Esophageal squamous cell carcinoma(ESCC)is a common malignant tumor with insidious early symptoms and a poor prognosis.In traditional Chinese medicine(TCM),ESCC is classified as"ye ge."Drawing on clinical experience,we believe that kidney deficiency leads to the deficiency of vital qi and immune dysfunction,providing the foundation for cancerous growth by depleting qi and damaging essence,toxic stasis and stagnation,forming a local hypoxic and acidic microenvironment that promotes tumor invasion,metastasis,and recurrence.Considering the effect of modern comprehensive treatments,the occurrence and development of ESCC are summarized as kidney deficiency being the root cause and toxic stasis being the driving force.The pathogenesis and treatment of ESCC in the preoperative,postoperative,and non-surgical treatment stages are discussed.The pathogenesis of the disease is summarized as follows:preoperatively,toxicity and stasis intertwine,depleting the kidney;postoperatively,the kidney loses its vitality,allowing various pathogenic factors to persist;during non-operative treatment,vital qi and pathogens contend,resulting in entrenched toxicity.During the preoperative neoadjuvant phase,therapy should resolve stasis,eliminate toxins,enhance kidney function,tonify essence,and support the body.During the postoperative adjuvant phase,therapy should strengthen the root and consolidate the foundation while detoxifying and expelling stasis.The non-surgical treatment stage uses"balanced interruption,"targeting tumor progression and metastasis by harmonizing yin and yang,thus preventing recurrence.This article will provide insights into the integrative Chinese-Western management of ESCC.

The Shanghai-style pediatric Tuina(Chinese therapeutic massage)school,a renowned academic school of pediatric Tuina in China,was founded by Professor JIN Yicheng,a mentor of the National Senior Traditional Chinese Medicine(TCM)Experts'Clinical Experience Inheritance Class and a distinguished TCM practitioner in Shanghai.This academic school has now been perpetuated through four generations.Prof.JIN Yicheng,a pioneering leader in modern China's pediatric Tuina,has dedicated sixty years to medical practice with unwavering benevolence and adherence to"principled innovation".While delving into traditional and ancient teachings,he has also embraced contemporary advancements.Building upon the essence of traditional pediatric Tuina,he integrated distinctive techniques from various Tuina schools,including the Yi Zhi Chan Tuina school,rolling manipulation Tuina school,and Neigong Tuina school.He also assimilated the quintessence of historical pediatric Tuina literature,the experience of modern Shanghai-based pediatric Tuina masters,and folk techniques while incorporating his years of clinical insights.This synthesis finally led to the formulation of the academic thought of"reinforcing healthy Qi and unblocking regulation"in Shanghai-style pediatric Tuina that guides clinical practice.Specifically,he comprehensively applies techniques such as"unblocking regulation of Zang-Fu organs","unblocking regulation of the four seas","unblocking regulation of the water and fire",and"unblocking regulation of the back"to the prevention and treatment of pediatric diseases across internal medicine,external medicine,orthopedics,and otolaryngology,which has significantly enhanced clinical efficacy and expanded the applicable age range and scope of Tuina for pediatric health issues,more aligning with the characteristics of children and adolescents'health challenges and current clinical demands,and paving a new way in preserving and developing traditional pediatric Tuina.

