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DR Michael H Pfeiffer Website - Con-Drug-Scientist PDF
DR Michael H Pfeiffer Website - Con-Drug-Scientist PDF
THE CON
Mr. Michael H. Pfeiffer conducted a full schedule of research for 6 years at the institute of physiology and
neuroscience laboratory at Charite Hospital at Humboldt University in Berlin at the same time that he
claims to have been a full time medical student at the same university.
1994-1999
PhD (Research Degree), May 1999, from Laboratory of Professor Dr. Uwe Heinemann Institute of
Physiology at the Medical Faculty of Charité, Humboldt University, Berlin, Germany
"Neuronal and gilal GABA-transporter and and their junction in the transition form
pharmacosensitive to pharmacoresistant forms of epileptiform activity in the
temporal lobe of the rat in vitro."
Pfeiffer, M., Draguhn, A., Meierkord, H. & Heinemann, U. (1996). Effects of gamma-aminobutyric acid (GABA) agonists and GABA
uptake inhibitors on pharmacosensitive and pharmacoresistant epileptiform activity in vitro. British Journal of Pharmacology
119(3):569-77.
Source Abt. Neurophysiologie, Humboldt-Universität zu. Berlin, Germany; British Journal of Pharmacology 1996
Oct;119(3):569-77. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1915701/?tool=pubmed)
PhD Research Source of funds: Deutche Forschungsgemeinschaft (DFG) The German Research Council - Research
Collaboration Center - no. SBF 506
Abstract: Lowering of the extracellular Mg(2+)-concentration induces various patterns of epileptiform activity in
combined rat entorhinal cortex-hippocampal brain slices. After a prolonged period of exposure to Mg(2+)-free
medium seizure-like events in the entorhinal cortex change to a state of late recurrent discharges which cannot
be blocked by clinically available antiepileptic drugs. This late epileptiform activity thus represents a useful
model to test the effects of new anticonvulsant substances. 2. A mechanism possibly underlying the
development of sustained seizure-like activity is the loss of synaptically released gamma-aminobutyric acid
(GABA). Drugs which increase the amount of GABA available in presynaptic endings might thus be useful in the
treatment of these therapeutically complicated forms of epilepsy. 3. Therefore, we studied the effects of various
substances increasing GABA-mediated inhibition on early and late forms of epileptiform activity. GABA and the
GABAA receptor agonist muscimol blocked both the pharmacosensitive discharges in the hippocampus and
entorhinal cortex as well as the late recurrent discharges in the medial entorhinal cortex. The GABAB receptor
agonist baclofen blocked the recurrent short discharges very potently, but did not consistently block seizure-like
events and late recurrent discharges in the entorhinal cortex. 4. GABA uptake blockers showed a differential
potency to block the various discharge patterns. Whereas nipecotic acid and beta-alanine suppressed all forms
of epileptiform activity albeit at high concentrations (1-5 mM), tiagabine was much more potent in blocking the
hippocampal recurrent short discharges and the seizure-like events in the medial entorhinal cortex, but could not
block the late recurrent discharges. 5. Our data support the idea that prolonged neuronal overactivity might result
in a loss of synaptically available GABA. Selective block of uptake into glia cells or substitution of the transmitter
may therefore be an efficient strategy for the treatment of severe prolonged epileptic discharges whereas block
of neuronal GABA uptake fails to counteract synchronized discharges in this situation.
Note: Michael H Pfeiffer Research - German Research Collaboration Grant 506 (1997-2003) given to Prof. Dr. med Peter
T. Daniel Director Molecular Hematology and Oncology, Charité - Humboldt University Campus Berlin, Germany
Publication: Cell Death and Differentiation (2003) 10, 461–467. Combined p53/Bax mutation results in extremely poor
prognosis in gastric carcinoma with low microsatellite instability Edited by V De LaurenziA Mrózek1, H Petrowsky 3,
I Sturm1, J Kraus2, S Hermann1, S Hauptmann2, M Lorenz3, B Dörken1 and Peter T Daniel, German Research Grant
SBF 506
Congress of the Society of Neuroscience in Berlin, Germany,1996: 'Effects of GABA uptake inhibitors on
different patterns of low magnesium induced epileptiform activity in rat entorhinal cortex-hippocampal
slices" in Symposium: "Entoriiinal-hippocampal interactions: From cellular mechanisms to clinical
aspects"
Meeting of the Graduate Program "Mechanisms of Damage in CNS Disease - Application of Imaging
Techniques" in Eggsdorf, Germany,1996:
Mr. Pfeiffer’s Thesis records from the German National Library show he did receive a PhD.
Strong evidence indicates that Michael Herbert Pfeiffer is trained as a human experimental drug
researcher/ scientist (PhD in medical neurophysiology) from the Institute of Physiology
(Neurophysiology) in the Medical School at Charite, Humboldt University Hospital. He who has used
people in the USA misunderstanding of the German educational and medical systen background to falsely
receive a medical license for practicing medicine without proper medical training credentials.
PhD RESEARCH PUBLICATIONS
1996-1999 THE CON– REINVENTING – FROM
SCIENTIST TO FAKE PHYSICIAN
“Look for Publications of M. Pfeiffer in PubMed”
Born 18 February 1963 in Nuremberg,
Journals with Michael Pfeiffer's Research
(Full publications below to download) Germany.
Sleziki KI, Cho YW, Yi SD, Brock MS, Pfeiffer 01 October 1995 to December 1995
MH, Mcvearry KM, Tractenberg RE,
Motamedi, GK (2009). Department of Graduate Student Scholarship
Neurology, Georgetown University Medical
Center, Washington, DC, USA. Incident of
atypical handedness in epilepsy and its 1996 - Year 3 - The Active Student
association with clinical factors. Epilepsy Researcher Year
Behaviour, 2009 Oct. 16(2):330-4. Epub 2009
Aug 28. PMID: 19716770.
PhD Student – Year 3- Programme at Charite
uner Uwe Heinmann, Physiology Institute,