Study on the Effect of Polyamine Water Treatment Agent on Metal Corrosion Inhibition in Boiler Steam-Water System.

A polyamine water treatment agent was prepared with the film-forming amine (N-oleyl-1,3-propylenediamine) and the neutralizing amine (cyclohexanamine) under optimal conditions. The copper sulfate liquid drop experiment showed that a protective film was formed by the polyamine water treatment agent on carbon steel. The analyses of the polarization curve and electrochemical impedance spectroscopy of carbon steel indicated that the polyamine water treatment agent exhibited geometric effects, which could inhibit both anode and cathode reactions of carbon steel, and the corrosion inhibition effect of the polyamine water treatment agent showed an extreme-concentration phenomenon. A metal corrosion experiment in a simulated boiler steam-water system indicated that the polyamine water treatment agent mitigated the corrosion of carbon steel at different temperatures, and the corrosion inhibition rates of the polyamine water treatment agent in liquid and gas environments at 150 °C were 53.84% and 67.43%, respectively, better than that at 350 °C. SEM-EDS characterization indicated that the formation of the corrosion product, iron oxide, on the carbon steel was reduced with the addition of the polyamine water treatment agent in the simulated boiler steam-water system.

TFR1 knockdown alleviates iron overload and mitochondrial dysfunction during neural differentiation of Alzheimer's disease-derived induced pluripotent stem cells by interacting with GSK3B.

Iron metabolism disorders are implicated in the pathogenesis of Alzheimer's disease (AD). It was previously reported that transferrin receptor (TFR1) expression was upregulated in AD mouse model. However, the precise biological functions of TFR1 in AD progression remains unclear. Herein, we observed a gradual increase in TFR1 protein expression during the differentiation of AD patient-derived induced pluripotent stem cells (AD-iPS). TFR1 knockdown inhibited the protein expression of ferritin and ferritin heavy chain 1 (FTH1), enhanced the expression of ferroportin 1 (FPN1), and decreased intracellular levels of total iron, labile iron, and reactive oxygen species (ROS). Moreover, TFR1 knockdown improved mitochondrial membrane potential (MMP), increased adenosine triphosphate (ATP) content, downregulated mitochondrial fission proteins, and upregulated mitochondrial fusion proteins. TFR1 knockdown alleviated iron overload and mitochondrial dysfunction in neural cells differentiated from AD-iPS, while TFR1 overexpression showed the opposite results. Additionally, TFR1interacted with glycogen synthase kinase 3 beta (GSK3B) and promoted GSK3B expression. GSK3B overexpression reversed the inhibitory effects of TFR1 knockdown on iron overload and mitochondrial dysfunction in AD-iPS differentiated neural cells. In conclusion, TFR1 knockdown alleviated iron overload and mitochondrial dysfunction in neural cells differentiated from AD-iPS by promoting GSK3B expression. Our findings provide a potential therapeutic target for the treatment of AD.

Case Report: A case of spinal muscular atrophy with extensively drug-resistant Acinetobacter baumannii pneumonia treated with nebulization combined with intravenous polymyxin B: experience and a literature review.

Spinal muscular atrophy (SMA) is a neurodegenerative disease that results in progressive and symmetric muscle weakness and atrophy of the proximal limbs and trunk due to degeneration of spinal alpha-motor neurons. Children are classified into types 1-3, from severe to mild, according to the time of onset and motor ability. Children with type 1 are the most severe, are unable to sit independently, and experience a series of respiratory problems, such as hypoventilation, reduced cough, and sputum congestion. Respiratory failure is easily complicated by respiratory infections and is a major cause of death in children with SMA. Most type 1 children die within 2 years of age. Type 1 children with SMA usually require hospitalization for lower respiratory tract infections and invasive ventilator-assisted ventilation in severe cases. These children are frequently infected with drug-resistant bacteria due to repeated hospitalizations and require long hospital stays requiring invasive ventilation. In this paper, we report a case of nebulization combined with intravenous polymyxin B in a child with spinal muscular atrophy with extensively drug-resistant Acinetobacter baumannii pneumonia, hoping to provide a reference for the treatment of children with extensively drug-resistant Acinetobacter baumannii pneumonia.

