Enhanced Corrosion Inhibition of Q235 Steel by N,S Co-Doped Carbon Dots: A Sustainable Approach for Industrial Pickling Corrosion Inhibitors.

A high yield of environmentally friendly N,S-codoped (N,S-CDs) and N-doping carbon points (N-CDs) carbon dots was achieved through a biochemical oxidation reaction at room temperature in this study. Acetaldehyde, sodium hydroxide, benzotriazole (BTA), and 2-mercaptobenzimidazole (MB) with a similar structure were used as raw materials. The microstructure and properties of the corrosion inhibitor for Q235 steel were evaluated by various experiments. The results demonstrated enhanced corrosion inhibition rates of the N,S-CDs compared to the N-CDs using electrochemical tests (93.83% vs 77.65%) and weight loss experiments (96.35% vs 91.65%) at 50 mg/L, respectively, compared to the blank material, indicating that N,S codoping can significantly improve the corrosion inhibition effect of carbon dots. The significant improvements were attributed to the formation of dense adsorption films and the hydrophobic properties of N and S-CDs nanoparticles on the steel surface, leading to an effective barrier against corrosion. The findings from this study provide important experimental data for potential industrial applications and hold important practical value in the field of pickling corrosion inhibitors.

Neural pathways from hypothalamic orexin neurons to the ventrolateral preoptic area mediate sleep impairments induced by conditioned fear.

Introduction: Fear and sleep impairments common co-exist, but the underlying mechanisms remain unclear. Hypothalamic orexinergic neurons are involved in the regulation of sleep-wake and fear expression. The ventrolateral preoptic area (VLPO) is an essential brain region to promote sleep, and orexinergic axonal fibers projecting to the VLPO are involved in the maintenance of sleep-wake. Neural pathways from hypothalamic orexin neurons to the VLPO might mediate sleep impairments induced by conditioned fear. Methods: To verify above hypothesis, electroencephalogram (EEG) and electromyogram (EMG) were recorded for analysis of sleep-wake states before and 24 h after conditioned fear training. The retrograde tracing technique and immunofluorescence staining was used to identify the projections from the hypothalamic orexin neurons to the VLPO and to observe their activation in mice with conditioned fear. Moreover, optogenetic activation or inhibition of hypothalamic orexin-VLPO pathways was performed to observe whether the sleep-wake can be regulated in mice with conditioned fear. Finally, orexin-A and orexin receptor antagonist was administered into the VLPO to certify the function of hypothalamic orexin-VLPO pathways on mediating sleep impairments induced by conditioned fear. Results: It was found that there was a significant decrease in the non-rapid eye movement (NREM) and rapid eye movement (REM) sleep time and a significant increase in the wakefulness time in mice with conditioned fear. The results of retrograde tracing technique and immunofluorescence staining showed that hypothalamic orexin neurons projected to the VLPO and observed the CTB labeled orexin neurons were significantly activated (c-Fos+) in the hypothalamus in mice with conditioned fear. Optogenetic activation of hypothalamic orexin to the VLPO neural pathways significantly decreased NREM and REM sleep time and increased wakefulness time in mice with conditioned fear. A significant decrease in NREM and REM sleep time and an increase in wakefulness time were observed after the injection of orexin-A into the VLPO, and the effects of orexin-A in the VLPO were blocked by a pre-administrated dual orexin antagonist (DORA). Conclusion: These findings suggest that the neural pathways from hypothalamic orexinergic neurons to the VLPO mediate sleep impairments induced by conditioned fear.

One-Pot Hydrothermal Synthesized Nitrogen and Sulfur Codoped Carbon Dots for Acid Corrosion Inhibition of Q235 Steel.

N and S codoped carbon dots having good water solubility have been successfully made by a novel hydrothermal method and characterized by FTIR, XPS, and TEM. The as-synthesized CDs were carbon particles rich in polar functional groups less than 10 nm in size. Electrochemical measurements, gravimetry, and surface analysis methods were utilized to examine the inhibition characteristics and adsorption mechanism of CDs on the carbon steel in acid pickling solutions. Electrochemical measurements verified that the CDs displayed adequate protection with high inhibition efficiency of 97.8%. The long-term weight-loss experiments up to 72 h further confirmed the excellent corrosion inhibition at room temperature and 313 K. The results presented are helpful for the formulation of more effective acid pickling corrosion inhibitors.

