ObjectiveTo systematically elucidate the accumulation characteristics of secondary metabolites in the stems and leaves of Panax ginseng with different stem colors. MethodsUltra-high-performance liquid chromatography-triple quadrupole-tandem mass spectrometry （UHPLC-QqQ-MS） was employed to determine the of 22 ginsenosides in the stems and leaves of 2- to 5-year-old P. ginseng plants with green and purple stems. Principal component analysis （PCA）， orthogonal partial least squares-discriminant analysis （OPLS-DA）， and one-way analysis of variance （ANOVA） were performed to explore the distribution patterns of ginsenosides from three dimensions： tissue distribution， growth duration， and stem color. Results① Tissue distribution： Leaves served as the primary organ for ginsenoside accumulation， exhibiting significantly higher total ginsenoside content than stems， which indicated distinct tissue-specific distribution of ginsenosides. ② Growth duration： Ginsenoside levels in stems generally peaked in the 2-year-old plants before stabilizing， while those in leaves displayed a declining-rebounding pattern， indicating that the 2-year-old plants （harvest stage） was a critical time point for the resurgence of leaf ginsenosides. ③ Stem color： A stage-specific correlation was observed between stem color and ginsenoside accumulation. In stems， the early-growth stage （2-year-old） of purple-stemmed plants exhibited higher content of specific ginsenosides （e.g.， ginsenoside Rk₁ and notoginsenoside R₁）， which may be associated with its stronger early-stage stress resistance. In leaves， the content of core ginsenosides （e.g.， ginsenosides Re and Rd） in 5-year-old plants with green stems showed a surpassing trend， demonstrating higher potential of resource development. ConclusionThe accumulation of ginsenosides in P. ginseng stems and leaves is multidimensionally regulated by tissue type， growth duration， and stem color phenotypes. Purple-stemmed plants exhibit early-stage specific ginsenoside accumulation and stress resistance potential， whereas green-stemmed plants are more advantageous for core leaf ginsenoside development at the harvest stage. The findings confirm that aboveground stem color can serve as a biomarker for directed breeding and efficient resource utilization of P. ginseng.

ObjectiveTo systematically elucidate the accumulation characteristics of secondary metabolites in the stems and leaves of Panax ginseng with different stem colors. MethodsUltra-high-performance liquid chromatography-triple quadrupole-tandem mass spectrometry （UHPLC-QqQ-MS） was employed to determine the of 22 ginsenosides in the stems and leaves of 2- to 5-year-old P. ginseng plants with green and purple stems. Principal component analysis （PCA）， orthogonal partial least squares-discriminant analysis （OPLS-DA）， and one-way analysis of variance （ANOVA） were performed to explore the distribution patterns of ginsenosides from three dimensions： tissue distribution， growth duration， and stem color. Results① Tissue distribution： Leaves served as the primary organ for ginsenoside accumulation， exhibiting significantly higher total ginsenoside content than stems， which indicated distinct tissue-specific distribution of ginsenosides. ② Growth duration： Ginsenoside levels in stems generally peaked in the 2-year-old plants before stabilizing， while those in leaves displayed a declining-rebounding pattern， indicating that the 2-year-old plants （harvest stage） was a critical time point for the resurgence of leaf ginsenosides. ③ Stem color： A stage-specific correlation was observed between stem color and ginsenoside accumulation. In stems， the early-growth stage （2-year-old） of purple-stemmed plants exhibited higher content of specific ginsenosides （e.g.， ginsenoside Rk₁ and notoginsenoside R₁）， which may be associated with its stronger early-stage stress resistance. In leaves， the content of core ginsenosides （e.g.， ginsenosides Re and Rd） in 5-year-old plants with green stems showed a surpassing trend， demonstrating higher potential of resource development. ConclusionThe accumulation of ginsenosides in P. ginseng stems and leaves is multidimensionally regulated by tissue type， growth duration， and stem color phenotypes. Purple-stemmed plants exhibit early-stage specific ginsenoside accumulation and stress resistance potential， whereas green-stemmed plants are more advantageous for core leaf ginsenoside development at the harvest stage. The findings confirm that aboveground stem color can serve as a biomarker for directed breeding and efficient resource utilization of P. ginseng.

