OBJECTIVE To analyze occupational exposure to sharps injuries among medical staff in different posi-tions in a three-A hospital.METHODS A retrospective collection of all sharps injury cases reported from 2018 to 2023 in a general hospital was conducted.The basic characteristics,high-risk links,involved instruments,post-exposure emergency treatment and follow-up situations were analyzed,while sharps injury characteristics of medi-cal staff in different positions were classified and discussed.RESULTS Over six years,340 sharps injuries occurred with the highest incidence among interns(2.70 cases/100 FTE·year)and the lowest among logistics staff(1.05 cases/100 FTE·year).Jun.was the month with the highest incidence,averaging 7.33 cases.High-risk links in-cluded instruments handling,placing instruments into sharp containers and removing needles from rubber or other barriers,accounting for 76.47%.Nurses experienced injuries mostly occurred in general wards and were related to scalp needles;doctors mostly occurred in operating rooms and were due to surgical instruments;interns were pri-marily injured by blood collection needles;pharmacists and medical technicians were related to ampoule handling;while logistical staff were mostly injured by hollow needles and glass fragments from waste disposal.Nurses and doctors were the main injured groups,with a higher incidence among females(25-<35 years)and males(less than five years of work experience).The exposure source was mainly hepatitis B virus(HBV)infection.Post-ex-posure treatment was primarily standardized emergency treatment,but a higher proportion of non-standardized treatment was observed among logistics staff.Follow-up reports showed that interns and logistical staff had lower submission rates and lower training coverage.CONCLUSIONS Significant differences exist in sharps injury charac-teristics among medical staff in different positions.Attention should be paid to position-specific high-risk links and instruments.Targeted training and occupational health management should be strengthened to effectively prevent occupational exposure.

ObjectiveTo investigate the mechanism by which 2，3，5，4'-tetrahydroxyldiphenylethylene-2-O-glucoside （THSG） mitigates cerebral ischemia/reperfusion （CI/R） injury by regulating mitochondrial calcium overload and promoting mitophagy. MethodsSixty male SD rats were randomized into sham， model， SAS （40 mg·kg^-1）， and low-， medium- and high-dose （10， 20， 40 mg·kg^-1， respectively） THSG groups， with 10 rats in each group. The middle cerebral artery occlusion/reperfusion （MCAO/R） model was established by the modified Longa suture method. An oxygen-glucose deprivation/reoxygenation （OGD/R） model was constructed in PC12 cells. Neurological deficits were assessed via Zea Longa scoring， and cerebral infarct volume was measured by 2，3，5-triphenyltetrazolium chloride （TTC） staining. Structural and functional changes of cortical neurons in MCAO/R rats were assessed by hematoxylin-eosin and Nissl staining. PC12 cell viability was detected by cell counting kit-8 （CCK-8） assay， and mitochondrial calcium levels were quantified by Rhod-2 AM. Immunofluorescence was used to detect co-localization of PTEN-induced kinase 1 （PINK1） and leucine zipper/EF-hand-containing transmembrane protein 1 （LETM1） in neurons. Transmission electron microscopy （TEM） was employed to observe mitochondrial morphology in neurons. Western blot was employed to analyze the expression of translocase of outer mitochondrial membrane 20 （TOMM20）， autophagy-associated protein p62， microtubule-associated protein light chain 3 （LC3）， cysteinyl aspartate-specific proteinase-9 （Caspase-9）， B-cell lymphoma 2-associated protein X （Bax）， and cytochrome C （Cyt C）. ResultsCompared with the sham group， the model group exhibited increased infarct volume （P<0.01） and neurological deficit scores （P<0.01）， neuronal structure was disrupted with reduced Nissl bodies. （P<0.01）， mitochondrial swelling/fragmentation， decreased PINK1/LETM1 co-localization （P<0.01）， upregulated protein levels of LC3Ⅱ/LC3Ⅰ， TOMM20， Caspase-9， Bax， and Cyt C （P<0.01）， downregulated protein level of p62 （P<0.05）， weakened PC12 viability （P<0.01）， and elevated mitochondrial calcium level （P<0.01）. Compared with the model group， THSG and SAS groups showed reduced infarct volumes （P<0.05，P<0.01） and neurological deficit scores （P<0.05，P<0.01）， mitigated mitochondrial damage， and increased PINK1/LETM1 co-localization （P<0.01）. Medium/high-dose THSG and SAS alleviated the neurological damage， increased Nissl bodies （P<0.05，P<0.01）， downregulated the protein levels of p62， TOMM20， Caspase-9， Bax， and Cyt C （P<0.05，P<0.01）， and elevated the LC3Ⅱ/LC3Ⅰ level （P<0.05，P<0.01）. High-dose THSG enhanced PC12 cell viability （P<0.01）， increased PINK1/LETM1 co-localization （P<0.01）， and reduced mitochondrial calcium （P<0.01）. ConclusionTHSG may exert the neuroprotective effect on CI/R injury by activating the PINK1-LETM1 signaling pathway， reducing the mitochondrial calcium overload， and promoting mitophagy.

