Relationship between Monocytes and Stenosis-Related Autologous Arteriovenous Fistula Dysfunction.

BACKGROUND: Arteriovenous fistula (AVF) is considered to be the best choice of vascular access, but the maturation rate and patency rate of AVF are not satisfactory. Many studies have explored the influencing factors of AVF failure but do not involve the direct relationship between monocyte count and AVF failure. This study aims to explore the relationship between monocyte count and AVF dysfunction related to stenosis. METHODS: From September 2017 to September 2018, basic clinical data and laboratory parameters of patients were collected. All included patients were followed up to September 2019. The stenosis-related AVF failure events that occurred after the patient included in the study and the time of their occurrence were recorded. All patients were divided into 3 groups based on the tertile of monocyte count. Kaplan-Meier method was used to compare the patency rate of AVF in each group. The effects of variables on AVF failure were analyzed. A multivariate Cox regression model with p < 0.05 was included in the univariate Cox regression analysis. RESULTS: A total of 120 patients were included in this study. According to the recorded baseline monocyte count levels, they were divided into 3 groups according to their tertiles, 34 cases in the T1 group (T1 < 0.32 × 109/L), 44 cases in the T2 group (0.32 ≤ T2 < 0.51 × 109/L), and 42 cases in T3 group (T3 ≥0.51 × 109/L). After a median follow-up of 20 months, a total of 31 AVF failure events occurred. Kaplan-Meier survival curves showed that patients with a baseline monocyte count ≥0.51 × 109/L had the lowest patency rate of AVF (log-rank test χ2 = 7.525, p = 0.023). After adjusting to basic clinical data and biochemical indicators, there were statistically significant differences in patency rates of the 3 groups (hazard ratio = 2.774, 95% CI = 1.092-7.043). CONCLUSION: Monocyte count ≥0.51 × 109/L is an independent risk factor for AVF failure, and AVF failure caused by monocytes may be driven by inflammation.

Effects of delayed motherhood on hippocampal gene expression in offspring rats.

While many studies have examined the pregnancy and health-related outcomes of delayed motherhood for women, less is known concerning the potential consequences for their children. This study aims to investigate the effect of delayed motherhood on the hippocampus at the whole genome level. Sprague-Dawley rat females, either at the age of 3 or 12 months, were individually housed with a randomly selected 3-month-old male. The rat whole genome expression chips were used to detect gene expression differences in the hippocampus of newborn rats. The gene expression profile was studied through gene ontology and signal pathway analyses. qRT-PCR was used to determine the mRNA expression of solute carrier family 2 (SLC2A1) and S-phase kinase-associated protein 2 (SKP2). Western blot was used to detect the protein expression of SKP2. Compared to the control group, 1291 differentially expressed genes were detected, including 635 up-regulated genes and 656 down-regulated genes. These differential expressed genes were involved in 110 significant biological process and nine significant signaling pathways, in which the pathway in cancer is the most changed pathway. For SKP2 (up-regulated) and SLC2A1 (up-regulated) genes which were relevant to the pathway in cancer, qRT-PCR results were consistent with gene chip assay results. The upregulation of SKP2 was also demonstrated at protein level. In conclusion, delayed motherhood led to unique patterns of hippocampal gene expression in offspring and the newly identified genes afford a quantitative view of the changes which enable deeper insights into the molecular basis underlying the role of delayed motherhood.

Precisely Constructing Orbital-Coupled Fe─Co Dual-atom Sites for High-Energy-Efficiency Zn-Air/Iodide Hybrid Batteries.

Rechargeable Zn-air batteries (ZABs) are promising for energy storage and conversion. However, the high charging voltage and low energy efficiency hinder their commercialization. Herein, these challenges are addressed by employing precisely constructed multifunctional Fe-Co diatomic site catalysts (FeCo-DACs) and integrating iodide/iodate redox into ZABs to create Zinc-air/iodide hybrid batteries (ZAIHBs) with highly efficient multifunctional catalyst. The strong coupling between the 3d orbitals of Fe and Co weakens the excessively strong binding strength between active sites and intermediates, enhancing the catalytic activities for oxygen reduction/evolution reaction and iodide/iodate redox. Consequently, FeCo-DACs exhibit outstanding bifunctional oxygen catalytic activity with a small potential gap (ΔE = 0.66 V) and outstanding stability. Moreover, an outstanding catalytic performance toward iodide/iodate redox is obtained. Therefore, FeCo-DAC-based ZAIHBs exhibit high energy efficiency of up to 75% at 10 mA cm-2 and excellent cycling stability (72% after 500 h). This research offers critical insights into the rational design of DACs and paves the way for high-energy efficiency energy storage devices.

