Increased apoptosis during morphogenesis of the lower cheek teeth in tabby/EDA mice

In wild-type (WT) mice, epithelial apoptosis is involved in reducing the embryonic tooth number and the mesial delimitation of the first molar. We investigated whether apoptosis could also be involved in the reduction of tooth number and the determination of anomalous tooth boundaries in tabby (Ta)/EDA mice. Using serial histological sections and computer-aided 3D reconstructions, we investigated epithelial apoptosis in the lower cheek dentition at embryonic days 14.5-17.5. In comparison with WT mice, apoptosis was increased mainly mesially in Ta dental epithelium from day 15.5. This apoptosis showed a similar mesio-distal extent in all 5 morphotypes (Ia,b,c and IIa,b) of Ta dentition and eliminated the first cheek tooth in morphotypes IIa,b. Apoptosis did not appear to play any causal role in positioning inter-dental gaps. Analysis of the present data suggests that the increased apoptosis in Ta mice is a consequence of impaired tooth development caused by a defect in segmentation of dental epithelium.     

Effect of Ankaferd Blood Stopper on air leakage in the lung and prevention of bleeding: an experimental study

Background  

Air leakage and hemorrhage are important causes of morbidity and mortality in operations and traumas of the lung. Ankaferd Blood Stopper is a herbal product used for stopping hemorrhage. In our study, we investigated the efficacy of Ankaferd Blood Stopper in the prevention of air leakage in the lung and bleeding.     

Anti-inflammatory activity of bis(3-aryl-3-oxo-propyl)methylamine hydrochloride in rat

In this study the effects of compound B1, bis(3-aryl-3-oxo-propyl)methylamine hydrochloride, and an anti-inflammatory drug, indomethacin, were tested by carrageenan-induced paw edema and cotton pellet granuloma tests, for effects on acute and chronic phases of inflammation, respectively. Their effects on vascular permeability were also determined by hyaluronidase-induced capillary permeability test. Anti-inflammatory activity of B1 was compared with indomethacin. B1 decreased the carrageenan-induced paw edema by 49%, 35%, and 47% at 50, 100, and 200 mg kg(-1) doses, respectively, while this decrease was 82% by indomethacin at 20 mg kg(-1) dose. Antiproliferative effects in cotton pellet test of B1 at 50 mg kg(-1) and indomethacin at 20 mg kg(-1) doses were 44% and 43%, respectively. Indomethacin but not B1 inhibited the hyaluronidase-induced increase in capillary permeability. Our results suggest that B1 inhibits both acute and chronic phases of inflammation probably by an effect not mediated by prevention of increased capillary permeability. Especially, its anti-inflammatory activity against chronic phase of inflammation was comparable with that of indomethacin. Further detailed studies are needed to clarify the mechanism(s) of action responsible for the anti-inflammatory activity of B1.     

Antiulcer activity of fluvoxamine in rats and its effect on oxidant and antioxidant parameters in stomach tissue

Background  

Although many drugs are available for the treatment of gastric ulcers, often these drugs are ineffective. Many antidepressant drugs have been shown to have antiulcer activity in various models of experimental ulcer. One such drug, the antidepressant mirtazapine, has been reported to have an antiulcer effect that involves an increase in antioxidant, and a decrease in oxidant, parameters. To date, however, there is no information available regarding the antiulcer activity for a similar antidepressant, fluvoxamine. This study aimed to investigate the antiulcer effects of fluvoxamine and to determine its relationship with antioxidants.     

