gebhart/patrepeval huggingface dataset:
Tissue-specific gene activation by MyoD: determination of specificity by cis-acting repression elements. (1994)

MyoD is a muscle-specific transcriptional activator; E12 is a B-cell activator. An IgH enhancer is activated almost 100-fold by E12 but not at all by Myo; an MCK enhancer is activated almost 1000-fold by MyoD and not at all by E12. MyoD and E12 are both basic helix-loop-helix proteins that bind to similar E-box sequences (CANNTG); the IgH enhancer contains the same E boxes as the MCK enhancer, yet each retains exclusive specificity for either E12 or MyoD, respectively. We show that the IgH enhancer contains a cis-acting negative element that is directed at MyoD, but not at E12. This repression requires the mu E5 E box within the IgH enhancer; however, the specificity for repression, as opposed to activation, is associated with 2 bp flanking each side of the mu E5 E box. The target for repression of MyoD in the IgH enhancer is the bHLH region of MyoD. Our results suggest that MyoD only activates myogenic genes because nonmuscle enhancers that contain E boxes also contain negative elements that prevent MyoD activity.
Characterization of the zinc finger protein encoded by the WT1 Wilms' tumor locus. (1991)

We analysed the biochemical properties of the transcription factor encoded by the putative tumor-suppressor gene present at the WT1 Wilms' tumor locus. A gene containing the full-length amino acid coding sequence of human wt1 was reconstructed from synthetic oligonucleotides and cloned into expression vectors for in vitro and in vivo protein synthesis. Polyclonal rabbit antibodies specific for the WT1 protein were raised to an Escherichia coli-produced 91 amino acid N-terminal segment and to a 136 amino acid C-terminal segment, which contains the zinc finger domain. WT1 produced by in vitro translation migrated as a 52 kDa protein on sodium dodecylsulfate-polyacrylamide gels and bound to the EGR consensus sequence in gel-retardation assays. Expression of the wt1 gene via transient transfection in COS-1 cells revealed a 52 kDa protein which was immunoprecipitated by both the N-terminal- and C-terminal-specific antisera. Immunofluorescence studies of wt1-transfected COS-1 cells revealed that the WT1 protein was localized to the nucleus. Metabolic labeling with [32P]orthophosphate failed to reveal significant phosphorylation of the WT1 protein in COS-1 cells. Two immunoreactive WT polypeptides of 52 and 54 kDa were observed in murine embryonic stem cells and COS-1 kidney cells and may represent previously identified splicing variants of WT1. These antisera should be useful in characterizing the structure and function of the WT1 protein in human Wilms' tumor specimens.
A Combination Of Amoxicillian And Clavulanic Acid In The Treatment Of Impetigo In Children (1998)

Amoxicillin plus clavulanic acid (ACA) a combination of potentially effective antibiotic against beta-lactamase producing bacteria was compared with that of amoxicillin, erythomycin and co-trimoxazole in an open label, randomized trial in 100 children with mild to severe impetigo. 22&#x0025; children had mild, 25&#x0025; had moderate and 53&#x0025; children had severe impetigo. Pure growth of S. aureus was isolated in 68&#x0025; children, S.pyogenes in 26&#x0025; and both staphyto and streptococci in 6&#x0025; children. In mild to moderate infection 100&#x0025; children receiving ACA were cured clinically after first week, whereas 7 out of 15(46.6&#x0025;) children in amoxicillin group, 7 out of 13(53.1&#x0025;) children in erythromycin group and 4 out 12 (33.3&#x0025;) children in co-trimoxazole group showed clinical cure after first week. In severe impetigo 46.1&#x0025; children receiving ACA, 20&#x0025; children in amoxicillin group, 16.6&#x0025; children inerythromycin group and 7.6&#x0025; in co-trimoxazole group showed clinical cure on therapy after one week. ACA was well tolerated in children.
Distinct phenotypic and functional features of CADASIL mutations in the Notch3 ligand binding domain (2009)

