“炎-癌转化”是宫颈由高危型人乳头瘤病毒(high-risk human papillomavirus,HR-HPV)感染发展至宫颈癌的重要机制之一。持续性宫颈HR-HPV感染作为宫颈癌的重要诱因,其引起的局部非可控性炎症微环境是宫颈癌发生的内在机制。“炎-癌转化...“炎-癌转化”是宫颈由高危型人乳头瘤病毒(high-risk human papillomavirus,HR-HPV)感染发展至宫颈癌的重要机制之一。持续性宫颈HR-HPV感染作为宫颈癌的重要诱因,其引起的局部非可控性炎症微环境是宫颈癌发生的内在机制。“炎-癌转化”的宏观及微观病理过程均与中医“湿热蕴毒”的病机演变相契合,湿热聚结为“炎-癌转化”的驱动因素;湿热久蕴致脾虚肝郁为其病机演变特征;湿热久稽,肝脾失调,瘀滞蕴结胞门,终成“癌毒”。持续性宫颈HR-HPV感染所致的“炎-癌转化”进程主要责之于中医的湿、热、虚、毒病理因素。调控持续性宫颈HR-HPV感染炎性微环境为宫颈癌防治的重要途径。临证时以清热燥湿、健脾疏肝为核心治法,攻伐有道、内外同调,以截断“炎-癌转化”的进程。基于“湿热蕴毒”探讨持续性宫颈HR-HPV感染“炎-癌转化”进程,可为中医防治宫颈癌及中医药干预“炎-癌转化”提供思路。展开更多
Background Most patients with acute myelogenous leukemia （AML） suffer from disordered hemostasis. We have previously shown that annexin II （Ann II）, a high-affinity co-receptor for plasminogen/tissue plasminogen a...Background Most patients with acute myelogenous leukemia （AML） suffer from disordered hemostasis. We have previously shown that annexin II （Ann II）, a high-affinity co-receptor for plasminogen/tissue plasminogen activator, plays a central role in primary hyperfibrinolysis in patients with acute promyelocytic leukemia （APL）. The expression of Ann II in cells from patients with major subtypes of AML and the effect of arsenic trioxide （As203） on Ann II expression in AML cells were investigated to determine whether As203-mediated downregulation of Ann II could restore hemostatic stability. Methods A total of 103 patients （48 females and 55 males; age, 19-58 years） were included. Plasma samples were collected before and after treatment as well as after complete remission. Ann II and plasminogen activation were measured in leukemic cells during treatment with 1 pmol/L As203. Results Before AS203 treatment, Ann II mRNA expression （real-time PCR） was the highest in M3 cells （P 〈0.05）, higher in M5 cells than that in M1, M2, M4, and M6 cells （P〈0.001）, and positively correlated with Ann II protein expression （flow cytometry） （r=0.752, P 〈0.01）. Exposure for up to 120 hours to As203 （1 μmol/L） had no significant effect on Ann II protein in M1 and M2 leukemic cells, but decreased Ann II protein expression twofold within 48 hours of exposure in M3 cells （P 〈0.05） and twofold within 96 hours in M5 cells （P 〈0.05）. The rate of plasmin generation was higher in APL, M5, and M4 cells than in M1, M2, and M6 cells. Conclusions As203 may reduce hyperfibrinolysis in AML by downregulation of Ann 11. Furthermore, As2O3 affects more than one form of AML （APL, M4 and M5）, suggesting its potential role in their management.展开更多
文摘“炎-癌转化”是宫颈由高危型人乳头瘤病毒(high-risk human papillomavirus,HR-HPV)感染发展至宫颈癌的重要机制之一。持续性宫颈HR-HPV感染作为宫颈癌的重要诱因,其引起的局部非可控性炎症微环境是宫颈癌发生的内在机制。“炎-癌转化”的宏观及微观病理过程均与中医“湿热蕴毒”的病机演变相契合,湿热聚结为“炎-癌转化”的驱动因素;湿热久蕴致脾虚肝郁为其病机演变特征;湿热久稽,肝脾失调,瘀滞蕴结胞门,终成“癌毒”。持续性宫颈HR-HPV感染所致的“炎-癌转化”进程主要责之于中医的湿、热、虚、毒病理因素。调控持续性宫颈HR-HPV感染炎性微环境为宫颈癌防治的重要途径。临证时以清热燥湿、健脾疏肝为核心治法,攻伐有道、内外同调,以截断“炎-癌转化”的进程。基于“湿热蕴毒”探讨持续性宫颈HR-HPV感染“炎-癌转化”进程,可为中医防治宫颈癌及中医药干预“炎-癌转化”提供思路。
文摘Background Most patients with acute myelogenous leukemia （AML） suffer from disordered hemostasis. We have previously shown that annexin II （Ann II）, a high-affinity co-receptor for plasminogen/tissue plasminogen activator, plays a central role in primary hyperfibrinolysis in patients with acute promyelocytic leukemia （APL）. The expression of Ann II in cells from patients with major subtypes of AML and the effect of arsenic trioxide （As203） on Ann II expression in AML cells were investigated to determine whether As203-mediated downregulation of Ann II could restore hemostatic stability. Methods A total of 103 patients （48 females and 55 males; age, 19-58 years） were included. Plasma samples were collected before and after treatment as well as after complete remission. Ann II and plasminogen activation were measured in leukemic cells during treatment with 1 pmol/L As203. Results Before AS203 treatment, Ann II mRNA expression （real-time PCR） was the highest in M3 cells （P 〈0.05）, higher in M5 cells than that in M1, M2, M4, and M6 cells （P〈0.001）, and positively correlated with Ann II protein expression （flow cytometry） （r=0.752, P 〈0.01）. Exposure for up to 120 hours to As203 （1 μmol/L） had no significant effect on Ann II protein in M1 and M2 leukemic cells, but decreased Ann II protein expression twofold within 48 hours of exposure in M3 cells （P 〈0.05） and twofold within 96 hours in M5 cells （P 〈0.05）. The rate of plasmin generation was higher in APL, M5, and M4 cells than in M1, M2, and M6 cells. Conclusions As203 may reduce hyperfibrinolysis in AML by downregulation of Ann 11. Furthermore, As2O3 affects more than one form of AML （APL, M4 and M5）, suggesting its potential role in their management.
