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Hollow graphitic porous carbon nanosphere (CNS) materials are synthesized from polymerization of resorcinol (R) and formaldehyde (F) in the presence of templating iron polymeric complex (IPC), followed by carbonization treatment. The effect of rapid heating in the carbonization process is investigated for the formation of hollow graphitic carbon nanospheres. The resulting CNS from rapid heating was characterized for its structure and properties by transmission electron microscope (TEM), x-ray diffraction (XRD), Raman spectroscopy, bulk conductivity measurement and Brunauer-Emmett-Teller (BET) surface area. Hollow graphitic CNS with reduced degree of agglomeration is observed under rapid heating during the carbonization process when compared to the CNS synthesized using the standard slow heating approach. Key words: carbon nanosphere (CNS), rapid pyrolytic carbonization, agglomeration

Single-crystal Ni-rich cathode material LiNi0.88Co0.09Al0.03O2 (SC) was synthesized by a high-temperature solid-state calcination method. Physicochemical properties of primary and delithiated SC samples were investigated by X-ray diffractometry, X-ray photoelectron spectroscopy, and transmission electron microscopy. Electrochemical performance was characterized by long-term cycling, cyclic voltammetry, and in-situ impedance spectroscopy. The results indicated that high temperature rendered layered oxides to lose lithium/oxygen in the interior and exterior, and induced cationic disordering. Besides, the solid-phase synthesis process promoted phase transformation for electrode materials, causing the coexisting multi-phase in a single particle. High temperature can foster the growth of single particles, but it caused unstable structure of layered phase.

Ni-rich cathodes exhibit appealing properties, such as high capacity density, low cost, and prominent energy density. However, the inferior ionic conductivity and bulk structural degradation become bottlenecks for Ni-rich cathodes and severely limit their commercial utilization. Traditional coating and doping methods suffer fatal drawbacks in functioning as a unit and cannot radically promote material performance to meet the needs of Li-ion batteries (LIBs). Herein, we successfully devised an ingenious and facile synthetic method to establish Ni-rich oxides with a La2Zr2O7 coating and Zr doping. The coating layer improves the ion diffusion kinetics and enhances Li-ion transportation while Zr doping effectively suppresses the phase transition of LiNi0.8Co0.1Mn0.1O2 cathode. Owing to the synergetic effect of Zr doping and La2Zr2O7 coating, the modified material shows prominent initial discharge capacity of 184.7 mAh g−1 at 5 °C and maintains 177.5 mAh g−1 after 100 cycles at 1 °C. Overall, the proposed feasible electrode design method can have a far-reaching impact on further fabrication of advanced cathodes for high-performance LIBs.

An experimental study is conducted on the qualitative visualization of the flow field in separation and reattachment flows induced by an incident shock interaction by several techniques including shear-sensitive liquid crystal coating (SSLCC), oil flow, schlieren, and numerical simulation. The incident shock wave is generated by a wedge in a Mach 2.7 duct flow, where the strength of the interaction is varied from weak to moderate by changing the angle of attack α of the wedge from 8° and 10° to 12°. The stagnation pressure upstream was set to approximately 607.9 kPa. The SSLCC technique was used to visualize the surface flow characteristics and analyze the surface shear stress fields induced by the initial incident shock wave over the bottom wall and sidewall experimentally which resolution is 3500 × 200 pixels, and the numerical simulation was also performed as the supplement for a clearer understanding to the flow field. As a result, surface shear stress over the bottom wall was visualized qualitatively by SSLCC images, and flow features such as separation/reattachment and the variations of position/size of separation bubble with wedge angle were successfully distinguished. Furthermore, analysis of shear stress trend over the bottom wall by a hue value curve indicated that the relative magnitude of shear stress increased significantly downstream of the separation bubble compared with that upstream. The variation trend of shear stress was consistent with the numerical simulation results, and the error of separation position was less than 2 mm. Finally, the three-dimensional schematic of incident shock-induced interaction has been achieved by qualitative summary by multiple techniques, including SSLCC, oil flow, schlieren, and numerical simulation.

