Regenerated Graphite Electrodes with Reconstructed Solid Electrolyte Interface and Enclosed Active Lithium Toward >100% Initial Coulombic Efficiency.

Solid electrolyte interface (SEI) is arguably the most important concern in graphite anodes, which determines their achievable Coulombic efficiency (CE) and cycling stability. In spent graphite anodes, there are already-formed (yet loose and/or broken) SEIs and some residual active lithium, which, if can be inherited in the regenerated electrodes, are highly desired to compensate for the lithium loss due to SEI formation. However, current graphite regenerated approaches easily destroy the thin SEIs and residue active lithium, making their reuse impossible. Herein, this work reports a fast-heating strategy (e.g., 1900 K for ≈150 ms) to upcycle degraded graphite via instantly converting the loose original SEI layer (≈100 nm thick) to a compact and mostly inorganic one (≈10-30 nm thick with a 26X higher Young's Modulus) and still retaining the activity of residual lithium. Thanks to the robust SEI and enclosed active lithium, the regenerated graphite exhibited 104.7% initial CE for half-cell and gifted the full cells with LiFePO4 significantly improved initial CE (98.8% versus 83.2%) and energy density (309.4 versus 281.4 Wh kg-1 ), as compared with commercial graphite. The as-proposed upcycling strategy turns the "waste" graphite into high-value prelithiated ones, along with significant economic and environmental benefits.

The important role of starch fine molecular structures in starch gelatinization property with addition of sugars/sugar alcohols.

The relationship between the fine structure of starch and its gelatinization properties is not well studied, particularly in relation to the influence of sugar or sugar alcohol. In this study, seven starches with distinct molecular structures were investigated to determine how different sugars and sugar alcohols affect their gelatinization properties. The inclusion of sugars and sugar alcohols resulted in a significant elevation of starch gelatinization temperatures (∼ 8 °C), especially with sucrose, isomaltose and isomalt. Nevertheless, the influence of these sugars/ sugar alcohols on the gelatinization temperature range and enthalpy change varied depending on the particular starch varieties. According to the correlation analysis, sugars and sugar alcohols mainly exert their impact on the starch gelatinization temperature range and enthalpy change by possibly interacting with amylose chains possessing a degree of polymerization ranging from 100 to 1000 (p < 0.05) and inhibiting the amylose leaching during gelatinization. These findings help a better understanding of the complex relationship between starch fine structure and gelatinization properties under the influence of sugars and sugar alcohols.

Air-Stable Li2S Cathodes Enabled by an In Situ-Formed Li+ Conductor for Graphite-Li2S Pouch Cells.

Using Li2S cathodes instead of S cathodes presents an opportunity to pair them with Li-free anodes (e.g., graphite), thereby circumventing anode-related issues, such as poor reversibility and safety, encountered in Li-S batteries. However, the moisture-sensitive nature of Li2S causes the release of hazardous H2S and the formation of insulative by-products, increasing the manufacturing difficulty and adversely affecting cathode performance. Here, Li4SnS4, a Li+ conductor that is air-stable according to the hard-soft acid-base principle, is formed in situ and uniformly on Li2S particles because Li2S itself participates in Li4SnS4 formation. When exposed to air (20% relative humidity), the protective Li4SnS4 layer maintains its components and structure, thus contributing to the enhanced stability of the Li2S@Li4SnS4 composite. In addition, the Li4SnS4 layer can accelerate the sluggish conversion of Li2S because of its favorable interfacial charge transfer, and continuously confine lithium polysulfides owing to its integrity during electrochemical processes. A graphite-Li2S pouch cell containing a Li2S@Li4SnS4 cathode is constructed, which shows stable cyclability with 97% capacity retention after 100 cycles. Hence, combining a desirable air-stable Li2S cathode and a highly reversible Li-free configuration offers potential practical applications of graphite-Li2S full cells.

Association of Anxiety and Depressive Symptoms with Thyroid Hormone Concentrations in Patients with Primary Bone Tumors.

