1147 amount of
electrolytes present in the body. However, sophisticated whole body-measurement of electrolytes is not possible in most clinical situations, and in practice the main problem is to know how far an observed serum-
calciferol. This conclusion is not supported by data from two of our patients, children with cystinosis and rickets. In these patients the steady-state plasma levels of 25-hydroxyvitamin D (25-OH D) were measured while 25-H.C.C. was being used in treatment. Later the levels were measured while vitamin Dand vitamin D3, respectively, were being administered. All medications were given orally. The findings were:
electrolyte
pattern should influence management in a particular case. If the " sick cell " hypothesis is correct, then it might be expected that many of the observed electrolyte disturbances would be corrected simply by treating the underlying illness. This is indeed often found to be the case. In many other instances, the addition of potassium supplements (or stopping thiazide diuretics if these drugs are being given) corrects not only hypokalsemia but also quite severe hyponatraemia. Trinity Hospital, 19 Trinity Road, Taunton, Somerset.
*
osteomalacia the curative dosages of native ergocalciferol and cholecalciferol or of 25 hydroxyergocalciferol and 25 hydroxycholecalciferol administered by the same route must be compared directly.
uraemic
In January of this year a 3-month-old child was sent into this hospital with a history of an apnoeic attack following a coughing spasm in the second week of what sounded like whooping-cough.
University College Hospital Medical School, University Street,
The elder sister of this child had had a similar illness for the previous three weeks. The mother had treated this apnoeic attack by placing the child under a cold water tap. By the time he was admitted he was well and the chest was clear apart from a few crepitations at the bases. Immediately after admission he had a generalised convulsion with clonic spasms of all limbs, for which he had to be intubated, given intravenous diazepam, and ventilated. Fundoscopy at this time was normal, as was the cerebrospinal fluid. It was thought that he may have had an intracerebral bleed (or possibly an encephalopathy) secondary to his whoopingcough. However, a sample of blood taken before this convulsion showed severe hyponatraemia (116 meq. per 1.) and severe hypochlorsemia (80 meq. per 1.). On requestioning the parents, it appeared that vomiting had been very frequent in the previous two weeks and it would appear likely that the child had developed hyponatrsemia secondary to the vomiting, which in turn was secondary to the pertussis, the hyponatraemia being responsible for the convulsion before admission and for the alarming convulsion in the He was treated with intermittent positive-pressure ward. ventilation and intravenous fluid therapy, and electrolytes rapidly returned to normal. Six hours after admission the convulsions had stopped, and the child was taken off the ventilator two days after admission. He was also given chloramphenicol and made a good recovery, although for the next two weeks he had obvious paroxysmal
PARACETAMOL MEASUREMENT SIR,—Prescott and Matthew2 believe that cysteamine is the treatment of choice for paracetamol poisoning, but the safety of cysteamine in man has yet to be established. Since only about 1% of those who take a paracetamol overdose die,3 it is important to ensure that cysteamine is only administered to those patients who really need it.4 The plasma-paracetamol level has been shown to be a reasonably reliable predictor for subsequent hepatic necrosis, and, since cysteamine should be given within 10 hours of paracetamol ingestion3asimple, reliable, and rapid method of estimating it is needed. The following is such a method, and is based on a recently reported colorimetric method.7 1 ml. of
plasma is added to a 25 ml. stoppered centrifuge containing 2 ml. 10% trichloroacetic acid. After thorough mixing, the tube is centrifuged briefly and the clear supernatant decanted into a 25 ml. test-tube containing 1 ml. 6N hydrochloric acid and 2 ml. 10% sodium nitrite. After allowing the contents to stand for 2 minutes, 2 ml. of 15% sulphamic acid is added carefully, followed by 5 ml. 10% NaOH. The ensuing yellow colour is measured at 430 nm. against a reagent blank
tube
seemed to be a minor epidemic of whooping-cough in this area at the time seem to confirm the diagnosis as pertussis complicated by hyponatraemic convulsions. ,
J. R. HARPER M. J. MAGUIRE.
VITAMIN-D METABOLISM IN CHRONIC RENAL FAILURE
SIR,-Dr Eastwood and Professor de Wardener (April 26, p. 981) found that the parenteral administration of 40 µg. per day of hydroxycholecalciferol (25-H.c.c.) healed
osteomalacia in chronic renal failure and imply that this is equivalent to giving the patients a similar dose of chole-
C. E. DENT MERCEDES DOMENECH J. M. GERTNER.
London WC1E 6JJ.
