gebhart/patrepeval huggingface dataset:
Unique Ability of Integrin αvβ3 to Support Tumor Cell Arrest under Dynamic Flow Conditions (2002)

Shear-resistant arrest of circulating tumor cells is required for metastasis from the blood stream. Arrest during blood flow can be supported by tumor cell interaction with attached, activated platelets. This is mediated by tumor cell integrin alpha(v)beta3 and cross-linking plasma protein ligands. To analyze the mechanism of tumor cell ligand interactions under dynamic flow conditions, we used real-time video microscopy and tested human melanoma cell binding to fibrinogen, von Willebrand Factor, or fibronectin matrices in a buffer perfusion system. When perfused at venous flow, melanoma cells arrested abruptly and began to spread immediately. This was uniquely mediated by integrin alpha(v)beta3 on all tested ligands, and required alpha(v)beta3 activation and actin polymerization. Under static conditions, alpha(v)beta3 cooperated with alpha(v)beta1 and alpha5beta1 in supporting melanoma cell adhesion to fibronectin. But even when activated, beta1 integrins did not contribute to melanoma cell arrest during flow. Soluble ligand served as a cross-linker between attached and circulating tumor cells and enhanced melanoma cell arrest. Cohesion of activated melanoma cells was restricted to the matrix surface and did not occur in suspension. We conclude that the presence of alpha(v)beta3 in a functionally activated state provides a unique advantage for circulating tumor cells by promoting tumor cell arrest in the presence of flow-dependent shear forces.
Thin film solar cells on glass by transfer of monocrystalline Si films (1999)

Thin film solar cells based on monocrystalline Si films are transferred to a glass superstrate. Chemical vapor deposition serves to epitaxially deposit Si on quasi‐monocrystalline Si films obtained from thermal crystallization of a double layer porous Si film on a Si wafer. A separation layer that forms during this crystallization process allows one to separate the epitaxial layer on top of the quasi‐monocrystalline film from the starting Si wafer. We presently achieve an independently confirmed solar cell conversion efficiency of 9:26%. Ray tracing studies in combination with electrical device simulation indicate an efficiency potential of around 17% using simple device processing and moderate assumptions on minority carrier lifetime and surface recombination.
Shotgun Protein Sequencing with Meta-contig Assembly (2012)

Full-length de novo sequencing from tandem mass (MS/MS) spectra of unknown proteins such as antibodies or proteins from organisms with unsequenced genomes remains a challenging open problem. Conventional algorithms designed to individually sequence each MS/MS spectrum are limited by incomplete peptide fragmentation or low signal to noise ratios and tend to result in short de novo sequences at low sequencing accuracy. Our shotgun protein sequencing (SPS) approach was developed to ameliorate these limitations by first finding groups of unidentified spectra from the same peptides (contigs) and then deriving a consensus de novo sequence for each assembled set of spectra (contig sequences). But whereas SPS enables much more accurate reconstruction of de novo sequences longer than can be recovered from individual MS/MS spectra, it still requires error-tolerant matching to homologous proteins to group smaller contig sequences into full-length protein sequences, thus limiting its effectiveness on sequences from poorly annotated proteins. Using low and high resolution CID and high resolution HCD MS/MS spectra, we address this limitation with a Meta-SPS algorithm designed to overlap and further assemble SPS contigs into Meta-SPS de novo contig sequences extending as long as 100 amino acids at over 97% accuracy without requiring any knowledge of homologous protein sequences. We demonstrate Meta-SPS using distinct MS/MS data sets obtained with separate enzymatic digestions and discuss how the remaining de novo sequencing limitations relate to MS/MS acquisition settings.
Flow sorting of X and Y chromosome‐bearing spermatozoa into two populations (1987)

