gebhart/patrepeval huggingface dataset:
Homeodomain‐containing protein HOXB9 regulates expression of growth and angiogenic factors, facilitates tumor growth in vitro and is overexpressed in breast cancer tissue (2012)

HOXB9 is a homeobox-containing gene and is critical for the development of mammary gland and sternum. HOXB9 is also regulated by estrogen and is critical for angiogenesis. We investigated the biochemical roles of HOXB9 and its homeodomain in cell-cycle progression and tumorigenesis. Our studies demonstrated that HOXB9 is overexpressed in breast cancer tissue. HOXB9 overexpression stimulated 3D formation in soft agar assay. HOXB9 binds to the promoters of various tumor growth and angiogenic factors and regulates their expression. The homeodomain of HOXB9 plays crucial roles in transcriptional regulation of tumor growth factors and also in 3D colony formation, indicating crucial roles of the HOXB9 homeodomain in tumorigenesis. Overall, we demonstrated that HOXB9 is a critical regulator of tumor growth factors and is associated with tumorigenesis.
Review of current classifications for diverticular disease and a translation into clinical practice (2011)

A three-stage model is advanced for a renewed and comprehensive classification system for diverticular disease, incorporating up-to-date imaging and treatment modalities.
Progress and Challenges in AAV-Mediated Gene Therapy for Duchenne Muscular Dystrophy (2011)

Duchenne muscular dystrophy (DMD) is the most common form of childhood muscular dystrophy. DMD is an X-linked recessive disorder with an incidence of one in 3500 live male births (Emery, 1991). DMD causes progressive degeneration and regeneration of skeletal and cardiac muscles due to mutations in the dystrophin gene, which encodes a 427-kDa subsarcolemmal cytoskeletal protein (Hoffman et al., 1987). DMD is associated with severe, progressive muscle weakness and typically leads to death between the ages of 20 and 35 years. Due to recent advances in respiratory care, much attention is now focused on treating the cardiac conditions suffered by DMD patients.
Siderophore Peptide, a New Type of Post-translationally Modified Antibacterial Peptide with Potent Activity (2004)

Microcin E492 (MccE492, 7886 Da), the 84-amino acid antimicrobial peptide from Klebsiella pneumoniae, was purified in a post-translationally modified form, MccE492m (8717 Da), from culture supernatants of either the recombinant Escherichia coli VCS257 strain harboring the pJAM229 plasmid or the K. pneumoniae RYC492 strain. Chymotrypsin digestion of MccE492m led to the MccE492m-(74-84) C-terminal fragment that carries the modification and that was analyzed by mass spectrometry and nuclear magnetic resonance at natural abundance. The 831-Da post-translational modification consists of a trimer of N-(2,3-dihydroxybenzoyl)-l-serine linked via a C-glycosidic linkage to a beta-d-glucose moiety, itself linked to the MccE492m Ser-84-carboxyl through an O-glycosidic bond. This modification, which mimics a catechol-type siderophore, was shown to bind ferric ions by analysis of the collision-induced dissociation pattern obtained for MccE492m-(74-84) by electrospray ion trap mass spectrometry experiments in the presence of FeCl(3). By using a series of wild-type and mutant isogenic strains, the three catechol-type siderophore receptors Fiu, Cir, and FepA were shown to be responsible for the recognition of MccE492m at the outer membrane of sensitive bacteria. Because MccE492m shows a broader spectrum of antibacterial activity and is more potent than MccE492, we propose that by increasing the microcin/receptor affinity, the modification leads to a better recognition and subsequently to a higher antimicrobial activity of the microcin. Therefore, MccE492m is the first member of a new class of antimicrobial peptides carrying a siderophore-like post-translational modification and showing potent activity, which we term siderophore-peptides.
p27Kip1 in Stage III Colon Cancer: Implications for Outcome following Adjuvant Chemotherapy in Cancer and Leukemia Group B Protocol 89803 (2009)

Loss of p27 is associated with reduced survival in stage III colon cancer but by itself does not indicate a significant difference in outcome between patients treated IFL or 5-fluorouracil/leucovorin.
Overexpression of the oncogenic kinase Pim-1 leads to genomic instability. (2003)

