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metals on myocardiopathy and other ursemic manifestationsare now being investigated.Department of Medicine,Karolinska Hospital,S-104 01 Stockholm, Sweden

L. E. LINSK. PEHRSSON

CHILDREN’S USE OF HEARING-AIDS

SIR,-We are evaluating N.H.S. hearing aids (mainly thepostaural OL67, B.E.ll, and B.E.12) issued to children in theReading area. We assess the electroacoustic performance of theaids three months to a year after issue with a Bruel and Kiaerhearing-aid test box, and at the same time we evaluate thechild’s use of the aid in hearing speech. We use sentences’ asthe speech signal and cafeteria noise (speech babble) as thenoise source. The child is asked to listen to and repeat backsentences presented through a loudspeaker 1. 2m to his frontin a large partially sound-damped room. In the noisy condi-tion, cafeteria noise at -5 dB relative to the speech signal isemitted from a loudspeaker 1.2m behind the child. We set thenoise 5 dB below the speech signal on the grounds that in noisyconditions a speaker will raise his voice above the background.We are concentrating on children aged 10-16 years.From patients’ notes we selected 87 children. 17 were un-

suitable because of behaviour problems, multiple handicapand poor language skills, and of the remainder only 37attended for assessment. Their range of pure-tone hearing loss(better ear) was 14-80 (mean 43) dB. For listening to sen-tences with and without hearing-aids in the quiet, the resultswere: 1 patient gained >30 dB when wearing his aid, 6 pa-tients gained 20-29 dB when wearing their aids, 11 patientsgained 10-19 dB, 12 patients gained 0-9 dB, and 7 patientsdid worse (2-9 dB worse) with their aid. The test/retest errorfor each patient was 2-3 dB. All patients did worse in the pre-sence of cafeteria noise, as expected. Only one of the thirty-seven aids was badly malfunctioning. The average electro-acoustic gain at 1 kHz of the aid as worn was 18 dB (abouthalf the maximum), with a range of 1-38 dB.From these preliminary data we draw the following tenta-

tive conclusions:

(1) Our formal speech testing, which requires considerabletime, concentration by the patient, and linguistic skills, is notsuited to the assessment of a significant proportion (17 out of87) of hearing-aided children.(2) On telephoning parents of 10 non-attenders we found thatthe children were not using their aids or had thrown themaway because they were of little help or for cosmetic reasons.(3) In quiet conditions only 1 patient achieved a speech intel-ligibility gain approaching the maximum possible electroacous-tic gain (about 38 dB).(4) Hearing-aid wearers have difficulties in listening in noisysurrounds.2(5) The range of electro acoustic gain of the aids as worn waswide, with an average gain setting of half the maximum. Thisconfirms previous reports.3 The electroacoustic gain was notalways related to the speech intelligibility gain.

This preliminary survey suggests that, although some

children can obtain substantial advantage from their postauralaids for listening to speech in the quiet, most patients showonly a modest advantage, and some are actually worse off. Ourfindings accord with the provisional results of a similar studyin progress in the North of England so the situation in Read-ing probably reflects the national picture.

Audiology Unit,Royal Berkshire Hospital,Reading RG1 5AN

JOHN BENCHTERRY WATSONTREVOR DOWDING

1. Fry, D. B. Lancet, 1961, ii, 197.2. Briskey, R. J. in Handbook of Clinical Audiology (edited by J. Katz), p. 592.

Baltimore, 1972.3. Yantis, P. A., Millin, J., Shapiro, I. J. Speech Hear. Res. 1966, 9, 178.4. Newall, P. Personal communication.

DELAYED WOUND HEALING IN JAUNDICED RATS

SIR Jaundice seems to delay wound healing in both pa-tients and laboratory animals, but the mechanism is obscure.’

’

Since delay may be due to interference with cell division wehave made cytokinetic studies, using vincristine to arrest

mitosis in metaphase2 and bileduct ligation to induce jaundice.24 adult female Sprague-Dawley rats weighing 180-200 g

were divided into two groups. In the first group jaundice wasinduced by ligation and division of the common bileduct,while in the second, preparation of controls was similar butligation was omitted. After 6 days serum-bilirubin in the jaun-diced group reached 178 ±22 p.mol/1. Two animals from eachgroup were killed at 9 A.M. by cervical dislocation and all the

Mitotic index of colonic epithelium in jaundiced and control rats beforeand after vincristine.Vertical bars represent standard errors.

others were injected with vincristine, 1 mg/kg body-weight,before being killed in pairs after 13, 30, 45, and 60 min. Speci-mens from cxcum and ascending colon were fixed m Carnoy’sfluid for 6 h, embedded in paraffin wax, and sections were cuttransversely at 4µm and stained with Harris’s haematoxyhn.Only crypts seen in complete longitudinal profile were selectedand in each section three groups of 1000 cells were countedfrom the bottom upwards, noting the number and positions ofthe nuclei. In the 4 animals not given vincristine all stages ofmitosis were included, but in those given the drug only pro-phases and metaphases were seen. The results are tabulated toshow that the mitotic-rate is significantly increased in the jaun-diced animals (figure).The results are the reverse of what we originally expected:

instead of a reduction of mitotic activity, jaundice seems tohave induced an increase. This frequency of figures may bemisleading and result from an arrest of mitosis which recallsthe appearance of the liver in patients dying with jaundice dueto leptospirosis (Weil’s disease).3 Bileduct ligation, however,has altered not only the milieu interieur and the bilirubin towhich the colonic epithelium is exposed, but also the externalenvironment, the gut lumen. Recent research into the aoologyof large-bowel cancer has suggested that bile acids are

degraded by faecal bacteria into carcinogens,4 and bileduct

ligation will have largely excluded these from the bowel m thejaundiced animals. Further work is being undertaken on

1. Bayer, I., Ellis, H. Br. J. Surg. 1976, 63, 392.2. Wright, N., Morley, A., Appleton, D. Cell Tissue Kinet. 1972, 5, 351.3. Weinbren, H. K. in Systemic Pathology (edited by G. Payling Wright and

W. St. C. Symmers); p. 629. London, 1966.4. Hill, M. J. Cancer, Philad. 1974, 34, 815.