Moderate Traumatic Brain Injury Causes Acute Dendritic and Synaptic Degeneration in the Hippocampal Dentate Gyrus

Hippocampal injury-associated learning and memory deficits are frequent hallmarks of brain trauma and are the most enduring and devastating consequences following traumatic brain injury (TBI). Several reports, including our recent paper, showed that TBI brought on by a moderate level of controlled cortical impact (CCI) induces immature newborn neuron death in the hippocampal dentate gyrus. In contrast, the majority of mature neurons are spared. Less research has been focused on these spared neurons, which may also be injured or compromised by TBI. Here we examined the dendrite morphologies, dendritic spines, and synaptic structures using a genetic approach in combination with immunohistochemistry and Golgi staining. We found that although most of the mature granular neurons were spared following TBI at a moderate level of impact, they exhibited dramatic dendritic beading and fragmentation, decreased number of dendritic branches, and a lower density of dendritic spines, particularly the mushroom-shaped mature spines. Further studies showed that the density of synapses in the molecular layer of the hippocampal dentate gyrus was significantly reduced. The electrophysiological activity of neurons was impaired as well. These results indicate that TBI not only induces cell death in immature granular neurons, it also causes significant dendritic and synaptic degeneration in pathohistology. TBI also impairs the function of the spared mature granular neurons in the hippocampal dentate gyrus. These observations point to a potential anatomic substrate to explain, in part, the development of posttraumatic memory deficits. They also indicate that dendritic damage in the hippocampal dentate gyrus may serve as a therapeutic target following TBI

Network Pharmacology and In Vivo experiment-Based Strategy to Investigate Mechanisms of JinFangFuZiLiZhong Formula for Ulcerative Colitis

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Downregulation of ST6GAL2 Correlates to Liver Inflammation and Predicts Adverse Prognosis in Hepatocellular Carcinoma

Ruijia Liu,1,2,* Xudong Yu,1,* Xu Cao,1,2 Xuyun Wang,3 Yijun Liang,2 Wenying Qi,1,2 Yong’an Ye,1,2 Xiaobin Zao1,2,4 1Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, People’s Republic of China; 2Institute of Liver Diseases, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, People’s Republic of China; 3Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, People’s Republic of China; 4Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xiaobin Zao, Assistant Researcher, Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, 5 Haiyuncang Road, Dongcheng District, Beijing, 100700, People’s Republic of China, Tel +86-10-8401-3194, Email [email protected]: ST6 Beta-Galactoside Alpha-2,6-Sialyltransferase 2 (ST6GAL2), a member of the sialic acid transferase family, is differentially expressed in diverse cancers. However, it remains poorly understood in tumorigenesis and impacts on immune cell infiltration (ICI) in hepatocellular carcinoma (HCC).Patients and Methods: Herein, the expression, diagnosis, prognosis, functional enrichment, genetic alterations, immune characteristics, and targeted drugs of ST6GAL2 in HCC were researched by conducting bioinformatics analysis, in vivo, and in vitro experiments.Results: ST6GAL2 was remarkably decreased in HCC compared to non-tumor tissues, portending a poor prognosis associated with high DNA methylation levels. Functional enrichment and GSVA analyses revealed that ST6GAL2 might function through the extracellular matrix, PI3K-Akt signaling pathways, and tumor inflammation signature. We found that ST6GAL2 expression was proportional to ICI, immunostimulator, and immune subtypes. ST6GAL2 expression first increased and then decreased during the progression of liver inflammation to HCC. The dysfunctional experiment indicated that ST6GAL2 might exert immunosuppressive effects during HCC progression through regulating ICI. Several broad-spectrum anticancer drugs were obtained by drug sensitivity prediction analysis of ST6GAL2.Conclusion: In conclusion, ST6GAL2 was a reliable prognostic biomarker strongly associated with ICI, and could be a potential immunotherapeutic target for HCC.Keywords: hepatocellular carcinoma, ST6GAL2, prognosis, immune cell infiltration, biomarke

Identifying electrochemical effects in a thermal-electrochemical co-driven system for CO2 capture

Currently, the most promising amine absorption system for CO capture still faces the challenges of heavy steam consumption and a high energy penalty. Thus, a new thermal-electrochemical co-driven system (TECS) for CO capture was developed to resolve these problems. In the TECS, unknown electrochemical behaviors are quite essential to assess the CO capture performance. Electrochemical experiments were designed using response surface methodology (RSM) to identify electrochemical effects. The results show that the cathode process is slow and difficult, which is the main limitation in improving the performance of the TECS. Forced convection is necessary to improve the diffusion-controlled process and accelerate desorption. Four factors (Cu(II) molality, CO loading, temperature, KNO molality) play an auxo-action role in determining anode and cathode reaction rates. A regression model is developed based on the experimental data, and optimum operating conditions are obtained. Regeneration energy consumption reaches about 1.3 GJ per t CO, a decline of up to 70% compared with the traditional process. In addition, preliminary CO desorption experiments suggest that the mass transfer ascribed to the electrochemical process accounts for over 50% of the overall mass transfer coefficient in the CO desorption process

Exploiting an alternative CO2 absorption process by efficient solvent mixture

CO2 capture greatly helps with greenhouse gas mitigation. Chemical and physical absorption can control CO2 emission, but these methods are costly. To reduce the cost, an efficient solvent mixture of tetramethylammonium hydroxide (TAMH), tetramethylene sulfone (TMS), and ethylene glycol (EG) is assessed. Gas-liquid equilibrium, reaction kinetics, and mass transfer models are developed and validated by experiments. Henrys constant, reaction kinetics, and mass transfer coefficients between CO2 and TAMH-TMS-EG are identified. CO2 loading and mass transfer coefficient are, respectively, obtained as 0.55 mol/molTAMH and 4.02kmol/m2/s/kPa, which are on average 25% and 34% higher than the typical MEA process. The theoretical energy consumption amount for desorption of TAMH-TMS-EG-CO2 solutions is identified as 1.11 GJ/t to 1.34GJ/t. Minimum mass transfer resistance is determined at 40% to 80% TMS fraction. A temperature bulge shift and improvement in the interface characteristics enhance mass transfer due to uniform temperature field and good gas and liquid countercurrent contact

Characterization of the Highly Regulated Antigen BBA05 in the Enzootic Cycle of Borrelia burgdorferi▿

Dramatic alteration of surface lipoprotein profiles is a key strategy that Borrelia burgdorferi, the Lyme disease pathogen, has evolved for adapting to the diverse environments of arthropod and mammalian hosts. Several of these differentially expressed lipoproteins have been shown to play important roles in the enzootic cycle of B. burgdorferi. The BBA05 protein is a previously identified putative lipoprotein (P55 or S1 antigen) that elicits antibody responses in mammals. Recent microarray analyses indicate that the BBA05 gene is differentially expressed by many environmental factors, including temperature. However, the role of the BBA05 protein in the life cycle of B. burgdorferi has not been elucidated. Here we show that expression of the BBA05 gene was exclusively induced in feeding nymphal ticks during the spirochetal transmission from ticks to mammals. Upon generating a BBA05 mutant in an infectious strain of B. burgdorferi, we showed that the BBA05 mutant remained capable of establishing infection in mice, being acquired by ticks, persisting through tick molting, and reinfecting new mammalian hosts. These results indicate that, despite being a highly conserved and regulated antigen, the BBA05 protein has a nonessential role in the transmission cycle of B. burgdorferi, at least in the animal model