gebhart/patrepeval huggingface dataset:
DeepShift: Towards Multiplication-Less Neural Networks (2021)

The high computation, memory, and power budgets of inferring convolutional neural networks (CNNs) are major bottlenecks of model deployment to edge computing platforms, e.g., mobile devices and IoT. Moreover, training CNNs is time and energy-intensive even on high-grade servers. Convolution layers and fully connected layers, because of their intense use of multiplications, are the dominant contributor to this computation budget.We propose to alleviate this problem by introducing two new operations: convolutional shifts and fully-connected shifts which replace multiplications with bitwise shift and sign flipping during both training and inference. During inference, both approaches require only 5 bits (or less) to represent the weights. This family of neural network architectures (that use convolutional shifts and fully connected shifts) is referred to as DeepShift models. We propose two methods to train DeepShift models: DeepShift-Q which trains regular weights constrained to powers of 2, and DeepShift-PS that trains the values of the shifts and sign flips directly.Very close accuracy, and in some cases higher accuracy, to baselines are achieved. Converting pre-trained 32-bit floating-point baseline models of ResNet18, ResNet50, VGG16, and GoogleNet to DeepShift and training them for 15 to 30 epochs, resulted in Top-1/Top-5 accuracies higher than that of the original model. Last but not least, we implemented the convolutional shifts and fully connected shift GPU kernels and showed a reduction in latency time of 25% when inferring ResNet18 compared to unoptimized multiplication-based GPU kernels. The code can be found at https://github.com/mostafaelhoushi/DeepShift.
Cells that register logical relationships among proteins (1997)

Two-hybrid methods have augmented the classical genetic techniques biologists use to assign function to genes. Here, we describe construction of a two-bait interaction trap that uses yeast cells to register more complex protein relationships than those detected in existing two-hybrid systems. We show that such cells can identify bridge or connecting proteins and peptide aptamers that discriminate between closely related allelic variants. The protein relationships detected by these cells are analogous to classical genetic relationships, but lend themselves to systematic application to the products of entire genomes and combinatorial libraries. We show that, by performing logical operations on the phenotypic outputs of these complex cells and existing two-hybrid cells, we can make inferences about the topology and order of protein interactions. Finally, we show that cells that register such relationships can perform logical operations on protein inputs. Thus these cells will be useful for analysis of gene and allele function, and may also define a path for construction of biological computational devices.
Genome‐wide expression analysis of Middle Eastern papillary thyroid cancer reveals c‐MET as a novel target for cancer therapy (2007)

In an attempt to find genes that may be of importance in malignant progression of papillary thyroid carcinoma (PTC) in the Middle East, which therefore can be targeted in cancer therapy, we screened and validated the global gene expression in PTC using cDNA expression arrays and immunohistochemistry (IHC) on tumour tissue microarrays. Twenty-nine PTC tissue specimens were compared with seven non-cancerous thyroid specimens by use of cDNA microarray. Results for selected genes were confirmed by quantitative real-time PCR. Protein expression of selected genes was further studied using a tissue microarray consisting of 536 PTCs and compared with histologically non-cancerous tissue samples. One hundred and ninety-six genes were overexpressed in PTC tissues relative to non-cancerous thyroid tissues. The genes that were up-regulated in PTC were involved in cell cycle regulation, cell signaling, and oncogenesis. Among these genes, c-MET was identified by immunohistochemical methods as a protein that is overexpressed in 37% of PTCs and was significantly associated with more aggressive behaviour, eg higher stage, nodal involvement, and tall cell variant (p value = 0.01, 0.01 and 0.04, respectively). In this study, 55% of the PTC cases expressed activated AKT (P-AKT), which suggests that activated AKT may play an important role in PTC tumourigenesis. The fact that most of the PTC cases that had activated AKT showed overexpression of c-MET (p = 0.027) leads us to hypothesize that c-MET may be an alternative mechanism of AKT activation in Middle Eastern PTCs. Finally, our data suggest that c-MET dysregulation is associated with aggressive behaviour and may serve as a molecular biomarker and potential therapeutic target in this disease.
Substrate effect on the optical response of silver nanoparticles (2004)

