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I build a two-country general oligopolistic equilibrium model, in which sectors differ in emissions and technologies, and pollution can be transboundary. I derive the optimal bilateral environmental policy for the economy as a whole, for the cases in which the environmental damage either linearly or quadratically increases in total pollution. The analysis highlights that the optimal emission tax can even be negative, and bilateral trade liberalization should be matched with either a rise or a fall in the optimal emission tax. The moments of the emission distribution and technology distribution across sectors are fundamental to implement optimal environmental policies.

Background HCV can lead to both chronic liver disease and B-cell lymphoproliferative disorders. A strong association exists between HCV and mixed cryoglobulinaemia (MC). Methods Anti-nuclear antibodies (ANA), rheumatoid factor Ig-G (RF-IgG), free light chain κ and λ (FLC-κ, FLC-λ) levels and κ/λ ratio were evaluated in 50/420 subjects unexpectedly resulted anti-HCV positive after routine screenings for non-hepathological procedures. Results Three/fifty patients had HCV-RNA undetectable in the serum and were excluded from the analysis. Thirty-nine/fifty patients had laboratory evidence of circulating cryoglobulins without liver disease and MC-related symptoms. Among them, 17 resulted ANA-positive. The mean cryocrit was higher in ANA-positive patients, while no other demographic/clinical differences were observed between the groups. Significantly higher levels of RF-IgG were observed in ANA-positive vs ANA-negative patients. κ and λ FLC were higher in ANA-positive patients. A ROC analysis, based on ANA-positivity vs ANA-negativity, confirmed a high sensitivity and specificity of RF-IgG test. Conclusions Published data concerning MC come mostly from symptomatic vasculitis. We analyzed HCV-patients without MC symptoms, founding cryoglobulins in the majority of them. The increased levels of FR-IgG and FLC in CGs-ANA-positive patients, suggest these test could be used to identify a state of silent autoimmune and/or lymphoproliferative condition before the transition to a frank disease in naive HCV-patients without symptoms of extrahepatic manifestations.

This paper combines solar photovoltaic (PV) to wastewater treatment plants (WWTPs). A new methodology is proposed to design solar PV to reduce energy consumptions of aeration thanks in WWTPs. New analytical equations and parameters, based on the air temperatures, solar irradiations, biological kinetics, dissolved oxygens, mechanical oxygenations, are introduced to obtain the peak power of PV that maximize the auto-consumptions of aeration blowers installed in the oxidation tanks of WWTPs. The method allows a direct preliminary design and a calibrated estimation for energy power. To justify this method, three aspect are mainly discussed: (i) the oxidation tanks consume up to 30% of the energy of a WWTP; (ii) the temperature of wastewater is variable during the year, in the smaller WWTPs; (iii) the dissolved oxygen reduces, increasing temperature of wastewater. This methodology will support the sector in making decision over PV investments, helping wastewater utilities to consider sustainable management practices. Therefore, a further contribute to develop the integration of renewable energy sources combined with wastewater sectors is activated.

We investigated the relationship of metabolic syndrome (MetS) and its individual components with incidence of mild cognitive impairment (MCI) and its progression to dementia in a large longitudinal Italian population-based sample with a 3.5-year follow-up. A total of 2097 participants from a sample of 5632 65-84-year-old subjects from the Italian Longitudinal Study on Aging were evaluated. MetS was defined according to the Third Adults Treatment Panel of the National Cholesterol Education Program criteria. MCI, dementia, Alzheimer's disease (AD), and vascular dementia (VaD) were classified using current published criteria. Among MCI patients those with MetS (N=49) had a higher risk of progression to dementia (HR, 4.40; 95% CI, 1.30-14.82) compared with those without MetS (N=72). After a multivariate adjustment, the risk in MCI patients with MetS approximately doubled (multivariate adjusted HR, 7.80, 95% CI 1.29-47.20) compared with those MCI without MetS. Finally, among non-cognitively impaired individuals there were no significant differences in risks of developing MCI in those who were affected by MetS (N=608) in comparison with those without MetS (N=837), as well as excluding those individuals with undernutrition or low inflammatory status with or without undernutrition. In our population, among MCI patients the presence of MetS independently predicted an increased risk of progression to dementia over 3.5 years of follow-up.