Nervous system manifestations related to COVID-19 and their possible mechanisms.

In December 2019, the novel coronavirus disease (COVID-19) due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection broke. With the gradual deepening understanding of SARS-CoV-2 and COVID-19, researchers and clinicians noticed that this disease is closely related to the nervous system and has complex effects on the central nervous system (CNS) and peripheral nervous system (PNS). In this review, we summarize the effects and mechanisms of SARS-CoV-2 on the nervous system, including the pathways of invasion, direct and indirect effects, and associated neuropsychiatric diseases, to deepen our knowledge and understanding of the relationship between COVID-19 and the nervous system.

NDRG4 Alleviates Aß1-40 Induction of SH-SY5Y Cell Injury via Activation of BDNF-Inducing Signalling Pathways.

We explored the functions and mechanisms of N-myc downstream-regulated gene 4 (NDRG4) in an amyloid beta 1-40 induced Alzheimer's disease cell model. The levels of total and phosphorylated Tau protein were significantly up-regulated and cell activity was decreased with increasing Aß1-40 treatment in SH-SY5Y cells. The expression of NDRG4 mRNA and protein levels were significantly decreased that induced by Aß1-40 in these cells. NDRG4 overexpression significantly alleviated Aß1-40-induced SH-SY5Y apoptosis rates and caspases-3/7 activities. Equally, Reactive oxygen species, Mitochondrial membrane potential and Microscale malondialdehyde levels were significantly down-regulated, and Superoxide dismutase activity was increased by NDRG4 overexpression. BDNF protein level and phosphorylation levels of AKT and ERK1/2 were enhanced by NDRG4 overexpression. We also determined that the inhibitory effects of NDRG4 on cell apoptosis and Reactive oxygen species release were partially reversed by BDNF silencing, and by application of the PI3K specific inhibitor (LY294002) or ERK inhibitor (PD98059). These data indicate that NDRG4 attenuates Aß1-40-induced cell apoptosis and Reactive oxygen species release release, as well as oxidative stress injury. These effects may be mediated through BDNF-induced PI3K/AKT and MEK/ERK pathways.

Effects of temperature and humidity on the performance of a PECH polymer coated SAW sensor.

The influences of environment, such as temperature, humidity and interfering gases, on the performance of a surface acoustic wave (SAW) sensor in the detection of 2-chloroethyl ethyl sulfide (CEES) were invested. The 150 MHz SAW dual delay lines were used, coated with a poly(epichlorohydrin) (PECH) thin layer, and CEES was detected under different concentrations. Linear correlation between the frequency-shift and the exposure time of the sensor to CEES could be observed, and the limit of CEES could be detected as low as 1.5 mg m-3. Under different temperature (0-50 C°) and humidity (30-80% RH) conditions, CEES was detected by the fabricated SAW sensor coated with PECH, the frequency shifts were measured and the performance of the sensor was evaluated. The results proved that temperature and humidity were the most important factors to influence the performance of SAW sensors; with the decreasing of temperature and the increasing of humidity, there would be larger frequency shifts. In the interference experiments, it was found that most gases existing in the environment in high concentrations would not influence the detection of CEES. Then, the SAW sensor having been fabricated was kept under the conditions of 25 °C and 35% RH for 18 months to further verify the quality, and CEES was detected every so many months. It proved that the performance of the sensor would decrease about 16.39% after 18 months. Although it reflected the attenuation of the sensor to some extent, the sensor was still in good condition. Additionally, the related mechanisms were also discussed.

A Novel Surface Acoustic Wave Sensor Array Based on Wireless Communication Network.

