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[Display omitted] • The PEI-Im-CTG CEMs were modified via Debus-Radziszewski in-situ crosslinking. • The PEI-Im layer had rigid structure and strong cation-surface interaction. • The PEI-Im-CTG membrane exhibited high permselectivity between Li+ and Mg2+. • The PEI-Im-CTG membrane showed a high Li+ purity during two-stage ED process. Lithium extraction from salt-lakes is a crucial way to solve the global shortage of lithium resources. With high sustainability and efficient ion separation, electrodialysis (ED) has a high potential for lithium extraction from salt-lakes, yet suffering from the challenges of cation-cation selectivity. In this work, a facile Debus-Radziszewski in-situ cross-linking approach was proposed to construct a polyethyleneimine modification layer containing imidazole groups (PEI-Im) on a common cation exchange membrane (commercial membrane, i.e., CTG membrane) surface to enhance the lithium selectivity. The pore size, architecture rigidity and charged characteristic of this PEI-Im layer were controlled via adjusting the reaction conditions. The resultant membrane (PEI-Im-CTG) exhibited high Li+ permeation rate (0.89 mol·m−2·h−1) and excellent Li+/Mg2+ permselectivity (13.1), which are 4.0 times and 19.8 times higher than that of the pristine CTG membrane, respectively. Moreover, the PEI-Im-CTG membrane based two-stage ED process showed a high Li+ purity (∼99.90 %) and low energy consumption (∼0.158 kWh·mol-1Li+) for Li+ extraction from simulated salt-lakes. This work offers a facile and effective strategy for membrane modification with high Li+ selectivity, which is promising in lithium extraction from salt-lakes. [ABSTRACT FROM AUTHOR]

Background: Direct moxibustion (DM) is reported to be useful for cervical spondylotic radiculopathy (CSR), but the analgesic mechanism remains unknown. Autophagy plays a protective role in neuronal apoptosis, Act A/Smads signaling pathway has been confirmed to be associated with the activation of autophagy. The study aimed to explore the effect of DM on autophagy in rats with CSR and the involvement of Act A/Smads signaling pathway. Methods: Rats were randomly divided into Sham, CSR, CSR + DM, CSR + DM + 3‐MA (PI3K inhibitor), and CSR + DM + SB (Act A inhibitor) group. Three days after establishment of CSR model with a fish line inserted under the axilla of the nerve roots, DM at Dazhui (GV14) was performed six times once for seven consecutive days. Western blot and immunofluorescence staining were used to observe the expression of the neuronal autophagy molecule LC3II/I, Atg7, and Act A/Smads signaling molecule Act A, p‐Smad2, and p‐Smad3. Bcl‐2/Bax mRNA expression was measured by real time PCR. Results: DM improved the pain threshold and motor function of CSR rats and promoted the expression of Act A, p‐Smad2, p‐Smad3, LC3II/I, and Atg7 in the entrapped‐nerve root spinal dorsal horn. DM reduced the expression of Bax mRNA and decreased the number of apoptotic neurons. 3‐MA and Act A inhibitor SB suppressed the expression of above‐mentioned proteins and reduced the protective effect of DM on apoptotic neurons. Conclusion: DM exerts analgesic effects by regulating the autophagy to reduce cell apoptosis and repair nerve injury, and this feature may be related to the Act A/Smads signaling pathway. [ABSTRACT FROM AUTHOR]

In order to resolve the situations of nonuniform coolant flow distribution and insufficient vortex suppression, the existing Pressurized Water Reactor (PWR) usually adopts complex coolant mixing structures. However, those structures will greatly increase the complexity and maintenance cost of the system. To solve this problem, a trimming-based design method is proposed in this paper for the complex system and applies it to the design process of the PWR coolant flow distribution device. The function model of the coolant flow distribution system is built based on its functional analysis, and, according to the result of the component feature analysis, the columns and part of the basket are trimmed in order to simplify the overall structure of the system. To further solve the technical contradictions occurred in the simplified system, the contradiction solving tools of TRIZ theory are adopted. By setting the stereo flow equalizing plate, which can strengthen the function of flow distribution and vortex suppression, a coolant flow distribution device for PWR based on dome structure is obtained finally. This device owns a simple structure with good effect on coolant flow distribution and vortex suppression, which can achieve the goal of uniform coolant flow distribution of the system effectively. [ABSTRACT FROM AUTHOR]

Polyamide (PA) thin film nanocomposite (TFN) reverse osmosis (RO) membranes have been vigorously developed, which could be used in saline water desalination, wastewater treatment and chemicals separation and purification. Aiming at further improving the TFN RO membrane comprehensive performances, such as the perm-selectivity, stability and anti-fouling/-microbial properties remains a great challenge. Herein, we proposed a biomimetic nanoparticle redox strategy to in-situ integration of multiple functional nanoparticles, i.e., biomimetic nanoparticles (BNPs) and silver (Ag) nanoparticles into the PA matrix for simultaneously regulating the membrane microstructure and optimizing the surface property. A much hydrophilic selective layer with interior transporting channel structure renders the resultant RO membrane PA-BNP-Ag with an enhanced water permeance of ∼4.2 L m−2·h−1bar−1 without sacrificing NaCl rejection (∼98.1%). The BNPs induce Ag nanoparticles uniformly distributed within the PA matrix, which significantly improves the membrane anti-fouling/-bacterial property. The water flux recovery ratio of PAM-BNP-Ag was improved to be higher than 96% during several cycles filtration of saline solution containing bovine serum albumin foulants. More importantly, the membrane sterilization rate against Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) achieves nearly 100%. This work provides a new strategy for the construction of advanced PA TFN membranes with both high perm-selectivity and anti-fouling/-microbial property in RO desalination. [Display omitted] • The TFN RO membrane was fabricated with in-situ integration of multiple functional nanoparticles. • The TFN RO membrane with high hydrophilic surface and tunable microstructure. • The TFN RO membrane exhibits both high water permeance and NaCl rejection. • The TFN RO membrane represents excellent anti-fouling/-bacterial property. [ABSTRACT FROM AUTHOR]

Obesity is characterized by aberrant fat accumulation. However, the intracellular signaling pathway that senses dietary fat and leads to fat storage remains elusive. Here, we have observed that the levels of histone deacetylase 6 (HDAC6) and the related family member HDAC10 are markedly reduced in adipose tissues of obese animals and humans. Mice with adipocyte-specific depletion of Hdac6 exhibited increased fat accumulation and reduced insulin sensitivity. In normal adipocytes, we found that reversal of P300/CBP-associated factor-induced (PCAF-induced) acetylation at K56 on cell death-inducing DFFA-like effector C (CIDEC, also known as FSP27) critically regulated lipid droplet fusion and lipid storage. Importantly, HDAC6 deacetylates CIDEC, leading to destabilization and reduced lipid droplet fusion. Accordingly, we observed elevated levels of CIDEC and its acetylated form in HDAC-deficient adipocytes as well as the adipose tissue of obese animals and humans. Fatty acids (FAs) prevented CIDEC deacetylation by promoting the dissociation of CIDEC from HDAC6, which resulted in increased association of CIDEC with PCAF on the endoplasmic reticulum. Control of CIDEC acetylation required the conversion of FAs to triacylglycerols. Thus, we have revealed a signaling axis that is involved in the coordination of nutrient availability, protein acetylation, and cellular lipid metabolic responses. [ABSTRACT FROM AUTHOR]

