Microbiome modulation in inflammatory diseases: Progress to microbiome genetic engineering.

Recent developments in sequencing technology and analytical approaches have allowed researchers to show that the healthy gut microbiome is very varied and capable of performing a wide range of tasks. The importance of gut microbiota in controlling immunological, neurological, and endocrine function is becoming well-recognized. Thereby, numerous inflammatory diseases, including those that impact the gastrointestinal system, as well as less obvious ones, including Rheumatoid arthritis (RA), cancer, gestational diabetes (GD), type 1 diabetes (T1D), and type 2 diabetes (T2D), have been linked to dysbiotic gut microbiota. Microbiome engineering is a rapidly evolving frontier for solutions to improve human health. Microbiome engineering seeks to improve the function of an ecosystem by manipulating the composition of microbes. Thereby, generating potential therapies against metabolic, inflammatory, and immunological diseases will be possible through microbiome engineering. This essay first provides an overview of the traditional technological instruments that might be used for microbiome engineering, such as Fecal Microbiota Transplantation (FMT), prebiotics, and probiotics. Moreover, we will also discuss experimental genetic methods such as Metagenomic Alteration of Gut microbiome by In situ Conjugation (MAGIC), Bacteriophage, and Conjugative plasmids in manipulating intestinal microbiota.

An interplay between non-coding RNAs and gut microbiota in human health.

Humans have a complicated symbiotic relationship with their gut microbiome, which is postulated to impact host health and disease broadly. Epigenetic alterations allow host cells to regulate gene expression without altering the DNA sequence. The gut microbiome, offering environmental hints, can influence responses to stimuli by host cells with modifications on their epigenome and gene expression. Recent increasing data suggest that regulatory non-coding RNAs (miRNAs, circular RNAs, and long lncRNA) may affect host-microbe interactions. These RNAs have been suggested as potential host response biomarkers in microbiome-associated disorders, including diabetes and cancer. This article reviews the current understanding of the interplay between gut microbiota and non-coding RNA, including lncRNA, miRNA, and circular RNA. This can lead to a profound understanding of human disease and influence therapy. Furthermore, microbiome engineering as a mainstream strategy for improving human health has been discussed and confirms the hypothesis about a direct cross-talk between microbiome composition and non-coding RNA.

MicroRNA-206 in human cancer: Mechanistic and clinical perspectives.

MicroRNAs (miRNAs), small non-coding RNAs approximately 20-25 nt in length, play important roles via directly binding to the corresponding 3' UTR of target mRNAs. Recent research has shown that miRNAs cover a wide range of diseases, including several types of cancer. It is interesting to note that miR-206 operates as a tumor suppressor and is downregulated in abundant cancer types, such as breast cancer, lung cancer, colorectal cancer, and so forth. Interestingly, a growing number of studies have also reported that miR-206 could function as an oncogene and promote tumor cell proliferation. Thereby, miR-206 may act as either oncogenes or tumor suppressors under certain conditions. In addition, it was widely acknowledged that restoring tumor-suppressor miR-206 has emerged as an unconventional cancer therapy strategy. Therefore, miR-206 might be a newfangled procedure for achieving a more significant treatment outcome for cancer patients. This review summarizes the role of miR-206 in several cancer types and the contributions made between miR-206 and the diagnosis, treatment, and drug resistance of solid tumors.

Progress toward molecular therapy for diabetes mellitus: A focus on targeting inflammatory factors.

Diabetes mellitus (DM) has been the most prevalent global metabolic disease, turning into a serious risk for human health. Several researches have recorded a role for inflammation and immunity in the pathogenesis of both in T1DM and in T2DM. Lots of chemical agents are available to control and to cure diabetic patients, which are not always sufficient for euglycemia maintenance and late stage diabetic complications avoidance. Therefore, newborn therapeutic methods to refine clinical outcomes in DM are required. Nucleic-acid-based therapy also known as gene expression level regulator within the target cells has been calculated to be promising in various diseases. Thus, pronounced attempts have been dedicated to develop new targeted molecular therapy aimed at improving insulin resistance in DM. This review mainly focuses on recent progress in DM molecular therapy and whether, has potential efficacy against inflammatory mediators involved in DM.

Is there any relationship between mutation in CPS1 Gene and pregnancy loss?

BACKGROUND: Carbamoyl phosphate synthetase 1 (CPS1) is a liver-specific enzyme with the lowest enzymatic rate, which determines the overall rate of the other reactions in the pathway that converts ammonia to carbamoyl phosphate in the first step of the urea cycle. Carbamoyl phosphate synthetase 1 deficiency (CPS1D), which usually presents as lethal hyperammonemia, is a rare autosomal recessive hereditary disease. CASE: We report a case of a two-day-old female neonate with lethal hyperammonemia. The newborn infant was presented with hyperammonemia (34.7 µ g/ml; reference range 1.1-1.9). In Plasma amino acid analysis, there was a significant elevated levels of alanine (3,004 µ mol/L; reference range, 236-410 µ mol/L), glutamine (2,256 µ mol/L; reference range, 20-107 µ mol/L), asparagine (126 µ mol/L; reference range, 30-69 µ mol/L), glutamic acid (356 µ mol/L; reference range, 14-192 µ mol/L), aspartic acid (123 µ mol/L; reference range, 0-24 µ mol/L), and lysine (342 µ mol/L; reference range, 114-269 µ mol/L). We cannot diagnose the urea cycle disorder (UCD) CPS1D properly only based on the quantity of biochemical intermediary metabolites to exclude other UCDs with similar symptoms. Following next generation sequencing determined one homozygous mutation in CPS1 gene and also this mutation was determined in her parents. The identified mutation was c.2758G > C; p.Asp920His, in the 23 exon of CPS1. This novel homozygous mutation had not been reported previously. CONCLUSION: We applied whole exome sequencing successfully to diagnose the patient with CPS1D in a clinical setting. This result supports the clinical applicability of whole exome sequencing for cost-effective molecular diagnosis of UCDs.