To verify the accuracy of a Non-Contact Sleep Monitoring Mattress (NCSMM) based on body movement during sleep in assessing sleep quality of patients before neurosurgery in order to provide a more portable and efficient assessment tool for clinical staff.

A single-arm trial was conducted on 114 inpatients admitted in our department selected with convenience sampling. Sleep quality data of 1 night were collected through 5 sleep quality assessment tools, including NCSMM, polysomnography (PSG), Patient-Reported Outcome Measurement Information System (PROMIS) Sleep Disturbance scale, Richards-Campbell Sleep Scale (RCSQ), and a wearable device (smart watch for body movements and sleep quality monitoring). The sleep efficiency (≤85%) obtained by PSG was used as the diagnostic standard for sleep disorders. The area under the receiver operating characteristic curve (AUC), sensitivity, specificity, positive predictive value, negative predictive value, and Youden index were calculated for the other 4 tools to evaluate and compare their diagnostic effectiveness.

The AUC value for NCSMM, PROMIS, RCSQ and smart watch was 0.788 (95%CI: 0.687~0.888, P<0.001), 0.664 (95%CI: 0.543~0.784, P=0.02), 0.723 (95%CI: 0.600~0.846, P=0.001) and 0.750 (95%CI: 0.654~0.846, P<0.001), respectively. The diagnostic accuracy rate was 0.774, 0.559, 0.742 and 0.602, with corresponding Youden index value of 0.488, 0.321, 0.456, and 0.459. NCSMM demonstrated the best AUC value, sensitivity and Youden index when compared with the other 3 tools.

NCSMM shows high accuracy in assessing sleep quality in pre-neurosurgery inpatients, and it is a viable portable and efficient assessment tool in clinical practice.

To explore the effect and preliminary mechanism of the plant-derived immunostimulatory molecule, ophiopogonin, on enhancing the immune response of a subunit vaccine with the receptor-binding domain (RBD) of coronavirus spike protein as the antigen.

CCK-8 assay was used to determine the cytotoxicity of ophiopogonin D' (OPD') on bone marrow-derived dendritic cells (BMDCs). Female Balb/c mice were randomly divided into RBD, RBD/OPD', RBD/Alum, and control groups. The immunization dose was 5 μg of antigen per mouse and 100 μg of adjuvant per mouse, and immunization was carried out according to the intramuscular injection immunization procedure on days 0, 21, and 42. The titers of specific IgG and its subtype antibodies were detected by ELISA. The cytokine levels in the supernatant of splenocytes were detected using ELISA. The number of splenocytes secreting IFN-γ was detected by ELISpot. Laser confocal microscopy was employed to observe the uptake of antigen by BMDCs. The phagocytic ability of BMDCs for antigen was quantitatively analyzed by flow cytometry. The mechanism of its enhanced immune effect was preliminarily explored using transcriptomics technology combined with bioinformatics research.

When the concentration of OPD' was less than 5 μg/mL, the survival rate of BMDCs was 100%. After a single intramuscular injection in mice, except for a slight decrease in body weight, the other biochemical indicators were within corresponding normal ranges. After intramuscular injection immunization of the vaccine, the titers of serum-specific IgG, IgG1, and IgG2a in the RBD/OPD' group were significantly higher than those in the RBD group (P<0.05). Compared with the RBD group, the RBD/OPD' group induced a high-level Th1 cell immune response of IL-1β, TNF-α, and IFN-γ (P<0.01) and had more lymphocytes secreting IFN-γ (P<0.001). Laser confocal microscopy displayed that BMDCs took up more antigens after OPD' treatment, which was further confirmed with flow cytometry in quantitative analysis on antigen uptake rate (P<0.01). Transcriptomics results indicated that there was more significant enrichment of the PPAR signaling pathway in the RBD/OPD' group than the RBD group, suggesting that OPD' may activate the PPAR signaling pathway to exert its adjuvant effect.

OPD' effectively enhances the immune response of the RBD subunit vaccine, and its action mechanism may be related to the activation of the PPAR signaling pathway.

To investigate the characteristics of attentional bias towards cancer-related stimuli in breast cancer patients with fear of cancer recurrence (FCR) under subthreshold and suprathreshold stimulus conditions.

