Different Mechanisms Of Damage Research Articles

Analysis of asphalt microscopic and force curves under water-temperature coupling with AFM

Asphalt, as a crucial material in road construction, is affected by external environmental factors, among which water and temperature are the primary causes of water damage to asphalt pavements. Different hydro-thermal environments can cause varying types of damage to asphalt or the asphalt-aggregate interface. To analyze the micro-performance changes of different types of asphalt under various hydro-thermal environments, this study conducts tests onPG64–22 matrix asphalt, PG76–22 SBS-modified asphalt and PG82–34 high viscosity asphalt under different hydro-thermal coupling and freeze-thaw cycle conditions using Atomic Force Microscopy (AFM). The analysis is based on the obtained micro-morphology images and mechanical properties, exploring the impact mechanisms of different hydro-thermal environments on various asphalts. Results show that under different hydro-thermal conditions, the three asphalts exhibit different morphological changes: the asphalt surface's “bee-shaped structure” is gradually destroyed after hydro-thermal coupling, while a “disappearance-reappearance” phenomenon is observed under freeze-thaw cycles. Moreover, the roughness of the two modified asphalts shows a different trend from that of the matrix asphalt, indicating that the modifier alters the micro-structure of asphalt to some extent. Under hydro-thermal coupling, the adhesion force of the three asphalts decreases linearly, with matrix asphalt decreasing by 89.2% after 3 hours, SBS modified asphalt by 63.1%, and high-viscosity asphalt by 23.9%, showing that high-viscosity asphalt has better waterproof and heat-resistant performance. During freeze-thaw cycles, the adhesion force between the asphalt and the tip shows varying degrees of recovery. Additionally, there are differences in adhesion force across different areas of the asphalt surface, which tend to diminish with hydro-thermal coupling or freeze-thaw cycles. These results indicate that hydro-thermal coupling and freeze-thaw cycles have different mechanisms of damage to the internal structure of asphalt, providing important data for understanding the damage mechanisms in depth.

Oxidative Stress Damage of Iron Overload on Bone Marrow Erythropoiesis, Heart and Liver in Non-Transfusion Dependent Thalassemia

Background: Non-transfusion-dependent thalassemia (NTDT) characterized by ineffective hematopoiesis and increased intestinal iron absorption, and excessive iron deposits in the bone marrow, heart, and liver, causing progressive organ damage. It has been reported that oxidative stress damage caused by iron overload could induce apoptosis or ferroptosis. However, the related studies and mechanisms are not well unknown in NTDT disorders. Aims: To investigate the effects of iron overload on bone marrow erythropoiesis, heart and liver in NTDT patients and Hbb th3(th3/+) mice. Methods: Patients (19-47 y of age) and 12-month-old Hbb th3(th3/+) mice with NTDT were selected as thalassemia group, healthy human and normal mice were selected as control group. Iron overload related indexes, bone marrow erythropoiesis, oxidative stress, apoptosis and ferroptosis of each sample were detected by Elisa, flow cytometry, RT-PCR and Weston blot methods, respectively. Results: Compared with the control group, Serum ferritin is significantly increased in NTDT group, and there is imbalance of iron metabolism. And in NTDT patients, liver and myocardial iron deposition was assessed by MRI analysis, resonance results suggest that the degree of iron overload in liver is more significant than that in heart. The damage of erythropoiesis in NTDT group was more severe than that in control group, which showed active erythropoiesis, and the differentiation of erythroid precursor cells stagnated in early stage of erythroid precursor cells, and there were maturation disorders. The oxidative stress-related indexes reactive oxygen species (ROS), lipid peroxidation and malondialdehyde (MDA) induced by iron overload were also significantly increased in the NTDT group. However, significant signs of apoptosis were observed in the bone marrow of the NTDT group, including increased proportion of apoptotic cells, signs of apoptosis were mainly observed in the mitochondria of erythroid colony electron microscopy, and the level of GPX4 that is a key indicator of ferroptosis, was increased. But the expression of GPX4, VDAC2 and SLC7A11 of ferroptosis was decreased in the heart and liver with heavy iron deposition, and the signs of ferroptosis were also observed under electron microscopy. Summary/Conclusion: Our study found that there are differences in iron overload and injury performance among different organs in NTDT. Oxidative stress caused by iron overload in the bone marrow impairs erythropoiesis mainly through apoptosis, whereas signs of ferroptosis were observed in the liver and heart of Hbb th3(th3/+) mice.These results suggest that with the gradual accumulation of iron circulation, the damage is a dynamic process, and different organs show different signs of damage, which may be related to the different mechanisms of damage, tolerance and compensation of organs, but further studies are needed to confirm.