Mechanistic investigations have shown that, upon agonist activation, hydroxy-carboxylic acid receptor-1(HCA1) couples to a Gi protein and inhibits adenylate cyclase activity, leading to inhibition of liberation of free fatty acid. However, the underlying molecular mechanisms for HCA1 signaling remain largely unknown. Using CHO-K1 cells stably expressing HCA1, and L6 cells, which endogenously express rat HCA1 receptors, we found that activation of ERK1/2 by HCA1 was rapid, peaking at 5 min, and was significantly blocked by pertussis toxin. Furthermore, time course experiments with different kinase inhibitors demonstrated that HCA1 induced ERK1/2 activation via the extracellular Ca2+, PKC and IGF-I receptor transactivation-dependent pathways. In addition, we observed that pretreated the cells with M119K, an inhibitor of Gβγ subunit-dependent signaling, effectively attenuated the ERK1/2 activation triggered by HCA1, suggesting a critical role for βγ-subunits in HCA1-activated ERK1/2 phosphorylation. Furthermore, the present results also indicated that the arrestin2/3 were not required for ERK1/2 activation. In conclusion, our findings demonstrate that upon binding to agonist, HCA1 receptors initially activate Gi, leading to dissociation of the Gβγ subunit from activated Gi, and subsequently induce ERK1/2 activation via two distinct pathways: one PKC-dependent pathway and the other IGF-IR transactivation-dependent pathway. Our results provide the first in-depth evidence that defines the molecular mechanism of HCA1-mediated ERK1/2 activation. [ABSTRACT FROM AUTHOR]

Calsequestrin 1 (CASQ1) is the most crucial Ca2+ binding protein localized in the sarcoplasmic reticulum (SR) of skeletal muscle. With high capacity and low affinity for Ca2+, CASQ1 plays a significant role in maintaining a large amount of Ca2+ necessary for muscle contraction. However, only five mutations in CASQ1 have been identified to date. Here, we report a 42‐year‐old Chinese female patient who presented with a 12 years history of slowly progressive upper limb weakness, predominantly affecting distal muscles, which was uncommon comparing to other CASQ1‐related patients. Next‐generation sequencing (NGS) analysis revealed a novel heterozygous mutation (c.766G > A, p.Val256Met) in CASQ1. Functional studies confirmed the likely pathogenicity of this variant. Muscle histopathology revealed rare optically empty vacuoles in myofibers and atypical eosinophilic granules in the cytoplasm, which has not been observed before. We also performed a literature review on all the pathogenic mutations in CASQ1 and summarized their genetic and clinical characteristics. This is the first report on CASQ1‐related myopathy from China, further expanding the mutation spectrum of CASQ1 gene and provides new insights into the function of CASQ1. [ABSTRACT FROM AUTHOR]

This paper presents a preliminary study on the evaluation of an innovative energy dissipation system with shape memory alloys (SMAs) for structural seismic protection. A recentering shapememory alloy damper (RSMAD), in which superelastic nitinol wires are utilized as energy dissipation components, is proposed. Improved constitutive equations based on Graesser and Cozzarelli model are proposed for superelastic nitinol wires used in the damper. Cyclic tensile-compressive tests on the damper with various prestrain under different loading frequencies and displacement amplitudes were conducted. The results show that the hysteretic behaviors of the damper can bemodified to best fit the needs for passive structural control applications by adjusting the pretension of the nitinol wires, and the damper performance is not sensitive to frequencies greater than 0.5Hz. To assess the effectiveness of the dampers for structural seismic protection, nonlinear time history analysis on a ten-story steel frame with and without the dampers subjected to representative earthquake ground motions was performed. The simulation results indicate that superelastic SMA dampers are effective in mitigating the structural response of building structures subjected to strong earthquakes. [ABSTRACT FROM AUTHOR]

Shapememory alloys (SMAs) are a relatively new class of functional materials, exhibiting special thermo mechanical behaviors, such as shapememory effect and superelasticity, which enable their applications in seismic engineering as energy dissipation devices. This paper investigates the properties of superelastic NiTi shape memory alloys, emphasizing the influence of strain rate on superelastic behavior under various strain amplitudes by cyclic tensile tests. A novel constitutive equation based on Graesser and Cozzarelli's model is proposed to describe the strain-rate-dependent hysteretic behavior of superelastic SMAs at different strain levels. A stress variable including the influence of strain rate is introduced into Graesser and Cozzarelli's model. To verify the effectiveness of the proposed constitutive equation, experiments on superelastic NiTi wires with different strain rates and strain levels are conducted. Numerical simulation results based on the proposed constitutive equation and experimental results are in good agreement. The findings in this paper will assist the future design of superelastic SMA-based energy dissipation devices for seismic protection of structures. [ABSTRACT FROM AUTHOR]

Background: Mesenchymal stem cells (MSCs) promote tumor growth by differentiating into carcinoma-associated fibroblasts (CAFs) and composing the tumor microenvironment. However, the mechanisms responsible for the transition of MSCs to CAFs are not well understood. Exosomes regulate cellular activities by mediating cell-cell communication. In this study, we aimed to investigate whether cancer cell-derived exosomes were involved in regulating the differentiation of human umbilical cord-derived MSCs (hucMSCs) to CAFs. Methodology/Principal Findings: We first showed that gastric cancer cell-derived exosomes induced the expression of CAF markers in hucMSCs. We then demonstrated that gastric cancer cell-derived exosomes stimulated the phosphorylation of Smad-2 in hucMSCs. We further confirmed that TGF-β receptor 1 kinase inhibitor attenuated Smad-2 phosphorylation and CAF marker expression in hucMSCs after exposure to gastric cancer cell-derived exosomes. Conclusion/Significance: Our results suggest that gastric cancer cells triggered the differentiation of hucMSCs to CAFs by exosomes-mediated TGF-β transfer and TGF-β/Smad pathway activation, which may represent a novel mechanism for MSCs to CAFs transition in cancer. [ABSTRACT FROM AUTHOR]

Cancer stem cells (CSCs) have the characteristics of self-renewal, unlimited proliferation, and initiating new tumors. However, the origin of CSCs is still controversial. F6, a tumor cell line transformed from human fetal mesenchymal stem cells, was established in our previous study. Whether CSCs exist in this mutated cell line remains unclear. In the present study, we isolated CSCs from F6 cells based on CD133 expression using flow cytometry and investigated the biological characteristics of CD133+ F6 cells (F6-CD133+). We observed that the F6-CD133+ cells grew faster and had a higher capacity of colony formation than the F6-CD133− cells and parental F6 cells in vitro. In addition, F6-CD133+ cells had a higher tumorigenic ability than F6-CD133− cells in vivo since 1,000 F6-CD133+ cells were able to form tumors in nude mice. Cell viability assay revealed that F6-CD133+ cells were more sensitive to cisplatin while less to 5-fluorouracil. Furthermore, gene expression profile analysis showed that there were 673 differentially expressed genes between F6-CD133+ and F6-CD133− cells, many of which were involved in key cell signaling pathways. Taken together, our findings confirm that F6 cells contain a population of CSCs that contribute to its heterogeneity and tumorigenic potential, indicating that transformed stem cells could be the source of CSCs, and targeting this population may lead to more effective tumor treatments. [ABSTRACT FROM AUTHOR]