Aneuploidy and chromosomal aberrations are hallmarks of most human epithelial malignancies. Here we show that overexpression of the oncogenic kinase Pim-1 in human prostate epithelial cells induces genomic instability by subverting the mitotic spindle checkpoint. Cells overexpressing Pim-1 have a defect in the mitotic spindle checkpoint, abnormal mitotic spindles, centrosome amplification, and chromosome missegregation. Polyploidy and aneuploidy ensue due to a delay in completing cytokinesis. These results define a novel role for elevated Pim-1 expression in promoting genomic instability in human prostate tumors.
IL-22, in contrast to IL-10, does not induce Ig production, due to absence of a functional IL-22 receptor on activated human B cells (2002)

IL-22 is an IL-10 homologue that binds to and signals via the class II cytokine receptor (R) heterodimer IL-22RA1/CFR2-4 (IL-10R2), the latter chain being part of the IL-10R complex. Here, we report that, despite its structural similarity with IL-10, as well as its use of the common IL-10R2 chain, IL-22, in contrast to IL-10, is unable to induce Ig production by activated human B cells. Whereas culture of anti-CD40 mAb-stimulated splenic or tonsillar B cells in the presence of rIL-10 resulted in the production of IgG, IgG1, IgG3 and IgA, rIL-22, at concentrations ranging from 4 to 100 ng/ml, did not induce the production of any of these isotypes. Moreover, unlike rIL-10 which enhanced rIL-4-induced IgG4 and IgE production, rIL-22 was ineffective. Although activated B cells expressed transcripts for a soluble IL-22-binding protein (IL-22RA2), no mRNA for a transmembrane IL-22R (IL-22RA1) could be detected. The latter result was confirmed by the demonstration that rIL-22 failed to induce activation of STAT-3 and -5 in resting or activated B cells. Together, these data show that IL-22, in contrast to its homologue IL-10, is not involved in the immunological activity of B cells, which is due to the absence of a functional IL-22R at the surface of these cells.
Prorenin Receptor Is Essential for Podocyte Autophagy and Survival (2011)

The prorenin receptor (PRR) is highly expressed in podocytes, but its role in the maintenance of podocyte function is unknown. Here we generated podocyte-specific PRR-knockout mice and found that these animals died between 2 to 3 wk after birth. Within 14 d, PRR-knockout mice developed nephrotic syndrome, albuminuria with podocyte foot-process fusion, and cytoskeletal changes. Podocyte-specific PRR deletion also led to disturbed processing of multivesicular bodies and enrichment of autophagosomal (LC3) and lysosomal (LAMP2) markers, indicating a functional block in autophagosome-lysosome fusion and an overload of the proteasomal protein-degradation machinery. In vitro, PRR knockdown and pharmacologic blockade of vacuolar H(+)-ATPases, which associate with the PRR, increased vesicular pH, led to accumulation of LC3-positive and LAMP2-positive vesicles and altered the cytoskeleton. Taken together, these results suggest that the PRR is essential for podocyte function and survival by maintaining autophagy and protein-turnover machinery. Furthermore, PRR contributes to the control of lysosomal pH, which is important for podocyte survival and cytoskeletal integrity.
Rethinking Data Management for Storage-centric Sensor Networks. (2007)

Enamel is the structure that covers the entire clinical crown of a tooth. It enables to chew and crush food, and gives a final shape to the crowns of teeth. To evaluate calcium and magnesium contents in tooth enamel and analyse relationships between the study minerals extracted human permanent teeth were cut at every 150 microns and subjected into acid biopsy. The amounts of calcium and magnesium were assessed in the laboratory using atomic absorption spectroscopy with an air/acetylene flame. The lowest calcium and magnesium contents were found on the enamel surface of the teeth. Statistically significant correlation between the calcium and magnesium concentrations was found at a depth between 150 and 900 µm. Calcium and magnesium contents increased with increasing enamel depth. Calcium and magnesium deposits appeared to be stable through all the enamel layers studied. It would be suggested that mineralization/demineralization affect only external layer of the enamel, whereas deeper layers are not affected by these processes.
Effect of fatty acids on endothelium-dependent relaxation in the rabbit aorta (2006)

