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E Maioli

Publications and source records attributed to E Maioli.

23 records · Page 2Linked to original sources
PubMed1987

Studies on tumor necrosis factor (TNF): II. Metabolic fate and distribution of human recombinant TNF.

We have evaluated the fate of cold and 125I- human recombinant tumor necrosis factor (RTNF) using isolated organs such as rabbit and monkey livers and rabbit kidney and lungs. We have also evaluated the body distribution of the total radioactivity after iv administration of 125I-RTNF in the rabbits. Monkey and rabbit livers play little catabolic role for RTNF. Lungs do not catabolize TNF at all, while the kidney appears to be the main catabolic organ. Accordingly, the body distribution of 125I-RTNF shows that most of the radioactivity is concentrated in the kidneys.

Animals↗
PubMed1983

Salmon calcitonin and cGMP production by human kidney: studies in vivo and in vitro.

In order to evaluate whether or not the action of salmon calcitonin (sCT) at the kidney level could be mediated through specific receptors for the hormone, we have studied the effects of sCT infusions on urinary excretion of cyclic nucleotides in humans. Parallel in vitro studies have been conducted by evaluating the effects of sCT on cyclic nucleotide levels in primary cultures of cortical and medullary human kidney cells. In vivo experiments showed that sCT induced an increase in cGMP in human urine, which was rapid and short-lasting, being superimposable on the increase of urinary excretion of calcium and magnesium. The increase of inorganic phosphate urinary excretion was delayed and appeared to parallel that of urinary cAMP. On the other hand, our in vitro experiments showed that sCT stimulated the guanylate cyclase-cGMP system of human kidney cortical cells at nanomolar concentrations, while higher concentrations of the hormone were required to activate the adenylate cyclase-cAMP system. In addition, sCT was not able to significantly modify the cellular levels of either nucleotide in human kidney medullary cells. Present data demonstrated a direct effect of sCT on human kidney cortical cGMP production, while the efficacy of sCT on the kidney cortex adenylate cyclase-cAMP system appears to be delayed and/or reduced.

Aged↗
PubMedDate not supplied

Microfilament organization in human platelets.

Morphological and biochemical studies suggest that actin in human platelets polymerizes from monomers or oligomers into long filaments more tightly structured in activated than in resting platelets. The polymerization and reorganization of actin filaments are regulated by cellular proteins. Profilin prevents actin polymerization by forming tight complexes with monomeric actin; gelsolin acts both severing filaments and inhibiting their elongation by capping at the barbed end; other actin-binding proteins nucleate polymerization and cross-link actin filaments into networks or bundles. The changes in the actin assembly state, which are under the control of calcium, seem essential for pseudopodal formation. Other platelet processes, such as granule centralization and contractile gel formation, are due to calcium-dependent actin-myosin interaction. In addition, Ca++ seems to inhibit through calmodulin the binding of caldesmon to actin, allowing actin linkage to myosin in a 'flip-flop' fashion.

Actins↗