OBJECTIVE To optimize the prescription pre-review system in our hospital and evaluate its application effects. METHODS Aiming at the problems of imperfect rule base and high false positive rate in the early operation of the system， optimization measures were taken， including improving the content of the rule base， adjusting the interception level and prompt mode， refining the working model of prescription review pharmacists， and strengthening clinical communication. A retrospective cohort study was conducted， with prescription data from June to December 2023 （before optimization） as the control group and June to December 2024 （after optimization） as the observation group. Through inter group comparative analysis， the actual effect of optimizing the prescription pre-approval system was evaluated. RESULTS The prescription qualified rate increased from （82.51± 4.04）% before optimization to （90.98±1.55）% after optimization； the false positive rate decreased from （20.87±1.64）% before optimization to （7.41±2.04）% after optimization. The monthly range of prescription qualified rate narrowed from 10.24% to 4.11%， and the coefficient of variation decreased from 4.92% to 1.73%. The monthly range of false positive rate slightly increased from 4.40% to 5.34%， the coefficient of variation rose from 8.32% to 26.18%. CONCLUSIONS Through multi-dimensional optimizations of the prescription pre-review system in our hospital， its prescription review efficiency has been significantly enhanced， the quality of prescriptions has steadily improved， and the accuracy of reviews has notably improved.

Gliomas, with their infiltrative growth and malignant potential, present considerable therapeutic challenges. Maximal safe resection is essential for optimizing patient survival and quality of life. Despite this, existing intraoperative visualization techniques suffer from limited sensitivity and accuracy. Label-free Raman spectroscopy has emerged as a non-invasive, rapidly diagnostic, and highly accurate technique. It accurately diagnoses tumors, identifies infiltration margins, and classifies molecular subtypes, enhancing the precision of glioma surgery. This review summarizes the latest advances and applications of label-free Raman spectroscopy in glioma surgery.

AIM:To study the protective effect of transient receptor potential vanilic acid subtype 1(TRPV1)agonist capsaicin(CAP)on traumatic blood loss shock rats,and to further explore its possible mechanism by network pharmacology.METHODS:Forty-five SD rats were divided into 5 groups by random number table method:normal group,shock group,lactated Ringer's solution(LR)group,CAP pretreatment(single administration before shock)group,CAP pre-final administration(twice administration before and after shock)group,with 9 rats in each group for survival observation.Then 32 SD rats were divided into 4 groups according to the results of survival experiment:normal group,shock group,LR group,CAP pre-final administration group,with 8 rats in each group for blood pressure,hemodynamics,arterial blood gas,vascular reactivi-ty and hepaticand renal blood flow.At the same time,the potential mechanism of CAP in the treat-ment of traumatic hemorrhagic shock was investi-gated by network pharmacology.Furthermore,ap-ply the dataset to validate and analyse the diagnos-tic value of the hub genes.RESULTS:Rats in shock group died within hours of the completion of the shock model,and the mean survival time was 1.25(0.42,6.21)h.LR resuscitation could improve the survival of rats to some extent.The survival rate and survival time of rats in the CAP pretreatment group were slightly increased as compared with the LR group,while twice administration of CAP be-fore and after shock(CAP pre-final administration)resulted in better outcomes than LR resuscitation alone.Further results indicated that CAP pre-final administration significantly reduced the blood lac-tic acid level,improved the vasoconstrictive and di-astolic reactivity,and increased the liver and kidney blood flow of shock rats as compared with LR group.The improvement of hemodynamics and blood gas indexes in CAP group was slightly higher than LR group,but there was no statistical signifi-cance.A total of 37 genes related to CAP anti-trau-matic hemorrhage shock were obtained by net-work pharmacology.KEGG enrichment analysis showed that the Ca ion signaling pathway and Ras signaling pathway were significantly enriched.Vali-dation of the dataset showed that the expression levels of CXCR4,NF-kB1,GFPA and NTF3 hub gene were significantly different in the normal and shock groups,and that CXCR4 has a high diagnostic value for traumatic haemorrhagic shock.CONCLUSIONS:CAP,the TRPV1 agonist,significantly improved vas-cular function,increased organ blood flow,and cor-rected the lactic acidosis in rats with traumatic hemorrhagic shock,thus markedly improved the survival outcomes.The mechanism may be related to Ca ion signal pathway and Ras signal pathway.CXCR4,NF-kB1,GFPA and NTF3 may be having an important role in it.

