Dry heat loss in incubator: comparison of two premature newborn sized manikins

Keeping premature newborns warm is crucial for their survival. Their ability to prevent excessive heat loss to the environment and to control their body temperature is limited. The risk of hypothermia is particularly important for low-birth-weight newborns with a large body surface area in relation to their mass of heat-producing tissues. The present study was performed to assess the body heat loss difference between small and large body-size premature newborns using two anthropomorphic thermal manikins of premature newborns of 900 g and 1,800 g (respective body surface areas of 0.086 and 0.150 m²). The dry heat loss from the six body segments of the small manikin (S) was measured and compared with that of the large manikin (L). The two manikins were exposed to five different environmental temperatures ranging between 29 and 35°C in a single-walled, air-heated closed incubator. The magnitudes of heat loss decreased significantly by 20.4% between the two manikins [small manikin 110.1 (44.3) W/m² vs large manikin 87.6 (25.8) W/m², mean values with one standard deviation]. The results obtained from the comparison of the heat loss measures from the two manikins confirm the fact that the heat loss increases with an increase in the ratio of the body surface area to body mass. The thermal manikin appears to provide an accurate method for the assessment of thermal conditions in neonatal care.     

Cyclic AMP dependent,constitutive thermotolerance in the adenylate cyclase-deficient cr-1 (crisp) mutant of Neurospora crassa

Summary We investigated the heat shock response of the adenylate cyclase deficient mutant cr-1 (crisp) of Neurospora crassa. This strain was observed to be much more resistant to a lethal temperature of 50 °C than the wild type. This constitutive thermotolerance was absent in cr-1 conidiospores raised on cyclic AMP (cAMP, 2.5 mM) supplemented solid medium, but was partially restored when the conidiospores were germinated at 30 °C, a temperature which fails to induce thermotolerance in the wild-type strain. Two other crisp-like Neurospora mutants, cr-2 and cr-3 which, in contrast to cr-1, contain normal levels of cAMP, did not exhibit the thermotolerance phenomenon observed for cr-1. A cr-1, pe, fl (crisp-microconidial) strain also lacked the ability to tolerate a lethal heat treatment. Our results demonstrate that the adenylate cyclase deficient cr-1 mutant of Neu-rospora crassa expresses a constitutive thermotolerant phenotype as a consequence of its primary genetic defect: low levels of cAMP.     

The response of heat shock proteins 25 and 72 to ischaemia in different kidney zones

 Induction of heat shock proteins (HSPs) following cell injury contributes to the protection of vital cell functions. It was, therefore, of interest to study the effects of transient renal ischaemia on the abundance and distribution of two HSPs, HSP25 and HSP72, in renal tissue using Western-blot techniques. Analyses were performed on the supernatant (HSP25, HSP72) and pellet (HSP25) of homogenates obtained from cortex (CX) and outer (OM) and inner (IM) medulla of the rat kidney immediately after 60 min of ischaemia followed by varying periods of reperfusion. Ischaemia of the left kidney caused HSP25 contents to decrease in CX, OM and IM by 73, 89 and 54% respectively, compared with the corresponding zones of the contralateral control kidney. This initial decrease in supernatant HSP25 was accompanied by an increased abundance of HSP25 in the pellet. Following reperfusion, HSP25 contents in the supernatant gradually increased in CX and OM, reaching, after 24 h, values that were 5.4- and 2.5-fold higher, respectively, than those in the control kidneys. After 7 or 14 days of reperfusion, HSP25 contents had not completely normalised in CX, but had reached control levels in OM. In IM, the HSP25 content remained below control throughout the entire reperfusion period. HSP72 (supernatant) was below the detection limit in the CX of the control kidney. Similar to the level of HSP25, that of HSP72 was also markedly lower in OM and IM immediately after ischaemia. The intrarenal distribution of HSP72 and the sequence of zonal changes in HSP72 contents were similar to those observed for HSP25. These results are compatible with the view that, during ischaemia and the initial reperfusion period, HSP25 migrates from the cytoplasmic compartment (supernatant) into the nucleus and/or associates with cytoskeletal structures. The observation that both HSP25 and HSP72 are transiently induced in CX and OM, but not in IM, may be explained by the fact that, while all kidney cells are exposed to ischaemic stress, only inner medullary cells experience a major postischaemic attenuation of osmotic stress. Received: 11 February 1997 / Received after revision and accepted: 26 March 1997     

VP-16诱导细胞凋亡及其细胞核基质中热休克蛋白表达的研究

目的　研究VP 16诱导HL 6 0细胞凋亡的变化特点以及凋亡细胞及核基质中热休克蛋白 (HSP)表达的变化。　方法　琼脂糖凝胶电泳观察凋亡细胞基因组DNA断裂 ;TUNEL法观察凋亡细胞的形态学变化 ;用免疫印迹方法显示凋亡细胞核基质蛋白、细胞总蛋白中HSP表达的差异。　结果　VP 16作用HL 6 0细胞 0 5h出现早期凋亡特征。作用 4h可见明显的DNA梯状条带。与未凋亡的细胞比较 ,凋亡细胞核基质蛋白中HSP70和HSC70表达明显上调 ;VP 16作用 2、3及 4h细胞总蛋白中HSP70的表达随时间延长略显增加 ;诱导 2 2h比诱导 4h时去除VP 16后孵至 2 2h凋亡细胞总蛋白HSP70表达量增强了 3 4倍。　结论　 1 HL 6 0细胞早期凋亡形态出现在DNA梯状条带形成之前。 2 凋亡细胞核基质中HSP70、HSC70的表达明显增加 ,经 2、3及 4h作用的细胞总蛋白中HSP70表达差异不显著。这提示细胞凋亡后HSP70的活性位点主要位于核基质上。 3 VP 16作用细胞时间增长至2 2h ,HSP的保护作用可能消失     