Cerebral malaria, a severe form of the disease, is one of the most severe complications of infection with Plasmodium parasites and a leading cause of malaria mortality. Currently available antimalarial therapy has proven insufficient to prevent neurological complications and death in all cases of cerebral malaria. Souza and colleagues observed that transplantation of bone marrow-derived mesenchymal stromal cells (BM-MSCs) increased survival, reduced parasitemia, decreased malaria pigment accumulation in the spleen, liver and kidney, elevated Kupffer cell count in liver, alleviated renal injury and lung inflammation, and improved lung mechanics in an experimental mouse model of cerebral malaria. Although plenty of challenges lie ahead, their findings show the promise of BM-MSC therapy for the treatment of cerebral malaria. [ABSTRACT FROM AUTHOR]

Studies the controllability and observability issues for a linear time-varying impulsive control system. Variation of parameter for impulsive control systems; Modeling of complex dynamical behaviors of the system.

Cerebral malaria, a severe form of the disease, is one of the most severe complications of infection with Plasmodium parasites and a leading cause of malaria mortality. Currently available antimalarial therapy has proven insufficient to prevent neurological complications and death in all cases of cerebral malaria. Souza and colleagues observed that transplantation of bone marrow-derived mesenchymal stromal cells (BM-MSCs) increased survival, reduced parasitemia, decreased malaria pigment accumulation in the spleen, liver and kidney, elevated Kupffer cell count in liver, alleviated renal injury and lung inflammation, and improved lung mechanics in an experimental mouse model of cerebral malaria. Although plenty of challenges lie ahead, their findings show the promise of BM-MSC therapy for the treatment of cerebral malaria. [ABSTRACT FROM AUTHOR]

Simple Summary: The melon fly, Zeugodacus cucurbitae, is an important agricultural pest. At present, chemical pesticide treatment is the main method for field control, but this promotes pesticide resistance by Z. cucurbitae, because of its frequent use. ABC transporters are involved in detoxification metabolism, but few studies have yet considered their expression in melon fly. In this study, we identified the ABC transporters genes at a genome-wide level in melon fly, and analysed their spatiotemporal expression patterns, as well as changes in expression after insecticides treatments. A total of 49 ABC transporters were identified, and their expression levels varied at different developmental stages and between tissues. After three insecticides treatment, ZcABCB7 and ZcABCC2 were up-regulated. After β-cypermethrin induction, tissues were dissected at 12, 24 and 48 h, and the expression levels of a number of ABC genes were highly expressed within the fat body. From these results, we conclude that ZcABCB7 and ZcABCC2 may be involved in detoxification metabolism, and that the fat body is the main tissue that plays this role. The ATP-binding cassette (ABC) transporter is a protein superfamily that transports specific substrate molecules across lipid membranes in all living species. In insects, ABC transporter is one of the major transmembrane protein families involved in the development of xenobiotic resistance. Here, we report 49 ABC transporter genes divided into eight subfamilies (ABCA-ABCH), including seven ABCAs, seven ABCBs, 10 ABCCs, two ABCDs, one ABCE, three ABCFs, 16 ABCGs, and three ABCHs according to phylogenetic analysis in Zeugodacus cucurbitae, a highly destructive insect pest of cucurbitaceous and other related crops. The expressions level of 49 ABC transporters throughout various developmental stages and within different tissues were evaluated by quantitative transcriptomic analysis, and their expressions in response to three different insecticides were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). These ABC transporter genes were widely expressed at developmental stages but most highly expressed in tissues of the midgut, fat body and Malpighian tube. When challenged by exposure to three insecticides, abamectin, β-cypermethrin, and dinotefuran, the expressions of ZcABCB7 and ZcABCC2 were significantly up-regulated. ZcABCB1, ZcABCB6, ZcABCB7, ZcABCC2, ZcABCC3, ZcABCC4, ZcABCC5, and ZcABCC7 were significantly up-regulated in the fat body at 24 h after β-cypermethrin exposure. These data suggest that ZcABCB7 and ZcABCC2 might play key roles in xenobiotic metabolism in Z. cucurbitae. Collectively, these data provide a foundation for further analysis of ABCs in Z. cucurbitae. [ABSTRACT FROM AUTHOR]

Extracellular vesicles (EVs) in the field of spinal cord injury (SCI) have garnered significant attention for their potential applications in diagnosis and therapy. However, no bibliometric assessment has been conducted to evaluate the scientific progress in this area. A search of articles in Web of Science (WoS) from January 1, 1991, to May 1, 2023, yielded 359 papers that were analyzed using various online analysis tools. These articles have been cited 10,842 times with 30.2 times per paper. The number of publications experienced explosive growth starting in 2015. China and the United States led this research initiative. Keywords were divided into 3 clusters, including "Pathophysiology of SCI", "Bioactive components of EVs", and "Therapeutic effects of EVs in SCI". By integrating the average appearing year (AAY) of keywords in VoSviewer with the time zone map of the Citation Explosion in CiteSpace, the focal point of research has undergone a transformative shift. The emphasis has moved away from pathophysiological factors such as "axon", "vesicle", and "glial cell" to more mechanistic and applied domains such as "activation", "pathways", "hydrogels" and "therapy". In conclusions, institutions are expected to allocate more resources towards EVs-loaded hydrogel therapy and the utilization of innovative materials for injury mitigation. [ABSTRACT FROM AUTHOR]

How to efficiently and physically integrate the soil water dynamics with groundwater flow processes has drawn much attention. We present a coupled soil water-groundwater model, considering the two-way feedback coupling scheme, and verified its performance using two synthetic cases (using the fully 3D variably saturated flow (VSF) model simulations as the 'reference') and one real catchment 25 case (using the groundwater table depth and soil moisture profile measurements). By the cross-validation between the observations and various model simulations, the two-way coupling approach is proven physically accurate and is applicable for large-scale groundwater flow problems. Compared to the simulation by groundwater model alone (i.e., only MODFLOW), the coupling of MODFLOW with one soil column reduced the overestimation of groundwater table simulation (taking the VSF model simulations as the reference). The results were further improved as more soil columns were used to represent the heterogeneous soil watergroundwater interactions. Compared to the HYDRUS-MODFLOW, the two-way coupling approach produces a similar spatial distribution of hydraulic heads while better performs in mimicking the temporal dynamics of groundwater table depth and soil moisture profiles. We attribute the better performance to the different coupling strategies across the soil-water and groundwater interface. It is thus suggested to adopt the two-way feedback coupling scheme, together with the moving phreatic boundary and multi-scale water balance analysis, to maintain physical consistency and reduce coupling errors. The realistic implementation of the vadose zone processes (with STEMMUS), coupling approach, and spatiotemporal heterogeneity of soil water-groundwater interactions were demonstrated critical to accurately represent an integrated soil water-groundwater system. The developed STEMMUS-MODFLOW model can be further equipped with different complexities of soil physics (e.g., coupled soil water and heat transfer, freeze-thaw, airflow processes), surface hydrology (snowfall, runoff), soil and plant biogeochemical processes, towards an integrated "from bedrock to atmosphere" modeling framework. [ABSTRACT FROM AUTHOR]