Objective:To assess the efficacy and safety profile of antaitasvir phosphate combined with yiqibuvir in the treatment of chronic hepatitis C (CHC) of various genotypes, without cirrhosis or with compensated cirrhosis.Methods:394 cases with CHC from 22 centers were collected from October 2021 to April 2023. They were randomly assigned to receive either the experimental drugs (antaitasvir phosphate 100 mg+yiqibuvir 600 mg) or placebo treatment in a 3∶1 ratio. The patients were administered drugs once a day for 12 consecutive weeks, and then followed up for 24 weeks after treatment cessation. All subjects were unblinded at the four-week follow-up following drug discontinuation, with the experimental drug group continuing to complete subsequent post-discontinuation follow-up. The placebo group was switched to receive the experimental drugs for a repeated 12-week treatment period and followed up for another 24 weeks after discontinuation of the drug (placebo delayed treatment phase).The sustained virologic response rate (SVR12) was observed for subjects in the double-blind phase and the placebo delayed-treatment phase at 12 weeks after treatment cessation.Virological resistance analysis was performed on subjects who failed treatment. The primary efficacy endpoint was SVR12. The number and percentage of subjects who achieved "HCV RNA

Objective To investigate the in vitro drug release behavior of hydroxyapatite-wedelolactone(Hap-Wed)and its effect on promoting osteogenic differentiation of bone marrow mesenchymal stem cells(BMSCs).Methods The in vitro release behavior of Hap-Wed fusion materials was detected by chromatographic technique.After the cells were passed continuously up to the third generation,they were divided into:① control group:complete medium;② Os group:osteogenic inducer(1mmol/L dexamethasone,10mmol/L vitamin C,1mol/L β-glycerol phosphate);③ Wed group:1μg/ml Web and osteogenic inducer were added to the complete medium;④ Hap-Web group:1 μg/ml Web,osteogenic inducer and Hap were added to the complete medium.Alkaline phosphates(ALP)activity assay,alizarin red S staining assay,real-time quantitative polymerase chain reaction(RT-qPCR)detection of osteocalcin,Osterix and Runx2 gene expression,analysis of Hap-Wed on BMSCs osteoblast differentiation.Results Hap-Wed fusion material released the drug slowly.Compared with control group,the number of ALP staining and the number of calcified nodules increased significantly in Hap-Wed experimental group.The Hap-Wed experimental group increased gene expression of osteocalcin,Osterix and Runx2.Conclusion Hap-Wed fusion material can slow and effective stimulation of osteoblast differentiation,which may provide a promising application prospect for the future development of the carrier material.

AIM:This study aims to investigate the effects of aerobic exercise on hypothalamic autophagy and central leptin resistance in obese mice,and to explore the potential mechanisms.METHODS:Forty male C57BL/6J mice,aged 7 to 8 weeks,were randomly assigned to 5 groups:normal control(CON)group,high-fat diet(HFD)group,HFD+exercise(HFD+Exe)group,HFD+phosphate-buffered saline(PBS)group,and HFD+rilmenidine(autophagy ago-nist)group,with 8 mice in each group.Additionally,twelve fibronectin type Ⅲ domain-containing protein 5(Fndc5)gene(encoding irisin precursor protein)knockout(Fndc5 KO)mice were randomly allocated to Fndc5 KO+HFD group and Fndc5 KO+HFD+Exe group,with 6 mice in each group.All mice were fed for 28 weeks.The mice in CON group re-ceived a normal diet,while those in the remaining groups were provided with an HFD.The mice in HFD+Exe and Fndc5 KO+HFD+Exe groups engaged in aerobic treadmill exercise while continuing an HFD from weeks 17 to 28.The mice in HFD+PBS group received intraperitoneal injections of PBS as a control,while those in HFD+rilmenidine group received in-traperitoneal injections of rilmenidine(10 mg?kg-1?d-1),4 times a week over a total duration of 12 weeks(weeks 17 to 28).Following the intervention,serum metabolite levels,as well as concentrations of leptin and irisin,were quantified by ELISA.Morphological alterations in the liver and white adipose tissues were evaluated through oil red O staining and he-matoxylin-eosin(HE)staining.Western blot was utilized to assess the hypothalamic protein levels of autophagy markers,autophagy-related protein 7(ATG7),beclin-1,microtubule-associated protein 1 light chain 3(LC3)and p62,and leptin resistance markers,suppressor of cytokine signaling 3(SOCS3)and protein tyrosine phosphatase 1B(PTP1B).RE-SULTS:Observations of mouse phenotypes indicated that HFD feeding significantly increased body weight,blood lipid content and serum leptin level(P<0.05).The results of HE and oil red O staining demonstrated that HFD feeding marked-ly promoted lipid accumulation in the liver and caused ballooning of white adipocytes.Western blot analyses revealed that HFD feeding significantly down-regulated the protein levels of ATG7,beclin-1 and LC3-Ⅱ/LC3-I,but up-regulated the pro-tein level of p62(P<0.05),thus reducing cellular autophagy capacity.Furthermore,HFD feeding elevated the protein levels of leptin resistance markers SOCS3 and PTP1B(P<0.05).Aerobic exercise and autophagy agonist were found to partially reverse these changes,enhancing cellular autophagy capacity and alleviating leptin resistance.However,these effects were diminished after knockout of Fndc5 gene,further substantiating the role of irisin in exercise-mediated en-hancement of cellular autophagy and attenuation of leptin resistance.CONCLUSION:Aerobic exercise alleviates hypo-thalamic autophagy defect and central leptin resistance in obese mice,which may be associated with exercise-induced irisin.

