At low pulsing frequency, there are few such frequencies. At high pulsing frequency, there are many more such slowly relaxing terms present. It is these slowly relaxing terms that give rise to the characteristic increase in signal observed in a CPMG experiment. PARP inhibitor An expression for the effective transverse relaxation rate of the ground state ensemble is sought: equation(1) R2,eff=-1TrellnIG(Trel)IG(0)where Trel   is the total time of the concatenated CPMG elements and IG   specifies the signal intensity from the observed ground state at the specified times. In order to calculate the relevant signal intensities a

kinetic model for the exchange process and types of magnetisation present need to be specified. The simplest and most widely encountered kinetic scheme is the two-site case for in-phase magnetisation. Here, a ground state and an excited state undergo the conformational rearrangement G⇄kEGkGEE. In this scheme, the exchange rate kEX   = kEG   + kGE   and the fractional populations of the excited (PE  ) and ground (PG  ) states are given by kGE  /kEX   and kEG  /kEX   respectively. The CPMG experiment consists of a number of free precession elements interspersed with 180° pulses. To evaluate Cyclopamine their combined effect, how magnetisation evolves in the absence of pulses needs first

to be calculated. This is accomplished most conveniently using the shift basis (I  + = Ix   + iIy   and I  −   = Ix   − iIy  ) using a modified Bloch–McConnell equation [33]: equation(2) ddtIG+IE+=R+IG+IE+where E   and G   denote the magnetisation on the excited and ground states, respectively. The evolution matrix is: equation(3) R+=-kGE-R2GkEGkGE-kEG-R2E-iΔωR  2G   and R  2E   specify the intrinsic RG7420 relaxation of the ground and excited states respectively, and Δω   is the chemical shift difference between the ground and excited states in rad s−1. The solution for Eq. (2) is: equation(4) I(t)=eR+tI(0)=OI(0)I(t)=eR+tI(0)=OI(0)where I  (0) are I  (t  ) specify the magnetisation on the ground and excited states at time zero and t   respectively. Initially the system

is in equilibrium, and so I(0)†=(PG,PE)I(0)†=(PG,PE) where †† indicates a transpose. The derivation of I(t) first requires the well known matrix O (Eq. (17)) that determines how magnetisation evolves during free precession [2]. In the shift basis, the effect of a 180° on-resonance ideal pulse switches magnetisation on I+ terms to I−, leading magnetisation to evolve according to the complex conjugate of R+ (Eq. (3)), (R+)*. Following a 180° pulse therefore, magnetisation will evolve according to the matrix O*. By applying Eq. (4) iteratively, taking the complex conjugate where appropriate, an expression that represents the entire CPMG experiment can be built. This, when used with Eq. (1) enables us to derive an expression for R2,eff. The matrix M that represents the CPMG experiment will enable us to evaluate I(t) = MI(0).

Not only suspicious areas for microscopic disease can be boosted but also critical normal structures such as bowel, nerves, and ureters can be protected from unnecessary radiation. The DP expands the limitation of the retangular HAM applicator and makes it possible http://www.selleckchem.com/Androgen-Receptor.html to create more geometrically complex treatment areas. However, this entails the use of a template to delineate the target

area as well as more complex treatment planning, which could potentially result in a slightly lengthened procedure; thus, one should carefully identify the ideal candidate to use this nonuniform HDR-IORT technique. Finally, another drawback of this more complicated approach is that there is a greater potential for error regarding directionality of the HAM because it was no longer a uniform dose distribution. Although other centers have advocated IOERT [2], [9] and [10], this technique Selleckchem Erlotinib is not always feasible in certain sites owing to anatomic limitations [3] and [8]. Moreover, IOERT does not allow “DP” in the same manner achieved

by HDR-IORT using the HAM applicator. Harrison et al. (4) initially described our results using the HAM applicator to deliver HDR-IORT in 1995. In our experience, this flexible applicator is more advantageous because it can be molded to the tumor bed and allows more conformal treatment on curved surfaces. Moreover, the technique is relatively simple and the time to position the applicator is low. Lead shields and wet lap pads are often used to protect and displace normal organs from the target area to reduce the dose to the radiosensitive organs and structures in the pelvis. Nevertheless, complications such as ureteral stenosis, bowel obstruction, and neuropathy have been previously reported (11); thus lead shields and lap pads may not be sufficient to