BACKGROUND: Timely identification and intervention of psychological disorders bear significant import in ameliorating the ensuing therapeutic trajectories in primary bone tumor patients. Moreover, perturbations in thyroxine and thyroid-stimulating hormone (TSH) levels have been linked to manifestations of depressive and anxiety-related symptoms. However, the precise interplay governing the nexus of anxiety, depression, and the levels of thyroxine and TSH within the context of primary bone tumor patients remains presently unexplored. OBJECTIVE: The objective of this study is to investigate the potential correlation between the hypothalamus- pituitary-thyroxine (HPT) axis and the depressive as well as anxious states observed in patients afflicted with bone tumors. METHODS: Patients with primary bone tumors were required to accept the assessments of anxiety and depressive symptoms as well as thyroid axis hormone concentrations. The depressive and anxiety symptoms were assessed using the Hamilton Depression Rating Scale (HAMD) and the Hamilton Anxiety Scale (HAMA) score. During each follow-up, peripheral venous blood samples were collected for subsequent analysis using radioimmunoassay methods to measure serum- free T3, free T4, and TSH levels, with the calculated free T3 to free T4 ratio indicating peripheral free T4 to free T3 conversion. Tests for trend were conducted to assess thyroid axis hormone concentrations, HAMA scores, and HAMD scores, while the correlation between HAMA or HAMD scores and thyroid axis hormone concentrations was examined through univariate regression analyses. RESULTS: The study included 30 primary bone tumor patients. Initial high HAMA and HAMD scores decreased over a year after surgery (P < 0.05), reflecting diminishing anxiety and depression. TSH levels reduced postoperatively, contrasting with increased free-T3 and free-T4 levels (p < 0.01). Multivariate analysis affirmed that positive correlations were noted between TSH and anxiety/depression scores, while free-T3 correlated negatively, adjusted for demographic factors (p < 0.05). No significant associations emerged between HAMA/HAMD scores and free-T4 or free-T3 to free-T4 ratio (p > 0.05). CONCLUSION: The early identification of the low T3 syndrome could prove instrumental in both intervening and preventing adverse emotional states associated with primary bone tumors.

Li2Se as a Cathode Prelithiation Additive for Lithium-Ion Batteries.

In conventional lithium-ion batteries (LIBs), active lithium (Li) ions, which function as charge carriers and could only be supplied by the Li-containing cathodes, are also consumed during the formation of the solid electrolyte interphase. Such irreversible Li loss reduces the energy density of LIBs and is highly desired to be compensated by prelithiation additives. Herein, lithium selenide (Li2Se), which could be irreversibly converted into selenide (Se) at 2.5-3.8 V and thus supplies additional Li, is proposed as a cathode prelithiation additive for LIBs. Compared with previously reported prelithiation reagents (e.g., Li6CoO4, Li2O, and Li2S), the delithiation of Li2Se not only delivers a high specific capacity but also avoids gas release and incompatibility with carbonate electrolytes. The electrochemical characterizations show that with the addition of 6 wt % Li2Se to the LiFePO4 (LFP) cathodes, a 9% increase in the initial specific capacity in half Li||LFP cells and a 19.8% increase in the energy density (based on the total mass of the two electrodes' materials) could be achieved without sacrificing the other battery performance. This work demonstrates the possibility to use Li2Se as a high-efficiency prelithiation additive for LIBs and provides a solution to the high-energy LIBs.

Electrochemical Reactivation of Dead Li2 S for Li-S Batteries in Non-Solvating Electrolytes.

The use of non-solvating, or as-called sparingly-solvating, electrolytes (NSEs), is regarded as one of the most promising solutions to the obstacles to the practical applications of Li-S batteries. However, it remains a puzzle that long-life Li-S batteries have rarely, if not never, been reported with NSEs, despite their good compatibility with Li anode. Here, we find the capacity decay of Li-S batteries in NSEs is mainly due to the accumulation of the dead Li2 S at the cathode side, rather than the degradation of the anodes or electrolytes. Based on this understanding, we propose an electrochemical strategy to reactivate the accumulated Li2 S and revive the dead Li-S batteries in NSEs. With such a facile approach, Li-S batteries with significantly improved cycling stability and accelerated dynamics are achieved with diglyme-, acetonitrile- and 1,2-dimethoxyethane-based NSEs. Our finding may rebuild the confidence in exploiting non-solvating Li-S batteries with practical competitiveness.

