gebhart/patrepeval huggingface dataset:
Space-time coded modulation for high data rate wireless communications (2002)

This paper presents the theory and practice of a new advanced modem technology suitable for high data rate wireless communications and presents its performance over a frequency-flat Rayleigh fading channel. The new technology is based on space-time coded modulation (STCM) with multiple transmit and/or multiple receive antennas and orthogonal pilot sequence insertion (O-PSI). In this approach data is encoded by a space-time channel encoder and the output of the encoder is split into N streams to be simultaneously transmitted using N transmit antennas. The transmitter inserts periodic orthogonal pilot sequences in each of the simultaneously transmitted bursts. The receiver uses those pilot sequences to estimate the fading channel. When combined with an appropriately designed interpolation filter, accurate channel state information (CSI) can be estimated for the decoding process. Simulation results of the proposed modem as applied to the IS-136 cellular standard are presented. We present the frame error rate (FER) performance as a function of the signal to noise ratio (SNR) and Doppler spread in the presence of timing and frequency offset errors. Simulation results show that, for example, for 10% FER, data rates up to 54 kbps per a 30 kHz channel can be supported at a SNR of 11.7 dB and a Doppler spread of 180 Hz using a 32-state 8-PSK space-time code with 2 transmit and 2 receive antennas. Simulation results for other cases are also provided.
Dynamic, inter-subunit interactions between the N-terminal and central mutation regions of cardiac ryanodine receptor (2010)

Naturally occurring mutations in the cardiac ryanodine receptor (RyR2) have been linked to certain types of cardiac arrhythmias and sudden death. Two mutation hotspots that lie in the N-terminal and central regions of RyR2 are predicted to interact with one another and to form an important channel regulator switch. To monitor the conformational dynamics involving these regions, we generated a fluorescence resonance energy transfer (FRET) pair. A yellow fluorescent protein (YFP) was inserted into RyR2 after residue Ser437 in the N-terminal region, and a cyan fluorescent protein (CFP) was inserted after residue Ser2367 in the central region, to form a dual YFP- and CFP-labeled RyR2 (RyR2(S437-YFP/S2367-CFP)). We transfected HEK293 cells with RyR2(S437-YFP/S2367-CFP) cDNAs, and then examined them by using confocal microscopy and by measuring the FRET signal in live cells. The FRET signals are influenced by modulators of RyR2, by domain peptides that mimic the effects of disease causing RyR2 mutations, and by various drugs. Importantly, FRET signals were also readily detected in cells co-transfected with single CFP (RyR2(S437-YFP)) and single YFP (RyR2(S2367-CFP)) labeled RyR2, indicating that the interaction between the N-terminal and central mutation regions is an inter-subunit interaction. Our studies demonstrate that FRET analyses of this CFP- and YFP-labeled RyR2 can be used not only for investigating the conformational dynamics associated with RyR2 channel gating, but potentially, also for identifying drugs that are capable of stabilizing the conformations of RyR2.
Preparation and evaluation in vitro and in vivo of polylactic acid microspheres containing dibucaine. (1982)

DL-Polylactic acid microspheres containing dibucaine were prepared, and release patterns of dibucaine from the microspheres as well as the local anesthetic effects of the drug in the microspheres were examined. The influences of nonsolvents and dibucaine concentration at preparation on the characteristics and dibucaine contents of the microspheres were investigated. Higher pH in nonsolvents and higher dibucaine concentration at preparation resulted in increased dibucaine contents in the microspheres. The release patterns of dibucaine from microspheres varied significantly among microspheres with different dibucaine contents, and the release mechanisms of dibucaine from microspheres were greatly influenced by disintegration of the microspheres. The local anesthetic effects of 0.1 ml aliquots of dibucaine hydrochloride solutions were examined at four concentrations in vivo. Then, the local anesthetic effects of dibucaine in microspheres were compared with those of the above solutions in relation to the release rate of dibucaine from microspheres in vitro. The more the amount of dibucaine, the stronger was the local anesthetic effect. The local anesthetic effect of dibucaine in microspheres lasted much longer (300 h) than that of dibucaine hydrochloride solutions. The profile of local anesthetic effect of dibucaine in microspheres in vivo was different from the release profile in vitro.
Molecular determinants of protein half‐lives in eukaryotic cells (1987)

