Offset integrity reduces environmental risk: Using lessons from biodiversity and carbon offsetting to inform water quality offsetting in the catchments of the Great Barrier Reef.

Environmental offsetting has been developed as a mechanism to facilitate the benefits from economic development while avoiding or minimizing environmental harm. This is achieved by compensating for environmental impacts at one location by generating equivalent environmental improvements elsewhere. However, experience with biodiversity and carbon offsetting indicates it can be difficult to ensure the integrity of offsets. Under recent legislation in the catchments of the Great Barrier Reef (GBR), Australia, it is mandatory for water quality emissions from new or expanded point source development to be offset by reducing pollution elsewhere, frequently through reducing non-point source pollution (NPSP). Therefore, informed by experience with biodiversity and carbon offsetting, we summarised sources of uncertainty in NPSP reduction that would influence water quality offset integrity; estimated the maximum potential demand for water quality offsets from sewage treatment plants, the largest point source emitter of total nitrogen (TN) in the GBR catchments, between 2018 and 2050; and discussed the implications of both on the ability of offsetting to counterbalance the impact of economic development in catchments where nitrogen loads have a large influence on the health of important GBR ecosystems. The catchments surrounding the population centres of Cairns and Mackay had both a potentially high future demand for nitrogen water quality offsets and nitrogen loads with a strong influence on the health of the GBR. Consequently, any low integrity water quality offsets in these catchments could jeopardise progress toward the water quality improvements needed to ensure the continued health of the GBR. Water quality offsetting has numerous strengths as a policy instrument however substantial uncertainties remain related to environmental outcomes. Until further research can reduce these uncertainties, water quality offsets that are implemented near increased point source emissions and have a high certainty of effectiveness may provide a balance between scientific rigour and policy workability.

Análise do perfil do paciente portador de doenca osteomuscular relacionada ao trabalho (DORT) e usuário do serviço de saúde do trabalhador do SUS em Belo Horizonte / Analysis of the patient`s profile who bears DORT and is watched by the worker`s health reference center of general health service from Belo Horizonte

O presente trabalho pretende descrever o perfil do paciente portador de DORT atendido pelo Sistema Unico de Saude(SUS) em Belo Horizonte. Conhece-lo e de fundamental importancia, pois essas patologias sao responsaveis por cerca de (85 por cento) dos afastamentos do trabalho alem, de causarem grandes impactos psicologicos e socioeconomicos. Realizou-se o levantamento de 145 prontuarios de pacientes do Centro de Referencia de Saude ddo Trabalhador (CERSAT), no periodo de 1998 a 2001. Dados como sexo, faixa etaria, escolaridade, profissao, situacao de trabalho e diagnosticos foram analisados. Os resultados apontam que as DORT acometem mais as mulheres entre 21 e 50 anos de idade com baixo grau de escolaridade. Dados importantes foram observados no item ``diagnosticos``, pois estes tem-se mostrado inconclusivos, impedindo intervencao fisioterapica adequada. Constatou-se, contudo, que as tendinites continuam sendo as mais frequentes (49 por cento) e que as tenossinovites, as epicondilites e a fibromialgia tem aumentado nos ultimos anos, sendo que, na maioria dos casos, os pacientes chegam ao tratamento em fases avancadas. Essa situacao e um problema de saude publicae tem trazido prejuizos aos trabalhadores, tornando evidente a importancia de conhecer as necessidades dos pacientes e de oferecer-lhes tratamento mais adequado

Protein kinases selectively modulate apoptosis in the developing retina in vitro.

