Polymer-induced adhesion of endothelial cells.

The effects of neutral dextran concentration and molecular mass on the adhesion of endothelial cells (EC) to siliclad-covered glass surfaces were studied using interference reflection microscopy (IRM). Results indicate that close contact of the EC to the glass slides is markedly enhanced in the presence of 500 kDa dextran, with this increase reflected by both the speed of forming close contact as well as the size of the contact area. This increased adhesion is attributed to the reduction in surface concentrations of large polymers and, therefore, to the attractive forces caused by depletion interaction. Our findings suggest that depletion could play an important role in cell-cell or cell-surface interactions via accelerating and enhancing close contacts. This interaction should thus be considered in vivo and in vitro for specific potential applications, such as cell culture and cell adhesion to biomimetic surfaces. It should therefore be of particular interest in a wide range of biomedical applications.

Auricular Reconstruction in Adult Patients With Unprepared Congenital Microtia: A Single Institution's Experience.

METHODS: From January 2015 to January 2021, auricular reconstruction was performed in 38 adult patients (39 ears) of congenital microtia based on autologous costal cartilage. The whole procedure was divided into 2 stages: stage I, the individualized framework carved with autologous costal cartilage was inserted into subcutaneous pocket in the mastoid region; then, the earlobe was transposed backward; and stage II, ear elevation, harvesting the retroauricular fascial flap to cover the support scaffold and closing the defect with free skin graft, was performed. RESULTS: All patients successfully underwent ear reconstruction. The follow-up time ranged from 3 months to 3 years. Infection occurred in 1 patient. The ear frameworks were partially broken at the helix in 4 cases. Retroauricular graft skin survival was poor in 1 patient. Retroauricular hypertrophic scars occurred in 2 cases. Bad projection of the reconstructed ear occurred in 1 case. Totally 38 patients were satisfied with the results. CONCLUSIONS: According to the physiological characteristics of the costal cartilage and skin soft tissues of adult patients, improvements are made to details based on the Nagata's method, so that the adult patients with microtia can obtain satisfactory surgical results.

A novel study for joint toxicity of typical aromatic compounds in coal pyrolysis wastewater by Tetrahymena thermophile.

The coal pyrolysis wastewater (CPW) contributed to aquatic environment contamination with amount of aromatic pollutants, and the research on joint toxicity of the mixture of aromatic compounds was vital for environmental protection. By using Tetrahymena thermophile as non-target organism, the joint toxicity of typical nonpolar narcotics and polar narcotics in CPW was investigated. The results demonstrated that the nonpolar narcotics exerted chronic and reversible toxicity by hydrophobicity-based membrane perturbation, while polar narcotics performed acute toxicity by irreversible damage of cells. As the most hydrophobic nonpolar narcotics, indole and naphthalene caused the highest joint toxicity in 24 h with the lowest EC50mix (24.93 mg/L). For phenolic compounds, the combination of p-cresol and p-nitrophenol also showed the top toxicity (EC50mix = 10.9 mg/L) with relation to high hydrophobicity, and the joint toxicity was obviously stronger and more acute than that of nonpolar narcotics. Furthermore, by studying the joint toxicity of nonpolar narcotics and polar narcotics, the hydrophobicity-based membrane perturbation was the first step of toxicity effects, and afterwards the acute toxicity induced by electrophilic polar substituents of phenols dominated joint toxicity afterwards. This toxicity investigation was critical for understanding universal and specific effects of CPW to aquatic organisms.

Topovectorial mechanisms control the juxtamembrane proteolytic processing of Nrf1 to remove its N-terminal polypeptides during maturation of the CNC-bZIP factor.

