gebhart/patrepeval huggingface dataset:
In vitro and in vivo evaluation in dogs of a miniaturized glucose sensor. (1992)

A miniaturized glucose sensor was developed, consisting of a platinum wire entirely coated with teflon, except for a 1 mm section near its extremity where glucose oxidase is immobilized. The in vitro sensitivity to glucose of the sensors was 2.3 +/- 0.4 nA/mM, mean +/- SEM (n = 23). These sensors were implanted in the subcutaneous tissue of normal beagles. Two consecutive glucose infusions (15-30 mg/kg/min) were performed. The current generated by the sensor was used for calculation of the sensitivity coefficient (SC) (nA/mM), and the background current in the absence of glucose (lo) (nA). These parameters were used for determination of the apparent subcutaneous glucose concentration. The in vivo sensitivity was less than the in vitro sensitivity (0.5 +/- 0.1 vs. 2.2 +/- 0.2; n = 12 comparisons; p less than 0.01). Stability of sensor function was demonstrated by the absence in variation of SC and lo, calculated from the different plateaus obtained during the glucose infusions. This study provides a simple method for evaluating in vivo the function of a miniaturized sensor implanted in subcutaneous tissue.
Acoustic actuated fluorescence activated sorting of microparticles (2014)

In this paper, we present a fluorescence activated sorter realized in a continuous flow microfluidic chip. Sorting is achieved by deflecting a focused particle stream with short acoustic bursts (2.5 ms), in a fluorescence activated configuration. The system utilizes two-dimensional acoustic pre-focusing, using a single actuation frequency, to position all particles in the same fluid velocity regime at flow rates up to 1.7 mL min(-1). Particles were sorted based on their fluorescence intensities at throughputs up to 150 particles s(-1). The highest purity reached was 80% when sorting at an average rate of 50 particles s(-1). The average recovery of a sort was 93.2 ± 2.6%. The presented system enables fluorescence activated cell sorting in a continuous flow microfluidic format that allows aseptic integration of downstream microfluidic functionalities, opening for medical and clinical applications.
Developmental Stage of the Rat Mammary Gland as Determinant of Its Susceptibility to 7, 12-Dimethylbenz[<italic>a</italic>]anthracene<xref ref-type="fn" rid="FN2">2</xref> (1978)

Postnatal development of the mammary gland was studied in 80 noninbred Sprague-Dawley virgin rats ranging in age from 2 to 112 days, and the changes induced by 7,12-dimethylbenz[a]anthracene (DMBA) were studied in 60 noninbred Sprague-Dawley virgin rats that, at the age of 55 days, were inoculated intragastrically with 10 mg DMBA/100 g body weight. To correlate the sequential structural changes in the two groups, animals of both groups were killed weekly and their mammary glands removed and processed for wholemount. Terminal endbuds (TEB), terminal ducts (TD), alveolar buds (AB), and lobules per square millimeter were counted in wholemount preparations under a stereomicroscope. During postnatal development, the mammary gland tree grew by sprouting numerous ducts ending in club-shaped TEB. The density of TEB reached a peak when the rats were 21 days old (25 +/- 2 TEB/mm2), decreased sharply until the animals were 63 days old, and then decreased slowly until they were 84 days of age. The number of TEB decreased because of their differentiation mainly into AB or their evolution to TD. AB later differentiated into lobules. AB increased in number steadily to a plateau when the animals were 70--84 days old. After DMBA was administered to the rats at 55 days of age, the number of TEB remained higher than that in the control animals and the TEB became larger and had higher mitotic activities. Such TEB were called intraductal proliferations (IDP); they evolved to adenocarcinomas. DMBA increased the number of TD and decreased the number of AB and lobules in relation to the control animals. These findings led to the conclusion that DMBA administration to 55-day-old rats alters the differentiation of TEB leads to AB leads to lobules, inducing instead the sequence TEB leads to IDP leads to adenocarcinoma.
Non-Hodgkin's lymphoma: Patterns of relapse from complete remission after combination chemotherapy (1975)

