77
sensitivity in rabbits."," In all these situations it was possible to demonstrate a reduction in distensibility of the appropriate vessel wall. It is unlikely that atheroma would play a role at the arteriolar level, but it seems probable that more diffuse vascular disease of the type found in nephrosclerosis might well influence juxtaglomerular baroreceptor activity. IMPLICATIONS
Differences in the natural history of the renin-
subgroups of hypertension are readily comprehensible, since selection of patients with low-renin hypertension will automatically select individuals who have benign nephrosclerosis. Additionally, patients may be diluted by borderline hypertensives who have nephrosclerosis due to ageing rather than hypertension. The factors which determine this lesion are complex and uncertain,23 but it may be related to duration, lability, and severity of hypertension as well as the patient’s age. However, patients with fibrinoid necrosis of the vessel wall due to malignant hypertension are likely to belong to a different renin subgroup unless they have previously passed through a phase of " benign " essential hypertension. The exceptionally good response to diuretic therapy is readily understood. Studies with angiotensin inhibitors indicate that elevation of circulating-renin levels plays an important role in maintaining bloodpressure in the face of sodium depletion both in man. and in the laboratory animal.’ When this response is impaired, it is therefore reasonable to anticipate that more profound fall in blood-pressure would take place. "
"
This need not indicate that fluid retention is responsible for the hypertension. Demonstration of a specifically beneficial effect of spironolactone, as compared with other diuretics, might constitute evidence against the present hypothesis. This claim is, however, unsubstantiated.6 REFERENCES 1. Helmer, O. M. Can. med. Ass. J. 1964, 90, 221. 2. Crane, M. G., Harris, J. J., Johns, V. J. Am. J. Med. 1972, 52, 457. 3. Jose, A., Crout, J. R., Kaplan, N. M. Ann. intern. Med. 1970, 72, 9. 4. Kuchel, O., Fishman, L. M., Liddle, G. W., Michelakis, A. ibid. 1967, 67, 791. 5. Brunner, H. R., Laragh, J. H., Baer, L., Newton, M. A., Goodwin, F. T., Krakoff, L. R., Bard, R. H., Buhler, F. R. New Engl. J. Med. 1972, 286, 441. 6. Dunn, M. J., Tannen, R. L. Kidney Int. 1974, 5, 317. 7. Davis, J. O. Am. J. Med. 1973, 55, 333. 8. Thurau, K. W. C., Dahlheim, H., Grüner, A., Mason, J., Granger, P. Circulation Res. 1972, 30-31, suppl. 2, p. 182. 9. Blaine, E. H., Davis, J. O., Prewitt, R. L. Am. J. Physiol. 1971, 220, 1593. 10. Chobanian, A. V., Burrows, B. A., Hollander, W. J. clin. Invest. 1961, 40, 416. 11. Melby, J. C., Dale, S. L., Wilson, T. E. Circulation Res. 1971,
28-29, suppl. 2, p. 143. Laragh, J. H. Am. J. Med. 1973, 55, 261. Woods, J. W., Liddle, G. W., Stant, E. G., Michelakis, A. M., Brill, A. B. Archs intern. Med. 1969, 123, 366. 14. Lebel, M., Schalekamp, M. A., Beevers, D. G., Brown, J. J., Davies, D. L., Fraser, R., Kremer, D., Lever, A. F., Morton, J. J., Robertson, J. I. S., Tree, M., Wilson, A. Lancet, 1974, ii, 308. 15. Schalekamp, M. A., Lebel, M., Beevers, D. G., Fraser, R., Kolsters, G., Birkenhager, W. H. ibid. p. 310. 16. Birkenhager, W. H., Schalekamp, M. A. D. H., Krauss, X. H., Kolsters, G., Schalekamp-Kuyken, M. P. A., Kroon, B. J. M., Teulings, F. A. G. Eur. J. clin. Invest. 1972, 2, 115. 17. Tuck, M., Williams, C. H., Cain, J. P., Sullivan, J. M., Dluhy, R. G. Am. J. Cardiol. 1973, 32, 637. 18. Brown, J. J., Lever, A. F., Robertson, J. I. S., Schalekamp, M. A. Lancet, 1974, ii, 320.
