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At least 19 recordsLinked to original sources

PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗

PubMed2026

Relationships among mechanisms in psychosocial treatments for chronic pain: mechanism to mechanism lagged effects and relationships with outcomes.

Results suggest that psychosocial treatments for chronic pain work via several mechanisms, and that they often do so to similar degrees and in similar ways. Extant research, however, has focused on individual and/or independent effects of mechanisms on outcomes. Whether successful outcomes are also partly because of sequential and meaningful relationships among and between mechanisms-mechanism-to-mechanism effects-has not been examined. Secondary analyses were conducted of an RCT that compared cognitive therapy, mindfulness-based stress reduction, and behavior therapy to treatment as usual in a sample (N = 521) of people with chronic low back pain. Results of hierarchical linear modeling revealed that (1) Treatment Condition × Mechanism interactions predicting changes in other mechanisms were nonsignificant; (2) lagged prior session mechanism changes predicted next session changes in another mechanism; (3) lagged relationships between pain catastrophizing and pain self-efficacy were reciprocal, whereas links between lagged pain catastrophizing and mindfulness changes and lagged pain catastrophizing changes and behavioral activation changes were unidirectional; and (4) individual differences in the strengths of mechanism-to-mechanism relationships predicted pre- to post-treatment changes in outcomes. Results reveal heretofore hidden therapeutic processes that cognitive therapy, mindfulness-based stress reduction, and behavior therapy may share. Namely, that mechanism-to-mechanism lagged effects do indeed emerge beyond mechanism-to-outcome effects. Findings show not only that mechanisms may change in definable sequences relative to each other but that individual differences in the strengths of mechanism-to-mechanism relationships may themselves be predictive of outcomes.

Humans↗

PubMed1990

Cytolytic mechanisms of activated macrophages. Tumor necrosis factor and L-arginine-dependent mechanisms act synergistically as the major cytolytic mechanisms of activated macrophages.

We examined the cytolytic mechanisms of activated macrophages by using proteose peptone- or thioglycollate broth-induced mouse peritoneal macrophages or mouse macrophage hybridomas as effector cells, L.P3 cells, a clone of L929 cells, and P815 cells as target cells, and IFN-gamma and LPS as activators. It was determined that TNF is the main cytolytic molecule against L.P3 cells from the following results: 1) activated macrophages can produce TNF; 2) TNF shows cytotoxic activity against L.P3 cells; 3) the addition of anti-TNF antibody inhibited most of the cytolytic activity of activated macrophages against L.P3 cells. On the other hand, it was concluded that the main cytolytic mechanism against P815 cells is the production of NO2-/NO3- from L-arginine, from the following results: 1) activated macrophages can produce NO2-; 2) NaNO2 shows high cytotoxic activity against P815 cells; 3) the depletion of L-arginine from the medium inhibited most of the cytolytic activity of activated macrophages against P815 cells and NO2- production by activated macrophages. In this study, however, cytostatic effects of L-arginine-dependent effector mechanism were not studied. Thus, these results show that activated macrophages can express at least two cytolytic mechanisms independently, namely, the one that appears to be mediated by the L-arginine-dependent effector mechanism and the second that appears to be mediated directly by TNF. Furthermore, it was demonstrated that TNF and L-arginine-dependent NO2- production act synergistically as killing mechanisms of activated macrophages. These mechanisms can explain the cytolytic activity of activated macrophages against a variety of target cells.

Animals↗

PubMed1997

The mechanism of thioredoxin reductase from human placenta is similar to the mechanisms of lipoamide dehydrogenase and glutathione reductase and is distinct from the mechanism of thioredoxin reductase from Escherichia coli.

