1.Chloroplast genome structure of Artemisia vestita and its significance for species identification
Jin-ren LI ; Na-jia SUOLANG ; Zhi-li ZHAO ; Dol-kar MIGMAR ; ALA Kelsang GYAB ; Liang-hong NI
Chinese Traditional Patent Medicine 2025;47(6):1901-1909
AIM To sequence the chloroplast genome of Artemisia vestita Wall.ex Bess.METHODS Based on ethnobotanical surveys,sample collection and original plant identification were carried out.The chloroplast genome was sequenced using the Illumina platform,followed by assembly and annotation.A comprehensive comparative analysis was conducted with six Artemisia species.The maximum likelihood(ML)phylogenetic tree was constructed based on the chloroplast genome sequences of A.vestita and 32 other Asteraceae species,with Leptocodon hirsutus D.Y.Hong of Campanulaceae as outgroup.RESULTS The chloroplast genome of A.vestita was 151 204 bp in length,including a small single-copy region of 18 331 bp,a large single-copy region of 82 949 bp,and inverted repeat regions of 24 962 bp,with a total GC content of 37.45%.134 genes were annotated,including 89 protein-coding genes,8 ribosomal RNA genes,and 37 transfer RNA genes.A total of 67 SSRs and 44 LSRs were detected in the chloroplast genome.Comparative analysis with closely related species of Artemisia revealed 3 highly variable genes(clpP,rpl36,ycf1)and 6 highly variable intergenic regions(trnK-UUU-matK,rps18-rpl20,rpl36-infA,rpl14-rpl16,rpl16-rpl3 and trnL-UAG-ccsA),which could serve as candidate DNA barcodes for Artemisia identification.Phylogenetic analysis showed that Artemisia formed a highly supportive monophyletic group,with A.vestita and A.gmelinii Web.ex Stechm.being closely related.CONCLUSION This study may provide fundamental data for phylogenetic analysis of Artemisia,taxonomic identification and DNA barcoding construction of Tibetan herb.
2.Chloroplast genome structure of Artemisia vestita and its significance for species identification
Jin-ren LI ; Na-jia SUOLANG ; Zhi-li ZHAO ; Dol-kar MIGMAR ; ALA Kelsang GYAB ; Liang-hong NI
Chinese Traditional Patent Medicine 2025;47(6):1901-1909
AIM To sequence the chloroplast genome of Artemisia vestita Wall.ex Bess.METHODS Based on ethnobotanical surveys,sample collection and original plant identification were carried out.The chloroplast genome was sequenced using the Illumina platform,followed by assembly and annotation.A comprehensive comparative analysis was conducted with six Artemisia species.The maximum likelihood(ML)phylogenetic tree was constructed based on the chloroplast genome sequences of A.vestita and 32 other Asteraceae species,with Leptocodon hirsutus D.Y.Hong of Campanulaceae as outgroup.RESULTS The chloroplast genome of A.vestita was 151 204 bp in length,including a small single-copy region of 18 331 bp,a large single-copy region of 82 949 bp,and inverted repeat regions of 24 962 bp,with a total GC content of 37.45%.134 genes were annotated,including 89 protein-coding genes,8 ribosomal RNA genes,and 37 transfer RNA genes.A total of 67 SSRs and 44 LSRs were detected in the chloroplast genome.Comparative analysis with closely related species of Artemisia revealed 3 highly variable genes(clpP,rpl36,ycf1)and 6 highly variable intergenic regions(trnK-UUU-matK,rps18-rpl20,rpl36-infA,rpl14-rpl16,rpl16-rpl3 and trnL-UAG-ccsA),which could serve as candidate DNA barcodes for Artemisia identification.Phylogenetic analysis showed that Artemisia formed a highly supportive monophyletic group,with A.vestita and A.gmelinii Web.ex Stechm.being closely related.CONCLUSION This study may provide fundamental data for phylogenetic analysis of Artemisia,taxonomic identification and DNA barcoding construction of Tibetan herb.
3.Heart Yin deficiency and cardiac fibrosis: from pathological mechanisms to therapeutic strategies.