An analysis of patterns of relapse from complete remission in patients with non-Hodgkin's lymphoma treated with combination chemotherapy has demonstrated differences between histologic subgroups. Patients with diffuse histiocytic lymphoma who achieved a histologically proven complete remission after 6 months of treatment without maintenance have remained disease-free whereas those with nodular poorly differentiated lymphocytic and diffuse well-differentiated lymphocytic lymphomas have demonstrated a pattern of continuous late recurrence. The initial sites of relapse from complete remission in lymphocytic lymphoma were lymph nodes and bone marrow which were involved prior to treatment. Aggressive attempts at remission induction appear warranted in patients with diffuse histiocytic lymphoma because of the potential for extended disease-free survival. Patients with nodular poorly differentiated lymphocytic lymphoma may benefit from the use of maintenance chemotherapy, or radiotherapy to regions of previously known involvement after initiation of remission with chemotherapy.
Craniocerebral Trauma: Protection and Retrieval of the Neuronal Population after Injury (1998)

The understanding of traumatic brain damage that is being gained from recent research is widening and broadening perspectives from the traditional focus on mechanical, vascular, and metabolic effects to encompass wider, neurobiological issues, drawn from the fields of neurodevelopment, neuroplasticity, neurodegeneration, and neurogenetics. Neurotrauma is a fascinating area of neuroscience research, with promise for the translation of knowledge to improved clinical management and outcome.
Hydrophobicity of Bacillus and Clostridium spores (1990)

The hydrophobicities of spores and vegetative cells of several species of the genera Bacillus and Clostridium were measured by using the bacterial adherence to hexadecane assay and hydrophobic interaction chromatography. Although spore hydrophobicity varied among species and strains, the spores of each organism were more hydrophobic than the vegetative cells. The relative hydrophobicities determined by the two methods generally agreed. Sporulation media and conditions appeared to have little effect on spore hydrophobicity. However, exposure of spore suspensions to heat treatment caused a considerable increase in spore hydrophobicity. The hydrophobic nature of Bacillus and Clostridium spores suggests that hydrophobic interactions may play a role in the adhesion of these spores to surfaces.
Multiple polymorphic sites in factor X locus (1988)

The structure of factor X (FX) gene was analyzed in five FX deficient pedigrees with four different variants of the disease, as well as in 50 normal subjects. Genomic DNA from the deficient patients and the normal controls was digested with 12 restriction endonucleases and hybridized with a FX cDNA probe. The results seemingly exclude gross gene deletions or rearrangements in the deficient patients. A variety of polymorphic sites (ie, EcoRI, HindIII, PstI, PvuII, TaqI) was observed within the FX locus and their relative frequency was established. Intriguingly, a highly polymorphic region for the PvuII endonuclease was identified and located approximately 3 kilobases (kb) from the last 3′ exon. These polymorphisms allowed us to analyze the allelic segregation in a FX deficient family and to identify a homozygous subject.
Degradation of rRNA in interferon-treated vaccinia virus-infected cells. (1984)

In interferon-treated mouse L cells, following infection with a DNA-containing virus, vaccinia, synthesis of unique 2'-5'-linked oligonucleotides of the general formula ppp5'A2'(p5'A)n, abbreviated as 2-5A, was detected by competition radiobinding assay. In addition, degradation of rRNA into discrete and characteristic products, similar to those produced by 2-5A-activated endonuclease, was observed. The degradation of rRNA may represent a significant component of antiviral action of interferon in vaccinia virus-infected cells.
Differential regulation of interferon‐induced mRNAs and c‐myc mRNA by α‐ and γ‐interferons (1985)

The extent and kinetics of induction have been determined for eight mRNAs induced by alpha- and gamma-interferons in HeLa cells. The mRNAs which code for a 2-5A synthetase, metallothionein II, HLA class I antigen and five unknown proteins were induced 2 - greater than 100-fold by alpha-interferons. In the continued presence of alpha-interferon some mRNAs were maintained at the induced levels until at least 40 h, whereas others were induced only transiently. When the effects of alpha- and gamma-interferons were compared, the induced levels and kinetics were very similar for one mRNA (1-8) but were significantly different for the others. One mRNA (6-16) was induced more than 100-fold by alpha-interferon but not significantly by gamma-interferon. Parallel analysis of the level of c-myc mRNA showed it to decrease twofold in response to alpha-interferon, but to increase more than threefold in response to gamma-interferon, despite a more profound inhibition of cell growth by the latter. There must, therefore, be differences in how the levels of different mRNAs are sustained by alpha-interferons and how alpha- and gamma-interferons regulate the levels of the same mRNAs.
Quantum cryptographic device using single-photon phase modulation (1999)

