OBJECTIVE To investigate the current status of hospital-associated infections,distribution of infection cases in departments,infection sites and pathogens so as to achieve the rational allocation of resources and provide data support for continuous improvement of medical quality.METHODS From 2019 to 2023,the relevant data in-cluding the departments of hospitalized patients with the infections,time of infections,infection sites and patho-gens were collected from all of the infection patients of Hohhot First Hospital by Xinglin nosocomial infection teal-time monitoring system and were statistically analyzed.RESULTS There were 1802 cases of hospital-associated infec-tions in total from 2019 to 2023,and the average incidence rate of infection was 1.18％.The average incidence of hospi-tal-associated infections exceeded 3％in 6 of 36 departments from 2019 to 2023(584 cases in total,accounting for 32.41％among all the cases),and the incidence of hospital-associated infections showed an upward trend in intensive care unit(ICU)(x2=4.125,P=0.042).The 3 major infection sites of the patients with hospital-associated infections were as follow:the patients with respiratory system infection accourted for 66.35％,the patients with urinary system infec-tions accounted for 19.39％,the patients with blood system infections 3.33％.Klebsiella pneumoniae,Escherichia coli and Acinetobacter baumannii ranked the top 3 species of pathogens causing the hospital-associated infection,accounting for 17.68％,12.25％and 11.33％,respectively.CONCLUSIONS The incidence of hospital-associated infections shows an upward trend in recent years.It is necessary to strengthen the comprehensive and meticulous management of the infec-tions and take full advantage of information surveillance data so as to further improve the medical quality and safety.

OBJECTIVE To investigate the current status of hospital-associated infections,distribution of infection cases in departments,infection sites and pathogens so as to achieve the rational allocation of resources and provide data support for continuous improvement of medical quality.METHODS From 2019 to 2023,the relevant data in-cluding the departments of hospitalized patients with the infections,time of infections,infection sites and patho-gens were collected from all of the infection patients of Hohhot First Hospital by Xinglin nosocomial infection teal-time monitoring system and were statistically analyzed.RESULTS There were 1802 cases of hospital-associated infec-tions in total from 2019 to 2023,and the average incidence rate of infection was 1.18％.The average incidence of hospi-tal-associated infections exceeded 3％in 6 of 36 departments from 2019 to 2023(584 cases in total,accounting for 32.41％among all the cases),and the incidence of hospital-associated infections showed an upward trend in intensive care unit(ICU)(x2=4.125,P=0.042).The 3 major infection sites of the patients with hospital-associated infections were as follow:the patients with respiratory system infection accourted for 66.35％,the patients with urinary system infec-tions accounted for 19.39％,the patients with blood system infections 3.33％.Klebsiella pneumoniae,Escherichia coli and Acinetobacter baumannii ranked the top 3 species of pathogens causing the hospital-associated infection,accounting for 17.68％,12.25％and 11.33％,respectively.CONCLUSIONS The incidence of hospital-associated infections shows an upward trend in recent years.It is necessary to strengthen the comprehensive and meticulous management of the infec-tions and take full advantage of information surveillance data so as to further improve the medical quality and safety.

Objective To explore the relationship between plantar fascia stiffness and windlass mechanism and their impact on the arch,and provide a biomechanical mechanism explanation for plantar fascia and arch-related diseases.Methods A foot-plate model with 30° flexion angle at the metatarsophalangeal joint was constructed.The musculoskeletal model combined with the three-dimensional finite element analysis method was used,and the dynamic data of the foot during walking at the speed of 5 km/h was obtained using dual fluoroscopic imaging system(DFIS).The finite element model was verified,and the influence of plantar fascia stiffness on the capstan mechanism and arch-related mechanical parameters was explored.Results The finite element simulation analysis results were highly consistent with the foot data obtained by DFIS,confirming the validity of the model.With the increase of plantar fascia stiffness,the windlass effect and the stiffness of the longitudinal arch of the foot both showed an increasing trend,but the flexion angle of the metatarsophalangeal joint decreased,the distal stress of the plantar fascia gradually decreased,and the proximal stress increased;when the plantar fascia stiffness was 25％-150％,the width of the transverse arch of the foot increased with the increase of plantar fascia stiffness,while the height of the transverse arch decreased with the increase of plantar fascia stiffness;when the plantar fascia stiffness was 150％-200％,the width of the transverse arch of the foot decreased,the height increased,and the stiffness also increased.Conclusions An increase in plantar fascia stiffness can enhance the windlass mechanism to some extent,but it also leads to a reduction in metatarsophalangeal joint flexion.The stiffness of the plantar fascia affects the metatarsophalangeal joint flexion,thereby impacting the windlass mechanism and the distal tensile force of the plantar fascia.Together with the ground reaction force at the distal end of the metatarsals,these factors collectively influence the stiffness of the transverse arch of the foot.

