Parameter-Efficient Tuning with Special Token Adaptation

Parameter-efficient tuning aims at updating only a small subset of parameters when adapting a pretrained model to downstream tasks. In this work, we introduce PASTA, in which we only modify the special token representations (e.g., [SEP] and [CLS] in BERT) before the self-attention module at each layer in Transformer-based models. PASTA achieves comparable performance to fine-tuning in natural language understanding tasks including text classification and NER with up to only 0.029% of total parameters trained. Our work not only provides a simple yet effective way of parameter-efficient tuning, which has a wide range of practical applications when deploying finetuned models for multiple tasks, but also demonstrates the pivotal role of special tokens in pretrained language models

Controlled epitaxial graphene growth within amorphous carbon corrals

Structured growth of high quality graphene is necessary for technological development of carbon based electronics. Specifically, control of the bunching and placement of surface steps under epitaxial graphene on SiC is an important consideration for graphene device production. We demonstrate lithographically patterned evaporated amorphous carbon corrals as a method to pin SiC surface steps. Evaporated amorphous carbon is an ideal step-flow barrier on SiC due to its chemical compatibility with graphene growth and its structural stability at high temperatures, as well as its patternability. The amorphous carbon is deposited in vacuum on SiC prior to graphene growth. In the graphene furnace at temperatures above 1200$^\circ$C, mobile SiC steps accumulate at these amorphous carbon barriers, forming an aligned step free region for graphene growth at temperatures above 1330$^\circ$C. AFM imaging and Raman spectroscopy support the formation of quality step-free graphene sheets grown on SiC with the step morphology aligned to the carbon grid

An improved prediction of the effective range of stress intensity factor in fatigue crack growth

This paper will summarise the results obtained to date and which demonstrate that the mesoscale CJP model of crack tip fields is capable of providing an improved correlation of fatigue crack growth rates across a range of stress ratios and specimen geometries, compared with the standard stress intensity factor calculations

Role of Aβ-RAGE interaction in oxidative stress and cPLA2 activation in astrocytes and cerebral endothelial cells

Blood–brain barrier (BBB) dysfunctions have been implicated in the progression of Alzheimer's disease. Cerebral endothelial cells (CECs) and astrocytes are the main cell components of the BBB. Although amyloid-β oligomers (Aβ42) have been reported to mediate oxidative damage to the CECs and astrocytes and trigger the downstream mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, the cell surface binding site for Aβ42 and exact sequence of these events have yet to be elucidated. In this study, the receptor for advanced glycation endproducts (RAGE) was postulated to function as a signal transducing cell surface receptor for Aβ42 to induce reactive oxygen species (ROS) generation from NADPH oxidase and trigger downstream pathways for the phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). We found that Aβ42 competed with the anti-RAGE antibody (AbRAGE) to bind to RAGE on the surfaces of CECs and primary astrocytes. In addition, AbRAGE abrogate Aβ42-induced ROS production and the colocalization between the cytosolic (p47-phox) and membrane (gp91-phox) subunits of NADPH oxidase in both cell types. AbRAGE as well as NADPH oxidase inhibitor and ROS scavenger suppressed Aβ42-induced ERK1/2 and cPLA2 phosphorylation in CECs. At the same time, only AbRAGE, but neither NADPH oxidase inhibitor nor ROS scavenger, inhibited the ERK1/2 pathway and cPLA2 phosphorylation in primary astrocytes. Therefore, this study demonstrates that NADPH oxidase complex assembly and ROS production are not required for Aβ42 binding to RAGE at astrocytic surface leading to sequential phosphorylation of ERK1/2 and cPLA2, and suggests the presence of two different RAGE-dependent downstream pathways in the CECs and astrocytes

Role of Aβ-RAGE interaction in oxidative stress and cPLA2 activation in astrocytes and cerebral endothelial cells

