POZ Community Forums
Meds, Mind, Body & Benefits => Nutrition & HIV => Topic started by: bimazek on February 11, 2007, 03:49:21 pm
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blackberries, raspberries strawberries, and pomegranates
when i eat blackberries, raspberries strawberries, and pomegranates either fresh or at bottom of my yogurt i feel good the next day or two or three. I know that this is physical and not placebo. if you are living with this disease you know there are things that suppress and help...
What are your experiences with blackberries, raspberries strawberries, and pomegranates???
i even found that it only happens when i eat the seeds, which are hard, and end up at bottom of my protein shake, if i eat them i feel good, if i throw those seeds out i have less effect,
so i decided this morning to find out what is in the seed of blackberries, raspberries ...
i did a google search, and quickly found that Ellagic acid is mentioned over and over, there could be other things... but look what i found quickly... and look what i found about... amazing stuff
Ellagic acid is an antioxidant, been said to reduce heart disease, birth defects, liver problems, and to promote wound healing. (if our gut is in constant oxidative stress wouldnt we need more wound healing?)
then here is the clincher...
at the end of the wikipedia article ... it said...
"Clinical tests on cultured human cells also show that ellagic acid prevents the destruction of the p53 gene by cancer cells. Additional studies suggest that one of the mechanisms by which ellagic acid inhibits mutagenesis and carcinogenesis is by forming adducts with DNA, thus masking binding sites to be occupied by the mutagen or carcinogen." (could it be masking or blocking a binding site in hiv?)
when i saw that p53 i almost dropped out of my chair as that is the gene that is involved in hiv in a number of ways that are outlined below... and p53 has been coming up in alot of breakthroughs and new hiv studies...
LOOK IN THESE new hiv studies that have found p53 link with IL-7 CD4 CD8
scan for p53.....
and when u combine this with new info on...IL-7, FasL, pd-1 in my posts here...
seems like eating blackberries, raspberries strawberries, and pomegranates can only help maintain some health in hiv disease.
What are your experiences with blackberries, raspberries strawberries, and pomegranates???
IL-7 ellagic acid
http://scholar.google.com/scholar?hl=en&lr=&q=+il-7+ellagic+acid&btnG=Search
Fas
http://forums.poz.com/index.php?topic=7935.0
pd-1
http://forums.poz.com/index.php?topic=7475.0
IL-7
http://forums.poz.com/index.php?topic=8773.0
hiv initiates t cell death via p53
p53 in mediating cell cycle block and/or apoptosis by HIV
p53 repression of HIV driven transcription
http://scholar.google.com/scholar?q=hiv+p53+&hl=en&lr=&btnG=Search
http://scholar.google.com/scholar?hl=en&q=hiv+ellagic&spell=1
Inhibitory Effects of Egyptian Folk Medicines on HIV Reverse Transcriptase ...
11 compounds were isolated and identified gallic acid,ellagic acid
wikipedia... excerpt...
Ellagic acid is a polyphenol antioxidant found in numerous fruits and vegetables including raspberries, strawberries, cranberries, walnuts, pecans, pomegranates. Plants produce ellagic acid and glucose that combine to form ellagitannins, which are water soluble compounds that are easier for animals and humans to absorb into their diets.
Ellagic Acid and cancer Overview
Research in cell cultures and lab animals has found that ellagic acid may slow the growth of some tumors caused by certain carcinogens. While this is promising, at this time there is no reliable evidence from human studies showing that ellagic acid in any form can prevent or treat cancer
Ellagic acid seems to have some anti-cancer properties. It can act as an antioxidant, and has been found to cause apoptosis (cell death) in cancer cells in the lab.[3]There are also reports that ellagic acid may help the liver to break down or remove some cancer-causing substances from the blood
Some supporters have claimed these results mean that ellagic acid can prevent or treat cancer in humans. This has not been proven. Unfortunately, many substances showing promise against cancer in lab and animal studies have not been found to be useful in people. Ellagic acid has also been said to reduce heart disease, birth defects, liver problems, and to promote wound healing. There are no results from human studies to support these claims at this time.
The Hollings Cancer Institute at the University of South Carolina has conducted a double blind study on a group of 500 cervical cancer patients that gained a lot of attention. Nine years of study have shown that a natural product called ellagic acid is causing G-arrest within 48 hours (inhibiting and stopping mitosis - cancer cell division), and apoptosis (normal cell death) within 72 hours, for breast, pancreas, esophageal, skin, colon and prostate cancer cells.[5]
Clinical tests on cultured human cells also show that ellagic acid prevents the destruction of the p53 gene by cancer cells. Additional studies suggest that one of the mechanisms by which ellagic acid inhibits mutagenesis and carcinogenesis is by forming adducts with DNA, thus masking binding sites to be occupied by the mutagen or carcinogen. Ellagic acid can be found in different foods.
