gebhart/patrepeval huggingface dataset:
Partial inhibition of the human immunodeficiency virus type 1 protease results in aberrant virus assembly and the formation of noninfectious particles (1993)

The production of infectious particles by human immunodeficiency virus type 1 is dependent on the accurate cleavage of its Gag and Gag/Pol precursors by a virally encoded protease. In the absence of protease activity, morphologically abnormal particles which are noninfectious are formed. Recently, inhibitors of the protease of human immunodeficiency virus type 1 have been developed as potential therapeutic agents. We have examined the basis for the loss of infectivity at the limiting inhibitor concentrations that are likely to be achieved in clinical settings. We found that subtle defects in processing are correlated with profound deficits in infectivity. Further, we correlated this partially disrupted processing with an altered virion morphology. These data suggest that accurate and complete processing is essential to the formation of infectious, morphologically normal virions and that the pathway by which these precursors are processed and assembled is sensitive to partial inhibition of the protease by an inhibitor disproportionate to the effect of the inhibitor on the viral protease itself.
Canonical packet transmission on the ISI channel with Gaussian noise (2002)

Generalized decision feedback equalization (GDFE) enables canonical transmission on channels with intersymbol interference and Gaussian noise. There are several special cases of the GDFE, two of which are reviewed: vector-coding (VC) and packet decision feedback. Under special circumstances described, the packet DFE reduces to the well-known DFE as the delay and packet length go to infinity. Under the well-known situation where cyclic-prefixed packet transmission is used, VC reduces to the ADSL standard transmission method known as DMT.
Microphase separation in correlated random copolymers: Mean-field theory and fluctuation corrections (1998)

The behavior of a random $\mathrm{AB}$ multiblock copolymer melt with a Markovian sequence of monomers has been studied in the region where the spatially homogeneous state loses its stability. We use a generalization of the weak crystallization theory to the case of a polydisperse system. In the framework of both mean-field and Brazovski\ifmmode \breve{\imath}\else \u{\i}\fi{} approximations phase diagrams of such a system are constructed. It is shown that the major difference of these diagrams from the monodisperse ones is the presence of regions where two phases with different symmetry of the superlattice (lamellar, hexagonal, and bcc) coexist with each other in the finite temperature range. We show that the account of fluctuations alters the phase diagram near the critical point in comparison with the mean-field picture. In particular, in addition to ``windows'' of direct transitions from disordered to lamellar and hexagonal phases, three phase lines appear, where one of the two coexisting phases changes its symmetry. We demonstrate also that the period of the superstructures varies continuously with the temperature variation.
Plastic-adherent progenitor cells in human bone marrow. (1987)

Human bone marrow contains plastic-adherent hemopoietic progenitor cells whose plating efficiency is increased by brief (2 h) exposure to methylprednisolone (MP). When subsequently covered with methylcellulose medium, they form colonies of monoblastoid cells. Colony size, but not number, and mature cell production are increased by erythropoietin (epo) and granulocyte-macrophage colony-stimulating factor (GM-CSF). However, colonies do not grow under serum-free conditions. The resistance of plastic-adherent progenitors to treatment with 5-fluorouracil (5FU), their growth pattern, and their capacity to produce granulocytic and erythroid colonies on replating, suggest that they may be similar to the primitive, 5FU-resistant, plastic-adherent progenitor cells (HPP-CFC) in murine marrow.
Using Context to Create Semantic 3D Models of Indoor Environments (2010)

Semantic 3D models of buildings encode the geometry as well as the identity of key components of a facility, such as walls, floors, and ceilings. Manually constructing such a model is a time-consuming and error-prone process. Our goal is to automate this process using 3D point data from a laser scanner. Our hypothesis is that contextual information is important to reliable performance in unmodified environments, which are often highly cluttered. We use a Conditional Random Field (CRF) model to discover and exploit contextual information, classifying planar patches extracted from the point cloud data. We compare the results of our context-based CRF algorithm with a context-free method based on L2 norm regularized Logistic Regression (RLR). We find that using certain contextual information along with local features leads to better classification results.
Autologous Free Dermal Fat Graft: Reconstruction of Facial Contour Defects (1995)

