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At least 505 records · Page 28Linked to original sources
PubMed1991

Pharmacological versus binding analysis of receptor systems: how do they interplay? Myometrial cell receptors for oxytocin as a paradigm.

Binding studies in various biological systems frequently indicate the presence of several binding sites for a biologically active ligand. They differ in their affinity for the ligand in question, binding capacity, and Hill coefficient, which suggests differences in the mechanisms of the binding site-ligand interactions. Identification of the 'true' receptors (sites initiating a cellular response) appears to be difficult. Three clusters of binding sites for oxytocin were found on rat myometrial cells. The oxytocin receptor seems to be linked to the medium-affinity site; the cooperation between the high- and medium-affinity sites in eliciting the uterotonic response seems likely, but lacks experimental proof. Dose-response analysis in partially irreversibly inhibited uterus preparations, the method of equipotent doses (Furchgott-Bursztyn method), and structure-activity analysis of oxytocin-like peptides acting as competitive inhibitors of oxytocin, turned out to be suitable for pharmacological analysis of this receptor system.

Animals↗
PubMed1997

Chemotherapeutic treatments: a study of the interplay among drug resistance, toxicity and recuperation from side effects.

A system of differential equations for the control of tumor growth cells in a cycle nonspecific chemotherapy is analyzed. Spontaneously acquired drug resistance is taken into account, and a criterion for the selection of chemotherapeutic treatment is used. This criterion purports to describe the possibility of improvement of the patient's health when treatment is discontinued. Contrary to our early results which also take drug resistance into account, in this context strategies of continuous chemotherapy in which rest periods take part may be better than maximum drug concentration throughout the treatment (which appears to be in accordance with clinical practice). This bears out our previous conjecture that when drug resistance is accounted for, the imperfections in the usual modelling of treatment criteria, which in general do not allow for patient recuperation, ruled out the possibility of rest periods in optimal continuous chemotherapy.

Antineoplastic Agents↗
PubMed1998

The interplay of T cell responses to viral and autoimmune epitopes.

The examination of the immune T cell response to herpes simplex virus (HSV) antigen glycoprotein D (gD) in an ongoing infection has revealed a uniquely broad range of antigenic determinants seen. This has been shown in the murine T cell response to gD determinants where over 60% of the overlapping peptides are recognized as opposed to 1 of 30 peptides seen when gD was injected in Freund's adjuvant. This has also been seen in the response to local autoantigens when the HSV infection is produced by corneal scarification. Furthermore, analysis of the response to the autoantigen, Golli myelin basic protein (MBP), present in the developing thymus is explored.

Animals↗
PubMed1998

Pathogenic Neisseria--interplay between pro- and eukaryotic worlds.

The pathogenic Neisseria species constitute a multi-faceted infection model of a highly adapted pathogen-host relationship. Several bacterial and host-cell factors involved in the cellular cross-talk have been recently unraveled. Using Neisseria gonorrhoeae as a prototype, several structurally variable surface proteins, including pili and Opa proteins, have been revealed as adhesins recognizing distinct host-cell receptors. The Opa proteins, in particular, are important in facilitating interaction with heparan sulfate proteoglycan receptors and members of the CD66 and integrin receptor families. These interactions not only enable the pathogens' anchoring, and penetration into, the human mucosa but also stimulate cellular signaling cascades involving the phosphatidylcholine-dependent phospholipase C, acidic sphingomyelinase and protein kinase C in epithelial cells, and Src-related kinases, Rac1, p21-activated kinase and Jun N-terminal kinase in phagocytic cells. Activation of these pathways is essential for the entry and intracellular accommodation of the pathogens but also leads to an early induction of cytokine release, thus priming the immune response. It is believed that detailed knowledge of cellular signaling cascades activated by infection will aid us in applying known and novel interfering drugs, in addition to classical antibiotic therapy, to the therapeutic and prophylactic treatment of persistent or otherwise difficult-to-treat bacterial infections.

Epithelial Cells↗
PubMed1976

The positive control of cell proliferation by the interplay on calcium ions and cyclic nucleotides. A review.

