Management of Acid Mine Drainage within a Wetland in the Tarkwa Area

Acid Mine Drainage (AMD) is an environmental phenomenon that is being experienced by some surface mining companies in Ghana. Consequently, there is the need to generate information and expand local expertise base in handling this phenomenon. This work explored the sustainable anaerobic wetland mitigation method for the management of this phenomenon.Results of water analysis showed that the pH at the acidic effluent discharge area is 4.4 but then it increased gradually to pH of 7.5 in the wetland. The study identified a sulphate reducing bacterium (Desulfovibrio desulfuricans) inthe wetland, whose activity produced OH- ions that raised the pH of the acidic effluent resulting in the precipitation of heavy metals like iron, lead and nickel. Consequently, if the natural anaerobic remediation is engineered, the effluent from the AMD can be treated and discharged without causing any significant adverse impact to the geo-environmen

Land Use Changes within the Bogoso-Prestea Gold Concession, South West Ghana

Mining activities have existed in the Bogoso-Prestea area for over a century. The high demand for gold has led to intense mining activities in the area and has resulted in land use changes. This study evaluated a total area of 4 379.93 ha within the Bogoso-Prestea Gold Concession that has experienced land use change due to mining using estimation of areas and analysis of land use flows over a period of twenty years ie.1986 - 2006. Results from the study revealed that mining increased in land coverage from 4.69 ha in 1986 to 530.84 ha in 2006, an increase to 12.1% of the study area. Settlements increased to 4.95% in 2006 as compared to 0.41% in 1986, showing a significant rural migration primarily due to mining. Agricultural land use reduced from 97.8% in 1986 to 82.7% in 2006. The study also revealed that land use due to mining increased by only 0.67 % between 1996 and 2006 and if this trend continues, then land use due to mining under the prevailingconditions might not introduce any significant increment between 2006 and 2016

DRAM-3 modulates autophagy and promotes cell survival in the absence of glucose

Macroautophagy is a membrane-trafficking process that delivers cytoplasmic constituents to lysosomes for degradation. The process operates under basal conditions as a mechanism to turnover damaged or misfolded proteins and organelles. As a result, it has a major role in preserving cellular integrity and viability. In addition to this basal function, macroautophagy can also be modulated in response to various forms of cellular stress, and the rate and cargoes of macroautophagy can be tailored to facilitate appropriate cellular responses in particular situations. The macroautophagy machinery is regulated by a group of evolutionarily conserved autophagy-related (ATG) proteins and by several other autophagy regulators, which either have tissue-restricted expression or operate in specific contexts. We report here the characterization of a novel autophagy regulator that we have termed DRAM-3 due to its significant homology to damage-regulated autophagy modulator (DRAM-1). DRAM-3 is expressed in a broad spectrum of normal tissues and tumor cells, but different from DRAM-1, DRAM-3 is not induced by p53 or DNA-damaging agents. Immunofluorescence studies revealed that DRAM-3 localizes to lysosomes/autolysosomes, endosomes and the plasma membrane, but not the endoplasmic reticulum, phagophores, autophagosomes or Golgi, indicating significant overlap with DRAM-1 localization and with organelles associated with macroautophagy. In this regard, we further proceed to show that DRAM-3 expression causes accumulation of autophagosomes under basal conditions and enhances autophagic flux. Reciprocally, CRISPR/Cas9-mediated disruption of DRAM-3 impairs autophagic flux confirming that DRAM-3 is a modulator of macroautophagy. As macroautophagy can be cytoprotective under starvation conditions, we also tested whether DRAM-3 could promote survival on nutrient deprivation. This revealed that DRAM-3 can repress cell death and promote long-term clonogenic survival of cells grown in the absence of glucose. Interestingly, however, this effect is macroautophagy-independent. In summary, these findings constitute the primary characterization of DRAM-3 as a modulator of both macroautophagy and cell survival under starvation conditions

Inhibition of autophagy, lysosome and VCP function impairs stress granule assembly

Stress granules (SGs) are mRNA-protein aggregates induced during stress, which accumulate in many neurodegenerative diseases. Previously, the autophagy-lysosome pathway and valosin-containing protein (VCP), key players of the protein quality control (PQC), were shown to regulate SG degradation. This is consistent with the idea that PQC may survey and/or assist SG dynamics. However, despite these observations, it is currently unknown whether the PQC actively participates in SG assembly. Here, we describe that inhibition of autophagy, lysosomes and VCP causes defective SG formation after induction. Silencing the VCP co-factors UFD1L and PLAA, which degrade defective ribosomal products (DRIPs) and 60S ribosomes, also impaired SG assembly. Intriguingly, DRIPs and 60S, which are released from disassembling polysomes and are normally excluded from SGs, were significantly retained within SGs in cells with impaired autophagy, lysosome or VCP function. Our results suggest that deregulated autophagy, lysosomal or VCP activities, which occur in several neurodegenerative (VCP-associated) diseases, may alter SG morphology and composition

Autophagy fights disease through cellular self-digestion

Autophagy, or cellular self-digestion, is a cellular pathway involved in protein and organelle degradation, with an astonishing number of connections to human disease and physiology. For example, autophagic dysfunction is associated with cancer, neurodegeneration, microbial infection and ageing. Paradoxically, although autophagy is primarily a protective process for the cell, it can also play a role in cell death. Understanding autophagy may ultimately allow scientists and clinicians to harness this process for the purpose of improving human health.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62766/1/nature06639.pd