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an autosomal dominant small-vessel disease of the brain caused by mutations in the NOTCH3 receptor. The highly stereotyped nature of the mutations, which alter the number of cysteine residues within the epidermal growth factor-like repeats (EGFR), predicts that all mutations share common mechanisms. Prior in vitro assays and genetic studies in the mouse support the hypothesis that common mutations do not compromise canonical Notch3 function but instead convey a non-physiological and deleterious activity to the receptor through the unpaired cysteine residue. Intriguingly, in vitro studies predict that mutations located in the Delta/Serrate/LAG-2 ligand binding domain-(EGFR10-11) may result in a loss of Notch3 receptor function. However, the in vivo relevance and functional significance of this with respect to the pathogenic mechanisms and clinical expression of the disease remain largely unexplored. To ascertain, in vivo, the functional significance of EGFR10-11 mutations, we generated transgenic mice with one representative mutation (C428S) in EGFR10 of Notch3. These mice, like those with a common R90C mutation, developed characteristic arterial accumulation of Notch3 protein and granular osmiophilic material upon aging. By introducing the mutant C428S transgene into a Notch3 null background, we found that, unlike the R90C mutant protein, the C428S mutant protein has lost wild-type Notch3 activity and exhibited mild dominant-negative activity in three different biological settings. From a large prospectively recruited cohort of 176 CADASIL patients, we identified 10 patients, from five distinct pedigrees carrying a mutation in EGFR10 or 11. These mutations were associated with significantly higher Mini-Mental State Examination and Mattis Dementia Rating Scale scores (P < 0.05), when compared with common mutations. Additionally, we found a strong effect of this genotype on the burden of white matter hyperintensities (P < 0.01). Collectively, these results highlight distinctive functional and phenotypic features of EGFR10-11 mutations relative to the common CADASIL mutations. Our findings are compatible with the hypothesis that EGFR10-11 mutations cause the disease through the same gain of novel function as the common mutations, and lead us to propose that reduced Notch3 signalling acts as a modifier of the CADASIL phenotype.
Molecular Characterization of Breast Cancer with High-Resolution Oligonucleotide Comparative Genomic Hybridization Array (2009)

The present study identified dysregulated genes that could classify breast cancer and may represent novel therapeutic targets for molecular subsets of cancers.
[Congenital neuromyotonia. Retrospective study of 4 cases]. (1999)

Congenital neuromyotonia is a clinically heterogeneous syndrome with uniform electrophysiological features that permit its qualification.
Noninvasive, Transthoracic, Low-Frequency Ultrasound Augments Thrombolysis in a Canine Model of Acute Myocardial Infarction (2000)

In vivo, the noninvasive transthoracic application of low-frequency ultrasound (1) greatly augments the efficacy of t-PA-mediated thrombolysis, (2) seems safe, and (3) has substantial potential as a noninvasive adjunct to improve coronary patency without increasing the risk of bleeding.
Central Corneal Thickness Measurement with a Retinal Optical Coherence Tomography Device Versus Standard Ultrasonic Pachymetry (2001)

Imaging of the human cornea can be performed by a standard retinal OCT device, and OCT measurement of CCT shows excellent correlation to values obtained by PACH, giving similar readings separated by a constant difference. In corneal edema, the difference between the two methods is additionally increased, but continues to demonstrate excellent consistency.
Innate Immune Suppression Enables Frequent Transfection with RNA Encoding Reprogramming Proteins (2010)

Our results demonstrate that suppressing innate immunity enables frequent transfection with protein-encoding RNA. This technique represents a versatile tool for investigating expression dynamics and protein interactions by enabling precise control over levels and timing of protein expression. Our finding also opens the door for the development of reprogramming and directed-differentiation methods based on long-RNA transfection.
Development of a single-chain, quasi-dimeric zinc-finger nuclease for the selective degradation of mutated human mitochondrial DNA (2008)

The selective degradation of mutated mitochondrial DNA (mtDNA) molecules is a potential strategy to re-populate cells with wild-type (wt) mtDNA molecules and thereby alleviate the defective mitochondrial function that underlies mtDNA diseases. Zinc finger nucleases (ZFNs), which are nucleases conjugated to a zinc-finger peptide (ZFP) engineered to bind a specific DNA sequence, could be useful for the selective degradation of particular mtDNA sequences. Typically, pairs of complementary ZFNs are used that heterodimerize on the target DNA sequence; however, conventional ZFNs were ineffective in our system. To overcome this, we created single-chain ZFNs by conjugating two FokI nuclease domains, connected by a flexible linker, to a ZFP with an N-terminal mitochondrial targeting sequence. Here we show that these ZFNs are efficiently transported into mitochondria in cells and bind mtDNA in a sequence-specific manner discriminating between two 12-bp long sequences that differ by a single base pair. Due to their selective binding they cleave dsDNA at predicted sites adjacent to the mutation. When expressed in heteroplasmic cells containing a mixture of mutated and wt mtDNA these ZFNs selectively degrade mutated mtDNA, thereby increasing the proportion of wt mtDNA molecules in the cell. Therefore, mitochondria-targeted single-chain ZFNs are a promising candidate approach for the treatment of mtDNA diseases.
Using wireless Ethernet for localization (2003)

