A genetic study on subtropical Anadenanthera colubrina (Vell.) Brenan var. cebil (Griseb.) Altschul tree from Northwestern Argentina

Anadenanthera colubrina (Vell.) Brenan var. cebil (Griseb.) Altschul is a tree species in South America important for its cultural, economic, and medicinal uses. In addition, it represents a trace in memory of the forests that have decreased over the years and for this reason it is not only interesting to study but also important to preserve the tree species for future generations. In this paper, we have characterized the genetic diversity of four populations. We collected seeds from four different sites: San Bernardo (B), El Cebilar (C), Met\ue1n (M), and El Gallinato (G) in Salta Province, North Argentina. We then compared the intergenic transcribed sequences of ribosomal DNA, a known genetic molecular marker. Our previous results, obtained through the morphological and genetic analysis of only four individuals (one for each zone), have showed that the individuals from B and M sites were more similar to each other as well as the individuals from G and C sites. In this paper, a larger number of individuals (25) were characterized and their phylogenetic relationships were computed. The results confirmed the previously found similarities

A rapid spectroscopic method to detect the fraudulent treatment of tuna fish with carbon monoxide

Carbon monoxide (CO) can be used to treat fresh meat and fish in order to retain its 'fresh' red colour appearance for a longer period of time. In fact, upon aging, myoglobin is oxidized to met-myoglobin with the concomitant blue-shift and broadening of the Soret maximum, which brings about a change in the colour of the fish, revealing that it is no longer fresh. The use of carbon monoxide, which reacts with the oxy-myoglobin to form a fairly stable cherry red carboxy-myoglobin complex may mask spoilage, because the CO-complex can be stable beyond the microbiological shelf life of the meat. The presence of CO in tuna fish has been investigated by optical spectroscopy as the formation of the CO adduct can be easily detected by the combined analysis of electronic absorption spectra in their normal and second derivative modes, monitoring the intense Soret band at 420 nm. The presence of met- and oxy-myoglobin can obscure the presence of small amounts of the CO adduct; however, it can be revealed by chemically reducing the met- and oxy-forms to the deoxy-form in an anaerobic environment. This spectroscopic method provides a qualitatively rapid laboratory screening procedure for food control to unmask the presence of CO in frozen or fresh fish. (c) 2006 Elsevier Ltd. All rights reserved

Lipoprotein abnormalities in chronic kidney disease and renal transplantation

Chronic kidney disease (CKD) is one of the most important risk factors for cardiovascular disease (CVD). Despite the kidney having no direct implications for lipoproteins metabolism, advanced CKD dyslipidemia is usually present in patients with CKD, and the frequent lipid and lipoprotein alterations occurring in these patients play a role of primary importance in the development of CVD. Although hypertriglyceridemia is the main disorder, a number of lipoprotein abnormalities occur in these patients. Different enzymes pathways and proteins involved in lipoprotein metabolism are impaired in CKD. In addition, treatment of uremia may modify the expression of lipoprotein pattern as well as determine acute changes. In renal transplantation recipients, the main lipid alteration is hypercholesterolemia, while hypertriglyceridemia is less pronounced. In this review we have analyzed lipid and lipoprotein disturbances in CKD and also their relationship with progression of renal disease. Hypolipidemic treatments may also change the natural history of CVD in CKD patients and may represent important strategies in the management of CKD patients

Somatostatin: A Novel Substrate and a Modulator of Insulin-Degrading Enzyme Activity

Insulin-degrading enzyme (IDE) is an interesting pharmacological target for Alzheimer's disease (AD), since it hydrolyzes beta-amyloid, producing non-neurotoxic fragments. It has also been shown that the somatostatin level reduction is a pathological feature of AD and that it regulates the neprilysin activity toward beta-amyloid. In this work, we report for the first time that IDE is able to hydrolyze somatostatin [k(cat) (s(-1)) = 0.38 (+/-0.05); K-m (M) = 7.5 (+/-0.9) x 10(-6)] at the Phe6-Phe7 amino acid bond. On the other hand, somatostatin modulates IDE activity, enhancing the enzymatic cleavage of a novel fluorogenic beta-amyloid through a decrease of the K-m toward this substrate, which corresponds to the 10-25 amino acid sequence of the A beta(1-40). Circular dichroism spectroscopy and surface plasmon resonance imaging experiments show that somatostatin binding to IDE brings about a concentration-dependent structural change of the secondary and tertiary structure(s) of the enzyme, revealing two possible binding sites. The higher affinity binding site disappears upon inactivation of IDE by ethylenediaminetetra acetic acid, which chelates, the catalytic Zn2+ ion. As a whole, these features suggest that the modulatory effect is due to an allosteric mechanism: somatostatin binding to the active site of one IDE subunit (where somatostatin is cleaved) induces an enhancement of IDE proteolytic activity toward fluorogenic beta-amyloid by another subunit. Therefore, this investigation on IDE-somatostatin interaction contributes to a more exhaustive knowledge about the functional and structural aspects of IDE and its pathophysiological implications in the amyloid deposition and somatostatin homeostasis in the brain. (C) 2008 Elsevier Ltd. All rights reserved

A Novel WAC Loss of Function Mutation in an Individual Presenting with Encephalopathy Related to Status Epilepticus during Sleep (ESES)

WAC (WW Domain Containing Adaptor With Coiled-Coil) mutations have been reported in only 20 individuals presenting a neurodevelopmental disorder characterized by intellectual disability, neonatal hypotonia, behavioral problems, and mildly dysmorphic features. Using targeted deep sequencing, we screened a cohort of 630 individuals with variable degrees of intellectual disability and identified five WAC rare variants: two variants were inherited from healthy parents; two previously reported de novo mutations, c.1661_1664del (p.Ser554*) and c.374C>A (p.Ser125*); and a novel c.381+2T>C variant causing the skipping of exon 4 of the gene, inherited from a reportedly asymptomatic father with somatic mosaicism. A phenotypic evaluation of this individual evidenced areas of cognitive and behavioral deficits. The patient carrying the novel splicing mutation had a clinical history of encephalopathy related to status epilepticus during slow sleep (ESES), recently reported in another WAC individual. This first report of a WAC somatic mosaic remarks the contribution of mosaicism in the etiology of neurodevelopmental and neuropsychiatric disorders. We summarized the clinical data of reported individuals with WAC pathogenic mutations, which together with our findings, allowed for the expansion of the phenotypic spectrum of WAC-related disorders