gebhart/patrepeval huggingface dataset:
Bombesin stimulates human nasal mucous and serous cell secretion in vivo (1992)

Bombesin, gastrin-related peptide (GRP), and related peptides sharing the common carboxyterminal sequence stimulate lactoferrin (serous cell marker) and glycoconjugate (mucous cell and goblet cell marker) release from human nasal mucosal explants in vitro. In vivo, GRP released from trigeminal sensory nerves may act upon GRP-bombesin binding sites on respiratory epithelial cells and submucosal glands. To determine whether GRP-bombesin can stimulate nasal secretion in vivo, bombesin was administered to eight normal subjects by unilateral, topical administration. Secretions from both nostrils were collected for measurement of total protein, lysozyme, hexose-containing glycoconjugates, and albumin (marker of vascular permeability). Baseline secretions contained 72.0 +/- 17.3 micrograms/ml of total protein, 14 +/- 2 micrograms/ml of lysozyme, 113 +/- 44 micrograms/ml of hexose-containing glycoconjugates, and 7.8 +/- 3.4 micrograms/ml of albumin. Hexose-containing glycoconjugate secretion was significantly increased after 1 nmol (385 +/- 63 micrograms/ml, P less than 0.001 by analysis of variance), 10, 100, and 1,000 nmol of bombesin, but the secretion was not dose dependent. Significant lysozyme (24 +/- 3 micrograms/ml, P less than 0.05) and total protein (155 +/- 23 micrograms/ml, P less than 0.01) secretion occurred after 1,000 nmol. No statistically significant changes in albumin secretion occurred at any dose. Saline had no significant effects on secretion. Therefore, bombesin stimulated secretion from submucosal glands and possibly epithelial cells in the human nose without affecting vascular permeability.
Green and controlled synthesis of gold and platinum nanomaterials using vitamin B2: density-assisted self-assembly of nanospheres, wires and rods (2006)

For the first time, we report efficient density-assisted self-assembly synthesis of gold and platinum nanospheres, nanowires and nanorods using vitamin B2 (riboflavin) at room temperature without employing any special capping or dispersing agent; this environmentally benign and general approach affords a facile entry to production of shape-selective Au and Pt noble nanostructures, which can be extended to silver and palladium nanostructures.
Efficacy of an Adjuvanted Middle East Respiratory Syndrome Coronavirus Spike Protein Vaccine in Dromedary Camels and Alpacas (2019)

MERS-CoV is present in dromedary camels throughout the Middle East and Africa. Dromedary camels are the primary zoonotic reservoir for human infections. Interruption of the zoonotic transmission chain from camels to humans, therefore, may be an effective strategy to control the ongoing MERS-CoV outbreak. Here we show that vaccination with an adjuvanted MERS-CoV Spike protein subunit vaccine confers complete protection from MERS-CoV disease in alpaca and results in reduced and delayed viral shedding in the upper airways of dromedary camels. Protection in alpaca correlates with high serum neutralizing antibody titers. Lower titers of serum neutralizing antibodies correlate with delayed and significantly reduced shedding in the nasal turbinates of dromedary camels. Together, these data indicate that induction of robust neutralizing humoral immune responses by vaccination of naïve animals reduces shedding that potentially could diminish the risk of zoonotic transmission.
Morning bright light therapy for sleep and behavior disorders in elderly patients with dementia (1994)

Fourteen inpatients with dementia showing sleep and behavior disorders (average age = 75 years), and 10 control elderly people (average age = 75 years) were carefully observed for 2 months. Four weeks of morning light therapy markedly improved sleep and behavior disorders in the dementia group. The measurement of sleep time and the serum melatonin values suggests that sleep and behavior disorders in the dementia group are related to decreases in the amplitude of the sleep-wake rhythm and decreases in the levels of melatonin secretions. Morning light therapy significantly increased total and nocturnal sleep time and significantly decreased daytime sleep time. These results indicate that morning bright light is a powerful synchronizer that can normalize disturbed sleep and substantially reduce the frequency of behavior disorders in elderly people with dementia.
Erwiniachrysanthemi HarpinEch: An Elicitorof the Hypersensitive Response that Contributesto Soft-Rot Pathogenesis (1995)