Calcium, cyclic AMP, and cyclic GMP do not seem to be involved in proliferative activation of postmitotic differentiated cells. Instead, they are intracycle regulators, and we propose the following working model of their control of the initiation of DNA synthesis. While a role for cyclic GMP cannot yet be defined, a brief postmitotic burst of its synthesis might serve to prevent certain activated cells (e.g. 3T3 mouse cells) from being diverted into a nonproliferating (but still activated) G0 state (Figs. 1 and 17). In a latter part of the G1 phase, something happens to stimulate briefly the synthesis of cyclic AMP which, in turn, drives calcium ions from the mitochondria into the cytosol to activate newly synthesized thymidylate synthetase (or other primed enzymic assemblies) (Fig. 1). Having "turned on" their target enzymes, the accumulated cyclic AMP is destroyed and the excess calcium ions are reaccumulated by the mitochondria to avoid interfering with succeeding reactions. This model predicts that persistent changes in cyclic AMP metabolism and the respiration-linked, calcium-accumulating (ion-buffering) activity of mitochondria may be responsible for the sustained growth of tumors.

Acetylcholine↗
PubMed2005

[Atherogenesis: interplay between cholesterol, inflammation and coagulation].

It is now generally accepted that, in addition to hypercholesterolemia, pro-inflammatory and procoagulatory factors play a major role in atherogenesis. Risk factors such as smoking, hypertension, diabetes and renal diseases alter lipoprotein profile and composition thus rendering them susceptible to modification. Modified lipoproteins induce local inflammation possibly due to activation of nuclear factor (NF-)kappaB and subsequent expression of adhesion molecules, release of pro-inflammatory cytokines, growth factors and mitogens, which are mediators for cell growth, proliferation and lipid deposition. Furthermore, activation of collagenases and proteases in combination with prothrombotic processes attenuate clot formation, plaque rupture and occlusion of vessels. Clinical as well as experimental studies suggest that elevated levels of pro-inflammatory markers may have a diagnostic potential. Thus, a therapeutic approach which modulates circulating cholesterol levels and improves pro-inflammatory and procoagulatory situation may prove beneficial as adjuvant therapy in atherosclerotic disease.

Atherosclerosis↗
PubMed2002

Insulin regulation of glucose uptake: a complex interplay of intracellular signalling pathways.

Insulin-stimulated glucose uptake in adipose tissue and striated muscle is critical for reducing post-prandial blood glucose concentrations and the dysregulation of this process is one hallmark of Type II (non-insulin-dependent) diabetes mellitus. It has been well established that the insulin-stimulated redistribution of the insulin responsive glucose transporter, GLUT-4, from intracellular storage sites to the plasma membrane depends on the production of phosphoinositide 3,4,5 trisphosphate by the Class IA Phosphatidylinositol 3' kinase. Recent discoveries however, have shown the presence of a second insulin signalling pathway leading to GLUT-4 translocation, a pathway dependent on insulin receptor signalling emanating from caveolae or lipid rafts at the plasma membrane. This pathway begins with the phosphorylation of the adaptor protein Cbl by the insulin receptor, and results in the activation of a small GTP binding protein, TC10, a member of the Rho family. TC10 is able to modulate actin structure in 3T3L1 adipocytes, and its overexpression inhibits insulin-stimulated GLUT-4 translocation, an inhibition completely dependent on localization of TC10 to the caveolae or lipid rafts. The spatial compartmentalization of insulin signalling from caveolae or lipid rafts provides a novel signalling pathway that functions in concert with general signalling mechanisms in the control of actin dynamics regulating insulin-dependent GLUT-4 translocation.

Animals↗
PubMed2002

Anticipatory control of center of mass and joint stability during voluntary arm movement from a standing posture: interplay between active and passive control.

