gebhart/patrepeval huggingface dataset:
Inhibition of Human Immunodeficiency Virus Type 1 Replication prior to Reverse Transcription by Influenza Virus Stimulation (2000)

It is now recognized that, in addition to drug-mediated therapies against human immunodeficiency virus type 1 (HIV-1), the immune system can exert antiviral effects via CD8(+) T-cell-generated anti-HIV factors. This study demonstrates that (i) supernatants from peripheral blood mononuclear cells (PBMC) stimulated with influenza A virus inhibit replication of CCR5- and CXCR4-tropic HIV-1 isolates prior to reverse transcription; (ii) the HIV-suppressive supernatants can be generated by CD4- or CD8-depleted PBMC; (iii) this anti-HIV activity is partially due to alpha interferon (IFN-alpha), but not to IFN-gamma, IFN-beta, the beta-chemokines MIP-1alpha, MIP-1beta, and RANTES, or interleukin-16; (iv) the anti-HIV activity is generated equally well by PBMC cultured with either infectious or UV-inactivated influenza A virus; and (v) the antiviral activity can be generated by influenza A-stimulated PBMC from HIV-infected individuals. These findings represent a novel mechanism for inhibition of HIV-1 replication that differs from the previously described CD8 anti-HIV factors (MIP-1alpha, MIP-1beta, RANTES, and CD8 antiviral factor).
3D User Interfaces: New Directions and Perspectives (2008)

Three-dimensional user interfaces (3D UIs) let users interact with virtual objects, environments, or information using direct 3D input in the physical and/or virtual space. In this article, the founders and organizers of the IEEE Symposium on 3D User Interfaces reflect on the state of the art in several key aspects of 3D UIs and speculate on future research.
Clinical Evaluation of 61 Patients with Pulmonary Aspergilloma. (2000)

Pulmonary aspergilloma usually occurs in elderly patients with old tuberculosis and respiratory failure. Many cases did not respond to antifungal therapy with itraconazole or amphotericin B. Our analysis indicates that more effective and appropriate therapeutic regimens are needed for the treatment of patients with pulmonary aspergilloma.
MEK Inhibition, Alone or in Combination with BRAF Inhibition, Affects Multiple Functions of Isolated Normal Human Lymphocytes and Dendritic Cells (2014)

Combination therapy with BRAF and MEK inhibition is currently in clinical development for the treatment of BRAF-mutated malignant melanoma. BRAF inhibitors are associated with enhanced antigen-specific T-lymphocyte recognition in vivo. Consequently, BRAF inhibition has been proposed as proimmunogenic and there has been considerable enthusiasm for combining BRAF inhibition with immunotherapy. MEK inhibitors inhibit ERK phosphorylation regardless of BRAF mutational status and have been reported to impair T-lymphocyte and modulate dendritic cell function. In this study, we investigate the effects on isolated T lymphocytes and monocyte-derived dendritic cells (moDC) of a MEK (trametinib) and BRAF (dabrafenib) inhibitor combination currently being evaluated in a randomized controlled clinical trial. The effects of dabrafenib and trametinib, alone and in combination, were studied on isolated normal T lymphocytes and moDCs. Lymphocyte viability, together with functional assays including proliferation, cytokine production, and antigen-specific expansion, were assessed. MoDC phenotype in response to lipopolysaccharide stimulation was evaluated by flow cytometry, as were effects on antigen cross-presentation. Dabrafenib did not have an impact on T lymphocytes or moDCs, whereas trametinib alone or in combination with dabrafenib suppressed T-lymphocyte proliferation, cytokine production, and antigen-specific expansion. However, no significant decrease in CD4(+) or CD8(+) T-lymphocyte viability was observed following kinase inhibition. MoDC cross-presentation was suppressed in association with enhanced maturation following combined inhibition of MEK and BRAF. The results of this study demonstrate that MEK inhibition, alone or in combination with BRAF inhibition, can modulate immune cell function, and further studies in vivo will be required to evaluate the potential clinical impact of these findings.
The Association of Atopobium vaginae and Gardnerella vaginalis with Bacterial Vaginosis and Recurrence after Oral Metronidazole Therapy (2006)

Infection with A. vaginae is more specific for BV than infection with G. vaginalis. The higher recurrence rates in women in whom both A. vaginae and G. vaginalis were detected suggest that A. vaginae makes a significant contribution to BV. However, its etiological role remains unclear.
Trichostatin A and trapoxin: Novel chemical probes for the role of histone acetylation in chromatin structure and function (1995)

