Growth and carbon stock change in eucalypt woodlands in northeast Australia: ecological and greenhouse sink implications

Data from 57 permanent monitoring sites are used to document the growth in woody vegetation and estimate the carbon sink in 27 M ha of eucalypt woodlands (savannas), contained within c. 60 M ha of grazed woodlands in Queensland (northeast Australia). The study sites are shown to be representative of the environment and structure of the eucalypt woodlands in the defined study area. Mean basal area increment for all live woody plants in 30 long‐term sites, with an average initial basal area of 11.86 ± 1.38 (SE) m² ha^?1, was 1.06 m² ha^?1 over a mean 14 years timeframe. The majority of the measurement period, commencing between 1982 and 1988, was characterized by below‐average rainfall. The increase in live tree basal area was due primarily to growth of existing trees (3.12 m² ha^?1) rather than establishment of new plants (0.25 m² ha^?1) and was partly offset by death (2.31 m² ha^?1). A simple but robust relationship between stand basal area and stand biomass of all woody species was developed for the eucalypt dominant woodlands. Analysis of above‐ground carbon stocks in live and standing dead woody plants gave a mean net above‐ground annual carbon increment for all 57 sites of 0.53 t C ha^?1 y^?1, similar to values estimated elsewhere in world savannas. Published root : shoot ratios were used to infer C flux in woody root systems on these sites. This results in an estimated sink in above‐ and below‐ground biomass of 18 Mt C y^?1 over the eucalypt woodlands studied, and potentially up to 35 Mt C y^?1 if extended to all grazed woodlands in Queensland. It is suggested that introduction of livestock grazing and altered fire regimes have triggered the change in tree‐grass dominance in these woodlands. Thus, change in carbon stocks in the grazed woodlands of Queensland is identified as an important component of human‐induced greenhouse gas flux in Australia, equivalent in magnitude to c. 25% of the most recently published (1999) total estimated national net emissions. The latter inventory takes into account emissions from land clearing, but does not include the sink identified in the present study. This sequestration also represents a small but significant contribution to the global terrestrial carbon sink.     

Tau Proteins and Tauopathies in Alzheimer’s Disease

Alzheimer’s disease (AD) is characterized by progressive memory loss and cognitive function deficits. There are two major pathological hallmarks that contribute to the pathogenesis of AD which are the presence of extracellular amyloid plaques composed of amyloid-β (Aβ) and intracellular neurofibrillary tangles composed of hyperphosphorylated tau. Despite extensive research that has been done on Aβ in the last two decades, therapies targeting Aβ were not very fruitful at treating AD as the efficacy of Aβ therapies observed in animal models is not reflected in human clinical trials. Hence, tau-directed therapies have received tremendous attention as the potential treatments for AD. Tauopathies are closely correlated with dementia and immunotherapy has been effective at reducing tau pathology and improving cognitive deficits in animal models. Thus, in this review article, we discussed the pathological mechanism of tau proteins, the key factors contributing to tauopathies, and therapeutic approaches for tauopathies in AD based on the recent progress in tau-based research.     

A new method for studying the genetic control of specific mitochondrial proteins in Paramecium aurelia

Summary Mitochondria from one syngen (or sub-species) of Paramecium aurelia have been introducted into a different syngen by preparing erythromycin-resistant mitochondria from syngen 1 and micro-injecting them into erythromycin-sensitive syngen 7 cells. The recipient sensitive cells were then placed in erythromycin to inhibit the replication of the sensitive mitochondria. Such selected clones contain a syngen 7 nucleus but a mitochondrial genome which is derived from syngen 1 erythromycin-resistant mitochondria.Using this method it has been shown that the mitochondrial enzyme fumarase is not coded by the mitochondrial genome, and by implication, is coded by the nuclear genome. The use of this technique as a method for determining if specific mitochondrial proteins are controlled by nuclear or mitochondrial genes is discussed.     

Coproporphyrinogenase activities in extracts of Rhodopseudomonas spheroides and Chromatium strain D

1. The anaerobic coproporphyrinogenase activity in an extract of Rhodopseudomonas spheroides is inhibited by 1,10-phenanthroline, alphaalpha'-bipyridyl, flavins, 2,4-dinitrophenol and 1,4-naphthaquinone. These compounds have no effect on the aerobic coproporphyrinogenase activity. 2. On removal of small-molecular-weight material from a crude extract, the anaerobic system becomes very unstable; it can be stabilized by adding succinate. Now nicotinamide nucleotides, in addition to Mg(2+), ATP and methionine, are required for protoporphyrin to be formed. 3. A mechanism for the anaerobic reaction is proposed, based on the cofactor requirements and the effect of inhibitors. 4. The enzyme responsible for aerobic activity has been partially purified and some of its properties are reported. 5. A crude extract of Chromatium strain D also exhibits coproporphyrinogenase activity under anaerobic conditions in the presence of S-adenosylmethionine or ATP plus methionine. The requirement for other cofactors is variable.