The way cancer kills a person is more brutal then cartels

[TsarTsar444]

When it metastasizes in your bones...It literally starts breaking them from the growth everywhere in your whole body, one of the most painful ways to die, easily in the top 5, imagine seeing your son, daughter or parents going through this jfl, even cartels cutting you limb from limb is less painful, but no cuck will tell you this. Jfl at cancer still not being curable easily, what a clown world, same for noorwoding.

But muh Mars landing 2024 NASA funding is soo cool sweety, heking Elon Musk

 

[stuckneworleans]

Cancer is a trillion dollar industry. Imagine thinking the patient's health is the priority in modern medicine.

 

[Deleted member 11414]

one of my childhood best friends has cancer, its really sad, he's like the most kind hearted person you'll ever meet as well

 

[Deleted member 5189]

its the treatment for cancer that kills them.

 

[Deleted member 5189]

one of my childhood best friends has cancer, its really sad, he's like the most kind hearted person you'll ever meet as well

thx bro

 

[Albeacho]

one of my childhood best friends has cancer, its really sad, he's like the most kind hearted person you'll ever meet as well

 

[TsarTsar444]

Cancer is a trillion dollar industry. Imagine thinking the patient's health is the priority in modern medicine.

Brutal, they will never find a super effective cheap treatment then, jfl at these cucks

 

[Ronnie Kray]

Better than inceldom

 

[TsarTsar444]

Better than inceldom

Cope, you can do surgeries, roid, dark triad cartel max etc. Lot of options, being eaten alive from your own cells for months and not being able to do anything about it is bruuuutall

 

[Ronnie Kray]

Cope, you can do surgeries, roid, dark triad cartel max etc. Lot of options, being eaten alive from your own cells for months and not being able to do anything about it is bruuuutall

Of course chad

 

[goat2x]

i had one of my family member dying from cancer

seeing it slowly consuming them away is brutal

lack of hair, shit collagen, wrinkles, they become skinny and quiet

its like they are slowly walking to the grave tbh

 

[Jason Voorhees]

The black plague was more brutal imo

 

[( ( ( d[-_-]b ) ) )]

i had one of my family member dying from cancer

seeing it slowly consuming them away is brutal

lack of hair, shit collagen, wrinkles, they become skinny and quiet

its like they are slowly walking to the grave tbh

Same here man.

 

[TsarTsar444]

The black plague was more brutal imo

No, it has 90% cure rate today, much more then cancer, also it kills you in a few days. How cancer kills is skewed because cancer patients are pumped up with opoids, but without them its much more brutal then black death, jfl its literally breaking your bones for days slowly

 

[Jason Voorhees]

No, it has 90% cure rate today, much more then cancer, also it kills you in a few days. How cancer kills is skewed because cancer patients are pumped up with opoids, but without them its much more brutal then black death, jfl its literally breaking your bones for days slowly

What Cancer are u talking about?

 

[TsarTsar444]

What Cancer are u talking about?

Majority of them, they all have the same symptoms in the late stage when they metastasize in your bones, its completely over when it reaches the bones

 

[Adriana Lima]

damm @Hozay better step up your game

 

[BigJimsWornOutTires]

People are a cancer.

 

[Deleted member 11414]

what type and stage is it? do doctors think hes gonna live long?

its adrenaline glands and idk what stage it is but he's been in chemo for a while and he has a good chance of surviving its still brutal though

 

[Deleted member 11414]

hope he recovers ngl.

me too, he's probably one of the nicest people i've ever met and he's the kind of person who just has zero hate in him what so ever

 

[coolguy1]

Eat cow shit to give yourself salmonella
source: Aajonus

 

[Deleted member 5189]

Eat cow shit to give yourself salmonella
source: Aajonus

salmonella sounds like a nice name for a girl tbh

 

[mogstar]

its the treatment for cancer that kills them.

Care to elaborate genius ?

 

[Deleted member 5189]

Care to elaborate genius ?

 

[Deleted member 6403]

PUFAs and estrogen cause cancer. Serious.

 

[TsarTsar444]

PUFAs and estrogen cause cancer. Serious.

Women get less cancer then men i think, so its not true, women live longer

 

[coolguy1]

Wtf just happened there?

