BACKGROUND:3D-printed bone tissue engineering scaffolds have obvious advantages in the research and clinical treatment of bone defect repair.As one of the important raw materials for 3D printed bone scaffolds,poly-L-lactic acid has a great potential for application in performing bone defect repair,but clinical patients with different bone defect causative factors have different requirements for the comprehensive performance of poly-L-lactic acid bone scaffolds.OBJECTIVE:To summarize and review the development of 3D printing technology and poly-L-lactic acid scaffolds and the design strategies chosen for scaffolds for bone repair in the setting of bone diseases such as osteomyelitis,bone tumor,osteonecrosis,and osteoporosis.METHODS:Literature from CNKI,WanFang,PubMed,Science Direct,and Web of Science databases were searched and screened from 1994 to 2024.Search terms were"3D printing,polylactic acid,bone tissue engineering scaffold,osteomyelitis,bone tumor,osteonecrosis,osteoporosis,bone defect"in Chinese and English.The screened 62 articles were systematically summarized and analyzed.RESULTS AND CONCLUSION:(1)Poly-L-lactic acid is considered to be an ideal raw material for artificial bone scaffold design due to its non-toxicity,processability,biocompatibility,and ability to self-degrade in the human environment.The application of 3D printing technology has enabled poly-L-lactic acid bone scaffolds to meet the multilayered and porous structural design requirements of biomimetic artificial bone repair materials,and to optimize the mechanical properties for better bone repair.(2)According to different bone disease microenvironments,timely adjustment of the functional design of poly-L-lactic acid scaffolds is important for the comprehensive osteogenic efficacy of the scaffolds.The article discusses the application of poly-L-lactic acid scaffolds in bone disease environments such as osteomyelitis,bone tumor,osteonecrosis,and osteoporosis,and highlights the importance of rationally grasping the timing of bone disease treatment and bone tissue regeneration for bone defects caused by different bone diseases.(3)Although poly-L-lactic acid scaffolds show potential in bone repair,there are still some problems,such as the need to further optimize the structural design of the scaffolds to fit new bone regeneration,enhance the bioactivity of the scaffolds,and take into account other functions(e.g.,antimicrobial,anti-tumor,and anti-osteoporosis)in order to adapt to the needs of bone tissue repair in different pathological environments.

BACKGROUND:3D-printed bone tissue engineering scaffolds have obvious advantages in the research and clinical treatment of bone defect repair.As one of the important raw materials for 3D printed bone scaffolds,poly-L-lactic acid has a great potential for application in performing bone defect repair,but clinical patients with different bone defect causative factors have different requirements for the comprehensive performance of poly-L-lactic acid bone scaffolds.OBJECTIVE:To summarize and review the development of 3D printing technology and poly-L-lactic acid scaffolds and the design strategies chosen for scaffolds for bone repair in the setting of bone diseases such as osteomyelitis,bone tumor,osteonecrosis,and osteoporosis.METHODS:Literature from CNKI,WanFang,PubMed,Science Direct,and Web of Science databases were searched and screened from 1994 to 2024.Search terms were"3D printing,polylactic acid,bone tissue engineering scaffold,osteomyelitis,bone tumor,osteonecrosis,osteoporosis,bone defect"in Chinese and English.The screened 62 articles were systematically summarized and analyzed.RESULTS AND CONCLUSION:(1)Poly-L-lactic acid is considered to be an ideal raw material for artificial bone scaffold design due to its non-toxicity,processability,biocompatibility,and ability to self-degrade in the human environment.The application of 3D printing technology has enabled poly-L-lactic acid bone scaffolds to meet the multilayered and porous structural design requirements of biomimetic artificial bone repair materials,and to optimize the mechanical properties for better bone repair.(2)According to different bone disease microenvironments,timely adjustment of the functional design of poly-L-lactic acid scaffolds is important for the comprehensive osteogenic efficacy of the scaffolds.The article discusses the application of poly-L-lactic acid scaffolds in bone disease environments such as osteomyelitis,bone tumor,osteonecrosis,and osteoporosis,and highlights the importance of rationally grasping the timing of bone disease treatment and bone tissue regeneration for bone defects caused by different bone diseases.(3)Although poly-L-lactic acid scaffolds show potential in bone repair,there are still some problems,such as the need to further optimize the structural design of the scaffolds to fit new bone regeneration,enhance the bioactivity of the scaffolds,and take into account other functions(e.g.,antimicrobial,anti-tumor,and anti-osteoporosis)in order to adapt to the needs of bone tissue repair in different pathological environments.

