gebhart/patrepeval huggingface dataset:
Impaired erythrocytes deformability in H 2 O 2 -induced oxidative stress: Protective effect of L-carnosine (2008)

Impaired red blood cell deformability is a hemorheological perturbation induced by many kinds of diseases. An increase in free radicals causes a reduction in erythrocyte flexibility and deformability. Carnosine is a dipeptide abundant in skeletal muscle and brain of humans. One of the main function of carnosine is its antioxidant and free-radical scavenger effect. In this study our aim is to investigate the protective effect of L-carnosine on RBCs in H(2)O(2)-induced oxidative stress in vitro conditions. Twenty male wistar albino rats, 10 were 3 months old, 10 were 12 months old used. The blood from each rat were divided into ten tubes and these blood samples divided into two groups. The first tube of the first group was the control and the rest 4 tubes were treated with different concentrations of L-carnosine. All tubes in the second group were incubated with H(2)O(2) additively. The deformability indexes of the erythrocytes were measured by a laser diffractometer (Myrenne Rheodyne SSD).L-carnosine has improved the RBC deformability significantly which is impaired by H(2)O(2) treatment (p<0.05). Increase in deformability is more significant in young rat group when compared to old rat group.L-carnosine, as an antioxidant molecules, has a dose dependent positive effect on RBC deformability and has improved or protect the deformability of erythrocytes, especially in young rat group which impaired by H(2)O(2)-induced oxidative stress in vitro conditions. The results of this study first suggest that L-carnosine supplemention can be used to improve the RBC quality or to protect them from oxidative damage in survival of RBC in the circulation.
Heats of Combustion and Formation of New Energetic Thermoplastic Elastomers Based on GAP, PolyNIMMO and PolyGLYN (2003)

Abstract Heats of combustion and formation of various energetic thermoplastic elastomers (ETPE), corresponding to linear copolyurethanes based on an energetic prepolymer and a diisocyanate, were measured by a calorimetric method. These ETPEs were synthesized from three different molecular weights of glycidyl azide polymer, from poly(3‐nitratomethyl‐3‐methyloxetane) and from poly glycidyl nitrate. The prepolymers were also analyzed for comparison with the corresponding ETPEs. A significant difference of the heats of formation was observed between the prepolymers and their ETPEs, while the heats of combustion were similar.
The time-delayed inverted pendulum: Implications for human balance control (2009)

The inverted pendulum is frequently used as a starting point for discussions of how human balance is maintained during standing and locomotion. Here we examine three experimental paradigms of time-delayed balance control: (1) mechanical inverted time-delayed pendulum, (2) stick balancing at the fingertip, and (3) human postural sway during quiet standing. Measurements of the transfer function (mechanical stick balancing) and the two-point correlation function (Hurst exponent) for the movements of the fingertip (real stick balancing) and the fluctuations in the center of pressure (postural sway) demonstrate that the upright fixed point is unstable in all three paradigms. These observations imply that the balanced state represents a more complex and bounded time-dependent state than a fixed-point attractor. Although mathematical models indicate that a sufficient condition for instability is for the time delay to make a corrective movement, tau(n), be greater than a critical delay tau(c) that is proportional to the length of the pendulum, this condition is satisfied only in the case of human stick balancing at the fingertip. Thus it is suggested that a common cause of instability in all three paradigms stems from the difficulty of controlling both the angle of the inverted pendulum and the position of the controller simultaneously using time-delayed feedback. Considerations of the problematic nature of control in the presence of delay and random perturbations ("noise") suggest that neural control for the upright position likely resembles an adaptive-type controller in which the displacement angle is allowed to drift for small displacements with active corrections made only when theta exceeds a threshold. This mechanism draws attention to an overlooked type of passive control that arises from the interplay between retarded variables and noise.
PHYSICAL UNCLONABLE FUNCTION HARDWARE KEYS UTILIZING KIRCHHOFF-LAW-JOHNSON-NOISE SECURE KEY EXCHANGE AND NOISE-BASED LOGIC (2013)

