顶空毛细管气相色谱法测定头孢他美钠中4种有机溶剂的残留量

采用顶空毛细管气相色谱法,测定了头孢他美钠中乙醇、丙酮、二氯甲烷和四氢呋喃四种溶剂的残留量.用DB-624毛细管气相色谱柱顶空进样法,FID检测器.乙醇、丙酮、二氯甲烷和四氢呋喃的线性范围分别为0.2～7.0 mg·mL-1(r=0.9995),0.2～7.0 mg·mL-1(r=0.9994),0.03～1.0mg·mL-1(r=0.9993),0.02～0.9 mg·mL-1(r=0.9994);乙醇、丙酮、二氯甲烷和四氢呋喃的平均回收率分别为100.5%、99.6%、99.0%、98.4%;RSD(n=5)分别为1.2%、2.3%、1.8%、2.8%.本方法简单、准确、灵敏度高、重现性好,适用于头孢他美钠中有机溶剂残留量的测定.     

Long-term haematopoietic reconstitution by Trp53-/-p16Ink4a-/-p19Arf-/- multipotent progenitors

Haematopoiesis is maintained by a hierarchical system where haematopoietic stem cells (HSCs) give rise to multipotent progenitors, which in turn differentiate into all types of mature blood cells. HSCs maintain themselves for the lifetime of the organism because of their ability to self-renew. However, multipotent progenitors lack the ability to self-renew, therefore their mitotic capacity and expansion potential are limited and they are destined to eventually stop proliferating after a finite number of cell divisions. The molecular mechanisms that limit the proliferation capacity of multipotent progenitors and other more mature progenitors are not fully understood. Here we show that bone marrow cells from mice deficient in three genes genetically downstream of Bmi1--p16Ink4a, p19Arf and Trp53 (triple mutant mice; p16Ink4a and p19Arf are alternative reading frames of the same gene (also called Cdkn2a) that encode different proteins)--have an approximately 10-fold increase in cells able to reconstitute the blood long term. This increase is associated with the acquisition of long-term reconstitution capacity by cells of the phenotype c-kit+Sca-1+Flt3+CD150-CD48-Lin-, which defines multipotent progenitors in wild-type mice. The pattern of triple mutant multipotent progenitor response to growth factors resembles that of wild-type multipotent progenitors but not wild-type HSCs. These results demonstrate that p16Ink4a/p19Arf and Trp53 have a central role in limiting the expansion potential of multipotent progenitors. These pathways are commonly repressed in cancer, suggesting a mechanism by which early progenitor cells could gain the ability to self-renew and become malignant with further oncogenic mutations.