876 theoretical nor experimental evidence to support its use and demands large resources of valuable blood-products. In paraquat poisoning, rational treatment-namely, gastrointestinal absorbents and hxmodialysis/perfusion-is already available. These treatments may require sophisticated apparatus but the economic drain in their use is probably less than for plasma-
pheresis.
Their location incertain
specialised
units has the
additional advantage of allowing the study of sufficient numbers of patients to expand our knowledge of paraquat
pharmacokinetics and treatment. K.R.U.F. Institute of Renal
J. MILLER
Disease,
E. SANDERS
Royal Infirmary,
D. WEBB
Z Cardiff CF2 15
IN-VITRO IMMUNOLOGICAL ASSAY FOR DIAGNOSIS OF CŒLIAC DISEASE
interested in the paper by Dr Ashkenazi and colleagues (March 25, p. 627) on the production of leucocytemigration-inhibition factor (L.LF.) by codiac peripheral-blood lymphocytes challenged in vitro with a gluten fraction. Their patients were essentially children; earlier reportsl-5 of gluteninduced L.I.F. release by leucocytes have been based on work on adults with coeliac disease. To date, reports have consistently shown the specificity of this leucocyte migration inhibition (L.M.I.) with respect to coeliac disease, but, with one exception,3 have failed to assess its specificity in terms of other dietary
SIR,-We
were
antigens. FREQUENCY
OF L.M.I. TO THREE ANTIGENS IN C(ELM
OTHER GASTROINTESTINAL
DISEASE,
DISEASE,
AND CONTROLS
*For of-gliadin, migration inhibition was taken as a mean migration index (6 replicates per antigen dilution) below the 2 s.D. range (0.89-1.25) derived from the healthy staff control group. For oc-lactalbumin and a.c.., a migration index below 0.80 was considered to represent significant inhibition.
We have looked at both the antigen and disease specificity of this in-vitro assay system.6 L.M.I. to ot-giiadin, a-lactalbumin, and B.C.G. has been studied in five groups (table), including untreated coeliacs ingesting a normal diet and coeliacs who had been on a strict gluten-free diet for over 6 months. L.M.I. to B.C.G. was similar in all groups, confirming the potentially normal responsiveness of coeliac leucocytes in this test. L.M.I. to an a-gliadin fraction known to be toxic to cceliac patients in remission’ was virtually specific for coeliac disease. While these differences between coeliacs and other subjects could result from non-specific intestinal permeability to many dietary antigens secondary to the villous atrophy, this seems unlikely in view of the absence of any significant differences in the fre1. Bullen, A. W., Losowsky, M. S. Gut, 1976, 17, 813. 2. Douwes, F. R. Lancet, 1976, ii, 1353. 3. Asquith, P., Haeney, M. R. Gut, 1977, 18, A942. 4. Douwes, F. R., Lippmann-Nielsen, I., Hanke, R. Dt. med. Wschr. 1977,
102, 721. 5. Bullen, A. W., Losowsky, M. S. Gut, 1978, 19, 126. 6. Haeney, M. R., Asquith, P. in Perspectives in Coeliac Disease (edited by B. McNicholl, C. F. McCarthy, and P. F. Fottrell). Lancaster (in the press). 7. Schneider, R., Kendall, M. J., Hawkins, C. F. in Cœliac Disease: Proceedmgs of the Second International Cœliac Symposium (edited by W. Th. J. M. Hekkens and A. S. Peña); p. 72. Leiden, 1974.
quency of
L.M.I. to a-lactalbumin. Our results are in broad with those of Ashkenazi et al. but additionally sugagreement gest that L.M.I. is likely to be specific for a-gliadin. However, our findings do differ in one interesting respect. We found that L.M.I. to ot-gliadin was more common in treated than in untreated coeliacs, and have suggested that this may be due to a redistribution of lymphocytes after antigen withdrawal. A similar hypothesis was proposed to explain comparable results of lymphocyte transformation by gluten in cceliacs ingesting normal or gluten-free diets.8 L.M.I. to a-gliadin may be due to factors other than L.LF. generated by the activation of sensitised T lymphocytes, including antigen-antibody complexes9 or L.I.F. release by B cells.1o Despite these alternative explanations, L.M.I. to antigenic challenge shows a qualitative correlation with in-vivo cell-mediated immunity in the host.
