Improved value and carbon footprint by complete utilization of corncob lignocellulose

Lignocellulose, as the most abundant type of inedible biomass, is considered as a promising renewable feedstock for making fuels, chemicals, and materials. However, its complex structure makes most of current biorefinery processes suffer from low resource utilization rates, high energy consumption or ill-defined market orientation of the obtained products. Here, we propose and evaluate the EXA (Ethanol, Xylose, Adhesive) biorefinery strategy based on current xylose industry. This process integrates four conversion and separation stages to consecutively produce ethanol, xylose, and adhesive with total carbon utilization of 79.6%. The key innovation is the establishment of an easy-to-operate process for direct production of high-quality adhesive from a lignin-rich liquid fraction that makes the overall process significantly more sustainable. Techno-economic analysis (TEA) shows that the revenue of proposed EXA process increases more than 110 times compares with the current process and life cycle assessment (LCA) demonstrates a much lower CO2 footprint from an environmental burden per unit of revenue perspective

Simplified Attitude Determination Algorithm Using Accelerometer and Magnetometer with Extremely Low Execution Time

Accelerometer-magnetometer attitude determination is a common and vital medium processing technique in industrial robotics and consumer electronics. In this paper, we report a novel analytic attitude solution to the accelerometer-magnetometer combination in the sense of Wahba’s problem. The Davenport matrix is analytically given and its eigenvalues are computed. Through derivations, the eigenvalues are simplified to very short expressions. Then, the corresponding eigenvectors are given accordingly via matrix row operations. The system is highly optimized based on the factorization and simplification of the obtained row-echelon form, which makes it computationally fast in practice. In this way, it is named as the fast accelerometer-magnetometer combination (FAMC). Experiments on the correctness and advantages of the proposed solution are conducted. The results show that compared with conventional solutions, the proposed analytic solution is not only correct and accurate, but to our knowledge, the most time efficient as well

The impact of masticatory dysfunction caused by occlusal disharmony on cognitive function

As the world’s population ages, age-related cognitive decline and dementia are becoming important challenges for geriatric care. Despite the ongoing search for solutions to address cognitive decline, effective interventions have not yet been established. There is increasing evidence from clinical, epidemiological, and animal studies that masticatory dysfunction due to occlusal disharmony is a risk factor for cognitive decline and an increased incidence of dementia. The mechanisms may involve altered nutritional intake, decreased cerebral blood flow, chronic stress, and hippocampal morphological function. These findings suggest that maintaining and adequately restoring the entire masticatory system has a positive impact for the prevention of cognitive decline

CypD induced ROS output promotes intracranial aneurysm formation and rupture by 8-OHdG/NLRP3/MMP9 pathway

Reactive Oxygen Species (ROS) are widely accepted as a pernicious factor in the progression of intracranial aneurysm (IA), which is eminently related to cell apoptosis and extracellular matrix degradation, but the mechanism remains to be elucidated. Recent evidence has identified that enhancement of Cyclophilin D (CypD) under stress conditions plays a critical role in ROS output, thus accelerating vascular destruction. However, no study has confirmed whether cypD is a detrimental mediator of cell apoptosis and extracellular matrix degradation in the setting of IA development. Our data indicated that endogenous cypD mRNA was significantly upregulated in human IA lesions and mouse IA wall, accompanied by higher level of ROS, MMPs and cell apoptosis. CypD−/− remarkably reversed vascular smooth muscle cells (VSMCs) apoptosis and elastic fiber degradation, and significantly decreased the incidence of aneurysm and ruptured aneurysm, together with the downregulation of ROS, 8-OHdG, NLRP3 and MMP9 in vivo and vitro. Furthermore, we demonstrated that blockade of cypD with CsA inhibited the above processes, thus preventing IA formation and rupture, these effects were highly dependent on ROS output. Mechanistically, we found that cypD directly interacts with ATP5B to promote ROS release in VSMCs, and 8-OHdG directly bind to NLRP3, which interacted with MMP9 to increased MMP9 level and activity in vivo and vitro. Our data expound an unexpected role of cypD in IA pathogenesis and an undescribed 8-OHdG/NLRP3/MMP9 pathway involved in accelerating VSMCs apoptosis and elastic fiber degradation. Repressing ROS output by CypD inhibition may be a promising therapeutic strategy for prevention IA development

