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PubMed1987

[Acceleration behavior in the antepartum cardiotocogram and the condition of the newborn infant].

The prognostic value of fetal heart accelerations in the antepartal cardiotocogram (CTG) is analyzed with regard to fetal outcome. A total of 560 CTGs made one week before delivery were divided into five groups: newborns with cord around the neck, newborns with acidosis, newborns with fetal growth retardation, newborns with low Apgar scores at 1 and 5 minutes (Apgar-7), normal newborns as control group. In contrast to other publications, the present authors did not find accelerations in the antepartal CTG to be a definite positive prognostic sign. These observations indicate that fetal heart acceleration evaluation should not be included in a fetal heart score in the antepartal CTG.

Acidosis↗

PubMed1978

Myasthenic antibodies cross-link acetylcholine receptors to accelerate degradation.

The decrease of acetylcholine receptors at neuromuscular junctions of myasthenic patients has been attributed to an antibody-mediated autoimmune process that accelerates receptor degradation. We studied the mechanism of this process in skeletal-muscle cultures, using intact antibodies and antibody fragments. Addition of myasthenic IgG or its divalent fragment, F(ab')2, to cultures accelerated the rate of acetylcholine-receptor degradation threefold. By contrast, the monovalent fragment, Fab, from myasthenic serum had no effect on degradation, although it bound to acetylcholine receptors. Addition of a second, "piggyback" antibody to cross-link the Fab:receptor complexes resulted in a threefold increase of the degradation rate. Similarly, when acetylcholine receptors with bound alpha-bungarotoxin were cross-linked by the addition of specific antibody against alpha-bungarotoxin, the degradation rate increased approximately threefold. The effect of myasthenic patients' antibodies in accelerating degradation of acetylcholine receptors is attributed to their ability to cross-link the receptors.

Autoantibodies↗

PubMed2005

Application of accelerated molecular dynamics schemes to the production of amorphous silicon.

The evolving nature of a Stillinger-Weber modeled silicon glass is studied using two accelerated molecular dynamics scheme, specifically, hyperdynamics and self-guided algorithms due to Voter and due to Wu and Wang, respectively. We obtain an acceleration of the dynamics, a "boost," on the order of 20 without incurring any significant computational overhead. The validity of the results using accelerated methods is provided by comparison to a conventional molecular dynamics (MD) algorithm simulated under constant temperature conditions for more than 100 ns. We found that performing a sensitivity analysis of the effect of the parameters lambda and t1 before applying the self-guided MD scheme was important. Values of lambda greater than 0.1 and t1 equal to 1 ps were found to give improved structural evolution as compared to a conventional MD scheme. The hyperdynamics approximation scheme was found to be effective in obtaining boosts in the range of 4-12 for a small system without changing the dynamics of the evolution. However, for a large system size such an approach introduces significant perturbations to the pertinent equations of motion.

Algorithms↗

PubMed2006

Accelerated molecular dynamics simulation of the thermal desorption of n-alkanes from the basal plane of graphite.

We utilize accelerated molecular dynamics to simulate alkane desorption from the basal plane of graphite. Eight different molecules, ranging from n-pentane to n-hexadecane, are studied in the low coverage limit. Acceleration of the molecular dynamics simulations is achieved using two different methods: temperature acceleration and a compensating potential scheme. We find that the activation energy for desorption increases with increasing chain length. The desorption prefactor increases with chain length for molecules ranging from pentane to decane. This increase subsides and the value of the preexponential factor fluctuates about an apparently constant value for decane, dodecane, tetradecane, and hexadecane. These trends are consistent with data obtained in experimental temperature-programed desorption (TPD) studies. We explain the dependence of the preexponential factor on alkane chain length by examining conformational changes within the alkane molecules. For the shorter molecules, torsional motion is not activated over experimental temperature ranges. These molecules can be treated as rigid rods and their partial loss in translational and rotational entropies upon adsorption increases as chain length increases, leading to an increasing preexponential factor. At their typical TPD peak temperatures, torsions are activated in the longer adsorbed chain molecules to a significant extent which increases with increasing chain length, increasing the entropy of the adsorbed molecule. This increase counteracts the decrease in entropy due to a loss of translation and rotation, leading to a virtually constant prefactor.