Mutants of the soft-rot pathogen Erwinia chrysanthemi EC16 that are deficient in the production of the pectate lyase isozymes PelABCE can elicit the hypersensitive response (HR) in tobacco leaves. The hrpNEch gene was identified in a collection of cosmids carrying E. chrysanthemi hrp genes by its hybridization with the Erwinia amylovora hrpNEa gene. hrpNEch appears to be in a monocistronic operon, and it encodes a predicted protein of 340 amino acids that is glycine-rich, lacking in cysteine, and highly similar to HrpNEa in its C-terminal half. Escherichia coli DH5 alpha cells expressing hrpNEch from the lac promoter of pBluescript II accumulated HrpNEch in inclusion bodies. The protein was readily purified from cell lysates carrying these inclusion bodies by solubilization in 4.5 M guanidine-HCl and reprecipitation upon dialysis against dilute buffer. HrpNEch suspensions elicited a typical HR in tobacco leaves, and elicitor activity was heat-stable. Tn5-gusA1 mutations were introduced into the cloned hrpNEch and then marker-exchanged into the genomes of E. chrysanthemi strains AC4150 (wild type), CUCPB5006 (delta pelABCE), and CUCPB5030 (delta pelABCE outD::TnphoA). hrpNEch::Tn5-gusA1 mutations in CUCPB5006 abolished the ability of the bacterium to elicit the HR in tobacco leaves unless complemented with an hrpNEch subclone. An hrpNEch::Tn5-gusA1 mutation also reduced the ability of AC4150 to incite infections in witloof chicory leaves, but it did not reduce the size of lesions that did develop. Purified HrpNEch and E. chrysanthemi strains CUCPB5006 and CUCPB5030 elicited HR-like necrosis in leaves of tomato, pepper, African violet, petunia, and pelargonium, whereas hrpNEch mutants did not.(ABSTRACT TRUNCATED AT 250 WORDS)
Quorum-Sensing Regulation of the Production of Blp Bacteriocins in Streptococcus thermophilus (2007)

The blp gene cluster identified in the genome sequences of Streptococcus thermophilus (blp(St)) LMG18311, CNRZ1066, and LMD-9 displays all the characteristics of a class II bacteriocin locus. In the present study, we showed that the blp(St) locus is only fully functional in strain LMD-9 and regulates the production of antimicrobial peptides that inhibit strains LMG18311 and CNRZ1066. The blp(St) cluster of LMD-9 contains 23 genes that are transcriptionally organized in six operons: blpABC(St) (peptide transporter genes and pheromone gene); blpRH(St) (two-component regulatory system genes); blpD(St)-orf1, blpU(St)-orf3, and blpE-F(St) (bacteriocin precursors and immunity genes); and blpG-X(St) (unknown function). All the operons, except the regulatory unit blpRH(St), were shown to be coregulated at the transcriptional level by a quorum-sensing mechanism involving the mature S. thermophilus pheromone BlpC* (BlpC*(St)), which was extracellularly detected as two active forms (30 and 19 amino acids). These operons are differentially transcribed depending on growth phase and pheromone concentration. They all contain a motif with two imperfect direct repeats in their mapped promoter regions that could serve as binding sites of the response regulator BlpR(St). Through the construction of deletion mutants, the blp(St) locus of strain LMD-9 was shown to encode all the essential functions associated with bacteriocin production, quorum-sensing regulation, and immunity.
Triple-Helix Formation Induces Recombination in Mammalian Cells via a Nucleotide Excision Repair-Dependent Pathway (2000)

The ability to stimulate recombination in a site-specific manner in mammalian cells may provide a useful tool for gene knockout and a valuable strategy for gene therapy. We previously demonstrated that psoralen adducts targeted by triple-helix-forming oligonucleotides (TFOs) could induce recombination between tandem repeats of a supF reporter gene in a simian virus 40 vector in monkey COS cells. Based on work showing that triple helices, even in the absence of associated psoralen adducts, are able to provoke DNA repair and cause mutations, we asked whether intermolecular triplexes could stimulate recombination. Here, we report that triple-helix formation itself is capable of promoting recombination and that this effect is dependent on a functional nucleotide excision repair (NER) pathway. Transfection of COS cells carrying the dual supF vector with a purine-rich TFO, AG30, designed to bind as a third strand to a region between the two mutant supF genes yielded recombinants at a frequency of 0.37%, fivefold above background, whereas a scrambled sequence control oligomer was ineffective. In human cells deficient in the NER factor XPA, the ability of AG30 to induce recombination was eliminated, but it was restored in a corrected subline expressing the XPA cDNA. In comparison, the ability of triplex-directed psoralen cross-links to induce recombination was only partially reduced in XPA-deficient cells, suggesting that NER is not the only pathway that can metabolize targeted psoralen photoadducts into recombinagenic intermediates. Interestingly, the triplex-induced recombination was unaffected in cells deficient in DNA mismatch repair, challenging our previous model of a heteroduplex intermediate and supporting a model based on end joining. This work demonstrates that oligonucleotide-mediated triplex formation can be recombinagenic, providing the basis for a potential strategy to direct genome modification by using high-affinity DNA binding ligands.
Dielectric relaxation and Schottky conduction of IR laser irradiated Makrofol‐DE polycarbonate (2011)