The topobiological behaviour of Nrf1 dictates its post-translational modification and its ability to transactivate target genes. Here, we have elucidated that topovectorial mechanisms control the juxtamembrane processing of Nrf1 on the cyto/nucleoplasmic side of endoplasmic reticulum (ER), whereupon it is cleaved and degraded to remove various lengths of its N-terminal domain (NTD, also refolded into a UBL module) and acidic domain-1 (AD1) to yield multiple isoforms. Notably, an N-terminal ~12.5-kDa polypeptide of Nrf1 arises from selective cleavage at an NHB2-adjoining region within NTD, whilst other longer UBL-containing isoforms may arise from proteolytic processing of the protein within AD1 around PEST1 and Neh2L degrons. The susceptibility of Nrf1 to proteolysis is determined by dynamic repositioning of potential UBL-adjacent degrons and cleavage sites from the ER lumen through p97-driven retrotranslocation and -independent pathways into the cyto/nucleoplasm. These repositioned degrons and cleavage sites within NTD and AD1 of Nrf1 are coming into their bona fide functionality, thereby enabling it to be selectively processed by cytosolic DDI-1/2 proteases and also partiality degraded via 26S proteasomes. The resultant proteolytic processing of Nrf1 gives rise to a mature ~85-kDa CNC-bZIP transcription factor, which regulates transcriptional expression of cognate target genes. Furthermore, putative ubiquitination of Nrf1 is not a prerequisite necessary for involvement of p97 in the client processing. Overall, the regulated juxtamembrane proteolysis (RJP) of Nrf1, though occurring in close proximity to the ER, is distinctive from the mechanism that regulates the intramembrane proteolytic (RIP) processing of ATF6 and SREBP1.

Mechanisms controlling the multistage post-translational processing of endogenous Nrf1α/TCF11 proteins to yield distinct isoforms within the coupled positive and negative feedback circuits.

To gain a better understanding of the multistep processing of Nrf1 to yield various isoforms with confused molecular masses, we herein establish a generally acceptable criterion required for identification of its endogenous full-length proteins and derivative isoforms expressed differentially in distinct experimental cell lines. Further work has been focused on the molecular mechanisms that dictate the successive post-translational modifications (i.e. glycosylation by OST, deglycosylation by NGLY, and ubiquitination by Hrd1) of this CNC-bZIP protein and its proteolytic processing to give rise to multiple proteoforms. Several lines of experimental evidence have demonstrated that the nascent Nrf1α/TCF11 polypeptide (non-glycosylated) is transiently translocated into the endoplasmic reticulum (ER), in which it becomes an inactive glycoprotein-A, and is folded in a proper topology within and around membranes. Thereafter, dynamic repositioning of the ER-resident domains in Nrf1 glycoprotein is driven by p97-fueled retrotranslocation into extra-ER compartments. Therein, Nrf1 glycoprotein is allowed for deglycosylation digestion by glycosidases into a deglycoprotein-B and its progressive proteolytic processing by cytosolic DDI-1/2 and proteasomes so as to generate N-terminally-truncated protein-C/D. This processing is accompanied by removal of a major N-terminal ~12.5-kDa polypeptide from Nrf1α. Interestingly, our present study has further unraveled that there exist coupled positive and negative feedback circuits between Nrf1 and cognate target genes, including those encoding its regulators p97, Hrd1, DDI-1 and proteasomes. These key players are differentially or even oppositely involved in diverse cellular signaling responses to distinct extents of ER-derived proteotoxic and oxidative stresses induced by different concentrations of proteasomal inhibitors.

Modified 2-Stage Method for Auricular Reconstruction.

BACKGROUND: Auricular reconstruction is one of the most challenging procedures in the field of plastic surgery. The aims of this study were to apply the modified 2-stage method to perform auricular reconstruction and to summarize the clinical experience in the past 10 years. METHODS: Auricular reconstruction was performed in 243 patients (total 254 ears) of congenital microtia using autologous costal cartilage. The whole procedure is divided into 2 stages. Stage I: the individualized framework fabricated with autologous costal cartilage is inserted into subcutaneous pocket in the mastoid region, and then the earlobe was transposed backward to connect with the lower part of the framework. The second-stage surgery mainly includes the following main contents: ear elevation, fixing the bracket behind the reconstructed ear framework, harvesting the retroauricular fascial flap to cover the bracket, and closing the defect with free skin grafts. RESULTS: A total of 243 patients (254 ears) of congenital microtia underwent ear reconstruction. The follow-up time ranged from 6 months to 4 years; 220 patients were satisfied with the results. Surgery-related complications such as infection, partial skin graft necrosis, flap necrosis, bad projection of the constructed auricle, and extrusion of cartilage occurred in 24 cases, and hypertrophic scars occurred in 16 patients. CONCLUSIONS: This modified 2-stage method for auricle reconstruction can receive acceptable results and fewer complications; furthermore, it is relatively simple and easy to master. The 10-year experience validates that this modified method is an ideal method in auricular reconstruction.

