Self-Powered Programmable van der Waals Photodetectors with Nonvolatile Semifloating Gate.

Tunable photovoltaic photodetectors are of significant relevance in the fields of programmable and neuromorphic optoelectronics. However, their widespread adoption is hindered by intricate architectural design and energy consumption challenges. This study employs a nonvolatile MoTe2/hexagonal boron nitride/graphene semifloating photodetector to address these issues. Programed with pulsed gate voltage, the MoTe2 channel can be reconfigured from an n+-n to a p-n homojunction and the photocurrent transition changes from negative to positive values. Scanning photocurrent mapping reveals that the negative and positive photocurrents are attributed to Schottky junction and p-n homojunction, respectively. In the p-n configuration, the device demonstrates self-driven, linear, rapid response (∼3 ms), and broadband sensitivity (from 405 to 1500 nm) for photodetection, with typical performances of responsivity at ∼0.5 A/W and detectivity ∼1.6 × 1012 Jones under 635 nm illumination. These outstanding photodetection capabilities emphasize the potential of the semifloating photodetector as a pioneering approach for advancing logical and nonvolatile optoelectronics.

Lithography-free and high-efficiency preparation of black phosphorous devices by direct evaporation through shadow mask.

Two-dimensional (2D) materials including black phosphorus (BP) have been extensively investigated because of their exotic physical properties and potential applications in nanoelectronics and optoelectronics. Fabricating BP based devices is challenging because BP is extremely sensitive to the external environment, especially to the chemical contamination during the lithography process. The direct evaporation through shadow mask technique is a clean method for lithography-free electrode patterning of 2D materials. Herein, we employ the lithography-free evaporation method for the construction of BP based field-effect transistors and photodetectors and systematically compare their performances with those of BP counterparts fabricated by conventional lithography and transfer electrode methods. The results show that BP devices fabricated by direct evaporation method possess higher mobility, faster response time, and smaller hysteresis than those prepared by the latter two methods. This can be attributed to the clean interface between BP and evaporated-electrodes as well as the lower Schottky barrier height of 20.2 meV, which is given by the temperature-dependent electrical results. Furthermore, the BP photodetectors exhibit a broad-spectrum response and polarization sensitivity. Our work elucidates a universal, low-cost and high-efficiency method to fabricate BP devices for optoelectronic applications.

lncRNA NEAT1 prompts autophagy and apoptosis in MPTP-induced Parkinson's disease by impairing miR-374c-5p.

Long non-coding RNAs (lncRNAs) play biological roles in brain disorder and neurodegenerative diseases. As the functions of lncRNA NEAT1 in Parkinson's disease (PD) remain unknown, in the present study, we aimed to explore the roles and underlying molecular mechanisms of NEAT1 in PD. A PD mouse model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and a cell model of SH-SY5Y induced by N-methyl-4-phenylpyridinium (MPP+) were established. The ratio of tyrosine hydroxylase (TH+) cells was determined by immunofluorescence assay, and the behavioral changes in mice were observed using pole tests and rotarod tests. The cellular viability and apoptosis of SH-SY5Y were detected by MTT assay and flow cytometric analysis, respectively, and the number of autophagosomes was subsequently measured by transmission electron microscopy. High-performance liquid chromatography was performed to detect the content of dopamine, and a dual-luciferase reporter assay was used to clarify the target of NEAT1 simultaneously. The results demonstrated that the level of NEAT1 was upregulated in the MPTP-induced PD mice, dopamine neurons, and the SH-SY5Y cells treated with MPP+, whereas the level of miR-374c-5p was downregulated. NEAT1 level was positively correlated with MPP+ in a concentration-dependent manner. NEAT1 inhibition efficiently facilitated cell proliferation but inhibited apoptosis and autophagy in the MPP+-treated SH-SY5Y cells. Additionally, silencing of NEAT1 increased the TH+ rate of neurons and suppressed autophagy greatly in PD mice. As a possible target of NEAT1, miR-374c-5p could impact on the apoptosis and autophagy of the SH-SY5Y cells. NEAT1 inhibition upregulated the expression of miR-374c-5p, enhanced SH-SY5Y cell viability, and repressed autophagy and apoptosis in MPTP-induced PD mice. These findings indicated a potential therapeutic role of NEAT1 in treating PD.

