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Long-term sensitization of cardiovascular stress responses after a single stressful experience.

There is evidence that the experience of traumatic events may play a role in the pathogenesis of somatic diseases, including cardiovascular disorders. In this study, telemetry was used to investigate the long-term effects of a single stressful experience on cardiovascular and behavioral responses to novel challenges 2 weeks later. Rats were exposed to footshocks and tested for sensitization using the following challenges: novel cylinder (Day 14); shock prod acquisition test (Day 15); and shock prod retention test (Day 16). No difference in basal somatomotor activity (SA), heart rate (HR) and blood pressure between preshocked rats and control rats was found. However, preshocked rats displayed an enhanced blood pressure response compared to controls during the shock prod acquisition test and the shock prod retention test. No differential increase in HR response between both groups was found. During the novel cylinder test, the preshocked rats displayed less SA while no behavioral differences were found in the shock prod acquisition test and the shock prod retention test. We conclude that a single stressful experience induces long-term sensitization of blood pressure responses to novel challenges that are not necessarily linked to sensitized behavioral responses. The footshock model may be a useful model to study autonomic hyperresponsivity found in posttraumatic stress disorder (PTSD).

Animals↗

The comparison of uncoupling activity of constituently synthesised and stress-induced forms of winter rye stress uncoupling protein CSP 310.

A difference between the uncoupling action of constituently synthesised and stress-induced forms of winter rye stress uncoupling protein CSP 310 on winter wheat mitochondria in vitro was found from the initiation of incubation. The uncoupling activity of CSP 310 depended on its concentration in the incubation media. The addition of anti-CSP 310 antiserum to isolated mitochondria from stressed winter rye shoots caused coupling of oxidation and phosphorylation. Western-blot analysis did not locate dehydrins K-segment in CSP 310 subunits.

Journal Article↗

Head-to-head comparison of exercise stress testing, pharmacologic stress echocardiography, and perfusion tomography as first-line examination for chest pain in patients without history of coronary artery disease.

BACKGROUND: To overcome the relatively low accuracy of exercise stress testing (EST) in detecting coronary artery disease (CAD), both echocardiography and perfusion scintigraphy have been evaluated in conjunction with pharmacologic stress, but there is still uncertainty of the relative value of these tests as possible first-line examinations for suspected CAD. This study evaluated the accuracy of EST, dipyridamole and dobutamine stress echocardiography (DIP-ECHO, DOB-ECHO), and dipyridamole and dobutamine technetium 99m sestamibi tomography (DIP-MIBI, DOB-MIBI) for the detection of CAD in patients evaluated for the first time because of chest pain. METHODS AND RESULTS: Sixty patients underwent EST, DIP-ECHO, DOB-ECHO, DIP-MIBI, and DOB-MIBI. Echocardiographic images were acquired simultaneously with sestamibi injections, and the scintigraphic images were collected 1 hour later. Coronary angiography was performed within 15 days. Out of 33 patients with significant (>70%) coronary stenoses, 19 (58%) were correctly identified by EST, 18 (55%) by DIP-ECHO, 20 (61%) by DOB-ECHO, 32 (97%) by DIP-MIBI, and 30 (91%) by DOB-MIBI (p < 0.005 for MIBI vs EST and ECHO). The specificity of EST was 67% (p < 0.05 vs ECHO and MIBI), 96%, 96%, 89%, and 81%, respectively. Of the 62 stenotic coronary arteries, 20 (32%) were correctly identified by DIP-ECHO, 24 (39%) by DOB-ECHO, 48 (77%) by DIP-MIBI, and 45 (73%) by DOB-MIBI. The sensitivity of the imaging techniques in predicting the presence of multivessel disease was 14% and 29% for DIP and DOB-ECHO compared with 48% and 57% for DIP and DOB-MIBI. CONCLUSIONS: Our results confirm the limited reliability of EST in detecting CAD and the good diagnostic value of DIP and DOB-MIBI. Conversely, the lower sensitivity and the poorer capability to recognize multivessel CAD do not support the role of either DIP or DOB-ECHO as first-line examination for suspected CAD.

Chest Pain↗

Rapid deubiquitination of nucleosomal histones in human tumor cells caused by proteasome inhibitors and stress response inducers: effects on replication, transcription, translation, and the cellular stress response.

