Changes in the Activities of Aldolase and of D-Glyceraldehyde-3-Phosphate Dehydrogenase during the Mitotic Cycle in Microspores of Lilium longiflorum

Microspores of Lilium longiflorum were isolated at various stages of development surrounding the mitotic interval and were analyzed for changes in the activities of D-glyceraldehyde-3-phosphate dehydrogenase and aldolase. Fructose 1,6 diphosphate was used as substrate. Activities were measured by the increase in optical density due to the reduction of diphosphopyridine nucleotide. It was found that mitosis occurs during the minimal activity of both aldolase and D-glyceraldehyde-3-phosphate, thus indicating that heightened glycolytic capacity is not necessarily related to mitosis. It was also found that soluble-SH levels were highest when the enzymes were least active. It appeared, therefore, that the "—SH enzymes" are not necessarily activated intracellularly by high concentrations of soluble thiol. These results are discussed in connection with the theory that soluble-SH compounds stimulate glycolysis and in this way initiate mitosis.     

Segmentation and the development of the vertebrate nervous system

1. Recent experiments on the development of neural segmentation in chick embryos are reviewed. 2. Segmentation of the spinal peripheral nerves is governed by a subdivision of the somite-derived sclerotome into anterior and posterior halves. Migrating neural crest cells and outgrowing motor axons are confined to the anterior sclerotome as a result, in part, of inhibitory interactions with posterior sclerotome cells. 3. The sclerotomal distribution of certain molecules known to influence growing nerve cells in vitro, namely laminin, fibronectin, N-CAM, N-Cadherin and J1/tenascin/cytotactin, suggest that these molecules play no critical role in determining the preference of nerve cells for anterior sclerotome. 4. Peanut agglutinin (PNA) recognises cell surface-associated components on posterior cells which, when incorporated into liposomes, cause the abrupt collapse of sensory growth cones in vitro. The PNA receptor(s) may be inhibitory for nerve cells in vivo. 5. The chick hindbrain epithelium is segmented early in its development. Each branchiomotor nucleus in the series of cranial nerves V, VII and IX derives from a pair of segments lying in register with an adjacent branchial arch. Neurogenesis of motor and reticular axons begins in alternate segments, suggesting parallels with insect pattern formation.     

Putative enkephalin precursors in bovine adrenal medulla.

Extracts from bovine adrenal medulla and adrenal medullary chromaffin granules were found to contain three proteins, 20,000, 10,000 and 5,000 approximate molecular weights which yield tryptic peptides with opioid activity. The opioid activity of these peptides was demonstrated with a radioreceptor assay and two radioimmunoassays. The three proteins yield the same active peptides all of which are chromatographically distinct from the tryptic opioid nonapeptide β-LPH 61–69, generated by trypsin digestion of pituitary endorphins and their precursors. Furthermore, these endorphins and their precursors do not appear to be present in the adrenal medulla. These findings further support the hypothesis that the enkephalin biosynthetic pathway is distinct from that leading to β-endorphin.     

Comparative trial of volunteer and professional treatments of dysphasia after stroke.

A study of the treatment of dysphasia after stroke compared the progress of two groups of disabled patients. One received conventional treatment from qualified speech therapists and the other from non-professional volunteers. Methods of assessing communication difficulties were also compared and the impact of aphasic illness on families examined. No important differences in the results of treatment were seen between the two groups. The volunteers, however, often had to assume some of the responsibilities of social workers, and transport to hospital created practical and economic problems. It is concluded that the two forms of treatment provide essentially the same benefit, although doubt must still remain because relatively few patients were studied.     

Isolation and sequence of a non-opioid peptide derived from proenkephalin

A non-opioid peptide derived from adrenal proenkephalin has been isolated and sequenced. The sequence of this peptide is Ser-Pro-His-Leu-Glu-Asp-Glu-Thr-Lys-Glu-Leu-Gln (Proenkephalin 168-180). This sequence represents the portion of Peptide I that is cleaved to yield Peptide E. This peptide is processed in a similar manner to the opioid peptides and is present at approximately the same level as Peptide E.     

Tumor cells enhance their own CD44 cleavage and motility by generating hyaluronan fragments

Hyaluronan (HA) is an extracellular matrix glycosaminoglycan that interacts with cell-surface receptors, including CD44. Although HA usually exists as a high molecular mass polymer, HA of a much lower molecular mass that shows a variety of biological activities can be detected under certain pathological conditions, particularly in tumors. We previously reported that low molecular weight HAs (LMW-HAs) of a certain size range induce the proteolytic cleavage of CD44 from the surface of tumor cells and promote tumor cell migration in a CD44-dependent manner. Here, we show that MIA PaCa-2, a human pancreatic carcinoma cell line, secreted hyaluronidases abundantly and generated readily detectable levels of LMW-HAs ranging from approximately 10- to 40-mers. This occurred in the absence of any exogenous stimulation. The tumor-derived HA oligosaccharides were able to enhance CD44 cleavage and tumor cell motility. Inhibition of the CD44-HA interaction resulted in the complete abrogation of these cellular events. These results are consistent with the concept that tumor cells generate HA oligosaccha-rides that bind to tumor cell CD44 through the expression of their own constitutive hyaluronidases. This enhances their own CD44 cleavage and cell motility, which would subsequently promote tumor progression. Such an autocrine/paracrine-like process may represent a novel activation mechanism that would facilitate and promote the malignant potential of tumor cells.     

RAGE mediates amyloid-beta peptide transport across the blood-brain barrier and accumulation in brain

Amyloid-beta peptide (Abeta) interacts with the vasculature to influence Abeta levels in the brain and cerebral blood flow, providing a means of amplifying the Abeta-induced cellular stress underlying neuronal dysfunction and dementia. Systemic Abeta infusion and studies in genetically manipulated mice show that Abeta interaction with receptor for advanced glycation end products (RAGE)-bearing cells in the vessel wall results in transport of Abeta across the blood-brain barrier (BBB) and expression of proinflammatory cytokines and endothelin-1 (ET-1), the latter mediating Abeta-induced vasoconstriction. Inhibition of RAGE-ligand interaction suppresses accumulation of Abeta in brain parenchyma in a mouse transgenic model. These findings suggest that vascular RAGE is a target for inhibiting pathogenic consequences of Abeta-vascular interactions, including development of cerebral amyloidosis.