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Background:

MicroRNA-155 (miR-155) is a pro-inflammatory molecule implicated in autoimmune and inflammatory diseases, including inflammatory bowel disease (IBD). This study evaluated circulating miR-155 expression in IBD patients versus healthy controls and its association with clinical markers.

Methods:

Thirty IBD patients (20 ulcerative colitis [UC], 10 Crohn’s disease [CD]) and 20 age- and sex-matched healthy controls were enrolled. Plasma miR-155 levels were measured using qRT-PCR. Clinical data included C-reactive protein (CRP), fecal calprotectin, and Mayo score (for UC). Analyses were conducted using SPSS v26.0.

Results:

miR-155 expression was significantly elevated in IBD patients (median fold change: UC = 24.2, CD = 37.5, controls = 1.00; p < 0.0001). No significant difference was observed between UC and CD groups. miR-155 positively correlated with fecal calprotectin (ρ = 0.475, p = 0.008) and Mayo score in UC patients (ρ = 0.748, p < 0.001).

Conclusion:

Circulating miR-155 is significantly overexpressed in IBD and correlates with intestinal inflammation and disease activity, supporting its utility as a non-invasive biomarker.

Inflammatory bowel disease (IBD) is a persistent inflammatory illness of the gastrointestinal tract (GIT) triggered by an inappropriate immune response to environmental stimuli in genetically predisposed persons. Unfortunately, IBD patients' quality of life is negatively impacted by the symptoms associated with the disease. The exact etiology of IBD pathogenesis is not fully understood, but the emerging research indicated that the microRNA (miRNA) plays an important role. miRNAs have been documented to possess a significant role in regulating pro- and anti-inflammatory pathways, in addition to their roles in several physiological processes, including cell growth, proliferation, and apoptosis. Variations in the miRNA profiles might be a helpful prognostic indicator and a valuable tool in the differential diagnosis of IBD. Most interestingly, these miRNAs have a promising therapeutic target in several pre-clinical animal studies and phase 2 clinical studies to alleviate inflammation and improve patient's quality of life. This comprehensive review discusses the current knowledge about the significant physiological role of different miRNAs in the health of the intestinal immune system and addresses the role of the most relevant differentially expressed miRNAs in IBD, identify their potential targets, and emphasize their diagnostic and therapeutic potential for future research.

Introduction: CD34+CD38-stem cells were identified as the most related markers to acute myeloid leukemia (AML) progression, resistance, and relapse. However, there is still a lack of published data identifying the level of CD34 and CD38 during induction chemotherapy and after complete remission. Objectives: This study aimed to evaluate the levels of CD34+CD38+progenitor cells and CD34+CD38-stem cells in AML patients at diagnosis and after induction chemotherapy. Patients and Methods: This is a prospective cohort study. Both CD34 and CD38 cell markers were identified using f low cytometry in newly diagnosed AML patients and after induction chemotherapy. Results: Forty newly diagnosed AML patients (27 males and 13 females) were followed up after induction chemotherapy. Results revealed a statistically significant decline (P ≤ 0.05) in CD34+CD38-stem cell levels as well as in CD34+CD38+progenitor cell levels in AML patients who achieved complete or incomplete remission compared to newly diagnosed AML patients. Besides, age and CD34+CD38-stem cells exhibited a statistically significant positive correlation at diagnosis. Conclusion: Our study showed CD34+CD38-stem cells are associated with disease progression and poor survival in AML patients. We concluded that, CD34 and CD38 are promising follow-up markers for AML patients on induction chemotherapy. In order to keep AML patients in full remission and increase their chances of survival, medications that target leukemic stem cells (LSCs) should be used in conjunction with the usual chemotherapy that targets blasts.