Manf Enhances the Pyroptosis Inhibition of Bone Marrow-derived Mesenchymal Stem Cells to Relieve Cerebral Infarction Injury.

Cerebral infarction is a common disease characterized by high mortality, a narrow therapeutic window, and limited therapeutic options. Recently, cell therapy based on gene modification has brought a glimmer of hope to the treatment of cerebral infarction although the explicit underlying mechanism is beyond being well dissected. In the present study, we constructed an animal model of middle cerebral artery occlusion (MCAO), compared differentially expressed genes (DEGs) between the sham and MCAO groups by single-cell RNA sequencing (scRNA-seq) to explore the potential cell death-related pathways involved in cerebral infarction, and transfected Manf into BMSCs by lentivirus. Subsequently, we injected BMSCs (bone marrow-derived mesenchymal stem cells), Manf-modified BMSCs, or lentivirus encoding Manf into the brain. Their effects on MANF content, apoptosis, pyroptosis, infarct volume in the brain, and neurological function were evaluated after MCAO. We found that the DEGs upregulated in four major cell clusters after MCAO and were enriched with not only apoptosis, ferroptosis, and necroptosis but also with pyroptosis-related pathways. In addition, transfection of Manf into BMSCs significantly increased the expression and secretion of MANF in BMSCs; BMSCs, Manf-modified BMSCs, and Manf treatment all resulted in an increase in Manf content in the brain, a decrease in the expression of apoptosis- and pyroptosis-related molecules, a reduction in infarct volume, and an improvement in neurological function after MCAO. Moreover, Manf-modified BMSCs have the strongest therapeutic effect. Collectively, Manf-modified BMSCs ameliorate ischemic injury after cerebral infarction by repressing apoptosis- and pyroptosis-related molecules, which represents a new cell therapy strategy for cerebral infarction.

Identification of pyroptosis-related immune signature and drugs for ischemic stroke.

Background: Ischemic stroke (IS) is a common and serious neurological disease, and multiple pathways of cell apoptosis are implicated in its pathogenesis. Recently, extensive studies have indicated that pyroptosis is involved in various diseases, especially cerebrovascular diseases. However, the exact mechanism of interaction between pyroptosis and IS is scarcely understood. Thus, we aimed to investigate the impact of pyroptosis on IS-mediated systemic inflammation. Methods: First, the RNA regulation patterns mediated by 33 pyroptosis-related genes identified in 20 IS samples and 20 matched-control samples were systematically evaluated. Second, a series of bioinformatics algorithms were used to investigate the contribution of PRGs to IS pathogenesis. We determined three composition classifiers of PRGs which potentially distinguished healthy samples from IS samples according to the risk score using single-variable logistic regression, LASSO-Cox regression, and multivariable logistic regression analyses. Third, 20 IS patients were classified by unsupervised consistent cluster analysis in relation to pyroptosis. The association between pyroptosis and systemic inflammation characteristics was explored, which was inclusive of immune reaction gene sets, infiltrating immunocytes and human leukocyte antigen genes. Results: We identified that AIM2, SCAF11, and TNF can regulate immuno-inflammatory responses after strokes via the production of inflammatory factors and activation of the immune cells. Meanwhile, we identified distinct expression patterns mediated by pyroptosis and revealed their immune characteristics, differentially expressed genes, signaling pathways, and target drugs. Conclusion: Our findings lay a foundation for further research on pyroptosis and IS systemic inflammation, to improve IS prognosis and its responses to immunotherapy.

Pramipexole Inhibits Neuronal Apoptosis in Rats with Parkinson's Disease.

