Serum levels of IGF1 are a useful predictor of retinopathy of prematurity

Objective: To ascertain whether insulin‐like growth factor 1 (IGF1) is associated with retinopathy of prematurity (ROP) and is a useful predictor of the disease. Although its aetiopathogenesis is multifactorial, development of the disease appears to be related to a deficiency in IGF1, a hormone that acts together with vascular endothelial growth factor in the normal angiogenesis in the retina. Design: Prospective study for a 30‐month period. Participants: A total of 74 premature newborn babies, of less than 1500 g and/or 32 weeks’ gestational age or less. Testing: To determine the development and severity of ROP. Main outcome measures: Serum levels of IGF1 were measured once a week from birth until 40 weeks corrected gestational age in each subject. Results: Of our subjects, 32.4% developed some form of ROP, and all those ROP patients had the following characteristics at birth (median ± standard deviation scores): low weight (1098 ± 188 vs. 1393 ± 285 g), short length (36.74 ± 1.77 vs. 38.89 ± 3.08 cm), small cranial perimeter (26.03 ± 1.74 vs. 27.93 ± 1.81 cm) and young gestational age (29.7 ± 1.78 vs. 31.3 ± 1.79 weeks) (p < 0.05). Other factors previously associated with ROP that were also observed with statistically significant frequency in our ROP patients were bronchopulmonary dysplasia, intracranial haemorrhage, the need for erythrocyte transfusion or treatment with erythropoietin and sepsis (all p < 0.05). Levels of IGF1 at the 3rd week post‐partum, independent of gestational age at birth, were clearly lower in the group who developed ROP (29.13 vs. 43.16 ng/mL, p < 0.05). A value of 30 ng/mL of IGF1 in the third week post‐partum was found to have a 90% sensitivity in the diagnosis of ROP. A rapid rise in IGF1 levels between the 3rd and 5th weeks appeared to be related to the development of a higher stage of ROP. Conclusion: Determination of IGF1 serum levels in the 3rd week post‐partum, independent of gestational age at birth, provides a sufficient and reliable prognostic tool and allows the identification of a group of patients at high risk of developing the disease.     

Normal and degenerative posterior spinal structures: MR imaging

A retrospective study of the magnetic resonance (MR) images of the lumbar spines of 13 healthy subjects and 30 patients with degenerative changes was done. In the healthy subjects, the vertebral facets, thickness of the cartilage and ligamentum flavum, signal characteristics of the bone marrow, and size of the spinal canal were studied. In the patients with degenerative changes in one of these structures, MR images in the sagittal plane were useful in demonstrating hypertrophy of the ligamentum flavum or the vertebral facets, in grading the degree of foraminal stenosis, and in measuring the sagittal diameter of the spinal cord. MR images in the axial plane facilitated detailed analysis of the facet joint and more accurate measurements of the thickness of the ligamentum flavum and spinal canal diameter. MR images were compared with computed tomography scans in 12 patients.     

聚乙二醇干扰素α-2b或α-2a与利马韦林联合治疗丙型肝炎疗效比较

背景及目的：丙型肝炎的治疗指南推荐聚乙二醇干扰素α-2b或α-2a联合利巴韦林治疗.但是,这两种方案并没有进行充分地比较,本研究通过临床观察对其疗效进行分析探讨.     