The only established difference on which to base the separation of X and Y chromosome-bearing spermatozoa is chromosomal constitution. This difference is quantifiable both from chromosome morphology (karyotype) and from DNA content. Flow cytometric techniques were used to measure relative DNA content of the X and Y populations and to flow-sort spermatozoa from Chinchilla laniger. Epididymal spermatozoa were recovered in PBS, fixed in 80% ethanol, treated with papain and dithioerythritol, and stained for DNA with Hoechst 33342. Sperm nuclei were analyzed and sorted on an EPICS V flow cytometer/cell sorter, modified specifically for spermatozoa. Two clearly resolved peaks (coefficient of variation less than 1.5%) with approximately 7.5% difference in DNA content between X and Y chromosome-bearing spermatozoa were evident. Sperm nuclei were sorted from a portion of the X and Y peaks at a rate of 55 nuclei/sec for each population. Purities of individual X and Y populations averaged 95% as determined by reanalysis of the sorted populations. Successful sorting of Chinchilla X and Y chromosome-bearing spermatozoa into separate populations may aid in the identification of a biochemical marker that could be used to discriminate between the two sperm populations and lead to a practical procedure for sexing spermatozoa.
Polarimetric imaging of uterine cervix: a case study (2013)

We present a preliminary investigation of macroscopic polarimetric imaging of uterine cervix. Orthogonal state contrast (OSC) images of healthy and anomalous cervices have been taken in vivo at 550 nm. Four ex vivo cervix samples have been studied in full Muller polarimetry, at 550 nm and 700 nm, and characterized in detail by standard pathology. One sample was totally healthy, another one carried CIN lesions at very early stage (CIN1) in its visible exocervical region, while for the other two samples more advanced (CIN3) lesions were present, together with visible glandular epithelium (ectropion). Significant birefringence has been observed in the healthy regions of all six samples, both in vivo and ex vivo. Standard treatments of the Mueller images of the ex vivo samples allowed to quantify both retardation and depolarization. Retardation reached 60° in healthy regions, and disappeared in the anomalous regions of the other three ex vivo samples. The depolarization power was largest in healthy regions, and lower in CINs and ectropion. Possible origins of the observed effects are briefly discussed.
In vivo friction properties of human skin (1999)

In vivo frictional properties of human skin and five materials, namely aluminium, nylon, silicone, cotton sock, Pelite, were investigated. Normal and untreated skin over six anatomic regions of ten normal subjects were measured under a controlled environment. The average coefficient of friction for all measurements is 0.46+/-0.15 (p<0.05). Among all measured sites, the palm of the hand has the highest coefficient of friction (0.62+/-0.22). For all the materials tested, silicone has the highest coefficient of friction (0.61+/-0.21), while nylon has the lowest friction (0.37+/-0.09).
Phase I/II study of novel HLA-A24 restricted DEPDC1 and MPHOSPH1 peptide vaccine for bladder cancer. (2010)

e13122 Background: We had previously reported that M-phase phosphoprotein 1 (MPHOSPH1) and DEP domain containing 1 (DEPDC1) were identified as oncogenes by genome-wide expression profile analysis of bladder cancer by cDNA microarray. We also identified that MPHOSPH1 and DEPDC1 derived epitope peptides, which induce specific cytotoxic T lymphocytes (CTL) against bladder cancer expressing MPHOSPH1 and DEPDC1 in HLA-A24 restricted fashion. We conducted a phase I/II study of a vaccine treatment using these novel peptides and assessed both the safety and efficacy for patients with advanced bladder cancer. Methods: The main eligibility criteria was advanced bladder cancer patients who already resistant to the standard chemotherapies or radiotherapy, having HLA-A*2402 genotype and expression of MPHOSPH1 or DEPDC1 on tumor tissues by immunohistochemistry. MPHOSPH1-278 (IYNEYIYDL) and/or DEPDC1-294 (EYYELFVNI) peptides (each of 1mg/body) were subcutaneously injected with Montanide ISA 51 adjuvant. Patients were vaccinated on day 1, 8, 15, and 22 of each 28-day treatment cycles. The primary endpoint was evaluation of safety and the secondary end points were immunological and clinical response. Results: Six patients were enrolled in phase I part. Vaccinations were well tolerated without serious adverse events. Inductions of antigen-specific CTL response were recognized in four out of six patients. A total of 15 patients were enrolled in the phase I/II study. One patient with multiple lung metastasis and another two patients with bladder invasion showed objective response with necrosis in image analysis. The clinical and immunological reaction was recognized for synchronization. Six patients showed stable disease for more than 4 months. Conclusions: Our experience data suggest that novel MPHOSPH1 and DEPDC1 epitope peptide vaccine treatment is tolerable and may be an effective for patients with bladder cancer. As the next study, peptide vaccine against recurrence prevention after TUR for non-muscle-invasive bladder cancer is now in progress. No significant financial relationships to disclose.
Mast cell involvement in normal human skin wound healing: expression of monocyte chemoattractant protein-1 is correlated with recruitment of mast cells which synthesize interleukin-4in vivo (2000)