Photocatalytic degradation of tetracycline hydrochloride by a Fe3O4/g-C3N4/rGO magnetic nanocomposite mechanism: modeling and optimization.

The photocatalytic degradation of antibiotics requires a good separation efficiency of photogenerated electron-hole pairs and a wide visible light absorption range. Current studies have discussed the successful preparation of ferroferric oxide/graphite carbon nitride/reduced graphene oxide (Fe3O4/g-C3N4/rGO). The phase structure and morphology of the Fe3O4/g-C3N4/rGO composites were characterized by XRD, HR-TEM, SEM, and EDS. The obtained composites were used to degrade tetracycline hydrochloride (TCH) to evaluate its photocatalytic activity. The effects of four variables on the degradation of TCH were analyzed by the response surface method and artificial intelligence (gradient regression tree, random forest, artificial neural network, etc.). The results showed that the graphite carbon nitride in the catalyst maintained its original structure and that the photocatalytic activity was significantly improved. The degradation rate of TCH was 86.7% under the optimal conditions (the Fe3O4/g-C3N4/rGO dosage was 0.1 g, pH = 7.0, the initial concentration of TCH was 20 mg/L, and the visible light irradiation time was 60 min). At the same time, the degradation rate of TCH changed little after the material was used five times, which indicates that the stability and recyclability of the Fe3O4/g-C3N4/rGO photocatalyst were excellent. Finally, a possible photocatalytic mechanism of the Fe3O4/g-C3N4/rGO photocatalyst is proposed in this paper.

Graphene-based photocatalytic nanocomposites used to treat pharmaceutical and personal care product wastewater: A review.

Photocatalytic technology has been widely studied by researchers in the field of environmental purification. This technology can not only completely convert organic pollutants into small molecules of CO2 and H2O through redox reactions but also remove metal ions and other inorganic substances from water. This article reviews the research progress of graphene-based photocatalytic nanocomposites in the treatment of wastewater. First, we elucidate the basic principles of photocatalysis, the types of graphene-based nanocomposites, and the role of graphene in photocatalysis (e.g., graphene can accelerate the separation of photon-hole pairs and increase the intensity and range of light absorption). Second, the preparation, characterization, and application of composites in wastewater are introduced. We also discuss the kinetic model of the photocatalytic degradation of pollutants. Finally, the enhancement mechanism of graphene in terms of photocatalysis is not completely clear, and graphene-based photocatalysts with high catalytic efficiency, low cost, and large-scale production have not yet appeared, so there is an urgent need for more extensive and in-depth research.

Cancer-induced bone pain sequentially activates the ERK/MAPK pathway in different cell types in the rat spinal cord.

BACKGROUND: Previous studies have demonstrates that, after nerve injury, extracellular signal-regulated protein kinase (ERK) activation in the spinal cord-initially in neurons, then microglia, and finally astrocytes. In addition, phosphorylation of ERK (p-ERK) contributes to nociceptive responses following inflammation and/or nerve injury. However, the role of spinal cells and the ERK/MAPK pathway in cancer-induced bone pain (CIBP) remains poorly understood. The present study analyzed activation of spinal cells and the ERK/MAPK pathway in a rat model of bone cancer pain. RESULTS: A Sprague Dawley rat model of bone cancer pain was established and the model was evaluated by a series of tests. Moreover, fluorocitrate (reversible glial metabolic inhibitor) and U0126 (a MEK inhibitor) was administered intrathecally. Western blots and double immunofluorescence were used to detect the expression and location of phosphorylation of ERK (p-ERK). Our studies on pain behavior show that the time between day 6 and day 18 is a reasonable period ("time window" as the remaining stages) to investigate bone cancer pain mechanisms and to research analgesic drugs. Double-labeling immunofluorescence revealed that p-ERK was sequentially expressed in neurons, microglia, and astrocytes in the L4-5 superficial spinal cord following inoculation of Walker 256 cells. Phosphorylation of ERK (p-ERK) and the transcription factor cAMP response element-binding protein (p-CREB) increased in the spinal cord of CIBP rats, which was attenuated by intrathecal injection of fluorocitrate or U0126. CONCLUSIONS: The ERK inhibitors could have a useful role in CIBP management, because the same target is expressed in various cells at different times.

Carbon-Based Nanocomposites as Fenton-Like Catalysts in Wastewater Treatment Applications: A Review.

