BACKGROUND/OBJECTIVES: Numbers of epidemiological studies assessing coffee consumption and serum lipids have yielded inconsistent results. We aimed to evaluate the effects of coffee intake on serum lipids. SUBJECTS/METHODS: We searched several English and Chinese electronic databases up to September 2011 for randomized controlled trials of coffee on serum lipids. Weighted mean effect size was calculated for net changes in serum lipids by using random-effect models or fixed-effect models. Subgroup and meta-regression analyses were conducted to explore possible explanations for heterogeneity among trials. RESULTS: Twelve studies conducted in Western countries with a total of 1017 subjects were identified. Meta-analyses showed, on average, drinking coffee for 45 days was associated with an increase of 8.1 mg/dl (95% confidence interval (CI): 4.5, 11.6; Po0.001) for total cholesterol (TC), 5.4 mg/dl (95% CI: 1.4, 9.5; P ¼ 0.009) for low-density lipoprotein cholesterol (LDL-C) and 12.6 mg/dl (95% CI: 3.5, 12.6; P ¼ 0.007) for triglyceride (TG). The increase in TC were greater in trials using unfiltered coffee and caffeinated coffee as the treatment group. Those who had hyperlipidemia were more sensitive to the cholesterol-raising effect of coffee. Meta-regression analysis revealed a positive dose-response relation between coffee intake and TC, LDL-C and TG. CONCLUSION: The intake of coffee especially unfiltered coffee is contributed significantly to the increase in TC, LDL-C and TG, and the changes were related to the level of intake. Studies of coffee intake on serum lipids in Asian populations should be performed. Keywords: coffee; caffeine; lipids; meta-analysis; randomized controlled trials INTRODUCTIONCoffee is one of the most commonly consumed beverages and even small health effects of coffee could have considerable public health consequences. Controversies regarding its risks and benefits still exist as substances in coffee may have either unfavorable or beneficial effects on the cardiovascular system. 1 A large body of epidemiology studies, including recent studies, [2][3][4][5] examining the association between coffee consumption and serum lipids have yielded inconsistent results.A meta-analysis of nine randomized controlled trials (RCTs) published before December 1998 concluded that consumption of unfiltered, but not filtered, coffee increased serum levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C). 6 However, this meta-analysis was only based on English-language literature and the authors failed to include two important RCTs, 7,8 which included 345 participants. In addition, the active factors such as caffeine and coffee oils, which were responsible for the plasma lipoprotein-increasing effect of coffee, were not determined.To determine the effect of caffeinated coffee and decaffeinated coffee consumption on plasma lipoprotein cholesterol levels in healthy men, Fried et al. 9 performed a RCT by three intervention coffee including 720 ml/day of caffeinated coffee, 360 ml/day o...
Background:Little is known about the tumour suppressive proteins and the underlying mechanisms that suppress colon cancer progression. Homeodomain-containing transcription factor HOXB9 plays an important role in embryogenesis and cancer development. We here aim to uncover the potential role of HOXB9 in the regulation of colon adenocarcinoma progression including epithelial-to-mesenchymal transition.Methods:HOXB9 expression in colon adenocarcinoma cells and patients was analysed by western blot and immunohistochemistry separately. Correlation between HOXB9 expressions with patients' survival was assessed by Kaplan–Meier analysis. HOXB9-regulated target gene expression was determined by RNA sequencing in HOXB9-overexpressing colon adenocarcinoma cells.Results:Elevated HOXB9 expression was identified in well-differentiated colon adenocarcinoma patients and was associated with a better overall patients' survival. Overexpression of HOXB9 inhibited colon adenocarcinoma cell growth, migration, invasion in vitro and tumour growth, liver as well as lung metastases in nude mice; whereas silencing HOXB9 promoted these functions. HOXB9 promoted colon adenocarcinoma differentiation via a mechanism that stimulates mesenchymal-to-epithelial transition, involving downregulation of EMT-promoting transcriptional factors including Snail, Twist, FOXC2 and ZEB1 and upregulation of epithelial proteins including E-cadherin, claudins-1, -4, -7, occludin and ZO-1.Conclusions:HOXB9 is a novel tumour suppressor that inhibits colon adenocarcinoma progression by inducing differentiation. Elevated expression of HOXB9 predicts a longer survival in colon adenocarcinoma patients.
A genome-wide differential expression of long noncoding RNAs (lncRNAs) was identified in blood specimens of autism spectrum disorder (ASD). A total of 3929 lncRNAs were found to be differentially expressed in ASD peripheral leukocytes, including 2407 that were upregulated and 1522 that were downregulated. Simultaneously, 2591 messenger RNAs (mRNAs), including 1789 upregulated and 821 downregulated, were also identified in ASD leukocytes. Functional pathway analysis of these lncRNAs revealed neurological pathways of the synaptic vesicle cycling, long-term depression and long-term potentiation to be primarily involved. Thirteen synaptic lncRNAs, including nine upregulated and four downregulated, and 19 synaptic mRNAs, including 12 upregulated and seven downregulated, were identified as being differentially expressed in ASD. Our identification of differential expression of synaptic lncRNAs and mRNAs suggested that synaptic vesicle transportation and cycling are important for the delivery of synaptosomal protein(s) between presynaptic and postsynaptic membranes in ASD. Finding of 19 lncRNAs, which are the antisense, bi-directional and intergenic, of HOX genes may lead us to investigate the role of HOX genes involved in the development of ASD. Discovery of the lncRNAs of SHANK2-AS and BDNF-AS, the natural antisense of genes SHANK2 and BDNF, respectively, indicates that in addition to gene mutations, deregulation of lncRNAs on ASD-causing gene loci presents a new approach for exploring possible epigenetic mechanisms underlying ASD. Our study also opened a new avenue for exploring the use of lncRNA(s) as biomarker(s) for the early detection of ASD.
Inducing senescence in cancer cells is an effective approach to suppress cancer growth, and it contributes significantly to the efficacy of therapeutic drugs. Previous studies indicated that transcription factors NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells) and C/EBPβ (CCAAT/enhancer-binding protein-β) play a critical role in the establishment of senescence by upregulating proinflammatory cytokines, notably interleukin-6 (IL-6) and interleukin-8 (IL-8). However, it is not clear how these two factors are activated in response to senescence-inducing stimuli and subsequently regulate gene transcription. Here, we reveal Bcl-2-associated transcription factor 1 (Bclaf1) as a novel player in the therapeutic drug doxorubicin-induced senescence (TIS) in multiple cancer cells. Bclaf1 is upregulated through the ATM/Nemo/NF-κB pathway during TIS and is a direct target of p65 and c-Rel. The induction of Bclaf1 by NF-κB is essential for C/EBPβ upregulation and IL-6/IL-8 transcription during TIS. Bclaf1 can interact with the leucine zipper region of C/EBPβ and cooperate with C/EBPβ to upregulate IL-8. Furthermore, we show that Bclaf1 is required for the effectiveness of doxorubicin (Dox) treatment-induced tumor suppression in a xenograft tumor model. These finding suggest that Bclaf1 plays a crucial role in transducing the senescence-inducing signal from NF-κB to C/EBPβ during TIS, thus amplifying the signals for the establishment of senescence. Given the recent revelation that Bclaf1 is involved in tumorigenesis, our data indicate that the responsiveness of Bclaf1 to NF-κB may determine the effectiveness of therapeutic drugs.
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