AIM:This study aims to investigate the effects of aerobic exercise on hypothalamic autophagy and central leptin resistance in obese mice,and to explore the potential mechanisms.METHODS:Forty male C57BL/6J mice,aged 7 to 8 weeks,were randomly assigned to 5 groups:normal control(CON)group,high-fat diet(HFD)group,HFD+exercise(HFD+Exe)group,HFD+phosphate-buffered saline(PBS)group,and HFD+rilmenidine(autophagy ago-nist)group,with 8 mice in each group.Additionally,twelve fibronectin type Ⅲ domain-containing protein 5(Fndc5)gene(encoding irisin precursor protein)knockout(Fndc5 KO)mice were randomly allocated to Fndc5 KO+HFD group and Fndc5 KO+HFD+Exe group,with 6 mice in each group.All mice were fed for 28 weeks.The mice in CON group re-ceived a normal diet,while those in the remaining groups were provided with an HFD.The mice in HFD+Exe and Fndc5 KO+HFD+Exe groups engaged in aerobic treadmill exercise while continuing an HFD from weeks 17 to 28.The mice in HFD+PBS group received intraperitoneal injections of PBS as a control,while those in HFD+rilmenidine group received in-traperitoneal injections of rilmenidine(10 mg?kg-1?d-1),4 times a week over a total duration of 12 weeks(weeks 17 to 28).Following the intervention,serum metabolite levels,as well as concentrations of leptin and irisin,were quantified by ELISA.Morphological alterations in the liver and white adipose tissues were evaluated through oil red O staining and he-matoxylin-eosin(HE)staining.Western blot was utilized to assess the hypothalamic protein levels of autophagy markers,autophagy-related protein 7(ATG7),beclin-1,microtubule-associated protein 1 light chain 3(LC3)and p62,and leptin resistance markers,suppressor of cytokine signaling 3(SOCS3)and protein tyrosine phosphatase 1B(PTP1B).RE-SULTS:Observations of mouse phenotypes indicated that HFD feeding significantly increased body weight,blood lipid content and serum leptin level(P<0.05).The results of HE and oil red O staining demonstrated that HFD feeding marked-ly promoted lipid accumulation in the liver and caused ballooning of white adipocytes.Western blot analyses revealed that HFD feeding significantly down-regulated the protein levels of ATG7,beclin-1 and LC3-Ⅱ/LC3-I,but up-regulated the pro-tein level of p62(P<0.05),thus reducing cellular autophagy capacity.Furthermore,HFD feeding elevated the protein levels of leptin resistance markers SOCS3 and PTP1B(P<0.05).Aerobic exercise and autophagy agonist were found to partially reverse these changes,enhancing cellular autophagy capacity and alleviating leptin resistance.However,these effects were diminished after knockout of Fndc5 gene,further substantiating the role of irisin in exercise-mediated en-hancement of cellular autophagy and attenuation of leptin resistance.CONCLUSION:Aerobic exercise alleviates hypo-thalamic autophagy defect and central leptin resistance in obese mice,which may be associated with exercise-induced irisin.

