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Light-Burned Magnesia (LBM) activated Ground Granulated Blast Furnace Slag (GGBS) is established as a promising and robust binder for soil stabilization. However, its durability in saline environments subjected to freeze-thaw (F-T) cycles lacks systematic investigation. To validate its potential for subgrade engineering in seasonally frozen regions, this study evaluates the mechanical and microscopic properties of LBM-GGBS solidified saline soil under F-T cycling. The effects of LBM and GGBS on the unconfined compressive strength (UCS), permeability coefficient, Cl − leaching and microstructures of solidified saline soil after different F-T cycles (0, 2, 4, 6, 8, and 10) were examined. The results showed that increasing the LBM-GGBS content significantly enhanced the soil’s resistance to F-T cycles. With a 12% LBM-GGBS content and a GGBS/LBM ratio of 7 (determined as the optimal mix proportion), the solidified soil reached a residual strength of 3 MPa after 10 F-T cycles, which was four times the strength required for the upper base layer of highway pavement subgrade. Microscopic analysis revealed that the LBM-GGBS solidified soil exhibited a dense structure with calcium silicate hydrate (C-S-H), magnesium silicate hydrate (M-S-H), hydrotalcite, and Kuzel salt as the primary reaction products. The formation of these hydration products significantly densified the structure, thereby increasing the strength and improving the F-T resistance of the solidified soil. Furthermore, ~ 75% of Cl − in the original saline soil could be stabilized even after multiple F-T cycles. These findings elucidate the micro-mechanism of chloride stabilization under freezing conditions and provide a robust theoretical foundation for utilizing LBM-GGBS to mitigate saline soil hazards in seasonally frozen regions.

The aim of this study was to compare the microbial community structure and diversity in powdery mildew-infected and noninfected strawberry plant rhizosphere soils in the greenhouse based on variations in the 16S rRNA gene V3–V4 and fungal ITS2 regions by Illumina amplicon sequencing. Powdery mildew infection reduced the number of operational taxonomic units (OTUs) and prokaryotic and fungal community richness/diversity indexes in the rhizosphere soils compared with those in healthy plant soils. Furthermore, 3543 prokaryotic and 581 fungal OTUs were obtained at the 97% similarity level. Proteobacteria, Actinobacteria, Bacteroidetes, Acidobacteria, and Chloroflexi were the dominant bacterial phyla; Woesearchaeota_DHVEG-6, Bathyarchaeota, and Thaumarchaeota were the dominant archaea; and Ascomycota, Basidiomycota, unclassified_fungi, and Zygomycota were the dominant fungal phyla. Their proportions differed significantly among samples. Wolbachia, Devosia, Pseudolabrys, Streptomyces, and Rhizomicrobium were the most abundant bacterial genera; their proportions differed significantly among samples. Most Pseudomonas, Streptomyces, and ‘norank’ group members might be potential antagonistic microorganisms of powdery mildew pathogens, and Wolbachia and Rickettsia might be pathogen-transmitting vectors. Microascus, Clitopilus, and Ciliophora were the dominant fungi, and their community structures and abundances significantly differed among samples. Microascus, Talaromyces, Zopfiella, and Cryptococcus were relatively more abundant in the powdery mildew-infected strawberry plant rhizosphere soils. Fusarium, Trichoderma, Clitopilus, and ‘unclassified’ group members may be potential antagonistic populations. The results suggested that powdery mildew-infected strawberry fruits and plants cannot be consumed. This report is the first study to illustrate differences in the rhizosphere soil prokaryotic and fungal communities between powdery mildew-infected and noninfected strawberry plants in a greenhouse.

