gebhart/patrepeval huggingface dataset:
Intelligent Video Surveillance (2009)

From the streets of London to&nbsp;subway stations in New York City, hundreds of thousands of surveillance cameras ubiquitously collect hundreds of thousands of videos, often running 24/7. How can such vast volumes of video data be stored, analyzed, indexed, and searched? How can advanced video analysis and systems autonomously recognize people and
Focused ultrasound-mediated suppression of chemically-induced acute epileptic EEG activity (2011)

These results revealed that low-intensity, pulsed FUS sonication suppressed the number of epileptic signal bursts using acute epilepsy model in animal. Due to its non-invasiveness and spatial selectivity, FUS may offer new perspectives for a possible non-invasive treatment of epilepsy.
Expression of genes for the alpha and beta subunits of the Na,K-ATPase in normal and drug resistant cells. (1987)

The studies described in this report show that the genes for sodium, potassium-ATPase exhibit more complexity than was originally expected on the basis of studies of the Na,K-ATPase proteins or their transport activities. First, there are at least three isoforms of the alpha subunit. Second, expression of the beta subunit, although apparently always leading to the same protein product, involves complex variability in the sizes and predominance of different mRNA classes. The biologic basis for this heterogeneity of mRNA transcripts is not known. Third, ouabain resistance in at least one cell line, the human Hela C+ cell line, involves amplification of two independent genetic units, the alpha and beta subunit genes, as well as high levels of expression of the mRNAs. These results serve as strong evidence for the importance of the beta subunit, although no discrete functions have yet been assignable to this protein. It is otherwise difficult to understand why the alpha and beta subunits are both amplified in these cells, and both decline upon withdrawal of the selective agent. On the basis of evidence gathered in our laboratory and that of other groups, we conclude that the genetic basis for sodium transport in eukaryotic tissues is far more complex than previously anticipated. There appears to be a need for specialization of sodium, potassium-ATPases in different tissues and for complex generation of multiple beta-subunit mRNA species. Our molecular genetic approach has also allowed us to demonstrate that there is probably an important role played by the beta-subunit in Na,K-ATPase function.(ABSTRACT TRUNCATED AT 250 WORDS)
An identity concerning controllability observability and coprimeness of linear systems and its applications (2007)

任何东西说空格实现，这在这篇论文被显示出(一， b ， c )给定的转移函数 T =(β( s ))/(α( s ))与α( s ) monic 和暗淡(A)= deg (α( s ))，满足身份β( A )= Q_c (一， b )S_ αQ _o (一， c )在哪儿 Q_c (一， b )并且 Q_o (一， c )是可控制性矩阵和矩阵三元组的 observability 矩阵(一， b ， c )，分别地并且S_α 是一个非退化的对称的矩阵。如此的身份给在州的空格描述和对的转移函数描述之间的一种深关系单个输入单个产量(SISO ) 线性系统。作为一个直接结论，如果并且仅当分子和转移功能的分母是警察白霜，我们到达任何转移功能的一条认识是最小的著名结果。如此的结果也被扩大到 SISO 描述符线性系统大小写。作为一应用程序，变换矩阵方程斧子 = X A 的一个完全的答案被建议并且线性系统被考虑的多输入多产量(MIMO ) 的最小的实现。
Location, Location, Location: Is Membrane Partitioning Everything When It Comes to Innate Immune Activation? (2011)

In the last twenty years, the general view of the plasma membrane has changed from a homogeneous arrangement of lipids to a mosaic of microdomains. It is currently thought that islands of highly ordered saturated lipids and cholesterol, which are laterally mobile, exist in the plane of the plasma membrane. Lipid rafts are thought to provide a means to explain the spatial segregation of certain signalling pathways emanating from the cell surface. They seem to provide the necessary microenvironment in order for certain specialised signalling events to take place, such as the innate immune recognition. The innate immune system seems to employ germ-lined encoded receptors, called pattern recognition receptors (PRRs), in order to detect pathogens. One family of such receptors are the Toll-like receptors (TLRs), which are the central "sensing" apparatus of the innate immune system. In recent years, it has become apparent that TLRs are recruited into membrane microdomains in response to ligands. These nanoscale assemblies of sphingolipid, cholesterol, and TLRs stabilize and coalesce, forming signalling platforms, which transduce signals that lead to innate immune activation. In the current paper, we will investigate all past and current literature concerning recruitment of extracellular and intracellular TLRs into lipid rafts and how this membrane organization modulates innate immune responses.
Efficient construction of cDNA libraries in plasmid expression vectors using an adaptor strategy (1986)

