三种水产药物对近江牡蛎(Crassostrea ariakensis)的影响

用3种水产药物硫酸铜、孔雀石绿、甲醛分别设置浓度梯度,对正常和天然患病近江牡蛎进行处理,连续观察7d,发现3种药物对正常近江牡蛎的影响强度为孔雀石绿〉甲醛〉硫酸铜。对患病近江牡蛎的致死率显著高于对正常近江牡蛎的致死率,即使用同一药物的更低浓度处理患病近江牡蛎,其死亡率也显著高于更高浓度处理的正常近江牡蛎的死亡率。在患病近江牡蛎药物处理实验中,对照组有明显死亡,但死亡率低于药物处理组。实验结果表明水产药物残留对近江牡蛎,特别是对患病近江牡蛎有较大影响,会导致其死亡率明显上升,这也可能是引起近江牡蛎大规模死亡的原因之一。     

短期高温对梨小食心虫成虫存活率和适应性的影响（英文）

【目的】梨小食心虫Grapholita molesta （Busck）（鳞翅目：卷蛾科）是一种世界性的害虫,能使蔷薇科的果树严重减产。本研究旨在评估此害虫的耐热性及适应性。【方法】将梨小食心虫成虫暴露在不同温度（36, 38, 40, 42, 44 和46℃）和不同暴露时间（0.5, 1, 2, 4和8 h）下,测定其存活率以及短期高温（38或40℃热驯化1 h）对其热耐受力、寿命、生殖力及卵孵化率的影响。【结果】随着高温暴露时间的延长,梨小食心虫成虫存活率下降。在38或40℃热驯化1 h后,能显著提高梨小食心虫成虫在42℃下2 h的存活率（P<0.05）。在41℃处理1 h,梨小食心虫出现热休克现象,其寿命显著延长,但产卵量显著下降。进一步的试验证明雄虫受高温影响较大,导致与其配对后的雌虫产卵量降低。然而,不论亲代受到怎样的热刺激,其后代的孵化率均不受影响。【结论】结果说明,超过41℃,1 h的高温能对梨小食心虫带来负面影响,但梨小食心虫成虫有适应高温的潜力。     

短时间高温处理对棉蚜存活的影响

为探索棉蚜Aphis gossypii Glover种群动态与高温的关系,研究了不同温度(30、34、38、42、46℃)、不同处理时间(1、2、5、8h)对棉蚜存活的影响。结果表明:在同一处理时间条件下,棉蚜的存活率随着温度的升高而降低;在同一处理温度下,棉蚜的存活率随处理时间的延长而降低。30～38℃温度范围内,棉蚜存活率降低缓慢,从42℃开始棉蚜的存活率迅速降低。棉蚜半数致死温度随着处理时间的延长而降低;相同处理时间条件下,若蚜半数致死温度高于成蚜,若蚜较成蚜更耐高温。     

短时高温对莲草直胸跳甲成虫存活及繁殖的影响

采用短时高温处理研究了40～47℃高温对莲草直胸跳甲Agasicles hygrophila Selma & Vogt成虫存活以及40～44℃对雌成虫繁殖的影响。结果表明:(1)处理1h后,随着温度的上升,莲草直胸跳甲雌雄成虫的存活率均随着温度的上升而下降,44℃时,雌成虫的存活率开始显著高于雄成虫;处理温度为40℃时,雌雄成虫存活率也随着处理时间的延长而下降,7h时,雌成虫的存活率开始显著高于雄成虫。此外,雌成虫致死90%的温度和时间分别高于雄成虫1.31℃和1.29h,均表明雌成虫的耐热能力比雄成虫强,但差异仅在胁迫强度偏大时表现为显著;(2)40～44℃短时高温影响莲草直胸跳甲成虫的繁殖。与对照处理相比,40、42和44℃高温处理1h后,雌成虫的寿命和产卵量变化不显著,但均引起了其产卵前期的延长和10日龄成虫产卵停滞,44℃时,平均停滞时间达2.62d,子代卵的孵化率则从40℃的88.67%下降到44℃的79.84%,44℃时显著低于对照。     

温度胁迫下越冬松针瘿蚊(Thecodiplosis japonensis)幼虫的生理生化机制(英文)