Cystatin C as a potential therapeutic mediator against Parkinson's disease via VEGF-induced angiogenesis and enhanced neuronal autophagy in neurovascular units

AbstractCystatin C (CYS C, Cst3) is an endogenous cysteine protease inhibitor that plays neuroprotective roles in neurodegenerative diseases. We aimed to explore the association of CYS C with Parkinson’s disease (PD) models and investigate its involvement in the role of neurovascular units (NVUs) in PD neuro-pathogenesis. We used A53T α-synuclein (SNCA) transgenic mice and 6-hydroxydopamine-lesioned DAergic PC12 cells as experimental PD models to investigate the mechanisms behind this association. The injections of CYS C were administered to the right substantia nigra (SN) of A53T SNCA transgenic mice to measure the effects of CYS C in transgenic A53T SNCA mice. To explore the angiogenesis in vivo and in vitro, we used the chick embryo chorioallantoic membrane (CAM) assay and tube formation (TF) assay. We found that CYS C has a neuroprotective effect in this in vivo PD model. We observed increased VEGF, NURR1 and autophagy markers LC3B and decreased SNCA and apoptosis marker cleaved CASP3 in different brain regions of CYS C-treated A53T SNCA transgenic mice. In vitro, we observed that CYS C-induced VEGF, a secreted protein, attenuated 6-OHDA-lesioned DAergic PC12 cell degeneration by regulating p-PKC-α/p-ERK1/2-Nurr1 signaling and inducing autophagy. VEGF-mediated angiogenesis was markedly enhanced in the conditioned media of 6-OHDA-lesioned PC12 cells with CYS C-overexpression, whereas blockage of autophagy in CYS C-overexpressing PC12 cells significantly downregulated VEGF expression and the associated angiogenesis. Our data indicate that CYS C displays dual neuronal–vascular functions, promoting PC12 cell survival and angiogenesis via regulating the level of secreted VEGF in NVUs. Our study provides evidence that may aid in the development of an alternative approach for the treatment of PD through modulation of CYS C-mediated neuronal-vascular pathways.</jats:p

A Mendelian randomisation, propensity score matching study to investigate causal association between serum homocysteine and intracranial aneurysm

Background and purpose Recent observational studies have reported that serum total homocysteine (tHcy) is associated with intracranial aneurysms (IAs). However, the causal effect of tHcy on IAs is unknown. We leveraged large-scale genetic association and real-world data to investigate the causal effect of tHcy on IA formation.Methods We performed a two-sample Mendelian randomisation (MR) using publicly available genome-wide association studies summary statistics to investigate the causal relationship between tHcy and IAs, following the recommendations of the Strengthening the Reporting of Observational Studies in Epidemiology-MR statement. Furthermore, a propensity score matching (PSM) analysis was conducted to evaluate the detailed effects of tHcy on risk of IA formation by utilizing real-world multicentre data, including 9902 patients with and without IAs (1:1 matched). Further interaction and subgroup analyses were performed to elucidate how tHcy affects risk of IA formation.Results MR analyses indicated that genetically determined tHcy was causally associated with IA risk (OR, 1.38, 95% CI 1.07 to 1.79; p=0.018). This is consistent with the more conservative weighted median analysis (OR, 1.41, 95% CI 1.03 to 1.93; p=0.039). Further sensitivity analyses showed no evidence of horizontal pleiotropy or heterogeneity of single nucleotide polymorphisms in causal inference. According to the PSM study, we found that, compared with low tHcy (≤15 µmol/L), moderate tHcy (&gt;15–30 µmol/L) (OR 2.13, 95% CI 1.93 to 2.36) and high tHcy (&gt;30 µmol/L) (OR 3.66, 95% CI 2.71 to 4.95) were associated with a higher IA risk (p trend &lt;0.001). Subgroup analyses demonstrated significant ORs of tHcy in each subgroup when stratified by traditional cardiovascular risk factors. Furthermore, there was also a synergistic effect of tHcy and hypertension on IA risk (p interaction &lt;0.001; the relative excess risk due to interaction=1.65, 95% CI 1.29 to 2.01).Conclusion Both large-scale genetic evidence and multicentre real-world data support a causal association between tHcy and risk of IA formation. Serum tHcy may serve as a biomarker to identify high-risk individuals who would particularly benefit from folate supplementation