The influence of the rammed stone column formation on strength parameters of the surrounding soil

This paper presents the results of field tests performed to examine the influence of the rammed stone column formation process on the surrounding soil. The influence is expressed by cohesion and internal friction angle changes. These parameters were determined in cone penetration test (CPTU) performed during and after the stone column formation process. The conducted tests have shown that the process of column formation affects the strength parameters of the surrounding soil. These changes are complex and come from a number of factors such as initial in situ soil characteristics, distance from the column and time. The field tests indicated a decrease in strength parameters during column formation process. Subsequently, when soil structure is rebuilt and consolidation process takes place, the strength parameters increase

Numerical analysis of consolidation of embankment subsoil reinforced with dynamic replacement stone columns

The paper presents a comparative analysis of the consolidation of soil under a road embankment reinforced with stone columns. The results were obtained from the most common analytical and numerical methods applied in driven column dimensioning. The analytical approach exploits Terzaghi’s one-dimensional theory and Barronʼs three-dimensional theory. The numerical calculations reflected the particular stages of the embankment construction in various two- and three-dimensional systems. The geotechnical parameters that were crucial for the research were determined on the basis of geoengineering documentation, laboratory and field studies. The paper begins with a short introduction presenting the dynamic replacement method

Hydrogen sulphide production in healthy and ulcerated gastric mucosa of rats

Hydrogen sulphide (H2S) is produced endogenously via two enzymes dependent on pyridoxal phosphate (PLP): cystathionine beta-synthase (CBS, EC 4.2.1.22), cystathionase γ-liase (CTH, EC 4.4.1.1), and a third, 3-mercaptopyruvate sulfurtransferase (MPST, EC 2.8.1.2). H2S strengthens the defence mechanisms of the gastric mucosal barrier, and plays an important role in gastroprotection, including the increased resistance to damage caused by various irritants and non-steroidal anti-inflammatory drugs. The study was conducted to determine the role of H2S in ulcerated gastric mucosa of rats caused by immobilization in cold water (WRS). The activity and expression of γ-cystathionase, cystathionine β-synthase, 3-mercaptopyruvate sulfurtransferase, and rhodanese was compared with healthy mucosa, together with H2S generation, and cysteine, glutathione, and cystathionine levels. The results showed that the defence mechanism against stress is associated with stimulation of the production of H2S in the tissue and confirmed the observed advantageous effect of H2S on healing of gastric ulcers. In case of animals pretreated with exogenous sources of H2S and NaHS, and some changes observed in the ulcerated gastric mucosa tend to return to values found in the healthy tissue, a finding that is in accordance with the previously determined gastroprotective properties of H2S. The results presented in this paper point to the possible role of rhodanese in H2S production in the gastric mucosa of rats, together with the earlier mentioned three enzymes, which are all active in this tissue

Hydrogen Sulfide and Carbon Monoxide Protect Gastric Mucosa Compromised by Mild Stress Against Alendronate Injury

Background Alendronate is an inhibitor of osteoclast-mediated bone resorption, but its clinical utility is limited due to gastrointestinal complications including bleeding erosions. Aims We studied whether potent vasodilators hydrogen sulfide (H2S) and carbon monoxide (CO) can protect against alendronate-induced gastric lesions in rats exposed to mild stress. Methods Three series (A, B, and C) of Wistar rats received alendronate (150-700 mg/kg i.g., series A) with or without NaHS (5 mg/kg), H2S donor or CORM-2 (5 mg/kg) releasing CO administered i.g. 30 min before alendronate administration (series B) in rats exposed for 3 days before alendronate administration to mild stress (series C). The area of gastric lesions was assessed by planimetry, the gastric blood flow (GBF) was determined by H2-gas clearance technique, and H2S production via CSE/CBS/3- MST activity and the gastric expression of HO-1, HO-2, HIF-1a, NF-jB, iNOS, COX-2, IL-1b, TNF-a, GPx-1 and SOD-2 were analyzed by qPCR or Western blot. Results Alendronate dose-dependently produced gastric mucosal lesions and significantly decreased GBF, and these effects were exacerbated by mild stress. NaHS and CORM2 significantly reduced the alendronate-induced gastric lesions in non-stressed and stressed animals, but only NaHS but not CORM-2 raised H2S production. NaHS and CORM-2 inhibited gastric expression of HIF-1a protein and HO-1, HIF-1a, NF-jB, COX-2, iNOS, IL-1b, TNF-a mRNAs but failed to affect those of HO-2, GPx-1, and SOD-2. Conclusion Both H2S and CO released from their donors, NaHS and CORM-2, protect gastric mucosa compromised by stress against alendronate-induced gastric damage via mechanism involving downregulation of HIF-1a, NF-jB and proinflammatory factors COX-2, iNOS, IL-1b, and TNF-a

