gebhart/patrepeval huggingface dataset:
High-Sn-content GeSn Alloy towards Room-temperature Mid Infrared Laser (2018)

Si photonics is a rapidly expanding technology that integrates photonic circuits onto a Si substrate. The integration of Si electronics and photonics has been a successful technology for a wide range of applications. Group-IV alloy GeSn has drawn great attentions as a complementary metal–oxide–semiconductor compatible optoelectronic material for Si photonics. The devices based on GeSn alloy could be monolithically integrated into well-established and high-yield Si integrated circuits, which is favorable for chip-scale Si photonics featuring smaller size, lower cost, and higher reliability. The relaxed GeSn with high material quality and high Sn composition is highly desirable to cover mid-infrared wavelength. A systematic study of GeSn strain relaxation mechanism and its effects on Sn incorporation during the epitaxy via chemical vapor deposition was conducted. It was discovered that Sn incorporation into Ge lattice sites is limited by high compressive strain rather than historically acknowledged chemical reaction dynamics, which was also confirmed by Gibbs free energy calculation. Following the discovered growth mechanism, a world-record Sn content of 22.3% was achieved. Even higher Sn content could be obtained if further continuous growth with the same recipe is conducted. The GeSn laser with higher Sn content is highly desired to cover longer wavelength in mid-infrared. This work demonstrated optically pumped edge-emitting GeSn lasers under two different pumping lasers with 1064 and 1950 nm wavelengths. The device structure featured Sn compositional graded with the maximum Sn content of 22.3%. Under the 1950 nm pumping laser, the GeSn laser achieved the world-record near room temperature lasing (270 K). The corresponding lasing wavelength has been extended up to 3442 nm, an unprecedented GeSn lasing wavelength so far in the world. The GeSn/GeSn/GeSn single and double quantum wells were also investigated to further improve laser performance. The unintentional Ge interlayer between barrier and well region of QW structure was removed by introducing the GeSn with variable Sn content as the buffer layer. As a result, the QW structure was demonstrated as the true type-I and direct bandgap structure, which is advantageous for the optoelectronic devices.
Blending with Non‐responsive Polymers to Incorporate Nanoparticles into Shape‐Memory Materials and Enable Photothermal Heating: The Effects of Heterogeneous Temperature Distribution (2014)

Blending a shape‐memory polymer (SMP) (e.g., thermoplastic polyurethane) with an immiscible carrier polymer (e.g., poly(ethylene oxide) (PEO) or poly(vinyl alcohol) (PVA)) containing dispersed metal nanoparticles (AuNPs) is a simple approach to enable actuation via photothermal heating. For blends containing up to 90% carrier polymer, the shape‐memory capability can be thermally triggered either conventionally or utilizing internal heating via application of light that is resonant with the particle's surface plasmon resonance. When incorporating nanoparticles in this manner, neither chemical modification of the shape‐memory moiety nor solvation of the SMP is necessary. Actuation times are determined by the particular heterogeneous temperature distribution, which generally occurs under both conventional and photothermal heating methods, but with different spatial patterns. Blending an SMP with PEO containing AuNPs imposes a higher transition temperature (the melting point of PEO), enabling heat generated within the nanoparticle‐containing regions to equilibrate throughout the sample, resulting in performance under photothermal conditions comparable with that achieved in a conventional heating approach. SMP:PVA blends actuate at the SMP transition temperature and the response depends on the size of phase segregation between the PVA and SMP; when decreasing the characteristic size of the segregated regions, heat is efficiently transferred and optimal photothermal performance is observed. image
Beneficial behavioral effects of chronic cerebral dopamine neurotrophic factor (CDNF) infusion in the N171-82Q transgenic model of Huntington’s disease (2023)

