Femur bone densities

Femur bone densities

1662 Ethics of experiments in animals SiR,—Your May 22 editorial contains some remarkable assertions, especially about man’s evolutionary status as c...

177KB Sizes 2 Downloads 80 Views

1662

Ethics of experiments in animals SiR,—Your May 22 editorial contains some remarkable assertions, especially about man’s evolutionary status as champion predator. You should be well aware that evolution can only be viewed with hindsight, and whether our species’ rapacious predatory record will prove successful in the long term can only be speculation. Furthermore, the notion that ethics and morals can be dismissed before the throne of evolution is fascistic. Similar arguments have been used by white men to justify slavery and genocide of native peoples. Turning to the issue of the care of laboratory animals, you suggest that "the needs of the animal must come first". These needs must include the needs to live a natural life and not be used for invasive procedures or be kept in restrictive confinement. I have no knowledge of conditions in the University of Guelph. However, several investigations by animal rights workers in the UK have uncovered appalling conditions of animal housing that fail to meet Home Office guidelines, inadequate staff training, and poor animal handling.l,2 In the case of one supplier of primates, this failure has been acknowledged by the UK Home Office.3 The British Union for the Abolition of Vivisection does not believe that the needs of animals can be adequately met under present UK laws and monitoring systems. The Lancet should be calling not for slightly improved laboratory conditions, but a massive reduction in animal use, and a shift of resources to issues of relevance to human health. British Union for the Abolition of Vivisection, 16a Crane Grove, London N7 8LB, UK

DONAL CRAWFORD

1. British Union for the Abolition of Vivisection. The use of primates for research in the United Kingdom. London: BUAV, 1992. 2. Brtitish Union for the Abolition of Vivisection. A report into Wickham Laboratories Ltd. London: BUAV, 1993. 3. Wardle C. Primates (Allegations) [Written Answer to Parliamentary Question]. Official Report, Dec 3, 1992: c215-16.

Femur bone densities SIR,-Ms Lees and colleagues (March 13, p 673) establish that the bone density in femora from 18th and 19th century burials in Christ Church, Spitalfields, London, was greater than that in present day women, and relate their data to a current increased incidence of hip fractures. They suggest that the difference, present at puberty and persisting beyond the menopause, is due to the greater physical activity imposed on women of the earlier

period. Ivanhoe had earlier studied a similar 18th century population from Saint Bride’s columbarium in the Fleet Street area.! Thin sections of the first and third molars allowed him to demonstrate in roughly half the skeletons the residual lesions of sunlight deficiency rickets that had developed between infancy and age ten. At that time the hours of insolation became adequate to the need, and the skeletal lesions healed. During healing, rachitic long bones become harder and denser than normal, appearing ebumated or ivory-like to older pathologists. These robust bones of healed rickets provide an explanation for Lees and co-workers’ findings. Virchow, it is worth noting, provided a precedent for the suggestion when he held that the simian cast to bones of Neanderthal man reflected not a separate line in the evolution of Homo but rickets in man living during the Wiirm ice age. A more comprehensive description of the bones would probably reinforce one explanation or the other. Did any of the femora excluded from the Christ Church study show hip or knee deformities, bowing, or other stigmata of childhood rickets? My observer bias forbids any attempt at interpreting Lees’ fig 1. Department of Pharmacology, University of California, San Francisco, California 94143, USA

FREDERICK H. MEYERS

Interglobular dentine in first and third molars: relation to hours of sunshine during growth in two archeological populations from England. Calcif Tissue Int

1. Ivanhoe F.

1982; 34: 136-44. 2. Ivanhoe F. Was Virchow

right about Neanderthal? Nature 1970; 227: 577-79.

Paracelsus SIR,-As an addition to Professor Feder’s thoughtful article on (May 29, p 1396), I would like to draw attention to one

Paracelsus

giant predecessor of medicine. In his third "defension" from August 19, 1538, he declared "Everything is a poison, the dose alone makes a thing not a poison".1 This statement contains a central concept of modem experimental and clinical pharmacology and toxicology-namely, the dose-effect relationship, a principle of relevance not only to theoreticians but also to clinicians. It appears to be the most durable consequence of, and could well be considered to be a "surviving paradigma" of, Paracelsus. most important finding of this

Zentrum für Kardiovaskulare 6500 Mainz, Germany

Pharmakologie,

GUSTAV G. BELZ

K, ed. Theophrast von Hohenheim (Paracelsus): Sieben Defensiones (Antwort auf etliche Verunglimfungen seiner Misgonner). Leipzig: J A Barth,

1. Sudhoff

1915: 25.

Reappraisal of endotoxin in gram-negative sepsis? to compare the "classical" view on the of events leading to gram-negative sepsis, organ failure, and

SIR,-We should like course

death with that proposed by Dr Hurley (May l,p 1133). Classically, endotoxins are thought to play a central part in gram-negative sepsis by their induction of toxic amounts of cytokines, which cause the clinical symptoms. Hurley suggests that endotoxin in the bloodstream is an epiphenomenon accompanying the transition of bacteria to their cell-wall deficient L-forms, and that it is these L-forms that are responsible for the symptoms. Unless one wants to deny the involvement of cytokines in the course of gram-negative sepsis, one is left with the question: which cellular component of the L-form is responsible for the induction of cytokines? L-forms lack a rigid cell wall, are deficient in peptidoglycan, and possess a single membrane directly surrounding the cytoplasm. This membrane contains endotoxins ; although on a cell-to-cell basis, L-forms contain less, they were sometimes found to be more endotoxic than complete bacterial There is evidence that L-forms shed more endotoxins that parent bacterial Thus, transition to L-fonns is not necessarily followed by a halt in the release of endotoxins. For the L-form concept to be relevant to the understanding of gramnegative sepsis it is not necessary to dismiss the part played by endotoxin. The word "endotoxin" may be a misnomer, but we think that there is sufficient evidence obtained by injecting endotoxins into healthy volunteers to prove that it can give rise to the clinical symptoms of gram-negative sepsis. In our opinion, the novel hypothesis of Hurley is not a reappraisal of the role of endotoxins, but a reappraisal of the bacterial form giving rise to those endotoxins-ie, possibly L-fonns.

Vrije Universiteit,

J. APPELMELK J. DE GRAAFF L. G. THIJS

1081 BT Amsterdam, Netherlands

D. M. MACLAREN

B. Department of Medical Microbiology and Intensive Care Unit,

1. Mattman L. Cell wall deficient forms. Cleveland: CRC Press, 1974:90 and 199.

Tuberculosis in India: question of

compliance SiR,—The figure of 500 000 Indians dying every year from tuberculosis reported by Mangla (May 1, p 1142) makes it clear that three decades of National Tuberculosis Control Programme in India has achieved little-either in reduction in incidence or prevalence. However, the reasons for non-compliance reported by Mangla are ambiguous. Poor performance of this programme is due to very high (more than 50%) rate of default in treannent.1-3 Some of the causes of default, such as socioeconomic conditions, cannot be changed in the foreseeable future. Nevertheless, one important factor-prolonged duration of treatment—can be tackled immediately if short-course chemotherapy is introduced. In fact,