 

[Deleted member 6403]

Women get less cancer then men i think, so its not true, women live longer

The study only focuses on the lymphatic system and its cells, but the principle is general and has been observed in other organ/tissue cells. The most obvious example is cancer - no matter which organ it occurs in, the tumor is composed of de-differentiated cells not unlike the stem cells from which all other tissues/organs develop. In fact, the developing embryo can be viewed as a massive tumor, which is under the control of powerful differentiating fields produced by the mother's organism, placenta, etc. When those differentiating fields are lost/weakened in an adult organism then various developmental pathologies start to manifest including protein misfolding/accumulation, fibrosis and, of course, cancer. The study below demonstrates that all that is needed for such de-differentiation to occur is loss of mitochondrial function (and as such OXPHOS). In other words, the morphogenetic fields (and thus the cell's fate, in the authors' own words) require efficient energy production and without this energy the cells quickly revert to their primordial, de-differentiated, ravenous, growing state (e.g. cancer).

Mitochondrial respiration controls the Prox1-Vegfr3 feedback loop during lymphatic endothelial cell fate specification and maintenance | Science Advances
Mitochondria play key role in lymphatic development

"..."For the first time, we've defined that mitochondria activities are also required for cell fate—a concept that a few years ago was unthinkable," said Oliver, who is also a professor of Medicine in the Division of Nephrology and Hypertension and director of the Center for Vascular and Developmental Biology at the Feinberg Cardiovascular and Renal Research Institute. "We believe this is probably a more common functional role—cell specification and migration happens in a variety of cell types and tissues."

"...Navdeep Chandel, Ph.D., the David W. Cugell, MD, Professor of Medicine in the Division of Pulmonary and Critical Care, a professor of Biochemistry and Molecular Genetics and co-author of the study, previously discovered that deletion of mitochondrial complex III in blood endothelial cells of young mice affected the endothelial cells' proliferation and migration. "I was surprised by those results from Navdeep's lab because I believed that without mitochondrial respiration those cells would die," Oliver said. Oliver, along with Wanshu Ma, Ph.D., a postdoctoral fellow in the Oliver laboratory and lead author of the study, removed mitochondrial complex III—a structure essential for cellular respiration —from lymphatic endothelial cells in mouse embryos. Surprisingly, the investigators found that without mitochondria complex III, the number of lymphatic progenitor cells was greatly reduced, and those that did leave the vein quickly lost their lymphatic cell fate by reverting back to their original blood vasculature phenotype. This was caused by downregulation of VEGFR3, which in turn downregulates Prox1, a master regulator constantly required to maintain lymphatic cell fate, according to Ma. "These cells are losing the very features that make them lymphatics," Ma said. Using several experimental approaches, the scientists also discovered that without mitochondrial complex III and cellular respiration, certain metabolic byproducts were missing from the cells, which acted as a signal that enough lymphatic endothelial progenitor cells have left the vein and the Prox1-VEGFR3 feedback loop can shut down. "This is probably a general sensor of the metabolic status of the cell, somehow capable of sensing the micro-environment and detecting what the cells need to do," Oliver said. While this study only examined lymphatic endothelial cell development, Oliver said he believes that mitochondria are likely vital for this process elsewhere, and Chandel has shown that similar signaling is crucial for stem cell development and in tumor formation. "We believe this is a more global phenomenon—not just regarding lymphatics, but for every differentiating cell type," Oliver said.

 

[Deleted member 6403]

Women get less cancer then men i think, so its not true, women live longer

As the study below discusses, all PUFA, but especially omega-3, are about as potent as glucocorticoids in inducing T-cell death. Modern medicine has already recognized that anything that suppresses T-cell formation likely increases cancer risk, and some of the most promising cancer therapies to get recently approved are precisely T-cell activity boosters (e.g. Opdivo). Hopefully, the study below will give all PUFA fans a pause and reconsideration before they continue consuming this carcinogenic, immunosuppressive poison.

