Mohamed N Ahmed
- Associate Professor, Pediatrics
- Chief, Division of Neonatology
- Member of the Graduate Faculty
Contact
- (520) 626-6627
- Arizona Health Sciences Center, Rm. 4341A
- Tucson, AZ 85724
- mahmed1@arizona.edu
Degrees
- Ph.D.
- Suez Canal University, Ismailia, Egypt
- M.D.
- Suez Canal University, Ismailia, Egypt
Licensure & Certification
- AZ Medical License (2022)
Interests
No activities entered.
Courses
2023-24 Courses
-
Advanced Neonatology
PED 840B (Spring 2024) -
Advanced Neonatology
PED 840B (Fall 2023)
2022-23 Courses
-
Advanced Neonatology
PED 840B (Fall 2022)
2021-22 Courses
-
Dissertation
CTS 920 (Spring 2022)
2020-21 Courses
-
Advanced Neonatology
PED 840B (Spring 2021)
Scholarly Contributions
Journals/Publications
- Kylat, R. I., & Ahmed, M. N. (2022). Neonatal testicular torsion. African journal of paediatric surgery : AJPS, 19(1), 1-4.More infoRotation of the testis around the axis of the spermatic cord results in tissue ischaemia and testicular torsion (TT). TT in the newborn infant in the 1st month of life is referred to as neonatal TT (NTT) or perinatal TT and occurs in 6.1/100, 000 live births. The true incidence could be higher as some of these occur prenatally and can be asymptomatic. TT can be extravaginal, intravaginal and mesorchial and NTT is usually extravaginal. Physical examination can be adequate for the diagnosis, and utility of ultrasound (US) is mainly to exclude other conditions. If the timing of the torsion is prenatal, the testicle may not be salvageable. But, in certain situations, these could be asymptomatic bilateral TT. When the timing of torsion is not simultaneous (asynchronous torsion) early contralateral orchiopexy done at the time of exploration would prevent the occurence of asynchronous torsion. Non.operative maneuvres to detorse in NTT are not successful and not recommended. This review focuses on the diagnostic approach and management.
- Ahmed, M., Zaghloul, N., Zimmerman, P., Casanova, N. G., Sun, X., Song, J. H., Hernon, V. R., Sammani, S., Rischard, F., Rafikova, O., Rafikov, R., Makino, A., Kempf, C. L., Camp, S. M., Wang, J., Desai, A. A., Lussier, Y., Yuan, J. X., & Garcia, J. G. (2021). Endothelial eNAMPT drives EndMT and preclinical PH: rescue by an eNAMPT-neutralizing mAb. Pulmonary circulation, 11(4), 20458940211059712.More infoPharmacologic interventions to halt/reverse the vascular remodeling and right ventricular dysfunction in pulmonary arterial hypertension (PAH) remains an unmet need. We previously demonstrated extracellular nicotinamide phosphoribosyltransferase (eNAMPT) as a DAMP (damage-associated molecular pattern protein) contributing to PAH pathobiology via TLR4 ligation. We examined the role of endothelial cell (EC)-specific eNAMPT in experimental PH and an eNAMPT-neutralizing mAb as a therapeutic strategy to reverse established PH. Hemodynamic/echocardiographic measurements and tissue analyses were performed in Sprague Dawley rats exposed to 10% hypoxia/Sugen (three weeks) followed by return to normoxia and weekly intraperitoneal delivery of the eNAMPT mAb (1 mg/kg). WT C57BL/6J mice and conditional EC-cNAMPT mice were exposed to 10% hypoxia (three weeks). Biochemical and RNA sequencing studies were performed on rat PH lung tissues and human PAH PBMCs. Hypoxia/Sugen-exposed rats exhibited multiple indices of severe PH (right ventricular systolic pressure, Fulton index), including severe vascular remodeling, compared to control rats. PH severity indices and plasma levels of eNAMPT, IL-6, and TNF- were all significantly attenuated by eNAMPT mAb neutralization. Compared to hypoxia-exposed WT mice, cNAMPT KO mice exhibited significantly reduced PH severity and evidence of EC to mesenchymal transition (EndMT). Finally, biochemical and RNAseq analyses revealed eNAMPT mAb-mediated rectification of dysregulated inflammatory signaling pathways (TLR/NF-κB, MAP kinase, Akt/mTOR) and EndMT in rat PH lung tissues and human PAH PBMCs. These studies underscore EC-derived eNAMPT as a key contributor to PAH pathobiology and support the eNAMPT/TLR4 inflammatory pathway as a highly druggable therapeutic target to reduce PH severity and reverse PAH.