12. 13.
ROLE OF Fc RECEPTORS IN HERPES SIMPLEX VIRUS INFECTION ALAN S. RABSON JOSE C. COSTA Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014, U.S.A.
It is suggested that Fc receptors which Sum ary appear on the surface of cells infected by herpes-simplex virus confer a biological advantage on the virus—perhaps by binding immunoglobulin
molecules or surface, thus
antigen-antibody complexes on the cell blocking viral antigenic sites, or by consuming antibody directed at surface viral antigen or by modifying replication of the virus. RECEPTORS for the Fc portion of immunoglobulins the surface of cells have been known for some time, but their precise biological function and significance in some of the cell types in which they are readily demonstrable are still unclear. In 1964 Watkins reported that sheep red blood-cells (R.B.C.) coated with anti-sheep R.B.c. antibody adsorbed to herpes-simplex virus (H.S.v.) infected cells but not to uninfected cells.l Later Yasuda and Milmgrom showed that this haemadsorption was mediated through a bond between the Fc fragment of the antibody coating the R.B.c. and an Fc receptor site which developed on the surface of the H.s.v.-infected cell.2 This development of an Fc receptor takes place early in the infectious cycle and may be due to uncovering of a cell receptor or the inserting of a viralcoded protein with receptor properties into the cell membrane. What is the biological significance of an Fc receptor in an H.s.v.-infected cell? When a cell supports replication of H.s.v. particles, virus-specific antigens appear on the cell membrane well before the viral replication cycle is complete 3 These antigens render the infected cell susceptible to recognition and destruction by the host immunological response. Such cells can be destroyed in four waysby antibody and complement mediated cell lysis,’ by the interaction of antibody, complement, and leucocytes,3 by specific cell-mediated Iysis,5 or by the synergistic effect of antibody and non-immune effector cells (antibody-dependent cell-mediated toxicity).6,7 It on
Brunner, H. R., Sealey, J. E., Laragh, J. H. Hypertension Manual (edited by J. H. Laragh); p. 71. New York, 1974. 20. Mroczek, W. J., Finnerty, F. A., Catt, K. J. Lancet, 1973, ii, 464. 21. Papper, S., Vaamonde, C. A. in Diseases of the Kidney (edited by M. B. Strauss and L. G. Welt).; p. 735. Boston, 1971. 22. Bell, E. T., Clawson, B. J. Archs Path. 1928, 5, 939. 23. Tracy, R. E., Toca, V. T. Lab. Invest. 1974, 30, 30. 24. Smith, J. P. J. Path. Bact. 1955, 69, 147. 25. Bell, E. T. Renal Diseases. Philadelphia, 1946. 26. Sambhi, M. P., Crane, M. G., Genest, J. Ann. intern. Med. 1973, 79, 411. 27. Crane, M. G., Harris, J. J., Johns, V. J. Am. J. Med. 1972, 52, 457. 28. Spark, R. F., O’Hare, C. M., Regan, R. M. Archs intern. Med. 1974, 133, 205. 29. Angell-James, J. E. Circulation Res. 1973, 32, 149. 30. Angell-James, J. E. J. Physiol., Lond. 1971, 217, 30P. 31. Angell-James, J. E. Circulation Res. 1974, 34, 27. 32. Haber, E., Sancho, J. Re. R., Barger, A. C. Third meeting of International Society of Hypertension, Milan, 1974. Clin. Sci. mol. med. (in the press). 33. Gavras, H., Brunner, H. R., Vaughan, E. D., Laragh, J. H. Science, 1973, 180, 1369. 19.