Polyunsaturated fatty acids, membrane organization, T cells, and antigen presentation

'"...Although the studies are not conclusive and there are conflicting reports (17), the n−3 PUFAs decrease specific disease symptoms and the need for antiinflammatory drugs for patients with chronic inflammatory diseases (6, 18). n−3 Fatty acids may be immunosuppressive agents for a variety of inflammatory ailments, including Crohn disease, atherosclerosis, colitis, graft-versus-host disease, rheumatoid arthritis, psoriasis, multiple sclerosis, asthma, and systemic lupus erythematosus (19–28). "

"...A series of studies from Kleinfeld’s laboratory (55) showed that unsaturated free fatty acids (FFAs) could inhibit specific aspects of cytotoxic T cell function by perturbing membranes. Initially, it was shown that short-term exposure of murine allogeneic effector T cells to low levels of unsaturated FFAs (<10 μmol/L), including PUFAs, inhibited lysis of target APCs. The change in lysis of target cells was a direct consequence of the FFA added to the CTLs, because lysis could be inhibited by extracting the unsaturated FFA with bovine serum albumin before CTL-target conjugation (55). Specific aspects of T cell function inhibited by unsaturated lipids included the initial rise in intracellular [Ca2+] on conjugate formation, protein phosphorylation events, and subsequent CTL esterase release. On the other hand, release of inositol phosphates and binding to target cells were unaffected (55–59). Because the inhibition in CTL calcium release linearly correlated with the decrease in membrane acyl chain order induced by the presence of increasing unsaturation in the plasma membrane (56), it was hypothesized that modulation of membrane structure affected T cell Ca2+ signaling. Information on the effects of PUFAs on the T cell calcium response has continued to grow (60, 61). For example, Stulnig et al (61) showed that administration of PUFAs reduced the calcium response dose dependently in vitro on stimulation of Jurkat T lymphocytes. Although no change was observed with the saturated palmitic acid, maximal effects were observed with GLA and DGLA and modest effects with EPA and AA."

"...Some of the in vivo or ex vivo data on PUFAs and T cell function are consistent with findings from cell culture. For example, healthy persons infused with lipids to elevate serum PUFAs had a reduced calcium response of their CD4+ and CD8+ T cells (61). Also, feeding mice n−3 PUFAs, predominately DHA, lowered the proliferative response of splenic T lymphocytes on in vitro stimulation through CD28 and the TCR/CD3 complex (74)...Inner leaflet lipids (eg, PEs and PSs) isolated from mice fed diets rich in fish oils were enriched with PUFAs to a greater extent than were outer leaflet lipids (77, 78). Surprisingly, it was also observed that the sphingomyelin content of DRM fractions was significantly (≈30%) lower in fish oil–fed mice than in control corn oil–fed animals (77, 78). In the same study, recruitment of PKCθ into rafts of T cells from mice fed diets supplemented with fish oils or purified DHA was inhibited relative to cells isolated from mice fed corn oil. In addition, receptor-induced activation of the transcription factors AP-1 and nuclear transcription factor κB was lowered and, consequently, IL-2 production and T cell proliferation were inhibited in cells isolated from fish oil–fed mice (78). Fish oil–fed mice also show elevated concentrations of Fas colocalization with raft molecules in naive T cells (78). In light of data that showed that n−3 PUFAs enhanced activation induced cell death in T cells (79), it was speculated that Fas relocalization by PUFAs may be yet another mechanism by which n−3 PUFAs inhibit T cell activity (78, 80)."

"...

