JOURNAL OF FOOD PROCESS ENGINEERING, Issue 1 2004
J.S. ROBERTS
ABSTRACT Fuji, McIntosh, and Red Delicious apple mashes were heated in a 2450 MHz oven to achieve bulk temperatures of 40, 50, 60, and 70C. Three kilograms of mash at a depth of 0.016 m heated using 1500 W were the optimum parameters to heat apple mash in the microwave. Variety of the apple mash was shown not to have a significant effect on the heating performance. Comparing actual bulk temperature to the predicted bulk temperatures of 40, 50, 60, and 70C showed reproducibility of heating these mashes using microwave energy. Average variation between actual and predicted bulk temperatures were 1.48C for the Fuji mash, 0.98C for the McIntosh mash, and 1.13C for the Red Delicious mash. In addition, regional heating was investigated and four distinct regions of heating were observed: the corner, the edge, the middle, and the center. Color and moisture content of the mash were also measured and compared to unheated mash at 21C. [source]

EFFECT OF PRETREATMENT ON DRYING TIME AND QUALITY OF CHILLI PEPPER

JOURNAL OF FOOD PROCESSING AND PRESERVATION, Issue 4 2010
T.Y. TUNDE-AKINTUNDE
ABSTRACT A study was carried out on the effect of various pretreatments and drying methods on drying time and quality of chilli pepper. Chilli peppers were pretreated with different blanching types and concentrations of osmotic sugar solutions (60 and 70°Brix), and were dried afterward. Results indicated that the pretreated peppers dried faster than the untreated ones. The peppers soaked in osmotic solution of 70°Brix had the lowest drying time, which decreased by a variation of 33.3,41.7%, compared with the dried untreated peppers that had the highest drying time. Solar-dried peppers had higher nutritional content than peppers dried from the other methods, while the oven-dried pepper samples had the lowest vitamin A and vitamin C contents. PRACTICAL APPLICATIONS Drying gives dried samples lower nutritional quality than fresh samples because of physiological changes that takes place. Pretreatments of pepper by steam and by water blanching are common methods, but osmotic dehydration also has a significant effect on the quality of dried foods. The effect of the pretreatments and drying methods on the drying rate and nutritional quality of dried pepper were investigated. Osmotically dehydrated samples had the lowest drying time, while pretreated samples dried faster than untreated samples generally. The nutritional quality of the dried samples, however, varied with the different pretreatment methods. This indicates that pretreatment enhances drying rate and also affects the quality of the final dried product. Dried pepper can thus be pretreated with blanching or dipping in osmotic solutions for products of higher nutritional quality. This will give dried pepper that will meet the nutritional requirement of the consumers better than untreated dried pepper. [source]

EFFECTS OF PRETREATMENT WITH ROSEMARY (ROSMARINUS OFFICINALIS L.) IN THE PREVENTION OF LIPID OXIDATION IN SALTED TILAPIA FILLETS

JOURNAL OF FOOD QUALITY, Issue 5 2008
M. DA SILVA AFONSO
ABSTRACT To delay lipid oxidation during meat processing, synthetic antioxidants have been used in the food industry, but the consumers' concern over their toxicity increased interest in research with natural antioxidants. The aim of this work was to analyze the water activity (Aw), thiobarbituric acid reactive substances (TBARS), moisture and trichloroacetic acid-soluble nitrogen (TCASN) in brined tilapia fillets treated or pretreated with natural rosemary extract (Rosmarinus officinalis) and stored for 240 days at ,18C. Higher Aw (0.900 ± 0.010) and moisture (70.13 ± 0.20) values were observed in the pretreated fillets. The TBARS values in the treatment (3.31 ± 0.79) and pretreatment (3.39 ± 0.53) were half the value of the control treatment (6.14 ± 1.21) at 240 days. Statistical differences were observed in TCASN values in 180 (0.112 ± 0.020) and 240 (0.132 ± 0.017) days, with the pretreatment showing a more protective effect in protein oxidation. In this study, rosemary proved to be protective during the frozen storage, especially when its extract was used as pretreatment, before the salting process. PRACTICAL APPLICATIONS Fish consumption is highly elastic, because the annual average consumption of seafood per person in Brazil is only 6.8 kg. The federal government has set a goal to increase it to 12 kg by 2007. Salting is an older food preservation process still used today, and is extremely important because, despite advances in food technology, increased monitoring and improved knowledge, it is emphasized as an easy, cheap and effective process that does not require refrigeration. Tilapia is a highly prolific fish, with a production volume that is increasingly higher each year in Brazil. Therefore, it calls for interesting research to allow an increased shelf life for this species. [source]

THE EFFECT OF PRETREATMENT OF SHREDDED CELERIAC USING SOLUTIONS OF ENZYMATIC BROWNING INHIBITORS ON THE QUALITY OF MINIMALLY PROCESSED PRODUCT

JOURNAL OF FOOD QUALITY, Issue 5 2007
BIETA, RADZIEJEWSKA-KUBZDELA EL
ABSTRACT The study investigated the effect of soaking celeriac flakes in solutions containing various concentrations of enzymatic browning inhibitors on the quality of stored minimally processed product. Ascorbic acid (0.2,0.5%), 4-hexylresorcinol (0.003,0.01%), sodium chloride (0.1,0.5%) and sodium lactate (2,3%) were used as browning inhibitors. On the basis of the conducted tests, it was found that among the applied browning inhibitors, only ascorbic acid had an advantageous effect on the quality of stored celeriac flakes. Along with an increase in its concentration in the solution (0.2,0.5%) used for the pretreatment of the flakes, the value of color parameter a* decreased, while the value of parameter b* increased. At the concentration of ascorbic acid in the solution exceeding 0.25%, flake color in the sensory examination was evaluated as desirable. An increase of ascorbic acid concentration in the solution in the range from 0.2 to 0.4% resulted in a decrease in the total mesophilic and psychrophilic bacteria counts, respectively, by 3 and 1 log cfu/g of the stored product. PRACTICAL APPLICATIONS Minimal processing of celeriac provides convenience for consumers and many economic benefits for producers. Minimal processing of celeriac can induce disadvantageous changes in tissue, which may lead to darkening of the flakes and deterioration of product sensory attributes. Moreover, shredded raw material constitutes an excellent medium for the development of microorganisms. This article contains information about the effectiveness of enzymatic browning inhibitors for extending the shelf life of celeriac flakes. We show a range of concentrations of inhibitors, which improve the preservation of color, intrinsic taste and microbial quality of minimally processed celeriac. [source]