Reversible acetylation at the epsilon-amino group of lysines located at the conserved domain of core histones is supposed to play an important role in the regulation of chromatin structure and its transcriptional activity. One promising strategy for analyzing the precise function of histone acetylation is to block the activities of acetylating or deacetylating enzymes by specific inhibitors. Recently, two microbial metabolites, trichostatin A and trapoxin, were found to be potent inhibitors of histone deacetylases. Trichostatin A reversibly inhibits the mammalian histone deacetylase, whereas trapoxin causes inhibition through irreversible binding to the enzyme. The histone deacetylase from a trichostatin A-resistant cell line is resistant to trichostatin A, indicating that the enzyme is the primary target. Both of the agents induce a variety of biological responses of cells such as induction of differentiation and cell cycle arrest. Trichostatin A and trapoxin are useful in analyzing the role of histone acetylation in chromatin structure and function as well as in determining the genes whose activities are regulated by histone acetylation.
Activating agents and protecting groups (1999)

Partial table of contents: Acetic Anhydride. Acetyl Chloride (+ co-reactants). Aluminum Chloride. Boron Trifluorideetherate. Bromodimethylborane. 2,2-Dimethyl-1,3-propanediol. Dimethyl Sulfate. Diphenylbis(1,1,1,3,3,3-hexafluoro-2-phenyl-2-propoxy)-sulfirane. Ethylaluminum Dichloride. N-Ethylbenzisoxazolium Tetrafluoroborate. Hydrazine. 1-Hydroxybenzotriazole. Lithium Bromide. Lithium Chloride. Lithium Iodide. Montmorillonite K-10. 2-Morpholinoethyl Isocyanide. Phenyl Phosphorodi(1-imidazolate). Phosgene. 1,3-Propanediol. 1,3-Propanedithiol. Silver(I) Tetrafluoroborate. Triethylaluminum. Triethyl Orthoformate. Trifluoroacetic Anhydride. Zinc Bromide. Zinc Chloride. Zinc Iodide. Zinc Bis(p-toluenesulfonate). List of Contributors. Indexes.
Influence of meal composition on postprandial peripheral plasma concentrations of vasoactive peptides in man (1996)

In a randomized cross-over study healthy non-obese male human subjects received standardized isocaloric, isovolumetric meals consisting of either carbohydrate, protein or fat and a non-caloric control meal consisting of an equal volume of water. Peripheral venous plasma concentrations of calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP), and peptide YY (PYY) were measured pre- and postprandially. Plasma CGRP concentrations were lowered following the protein meal and following the fat meal, but remained unaltered after carbohydrate or water ingestion. Plasma VIP concentrations increased slightly following the carbohydrate meal and following water loading. The PYY concentrations increased after the protein and the carbohydrate meal and a slight rise was observed following fat ingestion. Water loading did not affect the plasma level of PYY. We conclude that the postprandial peripheral plasma concentrations of CGRP, VIP and PYY are dependent on the caloric meal composition. The VIP, but not the CGRP and PYY concentrations seem to be influenced by gastric distension. The physiological significance of the postprandial alterations in peripheral concentrations of these peptides is at present uncertain.
Sudden infant death in a patient with FGFR3 P250R mutation (2006)

P250R mutation in the FGFR3 gene also known as Muenke syndrome is associated with coronal craniosynostosis, sensorineural deafness, craniofacial, and digital abnormalities. We report a family with this mutation associated with sudden death in an affected newborn, most probably due to upper airway obstruction.
Experimental Study of Circulation Control Wings at Low Reynolds Numbers (2014)

The objective of this research is to design, develop and compare the effectiveness of upper slot blowing on three Circulation Control Wings (CCWs) and to find the configuration that gives the best lift augmentation. A low-speed wind-tunnel experimental study is undertaken to evaluate the effect of upper slot blowing along the span over four different Trailing-Edge (TE) Coanda surfaces on three 3-D CCWs for the purpose of lift augmentation. Wind tunnel tests are conducted at Mach numbers of 0.022, 0.024, 0.029 and 0.04, at Reynolds numbers of 0.67 × 10 to 1.26 × 10 with moment coefficients of blowing from 0.0 to 0.011. It is found that the (2:1) Coanda surface configuration is the most effective in all three CCWs. At Ma = 0.022 and α = 18, the (2:1) Coanda surface on the symmetrical NACA0015 CCW gives the maximum ∆CL = 0.2 at Cμ = 0.011. The maximum lift augmentation ratio of 61 is observed with the (2:1) Coanda surface on the S8036 CCW at α = 2.
Electroporation Protocols for Microorganisms (1995)

