OBJECTIVE To clarify the current development status of clinical pharmacist training bases and the pharmacist workforce in China， and to provide evidence for standardizing base construction and promoting the high-quality development of hospital pharmacy. METHODS Questionnaires were distributed to all clinical pharmacist training bases for urgently-needed health professionals and clinical pharmacist training bases under the Chinese Hospital Association that had been approved by the end of 2023 to collect data including base profiles and pharmacist staffing conditions. Expert teams carried out field investigations to verify the collected data. Descriptive statistical analyses were conducted on the quantity， type and regional distribution of training bases， and the influencing factors of pharmacist staffing in the bases were analyzed. RESULTS Field surveys were completed covering 297 training bases across 31 provincial-level administrative regions. Among the base hospitals， 87.88% were Grade A tertiary general hospitals， and 65.32% were located in provincial capitals. The eastern region had the largest number of bases （136， accounting for 45.79%）， followed by the western region （79， 26.60%）. Great disparities existed among provinces in terms of base quantity and hospital scale. The median proportion of pharmaceutical technical personnel in base hospitals was 4.05%， and the median number of clinical pharmacists per 100 hospital beds was 0.53. Both indicators reached the highest in the eastern region （0.57， 4.43%） and the lowest in the northeastern region （0.45， 3.01%）. A total of 3 627 full-time clinical pharmacists were employed in all surveyed bases， among whom 83.68% held clinical pharmacist training certificates， 35.43% possessed senior professional titles， and 78.19% had postgraduate or higher educational background. The total annual training capacity of the surveyed bases was 4 291 trainees， with obvious differences in annual training capacity across regions and provinces. Training specialties covered 19 specialized disciplines plus one general discipline， and no province could deliver training for all 20 specialties simultaneously. Multivariate Logistic regression analysis showed that geographic region exerte d a significant impact on the proportion of pharmaceutical technical personnel （≥4%） （ P ＜0.05）， while the approval time of training bases and hospital scale had significant effects on the number of clinical pharmacists per 100 beds （≥0.6） （ P ＜0.05）. CONCLUSIONS China’s clinical pharmacist training system has basically matured and taken initial shape. The distribution of clinical pharmacist training resources is generally consistent with regional population and economic development levels. However， the allocation of pharmaceutical staff and clinical pharmacists has not yet met national standards and clinical service demands.

OBJECTIVE To clarify the current development status of clinical pharmacist training bases and the pharmacist workforce in China， and to provide evidence for standardizing base construction and promoting the high-quality development of hospital pharmacy. METHODS Questionnaires were distributed to all clinical pharmacist training bases for urgently-needed health professionals and clinical pharmacist training bases under the Chinese Hospital Association that had been approved by the end of 2023 to collect data including base profiles and pharmacist staffing conditions. Expert teams carried out field investigations to verify the collected data. Descriptive statistical analyses were conducted on the quantity， type and regional distribution of training bases， and the influencing factors of pharmacist staffing in the bases were analyzed. RESULTS Field surveys were completed covering 297 training bases across 31 provincial-level administrative regions. Among the base hospitals， 87.88% were Grade A tertiary general hospitals， and 65.32% were located in provincial capitals. The eastern region had the largest number of bases （136， accounting for 45.79%）， followed by the western region （79， 26.60%）. Great disparities existed among provinces in terms of base quantity and hospital scale. The median proportion of pharmaceutical technical personnel in base hospitals was 4.05%， and the median number of clinical pharmacists per 100 hospital beds was 0.53. Both indicators reached the highest in the eastern region （0.57， 4.43%） and the lowest in the northeastern region （0.45， 3.01%）. A total of 3 627 full-time clinical pharmacists were employed in all surveyed bases， among whom 83.68% held clinical pharmacist training certificates， 35.43% possessed senior professional titles， and 78.19% had postgraduate or higher educational background. The total annual training capacity of the surveyed bases was 4 291 trainees， with obvious differences in annual training capacity across regions and provinces. Training specialties covered 19 specialized disciplines plus one general discipline， and no province could deliver training for all 20 specialties simultaneously. Multivariate Logistic regression analysis showed that geographic region exerte d a significant impact on the proportion of pharmaceutical technical personnel （≥4%） （ P ＜0.05）， while the approval time of training bases and hospital scale had significant effects on the number of clinical pharmacists per 100 beds （≥0.6） （ P ＜0.05）. CONCLUSIONS China’s clinical pharmacist training system has basically matured and taken initial shape. The distribution of clinical pharmacist training resources is generally consistent with regional population and economic development levels. However， the allocation of pharmaceutical staff and clinical pharmacists has not yet met national standards and clinical service demands.