PRETREATMENT WITH INTRAVENOUS ASCORBIC ACID PRESERVES ENDOTHELIAL FUNCTION DURING ACUTE HYPERGLYCAEMIA (R1)

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2005
Brian A Mullan
SUMMARY 1.,Acute hyperglycaemia may impair endothelial function. Ascorbic acid (AA), administered intra-arterially, has been reported to improve endothelium-dependent vasodilatation during a forearm hyperglycaemic clamp. Using a randomized, double-blind, placebo-controlled, cross-over study, we investigated the potential for intravenous ascorbic acid to modify the endothelial response to acute systemic hyperglycaemia in humans. 2.,Nine healthy male volunteers were recruited from the hospital staff. Endothelial function was determined by measuring the forearm blood flow responses to intrabrachial infusions of endothelium-dependent (ED) and endothelium-independent (EID) vasodilators. The endothelial function index (EFI) was derived from the ratio of ED and EID vasodilatation. Haemodynamic and endothelial function measurements were performed at baseline and then repeated 2 h after a systemic hyperglycaemic clamp (14 mmol/L). The subjects, studied on two separate occasions, were randomized to placebo or 2 g intravenous ascorbic acid prior to the initiation of hyperglycaemia. 3.,After systemic hyperglycaemia with placebo pretreatment, the EFI fell from 1.08 ± 0.21 to 0.74 ± 0.13 (difference (95% confidence interval): 0.34 (0.20, 0.47); P < 0.001). When subjects were pretreated with ascorbic acid, the EFI was not affected by hyperglycaemia (1.11 ± 0.21 to 1.12 ± 0.17; P = 0.938). This difference between placebo and ascorbic acid was significant (P < 0.001). Plasma ascorbate concentrations decreased during hyperglycaemia and correlated directly with the reduction in the EFI (r = 0.798; P < 0.001). 4.,Pretreatment with an intravenous bolus of ascorbic acid can prevent endothelial dysfunction during acute systemic hyperglycaemia. Therefore, ascorbic acid may have potential therapeutic use in clinical situations where acute hyperglycaemia may be a complication. [source]

Pretreatment with insulin before ischaemia reduces infarct size in Langendorff-perfused rat hearts

ACTA PHYSIOLOGICA, Issue 2 2009
B. N. Fuglesteg
Abstract Aim:, To compare the possible role of Akt and mammalian target of rapamycin (mTOR) in mediating cardioprotection against ischaemia under three different conditions: (1) During ischaemic preconditioning (IPC), (2) when insulin was given as a pretreatment agent (InsPC) and (3) when insulin was given as a reperfusion cell survival agent (InsR). Methods:, Isolated perfused rat hearts were subjected to IPC (3 × 5 min) or InsPC (50 mU mL,1; 3 × 5 min), before 30 min of regional ischaemia followed by 120 min of reperfusion ± 1L-6-hydroxymethyl- chiro -inositol-2 - [(R)-2- O -methyl-3- O -octadecylcarbonate] (HIMO) (20 ,m; Akt inhibitor) or rapamycin (1 nm; mTOR inhibitor). In addition, insulin (3 mU mL,1) was given at the onset of reperfusion, ±HIMO or rapamycin. Risk zone (R) and infarct size (I) were determined with Evans blue and tetrazolium staining respectively. Western blot analysis was performed on tissue from Langendorff-perfused rat hearts and cell lysates from cultured HL1 cells. Results:, IPC, InsPC and InsR treatment resulted in a significant reduction in infarct size compared to controls (all P < 0.05). This protective effect of IPC and insulin was abolished by the inhibitors. However, the putative Akt inhibitor, although capable of abolishing cardioprotection induced by insulin, was not able to inhibit insulin-induced phosphorylation of Akt in Langendorff-perfused rat hearts and cultured HL1 cells. The target for this compound therefore remains to be determined. Conclusion:, IPC and insulin (either as InsPC or InsR) appear to activate mTOR, and this kinase seems to play an essential role in cardioprotection against ischaemia and reperfusion injury as rapamycin blocked the protection. [source]

An actin-stabilizing peptide conjugate deduced from the major outer sheath protein of the bacterium Treponema denticola

CYTOSKELETON, Issue 9 2007
Mohsen Amin
Abstract A synthetic peptide conjugated to bovine serum albumin, P34BSA, based on a 10-mer in the deduced amino acid sequence of the major outer sheath protein of Treponema denticola, was found to stabilize actin filaments of fibroblasts. Pretreatment of cells with P34BSA inhibited the actin disruption induced by cytochalasin D and latrunculin B. P34BSA was taken up by the cells and localized among actin filaments. P34BSA bound actin from fibroblast lysates, and cell exposure to P34BSA led to the activation of RhoA, a key regulator of actin filament assembly in fibroblasts. Exposure of fibroblasts to P34BSA retarded their migration on a collagen substratum. P34BSA also inhibited chemotaxis of murine neutrophils. Our findings with a novel peptide conjugate imply that bacterial proteins known to perturb the cytoskeleton represent a rich source of molecular models upon which to design synthetic reagents for modulating actin-dependent cellular functions. Cell Motil. Cytoskeleton 2007. © 2007 Wiley-Liss, Inc. [source]

Retinoids and Wound Healing

DERMATOLOGIC SURGERY, Issue 10 2006
MARK ABDELMALEK MD
BACKGROUND Retinoids are widely used in dermatology and may play a role in wound healing. The exact role of retinoids in wounds is confusing and controversial, however. Systemic retinoids are presumed to be detrimental to wound healing; however, this standard is based on isolated reports. OBJECTIVE The objective was to provide a critical review of the available literature regarding the role of both topical and systemic retinoids in various aspects of wound healing. CONCLUSIONS Pretreatment with retinoids likely promotes wound healing after facial resurfacing procedures and full- or partial-thickness wounds. While the evidence is mixed regarding the effects of retinoids applied to fresh and healing wounds, the majority of the evidence available shows favorable wound-healing properties in this setting. The medical,legal standard regarding the avoidance of facial resurfacing and surgical procedures in patients on or recently completing a course of systemic retinoids was likely prematurely established. [source]