whooping-cough with, initially, frequent apnoeic attacks, paroxysms of coughing, and a typical whoop. A chest X-ray showed inflammatory changes throughout the right lung, which cleared. The diagnosis was not confirmed bacteriologically, but the child’s subsequent course, his sister’s illness, and what
Hospital,
Stamp.
In order to make a valid comparison of the relative efficacy of ergocalciferol (D2) and cholecalciferol (Dg) in
SIR,-Convulsions are a recognised complication of whooping-cough, as is vomiting and metabolic alkalosis, even to the point of tetany. These may, however, combine to present in an alarming fashion, as in the following case.
General
C. B.
Thus, in patient 1 the plasma level showed little change when 25 times by weight the dose of Da was substituted for 25-H.C.C.; while in patient 2 a six-fold increase in dosage led to a three-fold fall in plasma 25-OH D level. This is probably the result of poor conversion of vitamin D and D 3 to the 25 hydroxylated form as a result of feedback inhibition of hepatic calciferol 25-hydroxylase by the high circulating levels of 25-OH D.1
P. F. ROE.
HYPONATRÆMIA AND CONVULSIONS IN WHOOPING-COUGH
Northampton NN1 5BD.
Kindly determined by Dr T.
of water. The calibration jjLg. per ml. plasma.
curve
is linear
over
the range 100-500
The method takes 5-10 minutes and all reagents are standard laboratory issue, readily made up, and stable with the exception of the nitrite reagent, which should be made up immediately before use. The possibility of providing the reagents in the form of a test kit for rapid in-ward assays is being pursued. Olmdahl, J. L., De Luca, H. F. Physiol. Rev. 1973, 53, 327. Prescott, L. F., Matthew, H. Lancet, 1974, i, 998. Wright, N. Prescribers J. 1974, 14, 78. Gazzard, B. G., Murray-Lyon, I. M., Davis, M., Thompson, R. P. H., Williams, R., Goulding, R. Lancet, 1974, i, 864. 5. Stewart, M. J. ibid. p. 1162. 6. Prescott, L. F., Swainson, C. P., Forrest, A. R. W., Newton, R. W., Wright, N., Matthew, H. ibid. p. 588. 7. Chefetz, L., Daly, R. E., Schriftman, H., Lomner, J. J. J. pharm. Sci. 1971, 60, 463.
1. 2. 3. 4.
1148 The reaction is specific for paracetamol, and there is no interference from the sulphate and glucuronide conjugates of paracetamol. In addition, presence of the following substances at the 50 (1.g. per ml. level does not interfere
Obituary WILLIAM
with the reaction:
amitryptiline, amphetamine, caffeine, chlordiazepoxide, chlormezanone, chlorpromazine, chlorpropamide, cocaine, diazepam, diphenhydramine, diphenyldantoin, dihydrocodeine, imipramine, indomethacin, lorazepam, meprobamate, methadone, methaqualone, morphine, nitrazepam, oxypertine, pentazocine, pentobarbitone, promethazine, salicylate, strychnine, theophylline, tolbutamide. Metabolic Studies Department, Sterling-Winthrop Research and
Development Division, Edgefield Avenue, Newcastle upon Tyne NE3 3TT.
JOHN P. GLYNN STEPHEN E. KENDAL.