Nach Is a Novel Subgroup at an Early Evolutionary Stage of the CNC-bZIP Subfamily Transcription Factors from the Marine Bacteria to Humans.

Normal growth and development, as well as adaptive responses to various intracellular and environmental stresses, are tightly controlled by transcriptional networks. The evolutionarily conserved genomic sequences across species highlights the architecture of such certain regulatory elements. Among them, one of the most conserved transcription factors is the basic-region leucine zipper (bZIP) family. Herein, we have performed phylogenetic analysis of these bZIP proteins and found, to our surprise, that there exist a few homologous proteins of the family members Jun, Fos, ATF2, BATF, C/EBP and CNC (cap'n'collar) in either viruses or bacteria, albeit expansion and diversification of this bZIP superfamily have occurred in vertebrates from metazoan. Interestingly, a specific group of bZIP proteins is identified, designated Nach (Nrf and CNC homology), because of their strong conservation with all the known CNC and NF-E2 p45 subunit-related factors Nrf1 and Nrf2. Further experimental evidence has also been provided, revealing that Nach1 and Nach2 from the marine bacteria exert distinctive functions, when compared with human Nrf1 and Nrf2, in the transcriptional regulation of antioxidant response element (ARE)-battery genes. Collectively, further insights into these Nach/CNC-bZIP subfamily transcription factors provide a novel better understanding of distinct biological functions of these factors expressed in distinct species from the marine bacteria to humans.

MicroRNA 26a prolongs skin allograft survival and promotes regulatory T cell expansion in mice.

MicroRNA 26a (Mir-26a) has been reported to play functions in cellular differentiation, cell growth, cell apoptosis, and metastasis. However, the role of Mir-26a in transplant rejection has never been investigated. Full-thickness skin grafts 1-2 cm in diameter were obtained from the tail-skin CBA/J donor mice and transplanted onto the back of wild-type C57Bl/6 recipient mice. Vectors encoding pre-Mir-26a (LV-26a) and an empty lentiviral vector (LV-Con) delivered approximately 2 × 10(7) transforming units of recombinant lentivirus were injected to mice once through the tail vein. Mir-26a overexpression results in prolonged skin allograft survival (MST = 9.5 days in LV-Con mice; MST = 22 days in LV-26a mice. P < 0.01) and promoted regulatory T cells (Tregs) expansion. The prolonged skin allograft survival induced by LV-26a was abrogated by depletion of Tregs with anti-CD25 antibodies. Mir-26a significantly promoted IL-10 expression and suppressed the expression of IL-6, IL-17, and IFN-γ. Furthermore, IL-6 overexpression led to complete suppression of the Mir-26a-induced upregulation of Foxp3. The prolonged allograft survival induced by LV-Mir-26a was also completely abrogated by IL-6 overexpression. In conclusion, Mir-26a prolongs skin allograft survival and promotes Tregs expansion in part through inhibition of IL-6 expression.

NFE2L1/Nrf1 serves as a potential therapeutical target for neurodegenerative diseases.

The failure of the proper protein turnover in the nervous system is mainly linked to a variety of neurodegenerative disorders. Therefore, a better understanding of key protein degradation through the ubiquitin-proteasome system is critical for effective prevention and treatment of those disorders. The proteasome expression is tightly regulated by a CNC (cap'n'collar) family of transcription factors, amongst which the nuclear factor-erythroid 2-like bZIP factor 1 (NFE2L1, also known as Nrf1, with its long isoform TCF11 and short isoform LCR-F1) has been identified as an indispensable regulator of the transcriptional expression of the ubiquitin-proteasome system. However, much less is known about how the pivotal role of NFE2L1/Nrf1, as compared to its homologous NFE2L2 (also called Nrf2), is translated to its physiological and pathophysiological functions in the nervous system insomuch as to yield its proper cytoprotective effects against neurodegenerative diseases. The potential of NFE2L1 to fulfill its unique neuronal function to serve as a novel therapeutic target for neurodegenerative diseases is explored by evaluating the hitherto established preclinical and clinical studies of Alzheimer's and Parkinson's diseases. In this review, we have also showcased a group of currently available activators of NFE2L1, along with an additional putative requirement of this CNC-bZIP factor for healthy longevity based on the experimental evidence obtained from its orthologous SKN1-A in Caenorhabditis elegans.