AIM:To study the protective effect of transient receptor potential vanilic acid subtype 1(TRPV1)agonist capsaicin(CAP)on traumatic blood loss shock rats,and to further explore its possible mechanism by network pharmacology.METHODS:Forty-five SD rats were divided into 5 groups by random number table method:normal group,shock group,lactated Ringer's solution(LR)group,CAP pretreatment(single administration before shock)group,CAP pre-final administration(twice administration before and after shock)group,with 9 rats in each group for survival observation.Then 32 SD rats were divided into 4 groups according to the results of survival experiment:normal group,shock group,LR group,CAP pre-final administration group,with 8 rats in each group for blood pressure,hemodynamics,arterial blood gas,vascular reactivi-ty and hepaticand renal blood flow.At the same time,the potential mechanism of CAP in the treat-ment of traumatic hemorrhagic shock was investi-gated by network pharmacology.Furthermore,ap-ply the dataset to validate and analyse the diagnos-tic value of the hub genes.RESULTS:Rats in shock group died within hours of the completion of the shock model,and the mean survival time was 1.25(0.42,6.21)h.LR resuscitation could improve the survival of rats to some extent.The survival rate and survival time of rats in the CAP pretreatment group were slightly increased as compared with the LR group,while twice administration of CAP be-fore and after shock(CAP pre-final administration)resulted in better outcomes than LR resuscitation alone.Further results indicated that CAP pre-final administration significantly reduced the blood lac-tic acid level,improved the vasoconstrictive and di-astolic reactivity,and increased the liver and kidney blood flow of shock rats as compared with LR group.The improvement of hemodynamics and blood gas indexes in CAP group was slightly higher than LR group,but there was no statistical signifi-cance.A total of 37 genes related to CAP anti-trau-matic hemorrhage shock were obtained by net-work pharmacology.KEGG enrichment analysis showed that the Ca ion signaling pathway and Ras signaling pathway were significantly enriched.Vali-dation of the dataset showed that the expression levels of CXCR4,NF-kB1,GFPA and NTF3 hub gene were significantly different in the normal and shock groups,and that CXCR4 has a high diagnostic value for traumatic haemorrhagic shock.CONCLUSIONS:CAP,the TRPV1 agonist,significantly improved vas-cular function,increased organ blood flow,and cor-rected the lactic acidosis in rats with traumatic hemorrhagic shock,thus markedly improved the survival outcomes.The mechanism may be related to Ca ion signal pathway and Ras signal pathway.CXCR4,NF-kB1,GFPA and NTF3 may be having an important role in it.

Objective To investigate the in vitro drug release behavior of hydroxyapatite-wedelolactone(Hap-Wed)and its effect on promoting osteogenic differentiation of bone marrow mesenchymal stem cells(BMSCs).Methods The in vitro release behavior of Hap-Wed fusion materials was detected by chromatographic technique.After the cells were passed continuously up to the third generation,they were divided into:① control group:complete medium;② Os group:osteogenic inducer(1mmol/L dexamethasone,10mmol/L vitamin C,1mol/L β-glycerol phosphate);③ Wed group:1μg/ml Web and osteogenic inducer were added to the complete medium;④ Hap-Web group:1 μg/ml Web,osteogenic inducer and Hap were added to the complete medium.Alkaline phosphates(ALP)activity assay,alizarin red S staining assay,real-time quantitative polymerase chain reaction(RT-qPCR)detection of osteocalcin,Osterix and Runx2 gene expression,analysis of Hap-Wed on BMSCs osteoblast differentiation.Results Hap-Wed fusion material released the drug slowly.Compared with control group,the number of ALP staining and the number of calcified nodules increased significantly in Hap-Wed experimental group.The Hap-Wed experimental group increased gene expression of osteocalcin,Osterix and Runx2.Conclusion Hap-Wed fusion material can slow and effective stimulation of osteoblast differentiation,which may provide a promising application prospect for the future development of the carrier material.

Gliomas, with their infiltrative growth and malignant potential, present considerable therapeutic challenges. Maximal safe resection is essential for optimizing patient survival and quality of life. Despite this, existing intraoperative visualization techniques suffer from limited sensitivity and accuracy. Label-free Raman spectroscopy has emerged as a non-invasive, rapidly diagnostic, and highly accurate technique. It accurately diagnoses tumors, identifies infiltration margins, and classifies molecular subtypes, enhancing the precision of glioma surgery. This review summarizes the latest advances and applications of label-free Raman spectroscopy in glioma surgery.