Electroporation is one of the most widespread techniques used in modem molecular genetics. It is most commonly used to introduce DNA into cells for investigations of gene structure and function, and i
An Extended AE-Rich N-Terminal Trunk in Secreted Pineapple Cystatin Enhances Inhibition of Fruit Bromelain and Is Posttranslationally Removed during Ripening (2009)

Phytocystatins are potent inhibitors of cysteine proteases and have been shown to participate in senescence, seed and organ biogenesis, and plant defense. However, phytocystatins are generally poor inhibitors of the cysteine protease, bromelain, of pineapple (Ananas comosus). Here, we demonstrated that pineapple cystatin, AcCYS1, inhibited (>95%) stem and fruit bromelain. AcCYS1 is a unique cystatin in that it contains an extended N-terminal trunk (NTT) of 63 residues rich in alanine and glutamate. A signal peptide preceding the NTT is processed in vitro by microsomal membranes giving rise to a 27-kD species. AcCYS1 mRNA was present in roots and leaves but was most abundant in fruit. Using immunofluorescence and immunoelectron microscopy with an AcCYS1-specific antiserum, AcCYS1 was found in the apoplasm. Immunoblot analysis identified a 27-kD protein in fruit, roots, and leaves and a 15-kD species in mature ripe fruit. Ripe fruit extracts proteolytically removed the NTT of 27-kD AcCYS1 in vitro to produce the 15-kD species. Mass spectrometry analysis was used to map the primary cleavage site immediately after a conserved critical glycine-94. The AE-rich NTT was required to inhibit fruit and stem bromelain (>95%), whereas its removal decreased inhibition to 20% (fruit) and 80% (stem) and increased the dissociation equilibrium constant by 1.8-fold as determined by surface plasmon resonance assays. We propose that proteolytic removal of the NTT results in the decrease of the inhibitory potency of AcCYS1 against fruit bromelain during fruit ripening to increase tissue proteolysis, softening, and degradation.
Transport characteristics of a novel peptide platform for CNS therapeutics (2009)

New and effective therapeutics that cross the blood-brain barrier (BBB) are critically needed for treatment of many brain diseases. We characterize here a novel drug development platform that is broadly applicable for the development of new therapeutics with increased brain penetration. The platform is based on the Angiopep-2 peptide, a sequence derived from ligands that bind to low-density lipoprotein receptor-related protein-1 (LRP-1), a receptor expressed on the BBB. Fluorescent imaging studies of a Cy5.5Angiopep-2 conjugate and immunohistochemical studies of injected Angiopep-2 in mice demonstrated efficient transport across the BBB into brain parenchyma and subsequent co-localization with the neuronal nuclei-selective marker NeuN and the glial marker glial fibrillary acidic protein (GFAP). Uptake of [(¹²⁵I]-Angiopep-2 into brain endothelial cells occurred by a saturable mechanism involving LRP-1. The primary sequence and charge of Angiopep-2 were crucial for its passage across the BBB. Overall, the results demonstrate the significant potential of this platform for the development of novel neurotherapeutics.
Platelet–cancer interactions: mechanisms and pharmacology of tumour cell‐induced platelet aggregation (2004)

During haematogenous metastasis, cancer cells migrate to the vasculature and interact with platelets resulting in tumour cell-induced platelet aggregation (TCIPA). We review: 1. The biological and clinical significance of TCIPA; 2. Molecular mechanisms involved in platelet aggregation by cancer cells; 3. Strategies for pharmacological regulation of these interactions. We conclude that pharmacological regulation of platelet-cancer cell interactions may reduce the impact of TCIPA on cancer biology.
Prospective Randomized Feasibility Study Assessing the Effect of Cyclic Sacral Neuromodulation on Urinary Urge Incontinence in Women (2017)

The results suggest that patients with overactive bladder who have been implanted with sacral neuromodulation devices and are receiving substantial benefit may perceive further optimization by switching to cycling settings.
The acute-phase protein alpha 1-antitrypsin inhibits growth and proliferation of human early erythroid progenitor cells (burst-forming units-erythroid) and of human erythroleukemic cells (K562) in vitro by interfering with transferrin iron uptake (1994)

