gebhart/patrepeval huggingface dataset:
Factors Affecting Dystocia and the Effects of Dystocia on Subsequent Reproduction in Beef Cattle (1973)

Calving and subsequent breeding information were obtained on 1889 Hereford and Angus cows bred to bulls representing the Hereford, Angus, Jersey, South Devon, Limousin, Simmental and Charolais breeds. The influence of sire breed, dam breed, dam age, calf sex and calf birth weight on the occurrence of dystocia and the effects of dystocia on subsequent reproductive performance were examined. Sire breed, dam breed, dam age and calf sex were significant (P<.005) sources of variation associated with dystocia when birth weight was not included in the analysis. The regression of birth weight on calving difficulty was a significant (P<.005) source of variation and calving difficulty increased 2.30 ± 0.21% for each kilogram increase in birth weight. When birth weight was held constant in the analysis, dam age was the only main effect significantly (P<.005) associated with percent calving difficulty. Calves sired by Charolais, Simmental, Limousin and South Devon bulls experienced significantly (P<.01) more calving difficulty (30.90±2.41, 32.66±3.09, 30.78±3.19 and 32.34±5.19%) than those sired by Hereford, Angus and Jersey bulls (15.78+-2.27, 9.90±2.55 and 6.46±3.61%). Percent calving difficulty was higher (P<.05) in Hereford-than in Jersey-sired calves. No significant differences in percent calving difficulty were found among the Charolais-, Simmental-, Limousin- and South Devon-sired calves nor between the Angus- and Jersey-sired calves. Dystocia in 2-year-old cows was 36.03±2.96% higher than in 3-year-olds and 44.62± 2.99% higher than in 4 and 5-year-olds. Percent dystocia was 8.59±3.39% higher (P<.05) in 3-year-old than in 4- and 5-year-old cows. Hereford cows had more (P<.005) calving difficulty than Angus cows, 34.78±3.19 compared to 27.02±3.13%. Dystocia was not significantly different between crossbred and straightbred calves, but crossbred calves were 1.55±0.26 kg heavier at birth than straightbreds. Male calves were heavier (P<.005) at birth than female calves, 35.12±1.82 compared to 32.10±1.81 kg, and experienced more (P<.005) dystocia, 28.40±1.71 compared to 16.98±1.70%. There was a higher percentage of calving difficulty in male births than in female births for all ages of cows, but the magnitude of the differences between sexes was greater in 2-year-old cows than in the other age groups. Dystocia had a signicant (P<.005) effect on the percentage of cows detected in estrus during the 45-day AI period, conception rate to AI and total conception rate. Fewer (14.4%) cows experiencing dystocia were detected in estrus during the AI period than those with no dystocia. In all cows, dystocia resulted in a 15.6% lower conception rate to AI and a 15.9% lower overall conception rate. The 2-year-old cows had a lower estrus detection rate, a lower conception rate during the AI period and a longer interval from calving to first breeding and from calving to conception than the 3-, 4- and 5-year-old cows.
Lattice defects in microtubules: protofilament numbers vary within individual microtubules (1992)

We have used cryo-electron microscopy of vitrified specimens to study microtubules assembled both from three cycle purified tubulin (3x-tubulin) and in cell free extracts of Xenopus eggs. In vitro assembled 3x-tubulin samples have a majority of microtubules with 14 protofilaments whereas in cell extracts most microtubules have 13 protofilaments. Microtubule polymorphism was observed in both cases. The number of protofilaments can change abruptly along individual microtubules usually by single increments but double increments also occur. For 3x-tubulin, increasing the magnesium concentration decreases the proportion of 14 protofilament microtubules and decreases the average separation between transitions in these microtubules. Protofilament discontinuities may correspond to dislocation-like defects in the microtubule surface lattice.
Electronic thermal conductivity and the Wiedemann-Franz law for unconventional superconductors (1996)

