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Archive for March, 2010

Contraversial effect of estrogen on Atherosclerosis and Thrombosis

Estrogen is known to protect premenopausal women from cardiovascular
disease such as Atherosclerosis. However I’ve heard that Estrogen
incleases thrombosis.

Could you explain this paradoxical results to me?
Thanks

.
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Magnetic resonance imaging of brain iron

NMR Biomed. 2004 Nov 3;17(7):433-445 [Epub ahead of print] Links

High-field magnetic resonance imaging of brain iron: birth of a biomarker?

Schenck JF, Zimmerman EA.

General Electric Global Research Center, Schenectady, New York, USA.

The brain has an unusually high concentration of iron, which is distributed in
an unusual pattern unlike that in any other organ. The physiological role of
this iron and the reasons for this pattern of distribution are not yet
understood. There is increasing evidence that several neurodegenerative
diseases are associated with altered brain iron metabolism. Understanding these
dysmetabolic conditions may provide important information for their diagnosis
and treatment. For many years the iron distribution in the human brain could be
studied effectively only under postmortem conditions. This situation was
changed dramatically by the finding that T(2)-weighted MR imaging at high field
strength (initially 1.5 T) appears to demonstrate the pattern of iron
distribution in normal brains and that this imaging technique can detect
changes in brain iron concentrations associated with disease states. Up to the
present time this imaging capability has been utilized in many research
applications but it has not yet been widely applied in the routine diagnosis
and management of neurodegenerative disorders. However, recent advances in the
basic science of brain iron metabolism, the clinical understanding of
neurodegenerative diseases and in MRI technology, particularly in the
availability of clinical scanners operating at the higher field strength of 3
T, suggest that iron-dependent MR imaging may soon provide biomarkers capable
of characterizing the presence and progression of important neurological
disorders. Such biomarkers may be of crucial assistance in the development and
utilization of effective new therapies for Alzheimer’s and Parkinson’s
diseases, multiple sclerosis and other iron-related CNS disorders which are
difficult to diagnose and treat. Copyright (c) 2004 John Wiley & Sons, Ltd.

PMID: 15523705 [PubMed - as supplied by publisher]

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——

Who loves ya.
Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking

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Please Help

Hi.  I am desperate for some help, so could everyone please take a
look at my website.  I promise I’m not selling anything, nor is it a
cam site http://pleasehelpme.20megsfree.com/

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Valve incompetence – a dynamic hypothesis

A possible cause for valve incompetence.

The idea is that during valsalva maneuver, which many of us are
performing some times even unconsciously some more often than others
and some more intensely than others, the intra abdominal pressure
(IAP) may increase to values up to 340 mm/Hg.

"To my knowledge, it has not been demonstrated that sneezing or
coughing leads to a higher IAP than a valsalva maneuver. Instead, the
highest IAP values have been found during valsalva maneuvers (Harman
et al. 1988: 277 mm Hg; McGill and Sharratt 1990: 340 mm Hg). A
valsalva maneuver is the voluntary pressurization of the abdominal
cavity, with a closed glottis (to keep the intrathoracic pressure
high, and therefore to support the diaphragm), and a contraction of
all muscles contributing to IAP: diaphragm, transversus abdominis,
partly the obliques, and the pelvic floor musculature. So why should a
valsalva maneuver ("sustained"??) has a different effect than
sneezing/coughing?"
from
http://isb.ri.ccf.org/biomch-l/archives/biomch-l-1999-04/00036.html

The interesting thing is that according to some articles on the net,
arterial blood pressure may increase to similar values.

"The Valsalva maneuver or holding the breath while performing an
exercise can increase blood pressure to extremely high and dangerous
levels. Blood pressures of nearly 400/350 have been recorded during
such actions. Existing aneurisms can burst, blood vessels in the eye
can rupture and even retinas can tear (Valsalva Retinopathy). This is
a common and dangerous practice. It is also the job of the trainer or
spotter to recognize when the breath is being held and bring it to the
exerciser’s attention immediately."
from
http://www.siliconcentral.info/sc309.htm
(last paragraph)

That would also explain why intra cranial pressure durring sneezing
increases to values up to 50 mm/Hg.

