Purpose To explore the expression level of let-7b-5p in glioma and its effects and potential mecha-nisms on U251 cell growth.Methods The expression of let-7b-5p in glioma was detected using qRT-PCR.Data from the CGGA database were analyzed to examine the relationship between the let-7b-5p expression levels,WHO grade and overall survival rates of glioma patients.Transient transfection was used to downregulate the expression of let-7b-5p and IGF1R in U251 cells.The role and potential mechanism of let-7b-5p in the U251 cell were evaluated using qRT-PCR,CCK8 assays,clone formation assays,Western blotting,and double luciferase reporter assays.Results The expres-sion of let-7b-5p in glioma cells(A172:3.64±0.64,V251:4.56±0.52,U87-MG:3.31±0.50)and tissues(2.18±0.22)was significantly higher than that in astrocytes(HMC3:1.00±0.21,P＜0.05 or P＜0.01)and nor-mal brain tissues(1.01±0.19,P＜0.05).Let-7b-5p expression was negatively correlated with WHO grades but pos-itively correlated with survival rates in primary and recurrent glioma patients(P＜0.000 1 and P=0.028,respective-ly).Knockdown of let-7b-5p in U251 cells significantly promoted the growth of glioma cells(CCK8:knockdown group 126.00±12.09 vs miR-NC group 90.93±5.13,P＜0.05)and activated PI3K/AKT signal pathway.Suppressing IGF1R expression in U251 cells reversed the effects of let-7b-5p knockdown on glioma cell growth[CCK8:let-7b-5p knockdown+IGF1R knockdown group(92.08±6.14)vs let-7b-5p knockdown+sh-NC group(116.67.08±8.50)]and PI3K/AKT signal pathway activation.Conclusion Let-7b-5p functions as a tumor suppressor gene in glioma.It may regulate glioma cell growth by targeting IGF1R and modulating PI3K/AKT signal pathway.

Clinical pharmacist training is an important way to strengthen the clinical pharmacist team's construction and improve their pharmaceutical service capabilities and levels.The Pharmacy Administration and Pharmacy Practice in Healthcare Institutions-Part 4-8-1:Pharmacy Administration-Pharmacy Training Management-Clinical Pharmacist Training was based on the relevant requirements of the current clinical pharmacist training system of the Chinese Hospital Association,and formulated by sor-ting out relevant materials,such as standards,policies and regulations,technical specifications,literature,the current situation of clinical pharmacist training in China,and expert opinions.A total of 15 key elements of clinical pharmacist training were selected and divided into three aspects(base management,training process and assessment,and the quality management,evaluation and improvement).This article mainly introduced the construction method and content of the clinical pharmacist training standard,to deepen the understanding of the standard for relevant units and to promote the implementation of the standard.

AIM:To explore the effect and mecha-nism of ethanol extract of Angelica sinensis(Oliv.)Diels(EEA)on cell proliferation and apoptosis in B16-F10 melanoma cells.METHODS:Cell viability was analyzed by MTT method.Cell proliferation was detected by colony formation assay.The invert-ed microscope was used to observe the changes of cell growth confluence and morphology.Hoechst 33342 staining was used to detect cell apoptosis.Flow cytometry(FCM)was used to detect cell cycle and apoptosis.Transmission electron microscopy(TEM)was used to observe the changes of cell mi-tochondrial structure.Western blot was used to de-tect the expression levels of cell cycle,apoptosis,mitochondrial biogenesis,and mitochondrial dy-namics-related proteins.RESULTS:Compared with the blank control group,the cell viability of B16-F10 melanoma cells was reduced after EEA(10-400μg/mL)treatment for 24 h and 48 h,respectively(P＜0.05,P＜0.01).The decreased cell growth conflu-ence,morphological changes such as shrinkage,rounding,and reduction in the volume,and apop-totic morphologic changes such as chromatin con-densation were observed after EEA(100 μg/mL and 200 μg/mL)treatment for 24 h.The number of cell clones was decreased after EEA(10-200 μg/mL)treatment for 14 d(P＜0.01).The morphology of mitochondria became more round and shorter,and the inner mitochondrial matrices were either damaged or absent after 200 μg/mL EEA treatment for 24 h.The ratio of cells in G0/G1 phase and the early apoptosis rate of cells were higher than those of the blank control group(P＜0.01)after EEA(20-200 μg/mL)treatment for 24 h.Western blot re-sults showed that compared with the blank control group,the protein expression levels of cleaved cas-pase-9,Bax,DRP1,and FIS1 were up-regulated(P＜0.05,P＜0.01),and the protein expression levels of cyclin D1,cyclin E,CDK2,CDK4,Bcl-2,Bad,Bcl-XL,SIRT1,PGC-1α,NRF1,TFAM,MFN2,and OPA1 were down-regulated(P＜0.05,P＜0.01).CONCLUSION:EEA has an inhibitory effect on the proliferation of B16-F10 melanoma cells,which may be related to the induction of G1/S cell cycle arrest and mito-chondrial apoptotic pathway,and the disruption of mitochondrial biogenesis and mitochondrial dy-namics.

