gebhart/patrepeval huggingface dataset:
Effect of sialic acid content on glycoprotein pI analyzed by two‐dimensional electrophoresis (2010)

2-DE is broadly used for quantitative analysis of differential protein expression in complex mixtures such as serum samples or cell lysates. PTMs directly influence the 2-DE pattern, and knowledge of the rules of protein separation is required in order to understand the protein distribution in a 2-DE gel. Glycosylation is the most common PTM and can modify both the molecular weight and the pI of a protein. In particular, the effect of charged monosaccharides (mainly sialic acids, SAs) on the 2-DE pattern of a protein is of major interest since changes in sialylation are regularly observed in comparative studies. Little is known about the pI shift of a glycoprotein induced by the presence of SAs, or whether this shift is the same for all glycoproteins. To address this issue, this study examined the influence of SA on the 2-DE pattern of three serum glycoproteins (haptoglobin, α1-antitrypsin and ribonuclease 1), which N-glycan chains had been previously characterised, and reviewed existing bibliographic data. The SA content of the different glycoforms of a glycoprotein showed a negative linear correlation with the pI, although the slope varied among the studied glycoproteins. We also described a positive correlation between the protein pI and the pI decrease per SA molecule.
Controlling crystal architecure in molecular solids: the supramolecular approach (2001)

The properties of molecular solids are well known to depend not only on the structure of the molecule itself, but also on the three-dimensional architecture adopted during crystallization. Such is the variation in properties with crystal structure that the existence of different polymorphs can, for example, switch on and off photoinduced reactions as well as profoundly affect the pharmaceutical activity of drugs [1–3].
Long-acting progestational agents; 17-ethinyl-19-nortestosterone enanthate, 17 alpha-hydroxyprogesterone caproate and 17-alpha-hydroxy-progesterone acetate. (1957)

The effects of the parenterally administered contraceptive agents 17-ethinyl-19-nortestestosterone enanthate (ENE) 17-alpha-hydroxyprogesterone caproate (AHC) and 17-alpha-hydroxyprogesterone acetate (AHA) on the endometrium vaginal epithelium basal body temperature and cervical mucus were studied in 3 surgical castrates. All of the agents produced secretory changes of the endometrium regression of epithelial proliferation of vaginal cells elevation of body temperature and abolition of cervical fern phenomenon and uterine bleeding. ENE was the most potent of the 3 agents. However AHC and AHA seemed to be more useful for cyclic therapy since the action of ENE was too extended. Progestational withdrawal bleeding occurred 13-15 days after a single injection of AHA or AHC while withdrawal bleeding after an ENE injection occurred 25-28 days after administration. The duration of the effect varied with the dosage. It appeared that a single injection of 150 mg ENE produced effects similar to 350 mg doses of AHC or AHA. No side effects were observed during any of the tests.
Rapid Isolation And Purification Of Mitochondria For Transplantation By Tissue Dissociation And Differential Filtration (2014)

Previously described mitochondrial isolation methods using differential centrifugation and/or Ficoll gradient centrifugation require 60 to 100 min to complete. We describe a method for the rapid isolation of mitochondria from mammalian biopsies using a commercial tissue dissociator and differential filtration. In this protocol, manual homogenization is replaced with the tissue dissociator's standardized homogenization cycle. This allows for uniform and consistent homogenization of tissue that is not easily achieved with manual homogenization. Following tissue dissociation, the homogenate is filtered through nylon mesh filters, which eliminate repetitive centrifugation steps. As a result, mitochondrial isolation can be performed in less than 30 min. This isolation protocol yields approximately 2 x 10(10) viable and respiration competent mitochondria from 0.18 ± 0.04 g (wet weight) tissue sample.
Fenoxaprop Interactions for Barnyardgrass (Echinochloa crus-galli) Control in Rice (2005)

