tbuckley/cabot-search huggingface dataset:
Molecular Population Genetics of Herbivore-induced Protease Inhibitor Genes in European Aspen (Populus tremula L., Salicaceae)
Authors: Pär K. Ingvarsson
Journal: Molecular Biology and Evolution (2005)

Plants defend themselves against the attack of natural enemies by using an array of both constitutively expressed and induced defenses. Long-lived woody perennials are overrepresented among plant species that show strong induced defense responses, whereas annual plants and crop species are underrepresented. However, most studies of plant defense genes have been performed on annual or short-lived perennial weeds or crop species. Here I use molecular population genetic methods to survey six wound-inducible protease inhibitors (PIs) in a long-lived woody, perennial plant species, the European aspen (Populus tremula), to evaluate the likelihood of either recurrent selective sweeps or balancing selection maintaining amino acid polymorphisms in these genes. The results show that none of the six PI genes have reduced diversities at synonymous sites, as would be expected in the presence of recurrent selective sweeps. However, several genes show some evidence of nonneutral evolution such as enhanced linkage disequilibrium and a large number of high-frequency-derived mutations. A group of at least four Kunitz trypsin inhibitor genes appear to have experienced elevated levels of nonsynonymous substitutions, indicating allelic turnover on an evolutionary timescale. One gene, TI1, has enhanced levels of intraspecific polymorphism at nonsynonymous sites and also has an unusual haplotype structure characterized by two divergent haplotypes occurring at roughly equal frequencies in the sample. One haplotype has very low levels of intraallelic nucleotide diversity, whereas the other haplotype has levels of diversity comparable to other genes in P. tremula. Patterns of sequence diversity at TI1 do not fit a simple model of either balancing selection or recurrent selective sweeps. This suggests that selection at TI1 is more complex, possibly involving allelic cycling.
Circulating tumor cells in colorectal cancer: correlation with clinical and pathological variables
Authors: J. Sastre, M.L. Maestro, J. Puente, S. Veganzones, R. Alfonso, S. Rafael, J.A. García-Saenz, M. Vidaurreta, M. Martín, M. Arroyo, M.T. Sanz-Casla, E. Díaz-Rubio
Journal: Annals of Oncology (2008)
Central nervous system mechanisms involved in inhibition of renal sympathetic nerve activity induced by arginine vasopressin.
Authors: S Suzuki, A Takeshita, T Imaizumi, Y Hirooka, M Yoshida, S Ando, M Nakamura
Journal: Circulation Research (1989)

Previous studies have suggested that intravenous infusion of arginine vasopressin (AVP) inhibits sympathetic nerve activity (SNA) in rabbits by its action at the brainstem. This study aimed to determine, first, whether this action of AVP depended on functioning baroreflex mechanisms. The second aim was to determine the role of the nucleus tractus solitarii (NTS) in mediating this action of AVP. Experiments were performed in rabbits anesthetized with alpha-chloralose. Intravenous infusions of AVP (1, 3, and 10 mU/kg/min) resulted in progressive inhibition of renal SNA in rabbits with intact arterial baroreceptors and vagal afferents as well as in rabbits with sinoaortic denervation and bilateral vagotomy. The magnitudes of renal SNA inhibition evoked with AVP were comparable in the two groups. Renal SNA inhibition evoked with AVP at doses of 1 and 3 mU/kg/min in rabbits after sinoaortic denervation and vagotomy was totally blocked by chemical lesions with kainic acid of the bilateral NTS or the area postrema. Lesions of the NTS or the area postrema markedly attenuated (by about 60%) but did not totally block the response evoked with AVP at a dose of 10 mU/kg/min. AVP microinjected directly into the NTS did not evoke changes in renal SNA or arterial pressure, whereas AVP microinjected into the area postrema suppressed renal SNA. These results suggest that intravenous AVP at lower doses inhibited renal SNA by causing excitation of the NTS neurons, and this action of AVP did not depend on functioning baroreflex mechanisms. The second suggestion is that the NTS was unlikely to be the site where AVP directly interacted but instead received a neural connection, presumably from the area postrema, where AVP might directly interact.
Influence of HLA-class II incompatibility between mother and fetus on the development and course of rheumatoid arthritis of the mother
Authors: I E van der Horst-Bruinsma, R R P de Vries, P D M de Buck, P W van Schendel, F C Breedveld, G M T. Schreuder, J M W Hazes
Journal: Annals of the Rheumatic Diseases (1998)