Low levels of mouse sperm chromatin fragmentation delay embryo development.

We previously demonstrated that MnCl2 induces double-stranded DNA breaks in sperm in a process that we term as sperm chromatin fragmentation. Here, we tested if the levels of double-stranded DNA breaks were corelated to the concentration of MnCl2, and we compared this to another agent that causes single-stranded DNA breaks, H2O2. We found that both methods have the advantage of inducing DNA breaks in a concentration-dependent manner. Mouse sperm were treated with varying concentrations of either H2O2 or MnCl2, and the DNA damage was assessed by pulse-field gel electrophoresis, and the alkaline and neutral comet assays. Oocytes were injected with either treated sperm and the resulting embryos analyzed with an embryoscope to detect subtle changes in embryonic development. We confirmed that H2O2 treatment induced primarily single-stranded DNA breaks and MnCl2 induced primarily double-stranded DNA breaks, indicating different mechanisms of damage. These sperm were injected into oocytes, and the development of the resulting embryos followed with an embryoscope equipped with time lapse recording. We found that aberrations in early embryonic development by day 2 with even the lowest levels of DNA damage and that the levels of embryonic aberrations correlated to the concentration of either H2O2 or MnCl2. Low levels of H2O2 caused significantly more aberrations in embryonic development than low levels of MnCl2 even though the levels of DNA damage as measured by comet assays were similar. These data demonstrate that even low levels of sperm DNA damage cause delays and arrests in embryonic development.

Alterations in cortical morphometry of the contralesional hemisphere in children, adolescents, and young adults with perinatal stroke

Perinatal stroke causes most hemiparetic cerebral palsy and cognitive dysfunction may co-occur. Compensatory developmental changes in the intact contralesional hemisphere may mediate residual function and represent targets for neuromodulation. We used morphometry to explore cortical thickness, grey matter volume, gyrification, and sulcal depth of the contralesional hemisphere in children, adolescents, and young adults after perinatal stroke and explored associations with motor, attention, and executive function. Participants aged 6–20 years (N = 109, 63% male) with unilateral perinatal stroke underwent T1-weighted imaging. Participants had arterial ischemic stroke (AIS; n = 36), periventricular venous infarction (PVI; n = 37) or were controls (n = 36). Morphometry was performed using the Computational Anatomy Toolbox (CAT12). Group differences and associations with motor and executive function (in a smaller subsample) were assessed. Group comparisons revealed areas of lower cortical thickness in contralesional hemispheres in both AIS and PVI and greater gyrification in AIS compared to controls. Areas of greater grey matter volume and sulcal depth were also seen for AIS. The PVI group showed lower grey matter volume in cingulate cortex and less volume in precuneus relative to controls. No associations were found between morphometry metrics, motor, attention, and executive function. Cortical structure of the intact contralesional hemisphere is altered after perinatal stroke. Alterations in contralesional cortical morphometry shown in perinatal stroke may be associated with different mechanisms of damage or timing of early injury. Further investigations with larger samples are required to more thoroughly explore associations with motor and cognitive function.