Objective:To investigate the effects and underlying mechanisms of the hypoxia-inducible factor-1α (HIF-1α) agonist Roxadustat in alleviating pulmonary ischemia-reperfusion injury (IRI) in mice.Method:This study consisted of both in vivo and in vitro experiments. Thirty-six male C57/BL6 mice (6~8 weeks old) were used. In the animal experiments, 20 mice underwent left pulmonary artery ligation to establish the IRI model and were divided into reperfusion groups of 0, 1, 2, or 4 hours (IR-0/1/2/4 h, n=4 each), with a sham group ( n=4) as control. Temporal and spatial changes in pulmonary HIF-1α expression were analyzed. Another 16 mice were randomized into four groups: sham ( n=4), I/R+vehicle (DMSO, n=4), and I/R+Roxadustat treatment at 25 mg/kg or 50 mg/kg (I/R+ROX-LD, I/R+ROX-HD, n=4 each). Roxadustat or DMSO was administered intraperitoneally once daily for 5 days before surgery. Lung injury, inflammation, and endothelial apoptosis were subsequently assessed. In the cell experiments, human umbilical vein endothelial cell (HUVEC) was subjected to hypoxia-reoxygenation (H/R) to determine the time course of HIF-1α expression. Cells pretreated with Roxadustat (25 μmol) were then exposed to H/R, and HIF-1α expression and apoptosis were analyzed. To verify the role of HIF-1α, siRNA knockdown of HIF-1α mRNA was performed before Roxadustat pretreatment and H/R exposure. Result:In vivo, pulmonary HIF-1α mRNA expression increased progressively after reperfusion, while protein expression peaked early and subsequently declined ( P<0.05). Immunofluorescence staining revealed HIF-1α predominantly localized to pulmonary endothelial cells following I/R. Compared with the I/R+DMSO group, Roxadustat (both doses) upregulated HIF-1α expression in lung tissue. In vitro, HIF-1α mRNA expression increased continuously after H/R, while protein levels first rose and then decreased ( P<0.05). Roxadustat pretreatment upregulated Bcl-2 and downregulated Bax and cleaved caspase-3 compared with the H/R group ( P<0.05). HIF-1α knockdown reversed these effects, resulting in decreased Bcl-2 and increased Bax and cleaved caspase-3 expression relative to the Roxadustat-treated group. Conclusion:The HIF-1α agonist Roxadustat inhibits vascular endothelial apoptosis, alleviates endothelial injury, reduces inflammatory cell infiltration in lung tissue, and lowers inflammatory responses in mice with pulmonary ischemia-reperfusion injury.

Immunogenic cell death(ICD)is a form of cell death that can activate the immune system,especially in the treatment of cancer.ICD can enhance the recognition of tumors by the immune system and the release of damage associated molecular patterns(DAMPs),to achieve tumor cell death.Oncolytic viruses(OVs)can selectively infect and kill tumor cells without damaging normal cells.OVs are type Ⅱ ICD inducers that induce ICD in tumor cells by targeting the endoplasmic reticulum.Here,we review the characteristics of ICD and the mechanism of ICD induction by OVs.We also review the latest clinical progress involving ICD and discuss future treatment strategies for tumors.