A total of 94 female breast cancer patients admitted in First Affiliated Hospital of Army Medical University from September 2022 to March 2023 were recruited to complete the Fear of Cancer Recurrence Inventory-Short Form (FCRI-SF) and the dot-probe task. According to the FCRI-SF cut-off score of 13, they were divided into clinical and non-clinical FCR groups, with 47 cases in each group. One-sample t-test and repeated-measures ANOVA were used to statistically analyze the subjects in the 2 groups in terms of attentional bias score, attentional orienting score and attentional disengagement difficulty score.

The patients in the clinical FCR group showed a significant attentional bias toward cancer-related negative words (P<0.05). Under the subthreshold stimulus condition, its main component was attentional orienting to cancer-related negative words (P<0.05). In the suprathreshold stimulus condition, the main components were attentional orienting to neutral words matched by cancer-related negative words and difficulty in attentional disengagement from cancer-related negative words as well as attentional avoidance for cancer-related positive words (P<0.05).

Breast cancer patients with clinical FCR have an attentional bias toward cancer-related negative stimuli. Reducing their attention to cancer-related negative stimuli may be an effective measure to reduce FCR level in the patients.

To identify and delineate the developmental trajectories of depressive symptoms in the middle-aged and elderly population in China, and to explore the risk factors for depressive symptom trajectories in China's middle-aged and elderly population.

According to our inclusion and exclusion criteria, 7 600 participants were subjected based on the data from the China Health and Aged Care Tracking Survey (CHARLS) published by Peking University. The data from 5 waves of the survey from 2011 to 2023 were collected and analyzed with latent growth curve model (LGCM), latent class growth model (LGCM) to identify the developmental trajectories of depressive symptoms in the participants. Multicategorical logistic regression analyses were conducted to analyze whether gender, marital status, educational level, urban/rural residence, annual income, self-rated health status, and childhood bullying experience were risk factors for different trajectories of depressive symptoms.

Two developmental trajectories of depressive symptoms were identified and classified in this study, that is, low-level stable (n=5 545, 72.96%) and high-level ascending (n=2 055, 27.04%). With the low-level stable group as a reference, multicategorical logistic regression analysis revealed that female (OR=1.373, 95CI%: 1.191~1.584, P<0.001), residence of rural area (OR=1.634, 95CI%: 1.410~1.895, P<0.001), and poor self-rated health status (OR=2.059, 95%CI: 1.890~2.243, P<0.001), and experience of childhood bullying (OR=1.76, 95%CI: 1.489~2.080, P<0.001) were associated with an increased risk of high-level ascending trajectory of depression.

There are 2 different trajectories of depressive mood in Chinese middle-aged and elderly population. And poor self-rated health status, history of childhood bullying, being female, and residence of rural area are risk factors for a high-level ascending trajectory of depressive symptoms.

To explore the causal relationships of anxiety, depression and neuroticism with recurrent spontaneous abortion (RSA).

Genome-wide association study (GWAS) data were used to extract single nucleotide polymorphisms (SNPs) closely related to anxiety, depression and neuroticism as instrumental variables (IVs). Inverse variance weighting (IVW), weighted median estimator (WME), weighted mode (WM) and Mendelian randomization (MR)-Egger regression were employed for MR analysis to evaluate the causal effects of anxiety, depression and neuroticism with RSA, and to analyze heterogeneity, gene pleiotropy and sensitivity.

A total of 46 SNPs were extracted from GWAS data as IVs (5 anxiety SNPs, 9 depression SNPs, and 32 neuroticism SNPs). IVW, WME, WM and MR-Egger regression analysis revealed that the odds ratio (OR) and 95% confidence interval (CI) of anxiety data were 1.07 (0.86-1.32), 1.10 ( 0.85-1.43), 1.14 (0.81-1.59) and 1.18 (0.53-2.61); those of depression data were 1.11 (0.93-1.32), 1.05 (0.83-1.32), 0.96 (0.67-1.38) and 0.57 (0.25-1.31); those of neuroticism data were 1.01 (0.75-1.36), 1.07 (0.73-1.56), 1.02 (0.49-2.12) and 2.40 (0.46-12.44), but none of the above causal analyses were statistically significant (all P>0.05). After reliability analysis, the Cochran's Q test for heterogeneity evaluation was not significant (P>0.05), the MR-Egger regression intercepts for gene pleiotropy evaluation were all close to 0 (P>0.05), and the sensitivity evaluation "Leave-one-out" test also shows that the combined causal effect values are similar.

