Eat your green roughage.
Lecithin has been compared to tetracycline as a .. standin.

"Lecithin therapy"
"Significantly attenuated by tetracycline, but not by penicillin"

Arthritis Rheum. 2007 Nov 29;56(12):3940-3948 [Epub ahead of print]
Links
Circulating levels of tumor necrosis factor receptors are highly
predictive of mortality in patients with rheumatoid arthritis.
Mattey DL, Glossop JR, Nixon NB, Dawes PT.
University Hospital of North Staffordshire, Hartshill, Stoke‐on‐Trent,
Staffordshire, UK, and Keele University, Keele, Staffordshire, UK.

OBJECTIVE:
To investigate whether circulating levels of soluble tumor necrosis
factor receptors (sTNFR) are predictive of mortality in rheumatoid
arthritis (RA).
METHODS:
Levels of sTNFRI and sTNFRII at study entry were quantified using
enzyme-linked immunosorbent assays in sera from 401 white patients
with RA followed up for 13 years. Patients were tracked via the
National Health Service Central Register, and the relationship between
sTNFR levels and mortality was analyzed using a Cox proportional
hazards regression model. Hazard ratios (HRs) and 95% confidence
intervals (95% CIs) were calculated.
RESULTS:
At the end of the followup period, 132 (32.9%) of 401 patients had
died. Of these, 64 (48.5%) died of cardiovascular disease (CVD).
Significant associations between all-cause mortality and baseline
levels of sTNFRI and sTNFRII were identified in men (HR 1.7 [95% CI
1.2-2.4] and HR 1.18 [95% CI 1.05-1.32], respectively) and women (HR
1.33 [95% CI 0.99-1.8] and HR 1.14 [95% CI 1.02-1.28], respectively).
Analysis including levels of both sTNFRI and sTNFRII indicated that
the sTNFRII level was the best overall predictor of mortality.
Multivariate analysis also revealed that the sTNFRII level was a
predictor of all-cause and CVD mortality independently of age, sex,
disease duration, C-reactive protein level, erythrocyte sedimentation
rate, rheumatoid factor, nodular disease, modified Health Assessment
Questionnaire score, taking CVD drugs, and smoking.
CONCLUSION:
Our data indicate that serum levels of sTNFR are powerful predictors
of mortality in RA. Elevated levels are particularly associated with
mortality due to CVD and may be useful for identifying patients at
increased risk of premature death.

PMID: 18050238 [PubMed - as supplied by publisher]
----------------------------------------------------------------

----------------------------------------------------------------
<<snip>>
The endotoxin-stimulated tumor necrosis factor-alpha release is
decreased by dilinoleoylphosphatidylcholine, the active
phosphatidylcholine (PC) species of polyenylphosphatidylcholine
(PPC).
<<snip>>

Alcohol. 2004 Aug;34(1):9-19. Related Articles, Links

Alcoholic fatty liver: its pathogenesis and mechanism of progression
to
inflammation and fibrosis.

Lieber CS.

Bronx Veterans Affairs Medical Center, Bronx, NY 10468, USA; Mount
Sinai School of Medicine, New York, NY 10029, USA.

Liver disease in the alcoholic is due not only to malnutrition but
also
to ethanol's hepatotoxicity linked to its metabolism by means of the
alcohol dehydrogenase and cytochrome P450 2E1 (CYP2E1) pathways and
the
resulting production of toxic acetaldehyde. In addition, alcohol
dehydrogenase-mediated ethanol metabolism generates the reduced form
of
nicotinamide adenine dinucleotide (NADH), which promotes steatosis by
stimulating the synthesis of fatty acids and opposing their
oxidation.
Steatosis is also promoted by excess dietary lipids and can be
attenuated by their replacement with medium-chain triglycerides.
Through reduction of pyruvate, elevated NADH also increases lactate,
which stimulates collagen synthesis in myofibroblasts. Furthermore,
CYP2E1 activity is inducible by its substrates, not only ethanol but
also fatty acids. Their excess and metabolism by means of this
pathway
generate release of free radicals, which cause oxidative stress, with
peroxidation of lipids and membrane damage, including altered enzyme
activities. Products of lipid peroxidation such as 4-hydroxynonenal
stimulate collagen generation and fibrosis, which are further
increased
through diminished feedback inhibition of collagen synthesis because
acetaldehyde forms adducts with the carboxyl-terminal propeptide of
procollagen in hepatic stellate cells. Acetaldehyde is also toxic to
the mitochondria, and it aggravates their oxidative stress by binding
to reduced glutathione and promoting its leakage. Oxidative stress
and
associated cellular injury promote inflammation, which is aggravated
by
increased production of the proinflammatory cytokine tumor necrosis
factor-alpha in the Kupffer cells. These are activated by induction
of
their CYP2E1 as well as by endotoxin. The endotoxin-stimulated tumor
necrosis factor-alpha release is decreased by
dilinoleoylphosphatidylcholine, the active phosphatidylcholine (PC)
species of polyenylphosphatidylcholine (PPC). Moreover, defense
mechanisms provided by peroxisome proliferator-activated receptor
alpha
and omega fatty acid oxidation are readily overwhelmed, particularly
in
female rats and also in women who have low hepatic induction of fatty
acid-binding protein (L-FABPc). Accordingly, the intracellular
concentration of free fatty acids may become high enough to injure
membranes, thereby contributing to necrosis, inflammation, and
progression to fibrosis and cirrhosis. Eventually, hepatic
S-adenosylmethionine and PCs become depleted in the alcoholic, with
impairment of their multiple cellular functions, which can be
restored
by PC replenishment. Thus, prevention and therapy opposing the
development of steatosis and its progression to more severe injury
can
be achieved by a multifactorial approach: control of alcohol
consumption, avoidance of obesity and of excess dietary long-chain
fatty acids, or their replacement with medium-chain fatty acids, and
replenishment of S-adenosylmethionine and PCs by using PPC. Progress
in
the understanding of the pathogenesis of alcoholic fatty liver and
its
progression to inflammation and fibrosis has resulted in prospects
for
their better prevention and treatment.