OBJECTIVE To investigate the current status of quality management in clinical pharmacist training bases in China， and to provide references for the standardized development and improvement of these bases. METHODS A combined approach of questionnaire survey and on-site investigation was adopted， targeting the healthcare highly sought-after talent （clinical pharmacist） training bases in 31 provinces of China as well as the clinical pharmacist training bases affiliated with the Chinese Hospital Association. A training quality management evaluation index system consisting of 25 tertiary indicators was established. Investigations were conducted from two dimensions： structural quality of training and quality management of training processes. Data were statistically analyzed using descriptive statistical methods. RESULTS On-site investigations were completed for 297 clinical pharmacist training bases across the 31 provinces， among which 284 were affiliated with the Chinese Hospital Association and 271 were healthcare highly sought-after talent （clinical pharmacist） training bases. In terms of structural quality， the core indicator compliance rate for hospital-level training systems exceeded 80%， the rate of special fund utilization for designated purposes reached 80.13%， and the overall compliance rate for software and hardware facilities surpassed 88%. A total of 1 348 preceptors were employed across the training bases， among whom those with senior professional titles and full-time specialist clinical pharmacists as lead preceptors accounted for 62.91% and 94.36%， respectively. Regarding process quality， the compliance rate for “establishment of clinical practice teaching groups in accordance with regulations during clinical department rotations” was 85.19%， and 79.80% and 76.09% of the bases were found to implement strict confidentiality in theoretical examinations and meet the required scale of assessment cases， respectively. However， formal documents of corresponding training management regulations were formulated in only 57.91% of the bases， and the completeness and standardization rate of training manual completion was merely 47.47%. In addition， considerable disparities in quality management levels were observed among provinces， with issues in training process quality being particularly prominent. CONCLUSIONS The management system， hardware facilities， and preceptor staffing of clinical pharmacist training bases in China are relatively well-established， yet notable variations in quality management exist among training bases across different provinces.

ObjectiveTo investigate the ameliorative effect of paeonol on acute alcohol-induced hepatic inflammation in mice via the regulation of the short-chain fatty acids （SCFAs）-specific receptor GPR43/mitogen-activated protein kinase （MAPK） signaling pathway. MethodsC57BL/6 mice were randomly divided into five groups： blank control group， model group， low-dose paeonol group （120 mg·kg^-1）， high-dose paeonol group （480 mg·kg^-1）， and silybin group （36.8 mg·kg^-1）. A mouse model of alcohol-induced liver disease （ALD） was established by ad libitum administration of a Lieber-DeCarli alcohol liquid diet. Serum lipid levels， liver function， inflammatory cytokines， and oxidative stress markers were measured. Liver hematoxylin-eosin （HE） staining and Oil Red O staining were performed to validate successful modeling. Western blot analysis was used to assess the expression levels of zonula occludens-1 （ZO-1）， Claudin-1， and proteins related to the GPR43/MAPK signaling pathway in the colonic tissue. Immunohistochemistry was employed to detect the protein expression of GPR43， ZO-1， and Claudin-1 in the colon. Then 16S rDNA sequencing was performed to analyze differences in intestinal flora between the model group and the high-dose paeonol group. Additionally， fecal microbiota transplantation （FMT） experiments were conducted to validate the regulatory effect of paeonol on ALD via modulation of intestinal flora. ResultsCompared with the blank control group， the model group showed significantly elevated serum lipid levels， oxidative stress， and inflammatory cytokine expression （P<0.01）. Liver histology revealed increased inflammatory infiltration and lipid droplet accumulation. Colonic mucosal injury and impaired intestinal barrier function were observed. Levels of MAPK pathway-related proteins in the colonic tissue were upregulated （P<0.01）， while GPR43， ZO-1， and Claudin-1 protein expression levels were significantly decreased （P<0.01）. The composition and abundance of the intestinal flora were markedly altered， with a reduced Bacteroidetes-to-Firmicutes ratio and decreased relative abundances of Eubacterium， Parabacteroides， Erysipelothrix， and Adlercreutzia， alongside increased abundances of Clostridium butyricum， Enterococcus， and Helicobacter pylori in the model group. Compared with the model group， paeonol significantly reduced serum lipid levels， oxidative stress responses， and the expression of inflammatory cytokines in ALD mice （P<0.05， P<0.01）. It also attenuated hepatic lipid accumulation， restored intestinal barrier function， and repaired the structural integrity of liver and colonic tissues. The protein expression levels of ZO-1， Claudin-1， and GPR43 in the colonic tissue were significantly increased （P<0.05， P<0.01）， while those of MAPK pathway-related proteins were significantly decreased （P<0.05， P<0.01）. The intestinal flora dysbiosis was effectively alleviated， rendering its composition closer to that of normal mice. The efficacy of paeonol in modulating ALD was further confirmed by FMT experiments， supporting its mechanistic involvement in the SCFAs-GPR43/MAPK signaling pathway. ConclusionPaeonol exerts a protective effect against ALD in mice， which may be mediated through regulation of the SCFAs-GPR43/MAPK signaling pathway， thereby achieving anti-inflammatory effects and improving intestinal barrier function.

