Optimal power-heat-carbon scheduling strategy for interconnected heterogeneous multi-microgrid considering hydrogen fuel cell vehicles.

The scale of multi-microgrid (MMG) and hydrogen fuel cell vehicles (HFCVs) is increasing dramatically with the increase in the new energy penetration ratio, and developing an integrated energy system containing a multi-microgrid for hydrogen fuel vehicles brings great challenges to power grid operation. Focusing on the difficulties of the access of multiple microgrids for the low-carbon and economic operation of the system, this paper proposes an optimal interconnected heterogeneous multi-microgrid power-heat-carbon scheduling strategy for hydrogen-fueled vehicles. Firstly, an HFCV model is established, and then an optimal scheduling model is constructed for the cooperative trading of power-heat-carbon in a multi-microgrid, on the basis of which the low-carbon economic operation of the multi-microgrid is realized. The results of the case study show that the scheduling strategy in this paper reduces carbon emissions by about 7.12% and costs by about 3.41% compared with the independent operation of the multi-microgrid. The degrees of interaction of each multi-microgrid are also analyzed under different HFCV penetration rates.

Mechanisms of change in gel water-holding capacity of myofibrillar proteins affected by lipid oxidation: The role of protein unfolding and cross-linking.

This work explored the effects of protein unfolding and cross-linking induced by lipid oxidation (linoleic acid, OLA) on the gel water-holding capacity (WHC) of beef myofibrillar proteins (MP). Medium concentration of OLA (≤6 mM) caused the increase of gel WHC from 55.2% to 65.1%, while relative high OLA concentration (>6 mM) decreased the gel WHC. When the OLA concentrations increased from 0 to 10 mM, the population of immobile water of gel decreased from 92.91% to 78.97%, whereas that of free water increased from 6.13% to 19.80%, suggesting that OLA treatment regardless concentration was harmful for gel WHC. However, medium OLA concentrations (≤6 mM) caused the shifting of α-helixes to ß-sheets in MP gel, exerting positive effect on gel WHC. Protein unfolding and cross-linking jointly determined the increased gel WHC at moderate oxidative modification. Additionally, the protein aggregation at high OLA concentration resulted in decreased gel WHC.

Weight loss effect of sweet orange essential oil microcapsules on obese SD rats induced by high-fat diet.

Obesity is one of the most common and major health concerns worldwide. Weight management through dietary supplements with natural plant extracts has become the focus of current research. Sweet orange essential oil (SOEO) is a natural plant extract, with many bioactivities. In order to evaluate the weight loss effect of SOEO microcapsules and investigate the underlying mechanism, we fed high-fat diet-induced obese SD rats with SOEO microcapsules for 15 days and found that SOEO microcapsules reduced body weight gain by 41.4%, decreased total cholesterol level, alleviated liver and adipose tissue pathological alteration. The results of fluorescence quantitative PCR revealed that decreasing the expression of peroxisome proliferators-activated receptor-γ, upregulating of uncoupling protein 2, hormone sensitive lipase and carnitine palmitoyltransferase I, inhibiting the expression of acetyl-CoA carboxylase appear to be the mechanism of SOEO microcapsules to lose weight. This study suggests that SOEO microcapsule is a potential dietary supplement for weight loss. Abbreviations: SOEO: sweet orange essential oil; TC: total cholesterol; TG: triglyceride; LDL-c: low-density lipoprotein cholesterol; HDL-c: high-density lipoprotein cholesterol; PPARα: peroxisome proliferators-activated receptor-α; PPARγ: peroxisome proliferators-activated receptor-γ; UCP2: uncoupling protein 2; HSL: hormone sensitive lipase; CPT1: carnitine palmitoyltransferase I; ACC: acetyl-CoA carboxylase; NPY: neuropeptide Y; LEP: leptin; INS: insulin; ALT: alanine aminotransferase; AST: aspartate aminotransferase.

Microcapsule of sweet orange essential oil changes gut microbiota in diet-induced obese rats.