The proteasome inhibitors, lactacystin and N-acetyl-leucyl-leucyl-norlucinal, caused a rapid and near-complete loss of approximately 22-23-kDa ubiquitinated nucleoproteins, which we have identified as monoubiquitinated nucleosomal histones H2A and H2B by immunological and two-dimensional electrophoretic techniques. In human SKBr3 breast tumor cells, depletion of monoubiquitinated histones by the proteasome inhibitors coincided with the accumulation of high molecular weight ubiquitinated proteins in both nucleoprotein and cytosolic fractions and decreased unconjugated ubiquitin in the cytosol, without changes in the nonubiquitinated core histones. Unconjugated ubiquitin was not detected in isolated tumor cell nuclei. A similar loss in monoubiquitinated histones occurred in cells harboring a defective, temperature-sensitive mutation of the ubiquitin-activating E1 enzyme, after these cells were elevated from 33 degrees C to the non-permissive temperature of 39 degrees C. DNA replication and RNA transcription were decreased by the proteasome inhibitors most strongly after 90% of the ubiquitin had been removed from ubiquitinated histones H2A and H2B, suggesting a relationship between the nucleosomal histone ubiquitin status and the processing of genetic information. Interestingly, although both proteasome inhibitors caused a generalized decrease in methionine incorporation into proteins, they strongly induced the synthesis of the hsp72 and hsp90 stress proteins. Finally, treating cells with heat-shock at 43 degrees C, with stress response-provoking chemicals or with several other proteasome inhibitors caused ubiquitinated proteins to accumulate, depleted free ubiquitin, and concomitantly decreased nucleosomal monoubiquitinated histones. These results suggest that deubiquitination of nucleosomal histones H2A and H2B may play a previously unrecognized role in the cellular stress response, as well as in the processing of chromatin, and emphasize the important role of the proteasome in cellular homeostasis.

Acetylcysteine↗

Tc-99m tetrofosmin myocardial SPECT perfusion imaging: comparison of rest-stress and stress-rest protocols.

AIM: The purpose of this study was to evaluate the diagnostic value of Tc-99m tetrofosmin SPECT myocardial perfusion scintigraphy rest/stress and stress/rest protocols for the assessment of coronary artery disease (CAD). METHODS: 65 patients underwent both rest and stress SPECT imaging in a one-day protocol and coronary angiography within 2 months before or after scintigraphy. Scintigraphic data was obtained according to two different protocols; 1) rest-stress (n = 18) and 2) stress-rest (n = 47). RESULTS: Scintigraphic evidence for myocardial ischaemia was found in 36 patients (55%). The overall sensitivity to detect CAD (> 50% luminal stenosis) was 94% (34/36), specificity 66% (19/24), positive predictive value 77%, negative predictive value 90%. The sensitivity to detect CAD for protocols 1 and 2 were 100% and 93%, specificity 56% and 70%, positive predictive value 69% and 81% and negative predictive value 100% and 88%, respectively. The left anterior descending coronary artery showed a sensitivity (overall, protocol 1 & 2) of 78%, 75% (3/4) and 79% (15/19) and a specificity of 71%, 64% (9/14) and 75% (21/28). The right coronary artery showed a sensitivity (overall, protocol 1 & 2) of 91%, 100% (6/6) and 88% (14/16) and a specificity of 70%, 92% (11/12) and 61% (19/31). The left circumflex coronary artery showed a sensitivity (overall, protocol 1 & 2) of 50%, 67% (2/3) and 46% (6/13) and a specificity of 94%, 100% (15/15) and 91% (31/34). CONCLUSION: Tc-99m tetrofosmin appears to be a valuable tool in predicting significant CAD. The sensitivity and the positive predictive value are high, making this test highly appropriate for the diagnosis of CAD. The diagnostic value of the individual coronary arteries is high to moderate. No significant differences were found between both protocols.

Adult↗

Comparison of dobutamine stress echocardiography and exercise stress Thallium-201 SPECT for detection of myocardial ischemia after acute myocardial infarction treated with thrombolysis.