ObjectiveTo investigate the ameliorative effect of paeonol on acute alcohol-induced hepatic inflammation in mice via the regulation of the short-chain fatty acids （SCFAs）-specific receptor GPR43/mitogen-activated protein kinase （MAPK） signaling pathway. MethodsC57BL/6 mice were randomly divided into five groups： blank control group， model group， low-dose paeonol group （120 mg·kg^-1）， high-dose paeonol group （480 mg·kg^-1）， and silybin group （36.8 mg·kg^-1）. A mouse model of alcohol-induced liver disease （ALD） was established by ad libitum administration of a Lieber-DeCarli alcohol liquid diet. Serum lipid levels， liver function， inflammatory cytokines， and oxidative stress markers were measured. Liver hematoxylin-eosin （HE） staining and Oil Red O staining were performed to validate successful modeling. Western blot analysis was used to assess the expression levels of zonula occludens-1 （ZO-1）， Claudin-1， and proteins related to the GPR43/MAPK signaling pathway in the colonic tissue. Immunohistochemistry was employed to detect the protein expression of GPR43， ZO-1， and Claudin-1 in the colon. Then 16S rDNA sequencing was performed to analyze differences in intestinal flora between the model group and the high-dose paeonol group. Additionally， fecal microbiota transplantation （FMT） experiments were conducted to validate the regulatory effect of paeonol on ALD via modulation of intestinal flora. ResultsCompared with the blank control group， the model group showed significantly elevated serum lipid levels， oxidative stress， and inflammatory cytokine expression （P<0.01）. Liver histology revealed increased inflammatory infiltration and lipid droplet accumulation. Colonic mucosal injury and impaired intestinal barrier function were observed. Levels of MAPK pathway-related proteins in the colonic tissue were upregulated （P<0.01）， while GPR43， ZO-1， and Claudin-1 protein expression levels were significantly decreased （P<0.01）. The composition and abundance of the intestinal flora were markedly altered， with a reduced Bacteroidetes-to-Firmicutes ratio and decreased relative abundances of Eubacterium， Parabacteroides， Erysipelothrix， and Adlercreutzia， alongside increased abundances of Clostridium butyricum， Enterococcus， and Helicobacter pylori in the model group. Compared with the model group， paeonol significantly reduced serum lipid levels， oxidative stress responses， and the expression of inflammatory cytokines in ALD mice （P<0.05， P<0.01）. It also attenuated hepatic lipid accumulation， restored intestinal barrier function， and repaired the structural integrity of liver and colonic tissues. The protein expression levels of ZO-1， Claudin-1， and GPR43 in the colonic tissue were significantly increased （P<0.05， P<0.01）， while those of MAPK pathway-related proteins were significantly decreased （P<0.05， P<0.01）. The intestinal flora dysbiosis was effectively alleviated， rendering its composition closer to that of normal mice. The efficacy of paeonol in modulating ALD was further confirmed by FMT experiments， supporting its mechanistic involvement in the SCFAs-GPR43/MAPK signaling pathway. ConclusionPaeonol exerts a protective effect against ALD in mice， which may be mediated through regulation of the SCFAs-GPR43/MAPK signaling pathway， thereby achieving anti-inflammatory effects and improving intestinal barrier function.

