At the recent tuberous sclerosis complex consensus conference, the clinical diagnostic criteria for tuberous sclerosis complex were simplified and revised to reflect both new clinical information about tuberous sclerosis complex and an improved understanding of the disorder derived from molecular genetic studies. Based on this new information, some clinical signs once regarded as pathognomonic for tuberous sclerosis complex are now known to be less specific. No single sign is present in all affected patients, and there is no proof that any single clinical or radiographic sign is absolutely specific for tuberous sclerosis complex. Accordingly, the clinical and radiographic features of tuberous sclerosis complex have now been divided into major and minor categories based on the apparent degree of specificity for tuberous sclerosis complex of each feature. A definitive diagnosis of tuberous sclerosis complex now requires two or more distinct types of lesions, rather than multiple lesions of the same type in the same organ system. Although diagnosis on purely clinical grounds can continue to be difficult in a few patients, there should be little doubt about the diagnosis for those individuals who fulfill these strict criteria. Couples with more than one child with tuberous sclerosis complex, no extended family history, and no clinical features of tuberous sclerosis complex are more likely to have germline mosaicism for tuberous sclerosis than nonexpression of the mutation. Germline mosaicism, while fortunately rare, will not be suspected from either diagnostic criteria or molecular testing until a couple has multiple affected children. Genetic counseling for families with one affected child should include a small (1% to 2%) possibility of recurrence, even for parents who have no evidence of tuberous sclerosis complex after a thorough diagnostic evaluation.

The cellular basis of immunological memory remains a controversial issue. Here we show that basophils bound large amounts of intact antigens on their surface and were the main source of interleukins 6 and 4 in the spleen and bone marrow after restimulation with a soluble antigen. Depletion of basophils resulted in a much lower humoral memory response and greater susceptibility of immunized mice to sepsis induced by Streptococcus pneumoniae. Adoptive transfer of antigen-reactive basophils significantly increased specific antibody production, and activated basophils, together with CD4(+) T cells, profoundly enhanced B cell proliferation and immunoglobulin production. These basophil-dependent effects on B cells required interleukins 6 and 4 and increased the capacity of CD4(+) T cells to provide B cell help. Thus, basophils are important contributors to humoral memory immune responses.

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E 1993. Salt-induced oxidative stress mediated by activated oxvgen species in pea leaf mitochondria. -Physiol. Plant. 89: 103-110.The effect in vivo of salt stress on the activated oxygen metabolism of mitochondria, was studied in leaves from two NaCI-treated cultivars of Pisum sativum L. with different sensitivity to NaCl. In mitochondria from NaCI-sensitive plants, salinity brought about a significant decrease of Mn-SOD (EC 1.15.1.1) Cu,Zn-SOD I (EC 1.15.1.1) and fumarase (EC 4.2.1.2) activities. Conversely, in salt-tolerant plants NaCl treatment produced an increase in the mitochondrial Mn-SOD activity and, to a lesser extent, in fumarase activity. In mitochondria from both salt-treated cultivars, the internal H^O, concentration remained unchanged. The NADH-and succinatedependent generation of O\ radicals by submitochondrial particles and the lipid peroxidation of mitochondrial membranes, increased as a result of salt treatment, and these changes were higher in NaCl-sensitive than in NaCt-tolerant plants. Accordingly, the enhanced rates of superoxide production by mitochondria from saltsensitive plants were concomitant with a strong decrease in the mitochondrial Mn-SOD activity, whereas NaCl-tolerant plants appear to have a protection mechanism against salt-induced increased Oi" production by means of the induction of the mitochondrial Mn-SOD activity. These results indicate that in the subcellular toxicity of NaCl in pea plants, at.i"he level of mitochondria, an oxidative stress mechanism mediated by superoxide radicals is involved, and also imply a function for mitochondrial Mn-SOD in the molecular mechanisms of plant tolerance to NaCl.