tbuckley/cabot-search huggingface dataset:
Ancient Properties of Spider Silks Revealed by the Complete Gene Sequence of the Prey-Wrapping Silk Protein (AcSp1)
Authors: Nadia A. Ayoub, Jessica E. Garb, Amanda Kuelbs, Cheryl Y. Hayashi
Journal: Molecular Biology and Evolution (2012)

Spider silk fibers have impressive mechanical properties and are primarily composed of highly repetitive structural proteins (termed spidroins) encoded by a single gene family. Most characterized spidroin genes are incompletely known because of their extreme size (typically >9 kb) and repetitiveness, limiting understanding of the evolutionary processes that gave rise to their unusual gene architectures. The only complete spidroin genes characterized thus far form the dragline in the Western black widow, Latrodectus hesperus. Here, we describe the first complete gene sequence encoding the aciniform spidroin AcSp1, the primary component of spider prey-wrapping fibers. L. hesperus AcSp1 contains a single enormous (∼19 kb) exon. The AcSp1 repeat sequence is exceptionally conserved between two widow species (∼94% identity) and between widows and distantly related orb-weavers (∼30% identity), consistent with a history of strong purifying selection on its amino acid sequence. Furthermore, the 16 repeats (each 371–375 amino acids long) found in black widow AcSp1 are, on average, >99% identical at the nucleotide level. A combination of stabilizing selection on amino acid sequence, selection on silent sites, and intragenic recombination likely explains the extreme homogenization of AcSp1 repeats. In addition, phylogenetic analyses of spidroin paralogs support a gene duplication event occurring concomitantly with specialization of the aciniform glands and the tubuliform glands, which synthesize egg-case silk. With repeats that are dramatically different in length and amino acid composition from dragline spidroins, our L. hesperus AcSp1 expands the knowledge base for developing silk-based biomimetic technologies.
Laparoendoscopic Single-site and Natural Orifice Transluminal Endoscopic Surgery in Urology: A Critical Analysis of the Literature
Authors: Riccardo Autorino, Jeffrey A. Cadeddu, Mihir M. Desai, Matthew Gettman, Inderbir S. Gill, Louis R. Kavoussi, Estevão Lima, Francesco Montorsi, Lee Richstone, Jens U. Stolzenburg, Jihad H. Kaouk
Journal: European Urology (2010)
Outcomes of noncardiac, nonobstetric surgery in patients with PAH: an international prospective survey
Authors: Stephanie Meyer, Vallerie V. McLaughlin, Hans-Juergen Seyfarth, Todd M. Bull, Carmine D. Vizza, Mardi Gomberg-Maitland, Ioana R. Preston, Joan A. Barberà, Paul M. Hassoun, Michael Halank, Xavier Jaïs, Nils Nickel, Marius M. Hoeper, Marc Humbert
Journal: European Respiratory Journal (2012)

We conducted an international, prospective, 3-year questionnaire-based survey among 11 pulmonary hypertension centres to assemble data from patients with pulmonary arterial hypertension (PAH) undergoing noncardiac and nonobstetric surgery. Data were collected between July 2007 and June 2010 from 114 patients with PAH (70% female, mean age 57 years) who underwent major surgery. At the time of surgery, 43% were in functional class III/IV. 82% of the interventions were performed under general anaesthesia and 18% under spinal anaesthesia. Major complications occurred in seven (6.1%) of the patients, of whom four died, resulting in an overall perioperative mortality rate of 3.5%. The mortality rate was 15% (two out of 13) in emergency procedures, compared with 2% (two out of 101) in nonemergency procedures (p=0.01). Risk factors for major complications were an elevated right atrial pressure (OR 1.1, 95% CI 1.0–1.3; p=0.01), a 6-min walking distance &lt;399 m at the last preoperative assessment (OR 2.2, 95% CI 1.1–3.7; p=0.04), the perioperative use of vasopressors (OR 1.5, 95% CI 1.2–2.7; p=0.03) and the need for emergency surgery (OR 2.4, 95% CI 1.4–3.6; p=0.01). Major surgery in patients with PAH continues to be a high-risk procedure, particularly when emergency interventions are needed.
Humoral Autoimmune Manifestation in Subacute Thyroiditis
Authors: H. Bliddal, K. Bech, U. Feldt‐Rasmussen, M. Høier‐Madsen, B. Thomsen, H. Nielsen
Journal: Allergy (1985)