We use the quasiclassical theory of superconductivity to calculate the electronic contribution to the thermal conductivity. The theory is formulated for low temperatures when heat transport is limited by electron scattering from random defects and for superconductors with nodes in the order parameter. We show that certain eigenvalues of the thermal conductivity tensor are universal at low temperature, ${\mathit{k}}_{\mathit{BT}}$\ensuremath{\ll}\ensuremath{\gamma}, where \ensuremath{\gamma} is the bandwidth of impurity bound states in the superconducting phase. The components of the electrical and thermal conductivity also obey a Wiedemann-Franz law with the Lorenz ratio L(T)=\ensuremath{\kappa}/\ensuremath{\sigma}T given by the Sommerfeld value of ${\mathit{L}}_{\mathit{S}}$=(${\mathrm{\ensuremath{\pi}}}^{2}$/3)(${\mathit{k}}_{\mathit{B}}$/e${)}^{2}$ for ${\mathit{k}}_{\mathit{BT}}$\ensuremath{\ll}\ensuremath{\gamma}. For intermediate temperatures the Lorenz ratio deviates significantly from ${\mathit{L}}_{\mathit{S}}$, and is strongly dependent on the scattering cross section, and qualitatively different for resonant vs nonresonant scattering. We include comparisons with other theoretical calculations and the thermal conductivity data for the high-${\mathit{T}}_{\mathit{c}}$ cuprate and heavy fermion superconductors. \textcopyright{} 1996 The American Physical Society.
Rhodium complex-catalyzed desilylative cyclocarbonylation of 1-aryl-2-(trimethylsilyl)acetylenes: a new route to 2,3-dihydro-1H-inden-1-ones (1993)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTRhodium complex-catalyzed desilylative cyclocarbonylation of 1-aryl-2-(trimethylsilyl)acetylenes: a new route to 2,3-dihydro-1H-inden-1-onesRyo Takeuchi and Hiroyuki YasueCite this: J. Org. Chem. 1993, 58, 20, 5386–5392Publication Date (Print):September 1, 1993Publication History Published online1 May 2002Published inissue 1 September 1993https://pubs.acs.org/doi/10.1021/jo00072a020https://doi.org/10.1021/jo00072a020research-articleACS PublicationsRequest reuse permissionsArticle Views739Altmetric-Citations42LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Highly Pathogenic Simian Immunodeficiency Virus mne Variants That Emerge during the Course of Infection Evolve Enhanced Infectivity and the Ability To Downregulate CD4 but Not Class I Major Histocompatibility Complex Antigens (2002)

The replicative, cytopathic, and antigenic properties of simian immunodeficiency virus (SIV) variants influence its replication efficiency in vivo. To further define the viral properties and determinants that may be important for high-level replication in vivo and progression to AIDS, we compared a minimally pathogenic SIVmne molecular clone with two highly pathogenic variants cloned from late stages of infection. Both variants had evolved greater infectivity than the parental clone due to mutations in nef. Interestingly, a pol determinant in one of the highly pathogenic variants also contributed to its increased infectivity. Furthermore, because replication in vivo may also be influenced by the ability of a virus to evade the cellular immune response of the host, we examined whether the variants were more capable of downregulating surface expression of class I major histocompatibility complex (MHC). Decreased MHC class I expression was not observed in cells infected with any of the viruses. Furthermore, the Nef proteins of the highly pathogenic variants only slightly reduced surface MHC class I expression in transfected cells, although they efficiently downregulated CD4. Together, these data demonstrate that mutations which can enhance viral infectivity, as well as CD4 downregulation, may be important for efficient replication of SIV in the host. However, Nef-mediated reduction of MHC class I expression does not appear to be critical for the increased in vivo replicative ability of highly pathogenic late variants.
Transitions between lung cancer phenotypes--implications for tumor progression. (1991)

Progression from a treatment-sensitive to a treatment-resistant tumor state is a virtually universal phenomenon in patients with small-cell lung carcinoma (SCLC). In such individuals, this tumor progression may involve transitions from a SCLC to a non-SCLC lung cancer phenotype. We are investigating the cell and molecular biology aspects of these transitions and have derived a cell culture model of one such change, oncogene-induced transition of SCLC to the large-cell undifferentiated lung cancer phenotype. Here we discuss the potential implication of this model for understanding the cell lineage and molecular events regulating normal bronchial epithelial cell differentiation and their relationships to the histogenesis and behavior of lung cancers.
Limiting factors for maximum oxygen uptake and determinants of endurance performance (2000)

In the exercising human, maximal oxygen uptake (VO2max) is limited by the ability of the cardiorespiratory system to deliver oxygen to the exercising muscles. This is shown by three major lines of evidence: 1) when oxygen delivery is altered (by blood doping, hypoxia, or beta-blockade), VO2max changes accordingly; 2) the increase in VO2max with training results primarily from an increase in maximal cardiac output (not an increase in the a-v O2 difference); and 3) when a small muscle mass is overperfused during exercise, it has an extremely high capacity for consuming oxygen. Thus, O2 delivery, not skeletal muscle O2 extraction, is viewed as the primary limiting factor for VO2max in exercising humans. Metabolic adaptations in skeletal muscle are, however, critical for improving submaximal endurance performance. Endurance training causes an increase in mitochondrial enzyme activities, which improves performance by enhancing fat oxidation and decreasing lactic acid accumulation at a given VO2. VO2max is an important variable that sets the upper limit for endurance performance (an athlete cannot operate above 100% VO2max, for extended periods). Running economy and fractional utilization of VO2max also affect endurance performance. The speed at lactate threshold (LT) integrates all three of these variables and is the best physiological predictor of distance running performance.
Immune regulation by 4‐1BB and 4‐1BBL: complexities and challenges (2009)