Loss of Nrf1 rather than Nrf2 leads to inflammatory accumulation of lipids and reactive oxygen species in human hepatoma cells, which is alleviated by 2-bromopalmitate.

Since Nrf1 and Nrf2 are essential for regulating the lipid metabolism pathways, their dysregulation has thus been shown to be critically involved in the non-controllable inflammatory transformation into cancer. Herein, we have explored the molecular mechanisms underlying their distinct regulation of lipid metabolism, by comparatively analyzing the changes in those lipid metabolism-related genes in Nrf1α-/- and/or Nrf2-/- cell lines relative to wild-type controls. The results revealed that loss of Nrf1α leads to lipid metabolism disorders. That is, its lipid synthesis pathway was up-regulated by the JNK-Nrf2-AP1 signaling, while its lipid decomposition pathway was down-regulated by the nuclear receptor PPAR-PGC1 signaling, thereby resulting in severe accumulation of lipids as deposited in lipid droplets. By contrast, knockout of Nrf2 gave rise to decreases in lipid synthesis and uptake capacity. These demonstrate that Nrf1 and Nrf2 contribute to significant differences in the cellular lipid metabolism profiles and relevant pathological responses. Further experimental evidence unraveled that lipid deposition in Nrf1α-/- cells resulted from CD36 up-regulation by activating the PI3K-AKT-mTOR pathway, leading to abnormal activation of the inflammatory response. This was also accompanied by a series of adverse consequences, e.g., accumulation of reactive oxygen species (ROS) in Nrf1α-/- cells. Interestingly, treatment of Nrf1α-/- cells with 2-bromopalmitate (2BP) enabled the yield of lipid droplets to be strikingly alleviated, as accompanied by substantial abolishment of CD36 and critical inflammatory cytokines. Such Nrf1α-/- -led inflammatory accumulation of lipids, as well as ROS, was significantly ameliorated by 2BP. Overall, this study provides a potential strategy for cancer prevention and treatment by precision targeting of Nrf1, Nrf2 alone or both.

Complete genome sequence and anti-obesity potential of Lactiplantibacillus plantarum HOM2217 in 3T3-L1 cells and high-fat diet-fed rats.

The global prevalence of obesity is rising year by year, which has become a public health problem worldwide. Many animal and clinical studies have shown that Lactiplantibacillus plantarum is considered an ideal probiotic and potential supplement for the treatment of obesity. In this study, we aimed to complete the genome sequence of L. plantarum HOM2217, which was isolated from human milk, and study its physiological characteristics and anti-obesity effects in 3T3-L1 cells and rats fed a high-fat diet (HFD) to determine its potential as a starter for functional food products. Whole-genome analysis demonstrated that HOM2217 contained a single circular chromosome of 3,267,529 bp with a GC content of 44.5% and one plasmid (62,350 bp) with a GC content of 38.5%. Compared to the reference strains, HOM2217 demonstrated superior tolerance to gastrointestinal conditions, higher adhesion to intestinal epithelial cell lines, potent antimicrobial activity against Enterobacter cloacae ATCC 13047, and effective cholesterol removal ability in vitro. Treatment with heat-killed HOM2217 significantly reduced lipid accumulation and intracellular triglyceride production in 3T3-L1 adipocytes. Daily treatment of HFD-fed rats with HOM2217 for 7 weeks decreased body weight, body weight gain, and body fat without changes in food intake. HOM2217 also significantly increased the serum high-density lipoprotein cholesterol (HDL-C) level, decreased the serum tumor necrosis factor (TNF-α) and increased short-chain fatty acid (SCFA) (formic acid, acetic acid, and butyric acid) levels in the cecum. Thus, HOM2217 could potentially prevent obesity in rats by inhibiting inflammatory responses and regulating lipid metabolism and SCFAs expression. Therefore, HOM2217 has potential as an alternative treatment for obesity.

