Suplementación dietética con aguas residuales de una fábrica productora de caramelo y su efecto sobre el crecimiento de cerdos destetados y componentes del eje de factores de crecimiento semejantes a insulina

An experiment was conducted to evaluate the expression of insulin-like growth factor-I (IGF-I) and IGF-binding proteins (IGFBPs -II and -III) in response to a 10% inclusion of caramel plant wastewater (CPWW) in weaning pig diets; the objective was to assess associations between those growthrelated proteins to feed intake (Fl) and body weight gain (BWG). Sixteen purebred Landrace piglets were randomly distributed among eight pens (a gilt and boar per pen) and assigned to one of two treatments: 0% (control) and 10% inclusion of CPWW. During four consecutive weeks, live weight and Fl were recorded. Blood samples were drawn by jugular venipuncture during the first, second, and third weeks of the experiment and serum levels of IGF-I, IGFBP-II and IGFBP-III were determined. Feed intake, BWG and feed efficiency (FE) were not affected (P > 0.05) by the addition of 10% CPWW tothe diet, nor was animal health status visibly affected. Serum IGF-I levels were higher in control animals (P < 0.05) and increased from d 14 to d 28 of the experimental period (P < 0.05). Weekly increases were observed for IGFBP- III (P < 0.05) whereas IGFBP-II circulating levels decreased from d 14 to d 28 of the post-weaning test period. Simple correlation analysis revealed that there was a positive association between circulating levels of IGF-I and IGFBP-III (r = 0.88; P < 0.0001). However, the opposite was observed between these two and IGFBP-II (r = -0.84, P < 0.0001; r = -0.67, P < 0.0025, respectively). The changes observed in circulating levels of IGF-I, IGFBP-III and IGFBP-II were associated with weekly increases in Fl and BWG that occurred during the entire experimental period (P < 0.05). Se realizó un experimento para determinar si la inclusión de un 10% de aguas residuales de una fábrica de caramelo (CPWW, por sus siglas en inglés) en la dieta de cerdos post-destete resulta en cambios en los niveles del factor de crecimiento semejante a insulina-l (IGF-I, por sus siglas en inglés) y proteínas fijadoras de IGF (IGFBPs-ll y -III, por sus siglas en inglés) en la sangre, y si éstos se asocian a diferencias en consumo de alimento (CA), ganancia en peso (GP), y eficiencia de conversión (EC). Dieciséis cerdos de raza Landrace se distribuyeron al azar entre ocho jaulas (una cerda y un cerdo por jaula) y se asignaron a uno de dos tratamientos: 0% (control) y 10% de inclusión de CPWW. Durante cuatro semanas consecutivas se registró el peso vivo y el consumo de alimento de los animales. Se recolectaron muestras de sangre a través de sangrado yugular durante la primera, segunda y tercera semana del experimento y se determinaron los niveles de IGF-I, IGFBP-II y IGFBP-III en el suero. No hubo efecto significativo de la adición de 10% CPWW en la dieta sobre CA, GP y EC (P > 0.05). Mediante apreciación visual se determinó que la inclusión de CPWW no tuvo efectos adversos en la salud de los animales. Los niveles de IGF-I fueron más altos para los animales control (P < 0.05) y aumentaron del día 14 al día 28 del periodo post-destete (P < 0.05). Se observó un aumento semanal en los niveles de IGFBP-III (P < 0.05), mientras que los niveles de IGFBP-II disminuyeron a partir del día 14 al día 28 (P < 0.05). El análisis de correlación simple reveló que existe una asociación positiva entre los niveles de IGF-I y IGFBP-III circulando en la sangre (r = 0.88; P < 0.0001). Sin embargo, se observó un efecto opuesto entre éstos y IGFBP-II (r = -0.84, P < 0.0001; r = -0.67, P < 0.0025, respectivamente). Los cambios observados en los niveles sanguíneos de IGF-I, IGFBP-III y IGFBP-II se asociaron a aumentos semanales en CA y GP que ocurrieron durante todo el periodo experimental (P < 0.05)