We describe a method for the construction of large DNA fragment libraries in plasmid vectors, in which complementary, single-stranded extensions are ligated onto both vector and insert DNA using un-phosphorylated adaptor oligonucleotides. Special consideration has been taken of the requirements of expression screening as follows: cDNA synthesis using random oligonucleotide primers is described which maximises the probability of obtaining open reading frame fragments from large mRNA molecules, the adaptors use codons found in high abundance E. coli proteins to minimise problems of premature termination when using strong promoters, and the sequence encoded by the adaptors, when cloned into the bacterial expression vector pEX1, promotes a surface location for the foreign antigenic determinant where it is accessible to antibodies used for screening.
Auditory Neuropathy Spectrum Disorder due to Two Novel Compound Heterozygous OTOF Mutations in Two Chinese Families (2019)

Auditory neuropathy spectrum disorder (ANSD), also called auditory neuropathy (AN), is a unique type of prelingual hearing impairment. Up to 10% of deaf infants and children are affected by this disease. Mutation of the <i>OTOF</i> gene which encodes otoferlin is the common cause of congenital nonsyndromic ANSD. To date, over 110 mutations have been identified in the <i>OTOF</i> gene according to the Human Gene Mutation Database (HGMD). Here, next-generation sequencing (NGS) revealed that the compound heterozygous mutations c.4748G>A/c.2523+1G>T and c.5248G>C/c.5098G>C of the <i>OTOF</i> gene were present in two Chinese ANSD patients. Each patient had a known pathogenic mutation (c.4748G>A or c.5098G>C) and a novel mutation (c.2523+1G>T or c.5248G>C). Comparative amino acid sequence analysis across different species revealed that the residues at these novel mutation sites are evolutionarily highly conservative. This indicated that the novel mutations were possible causes of the disorder in the patients. Our findings extend the <i>OTOF</i> mutation spectrum and further confirm the role of the <i>OTOF</i> gene in ANSD.
Structural Changes of Ag Single Crystals by Exposure to Hyper-thermal Atomic Oxygen (2004)

Extended abstract of a paper presented at Microscopy and Microanalysis 2004 in Savannah, Georgia, USA, August 1–5, 2004.
Analyzing & designing the security of shared resources on smartphone operating systems (2018)

Smartphone penetration surpassed 80% in the US and nears 70% in Western Europe. In fact, smartphones became the de facto devices users leverage to manage personal information and access external data and other connected devices on a daily basis. To support such multi-faceted functionality, smartphones are designed with a multi-process architecture, which enables third-party developers to build smartphone applications which can utilize smartphone internal and external resources to offer creative utility to users. Unfortunately, such third-party programs can exploit security inefficiencies in smartphone operating systems to gain unauthorized access to available resources, compromising the confidentiality of rich, highly sensitive user data.