"Intracranial pressure is not a constant value but is variable. It can
increases sharply with coughing and sneezing, up to 50 or 60 mm/Hg to
settle down to normal values in a short time."
from
http://www.health.adelaide.edu.au/paed-neuro/pressure.html

Using simple logic, one can assume that the venous pressure may
increase to similar values (340 mm/Hg), since simple hydraulics tell
us that the extra arterial pressure during valsalva is created by the
same intra abdominal pressure squeezing both the central arteries and
veins, and that would be the reason that valves will fail along the
veins starting with the ones close to abdomen/thorax and not
surrounded by muscles (saphenous, jugular, etc.)

I am wandering if anyone has ever dynamically measured the venous
pressure before the jugular valve during valsalva and in general.

No need to mention in this hypothesis what happens to someone if has
jugular valve incompetence and sneezes. (It may be possible that
dynamic increase of the blood pressure in the vein to occur at such
values that will temporarily close the failing valve.)

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Dissertation suggestions , please !

Hi group,

I’ve got to do a dissertation in integrated pathology.  Was wondering if
anyone could offer any suggestions to topics they think are interesting and
are research worthy.  Also, would appreciate if you could give me any URL
links to any such sites that give information to dissertation writing in
this field.

Thanks in advance

JB

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Vitamin E and Heart Disease and Mortality… too much Testosterone

Vitamin E and Heart Disease and Mortality… too much Testosterone?

Copyright 2004, James Michael Howard, Fayetteville, Arkansas, U.S.A.

While controversial, support exists that testosterone increases
mortality in men and women.  Testosterone is not "the male hormone,"
males simply produce more of it.  Increased "morbidity and mortality"
are a concern for women with androgen excess (Am J Med. 1995 Jan
16;98(1A):137S-143S).

Vitamin E stimulates testosterone production in men (Endocrinol Jpn.
1982 Jun;29(3):287-92).  (I could not find a connection in women.)  If
testosterone really does have a connection with increased morbidity
and mortality, it may be that the increased mortality now attributed
to excess vitamin E may be due to increased levels of testosterone.

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Why There are Two Peaks of Death and Disease in Older Age

Why There are Two Peaks of Death and Disease in Older Age

Copyright, 2004, James Michael Howard, Fayetteville, Arkansas, U.S.A.

It is my hypothesis that DHEA was selected by evolution because it
optimizes replication and transcription of DNA.  Therefore, all genes
and tissues are activated by DHEA.  I think the rise of DHEA caused
the evolution of mammals (Hormones in Mammalian Evolution, Rivista di
Biologia / Biology Forum 2001; 94: 177-184).  DHEA production may be
involved in the pattern described by Dr. Steven Frank: "Humans die at
an increasing rate until late in life, when mortality rates level
off." ("A Multistage Theory of Age-specific Acceleration in Human
Mortality," BMC Biology 2004; 2: 16, an online journal)

DHEA is very high through the first month of life, followed by a
severe decline until ages 5-7 years (adrenarche), whereupon it
increases rapidly until age 20-25 years, then declines again, reaching
very low levels in old age.

I suggest this represents the onset of neonatal production of DHEA
which triggers rapid growth and development, especially in the brain.
This rapid growth of the brain causes the decline of "measurable"
levels of DHEA prior to adrenarche.  The brain literally absorbs the
available DHEA for growth and development.  Once the brain begins to
finalize growth and development, measurable levels of DHEA reappear
and adrenarche begins.  This frees DHEA for growth and development of
the body, which, when near completion, again allows DHEA for
activation of the brain centers which control puberty.  (This is the
basis for a switch from growth and development to activation and
maintenance.)  Availability of DHEA is first used for the brain, then
the body, and is then used for activation of puberty.  DHEA continues
production until our reproduction is completed, then it declines.
There is no need to continue DHEA production after reproduction and
children are able to exist without parents.  DHEA production begins to
decline thereafter; activation of all tissues declines
correspondingly.  I think the loss of DHEA results in aging.  (DHEA
declines in AIDS; I think AIDS represents premature aging because of
this abnormal decline of DHEA.)

