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Objective: To explore the psychological personality characteristics of transgender groups and to determine whether these characteristics differ according to sociodemographic factors. Methods: This cross-sectional study was conducted between January 2021 and April 2023 at a psychosexual outpatient clinic in a psychiatric hospital in Beijing, China. In total, 481 individuals were included in this study, and demographic information was collected using a self-administered general questionnaire. Psychological personality traits were assessed using the Minnesota Multiphasic Personality Inventory (MMPI). Results: The mean scores of the assigned male at birth (AMAB) group were significantly higher than those of the male controls for all 10 clinical factors of the MMPI (p < 0.01 or p < 0.001). The scores for both the Masculinity-femininity (Mf) and Depression (D) factors in the AMABs group exceeded the clinical threshold (T > 60) and were the highest and second-highest scores on the entire scale, respectively. Individuals assigned female at birth (AFAB) had significantly higher scores than female controls for Hysteria (Hy), Psychopathic Deviate (Pd), and Hypomania (Ma) (p < 0.05, p < 0.01, and p < 0.001, respectively). There were significant differences in the rates of abnormal values for the various factors of the MMPI (T > 60) according to gender, age, and education (p < 0.05, p < 0.01, and p < 0.001, respectively). Compared to AFABs, AMABs had higher rates of abnormal scores (T > 60) on the Hypochondriasis (Hs), D, Hy, Mf, Paranoia (Pa), Psychasthenia (Pt), Schizophrenia (Sc), and Social Introversion (Si) scales (p < 0.05, p < 0.01, and p < 0.001, respectively). Second, the transgender group aged ≤25 years had higher rates of abnormal scores (T > 60) on the Hs, D, Hy, Pd, Pa, Pt, Sc, and Ma scales (p < 0.05, p < 0.01, and p < 0.001, respectively). Finally, outliers (T > 60) for the Hs, D, Hy, Pd, Pa, Pt, Ma, and Si factors were more prevalent among those with a primary to high school level of education (p < 0.05, p < 0.01, and p < 0.001, respectively). Conclusion: Assigned male at births may have a variety of psychological vulnerabilities, and there is a need to focus especially on those with a primary to high school level of education, those aged ≤25 years, and transgender females.

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BACKGROUND: Although many molecules have been investigated as biomarkers for spinal cord injury (SCI) or ischemic stroke, none of them are specifically induced in central nervous system (CNS) neurons following injuries with low baseline expression. However, neuronal injury constitutes a major pathology associated with SCI or stroke and strongly correlates with neurological outcomes. Biomarkers characterized by low baseline expression and specific induction in neurons post-injury are likely to better correlate with injury severity and recovery, demonstrating higher sensitivity and specificity for CNS injuries compared to non-neuronal markers or pan-neuronal markers with constitutive expressions. METHODS: In animal studies, young adult wildtype and global Atf3 knockout mice underwent unilateral cervical 5 (C5) SCI or permanent distal middle cerebral artery occlusion (pMCAO). Gene expression was assessed using RNA-sequencing and qRT-PCR, while protein expression was detected through immunostaining. Serum ATF3 levels in animal models and clinical human samples were measured using commercially available enzyme-linked immune-sorbent assay (ELISA) kits. RESULTS: Activating transcription factor 3 (ATF3), a molecular marker for injured dorsal root ganglion sensory neurons in the peripheral nervous system, was not expressed in spinal cord or cortex of naïve mice but was induced specifically in neurons of the spinal cord or cortex within 1 day after SCI or ischemic stroke, respectively. Additionally, ATF3 protein levels in mouse blood significantly increased 1 day after SCI or ischemic stroke. Importantly, ATF3 protein levels in human serum were elevated in clinical patients within 24 hours after SCI or ischemic stroke. Moreover, Atf3 knockout mice, compared to the wildtype mice, exhibited worse neurological outcomes and larger damage regions after SCI or ischemic stroke, indicating that ATF3 has a neuroprotective function. CONCLUSIONS: ATF3 is an easily measurable, neuron-specific biomarker for clinical SCI and ischemic stroke, with neuroprotective properties. HIGHLIGHTS: ATF3 was induced specifically in neurons of the spinal cord or cortex within 1 day after SCI or ischemic stroke, respectively. Serum ATF3 protein levels are elevated in clinical patients within 24 hours after SCI or ischemic stroke. ATF3 exhibits neuroprotective properties, as evidenced by the worse neurological outcomes and larger damage regions observed in Atf3 knockout mice compared to wildtype mice following SCI or ischemic stroke.