Background Anti-nuclear antibodies are immunoglobulins directed against nuclear antigens. They are associated with many autoimmune disorders, but are frequently found in patients infected with hepatitis C virus, possibly indicating an underlying common origin. Likewise, mixed cryoglobulinemia often accompanies autoimmune diseases and hepatitis C infection. Aim To compare anti-nuclear antibodies and immunoglobulin content of cryoprecipitates from hepatitis C virus-positive patients in order to assess their predictive value in the onset of hepatitis C virus-driven extrahepatic disorders. Methods Serum from 40 hepatitis C virus-positive patients and 50 controls with rheumatoid arthritis was processed for cryoglobulin detection: all subjects presented with Type III mixed cryoglobulinemia. Immunoglobulin content and immunoglobulin subclasses of cryoprecipitates were assessed by immunofixation and tested by ELISA for rheumatoid factor. Cryoprecipitates were also analysed for anti-nuclear antibodies by indirect immuno-fluorescence to identify specific patterns typical of each condition. Results Anti-nuclear antibody patterns differed significantly; 26 infected subjects (65%) were IgG3 positive: of these, 25 were also anti-nuclear antibody-positive (96.1%). Conclusions IgG3 are autoreactive clones unrelated to viral recognition and possibly involved in autoimmune disorders. Altogether, these results may represent useful diagnostic device for early detection of hepatitis C virus-induced autoimmune diseases.

Deficits in executive functions are key features of schizophrenia. Rodent behavioral paradigms used so far to find animal correlates of such deficits require extensive effort and time. The puzzle box is a problem-solving test in which mice are required to complete escape tasks of increasing difficulty within a limited amount of time. Previous data have indicated that it is a quick but highly reliable test of higher-order cognitive functioning. We evaluated the use of the puzzle box to explore executive functioning in five different mouse models of schizophrenia: mice with prefrontal cortex and hippocampus lesions, mice treated sub-chronically with the NMDA-receptor antagonist MK-801, mice constitutively lacking the GluA1 subunit of AMPA-receptors, and mice over-expressing dopamine D2 receptors in the striatum. All mice displayed altered executive functions in the puzzle box, although the nature and extent of the deficits varied between the different models. Deficits were strongest in hippocampus-lesioned and GluA1 knockout mice, while more subtle deficits but specific to problem solving were found in the medial prefrontal-lesioned mice, MK-801-treated mice, and in mice with striatal overexpression of D2 receptors. Data from this study demonstrate the utility of the puzzle box as an effective screening tool for executive functions in general and for schizophrenia mouse models in particular.

Drugs currently used in the treatment of cognitive impairment and dementia have a very limited therapeutic value, suggesting the necessity to potentially individualize new strategies able to prevent and to slow down the progression of predementia and dementia syndromes. An increasing body of epidemiological evidence suggested that elevated saturated fatty acids (SFA) could have negative effects on age-related cognitive decline (ARCD) and mild cognitive impairment (MCI). Furthermore, a clear reduction of risk for cognitive decline has been found in population samples with elevated fish consumption, high intake of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA), particularly n-3 PUFA. Epidemiological findings demonstrated that high PUFA intake appeared to have borderline non-significant trend for a protective effect against the development of MCI. Several hypotheses could explain the association between dietary unsaturated fatty acids and cognitive functioning, including mechanisms through the co-presence of antioxidant compounds in food groups rich in fatty acids, via atherosclerosis and thrombosis, inflammation, accumulation of b-amyloid, or via an effect in maintaining the structural integrity of neuronal membranes, determining the fluidity of synaptosomal membranes that thereby regulate neuronal transmission. However, recent findings from clinical trials with n-3 PUFA supplementation showed efficacy on depressive symptoms only in non-apolipoprotein E (APOE) epsilon4 carriers, and on cognitive symptoms only in very mild Alzheimer's disease (AD) subgroups, MCI patients, and cognitively unimpaired subjects non-APOE epsilon4 carriers. These data together with epidemiological evidence support a possible role of fatty acid intake in maintaining adequate cognitive functioning and possibly for the prevention and management of cognitive decline and dementia, but not when the AD process has already taken over.

