RESUMEN
Ant behavior relies on a collection of natural products, from following trail pheromones during foraging to warding off potential predators. How nervous systems sense these compounds to initiate a behavioral response remains unclear. Here, we used Caenorhabditis elegans chemotaxis assays to investigate how ant compounds are detected by heterospecific nervous systems. We found that C. elegans avoid extracts of the pavement ant ( Tetramorium immigrans ) and either osm-9 or tax-4 ion channels are required for this response. These experiments were conducted in an undergraduate laboratory course, demonstrating that new insights into interspecies interactions can be generated through genuine research experiences in a classroom setting.
RESUMEN
Arsenic iron removal plants (AIRPs) are used in some locations in Bangladesh to remove arsenic from groundwater to provide access to safer drinking water. In this study, the influence of orthophosphate in influent water on the performance of 21 (of 105) AIRPs installed in the Manikganj District was evaluated. The degree of aeration was also estimated, and the role of dissolved oxygen in AIRP performance is discussed. AIRP installations were done by a local non-governmental organization (The Society for People's Action in Change and Equity) with financial assistance from the Australian High Commission, Dhaka under the Direct Aid Program of the Australian Government. The presence of orthophosphate in the influent did not influence arsenic removal efficiency in the tested AIRPs, likely due to the high iron concentrations at all sites. The high iron provides adequate surface area for both orthophosphate and arsenic to be removed. Orthophosphate co-precipitated with iron oxides much more quickly than arsenic, in one cleaning cycle study, and is expected to play a more significant role in interfering with arsenic removal at sites with much lower iron concentrations. The aeration trays studied are estimated to introduce at least 2.4-3.7 mg/L of dissolved oxygen. In normal operation, sufficient oxygen is introduced through the aeration tray to fully oxidize all influent iron. The AIRPs studied show promise for use in areas of Bangladesh with high natural iron, where users are concerned with arsenic, iron, or both, in their drinking water.
Asunto(s)
Arsénico/química , Hierro/química , Oxígeno/química , Fosfatos/química , Purificación del Agua/instrumentación , Purificación del Agua/métodos , Adsorción , Aniones/química , Bangladesh , Oxidación-Reducción , Contaminantes Químicos del Agua/química , Abastecimiento de AguaRESUMEN
Novel therapeutic approaches using stem cell transplantation to treat neurodegenerative diseases have yielded promising results. However, survival of stem cells after transplantation has been very poor in animal models, and considerable efforts have been directed at increasing the viability of engrafted stem cells. Therefore, understanding the mechanisms that regulate survival and death of neural stem cells is critical to the development of stem cell-based therapies. Hippocampal neural (HCN) stem cells derived from the adult rat brain undergo cell death following insulin withdrawal, which is associated with downregulation of antiapoptotic Bcl-2 family members. To understand the type of cell death in HCN cells following insulin withdrawal, apoptosis markers were assessed. Of note, DNA fragmentation or caspase-3 activation was not observed, but rather dying cells displayed features of autophagy, including increased expression of Beclin 1 and the type II form of light chain 3. Electron micrographs showed the dramatically increased formation of autophagic vacuoles with cytoplasmic contents. Staurosporine induced robust activation of caspase-3 and nucleosomal DNA fragmentation, suggesting that the machinery of apoptosis is intact in HCN cells despite the apparent absence of apoptosis following insulin withdrawal. Autophagic cell death was suppressed by knockdown of autophagy-related gene 7, whereas promotion of autophagy by rapamycin increased cell death. Taken together, these data demonstrate that HCN cells undergo a caspase-independent, autophagic cell death following insulin withdrawal. Understanding the mechanisms governing autophagy of adult neural stem cells may provide novel strategies to improve the survival rate of transplanted stem cells for treatment of neurodegenerative diseases. Disclosure of potential conflicts of interest is found at the end of this article.
Asunto(s)
Células Madre Adultas/citología , Autofagia , Hipocampo/citología , Insulina/deficiencia , Neuronas/citología , Células Madre/citología , Animales , Apoptosis , Proliferación Celular , Células Cultivadas , Regulación hacia Abajo , Inmunohistoquímica , Proteínas de Filamentos Intermediarios/metabolismo , Proteínas del Tejido Nervioso/metabolismo , Nestina , Neuronas/ultraestructura , Ratas , Células Madre/ultraestructura , Vacuolas/ultraestructura , Proteína bcl-X/metabolismoRESUMEN
The objective of this study was to determine if the phosphodiesterase 5 (PDE-5) inhibitor, sildenafil, could be used as a neuroprotective agent in a chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) murine model of Parkinson's disease. The underlying hypothesis of these studies is that blockade of PDE-5 catabolism of cGMP will attenuate the loss of nigrostriatal dopamine (NSDA) neurons following chronic neurotoxin exposure. Chronic MPTP-treated mice were administered sildenafil using three different regimens. Animals were: 1) treated with sildenafil and then exposed to chronic MPTP; 2) treated concurrently with sildenafil and MPTP; and 3) first exposed to MPTP and subsequently treated with sildenafil. End points of neurotoxicity included dopamine (DA) and tyrosine hydroxylase (TH) concentrations in NSDA axon terminals in the striatum, and stereological cell counts of TH immunoreactive neurons in the substantia nigra. Results reveal that sildenafil did not prevent neurotoxicity produced by chronic MPTP exposure regardless of the treatment paradigms employed. On the other hand, sildenafil did not produce any deleterious effect on NSDA neuron function nor did it potentiate the neurotoxic effects of MPTP. These results suggest that sildenafil would not accelerate DA cell loss when used as a treatment for erectile dysfunction in men diagnosed with Parkinson's disease.