Multiple pathways of intracellular protein breakdown operate within cells, and the activities of different pathways can be regulated under different physiological conditions. Recent studies suggest that molecular determinants within proteins target them for different pathways of proteolysis. Proteins that are partially unfolded and have an unblocked amino-terminal amino acid with a bulky side chain appear to be good substrates for cytosolic, ubiquitin-mediated pathways of proteolysis. Certain modifications of internal residues such as oxidation of methionines also increase the susceptibility of certain proteins to ubiquitin-mediated proteolysis. Rapidly degraded normal proteins contain peptide regions rich in proline, glutamate, serine, and threonine (PEST regions). The pathway of degradation for these proteins has not been established, but they may be good substrates for calcium-activated proteases. In addition, a lysosomal pathway of protein degradation is activated when serum is withdrawn from cultured cells and is selective for cytosolic proteins containing peptide regions similar to Lys-Phe-Glu-Arg-Gln (KFERQ). This short review summarizes our current understanding of mechanisms of protein breakdown in eukaryotes and evaluates potential molecular determinants of protein half-lives.
A Dynamic Programming Approach to De Novo Peptide Sequencing via Tandem Mass Spectrometry (2001)

Tandem mass spectrometry fragments a large number of molecules of the same peptide sequence into charged molecules of prefix and suffix peptide subsequences and then measures mass/charge ratios of these ions. The de novo peptide sequencing problem is to reconstruct the peptide sequence from a given tandem mass spectral data of k ions. By implicitly transforming the spectral data into an NC-spectrum graph G (V, E) where /V/ = 2k + 2, we can solve this problem in O(/V//E/) time and O(/V/2) space using dynamic programming. For an ideal noise-free spectrum with only b- and y-ions, we improve the algorithm to O(/V/ + /E/) time and O(/V/) space. Our approach can be further used to discover a modified amino acid in O(/V//E/) time. The algorithms have been implemented and tested on experimental data.
MUC1 dysregulation as the consequence of a t(1;14)(q21;q32) translocation in an extranodal lymphoma (2000)

Cytogenetic abnormalities at chromosome 1q21 are among the most common lesions in diffuse large-cell lymphoma and have been associated with a poor prognosis. A novel cell line, SKI-DLCL-1, was established from ascitic fluid that carries a t(1;14)(q21;q32) chromosomal translocation. Using pulsed-field gel electrophoresis, the breakpoint on the IgH locus mapped to a gamma locus between C1 and C2. A cosmid library was prepared from SKI-DLCL-1, and Cγ-positive clones spanning the breakpoint were identified by screening with fluorescence in situ hybridization. The breakpoint occurs 860 bp downstream of the 3′ UTR of the MUC1 gene. The break appears to be a staggered double-strand break consistent with an error in immunoglobulin class switching. The MUC1 gene is highly transcribed and translated, and the protein is highly glycosylated. It is postulated that MUC1 expression is brought under the control of the 3′E enhancer. MUC1 lies in a region of chromosome 1 characterized by an unusually high density of genes, with 7 known genes in a region of approximately 85 kb. To determine whether there was a pleiotropic effect of the expression of genes in the region as a consequence of the translocation, the expression of 6 additional genes was assessed. None of the other genes in this region (CLK2, propin, COTE1, GBA, metaxin, and thrombospondin 3) are overexpressed in SKI-DLCL-1. Thus, the translocation t(1;14)(q21;q32) seen in both the primary tumor and the derived cell line results in the marked overexpression of MUC1 without affecting the expression of other genes in the region.
Novel Allergen Structures with Tandem Amino Acid Repeats Derived from German and American Cockroach (1998)

Cockroaches produce potent allergens that are an important cause of asthma. The two principal domiciliary cockroach species, Blattella germanica and Periplaneta americana, secrete major allergens, Bla g 1 and Per a 1. Here, we report the molecular cloning of three Bla g 1 cDNA clones, which showed 70% amino acid sequence identity with Per a 1. Plaque immunoassays with human IgE antibodies or murine monoclonal antibodies showed that these allergens were antigenically cross-reactive. The Bla g 1 sequences also showed homology to five previously undefined cockroach allergen sequences. An unusual feature of all these sequences was that they contained multiple tandem amino acid repeats of approximately 100 amino acid residues. Between one and seven repeat units were identified by dot-plot matrix analysis. The sequences also showed homology to a mosquito protein involved in digestion (ANG12 precursor) and to mitochondrial energy transfer proteins. High levels of Bla g 1 were found in cockroach hindgut and proventriculus. Amino acid sequencing of natural Bla g 1 and Per a 1 suggested that these allergens are cleaved by trypsin-like enzymes following secretion into the digestive tract. The repeat sequences appear to have evolved by duplication of an ancestral amino acid domain, which may have arisen from the mitochondrial energy transfer proteins.
Recent progress on upgrading of bio-oil to hydrocarbons over metal/zeolite bifunctional catalysts (2017)

