Asif Ahmed (scientist)

Last updated

Asif Ahmed
Asif Ahmed Academic.jpg
Asif Ahmed at the Aston University in 2016
Nationality British
Alma mater
Scientific career
Fields Preeclampsia
Institutions
Thesis Platelet abnormalities in cardiopulmonary bypass surgery (1989)
Doctoral advisors
  • Paul Salmon
  • Michael Hobsley
Other academic advisors

Asif Ahmed FRSB is a British-Indian vascular scientist, [1] whose research focuses on reducing the risk of mortality and morbidity in pregnancy. [2] He is the founder and former Pro-Vice-Chancellor and Executive Dean of Aston Medical School, Birmingham, [3] and established the Aston Medical Research Institute, a university-wide multidisciplinary translational research entity at Aston University. [4]

Contents

Education and career

Asif Ahmed went to a local comprehensive Aylward School in North London and was subsequently educated at King's College London where he gained his undergraduate degree in pharmacology. He was awarded a Ph.D. for his work on platelet abnormalities in cardiopulmonary bypass surgery from University College London in 1989. [5]

From 1989 to 1993, he was a Postdoctoral Research Fellow at the University of Cambridge and went on to work at The University of Birmingham, being promoted to Professor of Reproductive Physiology in 1998. From 2009 to 2011 he was a Visiting Professor at Stanford University School of Medicine. [6]

He held the Inaugural Gustav Born Chair of Vascular Biology [7] and was appointed as the Assistant Principal for International Postdoctoral Training at the University of Edinburgh in 2010. [8] Ahmed joined Aston University as the first Pro-Vice-Chancellor for Health in October 2012. [9] He was elected as a Fellow of the Royal Society of Biology in 2013.

As of 2021, he is Senior Advisor to the President and Vice-Chancellor at the University of Southampton. [10]

Research

Ahmed's laboratory has studied vascular growth factors in pregnancy and preeclampsia. [11] Research topics include the enzyme placental heme oxygenase (HO), [12] carbon monoxide (CO), [13] [14] and soluble Flt-1. [15] [16]

Related Research Articles

<span class="mw-page-title-main">Pre-eclampsia</span> Hypertension occurring during pregnancy

Pre-eclampsia is a multi-system disorder specific to pregnancy, characterized by the onset of high blood pressure and often a significant amount of protein in the urine. When it arises, the condition begins after 20 weeks of pregnancy. In severe cases of the disease there may be red blood cell breakdown, a low blood platelet count, impaired liver function, kidney dysfunction, swelling, shortness of breath due to fluid in the lungs, or visual disturbances. Pre-eclampsia increases the risk of undesirable as well as lethal outcomes for both the mother and the fetus including preterm labor. If left untreated, it may result in seizures at which point it is known as eclampsia.

<span class="mw-page-title-main">Pulmonary hypertension</span> Increased blood pressure in lung arteries

Pulmonary hypertension is a condition of increased blood pressure in the arteries of the lungs. Symptoms include shortness of breath, fainting, tiredness, chest pain, swelling of the legs, and a fast heartbeat. The condition may make it difficult to exercise. Onset is typically gradual. According to the definition at the 6th World Symposium of Pulmonary Hypertension in 2018, a patient is deemed to have pulmonary hypertension if the pulmonary mean arterial pressure is greater than 20mmHg at rest, revised down from a purely arbitrary 25mmHg, and pulmonary vascular resistance (PVR) greater than 3 Wood units.

<span class="mw-page-title-main">Endothelial dysfunction</span>

In vascular diseases, endothelial dysfunction is a systemic pathological state of the endothelium. Along with acting as a semi-permeable membrane, the endothelium is responsible for maintaining vascular tone and regulating oxidative stress by releasing mediators, such as nitric oxide, prostacyclin and endothelin, and controlling local angiotensin-II activity.

<span class="mw-page-title-main">Nitric oxide synthase</span> Enzyme catalysing the formation of the gasotransmitter NO(nitric oxide)

Nitric oxide synthases (NOSs) are a family of enzymes catalyzing the production of nitric oxide (NO) from L-arginine. NO is an important cellular signaling molecule. It helps modulate vascular tone, insulin secretion, airway tone, and peristalsis, and is involved in angiogenesis and neural development. It may function as a retrograde neurotransmitter. Nitric oxide is mediated in mammals by the calcium-calmodulin controlled isoenzymes eNOS and nNOS. The inducible isoform, iNOS, involved in immune response, binds calmodulin at physiologically relevant concentrations, and produces NO as an immune defense mechanism, as NO is a free radical with an unpaired electron. It is the proximate cause of septic shock and may function in autoimmune disease.

