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FLOWER VASES AS RESERVOIRS OF PATHOGENS
359 prepared in c.s.F. obtained from the of digoxin therapy. On the above regimen for maintenance therapy, plasmadigoxin levels ranged from 1-5 to 2-1 4ng. per ml., which is The c.s.F.-digoxin within the normal therapeutic ranged concentration was less than 0-2 ng. per ml. on one occasion, and undetectable on all other occasions. The c.s.F. pressures remained abnormally high-260-350 mm. C.S.F.-and little different from those recorded on steroid therapy alone or on no drug therapy. With the reintroduction of steroids the patient gained weight, but he remained symptomless, no digoxin side-effects were encountered, and clinical examination showed no change. Plasma sodium, potassium, and urea levels, as well as c.s.F. sodium, potassium, and magnesium levels, remained unaltered, as did serial electrocardiograms. standards for this
patient before the
were
start
C.s.F. secretion from the choroid plexus is believed to be an active process associated with a sodium/potassiumactivated adenosine triphosphatase which in certain circumstances is inhibited by cardiac glycosides.5 It might be deduced from this that digoxin would reduce the raised c.s.F. pressure in conditions such as B.I.H., but this has not been substantiated in the present report. We have also failed to detect significant amounts of digoxin in C.s.F., which is at variance with the findings of Bertler et al .,2 who detected it in infants, with a plasma/c.s.F. ratio of 3/1-4/1, using a modified 86Rb method for digoxin
assay.
Although digoxin, in a comparatively high daily dose, failed to lower the C.S.F. pressure in this case of B.I.H., a beneficial effect remains possible in other cases of raised intracranial pressure. Comparison of our case with those of Neblett et al.l is difficult, because these workers do not state what were their " normal " doses of digoxin. National Hospital for Nervous Diseases, London WC1N 3BG.
Queen Square,
G. D. SCHOTT.
Poisons Unit,
Guy’s Hospital,
D. HOLT.
London SE1 9RT.
1. Neblett, C. R., McNeel, D. P., Waltz, T. A., Jr., Harrison, G. M. Lancet, 1972, ii, 1008. 2. Bertler, Å., Andersson, K.-E., Wettrell, G. ibid. 1973, ii, 1453. 3. Smith, T. W., Butler, V. P., Haber, E. New Engl. J. Med. 1969, 4.
281, 1212. Chamberlain, D. A., White, Br. med. J. 1970, iii, 429.
5. Davson, H. 1967.
R.
J., Howard, M. R., Smith, T. W.
Physiology of the Cerebrospinal Fluid; p. 137. London,
SCREENING FOR TAY-SACHS DISEASE SIR,-Professor Edwards (Nov. 17, p. 1143) is in error when he states that selective feticide has rabbinical approval. To eliminate Tay-Sachs disease by " selective termination of affected pregnancies "1 is unacceptable in Judaism. Recourse to abortion in circumstances where the unborn fetus is determined to have Tay-Sachs disease is not permissible in traditional Jewish law unless a threat to the mother’s life exists. Furthermore, since no therapeutic advantage is obtained by amniocentesis carried out solely for the purpose of diagnosing a severe genetic defect such as Tay-Sachs disease, it poses an unnecessary risk to both mother and fetus and would hence be prohibited. Amniocentesis performed to diagnose a condition such as bloodgroup incompatibility for which medical therapy is available, not only may but must be performed by the physician, even repeatedly in Jewish law, as part of good medical practice. The reproductive patterns of Jewish families must be influenced as much by ethical and religious considerations, such as the Biblical commandment to procreate, as by medical and genetic factors. Queens Hospital Center, New York 11432,
Queens,
U.S.A. 1.
Glazerman,
L. R. New
FRED ROSNER.
Engl. J. Med. 1973, 289, 754.
FLOWER VASES AS RESERVOIRS OF PATHOGENS
SIR,—David Taplin and Patricia Mertz1 report large numbers of potentially pathogenic bacteria in water from flower vases. In 1963 Smellie and Brincklow2 recommended addition of chlorhexidine (’Hibitane’), 1 ml. of 5% solution to 500 ml. tap-water, which inhibited the growth of microorganisms and furthermore delayed decomposition and obviated the necessity for changing the water. The findings were reproduced by Marie Christensen. We have used chlorhexidine in 0-02% solution for flower water in our hospital since 1967 and we have never been able to culture pathogenic bacteria from flower vases. Department of Bacteriology and KIRSTEN STÆHR JOHANSEN Intensive-care Unit, HELGA LAURSEN Frederiksberg Hospital, BENDT J. WILHJELM. Copenhagen, Denmark. 1. Taplin, D., Mertz, P. Lancet, 1973, ii, 1279. 2. Smellie, H., Brincklow, P. ibid. 1963, ii, 777. 3. Petersen, M. Tidsskr. Sygepleje. 1969, p. 259.
