioral and Brain Sciences (2012)

Abstract We find problems with Vaesen's treatment of the primatological research, in particular his analysis of foresight, function representation, and social intelligence. We argue that his criticism of research on foresight in great apes is misguided. His claim that primates do not attach functions to particular objects is also problematic. Finally, his analysis of theory of mind neglects many distinctions.
Sustained Improvement After Combined Anterior Mitral Leaflet Extension and Myectomy in Hypertrophic Obstructive Cardiomyopathy
Authors: Chris van der Lee, Marcel J.M. Kofflard, Lex A. van Herwerden, Willem B. Vletter, Folkert J. ten Cate
Journal: Circulation (2003)

Background— Mitral leaflet extension (MLE) combined with septal myectomy is a new surgical approach to treat hypertrophic obstructive cardiomyopathy (HOCM) and an enlarged mitral leaflet area. The study presents the long-term clinical results and outcome of this technique. Methods and Results— MLE entails grafting a glutaraldehyde-preserved autologous pericardial patch onto the center portion of the anterior mitral valve leaflet. Twenty-nine patients with HOCM were studied. Mean follow-up (±SD) was 3.4±2.1 years (range 3 months to 7.7 years). The preoperative calculated mitral leaflet area was 16.7±3.4 cm 2 . New York Heart Association functional class improved significantly from 2.8±0.4 to 1.3±0.4 ( P &lt;0.05), width of the interventricular septum decreased from 23±4 to 17±2 mm ( P &lt;0.05), left ventricular outflow tract gradient decreased from 100±20 to 17±14 mm Hg ( P &lt;0.01), severity of mitral regurgitation graded on a scale from 0 to 4+ decreased from 2.5±0.9 to 0.5±0.6 ( P &lt;0.01), and severity of the systolic anterior motion of the mitral valve graded on a scale from 0 to 3+ decreased from 2.9±0.3 to 0.5±0.7 ( P &lt;0.01) postoperatively. There were no deaths associated with surgery. Conclusions— Long-term follow-up shows sustained improvement in functional status, reduction of outflow tract obstruction, and attenuation of mitral regurgitation and systolic anterior motion of the mitral valve. In this respect, the new technique widens the surgical applications in HOCM.