Structure,activity relationships of isoeugenol-based chlorophenylpiperazine derivatives on serotonergic/adrenergic receptor, platelet aggregation, and lipid peroxidation

DRUG DEVELOPMENT RESEARCH, Issue 5 2010
Kuo-Ping Shen
Abstract Three isoeugenol-based eugenosedin chlorphenylpiperazine derivatives, Eu-A, Eu-B, and Eu-C, were synthesized and tested for their serotonergic, adrenergic antagonist, antioxidant, and anti-aggregation activities. In radioligand binding assays, all three agents displayed significant binding affinities on ,1, ,2, ,1, 5-HT1B, and 5-HT2A receptors. In human platelet, they inhibited epinephrine and 5-HT-induced aggregation, and in human platelet with ,2 and 5-HT2A receptors they had a competitive binding effect. Eu-B and Eu-C were more potent than Eu-A. All compounds had antioxidant effects derived from aryloxypropanolamine. Eu- A, Eu-B, or Eu-C (1, 3, 5,mg/kg iv) given to normotensive Wistar rats produced a dose-dependent decrease in mean arterial blood pressure and heart rate and when injected into the cisternum, Eu-A, Eu-B, or Eu-C (0.3, 0.03,µmol) increased blood pressure within 15,min. Pretreatment with any of the three agents inhibited clonidine (38,pmol)-induced hypotension. In vitro experiments, Eu-A, Eu-B, or Eu-C (1, 10, and 100,µM) competitively antagonized norepinephrine-, clonidine-, and 5-HT (10,8,10,4,M)-induced vasocontraction in isolated rat aorta, and competitively antagonized isoproterenol (10,8,10,4,M)-induced positive inotropic effects in a concentration-dependent manner in the isolated rat left atrium. In isolated rabbit ear arteries sensitized with 16,mM K+, all three agents antagonized 5-nonyloxytryptamine- and 5-HT-induced vasocontractions. These findings show that Eu-A, Eu-B, and Eu-C possess functional ,1, ,2, ,1, 5-HT1B, and 5-HT2A receptor blocking activities. In conclusion, the changes in the position of chloride at phenylpiperazine influenced the serotonergic receptor, adrenoceptor antagonistic activities, but not anti-aggregation and antioxidant activities. Drug Dev Res 71:1,9, 2010. © 2010 Wiley-Liss, Inc. [source]

The Influence of the Cathodic Pretreatment on the Electrochemical Detection of Dopamine by Poly(1-aminoanthracene) Modified Electrode

ELECTROANALYSIS, Issue 19 2010
Estela de Pieri Troiani
Abstract In this study we demonstrated the influence of the cathodic pretreatment of poly(1-aminoanthracene) (PAA) electropolymerized on a platinum electrode for determination of dopamine (DA). The DA electrochemical response was obtained after a cathodic pretreatment of the PAA electrode which consisted of applying a potential of ,0.7,V (vs. Ag/AgCl) for 3,s before each measurement. The pretreatment of the electrode changed the PAA electrocatalytic properties so that the electrode began to present electrochemical response to DA without interference of ascorbic acid (AA). The anodic peak currents determined by differential pulse voltammetry using pretreated PAA showed a linear dependence on the DA concentration from 0.56 to 100,µM with a detection limit of 0.13,µM and a correlation coefficient of 0.9986. The electrode exhibits a relative standard deviation of 1.2,% for ten successive measurements of a 0.5,mM DA solution. The analysis by scanning electron microscopy and atomic force microscopy show a homogeneous and nanostructured film with globular structures with diameter of about 20,nm. The analytical results obtained for DA determination at a pretreated PAA electrode in pharmaceutical formulation sample were in good agreement with those obtained by a comparative procedure at a 95,% confidence level. PAA electrode after the pretreatment showed electrochemical responses to DA with excellent selectivity, sensitivity, and high stability without interference of AA. [source]

Multiple-point electrochemical detection for a dual-channel hybrid PDMS-glass microchip electrophoresis device

ELECTROPHORESIS, Issue 19 2009
Mario Castaño-Álvarez
Abstract A new PDMS-based dual-channel MCE with multiple-point amperometric detection has been evaluated. Electrophoresis has been optimised in a single-channel device. Pretreatment with 0.1,M NaOH is very important for increasing and stabilising the EOF. The precision is adequate for a day's work in terms of both peak current and migration time. The RSD of the peak current for five successive signals was 1.9, 2.4 and 3.1% for dopamine, p- aminophenol and hydroquinone. RSD for the migration time was always less than 1.3%, which demonstrates the stability of the EOF and the possibility of running multiple experiments in the same microchip. The adequate inter-microchip precision as well as the rapid and simple manufacturing procedure indicates the disposable nature of the PDMS microchips. A dual-channel device with very simple multiple-point amperometric detection is proposed here. Elasticity of the PDMS allows removing the polymer slightly and aligning gold wires working electrodes. Injection can be performed from each of the sample reservoirs or from both simultaneously. The distance between the separation channels is critical for obtaining adequate signals as well as the introduction of a high-voltage electrode in the buffer reservoir. Simultaneous measurement of the same analytes in both channels is possible by applying the same potential. Moreover, since no cross-separation is produced, different analytes or samples can be simultaneously measured. [source]

Protective effect of the cruciferous vegetable mustard leaf (Brassica campestris) against in vivo chromosomal damage and oxidative stress induced by ,-radiation and genotoxic chemicals

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 5 2008
Ashu B. Tiku
Abstract We evaluated the possible protective effect of the popular Indian cruciferous vegetable mustard leaf (Brassica campestris) against chromosomal damage and oxidative stress induced by ,-radiation, cyclophosphamide (CPH) and urethane (URE), in mice. In vivo bone marrow micronucleus test was performed to assess chromosomal damage, and oxidative stress was monitored by estimating the changes in lipid peroxidation and the status of glutathione (GSH) as well as redox cycle antioxidants. Pretreatment with 50,250 mg/kg body wt of mustard leaf extract (MLE) for seven days significantly reduced the frequencies of micronuclei induced by ,-radiation, CPH and URE. The protective effect against chromosomal damage was associated with modulation of lipid peroxidation as well as an increase in GSH and the GSH-dependent enzyme glutathione S -transferase (GST). Mass spectral analysis showed the presence of glucosinolates in MLE used for the pretreatment of mice. These findings indicate that intake of the green leafy cruciferous vegetable mustard leaf can lead to protection against in vivo genotoxicity and oxidative stress. Environ. Mol. Mutagen., 2008. © 2008 Wiley-Liss, Inc. [source]

