Response of stress-susceptible and stress-resistant Hampshire pigs to electrical stress. II. Effects on blood cells and blood minerals.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We have previously shown that an outer membrane protein, SspA, is prominently induced by salt stress in a photosynthetic bacterium, Rhodobacter sphaeroides f. sp. denitrificans IL106 (R. sphaeroides). In this study, we investigated the physiological role of SspA under various stress conditions. Using recombinant SspA expressed in Escherichia coli as an antigen, the polyclonal antiserum of SspA was prepared. Western blot analysis demonstrated that SspA was highly induced by salt stress under both anaerobic and aerobic conditions. SspA was also induced, but to a lesser extent, by osmotic and acid stress. It is reduced under heat and cold compared to non-stressed conditions. While sspA-disrupted R. sphaeroides grew normally under anaerobic conditions in either the presence or absence of stress, it displayed significantly retarded growth under aerobic conditions in the dark, especially when osmotic or salt stress were imposed. In addition, the sspA disruptant, but not the wild type, formed cell aggregates when grown under both anaerobic and aerobic conditions, and this phenotype was significantly enhanced under salt-stressed aerobic conditions. Together, our findings suggest that SspA is critical under salt-stressed, aerobic growth conditions.
The analysis of wall motion abnormalities with dobutamine stress echocardiography is an established method for the detection of myocardial ischemia. With ultrafast magnetic resonance tomography, the application of identical stress protocols as used for echocardiography is possible. In 208 consecutive patients (147 M, 61 F) with suspected coronary artery disease, dobutamine stress echocardiography partially using harmonic imaging and dobutamine stress magnetic resonance tomography (DSMR) were performed prior to cardiac catheterization. DSMR images were acquired during short breath holds in 3 short axis-, a 4-, and a 2-chamber view using a turbo gradient echo technique. Patients were examined at rest and during a standard dobutamine-atropine scheme until submaximal heart rate was reached. Regional wall motion was assessed in a 16 segment model. Significant coronary heart disease was defined as angiographic >/=50% diameter stenosis. With DSMR, significantly more patients yielded very good (69%) or good (13%) image quality in comparison with dobutamine stress echocardiography (20% and 31%, p<0. 05). Moderate image quality occurred in 16% with MR and 41% with dobutamine stress echocardiography (p<0.05), 2% and 8% were non-diagnostic. With each technique 18 patients could not be examined (DSE: emphysema: 10, adipositas: 8, DSMR: claustrophobia: 11, adipositas: 6, contraindication: 1). Four patients did not reach target heart rate. In 107 patients, significant coronary artery disease was found. With DSMR sensitivity was 88.7% (dobutamine stress echocardiography: 74.3%; p<0.05) and specificity 85.7% (dobutamine stress echocardiography: 69.8%; p <0.05). This difference was most pronounced in the group with moderate echocardiographic image quality. High dose DSMR is superior to dobutamine stress echocardiography and can replace this technique especially in patients with moderate echocardiographic image quality.
The chronic stress state has previously been defined as persistent visceral arousal coupled with behavioral abnormalities. To determine the number of stressor exposures necessary to induce a chronic stress state, male rats were given 2 hours of inescapable shock on 10, 7, 4, or 3 consecutive days. The 3-day stress group had the most pervasive changes in the variables measured: persistently elevated basal plasma corticosterone (CORT), continued weight loss in the post-stressor period, and abnormal behavior. More exposures to the stress regimen did not produce higher CORT levels or greater behavioral changes. Acutely stressed rats, exposed to 1 day of inescapable shock, had persistent CORT elevations without the other changes seen in the 3-day stress group. The data suggest that 3 days of our stress regimen are sufficient to produce a state of chronic stress and that some signs of this state begin to appear as early as the first exposure to our inescapable stress regimen.