Upgrading of bio-oil over metal/zeolite bi-functional catalysts, is of high necessity and popularity in converting biomass to high-quality hydrocarbons (transportation fuels and petrochemicals) to reduce the overall CO<sub>2</sub> emissions of fossil based materials.
The Insulinotropic Effect of Acute Exendin-4 Administered to Humans: Comparison of Nondiabetic State to Type 2 Diabetes (2002)

Exendin-4 is a potent and long-acting agonist of the glucagon-like peptide-1 (GLP-1) receptor. GLP-1 is an insulinotropic gut peptide and is being evaluated for the regulation of plasma glucose in type 2 diabetes. The purpose of the present study was to ascertain whether exendin-4 is insulinotropic and whether it has long-lived biological effects in nondiabetic and type 2 diabetic subjects. Because incretins are glucose dependent with respect to their insulin-releasing capacity, we used the hyperglycemic glucose clamp technique to begin to address these issues in two separate protocols. In one protocol, we infused exendin-4 (0.15 pmol x kg(-1) x min(-1)) in seven nondiabetic and seven type 2 diabetic subjects during the second hour of a 5-h hyperglycemic clamp in which fasting plasma glucose was raised by 5.4 mmol/liter. The second protocol was identical to the first except that plasma glucose was allowed to fall to the fasting levels during the fourth hour and again raised by 5.4 mmol/liter during the fifth hour in four nondiabetic and four diabetic subjects. With the initiation of exendin-4 infusion at 60 min, plasma insulin response was potentiated 4- to 5-fold in both groups. Despite termination of exendin-4 at the end of the second hour, the insulin levels remained elevated for several hours and hyperglycemia was maintained. All volunteers ate a meal 5.5 h after inducing hyperglycemia. Postprandial plasma glucose, insulin, and GLP-1 did not rise in any subject, possibly because of delayed gastric emptying by exendin-4 even though its infusion had been terminated 4 h previously. We concluded that exendin-4 is a potent and long-lasting insulinotropic agent in nondiabetic and diabetic subjects.
WNT16B Is a New Marker of Cellular Senescence That Regulates p53 Activity and the Phosphoinositide 3-Kinase/AKT Pathway (2009)

Senescence is a tumor suppression mechanism that is induced by several stimuli, including oncogenic signaling and telomere shortening, and controlled by the p53/p21(WAF1) signaling pathway. Recently, a critical role for secreted factors has emerged, suggesting that extracellular signals are necessary for the onset and maintenance of senescence. Conversely, factors secreted by senescent cells may promote tumor growth. By using expression profiling techniques, we searched for secreted factors that were overexpressed in fibroblasts undergoing replicative senescence. We identified WNT16B, a member of the WNT family of secreted proteins. We found that WNT16B is overexpressed in cells undergoing stress-induced premature senescence and oncogene-induced senescence in both MRC5 cell line and the in vivo murine model of K-Ras(V12)-induced senescence. By small interfering RNA experiments, we observed that both p53 and WNT16B are necessary for the onset of replicative senescence. WNT16B expression is required for the full transcriptional activation of p21(WAF1). Moreover, WNT16B regulates activation of the phosphoinositide 3-kinase (PI3K)/AKT pathway. Overall, we identified WNT16B as a new marker of senescence that regulates p53 activity and the PI3K/AKT pathway and is necessary for the onset of replicative senescence.
Neutrophil recruitment in Clostridium difficile toxin A enteritis in the rabbit. (1994)