BackgroundWith the rapid development of the networking technologies， internet addiction has increasingly become a serious mental health issue. Previous studies have revealed the link between childhood trauma and internet addiction， while the mediating role of perceived stress in this link is not yet clear. ObjectiveTo investigate the role of medical students' perceived stress in the relationship between childhood trauma and internet addiction， so as to provide references for the intervention of internet addiction. MethodsFrom February to March 2023， a random sampling technique was used to select 1 232 undergraduate students from the School of Clinical Medical Sciences of Southwest Medical University as research subjects. The Childhood Trauma Questionnaire-Short Form （CTQ-SF）， Perceived Stress Scale （PSS）， Internet Gaming Disorder Scale （IGDS）， and Bergen Social Media Addiction Scale （BSMAS） were used for assessment. Pearson's correlation coefficients were calculated. The mediation effect of perceived stress in the relationship between childhood trauma and internet addiction was tested using Model 4 in the SPSS Process 4.1， and Bootstrapping procedure involving 5 000 replicates was employed to confirm the statistical significance. ResultsA total of 1 016 （82.47%） valid completed questionnaires were gathered. The CTQ-SF scores of medical students were positively correlated with PSS scores， IGD scores， and BSMAS scores （r=0.583， 0.474， 0.465， P<0.01）. PSS scores were positively correlated with IGD scores and BSMAS scores （r=0.369， 0.479， P<0.01）. Childhood trauma in medical students was found to positively predict perceived stress （β=0.191， P<0.01）， social media addiction （β=0.160， P<0.01）， and internet gaming disorder （β=0.106， P<0.01）. Perceived stress played a significant mediating role in the relationship between childhood trauma and internet gaming disorder， indirect effect value was 0.018 （95% CI： 0.009~0.027）， accounting for 16.98%. Perceived stress also exhibited a significant mediating role in the relationship between childhood trauma and social media addiction， indirect effect value was 0.063 （95% CI： 0.048~0.079）， accounting for 39.38%. ConclusionChildhood trauma in medical students may affect internet gaming disorder and social media addiction through perceived stress. ［Funded by 2022 Annual Research Project of Sichuan Applied Psychology Research Center，（number，CSXL-22102）］

The purpose of this investigation was to elucidate the clinical characteristics and genetic underpinnings of a pediatric patient with neurodevelopmental disorder with ataxic gait, absent speech, and decreased cortical white matter (NDAGSW, OMIM#617807). The affected individual, a 1-year-9-month-old male, displayed physical development retardation and distinctive facial features, notably periorbital puffiness, upward-gazing palpebral fissures, a shortened philtrum, a tented mouth, and conical-shaped digits. Clinically, the patient presented with profound global developmental retardation, marked language deficits, hypotonia, and an ataxic gait. Subtle, non-diagnostic alterations were identified in cranial magnetic resonance imaging and visual evoked potential assessments. The trio-whole exome sequencing analysis revealed a de novo heterozygous mutation, c.202G>A (p.A68T), within the RAB11B gene, a known pathogenic variant linked to NDAGSW. Neurodevelopmental disorders due to RAB11B gene variants are rare disorders with clinical manifestations of severe mental retardation, aphasia, motor retardation, gait abnormalities with peculiar phenotypical features, structural abnormalities of the brain, and reduced cerebral white matter, cerebellar hypoplasia, and hypoplasia of the corpus callosum as seen on cranial imaging. Based on the characteristics of the disease, the heterozygous missense mutation c.202G>A (p.Ala68Thr) in the RAB11B gene was identified as the genetic etiology of the child.