SURVIVAL OF THE GENETICALLY INCOMPATIBLE FETAL GRAFT
SIR,—Dr Finn (April 12, p. 835) proposed an attractive hypothesis to account for the non-rejection of the fetal allograft. He postulated that shared surface-repellent molecules prevent competent cells.
contact
of maternal and fetal immuno,
We have previously suggested that oc-fetoprotein (A.F.P.) could potentially abrogate maternal lymphocyte immune 1 Murgita and Tomasi 2,3 responses against the fetus. demonstrated suppression of humoral immune responses, mixed lymphocyte reactivity, and mitogen-induced lymphocyte transformation by A.F.P. A.F.P. may serve as a natural immunosuppressive agent that abrogates potentially harmful maternal immune responses. A.F.P. is a major serum-protein in the fetus which crosses the placental barrier to the maternal circulation where it could serve as
immunosuppressive agent.4 Furthermore, A.F.P. may inhibit lymphopoiesis: we have reported a patient with haemochromatosis and lymphocytosis who developed an A.F.P.-positive hepatocellular carcinoma and lymphopenia. Her total lymphocyte counts during a 24-year period were 2305 per c.mm. at 37 years of age, 10,089 per c.mm. at 46 years, 9920 per c.mm. at
an
54 years, and then plummeted to 1366 per c.mm. after the appearance of an A.F.P.-synthesising hepatoma. The lymphopenia may have resulted from factors other than A.F.P., but this speculation merits consideration. Other mechanisms in addition to surface-repellent molecules need to be considered to explain the non-rejection of the fetus. We have suggestedthat combined fail-safe mechanisms, including placental barriers, blocking antibodies, hormones, and possibly A.F.P. and other fetal proteins 6 may act concertedly to prevent maternal rejection of the fetus. The placenta is an endocrine organ strategically placed to optimise the impact of the immunosuppressive effect of oestrogen, progesterone, cortisol, prolactin, and chorionic gonadotrophin.7-1o Commonwealth of Massachusetts Medical Center, 55 Lake Avenue North, Worcester, Massachusetts 01605, U.S.A.
M.D., Hon.D.Sc.Belf., D.Sc.Glasg., F.R.C.S., F.R.C.O.G., F.R.S.E.
Prof. William Hamilton, professor emeritus of anatomy in the University of London since 1971, died on May 3 at the age of 71. The passing of this distinguished anatomist and embryologist will be mourned by the many, at home and abroad, who have a vivid recollection of him as teacher, colleague, or friend. the Queen’s of exceptional honours in the B.SC. examination in 1926, and in the M.B. in 1929. He proceeded to the M.sc. in 1931 and then went as a lecturer in anatomy to Glasgow University, where he was awarded the D.sc. degree in 1934, and where, under the influence of Thomas Hastie Bryce, he developed his life-long passion for embryology. From Glasgow he went to St. Thomas’s Hospital Medical School as deputy director of anatomy, and he was appointed to the chair of anatomy in the University of London at St. Bartholomew’s Hospital Medical College in 1936. In 1945 he returned to Glasgow as regius professor of anatomy, but personal reasons, combined with the prospect of starting up a new department, led him to accept the appointment to the newly created chair of anatomy at Charing Cross Hospital Medical School in 1947, and he remained in post there until his retirement in 1970. During this period he was president of the Anatomical Society of Great Britain and Ireland in 1953-55. As dean of Charing Cross Hospital Medical School in 1956-62, he succeeded in obtaining for the school chairs in obstetrics and gynaecology, surgery, and medicine, in that order, over the short space of 3 years. It was also during his deanship that plans were laid for the new hospital and medical school at Fulham, and he played a leading part in determining the existing integrated pattern of buildings. In 1933 he married Maimie, only daughter of Samuel Young of Belfast; and it was a source of great joy to him that his four sons all became members of the medical profession (two of them are consultant surgeons), and that his daughter became a distinguished dental pathologist. He received his medical education
University, Belfast where, in a brilliance, he obtained first-class
1. Purtilo, D. T., Hallgren, H. M., Yunis, E. J. Lancet, 1972, i, 769. 2. Murgita, R. A., Tomasi, T. B.J. exp. Med. 1975, 141, 269. 3. Murgita, R. A., Tomasi, T. B. ibid. p. 440. 4. Purtilo, D. T., Yunis, E. J. Lab. Invest. 1971, 25, 291. 5. Purtilo, D. T., Kersey, J. H., Hallgren, H. M., Fox, K. R., Yunis,’ E. J. Am. J. clin. Path. 1973, 59, 295. 6. Gaugas, J. M. Transplantation, 1974, 18, 538. 7. Medawar, P. B., Sparrow, E. M. J. Endocr. 1956, 14, 240. 8. Waltman, S. R., Burde, R. M., Berrios, J. Transplantation, 1971, 11, 194. 9. Munroe, J. J. J. reticuloendothelial Soc. 1971, 9, 361. 10. Han, T. Clin. exp. Immun. 1974, 18, 529.
