Skin Sensitization in School Children in Northern and Southern Norway

It has been suggested that environmental exposures and living conditions can explain some of the worldwide variation in atopic disorders. Norway has large environmental contrasts within the country. We compared skin prick sensitization rates among school children living in the southern subarctic and in the northern artic part of Norway. Approximately one quarter of the children were sensitized, mostly against pollen and animal dander, while mite and mould sensitization seemed to be a minor problem. Sensitization rates and profiles were similar in the north and south despite differences in living conditions and environmental exposures.     

Unraveling toxicological mechanisms and predicting toxicity classes with gene dysregulation networks

The use of genes for distinguishing classes of toxicity has become well established. In this paper we combine the reconstruction of a gene dysregulation network (GDN) with a classifier to assign unseen compounds to their appropriate class. Gene pairs in the GDN are dysregulated in the sense that they are linked by a common expression pattern in one class and differ in this pattern in another class. The classifier gives a quantitative measure on this difference by its prediction accuracy. As an in‐depth example, gene pairs were selected that were dysregulated between skin cells treated with either sensitizers or irritants. Pairs with known and novel markers were found such as HMOX1 and ZFAND2A, ATF3 and PPP1R15A, OXSR1 and HSPA1B, ZFP36 and MAFF. The resulting GDN proved biologically valid as it was well‐connected and enriched in known interactions, processes and common regulatory motifs for pairs. Classification accuracy was improved when compared with conventional classifiers. As the dysregulated patterns for heat shock responding genes proved to be distinct from those of other stress genes, we were able to formulate the hypothesis that heat shock genes play a specific role in sensitization, apart from other stress genes. In conclusion, our combined approach creates added value for classification‐based toxicogenomics by obtaining novel, well‐distinguishing and biologically interesting measures, suitable for the formulation of hypotheses on functional relationships between genes and their relevance for toxicity class differences. Copyright © 2012 John Wiley & Sons, Ltd.     

Continuing Education for Forest Managers

Changing community attitudes are leading to a wider acceptance of the need for continuing education. Universities offering professional degree courses have a responsibility for continuing education in the subject-areas covered by their undergraduate curricula, which could be discharged in one or more ways, e.g. short refresher courses to keep practitioners abreast of developing theory and practice, or longer recurrent study programs leading to further formal qualifications. However the responsibility for continuing education must be shared by employing agencies and professional societies. The Institute of Foresters in particular should be concerned with ensuring that adequate opportunities exist for further education of its corporate membership. The needs and likely demands of foresters for continuing education are considered, and suggestions outlined for future developments.     

An Experimental Model of Heat Storage in Working Firefighters

Objective. Develop experimental models to study uncompensable heat stress (UCHS) in working firefighters (FFs). Methods. FFs ingested core temperature (Tc) capsules prior to performing sequential tasks in 40°C andpersonal protective ensemble (PPE), or 18°C andno PPE. Both trials were conducted in an environmental chamber with FFs using self-contained breathing apparatus (SCBA). Results. FFs exercising in heat andPPE reproduced UCHS conditions. For every FF in both trials for whom the capsules worked, Tc was elevated, andTc_max occurred after completion of study protocol. Trials with PPE resulted in a mean maximum temperature of 38.94°C (± 0.37°C); Tc_max reached 40.4°C. Without PPE, maximum Tc averaged 37.79°C (± 0.07°C). Heat storage values ranged from 131 to 1205 kJ, averaging 578 kJ (± 151.47kJ) with PPE and210.83 kJ (± 21.77kJ) without PPE. Conclusions. An experimental model has been developed that simulates the initial phases of an interior fire attack to study the physiology of UCHS in FF. The hot environment andPPE increase maximum Tc andheat storage over that due to the exertion required to perform the tasks andmay decrease time to volitional fatigue. This model will permit controlled studies to optimize work-rest cycles, rehab conditions, andphysical conditioning of FFs.     

高温及游泳对腹腔巨噬细胞的影响

我们采用电子显微镜等技术研究了高温及游泳对SD大鼠腹腔巨噬细胞超微结构和功能的影响。结果表明外界高温(40℃)能使大鼠体温急剧升高(Y=0.05074+37.92),游泳时间明显缩短(P<0.01),显著抑制巨噬细胞变形、游走及吞噬能力,促进巨噬细胞出现空泡变性,游泳能加重上述变化。在受热后24h,巨噬细胞吞噬能力基本恢复,而空泡变性无明显改变。     

严重创伤早期大鼠下丘脑HSP70与iNOS表达与分布的时效关系

目的研究严重创伤早期大鼠下丘脑热休克蛋白(HSP)70与诱导型一氧化氮合酶(iNOS)转录表达变化分布和意义.方法采用BIM-Ⅲ型生物撞击机致大鼠胸部严重撞击伤,并造成单侧股骨骨折,运用S-ABC免疫组化、原位杂交技术测定下丘脑HSP70与iNOS及其mRNA的转录表达水平.结果正常对照组HSP70低水平表达,在伤后1小时即开始明显增高(P＜0.05),6小时达到峰值为正常的18倍,12小时后开始下降,24小时时主要集中在室旁核内;iNOS无基础表达,在伤后1小时开始出现,随HSP70同步增高,8小时达到高峰,较1小时时增加13倍.两者相关系数r=0.97601.结论严重创伤后早期下丘脑内HSP70和iNOS过度表达, 在严重创伤应激时下丘脑的损伤与抗损伤机制中起重要作用.     