Insights into the newly synthesized N-doped carbon dots for Q235 steel corrosion retardation in acidizing media: A detailed multidimensional study.

N-doped carbon quantum dots (NCQDs) were synthesized by a hydrothermal method using folic acid and o-phenylenediamine as precursors. The inhibition behaviour of the NCQDs on Q235 steel in 1 M HCl solution was appraised through electrochemical impedance spectroscopy (EIS), potentiodynamic polarization curves (PDP), and surface analysis. The results demonstrated that the synthesized NCQDs had an effective anticorrosion effect on Q235 steel, and the corrosion inhibition efficiency of 150 mg/L NCQDs reached 95.4%. Additionally, the analysis of the PDP corrosion potential changes indicated that the NCQDs acted as a mixed corrosion inhibitor. Moreover, the NCQDs adsorbed onto the surface of steel by coordinating its electron-rich atoms with the iron metal to form a protective film, which slowed the dissolution reaction of the anodic metal to achieve corrosion inhibition. The adsorption mechanism of the NCQDs was consistent with Langmuir adsorption, including physical and chemical adsorption. Therefore, this work can inspire and facilitate, to a certain extent, the future application of doped carbon quantum dots as efficient corrosion inhibitors in pickling solutions.

Synthesis and Structure of Water-Soluble Sb Quantum Dots and Enhanced Corrosion Inhibition Performance and Mechanisms.

Generally, single organic or inorganic inhibitors could effectively inhibit corrosion for metallic materials; however, there are rarely reports about the hybrid corrosion inhibitors consisting of organic and inorganic inhibitors. Thus, in this work, we synthesize a hybrid environment-friendly water-soluble corrosion inhibitor (Sb quantum dots) containing Sb, Sb2O3, Sb2O4, and carbon using the electrochemical exfoliation method. The inhibition effectiveness in short- and long-term immersion tests is measured using electrochemical methods, weight loss, and surface analysis. The results exhibit that the corrosion inhibition efficiency sensitively relates to the concentration of Sb quantum dots (SQDs), which achieves the largest value as the concentration of SQDs increases to 200 mg/L. Atomic force microscopy, scanning electron microscopy, and contact angle analysis reveal that the SQDs well-disperse on and cover the Q235 steel surface at 200 mg/L. According to the Langmuir adsorption data, the physicochemical adsorption and effective antioxidation of SQDs on the passivated Q235 steel surface are in charge of the effective corrosion inhibition efficiency in 0.5 M H2SO4 solution.

In Situ Friction-Induced Graphene Originating from Methanol at the Sliding Interface between the WC Self-Mated Tribo-Pair and Its Tribological Performance.

Alcohols are reported to have superlubricity at low loads during sliding; however, their lubricity under high loads has rarely been reported. Meanwhile, the lubrication mechanism of alcohols under high loads is still not well understood. Here, we first report the lubricity of methanol under 98 N and 1450 rpm and demonstrate the formation of graphene and fullerene-like nanostructures induced by tribochemical reactions. Results show that the lubrication mechanism was mainly attributed to the friction-induced graphene under boundary lubrication condition. Besides that, the wear rate of a YG8 hard alloy ball mainly occurred at the run-in processes, and the friction-induced graphene effectively inhibited further wear after the run-in processes. The formation mechanism of graphene was well investigated, and the flash temperature rise and catalyst (WC, WO2, and WO3) were the major causes for the formation of graphene.

Combination of BMSCs-laden acellular nerve xenografts transplantation and G-CSF administration promotes sciatic nerve regeneration.

