Expression analysis of genes involved in collagen cross‐linking and its regulation in traumatic anterior shoulder instability

The molecular alterations involved in the capsule deformation presented in shoulder instability patients are poorly understood. Increased TGFβ1 acts as a signal for production of matrix macromolecules by fibrogenic cells at joint injury sites. TGFβ1, through its receptor TGFβR1, regulates genes involved in collagen cross‐linking, such as LOX, PLOD1, and PLOD2. We evaluated TGFβ1, TGFβR1, LOX, PLOD1, and PLOD2 gene expression in the antero‐inferior (macroscopically injured region), antero‐superior and posterior regions of the glenohumeral capsule of 29 shoulder instability patients and eight controls. We observed that PLOD2 expression was increased in the anterior‐inferior capsule region of the patients compared to controls. LOX expression tended to be increased in the posterior portion of patients. Patients with recurrent shoulder dislocation presented upregulation of TGFβR1 in the antero‐inferior capsule portion and of PLOD2 in the posterior region. Conversely, LOX was increased in the posterior portion of the capsule of patients with a single shoulder dislocation episode. In the antero‐inferior, LOX expression was inversely correlated and TGFβR1 was directly correlated with the duration of symptoms. In the posterior region, PLOD2, TGFβ1, and TGFβR1 were directly correlated with the duration of symptoms. In conclusion, PLOD2 expression was increased in the macroscopically injured region of the capsule of patients. Upregulation of TGFβ1, TGFβR1, and PLOD2 seems to be related with the maintenance of disease symptoms, especially in the posterior region. LOX upregulation seems to occur only in the initial phase of the affection. Therefore, TGFβ1, TGFβR1, LOX, and PLOD2 may play a role in shoulder instability. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:510–517, 2016.     

Fathers’ parenting self-efficacy during the transition to parenthood

Background: Little is known about the development of fathers’ parenting self-efficacy during the transition to parenthood.

Objectives: To analyse (1) fathers’ parenting self-efficacy developmental path and (2) the effects of anxious and depressive symptoms and coparenting support on fathers’ parenting self-efficacy developmental path, from the first trimester of pregnancy to 6 months postpartum.

Methods: Eighty-six fathers recruited at the first trimester of pregnancy completed self-report measures of anxious and depressive symptoms, coparenting support and parenting self-efficacy at the first and third trimesters of pregnancy, and at 1 and 6 months postpartum. Growth curve models were performed.

Results: An increase in fathers’ parenting self-efficacy was found from the first trimester of pregnancy to 6 months postpartum. The main effects of anxious symptoms and interaction effects of anxious symptoms and time were found on fathers’ parenting self-efficacy. Fathers with higher anxious symptoms revealed lower levels of parenting self-efficacy at the first trimester of pregnancy and a lower increase of parenting self-efficacy from this time to 6 months postpartum. The main effects of coparenting support were found in fathers’ parenting self-efficacy. At the first trimester of pregnancy, fathers who perceived more coparenting support revealed higher levels of parenting self-efficacy.

Conclusion: The present study may contribute to the literature by describing fathers’ parenting self-efficacy developmental path and the effects of anxious symptoms and coparenting support on fathers’ parenting self-efficacy developmental path during the transition to parenthood.     

The Effect of High‐Mobility Group Box 1 in Rat Steatotic and Nonsteatotic Liver Transplantation From Donors After Brain Death

High‐mobility group box 1 (HMGB1) has been described in different inflammatory disorders, and the deleterious effects of brain death (BD) may counteract the protection conferred by ischemic preconditioning (IP), the only surgical strategy that is being applied in clinical liver transplantation. Our study examined how HMGB1 may affect preconditioned and unpreconditioned steatotic and nonsteatotic liver grafts from donors after BD (DBDs) for transplantation. HMGB1 was pharmacologically modulated in liver grafts from DBDs, and HMGB1‐underlying mechanisms were characterized. We found that BD decreased HMGB1 in preconditioned and unpreconditioned livers and was associated with inflammation and damage. Exogenous HMGB1 in DBDs activates phosphoinositide‐3‐kinase and Akt and reduces hepatic inflammation and damage, increasing the survival of recipients. Combination of IP and exogenous HMGB1 shows additional benefits compared with HMGB1 alone. This study provides new mechanistic insights into the pathophysiology of BD‐derived liver graft damage and contributes to the development of novel and efficient strategies to ultimately improve liver graft quality.     

Anosmin-1 over-expression increases adult neurogenesis in the subventricular zone and neuroblast migration to the olfactory bulb

New subventricular zone (SVZ)-derived neuroblasts that migrate via the rostral migratory stream are continuously added to the olfactory bulb (OB) of the adult rodent brain. Anosmin-1 (A1) is an extracellular matrix protein that binds to FGF receptor 1 (FGFR1) to exert its biological effects. When mutated as in Kallmann syndrome patients, A1 is associated with severe OB morphogenesis defects leading to anosmia and hypogonadotropic hypogonadism. Here, we show that A1 over-expression in adult mice strongly increases proliferation in the SVZ, mainly with symmetrical divisions, and produces substantial morphological changes in the normal SVZ architecture, where we also report the presence of FGFR1 in almost all SVZ cells. Interestingly, for the first time we show FGFR1 expression in the basal body of primary cilia in neural progenitor cells. Additionally, we have found that A1 over-expression also enhances neuroblast motility, mainly through FGFR1 activity. Together, these changes lead to a selective increase in several GABAergic interneuron populations in different OB layers. These specific alterations in the OB would be sufficient to disrupt the normal processing of sensory information and consequently alter olfactory memory. In summary, this work shows that FGFR1-mediated A1 activity plays a crucial role in the continuous remodelling of the adult OB