Of six p53-derived peptides possessing an HLA-A24 binding motif, the p53 peptide 125-134 (p53(125-134)) was found to have a high binding capacity and induced peptide-specific CTLs from peripheral blood mononuclear cells, using peptide-pulsed autologous dendritic cells and subsequent cultivation with cytokines interleukin 2 and interleukin 7.
Elevation of CD95 [?] expression by DNA-damaging drugs was notably blocked in MCF-7 cells expressing the human papillomavirus type 16 E6 protein (E6 [?] cells) which prevented p53 accumulation upon DNA damage.
Triggering of Fas (CD95) by its ligand (FasL) rapidly induces cell death via recruitment of the adaptor protein Fas-associated death domain (FADD), resulting in activation of a caspase cascade.
FAP-1 binds to FAS in a ligand-dependent manner and forms a signaling complex that modulates the ability of astrocytoma cells to undergo FAS ligand (FASL)-mediated cell death.
CD95 ligand (CD95L induced mitochondrial cytochrome c [?] release and processing of caspases 3, 7, 8 and 9 in LN-18 cells in the absence of an inhibitor of protein synthesis, cycloheximide (CHX).
The present investigation shows that IFN-alpha induces autocrine cell suicide of Daudi cells by a cross-talk between the CD95 [?] receptor and TNF-alpha.
p53-mediated up-regulation of CD95 [?] is not involved in genotoxic drug-induced apoptosis of human breast tumor cells.
These areas include host genetic predispositions, tumor cytogenetics, molecular genetics (including the Rb, p53, RECQ helicase, and telomere pathways), and metastatic factors (ezrin, annexin 2, chemokine receptor 4, Fas/FasL pathways) that may contribute to both the initiation and the progression of tumor formation.
In the hypothesis that the proinflammatory cytokines and lipopolysaccharide (LPS) in gram-negative sepsis can directly cause renal tubular cell apoptosis via Fas- and caspase-mediated pathways, we examined apoptosis and Fas, Fas ligand, FADD expression, as well as PARP cleavage in cultured human proximal tubular cells under the cytokine and LPS-stimulated conditions.
in contrast, in intermediate CD4(+) CD8(-) CD3(-) thymocytes, the other subpopulation known to allow virus replication, TEC or IL-7 has little or no effect on CXCR4 expression and signaling.
IL-7 induced T-cell proliferation and up-regulated CXCR4 expression in peripheral blood mononuclear cells in vitro.
Both SDF-1alpha and IL-7 plasma levels correlated negatively with the percentage of all subsets of leukocytes expressing CXCR4, across the study groups regardless of the presence or absence of disease.
In addition, IL-7 [?]-induced proliferation but not survival of the developing thymic progenitor cells was strongly inhibited by IFN-alpha.
These results suggest that IL-7 [?]-mediated STAT5 activation is essential for long-term survival of naive CD4 cells after export from thymus, and that another SOCS1-sensitive cytokine is critical for short-term naive T cell survival.
The results show that IL-7 [?] up-regulates MUC1 on CD4+, CD8+, CD25+, CD69+, naive CD45RA+, and memory CD45RO+ T cells.
We show that IL-7 [?] activates PKB [?] and STAT5 in human thymocytes.
These experiments revealed that PI-3K [?]/PKB [?] activation is essential for the survival and proliferation of T cell precursors and suggest that STAT5 activated by IL-7 [?] mediates T cell differentiation.
A murine cell line (IxN/2b) absolutely dependent upon exogenous IL-7 for continued growth has been obtained that expresses lymphoid precursor and class I MHC antigens and also contains a rearranged mu heavy chain.
Thus, the signaling pathways initiated via the p90 [?] IL-7R-associated src kinases are unlikely to be solely responsible for the proliferation of only activated T cells in response to IL-7 [?].
We observed that the stromal cell-derived cytokine interleukin 7 (IL-7) enhances the expression of CD19 molecules on progenitor B-lineage cells in human bone marrow samples and downregulates the expression of terminal deoxynucleotidyl transferase (TdT) and the recombinase-activating genes RAG-1 and RAG-2.
Hence, we identified p59fyn and p53/56lyn to be stimulated by IL-7 [?].
Specific inhibition of IL-7-induced Jak kinase activity ablates p85 [?] tyrosine phosphorylation, subsequent P13 kinase activation, and, ultimately, proliferation.