松针瘿蚊是韩国林业爆发性害虫,以 ３龄老熟幼虫在地表越冬。经冷休克（－１０ ℃和－５ ℃）和热休克（３７℃、４０℃和４５℃）处理的越冬幼虫与正常幼虫具有相同的过冷却点,保持在－２０℃左右。温度胁迫可以提高对亚致死温度（－１５℃、３ ｈ）的耐受性。对于存活率的提高,冷休克处理比热休克处理更有效。这是冷热休克能同时提高虫体亚致死温度的耐受性的第三例报道。在冷休克（－１０℃）和热休克（４０℃和４５℃）处理后,老熟幼虫表达一种特异的胁迫蛋白,分子量为 ８３ ｋＤ。本文还研究了温度胁迫对越冬老熟幼虫体内酶促与非酶促抗氧化系统的影响。温度胁迫使老熟幼虫产生氧化胁迫,而快速冷耐受（ｒａｐｉｄ ｃｏｌｄｈａｒａｅｎｉｎｇ）处理,由于体内谷胱甘肽含量的提高以及谷胱甘肽还原酶活性的增高,使之不发生氧化胁迫反应。     

短时高温对意大利蝗存活和生殖的影响

【目的】明确短时高温对意大利蝗Calliptamus italicus(L.)存活和生殖的影响,为气候变暖趋势下意大利蝗灾害的预测预报及综合防治提供理论依据。【方法】采集初羽化24h内的意大利蝗雌雄成虫,于30℃光照培养箱中饲养。设置4个温度处理组,分别为33、36、39、42℃,每日处理4h,之后放回30℃光照培养箱中继续饲养。未经过短时高温处理的意大利蝗为对照组。观察记录各组意大利蝗存活率、寿命、产卵前期、产卵期、单雌产卵量、卵巢发育情况及卵巢中卵黄蛋白含量,并分析变化规律。【结果】短时高温对意大利蝗成虫存活率无显著影响,但对其寿命有显著影响(P0.01),其中33℃处理4h,意大利蝗雌雄成虫寿命显著延长(P0.01),而36~42℃范围内处理4h,意大利蝗雌雄成虫寿命显著缩短(P0.01)。短时高温对意大利蝗产卵前期有显著影响(P0.05),随温度升高,产卵前期缩短,但对产卵期没有显著影响(P0.05)。短时高温对意大利蝗单雌产卵量有显著影响(P0.01),其中33℃处理组单雌产卵量为(57.6±2.4)粒,显著高于对照组(P0.01),36~42℃范围内,随温度升高单雌产卵量显著降低(P0.01)。短时高温对意大利蝗卵巢长度、鲜重及发育历期有显著影响(P0.01),但对卵巢宽度没有显著影响(P0.05),且随温度升高,卵巢长度、宽度、鲜重及发育历期均呈下降趋势。短时高温可使卵黄蛋白在卵巢中提前沉积,并对其含量(峰值)有显著影响(P0.01),其中33℃处理组卵黄蛋白含量(峰值)为(49.795±6.253)mg/mL,显著高于对照组(P0.01),36~42℃范围内处理4h,卵黄蛋白含量(峰值)显著减少(P0.01)。【结论】33℃处理4h,意大利蝗存活及生殖特性显著提高,而36℃及以上高温对意大利蝗生长繁殖产生不利影响。     

麻醉对大鼠应激反应的影响

用40、42、44℃分别处理清醒状态和麻醉状态大鼠30min,于正常饲养条件下恢复24h后,检测其肝脏热休克蛋白70（HSP70）的表达差异及酸性和中性蛋白水解酶活性变化。结果表明,当热休克温度为40-44℃时,清醒状态大鼠肝脏的HSP70合成能力逐渐下降,而麻醉大鼠肝脏HSP70合成能力逐渐增加,在42℃热休克条件下,麻醉状态大鼠肝脏的酸性蛋白水解酶活性最强,在44℃热休克条件下,清醒状态大鼠肝脏的酸性蛋白水解酶活性最强,在40-44℃热休克条件下,麻醉状态和清醒状态大鼠肝脏的45kD中性蛋白水解酶活性与对照相似,但40kD的中性蛋白水解酶活性随热休克温度升高而降低,另外,40℃热休克诱导麻醉状态大鼠肝脏出现一个高活性的35kD中性蛋白水解酶,根据实验结果推测,麻醉状态大鼠肝脏的热耐受性大于清醒大鼠,大鼠的热休克反应受整体水平和细胞水平的双重调控,并涉及除HSP70合成以外的其他生化活动。     