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BACKGROUND: Trans persons' physical and mental health is easily affected by the attitude of those around them. However, China currently lacks a valid psychometric instrument to investigate people's attitudes toward trans persons. Therefore, this study modifies the English version of the Transgender Attitudes and Beliefs Scale (TABS) to suit the Chinese context. It subsequently examines the reliability and validity of the Chinese version of the TABS. METHODS: This study recruited 1164 university students, aged 18-25 years, from 7 regions of China. SPSS26.0 and AMOS24.0 were used for data statistical analysis. Critical ratio method and correlation coefficient method were used for item analysis. Exploratory factor analysis and confirmatory factor analysis were used to test the structural validity of the Chinese version of Transgender Beliefs and Attitudes Scale, and the internal consistency reliability of the scale was tested. RESULTS: The TABS-C contains 26 items with 3 factors. The Cronbach's alpha was 0.957 for the total scale and 0.945, 0.888, and 0.885 for the 3 factors. The half-point reliability of the scale was 0.936, and the retest reliability was 0.877. The Pearson correlation coefficients for the 3 factors and the total scale score ranged from 0.768 to 0.946. CONCLUSION: The TABS-C has reliable psychometric properties and is suitable for usage among college students in the Chinese context.

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Objective@#To investigate the prevalence of depression and anxiety among transgender populations and the correlation with defense mechanism, so as to provide the evidence for improving mental health among transgender populations. @*Methods@#Transgender populations that visited Psychosexual Outpatient Department of Beijing Huilongguan Hospital for the first time from December 2020 to December 2021 were enrolled. Participants' demographics, depression, anxiety and type of defense mechanisms were collected using self-designed questionnaires, Self-rating Depression Scale, Self-rating Anxiety Scale and Defense Style Questionnaire (DSQ). Factors affecting depression and anxiety were identified using a multivariable logistic regression model. @*Results@#Totally 126 transgender individuals were enrolled, including 95 men (75.40%) with a mean age of (21.53±4.55) years and 31 women (24.60%) with a mean age of (23.58±5.55) years. The prevalence of depression was 46.83% among participants, including 44.07% of participants with mild depression, 30.51% with moderate depression and 25.42% with severe depression, and the prevalence of anxiety was 26.19% among participants, including 60.61% of participants with mild anxiety, 21.21% with moderate anxiety and 18.18% with severe anxiety. The detection of depression was 54.74% among men and 22.58% among women (P<0.05), and the detection of both depression (62.79% vs. 38.55%, P<0.05) and anxiety (41.86% vs. 18.07%, P<0.05) was significantly higher among transgender populations with self-injury or suicide behaviors than among those without. Multivariable logistic regression analysis showed that immature defense mechanisms increased the risk of depression (OR=1.034, 95%CI: 1.018-1.051) and anxiety (OR=1.031, 95%CI: 1.014-1.049) among transgender populations, while mature defense mechanisms reduced the risk of depression (OR=0.887, 95%CI: 0.832-0.946) and anxiety (OR=0.878, 95%CI: 0.821-0.938) among transgender populations.@*Conclusions@#The prevalence of depression and anxiety was 46.83% and 26.19% among transgender populations included in this study. Mature defense mechanisms are beneficial to reduce the risk of depression and anxiety among transgender populations. Key words： transgender population depression anxiety defense mechanism

