bluuebunny/crossref_metadata_2025_split huggingface dataset:
Studies on Mechanisms Involved in Hypoglycemia-Induced Platelet Activation
Authors: Trovati Mariella , Anfossi Giovanni , Cavalot Franco , Vitali Sara , Massucco Paola , Mularoni Elena , Schinco Piercarla , Tamponi Giacomo , Emanuelli Giorgio 
Published: September 2013

The aim of our study was to investigate the mechanisms involved in hypoglycemia-induced platelet activation. Sixteen healthy male subjects received a 60-min intravenous infusion of human regular insulin at the rate of 64 mU · m−2 · min−1: throughout 150 min, we serially measured plasma concentrations of glucose, insulin, and counterregulatory hormones; platelet sensitivity to ADP, thrombin and platelet-activating factor; plasma concentrations of platelet markers for specific proteins of in vivo release reaction (β-thromboglobulin and platelet factor 4). Our study showed that insulin-induced hypoglycemia causes a significant increase in platelet sensitivity to aggregating agents in vitro and a platelet release reaction in vivo. Hypoglycemia-induced platelet activation was not correlated with plasma glucose concentrations at nadir and occurred before the increase of plasma growth hormone and cortisol.
To further elucidate the mechanisms of hypoglycemia-induced platelet activation, we incubated in vitro platelet-rich plasma (PRP) of seven fasting healthy subjects with the same concentrations of insulin, epineph-rine, glucagon, growth hormone, and cortisol measured in vivo during insulin-induced hypoglycemia. Only epinephrine was able to increase platelet sensitivity to aggregating agents. To investigate the role of α-adrenergic receptors in this phenomenon, we also studied four healthy subjects on another occasion, repeating the above-described insulin infusion together with intravenous infusion of phentolamine (–15 to + 150 min), 5 mg over 2 min followed by 500 μg/min. α-Blockade was able to suppress hypoglycemia-induced increase of platelet sensitivity to aggregating agents. A further study in vitro confirmed these results obtained in vivo, showing that incubation with phentolamine is able to inhibit the epinephrine-induced increase of platelet aggregation in response to ADP, thrombin, and platelet-activating factor.
In conclusion, insulin-induced hypoglycemia deeply influences platelet function, causing an increase of platelet sensitivity to aggregating agents in vitro and a release reaction in vivo. Through α-adrenoreceptors, epinephrine is responsible for the hypoglycemia-induced increase of platelet aggregation in response to ADP, thrombin, and platelet-activating factor.
Insulin-Receptor Development in Normal and Diabetic Pregnancies: Role of Membrane Fluidity
Authors: Neufeld N D , Corbo L M 
Published: September 2013

In the hyperinsulinemic offspring of the diabetic mother, both significant macrosomia and postnatal hypoglycemia are thought to be due to increased insulin sensitivity. The purpose of this study is to characterize changes in insulin-receptor development in fetal offspring of an experimental model of diabetic pregnancy. Two groups of Sprague-Dawley female rats were studied after timed mating. Both groups received injections of either vehicle (controls) or streptozocin (diabetic), 40 mg/100 g body wt, on day 7 of pregnancy and were killed at either 17, 20, or 21 days of gestation. Maternal and fetal blood were assayed for glucose and insulin, and fetal liver membranes were prepared for 125I-labeled insulin binding, lipid composition, and fluorescence polarization studies with the probe 1,6-diphenyl-1,3,5-hexatriene (DPH).
Maternal and pooled fetal glucose levels were elevated in streptozocin-treated rats; however, pooled fetal insulin values were not elevated in the offspring of diabetic animals compared with controls (33 ± 1 vs. 50 ± 5 μU/ml). 125I-insulin binding was greater in fetal offspring of diabetic (FO) rat membranes at each gestational age studied [P &lt; .001 by analysis of variance (ANOVA)] due to significantly greater numbers of both high- and low-affinity receptors. The highest insulinbinding capacity was seen on membranes obtained from FD rats at day 21 (9.92 M · L1 · 100 μg membranes1 vs. 6.38 M · L1 · 100 μg protein1 in fetal control (FC) rats. At each gestational age, membranes from FDs had lower values for fluorescence polarization (using the probe DPH) than did gestational-age-matched controls. These values suggest that membrane fluidity was lower in membranes from the FD group. Lipid analyses of plasma membranes showed significantly higher levels of phospholipid-to-protein ratios in samples from 20- and 21-day FD rats than in matched controls (0.297 ± 0.032 and 0.0547 ± 0.116 vs. 0.193 ± 0.001 and 0.261 ± 0.016, P &lt; .05 by ANOVA). Significant correlations existed between insulin tracer binding and fluorescence polarization (FP) (r = −.82, P &lt; .05) and between insulin-binding capacity and flow activation energy, a measurement derived from FP data obtained over a range of temperatures (r = − .95, P &lt; .005).
In summary, experimental diabetic pregnancy was associated with increased expression of insulin receptors on hepatic plasma membranes. This could be correlated with certain physical properties of the membrane related to lipid content and composition. The data did not exclude the possibility that other factors such as different rates of receptor synthesis and/or degradation could be operative in fetal development in diabetic pregnancy.
Inhibition of Glycogenolysis and Glycogen Phosphorylase by Insulin and Proinsulin in Rat Hepatocyte Cultures
Authors: Hartmann Heinz , Probst Irmelin , Jungermann Kurt , Creutzfeldt Werner 
Published: September 2013