In order to compare the ability of dobutamine stress echocardiography (DSE) and exercise Thallium-201 SPECT to detect myocardial ischemia in patients with myocardial infarction (MI) treated with thrombolysis, 43 prospectively selected patients with MI treated with thrombolysis underwent within 1 month from MI DSE, stress-redistribution-reinjection Thallium-201 SPECT and coronary angiography. The echocardiographic and scintigraphic images were analyzed for the presence of myocardial ischemia using a 11-segment left ventricular model. DSE and exercise Thallium-201 SPECT detected myocardial ischemia in the infarct zone in 72% and 72% (31/43) of patients and ischemia at a distance in 12% (5/43) and 19% (8/43) of patients with a concordance of 67% and 88%, respectively. A significant agreement between DSE and exercise Thallium SPECT was found in the evaluation of the extent of both myocardial necrosis and stress-induced myocardial ischemia. DSE and exercise Thallium SPECT showed similar sensitivity (79 vs 76%), specificity (60 vs 60%) and accuracy (77 vs 74%) for detection of a critical stenosis of the infarct-related artery; there was also no significant difference between the tests in sensitivity, specificity and accuracy for detection of the multivessel disease. In conclusion, initially after thrombolyzed MI, DSE and exercise Thallium-201 SPECT detect myocardial ischemia in the infarct zone in a high proportion of patients and show a similar accuracy for the diagnosis of a critical stenosis of the infarct-related coronary artery and of the multivessel disease.

Aged↗

Sensation seeking, stress, and adolescent injuries: a test of stress-buffering, risk-taking, and coping skills hypotheses.

The potential stress-buffering effects of sensation seeking were assessed in a prospective study involving high school athletes. A significant positive relation between major negative sport-specific life events and subsequent injury time-loss occurred only for athletes low in sensation seeking. No evidence was obtained for a competing hypothesis that high sensation seeking would constitute an injury vulnerability factor by increasing risk-taking behaviors. Although low sensation seekers reported poorer stress management coping skills, there was no evidence that differences in coping efficacy mediated the injury vulnerability difference. Results indicate that sensation seeking is a stress-resiliency factor and suggest the utility of assessing relations between life stressors and outcomes that occur within the same environmental context.

Adaptation, Psychological↗

Effects of time of testing, stress level, and number of conditioning days on naloxone sensitivity of conditioned stress-induced analgesia in rats.

Controversy exists as to whether conditioned stress-induced analgesia (CSIA) utilizes opioid or nonopioid mechanisms. In two experiments, both an anticipatory conditioned stimulus (CS) and a shock-associated CS were used. The duration of exposure to the anticipatory CS was long, as in studies reporting opioid CSIA, whereas the duration of the shock-associated CS was short, as in studies reporting nonopioid CSIA. In addition, the effects of unconditioned stimulus (UCS) strength were investigated by using three levels of footshock (no, moderate, and high), and the development of CSIA was monitored by using different levels of training (1 to 6 days). CSIA, measured in both anticipatory and postexposure test periods, was found to be relatively stable across tail-flick trials within days and insensitive to strength of shock. As training progressed, CSIA increased with repeated CS-UCS pairings. We tested for opioid involvement using naloxone and found opioid and nonopioid mechanisms underlying CSIA; these mechanisms combined to form a stable level of analgesia. Our data suggest that stress level and amount of training interact to activate opioid and nonopioid mechanisms of CSIA. Apparent discrepancies in previous studies regarding naloxone sensitivity of CSIA may therefore be attributable to differences in stress levels, test periods and durations of exposure to shock-related cues.

Animals↗

Requirement of the p38 mitogen-activated protein kinase signalling pathway for the induction of the 78 kDa glucose-regulated protein/immunoglobulin heavy-chain binding protein by azetidine stress: activating transcription factor 6 as a target for stress-induced phosphorylation.

Malfolded protein formation and perturbance of calcium homoeostasis results in the induction of the endoplasmic reticulum (ER) chaperone protein, namely the 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein. Various ER stress inducers can activate grp78, but signal transduction mechanisms are not well understood. We report in the present study that the induction of endogenous grp78 mRNA by the amino acid analogue azetidine (AzC) requires the integrity of a signal transduction pathway mediated by p38 mitogen-activated protein kinase (p38 MAPK). In contrast, induction of grp78 by thapsigargin that depletes the ER calcium storage can occur even when the p38 MAPK pathway is blocked. Treatment of cells with AzC results in the sustained activation of p38 MAPK. We identified an ER transmembrane activating transcription factor 6 (ATF6) as a target of p38 MAPK phosphorylation in AzC-treated cells. ATF6 undergoes proteolytic cleavage on AzC treatment, releasing a nuclear form that is an activator of the grp78 promoter. We show here that constitutively active mitogen-activated protein kinase kinase 6, a selective p38 MAPK activator, enhances the ability of the nuclear form of ATF6 to transactivate the grp78 promoter. Our results provide direct evidence that different ER stress inducers use diverse pathways to activate grp78 and that in addition to activation by proteolytic cleavage, ATF6 undergoes specific ER stress-induced phosphorylation. We propose that phosphorylation of ATF6 is a novel mechanism for augmenting its potential as a transcription activator.