Objective:To investigate the effect of myo-inositol on the reactivation of ocular dominance plasticity in the visual cortex of adult mice and its mechanisms.Methods:Thirty-two male SPF-grade C57BL/6J mice at postnatal day 60 (P60) were randomly divided into four groups using a random number table: normal control group, monocular form deprivation (MD) group, myo-inositol group (myo-inositol administered to normal mice), and MD+ myo-inositol group (myo-inositol administered to MD mice), with 8 mice in each group.The right eyes of MD group and MD+ myo-inositol group received MD on P60.Mice in each group were housed until P64 when pattern visual evoked potential (P-VEP) recordings were performed in both eyes.The amplitude and peak time of P100 wave were measured, and the contralateral/ipsilateral ratio (C/I) was calculated to evaluate the shift of ocular dominance.Twenty-four mice were randomly divided into MD group and MD+ myo-inositol group using the random number table method, with 12 mice in each group.RNA was extracted from the visual cortex of the two groups of mice, and transcriptomic sequencing and bioinformatics analysis were performed to screen differentially expressed genes.Six mice were randomly divided into MD group and MD+ myo-inositol group using the random number table method, with 3 mice in each group, and the expression changes of differentially expressed genes cell communication network factor 1( CCN1), fatty acid binding protein 7( Fabp7) and galectin-3 binding protein ( Lgals3bp) were verified by real-time fluorescence quantitative PCR.This study adhered to the Regulations on the Administration of Laboratory Animals (2017 Edition), and the research protocol was approved by the Animal Ethics Committee of Tianjin Medical University (No.TMUaMEC2022004). Results:The P-VEP results showed that the right eye P100 amplitudes in the normal control, MD, myo-inositol and MD+ myo-inositol groups were (89.04±19.87), (83.04±9.42), (88.14±21.75) and (61.75±15.42)μV, and the P100 wave peak time were (102.40±5.64), (101.50±8.26), (101.33±8.66) and (111.30±7.17)ms, and C/I were 2.38±0.17, 2.35±0.22, 2.41±0.31, and 1.65±0.24, respectively, with statistically significant overall differences ( F=5.844, 2.221, 16.634; all P<0.05).Compared with the normal control group, MD group and myo-inositol group, the MD+ myo-inositol group had a significant decrease in the P100 wave amplitude in the right eye, a significant prolongation of the P100 wave peak time, and a significant decrease in the C/I, with statistically significant differences (all P<0.05).There was no significant difference in P100 wave amplitude or peak time in the left eyes among the normal control, MD, myo-inositol and MD+ myo-inositol groups ( F=0.249, 1.356; both P>0.05).The transcriptome sequencing results showed that there were significant differences in the expression of 93 genes between the MD+ myo-inositol group and the MD group, among which the differential expression of CCN1, Fabp7 and Lgals3bp genes related to visual plasticity was particularly significant.The real-time fluorescence quantitative PCR results verified that the expression of CCN1 in the MD+ myo-inositol group was significantly decreased, and the expression of Fabp7 and Lgals3bp was significantly increased, with statistically significant differences ( t=17.561, 9.237, 12.710; all P<0.001). Conclusions:Myo-inositol can effectively reactivate ocular dominance plasticity in the visual cortex in adult mice, and may mediate this process by regulating the expression of specific genes CCN1, Fabp7, and Lgals3bp.

Objective:To explore the effects of microRNA-221(miR-221)on inflammation and fibrosis induced by lipopoly-saccharide(LPS)in rat cardiomyocytes and the regulatory role of phosphatidylinositol 3-kinase(PI3K)/seronine/threonine protein kinase(AKT)signaling pathway.Methods:Cultured rat myocardial H9C2 cells in vitro,they were divided into control group(no inter-vention),LPS group(10 μg/ml LPS),experimental group(10 μg/ml LPS+10,20,40,80 μmol/L baicalin),mimics NC group(10 μg/ml LPS+mimics NC transfection),miR-221 mimics group(10 μg/ml LPS+transfection miR-221 mimics),inhibitor NC group(10 μg/ml LPS+transfection inhibitor NC),miR-221 inhibitor group(10 μg/ml LPS+transfection miR-221 inhibitor),10+miR-221 mimics group(10 μg/ml LPS+10 μmol/L baicalin+transfection miR-221 mimics)and 10+miR-221 inhibitor group(10 μg/ml LPS+10 μmol/L baicalin+transfection miR-221 inhibitor)were treated for 24 h.Real-time quantitative fluorescence PCR(RT-qPCR),ELISA,CCK-8,5-acetyne-2'-deoxyuracil nucleoside(EdU)and Transwell chamber methods were used to determine the expression level of miR-221,the expression levels of inflammatory factors,cell viability,cell proliferation and migration ability,Western blot was used to determine the expression levels of EMT-related proteins[E-cadherin,N-cadherin,Vimentin,fibronectin(FN)]and PI3K/AKT pathway related proteins.Results:Cell viability increased in LPS+10 group(P<0.05),so LPS+10 group was selected for follow-up experiment.The results of miR-221 level showed that miR-221 mimics group was higher than mimics NC group(P<0.05),miR-221 inhibitor group was lower than inhibitor NC group(P<0.05).Transfection of miR-221mimics group and miR-221 inhibitor group was successful.Compared with control group,cell proliferation rate and E-cadherin protein level in LPS group were decreased(P<0.05).The expression level of miR-221,cell migration number,IL-6 and TNF-α levels,and the protein levels of p-PI3K,p-AKT,N-cadherin,FN and Vimentin were increased(P<0.05).Compared with LPS group,LPS+10 group significantly reversed the changes of the above indexes(P<0.05).Compared with LPS+10 group,10+miR-221 mimics group reduced the above effect of baicalin in LPS-induced cells(P<0.05).However,miR-221 inhibitor of 10+miR-221 inhibitor group enhanced the above effect of baicalin in LPS-induced cells(P<0.05).Conclusion:Baicalin can inhibit the effects of LPS-induced myocyte H9C2 migration,inflammation and fibrosis and promote their proliferation by down-regulating the expression of miR-221,and its mechanism may be related to the inhibi-tion of PI3K/AKT signaling pathway.