INtervention for Cognitive Reserve Enhancement in Delaying the Onset of Alzheimer\u27s Symptomatic Expression (INCREASE), a Randomized Controlled Trial: Rationale, Study Design, and Protocol

BACKGROUND: The course of Alzheimer\u27s disease (AD) includes a 10-20-year preclinical period with progressive accumulation of amyloid β (Aβ) plaques and neurofibrillary tangles in the absence of symptomatic cognitive or functional decline. The duration of this preclinical stage in part depends on the rate of pathologic progression, which is offset by compensatory mechanisms, referred to as cognitive reserve (CR). Comorbid medical conditions, psychosocial stressors, and inappropriate medication use may lower CR, hastening the onset of symptomatic AD. Here, we describe a randomized controlled trial (RCT) designed to test the efficacy of a medication therapy management (MTM) intervention to reduce inappropriate medication use, bolster cognitive reserve, and ultimately delay symptomatic AD. METHODS/DESIGN: Our study aims to enroll 90 non-demented community-dwelling adults ≥ 65 years of age. Participants will undergo positron emission tomography (PET) scans, measuring Aβ levels using standardized uptake value ratios (SUVr). Participants will be randomly assigned to MTM intervention or control, stratified by Aβ levels, and followed for 12 months via in-person and telephone visits. Outcomes of interest include: (1) medication appropriateness (measured with the Medication Appropriateness Index (MAI)); (2) scores from Trail Making Test B (TMTB), Montreal Cognitive Assessment (MoCA), and California Verbal Learning Test (CVLT); (3) perceived health status (measured with the SF-36). We will also evaluate pre- to post-intervention change in: (1) use of inappropriate medications as measured by MAI; 2) CR Change Score (CRCS), defined as the difference in scopolamine-challenged vs unchallenged cognitive scores at baseline and follow-up. Baseline Aβ SUVr will be used to examine the relative impact of preclinical AD (pAD) pathology on CRCS, as well as the interplay of amyloid burden with inappropriate medication use. DISCUSSION: This manuscript describes the protocol of INCREASE ( INtervention for Cognitive Reserve Enhancement in delaying the onset of Alzheimer\u27s Symptomatic Expression ): a randomized controlled trial that investigates the impact of deprescribing inappropriate medications and optimizing medication regimens on potentially delaying the onset of symptomatic AD and AD-related dementias. TRIAL REGISTRATION: ClinicalTrials.gov, NCT02849639. Registered on 29 July 2016

Environmental risk factors for dementia: a systematic review

Background - Dementia risk reduction is a major and growing public health priority. While certain modifiable risk factors for dementia have been identified, there remains a substantial proportion of unexplained risk. There is evidence that environmental risk factors may explain some of this risk. Thus, we present the first comprehensive systematic review of environmental risk factors for dementia. Methods - We searched the PubMed and Web of Science databases from their inception to January 2016, bibliographies of review articles, and articles related to publically available environmental data. Articles were included if they examined the association between an environmental risk factor and dementia. Studies with another outcome (for example, cognition), a physiological measure of the exposure, case studies, animal studies, and studies of nutrition were excluded. Data were extracted from individual studies which were, in turn, appraised for methodological quality. The strength and consistency of the overall evidence for each risk factor identified was assessed. Results - We screened 4784 studies and included 60 in the review. Risk factors were considered in six categories: air quality, toxic heavy metals, other metals, other trace elements, occupational-related exposures, and miscellaneous environmental factors. Few studies took a life course approach. There is at least moderate evidence implicating the following risk factors: air pollution; aluminium; silicon; selenium; pesticides; vitamin D deficiency; and electric and magnetic fields. Conclusions - Studies varied widely in size and quality and therefore we must be circumspect in our conclusions. Nevertheless, this extensive review suggests that future research could focus on a short list of environmental risk factors for dementia. Furthermore, further robust, longitudinal studies with repeated measures of environmental exposures are required to confirm these associations