The tumor necrosis factor receptor family member 4-1BB plays a key role in the survival of activated and memory CD8(+) T cells. Depending on the disease model, 4-1BB can participate at different stages and influence different aspects of the immune response, likely due to the differential expression of receptor and ligand relative to other costimulatory molecules. Studies comparing mild versus severe influenza infection of mice suggest that the immune system uses inducible receptors such as 4-1BB to prolong the immune response when pathogens take longer to clear. The expression of 4-1BB on diverse cell types, evidence for bidirectional as well as receptor-independent signaling by 4-1BBL, the unexpected hyperproliferation of 4-1BB-deficient T cells, and complex effects of agonistic anti-4-1BB therapy have revealed additional roles for the 4-1BB/4-1BBL receptor/ligand pair in the immune system. In this review, we discuss these diverse roles of 4-1BB and its ligand in the immune response, exploring possible mechanisms for the observed complexities and implications for therapeutic applications of 4-1BB/4-1BBL.
Evidence for nifU and nifS Participation in the Biosynthesis of the Iron-Molybdenum Cofactor of Nitrogenase (2007)

The nifU and nifS genes encode the components of a cellular machinery dedicated to the assembly of [2Fe-2S] and [4Fe-4S] clusters required for growth under nitrogen-fixing conditions. The NifU and NifS proteins are involved in the production of active forms of the nitrogenase component proteins, NifH and NifDK. Although NifH contains a [4Fe-4S] cluster, the NifDK component carries two complex metalloclusters, the iron-molybdenum cofactor (FeMo-co) and the [8Fe-7S] P-cluster. FeMo-co, located at the active site of NifDK, is composed of 7 iron, 9 sulfur, 1 molybdenum, 1 homocitrate, and 1 unidentified light atom. To investigate whether NifUS are required for FeMo-co biosynthesis and to understand at what level(s) they might participate in this process, we analyzed the effect of nifU and nifS mutations on the formation of active NifB protein and on the accumulation of NifB-co, an isolatable intermediate of the FeMo-co biosynthetic pathway synthesized by the product of the nifB gene. The nifU and nifS genes were required to accumulate NifB-co in a nifN mutant background. This result clearly demonstrates the participation of NifUS in NifB-co synthesis and suggests a specific role of NifUS as the major provider of [Fe-S] clusters that serve as metabolic substrates for the biosynthesis of FeMo-co. Surprisingly, although nifB expression was attenuated in nifUS mutants, the assembly of the [Fe-S] clusters of NifB was compensated by other non-nif machinery for the assembly of [Fe-S] clusters, indicating that NifUS are not essential to synthesize active NifB.
Pseudo-von Willebrand disease: a mutation in the platelet glycoprotein Ib alpha gene associated with a hyperactive surface receptor (1993)

Pseudo (platelet-type)-von Willebrand disease is an autosomal dominant bleeding disorder caused by the hyperfunction of a receptor on the platelet surface. The abnormal receptor, glycoprotein Ib, displays increased affinity for its ligand, von Willebrand factor. Four members (normal mother/affected father/two affected daughters) of a family with pseudo-von Willebrand disease were studied to determine the molecular genetic basis for their congenital platelet defect. Segments of the platelet glycoprotein Ib alpha gene were amplified by means of the polymerase chain reaction, cloned, and sequenced. A point mutation (A to G, codon 239) was found in segments from the affected individuals but not from the normal. The mutation results in a single amino acid substitution (valine-mutant for methionine-normal) at residue 239 within the Ib alpha binding site for von Willebrand factor. Both the mutant and the normal sequence were found in affected individuals, suggesting a heterozygous state. Amplified DNA from family members and from 58 normal individuals was analyzed by allele-specific oligonucleotide hybridization. Only the normal sequence was found in the mother and the normal individuals, whereas both the normal and the mutant alleles were found in the affected family members. The described mutation is associated with the pseudo-von Willebrand disease phenotype seen in this kindred. The resultant single amino acid substitution in glycoprotein Ib alpha relates to increased receptor function and to excessive binding of von Willebrand factor to the platelet surface.
Genotyping single nucleotide polymorphisms by mass spectrometry (2002)

In the last decade, the demand for high-throughput DNA analysis methods has dramatically increased, mainly due to the advent of the human genome sequencing project that is now nearing completion. Even though mass spectrometry did not contribute to that project, it is clear that it will have an important role in the post-genome sequencing era, in genomics and proteomics. In genomics, mainly matrix-assisted laser desorption/ionization (MALDI) mass spectrometry will contribute to large-scale single nucleotide polymorphism (SNP) genotyping projects. Here, the development and history of DNA analysis by mass spectrometry is reviewed and put into the context with the requirements of genomics. All major contributions to the field and their status and limitations are described in detail.
Tunable coupling of qubits: Nonadiabatic corrections (2006)

