Antimicrobial resistance(AMR)has been a difficult problem of globally public health that can threaten human health.If its spread could not be effectively curbed,it will lead to increasing limitation in the options of clinical treatment.In the increasingly complex environment of diagnosis and treatment of infectious diseases,it is particularly urgent to build a rapid,accurate and widely popularized diagnosis system for pathogen,which is the key prerequisite of realizing accurate assessment for susceptibility of antimicrobial drug.This article comprehensively reviewed the main rapid diagnostic techniques currently used in AMR monitoring and detecting for antimicrobial susceptibility on the basis of the above conditions.It not only provided a detailed analysis of molecular typing methods represented by gene sequencing and phenotype identification methods based on conventional culture,but also focused on a new joint diagnostic strategy that combined genomic information with functional verification.Through comparative study for various technical principles,operating procedures and clinical applicability,the purpose of this paper was to provide scientific basis for optimizing the rapid detection scheme of drug susceptibility in clinical microbiology laboratories,and promote a comprehensive improvement of the level of diagnosis and treatment for infectious diseases,and ultimately improve the multi-layered network system of prevention and control for nosocomial infection.

Objective:To compare the efficacy of oliceridine and sufentanil when combined with propofol for painless gastroscopy.Methods:In this randomized controlled trial, 66 patients of either sex, aged 18-64 yr, with a body mass index of 18-26 kg/m 2, of American Society of Anesthesiologists Physical Status classification Ⅰor Ⅱ, scheduled for elective painless gastroscopy from September 2024 to November 2024, were divided into 2 groups ( n=33 each) using a table of computer-generated random numbers: sufentanil combined with propofol group (SP group) and oliceridine combined with propofol group (OP group). Sufentanil 0.1 μg/kg was intravenously injected in group SP, oliceridine 0.02 mg/kg was intravenously injected in group OP, and 1 min later propofol 2 mg/kg was intravenously injected in both groups. When the modified Observer′s Assessment of Alertness and Sedation score ≤ 1, the painless gastroscopy was performed. Heart rate, mean arterial pressure and peripheral oxygen saturation were recorded on admission to the operating room, immediately after insertion of the gastroscope, and at the end of procedure. The success of sedation, time of gastroscopy, emergence time, consumption of propofol and use of vasoactive drugs were recorded. The occurrence of adverse events such as respiratory depression, hypotension, dizziness and nausea was also recorded. Results:Compared with group SP, the incidence of respiratory depression was significantly decreased in group OP ( P<0.05). There was no statistically significant difference in the incidence of hypotension, dizziness and nausea and heart rate, mean arterial pressure and peripheral oxygen saturation at different time points between the two groups ( P>0.05). Conclusions:Oliceridine provides better efficacy than sufentanil when combined with propofol in painless gastroscopy.

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.

