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In recent years, the contraction of a disease and the death of sickness that have much influence on dietary life increase in the middle-age person, born in one figure of Showa. The authors investigated their consciousness of health and dietary life, the state of health, and the action of dietary life and others on 1000 middle-age persons, in order to obtain the basic data that are useful to increasing of the atention to nutritive problem and are helpful to spread the thought of "Promotion of Health". The results obtained are as follows ; 1. Many people have normal values in obesity degree but the distribution incline a little toward the fatness. 2. The rate of hypertensive is 12% and the border of hypertension is even 26% except the indistinctness. In the first half of the 50\u27s of the age the border is clearly increased as compared with that in the latter half of the 40\u27s. 3. The number of times of measuring of the blood pressure is more than twice a year and less than once a month, and the place of measuring is usually in a hospital. 4. The diseases attacked in the last five years are plenty of stomach-duodenal ulcer and hypertension. 5. Many people take the medical advices on the diseases of stomach and breast, on the other hand few people on the heart-vascular

Mutations in lipid transporter ABCA12 in harlequin ichthyosis and functional recovery by corrective gene transfer

Harlequin ichthyosis (HI) is a devastating skin disorder with an unknown underlying cause. Abnormal keratinocyte lamellar granules (LGs) are a hallmark of HI skin. ABCA12 is a member of the ATP-binding cassette transporter family, and members of the ABCA subfamily are known to have closely related functions as lipid transporters. ABCA3 is involved in lipid secretion via LGs from alveolar type II cells, and missense mutations in ABCA12 have been reported to cause lamellar ichthyosis type 2, a milder form of ichthyosis. Therefore, we hypothesized that HI might be caused by mutations that lead to serious ABCA12 defects. We identify 5 distinct ABCA12 mutations, either in a compound heterozygous or homozygous state, in patients from 4 HI families. All the mutations resulted in truncation or deletion of highly conserved regions of ABCA12. Immunoelectron microscopy revealed that ABCA12 localized to LGs in normal epidermal keratinocytes. We confirmed that ABCA12 defects cause congested lipid secretion in cultured HI keratinocytes and succeeded in obtaining the recovery of LG lipid secretion after corrective gene transfer of ABCA12. We concluded that ABCA12 works as an epidermal keratinocyte lipid transporter and that defective ABCA12 results in a loss of the skin lipid barrier, leading to HI. Our findings not only allow DNA-based early prenatal diagnosis but also suggest the possibility of gene therapy for HI