Intrauterine Inflammation Leads to Select Sex- and Age-Specific Behavior and Molecular Differences in Mice.

Sex-specific differences in behavior have been observed in anxiety and learning in children exposed to prenatal inflammation; however, whether these behaviors manifest differently by age is unknown. This study assesses possible behavioral changes due to in utero inflammation as a function of age in neonatal, juvenile, and adult animals and presents potential molecular targets for observed differences. CD-1 timed pregnant dams were injected in utero with lipopolysaccharide (LPS, 50 μg/animal) or saline at embryonic day 15.

Intra-Tumoral Nerve-Tracing in a Novel Syngeneic Model of High-Grade Serous Ovarian Carcinoma.

Dense tumor innervation is associated with enhanced cancer progression and poor prognosis. We observed innervation in breast, prostate, pancreatic, lung, liver, ovarian, and colon cancers. Defining innervation in high-grade serous ovarian carcinoma (HGSOC) was a focus since sensory innervation was observed whereas the normal tissue contains predominantly sympathetic input.

IFNγ-Producing γ/δ T Cells Accumulate in the Fetal Brain Following Intrauterine Inflammation.

Intrauterine inflammation impacts prenatal neurodevelopment and is linked to adverse neurobehavioral outcomes ranging from cerebral palsy to autism spectrum disorder. However, the mechanism by which a prenatal exposure to intrauterine inflammation contributes to life-long neurobehavioral consequences is unknown. To address this gap in knowledge, this study investigates how inflammation transverses across multiple anatomic compartments from the maternal reproductive tract to the fetal brain and what specific cell types in the fetal brain may cause long-term neuronal injury.

Surface modification on MoO/Mo(110) induced by a local electric potential.

Oxygen adatoms on the MoO/Mo(110) surface are observed to be removed when a sufficiently large bias is applied between the scanning tunneling microscope tip and the surface. Experimental observations, such as the bias polarity dependence of adatom removal and the observation of an intermediate state, indicate that the adatom penetrates the surface oxide layer. Through the comparison of finite element method simulations with various experimental relationships, the electric field is concluded to be the sole contributor to adatom penetration into the surface oxide layer.

The Absence of TLR4 Prevents Fetal Brain Injury in the Setting of Intrauterine Inflammation.

Background: Exposure to intrauterine inflammation during pregnancy is linked to brain injury and neurobehavioral disorders in affected children. Innate immunity, specifically Toll-like receptor (TLR) signaling pathways are present throughout the reproductive tract as well as in the placenta, fetal membranes, and fetus. The TLR pathways are mechanistically involved in host responses to foreign pathogens and may lead to brain injury associated with prenatal inflammation.

Intrauterine inflammation reduces postnatal neurogenesis in the hippocampal subgranular zone and leads to accumulation of hilar ectopic granule cells.

Prenatal inflammation is associated with poor neurobehavioral outcomes in exposed offspring. A common route of exposure for the fetus is intrauterine infection, which is often associated with preterm birth. Hippocampal development may be particularly vulnerable to an inflammatory insult during pregnancy as this region remains highly neurogenic both prenatally and postnatally.

Exposure to intrauterine inflammation alters metabolomic profiles in the amniotic fluid, fetal and neonatal brain in the mouse.

Introduction: Exposure to prenatal inflammation is associated with diverse adverse neurobehavioral outcomes in exposed offspring. The mechanism by which inflammation negatively impacts the developing brain is poorly understood. Metabolomic profiling provides an opportunity to identify specific metabolites, and novel pathways, which may reveal mechanisms by which exposure to intrauterine inflammation promotes fetal and neonatal brain injury.

Day-night cycles and the sleep-promoting factor, Sleepless, affect stem cell activity in the Drosophila testis.

Adult stem cells maintain tissue integrity and function by renewing cellular content of the organism through regulated mitotic divisions. Previous studies showed that stem cell activity is affected by local, systemic, and environmental cues. Here, we explore a role of environmental day-night cycles in modulating cell cycle progression in populations of adult stem cells.

Oxygen doping of HTSC and resistive switching in HTSC-based heterostructures.

The studies of the bipolar resistive switching effect in thin film heterojunctions (YBa2Cu3O7-δ /Ag) and (Nd 2-x Ce x CuO4-y /Ag) have exhibited the role of oxygen as a doping element in hole- and electron-doped HTSC compounds.

JAK-STAT signal inhibition regulates competition in the Drosophila testis stem cell niche.

Adult stem cells often reside in local microenvironments, or niches. Although niches can contain multiple types of stem cells, the coordinate regulation of stem cell behavior is poorly understood. In the Drosophila testis, Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling is directly required for maintenance of the resident germline and somatic stem cells.

The origin of islet-like cells in Drosophila identifies parallels to the vertebrate endocrine axis.

Single-cell resolution lineage information is a critical key to understanding how the states of gene regulatory networks respond to cell interactions and thereby establish distinct cell fates. Here, we identify a single pair of neural stem cells (neuroblasts) as progenitors of the brain insulin-producing neurosecretory cells of Drosophila, which are homologous to islet beta cells. Likewise, we identify a second pair of neuroblasts as progenitors of the neurosecretory Corpora cardiaca cells, which are homologous to the glucagon-secreting islet alpha cells.

Novel regulators revealed by profiling Drosophila testis stem cells within their niche.

Stem cells are defined by the fact that they both self-renew, producing additional stem cells, and generate lineal descendants that differentiate into distinct functional cell types. In Drosophila, a small germline stem cell population is influenced by a complex microenvironment, the stem cell niche, which itself includes a somatic stem cell population. While stem cells are unique, their immediate descendants retain considerable stem cell character as they mitotically amplify prior to differentiation and can be induced to de-differentiate into stem cells.