Prenatal alcohol exposure promotes NLRP3 inflammasome-dependent immune actions following morphine treatment and paradoxically prolongs nerve injury-induced pathological pain in female mice.

Background: Neuroimmune dysregulation from prenatal alcohol exposure (PAE) may contribute to neurological deficits associated with fetal alcohol spectrum disorders (FASD). PAE is a risk factor for developing peripheral immune and spinal glial sensitization and release of the proinflammatory cytokine IL-1β, which lead to neuropathic pain (allodynia) from minor nerve injury. Although morphine acts on μ-opioid receptors, it also activates immune receptors, TLR4, and the NLRP3 inflammasome that induces IL-1β.

Brain structural differences in children with fetal alcohol spectrum disorder and its subtypes.

Introduction: The teratogenic effects of prenatal alcohol exposure (PAE) have been examined in animal models and humans. The current study extends the prior literature by quantifying differences in brain structure for individuals with a fetal alcohol spectrum disorder (FASD) compared to typically developing controls, as well as examining FASD subtypes. We hypothesized the FASD group would reveal smaller brain volume, reduced cortical thickness, and reduced surface area compared to controls, with the partial fetal alcohol syndrome (pFAS)/fetal alcohol syndrome (FAS) subtypes showing the largest effects and the PAE/alcohol-related neurodevelopmental disorder (ARND) subtype revealing intermediate effects.

Prenatal alcohol exposure alters mRNA expression for stress peptides, glucocorticoid receptor function and immune factors in acutely stressed neonatal brain.

Background: The amygdala, hippocampus and hypothalamus are critical stress regulatory areas that undergo functional maturation for stress responding initially established during gestational and early postnatal brain development. Fetal alcohol spectrum disorder (FASD), a consequence of prenatal alcohol exposure (PAE), results in cognitive, mood and behavioral disorders. Prenatal alcohol exposure negatively impacts components of the brain stress response system, including stress-associated brain neuropeptides and glucocorticoid receptors in the amygdala, hippocampus and hypothalamus.

Comparison of Astigmatism Prediction Accuracy for Toric Lens Implantation from Two Swept-Source Optical Coherence Tomography Devices.

Purpose: To compare the astigmatism prediction accuracy for toric intraocular lens (IOL) implantation between two swept-source optical coherence tomography (SS-OCT) devices: Argos (Movu, a Santec Company) and the IOLMaster 700 (Carl Zeiss Meditec).

Methods: This was a retrospective chart review of 59 eyes (44 patients) with corneal astigmatism and cataract that underwent cataract surgery or refractive lens exchange surgery with a toric IOL. Biometry was performed on all patients prior to cataract surgery and the Barrett toric IOL calculator was used.

Sex differences in the cognitive function of first-diagnosed, drug-naïve depressed patients: An observational case-control study.

Background: Major depressive disorder (MDD) is a severe mental illness with high prevalence and recurrence rates. Cognitive impairments are found in most depressed patients, but systematic assessment of sex differences in cognitive deficits remains to be investigated.

Methods: A total of 69 first-diagnosed, drug-naïve depressed outpatients (males/females = 28/41; average age: 27.

Targeting the β2-integrin LFA-1, reduces adverse neuroimmune actions in neuropathic susceptibility caused by prenatal alcohol exposure.

Recently, moderate prenatal alcohol exposure (PAE) was shown to be a risk factor for peripheral neuropathy following minor nerve injury. This effect coincides with elevated spinal cord astrocyte activation and ex vivo immune cell reactivity assessed by proinflammatory cytokine interleukin (IL) -1β protein expression. Additionally, the β2-integrin adhesion molecule, lymphocyte function-associated antigen-1 (LFA-1), a factor that influences the expression of the proinflammatory/anti-inflammatory cytokine network is upregulated.