Hypertension is the most prevalent chronic disease and a risk factor for various diseases. Although its mechanisms and therapies are constantly being updated and developed, they are still not fully clarified. In recent years, novel gut microbiota and its metabolites have attracted widespread attention. It is strongly linked with physiological and pathological systems, especially TMA and TMAO. TMA is formed by intestinal microbial metabolism of choline and L-carnitine and converted into TMAO by FMO3. This paper collected and collated the latest researches and mainly discussed the following four parts. It introduced gut microbiota; provided a focus on TMA, TMA-producing bacteria, and TMAO; summarized the alternations in hypertensive patients and animals; discussed the mechanisms of TMAO with two respects; and summarized the regulatory factors may be as new interventions and therapies of hypertension. And, more relevant studies are still prospected to be accomplished between hypertension and TMA/TMAO for further clinical services.

The Gly-Asp-Ser-Leu (GDSL)-lipase family is a large subfamily of lipolytic enzymes that plays an important role in plant growth and defense against environmental stress. However, little is known about their function in pecans (Carya illinoensis K. Koch). In this study, 87 CilGDSLs were identified and divided into 2 groups and 12 subgroups using phylogenetic analysis; members of the same sub-branch had conserved gene structure and motif composition. The majority of the genes had four introns and were composed of an α-helix and a β-strand. Subcellular localization analysis revealed that these genes were localized in the extracellular matrix, chloroplasts, cytoplasm, nucleus, vacuole, and endoplasmic reticulum, and were validated by transient expression in tobacco mesophyll cells. Furthermore, the analysis of the promoter cis-elements for the CilGDSLs revealed the presence of plant anaerobic induction regulatory, abscisic acid response, light response elements, jasmonic acid (JA) response elements, etc. The qRT-PCR analysis results in “Pawnee” with salt treatment showed that the CilGDSL42.93 (leaf) and CilGDSL39.88 (root) were highly expressed in different tissues. After salt stress treatment, isobaric tags for relative and absolute quantitation (iTRAQ) analysis revealed the presence of a total of ten GDSL proteins. Moreover, the weighted gene co-expression network analysis (WGCNA) showed that one set of co-expressed genes (module), primarily CilGDSL41.11, CilGDSL39.49, CilGDSL34.85, and CilGDSL41.01, was significantly associated with salt stress in leaf. In short, some of them were shown to be involved in plant defense against salt stress in this study.

Background Nonobstructive azoospermia (NOA) is one of the most difficult forms of male infertility to treat, and its pathogenesis is still unclear. miRNAs can regulate autophagy by affecting their target gene expression. Our previous study found that miR-188-3p expression in NOA patients was low. There are potential binding sites between the autophagy gene ATG7 and miR-188-3p. This study aimed to verify the binding site between miR-188-3p and ATG7 and whether miR-188-3p affects autophagy and participates in NOA by regulating ATG7 to influence the autophagy marker genes LC3 and Beclin-1. Methods Testicular tissue from 16 NOA patients and 16 patients with normal spermatogenesis and 5 cases in each group of pathological sections were collected. High-throughput sequencing was performed to detect mRNA expression differences. Quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, immunohistochemical staining and immunofluorescence were used to detect protein localization and expression. Autophagosome changes were detected by electron microscopy. The targeting relationship between miR-188-3p and ATG7 was confirmed by a luciferase assay. Results ATG7 protein was localized in the cytoplasm of spermatogenic cells at all levels, and the ATG7 gene (p = 0.019) and protein (p = 0.000) were more highly expressed in the NOA group. ATG7 expression after overexpression/inhibition of miR-188-3p was significantly lower (p = 0.029)/higher (p = 0.021) than in the control group. After overexpression of miR-188-3p, the ATG7 3'UTR-WT luciferase activity was impeded (p = 0.004), while the ATG7 3'UTR-MUT luciferase activity showed no significant difference (p = 0.46). LC3 (p = 0.023) and Beclin-1 (p = 0.041) expression in the NOA group was significantly higher. LC3 and Beclin-1 gene expression after miR-188-3p overexpression/inhibition was significantly lower (p = 0.010 and 0.024, respectively) and higher (p = 0.024 and 0.049, respectively). LC3 punctate aggregation in the cytoplasm decreased after overexpression of miR-188-3p, while the LC3 punctate aggregation in the miR-188-3p inhibitor group was higher. The number of autophagosomes in the miR-188-3p mimic group was lower than the number of autophagosomes in the mimic NC group. Conclusions LC3 and Beclin-1 were more highly expressed in NOA testes and negatively correlated with the expression of miR-188-3p, suggesting that miR-188-3p may be involved in the process of autophagy in NOA. miR-188-3p may regulate its target gene ATG7 to participate in autophagy anDual luciferase experiment d affect the development of NOA.