<h3>OBJECTIVE</h3> To assess the relation between the course of rheumatoid arthritis (RA) during pregnancy or the onset of RA postpartum and DRB1, DQA1, and DQB1 incompatibilities between mother and child. <h3>METHODS</h3> In 45 pregnancies of 33 RA patients the course of RA was related to the number of class II incompatibilities. Furthermore class II incompatibilities in 16 pregnancies followed by RA onset were compared with those in 87 control pregnancies. <h3>RESULTS</h3> The risk of a favourable compared with an unfavourable course was 0.95, 2.67, and 2.38 in case of DRB1, DQA1, and DQB1 incompatibility respectively. DQA1 and DQB1 incompatibilities were seen more often in the 10 pregnancies followed by RA onset within three months than in control pregnancies (OR 8.02, 95% CI 0.97, 66.06 and OR 8.79 95% CI 1.07, 72.46 respectively). <h3>CONCLUSIONS</h3> DQA1 and DQB1 incompatibility between mother and child seems to have a favourable effect on the course of RA and may postpone the risk of RA onset during pregnancy.
Phase I trial combining temozolomide plus lapatinib for the treatment of brain metastases in patients with HER2-positive metastatic breast cancer: the LAPTEM trial
Authors: E. de Azambuja, D. Zardavas, M. Lemort, J. Rossari, C. Moulin, A. Buttice, V. D'Hondt, F. Lebrun, Y. Lalami, F. Cardoso, C. Sotiriou, T. Gil, D. Devriendt, M. Paesmans, M. Piccart-Gebhart, A. Awada
Journal: Annals of Oncology (2013)
Alpha 1-adrenoreceptor blockade reduces the angiotensin II-induced vascular smooth muscle cell DNA synthesis in the rat thoracic aorta and carotid artery.
Authors: E M van Kleef, J F Smits, J G De Mey, J P Cleutjens, D M Lombardi, S M Schwartz, M J Daemen
Journal: Circulation Research (1992)

We explored effects of alpha 1-adrenoreceptor blockade with prazosin on the increased vascular smooth muscle cell (SMC) DNA synthesis induced by angiotensin II (Ang II) in rats. Ang II was infused with or without prazosin or its solvent. Observations were compared with those in rats receiving saline or solvent. In group A, Ang II was infused for 2 weeks by subcutaneously implanted osmotic minipumps at a rate of 35 ng/100 g per minute. Group B received Ang II together with the alpha 1-adrenoreceptor antagonist prazosin (0.35 micrograms/100 g per minute). Group C received Ang II and 50% dimethyl sulfoxide (DMSO), the solvent of prazosin; group D received 50% DMSO; and group E received 0.9% NaCl (Ang II vehicle). All animals were infused with 5-bromo-2'-deoxyuridine for 2 weeks via separate minipumps to measure DNA synthesis. Ang II significantly increased the fraction of DNA synthesizing SMCs in the media of the thoracic aorta from 0.4 +/- 0.1% (mean +/- SD) in group E (n = 6) to 10.8 +/- 7.0% in group A (n = 8). Addition of prazosin to Ang II reduced the labeling fraction of SMCs to 3.0 +/- 2.2% (group B, n = 9). The remaining SMC DNA synthesis in the prazosin-treated group was probably due to the effects of the solvent of prazosin, i.e., 50% DMSO, since infusion of 50% DMSO alone increased the labeling fraction to 4.1 +/- 2.0% (group D, n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)
Histamine and tryptase modulate asthmatic airway smooth muscle GM-CSF and RANTES release
Authors: J. Chhabra, Y-Z. Li, H. Alkhouri, A. E. Blake, Q. Ge, C. L. Armour, J. M. Hughes
Journal: European Respiratory Journal (2007)