IEEE 802.11b wireless Ethernet is rapidly becoming the standard for in-building and short-range wireless communication. Many mobile devices such as mobile robots, laptops and PDAs already use this protocol for wireless communication. Many wireless Ethernet cards measure the signal strength of incoming packets. This paper investigates the feasibility of implementing a localization system using this sensor. Using a Bayesian localization framework, we show experiments demonstrating that off-the-shelf wireless hardware can accurately be used for location sensing and tracking with about one meter precision in a wireless-enabled office building.
An efficient multi-frame dynamic search range motion estimation for H.264 (2007)

H.264/AVC achieves higher compression efficiency than previous video coding standards. However, this comes at the cost of increased complexity due to the use of variable block size motion estimation and long-term memory motion compensated prediction (LTMCP). In this paper, an efficient multi-frame dynamic search range motion estimation algorithm is proposed. This algorithm can adjust the spatial search range and temporal search range according to the video content dynamically. This algorithm can be on the top of many other fast motion estimation (Fast ME) algorithms. Compared with the constant search range scheme used by multi-frame UMHexagonS algorithm, the proposed algorithm can be 4.86 time faster, with negligible degradation of video quality.
EMOTION-PROCESSING BIASES AND RESTING EEG ACTIVITY IN DEPRESSED ADOLESCENTS (2015)

Depressed female adolescents were characterized by emotion-processing biases in favor of sad emotions and reduced recognition of happiness, especially when cues of happiness were subtle. Blunted recognition of happy was associated with left DLPFC resting hypoactivity.
The generation of diffusion Markovian processes with probability density function defined on part of the real axis (1996)

The correlated random process is represented as a solution of a stochastic differential first-order equation (SDE). The case of processes with a probability density function defined on a semi-infinite or finite range is considered. The limitation of the range of the simulated process requires modification of the specific structure of the SDE. The approach presented provides excellent results in modeling significant non-Gaussian processes with approximately an exponential correlation function. It is validated by direct numerical simulation of a uniformly distributed correlated process.
Ultrastructure of the Blood and Lymphatic Capillaries of the Respiratory Tissue During Inflammation and Endobronchial Laser Therapy (2000)

For wide application of low-energy laser irradiation in the pulmonary clinic, study of the structural basis of the therapeutic effect is necessary. The aim of this research is to describe the structural changes of the blood and lymphatic capillaries in the respiratory tissues during inflammation and following laser biostimulation. Comparative ultrastructural study was carried out on 127 open respiratory biopsy specimens from 45 patients with infectious-destructive lung diseases. These patients were divided into two groups, depending on tactic of pre-operative therapy: patients treated by only traditional anti-inflammatory measures and patients receiving additional laser therapy. Heightened permeability of the blood capillary endotheliocytes was noted as the initial stage in the development of the inflammatory reaction. Intensification of the process of permeability is accompanied by interstitial edema, deformation of the interalveolar septa, and structural disorganization of alveolar epithelium cells. Local lesions of microcirculation result in tissue hypoxia and induce processes of fibrosis. Laser biostimulation promotes reversion of the inflammatory process and stabilizes fibroplastic processes. Basic principles of pathogenetic therapy were stated. It was shown that low-energy laser irradiation satisfies these requirements as an additional method in the therapy of destructive lung diseases.
Leucine-tRNA Initiates at CUG Start Codons for Protein Synthesis and Presentation by MHC Class I (2012)