Lipofuscin is an autofluorescent (AF) pigment formed by lipids and misfolded proteins that accumulates in post-mitotic cells with advanced age. Here we immunophenotyped microglia in the brain of old C57BL/6 mice (>18 months-old) and demonstrate that in comparison to young mice, one third of old microglia are AF, characterized by profound changes in lipid and iron content, phagocytic activity, and oxidative stress. Pharmacological depletion of microglia in old mice eliminated the AF microglia following repopulation and reversed microglial dysfunction. Age-related neurological deficits and neurodegeneration after traumatic brain injury (TBI) were attenuated in old mice lacking AF microglia. Furthermore, hyperphagocytic activity and lipid accumulation in microglia persisted for up to one year after TBI, were modified by Apoe4 genotype, and chronically driven by phagocyte-mediated oxidative stress. Thus, AF may reflect a pathological state in aging microglia associated with hyperphagocytosis and inflammatory neurodegeneration that can be further accelerated by TBI.TeaserTraumatic brain injury accelerates age-related pathological phagocytosis and lipofuscin formation in microglia.

Background Based on amyloid cascade and tau hypotheses, protein biomarkers of different Aβ and tau species in cerebrospinal fluid (CSF) and blood/plasma/serum have been examined to correlate with brain pathology. Recently, unbiased proteomic profiling of these human samples has been initiated to identify a large number of novel AD biomarker candidates, but it is challenging to define reliable candidates for subsequent large-scale validation. Methods We present a comprehensive strategy to identify biomarker candidates of high confidence by integrating multiple proteomes in AD, including cortex, CSF and serum. The proteomes were analyzed by the multiplexed tandem-mass-tag (TMT) method, extensive liquid chromatography (LC) fractionation and high-resolution tandem mass spectrometry (MS/MS) for ultra-deep coverage. A systems biology approach was used to prioritize the most promising AD signature proteins from all proteomic datasets. Finally, candidate biomarkers identified by the MS discovery were validated by the enzyme-linked immunosorbent (ELISA) and TOMAHAQ targeted MS assays. Results We quantified 13,833, 5941, and 4826 proteins from human cortex, CSF and serum, respectively. Compared to other studies, we analyzed a total of 10 proteomic datasets, covering 17,541 proteins (13,216 genes) in 365 AD, mild cognitive impairment (MCI) and control cases. Our ultra-deep CSF profiling of 20 cases uncovered the majority of previously reported AD biomarker candidates, most of which, however, displayed no statistical significance except SMOC1 and TGFB2. Interestingly, the AD CSF showed evident decrease of a large number of mitochondria proteins that were only detectable in our ultra-deep analysis. Further integration of 4 cortex and 4 CSF cohort proteomes highlighted 6 CSF biomarkers (SMOC1, C1QTNF5, OLFML3, SLIT2, SPON1, and GPNMB) that were consistently identified in at least 2 independent datasets. We also profiled CSF in the 5xFAD mouse model to validate amyloidosis-induced changes, and found consistent mitochondrial decreases (SOD2, PRDX3, ALDH6A1, ETFB, HADHA, and CYB5R3) in both human and mouse samples. In addition, comparison of cortex and serum led to an AD-correlated protein panel of CTHRC1, GFAP and OLFM3. In summary, 37 proteins emerged as potential AD signatures across cortex, CSF and serum, and strikingly, 59% of these were mitochondria proteins, emphasizing mitochondrial dysfunction in AD. Selected biomarker candidates were further validated by ELISA and TOMAHAQ assays. Finally, we prioritized the most promising AD signature proteins including SMOC1, TAU, GFAP, SUCLG2, PRDX3, and NTN1 by integrating all proteomic datasets. Conclusions Our results demonstrate that novel AD biomarker candidates are identified and confirmed by proteomic studies of brain tissue and biofluids, providing a rich resource for large-scale biomarker validation for the AD community.

