Grafted fat has many attributes of an ideal filler, but the results, like those of any procedure, are technique dependent. Fat grafting remains shrouded in the stigma of variable results experienced by most plastic surgeons when they first graft fat. However, many who originally reported failure eventually report success after altering their methods of harvesting, refinement, and placement. Many surgeons have refined their techniques to obtain long-term survival and volume replacement with grafted fat. They have observed that transplanted fat not only adjusts facial and body proportion but also improves surrounding tissues into which the fat is placed. They have noted not only the improvement in the quality of aging skin and scars but also a remarkable improvement in conditions such as radiation damage, chronic ulceration, breast capsular contracture, and damaged vocal cords. The mechanism of fat graft survival is not clear, and the role of adipose-derived stem cells and preadipocytes in fat survival remains to be determined. Early research has indicated the possible involvement of more undifferentiated cells in some of the observed effects of fat grafting on surrounding tissues. Of particular interest is the research that has pointed to the use of stem cells to repair and even to become bone, cartilage, muscle, blood vessels, nerves, and skin. Further studies are essential to understand grafted fat tissue.

Employing acquisition jnterstimulus intervals (ISIs) of 200 and 700 msec, and three subsequent ISI shift conditions (fixed, gradual, and abrupt) with two directions of ISI shift (short to long and long to short) the study revealed: (a) the 200-msec. ISI resulted in fewer trials to the first OR and a higher overall level of percentage CRs; (6) percentage CRs under the shortto-long ISI shift fell significantly below the long-to-short and fixed ISI conditions; and (c) CR onset latency, CR peak latency, and OR topography altered in the direction of ISI shift. It was concluded that the instrumental response-shaping hyopthesis cannot presently account for major portions of the percentage CR data.

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1. We have attempted to reduce dapsone‐dependent methaemoglobinaemia formation in six dermatitis herpetiformis patients stabilised on dapsone by the co‐administration of cimetidine. 2. In comparison with control, i.e. dapsone alone, methaemoglobinaemia due to dapsone fell by 27.3 +/‐ 6.7% and 26.6 +/‐ 5.6% the first and second weeks after commencement of cimetidine administration. The normally cyanotic appearance of the patient on the highest dose of dapsone (350 mg day‐ 1), underwent marked improvement. 3. There was a significant increase in the trough plasma concentration of dapsone (2.8 +/‐ 0.8 x 10(‐5)% dose ml‐1) at day 21 in the presence of cimetidine compared with control (day 7, 1.9 +/‐ 0.6 x 10(‐5)% dose ml‐1, P less than 0.01). During the period of the study, dapsone‐mediated control of the dermatitis herpetiformis in all six patients was unchanged. 4. Trough plasma concentrations of monoacetyl dapsone were significantly increased (P less than 0.05) at day 21 (1.9 +/‐ 1.0 x 10(‐5)% dose ml‐ 1) compared with day 7 (1.6 +/‐ 0.9 x 10(‐5)% dose ml‐1:control). 5. Over a 12 h period, 20.6 +/‐ 8.9% (day 0) of a dose of dapsone was detectable in urine as dapsone hydroxylamine. Significantly less dapsone hydroxylamine was recovered from urine at day 14 (15.0 +/‐ 8.4) in the presence of cimetidine, compared with day 0 (control: P less than 0.05). 6. The co‐administration of cimetidine may be of value in increasing patient tolerance to dapsone, a widely used, effective, but comparatively toxic drug.