Degranulating mast cells are increased in the airway smooth muscle (ASM) of asthmatics, where they may influence ASM function. The aim of the present study was to determine whether histamine and tryptase modulate ASM cell granulocyte-macrophage colony-stimulating factor (GM-CSF) and RANTES (regulated on activation, normal T-cell expressed and secreted) release and also to examine which receptors are involved in this release. Confluent, quiescent ASM cells from asthmatic and nonasthmatic donors were treated with histamine (1 μM–100 μM) with and without histamine receptor antagonist pre-treatment, or the protease-activated receptor (PAR)-2 agonists tryptase (0.5–5 nM) and SLIGKV (100 and 400 μM). The cells were then stimulated with interleukin (IL)-1β and/or tumour necrosis factor (TNF)-α (10 ng·mL −1 ) or left unstimulated for 24 h. Release of GM-CSF and RANTES was determined by ELISA and prostaglandin (PG)E 2 measured by enzyme immunoassay. Neither histamine nor tryptase induced ASM GM-CSF or RANTES secretion. However, histamine increased IL-1β-induced GM-CSF release and markedly reduced TNF-α-induced RANTES release by both asthmatic and nonasthmatic cells to a similar extent, but did not modulate PGE 2 release. All changes involved activation of the histamine H1 receptor as they were partially or fully blocked by chlorpheniramine, but not ranitidine. Tryptase, via its proteolytic activity, also potentiated GM-CSF, but not RANTES, release from asthmatic and nonasthmatic ASM cells induced by both cytokines. PAR-2 involvement in the tryptase potentiation was unlikely because SLIGKV had no effect. In conclusion, mast cells, through histamine and tryptase, may locally modulate airway smooth muscle-induced inflammation in asthma.
Vitronectin expression in primary lung cancer
Authors: Lina M. Salazar-Pelaez, Magda C. Ledesma, Ana M. Herrera
Journal: European Respiratory Journal (2012)

Rationale 

Vitronectin (Vn) plays a role in extracellular matrix (ECM) remodeling during tumorigenesis. Vn is present in human bronchial submucosal glands and it is secreted by A549 lung adenocarcinoma cell line. However, whether Vn is differentially expressed in tissues of primary lung cancer has not been explored.

Methods 

Lung tissue from 22 primary lung carcinoma and 36 non-lung cancer subjects were obtained from fibrobronchoscopy. Sections were analyzed by histo- immunohistochemical methods. The total area occupied by ECM, surface and glandular epithelium, as well as the percentage area occupied by Vn at each of these localizations were measured. Chi-square, t-student, U-Mann Whitney and ANOVA tests were used in group comparisons. Statistical significance was tested at P<0.05.

Results 

Vn expression was observed in bronchial glandular and surface epithelium, as well as in ECM (Figure 1). In total, the average area of ECM, surface or glandular epithelium was 0.289mm2 (± 0.032), 0.043mm2 (±0.009), 0.084mm2 (±0.031), respectively. The percentage area occupied by Vn in ECM, surface or glandular epithelium, was 4.899 (±1.186), 7.279 (±1.623), 3.285 (±1.038), respectively; with not significant statistical differences between lung cancer and non-cancer subjects or within different types primary lung cancer.

![Figure][1] 



Conclusion 

There were no statistically significant differences in Vn expression between lung cancer and non-cancer subjects, or within primary lung carcinomas.

 [1]: pending:yes
Allergic contact and photocontact dermatitis due to psoralens in patients with psoriasis treated with topical PUVA
Authors: A. TAKASHIMA, K. YAMAMOTO, S. KIMURA, Y. TAKAKUWA, N. MIZUNO
Journal: British Journal of Dermatology (1991)

Summary The incidence and clinical features of allergic contact and/or photocontact dermatitis due to psoralens were examined in 371 patients with psoriasis treated with topical PUVA. The psoralen derivatives used in the study were 8-methoxypsoralen (8MOP), 3-carbethoxypsoralen (3CPs), 4,6,4′-trimethylangelicin (TMA) and 7-methyl pyridopsoralen (MPP). Of 371 patients treated with 8MOP, three (0.8%) developed an acute dermatitis in the PUVA-treated areas. This incidence was significantly lower (P<0.01) than that for 3CPs (four of 10 patients) or that for TMA (six of 17 patients). None of the seven patients receiving MPP on PUVA had a reaction. It was confirmed that these dermatitis reactions were due to contact and/or photocontact allergy to psoralens by several methods that included patch and photopatch tests, photopatch test mapping, determination of the minimal erythema dose (MED) and immunohistochemistry.
The State of the World’s Refugees
Authors: Paul B. Spiegel
Journal: JAMA (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Glucose Modulation of Amino Acid-Induced Glucagon and Insulin Release in the Isolated Perfused Rat Pancreas
Authors: Anthony S. Pagliara, Susan N. Stillings, Barbara Hover, Duane M. Martin, Franz M. Matschinsky
Journal: Journal of Clinical Investigation (1974)