Similarly, IL-7 [?] enhanced IL-4-induced Ig production in the presence of CD4+ T cells.
IL-7 [?]-driven proliferation is mediated via high affinity IL-7R, and accordingly, Scatchard analysis revealed that, like the p90 [?] IL-7R, the p76 IL-7R bound IL-7 [?] with dual (high; Kd 38 pM and low; Kd 360 pM) affinity.
Although IRS-1 displays a higher degree of basal association, IL-7 [?] induces a much greater increase in the activity associated with IRS-2.
The adhesion molecules LFA-1 [?] and VLA-4 were responsible for the augmented adhesiveness of activated CD4+CD23+ T cells cultured in the presence of IL-7.
Furthermore, PHA activated CD4+ T cells cultured in the presence of IL-7 [?] are polarized to a Th-2 pattern of cytokine production.
On the other hand, a number of molecules co-immunoprecipitated with CDK4 were enhanced in the lysate of IL-7 [?]-stimulated B precursor cells.
Interleukin-7 enhances colony growth and induces CD20 antigen of a Ph+ acute lymphoblastic leukemia cell line, OM9;22.
In liquid culture, more than 80% of IL-7-treated OM9;22 cells express CD20 antigen but fail to express surface immunoglobulins or cytoplasmic mu-chain, indicating that the cells have a potential of limited maturation by IL-7.
In conclusion, MSC [?] mediated IL-7 gene therapy and may be a more feasible strategy to restore immune function following allo-TCD-BMT.
The presence of IL-7 or IL-7R blocking antibodies in lympho-epithelial co-cultures consistently reduced the TEC [?]-mediated apoptosis inhibition in T-ALL blasts (70% decrease).
Previously, we have shown that IL-7 increases viability and proliferation of T cell acute lymphoblastic leukemia (T-ALL) cells by up-regulating Bcl-2 and down-regulating the cyclin-dependent kinase inhibitor p27kip1.
production of interleukin-7 in human intestinal epithelial cells.
Of six p53-derived peptides possessing an HLA-A24 binding motif, the p53 peptide 125-134 (p53(125-134)) was found to have a high binding capacity and induced peptide-specific CTLs from peripheral blood mononuclear cells, using peptide-pulsed autologous dendritic cells and subsequent cultivation with cytokines interleukin 2 and interleukin 7.
Elevation of CD95 [?] expression by DNA-damaging drugs was notably blocked in MCF-7 cells expressing the human papillomavirus type 16 E6 protein (E6 [?] cells) which prevented p53 accumulation upon DNA damage.
Triggering of Fas (CD95) by its ligand (FasL) rapidly induces cell death via recruitment of the adaptor protein Fas-associated death domain (FADD), resulting in activation of a caspase cascade.
FAP-1 binds to FAS in a ligand-dependent manner and forms a signaling complex that modulates the ability of astrocytoma cells to undergo FAS ligand (FASL)-mediated cell death.
CD95 [?] ligand (CD95L [?]) induced mitochondrial cytochrome c [?] release and processing of caspases 3, 7, 8 and 9 in LN-18 cells in the absence of an inhibitor of protein synthesis, cycloheximide (CHX).
The present investigation shows that IFN-alpha induces autocrine cell suicide of Daudi cells by a cross-talk between the CD95 [?] receptor and TNF-alpha.
p53-mediated up-regulation of CD95 [?] is not involved in genotoxic drug-induced apoptosis of human breast tumor cells.
These areas include host genetic predispositions, tumor cytogenetics, molecular genetics (including the Rb, p53, RECQ helicase, and telomere pathways), and metastatic factors (ezrin, annexin 2, chemokine receptor 4, Fas/FasL pathways) that may contribute to both the initiation and the progression of tumor formation.
In the hypothesis that the proinflammatory cytokines and lipopolysaccharide (LPS) in gram-negative sepsis can directly cause renal tubular cell apoptosis via Fas- and caspase-mediated pathways, we examined apoptosis and Fas, Fas ligand, FADD expression, as well as PARP cleavage in cultured human proximal tubular cells under the cytokine and LPS-stimulated conditions.
The CD56+ cells expressed high levels of IL-2R alpha and 75-kDa TNFR in response to IL-12, comparable to what was registered with IL-2 and IL-7 [?].
Of six p53-derived peptides possessing an HLA-A24 binding motif, the p53 peptide 125-134 (p53(125-134)) was found to have a high binding capacity and induced peptide-specific CTLs from peripheral blood mononuclear cells, using peptide-pulsed autologous dendritic cells and subsequent cultivation with cytokines interleukin 2 and interleukin 7.