at
career
T. W. G. writes: " With the late J. D. Boyd, his life-long friend and colleague, Hamilton did as much as anybody to establish embryology as a basic science of particular relevance to medicine. As a professor of anatomy he was the protagonist of innovations in teaching which resulted in the human body being presented to medical students as a dynamic, developing, functioning, and eventually ageing entity in which structure and function are closely related. The clinical relevance of what he taught was always prominent; and he did much to make radiological and surface anatomy integral parts of the preclinical course. Hamilton understood fully the processes of producing books, and any book associated with his name was of a very high standard, largely because he had familiarised himself with the art of illustration and the techniques of printing and plate-making. His main efforts in this area were directed to Human Embryology (now in its 4th edition), Surface and Radiological Anatomy (now in its 5th edition), and a comprehensive work on the human placenta. He edited a textbook of topographical anatomy, the 2nd edition of which he was hoping to see published in the autumn. In recent years he had been heavily involved in producing films for teaching, in which developmental "
DAVID T. PURTILO.
JAMES HAMILTON
electrolytes present in the body. However, sophisticated whole body-measurement of electrolytes is not possible in most clinical situations, and in practice the main problem is to know how far an observed serum-
calciferol. This conclusion is not supported by data from two of our patients, children with cystinosis and rickets. In these patients the steady-state plasma levels of 25-hydroxyvitamin D (25-OH D) were measured while 25-H.C.C. was being used in treatment. Later the levels were measured while vitamin Dand vitamin D3, respectively, were being administered. All medications were given orally. The findings were:
electrolyte
pattern should influence management in a particular case. If the " sick cell " hypothesis is correct, then it might be expected that many of the observed electrolyte disturbances would be corrected simply by treating the underlying illness. This is indeed often found to be the case. In many other instances, the addition of potassium supplements (or stopping thiazide diuretics if these drugs are being given) corrects not only hypokalsemia but also quite severe hyponatraemia. Trinity Hospital, 19 Trinity Road, Taunton, Somerset.
*
osteomalacia the curative dosages of native ergocalciferol and cholecalciferol or of 25 hydroxyergocalciferol and 25 hydroxycholecalciferol administered by the same route must be compared directly.
uraemic
In January of this year a 3-month-old child was sent into this hospital with a history of an apnoeic attack following a coughing spasm in the second week of what sounded like whooping-cough.
