Mild Gestational Hypothyroidism in Mice Has Transient Developmental Effects and Long-Term Consequences on Neuroendocrine Systems.

Thyroid hormones (TH) play a key role in fetal brain development. While severe thyroid dysfunction, has been shown to cause neurodevelopmental and reproductive disorders, the rising levels of TH-disruptors in the environment in the past few decades have increased the need to assess effects of subclinical (mild) TH insufficiency during gestation. Since embryos do not produce their own TH before mid-gestation, early development processes rely on maternal production.

Preclinical Evidence for a Drug-Drug Interaction Between Cannabinol and Melatonin.

The worldwide legalization of medicinal cannabis has led to an increased use of products made by commercial operators. These products often contain minor cannabinoids such as cannabinol (CBN) which are advertised to improve sleep. Products are also available in which CBN is combined with conventional therapies, with a common product containing both CBN and the widely used sleep-aid melatonin.

New Onset Diabetes in Pancreatic Adenocarcinoma Does Not Correlate With Molecular Subtype.

Background And Objectives: Studies show that new onset diabetes mellitus (DM) (NOD) predates the diagnosis of PDAC by up to 2 years. Two tumor-intrinsic molecular subtypes of PDAC that are prognostic and predictive of chemotherapy response have been described and validated. We hypothesize that patients with NOD may have different molecular subtypes and prognoses.

A high seizure burden increases brain concentrations of specialized pro-resolving mediators in the Scn1a mouse model of Dravet syndrome.

Objective: Dravet syndrome is a severe, intractable epilepsy in which 80 % of patients have a de novo mutation in the gene SCN1A. We recently reported that a high seizure burden increased hippocampal concentrations of an array of pro-inflammatory prostaglandins in the Scn1a mouse model of Dravet syndrome. This raised the possibility that a high seizure burden might also trigger the accumulation of specialized pro-resolving mediators that facilitate the resolution of neuroinflammation and brain repair.