Wyniki wyszukiwania

1

Veterinary interlocking nailing and its augmentation for fracture repair

100%

Patil D. B., Adamiak Z., Piorek A.

Polish Journal of Veterinary Sciences

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2008

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tom 11

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nr 2

187-191

The present review informs about the current status regarding use of interlocking nailing for fracture repair in animals. The clinical limitations of interlocking nailing and its subsequent improvement by evolving novel nail design or supplementation with type I ESF using hybrid nail bolt/ESF pin has been dealt. The biomechanical and clinical evaluation of novel interlocking nail supplements and its possible clinical use is included.

2

Augmentation of the NO-cGMP cascade induces anxiogenic-like effect in mice

100%

Volke V., Wegener G., Vasar E.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 4

Several studies have reported the anxiolytic-like effects of various nitric oxide synthase inhibitors in distinct animal models. However, in the context of anxiety, the possible involvement of cyclic GMP, believed to be one of the main targets of NO, remains obscure. Cyclic GMP is degraded by the specific phosphodiesterases in the brain. Therefore, we studied the effect of the selective phosphodiesterase type 5 inhibitor sildenafil in the mouse elevated plus-maze test of anxiety and in the open field test of locomotion. We found that sildenafil (0.05-10 mg/kg i.p.) alone did not affect the behavior of animals in the plus-maze or open field tests, but the anxiogenic beta-carboline DMCM given in a subconvulsive dose (2 mg/kg i.p.) decreased the time spent on open arms in the elevated plus-maze. Treatment with the NO precursor L-arginine (200 mg/kg i.p.) did not modify the behavior of animals in the plus-maze, however, when sildenafil (1 mg/kg i.p.) was administered in combination with L-arginine (200 mg/kg i.p.), both the time spent on the open arms and the percentage of open arm visits were significantly decreased. We conclude that augmentation of the NO-cGMP cascade induces anxiogenic-like effect in mice.

3

Superoxide dismutase mimetic modulates hyperoxic augmentation of the diaphragmatic response to poikilocapnic hypoxia in non-vagotomized rats

84%

Budzinska K., Ilasz R.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 6

163-172

4

Controlling pear psyllids by mass-releasing Anthocoris nemoralis and A.nemorum [Heteroptera: Anthocoridae]

84%

Sigsgaard L., Esbjerg P., Philipsen H.

Journal of Fruit and Ornamental Plant Research

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2006

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tom 14

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nr Suppl.3

5

Alpha-1 antitrypsin: a potent anti-inflammatory and potential novel therapeutic agent

67%

Bergin D. A., Hurley K., McElvaney N. G., Reeves E. P.

Archivum Immunologiae et Therapiae Experimentalis

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2012

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tom 60

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nr 2

6

Augmentation of ventral tegmental area stimulation-induced feeding by both stimulation and lesion of the contralateral ventral tegmental area in the rat

67%

Maliszewska-Scislo M., Trojniar W.

Acta Neurobiologiae Experimentalis

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1999

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tom 59

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nr 4

7

Paradoxical augmentation of bradykinin-induced vasodilatation by xanthine-xanthine oxidase-derived free radicals in isolated guinea pig heart

67%

Olszanecki R., Kozlovski V. I., Chlopicki S., Gryglewski R. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,1

Increased generation of reactive oxygen species contribute to endothelial dysfunction in atherosclerosis, hypertension and heart failure. Recently, it was suggested that bursts of superoxide anions may inactivate endothelial surface-bound enzymes such as angiotensin converting enzyme (ACE). Here, we tested effects of xanthine/xanthine oxidase-derived superoxide anions on vascular responses and ACE activity in the isolated guinea pig heart. We analysed effects of intracoronary infusion of low concentration of xanthine oxidase (10 mU/ml) in the presence of xanthine (0,5 mM) (X/XO) on bradykinin, other endothelium-dependent and independent vasodilators (acetylcholine, ADP, SNAP), as well as vasoconstrictor responses to angiotensin I and angiotensin II. Surprisingly, X/XO significantly augmented coronary response to bradykinin without an effect on responses to ADP, acetylcholine, SNAP, angiotensin I and angiotensin II. In contrast, inhibition of ACE by perindoprilate (100 nM) resulted in augmentation of bradykinin-induced vasodilatation as well as diminution of angiotensin I-evoked vasoconstriction without an influence on other responses. In summary, in the isolated guinea pig heart, X/XO-derived free radicals selectively augmented coronary vasodilator response to bradykinin, which cannot be explained by X/XO- induced derangement of ACE. The mechanism of this paradoxical phenomenon, which might represent a defensive response of the coronary circulation to oxidative stress requires further investigations.