Investigation of (d, 3n) reaction cross section using theoretical nuclear codes calculations on some nuclear materials.

It is important to examine the effects of the nuclear reaction, which is used as a building material in nuclear reactors. Nuclear reactions occur as a result of the interaction between incident particles with the target nuclei. The charged particle-induced reactions have prime importance in understanding the reaction mechanism which can be applicable to understand the particles resulting from the reaction. It is useful to develop shielding the particle accelerators and fusion reactors. The present study contributes to providing the theoretical prediction of excitation functions for 112Cd (d, 3n)111In, 141Pr (d, 3n)140Nd, 167Er (d, 3n)166Tm, 197Au (d, 3n)196Hg and 209Bi (d, 3n)208Po reactions using theoretical model codes such as TALYS-1.95, EMPIRE-3.2.3, and ALICE-2014 within the incident deuteron energy range of threshold energy to 50 MeV. Also, newly developed (d, 3n) cross-section formula (Kavun, 2020) calculations have been performed for these reactions at 20 MeV of deuteron energy. Lastly, all calculated results have been compared with one another and with the previously published experimental data of the EXFOR database.

Measurement of 232Th and 238U neutron capture cross-sections in the energy range 5-17 MeV.

The neutron capture cross sections of 232Th and 238U at the average neutron energies of 5.08 ±â€¯0.17, 8.96 ±â€¯0.77, 12.47 ±â€¯0.83, and 16.63 ±â€¯0.95 MeV have been measured by using the activation technique and off-line γ-ray spectroscopy. The 232Th and 238U were irradiated with neutrons produced from the 7Li(p, n) reaction using the proton energies of 7, 11, 15 and 18.8 MeV from the 14UD BARC-TIFR Pelletron facility in Mumbai, India. Detailed covariance analysis was also performed to evaluate the uncertainties in the measured cross-sections. The excitation function of the 232Th(n, γ) and 238U(n, γ) reactions were calculated using the theoretical model code TALYS-1.9. The experimental and theoretical results from the present work were compared with the ENDF/B-VII-1 and JENDL-4.0 nuclear data libraries and were found to be in good agreement.

Evaluation of Emblica officinalis fruit powder as a growth promoter in commercial broiler chickens.

AIM: The present study was conducted to evaluate the dietary addition of Emblica officinalis (Amla) fruit powder as a growth promoter in commercial broiler chickens. MATERIALS AND METHODS: An experiment was conducted on 135 commercial broiler chicks (Ven-Cobb 400 strain) divided into three groups with three replicates of 15 chicks each. Three treatment groups were as follows - T1: Basal diet as per BIS standards; T2: Basal diet supplemented with 0.4% of E. officinalis fruit powder; and T3: Basal diet supplemented with 0.8% of E. officinalis fruit powder. RESULTS: The average body weights at the end of the 6(th) week were significantly higher (p<0.05) in groups T2 and T3 compared to group T1. Feed intake, feed conversion ratio and feed cost per kg live weight production were similar among the treatment groups. The net profit per bird was the highest in group T2 (Rs. 19.22/bird) followed by group T3 (Rs. 17.86/bird) and the lowest in group T1 (Rs. 14.61/bird). CONCLUSION: Based on the results of the present study, it was concluded that dietary addition of E. officinalis (Amla) fruit powder had a positive effect on growth performance and net profit per bird in commercial broiler chickens.

TNF-α-induces airway hyperresponsiveness to cholinergic stimulation in guinea pig airways.

BACKGROUND AND PURPOSE: TNF-α is an inflammatory cytokine implicated in the pathogenesis of asthma and it causes airway inflammation, bronchoconstriction and airway hyperresponsiveness to a number of spasmogens following inhalation. EXPERIMENTAL APPROACH: We compared contractions of guinea pig isolated trachea incubated with saline or TNF-α for 1, 2 or 4 days to electrical field stimulation (EFS), 5-HT or methacholine. In addition, we compared bronchoconstriction in anaesthetized guinea pigs 6 h after intratracheal instillation of saline or TNF-α to vagal nerve stimulation, i.v. 5-HT or methacholine. Differential counts were performed on the bronchoalvelolar lavage fluid (BALF). KEY RESULTS: Maximum contractions to methacholine, 5-HT and EFS were not different between freshly prepared and saline-incubated tissues. Exposure to TNF-α concentration-dependently potentiated contractions to 5-HT and EFS, but not methacholine. All contractions were atropine-sensitive, but not hexamethonium-sensitive. 5-HT-evoked contractions were inhibited by ketanserin or epithelial denudation. Only EFS-evoked contractions were tetrodotoxin-sensitive. Vagal stimulation, i.v. 5-HT or MCh caused a significant atropine-sensitive, frequency- and dose-dependent bronchoconstriction and decreased blood pressure similarly in both saline and TNF-α pre-treated animals. TNF-α potentiated the bronchoconstriction to vagal stimulation and 5-HT, but not MCh. The BALF from saline-treated animals contained predominantly macrophages, whereas that from TNF-α-treated animals contained neutrophils. CONCLUSIONS AND IMPLICATIONS: TNF-α caused airway hyperresponsiveness to nerve stimulation in vivo and increased contractility in vitro. However, responsiveness to MCh was unchanged, suggesting a pre-synaptic action of TNF-α on parasympathetic nerves. TNF-α-induced airway hyperresponsiveness to 5-HT suggested an increased 5-HT(2A) receptor-mediated acetylcholine release from epithelial cells.

