Winston Salem State University - Biology
Home Schooling
Guilford Technical Community College
Evidence Based STEM teaching
Design and Interpretation of Clinical Trials
Johns Hopkins University via Coursera
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What is Data Science?
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Coursera (IBM)
Archive Vision and Change Scholar
American Physiological Society
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Epigenetic Control of Gene Expression
University of Melbourne (via Coursera)
Online Teaching Essentials
The City University of New York
Columbia University
Brooklyn College
Winston-Salem State University
New Mexico Highlands University
New York City Metropolitan Area
Lecturer (Doctoral Schedule) and Coordinator of Core Biology
Brooklyn College
WSSU is an HBCU mainly emphasizing teaching but moving more in a research direction. I am working on the forefront of both the teaching and research priorities. On the teaching
I am curious in why the traditional techniques I learned by are not as effective as before
and am one of the leaders in trying new approaches and technologies to student learning
especially to non-biology majors. I am also
with some of my colleagues
designing new topical non-major courses
such as environmental biology
human biology and disease
and human reproduction and development. I personally designed or co-designed two of those courses. I have also reviewed and edited a number of non-major textbooks and lab books. For research my main interest is in hormonal modulation of neurotransmitter systems. My main hormones of interest are insulin
cortisols
and progesterones. My research may have implications in diabetes
food intake
inflammation and autoimmunity
PMDD
anxiety
stress
and effects of environmental exposure to hormone mimetics. I am also screening potential drugs designed for other neurotransmitter systems for cross-effects at GABA-A receptors.
Winston-Salem State University
Adjunct Professor
I taught Anatomy and Physiology I lecture and lab
including the cat dissections
Guilford Technical Community College
New Mexico Highlands University
Las Vegas
NM
Recruited via an NIH grant. I started the steroid work I have recently expanded and published.\nTaught biomolecules
endocrinology
graduate and undergraduate cell biology
graduate genes and disease seminar; and a mixed graduate/undergraduate new course in neurobiology.
Assistant Professor of Cell Biology
I worked on my research project on the effects of different drugs on the shape of the GABA-A receptor.
Columbia University
Mount Ida College
Newton
MA
In charge of Natural and Applied Sciences
biology
chemistry
forensic science
and environmental sustainability
including all faculty
annual reports
assessment
budgets
and hiring.
Associate Professor and Chair of Natural and Applied Sciences
PhD
The Integrated Program. Gave experience in microbiology
genetics
cancer
and development as well as the neuroscience/hormone related work I currently do.
Cellular
Molecular and Biophysical Studies
Cellular Membranes and Organelles
Cell and Tissue Culture
Eukaryotic Molecular Biology
Immunology and Serology
Biology of Cancer
Advanced Biochemistry
Calculus for Business
Economics and Biology
Cell Ultrastructure and Function
General Physiology
Intro to Pharmacology
Classroom Management
Genetics
Advanced Cell and Developmental Biology
General Ecology
Cytogenetics
Chemistry II
Calculus II
Education Practicum
Immunology
Coursera (University of Toronto)
Bioinfomatic Methods I
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Rutgers University
National Institutes of Health
Guilford Technical Community College
I taught Labs for General Biology
Molecular Biology
and Genetics.
Rutgers University
Marymount Manhattan College
Greater New York City Area
Teaching Anatomy
Evolution
and Drugs and Brain.
Visiting Associate Professor of Biology
Special pharmacology research fellow in NINDS/NIGMS working on dopamine receptor pharmacology
desensitization
and signaling.
National Institutes of Health
Society for Neuroscience
American Association for the Advancement of Science
Attending various meetings and workshops for major and course curriculum redesign based current research and in Vision and Change.
AAC&U and PKAL
Member
American Society for Pharmacology and Experimental Therapeutics
English
Global Medical Discovery Article of Interest:
For Williams DB (2011) A mutant residue in the third transmembrane region of the GABA-A alpha1 subunit causes increased agonistic neurosteroid responses. Neurochem Int. 58: 794-803. (doi:10.1016/j.neuint.2011.03.005)
Tri Beta
Induction as honorary member
Research Highlighted in Target Intelligence Service
For Williams DB (2011) A mutant residue in the third transmembrane region of the GABA-A alpha1 subunit causes increased agonistic neurosteroid responses. Neurochem Int. 58: 794-803. (doi:10.1016/j.neuint.2011.03.005)
Faculty of 1000
MS
Teaching assistant for genetics
general biology
molecular biology
\nMasters' research on hormone effects on GABA-A receptor ligand binding.\n
Biology
Coral Lansbury Award for Best Graduate Student
BA
Biology
Rahman Award as top biology student.\nAthenaeum Honor Society
I was co-valedictorian.