The writing of pharmacist-managed clinics documents （hereinafter referred to as “outpatient medication record”） is a necessary part of pharmacist-managed clinics service. Outpatient medication record is an important carrier to reflect the quality of pharmacist-managed clinics service. The Chinese Hospital Association Pharmaceutical Specialized Committee was entrusted by the Pharmaceutical Administration Department of the National Health Commission to lead the formulation of the Guidelines for the Pharmacist-managed Clinics Service and Document Writing and Usage （Reference） （hereinafter referred to as Guidelines） according to the compilation method of group standards and the technical route of “documentation combing→framework establishment→draft writing→opinion collection→Guidelines formation”. The Guidelines standardizes the basic requirements of pharmacist-managed clinics record management and the basic content of record， and provides a general template and two specialized templates including pregnant and lactating pharmacist-managed clinics record template and cough and asthma pharmacist-managed clinics record template， which provides a reference for medical institutions to write pharmacist-managed clinics record. This paper introduces the formulation process of Guidelines and analyzes the key contents of Guidelines， which is helpful for the application practice of Guidelines and further improves the quality of pharmacist-managed clinics work.

Objective To establish a model of indirectly induced respiratory tract infection with influenza A subtypes H1N1 and H3N2 in animals,to screen influenza virus hosts,and to provide theoretical support for the clinical control of influenza viruses.Methods Fifty BALB/c mice and 50 Hartley guinea pigs were randomly divided into five groups(10 animals/group for each species):normal control group,virus infects 1 group,virus infects 2 group,close transmission 1 group,and close transmission 2 group.Mice and guinea pigs in virus infects 1 and 2 groups were administered influenza A(H1N1)and influenza A(H3N2)viruses via nasal drip.For both virus infects 1 and 2 groups,animals were housed together with those in the close transmission group at a 1∶1 ratio on the following day.On day 7,the lung function,viral titer and viral load of the nasal tissue,trachea,and lung tissue of each group were measured,and pathological changes of the trachea and lung tissue of animals in the close transmission group were evaluated.Results In mice,the viral titers and viral loads of nasal,tracheal,and lung tissues of virus infects 1 and 2 and the closely transmitted groups 1 and 2 were significantly higher(P＜0.01),pathological scores of the trachea and lung tissues were significantly higher(P＜0.01),and the FVC and FEV20 of virus infects l and 2 groups were significantly lower(P＜0.01)than those in the normal control group.The nasal tissue,trachea and lung tissues of guinea pigs in virus infects 1 and 2 groups and close transmission groups 1 and 2 showed significantly higher viral titers and viral loads(P＜0.01),significantly higher trachea and lung histopathological scores(P＜0.01),and significantly lower FVC and FEV200(P＜0.01)than those of the normal control group.Conclusions In this study,influenza A subtypes H1N1 and H3N2 were used to indirectly induce respiratory tract infections in mice and guinea pigs for analyses of animal lung function,respiratory viral titers,viral load,and pathology.The animal models of the indirect transmission of influenza viruses in the respiratory tract had certain limitations;for example,influenza viruses were transmitted less efficiently among mice than among guinea pigs.The guinea pig model was stable.These findings confirm that guinea pigs are suitable hosts for efficient virus replication and transmission.

Objective:To elucidate the mechanism by which Clostridium butyricum alleviates atopic dermatitis (AD) from three aspects: immune cells, gut microbiota, and the metabolites of gut microbiota, short-chain fatty acids (SCFAs), and provide a theoretical reference for clinical probiotic-assisted treatment of AD. Methods:A model of 2, 4-dinitrochlorobenzene (DNCB)-induced AD was established using BALB/c mice. Three groups including control group, AD group, and Clostridium butyricum intervention group were set up with 20 mice in each group. The dermatitis score, scratching score, pathological conditions and mast cell infiltration at the lesion site, and the levels of cytokines related to Th1/Th2 and Th17/Treg as well as IgE levels in serum samples were analyzed. Gut microbiota was detected by 16S rRNA gene sequencing. The contents of SCFAs in mouse fecal samples were detected by gas chromatography-mass spectrometry. Spearman correlation analysis was performed to investigate the correlation between the cytokines related to Th1/Th2 and Th17/Treg, gut microbiota, and SCFAs. Comparisons between groups were performed using one-way analysis of variance with Turkey post hoc test correction. Results:Clostridium butyricum intervention down-regulated various inflammatory indexes and alleviated pathological changes in AD mice, elevated the levels of IFN-γ ( P<0.05) and IL-10 ( P<0.01), reduced the levels of IL-4, IL-17 and IgE ( P<0.01), and maintained the balance of Th1/Th2 ( P<0.01) and Th17/Treg ( P<0.001). Besides, the intervention improved intestinal dysbiosis by decreasing the abundance of conditionally pathogenic bacteria such as Prevotellaceae_ UCG-001 ( P<0.01) and increasing the abundance of beneficial bacteria such as Lachnospiraceae_ NK4A136_ group and norank_ f_ Oscillospiraceae ( P<0.05), and enhanced the production of SCFAs ( P<0.05). Correlation analysis showed that allergy-associated immune cytokines were strongly correlated with the composition of gut microbiota and the content of SCFAs. Conclusions:Clostridium butyricum may regulate the microbiota-SCFAs signaling response by inhibiting the colonization of harmful bacteria and increasing the abundance of beneficial bacteria. This, in turn, increases the level of SCFAs, decreases the number of pro-inflammatory cytokines, and maintains the balance of Th1/Th2 and Th17/Treg in the body. Therefore, Clostridium butyricum may alleviate allergic diseases.