78
is plausible that the two last mechanisms could be interfered with by binding of immunoglobulins or antigen-antibody complexes through the Fc fragment to the cell Fc site. The presence of immunoglobulin molecules or antigen-antibody complexes attached to the cell surface could mask the H.s.v. surface antigen and block recognition and subsequent cell destruction. Furthermore, the binding of an H.s.v. antibody molecule through the Fc fragment instead of the Fab terminal would diminish the possibilities for activation In that way the Fc of the complement ;system. consume " receptor could " antibody directed to the H.s.v. membrane antigen and render it inefficient to mediate complement-dependent lysis. In addition to the possibility that the presence of an Fc receptor on the surface of an H.s.v.-infected cell could be an advantage to the virus by protecting the host cell from destruction, the occupation of Fc receptor sites might modify the replication of the virus. One would predict that it would be of advantage to the virus to modify the late phases of the replicative cycle so as not to cause abrupt cell lysis. All the speculations developed above can be experimentally tested. If some of the functions of the Fc receptor site can be demonstrated in the laboratory, it would become justifiable to think that the ability to develop an Fc receptor on the surface of an infected cell early in the replication cycle represents a selective advantage for a given virus. REFERENCES
Watkins, J. F. Nature, 1964, 251, 542. Yasuda, J., Milmgrom, F. Int. Archs Allergy, 1968, 33, 151. Lodmell, D. L., Niwa, A., Hayashi, K., Notkins, A. L. J. exp. Med. 1973, 137, 706. 4. Smith, J. W., Adam, E., Melnick, J. L., Rawls, W. E. J. Immun. 1972, 109, 554. 5. Speel, L. F., Osborn, J. E., Walker, D. L. ibid. 1968, 101, 409. 6. Shore, S. L., Nahmias, A. J., Starr, S. E., Wood, P. A., McFarlin, D. E. Nature, 1974, 251, 350. 7. Rager-Zisman, B., Bloom, B. R. ibid. p. 542. 1. 2. 3.
mind will be stimulated by the stark comparison look further and start another great advance, comparable that resulting from the identification of specific chemical allergens. Until primary irritant effects are understood better, the subject of contact dermatitis will remain a medicolegal morass. There are some trivial blemishes. Most of the spelling mistakes are merely irritating (though " serum " for " sebum " on p. 11 could confuse). The style, in general excellent, relapses sometimes, clouding the meaning in a book which, being succinct, ought to be crystal clear. The detailed information is impeccable, but a reference to Candida albicans in the xtiology of sore mouth associated with dentures would be desirable. The index is good. It is a superb and beautifully produced little book that is truly pocketable. It is a must for clinical dermatologists, industrial medical officers, and employment advisers; and it should be consulted by a very wide readership in hospital (including medical students), general practice, the Law, and industry.
inquiring to to
Iron in
Biochemistry
and Medicine
Edited by A. JACOBS and M. WoRwooD, Welsh National School of Medicine. London and New York: Academic Press. 1974. Pp. 769. £15.20; $39.25.
EDITED
by Professor Jacobs and Dr Worwood, this multidisciplinary book on iron metabolism includes the chemistry of iron, its absorption, transport, utilisation, and storage in the body, and many different aspects of ha:m metabolism. Four chapters deal with erythropoiesis, tissue effects, and the epidemiology of iron deficiency and its treatment: there is also a chapter on iron metabolism in infancy and childhood. Other chapters deal with oxygen carriage, cytochromes, non-hsem proteins, iron in the reticuloendothelial system, iron overload, iron and infection, and genetic abnormalities of iron metabolism in animals. In other words, most aspects of iron metabolism are covered. Five of the twenty chapters come from Cardiff, reflecting the special interests of Professor Jacobs in iron metabolism, and the other fifteen come from experts in England, Scotland, Denmark, South Africa, Canada, and the United States. It is a tribute to the contributors, but more especially to the two editors, that the extensive references given at the end of each chapter include some dated 1973. This is an excellent reference book, full of useful up-to-date information.
Reviews of Books
A Manual of Head
Manual of Contact Dermatitis SIGFRID
FREGERT.
Copenhagen: Munksgaard.