Successful long-term augmentation of facial contour defects may be achieved with autologous FDFGs in an appropriate patient population. Careful patient selection and proper surgical technique are essential for satisfactory long-term results. Guidelines are provided for the augmentation of facial contour defects with autologous FDFGs.
Growth factor supplemented matrigel improves ectopic skeletal muscle formation—a cell therapy approach (2001)

Following damage to skeletal muscle, satellite cells become activated, migrate towards the injured area, proliferate, and fuse with each other to form myotubes which finally mature into myofibers. We tested a new approach to muscle regeneration by incorporating myoblasts, with or without the exogenous growth factors bFGF or HGF, into three-dimensional gels of reconstituted basement membrane (matrigel). In vitro, bFGF and HGF induced C2C12 myoblast proliferation and migration and were synergistic when used together. In vivo, C2C12 or primary i28 myoblasts were injected subcutaneously together with matrigel and growth factors in the flanks of nude mice. The inclusion of either bFGF or HGF increased the vascularization of the gels. Gels supplemented with bFGF showed myogenesis accompanied by massive mesenchymal cell recruitment and poor organization of the fascicles. Samples containing HGF showed delayed differentiation with respect to controls or bFGF, with increased myoblast proliferation and a significantly higher numbers of cells in myotubes at later time points. HGF samples showed limited mesenchymal cell infiltration and relatively good organization of fascicles. The use of both bFGF and HGF together showed increased numbers of nuclei in myotubes, but with bFGF-mediated fibroblast recruitment dominating. These studies suggest that an appropriate combination of basement membrane components and growth factors could represent a possible approach to enhance survival dispersion, proliferation, and differentiation of myogenic cells during muscle regeneration and/or myoblast transplantation. This model will help develop cell therapy of muscle diseases and open the future to gene therapy approaches. J. Cell. Physiol. 186:183–192, 2001. © 2001 Wiley-Liss, Inc.
Cellular patterns of insulin-like growth factor system gene expression in murine chondrogenesis and osteogenesis. (1995)

In situ hybridization histochemistry was used to map cellular patterns of gene expression for the insulin-like growth factor (IGF) system in developing murine skeleton from embryonic day 15 (E15) through postnatal day 25 (P25). IGF-I receptor and IGF-II receptor messenger RNAs (mRNAs) are both selectively concentrated in developing chondrocytes and osteoblasts. IGF-II and IGF-binding protein-5 and -6(IGFBP-5 and -6) mRNAs are abundant in mesenchymal condensations and chondroblasts on E15. Chondrocyte IGF-II mRNA levels remain high, but IGFBP-5 and -6 mRNAs decline significantly as cartilage matures. Low levels of IGFBP-6 mRNA are detected in postnatal chondrocytes up to at least P25, but IGFBP-5 mRNA is no longer detected in chondrocytes after E18. IGF-I and IGFBP-2, -3, and -4 mRNAs are detected in surrounding mesenchymal tissue, but are not detected in mesenchymal condensations or chondrocytes at any stage of development. IGFBP-3 mRNA is localized in sprouting capillaries invading the perichondrium and periosteum throughout development. IGF-I, IGF-II, and IGFBP-2, -4, -5, and -6 mRNAs are detected in osteoblasts localized in zones of endochondral ossification from E18 to at least P25. IGFBP-1 mRNA is not detected in cartilage or bone cells at any stage of development. These data confirm the recent report by Shinar et al. that IGF-II, but not IGF-I, mRNA is detected in rat chondrocytes in vivo and show that this pattern also applies to the mouse. The present study demonstrates, for the first time, the cell-specific patterns of IGF-I and -II receptor and IGFBP-2 to -6 gene expression during the processes of chondro- and osteogenesis in vivo. Interestingly, IGF-II, both IGF receptors, and IGFBP-5 and -6 are simultaneously coexpressed in chondrocyte precursors early in skeletal development, suggesting functional interactions between these specific factors in chondrogenesis. Both IGFs, both IGF receptors, and IGFBP-2, -4, -5, and -6 are all expressed in osteoblasts, providing evidence for potential local interactions between these IGF system components in osteogenesis. Thus, 9 of 10 known components of the IGF system demonstrate dynamic cell-specific patterns of gene expression during chondro- and osteogenesis, supporting the view that the IGF system has a complex and integral role within the developing skeleton.
Ketamine hydrochloride in the treatment of phantom limb pain (1993)