Journal Article↗

PubMed2003

Functional appliance therapy accelerates and enhances condylar growth.

The present study was designed to quantitatively assess the temporal pattern of expression of Sox 9, the regulator of chondrocyte differentiation and type II collagen, the major component of the cartilage matrix during forward mandibular positioning, and compare it with the expression during natural growth. Female Sprague-Dawley rats, 5 weeks old, were used. Results showed that the expression of Sox 9 and type II collagen are accelerated and enhanced when the mandible is positioned forward. Furthermore, we monitored the amount of new bone formation during mandibular advancement and after the removal of bite-jumping appliances. A substantial increase was observed in the amount of newly formed bone when the mandible was positioned forward. No significant difference in new bone formation could be found after the appliance was removed when compared with natural growth. Thus, functional appliance therapy accelerates and enhances condylar growth by accelerating the differentiation of mesenchymal cells into chondrocytes, leading to an earlier formation and increase in amount of cartilage matrix. This enhancement of growth did not result in a subsequent pattern of subnormal growth for most of the growth period; this indicates that functional appliance therapy can truly enhance condylar growth.

Activator Appliances↗

PubMed2006

Normal-repeat-length polyglutamine peptides accelerate aggregation nucleation and cytotoxicity of expanded polyglutamine proteins.

The dependence of disease risk and age-of-onset on expanded CAG repeat length in diseases like Huntington's disease (HD) is well established and correlates with the repeat-length-dependent nucleation kinetics of polyglutamine (polyGln) aggregation. The wide variation in ages of onset among patients with the same repeat length, however, suggests a role for modifying factors. Here we describe the ability of normal-length polyGln repeat sequences to greatly accelerate the nucleation kinetics of an expanded polyGln peptide. We find that normal-length polyGln peptides enhance the in vitro nucleation kinetics of a Q(47) peptide in a concentration-dependent and repeat-length-dependent manner. In vivo, we show that coexpression of a Q(20) sequence in a Drosophila model of HD expressing Htt exon 1 protein with an Q(93) repeat accelerates both aggregate formation and neurotoxicity. The accelerating effect of short polyGln peptides is attributable to the promiscuity of polyGln aggregate elongation and reflects the intimate relationship between nucleus formation and early elongation events in establishing nucleation kinetics. The results suggest that the overall state of the polyGln protein network in a cellular environment may have a profound effect on the toxic consequences of polyGln expansion and thus may serve as a genetic modifier of age of onset in HD.

Animals↗

PubMed2006

Klf4 and corticosteroids activate an overlapping set of transcriptional targets to accelerate in utero epidermal barrier acquisition.

Premature infants are at an increased risk for infections and dehydration because of incomplete development of the epidermis, which attains its essential function as a barrier only during the last stages of in utero development. When a premature birth is anticipated, antenatal corticosteroids are administered to accelerate lung epithelium differentiation. One pleiotropic, but beneficial, effect of antenatal corticosteroids is acceleration of skin barrier establishment by an unknown mechanism. In mice, the transcription factor Klf4 is both necessary and sufficient, within a developmental field of competence, to establish this skin barrier, as demonstrated by targeted ablation and transgenic expression of Klf4, respectively. Here, we report that Klf4 and corticosteroid treatment coordinately accelerate barrier acquisition in vivo. Transcriptional profiling reveals that the genes regulated by corticosteroids and Klf4 during the critical window of epidermal development significantly overlap. KLF4 activates the proximal promoters of a significant subset of these genes. Dissecting the intersection of the genetic and pharmacological pathways, regulated by KLF4 and corticosteroids, respectively, leads to a mechanistic understanding of the normal process of epidermal development in utero.