Mast cells (MCs) are known as key cells of immediate type hypersensitivity reactions. It has recently been shown that MCs regulate fibroblast proliferation by heterotypic cell-cell contact and secretion of interleukin-4 (IL-4) in vitro. It was therefore hypothesized that MCs may contribute to wound repair in vivo. Using immunohistology and in situ hybridization, the time course of mast cell recruitment and the expression of MC-attractant chemokines were analysed in a human skin wound-healing model, and the production of IL-4 by MCs in vivo was investigated. The data obtained indicate that the five-fold increase of the tryptase+ MCs at the fibrotic border of the wound within the first 10 days is the result of increased recruitment/survival of MCs or MC precursors, but not of increased local proliferation. Recruitment of MCs is paralleled by the expression of monocyte chemoattractant protein-1 (MCP-1), but not by other chemokines such as RANTES (regulated on activation, normal T cell expressed and secreted) and/or MIP (macrophage inflammatory protein)-1alpha/beta. Notably, 60-70% of MCs exhibited strong and selective IL-4 immunoreactivity, whereas other resident and passenger cells were rather quiescent. The data suggest that MC contribute significantly to the cytokine network of wound repair via MC-derived IL-4 and stimulation of fibroblast proliferation.
Antitumor Activity and Its Properties of Eubacterium lentum (1988)

In the present study, some basic effects of Eubacterium lentum (TYH-11), isolated from normal intestinal flora, upon the immune system and various experimental tumor cell lines were investigated. E. lentum showed no direct cytotoxicity against Ehrlich ascites tumor, while Serratia marcescens (TY-142) did show direct cytotoxicity. E. lentum presented striking antitumor activity which differed according to the injection route and time. This strain showed antitumor activity against 11 experimental tumor cell lines including Ehrlich ascites tumor, Meth-A, etc., but not against EL4 or Lewis lung carcinoma. The antitumor activity in this strain was recognized to lie in the cell wall and granular fractions. The effect of this strain on the immune system was studied by using plaque formation and the footpad reaction. When mice received 5 injections of E. lentum, the plaque number increased to treble the control level. Spleen weight was also increased following administration of E. lentum. In normal and tumor-bearing mice immunized with SRBC alone, the footpad reaction was increased significantly to the control level by administration of E. lentum.
Physiological Functions of Glucocorticoids in Stress and Their Relation to Pharmacological Actions* (1984)

Almost any kind of threat to homeostasis or stress will cause plasma glucocorticoid levels to rise. The increased levels have traditionally been ascribed the physiological function of enhancing the organism's resistance to stress, a role well recognized in glucocorticoid therapy. How the known physiological and pharmacological effects of glucocorticoids might accomplish this function, however, remains a mystery. A generalization that is beginning to emerge is that many of these effects may be secondary to modulation by glucocorticoids of the actions of numerous intercellular mediators, including established hormones, prostaglandins and other arachidonic acid metabolites, certain secreted neutral proteinases, lymphokines, and a variety of bioactive peptides. These mediators participate in physiological mechanisms--endocrine, renal, immune, neural, etc.--that mount a first line of defense against such challenges to homeostasis as hemorrhage, metabolic disturbances, infection, anxiety, and others. Contrary to the traditional view that glucocorticoids enhance these defense mechanisms, however, it has become increasingly clear that glucocorticoids at moderate to high levels generally suppress them. This paradox, which first emerged when glucocorticoids were discovered to be antiinflammatory agents, remains a major obstacle to a unified picture of glucocorticoid function. We propose that stress-induced increases in glucocorticoid levels protect not against the source of stress itself but rather against the body's normal reactions to stress, preventing those reactions from overshooting and themselves threatening homeostasis. This hypothesis, the seeds of which are to be found in many discussions of particular glucocorticoid effects, immediately accounts for the paradox noted above. Furthermore, it provides glucocorticoid physiology with a unified conceptual framework that can accommodate such apparently unrelated physiological and pharmacological effects as those on carbohydrate metabolism, inflammatory processes, shock, and water balance. It also leads us to suggest that some of the enzymes rapidly induced by glucocorticoids, such as glutamine synthetase, detoxify mediators released during stress-induced activation of primary defense mechanisms. These mediators would themselves lead to tissue damage if left unchecked.
Molecular Approaches towards the Inhibition of the Signal Transducer and Activator of Transcription 3 (Stat3) Protein (2008)

