A5030835498- Hemoglobinopathies and Related Disorders
- Erythrocyte Function and Pathophysiology
- Epigenetics and DNA Methylation
- Ethics and Legal Issues in Pediatric Healthcare
- IL-33, ST2, and ILC Pathways
- Vitamin K Research Studies
- Hemoglobin structure and function
- Immune Cell Function and Interaction
- Folate and B Vitamins Research
- Hematopoietic Stem Cell Transplantation
- Immune cells in cancer
- RNA Interference and Gene Delivery
- Inflammatory mediators and NSAID effects
- Inflammasome and immune disorders
- Natural Compounds in Disease Treatment
- Neurological Disorders and Treatments
- Plant biochemistry and biosynthesis
- DNA and Nucleic Acid Chemistry
- Heme Oxygenase-1 and Carbon Monoxide
- Acute Lymphoblastic Leukemia research
- Reproductive Biology and Fertility
- DNA Repair Mechanisms
- Porphyrin Metabolism and Disorders
- Genetics and Neurodevelopmental Disorders
- Peroxisome Proliferator-Activated Receptors
University of Pittsburgh
2021-2025
West Virginia University
2019-2021
University of Dhaka
2018-2019
BRAC University
2019
Abstract The transcriptional repressor Hairy Enhancer of Split 1 (HES1) plays an essential role in the development many organs by promoting maintenance stem/progenitor cells, controlling reversibility cellular quiescence, and regulating both cell fate decisions. Deletion Hes1 mice results severe defects multiple is lethal late embryogenesis. Here we have investigated HES1 hematopoiesis using a hematopoietic lineage-specific knockout mouse model. We found that while dispensable for...
Background: Americans of African ancestry (AA) show disparities in ischemic stroke when compared to Euro-Americans: two-fold more prevalence and mortality, greater disability post-stroke complications, slower recovery. Thromboembolic involves platelet hyperactivity, which stroke-related oxidative stress promotes. The nitric oxide (NO)-soluble guanylate cyclase (sGC)-guanosine 3',5'-cyclic monophosphate (cGMP) pathway regulates vascular homeostasis. Oxidized (Fe 3+ ) sGC heme is...
Objectives: Inflammation is our body’s normal defense mechanism, but in some cases, it may be responsible for causing different kinds of disorders. Several antiinflammatory drugs are present the treatment these disorders; however, conventional anti-inflammatory cause side effects when used long term and therefore, better to use them a low dose shorter duration time. This study was designed find out whether there an augmentation therapeutic effectiveness like diclofenac sodium (NSAID),...
Abstract Chemoresistance posts a major hurdle for treatment of acute leukemia. There is increasing evidence that prolonged and intensive chemotherapy often fails to eradicate leukemic stem cells, which are protected by the bone marrow niche can induce relapse. Thus, new therapeutic approaches overcome chemoresistance urgently needed. By conducting an ex vivo small molecule screen, here we have identified Quinacrine (QC) as sensitizer Cytarabine (AraC) in treating lymphoblastic leukemia...
The crosstalk between the BM microenvironment (niche) and hematopoietic stem cells (HSCs) is critical for HSC regeneration. Here, we show that in mice, deletion of Fanconi anemia (FA) genes Fanca Fancc dampened regeneration through direct effects on HSCs indirect niche cells. FA showed persistent upregulation Wnt target Prox1 response to total body irradiation (TBI). Accordingly, lineage-specific improved long-term repopulation irradiated HSCs. Forced expression WT mimicked defective...
NOD-like receptor 12 (NLRP12) is a member of the nucleotide-binding domain and leucine-rich repeat containing inflammasome family that plays central role in innate immunity. We previously showed DNA damage upregulated NLRP12 hematopoietic stem cells (HSCs) mice deficient repair gene Fanca. However, HSC maintenance not known. Here, we show persistent damage-induced improves function both mouse human models deficiency aging. Specifically, treatment Fanca-/- with cross-linker mitomycin C or...
Summary The Fanconi anaemia protein FANCD2 suppresses PPAR Ɣ to maintain haematopoietic stem cell’s (HSC) function; however, the underlying mechanism is not known. Here we show that acts in concert with Notch target HES1 suppress inflammation‐induced HSC maintenance. Loss of exacerbates ‐KO defects. However, deletion does cause more severe inflammation‐mediated defects mice, indicating both and are required for limiting detrimental effects inflammation on HSCs. Further analysis shows...