In order to separate chiral D-phenylalanine from L-phenylalanine,the enzyme catalytic method by papain and immobilized papain were used in this investigation.It indicated that the yield rate of N-acetyl-DL-phenylalanine synthesized from DL-phenylalanine was 88.7%.The ionic strength was the strongest influencing factor in the synthesis of N-acetyl-L-phenylalanylaniline by both papain and immobilized papain on sodium alginate-ehitosan(IPSAC).But the reaction temperature was the strongest influencing factor in the synthesis by immobilized papain on nylon cloth(IPN).The ionic strength and the pH were the important influencing factors in the synthesis.The yield rates of the best synthesis system of N-acetyl-L-phenylalanylaniline by papain,IPSAC,IPN were 61.2%,54.7%,36.3%,respectively.The yield rate of L-phenylalanine from N-acetyl-L-phenylalanylaniline hydrolyzation was 59.2%.The optical purity of the product was 96.6%.The vield rate of D-phenylalanine from N-acetyl-D-phenylalanine hydrolyzation was 61.7%.The optical purity was 95.7%.

Objective To evaluate the ultrasonic feature and clinical significance of persistent left superior vena cava(PLSVC)in fetal life.Methods Fetal echocardiography was performed in 3368 fetuses.Thirty-one fetuses of PLSVC were confirmed.Results The dilated coronary sinus was observed in 30 of 31 fetuses.Congenital heart defects were presented in 14 of these cases,and extracardiac anomalies were presented in 6 fetuses.Both congenital heart defects and extracardiac anomalies were observed in 4 fetuses.Conclusions PLSVC is always associated with congenital heart defects.The prognosis Of affected fetuses largely depends on whether or not the PLSVC is associated with a congenital heart defect.Prenatal diagnosis of PLSVC can help US plan perinatal counseling and ameliorate the postnatal course.

OBJECTIVE To study the mitochondrial toxicity effect of Radix Aconiti Lateralis Praepa?rata(Fuzi)on H9c2 cardiomyocytes. METHODS H9c2 cells were exposed to Fuzi decoction 6.25, 12.5,25,50 and 100 g·L-1 for 24 h. Fluorescence staining and CCK-8 assay were used to detect cell viability. H9c2 cells were exposed to Fuzi decoction 6.25,12.5 and 25 g · L-1 for 24 h,while the effect on mitochondrial membrane potential and reactive oxygen species(ROS)was detected by flow cytometry. The fluorescence molecular probe and laser scanning confocal microscope were used to observe the effect on Ca2+ in cells,Ca2+ and superoxide in mitochondria. The effect on ATP concentration in cells was detected via firefly luciferin and the expression of Pgc-1α,Bcl-2 and Bax mRNA evaluated by real-time PCR,while the expression of Pgc-1α protein was measured by Western blotting. RESULTS H9c2 cell viability was significantly inhibited by Fuzi decoction 12.5-100 g · L-1(P<0.05,P<0.01). The IC50 value was 47.4669 g · L-1,while the 95%confidence limit was 32.5997-69.1145 g · L-1. After treatment with Fuzi decoction 25 g · L-1 ,the fluorescence intensity of ROS in the normal control group increased from 204±67 to 454±78(P<0.05),that of mitochondrial superoxide increased from 5.4±1.8 to 26.8±8.5 (P<0.01),mitochondrial membrane potential decreased from 1.7±0.5 to 0.8±0.4(P<0.05),the fluores?cence intensity of intracellular Ca2+increased from 7.8±0.8 to 22.1±0.5(P<0.05)while that of mitochon?drial Ca2+decreased from 38.0±4.3 to 9.2±1.6(P<0.01),and intracellular ATP concentration decreased from (10.6 ± 0.4)μmol · g-1 to (5.3 ± 1.1)μmol · g-1 protein (P<0.05). qPCR and Western blotting test results showed that compared with the normal control group ,Pgc-1αand Bcl-2 mRNA relative expression level in Fuzi decoction 25 g·L-1 group was decreased from 1.00±0.10 and 1.00±0.10 to 0.09±0.06(P<0.01)and 0.43±0.06(P<0.01),respectively, while the relative expression of Bax mRNA was increased from 1.00 ± 0.03 to 1.17 ± 0.06 (P<0.05),and the expression of Pgc-1α protein was decreased from 0.906±0.034 to 0.541±0.003(P<0.01). CONCLUSION Fuzi has some mitochondrial toxicity to cardiomy?opathy. This effect arises from the combined action of different mechanisms. Mitochondrial toxicity of myocytes may account for the cardiac toxicity of Fuzi.