Mild traumatic brain injury (mTBI) induced by low-intensity blast (LIB) is a serious health problem affecting military service members and veterans. Our previous reports using a single open-field LIB mouse model showed the absence of gross microscopic damage or necrosis in the brain, while transmission electron microscopy (TEM) identified ultrastructural abnormalities of myelin sheaths, mitochondria, and synapses. The neurovascular unit (NVU), an anatomical and functional system with multiple components, is vital for the regulation of cerebral blood flow and cellular interactions. In this study, we delineated ultrastructural abnormalities affecting the NVU in mice with LIB exposure quantitatively and qualitatively. Luminal constrictive irregularities were identified at 7 days post-injury (DPI) followed by dilation at 30 DPI along with degeneration of pericytes. Quantitative proteomic analysis identified significantly altered vasomotor-related proteins at 24 h post-injury. Endothelial cell, basement membrane and astrocyte end-foot swellings, as well as vacuole formations, occurred in LIB-exposed mice, indicating cellular edema. Structural abnormalities of tight junctions and astrocyte end-foot detachment from basement membranes were also noted. These ultrastructural findings demonstrate that LIB induces multiple-component NVU damage. Prevention of NVU damage may aid in identifying therapeutic targets to mitigate the effects of primary brain blast injury.

Traumatic brain injury (TBI) is a leading cause of death and long-term disability. Following the initial insult, severe TBI progresses to a secondary injury phase associated with biochemical and cellular changes. The secondary injury is thought to be responsible for the development of many of the neurological deficits observed after TBI and also provides a window of opportunity for therapeutic intervention. Matrix metalloproteinase-9 (MMP-9 or gelatinase B) expression is elevated in neurological diseases and its activation is an important factor in detrimental outcomes including excitotoxicity, mitochondrial dysfunction and apoptosis, and increases in inflammatory responses and astrogliosis. In this study, we used an experimental mouse model of TBI to examine the role of MMP-9 and the therapeutic potential of SB-3CT, a mechanism-based gelatinase selective inhibitor, in ameliorating the secondary injury. We observed that activation of MMP-9 occurred within one day following TBI, and remained elevated for 7 days after the initial insult. SB-3CT effectively attenuated MMP-9 activity, reduced brain lesion volumes and prevented neuronal loss and dendritic degeneration. Pharmacokinetic studies revealed that SB-3CT and its active metabolite, p-OH SB-3CT, were rapidly absorbed and distributed to the brain. Moreover, SB-3CT treatment mitigated microglial activation and astrogliosis after TBI. Importantly, SB-3CT treatment improved long-term neurobehavioral outcomes, including sensorimotor function, and hippocampus-associated spatial learning and memory. These results demonstrate that MMP-9 is a key target for therapy to attenuate secondary injury cascades and that this class of mechanism-based gelatinase inhibitor-with such desirable pharmacokinetic properties-holds considerable promise as a potential pharmacological treatment of TBI.

Background Cerebral ischemia has been shown to induce activation of matrix metalloproteinases (MMPs), particularly MMP-9, which is associated with impairment of the neurovasculature, resulting in blood–brain barrier breakdown, hemorrhage and neurodegeneration. We previously reported that the thiirane inhibitor SB-3CT, which is selective for gelatinases (MMP-2 and −9), could antagonize neuronal apoptosis after transient focal cerebral ischemia. Results Here, we used a fibrin-rich clot to occlude the middle cerebral artery (MCA) and assessed the effects of SB-3CT on the neurovasculature. Results show that neurobehavioral deficits and infarct volumes induced by embolic ischemia are comparable to those induced by the filament-occluded transient MCA model. Confocal microscopy indicated embolus-blocked brain microvasculature and neuronal cell death. Post-ischemic SB-3CT treatment attenuated infarct volume, ameliorated neurobehavioral outcomes, and antagonized the increases in levels of proform and activated MMP-9. Embolic ischemia caused degradation of the neurovascular matrix component laminin and tight-junction protein ZO-1, contraction of pericytes, and loss of lectin-positive brain microvessels. Despite the presence of the embolus, SB-3CT mitigated these outcomes and reduced hemorrhagic volumes. Interestingly, SB-3CT treatment for seven days protected against neuronal laminin degradation and protected neurons from ischemic cell death. Conclusion These results demonstrate considerable promise for the thiirane class of selective gelatinase inhibitors as potential therapeutic agents in stroke therapy.

