[Psychotherapy prognostic factors for personality disorders (PD) treatment: The role of self-reported questionnaires].

Objectives Dropout rates in psychotherapy are known to be high in patients with personality disorders (PD; ranging from 25% and 64% for Borderline PD). Faced with this observation, the Treatment Attrition-Retention Scale for Personality Disorders (TARS-PD; Gamache et coll., 2017) was developed to precisely identify patients with PD at high risk of abandoning therapy based on 15 criteria, regrouped in 5 factors: Pathological Narcissism, Antisocial/Psychopathy, Secondary Gain, Low Motivation, and Cluster A Features.

Interferon-β suppresses murine Th1 cell function in the absence of antigen-presenting cells.

Interferon (IFN)-β is a front-line therapy for the treatment of the relapsing-remitting form of multiple sclerosis. However, its immunosuppressive mechanism of function remains incompletely understood. While it has been proposed that IFN-β suppresses the function of inflammatory myelin antigen-reactive T cells by promoting the release of immunomodulatory cytokines such as IL-27 from antigen-presenting cells (APCs), its direct effects on inflammatory CD4+ Th1 cells are less clear.

Degradation of S-RNase in compatible pollen tubes of Solanum chacoense inferred by immunogold labeling.

The flowering plant Solanum chacoense uses an S-RNase-based self-incompatibility system in order to reject pollen that shares the same genes at the S-locus (S-haplotype) with the style (an incompatible reaction). Two different models have been advanced to explain how compatible pollen tubes are protected from the cytotoxic effects of the S-RNase, sequestration of the S-RNase in a vacuolar compartment or degradation of the S-RNase in the cytoplasm. Here, we examine the subcellular distribution of an S11-RNase 18 and 24 h post pollination (hpp) in compatible and incompatible crosses by immunogold labeling and transmission electron microscopy.

eEF1A is an S-RNase binding factor in self-incompatible Solanum chacoense.

Self-incompatibility (SI) is a genetic mechanism that allows flowering plants to identify and block fertilization by self-pollen. In the Solanaceae, SI is controlled by a multiallelic S-locus encoding both S-RNases and F-box proteins as female and male determinants, respectively. S-RNase activity is essential for pollen rejection, and a minimum threshold value of S-RNases in the style is also required.

The combination of valacyclovir with an anti-TNF alpha antibody increases survival rate compared to antiviral therapy alone in a murine model of herpes simplex virus encephalitis.

The added benefit of combining valacyclovir (VACV), an antiviral agent, with etanercept (ETA), an anti-tumor necrosis factor alpha (TNF-α) antibody, for the treatment of herpes simplex virus type 1 (HSV-1) encephalitis (HSE) was evaluated in a mouse model. BALB/c mice were infected intranasally with 1.85 × 104 plaque forming units of HSV-1.

Both TRIF and IPS-1 adaptor proteins contribute to the cerebral innate immune response against herpes simplex virus 1 infection.

Toll-like receptors (TLRs) and RNA helicases (RLHs) are important cell sensors involved in the immunological control of viral infections through production of type I interferon (IFN). The impact of a deficiency in the TRIF and IPS-1 adaptor proteins, respectively, implicated in TLR3 and RLH signaling pathways, was investigated during herpes simplex virus 1 (HSV-1) encephalitis. TRIF(-/-), IPS-1(-/-), and C57BL/6 wild-type (WT) mice were infected intranasally with 7.

A new dual-specific incompatibility allele revealed by absence of glycosylation in the conserved C2 site of a Solanum chacoense S-RNase.

The stylar determinant of gametophytic self-incompatibility (GSI) in Solanaceae, Rosaceae, and Plantaginaceae is an S-RNase encoded by a multiallelic S-locus. The primary structure of S-RNases shows five conserved (C) and two hypervariable (HV) regions, the latter forming a domain implicated in S-haplotype-specific recognition of the pollen determinant to SI. All S-RNases are glycosylated at a conserved site in the C2 region, although previous studies have shown that N-linked glycans at this position are not required for S-haplotype-specific recognition and pollen rejection.

Modulation of TLR9 response in a mouse model of herpes simplex virus encephalitis.

We evaluated the effects of agonists and antagonist of toll-like receptor (TLR) 9 in comparison with a TLR3 agonist in a mouse model of herpes simplex virus type 1 (HSV-1) encephalitis (HSE). BALB/c mice received a single intranasal dose of either a TLR3 agonist (polyinosinic:polycytidylic acid; PIC), TLR9 agonists (oligodeoxynucleotides (ODNs) 1585, 1826 or 2395) or a TLR9 antagonist (ODN 2088), 1 day before and, for selected groups, 3 days after infection with HSV-1. Mice that received the pre-treatment with vehicle, PIC, ODNs 1585, 1826, 2395 and 2088 before infection had survival rates of 25%, 65%, 55%, 40%, 55% and 30%, respectively (P<0.

A time course of GFP expression and mRNA stability in pollen tubes following compatible and incompatible pollinations in Solanum chacoense.

The self-incompatibility (SI) reaction in the Solanaceae involves molecular recognition of stylar haplotypes by pollen and is mediated by the S-locus from which a stylar-localized S-RNase and several pollen-localized F-box proteins are expressed. S-RNase activity has been previously shown to be essential for the SI reaction, leading to the hypothesis that pollen rejection in incompatible crosses is due to degradation of pollen RNA. We used pollen expressing the fluorescent marker GFP, driven by the LAT52 promoter, to monitor the accumulation of mRNA and protein in pollen after compatible and incompatible pollinations.

Impact of deficiency in CCR2 and CX3CR1 receptors on monocytes trafficking in herpes simplex virus encephalitis.

The role played by resident microglia and by the infiltration of peripheral monocytes/macrophages in the innate immune response during herpes simplex virus type 1 (HSV-1) encephalitis was evaluated in mice deficient for the CCR2 and CX3CR1 receptors. CCR2(-/-), CX3CR1(-/-) and C57BL/6 wild-type (WT) male mice were infected intranasally with 7×10(5) p.f.

Glaucoma-associated WDR36 variants encode functional defects in a yeast model system.

Primary open-angle glaucoma (POAG) is a leading cause of blindness worldwide. POAG is associated with a characteristic progression of changes to ocular morphology and degeneration at the optic nerve head with the loss of visual fields. Physical mapping efforts identified genomic loci in which to search for causative POAG gene mutations.

Effect of pretreatment with toll-like receptor agonists in a mouse model of herpes simplex virus type 1 encephalitis.

Background: We evaluated the effect of pretreatment with Toll-like receptor (TLR) agonists in a mouse model of herpes simplex virus type 1 (HSV-1) encephalitis.

Methods: BALB/c mice received a single intraperitoneal or intranasal injection of polyinosinic:polycytidylic acid (poly I:C), a TLR3 agonist; lipopolysaccharide (LPS), a TLR4 agonist; oligodeoxynucleotide (ODN), a TLR9 agonist; or control vehicle. Twenty-four hours later, animals were infected with 5000 plaque-forming units of HSV-1.