A novel crosstalk between Nrf2 and Smad2/3 bridged by two nuanced Keap1 isoforms with their divergent effects on these distinct family transcription factors.

The Keap1-Nrf2 signalling to transcriptionally regulate antioxidant response element (ARE)-driven target genes has been accepted as key redox-sensitive pathway governing a vast variety of cellular stresses during healthy survival and disease development. Herein, we identified two nuanced isoforms α and ß of Keap1 in HepG2 cells, arising from its first and another in-frame translation starting codons, respectively. In identifying those differential expression genes monitored by Keap1α and/or Keap1ß, an unusual interaction of Keap1 with Smad2/3 was discovered by parsing transcriptome sequencing, Keap1-interacting protein profiling and relevant immunoprecipitation data. Further examination validated that Smad2/3 enable physical interaction with Keap1, as well as its isoforms α and ß, by both EDGETSD and DLG motifs in the linker regions between their MH1 and MH2 domains, such that the stability of Smad2/3 and transcriptional activity are enhanced with their prolonged half-lives and relevant signalling responses from the cytoplasmic to nuclear compartments. The activation of Smad2/3 by Keap1, Keap1α or Keap1ß was much likely contributable to a coordinative or another competitive effect of Nrf2, particularly in distinct Keap1-based cellular responses to its cognate growth factor (i.e. TGF-ß1) or redox stress (e.g. stimulated by tBHQ and DTT). Overall, this discovery presents a novel functional bridge crossing the Keap1-Nrf2 redox signalling and the TGF-ß1-Smad2/3 pathways so as to coordinately regulate the healthy growth and development.

Nrf1 is not a direct target gene of SREBP1, albeit both are integrated into the rapamycin-responsive regulatory network in human hepatoma cells.

The essential role of protein degradation by ubiquitin-proteasome system is exerted primarily for maintaining cellular protein homeostasis. The transcriptional activation of proteasomal genes by mTORC1 signaling depends on Nrf1, but whether this process is directly via SREBP1 remains elusive. In this study, our experiment evidence revealed that Nrf1 is not a direct target of SREBP1, although both are involved in the rapamycin-responsive regulatory networks. Closely scrutinizing two distinct transcriptomic datasets unraveled no significant changes in transcriptional expression of Nrf1 and almost all proteasomal subunits in either siSREBP2-silencing cells or SREBP1-∕-MEFs, when compared to equivalent controls. However, distinct upstream signaling to Nrf1 dislocation by p97 and its processing by DDI1/2, along with downstream proteasomal expression, may be monitored by mTOR signaling, to various certain extents, depending on distinct experimental settings in different types of cells. Our further evidence has been obtained from DDI1-∕-(DDI2insC) cells, demonstrating that putative effects of mTOR on the rapamycin-responsive signaling to Nrf1 and proteasomes may also be executed partially through a DDI1/2-independent mechanism, albeit the detailed regulatory events remain to be determined.

Improving the aging aroma profiles of Italian Riesling and Petit Verdot Wines: Impact of spontaneous and inoculated fermentation processes.

The study employed gas chromatography-ion mobility spectrometry to differentiate between wines undergoing spontaneous fermentation and inoculated fermentation, with aging periods of 3, 9, and 15 months. The results indicate that throughout the three aging periods, there was a notable increase in the levels of ethyl hexanoate (Monomer, M), 2-methyl butanal, ethyl octanoate (M), ethyl octanoate (Dimer, D), propyl acetate, and 3-methylbutanal in the spontaneous Italian Riesling wine (RS). Furthermore, the compounds isoamyl acetate (M), ethyl formate (D), 4-methyl-2-pentanone (M), and ethyl formate (M) demonstrated the highest concentrations at 15 months in RS, accordingly, these compounds displayed a consistent upward trend throughout the aging period. A total of 14 volatile compounds exhibited an upward trend from 3 to 15 months in the spontaneous fermentation of Petit Verdot Wine (VS). Subsequently, these compounds attained their maximum levels. Spontaneous fermentation effectively enhances the aromatic characteristics of wines, consequently improving their capacity for aging.

High-Speed Dicing of SiC Wafers with 0.048 mm Diamond Blades via Rolling-Slitting.