激光汽化活体生物组织的传热过程分析

目的：研究激光汽化生物活体组织的传热过程及其影响因素，方法：基于血液灌注率温度依赖型Pennes生物传热方程，建立激光与生物活体组织热相互作用的一般模型，研究组织表面发生汽化相变，中间组织出现热凝结，内层组织发生温升的过程，由此探讨组织中的激光传输特性，以及血液灌注率和边界冷却等因素的影响情况。结果：通过数值计算，得出活体组织表面汽化速度及内部温度分布，研究表明，活体组织对不同激光的吸收能力，血液灌注率与边界冷却放松择组织汽化速度，组织凝结过程及温度分布有显著影响。结论：该模型可用于预测激光汽化蚀除组织的过程，分析结果对激光临床应用具有理论指导意义。     

Ergothioneine pretreatment protects the liver from ischemia-reperfusion injury caused by increasing hepatic heat shock protein 70

BACKGROUND: Reperfusion of the liver after ischemia induces the expression of the heat shock genes and the synthesis of the heat shock proteins (HSP). We studied the effects of the natural antioxidant ergothioneine (EGT) treatment on the expression of HSP70 in ischemic-reperfused (IR) liver. METHODS: Adult male Wistar rats were randomly divided into three groups: Sham group given standard laboratory chow and water for 3 weeks followed by sham operation; Control group given standard laboratory chow and water for 3 weeks followed by liver IR injury; EGT group given standard laboratory chow supplementation l-ergothioneine (1.2 mg/kg/d body weight) administered by gavage and water for 3 weeks followed by liver IR injury. Ten rats from each group were killed to determine serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactic dehydrogenase (LDH), tissue malondialdehyde (MDA), HSP70 levels, and histologic changes at 30, 60, and 120 min of reperfusion, respectively. Survival was followed for 1 week. RESULTS: IR caused significant increase in serum AST, ALT, LDH, and tissue MDA levels. As compared with the control group, animals treated with EGT experienced a significant decrease in serum AST, ALT, and LDH levels in all reperfusion periods. Tissue MDA levels in animals receiving EGT were significantly reduced as compared with control group at 30 min and 60 min after reperfusion. After ischemia, reperfusion caused a remarkable production of HSP70 in the control group. When the rats were pretreated with EGT, the levels of HSP70 increased significantly in their livers after reperfusion compared with the control group. Liver injury in the EGT-treated animals was lower to that in the control group. The 7-day survival rate was significantly improved (from 50% to 80%) by EGT pretreatment. CONCLUSION: HSP70 has been shown to induce tolerance against warm IR injury in rat livers. EGT pretreatment protects the liver from IR injury by over-expression of HSP and the subsequent suppression of lipid peroxidation.     

MK2 plays an important role for the increased vascular permeability that follows thermal injury

We previously reported Rho kinase is involved in vessel hyper-permeability caused by burns. Here we further explore the Rho kinase downstream signaling, it is found that its specific inhibitor Y27632 significantly diminishes the activation of JNK and p38 MAPKs but not ERK that induced by serum from burned rats (burn-serum). JNK activation was found involved in the expression of HUVEC adhesion molecules following thermal injury, although not in the process of stress fiber formation. Inhibition of various MAPKs by specific inhibitors showed that SB203580 (inhibitor of p38), but neither SP600125 (inhibitor of JNK) nor PD98059 (inhibitor of ERK), abolish activation of the p38 downstream kinase MK2. Demonstration of stress fibers by fluorescent-labeled phalloidin showed that inhibition of MK2, either by its specific inhibitor or by dominant negative adeno-viral-carried constructs, significantly reduced burn-serum-induced HUVEC stress-fiber formation, while inhibition of another downstream p38 MAPK kinase, PRAK, had no such effects. Transfection of dominant negative adeno-viral MK2 (Ad-MK2(A)) significantly inhibited thermal injury-induced blood vessel hyper-permeability in rats and, moreover, prolonged the survival of burned rats beyond 72 h following thermal injury. One of the mechanisms behind these phenomena is that Ad-MK2(A) causes a significant depression of burn-serum-induced HSP27-phosphorylation, while the adeno-viral transported dominant negative PRAK (Ad-PRAK(A)) does not block. Although the effect of blockade of MK2 through its adeno-viral approach requires further study and investigation of alternatives to know for sure, we may have found a new pathway behind thermal-injury-induced blood vessel hyper-permeability, namely: Rho kinase > p38 > MK2 > HSP27.     

Large-conductance Ca2+-activated K+ channel involvement in suppression of cerebral ischemia/reperfusion injury after electroacupuncture atShuigou (GV26) acupoint in rats

Excess activation and expression of large-conductance Ca2+-activated K+ channels (BKCa channels) may be an important mechanism for delayed neuronal death after cerebral ischemia/reperfusion injury. Electroacupuncture can regulate BKCa channels after cerebral ischemia/reperfusion injury, but the precise mechanism remains unclear. In this study, we established a rat model of cerebral ischemia/reperfusion injury. Model rats received electroacupuncture of 1 mA and 2 Hz atShuigou (GV26) for 10 minutes, once every 12 hours for a total of six times in 72 hours. We found that in cerebral ischemia/reperfusion injury rats, ischemic changes in the cerebral cortex were mitigated after electroacupuncture. Moreover, BKCa channel protein and mRNA expression were reduced in the cerebral cortex and neurological function noticeably improved. These changes did not occur after electroacupuncture at a non-acupoint (5 mm lateral to the left side of Shuigou). Thus, our ifndings indicate that electroacupuncture atShuigou improves neurological function in rats following cerebral ischemia/reperfu-sion injury, and may be associated with down-regulation of BKCa channel protein and mRNA expression. Additionally, our results suggest that theShuigou acupoint has functional speciifcity.