1. 1) PUFA incorporation disrupts sphingomyelin-cholesterol microdomain formation and alters signal transduction. A perturbation in the stability of liquid ordered microdomains by PUFAs changes the distribution of proteins between domains as readout by localization to either DRMs or DSMs (assuming that detergent extraction is some crude representation of differing membrane heterogeneities). The physical disruption would be driven by the low affinity of cholesterol for PUFA acyl chains. Disruption of liquid ordered domains by PUFAs may also explain the reduction in sphingomyelin concentrations in DRM fractions in ex vivo studies (77). Indeed, raft disruption by cholesterol depletion has been shown to effect cellular signaling (141).
2. 2) DRMs may not accurately depict the differing types of lipid microdomains that may sequester into these fractions. It has become increasingly clear from cell studies that raft microdomains may exist as nanoclusters <5 nm, with a few glycosylphosphatidylinositol-anchored proteins in each cluster (142). It has been suggested that there is tremendous heterogeneity in DRM microdomains (51) and it is reasonable to speculate that PUFA microdomains may exist on a nanometer scale (143). Therefore, PUFA-rich microdomains may show up in DRM fractions but may still segregate from liquid ordered domains based on steric incompatibility between cholesterol and PUFAs. These interactions may trigger protein displacement and loss of function.
3. 3) On dietary intake, most PUFAs are esterified to phospholipids in the sn-2 position, with saturated acyl chains in the sn-1 position. Therefore, the sn-1 chains may participate in microdomain formation with cholesterol and exclude PUFAs, as suggested by the work of Huster et al (1998). However, during detergent extraction, the high affinity between the sn-1 chain and cholesterol may result in PUFA enrichment in the DRM fraction. Even though biochemical analysis of DRMs shows substantial amounts of PUFAs, they are not directly involved in the formation of liquid ordered domains.
4. 4) PUFA incorporation into cells drives cholesterol from the outer to the inner leaflet (144, 145). The efflux of cholesterol may drive changes in outer and inner leaflet microdomain formation. The signaling complexes of the inner leaflet may respond to a reduction in cholesterol concentrations and alter T cell signaling. Our laboratory has shown that cholesterol depletion can result in a reorganization of the actin cytoskeleton (106). Perhaps PUFA-induced changes in cholesterol also alter the organization of the cytoskeleton, which could modify cellular signaling."

"...As the data grow on how select PUFAs may modulate inflammatory and autoimmune diseases, there is a growing need for elucidating the underlying molecular mechanisms. An understanding of the effect of PUFAs at the level of T cell membrane organization is only starting to emerge, whereas relatively little is known about membrane modulation of APCs. The data from cellular and animal studies tell us that PUFAs induce changes in localization of proteins from DRM to DSM fractions, which has measurable consequences for T cell signaling and proliferation. However, the mechanisms by which PUFAs induce changes in protein localization are not known, and it is here that model membrane experiments suggest testable hypotheses. We know that PUFA-containing phospholipids impart unique structural effects on bilayers, but what is required is better knowledge of how these effects translate into functional consequences at the cellular level. Further investigation at the interface between model bilayers and cellular systems may answer some questions regarding PUFA-raft interactions. How PUFAs modulate MHC conformation, vertical orientation, lateral organization, and trafficking—on the basis of literature reports and some data from our own laboratory—also requires extensive investigation at all levels, from synthetic bilayers to animal experiments. Because dietary intake of PUFAs will result in a distribution to virtually every cell of the body, the changes described above for APCs are also applicable to T cells. PUFA modification of cellular membranes may be an important target for immunosuppression."

 

[Deleted member 6403]

Women get less cancer then men i think, so its not true, women live longer

Apparently, mainstream medicine has managed to convinced the public somehow that there are carcinogenic and non-carcinogenic estrogens. An example of the former would be (17)-beta-estradiol and an example of the latter would be (17)-alpha-estradiol. The former is a strong agonist/activator of both estrogen receptors while the latter binds and interacts with those receptors very weakly. That is precisely the reason, medicine has been claiming that alpha-estradiol is non-carcinogenic. While beta-estradol has been officially labelled a "known carcinogen" by the National Institute of Environmental Health Sciences (NIEHS), which is a part of the National Institutes of Health (NIH) and as such Department of Health and Human Services (HHS), the alpha isomer has not. Now, the article is almost 17 years old and many things have changed since then. Namely, mainstream medicine has completely ignored the NIEHS announcement and has also been staging attacks on the results of the WHI studies that demonstrated beta-estradiol causes cancer, heart disease, strokes, dementia, etc. So, 17 years after the (still standing) official classification of estrogen as a carcinogen by the very "experts" we are all told to obey, the new position of those same experts is that neither the beta nor the alpha isomers of estradiol are carcinogenic. One of the main justifications given for the renewed promotion of estrogen is that it acts as an "antioxidant", yet the study below found the exact opposite - estrogen, by itself, can cause oxidative stress that is crucial for carcinogenesis. To me, at least, the evidence is quite clear and in plain sight - there is no such thing as a safe estrogen! Especially, in the presence of PUFA, which amplifies estrogen's genomic/receptor effects and also increases oxidative stress.

http://www.columbia.edu/cu/record/archives/vol28/vol28_iss16/Pg8-2816.pdf

"...It's disconcerting to think that a natural hormone circulating in significant amounts through the bodies of half the world's population is a carcinogen, but it's now official. In December, the National Institute of Environmental Health Sciences (NIEHS) added estrogen to its list of known cancer-causing agents. For years, estrogen has been a suspected carcinogen, since strong epidemiological evidence associates the hormone to breast, endometrial, and uterine cancers. Women who begin menstruating early, or who start menopause late, produce more estrogen over their lifetimes and have a higher risk of breast cancer. Recently, the clinical trial of estrogen plus progestin treatment therapy was terminated because of an increased risk of breast cancer."

