Degradation of communal rangelands in South Africa: towards an improved understanding to inform policy

In South Africa, the relative extent of range degradation under freehold compared to communal tenure has been strongly debated. We present a perspective on the processes that drive rangeland degradation on land under communal tenure. Our findings are based on literature as well as extensive field work on both old communal lands and ‘released’ areas, where freehold farms have been transferred to communal ownership. We discuss the patterns of degradation that have accompanied communal stewardship and make recommendations on the direction policy should follow to prevent further degradation and mediate rehabilitation of existing degraded land.Keywords: communal rangelands, land degradation, rehabilitation, social systemsAfrican Journal of Range & Forage Science 2013, 30(1&2): 57–6

Contributions of nitrogen deposition and forest regrowth to terrestrial carbon uptake

<p>Abstract</p> <p>Background</p> <p>The amount of reactive nitrogen deposited on land has doubled globally and become at least five-times higher in Europe, Eastern United States, and South East Asia since 1860 mostly because of increases in fertilizer production and fossil fuel burning. Because vegetation growth in the Northern Hemisphere is typically nitrogen-limited, increased nitrogen deposition could have an attenuating effect on rising atmospheric CO₂by stimulating the vegetation productivity and accumulation of carbon in biomass.</p> <p>Results</p> <p>This study shows that elevated nitrogen deposition would not significantly enhance land carbon uptake unless we consider its effects on re-growing forests. Our results suggest that nitrogen enriched land ecosystems sequestered 0.62–2.33 PgC in the 1980s and 0.75–2.21 PgC in the 1990s depending on the proportion and age of re-growing forests. During these two decades land ecosystems are estimated to have absorbed 13–41% of carbon emitted by fossil fuel burning.</p> <p>Conclusion</p> <p>Although land ecosystems and especially forests with lifted nitrogen limitations have the potential to decelerate the rise of CO₂concentrations in the atmosphere, the effect is only significant over a limited period of time. The carbon uptake associated with forest re-growth and amplified by high nitrogen deposition will decrease as soon as the forests reach maturity. Therefore, assessments relying on carbon stored on land from enhanced atmospheric nitrogen deposition to balance fossil fuel emissions may be inaccurate.</p

Vault changes after cyclopentolate instillation in eyes with posterior chamber phakic intraocular lens

Posterior chamber phakic intraocular lens (pIOL) implantation is a common option for correcting moderate-to-high ocular refractive defects. Because this pIOL is implanted on ciliary sulcus, the distance between the back surface of the pIOL and the anterior surface of the crystalline lens, that it is known as vault, should be measured in different conditions to ensure the technique's safety. Cyclopentolate is a drug that dilates the pupil and relaxes accommodation (cycloplegia). It is often used for different ocular examinations and for other medical purposes. However, there is no evidence of the effect of this drug on vault. This study quantified central vault changes associated with cyclopentolate instillation. We measured the vault under normal conditions (pre-cycloplegic instillation) and after instilling cyclopentolate on 39 eyes of 39 patients with implanted pIOL. Our results suggest that cyclopentolate instillation may induce changes to vault in eyes with implanted pIOL. These changes seem safe and are mainly associated with vault under normal conditions, but also with anterior chamber depth, pupillary diameter and pIOL size.- European Fund for Regional Development (FEDER) through the COMPETE Program and the Portuguese Foundation for Science and Technology (FCT) provided financial support in the framework of projects PTDC/SAU-BEB/098391/2008, PTDC/SAU-BEB/098392/2008 and the Strategic Project PEST-C/FIS/UI607/2011

Recognition of Depression in Older Medical Inpatients

BACKGROUND: Studies of recognition of depression in older (aged 65 or more) medical inpatients show low rates of recognition of depression by attending physicians. However, few studies have compared different measures of recognition of depression. OBJECTIVES: (1) To compare the validity of four indicators of recognition of depression and a global measure of recognition against a diagnosis of depression and (2) to explore the effect of patient characteristics on recognition of depression. METHODS: In a cohort of 264 medical inpatients 65 years and older (115 with major or minor depression, 78 with no depression), sensitivities, specificities, and diagnostic odds ratios (DOR) of 4 indicators of recognition (symptoms, diagnosis, treatment, and referral) and a global measure of recognition (any of the 4 indicators) were calculated. The associations between patient characteristics (age, sex, history of depression, antidepressant use before admission, severity of depression, comorbidity, duration of hospitalization, disability, and hospital of admission) and recognition were explored using multiple logistic regression. RESULTS: Less than half of the depressed patients were recognized. The indicator with the highest sensitivity was treatment (27.8%, 95% confidence interval [CI] 20.0–37.0), whereas the indicator with the best specificity was diagnosis (96.6%, 95% CI 91.9–98.7). The unadjusted DOR of global recognition was 2.6 (95% CI 1.5, 4.4). Less comorbidity, more severe depression symptoms, a history of depression, longer hospital stay, and antidepressant use before admission were significantly associated with better global recognition. CONCLUSION: Recognition of depression in elderly medical inpatients depends upon the indicator of recognition used

