gebhart/patrepeval huggingface dataset:
Sensitivity of CFP/YFP and GFP/mCherry pairs to donor photobleaching on FRET determination by fluorescence lifetime imaging microscopy in living cells (2006)

Fluorescent protein-based FRET is a powerful method for visualizing protein-protein interactions and biochemical reactions in living cells. It can be difficult, however, to avoid photobleaching when observing fluorescent cells under the microscope, especially those expressing CFP. We compared the sensitivity of two protein-based FRET pairs to light-induced fluorescence changes in the donor, on FRET determination by fluorescence lifetime imaging microscopy (FLIM). Thanks to the very low excitation light levels of the time- and space-correlated single photon counting (TSCSPC) method, FLIM acquisitions were achieved without donor photobleaching. Here, we show that photobleaching of CFP by a mercury lamp under the microscope induced a decrease in the mean fluorescence lifetime, which interfered with FRET determination between CFP and YFP. Importantly, the range of light-induced variation of the mean fluorescence lifetime of CFP was not proportional to the decrease in the steady state fluorescence intensity and varied from cell to cell. The choice of the CFP/YFP pair therefore requires that the cells be observed and analyzed at very low light levels during the whole FRET experiment. In contrast, the GFP/mCherry pair provided an accurate FRET measurement by FLIM, even if some GFP photobleaching took place. We thus demonstrate that CFP can be an unreliable donor for FRET determination in living cells, due to its photosensitivity properties. We demonstrate that the GFP/mCherry pair is better suited for FRET measurement by FLIM in living cells than the CFP/YFP pair.
Synthesis of Oligonucleotides Containing 3'-Alkyl Carboxylic Acids Using Universal, Photolabile Solid Phase Synthesis Supports (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSynthesis of Oligonucleotides Containing 3'-Alkyl Carboxylic Acids Using Universal, Photolabile Solid Phase Synthesis SupportsDong Jin Yoo and Marc M. GreenbergCite this: J. Org. Chem. 1995, 60, 11, 3358–3364Publication Date (Print):June 1, 1995Publication History Published online1 May 2002Published inissue 1 June 1995https://pubs.acs.org/doi/10.1021/jo00116a019https://doi.org/10.1021/jo00116a019research-articleACS PublicationsRequest reuse permissionsArticle Views452Altmetric-Citations47LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
The τ-Nitrogen of D2 Histidine 189 is the Hydrogen Bond Donor to the Tyrosine Radical YD• of Photosystem II (1997)

ADVERTISEMENT RETURN TO ISSUEPREVCommunicationNEXTThe τ-Nitrogen of D2 Histidine 189 is the Hydrogen Bond Donor to the Tyrosine Radical YD• of Photosystem IIKristy A. Campbell, Jeffrey M. Peloquin, Bruce A. Diner, Xiao-Song Tang, Dexter A. Chisholm, and R. David BrittView Author Information Department of Chemistry University of California Davis, California 95616 Central Research and Development Department Experimental Station, P.O. Box 80173 E. I. du Pont De Nemours & Company Wilmington, Delaware 19880-0173 Cite this: J. Am. Chem. Soc. 1997, 119, 20, 4787–4788Publication Date (Web):May 21, 1997Publication History Received25 February 1997Published online21 May 1997Published inissue 1 May 1997https://doi.org/10.1021/ja9706155Copyright © 1997 American Chemical SocietyRIGHTS & PERMISSIONSArticle Views274Altmetric-Citations64LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InReddit Read OnlinePDF (135 KB) Get e-AlertsSUBJECTS:Coupling reactions,Monomers,Nitrogen,Noncovalent interactions,Peptides and proteins Get e-Alerts
Evaluation of c-kit protein (CD117) expression in common salivary gland neoplasms (2014)

CD117 expression itself cannot be used as a marker in differential diagnosis of salivary gland neoplasms. However, the percentage of the CD117 immunoreactive cells and the staining intensities appeared to be important factors in distinguishing AdCC from PLGA and PA.
Inhibition of lung cancer cell growth and induction of apoptosis after reexpression of 3p21.3 candidate tumor suppressor gene SEMA3B (2001)