University College Hospital Medical School, University Street,
The elder sister of this child had had a similar illness for the previous three weeks. The mother had treated this apnoeic attack by placing the child under a cold water tap. By the time he was admitted he was well and the chest was clear apart from a few crepitations at the bases. Immediately after admission he had a generalised convulsion with clonic spasms of all limbs, for which he had to be intubated, given intravenous diazepam, and ventilated. Fundoscopy at this time was normal, as was the cerebrospinal fluid. It was thought that he may have had an intracerebral bleed (or possibly an encephalopathy) secondary to his whoopingcough. However, a sample of blood taken before this convulsion showed severe hyponatraemia (116 meq. per 1.) and severe hypochlorsemia (80 meq. per 1.). On requestioning the parents, it appeared that vomiting had been very frequent in the previous two weeks and it would appear likely that the child had developed hyponatrsemia secondary to the vomiting, which in turn was secondary to the pertussis, the hyponatraemia being responsible for the convulsion before admission and for the alarming convulsion in the He was treated with intermittent positive-pressure ward. ventilation and intravenous fluid therapy, and electrolytes rapidly returned to normal. Six hours after admission the convulsions had stopped, and the child was taken off the ventilator two days after admission. He was also given chloramphenicol and made a good recovery, although for the next two weeks he had obvious paroxysmal
PARACETAMOL MEASUREMENT SIR,—Prescott and Matthew2 believe that cysteamine is the treatment of choice for paracetamol poisoning, but the safety of cysteamine in man has yet to be established. Since only about 1% of those who take a paracetamol overdose die,3 it is important to ensure that cysteamine is only administered to those patients who really need it.4 The plasma-paracetamol level has been shown to be a reasonably reliable predictor for subsequent hepatic necrosis, and, since cysteamine should be given within 10 hours of paracetamol ingestion3asimple, reliable, and rapid method of estimating it is needed. The following is such a method, and is based on a recently reported colorimetric method.7 1 ml. of
plasma is added to a 25 ml. stoppered centrifuge containing 2 ml. 10% trichloroacetic acid. After thorough mixing, the tube is centrifuged briefly and the clear supernatant decanted into a 25 ml. test-tube containing 1 ml. 6N hydrochloric acid and 2 ml. 10% sodium nitrite. After allowing the contents to stand for 2 minutes, 2 ml. of 15% sulphamic acid is added carefully, followed by 5 ml. 10% NaOH. The ensuing yellow colour is measured at 430 nm. against a reagent blank
tube
seemed to be a minor epidemic of whooping-cough in this area at the time seem to confirm the diagnosis as pertussis complicated by hyponatraemic convulsions. ,
J. R. HARPER M. J. MAGUIRE.
VITAMIN-D METABOLISM IN CHRONIC RENAL FAILURE
SIR,-Dr Eastwood and Professor de Wardener (April 26, p. 981) found that the parenteral administration of 40 µg. per day of hydroxycholecalciferol (25-H.c.c.) healed
osteomalacia in chronic renal failure and imply that this is equivalent to giving the patients a similar dose of chole-
C. E. DENT MERCEDES DOMENECH J. M. GERTNER.
London WC1E 6JJ.
whooping-cough with, initially, frequent apnoeic attacks, paroxysms of coughing, and a typical whoop. A chest X-ray showed inflammatory changes throughout the right lung, which cleared. The diagnosis was not confirmed bacteriologically, but the child’s subsequent course, his sister’s illness, and what
Hospital,
Stamp.
In order to make a valid comparison of the relative efficacy of ergocalciferol (D2) and cholecalciferol (Dg) in
SIR,-Convulsions are a recognised complication of whooping-cough, as is vomiting and metabolic alkalosis, even to the point of tetany. These may, however, combine to present in an alarming fashion, as in the following case.
General
C. B.
Thus, in patient 1 the plasma level showed little change when 25 times by weight the dose of Da was substituted for 25-H.C.C.; while in patient 2 a six-fold increase in dosage led to a three-fold fall in plasma 25-OH D level. This is probably the result of poor conversion of vitamin D and D 3 to the 25 hydroxylated form as a result of feedback inhibition of hepatic calciferol 25-hydroxylase by the high circulating levels of 25-OH D.1
P. F. ROE.
HYPONATRÆMIA AND CONVULSIONS IN WHOOPING-COUGH
Northampton NN1 5BD.
