A review of phase change heat transfer in shape-stabilized phase change materials (ss-PCMs) based on porous supports for thermal energy storage

Latent heat thermal energy storage (LHTES) uses phase change materials (PCMs) to store and release heat, and can effectively address the mismatch between energy supply and demand. However, it suffers from low thermal conductivity and the leakage problem. One of the solutions is integrating porous supports and PCMs to fabricate shape-stabilized phase change materials (ss-PCMs). The phase change heat transfer in porous ss-PCMs is of fundamental importance for determining thermal-fluidic behaviours and evaluating LHTES system performance. This paper reviews the recent experimental and numerical investigations on phase change heat transfer in porous ss-PCMs. Materials, methods, apparatuses and significant outcomes are included in the section of experimental studies and it is found that paraffin and metal foam are the most used PCM and porous support respectively in the current researches. Numerical advances are reviewed from the aspect of different simulation methods. Compared to representative elementary volume (REV)-scale simulation, the pore-scale simulation can provide extra flow and heat transfer characteristics in pores, exhibiting great potential for the simulation of mesoporous, microporous and hierarchical porous materials. Moreover, there exists a research gap between phase change heat transfer and material preparation. Finally, this review outlooks the future research topics of phase change heat transfer in porous ss-PCMs

Self-Renewal and Differentiation Capacity of Urine-Derived Stem Cells after Urine Preservation for 24 Hours

The authors would like to thank Karl-Erik Andersson for his valuable comments and Ms. Karen Klein (Research Support Core, Wake Forest School of Medicine) for her editorial assistance with this manuscript.Administrative support: AA. Editorial help: AA. Conceived and designed the experiments: YYZ. Performed the experiments: RL GL YS SB. Analyzed the data: RL GL YS SB XL XZ HL YYZ. Contributed reagents/materials/analysis tools: AA. Wrote the paper: RL GL YYZ.Despite successful approaches to preserve organs, tissues, and isolated cells, the maintenance of stem cell viability and function in body fluids during storage for cell distribution and transportation remains unexplored. The aim of this study was to characterize urine-derived stem cells (USCs) after optimal preservation of urine specimens for up to 24 hours. A total of 415 urine specimens were collected from 12 healthy men (age range 20–54 years old). About 6×104 cells shed off from the urinary tract system in 24 hours. At least 100 USC clones were obtained from the stored urine specimens after 24 hours and maintained similar biological features to fresh USCs. The stored USCs had a “rice grain” shape in primary culture, and expressed mesenchymal stem cell surface markers, high telomerase activity, and normal karyotypes. Importantly, the preserved cells retained bipotent differentiation capacity. Differentiated USCs expressed myogenic specific proteins and contractile function when exposed to myogenic differentiation medium, and they expressed urothelial cell-specific markers and barrier function when exposed to urothelial differentiation medium. These data demonstrated that up to 75% of fresh USCs can be safely persevered in urine for 24 hours and that these cells stored in urine retain their original stem cell properties, indicating that preserved USCs could be available for potential use in cell-based therapy or clinical diagnosis.Yeshttp://www.plosone.org/static/editorial#pee

Nampt Expression Decreases Age-Related Senescence in Rat Bone Marrow Mesenchymal Stem Cells by Targeting Sirt1.

Senescence restricts the development of applications involving mesenchymal stem cells (MSCs) in research fields, such as tissue engineering, and stem cell therapeutic strategies. Understanding the mechanisms underlying natural aging processes may contribute to the development of novel approaches to preventing age-related diseases or slowing individual aging processes. Nampt is a rate-limiting NAD biosynthetic enzyme that plays critical roles in energy metabolism, cell senescence and maintaining life spans. However, it remains unknown whether Nampt influences stem cell senescence. In this study, the function of Nampt was investigated using a rat model of natural aging. Our data show that Nampt expression was significantly lower in MSCs obtained from aged rats than in those obtained from young rats during physiological aging. Reducing the level of Nampt in aged MSCs resulted in lower intracellular concentrations of NAD+ and downregulated Sirt1 expression and activity. After the Nampt inhibitor FK866 was added, young MSCs were induced to become aged cells. The enhanced senescence was correlated with NAD+ depletion and Sirt1 activity attenuation. In addition, Nampt overexpression attenuated cell senescence in aged MSCs. Our findings provide a new explanation for the mechanisms underlying stem cell senescence and a novel target for delaying stem cell senescence and preventing and treating age-related diseases

Metabolism: A Novel Shared Link between Diabetes Mellitus and Alzheimer’s Disease

