gebhart/patrepeval huggingface dataset:
Construction of a rice bacterial artificial chromosome library and identification of clones linked to the Xa‐21 disease resistance locus (1995)

A bacterial artificial chromosome (BAC) library consisting of 11,000 clones with an average DNA insert size of 125 kb was constructed from rice nuclear DNA. The BAC clones were stable in E. coli after 100 generations of serial growth. Transformation of the BAC clones by electroporation into E. coli was highly efficient and increased with decreasing size of the DNA inserts. The library was evaluated for the presence of organellar, repeated, and telomeric sequences. A very low percentage (< 0.3%) of the library consisted of chloroplast and mitochondrial clones. Eighteen BACs were identified that hybridized with an Arabidopsis telomere repeat. Sixteen BACs hybridized with the AA genome-specific repetitive sequence pOs48. Twelve clones were isolated that hybridized with three DNA markers linked to the Xa-21 disease resistance locus. The results indicate that the BAC system can be used to clone and manipulate large pieces of plant DNA efficiently.
Selective-Mapping Type Peak Power Reduction Techniques For Turbo Coded OFDM (2005)

In an earlier paper, a selective-mapping type turbo coded OFDM scheme was proposed, for which the interleaver of the encoder of the turbo coding can be varied to reduce the associated PAPR (peak to average power ratio) while the transmission of side information is not needed. In this paper, we propose two modified versions of that scheme. For the first, the variation of the interleaver of the turbo encoder is replaced by the variation of the bit permutation of the turbo codeword. For the second, the variation of the interleaver of the turbo encoder is replaced by the variation of a maximum-length sequence which is added to the turbo codeword. These two modified schemes can provide better PAPR reduction capability.
Influence of TPA (12-O-tetradodecanoyl-phorbol-13-acetate) on human B lymphocyte function. (1985)

The effect of the tumour-promoting agent TPA (12-0-tetra-dodecanoyl-phorbol-13-acetate) on the proliferation and Ig secretion response of blood and tonsil lymphocytes was investigated and compared to that of the T-cell-dependent polyclonal activators pokeweed mitogen (PWM) and group A streptococcal cell membranes (A-ScM) or the T-cell-independent B cell mitogen Staphylococcus aureus Cowan I (SAC) and a T-cell-independent B cell activator Klebsiella pneumoniae (Klebs M). In blood mononuclear cells (MNC), a rather weak, monocyte-dependent DNA synthetic response was observed after exposure to TPA, in comparison to PWM, A-ScM or SAC. Whereas highly purified B cells did not respond to TPA, purified T cells proliferated to a similar degree as unseparated MNC; moreover, the addition of T to B lymphocytes enhanced proliferation rates proportionally to the number of T cells added. This suggests that TPA acts as a polyclonal T cell activator (PTA) for human blood and tonsil cells. Similarly, TPA induced only small amounts of Ig secretion in blood and in tonsil MNC, as determined by an ELISA assay, and no significant Ig secretion in highly purified B cells. The rather weak B cell differentiation response was not due to a monocyte suppressor effect, since partially monocyte-depleted MNC or B cells responded similarly to the non-depleted cells. Thus, TPA cannot be considered as an alternative to other B cells stimulators, both with regard to DNA synthesis and Ig secretion.
Phthalascidin, a synthetic antitumor agent with potency and mode of action comparable to ecteinascidin 743 (1999)

A series of totally synthetic molecules that are structurally related to the marine natural product ecteinascidin 743 (Et 743) has been prepared and evaluated as antitumor agents. The most active of these, phthalascidin, is very similar to Et 743 with regard to in vitro potency and mode of action across a variety of cell types. The antiproliferative activity of phthalascidin (IC50 = 0.1-1 nM) is greater than that of the agents Taxol, camptothecin, adriamycin, mitomycin C, cisplatin, bleomycin, and etoposide by 1-3 orders of magnitude, and the mechanism of action is clearly different from these currently used drugs. Phthalascidin and Et 743 induce DNA-protein cross-linking and, although they seem to interact with topoisomerase (topo) I (but not topo II), topo I may not be the primary protein target of these agents. Phthalascidin and Et 743 show undiminished potency in camptothecin- and etoposide-resistant cells. Phthalascidin is more readily synthesized and more stable than Et 743, which is currently undergoing clinical trials. The relationship of chemical structure and antitumor activity for this class of molecules has been clarified by this study.
Human Bone Morphogenetic Protein Allografting for Reconstruction of Femoral Nonunion (2000)

