Imparting Outstanding Dispersibility to Nanoscaled 2D COFs for Constructing Organic Solvent Forward Osmosis Membranes.

In the context of thin-film nanocomposite membranes with interlayer (TFNi), nanoparticles are deposited uniformly onto the support prior to the formation of the polyamide (PA) layer. The successful implementation of this approach relies on the ability of nanoparticles to meet strict requirements regarding their sizes, dispersibility, and compatibility. Nevertheless, the synthesis of covalent organic frameworks (COFs) that are well-dispersed, uniformly morphological, and exhibit improved affinity to the PA network, while preventing agglomeration, remains a significant challenge. In this work, a simple and efficient method is presented for the synthesis of well-dispersed, uniformly morphological, and amine-functionalized 2D imine-linked COFs regardless of the ligand composition, group type, or framework pore size, by utilizing a polyethyleneimine (PEI) shielded covalent self-assembly strategy. Subsequently, the as-prepared COFs are incorporated into TFNi for the recycling of pharmaceutical synthetic organic solvents. After optimization, the membrane exhibits a high rejection rate and a favorable solvent flux, making it a reliable method for efficient organic recovery and the concentration of active pharmaceutical ingredient (API) from the mother liquor through an organic solvent forward osmosis (OSFO) process. Notably, this study represents the first investigation of the impact of COF nanoparticles in TFNi on OSFO performance.

A RhABF2/Ferritin module affects rose (Rosa hybrida) petal dehydration tolerance and senescence by modulating iron levels.

Plants often develop the capacity to tolerate moderate and reversible environmental stresses, such as drought, and to re-establish normal development once the stress has been removed. An example of this phenomenon is provided by cut rose (Rosa hybrida) flowers, which experience typical reversible dehydration stresses during post-harvest handling after harvesting at the bud stages. The molecular mechanisms involved in rose flower dehydration tolerance are not known, however. Here, we characterized a dehydration- and abscisic acid (ABA)-induced ferritin gene (RhFer1). Dehydration-induced free ferrous iron (Fe2+ ) is preferentially sequestered by RhFer1 and not transported outside of the petal cells, to restrict oxidative stresses during dehydration. Free Fe2+ accumulation resulted in more serious oxidative stresses and the induction of genes encoding antioxidant enzyme in RhFer1-silenced petals, and poorer dehydration tolerance was observed compared with tobacco rattle virus (TRV) controls. We also determined that RhABF2, an AREB/ABF transcription factor involved in the ABA signaling pathway, can activate RhFer1 expression by directly binding to its promoter. The silencing of RhABF2 decreased dehydration tolerance and disrupted Fe homeostasis in rose petals during dehydration, as did the silencing of RhFer1. Although both RhFer1 and Fe transporter genes are induced during flower natural senescence in plants, the silencing of RhABF2 or RhFer1 accelerates the petal senescence processes. These results suggest that the regulatory module RhABF2/RhFer1 contributes to the maintenance of Fe levels and enhances dehydration tolerance through the action of RhFer1 locally sequestering free Fe2+ under dehydration conditions, and plays synergistic roles with transporter genes during flower senescence.

NLRP3 inflammasome activation in mesenchymal stem cells inhibits osteogenic differentiation and enhances adipogenic differentiation.

Osteoporosis is one of the most common skeletal disease featured by osteopenia and adipose accumulation in bone tissue. NLRP3 inflammasome activation is an essential player in aging-related chronic diseases like osteoporosis, particularly due to the causal caspase-1 activation and its correlation to adipose accumulation in bone tissue. Moreover, the expression of anti-aging/senescence SIRT1 was reported to decline along with aging. As the major cellular contributor of bone formation, mesenchymal stem cells (MSCs) are multipotent stem cells processing mutually exclusive differentiatability toward osteocytes or adipocytes. Therefore, we hypothesized that NLRP3 inflammasome activation promotes adipogenesis and repress osteogenesis in MSCs via inhibiting SIRT1 expression. We activated NLRP3 inflammasome in human MSCs via lipopolysaccharide and palmitic acid (LPS/PA) treatment for self-renewal maintenance, adipogenic differentiation or osteogenic differentiation. LPS/PA treatment significantly increased NLRP3 expression, decreased SIRT1 expression and promoted caspase-1 activity in MSCs. LPS/PA treatment also boosted adipogenesis of MSCs and suppressed osteogenesis. Moreover, inhibition of caspase-1 activity repressed adipogenic differentiation and partially improved osteogenic differentiation of MSCs with LPS/PA treatment. Our study demonstrated the pivotal roles of NLRP3 inflammasome and downstream mediator caspase-1 for the progress of osteo-differentiation MSCs, and offered novel therapeutic target of treatment for osteoporosis.