Evaluation of the radioprotective effect of Liv 52 in mice

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 7 2006
Ganesh C. Jagetia
Abstract Liv 52 is a mixture of botanicals that is used clinically to treat various hepatic disorders. In this study, the radioprotective activity of Liv 52 was evaluated in mice given whole-body exposure to different doses of ,-radiation. In addition, a series of studies was conducted to explore the mechanism of radioprotection. Radioprotection was evaluated by the ability of Liv 52 to reduce both the frequency of bone marrow micronucleated erythrocytes and the lethality produced by 60Co ,-radiation. Mice were treated by oral gavage once daily for seven consecutive days with 500 mg/kg body weight Liv 52 or carboxymethylcellulose vehicle prior to radiation. Micronucleated polychromatic erythrocytes (MPCEs), micronucleated normochromatic erythrocytes (MNCEs), and the PCE/NCE ratio were measured at 0.25,14 days after exposure to whole-body radiation doses of 0, 0.5, 1.5, 3.0, or 4.5 Gy; animal survival was monitored after doses of 7, 8, 9, 10, 11, or 12 Gy. Pretreatment of mice with Liv 52 significantly reduced the frequency of radiation-induced MPCEs and MNCEs. Irradiation reduced the PCE/NCE ratio in a dose-related manner for up to 7 days following irradiation; Liv 52 pretreatment significantly mitigated against these reductions. Liv 52 treatment also reduced the symptoms of radiation sickness and increased mouse survival 10 and 30 days after irradiation. Liv 52 pretreatment elevated the levels of reduced glutathione (GSH), increased the activities of glutathione transferase, GSH peroxidase, GSH reductase, superoxide dismutase, and catalase, and lowered lipid peroxidation (LPx) and the activities of alanine amino transferase and aspartate aminotransferase 30 min after exposure to 7 Gy of ,-radiation. Liv 52 pretreatment also reduced radiation-induced LPx and increased GSH concentration 31 days following the exposure. The results of this study indicate that pretreatment with Liv 52 reduces the genotoxic and lethal effects of ,-irradiation in mice and suggest that this radioprotection may be afforded by reducing the toxic effects of the oxidative products of irradiation. Environ Mol. Mutagen., 2006. © 2006 Wiley-Liss, Inc. [source]

The Effects of Ascorbic Acid on Penicillin-induced Epileptiform Activity in Rats

EPILEPSIA, Issue 7 2007
Mustafa Ayyildiz
Summary:,Purpose: Epileptic seizure results from excessive discharge in a population of hyperexcitable neurons. A number of studies help to document the effects of active oxygen free radical scavengers such as ,-tocopherol or ascorbic acid (vitamin C). In the present study, we examined the effects of ascorbic acid, at the six different doses, on penicillin-induced epileptiform activity. Methods: A single microinjection of penicillin (2.5 ,l, 500 units, intracortically) into the left sensorimotor cortex induced epileptiform activity within 2,5 min, progressing to full seizure activity lasting ,3,5 h. In the first set of experiments, 30 min after penicillin injection, six different doses of ascorbic acid (25, 50, 100, 200, 400, or 800 mg/kg) were administered intraperitoneally (IP). The other group of animals received the effective dose of ascorbic acid (100 mg/kg, IP) for 7 days. Ascorbic acid administration was stopped 24 h before penicillin treatment. Another group of rats received the effective dose of ascorbic acid (100 mg/kg, IP) 30 min before penicillin treatment. In the second set of experiments, the lipid peroxidation (MDA) and reduced glutathione (GSH) levels of brain were measured in the control, control + ascorbic acid, penicillin, and penicillin + ascorbic acid groups. Results: Ascorbic acid, at the low dose (50, 100 mg/kg, 30 min after penicillin injection), decreased both the frequency and amplitude of penicillin-induced epileptiform activity in rats. Ascorbic acid, at intermediate doses (200, 400 mg/kg, 30 min after penicillin injection), decreased the frequency of epileptiform activity without changing the amplitude. Ascorbic acid, at the lowest dose (25 mg/kg) and highest dose (800 mg/kg) (30 min after penicillin injection), did not change either the frequency or amplitude of epileptiform activity. Ascorbic acid, at the low dose (100 mg/kg) was the most effective dose in changing the frequency and amplitude of penicillin-induced epileptiform activity. Pretreatment with ascorbic acid (100 mg/kg) 30 min before penicillin treatment caused a significant delay in the onset of penicillin-induced epileptiform activity. Pretreatment with ascorbic acid (100 mg/kg) for 7 days did not change the latency of epileptiform activity. The most effective dose of ascorbic acid (100 mg/kg) prevented both the decrease in GSH level and the increase in lipid peroxidation level (MDA) occurring after penicillin-induced epileptiform activity. Conclusions: These data indicate that ascorbic acid has neuroprotective activity against penicillin-induced epileptiform electrocorticogram activity. [source]

The "Forgotten" Cross-Tolerance Between Phenobarbital and Primidone: It Can Prevent Acute Primidone-Related Toxicity

EPILEPSIA, Issue 10 2000
Andres M. Kanner
Summary Purpose: We report on the effect that pretreating patients with phenobarbital has on averting adverse events when primidone is introduced. Methods: Thirty patients with intractable partial epilepsy were pretreated with phenobarbital before starting primidone. Therapy with primidone was started at a dosage of 500 mg/day, and the phenobarbital was stopped. The primidone dose was then increased by 125 to 250 mg every 3 weeks until adverse events or a seizure-free state was reached. All previous antiep-ileptic medications were tapered down to yield a primidone monotherapy regimen. Results: Twenty-six patients (87%) tolerated the introduction of primidone with minimal or no adverse events. Only one patient had to discontinue primidone during the initial 4 weeks because of severe dizziness. This was the only patient in whom primidone monotherapy could not be reached because of adverse events. Three other patients experienced dizziness severe enough to interfere with their activities. This symptom disappeared in two patients after the dose was lowered; in the other patient, primidone was stopped and phenobarbital was restarted for another 4 days. No symptoms recurred when primidone was reintroduced on the fifth day. Conclusions: Pretreatment with phenobarbital can minimize the occurrence of intolerable adverse events associated with the introduction of primidone. [source]