Molecular approaches towards Stat3 inhibition: Stat3 inhibition represents an exciting new approach to the treatment of cancer. The advances in the direct molecular inhibition of Stat3 are highlighted through discussion of the various inhibitors currently under investigation, including peptide sequences, peptidomimetics, small molecules and platinum-based agents.
A potent inhibitor of endothelial cell proliferation is generated by proteolytic cleavage of the chemokine platelet factor 4. (1995)

Platelet factor 4 (PF-4) is an archetype of the "chemokine" family of low molecular weight proteins that play an important role in injury responses and inflammation. From activated human leukocyte culture supernatants, we have isolated a form of PF-4 that acts as a potent inhibitor of endothelial cell proliferation. The PF-4 derivative is generated by peptide bond cleavage between Thr-16 and Ser-17, a site located downstream from the highly conserved and structurally important CXC motif. The unique cleavage leads to a loss of one of the structurally important large loops in the PF-4 molecule and generation of an N terminus with basic residues that have the potential to interact with the acidic extracellular domain of the G-protein-coupled chemokine receptor. The N-terminal processed PF-4 exhibited a 30- to 50-fold greater growth inhibitory activity on endothelial cells than PF-4. Since endothelial cell growth inhibition is the only known cellular activity of the cleaved PF-4, we have designated this chemokine endothelial cell growth inhibitor. The N-terminal processing of PF-4 may represent an important mechanism for modulating PF-4 activity on endothelial cells during tissue injury, inflammation, and neoplasia.
Discrimination between Bacillus cereus and Bacillus thuringiensis using specific DNA probes based on variable regions of 16S rRNA (2006)

Identification of Bacillus cereus and differentiation between B. cereus and closely related species are currently based on biochemical tests. The main problem is to discriminate between B. cereus and B. thuringiensis. Sequencing part of the 16S rRNA showed that several B. cereus isolates present in food and involved in food poisoning, confirmed according to the classical biochemical methods, were in fact B. thuringiensis. As this organism is the most commonly used microbial insecticide worldwide, the results of this study emphasize the need for accurate identification methods and for careful screening of strains for use as insecticides. Therefore, specific DNA probes based on the variable region VI of 16S rRNA of B. cereus and B. thuringiensis were designed. The probes were used in hybridization experiments with the variable region amplified using the polymerase chain reaction. In this way, a rapid and sensitive method was developed to distinguish B. cereus and B. thuringiensis.
Detection of Rifampin Resistance in Mycobacterium tuberculosis in a Single Tube with Molecular Beacons (2001)

Current clinical assays for determining antibiotic susceptibility in Mycobacterium tuberculosis require many weeks to complete due to the slow growth of the bacilli. Here we demonstrate an extremely sensitive single-tube PCR assay that takes less than 3 h and reliably identifies rifampin-resistant M. tuberculosis in DNA extracted directly from sputum. Ninety-five percent of mutations associated with rifampin resistance occur in an 81-bp core region of the bacterial RNA polymerase gene, rpoB. All mutations that occur within this region result in rifampin resistance. The assay uses novel nucleic acid hybridization probes called molecular beacons. Five different probes are used in the same reaction, each perfectly complementary to a different target sequence within the rpoB gene of rifampin-susceptible bacilli and each labeled with a differently colored fluorophore. Together, their target sequences encompass the entire core region. The generation of all five fluorescent colors during PCR amplification indicates that rifampin-susceptible M. tuberculosis is present. The presence of any mutation in the core region prevents the binding of one of the molecular beacons, resulting in the absence of one of the five fluorescent colors. When 148 M. tuberculosis clinical isolates of known susceptibility to rifampin were tested, mutations associated with rifampin resistance were detected in 63 of the 65 rifampin-resistant isolates, and no mutations were found in any of the 83 rifampin-susceptible isolates. When DNA extracted directly from the sputum of 11 patients infected with rifampin-resistant tuberculosis was tested, mutations were detected in all of the samples. The use of this rapid assay should enable early detection and treatment of drug-resistant tuberculosis in clinical settings.
Furano compounds. XX. Synthesis of angular and linear furoxanthones (1972)