Diabetic wound is a complication of diabetes, which is difficult to heal and easy to turn into chronic wound. Compared with ordinary wound healing, diabetic wounds stay in the inflammatory stage and can not enter the proliferative stage. This is because the proportion of pro-inflammatory cytokines increases, leading to the imbalance of inflammatory cells and the accumulation of a large number of inflammatory factors. The production and release of inflammatory factors is closely related to pyroptosis. Pyroptosis is a kind of programmed death mode of inflammatory cells. Mediated by inflammasome, pyroptosis is transduced through typical and atypical inflammasome signaling pathways, resulting in the formation of pores on the cell membrane and inducing cell death. In this process, a large number of pro-inflammatory cytokines are released to maintain the inflammatory environment of wounds, hindering the development of diabetic wounds to the proliferative stage and remodeling stage, thus inhibiting the healing of diabetic wounds. This article reviews the mechanism of pyroptosis and its effect on diabetic wounds, the potential significance of inhibiting pyroptosis in the treatment of diabetic wounds, and the existing problems.

Combined with teaching practice, this study summarizes the teaching contents, methods and effect evaluation of pathological technology for professional postgraduates majoring in pathology. According to the basic conditions of postgraduates, the pathological technology training program has been formulated, student-centered heuristic teaching is carried out by using diversified teaching methods such as flipped classroom, interactive theoretical teaching is carried out by using the intelligent teaching platform, and practical teaching is carried out by using the problem-based learning mode, aiming to improve the theoretical literacy and practical level of pathological technology of professional postgraduates majoring in pathology, improve their clinical research thinking, and lay a foundation for clinical pathological diagnosis and scientific research in the future.

Objective To explore the mechanism underlying the protective effect of α2-macroglobulin (A2M) against glucocorticoid-induced femoral head necrosis. Methods In a human umbilical vein endothelial cell (HUVEC) model with injuries induced by gradient concentrations of dexamethasone (DEX;10-8-10-5 mol/L), the protective effects of A2M at 0.05 and 0.1 mg/mL were assessed by examining the changes in cell viability, migration, and capacity of angiogenesis using CCK-8 assay, Transwell and scratch healing assays and angiogenesis assay. The expressions of CD31 and VEGF-A proteins in the treated cells were detected using Western blotting. In BALB/c mouse models of avascular necrosis of the femoral head induced by intramuscular injections of methylprednisolone, the effects of intervention with A2M on femoral trabecular structure, histopathological characteristics, and CD31 expression were examined with Micro-CT, HE staining and immunohistochemical staining. Results In cultured HUVECs, DEX treatment significantly reduced cell viability, migration and angiogenic ability in a concentration- and time-dependent manner (P<0.05), and these changes were obviously reversed by treatment with A2M in positive correlation with A2M concentration (P<0.05). DEX significantly reduced the expression of CD31 and VEGF-A proteins in HUVECs, while treatment with A2M restored CD31 and VEGF-A expressions in the cells (P<0.05). The mouse models of femoral head necrosis showed obvious trabecular damages in the femoral head, where a large number of empty lacunae and hypertrophic fat cells could be seen and CD31 expression was significantly decreased (P<0.05). A2M treatment of the mouse models significantly improved trabecular damages, maintained normal bone tissue structures, and increased CD31 expression in the femoral head (P<0.05). Conclusion A2M promotes proliferation, migration, and angiogenesis of DEX-treated HUVECs and alleviates methylprednisolone-induced femoral head necrosis by improving microcirculation damages and maintaining microcirculation stability in the femoral head.

Objective:To explore the occurrence and influencing factors of post-burn psychological stress disorder in preschool children.Methods:This study was a multi-center cross-sectional survey. From January 2022 to February 2023, 85 preschool children (aged 1 to 6 years) with burns admitted to the Affiliated Hospital of North Sichuan Medical College, Nanchong Central Hospital, Suining Central Hospital, Guang'an People's Hospital, and Guangyuan Central Hospital who met the inclusion criteria were selected as respondents. A self-made general information questionnaire was used to investigate the children's general data including gender, age group, residential area, main caregiver and their education level, and family type, as well as the injury condition including cause of injury and burn severity. The Child Stress Disorders Checklist was used to investigate the occurrence of psychological stress disorder in children at 3 days to 1 month after injury, and the incidence rate was calculated. The children were classified according to their general data and injury condition, and the occurrence of psychological stress disorder in children at 3 days to 1 month after injury was recorded, and the influencing factors for post-burn psychological stress disorder in preschool children were screened.Results:A total of 85 questionnaires were distributed and 85 valid questionnaires were recovered, with an effective recovery rate of 100%. Among the children, there were 45 boys and 40 girls, with most children aged 1 to 3 years. There were slightly more children in rural areas than in cities. About half of the children were mainly cared for by their parents and grandparents, respectively, and the education level of the main caregivers was mainly high school/technical secondary school. The family type was mainly core family and extended family. The main cause of injury was hydrothermal scald, and the severity of burns was mainly moderate. The incidence rate of psychological stress disorder in this group of children at 3 days to 1 month after injury was 34.12% (29/85). There were statistically significant differences in the occurrence of psychological stress disorder in children with different age groups, causes of injuries, and burn severity at 3 days to 1 month after injury (with χ2 values??of 9.18, 7.80, and 25.47, respectively, P<0.05); there were no statistically significant differences in the occurrence of psychological stress disorder in children with different genders, residential area, main caregivers, main caregivers' education levels, or family types at 3 days to 1 month after injury ( P>0.05). Multivariate logistic regression analysis showed that age group and burn severity were independent influencing factors for the occurrence of psychological stress disorder in preschool children after burns (with odds ratios of 8.21 and 33.99, respectively, and 95% confidence intervals of 1.57-43.04 and 5.55-207.93, respectively, P<0.05), the older the child and the more severe the burn, the higher the possibility of the occurrence of psychological stress disorder. Conclusions:The incidence rate of psychological stress disorder is high in preschool children after burns. Age group and burn severity are independent influencing factors for the occurrence of post-burn psychological stress disorder in this type of children.