3T3 Cells↗

Alterations in the accumulation of adenylylated nucleotides in heavy-metal-ion-stressed and heat-stressed Synechococcus sp. strain PCC 6301, a cyanobacterium, in light and dark.

Heavy-metal-ion- (Cd2+, Cu2+, Pb2+, Hg2+ and Zn2+) or heat (50 degrees C)-stress treatments of the unicellular cyanobacterium Synechococcus sp., strain PCC 6301, under both light and dark conditions led to the accumulation of bis(5'-nucleosidyl)oligophosphates: Ap4A, Ap4G, Ap3A, Ap3G and Ap3Gp2. Under light regimens, the accumulation of Ap4A and Ap4G is more characteristic of heavy-metal-ion-stressed cells, whereas the accumulation of Ap3A, Ap3G and Ap3Gp2 is the dominant feature of heavy-metal-ion or heat-shock treatment during energy deprivation (i.e. in the dark). This accumulation of bisnucleoside oligophosphates supports a model whereby the adenylylated nucleotides are synthesized by the backward reaction of tRNA-aminoacyl synthetases. These nucleotides may also act to switch or modulate cyanobacterial responses under various environmental stress conditions.

Adenine Nucleotides↗

Stress radionuclide imaging versus stress echocardiography: a framework for comparisons.

Comparisons of stress-imaging procedures require analyses based on their 2 principal applications: diagnostic and prognostic assessments. Besides comparing results reported in the literature--in which differences have been reported in the ability of stress nuclear versus stress echocardiographic imaging to predict a low risk of cardiac events-other factors often not reported may be important in discerning the relative efficacy of these tests. These include consideration of how these tests perform in specific, individualized patient scenarios; the effect of on-going technical advances on test usefulness; and evaluation of test worthiness according to such factors as cost-effectiveness and the magnitude of incremental test information that is provided. Furthermore, it is important to distinguish between a test's efficacy (ie, its intrinsic accuracy) and its effectiveness (ie, how it performs in the real world of clinical practice).

Coronary Disease↗

Cellular stress induces the tyrosine phosphorylation of caveolin-1 (Tyr(14)) via activation of p38 mitogen-activated protein kinase and c-Src kinase. Evidence for caveolae, the actin cytoskeleton, and focal adhesions as mechanical sensors of osmotic stress.

Environmental stressors have been recently shown to activate intracellular mitogen-activated protein (MAP) kinases, such as p38 MAP kinase, leading to changes in cellular functioning. However, little is known about the downstream elements in these signaling cascades. In this study, we show that caveolin-1 is phosphorylated on tyrosine 14 in NIH 3T3 cells after stimulation with a variety of cellular stressors (i.e. high osmolarity, H2O2, and UV light). To detect this phosphorylation event, we employed a phosphospecific monoclonal antibody probe that recognizes only tyrosine 14-phosphorylated caveolin-1. Since p38 MAP kinase and c-Src have been previously implicated in the stress response, we next assessed their role in the tyrosine phosphorylation of caveolin-1. Interestingly, we show that the p38 inhibitor (SB203580) and a dominant-negative mutant of c-Src (SRC-RF) both block the stress-induced tyrosine phosphorylation of caveolin-1 (Tyr(P)(14)). In contrast, inhibition of the p42/44 MAP kinase cascade did not affect the tyrosine phosphorylation of caveolin-1. These results indicate that extracellular stressors can induce caveolin-1 tyrosine phosphorylation through the activation of well established upstream elements, such as p38 MAP kinase and c-Src kinase. However, heat shock did not promote the tyrosine phosphorylation of caveolin-1 and did not activate p38 MAP kinase. Finally, we show that after hyperosmotic shock, tyrosine-phosphorylated caveolin-1 is localized near focal adhesions, the major sites of tyrosine kinase signaling. In accordance with this localization, disruption of the actin cytoskeleton dramatically potentiates the tyrosine phosphorylation of caveolin-1. Taken together, our results clearly define a novel signaling pathway, involving p38 MAP kinase activation and caveolin-1 (Tyr(P)(14)). Thus, tyrosine phosphorylation of caveolin-1 may represent an important downstream element in the signal transduction cascades activated by cellular stress.

3T3 Cells↗

Sarco/endoplasmic reticulum calcium ATPase-2 expression is regulated by ATF6 during the endoplasmic reticulum stress response: intracellular signaling of calcium stress in a cardiac myocyte model system.