Objective:To explore the intervention mechanism of Clostridium butyricum on asthma from the perspective of im-mune inflammation and pulmonary flora,and to provide a new scheme for the prevention and treatment of asthma.Methods:Mice were randomly divided into Clostridium butyricum(CM)group,asthma model group(Model)and normal control group(Control),with 16 mice in each group.The model group and CM group were sensitized by ovalbumin(OVA)and stimulated by continuous atomi-zation of 1%OVA solution to establish asthma mouse model,and the control group was replaced by normal saline.Mice in CM group were administrated with CM solution at 1×109 CFU/d.The total number of white blood cells in bronchoalveolar lavage fluid(BALF)was counted.Eosinophil number(EOS)was counted by Wright-Giemsa staining.The pathological changes of lung tissue were ob-served by HE staining and PAS staining.Serum levels of IL-4,IgE and IFN-γ were determined by ELISA.Mouse lung microflora was analyzed by 16S rRNA.Results:Compared with Model group,white blood cells and EOS inflammatory cells in CM group were signifi-cantly decreased(P<0.05),lung inflammatory cell infiltration and goblet cell proliferation were significantly reduced,serum IL-4 and IgE levels were significantly decreased(P<0.05),IFN-γ levels were significantly increased(P<0.05),and Th1/Th2 balance was maintained.The abundance of Proteobacteria and Escherichia-Shigella in the lung of mice were significantly decreased,and correlation analysis showed that the decrease of IL-4 and IgE levels were positively correlated with the increase of Escherichia-Shigella abundance(P<0.05,r>0.9).Conclusion:Clostridium butyricum intervention can change the composition of lung flora,regulate immune cells and cytokines,maintain Th1/Th2 balance,so as to reduce the OVA-induced pulmonary inflammation of allergic asthma.

Objective:To explore the intervention mechanism of Clostridium butyricum on asthma from the perspective of im-mune inflammation and pulmonary flora,and to provide a new scheme for the prevention and treatment of asthma.Methods:Mice were randomly divided into Clostridium butyricum(CM)group,asthma model group(Model)and normal control group(Control),with 16 mice in each group.The model group and CM group were sensitized by ovalbumin(OVA)and stimulated by continuous atomi-zation of 1%OVA solution to establish asthma mouse model,and the control group was replaced by normal saline.Mice in CM group were administrated with CM solution at 1×109 CFU/d.The total number of white blood cells in bronchoalveolar lavage fluid(BALF)was counted.Eosinophil number(EOS)was counted by Wright-Giemsa staining.The pathological changes of lung tissue were ob-served by HE staining and PAS staining.Serum levels of IL-4,IgE and IFN-γ were determined by ELISA.Mouse lung microflora was analyzed by 16S rRNA.Results:Compared with Model group,white blood cells and EOS inflammatory cells in CM group were signifi-cantly decreased(P<0.05),lung inflammatory cell infiltration and goblet cell proliferation were significantly reduced,serum IL-4 and IgE levels were significantly decreased(P<0.05),IFN-γ levels were significantly increased(P<0.05),and Th1/Th2 balance was maintained.The abundance of Proteobacteria and Escherichia-Shigella in the lung of mice were significantly decreased,and correlation analysis showed that the decrease of IL-4 and IgE levels were positively correlated with the increase of Escherichia-Shigella abundance(P<0.05,r>0.9).Conclusion:Clostridium butyricum intervention can change the composition of lung flora,regulate immune cells and cytokines,maintain Th1/Th2 balance,so as to reduce the OVA-induced pulmonary inflammation of allergic asthma.