Cardiorespiratory treatments as modifiers of the relationship between particulate matter and health: a case-only analysis on hospitalized patients in Italy.

Background: A few panel and toxicological studies suggest that health effects of particulate matter (PM) might be modified by medication intake, but whether this modification is confirmed in the general population or for more serious outcomes is still unknown.

Objectives: We carried out a population-based pilot study in order to assess how pre-hospitalization medical treatments modify the relationship between PM<10 μm in aerodynamic diameter (PM10) and the risk of cardiorespiratory admission.

Methods: We gathered information on hospitalizations for cardiorespiratory causes, together with pre-admission pharmacological treatments, that occurred during 2005 in seven cities located in Lombardy (Northern Italy).

Neuronal drug transporters in platinum drugs-induced peripheral neurotoxicity.

To gain a better insight into the neurotoxicity of platinum drugs, it is important to increase our knowledge over the phenomena allowing their entry into dorsal root ganglia neurons. A deeper understanding of platinum-drug transport mechanisms in neurons would represent not only a step forward in the pathogenetic interpretation of their neurotoxicity, but would also disclose possible treatment options to prevent this severe side-effect achievable through modulation of transporter activity. Copper transporters and organic cation transporters have been identified as putative targets for the pharmacological modulation of neuronal cell accumulation of platinum drugs and damage, and this possibility has been demonstrated by animal studies.

Aβ42 production in brain capillary endothelial cells after oxygen and glucose deprivation.

Although the diverse triggers of AD are still under debate, the hypothesis of the contribution of cerebrovascular deficiencies has emerged in recent years. Cerebrovascular dysfunction may precede cognitive decline and onset of neurodegeneration. Indeed, the toxic Aβ(42) aggregates constituting senile plaques, one of AD hallmarks, is often detected as amorphous material or fine fibrils in the brain capillary of AD patients.

A panel of macroautophagy markers in lymphomonocytes of patients with amyotrophic lateral sclerosis.

A potential role for macroautophagy dysfunction in the pathogenesis of amyotrophic lateral sclerosis (ALS) was hypothesized after the demonstration that selected markers are up-regulated in post mortem samples obtained from both patients and animal models of disease. We hypothesized that a putative dysfunction of this catabolic pathway could be operative also in peripheral blood mononuclear cells (PBMC) obtained from ALS patients, since these cells represent an accessible model for studying molecular pathogenesis events in neuropsychiatric disorders. Beclin-1 and LC3II immunoreactivity were assessed in PBMC from 15 ALS patients and 15 controls by Western blot analysis.

Enhanced folate binding of cultured fibroblasts from Alzheimer's disease patients.

We compared the levels of serum folate from Alzheimer's disease (AD) patients and from age-matched healthy subjects and used primary cultures of fibroblasts, obtained from the two groups, to assess possible differences in their ability to bind folate. The results show that the levels of circulating folate are significantly (p<0.01; n=30) lower in AD patients than in controls (4.