We have previously shown that the hepatic acute-phase protein alpha 1-antitrypsin (alpha 1-AT) inhibits transferrin (tf) binding to its receptor (tfR) of human placental membranes. To evaluate the possibility that this interaction can explain the pathophysiology of the changes in iron metabolism in the course of chronic disease, subsequently leading to anemia in chronic disease (ACD), we examined the effect of alpha 1-AT on cells of the erythroid cell line. alpha 1-AT completely prevented tf binding to tfR on K562 human erythroleukemic cells and on reticulocytes. This inhibitory potency was dose-dependent and competitive, as proved in equilibrium saturation and kinetic studies. The cytokines interleukin-1 (IL-1), IL-6, and tumor necrosis factor alpha showed no such effect. Internalization of the tf-tfR complex was inhibited with alpha 1-AT in a dose-dependent manner. Furthermore, alpha 1-AT profoundly reduced the growth of K562 cells as well as their proliferation, albeit to a lesser degree. Growth of early erythroid progenitor cells (burst-forming units-erythroid) was significantly suppressed by alpha 1-AT, but no effect on the growth of late erythroid progenitor cells (colony-forming units-erythroid) was detected. These inhibitions of alpha 1-AT were seen in high physiologic concentrations attained in the course of acute-phase situations. These data show that alpha 1-AT might be a mediator of the changes in iron metabolism that are characteristic of clinical findings in the course of ACD.
Human StarD5, a cytosolic StAR-related lipid binding protein (2005)

Recently identified StarD5 belongs to the StarD4 subfamily, a subfamily of steroidogenic acute regulatory related lipid transfer (START) domain proteins that includes StarD4 and StarD6, proteins whose functions remain unknown. The objective of this study was to confirm StarD5's protein localization and sterol binding capabilities as measures to pursue function. Using rabbit polyclonal antibody against newly purified human histidine-tagged/StarD5 protein, StarD5 was detected in human liver. In parallel studies, increased expression of StarD5 in primary hepatocytes led to a marked increase in microsomal free cholesterol. Cell fractionation studies demonstrated StarD5 protein in liver cytosolic fractions only, suggesting StarD5 as a directional cytosolic sterol carrier. Supportive in vitro binding assays demonstrated a concentration-dependent binding of cholesterol by StarD5 similar to that of the cholesterol binding START domain protein StarD1. In contrast to selective cholesterol binding by StarD1, StarD5 bound the potent regulatory oxysterol, 25-hydroxycholesterol, in a concentration-dependent manner. StarD5 binding appeared selective for cholesterol and 25-hydroxycholesterol, as no binding was observed for other tested sterols. The ability of StarD5 to bind not only cholesterol but also 25-hydroxycholesterol, a potent inflammatory mediator and regulatory oxysterol, raises basic fundamental questions about StarD5's role in the maintenance of cellular cholesterol homeostasis.
Association between v-Src and Protein Kinase C δ in v-Src-transformed Fibroblasts (1997)

In response to the kinase activity of v-Src there is an increase in the membrane association of the novel protein kinase C (PKC) isoform PKC delta (Zang, Q., Frankel, P., and Foster, D. A. (1995) Cell Growth Differ. 6, 1367-1373). We report here that in v-Src-transformed cells PKC delta co-immunoprecipitates with v-Src and is phosphorylated on tyrosine. The tyrosine-phosphorylated PKC delta had reduced enzymatic activity relative to the non-tyrosine-phosphorylated PKC delta from v-Src-transformed cells. The association between Src and PKC delta was dependent upon both an active Src kinase and membrane association. The association between c-Src Y527F and PKC delta was substantially enhanced by mutating a PKC phosphorylation site at Ser-12 in Src to Ala indicating that PKC delta phosphorylation of Src at Ser-12 destabilizes the interaction, possibly in a negative feedback loop. These data demonstrate that upon recruitment of PKC delta to the membrane in v-Src-transformed cells there is the formation of a Src.PKC delta complex in which PKC delta becomes phosphorylated on tyrosine and down-regulated.
Brightly-Luminescent and Color-Tunable Colloidal CH3NH3PbX3 (X=Br, I, Cl) Quantum Dots: Potential Alternatives for Display Technology (2015)