The metabolic syndrome, Type II (non-insulin-dependent) diabetes and obesity are associated with endothelial dysfunction and increased plasma concentrations of NEFAs (non-esterified fatty acids; free fatty acids). The present study was undertaken to define the inhibitory effects of saturated NEFAs on EDR (endothelium-dependent relaxation). Experiments were performed in rings of rabbit aorta to establish (i) dose-response relationships, (ii) the effect of chain length, (iii) the effect of the presence of double bonds, (iv) reversibility and time course of inhibition, and (v) the effect on nitric oxide production. Aortic rings were incubated (1 h) with NEFA-albumin complexes derived from lauric (C(12:0)), myristic (C(14:0)), palmitic (C(16:0)), stearic (C(18:0)) and linolenic (C(18:3)) acids. EDR induced by acetylcholine (0.1-10 mumol/l) was measured after pre-contraction with noradrenaline. Inhibition of EDR was dose-dependent (0.5-2 mmol/l NEFA), and the greatest inhibition (51%) was observed with stearic acid (2 mmol/l). Lauric acid had the smallest inhibitory effect. The inhibitory effects were always reversible and were evident after 15 min of incubation. Linolenic acid caused a significantly lower inhibition of EDR than stearic acid. SOD (superoxide dismutase) restored the inhibitory effect caused by NEFAs, suggesting the involvement of ROS (reactive oxygen species) in removing nitric oxide. The nitric oxide concentration measured after exposure of the rings to acetylcholine was lower after incubation with NEFAs than with Krebs buffer alone. This finding is consistent with removal of nitric oxide by ROS. This claim was supported by the demonstration of increased concentrations of nitrated tyrosine in the rings incubated with NEFAs.
Circulating Epstein–Barr Virus in Children Living in Malaria‐Endemic Areas (2005)

Children living in malaria-endemic regions have high incidence of Burkitt's lymphoma (BL), the aetiology of which involves Plasmodium falciparum malaria and Epstein-Barr virus (EBV) infections. Acute malarial infection impairs the EBV-specific immune responses with the consequent increase in the number of EBV-carrying B cells in the circulation. To further understand the potential influence of malarial infection on the EBV persistence in children living in malaria-endemic areas, we studied the occurrence and quantified cell-free EBV-DNA in plasma from 73 Ghanaian children with and without acute malarial infection. Viral DNA was detected in 40% of the samples (47% in the malaria-infected and 34% in the nonmalaria group) but was absent in plasma from Ghanaian adults and healthy Italian children. These findings provide evidence that viral reactivation is common among children living in malaria-endemic areas, and may contribute to the increased risk for endemic BL. The data also suggest that the epidemiology of EBV infection and persistence varies in different areas of the world.
Regulation of Sodium-Dependent Phosphate Transport by Parathyroid Hormone in Opossum Kidney Cells: Adenosine 3 ′,5 ′-Monophosphate-Dependent and -Independent Mechanisms* (1988)

The hormonal regulation of Na+-dependent phosphate transport was studied in opossum kidney (OK) cells. PTH caused time- and concentration-dependent decreases in Na+-dependent phosphate transport, with 10 pM PTH-(1-34) producing a 19% decline in phosphate transport. The EC50 for PTH inhibition of phosphate transport was 50 pM. Kinetic analyses of phosphate transport indicated that PTH decreased the maximum velocity without affecting the Km for phosphate. PTH increased cAMP formation with an EC50 of 10 nM. 8-Bromo-cAMP and (Bu)2cAMP also inhibited phosphate transport. Forskolin increased cAMP formation and decreased phosphate transport, whereas the cyclase-inactive forskolin analog 1,9-dideoxyforskolin also inhibited phosphate transport. The PTH analog [8,18-norleucine,34-tyrosinamide]PTH-(3-34) reduced phosphate transport at concentrations from 10 nM to 30 microM, but did not increase cAMP formation at concentrations up to 10 microM. The adenylate cyclase inhibitor 2',5'-dideoxyadenosine produced concentration-dependent decreases in PTH-stimulated cAMP formation, but did not influence PTH inhibition of Na+-dependent phosphate transport. Vasoactive intestinal polypeptide and prostaglandin E1 increased cAMP formation in OK cells, but were weak inhibitors of phosphate transport. This study suggests that cAMP may not be the only transmembrane signaling mechanism involved in the regulation of Na+-dependent phosphate transport by PTH-(1-34) in OK cells.
Reversing Quantum Trajectories with Analog Feedback (2014)

