Serumski srčani troponin I kao biljeg srčane degeneracije uzrokovane pokusnim trovanjem ovaca salinomicinom.

Salinomycin is an ionophore with antimicrobial properties. It is a dietary additive used as a growth promoter for ruminants and as a coccidiostat in chickens. However, over-dosage or misuse situations can lead to a series of toxic syndromes. Cardiac troponin I (cTnI) is the part of the troponin complex (I, C and T) within the sarcomere in myocardial cells that regulates contraction of the heart muscle. cTnI is released from injured myocardiocytes into circulation, so it can be a specifific biomarker in myocardial necrosis. The purpose of this study is to propose cTnI for diagnostic cardiac degeneration induced by experimental toxicosis with salinomycin in sheep. Twenty Iranian mixed breed adult female fat-tailed sheep (BW: 33.3 ± 3.4 kg) were used in this study. The sheep were randomly divided in to five equal groups. Group I (control) received 20 mL normal Saline. Groups II, III, IV and V were orally administered 1 mg/kg (twice a day for two days), 2, 3 and 4 mg/kg (once a day for two days) salinomycin, respectively. Following drug administration, blood samples were collected at different time intervals (2, 5, 8, 14 and 21 days) in order to determine various biochemical parameters (cTnI, CK, LDH, ALT and AST). In all groups, the heart sounds of the animals were carefully heard and electrocardiogram (ECG) was taken to determine the type of probable arrhythmia. The results illustrated a significant increase in the activity of cTnI. Numerous arrhythmias were recorded, such as: sinus tachycardia, supraventricular tachycardia, sinus arrhythmia and supraventricular premature contraction. All animals with arrhythmias showed a significant increase in the activity of cTnI. Cardiac muscle necrosis observed macroscopically on post mortem examination revealed myocardial degeneration. Overall, the results of this study indicate that cTnI may be considered as a valuable biomarker in diagnosing cardiac degeneration due to salinomycin toxicosis.Salinomicin je ionofor s antimikrobnim svojstvima. Rabi se kao dodatak hrani koji u preživača ima ulogu promotora rasta, a u pilića ulogu kokcidiostatika. Prevelike količine i pogrešna uporaba salinomicina mogu dovesti do teških sindroma trovanja. Srčani troponin I (cTnI) je dio troponinskog kompleksa (I, C i T), unutar sarkomere srčanih mišićnih stanica, koji regulira kontrakcije srčanog mišića. Budući da se oslobađa iz oštećenih miokardiocita u krvotok, cTnI može biti specifičan biomarker kod nekroze srčanog mišića. Svrha istraživanja bila je predložiti da se cTnI primjeni u dijagnostici srčane degeneracije uzrokovane pokusnim trovanjem ovaca salinomicinom. U istraživanje je bilo uključeno 20 odraslih, masnorepih ovaca, križanki iranskih pasmina (TM: 33,3 ± 3,4 kg). Ovce su metodom slučajnog izbora bile podijeljene u pet skupina iste veličine. Skupina I (kontrola) dobila je 20 mL otopine soli. Skupine II, III, IV i V dobile su oralnim putem salinomicin i to u količini od 1 mg/kg (dva puta dnevno kroz dva dana), odnosno 2, 3 i 4 mg/kg (jednom dnevno kroz dva dana). Odmah nakon toga uzimani su uzorci krvi u različitim vremenskim razmacima (2, 5, 8, 14 i 21 dana) s ciljem određivanja različitih biokemijskih pokazatelja (cTnI, CK, LDH, ALT i AST). U svim skupinama pažljivo su osluškivani srčani tonovi i određivan elektrokardiogram s ciljem otkrivanja tipa moguće srčane aritmije. Rezultati pokazuju značajno povećanje aktivnosti cTnI. Zabilježene su i mnoge aritmije kao što su sinusna tahikardija, supraventrikularna tahikardija, sinusna aritmija i supraventrikularna preuranjena kontrakcija. Sve su životinje uz aritmiju očitovale i značajno povećanje aktivnosti cTnI. Razudbom nakon uginuća makroskopski je opažena nekroza i degeneracija srčanog mišića. Zaključno, rezultati istraživanja pokazuju da cTnI može biti vrijedan biomarker u dijagnostici srčane degeneracije prouzročene trovanjem salinomicinom

Serum cardiac troponin I as a biomarker in cardiac degeneration following experimental salinomycin toxicosis

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In vitroantibacterial effect of wasp (Vespa orientalis) venom

