The Indian peafowl (Pavo cristanus) is native to South Asia and is the national bird of India. Here we present a draft genome sequence of the male blue peacock using Illumina and Oxford Nanopore technology (ONT). ONT sequencing gave ∼2.3-fold sequencing coverage, whereas Illumina generated 150–base pair paired-end sequence data at 284.6-fold coverage from 5 libraries. Subsequently, we generated a 0.915-gigabase pair de novo assembly of the peacock genome with a scaffold N50 of 0.23 megabase pairs (Mb). We predict that the peacock genome contains 23,153 protein-coding genes and 75.3 Mb (7.33%) of repetitive sequences. We report a high-quality assembly of the peacock genome using a hybrid approach of sequences generated by both Illumina and ONT. The long-read chemistry generated by ONT was useful for addressing challenges related to de novo assembly, particularly at regions containing repetitive sequences spanning longer than the read length, and which could not be resolved with only short-read–based assembly. Contig assembly of Illumina short reads gave an N50 of 1,639 bases, whereas with ONT, the N50 increased by >9-fold to 14,749 bases. The initial contig assembly based on Illumina sequencing reads alone gave 685,241 contigs. Further scaffolding on assembled contigs using both Illumina and ONT sequencing reads resulted in a final assembly of 15,025 super-scaffolds, with an N50 of ∼0.23 Mb. Ninety-five percent of proteins predicted by homology matched with those in a public repository, verifying the completeness of our assembly. Like other phylogenetic studies of avian conserved genes, we found P. cristatus to be most closely related to Gallus gallus, followed by Meleagris gallopavo and Anas platyrhynchos. Compared with the recently published peacock genome assembly, the current, superior, hybrid assembly has greater sequencing depth, fewer non-ATGC sequences, and fewer scaffolds.

SKP2 (S-phase kinase-associated protein 2) is a member of the F-box family of substrate-recognition subunits in the SCF ubiquitin-protein ligase complexes. It is associated with ubiquitin-mediated degradation in the mammalian cell cycle components and other target proteins involved in cell cycle progression, signal transduction, and transcription. Being an oncogene in solid tumors and hematological malignancies, it is frequently associated with drug resistance and poor disease outcomes. In the current review, we discussed the novel role of SKP2 in different hematological malignancies. Further, we performed a limited in-silico analysis to establish the involvement of SKP2 in a few publicly available cancer datasets. Interestingly, our study identified Skp2 expression to be altered in a cancer-specific manner. While it was found to be overexpressed in several cancer types, few cancer showed a down-regulation in SKP2. Our review provides evidence for developing novel SKP2 inhibitors in hematological malignancies. We also investigated the effect of SKP2 status on survival and disease progression. In addition, the role of miRNA and its associated families in regulating Skp2 expression was explored. Subsequently, we predicted common miRNAs against Skp2 genes by using miRNA-predication tools. Finally, we discussed current approaches and future prospective approaches to target the Skp2 gene by using different drugs and miRNA-based therapeutics applications in translational research.

Objective: Pabda (Ompok bimaculatus) is a freshwater catfish, largely available in Asian countries, especially in Bangladesh, India, Pakistan and Nepal. This fish is highly valued for its fabulous taste and high nutritional value and is very popular as a rich source of proteins, omega-3 and omega-6 fatty acids, vitamins and mineral for growing children, pregnant females and elders. We performed de-novo sequencing of Ompok bimaculatus using a hybrid approach and present here a draft assembly for this species for the first time. Data Description: The genome of Ompok bimaculatus (Fig. 1: Table 1, Data file 3) from Ganges river, has been sequenced by hybrid approach using Illumina short reads and PacBio long reads followed by structural annotations. The draft genome assembly was found to be 718 Mb with N50 size of 81 kb. MAKER gene annotation tool predicted 21,371 genes.

Objective Hemoglobin A1c (HbA1c) level remains the gold standard test for the assessment of glycemic control, and it reflects the mean glucose values in the previous 3-month period. HbA1c is expressed as a percentage, whereas the monitoring and treatment of diabetes are based on blood glucose levels expressed as mg/dL. It is appropriate to make it easy for the patient to understand both random blood sugar (RBS) and estimated average glucose (eAG) expressed with the same units. This will enhance the usefulness of eAG. This article determines the statistical correlation between eAG derived from HBA1C with RBS values both in diabetic and prediabetic subjects. Methods The RBS and HbA1c levels of 178 males and 283 females (12–90 years) were obtained and the eAG levels were calculated using Nathan's regression equation. The samples were divided into four groups based on HbA1c levels—group 1: HbA1c greater than 9%, group 2: HbA1c 6.5 to 9%, group 3: HbA1c 5.7 to 6.4%; and group 4: HbA1c less than 5.7%. Results There was a statistically significant positive correlation between RBS and eAG values for the study group 1 and 2. Also, the median values of RBS and eAG showed a significant difference (p < 0.001). Conclusion As the association between the RBS and eAG levels is strong in a fairly and poorly controlled diabetic population, reporting the eAG level together with the HbA1c level at no additional cost may assist in effective blood glucose control in clinical care. However, eAG and RBS values cannot be used interchangeably.

While considerable information exists on the ten-eleven translocation 2 (TET2) mutational landscape in AML, the information on TET2 expression is limiting. So, we aimed to study the TET2 expression at mRNA and protein levels in AML patients compared to healthy controls. To achieve this, we recruited 70 non-M3, de novo AML patients and 20 healthy controls. The expression of TET2 was checked at mRNA and protein levels by qPCR and ELISA respectively and the TET activity was checked by the 5-hmC assay. TET2 mRNA expression was correlated with clinicopathological parameters and overall survival. We found a significant downregulation of TET2 mRNA and protein and significantly lower DNA 5-hmC levels in AML patients compared to controls. TET2 downregulation was more in patients with high blast counts and patients of the adverse-risk ELN category. We also found a significant upregulation of DNMT1 and DNMT3a suggesting a hypermethylation phenotype in de novo AML.

A healthy host-microbiome relationship, crucial for intestinal homeostasis, is established early in postnatal life. Imbalance in the neonatal microbiome may lead to the development of chronic pathological conditions later in life. Dysbiosis of the gut microbiota is increasingly being linked to the etiology of both intestinal and systemic illnesses such as irritable bowel disease (IBD), cardiovascular diseases and diabetes, as well as kidney and neurological disorders. Gut dysbiosis also leads to the development of colorectal cancer (CRC). Despite substantial research, little is known about the interactions between microorganisms, their hosts, and their environments, or whether dysbiosis is a cause or consequence of disease. According to a recent hypothesis, bacterial species living in the mucus layer of the colon may determine whether cellular homeostasis is retained or inflammatory processes are elicited, either through direct interaction with intestinal epithelium or indirectly via bacterial metabolites. Recently, high throughput deep-sequencing technology has enabled the characterization of the microbiota in patients suffering from intestinal or extra-intestinal disorders, and a strong association between dysbiosis and disease development was found. However, specific disease drivers still need to be identified in most cases. Small compounds and metabolites produced by gut bacterial flora act as signaling molecules, such as neurotransmitters and neuropeptides that can profoundly influence host physiology. These metabolites play a crucial role in modulating gut-brain crosstalk. There is growing evidence that neurological disorders such as Alzheimer's disease, Parkinson’s and others, may originate or be exaggerated in response to microbial dysbiosis either directly or indirectly interfering with the drugs through metabolites. The present evidence on the role of the gut microbiota in disease development and drug metabolism is summarized in this review. Based on available studies, we can explore the potential of gut flora to alleviate disease progression.