Tumor microenvironment(TME)is the living environment of tumor cells.The immune cells contained in TME are reprogrammed into tumor-promoting states due to various factors.Inhibiting this reprogramming effect of TME is an innovative strategy for treating tumors.As an essential factor in spindle assembly,TPX2 is considered to be a gene that promotes cancer cell proliferation and plays a role in cell response to replication stress.Highly expressed TPX2 in tumor cells promotes tumor growth through a variety of pathways,and these pathways can promote the tumor-promoting activity of immune cells in TME.Therefore,TPX2 may be a regulatory gene of TME.This paper discusses the possible mechanism of TPX2 involved in the regulation of TME by discussing the pathway medi-ated by TPX2 and the regulation of immune cells infiltrated in TME,and provides ideas for subsequent research directions.

BACKGROUND:Synovitis is involved in all stages of osteoarthritis and is a key factor contributing to the development of osteoarthritis.Studies have shown that circular RNA(circRNA)plays an important role in the proliferation,apoptosis and extracellular matrix degradation of synovial cells and chondrocytes.OBJECTIVE:To observe the effects of circRNA SEC24A on the interleukin-1β-induced proliferation,apoptosis,and expression of inflammatory factors in human synovial fibroblasts.METHODS:Human synovial fibroblasts were divided into four groups,including control group,interleukin-1β group,empty vector group,and sh-circSEC24A group.Except for the control group,the other three groups were induced with 10 ng/mL interleukin-1β for 24 hours to establish inflammatory cell models;the empty vector group and sh-circSEC24A group were infected with empty vector virus and lentiviral vector knocking down circSEC24A.CCK-8 assay was used to detect cell proliferation.Flow cytometry was used to detect cell apoptosis.ELISA was used to detect the levels of matrix metalloproteinase-9,matrix metalloproteinase-13,interleukin-6,and tumor necrosis factor-α in cell supernatant.Western blot assay was used to detect the relative expression levels of Bax,Bcl-2,matrix metalloproteinase-9,matrix metalloproteinase-13,casepase3,cleaved-casepase3,casepase8,and cleaved-casepase8 proteins in cells.RESULTS AND CONCLUSION:(1)qRT-PCR results showed that compared with the normal group,the expression of circSEC24A in human synovial fibroblasts induced by interleukin 1β was significantly up-regulated.(2)The absorbance value of cells in the sh-circSEC24A group detected by CCK-8 assay was significantly higher than that of interleukin 1β group and empty vector group(P＜0.05).The apoptosis rate of sh-circSEC24A group detected by flow cytometry was significantly lower than that of interleukin 1β group and empty vector group(P＜0.05).(3)The levels of tumor necrosis factor α and interleukin 6 in the supernatant of human synovial fibroblasts in the sh-circSEC24A group detected by ELISA were significantly lower than those in the interleukin 1β group and the empty vector group(P＜0.01,P＜0.001).(4)Western blot assay results showed that compared with the interleukin 1β group and the empty vector group,the expression of the pro-apoptotic factor Bax protein in the sh-circSEC24A group significantly decreased,and the expression of the anti-apoptotic factor Bcl-2 protein increased significantly(P＜0.05);apoptosis and related activating factors cleaved-casepase3 and cleaved-casepase8 protein expressions were both reduced(P＜0.05).(5)ELISA and western blot assay results showed that compared with the interleukin 1β group and the empty vector group,the sh-circSEC24A group had lower levels of matrix metalloproteinase 9 and matrix metalloproteinase 13 protein(P＜0.05).These findings indicated that the expression of circSEC24A was abnormally increased in human synovial fibroblasts induced by interleukin 1β.Knocking down circSEC24A expression could promote the proliferation of human synovial fibroblasts and inhibit apoptosis,inflammatory factor release,and extracellular matrix degradation,suggesting that circSEC24A may be an important intervention target for early osteoarthritis.

