Transcriptional Profiling of the Small Intestine and the Colon Reveals Modulation of Gut Infection with According to the Vitamin A Status.

Vitamin A (VA) deficiency and diarrheal diseases are both serious public health issues worldwide. VA deficiency is associated with impaired intestinal barrier function and increased risk of mucosal infection-related mortality. The bioactive form of VA, retinoic acid, is a well-known regulator of mucosal integrity.

Priming with Retinoic Acid, an Active Metabolite of Vitamin A, Increases Vitamin A Uptake in the Small Intestine of Neonatal Rats.

Given that combined vitamin A (VA) and retinoic acid (RA) supplementation stimulated the intestinal uptake of plasma retinyl esters in neonatal rats, we administrated an RA dose as a pretreatment before VA supplementation to investigate the distinct effect of RA on intestinal VA kinetics. On postnatal days (P) 2 and 3, half of the pups received an oral dose of RA (RA group), while the remaining received canola oil as the control (CN). On P4, after receiving an oral dose of H-labeled VA, pups were euthanized at selected times ( = 4-6/treatment/time) and intestine was collected.

RNAseq studies reveal distinct transcriptional response to vitamin A deficiency in small intestine versus colon, uncovering novel vitamin A-regulated genes.

Vitamin A (VA) deficiency remains prevalent in resource limited areas. Using Citrobacter rodentium infection in mice as a model for diarrheal diseases, previous reports showed reduced pathogen clearance and survival due to vitamin A deficient (VAD) status. To characterize the impact of preexisting VA deficiency on gene expression patterns in the intestines, and to discover novel target genes in VA-related biological pathways, VA deficiency in mice were induced by diet.

A Novel CDK2/9 Inhibitor CYC065 Causes Anaphase Catastrophe and Represses Proliferation, Tumorigenesis, and Metastasis in Aneuploid Cancers.

Cyclin-dependent kinase 2 (CDK2) antagonism inhibits clustering of excessive centrosomes at mitosis, causing multipolar cell division and apoptotic death. This is called anaphase catastrophe. To establish induced anaphase catastrophe as a clinically tractable antineoplastic mechanism, induced anaphase catastrophe was explored in different aneuploid cancers after treatment with CYC065 (Cyclacel), a CDK2/9 inhibitor.

Perturbed Vitamin A Status Induced by Iron Deficiency Is Corrected by Iron Repletion in Rats with Pre-Existing Iron Deficiency.

Background: Although iron deficiency is known to interrupt vitamin A (VA) metabolism, the ability of iron repletion to restore VA metabolism and kinetics in iron-deficient rats is not well understood.

Objectives: In the present study, we examined the effects of dietary iron repletion on VA status in rats with pre-existing iron deficiency.

Methods: Weanling Sprague-Dawley rats were fed a VA-marginal diet (0.

Using the human CYP26A1 gene promoter as a suitable tool for the determination of RAR-mediated retinoid activity.

We have used a shortened construct form of the CYP26A1 gene promoter, in a promoter-less vector with either luciferase (known as E4) or a red fluorescent protein, RFP (known as E4.2) as the reporter gene and examined their responses to retinoids in transfected HepG2 and HEK293T cells. The promoter responded linearly to a wide concentration range of at-RA in cells cotransfected with retinoic acid receptors (RAR).

Dietary Iron Repletion Stimulates Hepatic Mobilization of Vitamin A in Previously Iron-Deficient Rats as Determined by Model-Based Compartmental Analysis.

Background: Iron deficiency can result in hyporetinolemia and hepatic vitamin A (VA) sequestration.

Objectives: We used model-based compartmental analysis to determine the impact of iron repletion on VA metabolism and kinetics in iron-deficient rats.

Methods: At weaning, Sprague-Dawley rats were assigned to either a VA-marginal diet (0.

CYP26A1 gene promoter is a useful tool for reporting RAR-mediated retinoid activity.

Of numerous genes regulated by retinoic acid (RA), CYP26A1 is the most inducible gene by RA. In this study, we have used a shortened construct form, E4, of the CYP26A1 gene promoter, in a promoter-less vector with either luciferase or red fluorescent protein (RFP) as the reporter gene and have tested its responses to retinoids in transfected HepG2 and HEK293T cells. The promoter responded linearly to a wide concentration range of RA in cells cotransfected with retinoic acid receptors.

Vitamin A status affects weight gain and hepatic glucose metabolism in rats fed a high-fat diet.

Whether vitamin A (VA) has a role in the development of metabolic abnormalities associated with intake of a high-fat diet (HFD) is unclear. Sprague-Dawley rats after weaning were fed an isocaloric VA sufficient HFD (VAS-HFD) or a VA deficient HFD (VAD-HFD) for 8 weeks. Body mass, food intake, liver and adipose tissue mass, and the hepatic expression levels of key proteins for metabolism were determined.

Retinoic Acid Mediated Clearance of in Vitamin A Deficient Mice Requires CD11b+ and T Cells.

Vitamin A deficiency affects over 250 million preschool-age children worldwide and is associated with increased childhood mortality and risk of developing enteric infections. Vitamin A deficient (A-) mice developed chronic infection. A single oral dose of retinoic acid (RA) at d7 post-infection was sufficient to induce clearance of the pathogen in A- mice.

A spatiotemporally controllable chemical gradient generator via acoustically oscillating sharp-edge structures.

The ability to generate stable, spatiotemporally controllable concentration gradients is critical for resolving the dynamics of cellular response to a chemical microenvironment. Here we demonstrate an acoustofluidic gradient generator based on acoustically oscillating sharp-edge structures, which facilitates in a step-wise fashion the rapid mixing of fluids to generate tunable, dynamic chemical gradients. By controlling the driving voltage of a piezoelectric transducer, we demonstrated that the chemical gradient profiles can be conveniently altered (spatially controllable).

An acoustofluidic sputum liquefier.

We demonstrate the first microfluidic-based on-chip liquefaction device for human sputum samples. Our device is based on an acoustofluidic micromixer using oscillating sharp edges. This acoustofluidic sputum liquefier can effectively and uniformly liquefy sputum samples at a throughput of 30 μL min(-1).

Paradoxical effects of all-trans-retinoic acid on lupus-like disease in the MRL/lpr mouse model.

Roles of all-trans-retinoic acid (tRA), a metabolite of vitamin A (VA), in both tolerogenic and immunogenic responses are documented. However, how tRA affects the development of systemic autoimmunity is poorly understood. Here we demonstrate that tRA have paradoxical effects on the development of autoimmune lupus in the MRL/lpr mouse model.

A reliable and programmable acoustofluidic pump powered by oscillating sharp-edge structures.

We present a programmable acoustofluidic pump that utilizes the acoustic streaming effects generated by the oscillation of tilted sharp-edge structures. This sharp-edge-based acoustofluidic pump is capable of generating stable flow rates as high as 8 μL min(-1) (~76 Pa of pumping pressure), and it can tune flow rates across a wide range (nanoliters to microliters per minute). Along with its ability to reliably produce stable and tunable flow rates, the acoustofluidic pump is easy to operate and requires minimum hardware, showing great potential for a variety of applications.