1. Sixty-one cases of compression of the ulnar nerve are reported, forty at the elbow and twenty-one at the wrist. Although contributory factors may include deformity, osteoarthritis, injury, ganglia and other tumours, the narrow anatomical confines of the nerve at these two levels are noteworthy and alone may produce nerve compression.

2. Careful clinical examination will usually determine the level of involvement if not the exact pathology. Surgical exploration is indicated both as a diagnostic and therapeutic procedure in most cases.

3. Following removal of the compressing agent rapid recovery occurred in most cases.

1. The clinical features, diagnosis and treatment of osteomalacia are discussed in relation to thirty-seven recently recognised cases. It is suggested that this disease is not uncommon in elderly women, among whom it is liable to be confused with senile osteoporosis. Osteomalacia may be distinguished by, firstly, the history, in which persistent skeletal pain of long duration and muscular weakness are typical of osteomalacia, but not of osteoporosis in which transient episodes of pain usually associated with a fracture are more characteristic. There is a high incidence of previous gastric surgery in the osteomalacia patients. Secondly, the physical examination shows skeletal tenderness in osteomalacia but this is not a particular feature of osteoporosis. A shuffling "penguin gait" suggests osteomalacia. Thirdly, the biochemistry shows a low plasma calcium and phosphate, and raised alkaline phosphatase levels commonly in osteomalacia but these are usually normal in osteoporosis. Reduced twenty-four-hour urinary calcium is characteristic of osteomalacia but not of osteoporosis. Fourthly, radiology will show diminished bone density which is common to both diseases, but if the changes are more marked in the peripheral bones than in the axial skeleton osteomalacia is suggested; the opposite is typical of osteoporosis. Skeletal deformity without fracture suggests osteomalacia, as do stress fractures and greenstick fractures in the elderly. Looser's zones are diagnostic of osteomalacia in which they are the most important radiological feature. Finally, histology will show the presence of excess osteoid tissue in undecalcified sections of bone in osteomalacia. This may be the earliest and most sensitive index of the disease and biopsy is indicated in all doubtful cases.

2. The etiology is discussed and it is suggested that a dietary deficiency of vitamin D, limited exposure to sunlight and mild degrees of malabsorption may all be important either alone or in combination. No satisfactory explanation is offered for the predominant female incidence.

3. A practical method of treatment is given and the dangers of uncontrolled administration of vitamin D indicated.

4. Treatment of osteomalacia is rapidly and consistently successful, and well justifies a thorough screening of all elderly patients presenting with weakness, skeletal pain, pathological fractures or with diminished radiographic density of bone.

1. Homografts of eighteen-day-old foetal femora in pure strains of mice showed no fundamental difference in behaviour from grafts of more mature bone and cartilage.

2. Growth of bone was limited to a short period after transplantation and was abolished by previous immunisation. Cartilage growth alone was responsible for the increase in size of these transplants and did not appear to be influenced by the presence of immunity.

3. There is no reason to suppose that bone from an immature source is likely to behave more favourably than more mature bone homografts in clinical use.

4. The limited growth of cartilage and the total failure of bone survival in the heterografts indicate an immune reaction ofa different order from that which develops against the homograft.

5. The different effect of the homograft immune reaction on cartilage and bone enabled certain conclusions to be drawn concerning the part played by these two tissues in determining the form of a bone. Cartilage growth and development is shown to be regulated in large part by intrinsic factors. Bone growth and form on the other hand is shown to be dependent largely upon extrinsic influences.

1 . Fresh bone autografts to a muscle bed in the rat gave rise to vigorous new bone formation from about the fourth day. The graft took the form of a hollow ossicle with central bone marrow at eighteen days: it became progressively more regular in outline and was still present at six months.

2. Fresh bone homografts produced two separate phases of new bone formation–early and late. In the early phase non-lamellar woven bone appeared at about the fourth day, continued to grow until eight days, and subsequently died. It arose from osteogenic cells of the homograft. In the late phase, which developed in relation to a few grafts after four weeks, the new bone was lamellar in character, and remained closely applied to the graft surface. Evidence is presented that this bone arose by metaplasia of the host connective tissues at the graft site. There was a local inflammatory response to the bone homograft.

3. Both phases of homograft new bone formation were abolished if the animal was prepared by a skin homograft from the same donor four weeks before, but not if four months elapsed between the two grafting procedures.

4. Freeze-dried bone homografts did not give rise to the early phase of homograft new bone but produced a few examples of the late phase after five months. The inflammatory response was less intense with freeze-dried homografts than with fresh homografts.

5. Skin homografts three weeks after fresh bone homografts from the same donor underwent an early rejection at five to six days.

6. Skin homografts three weeks after freeze-dried bone homografts from the same donor had a mean survival time of twelve days, which was significantly longer than the mean survival time of l0·9 days in normal rats.