gebhart/patrepeval huggingface dataset:
Validation and Clinical Utility of a 70-Gene Prognostic Signature for Women With Node-Negative Breast Cancer (2006)

The 70-gene signature adds independent prognostic information to clinicopathologic risk assessment for patients with early breast cancer.
The Effect of the Frequency of Subcutaneous Insulin-Like Growth Factor-1 Administration on Weight Gain in Growth Hormone Deficient Mice (1991)

To ascertain the frequency of subcutaneous IGF-1 administration necessary to promote growth we examined the weight gain of male homozygous lit/lit mice in response to either sc. IGF-1 or bovine GH administration. Lit/lit mice showed a dose dependent response to treatment with GH. Bovine GH induced a response in body weight gain within 3 days of the start of treatment. Following a single subcutaneous injection of IGF-1, plasma IGF-1 levels were elevated for 4-6 hours. Three treatment schedules for IGF-1 were used (once daily, twice daily and four times daily), each employing the same total daily dose of IGF-1 (30 micrograms). With IGF-1 treatment, a significant effect on body weight gain was obtained when administered four times daily. The growth rate with IGF-1 treatment 6 hourly was similar to that observed following treatment with bGH (10 micrograms sc daily). Twelve hourly IGF-1 administration only had a significant effect on body weight gain when weight was measured in the evening. Lit/lit mice treated once daily with 30 micrograms IGF-1 had no weight gain response and became severely hypoglycaemic. Frequent subcutaneous IGF-1 administration is one approach to growth enhancement in GH deficiency; higher doses administered less frequently do not promote growth and may cause hypoglycaemia.
DISTRIBUTION OF P2X RECEPTORS IN THE URINARY BLADDER AND THE URETER OF THE RAT (2000)

Having established the distribution of P2X receptors in normal animal bladder and ureter tissue, it is now possible to perform comparable investigations on normal and diseased human tissue to establish a possible role of P2X receptors in pathogenic events.
Direct and Indirect Inhibition of Ovulation in Rats by an Antagonist of Luteinizing Hormone-Releasing Hormone* (1985)

The importance of a central or peripheral site of action in the blockade of ovulation induced by LHRH antagonists was investigated. To determine if hCG could induce ovulation in cycling animals given antiovulatory doses of 10 or 100 micrograms [N-Ac-D-p-Cl-Phe1,D-p-Cl-Phe2,D-Trp3,D-Arg6,D-Ala10] LHRH, the antagonist was injected at 1200 h of proestrus followed by varying doses of hCG at 1600 h. hCG did induce ovulation in animals given the analog, which suggested that the antagonist acted primarily at the hypothalamus-pituitary level to inhibit ovulation; however, 20 IU hCG induced ovulation in all animals given 10 micrograms antagonist, but 40 IU were required for the same effect in animals injected with 100 micrograms. To test whether hormone secretion was differentially affected by the two doses of antagonist, animals were injected with antagonist at 1200 h of proestrus, and groups were killed at 1- or 2-h intervals through 2100 h. Both 10 and 100 micrograms antagonist suppressed serum LH, FSH, progesterone, and estradiol levels to the same degree. Therefore, no differences in these hormones were detected that could account for the increased hCG required to induce ovulation in the 100 micrograms-treated animals. We next examined the ability of the antagonist to inhibit ovulation in animals hypophysectomized at day 24 of age and injected with 25 IU PMSG 7 days later and 30 or 50 IU hCG 48 h after PMSG. When the antagonist was given 4 h before 50 IU hCG, the antagonist did not completely inhibit ovulation even at 100 or 1000 micrograms/rat. When hCG was reduced to 30 IU, 100 micrograms antagonist induced a partial inhibition of ovulation, and 1000 micrograms induced a complete blockade. These results suggest that the LHRH antagonists primarily act centrally to inhibit ovulation, but they make the ovaries less responsive to hCG stimulation and can directly inhibit ovulation at high doses.
Genomic structure of an integrin alpha subunit, the leukocyte p150,95 molecule. (1990)

