Virgin olive oil and a Mediterranean diet fight heart disease by changing how our genes function

"New research in the FASEB Journal suggests that the polyphenols in virgin olive oil modify the expression of atherosclerosis-related genes, leading to health benefits" Read more....Virgin olive oil and a Mediterranean diet fight heart disease by changing how our genes function:

Testosterone suppresses oxidative stress in human neutrophils

Testosterone suppresses oxidative stress in human neutrophils

Leptin Administration Downregulates the Increased Expression Levels of Genes Related to Oxidative Stress and Inflammation in the Skeletal Muscle of ob/ob Mice

Leptin Administration Downregulates the Increased Expression Levels of Genes Related to Oxidative Stress and Inflammation in the Skeletal Muscle of ob/ob Mice

Homocysteine and Hypertension in Diabetes: Does PPARγ Have a Regulatory Role?

Homocysteine and Hypertension in Diabetes: Does PPARγ Have a Regulatory Role?

Female Hormones May Contribute to Sexual Dimorphism in TMJ~!

Comment: I suspect this is going to has implications on other pain conditions as well, especially those under the environmental illness umbrella like CFS and fibromyalgia....

"hippocampal TRPV1 can modulate central pain processing and estradiol may contribute to the sexual dimorphism of TMD pain sensitivity through upregulation of TRPV1 expression in the hippocampus"

Link:CiteULike: 17-beta-Estradiol Enhanced Allodynia of Inflammatory Temporomandibular Joint through Upregulation of Hippocampal TRPV1 in Ovariectomized Rats:

Sleep and Brain Energy Levels: ATP Changes during Sleep

Sleep and Brain Energy Levels: ATP Changes during Sleep

Dopamine, Time, and Impulsivity in Humans

Dopamine, Time, and Impulsivity in Humans

The BDNF Val66Met Polymorphism Impairs NMDA Receptor-Dependent Synaptic Plasticity in the Hippocampus

"Consistent with the NMDA receptor-dependent synaptic plasticity impairment, we observed a significant decrease in NMDA receptor neurotransmission in the CA1 pyramidal neurons of BDNFMet/Met mice. Thus, these results show that the BDNF Val66Met polymorphism has a direct effect on NMDA receptor transmission, which may account for changes in synaptic plasticity in the hippocampus."

Link:CiteULike: The BDNF Val66Met Polymorphism Impairs NMDA Receptor-Dependent Synaptic Plasticity in the Hippocampus:

Brain Chemical Makes Us More Impulsive

Brain Chemical Makes Us More Impulsive

Heavy Metals, Metallothionein and Regulation by Nrf2

Metallothionein: protein that modulates internal stores of heavy metals. Alterations in function have been recently implicated in autism as well as, other conditions where metals may be a factor including metabolic impairments and Alzheimer's.

In several past blogs, we have discussed health benefits of broccoli because it elevates the Nrf2 antioxidant system. In contrast to the preceding blog where it was noted that metallothioneins can inhibit GSK-3b which is an off/on switch for Nrf2 it has also be demonstrated that metalloproteins can be regulated by Nrf2. In 2005, Yeh's study suggested that sulphoraphane, "strongly suggest that at low concentrations of sulforaphane, activation of MAPKs such as ERK and p38 pathway lead to Nrf2-mediated metallothionein gene expression." One can assume from this that conditions that impair the Nrf2 system may lead to possible accumulation of toxic amounts of metals that can impair any number of metabolic processes. Such conditions include methylation, nutrition and other genetic factors such as polymorphisms, for example. Of course, this does not exclude factors that impair metallothionein on its own.

Notes:

• metallothionein expression needs to be tightly regulated because underexpression or overexpression can help mitigte or enhance disease.

HEIRS Library Tags: heavy metals, sulphoraphane (sulforaphane), Nrf2*****Sign up to receive alerts of heavy metal articles

            Blog Tags: Broccoli, sulforaphane, Nrf2

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Raymond, A. D., Gekonge, B., Giri, M. S., Hancock, A., Papasavvas, E., Chehimi, J., Kossevkov, A. V., Nicols, C., Yousef, M., Mounzer, K., Shull, J., Kostman, J., Showe, L., and Montaner, L. J. (2010). Increased metallothionein gene expression, zinc, and zinc-dependent resistance to apoptosis in circulating monocytes during hiv viremia. Journal of leukocyte biology.

http://www.citeulike.org/user/HEIRS/article/7369487


Yeh, C.-T. and Yen, G.-C. (2005). Effect of sulforaphane on metallothionein expression and induction of apoptosis in human hepatoma hepg2 cells. Carginogenesis Advance Access.

http://www.citeulike.org/user/HEIRS/article/7369321

Sabolić, I., Breljak, D., Skarica, M., and Herak-Kramberger, C. M. (2010). Role of metallothionein in cadmium traffic and toxicity in kidneys and other mammalian organs. Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine.

http://www.citeulike.org/user/HEIRS/article/7369302

TLRs Regulates Reactions to Particulate Matter and Other Contaminant Considerations~!