稻纵卷叶螟幼虫驯化产生的热适应能力的继代效应

摘要: 【目的】在全球不断变暖背景下,昆虫受到热胁迫的频率不断增加。短期内反复受到热胁迫会使昆虫产生热适应性,但是昆虫热驯化所产生的耐热能力的传代效应还不完全清楚。稻纵卷叶螟Cnaphalocrocis medinalis是水稻上的重要害虫,对其幼虫在特定温度下进行几代热锻炼可提高其对高温的适应能力。本研究旨在摸清稻纵卷叶螟热适应的传代能力,为在全球变暖形势下以温度因子预测其种群发展趋势提供指导。【方法】将实验室内分别经39℃和41℃连续锻炼30代建立的稻纵卷叶螟热锻炼品系HA39和HA41以及非锻炼品系HA27的1-5龄期幼虫在不同温度(36℃和41℃)下进行不同时长(1~144 h)的暴露处理,调查幼虫的存活率,确定热锻炼品系幼虫的耐热能力;采用两品系间杂交实验测定HA39和HA27各交配组合的繁殖力及后代3龄幼虫的耐热能力;对HA39停止高温锻炼,并测定停止锻炼2代后3龄幼虫的耐热能力。【结果】稻纵卷叶螟3龄幼虫经历多代次短期热锻炼不仅可提高该龄幼虫的高温适应力,而且可提高其他龄期幼虫对特定高温的耐受能力,表现为HA39和HA41在36或41℃下处理特定时长的存活率显著高于HA27。锻炼高温的不同,幼虫获得的热耐受能力也有差异。39℃下锻炼可提高4龄幼虫在36℃下暴露2和4 d以及5龄幼虫在41℃下暴露5和6 h时的存活率,但41℃下锻炼则不可。HA39和HA27的自交及杂交后代的繁殖力之间均无显著差异,杂交后代3龄幼虫在41℃下处理5和6 h时的存活率与HA39自交后代的相当,并且显著高于HA27自交后代的,幼虫通过热锻炼获得的耐热能力可从亲本遗传给后代。停止热锻炼2代后,在39℃下处理4 h时HA39 3龄幼虫的存活率显著高于HA27的,但39℃下其余处理时间以及36和41℃下处理1~7 h HA39 3龄幼虫的存活率均与HA27的无显著差异,表明幼虫热锻炼产生的耐热能力在停止锻炼后2代仍可部分保持。【结论】稻纵卷叶螟幼虫的热适应能力具有继代效应。经过长期的气候变暖适应后,稻纵卷叶螟种群的热适应能力很可能在不断增强,从而夏季高温对其种群的抑制作用减弱,其种群暴发频率增加。     

热休克预处理对TNF-α诱导的RAW264.7巨噬细胞迁移的影响

热休克反应是机体中一个重要的内源性保护机制,但其对TNF-α诱导的单核/巨噬细胞迁移有无影响目前尚不清楚.采用酶联免疫吸附实验观察TNF-α(20μg/L)刺激RAW264.7巨噬细胞4h后炎症因子IL-1β、IL-6、IL-15的表达情况;Western blot验证热休克预处理诱导热休克蛋白表达的增加;利用细胞趋化实验观察热休克预处理(42℃,1h)对TNF-α所致巨噬细胞迁移的影响.研究发现,TNF-α可明显促进RAW264.7细胞株中IL-1β、IL-6、IL-15等炎症因子的释放;热休克预处理诱导热休克蛋白HSP70、HSP90、HSP25表达增加;细胞趋化实验发现TNF-α处理的RAW264.7细胞迁移能力较正常对照组明显增强,而热休克预处理组巨噬细胞的迁移能力较单纯TNF-α处理组明显减弱.上述结果表明,热休克预处理抑制TNF-α所致巨噬细胞的迁移.     

近江牡蛎吊养养成技术标准

近江牡蛎是我国重要的养殖经济贝类,其养殖历史约两个世纪,但是,一直缺乏该牡蛎的养殖技术规范(标准)。为了近江牡蛎优质高产,特制定了该牡蛎吊养技术标准。该标准由以下几个方面组成:养殖条件,包括养殖环境、海水温度范围(6-32℃)、海水深度(低潮线以下2-8m)、盐度(8‰-30‰),吊养设施结构,吊养方法,饲养过程中的管理和起捕条件与方法等等。     

Heat shock protein (hsp70) expression and thermal tolerance in sublethally heat-shocked eastern oysters Crassostrea virginica infected with the parasite Perkinsus marinus

