Age and phenology control photosynthesis and leaf traits in the understory woody species, Rhamnus cathartica and Prunus serotina.

Understory plants are often inadequately represented or neglected within analyses of forest ecosystem productivity. Further, the potential impacts of the biological factors of age class and growth form on carbon cycling physiology, and how it may vary across the growing season and amongst species of different native/non-native status, have not been thoroughly considered. Our study examines photosynthesis and associated physical leaf traits in two understory woody species, Rhamnus cathartica, introduced and invasive in North America, and Prunus serotina, a common subcanopy species native to North America. We estimated leaf-level photosynthesis as measured through light and carbon dioxide response curves, dark-adapted chlorophyll fluorescence and leaf traits (leaf mass per area and stomatal density) for each combination of species and age class at plots in the understory of a temperate deciduous research forest in the US Upper Midwest at two time points during the growing season, late spring (late May) and mid-summer (mid-July). Carbon assimilation rates from light response curves (A sat, A 400) and fluorescence capacity estimate F v/F m all increased between the two measurement points in both species and age class. Estimates of carbon reaction capacity (V cmax and J max) exhibited a different directional response to seasonal development, declining in seedlings of both species and P. serotina trees (~8-37 % reduction in V cmax, ~9-34 % reduction in J max), though increased in trees of R. cathartica (+24 % in V cmax, +9 % in J max). Divergent responses in photosynthetic parameters amongst these factors may be explained by species differences in leaf mass per area and stomatal density, which together are likely influenced by both growth form, canopy position and ontogeny. Overall, we believe our findings suggest complex, varied influences on photosynthesis that indicate environmental and biological plasticity which may contribute to the historic and continued expansion of R. cathartica in the US Upper Midwest region.

Nociceptor neurons direct goblet cells via a CGRP-RAMP1 axis to drive mucus production and gut barrier protection.

Neuroepithelial crosstalk is critical for gut physiology. However, the mechanisms by which sensory neurons communicate with epithelial cells to mediate gut barrier protection at homeostasis and during inflammation are not well understood. Here, we find that Nav1.8+CGRP+ nociceptor neurons are juxtaposed with and signal to intestinal goblet cells to drive mucus secretion and gut protection. Nociceptor ablation led to decreased mucus thickness and dysbiosis, while chemogenetic nociceptor activation or capsaicin treatment induced mucus growth. Mouse and human goblet cells expressed Ramp1, receptor for the neuropeptide CGRP. Nociceptors signal via the CGRP-Ramp1 pathway to induce rapid goblet cell emptying and mucus secretion. Notably, commensal microbes activated nociceptors to control homeostatic CGRP release. In the absence of nociceptors or epithelial Ramp1, mice showed increased epithelial stress and susceptibility to colitis. Conversely, CGRP administration protected nociceptor-ablated mice against colitis. Our findings demonstrate a neuron-goblet cell axis that orchestrates gut mucosal barrier protection.

ChABC infusions into medial prefrontal cortex, but not posterior parietal cortex, improve the performance of rats tested on a novel, challenging delay in the touchscreen TUNL task.