ObjectiveTo investigate the mechanism by which 2，3，5，4'-tetrahydroxyldiphenylethylene-2-O-glucoside （THSG） mitigates cerebral ischemia/reperfusion （CI/R） injury by regulating mitochondrial calcium overload and promoting mitophagy. MethodsSixty male SD rats were randomized into sham， model， SAS （40 mg·kg^-1）， and low-， medium- and high-dose （10， 20， 40 mg·kg^-1， respectively） THSG groups， with 10 rats in each group. The middle cerebral artery occlusion/reperfusion （MCAO/R） model was established by the modified Longa suture method. An oxygen-glucose deprivation/reoxygenation （OGD/R） model was constructed in PC12 cells. Neurological deficits were assessed via Zea Longa scoring， and cerebral infarct volume was measured by 2，3，5-triphenyltetrazolium chloride （TTC） staining. Structural and functional changes of cortical neurons in MCAO/R rats were assessed by hematoxylin-eosin and Nissl staining. PC12 cell viability was detected by cell counting kit-8 （CCK-8） assay， and mitochondrial calcium levels were quantified by Rhod-2 AM. Immunofluorescence was used to detect co-localization of PTEN-induced kinase 1 （PINK1） and leucine zipper/EF-hand-containing transmembrane protein 1 （LETM1） in neurons. Transmission electron microscopy （TEM） was employed to observe mitochondrial morphology in neurons. Western blot was employed to analyze the expression of translocase of outer mitochondrial membrane 20 （TOMM20）， autophagy-associated protein p62， microtubule-associated protein light chain 3 （LC3）， cysteinyl aspartate-specific proteinase-9 （Caspase-9）， B-cell lymphoma 2-associated protein X （Bax）， and cytochrome C （Cyt C）. ResultsCompared with the sham group， the model group exhibited increased infarct volume （P<0.01） and neurological deficit scores （P<0.01）， neuronal structure was disrupted with reduced Nissl bodies. （P<0.01）， mitochondrial swelling/fragmentation， decreased PINK1/LETM1 co-localization （P<0.01）， upregulated protein levels of LC3Ⅱ/LC3Ⅰ， TOMM20， Caspase-9， Bax， and Cyt C （P<0.01）， downregulated protein level of p62 （P<0.05）， weakened PC12 viability （P<0.01）， and elevated mitochondrial calcium level （P<0.01）. Compared with the model group， THSG and SAS groups showed reduced infarct volumes （P<0.05，P<0.01） and neurological deficit scores （P<0.05，P<0.01）， mitigated mitochondrial damage， and increased PINK1/LETM1 co-localization （P<0.01）. Medium/high-dose THSG and SAS alleviated the neurological damage， increased Nissl bodies （P<0.05，P<0.01）， downregulated the protein levels of p62， TOMM20， Caspase-9， Bax， and Cyt C （P<0.05，P<0.01）， and elevated the LC3Ⅱ/LC3Ⅰ level （P<0.05，P<0.01）. High-dose THSG enhanced PC12 cell viability （P<0.01）， increased PINK1/LETM1 co-localization （P<0.01）， and reduced mitochondrial calcium （P<0.01）. ConclusionTHSG may exert the neuroprotective effect on CI/R injury by activating the PINK1-LETM1 signaling pathway， reducing the mitochondrial calcium overload， and promoting mitophagy.