Kindly determined by Dr T.
of water. The calibration jjLg. per ml. plasma.
curve
is linear
over
the range 100-500
The method takes 5-10 minutes and all reagents are standard laboratory issue, readily made up, and stable with the exception of the nitrite reagent, which should be made up immediately before use. The possibility of providing the reagents in the form of a test kit for rapid in-ward assays is being pursued. Olmdahl, J. L., De Luca, H. F. Physiol. Rev. 1973, 53, 327. Prescott, L. F., Matthew, H. Lancet, 1974, i, 998. Wright, N. Prescribers J. 1974, 14, 78. Gazzard, B. G., Murray-Lyon, I. M., Davis, M., Thompson, R. P. H., Williams, R., Goulding, R. Lancet, 1974, i, 864. 5. Stewart, M. J. ibid. p. 1162. 6. Prescott, L. F., Swainson, C. P., Forrest, A. R. W., Newton, R. W., Wright, N., Matthew, H. ibid. p. 588. 7. Chefetz, L., Daly, R. E., Schriftman, H., Lomner, J. J. J. pharm. Sci. 1971, 60, 463.
1. 2. 3. 4.
1148 The reaction is specific for paracetamol, and there is no interference from the sulphate and glucuronide conjugates of paracetamol. In addition, presence of the following substances at the 50 (1.g. per ml. level does not interfere
Obituary WILLIAM
with the reaction:
amitryptiline, amphetamine, caffeine, chlordiazepoxide, chlormezanone, chlorpromazine, chlorpropamide, cocaine, diazepam, diphenhydramine, diphenyldantoin, dihydrocodeine, imipramine, indomethacin, lorazepam, meprobamate, methadone, methaqualone, morphine, nitrazepam, oxypertine, pentazocine, pentobarbitone, promethazine, salicylate, strychnine, theophylline, tolbutamide. Metabolic Studies Department, Sterling-Winthrop Research and
Development Division, Edgefield Avenue, Newcastle upon Tyne NE3 3TT.
JOHN P. GLYNN STEPHEN E. KENDAL.
SURVIVAL OF THE GENETICALLY INCOMPATIBLE FETAL GRAFT
SIR,—Dr Finn (April 12, p. 835) proposed an attractive hypothesis to account for the non-rejection of the fetal allograft. He postulated that shared surface-repellent molecules prevent competent cells.
contact
of maternal and fetal immuno,
We have previously suggested that oc-fetoprotein (A.F.P.) could potentially abrogate maternal lymphocyte immune 1 Murgita and Tomasi 2,3 responses against the fetus. demonstrated suppression of humoral immune responses, mixed lymphocyte reactivity, and mitogen-induced lymphocyte transformation by A.F.P. A.F.P. may serve as a natural immunosuppressive agent that abrogates potentially harmful maternal immune responses. A.F.P. is a major serum-protein in the fetus which crosses the placental barrier to the maternal circulation where it could serve as
immunosuppressive agent.4 Furthermore, A.F.P. may inhibit lymphopoiesis: we have reported a patient with haemochromatosis and lymphocytosis who developed an A.F.P.-positive hepatocellular carcinoma and lymphopenia. Her total lymphocyte counts during a 24-year period were 2305 per c.mm. at 37 years of age, 10,089 per c.mm. at 46 years, 9920 per c.mm. at
an
54 years, and then plummeted to 1366 per c.mm. after the appearance of an A.F.P.-synthesising hepatoma. The lymphopenia may have resulted from factors other than A.F.P., but this speculation merits consideration. Other mechanisms in addition to surface-repellent molecules need to be considered to explain the non-rejection of the fetus. We have suggestedthat combined fail-safe mechanisms, including placental barriers, blocking antibodies, hormones, and possibly A.F.P. and other fetal proteins 6 may act concertedly to prevent maternal rejection of the fetus. The placenta is an endocrine organ strategically placed to optimise the impact of the immunosuppressive effect of oestrogen, progesterone, cortisol, prolactin, and chorionic gonadotrophin.7-1o Commonwealth of Massachusetts Medical Center, 55 Lake Avenue North, Worcester, Massachusetts 01605, U.S.A.
