depolarizations, decreased K+ conductance and
 Gastaut H, Tassinari CA, editors. Handbook of Electro-
enhancement of excitatory signals such as Gluta-
encephalography and Clinical Neurophysiology, part A, vol. 13. Amsterdam: Elsevier Scientific Publishing Company;
mate . Serotonin plays a dual (may be synergis-
tic effect) role in increasing susceptibility to
 Shouse MN, Staba R, Farber PR. Physiological basis: how
seizures. Firstly through 5-HT 2A receptors (as men-
NREM sleep components can promote and REM sleep
tioned above) and secondly through its effects on
components can suppress seizure discharge propagation.
sleep; on the one hand, it promotes NREM sleep
Clin Neurophysiol 2000;111(Suppl. 2):S9–S18.
 Murphy M, Donovan S. The Physical and Psychological
(NREM increases susceptibility to seizures), while
Effects of Meditation. Big Sur, CA: Esalen Institute; 1989.
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 Pacia SV, Ebersole JS. Intracranial substrates of scalp ictal
REM initiation and PGO wave generation, the latter
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two supposed to be potent anti-epileptic.
Thus, the evidences put forward do support the
 Gastaut H, Tassinari CA, editors. Handbook of Electro-
encephalography and clinical neurophysiology, part A, vol.
possibility of risk of epileptogenesis during medita-
13. Amsterdam: Elsevier Scientific Publishing Company;
tion as hypothesized in my article at the same time
refuting the objections and controversies raised in
 Persinger MA. Transcendental meditation (TM) and general
meditation are associated with enhanced complex partial
Finally, funded by the Indian government, a ten-
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* Address: ‘‘8, 10’’ C-Block, Near Paliwal Health Club, Haris-
seizures during the sleep-wake cycle: Differences by
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Salmeterol and paroxetine: More evidencefor paradoxical medicine
Lurie and Wolfe of Public Citizen recently suggested
discussions have focused on incomplete disclosure,
in the Lancet that Glaxo SmithKline (GSK) bundled
we remain intrigued by the possibility that chronic
post-trial data with trial data that effectively down-
use of these drugs can produce an exacerbation of
played the risk of death with use of salmeterol .
the underlying condition. In the case of paroxetine,
Similar claims were recently levied against GSK only
the phenomenon of serotonin withdrawal syndrome
last year with respect to studies of paroxetine in
has become increasingly recognized, and, as such
children and adolescents in which data on suicide
may have contributed to an increased risk of morbid-
was not initially fully disclosed [2,3]. While these
ity and mortality. In the case of salmeterol, although
the beta-agonist may have directly produced some
 Is GSK guilty of fraud? Lancet 2004;363(9425):1919.
of the witnessed sequelae, this putative risk may
 Hay A. Questions about SSRI antidepressant drug regulation.
actually be less than what has been traditionally pre-
 Murray JJ. Cardiovascular risks associated with beta-agonist
sumed . However, an additional explanation may
therapy. Chest 2005;127(6):2283–5.
merit consideration—the idea that paradoxical ef-
 Doux JD, Bazar KA, Lee PY, Yun AJ. Can chronic use of
fects caused from interval withdrawal between
anti-inflammatory agents paradoxically promote chronic
times of administration may have caused autonomic
inflammation through compensatory host response. MedHypotheses 2005;65(2):389–91.
remodeling and patient deaths. If so, beta-agonists
 Yun AJ, Lee PY, Doux JD. Paradoxical inflammation revis-
may potentially represent the fourth class of drugs
ited: muraglitazar and cardiovascular risk. Med Hypotheses
to show paradoxical responses that did not emerge
initially with shorter term trials and that only be-
 Yun AJ, Lee PY, Bazar KA. Paradoxical strategy for treating
came revealed with chronic use. Each of these drug
chronic diseases where the therapeutic effect is derivedfrom compensatory response rather than drug effect. Med
categories has an entirely independent mechanism
of action—we have previously discussed cyclooxygen-ase-2 inhibitors  and more recently the PPAR ago-
nist muraglitazar . Given such a consistent
pattern of behavior for different types of medica-
tions, we believe that this phenomenon warrants a
more fundamental explanation—namely that we are
witnessing paradoxical medicine in action , but
as a detriment rather than as a benefit.
E-mail address: [email protected] (A.J. Yun)
 Lurie P, Wolfe SM. Misleading data analyses in salmeterol
(SMART) study. Lancet 2005;366(9493):1261–2. discussion
Tumor-causing plant bacteria may infect animals
Agrobacterium tumefaciens is a well known phytop-
potential infectivity and oncogenetic flow between
atogen; it is a soil bacterium that causes plant’s tu-
Agrobacterium and animals in vivo .
mors disease called Crown Galls . The microbe
After 120 days of wild Agrobacterium injection
contains a DNA plasmid called DNA Ti (tumor induc-
on wounded Chrisantemum maximum, galls are
ing) . The bacterium is introduced in a wounded
evident and pathologically confirmed. Then, we
plant and the plasmid is then integrated in to the
treated 40 SWISS mice, 8 mice each group, with
cell plant genome and overproduces growth regula-
A. tumefaciens cultured: Orally, SC and intraperi-
tors (auxins and cytokines) that can initiate the
toneal injections weekly shaved skin and topicated
Crown Gall  disease. The growth regulators are
with crown galls bacteria and only shaved as con-
also present in mammal’s metabolism. Discovered
trol. After 11 weeks, skin lesions and regionally
by Erwin Smith (1854–1927) [2–5], we know now
nodes are evident in 6–8 mice in shaved and topi-
that the soil bacterium may jump Kingdoms . In
cated group. At optical microscope, H–E · 450,
2001, Vitaly Citovsky from the State University of
lymphoid hyperplasia, neoangiogenesis and neofi-
New York and colleagues found that the plant bacte-
brinogenesis are confirmed. After 18 weeks, multi-
rium was able to attach human cells in vitro and in-
ple tumors and distant metastasis are seen, due to
sert its DNA as it does with plant cells . Recently,
hyperplasia and mesenchymal metaplasia.
the soil microbe has been isolated from blood sam-
Our observations confirmed in vivo the pathoge-
ples of cancer patients [10–12]. We are studying the
nicity of A. tumefaciens on mammals and we think
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