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The dynamic interplay between Western medicine and the complementary and alternative medicine movement: how activists perceive a range of responses from physicians and hospitals.

Scholars must examine the dynamic relationship between activists and organisational actors, because all social movements interact in some way with the institutions they seek to change, and because activists engage in ongoing attempts to shape these interactions. Using data from the complementary and alternative medicine (CAM) movement in California and hospitals in New York and Massachusetts, I identify how physicians and hospitals respond to the CAM movement, and how activists perceive each response. Using social movement and institutional theories, this study illustrates that social movements can penetrate and reshape formal organisations, because established organisations have permeable boundaries. Organisational responses to activism can take the form of avoidance, compromise, acquiescence, manipulation or defiance. Activists vary in their response to these outcomes, because activists are not unanimous in their goals. These outcomes result from continual negotiation between CAM activists and organisational actors, and within each group. Thus, the outcomes are constantly evolving.

Attitude of Health Personnel↗

Interplay between superantigens and immunoreceptors.

Superantigens (SAGs) cause a massive T-cell proliferation by simultaneously binding to major histocompatibility complex (MHC) class II on antigen-presenting cells and T-cell receptors (TCRs) on T cells. These T-cell mitogens can cause disease in host, such as food poisoning or toxic shock. The best characterized groups of SAGs are the bacterial SAGs secreted by Staphylococcus aureus and Streptococcus pyogenes. Despite a common overall three-dimensional fold of these SAGs, they have been shown to bind to MHC class II in different ways. Recently, it has also been shown that SAGs have individual preferences in their binding to the TCRs. They can interact with various regions of the variable beta-chain of TCRs and at least one SAG seems to bind to the alpha-chain of TCRs. In this review, different subclasses of SAGs are classified based upon their binding mode to MHC class II, and models of trimolecular complexes of MHC-SAG-TCR molecules are described in order to reveal and understand the complexity of SAG-mediated T-cell activation.

Amino Acid Sequence↗

Integrating temporal biases: the interplay of focal thoughts and accessibility experiences.

We provide an integrative account of temporal biases (confidence changes, planning fallacy, impact bias, and hindsight bias). Students listed either 3 or 12 thoughts about success or failure before an upcoming real-life exam or immediately after learning their grades. Previous explanations had focused on how thought content alone (what comes to mind) influences temporal biases. We found, however, an interaction between thought content and accessibility experiences (how easily or difficultly thoughts come to mind). Thinking about 3 ways to succeed (success was easy to bring to mind) was equivalent to thinking about 12 ways to fail (failure was difficult to bring to mind), and conversely, thinking about 3 ways to fail was equivalent to thinking about 12 ways to succeed. In no case was thought content alone sufficient to predict the biases. These results have implications for debiasing strategies and other judgments over time.

Affect↗

Dancing with the enemy: the interplay of herpes simplex virus with dendritic cells.

Summary Herpes simplex virus (HSV) represents a smart pathogen, which displays both lytic and latent modes of interaction with its natural human host. In order to be optimally equipped for immune evasion and to reply to any attacks of the host during reactivation, HSV has developed a multitude of cleverly devised defence strategies. Dendritic cells (DC) as antigen-presenting cells located at the border zones of the body and the environment have been shown to play a crucial role as one of the first cells interacting with HSV beside epithelial cells, on one hand, and as important controllers of the viral spreading on the other hand. Here, we provide a research update about the interaction of HSV with DC and summarize the latest proceedings in this field.

Antigens, CD↗

Sensitivity of Escherichia coli to various beta-lactams is determined by the interplay of outer membrane permeability and degradation by periplasmic beta-lactamases: a quantitative predictive treatment.