Phosphatase and tensin homologue (PTEN)-induced putative kinase 1 reduces pancreatic ß-cells apoptosis in glucotoxicity through activation of autophagy.

Chronic elevated glucose is harmful to pancreatic ß-cells, resulting in pancreatic ß-cells dysfunction and apoptosis. Understanding the molecular mechanisms associated with ß-cells survival is pivotal for the prevention of ß-cells injury caused by glucotoxicity. The role of Phosphatase and tensin homologue (PTEN)-induced putative kinase 1 (PINK1) in the fate of pancreatic ß-cells constantly exposed to high glucose was studied. Sustained high glucose increased PINK1 protein expression both in rat pancreatic ß-cells and INS-1 ß-cells, and that this increase can be inhibited by PINK1 knockdown and further enhanced by PINK1 over-expression. PINK1 deficiency aggravated glucotoxicity-induced pancreatic ß-cells apoptosis and inhibition of autophagy whereas PINK1 could reverse these adverse effects. This study provides fundamental data supporting the potential protective role of PINK1 as a new therapeutic target necessary to preserve ß-cells survival under non-physiological hyperglycemia conditions.

Ginsenoside Rh2 inhibits proliferation and induces apoptosis in human leukemia cells via TNF-α signaling pathway.

Ginsenoside Rh2, a triterpene saponin extracted from Panax ginseng, exhibits pharmacological activity against multiple cancers. However, the anticancer mechanism of ginsenoside Rh2 is unclear. In this study, we found that ginsenoside Rh2 effectively inhibits growth and induces apoptosis of HL-60 cells. Using microarray technology, we found that tumor necrosis factor-α (TNF-α) is clearly up-regulated. Furthermore, anti-TNF-α antibody relieved the Rh2-induced HL-60 cell apoptosis via suppression of caspase-8, caspase-9, and caspase-3 activation. In addition, TNF-α up-regulation was also observed in other Rh2-treated cancer cell lines. These results demonstrate that TNF-α plays a key role in ginsenoside Rh2-induced cell apoptosis.

[Effect of curcumin on the expression of p-STAT3 and IκB in db/db mice].

OBJECTIVE: To determine the effect of curcumin on diabetic nephropathy in db/db mice and its possible mechanism. METHODS: Ten female db/db mice were randomly divided into 2 groups: one was treated with curcumin at 200 mg/(kg.d) and the other was a placebo group. Five age-matched db/m mice were grouped as the controls. In the curcumin group, curcumin was administered to db/db mice for 18 weeks. At the end of the experiment, the blood glucose and albumin were measured, and the kidney tissue sections were stained with PAS to observe the pathological changes. The expression of collagen IV and FN in the kidney was detected by immunohitochemistry staining. Western blot was used to detect the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and IκB in the kidney. RESULTS: Compared with db/m mice, the weight and blood glucose of db/db mice were markedly increased, accompanied with heavy proteinuria, glomerulus hypertrophy, mesangial area expansion, thickening of basement membrane and ECM deposition. The phosphorylation of STAT3 was upregulated and the degradation of IκB was increased. Compared with the db/db mice, curcumin significantly decreased the urinary albumin, inhibited the phosphorylation of STAT3 and the degradation of IκB, and reduced the expression of collagen IV and FN in the kidney. CONCLUSION: Curcumin can obviously decrease albuminuria and attenuate glomerular sclerosis in diabetic db/db mice by inhibiting phosphorylation of STAT3 and degradation of IκB.

Hsa_circ_0010023 promotes the development of papillary thyroid carcinoma by sponging miR-1250-5p.