The recently described transcription factor, ATF6, mediates the expression of proteins that compensate for potentially stressful changes in the endoplasmic reticulum (ER), such as reduced ER calcium. In cardiac myocytes the maintenance of optimal calcium levels in the sarcoplasmic reticulum (SR), a specialized form of the ER, is required for proper contractility. The present study investigated the hypothesis that ATF6 serves as a regulator of the expression of sarco/endoplasmic reticulum calcium ATPase-2 (SERCA2), a protein that transports calcium into the SR from the cytoplasm. Depletion of SR calcium in cultured cardiac myocytes fostered the translocation of ATF6 from the ER to the nucleus, activated the promoter for rat SERCA2, and led to increased levels of SERCA2 protein. SERCA2 promoter induction by calcium depletion was partially blocked by dominant-negative ATF6, whereas constitutively activated ATF6 led to SERCA2 promoter activation. Mutation analyses identified a promoter-proximal ER stress-response element in the rat SERCA2 gene that was required for maximal induction by ATF6 and calcium depletion. Although this element was shown to be responsible for all of the effects of ATF6 on SERCA2 promoter activation, it was responsible for only a portion of the effects of calcium depletion. Thus, SERCA2 induction in response to calcium depletion appears to be a potentially physiologically important compensatory response to this stress that involves intracellular signaling pathways that are both dependent and independent of ATF6.

Activating Transcription Factor 6↗

Epigenomic stress response. Knockdown of DNA methyltransferase 1 triggers an intra-S-phase arrest of DNA replication and induction of stress response genes.

The DNA methylation pattern is an important component of the epigenome that regulates and maintains gene expression programs. In this paper, we test the hypothesis that vertebrate cells possess mechanisms protecting them from epigenomic stress similar to DNA damage checkpoints. We show that knockdown of DNMT1 (DNA methyltransferase 1) by an antisense oligonucleotide triggers an intra-S-phase arrest of DNA replication that is not observed with control oligonucleotide. The cells are arrested at different positions throughout the S-phase of the cell cycle, suggesting that this response is not specific to distinct classes of origins of replication. The intra-S-phase arrest of DNA replication is proposed to protect the genome from extensive DNA demethylation that could come about by replication in the absence of DNMT1. This protective mechanism is not induced by 5-aza-2'-deoxycytidine, a nucleoside analog that inhibits DNA methylation by trapping DNMT1 in the progressing replication fork, but does not reduce de novo synthesis of DNMT1. Our data therefore suggest that the intra-S-phase arrest is triggered by a reduction in DNMT1 and not by demethylation of DNA. DNMT1 knockdown also leads to an induction of a set of genes that are implicated in genotoxic stress response such as NF-kappaB, JunB, ATF-3, and GADD45beta (growth arrest DNA damage 45beta gene). Based on these data, we suggest that this stress response mechanism evolved to guard against buildup of DNA methylation errors and to coordinate inheritance of genomic and epigenomic information.

Cell Division↗

Deficiency of the stress kinase p38alpha results in embryonic lethality: characterization of the kinase dependence of stress responses of enzyme-deficient embryonic stem cells.

The mitogen-activated protein (MAP) kinase p38 is a key component of stress response pathways and the target of cytokine-suppressing antiinflammatory drugs (CSAIDs). A genetic approach was employed to inactivate the gene encoding one p38 isoform, p38alpha. Mice null for the p38alpha allele die during embryonic development. p38alpha(1/)- embryonic stem (ES) cells grown in the presence of high neomycin concentrations demonstrated conversion of the wild-type allele to a targeted allele. p38alpha(-/)- ES cells lacked p38alpha protein and failed to activate MAP kinase-activated protein (MAPKAP) kinase 2 in response to chemical stress inducers. In contrast, p38alpha(1/+) ES cells and primary embryonic fibroblasts responded to stress stimuli and phosphorylated p38alpha, and activated MAPKAP kinase 2. After in vitro differentiation, both wild-type and p38alpha(-/)- ES cells yielded cells that expressed the interleukin 1 receptor (IL-1R). p38alpha(1/+) but not p38alpha(-/)- IL-1R-positive cells responded to IL-1 activation to produce IL-6. Comparison of chemical-induced apoptosis processes revealed no significant difference between the p38alpha(1/+) and p38alpha(-/)- ES cells. Therefore, these studies demonstrate that p38alpha is a major upstream activator of MAPKAP kinase 2 and a key component of the IL-1 signaling pathway. However, p38alpha does not serve an indispensable role in apoptosis.