In Gram-negative bacteria, beta-lactam antibiotics must overcome two barriers, the outer membrane and the periplasmic beta-lactamase, before they reach the targets of their action, penicillin-binding proteins. Although the barrier property of the outer membrane and catalytic property of the beta-lactamases have been studied and their significance in creating beta-lactam resistance emphasized, the interaction between these two barriers has not been treated quantitatively. Such treatment shows that the sensitivity, to a variety of beta-lactams, of the Escherichia coli K-12 cells containing very different levels of chromosomally coded AmpC beta-lactamase, or a plasmid-coded TEM-type beta-lactamase, can be predicted rather accurately from the penetration rate through the outer membrane and the hydrolysis rate in the periplasm. We further propose a new parameter, 'target access index', which is a quantitative expression of the result of interaction between the two barriers, and reflects the probability of success for the antibiotic to reach the targets.

Anti-Bacterial Agents↗

Interplay between primase and replication factor C in the hyperthermophilic archaeon Sulfolobus solfataricus.

The heterodimeric primase from the hyperthermophilic archaeon Sulfolobus solfataricus synthesizes long RNA and DNA products in vitro. How primer synthesis by primase is coupled to primer extension by DNA polymerase in this organism is unclear. Here we show that the small subunit of the clamp loader replication factor C (RFC) of S. solfataricus interacted with both the catalytic and non-catalytic subunits of the primase by yeast two-hybrid and co-immunoprecipitation assays. Further, the primase-RFC interaction was also identified in the cell extract of S. solfataricus. Deletion analysis indicated that the small subunit of RFC interacted strongly with the N-terminal domain of the catalytic subunit of the primase. RFC stimulated dinucleotide formation but decreased the amount of primers synthesized by the primase. The inhibition of primer synthesis is consistent with the observation that RFC reduced the affinity of the primase for DNA templates. On the other hand, primase stimulated the ATPase activity of RFC. These findings suggest that the primase-RFC interaction modulates the activities of both enzymes and therefore may be involved in the regulation of primer synthesis and the transfer of primers to DNA polymerase in Archaea.

Adenosine Triphosphatases↗

Regulation of IgG-IgM interplay by antibody specificity in human K-cell-mediated cytotoxicity.

IgM antibodies, by themselves unable to induce human K-cell-mediated cytotoxicity, enhanced the lysis of TNP-coated bovine erythrocytes (TNP-Eb) induced by suboptimal concentrations of IgG antibodies. The antibodies used were directed against either TNP or intrinsic Eb antigens. The best enhancement of antibody-dependent cell-mediated cytotoxicity (ADCC) was obtained when IgG and IgM antibodies had different specificities. IgM antibodies with specificity similar to that of the IgG antibodies often inhibited rather than enhanced cytolysis. By using 125I-labelled anti-DNP IgG, the number of IgG/TNP-Eb was determined. Under the present conditions, at least 9000 IgG molecules/TNP-Eb were required for K-cell-mediated lysis in the absence of IgM. In the presence of IgM antibody concentrations optimal for enhancement of ADCC, the minimal number of IgG molecules required for induction of ADCC was 30-100 times lower. No enhancement of cytotoxicity was seen with more than the optimal concentration of IgM even when IgG binding to the target cells was not reduced by IgM. This suggested that induction of ADCC was dependent on contiguous IgG-Fc receptor interactions, which were inhibited owing to steric hindrance by excessive amounts of IgM in the critical contact areas between effector cells and target cells.

Animals↗

Type III effectors orchestrate a complex interplay between transcriptional networks to modify basal defence responses during pathogenesis and resistance.