Furthermore, IELs constitutively expressed the IL-18 receptor in addition to the IL-2 and IL-7 receptors.
Granzyme expression occurs early in cells cultured with IL2 but its presence did not correlate with lytic function; CD56+ cells grown in the presence of IL7 express these enzymes and perforin after longer periods of culture, but lack the ability to lyse NK targets.
We demonstrate that although untreated or IL-2-treated naive T cells are not productively infected by HIV, IL-7 pretreatment mediated the productive infection of laboratory-adapted, M-tropic, and primary isolates of HIV as determined by p24 core antigen production.
IL-2, IL-4 and IL-7 [?] increased uPAR presentation on 20 to 50% of the T cell population, and combined stimulation of bulk cultures demonstrated an additive effect of IL-2 and IL-7 [?], whereas the response to each of the two was inhibited by IL-4.
Induction of T-cell pore-forming protein (PFP) mRNA and cytotoxic potential by IL-7 [?] was both slow and minor compared with that observed in IL-2-cultured T cells.
When cultured in the presence of interleukin 7 or interleukin 2, these thymocytes gave rise to 30-60% CD3/TCR gamma delta medium and high cells (60-70% expressing V delta 1) seen as discrete populations.
In addition to regulating various functions, it is concluded that IL-2 and IL-7 [?] have the ability to prevent PCD in NK cells.
The IL receptor common gamma (gamma c) chain is required for the formation of high affinity cytokine receptor complexes for IL-2 [?], IL-4, IL-7 [?], IL-9 [?], and IL-15 [?], and for signals regulating cell survival, growth, and differentiation.
Finally, we show that IL-2, IL-7 [?], and IL-15, but not IL-21, reverse the anergic phenotype of CD4(+)CD25(+) T cells.
IL-2 or IL-7 [?] was effective in increasing melanoma-specific cytotoxic T lymphocyte (CTL) activity in cultures where CD8 T cells were predominant, whereas IL-4 followed by IL-2 was most effective in cultures where CD4 T cells predominated.
We therefore examined levels of the T-cell trophic cytokines IL-2, IL-4, IL-7 [?], IL-12, IL-13, and IL-15 in plasma in 93 CTCL patients and healthy controls.
METHODS: Duodenal biopsy specimens (14 treated and 13 untreated celiac patients, 7 controls) were cultured in vitro for 24 hours with or without gliadin (1 mg/mL), IL-15, IL-7, IL-4, or IL-2 (10 ng/mL).
One gene induced by IL-2, IL-7, and IL-15 but not IL-4 was dual-specificity phosphatase 5 (DUSP5).
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Compared to the effects of IL-2, IL-7 induced lower, but substantial levels of granulocyte-macrophage colony-stimulating factor (GM-CSF) mRNA, and IL-7 was a more potent GM-CSF-inducing stimulus than IL-12.
Addition of FLT-3 ligand to IL-2, IL-7 [?] SCF, and stromal factors are important in early stages of NK development.
Our data suggest that the expression of both CD80 and IL-2 plus IL-7 [?] can enhance the efficacy of tumor vaccines. In the present study, we found that IL-7 [?] was significantly more effective at enhancing HIV-1 proviral reactivation than either IL-2 alone or IL-2 combined with phytohemagglutinin (PHA) in CD8-depleted PBMCs.
The requirement for IL-2 and CD28 signals is not linked to promoting T-cell division and expansion but most likely due to their capacity to (i) promote effector cell differentiation; (ii) induce survival proteins, and, as we discuss in more detail; (iii) program expression of receptors for 'memory survival factors' such as IL-7 .
IL-2 and IL-15 prevented the spontaneous death of CD4+ and CD8+ T cells, whereas IL-10 prevented only CD8 T-cell death and IL-7 [?] had no effect on T-cell death.
The CD56+ cells expressed high levels of IL-2R alpha and 75-kDa TNFR in response to IL-12, comparable to what was registered with IL-2 and IL-7 [?]. Of six p53-derived peptides possessing an HLA-A24 binding motif, the p53 peptide 125-134 (p53(125-134)) was found to have a high binding capacity and induced peptide-specific CTLs from peripheral blood mononuclear cells, using peptide-pulsed autologous dendritic cells and subsequent cultivation with cytokines interleukin 2 and interleukin 7.
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the drink company named "Naked" sells a pomegranate juice and it tastes just like kool-aid. after i drink it i feel fresh and in a good mood. same is true after i eat fresh blueberries and fresh pineapple. oh yeah, green apples too
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I have blackberries, raspberries strawberries, on a regular basis, depending on availability in the super markets. all that is good for ya. Some people may have an allergic reaction to strawberries though.