BACKGROUND: Papillary thyroid cancer (PTC) is the most common thyroid tumor (TC). However, there is still a lack of effective indicators for PTC detection and prognosis. We intended to find a novel tumor marker for the progression of PTC. METHODS: The expression of circRNAs was measured by quantitative real-time polymerase chain reaction (qRT-PCR). SiRNA transfection was used to knockdown the expression of hsa_circ_0010023 in K1 cells. Cell proliferation was evaluated using cell counting and CCK8. Cell apoptosis was analyzed using flow cytometry. Hsa_circ_0010023 downstream pathways were predicted with bio-informatics analysis. The miR-1250-5p and MAPK1 were measured by qRT-PCR. The interaction between miR-1250-5p and hsa_circ_0010023 was vertified by dual-luciferase reporter assay. RESULTS: Among the four circRNAs screened, only hsa_circ_0010023 and hsa_circ_0128482 were highly expressed in PTC (P < 0.05). The expression of hsa_circ_0010023 was significantly correlated with lymph node metastasis and extrathyroid infiltration (P < 0.05). Compared with the control group, the cell proliferation of the si-circ-0010023 group was significantly inhibited (P < 0.05). Knockdown of hsa_circ_0010023 promotes apoptosis of K1 cells (P < 0.001). The expression of hsa_circ_0010023 was negatively correlated with miR-1250-5p and positively correlated with MAPK1. MiR-1250-5p overexpression significantly reduced the luciferase activity of wild type plasmid (hsa_circ_0010023 WT), but not that of mutant type plasmid (hsa_circ_0010023 MUT). CONCLUSION: The expression level of hsa_circ_0010023 was positive related to the progression of PTC, and hsa_circ_0010023 may promote PTC through sponging miR-1250-5p. Hsa_circ_0010023 may be a potential bio-marker for the diagnosis of PTC.

Shift work promotes adipogenesis via cortisol-dependent downregulation of EGR3-HDAC6 pathway.

The disruption of circadian rhythms caused by long-term shift work can cause metabolic diseases such as obesity. Early growth response 3 (EGR3) is a member of early growth response (EGR) family, which is involved in several cellular responses, had been reported as a circadian rhythm gene in suprachiasmatic nucleus. In this research, EGR3 was found to be widely expressed in the different tissue of human and mice, and downregulated in adipose tissue of obese subjects and high-fat diet mice. Moreover, EGR3 was found negatively regulated by cortisol. In addition, EGR3 is a key negative modulator of hADSCs and 3T3-L1 adipogenesis via regulating HDAC6, which is a downstream target gene of EGR3 and a negative regulator of adipogenesis and lipogenesis. These findings may explain how circadian rhythm disorder induced by shift works can cause obesity. Our study revealed a potential therapeutic target to alleviate metabolic disorders in shift workers and may provide better health guidance to shift workers.

Region-Specific CD16+ Neutrophils Promote Colorectal Cancer Progression by Inhibiting Natural Killer Cells.

The colon is the largest compartment of the immune system, with innate immune cells exposed to antigens in the environment. However, the mechanisms by which the innate immune system is instigated are poorly defined in colorectal cancer (CRC). Here, a population of CD16+ neutrophils that specifically accumulate in CRC tumor tissues by imaging mass cytometry (IMC), immune fluorescence, and flow cytometry, which demonstrated pro-tumor activity by disturbing natural killer (NK) cells are identified. It is found that these CD16+ neutrophils possess abnormal cholesterol accumulation due to activation of the CD16/TAK1/NF-κB axis, which upregulates scavenger receptors for cholesterol intake including CD36 and LRP1. Consequently, these region-specific CD16+ neutrophils not only competitively inhibit cholesterol intake of NK cells, which interrupts NK lipid raft formation and blocks their antitumor signaling but also release neutrophil extracellular traps (NETs) to induce the death of NK cells. Furthermore, CD16-knockout reverses the pro-tumor activity of neutrophils and restored NK cell cytotoxicity. Collectively, the findings suggest that CRC region-specific CD16+ neutrophils can be a diagnostic marker and potential therapeutic target for CRC.