Regional Immunology Unit, and Metabolic Research Unit, East Birmingham Hospital, Birmingham B9 5ST
M. R. HAENEY
P. ASQUITH
BONE-MARROW TRANSPLANTATION IN ACUTE LEUKÆMIA
SIR,-Commenting upon the report by the U.C.L.A. BoneTransplant Team,’ Dr Catovsky and his colleagues (Feb. 4, p. 266) ask "Did the controls receive the most intensive treatment, short of total-body irradiation, that could be safely administered without the support of a marrow graft?". marrow
This
cannot be answered: if the patient did not surthe was obviously too intensive, but if the patreatment vive, tient lives there is no way to know whether or not more therapy could have been tolerated. The principal objective of the marrow-transplantation approach is the administration of "supralethal" antileukaemic therapy with subsequent avoidance of death from marrow aplasia by transplantation of a "new" bone-marrow. We have reported long-term survival in patients with relapsed acute leukaemia, both lymphoblastic and myeloid, treated by intensive chemotherapy, total-body irradiation, and bone-marrow transplantation.2,6of 16 recipients of syngeneic marrow and 14 of 110 recipients of allogeneic marrow are still alive, without leukaemia, 2t to 7y years later. Actuarial analysis4 of the probability of being in remission indicated a constant rate of relapse for the first 2 years. Thereafter, the relapse-rate became very low, indicating a high probability that these long-term survivors are cured of their diseaseespecially since all the living patients are well out on the plateau of the curve. Powles6 has pointed out that a similar analysis of patients treated with chemotherapy shows a continued risk of relapse with time measured over years. Of course, with a constant rate of relapse (or death) there would always be a few long-term survivors if one starts with a sufficiently large number of patients. An actuarial analysis of survival after first relapse of the 150 patients mentioned by Catovsky et al. would be of interest.
question
Fred Hutchinson Cancer Research Center, Seattle, Washington 98104, U.S.A.
E. DONNALL THOMAS
8. Asquith, P. ibid. p. 242. 9. Spitler, L., Huber, H., Fudenberg, H. H. J. Immun. 1969, 102, 404. 10. Rocklin, R. E., MacDermott, R. P., Chess, L., Schlossman, S. F., David, J. R. J. exp. Med. 1974, 140, 1303. 11. David, J. R., David, R. R. Progr. Allergy, 1972, 16, 300. 1. U.C.L.A. Bone-marrow Transplant Team Lancet, 1977, ii, 1197. 2. Thomas, E. D., and others Blood, 1977, 49, 511. 3. Fefer, A., Buckner, C. D., Thomas, E. D., Cheever, M. A., Clift, R. A., Glucksberg, H., Neiman, P. E., Storb, R. New Engl. J. Med. 1977, 297, 146. 4. Kaplan, E. L., Meier, P. J. Am. statist. Ass. 1958, 53, 457. 5. Thomas, E. D., Flournoy, N., Buckner, C. D., Clift, R. A., Fefer, A., Neiman, P. E., Storb, R. Leukemia Res. 1977, 1, 67. 6. Powles, R. L. Biomedicine, 1976, 24, 327.