We study the influence of a substrate on the surface plasmon resonance absorption in silver nanoparticles depending on the distance between the nanoparticles and the substrate. The experimentally observed red shift of the resonant absorption is explained in the frame of the image-induced charges at the interface between the ambient medium and the substrate. The influence of a metallic substrate is negligible when the clusters are at a distance d>2R from the substrate. A dielectric substrate has much less influence on the optical response of silver clusters than a metallic one.
Crystal Structure Determination ofEscherichia coliClpP Starting from an EM-Derived Mask (1998)

Large ATP-dependent proteolytic complexes carry out the majority of intracellular proteolysis. To begin to understand the function of these proteases at a structural level, we have combined the information from a number of biophysical techniques such as electron microscopy (EM), small-angle scattering, and x-ray crystallography. In this study, we exploited the inherent symmetry of Escherichia coli ClpP, the proteolytic component of the ClpAP/XP ATP-dependent protease, to determine its x-ray crystal structure to 2.3-A resolution starting with a phase set derived from a low-resolution mask obtained from EM and small-angle x-ray scattering analysis. Sevenfold and 14-fold noncrystallographic symmetry averaging facilitated phase extension beyond 20 A and in combination with mask redetermination and matrix refinement was sufficient for completely determining the structure. The structure of ClpP is a homo-tetradecamer composed of two heptameric rings enclosing a cavity of approximately 50 A in diameter that compartmentalizes the 14 serine proteolytic active sites. Comparison of the ClpP structure with those of the 20S proteasome and HslV reveals a striking example of evolutionary convergence, despite them being unrelated in sequence and fold. Moreover, similarity in their overall architecture suggests a common model for their action.
Programmed death 1 signaling on chronic myeloid leukemia–specific T cells results in T-cell exhaustion and disease progression (2009)

Chronic myeloid leukemia (CML) is a malignant myeloproliferative disease with a characteristic chronic phase (cp) of several years before progression to blast crisis (bc). The immune system may contribute to disease control in CML. We analyzed leukemia-specific immune responses in cpCML and bcCML in a retroviral-induced murine CML model. In the presence of cpCML and bcCML expressing the glycoprotein of lymphocytic choriomeningitis virus as a model leukemia antigen, leukemia-specific cytotoxic T lymphocytes (CTLs) became exhausted. They maintained only limited cytotoxic activity, and did not produce interferon-gamma or tumor necrosis factor-alpha or expand after restimulation. CML-specific CTLs were characterized by high expression of programmed death 1 (PD-1), whereas CML cells expressed PD-ligand 1 (PD-L1). Blocking the PD-1/PD-L1 interaction by generating bcCML in PD-1-deficient mice or by repetitive administration of alphaPD-L1 antibody prolonged survival. In addition, we found that PD-1 is up-regulated on CD8(+) T cells from CML patients. Taken together, our results suggest that blocking the PD-1/PD-L1 interaction may restore the function of CML-specific CTLs and may represent a novel therapeutic approach for CML.
Induction of expression of osteopontin (OPN; secreted phosphoprotein) in metastatic, ras-transformed NIH 3T3 cells. (1992)

We have previously shown that transfection of NIH 3T3 cells with the T24 H-ras oncogene converts the cells to a tumorigenic and metastatic phenotype, in proportion to levels of ras expression. We hypothesize that ras-induced increases in malignancy occur via altered expression of various genes. We have identified OPN (osteopontin; also known as Secreted Phosphoprotein, 2ar, Eta-1, and transformation-associated phosphoprotein) as a ras-induced gene in these cells. We report here that expression of OPN RNA and secretion of OPN protein are increased in a series of ras-transformed NIH 3T3 cells, in proportion to levels of expression of ras. Detection of secreted OPN protein was facilitated by a barium citrate precipitation procedure. Although the function of this protein in tumor cells is not known, OPN contains a conserved GRGDS (glycine-arginine-glycine-aspartic acid-serine) amino acid sequence, which may function as a cell attachment site for this protein. We speculate that increased expression of OPN contributes to the increased malignancy of ras oncogene-transformed NIH 3T3 cells, perhaps by alterations in either adhesive properties or integrin-mediated signal transduction pathways.
A micropower low-noise monolithic instrumentation amplifier for medical purposes (1987)