Perineuronal nets (PNNs) are specialized extracellular matrix structures that surround subsets of neurons throughout the central nervous system (CNS). They are made up of chondroitin sulfate proteoglycans (CSPGs), hyaluronan, tenascin-R, and many other link proteins that together make up their rigid and lattice-like structure. Modulation of PNNs can alter synaptic plasticity and thereby affect learning, memory, and cognition. In the present study, we degraded PNNs in the medial prefrontal (mPFC) and posterior parietal (PPC) cortices of Long-Evans rats using the enzyme chondroitinase ABC (ChABC), which cleaves apart CSPGs. We then measured the consequences of PNN degradation on spatial working memory (WM) with a trial-unique, non-matching-to location (TUNL) automated touchscreen task. All rats were trained with a standard 6 sec delay and 20 sec inter-trial interval (ITI) and then tested under four different conditions: a 6 sec delay, a variable 2 or 6 sec delay, a 2 sec delay with a 1 sec ITI (interference condition), and a 20 sec delay. Rats that received mPFC ChABC treatment initially performed TUNL with higher accuracy, more selection trials completed, and fewer correction trials completed compared to controls in the 20 sec delay condition but did not perform differently from controls in any other condition. Rats that received PPC ChABC treatment did not perform significantly differently from controls in any condition. Posthumous immunohistochemistry confirmed an increase in CSPG degradation products (C4S stain) in the mPFC and PPC following ChABC infusions while WFA staining intensity and parvalbumin positive neuron number were decreased following mPFC, but not PPC, ChABC infusions. These findings suggest that PNNs in the mPFC play a subtle role in spatial WM, but PNNs in the PPC do not. Furthermore, it appears that PNNs in the mPFC are involved in adapting to a challenging novel delay, but that they do not play an essential role in spatial WM function.

Non-small-cell lung cancer cell lines A549 and NCI-H460 express hypoxanthine guanine phosphoribosyltransferase on the plasma membrane.

In both males and females, lung cancer is one of the most lethal cancers worldwide and accounts for >30% of cancer-related deaths. Despite advances in biomarker analysis and tumor characterization, there remains a need to find suitable biomarker antigen targets for treatment in late-stage lung cancer. Previous research on the salvage pathway enzyme TK1 shows a unique relationship with cancer patients as serum levels are raised according to cancer grade. To expand this analysis, the other salvage pathway enzymes were evaluated for possible upregulation within lung cancer. Adenine phosphoribosyltransferase, deoxycytidine kinase, and hypoxanthine guanine phosphoribosyltransferase (HPRT) were assessed for their presentation on two non-small-cell lung cancer cell lines NCI-H460 and A549. In the present study, we show that deoxycytidine kinase and adenine phosphoribosyltransferase have no significant relationship with the membrane of NCI-H460 cells. However, we found significant localization of HPRT to the membrane of NCI-H460 and A549 cells. When treated with anti-HPRT antibodies, the average fluorescence of the cell population increased by 24.3% and 12.9% in NCI-H460 and A549 cells, respectively, in comparison with controls. To ensure that expression was not attributed to cytoplasmic HPRT, confocal microscopy was performed to visualize HPRT binding on the plasma membrane. After staining NCI-H460 cells treated with both fluorescent antibodies and a membrane-specific dye, we observed direct overlap between HPRT and the membrane of the cancer cells. Additionally, gold-conjugated antibodies were used to label and quantify the amount of HPRT on the cell surface using scanning electron microscopy and energy-dispersive analysis X-ray. Further confirming HPRT presence, the gold weight percentage of the sample increased significantly when NCI-H460 cells were exposed to HPRT antibody (P=0.012) in comparison with isotype controls. Our results show that HPRT is localized on the surface of these non-small-cell lung cancer cell lines.

Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.HttQ111/+ model of Huntington's disease.

We investigated the appearance and progression of disease-relevant signs in the B6.HttQ111/+ mouse, a genetically precise model of the mutation that causes Huntington's disease (HD). We find that B6.HttQ111/+ mice are healthy, show no overt signs of central or peripheral inflammation, and no gross motor impairment as late as 12 months of age. Behaviorally, we find that 4-9 month old B6.HttQ111/+ mice have normal activity levels and show no clear signs of anxiety or depression, but do show clear signs of reduced motivation. The neuronal density, neuronal size, synaptic density and number of glia is normal in B6.HttQ111/+ striatum, the most vulnerable brain region in HD, up to 12 months of age. Despite this preservation of the synaptic and cellular composition of the striatum, we observe clear progressive, striatal-specific transcriptional dysregulation and accumulation of neuronal intranuclear inclusions (NIIs). Simulation studies suggest these molecular endpoints are sufficiently robust for future preclinical studies, and that B6.HttQ111/+ mice are a useful tool for modeling disease-modifying or neuroprotective strategies for disease processes before the onset of overt phenotypes.