Effects of endothelin-1 on portal-systemic collaterals of common bile duct-ligated cirrhotic rats

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 4 2004
C.-C. Chan
Abstract Background/Aims, Endothelin-1 (ET-1) may induce intrahepatic vasoconstriction and consequently increase portal pressure. Endothelin-1 has been shown to exert a direct vasoconstrictive effect on the collateral vessels in partially portal vein-ligated rats with a high degree of portal-systemic shunting. This study investigated the collateral vascular responses to ET-1, the receptors in mediation and the regulation of ET-1 action by nitric oxide and prostaglandin in cirrhotic rats with a relatively low degree of portal-systemic shunting. Methods, The portal-systemic collaterals of common bile duct-ligated (BDL) cirrhotic rats were tested by in situ perfusion. The concentration-response curves of collaterals to graded concentrations of ET-1 (10,10,10,7 m) with or without BQ-123 (ETA receptor antagonist, 2 × 10,6 m), BQ-788 (ETB receptor antagonist, 10,7 m) or both were recorded. In addition, the collateral responses to ET-1 with preincubation of N, -nitro-L-arginine (NNA, 10,4 M), indomethacin (INDO, 10,5 M) or in combination were assessed. Results, Endothelin-1 significantly increased the perfusion pressures of portal-systemic collaterals. The ET-1-induced constrictive effects were inhibited by BQ-123 or BQ-123 plus BQ-788 but not by BQ-788 alone. The inhibitory effect was greater in the combination group. Pretreatment of NNA or NNA plus INDO equivalently enhanced the response of ET-1 while pretreatment of INDO alone exerted no effect. Conclusion, Endothelin-1 has a direct vasoconstrictive effect on the collaterals of BDL cirrhotic rats, mainly mediated by ETA receptor. Endogenous nitric oxide may play an important role in modulating the effects of ET-1 in the portal-systemic collaterals of BDL cirrhotic rats. [source]

Signaling events leading to the curative effect of cystatin on experimental visceral leishmaniasis: Involvement of ERK1/2, NF-,B and JAK/STAT pathways

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 3 2009
Susanta Kar
Abstract Curative effect of cystatin, a natural cystein protease inhibitor, on experimental visceral leishmaniasis was associated with strong upregulation of iNOS. The transductional mechanisms underlying this cellular response was investigated in the murine macrophage cell line RAW 264.7 and in the BALB/c mouse model of visceral leishmaniasis. Cystatin synergizes with IFN-, in inducing ERK1/2 phosphorylation and NF-,B DNA-binding activity. Pretreatment of cells with specific inhibitors of NF-,B or ERK1/2 pathway blocked the cystatin plus IFN-,-inducible NF-,B activity and markedly reduced the expression of iNOS at both mRNA and protein levels. Silencing of mitogen- and stress-activated protein kinase 1 significantly reduced cystatin-mediated NF-,B-dependent iNOS gene transcription suggesting the involvement of mitogen- and stress-activated protein kinase 1 activation in ERK1/2 signaling. DNA binding as well as silencing experiments revealed the requirement of IFN-,-mediated JAK-STAT activation even though cystatin did not modulate this signaling cascade by itself. In the in vivo situation, key steps in the activation cascade of NF-,B, including nuclear translocation of NF-,B subunits, I,B phosphorylation and I,B kinase, are all remarkably enhanced in Leishmania -infected mice by cystatin. Understanding the molecular mechanisms through which cystatin modulates macrophage effector responses will contribute to better define its potential for macrophage-associated diseases, in general. [source]

Hierarchy of eosinophil chemoattractants: role of p38 mitogen-activated protein kinase

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 9 2006
Petra Schratl
Abstract Several chemoattractants can regulate the recruitment of eosinophils to sites of inflammation, but the hierarchy among them is unknown. We observed here that eosinophil chemotaxis towards eotaxin or 5-oxo-6,8,11,14-eicosatetraenoic acid (5-oxo-ETE) was amplified up to sixfold in the presence of prostaglandin (PG) D2. This effect was only seen in eosinophils, and not in neutrophils or basophils. Pretreatment with the chemoattractant receptor-homologous molecule expressed on TH2 cells (CRTH2) antagonist ramatroban prevented the PGD2 enhancement of eosinophil migrations. In contrast, eotaxin or 5-oxo-ETE inhibited the migration of eosinophils towards PGD2. 5-oxo-ETE enhanced the chemotaxis to eotaxin, while eotaxin had no effect on 5-oxo-ETE-induced migration. 5-oxo-ETE induced the phosphorylation of p38 mitogen-activated protein kinase, and inhibition of p38 mitogen-activated protein kinase by SB-202190 converted the effect of 5-oxo-ETE on the chemotaxis to PGD2 from inhibition to enhancement. The presence of blood or plasma markedly decreased the sensitivity of eosinophils to eotaxin or 5-oxo-ETE, while responses to PGD2 were unaltered. In conclusion, PGD2 might be an initial chemoattractant, since it maintains its potency in the circulation and augments the responsiveness of eosinophils to other chemoattractants. In contrast, eotaxin seems to be an end-point chemoattractant, since it has reduced efficacy in blood and is capable of down-modulating eosinophil responsiveness to other chemoattractants. [source]

Role of the monomeric GTPase Rho in hematopoietic progenitor cell migration and transplantation

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 1 2006
Stephan Göttig
Abstract To investigate the role of the monomeric guanosine triphosphatase (GTPase) Rho on migration of hematopoietic progenitor cells (HPC), we employed different clostridial toxins which inhibit the Rho family of GTPases. Pretreatment with C2I-C3, a cell-accessible C3 transferase fusion protein that targets Rho, increased chemokinetic migration of the factor-dependent multipotent cell line Factor Dependent Cell Paterson with mixed lineage differentiation potential (FDCP-mix) and of primary lineage marker-depleted HPC in vitro. In contrast, treatment with lethal toxin (LT) from Clostridium sordellii, which predominantly inactivates Rac, and with toxin,B from C.,difficile, which inactivates Rho, Rac and Cdc42, decreased in vitro migration. When HPC pretreated with LT or toxin,B were transplanted into mice, homing to the bone marrow was impaired, whereas C2I-C3 treatment did not alter HPC homing. However, in a competitive hematopoietic repopulation experiment in C57BL/6 mice, pretreatment of bone marrow cells with any of the inhibitors, including the Rho inhibitor C2I-C3, resulted in suppressed donor-type hematopoiesis. Our data indicate that whereas Rac supports HPC cell cycling, migration, short-term homing and hematopoietic regeneration, Rho coordinates down-regulation of HPC migration and is required for hematopoietic regeneration. [source]

