Vorticity flux through the Yucatan Channel and Loop Current variability in the Gulf of Mexico
[1] Recent observations (the CANEK Program [Candela et al., 2002]) suggest that potential vorticity (PV) flux anomaly (VFA) at Yucatan Channel may serve as a useful indicator of Loop Current variability, including Loop Current extension, retraction, and eddy shedding. Intuitively, anticyclonic VFA extends the Loop Current into the Gulf of Mexico and cyclonic VFA causes retraction or even shedding. However, this intuition is inconsistent with PV conservation. The problem is reexamined here by careful analyses of the relation between VFA and Loop Current variability using (1) the results of a 15-year numerical simulation of shedding specified with simple forcing, and (2) CANEK and satellite observations. Both model and observations indicate that Loop Current eddy shedding or retraction tends to occur shortly (1� 2 months) after the influx of VFA at Yucatan has turned anticyclonic, and that these events are sometimes preceded by a more prolonged period of influx of cyclonic VFA. These findings suggest that contrary to intuition, influx of cyclonic VFA tends to extend the Loop Current into the Gulf, thus making the Loop Current more susceptible to retract or shed an eddy, and influx of anticyclonic VFA may then ‘‘trigger’’ retraction or eddy shedding. However, the Loop Current’s behaviors are much more complex than can be prescribed by these simple rules. A much longer observational data set, coupled with more refined model experiments and sophisticated analyses, is required to further quantify the phenomenon. INDEX TERMS: 4520 Oceanography: Physical: Eddies and mesoscale processes; 4255 Oceanography: General: Numerical modeling; 4576 Oceanography: Physical: Western boundary currents; 4243 Oceanography: General: Marginal and semienclosed seas; KEYWORDS: vorticity flux, Loop Current, Yucatan Channel Citation: Oey, L.-Y. (2004), Vorticity flux through the Yucatan Channel and Loop Current variability in the Gulf of Mexico, J. Geophys. Res., 109, C10004, doi:10.1029/2004JC002400.
A model study of the vertically integrated transport variability through the Yucatan Channel: Role of Loop Current evolution and flow compensation around Cuba
[1] In the paper “A model study of the vertically integrated 
transport variability through the Yucatan Channel: Role of 
Loop Current evolution and flow compensation around 
Cuba” by Lin et al. (Journal of Geophysical Research, 114, 
C08003, doi:10.1029/2008JC005199, 2009), in the last 
sentence of paragraph 31, the word “westward” in “drives 
enhanced westward” should be “eastward.”
Protective effect of ginsenoside Re on acute gastric mucosal lesion induced by compound 48/80
The protective effect of ginsenoside Re, isolated from ginseng berry, against acute gastric mucosal lesions was examined in rats with a single intraperitoneal injection of compound 48/80 (C48/80). Ginsenoside Re (20 mg/kg or 100 mg/kg) was orally administered 0.5 h prior to C48/80 treatment. Ginsenoside Re dose-dependently prevented gastric mucosal lesion development 3 h after C48/80 treatment. Increases in the activities of myeloperoxidase (MPO; an index of neutrophil infiltration) and xanthine oxidase (XO) and the content of thiobarbituric acid reactive substances (TBARS; an index of lipid peroxidation) and decreases in the contents of hexosamine (a marker of gastric mucus) and adherent mucus, which occurred in gastric mucosal tissues after C48/80 treatment, were significantly attenuated by ginsenoside Re. The elevation of Bax expression and the decrease in Bcl2 expression after C48/80 treatment were also attenuated by ginsenoside Re. Ginsenoside Re significantly attenuated all these changes 3 h after C48/80 treatment. These results indicate that orally administered ginsenoside Re protects against C48/80-induced acute gastric mucosal lesions in rats, possibly through its stimulatory action on gastric mucus synthesis and secretion, its inhibitory action on neutrophil infiltration, and enhanced lipid peroxidation in the gastric mucosal tissue.