The Phenotypic and Genetic Spectrum of Paroxysmal Kinesigenic Dyskinesia in China.

BACKGROUND: Paroxysmal kinesigenic dyskinesia is a spectrum of involuntary dyskinetic disorders with high clinical and genetic heterogeneity. Mutations in proline-rich transmembrane protein 2 have been identified as the major pathogenic factor. OBJECTIVES: We analyzed 600 paroxysmal kinesigenic dyskinesia patients nationwide who were identified by the China Paroxysmal Dyskinesia Collaborative Group to summarize the clinical phenotypes and genetic features of paroxysmal kinesigenic dyskinesia in China and to provide new thoughts on diagnosis and therapy. METHODS: The China Paroxysmal Dyskinesia Collaborative Group was composed of departments of neurology from 22 hospitals. Clinical manifestations and proline-rich transmembrane protein 2 screening results were recorded using unified paroxysmal kinesigenic dyskinesia registration forms. Genotype-phenotype correlation analyses were conducted in patients with and without proline-rich transmembrane protein 2 mutations. High-knee exercises were applied in partial patients as a new diagnostic test to induce attacks. RESULTS: Kinesigenic triggers, male predilection, dystonic attacks, aura, complicated forms of paroxysmal kinesigenic dyskinesia, clustering in patients with family history, and dramatic responses to antiepileptic treatment were the prominent features in this multicenter study. Clinical analysis showed that proline-rich transmembrane protein 2 mutation carriers were prone to present at a younger age and have longer attack duration, bilateral limb involvement, choreic attacks, a complicated form of paroxysmal kinesigenic dyskinesia, family history, and more forms of dyskinesia. The new high-knee-exercise test efficiently induced attacks and could assist in diagnosis. CONCLUSIONS: We propose recommendations regarding diagnostic criteria for paroxysmal kinesigenic dyskinesia based on this large clinical study of paroxysmal kinesigenic dyskinesia. The findings offered some new insights into the diagnosis and treatment of paroxysmal kinesigenic dyskinesia and might help in building standardized paroxysmal kinesigenic dyskinesia clinical evaluations and therapies. © 2020 International Parkinson and Movement Disorder Society.

Oridonin suppresses autophagy and survival in rheumatoid arthritis fibroblast-like synoviocytes.

Context: Oridonin exhibits various pharmacological and physiological activities, including antioxidant, antibacterial, anti-inflammatory, pro-apoptotic, anticancer and neurological effects. However, its role in rheumatoid arthritis (RA) is yet to be revealed.Objective: We evaluated the effects of oridonin on the survival and autophagy of RA-fibroblast-like synoviocytes (FLSs).Materials and methods: RA-FLSs were treated with oridonin at serial concentrations of 0, 2, 4, 6, 8 and 10 µg/mL for 24, 48 and 72 h. Then, cell proliferation and apoptosis were measured. A GFP-LC3 plasmid was transfected into the cells to determine autophagy.Results: Oridonin suppressed RA-FLS proliferation in a dose-dependent manner. The half maximal inhibitory concentrations (IC50) of oridonin at 24, 48 and 72 h were 8.28, 7.88 and 8.35 µg/mL, respectively. Treatment with oridonin for 24 h increased apoptosis by 4.1%, and increased the protein levels of Bax and cleaved caspase-3 but significantly decreased the levels of IL-1ß in the culture supernatant (p < 0.05). In addition, 6 h of oridonin treatment significantly decreased the number of GFP-LC3 punctate dots and inhibited the protein levels of ATG5 and Beclin1 by 80.01% and 42.12%, respectively. Chloroquine (CQ) significantly reinforced the effects of oridonin on inhibition of autophagy, suppression of proliferation, and induction of apoptosis in RA-FLSs (p < 0.05).Conclusions: Our results indicate that treatment with oridonin in combination with CQ inhibits autophagy and cell proliferation and induces apoptosis in RA-FLSs more effectively than treatment oridonin alone. This finding indicates that oridonin is a potential therapeutic agent for RA.