Objective:To investigate the effect of myo-inositol on the reactivation of ocular dominance plasticity in the visual cortex of adult mice and its mechanisms.Methods:Thirty-two male SPF-grade C57BL/6J mice at postnatal day 60 (P60) were randomly divided into four groups using a random number table: normal control group, monocular form deprivation (MD) group, myo-inositol group (myo-inositol administered to normal mice), and MD+ myo-inositol group (myo-inositol administered to MD mice), with 8 mice in each group.The right eyes of MD group and MD+ myo-inositol group received MD on P60.Mice in each group were housed until P64 when pattern visual evoked potential (P-VEP) recordings were performed in both eyes.The amplitude and peak time of P100 wave were measured, and the contralateral/ipsilateral ratio (C/I) was calculated to evaluate the shift of ocular dominance.Twenty-four mice were randomly divided into MD group and MD+ myo-inositol group using the random number table method, with 12 mice in each group.RNA was extracted from the visual cortex of the two groups of mice, and transcriptomic sequencing and bioinformatics analysis were performed to screen differentially expressed genes.Six mice were randomly divided into MD group and MD+ myo-inositol group using the random number table method, with 3 mice in each group, and the expression changes of differentially expressed genes cell communication network factor 1( CCN1), fatty acid binding protein 7( Fabp7) and galectin-3 binding protein ( Lgals3bp) were verified by real-time fluorescence quantitative PCR.This study adhered to the Regulations on the Administration of Laboratory Animals (2017 Edition), and the research protocol was approved by the Animal Ethics Committee of Tianjin Medical University (No.TMUaMEC2022004). Results:The P-VEP results showed that the right eye P100 amplitudes in the normal control, MD, myo-inositol and MD+ myo-inositol groups were (89.04±19.87), (83.04±9.42), (88.14±21.75) and (61.75±15.42)μV, and the P100 wave peak time were (102.40±5.64), (101.50±8.26), (101.33±8.66) and (111.30±7.17)ms, and C/I were 2.38±0.17, 2.35±0.22, 2.41±0.31, and 1.65±0.24, respectively, with statistically significant overall differences ( F=5.844, 2.221, 16.634; all P<0.05).Compared with the normal control group, MD group and myo-inositol group, the MD+ myo-inositol group had a significant decrease in the P100 wave amplitude in the right eye, a significant prolongation of the P100 wave peak time, and a significant decrease in the C/I, with statistically significant differences (all P<0.05).There was no significant difference in P100 wave amplitude or peak time in the left eyes among the normal control, MD, myo-inositol and MD+ myo-inositol groups ( F=0.249, 1.356; both P>0.05).The transcriptome sequencing results showed that there were significant differences in the expression of 93 genes between the MD+ myo-inositol group and the MD group, among which the differential expression of CCN1, Fabp7 and Lgals3bp genes related to visual plasticity was particularly significant.The real-time fluorescence quantitative PCR results verified that the expression of CCN1 in the MD+ myo-inositol group was significantly decreased, and the expression of Fabp7 and Lgals3bp was significantly increased, with statistically significant differences ( t=17.561, 9.237, 12.710; all P<0.001). Conclusions:Myo-inositol can effectively reactivate ocular dominance plasticity in the visual cortex in adult mice, and may mediate this process by regulating the expression of specific genes CCN1, Fabp7, and Lgals3bp.

