In Vitro Testing to Aflatoxin Binding by Glucomannan Yeast Product and Glucomannan Extract from Amorphophallus oncophyllus

The aim of research was to test the capability of glucomannan yeast product (GYP) and glucomannan resulted from Amorphophallus oncophyllus extraction (GRE) to bind aflatoxin in in vitro testing. Before in vitro testing, both GYP and GRE were analyzed to determine proximate analysis, glucose, and mannose concentrations. In vitro testing used aflatoxin, binder and gastro intestinal fluid in 3% ringer solution. The weights of binders were 41.05; 82.1; 123.15; and 164.2 mg and weight of aflatoxin was 0.1642 µg of each tube. The results showed that the percentage of aflatoxin bound increased by the increasing weight either glucomannan from yeast product or glucomannan resulted from A. oncophylus extraction. The percentages of aflatoxin binding with binder of both glucomannan yeast product were 19.72%; 21.51%; 42.25%; 46.35% and glucomannan from A. oncophyllus extraction were 4.08%; 28.72%; 36.73%; and 89.07%, consecutively. There were positive correlations (

Pengaruh Subtitusi Tepung Bayam Merah dan Tepung Kacang Merah terhadap Uji Organoleptik dan Kandungan Gizi Cookies

Abstrak Status gizi ibu menjadi salah satu faktor yang menentukkan pertumbuhan perkembangan janin termasuk berat dan panjang saat lahir. Salah satu upaya yang dapat dilakukan adalah dengan pemberian makanan tambahan (PMT) yang kaya Fe. PMT dapat disajikan dalam bentuk makanan pokok maupun selingan dengan bahan baku pangan lokal. Produk PMT yang baru adalah pemberian Cookies kaya Fe dengan formulasi penambahan bayam merah dan kacang merah. Cookies menjadi pilihan karena berbahan dasar tepung terigu yang sudah dikenal masyarakat luas, dapat langsung dikonsumsi, kadar airnya rendah sehingga tahan lama, teksturnya digemari karena renyah, dan mudah dibuat, disamping membantu mencukupi kebutuhan energi dan zat besi untuk ibu hamil.Tujuan penelitian ini adalah untuk mengetahaui pengaruh subtitusi tepung bayam merah dan tepung kacang merah terhadap uji organoleptik dan kandungan gizi cookies. Jenis penelitian ini menggunakan Rancangan acak lengkap (RAL) dengan 4 perlakuan P1 (30 % & 5 %), P2 ( 40 % & 10 %), P3 (50 % & 15 %). Hasil penelitian didapatkan ada perbedaan aroma dan tekstur pada perlakuan P1, P2 dan P3 dimana P Value < 0.05, dan tidak ada perbedaan kualitas untuk rasa dan warna pada perlakuan P1, P2 dan P3 dimana P Value > 0.05. untuk hasil uji kandungan gizi terdapat perbedaan yang nyata dimana dalam perlakuan P1 sampai P3 kandungan protein lebih tinggi pada perlakuan P3 dengan nilai 8.89 kal/100 gr bahan makanan. &nbsp

Early Impacts of COVID-19 on Nutrition Intake and Household Dietary Diversity in Kupang District, East Nusa Tenggara, Indonesia

One of the social problems solving the direct impact on the community is overcoming household food security due to the COVID-19 pandemic. This study aims to analyze household food security during the COVID-19 pandemic and link it to the nutrient intake and nutritional status of children under five in the Kupang district area. This cross-sectional study is based on a survey conducted on the Timorese population in Kupang, East Nusa Tenggara, Indonesia, from May to October 2021. Data on household dietary diversity was collected through the 24-hour food recall using the household dietary diversity score (HDDS). The study sample was taken from Timorese population families with toddlers under five years, and 1,444 families voluntarily participated in this study. Subjects were taken at each public health using a simple random method. This study analyzes the Spearman correlation test with the HDDS and the proportion of food expenditure. A 63% of households had a balance of less cost (<50%) with an average of 63.9. Generally, households (90.4%) had a pretty good diet diversity score. Food groups that were relatively highly consumed by most households included cereals (100%), sugar and sweeteners (90.2%), oils and fats (93.7%), seasonings, and spices (89.4%). A significant effect with p<0.05 was on HDDS during the COVID-19 pandemic. The food consumption score is another indicator widely used in determining household food security. Therefore, it is necessary to revalidate tests in further studies of these indicators

Inborn and acquired metabolic defects in cancer

The observation that altered metabolism is the fundamental cause of cancer was made by Otto Warburg nearly a century ago. However, the subsequent identification of oncogenes and tumor suppressor genes has displaced Warburg's theory pointing towards genetic aberrations as the underlining cause of cancer. Nevertheless, in the last decade, cancer-associated mutations have been identified in genes coding for tricarboxylic acid cycle (TCA cycle, also known as Krebs cycle) and closely related enzymes that have essential roles in cellular metabolism. These observations have revived interest in Warburg's hypothesis and prompted a flurry of functional studies in the hope of gaining mechanistic insight into the links between mitochondrial dysfunction, metabolic alterations, and cancer. In this review, we discuss the potential pro-oncogenic signaling role of some TCA cycle metabolites and their derivatives (oncometabolites). In particular, we focus on their effects on dioxygenases, a family of oxygen and α-ketoglutarate-dependent enzymes that control, among other things, the levels and activity of the hypoxia-inducible transcription factors and the activity of DNA and histone demethylases