The eukaryotic calcium/calmodulin-dependent protein phosphatase calcineurin is crucial for the environmental adaption of fungi. However, the mechanism of coordinate regulation of the response to salt stress by calcineurin and the high-affinity calcium channel CchA in fungi is not well understood. Here we show that the deletion of cchA suppresses the hyphal growth defects caused by the loss of calcineurin under salt stress in Aspergillus nidulans. Additionally, the hypersensitivity of the ΔcnaA strain to extracellular calcium and cell-wall-damaging agents can be suppressed by cchA deletion. Using the calcium-sensitive photoprotein aequorin to monitor the cytoplasmic Ca2+ concentration ([Ca2+]c) in living cells, we found that calcineurin negatively regulates CchA on calcium uptake in response to external calcium in normally cultured cells. However, in salt-stress-pretreated cells, loss of either cnaA or cchA significantly decreased the [Ca2+]c, but a deficiency in both cnaA and cchA switches the [Ca2+]c to the reference strain level, indicating that calcineurin and CchA synergistically coordinate calcium influx under salt stress. Moreover, real-time PCR results showed that the dysfunction of cchA in the ΔcnaA strain dramatically restored the expression of enaA (a major determinant for sodium detoxification), which was abolished in the ΔcnaA strain under salt stress. These results suggest that double deficiencies of cnaA and cchA could bypass the requirement of calcineurin to induce enaA expression under salt stress. Finally, YvcA, a member of the transient receptor potential channel (TRPC) protein family of vacuolar Ca2+ channels, was proven to compensate for calcineurin-CchA in fungal salt stress adaption. [ABSTRACT FROM AUTHOR]

Statistical analyses, a Piper diagram, the saturation index and the correlations of chemical parameters were used to reveal the hydrogeochemistry and hydrogeochemical evolution of shallow groundwater in the southern part of the Zhongwei section of the Yellow River alluvial plain. The water quality for agricultural and domestic uses was also assessed in the study. The results suggest that the shallow groundwater in the study area is fresh to moderately mineralized water. Higher Ca2+ and HCO3- are observed in the less mineralized water, whereas Na+ and SO42- are common ions in the highly mineralized water. The major hydrochemical facies for groundwater with total dissolved solids (TDS) <1 g/L are HCO3-Ca·Mg and HCO3-Ca·Na·Mg, and for groundwater with TDS > 1 g/L, SO4·Cl-Na and SO4·Cl-Na·Mg·Ca are the predominant hydrochemical types. The main reactions in the groundwater system are the dissolution/precipitation of gypsum, fluorite, halite, calcite and dolomite. Cation exchange is also important in controlling the groundwater chemistry. The water samples assessed in the paper are of acceptable quality for agricultural use, but most of them are not fit for direct human consumption (drinking). TDS, total hardness (TH), Cl- and SO42- are the main indices that result in the poor drinking water quality. [ABSTRACT FROM AUTHOR]

The article presents Engineered neutrophil-derived exosome-like vesicles for targeted cancer therapy. Topics discussed include Neutrophils are the most abundant innate immune cells in human circulation; however, their derived exosomes have been rarely studied for tumor treatment; and reported that exosomes from neutrophils (N-Ex) induce tumor cell apoptosis by delivering cytotoxic proteins and activating caspase signaling pathway.

Many insects possess a sexual communication system that is vulnerable to chemical espionage by parasitic wasps. We recently discovered that a hitch-hiking (H) egg parasitoid exploits the antiaphrodisiac pheromone benzyl cyanide (BC) of the Large Cabbage White butterfly Pieris brassicae. This pheromone is passed from male butterflies to females during mating to render them less attractive to conspecific males. When the tiny parasitic wasp Trichogramma brassicae detects the antiaphrodisiac, it rides on a mated female butterfly to a host plant and then parasitizes her freshly laid eggs. The present study demonstrates that a closely related generalist wasp, Trichogramma evanescens, exploits BC in a similar way, but only after learning. Interestingly, the wasp learns to associate an H response to the odors of a mated female P. brassicae butterfly with reinforcement by parasitizing freshly laid butterfly eggs. Behavioral assays, before which we specifically inhibited long-term memory (LTM) formation with a translation inhibitor, reveal that the wasp has formed protein synthesis-dependent LTM at 24 h after learning. To our knowledge, the combination of associatively learning to exploit the sexual communication system of a host and the formation of protein synthesis-dependent LTM after a single learning event has not been documented before. We expect it to be widespread in nature, because it is highly adaptive in many species of egg parasitoids. Our finding of the exploitation of an antiaphrodisiac by multiple species of parasitic wasps suggests its use by Pieris butterflies to be under strong selective pressure. [ABSTRACT FROM AUTHOR]

Acquired lymphedema is a complex disease caused by cancer treatment or parasitic infection and few effective treatments are available for lymphedema.1-3 It is urgently needed to develop new experimental approaches and therapeutic strategies.3 In this study, we address a new role and mechanism of MSC-ex (human umbilical cord Wharton's jelly mesenchymal stem cells derived exosome) in lymphedema treatment. MSC-ex treatment promoted lymphatic drainage in lymphedema mice as injected methylene blue across the site of incision at week 6, which was not found in PBS treated mice (Figure 1J). As lymphangiogenesis is crucial in lymphedema development after lymphatic ablation,4,5 we analyzed the lymphatic anatomy and lymphangiogenesis in MSC-ex treated animals. [Extracted from the article]

The Tibetan Plateau is the source of most of Asia's major rivers and has been called the Asian Water Tower. Detailed knowledge of its hydrogeology is paramount to enable the understanding of groundwater dynamics, which plays a vital role in headwater areas like the Tibetan Plateau. Nevertheless, due to its remoteness and the harsh environment, there is a lack of field survey data to investigate its hydrogeology. In this study, borehole core lithology analysis, altitude survey, soil thickness measurement, hydrogeological survey, and hydrogeophysical surveys (e.g., Magnetic Resonance Sounding – MRS, Electrical Resistivity Tomography – ERT, and Transient Electromagnetic – TEM) were conducted in the Maqu catchment within the Yellow River Source Region (YRSR). The soil thickness measurements were done in the western mountainous area of the catchment, where hydrogeophysical surveys were difficult to be carried out. The results indicate soil thicknesses are within 1.2 m in most cases, and the soil thickness decreases as the slope increases. The hydrogeological survey reveals that groundwater flows from the west to the east, recharging the Yellow River. The hydraulic conductivity ranges from 0.2 m/d to 12.4 m/d. The MRS soundings results, i.e., water content and hydraulic conductivity, confirmed the presence of unconfined aquifer in the flat eastern area. The depth of the Yellow River deposits was derived at several places in the flat eastern area based on TEM results. These survey data and results can be used to develop integrated hydrological modeling and water cycle analysis to improve a full–picture understanding of the water cycle at the Maqu catchment in the YRSR. The raw data set is freely available at https://doi.org/10.17026/dans-z6t-zpn7 (Li et al., 2020). [ABSTRACT FROM AUTHOR]

