The variation with pH of the surface potentials of spread monolayers of weak acids or bases may be used to calculate the intrinsic ionization constants of the film-forming molecules. The method is valid for condensed monolayers at the air/water interface for regions of a low degree of ionization only. The intrinsic constants for stearic acid and nonadecylamine monolayers are similar to the ionization constants for short-chain fatty acids and amines in aqueous solution. The relations between this and other methods of treating the ionization of a weak acid or base in a surface are discussed.

In the rabbit 2:3:5:6-tetrachloronitrobenzene is metabolized by reduction of the nitro group, hydroxylation and mercapturic acid formation (Bray, Hybs, James & Thorpe, 1953). The last reaction is of particular interest since it is accompanied by loss of a nitro group directly attached to the benzene ring. Two further examples of this type of reaction were encountered when pentachloronitrobenzene and 2:3:4:6-tetrachloronitrobenzene were given to rabbits (Betts, James & Thorpe, 1953). A more detailed study of the metabolism of these two compounds is now reported. The stability of the nitro group in pentachloro-, the tetrachloro-and three trichloro-nitrobenzenes has been examined in relation to formation of mercapturic acids from the highly chlorinated nitrobenzenes. METHODS Melting points are uncorrected. Materials. Pentachloronitrobenzene, m.p. 1460, was supplied by Bayer Agriculture Ltd. and Hickson and Welch Ltd. and 2:3:5:6-tetrachloronitrobenzene, m.p. 990, by Bayer Agriculture Ltd. 2:3:4:6-Tetrachloronitrobenzene, m.p. 410, was prepared from 2:4:6-trichloroaniline, which was converted by a Sandmeyer reaction into 1:2:3:5tetrachlorobenzene; this was nitrated by refluxing for 0-5 hr. with HNO3 (sp.gr. 1-52) to give 2:3:4:6-tetrachloronitrobenzene. (Details were kindly supplied by Dr M.

Insulin or exercise stimulates skeletal muscle glucose transport, most likely by increasing both the number and activity of glucose transporters in the plasma membrane. Skeletal muscle glucose transport of genetically obese Zucker rats (fa/fa) displays a severe insulin resistance that results, at least in part, from a failure of net transporter translocation to the cell membrane (King, P., E. D. Horton, M. Hirshman, and E. S. Horton. J. Clin, Invest. 90: 1568-1575, 1992). The purpose of the present study was to determine if the obese rat muscle was also resistant to the action of acute exercise to increase glucose transport and, if so, to determine if the defect involved transporter translocation as seen in the resistance to insulin. The muscle glucose transport system was investigated in plasma membranes isolated from postprandial, sedentary or acutely exercised, lean and obese Zucker rats. Measurements of D- and L-glucose uptake by membrane vesicles under equilibrium exchange conditions indicated that an acute bout of exercise resulted in a threefold increase in the maximum velocity (Vmax) for lean animals (5.7 vs. 17.6 nmol.mg protein-1.min-1) and a 4.5-fold increase in the Vmax for obese rats (4.1 vs. 18.6 nmol.mg protein-1.min-1). For both lean and obese animals, this increase in transport was associated with an increase in transporter number measured by cytochalasin B binding (1.6- and 2.2-fold, respectively) and with an increase in the average carrier turnover number (1.9- and 2.0-fold, respectively). The results indicate that, unlike a maximal insulin stimulus, acute exercise of the obese Zucker rat promotes both transporter translocation and transporter activation in skeletal muscle.

Summary A chronic degenerative neurological disorder is described which is characterized by tics, grimacing, involuntary movements, a severe disturbance of swallowing and a concurrent malformation of the erythrocytes. This condition is clearly different from familial hypo-betalipoproteinaemia and abetalipoproteinaemia, the two previously described neurological disorders associated with abnormal red cells.

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