We report a particular implementation of a quantum cryptographic device operating at 1540-nm wavelength and involving interference between phase-modulated sidebands produced by a pair of phase modulators in the transmitting and receiving modules. The principle of operation is described in terms of both classical and quantum optics. The method has been demonstrated experimentally using a strongly attenuated semiconductor laser diode. Single photon interference has been obtained with a fringe visibility greater than 90%, indicating that the system can be used for quantum key distribution.
Ribosomal Alterations Contribute to Bacterial Resistance against the Dipeptide Antibiotic TAN 1057 (2004)

TAN 1057-resistant Staphylococcus aureus and Escherichia coli strains were selected to elucidate the mechanism of resistance and the mode of action of this dipeptide antibiotic. Cell-free translation with isolated ribosomes and S150 fractions from sensitive and resistant S. aureus strains demonstrated that alterations in the ribosomes contribute to the resistance of the bacteria.
Alefacept selectively promotes NK cell‐mediated deletion of CD45R0+ human T cells (2003)

Modulation of the immune response using immunoglobulin fusion proteins has shown great promise for clinical immunotherapy of autoimmune diseases. Alefacept is an immunoglobulin fusion protein composed of the first extracellular domain of human LFA-3 fused to the hinge, C(H)2 and C(H)3 domains of human IgG(1). Alefacept has previously been reported to inhibit T cell proliferation. Here, we analyzed the effects of alefacept on lymphocytes in vitro and characterized the role of autologous NK cells in its mechanism of action. Alefacept, but not a C(H)2 binding mutant of Alefacept, inhibited CD3-induced T cell proliferation only in the presence of live NK cells, consistent with an important role for FcgammaR engagement. Alefacept caused preferential depletion of CD69+CD45R0+CD25+ T cell subsets. Cytotoxicity assays revealed that alefacept, but not the C(H)2 binding mutant, induced NK cell-mediated death of activated T cells and sorting into CD45R0+ and CD45RA+ subpopulations showed that lymphocyte deletion occurred preferentially in the CD45R0+ subset. Activated CD45R0+ cells expressed higher levels of CD2 than CD45R0- cells, providing a possible explanation for the selective targeting of this subset. Our results suggest that selective targeting of CD45R0+ T cells by NK cells represents a potential therapeutic mechanism of action of alefacept.
Microwave operation and modulation of a transistor laser (2005)

The microwave operation and modulation (3GHz) of an InGaP∕GaAs heterojunction bipolar transistor (HBT) laser is reported. The HBT layer structure is in the form of an optical waveguide (with cleaved ends) that also includes an InGaAs recombination quantum well in the p-type base region to improve the recombination radiation properties. The shift in HBT laser operation from spontaneous to stimulated emission is manifest as a distinct change in the HBT current–voltage characteristics, specifically a decrease in the common-emitter current gain (βdc=IC∕IB) and the occurrence of even a more striking peak in the small signal (ac) gain βac=ΔIC∕ΔIB.
ATP-dependent incorporation of 20S protease into the 26S complex that degrades proteins conjugated to ubiquitin. (1989)

Previous studies have indicated that the ATP-dependent 26S protease complex that degrades proteins conjugated to ubiquitin is formed by the assembly of three factors in an ATP-requiring process. We now identify one of the factors as the 20S "multicatalytic" protease, a complex of low molecular weight subunits widely distributed in eukaryotic cells. Comparison of the subunit compositions of purified 20S and 26S complexes indicates that the former is an integral part of the latter. By the use of detergent treatment to activate latent protease activity, we show that the 20S protease becomes incorporated into the 26S complex in the ATP-dependent assembly process. It thus seems that the 20S protease is the "catalytic core" of the 26S complex of the ubiquitin proteolytic pathway.
FGFR4 signaling is a necessary step in limb muscle differentiation (2002)