Injuries in General Surgery
GRAHAM MARTIN, F.R.C.S., Wellington Hospital, Wellington, New Zealand. London: Heinemann. 1974. Pp. 158. E2. 1974.
Pp. 107. D. kr. 48. NEITHER simplicity nor humility, which are prime features of this manual, are glamorous virtues, so that some readers may feel that they have been told to go and wash themselves in Jordan seven times; but the discerning will recognise a pearl of great price. All the important practical aspects of contact dermatitis are covered in 107 pages. The information includes the nature and habitats of the commonest allergens, details of patch-testing and photo patch-testing techniques (with a table of recommended strengths for test allergens), and brief sections on prevention, treatment, and (very important) rehabilitation. There is no comparable source of such concise and reliable information. Dr Fregert has written this book on behalf of the International Contact Dermatitis Research Group. The advantages of recognising and understanding contact dermatitis are beginning to filter through to clinical dermatologists: this manual should catalyse the process. The strong light cast on the subject emphasises the contrast between the clear facts known about allergic contact dermatitis and the vague theories of irritant and toxic dermatitis; perhaps some
THIS manual aims to be a straightforward guide to the general surgeon who has to take responsibility for head injuries. It is succinct and well illustrated, describing all the important steps in management, both medical and surgical, from the acute situation to the problems of rehabilitation. The complications are also described, and clear guidance is given about their treatment. Each chapter ends with multiple-choice questions to test the reader’s comprehension. Although one might quibble with a number of small points, usually of emphasis, it is a book to be strongly recommended, not only to the readers for whom it was designed but also to nurses, medical students, and junior staff who wish to improve their understanding and treatment of these important injuries. New Editions ECG Case Studies. 2nd ed. By Julian Frieden and Ira L. Rubin. Flushing, N.Y.: Medical Examination Publishing. London: Kimpton. 1974. Pp. 284.$7.50; E3.40.
Histology. 7th ed. By Arthur W. Ham. Philadelphia: Lippincott. Oxford: Blackwell. 1974. Pp. 1006.$24.75; &12.40.
sensitivity in rabbits."," In all these situations it was possible to demonstrate a reduction in distensibility of the appropriate vessel wall. It is unlikely that atheroma would play a role at the arteriolar level, but it seems probable that more diffuse vascular disease of the type found in nephrosclerosis might well influence juxtaglomerular baroreceptor activity. IMPLICATIONS
Differences in the natural history of the renin-
subgroups of hypertension are readily comprehensible, since selection of patients with low-renin hypertension will automatically select individuals who have benign nephrosclerosis. Additionally, patients may be diluted by borderline hypertensives who have nephrosclerosis due to ageing rather than hypertension. The factors which determine this lesion are complex and uncertain,23 but it may be related to duration, lability, and severity of hypertension as well as the patient’s age. However, patients with fibrinoid necrosis of the vessel wall due to malignant hypertension are likely to belong to a different renin subgroup unless they have previously passed through a phase of " benign " essential hypertension. The exceptionally good response to diuretic therapy is readily understood. Studies with angiotensin inhibitors indicate that elevation of circulating-renin levels plays an important role in maintaining bloodpressure in the face of sodium depletion both in man. and in the laboratory animal.’ When this response is impaired, it is therefore reasonable to anticipate that more profound fall in blood-pressure would take place. "