Objective:To investigate the expressions of cystathionine-β-synthase(CBS)and cystathionine-γ-lyase(CSE)and their effects on the malignant biological behaviours of breast cancer cells,and to elucidate their mechanisms.Methods:The breast cancer tissue and paracancerous normal tissue from 15 cases of patients were selected,and RT-qPCR and Western blotting methods were used to detect the mRNA and protein expression levels of CBS and CSE in breast cancer tissue,paracancerous normal tissue,MCF-7 cells,and MDA-MB-231 cells.The MCF-7 cells were divided into siNC group(transfected with siNC)and siCBS group(transfected with siCBS),and the MDA-MB-231 cells were divided into ovNC group(transfected with CSE over-expression empty plasmid)and ovCSE group(transfected with CSE over-expression plasmid).CCK8 assay was used to detect the proliferation activities of breast cancer cells in various groups,Transwell assay was used to detect the numbers of migration and invasion cells in various groups,and Western blotting method was used to detect the protein expression levels of E-cadherin,N-cadherin and Vimentin proteins in the breast cancer cells in various groups.Results:Compared with paracancerous normal tissue,the expression levels of CBS and CSE mRNA and proteins in breast cancer tissue were increased(P＜0.05 or P＜0.01).Compared with MDA-MB-231 cells,the CBS mRNA expression level in the MCF-7 cells was increased(P＜0.05);compared with MCF-7 cells,the expression level of CSE protein in the MDA-MB-231 cells was decreased(P＜0.05).Compared with siNC group,the proliferation activity,the numbers of migration and invasion cells,the expression levels of N-cadherin and Vimentin proteins in the MCF-7 cells in siCBS group were significantly decreased(P＜0.05),and the expression level of E-cadherin protein was increased(P＜0.05).Compared with ovNC group,the proliferation activity,the numbers of migratoin and invasion cells,and the expression levels of N-cadherin and Vimentin proteins in the MDA-MB-231 cells in ovCSE group were increased(P＜0.05),while the expression level of E-cadherin protein was significantly decreased(P＜0.05).Conclusion:The expressions of CBS and CSE are upregulated in breast cancer tissue,and high levels of CBS and CSE promote proliferation,migration,invasion and epithelial-mesenchymal transition(EMT)of breast cancer cells.

Forensic microbiology,a pivotal discipline within forensic science,focuses on microorganisms as the primary subject of study and applies life science technologies to analyze microbial evidence in criminal and civil investigations.Tissue source inference plays a crucial role in forensic investigations,facilitating case assessment and crime scene reconstruction.The application of microbiome analysis in tissue source inference benefits from the tissue specificity and spatiotemporal stability of human microbial communities.This article provides a systematic review of recent advances in tissue source inference based on microbiome analysis,covering technological development,research trends,and practical applications.Finally,the challenges confronted in practice in forensic microbiology and the future prospects for its development are summarized.

Objective To analyze the changes in angiopoietin-2(Ang-2)levels before and after microwave ablation(MWA)in patients with high-risk pulmonary nodule and its impact on postoperative recurrence.Method A total of 94 patients with high-risk pulmonary nodules admitted to Guizhou Aerospace Hospital from December 2019 to December 2021 were included and categorized into a recurrence group(n=30)and a non-recurrence group(n=64).Clinical data was compared between the two groups.Pearson correlation analysis was used to analyze the correlation between pre-treatment angiopoietin-2(Ang-2)levels and CT parameters.Logistic regression model,restricted cubic splines,threshold effect analysis,and receiver operating characteristic(ROC)curve were used to analyze the relationship between pre-treatment Ang-2 levels and postoperative recurrence.Kaplan-Meier survival curves were used to analyze the differences in overall survival among patients with different Ang-2 levels.Cox regression model was used to analyze the factors affecting patients'survival.Result Compared to pre-treatment levels within the same group,Ang-2 levels in both groups decreased significantly,with statistically significant differences(P<0.05).Pearson correlation analysis showed that pre-treatment Ang-2 levels were positively correlated with BF,BV,PS,and MTT.Ang-2 level was independently associated with postoperative recurrence.Results of ROC analysis indicated that pre-treatment Ang-2 had certain predictive value for postoperative recurrence(area under the curve=0.789).Restricted cubic spline analysis revealed a nonlinear dose-response relationship between pre-treatment Ang-2 and postoperative recurrence(P<0.05).Threshold effect analysis identified that the inflection point of Ang-2 affecting recurrence as 1905.41 pg/mL.Survival analysis demonstrated that the median overall survival of patients in the Ang-2<1905.41 pg/mL group was longer than that in the Ang-2≥1905.41 pg/mL group(P=0.039).Furthermore,Ang-2≥1905.41 pg/mL was an independent factor affecting patients'survival time.Conclusion The levels of Ang-2 decreased significantly in patients with high-risk pulmonary nodules after MWA,and pre-treatment Ang-2 level has certain predictive value for postoperative recurrence.

