Discrimination of land-use types in a catchment by energy dispersive X-ray fluorescence and principal component analysis.

Differences in composition and chemical elemental concentration are important information for soil samples classification. The objective of this study is to present a direct methodology, that is non-destructive and without complex sample preparation, in order to discriminate different land-use types and soil degradation, employing energy dispersive X-ray fluorescence and multivariate analysis. Sample classification results from principal component analysis, utilizing spectral data and elemental concentration values demonstrate that the methodology is efficient to discriminate different land-use types.

Reactive astrocytes and Wnt/ß-catenin signaling link nigrostriatal injury to repair in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease.

Emerging evidence points to reactive glia as a pivotal factor in Parkinson's disease (PD) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse model of basal ganglia injury, but whether astrocytes and microglia activation may exacerbate dopaminergic (DAergic) neuron demise and/or contribute to DAergic repair is presently the subject of much debate. Here, we have correlated the loss and recovery of the nigrostriatal DAergic functionality upon acute MPTP exposure with extensive gene expression analysis at the level of the ventral midbrain (VM) and striata (Str) and found a major upregulation of pro-inflammatory chemokines and wingless-type MMTV integration site1 (Wnt1), a key transcript involved in midbrain DAergic neurodevelopment. Wnt signaling components (including Frizzled-1 [Fzd-1] and ß-catenin) were dynamically regulated during MPTP-induced DAergic degeneration and reactive glial activation. Activated astrocytes of the ventral midbrain were identified as candidate source of Wnt1 by in situ hybridization and real-time PCR in vitro. Blocking Wnt/Fzd signaling with Dickkopf-1 (Dkk1) counteracted astrocyte-induced neuroprotection against MPP(+) toxicity in primary mesencephalic astrocyte-neuron cultures, in vitro. Moreover, astroglial-derived factors, including Wnt1, promoted neurogenesis and DAergic neurogenesis from adult midbrain stem/neuroprogenitor cells, in vitro. Conversely, lack of Wnt1 transcription in response to MPTP in middle-aged mice and failure of DAergic neurons to recover were reversed by pharmacological activation of Wnt/ß-catenin signaling, in vivo, thus suggesting MPTP-reactive astrocytes in situ and Wnt1 as candidate components of neuroprotective/neurorescue pathways in MPTP-induced nigrostriatal DAergic plasticity.

[Effect of treatment with a food supplement (containing: selected sea fish cartilage, vitamin C, vitamin E, folic acid, zinc, copper) in women with iron deficiency: double blind, randomized, placebo-controlled trial]. / Ruolo cardine dell'assunzione di un integratore alimentare (contenente idrolizzato di cartilagine di pesce marino, vitamina C,vitamina E, acido folico, zinco, rame) nel trattamento della sideropenia in un gruppo di pazienti in etá fertile.

AIM: The term iron deficiency is used to indicate a condition in which the content of iron (Fe) in the organism is low, even before the consequent reduction in erythropoiesis comes about. This clinical situation is very frequent in patients in fertile age. The therapy commonly used (Fe salts) is often poorly tolerated. The use of a food supplement containing nutrients useful for improving the bioavailability of Fe and that is well tolerated can represent a valid alternative to iron therapy. METHODS: The present study examines 49 fertile women with iron deficiency, of normal weight and not undergoing estroprogestin treatment. The patients underwent 3 assessments: basal, after 30 and after 60 days to determine their complete haemochrome, blood iron, blood ferritin, blood transferrin, iron binding capacity, folates, TSH, FT3, and FT4. Following the basal assessment, patients were randomly assigned to 1 of 2 treatment groups: treatment A (25 patients): food supplement containing hydrolyzed sea fish cartilage, vitamin C, vitamin E, folic acid, zinc, copper (Captafer); treatment B (24 patients): placebo. RESULTS: The patients were then subdivided into 2 groups according to the basal blood iron (<60 microg/dL) or blood ferritin (<20 ng/mL) values. In the group presenting blood iron of <60 microg/dL only treatment A supplement produced a significant improvement in blood iron after 30 (P<0.001) and after 60 (P<0.005) days of treatment. The group with basal blood ferritin of <20 ng/mL presented blood iron levels of >60 microg/dL; in these patients after 60 days of treatment with the supplement, there was a significant increase in blood ferritin (P<0.05); the patients treated with placebo, on the other hand, did not show any significant difference compared to basal values. CONCLUSIONS: This study has shown that, in patients with iron deficiency, the use of a food supplement, consisting of nutrients that improve the bioavailability of Fe, leads to a significant improvement in blood iron and blood ferritin levels.

