[Objective]To systematically review the records of Centipeda minima in historical herbal literature,investigating its botanical origins,medicinal history,etc.,to clarify its name,origin,medicinal properties and therapeutic effects,providing references for clinical applications.[Methods]A systematic review of historical herbal literature was conducted,combined with modern herbal texts such as the Chinese Pharmacopoeia and Chinese Materia Medica.Based on the textual records and illustrations from various herbal texts,a systematic investigation of Centipeda minima was carried out.[Results]Centipeda minima was first recorded in the Tang Dynasty's Diet Therapy Materia Medica under the name"Shihusui",and was later named for the"Centipeda minima"characteristic.There was confusion about its origins in the herbal medicines of the past dynasties.During the Ming and Qing Dynasties,the characteristics of its Compositae plant(Centipe daminima)were gradually clarified.The drawings in the Qing Dynasty's An Illustrated Book of Plants was highly consistent with modern authentic products.The controversy over nature and taste had shifted from the early"cold nature"to the consensus that"warm and non-toxic",and modern pharmacopoeia follows this theory.The efficacy has expanded from"clearing nasal orifices and spitting wind and phlegm"in the Tang Dynasty to"dispelling sores and swelling,treating hemorrhoids and removing eye fog"in the Ming and Qing Dynasties.In modern times,it focused on the three major functions of"dissipating wind and cold,clearing nasal orifices and relieving cough".[Conclusion]Clarifying the development context of the name evolution,origin controversy,property and toxicity,taste toxicity and efficacy indication of Centipeda minima can provide historical basis and theoretical support for its modern clinical application and in-depth research.Future research should focus on multi-disciplinary integration and further explore its scientific connotation and clinical value.

Background and Objectives: Heart failure is a potentially fatal event caused by diverse cardiovascular diseases, leading to high morbidity and mortality. Histone deacetylase (HDAC) inhibitors positively influence cardiac hypertrophy, fibrosis, hypertension, myocardial infarction, and heart failure, causing some side effects. We aimed to investigate the effect of the novel HDAC inhibitor YAK577 on the heart failure mouse model and its underlying mechanism. Methods: New hydroxamic acid YAK577 was prepared via methyl-2,3-diphenylpropanoate synthesis using carboxylic acids. We used a micro-osmotic pump, including isoproterenol (ISO; 80 mg/kg/day), to induce a heart failure with reduced ejection fraction. Cardiac hypertrophy was assessed by heart weight to body weight ratio and cross-sectional area.The left ventricular (LV) function was assessed by echocardiography. Fibrosis was evaluated using picrosirius red staining. Overexpression and knockdown experiments were performed to investigate the association between HDAC8 and matrix metalloproteinase 12 (MMP12). Results: YAK577 treatment restored ISO-induced reduction in LV fractional shortening and ejection fraction (n=9–11). YAK577 significantly downregulated cardiac hypertrophy marker genes (natriuretic peptide B, NPPB, and myosin heavy chain 7, MYH7) and cardiomyocyte size in vitro but not in vivo. YAK577 ameliorated cardiac fibrosis and fibrosis-related genes in vivo and in vitro. Additionally, YAK577 reduced elevated HDAC8 and MMP12 mRNA and protein expressions in ISO-infused mice, H9c2 cells, and rat neonatal cardiomyocytes.HDAC8 overexpression stimulated MMP12 and NPPB mRNA levels, while HDAC8 knockdown downregulated these genes. Conclusions YAK577 acts as a novel heart failure drug through the HDAC8/MMP12 pathway.