The inhibitory action of insulin and proinsuiin on basal and glucagon-activated glycogenolysis was studied in cultured rat hepatocytes containing [14C]glycogen. Insulin or proinsuiin given as sole hormones in the presence of 5 mM glucose decreased basal release of [14C]glucose from [14C]glycogen to 20%. Half-maximal effective concentration of insulin was ∼0.15 nM and of proinsuiin was ∼5 nM. Inhibition of [14C]lactate release from [14C]glycogen required slightly higher hormone concentrations with a similar difference in potency for insulin and proinsuiin.
The glucagon-stimulated release of [14C]glucose was completely blocked by insulin or proinsuiin with half-maximal effective concentrations of ∼0.2 and 8 nM, respectively. In contrast, release of [14C]lactate in the presence of glucagon was increased slightly by insulin and proinsuiin.
Basal and glucagon-activated phosphorylase activity was inhibited by ∼50% in a dose-dependent manner by both hormones, with differences in potency similar to those for the inhibition of glycogenolysis.
These data point to a direct regulatory role of insulin in the control of hepatic glycogen breakdown even when acting as sole hormone. The results do not support the notion of a preferential inhibitory potency of proinsuiin on hepatic glycogenolysis.
Acquisition and persistence of antimicrobial-resistant bacteria isolated from dogs and cats admitted to a veterinary teaching hospital
Authors: Hamilton Elizabeth , Kruger John M. , Schall William , Beal Matthew , Manning Shannon D. , Kaneene John B. 
Published: September 2013

Abstract
Objective—To assess antimicrobial resistance among bacteria isolated from dogs and cats admitted to a veterinary teaching hospital (VTH), determine the incidence of acquisition of and frequency of persistent colonization by antimicrobial-resistant organisms among these animals, and identify risk factors associated with these variables.
Design—Prospective longitudinal study.
Animals—622 dogs and 92 cats admitted to a VTH and expected to stay ≥ 48 hours.
Procedures—Samples were collected with rectal and nasal or oropharyngeal swabs at admission and discharge. Isolates of enterococci, staphylococci, and Escherichia coli were tested for antimicrobial resistance via microbroth dilution methods. A subset of isolates was analyzed with pulsed-field gel electrophoresis and multilocus sequence typing. Significant trends in proportions of organisms with antimicrobial resistance over the 3-year study period were assessed.
Results—The proportion of staphylococci with antimicrobial resistance increased, whereas the proportion of E coli with resistance decreased, over time; resistance among enterococci was more variable. For 506 dogs with paired admission and discharge samples, multidrug-resistant (MDR) E coli was acquired by 40 (8%) and methicillin-resistant Staphylococcus aureus (MRSA) was acquired by 7 (1.4%); hospitalization for > 3 days was significantly associated with both variables. Most (5/7 isolates) acquired MRSA was of sequence type (ST) 5.
Conclusions and Clinical Relevance—Extended hospitalization was associated with increased risk of acquiring MDR E coli or MRSA, although few animals acquired MRSA. It is unclear whether associations were confounded by illness severity or use of infection control measures. Additionally, MRSA of ST5, which has been associated with small animal medicine, was the most commonly acquired MRSA in this study.
Le printemps des partis ? Le rôle des organisations partisanes égyptiennes dans les élections législatives
Authors: Steuer Clément 
Published: September 2013