The smartphone ecosystem, is designed such that users can readily install and replace applications on their smartphones. This facilitates users’ efforts in customizing the capabilities of their smartphones tailored to their needs. Statistics report an increasing number of available smartphone applications— in 2017 there were approximately 3.5 million third-party apps on the official application store of the most popular smartphone platform. In addition we expect users to have approximately 95 such applications installed on their smartphones at any given point. However, mobile apps are developed by untrusted sources. On Android—which enjoys 80% of the smartphone OS market share—application developers are identified based on self-sign certificates. Thus there is no good way of holding a developer accountable for a malicious behavior. This creates an issue of multi-tenancy on smartphones where principals from diverse untrusted sources share internal and external smartphone resources. Smartphone OSs rely on traditional operating system process isolation strategies to confine untrusted third-party applications. However this approach is insufficient because incidental seemingly harmless resources can be utilized by untrusted tenants as side-channels to bypass the process boundaries. Smartphones also introduced a permission model to allow their users to govern third-party application access to system resources (such as camera, microphone and location functionality). However, this permission model is both coarse-grained and does not distinguish whether a permission has been declared by a trusted or an untrusted principal. This allows malicious applications to perform privilege escalation attacks on the mobile platform. To make things worse, applications might include third- party libraries, for advertising or common recognition tasks. Such libraries share the process address space with their host apps and as such can inherit all the privileges the host app does. Identifying and mitigating these problems on smartphones is not a trivial process. Manual analysis on its own of all mobile apps is cumbersome and impractical, code analysis techniques suffer from scalability and coverage issues, ad-hoc approaches are impractical and susceptible to mistakes, while sometimes vulnerabilities are well…
Interleukin-2 and alpha/beta interferon down-regulate hepatitis B virus gene expression in vivo by tumor necrosis factor-dependent and -independent pathways (1994)

We have recently reported that administration of recombinant tumor necrosis factor alpha (TNF-alpha) to hepatitis B virus (HBV) transgenic mice reduces the hepatic steady-state content of HBV-specific mRNA by up to 80% in the absence of liver cell injury. In the current study, we analyzed the regulatory effects of several other inflammatory cytokines in the same transgenic model system. Hepatic HBV mRNA content was reduced by up to 90% following administration of a single noncytopathic dose (100,000 U) of interleukin 2 (IL-2). Comparable effects were produced by administration of alpha and beta interferons (IFN-alpha and IFN-beta), but only after multiple injections of at least 500,000 U per mouse. Importantly, the regulatory effect of IL-2 was completely blocked by the prior administration of antibodies to tumor necrosis factor alpha (TNF-alpha), which did not block the effect of IFN-alpha or IFN-beta. In contrast to these observations, recombinant IFN-gamma, IL-1, IL-3, IL-6, TNF-beta, transforming growth factor beta, and granulocyte-monocyte colony-stimulating factor were inactive in this system. These results suggest that selected inflammatory cytokines can down-regulate HBV gene expression in vivo by at least two pathways, one that is dependent on TNF-alpha and another that is not. These results imply that antigen-nonspecific products of the intrahepatic HBV-specific inflammatory response may contribute to viral clearance or persistence during HBV infection.
The cellular and molecular events of central nervous system remyelination (1990)

Central nervous system (CNS)* regeneration is a subject of great interest, particularly in diseases causing a dramatic loss of neurons. However, some CNS diseases do not affect neurons but damage other cells, such as the myelin-forming cells--called oligodendrocytes--which are also crucial to the harmonious function of the nervous system. Diseases in which oligodendrocytes and myelin are attacked can cause devastating neurological dysfunction which is sometimes followed by recovery and myelin repair or remyelination. The question of the regeneration potential of oligodendrocytes in experimental and human demyelinating diseases such as multiple sclerosis has been debated for a long time. Present evidence suggests that oligodendrocyte precursor cells persist in the adult CNS and that oligodendrocyte regeneration can occur but may be limited by ongoing disease processes. Here we will briefly review recent advances which have broadened our understanding of the cellular and molecular events of CNS remyelination.
RLIP76: A Target for Kidney Cancer Therapy (2009)

RLIP76 is a multifunctional transporter protein that serves as an energy-dependent efflux mechanism for endogenously generated toxic metabolites as well as exogenous toxins, including chemotherapy drugs. Our recent studies in cultured cells, syngeneic animal tumor model, and in xenograft model have shown that RLIP76 serves a major cancer-specific antiapoptotic role in a wide variety of histologic types of cancer, including leukemia, melanoma, colon, lung, prostate, and ovarian cancer. Results of present studies in cell culture and xenograft model of Caki-2 cells show that RLIP76 is an important anticancer for kidney cancer because inhibition of RLIP76 function by antibody or its depletion by small interfering RNA or antisense DNA caused marked and sustained regression of established human kidney xenografts of Caki-2 cells in nude mouse.
Segregation and rearrangement of coamplified genes in different lineages of mutant cells that overproduce adenylate deaminase. (1986)