Huntington's disease (HD) is a progressive inherited neurological disease characterized by the degeneration of basal ganglia and the accumulation of mutant huntingtin (mHtt) aggregates in specific brain areas. Currently, there is no treatment for halting the progression of HD. Cerebral dopamine neurotrophic factor (CDNF) is a novel endoplasmic reticulum located protein with neurotrophic factor properties that protects and restores dopamine neurons in rodent and non-human primate models of Parkinson's disease. Our recent study showed that CDNF improves motor coordination and protects NeuN positive cells in a Quinolinic acid toxin rat model of HD. Here we have investigated the effect of chronic intrastriatal CDNF administration on behavior and mHtt aggregates in the N171-82Q mouse model of HD. Data showed that CDNF did not significantly decrease the number of mHtt aggregates in most brain regions studied. Notably, CDNF significantly delayed the onset of symptoms and improved motor coordination in N171-82Q mice. Furthermore, CDNF increased BDNF mRNA level in hippocampus in vivo in the N171-82Q model and BDNF protein level in cultured striatal neurons. Collectively our results indicate that CDNF might be a potential drug candidate for the treatment of HD.
The effect of atropine on acetylcholine action at the neuromuscular junction (1973)

Abstract The action of atropine at the motor end plate was studied by measuring its effect on acetylcholine-induced fluctuations of membrane potential (‘acetylcholine noise’). Atropine, in contrast to curare, modifies the elementary depolarization produced by the impact of acetylcholine molecules; it reduces the voltage amplitude and shortens the underlying ionic current pulse.
Particulate matter causes skin barrier dysfunction (2021)

The molecular mechanisms that underlie the detrimental effects of particulate matter (PM) on skin barrier function are poorly understood. In this study, the effects of PM2.5 on filaggrin (FLG) and skin barrier function were investigated in vitro and in vivo. The levels of FLG degradation products, including pyrrolidone carboxylic acid, urocanic acid (UCA), and cis/trans-UCA, were significantly decreased in skin tape stripping samples of study subjects when they moved from Denver, an area with low PM2.5, to Seoul, an area with high PM2.5 count. Experimentally, PM2.5 collected in Seoul inhibited FLG, loricrin, keratin-1, desmocollin-1, and corneodesmosin but did not modulate involucrin or claudin-1 in keratinocyte cultures. Moreover, FLG protein expression was inhibited in human skin equivalents and murine skin treated with PM2.5. We demonstrate that this process was mediated by PM2.5-induced TNF-α and was aryl hydrocarbon receptor dependent. PM2.5 exposure compromised skin barrier function, resulting in increased transepidermal water loss, and enhanced the penetration of FITC-dextran in organotypic and mouse skin. PM2.5-induced TNF-α caused FLG deficiency in the skin and subsequently induced skin barrier dysfunction. Compromised skin barrier due to PM2.5 exposure may contribute to the development and the exacerbation of allergic diseases such as atopic dermatitis.
Heat Resistant Adhesion and Melt Rheology of the Polymer Complex between lonomer and Polyamide Oligomer (1986)

Polyamide chain was introduced in the Zn ion ionomer made from ethylene-methacrylic acid copolymer and its effect on the heat resistant adhesive properties was investigated. The heat resistant temperature of the ionomer was enormously improved by compounding 5-20wt% of polyamide oligomer with primary amino end group into the ionomer. The resulting composite was thermoplastic and exhibited unusual thermo-adhesion behavior. Although the composite was capable of thermo-adhesion at the temperature as low as that for the component ionomer, it did not creep significantly up to the temperature considerably higher than the adhesion temperature.To clarify the cause and mechanisms of this unusual function, rheological measurements were made on the composite. The following features were revealed. The composite exhibited highly non-Newtonian flow behavior in the temperature range between the melting point of the component ionomer (85-105°C) and that of polyamide oligomer (180-215°C). The viscosity of the composite was much higher than that of the ionomer at low shear rates, leading to the improved heat resistant adhesive properties. With increasing shear rates, the viscosity of the composite decreased down to that of the ionomer, leading to the ease of thermo-processing and adhesion of the composite.In the composite, ammine complex salt was formed between Zn ionomer and polyamide oligomer through coordination of amino end group of the latter to zinc carboxylate of the former. In the above-mentioned temperature range, microphase-separated structures were formed in the composite. The solid phase microdomains of polyamide chains were dispersed in molten matrix of ionomer, and these phases were connected by coordination ionic bond. The thermoplastic and non-Newtonian behavior of the composite resulted from the destruction of the microdomains under high shear rates and the decrease of the ionic bond strength under high shear rates and high temperature.
Discovery of 3,3‐Dimethyl‐5‐hydroxypipecolic Hydroxamate‐Based Inhibitors of Aggrecanase and MMP‐13. (2005)

