ObjectiveTo explore the protective effect and underlying mechanism of Gegen Qinliantang on cognitive function in db/db mice with diabetic cognitive impairment （DCI）. MethodsThirty-two 8-week-old male db/db mice were randomly assigned to the model group， dapagliflozin group （1.0 mg·kg^-1·d^-1）， low-dose Gegen Qinliantang group （6.24 g·kg^-1·d^-1）， and high-dose Gegen Qinliantang group （24.96 g·kg^-1·d^-1）. Eight db/m mice served as the normal group. All mice were administered the corresponding treatment once daily by gavage for 10 consecutive weeks. Body weight and fasting blood glucose （FBG） were dynamically monitored. The Morris water maze test was used to evaluate cognitive function. Hematoxylin-eosin （HE） staining and Nissl staining were used to observe pathological changes in the hippocampus. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in hippocampal tissue. Immunofluorescence double staining was used to detect the co-expression of M1 microglial marker CD16/32 and ionized calcium-binding adapter molecule 1 （IBA1） in the hippocampus. Western blot analysis was performed to detect the protein expression of postsynaptic density protein 95 （PSD-95）， synapsin （SYN）， nuclear factor-κB p65 （NF-κB p65）， and phosphorylated NF-κB p65 （p-NF-κB p65） in the hippocampus. ResultsCompared with the normal group， the model group showed significantly increased body weight and FBG levels （P<0.01）， significantly prolonged escape latency and reduced platform crossings in the Morris water maze test （P<0.01）， disordered arrangement of hippocampal neurons， nuclear pyknosis， increased neuronal necrosis， reduced Nissl bodies， decreased expression of synaptic proteins PSD-95 and SYN （P<0.01）， increased CD16/32⁺ /IBA1⁺ positive rate， elevated levels of TNF-α and IL-1β， and an increased p-NF-κB p65/NF-κB p65 ratio （P<0.01）. Compared with the model group， the dapagliflozin group exhibited significantly reduced FBG levels at weeks 5 and 10 （P<0.05， P<0.01） and increased body weight. The high-dose Gegen Qinliantang group showed significantly reduced FBG at week 10 （P<0.05）. Escape latency was significantly reduced on days 3 and 5 of the water maze test in the dapagliflozin group and on day 5 in the high-dose Gegen Qinliantang group （P<0.05）. Platform crossings were significantly increased in both the dapagliflozin group and the high-dose Gegen Qinliantang group （P<0.05）. Hippocampal pathological damage was alleviated to varying degrees in the dapagliflozin group and the low- and high-dose Gegen Qinliantang groups， with significantly increased expression of PSD-95 and SYN （P<0.01）. Further studies revealed that both low- and high-dose Gegen Qinliantang reduced hippocampal IL-1β levels and the CD16/32⁺/IBA1⁺ positive rate of microglia， while the high-dose group also significantly reduced hippocampal TNF-α levels and the p-NF-κB p65/NF-κB p65 （P<0.05， P<0.01）. ConclusionGegen Qinliantang can improve hyperglycemia， cognitive dysfunction， and synaptic damage in DCI， inhibit M1 polarization of microglia and neuroinflammation， and its mechanism may be related to the inhibition of NF-κB activation.

