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This study aimed to explore the pathway from childhood trauma to nonsuicidal self-injury (NSSI) in adolescents with major depressive disorder (MDD) and to examine the chain-mediating role of psychological resilience and depressive symptoms in this pathway. A total of 391 adolescents with MDD were recruited in the present study. The Chinese version of the Childhood Trauma Questionnaire-Short Form (CTQ-SF), the Chinese version of the Symptoms Check List-90 (SCL-90), the Chinese version of the Conner-Davidson Resilience Scale (CD-RISC), and the Ottawa Self-Injury Inventory Chinese Revised Edition (OSIC) were used to evaluate childhood trauma, depressive symptoms, psychological resilience and NSSI, respectively. Our results showed that 60.87% of adolescents with MDD had NSSI in the past month. Childhood trauma frequency was negatively correlated with psychological resilience but positively correlated with depressive symptoms and NSSI severity in adolescents with MDD. The stepwise logistic regression analysis identified that age, childhood trauma and depressive symptoms could independently predict the occurrence of NSSI, and the three-step hierarchical regression showed that childhood trauma, psychological resilience and depressive symptoms were all significantly associated with NSSI frequency in adolescents with MDD. Furthermore, the chain-mediation analysis revealed that psychological resilience and depression serially mediated the relationship between childhood trauma and NSSI in adolescents with MDD. Interventions targeted at improving resilience and depression may mitigate the impact of childhood trauma severity on NSSI risk in adolescents with MDD.
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Objective: To observe the levels of serum 3-nitrotyrosine (3-NT), neuronal PAS domain protein 4 (NPASDP-4), and S100ß protein in patients diagnosed with cerebral infarction and analyze their correlation with cognitive dysfunction in these patients. Methods: The study included a cohort of 158 patients suffering from cerebral infarction who were admitted to the Liwan District Hospital of Traditional Chinese Medicine between January 2021 and December 2022. After stabilizing vital signs, all patients underwent the Montreal Cognitive Assessment (MoCA) to assess their cognitive function. Based on the assessment results, they were divided into two groups: the cognitive dysfunction group (121 cases) and the normal cognitive function group (37 cases). The baseline characteristics and serum levels of 3-NT, neuronal PAS domain protein 4 (NPASDP-4), and S100ß protein were compared in the patient cohorts. Furthermore, the correlation between these three indicators and cognitive function in patients suffering from cerebral infarction was analyzed. A logistic regression model was constructed to analyze how serum levels of 3-NT, NPASDP-4, and S100ß protein levels affected cognitive function in patients suffering from cerebral infarction. ROC curve analysis was conducted to assess the predictive value of serum 3-NT, NPASDP-4, and S100ß protein levels for cognitive function in patients suffering from cerebral infarction. Results: Among the 158 patients with cerebral infarction, 121 (76.58%) had cognitive dysfunction, while 37 (23.42%) had normal cognitive function. The levels of 3-NT, NPASDP-4, and S100ß protein were found to be significantly higher in the cognitive dysfunction group compared to the normal cognitive function group (t = 5.788, 7.774, 6.460; P = .000, .000, .000). The point-biserial correlation analysis results showed a positive correlation between serum levels of 3-NT, NPASDP-4, and S100ß protein and the occurrence of cognitive dysfunction in patients suffering from cerebral infarction (r=0.420, 0.529, 0.424; P = .000, .000, .000). The logistic regression model demonstrated that serum levels of 3-NT(95%CI: 1.299-2.603), NPASDP-4(95%CI: 1.487-3.386), and S100ß protein(95%CI: 1.153-8.746) were risk factors for cognitive dysfunction in patients suffering from cerebral infarction (OR=1.839, 2.244, 1.429; P = .001, .000, .240). ROC curve analysis demonstrated that serum 3-NT, NPASDP-4, and S100ß protein levels exhibited a certain predictive value for cognitive function in patients with cerebral infarction (AUC = 0.789, 0.881, 0.820). Conclusion: Serum levels of 3-NT, NPASDP-4, and S100ß protein are closely related to the cognitive function of patients with cerebral infarction, and abnormal changes in these levels may exacerbate cognitive dysfunction in these patients.