In chick embryos, most if not all, replicating myoblasts present within the skeletal muscle masses express high levels of the FGF receptor FREK/FGFR4, suggesting an important role for this molecule during myogenesis. We examined FGFR4 function during myogenesis, and we demonstrate that inhibition of FGFR4, but not FGFR1 signaling, leads to a dramatic loss of limb muscles. All muscle markers analyzed (such as Myf5, MyoD and the embryonic myosin heavy chain) are affected. We show that inhibition of FGFR4 signal results in an arrest of muscle progenitor differentiation, which can be rapidly reverted by the addition of exogenous FGF, rather than a modification in their proliferative capacities. Conversely, over-expression of FGF8 in somites promotes FGFR4 expression and muscle differentiation in this tissue. Together, these results demonstrate that in vivo, myogenic differentiation is positively controlled by FGF signaling, a notion that contrasts with the general view that FGF promotes myoblast proliferation and represses myogenic differentiation. Our data assign a novel role to FGF8 during chick myogenesis and demonstrate that FGFR4 signaling is a crucial step in the cascade of molecular events leading to terminal muscle differentiation.
BCL-2 family proteins as 5-Azacytidine-sensitizing targets and determinants of response in myeloid malignancies (2014)

Synergistic molecular vulnerabilities enhancing hypomethylating agents in myeloid malignancies have remained elusive. RNA-interference drug modifier screens identified antiapoptotic BCL-2 family members as potent 5-Azacytidine-sensitizing targets. In further dissecting BCL-XL, BCL-2 and MCL-1 contribution to 5-Azacytidine activity, siRNA silencing of BCL-XL and MCL-1, but not BCL-2, exhibited variable synergy with 5-Azacytidine in vitro. The BCL-XL, BCL-2 and BCL-w inhibitor ABT-737 sensitized most cell lines more potently compared with the selective BCL-2 inhibitor ABT-199, which synergized with 5-Azacytidine mostly at higher doses. Ex vivo, ABT-737 enhanced 5-Azacytidine activity across primary AML, MDS and MPN specimens. Protein levels of BCL-XL, BCL-2 and MCL-1 in 577 AML patient samples showed overlapping expression across AML FAB subtypes and heterogeneous expression within subtypes, further supporting a concept of dual/multiple BCL-2 family member targeting consistent with RNAi and pharmacologic results. Consequently, silencing of MCL-1 and BCL-XL increased the activity of ABT-199. Functional interrogation of BCL-2 family proteins by BH3 profiling performed on patient samples significantly discriminated clinical response versus resistance to 5-Azacytidine-based therapies. On the basis of these results, we propose a clinical trial of navitoclax (clinical-grade ABT-737) combined with 5-Azacytidine in myeloid malignancies, as well as to prospectively validate BH3 profiling in predicting 5-Azacytidine response.
The Acquisition of hMLH1 Methylation in Plasma DNA after Chemotherapy Predicts Poor Survival for Ovarian Cancer Patients (2004)

Aberrant epigenetic regulation, such as CpG island methylation and associated transcriptional silencing of genes, has been implicated in a variety of human diseases, including cancer. Methylation of genes involved in apoptosis, including the DNA mismatch repair (MMR) gene hMLH1, can occur in tumor models of resistance to chemotherapeutic drugs. However, the relevance for acquired resistance to chemotherapy of patients' tumors remains unsubstantiated. Plasma DNA from cancer patients, including those with ovarian cancer, often contains identical DNA changes as the tumor and provides a means to monitor CpG island methylation changes. We have examined plasma DNA of patients with epithelial ovarian cancer enrolled in the SCOTROC1 Phase III clinical trial for methylation of the hMLH1 CpG island before carboplatin/taxoid chemotherapy and at relapse. Methylation of hMLH1 is increased at relapse, and 25% (34 of 138) of relapse samples have hMLH1 methylation that is not detected in matched prechemotherapy plasma samples. Furthermore, hMLH1 methylation is significantly associated with increased microsatellite instability in plasma DNA at relapse, providing an independent measure of function of the MMR pathway. Acquisition of hMLH1 methylation in plasma DNA at relapse predicts poor overall survival of patients, independent from time to progression and age (hazard ratio, 1.99; 95% confidence interval, 1.20-3.30; P = 0.007). These data support the clinical relevance of acquired hMLH1 methylation and concomitant loss of DNA MMR after chemotherapy of ovarian cancer patients. DNA methylation changes in plasma provide the potential to define patterns of methylation during therapy and identify those patient populations who would be suitable for novel epigenetic therapies.
Identification of a novel G-protein coupled receptor expressed in distinct brain regions and a defined olfactory zone. (1998)