À la faveur de la nouvelle législation encadrant les organisations partisanes et les opérations électorales, les partis politiques égyptiens ont dominé les premières élections législatives post-révolutionnaires, au détriment notamment des élites locales traditionnelles et des hommes d’affaires. Le système partisan égyptien ne s’est néanmoins pour l’instant que partiellement autonomisé. Durant la campagne, les partis se sont révélés extrêmement dépendants de toute une variété d’organisations leur préexistant : clientèles, tribus, entreprises, syndicats, mouvements révolutionnaires, Églises, et surtout confrérie des Frères musulmans et organisation de la Prédication salafiste. Ce manque d’institutionnalisation ne doit cependant pas masquer le fait que les partis ont joué un rôle central dans ces élections, à tel point que cette situation a motivé l’arrêt de la Haute Cour Constitutionnelle qui a entraîné la dissolution de l’Assemblée du peuple en juin 2012.
Morsi au pouvoir : scénario d'une transition à l'égyptienne
Authors: Azab Lamiss 
Published: September 2013

Le 24 juin 2012, les Égyptiens ont choisi le candidat des Frères Musulmans à la présidentielle, Mohamed Morsi, pour inaugurer cette deuxième République égyptienne. Dans un contexte fortement marqué par l’instabilité institutionnelle et la fragilité constitutionnelle, par le chaos sécuritaire et l’omniprésence du militaire, il reste difficile d’évaluer le processus de transition démocratique. En revenant sur le champ politique égyptien au lendemain des législatives et en reprenant les « surprises » des présidentielles, certains choix électoraux sont mis en lumière pour nuancer les propos selon lesquels l’Égypte serait sortie de la dictature militaire pour entrer, de son propre gré, dans la dictature islamique. Une analyse fondée sur le terrain et limitée aux facteurs internes permet de proposer un éclairage sur les mécanismes socioculturels propres au champ égyptien. Il en ressort que les électeurs ont plutôt voté contre un retour de l’ancien régime que pour un programme politique à référent islamique.
Initiatives de transition : la question politique
Authors: Jonet Christian , Servigne Pablo 
Published: September 2013

Puissant outil de mobilisation citoyenne suscitant un intérêt croissant du public et des médias, les initiatives de transition troublent les sensibilités de gauche par leur silence remarqué sur la question des inégalités et des luttes sociales. Le mouvement est-il « apolitique » ? N’est-il pas au contraire pleinement politique ? Quelles opportunités et quels risques comportent ces nouvelles pratiques et cette manière de concevoir la politique ?
Pour une transition écologique à visée sociétale
Authors: Laigle Lydie 
Published: September 2013

Les experts nous expliquent que le pétrole va manquer, que le carbone est nocif, que les inégalités augmentent. Mais le lien entre ces constats statistiques et dispersés et les activités quotidiennes est souvent extrêmement ténu. Comment mettre en place des activités qui inversent les tendances néfastes ? Un message ressort cependant, d’une manière générale : cette dispersion et incohérence des institutions établies risquent de durer, chacun préservant son pré carré, avec la force de l’inertie. Le renvoi de questions politiques à l’expertise technique ne correspond-il pas à cela : une volonté institutionnelle d’éviter toute remise en cause des compétences acquises ? L’action instituante doit donc prendre le relais, et poser les jalons de nouvelles institutions. D’abord locales et extrêmement plastiques, peu stabilisées, elles croissent discrètement à l’ombre de leurs aînées, et ambitionnent de les remplacer.
« Plutôt que d'avoir une indignation globale, il vaut mieux agir »
Authors: Lagneau Antoine , Massiah Gus , Karakartal Elif 
Published: September 2013

Miguel Benasayag, philosophe, psychanalyste et essayiste franco-argentin, militant guévariste durant la dictature en Argentine (PRT-ERP), s’inscrit dans la mouvance libertaire. Critique envers « la militance triste », méfiant vis-à-vis des partis, il revient sur son expérience dans la guérilla et sur ses idées développées par la suite dans Pour une nouvelle radicalité 1 . Du collectif Malgré Tout à son travail actuel avec le mouvement coopérativiste en Italie, il détaille pour Mouvements ses différents engagements fondés sur l’expérimentation (théorique et pratique) et formule des hypothèses sur les nouvelles ontologies en cours d’émergence : quelle sera donc cette « nouvelle bête » qui marquera notre époque comme les figures de Dieu, puis celle de l’Homme, avaient marqué les précédentes ?
Both MC5r and A2Ar Are Required for Protective Regulatory Immunity in the Spleen of Post–Experimental Autoimmune Uveitis in Mice
Authors: Lee Darren J. , Taylor Andrew W. 
Published: September 2013