Cerebral tissues from archaeological human remains are extremely rare findings. Hereby, we report a multidisciplinary study of a unique case of a left cerebral hemisphere from a 13th century AD child, found in north-western France. The cerebral tissue-reduced by ca. 80% of its original weight-had been fixed in formalin since its discovery. However, it fully retained its gross anatomical characteristics such as sulci, and gyri; the frontal, temporal and occipital lobe as well as grey and white matter could be readily recognised. Neuronal remains near the hippocampus area and Nissl bodies from the motor cortex area were observed (Nissl, Klüver-Barrera staining). Also, computed tomography (CT) and magnetic resonance imaging (T1, proton density, ultra short echo time sequences) were feasible. They produced high quality morpho-diagnostic images. Both histological and radiological examinations could not confirm the pathologist's previously suggested diagnosis of cerebral haemorrhage as the cause of death. Reproducible cloned mtDNA sequences were recovered from the skeleton but not from the brain itself. This was most likely due to the combined effect of formaldehyde driven DNA-DNA and/or DNA-protein cross-linking, plus hydrolytic fragmentation of the DNA. The chemical profile of the brain tissue, from gas-chromatography/mass-spectroscopy analysis, suggested adipocerous formation as the main aetiology of the mummification process. The hereby presented child brain is a unique paleo-case of well-preserved neuronal cellular tissue, which is a conditio sine qua non for any subsequent study addressing wider perspectives in neuroscience research, such as the evolution of brain morphology and pathology.

Previous studies examining the association between the interleukin 6 (IL-6)-174 C/G polymorphism and Alzheimer's disease (AD) have yielded conflicting results. Furthermore, the C allele of the IL-6 variable number of tandem repeats (VNTR) polymorphism was associated with a delayed onset and a decreased risk of AD.A total sample of 149 AD patients, and 298 age- and sex-matched unrelated caregivers from Apulia, southern Italy, were genotyped for the apolipoprotein E (APOE) polymorphism, the VNTR polymorphism in the 3' flanking region, and the -174G/C single-nucleotide polymorphism (SNP) in the promoter region of IL-6 gene on chromosome 7. Furthermore, we performed a haplotype analysis on these two polymorphisms on IL-6 locus.IL-6 VNTR and -174G/C allele and genotype frequencies were similar between AD patients and controls, also after stratification for late-onset (or =65 years) and early-onset (65 years) or APOE epsilon4 status. Furthermore, there was no evidence of linkage disequilibrium between the VNTR and -174G/C polymorphisms, not supporting a previous reported additive effect of both IL-6 polymorphisms on AD risk.Our findings did not support a role of IL-6-174 G/C and IL-6 VNTR polymorphisms in the risk of sporadic AD in southern Italy, suggesting that these polymorphisms of IL-6 gene were at most weak genetic determinants of AD.

Clinical and epidemiologic research has focused on the identification of risk factors that may be modified in predementia syndromes, at a preclinical and early clinical stage of dementing disorders, with specific attention to the role of depression. Our goal was to provide an overview of these studies and more specifically to describe the prevalence and incidence of depression in individuals with mild cognitive impairment (MCI), the possible impact of depressive symptoms on incident MCI, or its progression to dementia and the possible mechanisms behind the observed associations. Prevalence and incidence of depressive symptoms or syndromes in MCI vary as a result of different diagnostic criteria and different sampling and assessment procedures. The prevalence of depression in individuals with MCI was higher in hospital-based studies (median: 44.3%, range: 9%-83%) than in population-based studies (median: 15.7%, range: 3%-63%), reflecting different referral patterns and selection criteria. Incidence of depressive symptoms varied from 11.7 to 26.6/100 person-years in hospital-based and population-based studies. For depressed normal subjects and depressed patients with MCI, the findings on increased risk of incident MCI or its progression to dementia were conflicting. These contrasting findings suggested that the length of the follow-up period, the study design, the sample population, and methodological differences may be central for detecting an association between baseline depression and subsequent development of MCI or its progression to dementia. Assuming that MCI may be the earliest identifiable clinical stage of dementia, depressive symptoms may be an early manifestation rather than a risk factor for dementia and Alzheimer disease, arguing that the underlying neuropathological condition that causes MCI or dementia also causes depressive symptoms. In this scenario, at least in certain subsets of elderly patients, late-life depression, MCI, and dementia could represent a possible clinical continuum.

