Re: Interesting abstract on borrelia, need comments please

[Guest guest]

that is interesting. was he ever on rx antivirals?

Natasa

>

> Natasa,

>

> Thank you for your post. Hmmm... It seems that I need to increase the

dosage of L-lysine again. L-lysine is involved in the structural repair

of damaged blood vessels. Ingvar was on high dose vitamin C and

L-lysine for a short period of time in 2006. That was my attempt to

treat his CMV and EBV. He was doing really well at that time. Out of

curiosity I collected his urine sample for UTM, when he was not

chelated. His UTM reflected elevated level of Mercury without use of

any metal chelator.

>

> Limin

>

>

>

> From: natasa778

> Sent: Thursday, January 08, 2009 04:16

> To: BorreliaMultipleInfectionsAndAutism

> Subject: Interesting abstract on

borrelia, need comments please

>

>

>

> Hi Tami and others, I came across this recent paper abstract on

borrelia, and found it quite interesting. it shows DIRECT damage induced

by bb (that is not through inflammatory cytokines produced by the host

defence system) on the vessels that line the blood. This offers an

explanation of how bb could cause leaky gut and esp breakdown of blood

brain barrier.

>

> They notice that this damage is induced only by virulent strain of bb,

not by avirulent one. Are the lab lyme tests that are available at the

moment capable of establishing virulence of the strains found? sorry if

this is common knowledge, it is new to me

>

> also, when treating for lyme, is it possible/documented that bb could

be provoked to change into more virulent forms? there was a thread

recently on 'awakening' lyme symptoms through supplements. Any thoughts?

>

> Natasa

>

>

> PLoS ONE. 2008;3(12):e4101. Epub 2008 Dec 31.

> Spent culture medium from virulent Borrelia burgdorferi increases

permeability of individually perfused microvessels of rat mesentery.

> Zhou X, ...Department of Physiology and Pharmacology, West Virginia

University, town, WV, USA.

> BACKGROUND: Lyme disease is a common vector-borne disease caused by

the spirochete Borrelia burgdorferi (Bb), which manifests as systemic

and targeted tissue inflammation. Both in vitro and in vivo studies have

shown that Bb-induced inflammation is primarily host-mediated, via

cytokine or chemokine production that promotes leukocyte

adhesion/migration. Whether Bb produces mediators that can directly

alter the vascular permeability in vivo has not been investigated. The

objective of the present study was to investigate if Bb produces a

mediator(s) that can directly activate endothelial cells resulting in

increases in permeability in intact microvessels in the absence of blood

cells. METHODOLOGY/PRINCIPAL FINDINGS: The effects of cell-free, spent

culture medium from virulent (B31-A3) and avirulent (B31-A) B.

burgdorferi on microvessel permeability and endothelial calcium

concentration, [Ca(2+)](i), were examined in individually perfused rat

mesenteric venules. Microvessel permeability was determined by measuring

hydraulic conductivity (Lp). Endothelial [Ca(2+)](i), a necessary signal

initiating hyperpermeability, was measured in Fura-2 loaded

microvessels. B31-A3 spent medium caused a rapid and transient increase

in Lp and endothelial [Ca(2+)](i). Within 2-5 min, the mean peak Lp

increased to 5.6+/-0.9 times the control, and endothelial [Ca(2+)](i)

increased from 113+/-11 nM to a mean peak value of 324+/-35 nM. In

contrast, neither endothelial [Ca(2+)](i) nor Lp was altered by B31-A

spent medium. CONCLUSIONS/SIGNIFICANCE: A mediator(s) produced by

virulent Bb under culture conditions directly activates endothelial

cells, resulting in increases in microvessel permeability. Most

importantly, the production of this mediator is associated with Bb

virulence and is likely produced by one or more of the 8 plasmid(s)

missing from strain B31-A. PMID: 19116656

>

[Guest guest]

No, Ingvar has never been on any prescribed drug since birth.

Limin

--------------------------------------------------

Sent: Friday, January 09, 2009 09:21

To: <BorreliaMultipleInfectionsAndAutism >

Subject: Re: Interesting abstract on

borrelia, need comments please

> that is interesting. was he ever on rx antivirals?