Objective To investigate the coagulation abnormalities and molecular genetic characteristics of a family with asymptomatic inherited fibrinogen disorders(IFD).Methods The clinical data of a family with IFD,including 5 individuals from two generations,were collected.Their peripheral blood coagulation indicators were detected.The coding sequences of FGA,FGB and FGG genes were amplified by PCR and Sanger sequencing was used to identify the candidate variants,which were further validated in the family mem-bers.The bioinformatic software was used to analyze the pathogenicity and conservation of the missense mutation and its effect on the spatial structure and function of the protein.Results The IFD patients had significantly low fibrinogen antigen(Fg:Ag)concentration and fibrinogen coagulation(Fg:C)activity concentration as well as prolonged thrombin time(TT),while coagulation indicators of the unaffected relatives were normal.The results of Sanger sequencing showed that all IFD patients carried a heterozygous missense variant of c.1001A>C(p.Asn334Thr)in the FGG gene.The bioinformatic analysis suggested that Asn334Thr was a pathogenic variant,while homology analysis indicated that the Asn334 locus was highly conserved in evolution.The analysis of protein spatial structure showed that the Asn334Thr mutation altered hydrogen bonds between amino acids.Conclusion The heterozygous missense variant c.1001A>C(p.Asn334Thr)in the FGG gene may be the pathogenic cause of the proband.The finding enriches the spectrum of FGG gene mutations and provides experimental evidence for the genetic counseling of affected families.

Objective To explore the relationship between plantar fascia stiffness and windlass mechanism and their impact on the arch,and provide a biomechanical mechanism explanation for plantar fascia and arch-related diseases.Methods A foot-plate model with 30° flexion angle at the metatarsophalangeal joint was constructed.The musculoskeletal model combined with the three-dimensional finite element analysis method was used,and the dynamic data of the foot during walking at the speed of 5 km/h was obtained using dual fluoroscopic imaging system(DFIS).The finite element model was verified,and the influence of plantar fascia stiffness on the capstan mechanism and arch-related mechanical parameters was explored.Results The finite element simulation analysis results were highly consistent with the foot data obtained by DFIS,confirming the validity of the model.With the increase of plantar fascia stiffness,the windlass effect and the stiffness of the longitudinal arch of the foot both showed an increasing trend,but the flexion angle of the metatarsophalangeal joint decreased,the distal stress of the plantar fascia gradually decreased,and the proximal stress increased;when the plantar fascia stiffness was 25％-150％,the width of the transverse arch of the foot increased with the increase of plantar fascia stiffness,while the height of the transverse arch decreased with the increase of plantar fascia stiffness;when the plantar fascia stiffness was 150％-200％,the width of the transverse arch of the foot decreased,the height increased,and the stiffness also increased.Conclusions An increase in plantar fascia stiffness can enhance the windlass mechanism to some extent,but it also leads to a reduction in metatarsophalangeal joint flexion.The stiffness of the plantar fascia affects the metatarsophalangeal joint flexion,thereby impacting the windlass mechanism and the distal tensile force of the plantar fascia.Together with the ground reaction force at the distal end of the metatarsals,these factors collectively influence the stiffness of the transverse arch of the foot.

Objective To investigate the coagulation abnormalities and molecular genetic characteristics of a family with asymptomatic inherited fibrinogen disorders(IFD).Methods The clinical data of a family with IFD,including 5 individuals from two generations,were collected.Their peripheral blood coagulation indicators were detected.The coding sequences of FGA,FGB and FGG genes were amplified by PCR and Sanger sequencing was used to identify the candidate variants,which were further validated in the family mem-bers.The bioinformatic software was used to analyze the pathogenicity and conservation of the missense mutation and its effect on the spatial structure and function of the protein.Results The IFD patients had significantly low fibrinogen antigen(Fg:Ag)concentration and fibrinogen coagulation(Fg:C)activity concentration as well as prolonged thrombin time(TT),while coagulation indicators of the unaffected relatives were normal.The results of Sanger sequencing showed that all IFD patients carried a heterozygous missense variant of c.1001A>C(p.Asn334Thr)in the FGG gene.The bioinformatic analysis suggested that Asn334Thr was a pathogenic variant,while homology analysis indicated that the Asn334 locus was highly conserved in evolution.The analysis of protein spatial structure showed that the Asn334Thr mutation altered hydrogen bonds between amino acids.Conclusion The heterozygous missense variant c.1001A>C(p.Asn334Thr)in the FGG gene may be the pathogenic cause of the proband.The finding enriches the spectrum of FGG gene mutations and provides experimental evidence for the genetic counseling of affected families.

Tumor microenvironment(TME)is the living environment of tumor cells.The immune cells contained in TME are reprogrammed into tumor-promoting states due to various factors.Inhibiting this reprogramming effect of TME is an innovative strategy for treating tumors.As an essential factor in spindle assembly,TPX2 is considered to be a gene that promotes cancer cell proliferation and plays a role in cell response to replication stress.Highly expressed TPX2 in tumor cells promotes tumor growth through a variety of pathways,and these pathways can promote the tumor-promoting activity of immune cells in TME.Therefore,TPX2 may be a regulatory gene of TME.This paper discusses the possible mechanism of TPX2 involved in the regulation of TME by discussing the pathway medi-ated by TPX2 and the regulation of immune cells infiltrated in TME,and provides ideas for subsequent research directions.

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