"...To see if cancer-causing estrogens need oxygen radicals to produce tumors, Bhat implanted pellets of the hormone in hamsters that are susceptible to estrogen-induced kidney cancer. This model is widely used as an animal model of hormonal cancer. As expected, when the carcinogenic 17beta-estradiol (E2) was used, nearly all hamsters with the pellets developed cancer within seven months. E2 promotes cell proliferation and produces oxygen radicals when metabolized by the cell."

"...Also, as expected, none of the hamsters developed kidney cancer when a non-carcinogenic estrogen, 17-alpha-ethinyl-estradiol (EE) was implanted. EE acts through estrogen receptors to create new cells like E2, but unlike E2, is poorly broken down and does not produce oxygen radicals. But when EE was combined with a non-estrogen molecule that generates oxygen radicals, 30 percent of the hamsters developed kidney cancer within seven months."

"...But it also suggests that reputedly "safe" estrogens that are touted as replacements for the estrogens in hormone replacement therapy may not be so safe after all. "If we have oxidative stress in cells from other chemicals, then women are at risk for cancer even with estrogens that are considered non-carcinogenic," Bhat says. "The therapy may be safer if taken with antioxidants, but more research is needed to make safe and more effective antioxidants."

 

[Deleted member 5189]

The study only focuses on the lymphatic system and its cells, but the principle is general and has been observed in other organ/tissue cells. The most obvious example is cancer - no matter which organ it occurs in, the tumor is composed of de-differentiated cells not unlike the stem cells from which all other tissues/organs develop. In fact, the developing embryo can be viewed as a massive tumor, which is under the control of powerful differentiating fields produced by the mother's organism, placenta, etc. When those differentiating fields are lost/weakened in an adult organism then various developmental pathologies start to manifest including protein misfolding/accumulation, fibrosis and, of course, cancer. The study below demonstrates that all that is needed for such de-differentiation to occur is loss of mitochondrial function (and as such OXPHOS). In other words, the morphogenetic fields (and thus the cell's fate, in the authors' own words) require efficient energy production and without this energy the cells quickly revert to their primordial, de-differentiated, ravenous, growing state (e.g. cancer).

Mitochondrial respiration controls the Prox1-Vegfr3 feedback loop during lymphatic endothelial cell fate specification and maintenance | Science Advances
Mitochondria play key role in lymphatic development

"..."For the first time, we've defined that mitochondria activities are also required for cell fate—a concept that a few years ago was unthinkable," said Oliver, who is also a professor of Medicine in the Division of Nephrology and Hypertension and director of the Center for Vascular and Developmental Biology at the Feinberg Cardiovascular and Renal Research Institute. "We believe this is probably a more common functional role—cell specification and migration happens in a variety of cell types and tissues."

"...Navdeep Chandel, Ph.D., the David W. Cugell, MD, Professor of Medicine in the Division of Pulmonary and Critical Care, a professor of Biochemistry and Molecular Genetics and co-author of the study, previously discovered that deletion of mitochondrial complex III in blood endothelial cells of young mice affected the endothelial cells' proliferation and migration. "I was surprised by those results from Navdeep's lab because I believed that without mitochondrial respiration those cells would die," Oliver said. Oliver, along with Wanshu Ma, Ph.D., a postdoctoral fellow in the Oliver laboratory and lead author of the study, removed mitochondrial complex III—a structure essential for cellular respiration —from lymphatic endothelial cells in mouse embryos. Surprisingly, the investigators found that without mitochondria complex III, the number of lymphatic progenitor cells was greatly reduced, and those that did leave the vein quickly lost their lymphatic cell fate by reverting back to their original blood vasculature phenotype. This was caused by downregulation of VEGFR3, which in turn downregulates Prox1, a master regulator constantly required to maintain lymphatic cell fate, according to Ma. "These cells are losing the very features that make them lymphatics," Ma said. Using several experimental approaches, the scientists also discovered that without mitochondrial complex III and cellular respiration, certain metabolic byproducts were missing from the cells, which acted as a signal that enough lymphatic endothelial progenitor cells have left the vein and the Prox1-VEGFR3 feedback loop can shut down. "This is probably a general sensor of the metabolic status of the cell, somehow capable of sensing the micro-environment and detecting what the cells need to do," Oliver said. While this study only examined lymphatic endothelial cell development, Oliver said he believes that mitochondria are likely vital for this process elsewhere, and Chandel has shown that similar signaling is crucial for stem cell development and in tumor formation. "We believe this is a more global phenomenon—not just regarding lymphatics, but for every differentiating cell type," Oliver said.

