环青海湖地区重点人群投服碘油丸前后碘营养状况的调查

目的了解青海省环湖地区重点人群的碘营养状况,以及服用碘油丸后的变化情况,为今后在青海省推广碘盐困难地区和边远地区对重点人群投放碘油丸提供可靠的理论依据。方法盐碘检测采用半定量方法进行;尿碘检测采用WS／T 107-1999标准进行:水碘检测采用砷铈氧化还原法;8-10岁学龄儿童甲状腺检查采用触诊法进行。结果环湖地区孕妇、哺乳妇女尿碘中位数分别为96．0、90．6μg／L,8-10岁儿童、育龄妇女的尿碘中位数虽高于100μg／L,但<50μg／L的比例均>20％;服碘油丸前农牧区儿童、妇女的碘营养水平较城镇低,尿碘中位数均<80 μg／L。服药后5组重点人群的尿碘水平均有不同程度的提高,以农牧区的提高最明显。结论青海省环湖地区5组重点人群的碘营养状况不理想,以孕妇、哺乳妇女缺碘最严重,8-10 岁儿童的尿碘水平不能完全反映其他重点人群的碘营养水平。     

Granulocyte colony-stimulating factor (G-CSF) production and G-CSF receptor structure in patients with congenital neutropenia

Congenital neutropenia (Kostmann's syndrome [KS]) is an autosomal recessive syndrome that is characterized by profound neutropenia, resulting in major clinical infections and death. Since the neutropenia and symptoms in KS improve in response to exogenous administration of granulocyte colony-stimulating factor (G-CSF), we studied bone marrow cytokine (G-CSF, granulocyte-macrophage CSF [GM-CSF], and interleukin- 6) production under both basal and stimulated conditions. No differences in G-CSF, GM-CSF, or IL-6 gene expression were found in bone marrow stromal cells between normal controls and KS patients, and all three cytokines were detected by enzyme-linked immunosorbent assay (ELISA) in medium conditioned by bone marrow stromal cells from normal donors and patients with KS. Each KS patient tested had detectable, functional G-CSF in their own serum before exogenous G-CSF administration. Since G-CSF production appeared normal in KS patients, we then asked whether we could detect structural defects in the signaling portion of G-CSF receptor genes. Polymerase chain reaction (PCR) amplification of the G-CSF receptor transmembrane region alone, and of the transmembrane plus cytosolic portions of the receptor, yielded the size products predicted from the sequences of the normal G- CSF receptor. Single-strand conformational polymorphism (SSCP) analysis of G-CSF receptor PCR products demonstrated no variance in structural conformation between KS patients and normal subjects. These results demonstrate that bone marrow stromal cells in patients with KS secrete normal concentrations of functional G-CSF and suggest that the neutropenia in KS patients is caused by an inability of neutrophilic progenitor and precursor cells to respond to normal, physiologic levels of G-CSF. Such a defect, clinically responsive to pharmacologic doses of G-CSF, might be caused by defects in the post-G-CSF receptor signal transduction pathway.     

Cell kinetic responses in childhood acute nonlymphocytic leukemia during high-dose therapy with cytosine arabinoside

Sequential bone marrow aspirates obtained from 10 children with relapsed acute nonlymphocytic leukemia (ANLL) after a high dose of cytosine arabinoside (Ara-C; 1000 mg/sq m) were analyzed by flow cytophotometry. The drug causing elimination of proliferating cells followed by a synchronous wave of cell recruitment. Among individual patients, considerable variation was observed in the degree of recruitment as well as in the time of appearance of the recruitment maximum (range 17-36 hr). However, both parameters appeared inversely correlated with the proliferative status in the bone marrow before treatment. In 6 other patients, cell kinetic responses were studied during treatment with repeated Ara-C injections scheduled individually according to the expected optima of recruitment. Waves of recruitment could be observed during 4-5 consecutive injections. The results suggest that in childhood ANLL, characteristic and individual cytokinetic responses to treatment with high-dose Ara-C can be monitored during therapy. These observations may allow the development of individual treatment schedules.     

p53基因和血清P53抗体表达与原发性肝癌分化程度的关系

约50%人肿瘤有肿瘤抑制基因p53的突变,并且表达异常的P53蛋白,刺激机体产生自身体液免疫,故在血清中可检测到P53抗体.     

Interleukin-6 synergizes with M-CSF in the formation of macrophage colonies from purified human marrow progenitor cells

We examined the in vitro stimulative effects of recombinant human interleukin-6 (IL-6, or interferon-beta 2) on purified human bone marrow progenitor cells. IL-6 alone or in combination with erythropoietin (Epo), IL-3, GM-CSF, or G-CSF did not induce colony formation. However, IL-6 strongly synergized with M-CSF in stimulating macrophage colony formation (colony numbers and size). The magnitude of IL-6 synergism with M-CSF was dose dependent; maximal potentiation of M- colony formation was evident at approximately 100 to 1,000 U/mL IL-6. When the addition of IL-6 to M-CSF-supplemented cultures was delayed for more than one day after the beginning of culture, enhancement of macrophage colony formation was lost. IL-6 stimulation of M-CSF- responsive colony formation was not apparent when nonpurified marrow cells were plated, most likely due to endogenous IL-6 release. These observations suggest that IL-6, in addition to playing a role in B- lymphocyte proliferation can potentiate the human immune defence mechanism by stimulating monocyte-macrophage development as well.