Anticipatory control of upright posture is the focus of this study that combines experimental and modeling work. Individuals were asked to raise or lower their arms from two initial postures such that the final posture of the arm was at 90 degrees with respect to the body. Holding different weights in the hand varied the magnitude of perturbation to postural stability generated by the arm movement. Whole body kinematics and ground reaction forces were measured. Inverse dynamic analysis was used to determine the internal joint moments at the shoulder, hip, knee and ankle, and reaction forces at the shoulder. Center of mass (COM) of the arm, posture (rest of the body without the arms) and whole body (net COM) were also determined. Changes in joint moment at the hip, knee and ankle revealed a significant effect of the direction of movement. The polarities of the joint moment response were appropriate for joint stabilization. Net COM change showed a systematic effect of the direction of movement even though the arm COM was displaced by the same amount and in the same direction for both arm raising and lowering conditions. In order to determine the effects of the passive forces and moments on the posture COM, the body was modeled as an inverted pendulum. The model was customized for each participant; the relevant model parameters were estimated from data obtained from each trial. The ankle joint stiffness and viscosity were adjusted to ensure postural equilibrium prior to arm movement. Joint reactive forces and moments generated by the arm movements were applied at the shoulder level of this inverted pendulum; these were the only inputs and no active control was included. The posture COM profile from the model simulation was calculated. Results show that simulated posture COM profile and measured posture COM profile are identical for about 200 ms following the onset of arm movement and then they deviate. Therefore, the initial control of COM is passive in nature and the observed joint moment response is for joint stabilization and not for the control of COM.

Adaptation, Physiological↗
PubMed2006

The interplay between strategic and adaptive control mechanisms in plastic recalibration of locomotor function.

We have previously shown that viewing simulated rotary self-motion during treadmill locomotion causes immediate strategic modifications (Richards et al. in Presence Teleoper Vir Real 13:371-384, 2004) as well as an after effect reflecting adaptive modification of the control of position and trajectory during over-ground locomotion (Mulavara et al. in Exp Brain Res 166:210-219, 2005). The process of sensorimotor adaptation is comprised of both strategic and adaptive control mechanisms. Strategic control involves cognitive, on-line corrections to motor outputs once one is aware of a sensory discordance. Over an extended period of exposure to the sensory discordance, new strategic sensorimotor coordination patterns are reinforced until they become more automatic, and therefore adaptive in nature. The objective of this study was to investigate how strategic changes in trunk control during exposure to simulated rotary self-motion during treadmill walking influences adaptive modification of locomotor heading direction during over-ground stepping. Subjects (n = 10) walked on a motorized linear treadmill while viewing a wide field-of-view virtual scene for 24 min. The scene was static for the first 4 min and then, for the last 20 min, depicted constant rate self-motion equivalent to walking in a counter-clockwise, circular path around the perimeter of a room. Subjects performed five stepping trials both before and after the exposure period to assess after effects. Results from our previous study showed a significant change in heading direction (HD) during post-exposure step tests that was opposite to the direction in which the scene rotated during the adaptation period. For the present study, we quantified strategic modifications in trunk movement control during scene exposure using normalized root mean square (R(P)) variation of the subject's 3D trunk positions and normalized sum of standard deviations (R (O)) variation of 3D trunk orientations during scene rotation relative to that during static scene presentation. Associated 95% confidence intervals, CI(P) and CI(O), were calculated to investigate the variation of strategic modifications during scene exposure. Repeated measures ANOVA and individual subject regression analyses showed that R(P) and R(O) (i.e. strategic modifications) for trunk fore/aft (X) positions and yaw rotations, respectively, decreased significantly over the exposure period. Furthermore, we found a significant correlation between the magnitude change in HD and the rate at which the variation of strategic modifications in trunk X decreased. We also found evidence of a correlation between HD and the rate at which strategic modifications in trunk yaw decreased. We infer that adaptive recalibration of locomotor trajectory using optic flow stimuli depends on the rate at which kinematic variability associated with strategic control is reduced.

Adaptation, Physiological↗
PubMed2003

The human red cell voltage-regulated cation channel. The interplay with the chloride conductance, the Ca(2+)-activated K(+) channel and the Ca(2+) pump.

The activation/deactivation kinetics of the human erythrocyte voltage-dependent cation channel was characterized at the single-channel level using inside-out patches. It was found that the time dependence for voltage activation after steps to positive membrane potentials was slow ( t(1/2) about 30 s), whereas the deactivation was fast ( t(1/2) about 15 ms). Both activation and deactivation of this channel were also demonstrated in intact red cells in suspension. At very positive membrane potentials generated by suspension in extracellular low Cl(-) concentrations, the cation conductance switched on with a time constant of about 2 min. Deactivation of the cation channel was clearly demonstrated during transient activation of the Gárdos channel elicited by Ca(2+) influx via the cation channel and ensuing efflux via the Ca(2+) pump. Thus, the voltage-dependent cation channel, the Gárdos channel and the Ca(2+) pump constitute a coupled feedback-regulated system that may become operative under physiological conditions.

