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Abstract: The seasonal and interannual changes in surface nutrients, dissolved inorganic carbon (DIC) and total alkalinity (TA) were recorded in the North Pacific (30–54°N) from 1995 to 2001. This study focuses on the region north of the subarctic boundary (∼40°N) where there was extensive monthly coverage of surface properties. The nutrient cycles showed large interannual variations in the eastern and western subarctic gyres. In the Alaska Gyre the seasonal depletion of nitrate (ΔNO3) increased from 8–14 µmol kg−1 in 1995–1999 to 21.5 µmol kg−1 in 2000. In the western subarctic the shifts were similar in amplitude but more frequent. The large ΔNO3 levels were associated with high silicate depletions, indicating enhanced diatom production. The seasonal DIC:NO3 drawdown ratios were elevated in the eastern and central subarctic due to calcification. In the western subarctic and the central Bering Sea calcification was significant only during 1997 and/or 1998, two El Niño years. Regional C/N stoichiometric molar ratios of 5.7 to 7.0 (>40°N) were determined based on the years with negligible or no calcification. The annual new production (NPa) based on ΔNO3 and these C/N ratios showed large interannual variations. NPa was usually higher in the western than in the eastern subarctic. However, values of 84 gC m−2yr−1 were found in the Alaska Gyre in 2000 which is similar to that in the most productive provinces of the northern North Pacific. There were also large increases in NPa around the Alaska Peninsula in 1997 and 1998. Finally, the net removal of carbon by the biological pump was estimated as 0.72 Gt C yr−1 in the North Pacific (>30°N).

Unambiguous syntheses of four unreported monomethylated derivatives of 3-phenyldihydro-1,2,4-triazin-6(1H)-ones, namely, the 1-methyl (2), 2-methyl (3), 4-methyl (4) and the imidic O-methyl derivative (5), are described. Regioselectivity was achieved for the synthesis of (2) by addition of ethyl glycinate to the 1,3-dipolar nitrile imine derived from N- methylbenzohydrazonoyl bromide hydrobromide (8). The key step for the synthesis of (3) was addition of benzyl 3-methylcarbazate (14) to ethyl N-[ chloro (phenyl) methylene ] glycinate (15b). The 4-methyl compound (4) was prepared by cycloaddition of ethyl N-( thiobenzoyl ) sarcosinate (21) with hydrazine hydrate, and the O-methyl compound (5) was prepared by reaction of sodium methoxide with 6-chloro-3-phenyl-4,5-dihydro-1,2,4-triazine (23).

An unambiguous synthesis of the published structure for the natural product sinharine (1) showed that the assignment was incorrect. (E)-3-( Methylthio )-N-(2-phenylethyl) propenamide (4) was proposed as an alternative structure and this was confirmed by synthesis. Similarly the literature proposal for the structure of methylsinharine was reviewed and the natural product tentatively reassigned as (E)-N-methyl-3-( methylthio )-N-(2-phenylethyl) propenamide.

Several derivatives of the novel 1,4,2-oxathiazin-6(5H)-one system were prepared by reaction of mercapto carboxylic acids with substituted carbohydroximoyl chlorides and subsequent cyclization of the resulting oxime acid with dicyclohexylcarbodiimide . The stability of the 1,4,2-oxathiazin-6(5H)-one system to acid and base conditions as well as to various nucleophiles was investigated.

The results of the work on experimental rickets in rats have shown that rickets can be produced by diets which are poor in phosphorus and rich in calcium or diets which are poor in calcium and rich in phosphorus. A condition produced in that manner can be prevented or restored to normal by exposing the animals to a sufficient amount of light of certain wave lengths or by administering cod liver oil which contains a substance that affects the calcium and phosphorus metabolism. There is no evidence at present that this substance regularly occurs in natural foodstuffs, and, therefore, there seems no valid reason to put it into the class of vitamins. Until it has been shown that the curative agent in cod liver oil is a component of normal foods, we cannot assume that rickets is due to a vitamin deficiency. This, then, leaves us, in spite of the accumulated data on experimental rickets in animals, without any definite information as to the physiological changes which lead to rickets in children since children will develop rickets on diets well balanced with regard to calcium and phosphorus. It is important, therefore, to learn more concerning other factors which influence rickets-production, in order to gain an understanding of the possible causes of human rickets when it is produced under conditions where dietary factors cannot be held responsible. We believe that we have obtained evidence of a factor not taken into consideration in the recent work on experimental rickets.Ernst Schlossl in one of his monographic papers on rickets has called attention to the fact that contrary to the hypothesis held at one time, according to which rickets is due to an acidosis, it is found that rickets seems to develop more frequently under conditions rather the opposite of an acidosis.