Advanced oxidation (e.g., fenton-like reagent oxidation and ozone oxidation) is a highly important technology that uses strong oxidizing free radicals to degrade organic pollutants and mineralize them. The fenton-like reactions have the characteristics of low cost, simple operation, thorough reaction and no secondary pollution. Fenton-like reagents refer to a strong oxidation system composed of transition metal ions (e.g., Fe3+, Mn2+ and Ag+) and oxidants (hydrogen peroxide, potassium persulfate, sodium persulfate, etc). Graphene and carbon nanotube possess a distinctive mechanical strength, flexibility, electrical and thermal conductivity and a very large specific surface area, which can work as an excellent carrier to disperse the catalyst and prevent its agglomeration. Fullerene can synergize with iron-based materials to promote the reaction of hydroxyl groups with organic pollutants and enhance the catalytic effect. Fenton-like catalysts influence the catalytic behavior by inducing electron transfer under strong interactions with the support. Due to the short lifespan of free radicals, the treatment effect is usually enhanced with the assistance of external conditions (ultraviolet and electric fields) to expand the application of fenton-like catalysts in water treatment. There are mainly light-fenton, electro-fenton and photoelectric-fenton methods. Fenton-like catalysts can be prepared by hydrothermal method, impregnation and coordination-precipitation approaches. The structures and properties of the catalysts are characterized by a variety of techniques, such as high-resolution transmission electron microscopy, high-angle annular dark-field scanning transmission electron microscopy and X-ray absorption near-edge structure spectroscopy. In this paper, we review the mechanisms, preparation methods, characterizations and applications status of fenton-like reagents in industrial wastewater treatment, and summarize the recycling of these catalysts and describe prospects for their future research directions.

[Antioxidant xanthones from Securidaca inappendiculata].

OBJECTIVE: To study the antioxidant constituents from the roots of Securidaca inappendiculata. METHOD: The bioassay-guided isolation of antioxidant constituents was carried out by the column chromatographic techniques. The combination of IR, MS, NMR and 2D-NMR spectroscopics methods was used to identify their structures. RESULT: Two new xanthones, 1, 2, 5-trihydroxy-6, 8-dimethoxy-9H-xanthen-9-one(1), 1, 5-dihydroxy-2, 6, 8-trimethoxy-9H-xanthen-9-one (2), along with seven known ones, 3, 8-dihydroxy-1, 4-dimethoxy-9H-xanthen-9-one(3), 4, 6-dihydroxy-1, 5, 7-trimethoxy-9H-xanthen-9-one(4), 7-hydroxy-1, 2, 3, 8-tetramethoxy-9H-xanthen- 9-one(5), 1, 7-dihydroxy-9H-xanthen-9-one(6), 4-hydroxy-3, 7-dimethoxy-9H-xanthen-9-one(7), 1,7-dimethoxy-9H-xanthen-9-one(8) and aucuparin(9), were isolated from the roots of S. inappendiculata. CONCLUSION: Compounds 1 and 2 were new xanthones, and compound 3 was isolated as a natural product for the first time, and compounds 4 and 6 were isolated for the first time from this genus. The antioxidant activities of all compounds were evaluated by ABTS, FRAP and DPPH assays respectively. Compound 9 showed significant activity by the ABTS and FRAP assays. Compound 1 showed significant activity with IC50 value of 0.31 mg x L(-1) in DPPH assay. Scavenging capacity of all compounds determined by all assays were well correlated between ABTS and FRAP assay (r = 0.9555).

Role of autophagy on bone marrow mesenchymal stem­cell proliferation and differentiation into neurons.

The purpose of the present study was to investigate the role of autophagy on rat bone marrow mesenchymal stem cell (BMSC) proliferation, apoptosis and differentiation into neurons. After treatment with rapamycin, 3-methyladenine (3-MA) or chloroquine, the cell cycle, apoptosis, expression of neuron-specific enolase (NSE) and the mean fluorescence intensity (MFI) of Notch1 in BMSCs were examined by flow cytometry. The expression of microtubule-associated protein 2 (MAP2), Notch1 and Hes1 was investigated by western blot analysis. The results showed that after induction of autophagy using rapamycin, the proliferation of BMSCs was inhibited. Furthermore, the S-phase population was significantly decreased compared to that in the control group (P<0.05). In addition, the percentage of NSE-positive cells and the expression of MAP2 were significantly increased compared to those in the control group (P<0.05). The MFI of Notch1 was markedly upregulated compared to that in the control group (P<0.05). When autophagy was inhibited by 3-MA or chloroquine, the percentage of apoptotic cells and NSE-positive cells as well as the expression of MAP2 were markedly reduced compared to those in the control group (P<0.05). Furthermore, western blot analysis showed that Notch1 and Hes1 were decreased in the rapamycin-treated group, while they were not affected by 3-MA or chloroquine. The present study indicated that induction of autophagy in BMSCs decreased their S-phase population, promoted their differentiation into neurons and promoted the expression of NSE and MAP2. The mechanisms underlying this process may be linked to the regulation of autophagy-induced inhibition of the Notch1 signaling pathway.