Adaptation, Physiological↗
PubMed2003

Nonrandom intragenic variations in patterns of codon bias implicate a sequential interplay between transitional genetic drift and functional amino acid selection.

Although most codon third bases appear to be functionless, the synonymous codons so defined exhibit a strikingly nonrandom distribution (codon bias) within human and other genes. To examine this phenomenon further, we generated a database of DNA sequences encoding human transmembrane cell-surface receptor proteins. Using this database we show here that the guanine and cytosine content of codon third bases (GC3) varies intragenically with the nature of the specified receptor domains (transmembrane > extracellular > intracellular domains; p < 0.001), the phenotype of the encoded amino acids (hydrophobic > hydrophilic > neutral amino acids; p < 0.001), and the receptor affiliation of the transmembrane (G-protein-coupled receptors > receptor tyrosine kinases; p < 0.001). Within gene regions specifying transmembrane domains, GC3 declines as domain functionality becomes redundant with increasing hydrophobicity (p < 0.001). Codons containing the second-base cytosine (XCZ, which encodes neutral amino acids) are selectively depleted of third-base adenine content (A3: XCA codons) when encoding transmembrane domain residues, consistent with positive selection for transitional mutation of XCG to XTG (which encodes hydrophobic amino acids) rather than to the synonymous XCA. Supporting this XCG --> XTG mechanism of codon bias, the G3:A3 ratio of codons specifying the transmembrane amino acid glycine (GGZ) is intermediate between that of its functional homolog alanine (GCZ) and that of hydrophobic valine (GTZ), even though the C3:T3 ratios are similar. Conversely, nearest-neighbor analysis of third bases 5' to codons specifying valine and leucine (CTZ) confirms a significant difference in C3:T3 but not G3:A3 ratios (i.e., C3/G1 --> T3/G1 > C3/A1; p < 0.001), consistent with the functionally advantageous retention of hydrophobic residues. These data raise the possibility that patterns of intragenic codon bias reflect a balance between negative and positive selection, suggesting in turn that analysis of codon third-base usage may help to predict the functional significance of encoded products.

Amino Acids↗
PubMed2002

Neurofibromatosis type 1, hyperparathyroidism, and osteosarcoma: interplay?

Neurofibromatosis type 1 (NF 1) is a syndrome with a predisposition for benign and malignant tumor development. Of the malignant neoplasms, osteogenic sarcomas are rare but have been described. There are some reports of patients with neurofibromatosis type 1 with a parathyroid adenoma and hyperparathyroidism. Also, there are studies that imply that the parathyroid hormone plays a role in the regulation and modulation of oseogenic sarcomas in vitro. We report about a 50-year-old female suffering from neurofibromatosis type 1, with a 3-year documented history of untreated hyperparathyroidism and a parathyroid adenoma. The patient developed a mandibular osteogenic sarcoma. To our knowledge, this is the first reported case occurring in the mandible. The unusual tumor site for a patient with neurofibromatosis type 1, the conjugation with hyperparathyroidism and the rapid growth of an osteogenic sarcoma are intriguing.

Bone Neoplasms↗
PubMed2006

Chiasma formation: chromatin/axis interplay and the role(s) of the synaptonemal complex.

Meiotic recombination proceeds in biochemical complexes that are physically associated with underlying chromosome structural axes. In this study, we discuss the organizational basis for these axes, the timing and nature of recombinosome/axis organization with respect to the prophase program of DNA and to structural changes, and the possible significance of axis organization. Furthermore, we discuss implications and extensions of our recently proposed mechanical model for chiasma formation. Finally, we give a broader consideration to past and present models for the role of the synaptonemal complex.

Chromatin↗
PubMed2002

Interplay among the changes of muscle strength, cross-sectional area and maximal explosive power: theory and facts.

