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ALLOGRAFT rejection is usually grouped with delayed hypersensitivity, acquired cellular resistance to infection and some types of auto-immune disease as a form of cell-mediated immunity, implying that all these phenomena may share a common immunological mechanism. The rejection of skin allografts is generally accompanied by the development of delayed-type hypersensitivity to graft antigens. Reactions having the time-course and macroscopic and microscopic features of skin reactions in delayed-type hypersensitivity have been elicited by injecting donor antigen (in the form of lymphoid cells or extracts thereof) into sensitized humans, guinea-pigs, hamsters, dogs and rats1–3. Similar reactions could not be elicited in mice1. Here we describe the induction of delayed hypersensitivity reactions in the footpads of mice. Because resistance to isografts of chemically induced tumours in mice may also be a form of cell mediated immunity4, we have also tested whether similar reactions can be elicited after tumour isografting in mice.

Cirrhosis following small-bowel bypass with jejunocolic anastomosis for obesity is well recognized (1-7). Opinions differ concerning permanent liver damage following jejunoileal bypass, but most of the evidence supports jejunoileal bypass as being relatively safe (816) and there are only one or two well documented cases of death from cirrhosis following jejunoileal shunt (15, 17). We report another such case.

The e.s.r. spectra of α- and of β-naphthoxyl radicals have been obtained and analysed. Unambiguous assignments of the coupling constants have been found by getting spectra from a number of substituted naphthols and these have been confirmed by generating radicals from the dihydroxynaphthalenes in acid solution and analysing the corresponding e.s.r. spectra.