Thioredoxin reductase, lipoamide dehydrogenase, and glutathione reductase are members of the pyridine nucleotide-disulfide oxidoreductase family of dimeric flavoenzymes. The mechanisms and structures of lipoamide dehydrogenase and glutathione reductase are alike irrespective of the source (subunit M(r) approximately 55,000). Although the mechanism and structure of thioredoxin reductase from Escherichia coli are distinct (M(r) approximately 35,000), this enzyme must be placed in the same family because there are significant amino acid sequence similarities with the other two enzymes, the presence of a redox-active disulfide, and the substrate specificities. Thioredoxin reductase from higher eukaryotes on the other hand has a M(r) of approximately 55,000 [Luthman, M. & Holmgren, A. (1982) Biochemistry 21, 6628-6633; Gasdaska, P. Y., Gasdaska, J. R., Cochran, S. & Powis, G. (1995) FEBS Lett 373, 5-9; Gladyshev, V. N., Jeang, K. T. & Stadtman, T.C. (1996) Proc. Natl. Acad. Sci. USA 93, 6146-6151]. Thus, the evolution of this family is highly unusual. The mechanism of thioredoxin reductase from higher eukaryotes is not known. As reported here, thioredoxin reductase from human placenta reacts with only a single molecule of NADPH, which leads to a stable intermediate similar to that observed in titrations of lipoamide dehydrogenase or glutathione reductase. Titration of thioredoxin reductase from human placenta with dithionite takes place in two spectral phases: formation of a thiolate-flavin charge transfer complex followed by reduction of the flavin, just as with lipoamide dehydrogenase or glutathione reductase. The first phase requires more than one equivalent of dithionite. This suggests that the penultimate selenocysteine [Tamura, T. & Stadtman, T.C. (1996) Proc. Natl. Acad. Sci. USA 93, 1006-1011] is in redox communication with the active site disulfide/dithiol. Nitrosoureas of the carmustine type inhibit only the NADPH reduced form of human thioredoxin reductase. These compounds are widely used as cytostatic agents, so this enzyme should be studied as a target in cancer chemotherapy. In conclusion, three lines of evidence indicate that the mechanism of human thioredoxin reductase is like the mechanisms of lipoamide dehydrogenase and glutathione reductase and differs fundamentally from the mechanism of E. coli thioredoxin reductase.

Dihydrolipoamide Dehydrogenase↗

PubMed1985

Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XIV. Mutational and non-mutational mechanisms as subsets of a more general mechanism. Part C. A defined cancer mutation.

The results of applying a mechanism of ethionine-induced embryonic gene derepressions to explain similar features found in hereditary tyrosinemia have been extended to a well defined cancer mutation. In all three cases, the described mechanism is compatible with the explanation for the etiology of embryonic like phenotypic expressions in cells and potentially for the carcinogenic process. The essence of the formulated process for a human bladder carcinoma mutation in the ras gene for a protein phosphokinase states that a specific proto-oncogene is mutated to an oncogene by various known processes. The protein phosphokinase that has an altered specificity resulting in anomalous phosphorylation of important regulating proteins by a non-mutation mechanism, i.e. by ethionine, would produce the same effect in a hypomethylated state of deoxyribonucleic acid causing an embryonic type protein phosphokinase gene to become activated. These embryonic oncogenes are supersensitive to methylation control mechanisms--thus the link between non-mutation and mutation type mechanisms.

Carcinogens↗

PubMed1998

Catalytic mechanism of aldose reductase studied by the combined potentials of quantum mechanics and molecular mechanics.

The catalytic reduction of D-glyceraldehyde to glycerol by aldose reductase has been investigated with the combined potentials of quantum mechanics (QM) and molecular mechanics (MM) to resolve the question of whether Tyr48 or His110 serves as the proton donor during catalysis. Site directed mutagenesis studies favor Tyr48 as the proton donor while the presence of a water channel linking the N delta 1 of His110 to the bulk solvent suggests that His110 is the proton donor. Utilizing the combined potentials of QM and MM, the binding mode of substrate D-glyceraldehyde was investigated by optimizing the local geometry of Asp43, Lys77, Tyr48, His110 and NADPH at the active site of aldose reductase. Reaction pathways for the reduction of D-glyceraldehyde to glycerol were then constructed by treating both Tyr48 and His110 as proton donors. Comparison of energetics obtained from the reaction pathways suggests His110 to be the proton donor. Based on these findings, a reduction mechanism of D-glyceraldehyde to glycerol is described.

Aldehyde Reductase↗

PubMed2007

Simulated scaling method for localized enhanced sampling and simultaneous "alchemical" free energy simulations: a general method for molecular mechanical, quantum mechanical, and quantum mechanical/molecular mechanical simulations.

