Various infusion solutions are used during preoperative hemodilution or for substituting intraoperative blood loss. We examined the influence of saline 0.9%, albumin 5%, dextran 6%, gelatin 3.5% and hydroxyethyl starch 6% (HES, mw 40,000 and 450,000) on primary hemostasis using the In-vitro bleeding test (IVBT) on composed blood samples of different hematocrit but constant platelet concentration. All infusion solutions tested caused longer bleeding times, depending on the volume used. Saline and albumin had the strongest effect, whereas high molecular weight HES or dextran showed hardly any impairment, if used in a quantity of less than 20% of the blood volume. Autologous plasma seems to be the best substitute in hemodiluted patients, at least if more than 20% of the blood volume has to be substituted by infusion solutions.
It is now well established in normal humans and mice that purification of IgG from serum unmasks their autoantibody activity. Mercuric chloride (HgCl2 ) induces in Brown-Norway (BN) rats a Th2-dependent polyclonal B cell activation, a huge increase in serum IgE and IgG1 concentrations, the production of numerous autoantibodies and an autoantibody-mediated glomerulonephritis. In the present study we have compared the IgG autoantibody activity in the serum and in the purified IgG fraction from normal and HgCl2 -injected BN rats. IgG autoantibodies were found to be masked in normal serum by non-immunoglobulin (non-Ig) serum proteins and, provided these IgG did not encounter normal serum proteins, they could bind to glomerular antigens as assessed by immunofluorescence in a unilateral perfused kidney model. As a consequence of HgCl2 -induced polyclonal activation of B cells, IgG autoantibodies were no longer complexed to non-Ig serum proteins, they were easily detected in the serum and could therefore reach their glomerular target. However, these autoantibodies could still be blocked by normal non-Ig serum proteins not only in vitro but also in a unilateral perfused kidney model so that their binding to glomerular antigens could be prevented. These findings indicate that the ratio between autoantibody level and the amount of non-Ig serum proteins may be crucial in autoantibody-mediated autoimmune diseases.
Abstract Background Opiates act through opioid receptors to diminish pain. Here, we investigated whether mu ( MOR ) and delta ( DOR ) receptor endogenous activity assessed in the whole mouse body or in particular at peripheral receptors on primary nociceptive neurons, control colonic pain. Methods We compared global MOR and DOR receptor knockout ( KO ) mice, mice with a conditional deletion of MOR and DOR in Nav1.8‐positive nociceptive primary afferent neurons ( cKO ), and control floxed mice of both genders for visceral sensitivity. Visceromotor responses to colorectal distension ( CRD ) and macroscopic colon scores were recorded on naïve mice and mice with acute colitis induced by 3% dextran sodium sulphate ( DSS ) for 5 days. Transcript expression for opioid genes and cytokines was measured by quantitative RT ‐ PCR . Results Naïve MOR and DOR global KO mice show increased visceral sensitivity that was not observed in cKO mice. MOR and preproenkephalin (Penk) were the most expressed opioid genes in colon. MOR KO mice had augmented kappa opioid receptor and Tumour‐Necrosis‐Factor‐α and diminished Penk transcript levels while DOR , preprodynorphin and Interleukin‐1β were unchanged. Global MOR KO females had a thicker colon than floxed females. No alteration was detected in DOR mutant animals. A 5‐day DSS treatment led to comparable hypersensitivity in the different mouse lines. Conclusion Our results suggest that mu and delta opioid receptor global endogenous activity but not activity at the peripheral Nav1.8 neurons contribute to visceral sensitivity in naïve mice, and that endogenous MOR and DOR tones were insufficient to elicit analgesia after 5‐day DSS ‐induced colitis. Significance Knockout mice for mu and delta opioid receptor have augmented colon sensitivity in the CRD assay. It shows endogenous mu and delta opioid analgesia that may be explored as potential targets for alleviating chronic intestinal pain.
Les dispositifs de realite virtuelle sont progressivement integres dans differents programmes de reeducation (Fuchs & Chretien, 2018). C’est le cas par exemple des visiocasques utilises dans des therapies innovantes pour encourager la motivation des patients. Cependant, la tolerance et les effets lies a l’exposition aux Environnements Virtuels (EV) sont peu evalues. Cette etude s’interesse a la relation entre l’âge, les reactions posturales, et les cybermalaises induits lors de 5 expositions successives de 250 secondes chacune chez 86 personnes (âgees de 21 a 86 ans). Les participants ont d’abord repondu a un questionnaire concernant le mal des transports (Golding, 1998), puis, apres la 1ere et la 5eme exposition a l’EV, a un questionnaire concernant les cybermalaises (Kennedy et al., 1993). Dans notre echantillon, les scores sur le cybermalaise et le mal des transports sont independants de l’âge. L’EV comportait entre autre une translation avant (TAV) et une translation arriere (TAR). Une augmentation de la Longueur (LCP) et de la Vitesse (VCP) du Centre des Pressions (CP) (valeur avant et apres les translations) est observee (p < 0.05) lors des TAV et TAR. Une adaptation des reactions posturales (comparaison des expositions 1 et 5) est egalement mise en evidence (p < 0.05) pour les TAV et TAR. Une adaptation significative a la perturbation est observee pour LCP et VCP de la TAV (interaction : F (1, 85) = 4.37, p < 0.05 ; F (1, 85) = 4.36, p < 0.05), mais pas pour la TAR. Si LCP et VCP sont correles a l’âge lors de la premiere exposition (pour TAV et TAR), ce n’est plus le cas pour TAV apres la 5eme exposition. Parallelement, le sentiment de cybermalaise augmente avec la duree d’exposition a l’EV (F (1, 85) = 6.28, p < 0.05), et ce independamment de l’âge. Ainsi, alors qu’une adaptation posturale en realite virtuelle est observee, le sentiment de cybermalaise, lui, augmente avec la duree d’exposition quel que soit l’âge.
References :
Fuchs, P., & Chretien, L., (2018). Theories de la realite virtuelle : les veritables usages. Mines ParisTech.
Golding, J. F. (1998). Motion sickness susceptibility questionnaire revised and its relationship to other forms of sickness. Brain research bulletin, 47(5), 507-516.
Kennedy, R.S., Lane, N.E., Berbaum, K.S., & Lilienthal, M.G. (1993). Simulator Sickness Questionnaire: An enhanced method for quantifying simulator sickness. International Journal of Aviation Psychology, 3(3), 203-220.
ABSTRACT NOD2 mutations are key risk factors for Crohn’s disease (CD). NOD2 contributes to intestinal homeostasis by regulating innate and adaptive immunity together with intestinal epithelial function. However, the roles of NOD2 during gut inflammation is not known. We initially observed that NOD2 expression was increased in epithelial cells remote from inflamed areas in CD patients. To explore this finding, Nod2 mRNA expression, inflammation and gut permeability were examined in the small bowel of wild-type (WT), Nod2 knockout and Nod2 mutant mice after rectal instillation of 2,4,6-trinitrobenzene sulfonic acid (TNBS). In WT mice, Nod2 upregulation remote to rectal injury was associated with pro-inflammatory cytokine expression, recirculating CD4 + T-cells, increased paracellular permeability and myosin like chain kinase activity. Nod2 knockout or mutation led to duodenitis and ileitis demonstrating the remote protective role of Nod2. Bone morrow stem cell (BMSC) transplantations indicated that the small intestinal inflammation was due to NOD2 loss in both hematopoietic and non-hematopoietic compartments. As a whole, WT but not mutant NOD2 prevents disease extension at sites remote from the initial intestinal injury.
