Macrophages are innate immune cells connected with the development of inflammation. Retinoic acid has previously been proved to have anti-inflammatory and anti-arthritic properties. However, the exact mechanism through which retinoic acid modulates arthritis remains unclear. This study aimed to investigate whether retinoic acid ameliorates rheumatoid arthritis by modulating macrophage polarization. This study used retinoic acid to treat mice with adjuvant arthritis and evaluated anti-inflammatory effects by arthritis score, thermal nociceptive sensitization test, histopathologic examination and immunofluorescence assays. In addition, its specific anti-arthritic mechanism was investigated by flow cytometry, cell transfection and inflammatory signaling pathway assays in RAW264.7 macrophages in vitro. Retinoic acid significantly relieved joint pain and attenuated inflammatory cell infiltration in mice. Furthermore, this treatment modulated peritoneal macrophage polarization, increased levels of arginase 1, as well as decreased inducible nitric oxide synthase expression. In vitro, we verified that retinoic acid promotes macrophage transition from the M1 to M2 type by upregulating mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression and inhibiting P38, JNK and ERK phosphorylation in lipopolysaccharide-stimulated RAW264.7 cells. Notably, the therapeutic effects of retinoic acid were inhibited by MKP-1 knockdown. Retinoic acid exerts a significant therapeutic effect on adjuvant arthritis in mice by regulating macrophage polarization through the MKP-1/MAPK pathway, and play an important role in the treatment of rheumatic diseases.

Objective To design an intelligent monitoring platform for adverse drug reactions(ADRs)to solve the problems of the traditional ADR monitoring mode.Methods The ADR intelligent monitoring platform was designed based on artificial intelligence and big data technologies,which was developed with Browser/Server(B/S)architecture,C#programming language and.NET development tool.There were five functional modules involved in the platform for ADR knowledge base,monitoring rule setting,intelligent monitoring,report management and statistical analysis.Results The platform realized the full-process management of ADR intelligent monitoring,reporting,review and statistical analysis,which enhanced the ADR report in quantity,quality and timeliness.Conclusion The platform contributes to improving the monitoring of ADR and patient medication safety.[Chinese Medical Equipment Journal,2025,46(9):33-38]

Objective:To evaluate the relationship between transverse sinus stenosis (TSS) and cerebral blood flow in normal adults based on four-dimensional flow (4D Flow) MRI.Methods:The study was a cross-sectional study. Totally 81 normal volunteers who underwent magnetic resonance venography (MRV) and 4D Flow MRI were prospectively enrolled at Beijing Friendship Hospital, Capital Medical University from January 2020 to December 2022. Based on MRV evaluation of transverse sinus dysplasia, the volunteers were divided into a dysplasia group (26 cases) and a non-dysplasia group (55 cases); The area of the stenosis and the normal transverse sinus at the distal end were measured. The degree of TSS and the bilateral average transverse sinus stenosis (BA-TSS) were calculated. TSS was determined using TSS levels of 1/3, 1/2, and 2/3 as thresholds, and was divided into three groups: no TSS group, unilateral TSS group, and bilateral TSS group, with 28, 39, and 14 cases, 37, 37, and 7 cases, and 43, 36, and 2 cases, respectively. Based on 4D Flow MRI, the blood flow of the internal carotid artery, vertebral artery, superior sagittal sinus, straight sinus, and transverse sinus distal and proximal ends were measured. The cerebral blood flow (bilateral internal carotid artery blood flow+bilateral vertebral artery blood flow), venous sinus return blood flow 1 (superior sagittal sinus blood flow+straight sinus blood flow), return blood flow 2 (sum of bilateral transverse sinus distal end blood flow), return blood flow 3 (sum of bilateral transverse sinus proximal end blood flow), and the ratio of return blood flow to cerebral blood flow were calculated. Independent sample t-test was used to compare the differences between the group with and without transverse sinus dysplasia; Single factor analysis of variance was used to compare the differences between the TSS free group, unilateral TSS group, and bilateral TSS group. Based on single factor linear regression, the relationships between BA-TSS and blood flow parameters were analyzed.Results:There was no statistically significant difference in various blood flow parameters between the group with and without transverse sinus dysplasia (all P>0.05). When using 1/3, 1/2, and 2/3 as thresholds, there was no statistically significant difference in various blood flow parameters between the non TSS group, unilateral TSS group, and bilateral TSS group (all P>0.05). BA-TSS was linearly positively correlated with cerebral blood flow (β=0.986, 95% CI 0.108-1.865, P=0.028), but not linearly correlated with return blood flow 1, 2, and 3 (all P>0.05). The degree of BA-TSS was linearly negatively correlated with return blood flow 1/cerebral blood flow (β=-0.001, 95% CI -0.002-0, P=0.009) and return blood flow 2/cerebral blood flow (β=-0.001, 95% CI -0.002-0, P=0.018), but not with return blood flow 3/cerebral blood flow ( P=0.076). Conclusion:The BA-TSS degree in normal adults is positively correlated with cerebral blood inflow and negatively correlated with the proportion of venous sinus outflow.