There dose not exist causal relationships of anxiety, depression and neuroticism with RSA. The reliability test shows that the results are relatively robust.

To investigate the therapeutic efficacy of artesunate (AS) on polycystic ovary syndrome (PCOS) in mice and explore the potential mechanism primarily.

‍Twenty-five female C57BL/6J mice were randomly divided into Control group, model group (PCOS group), low- and high-dose AS groups (AS15 and AS30 groups) and metformin group (Met group). In addition to the Control group, the mouse model of PCOS was established by subcutaneous injection of dehydroepiandrosterone (DHEA, 60 mg/kg) following by a high-fat diet for 21 d. After modeling, AS of 15 and 30 mg/kg was intraperitoneally injected into the mice of the AS15 and AS30 groups, respectively, and 200 mg/kg Met was given to those of the Met group by gavage, once per day, for 6 weeks. ELISA was used to detect serum testosterone (T), fasting insulin (FINS), luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and the LH/FSH ratio was calculated. The levels of fasting blood glucose (FBG), triglyceride (TG) and total cholesterol (TC) were detected by automatic biochemical analyzer, and the homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. The estrous cycle was observed, and HE staining was performed for pathological changes in the ovary and uterus. Immunofluorescence assay was employed to measure the expression of p-eIF2α, ATF4 and CHOP in the ovarian tissue. After steroidogenic human granulosa-like tumor cell line KGN were exposed to 100 μmol/L DHEA to simulate the hyperandrogen environment of PCOS, and then treated with 5 and 10 μg/mL AS for 24 h, the protein levels of endoplasmic reticulum stress signaling pathway was detected by Western blotting.

‍Compared with the Control group, the PCOS mice had disturbed estrous cycle, polycystic changes in the ovaries, and significantly increased serum T level and LH/FSH ratio (P<0.05), and obviously elevated HOMA-IR, TC and TG levels in terms of metabolism (P<0.01). The expression levels of p-eIF2α, ATF4 and CHOP were notably up-regulated in the ovarian granulosa cells of PCOS mice and KGN cells after DHEA exposure (P<0.05). Additionally, AS treatment attenuated the pathological changes of ovary and uterine expression, decreased the serum T level and the LH/FSH ratio (P<0.05), and reduced HOMA-IR, TC and TG levels (P<0.05) when compared with the PCOS mice. Moreover, the expression levels of p-eIF2α, ATF4 and CHOP were significantly down-regulated after AS treatment in both ovarian granulosa cells of PCOS mice and KGN cells (P<0.05).

‍AS significantly improves glycolipid metabolic disorder and reproductive dysfunction in PCOS mice, which may be associated with its suppressing endoplasmic reticulum stress by inhibiting the PERK/eIF2α/ATF4/CHOP pathway.

To screen the targets related to the metabolic enzymes involved in the cholesterol synthesis pathway that inhibits the polarization of macrophages towards M1 phenotype, and verify the intervention effects and underlying mechanisms in colorectal cancer cells.

Mouse colorectal cancer MC38 cells were divided into control group (si-NC) and experimental groups (the expression of enzymes in cholesterol synthesis pathway was interfered with siRNA for corresponding targets). RT-qPCR was used to detect the mRNA levels of corresponding targets in MC38 cells after transfection. After peritoneal macrophages were extracted from male C57BL/6 mice (6 weeks old, weighing 13~18 g), the macrophages were then treated with the conditioned media of MC38 cells transfected with different siRNAs for 48 h. RT-qPCR was employed to detect the mRNA levels of IL-1β, IL-6 and TNF-α in the macrophages so as to evaluate the effect of the culture media on the M1 polarization. MC38 cells were divided into control groups (OE-NC and sh-NC), farnesyl-diphosphate farnesyltransferase 1 (FDFT1) overexpression group (OE-FDFT1) and FDFT1 knockdown group (sh-FDFT1). RT-qPCR was applied to detect the mRNA expression of FDFT1, and Western blotting was conducted to measure the protein level of FDFT1. C57BL/6 mice were subjected randomly to construct a subcutaneous tumor-bearing model and a model of intraperitoneal metastatic tumor (n=5) respectively. The growth of tumor mass was then measured. Flow cytometry was used to observe the proliferation and apoptosis of MC38 cells, and Transwell assay to detect migration ability of MC38 cells. Five C57BL/6 macrophage-depleted mice (established with injection of clodronate liposome suspension through tail vein) received intraperitoneal implantation to construct a metastasis model, and then the obtained tumor masses were then weighted.