A novel surface acoustic wave (SAW) sensor array based on wireless communication network is prepared. The array is composed of four SAW sensors, a wireless communication network module, and a global positioning system (GPS) module. The four SAW sensors of the array are coated with triethanolamine, polyepichlorohydrin, fluoroalcoholpolysiloxane, and L-glutamic acid hydrochloride to detect hydrogen sulfide (H2S), 2-chloroethyl ethyl sulfide (CEES), dimethylmethylphosphonate (DMMP), and ammonia (NH3) at film thicknesses of 50⁻100 nm. The wireless communication network module consists of an acquisition unit, a wireless control unit, and a microcontroller unit. By means of Zigbee and Lora technologies, the module receives and transmits the collected data to a PC work station in real-time; moreover, the module can control the sensor array's working mode and monitor the working status. Simultaneously, the testing location is determined by the GPS module integrated into the SAW sensor array. H2S, CEES, DMMP, and NH3 are detected in 300 m at different concentrations. Given the practical future application in environment in the future, the low, safe concentrations of 1.08, 0.59, 0.10, and 5.02 ppm for H2S, CEES, DMMP, and NH3, respectively, are detected at the lowest concentration, and the sensitivities of different sensors of the sensor array are 32.4, 14.9, 78.1 and 22.6 Hz/ppm, respectively. With the obtained fingerprints and pattern recognition technology, the detected gases can be recognized.

LanCL1 attenuates ischemia-induced oxidative stress by Sirt3-mediated preservation of mitochondrial function.

Lanthionine synthetase C-like protein 1 (LanCL1) is homologous to prokaryotic lanthionine cyclases, and has been shown to have novel functions in neuronal redox homeostasis. A recent study showed that LanCL1 expression was developmental and activity-dependent regulated, and LanCL1 transgene protected neurons against oxidative stress. In the present study, the potential protective effects of LanCL1 against ischemia was investigated in an in vitro model mimicked by oxygen and glucose deprivation (OGD) in neuronal HT22 cells. We found that OGD exposure induced a temporal increase and persistent decreases in the expression of LanCL1 at both mRNA and protein levels. Overexpression of LanCL1 by lentivirus (LV-LanCL1) transfection preserved cell viability, reduced lactate dehydrogenase (LDH) release and attenuated apoptosis after OGD. These protective effects were accompanied by decreased protein radical formation, lipid peroxidation and mitochondrial dysfunction. In addition, LanCL1 significantly stimulated mitochondrial enzyme activities and SOD2 deacetylation in a Sirt3-dependent manner. The results of western blot analysis showed that LanCL1-induced activation of Sirt3 was dependent on Akt-PGC-1α pathway. Knockdown of PGC-1α expression using small interfering RNA (siRNA) or blocking Akt activation using specific antagonist partially prevented the protective effects of LanCL1 in HT22 cells. Taken together, our results show that LanCL1 protects against OGD through activating the Akt-PGC-1α-Sirt3 pathway, and may have potential therapeutic value for ischemic stroke.

Long Noncoding RNA SNHG1 Promotes Neuroinflammation in Parkinson's Disease via Regulating miR-7/NLRP3 Pathway.

Parkinson's disease (PD) is the second most common neurodegenerative disorders. Neuroinflammation plays an important role in the pathogenesis of PD. Long noncoding RNA small nucleolar RNA host gene 1 (SNHG1) was elevated in the brain specimens of PD patients and MPP+-treated SH-SY5Y cells. The expression of mouse Snhg1 and miR-7 was firstly determined in lipopolysaccharide (LPS)-induced BV2 cells. The role and mechanism of SNHG1 in the neuroinflammation of PD were investigated using gain- and loss-of function approaches both in vitro and in vivo. Snhg1 expression was elevated, whereas miR-7 reduced in LPS-induced BV2 cells. Upregulation of Snhg1 elevated, and Snhg1 knockdown suppressed LPS-induced BV2 microglial activation and inflammation. miR-7 reversed, while anti-miR-7 further enhanced the effects of Snhg1 on BV2 cells. Furthermore, we found that Snhg1 functioned as a competing endogenous RNA for miR-7 to regulate nod-like receptor protein 3 (NLRP3) expression, leading to the activation of NLRP3 inflammasome. In the microglial culture supernatant transfer model, knockdown of Snhg1 or NLRP3 in LPS-stimulated BV2 cells inhibited primary neurons from apoptosis and elevated caspase-3 activity. Additionally, Snhg1 was increased in MPTP-induced PD mouse models. Downregulation of Snhg1 elevated miR-7 expression, suppressed the activation of microglia and NLRP3 inflammasome as well as dopaminergic neuron loss in the midbrain substantia nigra pars compacta in MPTP-treated mice. In conclusion, our study suggests that SNHG1 promotes neuroinflammation in the pathogenesis of PD via modulating miR-7/NLRP3 pathway.