Analysis of Chlamydia pneumoniae-specific oligoclonal bands in multiple sclerosis and other neurologic diseases.

OBJECTIVE: Paired serum and cerebrospinal fluid (CSF) specimens were investigated for Chlamydia pneumoniae-specific oligoclonal bands (OCBs) to determine band specificity in multiple sclerosis (MS). MATERIAL AND METHODS: Serum and CSF samples were collected from patients with relapsing-remitting MS (n = 56), other inflammatory (n = 18) or non-inflammatory (n = 15) neurologic diseases, and from 10 healthy controls. OCBs were determined with affinity immunoblotting of C. pneumoniae-specific IgG onto antigen-coated nitrocellulose paper after protein separation with agarose isoelectric focusing. RESULTS: Chlamydia pneumoniae-specific OCBs were present in 5 of 56 patients with MS, and in 3 of 18 patients with other inflammatory neurologic diseases. CONCLUSIONS: The intrathecal production of C. pneumoniae-specific oligoclonal IgG occurs in a minority of patients with MS. This intrathecal anti-C. pneumoniae reactivity is likely part of a polyspecific humoral immune response in MS.

Interferon gamma and interleukin 4 producing T cells in peripheral blood of multiple sclerosis patients undergoing immunomodulatory treatment.

Intracellular cytokine flow cytometry was used to analyse the percentages of interferon (IFN) gamma and interleukin (IL)-4 producing T cells in the peripheral blood of multiple sclerosis patients, before and after immunomodulatory treatment, and of healthy controls. After six months of treatment, different doses of IFN beta1a (Avonex or Rebif) decreased CD4+ (Th1, Th2) and CD8+ (Tc1) cells to a similar extent, without affecting the Th1/Th2 ratio. These T cell subsets were unmodified after nine months of glatiramer acetate (Copaxone) treatment, and after six day courses of high dose 6-methylprednisolone. The data suggest that IFN beta1a produces sustained downmodulation of IFN gamma and IL-4 producing T cells in vivo, which may contribute to its therapeutic efficacy; that glatiramer acetate possibly acts without altering non-specific cellular immunity; and that glucocorticoid induced lymphocytopenia does not affect the percentages of Th1, Th2, and Tc1 cells; at least in the periphery, none of the treatments caused a Th1 to Th2 shift that could account for their respective therapeutic effects.

Serum and CSF levels of MCP-1 and IP-10 in multiple sclerosis patients with acute and stable disease and undergoing immunomodulatory therapies.

The two chemokines, monocyte chemoattractant protein (MCP)-1 and gamma-interferon inducible protein (IP)-10, are thought to be involved in the pathogenesis of multiple sclerosis (MS). We measured MCP-1 and IP-10 levels in serum and CSF samples from 38 acute and 25 stable MS patients and from 40 controls. The latter consisted in patients with other inflammatory neurological diseases (OIND) or with non-inflammatory neurological diseases, and healthy controls. CSF MCP-1 levels exceeded those found in serum in all the patients studied as well as in healthy controls. CSF MCP-1 levels were significantly lower in acute MS [468+/-(S.E.M.) 18 pg/ml] than in stable MS (857+/-104 pg/ml). When detectable, serum and CSF IP-10 levels were significantly higher in acute MS (serum 331+/-66 pg/ml; CSF 118+/-16 pg/ml) than in stable MS (serum 69+/-7 pg/ml; CSF 25+/-2 pg/ml). Among OIND patients, those with HIV-1-associated dementia showed high serum and CSF levels of both MCP-1 and IP-10. Those with encephalitis showed high serum and CSF levels of IP-10 and CSF mononuclear pleiocytosis. We also evaluated the effects of 6-methylprednisolone or IFN-beta1a therapy on circulating MCP-1 and IP-10 levels. Neither MCP-1 nor IP-10 post-therapy levels varied significantly from baseline values. Our findings suggest that (a) MCP-1 could be constitutively produced within the brain; (b) MCP-1 and IP-10 CSF levels in acute MS vary significantly from those in stable MS, and these variations are inverse; and (c) current MS therapies do not modify circulating levels of MCP-1 and IP-10.

Interferon-gamma and interleukin-4-producing T cells in peripheral blood of multiple sclerosis patients.