protect adjacent highly radiosensitive structures, and the use of the HAM applicator for dose de-escalation should be encouraged to avoid Methocarbamol high doses to areas at higher risk of complication. The potential for severe late complications related to a single high dose remains a concern [8] and [12] because the classic principles of radiobiology, sublethal damage repair, reoxygenation of hypoxic cells, and redistribution of cells in the cell cycle are not exploited. Haddock et al. (2) reported in reirradiated patients with colorectal cancer using IOERT that doses exceeding 12.5 Gy in a single fraction were associated with increased incidence and severity of neuropathy. Other common IOERT-related complications included wound infection, gastrointestinal tract fistula, and ureteral obstruction.

Apart from radioactivity, there are chemicals, which were spread all over the region,

that should be measured in the coastal and terrestrial locations of tsunami hit areas. For example, the tsunami caused by the Great Eastern Japan Earthquake inundated a total area of approximately 470 km2 in Japan. The earthquake and the tsunami caused destruction or damage of 125,000 buildings, heavy damage to roads and railways. During these incidents many electrical generators were taken down. The waves swept away thousands of cars and other vehicles and flooded various buildings as they traveled inland. Some small towns in the tsunami hit areas were destroyed entirely, thus carrying away a variety of materials http://www.selleckchem.com/products/dabrafenib-gsk2118436.html Omipalisib nmr with them

and scattered them all over the tsunami hit areas. The degree and extent of damage was enormous and the worst affected coastal towns were left as only piles of rubble, with almost no parts of any structure left standing. Even some of the anti-tsunami seawalls collapsed. To date, there are trillions of pieces of composite rubble, comprising more than 25 million tons, are laying in the tsunami hit areas, waiting to be disposed of by the agencies involved in this job. The complexity of the waste to be disposed may pose a serious threat of environmental pollution, which should also be monitored along with the effects of nuclear disaster. Northern Japan, where the tsunami hit, has a cold

climate and almost all the buildings were built with wood and 3-oxoacyl-(acyl-carrier-protein) reductase cement and were invariably packed with variety of heat insulating materials containing flame retardants to keep the houses warm and also to prevent accidental fire. All these materials are now being inundated by seawater containing halide ions. All these wood and allied material are now soaked by seawater and even after drying they will contain enough chlorine and bromine to form chlorinated and brominated dioxins and related chemicals, if they are burnt under low temperature conditions. Along with these, large quantities of BFRs (brominated flame retardants) and other POPs chemicals like PCBs will also be released during such burning of waste. Such an enormous quantity of burnable material, if they can be segregated at all, cannot be handled by the high quality incinerator facilities, and this may lead to low temperature burning. The agencies involved in the disposal of these materials are now considering various means for doing this, but if this takes a long time, the public have to resort to open burning of the rubble around their destroyed houses, in small heaps. On the other hand, if these wastes can be land-filled at all, again there will be long lasting contamination of nearby aquatic and terrestrial environments, by leaching and land runoff of complex chemical mixtures.

3. The Rhetorical Structure Theory [25] and [26] framework provides a well defined way of expressing discourse-level rhetorical relationships between utterances. The textual realisation IWR-1 of RST relations is not domain-specific, therefore the specific generation rules can be applied equally for the generation of medical summaries as well as any other type of English text. The RST framework is particularly suited to our specific application since the relations between chronicle events map naturally to RST schemas

(e.g., we express facts such as inference (an event led to another) or causality (an event causes another)). Saying it: Starting from a plan distributing the content among paragraphs and sentences, with some linking phrases and formatting already specified, a template-based grammar generates the surface forms of the sentences, producing as output a complete specification of the text. In our example, a template would map the domain-specific relationship inferences(biopsy, cancer) The text generation system uses two types selleck products of grammar rules for realising the summaries. Firstly,

a large standard generative grammar for English phrases and sentences, which consists of generic rules such as: definite noun phrases = [definite article] + [determiner] + [noun] (for phrases) or causal relation = main clause + causal connector + subordinate clause (for sentences). This helps generating constructs such as “the clinical diagnosis” or “the patient underwent chemotherapy because of the cancer”. These rules are static and independent of any new information available to the generation system, therefore no effort is involved