Adrenal Cortex Hormones↗

PubMed2001

Acceleration of atherogenesis by COX-1-dependent prostanoid formation in low density lipoprotein receptor knockout mice.

The cyclooxygenase (COX) product, prostacyclin (PGI(2)), inhibits platelet activation and vascular smooth-muscle cell migration and proliferation. Biochemically selective inhibition of COX-2 reduces PGI(2) biosynthesis substantially in humans. Because deletion of the PGI(2) receptor accelerates atherogenesis in the fat-fed low density lipoprotein receptor knockout mouse, we wished to determine whether selective inhibition of COX-2 would accelerate atherogenesis in this model. To address this hypothesis, we used dosing with nimesulide, which inhibited COX-2 ex vivo, depressed urinary 2,3 dinor 6-keto PGF(1alpha) by approximately 60% but had no effect on thromboxane formation by platelets, which only express COX-1. By contrast, the isoform nonspecific inhibitor, indomethacin, suppressed platelet function and thromboxane formation ex vivo and in vivo, coincident with effects on PGI(2) biosynthesis indistinguishable from nimesulide. Indomethacin reduced the extent of atherosclerosis by 55 +/- 4%, whereas nimesulide failed to increase the rate of atherogenesis. Despite their divergent effects on atherogenesis, both drugs depressed two indices of systemic inflammation, soluble intracellular adhesion molecule-1, and monocyte chemoattractant protein-1 to a similar but incomplete degree. Neither drug altered serum lipids and the marked increase in vascular expression of COX-2 during atherogenesis. Accelerated progression of atherosclerosis is unlikely during chronic intake of specific COX-2 inhibitors. Furthermore, evidence that COX-1-derived prostanoids contribute to atherogenesis suggests that controlled evaluation of the effects of nonsteroidal anti-inflammatory drugs and/or aspirin on plaque progression in humans is timely.

6-Ketoprostaglandin F1 alpha↗

PubMed2003

Solution structure of a functionally active fragment of decay-accelerating factor.

The second and third modules of human decay accelerating factor (DAF) are necessary and sufficient to accelerate decay of the classical pathway (CP) convertase of complement. No structure of a mammalian protein with decay-accelerating activity has been available to date. We therefore determined the solution structure of DAF modules 2 and 3 (DAF approximately 2,3). Structure-guided analysis of 24 mutants identified likely contact points between DAF and the CP convertase. Three (R96, R69, and a residue in the vicinity of L171) lie on DAF approximately 2,3's concave face. A fourth, consisting of K127 and nearby R100, is on the opposite face. Regions of module 3 remote from the semiflexible 2-3 interface seem not to be involved in binding to the CP convertase. DAF thus seems to occupy a groove on the CP convertase such that both faces of DAF close to the 2-3 junction (including a positively charged region that encircles the protein at this point) interact simultaneously. Alternative pathway convertase interactions with DAF require additional regions of CCP 3 lying away from the 2-3 interface, consistent with the established additional requirement of module 4 for alternative pathway regulation.

Binding Sites↗

PubMed1989

Binding of hormone accelerates the kinetics of glucocorticoid and progesterone receptor binding to DNA.

Steroid hormone receptors induce genes by virtue of their interaction with DNA regulatory sequences. The hormonal response of a particular gene in vivo correlates with binding of the hormone to the receptor and supposedly reflects the degree of occupancy of the corresponding DNA regulatory sequences. However, in vitro the steroid-free glucocorticoid and progesterone receptors bind specifically to the regulatory sequences of mouse mammary tumor virus, thus raising questions on the role of the hormone in DNA binding in vivo. By using monoclonal antibodies, gel retardation assays, and filter binding techniques we show here that binding of a functional steroid to either the glucocorticoid or the progesterone receptors influences the kinetics of the protein-DNA interaction in vitro. In the presence of hormone the on rate of receptor binding to DNA fragments with or without regulatory sequences is accelerated 2- to 5-fold, and the off rate is accelerated 10- to 20-fold. The receptors complexed to an antihormone bind to DNA with kinetics intermediate between those of the steroid-free and the hormone-bound protein. Thus, ligand binding accelerates the kinetics of receptor binding to DNA and this could partly account for the behavior of the hormone receptor observed in vivo.