The genomic structure of integrins is important to our understanding of the evolution of this complex family. The alpha subunit of the leukocyte integrin p150,95 (CD11c) is a transmembrane polypeptide of 1144 residues whose long extracellular region contains three putative divalent cation binding repeats and a 200- amino acid inserted or "I" domain. The p150,95 alpha subunit gene extends over 25 kilobases and is comprised of at least 31 exons grouped in five clusters. The I domain, which is only present in some integrins and is homologous to domains in von Willebrand factor, cartilage matrix protein, complement factor B and the alpha 1 and alpha 2 chains of collagen type VI, is distributed in four exons. Each one of the three divalent cation binding repeats is encoded by a separate exon. Surprisingly, a sequence homologous to the first two putative divalent cation binding repeats is present in an inverted orientation in the intron following the last exon of the I domain. Both the signal peptide and the transmembrane domain are split in two exons. Putative proteolytic cleavage sequences in other integrin alpha subunits align as inserts within the p150,95 alpha subunit gene falling at exon boundaries. The organization of the p150,95 alpha subunit gene provides further insights into the structure and evolution of the integrins.
Hyperamylinemia, hyperinsulinemia, and insulin resistance in genetically obese LA/N-cp rats. (1992)

The experimental evidence supporting a direct role for hyperinsulinemia as a cause of insulin resistance remains equivocal. Amylin, an islet beta-cell peptide cosecreted with insulin in response to nutrient stimuli, causes insulin resistance when infused into intact animals or applied to isolated skeletal muscles. We compared measures of amylin and insulin gene expression between control and genetically obese, insulin-resistant Lister Albany/NIH-(LA/N-cp) rats. Pancreatic amylin messenger RNA levels were increased 7.8 +/- 0.7-fold (mean +/- SEM), and plasma amylin-like immunoreactive material was increased 10.9 +/- 1.1-fold (LA/N-lean, 14 +/- 4 pM; LA/N-cp, 153 +/- 16 pM; p less than 0.0001) in obese rats. Pancreatic insulin I mRNA levels were increased 7.4 +/- 0.5-fold, and plasma insulin levels 20.0 +/- 5.0-fold, in these rats (LA/N-lean, 308 +/- 84 pM; LA/N-cp 6,120 +/- 1,540 pM; p less than 0.0001). The EC50 for insulin-stimulated incorporation of glucose into glycogen was about fourfold higher in muscles isolated from obese rats. The present results, coupled with previous observations, support the hypothesis that hyperamylinemia, rather than hyperinsulinemia per se, could have directly caused the insulin resistance in the obese LA/N-cp rats. Hyperamylinemia needs to be considered in future experimental studies probing the relation between hyperinsulinemia and insulin resistance.
Pairing Symmetry in Single-Layer Tetragonal Tl 2 Ba 2 CuO β+δ Superconductors (1996)

A high-resolution scanning superconducting quantum interference device microscopy study of tetragonal single-layer Tl 2 Ba 2 CuO 6+δ films, deposited on tricrystal SrTiO 3 substrates, demonstrates the effect of spontaneously generated half flux quanta. This observation shows that in addition to YBa 2 Cu 3 O 7 , the order parameter symmetry in Tl 2 Ba 2 CuO 6+δ is consistent with that of a d x 2 - y 2 pair state. This result also rules out any bilayer or twinning effects and any pairing that is incompatible with the fourfold rotational symmetry as in the Tl 2 Ba 2 CuO 6+δ superconducting system.
Low-dose Interleukin-2 in the Treatment of Autoimmune Disease (2014)

CD4+ regulatory T cells (Tregs) act to maintain peripheral immune tolerance. Decreased numbers or defective function of Tregs has been implicated in the pathogenesis of various autoimmune diseases. Interleukin-2 (IL-2) at high doses is approved by the US Food and Drug Administration (FDA) as an immune stimulant to induce anti-tumor cytotoxicity. However, at physiologic doses, IL-2 is necessary for the expansion and function of Tregs. Treatment with low-dose IL-2 can selectively enhance Treg function while avoiding the activation of effector T cells and ameliorate immune inflammation. Administration of low doses of IL-2 to patients suffering from chronic graft versus host disease (cGvHD) or chronic hepatitis C-mediated vasculitis resulted in significant clinical benefit, which was linked to improved Treg cell function. Preclinical studies suggest that low-dose IL-2 may offer benefit in other autoimmune diseases including systemic lupus erythematosus and type 1 diabetes. Ongoing preclinical and clinical studies indicate a wider potential role for low-dose IL-2 based Treg therapeutics in human autoimmune diseases.
InGaN-CdSe-ZnSe quantum dots white LEDs (2005)