"
This need not indicate that fluid retention is responsible for the hypertension. Demonstration of a specifically beneficial effect of spironolactone, as compared with other diuretics, might constitute evidence against the present hypothesis. This claim is, however, unsubstantiated.6 REFERENCES 1. Helmer, O. M. Can. med. Ass. J. 1964, 90, 221. 2. Crane, M. G., Harris, J. J., Johns, V. J. Am. J. Med. 1972, 52, 457. 3. Jose, A., Crout, J. R., Kaplan, N. M. Ann. intern. Med. 1970, 72, 9. 4. Kuchel, O., Fishman, L. M., Liddle, G. W., Michelakis, A. ibid. 1967, 67, 791. 5. Brunner, H. R., Laragh, J. H., Baer, L., Newton, M. A., Goodwin, F. T., Krakoff, L. R., Bard, R. H., Buhler, F. R. New Engl. J. Med. 1972, 286, 441. 6. Dunn, M. J., Tannen, R. L. Kidney Int. 1974, 5, 317. 7. Davis, J. O. Am. J. Med. 1973, 55, 333. 8. Thurau, K. W. C., Dahlheim, H., Grüner, A., Mason, J., Granger, P. Circulation Res. 1972, 30-31, suppl. 2, p. 182. 9. Blaine, E. H., Davis, J. O., Prewitt, R. L. Am. J. Physiol. 1971, 220, 1593. 10. Chobanian, A. V., Burrows, B. A., Hollander, W. J. clin. Invest. 1961, 40, 416. 11. Melby, J. C., Dale, S. L., Wilson, T. E. Circulation Res. 1971,
28-29, suppl. 2, p. 143. Laragh, J. H. Am. J. Med. 1973, 55, 261. Woods, J. W., Liddle, G. W., Stant, E. G., Michelakis, A. M., Brill, A. B. Archs intern. Med. 1969, 123, 366. 14. Lebel, M., Schalekamp, M. A., Beevers, D. G., Brown, J. J., Davies, D. L., Fraser, R., Kremer, D., Lever, A. F., Morton, J. J., Robertson, J. I. S., Tree, M., Wilson, A. Lancet, 1974, ii, 308. 15. Schalekamp, M. A., Lebel, M., Beevers, D. G., Fraser, R., Kolsters, G., Birkenhager, W. H. ibid. p. 310. 16. Birkenhager, W. H., Schalekamp, M. A. D. H., Krauss, X. H., Kolsters, G., Schalekamp-Kuyken, M. P. A., Kroon, B. J. M., Teulings, F. A. G. Eur. J. clin. Invest. 1972, 2, 115. 17. Tuck, M., Williams, C. H., Cain, J. P., Sullivan, J. M., Dluhy, R. G. Am. J. Cardiol. 1973, 32, 637. 18. Brown, J. J., Lever, A. F., Robertson, J. I. S., Schalekamp, M. A. Lancet, 1974, ii, 320.
12. 13.
ROLE OF Fc RECEPTORS IN HERPES SIMPLEX VIRUS INFECTION ALAN S. RABSON JOSE C. COSTA Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014, U.S.A.
It is suggested that Fc receptors which Sum ary appear on the surface of cells infected by herpes-simplex virus confer a biological advantage on the virus—perhaps by binding immunoglobulin
molecules or surface, thus
antigen-antibody complexes on the cell blocking viral antigenic sites, or by consuming antibody directed at surface viral antigen or by modifying replication of the virus. RECEPTORS for the Fc portion of immunoglobulins the surface of cells have been known for some time, but their precise biological function and significance in some of the cell types in which they are readily demonstrable are still unclear. In 1964 Watkins reported that sheep red blood-cells (R.B.C.) coated with anti-sheep R.B.c. antibody adsorbed to herpes-simplex virus (H.S.v.) infected cells but not to uninfected cells.l Later Yasuda and Milmgrom showed that this haemadsorption was mediated through a bond between the Fc fragment of the antibody coating the R.B.c. and an Fc receptor site which developed on the surface of the H.s.v.-infected cell.2 This development of an Fc receptor takes place early in the infectious cycle and may be due to uncovering of a cell receptor or the inserting of a viralcoded protein with receptor properties into the cell membrane. What is the biological significance of an Fc receptor in an H.s.v.