• 한국조류학회지
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• 제25권2호
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• pp.82-86
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• 2018

플라스틱 유색가락지는 수많은 생태학 및 조류학 현장 연구에 흔히 사용되고 있으나, 참새목 조류에서 유색가락지로 인한 부상에 대한 기록은 드문 실정이다. 본 연구는 전남 신안군 홍도에서의 가락지 부착조사 과정에서 최초 포획된 날로부터 596일 후 재포획 된 흰배지빠귀(Turdus pallidus)가 분할식 다빅(Darvic) 유색가락지로 인해 발가락이 소실되었음을 확인하고 이를 처음으로 보고한다. 또 인접한 흑산도에서는 포획된 지 135일 후에 재관찰된 검은이마직박구리(Pycnonotus sinensis)의 왼쪽 뒷발가락이 유색가락지 안쪽에 끼어있는 사례도 함께 확인하였다. 유색가락지를 부착한 산새류 1,900여 개체에서 확인된 두 사례를 바탕으로, 향후 유색가락지의 사용과 부착에 있어서 일반적인 유색가락지 부착지침을 따르는 신중한 접근법을 강조한다.

• Environmental Analysis Health and Toxicology
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• 제21권1호
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• pp.87-92
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• 2006

This study was done to investigate the protective effect of novel 9-amino-1, 2, 3, 4-tetrahydroacridine derivatives on the hepatoprotective effect intoxicated rats induced by carbon tetrachloride ($CCl_4$). A series of currently derivatives of 9-amino-1, 2, 3, 4-tetrahydroacridine have been prepared through the alkly substitution or the ring expansion for the treatment of the Alzheimer's disease. The activities of aminotransferase (aspartate and alanine) and contents of alkaline phosphatase, triglyceride and glutathione S-transferase in 9-amino-1, 2, 3, 4-tetrahydroacridine derivatives pretreated rats were significantly decreased compared to the only carbon tetrachloride treated rats but the contents of cholesterol were increased compared to the only $CCl_4$ treated rats. The result indicated that 9-amino-1, 2, 3, 4-tetrahydroacridine derivatives showed hepatoprotective effect in $CCl_4$ treated rats.

• Biomolecules & Therapeutics
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• 제22권5호
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• pp.420-425
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• 2014

Esophageal reflux of gastric contents causes esophageal mucosal damage and inflammation. Recent studies show that oxygen-derived free radicals mediate mucosal damage in reflux esophagitis (RE). Chlorogenic acid (CGA), an ester of caffeic acid and quinic acid, is one of the most abundant polyphenols in the human diet and possesses anti-inflammatory, antibacterial and anti-oxidant activities. In this context, we investigated the effects of CGA against experimental RE in rats. RE was produced by ligating the transitional region between the forestomach and the glandular portion and covering the duodenum near the pylorus ring with a small piece of catheter. CGA (10, 30 and 100 mg/kg) and omeprazole (positive control, 10 mg/kg) were administered orally 48 h after the RE operation for 12 days. CGA reduced the severity of esophageal lesions, and this beneficial effect was confirmed by histopathological observations. CGA reduced esophageal lipid peroxidation and increased the reduced glutathione/oxidized glutathione ratio. CGA attenuated increases in the serum level of tumor necrosis factor-${\alpha}$, and expressions of inducible nitric oxide synthase and cyclooxygenase-2 protein. CGA alleviates RE-induced mucosal injury, and this protection is associated with reduced oxidative stress and the anti-inflammatory properties of CGA.

• The Korean Journal of Pain
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• 제23권1호
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• pp.1-10
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• 2010

Background: Recent studies indicate that reactive oxygen species (ROS) are involved in persistent pain, including neuropathic and inflammatory pain. Since the data suggest that ROS are involved in central sensitization, the present study examines the levels of activated N-methyl-D-aspartate (NMDA) receptors in the dorsal horn after an exogenous supply of three antioxidants in rats with chronic post-ischemia pain (CPIP). This serves as an animal model of complex regional pain syndrome type-I induced by hindpaw ischemia/reperfusion injury. Methods: The application of tight-fitting O-rings for a period of three hours produced CPIP in male Sprague-Dawley rats. Allopurinol 4 mg/kg, allopurinol 40 mg/kg, superoxide dismutase (SOD) 4,000 U/kg, N-nitro-L-arginine methyl ester (L-NAME) 10 mg/kg and SOD 4,000 U/kg plus L-NAME 10 mg/kg were administered intraperitoneally just after O-ring application and on the first and second days after reperfusion. Mechanical allodynia was measured, and activation of the NMDA receptor subunit 1 (pNR1) of the lumbar spinal cord (L4-L6) was analyzed by the Western blot three days after reperfusion. Results: Allopurinol reduced mechanical allodynia and attenuated the enhancement of spinal pNR1 expression in CPIP rats. SOD and L-NAME also blocked spinal pNR1 in accordance with the reduced mechanical allodynia in rats with CPIP. Conclusions: The present data suggest the contribution of superoxide, produced via xanthine oxidase, and the participation of superoxide and nitric oxide as a precursor of peroxynitrite in NMDA mediated central sensitization. Finally, the findings support a therapeutic potential for the manipulation of superoxide and nitric oxide in ischemia/reperfusion related pain conditions.