Objective:To investigate the role of cyclooxygenase-2 (COX-2) in glycochenodeoxycholic acid (GCDC)-induced apoptosis of mouse extrahepatic biliary epithelial cells (EBECs) and clarify its possible mechanism.Methods:EBECs were cultured in vitro and infected with RNAi-COX-2 lentivirus (GCDC+ shCOX-2 group). EBECs were then treated with different concentrations (0, 25, 50, 100, 200, 400, 800 μmol/L) of GCDC (GCDC group). Cell proliferation activity was detected by cell counting kit-8 (CCK-8) assay; lactate dehydrogenase (LDH) release rate was measured by colorimetry; apoptosis was analyzed by flow cytometry; caspase-3 activity was detected by fluorescent probe method; COX-2 mRNA expression was determined by real-time quantitative polymerase chain reaction (qRT-PCR); protein levels of COX-2, autophagy-related proteins LC3, p62, Beclin-1, and apoptosis-related proteins Bax, Bcl-2, cleaved caspase-3 were evaluated by Western blot.Results:Compared with the 0 μmol/L GCDC group, the apoptosis level, LDH release rate, and caspase-3 activity in the 50, 100, and 200 μmol/L GCDC groups gradually increased (all P<0.05) in a concentration-dependent manner. After RNAi-COX-2 lentivirus infection, COX-2 mRNA and protein expression levels in EBECs significantly decreased (all P<0.05). Compared with the GCDC group, the apoptosis rate of EBECs in the GCDC+ shCOX-2 group significantly decreased ( P<0.05). The GCDC+ shCOX-2 group showed increased cell proliferation activity, downregulated protein expressions of Bax, cleaved caspase-3, and p62, and upregulated protein expressions of Bcl-2, LC3 II/I, and Beclin-1 (all P<0.05). Conclusions:Inhibition of COX-2 improves GCDC-induced apoptosis of EBECs, and the mechanism may be related to the activation of the autophagy pathway.

Objective:To investigate the role of cyclooxygenase-2 (COX-2) in glycochenodeoxycholic acid (GCDC)-induced apoptosis of mouse extrahepatic biliary epithelial cells (EBECs) and clarify its possible mechanism.Methods:EBECs were cultured in vitro and infected with RNAi-COX-2 lentivirus (GCDC+ shCOX-2 group). EBECs were then treated with different concentrations (0, 25, 50, 100, 200, 400, 800 μmol/L) of GCDC (GCDC group). Cell proliferation activity was detected by cell counting kit-8 (CCK-8) assay; lactate dehydrogenase (LDH) release rate was measured by colorimetry; apoptosis was analyzed by flow cytometry; caspase-3 activity was detected by fluorescent probe method; COX-2 mRNA expression was determined by real-time quantitative polymerase chain reaction (qRT-PCR); protein levels of COX-2, autophagy-related proteins LC3, p62, Beclin-1, and apoptosis-related proteins Bax, Bcl-2, cleaved caspase-3 were evaluated by Western blot.Results:Compared with the 0 μmol/L GCDC group, the apoptosis level, LDH release rate, and caspase-3 activity in the 50, 100, and 200 μmol/L GCDC groups gradually increased (all P<0.05) in a concentration-dependent manner. After RNAi-COX-2 lentivirus infection, COX-2 mRNA and protein expression levels in EBECs significantly decreased (all P<0.05). Compared with the GCDC group, the apoptosis rate of EBECs in the GCDC+ shCOX-2 group significantly decreased ( P<0.05). The GCDC+ shCOX-2 group showed increased cell proliferation activity, downregulated protein expressions of Bax, cleaved caspase-3, and p62, and upregulated protein expressions of Bcl-2, LC3 II/I, and Beclin-1 (all P<0.05). Conclusions:Inhibition of COX-2 improves GCDC-induced apoptosis of EBECs, and the mechanism may be related to the activation of the autophagy pathway.

The purpose of this investigation was to elucidate the clinical characteristics and genetic underpinnings of a pediatric patient with neurodevelopmental disorder with ataxic gait, absent speech, and decreased cortical white matter (NDAGSW, OMIM#617807). The affected individual, a 1-year-9-month-old male, displayed physical development retardation and distinctive facial features, notably periorbital puffiness, upward-gazing palpebral fissures, a shortened philtrum, a tented mouth, and conical-shaped digits. Clinically, the patient presented with profound global developmental retardation, marked language deficits, hypotonia, and an ataxic gait. Subtle, non-diagnostic alterations were identified in cranial magnetic resonance imaging and visual evoked potential assessments. The trio-whole exome sequencing analysis revealed a de novo heterozygous mutation, c.202G>A (p.A68T), within the RAB11B gene, a known pathogenic variant linked to NDAGSW. Neurodevelopmental disorders due to RAB11B gene variants are rare disorders with clinical manifestations of severe mental retardation, aphasia, motor retardation, gait abnormalities with peculiar phenotypical features, structural abnormalities of the brain, and reduced cerebral white matter, cerebellar hypoplasia, and hypoplasia of the corpus callosum as seen on cranial imaging. Based on the characteristics of the disease, the heterozygous missense mutation c.202G>A (p.Ala68Thr) in the RAB11B gene was identified as the genetic etiology of the child.