gebhart/patrepeval huggingface dataset:
Organization and Expression of Calicivirus Genes (2000)

The application of molecular techniques to the characterization of caliciviruses has resulted in an extensive database of sequence information. This information has led to the identification of 4 distinct genera. The human enteric caliciviruses have been assigned to 2 of these genera. This division is reflected not only in sequence diversity but in a fundamental difference in genome organization. Complete genome sequences are now available for 5 enteric caliciviruses and demonstrate that human and animal enteric caliciviruses are phylogenetically closely related. Currently, there is no cell culture system for the human viruses; therefore, studies have relied on heterologous expression and in vitro systems. These studies have shown that in both human and animal viruses the viral nonstructural proteins are produced from a polyprotein precursor that is cleaved by a single viral protease. The purpose of this article is to provide an overview of the current knowledge of genome structure and gene expression in the enteric caliciviruses.
New Hope for Liver Xenotransplantation (2016)

Department of Surgery, Indiana University, School of Medicine, Indianapolis, IN. [email protected]. Disclosure: Joseph Tector has founded Xenobridge llc and has applied for patents related to xenotransplantation.
Treatment of eosinophilic esophagitis: is oral viscous budesonide superior to swallowed fluticasone spray? (2011)

Eosinophilic esophagitis (EoE) is an immunologic reaction to ingested or inhaled allergens characterized by esophageal eosinophilia and gastrointestinal symptoms. In adults, this disease is more common in men than women, with a mean age of onset of 38 years. Recent data show that EoE is increasing in prevalence, with an incidence of 6–30 cases per 100,000 individuals.1
Quantum Correlations in Two-Particle Anderson Localization (2010)

We predict quantum correlations between noninteracting particles evolving simultaneously in a disordered medium. While the particle density follows the single-particle dynamics and exhibits Anderson localization, the two-particle correlation develops unique features that depend on the quantum statistics of the particles and their initial separation. On short time scales, the localization of one particle becomes dependent on whether or not the other particle is localized. On long time scales, the localized particles show oscillatory correlations within the localization length. These effects can be observed in Anderson localization of nonclassical light and ultracold atoms.
CD32B is highly expressed on clonal plasma cells from patients with systemic light-chain amyloidosis and provides a target for monoclonal antibody–based therapy (2008)

Despite advances in therapy, many patients with systemic light-chain amyloidosis (AL) die within 3 years from diagnosis. The humanized 2B6 monoclonal antibody (MoAb) is specific for the low-affinity IgG Fc receptor CD32B and effective in a human CD32B+ B-cell lymphoma murine xenograft model. Because MoAb therapy could improve outcomes in AL, we studied CD32B expression by clonal plasma cells obtained from 48 patients with AL. Transcript profiling showed that expression of CD32B was significantly higher than expression of all other Fc receptor family members. Reverse-transcriptase polymerase chain reaction (RT-PCR) using double-enriched CD138+ plasma cells showed uniform expression of the stable cell surface CD32B1 isoform at diagnosis and relapse, and flow cytometry showed intense CD32B cell surface staining on 99% of CD138+ plasma cells at diagnosis and relapse. These data provide a rationale for the novel therapeutic targeting of CD32B using the humanized 2B6 MoAb in patients with systemic AL-amyloidosis.
Rapid and sensitive nonradioactive detection of mutant K-ras genes via 'enriched' PCR amplification. (1991)

We have developed a rapid and highly sensitive nonradioactive method for the detection of a mutant codon 12 human c-K-ras allele in the presence of as many as 10(4) copies of the wild type codon 12 allele. This sensitivity is achieved by selective polymerase chain reaction (PCR) amplification of mutant K-ras gene sequences employing a two stage procedure. The first stage entails the amplification of both K-ras mutant and wild type codon 12 sequences, followed by a selective restriction enzyme digestion of only wild type sequences. The second stage involves a subsequent amplification of undigested amplified fragments, enriched in mutant codon 12 sequences. These products are subject to restriction length polymorphism analysis for the detection of point mutations at codon 12. This technique is rapid, nonradioactive, and eliminates the need for either oligonucleotide hybridization or DNA sequencing. Variations of this selective amplification procedure may prove promising for the detection of specific point mutations in heterogenous cell populations.
Thermal Inactivation of Pectin Methylesterase, Polygalacturonase, and Peroxidase in Tomato Juice (2002)

