1,223 research outputs found

    Don't stop taking aspirin [Letter]

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    Dairy foods and body mass index over 10-year: evidence from the Caerphilly Prospective Cohort Study

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    The association between dairy product consumption and body mass index (BMI) remains controversial. The aim of the present study was to investigate the association between total dairy, milk, cheese, cream and butter consumption and BMI change over a 10-year follow-up by using long-term follow-up cohort data from the Caerphilly Prospective Cohort Study (CAPS). The CAPS included 2512 men aged 45⁻59 years at baseline, who were followed up at 5-year intervals for over 20-year. A semi-quantitative food frequency questionnaire estimated the intake of dairy consumption, including milk, cheese, cream and butter at baseline, 5-year and 10-year follow-up. In total, men free of cardiovascular disease, diabetes and cancer ( = 1690) were included in current analysis. General linear regression and logistic regression were used for data analysis. The results showed higher cheese consumption was associated with lower BMI at the 5-year follow-up ( = 0.013). There was no evidence that higher consumption of total dairy, milk, cream and butter were significantly associated with BMI during the over the 10-year following-up. This study suggest that cheese consumption have beneficial effects on lowering BMI, which needs further investigation

    Stimulation of Activin A/Nodal signaling is insufficient to induce definitive endoderm formation of cord blood-derived unrestricted somatic stem cells

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    Introduction: Unrestricted somatic stem cells (USSC) derived from umbilical cord blood are an attractive alternative to human embryonic stem cells (hESC) for cellular therapy. USSC are capable of forming cells representative of all three germ line layers. The aim of this study was to determine the potential of USSC to form definitive endoderm following induction with Activin A, a protein known to specify definitive endoderm formation of hESC. Methods: USSC were cultured for (1) three days with or without 100 ng/ml Activin A in either serum-free, low-serum or serum-containing media, (2) three days with or without 100 ng/ml Activin A in combination with 10 ng/ml FGF4 in pre-induction medium, or (3) four days with or without small molecules Induce Definitive Endoderm (IDE1, 100 nM; IDE2, 200 nM) in serum-free media. Formation of definitive endoderm was assessed using RT-PCR for gene markers of endoderm (Sox17, FOXA2 and TTF1) and lung epithelium (surfactant protein C; SPC) and cystic fibrosis transmembrane conductance regulator; CFTR). The differentiation capacity of Activin A treated USSC was also assessed. Results: Activin A or IDE1/2 induced formation of Sox17+ definitive endoderm from hESC but not from USSC. Activin A treated USSC retained their capacity to form cells of the ectoderm (nerve), mesoderm (bone) and endoderm (lung). Activin A in combination with FGF4 did not induce formation of Sox17+ definitive endoderm from USSC. USSC express both Activin A receptor subunits at the mRNA and protein level, indicating that these cells are capable of binding Activin A. Conclusions: Stimulation of the Nodal signaling pathway with Activin A or IDE1/2 is insufficient to induce definitive endoderm formation from USSC, indicating that USSC differ in their stem cell potential from hESC

    Aspirin and cancer survival: a systematic review and meta-analyses of 118 observational studies of aspirin and 18 cancers.

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    BackgroundDespite the accumulation of research papers on aspirin and cancer, there is doubt as to whether or not aspirin is an acceptable and effective adjunct treatment of cancer. The results of several randomised trials are awaited, and these should give clear evidence on three common cancers: colon, breast and prostate. The biological effects of aspirin appear likely however to be of relevance to cancer generally, and to metastatic spread, rather than just to one or a few cancers, and there is already a lot of evidence, mainly from observational studies, on the association between aspirin and survival in a wide range of cancers.AimsIn order to test the hypothesis that aspirin taking is associated with an increase in the survival of patients with cancer, we conducted a series of systematic literature searches to identify clinical studies of patients with cancer, some of whom took aspirin after having received a diagnosis of cancer.ResultsThree literature searches identified 118 published observational studies in patients with 18 different cancers. Eighty-one studies report on aspirin and cancer mortality and 63 studies report on all-cause mortality. Within a total of about a quarter of a million patients with cancer who reported taking aspirin, representing 20%-25% of the total cohort, we found aspirin to be associated with a reduction of about 20% in cancer deaths (pooled hazard ratio (HR): 0.79; 95% confidence intervals: 0.73, 0.84 in 70 reports and a pooled odds ratio (OR): 0.67; 0.45, 1.00 in 11 reports) with similar reductions in all-cause mortality (HR: 0.80; 0.74, 0.86 in 56 studies and OR: 0.57; 0.36, 0.89 in seven studies). The relative safety of aspirin taking was examined in the studies and the corresponding author of every paper was written to asking for additional information on bleeding. As expected, the frequency of bleeding increased in the patients taking aspirin, but fatal bleeding was rare and no author reported a significant excess in fatal bleeds associated with aspirin. No author mentioned cerebral bleeding in the patients they had followed.ConclusionsThere is a considerable body of evidence suggestive of about a 20% reduction in mortality in patients with cancer who take aspirin, and the benefit appears not to be restricted to one or a few cancers. Aspirin, therefore, appears to deserve serious consideration as an adjuvant treatment of cancer, and patients with cancer, and their carers, have a right to be informed of the available evidence