A study was conducted in 2000 and 2001 to evaluate interaction of fenoxaprop with other herbicides for barnyardgrass control in rice. Changes in herbicide interaction over time were also evaluated, and herbicide combinations were ranked on the basis of compatibility. Fenoxaprop at 0.075 kg/ha plus bentazon or propanil plus molinate resulted in an additive response for barnyardgrass control at 10, 20, and 30 d after treatment (DAT); however, when the rate of fenoxaprop increased to 0.089 kg/ha, an antagonistic effect was found. Carfentrazone and halosulfuron consistently antagonized the activity of fenoxaprop at both rates on barnyardgrass. Bensulfuron at 10 and 20 DAT and triclopyr at 20 DAT were antagonistic to fenoxaprop. An increase in interaction over time was detected when fenoxaprop at 0.089 kg/ha was applied in mixture with carfentrazone at 0.04 kg/ha or halosulfuron at 0.05 kg/ha. These results indicate that propanil plus molinate and bentazon are more compatible with fenoxaprop at 0.075 kg/ha for barnyardgrass control, whereas bensulfuron, carfentrazone, halosulfuron, and triclopyr can antagonize fenoxaprop activity on barnyardgrass.
Implantation of Bone Marrow Mononuclear Cells Into Ischemic Myocardium Enhances Collateral Perfusion and Regional Function via Side Supply of Angioblasts, Angiogenic Ligands, and Cytokines (2001)

BMI may constitute a novel safety strategy for achieving optimal therapeutic angiogenesis by the natural ability of the BM cells to secrete potent angiogenic ligands and cytokines as well as to be incorporated into foci of neovascularization.
Randomized discontinuation trial of sorafenib (BAY 43-9006) (2006)

With the increasing interest in development of cytostatic anticancer drugs, the randomized discontinuation trial (RDT) design has been proved to be useful in the evaluation of their clinical activity. In the June 1, 2006 issue of the Journal of Clinical Oncology, a study by Ratain et al. uses RDT in a phase-II placebo controlled study to evaluate the efficacy of sorafenib (BAY 43-9006) in patients with metastatic renal cell carcinoma (RCC). The results from their investigation affirm the merits of the RDT in testing the efficacy of cytostatic drugs and also prove the significant disease-stabilizing activity and tolerability of sorafenib in metastatic renal cell carcinoma.
Adenoviral and adeno-associated viral vector mediated gene transfer in the guinea pig cochlea (2002)

Peripheral sensorineural hearing loss is a very common inner ear disorder affecting nearly 10% of the population. At present there is no cure for this disorder but gene therapy has been suggested as a potentially effective method for clinical treatment in the future. Thus we investigated the effectiveness of adenoviral (Ad) and adeno-associated viral (AAV) vectors to transduce the cochlea of guinea pigs. After direct injection into the basal turn of the cochlea, we found that both Ad and AAV vectors coding for the reporter genes lacZ or GFP readily transduced spiral ganglion cells. In addition, some transgene expression was detected in the stria vascularis after AAV-GFP injection. Gene expression persisted at least 8 weeks after viral vector injection. Present findings will help to develop future gene therapy protocols in the inner ear by using Ad and AAV coding for neurotrophins such as NT-3, BDNF, GDNF and VEGF.
Two species of human CRK cDNA encode proteins with distinct biological activities. (1992)

Two distinct human CRK cDNAs, designated CRK-I and CRK-II, were isolated from human embryonic lung cells by polymerase chain reaction and by screening of a human placenta cDNA library, respectively. CRK-I differed from CRK-II in that it lacked a 170-nucleotide sequence, suggesting that CRK-I and CRK-II were the products of alternative splicing. The amino acid sequences deduced from these two cDNAs differed in the carboxyl termini and contained one SH2 and either one or two SH3 domains. RNAse protection analysis demonstrated both CRK-I and CRK-II mRNAs in various human cells. Three CRK proteins, of 42, 40, and 28 kDa, were identified in human embryonic lung cells by means of antibodies against the SH2 region and the SH3 region of the bacterially expressed CRK-I protein. Transient expression of CRK-I and CRK-II cDNAs in COS7 cells showed that the former encoded the 28-kDa protein and the latter encoded the 40- and 42-kDa proteins. All human cell lines so far examined expressed the 40-kDa protein; however, expression of the 28- and the 42-kDa proteins was variable. In a comparison of the biological activity of the two human CRK proteins, both proteins were stably expressed in rat 3Y1 cells. All cell lines expressing CRK-I protein showed altered morphology, proliferated in soft agar, and grew as massive tumors in nude mice. Although CRK-II-expressing cells showed a slight morphologic change, they did not make colonies in soft agar or grow in nude mice. These results demonstrate that the two species of human CRK cDNA encode proteins which differ in their biological activities.
TRF1 Controls Telomere Length and Mitotic Fidelity in Epithelial Homeostasis (2009)