Do multiple system atrophy and Parkinson's disease show distinct patterns of volumetric alterations across hippocampal subfields? An exploratory study.

OBJECTIVES: To investigate the volumetric alterations of hippocampal subfields and identify which subfields contribute to mild cognitive impairment (MCI) in multiple system atrophy (MSA) and Parkinson's disease (PD). METHODS: Thirty MSA-MCI, 26 PD-MCI, and 30 healthy controls were administered cognitive assessment, along with hippocampal segmentation using FreeSurfer 6.0 after a 3-T MRI scan. Regression analyses were performed between the volumes of hippocampal subfields and cognitive variables. RESULTS: Compared with healthy controls, the volume of the hippocampal fissure was enlarged in PD-MCI patients, while left Cornu Ammonis (CA2-CA3), bilateral molecular layer, bilateral hippocampus-amygdala transition area, right subiculum, right CA1, right presubiculum, right parasubiculum, and bilateral whole hippocampus were reduced in the MSA-MCI group. Moreover, volumetric reductions of the bilateral hippocampal tail, bilateral CA1, bilateral presubiculum, bilateral molecular layer, left CA2-CA3, left hippocampus-amygdala transition area, right parasubiculum, and bilateral whole hippocampus were found in MSA-MCI relative to the PD-MCI group. The volumes of the left CA2-CA3 (B = - 11.34, p = 0.006) and left parasubiculum (B = 4.63, p = 0.01) were respectively correlated with language and abstraction functions. The volumes of the left fimbria (B = 6.99, p = 0.002) and left hippocampus-amygdala transition area (B = 2.28, p = 0.009) were correlated with visuospatial/executive function. CONCLUSIONS: The MSA-MCI patients showed more widespread impairment of hippocampal subfields compared with the PD-MCI group, involving trisynaptic loop and amygdala-hippocampus interactions. The alteration of CA, hippocampus-amygdala transition area, and fimbria still requires further comparison between the two patient groups. KEY POINTS: • The atrophy patterns of hippocampal subfields differed between MSA and PD patients. • MSA has widespread change in trisynaptic loop and amygdala-hippocampus interactions. • The atrophy patterns may help to understand the differences of cognitive impairment in MSA and PD.

Plasmon-coupled charge transfer in WO3-x semiconductor nanoarrays: toward highly uniform silver-comparable SERS platforms.

Transition metal oxide semiconductors have been explored in surface-enhanced Raman scattering (SERS) active substrates, yet their detection sensitivity and enhancement effects are inferior. What's more, the reported fabrication technique ignored the effects of the electromagnetic mechanisms and was far from satisfactory for practical applications. Herein, we report on a convenient nanotechnique to fabricate large-area hexagon plum-blossom-like WO3-x nanoarrays based on aluminum nanobowl array substrates. Localized surface plasmon resonance can be increased via adjusting the time of tungsten magnetron sputtering with H2 annealing treatment. The introduction of a double-switch experiment demonstrates that localized surface plasmon-coupled photoinduced charge transfer can not only increase SERS enhancement comparable to similar silver nanostructures but also implement a low limit of detection below 10-9 M. A triple-switch experiment offers specific rules in the molecular detection of WO3-x semiconductors and important guidance for the fabrication of SERS-active semiconducting platforms.

The polymorphism of SREBF1 gene rs11868035 G/A is associated with susceptibility to Parkinson's disease in a Chinese population.

PURPOSE: To explore the potential association between the single-nucleotide polymorphism (SNP) of two functional genes (sterol regulatory element binding transcription factor1 [SREBF1] gene rs11868035 and USP25 gene rs2823357) and susceptibility to Parkinson's disease (PD) in people of Northeast China. METHODS: A number of 649 cases of PD from consecutive outpatient and inpatient ward of our hospital were included in this retrospective study, and 355 healthy people were also included as control group. The technique of Kompetitive Allele Specific PCR (KASP) was applied to determine the frequency distribution of genotype and allele gene of rs11868035 and rs2823357 in both groups. RESULTS: The significant association was observed for SREBF1 gene rs11868035 in G carriers in PD patients. The frequency of GA + GG genotype and G allele in PD group was significantly higher than in control group of SREBF1 gene rs11868035 (p<.001). PD patients with G/A variant got higher UPDRSII + III score and lower MMSE score than non-carriers, which was statistically different (p=.017, p=.003, respectively). As for USP25, there was no significant difference in the distributions of genotypes and alleles of rs2823357 between PD patients and controls (p>.05). CONCLUSIONS: Polymorphism of SREBF1 gene rs11868035 may increase susceptibility to PD in the northeastern Chinese population, while variant of USP25 gene rs2823357 may have no association with susceptibility to PD in northeastern Chinese. PD patients with G/A variant may worsen their motor and cognitive function disorder.