Background: Long non-coding RNAs (lncRNAs) are involved in many fundamental biological processes, such as transcription regulation, protein degradation, and cell differentiation. Information on lncRNA in the melon fly, Zeugodacus cucurbitae (Coquillett) is currently limited. Results: We constructed 24 RNA-seq libraries from eight tissues (midgut, Malpighian tubules, fat body, ovary, and testis) of Z. cucurbitae adults. A total of 3124 lncRNA transcripts were identified. Among those, 1464 were lincRNAs, 1037 were intronic lncRNAs, 301 were anti-sense lncRNAs, and 322 were sense lncRNAs. The majority of lncRNAs contained two exons and one isoform. Differentially expressed lncRNAs were analyzed between tissues, and Malpighian tubules versus testis had the largest number. Some lncRNAs exhibited strong tissue specificity. Specifically expressed lncRNAs were identified and filtered in tissues of female and male Z. cucurbitae based on their expression levels. Four midgut-specific lncRNAs were validated by quantitative real-time polymerase chain reaction (RT-qPCR), and the data were consistent with RNA-seq data. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of targets of midgut-specific lncRNAs indicated an enrichment of the metabolic process. Conclusions: This was the first systematic identification of lncRNA in the melon fly. Expressions of lncRNAs in multiple adult tissues were evaluated by quantitative transcriptomic analysis. These qualitative and quantitative analyses of lncRNAs, especially the tissue-specific lncRNAs in Z. cucurbitae, provide useful data for further functional studies. [ABSTRACT FROM AUTHOR]

Age-associated diseases, including vascular diseases, are on the rise with the increase in the aging population. However, the mechanisms of aging and age-associated vascular dysfunction remain to be fully elucidated. Replicative senescence of vascular smooth muscle cells (VSMCs) contributes to aging as well as age-associated vascular diseases. Rapamycin may delay aging-associated diseases via inhibition of the mammalian target of rapamycin (mTOR), but its role in VSMC aging has remained elusive. The present study investigated the involvement of mTOR signaling in replicative senescence of VSMCs. Replicative senescence was induced in human VSMCs by extended passages and identified by assessing the cell morphology, senescence-associated β-galactosidase activity, and p53 and p21 protein expression. Protein expression and phosphorylation were determined by western blot analysis. Significant senescence of VSMCs was observed in cells subjected to extended passaging (until passage 15). Significant decreases in adenosine monophosphate-activated protein kinase (AMPK)/tuberous sclerosis complex 2 (TSC2) phosphorylation, but significant increases in mTOR/ribosomal protein S6 kinase 1 (S6K1) phosphorylation, were observed in cells with replicative senescence compared with those in young cells. Pre-treatment of VSMCs with AMPK activator and mTOR inhibitor delayed replicative senescence and reversed changes in AMPKα, TSC2, mTOR and S6K1 phosphorylation in senescent VSMCs. The AMPK/TSC2/mTOR/S6K1 signaling axis was found to have an important role in regulating replicative senescence of human VSMCs. [ABSTRACT FROM AUTHOR]

Secreted effectors from Magnaporthe oryzae play critical roles in the interaction with rice to facilitate fungal infection and disease development. M. oryzae-secreted protein MoHrip1 can improve plant defense as an elicitor in vitro, however, its biological function in fungal infection is not clear. In this study, we found that the expression of mohrip1 was significantly induced in the stages of fungal penetration and colonization. Although dispensable for the growth and conidiation, MoHrip1 was necessary for the full virulence of M. oryzae. Deletion of mohrip1 remarkably compromised fungal virulence on rice seedlings and even on rice leaves with wounds. Rice sheath inoculation assay further demonstrated the defects of mohrip1-deleted mutants on penetration and proliferation in rice cells. Additionally, compared with WT and complementation strain, the inoculation of mohrip1-deleted mutants induced a higher expression of specific defense related genes and a higher production of specific defensive compounds in rice leaves. These data collectively indicated that MoHrip1 is necessary for fungal penetration and invasive expansion, and further full virulence of rice blast fungus. [ABSTRACT FROM AUTHOR]

Grain growth in porous ceramics is a complex process due to the variety of interactions between pores and grains. In this study, the pore deformation and grain boundary migration during porous ceramic sintering are simulated by the phase-field method, and the variety of diffusions during sintering is considered. Pores of different shapes and sizes are induced into the simulations to investigate the grain boundary migration and pore deformations during grain growth. Simulation results indicate that the porous microstructure is determined by the contacting mode between pore surface and grain boundaries, which is in good agreement with experimental observations. The efficiency of the grain boundary migration is analyzed via calculating the forces applied on the interfaces between grains and pores, and the mechanism of the pore deformation during grain boundary migration is discussed. Therefore, controlling the grain-pore microstructure by adjusting the synthesis process is essential to reach the desired mechanical and physical properties of sintered materials. [ABSTRACT FROM AUTHOR]

Objectives: Long noncoding RNAs (lncRNAs) play important roles in cancer development and progression. The deregulated expression of LINC00978 has been reported in human cancers. However, the expression pattern and biological roles of LINC00978 in gastric cancer (GC) remain unclear. In this study, we investigated the potential roles and clinical value of LINC00978 in gastric cancer. Materials and methods: QRT-PCR was performed to investigate the expression of LINC00978 in gastric cancer cell lines, tissues and serum samples. Cell counting, colony formation, transwell migration and matrigel invasion assays were performed to determine the effects of shRNA-mediated knockdown of LINC00978 on gastric cancer cell functions. In vivo tumour growth assay was also conducted. Flow cytometry, immunohistochemistry, western blot and qRT-PCR were used for potential mechanism study. Results: LINC00978 expression level was elevated in GC tumour tissues, serum samples and cell lines. The expression level of LINC00978 was significantly correlated with tumour size (P = 0.02), lymphatic metastasis (P = 0.009) and TNM stage (P = 0.009). LINC00978 knockdown inhibited the proliferation of GC cells by suppressing cell cycle progression and inducing apoptosis. LINC00978 knockdown also inhibited the migration and invasion of GC cells. In addition, LINC00978 knockdown inhibited the activation of TGF-β/ SMAD signalling pathway and the process of epithelial-mesenchymal transition (EMT) in GC cells. Moreover, the in vivo tumorigenicity of LINC00978 knockdown GC cells in mice was significantly decreased. Conclusions: LINC00978 promotes gastric cancer progression and may serve as a potential biomarker for GC. [ABSTRACT FROM AUTHOR]