To successfully infect a plant, bacterial pathogens inject a collection of Type III effector proteins (TTEs) directly into the plant cell that function to overcome basal defences and redirect host metabolism for nutrition and growth. We examined (i) the transcriptional dynamics of basal defence responses between Arabidopsis thaliana and Pseudomonas syringae and (ii) how basal defence is subsequently modulated by virulence factors during compatible interactions. A set of 96 genes displaying an early, sustained induction during basal defence was identified. These were also universally co-regulated following other bacterial basal resistance and non-host responses or following elicitor challenges. Eight hundred and eighty genes were conservatively identified as being modulated by TTEs within 12 h post-inoculation (hpi), 20% of which represented transcripts previously induced by the bacteria at 2 hpi. Significant over-representation of co-regulated transcripts encoding leucine rich repeat receptor proteins and protein phosphatases were, respectively, suppressed and induced 12 hpi. These data support a model in which the pathogen avoids detection through diminution of extracellular receptors and attenuation of kinase signalling pathways. Transcripts associated with several metabolic pathways, particularly plastid based primary carbon metabolism, pigment biosynthesis and aromatic amino acid metabolism, were significantly modified by the bacterial challenge at 12 hpi. Superimposed upon this basal response, virulence factors (most likely TTEs) targeted genes involved in phenylpropanoid biosynthesis, consistent with the abrogation of lignin deposition and other wall modifications likely to restrict the passage of nutrients and water to the invading bacteria. In contrast, some pathways associated with stress tolerance are transcriptionally induced at 12 hpi by TTEs.

Amino Acids, Aromatic↗

Control of blastema cell proliferation by possible interplay of calcium and cyclic nucleotides during newt limb regeneration.

The effects of the divalent cation ionophore A23187, papaverine, and chlorpromazine on the mitotic index and cyclic nucleotide levels in newt limb regeneration blastemata (Notophthalmus viridescens) were assessed. The results of the experiments suggest that an intracellular increase in divalent cation (Ca2+) concentration results in elevated cGMP levels, suppressed cAMP levels, and a corresponding increase in blastema cell proliferation. The results also suggest that the converse conditions, namely, calcium efflux or inhibition of calmodulin activation (i.e., inhibition of Ca2+ binding), yields elevated cAMP levels, suppressed cGMP levels, and a corresponding decrease in blastema cell divisions.

Adenosine Monophosphate↗

Electrostatic effects and the dynamics of enzyme reactions at the surface of plant cells. 3. Interplay between limited cell-wall autolysis, pectin methyl esterase activity and electrostatic effects in soybean cell walls.

Soybean cell walls display a process of autolysis which results in the release of reducing sugars from the walls. Loosening and autolysis of cell wall are involved in the cell-wall growth process, for autolysis is maximum during both cell extension and cell-wall synthesis. Autolysis goes to completion within about 50 h and is an enzymatic process that results from the activity of cell wall exo- and endo-glycosyltransferases. The optimum pH of autolysis is about 5. Increasing the ionic strength of the bulk phase where cell-wall fragments are suspended, results in a shift of the pH profile towards low pH. This is consistent with the view that at 'low' ionic strength, the local pH in the cell wall is lower than in the bulk phase. One of the main ideas of the model proposed in a preceding paper, is that pectin methyl esterase reaction, by building up a high fixed charge density, results in proton attraction in the wall. Low pH must then activate the wall loosening enzymes involved in autolysis and cell growth. This view may be directly confirmed experimentally. The pH of a cell-wall suspension, initially equal to 5, was brought to 8 for 20 min, then back to 5. Under these conditions, the rate of cell-wall autolysis was enhanced with respect to the rate of autolysis obtained with cell-wall fragments kept at pH 5. The pH response of the multienzyme plant cell-wall system basically relies on opposite pH sensitivities of the two types of enzymes involved in the growth process. Pectin methyl esterase, which generates the cell-wall Donnan potential, is inhibited by protons, whereas the wall-loosening enzymes involved in cell growth are activated by protons.

Autolysis↗

The relationship between electron flux and the redox poise of the quinone pool in plant mitochondria. Interplay between quinol-oxidizing and quinone-reducing pathways.