Abstract The three isomeric furoxanthones viz. 4‐methoxy‐2‐methyl‐5‐H‐furo[3,2‐b]xanthen‐5‐one 11 , 4‐methoxy‐2‐methyl‐11‐H‐furo [2,3‐a]xanthen‐11‐one 16 and 5‐methoxy‐2‐methyl‐6‐H‐furo[2,3‐c]‐xanthen‐6‐one 23 have been synthesised starting with 1,3‐dihydroxy xanthone and building a furan ring on the 2:3, 1:2, and 3:4 positions respectively after partial tosylation of the 3‐hydroxyl and following the sequence of reactions: allylation, C LAISEN rearrangement, acetylation, bromine addition and dehydrobromination with appropriate modification, viz. methylation and detosylation in the sequence depending on the individual case.
Phospholipid membrane permeability of peptide nucleic acid (1995)

Phospholipid vesicles (liposomes) as membrane models have been used to study the penetration properties of peptide nucleic acid (PNA), a new DNA analog in which the nucleobases are attached to a pseudo-peptide backbone. The liposomes were characterised by carboxyfluorescein efflux, light-scattering and cryogenic transmission electron microscopy. The liposome structure was found not to be affected by the incorporation of PNA or an oligonucleotide. Two 10-mer fluorescein-labelled PNAs were found to have low efflux rates (half-times of 5.5 and 11 days), comparable to that of a 10-mer oligonucleotide (half-time of 7 days). We conclude that passive diffusion of unmodified PNA over the lipid membrane is not likely to be an effective way of transport into biological cells.
Tyrosine phosphorylation and activation of JAK family tyrosine kinases by interleukin-9 in MO7E cells (1995)

Interleukin-9 (IL-9) is a T-cell-derived multifunctional cytokine that can stimulate the proliferation of a human megakaryocytic leukemia cell line, MO7E. Previous studies suggested that protein tyrosine phosphorylation may be involved in IL-9 signaling pathways. However, tyrosine kinases activated by IL-9 have not been identified. In this report we show that IL-9 induces tyrosine phosphorylation and activation of the JAK family tyrosine kinases including JAK1, JAK3, and Tyk2. The kinetic studies indicate that tyrosine phosphorylation and activation of JAK kinases induced by IL-9 occurred within 1 minute, peaked by 5 to 10 minutes, and persisted at least for 45 minutes. Furthermore, we show that signal transducers and activators of transcription (Stat) 91 or related protein and an 88-kD Stat 91-associated protein are rapidly tyrosine phosphorylated following IL-9 treatment. Gel shift assays confirm that nuclear extracts from MO7E cells stimulated with IL-9 specifically interact with a DNA element termed gamma activated site. These results suggest that actions of IL-9 may, in part, be mediated through JAK kinase-Stat signaling cascades.
Aggressive inherited and sporadic medullary thyroid carcinomas display similar oncogenic pathways (2009)

RET oncogene mutations are found in familial medullary thyroid carcinomas (MTC) and in one-third of sporadic cases. Oncogenic mechanisms involved in non-RET mutated sporadic MTC remain unclear. To study alterations associated with the development of both inherited and sporadic MTC, pangenomic DNA microarrays were used to analyze the transcriptome of 13 MTCs (four familial and nine sporadic). By using an ANOVA test, a list of 173 gene sequences with at least a twofold change expression was obtained. A subset of differentially expressed genes was controlled by real-time quantitative PCR and immunohistochemistry on a larger collection of MTCs. The expression pattern of those genes allowed us to distinguish two groups of sporadic tumors. The first group displays an expression profile similar to that expressed by inherited RET634 tumors. The second presents an expression profile close to that displayed by inherited RET918 tumors and includes tumors from patients with distant metastases. It is characterized by the overexpression of genes involved in proliferation and invasion (PTN, ESM1, and CEACAM6) or matrix remodeling (COL1A1, COL1A2, and FAP). Interestingly, RET918 tumors showed overexpression of the PTN gene, encoding pleiotrophin, a protein associated with metastasis. Using a MTC cell line, silencing of RET induced the inhibition of PTN gene expression. Overall, our results suggest that familial MTC and sporadic MTC could activate similar oncogenic pathways.