Depression, anxiety and apathy are ‘common neuropsychiatric symptoms (NPS) in Alzheimer’s disease (AD). We aimed to find regional gray matter (GM) volume difference of these symptoms, in AD patients compared to AD control, and investigate possible associations of GM atrophy with cognitive covariant. Study subjects were retrieved from the Alzheimer’s Disease Neuroimaging Initiative database. Thirty-five participants are AD control, 27 AD patients with anxiety, 19 with depression and 24 with apathy, ages ≥ 55.1 years. Recruited subjects had an assessment of their clinical and structural MRI data. GM differences and clinical data were analyzed using voxel-based morphometry and ANOVA with Scheffe post hoc test, respectively. We found significant GM volumes differences in the left insula, left parahippocampal, posterior cingulate and the bilateral putamen in the anxiety group. The results also revealed that the right parahippocampal, Brodmann area 38 and the middle frontal gyrus were significant in patients with depression. Significant results were with a p

Chronic neuroinflammation with sustained microglial activation occurs following severe traumatic brain injury (TBI) and is believed to contribute to subsequent neurodegeneration and neurological deficits. Microglia, the primary innate immune cells in brain, are dependent on colony stimulating factor 1 receptor (CSF1R) signaling for their survival. In this preclinical study, we examined the effects of delayed depletion of chronically activated microglia on functional recovery and neurodegeneration up to 3 months postinjury. A CSF1R inhibitor, Plexxikon (PLX) 5622, was administered to adult male C57BL/6J mice at 1 month after controlled cortical impact to remove chronically activated microglia, and the inhibitor was withdrawn 1-week later to allow for microglial repopulation. Following TBI, the repopulated microglia displayed a ramified morphology similar to that of Sham uninjured mice, whereas microglia in vehicle-treated TBI mice showed the typical chronic posttraumatic hypertrophic morphology. PLX5622 treatment limited TBI-associated neuropathological changes at 3 months postinjury; these included a smaller cortical lesion, reduced hippocampal neuron cell death, and decreased NOX2- and NLRP3 inflammasome-associated neuroinflammation. Furthermore, delayed depletion of chronically activated microglia after TBI led to widespread changes in the cortical transcriptome and altered gene pathways involved in neuroinflammation, oxidative stress, and neuroplasticity. Using a variety of complementary neurobehavioral tests, PLX5622-treated TBI mice also had improved long-term motor and cognitive function recovery through 3 months postinjury. Together, these studies demonstrate that chronic phase removal of neurotoxic microglia after TBI using CSF1R inhibitors markedly reduce chronic neuroinflammation and associated neurodegeneration, as well as related motor and cognitive deficits.SIGNIFICANCE STATEMENTTraumatic brain injury (TBI) is a debilitating neurological disorder that can seriously impact the patient's quality of life. Microglial-mediated neuroinflammation is induced after severe TBI and contributes to neurological deficits and on-going neurodegenerative processes. Here, we investigated the effect of breaking the neurotoxic neuroinflammatory loop at 1-month after controlled cortical impact in mice by pharmacological removal of chronically activated microglia using a colony stimulating factor 1 receptor (CSF1R) inhibitor, Plexxikon 5622. Overall, we show that short-term elimination of microglia during the chronic phase of TBI followed by repopulation results in long-term improvements in neurological function, suppression of neuroinflammatory and oxidative stress pathways, and a reduction in persistent neurodegenerative processes. These studies are clinically relevant and support new concepts that the therapeutic window for TBI may be far longer than traditionally believed if chronic and evolving microglial-mediated neuroinflammation can be inhibited or regulated in a precise manner.

Building individual brain networks form the single volume of anatomical MRI is a challenging task. Furthermore, the high-order connectivity of morphological networks remains unexplored. This paper aimed to investigate the individual high-order morphological connectivity from anatomical MRI. Towards this goal, a unified framework based on six feature distances (euclidean, seuclidean, mahalanobis, cityblock, minkowski, and chebychev) was proposed to derive high-order interregional morphological features. The test-retest datasets and the healthy aging datasets were applied to analyze the reliability and the inter-subject variability of the novel features. In addition, the predictive models based on these novel features were established for age estimation. The proposed six neuroanatomical features exhibited significant high-to-excellent reliability. Certain connections were significantly correlated to biological age based on the six novel metrics (p .05, FDR corrected). Moreover, the predicted age were significantly correlated to the original age in each regression task (r 0.5, p 10

