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New Study: Hypoxia is a marker in atherosclerotic plaques

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Good morning,

It is always wonderful to read new studies confirming the dangers of

low oxygen - hypoxia.

In the abstract cited below, hypoxia was found to be a key regulating

factor triggering inflammation as well as apoptosis in atherosclerotic

plaques.

Sally

J Vasc Surg. 2010 Aug 17. [Epub ahead of print]

Evidence for markers of hypoxia and apoptosis in explanted human carotid

atherosclerotic plaques.

(Department of Clinical and Experimental Medicine and Vascular Surgery, Section

of Pharmacology, School of Medicine, Messina, Italy.

Abstract

OBJECTIVE: Apoptosis and inflammation are important features of

atherosclerotic plaques. We investigated whether a common signal molecule can

trigger these two apparently separate pathways.

Hypoxia inducible factor (HIF-1alpha) is known to participate in

atherosclerosis and to stimulate apoptosis signal-regulating kinase 1 (ASK-1),

one of the mitogen-activated protein kinases, which is activated by various

extracellular stimuli and involved in a

variety of cellular function.

METHODS: We tested carotid artery specimens from 50 subjects who underwent

angioplasty and five age-matched controls for either Western blot or histologic

analysis. The hypoxic status was investigated by means of HIF-1alpha expression

in carotid specimens.

RESULTS: HIF-1alpha was significantly upregulated in carotid specimens with

respect to controls (P < .05), ASK-1 was detected in plaques of any composition

from lipidic to calcific, and this expression increased with the stage of the

plaque and with the expression of inflammatory (p-ERK, RANK-L, OPG) and

apoptotic molecules (caspase 9, p-p-38, and p-JNK).

CONCLUSION: Our data suggest that hypoxia is the key regulating factor that

triggers inflammation as well as apoptosis in human atherosclerotic plaque.

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Hypoxia, or oxygen shortage, assists plaque formation, and we already know the

major cause of hypoxia.

As a person ages, Plasmin, the only fibrinolytic enzyme, reduces in production.

Its function as a fibrionolytic is to specifically reduce fibrin, (as protease

reduces other protein) thus reducing spontaneous blood coagulation, called

coagulopathy, eroding clots, and reducing inflammation.

When plasmin is reduced, the blood thickens and slows, microcirculation is

reduced, and the blood's oxygen carrying capacity to the tissues is considerably

reduced. As general inflammation increases the it further reduces

microcirculation.

Allopathic medicine seeks to use Warfarin and Coumadin, a dangerous

anticoagulant that gives one a " poor prognosis " in the event of a haemorragic

stroke. Self-health followers instead use metabolic enzymes to reduce

inflammation and jack up the missing plasmin with almost identical enzymes that

have no known side effects and a huge therapeutic window.

Gooogle metabolic enzymes references for my article of several years ago on the

more wholistic approach of simply helping the body's natural fibrinolytic enzyme

plasmin do it's job. The approach actually works better than plasmin and also

increases plasmin output a bit as it goes. BlockBuster AllClear I discuss is the

best on the market IMO; the beauty of BlockBuster AllClear is that it contains

THREE fibrinolytics that work in synergy, also protease for protein, amylase for

starch, and importantly, lipase for fats, plaque included. It even carries a

money back guarantee that it'll work, a guarantee that is valid even for the buy

three get four sale, so save your empty bottles.

I'll place this link; Saul may remove it if the post is too commercial or my

insight and research have no value ;)

http://tinyurl.com/enzymetherapy

That said, I'm a proponent of ozone therapy as well. My wife Jo has been taking

ozone saunas steadily now 3 a week, for about 8 weeks; she's slimming again, has

only 10 pounds to go, and she looks 32 but just turned 49 :) I've done a short

BlockBuster AllClear program but she has not. For most of the details of her

anti-aging approach and mine, see my recent post on the Amegapacific group

http://groups.yahoo.com/group/amegapacific

all good,

Duncan

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