The dependence of electron flux through quinone-reducing and quinol-oxidizing pathways on the redox state of the ubiquinone (Q) pool was investigated in plant mitochondria isolated from potato (Solanum tuberosum cv. Bintje, fresh tissue and callus), sweet potato (Ipomoea batatas) and Arum italicum. We have determined the redox state of the Q pool with two different methods, the Q-electrode and Q-extraction techniques. Although results from the two techniques agree well, in all tissues tested (with the exception of fresh potato) an inactive pool of QH2 was detected by the extraction technique that was not observed with the electrode. In potato callus mitochondria, an inactive Q pool was also found. An advantage of the extraction method is that it permits determination of the Q redox state in the presence of substances that interfere with the Q-electrode, such as benzohydroxamate and NADH. We have studied the relation between rate and Q redox state for both quinol-oxidizing and quinone-reducing pathways under a variety of metabolic conditions including state 3, state 4, in the presence of myxothiazol, and benzohydroxamate. Under state 4 conditions or in the presence of myxothiazol, a non-linear dependence of the rate of respiration on the Q-redox state was observed in potato callus mitochondria and in sweet potato mitochondria. The addition of benzohydroxamate, under state 4 conditions, removed this non-linearity confirming that it is due to activity of the cyanide-resistant pathway. The relation between rate and Q redox state for the external NADH dehydrogenase in potato callus mitochondria was found to differ from that of succinate dehydrogenase. It is suggested that the oxidation of cytoplasmic NADH in vivo uses the cyanide-resistant pathway more than the pathway involving the oxidation of succinate. A model is used to predict the kinetic behaviour of the respiratory network. It is shown that titrations with inhibitors of the alternative oxidase cannot be used to demonstrate a pure overflow function of the alternative oxidase.

Benzoquinones↗

Regulation of mitochondrial biogenesis in Saccharomyces cerevisiae. Intricate interplay between general and specific transcription factors in the promoter of the QCR8 gene.

Transcription of the QCR8 gene, encoding subunit VIII of the Saccharomyces cerevisiae mitochondrial ubiquinol-cytochrome c oxidoreductase (QCR), is controlled by the carbon-source-dependent heme-activator protein complex HAP2/3/4 and the general transcriptional regulators autonomous replication-site-binding factor ABF1 and centromere-binding and promoter-binding factor CPF1. In this study, we investigate and dissect the relative contributions and mutual interactions of these regulators in transcriptional control. Transcription was analyzed both under steady-state conditions and during nutritional shifts, in hap delta mutants and after site-specific mutagenesis of the various binding sites in the chromosomal context of the QCR8 gene. We present evidence for both direct and indirect interactions between ABF1 and HAP2/3/4, and show that HAP2/3/4 is essential for a rapid transcriptional induction during transition from repressed to derepressed conditions. However, the activator is not the only determinant for carbon-source-dependent regulation, and we observe a functional difference between HAP2/3/4 and the HAP2/3 subcomplex. ABF1 is required for maintainance of basal repressed and derepressed transcription in the steady state of growth. The repressive action of the negative modulator CPF1 during escape from glucose repression is overcome through the cooperative action of ABF1 and HAP2/3/4. The implications of the intricate interactions of these DNA-binding regulators for control of expression of mitochondrial protein genes are discussed.

Base Sequence↗

Regulation of expression of the rat serine protease inhibitor 2.3 gene by glucocorticoids and interleukin-6. A complex and unusual interplay between positive and negative cis-acting elements.