Abstract For Abstract see ChemInform Abstract in Full Text.
Figure S1 from Blockade of Cell Volume Regulatory Protein NKCC1 Increases TMZ-Induced Glioma Apoptosis and Reduces Astrogliosis (2023)

&lt;p&gt;Fig. S1. Full-length western blots of glioma cells, mouse tissue and human tissue samples.&lt;/p&gt;
The ACE2‐deficient mouse: A model for a cytokine storm‐driven inflammation (2020)

Angiotensin converting enzyme 2 (ACE2) plays an important role in inflammation, which is attributable at least, in part, to the conversion of the pro-inflammatory angiotensin (Ang) II peptide into angiotensin 1-7 (Ang 1-7), a peptide which opposes the actions of AngII. ACE2 and AngII are present in many tissues but information on the cornea is lacking. We observed that mice deficient in the Ace2 gene (Ace2<sup>-/-</sup> ), developed a cloudy cornea phenotype as they aged. Haze occupied the central cornea, accompanied by corneal edema and neovascularization. In severe cases with marked chronic inflammation, a cell-fate switch from a transparent corneal epithelium to a keratinized, stratified squamous, psoriasiform-like epidermis was observed. The stroma contained a large number of CD11c, CD68, and CD3 positive cells. Corneal epithelial debridement experiments in young ACE2-deficient mice showed normal appearing corneas, devoid of haze. We hypothesized, however, that these mice are "primed" for a corneal inflammatory response, which once initiated, would persist. In vitro studies reveal that interleukins (IL-1a, IL-1b), chemokines (CCL2, CXCL8), and TNF-α, are all significantly elevated, resulting in a cytokine storm-like phenotype. This phenotype could be partially rescued by treatment with the AngII type 1 receptor (AT1R) antagonist, losartan, suggesting that the observed effect was mediated by AngII acting on its main receptor. Since the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes human ACE2 as the receptor for entry with subsequent downregulation of ACE2, corneal inflammation in Ace2<sup>-/-</sup> mice may have a similar mechanism with that in COVID-19 patients. Thus the Ace2<sup>-/-</sup> cornea, because of easy accessibility, may provide an attractive model to explore the molecular mechanisms, immunological changes, and treatment modalities in patients with COVID-19.
Polyoxovanadometalate‐Catalyzed Selective Epoxidation of Alkenes with Hydrogen Peroxide (2005)

The bis(μ-hydroxo)-bridged dioxovanadium site in [γ-1,2-H2SiV2W10O40]4− catalyzes the epoxidation of alkenes in the presence of only one equivalent of H2O2 with a high yield of epoxide, high efficiency of H2O2 utilization, unusual regioselectivity, and unprecedented diastereoselectivity (see picture).
Non-Phosphorylated Tau in Cerebrospinal Fluid is a Marker of Alzheimer’s Disease Continuum in Young Urbanites Exposed to Air Pollution (2018)