Thermal inactivation kinetics have been determined for pectin methylesterase (PME), polygalacturonase (PG), and peroxidase (POD) in tomato juice. Two parameters, the inactivation rate constant (k) at a reference temperature and the activation energy for inactivation (E(a)), were determined for each enzyme. For PME and PG, the k and E(a) values reported here do not agree with those in several previously published reports. These differences can be explained either by the differences in pH values used for inactivation determinations or by inadequacies in the heating methods used in some previous studies. POD showed simple first-order inactivation kinetics and was less thermally stable than either PME or PG. When different cultivars of tomatoes were evaluated, there was no difference in the thermal inactivation kinetics of these enzymes.
Clinical significance of HER-2/neu oncogene amplification in primary breast cancer. The South Australian Breast Cancer Study Group. (1993)

Although the follow-up duration of this study is relatively short, we conclude that HER-2/neu amplification is an independent predictor of shorter DFS in both node-negative and node-positive patients.
Peripheral glucose metabolism and insulin sensitivity in Alzheimer's disease (1993)

Twenty-four patients with Alzheimer's disease and matched controls were examined with reference to metabolic parameters such as peripheral insulin and glucose metabolism, serum lipid concentrations and blood pressure levels. Blood glucose levels and insulin response were measured during an intravenous glucose tolerance test and peripheral insulin sensitivity was estimated with the hyperinsulinemic euglycemic clamp technique. There were no differences recorded between the two groups in glucose metabolism, triglyceride, cholesterol or HDL-cholesterol levels. The patients with Alzheimer's disease had significantly lower blood pressure levels, which partly could be explained by ongoing treatment with neuroleptics and antidepressives. Previous findings of higher insulin levels in Alzheimer's disease could not be verified.
Expression of Cone-Photoreceptor–Specific Antigens in a Cell Line Derived from Retinal Tumors in Transgenic Mice (2004)

661W cells demonstrate cellular and biochemical characteristics exhibited by cone photoreceptor cells. These cells also resemble neuronal cells with their spindlelike processes and should serve as a useful alternative in vitro model for the study of cone photoreceptor cell biology and associated diseases.
Site-Specific PEGylation of Therapeutic Proteins (2015)

The use of proteins as therapeutics has a long history and is becoming ever more common in modern medicine. While the number of protein-based drugs is growing every year, significant problems still remain with their use. Among these problems are rapid degradation and excretion from patients, thus requiring frequent dosing, which in turn increases the chances for an immunological response as well as increasing the cost of therapy. One of the main strategies to alleviate these problems is to link a polyethylene glycol (PEG) group to the protein of interest. This process, called PEGylation, has grown dramatically in recent years resulting in several approved drugs. Installing a single PEG chain at a defined site in a protein is challenging. Recently, there is has been considerable research into various methods for the site-specific PEGylation of proteins. This review seeks to summarize that work and provide background and context for how site-specific PEGylation is performed. After introducing the topic of site-specific PEGylation, recent developments using chemical methods are described. That is followed by a more extensive discussion of bioorthogonal reactions and enzymatic labeling.
Exposure to Diethylstilbestrol During Pregnancy Permanently Alters the Ovary and Oviduct (1983)