Neutrophil infiltration is a prominent feature of Clostridium difficile-associated enteritis and colitis. The aim of this study was to examine the importance of neutrophil recruitment and neutrophil-mediated tissue damage in C. difficile toxin A-induced enteritis. Competitive binding experiments using purified 3H-toxin A demonstrated the presence of a single class of medium affinity receptors on rabbit neutrophils (Kd 7 x 10(-8) M). Pertussis toxin and the nonhydrolyzable GTP analog GTPgamma S both inhibited 3H-toxin A binding (by 56 and 65%, respectively), indicating that the rabbit neutrophil toxin A receptor is G protein linked. Toxin A elicited a dose-dependent (25-200 micrograms/ml) stimulation of neutrophil migration in vitro, and this functional effect was also pertussis toxin sensitive (69% inhibition). Treatment of neutrophils with R15.7, a blocking monoclonal antibody to the leuocyte adhesion molecule CD18, inhibited toxin A-stimulated neutrophil migration by 85% in vitro. Pretreatment of rabbits with R15.7 also prevented neutrophil infiltration of toxin A-exposed ileal loops in vivo as determined by histologic examination and by ileal tissue myeloperoxidase levels. Furthermore, R15.7 effected a substantial inhibition of fluid secretion (by 65%), mannitol permeability (by 66%), and histologic damage in toxin A-exposed ileal loops. Anti-CD18 (R15.7) had no inhibitory effect on cholera toxin enterotoxicity. These data demonstrate that C. difficile toxin A is a proinflammatory toxin whose enterotoxic effects are substantially dependent upon neutrophil recruitment.
Genetic Determinants Responsible for Acquisition of Dengue Type 2 Virus Mouse Neurovirulence (1998)

Studies conducted some 50 years ago showed that serial intracerebral passage of dengue viruses in mice selected for neurovirulent mutants that also exhibited significant attenuation for humans. We investigated the genetic basis of mouse neurovirulence of dengue virus because it might be directly or indirectly associated with attenuation for humans. Analysis of the sequence in the C-PreM-E-NS1 region of the parental dengue type 2 virus (DEN2) New Guinea C (NGC) strain and its mouse-adapted, neurovirulent mutant revealed that 10 nucleotide changes occurred during serial passage in mice. Seven of these changes resulted in amino acid substitutions, i.e., Leu55-Phe and Arg57-Lys in PreM, Glu71-Asp, Glu126-Lys, Phe402-Ile, and Thr454-Ile in E, and Arg105-Gln in NS1. The sequence of C was fully conserved between the parental and mutant DEN2. We constructed intertypic chimeric dengue viruses that contained the PreM-E genes or only the NS1 gene of neurovirulent DEN2 NGC substituting for the corresponding genes of DEN4. The DEN2 (PreM-E)/DEN4 chimera was neurovirulent for mice, whereas DEN2 (NS1)/DEN4 was not. The mutations present in the neurovirulent DEN2 PreM-E genes were then substituted singly or in combination into the sequence of the nonneurovirulent, parental DEN2. Intracerebral titration of the various mutant chimeras so produced identified two amino acid changes, namely, Glu71-Asp and Glu126-Lys, in DEN2 E as being responsible for mouse neurovirulence. The conservative amino acid change of Gu71-Asp probably had a minor effect, if any. The Glu126-Lys substitution in DEN2 E, representing a change from a negatively charged amino acid to a positively charged amino acid, most likely plays an important role in conferring mouse neurovirulence.
Measuring ease of breathing in young patients with cystic fibrosis (2002)

Our objective was to compare two new objective measures of ease of breathing with the visual analog scale (VAS). Twenty-eight patients with CF, 7-34 years old (FEV(1) 25-114% of predicted), enrolled. Ease of breathing was evaluated by a standard 10-cm VAS, maximum phonation (time, in seconds, to sustain the syllable "Ahh") using a single breath, and counting in a single breath at one number per second (Count) at rest, following 3 min of stepping exercise at 15 steps per minute (STEP15), and 3 min at 30 steps per minute (STEP30). Heart rate (HR) and oxyhemoglobin saturation (SaO(2)) were measured.HR and VAS increased significantly, and SaO(2), phonation, and Count decreased significantly from rest to STEP15 and STEP30. Phonation time correlated significantly (and inversely) with HR after exercise. Phonation time was positively correlated with SaO(2) at rest and after STEP30. Counts at rest and after STEP30 were significantly related to SaO(2). VAS showed no relationship to heart rate at rest or after exercise, but was related to SaO(2) at the end of STEP30. Test-retest reliability for three trials of phonation was 0.92, and for the five trials of counting was 0.93. Correlation coefficients for maximum phonation at rest, STEP15, and STEP30 on 2 separate days were 0.61, 0.94, and 0.91, respectively. Correlation coefficients for Count at rest, STEP15, and STEP30 on 2 separate days were 0.96, 0.94, and 0.94, respectively. Correlation coefficients for VAS at rest, STEP15, and STEP30 on 2 separate days were 0.25, 0.89, and 0.97, respectively. Thus both the maximum phonation and Count have good test-retest reliability within one session, and across 2 separate days, for both rest and exercise conditions. In conclusion, maximum phonation and Count are valid and reliable measures of ease of breathing; they reflect increasing work loads and show stronger correlations with heart rate and SaO(2) than does VAS. These measures could be an important tool for clinical research and patient care.
Prior Knowledge in Support Vector Kernels (1997)