Objective To explore the molecular mechanisms by which cucurbitacin B(CuB)regulates the mitochondrial ap-optosis pathway through the nicotinamide phosphoribosyltransferase(NAMPT)/forkhead transcription factor O subfamily member 3a(FoxO3a)axis to affect the biological function of non-small cell lung cancer(NSCLC)cells.Methods Gefitinib(GEF)and CuB were used to intervene in A549 cells.Network pharmacology was employed to analyze the targets and downstream pathways,and different vector-transfected cell groups were set up.Cell viability was detected by CCK-8 assay,cell invasion by Transwell assay,and cell apoptosis by flow cytometry.The mitochondrial membrane potential(MMP)level was measured using a JC-1 kit,and intracellular reactive oxygen species(ROS)levels were detected using a kit.Western blot was used to detect the expression of mitochondrial dynamics-related proteins(DRP1,Mfn1),as well as the protein levels of NAMPT and FoxO3a in A549 cells.The mRNA expression of NAMPT was detected by qRT-PCR.Additionally,a xenograft model in nude mice was es-tablished to verify the therapeutic effects of CuB in vivo.Results Compared with the control group,GEF and CuB intervention significantly inhibited the viability and invasion of A549 cells and induced cell apoptosis.Moreover,CuB intervention significant-ly decreased the MMP level,increased ROS concentration,and upregulated the expression of DRP1 while downregulating Mfn1 in A549 cells(P＜0.05).NAMPT,a therapeutic target,was highly expressed in A549 cells and was inhibited by CuB.Compared with the vector group,overexpression of NAMPT significantly promoted the growth of A549 cells and inhibited mitochondrial apoptosis.Compared with the vector+CuB(100 nmol/L)group,overexpression of NAMPT reversed the effects of CuB on A549 cells(P＜0.05).Compared with the si-NAMPT-NC group,silencing NAMPT significantly inhibited the growth of A549 cells and promoted mitochondrial apoptosis,while knockdown of FoxO3a enhanced the viability and invasion of A549 cells and re-versed the damaging effects of si-NAMPT on cancer cells(P＜0.05).In vivo experimental results showed that CuB inhibited tumor weight and volume in a dose-dependent manner.Conclusion CuB regulates the NAMPT-FoxO3a axis through the mito-chondrial apoptosis pathway to inhibit the progression of NSCLC both in vitro and in vivo.

Objective To explore the molecular mechanisms by which cucurbitacin B(CuB)regulates the mitochondrial ap-optosis pathway through the nicotinamide phosphoribosyltransferase(NAMPT)/forkhead transcription factor O subfamily member 3a(FoxO3a)axis to affect the biological function of non-small cell lung cancer(NSCLC)cells.Methods Gefitinib(GEF)and CuB were used to intervene in A549 cells.Network pharmacology was employed to analyze the targets and downstream pathways,and different vector-transfected cell groups were set up.Cell viability was detected by CCK-8 assay,cell invasion by Transwell assay,and cell apoptosis by flow cytometry.The mitochondrial membrane potential(MMP)level was measured using a JC-1 kit,and intracellular reactive oxygen species(ROS)levels were detected using a kit.Western blot was used to detect the expression of mitochondrial dynamics-related proteins(DRP1,Mfn1),as well as the protein levels of NAMPT and FoxO3a in A549 cells.The mRNA expression of NAMPT was detected by qRT-PCR.Additionally,a xenograft model in nude mice was es-tablished to verify the therapeutic effects of CuB in vivo.Results Compared with the control group,GEF and CuB intervention significantly inhibited the viability and invasion of A549 cells and induced cell apoptosis.Moreover,CuB intervention significant-ly decreased the MMP level,increased ROS concentration,and upregulated the expression of DRP1 while downregulating Mfn1 in A549 cells(P＜0.05).NAMPT,a therapeutic target,was highly expressed in A549 cells and was inhibited by CuB.Compared with the vector group,overexpression of NAMPT significantly promoted the growth of A549 cells and inhibited mitochondrial apoptosis.Compared with the vector+CuB(100 nmol/L)group,overexpression of NAMPT reversed the effects of CuB on A549 cells(P＜0.05).Compared with the si-NAMPT-NC group,silencing NAMPT significantly inhibited the growth of A549 cells and promoted mitochondrial apoptosis,while knockdown of FoxO3a enhanced the viability and invasion of A549 cells and re-versed the damaging effects of si-NAMPT on cancer cells(P＜0.05).In vivo experimental results showed that CuB inhibited tumor weight and volume in a dose-dependent manner.Conclusion CuB regulates the NAMPT-FoxO3a axis through the mito-chondrial apoptosis pathway to inhibit the progression of NSCLC both in vitro and in vivo.