White light-emitting diodes (WLEDs) were fabricated by combining blue InGaN chips with luminescent colloidal core-shell CdSe-ZnSe quantum dots (QDs). The core-shell CdSe-ZnSe QDs synthesized by thermal deposition approach exhibited high photoluminescence efficiency with a quantum yield more than /spl sim/40%, and size-tunable emission wavelengths from 510 to 620 nm. Three-band red-green-blue WLED was successfully assembled by blue InGaN chips and green-emitting and red-emitting CdSe-ZnSe QDs. Based on QDs with flexibly selected color, the WLEDs exhibited white light with a CIE-1931 coordinate of (0.33, 0.33) and color rendering index R/sub a/ of 91.
Expression of a cDNA encoding the human insulin receptor-related receptor. (1994)

The insulin receptor-related receptor (IRR) gene encodes a protein that is homologous to the receptors for insulin and insulin-like growth factor-I (IGF-I). We have cloned a full-length cDNA encoding the human IRR by screening a human kidney cDNA library. The nucleotide sequence of our cDNA is identical to the sequence predicted from the human IRR gene except for the presence of an insertion of 24 base pairs between exons 13 and 14. This insertion was caused by use of an alternative splice acceptor site in the 3' portion of intron 13. Interestingly, this alternative splicing occurs at a position at which alternative splicing of the homologous IGF-I receptor mRNA also occurs. We amplified human kidney IRR by the polymerase chain reaction to quantitate the proportion of transcripts which included the 24-nucleotide sequence between exons 13 and 14. Fewer than 10% of the transcripts contained this additional sequence. We expressed the IRR cDNA lacking the 24-base pair insert in NIH-3T3 cells to study the biosynthesis, tyrosine phosphorylation, and ligand binding properties of the IRR. Like receptors for insulin and IGF-I, the IRR was synthesized as a single polypeptide precursor that underwent proteolytic cleavage and glycosylation to yield an alpha subunit and a beta subunit. However, both subunits of the IRR had smaller apparent molecular mass than the homologous subunits of the insulin receptor (108,000 versus 135,000 for the alpha subunits and 66,000 versus 95,000 for the beta subunits). IRR tyrosine phosphorylation could be stimulated by vanadate plus H2O2, which have been demonstrated previously to increase the phosphotyrosine content of the insulin receptor tyrosine kinase. However, proinsulin, insulin, IGF-I, and IGF-II did not stimulate tyrosine phosphorylation of the IRR. We conclude that these peptides are not the ligands for the IRR.
GRIN2B mutations in west syndrome and intellectual disability with focal epilepsy (2013)

We identified GRIN2B gain-of-function mutations as a cause of West syndrome with severe developmental delay as well as of ID with childhood onset focal epilepsy. Severely disturbed channel function corresponded to severe clinical phenotypes, underlining the important role of facilitated NMDA receptor signaling in epileptogenesis.
Expression and Purification of a Soluble Functional form of the Platelet αIIbβ3 Integrin (1995)

Platelet glycoproteins alpha IIb and beta 3 are membrane proteins that associate to form a Ca(2+)-dependent heterodimer which constitutes an inducible member of the integrin family at the surface of the cell. To produce a soluble form of this complex, alpha IIb and beta 3 were both deleted of their transmembrane and cytoplasmic domains and were expressed in COS cells. Production of the truncated subunits and their mode of assembly were examined by immunoprecipitation experiments and compared to those of wild-type alpha IIb beta 3. Synthesis and processing of the truncated heterodimer proceeded via a pathway similar to that observed for the wild-type alpha IIb beta 3 in COS cells or in human megakaryocytes. The truncated beta 3 subunit associated with the Pro-truncated form of the alpha IIb subunit. This precursor form was not secreted. After proteolytic cleavage of the Pro-truncated alpha IIb, the mature heterodimer was secreted into the culture supernatant. To quantify the molar ratio of the various secreted soluble forms, an immunocapture assay was designed. All secreted tr-alpha IIb subunits associated with tr-beta 3. In contrast, tr-beta 3 was produced and secreted in excess as the free form. Immunoreactivity of the wild-type and soluble truncated complexes was identical since all the monoclonal antibodies used reacted with surface-located epitopes on both complexes. This indicated that the soluble truncated heterodimer adopted a native conformation. To purify this soluble heterodimer, tr-alpha IIb beta 3-containing culture supernatant was adsorbed on an RGDW-affinity column and eluted with a solution of the free peptide RGDW. In the RGD-eluted material, the amount of each subunit was stoichiometric, suggesting that the complex was not disrupted during purification. The capacity of the wild-type and truncated RGD-eluted complexes to interact with soluble fibrinogen was compared using a solid-phase immunocapture assay. tr-alpha IIb beta 3 and platelet alpha IIb beta 3 exhibited similar fibrinogen-binding capacity. For both complexes, these interactions were mediated by RGD and gamma fibrinogen signals.
A cloned Erwinia chrysanthemi Hrp (type III protein secretion) system functions in Escherichia coli to deliver Pseudomonas syringae Avr signals to plant cells and to secrete Avr proteins in culture (1998)