Three cases are described in which phantom limb pain was successfully treated with ketamine hydrochloride. Possible mechanisms for this observation are suggested.
Advanced real-time safety management system for construction sites (2008)

This paper reports the results of preliminary experiments concerning position tracking of workers in construction sites. The experiments are part of an ongoing research concerning the development of a new generation of advanced construction management systems allowing real-time monitoring and coordination of tasks, automatic health and safety management, on-site delivery of technical information, capture of as-built documentation, etc. This paper focuses on the development of a reliable methodology for real-time monitoring of workers’ and equipment’s position in outdoor construction sites through the application of technologies based on Ultra Wide Band (UWB). Guidelines for the design of the receivers’ topology will be addressed and the results of measurements done on a typical medium sized block of flats in different construction progress phases will be summed.
A New Family of Human Histone Deacetylases Related toSaccharomyces cerevisiae HDA1p (1999)

Histone deacetylases are the catalytic subunits of multiprotein complexes that are targeted to specific promoters through their interaction with sequence-specific DNA-binding factors. We have cloned and characterized a new human cDNA, HDAC-A, with homology to the yeast HDA1 family of histone deacetylases. Analysis of the predicted amino acid sequence of HDAC-A revealed an open reading frame of 967 amino acids containing two domains: a NH2-terminal domain with no homology to known proteins and a COOH-terminal domain with homology to known histone deacetylases (42% similarity to RPD3, 60% similarity to HDA1). Three additional human cDNAs with high homology to HDAC-A were identified in sequence data bases, indicating that HDAC-A itself is a member of a new family of human histone deacetylases. The mRNA encoding HDAC-A was differentially expressed in a variety of human tissues. The expressed protein, HDAC-Ap, exhibited histone deacetylase activity and this activity mapped to the COOH-terminal region (amino acids 495-967) with homology to HDA1p. In immunoprecipitation experiments, HDAC-A interacted specifically with several cellular proteins, indicating that it might be part of a larger multiprotein complex.
Linkage studies in familial Alzheimer disease: evidence for chromosome 19 linkage. (1991)

A genetic component in the etiology of Alzheimer disease (AD) has been supported by indirect evidence for several years, with autosomal dominant inheritance with age-dependent penetrance being suggested to explain the familial aggregation of affecteds. St. George Hyslop et al. reported linkage of familial AD (FAD) in four early-onset families (mean age at onset [M] less than 50 years). Subsequent studies have been inconsistent in their results; Goate et al. also reported positive lod scores. However, both Pericak-Vance et al.'s study of a series of mainly late-onset FAD families (M greater than 60 years) and Schellenberg et al.'s study failed to confirm linkage to chromosome 21 (CH21). These various studies suggest the possibility of genetic heterogeneity, with some families linked to CH21 and others unlocalized. Recently, St. George Hyslop et al. extended their analysis to include additional families. The extended analyses supported their earlier finding of linkage to CH21, while showing strong evidence of heterogeneity between early-onset (M less than 65 years) and late-onset (M greater than 60 years) FAD families. Because our families did not show linkage to CH21, we undertook a genomic search for an additional locus for FAD. Because of both the confounding factor of late age at onset of FAD and the lack of clear evidence of Mendelian transmission in some of our families, we employed the affected-pedigree-member (APM) method of linkage analysis as an initial screen for possible linkage. Using this method, we identified two regions suggesting linkage: the proximal long arm of chromosome 19 (CH19) and the CH21 region of FAD linkage reported by St. George Hyslop et al. Application of standard likelihood (LOD score) analysis to these data support the possibility of an FAD gene locate on CH19, particularly in the late-onset FAD families. These data further suggest genetic heterogeneity and delineate this region of CH19 as an area needing additional investigation in FAD.
Glyburide Decreases Insulin Requirement, Increases (β-Cell Response to Mixed Meal, and Does Not Affect Insulin Sensitivity: Effects of Short- and Long-Term Combined Treatment in Secondary Failure to Sulfonylurea (1987)