Blood–brain barrier (BBB) dysfunctions have been implicated in the progression of Alzheimer's disease. Cerebral endothelial cells (CECs) and astrocytes are the main cell components of the BBB. Although amyloid-β oligomers (Aβ42) have been reported to mediate oxidative damage to the CECs and astrocytes and trigger the downstream mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, the cell surface binding site for Aβ42 and exact sequence of these events have yet to be elucidated. In this study, the receptor for advanced glycation endproducts (RAGE) was postulated to function as a signal transducing cell surface receptor for Aβ42 to induce reactive oxygen species (ROS) generation from NADPH oxidase and trigger downstream pathways for the phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). We found that Aβ42 competed with the anti-RAGE antibody (AbRAGE) to bind to RAGE on the surfaces of CECs and primary astrocytes. In addition, AbRAGE abrogate Aβ42-induced ROS production and the colocalization between the cytosolic (p47-phox) and membrane (gp91-phox) subunits of NADPH oxidase in both cell types. AbRAGE as well as NADPH oxidase inhibitor and ROS scavenger suppressed Aβ42-induced ERK1/2 and cPLA2 phosphorylation in CECs. At the same time, only AbRAGE, but neither NADPH oxidase inhibitor nor ROS scavenger, inhibited the ERK1/2 pathway and cPLA2 phosphorylation in primary astrocytes. Therefore, this study demonstrates that NADPH oxidase complex assembly and ROS production are not required for Aβ42 binding to RAGE at astrocytic surface leading to sequential phosphorylation of ERK1/2 and cPLA2, and suggests the presence of two different RAGE-dependent downstream pathways in the CECs and astrocytes

Low energy laser light (632.8 nm) suppresses amyloid-β peptide-induced oxidative and inflammatory responses in astrocytes

Oxidative stress and inflammation are important processes in the progression of Alzheimer's disease (AD). Recent studies have implicated the role of amyloid β-peptides (Aβ) in mediating these processes. In astrocytes, oligomeric Aβ induces the assembly of NADPH oxidase complexes resulting in its activation to produce anionic superoxide. Aβ also promotes production of pro-inflammatory factors in astrocytes. Since low energy laser has previously been reported to attenuate oxidative stress and inflammation in biological systems, the objective of this study was to examine whether this type of laser light was able to abrogate the oxidative and inflammatory responses induced by Aβ. Primary rat astrocytes were exposed to Helium-Neon laser (λ=632.8 nm), followed by the treatment with oligomeric Aβ. Primary rat astrocytes were used to measure Aβ-induced production of superoxide anions using fluorescence microscopy of dihydroethidium (DHE), assembly of NADPH oxidase subunits by the colocalization between the cytosolic p47phox subunit and the membrane gp91phox subunit using fluorescent confocal microscopy, phosphorylation of cytosolic phospholipase A2 (cPLA2), and expressions of pro-inflammatory factors including interleukin-1β (IL-1β) and inducible nitric-oxide synthase (iNOS) using Western blot Analysis. Our data showed that laser light at 632.8 nm suppressed Aβ-induced superoxide production, colocalization between NADPH oxidase gp91phox and p47phox subunits, phosphorylation of cPLA2, and the expressions of IL-1β and iNOS in primary astrocytes. We demonstrated for the first time that 632.8 nm laser was capable of suppressing cellular pathways of oxidative stress and inflammatory responses critical in the pathogenesis in AD. This study should prove to provide the groundwork for further investigations for the potential use of laser therapy as a treatment for AD

Low energy laser light (632.8 nm) suppresses amyloid-β peptide-induced oxidative and inflammatory responses in astrocytes

Oxidative stress and inflammation are important processes in the progression of Alzheimer's disease (AD). Recent studies have implicated the role of amyloid β-peptides (Aβ) in mediating these processes. In astrocytes, oligomeric Aβ induces the assembly of NADPH oxidase complexes resulting in its activation to produce anionic superoxide. Aβ also promotes production of pro-inflammatory factors in astrocytes. Since low energy laser has previously been reported to attenuate oxidative stress and inflammation in biological systems, the objective of this study was to examine whether this type of laser light was able to abrogate the oxidative and inflammatory responses induced by Aβ. Primary rat astrocytes were exposed to Helium-Neon laser (λ=632.8 nm), followed by the treatment with oligomeric Aβ. Primary rat astrocytes were used to measure Aβ-induced production of superoxide anions using fluorescence microscopy of dihydroethidium (DHE), assembly of NADPH oxidase subunits by the colocalization between the cytosolic p47phox subunit and the membrane gp91phox subunit using fluorescent confocal microscopy, phosphorylation of cytosolic phospholipase A2 (cPLA2), and expressions of pro-inflammatory factors including interleukin-1β (IL-1β) and inducible nitric-oxide synthase (iNOS) using Western blot Analysis. Our data showed that laser light at 632.8 nm suppressed Aβ-induced superoxide production, colocalization between NADPH oxidase gp91phox and p47phox subunits, phosphorylation of cPLA2, and the expressions of IL-1β and iNOS in primary astrocytes. We demonstrated for the first time that 632.8 nm laser was capable of suppressing cellular pathways of oxidative stress and inflammatory responses critical in the pathogenesis in AD. This study should prove to provide the groundwork for further investigations for the potential use of laser therapy as a treatment for AD

