Use of Toll-Like Receptor Agonists to Induce Ectopic Lymphoid Structures in Myasthenia Gravis Mouse Models.

Myasthenia gravis (MG) is an autoimmune disease mediated by autoantibodies against the acetylcholine receptor (AChR) at the neuromuscular junction. MG symptoms are characterized by muscle weaknesses. The thymus of MG patients is very often abnormal and possesses all the characteristics of tertiary lymphoid organs such as neoangiogenesis processes, overexpression of inflammatory cytokines and chemokines, and infiltration of B lymphocytes leading to ectopic germinal center (GC) development.

Muscle satellite cells are functionally impaired in myasthenia gravis: consequences on muscle regeneration.

Myasthenia gravis (MG) is a neuromuscular disease caused in most cases by anti-acetyl-choline receptor (AChR) autoantibodies that impair neuromuscular signal transmission and affect skeletal muscle homeostasis. Myogenesis is carried out by muscle stem cells called satellite cells (SCs). However, myogenesis in MG had never been explored.

Preconditioned mesenchymal stem cells treat myasthenia gravis in a humanized preclinical model.

Myasthenia gravis (MG) with anti-acetylcholine receptor (AChR) Abs is an autoimmune disease characterized by severe defects in immune regulation and thymic inflammation. Because mesenchymal stem cells (MSCs) display immunomodulatory features, we investigated whether and how in vitro-preconditioned human MSCs (cMSCs) could treat MG disease. We developed a new humanized preclinical model by subcutaneously grafting thymic MG fragments into immunodeficient NSG mice (NSG-MG model).

Review on Toll-Like Receptor Activation in Myasthenia Gravis: Application to the Development of New Experimental Models.

Abnormal toll-like receptor (TLR) activation and uncontrolled resolution of inflammation are suspected to play a key role in the development of autoimmune diseases. Acquired myasthenia gravis (MG) is an invalidating neuromuscular disease leading to muscle weaknesses. MG is mainly mediated by anti-acetylcholine receptor (AChR) autoantibodies, and thymic hyperplasia characterized by ectopic germinal centers is a common feature in MG.

Novel CXCL13 transgenic mouse: inflammation drives pathogenic effect of CXCL13 in experimental myasthenia gravis.

Abnormal overexpression of CXCL13 is observed in many inflamed tissues and in particular in autoimmune diseases. Myasthenia gravis (MG) is a neuromuscular disease mainly mediated by anti-acetylcholine receptor autoantibodies. Thymic hyperplasia characterized by ectopic germinal centers (GCs) is a common feature in MG and is correlated with high levels of anti-AChR antibodies.

Role of IL-1β in experimental cystic fibrosis upon P. aeruginosa infection.

Cystic fibrosis is associated with increased inflammatory responses to pathogen challenge. Here we revisited the role of IL-1β in lung pathology using the experimental F508del-CFTR murine model on C57BL/6 genetic background (Cftr(tm1eur) or d/d), on double deficient for d/d and type 1 interleukin-1 receptor (d/d X IL-1R1-/-), and antibody neutralization. At steady state, young adult d/d mice did not show any signs of spontaneous lung inflammation.

Thymoma-associated myasthenia gravis: On the search for a pathogen signature.

Myasthenia gravis (MG) is an autoimmune disease mainly mediated by anti-acetylcholine receptor (AChR) antibodies. In the late onset, a thymoma, tumor of the thymus, is quite frequent. However, the events leading to thymoma and MG are not understood.

Effect of interfaces on the melting of PEO confined in triblock PS-b-PEO-b-PS copolymers.

Block copolymers form nanostructures that have interesting physical properties because they combine, for a single compound, the complementary features brought by each block. However, in order to fully exploit these properties, the physical state of each kind of domain must be precisely controlled. In this work, triblock PS-b-PEO-b-PS copolymers consisting of a central poly(ethylene oxide) (PEO) block covalently bonded to polystyrene (PS) blocks were synthesized by Atom Transfer Radical Polymerization.