A CMOS low-power low-noise monolithic instrumentation amplifier (IA) is described. The power drain is reduced by use of current feedback and by use of only single-stage operational transconductance amplifiers in the low-frequency loop. The bandwidth of the IA is designed for medical purposes (0.5-500 Hz) and it can produce variable gains of 14/20/26/40 dB, which are set by control software.
In vivo corrosion behavior of Mg‐Mn‐Zn alloy for bone implant application (2007)

Magnesium alloy has been implanted in rats to investigate the in vivo degradation behavior of magnesium for bone implant application. After 9 weeks postoperation, 100% implants were fixed and no inflammation was observed. Histological analysis showed new bone was formed around magnesium implant and no difference was found in the histological microstructure of the new bone and the cortical bone. A degradation or reaction layer, which was mainly composed of Ca, P, O, and Mg, was formed on the surface of magnesium alloy implants. High Ca content in the degradation layer displayed that magnesium could promote the deposition of Ca. Residual area calculation has showed that 10-17% magnesium alloy implant has been degraded in vivo. Compared with that of the controlled rats, no increase in serum magnesium and no disorder of kidney were observed after 15 weeks postoperation. After 18 weeks postoperation, 100% magnesium implants were fixed and no inflammation was observed. About 54% magnesium implant has degraded in vivo. Element analysis showed that Zn and Mn in Mg-Mn-Zn alloy distributed homogeneously in the residual magnesium implant, the degradation layer, and the surrounding bone tissue after 18 weeks implantation, indicating that Zn and Mn elements were easily absorbed by bioenvironment.
Maternal Experience Produces Long-Lasting Behavioral Modifications in the Rat. (2005)

From 5 to 22 months of age, cognitive and emotional responses of nulliparous, primiparous, and multiparous rats were assessed using a dry land maze (DLM) and an elevated plus-maze (EPM) at 4-month intervals. Parous rats exhibited improved spatial memory in the probe and competitive versions of the DLM, and more exploration in the EPM and a novel stimulus test relative to nulliparous females. The nulliparous females, however, outperformed parous rats during the DLM visual cue test at 17 months of age. At 23 months, no differences in stressed corticosterone levels or Golgi-stained hippocampal neurons were observed. Thus, cognitive and emotional modifications were observed in parous rats; the neurobiological mechanisms for these enduring effects, however, remain to be identified.
Assessment Methods and the Differential Diagnosis of Anxiety (1981)

Anxiety states are commonly encountered, especially in general practice. Some endocrine disorders have features in common with anxiety states, especially thyrotoxicosis and idiopathic hypoglycemia. Functional cardiovascular disorders merge into anxiety states and include a large number of ill-differentiated syndromes. Other causes of anxiety are the drug-associated conditions, such as amphetamine overdose and barbiturate withdrawal. Among neuropsychiatric illnesses, temporal lobe epilepsy and the postconcussional state commonly have anxiety as a prominent syndrome. Psychophysiological technique can be used to assess anxiety levels in a variety of clinical contexts but need cautious interpretation. Anxiety is most easily assessed using rating scales but potential users must be clear as to what they are trying to measure. For clinical anxiety assessed by the physician, the Hamilton Scale is appropriate; for self-assessments linear scales can be adapted.
Catalysis of a stereospecific bimolecular amide synthesis by an antibody. (1988)