Jia-Hui CHEN ; Si-Jing LI ; Xiao-Jiao ZHANG ; Zi-Ru LI ; Xing-Ling HE ; Xing-Ling CHEN ; Tao-Chun YE ; Zhi-Ying LIU ; Hui-Li LIAO ; Lu LU ; Zhong-Qi YANG ; Shi-Hao NI
China Journal of Chinese Materia Medica 2025;50(7):1987-1993
Cardiac fibrosis(CF) is a cardiac pathological process characterized by excessive deposition of extracellular matrix(ECM). When the heart is damaged by adverse stimuli, cardiac fibroblasts are activated and secrete a large amount of ECM, leading to changes in cardiac fibrosis, myocardial stiffness, and cardiac function declines and accelerating the development of heart failure. There is a close relationship between heart yin deficiency and cardiac fibrosis, which have similar pathogenic mechanisms. Heart Yin deficiency, characterized by insufficient Yin fluids, causes the heart to lose its nourishing function, which acts as the initiating factor for myocardial dystrophy. The deficiency of body fluids leads to stagnation of blood flow, resulting in blood stasis and water retention. Blood stasis and water retention accumulate in the heart, which aligns with the pathological manifestation of excessive deposition of ECM, as a tangible pathogenic factor. This is an inevitable stage of the disease process. The lingering of blood stasis combined with water retention eventually leads to the generation of heat and toxins, triggering inflammatory responses similar to heat toxins, which continuously stimulate the heart and cause the ultimate outcome of CF. Considering the syndrome of heart Yin deficiency, traditional Chinese medicine capable of nourishing Yin, activating blood, and promoting urination can reduce myocardial cell apoptosis, inhibit fibroblast activation, and lower the inflammation level, showing significant advantages in combating CF.
Humans
;
Fibrosis/drug therapy*
;
Animals
;
Yin Deficiency/metabolism*
;
Myocardium/metabolism*
;
Medicine, Chinese Traditional
;
Drugs, Chinese Herbal/therapeutic use*
4.Correlation between Serum FGF-23, HPSE Levels and Early Renal Impairment in Patients with Multiple Myeloma.
Li-Fang MA ; Yan YUN ; Yan-Qi LIU ; Xue-Qin BAI ; Wen-Juan NI ; Zhi-Qin LI ; Yan LU ; Zhe LI ; Jing LI ; Guo-Rong JIA
Journal of Experimental Hematology 2025;33(3):822-827
OBJECTIVE:
To investigate the relationship between serum levels of fibroblast growth factor-23 (FGF-23), heparanase (HPSE) and early renal impairment (RI) in patients with multiple myeloma (MM).
METHODS:
A retrospective analysis was conducted on the clinical data of 125 MM patients who were initially diagnosed in the Department of Hematology of the First Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology from June 2020 to June 2023. The patients were divided into RI group (>176.80 μmol/L) and non-RI group (≤176.80 μmol/L) based on their serum creatinine levels when diagnosed. The baseline data and laboratory indexes of the two groups were compared. The relationship between serum FGF-23, HPSE and early RI in MM patients was analyzed.
RESULTS:
Among 125 newly diagnosed MM patients, 33 cases developed early RI, accounting for 26.40%. The proportion of light chain type, blood urea nitrogen (BUN), blood uric acid, lactate dehydrogenase, FGF-23, and HPSE levels in RI group were higher than those in non-RI group (all P <0.05). There was no statistical significant difference in other data between the two groups (P >0.05). Multivariate logistic regression analysis showed that BUN, FGF-23 and HPSE were associated with early RI in MM patients (all P <0.05). The serum FGF-23 level was divided into Q1-Q4 groups by quartile, and the serum HPSE level was divided into q1-q4 groups. The correlation analysis showed that with the increase of serum FGF-23 and HPSE levels, the incidence of early RI increased (r =0.668, 0.592). Furthermore, logistic regression analysis showed that after controlling for confounding factors, elevated levels of serum FGF-23 and HPSE were still influencing factors for early RI in MM patients (OR>1, P <0.05). According to Pearson's linear correlation test, there was a positive correlation between serum FGF-23 level and HPSE level (r =0.373).
CONCLUSION
There is a certain correlation between serum levels of FGF-23, HPSE and early RI in MM patients, and the incidence of early RI is higher in patients with abnormally high levels of both.
Humans
;
Multiple Myeloma/complications*
;
Fibroblast Growth Factor-23
;
Retrospective Studies
;
Fibroblast Growth Factors/blood*
;
Glucuronidase/blood*
;
Male
;
Female
;
Middle Aged
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Renal Insufficiency/blood*
;
Aged
5.A preclinical evaluation and first-in-man case for transcatheter edge-to-edge mitral valve repair using PulveClip® transcatheter repair device.