Quantitative assessment of serial brain sections provides an objective measure of neurological events at cellular and molecular levels but is difficult to implement in experimental neuroscience laboratories because of variation from person-to-person and the time required for analysis. Whole slide imaging (WSI) technology, recently introduced for pathological diagnoses, offers an electronic environment and a variety of computational tools for performing high-throughput histological analysis and managing the associated information. In our study, we applied various algorithms to quantify histologic changes associated with brain injury and compared the results to manual assessment. WSI showed a high degree of concordance with manual quantitation by Pearson correlation and strong agreement using Bland-Altman plots in: (i) cortical necrosis in cresyl-violet-stained brain sections of mice after focal cerebral ischemia; (ii) intracerebral hemorrhage in ischemic mouse brains for automated annotation of the small regions, rather than whole hemisphere of the tissue sections; (iii) Iba1-immunoreactive cell density in the adjacent and remote brain regions of mice subject to controlled cortical impact (CCI); and (iv) neuronal degeneration by silver staining after CCI. These results show that WSI, when appropriately applied and carefully validated, is a highly efficient and unbiased tool to locate and identify neuropathological features, delineate affected regions and histologically quantify these events.

Based on 243 current valid distribution records for six wild strawberry species in China and data on 20 environmental variables, the geographical distributions of and potentially suitable areas for the wild strawberry species in Yunnan Province (China) under the current climate scenario were explored using the MaxEnt model and ArcGIS software, and major environmental variables affecting their geographical distributions were evaluated. In addition, the spatio-temporal dynamic patterns of the suitable areas for the six wild strawberry species in Yunnan Province in the 2050s and 2070s under the two climate models of RCP2.6 and RCP8.5 were predicted. Under the current climate scenario, the six wild strawberry species have suitable areas in Yunnan Province, which were mainly distributed in the high-altitude and low-temperature regions in the northwest and northeast, such as Diqing and Zhaotong. In addition, the average size of the highly suitable area for diploid wild strawberry species was greater than that for tetraploid species. Under the future climate scenarios, the average size of the highly suitable area for diploid species showed a tendency to expand, while that of tetraploid species showed a tendency to shrink. Altitude was a critical variable affecting the distribution of tetraploid species. Under the two future climate models of RCP2.6 and RCP8.5, the suitable areas for wild strawberry species shifted to the regions of high latitude, high altitude, and low temperature. In addition, the average distance in the shift of the suitable area for tetraploid strawberry species was greater than that for the suitable area for diploid strawberry species. The above results provide valuable information for the management and protection of the germplasm resources of Fragaria.

Excessive activation of gelatinases (MMP-2/-9) is a key cause of detrimental outcomes in neurodegenerative diseases. A single-dimension zymography has been widely used to determine gelatinase expression and activity, but this method is inadequate in resolving complex enzyme isoforms, because gelatinase expression and activity could be modified at transcriptional and posttranslational levels. In this study, we investigated gelatinase isoforms under in vitro and in vivo conditions using two-dimensional (2D) gelatin zymography electrophoresis, a protocol allowing separation of proteins based on isoelectric points (pI) and molecular weights. We observed organomercuric chemical 4-aminophenylmercuric acetate-induced activation of MMP-2 isoforms with variant pI values in the conditioned medium of human fibrosarcoma HT1080 cells. Studies with murine BV-2 microglial cells indicated a series of proform MMP-9 spots separated by variant pI values due to stimulation with lipopolysaccharide (LPS). The MMP-9 pI values were shifted after treatment with alkaline phosphatase, suggesting presence of phosphorylated isoforms due to the proinflammatory stimulation. Similar MMP-9 isoforms with variant pI values in the same molecular weight were also found in mouse brains after ischemic and traumatic brain injuries. In contrast, there was no detectable pI differentiation of MMP-9 in the brains of chronic Zucker obese rats. These results demonstrated effective use of 2D zymography to separate modified MMP isoforms with variant pI values and to detect posttranslational modifications under different pathological conditions.

