Mitigation and adaptation synergy in forest sector

Mitigation and adaptation are the two main strategies to address climate change. Mitigation and adaptation have been considered separately in the global negotiations as well as literature. There is a realization on the need to explore and promote synergy between mitigation and adaptation while addressing climate change. In this paper, an attempt is made to explore the synergy between mitigation and adaptation by considering forest sector, which on the one hand is projected to be adversely impacted under the projected climate change scenarios and on the other provide opportunities to mitigate climate change. Thus, the potential and need for incorporating adaptation strategies and practices in mitigation projects is presented with a few examples. Firstly, there is a need to ensure that mitigation programs or projects do not increase the vulnerability of forest ecosystems and plantations. Secondly, several adaptation practices could be incorporated into mitigation projects to reduce vulnerability. Further, many of the mitigation projects indeed reduce vulnerability and promote adaptation, for example; forest and biodiversity conservation, protected area management and sustainable forestry. Also, many adaptation options such as urban forestry, soil and water conservation and drought resistant varieties also contribute to mitigation of climate change. Thus, there is need for research and field demonstration of synergy between mitigation and adaptation, so that the cost of addressing climate change impacts can be reduced and co-benefits increased.     

Adult-onset GM2 gangliosidosis diagnosed in a fetus

Amniocentesis and subsequent tests are reported on a fetus conceived of a rare mating type: its mother has an intermediate level of β hexosaminidase A (HEX A), characteristic of carriers of Tay-Sachs disease (TSD), while the father suffers from an adult-onset GM₂ ganglio-sidosis (AOG) with severe HEX A deficiency. Activity of HEX A in the cultured fetal cells was very low when measured by the heat-inactivation method, thus showing the typical biochemical phenotype of TSD fetuses. However, upon separation of HEX isozymes by ion exchange chromatography, residual HEX A (17 per cent of total HEX) was demonstrated. Also in contrast to TSD fetuses, this fetus' fibroblasts were able to synthesize the precursor of a chains of HEX, and ultrastructural examination of its brain revealed few atypical lamellar bodies, unlike those found in TSD fetuses of the same gestational age. It is therefore concluded that the fetus was not affected with TSD, but rather with AOG.