Objective:To investigate the effects and underlying mechanisms of the hypoxia-inducible factor-1α (HIF-1α) agonist Roxadustat in alleviating pulmonary ischemia-reperfusion injury (IRI) in mice.Method:This study consisted of both in vivo and in vitro experiments. Thirty-six male C57/BL6 mice (6~8 weeks old) were used. In the animal experiments, 20 mice underwent left pulmonary artery ligation to establish the IRI model and were divided into reperfusion groups of 0, 1, 2, or 4 hours (IR-0/1/2/4 h, n=4 each), with a sham group ( n=4) as control. Temporal and spatial changes in pulmonary HIF-1α expression were analyzed. Another 16 mice were randomized into four groups: sham ( n=4), I/R+vehicle (DMSO, n=4), and I/R+Roxadustat treatment at 25 mg/kg or 50 mg/kg (I/R+ROX-LD, I/R+ROX-HD, n=4 each). Roxadustat or DMSO was administered intraperitoneally once daily for 5 days before surgery. Lung injury, inflammation, and endothelial apoptosis were subsequently assessed. In the cell experiments, human umbilical vein endothelial cell (HUVEC) was subjected to hypoxia-reoxygenation (H/R) to determine the time course of HIF-1α expression. Cells pretreated with Roxadustat (25 μmol) were then exposed to H/R, and HIF-1α expression and apoptosis were analyzed. To verify the role of HIF-1α, siRNA knockdown of HIF-1α mRNA was performed before Roxadustat pretreatment and H/R exposure. Result:In vivo, pulmonary HIF-1α mRNA expression increased progressively after reperfusion, while protein expression peaked early and subsequently declined ( P<0.05). Immunofluorescence staining revealed HIF-1α predominantly localized to pulmonary endothelial cells following I/R. Compared with the I/R+DMSO group, Roxadustat (both doses) upregulated HIF-1α expression in lung tissue. In vitro, HIF-1α mRNA expression increased continuously after H/R, while protein levels first rose and then decreased ( P<0.05). Roxadustat pretreatment upregulated Bcl-2 and downregulated Bax and cleaved caspase-3 compared with the H/R group ( P<0.05). HIF-1α knockdown reversed these effects, resulting in decreased Bcl-2 and increased Bax and cleaved caspase-3 expression relative to the Roxadustat-treated group. Conclusion:The HIF-1α agonist Roxadustat inhibits vascular endothelial apoptosis, alleviates endothelial injury, reduces inflammatory cell infiltration in lung tissue, and lowers inflammatory responses in mice with pulmonary ischemia-reperfusion injury.

Objective:To develop a treatment-related quality of life scale for Chinese patients with multiple myeloma (MM) and to test its reliability and validity.Methods:The initial scale was constructed through a literature search, Delphi expert correspondence, and cognitive testing. This study conducted a preliminary survey of 379 patients with MM and a formal survey of 865 patients from the hematology departments of 155 hospitals nationwide from February 2024 to March 2024. The final scale was obtained after conducting item analysis and reliability and validity tests on the initial scale.Results:The constructed scale contains 36 items covering six domains: physiological, psychological, social, treatment side effects, general health, and others. In the preliminary survey, the Cronbach’s alpha coefficient of each item ranged from 0.597 to 0.939, and the test-retest reliability was 0.747 ( P<0.001). Exploratory factor analysis extracted eight common factors with a cumulative variance contribution of 60.058%. In the formal survey, the Cronbach’s alpha coefficient of each item ranged from 0.484 to 0.930, and the test-retest reliability was 0.835 ( P<0.001). Confirmatory factor analysis revealed a comparative fit index of 0.750, a root-mean-square error of approximation of 0.090, and a root-mean-square residual of 0.067. Conclusion:The treatment-related quality of life scale for Chinese patients with MM designed in this study exhibited good reliability and validity, reflecting the impact of treatment on the quality of life of patients. This scale can provide a reference to clinicians for assessing the disease status of patients.

Transmissible gastroenteritis(TGE)is a highly contagious gastrointestinal disease of pigs caused by the transmissible gastroenteritis virus(TGEV).It results in severe diarrhea and high mortality in suckling piglets.As no specific treatment available,vaccination is considered to be one of the most cost-effective measures for preventing and controlling TGE.However,the immune protection provided by vaccines based on traditional TGEV strains is becoming inadequate due to the continuous emergence of strong and new strains of the virus,which poses a serious threat to the pig industry's health and development.Therefore,the development of new vaccines with im-proved efficiency and broad-spectrum coverage is urgently needed.This paper aims to summarize the pathogenic structural characteristics of TGEV,discuss the latest advancements in TGEV vac-cine research and development,and propose future strategies for the development of highly effec-tive TGEV vaccines.The findings of this paper can serve as a valuable reference for effectively pre-venting and controlling TGE in clinical practice.