Specific Autoantibodies and Microvascular Damage Progression Assessed by Nailfold Videocapillaroscopy in Systemic Sclerosis: Are There Peculiar Associations? An Update

Specific autoantibodies and nailfold videocapillaroscopy (NVC) findings are serum and morphological diagnostic hallmarks of systemic sclerosis (SSc) as well as useful biomarkers which stratify the microvascular progression and prognosis of patients. The aim of our narrative review is to provide an update and overview of the link between SSc-related autoantibodies, used in clinical practice, and microvascular damage, evaluated by NVC, by exploring the interaction between these players in published studies. A narrative review was conducted by searching relevant keywords related to this field in Pubmed, Medline and EULAR/ACR conference abstracts with a focus on the findings published in the last 5 years. Our search yielded 13 clinical studies and 10 pre-clinical studies. Most of the clinical studies (8/13, 61.5%) reported a significant association between SSc-related autoantibodies and NVC patterns: more specifically anti-centromere autoantibodies (ACA) were associated more often with an "Early" NVC pattern, whereas anti-topoisomerase autoantibodies (ATA) more frequently showed an "Active" or "Late" NVC pattern. Five studies, instead, did not find a significant association between specific autoantibodies and NVC findings. Among the pre-clinical studies, SSc-related autoantibodies showed different mechanisms of damage towards both endothelial cells, fibroblasts and smooth muscle vascular cells. The clinical and laboratory evidence on SSc-related autoantibodies and microvascular damage shows that these players are interconnected. Further clinical and demographic factors (e.g., age, sex, disease duration, treatment and comorbidities) might play an additional role in the SSc-related microvascular injury whose progression appears to be complex and multifactorial.

Phosphorylation of S6RP in peritubular capillaries of kidney grafts and circulating HLA donor-specific antibodies.

Antibody-mediated rejection (ABMR) caused by donor-specific HLA-antibodies (DSA) is a mediator of allograft loss after kidney transplantation (KT). DSA can activate microvascular endothelium damage through the mTOR pathway. In this study we assessed the mTOR pathway activation by DSA in KT with ABMR (ABMR + DSA+) compared to controls (ABMR-DSA-), biopsies with ABMR changes without DSA (ABMR + DSA-) and DSA without ABMR changes (ABMR-DSA+), and the potential modulation by mTOR inhibitors (mTORi). We evaluated 97 biopsies: 31 ABMR + DSA+, 33 controls ABMR-DSA-, 16 ABMR + DSA-, and 17 ABMR-DSA+ cases. Regarding immunosuppression of full ABMR + DSA+ and controls, 21 biopsies were performed under mTORi treatment (11 of them ABMR + DSA+ cases) and 43 without mTORi (20 of them ABMR + DSA+) so as to explore its effect on the mTOR pathway. Biopsies were stained for C4d, Ki67, and phosphorylated (p) S6RP, ERK, and mTOR by immunohistochemistry. Labeling was graded according to peritubular capillary staining. ABMR biopsies showed significantly higher C4d, p-S6RP, and Ki67 staining in peritubular capillaries (PTC) compared to controls, and light differences in p-ERK or p-mTOR. mTORi treatment did not modify p-S6RP, p-mTOR, and p-ERK staining. Diffuse p-S6RP in PTC in the biopsies significantly associated with circulating HLA-DSA independently of graft rejection, and with worse death-censored graft survival. These findings suggest that activation of endothelium through the mTOR pathway evidence different mechanisms of damage in ABMR + DSA+ and ABMR + DSA- despite similar histological injury.