To study the autoimmune manifestations in subacute thyroiditis (SAT), the patterns of thyroid antibodies, thyroglobulin and circulating immune complexes were investigated in 10 patients during the course of the disease. Eight patients were thyrotoxic at diagnosis, and became euthyroid during recovery with a median observation of 8 months (4–30 months). Thyroid stimulating immunoglobulins were measured as TSH binding inhibiting immunoglobulins (TBII) and as thyroid stimulating antibodies (TSAb). TBII were present in all patients at least once during the observation period and remained detectable in six patients after recovery. TSAb were detected in three patients without relation to the hyperthyroid state. Thyroglobulin antibodies (TgAb) were present in four patients and persisted in three, while microsomal antibodies (MAb) were negative. Thyroglobulin (Tg) in the TgAb negative patients (n = 6) was high at diagnosis (median 229 μg/1, range 55–375) and fell rapidly during the course of SAT. Circulating immune complexes (CIC), which were found in all patients, reached maximal levels shortly after the onset of the disease and persisted after recovery. No correlation could be demonstrated between the different thyroid antibodies, and there was no clear relation between the levels of CIC and presence of the autoantibodies. However, the changes in CIC paralleled the changes in TBII, and it is suggested that immune complex formation is a major feature of the regulatory mechanisms controlling the immune responses in SAT.
Midthigh Muscle Cross-Sectional Area Is a Better Predictor of Mortality than Body Mass Index in Patients with Chronic Obstructive Pulmonary Disease
Authors: Karine Marquis, Richard Debigaré, Yves Lacasse, Pierre LeBlanc, Jean Jobin, Guy Carrier, François Maltais
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

This study was undertaken to test the hypothesis that a reduction in midthigh muscle cross-sectional area obtained by CT scan (MTCSA(CT)) is a better predictor of mortality in chronic obstructive pulmonary disease (COPD) than low body mass index (BMI). We also wished to evaluate whether anthropometric measurements could be used to estimate MTCSA(CT). One hundred forty-two patients with COPD (age = 65 +/- 9 years, mean +/- SD, 26 F, BMI = 26 +/- 6 kg/m(2), FEV(1) = 42 +/- 16% predicted) were recruited from September 1995 to April 2000 with a mean follow-up of 41 +/- 18 months. The primary end-point was all-cause mortality during the study period. A Cox proportional hazards regression model was used to predict mortality using the following independent variables: age, sex, daily use of corticosteroid, FEV(1), DL(CO), BMI, thigh circumference, MTCSA(CT), peak exercise workrate, Pa(O2), and Pa(CO2). Only MTCSA(CT) and FEV(1) were found to be significant predictors of mortality (p = 0.0008 and p = 0.01, respectively). A second analysis was also performed with FEV(1) and MTCSA(CT) dichotomized. Patients were divided into four subgroups based on FEV(1) (< or >or= 50% predicted) and MTCSA(CT) (< or >or= 70 cm(2)). Compared with patients with an FEV(1) >or= 50% predicted and a MTCSA(CT) >or= 70 cm(2), those with an FEV(1) < 50% predicted and a MTCSA(CT) >or= 70 cm(2) had a mortality odds ratio of 3.37 (95% confidence interval, 0.41-28.00), whereas patients with an FEV(1) < 50% predicted and a MTCSA(CT) < 70 cm(2) had a mortality odds ratio of 13.16 (95% confidence interval, 1.74-99.20). MTCSA(CT) could not be estimated with sufficient accuracy from anthropometric measurements. In summary, we found in this cohort of patients with COPD that (1) MTCSA(CT) was a better predictor of mortality than BMI, and (2) MTCSA had a strong impact on mortality in patients with an FEV(1) < 50% predicted. These findings suggest that the assessment of body composition may be useful in the clinical evaluation of these patients.
The biological response modifier AM3 attenuates the inflammatory cell response and hepatic fibrosis in rats with biliary cirrhosis
Authors: A. Albillos, M. Nieto, M. Ubeda, L. Munoz, B. Fraile, E. Reyes, L. Lledo, I. Blanco, O. Pastor, C. Salas, M. Lario, J. Monserrat, R. Bataller, M. Alvarez-Mon
Journal: Gut (2010)