Stacking sequences of black phosphorous allotropes and the corresponding few-layer phosphorenes.

Possible bulk black phosphorus (BP) allotropes are constructed based on single-layer BP with various stacking sequences. Our stacking algorithm shows that there are eight possible allotropes with two stacking layers in their unit cells possessing relatively high symmetries, and six of them are retained after structural relaxation using a van der Waals correction of optB88-vdW. The AF, AG, and AH bulk structures are presented for the first time. The structural relationship of these configurations has been explained via an interlayer slipping process. The total energy of the AF allotrope is closest to the most stable bulk BP structure (AB stacking) among all explored 2-layer stacked bulk structures. The calculated band structure of the AF allotrope using HSE06 shows a direct band gap of 0.48 eV with anisotropic electronic structures. We also presented six possible BP allotropes with three stacking layers in their unit cells. The newly reported AAF and ABC stacked structures show semiconducting and metallic features, respectively. After the bulk structures were explored, we further built the corresponding few-layer phosphorene structures and investigated their electronic properties. The results show that all the few-layer phosphorenes show semiconducting features. The AE, AAE, and AEA phosphorenes have indirect band gaps while the other explored phosphorenes possess direct band gaps located at the Γ point.

Monocytes, microglia, and CD200-CD200R1 signaling are essential in the transmission of inflammation from the periphery to the central nervous system.

Peripheral inflammation is known to trigger neuroinflammation and neurodegenerative disease. However, the key components during the propagation of inflammation from the periphery to the central nervous system (CNS) remain unclear. Lipopolysaccharide (LPS) was administered to Sprague-Dawley rats to induce peripheral inflammation. An intravenous injection and an intranigral injection of clodronate liposomes were given to deplete monocytes and microglia, respectively. Recombinant CD200 fusion protein (CD200Fc) or an anti-CD200R1 antibody was injected into the substantia nigra to manipulate the involvement of CD200 and CD200R1. Immunohistochemistry and immunofluorescence staining were used to measure microglial activation and dopaminergic neuronal loss. The expression of brain pro-inflammatory cytokines (i.e., tumor necrosis factor alpha, IL-1ß) and CD200-CD200R1 signaling were measured by quantitative RT-PCR. Our data showed that the peripheral LPS injection activated the microglia and induced an increase in the levels of pro-inflammatory cytokines (i.e., tumor necrosis factor alpha, IL-1ß). The depletion of either monocytes or microglia suppressed these inflammatory effects that were induced by peripheral LPS administration. The peripheral LPS injection increased the expression of CD200 and CD200R1 in the substantia nigra. Dopaminergic neuronal loss induced by the peripheral LPS injection was accelerated by the blockade of CD200-CD200R1 signaling with an anti-CD200R1 antibody and attenuated by intensifying the signaling with CD200Fc. These results highlight the importance of monocytes, microglia, and CD200-CD200R1 signaling in the transmission of inflammation from the periphery to the CNS.

Peripheral immune tolerance alleviates the intracranial lipopolysaccharide injection-induced neuroinflammation and protects the dopaminergic neurons from neuroinflammation-related neurotoxicity.