Obesity is associated with the changes in gut microbiota. The aim of present study was to investigate the effects of sweet orange essential oil (SOEO) microcapsules on body weight and gut microbiota in obese rats induced by high-fat diet. By analyzing the body weight, fat rate and the sequence of cloned microbial small-subunit ribosomal RNA genes (16S rDNA) in rats fecal samples, we found that SOEO microcapsules decreased the body weight and increased the relative abundance of Bifidobacterium (genus-level) in gut microbiota. The analysis of endotoxin content proved that SOEO microcapsules protected gut barrier and decreased gut endotoxin levels by increasing the content of Bifidobacterium, then ameliorated low-grade inflammation, achieving the goal of losing weight. This might be the mechanism of SOEO microcapsules to lose body weight and provided a novel anti-obesity dietary supplement.

WIP1 phosphatase is a critical regulator of adipogenesis through dephosphorylating PPARγ serine 112.

WIP1, as a critical phosphatase, plays many important roles in various physiological and pathological processes through dephosphorylating different substrate proteins. However, the functions of WIP1 in adipogenesis and fat accumulation are not clear. Here, we report that WIP1-deficient mice show impaired body weight growth, dramatically decreased fat mass, and significantly reduced triglyceride and leptin levels in circulation. This dysregulation of adipose development caused by the deletion of WIP1 occurs as early as adipogenesis. In contrast, lentivirus-mediated WIP1 phosphatase overexpression significantly increases the adipogenesis of pre-adipocytes via an enzymatic activity-dependent mechanism. PPARγ is a master gene of adipogenesis, and the phosphorylation of PPARγ at serine 112 strongly inhibits adipogenesis; however, very little is known about the negative regulation of this phosphorylation. Here, we show that WIP1 phosphatase plays a pro-adipogenic role by interacting directly with PPARγ and dephosphorylating p-PPARγ S112 in vitro and in vivo.

WIP1 Phosphatase Plays a Critical Neuroprotective Role in Brain Injury Induced by High-Altitude Hypoxic Inflammation.

The hypobaric hypoxic environment in high-altitude areas often aggravates the severity of inflammation and induces brain injury as a consequence. However, the critical genes regulating this process remain largely unknown. The phosphatase wild-type p53-induced phosphatase 1 (WIP1) plays important roles in various physiological and pathological processes, including the regulation of inflammation in normoxia, but its functions in hypoxic inflammation-induced brain injury remain unclear. Here, we established a mouse model of this type of injury and found that WIP1 deficiency augmented the release of inflammatory cytokines in the peripheral circulation and brain tissue, increased the numbers of activated microglia/macrophages in the brain, aggravated cerebral histological lesions, and exacerbated the impairment of motor and cognitive abilities. Collectively, these results provide the first in vivo evidence that WIP1 is a critical neuroprotector against hypoxic inflammation-induced brain injury.

miR-210 protects renal cell against hypoxia-induced apoptosis by targeting HIF-1 alpha.

The kidney is vulnerable to hypoxia-induced injury. One of the mechanisms underlying this phenomenon is cell apoptosis triggered by hypoxia-inducible factor-1-alpha (HIF-1α) activation. MicroRNA-210 (miR-210) is known to be induced by HIF-1α and can regulate various pathological processes, but its role in hypoxic kidney injury remains unclear. Here, in both kinds of rat systemic hypoxia and local kidney hypoxia models, we found miR-210 levels were upregulated significantly in injured kidney, especially in renal tubular cells. A similar increase was observed in hypoxia-treated human renal tubular HK-2 cells. We also verified that miR-210 can directly suppress HIF-1α expression by targeting the 3' untranslated region (UTR) of HIF-1α mRNA in HK-2 cells in severe hypoxia. Accordingly, miR-210 overexpression caused significant inhibition of the HIF-1α pathway and attenuated apoptosis caused by hypoxia, while miR-210 knockdown exerted the opposite effect. Taken together, our findings verify that miR-210 is involved in the molecular response in hypoxic kidney lesions in vivo and attenuates hypoxia-induced renal tubular cell apoptosis by targeting HIF-1α directly and suppressing HIF-1α pathway activation in vitro.

[Establishment and evaluation of a murine model of brain injury induced by high altitude hypoxic inflammation].