Abstract The effect of IR laser pulses on the dielectric properties, X‐ray diffraction, Fourier transform infrared spectroscopy (FTIR), and I – V characteristics of Makrofol‐DE 1‐1 CC polycarbonate has been investigated in the temperature and frequency ranges of 300–375K and 10 kHz–4 MHz, respectively. IR laser fluencies are set from 0.47 to 7.07 J/cm 2 . Three relaxation processes namely, α, β, and γ have been obtained. The first process is due to the micro Brownian motion of the segmental parts of the main chain. The second process was assigned to the local motion of the dipoles within the crystalline phases of the sample. The third one was attributed to the crank shaft motion along the main chains of the Makrofol. X‐ray diffraction and FTIR spectroscopy have revealed that the irradiation of Makrofol at the fluence range 0.94–7.07 J/cm 2 causes crosslinking formation inside the sample. Reduction in crystallinity of Makrofol at higher IR laser doses is due to the crosslinking formation taking place within polymer matrix. At higher voltage, the conduction mechanism of Makrofol‐DE was identified as Shottky type. The attained results suggested strongly the applicability of Makrofol‐DE in IR laser pulses dosimetry. © 2011 Wiley Periodicals, Inc. J Appl Polym Sci, 2012
2‘,5‘-Oligoadenylate-dependent RNase L is a dimer of regulatory and catalytic subunits. (1993)

The subunit composition of RNase L, a key enzyme in the interferon system, has been characterized. RNase L was purified from human Daudi cells on a column of 2-5A-Sepharose and used to immunize Balb/c mice. A specific monoclonal antibody which recognizes a protein of 80 kDa has been isolated. This protein has been characterized and shown to be an RNA-binding protein with nuclease activity which is associated with, but distinct from, the 80-kDa 2-5A-binding protein known previously as RNase L. It is therefore proposed that the 2-5A-dependent RNase L is a complex of two distinct subunits: an 80-kDa RNA-binding protein (i.e. the catalytic subunit) and an 80-kDa 2-5A-binding protein (i.e. the regulatory subunit).
Phosphorylation of the RNA Polymerase II Carboxyl-Terminal Domain by CDK9 Is Directly Responsible for Human Immunodeficiency Virus Type 1 Tat-Activated Transcriptional Elongation (2002)

Stimulation of transcriptional elongation by the human immunodeficiency virus type 1 Tat protein is mediated by CDK9, a kinase that phosphorylates the RNA polymerase II carboxyl-terminal domain (CTD). In order to obtain direct evidence that this phosphorylation event can alter RNA polymerase processivity, we prepared transcription elongation complexes that were arrested by the lac repressor. The CTD was then dephosphorylated by treatment with protein phosphatase 1. The dephosphorylated transcription complexes were able to resume the transcription elongation when IPTG (isopropyl-beta-D-thiogalactopyranoside) and nucleotides were added to the reaction. Under these chase conditions, efficient rephosphorylation of the CTD was observed in complexes containing the Tat protein but not in transcription complexes prepared in the absence of Tat protein. Immunoblots and kinase assays with synthetic peptides showed that Tat activated CDK9 directly since the enzyme and its cyclin partner, cyclin T1, were present at equivalent levels in transcription complexes prepared in the presence or absence of Tat. Chase experiments with the dephosphorylated elongation transcription complexes were performed in the presence of the CDK9 kinase inhibitor DRB (5,6-dichloro-1-beta-D-ribofuranosyl-benzimidazole). Under these conditions there was no rephosphorylation of the CTD during elongation, and transcription through either a stem-loop terminator or bent DNA arrest sequence was strongly inhibited. In experiments in which the CTD was phosphorylated prior to elongation, the amount of readthrough of the terminator sequences was proportional to the extent of the CTD modification. The change in processivity is due to CTD phosphorylation alone, since even after the removal of Spt5, the second substrate for CDK9, RNA polymerase elongation is enhanced by Tat-activated CDK9 activity. We conclude that phosphorylation of the RNA polymerase II CTD by CDK9 enhances transcription elongation directly.
Detection and Quantification of Vascular Endothelial Growth Factor/Vascular Permeability Factor in Brain Tumor Tissue and Cyst Fluid (1994)