CircRNAs are a class of RNA molecules that structurally form closed loops. CircRNAs are abundant in eukaryotic transcripts and show certain levels of tissue and cell specificity. CircRNAs have been suggested to regulate gene expression at transcriptional, post-transcriptional, and translational levels. An increasing number of studies have shown that circRNAs play important roles in the development and progression of diseases including cancer. In particular, circRNAs have shown great potential in cancer diagnosis, prognosis, and therapy. In this review, we provide an overview of the biogenesis and characteristics of circRNAs, succinctly describe their functions, and comprehensively discuss about the recent advances in the roles of circRNAs in cancer with an emphasis on their clinical values. [ABSTRACT FROM AUTHOR]

Non-noble metal-based heterostructures have emerged as a promising strategy to construct high-efficient electrocatalysts for the Oxygen evolution reaction. Herein, we reported a three-dimensional core-shell heterostructures of NiTe/NiCo-LDH (NiCo layered double hydroxides) on the Ni foam to resolve the low electronic conductivity and self-aggregation of NiCo-LDH. This NiTe/NiCo-LDH electrocatalyst could be prepared from a two-step reaction as a hydrothermal reaction and electrodeposition approach. Benefiting from the existence of strong interface effects between the NiTe nanorod core and NiCo-LDH nanosheet shell, the NiTe/NiCo-LDH electrocatalyst exhibited superior activity for the Oxygen evolution reaction at a current density of 100 mA cm−2 with an overpotential of 376 mV in 1.0 M KOH solution, which was significantly smaller than that of a single component of NiTe (586 mV), NiCo-LDH (410 mV) and commercial RuO 2 (428 mV). Furthermore, the NiTe/NiCo-LDH catalyst indicated long-term stability after 24 h continuous working. Density functional theory computations unveil that the heterostructures modified the original electronic structures and weakened the atomic interaction in the LDH layers, which have effectively adjusted the d -band center of the catalytic active Co sites to the Fermi level. This work demonstrated an effective strategy of interfacial engineering to optimize electron transfer to boost Oxygen evolution reaction performance. [Display omitted] • Three-dimensional (3D) core-shell heterostructure of NiTe/NiCo-LDH on the NF is synthesized. • NiTe/NiCo-LDH electrocatalyst showed extraordinary OER activity and stability under alkaline condition. • The outstanding OER performance is mainly attributed to the synergetic effect between NiTe core and NiCo-LDH shell. • OER improvement mechanism is clarified through the experiment and theoretical calculation. [ABSTRACT FROM AUTHOR]

Background: The administration of cisplatin is limited due to its nephrotoxic side effects, and prevention of this nephrotoxicity of cisplatin is difficult. Mesenchymal stem cell (MSC)-derived exosomes have been implicated as a novel therapeutic approach for tissue injury. In this study, we demonstrated that the pretreatment of human umbilical cord MSC-derived exosomes (hucMSC-Ex) can prevent the development of cisplatin-induced renal toxicity by activation of autophagy in vitro and in vivo. Methods: In vitro, rat renal tubular epithelial (NRK-52E) cells were pre-incubated with exosomes from hucMSC or HFL1 (human lung fibroblast cells; as control) for 30 min, and 3-methyladenine (an autophagic inhibitor) and rapamycin (an autophagic inducer) for 1 h before cisplatin treatment for 8 h, respectively. Cells were harvested for apoptosis assay, enzyme-linked immunosorbent assay (ELISA), Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR). In vivo, we constructed cisplatin-induced acute kidney injury rat models. Prior to treatment with cisplatin for 0.5 h, hucMSC-Ex or HFL1-Ex were injected into the kidneys via the renal capsule. 3-methyladenine and rapamycin were injected under the kidney capsule before hucMSC-Ex. All animals were sacrificed at 3 days after cisplatin injection. Renal function, Luminex assay, tubular apoptosis and proliferation, and autophagy response were evaluated. Results: hucMSC-Ex inhibited cisplatin-induced mitochondrial apoptosis and secretion of inflammatory cytokines in renal tubular epithelial cells in vitro. hucMSC-Ex increased the expression of the autophagic marker protein LC3B and the autophagy-related genes ATG5 and ATG7 in NRK-52E cells. Rapamycin mimicked the effects of hucMSC-Ex in protecting against cisplatin-induced renal injury, while the effects were abrogated by the autophagy inhibitor 3-methyladenine in the animals. Conclusions: Our findings indicate that the activation of autophagy induced by hucMSC-Ex can effectively relieve the nephrotoxicity of cisplatin. Therefore, pre-treatment of hucMSC-Ex may be a new method to improve the therapeutic effect of cisplatin. [ABSTRACT FROM AUTHOR]

Background: Overexpression of cyclin D1 dependent kinases 4 and 6 (CDK4/6) is a common feature of many human cancers including leukemia. LEE011 is a novel inhibitor of both CDK4 and 6. To date, the molecular function of LEE011 in leukemia remains unclear. Methods: Leukemia cell growth and apoptosis following LEE011 treatment was assessed through CCK-8 and annexin V/propidium iodide staining assays. Cell senescence was assessed by β-galactosidase staining and p16INK4a expression analysis. Gene expression profiles of LEE011 treated HL-60 cells were investigated using an Arraystar Human LncRNA array. Gene ontology and KEGG pathway analysis were then used to analyze the differentially expressed genes from the cluster analysis. Results: Our studies demonstrated that LEE011 inhibited proliferation of leukemia cells and could induce apoptosis. Hoechst 33,342 staining analysis showed DNA fragmentation and distortion of nuclear structures following LEE011 treatment. Cell cycle analysis showed LEE011 significantly induced cell cycle G1 arrest in seven of eight acute leukemia cells lines, the exception being THP-1 cells. β-Galactosidase staining analysis and p16INK4a expression analysis showed that LEE011 treatment can induce cell senescence of leukemia cells. LncRNA microarray analysis showed 2083 differentially expressed mRNAs and 3224 differentially expressed lncRNAs in LEE011-treated HL-60 cells compared with controls. Molecular function analysis showed that LEE011 induced senescence in leukemia cells partially through downregulation of the transcriptional expression of MYBL2. Conclusions: We demonstrate for the first time that LEE011 treatment results in inhibition of cell proliferation and induction of G1 arrest and cellular senescence in leukemia cells. LncRNA microarray analysis showed differentially expressed mRNAs and lncRNAs in LEE011-treated HL-60 cells and we demonstrated that LEE011 induces cellular senescence partially through downregulation of the expression of MYBL2. These results may open new lines of investigation regarding the molecular mechanism of LEE011 induced cellular senescence. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cells (MSCs) are attractive seed cells for immunotherapy, tissue engineering and regenerative medicine due to their self-renewal and multidirectional differentiation abilities, diverse immunoregulatory functions and ease of isolation from a wide range of tissues. MSCs exert their immunoregulatory effect on immune cells via cell-to-cell contact and paracrine mechanisms. In turn, MSCs can also be modulated by immune cells. Macrophages are constantly present in the mucosa of the intestinal tract of mammals and play an important role in the development and progression of inflammatory bowel disease (IBD), a chronic and recurrent inflammatory disease of the gastrointestinal tract characterized by idiopathic mucosal inflammation. The increased morbidity and mortality of IBD have made it a disease hard to cure in the clinic. MSCs have emerged as an important tool for IBD therapy due to their abilities to differentiate into enterocyte-like cells and regulate inflammatory cells, especially macrophages. In this review, we discuss the recent advances in the interaction between MSCs and macrophages in diseases, with an emphasis on IBD. We propose that an optimized MSC-based therapy would provide a novel strategy for the treatment of IBD and the prevention of IBD-associated colorectal cancer (CRC). [ABSTRACT FROM AUTHOR]