- Bader, M. Y., Zaghloul, N., Repholz, A., Nagy, N., Ahmed, M. N., Thompson, L., & Kylat, R. I. (2021). A Retrospective Review Following the Addition of Clonidine to a Neonatal Abstinence Syndrome Treatment Algorithm. Frontiers in pediatrics, 9, 632836.More infoTo investigate the outcomes associated with the implementation of a neonatal abstinence syndrome (NAS) treatment algorithm utilizing dual therapy with morphine sulfate and clonidine in a level four neonatal intensive care unit (NICU). A cohort of neonates (≥35 weeks gestation) born at an academic tertiary medical center between January 1, 2015 and December 31, 2018 who were diagnosed with NAS were retrospectively evaluated following the implementation of a new NAS treatment algorithm. Neonates were categorized in two groups based on if they were treated pre- or post-implementation of the protocol. The primary efficacy outcome was length of hospital stay. Secondary outcomes included the incidence of adverse drug reactions, length of treatment for NAS, and maximum as well as total cumulative dose of each medication used to treat NAS. The implementation of this NAS treatment algorithm significantly reduced the length of hospital stay (30 days vs. 20 days, = 0.001). In addition, there was a significant decrease in duration of morphine sulfate exposure as well as cumulative dose of morphine required to successfully treat a neonate with NAS in the post-implementation group (26 days vs. 15 days, = 0.002 and 6.9 mg/kg vs. 3.4 mg/kg, = 0.031). Addition of clonidine to morphine sulfate as initial therapy for NAS significantly reduced the cumulative exposure as well as duration of exposure to morphine sulfate compared to morphine monotherapy and decrease length of hospital stay.
- Chester, A. H., McCormack, A., Miller, E. J., Ahmed, M. N., & Yacoub, M. H. (2021). Coronary vasodilation mediated by T cells expressing choline acetyltransferase. American journal of physiology. Heart and circulatory physiology, 321(5), H933-H939.More infoCD4 T cells expressing choline acetyltransferase (ChAT) have recently been shown to cause a drop in systemic blood pressure when infused into mice. The aim of this study was to determine if ChAT-expressing T cells could regulate coronary vascular reactivity. Preconstricted segments of epicardial and intramyocardial porcine coronary arteries relaxed in response to Jurkat T cells (JT) that overexpressed ChAT (JT cells). The efficacy of the JT cells was similar in epicardial and intramyocardial vessels with a maximum dilator response to 3 × 10 cells/mL of 38.0 ± 6.7% and 38.7 ± 7.25%, respectively. In contrast, nontransfected JT cells elicited a weak dilator response, followed by a weak contraction. The response of JT cells was dependent on the presence of the endothelial cells. In addition, the response could be significantly reduced by -nitro-l-arginine methyl ester (l-NAME) and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) in the presence of indomethacin. JT cells, but not JT cells, increased the expression of phosphorylated endothelial nitric oxide synthase (eNOS). JT cells contained significantly greater levels of acetylcholine compared with JT cells; however, the nonselective muscarinic antagonist atropine and the M receptor antagonist pirenzepine both failed to block the dilator effect of JT cells. Exogenously added acetylcholine induced only a weak relaxation (∼10%) at low concentrations, which became a contractile response at higher concentrations. These data illustrate the capacity for cells that express ChAT to regulate coronary vascular reactivity, via mechanisms that are dependent on interaction with the endothelium and in part mediated by the release of nitric oxide. This study shows ChAT-expressing T cells can induce vasodilation of the blood vessel in the coronary circulation and that this effect relies on a direct interaction between T cells and the coronary vascular endothelium. The study establishes a potential immunomodulatory role for T cells in the coronary circulation. The present findings offer an additional possibility that a deficiency of ChAT-expressing T cells could contribute to reduced coronary blood flow and ischemic events in the myocardium.
