Omega 3 and 6 oils for primary prevention of allergic disease: systematic review and meta-analysis

Background:  There is conflicting evidence on the use of omega 3 and omega 6 supplementation for the prevention of allergic diseases. We conducted a systematic review evaluating the effectiveness of omega 3 and 6 oils for the primary prevention of sensitization and development of allergic disorders.
Methods:  We searched The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, LILACS, PsycInfo, AMED, ISI Web of Science and Google Scholar for double-blind randomized controlled trials. Two authors independently assessed articles for inclusion. Meta-analyses were undertaken using fixed effects modelling, or random effects modelling in the event of detecting significant heterogeneity.
Results:  Of the 3129 articles identified, 10 reports (representing six unique studies) satisfied the inclusion criteria. Four studies compared omega 3 supplements with placebo and two studies compared omega 6 supplements with placebo. There was no clear evidence of benefit in relation to reduced risk of allergic sensitization or a favourable immunological profile. Meta-analyses failed to identify any consistent or clear benefits associated with use of omega 3 [atopic eczema: RR = 1.10 (95% CI 0.78–1.54); asthma: RR = 0.81 (95% CI 0.53–1.25); allergic rhinitis: RR = 0.80 (95% CI 0.34–1.89) or food allergy RR = 0.51 (95% CI 0.10–2.55)] or omega 6 oils [atopic eczema: RR = 0.80 (95% CI 0.56–1.16)] for the prevention of clinical disease.
Conclusions:  Contrary to the evidence from basic science and epidemiological studies, our systematic review and meta-analysis suggests that supplementation with omega 3 and omega 6 oils is probably unlikely to play an important role as a strategy for the primary prevention of sensitization or allergic disease.     

DNA microarrays detect effects of soil contamination on Arabidopsis thaliana gene expression

Soil contamination, such as heavy metals and benzene compounds, is a widespread problem on military installations. It is important to be able to determine the effects of soil contamination before any adverse effects appear in organisms in surrounding areas. We examined gene expression in Arabidopsis thaliana grown in soil from three sites at the Radford Army Ammunition Plant in Radford, Virginia, USA, using DNA microarrays. We analyzed soil, germination, and growth rate to compare with the microarray data. Soil contamination affected both external phenotype and gene expression. Plants grown in soil with high levels of contaminants were chloritic and were smaller than control plants grown in potting soil. Plants grown in soil with the highest copper concentration had the lowest growth rates and had genes up-regulated across several functional groups. Plants grown in soils with elevated lead had many genes down-regulated that were related to photosystem II, metabolism, cellular transport, and protein synthesis. Genes consistently up-regulated across most microarrays were genes related to photosystem I, genes related to water deprivation and oxidative stress response, heat shock proteins, and toxin catabolism genes such as glutathiones. DNA microarrays, in concert with a model genetic organism such as A. thaliana, were an effective assessment tool to determine the presence of toxic substances in soil at a site used for the production of military explosives.     

Coats-type retinal telangiectasia in case of Kabuki make-up syndrome (Niikawa-Kuroki syndrome)

PURPOSE: To report a case of Kabuki make-up syndrome (KMS) or Niikawa-Kuroki syndrome with Coats-type retinal telangiectasia, which has not been previously reported. METHODS: Observational case report. CONCLUSIONS: There have been only two reports of retinal pigmentation abnormalities and a single case of bilateral macular deposits in KMS, but this is the first report of a Coats type retinal telangiectasia. This case highlights the importance of thorough posterior segment examination in cases of KMS.     

Specific investigations in chronic urinary bilharziasis.

Seventy-two patients with histologically confirmed chronic urinary bilharziasis were studied for the reliability of some specific investigative tools in diagnosing this disease, namely urinalysis, serology, urography, and cystoscopy. Of the 72 patients 36 (50%) had hematuria and only 3 (4%) had ova of Schistosoma haematobium on urinalysis. Sixty-two patients (86%) had features of bilharziasis on intravenous urography (IVU). Of the remaining 10 patients with negative urography 6 underwent serology and all had positive results. Of the total patients 52 underwent serology and 49 had significant bilharzial antibody titer (94.2%). At cystoscopy all patients (100%) had features of bilharziasis. It is concluded that the most reliable diagnostic tools in chronic urinary bilharziasis are cystoscopy, serology, and to a lesser extent urography. Unlike early bilharziasis, chronic bilharziasis can be missed if total reliance is placed on urinalysis for screening a population at risk.     

Coats-Type Retinal Telangiectasia in Case of Kabuki Make-Up Syndrome (Niikawa-Kuroki Syndrome)

Purpose: To report a case of Kabuki make-up syndrome (KMS) or Niikawa-Kuroki syndrome with Coats-type retinal telangiectasia, which has not been previously reported. Methods: Observational case report. Conclusions: There have been only two reports of retinal pigmentation abnormalities and a single case of bilateral macular deposits in KMS, but this is the first report of a Coats type retinal telangiectasia. This case highlights the importance of thorough posterior segment examination in cases of KMS.     