BACKGROUND: Neuroinflammation plays a critical role in the onset and development of neurodegeneration disorders such as Parkinson's disease. The immune activities of the central nervous system are profoundly affected by peripheral immune activities. Immune tolerance refers to the unresponsiveness of the immune system to continuous or repeated stimulation to avoid excessive inflammation and unnecessary by-stander injury in the face of continuous antigen threat. It has been proved that the immune tolerance could suppress the development of various peripheral inflammation-related diseases. However, the role of immune tolerance in neuroinflammation and neurodegenerative diseases was not clear. METHODS: Rats were injected with repeated low-dose lipopolysaccharide (LPS, 0.3 mg/kg) intraperitoneally for 4 days to induce peripheral immune tolerance. Neuroinflammation was produced using intracranial LPS (15 µg) injection. Inflammation cytokines were measured using enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR). Microglial activation were measured using immunostaining of Iba-1 and ED-1. Dopaminergic neuronal damage was evaluated using immunochemistry staining and stereological counting of TH-positive neurons. Behavioral impairment was evaluated using amphetamine-induced rotational behavioral assessment. RESULTS: Compared with the non-immune tolerated animals, pre-treatment of peripheral immune tolerance significantly decreased the production of inflammatory cytokines, suppressed the microglial activation, and increased the number of dopaminergic neuronal survival in the substantia nigra. CONCLUSIONS: Our results indicated that peripheral immune tolerance attenuated neuroinflammation and inhibited neuroinflammation-induced dopaminergic neuronal death.

Peripheral Blood Monocyte Tolerance Alleviates Intraperitoneal Lipopolysaccharides-Induced Neuroinflammation in Rats Via Upregulating the CD200R Expression.

Neuroinflammation is an important pathogenesis of Parkinson's disease (PD). The peripheral immune system could produce profound effects on central immunities. The peripheral blood monocyte (PBM) immune tolerance is the refractoriness of immune system to avoid overactive peripheral inflammation. The PBM are also actively involved in central immune activities. There is evidence implying the probable failure of immune tolerance and impairment of CD200/CD200R signaling in PD patients. Here we aimed to explore the effects of PBM tolerance in peripheral LPS-induced neuroinflammation as well as the specific roles of CD200/CD200R pathway in PBM tolerance. We found that repeated intraperitoneal administration of 0.3 mg/kg LPS was able to induce the PBM tolerance. PBM tolerance reduced peripheral LPS-induced elevation of serum TNF-α, IL-1ß expression and TLR4 expression in PBM. PBM tolerance and PBM depletion alleviated peripheral LPS-induced neuroinflammation demonstrated by reduced proinflammatory cytokines in brain and blocked microglia activation. The CD200R expression in PBM was upregulated in PBM tolerance group after intraperitoneal administration of high-dose LPS in vivo and the blockade of CD200/CD200R interaction induced the failure of PBM tolerance in vitro. These results suggested the PBM tolerance could attenuate the peripheral LPS-induced neuroinflammation via upregulating the CD200R expression and the CD200/CD200R signaling played a key role in PBM tolerance. Effective regulation of the PBM in periphery may be a potential way to limit neuroinflammation while the CD200R on PBM could be used as a potential therapeutic target to alleviate neuroinflammation.

Using 'swallow-tail' sign and putaminal hypointensity as biomarkers to distinguish multiple system atrophy from idiopathic Parkinson's disease: A susceptibility-weighted imaging study.

OBJECTIVE: To investigate the value of 'swallow-tail' sign and putaminal hypointensity on 3 T susceptibility-weighted imaging (SWI) for distinguishing multiple system atrophy (MSA) from idiopathic Parkinson's disease (IPD). METHODS: Three groups - 39 MSA patients, 18 IPD patients,and 31 healthy controls (HCs) - were administered a 3 T SWI sequence to evaluate 'swallow-tail' sign and putaminal hypointensity using visual scales from 0 to 2 and 0 to 3 scores, respectively. The diagnostic accuracy of the two signs separately and combined was calculated using a receiver operating characteristic curve, with clinical diagnosis as the gold standard. RESULTS: The scores of 'swallow-tail' sign were lower in IPD than in MSA or in HCs, as well as for putaminal hypointensity in IPD or HCs than in MSA (p < 0.05). The sensitivity and specificity of 'swallow-tail' sign and putaminal hypointensity were 87.9% and 83.3%, and 35.9% and 100%, respectively, in the respective patient groups. The area under the curve of combined signs was increased from 0.85 ('swallow tail') or 0.68 (putaminal hypointensity) to 0.93. CONCLUSION: The combination of 'swallow-tail' sign and putaminal hypointensity can increase the accuracy of discriminating between MSA and IPD. KEY POINTS: • Differential diagnosis of MSA and IPD is still challenging in clinical practice. • Absence of 'swallow-tail' sign is a valuable biomarker for IPD on SWI. • Putaminal hypointensity is a valuable biomarker for MSA on SWI. • Combined 'swallow- tail' sign and putaminal hypointensity increase diagnostic accuracy.