Peripheral nerve gaps often lead to interrupted innervation, manifesting as severe sensory and motor dysfunctions. The repairs of the nerve injuries have not achieved satisfactory curative effects in clinic. The transplantation of bone marrow stromal cells (BMSCs)-laden acellular nerve xenografts (ANX) has been proven more effective than the acellular nerve allografting. Besides, granulocyte colony-stimulating factor (G-CSF) can inhibit inflammation and apoptosis, and thus is conducive to the microenvironmental improvement of axonal regeneration. This study aims to investigate the joint effect of BMSCs-seeded ANX grafting and G-CSF administration, and explore the relevant mechanisms. Adult SD rats were divided into five groups randomly: ANX group, ANX combined with G-CSF group, BMSCs-laden ANX group, BMSCs-laden ANX combined with G-CSF group, and autograft group. Eight weeks after transplantation, the detection of praxiology and neuroelectrophysiology was conducted, and then the morphology of the regenerated nerves was analyzed. The inflammatory response and apoptosis in the nerve grafts as well as the expression of the growth-promoting factors in the regenerated tissues were further assayed. G-CSF intervention and BMSCs implanting synergistically promoted peripheral nerve regeneration and functional recovery following ANX bridging, and the restoration effect was matchable with that of the autologous nerve grafting. Moreover, local inflammation was alleviated, the apoptosis of the seeded BMSCs was decreased, and the levels of the neuromodulatory factors were elevated. In conclusion, the union application of BMSCs-implanted ANX and G-CSF ameliorated the niche of neurotization and advanced nerve regeneration substantially. The strategy achieved the favorable effectiveness as an alternative to the autotransplantation.

Tribological and antioxidation properties study of two N-containing borate ester derivatives as additive in rapeseed oil.

Two kinds of phenol- and N- containing borate ester, BTEB and BMEB have good hydrolysis stability due to the B-N coordination bond. The PB value improved by 60.7% and 67.6% respectively at 0.5wt% BTEB, BMEB in rapeseed oil. Their antiwear effect increases with the increase of adding content, and BMEB is better than BTEB. The friction-reducing effect of BTEB is better than BMEB. All additives formed a protective film which containing BOx, FeOx and other organic nitrogen compounds. The better capacities of BMEB may due to the complex boundary lubricating film which contain ferrous sulfate, ferrous sulfide. All additives possessed good antioxidation effect, and it increased the oxidation activation energy than rapeseed oil by 51.15% and 78.82% respectively at 0.25wt%.

Evaluation of vitrification protocol of mouse ovarian tissue by effect of DNA methyltransferase-1 and paternal imprinted growth factor receptor-binding protein 10 on signaling pathways.

Transplantation of cryopreserved ovarian tissue has been considered as a promising way of fertility preservation for women. however, this cryopreservation method is prone to post-resuscitation follicle proliferation and oocyte development stagnation, affecting late transplant survival. To evaluate current vitrification works, we investigated the critical pathway alternations in vitrified-warmed juvenile 10-day-old mouse ovary. We showed a significant decrease of protein kinase B (Akt) and Mitogen-activated protein kinase (Mapk) phosphorylation, during which serine/threonine kinases play central roles in coordinating follicle and oocyte development and stress response. Inhibition of Akt and Mapk activity were associated with one of the imprinted insulin pathway negative regulatory genes, Growth factor receptor-binding protein 10 (Grb10) which remarkably increased in vitrified-warmed juvenile mouse ovary than that of fresh group (p < 0.05). RNAi-induced Grb10 down-regulation reversed the decrease in Akt and Mapk phosphorylation. The increase of Grb10 expression was partially caused by the hyper-methylation of the promoter region, associated with the decrease of follicular DNA methyltransferase (Dnmt) 1 protein in different stages of vitrified-warmed group, compared to fresh group (p < 0.05). The mRNA and protein expression of Dnmt1 in ovary of vitrified-warmed juvenile mouse were remarkably lower than those in fresh group (p < 0.05). Dnmt1 overexpression dramatically reversed Grb10 up-regulation and Akt and Mapk phosphorylation reduction. Taken together, our findings suggest that Grb10 expression might be helpful in evaluation of effectiveness of vitrification, and considered as a potential target for further vitrification protocols improvement in the future.