The role of erythropoietin in the protection of gastric mucosa from indometacin‐induced gastric injury and its relationship with oxidant and antioxidant parameters in rats

Objectives Erythropoietin has anti‐oxidative and anti‐inflammatory activity. We wanted to evaluate its activity in preventing damage to the gastric mucosa. Methods We examined the protective effect of erythropoietin on indometacin‐induced gastric mucosa damage in the rat stomach and compared its potency with that of famotidine. We also measured effects on oxidant and antioxidant parameters in the rat stomach. Key findings Famotidine and erythropoietin 2500 and 5000 IU/kg reduced the ulcer area by 98%, 31% and 58%, respectively, compared with the indometacin group. Superoxide dismutase activity and glutathione level were decreased and myeloperoxidase activity increased in the indometacin group compared with healthy rats. Famotidine and erythropoietin at all doses increased superoxide dismutase and glutathione levels significantly compared with the indometacin group. Myeloperoxidase activity was decreased by erythropoietin and famotidine. Conclusions These results support the view that erythropoietin counteracts the effects of indometacin in inducing gastric ulcer and could be used as a an antiulcer compound. Its antiulcer effect is less potent than that of famotidine. The antiulcerogenic effects of erythropoietin may be related to its intrinsic ability to sustain the activities of free‐radical scavenging enzymes and the bioavailability of glutathione.     

Synthesis and Biological Evaluation of Novel Bromophenol Derivatives as Carbonic Anhydrase Inhibitors

Here, we provide an alternative synthesis of the natural bromophenol 3,4‐dibromo‐5‐(2,3‐dibromo‐4,5‐dihydroxybenzyl)‐6‐(ethoxymethyl)benzene‐1,2‐diol ( 3 ) and the first synthesis of (4,5‐dihydroxy‐2‐methylphenyl)(3,4‐dihydroxyphenyl)methanone ( 18 ) and its brominated derivatives 19 – 21 . The compounds were characterized and tested against the two most studied members of the pH regulatory enzyme family, carbonic anhydrase (CA). The inhibitory potencies of the novel compounds and two natural bromophenols 2 , 3 were analyzed at the human isoforms hCA I and hCA II as targets and the K_I values were calculated. The K_I values of the novel compounds were measured in the range of 13.7–32.7 µM for the hCA I isozyme and 0.65–1.26 µM for the hCA II isozyme. The structurally related compound 14 was also tested in order to understand the structure–activity relationship, and the clinically used sulfonamide acetazolamide (AZA) was tested for comparison reasons. All of the compounds exhibited competitive inhibition with 4‐nitrophenylacetate as substrate. The compounds showed strong inhibitory activity against hCA I, being more effective as compared to the clinically used AZA (K_I: 36.2 µM), but rather less activity against hCA II.     

A comparative investigation of biochemical and histopathological effects of thiamine and thiamine pyrophosphate on ischemia–reperfusion induced oxidative damage in rat ovarian tissue

In this study, the biochemical and histopathological effects of thiamine and thiamine pyrophosphate on ischemia–reperfusion induced oxidative damage in rat ovarian tissue were investigated. Animals were divided into four groups of six rat each, ovarian ischemia–reperfusion (IR), 25 mg/kg thiamine + ovarian ischemia–reperfusion (TIR), 25 mg/kg thiamine pyrophosphate + ovarian ischemia–reperfusion (TPIR) and Sham group (SG). The results of the biochemical experiments have shown that the rat ovarian tissue with thiamine treatment, the level of MDA, GSH and the 8-hydroxyguanine are almost the same as the IR group; while in the group with thiamine pyrophosphate treatment, the level of MDA, GSH and the 8-hydroxyguanine are almost the same as the SG. Ovarian tissue of rats in the IR group were congested and dilated vessels, edema, hemorrhage, necrotic and apoptotic cells. In this group, the migration and the adhesion of the polymorphonuclear leucocytes to the endothelium were observed. Both ovaries in TPIR group, there was no difference according to the SG. Histopathology of ovarian tissues in the TIR group was almost the same with the IR group. Our results indicate that thiamine pyrophosphate significantly prevents the ischemia–reperfusion induced oxidative damage in ovarian tissue, whereas thiamine has no effect. In conclusion, we have found that thiamine pyrophosphate prevents oxidative damage due to ischemia–reperfusion injury, whereas thiamine does not have this effect. Furthermore, we have confirmed that the results of our biochemical analyses are in concordance with the histopathological findings.