This study aimed at developing a radiomics signature (R score) as prognostic biomarkers based on penumbra quantification and to validate the radiomics nomogram to predict the clinical outcomes for thrombolysis for acute ischemic stroke (AIS) patients. In total, 168 patients collected from seven centers were retrospectively included. A score of mismatch was defined as MIS. Based on a short-term clinical label, 456 radiomics features were evaluated with feature selection methods. R score was constructed with the selected features. To compare the predictive capabilities of the clinical factors, MIS, and R score, three nomograms were developed and evaluated, according to the short-term clinical assessment on day 7. Finally, the radiomics nomogram was validated by predicting the 3-month clinical outcomes of AIS patients, in an external cohort. R scores were found to be significantly higher in patients with favorable clinical outcomes in both training and validation datasets. The predictive value of the radiomics nomogram estimating favorable clinical outcomes was modest, with a concordance index (C-index) of 0.695 [95% confidence interval (CI) 0.667–0.723) in an external validation dataset. In addition, the area under curve (AUC) of the radiomics nomogram predicting favorable clinical outcome reached 0.886 (95% CI 0.809–0.963) on day 7 and 0.777 (95% CI 0.666–0.888) at 3 months. The radiomics signature is an independent biomarker for estimating the clinical outcomes in AIS patients. By improving the individualized prediction of the clinical outcome for AIS patients 3 months after onset, the radiomics nomogram adds more value to the current clinical decision-making process.

The aim of this study was to investigate the influence of microwave drying on the protein quality of japonica sorghum following an intermittent drying test. Using label-free technology and liquid chromatography-tandem mass spectrometry for proteomic analysis, the effects of microwave drying on sorghum differential protein expression, functional classification, and metabolic pathways were analyzed at the molecular level. After sorghum was dried using a microwave, 85 differential proteins were identified. Among them, 51 showed up-regulated expression while 34 had down-regulated expression. The up-regulation and down-regulation of differential protein expressions significantly changed them, and proteins with larger up-regulated and down-regulated expressions were postulated to affect biological and metabolic processes of sorghum during subsequent processing. Differential proteins were significantly (P ˂ 0.01) involved in metabolic pathways, such as carbon metabolism, glycolysis/gluconeogenesis, carbon fixation in photosynthetic organisms, biosynthesis of amino acids, amino sugar and nucleotide sugar metabolism, and the TCA cycle. For the protein interaction network, glyceraldehyde-3-phosphate dehydrogenase of the down-regulated proteins was postulated to be the key factor affecting the entire metabolic system or signal transduction pathway. Up-regulated proteins, including phosphoglycerate mutase and phosphopyruvate hydratase, as well as down-regulated proteins such as glyceraldehyde-3-phosphate dehydrogenase and fructose-bisphosphate aldolase, not only directly or indirectly affected a variety of metabolic processes, but were specifically closely related to glycolysis and glycometabolism. Overall, this study showed that among the related metabolic pathways, differential protein changes in glycometabolism pathways may have the greatest impact on metabolic processes. The research results discussed herein can provide theoretical support for the industrial application of microwave drying and deep processing of sorghum.

The complete chloroplast (cp) genome of Crassocephalum crepidioides was sequenced and assembled for the first time. In this study, the total genome size is 150,596 bp in length and demonstrates a typical quadripartite structure containing a large single copy (LSC, 82,575 bp) and a small single copy (SSC, 18,293 bp), separated by a pair of inverted repeats (IRa, IRb) of 24,864 bp. The G + C content of this cp genome was 37.21%. Gene annotation analysis identified 130 genes including 85 protein-coding genes, 37 transfer RNA, and 8 ribosomal RNA genes. The maximum-likelihood phylogenetic analysis result showed that C. crepidioides was closely related to Nannoglottis ravida in the phylogenetic relationship.

Antigen presenting cells (APCs) have been extensively studied for treating cancers and autoimmune diseases. Dendritic cells (DCs) are potent APCs that uptake and present antigens (Ags) to activate immunity or tolerance. Despite their active use in cellular immunotherapies, DCs face several challenges that hinder clinical translation, such as inability to control Ag dosing for tuning immune responses and low abundance in peripheral blood. B cells are a potential alternative to DCs, but their poor non-specific Ag uptake capabilities compromise controllable priming of T cells. We developed phospholipid-conjugated Ags (L-Ags) and lipid-polymer hybrid nanoparticles (L/P-Ag NPs) as Ag delivery platforms to expand the range of accessible APCs for use in priming CD4+and CD8+T cells. These delivery platforms were evaluated using DCs, CD40-activated B cells, and resting B cells as a diverse set of APCs to understand the impact of various Ag delivery mechanisms for generation of Ag-specific T cell responses. L-Ag delivery (termed depoting) of MHC class I and II-restricted Ags successfully loaded all APC types in a tunable manner and primed both Ag-specific CD8+and CD4+T cells, respectively. Incorporating L-Ags and polymer-conjugated Ags (P-Ag) into NPs can direct Ags to different uptake pathways to engineer the dynamics of presentation and shape T cell responses. DCs were capable of processing and presenting Ag delivered from both L- and P-Ag NPs yet B cells could only utilize Ag delivered from L-Ag NPs. Multivariate analysis of cytokines secreted from APC:T cell co-cultures indicated that L-Ag NPs primed different T cell responses than P-Ag NPs. Altogether, we show that L-Ags and P-Ags can be rationally paired within a single NP to leverage distinct delivery mechanisms to access multiple Ag processing pathways in two APC types, offering a modular delivery platform for engineering immunotherapies.

