The effects of the signs and structures of charged groups in modified β-cyclodextrins on their binding and catalytic properties were examined in aqueous solutions by using ammonium salt of mono(6-sulfonato-6-deoxy)-β-cyclodextrin and hydrogencarbonate salts of mono(6-trimethylammonio-6-deoxy)- and mono[6-(1-pyridinio)-6-deoxy]-β-cyclodextrins as charged hosts. An ionic guest was bound more strongly to an oppositely charged host than to an identically charged host. Binding constants for charged host-guest systems were affected by a change in the ionic strength and by the addition of dimethyl sulfoxide to an aqueous solution. The catalytic effects of the charged hosts on the alkaline hydrolyses of o-, m-, and p-acetoxybenzoic acids were also different from those of the parent β-cyclodextrin. These results could be explained in terms of electrostatic, steric, and hydrophobic interactions between the hosts and guests.
The serum of thyro‐parathyroidectomized dogs and cats produces some increase of excitability in the isolated nerve of the frog, but has no special effect on the contraction of isolated muscle, nor does it cause tremors in the frog's sartorius muscle. The serum of both thyroidectomized and normal dogs and cats has no effect or a very feeble (depressive or excitatory) effect on frog's nerve, thus showing itself much more inert than the serum of thyro‐parathyroidectomized animals. But on muscle the effect is the same in all. A solution of guanidine carbonate above.01 % causes some increase of nervous excitability, approaching that caused by the serum of the thyro‐parathyroidectomized animals. On muscle, guanidine carbonate solutions above .025 % show a depressive effect, while a .001 % solution produced no effect. None of the solutions of guanidine carbonate within the concentration range studied produced any spontaneous twitching in the muscle. It is already known that nerve is affected by a guanidine solution of lower concentration than affects muscles. In these experiments the muscle preparation was not denervated, so that the correct expression would be muscle with its neural elements. These experimental results taken in conjunction with the results of the ivestigations of previous workers on the problem of tetany give reason for supposing that the serum of animals in a condition of tetania parathyreopriva may contain some exciting substance which is present in just sufficient amount to affect the excitability of motor nerves but not of muscles. This conclusion is put forward with reserve, since my experiments on this subject are not yet complete. The similarity in the action on nerve and muscle of guanidine carbonate and or the serum from animals in a condition of tetania parathyreopriva lends support to the experimental conclusions adduced by previous investigators that some guanidine‐like body may be an agent in producing the hyperexcitability of peripheral motor nerves which occurs in the condition of tetany.
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