<h3>Background</h3> An inflammatory immune system response ensues in the liver and in the systemic circulation in cirrhosis, where it contributes to hepatic fibrosis and peripheral vasodilation. Modulation of the inflammatory response without increasing susceptibility to infection is a therapeutic target in cirrhosis. AM3 is a low-toxicity biological response modifier with regulatory effects on innate and adaptative immunity, and the ability to normalise the production of tumour necrosis factor α (TNFα). <h3>Aims</h3> This was an experimental study to investigate the effects of oral AM3 on the systemic and hepatic inflammatory response, liver fibrosis and on the haemodynamic abnormalities of portal hypertension in rats with biliary cirrhosis. <h3>Design</h3> Bile-duct ligated rats received a 3-week oral course of AM3 or placebo. <h3>Results</h3> In cirrhotic rats, AM3 blunted the inflammatory switch of circulating and intrahepatic monocytes and T-cells to TNFα and interferon γ (IFNγ) production, respectively. AM3 modified the intrahepatic polarisation pattern of the regulatory cytokines, decreasing the mRNA expression of transforming growth factor β1 (TGFβ1), interleukin 4 (IL4), and IFNγ, and increasing that of IL10. Total and IFNγ-producing natural killer (NK) cells were lowered by AM3 in the peripheral blood and liver of cirrhotic rats. The immunomodulatory effects of AM3 led to reduced hepatic fibrogenesis in cirrhotic rats, as shown by decreased area of liver fibrosis, hydroxyproline content and mRNA expression of procollagen α1(I). Besides, AM3 lowered portal pressure and systemic hyperaemia. <h3>Conclusions</h3> The biological response modifier AM3 reverses the concurrent inflammatory immune system activation in peripheral blood and liver of experimental established cirrhosis, which results in reductions of hepatic fibrosis, portal pressure and peripheral vasodilation.
PPARγ agonists inhibit angiogenesis by suppressing PKCα- and CREB-mediated COX-2 expression in the human endothelium
Authors: Egeria Scoditti, Marika Massaro, Maria Annunziata Carluccio, Alessandro Distante, Carlo Storelli, Raffaele De Caterina
Journal: Cardiovascular Research (2009)

AimsThe activation of peroxisome proliferator-activated receptor (PPAR)γ is known to inhibit angiogenesis. As a potential mechanism for this, we aimed at examining the effects of PPARγ agonists on the pro-angiogenic enzyme cyclooxygenase (COX)-2 in human endothelium.
Challenges of stop smoking cessation program regarding the ethical aspects of smoking cessation
Authors: Doina Adina Todea, Loredana Elena Rosca, Andreea Codruta Coman
Journal: European Respiratory Journal (2014)

The ethical aspects related to the approach of persons addicted to tobacco use are a particular problem and requires the knowledge and observance of the principles of bioethics in the control of tobacco use. A retrospective descriptive observational study was performed between 2008-2012 in 482 patients who voluntarily presented to the Service of Counseling for smoking cessation. Of all subjects 52.07% were male. 94.81% of the respondents were aged between 20-59 years. Male sex, adult age and the status of married person with children represent the prototype of the smoking patient who wishes to receive counseling. Among the reasons reported by the subjects regarding smoking cessation, the concern for health was ranked first (40.04%), followed by financial reasons (21.37%), the wish not to be nicotine dependent (11.20%), and the influence of the entourage (10.17%).The study shows the fact that persons who during counseling were found to have a moderate and high nicotine dependence using the Fagestrom test quantification were also those who were more subjectively aware of the severity of their status in relation to tobacco use (p
Angiotensin II–Induced Oxidative Stress Resets the Ca <sup>2+</sup> Dependence of Ca <sup>2+</sup> –Calmodulin Protein Kinase II and Promotes a Death Pathway Conserved Across Different Species
Authors: Julieta Palomeque, Omar Velez Rueda, Luciana Sapia, Carlos A. Valverde, Margarita Salas, Martin Vila Petroff, Alicia Mattiazzi
Journal: Circulation Research (2009)