C1 INACTIVATOR FROM CANCER CELLS SIR,-Blocking antibodies reacting in anti-antibody complexes may be responsible for defending neoplastic tissue against the humoral immunological system Instead of searching for this blocking mechanism in the humoral phase, I have tried to find a blocking factor on the cancer-cell membrane itself. Cl inactivator operates at the start of the complement system (i.e., in Cl activation of C4 and C2).4 Cl inactivator contains 12% hexose and 17% N-acetylneuraminic acid.s This accords with results for the sedimentation constant, spectrophotometric absorption, and immunoelectrophoretic patterns, which suggest that Cl inactivator is an alpha2
neuraminoglycoprotein,s Cl inactivator has been
found on the membrane of human-carcinoma and blast-leukxmia cells, using immunofluorescence and microfluorimetry.7,8 The presence of Cl inactivator on these cells represents a possible blocking mechanism, or more correctly an inhibiting mechanism.7,8 Therefore, it seemed reasonable to isolate and purify Cl inactivator from cancer cells. The carcinoma cells from pleural and ascites fluid from patients with carcinosis were cultured in Eagle’s minimum essential medium containing 15% inactivated fetal calf serum. Finally, the cells were cultured in convenient aminoacid media. The Cl inactivator from carcinoma cells was isolated from the media and purified by column chromatography. In this way, 3 different preparations were obtained: (1) from the. original ascites or pleural fluid; (2) from the Eagle medium; and (3) from the aminoacid medium. The 3 different preparations of C1 inactivator from carcinoma cells were compared with purified normal Cl inactivator from human serum. The methods used were: immunoelectrophoretic patterns; inhibition of human fibrinolysis; inhibition of complement activation; and inhibition of the Cl esterase effect on N-acetyl-L-tyrosine ethyl ester. The results of these investigations showed a striking similarity between Cl inactivator from the 3 carcinoma-cell preparations and the normal Cl inactivator. There was a difference with Freeman electrophoresis in which the normal Cl inactivator has a double peak. The first peak represents albumin-bound Cl inactivator and the second peak free CT. With the Cl inactivator from carcinoma-cell preparations there was no binding to albumin. The possible role of Cl inactivator from carcinoma cells in blocking or inhibiting the humoral immunological system was studied next. Human cancer cells were incubated with
patient before the
were
start
C.s.F. secretion from the choroid plexus is believed to be an active process associated with a sodium/potassiumactivated adenosine triphosphatase which in certain circumstances is inhibited by cardiac glycosides.5 It might be deduced from this that digoxin would reduce the raised c.s.F. pressure in conditions such as B.I.H., but this has not been substantiated in the present report. We have also failed to detect significant amounts of digoxin in C.s.F., which is at variance with the findings of Bertler et al .,2 who detected it in infants, with a plasma/c.s.F. ratio of 3/1-4/1, using a modified 86Rb method for digoxin
assay.
Although digoxin, in a comparatively high daily dose, failed to lower the C.S.F. pressure in this case of B.I.H., a beneficial effect remains possible in other cases of raised intracranial pressure. Comparison of our case with those of Neblett et al.l is difficult, because these workers do not state what were their " normal " doses of digoxin. National Hospital for Nervous Diseases, London WC1N 3BG.
Queen Square,
G. D. SCHOTT.
Poisons Unit,
Guy’s Hospital,
D. HOLT.
London SE1 9RT.
1. Neblett, C. R., McNeel, D. P., Waltz, T. A., Jr., Harrison, G. M. Lancet, 1972, ii, 1008. 2. Bertler, Å., Andersson, K.-E., Wettrell, G. ibid. 1973, ii, 1453. 3. Smith, T. W., Butler, V. P., Haber, E. New Engl. J. Med. 1969, 4.
281, 1212. Chamberlain, D. A., White, Br. med. J. 1970, iii, 429.
5. Davson, H. 1967.
R.
J., Howard, M. R., Smith, T. W.