M.D., Hon.D.Sc.Belf., D.Sc.Glasg., F.R.C.S., F.R.C.O.G., F.R.S.E.
Prof. William Hamilton, professor emeritus of anatomy in the University of London since 1971, died on May 3 at the age of 71. The passing of this distinguished anatomist and embryologist will be mourned by the many, at home and abroad, who have a vivid recollection of him as teacher, colleague, or friend. the Queen’s of exceptional honours in the B.SC. examination in 1926, and in the M.B. in 1929. He proceeded to the M.sc. in 1931 and then went as a lecturer in anatomy to Glasgow University, where he was awarded the D.sc. degree in 1934, and where, under the influence of Thomas Hastie Bryce, he developed his life-long passion for embryology. From Glasgow he went to St. Thomas’s Hospital Medical School as deputy director of anatomy, and he was appointed to the chair of anatomy in the University of London at St. Bartholomew’s Hospital Medical College in 1936. In 1945 he returned to Glasgow as regius professor of anatomy, but personal reasons, combined with the prospect of starting up a new department, led him to accept the appointment to the newly created chair of anatomy at Charing Cross Hospital Medical School in 1947, and he remained in post there until his retirement in 1970. During this period he was president of the Anatomical Society of Great Britain and Ireland in 1953-55. As dean of Charing Cross Hospital Medical School in 1956-62, he succeeded in obtaining for the school chairs in obstetrics and gynaecology, surgery, and medicine, in that order, over the short space of 3 years. It was also during his deanship that plans were laid for the new hospital and medical school at Fulham, and he played a leading part in determining the existing integrated pattern of buildings. In 1933 he married Maimie, only daughter of Samuel Young of Belfast; and it was a source of great joy to him that his four sons all became members of the medical profession (two of them are consultant surgeons), and that his daughter became a distinguished dental pathologist. He received his medical education
University, Belfast where, in a brilliance, he obtained first-class
1. Purtilo, D. T., Hallgren, H. M., Yunis, E. J. Lancet, 1972, i, 769. 2. Murgita, R. A., Tomasi, T. B.J. exp. Med. 1975, 141, 269. 3. Murgita, R. A., Tomasi, T. B. ibid. p. 440. 4. Purtilo, D. T., Yunis, E. J. Lab. Invest. 1971, 25, 291. 5. Purtilo, D. T., Kersey, J. H., Hallgren, H. M., Fox, K. R., Yunis,’ E. J. Am. J. clin. Path. 1973, 59, 295. 6. Gaugas, J. M. Transplantation, 1974, 18, 538. 7. Medawar, P. B., Sparrow, E. M. J. Endocr. 1956, 14, 240. 8. Waltman, S. R., Burde, R. M., Berrios, J. Transplantation, 1971, 11, 194. 9. Munroe, J. J. J. reticuloendothelial Soc. 1971, 9, 361. 10. Han, T. Clin. exp. Immun. 1974, 18, 529.
at
career
T. W. G. writes: " With the late J. D. Boyd, his life-long friend and colleague, Hamilton did as much as anybody to establish embryology as a basic science of particular relevance to medicine. As a professor of anatomy he was the protagonist of innovations in teaching which resulted in the human body being presented to medical students as a dynamic, developing, functioning, and eventually ageing entity in which structure and function are closely related. The clinical relevance of what he taught was always prominent; and he did much to make radiological and surface anatomy integral parts of the preclinical course. Hamilton understood fully the processes of producing books, and any book associated with his name was of a very high standard, largely because he had familiarised himself with the art of illustration and the techniques of printing and plate-making. His main efforts in this area were directed to Human Embryology (now in its 4th edition), Surface and Radiological Anatomy (now in its 5th edition), and a comprehensive work on the human placenta. He edited a textbook of topographical anatomy, the 2nd edition of which he was hoping to see published in the autumn. In recent years he had been heavily involved in producing films for teaching, in which developmental "
DAVID T. PURTILO.
JAMES HAMILTON