in Aprepitant enhancing the rules when new data becomes available to the system. The second set of generation rules are specific to the medical domain and more restricted in size. They govern the way the system expresses connections between words in the vocabulary, for example, the fact that the correct way of expressing an event of type surgical procedure is “the patient underwent surgery”. These rules are partially static in that they do not require re-writing or enhancing if we see new, unknown words which belong to a category known by the system (e.g., the fact that “mastectomy” is a brand new word of type surgical procedure doesn’t require rewriting the rules for surgical procedure. However, if the type of events in the Chronicle changes (e.g., if the system were to be applied to a new, non-medical, domain), we would need to manually create generation rules for each new type of event. Can these automatically generated summaries perform a useful role in the clinical setting? We explored this question through a formal study with twenty-one clinicians at a teaching hospital.

After 4 weeks of observation, a second cohort was assigned randomly to group 3 (BMS-791325 150 mg twice Natural Product Library daily for 24 weeks) or group 4 (BMS-791325 150 mg twice daily for 12 weeks). Patients were stratified by genotype 1a/1b, with 1b patient enrollment targeted between 25% and 38% or less of the total number of patients

in each group. The primary end point was an HCV-RNA level less than 25 IU/mL at SVR12. Other end points included analysis of HCV RNA at various time points during and after treatment, rates of viral breakthrough and relapse, and assessment of safety and tolerability. In the event of viral breakthrough (defined as confirmed increase in HCV-RNA level >1 log10 from nadir or confirmed HCV RNA level >25 IU/mL on or after week 8), patients were eligible to receive treatment intensification, defined as peginterferon alfa-2a (180 μg subcutaneously, once weekly) and ribavirin (1000 mg orally per day if patient weighed <75 kg, or 1200 mg orally per day if patient weighed >75 kg) in addition to continuation of the direct-acting antivirals for up to an additional 48 weeks. Blood samples were drawn at baseline, days 1-7, days 9, 11, 14, 21, 28, every week through week 8, then every 2 weeks until the end of

treatment, and post-treatment weeks 4, 12, 24, 36, and 48. HCV-RNA level was determined at a central laboratory using the COBAS TaqMan v2 assay (Roche Molecular Diagnostics, Pleasanton, CA), with a lower limit of quantitation AZD9291 ic50 of 25 IU/mL and a lower limit of detection of approximately 10 IU/mL. HCV genotypes were determined by polymerase chain reaction amplification and sequencing using the VERSANT HCV Amplification 2.0 Kit (LiPA) (Siemens, Munich, Germany). Tolmetin The host interleukin

(IL)28B genotype (rs12979860 single-nucleotide polymorphism) was determined by Monogram Biosciences (South San Francisco, CA) using a real-time polymerase chain reaction assay. All baseline samples were analyzed for polymorphisms in HCV NS3, NS5A, and NS5B associated with drug resistance using population sequencing (sensitivity, ≈20%). Safety and tolerability were measured by serious adverse events, treatment-emergent adverse events, discontinuations owing to adverse events, severity grade 3/4 adverse events, and severity grade 3/4 laboratory abnormalities. Vital sign and electrocardiographic measurements, physical examinations, and clinical laboratory results were assessed throughout the study. Binary antiviral activity end points were assessed using modified intent-to-treat methodology. Patients prescribed a different treatment as assigned for the whole treatment duration were analyzed based on actual treatment (as treated).

Via PubMed 5 reviews and 159 RCTs, via Embase 21 reviews and 202 RCTs, via Cinahl 344 reviews/RCTs, and via Pedro 7 reviews and 28 RCTs were found. Finally, no (Cochrane) reviews and 17 additional RCTs (14 via PubMed, 3 via Embase, 0 via Cinahl or Pedro) were included: 16 studied ESWT (10 for calcific and 6 for non-calcific tendinosis) and one studied Radial ShockWave Therapy (RSWT) for calicific tendinosis. RSWT is pneumatically generated with low- or medium-energy shockwaves (Cacchio et al., 2006) PCI 32765 and therefore should have a lower peak-pressure and longer rise-time than ESWT. Further, the focal

point is centred on the tip of the applicator instead of on the target zone, as is done in ESWT. Therefore, it is supposed to be less painful, of less risk and should target the calcification more effectively (Haake et al., 2002). The characteristics of the studies are described in Appendix II. Of the 17 RCTs, 10 were classified as high-quality selleck chemical and 7 as low-quality (Table 2) by using the list of Furlan et al. (2009) The most prevalent methodological flaws were ‘care giver’ (i.e. the one who provides the intervention) not blinded’ (65%), and ‘no intention-to-treat analysis’ (35%). Table 3 and Table 4 show the evidence for effectiveness we found in this study. A high-quality study (Gerdesmeyer