As the study below discusses, all PUFA, but especially omega-3, are about as potent as glucocorticoids in inducing T-cell death. Modern medicine has already recognized that anything that suppresses T-cell formation likely increases cancer risk, and some of the most promising cancer therapies to get recently approved are precisely T-cell activity boosters (e.g. Opdivo). Hopefully, the study below will give all PUFA fans a pause and reconsideration before they continue consuming this carcinogenic, immunosuppressive poison.

Polyunsaturated fatty acids, membrane organization, T cells, and antigen presentation

'"...Although the studies are not conclusive and there are conflicting reports (17), the n−3 PUFAs decrease specific disease symptoms and the need for antiinflammatory drugs for patients with chronic inflammatory diseases (6, 18). n−3 Fatty acids may be immunosuppressive agents for a variety of inflammatory ailments, including Crohn disease, atherosclerosis, colitis, graft-versus-host disease, rheumatoid arthritis, psoriasis, multiple sclerosis, asthma, and systemic lupus erythematosus (19–28). "

"...A series of studies from Kleinfeld’s laboratory (55) showed that unsaturated free fatty acids (FFAs) could inhibit specific aspects of cytotoxic T cell function by perturbing membranes. Initially, it was shown that short-term exposure of murine allogeneic effector T cells to low levels of unsaturated FFAs (<10 μmol/L), including PUFAs, inhibited lysis of target APCs. The change in lysis of target cells was a direct consequence of the FFA added to the CTLs, because lysis could be inhibited by extracting the unsaturated FFA with bovine serum albumin before CTL-target conjugation (55). Specific aspects of T cell function inhibited by unsaturated lipids included the initial rise in intracellular [Ca2+] on conjugate formation, protein phosphorylation events, and subsequent CTL esterase release. On the other hand, release of inositol phosphates and binding to target cells were unaffected (55–59). Because the inhibition in CTL calcium release linearly correlated with the decrease in membrane acyl chain order induced by the presence of increasing unsaturation in the plasma membrane (56), it was hypothesized that modulation of membrane structure affected T cell Ca2+ signaling. Information on the effects of PUFAs on the T cell calcium response has continued to grow (60, 61). For example, Stulnig et al (61) showed that administration of PUFAs reduced the calcium response dose dependently in vitro on stimulation of Jurkat T lymphocytes. Although no change was observed with the saturated palmitic acid, maximal effects were observed with GLA and DGLA and modest effects with EPA and AA."

"...Some of the in vivo or ex vivo data on PUFAs and T cell function are consistent with findings from cell culture. For example, healthy persons infused with lipids to elevate serum PUFAs had a reduced calcium response of their CD4+ and CD8+ T cells (61). Also, feeding mice n−3 PUFAs, predominately DHA, lowered the proliferative response of splenic T lymphocytes on in vitro stimulation through CD28 and the TCR/CD3 complex (74)...Inner leaflet lipids (eg, PEs and PSs) isolated from mice fed diets rich in fish oils were enriched with PUFAs to a greater extent than were outer leaflet lipids (77, 78). Surprisingly, it was also observed that the sphingomyelin content of DRM fractions was significantly (≈30%) lower in fish oil–fed mice than in control corn oil–fed animals (77, 78). In the same study, recruitment of PKCθ into rafts of T cells from mice fed diets supplemented with fish oils or purified DHA was inhibited relative to cells isolated from mice fed corn oil. In addition, receptor-induced activation of the transcription factors AP-1 and nuclear transcription factor κB was lowered and, consequently, IL-2 production and T cell proliferation were inhibited in cells isolated from fish oil–fed mice (78). Fish oil–fed mice also show elevated concentrations of Fas colocalization with raft molecules in naive T cells (78). In light of data that showed that n−3 PUFAs enhanced activation induced cell death in T cells (79), it was speculated that Fas relocalization by PUFAs may be yet another mechanism by which n−3 PUFAs inhibit T cell activity (78, 80)."