The rat serine protease inhibitor 2.3 gene (spi 2.3) is almost completely silent in normal animals and is transiently expressed during acute inflammation. It encodes a potential anti-elastase which is likely to play a major physiological role for the host defense. Two well-known inflammatory mediators, glucocorticoids and interleukin-6 (IL-6) activate the spi 2.3 promoter and increase steady-state levels of mRNA in cultured hepatocytes. GC activation is mediated by a single glucocorticoid-response element which seems to act autonomously. A unique array of four functional IL-6-response sites was identified in the spi 2.3 promoter. Three of them (C-II--IV) bear structural identity to the CCAAT/enhancer-binding-protein-binding site consensus sequence, whereas the fourth closely resembles the consensus kappa B nuclear factor recognition motif. The C-IV element, which is the most active, contains the motif 5'-CTGGGA and binds the IL-6-inducible acute-phase response factor present in liver nuclear extracts from inflamed rats. Both basal and IL-6-dependent activities of each individual cytokine-response element tested separately are strongly down regulated by a recently identified regulatory sequence, located in the 3' untranslated region of the spi 2.3 gene. However, this repressor element does not significantly affect overall IL-6-dependent spi 2.3 promoter activity. This suggests that, in the context of the active gene in vivo, all four IL-6-response sites, which are largely redundant, cooperate to overcome the strong repressive effect of the 3' untranslated region silencer and are needed to bring about a maximal IL-6 response. These data reveal a novel type of regulation of an acute-phase gene involving different classes of IL-6-response elements controlled by a repressor and acting in conjunction with a glucocorticoid-response element.

Animals↗

Frontier migration as a multi-stage phenomenon reflecting the interplay of macroforces and local conditions: the Ecuador Amazon.

"This paper considers frontier migration to the Ecuador Amazon as a multistage phenomenon, examining the entire migration stream from its origins in highland and coastal locales of Ecuador, to intermediate stops outside and within the Amazon, to final Amazon destinations. The approach is one where models pertaining to regional development, migration, and pioneer activity are treated as complementary to one another and meshed with a qualitative knowledge of place. It is shown that frontier settlement patterns reflect the composite of these models, a maturing space-economy, and the interaction of local characteristics with exogenous circumstances representing national and international contexts."

Americas↗

Interplay and interference of the carotid baroreceptors, central command, ergoreceptors on the peripheral vascular responses during static exercise.

1. The aim of the present study was to examine the influence of the carotid baroreceptors on the peripheral vascular responses during static exercise and its interference with the 'central command' and the ergoreceptors. 2. Ten healthy subjects performed an isometric handgrip with 30% of maximal voluntary contraction for 1.5 min. Five seconds prior to the end of the exercise the arterial circulation to the exercising forearm muscles was occluded for 1.5 min. The carotid baroreceptors were stimulated by neck suction at -40 mmHg for 0.5 min in each period, and also during control and recovery phase. Contralateral forearm and calf blood flow were measured simultaneously with ECG-triggered venous occlusion plethysmography. 3. The present findings suggest that there are 'central command' and ergoreceptors which modulate carotid baroreflex function to the afferent output to the heart and the peripheral circulation.

Adult↗

Pacemaking in the heart: the interplay of ionic currents.

1. There is still a degree of controversy about which currents drive pacemaking in the sinoatrial node or sinus venous. Early attempts to identify a single 'pacemaker current' in these tissues, based on voltage-clamp data, were largely unsuccessful, prompting the search for other mechanisms that may contribute to rhythmic activity. 2. Whole-cell patch-clamp recording from single cells isolated from the sinus venosus of the toad has shown that a voltage-dependent sodium current may play a role in pacemaking. This current has a transient component that contributes to the action potential upstroke and an inactivation-resistant component that contributes to the diastolic depolarization. The relative importance of this current in pacemaking is still controversial. 3. The development of computer models of pacemaking has contributed greatly to our understanding of how ionic currents can interact to produce rhythmic activity. Results are presented from one such model, 'Oxsoft Heart', to illustrate the different contributions of Ir and INa and to highlight the concept that pacemaking is driven by the integrated activity of many processes, rather than by any one current in particular. 4. Present models of pacemaking fail to accurately reproduce biological observations for certain situations. It is becoming clear that many processes contribute to pacemaking and have yet to be fully incorporated into models. Recent results regarding the role of intracellular calcium buffering and release and their implications, are discussed in this context. 5. The control of pacemaking by neurotransmitters is discussed. The limitations of single cell models in reproducing many of the complex responses to nerve stimulation of multicellular tissue, such as postinhibitory rebound, are discussed and possible improvements to models are suggested.

Animals↗