Background The emergence of antibacterial resistance against several classes of antibiotics is an inevitable consequence of drug overuse. As antimicrobial resistance spreads throughout the globe, new substances will always be necessary to fight against multidrug-resistant microorganisms. Venoms of many animals have recently gained attention in the search for new antimicrobials to treat infectious diseases. Thefore, the present study aimed to study the antibacterial effects of wasp (Vespa orientalis) crude venom. Two gram-positive bacteria (Staphylococcus aureus and Bacillus subtilis) and two gram-negative ones (Escherichia coli and Klesiella pneumonia) were compared for their sensitivity to the venom by determining the inhibition zone (Kirby-Bauer method) and minimum inhibitory concentration (MIC). A microbroth kinetic system based on continuous monitoring of changes in the optical density of bacterial growth was also used for determination of antimicrobial activity.Results The venom exhibited a well-recognized antimicrobial property against the tested bacterial strains. The inhibition zones were determined to be 12.6, 22.7, 22.4 and 10.2 mm for S. aureus, B. subtilis,E. coliand K. pneumonia, respectively. The corresponding MIC values were determined to be 64, 8, 64 and 128 μg/mL, respectively. The MIC50 and MIC90 values of the venom were respectively determined to be 63.6 and 107 μg/mL for S. aureus, 4.3 and 7.0 μg/mL for B. subtilis, 45.3 and 65.7 μg/mL for E. coli and 74.4 and 119.2 μg/mL for K. pneumonia. Gram-positive bacteria were generally more sensitive to the venom than gram-negative ones.Conclusions Results revealed that the venom markedly inhibits the growth of both gram-positive and gram-negative bacteria and could be considered a potential source for developing new antibacterial drugs

In vitro antihistamine-releasing activity of a peptide derived from wasp venom of Vespa orientalis

Objective: To investigate the antihistamine-releasing effect of a peptide isolated from wasp venom of Vespa orientalis. Methods: This peptide was separated from crude venom by chromatography methods and mass spectrometry. Then various concentrations (2, 4, 8, 16, 32, 64, 128 and 256 μmol/L) of the peptide were incubated with mast cells and lactate dehydrogenase assay was performed. Results: No significant effect was observed in lactate dehydrogenase absorbance under 128 μmol/L concentration. This implied that the peptide did not cause cell death in mast cells and consequently, histamine release did not happen. Moreover, the results showed the IC50 of mast cells degranulation at 126 μmol/L, which was approximately high implying that this peptide had high selectivity for normal cells and did not cause histamine release from these cells. Conclusions: This would be a great aim in new drug development, in which an agent acts potentially on its target tissue without activating the immune system

Impacted calculus within a urethral stent: A rare cause of urinary retention

An elderly male presented to the emergency department with acute urinary retention. He had poor flow of urine associated with serosanguinous discharge per urethra for 3 days duration. Earlier he underwent permanent metallic urethral stenting for post TURP bulbar urethral stricture. Plain X-ray of Pelvis showed an impacted calculus within the urethral stent in bulbar urethra. Urethrolitholapaxy was done with semirigid ureteroscope. Urethral stent was patent and well covered. Subsequently he had an uneventful recovery. We describe a unique case of acute urinary retention due to calculus impaction within a urethral stent

Modulation of ERK1/2 and Akt Pathways Involved in the Neurotrophic Action of Caffeic Acid Alkyl Esters

Neurodegenerative diseases affect millions of human lives all over the world. The number of afflicted patients is rapidly growing, and disease-modifying agents are urgently needed. Caffeic acid, an important member of the hydroxycinnamic acid family of polyphenols, has considerable neurotrophic effects. We have previously shown how caffeate alkyl ester derivatives significantly promote survival and differentiation in neuronal cells. In this study, the mechanisms by which these ester derivatives exert their neurotrophic effects are examined. A series of eight caffeic acid esters with different alkyl chain lengths, ranging from methyl (CAF1) to dodecyl esters (CAF8), were synthesized and studied for their influence on neurotrophic signaling pathways. Caffeate esters did not induce tropomyosin-receptor kinase A (TrkA) phosphorylation, which was assessed by immunoblotting up to a concentration of 25 µM. NIH/3T3 cells overexpressing TrkA were generated to further examine phosphorylation of this receptor tyrosine kinase. None of the esters induced TrkA phosphorylation in these cells either. Assessment of the effect of caffeate derivatives on downstream neurotrophic pathways by immunoblotting showed that the most potent esters, decyl caffeate (CAF7) and dodecyl caffeate (CAF8) caused extracellular signal-regulated kinase (ERK1/2) and Akt serine threonine kinase phosphorylation in PC12 cells at 5 and 25 µM concentrations. In conclusion, this study shows that caffeate esters exert their neurotrophic action by modulation of ERK1/2 and Akt signaling pathways in neuronal cells, and further demonstrates the potential therapeutic implications of these derivatives for neurodegenerative diseases