Caveolin 1 protein expression in renal cell carcinoma predicts survival

<p>Abstract</p> <p>Background</p> <p>Caveolae play a significant role in disease phenotypes such as cancer, diabetes, bladder dysfunction, and muscular dystrophy. The aim of this study was to elucidate the caveolin-1 <it>(</it>CAV1<it>) </it>protein expression in renal cell cancer (RCC) and to determine its potential prognostic relevance.</p> <p>Methods</p> <p>289 clear cell RCC tissue specimens were collected from patients undergoing surgery for renal tumors. Both cytoplasmic and membranous CAV1 expression were determined by immunohistochemistry and correlated with clinical variables. Survival analysis was carried out for 169 evaluable patients with a median follow up of 80.5 months (interquartile range (IQR), 24.5 - 131.7 months).</p> <p>Results</p> <p>A high CAV1 expression in the tumor cell cytoplasm was significantly associated with male sex (p = 0.04), a positive nodal status (p = 0.04), and poor tumor differentiation (p = 0.04). In contrast, a higher than average (i.e. > median) CAV1 expression in tumor cell membranes was only linked to male sex (p = 0.03). Kaplan-Meier analysis disclosed significant differences in 5-year overall (51.4 vs. 75.2%, p = 0.001) and tumor specific survival (55.3 vs. 80.1%, p = 0.001) for patients with higher and lower than average cytoplasmic CAV1 expression levels, respectively. Applying multivariable Cox regression analysis a high CAV1 protein expression level in the tumor cell cytoplasm could be identified as an independent poor prognostic marker of both overall (p = 0.02) and tumor specific survival (p = 0.03) in clear cell RCC patients.</p> <p>Conclusion</p> <p>Over expression of caveolin-1 in the tumour cell cytoplasm predicts a poor prognosis of patients with clear cell RCC. CAV1 is likely to be a useful prognostic marker and may play an important role in tumour progression. Therefore, our data encourage further investigations to enlighten the role of CAV1 and its function as diagnostic and prognostic marker in serum and/or urine of RCC patients.</p

Kinetic regulation of multi-ligand binding proteins

Background: Second messengers, such as calcium, regulate the activity of multisite binding proteins in a concentration-dependent manner. For example, calcium binding has been shown to induce conformational transitions in the calcium-dependent protein calmodulin, under steady state conditions. However, intracellular concentrations of these second messengers are often subject to rapid change. The mechanisms underlying dynamic ligand-dependent regulation of multisite proteins require further elucidation. Results: In this study, a computational analysis of multisite protein kinetics in response to rapid changes in ligand concentrations is presented. Two major physiological scenarios are investigated: i) Ligand concentration is abundant and the ligand-multisite protein binding does not affect free ligand concentration, ii) Ligand concentration is of the same order of magnitude as the interacting multisite protein concentration and does not change. Therefore, buffering effects significantly influence the amounts of free ligands. For each of these scenarios the influence of the number of binding sites, the temporal effects on intermediate apo- and fully saturated conformations and the multisite regulatory effects on target proteins are investigated. Conclusions: The developed models allow for a novel and accurate interpretation of concentration and pressure jump-dependent kinetic experiments. The presented model makes predictions for the temporal distribution of multisite protein conformations in complex with variable numbers of ligands. Furthermore, it derives the characteristic time and the dynamics for the kinetic responses elicited by a ligand concentration change as a function of ligand concentration and the number of ligand binding sites. Effector proteins regulated by multisite ligand binding are shown to depend on ligand concentration in a highly nonlinear fashion

Disease-Toxicant Interactions in Manganese Exposed Huntington Disease Mice: Early Changes in Striatal Neuron Morphology and Dopamine Metabolism