We report a nonhydrolytic bimolecular aminolysis reaction catalyzed by an antibody. The stereospecific formation of an amide from racemic lactone plus an aromatic amine is described by a random equilibrium bireactant kinetic sequence. The observed turnover rate may be approximated from the measured difference between the binding of reactants and the transition state analog.
Deep mixture density networks for acoustic modeling in statistical parametric speech synthesis (2014)

Statistical parametric speech synthesis (SPSS) using deep neural networks (DNNs) has shown its potential to produce naturally-sounding synthesized speech. However, there are limitations in the current implementation of DNN-based acoustic modeling for speech synthesis, such as the unimodal nature of its objective function and its lack of ability to predict variances. To address these limitations, this paper investigates the use of a mixture density output layer. It can estimate full probability density functions over real-valued output features conditioned on the corresponding input features. Experimental results in objective and subjective evaluations show that the use of the mixture density output layer improves the prediction accuracy of acoustic features and the naturalness of the synthesized speech.
Hough Forests for Object Detection, Tracking, and Action Recognition (2011)

Abstract—The paper introduces Hough forests, which are random forests adapted to perform a generalized Hough transform in an efficient way. Compared to previous Hough-based systems such as implicit shape models, Hough forests improve the performance of the generalized Hough transform for object detection on a categorical level. At the same time, their flexibility permits extensions of the Hough transform to new domains such as object tracking and action recognition. Hough forests can be regarded as task-adapted codebooks of local appearance that allow fast supervised training and fast matching at test time. They achieve high detection accuracy since the entries of such codebooks are optimized to cast Hough votes with small variance and since their efficiency permits dense sampling of local image patches or video cuboids during detection. The efficacy of Hough forests for a set of computer vision tasks is validated through experiments on a large set of publicly available benchmark data sets and comparisons with the state-of-the-art.
Extended phase I study of AS1411 in renal and non-small cell lung cancers (2006)

13098 Background: AS1411 is an oligonucleotide aptamer that binds to nucleolin, a protein expressed on the surface of tumor cells. A dose-escalating phase I trial in patients with various advanced cancers revealed no serious toxicities and consequently did not reach an MTD. There was evidence of activity, especially in renal cell carcinoma (RCC). This study has been reopened for further dose escalation to reach an optimal biological dose (OBD; unless an MTD is reached) in patients with RCC and non-small cell lung cancer (NSCLC). Methods: Patients had advanced RCC or NSCLC refractory to standard treatment. AS1411 was administered as a single continuous 7-day iv infusion, with the option of a second cycle. Patients were enrolled in cohorts of 3. If no serious toxicity was observed within 28 days, the dose was escalated to the next level. Toxicity was graded using the NCI CTCAE v3.0. The study plan was to enroll additional patients at the OBD such that a total of 12 RCC and 12 NSCLC patients received a 7-day infusion. Blood and urine samples were taken for pharmacokinetic analysis. Tumor responses were assessed every 28 days using the RECIST guidelines. Results: No serious adverse events have been observed up to a dose of 22mg/kg/day, which was associated with a mean peak plasma concentration of 1.5 μM. Response findings to date are as follows: of 5 RCC patients, 1 maintains a near-complete response 18 months after treatment, 3 have ongoing stable disease (SD; 1 at 3 months, 2 at 2 months) and a fourth had progressive disease (PD) at 2 months post-treatment; of 3 NSCLC patients, 1 has an ongoing SD and 2 had PDs at 1 month post-treatment. Recruitment and follow up continues. Conclusions: A 7-day infusion of AS1411 at 22mg/kg/day was not associated with any serious adverse events and achieved peak plasma concentrations in the range at which killing of various cancer cell lines is observed in vitro. A single further escalation is planned to reach a dose of 40mg/kg/day. Observation of additional cases of stable disease in RCC supports the previous observations of anti-cancer effects in this disease. [Table: see text]
An NFxB-like factor is essential but not sufficient for cytokine induction of endothelial leukocyte adhesion molecule 1 (ELAM-1) gene transcription (1991)