Compared with MC38 cells after si-NC transfection, the mRNA levels of corresponding targets in MC38 cells in the experimental groups were significantly reduced (P<0.05). Significant increases were found in the mRNA levels of IL-1β, IL-6 and TNF-α of the macrophages with FDFT1 interference than the control cells (P<0.05). There were no statistical differences in the proliferation, apoptosis and migration of MC38 cells in the control group (OE-NC and sh-NC) and the cells of the FDFT1 overexpression group and FDFT1 knockdown group (P>0.05). In both the subcutaneous tumor-bearing model and the model of intraperitoneal metastatic tumor, the mass weight was significantly heavier in the OE-FDFT1 group than the OE-NC group (P<0.01), and was notably smaller in the sh-FDFT1 group than the sh-NC group (P<0.01). For the macrophage-depleted mouse tumor model, no remarkable change was observed in the tumor weight between the OE-FDFT1 group and the OE-NC group as well as the sh-FDFT1 group and the sh-NC group.

FDFT1, the metabolic enzyme in the cholesterol synthesis pathway of colorectal cancer tumor cells, is a potential target for tumor immunotherapy targeting macrophages, which promotes tumor progression by regulating macrophages.

To explore the role and mechanism of warm malate ringer’s solution (MR) in resuscitation of the lethal triad caused by severe trauma.

A rat model of severe trauma was established in SPF-grade SD rats (half male and half female, weighing 200~220 g) using combined multiple injuries and hemorrhagic shock, and the rats were randomly divided into 8 groups (n=8): Sham group, only arterial and venous catheterization; Trauma (Tra) groups with different time points (10, 30, 60, 90, 120, 180 min) and a Trauma group that were observed without any treatment for 180 min after model establishment. The changes of activated clotting time (ACT), reaction time (R), maximum amplitude (MA), and rate of blood clot formation (Angle) at different time points were detected by using thromboelastography, and tail bleeding, core body temperature and arterial blood gas parameters, were also observed and detected. The plasma von Willebrand Factor (vWF) level, mitochondrial respiratory control ratio in pulmonary venous endothelium, and expression levels of vascular endothelial cadherin (VE-Cadherin), peroxisome proliferator activating receptor gamma coactivator 1α (PGC1α), dynamin-related protein 1 (Drp1), p-Drp1, and mitofusin 2 (Mfn2) were detected to evaluate the vascular endothelial injury and mitochondrial dysfunction. Another group of SD rats were randomly divided into severe trauma group (no treatment for 180 min after injury), and MR solution at room temperature and at 37 ℃ groups. MR solution at room temperature or at 37 ℃ was given to the rats using a medical blood transfusion apparatus at 60 min post-trauma. Above indicators were observed and detected to investigate the resuscitation effect of the MR solution.

Compared with the Sham group, the severely traumatic rats at 180 min after injury had significantly prolonged ACT and R values (P<0.05), shortened MA and decreased Angle values (P<0.05), extended tail bleeding time (P<0.05), lower partial pressure of carbon dioxide (PCO₂) and HCO{}_{\mathrm{3}}^{-} and base excess (BE) levels (P<0.05), and continuously increasing K⁺ (P<0.05) and decreasing Na⁺ (P<0.05) and Ca²⁺ levels (P<0.05). Additionally, plasma vWF level (P<0.05) and protein levels of VE-cadherin, PGC1α and Mfn2 in pulmonary vein endothelium were significantly reduced (P<0.05), the expression of p-Drp1 was enhanced and the mitochondrial respiration control rate was declined in the rats at 180 min after injury (P<0.05). MR solution resuscitation shortened tail bleeding time (P<0.05), increased core body temperature (P<0.05), elevated plasma vWF level (P<0.05), increased protein levels of VE-cadherin, PGC1α and Mfn2 (P<0.05), and decreased that of p-Drp1 protein expression (P<0.05) when compared with the rats at 180 min after severe traumatic injury. The above effects were more significant in the rats infused with the solution at 37 ℃ than those at room temperature.