In this study, an innovative fabrication method called rolling-slitting forming, which forms ultra-thin diamond blades, was presented for the first time. Furthermore, the feasibility of the rolling-slitting forming method when applied to silicon carbide wafer dicing blades was investigated; moreover, the cold-pressing blade samples were manufactured through the conventional process under the same sintering conditions to compare and analyze the manufacturing efficiency, organization and performance. The results show that the new method achieves high-precision and low-thickness dicing blades through continuous production without molds-with the thinnest blades being 0.048 mm thick. Furthermore, the rolling-slitting blade has a unique multiporous heat-conductive matrix structure and in-situ generated amorphous pyrolytic carbon, which can reduce the dicing resistance and contribute to a better cutting quality. In addition, the effects of the dicing parameters on SiC were investigated by using indications of spindle current, dicing chipping size and kerf width during the high dicing process. For a dicing depth of 0.2 mm, the ideal performance of dicing SiC with an ultra-thin blade was achieved at a spindle speed of 22,000 rpm and a feed rate of 5 mm/s. This research provides a new idea for the manufacturing of dicing blades, which can satisfy the demand for ultra-narrow dicing streets of high integration of ICs.

Nrf1 is an indispensable redox-determining factor for mitochondrial homeostasis by integrating multi-hierarchical regulatory networks.

To defend against a vast variety of challenges in oxygenated environments, all life forms have evolutionally established a set of antioxidants, detoxification, and cytoprotective systems during natural selection and adaptive survival, to maintain cell redox homeostasis and organ integrity in the healthy development and growth. Such antioxidant defense systems are predominantly regulated by two key transcription factors Nrf1 and Nrf2, but the underlying mechanism(s) for their coordinated redox control remains elusive. Here, we found that loss of full-length Nrf1 led to a dramatic increase in reactive oxygen species (ROS) and oxidative damages in Nrf1α-∕- cells, and this increase was not eliminated by drastic elevation of Nrf2, even though the antioxidant systems were also substantially enhanced by hyperactive Nrf2. Further studies revealed that the increased ROS production in Nrf1α-∕- resulted from a striking impairment in the mitochondrial oxidative respiratory chain and its gene expression regulated by nuclear respiratory factors, called αPalNRF1 and GABPNRF2. In addition to the antioxidant capacity of cells, glycolysis was greatly augmented by aberrantly-elevated Nrf2, so to partially relieve the cellular energy demands, but aggravate its mitochondrial stress. The generation of ROS was also differentially regulated by Nrf1 and Nrf2 through miR-195 and/or mIR-497-mediated UCP2 pathway. Consequently, the epithelial-mesenchymal transformation (EMT) of Nrf1α-∕- cells was activated by putative ROS-stimulated signaling via MAPK, HIF1α, NF-ƙB, PI3K and AKT, all players involved in cancer development and progression. Taken together, it is inferable that Nrf1 acts as a potent integrator of redox regulation by multi-hierarchical networks.

A Review of Spatter in Laser Powder Bed Fusion Additive Manufacturing: In Situ Detection, Generation, Effects, and Countermeasures.

Spatter is an inherent, unpreventable, and undesired phenomenon in laser powder bed fusion (L-PBF) additive manufacturing. Spatter behavior has an intrinsic correlation with the forming quality in L-PBF because it leads to metallurgical defects and the degradation of mechanical properties. This impact becomes more severe in the fabrication of large-sized parts during the multi-laser L-PBF process. Therefore, investigations of spatter generation and countermeasures have become more urgent. Although much research has provided insights into the melt pool, microstructure, and mechanical property, reviews of spatter in L-PBF are still limited. This work reviews the literature on the in situ detection, generation, effects, and countermeasures of spatter in L-PBF. It is expected to pave the way towards a novel generation of highly efficient and intelligent L-PBF systems.

The protective effect of EGB761 on vessels of denervated gastrocnemius in rats and its mechanism.