    Dairy foods and body mass index over 20-years: evidence from Caerphilly Prospective Study

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    The prevalence of obesity has reached epidemic proportions with more than 600 million adults worldwide classified as clinically obese (body mass index (BMI) ⩾ 30 kg/m2)(1). Among the various approaches to tackle obesity and its comorbidities, a heathy diet is one of the key determinants for reducing obesity(2). Given that dairy products are naturally rich in protein and essential micronutrients, including calcium, potassium and vitamin A(3), they are recommended as an integral part of a healthy diet by many countries(4). However, dairy is also a major contributor to saturated fatty acids (SFA) and energy intake(5), thus their role in development of obes- ity has been questioned and explored by several studies(6). We investigated the association between total dairy, milk, cheese, cream and butter consumption and BMI change over a 20-year follow-up using the Caerphilly prospective study (CAPS). The CAPS included 2512 men aged 45–59 years, who were followed up at 5-year intervals for over 20-years. The associations of total dairy, milk, cheese, cream and butter consumption with BMI were examined cross-sectionally at baseline and longitudinally at 5, 10, 15 and 20-years follow-ups. General linear regression and logistic regression were used for data analysis. Men free of cardiovascular disease and diabetes (n = 1704) were included in the current analysis. Higher cheese consumption was associated with lower BMI at the 5-year follow-up (P = 0·008) but not at later follow-ups. There was no evidence that higher consumption of dairy products was associated with increased BMI during the over 20-years follow-up, although total dairy (P = 0·002) and milk consumption (P < 0·001) were inversely associated with BMI at baseline. For the future studies, the association between cheese consumption and BMI requires further investigation

    The Lantern Vol. 30, No. 2, May 1963

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    • An Observation • Interim • The Collected Raid • Please • Love Me • Waiting With the Sun • Upon a Summit • A Hedonist Comments on His Religion • Like Ice • Dark Morning • So Soft the Breeze • The Heat of Youth • Solemnity • A Laugh • Peter Departinghttps://digitalcommons.ursinus.edu/lantern/1084/thumbnail.jp

    Aspirin and cancer: biological mechanisms and clinical outcomes

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    Evidence on aspirin and cancer comes from two main sources: (1) the effect of aspirin upon biological mechanisms in cancer, and (2) clinical studies of patients with cancer, some of whom take aspirin. A series of systematic literature searches identified published reports relevant to these two sources. The effects of aspirin upon biological mechanisms involved in cancer initiation and growth appear to generate reasonable expectations of effects upon the progress and mortality of cancer. Clinical evidence on aspirin appears overall to be favourable to the use of aspirin, but evidence from randomized trials is limited, and inconsistent. The main body of evidence comes from meta-analyses of observational studies of patients with a wide range of cancers, about 25% of whom were taking aspirin. Heterogeneity is large but, overall, aspirin is associated with increases in survival and reductions in metastatic spread and vascular complications of different cancers. It is important that evaluations of aspirin used as an adjunct cancer treatment are based upon all the available relevant evidence, and there appears to be a marked harmony between the effects of aspirin upon biological mechanisms and upon the clinical progress of cancer

    Healthy living and cancer: evidence from UK Biobank.

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    CONTEXT: UK Biobank is a prospective study of half a million subjects, almost all aged 40-69 years, identified in 22 centres across the UK during 2006-2010. OBJECTIVE: A healthy lifestyle has been described as 'better than any pill, and no side effects [5]. We therefore examined the relationships between healthy behaviours: low alcohol intake, non-smoking, healthy BMI, physical activity and a healthy diet, and the risk of all cancers, colon, breast and prostate cancers in a large dataset. METHOD: Data on lifestyle behaviours were provided by 343,150 subjects, and height and weight were measured at recruitment. 14,285 subjects were diagnosed with cancer during a median of 5.1 years of follow-up. RESULTS: Compared with subjects who followed none or a single healthy behaviour, a healthy lifestyle based on all five behaviours was associated with a reduction of about one-third in incident cancer (hazard ratio [HR] 0.68; 95% confidence intervals [CI] 0.63-0.74). Colorectal cancer was reduced in subjects following the five behaviours by about one-quarter (HR 0.75; 95% CI 0.58-0.97), and breast cancer by about one-third (HR 0.65; 95% CI 0.52-0.83). The association between a healthy lifestyle and prostate cancer suggested a significant increase in risk, but this can be attributed to bias consequent on inequalities in the uptake of the prostate specific antigen screening test. CONCLUSIONS: Taken together with reported reductions in diabetes, vascular disease and dementia, it is clearly important that every effort is taken to promote healthy lifestyles throughout the population, and it is pointed out that cancer and other screening clinics afford 'teachable moments' for the promotion of a healthy lifestyle
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