Semaphorins SEMA3B and its homologue SEMA3F are 3p21.3 candidate tumor suppressor genes (TSGs), the expression of which is frequently lost in lung cancers. To test the TSG candidacy of SEMA3B and SEMA3F, we transfected them into lung cancer NCI-H1299 cells, which do not express either gene. Colony formation of H1299 cells was reduced 90% after transfection with wild-type SEMA3B compared with the control vector. By contrast, only 30-40% reduction in colony formation was seen after the transfection of SEMA3F or SEMA3B variants carrying lung cancer-associated single amino acid missense mutations. H1299 cells transfected with wild-type but not mutant SEMA3B underwent apoptosis. We found that lung cancers (n = 34) always express the neuropilin-1 receptor for secreted semaphorins, whereas 82% expressed the neuropilin-2 receptor. Because SEMA3B and SEMA3F are secreted proteins, we tested conditioned medium from COS-7 cells transfected with SEMA3B and SEMA3F and found that medium from wild-type SEMA3B transfectants reduced the growth of several lung cancer lines 30-90%, whereas SEMA3B mutants or SEMA3F had little effect in the same assay. Sequencing of sodium bisulfite-treated DNA showed dense methylation of CpG sites in the SEMA3B 5' region of lung cancers not expressing SEMA3B but no methylation in SEMA3B-expressing tumors. These results are consistent with SEMA3B functioning as a TSG, the expression of which is inactivated frequently in lung cancers by allele loss and promoter region methylation.
Simultaneous structure and size–strain refinement by the Rietveld method (1990)

A new procedure for simultaneous refinement of structural and microstructural disorder parameters for polycrystalline materials is proposed. It is based on the Rietveld method combined with Fourier analysis for broadened peaks. Crystallite size and shape and r.m.s. microstrain are regarded as fitting parameters, replacing the well known formula of Caglioti, Paoletti & Ricci [Nucl. Instrum. Methods (1958), 3, 223–228] for the angular dependence of the peak width. In particular, from these microstructural disorder parameters, by inverting the Warren–Averbach procedure [Warren & Averbach (1950). J. Appl. Phys. 21, 595–599; (1952), 23, 1059] for a single peak, it is possible to obtain the parameters of the pseudo-Voigt (pV) functions employed to fit the experimental data. The anisotropy of the crystallite size and microstrain is also taken into account. The method has been tested on three materials with different degrees of crystallization: tetragonal ZrO2 (P42/nmc, a = 3.5961, c = 5.1770 Å, Vc = 66.95 Å3, Z = 2, Rwp = 0.077, M ≃100 Å, 〈∊2〉1/2 ≃ 3 × 10−3); tetragonal Zr0.82Ce0.18O2 (P42/nmc, a = 3.6419, c = 5.2440 Å, Vc = 69.556 Å3, Z = 2, Rwp = 0.0654, M ≃1000 Å, 〈∊2〉1/2 ≃8 × 10−4); α-Al2O3 (R{\bar 3}c, a = 4.7605, c = 12.9956 Å, Vc = 255.05 Å3, Z = 6, Rwp = 0.0684, M ≃ 1400 Å, 〈∊2〉1/2 ≃7 × 10−4).
Vaccination with Tumor Lysate-Pulsed Dendritic Cells Elicits Antigen-Specific, Cytotoxic T-Cells in Patients with Malignant Glioma (2004)

The primary goal of this Phase I study was to assess the safety and bioactivity of tumor lysate-pulsed dendritic cell (DC) vaccination to treat patients with glioblastoma multiforme and anaplastic astrocytoma. Adverse events, survival, and cytotoxicity against autologous tumor and tumor-associated antigens were measured. Fourteen patients were thrice vaccinated 2 weeks apart with autologous DCs pulsed with tumor lysate. Peripheral blood mononuclear cells were differentiated into phenotypically and functionally confirmed DCs. Vaccination with tumor lysate-pulsed DCs was safe, and no evidence of autoimmune disease was noted. Ten patients were tested for the development of cytotoxicity through a quantitative PCR-based assay. Six of 10 patients demonstrated robust systemic cytotoxicity as demonstrated by IFN-gamma expression by peripheral blood mononuclear cells in response to tumor lysate after vaccination. Using HLA-restricted tetramer staining, we identified a significant expansion in CD8+ antigen-specific T-cell clones against one or more of tumor-associated antigens MAGE-1, gp100, and HER-2 after DC vaccination in four of nine patients. A significant CD8+ T-cell infiltrate was noted intratumorally in three of six patients who underwent reoperation. The median survival for patients with recurrent glioblastoma multiforme in this study (n = 8) was 133 weeks. This Phase I study demonstrated the feasibility, safety, and bioactivity of an autologous tumor lysate-pulsed DC vaccine for patients with malignant glioma. We demonstrate for the first time the ability of an active immunotherapy strategy to generate antigen-specific cytotoxicity in brain tumor patients.
Inhibins and activins regulate mammary epithelial cell differentiation through mesenchymal-epithelial interactions (1997)