ObjectiveTo explore the protective effect and underlying mechanism of Gegen Qinliantang on cognitive function in db/db mice with diabetic cognitive impairment （DCI）. MethodsThirty-two 8-week-old male db/db mice were randomly assigned to the model group， dapagliflozin group （1.0 mg·kg^-1·d^-1）， low-dose Gegen Qinliantang group （6.24 g·kg^-1·d^-1）， and high-dose Gegen Qinliantang group （24.96 g·kg^-1·d^-1）. Eight db/m mice served as the normal group. All mice were administered the corresponding treatment once daily by gavage for 10 consecutive weeks. Body weight and fasting blood glucose （FBG） were dynamically monitored. The Morris water maze test was used to evaluate cognitive function. Hematoxylin-eosin （HE） staining and Nissl staining were used to observe pathological changes in the hippocampus. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in hippocampal tissue. Immunofluorescence double staining was used to detect the co-expression of M1 microglial marker CD16/32 and ionized calcium-binding adapter molecule 1 （IBA1） in the hippocampus. Western blot analysis was performed to detect the protein expression of postsynaptic density protein 95 （PSD-95）， synapsin （SYN）， nuclear factor-κB p65 （NF-κB p65）， and phosphorylated NF-κB p65 （p-NF-κB p65） in the hippocampus. ResultsCompared with the normal group， the model group showed significantly increased body weight and FBG levels （P<0.01）， significantly prolonged escape latency and reduced platform crossings in the Morris water maze test （P<0.01）， disordered arrangement of hippocampal neurons， nuclear pyknosis， increased neuronal necrosis， reduced Nissl bodies， decreased expression of synaptic proteins PSD-95 and SYN （P<0.01）， increased CD16/32⁺ /IBA1⁺ positive rate， elevated levels of TNF-α and IL-1β， and an increased p-NF-κB p65/NF-κB p65 ratio （P<0.01）. Compared with the model group， the dapagliflozin group exhibited significantly reduced FBG levels at weeks 5 and 10 （P<0.05， P<0.01） and increased body weight. The high-dose Gegen Qinliantang group showed significantly reduced FBG at week 10 （P<0.05）. Escape latency was significantly reduced on days 3 and 5 of the water maze test in the dapagliflozin group and on day 5 in the high-dose Gegen Qinliantang group （P<0.05）. Platform crossings were significantly increased in both the dapagliflozin group and the high-dose Gegen Qinliantang group （P<0.05）. Hippocampal pathological damage was alleviated to varying degrees in the dapagliflozin group and the low- and high-dose Gegen Qinliantang groups， with significantly increased expression of PSD-95 and SYN （P<0.01）. Further studies revealed that both low- and high-dose Gegen Qinliantang reduced hippocampal IL-1β levels and the CD16/32⁺/IBA1⁺ positive rate of microglia， while the high-dose group also significantly reduced hippocampal TNF-α levels and the p-NF-κB p65/NF-κB p65 （P<0.05， P<0.01）. ConclusionGegen Qinliantang can improve hyperglycemia， cognitive dysfunction， and synaptic damage in DCI， inhibit M1 polarization of microglia and neuroinflammation， and its mechanism may be related to the inhibition of NF-κB activation.

Objective To investigate the role and mechanism of NLRP3/Caspase-1/IL-1 β inflammasome pathway in the formation of aortic dissection in mice.Methods Fifty male C57BL/6 mice(3 weeks old,body weight 10～13 g)were divided into control group(n =10,normal diet),β-aminopropionitrile(BAPN)group[n =20,drink water containing 1 g/(kg·d)BAPN],and BAPN+MCC950 group[n=20,drink water containing 1 g/(kg·d)BAPN and intraperitoneal injection of 20 mg/(kg·d)NLRP3 inhibitor,MCC950]by random sampling.Water intake,body weight,incidence of aortic dissection and aortic dissection-related mortality were recorded.The inflammatory infiltration in the aorta was observed with HE staining,elastic fiber breakage was observed by elastic Van Gieson(EVG)staining,average fluorescence intensity of NLRP3,IL-1β,α-SMA and OPN was detected by immunofluorescence assay,and protein expression levels of NLRP3,Caspase-1,ASC,IL-1β,α-SMA and OPN were measured with Western blotting.Results No aortic dissection or death was observed in the control group.The BAPN group had an incidence of aortic dissection of 80％,aortic dissection-related mortality of 35％,and obvious broken elastic fibers and inflammatory infiltrate in the aortic wall,and increased expression levels of NLRP3,Caspase-1,ASC and IL-1 β,decreased contractile α-SMA and increased synthetic protein OPN when compared with the control group(P<0.05).While MCC950 treatment decreased the incidence of aortic dissection(80％vs 35％,P=0.004)and aortic dissection-related mortality(35％vs 15％,P=0.144),alleviated the broken elastic fibers and inflammatory infiltrate in the aortic wall,and down-regulated the expression of NLRP3,Caspase-1,ASC and IL-1β,enhanced contractile α-SMA and decreased the synthetic protein when compared with the BAPN group(P<0.05).Conclusion The occurrence of aortic dissection in mice is associated with activation of NLRP3/Caspase-1/IL-1 β inflammasome pathway.NLRP3 inhibitor,MCC950,can reduce the occurrence of aortic dissection and show a protective effect on blood vessels.

Galectin-9 （Gal-9） is a member of the galectin family that can specifically recognize and bind to galactosides. Recent studies have shown that Gal-9 is highly expressed in the liver and can help to maintain intrahepatic immune homeostasis and perform biological functions in various liver diseases. This article reviews the immunomodulatory functions of Gal-9 and its role in different liver diseases. Studies have shown that Gal-9 has important biological functions in different liver diseases through multiple pathways. Research on the specific immunomodulatory mechanisms and functions of Gal-9 may help to discover the therapeutic role of Gal-9 in liver diseases.

