Integrative metagenomic and lipidomic analyses reveal alterations in children with obesity and after lifestyle intervention.

Background: Despite emerging evidence linking alterations in gut microbiota to childhood obesity, the metabolic mechanisms linking gut microbiota to the lipid profile during childhood obesity and weight loss remain poorly understood.

Methodology: In this study, children with obesity were treated with lifestyle weight loss therapy. Metagenomics association studies and serum untargeted lipidomics analyses were performed in children with obesity and healthy controls before and after weight loss.

Adipose stem cells from type 2 diabetic mice exhibit therapeutic potential in wound healing.

Background: Diabetic patients suffer from impaired wound healing. Mesenchymal stem cell (MSC) therapy represents a promising approach toward improving skin wound healing through the release of soluble growth factors and cytokines that stimulate new vessel formation and modulate inflammation. Whether adipose tissue-derived MSCs (ASCs) from type 2 diabetes (T2D) donors are suitable for skin damage repair remains largely unknown.

SNHG16 promotes tumorigenesis and cisplatin resistance by regulating miR-338-3p/PLK4 pathway in neuroblastoma cells.

Background: Long noncoding RNA small nucleolar RNA host gene 16 (lncRNA SNHG16) has been revealed to be involved in the tumorigenesis of neuroblastoma. However, the role of SNHG16 in regulating cisplatin sensitivity in neuroblastoma remains largely unknown.

Methods: The expression of SNHG16, microRNA (miR)-338-3p and polo-like kinase 4 (PLK4) mRNA was measured using quantitative real-time polymerase chain reaction.

LncRNA KCNQ1OT1 contributes to the progression and chemoresistance in acute myeloid leukemia by modulating Tspan3 through suppressing miR-193a-3p.

Aims: Acute myeloid leukemia (AML) is an aggressive cancer that invariably produces drug resistance after treatment. The aim is to explore the role of lncRNA potassium voltage-gated channel subfamily Q member 1 overlapping transcript 1 (KCNQ1OT1) and associated novel mechanisms in the progression and chemoresistance of AML.

Main Methods: The expression of KCNQ1OT1, miR-193a-3p, and Tspan3 was measured by qRT-PCR.

Astragalus root extract inhibits retinal cell apoptosis and repairs damaged retinal neovascularization in retinopathy of prematurity.

Since the functions of Astragalus root extract in retinopathy remain to be unraveled, this study is performed to elucidate whether Astragalus root extract functions in retinal cell apoptosis and angiogenesis in retinopathy of prematurity (ROP). Newborn mice were selected for establishing mice models of oxygen-induced retinopathy (OIR), which were treated with high-, medium- or low-Astragalus root extract. Evans Blue (EB) was perfused to detect the blood retinal barrier.