脐血有核细胞移植治疗脑卒中的动物实验

目的:脐血有核细胞中富含多系前体细胞,具备改善受损神经系统功能的潜能。为此建立阻塞性脑卒中动物模型,探讨脐血有核细胞移植对其治疗的可行性。方法:实验于2004-09/2005-05在深圳市宝安区人民医院动物实验室完成。①实验材料:脐带血取自足月新生儿,由深圳宝安血站研究室提供,产妇及其家属均签署知情同意书。SD清洁级成年大鼠80只,随机取20只作为正常对照组,另60只以电凝法建立阻塞性脑卒中模型。剔除运动功能障碍不典型鼠后,随机取5只作为模型观察,余鼠按1∶1随机分为细胞移植组和模型对照组,当出现单只为尾数时,将其分配在细胞移植组。②实验方法:无菌抽取脐血20mL,加入乙二胺四乙酸抗凝,Ficoll法分离脐血有核细胞。造模后第10天,细胞移植组大鼠将头部固定,按前囟尾侧3.0mm,中线旁1.5mm,深度1.2mm注入1011L-1脐血有核细胞悬液5μL,1μL/min。模型对照组注射等量无细胞脐血清,正常对照组不给予任何干预。③实验评估:造模后4周,5只模型观察大鼠制作脑切片,行苏木精-伊红染色镜检。各组分别于细胞移植前、细胞移植后2,6周进行横木行走实验和触觉刺激试验,检测其运动和触觉功能的恢复。处死各组大鼠制作病理切片,免疫荧光检测脐血有核细胞在脑内生存和分化情况。结果:正常对照组、细胞移植组、模型对照组各20只、24只、24只进入结果分析。①阻塞性脑卒中模型大鼠病理特征:造模大鼠出现行为障碍,缺血部位出现中风囊,病理切片可见缺血坏死区等阻塞性脑卒中所致脑组织病理损伤。②运动和触觉功能测试:细胞移植前,细胞移植组与模型对照组大鼠的横木行走能力、撕胶纸能力均基本相似(P=0.05),且明显低于正常对照组(P<0.01)。移植后第2周,细胞移植组大鼠两项能力均明显强于模型对照组(P<0.05),但仍低于正常对照组(P<0.01)。移植后第6周,细胞移植组大鼠的横木行走能力明显改善,与正常对照组基本相似(P>0.05);撕胶纸能力仍低于正常对照组(P<0.01)。③阳性细胞免疫荧光检测:细胞移植组进针注射部位存在大量抗人RNP/CD45双阳性完整细胞,并向大脑中线、皮层梗死部位迁移。所植入的细胞约2.95%表达胶质纤维酸性蛋白,3.41%表达神经特异性烯醇化酶。结论:移植人脐血有核细胞能有效改善阻塞性脑卒中大鼠的运动和触觉功能缺陷。     

Lack of autologous mixed lymphocyte reaction in patients with chronic lymphocytic leukemia: evidence for autoreactive T-cell dysfunction not correlated with phenotype, karyotype, or clinical status

In the present study, there was a complete lack of autologous MLR between responding T cells or T subsets and unirradiated or irradiated leukemic B cells or monocytes in all 20 patients with CLL, regardless of disease status, stage, phenotype, or karyotype of the disease. The stimulating capacity of unirradiated CLL B cells and CLL monocytes or irradiated CLL B cells was significantly depressed as compared to that of respective normal B cells and monocytes in allogeneic MLR. The responding capacity of CLL T cells was also variably lower than that of normal T cells against unirradiated or irradiated normal allogeneic B cells and monocytes. The depressed allogeneic MLR between CLL B cells or CLL monocytes and normal T cells described in the present study could be explained on the basis of a defect in the stimulating antigens of leukemic B cells or monocytes. The decreased allogeneic MLR of CLL T cells might simply be explained by a defect in the responsiveness of T lymphocytes from patients with CLL. However, these speculations do not adequately explain the complete lack of autologous MLR in these patients. When irradiated CLL B cells or irradiated CLL T cells were cocultured with normal T cells and irradiated normal B cells, it was found that there was no suppressor cell activity of CLL B cells or CLL T cells on normal autologous MLR. Our data suggest that the absence or dysfunction of autoreactive T cells within the Tnon-gamma subset account for the lack of autologous MLR in patients with CLL. The possible significance of the autologous MLR, its relationship to in vivo immunoregulatory mechanisms, and the possible role of breakdown of autoimmunoregulation in the oncogenic process of certain lymphoproliferative and autoimmune diseases in man are discussed.