877
ARGENTINA, MEDICINE, AND THE WORLD CUP SiR,—Iam increasingly concerned at the number of doctors
disappeared in Argentina. I have written to the Argentinian ambassador asking for his reassurance that the allegations relating to these disappearing doctors are untrue, but I have had no reply. It seems to me that no doctor can now feel safe in Argentina. Medical advisers will be essential during the World Cup football matches to be held in Argentina this summer. Could I urge who have
doctors concerned to withdraw their services from World Cup football until the Argentinian Government desists in its policy of causing doctors to disappear without trace. General Infirmary, Leeds LS1 3EX
J. A. COTTERILL
Dr BEATRIZ
IPARRAGUIRRE DE WEINSTEIN, whose disappearreported by Dr Catovsky in our issue of March 25, has been released, after international pressure. On April 5 armed men halted an ambulance in Buenos Aires and seized Dr HILDA ERENU DE LIwSKI. Nothing more is ance was
known of her, and her husband, Dr NORBERTO IGNACIO LIwsKI, has also disappeared. A similar fate has overtaken Dr FRANCISCO MANUEL GARCIA FERNANDEZ. These 3 names must be added to Amnesty International’s March 28 list of at least 42 doctors and 35 medical students known to have been detained or who have disappeared since the military coup in
events of the past eight years have proved us to be entirely wrong in this respect. The demand for cyanocobalamin has persisted to such an extent that we have now restored it to our general list, and our justification for so doing lies in the belief that we, as pharmaceutical manufacturers, have an obligation to meet the requirements of prescribers for a B.P. drug whether or not we agree with their choice of such drug in a particular clinical situation.
min, but the
Pabyrn Laboratories, Paines and Byrne, Limited,
HÆMAGGLUTININ FROM HUMAN REOVIRUS-LIKE AGENT
SiR,—Hxmagglutinins have been prepared from cultured African green monkey kidney cells and bovine kidney cells2 infected with Nebraska calf diarrhoea virus. We have obtained a hasmagglutinin from the stools of infants and young children infected with human reovirus-like (H.R.v.L.) agent. Five 40 ml samples of watery stools were centrifuged at 5000 r.p.m. for 30 min at 4°C. The supernatant of each sample was centrifuged at 8000 r.p.m. for 30 min at 4°C. The second H.I. AND COMPLEMENT-FIXING
This list is maintained by the Latin American Research Department of Amnesty International, 10 Southampton
Street, London WC2 7HF,
to
whom
we are
grateful
for the
above information.-ED.L WHY HAS CYANOCOBALAMIN NOT BEEN WITHDRAWN?
SiR,-Dr Foulds and his colleagues (April 8, p. 777) ask why cyanocobalamin is still on the market. In 1970, following an earlier letter on the same subject by Foulds et al.1 this company withdrew from general sale its product Cobalin (injection cyanocobalamin B.P.). In view of the evidence of the superiority of hydroxocobalamin in the parenteral treatment of pernicious anaemia we had considered this course of action before 1970, but had deferred a final decision because the demand for cyanocobalamin continued unabated. After publication of the above plea’ for withdrawal of cyanocobalamin we felt sure that this preparation would be abandoned by clinicians in favour of hydroxocobala1. Foulds, W. S., Freeman, A. G., 35.
Phillips,
C. I., Wilson, J. Lancet, 1970, i,
(C.F.) ANTIBODY TITRES OF PAIRED
SERA FROM INFANTS AND YOUNG CHILDREN WITH ACUTE
Argentina two years ago. The detained doctors are: JORGE BEPRE (infectious diseases specialist, Cordoba, and secretary-general of the Assistant Doctors’ Union); CLAUDIO SANTIAGO BERMANN (psychiatrist, Cordoba); MARCOS BROSCHI (cardiologist, Cordoba); MARIO ROGER FALCO (neurosurgeon) ; OSCAR FATTORINI (surgeon); EDUARDO LLOSA (professor, and member of the Asociaci6n Trabajadores del Estado); MAGDALENA MAINER (Buenos Aires); ERNESTO SARAVI (obstetrician); CARLOS SASSETELLI (Cordoba; scientific secretary of the Argentine Federation of Psychiatry, central region). The doctors who have disappeared include: HoRACio JosE ALVEREZ, JAIME BARRERA ORO, NORMA LETICIA BATSCHE, HUGO FRANCISCO BELLAGAMBA, A. BONANO, ARTURO BRANDT, MARTA BREA, OFELIA ALICIA CASSANO, SAMUEL ALBERTO FALICOFF, RAUL HAROLDO FUENTES, EUGENIO FELix GALLINA (with his two medical student sons), BEATRIZ GALLINA, AUGUSTIN GOIBURU, EDUARDO MARIO KORIN, MANUEL LIBEROFF, EDUARDO MIGUEL O’NEILL, ALEJANDRO PASTORINI, ALBERTO JOSE PERGAMENTI, SYLVIA MONICA QUINTELA DALLASTA, JUAN CARLOS RISAU, JORGE MARIO ROITMAN, EDUARDO CARLOS SALA, GUILLERMO TAMBURNIN, BLANCA TARNOPOLSKY, PABLO DAVID TREJO VALLEJOS, JOSE LuÍs UJHELLY, MERCEDES- SALVADORA VEGA DE ESPECHE, GRACIELA VALLEJO, CATALINA VELAZCO DE MORINI, RUBEN MARIO DE ANGELIS, DANIEL RICARDO PEREZ, JORGE FALCONE, NORMA BEATRIZ LEIVA.