Physiology of the Cerebrospinal Fluid; p. 137. London,
SCREENING FOR TAY-SACHS DISEASE SIR,-Professor Edwards (Nov. 17, p. 1143) is in error when he states that selective feticide has rabbinical approval. To eliminate Tay-Sachs disease by " selective termination of affected pregnancies "1 is unacceptable in Judaism. Recourse to abortion in circumstances where the unborn fetus is determined to have Tay-Sachs disease is not permissible in traditional Jewish law unless a threat to the mother’s life exists. Furthermore, since no therapeutic advantage is obtained by amniocentesis carried out solely for the purpose of diagnosing a severe genetic defect such as Tay-Sachs disease, it poses an unnecessary risk to both mother and fetus and would hence be prohibited. Amniocentesis performed to diagnose a condition such as bloodgroup incompatibility for which medical therapy is available, not only may but must be performed by the physician, even repeatedly in Jewish law, as part of good medical practice. The reproductive patterns of Jewish families must be influenced as much by ethical and religious considerations, such as the Biblical commandment to procreate, as by medical and genetic factors. Queens Hospital Center, New York 11432,
Queens,
U.S.A. 1.
Glazerman,
L. R. New
FRED ROSNER.
Engl. J. Med. 1973, 289, 754.
FLOWER VASES AS RESERVOIRS OF PATHOGENS
SIR,—David Taplin and Patricia Mertz1 report large numbers of potentially pathogenic bacteria in water from flower vases. In 1963 Smellie and Brincklow2 recommended addition of chlorhexidine (’Hibitane’), 1 ml. of 5% solution to 500 ml. tap-water, which inhibited the growth of microorganisms and furthermore delayed decomposition and obviated the necessity for changing the water. The findings were reproduced by Marie Christensen. We have used chlorhexidine in 0-02% solution for flower water in our hospital since 1967 and we have never been able to culture pathogenic bacteria from flower vases. Department of Bacteriology and KIRSTEN STÆHR JOHANSEN Intensive-care Unit, HELGA LAURSEN Frederiksberg Hospital, BENDT J. WILHJELM. Copenhagen, Denmark. 1. Taplin, D., Mertz, P. Lancet, 1973, ii, 1279. 2. Smellie, H., Brincklow, P. ibid. 1963, ii, 777. 3. Petersen, M. Tidsskr. Sygepleje. 1969, p. 259.
C1 INACTIVATOR FROM CANCER CELLS SIR,-Blocking antibodies reacting in anti-antibody complexes may be responsible for defending neoplastic tissue against the humoral immunological system Instead of searching for this blocking mechanism in the humoral phase, I have tried to find a blocking factor on the cancer-cell membrane itself. Cl inactivator operates at the start of the complement system (i.e., in Cl activation of C4 and C2).4 Cl inactivator contains 12% hexose and 17% N-acetylneuraminic acid.s This accords with results for the sedimentation constant, spectrophotometric absorption, and immunoelectrophoretic patterns, which suggest that Cl inactivator is an alpha2
neuraminoglycoprotein,s Cl inactivator has been
found on the membrane of human-carcinoma and blast-leukxmia cells, using immunofluorescence and microfluorimetry.7,8 The presence of Cl inactivator on these cells represents a possible blocking mechanism, or more correctly an inhibiting mechanism.7,8 Therefore, it seemed reasonable to isolate and purify Cl inactivator from cancer cells. The carcinoma cells from pleural and ascites fluid from patients with carcinosis were cultured in Eagle’s minimum essential medium containing 15% inactivated fetal calf serum. Finally, the cells were cultured in convenient aminoacid media. The Cl inactivator from carcinoma cells was isolated from the media and purified by column chromatography. In this way, 3 different preparations were obtained: (1) from the. original ascites or pleural fluid; (2) from the Eagle medium; and (3) from the aminoacid medium. The 3 different preparations of C1 inactivator from carcinoma cells were compared with purified normal Cl inactivator from human serum. The methods used were: immunoelectrophoretic patterns; inhibition of human fibrinolysis; inhibition of complement activation; and inhibition of the Cl esterase effect on N-acetyl-L-tyrosine ethyl ester. The results of these investigations showed a striking similarity between Cl inactivator from the 3 carcinoma-cell preparations and the normal Cl inactivator. There was a difference with Freeman electrophoresis in which the normal Cl inactivator has a double peak. The first peak represents albumin-bound Cl inactivator and the second peak free CT. With the Cl inactivator from carcinoma-cell preparations there was no binding to albumin. The possible role of Cl inactivator from carcinoma cells in blocking or inhibiting the humoral immunological system was studied next. Human cancer cells were incubated with