P323 MYOCARDIAL INVOLVEMENT IN ANTI–PHOSPHOLIPID SYNDROME: A CASE OF A YOUNG BREASTFEEDING WOMAN

Abstract Introduction In Antiphospholipid Syndrome (APS) myocardial tissue can be involved through immune–mediated or thrombotic mechanisms, giving chest pain and increase of myocardial cytolysis markers. This may occur without any signs of myocardial injury at the moment of echocardiography, coronarography and cardiac magnetic resonance (CMR). The aim is to increase the awareness about this life–threating condition.Case summary. We present the case of 26–year–old woman few days after childbirth, affected by APS in anticoagulant therapy with previous deep vein thrombosis and without any other cardiovascular risk factors. She was symptomatic for intermittent chest–epigastric pain, fever and skin livedo reticularis. Lab Tests: TnI 750 ng/L, C–reactive protein 9.6 mg/dL, D–dimer 1693 µg/L; anemia; Antithyroid Antibodies and ANA 1:160 (SSB/LA). Blood cultures and COVID test were negative.Results. Echocardiography showed normal left/right ventricular function, but minimal pericardial effusion was present. Pulmonary Angio–CT revealed small thromboembolic event, ground–glass lungs compatible with hemorrhagic alveolitis.After a few days, the patient presented increased epigastric pain, headache, vomiting up to presenting a comatose state. Thrombotic or hemorrhagic events with cerebral CT and MR were excluded. Total–body CT was negative, except for peri–splenic and recto–uterine pouches.For the increase of TnI up to 4741 ng/L, the patient underwent coronary angiography which demonstrated non–obstructive coronary arteries. The assembled Neuro–Cardio–Rheumatology team suspected a rapidly developing Catastrophic APS which was developing quickly with multi–organ and life–threatening involvement.The patient underwent 4 cycles of plasmapheresis, intravenous human IgG and corticosteroids, with rapid clinical improvement. CMR subsequently demonstrated a small transmural late enhancement area on lateral left ventricle wall.The patient was discharged from the hospital on Day 6 post–therapies.Conclusions. APS may involve more organs, including myocardial tissue with different mechanisms of damage and high mortality rate. The presented case poses a multidisciplinary challenge, because thrombotic multiorgan microangiopathy may be not always diagnosed. Imaging methods such as CMR could be optimized with adenosine stress–CMR. Clinical attention is required among women with APS, to reach early diagnosis of myocardial thrombotic microangiopathy and to establish the best effective treatment.

Implementation of Tite Liner technique for maintenance and rehabilitation of a Colombian oil pipeline

One of the greatest challenges for petrochemical industry is corrosion prevention, mitigation and control, a phenomenon that generates a high negative impact due to materials degradation and that in recent years has increased as a result of multiphase fluids processing. Thus, there are different mechanisms of damage by internal corrosion that are generated during transport of multiphase fluids with high content of corrosive agents such as carbon dioxide, solid particles and sediments increased because of transport conditions. The technique Tite Liner was used for maintenance and repair of a Colombian oil pipeline with severe integrity problems. Equally, design and tuning of physical and chemical properties of the coating material was carried out, since they remained unchanged during thermofusion welding process, the initial compression for insertion in the system, the subsequent expansion to fit the pipeline internal dimensions and the system start up at high pressure. The experimental analysis displayed an improvement in the operational conditions of the line. This led to a decrease in the operating expenses of the pipeline, directing those assets in the physical recovery of other industrial equipment inherent to the hydrocarbon transportation process.

Bisphenol A and Bisphenol S Induce Endocrine and Chromosomal Alterations in Brown Trout.

Bisphenol A is a widely used compound found in large amount of consumer products. As concerns have been raised about its toxicological and public health effect, the use of alternatives to bisphenol A are now increasing. Bisphenol S is one of the analogues being used as a replacement for bisphenol A despite the fact that little is known about the effects of bisphenol S on living organisms. In this study, we investigated the potential endocrine and genotoxic effects of bisphenol A and bisphenol S in juvenile brown trout (Salmo trutta). The fish were exposed to the compounds for either 2 weeks or 8 weeks via sustained-release cholesterol implants containing doses of 2 mg/kg fish or 20 mg/kg fish of the substances. The effects on the thyroid hormone levels and the estrogenic disrupting marker vitellogenin were evaluated, along with the genotoxic markers micronucleated cells and erythrocyte nuclear abnormalities. An increase in plasma vitellogenin was observed in fish exposed to the high dose of bisphenol A for 2 weeks. At this experimental time the level of the thyroid hormone triiodothyronine (T3) in plasma was elevated after bisphenol S exposure at the high concentration, and paralleled by an increase of micronucleated cells. Moreover, bisphenol A induced an increase of micronuclei frequency in fish erythrocytes after the exposure at the lowest dose tested. Taken together the results indicate that both bisphenol A and its alternative bisphenol S cause endocrine disrupting and genotoxic effects in brown trout, although suggesting two different mechanisms of damage underlying bisphenol A and bisphenol S activity.