NADPH oxidase is a membrane-bound enzyme complex that faces the extracellular space. It can be found in the plasma membrane as well as in the membranes of phagosomes used by neutrophil white blood cells to engulf microorganisms. Human isoforms of the catalytic component of the complex include NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1, and DUOX2.

Soluble fms-like tyrosine kinase-1 is a tyrosine kinase protein with antiangiogenic properties. A non-membrane associated splice variant of VEGF receptor 1 (Flt-1), sFlt-1 binds the angiogenic factors VEGF and PlGF, reducing blood vessel growth through reduction of free VEGF and PlGF concentrations. In humans, sFlt-1 is important in the regulation of blood vessel formation in diverse tissues, including the kidneys, cornea, and uterus. Abnormally high levels of sFlt-1 have been implicated in the pathogenesis of preeclampsia.

<span class="mw-page-title-main">Heme oxygenase</span> Class of enzymes

Heme oxygenase, or haem oxygenase, is an enzyme that catalyzes the degradation of heme to produce biliverdin, ferrous ion, and carbon monoxide.

<span class="mw-page-title-main">Intrauterine hypoxia</span> Medical condition when the fetus is deprived of sufficient oxygen

Intrauterine hypoxia occurs when the fetus is deprived of an adequate supply of oxygen. It may be due to a variety of reasons such as prolapse or occlusion of the umbilical cord, placental infarction, maternal diabetes and maternal smoking. Intrauterine growth restriction may cause or be the result of hypoxia. Intrauterine hypoxia can cause cellular damage that occurs within the central nervous system. This results in an increased mortality rate, including an increased risk of sudden infant death syndrome (SIDS). Oxygen deprivation in the fetus and neonate have been implicated as either a primary or as a contributing risk factor in numerous neurological and neuropsychiatric disorders such as epilepsy, attention deficit hyperactivity disorder, eating disorders and cerebral palsy.

<span class="mw-page-title-main">Biliverdin reductase</span> Class of enzymes

Biliverdin reductase (BVR) is an enzyme found in all tissues under normal conditions, but especially in reticulo-macrophages of the liver and spleen. BVR facilitates the conversion of biliverdin to bilirubin via the reduction of a double-bond between the second and third pyrrole ring into a single-bond.

<span class="mw-page-title-main">Endothelial NOS</span> Protein and coding gene in humans

Endothelial NOS (eNOS), also known as nitric oxide synthase 3 (NOS3) or constitutive NOS (cNOS), is an enzyme that in humans is encoded by the NOS3 gene located in the 7q35-7q36 region of chromosome 7. This enzyme is one of three isoforms that synthesize nitric oxide (NO), a small gaseous and lipophilic molecule that participates in several biological processes. The other isoforms include neuronal nitric oxide synthase (nNOS), which is constitutively expressed in specific neurons of the brain and inducible nitric oxide synthase (iNOS), whose expression is typically induced in inflammatory diseases. eNOS is primarily responsible for the generation of NO in the vascular endothelium, a monolayer of flat cells lining the interior surface of blood vessels, at the interface between circulating blood in the lumen and the remainder of the vessel wall. NO produced by eNOS in the vascular endothelium plays crucial roles in regulating vascular tone, cellular proliferation, leukocyte adhesion, and platelet aggregation. Therefore, a functional eNOS is essential for a healthy cardiovascular system.

<span class="mw-page-title-main">VEGFR1</span> Protein-coding gene in the species Homo sapiens

Vascular endothelial growth factor receptor 1 is a protein that in humans is encoded by the FLT1 gene.

<span class="mw-page-title-main">Placental growth factor</span> Protein-coding gene in the species Homo sapiens

Placental growth factor(PlGF) is a protein that in humans is encoded by the PGF gene.

<span class="mw-page-title-main">PIGF</span> Protein-coding gene in the species Homo sapiens

Phosphatidylinositol-glycan biosynthesis class F protein is a protein that in humans is encoded by the PIGF gene.

<span class="mw-page-title-main">Zinc protoporphyrin</span> Chemical compound

Zinc protoporphyrin (ZPP) refers to coordination complexes of zinc and protoporphyrin IX. It is a red-purple solid that is soluble in water. The complex and related species are found in red blood cells when heme production is inhibited by lead and/or by lack of iron.

Central aortic blood pressure is the blood pressure at the root of aorta. Studies have shown the importance of central aortic pressure and its implications in assessing the efficacy of antihypertensive treatment with respect to cardiovascular risk factors. The traditional method of measuring blood pressure in the arms has been shown to underestimate the efficacy of medications such as amlodipine and overestimate the efficacy of those like atenolol. A clinical trial demonstrated that different medications for lowering blood pressure have different effects on the central aortic pressure and blood flow characteristics, despite producing similar branchial blood pressure readings. The study also indicated that the CAP is a better independent predictor of cardiovascular and kidney outcomes.