Objective The aim of the present cross-sectional study was to assess appetite and to examine at the same time the associations between self-reported appetite and orexigen (ghrelin) and anorexigen (free tryptophan, free tryptophan/large neutral amino acid ratios, low branched chain amino acid levels) substances in chronic hemodialysis patients. Design Cross-sectional study. Setting Patients were recruited from the Catholic University Outpatient Dialysis Clinic. Patients A total of 59 patients (32 men and 27 women) were included in this study. The mean age was 63.7 ± 13.9 years, and the mean dialytic age was 6.6 ± 5.1 years. Their mean body mass index of the study population was 25.1 ± 4.1 kg/m2. Methods The first question of the Hemodialysis (HEMO) Study Appetite questionnaire was used to assess the appetite of the hemodialysis patients. The multiple-choice answers for the first question, "During the past week, how would you rate your appetite?" were (1) very good, (2) good, (3) fair, (4) poor, or (5) very poor. Plasma amino acid concentrations were measured with the use of liquid chromatography. Ghrelin levels were measured with Ghrelin-RIA (Mediagnost). Results According to the questionnaire, in 16 of 59 (27.1%) hemodialysis patients, their appetite was very good (group 1); in 15 (25.4%), it was good (group 2); in another 15 (25.4%), it was fair (group 3); in 10 (16.9%), it was poor; and in 3 (5%), it was very poor. For statistical purposes, patients with a poor or very poor appetite were pooled together into a single group (group 4). Body mass index and serum albumin were significantly lower in patients with a fair and poor/very poor appetite than in patients with a very good or good appetite. According to the Subjective Global Assessment, all patients in groups A and B were well-nourished, whereas most patients in groups C (60%) and D (68%) were severely malnourished. Most of the comorbid conditions were significantly higher in patients of groups C and D. Branched chain amino acids were significantly lower in patients with a fair or poor/very poor appetite with respect to patients with a very good or good appetite. Free tryptophan levels were similar in the four groups of patients. The molar sum in plasma of the other large neutral amino acids (valine, leucine, isoleucine, tyrosin, phenylalanine) (large neutral amino acids) tended to be lower in patients with a fair and poor/very poor appetite than in patients with a very good or good appetite. However, the free tryptophan/large neutral amino acid ratio did not change significantly according to the appetite reported by the patients. Mean ghrelin levels were significantly higher in patients of group D than in other groups and in patients of groups B and C than in patients of group A. Conclusions The present study shows that poor appetite is associated with significantly lower branched chain amino acid levels but not with higher free tryptophan levels and higher free tryptophan/large neutral amino acid ratios in hemodialysis patients. In addition, significantly higher levels of ghrelin have been observed in patients with a poor/very poor appetite.

Catalase (CAT) −262 C/T promoter (rs1001179), cathepsin D (CTSD) exon 2 (rs17571), and apolipoprotein E (APOE) gene polymorphisms were studied in 242 patients with sporadic Alzheimer's disease (AD) and 421 unrelated age-, sex-, and ethnically matched control subjects from Apulia (Southern Italy). No statistically significant differences in CAT rs1001179 and CTSD rs17571 genotype and allele distribution between AD cases and healthy controls were observed for the whole AD sample, and when AD group was categorized by age at onset in early- and late-onset AD subsets. Furthermore, we did not find any statistically significant differences in rates between CAT rs1001179 and CTSD rs17571 genotypes and AD controlling for APOE e4 allele status. Our data, at present, do not support a role of two gene polymorphisms of the short arm of the chromosome 11, the CAT rs1001179 and CTSD rs17571, as a possible susceptibility factors for sporadic AD.