A preliminary analysis of the effect of the new rural cooperative medical scheme on inpatient care at a county hospital.

BACKGROUND: China in 2009 committed to reach universal health coverage by promoting three forms of health insurance; NCMS for the rural population, UEBMI for formally employed urban residents and URBMI for other urban residents. NCMS has expanded to near universal coverage in rural China since launching in 2003. The objective of this study aimed to assess the effect of NCMS on inpatient care utilization from 2003 to 2012 at Longyou county hospital, Zhejiang province. METHODS: The research was conducted at Longyou county, Zhejiang province. All registered inpatient admissions from January 1, 2003, to June 30, 2012, were included in the study. The PLSQL Developer software was used to select the interesting variables in the hospital information database and saved in an Excel 2003 file. The interesting variables included the patients' general information (name, gender, age, payment method), discharge diagnosis, length of hospital stay, and expenditure (total expenditure and out-of-pocket payment). Two common diseases (coronary arteriosclerotic disease and pneumonia) were selected as tracer conditions. RESULTS: 292,400 rural residents were enrolled in the Longyou county NCMS by 2011, 95.4% of the eligible population. A total of 145,744 inpatient admissions were registered from 1 January 2003 to 30 June 2012. The proportion of inpatients covered by NCMS increased from 30.3% in 2004 to 54.2% in 2012 while the proportion of inpatients covered by UEBMI increased from 7.7% in 2003 to 14.7% in 2012. The average expenditure for UEBMI insured inpatients was higher than the average for NCMS insured inpatients, although the gap was narrowing. The average length of hospital stay increased every year for all inpatients, but was higher for UEBMI inpatients than for NCMS insured inpatients. For both tracer conditions the results were similar to the above findings. CONCLUSIONS: NCMS has improved coverage height for its enrollees and resulted in increased cost of care per inpatient admission at the county hospital. However, wide differences persist between the two insurance systems in coverage height. Both systems are associated with increasing lengths of stay and rising cost per inpatient admission. We found that around 30% of inpatients were not covered by any of the two public health insurance systems, which calls for further studies.

Advances in Organoid Culture Research.

Organoids are powerful systems to facilitate the study of individuals' disorders and personalized treatments because they mimic the structural and functional characteristics of organs. However, the full potential of organoids in research has remained unrealized and the clinical applications have been limited. One of the reasons is organoids are most efficient grown in reconstituted extracellular matrix hydrogels from mouse-derived, whose poorly defined, batch-to-batch variability and immunogenicity. Another reason is that organoids lack host conditions. As a component of the tumor microenvironment, microbiota and metabolites can regulate the development and treatment in several human malignancies. Here, we introduce several engineering matrix materials and review recent advances in the coculture of organoids with microbiota and their metabolites. Finally, we discuss current trends and future possibilities to build more complex cocultures.

Utility of Large Diameter Visible Trephine in Percutaneous Endoscopic Lumbar Interbody Fusion: A Technical Report.

PURPOSE: In this study, a large diameter visible trephine was designed and used in percutaneous endoscopic lumbar interbody fusion to increase endoscopic bone decompression efficiency. Large diameter visible trephine-related technical notes and preliminary clinical experience are described. METHODS: A large diameter visible trephine was designed with normal diameter visible trephine as template. A total of 38 patients with lumbar degenerative diseases who underwent single-level percutaneous endoscopic lumbar interbody fusion with large or normal diameter visible trephine were included into a retrospective study. Operation time, bone decompression time, blood loss, intraoperative fluoroscopy, bone decompression fluoroscopy, and dura or nerve injury cases were recorded and analyzed statistically. Visual Analog Scale (VAS) scores and Oswestry Disability Index (ODI) were used to analyze the clinical outcomes of the 2 groups. RESULTS: The baseline data of the 2 groups were statistically similar. There was no significant difference in postoperative VAS and ODI scores between the 2 groups. Operation time and bone decompression time of large diameter visible trephine group were significantly shorter than that of normal diameter visible trephine group (P < 0.05). Intraoperative fluoroscopy times and bone decompression fluoroscopy times of large diameter visible trephine group were significantly more than that of normal diameter visible trephine group (P < 0.05). Blood loss of the 2 groups were not statistically different. There were no dura or nerve injury cases in the 2 groups. CONCLUSIONS: For percutaneous endoscopic lumbar interbody fusion, the large diameter visible trephine is a safe and efficient endoscopic bone decompression tool under fluoroscopic guidance.