To investigate whether sublethal heat shock protects Perkinsus marinus (Dermo)-infected oysters Crassostrea virginica from lethal heat stress, and the effects of P. marinus infection on sublethal heat shock response, oysters were first experimentally challenged with P. marinus. Then, when infections in oysters progressed to moderate levels (parasite burden = 10(4) to 10(5) cells g(-1) wet tissue weight), oysters were treated with a sublethal heat shock at 40 degrees C for 1 h (heat shock + Dermo challenge). Other treatment groups included heat-shocked, unchallenged (non-P. marinus challenged) oysters and non-heat-shocked, P. marinus-challenged and -unchallenged oysters. Thermal tolerance was compared among these treatments by administering a lethal heat treatment at 44 degrees C for 1 h, 7 d after sublethal heat shock. Sublethal heat shock enhanced survival to lethal heat treatment in both P. marinus-challenged and -unchallenged oysters. Although levels of hsp70 isoforms (hsp69 and hsp72) did not vary significantly by heat shock or infection with P. marinus, responses due to these treatments were apparent when comparing hsp70 levels within infected and uninfected oysters. Infection enhanced expression of hsp69, regardless of whether oysters were heat shocked or not. In uninfected oysters, hsp72 increased due to heat shock 2 and 7 d post heat shock. Overall, this study demonstrates that heat shock can improve survival in oysters, even in oysters infected with P. marinus. Expression of hsp70 varied among isoforms after sublethal and lethal heat shocks and in infected and uninfected oysters. The heat shock response was not negatively affected by P. marinus infection.     

Synergistic impacts of heat shock and spawning on the physiology and immune health of Crassostrea gigas: an explanation for summer mortality in Pacific oysters

Mass mortality is often observed in cultured oysters during the period following spawning in the summer season. To examine the underlying causes leading to this phenomenon, thermotolerance of the Pacific oyster Crassostrea gigas was assessed using pre- and postspawning oysters that were sequentially treated with sublethal (37 degrees C) and lethal heat shocks (44 degrees C). The effects were examined on a range of immune and metabolic parameters in addition to mortality rate. A preventative 37 degrees C significantly reduced oyster mortality after exposure to a second heat shock of 44 degrees C, but in postspawning oysters mortality remained at 80%, compared with < 10% in prespawning oysters. Levels of the 72 kDa and 69 kDa heat shock proteins were low in the gill tissue from postspawning oysters stimulated by heat shock, indicating spawning reduced heat shock protein synthesis. The postspawning oysters had depleted glycogen stores in the mantle tissue and reduced adenylate energy charge after heat shock, indicative of lower energy for metabolic activity. A cumulative effect of spawning and heat shock was observed on the immunocompetence of oysters, demonstrated by reduced hemocyte phagocytosis and hemolymph antimicrobial activity. These results support the hypothesis that the energy expended during reproduction compromises the thermotolerance and immune status of oysters, leaving them easily subject to mortality if heat stress occurs in postspawning stage. This study improves our understanding of oyster summer mortality and has implications for the long-term persistence of mollusks under the influence of global warming.     

Acquisition of thermotolerance in bay scallops, Argopecten irradians irradians, via differential induction of heat shock proteins

Many cells and organisms are rendered transiently resistant to lethal heat shock by short exposure to sublethal temperatures. This induced thermotolerance is thought to be related to increased amounts of heat shock proteins (HSPs) which, as molecular chaperones, protect cells from stress-induced damage. As part of a study on bivalve stress and thermotolerance, work was undertaken to examine the effects of sublethal heat shock on stress tolerance of juveniles of the northern bay scallop, Argopecten irradians irradians, in association with changes in the levels of cytoplasmic HSP70 and 40. Juvenile bay scallops heat-shocked at a sublethal temperature of 32 °C survived an otherwise lethal heat treatment at 35 °C for at least 7 days. As determined by ELISA, acquisition of induced thermotolerance closely paralleled HSP70 accumulation, whereas HSP40 accrual appeared less closely associated with thermotolerance. Quantification of scallop HSPs following lethal heat treatment, with or without conditioning, suggested a causal role for HSP70 in stress tolerance, with HSP40 contributing to a lesser, but significant extent. Overall, this study demonstrated that sublethal heat shock promotes survival of A. irradians irradians juveniles upon thermal stress and the results support the hypothesis that HSPs have a role in this induced thermotolerance. Exploitation of the induced thermotolerance response shows promise as a means to improve survival of bay scallops in commercial culture.     

Acute heat stress protects rats against endotoxin shock.