ME3738 protects from concanavalin,A-induced liver failure via an IL-6-dependent mechanism

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 8 2003
Christian Klein
Abstract ME3738 is a new compound that attenuates liver disease in several models of acute and chronic liver inflammation. We used the concanavalin,A (Con,A) model to elucidate the molecular mechanismsof ME3738 to block liver cell damage. Pretreatment of BALB/c mice with ME3738 prior to Con,A injection resulted in a significant reduction in liver injury. The protective effect of ME3738 prior to Con,A injection was associated with a reduction in IL-6 serum levels and NF-,B DNA binding in liver nuclear extracts. However, STAT3 DNA binding was induced via ME3738 prior to Con,A injection. Further analysis showed that ME3738 induces IL-6 serum levels and activates STAT3 DNA binding and target gene transcription. The relevance of this finding was assessed in IL-6,/, mice. Inthese animals, ME3738 induced no increase in IL-6 serum expression, and activation of IL-6-dependent pathways was not found. In addition, ME3738 did not protect IL-6,/, animals from Con,A-induced liver failure, while IL-6 injection was still effective. Therefore, we demonstrate that ME3738 triggers IL-6 expression, which activates pathways that are relevant to protect from Con,A-induced liver failure. [source]

Optimization of activated carbon-based decontamination of fish oil by response surface methodology

EUROPEAN JOURNAL OF LIPID SCIENCE AND TECHNOLOGY, Issue 7 2007
Åge Oterhals
Abstract The effect of activated carbon (AC) adsorption on the reduction of persistent organic pollutants (POP) in fish oil was studied based on response surface methodology at a 5-g/kg AC inclusion level. Pretreatment of the oil by alkali refining and bleaching increased the POP levels. The tested process variables (contact time and temperature) affected the AC adsorption rate and significant first- and second-order response models could be established. Polychlorinated dibenzo- p -dioxins and dibenzofurans (PCDD/F) showed a very rapid adsorption behavior and the concentration and toxic equivalent (TEQ) level could be reduced by 99%. Adsorption of dioxin-like polychlorinated biphenyls (DL-PCB) was less effective and depended on ortho substitution, i.e. non- ortho PCB were adsorbed more effectively than mono- ortho PCB with a maximum of 87 and 21% reduction, respectively, corresponding to a DL-PCB-TEQ reduction of 73%. A common optimum for both PCDD/F and DL-PCB adsorption could not be identified. AC treatment had no effect on the level of polybrominated diphenyl ether flame retardants. The differences in adsorption patterns may be explained based on molecular conformation. No change in oil quality could be observed based on oxidation parameters. Compliance with present PCDD/F and DL-PCB legislation levels in fish oil can be achieved based on AC adsorption. [source]

Oxidative stress on EAAC1 is involved in MPTP-induced glutathione depletion and motor dysfunction

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2008
Koji Aoyama
Abstract Excitatory amino acid carrier 1 (EAAC1) is a glutamate transporter expressed on mature neurons in the CNS, and is the primary route for uptake of the neuronal cysteine needed to produce glutathione (GSH). Parkinson's disease (PD) is a neurodegenerative disorder pathogenically related to oxidative stress and shows GSH depletion in the substantia nigra (SN). Herein, we report that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice, an experimental model of PD, showed reduced motor activity, reduced GSH contents, EAAC1 translocation to the membrane and increased levels of nitrated EAAC1. These changes were reversed by pre-administration of n-acetylcysteine (NAC), a membrane-permeable cysteine precursor. Pretreatment with 7-nitroindazole, a specific neuronal nitric oxide synthase inhibitor, also prevented both GSH depletion and nitrotyrosine formation induced by MPTP. Pretreatment with hydrogen peroxide, l -aspartic acid ,-hydroxamate or 1-methyl-4-phenylpyridinium reduced the subsequent cysteine increase in midbrain slice cultures. Studies with chloromethylfluorescein diacetate, a GSH marker, demonstrated dopaminergic neurons in the SN to have increased GSH levels after NAC treatment. These findings suggest that oxidative stress induced by MPTP may reduce neuronal cysteine uptake, via EAAC1 dysfunction, leading to impaired GSH synthesis, and that NAC would exert a protective effect against MPTP neurotoxicity by maintaining GSH levels in dopaminergic neurons. [source]

IP3 receptor in the hair cells of frog semicircular canal and its possible functional role

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2006
Maria Lisa Rossi
Abstract The presence and functional role of inositol trisphosphate receptors (IP3R) was investigated by electrophysiology and immunohistochemistry in hair cells from the frog semicircular canal. Intracellular recordings were performed from single fibres of the posterior canal in the isolated, intact frog labyrinth, at rest and during rotation, in the presence of IP3 receptor inhibitors and drugs known to produce Ca2+ release from the internal stores or to increase IP3 production. Hair cell immunolabelling for IP3 receptor was performed by standard procedures. The drug 2-aminoethoxydiphenyl borate (2APB), an IP3 receptor inhibitor, produced a marked decrease of mEPSP and spike frequency at low concentration (0.1 mm), without affecting mEPSP size or time course. At high concentration (1 mm), 2APB is reported to block the sarcoplasmic-endoplasmic reticulum Ca2+ -ATPase (SERCA pump) and increase [Ca2+]i; at the labyrinthine cytoneural junction, it greatly enhanced the resting and mechanically evoked sensory discharge frequency. The selective agonist of group I metabotropic glutamate receptors (RS)-3,5-dihydroxyphenylglycine (DHPG, 0.6 mm), produced a transient increase in resting mEPSP and spike frequency at the cytoneural junction, with no effects on mEPSP shape or amplitude. Pretreatment with cyclopiazonic acid (CPA, 0.1 mm), a SERCA pump inhibitor, prevented the facilitatory effect of both 2APB and DHPG, suggesting a link between Ca2+ release from intracellular stores and quantal emission. Consistently, diffuse immunoreactivity for IP3 receptors was observed in posterior canal hair cells. Our results indicate the presence and a possibly relevant functional role of IP3-sensitive stores in controlling [Ca2+]i and modulating the vestibular discharge. [source]