In the last decade, it has become more apparent the important role genes play in the development of late-onset Alzheimer's disease (AD). Great efforts, involving human genome scans and candidate gene studies, have been given towards identifying susceptibility genes for AD. A number of regions on different chromosomes have been reported to demonstrate linkage for AD. Of these, findings on chromosome 12 are some of the most compelling. Worldwide genetic association studies pre-dating and subsequent to recent linkage studies have identified and focused upon a number of genes that map to the areas of reported linkage on chromosome 12, however, analyses of those genes studied to date, on the whole, remain inconclusive and ambiguous. This paper reviews studies that have provided evidence of linkage for AD on chromosome 12 and in turn discusses the work conducted to date on candidate genes that have been identified and map to the chromosome 12 regions of interest.

With increasing emphasis on early diagnosis of Alzheimer disease (AD), clinical research has focused on the identification of risk factors that may be modified at a preclinical and early clinical stage of dementing disorders. Prevalence and incidence of different predementia syndromes vary as a result of different diagnostic criteria, as well as different sampling and assessment procedures. Particular interest in mild cognitive impairment (MCI) arises from the fact that MCI is thought to be a prodromal phase and therefore highly predictive of subsequent AD. Furthermore, many of the risk factors for cerebrovascular disease (CVD) and vascular dementia (VaD), including serum total cholesterol, hypertension, atherosclerosis, and apolipoprotein E (APOE) genotype have also been shown to increase the risk of AD. Both vascular factors and APOE epsilon4 allele have been associated with higher risk of AD. Some recent studies suggested further that CVD or vascular factors increased the risk of conversion of MCI to dementia. This review will focus on the possible role of vascular risk factors in modulating the risk of age-related cognitive decline, and the progression of predementia syndrome such as MCI to dementia.

The possible impact of diet, particularly the intake of fatty acids, on cognitive decline and dementia was addressed recently by several studies. We investigated the role of dietary fatty acids on the rate of mild cognitive impairment (MCI) in a population-based, prospective study carried out on 278 and 186 nondemented elderly subjects (65-84 years) at the 1st (1992-1993) and 2nd (1995-1996) survey from the cohort of Casamassima, Bari, Italy (n=704), one of the eight centers of the Italian Longitudinal Study on Aging. During the median follow-up of 2.6 years, 18 new events of MCI were diagnosed, and high polyunsaturated fatty acids (PUFA) intake appeared to be a protective factor against the development of MCI [hazard ratio (HR): 0.65, 95% confidence interval (CI): 0.43-0.98, trend-test, df=1, p

In recent years, there was an increasing interest on candidate genes may play an important role in the development of Alzheimer's disease (AD). Several genome wide screens have undertaken so far or expanded recently, and suggested a number of genomic areas that may contain novel susceptibility genes for AD, in particular most compelling have been the findings on chromosome 12. Polymorphisms in different susceptibility genes on chromosome 12 (A2M, LRP1, CP2 and OLR1) are now being suggested as possible genetic markers for increased risk of developing AD. However, many of these studies are controversial and have shown conflicting results. Thus far, the search for the chromosome 12 Alzheimer's gene must continue and there are several other genes in this region that we are looking at. In this article, we focused on the current knowledge of the genetics of familial late-onset and sporadic AD linked to the chromosome 12, and the future search for other candidate genes.

