Estimating transboundary transported anthropogenic sulfate deposition in Japan using the sulfur isotopic ratio.

High emissions of air pollutants from Northeast Asia are strongly influenced by air quality as well as by ecosystems. This study investigated the spatiotemporal variations in the sulfur isotopic ratio (δ34S) in atmospheric deposition at eleven monitoring stations in Japan from 2011 to 2016 and estimated the amount of transboundary transported anthropogenic sulfate (TRB) deposition using mass balance calculations. The δ34S of sulfate in precipitation ranged from -0.42 to +22.7‰. Sea salt (SS), TRB, and domestic anthropogenic sources (DOM) were the dominant sources of sulfate deposition in Japan. TRB sulfate deposition was largest on the Sea of Japan side, with an annual average value of 1.5 ±â€¯0.3-6.9 ±â€¯0.5 mg m-2 d-1 (36-44%), followed by Mt. Happo (4.5 ±â€¯0.1 mg m-2 d-1; 88%), the Pacific Ocean side (1.5 ±â€¯0.8, 4.3 ±â€¯0.9 mg m-2 d-1; 24-50%), and the remote islands in the North Pacific Ocean (1.1 ±â€¯0.2, 2.0 ±â€¯0.8 mg m-2 d-1; 19-32%). TRB sulfate deposition on the Sea of Japan side was 2-12 times higher in winter and 1-2 times higher in summer than that of DOM. In contrast, TRB sulfate deposition on the Pacific Ocean side was 1.5-3 times higher in summer than in winter due to high precipitation levels. In Tokyo, the annual contribution from DOM sulfate deposition is approximately three times higher than that from TRB. Annual TRB sulfate deposition is lowest at Ogasawara at 1.1 ±â€¯0.2 mg m-2 d-1, and the annual oceanic DMS contribution to sulfate deposition is high, accounting for 1.3 mg m-2 d-1 (20 ±â€¯6%). The contribution of Asian dust was estimated to be 1-5.2 mg m-2 d-1(3-6%), which occurred in a single Asian dust event on the Sea of Japan side.

A novel mutation of the ceruloplasmin gene in a patient with heteroallelic ceruloplasmin gene mutation (HypoCPGM).

We found a novel missense mutation in the ceruloplasmin (Cp) gene in a patient with the heteroallelic Cp gene mutation (HypoCPGM). The patient was a 72-year-old woman who came to our hospital with a 1-year history of postural tremor of the hands. The diagnosis was made based on serum Cp and copper readings which were about half the normal levels, as well as MRI tests of her brain which showed characteristics for hereditary ceruloplasmin deficiency (HCD), known to be caused by the homoallelic Cp gene mutation. Polymerase chain reaction (PCR)-direct sequencing analysis of the Cp gene of the patient revealed a novel point mutation, A to T, at nucleotide position 82 in Exon 1. This mutation changes the Ile28 codon (ATT) to a Phe codon (TTT) (missense mutation). PCR-restriction analysis with restriction enzyme Tsp EI for the mutation revealed that both the patient and her son were heterozygotes for the mutation.

[Composition of milk and electrophoretic analysis of milk casein in herbivorous voles (Microtus montebelli)].

Milk samples were collected from herbivorous voles (Microtus montebelli) and their compositions were analyzed. Total solids, fat, protein and ash concentrations of vole's milk were very higher than those of cow's milk. The lactose concentration was very lower than that of milk of cow or mouse. The electrophoretic patterns of milk casein of vole were different markedly from those of bovine, but resembled to those of mouse.

Pathological study of tracheal and pulmonary lesions in autopsy cases of congenital esophageal atresia.

One of the major causes of death in infants with congenital esophageal atresia is the lung complication. Analysis of the Annual of Pathological Autopsy Cases in Japan from 1966 to 1969 revealed that the lung complications were seen in 81% of total cases. We have carried out a detailed histological study of the trachea and lung in 4 infants who died of congenital esophageal atresia. In three of them, ciliated epithelium of the trachea was replaced by stratified squamous epithelium and the alveoli were filled with numerous foamy cells. There were only a little inflammatory change in sections studied. The constant association of these two lesions suggests cause-and-effect relationship, and we are inclined to think that retention of foamy cells in the alveoli is due to the impaired mucociliary transport mechanism in the respiratory tract.