Effects of heat on embryos and foetuses

Objectives : This paper reviews the effects of elevated maternal temperature on embryo and foetal development in experimental animals and in humans. Conclusions : Hyperthermia during pregnancy can cause embryonic death, abortion, growth retardation and developmental defects. Processes critical to embryonic development, such as cell proliferation, migration, differentiation and programmed cell death (apoptosis) are adversely affected by elevated maternal temperatures, showing some similarity to the effects of ionizing radiation. The development of the central nervous system is especially susceptible: a 2.5°C elevation for 1 h during early neural tube closure in rats resulted in an increased incidence of cranio-facial defects, and a 'spike' temperature elevation of 2-2.5°C in an exposure of 1 h during early neurogenesis in guinea pigs caused an increase in the incidence of microencephaly. However, in general, thresholds and dose-response relationships vary between species and even between different strains of the same species, depending on genotype. This precludes rigorous quantitative extrapolation to humans, although some general principles can be inferred. In humans, epidemiological studies suggest that an elevation of maternal body temperature by 2°C for at least 24 h during fever can cause a range of developmental defects, but there is little information on thresholds for shorter exposures. Further experimental and epidemiological studies are recommended, focusing on stage-specific developmental effects in the central nervous system using a variety of sensitive assays.     

Effects of Rauscher leukemia virus infection on BALB/c mouse embryos.

The effects of Rauscher leukemia virus (R-MuLV) infection on BALB/c mouse embryos were described. In mice infected with R-MuLV 12 days before mating, there were no embryos 8 days after possible conception, whereas in those infected either 8 days or 1 day before mating, pregnancy was established. The most striking effect of R-MuLV infection on the microscopic properties of the embryos was vast "apoptosis" in the mesoderm. The XC test with trypsinized embryo cells showed numerous polykaryons, which suggested that active leukemia virus was present in the embryonal tissue. Indirect immunofluorescence studies with specific rabbit antiserum to R-MuLV demonstrated the presence of virus antigens in the embryonal tissue. Vast immunofluorescence was also found in trophoblastic cells and embryonal membranes. We concluded that R-MuLV in BALB/c mice was transmitted from mother to embryo through the placenta and thereby caused excessive cell death, especially in the mesoderm.     

甲醛和苯联合染毒对小鼠胚胎的影响

目的： 研究甲醛和苯联合染毒对小鼠胚胎发育的影响。方法：将昆明孕鼠随机分为4组,每组10只。胚胎植入后进行不同浓度的甲醛和苯联合染毒,分别为对照组 (甲醛0 mg/m3、苯0 mg/m3)、低剂量组[甲醛 (0.10±0.01) mg/m3、苯 (0.11±0.01) mg/m3]、中剂量组[甲醛 (5.00±0.30) mg/m3、苯 (5.50±0.40) mg/m3]、高剂量组[甲醛 (10.00±0.50) mg/m3、苯 (11.00±0.50) mg/m3],每天染毒2 h,持续15 d。观察孕鼠一般情况,记录其生产情况及24 h存活仔鼠数目;称量仔鼠体质量、肝脏质量;并提取仔鼠肝脏总RNA,采用RT-PCR检测肝细胞中细胞周期调控基因Cdk2、CyclinE、Cdk7、CyclinH的表达情况。结果：高剂量组孕鼠平均体质量低于其余各组 (P<0.05),孕鼠、流产孕鼠数高于其他各组 (P<0.05),此外,高剂量组孕鼠产仔数及24 h存活仔鼠数也低于其他剂量组,差异均具有统计学意义 (P<0.05)。细胞周期调控基因Cdk2在中剂量组、高剂量组的表达高于对照组与低剂量组,CyclinE在高剂量组的表达高于其余各组,差异具均有统计学意义 (P<0.05)。Cdk7、CyclinH在各组中表达的差异均无统计学意义 (P>0.05)。结论：小鼠胚胎植入后,甲醛和苯联合可导致流产增加及胎鼠存活率降低,并引起仔鼠肝细胞中细胞周期调控异常。     

Effects of heat stress on cognitive performance: the current state of knowledge.

This paper discusses the current state of knowledge on the effects of heat stress on cognitive performance. Although substantial research has been performed, it has proven difficult to describe the literature findings in a systematic manner. This is due to the large number of factors that come into play, such as task type, exposure duration, skill and acclimatization level of the individual and due to the absence of a concise theory on which experimental work can be based. However, two trends have been identified. First, heat stress affects cognitive performance differentially, depending on the type of cognitive task. Secondly, it appears that a relationship can be established between the effects of heat stress and deep body temperature. A number of exposure limits have been proposed during the last decades. These limits are summarized in this paper, with a special emphasis on the most recent one derived by Hancock and Vasmatzidis. This limit, which employs an attentional resource approach, defines exposure duration thresholds as parallel lines. Although this approach appears to be the most promising thus far, it is concluded that much remains to be understood before a limit becomes universally acceptable.     

