Bioavailability of Oil-Based and β-Lactoglobulin-Complexed Vitamin A in a Rat Model

β-Lactoglobulin is capable of binding fat-soluble compounds including vitamin A palmitate and is suggested to specifically enhance intestinal uptake of retinol. In this study, bioavailability of a vitamin-A-retinyl palmitate complex in skim milk and in water-based liquids was investigated in vitamin-A-depleted rats. First, rats were fed a vitamin-A-free pellet diet for 6 wk and were thereafter gavage-fed with vitamin A in oil, vitamin-A-β-lactoglobulin complex, vitamin A in oil + skim milk, and vitamin-A-β-lactoglobulin + skim milk for 2 wk and 42 wk. Vitamin A repletion, as judged by vitamin A accumulation in serum and liver, occurred in all the treatments. Vitamin-A-β-lactoglobulin complex treatments had statistical equivalence with oil-based vitamin A treatments. In a second experiment, vitamin-A-depleted rats were fed UHT-processed skim milk fortified with either oil-based or freeze-dried β-lactoglobulin-complexed retinyl palmitate. Liver and serum vitamin A were analyzed by HPLC to indicate vitamin A status in the rats. Results showed no significant difference in bioavailability of retinyl palmitate from milk made with either regular oil-based or β-lactoglobulin-complexed fortifiers. The vitamin-A-β-lactoglobulin complex, being water soluble, may be useful for fortification of nonfat products.

Binder-Free Pellet Fabrication of Ultra-Fine Poly-Si Powder for Economical Production of Solar Grade Si Ingot

The consolidation process of ultra fine Si powders, generated as by-product during the decomposition process of silane gases, was systematically investigated for use as economical solar-grade feedstock. Si powder compacts were tried to fabricate by a consolidation process without a binding agent and then their density ratio and strength were evaluated. The Si powders in as-received state were not pure enough to be used alone as solar grade feedstock material. After the adequate chemical treatments, a sufficiently high purity above solar-grade was able to be achieved.

Ischemic preconditioning depends on interaction between mitochondrial KATP channels and actin cytoskeleton

Both mitochondrial ATP-sensitive K+(KATP) channels and the actin cytoskeleton have been proposed to be end-effectors in ischemic preconditioning (PC). For evaluation of the participation of these proposed end effectors, rabbits underwent 30 min of regional ischemia and 3 h of reperfusion. PC by 5-min ischemia + 10-min reperfusion reduced infarct size by 60%. Diazoxide, a mitochondrial KATP-channel opener, administered before ischemia was protective. Protection was lost when diazoxide was given after onset of ischemia. Anisomycin, a p38/JNK activator, reduced infarct size, but protection from both diazoxide and anisomycin was abolished by 5-hydroxydecanoate (5-HD), an inhibitor of mitochondrial KATP channels. Isolated adult rabbit cardiomyocytes were subjected to simulated ischemia by centrifuging the cells into an oxygen-free pellet for 3 h. PC was induced by prior pelleting for 10 min followed by resuspension for 15 min. Osmotic fragility was assessed by adding cells to hypotonic (85 mosmol) Trypan blue. PC delayed the progressive increase in fragility seen in non-PC cells. Incubation with diazoxide or pinacidil was as protective as PC. Anisomycin reduced osmotic fragility, and this was reversed by 5-HD. Interestingly, protection by PC, diazoxide, and pinacidil could be abolished by disruption of the cytoskeleton by cytochalasin D. These data support a role for both mitochondrial KATP channels and cytoskeletal actin in protection by PC.