As a chronic metabolic disease, diabetes mellitus (DM) is broadly characterized by elevated levels of blood glucose. Novel epidemiological studies demonstrate that some diabetic patients have an increased risk of developing dementia compared with healthy individuals. Alzheimer’s disease (AD) is the most frequent cause of dementia and leads to major progressive deficits in memory and cognitive function. Multiple studies have identified an increased risk for AD in some diabetic populations, but it is still unclear which diabetic patients will develop dementia and which biological characteristics can predict cognitive decline. Although few mechanistic metabolic studies have shown clear pathophysiological links between DM and AD, there are several plausible ways this may occur. Since AD has many characteristics in common with impaired insulin signaling pathways, AD can be regarded as a metabolic disease. We conclude from the published literature that the body’s diabetic status under certain circumstances such as metabolic abnormalities can increase the incidence of AD by affecting glucose transport to the brain and reducing glucose metabolism. Furthermore, due to its plentiful lipid content and high energy requirement, the brain’s metabolism places great demands on mitochondria. Thus, the brain may be more susceptible to oxidative damage than the rest of the body. Emerging evidence suggests that both oxidative stress and mitochondrial dysfunction are related to amyloid-β (Aβ) pathology. Protein changes in the unfolded protein response or endoplasmic reticulum stress can regulate Aβ production and are closely associated with tau protein pathology. Altogether, metabolic disorders including glucose/lipid metabolism, oxidative stress, mitochondrial dysfunction, and protein changes caused by DM are associated with an impaired insulin signal pathway. These metabolic factors could increase the prevalence of AD in diabetic patients via the promotion of Aβ pathology

Nicotinamide Mononucleotide Supplementation Improves Mitochondrial Dysfunction and Rescues Cellular Senescence by NAD⁺/Sirt3 Pathway in Mesenchymal Stem Cells

In vitro expansion-mediated replicative senescence has severely limited the clinical applications of mesenchymal stem cells (MSCs). Accumulating studies manifested that nicotinamide adenine dinucleotide (NAD+) depletion is closely related to stem cell senescence and mitochondrial metabolism disorder. Promoting NAD+ level is considered as an effective way to delay aging. Previously, we have confirmed that nicotinamide mononucleotide (NMN), a precursor of NAD+, can alleviate NAD+ deficiency-induced MSC senescence. However, whether NMN can attenuate MSC senescence and its underlying mechanisms are still incompletely clear. The present study herein showed that late passage (LP) MSCs displayed lower NAD+ content, reduced Sirt3 expression and mitochondrial dysfunction. NMN supplementation leads to significant increase in intracellular NAD+ level, NAD+/ NADH ratio, Sirt3 expression, as well as ameliorated mitochondrial function and rescued senescent MSCs. Additionally, Sirt3 over-expression relieved mitochondrial dysfunction, and retrieved senescence-associated phenotypic features in LP MSCs. Conversely, inhibition of Sirt3 activity via a selective Sirt3 inhibitor 3-TYP in early passage (EP) MSCs resulted in aggravated cellular senescence and abnormal mitochondrial function. Furthermore, NMN administration also improves 3-TYP-induced disordered mitochondrial function and cellular senescence in EP MSCs. Collectively, NMN replenishment alleviates mitochondrial dysfunction and rescues MSC senescence through mediating NAD+/Sirt3 pathway, possibly providing a novel mechanism for MSC senescence and a promising strategy for anti-aging pharmaceuticals

Nampt expression in MSCs obtained from young and old rats.

<p>Nampt protein levels were evaluated using Western blot analysis (A) and immunofluorescence (C). mRNA levels were detected using RT-qPCR (B). Nampt expression at both the protein and gene level were reduced in an age-dependent manner. Actin was used as the internal standard. The values shown indicate the mean ± SD (* p < 0.05, ** p< 0.01).</p

Inhibiting Nampt using FK866 increased cell senescence in MSCs obtained from the young group.

<p>Cells were treated with 10 nM FK866 for 72 h. (A) Unlike the controls, which displayed normal morphologies, the MSCs treated with FK866 were flattened and enlarged and displayed senescence-like morphological features. (B-C) SA-β-gal activity was then measured. The percentage of β-Gal-positive cells and their staining intensity were significantly higher in the FK866 group than in the control group. (D) pl6^INK4A and p21^WAF1/CIP1 expression levels were evaluated using RT-qPCR. When Nampt was inhibited using FK866 in MSCs obtained from young rats, the expression levels of both pl6^INK4A and p21^WAF1/CIP1 were upregulated. Furthermore, both intracellular NAD+ levels (E) and Sirt1 activity (F) were decreased in the FK866 treatment group compared to those in the control group. The values shown indicate the means ± SD (* p< 0.05, **p< 0.01).</p

Nampt overexpression attenuated cell senescence in MSCs obtained from the old group.

<p>Cells were transduced with the lentivirus system. (A) Fluorescence images showed that Nampt was successfully overexpressed in MSCs from old rats. LV-Nampt: lentivirus encoding Nampt; LV-Vector: lentivirus encoding enhanced green fluorescent protein (EGFP). (B) Nampt protein levels were confirmed using Western blot analysis. (C) Nampt mRNA levels were ascertained using RT-qPCR. (D) Nampt overexpression significantly decreased SA-β-gal activity in MSCs from old rats.</p