> Natasa

>

>

>>

>> Natasa,

>>

>> Thank you for your post. Hmmm... It seems that I need to increase the

> dosage of L-lysine again. L-lysine is involved in the structural repair

> of damaged blood vessels. Ingvar was on high dose vitamin C and

> L-lysine for a short period of time in 2006. That was my attempt to

> treat his CMV and EBV. He was doing really well at that time. Out of

> curiosity I collected his urine sample for UTM, when he was not

> chelated. His UTM reflected elevated level of Mercury without use of

> any metal chelator.

>>

>> Limin

>>

>>

>>

>> From: natasa778

>> Sent: Thursday, January 08, 2009 04:16

>> To: BorreliaMultipleInfectionsAndAutism

>> Subject: Interesting abstract on

> borrelia, need comments please

>>

>>

>>

>> Hi Tami and others, I came across this recent paper abstract on

> borrelia, and found it quite interesting. it shows DIRECT damage induced

> by bb (that is not through inflammatory cytokines produced by the host

> defence system) on the vessels that line the blood. This offers an

> explanation of how bb could cause leaky gut and esp breakdown of blood

> brain barrier.

>>

>> They notice that this damage is induced only by virulent strain of bb,

> not by avirulent one. Are the lab lyme tests that are available at the

> moment capable of establishing virulence of the strains found? sorry if

> this is common knowledge, it is new to me

>>

>> also, when treating for lyme, is it possible/documented that bb could

> be provoked to change into more virulent forms? there was a thread

> recently on 'awakening' lyme symptoms through supplements. Any thoughts?

>>

>> Natasa

>>

>>

>> PLoS ONE. 2008;3(12):e4101. Epub 2008 Dec 31.

>> Spent culture medium from virulent Borrelia burgdorferi increases

> permeability of individually perfused microvessels of rat mesentery.

>> Zhou X, ...Department of Physiology and Pharmacology, West Virginia

> University, town, WV, USA.

>> BACKGROUND: Lyme disease is a common vector-borne disease caused by

> the spirochete Borrelia burgdorferi (Bb), which manifests as systemic

> and targeted tissue inflammation. Both in vitro and in vivo studies have

> shown that Bb-induced inflammation is primarily host-mediated, via

> cytokine or chemokine production that promotes leukocyte

> adhesion/migration. Whether Bb produces mediators that can directly

> alter the vascular permeability in vivo has not been investigated. The

> objective of the present study was to investigate if Bb produces a

> mediator(s) that can directly activate endothelial cells resulting in

> increases in permeability in intact microvessels in the absence of blood

> cells. METHODOLOGY/PRINCIPAL FINDINGS: The effects of cell-free, spent

> culture medium from virulent (B31-A3) and avirulent (B31-A) B.

> burgdorferi on microvessel permeability and endothelial calcium

> concentration, [Ca(2+)](i), were examined in individually perfused rat

> mesenteric venules. Microvessel permeability was determined by measuring

> hydraulic conductivity (Lp). Endothelial [Ca(2+)](i), a necessary signal

> initiating hyperpermeability, was measured in Fura-2 loaded

> microvessels. B31-A3 spent medium caused a rapid and transient increase

> in Lp and endothelial [Ca(2+)](i). Within 2-5 min, the mean peak Lp

> increased to 5.6+/-0.9 times the control, and endothelial [Ca(2+)](i)

> increased from 113+/-11 nM to a mean peak value of 324+/-35 nM. In

> contrast, neither endothelial [Ca(2+)](i) nor Lp was altered by B31-A

> spent medium. CONCLUSIONS/SIGNIFICANCE: A mediator(s) produced by

> virulent Bb under culture conditions directly activates endothelial

> cells, resulting in increases in microvessel permeability. Most

> importantly, the production of this mediator is associated with Bb

> virulence and is likely produced by one or more of the 8 plasmid(s)

> missing from strain B31-A. PMID: 19116656

>>

>

>

>

> ------------------------------------

>

>

[Guest guest]

Interesting. Ginko just muscle tested for my dd.. I'm going to give

it a try. Thanks!! Robin

> > > >

> > > >

> > > > Hi Tami and others, I came across this recent paper abstract

on

> > > > borrelia, and found it quite interesting. it shows DIRECT

> damage

> > > induced

> > > > by bb (that is not through inflammatory cytokines produced by

> the

> > > host

> > > > defence system) on the vessels that line the blood. This

offers

> an

> > > > explanation of how bb could cause leaky gut and esp breakdown

> of

> > > blood

> > > > brain barrier.