Interactions between glucose and arginine and a mixture of 20 amino acids found in normal rat serum were studied in the isolated perfused rat pancreas of normal rats, with release of immunoreactive glucagon and insulin as parameters. Secretion of both pancreatic hormones was low during the steady state, whether glucose (5 mM) was included in the perfusion medium or not. This glucose concentration significantly stimulated insulin release twofold and resulted in an 80% inhibition of basal glucagon release. Arginine and the amino acid mixture were potent stimulants of both hormones. Secretion of both hormones followed identical biphasic response patterns after addition of arginine or the amino acid mixture. However, stimulation of insulin release occurred only when glucose was included, whereas both phases of glucagon release were elicited in the absence of glucose and markedly reduced in its presence. The dose-dependency curves of hormone release due to arginine on one hand and the amino acid mixture on the other differed substantially: with arginine, release of insulin and glucagon was linear between a concentration of 0.3 and 20 mM. In contrast, the amino acid mixture resulted in half-maximal release for both hormones between a concentration of 3 and 4.5 mM, and maximal release between 6 and 8 mM. The dose-dependencies of glucose modulation of α- and β-cell activity were also different: when the amino acid mixture was maintained at 15 mM and glucose varied (0-6.25 nM), no insulin release occurred until glucose was above 2.5 mM, whereas incremental inhibition of glucagon occurred through the complete dose range. It was also observed that glucose inhibition of amino acid-stimulated glucagon release was dissociated from glucose-dependent increase of insulin release.
Proteins ZNF198 and SUZ12 are down-regulated in hepatitis B virus (HBV) X protein-mediated hepatocyte transformation and in HBV replication
Authors: Wen-Horng Wang, Leo L. Studach, Ourania M. Andrisani
Journal: Hepatology (2011)

Chronic hepatitis B virus (HBV) infection is a major etiologic factor in hepatocellular carcinoma (HCC) pathogenesis, involving effects of chronic liver inflammation and of the weakly oncogenic HBV X protein (pX). pX-mediated hepatocyte transformation requires Polo-like kinase1 (Plk1) activity, but the mechanism is not fully understood. We identified by a genome-wide short hairpin RNA (shRNA) library screen the genes zinc finger, MYM-type 2 (ZNF198) and suppressor of zeste 12 homolog (Drosophila) (SUZ12) whose protein depletion rescues pX-expressing cells from DNA damage-induced apoptosis. ZNF198 and SUZ12 are components of chromatin remodeling complexes and associate with promyelocytic leukemia (PML) nuclear bodies. Knockdown of ZNF198 and SUZ12 by small interfering RNA (siRNA) reduced p53 stability and DNA repair, rescued pX-expressing hepatocytes from DNA damage-induced apoptosis, and increased pX-induced polyploidy and oncogenic transformation, suggesting ZNF198 and SUZ12 have a role in pX-mediated transformation. Interestingly, during pX-mediated transformation the protein but not messenger RNA (mRNA) levels of ZNF198 and SUZ12 progressively decreased, whereas Plk1 levels increased. Inhibition of Plk1 activity restored protein levels of ZNF198 and SUZ12. In addition, transfected Polo-box-domain (PBD) of Plk1 coimmunoprecipitated with ZNF198 and SUZ12, suggesting that these proteins are Plk1 substrates. Elevated Plk1 and reduced protein levels of ZNF198 and SUZ12 were also observed in human liver cancer cell lines derived from HBV-related tumors and in the presence of HBV replication. Importantly, knockdown by siRNA of ZNF198 and SUZ12 enhanced HBV replication.Reduced protein levels of ZNF198 and SUZ12 and elevated Plk1 occur during pX-mediated hepatocyte transformation in human liver cancer cell lines, as well as during HBV replication, underscoring the significance of these genes both in HBV-mediated HCC pathogenesis and HBV replication. We propose Plk1 activity down-regulates ZNF198 and SUZ12, thereby enhancing both HBV replication and pX-mediated oncogenic transformation.
Circulating regulatory anti–T cell receptor antibodies in patients with myasthenia gravis
Authors: Florence Jambou, Wei Zhang, Monique Menestrier, Isabelle Klingel-Schmitt, Olivier Michel, Sophie Caillat-Zucman, Abderrahim Aissaoui, Ludovic Landemarre, Sonia Berrih-Aknin, Sylvia Cohen-Kaminsky
Journal: Journal of Clinical Investigation (2003)

