Macroinvertebrate assemblages from a stream-wetland complex: a case study with implications for assessing restored hydrologic functions.

Legacies of past land use persist today in the form of incised, single-threaded stream channels with dramatically different hydrologic functions of pre-colonial stream valleys. Restoration practices that aim to return lost hydrologic functions by re-establishing floodplain and groundwater connections should result in stream habitat and biological assemblages that differ from modern, single-threaded channels. The aim of this case study was to identify attributes of macroinvertebrate assemblages that might serve as biological indicators of improved hydrologic functions following the restoration of a stream-wetland complex, similar to a Stage 0 restoration, of a headwater valley in the Western Allegheny region of the USA.

A Comparison of Hyporheic Transport at a Cross-Vane Structure and Natural Riffle.

While restoring hyporheic flowpaths has been cited as a benefit to stream restoration structures, little documentation exists confirming that constructed restoration structures induce comparable hyporheic exchange to natural stream features. This study compares a stream restoration structure (cross-vane) to a natural feature (riffle) concurrently in the same stream reach using time-lapsed electrical resistivity (ER) tomography. Using this hydrogeophysical approach, we were able to quantify hyporheic extent and transport beneath the cross-vane structure and the riffle.

Fractalkine over expression suppresses α-synuclein-mediated neurodegeneration.

In Parkinson's disease, α-synuclein is known to activate microglia and this activation has been proposed as one of the mechanisms of neurodegeneration. There are several signals produced by neurons that have an anti-inflammatory action on microglia, including CX3CL1 (fractalkine). We have shown that a soluble form of CX3CL1 is required to reduce neuron loss in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice and that fractalkine agonism can reduce neuron loss in a 6-hydroxydopamine lesion model.