Expression of NR1 and apoptosis levels in the hippocampal cells of mice treated with MK­801.

The aim of the present study was to investigate the characteristics of N­methyl­D­aspartate receptor R1 (NR1) expression and apoptosis in the nerve cells of the hippocampus in schizophrenia­like mice. C57BL/6 mice were randomly allocated to the following groups: i) Blank group; ii) MK­801 group; iii) MK­801+NMDA group, according to body weight. The NMDAR antagonist, MK­801 (0.6 mg/kg/d) was intraperitoneally injected daily for 14 days to induce a schizophrenia­like phenotype mouse model, and the effect of the NMDA injection via the lateral ventricle was observed. The results demonstrated that the number of NR1 positive cells in the MK­801 group increased in the CA1 and DG regions, indicating that NMDA may reverse this change. The level of damage decreased in the MK­801 treated group when compared with the blank group in the CA3 region. The protein expression of NR1 increased however, at the mRNA expression level, NR1 was lower in the MK­801 treated group when compared to the blank group; NMDA also reversed this change. In addition, early and total apoptosis detected in the hippocampal nerve cells was significantly increased in the MK­801 group when compared with the blank group, which was reversible following treatment with NMDA. These results indicated that NMDA may regulate the expression of NR1 and suppress apoptosis in hippocampal nerve cells in schizophrenia­like mice. Thus, NR1 may be a promising therapeutic target for the treatment of schizophrenia.

The Catalytically Lignan-Activation-Based Approach for the Synthesis of (epi)-Podophyllotoxin Derivatives.

Under the effect of a catalytic amount of Au(I) complex, 4-O-(2-cyclopropylethynyl)benzoyl-(epi)-podophyllotoxins, easily prepared via dehydrative condensation between (epi)-podophyllotoxin and ortho-cyclopropylethynylbenzoic acid, could efficiently couple with a variety of nucleophiles including alcohol, phenol, aniline, and carbon nucleophiles, all to provide (epi)-podophyllotoxin derivatives. Thus, the first catalytic and lignan-activation-based approach for (epi)-podophyllotoxin derivatization was established. Based on the new methodology, as well as the judicious choice of N3, AZMB, and Cbz protecting groups, an efficient approach forward was set. NK-611, an antitumoral agent at a phase II clinical trial was established, featuring an in situ anomerization of the hemiacetal OHs in the critical condensation step. Commencing from easily available starting material, the target molecule was obtained using the longest linear sequence of six steps and a 38% overall yield.

Synergistic effects of G-CSF and bone marrow stromal cells on nerve regeneration with acellular nerve xenografts.

Peripheral nerve defects result in severe denervation presenting sensory and motor functional incapacitation. Currently, a satisfactory therapeutic treatment promoting the repair of injured nerves is not available. As shown in our previous study, acellular nerve xenografts (ANX) implanted with bone marrow stromal cells (BMSCs) replaced allografts and promoted nerve regeneration. Additionally, granulocyte-colony stimulating factor (G-CSF) has been proven to mobilize supplemental cells and enhance vascularization in the niche. Thus, the study aimed to explore whether the combination of G-CSF and BMSC-laden ANX exhibited a synergistic effect. Adult Sprague-Dawley (SD) rats were randomly divided into five groups: ANX group, ANX combined with G-CSF group, BMSCs-laden ANX group, BMSCs-laden ANX combined with G-CSF group and autograft group. Electrophysiological parameters and weight ratios of tibialis anterior muscles were detected at 8 weeks post-transplantation. The morphology of the regenerated nerves was assayed, and growth-promoting factors present in the nerve grafts following G-CSF administration or BMSCs seeding were also investigated. Nerve regeneration and functional rehabilitation induced by the combination therapy were significantly advanced, and the rehabilitation efficacy was comparable with autografting. Moreover, the expression of Schwann cell markers, neurotrophic factors and neovessel markers in the nerve grafts was substantially increased. In conclusion, G-CSF administration and BMSCs transplantation synergistically promoted the regeneration of ANX-bridged nerves, which offers a superior strategy to replace autografts in repairing peripheral nerve injuries.