Highland Regional High School
JDRF
Parent Mentor and other activities
Cell Biology
Scientific Writing
Research
Curriculum Design and Assessment
Educational Assessment
Classroom
Pharmacology
Instructional Design
Genetics
Teaching
Cell Signaling
Cell Culture
Curriculum Development
College Teaching
Proposal Writing
Teaching Writing
Molecular Biology
Electrophysiology
Animal Welfare
University Teaching
Inhibitory effects if insulin on GABA-A currents modulated by the GABA-A alpha subunit
Insulin
when co-applied with GABA
can cause an inhibition of the induced current at GABAA receptors. Main methods: This study investigated that inhibitory effect of insulin at a variety of receptor isoforms
concentrating on α1
α2
and α4 containing receptors. Various isoforms were expressed in Xenopus oocytes and currents determined using two-electrode voltage clamp. Key findings: Submaximal GABA currents at all isoforms studied were inhibited by nanomolar concentrations of insulin. At α2 and α4 containing forms
insulin could inhibit maximal GABA currents. The ability to inhibit maximal currents
and the general potency and effects at submaximal currents paralleled the number of potential MAPK sites on the α subunits. Significance: The differences in insulin inhibition of GABA currents at different α containing GABAA receptors could be important in autocrine and paracrine control of hormone secretion in the pancreas
and in control of reward and food intake circuits of the brain.
Inhibitory effects if insulin on GABA-A currents modulated by the GABA-A alpha subunit
Pregnane derived steroids have agonistic and antagonistic actions at GABAA receptors. Putative binding sites for agonistic neurosteroids are located within the transmembrane (TM) regions. A mutation within the rat α1 TM3 region
S299C
caused the expressed receptors to have unusual and extreme sensitivity to agonistic neurosteroids. For mutant α1S299C receptors
with wild type β and γ subunits
expressed in Xenopus oocytes
steroids activated the GABAA receptors in the absence of GABA. Maximal steroid induced currents were about half of maximal GABA currents. The steroid activation was biphasic with EC50’s much lower than wild type
in subnanomolar and nanomolar concentrations
while the wild type had only one activation peak with near micromolar EC50. These currents could be blocked by both picrotoxin and an antagonist neurosteroid. The steroids did not seem to potentiate significantly submaximal GABA currents. The α1S299C mutation did not affect responses to the extracellularly acting partial agonist piperidine-4-sulfate. Substituted cysteine experiments indicate that this mutant can be modified by pCMBS- when the sulfhydryl reagent is added with the higher steroid concentration for activation but not the lower steroid concentration. The pCMBS- will also immediately block the high concentration steroid current. Taken together the data suggest that α1S299 is at least important in the in transduction of the steroid binding to the rest of the receptor.
A mutant residue in the third transmembrane region of the GABA-A alpha1 subunit causes increased agonistic neurosteroid responses.
In the CNS
GABA and insulin seem to contribute to similar processes
including neuronal survival; learning and reward; and energy balance and food intake. It is likely then that insulin and GABA may interact
perhaps at the GABAA receptor. One such interaction has already been described [33]; in it a micromolar concentration of insulin causes the insertion of GABAA receptors into the cell membrane
increasing GABA current. I have discovered another effect of insulin on GABAA currents. Using a receptor isoform α1β2γ2s that is the likely main neuronal GABAA isoform expressed recombinantly in Xenopus oocytes
insulin inhibits GABA induced current when applied simultaneously with low concentrations of GABA. Insulin will significantly inhibit currents induced by EC30-50 concentrations of GABA by about 40%. Insulin is potent in this effect; IC50’s of insulin in a two site model were found to be about 4.5 x10-10 M. The insulin effect on the GABA dose responses looked like that of a competitive antagonist. However
an effect of phosphorylation on the GABAA from the insulin receptor signal transduction pathway cannot yet be dismissed.
A novel
rapid inhibitory effect of insulin on α1β2γ2S γ-aminobutyric acid type A receptors.
\n\n\n\n
Letter to the Editor of Nexus Magazine
Continuing to gather preliminary data on histamine-GABA-A receptor ligand interactions.\n
Society for Neuroscience poster 2014
Williams
Daniel
Marymount Manhattan College
Mount Ida College
The following profiles may or may not be the same professor:
The following profiles may or may not be the same professor: