Research Terms
Industries
Issued Patents
¨ US Patent 7,357,950 B2 . Issued April 15, 2008 Topical treatment for dyshidrosis (pompholyx) and dry skin disorders
¨ US Patent 7,666,451 B2 Issued February 23, 2010: Method for Treatment of Pompholyx and Related Dry Skin Disorders.
Recent Publications
1. Mazzio, E, A. Becker and KFA Soliman. Inflammation and inducible nitric oxide synthase have no effect on monoamine oxidase activity in glioma cells. Biochem Pharmacol. 15:65:1719-1927 (2003).
2. Mazzio EA and KFA Soliman. Cytoprotection of pyruvic acid and reduced beta-nicotinamide adenine dinucleotide against hydrogen peroxide toxicity in neuroblastoma cells. Neurochem Res. 28(5):733-741 (2003).
3. Sircar R and KFA Soliman. Effects of postnatal PCP treatment on locomotor behavior and striatal D (2) receptor. Pharmacol Biochem Behav. 74(4):943-452(2003).
4. Mazzio and KFA Soliman. The role of glycolysis and gluconeogenesis in the cytoprotection of neuroblastoma cells against 1-methyl 4-phenylpyridinium ion toxicity. Neurotoxicology. 24:137-147 (2003).
5. Mazzio E and KFA Soliman Pyruvic acid cytoprotection against 1-methyl-4-phenylpyridinium, 6-hydroxydopamine and hydrogen peroxide toxicities in vitro. Neurosci Lett. 6; 337:77-80.
6. Mazzio, E; K J. Yoon and K FA. Soliman. Acetyl-
-carnitine cytoprotection against 1-methyl-4-phenylpyridinium toxicity in neuroblastoma cells, Biochemical Pharmacology, 66: 297-306 (2003)
7. Mazzio, E and K F A Soliman. Glioma cell capacity in removing generated reactive oxygen species. Journal of Applied Toxicology.24: 99-106 (2004)
8. Mazzio, E and K F A Soliman. Effect of enhancing mitochondrial oxidative phosphorylation with reducing equivalents and ubiquinone on 1-methyl-4-pheylpyridinium toxicity in neuroblastoma cells. Biochemical Pharmacology 67: 1167-1184 ( 2004)
9. Lee, E, H Chen, K R Shephard, N Lamango, K F A Soliman and CG Charlton. Inhibitory Effects of lysophosphatidylcholine on the dopaminergic system. Neurochemical Research 29: 1325-1334 (2004)
10. Lee, E, H Chen, K R Shephard, N Lamango, K F A Soliman and CG Charlton. The inhibitory role of methylation on the binding characteristics of dopamine receptors and transporter. Neuroscience Research 48: 335-344 (2004)
11. Mazzio E, R R. Reams and K F A Soliman. The role of oxidative stress, impaired glycolysis and mitochondrial respiratory redox failure in the cytotoxic effects of 6-hydroxydopamine in vitro. Brain Research 1004: 29-44 (2004)
12. Yoon K, K Redda E Mazzio, and KFA Soliman. Inhibitory effects of novel tetrahydropyridine derivatives on nitric oxide and reactive oxygen species in glioma cells. Drug Development Research 61:189-196 (2004)
13. Mazzio, E, MG Kolta, RR Reams, and K F A Soliman. Inhibitory effects of cigarette smoke on glial inducible nitric oxide synthase and lack of protective properties against oxidative neurotoxins in vitro. Neurotoxicology 26: 49-62 (2005)
14. Lee, E, K F A Soliman and C G Charlton. Lysophosphatidylcholine decreases locomotor activities and dopamine turnover rate in rats. Neurotoxicology26: 27-38 (2005)
15. Elsisi, N, S. Darling-Reed, EY Lee, E T Oriaku and K F Soliman. Ibuprofen and apigenin induce apoptosis and cell cycle arrest in activated microglia. Neuroscience Letters 375:91-96 (2005)
16. Lee, E, H Chen, K F A Soliman and CG Charlton: Effects of Homocysteine on the Dopaminergic System and behavior in Rodents. Neurotoxicology26: 361-371 (2005).
17. Lee, E, H. Chen, C. G. Charlton and KFA Soliman. The Role of Phospholipid Methylation in 1-Methyl-4-Phenyl-Pyridinium ion (MPP+) induced Neurotoxicity in PC12 cells. Neurotoxicology, 26, 945-957(2005)
18. K. R. Shepherd, E. Y. Lee , L. Schmued , S. F. Ali c, E.T. Oriaku , N. S. Lamango, K. F.A. Soliman , and C. G. Charlton .The potentiating effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on paraquat-induced neurochemical and behavioral changes in mice. Pharmacology Biochemistry Behavior 83:349-59 (2006)
19. Lee, E; Z. Williams C. Goodman, E.T. Oriaku, M. Thomas, C. Harris and KFA Soliman. Effects of NMDA Receptor Inhibition by Phencyclidine on the Neuronal Differentiation of PC12 Cells. Neurotoxicology. 27:558-66 (2006)
20. Williams, ZR; Goodman, CB and Soliman, KFA . Anaerobic Glycolysis Protection Against 1-methy 4-phenylpyridinium (MPP+) Toxicity in C6 Glioma Cells. In press. J Neurochemical Research (2007)
21. Mazzio, E and Soliman KF. In Vitro Screening for the Tumoricidal Properties of International Medicinal Herbs. Phytotherapy Research 23: 385-398 (2009).
22. Soliman, Y I; Mazzio, E Jackson T and Soliman KF "The effects of piroxicam in the attenuation of MPP+/MPTP toxicity in vitro and in vivo. Neurochemical Research 34:304-310 (2009).
23. Becker A, Soliman KF. The role of intracellular glutathione in inorganic mercury-induced toxicity in neuroblastoma cells. Neurochem Res. 34:1677-1684. 2009
24. Reams, R. R , D. Agrawal, M. B. Davis, S.Yoder, F. T. Odedina,, N. Kumar, J. M Higginbotham, T. Akinremi, S. Suther and K. F.A. Soliman. Microarray Comparison of Prostate Tumor Gene Expression In African-American and Caucasian American Males: A Pilot Project Study. BioMed Central 10:4 Supp 1S:3 (2009)
25. Mazzio E; Soliman KF. Evaluation of endogenous acidic metabolic products associated with anaerobic carbohydrate metabolism in tumor cells. Cell Biol Toxicology 26:177-188 (2010)
26. Mazzio, E A. Soliman Y I, Soliman K F A. Variable toxicological response to loss of OXPHOS through 1-methyl-4-phenylpyridinium-induced mitochondrial damage and hypoxia in diverse neural immortal cell lines . Cell Biology & Toxicology 26(6):527-39.Epub 2010 Apr 18.PMID: 20401737
27. Mazzio, E and Soliman KF. In Vitro Screening for the Tumoricidal Properties of International Medicinal Herbs. Part II. Phytotherapy Research. 2010 Jun 17. [Epub ahead of print]PMID: 20564497
28. Badisa RB, Darling-Reed SF, Soliman KF.The Protective Role of D: -Glucose Against 1-Methyl-4-Phenylpyridinium Ion (MPP (+)): Induced Mitochondrial Dysfunction in C6 Astroglial Cells. Neurochem Res. May 28. [Epub ahead of print]PMID: 20508987 (2010)
29. Mazzio, E A, F. Close and K. F.A. Soliman. The Biochemical and Cellular Basis for Nutraceutical Strategies to Attenuate Neurodegeneration in Parkinson’s Disease. Int. J. Mol. Sci. 12, 506-569 (2011)
American Physiological Society, Member; 1975 - present
, National Institutes of Health, National Institute of General Medical Sciences
, National Institutes of Health/National Center for Research Resources
; Pharmacy continuing education seminars; ;
Background:
Parkinson's disease (PD) is a complex neurodegenerative disorder involving
the predominant loss of dopaminergic neurons in the substantia nigra pars
compacta (SNc), subsequent decay of the nigrostriatal tract and associated
movement anomalies such as rigidity, bradykinesia and tremor. The foremost
pathological features associated with SNc dopaminergic degeneration are
mitochondrial abnormalities, ergogenic failure, excessive dopamine oxidation,
Lewy body deposition, inflammation, a-synuclein/ubiquinated protein
aggregation, heightened concentration of redox-active free iron and a gradual
loss of neuromelanin in and around the SNc. Susceptibility of these events
could be dependent upon a battery of genetic mutations (ie parkin, DJ-1,
PINK-I, LRRK2, park-1, ubiquitin-carboxy-terminal-hydrolase L1) or exposure
to environmental mitochondrial toxins, head trauma, viral/bacterial infections,
metals, antipsychotic/antidepressant drugs or rural/farm living
Statement of Problem:
Standard medical treatment for PD involves the use of therapeutics that
mitigate neurological effects through modulation/regulation of
neurotransmitter function (ie. levodopa/dopa-decarboxylase inhibitors
Sinemet and Madopar, dopamine agonists, catechol-o-methyltransferase
inhibitors, monoamine oxidase (MAO) inhibitors, anti-cholinergics and surgical
treatments. There is a need for nutritional formulations that could slow the
progressive nature of this disease, extending quality of life and rapid decline
with late stage onset.