A potential scaling version of simulated tempering is presented to efficiently sample configuration space in a localized region. The present "simulated scaling" method is developed with a Wang-Landau type of updating scheme in order to quickly flatten the distributions in the scaling parameter lambdam space. This proposal is meaningful for a broad range of biophysical problems, in which localized sampling is required. Besides its superior capability and robustness in localized conformational sampling, this simulated scaling method can also naturally lead to efficient "alchemical" free energy predictions when dual-topology alchemical hybrid potential is applied; thereby simultaneously, both of the chemically and conformationally distinct portions of two end point chemical states can be efficiently sampled. As demonstrated in this work, the present method is also feasible for the quantum mechanical and quantum mechanical/molecular mechanical simulations.

Algorithms↗

PubMed1984

Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XII mutational and non-mutational mechanism as subsets of a more general mechanism. Part A--Ethionine.

The ethionine-induced genic derepression mechanism is visualized as a secondary process that occurs after the S-adenosyl-L methionine pool concentrations are lowered to critical levels. Although DNA methylation has been shown to be correlated with genic activity, the times observed for inducement (3 days) of the alpha-fetoprotein gene and its reversibility (within 7 days) does not make it likely that alterations in the methylated status of DNA is involved. The specific mechanism is theorized to be as follows: the adenine moiety of S-adenosyl-L-methionine base-pairs with thymine of a specific structural area of the alpha-fetoprotein gene. The process is visualized as a frequent event during moments of structural relaxation of an otherwise hyperspiralized condition of the chromatin. This weak hydrogen bonding situation allows the methylation by protein methylases of a precursor chromatin protein that after methylation by the S-adenosyl-L-methionine which is base-paired to the specific DNA site, conformationally is set or locked into place and acts as a specific repressor for the alpha-fetoprotein gene. This subsequently disallows RNA polymerase activity of the region. During turnover of this chromatin protein the replacement of the methylated repressor is normally maintained. But if the S-adenosyl-L-methionine pool concentration is lowered to a level below that required for base-pairing by the adenine moiety, then the repressed conformational condition of the alpha-fetoprotein gene is altered allowing transcription. In this manner the correlation between low S-adenosyl-L-methionine and alpha-fetoprotein synthesis can be made.

Animals↗

PubMed1985

Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XIII. Mutational and non-mutational mechanisms as subsets of a more general mechanism. Part B--hereditary tyrosinemia.

In this mini-series three different examples of the etiology for the induction of alpha-fetoprotein and hepatocarcinogenesis have been chosen. The first paper describes the mechanism using the non-mutagen, ethionine. In this paper the mechanism is derived by virtue of a mutation that causes a deficiency in fumarylacetoacetate fumarylhydrolase activity with subsequent accumulation of fumarylacetoacetate that is an inhibitor of ATP: L-methionine S-adenosyltransferase. It is hypothesized that the chronically low levels of active methyl groups disallows base-pairing by the adenine moiety of S-adenosyl-L-methionine and the repressed conformation of the alpha-fetoprotein gene is altered and subsequent transcription takes place. The same or similar process occurs with the subset of genes (embryonically repressed) that as a special group of active genes gives embryonic features to a quasi-differentiated stem cell causing "dysdifferentiation" to a neoplastic state.

Amino Acid Metabolism, Inborn Errors↗

PubMed2004

Quantum mechanical/molecular mechanical investigation of the mechanism of C-H hydroxylation of camphor by cytochrome P450cam: theory supports a two-state rebound mechanism.

The stereospecific cytochrome P450-catalyzed hydroxylation of the C(5)-H((5-exo)) bond in camphor has been studied theoretically by a combined quantum mechanical/molecular mechanical (QM/MM) approach. Density functional theory is employed to treat the electronic structure of the active site (40-100 atoms), while the protein and solvent environment (ca. 24,000 atoms) is described by the CHARMM force field. The calculated energy profile of the hydrogen-abstraction oxygen-rebound mechanism indicates that the reaction takes place in two spin states (doublet and quartet), as has been suggested earlier on the basis of calculations on simpler models ("two-state reactivity"). While the reaction on the doublet potential energy surface is nonsynchronous, yet effectively concerted, the quartet pathway is truly stepwise, including formation of a distinct intermediate substrate radical and a hydroxo-iron complex. Comparative calculations in the gas phase demonstrate the effect of the protein environment on the geometry and relative stability of intermediates (in terms of spin states and redox electromers) through steric constraints and electronic polarization.