Abstract
The ocular microenvironment uses a poorly defined melanocortin 5 receptor (MC5r)-dependent pathway to recover immune tolerance following intraocular inflammation. This dependency is seen in experimental autoimmune uveoretinitis (EAU), a mouse model of endogenous human autoimmune uveitis, with the emergence of autoantigen-specific regulatory immunity in the spleen that protects the mice from recurrence of EAU. In this study, we found that the MC5r-dependent regulatory immunity increased CD11b+F4/80+Ly-6ClowLy-6G+CD39+CD73+ APCs in the spleen of post-EAU mice. These MC5r-dependent APCs require adenosine 2A receptor expression on T cells to activate EAU-suppressing CD25+CD4+Foxp3+ regulatory T cells. Therefore, in the recovery from autoimmune disease, the ocular microenvironment induces tolerance through a melanocortin-mediated expansion of Ly-6G+ regulatory APCs in the spleen that use the adenosinergic pathway to promote activation of autoantigen-specific regulatory T cells.
Inflammatory Responses Induced by Lipopolysaccharide Are Amplified in Primary Human Monocytes but Suppressed in Macrophages by Complement Protein C5a
Authors: Seow Vernon , Lim Junxian , Iyer Abishek , Suen Jacky Y. , Ariffin Juliana K. , Hohenhaus Daniel M. , Sweet Matthew J. , Fairlie David P. 
Published: September 2013

AbstractMonocytes and macrophages are important innate immune cells equipped with danger-sensing receptors, including complement and Toll-like receptors. Complement protein C5a, acting via C5aR, is shown in this study to differentially modulate LPS-induced inflammatory responses in primary human monocytes versus macrophages. Whereas C5a enhanced secretion of LPS-induced IL-6 and TNF from primary human monocytes, C5a inhibited these responses while increasing IL-10 secretion in donor-matched human monocyte-derived macrophages differentiated by GM-CSF or M-CSF. Gαi/c-Raf/MEK/ERK signaling induced by C5a was amplified in macrophages but not in monocytes by LPS. Accordingly, the Gαi inhibitor pertussis toxin and MEK inhibitor U0126 blocked C5a inhibition of LPS-induced IL-6 and TNF production from macrophages. This synergy was independent of IL-10, PI3K, p38, JNK, and the differentiating agent. Furthermore, C5a did not inhibit IL-6 production from macrophages induced by other TLR agonists that are selective for Toll/IL-1R domain–containing adapter inducing IFN-β (polyinosinic-polycytidylic acid) or MyD88 (imiquimod), demonstrating selectivity for C5a regulation of LPS responses. Finally, suppression of proinflammatory cytokines IL-6 and TNF in macrophages did not compromise antimicrobial activity; instead, C5a enhanced clearance of the Gram-negative bacterial pathogen Salmonella enterica serovar Typhimurium from macrophages. C5aR is thus a regulatory switch that modulates TLR4 signaling via the Gαi/c-Raf/MEK/ERK signaling axis in human macrophages but not monocytes. The differential effects of C5a are consistent with amplifying monocyte proinflammatory responses to systemic danger signals, but attenuating macrophage cytokine responses (without compromising microbicidal activity), thereby restraining inflammatory responses to localized infections.
IL-33 Markedly Activates Murine Eosinophils by an NF-κB–Dependent Mechanism Differentially Dependent upon an IL-4–Driven Autoinflammatory Loop
Authors: Bouffi Carine , Rochman Mark , Zust Christopher B. , Stucke Emily M. , Kartashov Andrey , Fulkerson Patricia C. , Barski Artem , Rothenberg Marc E. 
Published: September 2013

Abstract
Eosinophils are major effector cells in type 2 inflammatory responses and become activated in response to IL-4 and IL-33, yet the molecular mechanisms and cooperative interaction between these cytokines remain unclear. Our objective was to investigate the molecular mechanism and cooperation of IL-4 and IL-33 in eosinophil activation. Eosinophils derived from bone marrow or isolated from Il5-transgenic mice were activated in the presence of IL-4 or IL-33 for 1 or 4 h, and the transcriptome was analyzed by RNA sequencing. The candidate genes were validated by quantitative PCR and ELISA. We demonstrated that murine-cultured eosinophils respond to IL-4 and IL-33 by phosphorylation of STAT-6 and NF-κB, respectively. RNA sequence analysis of murine-cultured eosinophils indicated that IL-33 induced 519 genes, whereas IL-4 induced only 28 genes, including 19 IL-33–regulated genes. Interestingly, IL-33 induced eosinophil activation via two distinct mechanisms, IL-4 independent and IL-4 secretion/autostimulation dependent. Anti–IL-4 or anti–IL-4Rα Ab-treated cultured and mature eosinophils, as well as Il4- or Stat6-deficient cultured eosinophils, had attenuated protein secretion of a subset of IL-33–induced genes, including Retnla and Ccl17. Additionally, IL-33 induced the rapid release of preformed IL-4 protein from eosinophils by a NF-κB–dependent mechanism. However, the induction of most IL-33–regulated transcripts (e.g., Il6 and Il13) was IL-4 independent and blocked by NF-κB inhibition. In conclusion, we have identified a novel activation pathway in murine eosinophils that is induced by IL-33 and differentially dependent upon an IL-4 auto-amplification loop.
Disruption of the Complement Anaphylatoxin Receptor C5L2 Exacerbates Inflammation in Allergic Contact Dermatitis
Authors: Wang Ruobing , Lu Bao , Gerard Craig , Gerard Norma P. 
Published: September 2013