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Tibia fracture (BF) enhances stroke injury and post-stroke memory dysfunction in mouse. Reduction of neuroinflammation by activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) reduced acute neuronal injury and sensorimotor dysfunction in mice with BF 1-day after stroke. We hypothesize that reduction of neuroinflammation by activation of α-7 nAchR improves long-term memory function of mice with BF 6-h before stroke. The mice were randomly assigned to saline, PHA-568487 (α-7 nAchR agonist) and methyllycaconitine (antagonist) treatment groups. The sensorimotor function was tested by adhesive removal and corner tests at 3 days, the memory function was tested by Y-maze test weekly for 8 weeks and novel objective recognition test at 8 weeks post-injuries. We found PHA-568487 treatment reduced, methyllycaconitine increased the number of CD68+ cells in the peri-infarct and hippocampal regions, neuronal injury in the infarct region, sensorimotor and long-term memory dysfunctions. PHA-568487 treatment also reduced, while methyllycaconitine treatment increased atrophy of hippocampal granule cell layer and white matter damage in the striatum. In addition, PHA-568487 treatment increased neuron proliferation in granule cell layer. Our data indicated that reduction of neuroinflammation through activation of α-7 nAchR decreased neuronal damage, sensorimotor and long-term memory dysfunction of mice with BF shortly before stroke.

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[This corrects the article DOI: 10.3389/fnins.2020.00215.].

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Microemulsion cleaning method has been proved to be an effective way to clean oily sludge with low interfacial tension and high solubilizing ability for non-miscible liquids. In this paper, the percentage range of the microemulsion in the formulation was obtained by studying phase behavior of the microemulsion. The response surface method was used to model and optimize the microemulsion to obtain the best formulation: n-BuOH content at 9.89%, NaCl content at 2.24% and AES/APG ratio at 3.75, and the oil removal rate reached 97.28%. Meanwhile, the cleaning conditions of oil sludge were also optimized by the response surface method and the optimal cleaning parameters were determined as liquid-solid ratio at 4.2, stirring rate at 157 r·min-1, and stirring time at 38 min. In addition, some experiments were carried out to confirm the simulation results, affording the oil removal rate of 98.79%. SEM and FTIR confirmed that the oil on the sludge can be removed by microemulsion.

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BACKGROUND: Tibia fracture (BF) before stroke shortly causes long-term post-stroke memory dysfunction in mice. The mechanism is unclear. We hypothesize that BF enhances neuroinflammation and blood brain barrier (BBB) breakdown in the hippocampus and white matter (WM) damage. METHODS: Mice were assigned to groups: BF, stroke, BF+stroke (BF 6 h before stroke) and sham. BBB integrity was analyzed 3 days after the surgeries and WM injury was analyzed 3 days and 8 weeks after the surgeries. RESULTS: Stroke and BF+stroke groups had more activated microglia/macrophages and lower levels of claudin-5 in the ipsilateral hippocampi than the BF group. BF+stroke group had the highest number microglia/macrophages and the lowest level of claudin-5 among all groups and had fewer pericytes than BF group. Stroke and BF+stroke groups had smaller WM areas in the ipsilateral basal ganglia than the sham group 8 weeks after the injuries. The BF+stroke group also had smaller WM areas in the ipsilateral than sham and BF groups 3 days after the injuries and in the contralateral basal ganglia than stroke and BF groups 8 weeks after the injuries. CONCLUSIONS: BF exacerbates neuroinflammation and BBB leakage in the hippocampus and WM damage in basal ganglia, which could contribute to the long-lasting memory dysfunction in BF+stroke mice.