The interleukin 6 (IL-6) gene in humans is located in the short arm of chromosome 7 and has a-174 G/C polymorphism in its promoter region. The C allele at position-174 in the promoter of the interleukin 6 (IL-6) gene has been associated with reduced gene expression and reduced plasma levels of IL-6. Given the supposed role of several inflammatory mediators in neurodegeneration and Alzheimer's disease (AD), the IL-6-174 G/C promoter polymorphism has been associated with AD with contrasting findings. First aim of the present study was to investigate whether there was evidence in Southern Italy of an association between the IL-6-174 G/C promoter polymorphism and AD. Secondly, we also tested a possible effect of geographic genetic variations on existing reported associations comparing our results with the findings from published studies on other European populations. We examined apolipoprotein E (APOE) and IL-6-174 G/C promoter polymorphisms in a cohort of 168 sporadic AD patients and 220 sex- and age-matched nondemented controls from Southern Italy. No differences have been found in the IL-6-174 G/C promoter allele and genotype frequencies between AD patients and controls nor in early- and late-onset subsets of AD patients. No statistically significant differences in frequencies between IL-6-174 G/C promoter alleles and AD among APOE allele strata were found. Finally, comparing our results with the findings from other European populations, the IL-6*G/*G genotype frequency showed a statistically significant increasing trend from Northern to Southern regions of Europe in AD patients and controls, with a concomitant increase in IL-6*C/*G genotype frequency. Furthermore, an increasing geographical trend from North to South was found for the IL-6*G allele, with a concomitant inverse trend for IL-6*C allele. We suggest that regional European differences in genotype and allele frequencies of the IL-6-174 G/C promoter polymorphism may explain in part controversial findings on this polymorphism in AD in various European studies.

The lipoprotein Lp(a) with high plasma concentration is an independent genetic determinant for cardiovascular diseases. It was investigated as a quantitative factor of risk for myocardial infarction. A total of 345 Italian subjects, 127 Cases and 218 Controls, were studied. Lipids and lipoproteins were compared. Cases had atherogenic traits, such as lower HDL cholesterol and higher triglycerides than Controls. In particular, they had Lp(a) concentrations over the risk threshold, (median, 27 mg/dl in Cases vs 17 mg/dl in Controls; P = 0.0075, Mann-Whitney test) which confirmed the association of this parameter with the disease. Two main functional variants of the apo(a) gene, KringleIV and penta-nucleotide repeat, (PNR) were analyzed. Allele and genotype frequency distributions differed between Cases and Controls. Lp(a) concentrations differed according to PNR genotypes in Controls: subjects having alleles >8 showed lower Lp(a). This was not found in Cases. They had a higher prevalence of the smaller KringleIV alleles, the high Lp(a)-expressing ones. In Cases, genotypes consisting of two small KringleIV alleles were prevalently associated to PNR 8/9 and 8/10, thus preventing Lp(a) lowering. The putative apo(a) enhancer within LINE1 in the apo(a)-plasminogen intergenic region was investigated for functional polymorphisms. No variants that could be associated to the Lp(a) variability were found.

High levels of serum lipoprotein(a) [Lp(a)] have been associated with increased risk of coronary artery disease (CAD), but this association apparently is not confirmed in elderly people. We evaluated the interactions of Lp(a) with lipid and nonlipid CAD risk factors in a sample of subjects enrolled in the prevalence survey (1992 to 1993) of the Italian Longitudinal Study on Aging (ILSA). The entire population consisted of 5,632 elderly people, aged 65 to 84 years, randomly selected in 8 Italian municipalities. The present cross-sectional study included 400 free-living elderly subjects (74 +/- 6 years) from the randomized cohort of Casamassima (Bari, Southern Italy) (n = 704). The results showed that in the elderly population, high serum Lp(a) is a CAD risk factor dependent on type 2 diabetes mellitus and elevated low-density lipoprotein (LDL) cholesterol levels. In particular, the combined effect of high Lp(a) (or =20 mg/dl) and high LDL cholesterol (or =3.63 mmol/L [or =140 mg/dl]), increases coronary risk by 2.75 (95% confidence interval 7.70 to 0.99); finally, the effect of Lp(a)or =20 mg/dl and LDL cholesterolor =3.63 mmol/L (or =140 mg/dl), combined with type 2 diabetes mellitus, increases risk of CAD by 6.65 (95% confidence interval 35.40 to 1.25). In the elderly, elevated Lp(a) levels appear not to be an independent predictor of CAD, but this lipoprotein is a risk factor only in subjects with type 2 diabetes mellitus and elevated LDL cholesterol.

