Traumatic shock, one of leading causes of death in trauma patients, is characterized by abrupt onset, rapid progression, and poor prognosis. Failure to promptly identify and effectively intervene significantly increases its mortality rate. In recent years, with continuous advances in trauma medicine and ongoing optimization of management strategies, substantial progress has been made in the treatment of traumatic shock. However, no consensus has been reached on several key aspects of emergency care for these patients, including early identification of shock signs, clinical application of trauma assessment and management principles, appropriate selection of resuscitation techniques, and practical implementation of damage-control strategies, leading to considerable variability in resuscitation outcomes. To this end, the authors reviewed the recent advances in the management strategies for traumatic shock, aiming to provide a reference for clinical practice.

Traumatic shock, one of leading causes of death in trauma patients, is characterized by abrupt onset, rapid progression, and poor prognosis. Failure to promptly identify and effectively intervene significantly increases its mortality rate. In recent years, with continuous advances in trauma medicine and ongoing optimization of management strategies, substantial progress has been made in the treatment of traumatic shock. However, no consensus has been reached on several key aspects of emergency care for these patients, including early identification of shock signs, clinical application of trauma assessment and management principles, appropriate selection of resuscitation techniques, and practical implementation of damage-control strategies, leading to considerable variability in resuscitation outcomes. To this end, the authors reviewed the recent advances in the management strategies for traumatic shock, aiming to provide a reference for clinical practice.

Despite the great progress in the treatment of colorectal cancer (CRC), the current standard treatment protocols still have many limitations, and there is an urgent need for more effective biomarkers for personalized patient treatment. Circulating tumor DNA (ctDNA), as a dynamic, non-invasive liquid biopsy approach, overcomes the limitations of tissue biopsy in detecting tumor heterogeneity and molecular evolution. Current evidence from several studies suggests that ctDNA shows great promise in stratifying recurrence risk, guiding treatment decisions, and monitoring early recurrence. In addition, ctDNA can improve the efficiency of clinical research and drug development. However, the lack of standardisation of pre-ctDNA test variables and analysis procedures and the high technical costs limit its promotion and development. In this review, we summarize the available evidence on ctDNA in the clinical management of CRC and present its limitations and strategies for improvement.

Despite the great progress in the treatment of colorectal cancer (CRC), the current standard treatment protocols still have many limitations, and there is an urgent need for more effective biomarkers for personalized patient treatment. Circulating tumor DNA (ctDNA), as a dynamic, non-invasive liquid biopsy approach, overcomes the limitations of tissue biopsy in detecting tumor heterogeneity and molecular evolution. Current evidence from several studies suggests that ctDNA shows great promise in stratifying recurrence risk, guiding treatment decisions, and monitoring early recurrence. In addition, ctDNA can improve the efficiency of clinical research and drug development. However, the lack of standardisation of pre-ctDNA test variables and analysis procedures and the high technical costs limit its promotion and development. In this review, we summarize the available evidence on ctDNA in the clinical management of CRC and present its limitations and strategies for improvement.

Objective:To investigate mechanisms whereby phospholipase D1(PLD1)promotes pancreatic ductal adenocarcinoma(PDAC)progression.Methods:Targets were identified by screening the Genomic Spatial Event(GSE)database for genes differentially expressed in metastatic and primary tumors.Xenograft models were constructed by orthotopic injection of KPC cells into the mouse pancreas.Differential PLD1 expression in paired primary tumors and liver metastases derived from C57 mice and PDAC patients was confirmed using immunohistochemical staining.The effect of PLD1 expression on PDAC prognosis was assessed using a PDAC tissue microarray and clinical data.The effect of PLD1 expression on PDAC metastasis was assessed using transwell migration and scratch assays of cell lines ectopically expressing/silencing PLD1.The role of PLD1 in tumor metastasis was investigated using xenograft models constructed by orthotopic injection of PLD1-overexpression cell lines or vector control into the pancreas of C57 mice.Growth of primary tumors and liver metastases was monitored using bioluminescent imaging.The role of PLD1 in tumor progression was assessed using western blotting,transwell migration and scratch assays,and PLD1 enzyme-mutation cell lines.Downstream PLD1 target genes were identified using quantitative real-time PCR(qPCR),transcriptome sequencing,and response blocking.The effect of downstream target FSTL1 on liver metastasis in mice was assessed using bioluminescent imaging.Results:PLD1 expression was significantly higher in metastases than in primary tumors in KPC mice and patients.In the tissue microarray analysis,PLD1 expression was associated with diminished survival in PDAC patients;PLD1 overexpression in MIA PaCa-2 cells or knockdown in SW1990 cells could significantly affect the ability of invasion and migration.Xenograft models were established via orthotopic injections of the KPC cell line into the pancreas.Bioluminescent imaging demonstrated that PLD1 overexpression significantly increased signal intensity in the mouse liver(P<0.01);Treating the SW1990 cell line with PA and choline(PLD1 pathway products)did not restore loss of PDAC cell migration and invasion ability.Transwell and scratch assays in KRM,a PLD1 catalytic-mutation cell line,suggested that PLD1 activity is not required for PDAC metastasis;Transcriptome sequencing identified FSTL1 as a downstream molecule of PLD1.qPCR confirmed the consistency of mRNA levels between PLD1 and FSTL1.A blocking-rescue experiment suggested that FSTL1 is a downstream target of PLD1.A splenectomy metastasis model was constructed by injecting nude mice with tumor cells overexpressing FSTL1 and the results confirmed that overexpression of FSTL1 could induce liver metastases in PDAC cell due to tumor progression.Conclusion:PLD1 upregulates FSTL1 expression,promotes epithelial-mesenchymal transition of tumor cells,and enhances PDAC metastasis.Thus,PLD1 blockade could inhibit PDAC progression.