The endothelial leukocyte adhesion molecule 1 (ELAM-1) is transiently expressed specifically on the surface of cytokine-induced endothelial cells. We demonstrate that the transient expression of the protein is paralleled by an increase and decrease in transcription of the ELAM-1 gene. To identify the cis-acting transcription control regions within the ELAM-1 gene that are responsible for this cytokine-induced expression, we isolated and analyzed an ELAM-1 genomic clone containing sequences upstream of the transcription start site. We constructed a series of ELAM-1 deletion mutants linked to a reporter gene and analyzed their expression in both endothelial and non-endothelial cells. Results show that a fragment of 233 bp upstream of the transcription start site is sufficient to confer cytokine inducibility upon the reporter gene in both endothelial and non-endothelial cells. Further analysis defined two elements within this region that are involved in the cytokine inducibility of the ELAM-1 gene. One element lies within the -233 to -117 region, the other element represents an NF kappa B consensus binding site between nucleotides -94 to -85. Gel shift analysis reveals increased binding of an NF kappa B-like factor to this consensus sequence in extracts prepared from IL-1-induced endothelial cells. The results suggest that cytokine induction of ELAM-1 gene transcription is imparted by a combination of positive factors, one being an NF kappa B-like transcription factor, interacting with cis-acting elements within the enhancer/promoter of the gene.
Inhibition of Transforming Growth Factor-β1 Signaling Attenuates Ataxia Telangiectasia Mutated Activity in Response to Genotoxic Stress (2006)

Ionizing radiation causes DNA damage that elicits a cellular program of damage control coordinated by the kinase activity of ataxia telangiectasia mutated protein (ATM). Transforming growth factor beta (TGFbeta)-1, which is activated by radiation, is a potent and pleiotropic mediator of physiologic and pathologic processes. Here we show that TGFbeta inhibition impedes the canonical cellular DNA damage stress response. Irradiated Tgfbeta1 null murine epithelial cells or human epithelial cells treated with a small-molecule inhibitor of TGFbeta type I receptor kinase exhibit decreased phosphorylation of Chk2, Rad17, and p53; reduced gammaH2AX radiation-induced foci; and increased radiosensitivity compared with TGFbeta competent cells. We determined that loss of TGFbeta signaling in epithelial cells truncated ATM autophosphorylation and significantly reduced its kinase activity, without affecting protein abundance. Addition of TGFbeta restored functional ATM and downstream DNA damage responses. These data reveal a heretofore undetected critical link between the microenvironment and ATM, which directs epithelial cell stress responses, cell fate, and tissue integrity. Thus, Tgfbeta1, in addition to its role in homoeostatic growth control, plays a complex role in regulating responses to genotoxic stress, the failure of which would contribute to the development of cancer; conversely, inhibiting TGFbeta may be used to advantage in cancer therapy.
Repression of Prostaglandin Dehydrogenase by Epidermal Growth Factor and Snail Increases Prostaglandin E2 and Promotes Cancer Progression (2006)

Prostaglandin E(2) (PGE(2)), a proinflammatory bioactive lipid, promotes cancer progression by modulating proliferation, apoptosis, and angiogenesis. PGE(2) is a downstream product of cyclooxygenase (COX) and is biochemically inactivated by prostaglandin dehydrogenase (PGDH). In the present study, we investigated the mechanisms by which PGDH is down-regulated in cancer. We show that epidermal growth factor (EGF) represses PGDH expression in colorectal cancer cells. EGF receptor (EGFR) signaling induces Snail, which binds conserved E-box elements in the PGDH promoter to repress transcription. Induction of PGE(2) catabolism through inhibition of EGFR signaling blocks cancer growth in vivo. In human colon cancers, elevated Snail expression correlates well with down-regulation of PGDH. These data indicate that PGDH may serve a tumor suppressor function in colorectal cancer and provide a possible COX-2-independent way to target PGE(2) to inhibit cancer progression.