Fluorofenidone attenuates tubulointerstitial fibrosis by inhibiting TGF-ß(1)-induced fibroblast activation.

BACKGROUND: Novel therapeutic agents are urgently needed to combat renal fibrosis. The purpose of this study was to assess, using complete unilateral ureteral obstruction (UUO) in rats, whether fluorofenidone (AKF-PD) [1-(3-fluorophenyl)-5-methyl-2-(1H)-pyridone] inhibits renal fibrosis, and to determine whether it exerts its inhibitory function on renal fibroblast activation. METHODS: Sprague-Dawley rats were randomly divided into 3 groups: sham operation, UUO and UUO/AKF-PD (500 mg/kg/day). Renal function, tubulointerstitium damage index score, extracellular matrix (ECM) deposition, and the expressions of TGF-ß(1), collagen III, α-SMA, p-Smad2, p-Smad3, p-ERK1/2, p-JNK and p-p38 were measured. In addition, the expressions of α-SMA, fibronectin, CTGF, p-Smad2/3, p-ERK1/2, p-p38 and p-JNK were measured in TGF-ß(1)-stimulated normal rat renal fibroblasts (NRK-49F). RESULTS: AKF-PD treatment significantly attenuated tubulointerstitium damage, ECM deposition, the expressions of TGF-ß(1), collagen III, α-SMA, p-ERK1/2, p-p38 and p-JNK in vivo. In vitro, AKF-PD dose-dependently inhibited expressions of α-SMA, fibronectin and CTGF. Furthermore, AKF-PD did not inhibit Smad2/3 phosphorylation or nuclear accumulation, but rather attenuated ERK, p38 and JNK activation. CONCLUSION: AKF-PD treatment inhibits the progression of renal interstitial fibrosis in obstructed kidneys; this is potentially achieved by suppressing fibroblast activation. Therefore, AKF-PD is a special candidate for the treatment of renal fibrosis.

Fluorofenidone suppresses epithelial-mesenchymal transition and the expression of connective tissue growth factor via inhibiting TGF-beta/Smads signaling in human proximal tubular epithelial cells.

OBJECTIVES: The present study was designed to investigate the potential effects and mechanism of fluorofenidone (AKF-PD) on transforming growth factor beta1 (TGF-beta1)-induced tubular epithelial-mesenchymal transition (EMT) and the expression of connective tissue growth factor (CTGF) in human proximal tubular epithelial cells. METHODS: HK-2 cells were pretreated with AKF-PD, pirfenidone (PFD), Losartan, and SB431542 (an inhibitor of TGF-beta type I receptor). The pretreated HK-2 cells were subsequently co-treated with TGF-beta1 (5 ng/ml). The morphological changes of HK-2 cells were observed under an inverted microscope. Expression of alpha-SMA was detected by Western blot and immunofluorescence. The protein expression of ZO-1, fibronectin, CTGF, phosphorylated Smad2 (p-Smad2) and phosphorylated Smad3 (p-Smad3) were evaluated by Western blot. RESULTS: Through down-regulation of p-Smad2 and p-Smad3 proteins, AKF-PD significantly inhibited protein expression of alpha-SMA, fibronectin, and CTGF. Meanwhile, the depressed ZO-1 expression and morphological changes induced by TGF-beta1 were attenuated by AKF-PD. CONCLUSION: AKF-PD acts as an anti-fibrotic agent through blocking TGF-beta/Smads signaling and consequently inhibits TGF-beta1-induced EMT and CTGF expression in human proximal tubular epithelial cells.

Granulocytes Acquire Antiapoptosis Activity and Promote Tumor Growth during Tumor Progress.