Colorectal cancer stands as a leading cause of cancer-related morbidity and mortality globally,with liver metastases being a significant determinant of patient prognosis.Conventional diagnostic methods,includ-ing imaging studies and biomarker testing,frequently exhibit inadequate sensitivity and specificity,underscoring the necessity for more advanced technologies.Recent advancements in genomics,transcriptomics,proteomics,me-tabolomics,and epigenomics have revolutionized our understanding of the biological mechanisms driving colorectal cancer.These methodologies enable comprehensive analyses of genetic mutations,gene expression profiles,protein modifications,and metabolic reprogramming,all of which are pivotal to the metastatic process.This article high-lights the advanced capabilities of artificial intelligence(AI)technologies in processing complex multi-omics data,thereby enhancing diagnostic accuracy and supporting personalized treatment strategies.It also addresses the challenges AI encounters in multi-omics analyses,such as ensuring data quality,improving model interpretability,and facilitating clinical translation.Additionally,it explores the potential integration of emerging technologies like single-cell sequencing and spatial omics into large-scale,multicenter studies to further enhance the clinical utility of these tools.

Colorectal cancer stands as a leading cause of cancer-related morbidity and mortality globally,with liver metastases being a significant determinant of patient prognosis.Conventional diagnostic methods,includ-ing imaging studies and biomarker testing,frequently exhibit inadequate sensitivity and specificity,underscoring the necessity for more advanced technologies.Recent advancements in genomics,transcriptomics,proteomics,me-tabolomics,and epigenomics have revolutionized our understanding of the biological mechanisms driving colorectal cancer.These methodologies enable comprehensive analyses of genetic mutations,gene expression profiles,protein modifications,and metabolic reprogramming,all of which are pivotal to the metastatic process.This article high-lights the advanced capabilities of artificial intelligence(AI)technologies in processing complex multi-omics data,thereby enhancing diagnostic accuracy and supporting personalized treatment strategies.It also addresses the challenges AI encounters in multi-omics analyses,such as ensuring data quality,improving model interpretability,and facilitating clinical translation.Additionally,it explores the potential integration of emerging technologies like single-cell sequencing and spatial omics into large-scale,multicenter studies to further enhance the clinical utility of these tools.

OBJECTIVE To analyze occupational exposure to sharps injuries among medical staff in different posi-tions in a three-A hospital.METHODS A retrospective collection of all sharps injury cases reported from 2018 to 2023 in a general hospital was conducted.The basic characteristics,high-risk links,involved instruments,post-exposure emergency treatment and follow-up situations were analyzed,while sharps injury characteristics of medi-cal staff in different positions were classified and discussed.RESULTS Over six years,340 sharps injuries occurred with the highest incidence among interns(2.70 cases/100 FTE·year)and the lowest among logistics staff(1.05 cases/100 FTE·year).Jun.was the month with the highest incidence,averaging 7.33 cases.High-risk links in-cluded instruments handling,placing instruments into sharp containers and removing needles from rubber or other barriers,accounting for 76.47%.Nurses experienced injuries mostly occurred in general wards and were related to scalp needles;doctors mostly occurred in operating rooms and were due to surgical instruments;interns were pri-marily injured by blood collection needles;pharmacists and medical technicians were related to ampoule handling;while logistical staff were mostly injured by hollow needles and glass fragments from waste disposal.Nurses and doctors were the main injured groups,with a higher incidence among females(25-<35 years)and males(less than five years of work experience).The exposure source was mainly hepatitis B virus(HBV)infection.Post-ex-posure treatment was primarily standardized emergency treatment,but a higher proportion of non-standardized treatment was observed among logistics staff.Follow-up reports showed that interns and logistical staff had lower submission rates and lower training coverage.CONCLUSIONS Significant differences exist in sharps injury charac-teristics among medical staff in different positions.Attention should be paid to position-specific high-risk links and instruments.Targeted training and occupational health management should be strengthened to effectively prevent occupational exposure.