We explore methods for incorporating prior knowledge about a problem at hand in Support Vector learning machines. We show that both invari-ances under group transfonnations and prior knowledge about locality in images can be incorporated by constructing appropriate kernel functions.
Midkine in the progression of ratN-nitroso-N-methylurea-induced mammary tumors (1996)

Recent studies have implicated a role for midkine (MK) in cancer progression. This is based upon its structural homology with pleiotrophin, an angiogenic growth factor, and its ability to enhance fibrinolytic activity of bovine endothelial cells. To investigate whether MK plays a role in breast cancer, we examined MK mRNA expression in N-nitroso-N-methylurea-induced rat mammary tumors at various stages of tumor progression, including hormone independence and distant metastasis. Well-differentiated mammary adenocarcinomas showed levels of MK comparable to those of normal mammary gland. A 10- to 20-fold reduction in MK mRNA levels was observed in mammary tumors that had progressed to hormone independence and metastasis. The data suggest that loss of MK expression correlates with breast tumor progression. Treatment of rat mammary tumor cell lines with retinoic acid increased MK expression, decreased proliferation, and markedly reduced colony-forming efficiency in agar. This raises the possibility that agents that upregulate MK could have potential in prevention and therapy by causing breast cells to terminally differentiate.
Congenital Disorders of Glycosylation: A Rapidly Expanding Disease Family (2007)

Congenital disorders of glycosylation (CDG) are a large family of genetic diseases resulting from defects in the synthesis of glycans and in the attachment of glycans to other compounds. These disorders cause a wide range of human diseases, with examples emanating from all medical subspecialties. Since our 2001 review on CDG ( 36 ), this field has seen substantial growth: The number of N-glycosylation defects has doubled (from 6 to 12), five new O-glycosylation defects have been added to the two previously known ones, three combined N- and O-glycosylation defects have been identified, the first lipid glycosylation defects have been discovered, and a new domain, that of the hyperglycosylation defects, has been introduced. A number of CDG are due to defects in enzymes with a putative glycosyltransferase function. There is also a growing group of patients with unidentified defects (CDG-x), some with typical clinical presentations and others with presentations not seen before in CDG. This review focuses on the clinical, biochemical, and genetic characteristics of CDG and on advances expected in their future study and clinical management.
The MOS 36-Item Short-Form Health Survey (SF-36) (1993)

Cross-sectional data from the Medical Outcomes Study (MOS) were analyzed to test the validity of the MOS 36-Item Short-Form Health Survey (SF-36) scales as measures of physical and mental health constructs. Results from traditional psychometric and clinical tests of validity were compared. Principal components analysis was used to test for hypothesized physical and mental health dimensions. For purposes of clinical tests of validity, clinical criteria defined mutually exclusive adult patient groups differing in severity of medical and psychiatric conditions. Scales shown in the components analysis to primarily measure physical health (physical functioning and role limitations-physical) best distinguished groups differing in severity of chronic medical condition and had the most pure physical health interpretation. Scales shown to primarily measure mental health (mental health and role limitations-emotional) best distinguished groups differing in the presence and severity of psychiatric disorders and had the most pure mental health interpretation. The social functioning, vitality, and general health perceptions scales measured both physical and mental health components and, thus, had the most complex interpretation. These results are useful in establishing guidelines for the interpretation of each scale and in documenting the size of differences between clinical groups that should be considered very large.