Objective To extend the applicability of the Wolf Motor Function test (WMFT) to describe the residual functional abilities of moderate-to-severely affected stroke patients. The WMFT is a motor function test for mild to moderate upper extremity weakness in stroke patients, but it has not been routinely used for evaluation of more severe hemiparetic stroke patients due to its numerical characteristics. Design Data was collected as part of two double-blind sham controlled randomized interventional studies, the Transcranial Direct Current Stimulation (tDCS) in Chronic Stroke Recovery and tDCS Enhanced Stroke Recovery and Cortical Reorganization. Stroke patients were evaluated with the upper-extremity Fugl-Meyer (UFM) and the WMFT in the same setting prior to treatment. Setting University inpatient rehabilitation and outpatient clinic. Participants 32 stroke patients with moderate-to-severe hemiparesis enrolled in the tDCS in Chronic Stroke Recovery and tDCS Enhanced Stroke Recovery and Cortical Reorganization studies. Intervention Not applicable. Main Outcome Measures WMFT scores were calculated using 1) median performance times, 2) new calculation using the mean rate of performance. We compared the distribution of values from the two methods and examined the WMFT-UFM correlation for the traditional and the new calculation. Results WMFT rate values were more evenly distributed across their range than median WMFT time scores. The association between the WMFT rate and UFM was as good as the association between the median WMFT time scores and UFM (Spearman rs 0.84 vs −0.79). Conclusions The new WMFT mean rate of performance is valid and a more sensitive measure in describing the functional activities of the moderate to severely affected upper extremity of stroke subjects and avoids the pitfalls of the median WMFT time calculations.

Previously, we have shown that flies under-expressing the two mitochondrial peroxiredoxins (Prxs), dPrx3 and dPrx5, display increases in tissue-specific apoptosis and dramatically shortened life span, associated with a redox crisis, manifested as changes in GSH:GSSG and accumulation of protein mixed disulfides. To identify specific pathways responsible for the observed biological effects, we performed a transcriptome analysis. Functional clustering revealed a prominent group enriched for immunity-related genes, including a considerable number of NF-kB-dependent antimicrobial peptides (AMP) that are up-regulated in the Prx double mutant. Using qRT-PCR analysis we determined that the age-dependent changes in AMP levels in mutant flies were similar to those observed in controls when scaled to percentage of life span. To further clarify the role of Prx-dependent mitochondrial signaling, we expressed different forms of dPrx5, which unlike the uniquely mitochondrial dPrx3 is found in multiple subcellular compartments, including mitochondrion, nucleus and cytosol. Ectopic expression of dPrx5 in mitochondria but not nucleus or cytosol partially extended longevity under normal or oxidative stress conditions while complete restoration of life span occurred when all three forms of dPrx5 were expressed from the wild type dPrx5 transgene. When dPrx5 was expressed in mitochondria or in all three compartments, it substantially delayed the development of hyperactive immunity while expression of cytosolic or nuclear forms had no effect on the immune phenotype. The data suggest a critical role of mitochondria in development of chronic activation of the immune response triggered by impaired redox control.

Mitochondrial dysfunction often leads to neurodegeneration and is considered one of the main causes of neurological disorders, such as Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and other age-related diseases. Mitochondrial dysfunction is tightly linked to oxidative stress and accumulating evidence suggests the association between oxidative stress and neurological disorders. However, there is insufficient knowledge about the role of pro-oxidative shift in cellular redox and impairment of redox-sensitive signaling in the development of neurodegenerative pathological conditions. To gain a more complete understanding of the relationship between mitochondria, redox status, and neurodegenerative disorders, we investigated the effect of mitochondrial thiol-dependent peroxidases, peroxiredoxins (Prxs), on the physiological characteristics of flies, which change with pathologies such as PD, ALS and during aging. We previously found that through their ability to sense changes in redox and regulate redox-sensitive signaling, Prxs play a critical role in maintaining global thiol homeostasis, preventing age-related apoptosis and chronic activation of the immune response. We also found that the phenotype of flies under-expressing Prxs in mitochondria shares many characteristics with the phenotype of Drosophila models of neurological disorders such as ALS, including impaired locomotor activity and compromised redox balance. Here, we expanded the study and found that under-expression of mitochondrial Prxs leads to behavioral changes associated with neural function, including locomotor ability, sleep-wake behavior, and temperature-sensitive paralysis. We also found that under-expression of mitochondrial Prxs with a motor-neuron-specific driver, D42-GAL4, was a determining factor in the development of the phenotype of shortened lifespan and impaired motor activity in flies. The results of the study suggest a causal link between mitochondrial Prx activity and the development of neurological disorders and pre-mature aging.

Tidal wetlands are among the most effective natural ecosystems in sequestrating carbon on the planet, storing 0.4-6.5 Pg C globally (Duarte et al., 2013;Windham-Myers et al., 2018). However, their spatial extents have drastically reduced due to land-use change and rising sea levels (Lewis et al., 2019). Around 43%-48% of tidal wetlands in the U.S. are vulnerable to sea-level rise (Holmquist et al., 2021), which puts these significant carbon stocks at risk (Spivak et al., 2019). Even though tidal wetlands release relatively small amounts of methane (CH 4 ) compared to freshwater wetlands, the estimates of tidal wetlands' methane budgets are highly uncertain (±75%) on the global scale (Rosentreter et al., 2021). This uncertainty impedes our ability to inventory greenhouse gas budgets and thereby assess the radiative forcing of coastal wetlands (Holmquist et al., 2018). It also impedes our ability to represent tidal wetlands in Earth System Models (Ward et al., 2020). Improved accounting and