Long-term exposure to fine particulate matter (PM2.5) and ozone (O3) above USEPA standards is associated with Alzheimer's disease (AD) risk. Metropolitan Mexico City (MMC) children exhibit subcortical pretangles in infancy and cortical tau pre-tangles, NFTs, and amyloid phases 1-2 by the 2nd decade. Given their AD continuum, we measured in 507 normal cerebrospinal fluid (CSF) samples (MMC 354, controls 153, 12.82±6.73 y), a high affinity monoclonal non-phosphorylated tau antibody (non-P-Tau), as a potential biomarker of AD and axonal damage. In 81 samples, we also measured total tau (T-Tau), tau phosphorylated at threonine 181 (P-Tau), amyloid-β1-42, BDNF, and vitamin D. We documented by electron microscopy myelinated axonal size and the pathology associated with combustion-derived nanoparticles (CDNPs) in anterior cingulate cortex white matter in 6 young residents (16.25±3.34 y). Non-P-Tau showed a strong increase with age significantly faster among MMC versus controls (p = 0.0055). Aβ1 - 42 and BDNF concentrations were lower in MMC children (p = 0.002 and 0.03, respectively). Anterior cingulate cortex showed a significant decrease (p = <0.0001) in the average axonal size and CDNPs were associated with organelle pathology. Significant age increases in non-P-Tau support tau changes early in a population with axonal pathology and evolving AD hallmarks in the first two decades of life. Non-P-Tau is an early biomarker of axonal damage and potentially valuable to monitor progressive longitudinal changes along with AD multianalyte classical CSF markers. Neuroprotection of young urbanites with PM2.5 and CDNPs exposures ought to be a public health priority to halt the development of AD in the first two decades of life.
Sequential and parallel algorithms for frontier A* with delayed duplicate detection (2006)

We present sequential and parallel algorithms for Frontier A * (FA*) algorithm augmented with a form of Delayed Duplicate Detection (DDD). The sequential algorithm, FA*-DDD, overcomes the leak-back problem associated with the combination of FA * and DDD. The parallel algorithm, PFA*-DDD, is a parallel version of FA*-DDD that features a novel workload distribution strategy based on intervals. We outline an implementation of PFA*-DDD designed to run on a cluster of workstations. The implementation computes intervals at runtime that are tailored to fit the workload at hand. Because the implementation distributes the workload in a manner that is both automated and adaptive, it does not require the user to specify a workload mapping function, and, more importantly, it is applicable to arbitrary problems that may be irregular. We present the results of an experimental evaluation of the implementation where it is used to solve instances of the multiple sequence alignment problem on a cluster of workstations running on top of a commodity network. Results demonstrate that the implementation offers improved capability in addition to improved performance.
A web-based protein retrieval system by matching visual similarity (2005)

A Web-based three-dimensional (3D) protein retrieval system is available for protein structure data including all PDB and FSSP dataset. In this system, we use a visual-based matching method to compare the protein structure from multiple viewpoints. It takes less than three seconds for each query with 90% accuracy on the average
Predicting execution bottlenecks in map-reduce clusters (2012)

Extremely slow, or straggler, tasks are a major performance bottleneck in map-reduce systems. Hadoop infrastructure makes an effort to both avoid them (through minimizing remote data accesses) and handle them in the runtime (through speculative execution). However, the mechanisms in place neither guarantee the avoidance of performance hotspots in task scheduling, nor provide any easy way to tune the timely detection of stragglers. We suggest a machine-learning approach to address these problems, and introduce a slowdown predictor - an oracle to forecast how much slower a task will run on a given node, compared to similar tasks. Slowdown predictors can be embedded in the map-reduce infrastructure to improve the agility and timeliness of scheduling decisions. We provide initial evaluation to demonstrate the viability of our approach, and discuss the use cases for the new paradigm.
High Performance Beam Forming Network for Multi Contoured Beam Antennas (1986)

A compact Beam Forming Network (BFN) for contoured beam antennas has been developed and tested in the 10.9 to 12.8 GHz band (16%). The BFN components are designed with efficient electromagnetic tools to reduce the insertion loss and the amplitude and phase spreadings at the output ports. Particular care has been dedicated to the mechanical design in order to minimize the mass, to avoid critical resonances and thermal gradients. The BFN is composed of two independent sections connected together. These are the power divider section with sixteen output signals and the phase shifter section which establishes the correct phase distribution. The BFN utilizes as key components branch guide couplers and ireses phase shifters whose the predicted electrical characteristics are in excellent agreement with the experiments. Moreover an innovative technique is adopted to compensate the phase errors of the network in the relative wide band without additional tuning elements.
Recombinant Tissue-Type Plasminogen Activator in the Treatment of Acute Renal Artery Thrombosis After Kidney Transplantation (2010)