Neurochemical features of endomorphin-2-containing neurons in the submucosal plexus of the rat colon.

AIM: To investigate the distribution and neurochemical phenotype of endomorphin-2 (EM-2)-containing neurons in the submucosal plexus of the rat colon. METHODS: The mid-colons between the right and left flexures were removed from rats, and transferred into Kreb's solution. For whole-mount preparations, the mucosal, outer longitudinal muscle and inner circular muscle layers of the tissues were separated from the submucosal layer attached to the submucosal plexus. The whole-mount preparations from each rat mid-colon were mounted onto seven gelatin-coated glass slides, and processed for immunofluorescence histochemical double-staining of EM-2 with calcitonin gene-related peptide (CGRP), choline acetyltransferase (ChAT), nitric oxide synthetase (NOS), neuron-specific enolase (NSE), substance P (SP) and vasoactive intestinal peptide (VIP). After staining, all the fluorescence-labeled sections were observed with a confocal laser scanning microscope. To estimate the extent of the co-localization of EM-2 with CGRP, ChAT, NOS, NSE, SP and VIP, ganglia, which have a clear boundary and neuronal cell outline, were randomly selected from each specimen for this analysis. RESULTS: In the submucosal plexus of the mid-colon, many EM-2-immunoreactive (IR) and NSE-IR neuronal cell bodies were found in the submucosal plexus of the rat mid-colon. Approximately 6 ± 4.2 EM-2-IR neurons aggregated within each ganglion and a few EM-2-IR neurons were also found outside the ganglia. The EM-2-IR neurons were also immunopositive for ChAT, SP, VIP or NOS. EM-2-IR nerve fibers coursed near ChAT-IR neurons, and some of these fibers were even distributed around ChAT-IR neuronal cell bodies. Some EM-2-IR neuronal cell bodies were surrounded by SP-IR nerve fibers, but many long processes connecting adjacent ganglia were negative for EM-2 immunostaining. Long VIP-IR processes with many branches coursed through the ganglia and surrounded the EM-2-IR neurons. The percentages of the EM-2-IR neurons that were also positive for ChAT, SP, VIP or NOS were approximately 91% ± 2.6%, 36% ± 2.4%, 44% ± 2.5% and 44% ± 4.7%, respectively, but EM-2 did not co-localize with CGRP. CONCLUSION: EM-2-IR neurons are present in the submucosal plexus of the rat colon and express distinct neurochemical markers.

A novel tri-allelic insertion/deletion polymorphism in the promoter of p21(Waf1/Cip1) and the association with gastric cancer.

AIMS: p21(Waf1/Cip1) is a cyclin-dependent kinase inhibitor that is pivotal in arresting cellular growth in terminal cell differentiation and apoptosis. Thus, the existence of natural variants of p21(Waf1/Cip1) could be linked to specific cancer. The purpose of this report was to identify a novel tri-allelic insertion/deletion (INDEL) polymorphism (rs4135235) involving a poly-T sequence in the promoter region of p21(Waf1/Cip1) gene and to explore its role in gastric cancer (GC). METHOD: A total of unrelated 676 subjects (376 GC patients; 300 cancer-free controls) were enrolled in the study, and genomic DNA was obtained from each subject for genotyping. PCR-directed sequencing technique was used to detect the genotypes of the polymorphism. TA cloning was used to confirm the existence of three alleles. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by unconditional logistic regression analysis. RESULTS: Six genotypes (9T/9T, 10T/10T, 11T/11T, 9T/10T, 10T/11T, and 9T/11T) and three alleles (9Ts, 10Ts, and 11Ts) were identified among all study subjects. GC cases were different from the control group with over-representation of 9T/11T heterozygotes (19.7% vs. 12.3%) and under-representation of 10T/10T homozygotes (18.4% vs. 20.7%). Compared with those carrying 10T/10T, individuals with 9T/11T increased the susceptibility for GC (OR=1.797, 95%CI=1.065-3.031). CONCLUSION: Our findings confirmed the existence of a tri-allelic polymorphism in the promoter of p21(Waf1/Cip1). It has also shown the heterozygous genotype 9T/11T to be a potential risk factor for GC in the Chinese population.