Discovery of a Potent Pyrazolopyridine Series of γ-Secretase Modulators

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N-acetylcysteine attenuates dimethylnitrosamine induced oxidative stress in rats

Oxidative stress has been implicated in the pathogenesis and progression of various hepatic disorders and hence screening for a good hepatoprotective and antioxidant agent is the need of the hour. The present study was aimed to investigate the hepatoprotective and antioxidant property of N-acetylcysteine (NAC) against dimethylnitrosamine (DMN) induced oxidative stress and hepatocellular damage in male Wistar albino rats. Administration of single dose of DMN (5 mg/kg b.w.; i.p.) resulted in significant elevation in the levels of serum aspartate transaminase and alanine transaminase, indicating hepatocellular damage. Oxidative stress induced by DMN treatment was confirmed by an elevation in the status of lipid peroxidation (LPO) and reduction in the activities of enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase and in the levels of non-enzymic antioxidants, reduced glutathione, vitamin-C and vitamin-E in the liver tissue. DMN induced oxidative stress and hepatocellular membrane instability was further substantiated by a decline in the status of the membrane bound ATPases in the liver tissue. Post-treatment with NAC (50 mg/kg b.w.; p.o.) for 7 days effectively protected against the DMN induced insult to liver by preventing the elevation in the status of the serum marker enzymes and LPO, and restoring the activities of both the enzymic and non-enzymic antioxidants and membrane bound ATPases towards normalcy. These results demonstrate that NAC acts as a good hepatoprotective and antioxidant agent in attenuating DMN induced oxidative stress and hepatocellular damage.     

Anticancer effects of the p53 activator nutlin-3 in Ewing's sarcoma cells

Mutation of p53 is rare in Ewing’s sarcoma (ES), suggesting that targeting and activation of wild-type p53 may be an effective therapeutic strategy for ES. The recently developed small-molecule MDM2 inhibitor nutlin-3 restores wild-type p53 function, resulting in the inhibition of cancer cell growth and the induction of apoptosis. In the present study, we explored the responsiveness of ES cell lines with wild-type or mutated p53 to nutlin-3. We found that treatment with nutlin-3 increased p53 level and induced p53 target gene expression (MDM2, p21, PUMA) in ES cells with wild-type p53, but not in ES cells with mutated p53. Consistently, nutlin-3 elicited apoptosis only in wild-type p53 cells, as assessed by caspase-3 activity assay and flow cytometric analyses of mitochondrial depolarisation and DNA fragmentation. In addition, we found nutlin-3 to evoke cellular senescence, indicating that nutlin-3 induces pleiotropic anticancer effects in ES. Furthermore, combined treatment with nutlin-3 and an inhibitor of NF-κB produced synergistic antineoplastic activity in ES cells. Our findings suggest that the direct activation of p53 by nutlin-3 treatment may be a useful new therapeutic approach for patients with ES.     

Histone deacetylase inhibitors induce cell death and enhance the apoptosis-inducing activity of TRAIL in Ewing’s sarcoma cells

Purpose The present in vitro study was conducted to evaluate the effects of the histone deacetylase inhibitors (HDIs) suberoyl anilide hydroxamic acid (SAHA), sodium butyrate (NaB) and MS-275 applied as single agents or in combination with TRAIL in Ewing’s sarcoma. Methods Cytotoxic activities were assessed by cytofluorometric analysis of propidium iodide uptake, DNA fragmentation and mitochondrial depolarisation as well as by measuring caspase-9 and -3 activities. Cell-surface expression of TRAIL receptors was determined by cytofluorometry, and histone H4 acetylation was assessed by western blot. Results All three HDIs potently induced cell death in the two cell lines explored, SK-ES-1 and WE-68. However, they seemed to differ in their modes of action. SAHA and NaB induced mitochondrial depolarisation as well as caspase-9 and -3 activities, and their cytotoxic effects could be significantly reduced by the pan-caspase inhibitor z-VAD-fmk. MS-275 was a much weaker inducer of caspase-9 and -3 activities as well as mitochondrial injury; consistently, z-VAD-fmk had little effect on MS-275-mediated activities. Combined treatment of HDIs and TRAIL led to an additive effect in SK-ES-1 cells and a supra-additive effect in WE-68 cells. Yet, HDIs did not increase cell-surface expression of TRAIL receptor 2, but rather decreased it. Selective inhibition of caspase-8 in WE-68 cells and HDI treatment of CADO-ES-1 cells, a Ewing's sarcoma cell line deficient in caspase-8 expression, revealed that caspase-8 was not required for HDI-mediated apoptosis. Conclusions These results suggest that HDIs may be considered as a novel treatment strategy for Ewing’s sarcoma either applied as monotherapy or in combination with TRAIL.