-infected cell? When a cell supports replication of H.s.v. particles, virus-specific antigens appear on the cell membrane well before the viral replication cycle is complete 3 These antigens render the infected cell susceptible to recognition and destruction by the host immunological response. Such cells can be destroyed in four waysby antibody and complement mediated cell lysis,’ by the interaction of antibody, complement, and leucocytes,3 by specific cell-mediated Iysis,5 or by the synergistic effect of antibody and non-immune effector cells (antibody-dependent cell-mediated toxicity).6,7 It on
Brunner, H. R., Sealey, J. E., Laragh, J. H. Hypertension Manual (edited by J. H. Laragh); p. 71. New York, 1974. 20. Mroczek, W. J., Finnerty, F. A., Catt, K. J. Lancet, 1973, ii, 464. 21. Papper, S., Vaamonde, C. A. in Diseases of the Kidney (edited by M. B. Strauss and L. G. Welt).; p. 735. Boston, 1971. 22. Bell, E. T., Clawson, B. J. Archs Path. 1928, 5, 939. 23. Tracy, R. E., Toca, V. T. Lab. Invest. 1974, 30, 30. 24. Smith, J. P. J. Path. Bact. 1955, 69, 147. 25. Bell, E. T. Renal Diseases. Philadelphia, 1946. 26. Sambhi, M. P., Crane, M. G., Genest, J. Ann. intern. Med. 1973, 79, 411. 27. Crane, M. G., Harris, J. J., Johns, V. J. Am. J. Med. 1972, 52, 457. 28. Spark, R. F., O’Hare, C. M., Regan, R. M. Archs intern. Med. 1974, 133, 205. 29. Angell-James, J. E. Circulation Res. 1973, 32, 149. 30. Angell-James, J. E. J. Physiol., Lond. 1971, 217, 30P. 31. Angell-James, J. E. Circulation Res. 1974, 34, 27. 32. Haber, E., Sancho, J. Re. R., Barger, A. C. Third meeting of International Society of Hypertension, Milan, 1974. Clin. Sci. mol. med. (in the press). 33. Gavras, H., Brunner, H. R., Vaughan, E. D., Laragh, J. H. Science, 1973, 180, 1369. 19.
78
is plausible that the two last mechanisms could be interfered with by binding of immunoglobulins or antigen-antibody complexes through the Fc fragment to the cell Fc site. The presence of immunoglobulin molecules or antigen-antibody complexes attached to the cell surface could mask the H.s.v. surface antigen and block recognition and subsequent cell destruction. Furthermore, the binding of an H.s.v. antibody molecule through the Fc fragment instead of the Fab terminal would diminish the possibilities for activation In that way the Fc of the complement ;system. consume " receptor could " antibody directed to the H.s.v. membrane antigen and render it inefficient to mediate complement-dependent lysis. In addition to the possibility that the presence of an Fc receptor on the surface of an H.s.v.-infected cell could be an advantage to the virus by protecting the host cell from destruction, the occupation of Fc receptor sites might modify the replication of the virus. One would predict that it would be of advantage to the virus to modify the late phases of the replicative cycle so as not to cause abrupt cell lysis. All the speculations developed above can be experimentally tested. If some of the functions of the Fc receptor site can be demonstrated in the laboratory, it would become justifiable to think that the ability to develop an Fc receptor on the surface of an infected cell early in the replication cycle represents a selective advantage for a given virus. REFERENCES
Watkins, J. F. Nature, 1964, 251, 542. Yasuda, J., Milmgrom, F. Int. Archs Allergy, 1968, 33, 151. Lodmell, D. L., Niwa, A., Hayashi, K., Notkins, A. L. J. exp. Med. 1973, 137, 706. 4. Smith, J. W., Adam, E., Melnick, J. L., Rawls, W. E. J. Immun. 1972, 109, 554. 5. Speel, L. F., Osborn, J. E., Walker, D. L. ibid. 1968, 101, 409. 6. Shore, S. L., Nahmias, A. J., Starr, S. E., Wood, P. A., McFarlin, D. E. Nature, 1974, 251, 350. 7. Rager-Zisman, B., Bloom, B. R. ibid. p. 542. 1. 2. 3.