Effects on the expression of heat shock proteins by step-down heating and hypothermia in rat hepatoma cells with a different degree of heat sensitivity.

Thermosensitization induced by pretreatment at supra- and subnormal temperatures, rate of protein synthesis and expression of the major heat shock proteins under such conditions was investigated in relation to intrinsic heat sensitivity of rat hepatoma cells, i.e. Reuber H35 and HTC. The high degree of heat susceptibility of H35 cells was reflected by a high degree of thermosensitization after pretreatment by heat (step-down heating) at temperatures of 42-44 degrees C for 30 min or cold for 16 h at temperatures ranging from 0 to 25 degrees C. Sensitization under step-down heating conditions was found to be paralleled by a delayed recovery of protein synthesis. Despite an increased relative rate, enhancement of the absolute rate of synthesis of the major heat shock proteins, HSP28, HSP60, HSP68, HSP70, HSP84 and HSP100, was less pronounced during step-down exposure. Comparable results were obtained during recovery of sensitized H35 cells at 37 degrees C after exposure to heat following pretreatment at 0 degrees C. Furthermore, clear differences in the regulation of the specific HSP synthesis, depending on the particular treatment protocol, were observed.     

Effects of heat on mouse spermatogenesis monitored by flow cytometry

The effects of heat on mouse spermatogenesis have been determined using both testis weight and flow cytometrically determined DNA content distribution as experimental end-points. Temperatures of 38-42 degrees C and exposure times of 20-60 min have been tested. The results concerning the testis weight substantially confirm those reported by other authors (Hand et al. 1979). The measurement of DNA content distributions shows a relatively higher depletion, 14 days after treatment, of the cytometric compartment containing elongated spermatids in respect to that containing round spermatids. The analysis of the cytotoxic effects, monitored 14 vs. 28 days after treatment, as a function of the exposure time at a given temperature, or of the temperature for a fixed exposure time, indicates that, in the course of spermatogenesis, late spermatocytes are more sensitive to heat than differentiated spermatogonia. Following the approach based on flow cytometry, the effect of exposures as low as 20 min at 38 degrees C can be appreciated.     

Effects of heat on mouse spermatogenesis monitored by flow cytometry

The effects of heat on mouse spermatogenesis have been determined using both testis weight and flow cytometrically determined DNA content distribution as experimental end-points. Temperatures of 38–42°C and exposure times of 20–60 min have been tested. The results concerning the testis weight substantially confirm those reported by other authors (Hand et al. 1979). The measurement of DNA content distributions shows a relatively higher depletion, 14 days after treatment, of the cytometric compartment containing elongated spermatids in respect to that containing round spermatids. The analysis of the cytotoxic effects, monitored 14 vs. 28 days after treatment, as a function of the exposure time at a given temperature, or of the temperature for a fixed exposure time, indicates that, in the course of spermatogenesis, late spermatocytes are more sensitive to heat than differentiated spermatogonia. Following the approach based on flow cytometry, the effect of exposures as low as 20 min at 38°C can be appreciated.     

Effects of heat and other agents on amino acid uptake in Escherichia coli

In Escherichia coli K1060 grown at 37°C we observed that the uptake of both L-[³H]leucine and L-[³⁵S]methionine was inhibited by exposure of the cells to 48°C. The calcium channel Mockers diltiazem and verapamil, and the anti-arrhythmic agent quinidine, inhibited the uptake of L-[³H]leucine at both 37°C and 48°C. Verapamil also inhibited the uptake of L-[³⁵S]methionine at 37°C, but at 48°C protected against some of the heat-induced decrease in the uptake of this amino acid. The local anaesthetic procaine markedly inhibited the uptake of both labelled amino acids at temperatures between 37°C and 48°C. Amino acid uptake and cell killing were not correlated.     

Effects of heat and other agents on amino acid uptake in Escherichia coli

In Escherichia coli K1060 grown at 37 degrees C we observed that the uptake of both L-[3H]leucine and L-[35S]methionine was inhibited by exposure of the cells to 48 degrees C. The calcium channel blockers diltiazem and verapamil, and the anti-arrhythmic agent quinidine, inhibited the uptake of L-[3H]leucine at both 37 degrees C and 48 degrees C. Verapamil also inhibited the uptake of L-[35S]methionine at 37 degrees C, but at 48 degrees C protected against some of the heat-induced decrease in the uptake of this amino acid. The local anaesthetic procaine markedly inhibited the uptake of both labelled amino acids at temperatures between 37 degrees C and 48 degrees C. Amino acid uptake and cell killing were not correlated.     