Angiotensin (Ang) II-induced apoptosis was reported to be mediated by different signaling molecules. Whether these molecules are either interconnected in a single pathway or constitute different and alternative cascades by which Ang II exerts its apoptotic action, is not known.To investigate in cultured myocytes from adult cat and rat, 2 species in which Ang II has opposite inotropic effects, the signaling cascade involved in Ang II-induced apoptosis.Ang II (1 micromol/L) reduced cat/rat myocytes viability by approximately 40%, in part, because of apoptosis (TUNEL/caspase-3 activity). In both species, apoptosis was associated with reactive oxygen species (ROS) production, Ca(2+)/calmodulin-dependent protein kinase (CaMK)II, and p38 mitogen-activated protein kinase (p38MAPK) activation and was prevented by the ROS scavenger MPG (2-mercaptopropionylglycine) or the NADPH oxidase inhibitor DPI (diphenyleneiodonium) by CaMKII inhibitors (KN-93 and AIP [autocamtide 2-related inhibitory peptide]) or in transgenic mice expressing a CaMKII inhibitory peptide and by the p38MAPK inhibitor, SB202190. Furthermore, p38MAPK overexpression exacerbated Ang II-induced cell mortality. Moreover, although KN-93 did not affect Ang II-induced ROS production, it prevented p38MAPK activation. Results further show that CaMKII can be activated by Ang II or H(2)O(2), even in the presence of the Ca(2+) chelator BAPTA-AM, in myocytes and in EGTA-Ca(2+)-free solutions in the presence of the calmodulin inhibitor W-7 in in vitro experiments.(1) The Ang II-induced apoptotic cascade converges in both species, in a common pathway mediated by ROS-dependent CaMKII activation which results in p38MAPK activation and apoptosis. (2) In the presence of Ang II or ROS, CaMKII may be activated at subdiastolic Ca(2+) concentrations, suggesting a new mechanism by which ROS reset the Ca(2+) dependence of CaMKII to extremely low Ca(2+) levels.
Prognostic value of pretransplantation positron emission tomography using fluorine 18-fluorodeoxyglucose in patients with aggressive lymphoma treated with high-dose chemotherapy and stem cell transplantation
Authors: Karoline Spaepen, Sigrid Stroobants, Patrick Dupont, Peter Vandenberghe, Johan Maertens, Guy Bormans, José Thomas, Jan Balzarini, Christine De Wolf-Peeters, Luc Mortelmans, Gregor Verhoef
Journal: Blood (2003)
Remembering the Benefits of Vaccination
Authors: Kristen A. Feemster
Journal: JAMA Pediatrics (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 Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Journals 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) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2024 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 Pediatrics journal
Monocyte chemotactic peptide receptor. Functional characteristics and ligand-induced regulation.
Authors: J B Weinberg, J J Muscato, J E Niedel
Journal: Journal of Clinical Investigation (1981)

Monocytes, macrophages, and neutrophils will demonstrate several important cellular functions in response to synthetic formylated oligopeptides. N-formyl-norleucyl-leucyl-phenylalanyl-norleucyl-tyrosyl-lysine (fNLPNTL) was a potent chemoattractant for human blood monocytes; a 1.0-nM concentration induced a maximal chemotactic response. Binding of 125I-labeled fNLPNTL to the monocyte formyl peptide receptor was rapid, specific, and saturable at 4, 24, or 37 degrees C. At 4 degrees C, monocytes from several different donors demonstrated between 10,000 and 18,000 receptors/cell with a dissociation constant (Kd) of 1.7-2.7 nM. The association of the 125I peptide with the cells was irreversible at the elevated temperatures and exceeded the amount of surface receptor by approximately four-fold, suggesting receptor-mediated peptide endocytosis. Processing of rhodamine-labeled fNLPNTL by monocytes was observed directly by video intensification microscopy. At 37 degrees C, diffuse membrane fluorescence was seen initially, followed by rapid aggregation and internalization of the peptide. Monocytes incubated with fNLPNTL displayed a temperature dependent loss of surface binding capacity (receptor down-regulation). This decrease was due to a decrease in surface receptor number rather than to a decrease in receptor affinity. A dose-response curve for peptide-induced receptor down-regulation correlated with a dose-response curve for 125I-labeled fNLPNTL uptake, suggesting that each uptake event led to the loss of one surface receptor. Surface receptor replenishment following down-regulation was rapid and not dependent on new protein synthesis, but was inversely related to both the time and peptide concentration used to induce down-regulation. An exact correlation between receptor down-regulation and functional deactivation of the chemotactic response could not be demonstrated.
TSU68 Prevents Liver Metastasis of Colon Cancer Xenografts by Modulating the Premetastatic Niche
Authors: Masayoshi Yamamoto, Hirotoshi Kikuchi, Manabu Ohta, Toshiki Kawabata, Yoshihiro Hiramatsu, Kenji Kondo, Megumi Baba, Kinji Kamiya, Tatsuo Tanaka, Masatoshi Kitagawa, Hiroyuki Konno
Journal: Cancer Research (2008)