To explore the inhibition of pramipexole on the neuronal apoptosis and its influences on the expressions of brain tissue brain-derived neurotrophic factor (BDNF), and serum miR-103a and miR-30b and inflammatory factors in rats with Parkinson's disease. A total of 36 Sprague-Dawley rats were randomly divided into normal group (n = 12), model group (n = 12) and pramipexole group (n = 12). Compared with that in normal group, the positive expression of BDNF was substantially increased in model group and pramipexole group, and its positive expression in pramipexole group was notably higher than that in model group. The WB results revealed that compared with those in normal group, the relative protein expression levels of Bax and Bcl-2 were markedly increased and decreased, respectively, in the other two groups, and that pramipexole group exhibited a remarkable decline in the relative protein expression level of Bax and a considerable increase in that of Bcl-2, compared with model group. The relative expression levels of miR-103a and miR-30b in model and pramipexole groups were markedly higher than those in normal group, and pramipexole group had remarkably higher relative expression levels of miR-103a and miR-30b than model group. It was found through ELISA that model and pramipexole groups had markedly raised IL-1ß and IL-18 content compared with normal group, and their content in pramipexole group was remarkably lower than that in model group. Based on the TUNEL results, compared with that in normal group, the apoptosis rate of cells rose substantially in the other two groups, and the apoptosis rate in pramipexole group was notably lower than that in model group. Pramipexole may up-regulate the expressions of BDNF, miR-103a and miR-30b to inhibit the apoptosis and inflammation in Parkinson's disease model rats.

Plasma Concentration of Tumor Necrosis Factor-Stimulated Gene-6 as a Novel Diagnostic and 3-Month Prognostic Indicator in Non-Cardioembolic Acute Ischemic Stroke.

Background: Tumor necrosis factor-stimulated gene-6 (TSG-6) is a multifunctional, anti-inflammatory, and protective protein, while the association between TSG-6 and acute ischemic stroke (AIS) remains unclear in humans. This study aims to investigate the potential diagnostic and short-term prognosis predictive values of TSG-6 in non-cardioembolic AIS. Methods: A total of 134 non-cardioembolic AIS patients within 24 h after AIS onset and 40 control subjects were recruited. Using an AIS dataset from the Gene Expression Omnibus database and setting the median expression level of TNFAIP6 as the cutoff point, data were divided into TNFAIP6-high and TNFAIP6-low expression groups. Differently expressed genes (DEGs) were extracted to perform gene enrichment analysis and protein-protein interaction (PPI) network. Baseline data were analyzed in a four-group comparison plotted as plasma TSG-6 concentration median and 25th/75th percentiles. The correlative factors of 3-month outcome were evaluated by logistic regression. TSG-6 concentrations and TSG-6-to-interleukin-8 ratios were compared in a block design. A receiver-operating characteristic curve was used to analyze the detective value of TSG-6 and 3-month prognosis predictive values of TSG-6 and TSG-6-to-interleukin-8 ratio. Results: Non-cardioembolic AIS patients had significantly higher plasma TSG-6 levels than control subjects (P < 0.0001). The large-artery atherosclerosis group had significantly higher TSG-6 levels than the small-artery occlusion group (P = 0.0184). Seven hundred and eighty-two DEGs might be both AIS-related and TNFAIP6-correlated genes, and 17 targets were deemed AIS-related being closely relevant to TNFAIP6. Interleukin-8 was selected for further study. The National Institutes of Health Stroke Scale and the Acute Stroke Registry and Analysis of Lausanne scores at admission, lesion volume, neutrophil count, neutrophil-to-lymphocyte ratio, and interleukin-8 level were positively correlated with TSG-6 level, respectively (P < 0.0001). The unfavorable outcome group had meaningfully higher TSG-6 levels (P < 0.0001) and lower TSG-6-to-interleukin-8 ratios (P < 0.0001) than the favorable outcome group. After adjusting for confounding variables, elevated TSG-6 levels remained independently associated with 3-month poor prognosis of non-cardioembolic AIS (P = 0.017). In non-cardioembolic AIS, the cutoff values of TSG-6 concentration for detection and 3-month prognosis prediction and the TSG-6-to-interleukin-8 ratio for the 3-month prognosis prediction were 8.13 ng/ml [AUC, 0.774 (0.686-0.861); P < 0.0001], 10.21 ng/ml [AUC, 0.795 (0.702-0.887); P < 0.0001], and 1.505 [AUC, 0.873 (0.795-0.951); P < 0.0001]. Conclusions: Plasma TSG-6 concentration was a novel indicator for non-cardioembolic AIS diagnosis and 3-month prognosis. Elevated TSG-6-to-interleukin-8 ratio might suggest a 3-month favorable outcome.