The diabetic cognitive impairment(DCI)starts insidiously and can further develop into dementia.Early prevention and treatment are the key measure."Turbidity"refers to the body's metabolic products or the substances that cannot be transported and transformed normally,which is the breeding ground for DCI.The improper diet of diabetes patients leads to the imbalance of spleen and stomach absorption and induces the accumulation of essence into sugar turbidity.When the turbid remains for a long period of time,it will turn into phlegm,stasis,and turbid toxins and damage the clear orifice,resulting in cognitive impairment,which belongs to the category of"turbid evil invading the clear orifice".Neuroinflammation is a key factor inducing DCI,which is mainly regulated by meta-bolic reprogramming.As the direct product of metabolic reprogramming,lipid and lactate accumulation are key mediators of neuroin-flammation,along with high glucose,belonging to the category of"turbid evil"in traditional Chinese medicine.Metabolic reprogram-ming in the microenvironment of diabetes induces lactate and lipid accumulation,and mediates neuroinflammation,which is quite con-sistent with the development of TCM pathogenesis of"turbid evil invading the orifices".This paper aims to explore the modern biologi-cal understanding of the pathogenesis of turbid evil invading the clear orifice in DCI from the perspective of metabolic reprogramming,and to provide new ideas for its research of prevention and treatment in traditional Chinese medicine.

Objective To investigate the relationships between the expression levels of tumor necrosis factor receptor associated factor 4 (TRAF4) and ribosomal S6 protein kinase 4 (RSK4) protein in gastric cancer tissues and the recurrence after laparoscopic radical gastrectomy. Methods In total, 176 patients were divided into the recurrence and non-recurrence group, and the expression levels of TRAF4 and RSK4 protein in cancer and adjacent tissues and in gastric cancer tissues in the recurrence and non-recurrence group were compared. The influencing factor of recurrence and the efficacy of TRAF4 and RSK4 protein expression in predicting recurrence were analyzed. Results The positive expression rate of TRAF4 protein in gastric cancer tissues was higher than that in adjacent tissues (P < 0.05) and that in the recurrence group was higher than that in the non-recurrence group (P < 0.05). The positive expression rate of RSK4 protein in gastric cancer tissues was lower than that in adjacent tissues (P < 0.05) and that in the recurrence group was lower than that in non-recurrence group (P < 0.05). The largest tumor diameter 5 cm, poor differentiation, TNM Ⅲ stage, depth of invasion T3-T4, lymph node metastasis, absence of adjuvant chemotherapy after operation, positive expression of TRAF4 and RSK4 protein, and regular diet w influenced the post-operative recurrence (all P < 0.05). The accuracy of TRAF4 and RSK4 protein in gastric cancer tissues in combined predicting the recurrence was 83.52%. Conclusion The expression of TRAF4 protein is high, and the RSK4 protein is low in gastric cancer tissue, which are related to recurrence.

Objective:To investigate the status of grief among maternal spouse after perinatal loss, and analyze its influencing factors, so as to provide some reference for male grief supporting strategic.Methods:Using the convenient sampling method, 180 male spouses of hospitalized women in the Department of Obstetrics from Nanjing Maternity and Child Health Care Hospital from March to October 2022 were recruited. A cross-sectional survey was conducted by the general questionnaire, the Perinatal Grief Scale, the Family Adaptability and Cohesion Scale Ⅱ-Chinese Version, the Social Support Rating Scale, and the Simplified Coping Style Questionnaire.Results:The overall score of the Perinatal Grief Scale in male spouses of women who experienced a perinatal loss was (61.57 ± 14.14) points. The score of the Family Adaptability and Cohesion Scale Ⅱ-Chinese Version was (121 ± 14.42) points, the score of the Social Support Rating Scale was (34.23 ± 7.21) points, and the score of the Simplified Coping Style Questionnaire was (36.08 ± 7.64) points. Multiple linear regression analysis showed that participation in fetal interaction, loss of fetal age, social support and family adaptability were the main factors affecting male grief ( P<0.05). Conclusions:The grief among male spouses of women who experienced a perinatal loss is at a low level. The clinical medical staff can refer to the influencing factors and implement effective support, such as respecting the male's father status, coordinating social support resources, and improving the family's coping ability, in order to alleviate men's grief and help them return to normal life.

