Hemispheric dispersion of radioactive plume laced with fission nuclides from the Fukushima nuclear event

Radioactivities of particulate 131I and 137Cs released from the Fukushima nuclear accident were monitored in a regional aerosol network including two high mountain sites (central Taiwan and Tibetan Plateau). The results were integrated with data measured elsewhere around the world, with special focus on the mid-latitudes. The hemispheric transport of the Fukushima radiation clouds (FRCs) by the westerlies took $18 days, displaying an exponential-like decrease eastward, with a dilution factor of at least five orders of magnitude following a full circuit around the globe. The initial two waves of FRCs may travel at different atitudes: the first one at$3–4 km, whereas the second one up to 5 km or more. 131I and 137Cs were fractionated during transport, with 137Cs concentrated in the shallower layer, susceptible to depositional removal, while 131I moving faster and higher. This accident may be exemplified to identify some atmospheric processes on the hemispheric scale

KẾT QUẢ BƯỚC ĐẦU NGHIÊN CỨU TỐC ĐỘ LẮNG ĐỌNG, NGUỒN TRẦM TÍCH ĐÁY VỊNH HẠ LONG: DẤU HIỆU TỪ KHOÁNG VẬT SÉT, ĐỒNG VỊ 210Pb VÀ 137Cs

Ha Long bay is the World Natural Heritage, which annaually attracts a lot of foreign and domestic tourists. Nevertheless, in recent years, the landscape of Ha Long bay is devastated by many negative impacts-the shallowing of the bottom of bay is one of the great negative impacts. How is the shallowing of the bottom of Ha Long bay? What are reasons for the negative impacts? Based on the approach “source-to-sink” combined with results of clay mineral contents, results of 210Pb and 137Cs radionuclides, this study will contribute to clarifying the shallowing of the bottom of Ha Long bay. Results of smectite, illite and smectite/(illite+chlorite) ratios indicated that the sediment in Ha Long bay not only derives from the surrounding region of Ha Long bay but also derives from Red river system. Results of 210Pbex and 137Csex revealed the sedimentation rates in the Ha Long bay have varied between 0.47 - 0.75 cm/year over the last 100 years. It can be divided into four periods: period I (1920 - 1930); period II (1930 - 1960); period III (1960 - 1990); and period IV (1990 - 2011) with the average rate of 0.45 cm/year; 0.66 cm/year; 0.50 cm/year; and 0.85 cm/year respectively. The shallowing of the bottom of Ha Long bay was impacted by human activities such as building reservoirs, mining, urbanization or aquaculture etc.Vịnh Hạ Long là một trong những di sản thiên nhiên thế giới, hàng năm, vịnh thu hút nhiều du khách trong và ngoài nước. Tuy nhiên, trong những năm gần đây, cảnh quan vịnh bị tác động bởi hàng loạt các tác động tiêu cực - bồi lắng đáy vịnh là một trong những tác động tiêu cực lớn. Đáy vịnh Hạ Long bồi cạn ra sao? nguyên nhân nào gây ra? Theo cách tiếp cận từ nguồn cung cấp đến bồn lắng đọng trầm tích “source-to-sink” và phối hợp với kết quả thành phần khoáng vật sét và đồng vị phóng xạ 210Pb và 137Cs, nghiên cứu này sẽ góp phần là sáng tỏ vấn đề trên. Kết quả hàm lượng smectite, illite và chỉ số smectite/( illite+chlorite) chỉ thị: trầm tích chuyển vào vịnh Hạ Long không chỉ nhận từ vùng xung quanh vịnh mà nó còn nhận từ hệ thống sông Hồng. Kết quả 210Pb và 137Cs cho thấy: tốc độ lắng đọng trầm tích tại vịnh Hạ Long trong vòng 100 năm qua, dao động trong khoảng 0,47 - 0,75 cm/năm, và có thể chia làm 4 giai đoạn: giai đoạn I (từ năm 1920 - 1930), giai đoạn II (từ năm 1930 - 1960); giai đoạn III (1960 - 1990) và giai đoạn IV (từ năm 1990 - 2011) với tốc độ lắng đọng trung bình lần lượt là 0,45 cm/năm; 0,66 cm/năm; 0,50 cm/năm; và 0,85 cm/năm tương ứng. Các hoạt động của con người như: xây hồ chứa, khai thác mỏ, đô thị hóa, nuôi trồng thủy sản ... là nguyên nhân gây bồi cạn đáy vịnh

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field