Weak unclonable function (PUF) encryption key means that the manufacturer of the hardware can clone the key but not anybody else. Strong unclonable function (PUF) encryption key means that even the manufacturer of the hardware is unable to clone the key. In this paper, first we introduce an "ultra" strong PUF with intrinsic dynamical randomness, which is not only unclonable but also gets renewed to an independent key (with fresh randomness) during each use via the unconditionally secure key exchange. The solution utilizes the Kirchhoff-law-Johnson-noise (KLJN) method for dynamical key renewal and a one-time-pad secure key for the challenge/response process. The secure key is stored in a flash memory on the chip to provide tamper-resistance and nonvolatile storage with zero power requirements in standby mode. Simplified PUF keys are shown: a strong PUF utilizing KLJN protocol during the first run and noise-based logic (NBL) hyperspace vector string verification method for the challenge/response during the rest of its life or until it is re-initialized. Finally, the simplest PUF utilizes NBL without KLJN thus it can be cloned by the manufacturer but not by anybody else.
ISOLATE: a computational strategy for identifying the primary origin of cancers using high-throughput sequencing (2009)

Supplementary data are available at Bioinformatics online.
Expression of lipid body protein gene during maize seed development. Spatial, temporal, and hormonal regulation. (1988)

The storage lipids of seeds are packaged into lipid bodies, simple organelles containing a triacylglycerol core surrounded by a layer of phospholipids and proteins. A cDNA encoding the major protein from lipid bodies of maize (L3) was used as a hybridization probe to analyze the regulation of lipid body biosynthesis during seed development and germination. Immunofluorescent microscopy demonstrates that L3 protein accumulation is tissue-specific, confined to the embryo (scutellum and embryonic axis) and the aleurone layer of developing seed. Northern analyses show that L3 mRNA also accumulates to high levels in the embryo and is not found in any nonseed tissue. The steady-state level of L3 mRNA is developmentally regulated, increasing during early seed development and peaking at about the midpoint of seed development. It then decreases slowly, to 20% of the peak level, in the embryo of the mature seed and declines rapidly to undetectable levels as the seed germinates. The high level of L3 gene expression during seed development is not due to amplification of the L3 gene, since Southern analyses of maize genomic DNA indicate that the L3 gene has the same relatively low copy number throughout development (1-4 copies/haploid) genome). Rather, the increase in the steady-state level of L3 mRNA during seed development is transcriptionally regulated. The developmental changes in L3 mRNA levels are paralleled by changes in the transcription of the L3 gene, as measured by run-off transcription in isolated nuclei. The role of the plant growth regulator abscisic acid in regulating L3 gene expression was investigated. When the mature seed is allowed to imbibe in the presence of exogenous abscisic acid, germination is retarded, and the period of L3 gene expression is extended. The extended period of L3 gene expression in the presence of exogenous abscisic acid is due, at least in part, to a dramatic and specific increase in L3 gene transcription.
MediaAlert - a broadcast video monitoring and alerting system for mobile users (2005)

We present a system for automatic monitoring and timely dissemination of multimedia information to a range or mobile information appliances based on each user's interest profile. Multimedia processing algorithms detect and isolate relevant video segments from over twenty television broadcast programs based on a collection or words and phrases specified by the user. Content repurposing techniques are then used to convert the information into a form that is suitable for delivery to the user's mobile devices. Alerts are sent using a number of application messaging and network access protocols including email, short message service (SMS), multimedia messaging service (MMS), voice, session initiation protocol (SIP), fax, and pager protocols. The system is evaluated with respect to performance and user experiences. The MediaAlert system provides an effective and low-cost solution for the timely generation of alerts containing personal, business, and security information.
The insulin-sensitizing agent troglitazone improves metabolic and reproductive abnormalities in the polycystic ovary syndrome. (1996)