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A novel, Gram-stain-positive, rod-shaped, non-motile, non-spore-forming, obligately anaerobic bacterium, designated strain ZHW00191T, was isolated from human faeces and characterized by using a polyphasic taxonomic approach. Growth occurred at 25-45 °C (optimum, 37-42 °C), at pH 5.5-10.0 (optimum, pH 6.5-7.0) and with 0-2 % (w/v) NaCl (optimum, 0 %). The end products of glucose fermentation were acetic acid, isobutyric acid and isovaleric acid and a small amount of propionic acid. The dominant cellular fatty acids (>10 %) of strain ZHW00191T were C16 : 0, C18 : 1 ω9с and C18 : 2ω6,9с. Its polar lipid profile comprised diphosphatidylglycerol, phosphatidylglycerol, three unidentified phospholipids and ten unidentified glycolipids. Respiratory quinones were not detected. The cell-wall peptidoglycan contained meso-2,6-diaminopimelic acid, and the whole-cell sugars were ribose and glucose. The genomic DNA G+C content was 32.8 mol%. Analysis of the 16S rRNA gene sequence indicated that ZHW00191T was most closely related to Clostridium hiranonis TO-931T (95.3 % similarity). Average nucleotide identity (ANI) and digital DNA-DNA hybridization (dDDH) analyses with closely related reference strains indicated that reassociation values were both well below the thresholds of 95-96% and 70 % for species delineation, respectively. Based on phenotypic, chemotaxonomic and genetic studies, a novel genus, Peptacetobacter gen. nov., is proposed. The novel isolate ZHW00191T (=JCM 33482T=GDMCC 1.1530T) is proposed as the type strain of the type species Peptacetobacter hominis gen. nov., sp. nov. of the proposed new genus. Furthermore, it is proposed that Clostridium hiranonis be transferred to this novel genus, as Peptacetobacter hiranonis comb. nov.

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Background: The mechanism of post-stroke cognitive impairment (PSCI) has not been explained. We aimed to investigate whether miR-let-7i participates in the PSCI and illuminates its underlying role in oxygen-glucose deprivation (OGD)-induced cell apoptosis. Methods: Blood samples from 36 subjects with PSCI and 38 with post-stroke cognitive normality (Non-PSCI) were collected to evaluate the differential expression of miR-let-7 family members, using qRT-PCT analysis. Spearman correlation was performed to estimate the correlation between the miR-1et-7i level and Montreal Cognitive Assessment (MoCA) score. Treatment of SH-SY5Y cells with OGD was used to induce cell apoptosis in vitro. Effects of miR-let-7i on OGD-induced cell apoptosis was estimated after transfection. The target gene of miR-let-7i was analyzed by dual luciferase reporter gene assay. Results: The expression of miR-let-7i was up-regulated in PSCI patients compared with Non-PSCI (p < 0.001) and negatively correlated with MoCA score (r = -0.643, p < 0.001). When exposed to OGD, SH-SY5Y cells showed significant apoptosis accompanied by miR-let-7i up-regulation. In OGD-treated cells, miR-let-7i up-regulation was accompanied by cell apoptosis, while down-regulation showed the opposite effect. Luciferase reporter assay showed that Bcl-2 was a target gene of miR-let-7i. Western blot showed that miR-let-7i up-regulation promoted Bcl-2 expression, while qRT-PCR showed that miR-let-7i had no effect on Bcl-2 expression. Conclusion: miR-let-7i was overexpressed in PSCI patients and it could be used as a diagnostic biomarker for PSCI. We illuminated the potential mechanism that miR-let-7i alleviated OGD-induced cell damage by targeting Bcl-2 at the post-transcriptional level.

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Recent researches suggested that iron dysregulation play an important role in the pathogenesis of vascular dementia (VD). Iron deposition had been found in hippocampus in vascular dementia model in recent research. Nevertheless, the underlying mechanisms of iron deposition and its neurotoxicity in vascular dementia was still unclear. Thus, our research was aimed at whether the neurotoxicity of iron was associated with autophagy regulation. We established a chronic cerebral hypoperfusion model in the rat brain in order to mimic the vascular dementia using permanent bilateral common carotid artery occlusion (2VO). The preparation of iron overloaded rats model by intraperitoneal injection of iron dextran. Following, we tested the learning and memory function of each group using Morris Water Maze. Consequently, we analyzed the iron content and iron transport related molecules (TFR1, DMT1) in hippocampus. Furthermore, we examined the effect of iron deposition on autophagy-related molecules including AMPK, Beclin1 and LC3 and the number of autophagosomes in hippocampus. Last, we tested the apoptosis of neurons in hippocampus. We found that iron deposition in hippocampus in model groups which accompanied the decline of learning and memory function. And the expression of TFR1 and DMT1 were up-regulated in model groups. Moreover, iron deposition up-regulated the expression of AMPK, Beclin1 and LC3 and increase the number of autophagosomes in hippocampus. And the expression of Bax was up-regulated and Bcl-2 was down-regulated in iron deposition groups. To sum up, our data suggested that iron deposition increased AMPK/autophagy pathway associated molecules in the hippocampus and promoted neuronal apoptosis, which might be a new pathogenesis in vascular dementia.

