Productive replication of human adenoviruses in mouse epidermal cells

In contrast to most cells of mouse origin, cell lines derived from mouse epidermis are permissive for replication of human adenovirus type 5. The extent of epidermal cell differentiation correlated with the level of E1A expression and virus replication. Mouse epidermal cells may provide useful models for cancer therapy using replication-competent human adenoviruses.     

Evidence for a thiol reagent inhibiting choline acetyltransferase by reacting with the thiol group of coenzyme A forming a potent ingibitor.

Evidence is presented for the thiol reagent methyl methanethiolsulfonate inhibiting choline acetyltransferase (EC 2.3.1.6), not by reaction with an enzymic thiol group, but by reaction with the thiol group of CoA. The resulting CoA methyl disulfide is a potent inhibitor of this enzyme. Its action is reversed competitively by acetyl CoA.     

The chemistry of brown algae

The enormous and self-replenishing supplies—perhaps 200 or 300 million tons—of these seaweeds in the oceans of the world have been commercially exploited so far primarily in the production of alginic acid, but the other carbohydrates, proteins, lipids, vitamins, enzymes and antibacterial substances in them and discussed here may hold even greater values.     

Neuro-kardio-fazio-kutane Syndrome

Recently, neuro-cardio-facio-cutaneous (NCFC) syndromes were defined as a group of hereditary diseases with phenotypical overlap based on a similar pathogenetic mechanism. These syndromes are associated with increased signal transduction down the RAS-MAPK (RAS: rat sarcoma, MAPK: mitogen-activated protein kinase) pathway. Noonan, LEOPARD, cardio-facio-cutaneous, and Costello syndrome as well as neurofibromatosis type 1 and Legius syndrome belong to the NCFC diseases. Interdisciplinary health management is essential to determine and establish adequate medical diagnostics and treatment and to provide psychosocial support for affected patients and their families.     

Local anesthetics noncompetitively inhibit terbium binding to the exterior surface of nerve membrane vesicles

It has previously been shown that terbium binds to membrane vesicles prepared from the walking leg nerve of the lobster (Homarus americanus) with a high affinity K_d of 2.2 μM. Fluorescence of bound Tb³⁺ occurs via energy transfer from the aromatic residues of proteins (γ_ex = 280 nm; γ_em = 546 nm), and calcium inhibits Tb³⁺ binding competitively with a K_i of 1.8 mM. Displacement studies with EDTA demonstrate that more than 95% of the bound Tb³⁺ is at the vesicle exterior and is not being taken up by the vesicles. To investigate the putative role of Ca²⁺ in the interaction of local anesthetics with axonal membranes, lidocaine and the analogs GX-HCl and QX-314 were tested as inhibitors of Tb³⁺ binding. Inhibition by lidocaine is seen only at considerably higher doses (25 mM) than are required for conduction block of intact nerves (5 mM). Inhibition by lidocaine and the primary amine analog GX-HCl is entirely noncompetitive, whereas the quaternary ammonium derivative QX-314 appears to be a mixed competitive-noncompetitive inhibitor of Tb³⁺ binding. These data are not compatible with the hypothesis that there is a functionally essential cation binding site on the axonal membrane surface for which Ca²⁺ and local anesthetics compete, although local anesthetic action may be modified indirectly by altered calcium concentrations. Evidence is presented for a mechanism by which local anesthetics indirectly displace Tb³⁺ by altering the physical state of the axonal membrane.