The Hrp (type III protein secretion) system is essential for the plant parasitic ability of Pseudomonas syringae and most Gram-negative bacterial plant pathogens. AvrB and AvrPto are two P. syringae proteins that have biological activity when produced via heterologous gene expression inside plant cells or when produced by Hrp+ bacteria. Avr-like proteins, presumably injected by the Hrp system on bacterial contact with plant cells, appear to underlie pathogenic interactions, but none has been observed outside of the bacterial cytoplasm, and identifying novel genes encoding them is tedious and uncertain without a phenotype in culture. Here we describe a cloned Hrp secretion system that functions heterologously in Escherichia coli to secrete AvrB and AvrPto in culture and to promote AvrB and AvrPto biological activity in inoculated plants. The hrp gene cluster, carried on cosmid pCPP2156, was cloned from Erwinia chrysanthemi, a pathogen that differs from P. syringae in being host promiscuous. E. coli DH5alpha carrying pCPP2156, but not related Hrp-deficient cosmids, elicited a hypersensitive response in Nicotiana clevelandii only when also expressing avrB in trans. The use of pAVRB-FLAG2 and pAVRPTO-FLAG, which produce Avr proteins with a C-terminal FLAG-epitope fusion, enabled immunoblot detection of the secretion of these proteins to E. coli(pCPP2156) culture media. Secretion was Hrp dependent, occurred without leakage of a cytoplasmic marker, and did not occur with E. coli(pHIR11), which encodes a functional P. syringae Hrp system. E. coli(pCPP2156) will promote investigation of Avr protein secretion and systematic prospecting for the effector proteins underlying bacterial plant pathogenicity.
LocaLisa (1999)

This new technique enables accurate and reproducible real-time localization of electrode positions in cardiac mapping and ablation procedures. Its application does not distort the quality of electrograms and can be applied to any electrode catheter.
Generation of 2-nJ pulses from a femtosecond ytterbium fiber laser (2003)

We report a mode-locked ytterbium fiber laser that generates femtosecond pulses with energies as large as 2.2 nJ. This represents a 20-fold improvement in pulse energy compared with that of previously reported femtosecond Yb fiber lasers. The laser produces pulses as short as 52 fs, which are to our knowledge the shortest pulses to date from a Yb fiber laser. The laser is diode pumped by a wavelength-division multiplexing coupler, which leads to excellent stability.
Documenting the goals for monetary policy: some cross-country comparisons (2014)

Most central banks in advanced economies use published inflation targets to guide the day-to -day conduct of monetary policy. This article reviews the quite considerable differences in how various countries, which use quite similar operational targets, articulate what they expect from a central bank’s monetary policy.
Discrimination effects and sensitivity variations in matrix-assisted laser desorption/ionization (1997)

In matrix-assisted laser desorption/ionization (MALDI) the analyte signal produced depends strongly on the analyte and on the sample preparation procedure. Comparing the results obtained with the dried-drop method with the results obtained with a homogeneous sample preparation procedure, discrimination effects, as well as sensitivity variations, are shown to be dependent on the molecular weight of the analysed compounds. The signal obtained in MALDI is shown to be dependent on the hydrophobicity and basicity of the analyte. With the dried-drop method, in particular, evidence of peripheral sample deposition of hydrophilic compounds is shown. These last effects are due to mass transfer caused by differences in surface activities during solvent evaporation, and are known as Marangoni effects. © 1997 John Wiley & Sons, Ltd.
Molecular Population Genetics of Floral Homeotic Loci: Departures From the Equilibrium-Neutral Model at the APETALA3 and PISTILLATA Genes of Arabidopsis thaliana (1999)

