Lymphocyte predominance Hodgkin''s disease—an immunohistochemical study

Lymph node biopsies from 57 local and referred cases, previously diagnosed at Southampton between 1978 and 1987 as lymphocyte predominance Hodgkin's disease were examined using the monoclonal antibodies MT1, UCHL1, L26, LN-1, E29/68 (EMA), Leu-M1 (CD15) and Ber-H2 (CD30). Of the 34 cases with a nodular architecture, 21 (19 male, two female) contained polylobated Reed-Sternberg cell variants with a B-cell phenotype, which lacked expression of CD15. In all cases, the polylobated cells showed positive staining with L26 and LN-1. Six cases expressed EMA and three showed positive staining with Ber-H2. Two cases lacking polylobated cells were reclassified as reactive follicular hyperplasia with progressive transformation of germinal centres. The remaining 11 cases had an atypical immunophenotype and were reclassified, mainly as mixed cellularity Hodgkin's disease. In six cases, the lymph node architecture showed a mixture of nodular and diffuse growth patterns. Five of these cases contained polylobated cells with the typical morphology and immunophenotype of those seen in nodular lymphocyte predominance Hodgkin's disease. The sixth case contained cells expressing CD15, and was reclassified as nodular sclerosing Hodgkin's disease. Of the fifteen biopsies with a diffuse architecture, four contained polylobated B-cells lacking expression of CD15. These were considered to be diffuse lymphocyte predominance Hodgkin's disease. The remaining 11 cases were reclassified as either Hodgkin's disease, mixed cellularity or as T-cell lymphomas.     

Evolution of neural crest and placodes: amphioxus as a model for the ancestral vertebrate?

Recent studies of protochordates (ascidian tunicates and amphioxus) have given insights into possible ancestors of 2 of the characteristic features of the vertebrate head: neural crest and placodes. The neural crest probably evolved from cells on either side of the neural plate–epidermis boundary in a protochordate ancestral to the vertebrates. In amphioxus, homologues of several vertebrate neural crest marker genes ( BMP2/4 , Pax3/7 , Msx , Dll and Snail ) are expressed at the edges of the neural plate and/or adjacent nonneural ectoderm. Some of these markers are also similarly expressed in tunicates. In protochordates, however, these cells, unlike vertebrate neural crest, neither migrate as individuals through embryonic tissues nor differentiate into a wide spectrum of cell types. Therefore, while the protochordate ancestor of the vertebrates probably had the beginnings of a genetic programme for neural crest formation, this programme was augmented in the earliest vertebrates to attain definitive neural crest. Clear homologues of vertebrate placodes are lacking in protochordates. However, both amphioxus and tunicates have ectodermal sensory cells. In tunicates these are all primary neurons, sending axons to the central nervous system, while in amphioxus, the ectodermal sensory cells include both primary neurons and secondary neurons lacking axons. Comparisons of developmental gene expression suggest that the anterior ectoderm in amphioxus may be homologous to the vertebrate olfactory placode, the only vertebrate placode with primary, not secondary, neurons. Similarly, biochemical, morphological and gene expression data suggest that amphioxus and tunicates also have homologues of the adenohypophysis, one of the few vertebrate structures derived from nonneurogenic placodes. In contrast, the origin of the other vertebrate placodes is very uncertain.     

In Vivo Cultivation of Leukocytes in Diffusion Chambers: Requirement of Ascorbic Acid for Differentiation of Mononuclear Leukocytes to Fibroblasts

Studies were made to evaluate the influence of ascorbic acid upon thedifferentiation of mononuclear leukocytes to fibroblasts when cultivated indiffusion chambers, in vivo. Ascorbic acid-depleted leukocytes grown in ascorbic acid-deficient host guinea pigs developed into abnormal cellular formscharacterized by nuclear enlargement, multipolar mitoses, and giant formsThese changes could be reversed by treatment of the host guinea pigs withascorbic acid. The findings indicate a direct cellular role of ascorbic acidin the differentiation of mononuclear leukocytes to fibroblasts.

Submitted on April 12, 1961 Accepted on June 14, 1961     

SENSITIVE RADIOIMMUNOASSAY FOR SOMATOSTATIN USING N-[1251-TYR-SOMATOSTATIN AS LABELLED ANTIGEN

A sensitive radioimmunoassay for somatostatin using N-[125I]-Tyr-somatostatin is described and compared with that using [125I]-Tyr1-somatostatin. The minimum detectable amount of somatostatin using N-[125I]-Tyr-somatostatin as tracer was 0.1 to 0.5 pg, which is approximately 10-fold lower than the lower detection limit of the RIA using [125I]-Tyr1-somatostatin. Moreover, it was found that the shelf-life of N[125I]Tyr-somatostatin was prolonged in comparison with labelled Tyr1-somatostatin. Human pancreatic and gastric extracts displayed immunological similarity to synthetic somatostatin tetradecapeptide.     

Essential fatty acid deficient hairless mouse: a model of chronic epidermal hyperproliferation

Epidermal DNA synthesis has been shown to be increased approximately three-fold in hairless mice that were fed a diet deficient in essential fatty acids (EFA deficient) for 65 days, compared with animals fed a standard diet. Autoradiographic labelling indices showed a 330% increase in the EFA deficient mice over controls. The animals developed evidence of a diffuse thickening, scaling and loss of elasticity of the skin after 40 days on the EFA deficient diet. Histologically, the epidermis of the EFA deficient animals showed acanthosis, hypergranulosis, hyperkeratosis and increased intracellular epidermal spaces. Increased mitotic indices were found with Feulgen staining. This is further evidence that deficiencies of essential fatty acids are associated with disturbance of normal epidermal cell proliferation and control of keratinization. A single application of topical 0·1%. betamethasone valerate to EFA deficient mice reduced the epidermal DNA synthesis to that of normal diet mice. Ten percent linoleic acid topically over 2weeks also returned epidermal DNA synthesis to normal levels.