Objective:To compare the efficacy of oliceridine and sufentanil when combined with propofol for painless gastroscopy.Methods:In this randomized controlled trial, 66 patients of either sex, aged 18-64 yr, with a body mass index of 18-26 kg/m 2, of American Society of Anesthesiologists Physical Status classification Ⅰor Ⅱ, scheduled for elective painless gastroscopy from September 2024 to November 2024, were divided into 2 groups ( n=33 each) using a table of computer-generated random numbers: sufentanil combined with propofol group (SP group) and oliceridine combined with propofol group (OP group). Sufentanil 0.1 μg/kg was intravenously injected in group SP, oliceridine 0.02 mg/kg was intravenously injected in group OP, and 1 min later propofol 2 mg/kg was intravenously injected in both groups. When the modified Observer′s Assessment of Alertness and Sedation score ≤ 1, the painless gastroscopy was performed. Heart rate, mean arterial pressure and peripheral oxygen saturation were recorded on admission to the operating room, immediately after insertion of the gastroscope, and at the end of procedure. The success of sedation, time of gastroscopy, emergence time, consumption of propofol and use of vasoactive drugs were recorded. The occurrence of adverse events such as respiratory depression, hypotension, dizziness and nausea was also recorded. Results:Compared with group SP, the incidence of respiratory depression was significantly decreased in group OP ( P<0.05). There was no statistically significant difference in the incidence of hypotension, dizziness and nausea and heart rate, mean arterial pressure and peripheral oxygen saturation at different time points between the two groups ( P>0.05). Conclusions:Oliceridine provides better efficacy than sufentanil when combined with propofol in painless gastroscopy.

Antimicrobial resistance(AMR)has been a difficult problem of globally public health that can threaten human health.If its spread could not be effectively curbed,it will lead to increasing limitation in the options of clinical treatment.In the increasingly complex environment of diagnosis and treatment of infectious diseases,it is particularly urgent to build a rapid,accurate and widely popularized diagnosis system for pathogen,which is the key prerequisite of realizing accurate assessment for susceptibility of antimicrobial drug.This article comprehensively reviewed the main rapid diagnostic techniques currently used in AMR monitoring and detecting for antimicrobial susceptibility on the basis of the above conditions.It not only provided a detailed analysis of molecular typing methods represented by gene sequencing and phenotype identification methods based on conventional culture,but also focused on a new joint diagnostic strategy that combined genomic information with functional verification.Through comparative study for various technical principles,operating procedures and clinical applicability,the purpose of this paper was to provide scientific basis for optimizing the rapid detection scheme of drug susceptibility in clinical microbiology laboratories,and promote a comprehensive improvement of the level of diagnosis and treatment for infectious diseases,and ultimately improve the multi-layered network system of prevention and control for nosocomial infection.

Chemical cleaning and disinfection are crucial steps for eliminating infection in root canal treatment.However,irrigant selection or irrigation procedures are far from clear.The vapor lock effect in the apical region has yet to be solved,impeding irrigation efficacy and resulting in residual infections and compromised treatment outcomes.Additionally,ambiguous clinical indications for root canal medication and non-standardized dressing protocols must be clarified.Inappropriate intracanal medication may present side effects and jeopardize the therapeutic outcomes.Indeed,clinicians have been aware of these concerns for years.Based on the current evidence of studies,this article reviews the properties of various irrigants and intracanal medicaments and elucidates their effectiveness and interactions.The evolution of different kinetic irrigation methods,their effects,limitations,the paradigm shift,current indications,and effective operational procedures regarding intracanal medication are also discussed.This expert consensus aims to establish the clinical operation guidelines for root canal irrigation and a position statement on intracanal medication,thus facilitating a better understanding of infection control,standardizing clinical practice,and ultimately improving the success of endodontic therapy.

The overall health condition of patients significantly affects the diagnosis,treatment,and prognosis of endodontic diseases.A systemic consideration of the patient's overall health along with oral conditions holds the utmost importance in determining the necessity and feasibility of endodontic therapy,as well as selecting appropriate therapeutic approaches.This expert consensus is a collaborative effort by specialists from endodontics and clinical physicians across the nation based on the current clinical evidence,aiming to provide general guidance on clinical procedures,improve patient safety and enhance clinical outcomes of endodontic therapy in patients with compromised overall health.