Gang-Jun ZONG ; Jie-Wen DENG ; Ke-Yu CHEN ; Hua WANG ; Fei-Fei DONG ; Xing-Hua SHAN ; Jia-Feng WANG ; Ni ZHU ; Fei LUO ; Peng-Fei DAI ; Zhi-Fu GUO ; Yong-Wen QIN ; Yuan BAI
Journal of Geriatric Cardiology 2025;22(2):265-269
6.Preparation modification strategies for clinical treatment drugs of Parkinson's disease
Meng-jiao HE ; Yi-fang XIAO ; Xiang-an-ni KONG ; Zhi-hao LIU ; Xiao-guang WANG ; Hao FENG ; Jia-sheng TU ; Qian CHEN ; Chun-meng SUN
Acta Pharmaceutica Sinica 2024;59(3):574-580
Parkinson's disease (PD) is a chronic neurodegenerative disease. At present, levodopa and other drugs are mainly used for dopamine supplementation therapy. However, the absorption of levodopa in the gastrointestinal tract is unstable and its half-life is short, and long-term use of levodopa will lead to the end-of-dose deterioration, dyskinesia, the "ON-OFF" phenomenon and other symptoms. Therefore, new preparations need to be developed to improve drug efficacy, reduce side effects or improve compliance of patients. Based on the above clinical needs, this review briefly introduced the preparation modification strategies for the treatment of PD through case analysis, in order to provide references for the research and development of related preparations.
7.Effect of Chlorambucil Combined with Ibrutinib on Mantle Cell Lymphoma Cell Line Jeko-1 and Its Related Mechanism
Ni-Na CAI ; Wan-Yi LIU ; Zhi-Qiang LIU ; Jia-Hui GONG ; Yi-Ling LIN ; Ze-Chuan WANG ; Yue-Qin HUANG ; Jian-Xin GUO
Journal of Experimental Hematology 2024;32(1):132-137
Objective:To investigate the toxic effect of chlorambucil combined with ibrutinib on mantle cell lymphoma(MCL)cell line Jeko-1 and its related mechanism.Methods:The MCL cell line Jeko-1 was incubated with different concentrations of chlorambucil or ibrutinib or the combination of the two drugs,respectively.CCK-8 assay was used to detect the proliferation of the cells,and Western blot was used to measure the protein expression levels of BCL-2,caspase-3,PI3K,AKT and P-AKT.Results:After Jeko-1 cells were treated with chlorambucil(3.125,6.25,12.5,25,50 μmol/L)and ibrutinib(3.125,6.25,12.5,25,50 μmol/L)alone for 24,48,72h respectively,the cell proliferation was inhibited in a time-and dose-dependent manner.Moreover,the two drugs were applied in combination at low doses(single drug inhibition rate<50%),and the results showed that the combination of two drugs had a more significant inhibitory effect(all P<0.05).Compared with the control group,the apoptosis rate of the single drug group of chlorambucil(3.125,6.25,12.5,25,50 μmol/L)and ibutinib(3.125,6.25,12.5,25,50 μmol/L)was increased in a dose-dependent manner.The combination of the two drugs at low concentrations(3.125,6.25,12.5 μmol/L)could significantly increase the apoptosis rate compared with the corresponding concentration of single drug groups(all P<0.05).Compared with control group,the protein expression levels of caspase-3 in Jeko-l cells were upregulated,while the protein expression levels of BCL-2,PI3K,and p-AKT/AKT were downregulated after treatment with chlorambucil or ibrutinib alone.The combination of the two drugs could produce a synergistic effect on the expressions of the above-mentioned proteins,and the differences between the combination group and the single drug groups were statistically significant(all P<0.05).Conclusion:Chlorambucil and ibrutinib can promote the apoptosis of MCL cell line Jeko-1,and combined application of the two drugs shows a synergistic effect,the mechanism may be associated with the AKT-related signaling pathways.