In primary malignant brain tumors increased vascularity and marked edema strongly suggest a possible role of the vascular endothelial growth factor/vascular permeability factor (VEGF/VPF). This was confirmed by earlier in situ hybridization studies, by analysis of the expression of the mitogen in different subsets of glioblastoma cells, and by the fact that the VEGF/VPF receptor flt-1 (fms-like tyrosine kinase) is up-regulated in tumor cells in vivo. To assess and quantify the expression of the VEGF/VPF gene and of the receptor gene, 26 surgical specimens of brain tumor tissue from 24 patients were analyzed. In most malignant gliomas, the expression level of the VEGF/VPF gene is elevated and can be increased up to 20- to 50-fold in comparison with low-grade tumors. Using polymerase chain reaction-based amplification, it could be shown that the messenger RNAs of three different VEGF/VPF forms are synthesized in tumor tissue samples. Northern blot studies revealed that in some samples a significant expression of the gene coding for placenta growth factor, a growth factor closely related to VEGF/VPF, was observed. In addition, using a radioreceptor assay it was possible to detect high VEGF/VPF-like activity in the cyst fluids of brain tumors, indicating the accumulation of the mitogen and permeability factor in brain tumor cysts. Further investigations revealed that astrocytoma and glioblastoma cells in culture express the VEGF/VPF gene and secrete the VEGF/VPF protein, whereas gene expression of the two known VEGF/VPF receptors, kinase insert domain-containing receptor and flt-1, could not be detected. These data support previous reports, which stated that VEGF/VPF acts as a paracrine growth and permeability factor in brain tumors and may contribute to tumor growth by initiating tumor angiogenesis.
Glucose sensing in the intestinal epithelium (2003)

Dietary sugars regulate expression of the intestinal Na+/glucose cotransporter, SGLT1, in many species. Using sheep intestine as a model, we showed that lumenal monosaccharides, both metabolisable and nonmetabolisable, regulate SGLT1 expression. This regulation occurs not only at the level of transcription, but also at the post-transcriptional level. Introduction of d-glucose and some d-glucose analogues into ruminant sheep intestine resulted in > 50-fold enhancement of SGLT1 expression. We aimed to determine if transport of sugar into the enterocytes is required for SGLT1 induction, and delineate the signal-transduction pathways involved. A membrane impermeable d-glucose analogue, di(glucos-6-yl)poly(ethylene glycol) 600, was synthesized and infused into the intestines of ruminant sheep. SGLT1 expression was determined using transport studies, Northern and Western blotting, and immunohistochemistry. An intestinal cell line, STC-1, was used to investigate the signalling pathways. Intestinal infusion with di(glucos-6-yl)poly(ethylene glycol) 600 led to induction of functional SGLT1, but the compound did not inhibit Na+/glucose transport into intestinal brush-border membrane vesicles. Studies using cells showed that increased medium glucose up-regulated SGLT1 abundance and SGLT1 promoter activity, and increased intracellular cAMP levels. Glucose-induced activation of the SGLT1 promoter was mimicked by the protein kinase A (PKA) agonist, 8Br-cAMP, and was inhibited by H-89, a PKA inhibitor. Pertussis toxin, a G-protein (Gi)-specific inhibitor, enhanced SGLT1 protein abundance to levels observed in response to glucose or 8Br-cAMP. We conclude that lumenal glucose is sensed by a glucose sensor, distinct from SGLT1, residing on the external face of the lumenal membrane. The glucose sensor initiates a signalling pathway, involving a G-protein-coupled receptor linked to a cAMP-PKA pathway resulting in enhancement of SGLT1 expression.
The human asialoglycoprotein receptor is a possible binding site for low-density lipoproteins and chylomicron remnants (1991)