A composite inductive allograft consisting of an allogeneic, autolysed, antigen-free cortical bone carrier lyophilized with partially purified human bone morphogenetic protein was implanted in 30 consecutive femoral reconstructions that resulted from failure of fracture healing. There were 24 atrophic shortened femoral nonunions, four equal length femoral nonunions, and two femoral malunions. There were 10 men and 20 women with an average age of 47 years (range, 28-75 years). Allogeneic, autolysed antigen-free cortical bone was used as a structural alloimplant and as a delivery system for partially purified human bone morphogenetic protein. The composite implant of human bone morphogenetic protein/allogeneic, autolysed antigen-free cortical bone was used in conjunction with one-stage lengthening of the extremity, restoration of mechanical axis and rotational alignment. In 26 of 30 femurs, the human bone morphogenetic protein/allogeneic autolysed antigen-free cortical bone consisted of an allogeneic cortical bone implant incorporated into a one-stage lengthening of atrophic femoral nonunion. In four patients with equal length femoral nonunions, the human bone morphogenetic protein/allogeneic, autolysed antigen-free implant was placed as an medical femoral shaft onlay graft. Internal remodeling of the implant occurred within 8 to 12 weeks after implantation. Lengthening defects greater than 2 cm were supplemented with intercalary autogeneic bone graft. Twenty-four femurs healed at an average of 6 months at an average followup of 55 months. Four of six plate fatigue failures were salvaged with repeat plating. Two patients were lost to followup. The human bone morphogenetic protein/allogeneic, autolysed antigen-free bone allograft is an excellent structural and delivery system that induces host bone formation and implant remodeling allowing salvage of difficult femoral nonunions.
Characterization of Inhibin/Activin Subunit, Activin Receptor, and Follistatin Messenger Ribonucleic Acid in Human and Mouse Oocytes: Evidence for Activin's Paracrine Signaling from Granulosa Cells to Oocytes1 (1998)

Inhibin, activin, and follistatin (FS) are gonadal proteins that appear to have a role in regulating folliculogenesis through possible paracrine and/or autocrine interactions. To further examine the potential role of activin in oocyte-granulosa cell communication, we developed a sensitive reverse transcription-polymerase chain reaction protocol to analyze mRNA for the alpha, betaA, and betaB inhibin/activin subunits, FS, and the four activin receptor subtypes in individual human and mouse oocytes. The resulting expression pattern was further compared to that in human cumulus granulosa cells. Our results indicate that neither ssA nor betaB mRNA was detectable in any human or mouse oocyte, that alpha subunit was marginally present in some of the human oocytes, and that FS mRNA was detectable in human but not mouse oocytes. On the other hand, inhibin/activin subunit and FS mRNAs were abundantly expressed in cumulus cells. In addition, mRNAs for all four activin receptor subtypes (ActRIA, ActRIB, ActRIIA, and ActRIIB) were easily detectable in both oocytes and granulosa cells and appeared to be differentially expressed in oocytes during nuclear maturation. Finally, RNAs for both zona pellucida 3 and growth-differentiation factor-9, which were originally used as oocyte-specific markers, were detected in human but not mouse cumulus cells, although at lower levels than observed in oocytes. Taken together with previous studies, these results indicate that oocytes may be capable of responding to, but not synthesizing, activin.
Antibiotic Therapy, Endotoxin Concentration in Cerebrospinal Fluid, and Brain Edema in Experimental Escherichia coli Meningitis in Rabbits (1987)

We investigated the effect of cefotaxime and chloramphenicol on endotoxin concentrations in cerebrospinal fluid (CSF) and on the development of brain edema in rabbits with Escherichia coli meningitis. Both antibiotics were similarly effective in reducing bacterial titers. Cefotaxime, but not chloramphenicol, induced a marked increase of endotoxin in CSF, from log10 1.5 +/- 0.8 to log10 2.8 +/- 0.7 ng/ml (P less than .01). This result was associated with an increase in brain water content (405 +/- 12 g of water/100 g of dry weight compared with 389 +/- 8 g in untreated controls; P less than .01), whereas in animals treated with chloramphenicol, brain water content was identical to controls. The cefotaxime-induced increase in endotoxin concentration and brain edema were both neutralized by polymyxin B, which binds to the lipid A moiety of endotoxin, or by a monoclonal antibody to lipid A. These results indicate that treating gram-negative bacillary meningitis with selected antibiotics induces increased endotoxin concentrations in CSF that are associated with brain edema.
Hypoxia-Inducible Protein 2 ( HIG2 ), a Novel Diagnostic Marker for Renal Cell Carcinoma and Potential Target for Molecular Therapy (2005)