In this article, the author explains "it is plausible that PM2.5 contains bacterial or mycoplasma lipoproteins, which are known activators of TLR2 . Because PM2.5 contain high concentrations of a large number of metals. One or more of these metals could be involved in increased TLR2- mediated cytokine production triggered by microbial lipoprotein constituents of the PM2.5. In this regard, it is interesting that TLR2 has been implicated in proinflammatory cytokine expression by airway epithelial cells stimulated with air PM containing high amounts of metals. Another possibility is that PM2.5 cytokine-inducing effects are mediated by an indirect mechanism, via the generation of endogenous “danger” host molecules activating macrophages via TLR2."

Note: Recent findings by Notch show a potentiation effect between cyanobacteria and heavy metals and thus support an important mechanism although the mechanism remains to be elicited. In addition, one must always consider alterations in methylation which can be caused by endotoxin and heavy metals. Walsh and Usman demonstrated that in autism there is alterations in the functioning of metallotheinin protein which modulates and detoxifies metals. (Treat Autism and AD/HD, Wright) In other blogs, we have explained that metallotheinin inhibits GSK-3b (Wang)which can turn off the Nrf2 antioxidant system. This could explain why there are reports that the antioxidant system is negatively effected by metals (and by endotoxin)and thus, one must also consider that in mixed environmental pollutants, there is a reduction of function of this system. In addition, there is also potential that the AhR and metals interact to influence antioxidant and detoxification. These interactions of metals and the AhR are currently being investigated through a number of projects. (Korashy) Further study may shed more light on the interactions of the Nrf2 and AhR gene batteries and how they are effected by metals from environmental exposures.

Shoenfelt, J., Mitkus, R. J., Zeisler, R., Spatz, R. O., Powell, J., Fenton, M. J., Squibb, K. A., and Medvedev, A. E. (2009). Involvement of tlr2 and tlr4 in inflammatory immune responses induced by fine and coarse ambient air particulate matter. Journal of Leukocyte Biology, 86. http://www.citeulike.org/user/HEIRS/article/7367529

Vita. Hesham Korashy, PhD. Retrieved on June 29, 2010.
http://faculty.ksu.edu.sa/hkorashy/Pages/index.aspx

Notch, E. G., Miniutti, D. M., Berry, J. P., and Mayer, G. D. (2010). Cyanobacterial lps potentiates cadmium toxicity in zebrafish (danio rerio) embryos. Environmental toxicology.
http://www.citeulike.org/user/HEIRS/article/7367622

Heavy Metals. Treat Autism and ADHD. Retrieved on June 30, 2010. http://www.treatautism.ca/?page_id=126

Wang et al. Inactivation of GSK-3 by Metallothionein PreventsDiabetes-Related Changes in Cardiac EnergyMetabolism, Inflammation, Nitrosative Damage, and Remodeling. Diabetes. June 2009. Pgs. 1391-1402.

Wright, R. O. and Baccarelli, A. (2007). Metals and neurotoxicology. The Journal of Nutrition.
http://www.citeulike.org/user/HEIRS/article/7367642

Absence of TLR2 Protect Against Insulin Resistace from High Fat Diet~!

According to the author, this study presents evidence TLR2 is a molecular link between increased dietary lipid intake and the regulation of glucose homeostasis, via regulation of energy substrate utilisation and tissue inflammation.

HEIRS Health Research Blog: Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2

The Unexpected Role for the Aryl Hydrocarbon Receptor on Susceptibility to Experimental Toxoplasmosis

Toxoplasmosis is caused by infection with Toxoplasma gondii, an obligate intracellular parasite. The infection produces a wide range of clinical syndromes in humans, land and sea mammals, and various bird species.