Background Traumatic brain injury (TBI) accelerates risk for multiple Alzheimer's Disease and Related Dementias (ADRDs) featuring Tau protein hyperphosphorylation and tauopathy. Mild TBI (mTBI) causes a temporary disruption of brain function typically caused by blast, blow, or jolt to the head. While many individuals recover fully within a few weeks or months, some may experience long‐term cognitive deficits, but how TBI progresses to ADRDs including tauopathies remains complex and elusive. The present study identified the combinations of risk genes and timing of mTBI induced by open‐field blasts (OFB) that alter candidate fluid and imaging biomarkers involved, so that making early intervention possible to prevent or delay the progression of ADRD. Method human wild‐type Tau/CamKII bitransgenic (rT1) and Non‐carrier/non‐carrier mice were assigned randomly into two groups: OFB‐induced repetitive mTBI and sham control and evaluated for transgene and TBI‐dependent behavioral deficits at 3 months post‐injury. The brain tissues were collected for proteomics studies using high‐resolution label‐free global and phospho‐proteomics by liquid chromatography coupled with tandem mass spectrometry, followed by A.I. informed phenomic analysis integrating behavioral‐related proteomic datasets with human databases. Immunoblotting validated selected phenomics findings. Result We identified co‐expression subnetworks that were strongly correlated with PTSD‐like behavioral endophenotypes in humans including psychomotor agitation, fear response, and physical activity in rT1 mice following OFB‐induced repetitive mTBI. Biologically‐informed neural networks (BINN)‐enhanced eXplainable Artificial Intelligence (XAI) analysis of the differential expression (DE) profiles in human ADRD cohorts that differentiate symptomatic CTE and AD from asymptomatic AD and age‐matched human controls, identified overlapping networks in both mouse and human studies. Key proteins that regulate synaptic vesicle cycling, synaptic plasticity, and energy metabolism displayed DE in rT1 mice as a function of tau transgene and TBI interactions and drivers to accelerate their trajectory towards ADRD. Several of the TBI‐triggered DE proteins (YWHAG or 14‐3‐3 γ, HNRNPA2B1, and hexokinase), overlapped reported phosphoTau and Tau oligomer interactomes with proposed causal roles in metabolic deficits and neurodegeneration. Conclusion This study unveiled ADRD predictable converging molecular signatures that appear to drive the Tau‐TBI interaction conferring both chronic neuropsychiatric impairments and neurodegenerative disease progression, shedding light on the complex etiology of ADRD.

Traumatic brain injury (TBI) accelerates risk for multiple Alzheimer's Disease and Related Dementias (ADRDs) featuring Tau protein hyperphosphorylation and tauopathy. Mild TBI (mTBI) causes a temporary disruption of brain function typically caused by blast, blow, or jolt to the head. While many individuals recover fully within a few weeks or months, some may experience long-term cognitive deficits, but how TBI progresses to ADRDs including tauopathies remains complex and elusive. The present study identified the combinations of risk genes and timing of mTBI induced by open-field blasts (OFB) that alter candidate fluid and imaging biomarkers involved, so that making early intervention possible to prevent or delay the progression of ADRD. human wild-type Tau/CamKII bitransgenic (rT1) and Non-carrier/non-carrier mice were assigned randomly into two groups: OFB-induced repetitive mTBI and sham control and evaluated for transgene and TBI-dependent behavioral deficits at 3 months post-injury. The brain tissues were collected for proteomics studies using high-resolution label-free global and phospho-proteomics by liquid chromatography coupled with tandem mass spectrometry, followed by A.I. informed phenomic analysis integrating behavioral-related proteomic datasets with human databases. Immunoblotting validated selected phenomics findings. We identified co-expression subnetworks that were strongly correlated with PTSD-like behavioral endophenotypes in humans including psychomotor agitation, fear response, and physical activity in rT1 mice following OFB-induced repetitive mTBI. Biologically-informed neural networks (BINN)-enhanced eXplainable Artificial Intelligence (XAI) analysis of the differential expression (DE) profiles in human ADRD cohorts that differentiate symptomatic CTE and AD from asymptomatic AD and age-matched human controls, identified overlapping networks in both mouse and human studies. Key proteins that regulate synaptic vesicle cycling, synaptic plasticity, and energy metabolism displayed DE in rT1 mice as a function of tau transgene and TBI interactions and drivers to accelerate their trajectory towards ADRD. Several of the TBI-triggered DE proteins (YWHAG or 14-3-3 γ, HNRNPA2B1, and hexokinase), overlapped reported phosphoTau and Tau oligomer interactomes with proposed causal roles in metabolic deficits and neurodegeneration. This study unveiled ADRD predictable converging molecular signatures that appear to drive the Tau-TBI interaction conferring both chronic neuropsychiatric impairments and neurodegenerative disease progression, shedding light on the complex etiology of ADRD.