Objective:To explore the impact of different segmentation methods on differential diagnostic efficiency of 18F-FDG PET/MR radiomics to distinguish Parkinson′s disease (PD) from multiple system atrophy (MSA). Methods:From December 2017 to June 2019, 90 patients (60 with PD and 30 with MSA; 37 males, 53 females; age (55.8±9.5) years) who underwent 18F-FDG PET/MR in Union Hospital, Tongji Medical College, Huazhong University of Science and Technology were retrospectively collected. Patients were randomized to training set and validation set in a ratio of 7∶3. The bilateral putamina and caudate nuclei, as the ROIs, were segmented by automatic segmentation of brain regions based on anatomical automatic labeling (AAL) template and manual segmentation using ITK-SNAP software. A total of 1 172 radiomics features were extracted from T 1 weighted imaging (WI) and 18F-FDG PET images. The minimal redundancy maximal relevance (mRMR) and least absolute shrinkage and selection operator (LASSO) algorithm were used for features selection and radiomics signatures (Radscore) construction, with 10-fold cross-validation for preventing overfitting. The diagnostic performance of the models was assessed by ROC curve analysis, and the differences between models were calculated by Delong test. Results:There were 63 cases in training set (42 PD, 21 MSA) and 27 cases in validation set (18 PD, 9 MSA). The Radscore values were significantly different between the PD group and the MSA group in all training set and validation set of radiomics models ( 18F-FDG_Radscore and T 1WI_Radscore) based on automatic or manual segmentation methods ( z values: from -5.15 to -2.83, all P<0.05). ROC curve analysis showed that AUCs of 18F-FDG_Radscore and T 1WI_Radscore based on automatic segmentation in training and validation sets were 0.848, 0.840 and 0.892, 0.877, while AUCs were 0.900, 0.883 and 0.895, 0.870 based on manual segmentation. There were no significant differences in training and validation sets between Radiomics models based on different segmentation methods ( z values: 0.04-0.77, all P>0.05). Conclusions:The 18F-FDG PET/MR radiomics models based on different segmentation methods achieve promising diagnostic efficacy for distinguishing PD from MSA. The radiomics analysis based on automatic segmentation shows greater potential and practical value in the differential diagnosis of PD and MSA in view of the advantages including time-saving, labor-saving, and high repeatability.

Objectives:Microvascular obstruction (MVO) is a specific cardiac magnetic resonance (CMR) imaging feature in patients with acute myocardial infarction. The purpose of this study was to elucidate the predictive value of MVO in left ventricular adverse remodeling after primary percutaneous coronary intervention (PCI) in patients with acute ST-elevation myocardial infarction (STEMI).Methods:A total of 167 patients with STEMI undergoing primary PCI in the Chinese PLA General Hospital from 2016 to 2020 were enrolled in this prospective cohort study, the average age of study patients was 57±10 years old, with 151 males (90.4%) and 16 females (9.6%). The patients were divided into the MVO group ( n=81) and non-MVO group ( n=86) according to the presence or absence of MVO on CMR imaging, respectively. The primary endpoint of the study was the occurrence of left ventricular adverse remodeling, which was defined as an increase in left ventricular end diastolic volume (LVEDV) by >20% at 6 months after primary PCI compared with the baseline. Patients who completed follow-up were diagnosed as left ventricular adverse remodeling or no left ventricular adverse remodeling according to CMR. The baseline data, perioperative data, and related data of end points were compared between the MVO group and non-MVO group. Finally, the predictive value of MVO in left ventricular adverse remodeling was calculated by receiver operating characteristic curve analysis. Results:In the baseline data, preoperative thrombolysis in myocardial infarction (TIMI) flow ( χ2=13.74, P=0.003) and postoperative TIMI flow ( χ2=14.87, P=0.001) were both obviously decreased in the MVO group. After 6 months of follow-up, the incidence of left ventricular adverse remodeling in the MVO group was significantly higher than that in the non-MVO group [37.0%(27/73) vs. 18.9%(14/74), χ2=5.96, P=0.015]. The left ventricular end systolic volume at 6 months post infarction in the MVO group was significantly larger than that in the non-MVO group [(94±32) vs. (68±20) ml, t=-5.98, P<0.001], as well as the LVEDV [(169±38) vs. (143±29) ml, t=-4.74, P<0.001]. Receiver operating characteristic curve showed that the area under the curve of MVO size for predicting left ventricular adverse remodeling was 0.637. Conclusion:The risk of left ventricular adverse remodeling is significantly increased in patients with MVO after primary PCI for acute STEMI.

Correct neonatal resuscitation is the primary way to reduce perinatal mortality and neurological sequelae, and adequate preparation is essential. This article introduces the details for preparing neonatal resuscitation (including antenatal consultation) and ways to optimize the practice, aiming to improve the success rate of neonatal resuscitation.