Molecular variation in genes that regulate development provides insights into the evolutionary processes that shape the diversification of morphogenetic pathways. Intraspecific sequence variation at the APETALA3 and PISTILLATA floral homeotic genes of Arabidopsis thaliana was analyzed to infer the extent and nature of diversity at these regulatory loci. Comparison of AP3 and PI diversity with three previously studied genes revealed several features in the patterning of nucleotide polymorphisms common between Arabidopsis nuclear loci, including an excess of low-frequency nucleotide polymorphisms and significantly elevated levels of intraspecific replacement variation. This pattern suggests that A. thaliana has undergone recent, rapid population expansion and now exists in small, inbred subpopulations. The elevated intraspecific replacement levels may thus represent slightly deleterious polymorphisms that differentiate distinct ecotypes. The distribution of replacement and synonymous changes in AP3 and PI core and noncore functional domains also indicates differences in the patterns of molecular evolution between these interacting floral regulatory genes.
Convolutional Coding: Fundamentals and Applications (1997)

Here is an exceptional reference for gaining first-hand theoretical and practical knowledge of error-control coding and decoding. This book examines the principles of rate-compatible punctured convolutional codes as well as combined coding, modulation and equalization for intersymbol interference channels. The author supplies sample codes for software simulations of practical digital communication systems, covers each class of codes in detail, and provides examples and simulation results.
Immunogenic potentials of copolymer I in normal human lymphocytes (1985)

Copolymer I (COP I), a nonencephalitogenic polypeptide analogous to myelin basic protein, is currently being tested for possible effectiveness in treating MS. Peripheral blood mononuclear cells from normal human donors respond blastogenically to the L-form of COP I. This response was greater than that obtained with either bovine or guinea pig myelin basic protein (GPMBP), with no specificity for a particular T-cell subset. Analyses of culture supernatants demonstrated the presence of interleukin-2 and gamma interferon. Mononuclear cells from human fetal cord blood also responded blastogenically to COP I, but the magnitude of the response did not differ from that induced by GPMBP.
A Mitotic GlcNAcylation/Phosphorylation Signaling Complex Alters the Posttranslational State of the Cytoskeletal Protein Vimentin (2008)

O-linked beta-N-acetylglucosamine (O-GlcNAc) is a highly dynamic intracellular protein modification responsive to stress, hormones, nutrients, and cell cycle stage. Alterations in O-GlcNAc addition or removal (cycling) impair cell cycle progression and cytokinesis, but the mechanisms are not well understood. Here, we demonstrate that the enzymes responsible for O-GlcNAc cycling, O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) are in a transient complex at M phase with the mitotic kinase Aurora B and protein phosphatase 1. OGT colocalized to the midbody during telophase with Aurora B. Furthermore, these proteins coprecipitated with each other in a late mitotic extract. The complex was stable under Aurora inhibition; however, the total cellular levels of O-GlcNAc were increased and the localization of OGT was decreased at the midbody after Aurora inhibition. Vimentin, an intermediate filament protein, is an M phase substrate for both Aurora B and OGT. Overexpression of OGT or OGA led to defects in mitotic phosphorylation on multiple sites, whereas OGT overexpression increased mitotic GlcNAcylation of vimentin. OGA inhibition caused a decrease in vimentin late mitotic phosphorylation but increased GlcNAcylation. Together, these data demonstrate that the O-GlcNAc cycling enzymes associate with kinases and phosphatases at M phase to regulate the posttranslational status of vimentin.
Hereditary Pancreatitis and the Risk of Pancreatic Cancer (1997)

Patients with hereditary pancreatitis have a high risk of pancreatic cancer several decades after the initial onset of pancreatitis. A paternal inheritance pattern increases the probability of developing pancreatic cancer.
Bridging a generation gap (1990)

Rachael Smith and Judy Gillow describe the planning of a new course aimed at bridging the gap for pre-Project 2000 students