To determine the effects of transplacental exposure to diethylstilbestrol (DES) on the ovary and oviduct of the CD-1 mouse, timed pregnant mice were injected subcutaneously with DES (100 micrograms/kg) on Days 9 through 16 of gestation and female offspring sacrificed from 4 weeks to 10 months of age. Following DES exposure, ovarian alterations such as inflammation, a prominent interstitial compartment composed of medullary tubule-like structures, and intra- and para-ovarian cysts from mesonephric remnants were observed. In addition, there were oviductal abnormalities including malformation. As reported previously, the oviduct was closely adherent and coiled around the ovary in a similar position to that seen in the fetal mouse. This malformation was termed developmental arrest of the oviduct (DAO) and was a consistent finding in female offspring exposed prenatally to DES (100 micrograms/kg). Increased prevalence of salpingitis and microscopic alterations in the oviduct were also observed. Oviductal epithelium was mostly secretory type with basal vacuoles. In some cases, oviductal epithelium was hyperplastic and formed mucosal folds resembling glands which extended through the muscularis (diverticulosis). The extent of the adenomatous mucosal folds and the degree of extension through the muscularis increased with the age of the animal (100% at 10 months). Some characteristics of this abnormality resembled salpingitis isthmica nodosa, a lesion described in women which is associated with ectopic pregnancies and subfertility. Gross and microscopic changes in the oviduct were more consistent than were the changes among other portions of the reproductive tract of DES-treated mice previously reported. Since subfertility has been described in this mouse model as well as in prenatally DES-exposed women, the data presented in this report may help in evaluation of the reported reduced fertility in exposed patients as well as other infertility patients.
Evidence for B-lymphocyte mitogen activity in Borrelia burgdorferi-infected mice (1992)

Borrelia burgdorferi produces a mitogen for murine B lymphocytes which can be measured in vitro by polyclonal stimulation of proliferation and immunoglobulin production (R. Schoenfeld, B. Araneo, Y. Ma, L. Yang, and J. J. Weis, Infect. Immun. 60:455-464, 1992). Sonicated B. burgdorferi cells also stimulated IL-6 production by splenocyte cultures. We have used the murine model for Lyme disease described by Barthold et al. (S. W. Barthold, D. S. Beck, G. M. Hansen, G. A. Terwilliger, and K. D. Moody, J. Infect. Dis. 162:133-138, 1990) to determine whether the B. burgdorferi B-cell mitogen is expressed during active infection. To correlate arthritic changes with immune events, we have studied two strains of mice injected with B. burgdorferi; one of them, C3H/HeJ, developed severe disease, and the other, BALB/c, developed only mild disease. C3H/HeJ mice displayed a persistent 10-fold increase in circulating immunoglobulin G (IgG) levels, a 2-fold increase in IgM levels, and a 15-fold increase in peripheral lymph node B-cell numbers, providing evidence of mitogenic activity. Infected BALB/c mice also had evidence for mitogen activity, since the IgG level in serum increased three- to fourfold. The bulk of the increase in circulating IgG levels was not directed against B. burgdorferi antigens, supporting the occurrence of polyclonal B-cell activation. Analysis of IgG isotypes pointed out a contrast between C3H/HeJ and BALB/c mice in that levels of all isotypes were elevated somewhat in both strains of infected mice but IgG2a levels were much more dramatically increased in the C3H/HeJ mice (28-fold) than in the BALB/c mice (4-fold). In this study, interleukin-6 levels were found to be persistently elevated in the serum of infected C3H/HeJ mice. Interestingly, interleukin-6 levels in serum were much lower in the infected BALB/c mice. These findings indicate that the B. burgdorferi mitogen is active in infected animals and may contribute to the inflammatory and immune response to infection.
Beyond Trastuzumab: Overcoming Resistance to Targeted HER-2 Therapy in Breast Cancer (2009)

Overexpression of the human epidermal growth factor receptor 2 (HER-2) represents a biological subclass of breast cancer with distinct molecular alterations, clinical behavior, and response to systemic therapy. Trastuzumab is a monoclonal antibody directed against HER-2 which has revolutionized the management of both early and advanced breast cancer. It may exert its anti-cancer effects through inhibition of intracellular signaling, upregulation of p27, impaired angiogenesis, induction of immune-mediated destruction, and blockade of cleavage of the extracellular domain of HER-2. In spite of its robust clinical activity, most women with metastatic HER-2 overexpressing breast cancer eventually progress on trastuzumab therapy. Possible mechanisms of resistance include: altered receptor antibody interaction, PTEN loss and enhanced Akt signaling, p27 loss, signaling through other receptors. Preclinical experiments, clinical experience with the use of trastuzumab beyond progression, and a recent phase III clinical trial with Lapatinib, a dual EGFR/HER-2 tyrosine kinase inhibitor, demonstrate that the HER-2 signaling axis remains an important therapeutic target even after progression on trastuzumab. A variety of novel strategies are currently in development to exploit this pathway following the onset of resistance, such as receptor antibodies, sheddase inhibitors, signal transduction inhibitors, heat shock protein inhibitors, proteasome inhibitors, anti-angiogenic agents, and immune-stimulatory therapies, either as single agents or in combination with trastuzumab. Rational clinical trial design, with attention to appropriate patient selection and prospective collection of biological material, is needed to ensure that the new generation of anti-HER-2 targeted therapies realizes its promise in the treatment of trastuzumab-resistant disease.
ACAT inhibitors as antiatherosclerotic agents: Compounds and mechanisms (1994)