et al., 2003) (n = 96) compared high-ESWT (EFD: 0.32 mJ/mm2) to placebo for calcific supraspinatus tendinosis. At 3, 6, and 12 months follow-up, there were significant between-group differences in favour of the treatment group on pain, the total Constant Score, and on calcific deposit size (mm2). See Appendix II for the exact data. A low-quality study (Hsu et al., 2008) (n = 46) compared high-ESWT BCKDHA (EFD: 0.55 mJ/mm2) to placebo for calcifying shoulder tendinosis. The treatment group showed significant decrease on pain and the Constant score compared to the sham group at 3, 6 and 12 months follow-up. The calcium deposit width

reduction was bigger in the treatment group at 12 months, although no statistical comparisons were made between the groups. In conclusion, there is moderate evidence for effectiveness of ESWT compared with placebo in the short-, mid- and long-term. A low-quality RCT (Loew et al., 1999) (n = 80) studied high-ESWT-1-session versus high-ESWT-2-sessions versus no treatment for calcific shoulder tendinosis. There were no baseline differences on the Constant score; at 3 months follow-up significant higher Constant scores for the ESWT groups (63.7 (14.6) (mean (SD)) (high-ESWT-1-session), 68.5 (13.1) (high-ESWT-2-sessions), 47.8 (11.4) (no treatment)) was found. There is limited evidence for the effectiveness of high-ESWT (1 session and 2 sessions) compared to no treatment in the short-term. One low-quality RCT (Loew et al., 1999) studied effectiveness of high-ESWT-1-session versus high-ESWT-2-sessions.

377, p = 0.0136). Proteases inhibitor Lipoperoxidation

increased only at 25,000 IU/kg/day (F[3,24] = 3.517, p = 0.0304) and protein carbonylation increased at 12,500 and 25,000 IU/kg/day (F[3,24] = 5.508, p = 0.0050). Striatum of offsprings from retinyl palmitate treated dams showed significant alterations on the redox parameters analyzed (Table 4). CAT activity decreased in treated males at 12,500 and 25,000 IU/kg/day (according to two-way ANOVA the exposure to retinyl palmitate affect the result, F[3,48] = 6.171, p = 0.0012), but SOD activity did not change in both sexes at all doses. SOD/CAT ratio increased only in males at 25,000 IU/kg/day (F[3,48] = 2.934, p = 0.0427) and GST activity increased in treated males at 2500 and 25,000 IU/kg/day, but increased in females only at 25,000 IU/kg/day (F[3,48] = 11.92, p < 0.0001). TRAP decreased in both sexes at 12,500 and 25,000 IU/kg/day (F[3,48] = 11.24, p = 0.0001). Total reduced thiol content decreased only for males at 25,000 IU/kg/day (F[3,48] = 3.124, p = 0.0344) and lipoperoxidation increased in both sexes at the same dose (F[3,48] = 8.970, p = 0.0001). Protein carbonylation increased in males at 2500 and 25,000 IU/kg/day, but only in females at 25,000 IU/kg/day (F[3,48] = 5.008, p = 0.0039). Hippocampi of offsprings from selleck retinyl palmitate treated

dams showed significant alterations on the redox parameters analyzed (Table 5). CAT activity decreased in both sexes at all retinyl palmitate doses (according to two-way ANOVA the exposure to retinyl palmitate affect the result, F[3,48] = 15.57,

p < 0.0001), but SOD activity did not change at all doses. SOD/CAT ratio increased in males at all retinyl palmitate doses, but only increased in females at 12,500 and 25,000 IU/kg/day (F[3,48] = 11.98, p < 0.0001). GST activity did not change at all doses. TRAP and total reduced thiol content did not change. Lipoperoxidation increased in both sexes at all retinyl palmitate doses (F[3,48] = 16.34, p < 0.0001), but protein carbonylation only increased at 12,500 IU/kg/day in males and 25,000 IU/kg/day in females (F[3,48] = 5.056, p = 0.0040). Vitamin A exerts important roles in both development and Rutecarpine the adult brain, but excessive vitamin A intake may be teratogenic in humans (De Luca, 1991 and Lane and Bailey, 2005; McCaferry et al., 2005). Although the evidence of such effects for retinyl palmitate supplementation in humans is limited, there is a growing concern about the safety of retinyl palmitate supplementation during pregnancy and breastfeeding (Dolk et al., 1999, IVACG, 1998, Miller et al., 1998, Mills et al., 1997 and Ross et al., 2000). In general, human data regarding retinyl palmitate supplementation effects during pregnancy and breastfeeding are mostly in observational and epidemiological studies based in morphological endpoints.