Camphor↗

PubMed2006

A combined quantum mechanical and molecular mechanical study of the reaction mechanism and alpha-amino acidity in alanine racemase.

Combined quantum mechanical/molecular mechanical simulations have been carried out to investigate the origin of the carbon acidity enhancement in the alanine racemization reaction catalyzed by alanine racemase (AlaR). The present study shows that the enhancement of carbon acidity of alpha-amino acids by the cofactor pyridoxal 5'-phosphate (PLP) with an unusual, unprotonated pyridine is mainly due to solvation effects, in contrast to the intrinsic electron-withdrawing stabilization by the pyridinium ion to form a quinonoid intermediate. Alanine racemase further lowers the alpha-proton acidity and provides an overall 14-17 kcal/mol transition-state stabilization. The second key finding of this study is that the mechanism of racemization of an alanine zwitterion in water is altered from an essentially concerted process to a stepwise reaction by formation of an external aldimine adduct with the PLP cofactor. Finally, we have used a centroid path integral method to determine the intrinsic kinetic isotope effects for the two proton abstraction reactions, which are somewhat greater than the experimental estimates.

Alanine Racemase↗

PubMed1996

[Immunogenetic mechanisms in autoimmune processes: disorders of immune regulatory mechanisms, genetic determination of autoimmunity, effector mechanisms of autoimmune processes and their therapy].

Autoimmune disease represent a great social and medical problem. 5 to 7% of population suffer from these chronic debilitating disorders. Our knowledge about the immune system and the genetic determination of its components and processes has considerably increased in the fast few years. The purpose of the two articles on autoimmunity published in the previous and this issue is to offer a reader a topical status of the development in this field. Autoantigens, their presentation to T lymphocytes and superantigens were discussed in the first article. The breakdown of regulatory mechanisms of immunity, the genetic basis of autoimmunity, the effector mechanisms responsible for tissue damages and their therapy are reviewed in the presented article. (Tab. 4, Fig. 1.).

Autoimmune Diseases↗

PubMed2004

Reaction path potential for complex systems derived from combined ab initio quantum mechanical and molecular mechanical calculations.

Combined ab initio quantum mechanical and molecular mechanical calculations have been widely used for modeling chemical reactions in complex systems such as enzymes, with most applications being based on the determination of a minimum energy path connecting the reactant through the transition state to the product in the enzyme environment. However, statistical mechanics sampling and reaction dynamics calculations with a combined ab initio quantum mechanical (QM) and molecular mechanical (MM) potential are still not feasible because of the computational costs associated mainly with the ab initio quantum mechanical calculations for the QM subsystem. To address this issue, a reaction path potential energy surface is developed here for statistical mechanics and dynamics simulation of chemical reactions in enzymes and other complex systems. The reaction path potential follows the ideas from the reaction path Hamiltonian of Miller, Handy and Adams for gas phase chemical reactions but is designed specifically for large systems that are described with combined ab initio quantum mechanical and molecular mechanical methods. The reaction path potential is an analytical energy expression of the combined quantum mechanical and molecular mechanical potential energy along the minimum energy path. An expansion around the minimum energy path is made in both the nuclear and the electronic degrees of freedom for the QM subsystem internal energy, while the energy of the subsystem described with MM remains unchanged from that in the combined quantum mechanical and molecular mechanical expression and the electrostatic interaction between the QM and MM subsystems is described as the interaction of the MM charges with the QM charges. The QM charges are polarizable in response to the changes in both the MM and the QM degrees of freedom through a new response kernel developed in the present work. The input data for constructing the reaction path potential are energies, vibrational frequencies, and electron density response properties of the QM subsystem along the minimum energy path, all of which can be obtained from the combined quantum mechanical and molecular mechanical calculations. Once constructed, it costs much less for its evaluation. Thus, the reaction path potential provides a potential energy surface for rigorous statistical mechanics and reaction dynamics calculations of complex systems. As an example, the method is applied to the statistical mechanical calculations for the potential of mean force of the chemical reaction in triosephosphate isomerase.