Mass spectrometry (MS) has become a mainstream platform for comprehensive profiling of proteome, especially with the improvement of multiplexed tandem mass tag labeling coupled with two-dimensional liquid chromatography and tandem mass spectrometry (TMT-LC/LC-MS/MS). Recently, we have established a robust method for direct profiling of undepleted cerebrospinal fluid (CSF) proteome with the 16-plex TMTpro method, in which we optimized parameters in experimental steps of sample preparation, TMT labeling, LC/LC fractionation, tandem mass spectrometry, and computational data processing. The extensive LC fractionation not only enhances proteome coverage of the CSF but also alleviates ratio distortion of TMT quantification. The crucial quality control steps and improvements specific for the TMT16 analysis are highlighted. More than 3000 proteins can be quantified in a single experiment from 16 different CSF samples. This multiplexed method offers a powerful tool for profiling a variety of complex biofluids samples such as CSF, serum/plasma, and other clinical specimens.

Background: Myocardial infarction (MI) is closely related to heart failure and death. Cardiac fibrosis after MI is related to profound changes in cardiac structure and geometry, leading to decreased cardiac function. Unfortunately, effective therapies to prevent excessive cardiac fibrosis and improve cardiac function are limited. Consequently, new therapeutic strategies are urgently required to protect cardiac function after MI. Bakuchiol (BAK), extracted from the plant seeds of Psoralea corylifolia, has shown protective effects against pathological cardiac hypertrophy. However, it is unclear whether BAK could improve cardiac function and reduce cardiac fibrosis. Objective: To assess the reportability of bakuchiol as an alternative treatment against adverse cardiac remodeling after myocardial infarction. Methods: To address this question, a MI model was built on adult wild-type C57/BL 6N mice (male, 6–8 weeks, Zhejiang Vital River Laboratory Animal Technology Co., Ltd) by left coronary artery ligation and gavage with BAK (60 mg/kg/day) for 28 consecutive days. Chest cardiac ultrasonography was performed 7 and 28 days after MI using the Vevo 2100 system to assess ventricular shape and function in model mice. The effects of BAK on cardiac remodeling and function were assessed after MI. Effects of BAK on isoprenaline-induced cardiac fibroblast proliferation and migration were also studied. Results: ABAK can attenuate adverse cardiac remodeling and maintain left ventricular ejection fraction and fraction shortening. Furthermore, mice treated with BAK a showed lower fibrosis and wider left ventricular thickness than those without BAK. In addition, BAK can inhibit cardiac myofibroblast differentiation after MI. After stimulation with isoprenaline, BAK inhibited cardiac fibroblast proliferation and migration. At the molecular level, extracellular signal-regulated kinase 2 (ERK2) and transforming growth factor (TGF)-β1 were inhibited in both MI mice and isoprenaline-stimulated cardiac fibroblasts after BAK treatment. Conclusions: Our data suggest that BAK treatment, as a novel therapeutic strategy, protects against adverse cardiac remodeling and maintains cardiac function after MI, likely via the ERK2 and TGF-β1 signaling pathways. [Ethiop. J. Health Dev. 2021; 35(3):208-219] Key Words：Bakuchiol, myocardial infarction, cardiac fibrosis, cardiac fibroblast, ERK2, TGF-β1