Purpose To explore the expression level of let-7b-5p in glioma and its effects and potential mecha-nisms on U251 cell growth.Methods The expression of let-7b-5p in glioma was detected using qRT-PCR.Data from the CGGA database were analyzed to examine the relationship between the let-7b-5p expression levels,WHO grade and overall survival rates of glioma patients.Transient transfection was used to downregulate the expression of let-7b-5p and IGF1R in U251 cells.The role and potential mechanism of let-7b-5p in the U251 cell were evaluated using qRT-PCR,CCK8 assays,clone formation assays,Western blotting,and double luciferase reporter assays.Results The expres-sion of let-7b-5p in glioma cells(A172:3.64±0.64,V251:4.56±0.52,U87-MG:3.31±0.50)and tissues(2.18±0.22)was significantly higher than that in astrocytes(HMC3:1.00±0.21,P＜0.05 or P＜0.01)and nor-mal brain tissues(1.01±0.19,P＜0.05).Let-7b-5p expression was negatively correlated with WHO grades but pos-itively correlated with survival rates in primary and recurrent glioma patients(P＜0.000 1 and P=0.028,respective-ly).Knockdown of let-7b-5p in U251 cells significantly promoted the growth of glioma cells(CCK8:knockdown group 126.00±12.09 vs miR-NC group 90.93±5.13,P＜0.05)and activated PI3K/AKT signal pathway.Suppressing IGF1R expression in U251 cells reversed the effects of let-7b-5p knockdown on glioma cell growth[CCK8:let-7b-5p knockdown+IGF1R knockdown group(92.08±6.14)vs let-7b-5p knockdown+sh-NC group(116.67.08±8.50)]and PI3K/AKT signal pathway activation.Conclusion Let-7b-5p functions as a tumor suppressor gene in glioma.It may regulate glioma cell growth by targeting IGF1R and modulating PI3K/AKT signal pathway.

Clinical pharmacist training is an important way to strengthen the clinical pharmacist team's construction and improve their pharmaceutical service capabilities and levels.The Pharmacy Administration and Pharmacy Practice in Healthcare Institutions-Part 4-8-1:Pharmacy Administration-Pharmacy Training Management-Clinical Pharmacist Training was based on the relevant requirements of the current clinical pharmacist training system of the Chinese Hospital Association,and formulated by sor-ting out relevant materials,such as standards,policies and regulations,technical specifications,literature,the current situation of clinical pharmacist training in China,and expert opinions.A total of 15 key elements of clinical pharmacist training were selected and divided into three aspects(base management,training process and assessment,and the quality management,evaluation and improvement).This article mainly introduced the construction method and content of the clinical pharmacist training standard,to deepen the understanding of the standard for relevant units and to promote the implementation of the standard.

Intracranial atherosclerotic stenosis (ICAS) is one of the most common causes of ischemic stroke. Stenting is a treatment option for symptomatic ICAS, but it also has problems such as procedure-related complications and in-stent restenosis. This article reviews the application of stenting, particularly different stent systems, in patients with symptomatic ICAS.