We demonstrate the active suppression of transmon qubit dephasing induced by dispersive measurement, using parametric amplification and analog feedback. By real-time processing of the homodyne record, the feedback controller reverts the stochastic quantum phase kick imparted by the measurement on the qubit. The feedback operation matches a model of quantum trajectories with a measurement efficiency 0.5, consistent with the result obtained by postselection. We overcome the bandwidth limitations of the amplification chain by numerically optimizing the signal processing in the feedback loop and provide a theoretical model explaining the optimization result.
Clinical Cancer Research: The Next Decade (2005)

Ten years ago, Dr. John Mendelsohn and a talented editorial board set out to develop for AACR a journal that would offer a bridge between the important work being done in the laboratory and the pressing need of oncologists for up-to-the-minute information. By all measures of excellence, Clinical Cancer Research has succeeded beyond the original expectations of all involved. The journal has published many high-quality articles, and its impact factor puts it in the top tier of oncology journals. It has been my privilege to serve as Co-Deputy Editor with Dr. Waun Ki Hong.I now take on a new role for this important and prestigious journal. The thought of receiving the baton from the distinguished physician/scientists who brought the journal to this point is humbling, indeed. As the new Editor-in-Chief, I have assembled a group of notable Deputy Editors and Senior Editors and together we have defined a set of operating principles for Clinical Cancer Research:“CCR is responsible to its readers, contributors, and parent organization for the timely publication of information that will have major impact on the prevention, diagnosis, and treatment of cancer.If we remain true to these principles, our journal will continuously improve and make important contributions to the eradication of cancer.”At a recent editorial retreat of the Clinical Cancer Research editors, we unanimously approved two significant changes: You will also notice a change in the format of the Table of Contents. It has been redesigned to help readers quickly identify articles within their areas of interest. Major headings now include Cancer Prevention; Cancer Therapy; Imaging, Diagnosis, and Prognosis; and Human Cancer Biology. We also plan to introduce icons denoting pathways, modalities, or organ sites. We look forward to publishing your opinions expressed in Letters to the Editor or Brief Editorials on pressing topics.lThe Editors have instituted a formal nominating process for our editorial board to continuously refresh our reviewers and editorial content. We will continue to seek opportunities to publish supplements that address major topics in clinical/translational research. All supplements go through the same review process as submitted manuscripts.I thank the Publications Committee and the Board of Directors of the AACR for giving me this extraordinary opportunity. I look forward to your contributions and to hearing your opinions.
Real‐time Detection of Nucleotide Incorporation During Complementary DNA Strand Synthesis (2003)

Real-time observation of DNA strand synthesis by using a supercritical angle fluorescence detection apparatus for surface-selective fluorescence detection is described. DNA template molecules were immobilized on a glass surface and the synthesis of the complementary strand was observed after addition of enzyme, dTTP, dATP, dGTP, and fluorescently labeled dCTP (d, deoxy; TP, triphosphate; T, A, G, and C, nucleobases). The fluorescence increase during the Klenow-fragment-catalyzed polymerization depends on the number of labeled dCTP nucleotides incorporated. The efficiency of this reaction is of the same order of magnitude as that of a bimolecular hybridization reaction.
Phase 2 enzyme inducer sulphoraphane blocks prostaglandin and nitric oxide synthesis in human articular chondrocytes and inhibits cartilage matrix degradation (2012)

SFN inhibited a broad range of catabolic mechanisms in articular chondrocytes. SFN may be a safe and effective candidate drug for the inhibition of cartilage degradation in arthritic diseases.
Signaling pathways initiated by β-hydroxy-β-methylbutyrate to attenuate the depression of protein synthesis in skeletal muscle in response to cachectic stimuli (2007)