> > > >

> > > > They notice that this damage is induced only by virulent

strain

> > of

> > > bb,

> > > > not by avirulent one. Are the lab lyme tests that are

available

> > at

> > > the

> > > > moment capable of establishing virulence of the strains

found?

> > > sorry if

> > > > this is common knowledge, it is new to me

> > > >

> > > > also, when treating for lyme, is it possible/documented that

bb

> > > could be

> > > > provoked to change into more virulent forms? there was a

thread

> > > > recently on 'awakening' lyme symptoms through supplements.

Any

> > > thoughts?

> > > >

> > > > Natasa

> > > >

> > > > PLoS ONE. 2008;3(12):e4101. Epub 2008 Dec 31. Spent

> culture

> > > medium

> > > > from virulent Borrelia burgdorferi increases permeability of

> > > > individually perfused microvessels of rat mesentery. Zhou X

> > > > <http://www.ncbi.nlm.nih.gov/sites/entrez?

> > > Db=pubmed & Cmd=Search & Term=%22Z\

> > > > hou%20X%22%5BAuthor%

> > > 5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Results\

> > > >

> >

Panel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus> , ...Department

> > > of

> > > > Physiology and Pharmacology, West Virginia University,

> > town,

> > > WV,

> > > > USA.

> > > > BACKGROUND: Lyme disease is a common vector-borne disease

> caused

> > by

> > > the

> > > > spirochete Borrelia burgdorferi (Bb), which manifests as

> systemic

> > > and

> > > > targeted tissue inflammation. Both in vitro and in vivo

studies

> > have

> > > > shown that Bb-induced inflammation is primarily host-

mediated,

> via

> > > > cytokine or chemokine production that promotes leukocyte

> > > > adhesion/migration. Whether Bb produces mediators that can

> > directly

> > > > alter the vascular permeability in vivo has not been

> > investigated.

> > > The

> > > > objective of the present study was to investigate if Bb

> produces a

> > > > mediator(s) that can directly activate endothelial cells

> > resulting

> > > in

> > > > increases in permeability in intact microvessels in the

absence

> > of

> > > blood

> > > > cells. METHODOLOGY/PRINCIPAL FINDINGS: The effects of cell-

> free,

> > > spent

> > > > culture medium from virulent (B31-A3) and avirulent (B31-A) B.

> > > > burgdorferi on microvessel permeability and endothelial

calcium

> > > > concentration, [Ca(2+)](i), were examined in individually

> > perfused

> > > rat

> > > > mesenteric venules. Microvessel permeability was determined

by

> > > measuring

> > > > hydraulic conductivity (Lp). Endothelial [Ca(2+)](i), a

> necessary

> > > signal

> > > > initiating hyperpermeability, was measured in Fura-2 loaded

> > > > microvessels. B31-A3 spent medium caused a rapid and

transient

> > > increase

> > > > in Lp and endothelial [Ca(2+)](i). Within 2-5 min, the mean

> peak

> > Lp

> > > > increased to 5.6+/-0.9 times the control, and endothelial [Ca

> (2+)]

> > > (i)

> > > > increased from 113+/-11 nM to a mean peak value of 324+/-35

nM.

> In

> > > > contrast, neither endothelial [Ca(2+)](i) nor Lp was altered

by

> > B31-

> > > A

> > > > spent medium. CONCLUSIONS/SIGNIFICANCE: A mediator(s)

produced

> by

> > > > virulent Bb under culture conditions directly activates

> > endothelial

> > > > cells, resulting in increases in microvessel permeability.

Most

> > > > importantly, the production of this mediator is associated

with

> Bb

> > > > virulence and is likely produced by one or more of the 8

plasmid

> > (s)

> > > > missing from strain B31-A. PMID: 19116656

> > > >

> > >

> >

>