Objective: To analyze the trends in new diagnosis rates of HIV/AIDS cases in Huzhou City, Zhejiang Province from 2009 to 2023, so as to provide the basis for improving HIV/AIDS prevention and control strategies. Methods: Data of newly reported HIV/AIDS cases in Huzhou City from 2009 to 2023 were collected through the Chinese Disease Prevention and Control Information System. The new diagnosis rate was calculated as the ratio of newly reported HIV/AIDS cases within one year to the permanent resident population during the same period. The gender, age, and regional distribution characteristics of new diagnosis rates of HIV/AIDS cases were described. The trends were analyzed using average annual percent change (AAPC) and annual percent change (APC). Results: A total of 2 088 new HIV/AIDS cases were reported in Huzhou City from 2009 to 2023, with an average annual new diagnosis rate of 4.53/105. The new diagnosis rates showed an overall increasing trend from 2009 to 2023 (AAPC=12.745%, P<0.05), with rapid growth during 2009 to 2015 (APC=32.734%, P<0.05) but no significant trend during 2015 to 2023 (P>0.05). The average annual new diagnosis rate was significantly higher in males than in females (7.54/100 000 vs. 1.40/100 000, P<0.05). Male new diagnosis rate trend closely mirrored the overall population pattern, while females showed a continuous upward trend without clear inflection point (AAPC=12.575%, P<0.05). Age-specific analysis revealed average annual new diagnosis rates of 2.75/100 000, 6.16/100 000 and 3.83/100 000 for AIDS/HIV cases aged <25, 25-<50 and ≥50 years, respectively. The cases aged <25 years showed no significant trend (P>0.05), while the cases aged 25-<50 and ≥50 years followed patterns similar to the overall population. The average annual new diagnosis rates of HIV/AIDS cases in Wuxing District, Nanxun District, Deqing County, Changxing County and Anji County were 6.54/100 000, 3.43/100 000, 3.45/100 000, 3.56/100 000 and 4.94/100 000, respectively, showing overall upward trends (AAPC=9.672%, 27.599%, 11.800%, 18.896% and 10.254%, all P<0.05). Conclusions The new diagnosis rate of HIV/AIDS cases showed an overall upward trend in Huzhou City from 2009 to 2023. Cases are mainly concentrated among males, people aged 25-<50 years and Wuxing District, making them key targets for HIV/AIDS prevention and control.

Objective:To analyze the epidemiological and clinical characteristics of respiratory pathogens in China.Methods:This study was a cross-sectional study, which encompassed 19 core units of the clinical pathogen network and established a three-tiered clinical pathogen surveillance system. Thirty respiratory samples were collected every two weeks from various units from January to December 2024, and the clinical and pathogen diagnostic information were gathered. A total of 11 864 samples were tested using this system. The tier-1 clinical pathogen surveillance system covered influenza A virus (Flu-A), influenza B virus (Flu-B), respiratory syncytial virus (RSV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The tier-2 clinical pathogen surveillance system focused on 18 key respiratory pathogens. The tier-3 clinical pathogen surveillance system further clarified whether any emerging infectious diseases had occurred.Results:The tier-1 clinical pathogen surveillance system showed Flu-A predominated in December, Flu-B predominated in January, SARS-CoV-2 peaked in March and August, whereas RSV circulated sporadically throughout the year. Geographic trends were broadly consistent across the seven major regions, although Flu-A detection in December was notably higher in Northeast China (48.1%(111/231)) and East China (36.2%(148/409)), and RSV detection was concentrated in the Northwest and South China from January to March. Data from the tier-2 clinical pathogen surveillance system indicated that Streptococcus pneumoniae, Mycoplasma pneumoniae, rhinovirus, and adenovirus were detected year-round, of these, Streptococcus pneumoniae and rhinovirus showed elevated positive detection rates from August to September, while adenovirus peaked in January. Legionella pneumophila was not detected throughout the year, and other pathogens fluctuated throughout the year without a consistent pattern. The predominant etiologic agents of pediatric pneumonia were Mycoplasma pneumoniae (35.0%(105/300)), rhinovirus (25.7%(77/300)), and adenovirus (17.3%(52/300)), whereas adult pneumonia was mainly caused by Streptococcus pneumoniae (10.5%(29/277)), Staphylococcus aureus (6.9%(19/277)), Mycoplasma pneumoniae (6.9%(19/277)), and Flu-A (6.1%(17/277)). The tier-3 clinical pathogen surveillance system did not identify any emerging respiratory pathogens. Conclusion:Respiratory pathogens in China in 2024 exhibit distinct temporal and spatial distribution patterns and vary among different populations.

Background and Objectives: Heart failure is a potentially fatal event caused by diverse cardiovascular diseases, leading to high morbidity and mortality. Histone deacetylase (HDAC) inhibitors positively influence cardiac hypertrophy, fibrosis, hypertension, myocardial infarction, and heart failure, causing some side effects. We aimed to investigate the effect of the novel HDAC inhibitor YAK577 on the heart failure mouse model and its underlying mechanism. Methods: New hydroxamic acid YAK577 was prepared via methyl-2,3-diphenylpropanoate synthesis using carboxylic acids. We used a micro-osmotic pump, including isoproterenol (ISO; 80 mg/kg/day), to induce a heart failure with reduced ejection fraction. Cardiac hypertrophy was assessed by heart weight to body weight ratio and cross-sectional area.The left ventricular (LV) function was assessed by echocardiography. Fibrosis was evaluated using picrosirius red staining. Overexpression and knockdown experiments were performed to investigate the association between HDAC8 and matrix metalloproteinase 12 (MMP12). Results: YAK577 treatment restored ISO-induced reduction in LV fractional shortening and ejection fraction (n=9–11). YAK577 significantly downregulated cardiac hypertrophy marker genes (natriuretic peptide B, NPPB, and myosin heavy chain 7, MYH7) and cardiomyocyte size in vitro but not in vivo. YAK577 ameliorated cardiac fibrosis and fibrosis-related genes in vivo and in vitro. Additionally, YAK577 reduced elevated HDAC8 and MMP12 mRNA and protein expressions in ISO-infused mice, H9c2 cells, and rat neonatal cardiomyocytes.HDAC8 overexpression stimulated MMP12 and NPPB mRNA levels, while HDAC8 knockdown downregulated these genes. Conclusions YAK577 acts as a novel heart failure drug through the HDAC8/MMP12 pathway.