Development of a 3 RNA Binding Protein Signature for Predicting Prognosis and Treatment Response for Glioblastoma Multiforme.

Purpose: Glioblastoma multiforme (GBM) is the most widely occurring brain malignancy. It is modulated by a variety of genes, and patients with GBM have a low survival ratio and an unsatisfactory treatment effect. The irregular regulation of RNA binding proteins (RBPs) is implicated in several malignant neoplasms and reported to exhibit an association with the occurrence and development of carcinoma. Thus, it is necessary to build a stable, multi-RBPs signature-originated model for GBM prognosis and treatment response prediction. Methods: Differentially expressed RBPs (DERBPs) were screened out based on the RBPs data of GBM and normal brain tissues from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression Program (GTEx) datasets. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses on DERBPs were performed, followed by an analysis of the Protein-Protein Interaction network. Survival analysis of the DERBPs was conducted by univariate and multivariate Cox regression. Then, a risk score model was created on the basis of the gene signatures in various survival-associated RBPs, and its prognostic and predictive values were evaluated through Kaplan-Meier analysis and log-rank test. A nomogram on the basis of the hub RBPs signature was applied to estimate GBM patients' survival rates. Moreover, western blot was for the detection of the proteins. Results: BICC1, GNL3L, and KHDRBS2 were considered as prognosis-associated hub RBPs and then were applied in the construction of a prognostic model. Poor survival results appeared in GBM patients with a high-risk score. The area under the time-dependent ROC curve of the prognostic model was 0.723 in TCGA and 0.707 in Chinese Glioma Genome Atlas (CGGA) cohorts, indicating a good prognostic model. What was more, the survival duration of the high-risk group receiving radiotherapy or temozolomide chemotherapy was shorter than that of the low-risk group. The nomogram showed a great discriminating capacity for GBM, and western blot experiments demonstrated that the proteins of these 3 RBPs had different expressions in GBM cells. Conclusion: The identified 3 hub RBPs-derived risk score is effective in the prediction of GBM prognosis and treatment response, and benefits to the treatment of GBM patients.

Bone marrow mesenchymal stem cells induce M2 microglia polarization through PDGF-AA/MANF signaling.

BACKGROUND: Bone marrow mesenchymal stem cells (BMSCs) are capable of shifting the microglia/macrophages phenotype from M1 to M2, contributing to BMSCs-induced brain repair. However, the regulatory mechanism of BMSCs on microglia/macrophages after ischemic stroke is unclear. Recent evidence suggests that mesencephalic astrocyte-derived neurotrophic factor (MANF) and platelet-derived growth factor-AA (PDGF-AA)/MANF signaling regulate M1/M2 macrophage polarization. AIM: To investigate whether and how MANF or PDGF-AA/MANF signaling influences BMSCs-mediated M2 polarization. METHODS: We identified the secretion of MANF by BMSCs and developed transgenic BMSCs using a targeting small interfering RNA for knockdown of MANF expression. Using a rat middle cerebral artery occlusion (MCAO) model transplanted by BMSCs and BMSCs-microglia Transwell coculture system, the effect of BMSCs-induced downregulation of MANF expression on the phenotype of microglia/macrophages was tested by Western blot, quantitative reverse transcription-polymerase chain reaction, and immunofluorescence. Additionally, microglia were transfected with mimics of miR-30a*, which influenced expression of X-box binding protein (XBP) 1, a key transcription factor that synergized with activating transcription factor 6 (ATF6) to govern MANF expression. We examined the levels of miR-30a*, ATF6, XBP1, and MANF after PDGF-AA treatment in the activated microglia. RESULTS: Inhibition of MANF attenuated BMSCs-induced functional recovery and decreased M2 marker production, but increased M1 marker expression in vivo or in vitro. Furthermore, PDGF-AA treatment decreased miR-30a* expression, had no influence on the levels of ATF6, but enhanced expression of both XBP1 and MANF. CONCLUSION: BMSCs-mediated MANF paracrine signaling, in particular the PDGF-AA/miR-30a*/XBP1/MANF pathway, synergistically mediates BMSCs-induced M2 polarization.