We performed this study to investigate the hypothesis that insulin resistance plays a role in the pathogenesis of reproductive abnormalities in women with the polycystic ovary syndrome (PCOS). Twenty-five women with PCOS were enrolled in a double-blind randomized 3-month trial of two doses of the insulin-sensitizing agent, troglitazone, 21 of whom completed the study: 200 mg, n = 10; 400 mg, n = 11. Baseline hormonal parameters and glucose tolerance were compared with 12 age- and weight-matched ovulatory control women. There were no significant changes in body mass index during the study. Fasting (P < 0.01) and 2-h post-75-g glucose load insulin levels (P < 0.05), as well as integrated insulin responses to the glucose load, decreased (P < 0.05), and insulin sensitivity assessed by a frequently sampled iv glucose tolerance test increased significantly (P < 0.001) during troglitazone treatment. This was accompanied by significant decreases in the levels of nonsex hormone-binding globulin-bound testosterone (P < 0.01), dehydroepiandrosterone sulfate (P < 0.001), estradiol (P < 0.01), and estrone (P < 0.001). Stepwise regression analysis indicated that decreases in nonsex hormone-binding globulin testosterone levels were significantly correlated with decreases in integrated insulin responses to the glucose load (r2 0.44, P < 0.01). The only significant changes at the 200-mg troglitazone dose were an increase in insulin sensitivity (P < 0.05) and decreases in dehydro-epiandrosterone sulfate (P < 0.01) and estrone (P < 0.05) levels. At the 400-mg dose, in addition to the changes noted in the entire troglitazone treatment group, increases in the disposition index (the product of insulin sensitivity and secretion) achieved significance, as did decreases in androstenedione (P < 0.01) and LH (P < 0.05) levels and increases in sex hormone-binding globulin levels (P < 0.01). Two PCOS women had ovulatory menses. We conclude that 1) troglitazone improves total body insulin action in PCOS, resulting in lower circulating insulin levels; 2) insulin resistance, probably via hyperinsulinemia, results in a general augmentation of steroidogenesis and LH release in PCOS; and 3) insulin-sensitizing agents, such as troglitazone, may provide a novel therapy for PCOS.
From TCR Engagement to Minireview T Cell Activation: A Kinetic View of T Cell Behavior (1999)

Summary The three peculiar properties of T cell antigen recogni- Valitutti, S., Mueller, S., Dessing, M., and Lanzavecchia, A. (1996).J. Exp. Med. 183 , 1917–1921. tion, specificity, sensitivity, and context discrimination, Viola, A., and Lanzavecchia, A. (1996). Science 273 , 104–106. are dependent on the kinetics of TCR–ligand interaction Viola, A., Salio, M., Tuosto, L., Linkert, S., Acuto, A., and Lanzavec- andTcellstimulation.Theexquisitecapacitytodiscrimi- chia, A. (1997a). J. Exp. Med. 186 , 1775–1779. nate between homologous ligands can be understood Viola, A., Linkert, S., and Lanzavecchia, A. (1997b). Eur. J. Immunol. in terms of thresholds for TCR triggering, dependent on 27 , 3080–3083. multistep phosphorylation and recruiting events, that Xavier, R., Brennan, T., Li, Q., McCormack, C., and Seed, B. (1998). allow a kinetic discrimination of the ligand. The sensitiv- Immunity 8 , 723–732. ity of T cells can be explained by the fact that a single Zhang, W., Trible, R.P., and Samelson, L.E. (1998). Immunity
Synthesis and Characterization of Poly(l-glutamic acid) Gadolinium Chelate:  A New Biodegradable MRI Contrast Agent (2004)

Most currently evaluated macromolecular contrast agents for magnetic resonance imaging (MRI) are not biodegradable. The goal of this study is to synthesize and characterize poly(l-glutamic acid) (PG) gadolinium chelates as biodegradable blood-pool MRI contrast agents. Two PG chelates of gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA) were synthesized through the use of difunctional and monofunctional DTPA precursors. The conjugates were characterized with regard to molecular weight and molecular weight distribution, gadolinium content, relaxivity, and degradability. Distributions of the polymeric MRI contrast agents in various organs were determined by intravenous injection of (111)In-labeled polymers into mice bearing murine breast tumors. MRI scans were performed at 1.5 T in mice after bolus injection of the polymeric chelates. PG-Hex-DTPA-Gd, obtained from aminohexyl-substituted PG and DTPA-dianhydride, was partially cross-linked and was undegradable in the presence of cathepsin B. On the other hand, PG-Bz-DTPA-Gd synthesized directly from PG and monofunctional p-aminobenzyl-DTPA(acetic acid-tert-butyl ester) was a linear polymer and was degradable. The relaxivities of the polymers at 1.5 T were 3-8 times as great as that of Gd-DTPA. Both polymers had high blood concentrations and were primarily accumulated in the kidney. However, PG-Bz-DTPA-Gd was gradually cleared from the body and had significantly less retention in the blood, the spleen, and the kidney. MRI with PG-Bz-DTPA-Gd in mice showed enhanced vascular contrast at up to 2 h after the contrast agent injection. The ability of PG-Bz-DTPA-Gd to be degraded and cleared from the body makes it a favorable macromolecular MRI contrast agent.
Spread of human cancer cells occurs with probabilities indicative of a nongenetic mechanism (2005)