Potential Solution:
FAMU has developed and patented a nutraceutical formulation/vitamin that
PD patients can take orally, that could potentially slow/halt the
neurodegenerative process. The premise for the invention is based on
experimental findings of protective agents in a number of experimental
models that pertain specifically to PD. The formulation is comprised of a
proprietary blend of carboxylic acids, pyruvate, succinate, alpha.-ketoglutarate
and/or oxaloacetate, niacin/NADH, further combined with specific
macro/micronutrients, trace elements, amino acids, biochanin A ,butein
and/or concentrated plant sources.
Commercialization Status:
The product holds potential for development and commercialization with
specialty therapeutics in areas of PD. Currently, clinical trials would be
required.
Background:
Hand eczema is a widespread skin disorder, encompassing a variety of
diseases such as contact dermatitis and dyshidrosis (pompholyx). Dyshidrosis
itself is characterized by initial onset of blistering and dry cracked skin on the
hands or feet, affecting the tips and sides of fingers, toes, soles and palms.
The disease develops progressively to occupy larger surface area and
extensive pathological skin scaling, peeling, bleeding, deep fissures and open
wounds that in many cases do not heal. There is very little known about the
disease, other than a wide held believe it is due to stress, anxiety or contact
with some form of irritant or allergen.
Statement of Problem:
While topical steroidal or non-steroidal immuno-suppressive agents remain
the primary treatment for dyshidrosis, atopic dermatitis and psoriasis, they
don't address the etiology of the disease , in some cases are not effective or
only a temporary solution, and are known to lead to local and systemic side
effects with extended use. Skin conditions non-responsive to topical steroidal
creams render chronic long-term afflictions affecting quality of life. For the
case of dyshidrosis, confinement to white gloves, a potential loss of functional
utility of the hands and/or feet and avoiding direct contact with ubiquitous
substances such as soap, water and detergents.
Potential Solution:
FAMU has developed and patented an inside (oral nutritional) – outside
(topical) product for deep skin care originally designed for dyshidrosis. The
principles governing development of the topical/oral product combination
include capacity to [1] augment circulation or blood flow to hands and feet [2]
provide potent anti-microbial: anti-parasitic, anti-bacterial, anti-protozoal, anti-
fungal and anti-viral properties to destroy growth of invading pathogenic
organisms or unknown retroviruses [3] dermal anti-inflammatory agents [4]
cutaneous vasodilators [5] aloe vera and [6] contain constituents that destroy
or remove dead skin, which correlate with healing.
Commercialization Status:
The herbaceutix ™ Inside (Nutritional Supplement) - Outside (Cream) Skin
Care product line is currently in the early development stage but product is
market ready. The herbal extract formulations are safe, complete, and
prototypes can be manufactured on a small scale. We are seeking
collaborative partners or licensees in the Nutraceutical and/or HealthCare or
Topical Skin Care Industries to take these developments into
commercialization. The target market of this product is unique as it will not be
an anti-aging, moisturizing cream, but rather for adverse skin conditions that
affect quality of life.