Objective:To investigate mechanisms whereby phospholipase D1(PLD1)promotes pancreatic ductal adenocarcinoma(PDAC)progression.Methods:Targets were identified by screening the Genomic Spatial Event(GSE)database for genes differentially expressed in metastatic and primary tumors.Xenograft models were constructed by orthotopic injection of KPC cells into the mouse pancreas.Differential PLD1 expression in paired primary tumors and liver metastases derived from C57 mice and PDAC patients was confirmed using immunohistochemical staining.The effect of PLD1 expression on PDAC prognosis was assessed using a PDAC tissue microarray and clinical data.The effect of PLD1 expression on PDAC metastasis was assessed using transwell migration and scratch assays of cell lines ectopically expressing/silencing PLD1.The role of PLD1 in tumor metastasis was investigated using xenograft models constructed by orthotopic injection of PLD1-overexpression cell lines or vector control into the pancreas of C57 mice.Growth of primary tumors and liver metastases was monitored using bioluminescent imaging.The role of PLD1 in tumor progression was assessed using western blotting,transwell migration and scratch assays,and PLD1 enzyme-mutation cell lines.Downstream PLD1 target genes were identified using quantitative real-time PCR(qPCR),transcriptome sequencing,and response blocking.The effect of downstream target FSTL1 on liver metastasis in mice was assessed using bioluminescent imaging.Results:PLD1 expression was significantly higher in metastases than in primary tumors in KPC mice and patients.In the tissue microarray analysis,PLD1 expression was associated with diminished survival in PDAC patients;PLD1 overexpression in MIA PaCa-2 cells or knockdown in SW1990 cells could significantly affect the ability of invasion and migration.Xenograft models were established via orthotopic injections of the KPC cell line into the pancreas.Bioluminescent imaging demonstrated that PLD1 overexpression significantly increased signal intensity in the mouse liver(P<0.01);Treating the SW1990 cell line with PA and choline(PLD1 pathway products)did not restore loss of PDAC cell migration and invasion ability.Transwell and scratch assays in KRM,a PLD1 catalytic-mutation cell line,suggested that PLD1 activity is not required for PDAC metastasis;Transcriptome sequencing identified FSTL1 as a downstream molecule of PLD1.qPCR confirmed the consistency of mRNA levels between PLD1 and FSTL1.A blocking-rescue experiment suggested that FSTL1 is a downstream target of PLD1.A splenectomy metastasis model was constructed by injecting nude mice with tumor cells overexpressing FSTL1 and the results confirmed that overexpression of FSTL1 could induce liver metastases in PDAC cell due to tumor progression.Conclusion:PLD1 upregulates FSTL1 expression,promotes epithelial-mesenchymal transition of tumor cells,and enhances PDAC metastasis.Thus,PLD1 blockade could inhibit PDAC progression.

OBJECTIVE To investigate the drug resistance of ESBLs-producing Escherichia coli in community-acquired urinary tract infection for guiding the clinical drug-using.METHODS ATB-Expression analysis system was used for identification of bacteria,extra-susceptibility tests were detected by K-B method.RESULTS Totally 104 E.coli strains were detected,the isolation rate of ESBLs-producing E.coli was 13.5%,the resistant rates of E.coli were up to 70% to ampicillin,piperacillin and Co-trimoxazole,the resistant rate was up to 55% to ciprofloxacin and levofloxacin,and the susceptible rate was 100% to imipenem.CONCLUSIONS The E.coli is a main pathogen in community-acquired urinary tract infection,Its drug resistance is extremely severe.To enhance detecting drug resistance of pathogenic bacteria is of important significance for guiding the clinical rational drug-using and reducing drug-resistant strains.