There has been much uncertainty as to whether metastasis requires mutation at the time of spread. Here, we use clinical data to calculate the probability of the spread of melanoma and breast cancer cells. These calculations reveal that the probability of the spread of cancer cells is relatively high for small tumours (approximately 1 event of spread for every 500 cells for melanomas of 0.1 mm) and declines as tumours increase in size (approximately 1 event of spread for every 10(8) cells for melanomas of 12 mm). The probability of spread of breast cancer cells from the lymph nodes to the periphery is approximately 1 event of spread for every 10(8) cells in the nodal masses, which have a mean diameter of 5 mm, while the probability of spread of cancer cells from the breast to the periphery when the primary masses are 5 mm is also approximately 1 event of spread for every 10(8) cells. Thus, the occurrence of an event of spread from the breast to the lymph nodes appears not to increase the propensity of the progeny of those cells to spread from the lymph nodes to the periphery. These values indicate that the spread of human breast cancer and melanoma cells is unlikely to occur by a mechanism requiring mutation at the time of spread.
The stable maintenance system pem of plasmid R100: degradation of PemI protein may allow PemK protein to inhibit cell growth (1992)

We constructed plasmids carrying heat-inducible pemI and pemK genes, which were fused with the collagen-lacZ sequence in frame. The PemK-collagen-LacZ (PemK*) protein produced from the fusion gene upon heat induction inhibited the growth of cells and killed most of the cells in the absence of the PemI protein but did not do so in the presence of the PemI protein. This supports our previous assumption that the PemK protein inhibits cell division, leading to cell death, whereas the PemI protein suppresses the function of the PemK protein. We also constructed the plasmid carrying the heat-inducible pem operon which consists of the intact pemI gene and the pemK gene fused with collagen-lacZ. The simultaneously induced PemI and PemK* proteins did not inhibit the growth of cells. However, the temperature shift to 30 degrees C after induction of both proteins at 42 degrees C caused inhibition of cell growth and death of most cells. This suggests that the PemI protein is somehow inactivated upon the arrest of de novo synthesis of the PemI and PemK* proteins, allowing the PemK* protein to function. We observed that the PemI-collagen-LacZ (PemI*) protein was degraded faster than the PemK* protein, perhaps by the action of a protease(s). In fact, the lon mutation, which caused no apparent degradation of the PemI* protein, did not allow the PemK* protein to function, supporting the suggestion described above. Instability of the PemI protein would explain why the cells which have lost the pem+ plasmid are preferentially killed.
The antitumor monoclonal antibody 806 recognizes a high‐mannose form of the EGF receptor that reaches the cell surface when cells over‐express the receptor (2005)

Overexpression of the EGFR is commonly caused by EGFR gene amplification and is sometimes associated with expression of a variant EGFR (de2-7 EGFR or EGFRvIII) bearing an internal deletion in its extracellular domain. mAb 806 is a novel EGFR antibody with significant antitumor activity that recognizes both the de2-7 EGFR and a subset of the wild-type (wt) EGFR when overexpressed, but does not bind the EGFR expressed in normal tissues. Recently, we demonstrated that the mAb 806 epitope is restricted to a short cysteine loop of the EGFR (amino acids 287-302) that is only available for antibody binding in a transitional form of the receptor, which occurs as the receptor changes from its inactive tethered conformation to a dimeric untethered form. The truncation associated with the de2-7 EGFR mutation renders this receptor constitutively untethered, leading to increased binding of mAb 806. We now show that mAb 806 preferentially binds the immature high-mannose wt and de2-7 EGFR precursors normally located in the endoplasmic reticulum, indicating that this form of the wt EGFR is also constitutively untethered. Using the unique specificity of mAb 806, we clearly demonstrated the presence of these high-mannose EGFR precursors on the cell surface. Given that the high-mannose forms of the wt EGFR must be untethered they may contribute to the spontaneous EGFR signaling reported in cells overexpressing the receptor. These precursor forms of the EGFR thus represent novel tumor targets and contribute to the exceptional selectivity of mAb 806 for EGFR when overexpressed in cancer cells. As our observations are likely to apply to other receptors overexpressed in cancer, they suggest a strategy for developing antitumor antibodies even when the target receptor is expressed in normal tissue.
Genome changes and gene expression in human solid tumors (2000)

