Palatogenesis is a complex developmental process requiring temporospatially coordinated cellular and molecular events. The following review focuses on genetic, epigenetic, and environmental aspects directing palatal formation and their implication in orofacial clefting genesis. Essential for palatal shelf development and elevation (TGF-β, BMP, FGF, and WNT), the subsequent processes of fusion (SHH) and proliferation, migration, differentiation, and apoptosis of neural crest-derived cells are controlled through signaling pathways. Interruptions to these processes may result in the birth defect cleft lip and/or palate (CL/P), which happens in approximately 1 in every 700 live births worldwide. Recent progress has emphasized epigenetic regulations via the class of non-coding RNAs with microRNAs based on critically important biological processes, such as proliferation, apoptosis, and epithelial–mesenchymal transition. These environmental risks (maternal smoking, alcohol, retinoic acid, and folate deficiency) interact with genetic and epigenetic factors during palatogenesis, while teratogens like dexamethasone and TCDD inhibit palatal fusion. In orofacial cleft, genetic, epigenetic, and environmental impact on the complex epidemiology. This is an extensive review, offering current perspectives on gene-environment interactions, as well as non-coding RNAs, in palatogenesis and emphasizing open questions regarding these interactions in palatal development.
2‐Amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine (PhIP) is the most mass abundant heterocyclic aromatic amine in foods and is a colon‐specific carcinogen. We recently showed that PhIP‐DNA adducts in rat colon were reduced by 20% when the diet was supplemented with apiaceous vegetables (i.e., celery and parsnips) at a modest dose (21%, wt/wt) equivalent to a human intake of 1 cup/day (based on a 2,000 kcal diet). The mechanism of action, however, was not through a commonly hypothesized effect, inhibition of pro‐carcinogen activation. Thus, here we examine the effects of apiaceous vegetable intake on promising alternative mechanisms of dietary chemoprevention: 1) N‐ methyltransferase (NMT) protein expression, 2) gene expression of PhIP transporters, 3) expression of genes related to DNA damage signaling pathways, and 4) changes in the global microRNA (miRNA) profile in rat colon. Male Wistar rats fed either the American Institute for Nutrition (AIN)‐93G diet (n=6), or the AIN‐93G supplemented with apiaceous vegetables (API; n=7), received a single intraperitoneal injection of PhIP (10 mg PhIP/kg body weight) after 6 days of feeding. A negative control group was fed AIN‐93G and injected with DMSO (n=5). No difference in hepatic NMT protein expression was noted amongst the groups. There was a trend for increased colonic mRNA expression of p‐glycoprotein, a minor PhIP efflux transporter (1.5‐fold; P =0.075); mRNA expression of other colonic PhIP efflux transporters, BCRP and MRP2, was not changed. PCR array analysis revealed that mRNA expression of Pole and Rad18 , involved in DNA repair pathways and induced in response to DNA damage, was reduced by API (1.3‐fold for both; P <0.05). Also, in the global miRNA profiling analysis, 11 out of 421 miRNAs were either elevated or suppressed in response to apiaceous vegetable supplementation. In particular, miR‐19b‐3p and miR‐29b‐3p were increased by API diet (2.8‐ and 2.2‐fold increase, respectively, P <0.05). Predictions by Ingenuity Pathway Analysis suggest that these two miRNAs target BMPR2 and CCND1 , among others. Some evidence suggests BMPR2 may be oncogenic, and there are reports of a positive correlation between CCND1 overexpression and cancer onset. In conclusion, apiaceous vegetable intake had negligible effects on NMT protein and PhIP transporter gene expression, but did modify genes and miRNA with potential chemopreventive roles. Further investigations are warranted regarding the impact of apiaceous‐mediated modulation of Pole and Rad18 , and the net downstream effects of miRNA modulation as pertains to colon carcinogenesis. Support or Funding Information University of Minnesota Masonic Cancer Center
This study investigated the effects of roasting conditions on the physicochemical, taste, and volatile and odor-active compound (OAC) profiles of Coffea arabica L. At 150 ℃, roasting increased chlorogenic acid, total flavonoids, and caffeine concentrations. However, umami and sourness sensor decreased during the roasting process. At 210 ℃ roasting, total flavonoid and caffeine concentrations increased during the roasting process. Aldehydes, ketones, and sulfur-containing compounds dramatically increased during the roasting at 210 ℃ for 20 and 30 min in E-nose analysis. Pyrazines were mainly generated during the roasting at 210 ℃ for 20 and 30 min, and pyrazines showed the highest concentrations among all OACs in GC-olfactometry (GC-O) analysis. E-tongue data showed the separation of beans by roasting temperature. However, the E-nose and GC-O data showed the separation of beans by both roasting temperature and time via multivariate analysis. We identified similar results and patterns in the E-nose and GC-O analyses.
The fatty acid and volatile compound compositions of camellia oil were analyzed in this study. The impacts of the replacement of conventional vegetable oil with camellia oil on the sensory attributes of dried seaweed were also determined. C18:1 (83.59%), followed by C16:0 and C18:2, were the most abundant fatty acids in camellia oil. A total of 11 and 32 volatile compounds were identified in camellia oil and sesame oil, respectively. In the preference test, the camellia oil samples received a higher, although insignificant, liking rating in overall acceptability of appearance. Overall, there were no differences between the sensory attributes of camellia oil and sesame oil. This finding, combined with the unique fatty acid composition, thermal stability, and health benefits of camellia oil indicate that further study into the use of camellia oil in foods is warranted.
Genetically selected modern broiler chickens have acquired outstanding production efficiency through rapid growth and improved feed efficiency compared to unselected chicken breeds. Recently, we analyzed the transcriptome of breast muscle tissues obtained from modern pedigree male (PeM) broilers (rapid growth and higher efficiency) and foundational Barred Plymouth Rock (BPR) chickens (slow growth and poorer efficiency). This study was designed to investigate microRNAs that play role in rapid growth of the breast muscles in modern broiler chickens. In this study, differential abundance of microRNA (miRNA) was analyzed in breast muscle of PeM and BPR chickens and the results were integrated with differentially expressed (DE) mRNA in the same tissues. A total of 994 miRNA were identified in PeM and BPR chicken lines from the initial analysis of small RNA sequencing data. After filtering and statistical analyses, the results showed miR-2131-5p, miR-221-5p, miR-126-3p, miR-146b-5p, miR-10a-5p, let-7b, miR-125b-5p, and miR-146c-5p up-regulated whereas miR-206 down-regulated in PeM compared to BPR breast muscle. Based on inhibitory regulations of miRNAs on the mRNA abundance, our computational analysis using miRDB, an online software, predicated that 118 down-regulated mRNAs may be targeted by the up-regulated miRNAs, while 35 up-regulated mRNAs appear to be due to a down-regulated miRNA (i.e., miR-206). Functional network analyses of target genes of DE miRNAs showed their involvement in calcium signaling, axonal guidance signaling, and NRF2-mediated oxidative stress response pathways suggesting their involvement in breast muscle growth in chickens. From the integrated analyses of differentially expressed miRNA-mRNA data, we were able to identify breast muscle specific miRNAs and their target genes whose concerted actions can contribute to rapid growth and higher feed efficiency in modern broiler chickens. This study provides foundation data for elucidating molecular mechanisms that govern muscle growth in chickens.
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