We developed a ligand-assisted reprecipitation (LARP) strategy to fabricate brightly-luminescent and color-tunable colloidal CH3NH3PbX3 (X=Br, I, Cl) quantum dots and integrated them into wide color-gamut light-emitting diodes.
[A study on abnormal chondrocyte differentiation and abnormal expression of collagen types in articular cartilage from patients with Kaschin-Beck disease]. (1998)

The abnormal collagen pattern in the articular cartilage of KBD patients was similar to that seen in primary osteoarthritic cartilage, but having more pronounced type I collagen expression in the surface zone and no collagen expression in the chondronecrosis areas.
The foetal origins of the metabolic syndrome--a South African perspective. (2002)

The developing world is experiencing a rise in the prevalence of obesity, diabetes and cardiovascular disease to such an extent that it is often described as an epidemic. The most common explanation advanced for this phenomenon is the so-called epidemiological transition, with the biological basis of the thrifty genotype. The thrifty genotype theory suggests that genes derived from times of deprivation may result in adaptations that have adverse effects in times of plenty. However, a divergent theory is the so-called foetal origins of chronic disease, which ascribes the epidemic, in part, to an adverse intrauterine environment. There is compelling evidence, based on large numbers of epidemiological studies conducted in both developing and developed countries, that small size at birth in full-term pregnancies is linked with the subsequent development of the major features of the metabolic syndrome, namely glucose intolerance, increased blood pressure, dyslipidaemia and increased mortality from cardiovascular disease.
A specific promoter of the sensory cells of the inner ear defined by transgenesis (2001)

To date, no promoter sequence specific to the inner ear sensory cells (hair cells) has been reported. In an effort to understand the molecular mechanisms that determine hair cell fate in the inner ear, and with the goal of developing a valuable tool for gene therapy and for the generation of conditional knockouts, we initiated a search for cis-acting DNA sequences that regulate the expression of the murine Myo7a and human MYO7A genes. These genes encode the unconventional myosin VIIA which is expressed in hair cells and in some other epithelial cells. We generated lines of transgenic mice expressing the green fluorescent protein (GFP ) reporter gene under the control of several 5'-truncated versions of the Myo7a/MYO7A promoter region and intron 1. We obtained transgenic mice with a GFP expression restricted to the hair cells of the inner ear, cochlea and vestibule. Successive deletions of the promoter allowed us to define a minimal sequence of 118 bp that is sufficient, in the presence of intron 1, to target the transgene expression to hair cells. In addition, the deletion of intron 1 from the transgenes abolished hair cell expression, thus indicating the presence of a strong enhancer in the intron. This is the first report of regulatory sequences sufficient to target the expression of a gene exclusively in sensory cells of the inner ear. It also opens up the possibility for the analysis of the hair cell transcriptome.
Role of the Activation Loop Tyrosines in Regulation of the Insulin-like Growth Factor I Receptor-tyrosine Kinase (2006)

The tyrosine kinase activity of insulin-like growth factor I receptor (IGF1R) is under tight control. Ligand binding to the extracellular portion of IGF1R stimulates autophosphorylation at three sites (Tyr1131, Tyr1135, and Tyr1136) in the activation loop within the tyrosine kinase catalytic domain. Autophosphorylation at all three sites is required for maximum enzyme activity, and for IGF1-stimulated cellular activity of the receptor. Previous studies have not clarified the contributions of the individual tyrosines to enzymatic activation. Here, we produced single Tyr-to-Phe mutations at these positions, and compared activities of the purified kinase domains (unphosphorylated and phosphorylated) with wild-type IGF1R. Rates of autophosphorylation of the three mutants were more rapid than for wild-type IGF1R; this was most apparent for the Y1135F mutant. Substrate phosphorylation studies on the unphosphorylated forms of IGF1R confirmed that the value of Vmax for Y1135F was elevated relative to wild-type IGF1R, consistent with a disruption of an autoinhibitory interaction. In contrast, activity measurements on the fully phosphorylated enzymes indicated that kcat/Km values were lowered relative to wild-type IGF1R; this effect was most dramatic for Y1136F. We confirmed these findings using limited proteolysis and tryptophan fluorescence experiments. The results demonstrate that Tyr1135 plays a particularly important role in stabilizing the autoinhibited conformation of the activation loop, while Tyr1136 plays the key role in stabilizing the open, activated conformation of IGF1R.