Acute arterial thrombosis is an uncommon but potentially devastating consequence of kidney transplantation. Early recognition followed by thrombectomy may salvage the graft. We present a case of acute renal artery thrombosis after a living-related kidney transplant with successful treatment with operative thrombectomy and intraarterial infusion of recombinant tissue-type plasminogen activator.
Abstract 903: The IKKα kinase is a potential therapeutic target in K-Ras-induced lung cancer (2012)

Abstract Lung cancer is the leading cause of cancer deaths in the world. In lung cancer, K-Ras oncogenic mutations are widespread, and compounds used to target the biological activity of the Ras proteins failed in clinical trials. Therefore, it is imperative to identify novel therapeutic targets that reduce K-Ras-induced lung tumorigenesis. We have previously shown that K-Ras-induced lung tumorigenesis is potentiated by the subunit p65 of the transcription factor NF-κB; and that K-Ras-induced NF-κB activation in the lung requires IKKα. Therefore, we hypothesized the following: (1) the IKKα kinase promotes K-Ras-induced oncogenesis; and (2) pharmacological inhibition of IKKα activity will be beneficial therapeutically. We used genetic and/or pharmacological approaches to inactivate IKKα in primary lung epithelial cells transformed by K-Ras, as well as K-Ras-positive lung cancer cell lines, and determined that IKKα inhibiton reduces oncogenic properties in vitro. In addition we used a highly specific IKKα inhibitor (CmpdA, Bayer) to treat a K-Ras-induced lung cancer mouse model combined with loss of the tumor suppressor p53 (LSL-K-RasG12D/p53fl/fl). We chose this model for the following reasons: (1) K-Ras activation coupled to p53 loss leads to aggressive lung adenocarcinomas in mice that better resemble human lung tumors; (2) lung cancer patients harboring K-Ras oncogenic mutations frequently display p53 inactivation; and (3) it has been recently demonstrated that p53 loss can enhance NF-κB activation by K-Ras in lung tumors. To induce concomitant K-Ras activation and p53 loss in murine lung epithelial cells, we infected the lungs of LSL-K-RasG12D/p53fl/fl mice by intranasal administration of a Cre-expressing adenovirus (AdCre). Two treatment regimens were used to treat infected animals: CmpdA was either administered daily for 2 weeks immediately following AdCre infection or daily for 4 weeks starting 8 weeks post-infection. In either case, mice treated with CmpdA presented smaller and lower grade tumors than mice treated with placebo. These results show that IKKα promotes lung cancer growth and progression both in vitro and in vivo. In addition, we have shown that pharmacological administration of an IKKα inhibitor slows lung tumor growth and progression in vivo, supporting our hypothesis that IKKα inhibition therapy will have clinical benefits in lung cancer. This research is supported by a FAMRI YCSA Award and a FAPESP Young Investigator Award to DB and a NIH grant (CA73756) to AB. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 903. doi:1538-7445.AM2012-903
Q‐switched thulium–ytterbium co‐doped fibre laser using newly developed octagonal shaped inner cladding double‐clad active fibre and multi‐walled carbon nanotubes passive saturable absorber (2015)

Simple and low cost passive Q‐switched thulium–ytterbium co‐doped fibre lasers (TYFL) operating at 1977.5 nm is demonstrated using 905 nm multimode pumping, in conjunction with a multi‐walled carbon nanotubes (MWCNTs) saturable absorber. It uses a new octagonal shaped double‐clad thulium ytterbium co‐doped fibre, manufactured using a modified chemical vapour deposition process and a solution doping. The Tm 3+ and Yb 3+ cladding absorptions of the fibre are 0.325 and 3.3 dB/m at 790 nm and 976 nm, respectively. The MWCNTs composite is prepared by mixing the MWCNTs homogeneous solution with a diluted polyvinyl alcohol polymer solution before it is left to dry at room temperature to produce thin film. The film is sandwiched between two fibre connectors and integrated into the laser cavity for Q‐switching pulse generation. The repetition rate of the Q‐switching pulse can be tuned from 18.8 to 50.6 kHz while the pulse width reduces from 8.6 to 1.0 µs as the pump power increases from 1.6 to 2.3 W. At the pump power of 2.1 W, the TYFL produces the maximum pulse energy of 5.7 nJ.