Proteinuria and its relation to diverse biomarkers and body mass index in chronic hemodialysis.

Background: Certain adipokines exert direct effects on proteinuria, a cardiovascular risk factor ignored in hemodialysis. We measured different adipokines according to body mass index (BMI) in relation to proteinuria.

Methods: Patients numbered 57: group A (GA), BMI<25, n = 22; GB, BMI 25-30, n = 15; and GC, BMI > 30, n = 20.

Lack of dystrophin in mdx mice modulates the expression of genes involved in neuron survival and differentiation.

Duchenne muscular dystrophy is an X-linked disease characterized by progressive and lethal muscular wasting. Dystrophic patients, however, are also afflicted by several neurological disorders, the importance of which is generally underestimated. As promising therapies for muscles are currently in clinical trial stages, with the potential to provide an increase in the lifespan of young patients, determination of the genetic and molecular aspects characterizing this complex disease is crucial in order to allow the development of therapeutic approaches specifically designed for the nervous system.

Lack of dystrophin functionally affects α3β2/β4-nicotinic acethylcholine receptors in sympathetic neurons of dystrophic mdx mice.

In the sympathetic superior cervical ganglion (SCG), nicotinic acetylcholine receptors (nAChRs) mediate fast synaptic transmission. We previously demonstrated that in SCG neurons of mdx mice, an animal model for Duchenne muscular dystrophy, lack of dystrophin causes a decrease, compared to the wild-type, in post-synaptic nAChRs containing the α3 subunit associated with β2 and/or β4 (α3β2/β4-nAChRs), but not in those containing the α7 subunit. Here we show, by whole cell patch-clamp recordings from cultured SCG neurons, that both nicotine and acetylcholine-evoked currents through α3β2/β4-nAChRs are significantly reduced in mdx mice compared to the wild-type, while those through α7-nAChR are unaffected.

Components of the NGF signaling complex are altered in mdx mouse superior cervical ganglion and its target organs.

We previously reported that in the superior cervical ganglion (SCG) of dystrophic mdx mice, which lack full-length dystrophin, there is a loss of neurons projecting to SCG muscular targets, like the iris. Nonetheless, surviving neurons, innervating either iris or submandibular gland (SuGl), a SCG non-muscular target, underwent reduced axon defasciculation and terminal branching. Here we report that, during early post-natal development, levels of pro-apoptotic proNGF in mdx mouse iris, but not in the SuGl, are higher than in the wild-type.

Involvement of the plasminogen enzymatic cascade in the reaction to axotomy of rat sympathetic neurons.

Axotomy of superior cervical ganglion (SCG) neurons is characterized by peripheral regeneration of injured axons and temporary disassembly of the intraganglionic synapses, necessary for synaptic silencing. Both events require remodeling of the extracellular matrix achieved through controlled proteolysis of its components by different enzymatic systems. In this study, we investigate the involvement of the plasminogen enzymatic cascade in the response to axotomy of rat SCG neurons.