Structure, magnetic and transport properties of Ti-substituted La0.7Sr0.3MnO3

Ti-substituted perovskites, La0.7Sr0.3Mn1-xTixO3, with x between 0 to 0.20, were investigated by neutron diffraction, magnetization, electric resistivity, and magnetoresistance (MR) measurements. All samples show a rhombohedral structure (space group R3c) from 10 K to room temperature. At room temperature, the cell parameters a, c and the unit cell volume increase with increasing Ti content. However, at 10 K, the cell parameter a has a maximum value for x = 0.10, and decreases for x greater than 0.10, while the unit cell volume remains nearly constant for x greater than 0.10. The average (Mn,Ti)-O bond length increases up to x=0.15, and the (Mn,Ti)-O-(Mn,Ti) bond angle decreases with increasing Ti content to its minimum value at x=0.15 at room temperature. Below the Curie temperature T_C, the resistance exhibits metallic behavior for the x _ 0.05 samples. A metal (semiconductor) to insulator transition is observed for the x_ 0.10 samples. A peak in resistivity appears below T_C for all samples, and shifts to a lower temperature as x increases. The substitution of Mn by Ti decreases the 2p-3d hybridization between O and Mn ions, reduces the bandwidth W, and increases the electron-phonon coupling. Therefore, the TC shifts to a lower temperature and the resistivity increases with increasing Ti content. A field-induced shift of the resistivity maximum occurs at x less than or equal to 0.10. The maximum MR effect is about 70% for La0.7Sr0.3Mn0.8Ti0.2O3. The separation of TC and the resistivity maximum temperature Tmax enhances the MR effect in these compounds due to the weak coupling between the magnetic ordering and the resistivity as compared with La0.7Sr0.3MnO3.Comment: zip fil

Occultocarpon, a new monotypic genus of Gnomoniaceae on Alnus nepalensis from China

Microfungi in the Gnomoniaceae (Diaporthales, Ascomycetes) comprise species commonly reported as pathogens and endophytes on trees and herbaceous hosts primarily from temperate forests of North America, Europe, and Japan. The diversity of Gnomoniaceae in China is poorly known, although several plant families that occur there specifically the Betulaceae are considered important hosts. An exploratory trip to Yunnan, China, resulted in the discovery of several members of the Gnomoniaceae. In this paper a new monotypic genus, Occultocarpon and its species, O. ailaoshanense, are described and illustrated. A phylogeny based on three genes (LSU, rpb2, tef1-α) reveals that O. ailaoshanense belongs to the Gnomoniaceae and forms a branch distinct from the currently known genera. Occultocarpon ailaoshanense is characterized by perithecia with thin, central to eccentric necks in groups embedded in a stroma and oblong elliptical-elongated, one-septate ascospores. Occultocarpon ailaoshanense occurs on the bark of branches of Alnus nepalensis (Betulaceae) in Yunnan, ChinaMicrofungi in the Gnomoniaceae (Diaporthales, Ascomycetes) comprise species commonly reported as pathogens and endophytes on trees and herbaceous hosts primarily from temperate forests of North America, Europe, and Japan. The diversity of Gnomoniaceae in China is poorly known, although several plant families that occur there specifically the Betulaceae are considered important hosts. An exploratory trip to Yunnan, China, resulted in the discovery of several members of the Gnomoniaceae. In this paper a new monotypic genus, Occultocarpon and its species, O. ailaoshanense, are described and illustrated. A phylogeny based on three genes (LSU, rpb2, tef1-α) reveals that O. ailaoshanense belongs to the Gnomoniaceae and forms a branch distinct from the currently known genera. Occultocarpon ailaoshanense is characterized by perithecia with thin, central to eccentric necks in groups embedded in a stroma and oblong elliptical-elongated, one-septate ascospores. Occultocarpon ailaoshanense occurs on the bark of branches of Alnus nepalensis (Betulaceae) in Yunnan, Chin