The decline of DHEA reduces the activity level of all tissues.  (I
think the brain is especially able to use DHEA so the brain, usually,
declines last.  Remember the hypothetical use of DHEA for growth and
development of the brain.)  As an individual’s genome contains genes
that differ from that state most optimal for maintenance of the
person, the decline of DHEA will expose them, again, correspondingly.
That is, declining levels of DHEA are less able to participate in
activation of genes that differ from optimal configuration for
transcription.  These genes then increase the probability of
consequences of gene loss.  These consequences are exposed as DHEA
declines.  Many diseases and disorders manifest themselves with age.
Some of these cause death.

If a person does not carry genes that are prone to malfunction during
DHEA decline, then that person will live beyond the average age of
individuals who carry genes prone to the dire consequences of DHEA
decline.  These people exhibit the "normal" life span dependent upon
DHEA production.  At some point in old age, DHEA declines to the point
that brain function fails to maintain cardiovascular function.

I suggest the "early-life increase and late-life decrease in mortality
acceleration" may be explained by this combination of DHEA decline in
individuals with genes prone to malfunction and individuals who do not
carry these genes.

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blue prolene suture material left in abdominal…

I have blue prolene sutures left inside of me 4 inches below my
sternum and 2 inches above my belly button from an abdominal hernia
operation.  The original surgeon said they would dissolve.  They
didn’t dissolve.  It has been 3 years now.
Can these be harmful to me?  They poke a lot at my skin when I push
down on my abdomen and when I move my abdomen.
I know they are blue prolene sutures because I had another surgeon
remove some of them by clipping off the top of the sutures where they
protrude under my skin.  Now  I feel some of the ends coming through
different parts of my skin on the surface.

Are these blue prolene sutures typically used for abdominal hernias?
Or is this a mistake?  The surgeon who removed them said he would have
used
the sutures that dissolve because of complications with muscle tissue.

I am sure one of you have discovered some of these type of sutures in
your practice when examining a body.

Thanks.

Joe

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iron accumulation / AIDS / HIV-infected patients

<<snip>>
The iron accumulation found in these patients is instead caused by other
unknown mechanisms that need further studies to be clarified
<<snip>>

Biometals. 2004 Aug;17(4):443-50. Related Articles, Links  

Effects of AZT on cellular iron homeostasis.

Bozzi A, Brisdelli F, D’Alessandro AM, D’Andrea G, Lizzi AR, Rinaldi AC,
Oratore A.

Department of Biomedical Sciences and Technologies, University of L’Aquila, Via
Vetoio, Coppito 2, 67100 L’Aquila, Italy. bo…@cc.univaq.it

3′-azido-3′-deoxythymidine (AZT), the first chemotherapeutic drug approved by
FDA for treatment of HIV-infected patients and still used in combination
therapy, has been shown to induce, upon prolonged exposure, severe bone marrow
toxicity manifested as anemia, neutropenia and siderosis. These toxic effects
are caused by inhibition of heme synthesis and, as a consequence, transferrin
receptor (TfR) number appears increased and so iron taken up by cells. Since
iron overload can promote the frequency and severity of many infections,
siderosis is viewed as a further burden for AIDS patients. We have previously
demonstrated that AZT-treated K562 cells showed an increase of the number of
TfRs located on the surface of the plasma membrane without affecting their
biosynthesis, but slowing down their endocytotic pathway. In spite of the
higher number of receptors on the plasma-membrane of AZT-treated cells,
intracellular accumulation of iron showed a similar level in control and in
drug-exposed cells. The chelating ability of AZT and of its phosphorylated
derivatives, both in an acellular system and in K562 cells, was also checked.
The results demonstrated that AZT and AZTMP were uneffective as iron chelators,
while AZTTP displayed a significant capacity to remove iron from transferrin
(Tf). Our results suggest that AZT may be not directly involved in the iron
overloading observed upon its prolonged use in AIDS therapy. The iron
accumulation found in these patients is instead caused by other unknown
mechanisms that need further studies to be clarified.