Pomegranate , I take in the concentrated form. I try to remember to take once ounce per day.
Once ounce is equivalent to eating 15 pomegranates. My energy levels aren't too bad. I get the biggest boost, when I take Subligual - B-12. I feel a boost about 30 minutes after that. I haven't researched, exactly whats in all these fruits, but as I understand and read about them,, the antioxidant levels are good, that's why I eat them regularly. Also big into unsweetened Apple juice and grape juice. Orange juice is a little too acidic for me, but I will have it on occasion.
Ray
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Also try Black Current juice. it claims to have more antioxidants than the other berries alone.
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Apples, Grapes and blueberries are good sources of polyphenols -- according to sources... polyphenols inactive viruses in test tubes -- hope is it does the same in the blood.. i find it helpes me-- i'm sure all berries and fruits in these families do the same.
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thanks for the info... seems like there is lots of info on
polyphenol and hiv
http://scholar.google.com/scholar?q=polyphenol+hiv&hl=en&lr=&btnG=Search
Naturally derived anti-HIV agents. -
... Phytother. Res. 19, 557–581 (2005) FLAVONOIDS Flavonoids and related
polyphenols possess promis- ing anti-HIV activity. A number ...
Green tea polyphenol epigallocatechin gallate binding to CD4 as a model for the inhibition of HIV-1- …
- The Journal of Allergy and Clinical Immunology, 2004 - Elsevier... Abstract. Green tea polyphenol epigallocatechin gallate binding to CD4 as a model
for the inhibition of HIV-1-gp120 binding to CD4+ T cells
Polyphenols inhibit promotional phase of tumorigenesis: relevance of superoxide
radicals. Nutr. ... Inhibition of HIV infection by caffeoylquinic acid derivatives
When screening fruit juices for inhibitory activity against HIV- 1 using CD4 and ...
cacy is ascribed to its polyphenol compounds and possibly to other constituents ..
polyphenol in Foods
Notable sources of polyphenols include berries, tea, beer, wine, olive oil, chocolate/cocoa, walnuts, peanuts, yerba mate, and other fruits and vegetables. High levels of polyphenols can generally be found in the fruit skins.Health claims Main article: polyphenol antioxidant Research indicates that polyphenols may have antioxidant characteristics with potential health benefits. They may reduce the risk of cardiovascular disease and cancer.[2] polyphenols have also been investigated as a source of additional health benefit in organic produce, but no conclusion was made[3].It is believed that polyphenols can bind with nonheme iron (from plant sources) and decrease its absorption by the body by up to 50%
http://scholar.google.com/scholar?as_q=polyphenol+hiv&num=100&btnG=Search+Scholar&as_epq=&as_oq=&as_eq=&as_occt=any&as_sauthors=&as_publication=&as_ylo=2005&as_yhi=2007&as_allsubj=all&hl=en&lr=
Oxidative Stress and Therapeutic Approaches in HIV Dementia - group of 3 »
J Steiner, N Haughey, W Li, A Venkatesan, C … - Antioxid Redox Signal, 2006 - liebertonline.com
... Polyphenols also have antioxidant capabilities. HIV-positive patients who drank
fruit and vegetable juices had increased lym- phocyte proliferation, which ...
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Dried blueberries are great to reduce diarrhoea. Lots of vitamins, tannins and antioxidants.
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My experience with Berries and Pomegranates are they cost a fortune. lol
I do however notice that they definitely do a lot of good things.
Normally after having berries, I manage to sleep wonderfuly at night!
I notice they make you feel very "active" but not in an excessive way.
They're high in antioxidants and rare vitamins. They have high amounts of vitamin C.
If I had the money, I'd live off the stuff! ^^
Hugs,
Kent
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I've stopped eating regular cereal but buy a granola from one store and another store I find great berries dried and add them to the granola in a large container along with some nuts. Often I have blueberries cranberries and anything else that is on the store shelves in the mix. This really holds me for the morning instead of being hungry in 2 hours.
Lately tho I read a scientific research was trying to increase antioxidant effects and found a spash of alcohol greatly increases this with fruit. Somehow I don't think a jigger of vodka on my granola is a good rationalization to increase antioxidants.
glenn
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All make are ingredients for great sorbets. The nice thing is you can buy them in season and then store them when buying them is prohibitive. Also, Billberry, a relative of the blueberry, is also a great antioxidant and is available in pill form as well.
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i know they are expensive and i dont eat them as much because of that either
but i get them in yogurt, like raspberry and it is on bottom and the whole thing is like 50 cents including the raspberries
anyway
now my big thing is raw juise
see my post
carrot beet celery