In the retina of newborn rats there is evidence for two mechanisms of programmed cell death. Apoptosis of ganglion cells (RGCs) following axotomy depends on protein synthesis. In contrast, inhibition of protein synthesis leads to apoptosis in the neuroblastic layer (NBL). The induction of apoptosis following translational arrest suggests that post-translational modifications of apoptosis-associated proteins may be crucial to the cell death programs in the developing retina. We investigated the possible role of protein kinases upon apoptosis in retinal explants in vitro. An increase in the intracellular concentration of cAMP produced either by the adenylyl-cyclase activator forskolin (10 microM) or by 8-Br-cAMP (1 mM), prevented apoptosis induced in the NBL by inhibition of protein synthesis, but had no statistically significant effect upon RGC death. In contrast, neither 8-Br-cGMP (1 mM) nor the specific cGMP-phosphodiesterase inhibitor zaprinast (10-100 microM) had significant effects on apoptosis in the retina. The cAMP-phosphodiesterase inhibitors isobutylmethylxantine (IBMX, 0.1-1 mM) and Ro-201724 (50-200 microM) also prevented apoptosis in the NBL. The isoquinolinesulfonamide H89 (20 microM), a specific cAMP-dependent protein kinase inhibitor, partially reverted the protective effect of either forskolin or IBMX within the NBL. Neither 12-O-tetradecanoyl phorbol-13-acetate (TPA, 10 nM) nor bisindolylmaleimide (0.2-0.5 microM), respectively an activator and an inhibitor of protein kinase C had significant effects upon the retinal explants. The protein kinase inhibitor 2-aminopurine (2-AP, 10 mM) prevented apoptosis of axotomized ganglion cells and induced apoptosis in the NBL. Forskolin prevented the apoptosis induced by 2-AP in the NBL, whereas TPA had no effect. The effects of 2-AP were, however, not dependent on inhibition of protein synthesis. The data indicate that modulation of the activity of both cAMP-dependent protein kinase and several protein kinases sensitive to 2-aminopurine selectively affect apoptosis in distinct cell layers of the developing retina.

Death in a dish: controls of apoptosis within the developing retinal tissue.

Studies of programmed cell death in the developing retina in vitro are currently reviewed. The results of inhibiting protein synthesis in retinal explants indicate two mechanisms of apoptosis. One mechanism depends on the synthesis of positive modulators ('killer proteins'), while a distinct, latent mechanism appears to be continuously blocked by negative modulators. Extracellular modulators of apoptosis include the neurotrophic factors NT-4 and BDNF, while glutamate may have either a positive or a negative modulatory action on apoptosis. Several protein kinases selectively modulate apoptosis in distinct retinal layers. Calcium and nitric oxide were also shown to affect apoptosis in the developing retinal tissue. The protein c-Jun was found associated with apoptosis in various circumstances, while p53 seems to be selectively expressed in some instances of apoptosis. The results indicate that the sensitivity of each retinal cell to apoptosis is controlled by multiple, interactive, cell type- and context-specific mechanisms. Apoptosis in the retina depends on a critical interplay of extracellular signals delivered through neurotrophic factors, neurotransmitters and neuromodulators, several signal transduction pathways, and the expression of a variety of genes.

Death in dish: controls of apoptosis within the developing retinal tissue

Studies of programmed cell death in the developing retina in vitro are currently reviewed. The results of inhibiting protein synthesis in retinal explants indicate two mechanisms of apoptosis. One mechanism depends on the synthesis of positive modulators ('killer proteins'), while a distinct, latent mechanism appears to be continuously blocked by negative modulators. Extracellular modulators of apoptosis include the neurotrophic factors NT-4 and BDNF, while glutamate may have either a positive or a negative modulatory action on apoptosis. Several protein kinases selectively modulate apoptosis in distinct retinal layers. Calcium and nitric oxide were also shown to affect apoptosis in the developing retianl tissue. The protein c-Jun was found associated with apoptosis in various circumstances, while p53 seems to be selectively expressed in some instances of apoptosis. The results indicate that the sensitivity of each retinal cell to apoptosis is controlled by multiple, interactive, cell type- and context-specific mechanisms. Apoptosis in the retina depends on a critical interplay of extracellular signals delivered through neurotrophic factors, neurotransmitters and neuromodulators, several signal transduction pathways, and the expression of a variety of genes.