- Rajgarhia, A., Ayasolla, K. R., Zaghloul, N., Lopez Da Re, J. M., Miller, E. J., & Ahmed, M. (2021). Extracellular Superoxide Dismutase (EC-SOD) Regulates Gene Methylation and Cardiac Fibrosis During Chronic Hypoxic Stress. Frontiers in cardiovascular medicine, 8, 669975.More infoChronic hypoxic stress induces epigenetic modifications mainly DNA methylation in cardiac fibroblasts, inactivating tumor suppressor genes (RASSF1A) and activating kinases (ERK1/2) leading to fibroblast proliferation and cardiac fibrosis. The Ras/ERK signaling pathway is an intracellular signal transduction critically involved in fibroblast proliferation. RASSF1A functions through its effect on downstream ERK1/2. The antioxidant enzyme, extracellular superoxide dismutase (EC-SOD), decreases oxidative stress from chronic hypoxia, but its effects on these epigenetic changes have not been fully explored. To test our hypothesis, we used an model: wild-type C57B6 male mice (WT) and transgenic males with an extra copy of human hEC-SOD (TG). The studied animals were housed in hypoxia (10% O) for 21 days. The right ventricular tissue was studied for cardiac fibrosis markers using RT-PCR and Western blot analyses. Primary C57BL6 mouse cardiac fibroblast tissue culture was used to study the model, the downstream effects of RASSF-1 expression and methylation, and its relation to ERK1/2. Our findings showed a significant increase in cardiac fibrosis markers: Collagen 1, alpha smooth muscle actin (ASMA), and SNAIL, in the WT hypoxic animals as compared to the TG hypoxic group ( < 0.05). The expression of DNA methylation enzymes (DNMT 1&3b) was significantly increased in the WT hypoxic mice as compared to the hypoxic TG mice ( < 0.001). RASSF1A expression was significantly lower and ERK1/2 was significantly higher in hypoxia WT compared to the hypoxic TG group ( < 0.05). Use of SiRNA to block RASSF1A gene expression in murine cardiac fibroblast tissue culture led to increased fibroblast proliferation ( < 0.05). Methylation of the RASSF1A promoter region was significantly reduced in the TG hypoxic group compared to the WT hypoxic group (0.59 vs. 0.75, respectively). Based on our findings, we can speculate that EC-SOD significantly attenuates RASSF1A gene methylation and can alleviate cardiac fibrosis induced by hypoxia.
- Sheen, W., Ahmed, M., Patel, H., Codipilly, C. N., & Schanler, R. J. (2021). Is the Antioxidant Capacity of Stored Human Milk Preserved?. Breastfeeding medicine : the official journal of the Academy of Breastfeeding Medicine, 16(7), 564-567.More infoIn the neonatal intensive care unit (NICU) expressed mothers' milk usually is stored frozen until used. We found that when human milk was stored at -20°C for up to 9 months there were reduced bacterial counts and pH, increased free fatty acids, but unchanged immune proteins. Antioxidant protection is an important benefit of human milk. Few studies have evaluated long-term effects of cold storage on the antioxidant capacity of human milk. We hypothesized that the antioxidant capacity of human milk is affected adversely by long-term storage at -20°C. To study the impact of long-term cold storage on the oxidative capacity of human milk and the biological impact of these changes on macromolecular constituents of human milk. Freshly expressed milk was obtained from mothers in the NICU, stored at -20°C for 6 months, and compared with the baseline. Paired samples were analyzed for glutathione, hydrogen peroxide (HO), 8-isoprostane, catalase, and superoxide dismutase. There was no change in HO concentration between baseline and 6 months. Significant reductions from baseline in both catalase and superoxide dismutase concentrations and activities, total glutathione, oxidized glutathione, reduced glutathione, and the ratio of reduced to oxidized glutathione were observed (