Background and Objectives: Heart failure is a potentially fatal event caused by diverse cardiovascular diseases, leading to high morbidity and mortality. Histone deacetylase (HDAC) inhibitors positively influence cardiac hypertrophy, fibrosis, hypertension, myocardial infarction, and heart failure, causing some side effects. We aimed to investigate the effect of the novel HDAC inhibitor YAK577 on the heart failure mouse model and its underlying mechanism. Methods: New hydroxamic acid YAK577 was prepared via methyl-2,3-diphenylpropanoate synthesis using carboxylic acids. We used a micro-osmotic pump, including isoproterenol (ISO; 80 mg/kg/day), to induce a heart failure with reduced ejection fraction. Cardiac hypertrophy was assessed by heart weight to body weight ratio and cross-sectional area.The left ventricular (LV) function was assessed by echocardiography. Fibrosis was evaluated using picrosirius red staining. Overexpression and knockdown experiments were performed to investigate the association between HDAC8 and matrix metalloproteinase 12 (MMP12). Results: YAK577 treatment restored ISO-induced reduction in LV fractional shortening and ejection fraction (n=9–11). YAK577 significantly downregulated cardiac hypertrophy marker genes (natriuretic peptide B, NPPB, and myosin heavy chain 7, MYH7) and cardiomyocyte size in vitro but not in vivo. YAK577 ameliorated cardiac fibrosis and fibrosis-related genes in vivo and in vitro. Additionally, YAK577 reduced elevated HDAC8 and MMP12 mRNA and protein expressions in ISO-infused mice, H9c2 cells, and rat neonatal cardiomyocytes.HDAC8 overexpression stimulated MMP12 and NPPB mRNA levels, while HDAC8 knockdown downregulated these genes. Conclusions YAK577 acts as a novel heart failure drug through the HDAC8/MMP12 pathway.

Background and Objectives: Heart failure is a potentially fatal event caused by diverse cardiovascular diseases, leading to high morbidity and mortality. Histone deacetylase (HDAC) inhibitors positively influence cardiac hypertrophy, fibrosis, hypertension, myocardial infarction, and heart failure, causing some side effects. We aimed to investigate the effect of the novel HDAC inhibitor YAK577 on the heart failure mouse model and its underlying mechanism. Methods: New hydroxamic acid YAK577 was prepared via methyl-2,3-diphenylpropanoate synthesis using carboxylic acids. We used a micro-osmotic pump, including isoproterenol (ISO; 80 mg/kg/day), to induce a heart failure with reduced ejection fraction. Cardiac hypertrophy was assessed by heart weight to body weight ratio and cross-sectional area.The left ventricular (LV) function was assessed by echocardiography. Fibrosis was evaluated using picrosirius red staining. Overexpression and knockdown experiments were performed to investigate the association between HDAC8 and matrix metalloproteinase 12 (MMP12). Results: YAK577 treatment restored ISO-induced reduction in LV fractional shortening and ejection fraction (n=9–11). YAK577 significantly downregulated cardiac hypertrophy marker genes (natriuretic peptide B, NPPB, and myosin heavy chain 7, MYH7) and cardiomyocyte size in vitro but not in vivo. YAK577 ameliorated cardiac fibrosis and fibrosis-related genes in vivo and in vitro. Additionally, YAK577 reduced elevated HDAC8 and MMP12 mRNA and protein expressions in ISO-infused mice, H9c2 cells, and rat neonatal cardiomyocytes.HDAC8 overexpression stimulated MMP12 and NPPB mRNA levels, while HDAC8 knockdown downregulated these genes. Conclusions YAK577 acts as a novel heart failure drug through the HDAC8/MMP12 pathway.

