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An unusual neuropsychiatric disorder inherited in autosomal dominant fashion occurred in three successive generations of a family. Symptoms commenced late in the fifth decade in six affected patients and led to death in four to six years. The earliest and most prominent symptom was mental depression not responsive to antidepressant drugs or electroconvulsive therapy. This was accompanied by exhaustion, sleep disturbances, and marked weight loss. Later in the disease, symptoms of parkinsonism appeared, and respiratory failure occured terminally. The most recently affected family member was investigated biochemically late in his illness. Concentrations of taurine were greatly diminished in plasma and cerebrospinal fluid, and at autopsy, all regions of brain examined had a markedly reduced taurine content. Since taurine is a putative inhibitory synaptic transmitter, deficiency of brain taurine may possibly have caused the psychiatric and neurological manifestations of this disorder.

There are differences of opinion about the pathogenesis of Perthes' disease. All are agreed that it is due to ischaemia, but the cause of this and the size and number of infarctions are in dispute. Through the generosity of the contributors six whole femoral heads and core biopsies of five other cases have been studied radiographically and histologically. The findings ranged from an ischaemic arrest of ossification in the capital articular cartilage without infarction to multiple complete infarctions of the epiphysial bone. The ensuing reparative process contributes to the pathology, which is of a range to warrant grading or grouping.

Wound healing in the adult is commonly compromised by excessive scar formation. In contrast, fetal wound healing is a regenerative process characterised by the conspicuous absence of scarring. Available evidence suggests that phenotypic differences between fetal and adult fibroblasts are important determinants of these distinct modes of tissue repair. In this context, a number of groups (including our own) have documented differences between fetal and adult fibroblasts with respect to such potentially relevant characteristics as migratory activity, motogenic response to cytokines and the synthesis of motility factors, cytokines and matrix macromolecules. The oral mucosa appears to be a privileged site in the adult in that it continues to display a fetal‐like mode of wound healing. Data are presented in this review indicating that a subpopulation of gingival fibroblasts expresses several ‘fetal‐like’ phenotypic characteristics. These observations are discussed in terms of both the continued expression of a fetal‐like mode of wound healing in the oral mucosa and the possible differential involvement of distinct fibroblast subpopulations in the progression of periodontal disease.