Corrosion Resistance of Atomic Layer Deposition-Generated Amorphous Thin Films.

Atomic layer deposition (ALD) was used to prepare amorphous thin films of Al2O3, Nb2O5, and Ta2O5 on both silicon substrates and aluminum blocks. Etch rates in 10 M NH4OH were determined from X-ray reflectometry data collected as a function of time. Amorphous Al2O3 thin films were found to have an etch rate of 0.5 nm min-1 and an increase in roughness of ∼0.01 nm min-1. Electron microscopy data showed etch pits, consistent with the increase in roughness. Amorphous Nb2O5 and Ta2O5 films showed no appreciable etching or roughening over the course of a ∼500 h continuous immersion. An Nb2O5-coated aluminum block showed no corrosion after immersion in 10 M NH4OH for over 200 h, suggesting that the coatings were pinhole-free. These results suggest that amorphous ALD thin films of Nb2O5 and Ta2O5 are candidates as barrier layers for aluminum in caustic environments.

Synthesis of inorganic structural isomers by diffusion-constrained self-assembly of designed precursors: a novel type of isomerism.

The structure of precursors is used to control the formation of six possible structural isomers that contain four structural units of PbSe and four structural units of NbSe2: [(PbSe)1.14]4[NbSe2]4, [(PbSe)1.14]3[NbSe2]3[(PbSe)1.14]1[NbSe2]1, [(PbSe)1.14]3[NbSe2]2[(PbSe)1.14]1[NbSe2]2, [(PbSe)1.14]2[NbSe2]3[(PbSe)1.14]2[NbSe2]1, [(PbSe)1.14]2[NbSe2]2[(PbSe)1.14]1[NbSe2]1[(PbSe)1.14]1[NbSe2]1, [(PbSe)1.14]2[NbSe2]1[(PbSe)1.14]1[NbSe2]2[(PbSe)1.14]1[NbSe2]1. The electrical properties of these compounds vary with the nanoarchitecture. For each pair of constituents, over 20,000 new compounds, each with a specific nanoarchitecture, are possible with the number of structural units equal to 10 or less. This provides opportunities to systematically correlate structure with properties and hence optimize performance.

Designed synthesis, structure, and properties of a family of ferecrystalline compounds [(PbSe)(1.00)](m)(MoSe2)(n).

The targeted synthesis of multiple compounds with specific controlled nanostructures and identical composition is a grand challenge in materials chemistry. We report the synthesis of the new metastable compounds [(PbSe)1.00]m(MoSe2)n using precursors each designed to self-assemble into a specific compound. To form a compound with specific values for m and n, the number of atoms within each deposited elemental layer was carefully controlled to provide the correct absolute number of atoms to form complete layers of each component structural unit. On low-temperature annealing, these structures self-assemble with a specific crystallographic orientation between the component structural units with atomically abrupt interfaces. There is rotational disorder between the component structural units and between MoSe2 basal plane units within the MoSe2 layers themselves. The lead selenide constituent has a distorted rock salt structure exactly m bilayers thick leading to peaks in the off-axis diffraction pattern as a result of the finite size of and rotational disorder between the crystallites. The in-plane lattice parameters of the PbSe and MoSe2 components are independent of the value of m and n, suggesting little or no strain caused by the interface between them. These compounds are small band gap semiconductors with carrier properties dominated by defects and exhibit extremely low thermal conductivity as a result of the rotational disorder. The thermal conductivity can be tuned by varying the ratio of the number of ordered PbSe rock salt layers relative to the number of rotationally disordered MoSe2 layers. This approach, based on controlling the local composition of the precursor and low temperature to limit diffusion rates, provides a general route to the synthesis of new compounds containing alternating layers of constituents with designed nanoarchitecture.