, 2005). According to the LC/NE theory of the P3, these correlations result from a causal relationship: the NE impulse from the LC both causes

the synchronised depolarisation resulting in the scalp P3 as well as facilitating the behavioural response. Therefore, P3 and behaviour correlate on a single-trial level. Nieuwenhuis et al. (2005) propose that, following the decision about stimulus significance (categorisation Sunitinib cell line of the stimulus into a class of items requiring state transitions in light of the current strategy), an LC release of NE facilitates the selection of appropriate responses, regardless of the nature of the response (e.g. movements or memory updating). The P3’s RT-alignment also results from a causal relationship: NE from the LC facilitates state shifts and causes the P3. We thus focus on the LC/NE theory of the P3 here since this account is not only selleck chemicals llc neurobiologically explicit, but also, of the current P3 theories, it is the one that most directly predicts response-alignment. In our view, the previous findings outlined in Section 1.2 are consistent with the P600 as a marker of subjective significance of linguistic material, rather than of structural processing. Here, we put this hypothesis to a critical test by investigating if

the late positivity following structurally deviant linguistic material Pregnenolone shows the RT-alignment typical of the P3, as predicted by the P600-as-LC/NE-P3 hypothesis. RT alignment is neither a necessary nor an obvious feature of theories assuming that the P600 reflects linguistic processing or other aspects of stimulus analysis. Post-hoc additions to such theories could explain RT alignment of the P600. However, as discussed in Section 1.1, the relationship between P3 latency and RT is reliable. A dissociation between P600 latency and RT would falsify critical predictions of the P600-as-P3 hypothesis. Previous research demonstrated RT alignment of the error-related negativity (Debener et al., 2005) and

multiple members of the P3 family (Makeig et al., 2004), and onset alignment of N100/P100 (Jung et al., 2001). Cummings et al. (2006) found that a stimulus-interpretative component, the N400 (Kutas & Federmeier, 2011), is aligned to stimulus onset, not RT, thereby establishing that late, high-level components can be stimulus aligned. Previous sentence processing experiments lack the required information for investigating RT alignment of components. Either no overt task was used, or the task was delayed relative to the critical stimulus. We are not aware of previous electrophysiological sentence processing studies in which participants judged linguistic deviancy as soon as they detected the error, allowing for a correlation of RT and P600 latency. The present study aimed to fill this gap.

37v software. It was assumed that the darkest

gray received the highest encapsulation rate (total black). The background gray value was subtracted to correct the gray values of the implants. The colony was included see more as a random factor and treatments were analyzed by an ANOVA followed by an Unequal N HSD test at 5% probability. In this experiment, we used a fourth colony (colony D) to test the effects of removing bacteria on worker immunity. To kill the bacteria, we followed the methodology described by Poulsen et al. (2003a). We established six experimental treatments using workers with bacteria covering the whole body: (1) 22 without treatment, (2) 20 treated with a dry brush to remove their bacterial cover, (3) 20 treated with a wet (water only) brush, (4) 20 treated with a brush containing

a solution of penicillin G (622 mg/L), (5) 20 with a brush containing a solution of streptomycin sulfate (1230 mg/L) and (6) 20 treated with a brush containing a mixture of the two antibiotics. Ant workers were all about the same size (∼2.4 mm HW) and the brushing operation lasted approximately 10 s. Afterwards, all ants were marked with a dot of paint and placed in mini-colonies established in plastic pots containing 100 mL of fungus GKT137831 purchase garden and approximately 100 nestmate workers without visible bacteria coating. Ten days later, the marked workers were removed for an encapsulation assay, as described in Section 2.2. We verified that these marked workers did not show a visible white coating of bacteria in the integument, confirming that the treatments were effective. The groups