YAC128 Huntington's disease (HD) transgenic mice accumulate less manganese (Mn) in the striatum relative to wild-type (WT) littermates. We hypothesized that Mn and mutant Huntingtin (HTT) would exhibit gene-environment interactions at the level of neurochemistry and neuronal morphology. Twelve-week-old WT and YAC128 mice were exposed to MnCl2-4H2O (50 mg/kg) on days 0, 3 and 6. Striatal medium spiny neuron (MSN) morphology, as well as levels of dopamine (DA) and its metabolites (which are known to be sensitive to Mn-exposure), were analyzed at 13 weeks (7 days from initial exposure) and 16 weeks (28 days from initial exposure). No genotype-dependent differences in MSN morphology were apparent at 13 weeks. But at 16 weeks, a genotype effect was observed in YAC128 mice, manifested by an absence of the wild-type age-dependent increase in dendritic length and branching complexity. In addition, genotype-exposure interaction effects were observed for dendritic complexity measures as a function of distance from the soma, where only YAC128 mice were sensitive to Mn exposure. Furthermore, striatal DA levels were unaltered at 13 weeks by genotype or Mn exposure, but at 16 weeks, both Mn exposure and the HD genotype were associated with quantitatively similar reductions in DA and its metabolites. Interestingly, Mn exposure of YAC128 mice did not further decrease DA or its metabolites versus YAC128 vehicle exposed or Mn exposed WT mice. Taken together, these results demonstrate Mn-HD disease-toxicant interactions at the onset of striatal dendritic neuropathology in YAC128 mice. Our results identify the earliest pathological change in striatum of YAC128 mice as being between 13 to 16 weeks. Finally, we show that mutant HTT suppresses some Mn-dependent changes, such as decreased DA levels, while it exacerbates others, such as dendritic pathology

Painful and painless mutations of SCN9A and SCN11A voltage-gated sodium channels

Chronic pain is a global problem affecting up to 20% of the world’s population and has a significant economic, social and personal cost to society. Sensory neurons of the dorsal root ganglia (DRG) detect noxious stimuli and transmit this sensory information to regions of the central nervous system (CNS) where activity is perceived as pain. DRG neurons express multiple voltage-gated sodium channels that underlie their excitability. Research over the last 20 years has provided valuable insights into the critical roles that two channels, NaV1.7 and NaV1.9, play in pain signalling in man. Gain of function mutations in NaV1.7 cause painful conditions while loss of function mutations cause complete insensitivity to pain. Only gain of function mutations have been reported for NaV1.9. However, while most NaV1.9 mutations lead to painful conditions, a few are reported to cause insensitivity to pain. The critical roles these channels play in pain along with their low expression in the CNS and heart muscle suggest they are valid targets for novel analgesic drugs

Man and the Last Great Wilderness: Human Impact on the Deep Sea

The deep sea, the largest ecosystem on Earth and one of the least studied, harbours high biodiversity and provides a wealth of resources. Although humans have used the oceans for millennia, technological developments now allow exploitation of fisheries resources, hydrocarbons and minerals below 2000 m depth. The remoteness of the deep seafloor has promoted the disposal of residues and litter. Ocean acidification and climate change now bring a new dimension of global effects. Thus the challenges facing the deep sea are large and accelerating, providing a new imperative for the science community, industry and national and international organizations to work together to develop successful exploitation management and conservation of the deep-sea ecosystem. This paper provides scientific expert judgement and a semi-quantitative analysis of past, present and future impacts of human-related activities on global deep-sea habitats within three categories: disposal, exploitation and climate change. The analysis is the result of a Census of Marine Life – SYNDEEP workshop (September 2008). A detailed review of known impacts and their effects is provided. The analysis shows how, in recent decades, the most significant anthropogenic activities that affect the deep sea have evolved from mainly disposal (past) to exploitation (present). We predict that from now and into the future, increases in atmospheric CO2 and facets and consequences of climate change will have the most impact on deep-sea habitats and their fauna. Synergies between different anthropogenic pressures and associated effects are discussed, indicating that most synergies are related to increased atmospheric CO2 and climate change effects. We identify deep-sea ecosystems we believe are at higher risk from human impacts in the near future: benthic communities on sedimentary upper slopes, cold-water corals, canyon benthic communities and seamount pelagic and benthic communities. We finalise this review with a short discussion on protection and management methods