Excess Scattering Induced Loss at a Rough Surface Due to Partially Coherent Double-Reflection

Transmission (and retransmission) through rough surfaces degrades ultrasonic flaw detection and materials characterization. The flaw signal as well as reference signals (e.g. reflections from the front-surface or back-surface of the specimen) become difficult to interpret. In the simplest case, we make two assumptions in order to model the ultrasonic pulse-echo signal. Our first assumption is that the scatterer is large in the sense that it extends laterally for many surface correlation lengths. In this case, the signal has a small variance and is well described by its average value that will be referred to as the “specular” signal. Our second assumption is that the flaw is far from the surface, in a sense to be defined below. Given these two assumptions, the rough surface introduces a loss that is proportional to the square of the rms height, h, and the frequency, f. Further, the loss due to a double-transmission, L d , is just twice the loss due to a single-transmission, L s , i.e., L d ≈ 2 L s .</p

Pioglitazone, a specific ligand of peroxisome proliferator-activated receptor-gamma, protects pancreas against acute cerulein-induced pancreatitis

AIM: To determine the effect of pioglitazone, a specific peroxisome proliferator-activated receptor-γ (PPARγ) ligand, on the development of acute pancreatitis (AP) and on the expression of heat shock protein 70 (HSP70) in the pancreas. METHODS: AP was induced in rats by subcutaneous infusion of cerulein for 5 h. Pancreatic blood flow was measured by laser Doppler flowmetry. Plasma lipase activity, interleukin-1β (IL-1β) and IL-10 were determined. Pancreatic weight and histology were evaluated and pancreatic DNA synthesis and blood flow as well as pancreatic mRNA for IL-1β and HSP70 were assessed in rats treated with pioglitazone alone or in combination with cerulein. RESULTS: Pioglitazone administered (10-100 mg/kg i.g.) 30 min before cerulein, attenuated dose-dependently the pancreatic tissue damage in cerulein-induced pancreatitis (CIP) as demonstrated by the improvement of pancreatic histology, reduction in plasma lipase activity, plasma concentration of pro-inflammatory IL-1β and its gene expression in the pancreas and attenuation of the pancreatitis-evoked fall in pancreatic blood flow. CIP increased pancreatic HSP70 mRNA and protein expression in the pancreas and this effect was enhanced by pioglitazone treatment. CONCLUSION: Pioglitazone attenuates CIP and the beneficial effect of this pioglitazone is multifactorial probably due to its anti-inflammatory activities, to the suppression of IL-1β and to the overexpression of HSP70. PPARγ ligands could represent a new therapeutic option in the treatment of AP

Grapefruit-seed extract attenuates ethanol-and stress-induced gastric lesions via activation of prostaglandin, nitric oxide and sensory nerve pathways

AIM: Grapefruit-seed extract (GSE) containing flavonoids, possesses antibacterial and antioxidative properties but whether it influences the gastric defense mechanism and gastroprotection against ethanol- and stress-induced gastric lesions remains unknown. METHODS: We compared the effects of GSE on gastric mucosal lesions induced in rats by topical application of 100% ethanol or 3.5 h of water immersion and restraint stress (WRS) with or without (A) inhibition of cyclooxygenase (COX)-1 activity by indomethacin and rofecoxib, the selective COX-2 inhibitor, (B) suppression of NO-synthase with L-NNA (20 mg/kg ip), and (C) inactivation by capsaicin (125 mg/kg sc) of sensory nerves with or without intragastric (ig) pretreatment with GSE applied 30 min prior to ethanol or WRS. One hour after ethanol and 3.5 h after the end of WRS, the number and area of gastric lesions were measured by planimetry, the gastric blood flow (GBF) was assessed by H(2)-gas clearance technique and plasma gastrin levels and the gastric mucosal generation of PGE2, superoxide dismutase (SOD) activity and malonyldialdehyde (MDA) concentration, as an index of lipid peroxidation were determined. RESULTS: Ethanol and WRS caused gastric lesions accompanied by the significant fall in the GBF and SOD activity and the rise in the mucosal MDA content. Pretreatment with GSE (8-64 mg/kg i g) dose-dependently attenuated gastric lesions induced by 100% ethanol and WRS; the dose reducing these lesions by 50% (ID(50)) was 25 and 36 mg/kg, respectively, and this protective effect was similar to that obtained with methyl PGE2 analog (5 μg/kg i g). GSE significantly raised the GBF, mucosal generation of PGE(2), SOD activity and plasma gastrin levels while attenuating MDA content. Inhibition of PGE(2) generation with indomethacin or rofecoxib and suppression of NO synthase by L-NNA or capsaicin denervation reversed the GSE-induced protection and the accompanying hyperemia. Co-treatment of exogenous calcitonine gene-related peptide (CGRP) with GSE restored the protection and accompanying hyperemic effects of GSE in rats with capsaicin denervation. CONCLUSION: GSE exerts a potent gastroprotective activity against ethanol and WRS-induced gastric lesions via an increase in endogenous PG generation, suppression of lipid peroxidation and hyperemia possibly mediated by NO and CGRP released from sensory nerves

Testing QCD factorisation and charming penguins in charmless B→PV{\boldsymbol{B\to PV}}

We try a global fit of the experimental branching ratios and CP-asymmetries of the charmless $B\to PV$ decays according to QCD factorisation. We find it impossible to reach a satisfactory agreement, the confidence level (CL) of the best fit is smaller than .1 %. The main reason for this failure is the difficulty to accomodate several large experimental branching ratios of the strange channels. Furthermore, experiment was not able to exclude a large direct CP asymmetry in $\bar {B^0}\to\rho^+ \pi^-$, which is predicted very small by QCD factorisation. Trying a fit with QCD factorisation complemented by a charming-penguin inspired model we reach a best fit which is not excluded by experiment (CL of about 8 %) but is not fully convincing. These negative results must be tempered by the remark that some of the experimental data used are recent and might still evolve significantly.Comment: 21 pages, 4 figures; several typos corrected, added one footnote and two references, comments added about PQCD. To appear in Phys.Rev.