were compared by an ANOVA followed by an Unequal N HSD test at 5% probability. The aim of this study was to assess the metabolic rate and to infer ioxilan a possible energetic cost of maintaining ectosymbiotic bacteria. The production of carbon dioxide was measured in a carbon dioxide analyzer (TR 2; Sable System International, Las Vegas, Nevada, USA) using methods adapted from Hebling et al. (2000) and Guedes et al. (2006). A series of 25 mL flasks was used, each flask containing three workers (2.4 mm head capsule width) from each group (EXT, INB, and INØ) in a completely closed system. Carbon dioxide-free air was injected into the flasks for 2 min at 600 mL/min. An infrared reader was connected to the outlet of the system to quantify carbon dioxide (μmol). The test tubes were connected to the system for three hours before measurement of CO2 production from the workers, which was achieved by injection of CO2-free air into the vials for 2 min at a flow rate of 600 mL/min. This air flow directs CO2 to an infrared reader connected to the system and allows rapid quantification of the amount of CO2 produced on an hourly basis (in μmol). There were 14 replicates for each group, which were taken at the same proportion from three colonies (A, B, and C). In total, we took 42 workers from each colony.

Serial sections were equilibrated under identical conditions for 30 min at 37 °C in Krebs–HEPES buffer (in mM: 130 NaCl, 5.6 KCl, 2 CaCl2, 0.24 MgCl2, 8.3 HEPES, and 11 glucose, pH = 7.4). Fresh buffer containing DHE (2 μM) was applied topically to each tissue section, covered with a cover slip, incubated for 30 min in a light-protected humidified chamber at 37 °C, and then viewed with a inverted fluorescence microscope (NIKON Eclipse Ti-S, x40 objective) using the same imaging settings in the untreated and lead-treated rats. Fluorescence

was detected with a 568-nm long-pass filter. For quantification, eight frozen tissue segments per animal were sampled for each experimental condition and averaged. The mean fluorescence densities in the target region were calculated. All values are expressed as the mean ± standard error of the mean (SEM). Contractile responses to phenylephrine were expressed as a percentage of the Trichostatin A purchase Ganetespib maximal response induced by 75 mM KCl. Vasodilator responses to ACh or SNP were expressed as the percentage of relaxation of the previous contraction. For each concentration–response curve, the maximal effect (Rmax) and the concentration of agonist that produced 50% of the maximal response (log EC50) were calculated using non-linear regression analysis (GraphPad Prism,

GraphPad Software, Inc., San Diego, CA). The sensitivities of the agonists were expressed as pD2 (− log EC50). To compare the effects of L-NAME, TEA, 4-AP, IbTX, ChTX and apamin on the relaxation responses to ACh, some results were expressed as the differences in the area under the concentration–response curves (dAUC) for the control and experimental groups. These values indicate whether the magnitude of the effect of L-NAME, TEA, 4-AP, IbTX, ChTX and apamin is different in the untreated or lead-treated rats. The results were expressed as the mean ± SEM of the number of rats indicated (n). The differences were analyzed using Student’s t-test or two-way ANOVA followed by a Bonferroni test. P < 0.05 was considered to be significant. Lead acetate, l-phenylephrine hydrochloride,

ACh chloride, SNP, sodium pentobarbital, apocynin, SOD, catalase, OUA, L-NAME, TEA, 4-AP, IbTX, CbTX and apamin were purchased from Sigma-Aldrich (St. Louis, USA). The salts and reagents used were of analytical grade from Sigma-Aldrich and Merck (Darmstadt, Germany). Lead exposure unless did not affect the response to KCl (untreated E+: 3.46 ± 0.04 g, n = 38; lead-treated E+: 3.43 ± 0.11 g, n = 40; untreated E−: 3.49 ± 0.03 g, n = 20; lead-treated E−: 3.43 ± 0.09 g, n = 20; P > 0.05). Pre-contraction to phenylephrine used before performing ACh and SNP relaxation curves was similar in the groups (untreated E+: 2.46 ± 0.05 g, n = 10; lead-treated E+: 2.63 ± 0.03 g, n = 10; untreated E−: 2.55 ± 0.11 g, n = 10; lead-treated E−: 2.57 ± 0.04 g, n = 10 P > 0.05). However, this metal reduced vascular reactivity to phenylephrine in the aortic rings (Table 1).