Effects of mammalian in utero heat stress on adolescent body temperature

Abstract

In utero hyperthermia can cause a variety of developmental issues, but how it alters mammalian body temperature during adolescence is not well-understood. Study objectives were to determine the extent to which in utero hyperthermia affects future phenotypic responses to a heat load. Pregnant first parity pigs were exposed to thermal neutral (TN) or heat stress (HS) conditions during the entire gestation. Of the resultant offspring, 12 were housed in TN conditions, and 12 were maintained in HS conditions for 15 days. Adolescent pigs in HS conditions had increased rectal temperature and respiration rate (RR) compared to TN pigs, regardless of gestational treatment. Within the HS environment, no gestational difference in RR was detected; however, GHS pigs had increased rectal temperature compared to GTN pigs. As rectal temperature increased, GTN pigs had a more rapid increase in RR compared to the GHS pigs. Adolescent HS decreased nutrient intake, and body weight gain, but neither variable was statistically influenced by gestational treatments. In summary, in utero HS compromises the future thermoregulatory response to a thermal insult.     

Effects of pH on heat sensitization of mammalian cells with procaine hydrochloride

The enhancement of heat killing of CHO cells by treatment with 7 mM procaine HCl increased when cells were treated under alkaline conditions. Below a pH of 6.9, very little heat sensitization was observed; however, as the pH was increased to 7.4 and above, considerable heat sensitization occurred. There were no changes in intracellular pH at the beginning of heating that could be responsible for this phenomenon.     

Response of tumour-related and normal lymphocytes to antigens on fibroblasts from embryos of varying age.

The in vitro cytotoxic immune response of spleen lymphocytes from primiparous and tumour-related mice to embryonic cells from embryos of varying age and tumour cells has been investigated. The results indicate that lymphocytes from both primiparous and tumour-related (i.e., tumour-bearing or tumour-excised) animals give a response which is greater than that from cells from control mice ("virgin cells"). Moreover, in this putative anamnestic response the immune cells detect antigenic differences in the cell populations of embryos of varying age, which are not as readily demonstrable when cytotoxicity is derived from virgin cells. As a further indication of the in vivo priming to embryo-assoicated antigens, the data show that the precursors of cytotoxic cells apparently undergo a blastogenic response in the presence of embryo antigen, and revert to small quiescent cells when antigen is removed, in a way entirely analogous to that described for reactivity of mixed leucocyte cultures to antigens of the major histocompatibility complex. Finally, it seems that in animals immediately after removal of embryonic antigen (and to a lesser degree in virgin or late-embryo-immune mice) there exists a suppressor cell population which inhibits an anti-embryo cytotoxic response far more than an antiallograft response.     

热休克蛋白gp96对巨噬细胞功能的影响

背景与目的:热休克蛋白(heatshockprotein,HSP)gp96在抗原递呈和肿瘤特异性免疫治疗中具有重要作用,但其对巨噬细胞的作用机制尚待深入研究。本研究旨在探讨HSPgp96对小鼠腹腔巨噬细胞(peritonealelicitedmacrophages,PEMφ)功能的影响。方法:应用激光扫描共聚焦显微术,结合特异性荧光探针Fluo3-AM、DAF-FM-DA和H2DCF-DA,检测在HSPgp96作用下,腹腔巨噬细胞内钙离子(Ca2 )、一氧化氮(NO)和活性氧(ROS)的动态变化,并用荧光标记技术检测小鼠腹腔巨噬细胞MHCⅡ及CD86的表达强度和分布的变化。结果:小鼠腹腔巨噬细胞受HSPgp96刺激后,细胞内Ca2 、NO和ROS的生成量都快速升高,分别在刺激后30s、80s和580s时达峰值,增幅分别为(161.06±70.99)%、(77.58±31.17)%和(647.28±185.70)%。小鼠腹腔巨噬细胞受HSPgp96刺激后MHCⅡ阳性表达率:对照组为(40.9±3.5)%,HSPgp96(60mg/L)组为(61.8±5.1)%;CD86阳性表达率:对照组为(23.1±3.1)%,HSPgp96(60mg/L)组为(54.9±2.0)%。结论:HSPgp96在体外可使小鼠腹腔巨噬细胞内Ca2 、NO及ROS生成量明显增加;使抗原递呈分子MHCⅡ、CD86的表达明显上调。     

Effects of heat stress on cognitive performance: the current state of knowledge

This paper discusses the current state of knowledge on the effects of heat stress on cognitive performance. Although substantial research has been performed, it has proven difficult to describe the literature findings in a systematic manner. This is due to the large number of factors that come into play, such as task type, exposure duration, skill and acclimatization level of the individual and due to the absence of a concise theory on which experimental work can be based. However, two trends have been identified. First, heat stress affects cognitive performance differentially, depending on the type of cognitive task. Secondly, it appears that a relationship can be established between the effects of heat stress and deep body temperature. A number of exposure limits have been proposed during the last decades. These limits are summarized in this paper, with a special emphasis on the most recent one derived by Hancock and Vasmatzidis. This limit, which employs an attentional resource approach, defines exposure duration thresholds as parallel lines. Although this approach appears to be the most promising thus far, it is concluded that much remains to be understood before a limit becomes universally acceptable.