In 20 patients with non-insulin-dependent diabetes mellitus (NIDDM) and secondary failure to sulfonylurea, a double-blind randomized study was performed comparing two regimes: insulin plus placebo (IP) and insulin plus glyburide (IG). The protocol included two hospitalization periods (days 1-18 and 78-85) and follow-up at the outpatient clinic for 325 days. The metabolic control was kept as tight as possible. The subjects underwent normoglycemic clamp studies and meal tests with determination of insulin, C-peptide, glucagon, somatostatin, and gastric inhibitory polypeptide in plasma. On IG, they demonstrated marked and long-lasting improvement of metabolic control: HbA1c decreased from 11.1 +/- 0.3% on day 3 to 8.3 +/- 0.4% (P less than .001) on day 78 and 9.1 +/- 0.5% (P less than .001) on day 325. In subjects on IP, the corresponding values were 10.3 +/- 0.5, 8.4 +/- 0.4 (P less than .001), and 8.9 +/- 0.5% (P less than .05). Body weight increased by 6.0 +/- 1.5 kg (P less than .005) on IG and 2.9 +/- 2.1 kg (NS) on IP. The daily insulin requirement decreased on IG from 62.5 +/- 12.9 U/day on day 7 to 33.5 +/- 8.8 U/day on day 83 and 34.6 +/- 8.9 U/day on day 325. On IP the insulin requirement was almost constant: 62.0 +/- 10.7 U/day on day 7, 55.5 +/- 7.7 U/day on day 83, and 54.7 +/- 7.9 U/day on day 325. Insulin sensitivity measured with the hyperinsulinemic clamp (plasma insulin approximately equal to 130 microU/ml) was similar on IP and IG at the initiation of the study and was unchanged on days 18 and 85. A key observation of this study, although the mechanism is unclear, is that isoglycemic-meal-related insulin requirement was diminished by insulin treatment, indicating improvement of meal-related insulin sensitivity. Glyburide increased basal and meal-but not glucagon-stimulated insulin and C-peptide levels, and also augmented the effect of meals on somatostatin release. We conclude that in NIDDM, IG regime promptly and continuously decreased insulin requirement and improved metabolic control. This effect is, at least during the first 3 mo, mainly due to enhanced insulin secretion. IG and IP treatment had no effect on insulin sensitivity during hyperinsulinemic-normoglycemic clamp, whereas meal-related insulin sensitivity was augmented.
Syndromes of Androgen Resistance1 (1992)

Androgen resistance can be divided into two broad categories: deficiency in 5 alpha-reductase and defects in the androgen receptor. Studies of these two disorders have provided insight into both the normal pathway of androgen action and into the pathogenesis of abnormal sexual development. 5 alpha-Reductase deficiency is a rare autosomal recessive disorder involving the 5 alpha-reductase 2 enzyme; affected males exhibit a defect in virilization most evident as impairment of the virilization of the external genitalia and urogenital sinus. Disorders of the androgen receptor in genetic males cause a spectrum of developmental abnormalities that vary from phenotypic females to men with mild defects in virilization. On functional grounds we have divided these defects into absence of receptor function, qualitatively abnormal receptors, quantitative defects in receptor amount, and apparently normal receptor. Cloning of the cDNA for the receptor and application of the polymerase chain reaction techniques for sequencing of mutants made it possible to analyze these defects at the molecular level. It is now apparent that the functional categorization underestimated the complexity of the mutations. Indeed, major gene deletions and/or rearrangements, single amino acid substitutions, and premature termination codons all can cause variably severe functional abnormalities.
Internet Group Management Protocol, Version 3 (2002)

This document specifies Version 3 of the Internet Group Management Protocol, IGMPv3. IGMP is the protocol used by IPv4 systems to report their IP multicast group memberships to neighboring multicast routers. Version 3 of IGMP adds support for filtering, that is, the ability for a system to report interest in receiving packets *only* from specific source addresses, or from *all but* specific source addresses, sent to a particular multicast address. That information may be used by multicast routing protocols to avoid delivering multicast packets from specific sources to networks where there are no interested receivers.
Transforming growth factor β (TGFβ) causes a persistent increase in steady-state amounts of type I and type III collagen and fibronectin mRNAs in normal human dermal fibroblasts (1987)