The aim of this study was to develop a murine model of brain injury induced by high altitude hypoxic inflammation. In the study, we used a decompression chamber to mimic an acute hypobaric hypoxia, and 8-week-old male C57BL/6 mice were intraperitoneally injected with 5 mg/kg lipopolysaccharide (LPS) to induce inflammatory response. We determined the levels of pro-inflammatory factors (IL-6, TNF-α) and anti-inflammatory factor (IL-10) in mice serum using ELISA assays to confirm the high altitude hypoxic inflammation, and verified the brain injury after the inflammation using hematoxylin-eosin (HE) staining. The results showed that, among four experiment groups (ctrl, acute hypobaric hypoxia, LPS, and acute hypobaric hypoxia plus LPS groups), the acute hypobaric hypoxia plus LPS treatment group displayed the highest levels of IL-6, TNF-α, and IL-10. Meanwhile, the acute hypobaric hypoxia plus LPS treatment group showed the most severe cortex and hippocampus injuries, including cellular swelling, the widened pericellular spaces, angiogenesis, and shrunken neurons with darkly stained pyknotic nuclei, etc. Strikingly, nuclei ventrales posteriors thalami were found to be more sensitive to acute hypobaric hypoxia plus LPS treatment, and their destroy degrees were higher than those neurons in cortex and hippocampus. These results suggested that we established a reliable murine model of brain injury induced by high altitude hypoxic inflammation, and might be useful to the relevant studies.

Reduced Cerebral Oxygen Content in the DG and SVZ In Situ Promotes Neurogenesis in the Adult Rat Brain In Vivo.

Neurogenesis in the adult brain occurs mainly within two neurogenic structures, the dentate gyrus (DG) of the hippocampus and the sub-ventricular zone (SVZ) of the forebrain. It has been reported that mild hypoxia promoted the proliferation of Neural Stem Cells (NSCs)in vitro. Our previous study further demonstrated that an external hypoxic environment stimulated neurogenesis in the adult rat brain in vivo. However, it remains unknown how external hypoxic environments affect the oxygen content in the brain and result in neurogenesis. Here we use an optical fiber luminescent oxygen sensor to detect the oxygen content in the adult rat brain in situ under normoxia and hypoxia. We found that the distribution of oxygen in cerebral regions is spatiotemporally heterogeneous. The Po2 values in the ventricles (45∼50 Torr) and DG (approximately 10 Torr) were much higher than those of other parts of the brain, such as the cortex and thalamus (approximately 2 Torr). Interestingly, our in vivo studies showed that an external hypoxic environment could change the intrinsic oxygen content in brain tissues, notably reducing oxygen levels in both the DG and SVZ, the major sites of adult neurogenesis. Furthermore, the hypoxic environment also increased the expression of HIF-1α and VEGF, two factors that have been reported to regulate neurogenesis, within the DG and SVZ. Thus, we have demonstrated that reducing the oxygen content of the external environment decreased Po2 levels in the DG and SVZ. This reduced oxygen level in the DG and SVZ might be the main mechanism triggering neurogenesis in the adult brain. More importantly, we speculate that varying oxygen levels may be the physiological basis of the regionally restricted neurogenesis in the adult brain.

A method for establishing the high-altitude cerebral edema (HACE) model by acute hypobaric hypoxia in adult mice.

BACKGROUND: Exposure to acute hypobaric hypoxia (AHH) during ascent to high altitudes (>3500 m) is one of the main causes of acute mountain sickness (AMS) and high-altitude cerebral edema (HACE). Therefore, the aim of this study was to develop a model of HACE. NEW METHODS: We developed a model of HACE in mice using a decompression chamber with rapid ascent speed. RESULTS: Healthy male C57BL/6 mice were randomly divided into the control group and the AHH group. The AHH group was housed in a decompression chamber (at a velocity of 50 m/s within 5 min to 6000 m). Compared with the controls, brain water content was increased in the early stage (within 24 h) in the AHH group. After 72 h of exposure to AHH, there was a higher BBB permeability observed. In addition, the brain structure showed significant widening of the pericellular spaces and a dilatation of the cortical blood vessels after exposure to AHH, and some of the neurons appeared shrunken with darkly stained pyknotic nuclei, resulting in neuronal structural damage. Further, exposure to AHH also decreased cognitive function in the mice. COMPARISON WITH EXISTING METHODS: At present, there are no simple and rapid mouse models to study this syndrome in terms of its genetic basis, gene polymorphisms and susceptibility. CONCLUSION: Our findings show that AHH can increase BBB permeability and lead to cerebral edema in mice; thus, we provide an effective and stable model of HACE in mice.