Macrophages are innate immune cells connected with the development of inflammation. Retinoic acid has previously been proved to have anti-inflammatory and anti-arthritic properties. However, the exact mechanism through which retinoic acid modulates arthritis remains unclear. This study aimed to investigate whether retinoic acid ameliorates rheumatoid arthritis by modulating macrophage polarization. This study used retinoic acid to treat mice with adjuvant arthritis and evaluated anti-inflammatory effects by arthritis score, thermal nociceptive sensitization test, histopathologic examination and immunofluorescence assays. In addition, its specific anti-arthritic mechanism was investigated by flow cytometry, cell transfection and inflammatory signaling pathway assays in RAW264.7 macrophages in vitro. Retinoic acid significantly relieved joint pain and attenuated inflammatory cell infiltration in mice. Furthermore, this treatment modulated peritoneal macrophage polarization, increased levels of arginase 1, as well as decreased inducible nitric oxide synthase expression. In vitro, we verified that retinoic acid promotes macrophage transition from the M1 to M2 type by upregulating mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression and inhibiting P38, JNK and ERK phosphorylation in lipopolysaccharide-stimulated RAW264.7 cells. Notably, the therapeutic effects of retinoic acid were inhibited by MKP-1 knockdown. Retinoic acid exerts a significant therapeutic effect on adjuvant arthritis in mice by regulating macrophage polarization through the MKP-1/MAPK pathway, and play an important role in the treatment of rheumatic diseases.

Macrophages are innate immune cells connected with the development of inflammation. Retinoic acid has previously been proved to have anti-inflammatory and anti-arthritic properties. However, the exact mechanism through which retinoic acid modulates arthritis remains unclear. This study aimed to investigate whether retinoic acid ameliorates rheumatoid arthritis by modulating macrophage polarization. This study used retinoic acid to treat mice with adjuvant arthritis and evaluated anti-inflammatory effects by arthritis score, thermal nociceptive sensitization test, histopathologic examination and immunofluorescence assays. In addition, its specific anti-arthritic mechanism was investigated by flow cytometry, cell transfection and inflammatory signaling pathway assays in RAW264.7 macrophages in vitro. Retinoic acid significantly relieved joint pain and attenuated inflammatory cell infiltration in mice. Furthermore, this treatment modulated peritoneal macrophage polarization, increased levels of arginase 1, as well as decreased inducible nitric oxide synthase expression. In vitro, we verified that retinoic acid promotes macrophage transition from the M1 to M2 type by upregulating mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression and inhibiting P38, JNK and ERK phosphorylation in lipopolysaccharide-stimulated RAW264.7 cells. Notably, the therapeutic effects of retinoic acid were inhibited by MKP-1 knockdown. Retinoic acid exerts a significant therapeutic effect on adjuvant arthritis in mice by regulating macrophage polarization through the MKP-1/MAPK pathway, and play an important role in the treatment of rheumatic diseases.

Macrophages are innate immune cells connected with the development of inflammation. Retinoic acid has previously been proved to have anti-inflammatory and anti-arthritic properties. However, the exact mechanism through which retinoic acid modulates arthritis remains unclear. This study aimed to investigate whether retinoic acid ameliorates rheumatoid arthritis by modulating macrophage polarization. This study used retinoic acid to treat mice with adjuvant arthritis and evaluated anti-inflammatory effects by arthritis score, thermal nociceptive sensitization test, histopathologic examination and immunofluorescence assays. In addition, its specific anti-arthritic mechanism was investigated by flow cytometry, cell transfection and inflammatory signaling pathway assays in RAW264.7 macrophages in vitro. Retinoic acid significantly relieved joint pain and attenuated inflammatory cell infiltration in mice. Furthermore, this treatment modulated peritoneal macrophage polarization, increased levels of arginase 1, as well as decreased inducible nitric oxide synthase expression. In vitro, we verified that retinoic acid promotes macrophage transition from the M1 to M2 type by upregulating mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression and inhibiting P38, JNK and ERK phosphorylation in lipopolysaccharide-stimulated RAW264.7 cells. Notably, the therapeutic effects of retinoic acid were inhibited by MKP-1 knockdown. Retinoic acid exerts a significant therapeutic effect on adjuvant arthritis in mice by regulating macrophage polarization through the MKP-1/MAPK pathway, and play an important role in the treatment of rheumatic diseases.