Objective To investigate the molecular mechanisms by which SOX7 regulates the SHP-2/Wnt/β-cate-nin/ROS pathway,affecting the proliferation,invasion,and migration of colorectal cancer cells.Methods Twenty nude mice with subcutaneously transplanted tumor models were randomly divided into four groups:SOX7 NC(n=5),SOX mimic(n=5),SOX7 NC+PHPS1(n=5),and SOX7 mimic+PHPS1(n=5)to observe tumor growth.Human colorectal cancer cell line SW480 cells were transfected via lipofection and divided into six groups:SOX7 NC,SOX7 mimic,SOX7 NC+H2 O2,SOX7 mimic+H2O2,SOX7 NC+PHPS1,and SOX7 mimic+PHPS1.The ex-pression of SHP-2/Wnt/β-catenin/ROS pathway-related proteins in SW480 cells of each group was detected by Western blot.The invasion and migration capabilities of SW480 cells were assessed through scratch and Transwell invasion assays,while cell proliferation was evaluated using CCK-8.Results In vivo experiments demonstrated that tumors in the SOX7 mimic group were significantly smaller than those in the SOX7 NC group(P＜0.01).Tumors treated with PHPS1 intervention exhibited a significant increase in volume.There was no statistical significance in the difference in tumor volume between the SOX7 mimic+PHPS1 group and the SOX7 NC+PHPS1 group.In vitro experiments revealed that SOX7 mimic inhibited the expression of Wnt,β-catenin,NOX2,NOX4,PI3K,P-PI3K,AKT,P-AKT proteins(P＜0.01),and promoted the expression of p-SHP-2 protein(P＜0.01).The addition of hydrogen peroxide and SHP-2 inhibitor reversed the effects of SOX7 on SW480 cells(P＜0.05),and significantly promoted the expression levels of Wnt,β-catenin,NOX2,NOX4,PI3K,P-PI3K,AKT,P-AKT proteins,with no sig-nificant difference,while significantly reducing the expression levels of SHP-2,p-SHP-2 proteins,with no significant difference.PHPS1 inhibited the expression of SHP-2,p-SHP-2 proteins(P＜0.05)and upregulated the expression of Wnt,β-catenin,NOX2,NOX4,PI3K,P-PI3K,AKT,P-AKT proteins(P＜0.05).Scratch,Transwell invasion and migration assays,and CCK-8 experiments indicated that SOX7 suppressed the migration,invasion,and proliferation of SW480 cells through oxidative stress and the SHP-2 pathway(P＜0.01),while H2O2 and PHPS1 intervention promoted the migration,invasion,and proliferation of SW480 cells(P＜0.05).Conclusion SOX7 can suppress the proliferation,invasion,and migration of colorectal cancer by targeting the SHP-2/Wnt/β-catenin/ROS pathway.

ObjectiveTo investigate the mechanism of Baihuan Xiaoyao Decoction （Xiaoyaosan added with Lilii Bulbus and Albiziae Cortex） in alleviating depression-like behaviors of juvenile rats by regulating the polarization of microglia. MethodSixty juvenile SD rats were randomized into normal control， model， fluoxetine， and low-， medium-， and high-dose （5.36， 10.71， 21.42 g·kg^-1， respectively） Baihuan Xiaoyao decoction groups. The rat model of juvenile depression was established by chronic unpredictable mild stress （CUMS）. The sucrose preference test （SPT） was carried out to examine the sucrose preference of rats. Forced swimming test （FST） was carried out to measure the immobility time of rats. The open field test （OFT） was conducted to measure the total distance， the central distance， the number of horizontal crossings， and the frequency of rearing. Morris water maze （MWM） was used to measure the escape latency and the number of crossing the platform. The immunofluorescence assay was employed to detect the expression of inducible nitric oxide synthase （iNOS， the polarization marker of M1 microglia） and CD206 （the polarization marker of M2 microglia）. Real-time polymerase chain reaction was employed to determine the mRNA levels of iNOS， CD206， pro-inflammatory cytokines ［tumor necrosis factor （TNF）-α， interleukin （IL）-1β， and IL-6］ and anti-inflammatory cytokines （IL-4 and IL-10） in the hippocampus. Western blotting was employed to determine the protein levels of iNOS and CD206 in the hippocampus. The levels of IL-4 and IL-6 in the hippocampus were detected by enzyme-linked immunosorbent assay. ResultCompared with the normal control group， the model rats showed a reduction in sucrose preference （P<0.05）， an increase in immobility time （P<0.05）， decreased motor and exploratory behaviors （P<0.05）， and weakened learning and spatial memory （P<0.05）. In addition， the model rats showed up-regulated mRNA and protein levels of iNOS and mRNA levels of IL-1β， IL-6， and TNF-α （P<0.05）. Compared with the model group， Baihuan Xiaoyao decoction increased the sucrose preference value （P<0.05）， shortened the immobility time （P<0.01）， increased the motor and exploratory behaviors （P<0.05）， and improved the learning and spatial memory （P<0.01）. Furthermore， the decoction down-regulated the positive expression and protein level of iNOS， lowered the levels of TNF-α， IL-1β， and IL-6 （P<0.01）， promoted the positive expression of CD206， and elevated the levels of IL-4 and IL-10 （P<0.01） in the hippocampus of the high dose group. Moreover， the high-dose Baihuan Xiaoyao decoction group had higher sucrose preference value （P<0.01）， shorter immobility time （P<0.01）， longer central distance （P<0.01）， stronger learning and spatial memory （P<0.01）， higher positive expression and protein level of iNOS （P<0.01）， lower levels of TNF-α， IL-1β， and IL-6 （P<0.05， P<0.01）， lower positive expression and mRNA level of iNOS （P<0.05）， and higher levels of IL-4 and IL-10 （P<0.05， P<0.01） than the fluoxetine group. ConclusionBaihuan Xiaoyao decoction can improve the depression-like behavior of juvenile rats by inhibiting the M1 polarization and promoting the M2 polarization of microglia in the hippocampus.