Tunable surface-enhanced Raman scattering from high-density gold semishell arrays with controllable dimensions.

A convenient reproducible technique is reported for the fabrication of large-area gold semishell arrays by mechanically pressing porous anodic alumina (PAA) stamps into gold/polymer bilayer structures that serve as robust and cost-efficient surface-enhanced Raman-scattering (SERS) substrates. The surface structure can be tuned further to optimize the enhancement factor according to optional PAA fabrication parameters and imprinting pressures. Finite-difference time-domain calculations indicate that the structure may possess excellent SERS characteristics due to the high density and abundance of hot spots.

Dietary Copper Intake and Risk of Parkinson's Disease: a Cross-sectional Study.

Copper is an essential trace element for the human body. The epidemiological evidence for the association of dietary intake of copper with the risk of Parkinson's disease (PD) is limited. We conducted an evaluation of the cross-sectional data gathered from the National Health and Nutrition Examination Surveys spanning from 2007 to 2018, which comprised a total of 17,948 participants. To discern the distinct characteristics of the participants, we performed a univariate analysis and utilized a 1:2 ratio propensity score matching method to minimize the effects of selection bias. We employed weighted univariate as well as three multivariate logistic regression models both prior to and following matching, with the aim of examining the association between dietary copper intake and PD risk. Finally, we used the restricted cubic spline (RCS) methodology in order to investigate possible non-linear relationships. Furthermore, subgroup analysis was undertaken to elicit further understanding concerning the association between copper intake and PD. A negative correlation resulted between dietary copper intake and PD risk in both univariate and multivariate logistic regression models, prior to and following matching. Our findings demonstrate that there is a nonlinear, dose-dependent relationship between copper intake and PD, according to our RCS analysis. In subgroup analysis, copper intake was identified as an important protective factor for individuals who were non-Hispanic White, unmarried, and had completed higher education. Dietary copper intake was associated with the risk of PD. Supplementation of dietary copper may have potentially beneficial effects.

Small variation induces a big difference: the effect of polymerization kinetics of graphitic carbon nitride on its photocatalytic activity.

Graphitic carbon nitride (g-CN) has emerged as a promising visible-light-responsive photocatalyst, and its activity is highly sensitive to synthesis conditions. In this work, we attempt to correlate the photocatalytic activity of g-CN with its production yield, which is kinetically determined by the specific condensation process. Bulk g-CN samples were synthesized by the conventional condensation procedure, but in static air and flowing air, respectively. The one synthesized in static air showed a lower production yield with an increased specific surface area and preferential surface chemical states, corresponding to a significantly improved activity for photocatalytic hydrogen evolution (PHE) and dye degradation. We further synthesized a series of g-CN samples by merely changing the synthetic atmosphere, the ramping rate, and the loading amount of the precursor, and the difference in their PHE performance was found to be as high as 7.05 times. The notable changes in their production yields as well as the photocatalytic activities have been discussed from the point of view of polymerization reaction kinetics, and the self-generated NH3 atmosphere plays a crucial role.

The atomic structures of carbon nitride sheets for cathode oxygen reduction catalysis.

Carbon nitride sheets are promising Pt replacement materials for cathode oxygen reduction catalysis. Using first principles calculations with a global optimization method, we search for the most stable structures of the monolayer carbon nitrides at various C:N ratios. The results show that the larger the ratio, the more energetically favorable the obtained structures, and the more preferably for the C, N atoms to assume sp(2) configurations. A volcano shape is revealed for the curve of the representative O2 adsorption energies on the sheets vs. the ratios. In the ratio range of 2.0-3.0, the sheets not only have lower formation energies than the stable graphitic-C3N4, but also can potentially catalyze the oxygen reduction as efficiently as Pt.