F. P. DIGGINS
Perivale, Greenford, Middlesex UB6 7HG
NON-BACTERIAL GASTROENTERITIS
supernatant sucrose
was
further
a 10 and 50% carried out in a
purified by banding on
density gradient. Centrifugation
was
SW 27.1 rotor of a Beckman L2-65B ultracentrifuge at 74 000 g for 2 h at 4°C. The band at the interface was aspirated and centrifuged at 110 000 g for 2 h in a SW 50-1rotor of the same ultracentrifuge at 4°C. The sediment thus obtained was suspended in 1 ml of phosphate-buffered saline solution (P.B.S., pH 7-0) and centrifuged at 3000 r.p.m. for 10 min at 4°C. The supernatant was used as the haemagglutinin. For haemagglutination tests, 50 pi of serial twofold dilutions ofhxmagglutinin mixed with 25 pi of 0-5% chicken red bloodcells in P.B.s. The mixture was incubated at 40C for 1 h. The titre was expressed as the reciprocal of the highest antigen dilution showing complete hsemagglutination. The titres for the agglutinins from these five stools were 128, 64, 16, 2, and
pheresis.
Their location incertain
specialised
units has the
additional advantage of allowing the study of sufficient numbers of patients to expand our knowledge of paraquat
pharmacokinetics and treatment. K.R.U.F. Institute of Renal
J. MILLER
Disease,
E. SANDERS
Royal Infirmary,
D. WEBB
Z Cardiff CF2 15
IN-VITRO IMMUNOLOGICAL ASSAY FOR DIAGNOSIS OF CŒLIAC DISEASE
interested in the paper by Dr Ashkenazi and colleagues (March 25, p. 627) on the production of leucocytemigration-inhibition factor (L.LF.) by codiac peripheral-blood lymphocytes challenged in vitro with a gluten fraction. Their patients were essentially children; earlier reportsl-5 of gluteninduced L.I.F. release by leucocytes have been based on work on adults with coeliac disease. To date, reports have consistently shown the specificity of this leucocyte migration inhibition (L.M.I.) with respect to coeliac disease, but, with one exception,3 have failed to assess its specificity in terms of other dietary
SIR,-We
were
antigens. FREQUENCY
OF L.M.I. TO THREE ANTIGENS IN C(ELM
OTHER GASTROINTESTINAL
DISEASE,
DISEASE,
AND CONTROLS
*For of-gliadin, migration inhibition was taken as a mean migration index (6 replicates per antigen dilution) below the 2 s.D. range (0.89-1.25) derived from the healthy staff control group. For oc-lactalbumin and a.c.., a migration index below 0.80 was considered to represent significant inhibition.