[Overlapping Cervical Cell Image Segmentation Based on Bottleneck Detection and Watershed Algorithm].

This study proposes an image segmentation method based on bottleneck detection and watershed algorithm to solve the problem of overlapping cervical cell image. First, we use polygon approximation to get all feature points on the cell contour and then use bottleneck detection and ellipse fitting to obtain the correct split point pairs. Therefore, the approximate range of the overlapping region was determined. The watershed algorithm was used to obtain the internal boundary information for the gradient image of the region. Finally, the segmentation results of the overlapped cells were obtained by superimposing with the outer contour. The experimental results show that this algorithm can segment the contour of a single cell from the overlapping cervical cell images with good accuracy and integrity. The segmentation result is close to that of doctors' manual marking, and the segmentation result is better than other existing algorithms.

Over-Expression of TRPC6 via CRISPR Based Synergistic Activation Mediator in BMSCs Ameliorates Brain Injury in a Rat Model of Cerebral Ischemia/Reperfusion.

Stroke is a major life-threatening and disabling disease with a restricted therapeutic approach. Bone marrow stromal cells (BMSCs) possess proliferative ability and a multi-directional differentiation potential, and secrete a range of trophic/growth factors that can protect neurons after cerebral ischemia/reperfusion. Transient receptor potential canonical (TRPC) is a family of non-selective channels permeable to Ca2+, with several functions including neuronal survival. Over-expression of TRPC6, a subtype of the TRPC family, was shown to protect neurons against cerebral ischemia/reperfusion injury. However, it remains unclear whether over-expression of TRPC6 in BMSCs can further reduce brain injury after ischemia/reperfusion. In the present study, we report that over-expression of TRPC6 via a CRISPR-based synergistic activation mediator in BMSCs provided a greater reduction of brain injury in a rat model of ischemia/reperfusion. Further, the improved neurofunctional outcomes were associated with increased TRPC6 and brain derived neurotrophic factor expression levels. Overall, these data suggest that TRPC6 over-expressing BMSCs may be a promising therapeutic agent for ischemic stroke.

Combined bone marrow stromal cells and oxiracetam treatments ameliorates acute cerebral ischemia/reperfusion injury through TRPC6.

Ischemic stroke has become one of the leading causes of deaths and disabilities all over the world. In this study, we investigated the therapeutic effects of combined bone marrow stromal cells (BMSCs) and oxiracetam treatments on acute cerebral ischemia/reperfusion (I/R) injury. A rat model of middle cerebral artery occlusion (MCAO) followed by complete reperfusion, as well as a cortex neuron oxygen-glucose deprivation (OGD) model was established. When compared with BMSCs or oxiracetam monotherapy, combination therapy significantly improved functional restoration with decreased infarct volume in observed ischemic brain. We propose that it may occur through the transient receptor potential canonical (TRPC)6 neuron survival pathway. The increased expression of TRPC6 along with the reduction of neuronal cell death in the OGD cortex neurons and combination therapy group indicated that the TRPC6 neuron survival pathway plays an important role in the combined BMSCs and oxiracetam treatments. We further tested the activity of the calpain proteolytic system, and the results suggested that oxiracetam could protect the integrity of TRPC6 neuron survival pathway by inhibiting TRPC6 degradation. The protein levels of phospho-cAMP response element binding protein (p-CREB) were tested. It was found that BMSCs play a role in the activation of the TRPC6 pathway. Our study suggests that the TRPC6 neuron survival pathway plays a significant role in the protective effect of combined BMSCs and oxiracetam treatments on acute cerebral I/R injury. Combined therapy could inhibit the abnormal degradation of TRPC6 via decreasing the activity of calpain and increasing the activation of TRPC6 neuron survival pathway.