Granulocytes play important roles in cancer, and their apoptotic status is often changed by the influence of tumor environment. However, the changes and the function on granulocyte apoptosis in cancer are unclear. In this study, we used tumor-bearing mouse model and tumor patients to analyzed the apoptosis of granulocytes in different tissues by flow analysis and TUNEL fluorescence staining, and found that the percentage of apoptosis cells in granulocytes was significantly decreased in late-stage tumor-bearing mouse and patients. The in vitro co-culture experiment showed that these antiapoptotic granulocytes could significantly inhibit T cell proliferation, and RNA-seq proved that there was obvious difference on the transcriptome between these cells and control cells, particularly immune-related genes. What is important, adoptive transfer of these antiapoptotic granulocytes promoted tumor progress in mouse model. Conclusively, we found that granulocytes in late-stage tumor could delay the process of apoptosis, inhibit T cell proliferation, and acquire pro-tumor activity, which provides a new therapeutic target for tumor immunity.

Compound C attenuates NLRP3 inflammasome despite AMPK knockdown in LPS plus palmitate-induced THP-1 cells.

NLRP3 inflammasome is a key contributor to obesity-related insulin resistance and type 2 diabetes (T2D). Adenosine monophosphate-activated protein kinase (AMPK) is a principle intracellular energy sensor exerting protective effect against T2D. Strikingly, compound C, an inhibitor of AMPK, considerably inhibited the secretion of IL-1ß when THP-1 cells were stimulated with LPS plus palmitic acid (PA). The underlying mechanism was examined with respect to the effect of compound C on NLRP3 inflammasome, a multiprotein complex which controls the processing and production of IL-1ß. Interestingly, compound C significantly attenuated the activation of NLRP3 inflammasome. This phenomenon was reproduced in AMPK siRNA-transfected THP-1 cells, indicating that compound C exerts this function despite AMPK knockdown. Also, it significantly suppresses the mitochondria-generated reactive oxygen species (ROS) required for NLRP3 inflammasome activation. In conclusion, compound C was shown to significantly attenuate the NLRP3 inflammasome despite AMPK knockdown, rendering it as the novel target of compound C. Potentially, compound C attenuates NLRP3 inflammasome through the suppression of mitochondrial ROS production. These findings offer initial evidence into compound C as a novel pharmacological agent with significant therapeutic potential in NLRP3 inflammasome-related disorders, including obesity, insulin resistance, and T2D. Thus, further studies are essential to identify the effect of compound C on these diseases in vitro.

MicroRNA-139-5p upregulation is associated with diabetic endothelial cell dysfunction by targeting c-jun.

Dysfunction of endothelial cells (ECs) and their progenitor cells is an important feature of diabetic vascular disease. MicroRNA (miR)-139-5p is involved in inhibiting the metastasis and progression of diverse malignancies. However, the role of miR-139-5p in ECs still remains unclarified. Here we demonstrated that miR-139-5p expression was elevated in endothelial colony-forming cells (ECFCs) isolated from patients with diabetes, ECs derived from the aorta of diabetic rodents, and human umbilical vein endothelial cells (HUVECs) cultured in high glucose media. MiR-139-5p mimics inhibited tube formation, migration, proliferation, and down-regulated expression of c-jun, vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF)-B, in ECFCs and HUVECs, respectively; moreover, miR-139-5p inhibitors reversed the tendency. Further, gain- and-loss function experiments and ChIP assay indicated that miR-139-5p regulate functions of ECFCs by targeting c-jun-VEGF/PDGF-B pathway. In vivo experiments (Matrigel plug assay and hindlimb ischemia model) showed that miR-139-5p downregulation further promoted ECFC-mediated angiogenesis and blood perfusion. In conclusion, diabetes-mediated high miR-139-5p expression inhibits the c-jun-VEGF/PDGF-B pathway, thus decreasing ECFCs migration, tube formation and proliferation, which subsequently reduces ECs survival. Therefore, miR-139-5p might be an important therapeutic target in the treatment of diabetic vasculopathy in the future.

Responses of seed germination and shoot metabolic profiles of maize (Zea mays L.) to Y2O3 nanoparticle stress.