Inhibins and activins are members of the transforming growth factor beta (TGFbeta) family. Female mice in which both alleles encoding the inhibin betaB subunit have been deleted are unable to nurse their pups. We have now identified a cause of lactation failure in these mice. Ductal elongation and alveolar morphogenesis are retarded. During puberty and pregnancy, ductal outgrowth and alveolar development are limited and morphologically abnormal endbuds persist in the glands of postpartum females. The alveolar lumina fail to expand at parturition due to the absence of secreted milk. Transplantation experiments have been performed to determine whether the absence of systemic- or mammary-derived betaB subunits are the cause for the incomplete and aberrant development. While transplanted intact glands from wild-type mice grew normally in betaB-deficient hosts, betaB-deficient glands remained underdeveloped in wild-type hosts. However, betaB-deficient epithelium developed normally when transplanted into the fat pad of wild-type hosts. This demonstrates that ductal elongation and epithelial cell differentiation during puberty and pregnancy require activin/inhibin signalling from the stroma. The results further show that distinct, though related, activins and inhibins perform unique functions and are not able to compensate for the absence of activin B and AB and inhibin B in the process of mammogenesis. The betaB-deficient mice provide the first genetic evidence for stromal signalling in the adult mammary gland in vivo.
Breast cancer cells induce osteoblast apoptosis: A possible contributor to bone degradation (2003)

Breast cancer cells exhibit a predilection for metastasis to bone. There, the metastases usually bring about bone loss with accompanying pain and loss of function. One way that breast cancer cells disrupt the normal pattern of bone remodeling is by activating osteoclasts, the bone degrading cells. Nevertheless, targeting the osteoclasts does not cure the disease or result in bone repair. These observations indicate that osteoblast function also may be compromised. The objective of this study was to investigate the interaction of metastatic breast cancer cells with osteoblasts. Human metastatic breast cancer cells, MDA-MB-435 or MDA-MB-231, or their conditioned media were co-cultured with a human osteoblast line hFOB1.19. The breast cancer cells caused an increase in the prevalence of apoptotic osteoblasts. Apoptotic osteoblasts detected by the TUNEL assay or by caspase activity increased approximately two to fivefold. This increase was not seen with non-metastatic MDA-MB-468 cells. In an investigation of the mechanism, it was determined that the hFOB1.19 cells expressed fas and that fas was functional. Likewise the hFOB1.19 cells were susceptible to TNF-alpha, but this cytokine was not detected in the conditioned medium of the breast cancer cells. This study indicates that osteoblasts are the target of breast cancer cell-induced apoptosis, but fas/fas-ligand and TNF-alpha, two common initiators of cell death, are probably not involved in this aspect of the metastases/bone cell axis. There are several mechanisms that remain to be explored in order to determine how breast cancer cells bring about osteoblast apoptosis. Even though the specific initiator of apoptosis remains to be identified, the results of this study suggest that the mechanism is likely to be novel.
STAT3 is a potential modulator of HIF‐1‐mediated VEGF expression in human renal carcinoma cells (2005)