TRF1 is a component of the shelterin complex at mammalian telomeres; however, a role for TRF1 in telomere biology in the context of the organism is unclear. In this study, we generated mice with transgenic TRF1 expression targeted to epithelial tissues (K5TRF1 mice). K5TRF1 mice have shorter telomeres in the epidermis than wild-type controls do, and these are rescued in the absence of the XPF nuclease, indicating that TRF1 acts as a negative regulator of telomere length by controlling XPF activity at telomeres, similar to what was previously described for TRF2-overexpressing mice (K5TRF2 mice). K5TRF1 cells also show increased end-to-end chromosomal fusions, multitelomeric signals, and increased telomere recombination, indicating an impact of TRF1 on telomere integrity, again similar to the case in K5TRF2 cells. Intriguingly, K5TRF1 cells, but not K5TRF2 cells, show increased mitotic spindle aberrations. TRF1 colocalizes with the spindle assembly checkpoint proteins BubR1 and Mad2 at mouse telomeres, indicating a link between telomeres and the mitotic spindle. Together, these results demonstrate that TRF1, like TRF2, negatively regulates telomere length in vivo by controlling the action of the XPF nuclease at telomeres; in addition, TRF1 has a unique role in the mitotic spindle checkpoint.
Inhibition of gastric emptying by glucose depends on length of intestine exposed to nutrient (1989)

Nutrients inhibit gastric emptying in a dose-related fashion. We postulated that load-dependent gastric emptying results from the saturation of mucosal absorptive mechanisms, so that a longer length of the small intestine is exposed to unabsorbed nutrients as more nutrient enters the intestine to participate in this negative feedback. To test this idea, we limited exposure of 0.25 to 1.0 M glucose meals to various lengths of duodenum and jejunum in 17 dogs. The effects of these limited perfusions were then compared with experiments in which the whole gut (ALL) was exposed to the nutrient. Maximal inhibition was seen with 1.0 M meal and was similar with perfusions of 150 cm and ALL. By contrast, even with the 1.0 M load, no inhibition of gastric emptying was seen when glucose meal was confined to the first 15 cm of the proximal duodenum. Only 50-60% of maximal inhibition was observed during confinement of 1.0 M meal to the proximal 65 cm. We concluded that glucose sensors are present in both the proximal and the distal gut and the inhibition was related to the length of the small intestine exposed to glucose.
Rabbit myocardial 82Rb kinetics and a compartmental model for blood flow estimation (1989)

Quantification of regional myocardial blood flow (MBF) with rubidium-82 (82Rb) and positron emission tomography (PET) requires the validation of a tracer kinetic model that adequately describes the kinetics of 82Rb in tissue. We performed 134 82Rb kinetic experiments in 24 isolated, arterially perfused rabbit interventricular septa at different flow rates (0.5-4.5 ml.min-1.g-1) and under the following conditions: varied concentrations of glucose (2.8-11 mM), insulin (0-5 mU/ml), and potassium (5-8 mM); varied pH (7.2-7.8); varied workload; and the addition of acetylstrophanthidin (1.0 microM). The measured 82Rb tissue time-activity curves consisted of two exponential components, with half times inversely related to MBF. The size of the slow component decreased as MBF increased (from 70% at 0.3 ml.min-1.g-1 to 30% at 2.0 ml. min-1.g-1). The kinetics were not strongly dependent on the conditions studied and were consistent with a compartmental model containing two communicating compartments. The volume of the fast exchangeable compartment and the transport rate constant from the fast to the slow compartment were found to be independent of MBF. Values of MBF were estimated with the compartmental model from 82Rb kinetics, and they correlated well with the directly measured MBF (r = 0.91; slope = 1.03).
Levodopa and dopamine analogs: dihydroxy and trihydroxybenzylamines as novel quinol antitumor agents in experimental leukemia in vivo. (1981)