PMID: 15670660 [PubMed - in process]

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

<<snip>>
Lecithin therapy may be a useful adjuvant therapy  in patients with
severe
sepsis.
<<snip>>

Intensive Care Med. 2004 Mar 26 [Epub ahead of print] Related
Articles, Links

Effects of polyenylphosphatidylcholine on cytokines, nitrite/nitrate
levels,
antioxidant activity and lipid peroxidation in rats with sepsis.

Demirbilek S, Ersoy MO, Demirbilek S, Karaman A, Akin M, Bayraktar M,
Bayraktar
N.

Department of Anesthesiology and Reanimation, Medical School of Inonu
University, 44315, Malatya, Turkey.

OBJECTIVES.
To determine the effect of pretreatment with
polyenylphosphatidylcholine (lecithin, PPC) on plasma levels of tumor
necrosis
factor (TNF)-alpha, interleukin (IL)-6, IL-10, total nitrite/nitrate
(NOx), and
tissue levels of superoxide dismutase (SOD) and malondialdehyde (MDA)
in septic
rats.
DESIGN. Prospective, randomized, controlled animal study.
SETTING.
University laboratory.
SUBJECTS.
Forty-five Spraque-Dawley rats were divided
into three groups: group C, sham-operated; group S, sepsis; and group
P, sepsis
pretreated with PPC.
INTERVENTIONS.
Rats were made septic by cecal ligation and
puncture (CLP). Group P rats were treated with PPC (100 mg/day orally)
for 10
days before sepsis. Twenty-four hours later CLP, plasma concentrations
of
TNF-alpha, IL-6 and IL-10 and plasma levels of NOx were measured. SOD
and MDA
were determined in liver, lung and heart homogenates.
MEASUREMENTS AND MAIN
RESULTS.
All rats in group P survived during the 24-h observation time after
CLP, whereas survival rate in group S was 66.7% (10/15; P<0.05). PPC
significantly reduced plasma levels of TNF-alpha ( P=0.006), IL-6
( P=0.007),
IL-10 ( P=0.016), NOx ( P<0.001), and tissue levels of MDA ( P<0.001)
in group
P with respect to in group S. Tissue levels of SOD significantly
increased in
group P when compared with group S ( P<0.001).
CONCLUSIONS.
These results show
that PPC pretreatment exerts cumulative effects in decreasing the
levels of
cytokines, NOx, and tissue MDA concentrations, with a concomitant
increase in
survival in septic rats. Lecithin therapy may be a useful adjuvant
therapy in
controlling of the excessive production of the inflammatory cytokines
in
patients with severe sepsis.
DESCRIPTOR. SIRS/sepsis, experimental studies

PMID: 15045164 [PubMed - as supplied by publisher]
--------------------------------------------------------------------------

"PLA inhibitors including tetracyclin and the PLA substrate
phosphatidylcholine"

Int J Mol Med. 2007 Dec;20(6):913-8.Links
Phospholipase A as a potent virulence factor of Vibrio vulnificus.
Koo BS, Lee JH, Kim SC, Yoon HY, Kim KA, Kwon KB, Kim HR, Park JW,
Park BH.
Department of Biochemistry, Medical School and Institute for Medical
Sciences, Chonbuk National University, Jeonbuk 561-756, Korea.

Vibrio vulnificus infection has attracted special interest because of
its high mortality rate. However, the identification of its major
pathogenic determinant still remains obscure. In this study, a
cytolysin-negative mutant strain of V. vulnificus CVD707 was used to
determine the role of phospholipase A (PLA) in the pathogenesis of
this bacterial infection. The mutant strain caused the lysis of
erythrocytes in vitro and elevated plasma hemoglobin during the
infection in mice. Both the hemolytic and PLA activities were
dependent on calcium. Inhibition of hemolysis by PLA inhibitors
including tetracyclin and the PLA substrate phosphatidylcholine also
supports the possibility of membranous PLA as a major hemolytic
factor
in the cytolysin-deficient mutant. To identify the role of PLA in the
pathogenesis of V. vulnificus infection, the effects of tetracycline
on bacteria-induced macrophage cytotoxicity and lethality were
compared with those of penicillin, an antibiotic with no inhibitory
effect on PLA. Both the macrophage cytotoxicity and the lethality of
V. vulnificus CVD707 to mice were significantly attenuated by
tetracycline, but not by penicillin. However, bacterial counts in
culture medium and mouse blood revealed that penicillin was more
effective than tetracycline in killing bacteria under our
experimental
conditions. These results indicate that PLA activity is important in
V. vulnificus-induced cytotoxicity and lethality, suggesting a
crucial
role for PLA in the pathogenesis of V. vulnificus infection.

PMID: 17982702 [PubMed - in process]

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