血管内皮生长因子在妊高征胎盘中的表达研究

目的观察血管内皮生长因子(VEGF)在妊高征(PIH)胎盘中的表达情况.方法用免疫组织化学法,检测30例正常晚孕胎盘(对照组)和34例妊高征胎盘(妊高征组)中的VEGF表达水平,并作计算机图像分析,测定各组标本的阳性染色光度值.结果VEGF在正常晚孕胎盘和妊高征胎盘中均有表达,其分布基本一致,主要在滋养细胞、血管内皮及绒毛间质.计算机图像分析结果示,对照组VEGF阳性染色光度为0.23780±0.00434,妊高征组VEGF阳性染色光度为0.20688±0.01530,其中轻度0.22603±0.00828,中度0.20364±0.00365,重度0.19151±0.00441,妊高征组中VEGF表达明显低于对照组P＜0.01.且随妊高征病情的加重,VEGFF表达水平呈下降趋势.结论妊高征胎盘中VEGF表达水平降低可能与胎盘血管生成减少及胎盘滋养细胞侵入异常有关,在妊高征的发病中起重要作用.     

反义寡核苷酸对脑胶质瘤细胞生长抑制作用的动态研究

目的　探讨原癌基因 c- m yb反义寡核苷酸 (AON)对 C6脑胶质瘤细胞的体内生长抑制作用。方法　将 C6脑胶质瘤细胞接种于裸鼠皮下 ,当肿瘤长至 10 mm左右时随机分成 3组 (每组 12只 ) ,分别用 c- mybAON、正义寡核苷酸 (SON)和生理盐水瘤区原位注射 ,注药后 4、8、12和 16日各组处死动物 3只 ,动态观察肿瘤的体积、重量及病理学改变 ;用流式细胞仪检测肿瘤细胞的凋亡 ;以免疫组化方法分析各组的 c- m yb、bcl- 2蛋白阳性表达率。结果　 c- myb AON组的肿瘤体积抑制率分别为第 4天 6 6 .7% ,第 8天 71.4% ,第 12天 72 % ,第 16天73% ,与对照组相比 ,其生长抑制作用具有显著性 (P<0 .0 5 ) ;AON组凋亡细胞百分率为第 4天 3.4% ,第 8天 2 7.1% ,第 12天 46 .1% ,第 16天 48.4% ,是 SON组和对照组相应时段凋亡细胞的 3.5倍以上 (P<0 .0 5 ) ;AON组 c-myb和 bcl- 2蛋白阳性表达率较对照组有显著降低 (P<0 .0 5 ) ;且 AON治疗后的脑胶质瘤中见较多炎性细胞浸润和钙化灶。结论　 c- myb癌基因有可能成为反义基因治疗恶性脑胶质瘤的优选靶点之一     

Use of biologics in rotator cuff disorders: Current concept review

Poor tendon to bone healing following rotator cuff repair has led to the continued interest and investigation into biological augmentation. The biology of tendinopathy is not fully understood and consequently the availability of disease modifying therapeutic targets is limited. A ceiling of benefit has been reached by mechanical optimisation of rotator cuff repair and thus, in order to improve healing rates, a biological solution is required. This review focuses on the strategies to biologically augment rotator cuff disorders with an emphasis on rotator cuff repair. Leucocyte rich platelet rich plasma has been shown to improve healing rates without clinically relevant improvements in outcome scores. Similarly, improved healing rates have also been reported with bone marrow stimulation and in long-term follow-up with bone marrow concentrate. Extracellular matrix (ECM) and synthetic scaffolds can increase healing through mechanical and or biological augmentation. A potential third category of scaffold is bio-inductive and has no mechanical support. Studies involving various scaffolds have shown promising results for augmentation of large to massive tears and is likely to be most beneficial when tendon quality is poor, however level I evidence is limited.     

Biomechanical activity of the growth plate

Summary The authors analyze at several levels the biomechanical activity of the epiphyseal plate.From a histologic point of view, they show the role played by the different cell layers in growth.The rapid growth of long bones is well known in animals, not entirely in human beings. The factors involved in mechanical regulation of the epiphyseal plate are analyzed according to distraction and compression stresses. Other factors have also been reported (periosteum and muscle).Analysis of the literature reveals that biomechanical activity and the factors managing growth are not well known yet.A combined effort should be made to obtain better understanding of the surgical procedures carried out in pediatric orthopedics.