Objective To explore the mechanism underlying the protective effect of α2-macroglobulin (A2M) against glucocorticoid-induced femoral head necrosis. Methods In a human umbilical vein endothelial cell (HUVEC) model with injuries induced by gradient concentrations of dexamethasone (DEX;10-8-10-5 mol/L), the protective effects of A2M at 0.05 and 0.1 mg/mL were assessed by examining the changes in cell viability, migration, and capacity of angiogenesis using CCK-8 assay, Transwell and scratch healing assays and angiogenesis assay. The expressions of CD31 and VEGF-A proteins in the treated cells were detected using Western blotting. In BALB/c mouse models of avascular necrosis of the femoral head induced by intramuscular injections of methylprednisolone, the effects of intervention with A2M on femoral trabecular structure, histopathological characteristics, and CD31 expression were examined with Micro-CT, HE staining and immunohistochemical staining. Results In cultured HUVECs, DEX treatment significantly reduced cell viability, migration and angiogenic ability in a concentration- and time-dependent manner (P<0.05), and these changes were obviously reversed by treatment with A2M in positive correlation with A2M concentration (P<0.05). DEX significantly reduced the expression of CD31 and VEGF-A proteins in HUVECs, while treatment with A2M restored CD31 and VEGF-A expressions in the cells (P<0.05). The mouse models of femoral head necrosis showed obvious trabecular damages in the femoral head, where a large number of empty lacunae and hypertrophic fat cells could be seen and CD31 expression was significantly decreased (P<0.05). A2M treatment of the mouse models significantly improved trabecular damages, maintained normal bone tissue structures, and increased CD31 expression in the femoral head (P<0.05). Conclusion A2M promotes proliferation, migration, and angiogenesis of DEX-treated HUVECs and alleviates methylprednisolone-induced femoral head necrosis by improving microcirculation damages and maintaining microcirculation stability in the femoral head.

This paper summarizes clinical insights on treating the syndrome of coexisting dryness and dampness in Sjögren's syndrome （SS） based on the "three methods for liver diseases". It is proposed that the core pathogenesis of this subtype lies in the liver's failure to regulate and disperse， leading to fluid retention and transformation into dryness； disharmony between wood （liver） and earth （spleen）， resulting in internal generation of dryness and dampness； and liver impairment affecting the kidney， eventually causing extreme dryness to transform into dampness. This syndrome is thus characterized by disharmony between the liver and spleen， as well as dysfunction between ti （character， 体） and yong （function， 用）. Drawing from the Guide to Clinical Case （《临证指南医案》）， the "three methods for liver diseases" are applied as follows，i.e. using pungent and dispersing herbs to regulate the liver and resolve qi stagnation； using sweet and gentle herbs to soothe the liver and address the root of concurrent dryness and dampness； and using sour and purgative herbs to soften the liver and restore fluid balance. The coordinated use of these three methods， treating both ti and yong， facilitates the separation of dryness and dampness， providing a novel approach to syndrome differentiation and treatment for this subtype of SS.

Objective:To study the risk factors of surgical therapy in neonates with necrotizing enterocolitis (NEC).Methods:From January 2016 to July 2020, neonates with a confirmed diagnosis of NEC (Bell's Stage Ⅱ and above) admitted to our hospital were retrospectively enrolled. They were assigned into surgical group and conservative group according to whether surgeries were performed. The conditions during perinatal period, clinical characteristics and laboratory examinations at the onset of NEC were compared between the two groups. Multivariate Logistic regression analysis was used to determine the risk factors of surgical therapy.Results:A total of 177 neonates with NEC were identified, including 62 cases (35.0%) in the surgical group and 115 cases (65.0%) in the conservative group. Multivariate Logistic regression analysis showed that male gender ( OR=3.178,95% CI 1.457~6.929, P=0.004), comorbidity with shock ( OR=3.434, 95% CI 1.112~10.607, P=0.032), mechanical ventilation>7 d before NEC onset ( OR=3.663, 95% CI 1.098~12.223, P=0.035) and lymphocytes <2.0×10 9/L ( OR=4.121, 95% CI 1.801~9.430, P=0.001) at the onset of NEC were independent risk factors for surgical therapy. Conclusions:Male gender, comorbidity with shock, mechanical ventilation >7 d before NEC and lymphocytopenia at the onset are independent risk factors for surgical therapy in neonates with NEC (Stage Ⅱ and above).