Aberrantly enhanced vascular endothelial growth factor (VEGF) gene expression is associated with increased tumor growth and metastatic spread of solid malignancies, including human renal carcinomas. Persistent activation of STAT3 is linked to tumor-associated angiogenesis, but underlying mechanisms remain unclear. Therefore, we examined whether STAT3 modulates the stability and activity of hypoxia-inducible factor-1alpha (HIF-1alpha), and in turn enhances VEGF expression. We found that STAT3 was activated in ischemic rat kidneys and hypoxic human renal carcinoma cells. We also found that hypoxia-induced activation of STAT3 transactivated the VEGF promoter and increased the expression of VEGF transcripts. Consistent with these findings, STAT3 inhibition attenuated the hypoxic induction of VEGF. Interestingly, activated STAT3 increased HIF-1alpha protein levels due to the HIF-1alpha stability by blocking HIF-1alpha degradation and accelerated its de novo synthesis. The novel interaction of STAT3 with HIF-1alpha was identified in hypoxic renal carcinoma cells. Furthermore, hypoxia recruited STAT3, HIF-1alpha, and p300 to the VEGF promoter and induced histone H3 acetylation. Therefore, these findings provide compelling evidence that a causal relationship exists between STAT3 activation and HIF-1-dependent angiogenesis and suggest that therapeutic modalities designed to disrupt STAT3 signaling hold considerable promise for the blocking tumor growth and enhancing apoptosis of cancer cells and tissues.
Synthesis of N-Phenylsulfonyl Protected Furo[3,2-b]pyrroles (1994)

Protection of nitrogen atom of heterocyclic molecules, such as indole and pyrrole types, enables various reactions of these systems. N -Phenylsulfonyl derivatives, which have been widely used for this purpose, were prepared in the indole series by the reaction of N -sodium and N -lithium salts with benzenesulfonyl chloride. This method requires waterfree and oxygenfree conditions. On the other hand, the phase transfer catalysis conditions used in this work obviates these disadvantages. We therefore selected the latter method for the preparation of variously substituted 4-phenylsulfonylfuro[3,2- b ]pyrroles ( I - VII ) and 1-phenylsulfonylbenzo[ b ]furo[3,2- b ]pyrroles ( VIII - IX ).
ASSOCIATION OF INTRALEUKOCYTIC PLASMODIUM FALCIPARUM MALARIA PIGMENT WITH DISEASE SEVERITY, CLINICAL MANIFESTATIONS, AND PROGNOSIS IN SEVERE MALARIA (2003)

Peripheral parasite density of Plasmodium falciparum is used as an indicator of malaria disease severity, but does not quantify central sequestration, which is important in the pathogenesis of severe disease. Malaria pigment, recognizable within the cytoplasm of phagocytic cells by light microscopy may represent a peripheral marker for parasite biomass. One hundred seventy-two index cases of severe malaria and 172 healthy age-, residence-, and ethnicity-matched controls with uncomplicated malaria in Bandiagara, Mali were analyzed prospectively for presence of malaria pigment. The presence of polymorphonuclear cell (PMN) and monocyte pigment was strongly associated with severe disease compared with uncomplicated malaria. Total PMN pigment burden in children with severe malaria was higher in those with cerebral manifestations and with combined cerebral manifestations and severe anemia (hemoglobin < or = 5 g/dL) but was not associated with hyperparasitemia (> 500,000 asexual forms/mm3). Additionally, pigmented PMNs/mm3 was associated with a fatal outcome in patients with severe malaria. This study validates the presence of malaria pigment in monocytes and neutrophils as a marker for disease severity, and demonstrates that pigmented neutrophils are associated with cerebral malaria and with death in children with severe malaria.
Different Classes of Proteoglycans Contribute to the Attachment of Borrelia burgdorferi to Cultured Endothelial and Brain Cells (1998)