Objective:To develop a treatment-related quality of life scale for Chinese patients with multiple myeloma (MM) and to test its reliability and validity.Methods:The initial scale was constructed through a literature search, Delphi expert correspondence, and cognitive testing. This study conducted a preliminary survey of 379 patients with MM and a formal survey of 865 patients from the hematology departments of 155 hospitals nationwide from February 2024 to March 2024. The final scale was obtained after conducting item analysis and reliability and validity tests on the initial scale.Results:The constructed scale contains 36 items covering six domains: physiological, psychological, social, treatment side effects, general health, and others. In the preliminary survey, the Cronbach’s alpha coefficient of each item ranged from 0.597 to 0.939, and the test-retest reliability was 0.747 ( P<0.001). Exploratory factor analysis extracted eight common factors with a cumulative variance contribution of 60.058%. In the formal survey, the Cronbach’s alpha coefficient of each item ranged from 0.484 to 0.930, and the test-retest reliability was 0.835 ( P<0.001). Confirmatory factor analysis revealed a comparative fit index of 0.750, a root-mean-square error of approximation of 0.090, and a root-mean-square residual of 0.067. Conclusion:The treatment-related quality of life scale for Chinese patients with MM designed in this study exhibited good reliability and validity, reflecting the impact of treatment on the quality of life of patients. This scale can provide a reference to clinicians for assessing the disease status of patients.

OBJECTIVES: To investigate the role of activating transcription factor 3 (ATF3) in atherosclerotic plaques for regulating inflammatory responses during atherosclerosis (AS) progression. METHODS: Human coronary artery specimens from autopsy cases were examined for ATF3 protein expression and localization using immunofluorescence staining and Western blotting. Apolipoprotein E-deficient (ApoE^-/-) mouse models of AS induced by high-fat diet (HFD) feeding for 12 weeks were subjected to tail vein injection of adeno-associated virus serotype 9 (AAV9) to knock down ATF3 expression. After an additional 5 weeks of HFD feeding, the mice were euthanized for analyzing structural changes of the aortic plaques, and the expression levels of ATF3, inflammatory factors (CD45, CD68, IL-1β, and TNF-α), and NF-κB pathway proteins (P-IKKα/β and P-NF-κB p65) were detected. In the cell experiment, THP-1-derived foam cells were transfected with an ATF3-overexpressing plasmid or an ATF3-specific siRNA to validate the relationship between ATF3 and NF‑κB signaling. RESULTS: In human atherosclerotic plaques, ATF3 expression was significantly elevated and partially co-localized with CD68. ATF3 knockout in ApoE^-/- mice significantly increased aortic plaque volume, upregulated the inflammatory factors, enhanced phosphorylation of the NF‑κB pathway proteins, and increased the expressions of VCAM1, MMP9, and MMP2 in the plaques. In THP-1-derived foam cells, ATF3 silencing caused activation of the NF‑κB pathway, while ATF3 overexpression suppressed the activity of the NF-κB pathway. CONCLUSIONS AS promotes ATF3 expression, and ATF3 deficiency exacerbates AS progression by enhancing plaque inflammation via activating the NF-κB pathway, suggesting the potential of ATF3 as a therapeutic target for AS.
Animals ; Activating Transcription Factor 3/metabolism* ; Signal Transduction ; NF-kappa B/metabolism* ; Humans ; Mice ; Plaque, Atherosclerotic/metabolism* ; Inflammation/metabolism* ; Apolipoproteins E ; Atherosclerosis/metabolism* ; Diet, High-Fat

To summarize the clinical experience of Professor LIU Shangyi in treating pruritus vulvae. It is believed that women have the physiological characteristics of liver and kidney as the root， and their pubic area is easily attacked by wind-dampness pathogenic qi， so the core mechanism of pruritus vulvae is proposed as wind-dampness accumulation and deficiency of liver and kidney. The core treatment method is to dispel wind-dampness and nourish the liver and kidneys， and modify the Danggui Decoction （当归饮子） to form a self-prescribed Yinyang Formula （阴痒方） as the basic prescription to treat pruritus vulvaen.