Atherosclerosis is a major death cause in western industrialized countries. A diagnosing system, medical prevention, and treatment of atherosclerosis is not sufficient so far. A direct acting antiatherosclerotic agent is eagerly waited. ACAT inhibitor approach could provide such an agent. In the formation of atherosclerosis, cholesteryl esters, which are the lipids which accumulate in atheromatous plaques by an aid of macrophages and smooth muscle cells, forming foam cells, may play an important role. ACAT enzyme is responsible for the acylation of cholesterol to cholesteryl esters, a transformation which can be essential in not only cholesteryl esters accumulation at arterial walls but also the absorption of cholesterol in the intestine and the excretion of cholesterol in the liver. From these points, ACAT inhibitors might work against atherosclerosis in three different ways: first, cholesteryl ester accumulation inhibition at arterial walls could be a direct antiatherosclerotic effect; second, cholesterol absorption inhibition at the intestine; and third, cholesterol excretion acceleration at the liver, while the later two effects would result in a reduction of blood cholesterol level--a major risk factor of atherosclerosis. Taking account of this discussion, the ACAT inhibitors would be potent antiatherosclerotic agents. Medicinal research has been contributing full strength to produce an ultimate compound. These efforts should provide a drug which will be useful to patients.
A systematic review of reviews on the prevalence of anxiety disorders in adult populations (2016)

The prevalence of anxiety disorders is high in population subgroups across the globe. Recent research has expanded its focus to Asian countries, an increasingly greater number of physical and psychiatric conditions, and traumatic events associated with anxiety. Further research on illness trajectories and anxiety levels pre- and post-treatment is needed. Few studies have been conducted in developing and under-developed parts of the world and have little representation in the global literature.
CD66 nonspecific cross-reacting antigens are involved in neutrophil adherence to cytokine-activated endothelial cells. (1992)

Neutrophil adherence to cytokine-activated endothelial cell (EC) monolayers depends on the expression of the endothelial leukocyte adhesion molecule-1 (ELAM-1). The ligand for ELAM-1 is the sialylated Lewis-x antigen (SLe(x)) structure. The selectin LAM-1 (or LECAM-1) has been described as one of the SLe(x)-presenting glycoproteins involved in neutrophil binding to ELAM-1. Other presenter molecules have not yet been described. Our data demonstrate that the carcinoembryonic antigen (CEA)-like surface molecules on neutrophils--known as the nonspecific cross-reacting antigens (NCAs)--are involved in neutrophil adherence to monolayers of IL-1-beta-activated EC. The NCAs are recognized by CD66 (NCA-160 and NCA-90) and CD67 (NCA-95). Because NCA-95 and NCA-90 have previously been found to be phosphatidylinositol (PI)-linked, paroxysmal nocturnal hemoglobinuria (PNH) neutrophils (which lack PI-linked surface proteins) were tested as well. PNH neutrophils showed a diminished binding to activated EC. CD66 (on PNH cells still recognizing the transmembrane NCA-160 form) still inhibited the adherence of PNH cells to IL-1-beta-activated EC, but to a limited extent. Soluble CEA(-related) antigens inhibited normal neutrophil adherence as well, whereas neutrophil transmigration was unaffected. Sialidase-treatment as well as CD66 preclearing abolished the inhibitory capacity of the CEA(-related) antigens. The binding of soluble CEA antigens to IL-1-beta-pretreated EC was blocked by anti-ELAM-1. These soluble antigens, as well as the neutrophil NCA-160 and NCA-90, both recognized by CD66 antibodies, presented the SLe(x) determinant. Together, these findings indicate that the CD66 antigens (i.e., NCA-160/NCA-90) function as presenter molecules of the SLe(x) oligosaccharide structures on neutrophils that bind to ELAM-1 on EC.
Basic A1 Protein of the Myelin Membrane (1971)

