转移抑制基因nm23-H1在喉癌、下咽癌及其转移淋巴结中的表达

目的 :检测nm2 3-H1蛋白在喉癌、下咽癌及其淋巴结、声带息肉中的表达 ,阐明nm2 3-H1蛋白免疫反应下降与喉癌转移之间的关系。方法 :用常规链霉亲和素 -生物素 -过氧化物酶法 (SABC法 )nm2 3-H1多克隆抗体研究nm2 3-H1蛋白在 5 3例喉癌及其淋巴结、9例声带息肉中的表达。结果 :声带息肉及未转移淋巴结中均无基因产物的表达 ,喉癌及转移淋巴结中nm2 3-H1蛋白有不同程度的表达 ,喉癌的阳性表达率为 6 2 .5 % (n=32 ) ,转移淋巴结为 2 7.3% (n=11) ,差异有显著性 (P <0 .0 5 )。 结论 :在喉癌转移淋巴结中nm2 3-H1基因表达较在喉癌中显著下降 ,nm2 3-H1,基因可能在喉癌转移的发生机制中起作用     

Serum levels of the soluble low affinity receptor for IgE and soluble interleukin-2 receptor in childhood, and their relation to age, gender, atopy and allergic disease

Identifying immune factors associated with the development of atopy can enhance our understanding of the in vivo mechanisms involved and may have utility in paradigms designed to prevent disease. Two candidates sug-gested for such roles are the soluble low affinity receptor for IgE (sCD23) and the soluble interleukin-2 receptor (sCD25). To assess serum levels of these factors blood samples were collected at birth and at age 6 in a large nonselected population from Tucson, AZ. Log mean sCD23 and sCD25 lev-els decreased from birth to age 6, (for sCD23 0. 60 ffi 0. 26pg/l, n=340 and 0. 53 + 0. 28pg/l, n=333 and for sCD25 1. 95 i 0. 14pM. n=304 and 1. 86 ffi 0. 20pM, n=327. for the two ages respectively. Anglo children had lower sCD23 levels at birth compared to Hispanic children (p < 0.01); no effect of gender was observed. Skin test reactivity at age 6 was directly related to sCD25 levels at age 6 (p=0.007) and even levels at birth showed a similar trend (p=0.06). These relations were distinct from any relation to total se-rum IgE. No relation was observed with sCD23 levels for either skin test re-activity or serum IgE. The prevalences of asthma, rhinitis and eczema by age 6 were unrelated to sCD25 or sCD23 levels. The results indicate that soluble CD23 and CD25 have higher levels at birth than later in childhood and that the development of skin test reactivity may be associated with reg-ulatory mechanisms involving sCD25, whereas sCD23 was not similarly implicated.     

Sequential changes on23Na MRI after cerebral infarction

²³Na MRI changes from the acute to chronic phase were investigated in seven patients with cerebral in-farcts. They showed no signal increase during the first 13 h after the stroke and revealed a definite signal increase thereafter. This reached a maximum 45–82 h after stroke and became slightly less marked in the subactue and chronic phases, probably as a result of disappearance of cerebral oedema. In the early acute phase of stroke,²³Na MRI appears to fail to demonstrate Na⁺ increases in the ischaemic area, due presumably to the invisibility on MRI of intracellular²³Na in the intact brain. The increase more than 13 h after stroke, during which ischaemic cells are likely to die, is presumably because of increased visibility of intracellular²³Na in the dead cells.²³Na MRI is apparently insensitive to early ischaemic changes, but may be useful for assessing the cell viability in the ischaemic brain.     

肿瘤转移抑制基因nm23H_1产物在人鼻咽癌中表达的研究

采用ＳＰ免疫组化技术，以ＮＤＰＫ／ｎｍ２３Ｈ１特异的单克隆抗体为探针，对人鼻咽癌中ｎｍ２３Ｈ１的表达及其与颈淋巴结转移的关系进行了研究。结果：３１例鼻咽癌中ｎｍ２３Ｈ１基因产物表达的阳性率为４１．９％（１３／３１）。其中无转移组的阳性率为５２．３％（１１／２１），有转移组的阳性率为２０％（２／１０），两组间具有显著性差异（Ｐ＜０．０１），而在转移的颈淋巴结组织中ｎｍ２３Ｈ１产物表达极微或无表达，其阳性率为０，与无转移组比较有显著性差异（Ｐ＜０．０１）。上述结果说明，肿瘤转移抑制基因ｎｍ２３Ｈ１产物的表达，在无转移组呈高表达，在有转移组及淋巴结转移组中呈低表达，其表达与转移呈负相关，说明人鼻咽癌的转移与ｎｍ２３Ｈ１基因的低表达密切相关     

人肝癌组织nm23的表达及其与转移的关系

目的：研究ｎｍ２３基因在肝癌转移，发生，发展中的意义，方法：应用免疫组人技术（ＳＰ法）检测ｎｍ２３在２４例人肝癌组织的表达，结果ｎｍ２３在肝癌组织中较高表达，在癌旁组织中也有表达，在已发生临床转移的肝癌组织中ｎｍ２３的表达水平明显低于尚未发生转移，结论：ｎｍ２３在抑制肝癌转移中有一定的作用，但在肝癌转移过程显然尚有其他调节因素的存在。     

The effects of epidermal and fibroblast growth factors on the repair of corneal endothelial wounds in bovine corneas maintained in organ culture.

The effects of FGF and EGF on the repair process of the wounded endothelium of bovine corneas maintained in organ culture have been analyzed. Both EGF and FGF greatly accelerate the repair process of the corneal endothelium in vitro. Similar results were obtained when complete denudation of the endothelium was performed and cultured corneal endothelial cells were seeded at a final density of 3×10³/cm² on Descemet's membrane. Within 5 days a new endothelium with a morphology similar to that of intact corneal endothelium maintained in organ culture for the same period time was achieved. These results demonstrate, therefore, that either EGF or FGF can participate in the repair process of the corneal endothelium of corneas maintained in organ culture.     

Reversal of functional loss in the P23H-3 rat retina by management of ambient light

The present experiments were undertaken to test recovery of function in the retina of the rhodopsin-mutant P23H-3 rat, in response to the management of ambient light. Observations were made in transgenic P23H-3 and non-degenerative Sprague-Dawley albino (SD) rats raised to young adulthood in scotopic cyclic light (12h 5 lx "daylight", 12h dark). The brightness of the day part of the cycle was increased to 300 lx (low end of daylight range) for 1 week, and then reduced to 5 lx for up to 5 weeks. Retinas were assessed for the rate of photoreceptor death (using the TUNEL technique), photoreceptor survival (thickness of the outer nuclear layer), and structure and function of surviving photoreceptors (outer segment (OS) length, electroretinogram (ERG)). Exposure of dim-raised rats to 300 lx for 1 week accelerated photoreceptor death, shortened the OSs of surviving photoreceptors, and reduced the ERG a-wave, more severely in the P23H-3 transgenics. Returning 300 lx-exposed animals to 5 lx conditions decelerated photoreceptor death and allowed regrowth of OSs and recovery of the a-wave. Recovery was substantial in both strains, OS length in the P23H-3 retina increasing from 17% to 90%, and a-wave amplitude from 33% to 45% of control values. Thinning of the ONL over the 6 week period studied was minimal. The P23H-3 retina thus shows significant recovery of function and outer segment structure in response to a reduction in ambient light. Restriction of ambient light may benefit comparable human forms of retinal degeneration in two ways, by reducing the rate of photoreceptor death and by inducing functional recovery in surviving photoreceptors.