This study investigated the protective effect of EGB761 on blood vessels of denervated gastrocnemius of rat and its possible mechanism. Fifteen male adult SD rats were randomly divided into three groups: normal control group (n=3), control group (n=6) and EGB761-treated group (n=6). The rats in the control and EGB761-treated group underwent a neurotomy to bilateral sciatic nerves. Then, they were administered EGB761 [100 mg/(kg·d)] and isovolumic normal saline, respectively by gavage everyday. No treatment was given to the rats in the normal control group. Gastrocnemius was harvested at 1 and 3 week(s) postoperatively in each group. Immunohistochemical method was used to detect the ratio of capillary/fiber (CFR) of denervated gastrocnemius and the expression of VEGF, fetal liver kinase -1(Flk-1) receptor and HSP70 in the vascular wall. The results showed that in the normal control group, VEGF, Flk-1 and HSP70 were expressed in the vessel wall of gastrocnemius, with Flk-1 expressed only in the endothelial cell of vessels. CFR in the EGB761-treated group was significantly higher than that in the control group at 1 week and 3 week(s) after neurotomy. The expression of VEGF and Flk-1 in the vessel wall of both control and EGB761-treated group was much lower than that in the normal control group, and the expression of these proteins in the EGB761-treated group was decreased as compared with that in the control group. The expression of HSP70 in the vessel wall of both control and EGB761-treated groups was enhanced when compared with that in the normal control group, and it was substantially augmented in the EGB761-treated group in comparison to the control group. It was concluded that EGB761 has a protective effect on blood vessels of denervated gastrocnemius, which is related to the increased HSP70 expression but not the expression of VEGF and its receptor Flk-1.

Metagenomic analysis of aromatic ring-cleavage mechanism in nano-Fe3O4@activated coke enhanced bio-system for coal pyrolysis wastewater treatment.

In current study, nano-Fe3O4@activated coke enhanced bio-system (FEBS) under limited-oxygen condition was applied for efficient treatment of aromatic organics in coal pyrolysis wastewater. Metagenomic analyses revealed functional microbiome linkages and mechanism involved in aromatic ring-cleavage. Based on biodegradation efficiency in different reactors, FEBS supplementation conferred the best organic removal (avg. 92.29%). It also showed a remarkable advantage in biodegradability maintenance (>40%) over control reactors. Metagenomics profiling revealed the degradation processes were driven by Fe3O4 redox reactions and microbial biofilm, while the suspended sludge was the principal force for aromatic mineralization. Based on the analysis of functional species and genes, most bacteria cleaved the benzene ring preferably through the aerobic pathways, mediated by catechol 1, 2-dioxygenase, catechol 2, 3-dioxygenase and protocatechuate 3, 4-dioxygenase (66-84%). Ecological network showed that Comamonas testosterone-centered microbiome and Azotobacter linked to the nitrogen (N)-heterocyclic ring-cleavage. Network linkage further demonstrated that Alicycliphilus and Acidovorax were the key tone taxa involved in benzene ring-cleavage. Finally, combined with analysis of degradation products, bacteria degraded N-heterocyclic ring containing organic aromatic compounds (quinoline) mainly through anaerobic processes, whereas cleavage of benzene ring preferred aerobic pathways. The enriched functional species were the primary reason for the enhanced biodegradation in FEBS.

Ecological and functional research into microbiomes for targeted phenolic removal in anoxic carbon-based fluidized bed reactor (CBFBR) treating coal pyrolysis wastewater (CPW).

Powdered activated carbon (PAC), lignite activated coke (LAC) and Fe-C carriers were applied to enhance CBFBRs to degrade targeted phenolics. In start-up stage, PAC and LAC equipped CBFBRs with higher environment adaptability and phenolic degradation capacity for phenol (>96%), p-cresol (>91%) and 3, 5-dimethylphenol (>84%) in comparison to Fe-C carrier. In recovery stage, the superior performance was also identified for CBFBRs in basis of PAC and LAC than Fe-C-based reactor. However, the Fe-C carrier assisted CBFBR with more stable degradation performance under impact loading. By comparing microbiomes, significantly enriched Brachymonas (54.80%-68.81%) in CBFBRs exerted primary role for phenolic degradation, and positively contributed to microbial network. Meanwhile, Geobacter in Fe-C-based reactor induced excellent impact resistance by enhancing interspecific electron transfer among microbes. Furthermore, the investigation on functional genes related to phenolic degradation revealed that anaerobic pathway accounted for demethylation procedure, while aerobic pathways dominated the phenolic ring-cleavage process.