hich of the following will give well annotated metabolic pathway miRbase blastdb KEGG Ensembl

what is the experimental setups and methodologies employed in this paper to identify pathways, particularly through RNA sequencing

Scientists are interested in determining the underlying metabolic reprogramming events that lead to type 2 diabetes mellitus (T2DM), a disease characterized by insulin resistance and increased hepatic glucose production.  MicroRNAs (miRNAs) are a class of small noncoding RNAs implicated in T2DM pathology.  miR-26a, a member of the miR-26 family of miRNAs, has been shown to play a critical role in regulating hepatic glucose production and lipid metabolism.  miR-26a has also been implicated in the prevention of obesity-induced insulin resistance, as evidenced by decreased miR-26a expression in obese, leptin-deficient (ob/ob) mice compared to lean control mice.Experiment 1Researchers designed an experiment to promote obesity-induced insulin resistance in wild-type (WT) mice and Alb Tg mice, which express hepatic miR-26a at levels three-fold greater than WT.  WT mice and Alb Tg mice were fed either a standard healthy diet (SHD) or a high-fat diet (HFD) for 14 weeks.  All mice were then fasted for 13 hours and received an abdominal injection of a glucose preparation (2 g/kg of body weight).  The mice were then fasted for 10 hours to allow blood glucose levels to return to baseline, after which an insulin preparation (1 U/kg of body weight) was injected in the abdomen.  Blood samples were drawn from the tail veins of all specimens to assess serum glucose levels.  Figure 1 shows the experimental results for WT mice and Alb Tg mice fed a HFD.Figure 1  Effect of glucose and insulin administration on blood glucose of WT and Alb Tg mice fed a HFD.  (Note:  WT and Alb Tg mice fed a HFD had equal weight gain.)Experiment 2Blood samples were taken from fasting human adults, and levels of hepatic miR-26a were measured in comparison to a ubiquitously expressed reference gene, RNU24.  Figure 2 shows the miR-26a levels plotted against each subject's body mass index (BMI, the ratio of body mass to squared body height).Figure 2  Relationship between BMI and hepatic miR-26a expressionAdapted from Fu, X., Dong, B., Tian, Y., Lefebvre, P., Meng, Z., Wang, X., Pattou, F., Han, W., Wang, X., Lou, F., Jove, R., Staels, B., Moore, D.D., & Huang, W. (2015). MicroRNA-26a regulates insulin sensitivity and metabolism of glucose and lipids. The Journal of Clinical Investigation, 125(6), 2497–2509. Question 59One of the human study subjects with a BMI of 56 kg/m2 (Figure 2) is discovered to have a pathology similar to ob/ob mice.  Like ob/ob mice, individuals affected by this pathology exhibit normal weight at birth but become severely obese afterward and have undetectable levels of leptin in the serum.  What is the best explanation for the absence of serum leptin in this subject?A.Leptin cannot bind its receptor in the hypothalamus.B.Leptin cannot bind its receptor in the thyroid gland.C.Leptin cannot be secreted from gastric cells.D.Leptin cannot be secreted from adipocytes.

What is the role of that in RNA biochemistry?

Dear  Din,I recently invited you to review the above referenced manuscript.As you know, timely decisions are of utmost importance to authors. Unfortunately, I must now proceed with evaluating this manuscript without your input.I hope we will have the privilege of using your services in the future.Kind regards,Aamir Ahmad, PhDEditor-in-ChiefNon-coding RNA Research

Dear  Din,I recently invited you to review the above referenced manuscript.As you know, timely decisions are of utmost importance to authors. Unfortunately, I must now proceed with evaluating this manuscript without your input.I hope we will have the privilege of using your services in the future.Kind regards,Aamir Ahmad, PhDEditor-in-ChiefNon-coding RNA Resear