We have looked at both the antigen and disease specificity of this in-vitro assay system.6 L.M.I. to ot-giiadin, a-lactalbumin, and B.C.G. has been studied in five groups (table), including untreated coeliacs ingesting a normal diet and coeliacs who had been on a strict gluten-free diet for over 6 months. L.M.I. to B.C.G. was similar in all groups, confirming the potentially normal responsiveness of coeliac leucocytes in this test. L.M.I. to an a-gliadin fraction known to be toxic to cceliac patients in remission’ was virtually specific for coeliac disease. While these differences between coeliacs and other subjects could result from non-specific intestinal permeability to many dietary antigens secondary to the villous atrophy, this seems unlikely in view of the absence of any significant differences in the fre1. Bullen, A. W., Losowsky, M. S. Gut, 1976, 17, 813. 2. Douwes, F. R. Lancet, 1976, ii, 1353. 3. Asquith, P., Haeney, M. R. Gut, 1977, 18, A942. 4. Douwes, F. R., Lippmann-Nielsen, I., Hanke, R. Dt. med. Wschr. 1977,
102, 721. 5. Bullen, A. W., Losowsky, M. S. Gut, 1978, 19, 126. 6. Haeney, M. R., Asquith, P. in Perspectives in Coeliac Disease (edited by B. McNicholl, C. F. McCarthy, and P. F. Fottrell). Lancaster (in the press). 7. Schneider, R., Kendall, M. J., Hawkins, C. F. in Cœliac Disease: Proceedmgs of the Second International Cœliac Symposium (edited by W. Th. J. M. Hekkens and A. S. Peña); p. 72. Leiden, 1974.
quency of
L.M.I. to a-lactalbumin. Our results are in broad with those of Ashkenazi et al. but additionally sugagreement gest that L.M.I. is likely to be specific for a-gliadin. However, our findings do differ in one interesting respect. We found that L.M.I. to ot-gliadin was more common in treated than in untreated coeliacs, and have suggested that this may be due to a redistribution of lymphocytes after antigen withdrawal. A similar hypothesis was proposed to explain comparable results of lymphocyte transformation by gluten in cceliacs ingesting normal or gluten-free diets.8 L.M.I. to a-gliadin may be due to factors other than L.LF. generated by the activation of sensitised T lymphocytes, including antigen-antibody complexes9 or L.I.F. release by B cells.1o Despite these alternative explanations, L.M.I. to antigenic challenge shows a qualitative correlation with in-vivo cell-mediated immunity in the host.
Regional Immunology Unit, and Metabolic Research Unit, East Birmingham Hospital, Birmingham B9 5ST
M. R. HAENEY
P. ASQUITH
BONE-MARROW TRANSPLANTATION IN ACUTE LEUKÆMIA
SIR,-Commenting upon the report by the U.C.L.A. BoneTransplant Team,’ Dr Catovsky and his colleagues (Feb. 4, p. 266) ask "Did the controls receive the most intensive treatment, short of total-body irradiation, that could be safely administered without the support of a marrow graft?". marrow
This
cannot be answered: if the patient did not surthe was obviously too intensive, but if the patreatment vive, tient lives there is no way to know whether or not more therapy could have been tolerated. The principal objective of the marrow-transplantation approach is the administration of "supralethal" antileukaemic therapy with subsequent avoidance of death from marrow aplasia by transplantation of a "new" bone-marrow. We have reported long-term survival in patients with relapsed acute leukaemia, both lymphoblastic and myeloid, treated by intensive chemotherapy, total-body irradiation, and bone-marrow transplantation.2,6of 16 recipients of syngeneic marrow and 14 of 110 recipients of allogeneic marrow are still alive, without leukaemia, 2t to 7y years later. Actuarial analysis4 of the probability of being in remission indicated a constant rate of relapse for the first 2 years. Thereafter, the relapse-rate became very low, indicating a high probability that these long-term survivors are cured of their diseaseespecially since all the living patients are well out on the plateau of the curve. Powles6 has pointed out that a similar analysis of patients treated with chemotherapy shows a continued risk of relapse with time measured over years. Of course, with a constant rate of relapse (or death) there would always be a few long-term survivors if one starts with a sufficiently large number of patients. An actuarial analysis of survival after first relapse of the 150 patients mentioned by Catovsky et al. would be of interest.
question
Fred Hutchinson Cancer Research Center, Seattle, Washington 98104, U.S.A.