"...

1. 1) PUFA incorporation disrupts sphingomyelin-cholesterol microdomain formation and alters signal transduction. A perturbation in the stability of liquid ordered microdomains by PUFAs changes the distribution of proteins between domains as readout by localization to either DRMs or DSMs (assuming that detergent extraction is some crude representation of differing membrane heterogeneities). The physical disruption would be driven by the low affinity of cholesterol for PUFA acyl chains. Disruption of liquid ordered domains by PUFAs may also explain the reduction in sphingomyelin concentrations in DRM fractions in ex vivo studies (77). Indeed, raft disruption by cholesterol depletion has been shown to effect cellular signaling (141).
2. 2) DRMs may not accurately depict the differing types of lipid microdomains that may sequester into these fractions. It has become increasingly clear from cell studies that raft microdomains may exist as nanoclusters <5 nm, with a few glycosylphosphatidylinositol-anchored proteins in each cluster (142). It has been suggested that there is tremendous heterogeneity in DRM microdomains (51) and it is reasonable to speculate that PUFA microdomains may exist on a nanometer scale (143). Therefore, PUFA-rich microdomains may show up in DRM fractions but may still segregate from liquid ordered domains based on steric incompatibility between cholesterol and PUFAs. These interactions may trigger protein displacement and loss of function.
3. 3) On dietary intake, most PUFAs are esterified to phospholipids in the sn-2 position, with saturated acyl chains in the sn-1 position. Therefore, the sn-1 chains may participate in microdomain formation with cholesterol and exclude PUFAs, as suggested by the work of Huster et al (1998). However, during detergent extraction, the high affinity between the sn-1 chain and cholesterol may result in PUFA enrichment in the DRM fraction. Even though biochemical analysis of DRMs shows substantial amounts of PUFAs, they are not directly involved in the formation of liquid ordered domains.
4. 4) PUFA incorporation into cells drives cholesterol from the outer to the inner leaflet (144, 145). The efflux of cholesterol may drive changes in outer and inner leaflet microdomain formation. The signaling complexes of the inner leaflet may respond to a reduction in cholesterol concentrations and alter T cell signaling. Our laboratory has shown that cholesterol depletion can result in a reorganization of the actin cytoskeleton (106). Perhaps PUFA-induced changes in cholesterol also alter the organization of the cytoskeleton, which could modify cellular signaling."

"...As the data grow on how select PUFAs may modulate inflammatory and autoimmune diseases, there is a growing need for elucidating the underlying molecular mechanisms. An understanding of the effect of PUFAs at the level of T cell membrane organization is only starting to emerge, whereas relatively little is known about membrane modulation of APCs. The data from cellular and animal studies tell us that PUFAs induce changes in localization of proteins from DRM to DSM fractions, which has measurable consequences for T cell signaling and proliferation. However, the mechanisms by which PUFAs induce changes in protein localization are not known, and it is here that model membrane experiments suggest testable hypotheses. We know that PUFA-containing phospholipids impart unique structural effects on bilayers, but what is required is better knowledge of how these effects translate into functional consequences at the cellular level. Further investigation at the interface between model bilayers and cellular systems may answer some questions regarding PUFA-raft interactions. How PUFAs modulate MHC conformation, vertical orientation, lateral organization, and trafficking—on the basis of literature reports and some data from our own laboratory—also requires extensive investigation at all levels, from synthetic bilayers to animal experiments. Because dietary intake of PUFAs will result in a distribution to virtually every cell of the body, the changes described above for APCs are also applicable to T cells. PUFA modification of cellular membranes may be an important target for immunosuppression."