The Lyme disease spirochete, Borrelia burgdorferi, infects multiple tissues, such as the heart, joint, skin, and nervous system and has been shown to recognize heparan sulfate and dermatan sulfate proteoglycans. In this study, we examined the contribution of different classes of proteoglycans to the attachment of the infectious B. burgdorferi strain N40 to several immortalized cell lines and primary cultured cells, including endothelial cells and brain cells. Bacterial attachment was inhibited by exogenous proteoglycans or by treatment of host cells with inhibitors of proteoglycan synthesis or sulfation, indicating that proteoglycans play a critical role in bacterial binding to diverse cell types. Binding to primary bovine capillary endothelial cells or a human endothelial cell line was also inhibited by digestion with heparinase or heparitinase but not with chondroitinase ABC. In contrast, binding to glial cell-enriched brain cell cultures or to a neuronal cell line was inhibited by all three lyases. Binding of strain N40 to immobilized heparin could be completely inhibited by dermatan sulfate, and conversely, binding to dermatan sulfate could be completely blocked by heparin. As measured by 50% inhibitory dose, heparin was a better inhibitor of binding than dermatan sulfate, regardless of whether the substrate was heparin or dermatan sulfate. These results are consistent with the hypotheses that the species of proteoglycans recognized by B. burgdorferi vary with cell type and that bacterial recognition of different proteoglycans is mediated by the same bacterial molecule(s).
Development of Macrophages with Altered Actin Organization in the Absence of MafB (2006)

In the hematopoietic system the bZip transcription factor MafB is selectively expressed at high levels in monocytes and macrophages and promotes macrophage differentiation in myeloid progenitors, whereas a dominant-negative allele can inhibit this process. To analyze the requirement of MafB for macrophage development, we generated MafB-deficient mice and, due to their neonatal lethal phenotype, analyzed macrophage differentiation in vitro, in the embryo, and in reconstituted mice. Surprisingly we observed in vitro differentiation of macrophages from E14.5 fetal liver (FL) cells and E18.5 splenocytes. Furthermore we found normal numbers of F4/80(+)/Mac-1(+) macrophages and monocytes in fetal liver, spleen, and blood as well as in bone marrow, spleen, and peritoneum of adult MafB(-/-) FL reconstituted mice. MafB(-/-) macrophages showed intact basic macrophage functions such as phagocytosis of latex beads or Listeria monocytogenes and nitric oxide production in response to lipopolysaccharide. By contrast, MafB(-/-) macrophages expressed increased levels of multiple genes involved in actin organization. Consistent with this, phalloidin staining revealed an altered morphology involving increased numbers of branched protrusions of MafB(-/-) macrophages in response to macrophage colony-stimulating factor. Together these data point to an unexpected redundancy of MafB function in macrophage differentiation and a previously unknown role in actin-dependent macrophage morphology.
Multimarker assay for detection of endometrial cancer. (2006)

B18 Endometrial carcinoma is the most common gynecologic cancer. Lack of screening test for this type of cancer is associated with excess mortality for women who do not present with vaginal bleeding and other early warning signs for endometrial cancer. Although the prognosis for endometrial cancer is generally good, cancers identified at later stages are associated with high levels of morbidity and mortality. Therefore, prevention and early detection represent our best hope to overcome this disease. We hypothesize that a multi-marker panel would provide the requisite high sensitivity and specificity for early detection of endometrial cancer, to be utilized for screening of target populations. A panel of 64 biomarkers associated with endometrial cancers was analyzed in sera of patients with stages I-VI endometrial cancer and age-matched healthy women, utilizing a multiplex xMAP® bead-based immunoassay. The adaptive bandwidth kernel based density estimator combined with projection pursuit technique (ADEPT) and Monte-Carlo simulation was used to create a diagnostic model, based on the cross-validation set consisting of sera from 115 patients with endometrial cancer and 135 healthy women. Patients with endometrial cancer have significantly different expression patterns of several serum biomarkers than healthy individuals. We have identified an 8-biomarker panel that discriminated endometrial cancer cases from healthy controls with a sensitivity of greater than 99% at a specificity of 99% in a case/control cross-validation set. High degree discrimination between cancer and control groups indicates that serum cytokine profiles could potentially be used for development of blood-based diagnostic test for early detection of endometrial cancer. These studies demonstrate that combining the information in multiple markers using flexible statistical methods results in improved sensitivity while maintaining high specificity.
The Learning with Errors Problem (Invited Survey) (2010)

In this survey we describe the Learning with Errors (LWE) problem, discuss its properties, its hardness, and its cryptographic applications.
Gp91phox (NOX2) in classically activated microglia exacerbates traumatic brain injury (2010)

Classical activated microglia promote ROS formation through gp91phox and have an important role in brain damage following TBI. Modulating gp91phox and gp91phox -derived ROS may provide a new therapeutic strategy in combating post-traumatic brain injury.