Evidence for both inverse agonism at the cannabinoid CB1 receptor and the lack of an endogenous cannabinoid tone in the rat and guinea-pig isolated ileum myenteric plexus-longitudinal muscle preparation.

BACKGROUND AND PURPOSE: Cannabinoid receptor agonists reduce intestinal propulsion in rodents through the CB(1) receptor. In addition to its antagonistic activity at this receptor, rimonabant (N-(piperidino)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole-carboxyamide) alone augments intestinal transit. Using rat and guinea-pig ileum MPLM (myenteric plexus-longitudinal muscle) preparations, we investigated whether the latter effect was through inverse agonism or antagonism of endocannabinoid agonist(s). EXPERIMENTAL APPROACH: Inverse agonism was investigated by comparing the maximal enhancement of electrically evoked contractions of the MPLM by two CB(1) receptor antagonists, AM 251 (N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide) and O-2050 [(6aR,10aR)-3-(1-methanesulphonylamino-4-hexyn-6-yl)-6a,7,10,10a-tetrahydro-6,6,9-trimethyl-6-H-dibenzo[b,d]pyran], with that produced by rimonabant. To reveal ongoing endocannabinoid activity, effects of inhibiting endocannabinoid hydrolysis by fatty acid amide hydrolase (FAAH) using AA-5HT (arachidonyl-5-hydroxytryptamine), PMSF (phenylmethylsulphonyl fluoride) or URB-597 (3'-carbamoyl-biphenyl-3-yl-cyclohexylcarbamate), or putative uptake using VDM-11 [(5Z,8Z,11Z,14Z)-N-(4-hydroxy-2-methylphenyl)-5,8,11,14-eicosatetraenamide] was evaluated. KEY RESULTS: The presence of CB(1) receptors was revealed by antagonism of exogenous anandamide, arachidonylethanolamide (AEA) and WIN 55,212-2 [(R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)-pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate] by rimonabant. The rank order of potentiation of contractions was AM 251 > rimonabant > O-2050. Neither the FAAH inhibitors nor VDM-11 affected electrically evoked contractions. Each FAAH inhibitor increased the potency of AEA but not WIN 55,212-2. VDM-11 did not alter the inhibitory effect of AEA. CONCLUSIONS AND IMPLICATIONS: The different levels of maximal potentiation of contractions by the CB(1) receptor antagonists suggest inverse agonism. The potentiation of the action of AEA by the FAAH inhibitors showed that FAAH was present. The lack of effect of FAAH inhibitors and VDM-11 alone on electrically evoked contractions, and on the potency of exogenous AEA suggests that pharmacologically active endocannabinoids were not released and the endocannabinoid transporter was absent. Thus, the CB(1) receptor antagonists behave as inverse agonists.

Pharmacological characterization of cannabinoid receptor activity in the rat-isolated ileum myenteric plexus-longitudinal muscle preparation.

BACKGROUND AND PURPOSE: Cannabinoid effects on intestinal transit are commonly evaluated in rats. We characterized the cannabinoid receptors mediating the inhibitory effect of 5-(1,1-dimethylheptyl)-2-[5-hydroxy-2-(3-hydroxypropyl)-cyclohexyl]-phenol (CP 55,940), (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate (WIN 55,212-2), arachidonylethanolamide (AEA) and Delta(9)-tetrahydrocannabinol (Delta(9)-THC) on contractions of the rat ileum myenteric plexus-longitudinal muscle (MPLM) preparation. EXPERIMENTAL APPROACH: The interaction of each agonist was examined with the CB(1) and CB(2) receptor antagonist rimonabant and SR 144,528 respectively, on contractions elicited by electrical field stimulation (EFS) or exogenous ACh. The interaction of AEA with capsazepine, a TRPV(1) receptor antagonist, was also investigated. KEY RESULTS: EFS with single and trains of pulses evoked neurogenic ACh-mediated twitch and rebound contractions respectively. The rank order of potency for inhibition was CP 55,940 = WIN 55,212-2 > AEA > Delta(9)-THC and AEA > WIN 55,212-2 =Delta(9)-THC = CP 55,940 respectively. The stereoisomer WIN 55,212-3 was without effect. Rimonabant antagonized the inhibition of the twitches with pK(B) values of around 8.60, but only antagonized rebound contractions induced by WIN 55,212-2, AEA and Delta(9)-THC, with pA(2) values of around 6.80. Rimonabant increased the twitches but inhibited the rebound contractions. Contractions to exogenous ACh were not altered. These observations extended to the guinea pig ileum MPLM. CONCLUSIONS AND IMPLICATIONS: The rat MPLM contains CB(1) receptors and at least two non-CB(1)-non-CB(2)-non-TRPV(1) receptors attenuating EFS-evoked ACh-mediated contractions in an EFS frequency-dependent pre-synaptic and stereo-specific manner. Augmentation of the twitches by rimonabant may be through antagonism of an endocannabinoid tone or inverse agonism, whereas inhibition of the rebound contractions involved partial agonism.