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We use in situ synchrotron grazing incidence X-ray diffraction and X-ray reflectivity to investigate with high resolution the structure of a two-dimensional single layer of tantalum sulfide grown on a Au(111) surface and its evolution during intercalation by Cs atoms and deintercalation, which decouples and recouples the two materials, respectively. The grown single layer consists of a mixture of TaS2 and its S-depleted version, TaS, both aligned with gold, and forming moirés where 7 (respectively 13) lattice constants of the 2D layer almost perfectly match 8 (respectively 15) substrate lattice constants. Intercalation fully decouples the system by lifting the single layer by â¼370 pm and induces an increase of its lattice parameter by 1-2 picometers. The system gradually evolves, during cycles of intercalation/deintercalation assisted by an H2S atmosphere, toward a final coupled state consisting of the fully stoichiometric TaS2 dichalcogenide whose moiré is found very close to the 7/8 commensurability. The reactive H2S atmosphere appears necessary to achieve full deintercalation, presumably by preventing S depletion and the concomitant strong bonding with the intercalant. The structural quality of the layer improves during the cyclic treatment. In parallel, because they are decoupled from the substrate by the intercalation of cesium, some of the TaS2 flakes rotate by 30°. These produce two additional superlattices with characteristic diffraction patterns of different origins. The first is aligned with gold's high symmetry crystallographic directions and is a commensurate moiré ((6 × 6)-Au(111) coinciding with (3â3 × 3â3)R30°-TaS2). The second is incommensurate and corresponds to a near coincidence of (6 × 6) unit cells of 30°-rotated TaS2 with (4â3 × 4â3)Au(111) surface ones. This structure, which is less coupled to gold, might be related to the â¼(3× 3) charge density wave previously reported even at room temperature in TaS2 grown on noninteracting substrates. A (3 × 3) superstructure of 30°-rotated TaS2 islands is indeed revealed by complementary scanning tunneling microscopy.
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Background: Acupuncture is a well-known treatment option for ischemic stroke recovery, but evidence of its effectiveness remains limited. This is a randomized controlled trial to evaluate the effectiveness of acupuncture treatment for ischemic stroke rehabilitation. Methods: Rehabilitation training was provided to the control group. In acupuncture arm 1, these acupoints were derived from the ancient books, including GV20 (baihui), GV26 (shuigou), PC9 (zhongchong), ST6 (jiache), ST4 (dicang), LI15 (jianyu), LI11 (quchi), LI4 (hegu), GB30 (huantiao), GB31 (fengshi), GB34 (yanglingquan), and GB39 (xuanzhong). In acupuncture arm 2, the acupoints used were GV20 (baihui), PC6 (neiguan), LI11 (quchi), LI10 (shousanli), SJ5 (waiguan), LI4 (hegu), GB30 (huantiao), ST36 (zusanli), GB34 (yanglingquan), SP6 (sanyinjiao), ST41 (jiexi), and LR3 (taichong), which were extracted from Acupuncture and Moxibustion Science. After acupuncture, the needles were left in for 30 min and manually manipulated every 10 min. The three groups received treatment once a day, 5 times a week for 2 weeks. The primary outcome was the National Institutes of Health Stroke Scale (NIHSS), and the secondary outcomes were the Barthel Index (BI) and the Modified Ashworth Scale (MAS). Outcomes were measured in patients both before and after treatment. Results: A total of 497 patients with ischemic stroke were randomized into either arm 1 (159 cases), arm 2 (173 cases), or the control group (165 cases). After 2 weeks of treatment, the NIHSS scores for arm 1 were lower than those of the control group (P = 0.017); the BI scores were higher in arm two than that in the control group at T2 (P = 0.016) and follow-up (P = 0.020). Additionally, there was no significant difference between arm one and the control group for either the BI scores or the MAS scores (P > 0.05) and no significant difference between arm two and the control group for the MAS scores or the NIHSS scores (P > 0.05). Conclusion: The clinical efficacy of arm 1 and arm 2 (acupuncture groups) was superior to that of the control group, but there was no difference between the effects of the two acupuncture groups. Clinical Trial Registration: http://www.chictr.org.cn/index.aspx, identifier: ChiCTR-IOR-16008627.
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Xylose is one of the most abundant carbohydrates in nature, and widely used to produce bioethanol via fermentation in industry. Xylulose can produce two key enzymes: xylose reductase and xylitol dehydrogenase. Owing to the disparate cofactor specificities of xylose reductase and xylitol dehydrogenase, intracellular redox imbalance is detected during the xylose fermentation, resulting in low ethanol yields. To overcome this barrier, a common strategy is applied to artificially modify the cofactor specificity of xylose reductase. In this study, we utilized molecular simulation approaches to construct a 3D (three-dimensional) structural model for the NADP-dependent Pichia stipitis xylose reductase (PsXR). Based on the 3D model, the favourable binding modes for both cofactors NAD and NADP were obtained using the flexible docking procedure and molecular dynamics simulation. Structural analysis of the favourable binding modes showed that the cofactor binding site of PsXR was composed of 3 major components: a hydrophilic pocket, a hydrophobic pocket as well as a linker channel between the aforementioned two pockets. The hydrophilic pocket could recognize the nicotinamide moiety of the cofactors by hydrogen bonding networks, while the hydrophobic pocket functioned to position the adenine moiety of the cofactors by hydrophobic and Π-Π stacking interactions. The linker channel contained some key residues for ligand-binding; their mutation could have impact to the specificity of PsXR. Finally, it was found that any of the two single mutations, K21A and K270N, might reverse the cofactor specificity of PsXR from major NADP- to NADdependent, which was further confirmed by the additional experiments. Our findings may provide useful insights into the cofactor specificity of PsXR, stimulating new strategies for better designing xylose reductase and improving ethanol production in industry.