Dlk1 Is Necessary for Proper Skeletal Muscle Development and Regeneration

Delta-like 1homolog (Dlk1) is an imprinted gene encoding a transmembrane protein whose increased expression has been associated with muscle hypertrophy in animal models. However, the mechanisms by which Dlk1 regulates skeletal muscle plasticity remain unknown. Here we combine conditional gene knockout and over-expression analyses to investigate the role of Dlk1 in mouse muscle development, regeneration and myogenic stem cells (satellite cells). Genetic ablation of Dlk1 in the myogenic lineage resulted in reduced body weight and skeletal muscle mass due to reductions in myofiber numbers and myosin heavy chain IIB gene expression. In addition, muscle-specific Dlk1 ablation led to postnatal growth retardation and impaired muscle regeneration, associated with augmented myogenic inhibitory signaling mediated by NF-κB and inflammatory cytokines. To examine the role of Dlk1 in satellite cells, we analyzed the proliferation, self-renewal and differentiation of satellite cells cultured on their native host myofibers. We showed that ablation of Dlk1 inhibits the expression of the myogenic regulatory transcription factor MyoD, and facilitated the self-renewal of activated satellite cells. Conversely, Dlk1 over-expression inhibited the proliferation and enhanced differentiation of cultured myoblasts. As Dlk1 is expressed at low levels in satellite cells but its expression rapidly increases upon myogenic differentiation in vitro and in regenerating muscles in vivo, our results suggest a model in which Dlk1 expressed by nascent or regenerating myofibers non-cell autonomously promotes the differentiation of their neighbor satellite cells and therefore leads to muscle hypertrophy

The association of telomere length with substance use disorders: systematic review and meta-analysis protocol

BACKGROUND: The present protocol was designed for a systematic review and meta-analysis aimed at determining the association of telomere length with substance use disorders with the exclusion of nicotine addiction, and to identify potential moderators of the effect of telomere length. Such methodological information may provide guidance to improve the quality of future research on this important topic. METHODS: Potential studies will be identified through electronic databases (PubMed/MEDLINE, EMBASE, PsycINFO, and Web of Science) up from inception onwards. The inclusion criteria will include published or unpublished observational studies (cohort, case-control, and cross-sectional studies) reporting telomere length in adult patients with substance use disorder compared with a control group. Non-human studies or other study designs such as reviews, case-only, family-based, and/or population studies with only healthy participants will be excluded, as well as those focused solely on nicotine addiction. The main outcome will be telomere length in adults with substance use disorder (primary) and, specifically, in those with alcohol use disorder (secondary). Two investigators will independently evaluate the preselected studies for possible inclusion and will extract data following a standardized protocol. Disagreements will be resolved by consensus. The risk of bias of all included studies will be assessed using the Newcastle-Ottawa Quality Assessment Scale for non-randomized studies. Data will be converted into standardized mean differences as effect size index, and random-effects models will be used for the meta-analysis. Cochran's Q statistic, I(2) index, and visual inspection of the forest plot will be used to verify study heterogeneity. Subgroup analyses and meta-regressions will be conducted to ascertain heterogeneity. Several sensitivity analyses will be conducted to address the influence of potential confounding factors. Publication bias will be examined using the "funnel plot" method with Duval and Tweedie's trim-and-fill method and Egger test. DISCUSSION: This systematic review will assess the association of telomere length with substance use disorders aside from nicotine addiction. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration number CRD42019119785

The epigenetic landscape of renal cancer

This is an accepted manuscript of an article published by Nature in Nature Reviews: Nephrology on 28/11/2016, available online: https://doi.org/10.1038/nrneph.2016.168 The accepted version of the publication may differ from the final published version.The majority of kidney cancers are associated with mutations in the von Hippel-Lindau gene and a small proportion are associated with infrequent mutations in other well characterized tumour-suppressor genes. In the past 15 years, efforts to uncover other key genes involved in renal cancer have identified many genes that are dysregulated or silenced via epigenetic mechanisms, mainly through methylation of promoter CpG islands or dysregulation of specific microRNAs. In addition, the advent of next-generation sequencing has led to the identification of several novel genes that are mutated in renal cancer, such as PBRM1, BAP1 and SETD2, which are all involved in histone modification and nucleosome and chromatin remodelling. In this Review, we discuss how altered DNA methylation, microRNA dysregulation and mutations in histone-modifying enzymes disrupt cellular pathways in renal cancers