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C35H24CoN4O6, monoclinic, P21/n (no. 14), a = 11.444(2) Å, b = 11.648(2) Å, c = 21.478(4) Å, β = 97.05(3)°, V = 2841.5(10) Å3, Z = 4, Rgt(F) = 0.0849, wRref(F2) = 0.1393, T = 153(2) K.

The landscape of therapeutic deep brain stimulation (DBS) for locomotor function recovery is rapidly evolving. This review provides an overview of electrical neuromodulation effects on spinal cord injury (SCI), focusing on DBS for motor functional recovery in human and animal models. We highlight research providing insight into underlying cellular and molecular mechanisms. A literature review via Web of Science and PubMed databases from 1990 to May 29, 2024, reveals a growing body of evidence for therapeutic DBS in SCI recovery. Advances in techniques like optogenetics and whole-brain tractogram have helped elucidate DBS mechanisms. Neuronal targets sites for SCI functional recovery include the mesencephalic locomotor region (MLR), cuneiform nucleus (CNF), and nucleus raphe magnus (NRG), with pedunculopontine nucleus (PPN), periaqueductal gray (PAG), and nucleus ventroposterolateral thalami (VPL) for post-injury functional recovery treatment. Radiologically guided DBS optimization and combination therapy with classical rehabilitation have become an effective therapeutic method, though ongoing interventional trials are needed to enhance understanding and validate DBS efficacy in SCI. On the pre-clinical front, standardization of pre-clinical approaches are essential to enhance the quality of evidence on DBS safety and efficacy. Mapping brain targets and optimizing DBS protocols, aided by combined DBS and medical imaging, are critical endeavors. Overall, DBS holds promise for neurological and functional recovery after SCI, akin to other electrical stimulation approaches. [ABSTRACT FROM AUTHOR]

Immunohistochemical Strept Avidin Biotin-Peroxidase Complex (SABC) three-step method was used to investigate the distribution patterns and developmental changes of GnRH and GnRHR immunopositive (GnRH-ip and GnRHR-ip) cells in the pituitary of Ji Ning Gray goats during 0-180 days of age. The results showed that GnRH-ip and GnRHR-ip cells were detected only in the pars distalis of adenohypophysis. There were no positive cells in the pars intermedia and neurohypophysis. GnRH-ip and GnRHR-ip cells were not observed in the anterior pituitary at birth day and 30 days of age. At 60 days, a number of GnRH-ip and GnRHR-ip cells were found in the anterior pituitary. GnRH-ip cells were pale brown which scattered or clustered around the sinusoid capillary; GnRHR-ip cells were brown and the cytomembrane was darker. The size and percentage of GnRH-ip and GnRHR-ip cells increased with the age growth. The numbers of GnRH-ip and GnRHR-ip cells after sexual maturity were significantly bigger than that before sexual maturity. The results above suggested that GnRH and GnRHR in the pituitary of Ji Ning Gray goats play a pivotal role in the sexual development and sexual maturity.

C35H24CoN4O6, monoclinic, P21/n (no. 14), a = 11.444(2) Å, b = 11.648(2) Å, c = 21.478(4) Å, β = 97.05(3)°, V = 2841.5(10) Å3, Z = 4, Rgt(F) = 0.0849, wRref(F2) = 0.1393, T = 153(2) K. [ABSTRACT FROM AUTHOR]

The effect of copper and rare-earth elements on corrosion behavior of high silicon iron-based alloys in nitric acid was studied by means of static and loading current corrosion experiments. The anodic polarization curve was also made to discuss the corrosion mechanism. The examination on alloy microstructure and SEM corrosion pattern showed that when silicon content reached 14.5%, the Fe3Si phase appeared and the primary structure of the iron-base alloy was ferrite. When adding 4.57% copper in the iron alloy, its corrosion resistance in static diluted sulfuric acid was improved while its corrosion resistance and electrochemical corrosion properties in the nitric acid were decreased. In contrast, the addition of rare earth elements could improve the corrosion properties in all above conditions including in static diluted sulfuric acid and in nitric acid.