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Background. Parkinson's disease is a neurodegenerative disease in elder people, pathophysiologic basis of which is the severe deficiency of dopamine in the striatum. The purpose of the present study was to evaluate the neuroprotective effect of low-frequency rTMS on Parkinson's disease in model mice. Methods. The effects of low-frequency rTMS on the motor function, cortex excitability, neurochemistry, and neurohistopathology of MPTP-induced Parkinson's disease mice were investigated through behavioral detection, electrophysiologic technique, high performance liquid chromatography-electrochemical detection, immunohistochemical staining, and western blot. Results. Low-frequency rTMS could improve the motor coordination impairment of Parkinson's disease mice: the resting motor threshold significantly decreased in the Parkinson's disease mice; the degeneration of nigral dopaminergic neuron and the expression of tyrosine hydroxylase were significantly improved by low-frequency rTMS; moreover, the expressions of brain derived neurotrophic factor and glial cell line derived neurotrophic factor were also improved by low-frequency rTMS. Conclusions. Low-frequency rTMS had a neuroprotective effect on the nigral dopaminergic neuron which might be due to the improved expressions of brain derived neurotrophic factor and glial cell line-derived neurotrophic factor. The present study provided a theoretical basis for the application of low-frequency rTMS in the clinical treatment and recovery of Parkinson's disease.

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It has been well established that the mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) opener, diazoxide, has protective effects on the heart and brain following ischemia/reperfusion injury. However, the mechanism of the neuroprotective effects of diazoxide remains unclear. This study highlights the anti-apoptotic effects of the drug, which are mediated by specific regulation of apoptosis-inducing factor (AIF) in the process of oxygen and glucose deprivation (OGD)-induced apoptosis in SH-SY5Y cells. Our data showed that pretreatment with diazoxide in SH-SY5Y cells following OGD concentration-dependently increased cell viability. Compared to cells induced by OGD alone, cells pretreated with diazoxide displayed reduced rates of apoptosis, increased mitochondrial transmembrane potential (ΔΨm), and reduced AIF translocation to the cell nucleus. The protective effects of preconditioning with diazoxide were attenuated by 5-hydroxydecanoic acid (5-HD), a selective mitoK(ATP) channel antagonist. Meanwhile, cell death was blocked in OGD-induced cells stably transfected with the AIF-shRNA plasmid, and down-regulation of AIF reduced the diazoxide-mediated prevention of cell apoptosis as well as the loss of ΔΨm induced by OGD. Taken together, our results demonstrate for the first time that the AIF-mediated mitochondrial pathway plays a critical role in the protective effect of diazoxide against SH-SY5Y cell apoptosis induced by OGD. Diazoxide treatment might represent a novel therapeutic target for the treatment of ischemic cerebrovascular diseases.

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Although there is increasing evidence that the ATP sensitive potassium channel (K(ATP)) opener exhibits neuroprotective effects against ischaemic neural damage, little is known about the mechanism. Mitochondria play a key role in apoptosis by releasing many important factors, including cytochrome c and apoptosis-inducing factor, which in turn initiate the caspase-dependent and -independent mitochondrial pathway, respectively. In the present study, we sought to determine the locus that K(ATP) opener uses to mediate this protection in PC12 cells. We found that pre-treatment of PC12 cells with diazoxide (DZX), a mitochondrial ATP sensitive potassium channel (mitoK(ATP)) opener, dose-dependently increased cell viability under conditions of oxygen glucose deprivation (OGD). The protective effect of this pre-conditioning was attenuated by 5-hydroxydecanoic acid, a selective mitoK(ATP) blocker. The results showed that DZX inhibits the release of cytochrome c, the activation of caspase-3 and the release of AIF evoked by OGD. Taken together, our results demonstrate for the first time that activation of the mitoK(ATP) channel elicits protective effects against OGD-induced cell apoptosis by caspase-dependent and -independent mitochondrial pathways.

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