Adrenalectomy↗

PubMed1995

The acceleration and collimation of jets.

I will discuss several issues related to the acceleration, collimation, and propagation of jets from active galactic nuclei. Hydromagnetic stresses provide the best bet for both accelerating relativistic flows and providing a certain amount of initial collimation. However, there are limits to how much "self-collimation" can be achieved without the help of an external pressurized medium. Moreover, existing models, which postulate highly organized poloidal flux near the base of the flow, are probably unrealistic. Instead, a large fraction of the magnetic energy may reside in highly disorganized "chaotic" fields. Such a field can also accelerate the flow to relativistic speeds, in some cases with greater efficiency than highly organized fields, but at the expense of self-collimation. The observational interpretation of jet physics is still hampered by a dearth of unambiguous diagnostics. Propagating disturbances in flows, such as the oblique shocks that may constitute the kiloparsec-scale "knots" in the M87 jet, may provide a wide range of untapped diagnostics for jet properties.

Journal Article↗

PubMed1995

Accelerated hybridization of oligonucleotides to duplex DNA.

We report two strategies for accelerating the hybridization of oligonucleotides to DNA. We demonstrate that oligodeoxyribonucleotides and peptide nucleic acid oligomers hybridize to inverted repeats within duplex DNA by D-loop formation. Oligonucleotides and duplex template form an active complex, which can be recognized by T7 DNA polymerase to prime polymerization. Quantitation of polymerization products allowed the rate of hybridization to be estimated, and peptide nucleic acid oligomers and oligonucleotide-protein adducts anneal with association constants 500- and 12,000-fold greater, respectively, than the analogous unmodified oligonucleotides. Together, these results indicate that sequences within duplex DNA can be targeted by Watson-Crick base pairing and that chemical modifications can dramatically enhance the rate of strand association. These findings should facilitate targeting of oligomers for priming DNA polymerization, the detection of diagnostic sequences, and the disruption of gene expression. The observed acceleration of hybridization may offer a new perspective on the ability of RecA or other proteins to accelerate strand invasion.

Base Sequence↗

PubMed1995

Contraction accelerates myosin heavy chain synthesis rates in adult cardiocytes by an increase in the rate of translational initiation.

The purpose of this study was to determine the mechanism by which contraction acutely accelerates the synthesis rate of the contractile protein myosin heavy chain (MHC). Laminin-adherent adult feline cardiocytes were maintained in a serum-free medium and induced to contract at 1 Hz via electrical field stimulation. Electrical stimulation of contraction accelerated rates of MHC synthesis 28%, p < 0.05 by 4 h as determined by incorporation of [3H]phenylalanine into MHC. MHC mRNA expression as measured by RNase protection was unchanged after 4 h of electrical stimulation. MHC mRNA levels in messenger ribonucleoprotein complexes and translating polysomes were examined by sucrose gradient fractionation. The relative percentage of polysomebound MHC mRNA was equal at 47% in both electrically stimulated and control cardiocytes. However, electrical stimulation of contraction resulted in a reproducible shift of MHC mRNA from smaller polysomes into larger polysomes, indicating an increased rate of initiation. This shift resulted in significant increases in MHC mRNA levels in the fractions containing the larger polysomes of electrically stimulated cardiocytes as compared with nonstimulated controls. These data indicate that the rate of MHC synthesis is accelerated in contracting cardiocytes via an increase in translational efficiency.