The scale effect in composites: An explanation physically based on the different mechanisms of damage involved in failure

The strength of a lamina of a laminate was considered from almost the very beginning of the application of composites as a value depending on the lamina thickness. This was generically called scale effect, the value of the stress at the appearance of first damage in a lamina being identified as the in situ strength. The ultra-thin plies have allowed this first damage, typically transverse cracks in the 90-degree laminas, to be delayed.This study presents a completely physically based explanation of the scale effect in composites based on the key identification of two different failure mechanisms in the 90-degree lamina of a [0,90n]S laminate (here called progressive and explosive) that are triggered as a function of the morphology of the laminate. Their characterization is based on energy concepts and does not require either properties of difficult interpretations or fitting parameters.The study extends from plies of conventional thickness to ultra-thin plies. BEM models have been performed, correlating the predictions with experimental microscopic observations.Developing a physically based explanation of the scale effect is the first step towards identifying the parameters involved in the failure initiation. Once identified, these parameters can be measured.

Standing contact fatigue behavior of nitrided AISI 316L steels

In this work, an experimental-numerical evaluation of the standing contact fatigue testing of a nitrided AISI 316L steel was developed. The nitride layers were formed at the surface of an AISI 316L steel by a salt bath nitriding process at a temperature of 580 °C for 1, 3 and 5 h of exposure time, obtaining three different layer thicknesses. In order to know the mechanical response and the different mechanisms of damage associated with the standing contact fatigue test, Hertzian tests were performed on a MTS machine by cyclic loading of a sphere on a flat surface formed by the layer/substrate system. The standing contact fatigue test was developed through two main stages. First, the critical loads for each treatment condition were determined by monotonic tests, where the appearance of circular cracks was considered as the failure criterion. Subsequently, cyclic subcritical loads were applied at a frequency of 5 Hz. A numerical model based on the finite element method was developed to evaluate the stress field generated in the system by cyclic contact loads. The results indicate that the thinnest thickness of nitride layer exhibits better resistance to standing contact fatigue.

Modeling the Onset and Growth of Damage in Composite Cylinders under Lateral Pressure Loading Between Parallel Plates

The present study examines the experimental and numerical investigations of the behavior and initiation and the development of the filament wound glass fiber/polyester composite cylinders under the loading of the lateral pressure between the parallel rigid plates. According to ASTM D2412- 02 standard, the samples were organized between the parallel rigid plates under the pressured loading. In addition to conducting experimental tests, numerical simulation was performed using ABAQUS commercial software. In order to take into account the effects of the initiation and the development of damage, the 3D Hashin damage model has been utilized. To apply 3D Hashin damage model, a UMAT subroutine coding procedure was conducted using the Fortran 77 program. Using micro mechanical relations concerning the layers, the definition of mechanical properties and the fracture strength of the composite cylinder were separately obtained based on measuring fiber and resin properties and the relative standard. During the whole tests, experimental observations, including the level of failure due to loading and the cause of the occurrence of different mechanisms of damage, have been discussed. Comparison of the results of the experimental tests with the result of numerical simulation has an appropriate agreement with each other.

Influence of the inclusion shape and the constraints level on damage to the elementary cell

In this paper, a multi-scale analysis is presented for nucleation and growth of a microcrack in front of a macrocrack. The loading conditions of the elementary cell are determined at the mesoscopic level in order to perform an analysis of the microcrack growth at a microscopic level. Both the influence of the inclusion shape in the cell and the state of stress on the mechanism of material failure near the crack tip are analyzed. The relations between the mechanical properties of the inclusion and the matrix are determined, causing different mechanisms of damage to be experimentally observed.

The study of mechanisms of biological activity of copper oxide nanoparticle CuO in the test for seedling roots of Triticum vulgare.