Binding Sites↗

PubMed2006

Mechanical stimuli and nutrients regulate rapamycin-sensitive signaling through distinct mechanisms in skeletal muscle.

The mammalian target of rapamycin (mTOR) has been identified as a growth factor and nutrient-sensitive molecule that controls the translational machinery and cell growth. Rapamycin-sensitive (RS) signaling events have also been shown to be necessary for mechanical load-induced growth of skeletal muscle, but the mechanisms involved in the mechanical activation of RS signaling are not known. The finding that mechanical stimuli induce nutrient uptake in skeletal muscle raises the possibility that mechanically induced RS signaling is mediated via a nutrient-dependent mechanism. To investigate this hypothesis, skeletal muscles (ex vivo) were stimulated with nutrients or intermittent mechanical stretch and the phosphorylation of p70S6k [P-p70(389)], PKB [P-PKB], mTOR [P-mTOR(2481)], and p38 [P-p38] was assessed. In comparison to vehicle-treated controls, both nutrient and mechanical stimuli induced P-p70(389), neither stimulus altered P-PKB or P-mTOR(2481), and only mechanical stimuli induced P-p38. The nutrient and mechanically induced increase in P-p70(389) was blocked by rapamycin, but only nutrient-induced signaling to P-p70(389) was blocked by wortmannin. Furthermore, the mechanically induced increase in P-p70(389) was not impaired by the removal of exogenous nutrients. Taken together, these results indicate that exogenous nutrients are not required for mechanically induced RS signaling and that nutrient and mechanical stimuli activate RS signaling through distinct upstream mechanisms.

Amino Acids↗

PubMed1986

Contributions of glomerular and tubular mechanisms to antidiuresis in conscious domestic fowl.

Recently developed radioimmunoassay (RIA techniques were employed in a quantitative investigation of the renal actions of the avian antidiuretic hormone arginine vasotocin (AVT) in the conscious domestic fowl. Constant intravenous infusion of AVT at doses of 0.125-1.00 ng . kg-1 . min-1 was used to produce plasma AVT (PAVT) concentrations (verified by RIA) over the entire range of physiological PAVT levels in the domestic fowl. Comparison of the dose-response relationships between PAVT and glomerular and tubular mechanisms of antidiuresis revealed that tubular mechanisms are of primary importance and glomerular mechanisms of secondary importance in the conservation of water by the avian kidney. The greatest proportion of the total AVT-induced reduction in renal water excretion occurred at low physiological PAVT levels (less than 5 microU/ml), prior to any significant reduction in glomerular filtration rate (GFR), and appeared to be the exclusive result of tubular mechanisms of antidiuresis. At high PAVT levels (5-16 microU/ml), glomerular and tubular mechanisms overlapped, and their effects on water conservation could not be separated. Although GFR was reduced by nearly 30% at the highest dose of AVT, only minor additional amounts of water were conserved by the combined actions of glomerular and tubular mechanisms. The glomerular mechanisms appear to have only a minor secondary effect on water-conserving ability of the avian kidney.

Animals↗

PubMed2003

Mechanical influences on cells, tissues and organs - 'Mechanical Morphogenesis'.