Abstract
The complement anaphylatoxin C5a is a critical mediator of allergic contact dermatitis, bridging essential aspects of innate and adaptive immunity. This anaphylatoxin functions by interacting with two 7-transmembrane segment receptors, the C5aR and C5L2. The C5aR is a classical G protein coupled receptor, whereas C5L2 is deficient in coupling to G proteins because of variations in the sequence. Our previous work in human neutrophils revealed a unique role for C5L2 in negatively modulating anaphylatoxin receptor mediated cellular activation through interactions with β-arrestin. When C5L2 is deficient, C5aR-mediated β-arrestin signaling is greatly enhanced. The work described in this study was undertaken first to determine the effect of C5L2 deficiency in a murine model of contact sensitivity, and second to determine whether the resultant exacerbation of inflammatory parameters reflects a negative modulatory function of C5L2 on the C5aR. First, we find dramatic increases in inflammation in C5L2−/− animals compared with wild type mice. Second, these increases are completely reversed following administration of mAb against the C5aR. Thus, in allergic contact sensitivity, as in isolated human neutrophils, C5L2 functions to suppress C5a-C5aR–mediated responses, further underscoring its role as a negative regulator of anaphylatoxin activity.
Cutting Edge: TLR Signaling Licenses IRAK1 for Rapid Activation of the NLRP3 Inflammasome
Authors: Fernandes-Alnemri Teresa , Kang Seokwon , Anderson Connor , Sagara Junji , Fitzgerald Katherine A. , Alnemri Emad S. 
Published: September 2013

Abstract
Activation of the NLRP3 inflammasome by diverse stimuli requires a priming signal from TLRs and an activation signal from purinergic receptors or pore-forming toxins. In this study, we demonstrate, through detailed analysis of NLRP3 activation in macrophages deficient in key downstream TLR signaling molecules, that MyD88 is required for an immediate early phase, whereas Toll/IL-1R domain-containing adapter inducing IFN-β is required for a subsequent intermediate phase of posttranslational NLRP3 activation. Both IL-1R–associated kinase (IRAK) 1 and IRAK4 are critical for rapid activation of NLRP3 through the MyD88 pathway, but only IRAK1 is partially required in the Toll/IL-1R domain-containing adapter inducing IFN-β pathway. IRAK1 and IRAK4 are also required for rapid activation of NLRP3 by Listeria monocytogenes, as deletion of IRAK1 or IRAK4 led to defective inflammasome activation. These findings define the pathways that lead to rapid NLRP3 activation and identify IRAK1 as a critical mediator of a transcription-independent,inflammasome-dependent early warning response to pathogenic infection.
Endoscope-assisted External Approach for Lateral Lesions in Frontal Sinus
Authors: Shanbag Raghunath , Bidkar Vijay , Naik Ashok , Jalisatgi Roshan 
Published: September 2013

ABSTRACT

Background
Lesions of the frontal sinus (FS) are always a surgical challenge. Conventional endonasal endoscopic techniques do not provide complete access inside the FS. This is especially true with laterally placed lesions like mucocele or post-traumatic cerebrospinal fluid (CSF) leak from FS. Standard procedures like osteoplastic flap and endoscopic modified Lothrop are not feasible for these smaller unilateral lesions with normally functioning contralateral sinus.

Study design
Retrospective case study of laterally placed posterior table CSF leak and frontal mucocele were evaluated for their clinical presentation, radiological, operative findings and follow-up.

Conclusion
Complete external approaches to the lateral lesion of FS are associated with high morbidity. Ability of the endoscopes to visualize lateral and posterior extents of the FS directly through the brow incision helps in complete repair/ excision of these lesions without any difficulty.

How to cite this article
Shanbag R, Bidkar V, Naik A, Jalisatgi R. Endoscope-assisted External Approach for Lateral Lesions in Frontal Sinus. Clin Rhinol An Int J 2013;6(2):72-76.