Evaluation of the Braak staging of brain pathology with 1H-MRS in patients with Parkinson's disease.

The Braak staging of Parkinson's disease (PD) pathology is usually based on the brain autopsy, which has not been confirmed in living patients of PD. In this study, we investigated the metabolites of medulla oblongata, substantia nigra (SN), putamen, and motor cortex by measuring N-acetylaspartate (NAA), choline-containing compounds (Cho) and creatine (Cr) in 22 patients of PD and 15 age-matched healthy controls, using single-voxel 1H-magnetic resonance spectroscopy (1H-MRS). The results showed that NAA/Cr in SN was lower in PD group than that in control group (p=0.006), however, there was no difference for NAA/Cr and Cho/Cr between PD group and control group in other regions. In SN, NAA/Cr was negatively correlated with Unified Parkinson's Disease Rating Scale (UPDRS) (r=-0.743, p=0.002) and Hoehn-Yahr staging (r=-0.714, p=0.003), while Cho/Cr was positively correlated with UPDRS (r=0.850, p<0.001) and Hoehn-Yahr staging (r=0.647, p=0.009). In PD group, the variance of NAA/Cr in SN was significantly larger than that in other regions (p=0.005), but there was no difference for the variance of Cho/Cr among regions of interesting (ROIs) (p=0.267). These results indicate that SN is the most seriously injured region in PD, and the metabolites in SN measured by 1H-MRS is correlated with the severity of PD. However, the Braak staging of PD pathology is not validated by 1H-MRS.

[An integrated on-line processing method for spectrometric data based on wavelet transform and Gaussian fitting].

Miniature mobile field spectrometry is pivotal equipment for qualitative and quantitative in-situ analysis of chemical substances. To solve the problem of spectrum signal interfered by complicated noise, overlapped and irregular peak shape recognition, and quick monitoring, an integrated on-line processing method for spectrometric data based on wavelet transform and Gaussian fitting was developed. In this way, toluene and perfluorotributylamine were processed, and the results shows that the integrated method can powerfully and effectively eliminate the noise, retain the original feature, and correct the overlapped and asymmetrical peaks, which can improve the analysis accuracy of instrument, and also achieve data compression. In addition, the method satisfies the requirement of on-site analysis for mobile field spectrometry. For the processing of mass spectra of toluene, at the characteristic peaks of 91 and 92, the SNR increased 1.3 times compared to that of moving average smoothing method, while the error between original peaks and theoretic peaks decreased 3.6 times. In addition, Gaussian fitting described the multipoint mass spectra data by three Gaussian parameters, and achieved data compression. For the processing of mass spectrogram of perfluorotributylamine, the ratio of compression was 197 : 1.

[Mechanism of alopecia in patients with paraneoplastic pemphigus].

OBJECTIVE: To investigate the relationship between the levels of antidesmoglein (DSG) 1, 3 antibodies in the sera of patients with paraneoplastic pemphigus (PNP) and alopecia. METHODS: Sera from PNP patients, bullous pemphigoid patients, and normal healthy subjects were collected and 2 tissue samples from 2 healthy scalps were resected. Anti-DSG 1, 3 antibodies in the sera of PNP patients were detected by enzyme-linked immunosorbent assay (ELISA). Indirect immunofluorescent assay was used to detect whether the antibodies in the sera of PNP patients binds with the follicular epithelium of normal healthy scalp. RESULTS: Anti-DSG3 autoantibody was strongly positive and anti-DSG1 weakly positive in one patient, while both two antibodies were negative in the other patient. Their sera could bind to keratinocytes and follicular epithelium in human scalp. Immunofluorescent signals were found on the intercellular epidermal cell surface and outer root sheath of the follicular epithelium. However, the immunofluorescent signals in the section incubating with serum of bullous pemphigoid were only found on basal membrane zone. No signals were found in the section incubating with normal healthy serum. CONCLUSION: Alopecia in PNP patients are correlated with the anti-DSG3.