CKIP-1 suppresses the adipogenesis of mesenchymal stem cells by enhancing HDAC1-associated repression of C/EBPα.

Mesenchymal stem cells (MSCs) are considered as the developmental origin of multiple lineage cells including osteocytes, adipocytes, and muscle cells. Previous studies demonstrated that the PH domain-containing protein CKIP-1 plays an important role in the development of osteoblasts and cardiomyocytes. However, whether CKIP-1 is involved in the generation of adipocytes as well as the MSC differentiation remains unknown. Here we show that CKIP-1 is a novel regulator of MSCs differentiating into adipocytes. MSCs derived from CKIP-1-deficient mice display enhanced adipogenesis upon induction. Further analysis showed that CKIP-1 interacts with the histone deacetylase HDAC1 in the nucleus and inhibits the transcription of CCAAT/enhancer-binding protein α (C/EBPα), which is a crucial adipogenic transcription factor. Ectopic expression of CKIP-1 in a MSC-like cell line C3H/10T1/2 reduced the generation of adipocytes due to suppression of adipogenic factors, including C/EBPα. Moreover, CKIP-1-deficient mice showed an increase in body weight and white adipose tissue gains when fed on a high-fat diet. Collectively, these results suggest that CKIP-1 is a novel inhibitor of MSC-originated adipogenesis by enhancing HDAC1-associated repression of C/EBPα.

Murine calvaria-derived progenitor cells express high levels of osterix and lose their adipogenic capacity.

Though the mouse is the most widely used biomedical animal model, it is difficult to isolate murine mesenchymal stem cells (MSCs) from the bone marrow because of contamination by hematopoietic cells. The murine compact bone tissue of long bones is considered a novel and reliable source of MSCs with low hematopoietic cell contamination. We investigated whether the murine compact bone of the calvaria would be a promising source of MSCs due to its low bone marrow content. We isolated cells from both long bones and the calvaria using the same method. Although they shared morphological features and surface antigens similar to those of long bone-derived MSCs, the calvaria-derived cells highly expressed the osteogenic transcription factor osterix, lost their adipogenic capacity and gained a higher osteogenic capacity. These findings suggest that the cells that migrated from the calvaria were progenitor cells rather than MSCs and that the differentiation fate of mesenchymal stem/progenitor cells existing in different murine compact bone deposits is already committed.

A delivery system targeting bone formation surfaces to facilitate RNAi-based anabolic therapy.

Metabolic skeletal disorders associated with impaired bone formation are a major clinical challenge. One approach to treat these defects is to silence bone-formation-inhibitory genes by small interference RNAs (siRNAs) in osteogenic-lineage cells that occupy the niche surrounding the bone-formation surfaces. We developed a targeting system involving dioleoyl trimethylammonium propane (DOTAP)-based cationic liposomes attached to six repetitive sequences of aspartate, serine, serine ((AspSerSer)(6)) for delivering siRNAs specifically to bone-formation surfaces. Using this system, we encapsulated an osteogenic siRNA that targets casein kinase-2 interacting protein-1 (encoded by Plekho1, also known as Plekho1). In vivo systemic delivery of Plekho1 siRNA in rats using our system resulted in the selective enrichment of the siRNAs in osteogenic cells and the subsequent depletion of Plekho1. A bioimaging analysis further showed that this approach markedly promoted bone formation, enhanced the bone micro-architecture and increased the bone mass in both healthy and osteoporotic rats. These results indicate (AspSerSer)(6)-liposome as a promising targeted delivery system for RNA interference-based bone anabolic therapy.

[Advances on mutant p53 research].

Inactivation of tumor suppressor gene is a key event in carcinogenesis. p53 is one of the most important tumor suppressor genes in the genome, and its mutations are found in approximately 50% of human cancers. p53 mutation is also the main cause for human Li-Fraumeni syndrome. The vast majority of p53 mutations are missense mutations, and the corresponding mutant p53 proteins not only lose wild-type p53 tumor suppressor activities, but also gain new oncogenic properties favoring cancer development. Here, we mainly discussed the structural and functional alterations of mutant p53, the molecular mechanisms underlying gain of oncogenic functions, and the strategies and explorations of suppressing mutant p53 activities.