[Research of autophagy activity between rat bone marrow mesenchymal stem neural differentiation].

OBJECTIVE: To study the autophagy activity between rat bone marrow stem cells (BMSCs) neural differentiation in order to explore the mechanism involve in this process. METHODS: BMSCs were passed by 3 generation, then was induced with the revulsant 2% (DMSO) + 200 µmol/L (BHA), NSE expression was detected by immunocytochemical stain, the mRNA expression of autophagy associated genes L3B, Beclinl, Atg5, Atg7, Atg10 were detected by RT-PCR, the autophagy protein LC3B was examined by Western blot and flow cytometry analysis. RESULTS: BMSCs were passed by 3 generation, the purity of BMSCs could reach more than 90%, the morphology of cells were like fibroblasts, after the revulsant 2% DMSO + 200 µmol/L BRA induced, cells were extended long neurites, like nerve cells, positive rate of NSE staining was (83±5) %, RT-PCR results showed that the expression of autophagy associated genes LC3B, Beclinl, Atg5, Atg7 Atg0 were rised after BMSCs neural differentiation, Western blot analysis showed that the LC3B-II protein expression was increased after neural differentiation and the MFI of L3B was highten by flow cytometry. CONCLUSION: Autophagy is increased after rat BMSC neural differentiation.

Involvement of CX3CR1 in bone cancer pain through the activation of microglia p38 MAPK pathway in the spinal cord.

Previous studies have demonstrated that fractalkine, a newly discovered chemokine, is implicated in spinal cord neuron-to-microglia activation signaling as well as mediation of neuropathic and inflammatory pain via its sole receptor CX3CR1, which is specifically expressed on microglia. However, whether it is involved in bone cancer pain (BCP) and the underlying mechanisms have not been elucidated. In this study we utilized a Sprague-Dawley rat animal model, and our findings indicated that on day 6, 12, and 18 following bone cancer pain induced by Walker 256 cell inoculation, the expression level of CX3CR1 in the spinal cord gradually increased. Intrathecal injection of a neutralizing antibody against CX3CR1 not only delayed the initiation of mechanical allodynia, but also attenuated established pain sensitization of BCP rats. Furthermore, we demonstrated that blockade of CX3CR1 suppressed the activation of microglia and the expression of p38 mitogen-activated protein kinase (MAPK) in the spinal cord in BCP rats. These results suggest a new mechanism of BCP, in which the microglia CX3CR1/p38 signaling cascade potentially plays an important role in facilitating pain processing in BCP rats.

Tibia tumor-induced cancer pain involves spinal p38 mitogen-activated protein kinase activation via TLR4-dependent mechanisms.

Molecular mechanisms underlying bone cancer pain are poorly understood. Recently, p38 mitogen-activated protein kinase (MAPK) activation was shown to play a major role not only in the production of proinflammatory cytokines but also in the progression of inflammatory and neuropathic pain. We have demonstrated that tactile allodynia and spontaneous pain of female rats with tibia tumors were correlated with the increase of both phosphorylated-p38MAPK (p-p38MAPK) and proinflammatory cytokines (IL-1beta and TNF-alpha) in the spinal cord 6 days after Walker 256 cells' inoculation. This change was specific to bone cancer pain because rats without tibia tumors failed to show such an increase. On the other hand, a 3-day administration [4 microg/rat/day, intrathecally (i.t.)] of 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580), an inhibitor of p38MAPK, could suppress tactile allodynia and spontaneous pain of the bone cancer pain rats and decrease the phosphorylation of p38 as well as the expression of IL-1beta and TNF-alpha. To characterize the cellular events upstream of p38MAPK, we have examined the role of the toll-like receptor 4 (TLR4), which had been suggested to be involved in pain hypersensitivity. We found that prolonged knockdown of TLR4 during the 3-day administration of TLR4 small interfering RNA (siRNA; 2 microg/rat/day, i.t.) could attenuate hyperalgesia developed by Walker 256 cells' inoculation and decrease the phosphorylation of p38 as well as the increase of IL-1beta and TNF-alpha expression. These results demonstrate that TLR4-dependent phosphorylation of p38MAPK in spinal cord of rats might contribute to the development and maintenance of bone cancer pain, and p38MAPK and TLR4 would possibly be the potential targets for pain therapy.