Enhancement of learning behaviour by a potent nitric oxide-guanylate cyclase activator YC-1

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2005
Wei-Lin Chien
Abstract Memory is one of the most fundamental mental processes, and various approaches have been used to understand the mechanisms underlying this process. Nitric oxide (NO), cGMP and protein kinase G (PKG) are involved in the modulation of synaptic plasticity in various brain regions. YC-1, which is a benzylindazole derivative, greatly potentiated the response of soluble guanylate cyclase to NO (up to several hundreds fold). We have previously shown that YC-1 markedly enhances long-term potentiation in hippocampal and amygdala slices via NO-cGMP-PKG-dependent pathway. We here further investigated whether YC-1 promotes learning behaviour in Morris water maze and avoidance tests. It was found that YC-1 shortened the escape latency in the task of water maze, increased and decreased the retention scores in passive and active avoidance task, respectively. Administration of YC-1 30 min after foot-shock stimulation did not significantly affect retention scores in response to passive avoidance test. Administration of scopolamine, a muscarinic antagonist, markedly impaired the memory acquisition. Pretreatment of YC-1 inhibited the scopolamine-induced learning deficit. The enhancement of learning behaviour by YC-1 was antagonized by intracerebroventricular injection of NOS inhibitor L-NAME and PKG inhibitors of KT5823 and Rp-8-Br-PET-cGMPS, indicating that NO-cGMP-PKG pathway is also involved in the learning enhancement action of YC-1. YC-1 is thus a good drug candidate for the improvement of learning and memory. [source]

c-Src kinase activation regulates preprotachykinin gene expression and substance P secretion in rat sensory ganglia

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2003
Orisa J. Igwe
Abstract Increased synthesis of substance P (SP) in the dorsal root ganglia (DRG) and enhanced axonal transport to and secretion from the primary afferent sensory neurons might enhance pain signalling in the spinal dorsal horn by modifying pronociceptive pathways. IL-1, increases SP synthesis by enhancing the expression of preprotachykinin (PPT) mRNA encoding for SP and other tachykinins in the DRG. Stimulation of IL-1 receptor by IL-1, may induce the phosphorylation of tyrosine residues in many effector proteins through the activation of p60c-src kinase. The hypothesis that the synthesis of SP in and secretion from the primary sensory ganglia are regulated by the activation of p60c-src kinase induced by IL-1, was tested. Pretreatment of DRG neurons in culture with herbimycin A, genistein or PP2, three structurally different nonreceptor tyrosine kinase inhibitors that act by different mechanisms, decreased the kinase activity of p60c-src induced by the activation of IL-1 receptor. PP3, a negative control for the Src family of tyrosine kinase inhibitor PP2 had no effect. Herbimycin A and genistein also decreased IL-1,-induced expression of PPT mRNA-encoding transcripts and the levels of SP-li synthesized in the cells and secreted into the culture medium in a concentration-dependent manner. SB 203580 [a p38 mitogen-activated protein kinase (p38 MAPK) inhibitor] and PD 98059 (a p44/42 MAPK kinase inhibitor) were ineffective in modulating IL-1,-induced SP synthesis and secretion, and p60c-src kinase activity in DRG neurons. Whereas, IL-1 receptor antagonist and cycloheximide inhibited IL-1,-evoked secretion of SP-like immunoreactivity (SP-li), actinomycin D decreased it significantly but did not entirely abolish it. These findings show that phosphorylation of specific protein tyrosine residue(s) following IL-1 receptor activation might play a key role in IL-1, signalling to modulate PPT gene expression and SP secretion in sensory neurons. In view of the role of SP as an immunomodulator, these studies provide a new insight into neural-immune intercommunication in pain regulation in the sensory ganglia through the IL-1,-induced p60c-src activation. [source]

Conditional involvement of striatal serotonin3 receptors in the control of in vivo dopamine outflow in the rat striatum

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2003
Grégory Porras
Abstract Serotonin3 (5-HT3) receptors can affect motor control through an interaction with the nigrostriatal dopamine (DA) neurons, but the neurochemical basis for this interaction remains controversial. In this study, using in vivo microdialysis, we assessed the hypothesis that 5-HT3 receptor-dependent control of striatal DA release is conditioned by the degree of DA and/or 5-HT neuron activity and the means of DA release (impulse-dependent vs. impulse-independent). The different DA-releasing effects of morphine (1 and 10 mg/kg), haloperidol (0.01 mg/kg), amphetamine (1 and 2.5 mg/kg), and cocaine (10 and 20 mg/kg) were studied in the striatum of freely moving rats administered selective 5-HT3 antagonists ondansetron (0.1 mg/kg) or MDL 72222 (0.03 mg/kg). Neither of the 5-HT3 antagonists modified basal DA release by itself. Pretreatment with ondansetron or MDL 72222 reduced the increase in striatal DA release induced by 10 mg/kg morphine but not by 1 mg/kg morphine, haloperidol, amphetamine or cocaine. The effect of 10 mg/kg morphine was also prevented by intrastriatal ondansetron (1 µm) administration. Reverse dialysis with ondansetron also reduced the increase in DA release induced by the combination of haloperidol and the 5-HT reuptake inhibitor citalopram (1 mg/kg). Considering the different DA and 5-HT-releasing properties of the drugs used, our results demonstrate that striatal 5-HT3 receptors control selectively the depolarization-dependent exocytosis of DA only when central DA and 5-HT tones are increased concomitantly. [source]