Cells can sense changes in their mechanical environment and promote alterations and adaptations in tissue structure and function. Mechanical stimuli regulate such fundamental processes as cell division and differentiation and determine tissue form. The current editorial outlines the general scope of a subject area we have called 'mechanical morphogenesis'. We are promoting it as an area of special interest for future issues of the European Journal of Morphology. Clearly, mechanical loading is of pivotal importance to the development, function and repair of all tissues in the musculoskeletal system, including bone, ligament, tendon, skeletal muscle, intervertebral disc and meniscus. Bone in particular has attracted special interest and mechanical strain is central to both Wolff 's law and Frost's 'mechanostat' model of bone behaviour. But it is skeletal muscle that shows the most obvious and rapid response to altered load, with striated muscle fibres hypertrophing with strength-training programmes, and atrophing in the absence of adequate mechanical stimulation. Articular cartilage, together with tendons and ligaments is also responsive to changing exercise levels, and either abnormally high or low loads are detrimental. However, the influence of mechanical forces extends to many other organ systems, including the respiratory, cardiovascular, nervous and integumentary systems. The bronchial mucosa and the alveoli are subject to tensile and compressive loading during the volume changes that occur in respiration, and surface tension is also of paramount importance. The whole form of the cardiovascular system is driven by the haemodynamic influences of blood, and atherosclerosis has an underlying mechanical basis. The characteristic plaques tend to occur at sites of obvious mechanical significance - regions of arterial branching and curvature, where shear stress on the vessel wall may be low, but tensile stress high. Sensory perception by the nervous system has a well known mechanical basis and the cochlea is perhaps the most elaborate example of a site where sensory cells transduce mechanical forces and relay information to the brain. Mechanical force has also been proposed as a regulating factor in controlling axonal growth. Finally, the integumentary system has several structural adaptations that obviously relate to the influence of mechanical forces. The thickened layer of keratinised squames in the palms and soles is directly related to the high levels of shear at these locations.

Animals↗

PubMed2003

Ecotoxicity prediction using mechanism- and non-mechanism-based QSARs: a preliminary study.

In ecotoxicology, mechanism-based quantitative structure-activity relationships (QSARs) are usually developed with higher quality than QSARs without regard to toxicity mechanism. Correctly determining the mechanism of a compound, which is not always easy, is required to use mechanism-based QSARs for toxicity prediction. The mechanism determination step may introduce extra errors in addition to the intrinsic prediction errors of mechanism-based QSARs, thus compromising these QSARs' performance compared with QSARs regardless of mechanism. In this study, the mechanism identification-toxicity prediction (MI-TP) approach was compared with the direct toxicity prediction (DTP) approach using a data set containing phenol toxicity to Tetrahymena pyriformis. A statistical mechanism classification model for mechanism prediction, four mechanism-based QSARs and a single QSAR without discriminating between mechanisms were developed for toxicity prediction. Toxicity of phenols in an external data set was predicted following the MI-TP and DTP approaches. Results indicated that the mechanisms of several phenols in the external test set were incorrectly predicted which led to significant over- or under-estimation of their toxicity. Overall, the MI-TP approach did not yield more accurate toxicity prediction than the DTP approach.

Animals↗

PubMed2006

Preferences for mechanical ventilation among survivors of prolonged mechanical ventilation and tracheostomy.

BACKGROUND: Among survivors of prolonged mechanical ventilation, preferences for this treatment have rarely been explored. OBJECTIVES: To elicit preferences of survivors of prolonged mechanical ventilation (>or=7 days) and factors influencing these preferences. METHODS: A descriptive, cross-sectional survey design was used. Subjects were recruited from intensive care units in a tertiary care hospital and from long-term care facilities. Each subject (n = 30) was asked to reflect on the decision to use mechanical ventilation; rate current health, pain/discomfort in the intensive care unit and from mechanical ventilation, perceived family financial burden, and emotional/physical stress related to mechanical ventilation; identify changes that would influence preference for mechanical ventilation; and answer questions about quality of life, functional status, depressive symptoms, and communication. RESULTS: Most subjects (75.9%) would have chosen mechanical ventilation. Median days of mechanical ventilation and tracheostomy were greater for subjects who would have chosen mechanical ventilation (98.5 vs 70), as were median days of tracheostomy (102 vs 64). Patients who would not have chosen mechanical ventilation had more depressive symptoms and were more likely to be insured by Medicare. No other variables differed between groups. Patients who preferred mechanical ventilation would change their preference on the basis of their families' emotional/physical stress and financial burden. Patients who did not prefer mechanical ventilation would change their preference if the family financial burden and emotional/physical stress were reduced and current health improved. CONCLUSIONS: Most patients would have chosen mechanical ventilation. Survivors' preferences were influenced by their current health and families' financial burden and stress.

Adult↗