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The maternity care of deaf women is a subject which has received little attention, either within midwifery research, or within the arena of disability studies. Previous research has highlighted basic difficulties of access and information for such women. Midwives need to be aware of the challenges which can exist in ensuring deaf women can give informed consent, and that their rights and expectations under the Patient's Charter and Disability Discrimination Act are met. Failure of communication could potentially lead to a civil action for negligence. The use of relatives and friends for translation is still a common practice, but a case study illustrates the way in which this can distort even a relatively straightforward communication. Increasingly, the threat of litigation will probably lead to a growth in the availability of professional sign language interpreters, but maternity services may wish to consider the relative merits of different models for accessing these services.

On November 8 1995 the Disability Discrimination Act was passed by parliament making it '…unlawful to discriminate against disabled persons in connection with…the provision of goods, facilities and services…'. The aim of this article is to look at some of the possible implications of this legislation for health professionals in their dealings with one particular group of disabled people, namely the Deaf community whose first or preferred language is British Sign Language.

Although deaf women are usually seen as disabled, there is a movement among British Sign Language Users (BSL) to be seen instead as a linguistic minority. The deaf community itself is divided on this issue, and it is seen by some commentators on disability issues as inappropriate at a time when the meaning of the term ‘disability’ is itself being redefined positively. Access to services including sign language translation may depend on how these ‘labels’ are interpreted and used. Midwives should be sensitive to the woman's own, potentially ambiguous, view of herself as either having a disability or being a member of particular cultural and linguistic group.

Stabilization of equipment during endoscopic procedures frequently presents a problem. Most attempts to anchor a cystoscope have been cumbersome or have afforded transient stability. We describe an easily adjustable, flexible cystoscope holder that may be attached readily and locked in place after positioning. The unique open-sided clamp allows for a firm but delicate grasp of fiberoptic instruments. In addition to this function the flexible cystoscope holder may be adapted easily to become a surgical retractor. Our experience with this instrument has led to greater versatility during endoscopic and open procedures.

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.

Interactions between Bromobenzene Dose, Glutathione Concentrations, and Organ Toxicities in Single- and Multiple-Treatment Studies. KLUWE, W. M., MARONPOT, R. R., GREENWELL, A., AND HARRINGTON, F. (1984). Fundam. Appl. Toxicol. 4, 1019–1028. A single oral dose of 4.0 mmol/kg bromobenzene transiently depleted hepatic and renal reduced nonprotein sulfhydryl group (NPS) concentrations, caused hepatocellular necrosis, and increased serum glutamic-pyruvic transaminase activity in male Fischer 344 rats. The depletion of NPS had partially reversed by 24 hr, and NPS concentrations were approximately twice normal values by 48 hr post-treatment When the effects of single and repeated (once dairy for 2, 4, or 10 days) treatments with 4.0 mmol/kg were compared, it was apparent that the severity of hepatotoxicity lessened and the percentage depletions of hepatic and renal NPS concentrations decreased with increasing length of bromobenzene treatment There were essentially no signs of toxicity following the tenth treatment with 4.0 mmol/kg. Single-treatment studies indicated the following dose-response; 2.0 mmol/kg bromobenzene depleted liver NPS and was hepatotoxic 0.5 mmol/ kg caused a lesser depletion of liver NPS and was not (overtly) hepatotoxic, and 0.0625 mmol/ kg was the maximum dose that did not deplete liver NPS. The responses to single and multiple (ten) treatments with these representative doses were compared. Liver injury was observed after a single but not after the tenth daily treatment with 2.0 mmol/kg. Both the single and the tenth administrations of 2.0 mmol/kg depleted hepatic NPS, but the precentage of depletion was greater after the first than after the tenth dose. Liver injury was not detected with lower dose regimens. The patterns of NPS depletion in liver and kidney were similar after single or muliple (ten) treatments. The minimum NPS concentrations produced, however, were lower after single than after multiple treatments. The molar amounts of liver NPS depleted after the tenth treatment appeared to be equivalent to or greater than those after the first but prior bromobenzene exposure resulted in a higher concentration of tissue NPS being present at the time of the final treatment. Thus, the minimum tissue concentrations of NPS were greater after multiple treatments than after single treatments, despite the loss of equivalent amounts of NPS. It is concluded from these studies that repeated treatment produces resistance to bromobenzene hepatotoxicity. This protective adaptation may be due to a chemically induced increase in liver glutathione concentration

Application of Microencapsulation for Toxicology Studies. II. Toxicity of Microencapsulated Trichloroethylene in Fischer 344 Rats. MELNICK, R. L., JAMESON, C. W., GOEHL, T. J., MARONPOT, R. R., COLLINS, B. J., GREENWELL, A., HARRINGTON, F. W., WILSON, R. E., TOMAS-ZEWSKI, K. E., AND AGARWAL, D. K. (1987). Fundam. Appl. Toxicol. 8, 432–442. Gelatin–sorbitol microcapsules containing 44.1% trichloroethylene (TCE) were prepared and mixed in NIH-07 rodent meal diet and provided at microcapsule concentrations of 0 (untreated control group), 1.25,2.5, 5.0, or 10% (equivalent to 0, 0.55, 1.10, 2.21, or 4.41% TCE, respectively) to groups of 10 male F344 rats for 14 days. An additional control group received diets containing 5% empty capsules. For comparisons, TCE dissolved in corn oil was administered by gavage to different groups of 10 male rats for 14 consecutive days at dose levels adjusted to correspond to those in the feed study. Treatment-related deaths occurred only in the highest dose group of the gavage study. Body weight gain and feed consumption were reduced in high-dose groups of both the feed and gavage studies. There was no measurable loss of TCE in feed sampled from the cages during the study. Dose-related increases in organ (liver and kidney) weight/body weight ratios, individual cell necrosis in the liver, and hepatic microsomal NADPH cytochrome c re-ductase and peroxisomal palmitoyl-CoA oxidase and catalase activities were found in both the dosed-fed and gavage groups. Induction of cytochrome P-450 occurred only in the dosed-feed study. There were no significant compound-related pathologic lesions observed in the kidneys, the only other organ examined microscopically. Differences in lethality, cytochrome P-450 levels, and induction of microsomal or peroxisomal enzyme activities were attributed to differences in the method of dosing (gavage versus dosed-feed). The demonstration of no significant loss of TCE from the feed and of similar toxic effects produced by microencapsulated TCE via feed and TCE in corn oil via gavage indicate that microencapsulation can provide an excellent alternative exposure route for studying the oral toxicological properties of volatile chemicals, such as TCE, in rats.