Serum anti–T cell receptor (TCR) Ab’s are involved in immune regulation directed against pathogenic T cells in experimental models of autoimmune diseases. Our identification of a dominant T cell population expressing the Vβ5.1 TCR gene (TCRBV5-1), which is responsible for the production of pathogenic anti-acetylcholine receptor (AChR) autoantibodies in HLA-DR3 patients with early-onset myasthenia gravis (EOMG), prompted us to explore the occurrence, reactivity, and regulatory role of anti-TCR Ab’s in EOMG patients and disease controls with clearly defined other autoantibodies. In the absence of prior vaccination against the TCR, EOMG patients had elevated anti-Vβ5.1 Ab’s of the IgG class. This increase was restricted largely to EOMG cases with HLA-DR3 and with less severe disease, and it predicted clinical improvement in follow-up studies. EOMG patient sera containing anti-TCR Ab’s bound specifically the native TCR on intact Vβ5.1-expressing cells and specifically inhibited the proliferation and IFN-γ production of purified Vβ5.1-expressing cells to alloantigens in mixed lymphocyte reaction and the proliferation of a Vβ5.1-expressing T cell clone to an AChR peptide, indicating a regulatory function for these Ab’s. This evidence of spontaneously active anti-Vβ5.1 Ab’s in EOMG patients suggests dynamic protective immune regulation directed against the excess of pathogenic Vβ5.1-expressing T cells. Though not sufficient to prevent a chronic, exacerbated autoimmune process, it might be boosted using a TCR peptide as vaccine.
The Effect of Toll-Like Receptors and Toll-Like Receptor Genetics in Human Disease
Authors: Stavros Garantziotis, John W Hollingsworth, Aimee K. Zaas, David A. Schwartz
Journal: Annual Review of Medicine (2007)

Toll-like receptors (TLRs) enable innate immune recognition of endogenous and exogenous prototypic ligands. They also orchestrate innate and adaptive immune response to infection, inflammation, and tissue injury. Given their significance in the immune response, it is not surprising that genetic variations of TLRs can affect their function and by extension affect the response of the organism to environmental stimuli. The genetics of TLRs provides important insights in gene-environment interactions in health and disease, and it may enable scientists to assess patients' susceptibility to diseases or predict their response to treatments.
Reversible changes in serum immunoglobulin galactosylation during the immune response and treatment of inflammatory autoimmune arthritis
Authors: K Van Beneden, K Coppieters, W Laroy, F De Keyser, I E Hoffman, F Van den Bosch, B Vander Cruyssen, M Drennan, P Jacques, P Rottiers, G Verbruggen, R Contreras, N Callewaert, D Elewaut
Journal: Annals of the Rheumatic Diseases (2008)

<h3>Objectives:</h3> Improved DNA sequencer-aided fluorophore-assisted carbohydrate electrophoresis (DSA-FACE) technology was used to monitor the changes in the galactosylation status of serum immunoglobulins during the immune response and therapy of autoimmune arthritis. <h3>Methods:</h3> Collagen-induced arthritis (CIA) was induced in susceptible DBA/1 mice and the undergalactosylation status (UGS) of serum immunoglobulins was determined using the improved DSA-FACE technology. Prophylactic intravenous tolerisation with type II collagen as well as semitherapeutic treatment with dexamethasone (DEX) were performed and UGS was analysed. Next, the serum immunoglobulin glycosylation profiles of patients with rheumatoid arthritis (RA) and spondyloarthropathy (SpA) were studied and changes in the UGS scores during anti-tumour necrosis factor (TNF)α therapy followed. <h3>Results:</h3> In the longitudinal CIA study, the undergalactosylation state of immunoglobulins was found to be significantly correlated with the clinical arthritis scores. Upon collagen-specific tolerisation as well as glucocorticoid semitherapeutic treatment, improvement of the clinical arthritis scores correlated with decreased levels of UGS. It was also demonstrated that withdrawal of DEX was associated with an increased UGS score. Interestingly, reversibility in the UGS was also shown during treatment of patients with RA and SpA with anti-TNFα. <h3>Conclusions:</h3> These findings demonstrate that the UGS of serum immunoglobulins changes during the disease course of CIA and that this UGS is inhibited by antigen-specific and antigen-independent treatment procedures. The observation that Ig galactosylation is a reversible process is also documented during treatment of patients with RA and SpA with anti-TNFα.