Levodopa and dopamine demonstrate significant antitumor activity in several experimental systems. We have prepared the nonneurotoxic dihydroxybenzylamine (DHBA) analogs 2,3-DHBA, 3,4-DHBA, and 2,5-DHBA and the trihydroxy derivatives 2,3,4- and 3,4,5-trihydroxybenzylamine. These analogs demonstrated significant and reproducible antitumor activity in the ip P388 and L1210 lymphocytic leukemias. This activity was markedly increased when the drugs were given by multiple injections three times daily for 4 days. 3,4-DHBA and 2,3-DHBA resulted in 30% and 20% long-term survivors, respectively. There was a selective inhibition of thymidine incorporation and a relatively lesser effect on uridine and leucine incorporations. Inhibitory concentrations were between 0.1 and 1.0 mM. The trihydroxy derivatives were more potent, with inhibitory concentrations between 0.01 and 1.0 mM. Furthermore, the trihydroxy derivatives were also able to inhibit the incorporation of uridine and leucine as well as thymidine. The para derivative, 2,5-DHBA, although a potent inhibitor in vitro, was completely inactive in vivo. When L1210 and P388 tumor-bearing animals were given radioactive labeled thymidine in vivo following the administration of drugs. a selective inhibition of thymidine incorporation by tumor cells was observed, with essentially no effect on gut or bone marrow. Doses greater than 200 mg/kg completely suppressed the incorporation of radioactively labeled thymidine by tumor cells 1 hour after administration of drug. A similar dose response was observed in the more slowly growing P388 leukemia, suggesting that the antitumor effect did not strongly correlate with rate of the tumor. Since levodopa and dopamine are currently being evaluated in patients with metastatic melanoma, the availability of analogs with enhanced antitumor activity and broader antitumor spectrum are of interest.
A Snapshot Method to Provide Full Visibility for Functional Debugging Using FPGA (2005)

Until now, logic simulators are still the most popular verification tools. Although they can provide full controllability and observability during the verification process, the simulation speed is too slow for large amounts of input patterns. Using hardware emulation such as FPGA can have higher simulation speed. However, it is very hard to debug using this approach due to poor visibility in FPGAs. Therefore, in this paper, we propose another approach to "record" the internal behaviors of a FPGA and "replay" the interesting period of time in a software simulator. In this way, we can still have high simulation speed because most simulation efforts are still finished in FPGA. Moreover, full visibility and better debugging environment can be provided in the software simulation. The experimental results have shown the efficiency of using our approach.
Computer Based Behavioral Biometric Authentication via Multi-Modal Fusion (2013)

Biometric computer authentication has an advantage over password and access card authentication in that it is based on something you are, which is not easily copied or stolen. One way of performing biometric computer authentication is to use behavioral tendencies associated with how a user interacts with the computer. However, behavioral biometric authentication accuracy rates are much larger then more traditional authentication methods. This thesis presents a behavioral biometric system that fuses user data from keyboard, mouse, and Graphical User Interface (GUI) interactions. Combining the modalities results in a more accurate authentication decision based on a broader view of the user’s computer activity while requiring less user interaction to train the system than previous work. Testing over 30 users, shows that fusion techniques significantly improve behavioral biometric authentication accuracy over single modalities on their own. Two fusion techniques are presented, feature fusion and decision level fusion. Using an ensemble based classification method the decision level fusion technique improves the False Acceptance Rate (FAR) by 0.86 % and False Rejection Rate (FRR) by 2.98 % over the best individual modality. iv
Folic acid deficiency optic neuropathy: A case report (2008)

This case highlights an unusual presentation of folic acid deficiency that may present to the general physician.
Commonly Used Detergents (1998)

This appendix lists some common detergents along with useful information regarding the type of hydrophilic group (anionic, cationic, amphoteric, or nonionic), the critical micelle concentration (CMC) and the micelle molecular weight.
PDEF, a Novel Prostate Epithelium-specific Ets Transcription Factor, Interacts with the Androgen Receptor and Activates Prostate-specific Antigen Gene Expression (2000)

Prostate cancer, the most frequent solid cancer in older men, is a leading cause of cancer deaths. Although proliferation and differentiation of normal prostate epithelia and the initial growth of prostate cancer cells are androgen-dependent, prostate cancers ultimately become androgen-independent and refractory to hormone therapy. The prostate-specific antigen (PSA) gene has been widely used as a diagnostic indicator for androgen-dependent and -independent prostate cancer. Androgen-induced and prostate epithelium-specific PSA expression is regulated by a proximal promoter and an upstream enhancer via several androgen receptor binding sites. However, little progress has been made in identifying androgen-independent regulatory elements involved in PSA gene regulation. We report the isolation of a novel, prostate epithelium-specific Ets transcription factor, PDEF (prostate-derived Ets factor), that among the Ets family uniquely prefers binding to a GGAT rather than a GGAA core. PDEF acts as an androgen-independent transcriptional activator of the PSA promoter. PDEF also directly interacts with the DNA binding domain of androgen receptor and enhances androgen-mediated activation of the PSA promoter. Our results, as well as the critical roles of other Ets factors in cellular differentiation and tumorigenesis, strongly suggest that PDEF is an important regulator of prostate gland and/or prostate cancer development.
Ratiometric and photoconvertible fluorescent protein-based voltage indicator prototypes (2016)