Abstract The aim of this study was to investigate the inhibitory effect of TSU68 [(Z)-5-[(1,2-dihydro-2-oxo-3H-indol-3-ylidene)methyl]-2,4-dimethyl-1H-pyrrole-3-propanoic acid; SU6668], an inhibitor of vascular endothelial growth factor receptor 2, platelet-derived growth factor receptor β, and fibroblast growth factor receptor 1 (FGFR1), on colon cancer liver metastasis, and to test the hypothesis that TSU68 modulates the microenvironment in the liver before the formation of metastasis. First, we implanted the highly metastatic human colon cancer TK-4 orthotopically into the cecal walls of nude mice, followed by twice-daily administration of TSU68 (400 mg/kg/d) or vehicle. Five weeks of treatment with TSU68 significantly inhibited liver metastasis compared with the control group (P &amp;lt; 0.001). Next, we analyzed the gene expression profile in premetastatic liver using microarrays. Microarray and quantitative reverse transcription-PCR analysis showed that mRNA levels for the chemokine CXCL1 were significantly increased in tumor-bearing mice compared with non–tumor-bearing mice. Moreover, CXCL1 expression was significantly decreased by TSU68 treatment. CXCR2 expression was detected predominantly on tumor cells in orthotopic tumors compared with ectopic tumors. The number of migrating neutrophils in premetastatic liver was significantly decreased in the TSU68-treated group (P &amp;lt; 0.001). The amount of interleukin-12 (IL-12) p40 in the portal vein was significantly decreased by TSU68 (P = 0.02). Blockade of both CXCR2 and IL-12 p40 with a neutralizing antibody significantly inhibited liver metastasis. These results suggest that the CXCL1/CXCR2 axis is important in cancer metastasis and that TSU68 may modulate the premetastatic niche in the target organ through suppression of the inflammatory response, which might be an alternative mechanism used by antiangiogenic agents. [Cancer Res 2008;68(23):9754–62]
Effectiveness of an intervention led by lay health counsellors for depressive and anxiety disorders in primary care in Goa, India (MANAS): a cluster randomised controlled trial
Authors: Vikram Patel, Helen A Weiss, Neerja Chowdhary, Smita Naik, Sulochana Pednekar, Sudipto Chatterjee, Mary J De Silva, Bhargav Bhat, Ricardo Araya, Michael King, Gregory Simon, Helen Verdeli, Betty R Kirkwood
Journal: The Lancet (2010)
Dermal Connective Tissue Permeability in Rheumatoid Arthritics
Authors: A. Herp, J. Fabianek, A. Caltck, W. Pigman
Journal: Annals of the Rheumatic Diseases (1966)

Previous studies indicate thatthetransfer of proteins andother substances between synovial fluid andblood ismoreextensive forrheumatoid arthritics thanfornormalpersons (Harris, Millard, and Banerjee, 1958;Platt, Holley, andPigman, 1957; Michelazzi, 1943). Theprotein concentration in synovial fluid isalso higher forrheumatoid arthritics thanforhealthy individuals (Platt andothers, 1957; Decker, McKenzie, McGuckin,and Slocumb, 1959;Johansen andSylvest, 1961). Thesealterations suggest that afeature ofthis disease maybean enhanced  oftheconnective tissue. Thealtered permeability, inturn, could arise froma change ofthephysical state oftheground substance ofconnective tissue, particularly ofthehyaluronic acid, whichisespecially important forthephysical properties oftheground substance. Thisconcept is inagreement withtheobservations that thedegree of polymerization ofhyaluronic acid isdecreased inthe synovial fluid ofpatients withconnective tissue disease (Ragan andMeyer,1949; Sundblad, 1953; Bollet, 1956;Stafford, Niedermeier, Holley, and Pigman, 1964), since thesynovial fluid isprobably derived fromtheground substance. Thislaboratory hasbeenengaged forsometimein studying thenature oftheoxidative-reductive depolymerization (ORD-reaction) ofhyaluronic acidby autoxidants andtherelation ofthisreaction to catabolic processes (Pigman, Matsumura, andHerp, 1965). Several autoxidants andantioxidants (inhibitors) whichaffected theinvitro oxidative-reductive depolymerization ofhyaluronic acid(Pigman, Rizvi, andHolley, 1961; PigmanandRizvi, 1959) werealsofoundtoaffect invivoskinpermeability (Fabianek, Herp,andPigman, 1963; 1965). Thepresent paperreports dataonastudy ofthe permeability ofhumanskinforgroups ofhealthy subjects, hospitalized non-arthritic patients, and rheumatoid arthritic patients. Sincemostofthe arthritics wereonmedication atthetimeofexperimentation, theeffect oforal ingestion ofaspirin and other inhibitors ontheskinpermeability ofrats wasalso investigated.