To investigate the mechanism by which beta-hydroxy-beta-methylbutyrate (HMB) attenuates the depression of protein synthesis in the skeletal muscle of cachectic mice, a study has been carried out in murine myotubes in the presence of proteolysis-inducing factor (PIF). PIF inhibited protein synthesis by 50% within 4 h, and this was effectively attenuated by HMB (25-50 muM). HMB (50 muM) alone stimulated protein synthesis, and this was attenuated by rapamycin (27 nM), an inhibitor of mammalian target of rapamycin (mTOR). Further evidence for an involvement of this pathway was shown by an increased phosphorylation of mTOR, the 70-kDa ribosomal S6 kinase (p70(S6k)), and initiation factor 4E-binding protein (4E-BP1) and an increased association of eukaryotic initiation factor 2 (eIF4E) with eIF4G. PIF alone induced a transient (1-2 h) stimulation of phosphorylation of mTOR and p70(S6k). However, in the presence of HMB, phosphorylation of mTOR, p70(S6k), and 4E-BP1 was increased, and inactive 4E-BP1-eIF4E complex was reduced, whereas the active eIF4G.eIF4E complex was increased, suggesting continual stimulation of protein synthesis. HMB alone reduced phosphorylation of elongation factor 2, but this effect was not seen in the presence of PIF. PIF induced autophosphorylation of the double-strand RNA-dependent protein kinase (PKR), leading to phosphorylation of eIF2 on the alpha-subunit, which would inhibit protein synthesis. However, in the presence of HMB, phosphorylation of PKR and eIF2alpha was attenuated, and this was also observed in skeletal muscle of cachectic mice administered HMB (0.25 g/kg). These results suggest that HMB attenuates the depression of protein synthesis by PIF in myotubes through multiple mechanisms.
Challenges facing islet transplantation for the treatment of type 1 diabetes mellitus (2004)

Islet transplantation represents a most impressive recent advance in the search for a type 1 diabetes mellitus cure. While several hundred patients have achieved at least temporary insulin independence after receiving the islet “mini-organs” (containing insulin-producing β cells), very few patients remain insulin independent beyond 4 years after transplantation. In this review, we describe historic as well as technical details about the procedure and provide insight into clinical and basic research efforts to overcome existing hurdles for this promising therapy.
TGF-beta: problems and prospects. (1990)

TGF-beta research is proceeding at an exponential pace. Studies in this area have become increasingly relevant to many areas of cell regulation, continually providing new surprises and findings. One may confidently predict that TGF-beta will be one of the key molecules in future attempts to establish an integrated view of the processes whereby cells coordinate their own and mutual functions. We have seen only the beginning, and this minireview is only a glimpse.
Cancer and the gut microbiota: An unexpected link (2015)

Changes in the interactions among the gut microbiota, intestinal epithelium, and host immune system are associated with many diseases, including cancer. We discuss how environmental factors infuence this cross-talk during oncogenesis and tumor progression and how manipulations of the gut microbiota might improve the clinical activity of anticancer agents.
The (Pro)renin Receptor/ATP6AP2 is Essential for Vacuolar H + -ATPase Assembly in Murine Cardiomyocytes (2010)

Genetic ablation of Atp6ap2 created a loss-of-function model for V-ATPase. The gene product of ATP6AP2 is considered to act as in 2 ways: (1) as (P)RR, exerting a RAS-related function; and (2) as the V-ATPase-associated protein, exerting a non-RAS-related function that is essential for cell survival.
Scale‐up and optimization of an acoustic filter for 200 L/day perfusion of a CHO cell culture (2002)

Acoustic cell retention devices have provided a practical alternative for up to 50 L/day perfusion cultures but further scale-up has been limited. A novel temperature-controlled and larger-scale acoustic separator was evaluated at up to 400 L/day for a 10(7) CHO cell/mL perfusion culture using a 100-L bioreactor that produced up to 34 g/day recombinant protein. The increased active volume of this scaled-up separator was divided into four parallel compartments for improved fluid dynamics. Operational settings of the acoustic separator were optimized and the limits of robust operations explored. The performance was not influenced over wide ranges of duty cycle stop and run times. The maximum performance of 96% separation efficiency at 200 L/day was obtained by setting the separator temperature to 35.1 degrees C, the recirculation rate to three times the harvest rate, and the power to 90 W. While there was no detectable effect on culture viability, viable cells were selectively retained, especially at 50 L/day, where there was a 5-fold higher nonviable washout efficiency. Overall, the new temperature-controlled and scaled-up separator design performed reliably in a way similar to smaller-scale acoustic separators. These results provide strong support for the feasibility of much greater scale-up of acoustic separations.