Abstract Background Under conditions of salt stress, plants respond by initiating phosphorylation cascades. Many key phosphorylation events occur at the membrane. However, to date only limited sites have been identified that are phosphorylated in response to salt stress in plants. Results Membrane fractions from three-day and 200 mM salt-treated Arabidopsis suspension plants were isolated, followed by protease shaving and enrichment using Zirconium ion-charged magnetic beads, and tandem mass spectrometry analyses. From this isolation, 18 phosphorylation sites from 15 Arabidopsis proteins were identified. A unique phosphorylation site in 14-3-3-interacting protein AHA1 was predominately identified in 200 mM salt-treated plants. We also identified some phosphorylation sites in aquaporins. A doubly phosphorylated peptide of PIP2;1 as well as a phosphopeptide containing a single phosphorylation site (Ser-283) and a phosphopeptide containing another site (Ser-286) of aquaporin PIP2;4 were identified respectively. These two sites appeared to be novel of which were not reported before. In addition, quantitative analyses of protein phosphorylation with either label-free or stable-isotope labeling were also employed in this study. The results indicated that level of phosphopeptides on five membrane proteins such as AHA1, STP1, Patellin-2, probable inactive receptor kinase (At3g02880), and probable purine permease 18 showed at least two-fold increase in comparison to control in response to 200 mM salt-stress. Conclusion In this study, we successfully identified novel salt stress-responsive protein phosphorylation sites from membrane isolates of abiotic-stressed plants by membrane shaving followed by Zr4+-IMAC enrichment. The identified phosphorylation sites can be important in the salt stress response in plants.

Group A streptococcus (GAS) is a versatile pathogen that causes a wide spectrum of diseases in humans. Invading host cells is a known strategy for GAS to avoid antibiotic killing and immune recognition. However, the underlying mechanisms of GAS resistance to intracellular killing need to be explored. Endothelial HMEC-1 cells were infected with GAS, methicillin-resistant Staphylococcus aureus (MRSA) and Salmonella Typhimurium under nicotinamide (NAM)-supplemented conditions. The intracellular NAD+ level and cell viability were respectively measured by NAD+ quantification kit and protease-based cytotoxicity assay. Moreover, the intracellular bacteria were analyzed by colony-forming assay, transmission electron microscopy, and confocal microscopy. We found that supplementation with exogenous nicotinamide during infection significantly inhibited the growth of intracellular GAS in endothelial cells. Moreover, the NAD+ content and NAD+/NADH ratio of GAS-infected endothelial cells were dramatically increased, whereas the cell cytotoxicity was decreased by exogenous nicotinamide treatment. After knockdown of the autophagy-related ATG9A, the intracellular bacterial load was increased in nicotinamide-treated endothelial cells. The results of Western blot and transmission electron microscopy also revealed that cells treated with nicotinamide can increase autophagy-associated LC3 conversion and double-membrane formation during GAS infection. Confocal microscopy images further showed that more GAS-containing vacuoles were colocalized with lysosome under nicotinamide-supplemented conditions than without nicotinamide treatment. In contrast to GAS, supplementation with exogenous nicotinamide did not effectively inhibit the growth of MRSA or S. Typhimurium in endothelial cells. These results indicate that intracellular NAD+ homeostasis is crucial for controlling intracellular GAS infection in endothelial cells. In addition, nicotinamide may be a potential new therapeutic agent to overcome persistent infections of GAS. [ABSTRACT FROM AUTHOR]

Metal oxide semiconductor sensors based on nanocrystalline In2O3 and its composites are found to be very sensitive in detecting low-concentration (~ 5 ppm) gases such as ozone, nitrogen dioxide, formaldehyde and butane. Here, we successfully obtained fiber-shaped In2O3 crystalline nanofibers via electrospun and calcination routes. The gas sensing properties of the In2O3 nanofibers were studied by exposing them to the acetic acid vapor with different concentrations from 500 ppb to 2000 ppm at the optimum operating temperature (250 °C). The device possesses ultra-high response of 66.7 toward 2000 ppm acetic acid vapor, low response and recovery times of 25 s and 37 s (100 ppm), respectively, and significant selectivity to acetic acid at 100 ppm. In particular, the sensor based on In2O3 nanofibers has very low detection limit and can reach 500 ppb. Therefore, the presented In2O3 nanofiber sensor can be used in practice in acetic acid detection area in the future. [ABSTRACT FROM AUTHOR]