Vascular aging, a specific type of organic aging, is related to age-dependent changes in the vasculature, including atherosclerotic plaques, arterial stiffness, fibrosis, and increased intimal thickening. Vascular aging could influence the threshold, process, and severity of various cardiovascular diseases, thus making it one of the most important risk factors in the high mortality of cardiovascular diseases. As endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are the main cell biological basis of these pathology changes of the vasculature, the structure and function of ECs and VSMCs play a key role in vascular aging. MicroRNAs (miRNAs), small noncoding RNAs, have been shown to regulate the expression of multiple messenger RNAs (mRNAs) posttranscriptionally, contributing to many crucial aspects of cell biology. Recently, miRNAs with functions associated with aging or aging-related diseases have been studied. In this review, we will summarize the reported role of miRNAs in the process of vascular aging with special emphasis on EC and VSMC functions. In addition, the potential application of miRNAs to clinical practice for the diagnosis and treatment of cardiovascular diseases will also be discussed. [ABSTRACT FROM AUTHOR]

Background: Emerging evidence indicates that inappropriate cell-cell fusion might contribute to cancer progression. Similarly, mesenchymal stem cells (MSCs) can also fuse with other cells spontaneously and capable of adopting the phenotype of other cells. The aim of our study was to investigate the role of MSCs participated cell fusion in the tumorigenesis of gastric cancer.Methods: We fused human umbilical cord mesenchymal stem cells (hucMSCs) with gastric cancer cells in vitro by polyethylene glycol (PEG), the hybrid cells were sorted by flow cytometer. The growth and migration of hybrids were assessed by cell counting, cell colony formation and transwell assays. The proteins and genes related to epithelial- mesenchymal transition and stemness were tested by western blot, immunocytochemistry and real-time RT-PCR. The expression of CD44 and CD133 was examined by immunocytochemistry and flow cytometry. The xenograft assay was used to evaluation the tumorigenesis of the hybrids.Results: The obtained hybrids exhibited epithelial- mesenchymal transition (EMT) change with down-regulation of E-cadherin and up-regulation of Vimentin, N-cadherin, α-smooth muscle actin (α-SMA), and fibroblast activation protein (FAP). The hybrids also increased expression of stemness factors Oct4, Nanog, Sox2 and Lin28. The expression of CD44 and CD133 on hybrid cells was stronger than parental gastric cancer cells. Moreover, the migration and proliferation of heterotypic hybrids were enhanced. In addition, the heterotypic hybrids promoted the growth abilities of gastric xenograft tumor in vivo.Conclusions: Taken together, our results suggest that cell fusion between hucMSCs and gastric cancer cells could contribute to tumorigenic hybrids with EMT and stem cell-like properties, which may provide a flexible tool for investigating the roles of MSCs in gastric cancer. [ABSTRACT FROM AUTHOR]

Exosomes have emerged as a novel mode of intercellular communication. Exosomes can shuttle bioactive molecules including proteins, DNA, mRNA, as well as non-coding RNAs from one cell to another, leading to the exchange of genetic information and reprogramming of the recipient cells. Increasing evidence suggests that tumor cells release excessive amount of exosomes, which may influence tumor initiation, growth, progression, metastasis, and drug resistance. In addition, exosomes transfer message from tumor cells to immune cells and stromal cells, contributing to the escape from immune surveillance and the formation of tumor niche. In this review, we highlight the recent advances in the biology of exosomes as cancer communicasomes. We review the multifaceted roles of exosomes, the small secreted particles, in communicating with other cells within tumor microenvironment. Given that exosomes are cell type specific, stable, and accessible from body fluids, exosomes may provide promising biomarkers for cancer diagnosis and represent new targets for cancer therapy. [ABSTRACT FROM AUTHOR]

The fragile histidine triad (FHIT) gene is known to be a tumor suppressor gene and the abnormal methylation of FHIT has been identified in leukemia and several solid tumors. The transformation of the tumor F6 cell line from human fetal mesenchymal stem cells (FMSCs) was first reported in a previous study that also identified the presence of a population of cancer stem cells in the F6 cell line. However, the existence of the epigenetic changes during the transformation process have yet to be elucidated. To confirm the role of the FHIT gene in the transformation process of FMSC, the expression level and methylation status of the FHIT gene was examined in F6 tumor cells and FMSCs. Additionally, the alteration in cell morphology, the cell cycle and apoptosis in F6 cells following 5-Aza-CdR treatment was assessed. It was found that the FHIT gene was expressed in FMSCs, but not in F6 cells. The methylation-specific PCR results demonstrated that the promoter methylation of FHIT genes existed in the F6 cell line. Subsequent to treatment with 5-Aza-CdR the expression of FHIT genes was restored in F6 cells. In addition, the morphology of F6 cells was altered, and the cell cycle was arrested in the G2 phase, with the initiation of apoptosis. Overall, the present findings demonstrated that the FHIT gene was methylated in F6 cells and demethylation treatment lead to changes in the biological characteristics, thereby promoting the apoptosis of F6 cells. FHIT gene methylation may be one of the molecular events involved in the development and transformation of FMSCs into F6 tumor cells. [ABSTRACT FROM AUTHOR]

Human bone marrow mesenchymal stem cells (hBM-MSCs) favor tumor growth and metastasis in vivo and in vitro. Neovascularization is involved in several pathological conditions, including tumor growth and metastasis. Previous studies have demonstrated that human bone marrow MSC-derived conditioned medium (hBM-MSC-CM) can promote tumor growth by inducing the expression of vascular epidermal growth factor (VEGF) in tumor cells. However, the effect of BM-MSCs on tumor lymph vessel formation has yet to be elucidated. In the present study, the effect of BM-MSCs on processes involved in lymph vessel formation, including tube formation, migration and proliferation, was investigated in human-derived lymphatic endothelial cells (HDLECs). It was identified that hBM-MSC-CM promoted the tube formation and migration of HDLECs. In addition, tumor cells were revealed to participate in lymph vessel formation. In the present study, the SGC-7901, HGC-27 and GFP-MCF-7 cell lines were treated with hBM-MSC-CM. The results demonstrated that the expression of the lymph-associated markers, prospero homeobox protein 1 and VEGF receptor-3, were increased in the SGC-7901 and HGC-27 cell lines, but not in the GFP-MCF-7 cells. The tube formation assay demonstrated that the HGC-27 cells treated with hBM-MSC-CM for 20 days underwent tube formation. These findings indicate that hBM-MSC-CM can promote tube formation in HDLECs and HGC-27 cells, which may be associated with lymph vessel formation during tumor growth and metastasis. [ABSTRACT FROM AUTHOR]