E. DONNALL THOMAS
8. Asquith, P. ibid. p. 242. 9. Spitler, L., Huber, H., Fudenberg, H. H. J. Immun. 1969, 102, 404. 10. Rocklin, R. E., MacDermott, R. P., Chess, L., Schlossman, S. F., David, J. R. J. exp. Med. 1974, 140, 1303. 11. David, J. R., David, R. R. Progr. Allergy, 1972, 16, 300. 1. U.C.L.A. Bone-marrow Transplant Team Lancet, 1977, ii, 1197. 2. Thomas, E. D., and others Blood, 1977, 49, 511. 3. Fefer, A., Buckner, C. D., Thomas, E. D., Cheever, M. A., Clift, R. A., Glucksberg, H., Neiman, P. E., Storb, R. New Engl. J. Med. 1977, 297, 146. 4. Kaplan, E. L., Meier, P. J. Am. statist. Ass. 1958, 53, 457. 5. Thomas, E. D., Flournoy, N., Buckner, C. D., Clift, R. A., Fefer, A., Neiman, P. E., Storb, R. Leukemia Res. 1977, 1, 67. 6. Powles, R. L. Biomedicine, 1976, 24, 327.
877
ARGENTINA, MEDICINE, AND THE WORLD CUP SiR,—Iam increasingly concerned at the number of doctors
disappeared in Argentina. I have written to the Argentinian ambassador asking for his reassurance that the allegations relating to these disappearing doctors are untrue, but I have had no reply. It seems to me that no doctor can now feel safe in Argentina. Medical advisers will be essential during the World Cup football matches to be held in Argentina this summer. Could I urge who have
doctors concerned to withdraw their services from World Cup football until the Argentinian Government desists in its policy of causing doctors to disappear without trace. General Infirmary, Leeds LS1 3EX
J. A. COTTERILL
Dr BEATRIZ
IPARRAGUIRRE DE WEINSTEIN, whose disappearreported by Dr Catovsky in our issue of March 25, has been released, after international pressure. On April 5 armed men halted an ambulance in Buenos Aires and seized Dr HILDA ERENU DE LIwSKI. Nothing more is ance was
known of her, and her husband, Dr NORBERTO IGNACIO LIwsKI, has also disappeared. A similar fate has overtaken Dr FRANCISCO MANUEL GARCIA FERNANDEZ. These 3 names must be added to Amnesty International’s March 28 list of at least 42 doctors and 35 medical students known to have been detained or who have disappeared since the military coup in
events of the past eight years have proved us to be entirely wrong in this respect. The demand for cyanocobalamin has persisted to such an extent that we have now restored it to our general list, and our justification for so doing lies in the belief that we, as pharmaceutical manufacturers, have an obligation to meet the requirements of prescribers for a B.P. drug whether or not we agree with their choice of such drug in a particular clinical situation.
min, but the
Pabyrn Laboratories, Paines and Byrne, Limited,
HÆMAGGLUTININ FROM HUMAN REOVIRUS-LIKE AGENT
SiR,—Hxmagglutinins have been prepared from cultured African green monkey kidney cells and bovine kidney cells2 infected with Nebraska calf diarrhoea virus. We have obtained a hasmagglutinin from the stools of infants and young children infected with human reovirus-like (H.R.v.L.) agent. Five 40 ml samples of watery stools were centrifuged at 5000 r.p.m. for 30 min at 4°C. The supernatant of each sample was centrifuged at 8000 r.p.m. for 30 min at 4°C. The second H.I. AND COMPLEMENT-FIXING
This list is maintained by the Latin American Research Department of Amnesty International, 10 Southampton
Street, London WC2 7HF,
to
whom
we are
grateful
for the
above information.-ED.L WHY HAS CYANOCOBALAMIN NOT BEEN WITHDRAWN?