Four genes encoding proteins designated as W, X, Y1, and Y2 were found previously to be amplified at different levels in a Chinese hamster fibroblast mutant line selected for overproduction of adenylate deaminase. To gain information on the molecular mechanisms responsible, we studied the levels of amplification and the structures of these four genes in several lineages of mutant cells with comparable activities of adenylate deaminase, the selected enzyme. Only the W gene was amplified in all the lines. In one line, the X, Y1, and Y2 genes were coamplified, while in others either the Y1 gene or the pair X and Y2 were coamplified. The results were consistent with linkage of all the genes--in a particular order--in an amplifiable sequence with variable endpoints. Novel joints with a nonrandom distribution were observed. We frequently detected rearranged copies of the W gene, but very few novel joints were present in the other three genes in the six highly amplified lines examined. Some of the novel joints in gene W were highly amplified; they were generated by reamplification of a rearrangement that appeared at an early selection step. In some lines, reamplification was accompanied by deletion or mass correction of preexisting units. We discuss mechanisms which might account for these observations.
Antiallergic Effects of Terfenadine on Immediate Type Hypersensitivity Reactions (1987)

Terfenadine dose-dependently inhibited rat homologous PCA (2.5-10 mg/kg, p.o.) and experimentally-induced asthma in guinea pigs (0.5-5 mg/kg, p.o.). Similarly, metabolites I and II dose-dependently inhibited experimentally-induced asthma but their respective potencies were approximately 1/2 and 1/15th that of terfenadine. These results suggest that the metabolites contribute to the antiallergic effects of terfenadine. In ex vivo, terfenadine (5-20 mg/kg, p.o.) also inhibited the release of both antigen-induced histamine and SRS-A from sensitized guinea pig lung samples and that of histamine from rat peritoneal mast cells. Terfenadine dose-dependently increased the cAMP content in rat mast cells and in the lungs; in the latter, the augmented cAMP is associated with an increase in adenylate cyclase activity, but not with the inhibition of phosphodiesterase activity. The above evidence indicates that the inhibitory effects of terfenadine on mediator release from mast cells are in some way related to its antiallergic effects, and that an elevated cAMP content may be effective to enhance mediator release inhibition.
Mechanisms of anti-inflammatory and neuroprotective actions of PPAR-gamma agonists (2007)

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors of the nuclear hormone receptor superfamily. The 3 PPAR isoforms (alpha, delta/beta and gamma) are known to control many physiological functions including glucose absorption, lipid balance, and cell growth and differentiation. Of interest, PPAR-gamma activation was recently shown to mitigate the inflammation associated with chronic and acute neurological insults. Particular attention was paid to test the therapeutic potential of PPAR agonists in acute conditions like stroke, spinal cord injury (SCI) and traumatic brain injury (TBI), in which massive inflammation plays a detrimental role. While 15d-prostaglandin J2 (15d PGJ2) is the natural ligand of PPAR-gamma, the thiazolidinediones (TZDs) are potent exogenous agonists. Due to their insulin-sensitizing properties, 2 TZDs rosiglitazone and pioglitazone are currently FDA-approved for type-2 diabetes treatment. Recent studies from our laboratory and other groups have shown that TZDs induce significant neuroprotection in animal models of focal ischemia and SCI by multiple mechanisms. The beneficial actions of TZDs were observed to be both PPAR-gamma-dependent as well as -independent. The major mechanism of TZD-induced neuroprotection seems to be prevention of microglial activation and inflammatory cytokine and chemokine expression. TZDs were also shown to prevent the activation of pro-inflammatory transcription factors at the same time promoting the anti-oxidant mechanisms in the injured CNS. This review article discusses the multiple mechanisms of TZD-induced neuroprotection in various animal models of CNS injury with an emphasis on stroke.
A Novel Small-Molecule Inhibitor of Mcl-1 Blocks Pancreatic Cancer Growth In Vitro and In Vivo (2013)