Usefulness of cube copying in evaluating clinical profiles of patients with Parkinson disease.

OBJECTIVE: To clarify the relationship between the quantitatively assessed cube-copying test (CCT) and clinical profiles of cognitive and motor ability in Chinese patients with Parkinson disease (PD). METHODS: We gave the Montreal Cognitive Assessment (MoCA), which includes the CCT, to evaluate the cognitive function of 102 outpatients with PD. We also gave the Unified Parkinson's Disease Rating Scale (UPDRS) II and III and the Hoehn-Yahr scale to evaluate the patients' motor function and disease severity, respectively. We used Maeshima's method for quantitative assessment of the CCT, and calculated CCT errors by adding incomplete connections and plane-drawing errors. We divided the patients into 2 groups based on normal (no errors) versus abnormal (≥1 errors) CCT scores. RESULTS: We found 34 patients with normal scores and 68 with abnormal scores. The 2 groups had significant differences in age of onset, MoCA score, UPDRS II and III scores, and cognitive deterioration rate. CCT errors correlated inversely with cognitive domains except for orientation. Executive function was most commonly affected in both groups. We found correlations between numbers of CCT errors and left-limb movement, fine hand movement, postural instability and gait disorders, UPDRS II and III scores, and cognitive and motor deterioration rates. CONCLUSIONS: The quantitatively assessed CCT may be useful in estimating cognitive and motor dysfunction in patients with PD, and in monitoring disease progression.

Association of five SNPs at the PARK16 locus as a susceptibility locus with Parkinson's disease for forensic application.

To investigate the association of five SNPs (rs823083, rs708723, rs4951261, rs823076 and rs16856110) at the PARK16 locus with Parkinson's disease (PD), and to potentiate its forensic application. The genomic DNAs of 215 PD patients and 212 matched controls from the northern Han Chinese population were amplified in two independent PCR systems and subsequently genotyped by digestion with the three endonucleases (Hinf I, Nco I and Msp I ). The genetic parameters and association studies were carried out with SPSS 13.0, Haploview version 4.2 and PLINK 1.07 softwares. We detected accurately all genotypes in the five SNPs with multiplex PCR-RFLP and mismatched multiplex PCR-RFLP techniques. The genotypes of four SNPs, except for rs823083, were in Hardy-Weinberg equilibrium. The four SNPs, rs16856110, rs4951261, rs708723 and rs823076, which were in linkage equilibrium, should not be associated with PD (P-values ranging from 0.077 to 0.544). The SNPs investigated at the PARK16 locus were not found to be involved in PD-associated blocks in the northern Han Chinese population. The allele distributions of rs708723, rs4951261, rs823076 and rs16856110 in the northern Han Chinese population can be highly polymorphic, which can be applied to genetic analysis and forensic practices.

Association between blood selenium with parkinson's disease in the US (NHANES 2011-2020).

Selenium is an essential trace element for human health, playing a key role in regulating cellular oxidative stress, immune response, and inflammation. In recent years, the association between selenium and Parkinson's disease (PD) has aroused people's attention. The objective of this study is to investigate the relationship between blood selenium concentrations and PD risk in a sample of U.S. adults. A cross-sectional study was conducted using the National Health and Nutrition Examination Survey (NHANES) data from 2011-2020 and included 15,660 adults aged over 40 years old. Univariate logistic regression and multivariate logistic regression models were utilized to analyze the association between blood selenium concentrations and PD prevalence. Additionally, the restricted cubic spline (RCS) model was applied to investigate the dose-response relationships between blood selenium and PD. The findings indicated a link between elevated blood selenium levels and a reduced occurrence of Parkinson's disease (PD). Notably, this association between blood selenium and PD exhibited a non-linear pattern, wherein the decline in PD risk was more pronounced at higher selenium concentrations than at lower levels. An inflection point emerged at approximately 2.4 µmol/L, beyond which the rate of decline in risk significantly diminished with increasing selenium levels. A potential association between blood selenium concentrations and PD has been observed, with PD patients having lower blood selenium levels compared to non-PD patients. Higher levels of blood selenium may have a protective effect against PD. However, further prospective studies are needed to investigate the effect of blood selenium in PD patients and to determine causality.