Esophageal squamous cell carcinoma(ESCC)is a common malignant tumor with insidious early symptoms and a poor prognosis.In traditional Chinese medicine(TCM),ESCC is classified as"ye ge."Drawing on clinical experience,we believe that kidney deficiency leads to the deficiency of vital qi and immune dysfunction,providing the foundation for cancerous growth by depleting qi and damaging essence,toxic stasis and stagnation,forming a local hypoxic and acidic microenvironment that promotes tumor invasion,metastasis,and recurrence.Considering the effect of modern comprehensive treatments,the occurrence and development of ESCC are summarized as kidney deficiency being the root cause and toxic stasis being the driving force.The pathogenesis and treatment of ESCC in the preoperative,postoperative,and non-surgical treatment stages are discussed.The pathogenesis of the disease is summarized as follows:preoperatively,toxicity and stasis intertwine,depleting the kidney;postoperatively,the kidney loses its vitality,allowing various pathogenic factors to persist;during non-operative treatment,vital qi and pathogens contend,resulting in entrenched toxicity.During the preoperative neoadjuvant phase,therapy should resolve stasis,eliminate toxins,enhance kidney function,tonify essence,and support the body.During the postoperative adjuvant phase,therapy should strengthen the root and consolidate the foundation while detoxifying and expelling stasis.The non-surgical treatment stage uses"balanced interruption,"targeting tumor progression and metastasis by harmonizing yin and yang,thus preventing recurrence.This article will provide insights into the integrative Chinese-Western management of ESCC.

The Shanghai-style pediatric Tuina(Chinese therapeutic massage)school,a renowned academic school of pediatric Tuina in China,was founded by Professor JIN Yicheng,a mentor of the National Senior Traditional Chinese Medicine(TCM)Experts'Clinical Experience Inheritance Class and a distinguished TCM practitioner in Shanghai.This academic school has now been perpetuated through four generations.Prof.JIN Yicheng,a pioneering leader in modern China's pediatric Tuina,has dedicated sixty years to medical practice with unwavering benevolence and adherence to"principled innovation".While delving into traditional and ancient teachings,he has also embraced contemporary advancements.Building upon the essence of traditional pediatric Tuina,he integrated distinctive techniques from various Tuina schools,including the Yi Zhi Chan Tuina school,rolling manipulation Tuina school,and Neigong Tuina school.He also assimilated the quintessence of historical pediatric Tuina literature,the experience of modern Shanghai-based pediatric Tuina masters,and folk techniques while incorporating his years of clinical insights.This synthesis finally led to the formulation of the academic thought of"reinforcing healthy Qi and unblocking regulation"in Shanghai-style pediatric Tuina that guides clinical practice.Specifically,he comprehensively applies techniques such as"unblocking regulation of Zang-Fu organs","unblocking regulation of the four seas","unblocking regulation of the water and fire",and"unblocking regulation of the back"to the prevention and treatment of pediatric diseases across internal medicine,external medicine,orthopedics,and otolaryngology,which has significantly enhanced clinical efficacy and expanded the applicable age range and scope of Tuina for pediatric health issues,more aligning with the characteristics of children and adolescents'health challenges and current clinical demands,and paving a new way in preserving and developing traditional pediatric Tuina.