To identify molecules to serve as diagnostic markers for renal cell carcinoma (RCC) and as targets for novel therapeutic drugs, we investigated genome-wide expression profiles of RCCs using a cDNA microarray. We subsequently confirmed that hypoxia-inducible protein-2 (HIG2) was expressed exclusively in RCCs and fetal kidney. Induction of HIG2 cDNA into COS7 cells led to secretion of the gene product into culture medium and resulted in enhancement of cell growth. Small interfering RNA effectively inhibited expression of HIG2 in human RCC cells that endogenously expressed high levels of the protein and significantly suppressed cell growth. Moreover, addition of polyclonal anti-HIG2 antibody into culture medium induced apoptosis in RCC-derived cell lines. By binding to an extracellular domain of frizzled homologue 10 (FZD10), HIG2 protein enhanced oncogenic Wnt signaling and its own transcription, suggesting that this product is likely to function as an autocrine growth factor. ELISA analysis of clinical samples identified secretion of HIG2 protein into the plasma of RCC patients even at an early stage of tumor development, whereas it was detected at significantly lower levels in healthy volunteers or patients with chronic glomerulonephritis. The combined evidence suggests that this molecule represents a promising candidate for development of molecular-targeting therapy and could serve as a prominent diagnostic tumor marker for patients with renal carcinomas.
Fiber-based multispeckle detection for time-resolved diffusing-wave spectroscopy: characterization and application to blood flow detection in deep tissue (2007)

We present a technique for the measurement of temporal field autocorrelation functions of multiply scattered light with subsecond acquisition time. The setup is based on the parallel detection and autocorrelation of intensity fluctuations from statistically equivalent but independent speckles using a fiber bundle, an array of avalanche photodiodes, and a multichannel autocorrelator with variable integration times between 6.5 and 104 ms. Averaging the autocorrelation functions from the different speckles reduces the integration time in diffusing-wave spectroscopy experiments drastically, thus allowing us to resolve nonstationary scatterer dynamics with single-trial measurements. We present applications of the technique to the measurement of arterial and venous blood flow in deep tissue. We find strong deviations both of the shape and characteristic decay time of autocorrelation functions recorded at different phases of the pulsation cycle from time-averaged autocorrelation functions.
Photoimmunotherapy of Gastric Cancer Peritoneal Carcinomatosis in a Mouse Model (2014)

Photoimmunotherapy (PIT) is a new cancer treatment that combines the specificity of antibodies for targeting tumors with the toxicity induced by photosensitizers after exposure to near infrared (NIR) light. We performed PIT in a model of disseminated gastric cancer peritoneal carcinomatosis and monitored efficacy with in vivo GFP fluorescence imaging. In vitro and in vivo experiments were conducted with a HER2-expressing, GFP-expressing, gastric cancer cell line (N87-GFP). A conjugate comprised of a photosensitizer, IR-700, conjugated to trastuzumab (tra-IR700), followed by NIR light was used for PIT. In vitro PIT was evaluated by measuring cytotoxicity with dead staining and a decrease in GFP fluorescence. In vivo PIT was evaluated in a disseminated peritoneal carcinomatosis model and a flank xenograft using tumor volume measurements and GFP fluorescence intensity. In vivo anti-tumor effects of PIT were confirmed by significant reductions in tumor volume (at day 15, p<0.0001 vs. control) and GFP fluorescence intensity (flank model: at day 3, PIT treated vs. control p<0.01 and peritoneal disseminated model: at day 3 PIT treated vs. control, p<0.05). Cytotoxic effects in vitro were shown to be dependent on the light dose and caused necrotic cell rupture leading to GFP release and a decrease in fluorescence intensity in vitro. Thus, loss of GFP fluorescence served as a useful biomarker of cell necrosis after PIT.
Discussion: Vacuum Assisted Closure: Microdeformations of Wounds and Cell Proliferation (2004)

Chicago, Ill. Received for publication January 26, 2004. Robert F. Lohman, M.D., Department of Surgery, Section of Plastic Surgery, The University of Chicago, 5841 South Maryland Avenue, M/C 6035, Chicago, Ill. 606037, [email protected]
The biology of myeloid‐derived suppressor cells: The blessing and the curse of morphological and functional heterogeneity (2010)