Estimation of variability of retinal vessel network caused by pathology

Wstęp. W niniejszej pracy omówiono zagadnienie zmienności, czyli plastyczności sieci naczyń krwionośnych siatkówki, związane ze stanami patologicznymi. Wydaje się, że nawet wykształcona w rozwoju osobniczym sieć naczyń siatkówki może ulec zmianom kształtu, a zwłaszcza stopnia rozgałęzienia, zapewne pod wpływem czynników angiogennych wytwarzanych w przebiegu procesów patologicznych. Materiał i metody. Analiza fraktalna fotografii dna oka pozwoliła na wykazanie znamiennych różnic pomiędzy grupą kontrolną a chorymi na retinopatię cukrzycową, retinopatię nadciśnieniową oraz zmiany degeneracyjne plamki żółtej związane z wiekiem (AMD). Wyniki i analizę statystyczną oparto na obliczeniu wymiarów fraktalnych 173 fotografii dna oka pacjentów oraz osób z grupy kontrolnej. Przebadano 38 pacjentów z retinopatią cukrzycową, 31 osób z retinopatią nadciśnieniową, 32 chorych z jaskrą otwartego kąta, 39 pacjentów z AMD oraz 33 osoby z grupy kontrolnej. Wymiar fraktalny jest matematycznym parametrem opisującym stopień skomplikowania analizowanej sieci. Fotografie dna oka przetworzono cyfrowo, znormali-zowano i opracowano matematycznie. Zastosowano box counting method w celu obliczenia wymiarów fraktalnych. Wnioski. Taka analiza pozwala nie tylko na ocenę plastyczności i zmienności oraz stopnia skomplikowania sieci naczyniowej związanej ze stanami patologicznymi, ale umożliwia zastosowanie tej metody w diagnostyce okulistycznej.Background. The present study shows the plasticity of retinal vessel networks connected with pathology. It seems that even in adults, retinal vessel networks can change their shape and arborisation under the influence of angiogenic factors connected with pathological processes. Material and methods. Fractal analysis of photographs of vascular networks revealed significant differences between controls and diabetic retinopathy, hypertensive retinopathy and AMD (age related macular degeneration). The results are based on the analysis and calculations of fractal dimensions of 173 pathological and control photographs of retinal vessels. The following patients were included in the study: 38 diabetic retinopathy, 31 hypertensive retinopathy, 32 open-angle glaucoma, 39 AMD patients and 33 controls. The fractal dimension is the mathematical parameter describing the complexity of the analysed network. The obtained images of retinal vessel networks were digitised, normalised and processed mathematically. The box counting method was used for calculation of fractal dimensions. Conclusions. This analysis allows not only for description of the plasticity and complexity of retinal network as the effect of pathological conditions but also contains the potential to use this kind of analysis for diagnostic purposes

Exogenous asymmetric dimethylarginine (ADMA) in pathogenesis of ischemia-reperfusion-induced gastric lesions : interaction with protective nitric oxide (NO) and calcitonin gene-related peptide (CGRP)

Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide (NO) synthesis inhibitor and pro-inflammatory factor. We investigated the role of ADMA in rat gastric mucosa compromised through 30 min of gastric ischemia (I) and 3 h of reperfusion (R). These I/R animals were pretreated with ADMA with or without the combination of l-arginine, calcitonin gene-related peptide (CGRP) or a small dose of capsaicin, all of which are known to afford protection against gastric lesions, or with a farnesoid X receptor (FXR) agonist, GW 4064, to increase the metabolism of ADMA. In the second series, ADMA was administered to capsaicin-denervated rats. The area of gastric damage was measured with planimetry, gastric blood flow (GBF) was determined by H2-gas clearance, and plasma ADMA and CGRP levels were determined using ELISA and RIA. ADMA significantly increased I/R-induced gastric injury while significantly decreasing GBF, the luminal NO content, and the plasma level of CGRP. This effect of ADMA was significantly attenuated by pretreatment with CGRP, l-arginine, capsaicin, or a PGE2 analogue. In GW4064 pretreated animals, the I/R injury was significantly reduced and this effect was abolished by co-treatment with ADMA. I/R damage potentiated by ADMA was exacerbated in capsaicin-denervated animals with a further reduction of CGRP. Plasma levels of IL-10 were significantly decreased while malonylodialdehyde (MDA) and plasma TNF-α contents were significantly increased by ADMA. In conclusion, ADMA aggravates I/R-induced gastric lesions due to a decrease of GBF, which is mediated by a fall in NO and CGRP release, and the enhancement of lipid peroxidation and its pro-inflammatory properties

The protective role of carbon monoxide (CO) produced by heme oxygenases and derived from the CO-releasing molecule CORM-2 in the pathogenesis of stress-induced gastric lesions : evidence for non-involvement of nitric oxide (NO)

Carbon monoxide (CO) produced by heme oxygenase (HO)-1 and HO-2 or released from the CO-donor, tricarbonyldichlororuthenium (II) dimer (CORM-2) causes vasodilation, with unknown efficacy against stress-induced gastric lesions. We studied whether pretreatment with CORM-2 (0.1–10 mg/kg oral gavage (i.g.)), RuCl3 (1 mg/kg i.g.), zinc protoporphyrin IX (ZnPP) (10 mg/kg intraperitoneally (i.p.)), hemin (1–10 mg/kg i.g.) and CORM-2 (1 mg/kg i.g.) combined with NG-nitro-l-arginine (l-NNA, 20 mg/kg i.p.), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 mg/kg i.p.), indomethacin (5 mg/kg i.p.), SC-560 (5 mg/kg i.g.), and celecoxib (10 mg/kg i.g.) affects gastric lesions following 3.5 h of water immersion and restraint stress (WRS). Gastric blood flow (GBF), the number of gastric lesions and gastric CO and nitric oxide (NO) contents, blood carboxyhemoglobin (COHb) level and the gastric expression of HO-1, HO-2, hypoxia inducible factor 1α (HIF-1α), tumor necrosis factor α (TNF-α), cyclooxygenase (COX)-2 and inducible NO synthase (iNOS) were determined. CORM-2 (1 mg/kg i.g.) and hemin (10 mg/kg i.g.) significantly decreased WRS lesions while increasing GBF, however, RuCl3 was ineffective. The impact of CORM-2 was reversed by ZnPP, ODQ, indomethacin, SC-560 and celecoxib, but not by l-NNA. CORM-2 decreased NO and increased HO-1 expression and CO and COHb content, downregulated HIF-1α, as well as WRS-elevated COX-2 and iNOS mRNAs. Gastroprotection by CORM-2 and HO depends upon CO’s hyperemic and anti-inflammatory properties, but is independent of NO

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