鼠肝癌细胞的热休克蛋白诱导及其抗瘤机理研究

摸索鼠肝癌Ｈ２２细胞膜热休克蛋白７０最适的话导条件，并明确其体内外的抗瘤机理。方法用免疫荧光及ＦＣＭ光检测热休克Ｈ２２细胞膜ＨＳＰ７０蛋白的动态表达。并用ＭＭＣ灭活，热休克后的Ｈ２２细胞作抗原进行体内肿瘤免疫保护试验及体外肿瘤杀伤试验。     

人急性白血病淋巴细胞HSP70及 HSP70 mRNA的表达研究

目的：检测急性白血病病人血淋巴细胞热休克蛋白70（HSP70）及其mRNA的表达。方法：ELISA法检测HSP70,RT－PCR法检测HSP70 mRNA。结果：化疗前急性白血病病人淋巴细胞HSP70及mRNA明显低于正常人;而化疗后,急性白血病病人淋巴细胞HSP70及mRNA明显高于正常人（P＜0．01）,结论：HSP70与急性白血病癌细胞关系密切,对癌细胞起保护作用。     

实验性自身免疫性内耳病耳蜗热休克蛋白70的表达

目的　探讨自身免疫性内耳病模型动物耳蜗热休克蛋白的表达。方法　利用同种异体内耳抗原免疫豚鼠 ,以建立自身免疫性内耳病 (autoimmuneinnereardisease ,AIED)动物模型 ,并应用免疫组织化学及原位杂位技术 ,研究热休克蛋白 (heatshockprotein ,hsp) 70在正常对照组及AIED模型动物实验组耳蜗中的表达情况。结果　对照组豚鼠螺旋神经节细胞中存在hsp70样蛋白基础表达 ;实验组 2 8耳中 10耳 (35 7% )听阈提高≥ 10dB ;此组动物螺旋神经节细胞和血管纹、螺旋韧带hsp70及其mRNA表达明显增强。结论　以粗制膜迷路抗原免疫豚鼠 ,听阈提高动物hsp70在螺旋神经节细胞和血管纹、螺旋韧带合成增加。     

肿瘤热休克蛋白70-多肽复合物诱导特异性细胞毒T淋巴细胞产生的实验研究

目的　研究肿瘤细胞的热休克蛋白 70多肽复合物 (heatshockprotein 70peptide complexes ,HSP PC70 )诱导活化肿瘤特异性细胞毒T淋巴细胞 (cytotoxicTlymphocytes,CTL)的作用及该CTL的杀瘤效应。方法　利用细胞培养 ,流式细胞技术 ,蛋白质的分离纯化技术 ,电泳技术 ,Western blot检测方法 ,T淋巴细胞的诱导及体外扩增 ,酶标技术等 ,测定肿瘤HSP70 多肽复合物诱导活化小鼠体内CTL产生的作用。结果　HcaF细胞HSP PC70的自然表达率为 6 3.5 % ,热诱导后为 75 .5 % ;HcaF细胞的HSP PC70能够诱导活化肿瘤特异性的CTL ,该CTL在效靶比例为 5 0∶1、2 5∶1、12 .5∶1时于体外对HcaF细胞的杀伤效率分别为 84.2 %± 3.2 %、47.9%± 2 .6 %和 14.8%± 3.0 % ;该CTLCD3、CD8的阳性率分别为 93%± 7% ,92 %± 8% ;将活化的CTL注入荷瘤小鼠体内可见明显的治疗作用 ,注入 10 7CTL 4次后 ,10 0 %的小鼠获长期生存。结论　肿瘤来源的HSP PC70具有强大的免疫原性 ,可活化CD8 T淋巴细胞成为肿瘤特异性的CTL ,该CTL具有较高的体外杀瘤活性和良好的治疗作用。     

实热证、虚热证模型大鼠肝细胞琥珀酸脱氢酶活性研究

观察实热证、虚热证大鼠模型组与治疗组肝细胞线粒体琥珀酸脱氢酶(SDH)活性的变化。用紫外分光光度计测定肝细胞线粒体琥珀酸脱氢酶活性。结果表明：热证时(实热、虚热)SDH活性升高,经清热解毒、滋阴清热中药治疗后,SDH活性有所降低。说明：实热证、虚热证与机体能量代谢呈正相关,中药治疗有利于肝细胞线粒体呼吸亢进的恢复。     

锌对热应激大鼠热休克蛋白70mRNA表达的影响

目的：锌对热应激大鼠热休克蛋白７０ ｍ Ｒ Ｎ Ａ 表达的影响。方法：分别以高、中、低锌饲料（锌含量分别为９２２０、４５６１、２１７０ ｍ ｇ／ｋｇ 饲料）喂养３ 组大鼠,热暴露（干球４１５ ° Ｃ、湿球３２ ° Ｃ）３０ ｍ ｉｎ 时断头处死,应用 Ｎｏｒｔｈｅｒｎ 印迹杂交和斑点杂交检测热应激大鼠肝脏热休克蛋白７０ ｍ Ｒ Ｎ Ａ 的表达情况。结果：不经受热暴露的３ 组动物仅高锌组能检测到热休克蛋白７０ ｍ Ｒ Ｎ Ａ,而热暴露３０ ｍ ｉｎ 的３ 组动物均有热休克蛋白７０ ｍ Ｒ Ｎ Ａ 条带,且依锌水平不同,其表达强弱依次为高锌组强于中锌组,中锌组强于低锌组。结论：热应激时热休克蛋白７０ 基因的转录水平提高;锌通过活化热休克蛋白７０ 基因的转录而诱发热应激大鼠热休克蛋白７０ 的合成,从而使机体对热暴露产生更强的耐受力。