Noxious heat-induced CGRP release from rat sciatic nerve axons in vitro

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2001
S. K. Sauer
Abstract Noxious heat may act as an endogenous activator of the ionotropic capsaicin receptor (VR1) and of its recently found homologue VRL1, expressed in rat dorsal root ganglion cells and present along their nerve fibres. We have previously reported that capsaicin induces receptor-mediated and Ca++ -dependent calcitonin gene-related peptide (CGRP) release from axons of the isolated rat sciatic nerve. Here we extended the investigation to noxious heat stimulation and the transduction mechanisms involved. Heat stimulation augmented the CGRP release from desheathed sciatic nerves in a log,linear manner with a Q10 of ,,15 and a threshold between 40 and 42 °C. The increases were 1.75-fold at 42 °C, 3.8-fold at 45 °C and 29.1-fold at 52 °C; in Ca++ -free solution these heat responses were abolished or reduced by 71 and 92%, respectively. Capsazepine (10 µm) and Ruthenium Red (1 µm) used as capsaicin receptor/channel antagonists did not significantly inhibit the heat-induced release. Pretreatment of the nerves with capsaicin (100 µm for 30 min) caused complete desensitization to 1 µm capsaicin, but a significant heat response remained, indicating that heat sensitivity is not restricted to capsaicin-sensitive fibres. The sciatic nerve axons responded to heat, potassium and capsaicin stimulation with a Ca++ -dependent CGRP release. Blockade of the capsaicin receptor/channels had little effect on the heat-induced neuropeptide release. We conclude therefore that other heat-activated ion channels than VR1 and VRL1 in capsaicin-sensitive and -insensitive nerve fibres may cause excitation, axonal Ca++ influx and subsequent CGRP release. [source]

Differential roles of corticotropin-releasing factor receptor subtypes 1 and 2 in opiate withdrawal and in relapse to opiate dependence

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2000
Lin Lu
Abstract The possible effects on the morphine withdrawal signs of the nonspecific corticotropin-releasing factor (CRF) receptor antagonist ,-helical CRF, the selective CRF receptor subtype 1 antagonist CP-154,526 and the selective CRF receptor subtype 2 antagonist antisauvagine-30 (AS-30) were investigated in rats. The most withdrawal signs, including jumping, teeth chatter, writhing, shakes, lacrimation, piloerection, irritability and diarrhoea, were attenuated by pretreatment with ,-helical CRF (10 µg i.c.v.) and CP-154,526 (30 mg/kg i.p.). However, no morphine withdrawal signs except for diarrhea were significantly affected by pretreatment with AS-30 (10 µg, i.c.v.). To investigate the possible role of different CRFR antagonists (,-helical CRF, CP-154,526 and AS-30) in relapse to opiate dependence, the 28-day extinction of morphine-conditioned place preference (CPP) was used. The morphine-CPP disappeared following a 28-day extinction and then was reactivated by a single injection of 10 mg/kg morphine. Pretreatment with ,-helical CRF (10 µg, i.c.v.) and CP-154,526 (30 mg/kg, i.p.) could significantly block this reactivation of morphine-CPP. In contrast, pretreatment with AS-30 (1 or 10 µg i.c.v.) did not affect this reactivation of morphine-CPP. The present study demonstrated that activation of the CRF receptor is involved in morphine withdrawal signs and relapse to morphine dependence, and that the role of CRF receptor subtypes 1 and 2 in withdrawal and reactivation of morphine dependence is not identical. CRF receptor subtype 1, but not subtype 2, is largely responsible for the action of the CRF system on opiate dependence. These results suggest that the CRF receptor antagonists, particularly the CRF receptor subtype 1 antagonist, might be of some value in the treatment and prevention of drug dependence. [source]

N-methyl- d -aspartate enhancement of the glycine response in the rat sacral dorsal commissural neurons

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2000
Tian-.
Abstract The effect of N-methyl- d -aspartate (NMDA) on the glycine (Gly) response was examined in neurons acutely dissociated from the rat sacral dorsal commissural nucleus (SDCN) using the nystatin-perforated patch-recording configuration under voltage-clamp conditions. The application of 100 ,m NMDA to SDCN neurons reversibly potentiated Gly-activated Cl, currents (IGly) without affecting the Gly binding affinity and the reversal potential of IGly. A selective NMDA receptor antagonist, APV (100 ,m), blocked the NMDA-induced potentiation of IGly, whereas 50 ,m CNQX, a non-NMDA receptor antagonist, did not. The potentiation effect was reduced when NMDA was applied in a Ca2+ -free extracellular solution or in the presence of BAPTA AM, and was independent of the activation of voltage-dependent Ca2+ channels. Pretreatment with KN-62, a selective Ca2+,calmodulin-dependent protein kinase II (CaMKII) inhibitor, abolished the NMDA action. Inhibition of calcineurin (CaN) further enhanced the NMDA-induced potentiation of IGly. In addition, the GABAA receptor-mediated currents were suppressed by NMDA receptor activation in the SDCN neurons. The present results show that Ca2+ entry through NMDA receptors modulates the Gly receptor function via coactivation of CaMKII and CaN in the rat SDCN neurons. This interaction may represent one of the important regulatory mechanisms of spinal nociception. The results also suggest that GABAA and Gly receptors may be subject to different intracellular modulatory pathways. [source]

Flexural strength of glass fibre-reinforced posts bonded to dual-cure composite resin cements

EUROPEAN JOURNAL OF ORAL SCIENCES, Issue 2 2010
Peter Davis
Davis P, Melo LSD, Foxton RM, Sherriff M, Pilecki P, Mannocci F, Watson TF. Flexural strength of glass fibre-reinforced posts bonded to dual-cure composite resin cements. Eur J Oral Sci 2010; 118: 197,201. © 2010 The Authors. Journal compilation © 2010 Eur J Oral Sci The aims of this study were to evaluate the flexural strength of two different types of glass fibre-reinforced posts bonded to dual-cure composite resin cements. Forty glass methacrylate-based fibre posts (GC Fiber Post) and 20 glass fibre inter-polymerizing network posts (everStick POST) were divided into three groups. Group 1 contained 20 GC posts that were bonded to a dual-cure composite cement (UnifilCore). Group 2 contained 20 Stick Tech posts that had adhesive applied (Scotchbond Multipurpose resin) and were bonded to a dual-cure composite resin cement (RelyX Unicem). Group 3 contained 20 GC posts that were pretreated with a silane-coupling agent before being treated with resin and composite, as in group 1. A 4-point bend test was carried out to failure on all of the groups. Failure modes were determined using scanning electron microscopy. Pretreatment of the post surface with the silane-coupling agent did not increase the flexural strength. The flexural strength of the Stick Tech post was significantly lower than the flexural strength of the GC post. The mode of failure for the GC Posts was adhesive, whereas the Stick Tech posts failed cohesively. Different flexural strengths and failure modes were observed among the two fibre post,resin systems. [source]