To expand the toolbox of fluorescent protein-based voltage indicators, we explored two distinct protein design strategies. Using these design strategies, we created three new voltage indicators: a red intensiometric voltage indicator (tdFlicR Δ110AR), a green/red ratiometric voltage indicator (tdFlicR-VK-ASAP), and a green to red photoconvertible voltage indicator (FlicGR1).
Haemostatic Effects of Supraphysiological Levels of Testosterone in Normal Men (1995)

The effects of exogenous testosterone on the haemostatic system were studied in a group of 32 healthy men undergoing a clinical trial of hormonal male contraception. The men received 200 mg testosterone oenanthate (TE) weekly i.m., and plasma samples were taken pretreatment, at defined time points up to 52 weeks of treatment, and 4 and 8 weeks after discontinuing TE. This dose of TE caused a 2-fold increase in trough plasma testosterone levels. TE caused a fall in plasma fibrinogen concentration after 16 weeks of treatment. This was sustained for the duration of TE treatment and recovered to pretreatment levels during the recovery phase. There was also a sustained fall in the level of C4b binding protein which showed a rebound to levels above pretreatment during recovery. Levels of antithrombin III and prothrombin fragment F1.2 rose initially during TE treatment, and levels of protein C, protein S (free) and plasminogen activator inhibitor fell, but the concentrations of these factors all returned to pretreatment levels during continued treatment. There was no change in the plasma concentrations of beta-thromboglobulin, tissue plasminogen activator, protein S (total), or D-dimer. There was a sustained increase in haemoglobin concentration and haematocrit, without any change in platelet count. The observed changes were consistent with mild activation of the haemostatic system during initial treatment with testosterone. After several months the raised activation markers had returned to pretreatment levels indicating that a new equilibrium had been established which did not appear to be prothrombotic.(ABSTRACT TRUNCATED AT 250 WORDS)
Basic fibroblast growth factor binds to subendothelial extracellular matrix and is released by heparitinase and heparin-like molecules (1989)

Basic fibroblast growth factor (bFGF) exhibits specific binding to the extracellular matrix (ECM) produced by cultured endothelial cells. Binding was saturable as a function both of time and of concentration of 125I-bFGF. Scatchard analysis of FGF binding revealed the presence of about 1.5 X 10(12) binding sites/mm2 ECM with an apparent kD of 610nM. FGF binds to heparan sulfate (HS) in ECM as evidenced by (i) inhibition of binding in the presence of heparin or HS at 0.1-1 micrograms/mL, but not by chondroitin sulfate, keratan sulfate, or hyaluronic acid at 10 micrograms/mL, (ii) lack of binding to ECM pretreated with heparitinase, but not with chondroitinase ABC, and (iii) rapid release of up to 90% of ECM-bound FGF by exposure to heparin, HS, or heparitinase, but not to chondroitin sulfate, keratan sulfate, hyaluronic acid, or chondroitinase ABC. Oligosaccharides derived from depolymerized heparin, and as small as the tetrasaccharide, released the ECM-bound FGF, but there was little or no release of FGF by modified nonanticoagulant heparins such as totally desulfated heparin, N-desulfated heparin, and N-acetylated heparin. FGF released from ECM was biologically active, as indicated by its stimulation of cell proliferation and DNA synthesis in vascular endothelial cells and 3T3 fibroblasts. Similar results were obtained in studies on release of endogenous FGF-like mitogenic activity from Descemet's membranes of bovine corneas. It is suggested that ECM storage and release of bFGF provide a novel mechanism for regulation of capillary blood vessel growth. Whereas ECM-bound FGF may be prevented from acting on endothelial cells, its displacement by heparin-like molecules and/or HS-degrading enzymes may elicit a neovascular response.