We analyze the coupling of qubits mediated by a tunable and fast element beyond the adiabatic approximation. The nonadiabatic corrections are important and even dominant in parts of the relevant parameter range. As an example, we consider the tunable capacitive coupling between two charge qubits mediated by a gated Josephson junction, as suggested by Averin and Bruder. The nonadiabatic, inductive contribution persists when the capacitive coupling is tuned to zero. On the other hand, the total coupling can be turned off (in the rotating wave approximation) if the qubits are operated at symmetry points.
Phase I trial of recombinant human gamma-interferon and recombinant human tumor necrosis factor in patients with advanced gastrointestinal cancer. (1989)

Recombinant human gamma-interferon and recombinant human tumor necrosis factor are two representatives of a new class of antineoplastic agents. In vitro studies have suggested synergistic cytotoxic activities when the agents are combined. We report a phase I study of these two agents when administered daily for 5 consecutive days every 2 weeks in patients with advanced gastrointestinal cancers. Toxicity resulting from these agents was significant with hyperbilirubinemia representing the dose-limiting toxicity. Significant, although transient, myelosuppression was also observed. The maximal tolerated doses were 150 micrograms/m2/day for 5 days for each agent. Suggestive antineoplastic activity in biliary and pancreatic cancer was observed. Phase II trials of this combination are currently in progress.
Lipid droplet autophagy in the yeast Saccharomyces cerevisiae (2013)

Cytosolic lipid droplets (LDs) are ubiquitous organelles in prokaryotes and eukaryotes that play a key role in cellular and organismal lipid homeostasis. Triacylglycerols (TAGs) and steryl esters, which are stored in LDs, are typically mobilized in growing cells or upon hormonal stimulation by LD-associated lipases and steryl ester hydrolases. Here we show that in the yeast Saccharomyces cerevisiae, LDs can also be turned over in vacuoles/lysosomes by a process that morphologically resembles microautophagy. A distinct set of proteins involved in LD autophagy is identified, which includes the core autophagic machinery but not Atg11 or Atg20. Thus LD autophagy is distinct from endoplasmic reticulum-autophagy, pexophagy, or mitophagy, despite the close association between these organelles. Atg15 is responsible for TAG breakdown in vacuoles and is required to support growth when de novo fatty acid synthesis is compromised. Furthermore, none of the core autophagy proteins, including Atg1 and Atg8, is required for LD formation in yeast.
Kinase inhibitors for the treatment of inflammatory and autoimmune disorders (2008)

Drugs targeting inhibition of kinases for the treatment of inflammation and autoimmune disorders have become a major focus in the pharmaceutical and biotech industry. Multiple kinases from different pathways have been the targets of interest in this endeavor. This review describes some of the recent developments in the search for inhibitors of IKK2, Syk, Lck, and JAK3 kinases. It is anticipated that some of these compounds or newer inhibitors of these kinases will be approved for the treatment of rheumatoid arthritis, psoriasis, organ transplantation, and other autoimmune diseases.
Biliary epithelial cell antibodies induce expression of toll-like receptors 2 and 3: A mechanism for post–liver transplantation cholangitis? (2005)

Studies to determine the role of preformed antibodies to biliary epithelial cells (BECs) in liver transplant rejections have been initiated. However, the clinical importance of these antibodies in the posttransplantation period still remains to be elucidated. Reactivity to BECs isolated from a normal healthy liver was investigated in sera of 56 patients before and after liver transplantation (LTX) using flow cytometry. Functional capacity of BEC antibodies was determined by the ability to induce expression of Toll-like receptors (TLRs) on BECs. Cytokine and chemokine production induced by BEC antibodies was determined by enzyme-linked immunosorbent assay. In all, 7 patients (13%) had BEC antibodies only pre-LTX, 14 (25%) only after LTX, 18 (32%) both before and after LTX, and 17 (30%) had no detectable antibodies. Presence of preformed BEC antibodies correlated with acute rejections (P < 0.03). Deposition of immunoglobulins in bile ducts was detected in biopsies of patients during rejections. Significantly higher numbers of patients with post-LTX antibodies (9 of 32) developed cholangitis, compared with 0 of 17 without antibodies (P < 0.02). Specificity studies indicated that these antibodies were both non-HLA- and HLA-specific. Normal BECs expressed mRNA but not the proteins for the TLRs. However, treatment with F(ab')2 fragments of BEC antibodies induced protein expression of TLRs 2 and 3 and significantly high production of interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1alpha, epithelial neutrophil activating peptide (ENA)-78, and IL-8. In conclusion, BEC antibodies via induction of TLR2 and TLR3 expression, as well as inflammatory cytokine and chemokine production may induce epithelial cell inflammatory responses to bacterial components and contribute to posttransplantation cholangitis.