OBJECTIVES: To compare transesophageal atrial pacing stress echocardiography with dobutamine stress echocardiography for feasibility, safety, duration, patient acceptance and concordance in inducing wall motion abnormalities. BACKGROUND: Transesophageal atrial pacing is an effective method of increasing heart rate and has been used in the assessment of coronary artery disease. METHODS: Both tests were performed in sequence on the same patients in random order. Transesophageal atrial pacing stress echocardiography began at a heart rate of 10 beats/min above the baseline value and was increased by 20 beats/min every two min until 85% of the age-predicted maximum heart rate or another end point was reached. Dobutamine echocardiography was performed using three-min stages and a maximum dose of 40 microg/kg per min. Atropine (total dose < or =2 mg) was administered at the start of the 40 microg/kg per min stage if needed to augment heart rate or during pacing if Wenckebach heart block occurred. RESULTS: Transesophageal atrial pacing stress echocardiography was feasible in 100 of 104 patients (96%); the duration (8.6+/-3.6 min) was significantly shorter than that of dobutamine stress echocardiography (15.1+/-3.9 min) (p = 0.0001). With transesophageal atrial pacing stress echocardiography, the recovery period was shorter, symptoms and dysrhythmias were fewer, hypertension and hypotension were less common and target heart rate was more frequently achieved. No complications occurred with either test. Patient acceptance was satisfactory. Agreement between results of both tests was good for segmental wall motion scoring with a 16-segment model, scores 1 to 5 (kappa: rest, 0.79; peak, 0.57) and test interpretation (normal, ischemia, infarction or resting wall motion abnormality with ischemia) (kappa: 0.77). CONCLUSIONS: Transesophageal atrial pacing stress echocardiography is a feasible, well-tolerated alternative to dobutamine stress echocardiography. It can be performed rapidly and shows good agreement with dobutamine stress echocardiography in the induction of myocardial ischemia.
The role of an AAA protease FtsH (slr0228) in the turnover of the D1 protein was studied under moderate heat stress conditions using wild-type cells of the cyanobacterium Synechocystis PCC 6803 and the mutant cells lacking a homologue of FtsH (slr0228). When the growth temperature of the wild-type was shifted from 30 degrees C to 40 degrees C, growth and oxygen-evolving activity were partially inhibited. Under the same heat stress, growth of the mutant was inhibited more significantly (63% inhibition after 5 days heat stress, compared with 26% inhibition with the wild-type cells) and the oxygen-evolving activity was also impaired in parallel. With heat stress at 42 degrees C, the level of the D1 protein of wild type cells was decreased, whereas that in mutant cells was not. The responses of cyanobacterial cells to heat stress observed here are quite similar to those to light stress that were reported previously. From these results, we suggest that the FtsH protease (slr0228) is responsible for both the heat-induced and light-induced degradation of the D1 protein. Notably, the amount of FtsH increased when the wild-type cells were exposed to heat stress or light stress, indicating that the up-regulation of the FtsH protease in the thylakoids is crucial for the cyanobacterial cells to cope with these abiotic stresses.
Germination and subsequent hydroponic growth under salt stress (100 mmol/L NaCl) triggered an accumulation of six major stress proteins and resulted in a growth arrest of young seedlings of rice (Oryza sativa L.) cv. Bura Rata. Based on two-dimensional electrophoretic resolution, partial amino acid sequencing and immunodetection techniques, four of the salt stress-induced polypeptides were identified as LEA proteins. Under all experimental conditions wherein seedlings exhibited superior halotolerance, salt stress-induced LEA proteins were expressed at low levels. In contrast, accumulation of LEA proteins was found associated with growth arrest. When returned to non-saline media, seedlings stressed with salt for four days recovered immediately. Longer exposure to 100 mmol/L NaCl, however, progressively delayed recovery and reduced the number of seedlings which could recover from salt stress. Recovery from salt stress was consistently accompanied by degradation of the salt stress-induced LEA proteins. The results of this study show that LEA proteins accumulate during the salinity-triggered growth arrest of young Bura Rata seedlings and are mobilised during the recovery of seedlings from salinity stress.