8.Downregulation of MUC1 Inhibits Proliferation and Promotes Apoptosis by Inactivating NF-κB Signaling Pathway in Human Nasopharyngeal Carcinoma
Shou-Wu WU ; Shao-Kun LIN ; Zhong-Zhu NIAN ; Xin-Wen WANG ; Wei-Nian LIN ; Li-Ming ZHUANG ; Zhi-Sheng WU ; Zhi-Wei HUANG ; A-Min WANG ; Ni-Li GAO ; Jia-Wen CHEN ; Wen-Ting YUAN ; Kai-Xian LU ; Jun LIAO
Progress in Biochemistry and Biophysics 2024;51(9):2182-2193
ObjectiveTo investigate the effect of mucin 1 (MUC1) on the proliferation and apoptosis of nasopharyngeal carcinoma (NPC) and its regulatory mechanism. MethodsThe 60 NPC and paired para-cancer normal tissues were collected from October 2020 to July 2021 in Quanzhou First Hospital. The expression of MUC1 was measured by real-time quantitative PCR (qPCR) in the patients with PNC. The 5-8F and HNE1 cells were transfected with siRNA control (si-control) or siRNA targeting MUC1 (si-MUC1). Cell proliferation was analyzed by cell counting kit-8 and colony formation assay, and apoptosis was analyzed by flow cytometry analysis in the 5-8F and HNE1 cells. The qPCR and ELISA were executed to analyze the levels of TNF-α and IL-6. Western blot was performed to measure the expression of MUC1, NF-кB and apoptosis-related proteins (Bax and Bcl-2). ResultsThe expression of MUC1 was up-regulated in the NPC tissues, and NPC patients with the high MUC1 expression were inclined to EBV infection, growth and metastasis of NPC. Loss of MUC1 restrained malignant features, including the proliferation and apoptosis, downregulated the expression of p-IкB、p-P65 and Bcl-2 and upregulated the expression of Bax in the NPC cells. ConclusionDownregulation of MUC1 restrained biological characteristics of malignancy, including cell proliferation and apoptosis, by inactivating NF-κB signaling pathway in NPC.
9.Risk factors for bronchopulmonary dysplasia in twin preterm infants:a multicenter study
Yu-Wei FAN ; Yi-Jia ZHANG ; He-Mei WEN ; Hong YAN ; Wei SHEN ; Yue-Qin DING ; Yun-Feng LONG ; Zhi-Gang ZHANG ; Gui-Fang LI ; Hong JIANG ; Hong-Ping RAO ; Jian-Wu QIU ; Xian WEI ; Ya-Yu ZHANG ; Ji-Bin ZENG ; Chang-Liang ZHAO ; Wei-Peng XU ; Fan WANG ; Li YUAN ; Xiu-Fang YANG ; Wei LI ; Ni-Yang LIN ; Qian CHEN ; Chang-Shun XIA ; Xin-Qi ZHONG ; Qi-Liang CUI
Chinese Journal of Contemporary Pediatrics 2024;26(6):611-618
Objective To investigate the risk factors for bronchopulmonary dysplasia(BPD)in twin preterm infants with a gestational age of<34 weeks,and to provide a basis for early identification of BPD in twin preterm infants in clinical practice.Methods A retrospective analysis was performed for the twin preterm infants with a gestational age of<34 weeks who were admitted to 22 hospitals nationwide from January 2018 to December 2020.According to their conditions,they were divided into group A(both twins had BPD),group B(only one twin had BPD),and group C(neither twin had BPD).The risk factors for BPD in twin preterm infants were analyzed.Further analysis was conducted on group B to investigate the postnatal risk factors for BPD within twins.Results A total of 904 pairs of twins with a gestational age of<34 weeks were included in this study.The multivariate logistic regression analysis showed that compared with group C,birth weight discordance of>25%between the twins was an independent risk factor for BPD in one of the twins(OR=3.370,95%CI:1.500-7.568,P<0.05),and high gestational age at birth was a protective factor against BPD(P<0.05).The conditional logistic regression analysis of group B showed that small-for-gestational-age(SGA)birth was an independent risk factor for BPD in individual twins(OR=5.017,95%CI:1.040-24.190,P<0.05).Conclusions The development of BPD in twin preterm infants is associated with gestational age,birth weight discordance between the twins,and SGA birth.
10.Research status of targeting cancer-associated fibroblasts to overcome tumor drug resistance
Jia-ni ZHONG ; Zhi LI ; Jia CHEN ; Ze-ting YUAN ; Pei-hao YIN
The Chinese Journal of Clinical Pharmacology 2024;40(24):3648-3652
The tumor microenvironment(TME)exerts a profound impact on tumor cells,and cancer-associated fibroblasts(CAFs),as one of the most critical and abundant components of the TME,play a key role in tumor growth and development,stroma formation,as well as drug resistance and recurrence.CAFs actively partake in the development of tumor drug resistance via mechanisms such as secretion of soluble factors,exosome release,induction of epithelial-to-mesenchymal transition,regulation of vascular reconstruction,initiation of epigenetic modifications,facilitation of metabolic reprogramming,and sustenance of tumor stem cells.This paper reviews the origin of CAFs,their association with drug resistance,strategies against CAFs,and also discusses the future prospects and challenges of targeting CAFs,aiming to provide the basis for the therapeutic strategy of reversing tumor drug resistance by targeting CAFs.

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