45 research outputs found
Dairy products, dietary calcium and the risk of inflammatory bowel disease: results from a European prospective cohort investigation
Background: Dairy products may be involved in the etiology of inflammatory bowel disease by modulating gut microbiota and immune responses, but data from epidemiological studies examining this relationship are limited. We investigated the association between prediagnostic intake of these foods and dietary calcium, and the subsequent development of Crohn's disease (CD) and ulcerative colitis (UC). Methods: In total, 401,326 participants were enrolled in the European Prospective Investigation into Cancer and Nutrition cohort. At recruitment, consumption of total and specific dairy products (milk, yogurt, and cheese) and dietary calcium was measured using validated food frequency questionnaires. Cases developing incident CD (n = 110) or UC (n = 244) during follow-up were matched with 4 controls. Conditional logistic regression analyses were used to calculate odds ratios (ORs) with 95% confidence intervals (CIs), adjusted for total energy intake and smoking. Results: Compared with the lowest quartile, the ORs for the highest quartile of total dairy products and dietary calcium intake were 0.61 (95% CI, 0.32-1.19, p trend = 0.19) and 0.63 (95% CI, 0.28-1.42, p trend = 0.23) for CD, and 0.80 (95% CI, 0.50-1.30, p trend = 0.40) and 0.81 (95% CI, 0.49-1.34, p trend = 0.60) for UC, respectively. Compared with nonconsumers, individuals consuming milk had significantly reduced odds of CD (OR 0.30, 95% CI, 0.13-0.65) and nonsignificantly reduced odds of UC (OR 0.85, 95% CI, 0.49-1.47). Conclusions: Milk consumption may be associated with a decreased risk of developing CD, although a clear dose-response relationship was not established. Further studies are warranted to confirm this possible protective effect
Photography-based taxonomy is inadequate, unnecessary, and potentially harmful for biological sciences
The question whether taxonomic descriptions naming new animal species without type specimen(s) deposited in collections should be accepted for publication by scientific journals and allowed by the Code has already been discussed in Zootaxa (Dubois & NemĂ©sio 2007; Donegan 2008, 2009; NemĂ©sio 2009aâb; Dubois 2009; Gentile & Snell 2009; Minelli 2009; Cianferoni & Bartolozzi 2016; Amorim et al. 2016). This question was again raised in a letter supported
by 35 signatories published in the journal Nature (Pape et al. 2016) on 15 September 2016. On 25 September 2016, the following rebuttal (strictly limited to 300 words as per the editorial rules of Nature) was submitted to Nature, which on
18 October 2016 refused to publish it. As we think this problem is a very important one for zoological taxonomy, this text is published here exactly as submitted to Nature, followed by the list of the 493 taxonomists and collection-based
researchers who signed it in the short time span from 20 September to 6 October 2016
Plasma alkylresorcinol concentrations, biomarkers of whole-grain wheat and rye intake, in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort
Analysis of the Hindfoot Alignment Measured in 3D After a Medializing Calcaneal Osteotomy Using a Pre- and Postoperative Weightbearing CT
Category: Hindfoot Introduction/Purpose: An adult acquired flat foot (AAFD) is a complex 3D deformity. A medializing calcaneal osteotomy (MCO) is a surgical procedure frequently performed to correct the valgus alignment of the hindfoot in a stage II AAFD, when conservative measurements fail. However currently little is known on its accurate influence regarding the hindfoot alignment (HA). The aim is therefore to assess the influence of a MCO on the 3D HA using computer aided software analysis of the images retrieved from a weightbearing cone beam CT (WBCT). Methods: Twelve patients with a mean age of 49,4 years (range 18-67yrs) were prospectively included in a pre-post study design. Indications for surgical correction by a MCO with a solitary translation consisted of an AAFD stage II (N=10) and a posttraumatic valgus deformity (N=2). Fixation of the osteotomy was performed by a step-plate or double screw. WBCT was obtained pre- and post-operative. Images were subsequently segmented to allow a HA calculation in 3D(HA3D) by an angle between the anatomical tibia axis and the axis connecting the computed inferior calcaneuspoint and the centroid of the talus in the coronal plane based on a Cartesian coordinatesystem(Fig 1A, C). The tibia in the HA3D was separately assessed by the anatomical tibia axis (TAx 3D) and the axis to determine the tibial rotation(TR 3D) in the axial plane by connecting the computed most outer point of the anterior and posterior tubercle of the incisura fibularis(Fig 2A, D). Results: The mean medial translation of the calcaneal osteotomy during surgery was 5.72 mm (SD = 3.9). The mean HA3D pre-operatively equaled 18.21 degrees of valgus (SD = 6.6) and post-operatively 9.31 degrees of valgus (SD = 6.18). The Paired Studentâs t-test showed a significant correction of 8.89 degrees (95%CI [5.99, 