Three sets of ADCP data obtained from the upper ocean are used to examine possible influence of parametric subharmonic instability (PSI) at ϕc ≈ 13–15°N. Both kinetic‐energy and shear spectra at ϕc reveal that significant peaks appear at subharmonic frequencies of diurnal internal tides. Especially, the 0.5 K1 (subharmonic of K1 tides) can be trapped poleward of its critical latitude (14.52°N), significantly distinguished from wind generated near‐inertial internal waves. Moreover, the enhanced 0.5 K1 motions are more or less subject to a fortnightly spring‐neap circle. Relative to a higher latitude (say 18°N), diurnal motions at ϕc are greatly weakened. In contrast, small vertical‐scale motions in the inertial band and the shear induced by these motions are significantly enhanced. Likely, PSI mechanism plays an important role in these observations, whilst trapped sub‐inertial waves (0.5 K1) may be associated with the presence of negative sub‐inertial eddies.
Monotherapy of α‐glucosidase inhibitor (α‐GI) or dipeptidyl peptidase 4 (DPP4) inhibitor does not sufficiently minimize glucose fluctuations in the diabetic state. In the present study, we evaluated the combined effects of various of α‐GI inhibitors (acarbose, voglibose or miglitol) and sitagliptin, a DPP4 inhibitor, on blood glucose fluctuation, insulin and active glucagon‐like peptide‐1 (GLP‐1) levels after nutriment loading in mice. Miglitol and sitagliptin elicited a 47% reduction (P < 0.05) of the area under the curve of blood glucose levels for up to 2 h after maltose‐loading, a 60% reduction (P < 0.05) in the range of blood glucose fluctuation, and a 32% decrease in plasma insulin compared with the control group. All three of the combinations elicited a 2.5–4.9‐fold synergistic increase in active GLP‐1 (P < 0.05 vs control). Thus, combined treatment with the α‐GI miglitol, which more strongly inhibits the early phase of postprandial hyperglycemia, and DPP4 inhibitor yields both complementary and synergistic effects, and might represent a superior anti‐hyperglycemic therapy. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00081.x, 2011)
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