SiR,-Dr Foulds and his colleagues (April 8, p. 777) ask why cyanocobalamin is still on the market. In 1970, following an earlier letter on the same subject by Foulds et al.1 this company withdrew from general sale its product Cobalin (injection cyanocobalamin B.P.). In view of the evidence of the superiority of hydroxocobalamin in the parenteral treatment of pernicious anaemia we had considered this course of action before 1970, but had deferred a final decision because the demand for cyanocobalamin continued unabated. After publication of the above plea’ for withdrawal of cyanocobalamin we felt sure that this preparation would be abandoned by clinicians in favour of hydroxocobala1. Foulds, W. S., Freeman, A. G., 35.
Phillips,
C. I., Wilson, J. Lancet, 1970, i,
(C.F.) ANTIBODY TITRES OF PAIRED
SERA FROM INFANTS AND YOUNG CHILDREN WITH ACUTE
Argentina two years ago. The detained doctors are: JORGE BEPRE (infectious diseases specialist, Cordoba, and secretary-general of the Assistant Doctors’ Union); CLAUDIO SANTIAGO BERMANN (psychiatrist, Cordoba); MARCOS BROSCHI (cardiologist, Cordoba); MARIO ROGER FALCO (neurosurgeon) ; OSCAR FATTORINI (surgeon); EDUARDO LLOSA (professor, and member of the Asociaci6n Trabajadores del Estado); MAGDALENA MAINER (Buenos Aires); ERNESTO SARAVI (obstetrician); CARLOS SASSETELLI (Cordoba; scientific secretary of the Argentine Federation of Psychiatry, central region). The doctors who have disappeared include: HoRACio JosE ALVEREZ, JAIME BARRERA ORO, NORMA LETICIA BATSCHE, HUGO FRANCISCO BELLAGAMBA, A. BONANO, ARTURO BRANDT, MARTA BREA, OFELIA ALICIA CASSANO, SAMUEL ALBERTO FALICOFF, RAUL HAROLDO FUENTES, EUGENIO FELix GALLINA (with his two medical student sons), BEATRIZ GALLINA, AUGUSTIN GOIBURU, EDUARDO MARIO KORIN, MANUEL LIBEROFF, EDUARDO MIGUEL O’NEILL, ALEJANDRO PASTORINI, ALBERTO JOSE PERGAMENTI, SYLVIA MONICA QUINTELA DALLASTA, JUAN CARLOS RISAU, JORGE MARIO ROITMAN, EDUARDO CARLOS SALA, GUILLERMO TAMBURNIN, BLANCA TARNOPOLSKY, PABLO DAVID TREJO VALLEJOS, JOSE LuÍs UJHELLY, MERCEDES- SALVADORA VEGA DE ESPECHE, GRACIELA VALLEJO, CATALINA VELAZCO DE MORINI, RUBEN MARIO DE ANGELIS, DANIEL RICARDO PEREZ, JORGE FALCONE, NORMA BEATRIZ LEIVA.
F. P. DIGGINS
Perivale, Greenford, Middlesex UB6 7HG
NON-BACTERIAL GASTROENTERITIS
supernatant sucrose
was
further
a 10 and 50% carried out in a
purified by banding on
density gradient. Centrifugation
was
SW 27.1 rotor of a Beckman L2-65B ultracentrifuge at 74 000 g for 2 h at 4°C. The band at the interface was aspirated and centrifuged at 110 000 g for 2 h in a SW 50-1rotor of the same ultracentrifuge at 4°C. The sediment thus obtained was suspended in 1 ml of phosphate-buffered saline solution (P.B.S., pH 7-0) and centrifuged at 3000 r.p.m. for 10 min at 4°C. The supernatant was used as the haemagglutinin. For haemagglutination tests, 50 pi of serial twofold dilutions ofhxmagglutinin mixed with 25 pi of 0-5% chicken red bloodcells in P.B.s. The mixture was incubated at 40C for 1 h. The titre was expressed as the reciprocal of the highest antigen dilution showing complete hsemagglutination. The titres for the agglutinins from these five stools were 128, 64, 16, 2, and