[Objective]To systematically review the records of Centipeda minima in historical herbal literature,investigating its botanical origins,medicinal history,etc.,to clarify its name,origin,medicinal properties and therapeutic effects,providing references for clinical applications.[Methods]A systematic review of historical herbal literature was conducted,combined with modern herbal texts such as the Chinese Pharmacopoeia and Chinese Materia Medica.Based on the textual records and illustrations from various herbal texts,a systematic investigation of Centipeda minima was carried out.[Results]Centipeda minima was first recorded in the Tang Dynasty's Diet Therapy Materia Medica under the name"Shihusui",and was later named for the"Centipeda minima"characteristic.There was confusion about its origins in the herbal medicines of the past dynasties.During the Ming and Qing Dynasties,the characteristics of its Compositae plant(Centipe daminima)were gradually clarified.The drawings in the Qing Dynasty's An Illustrated Book of Plants was highly consistent with modern authentic products.The controversy over nature and taste had shifted from the early"cold nature"to the consensus that"warm and non-toxic",and modern pharmacopoeia follows this theory.The efficacy has expanded from"clearing nasal orifices and spitting wind and phlegm"in the Tang Dynasty to"dispelling sores and swelling,treating hemorrhoids and removing eye fog"in the Ming and Qing Dynasties.In modern times,it focused on the three major functions of"dissipating wind and cold,clearing nasal orifices and relieving cough".[Conclusion]Clarifying the development context of the name evolution,origin controversy,property and toxicity,taste toxicity and efficacy indication of Centipeda minima can provide historical basis and theoretical support for its modern clinical application and in-depth research.Future research should focus on multi-disciplinary integration and further explore its scientific connotation and clinical value.

Objective:To identify the relevant factors for the first-course remission of acute myeloid leukemia (AML) and to develop a predictive model as well as assess its predictive capability.Methods:Clinical data of 749 patients newly diagnosed with AML admitted to the Department of Hematology, the First Affiliated Hospital, Zhejiang University, School of Medicine from January 1, 2019, to April 30, 2023, were collected and randomly divided into training and validation sets. Multivariate logistic regression analysis was conducted to determine variables associated with complete remission in the first course of induction therapy, and a predictive model was established based on these variables. The receiver operating characteristic (ROC) curve of the predictive model was plotted, and the area under the curve (AUC) was calculated.Results:The indicators predicting the first remission course included peripheral blood white blood cell count during onset, CBF::MYH11 fusion gene, CEBPA bZIP region mutation, myelodysplastic syndrome-related gene mutation, and induction chemotherapy regimen selection as independent factors for the first remission course. The model’s area under the training and validation curves was 0.738 (95% CI: 0.696-0.780) and 0.726 (95% CI: 0.650-0.801), respectively. The Hosmer-Lemeshow test results yielded P-values of 0.993 and 0.335, respectively. Conclusion:In this study, the developed model demonstrates a strong predictive capability for the efficacy of the first course of patients with AML, providing valuable guidance to clinicians in assessing patient prognosis and selecting appropriate treatment strategies.

Obesity usually exacerbates the immunosuppressive tumor microenvironment (ITME), hindering CD8⁺ T cell infiltration and function, which further represents a significant barrier to the efficacy of immunotherapy. Herein, a multifunctional liposomal system (CR-Lip) for encapsulating celastrol (CEL) was utilized to remodel obesity-related ITME and improve cancer immunotherapy, wherein Ginsenoside Rg3 (Rg3) was detected interspersed in the phospholipid bilayer and its glycosyl exposed on the surface of the liposome. CR-Lip had a relatively uniform size (116.5 nm), facilitating favorable tumor tissue accumulation through the interaction between Rg3 and glucose transporter 1 overexpressed in obese tumor cells. Upon reaching the tumor region, CR-Lip was found to induce the immunogenic cell death (ICD) of HFD tumor cells. Notably, the level of PHD3 in HFD tumor cells was effectively boosted by CR-Lip to effectively block metabolic reprogramming and increase the availability of major free fatty acids fuel sources. In vivo, experiments studies revealed that the easy-obtained nano platform stimulated enhanced the production of various cytokines in tumor tissues, DC maturation, CD8⁺ T-cell infiltration, and synergistic anticancer therapeutic potency with aPD-1 (tumor inhibition rate = 82.1%) towards obesity-related melanoma. Consequently, this study presented an efficacious approach to tumor immunotherapy in obese mice by encompassing tumor eradication, inducing ICD, and reprogramming metabolism. Furthermore, it offered a unique insight into a valuable attempt at the immunotherapy of obesity-associated related tumors.