Myeloid-derived suppressor cells (MDSC) play an important role in the cellular network regulating immune responses in cancer, chronic infectious diseases, autoimmunity, and in other pathological conditions. Morphological, phenotypic and functional heterogeneity is a hallmark of MDSC. This heterogeneity demonstrates the plasticity of this immune suppressive myeloid compartment, and shows how various tumors and infectious agents can have similar biological effects on myeloid cells despite the differences in the factors that they produce to influence the immune system; however, such a heterogeneity creates ambiguity in the definition of MDSC as well as confusion regarding the origin and fate of these cells. In this review, we will discuss recent findings that help to better clarify these issues and to determine the place of MDSC within the myeloid cell lineage.
Treatment of acute respiratory distress syndrome with allogeneic adipose-derived mesenchymal stem cells: a randomized, placebo-controlled pilot study (2014)

Clinical trials.gov, NCT01902082.
Molecular mechanism of lysosomal sialidase deficiency in galactosialidosis involves its rapid degradation (1998)

Galactosialidosis is an inherited lysosomal storage disease caused by the combined deficiency of lysosomal sialidase and beta-galactosidase secondary to the deficiency of cathepsin A/protective protein, which is associated with sialidase and beta-galactosidase in a high-molecular weight (1.27MDa) complex. Clinical phenotypes of patients as well as the composition of compounds which are stored in patient's tissues implicate sialidase deficiency as the underlying pathogenic defect. The recent cloning and sequencing of lysosomal sialidase [Pshezhetsky, Richard, Michaud, Igdoura, Wang, Elsliger, Qu, Leclerc, Gravel, Dallaire and Potier (1997), Nature Genet. 15, 316-320] allowed us to study the molecular mechanism of sialidase deficiency in galactosialidosis. By Western blotting, using antibodies against the recombinant human enzyme, and by NH2-terminal sequencing, we showed that sialidase is synthesized as a 45.5 kDa precursor and after the cleavage of the 47-amino acid signal peptide and glycosylation becomes a 48.3 kDa mature active enzyme present in the 1.27 kDa complex. Transgenic expression of sialidase in cultured skin fibroblasts from normal controls and from galactosialidosis patients, followed by immunofluorescent and immunoelectron microscopy showed that in both normal and affected cells the expressed sialidase was localized on lysosomal and plasma membranes, but the amount of sialidase found in galactosialidosis cells was approximately 5-fold reduced. Metabolic labelling studies demonstrated that the 48.3 kDa mature active form of sialidase was stable in normal fibroblasts (half-life approximately 2.7 h), whereas in galactosialidosis fibroblasts the enzyme was rapidly converted (half-life approximately 30 min) into 38.7 and 24 kDa catalytically inactive forms. Altogether our data provide evidence that the molecular mechanism of sialidase deficiency in galactosialidosis is associated with abnormal proteolytic cleavage and fast degradation.
Structure−Activity Relationships for a Novel Series of Pyrido[2,3-d]pyrimidine Tyrosine Kinase Inhibitors (1997)

Screening of a compound library for inhibitors of the fibroblast growth factor (FGFr) and platelet-derived growth factor (PDGFr) receptor tyrosine kinases led to the development of a novel series of ATP competitive pyrido[2,3-d]pyrimidine tyrosine kinase inhibitors. The initial lead, 1-[2-amino-6-(2,6-dichlorophenyl)pyrido[2,3-d]pyrimidin-7-yl]-3- tert-butylurea (4b, PD-089828), was found to be a broadly active tyrosine kinase inhibitor. Compound 4b inhibited the PDGFr, FGFr, EGFr, and c-src tyrosine kinases with IC50 values of 1.11, 0.13, 0.45, and 0.22 microM, respectively. Subsequent SAR studies led to the synthesis of new analogs with improved potency, solubility, and bioavailability relative to the initial lead. For example, the introduction of a [4-(diethylamino)butyl]amino side chain into the 2-position of 4b afforded compound 6c with enhanced potency and bioavailability. Compound 6c inhibited PDGF-stimulated vascular smooth muscle cell proliferation with an IC50 of 0.3 microM. Furthermore, replacement of the 6-(2,6-dichlorophenyl) moiety of 4b with a 6-(3',5'-dimethoxyphenyl) functionality produced a highly selective FGFr tyrosine kinase inhibitor 4e. Compound 4e inhibited the FGFr tyrosine kinase with an IC50 of 0.060 microM, whereas IC50s for the inhibition of the PDGFr, FGFr, EGFr, c-src, and InsR tyrosine kinases for this compound (4e) were all greater than 50 microM.
Delivery of rapamycin‐loaded nanoparticle down regulates ICAM‐1 expression and maintains an immunosuppressive profile in human CD34+ progenitor‐derived dendritic cells (2007)