The negative effects of waterlogging can be effectively improved through the use of waterlogging-resistant rootstocks. However, the underlying physiological and molecular mechanisms of Chinese bayberry (Morella rubra) rootstock tolerance to waterlogging have not yet been investigated. This study aims to unravel the molecular regulation mechanisms underlying waterlogging-tolerant rootstocks. Two rootstocks, Morella cerifera (tolerant) and Morella rubra (sensitive), were selected for root zone hypoxia treatments, assessments of hormone levels and antioxidant enzyme activity, and transcriptomic analysis. While the contents of abscisic acid (ABA) and brassinosteroid (BR) in the roots of M. rubra decreased significantly after root zone hypoxia treatment, there were no significant changes in M. cerifera. Both the superoxide dismutase (SOD) activity and malondialdehyde (MDA) content increased in M. cerifera but were decreased in M. rubra. Transcriptome sequencing identified 1,925 (928 up- and 997 downregulated) and 733 (278 up- and 455 downregulated) differentially expressed genes (DEGs) in the two rootstocks. The gene set enrichment analysis showed that 84 gene sets were enriched after root zone hypoxia treatment, including 57 (35 up- and 22 downregulated) and 14 (five up- and nine downregulated) gene sets derived from M. cerifera and M. rubra, respectively, while the remaining 13 gene sets were shared. KEGG pathway analysis showed specific enrichment in six pathways in M. cerifera, including the mitogen-activated protein kinase (MAPK), tyrosine metabolism, glycolysis/gluconeogenesis, ribosome, cyanoamino acid metabolism, and plant-pathogen interaction pathways. Overall, these results provide preliminary insights into the molecular mechanisms of Chinese bayberry tolerance to waterlogging.

Levels of type 2 cytokines are elevated in the blood and intestinal tissues of ulcerative colitis (UC) patients in the active phase; this phenomenon indicates the participation of type 2 immune response in UC progression. The beneficial effects of melatonin in dextran sodium sulfate (DSS) and 2,4,6-trinitrobenzene sulfonic acid (TNBS) colitis models have been illustrated, but its role in the oxazolone (Oxa)-induced colitis model (driven by type 2 immune response) remains relatively unknown. We investigated the relationship between melatonin concentration and the severity of UC, revealing a significantly negative correlation. Subsequently, we investigated the effects of melatonin in Oxa-induced colitis mice and the potential underlying mechanisms. Administration of melatonin significantly counteracted body weight loss, colon shortening, and neutrophil infiltration in Oxa-induced colitis mice. Melatonin treatment mitigated Oxa-induced colitis by suppressing type 2 immune response. In addition, melatonin attenuated intestinal permeability by enhancing the expression of ZO-1 and occludin in colitis mice. Interestingly, the protective effect of melatonin was abolished when the mice were co-housed, indicating that the regulation of gut microbiota by melatonin was critical in alleviating Oxa-induced colitis. Subsequently, 16S rRNA sequencing was performed to explore the microbiota composition. Decreased richness and diversity of intestinal microbiota at the operational taxonomic unit (OTU) level resulted from melatonin treatment. Melatonin also elevated the abundance of Bifidobacterium, a well-known probiotic, and reduced proportions of several harmful bacterial genera, such as Desulfovibrio, Peptococcaceae, and Lachnospiraceae. Fecal microbiota transplantation (FMT) was used to explore the role of microbiota in the function of melatonin in Oxa-induced colitis. Microbiota transplantation from melatonin-treated mice alleviated Oxa-induced colitis, suggesting that the microbiome participates in the relief of Oxa-induced colitis by melatonin. Our findings demonstrate that melatonin ameliorates Oxa-induced colitis in a microbiota-dependent manner, suggesting the therapeutic potential of melatonin in treating type 2 immunity-associated UC.

To investigate the differentiation of regulatory T cells (Tregs) induced by methylprednisolone (MP) pulse therapy in patients with Systemic Lupus Erythematosus (SLE).We enrolled 30 patients with SLE and analyzed peripheral blood mononuclear cells (PBMCs) before and after MP pulse therapy. Peripheral Tregs, apoptosis of PBMCs subsets, and TGFβ production by monocytes was quantified by flow cytometry. Proliferation and IFN-γ production of CD4Peripheral Tregs was significantly increased after MP pulse therapy (6.76 ± 1.46% vs. 3.82 ± 1.02%, p 0.01), with an expansion of Nrp1MP pulse therapy induces CD4