Previous research has only examined perceptual deficits that are hypothesized in a model of stress and injury under laboratory-induced stress conditions. The generalizability of findings from such induced-stress conditions is limited beyond the laboratory. The current research examined the influence of life-event stress and hardiness on peripheral narrowing in a real-life stress situation. Athletes completed life-stress and hardiness questionnaires, along with measures of state anxiety and peripheral vision. The stress condition was obtained by assessing the athletes within 2 hours of a competition. The real-life stress condition had a larger effect on state anxiety and peripheral narrowing than the laboratory-induced situations used in previous research, with effect sizes twice and three times as large as those reported in the literature. All athletes experienced significant reductions in peripheral vision prior to competition, regardless of life-event stress or hardiness levels.
The impacts of drought on plant growth and development limit cereal crop production worldwide. Rice (Oryza sativa) productivity and production is severely affected due to recurrent droughts in almost all agroecological zones. With the advent of molecular and genomic technologies, emphasis is now placed on understanding the mechanisms of genetic control of the drought-stress response. In order to identify genes associated with water-stress response in rice, ESTs generated from a normalized cDNA library, constructed from drought-stressed leaf tissue of an indica cultivar, Nagina 22 were used. Analysis of 7794 cDNA sequences led to the identification of 5815 rice ESTs. Of these, 334 exhibited no significant sequence homology with any rice ESTs or full-length cDNAs in public databases, indicating that these transcripts are enriched during drought stress. Analysis of these 5815 ESTs led to the identification of 1677 unique sequences. To characterize this drought transcriptome further and to identify candidate genes associated with the drought-stress response, the rice data were compared with those for abiotic stress-induced sequences obtained from expression profiling studies in Arabidopsis, barley, maize, and rice. This comparative analysis identified 589 putative stress-responsive genes (SRGs) that are shared by these diverse plant species. Further, the identified leaf SRGs were compared to expression profiles for a drought-stressed rice panicle library to identify common sequences. Significantly, 125 genes were found to be expressed under drought stress in both tissues. The functional classification of these 125 genes showed that a majority of them are associated with cellular metabolism, signal transduction, and transcriptional regulation.
PURPOSE: Techniques designed to increase initial luminal diameter during stent implantation may ultimately lead to early restenosis by causing substantial vessel wall trauma and promoting neointimal hyperplasia. The purpose of this study was to evaluate the impact of stent oversizing on resultant arterial wall stress concentrations and examine the concept of a "stress threshold" for neointimal hyperplasia development. MATERIALS AND METHODS: A previously described three-dimensional large-strain hyperelastic numeric model was used to examine the nonlinear isotropic behavior of a 6-mm-diameter artery during stent deployment. An in situ axial prestretch of 10% and a mean arterial pressure of 100 mm Hg (13.3 kPa) were applied before stepwise expansion of a simulated Palmaz-Schatz stent to a diameter 30% greater than that of the native artery. The variation of arterial wall von Mises stresses with percentage diameter inflation was then compared with the known distribution of stent-induced neointimal hyperplasia. RESULTS: The order in which location-specific peak stresses exceeded a predetermined stress threshold was constant: the stent ends surpassed the threshold first, followed by the stent cross-links, then the stent struts, and finally the bare area between the stent struts. These locations corresponded in order to the most common locations of intimal proliferation after stent deployment. An exponential relationship between peak stress concentration and percent stent inflation was formulated. CONCLUSIONS: Stent-induced intramural stress injury beyond a certain threshold may cause early restenosis by triggering neointimal hyperplasia. Maximum stress concentrations increase exponentially with stent deployment diameter, highlighting the importance of minimal stent overexpansion and novel stent designs that specifically address peak stress reduction.
Water-deficit stresses preferentially reduce shoot growth, thereby disrupting the flow of carbohydrates from source leaves to the developing sinks. Here, we use a novel stress bioassay to dissect responses of field and greenhouse-grown cotton (Gossypium hirsutum) source leaves to water-deficit stresses. Fifth main stem leaf samples were harvested at sunrise and subjected to a prolonged elevated respiratory demand in the dark. Sucrose levels are lower in nonstressed cotton at sunrise compared to water-deficit stressed cotton, potentially predisposing the nonstressed tissue to succumb more rapidly. Tissue death was determined initially using the cell viability stain 2,3,5-triphenyltetrazolium chloride, but was determined in subsequent experiments by monitoring the decline in chlorophyll fluorescence yield. Fluorescence yield measurements were obtained within minutes of harvesting and individual samples were monitored over the time course of the treatment. Analyses of the time course and magnitude of chlorophyll fluorescence yield decline in samples from irrigated and dryland plots permitted the detection of stress responses within 24 h of the cessation of irrigation. The rate of fluorescence yield decline during the elevated respiratory demand treatment slowed as the water-deficit stress increased. Upon irrigation, the source leaves of the water-stressed plants recovered to prestress values within 4 d. Well-watered cotton overexpressing heat shock protein 101 had identical rates of fluorescence yield decline as nontransgenic cotton. These results suggest that the delayed decline in fluorescence yield of water-stressed tissue exposed to prolonged elevated respiratory demand can be used as a sensitive indicator of water-deficit stress responses.