Salvia miltiorrhiza is a perennial herb of the genus Salvia(Lamiaceae). As one of the earliest medicinal plants to undergo molecular biology research, it has gradually become a model plant for molecular biology of medicinal plants. With the gradual analysis of the genome of S. miltiorrhiza and the biosynthetic pathways of its main active components tanshinone and salvianolic acids, the transcriptional regulation mediated by transcription factors and related regulatory proteins has gradually become a new research focus. Due to the lack of scientific and unified naming of transcription factors and different research indexes in different literature, this paper systematically sorted out the transcription factors in different literature with the genomes of DSS3 from selfing for three generations and bh2-7 from selfing for six generations as reference. In total, 73 transcription factors and related regulatory proteins belonging to 13 gene families were identified. The effects of overexpression or gene silencing experiments on tanshinone and salvianolic acids were also analyzed. This study unified the identified transcription factors, which laid a foundation for further constructing the regulatory networks of secondary metabolites and insect or stress resistance and improving the quality of medicinal materials by using global transcriptional regulation engineering.
Salvia miltiorrhiza/chemistry* ; Plant Proteins/metabolism* ; Gene Expression Regulation, Plant ; Transcription Factors/metabolism* ; Abietanes/metabolism*

Objective To explore the relationship among sleep quality, fatigue and work-related musculoskeletal disorders (WMSDs) in firefighters, and to examine the mediating effect of fatigue between sleep quality and the risk of WMSDs. Methods A total of 271 firefighters from three prefecture-level cities in Jiangsu Province were selected as the study subjects by a convenient sampling method. The Chinese Musculoskeletal Disorders Questionnaire, Pittsburgh Sleep Quality Index (PSQI), and Fatigue Scale-14 were used to assess WMSDs, sleep quality and fatigue status among the study subjects. The effect of sleep quality and fatigue on WMSDs was analyzed, as well as the mediating role of fatigue between sleep quality and the risk of WMSDs. Results The annual prevalence of WMSDs among the firefighters was 68.6%. The firefighters who had poor and very poor sleep quality accounted for 36.2% and 7.7%, respectively. There were 88.6% of firefighters reported fatigue. The total scores of PSQI and fatigue of firefighters in WMSDs group were higher than those in non-WMSDs group (all P<0.01). Binary logistic regression analysis showed that the higher the total score of PSQI, the worse the sleep quality, and the higher the risk of WMSDs in firefighters (all P<0.01). The higher the total score of fatigue, the higher the risk of WMSDs (P<0.01), and the risk of WMSDs in the fatigue group was higher than that in the non-fatigue group among the firefighters (P<0.01). The direct effect of sleep quality on WMSDs in firefighters was 0.028 [95% confidence interval (CI): 0.012-0.050, P<0.01], and its indirect effect on WMSDs mediated by fatigue was 0.027 (95%CI: 0.018-0.040, P<0.01). Fatigue played a mediating role in sleep quality and WMSDs, with the mediating ratio of 0.491 (95%CI: 0.304-0.740, P<0.01). Conclusion Poor sleep quality and fatigue are related to an increased risk of WMSDs in firefighters in a dose-response manner. Fatigue plays a mediating role between sleep quality and the risk of WMSDs.

Macrophages are innate immune cells connected with the development of inflammation. Retinoic acid has previously been proved to have anti-inflammatory and anti-arthritic properties. However, the exact mechanism through which retinoic acid modulates arthritis remains unclear. This study aimed to investigate whether retinoic acid ameliorates rheumatoid arthritis by modulating macrophage polarization. This study used retinoic acid to treat mice with adjuvant arthritis and evaluated anti-inflammatory effects by arthritis score, thermal nociceptive sensitization test, histopathologic examination and immunofluorescence assays. In addition, its specific anti-arthritic mechanism was investigated by flow cytometry, cell transfection and inflammatory signaling pathway assays in RAW264.7 macrophages in vitro. Retinoic acid significantly relieved joint pain and attenuated inflammatory cell infiltration in mice. Furthermore, this treatment modulated peritoneal macrophage polarization, increased levels of arginase 1, as well as decreased inducible nitric oxide synthase expression. In vitro, we verified that retinoic acid promotes macrophage transition from the M1 to M2 type by upregulating mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression and inhibiting P38, JNK and ERK phosphorylation in lipopolysaccharide-stimulated RAW264.7 cells. Notably, the therapeutic effects of retinoic acid were inhibited by MKP-1 knockdown. Retinoic acid exerts a significant therapeutic effect on adjuvant arthritis in mice by regulating macrophage polarization through the MKP-1/MAPK pathway, and play an important role in the treatment of rheumatic diseases.