11.80], P<0.001). The mean TAX 3D pre-operatively was 6.80 degrees of valgus (SD = 3.38) and post-operatively 4.11 degrees of valgus (SD = 2.77), with a significant difference of 2.69 degrees (95%CI [1.79, 3.59], P <0.001). The mean TR3D pre-operatively was -27.11 degrees (SD = 4.77) and post-operatively - 28.80 degrees (SD = 5.98) and showed a significant difference of 1.69 degrees (95%CI [0.41, 2.97], P = 0,016). Conclusion: This study shows an effective correction of the valgus hindfoot in an AAFD. It appears that the correction is not only situated in the calcaneus but also to a lesser extent in the tibia and this resulted in 15% of the achieved HA correction. The novelty is the 3D weightbearing assessment of a hindfoot correction and the shown influence on the tibia. This information could be of use to take in to account when performing a pre-operative planning of a hindfoot deformity
Exposure to ambient air pollution and the risk of inflammatory bowel disease : a european nested case-control study
Industrialization has been linked to the etiology of inflammatory bowel disease (IBD).; We investigated the association between air pollution exposure and IBD.; The European Prospective Investigation into Cancer and Nutrition cohort was used to identify cases with Crohn's disease (CD) (n = 38) and ulcerative colitis (UC) (n = 104) and controls (n = 568) from Denmark, France, the Netherlands, and the UK, matched for center, gender, age, and date of recruitment. Air pollution data were obtained from the European Study of Cohorts for Air Pollution Effects. Residential exposure was assessed with land-use regression models for particulate matter with diameters of <10 Όm (PM10), <2.5 Όm (PM2.5), and between 2.5 and 10 Όm (PMcoarse), soot (PM2.5 absorbance), nitrogen oxides, and two traffic indicators. Conditional logistic regression analyses were performed to calculate odds ratios (ORs) with 95 % confidence intervals (CIs).; Although air pollution was not significantly associated with CD or UC separately, the associations were mostly similar. Individuals with IBD were less likely to have higher exposure levels of PM2.5 and PM10, with ORs of 0.24 (95 % CI 0.07-0.81) per 5 Όg/m(3) and 0.25 (95 % CI 0.08-0.78) per 10 Όg/m(3), respectively. There was an inverse but nonsignificant association for PMcoarse. A higher nearby traffic load was positively associated with IBD [OR 1.60 (95 % CI 1.04-2.46) per 4,000,000 motor vehicles Ă m per day]. Other air pollutants were positively but not significantly associated with IBD.; Exposure to air pollution was not found to be consistently associated with IBD
Fresh fruit consumption and all-cause and cause-specific mortality: findings from the China Kadoorie Biobank
Release of endogenous danger signals from HIFU-treated tumor cells and their stimulatory effects on APCs
Pharmacodynamics of Liposomal Amphotericin B and Flucytosine for Cryptococcal Meningoencephalitis: Safe and Effective Regimens for Immunocompromised Patients
Proteomic Bioprofiles and Mechanistic Pathways of Progression to Heart Failure The HOMAGE Study
Background Identifying the mechanistic pathways potentially associated with incident heart failure (HF) may provide a basis for novel preventive strategies. Methods and Results To identify proteomic biomarkers and the potential underlying mechanistic pathways that may be associated with incident HF defined as the first hospitalization for HF, a nested-matched case-control design was used with cases (incident HF) and controls (without HF) selected from 3 cohorts (>20â000 individuals). Controls were matched on cohort, follow-up time, age, and sex. Two independent sample sets (a discovery set with 286 cases and 591 controls and a replication set with 276 cases and 280 controls) were used to discover and replicate the findings. Two hundred fifty-two circulating proteins in the plasma were studied. Adjusting for the matching variables age, sex, and follow-up time (and correcting for multiplicity of tests), 89 proteins were found to be associated with incident HF in the discovery phase, of which 38 were also associated with incident HF in the replication phase. These 38 proteins pointed to 4 main network clusters underlying incident HF: (1) inflammation and apoptosis, indicated by the expression of the TNF (tumor necrosis factor)-family members; (2) extracellular matrix remodeling, angiogenesis and growth, indicated by the expression of proteins associated with collagen metabolism, endothelial function, and vascular homeostasis; (3) blood pressure regulation, indicated by the expression of natriuretic peptides and proteins related to the renin-angiotensin-aldosterone system; and (4) metabolism, associated with cholesterol and atherosclerosis. Conclusions Clusters of biomarkers associated with mechanistic pathways leading to HF were identified linking inflammation, apoptosis, vascular function, matrix remodeling, blood pressure control, and metabolism. These findings provide important insight on the pathophysiological mechanisms leading to HF. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02556450.status: publishe