Genome-wide analysis techniques such as chromosome painting, comparative genomic hybridization, representational difference analysis, restriction landmark genome scanning and high-throughput analysis of LOH are now accelerating high-resolution genome aberration localization in human tumors. These techniques are complemented by procedures for detection of differentially expressed genes such as differential display, nucleic acid subtraction, serial analysis of gene expression and expression microarray analysis. These efforts are enabled by work from the human genome program in physical map development, cDNA library production/sequencing and in genome sequencing. This review covers several commonly used large-scale genome and gene expression analysis techniques, outlines genomic approaches to gene discovery and summarizes information that has come from large-scale analyses of human solid tumors.
Mono-Iodoacetate-Induced Histologic Changes in Subchondral Bone and Articular Cartilage of Rat Femorotibial Joints: An Animal Model of Osteoarthritis (2003)

Osteoarthritis (OA) is a degenerative joint disease characterized by joint pain and a progressive loss of articular cartilage. Studies to elucidate the pathophysiology of OA have been hampered by the lack of a rapid, reproducible animal model that mimics both the histopathology and symptoms associated with the disease. Injection of mono-iodoacetate (MIA), an inhibitor of glycolysis, into the femorotibial joint of rodents promotes loss of articular cartilage similar to that noted in human OA. Here, we describe the histopathology in the subchondral bone and cartilage of rat (Wistar) knee joints treated with a single intra articular injection of MIA (1 mg) and sacrificed at 1, 3, 5, 7, 14, 28, and 56 days postinjection. Histologically, the early time points (days 1-7) were characterized by areas of chondrocyte degeneration/necrosis sometimes involving the entire thickness of the articular cartilage in the tibial plateaus and femoral condyles. Changes to the subchondral bone, as evidenced by increased numbers of osteoclasts and osteoblasts, were noted at by day 7. By 28 days, there was focal fragmentation and collapse of bony trabeculae with fibrosis and increased osteoclastic activity. By 56 days there were large areas of bone remodeling evidenced by osteoclastic bone resorption and newly formed trabeculae with loss of marrow hematopoietic cells. Subchondral cysts and subchondral sclerosis were present in some rats. In conclusion, intra-articular injection of MIA induces loss of articular cartilage with progression of subchondral bone lesions that mimic those of OA. This model offers a rapid and minimally invasive method to reproduce OA-like lesions in a rodent species.
A phase I and pharmacokinetic study of the mitochondrial-specific rhodacyanine dye analog MKT 077. (2000)

This Phase I study was performed to evaluate the tolerability and pharmacokinetic behavior of MKT-077, a water soluble rhodacyanine dye analogue, which partitions into tumor cell mitochondria where it is thought to act as a metabolic poison, leading to G1 arrest and apoptosis. Thirteen patients with advanced solid malignancies were treated with MKT-077 administered as a 30-min i.v. infusion weekly for 4 weeks every 6 weeks at doses ranging from 42 to 126 mg/m2/week. The principal toxicity was renal magnesium wasting, which was dose-limiting (grade 3) in one patient at each of the 84- and 126-mg/m2 dose levels. The other three patients at the 126-mg/m2 dose level developed grade 2 hypomagnesemia, which was cumulative in nature, improved with i.v. magnesium supplementation, and was controlled in two patients by the administration of prophylactic magnesium before and after treatment with MKT-077. Given the requirement for extensive monitoring of serum magnesium levels, dose escalation >126 mg/m2 was not considered feasible. Thus, the recommended dose for disease-oriented studies with this schedule of MKT-077 is 126 mg/m2/week. Pharmacokinetic studies revealed a prolonged terminal half-life (37 +/- 17 h) and a large volume of distribution (685 +/- 430 liters/m2). Clearance averaged 39 +/- 13 liters/h/m2. Peak MKT-077 plasma concentrations (1.2 +/-0.31 to 6.3 +/- 5.3 microg/ml) exceeded the IC50 concentrations required for human CX-1 colon, MCF-breast, CRL-1420 pancreas, EJ bladder, and LOX melanoma tumor cell lines in vitro (0.15-0.5 microg/ml). These results indicate that at the recommended dose level of 126 mg/m2/week of MKT-077, the toxicity profile was consistent with the preferential accumulation of the agent within tumor cell mitochondria, and biologically relevant plasma concentrations were achieved.