Binding and internalization of chylomicron remnants from rat mesenteric lymph by HepG2 cells was inhibited by both excess remnants and low-density lipoprotein (LDL) to the same extent. Ligand blots revealed binding of remnants and LDL to the LDL receptor. Measures regulating LDL receptor activity greatly influenced the binding of remnants: ethinyloestradiol, the hydroxymethylglutaryl-CoA reductase inhibitor pravastatin and the absence of LDL all increased binding, whereas high cell density or the presence of LDL decreased binding. Also, asialofetuin, asialomucin, the neoglycoprotein galactosyl-albumin and an antibody against the asialoglycoprotein receptor all decreased substantially the binding of remnants. At high cell density, binding internalization and degradation of chylomicron remnants was inhibited by up to 70-80%, yet binding of LDL was inhibited by no more than 20-30%. In cross-competition studies, the binding of 125I-asialofetuin was efficiently competed for by asialofetuin itself or by the antibody, and also by LDL and remnants, yet remnants displayed an approx. 100-fold higher affinity than LDL. Likewise, remnants of human triacylglycerol-rich lipoproteins and asialofetuin interfered with each others' binding to HepG2 cells or human liver membranes. It is concluded that the LDL receptor mediates the internalization of chylomicron remnants into hepatocytes depending on its activity, according to demand for cholesterol. Additionally, the asialoglycoprotein receptor may contribute to the endocytosis of LDL, but predominantly of chylomicron remnants.
Neutrophil gelatinase‐associated lipocalin (NGAL): A new marker of kidney disease (2008)

The incidence of both acute kidney injury (AKI, previously referred to as acute renal failure) and chronic kidney disease (CKD) is reaching epidemic proportions. In both situations, early intervention can significantly improve the prognosis. However, the paucity of early, predictive, non-invasive biomarkers has impaired our ability to institute potentially effective therapies for these common clinical conditions in a timely manner. The current status of one of the most promising novel biomarkers, namely neutrophil gelatinase-associated lipocalin (NGAL), is presented in this review. The evidence for the role of NGAL measurements in a variety of clinical situations leading to AKI (cardiac surgery, kidney transplantation, contrast nephropathy, haemolytic uraemic syndrome and in the intensive care setting) or to CKD (lupus nephritis, glomerulonephritides, obstruction, dysplasia, polycystic kidney disease, IgA nephropathy) is explored. The emerging utility of standardized clinical platforms for reliable measurement of NGAL in plasma (Triage NGAL Device; Biosite Incorporated) and urine (ARCHITECT analyzer; Abbott Diagnostics) is also discussed. It will be important in future studies to validate the sensitivity and specificity of NGAL concentration measurements in clinical samples from large cohorts and from multiple clinical situations. Such studies will be facilitated by the anticipated widespread availability of standardized commercial tools in the near future.
Core promoter: A critical region where the hepatitis B virus makes decisions (2014)

The core promoter (CP) of the viral genome plays an important role for hepatitis B virus (HBV) replication as it directs initiation of transcription for the synthesis of both the precore and pregenomic (pg) RNAs. The CP consists of the upper regulatory region and the basal core promoter (BCP). The CP overlaps with the 3'-end of the X open reading frames and the 5'-end of the precore region, and contains cis-acting elements that can independently direct transcription of the precore mRNA and pgRNA. Its transcription regulation is under strict control of viral and cellular factors. Even though this regulatory region exhibits high sequence conservation, when variations appear, they may contribute to the persistence of HBV within the host, leading to chronic infection and cirrhosis, and eventually, hepatocellular carcinoma. Among CP sequence variations, those occurring at BCP may dysregulate viral gene expression with emphasis in the hepatitis B e antigen, and contribute to disease progression. In this review these molecular aspects and pathologic topics of core promoter are deeply evaluated.
Interpretation of dislocation propagation velocities in strained GexSi1−x/Si(100) heterostructures by the diffusive kink pair model (1991)

Experimental measurements of misfit dislocation velocities, obtained from in situ transmission electron microscope observations of strained GexSi1−x/Si(100) heterostructures, are compared with predictions of the diffusive double-kink (or ‘‘kink pair’’) model of dislocation propagation. Good agreement is observed between experiment and theory for buried strained layers with applied stresses in the range of hundreds of MPa. For very thin uncapped strained layers, the diffusive double-kink model does not describe experimental data well. In these structures better agreement between experiment and theory is obtained if we model single-kink nucleation at the epilayer free surface. We compare our experimental data to those of other groups, and show how our modeling can reconcile apparently disparate trends deduced by these other groups.
Clinical features and management of benign prostatic hyperplasia (1999)

Benign prostatic hyperplasia represents the most common benign neoplastic condition afflicting men and has a major impact on the health of the population. It refers to a regional and nodular growth of stromal proliferation which, because of its proximity to the urethra, causes varying degrees of bladder outflow obstruction.