mind will be stimulated by the stark comparison look further and start another great advance, comparable that resulting from the identification of specific chemical allergens. Until primary irritant effects are understood better, the subject of contact dermatitis will remain a medicolegal morass. There are some trivial blemishes. Most of the spelling mistakes are merely irritating (though " serum " for " sebum " on p. 11 could confuse). The style, in general excellent, relapses sometimes, clouding the meaning in a book which, being succinct, ought to be crystal clear. The detailed information is impeccable, but a reference to Candida albicans in the xtiology of sore mouth associated with dentures would be desirable. The index is good. It is a superb and beautifully produced little book that is truly pocketable. It is a must for clinical dermatologists, industrial medical officers, and employment advisers; and it should be consulted by a very wide readership in hospital (including medical students), general practice, the Law, and industry.
inquiring to to
Iron in
Biochemistry
and Medicine
Edited by A. JACOBS and M. WoRwooD, Welsh National School of Medicine. London and New York: Academic Press. 1974. Pp. 769. £15.20; $39.25.
EDITED
by Professor Jacobs and Dr Worwood, this multidisciplinary book on iron metabolism includes the chemistry of iron, its absorption, transport, utilisation, and storage in the body, and many different aspects of ha:m metabolism. Four chapters deal with erythropoiesis, tissue effects, and the epidemiology of iron deficiency and its treatment: there is also a chapter on iron metabolism in infancy and childhood. Other chapters deal with oxygen carriage, cytochromes, non-hsem proteins, iron in the reticuloendothelial system, iron overload, iron and infection, and genetic abnormalities of iron metabolism in animals. In other words, most aspects of iron metabolism are covered. Five of the twenty chapters come from Cardiff, reflecting the special interests of Professor Jacobs in iron metabolism, and the other fifteen come from experts in England, Scotland, Denmark, South Africa, Canada, and the United States. It is a tribute to the contributors, but more especially to the two editors, that the extensive references given at the end of each chapter include some dated 1973. This is an excellent reference book, full of useful up-to-date information.
Reviews of Books
A Manual of Head
Manual of Contact Dermatitis SIGFRID
FREGERT.
Copenhagen: Munksgaard.
Injuries in General Surgery
GRAHAM MARTIN, F.R.C.S., Wellington Hospital, Wellington, New Zealand. London: Heinemann. 1974. Pp. 158. E2. 1974.
Pp. 107. D. kr. 48. NEITHER simplicity nor humility, which are prime features of this manual, are glamorous virtues, so that some readers may feel that they have been told to go and wash themselves in Jordan seven times; but the discerning will recognise a pearl of great price. All the important practical aspects of contact dermatitis are covered in 107 pages. The information includes the nature and habitats of the commonest allergens, details of patch-testing and photo patch-testing techniques (with a table of recommended strengths for test allergens), and brief sections on prevention, treatment, and (very important) rehabilitation. There is no comparable source of such concise and reliable information. Dr Fregert has written this book on behalf of the International Contact Dermatitis Research Group. The advantages of recognising and understanding contact dermatitis are beginning to filter through to clinical dermatologists: this manual should catalyse the process. The strong light cast on the subject emphasises the contrast between the clear facts known about allergic contact dermatitis and the vague theories of irritant and toxic dermatitis; perhaps some
THIS manual aims to be a straightforward guide to the general surgeon who has to take responsibility for head injuries. It is succinct and well illustrated, describing all the important steps in management, both medical and surgical, from the acute situation to the problems of rehabilitation. The complications are also described, and clear guidance is given about their treatment. Each chapter ends with multiple-choice questions to test the reader’s comprehension. Although one might quibble with a number of small points, usually of emphasis, it is a book to be strongly recommended, not only to the readers for whom it was designed but also to nurses, medical students, and junior staff who wish to improve their understanding and treatment of these important injuries. New Editions ECG Case Studies. 2nd ed. By Julian Frieden and Ira L. Rubin. Flushing, N.Y.: Medical Examination Publishing. London: Kimpton. 1974. Pp. 284.$7.50; E3.40.
Histology. 7th ed. By Arthur W. Ham. Philadelphia: Lippincott. Oxford: Blackwell. 1974. Pp. 1006.$24.75; &12.40.