Animals↗

PubMed1996

Accelerated evolution in inhibitor domains of porcine elafin family members.

Through the analysis of the porcine gene encoding the elastase inhibitor elafin, we demonstrated that there are at least three closely related members of the elafin family, and their genes have arisen by accelerated evolution. A porcine genomic DNA library was screened with a previously cloned human elafin cDNA probe, and several positive clones were obtained that can be distinguished by a combination of restriction enzymes. Sequence analysis of these clones revealed the presence of three homologous members whose genes, all consisting of three exons and two introns, are almost identical except the exon 2 sequences encoding the inhibitor domain called "WAP motif"; the intron sequences are related to each other with sequence similarities of 93-98%, whereas the exon 2 sequences exhibited only 60-77% similarities among the three members. The extreme divergence in the exon 2 sequences compared to the highly conserved intron sequences may be generated by accelerated mutations confined in a short stretch of the genes following recent duplication events of a single ancestral gene. An RNase protection assay indicated that the messages of the elafin family members are abundantly expressed in the trachea and intestine, suggesting that the most likely selective forces for the accelerated evolution are extrinsic proteinases produced by invasive microorganisms.

Amino Acid Sequence↗

PubMed1996

Molecular mechanism of tissue factor-mediated acceleration of factor VIIa activity.

The mechanism of the acceleration of the catalytic activity of factor VIIa (VIIa) in the presence of tissue factor (TF) was investigated. To explore the VIIa's site(s) that correlates with TF-mediated acceleration, zymogen VII, VIIa, and active site-modified VIIa were prepared, and dissociation constants (Kd) for their bindings to TF or soluble TF in solution were determined. We found that conversion of zymogen VII to VIIa led to an increase in affinity (DeltaDeltaG = 4.3-4.4 kJ/mol) for TFs. Dansyl-Glu-Gly-Arg chloromethyl ketone (DNS-EGRck) treatment of VIIa led to a further increase in the affinity (DeltaDeltaG = 7.3-12 kJ/mol). Neither removal of the Gla domain from VIIa nor truncation of the COOH-terminal membrane and cytoplasmic regions of TF affected the affinity enhanced after DNS-EGRck treatment of VIIa. Treatment of VIIa with (p-amidinophenyl)methanesulfonyl fluoride also enhanced its affinity for soluble TF, whereas treatment with 4-(2-aminoethyl)benzenesulfonyl fluoride, phenylmethylsulfonyl fluoride, or diisopropyl fluorophosphate had a slight effect on the affinity. On the other hand, DNS-EGRck and (p-amidinophenyl)methanesulfonyl fluoride treatments, but not diisopropyl fluorophosphate treatment, of VIIa led to protection of its alpha-amino group of Ile-153 from carbamylation. Protection of the alpha-amino group was consistent with formation of a critical salt bridge between Ile-153 and Asp-343 in the protease domain of VIIa. Therefore, TF may preferentially bind to the active conformational state of VIIa. When one assumes that free VIIa exists in equilibrium between minor active and dominant zymogen-like inactive conformational states, preferential binding of TF to the active state leads to a shift in equilibrium. We speculate that TF traps the active conformational state of VIIa and converts its zymogen-like state into an active state, thereby accelerating the VIIa activity.

Amino Acid Chloromethyl Ketones↗

PubMed1998

c-myc mRNA is down-regulated during myogenic differentiation by accelerated decay that depends on translation of regulatory coding elements.