The rapid development of nanotechnology raises questions assessment of their impact on living objects. In the present study, we evaluated the impact of nanoparticle (NP) CuO at concentrations ranging from 0.8 to 63.5g/l in the test on wheat seedlings Triticum vulgare during 1-72h. In the viability test (WST-test), cells were isolated from the roots of seedlings T. vulgare, 12h not observed increase reductase activity after 24h decreased rate of not more than 19% compared with the control. The number of dead cells in seedlings of T. vulgaris after exposure with CuO nanoparticles to the test with Evans blue increased by 5-15% compared to control. We observed that a significant increase in copper revenues leaves 4.5-8.9 times more in relation to the control and the roots-in 5-9.7 times. During the determined amount of active oxygen species, a significant proportional increase in the total pool of reactive oxygen species (ROS) in roots increased to 27.6% after exposure to NP CuO compared with the control. It is shown that in the introduction in medium, the NP CuO in the doses ranging from 3.2 to 63.5g/l leads to DNA fragmentation and increases the fragments less than 3000bp on 51.4-62.8%. The totality of our results influences nanoforms of copper oxide on the amount of ROS, and the viability of the genomic component of the cells shows different mechanisms of damage in the activation of a metabolic reaction, to determine the concentration of nano-CuO.

Early ultrastructural events of skeletal muscle damage following cardiotoxin-induced injury and glycerol-induced injury

In this study, we investigated the early changes of skeletal muscle damage in response to injuries induced by cardiotoxin (CTX) and glycerol by using both light microscopy and transmission electron microscopy. Normal, non-dystrophic, adult male mice were used in this study. Tibialis anterior (TA) muscles were injected either with CTX or glycerol. Samples were collected at intervals starting from 1h up to 4days after injury. Injured muscles were subjected to both histological and ultrastructural analyses. CTX-induced injury caused mitochondrial accumulation and swelling followed by lysis, while glycerol-induced injury caused accumulation of vesicles with focal disruption of the basal lamina, indicating that the injuries have different mechanisms of damage to myofibers. Moreover, inflammatory cells, including neutrophils and macrophages, were recruited earlier and in larger numbers after CTX-induced injury than after glycerol-induced injury. On the other hand, satellite cells (SCs) activation started at 6h after both injuries, as indicated by an increase in both the length and cytoplasmic-to-nuclear ratio. However, there were significantly longer SCs with a higher cytoplasmic-to-nuclear ratio in the CTX-injured muscles than in the glycerol-injured muscles at day 4. In conclusion, our results demonstrated a difference between CTX and glycerol in their damage to myofibers; CTX damages myofiber mitochondria, while glycerol damages the myofiber cell membrane and alters osmosis. In addition, CTX-induced injury caused earlier and more extensive inflammatory infiltration than did glycerol-induced injury. This study is the first study to shed light on the early events following skeletal muscle injury induced by CTX and glycerol.

Adsorbing/dissolving Lyoprotectant Matrix Technology for Non-cryogenic Storage of Archival Human Sera.

Despite abundant research conducted on cancer biomarker discovery and validation, to date, less than two-dozen biomarkers have been approved by the FDA for clinical use. One main reason is attributed to inadvertent use of low quality biospecimens in biomarker research. Most proteinaceous biomarkers are extremely susceptible to pre-analytical factors such as collection, processing, and storage. For example, cryogenic storage imposes very harsh chemical, physical, and mechanical stresses on biospecimens, significantly compromising sample quality. In this communication, we report the development of an electrospun lyoprotectant matrix and isothermal vitrification methodology for non-cryogenic stabilization and storage of liquid biospecimens. The lyoprotectant matrix was mainly composed of trehalose and dextran (and various low concentration excipients targeting different mechanisms of damage), and it was engineered to minimize heterogeneity during vitrification. The technology was validated using five biomarkers; LDH, CRP, PSA, MMP-7, and C3a. Complete recovery of LDH, CRP, and PSA levels was achieved post-rehydration while more than 90% recovery was accomplished for MMP-7 and C3a, showing promise for isothermal vitrification as a safe, efficient, and low-cost alternative to cryogenic storage.