Association between nucleotide-binding oligomerization domain protein 2 (NOD2) gene polymorphisms and Parkinson's disease (PD) susceptibility.

Objective: This study aimed to explore the association between single nucleotide polymorphisms (SNPs) of nucleotide-binding oligomerization domain protein 2 (NOD2) gene and Parkinson's disease susceptibility, including IVS4 + 10A > C (rs72796353) and a missense mutation at exon 9 (c.2857A > G p.K953E). Methods: Rs72796353 and c.2857A > G p.K953E polymorphisms of NOD2 gene were genotyped via polymerase chain reaction-restriction fragment length polymorphism in 125 cases with PD and 120 healthy controls. Genotype and allele frequencies differences of gene polymorphisms between the case and control groups were analyzed by the Chi-square test. Odds ratio (OR) and 95% confidence interval (95%CI) were used to indicate the relative susceptibility to PD. Furthermore, Hardy-Weinberg equilibrium (HWE) was evaluated by the χ2 test in controls. Results: Neither genotypes nor allele of rs72796353 was significantly different in cases and control groups (p > .05). Differently, AG/GG genotype of NOD2 2857 A > G polymorphism were associated with the increased risk of PD (OR = 2.486, 95%CI = 1.223-5.056), and G allele carriers were 2.563 times risk to suffer from PD (OR = 2.563, 95%CI = 1.310-5.013). Besides, AG genotype might be also a risk factor for PD. Conclusion: NOD2 c.2857A > G p.K953E polymorphism may be correlated with PD susceptibility in Chinese Han population, but not rs727796353. Further study should be conduct to certify this conclusion.

Probable RBD Associates with the Development of RLS in Parkinson's Disease: A Cross-Sectional Study.

OBJECTIVES: We aimed to investigate the prevalence of restless leg syndrome (RLS) and exploring the contributing factors that affect the development of RLS in Parkinson's disease (PD) patients. METHODS: A cross-sectional study was conducted consisting of 178 consecutive PD patients from our hospital between October 2015 and August 2016. We divided the participants into two groups, which were PD with RLS and PD with non-RLS. Then, we recorded their demographics and clinical data to draw a comparison between PD with RLS and PD with non-RLS. RESULTS: 23 (12.92%) were diagnosed with RLS among all the enrolled PD patients. Unified Parkinson's Disease Rating Scale III (UPDRS III) and Hamilton Depression Scale (HAMD) scores, probable rapid eye movement sleep behavior disorder (PRBD), and daily levodopa equivalent dose (LED) in the PD with the RLS group were significantly different from those in the PD with the non-RLS group. Daily LED and the scores of UPDRS III and HAMD in PD patients with RLS were all higher than those in PD patients with non-RLS. PRBD, daily LED, and HAMD scores were significantly independent factors contributing to the development of RLS (OR = 4.678, 95% CI 1.372~15.944, P = 0.014; OR = 1.003, 95% CI 1.001~1.005, P = 0.019; OR = 1.094, 95% CI 1.002~1.193, P = 0.045). The severity of RLS was positively correlated with the duration of PD and daily LED (r = 0.438, P = 0.036; r = 0.637, P = 0.001). CONCLUSION: PRBD existence, daily LED, and HAMD scores are independent factors for developing RLS in PD patients. PRBD existence is firstly proposed as an independent factor in developing RLS among PD patients. RLS severity in PD patients are positively associated with the duration of PD and daily LED.

Color Space Transformation-Based Smartphone Algorithm for Colorimetric Urinalysis.