Warm MR solution significantly improves the lethal triad in rats after severe trauma, which may be associated with its improving mitochondrial function and attenuating vascular endothelial damage.

‍To investigate the effect of dexmedetomidine （Dex） on bone loss in tail-suspended rats and primarily explore its regulatory mechanism on bone metabolism.

‍A total of 30 male rats were randomly divided into a control group，a model group，and a Dex group，with 10 animals in each group. Rat model of osteoporosis was established by hind limb suspension for 4 weeks. Dex at a dose of 10 μg/kg was given intraperitoneally，once every other day from the day of tail suspension. And equal amount of normal saline was given to the control and model group. Bone histological staining was used to observe the trabecular bone area fraction. Biomechanical three-point bending test was employed to measure the maximum load，stiffness，and fracture energy. Dual calcein/alizarin red fluorescence labeling and tartrate resistant acid phosphatase （TRAP） staining were applied respectively to detect the mineral apposition rate and bone formation rate as well as the number of osteoclasts on bone surfaces. Secondly，after primary osteoblasts were isolated from the tibiae of tail-suspended rats and then treated with 1 nmol/L Dex，the proportion of alkaline phosphatase （ALP）-positive osteoblasts and the activity of the enzyme were detected by ALP staining and activity test. qRT-PCR was applied to measure the expression of osteogenic activity-related factors，including osteocalcin （Ocn），Runt related transcription factor 2 （Runx2），Osterix protein （Osx），and type 1 collagen （Col1）.

‍The animal experiments revealed that Dex treatment significantly increased the tibial trabecular bone area fraction，inhibited the decrease in bone mechanical strength，and enhanced the mineralization deposition rate and new bone formation rate of trabecular bone in the tail-suspended rats （all P<0.001）. The in vitro experiments showed that Dex treatment obviously improved ALP activity and the number of ALP-positive osteoblasts in primary osteoblasts isolated from tail-suspended rats （P<0.01），and up-regulated the expression levels of osteogenic differentiation-related genes，such as Ocn，Runx2，Osx and Col1 （P<0.01）.

‍Dex exerts anti-bone loss effect in tail-suspended rats，which may be associated with its stimulation on osteoblast-mediated bone formation.

To identify the hub gene of fibroblast-like synoviocytes in rheumatoid arthritis (RA) and verify its impact on proliferation, migration and invasion of the cells.

Four independent synovial tissue microarray transcriptome sequencing datasets and one single cell sequencing dataset were downloaded from the Gene Expression Omnibus (GEO) database, and the hub gene of RA fibroblast-like synovial cells was identified by differential gene analysis, weighted gene co-expression network analysis (WGCNA) and single-cell sequencing data analysis. The expression of TNFAIP6 in human RA fibroblast-like synovial cell line MH7A was detected by RT-qPCR and Western blotting under simulated inflammatory environment. After MH7A cells were transfected with si-TNFAIP6, CCK-8 and Transwell assays were applied to detect the effects of silencing TNFAIP6 on the proliferation, migration and invasion abilities of MH7A cells.

With the aid of differential gene expression analysis, WGCNA, and single-cell sequencing data, we identified TNFAIP6 as the characteristic gene of RA fibroblast-like synoviocytes. RT-qPCR and Western blot assay demonstrated that TNFAIP6 was significantly highly expressed at mRNA and protein levels in MH7A cells stimulated with 10 ng/mL TNF-α when compared to the cells treated with PBS (P<0.05). CCK-8 and Transwell assays indicated that the silencing of TNFAIP6 markedly inhibited the proliferation, migration and invasion abilities of MH7A cells when compared with the control cells (FAM-si-NC,P<0.05).

TNFAIP6 is highly expressed specifically in RA fibroblast synoviocytes, which promotes the proliferation, migration and invasion, and may be the main contributor to the abnormal activation of RA fibroblast synoviocytes.