Using a high-throughput screening (HTS) approach, we have identified and validated several small-molecule Mcl-1 inhibitors (SMI). Here, we describe a novel selective Mcl-1 SMI inhibitor, 2 (UMI-77), developed by structure-based chemical modifications of the lead compound 1 (UMI-59). We have characterized the binding of UMI-77 to Mcl-1 by using complementary biochemical, biophysical, and computational methods and determined its antitumor activity against a panel of pancreatic cancer cells and an in vivo xenograft model. UMI-77 binds to the BH3-binding groove of Mcl-1 with Ki of 490 nmol/L, showing selectivity over other members of the antiapoptotic Bcl-2 family. UMI-77 inhibits cell growth and induces apoptosis in pancreatic cancer cells in a time- and dose-dependent manner, accompanied by cytochrome c release and caspase-3 activation. Coimmunoprecipitation experiments revealed that UMI-77 blocks the heterodimerization of Mcl-1/Bax and Mcl-1/Bak in cells, thus antagonizing the Mcl-1 function. The Bax/Bak-dependent induction of apoptosis was further confirmed using murine embryonic fibroblasts that are Bax- and Bak-deficient. In an in vivo BxPC-3 xenograft model, UMI-77 effectively inhibited tumor growth. Western blot analysis in tumor remnants revealed enhancement of proapoptotic markers and significant decrease of survivin. Collectively, these promising findings show the therapeutic potential of Mcl-1 inhibitors against pancreatic cancer and warrant further preclinical investigations.
Some Applications of Magnetic Resonance Imaging in Fluid Mechanics: Complex Flows and Complex Fluids (2008)

The review deals with applications of magnetic resonance imaging (MRI) techniques to study flow. We first briefly discuss the principles of flow measurement by MRI and give examples of some applications, such as multiphase flows, the MRI rheology of complex fluid flows, and blood flows in the human body.
Reliability, Reproducibility, and Validation of Five Major Histological Scoring Systems for Experimental Articular Cartilage Repair in the Rabbit Model (2011)

Histological evaluation of the repair tissue is a main pillar in the advancing field of experimental articular cartilage repair. Despite their widespread use, the major histological scoring systems for cartilage repair have seldom been validated. We tested the hypotheses (1) that elementary scores have a better reproducibility compared with more complex systems and (2) that the data from these different histological scores correlate with the DNA and proteoglycan contents of the repair tissue. A total of 1,165 observations of cartilage repair based on histological sections (n=233) from an experimental investigation on the repair of standardized osteochondral defects in vivo were made by three investigators with different levels of experience in cartilage research to determine the inter- and intra-observer reproducibility of elementary (Pineda and Wakitani score) and complex (O'Driscoll, Sellers, Fortier score) histological grading systems. DNA and proteoglycan contents of the repair tissues from simultaneously created defects were determined and correlated with histological (a) overall score values, (b) matrix staining, and (c) cellular characteristics of the five scores. Finally, applying the proteoglycan content as validating test, sensitivity, and specificity of the grading systems were assessed. All histological scores provided high intra- (Pearson r=0.92-0.99) and inter-observer reliability (intra-class correlation=0.94-0.99), low numerical intra- and inter-observer differences, and high internal correlations (Spearman's ρ=0.63-0.91). No disparity in reliability and reproducibility was detected between elementary and complex scores or between investigators with different levels of experience (all p>0.05). Individual histological overall score values did not correlate with proteoglycan contents but with DNA contents of the repair tissue (O'Driscoll, Wakitani, Sellers score). In all systems, proteoglycan contents did not correlate with matrix staining (all p>0.05), but histological cellular characteristics correlated with total cell numbers (p<0.001). These data indicate that both elementary and comprehensive histological scores are suited to quantify cartilage repair. Histological and biochemical evaluations may serve as complementary tools to assess articular cartilage repair in vivo.