A model has recently been proposed to predict the changes of mechanical power (W) during a maximal explosive effort (such as a standing high jump off both feet) following an adaptation (e.g. training/de-training). The model is based on the assumption that, all other things being equal (ceteris paribus), the predicted changes in W depend on the measured changes of muscle force (F) or cross-sectional area (CSA) only. It follows that, if the measured changes in W are not equal to those predicted by the model, factors other than a change in F (or CSA) must be responsible for this difference. The model does not allow the determination of factors specifically involved in the adaptation process but it helps in discriminating whether an adaptation has taken place at a local level (when the observed changes in F would be attributed to factors other than the observed changes in CSA, e.g. co-contractions, fibre type modifications...), or at a central level (when the observed changes in W would be attributed to other factors than the observed changes in F, e.g. co-ordination of multiple joints and muscle groups...), or in both regions. In this paper the model has been applied to data reported in the literature on disuse (BR, bed rest), de-conditioning (SF, space flight), strength training (ST) and de-training (DT). The results of these calculations have confirmed previous observations on the determinants of the adaptation process and further suggest: (1) that training for one specific motor task (e.g. ST) could affect the performance of a second task (e.g. a maximal explosive jump) but that, as soon as the trained motor task is terminated (DT), this ability is re-gained; and (2) that neuromuscular impairment in disuse (BR) is closer to de-training than to the de-conditioning brought about by weightlessness (SF).

Anatomy, Cross-Sectional↗
PubMed2000

Duplicated gene clusters suggest an interplay of glycogen and trehalose metabolism during sequential stages of aerial mycelium development in Streptomyces coelicolor A3(2).

DNA sequencing and operon disruption experiments indicate that the genes glgBI and glgBII, which code for the two developmentally specific glycogen branching enzymes of Streptomyces coelicolor A3(2) each form part of larger duplicated operons consisting of at least four genes in the order pep1-treS-pep2-glgB. The sequences of the TreS proteins are 73% identical (93% similar) to that of an enzyme that converts maltose into trehalose in Pinmelobacter, a distantly related actinomycete; and the Pep1 proteins show relatedness to the alpha-amylase superfamily. Disruptions of each operon have spatially specific effects on the nature of glycogen deposits, as assessed by electron microscopy. Upstream of the glgBI operon, and diverging from it, is a gene (glgP) that encodes a protein resembling glycogen phosphorylase from Thermatoga maritima and a homologue in Mycobacterium tuberculosis. These three proteins form a distinctive subgroup compared with glycogen phosphorylases from most other bacteria, which more closely resemble the enzymes from eukaryotes. Diverging from the glgBII operon, and separated from the pep1 gene by two very small ORFs, is a gene (glgX) encoding a probable glycogen debranching enzyme. It is suggested that most of these gene products participate in the developmentally modulated interconversion of immobile, inert glycogen reservoirs, and diffusible forms of carbon, both metabolically active (e.g. glucose-1-phosphate generated by glycogen phosphorylase) and metabolically inert but physiologically significant (trehalose).

Amino Acid Sequence↗
PubMed2002

Nuclear mitochondrial interplay in the modulation of the homopolymeric tract length heteroplasmy in the control (D-loop) region of the mitochondrial DNA.

We have studied the genetic characteristics of a homopolymeric tract length heteroplasmy associated with the 16189C variant in the mtDNA D-loop control region to identify the factor(s) involved in the generation of the length heteroplasmy. The relative proportion of the various lengths of the polycytosines (i.e., the pattern of the length heteroplasmy) is maintained in an individual, and previous evidence shows that it is regenerated de novo following cell divisions. The pattern is maintained in maternally related individuals, suggestive of mtDNA determinants. Of the 38 individuals with the 16189C variant studied, 39% were found to exhibit the (16180)AAACCCCCCCCCCC(16193) variant associated with A16183C polymorphism [(11C)-group], while 53% showed the (16180)AACCCCCCCCCCCC(16193) variant associated with a further A16182C polymorphism [(12C)-group]. Haplotype analysis of the mtDNA revealed a specific association of the longer mean length of the poly[C] in the (12C)-group with haplogroup B. A similar association was also observed in the (11C)-group, but with a novel haplogroup. Cybrid constructions revealed that the involvement of nuclear factor(s) in the generation of the length heteroplasmy is prominent in homopolymeric tract of eight cytosines. The nuclearly coded factor(s) is/are presumably related to the fidelity of the nuclearly coded components of the mitochondrial DNA replication machinery.

Base Sequence↗