Urine strips are widely applied for rapid analysis of various indexes of urine for clinical examinations. The tests mainly rely on the application of a urine analyzer, which suffers several drawbacks and cannot meet the requirements of point-of-care testing (POCT). The integration of a smartphone with a biosensor has recently attracted great attention. We herein propose a human vision-based smartphone algorithm for colorimetric analysis of various urine indexes. A CIEDE2000 formula in CIELab color space is applied for the evaluation of color difference, which may greatly improve the analytical performances of urine strips. The proposed algorithm also possesses merits such as good accuracy, quantitative analysis, and limited calculation task, which is suitable for the application with smartphone platform. Experimental results demonstrate that the proposed method shows excellent reliability compared with the urine analyzer and some other algorithms. In addition, human real samples are successfully analyzed with excellent accuracy. Therefore, this work provides a convenient colorimetric tool for POCT urine analysis.

Deviation of Spatial Representation and Asymmetric Saccadic Reaction Time in Hemi-Parkinson's Disease.

Background: Patients with Parkinson's disease (PD) commonly show spatially asymmetric behaviors, such as veering while attempting to walk in a straight line. While there is general agreement that the lateral motor dysfunction contributes to asymmetric behaviors in PD, it is dispute regarding whether the spatial perception is also biased. In addition, it is not clear whether PD impairs the speed of spatial information process, i.e., the efficiency of information process. Objectives: To assess the visuospatial representation and efficiency of spatial information processing in hemi-PD. Methods: Two saccadic tasks were employed: non-spatial cue evoked saccade and spatial cue evoked saccade. In the former task, an identical visual stimulus (appeared on the body mid-sagittal plane) was artificially associated with a fixed saccadic target (left or right) in a given session. In the latter task, subjects were instructed to make a rightward or leftward saccade based on the perceived location of a visual cue (left vs. right side of the body mid-sagittal plane). We estimated the location of subjective straight ahead (SSA) for each subject by using a psychometric fitting function to fit the location judgment results, enabling evaluation of the symmetry of representation between the left and right hemifields. In addition, since the locations of saccadic targets were same in these two tasks, thus, for each individual subject, the elongated saccadic reaction time (SRT) in the latter task, comparing with the former one, mainly reflects the time spent on judgment of the spatial location of visual cue, i.e., spatial perception. We also assessed the efficiency of spatial perception between two hemispheres, through comparing the normalized SRT (i.e., SRT difference between two tasks) between trials with leftward and rightward judgments. Results: Compared with healthy control subjects (HCs), the SSA was shifted to the contralesional side in both left onset PD (LPD, lesion of right substantia nigra) and right onset PD (RPD, lesion of left substantia nigra) patients. The process of spatial information was significantly longer when a spatial cue appeared in the contralesional hemifield. Conclusions: Patients with hemi-PD showed biased visuospatial representation between left and right hemifields and decreased the efficiency of spatial information processing in the contralesional side. Such results indicate that the hemi-PD impairs both spatial representation and the efficiency of spatial information process, which might contribute to asymmetric behaviors.

Effects of senescence and angiotensin II on expression and processing of amyloid precursor protein in human cerebral microvascular endothelial cells.

The present study was designed to determine the effects of senescence and angiotensin II (Ang II) on expression and processing of amyloid precursor protein (APP) in human brain microvascular endothelial cells (BMECs). Senescence caused a decrease in APP expression thereby resulting in reduced secretion of soluble APPα (sAPPα). In contrast, ß-site APP cleaving enzyme (BACE1) expression and production of amyloid ß (Aß)40 were increased in senescent endothelium. Importantly, in senescent human BMECs, treatment with BACE1 inhibitor IV inhibited Aß generation and increased sAPPα production by enhancing a disintegrin and metalloprotease (ADAM)10 expression. Furthermore, Ang II impaired expression of ADAM10 and significantly reduced generation of sAPPα in senescent human BMECs. This inhibitory effect of Ang II was prevented by treatment with BACE1 inhibitor IV. Our results suggest that impairment of α-processing and shift to amyloidogenic pathway of APP contribute to endothelial dysfunction induced by senescence. Loss of sAPPα in senescent cells treated with Ang II exacerbates detrimental effects of senescence on APP processing. Notably, inhibition of BACE1 has beneficial effects on senescence induced endothelial dysfunction. Reported findings may help to explain contributions of senescent cerebral microvascular endothelium to development of cerebral amyloid angiopathy and Alzheimer's disease (AD) pathology.