Abstract Twenty-seven tryptic peptides were isolated from the A1 protein from bovine spinal cord. These, together with 16 peptic peptides, were utilized to establish the complete amino acid sequence of the 170 residues of the A1 protein. Peptide T, derived from the A1 protein by cleavage of the carboxyl of the single tryptophan residue, was useful in positioning the peptides which comprise the COOH-terminal end. Seven chymotryptic and nine tryptic peptides were isolated from Peptide T. An unusual feature of the sequence is the methylated arginine residue at position 107 which is present as both the dimethyl and monomethyl derivatives. The methylated derivatives appear to be relatively resistant to tryptic hydrolysis. Located close to the methylated arginine residue is a Pro-Arg-Thr-Pro-Pro-Pro sequence, a structure which may induce a sharp bend in the molecule, suggesting a conformation more compatible with an open double chain structure than a random coil. The over-all sequence reveals no obvious periodicity but rather a general distribution of basic residues over the polypeptide chain, making the interaction with phospholipids within the myelin matrix highly probable. Several peptide segments of 9 residues exist, in which basic residues are missing; the somewhat nonpolar character of these regions suggests a possiblity for participation in nonpolar interactions.
Cloning of the luciferase structural genes from Vibrio harveyi and expression of bioluminescence in Escherichia coli (1984)

The DNA encoding the luciferase alpha and beta subunits in the luminous marine bacterium Vibrio harveyi (strain 392) is contained within a 4.0-kilobase HindIII fragment. DNA from V. harveyi was digested with HindIII, and the resulting fragments were inserted into the HindIII site of plasmid pBR322. The recombinant plasmids were introduced by transformation into Escherichia coli RR1. The colonies were supplied with n-decanal, the substrate for the bioluminescence reaction, and 12 colonies (of ca. 6000 total) were observed to luminesce brightly. One of the recombinant plasmids, pTB7, has been studied in detail. The high level of expression of bioluminescence in pTB7 was the result not of native V. harveyi promoters but rather of a promoter in pBR322 which is within the tetracycline resistance gene but oriented in the direction opposite to the transcription of the tetracycline gene. Using antiluciferase antibody to probe proteins transferred from sodium dodecyl sulfate-polyacrylamide gels to nitro-cellulose paper, we have shown that the E. coli transformants produce luciferase that cross-reacts with antiluciferase antibody and is the same molecular weight as V. harveyi luciferase. No alpha subunit could be detected by using antiluciferase antibody in lysates of a subclone, pTB104, which is identical with pTB7 except for deletion of the beta-subunit gene. Thus, the alpha subunit may be unstable and be degraded unless it is associated with beta. The bioluminescence emission spectra of V. harveyi and of E. coli transformants carrying pTB7 are indistinguishable.(ABSTRACT TRUNCATED AT 250 WORDS)
The role of the ubiquitination-proteasome pathway in breast cancer: Ubiquitin mediated degradation of growth factor receptors in the pathogenesis and treatment of cancer (2002)

Aberrant activity of growth factor receptors has been implicated in the pathogenesis of a wide variety of malignancies. The negative regulation of signaling by growth factor receptors is mediated in large part by the ubiquitination, internalization, and degradation of the activated receptor. Over the past few years, considerable insight into the mechanisms that control receptor downregulation has been gained. There are also data suggesting that mutations that lead to inhibition of downregulation of growth factor receptors could play a role in the pathogenesis of cancer. Therapies directed at enhancing the degradation of growth factor receptors offer a promising approach to the treatment of malignancies.
Justifying adverse actions with new scorecard technologies (2009)

It has been argued that flexible classification models such as neural networks, support vector machines, and random forests face resistance as credit scoring models because it is difficult to identify which characteristics contribute substantially to the overall scores. In fact, however, this is a misunderstanding arising from the fact that standard models are based on sums of transformations of the raw characteristics. We distinguish between the need to identify which characteristics contribute most to an individual‟s score and the need to identify which characteristics contribute to the performance of a scorecard. We describe solutions to these two problems, and illustrate by applying a range of scorecard approaches to some real credit card data.