The potential risks of rare-earth nanoparticles (RENPs) to plants in the environment are attracting increasing attention due to their wide-spread application. In this regard, little is known about the effects of Y2O3 NPs as an important member of RENPs on crop plants. Seed germination is vulnerable to environmental stress, which determines the growth and yield of crops. Here, maize seeds were exposed to a Y2O3 NP suspension (0-500 mg L-1) in the dark for 6 days. It was found that the Y2O3 NPs had no significant effect on the germination rates (>93%) in all treatments, but they could reduce seed vitality, delay germination, and inhibit seedling growth in a dose-dependent manner. Further, the inhibition effect of Y2O3 NPs on root elongation was much stronger than that on shoot elongation. Meanwhile, the activities of peroxidase (POD) and catalase (CAT) in shoots were enhanced with the increase in the Y2O3 NP concentration. A high-concentration (≥300 mg L-1) of Y2O3 NPs induced a significant increase in the malondialdehyde (MDA) level in shoots compared to the control, indicating that the membrane lipid peroxidation and permeability were enhanced. 1H NMR-based analysis showed that the polar metabolic profiles were altered significantly after treatment with 0, 10, and 500 mg L-1 of Y2O3 NPs, but there was no marked alteration observed for the non-polar metabolic profiles. The polar metabolites (e.g., sugars, amino acids, and most organic acids) showed a dose-dependent increase to Y2O3 NP stress, indicating that the metabolic pathways of carbohydrate metabolism, the tricarboxylic acid cycle (TCA), and amino acid synthesis were disturbed. There were significantly positive correlations found among the metabolites related with the antioxidant response and osmotic adjustment. The simultaneous accumulation of these metabolites possibly indicated the adaptation of the seedlings to stress at the cost of retarding glycolysis, TCA, and protein synthesis. The retarded effects finally inhibited the apparent growth of the seedlings. These findings reveal the phytotoxicity of Y2O3 NPs and provide physiological and biochemical and molecular-scale perspectives on the response of seedlings to stress.

Erratum to "Mesenchymal Stem Cells Coated by the Extracellular Matrix Promote Wound Healing in Diabetic Rats".

[This corrects the article DOI: 10.1155/2019/9564869.].

Profiling of differentially expressed genes in adipose tissues of multiple symmetric lipomatosis.

Multiple symmetric lipomatosis (MSL) is a rare disorder characterized by aberrant multiple and symmetric subcutaneous adipose tissue accumulation in the face, neck, shoulders, back, chest and abdomen, severely affecting the quality of life of patients. At present, precise MSL etiology and pathogenesis remain to be elucidated. The present study first utilized a digital gene expression technique with a next­generation sequencing platform to profile differentially expressed genes in three cases of MSL vs. normal control tissue. cDNA libraries from these tissue specimens were constructed and DNA sequenced for identification of differentially expressed genes, which underwent bioinformatic analysis using the Gene Ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) and protein­protein interaction (PPI) network analyses. As a result, a total of 859 differentially expressed genes were identified, including 308 upregulated genes (C19orf80, Apelin, C21orf33, FAM166B and HSD11B2 were mostly upregulated 6.984­, 4.670­, 4.412­, 3.693­ and 3.561­fold, respectively) and 551 downregulated genes [FosB proto­oncogene, AP­1 transcription factor subunit (FOSB), selectin (SEL) E, RAR related orphan receptor (ROR) B, salt inducible kinase (SIK)1 and epidermal growth factor­like protein (EGFL)6 were mostly downregulated ­9.845, ­8.243, ­8.123, ­7.702 and ­7.664 fold, respectively). The GO functional enrichment analysis demonstrated these differentially expressed genes were predominantly involved in biological processes and cellular components, while the KEGG pathway enrichment analysis demonstrated that ribosome, non­alcoholic fatty liver disease, human T­lymphotropic virus type 1 (HTLV­I) infection and Alzheimer's disease pathways were altered in MSL. The PPI network data demonstrated ubiquitin C (UBC), translocator protein (TSPO), Jun Proto­Oncogene, AP­1 Transcription Factor (JUN) and FOS were among these differentially expressed genes that participated in regulation of adipocyte differentiation, although no previous study has linked them to MSL. In conclusion, the present study profiled differentially expressed genes in MSL and identified gene pathways that may be associated with MSL development and progression.