<span class="mw-page-title-main">Placental disease</span> Medical condition

A placental disease is any disease, disorder, or pathology of the placenta.

Roland Stocker is a Swiss Australian biochemist who discovered the antioxidant activity of bilirubin. He is a former Olympic rower and has represented Switzerland at the 1980 Summer Olympics.

<span class="mw-page-title-main">Carbon monoxide-releasing molecules</span> Substances delivering CO within the body

Carbon monoxide-releasing molecules (CORMs) are chemical compounds designed to release controlled amounts of carbon monoxide (CO). CORMs are being developed as potential therapeutic agents to locally deliver CO to cells and tissues, thus overcoming limitations of CO gas inhalation protocols.

<span class="mw-page-title-main">Axel Haverich</span> German cardiac surgeon

Axel Haverich is a German cardiac surgeon.

<span class="mw-page-title-main">Pregnancy Outcome Prediction study</span>

The Pregnancy Outcome Prediction (POP) Study is a prospective cohort study of 4,512 women who have never given birth, recruited at the Rosie Hospital between January 2008 and July 2012.

References

  1. "Asif Ahmed". scholar.google.com. Retrieved 23 March 2023.
  2. "Cure for pre-eclampsia? Birmingham scientist offers hope for millions of women". 28 October 2020.
  3. Aston Medical School
  4. "Aston Medical Research Institute" . Retrieved 23 March 2023.
  5. "ORCID". orcid.org. Retrieved 23 March 2023.
  6. "Times Higher Education". 10 January 2013.
  7. "Gustav's Edinburgh Memories". The University of Edinburgh. Retrieved 23 March 2023.
  8. "University of Edinburgh" (PDF). Retrieved 23 March 2023.
  9. "Appointments". 10 January 2013.
  10. "Professor Asif Ahmed PhD". University of Southampton . Retrieved 11 December 2021.
  11. Ahmed, A; Dunk, C; Kniss, D; Wilkes, M (1997). "Role of VEGF receptor-1 (Flt-1) in mediating calcium-dependent nitric oxide release and limiting DNA synthesis in human trophoblast cells". Laboratory Investigation; A Journal of Technical Methods and Pathology. 76 (6): 779–91. PMID   9194854.
  12. Ahmed, A; Rahman, M; Zhang, X; Acevedo, C. H; Nijjar, S; Rushton, I; Bussolati, B; St John, J (2000). "Induction of placental heme oxygenase-1 is protective against TNFalpha-induced cytotoxicity and promotes vessel relaxation". Molecular Medicine. 6 (5): 391–409. doi:10.1007/bf03401783. PMC   1949957 . PMID   10952020.
  13. Cudmore, M; Ahmad, S; Al-Ani, B; Fujisawa, T; Coxall, H; Chudasama, K; Devey, L. R; Wigmore, S. J; Abbas, A; Hewett, P. W; Ahmed, A (2007). "Negative Regulation of Soluble Flt-1 and Soluble Endoglin Release by Heme Oxygenase-1". Circulation. 115 (13): 1789–97. doi: 10.1161/CIRCULATIONAHA.106.660134 . PMID   17389265.
  14. Wang, K; Ahmad, S; Cai, M; Rennie, J; Fujisawa, T; Crispi, F; Baily, J; Miller, M. R; Cudmore, M; Hadoke, P. W. F; Wang, R; Gratacos, E; Buhimschi, I. A; Buhimschi, C. S; Ahmed, A (2013). "Dysregulation of Hydrogen Sulfide Producing Enzyme Cystathionine -lyase Contributes to Maternal Hypertension and Placental Abnormalities in Preeclampsia". Circulation. 127 (25): 2514–22. doi: 10.1161/CIRCULATIONAHA.113.001631 . PMID   23704251.
  15. Ahmad, S; Ahmed, A (2004). "Elevated Placental Soluble Vascular Endothelial Growth Factor Receptor-1 Inhibits Angiogenesis in Preeclampsia". Circulation Research. 95 (9): 884–91. doi: 10.1161/01.RES.0000147365.86159.f5 . PMID   15472115.
  16. Thadhani, R; Kisner, T; Hangman, H; Bossung, V; Noack, S; Schaarschmidt, W; Jank, A; Kribs, A; Cornely, OA; Kreyssig, C; Hemphill, L; Rigby, AC; Khedkar, S; Lindner, TH; Mallmann, P; Stepan, H; Karumanchi, SA; Benzing, T (2011). "Pilot study of extracorporeal removal of soluble fms-like tyrosine kinase 1 in preeclampsia". Circulation. 124 (4): 940–50. doi: 10.1161/CIRCULATIONAHA.111.034793 . PMID   21810665.