Pro- and anti-inflammatory cytokines are thought to participate in the development and regulation of autoimmunity in multiple sclerosis (MS), a demyelinating disease of the central nervous system (CNS). We analysed the percentage of interferon (IFN)-gamma and interleukin (IL)-4-producing cells in the peripheral blood of both active and stable MS patients, and of healthy controls. After short-term stimulation, cytokine-producing cells were intracellularly stained and sorted. Significantly lower percentages of IFN-gamma and IL-4-producing T cells were found in stable MS patients than in controls, and in active than in stable patients. The diminution affected CD4(+) (Th1, Th2) and CD8(+) (Tc1) phenotypes. Tc2 cells were not detected. The Th1/Th2 ratio did not differ in active and stable MS, nor in controls. The fact that Th2 and Tc1 cell percentages were higher in stable than in active MS possibly indicates that these cells play a downmodulating role in the immune response. In contrast, a role in exacerbating the immune response is not attributable to Th1 cells, given their reduction in acute MS. Our data do not support the hypothesis that MS is a Th1/Th2 paradigmatic disease; rather, they suggest that sequestration in the CNS, or activation-induced apoptosis (whether in vivo or in vitro) may explain reduced levels of IFN-gamma and IL-4-producing subsets in the peripheral blood of clinically acute patients.

Chemoprevention of indirect and direct chemical carcinogenesis by carotenoids as oxygen radical quenchers.

Beta-carotene (BC) and canthaxanthine (CX), two carotenoids with and without pro-vitamin A activity, respectively, were found to help to prevent benzo[a]pyrene (BP)-induced skin carcinogenesis in the dark and BP photocarcinogenesis (UV 300-400 nm) when given as an oral supplement to female Swiss albino mice. The same experimental procedure was adapted to 8-methoxypsoralen (8-MOP) photoinduction of mammary carcinomas in mice. Here also, the two carotenoids were strongly antitumorigenic. Indeed, 8-MOP photomutagenesis, tested in S. typhimurium TA 102, appeared to depend on a two-step reaction, namely an oxygen-independent DNA-8-MOP photoadduct, followed by an oxygen-dependent second step, sensitive to carotenoids. This result suggests that dietary carotenoids (powerful antioxidant molecules) might prevent the carcinogenic risk caused by substances that are transformed into ultimate carcinogens by oxidative processes which are indirectly carcinogenic. Finally, to verify whether supplemental carotenoids can affect carcinogenesis where neither light excitation nor oxidative metabolic processes are involved, an experimental attempt was made on gastric carcinogenesis induced in rats by the direct carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The results demonstrate that supplemental carotenoids do not affect initiation and progression stages, but do prevent the progression stage of dysplasias to infiltrating gastric carcinomas. Thus, this provides strong presumptive evidence for oxygen radical involvement in the later stages of this neoplastic development, as recently reported in the literature. As far as mutagenicity in S. typhimurium is concerned, carotenoids do not exert, as expected, any protective effect on MNNG mutagenic activity. The above experimental data suggest that supplemental carotenoids, instead of sunscreen preparations, can be adopted by outdoor workers to prevent skin cancer. Accordingly, such natural antioxidants may be useful in human chemoprevention against neoplasias of the lung, breast, urinary bladder, and colon and rectum even after radical surgery.

Photocarcinogenesis by methoxypsoralen, neutral red, proflavine, and long UV radiation.

A study of the photosensitizing effects of 8-methoxypsoralen (MOP), neutral red (NR), and proflavine (PF) on the skin of female Swiss albino mice, strain 955, was carried out using fractionated exposure to long ultraviolet light (300-400 nm) and visible light (tungsten emission). The results (1) confirmed MOP photocarcinogenicity, (2) demonstrated that both NR and PF are photocarcinogens, and, further, (3) showed that the above UV light with 2.6% of fluence at 313 nm is a long-term carcinogenic agent even though the total dose of 313 nm was 100 times less than the minimal UV tumorigenic dose in mice. The tumors were mammary adenocarcinomas, carcinomas of skin appendages, carcino-mixo-sarcomas, lymphomas, and one case of thyroid adenocarcinoma. The implications of the above data regarding the controversy about oncogenic risks in photochemotherapy are discussed.

Dietary carotenoids block photocarcinogenic enhancement by benzo (a)pyrene and inhibit its carcinogenesis in the dark.

The carotenoids beta-carotene (C) and canthaxanthine (CX), with and without pro-vitamin A activity, respectively, when perorally administered to mice, markedly prevent benzo(a)pyrene photocarcinogenic enhancement (BP-PCE), continue to block such BP-PCE and protect significantly against BP carcinogenesis in mice maintained in the dark. These results appear relevant to both the pathogenesis of chemical carcinogenesis and rational programs of skin cancer prevention in humans.