Neurochemical phenotype and function of endomorphin 2-immunopositive neurons in the myenteric plexus of the rat colon.

The distribution and activity of endomorphins (EMs), which are endogenous µ-opioid receptor (MOR) ligands in the gastrointestinal tract (GI), are yet to be elucidated. The current study aimed to shed light on this topic. EM2 was expressed in the enteric neurons in the myenteric plexus of the mid-colon. Of the EM2-immunoreactive (EM2-IR) neurons, 53 ± 4.6%, 26 ± 4.5%, 26 ± 2.8% and 49 ± 4.2% displayed immunopositive staining for choline acetyl transferase (ChAT), substance P (SP), vasoactive intestinal peptide (VIP) and nitric oxide synthetase (NOS), respectively. A bath application of EM2 (2 µM) enhanced spontaneous contractile amplitude and tension, which were reversed by ß-FNA (an antagonist of MOR) but not NG-nitro-L-arginine methyl ether (L-NAME, a non-selective inhibitor of NOS) or VIP6-28 (an antagonist of the VIP receptor) in the colonic strips. EM2 significantly suppressed inhibitory junction potentials (IJPs) in 14 of the 17 examined circular muscle cells, and this effect was not antagonized by preincubation in L-NAME. EM2 was widely expressed in interneurons and motor neurons in the myenteric plexus and presynaptically inhibited fast IJPs, thereby enhancing spontaneous contraction and tension in the colonic smooth muscle.

Comparison of neuroprotective effects in ischemic rats with different hypothermia procedures.

OBJECTIVE: The neuroprotective effect of hypothermia has long been recognized. The aim of this work was to compare the neuroprotective effect of systemic, head and local vascular cooling hypothermia procedures in ischemic rats. METHODS: Stroke in Sprague-Dawley rats (n=64) was induced by a 3 hour right middle cerebral artery occlusion using an intraluminal filament. Before reperfusion, ischemic animals (n=16 in each group) received hypothermia (systemic, head or local vascular) or no treatment. Brain temperature, infarction volume (n=8 in each group) and functional outcome (n=8 in each group) were compared. RESULTS: Regarding brain temperature, vascular cooling significantly reduced the temperature of ischemic territory in cortex from 37.2 +/- 0.1 to 33.4 +/- 0.4 degrees C and in striatum from 37.5 +/- 0.2 to 33.9 +/- 0.4 degrees C within 5 minutes. This hypothermic condition remained for up to 60 minutes after reperfusion. However, systemic cooling reduced brain temperature at a similar level for six times longer. In the head cooling group, the target temperature was reached in 15 minutes, but returned to normal within 5 minutes. Although all hypothermia procedures induced neuroprotection, ischemic rats with vascular cooling showed significantly (p<0.001) better neuroprotection with 10.7 +/- 2.6% infarction, compared to 54.2 +/- 1.9% (no treatment), 37.1 +/- 1.0% (head cooling) and 29.1 +/- 3.4% (systemic cooling). Significantly (p<0.001) better effects on motor function were also detected in vascular cooling groups at 14 and 28 days. CONCLUSION: Vascular cooling appears to be the most effective in reducing infarct volume and improving functional outcome than the other two hypothermia methods in a rat ischemia/reperfusion model.

[Study of the volatilization inhibitor for formalin].

OBJECTIVE: To find an inhibitor to reduce the volatilization of formalin. METHOD: The saturated solution of sodium hydrosulphite (SHS) was sprayed on the surface of the anatomy specimens, then the concentration of formaldehyde in the air was tested. RESULTS: The concentration of formaldehyde in the air of SHS sprayed group [(3.10 +/- 1.22) mg/m3] was significantly lower than that of the control group [(8.36 +/- 4.11) mg/m3, P < 0.01]. CONCLUSION: SHS may be a volatilization inhibitor for formalin, which could reduce the concentration of formaldehyde in the air.