Murine C2C12 myoblasts induced to differentiate into multinucleated myotubes decrease their levels of c-myc mRNA 3-10-fold through posttranscriptional mechanisms that recognize regulatory elements contained in protein-coding sequences in exons 2 and 3 of the mRNA. To determine the mechanism by which these elements mediate c-myc mRNA down-regulation, we examined the regulation of mutant MYC and human beta-globin-MYC fusion mRNAs. Regulation of mRNAs containing MYC exon 2 or 3 is abolished by insertion of an upstream termination codon indicating that regulatory function depends on their translation. Exploiting this translation dependence, we show that pharmacologic inhibition of translation with cycloheximide abolishes the down-regulation of regulated MYC and globin-MYC mRNAs and induces their levels in differentiating C2C12 cells. We exclude the possibility that this induction in mRNA levels results from cycloheximide effects on transcription or processing of parts of the RNA other than the regulatory elements, leading to the conclusion that cycloheximide induction results from mRNA stabilization. We show that the magnitude of cycloheximide induction can be used to estimate turnover rates of mRNAs whose decay is translation-dependent. By using cycloheximide inducibility to examine turnover rates of MYC and globin-MYC mRNAs, we show that the MYC exon 2 and exon 3 regulatory elements, but not MYC 3'-untranslated region or chloramphenicol acetyltransferase coding sequences, mediate accelerated mRNA decay in differentiating, but not undifferentiated, C2C12 cells. We show that these regulatory elements must be translated to confer accelerated mRNA decay and that increased turnover occurs in the cytoplasm and not in the nucleus. Finally, using cycloheximide induction to examine mRNA half-lives, we show that mRNA turnover is increased sufficiently by mechanisms targeting the exon 2 and 3 regulatory elements to account for the magnitude of c-myc mRNA down-regulation during differentiation. We conclude from these results that c-myc mRNA down-regulation during myogenic differentiation is due to translation-dependent mechanisms that target mRNAs containing myc exon 2 and 3 regulatory elements for accelerated decay.

Animals↗

PubMed2000

Overexpression of a mammalian ethanolamine-specific kinase accelerates the CDP-ethanolamine pathway.

Ethanolamine kinase (EKI) is the first committed step in phosphatidylethanolamine (PtdEtn) biosynthesis via the CDP-ethanolamine pathway. We identify a human cDNA encoding an ethanolamine-specific kinase EKI1 and the structure of the EKI1 gene located on chromosome 12. EKI1 overexpression in COS-7 cells results in a 170-fold increase in ethanolamine kinase-specific activity and accelerates the rate of [3H]ethanolamine incorporation into PtdEtn as a function of the ethanolamine concentration in the culture medium. Acceleration of the CDP-ethanolamine pathway does not result in elevated cellular PtdEtn levels, but rather the excess PtdEtn is degraded to glycerophosphoethanolamine. EKI1 has negligible choline kinase activity in vitro and does not influence phosphatidylcholine biosynthesis. Acceleration of the CDP-ethanolamine pathway also does not change the rate of PtdEtn formation via the decarboxylation of phosphatidylserine. The data demonstrate the existence of separate ethanolamine and choline kinases in mammals and show that ethanolamine kinase can be a rate-controlling step in PtdEtn biosynthesis.

Amino Acid Sequence↗

PubMed2001

Accelerated G(1) phase progression induced by the human T cell leukemia virus type I (HTLV-I) Tax oncoprotein.

Tax, the human T cell leukemia virus type I oncoprotein, plays a crucial role in viral transformation and the development of the virally associated disease adult T cell leukemia. Because oncogenesis involves alterations in cell growth, it is important to examine the effects of Tax on cell cycle progression. Using a synchronized cell system, we have found that Tax expression accelerates G(1) phase progression and S phase entry with concomitant DNA replication. This accelerated progression is accompanied by an earlier onset of cdk2 kinase activity. In contrast to the shortening of G(1) phase, the length of S phase is unaffected by Tax expression. As a result of a more rapid cell cycle progression, cells expressing Tax exhibit faster growth kinetics and display an altered cell cycle distribution. Additionally, the decreased time allowed for growth in the presence of Tax results in a decreased cell size. Tax-associated acceleration of cell cycle progression may play a role in the ability of this viral oncoprotein to mediate cellular transformation and promote the development of human T cell leukemia virus type I-associated diseases.

CDC2-CDC28 Kinases↗