Effective immune surveillance by cytotoxic T cells requires newly synthesized polypeptides for presentation by major histocompatibility complex (MHC) class I molecules. These polypeptides are produced not only from conventional AUG-initiated, but also from cryptic non-AUG-initiated, reading frames by distinct translational mechanisms. Biochemical analysis of ribosomal initiation complexes at CUG versus AUG initiation codons revealed that cells use an elongator leucine-bound transfer RNA (Leu-tRNA) to initiate translation at cryptic CUG start codons. CUG/Leu-tRNA initiation was independent of the canonical initiator tRNA (AUG/Met-tRNA(i)(Met)) pathway but required expression of eukaryotic initiation factor 2A. Thus, a tRNA-based translation initiation mechanism allows non-AUG-initiated protein synthesis and supplies peptides for presentation by MHC class I molecules.
Immunoassay of Insulin-Like Growth Factor-Binding Protein-3 (IGFBP-3): New Means to Quantifying IGFBP-3 Proteolysis (2000)

Posttranslational modifications, particularly proteolysis, may play a significant role in the regulation of insulin-like growth factor (IGF)-binding protein-3 (IGFBP-3) physiology, and thus, measurement of modified variants of IGFBP-3 and/or their combination ratios may have important research and diagnostic relevance. Based on evaluation of a panel of monoclonal and polyclonal IGFBP-3 antibodies, we constructed three new enzyme-linked immunosorbent assays (ELISAs) using a common capture and polyclonal (ELISA-3) or monoclonal (ELISA-1 and -2) detection antibodies and evaluated them in a two-step colorimetric procedure. Evaluation of ELISA-1-3 demonstrated detection limit, dynamic range, overall precision, and recovery of the added IGFBP-3 to be generally less than 0.04 microg/L, 2-100 microg/L, less than 10%, and 91-113%, respectively. IGF-I and -II, and IGFBP-1, -2, -4, -5, and -6 did not interfere. In normal adult sera (n = 26), seminal plasma (n = 14), pregnancy sera (n = 30), and amniotic fluid (n = 30), ELISA-1-3 detected significantly different IGFBP-3 levels (by up to 6-fold, on the average), whereas levels in seminal plasma determined by ELISA-1 were undetectable. Comparison of the values obtained vs. corresponding levels by an established method (Diagnostic Systems Laboratories, Inc., active IGFBP-3 ELISA) were similarly sample dependent and, on the average, varied by up to 19-fold. Only ELISA-3 compared well with the Diagnostic Systems Laboratories, Inc., IGFBP-3 ELISA when samples from normal adults were analyzed. The observed variability could not be totally explained by 50% lower reactivity of ELISA-1-3 for glycosylated IGFBP-3 vs. the nonglycosylated form, and changes in phosphorylation had no effect on immunoreactivity. Evaluation of IGFBP-3 after proteolysis by seminal plasma, plasmin, or thrombin suggested recognition of intact IGFBP-3 by ELISA-1, whereas ELISA-3 appeared to measure intact and proteolyzed IGFBP-3 (total IGFBP-3) with similar potency. In contrast, levels determined by ELISA-2 increased severalfold, indicating preferential recognition of IGFBP-3 fragments. We propose that immunoassay capable of differential determination of IGFBP-3 variants may help better define the physiological importance and potential clinical value of IGFBP-3 measurements.
Successful management of polyneuropathy associated with IgM gammopathy of undetermined significance with antibody-based immunoadsorption. (2000)

Peripheral polyneuropathies associated with monoclonal IgM gammopathy of undetermined significance often have a progressive course and optimal treatment has not been established. We report on a patient diagnosed with polyneuropathy associated with benign IgM gammopathy, who was successfully treated with antibody-based immunoadsorption only. The neurological symptoms of the patient improved continuously over six months of treatment. Controlled trials should be performed to define this indication for antibody-based immunoadsorption therapy.
In vitro transcription of human mitochondrial DNA: accurate termination requires a region of DNA sequence that can function bidirectionally. (1986)

Mammalian mitochondrial genomes have a presumptive transcription termination site at the 16S rRNA-tRNALeu gene boundary. We have developed an in vitro system from human KB cells that terminates transcription at this gene boundary. By S1 nuclease protection, the 3' ends of terminated transcripts were mapped 3 and 4 base pairs upstream of the 16S rRNA-tRNALeu gene boundary, in agreement with in vivo data. By high-resolution sizing of transcripts, the 3' end was mapped 7 +/- 1 base pairs downstream from the gene boundary. Termination occurs with equal efficacy from transcriptional initiation at the heavy- or light-strand promoter. All template nucleotide sequence information necessary for termination appears to be located near the termination site itself. An unexpected observation is that the termination region functions bidirectionally.
Regulation of Macrophage Phagocytosis of Apoptotic Cells by cAMP (1998)