PCR-approaches with degenerated oligonucleotide primers have been employed in trying to identify novel members of the G-protein coupled receptor (GPCR) superfamily from rat brain. Screening a rat brain library with an amplification product showing some features of a GPCR gene led to the isolation of a full-length clone (RA1c); the encoded polypeptide comprises seven distinct hydrophobic stretches as well as several other hallmarks of GPCRs. Sequence comparison revealed a rather low but significant homology to GPCRs; RA1c shares about 30% sequence identity with various olfactory receptors and about 27% with several peptide receptors. By Northern blot and especially by in situ hybridization analysis it could be demonstrated that the RA1c receptor is expressed only in very distinct areas of the brain and in addition in a defined zone of the olfactory epithelium.
NOVEL EVIDENCE SUGGESTING AN ANTI‐OXIDANT PROPERTY FOR ERYTHROPOIETIN ON VANCOMYCIN‐INDUCED NEPHROTOXICITY IN A RAT MODEL (2007)

1. The aim of the present study was to investigate the role of oxidative stress in renal injury and to determine whether erythropoietin (EPO) acts as an anti-oxidant in vancomycin (VCM)-induced renal impairment. 2. Twenty-four rats were divided into three groups as follows: (i) control (Group 1); (ii) VCM treated (Group 2); and (iii) VCM + EPO treated (Group 3). Vancomycin (200 mg/kg, i.p.) was administered to Groups 2 and 3 for 7 days. Erythropoietin (150 IU/kg, i.p.) treatment was started 24 h before VCM and lasted for 7 days. On Day 8, renal tissues were excised and blood samples were collected. Serum creatinine and blood urea nitrogen were measured, along with renal malondialdehyde (MDA) levels, superoxide dismutase (SOD) and catalase (CAT) activity and tissue VCM levels. The kidneys were examined for any histopathological changes. 3. Renal MDA levels were found to be increased, whereas SOD and CAT activity was decreased, in the VCM-treated group compared with the control group. There was a marked decrease in MDA levels and an increase in SOD activity, but not CAT activity, after VCM + EPO treatment. Marked histopathological alterations, including interstitial oedema, tubular dilatation, tubular epithelial cell desquamation and vacuolization, were observed in VCM-treated rats. Histopathological changes were significantly improved after EPO administration. 4. In conclusion, the present data suggest that oxidative stress plays an important role in VCM-induced nephrotoxicity. Erythropoietin seems to act as an anti-oxidant, diminishing the toxic oxidative effects of VCM on renal tissues.
Sliced Inverse Regression for Dimension Reduction (1991)

Abstract Modern advances in computing power have greatly widened scientists' scope in gathering and investigating information from many variables, information which might have been ignored in the past. Yet to effectively scan a large pool of variables is not an easy task, although our ability to interact with data has been much enhanced by recent innovations in dynamic graphics. In this article, we propose a novel data-analytic tool, sliced inverse regression (SIR), for reducing the dimension of the input variable x without going through any parametric or nonparametric model-fitting process. This method explores the simplicity of the inverse view of regression; that is, instead of regressing the univariate output variable y against the multivariate x, we regress x against y. Forward regression and inverse regression are connected by a theorem that motivates this method. The theoretical properties of SIR are investigated under a model of the form, y = f(β 1 x, …, β K x, ε), where the β k 's are the unknown row vectors. This model looks like a nonlinear regression, except for the crucial difference that the functional form of f is completely unknown. For effectively reducing the dimension, we need only to estimate the space [effective dimension reduction (e.d.r.) space] generated by the β k 's. This makes our goal different from the usual one in regression analysis, the estimation of all the regression coefficients. In fact, the β k 's themselves are not identifiable without a specific structural form on f. Our main theorem shows that under a suitable condition, if the distribution of x has been standardized to have the zero mean and the identity covariance, the inverse regression curve, E(x | y), will fall into the e.d.r. space. Hence a principal component analysis on the covariance matrix for the estimated inverse regression curve can be conducted to locate its main orientation, yielding our estimates for e.d.r. directions. Furthermore, we use a simple step function to estimate the inverse regression curve. No complicated smoothing is needed. SIR can be easily implemented on personal computers. By simulation, we demonstrate how SIR can effectively reduce the dimension of the input variable from, say, 10 to K = 2 for a data set with 400 observations. The spin-plot of y against the two projected variables obtained by SIR is found to mimic the spin-plot of y against the true directions very well. A chi-squared statistic is proposed to address the issue of whether or not a direction found by SIR is spurious. Key Words: Dynamic graphicsPrincipal component analysisProjection pursuit