The purpose of this study was to determine 1) whether prior (24-h) heat stress could render rats cross-resistant to the lethal activity of bacterial lipopolysaccharide (LPS) and 2) whether this acquired state of resistance is associated with endotoxemia during the heat stress event. Four groups (n = 7/group) of rats were examined: 1) saline treated, 2) LPS treated, 3) heat stressed and saline treated, and 4) heat stressed and LPS treated. Saline or LPS (Escherichia coli, serotype 0111:B4, 20 mg/kg body wt) was given intravenously 24 h after exposure to heat (ambient temperature 47-50 degrees C, relative humidity 30%) for heat-stressed rats and at the same time of day for nonheated rats; survival was monitored for 48 h. Thermal responses were similar (P > 0.05); values for maximum core temperature (Tc) and time above Tc of 40 degrees C were 42.7 +/- 0.1 and 42.6 +/- 0.1 degrees C (SE) and 44.0 +/- 2.1 and 47.9 +/- 3.7 (SE) min for the heat-stressed saline-treated and heat-stressed LPS-treated rats, respectively. Administration of LPS to nonheated rats resulted in 71.4% (5 of 7 rats) lethality. In contrast, all (7 of 7) rats subjected to a single nonlethal heat stress event 24 h before LPS treatment survived (P < 0.05). Endotoxin was not detected in arterial plasma immediately after heat stress in rats (n = 6) exposed to a Tc of 42.9 +/- 0.1 degrees C. These findings demonstrate that acute heat stress can protect rats from the lethal activity of LPS.     

Induced thermotolerance and tissue Hsc70 in juvenile coho salmon, Oncorhynchus kisutch

We examined Hsc70 in gill, liver and caudal fin from coho salmon ( Oncorhynchus kisutch ) before (ambient, ~12 °C) and after a sublethal heat shock of 25 °C for 1 h. Increased levels were observed for at least 48 h in all three tissues. Attempts to demonstrate isoforms of this heat-shock protein were not successful using four different antibodies. However, one of these antibodies recognized isoforms in brine shrimp and oysters, two organisms in which the heat-shock response has been well characterized. Extracts of those organisms and coho salmon tissues were run on the same gels and evaluated on the same Western blots, at the same time. We believe that our results provide a reliable account of Hsc70 in these fish under these conditions. Limited experiments showed that induced thermotolerance was achieved in these coho salmon, lasting for about 1 week after the sublethal heat shock. These data suggest that increased levels of Hsc70 are correlated with induced thermotolerance in these fish.     

Induction of heat shock proteins by canavanine in Tetrahymena. No change in ATP levels measured in vivo by NMR

During induction of the heat shock response by temperature jump in the protozoan Tetrahymena, a decrease in cellular ATP levels occurs within minutes and cells become thermotolerant. Treatment of Tetrahymena with the amino acid analog canavanine also induces synthesis of heat shock proteins, but more slowly than by temperature jump. No changes in cellular ATP levels were observed during the course of canavanine induction of heat shock protein synthesis measured in vivo by the technique of 31P NMR spectroscopy. Tetrahymena do not become thermotolerant following induction of heat shock protein synthesis with canavanine. However, Tetrahymena will develop thermotolerance in the presence of canavanine if they are first subjected to a nonlethal temperature jump before exposure to a normally lethal temperature.     

Kinetics of thermally induced heat shock protein 27 and 70 expression by bone marrow-derived mesenchymal stem cells

Although bone marrow-derived mesenchymal stem cells (MSCs) are an attractive cell therapy candidate, their potential is limited by poor survival following transplantation. Over-expression of anti-apoptotic heat shock proteins using viral vectors can improve the survival of these cells under stressful conditions in vitro and in vivo. It is also possible to induce heat shock protein expression in many cell types by simply exposing them to a transient, nonlethal elevation in temperature. The response profile of MSCs to such a thermal stress has not yet been reported. Therefore, this study sought to determine the kinetics of thermally induced heat shock protein expression by MSCs in vitro. To determine if heat shock protein expression was a function of thermal stress exposure time, MSCs were exposed to 42°C for 15, 30, 45, and 60 min and were harvested 24 h later. To establish the time-course of heat shock protein expression, MSCs were heat shocked for 60 min and harvested 2, 24, 48, 72, 96, and 120 h later. The cells were then analyzed for Hsp27 and Hsp70 expression by Western blot. Densitometric analysis revealed that exposure to a thermal stress induced expression of both Hsp27 and Hsp70 and that the level of expression was dependant on stress exposure time. Following 60 min of heat stress, both Hsp27 and Hsp70 accumulated maximal expression after 48 h with both proteins returning to constitutive expression levels by 120 h. This study demonstrates that heat shock protein expression can be induced in MSCs by a simple thermal stress.