To summarize the rescue and care of a case of breath-holding attack caused by congenital contractures of limbs and face,hypotonia,and developmental delay(CLIFAHDD)syndrome.Key points of nursing:early identification and intervention of breath-holding attack in CLIFAHDD syndrome,and implementation of rapid reactive rescue;implementing individualized developmental care measures to avoid stimuli that induce breath-holding attack;paying attention to the assessment of oral feeding ability,strengthening the exercise of oral feeding ability and nutrition management;strengthening perioperative diversified airway management to prevent postoperative complications;the monitoring of early neurological and motor system development,and early start of rehabilitation care;doing a good job in health education for caregivers to help them master the first aid treatment and growth and development assessment methods in the event of a breath-holding attack.After 53 days of hospitalization,the patient was discharged.After being discharged from the hospital for more than 1 month,the patient had breath-holding attack 2～4 times a day.After being discharged from the hospital for more than 2 months,the patient had no breath-holding attack,and only had occasional convulsive seizures during sleep,which could be relieved spontaneously.

Objective To evaluate the efficacy and safety of transurethral resection of Prostate(TURP)combined with endocrine therapy in patients with advanced prostate cancer.Methods A retrospective analysis was conducted on 87 cases of late-stage prostate cancer with dysuria admitted between January 2014 and December 2017.We divided them into 2 groups.TURP group(n = 48)received transurethral resection of prostate,followed by regular endocrine therapy.The control group(n = 39)was only given regular endocrine therapy.Comparative analysis of indicators such as prostate-specific antigen before and after treatment,maximum urinary flow rate,residual urine volume,International Prostate Symptom Score(IPSS),and 5-year survival rate was performed between the two groups.Results Three months after TURP surgery,the symptoms of urinary difficulty significantly improved,and various indicators showed significant improvement compared to before the surgery.PSA levels also notably decreased compared to before the surgery.After 3 months of treatment,the TURP group showed significant improvements in IPSS,Qmax,RV,and PSA indicators compared to the control group(P<0.05).Both groups of patients experienced a gradual decrease in PSA levels after receiving standardized treatment.In the first 12 months of treatment,the PSA levels in the TURP group decreased more significantly compared to the control group,but after 12 months of treatment,the comparison difference was not statistically significant in the PSA levels between the two groups(P = 0.056).A 5-year follow-up comparison of the two groups of patients revealed that there was no statistically significant difference in survival(P = 0.734).Conclusion Transurethral resection of Prostate(TURP)combined with regular endocrine therapy can effectively improve the dysuria in prostate cancer patients,improve the quality of life of patients,and will not affect the five-year survival rate.TURP is a safe and effective treatment for advanced prostate cancer.