A total sample of 169 AD patients, and 264 age- and sex-matched unrelated caregivers from Apulia, southern Italy, were genotypized for alpha-2-macroglobulin (A2M) Val1000/Ile single-nucleotide polymorphism (SNP) (rs669), apolipoprotein E (APOE), and SNPs (+1073 and +1071) in the oxidized low-density lipoprotein receptor-1 (OLR1) gene on chromosome 12. A2M allele and genotype frequencies were similar between AD patients and controls, also after stratification for late onset (/=70 years) and early onset (70 years) or APOE varepsilon4 status. However, there was evidence in support of LD between the OLR1+1071, the OLR1+1073, and the rs669 SNPs, with T-C-A haplotype being associated with significant increased risk of AD in both the whole sample and when we stratified according to early and late onset AD subjects, with the allelic association with AD predominantly from the OLR1+1073 SNP, further supporting the role of OLR1 as a candidate risk gene for sporadic AD.

Higher total cholesterol, cognitive decline, and dementia Francesco Panza a,∗, Vincenzo Solfrizzi a, Alessia D’Introno a, Anna M. Colacicco a, Andrea Santamato b, Davide Seripa c, Alberto Pilotto c,d, Antonio Capurso a, Cristiano Capurso e a Department of Geriatrics, Center for Lipoprotein Metabolism, University of Bari, Policlinico, Piazza Giulio Cesare, 11, 70124 Bari, Italy b Department of Physical Medicine and Rehabilitation, University of Foggia, Foggia, Italy c Laboratory of Geriatrics and Gerontology, Department of Research, “Casa Sollievo dalla Sofferenza”, San Giovanni Rotondo, Foggia, Italy d Geriatric Unit, Department of Medical Sciences, IRCSS, “Casa Sollievo dalla Sofferenza”, San Giovanni Rotondo, Foggia, Italy e Department of Geriatrics, University of Foggia, Foggia, Italy

Potentiometric stripping analysis and constant current stripping analysis are proposed as routine methods for analysis of copper, zinc and selenium in plasma and urine samples. The analytical performance of these methods is comparable with that reported for atomic absorption spectrometry. However the low cost, greater simplicity of the apparatus, and the facility of execution make this methodology a valid candidate for routine application in Clinical Chemistry laboratories.

We studied centenarians to investigate the biological basis of human longevity focusing on the apolipoprotein A-IV and lipoprotein(a), potentially involved in the susceptibility to atherogenic mechanisms. We analyzed two restriction polymorphisms, HinfI347 (alleles +, -) and Fnu4HI360 (alleles 1, 2), and a VNTR (alleles 3, 4) at the 3' region of the apo A-IV gene. The allele frequencies, the lipoprotein concentrations and their association in centenarians and adults have been compared. In centenarians, the HinfI genotype distribution is different (P0.05) and the (+13) haplotype is prevalent (0.54 vs. 0.39), with a greater association of (+3), indicating the selection of a favourable allele. The lipoprotein modulation by the apo A-IV polymorphisms is suggested by significant associations in adults ((+/+) homozygotes have lower LDL-cholesterol and apo B than heterozygotes; (1/1) homozygotes have higher TG and apo B than heterozygotes), that in centenarians still exists as a trend. Centenarians show peculiar lipoprotein features: lower LDL-cholesterol (mean 103 vs. 115 mg/dl; P0.02), and higher lipoprotein(a) (median 17.5 vs. 4.5; P0.002). Large part of them (47%), especially the Hinf(+/+) and the (+13) homozygotes, have a lipoprotein(a)20 mg/dl, value considered as the threshold for atherogenic risk, surprisingly compatible with healthy longevity.

The Italian multicentric study on centenarians (IMSC) was aimed at assessing the level of preservation of the sense of taste, and at estimating to what extent the recognition of various gustative stimuli can give satisfaction and information regarding the surrounding environment for the centenarians. Taste sensitivity has been qualitatively established in a group of 126 Italian centenarians (mean age 101.9+/-1.4 years) and compared to that of a group of 100 elderly subjects (mean age 70.5+/-5.0 years). All the individuals included in the study groups had a mini mental state examination (MMSE) score larger than 19. The results revealed that taste sensitivity is significantly reduced in the centenarians; as a matter of fact, the elderly control subjects are able to perceive taste stimuli in 84.25+/-3.40% of the testing, while the centenarians were successful only in 74.23+/-6.19% of the experiments (P