Astrocytes and microglia engage in extensive and complex communication and mutual effect, which referrs to microglia-astrocyte crosstalk. Recent studies have highlighted that this crosstalk plays a pivotal role in neurodegenerative diseases, exerting either protective or detrimental effects. This review briefly introduces the molecular mechanism of microglia-astrocyte crosstalk and its research progress in Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis, and Parkinson's disease, aiming to provide new research directions and therapeutic targets for clinical improvement of neurodegenerative diseases from perspective of microglia-astrocyte crosstalk.

AIM:To explore the effect and mecha-nism of ethanol extract of Angelica sinensis(Oliv.)Diels(EEA)on cell proliferation and apoptosis in B16-F10 melanoma cells.METHODS:Cell viability was analyzed by MTT method.Cell proliferation was detected by colony formation assay.The invert-ed microscope was used to observe the changes of cell growth confluence and morphology.Hoechst 33342 staining was used to detect cell apoptosis.Flow cytometry(FCM)was used to detect cell cycle and apoptosis.Transmission electron microscopy(TEM)was used to observe the changes of cell mi-tochondrial structure.Western blot was used to de-tect the expression levels of cell cycle,apoptosis,mitochondrial biogenesis,and mitochondrial dy-namics-related proteins.RESULTS:Compared with the blank control group,the cell viability of B16-F10 melanoma cells was reduced after EEA(10-400μg/mL)treatment for 24 h and 48 h,respectively(P＜0.05,P＜0.01).The decreased cell growth conflu-ence,morphological changes such as shrinkage,rounding,and reduction in the volume,and apop-totic morphologic changes such as chromatin con-densation were observed after EEA(100 μg/mL and 200 μg/mL)treatment for 24 h.The number of cell clones was decreased after EEA(10-200 μg/mL)treatment for 14 d(P＜0.01).The morphology of mitochondria became more round and shorter,and the inner mitochondrial matrices were either damaged or absent after 200 μg/mL EEA treatment for 24 h.The ratio of cells in G0/G1 phase and the early apoptosis rate of cells were higher than those of the blank control group(P＜0.01)after EEA(20-200 μg/mL)treatment for 24 h.Western blot re-sults showed that compared with the blank control group,the protein expression levels of cleaved cas-pase-9,Bax,DRP1,and FIS1 were up-regulated(P＜0.05,P＜0.01),and the protein expression levels of cyclin D1,cyclin E,CDK2,CDK4,Bcl-2,Bad,Bcl-XL,SIRT1,PGC-1α,NRF1,TFAM,MFN2,and OPA1 were down-regulated(P＜0.05,P＜0.01).CONCLUSION:EEA has an inhibitory effect on the proliferation of B16-F10 melanoma cells,which may be related to the induction of G1/S cell cycle arrest and mito-chondrial apoptotic pathway,and the disruption of mitochondrial biogenesis and mitochondrial dy-namics.

Astrocytes and microglia engage in extensive and complex communication and mutual effect, which referrs to microglia-astrocyte crosstalk. Recent studies have highlighted that this crosstalk plays a pivotal role in neurodegenerative diseases, exerting either protective or detrimental effects. This review briefly introduces the molecular mechanism of microglia-astrocyte crosstalk and its research progress in Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis, and Parkinson's disease, aiming to provide new research directions and therapeutic targets for clinical improvement of neurodegenerative diseases from perspective of microglia-astrocyte crosstalk.

Astrocytes(AS)are the most abundant glial cells in the central nervous system and are involved in many physiological and pathological processes in the nervous system.Alterations in their phenotype are particularly important for the health of the CNS.Epigenetic mechanisms,including DNA methylation,histone modification,non-coding RNA regulation,and chromatin remodeling,are closely linked to alterations in AS proliferation,differentiation,inflammation,and other phenotypic features,but how these mechanisms function needs to be explored and summarized.By reviewing the recent advances in the role of epigenetic mechanisms in AS under various physiological and pathological states,we aim to provide new ideas for the understanding and treatment of related diseases.