A cross-investigation between thiamin deficiency and the physical condition of elderly people who require nursing care.

In recent years the occurrence of thiamin deficiency diseases has increased particularly among elderly people and there has been some speculation about whether or not any particular factors exist. In this study, we focused on elderly people requiring constant care in nursing homes and we conducted an accurate condition survey of total thiamin concentration in whole blood as a means of nutritional assessment. The total number of participants was 14 males and 60 females who were residing in a nursing home; they were aged between 65 and 105 y old. All of the subjects agreed to take part in our research. We conducted the following tests: anthropometric measurements, blood examination including total thiamin levels, and also physical functions such as in the level of nursing care required and tests of other physical conditions. The average±standard deviation of thiamin concentration was 22.4±8.9 ng/mL and the number of people with a deficient condition (less than 20 ng/mL) was 42, which was 56.8% of the total. From these results, the existence of thiamin deficiency is validated in more than half of the elderly people who require nursing care. On the other hand, the method of meal intake for all participants who have a thiamin deficiency was oral intake and for those who were non-deficient in thiamin, the percentage of tube feeding or nutritional supplementation intravenously was 37.5%, which was a significantly high value.

Bidirectional Ca2+ coupling of mitochondria with the endoplasmic reticulum and regulation of multimodal Ca2+ entries in rat brown adipocytes.

How the endoplasmic reticulum (ER) and mitochondria communicate with each other and how they regulate plasmalemmal Ca(2+) entry were studied in cultured rat brown adipocytes. Cytoplasmic Ca(2+) or Mg(2+) and mitochondrial membrane potential were measured by fluorometry. The sustained component of rises in cytoplasmic Ca(2+) concentration ([Ca(2+)](i)) produced by thapsigargin was abolished by removing extracellular Ca(2+), depressed by depleting extracellular Na(+), and enhanced by raising extracellular pH. FCCP, dinitrophenol, and rotenone caused bi- or triphasic rises in [Ca(2+)](i), in which the first phase was accompanied by mitochondrial depolarization. The FCCP-induced first phase was partially inhibited by oligomycin but not by ruthenium red, cyclosporine A, U-73122, a Ca(2+)-free EGTA solution, and an Na(+)-free solution. The FCCP-induced second phase paralleling mitochondrial repolarization was partially blocked by removing extracellular Ca(2+) and fully blocked by oligomycin but not by thapsigargin or an Na(+)-deficient solution, was accompanied by a rise in cytoplasmic Mg(2+) concentration, and was summated with a high pH-induced rise in [Ca(2+)](i), whereas the extracellular Ca(2+)-independent component was blocked by U-73122 and cyclopiazonic acid. The FCCP-induced third phase was blocked by removing Ca(2+) but not by thapsigargin, depressed by decreasing Na(+), and enhanced by raising pH. Cyclopiazonic acid-evoked rises in [Ca(2+)](i) in a Ca(2+)-free solution were depressed after FCCP actions. Thus mitochondrial uncoupling causes Ca(2+) release, activating Ca(2+) release from the ER and store-operated Ca(2+) entry, and directly elicits a novel plasmalemmal Ca(2+) entry, whereas Ca(2+) release from the ER activates Ca(2+) accumulation in, or release from, mitochondria, indicating bidirectional mitochondria-ER couplings in rat brown adipocytes.