Interface Engineering for Organic Electronics

The field of organic electronics has been developed vastly in the past two decades due to its promise for low cost, lightweight, mechanical flexibility, versatility of chemical design and synthesis, and ease of processing. The performance and lifetime of these devices, such as organic light‐emitting diodes (OLEDs), photovoltaics (OPVs), and field‐effect transistors (OFETs), are critically dependent on the properties of both active materials and their interfaces. Interfacial properties can be controlled ranging from simple wettability or adhesion between different materials to direct modifications of the electronic structure of the materials. In this Feature Article, the strategies of utilizing surfactant‐modified cathodes, hole‐transporting buffer layers, and self‐assembled monolayer (SAM)‐modified anodes are highlighted. In addition to enabling the production of high‐efficiency OLEDs, control of interfaces in both conventional and inverted polymer solar cells is shown to enhance their efficiency and stability; and the tailoring of source–drain electrode–semiconductor interfaces, dielectric–semiconductor interfaces, and ultrathin dielectrics is shown to allow for high‐performance OFETs.     

Thermal Expansion of Alkaline‐Doped Lanthanum Ferrite Near the Néel Temperature

The thermal expansion and magnetic behaviors of divalent, alkaline‐doped lanthanum ferrites (La_0.9M_0.1FeO₃, M=Ca, Sr, Ba) were assessed using a combination of dilatometry, magnetometry, time‐of‐flight neutron diffraction, and high‐temperature X‐ray diffraction. Néel temperatures were determined through vibrating sample magnetometry and correlated well with changes in thermal expansion behavior observed during both dilatometry and X‐ray diffraction. The Néel temperatures observed for pure, Ca‐doped, Sr‐doped, and Ba‐doped lanthanum ferrites were 471°C, 351°C, 465°C, and 466°C, respectively. The effect of divalent substitutions on the magnetic behavior are attributed to charge compensation mechanisms and structural changes in the material.     

Crosslinking effect on polydimethylsiloxane elastic modulus measured by custom‐built compression instrument

A macroscopic compression test utilizing a simple custom‐built instrument was employed to measure polydimethylsiloxane (PDMS) elastic modulus. PDMS samples with varying crosslinking density were prepared with the elastomer base to the curing agent ratio ranging from 5 : 1 to 33 : 1. The PDMS network elastic modulus varied linearly with the amount of crosslinker, ranging from 0.57 MPa to 3.7 MPa for the samples tested. PDMS elastic modulus in MPa can be expressed as 20 MPa/PDMS base to curing agent ratio. This article describes a simple method for measuring elastic properties of soft polymeric materials. © 2014 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2014 , 131, 41050.     

Multidimensional Phylogenetic Metrics Identify Class I Aminoacyl-tRNA Synthetase Evolutionary Mosaicity and Inter-Modular Coupling

The role of aminoacyl-tRNA synthetases (aaRS) in the emergence and evolution of genetic coding poses challenging questions concerning their provenance. We seek evidence about their ancestry from curated structure-based multiple sequence alignments of a structurally invariant “scaffold” shared by all 10 canonical Class I aaRS. Three uncorrelated phylogenetic metrics—mutation frequency, its uniformity, and row-by-row cladistic congruence—imply that the Class I scaffold is a mosaic assembled from successive genetic sources. Metrics for different modules vary in accordance with their presumed functionality. Sequences derived from the ATP– and amino acid– binding sites exhibit specific two-way coupling to those derived from Connecting Peptide 1, a third module whose metrics suggest later acquisition. The data help validate: (i) experimental fragmentations of the canonical Class I structure into three partitions that retain catalytic activities in proportion to their length; and (ii) evidence that the ancestral Class I aaRS gene also encoded a Class II ancestor in frame on the opposite strand. A 46-residue Class I “protozyme” roots the Class I tree prior to the adaptive radiation of the Rossmann dinucleotide binding fold that refined substrate discrimination. Such rooting implies near simultaneous emergence of genetic coding and the origin of the proteome, resolving a conundrum posed by previous inferences that Class I aaRS evolved after the genetic code had been implemented in an RNA world. Further, pinpointing discontinuous enhancements of aaRS fidelity establishes a timeline for the growth of coding from a binary amino acid alphabet.     

Nitrogen fixation and productivity of winter annual legume cover crops in Upper Midwest organic cropping systems

Nutrient Cycling in Agroecosystems - Legume cover crops can play a valuable role in maintaining and increasing soil quality and nitrogen availability, but are infrequently grown in the Upper...     

The Effects of Exercise and Activity-Based Physical Therapy on Bone after Spinal Cord Injury

Spinal cord injury (SCI) produces paralysis and a unique form of neurogenic disuse osteoporosis that dramatically increases fracture risk at the distal femur and proximal tibia. This bone loss is driven by heightened bone resorption and near-absent bone formation during the acute post-SCI recovery phase and by a more traditional high-turnover osteopenia that emerges more chronically, which is likely influenced by the continual neural impairment and musculoskeletal unloading. These observations have stimulated interest in specialized exercise or activity-based physical therapy (ABPT) modalities (e.g., neuromuscular or functional electrical stimulation cycling, rowing, or resistance training, as well as other standing, walking, or partial weight-bearing interventions) that reload the paralyzed limbs and promote muscle recovery and use-dependent neuroplasticity. However, only sparse and relatively inconsistent evidence supports the ability of these physical rehabilitation regimens to influence bone metabolism or to increase bone mineral density (BMD) at the most fracture-prone sites in persons with severe SCI. This review discusses the pathophysiology and cellular/molecular mechanisms that influence bone loss after SCI, describes studies evaluating bone turnover and BMD responses to ABPTs during acute versus chronic SCI, identifies factors that may impact the bone responses to ABPT, and provides recommendations to optimize ABPTs for bone recovery.     

Pep19 Has a Positive Effect on Insulin Sensitivity and Ameliorates Both Hepatic and Adipose Tissue Phenotype of Diet-Induced Obese Mice

Peptide DIIADDEPLT (Pep19) has been previously suggested to improve metabolic parameters, without adverse central nervous system effects, in a murine model of diet-induced obesity. Here, we aimed to further evaluate whether Pep19 oral administration has anti-obesogenic effects, in a well-established high-fat diet-induced obesity model. Male Swiss mice, fed either a standard diet (SD) or high-fat diet (HFD), were orally administrated for 30 consecutive days, once a day, with saline vehicle or Pep19 (1 mg/kg). Next, several metabolic, morphological, and behavioral parameters were evaluated. Oral administration of Pep19 attenuated HFD body-weight gain, reduced in approximately 40% the absolute mass of the endocrine pancreas, and improved the relationship between circulating insulin and peripheral insulin sensitivity. Pep19 treatment of HFD-fed mice attenuated liver inflammation, hepatic fat distribution and accumulation, and lowered plasma alanine aminotransferase activity. The inguinal fat depot from the SD group treated with Pep19 showed multilocular brown-fat-like cells and increased mRNA expression of uncoupling protein 1 (UCP1), suggesting browning on inguinal white adipose cells. Morphological analysis of brown adipose tissue (BAT) from HFD mice showed the presence of larger white-like unilocular cells, compared to BAT from SD, Pep19-treated SD or HFD mice. Pep19 treatment produced no alterations in mice behavior. Oral administration of Pep19 ameliorates some metabolic traits altered by diet-induced obesity in a Swiss mice model.