PMID: 15259365 [PubMed - in process]

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——

Who loves ya.
Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking

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iron chelation / neurodegenerative diseases

J Neural Transm. 2004 Oct-Nov;111(10-11):1455-71. Epub 2004 Apr 20. Links

Novel bifunctional drugs targeting monoamine oxidase inhibition and iron
chelation as an approach to neuroprotection in Parkinson’s disease and other
neurodegenerative diseases.

Youdim MB, Fridkin M, Zheng H.

Eve Topf and National Parkinson Foundation Centers of Excellence for
Neurodegenerative Diseases Research, and Department of Pharmacology,
Technion-Rapapport Faculty of Medicine, Haifa, Israel.

Iron has been shown to accumulates at site where neurons degenerate in
neurodegenerative diseases of Parkinson’s disease, Alzheimer’s disease,
Huntington disease, amyotrophic lateral sclerosis and Friedreich ataxia. Iron
is thought to participate or initiate oxidative stress via generation of
reactive oxygen species (ROS), such as hydroxyl radical. Iron chelators are
neuroprotective and prevent 6-hydroxydoapmine and MPTP dopaminergic
neurotoxicity in rats and mice. However, their action on monoamine oxidase
(MAO) A and B have not been determined previously since MAO-B inhibitors have
been shown to be neuroprotective in cellular and animal models of Parkinson’s
disease. The chelators 8-hydroxyquinoline, O-phenanthroline, 2,2′-dipyridyl,
U74500A and U74600F showed a preference for inhibition of rat brain
mitochondrial MAO-A over MAO-B. Their IC(50) ranged from 10(-3) M to 10(-6) M,
with 21-amino steroids (U74500A and U74006F) showing a greater selectivity and
potency for MAO-A. Desferrioxamine (desferal), a prototype potent iron
chelator, exhibited relatively poor MAO inhibitory. The inhibitions of MAO-A
and B by 21-amino steroids (Lazaroids) were time dependent and irreversible.
Those initiated by 8-hydroxyquinoline, 2,2′-dipyridyl and O-phenanthroline were
fully reversible by enzyme dilution experiments. Both Fe(2+) and Fe(3+) reverse
the MAO-A and B inhibition induced by the latter chelators, but not those
initiated by 21-amino steroids. The data infer that either the inhibition of
MAO by 21-amino steroids is either the resultant of their conversion to an
irreversible covalently bound ligand or that the iron chelation moiety and MAO
inhibitory activity in these compounds are not mutually shared. The results
suggest that bifunctional brain penetrable drugs with iron chelating property
and MAO inhibitory activity in could be the most feasible approach for
neuroprotection in neurodegenerative diseases. Such drug would prevent
participation of elevated iron in oxidative stress and formation of reactive
hydroxyl radical, via its interaction with H(2)O2 (Fenton chemistry), generated
as a consequence MAO and other oxidative enzyme reactions to generative
cytotoxic reactive hydroxyl radical. We have now developed several of these
compounds with neuroprotective, MAO inhibitory and iron chelating properties
from our prototype iron chelators, VK-28 possessing propargylamine moiety of
our anti-parkinson drug, rasagiline.

PMID: 15480846 [PubMed - in process]

————————————————————————–
——

Who loves ya.
Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking

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