Relationship between psychiatric status and frontal-subcortical systems in HIV-infected individuals.

Human immunodeficiency virus (HIV)-infected adults frequently evidence both neurocognitive and psychiatric dysfunction. It was hypothesized that apathy and irritability, but not anxiety and depression, are related to HIV effects on frontal-subcortical systems. This hypothesis was evaluated by determining the degree to which these psychiatric features are associated with neurocognitive functioning that is dependent upon frontal-subcortical circuitry and, therefore, thought to be sensitive to the central nervous system effects of HIV.

Adherence to antiretroviral medications in HIV: differences in data collected via self-report and electronic monitoring.

Controversy remains regarding the reliability of methods used to determine adherence to antiretroviral medication in HIV. In this study the authors compared adherence rates of 119 HIV-positive participants during a 6-month study, as estimated via electronic monitoring (EM) and self-report (SR). Adherence for both short (4-day) and long (4-week, or intervisit) periods was examined, as well as factors that underlie discrepancies between EM and SR.

Variations in patterns of highly active antiretroviral therapy (HAART) adherence.

Strict adherence to highly active antiretroviral therapy (HAART) is necessary for successful suppression of HIV replication. A large number of individuals are not adherent, however, and the reasons for non-adherence are varied and complex. We utilized cluster analyses to identify subgroups of adherers in a sample of 222 HIV positive individuals whose HAART use was electronically monitored.

Ocular toxoplasmosis in human immunodeficiency virus-infected patients.

The files of 45 human immunodeficiency virus-infected patients with ocular toxoplasmosis were reviewed, with a median follow-up of eight months. The condition was unilateral in 37 of the 45 patients (82%) and was bilateral in eight (18%). Inflammation of the anterior chamber and the vitreous was present in 32 of 53 eyes (60%) and 38 of 53 eyes (72%), respectively.

Foscarnet induction therapy for cytomegalovirus retinitis in AIDS: comparison of twice-daily and three-times-daily regimens.

We have evaluated the effects of induction therapy with foscarnet 100 mg/kg b.i.d.

Subacute inhalation toxicity of benzaldehyde in the Sprague-Dawley rat.

Benzaldehyde was administered by inhalation to female and male Sprague-Dawley rats for 14 consecutive days (low level: 500 ppm; medium level: 750 ppm; high level: 1000 ppm). Effects of this chemical were investigated during and at the end of the exposure period. Throughout the experiment, significant hypothermia and a reduction of motor activity were observed in all rats exposed to benzaldehyde and were accompanied in high-level rats by a severe impairment of the central nervous system, as evidenced by abnormal gait, tremors, and a positive Straub sign.

Efficacy and tolerance of intravitreal ganciclovir in cytomegalovirus retinitis in acquired immune deficiency syndrome.

Forty-four patients with acquired immune deficiency syndrome with cytomegalovirus (CMV) retinitis (64 eyes) intolerant of or refusing systemic antiviral therapy received 710 intravitreal injections of ganciclovir at the dosage of 400 micrograms per injection. The patients were followed for a mean period of 9 weeks. Induction therapy consisted of two injections a week until healing.

[Cytomegalovirus retinitis in AIDS. Treatment with intravitreal injections of ganciclovir].

Cytomegalovirus (CMV) retinitis is the most frequent ocular infection in AIDS, and it is responsible for blindness. Intravitreal injections of ganciclovir in doses of 400 g have been tried in patients who could not tolerate any systemic treatment. Induction therapy consists of 2 injections per week, followed by maintenance therapy with 1 injection per week.

Foscarnet in the treatment of cytomegalovirus retinitis in acquired immune deficiency syndrome.

Cytomegalovirus (CMV) retinitis is the major cause of visual loss in acquired immune deficiency syndrome (AIDS). Thirty-one patients with active CMV retinitis were treated with the new antiviral drug, Foscarnet (trisodium phosphonoformate). After a 3-week course of induction therapy, the retinitis improved in 29 of 31 patients (93.