It has been previously shown that transforming growth factor beta (TGF beta) is capable of stimulating fibroblast collagen and fibronectin biosynthesis. The purpose of this study was to examine the mechanisms involved in TGF beta stimulation of fibroblast biosynthetic activity. Our results indicate that TGF beta causes a marked enhancement of the production of types I and III collagens and fibronectin by cultured normal human dermal fibroblasts. The rate of collagen production by fibroblasts exposed to TGF beta was 2-3-fold greater than that of control cells. These effects were associated with a 2-3-fold increase in the steady-state amounts of types I and III collagen mRNAs and a 5-8-fold increase in the amounts of fibronectin mRNAs as determined by dot-blot hybridization with specific cloned cDNA probes. In addition, the increased production of collagen and fibronectin and the increased amounts of their corresponding mRNAs remained elevated for at least 72 h after removal of TGF beta. These findings suggest that TGF beta may play a major role in the normal regulation of extracellular matrix production in vivo and may contribute to the development of pathological states of fibrosis.
Auto-antibodies against oxidized LDL as a marker of coronary artery disease in patients with familial hypercholesterolaemia (2000)

Auto-antibodies to oxidized low-density lipoprotein (ox-LDL) are thought to play a pivotal role in the pathogenesis of atherosclerosis. This study investigates the value of auto-antibodies to ox-LDL as a predictive marker of atherosclerosis in patients with both homozygous and heterozygous familial hypercholesterolaemia (FH), who are known to suffer from severe premature atherosclerosis. The influences of well-established risk factors for atherosclerosis such as age, LDL-cholesterol levels and smoking on the results were also determined. Auto-antibody titres to ox-LDL and fasting lipid profiles were measured in 26 homozygous FH patients, 20 heterozygous FH patients without documented coronary artery disease (CAD), 24 heterozygotes with overt CAD and 10 healthy normocholesterolaemic controls. Carotid intima media thickness, used as an in vivo assessment of atherosclerosis, was also measured in the homozygous FH patients. Ox-LDL titres did not differ between the groups. There was also no association between ox-LDL titres and the LDL-cholesterol level (P=0.14), presence or absence of CAD (P=0.69), age (P=0.50), carotid intima-media thickness (P=0.51) or smoking (P=1.0). In conclusion, antibody titres against ox-LDL cannot be used as a predictive marker of the presence or severity of atherosclerosis in patients with FH.
Suppression of in vitro granulocytopoiesis by captopril and penicillamine. (1988)

The mechanisms underlying drug-induced neutropenia are poorly characterized. We have examined the mechanism of suppression of granulocytopoiesis by captopril and penicillamine using human and canine bone marrow cells in an in vitro culture system. Addition of captopril caused no significant change in granulocyte-macrophage colony formation at concentrations up to 30 micrograms/ml. In the presence of CuSO4 (1-3 micrograms/ml), however, captopril caused significant inhibition of colony growth (p less than 0.05). Penicillamine, another agent associated with neutropenia and, like captopril, having a reactive thiol group, also inhibited colony formation in the presence of copper. Chemical congeners of captopril lacking a reactive thiol group and enalaprilic acid, an alternative angiotensin-converting enzyme (ACE) inhibitor, failed to show inhibition, suggesting that the thiol group and not ACE inhibition was responsible. Analysis of day-7 colonies (98% neutrophilic) and day-21 colonies (37% neutrophilic, 30% macrophagic, 27% eosinophilic, and 6% mixed) showed that neutrophil-containing colonies, but not nonneutrophilic colonies were inhibited by the addition of captopril plus copper. Catalase totally reversed the inhibition of colony formation caused by these agents. Direct measurement of oxygen consumption in the presence of captopril showed marked enhancement with the addition of CuSO4 and a 48% reduction in the presence of added catalase. These data indicate that drugs with a reactive thiol group can interact with copper to generate H2O2, which can be toxic to neutrophilic progenitor cells. We postulate that this may be an important mechanism for drug-associated neutropenia and a general mechanism for drug-induced marrow cell injury.