Response of the cell membrane–cytoskeleton complex to osmotic and freeze/thaw stresses. Part 2: The link between the state of the membrane–cytoskeleton complex and the cellular damage

In an earlier paper [35], we examined the mutual interaction between the actin cytoskeleton and the cell membrane and explored the role this interaction plays during freeze/thaw. In this follow-up paper, we investigate the physical and chemical stresses induced by freeze/thaw and explore the different mechanisms of damage caused by these stresses. Our results showed that changes in cell volume during freeze/thaw and the unfrozen water content in the solution alter the cytoskeleton stiffness, and the available membrane material. Combined with unfavorable ice–membrane interactions and increasing membrane stiffness, increased de-structuring of the membrane (such as bleb and microvilli formation) synergistically act on the membrane–cytoskeleton system generating irreversible damage.

Design of damage tolerance in high-strength steels

AbstractWith the extensive application of advanced high-strength steels in various fields due to their excellent mechanical properties, industrial interest in the damage of advanced high-strength steels has increased in recent years. For these modern steels, due to their multiphase microstructure and different deformation mechanisms, the concept of damage must be re-examined. In this paper, the definition, length scale and different mechanisms of damage are introduced. Both the experimental evaluation of damage and the numerical damage models are briefly reviewed and compared. The approaches to improving damage tolerance are given in the framework of the damage tolerance design principle.

The Cardioprotective Effect of Brief Acidic Reperfusion after Ischemia in Perfused Rat Hearts is not Mimicked by Inhibition of the Na+/H+ Exchanger NHE1

Background: Ischemic postconditioning (PostC), i.e. brief ischemia-reperfusion cycles before full reperfusion, is protective against cardiac ischemia/reperfusion (I/R) injury. Inhibition of the Na⁺/H⁺ exchanger NHE1 and delayed intracellular pH-normalization have been proposed to underlie protection by PostC. Methods and Results: We used Langendorff perfused rat hearts exposed to 35 min global ischemia to show that 15 min acidic (pH 6.5) treatment at onset of reperfusion decreased infarct size and functional deterioration at least to the same extent as PostC. In contrast, NHE1 inhibition by EIPA was detrimental. To evaluate HL-1 atrial cardiomyocytes as a cellular model for PostC, we exposed the cells to simulated ischemia/reperfusion (I/R) mimicking that in perfused hearts. Necrosis and apoptosis induced by I/R were unaffected by 15 min of pH 6.0 at onset of reperfusion. I/R increased the activity of c-Jun N-terminal Kinase 1/2 (JNK1/2) and Akt, but not of p38 MAPK, with no further effect of acidic reperfusion or EIPA. Conclusion: In rat hearts, 15 min acidic reperfusion improves myocardial performance at least as much as does PostC, whereas NHE1 inhibition is detrimental. In contrast, in HL-1 cardiomyocytes, acidic reperfusion or NHE1 inhibition affect neither survival nor JNK1/2-, Akt-, and p38 MAPK activity after I/R, pointing to different mechanisms of damage and protection in these systems.

The response of barley to salinity stress differs between hydroponic and soil systems

Many studies on salinity stress assume that responses in hydroponics mimic those in soil. However, interactions between the soil solution and the soil matrix can affect responses to salinity stress. This study compared responses to salinity in hydroponics and soil, using two varieties of barley (Hordeum vulgare L.). The responses to salinity caused by high concentrations of Na+ and Cl– were compared to assess any consistent differences between hydroponics and soil associated with a cation and an anion that contribute to salinity stress. Concentrated nutrient solutions were also used to assess the effects of osmotic stress. The effects of salinity differed between the hydroponic and soil systems. Differences between barley cultivars in growth, tissue moisture content and ionic composition were not apparent in hydroponics, whereas significant differences occurred in soil. Growth reductions were greater under hydroponics than in soil at similar electrical conductivity values, and the uptake of Na+ and Cl– was also greater. The relative importance of ion exclusion and osmotic stress varied. In soil, ion exclusion tended to be more important at low to moderate levels of stress (EC at field capacity up to 10 dS m–1) but osmotic stress became more important at higher stress levels. High external concentrations of Cl– had similar adverse effects as high concentrations of Na+, suggesting that Cl– toxicity may reduce growth. Fundamental differences in salinity responses appeared between soil and solution culture, and the importance of the different mechanisms of damage varies according to the severity and duration of the salt stress.