Immune responses of dendritic cells (DCs) can be modulated by delivery of adjuvants to alter their maturation profile. The purpose of this study was to generate DCs from CD34(+) cells of human cord blood and characterize the effects of poly(D,L-lactic-co-glycolic acid) (PLGA)-nanoparticle encapsulated rapamycin in generating an immunosuppressive DC. Expression of ICAM-1 (intercellular adhesion molecule), a key molecule in DC-T cell interaction was increased in mature DCs in response to lipopolysaccharide (LPS). When rapamycin was encapsulated in the nanoparticle to maintain DCs in the immature state, ICAM-1 expression was down regulated. When delivered in the free form, rapamycin did not alter the expression of ICAM-1. Cytokine arrays exhibited an immunosuppressive profile of various cytokines in response to the nanoparticulate delivery of rapamycin. In addition, RT-PCR data demonstrated the presence of toll like receptor (TLR) 9 transcripts, although our DCs are myeloid in nature. In summary, our study demonstrates that DCs may be rendered immunosuppressive upon delivery of rapamycin-containing nanoparticles.
The Quantification of Fetomaternal Hemorrhage by an Enzyme‐Linked Antibody Test with Glutaraldehyde Fixation (1992)

A modified enzyme-linked antiglobulin test (ELAT) for quantifying D-positive red blood cells in the circulation of D-negative pregnant women is described. The antibody-antigen bond was stabilized and the problem of hemolysis eliminated by the use of 0.05% glutaraldehyde. The r value for the standardization curves for measuring cord RBC in mixtures was 0.98; coefficient of variation 5.8%. Reproducible quantitation of 0.125% D-positive cord RBC mixed with D-negative RBC was demonstrated. In comparative studies of artificial mixtures, Kleihauer-Betke results for more than 1% cord RBC were 50-100% greater than the true values. In several examples of large fetomaternal hemorrhages, the ELAT results matched the clinical data more closely than the Kleihauer-Betke based estimates. 2 ml of fetal RBC in a 1,600-ml red cell mass can be quantified using the modified ELAT.
Convergence of the NF‐κB and Interferon Signaling Pathways in the Regulation of Antiviral Defense and Apoptosis (2003)

The ubiquitously expressed interferon regulatory factor 3 (IRF-3) is directly activated following virus infection and functions as a key activator of the immediate-early Type 1 interferon (IFN) genes. Using DNA microarray analysis (8,556 genes) in Jurkat T cells inducibly expressing constitutively active IRF-3, several target genes directly regulated by IRF-3 were identified. Among the genes upregulated by IRF-3 were transcripts for a subset of known IFN-stimulated genes (ISGs), including ISG56, which functions as an inhibitor of translation initiation. Phosphorylation of C-terminal Ser/Thr residues--(382)GGASSLENTVDLHISNSHPLSLTSDQY(408)-is required for IRF-3 activation. Using C-terminal point mutations and a novel phosphospecific antibody, Ser396 was characterized as the minimal phosphoacceptor site required in vivo for IRF-3 activation following Sendai virus (SeV) infection, expression of viral nucleocapsid, or double-stranded RNA (dsRNA) treatment. The identity of the virus-activated kinase (VAK) activity that targets and activates IRF-3 and IRF-7 has remained a critical missing link in the understanding of interferon signaling. We report that the IKK-related kinases-IKKepsilon/TBK-1-are components of VAK that mediate IRF-3 and IRF-7 phosphorylation and thus functionally link the NF-kappaB and IRF pathways in the development of the antiviral response.
THE 1-DEOXY-D-XYLULOSE-5-PHOSPHATE PATHWAY OF ISOPRENOID BIOSYNTHESIS IN PLANTS (1999)

In plants the biosynthesis of prenyllipids and isoprenoids proceeds via two independent pathways: (a) the cytosolic classical acetate/mevalonate pathway for the biosynthesis of sterols, sesquiterpenes, triterpenoids; and (b) the alternative, non-mevalonate 1-deoxy-d-xylulose-5-phosphate (DOXP) pathway for the biosynthesis of plastidic isoprenoids, such as carotenoids, phytol (a side-chain of chlorophylls), plastoquinone-9, isoprene, mono-, and diterpenes. Both pathways form the active C5-unit isopentenyl diphosphate (IPP) as the precursor from which all other isoprenoids are formed via head-to-tail addition. This review summarizes current knowledge of the novel 1-deoxy-d-xylulose-5-phosphate (DOXP) pathway for isopentenyl diphosphate biosynthesis, apparently located in plastids. The DOXP pathway of IPP formation starts from D-glyceraldehyde-3-phosphate (GA-3-P) and pyruvate, with DOXP-synthase as the starting enzyme. This pathway provides new insight into the regulation of chloroplast metabolism.