Regulation of macrophage capacity to remove apoptotic cells may control the balance of apoptotic and necrotic leukocytes at inflamed foci and the extent of leukocyte-mediated tissue damage. Although the molecules involved in the phagocytic process are beginning to be defined, little is known about the underlying regulatory and signaling mechanisms controlling this process. In this paper, we have investigated the effects of treatment of human monocyte-derived macrophages with PGs and other agents that elevate intracellular cAMP on phagocytosis. PGE2 and PGD2 specifically reduced the proportion of macrophages that phagocytosed apoptotic cells. Similar results were obtained with the membrane-permeable cAMP analogues dibutyryl-cAMP and 8-bromo-cAMP but not with the cGMP analogue dibutyryl-GMP. Consistent with the observation that phagocytosis was inhibited by cAMP elevation, treatment of monocyte-derived macrophages with PGE2 resulted in rapid, transient increase in levels of intracellular cAMP. These effects were not due to nonspecific inhibition of monocyte-derived macrophage phagocytosis given that ingestion of Ig-opsonized erythrocytes was unaffected. Elevation of cAMP induced morphologic alterations indicative of changes in the adhesive status of the macrophage, including cell rounding and disassembly of structures that represent points of contact with substrate containing actin and talin. These results strongly suggest that rapid activation of cAMP signaling pathways by inflammatory mediators regulates processes that limit tissue injury and that modulation of cAMP levels represents an additional therapeutic target in the control of resolution of inflammation.
Enantioselective Synthesis of Axially Chiral Phthalides through Cationic [RhI(H8‐binap)]‐Catalyzed Cross Alkyne Cyclotrimerization (2004)

Easy access to axially chiral phthalides that bear one or two oxymethylene functionalities is provided by an enantioselective cross alkyne cyclotrimerization in the presence of the cationic complex [RhI{(S)-H8-binap}]+. The axial chirality is introduced during the formation of the benzene ring with high enantioselectivity.
Homeobox Gene Prx1 Is Expressed in Activated Hepatic Stellate Cells and Transactivates Collagen α1(I) Promoter (2008)

Hepatic stellate cells (HSCs) are mesenchymal cells of the liver, which are normally in quiescent state and synthesize tracing amounts of extracellular matrix proteins. Upon fibrogenic stimulus, HSCs become activated and increase synthesis of type I collagen 50-100 fold. Prx1 and Prx2 are two homeobox transcription factors which are required for mesenchymal tissue formation during embryogenesis. The present study shows that Prx1 mRNA is expressed in in vivo and in vitro activated HSCs, but not in quiescent HSCs. Prx1 is also expressed in fibrotic livers, while it is undetectable in normal livers. Overexpression of Prx1a in quiescent HSCs cultured in vitro induced collagen alpha1(I) mRNA and TGFbeta3 mRNA expression. Prx1 transactivated TGFbeta3 promoter 3 fold in transient transfection experiments. In the whole liver, Prx1a induced expression of collagen alpha1(I), alpha2(I), alpha1(III) and alpha-smooth muscle mRNAs, which are the markers of activation of HSCs. Prx1 also increased expression of collagen alpha1(I) mRNA after acute liver injury. This suggests that Prx1a promotes activation of HSCs and expression of type I collagen. Several regions in the collagen alpha1(I) promoter were identified which mediate transcriptional induction by Prx1. The regions are scattered throughout the promoter and individually have modest effects; however, the cumulative effect of all sequences is >50 fold. This is the first description of the effects of Prx1 in HSCs and in the liver, and identification of the two Prx1 target genes, which play a pivotal role in development of liver fibrosis, is a novel finding for liver pathophysiology.
Circulating DNA-Important Biomarker of Cancer (2012)

Circulating DNA as a very ideal non-invasive biomarker can easily be isolated from human plasma, serum and other body fluids Small amounts of free DNA circulate in both healthy and diseased human plasma/serum, but increased concentrations of DNA present in the plasma of cancer patients and miscellaneous diseases and physiological conditions, such as pregnancy, tissue trauma, Systemic Lupus Erythematosus (SLE), rheumatoid arthritis, glomerulonephritis, pancreatitis, cholelithiasis, inflammatory bowel disease, peptic ulcer disease, hepatitis and esophagitis This review discusses the progress of circulating DNA research and its application in diagnosis, monitoring and therapeutic application of cancer.