北欧湖泊鱼类状况调查:酸化、富营养化和放养活动对现有鱼类品种组成的影响

1995～1997年间对挪威、瑞典和芬兰的3821个湖泊的鱼类种群状况做了评估.采用分层随机抽样从芬诺斯堪的亚(芬兰、挪威、瑞典、丹麦的总称)所有面积≥0.04km2的126482个湖泊中选择调查湖泊.分析了湖泊的水化学,湖内鱼类状况则从邮件调查问卷中获得.鱼类种群损失发生最为频繁的地区在挪威南部酸化最严重的地区,而在芬诺斯堪的亚东部最少.根据调查问卷,鳟(Salmotrutta)、拟鲤(Rutilus rutilus)、北极红点鲑(Salvelinus alpinus)和鲈鱼(Percafluviatilis)鱼群损失的数量估计超过10000条.这些品种的鱼群潜在地受低碱性湖水影响的数量超过11000条.大约有3300个湖泊显示出总磷高于25μg/L,品种以鲤科鱼为主,这在芬诺斯堪的亚东部、芬兰西南最为明显.这次调查并未显示出鱼类品种由于富营养化而灭绝.1/3的湖泊人工放养了至少一个新的鱼类品种,最常放养的品种有鳟、白鲑(Coregonus lavaretus s.1.)、北极红点鲑、虹鳟(Oncorhynchusmykiss)、梭鲈(Stizostedion lucioperca)、茴鱼(Thymallus thymallus)、狗鱼(Esox lucius)、欧鳊(Abramis brama)、丁 (Tinca tinca)和欧 (Phoxinus phoxinus).在芬诺斯堪的亚湖泊,这些品种的人工放养量估计超过52000群.因此,北欧湖泊现有鱼类品种的数量最近受放养的影响超过了因环境变化如酸化等而损失造成的影响.     

陆地生态系统的恢复--模拟全球变化所引起的酸性输入减少和海盐输入增加的影响

到2010年<哥德堡议定书>正式实施时,欧洲自20世纪70年代末以来已减少的酸化硫和氮释放量将进一步减少.这里我们论述了通过使用应用于3个大型"清洁雨"实验(即分别在挪威里斯达尔谢伊阿[Risdalsheia],瑞典耶德松[Gardsjon]以及丹麦克洛斯特海泽[Klosterhede]的所谓"屋顶实验")的酸化模型MAGIC讨论恢复酸化陆地生态系统的结果.<哥德堡议定书>的实施将启动通过重建盐基饱和恢复上述3处土壤的进程.恢复率较低,在今后30年中,盐基饱和增加不足5%.气候引发的风暴严重性的加剧将增加海盐输入生态系统的量.这将为土壤提供额外的碱阳离子,并使恢复速度翻一番,同时还将随着沉积的碱阳离子与存储在土壤中的酸性交换导致高海盐输入之后的强酸性脉动.因此,酸化集水区土壤和径流的进一步恢复将取决于酸沉积下降的数量和速率,在近岸系统的情况下,还取决于海盐输入事件的频率和强度.     

Sectoral Trends and Driving Forces of Global Energy Use and Greenhouse Gas Emissions

Disaggregation of sectoral energy use and greenhouse gas emissions trends reveals striking differences between sectors and regions of the world. Understanding key driving forces in the energy end-use sectors provides insights for development of projections of future greenhouse gas emissions. This paper examines global and regional historical trends in energy use and carbon emissions in the industrial, buildings, transport, and agriculture sectors. Activity and economic drivers as well as trends in energy and carbon intensity are evaluated. We show that macro-economic indicators, such as GDP, are insufficient for comprehending trends and driving forces at the sectoral level. These indicators need to be supplemented with sector-specific information for a more complete understanding of future energy use and greenhouse gas emissions.     

Prenatal diagnosis of medium-chain acyl-CoA dehydrogenase (MCAD) deficiency in a family with a previous fatal case of sudden unexpected death in childhood

Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is a potentially fatal inherited disease with a carrier frequency of approximately 1:100 in most Caucasian populations. The disease is implicated in sudden unexpected death in childhood. A prevalent disease-causing point mutation (A985G) in the MCAD gene has been characterized, thus rendering diagnosis easy in the majority of cases. Since the clinical spectrum of MCAD deficiency ranges from death in the first days of life to an asymptomatic life, there are probably other genetic factors—in addition to MCAD mutations—involved in the expression of the disease. Thus, families who have experienced the death of a child from MCAD deficiency might have an increased risk of a seriously affected subsequent child. In such a family we have therefore performed a prenatal diagnosis on a chorionic villus sample by a highly specific and sensitive polymerase chain reaction (PCR) assay for the G985 mutation. The analysis was positive and resulted in abortion. We verified the diagnosis by direct analysis on blood spots and other tissue material from the aborted fetus and from family members.