Apparently, mainstream medicine has managed to convinced the public somehow that there are carcinogenic and non-carcinogenic estrogens. An example of the former would be (17)-beta-estradiol and an example of the latter would be (17)-alpha-estradiol. The former is a strong agonist/activator of both estrogen receptors while the latter binds and interacts with those receptors very weakly. That is precisely the reason, medicine has been claiming that alpha-estradiol is non-carcinogenic. While beta-estradol has been officially labelled a "known carcinogen" by the National Institute of Environmental Health Sciences (NIEHS), which is a part of the National Institutes of Health (NIH) and as such Department of Health and Human Services (HHS), the alpha isomer has not. Now, the article is almost 17 years old and many things have changed since then. Namely, mainstream medicine has completely ignored the NIEHS announcement and has also been staging attacks on the results of the WHI studies that demonstrated beta-estradiol causes cancer, heart disease, strokes, dementia, etc. So, 17 years after the (still standing) official classification of estrogen as a carcinogen by the very "experts" we are all told to obey, the new position of those same experts is that neither the beta nor the alpha isomers of estradiol are carcinogenic. One of the main justifications given for the renewed promotion of estrogen is that it acts as an "antioxidant", yet the study below found the exact opposite - estrogen, by itself, can cause oxidative stress that is crucial for carcinogenesis. To me, at least, the evidence is quite clear and in plain sight - there is no such thing as a safe estrogen! Especially, in the presence of PUFA, which amplifies estrogen's genomic/receptor effects and also increases oxidative stress.

http://www.columbia.edu/cu/record/archives/vol28/vol28_iss16/Pg8-2816.pdf

"...It's disconcerting to think that a natural hormone circulating in significant amounts through the bodies of half the world's population is a carcinogen, but it's now official. In December, the National Institute of Environmental Health Sciences (NIEHS) added estrogen to its list of known cancer-causing agents. For years, estrogen has been a suspected carcinogen, since strong epidemiological evidence associates the hormone to breast, endometrial, and uterine cancers. Women who begin menstruating early, or who start menopause late, produce more estrogen over their lifetimes and have a higher risk of breast cancer. Recently, the clinical trial of estrogen plus progestin treatment therapy was terminated because of an increased risk of breast cancer."

"...To see if cancer-causing estrogens need oxygen radicals to produce tumors, Bhat implanted pellets of the hormone in hamsters that are susceptible to estrogen-induced kidney cancer. This model is widely used as an animal model of hormonal cancer. As expected, when the carcinogenic 17beta-estradiol (E2) was used, nearly all hamsters with the pellets developed cancer within seven months. E2 promotes cell proliferation and produces oxygen radicals when metabolized by the cell."

"...Also, as expected, none of the hamsters developed kidney cancer when a non-carcinogenic estrogen, 17-alpha-ethinyl-estradiol (EE) was implanted. EE acts through estrogen receptors to create new cells like E2, but unlike E2, is poorly broken down and does not produce oxygen radicals. But when EE was combined with a non-estrogen molecule that generates oxygen radicals, 30 percent of the hamsters developed kidney cancer within seven months."

"...But it also suggests that reputedly "safe" estrogens that are touted as replacements for the estrogens in hormone replacement therapy may not be so safe after all. "If we have oxidative stress in cells from other chemicals, then women are at risk for cancer even with estrogens that are considered non-carcinogenic," Bhat says. "The therapy may be safer if taken with antioxidants, but more research is needed to make safe and more effective antioxidants."

 

[Deleted member 5189]

Wtf just happened there?

it was ded b4 they got there. although they go on to kill 3 chickens afterwards.

 

[coolguy1]

it was ded b4 they got there. although they go on to kill 3 chickens afterwards.

This nigga kinda sus ngl

 

[Deleted member 6403]

Proof?

 

[Deleted member 5189]

Proof?

wdym "Proof?" are you telling me you wrote all that yourself?

 

[Deleted member 5189]

View attachment 1207773
This nigga kinda sus ngl

i would

 

[Deleted member 6403]

wdym "Proof?" are you telling me you wrote all that yourself?

Is it not proof that supports my argument?

 

[Deleted member 5189]

Is it not proof that supports my argument?

 

[Enfant terrible]

i would just kill myself first tbh

 

[TsarTsar444]

i would just kill myself first tbh

Same tbh, but two things stop this for me, one is parents, second is God, jfl imagine God cucking you for eternity because of suicide, brutalllll