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Comportement biomécanique du cartilage de croissance. Incidences cliniques

Résumé Les auteurs analysent le comportement biomécanique du cartilage de croissance à plusieurs niveaux.Sur le plan histologique ils montrent le rôle joué dans la croissance par les différentes couches cellulaires.La vitesse de croissance des os longs est bien connue chez les animaux et difficile à apprécier chez l'homme. Les facteurs intervenant dans la régulation mécanique du cartilage sont analysés en fonction des contraintes en compression et en détraction. Les autres facteurs (périoste et muscle) sont rapportés.L'analyse de la littérature montre combien le comportement mécanique et les facteurs régissant la croissance sont mal connus et mériteraient un effort de recherche conjugué pour mieux comprendre la portée des gestes chirurgicaux en orthopédie infantile.

     

Effects of tri-iodothyronine (T3), insulin, insulin-like growth factor I (IGF-I) and transforming growth factor beta1 (TGFβ1) on the proportion of insulin cells in cultured embryonic chick pancreas

 With a view to ultimately identifying factors involved in the development of pancreatic insulin cells, we have cultured dorsal pancreatic buds from 5-day chick embryos on a basement membrane matrix (Matrigel) in a serum-free medium supplemented with selected factors. The endodermal components of the buds were freed of almost all the mesenchyme so as to eradicate as much as possible of this source of some such factors. In 7-day cultures, insulin and glucagon cells were demonstrated immunocytochemically; numbers of insulin cells were expressed as a percentage of insulin plus glucagon cell counts. Our standard medium contained insulin. Addition of tri-iodothyronine to this medium did not increase the proportion of insulin cells, but in combination with raised concentrations of glucose and essential amino acids it improved somewhat the marked increase previously recorded for these nutrient conditions. Omission of insulin from the standard medium greatly reduced the proportion of these cells; substitution of insulin by insulin-like growth factor I increased the proportion considerably more than did insulin. To test for an overall effect of growth factors, explants were cultured in standard medium on Matrigel containing reduced amounts of growth factors: the proportion of insulin cells proved to be increased over that reached on normal Matrigel. The suspicion that transforming growth factor β1, a component of Matrigel, might act to reduce the proportion of insulin cells was tested and found to be correct. It is suggested that the different factors studied here may affect either or both of proliferation and determination in the differentiation pathway of insulin vis-à-vis glucagon cells. Accepted: 13 March 1998     

The influence of sodium on growth in infancy

Sodium (Na) is an important growth factor, stimulating cell proliferation and protein synthesis and increasing cell mass. Sodium chloride (NaCl) deprivation inhibits growth, as reflected by reduced body and brain weight, length, muscle and brain protein and RNA content and brain lipid content compared with controls. This is not due to deficiency of other nutrients since control and experimental diets were identical except for NaCl content. Subsequent NaCl supplementation restores growth velocity to control values but does not induce catch-up growth. In humans, salt loss causes growth failure and subsequent salt repletion improves growth. Preterm infants <32 weeks' gestation at birth are renal salt losers in the first 2 weeks of post-natal life and are vulnerable to hyponatraemia. This can be prevented by increasing Na intake, which also produces accelerated weight gain that persists beyond the period of supplementation. Early nutrition in preterm infants can affect subsequent growth and also cognitive function: this is probably multifactorial, but NaCl intake differed substantially between study groups and is likely to be an important factor. The mechanism whereby Na promotes cell growth is not understood, but stimulation of the membrane Na⁺,H⁺-antiporter with alkalinization of the cell interior is a likely possibility.     

An unidentified macromolecular inhibitory constituent of calcium oxalate crystal growth in human urine

Summary We have detected and isolated a macromolecular constituent in normal human urine possessing calcium crystal growth inhibitory activity. The purification procedure consisted of two anion exchange chromatographies and one affinity chromatography. The crystal growth inhibitor was found to be heterogeneous in net charge as well as in size. It has not been identified. It is not an uronic acid-containing glycosaminoglycan, hitherto presumed to be responsible for the inhibitory activity. Whether an urinary fragment of inter--trypsin inhibitor is responsible has yet to be resolved.     

Growth hormone secretion in children and adolescents with familial tall stature

Sixty-five patients (22 boys and 43 girls) presenting with familial tall stature were investigated with regard to growth hormone (GH) secretion, both physiological and after stimulation with thyrotropin releasing hormone (TRH) and growth hormone relasing hormone (GHRH). Plasma insulin-like growth factor-I (IGF-I) was also measured. Two groups of patients were distinguished according to their physiological secretion of GH: a high secretory group (n=49) with a mean 24 h integrated concentration of GH (IC-GH) of 5.4±2.3 g/l per minute and a large number of peaks (5.1±1.6 in 24 h), and a low secretory group (n=16) with a mean 24 h IC-GH of 2.1±0.5 g/l per minute and few peaks (3.3±1.3 in 24h). Plasma IGF-I levels and GH peak values after the TRH test were significantly higher in the high secretory group. These results indicate that familial tall stature is the consequence either of hypersecretion of GH or of hypersensivity to this hormone (IGF-I levels being normal in spite of low GH levels).