An immortalized mouse fetal liver stromal cell line, named KM3, has demonstrated the potential to support the growth and maintenance of human embryonic stem cells (hESCs). In this study, the characteristics of KM3 cells were examined following cryopreservation at -70°C and in liquid nitrogen for 15, 30 and 60 days following treatment with 10 µg/ml mitomycin C. In addition, whether the KM3 cells were suitable for use as feeder cells to support the growth of hESCs was evaluated. The inhibition of mitosis without cell death was observed when the KM3 cells were treated with 10 µg/ml mitomycin C for 2 h. The morphology of the KM3 cells cryopreserved in liquid nitrogen for 60 days was not markedly changed, and the cell survival rate was 84.60±1.14%. By contrast, the survival rate of the KM3 cells was 66.40±2.88% following cryopreservation at -70°C for 60 days; the cells readily detached, were maintained for a shorter time, and had a reduced expression level of basic fibroblast growth factor. hESCs cultured on KM3 cells cryopreserved in liquid nitrogen for 60 days showed the typical bird's nest structure, with clear boundaries and a differentiation rate of 16.33±2.08%. The differentiation rate of hESCs cultured on KM3 cells cryopreserved at -70°C for 60 days was 37.67±3.51%. These results indicate that the cryopreserved KM3 cells treated with mitomycin C may be directly used in the subculture of hESCs, and the effect is relatively good with -70°C short-term or liquid nitrogen cryopreservation. [ABSTRACT FROM AUTHOR]

Introduction: Administration of bone marrow mesenchymal stem cells (MSCs) or secreted microvesicles improves recovery from acute kidney injury (AKI). However, the potential roles and mechanisms are not well understood. In the current study, we focused on the protective effect of exosomes derived from human umbilical cord mesenchymal stem cells (hucMSC-ex) on cisplatin-induced nephrotoxicity in vivo and in vitro. Methods: We constructed cisplatin-induced AKI rat models. At 24 h after treatment with cisplatin, hucMSC-ex were injected into the kidneys via the renal capsule; human lung fibroblast (HFL-1)-secreted exosomes (HFL-1-ex) were used as controls. All animals were killed at day 5 after administration of cisplatin. Renal function, histological changes, tubular apoptosis and proliferation, and degree of oxidative stress were evaluated. In vitro, rat renal tubular epithelial (NRK-52E) cells were treated with or without cisplatin and after 6 h treated with or without exosomes. Cells continued to be cultured for 24 h, and were then harvested for western blotting, apoptosis and detection of degree of oxidative stress. Results: After administration of cisplatin, there was an increase in blood urea nitrogen (BUN) and creatinine (Cr) levels, apoptosis, necrosis of proximal kidney tubules and formation of abundant tubular protein casts and oxidative stress in rats. Cisplatin-induced AKI rats treated with hucMSC-ex, however, showed a significant reduction in all the above indexes. In vitro, treatment with cisplatin alone in NRK-52E cells resulted in an increase in the number of apoptotic cells, oxidative stress and activation of the p38 mitogen-activated protein kinase (p38MAPK) pathway followed by a rise in the expression of caspase 3, and a decrease in cell multiplication, while those results were reversed in the hucMSCs-ex-treated group. Furthermore, it was observed that hucMSC-ex promoted cell proliferation by activation of the extracellular-signal-regulated kinase (ERK)1/2 pathway. Conclusions: The results in the present study indicate that hucMSC-ex can repair cisplatin-induced AKI in rats and NRK-52E cell injury by ameliorating oxidative stress and cell apoptosis, promoting cell proliferation in vivo and in vitro. This suggests that hucMSC-ex could be exploited as a potential therapeutic tool in cisplatin-induced nephrotoxicity. [ABSTRACT FROM AUTHOR]

A combined study of mineral O and Rb–Sr isotopes was carried out for a number of Mesozoic granitoids in China in order to compare the degree of O isotope equilibrium between coexisting minerals, with the validity of mineral Rb–Sr isochrons for granitoids. A scrutiny of both O isotope geothermometry and Rb–Sr internal isochron dating for corresponding minerals indicates that equilibrium O isotope fractionation between Rb–Sr isochron minerals corresponds to geologically meaningful isochron ages if the variation in 87Rb/86Sr ratio is big enough to provide reasonably small uncertainties in age. Significant deviation of the Rb–Sr isochron age from the actual age appears to depend on the difference in Sr isotopic composition between an external fluid and the igneous minerals. As a result, O isotope disequilibrium is often caused by interaction between the rock and the external fluid that results in mineral alteration. Post-magmatic alteration can cause isotope exchange between the minerals and an internally buffered fluid that is isotopically identical to the host rock. The O isotope composition of coexisting minerals in studied samples changed principally due to a decrease in temperature. Both Rb and Sr concentrations and the Sr isotope ratios of isochron minerals also changed due to the mixing of different Sr reservoirs. Nevertheless, the isochron age can remain unchanged if the mixing took place along the isochron chord between the internal fluid and the minerals from that newly altered minerals formed. This provides an insight into the effect of internal and external fluids on the validity of mineral Rb–Sr chronometry. In addition, an alternative approach is proposed to construct the cooling curve by a combined use of O isotope temperature and mineral isotope age for the granitoids of interest. Comparing with the traditional method using the empirical closure temperature for Rb–Sr chronometry, the proposed approach utilizes fewer variables with smaller uncertainties than the traditional way. [ABSTRACT FROM AUTHOR]

To investigate multitissue engraftment of human primitive hematopoietic cells and their differentiation in goats, human CD34+Lin- cord blood cells transduced with a GFP vector were transplanted into fetal goats at 45-55 days of gestation. GFP+ cells were detected in hematopoietic and nonhematopoietic organs including blood, bone marrow, spleen, liver, kidney, muscle, lung, and heart of the recipient goats (1.2-36% of all cells examined). We identified human β2 microglobulin-positive cells in multiple tissues. GFP+ cells sorted from the perfused liver of a transplant goat showed human insulin-like growth factor 1 gene sequences, indicating that the engrafted GFP+ cells were of human origin. A substantial fraction of cells engrafted in goat livers expressed the human hepatocyte-specific antigen, proliferating cell nuclear antigen, albumin, hepatocyte nuclear factor, and GFP. DNA content analysis showed no evidence for cellular fusion. Long-term engraftment of GFP+ cells could be detected in the blood of goats for up to 2 yr. Microarray analysis indicated that human genes from a variety of functional categories were expressed in chimeric livers and blood. The human/goat xenotransplant model provides a unique system to study the kinetics of hematopoietic stem cell engraftment, gene expression, and possible stem cell plasticity under noninjured conditions. [ABSTRACT FROM AUTHOR]