Objective To investigate the clinical features of multicentric reticulohistiocytosis (MRH). Methods The clinical manifestations, laboratory examination results and histologic characteristics of eleven patients with MRH were collected and compared with those of 33 patients with rheumatoid arthritis. Results In total, 72.7% of the MRH patients were women. The median age was 46 years (range 33–84 years). Diagnosed by specific pathologic features, all MRH patients exhibited cutaneous involvement. The dorsa of the hands, arms, face and auricle were the most commonly affected areas. Nodules were also located on the legs, scalp, trunk, neck, and even the hypoglossis and buccal mucosa. Ten MRH patients (90.9%) had symmetric polyarthritis. Compared with rheumatoid arthritis (RA) patients, MRH patients were more likely to have distal interphalangeal joint (DIP) involvement (63.6% vs 24.2%, P = 0.017) and less likely to have elbow (36.4% vs 72.7%, P = 0.003), ankle (45.5% vs 93.9%, P P = 0.009) involvement. Positivity for rheumatoid factor (RF) (36.4% vs 84.6%, P = 0.001) and anti-CCP antibody (9.1% vs 81.8%, P = 0.000), as well as the median RF titer [43.8 (31.7–61.0) vs 175.4 (21.3–940.3), P = 0.021], in MRH patients was lower than in RA patients. Elevation of the erythrocyte sedimentation rate (ESR) was also less common in MRH patients than in RA patients (36.4% vs 72.7%, P = 0.030). After treatment with median- to large-dose corticosteroids and disease-modifying antirheumatic drugs, 8 patients achieved complete remission and 2 patients partial remission (skin lesions ameliorated, joint lesions not ameliorated). Conclusion Always pathologically diagnosed, MRH is a systemic disease involving RA-like erosive polyarthritis and a specific distribution of skin nodules characterized by "coral beads". More DIP involvement and less elbow, ankle and MCP involvement are seen in MRH than in RA. In addition, less positivity and lower-titer RF, uncommon presence of anti-CCP antibodies and ESR elevation may be helpful to distinguish MRH from RA.

Vinylpyrazine compounds are widely present in foods, especially in hot-processed foods, as a class of flavor compounds; however, their formation mechanism in food systems is still unclear. Therefore, in this study, 2-vinylpyrazine and 2-vinyl-6-methylpyrazine were identified in the Maillard model reaction of D-glucose and glycine. The Maillard model reaction of glucose–glycine was constructed to explore the effects of reaction parameters on vinylpyrazines and the related products. The Maillard reaction of [U-13C6] glucose and glycine was established, and alkylpyrazines and formaldehyde were determined via isotope tracing technique as the precursors of vinylpyrazines. The formation of vinylpyrazines was verified by building a model reaction between alkylpyrazines and formaldehyde. The H/D exchange experiment confirmed that the active site of alkylpyrazines was on the methyl group, which was the reaction site for the condensation reaction of alkylpyrazines with formaldehyde. Results suggest that vinylpyrazines are formed by the condensation reaction of alkylpyrazines and formaldehyde.

It is expected, the growing demand for supercapacitor energy storage system (ESS) in which thousands of supercapacitor cells are connected as a stack for meeting the desired load power. The lifetime of ESS dramatically depends on the operating thermal effects of individual cells. In this paper, a temperature-suppression charging strategy is proposed for supercapacitor ESS to maximize its lifetime. First, the charging current and equivalent series resistance (ESR) construct the supercapacitor thermal model, and the ESR represents the degradation degree of the supercapacitor. Second, the maximization of system lifetime and equalization of unit degradation degree jointly form a convex optimization problem with the charging time constraint. The optimization problem is solved to obtain the equivalent charging current, which is realized through pulse width modulation (PWM) digital control. Simulation and experimental results show that the proposed method has the advantages of reducing ESS operating temperature and maximizing its lifetime.

In the hybrid energy storage system of electric vehicles, the main objective is to guarantee that the dc-bus voltage tracks the desired set point quickly and accurately. However, it is typically difficult for existing methods to provide both short settling time and small overshoot, which results in significant dc-bus voltage fluctuations. To address this issue, in this paper, we propose a predictive-set-point-modulation-based energy management control strategy. A lead-compensator-based predictive set-point modulation method is designed and integrated in the voltage control loop to improve the response speed. Theoretical analysis is carried out for the energy management system, and an explicit expression of the control parameters is derived. Moreover, an adaptive cutoff-frequency-based power allocation approach is proposed to guarantee that supercapacitors (SCs) can provide sustainable power supply in the long term. A laboratory testbed is built to verify the effectiveness of the proposed method. Experiment results show that the proposed method provides a lower dc-bus voltage fluctuation, higher SC capacity utilization, and a better protection for batteries, when compared with the conventional method.