Objective:To explore the effects of microRNA-221(miR-221)on inflammation and fibrosis induced by lipopoly-saccharide(LPS)in rat cardiomyocytes and the regulatory role of phosphatidylinositol 3-kinase(PI3K)/seronine/threonine protein kinase(AKT)signaling pathway.Methods:Cultured rat myocardial H9C2 cells in vitro,they were divided into control group(no inter-vention),LPS group(10 μg/ml LPS),experimental group(10 μg/ml LPS+10,20,40,80 μmol/L baicalin),mimics NC group(10 μg/ml LPS+mimics NC transfection),miR-221 mimics group(10 μg/ml LPS+transfection miR-221 mimics),inhibitor NC group(10 μg/ml LPS+transfection inhibitor NC),miR-221 inhibitor group(10 μg/ml LPS+transfection miR-221 inhibitor),10+miR-221 mimics group(10 μg/ml LPS+10 μmol/L baicalin+transfection miR-221 mimics)and 10+miR-221 inhibitor group(10 μg/ml LPS+10 μmol/L baicalin+transfection miR-221 inhibitor)were treated for 24 h.Real-time quantitative fluorescence PCR(RT-qPCR),ELISA,CCK-8,5-acetyne-2'-deoxyuracil nucleoside(EdU)and Transwell chamber methods were used to determine the expression level of miR-221,the expression levels of inflammatory factors,cell viability,cell proliferation and migration ability,Western blot was used to determine the expression levels of EMT-related proteins[E-cadherin,N-cadherin,Vimentin,fibronectin(FN)]and PI3K/AKT pathway related proteins.Results:Cell viability increased in LPS+10 group(P<0.05),so LPS+10 group was selected for follow-up experiment.The results of miR-221 level showed that miR-221 mimics group was higher than mimics NC group(P<0.05),miR-221 inhibitor group was lower than inhibitor NC group(P<0.05).Transfection of miR-221mimics group and miR-221 inhibitor group was successful.Compared with control group,cell proliferation rate and E-cadherin protein level in LPS group were decreased(P<0.05).The expression level of miR-221,cell migration number,IL-6 and TNF-α levels,and the protein levels of p-PI3K,p-AKT,N-cadherin,FN and Vimentin were increased(P<0.05).Compared with LPS group,LPS+10 group significantly reversed the changes of the above indexes(P<0.05).Compared with LPS+10 group,10+miR-221 mimics group reduced the above effect of baicalin in LPS-induced cells(P<0.05).However,miR-221 inhibitor of 10+miR-221 inhibitor group enhanced the above effect of baicalin in LPS-induced cells(P<0.05).Conclusion:Baicalin can inhibit the effects of LPS-induced myocyte H9C2 migration,inflammation and fibrosis and promote their proliferation by down-regulating the expression of miR-221,and its mechanism may be related to the inhibi-tion of PI3K/AKT signaling pathway.

Objective To analyze the current status of anti-bacterial activity of carbapenem-resistant Klebsiella pneumoniae and Escherichia coli clinically isolated from hospitalized patients,detect their related resistance genes,and provide reference for the clinical treatment of carbapenem resistant Enterobacteria(CRE)infections and the rational use of antibiotics.Methods A total of 400 non-repetitive isolates of Klebsiella pneumoniae and Escherichia coli isolated from clinical specimens of Punan Branch of Renji Hospital,Shanghai Jiao Tong University School of Medicine from January 2022 to December were collected.The minimum inhibitory concentrations of these strains against commonly used antibiotics were determined by the broth microdilution method.The carbapenemase and related resistance genes of CRE were detected by drug resistance phenotype testing and PCR.Results Among the 400 strains,51 strains were identified as CRE,accounting for 12.75%.Among these,49 strains produced carbapenemases,with 41 strains(80.39%)being CR Klebsiella pneumoniae and 10 strains(19.61%)being CR Escherichia coli.Among the CRE strains,34 strains(66.67%)carried blaKPC,13 strains(25.49%)carried blaNDM,and 2 strains(3.92%)carried blaOXA-48.Conclusion Compared with other commonly used antibiotics,colistin and tigecycline exhibited good in vitro antibacterial activity against carbapenemase-producing Klebsiella pneumoniae and Escherichia coli.In addition,there was good concordance between drug resistance phenotype testing and genotyping.Clinical microbiology laboratories could continuously monitor the drug resistance phenotype and genotype of CRE and develop appropriate treatment plans based on actual conditions.

Molecular typing of leukemia is the basis of risk assessment and treatment options. NUTM1 gene (15q14) rearrangement is a novel molecular type of acute B lymphoblastic leukemia (B-ALL), which is mainly found in children (≥1 year old) and infants (< 1 year old). The number of patients is slightly more in children than infants. However, in infantile ALL, NUTM1 rearrangement is the second most common molecular abnormality. These children respond well to conventional chemotherapy regimens and with a good prognosis. The number of leukemia patients with NUTM1 gene rearrangement is still small, and there is no relevant study or case report in China. NUT protein encoded by NUTM1 gene is a chromatin regulator, which is related to histone acetylation regulation and chromatin remodeling. This article aims to introduce the clinicopathological features, detection methods, possible tumorigenic mechanisms and therapeutic prospects of leukemia with NUTM1 gene rearrangement, to increase the understanding of this type of leukemia and provide reference for the precise molecular subtyping and treatment.