To understand low temperature and osmotic stress signaling in plants, we isolated and characterized two allelic Arabidopsis mutants, los5-1 and los5-2, which are impaired in gene induction by cold and osmotic stresses. Expression of RD29A-LUC (the firefly luciferase reporter gene under the control of the stress-responsive RD29A promoter) in response to cold and salt/drought is reduced in the los5 mutants, but the response to abscisic acid (ABA) remains unaltered. RNA gel blot analysis indicates that the los5 mutation reduces the induction of several stress-responsive genes by cold and severely diminishes or even completely blocks the induction of RD29A, COR15, COR47, RD22, and P5CS by osmotic stresses. los5 mutant plants are compromised in their tolerance to freezing, salt, or drought stress. los5 plants are ABA deficient, as indicated by increased transpirational water loss and reduced accumulation of ABA under drought stress in the mutant. A comparison with another ABA-deficient mutant, aba1, reveals that the impaired low-temperature gene regulation is specific to the los5 mutation. Genetic tests suggest that los5 is allelic to aba3. Map-based cloning reveals that LOS5/ABA3 encodes a molybdenum cofactor (MoCo) sulfurase. MoCo sulfurase catalyzes the generation of the sulfurylated form of MoCo, a cofactor required by aldehyde oxidase that functions in the last step of ABA biosynthesis in plants. The LOS5/ABA3 gene is expressed ubiquitously in different plant parts, and the expression level increases in response to drought, salt, or ABA treatment. Our results show that LOS5/ABA3 is a key regulator of ABA biosynthesis, stress-responsive gene expression, and stress tolerance.
The sigma(B)-dependent general stress regulon of Bacillus subtilis comprises more than 150 members. Induction of this regulon by imposition of environmental or metabolic stress confers multiple, nonspecific, and preemptive stress resistance to nongrowing, nonsporulated cells of B. subtilis. In this study we performed a regulon-wide phenotypic screening analysis to determine the stress sensitivity profiles of 94 mutants defective in candidate members of the general stress regulon that were previously identified in our transcriptional profiling study of the general stress response of B. subtilis. The phenotypic screening analysis included analysis of adaptation to a growth-inhibiting concentration of ethanol (10%, vol/vol) or NaCl (10%, wt/vol), severe heat shock (54 degrees C), and low temperature (survival at 4 degrees C and growth at 12.5 degrees C). Surprisingly, 85% of the mutants tested displayed increased sensitivity at an alpha confidence level of < or =0.01 to at least one of the four stresses tested, and 62% still exhibited increased sensitivity at an alpha of < or =0.001. In essence, we were able to assign 63 genes (28 genes with an alpha of < or =0.001) to survival after ethanol shock, 37 genes (28 genes with an alpha of < or =0.001) to protection from NaCl shock, 34 genes (24 genes with an alpha of < or =0.001) to survival at 4 degrees C, and 10 genes (3 genes with an alpha of < or =0.001) to management of severe heat shock. Interestingly, there was a substantial overlap between the genes necessary for survival during ethanol shock and the genes necessary for survival at 4 degrees C, and there was also an overlap between genes required for survival during ethanol shock and genes required for survival during NaCl shock. Our data provide evidence for the importance of the sigma(B) regulon at low temperatures, not only for growth but also for survival. Moreover, the data imply that a secondary oxidative stress seems to be a common component of the severe stresses tested.