Coenzyme Q and trace element contents of two antarctic fishes (Pagothenia bernacchii and Chionodraco hamatus) were investigated and compared with that of one temperate marine fish (Mugil cephalus). In particular, muscle and erythrocyte concentrations of coenzyme Q, vitamin E, selenium, copper and zinc were determined. Antarctic fishes showed, at the level of their muscles, higher levels of selenium, zinc and copper compared with M. cepalus. In antarctic fishes, in the place of Q10, the coenzyme Q form generally observed in temperature fishes, only the homolog coenzyme Q9 was found. This particular finding has been related to the difference in the crystallization temperature existing between CoQ10 and CoQ9. Moreover, the high levels of zinc and selenium, observed in C. hamatus, correlate very well with a recent report on the presence, in the liver of this fish, of a zinc-binding protein that, in addition, is characterized by an amino acid sequence closely similar to that of a selenium-containing protein isolated from ovine heart. All together, the results indicate, for the antarctic species, a high level of antioxidant defenses with respect to the mediterranean fish and may be considered as a stimulating basis for further studies on the oxidative metabolism of Antarctic organisms.

L-carnitine is an amino acid involved in the mechanism by which fatty acids are transported through the mitochondrial wall for oxidation. To determine whether the in vivo metabolism of lipoprotein(a) (Lp[a]) is linked to intramitochondrial oxidative metabolism, we investigated the effects of exogenously administered L-carnitine in patients with high serum concentrations of Lp(a). Eighteen outpatients received open-label treatment with L-carnitine 3 g/d for 8 weeks; 10 patients continued treatment for up to 16 weeks. Serum Lp(a) levels were decreased from a mean baseline value of 72.71 mg/dL by a mean of 14% after 4 weeks and 15% after 8 weeks in 18 patients and 13% after 12 weeks and 12% after 16 weeks of treatment in 10 patients ( P P

Coenzyme Q10 (CoQ10), vitamin E, triglycerides and conjugated dienes were measured in a group of 48 patients on chronic hemodialysis, in 15 uremic patients and in a control group of 10 normal subjects. CoQ10 levels were significantly lower (P < 0.001) in both hemodialytic and uremic patients compared with the normal group whereas triglycerides were significantly higher (P < 0.001) with respect to both normal subjects and uremic patients. Conjugated dienes were significantly higher (P < 0.001) in both hemodialytic and uremic patients with respect to normal subjects. The predialytic values of vitamin E were higher in hemodialytic patients with respect to both normal subjects and uremic patients whereas the postdialytic values were in the normal range. A restoration mechanism of vitamin E after hemodialytic treatment was hypothesized.

The action of simvastatin on serum lipids, lipoproteins, and apolipoproteins (apo) was investigated in 12 patients with primary moderate hypercholesterolemia in a double-blind, placebo-controlled protocol. After a 2-week placebo baseline and dietary stabilization period, 8 patients received simvastatin 10 mg/day and 4 patients received placebo under a double-blind design for 8 weeks; then all 12 were treated with simvastatin 10 mg/day in an open design for 8 weeks. In the group treated with simvastatin initially, at the end of the 16th week of therapy, simvastatin significantly reduced total cholesterol, low-density lipoprotein cholesterol, apo B, and apo E by 25%, 30%, 25%, and 18%, respectively. The results obtained confirm previous research by other authors and may suggest, furthermore, a mechanism of accelerated clearance of very-low-density lipoprotein remnants.

Mild cognitive impairment (MCI) is thought to be a prodromal phase of Alzheimer's disease, but in population-based studies MCI classification is less consistent than in clinical series, suggesting that MCI is a heterogeneous descriptor and the outcome at follow-up depends on which population is studied and how MCI is defined. We discussed in the present paper the issue of the heterogeneity of MCI and other predementia syndromes, both in clinical presentation and progression to dementia, supported by the findings of the Italian Longitudinal Study on Aging (ILSA) and other population-based and clinical-based studies.