Animals↗

Activation of the novel stress-activated protein kinase SAPK4 by cytokines and cellular stresses is mediated by SKK3 (MKK6); comparison of its substrate specificity with that of other SAP kinases.

A cDNA was cloned that encodes human stress-activated protein kinase-4 (SAPK4), a novel MAP kinase family member whose amino acid sequence is approximately 60% identical to that of the other three SAP kinases which contain a TGY motif in their activation domain. The mRNA encoding SAPK4 was found to be widely distributed in human tissues. When expressed in KB cells, SAPK4 was activated in response to cellular stresses and pro-inflammatory cytokines, in a manner similar to other SAPKs. SAPK4 was activated in vitro by SKK3 (also called MKK6) or when co-transfected with SKK3 into COS cells. SKK3 was the only activator of SAPK4 that was induced when KB cells were exposed to a cellular stress or stimulated with interleukin-1. These findings indicate that SKK3 mediates the activation of SAPK4. The substrate specificity of SAPK4 in vitro was similar to that of SAPK3. Both enzymes phosphorylated the transcription factors ATF2, Elk-1 and SAP-1 at similar rates, but were far less effective than SAPK2a (also called RK/p38) or SAPK2b (also called p38beta) in activating MAPKAP kinase-2 and MAPKAP kinase-3. Unlike SAPK1 (also called JNK), SAPK3 and SAPK4 did not phosphorylate the activation domain of c-Jun. Unlike SAPK2a and SAPK2b, SAPK4 and SAPK3 were not inhibited by the drugs SB 203580 and SB 202190. Our results suggest that cellular functions previously attributed to SAPK1 and/or SAPK2 may be mediated by SAPK3 or SAPK4.

Amino Acid Sequence↗

Activation of stress-activated protein kinase-3 (SAPK3) by cytokines and cellular stresses is mediated via SAPKK3 (MKK6); comparison of the specificities of SAPK3 and SAPK2 (RK/p38).

Stress-activated protein kinase-3 (SAPK3), a recently described MAP kinase family member with a wide-spread tissue distribution, was transfected into several mammalian cell lines and shown to be activated in response to cellular stresses, interleukin-1 (IL-1) and tumour necrosis factor (TNF) in a similar manner to SAPK1 (also termed JNK) and SAPK2 (also termed p38, RK, CSBP and Mxi2). SAPK3 and SAPK2 were activated at similar rates in vitro by SAPKK3 (also termed MKK6), and SAPKK3 was the only activator of SAPK3 that was induced when KB or 293 cells were exposed to cellular stresses or stimulated with IL-1 or TNF. Co-transfection with SAPKK3 induced SAPK3 activity and greatly enhanced activation in response to osmotic shock. These experiments indicate that SAPKK3 mediates the activation of SAPK3 in several mammalian cells. SAPK3 and SAPK2 phosphorylated a number of proteins at similar rates, including the transcription factors ATF2, Elk-1 and SAP1, but SAPK3 was far less effective than SAPK2 in activating MAPKAP kinase-2 and MAPKAP kinase-3. Unlike SAPK2, SAPK3 was not inhibited by the drug SB 203580. SAPK3 phosphorylated ATF2 at Thr69, Thr71 and Ser90, the same residues phosphorylated by SAPK1, whereas SAPK2 only phosphorylated Thr69 and Thr71. Our results suggest that cellular functions previously attributed to SAPK1 and/or SAPK2 may be mediated by SAPK3.

Animals↗

Body versus surface forces in continuum mechanics: is the Maxwell stress tensor a physically objective Cauchy stress?

The Maxwell stress tensor (MST) T(M) plays an important role in the dynamics of continua interacting with external fields, as in the commercially and scientifically important case of "ferrofluids." As a conceptual entity in quasistatic systems, the MST derives from the definition f(M)def=inverted Delta x T(M), where f(M)(x) is a physically objective volumetric external body-force density field at a point x of a continuum, derived from the solution of the pertinent governing equations. Beginning with the fact that T(M) is not uniquely defined via the preceding relationship from knowledge of f(M), we point out in this paper that the interpretation of T(M) as being a physical stress is not only conceptually incorrect, but that in commonly occuring situations this interpretation will result in incorrect predictions of the physical response of the system. In short, by elementary examples, this paper emphasizes the need to maintain the classical physical distinction between the notions of body forces f and stresses T. These examples include calculations of the torque on bodies, the work required to deform a fluid continuum, and the rate of interchange of energy between mechanical and other modes.

Journal Article↗