The Unexpected Role for the Aryl Hydrocarbon Receptor on Susceptibility to Experimental Toxoplasmosis: "The Unexpected Role for the Aryl Hydrocarbon Receptor on Susceptibility to Experimental Toxoplasmosis"

Toxoplasmosis. eMedicine. Retrieved on June 30, 2010. http://emedicine.medscape.com/article/229969-overview

Iron Mobilization and Induction of MPT in Acetaminophen-Induced Toxicity to Mouse Hepatocytes

"an increase of cytosolic chelatable ferrous iron occurs during acetaminophen hepatotoxicity, which triggers the MPT and cell killing. Disrupted lysosomes are the likely source of iron, and chelation of this iron decreases acetaminophen toxicity to hepatocytes."

Link: Lysosomal Iron Mobilization and Induction of the Mitochondrial Permeability Transition in Acetaminophen-Induced Toxicity to Mouse Hepatocytes -- Kon et al., 10.1093/toxsci/kfq175 -- Toxicological Sciences:

Genomic and Proteomic Responses to Environmentally Relevant Exposures to Dieldrin: Indicators of Neurodegeneration? -- Martyniuk et al., 10.1093/toxsci/kfq192 -- Toxicological Sciences

"sub-chronic exposure to dieldrin alters the abundance of mRNAs and proteins in the hypothalamus that are associated with cell metabolism, cell stability and integrity, stress, and DNA repair."

Link: Genomic and Proteomic Responses to Environmentally Relevant Exposures to Dieldrin: Indicators of Neurodegeneration? -- Martyniuk et al., 10.1093/toxsci/kfq192 -- Toxicological Sciences:

Nitrate in beetroot juice lowers blood pressure

Nitrate in beetroot juice lowers blood pressure

Ovarian transplantation restores fertility to old mice and also lengthens their lives

Ovarian transplantation restores fertility to old mice and also lengthens their lives

PROTECTIVE EFFECTS OF LACTOBACILLUS PARACASEI F19 IN A RAT MODEL OF OXIDATIVE AND METABOLIC HEPATIC INJURY.

The severity of liver and gut microbiota alterations induced by I/R was even greater in rats with liver inflammation and steatosis, i.e., MCD-fed animals. LP-F19 supplementation significantly reduced the harmful effects of I/R on the liver and on gut microbiota in both groups of rats, although the effect was slightly less in MCD-fed animals. In conclusion, LP-F19 supplementation, by restoring gut microbiota, attenuated I/R-related liver injury, particularly in the absence of steatosis.

CiteULike: PROTECTIVE EFFECTS OF LACTOBACILLUS PARACASEI F19 IN A RAT MODEL OF OXIDATIVE AND METABOLIC HEPATIC INJURY.: "Nardone, G., Compare, D., Liguori, E., Di Mauro, V., Rocco, A., Barone, M., Napoli, A., Lapi, D., Iovene, M. R. R., and Colantuoni, A. (2010). Protective effects of lactobacillus paracasei f19 in a rat model of oxidative and metabolic hepatic injury. American journal of physiology. Gastrointestinal and liver physiology."

For further reading: Library: Probiotics and Prebiotics
HEIRS Research Blog: Probiotics

Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2

In this study, we tested the hypothesis that HSV-induced neural cell oxidative tissue damage and cytotoxicity are mediated by microglial cell ROS through a TLR2-dependent mechanism. We detected elevated intracellular ROS in HSV-infected microglia obtained from wild-type mice. In contrast, the virus failed to induce ROS in microglia obtained from TLR2-/- mice. Additionally, compared to wild-type microglia, TLR2-/- microglia displayed attenuated HSV-induced lipid peroxidation and neurotoxicity. These studies demonstrate the importance of microglial cell TLR2 in inducing oxidative stress and neuronal damage in response to viral infection.

CiteULike: Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2: "Schachtele, S., Hu, S., Little, M., and Lokensgard, J. (2010). Herpes simplex virus induces neural oxidative damage via microglial cell toll-like receptor-2. Journal of Neuroinflammation, 7(1):35+."

Note: If high fat diets (HFD) influence the expression of TLR2 - one could assume that HFD may augment inflammatory responses. Diets that are lower in fat such as a typical Mediterranean Diet may reduce these inflammatory mediators and reduce symptoms. Other studies show that high glucose diets may also induce TLR expression (Dasu) and there is evidence that TR2 is necessary for development of the metabolic syndrome which makes one at higher risk for cardiovascular disease and diabetes (Himes).

For Further Reading: ImmunoGenetics in Autism, MCS and Cancer -- What Has Food Got To Do With It!

HEIRS Library Tags: TLR2


Dasu, M. R., Devaraj, S., Zhao, L., Hwang, D. H., and Jialal, I. (2008). High glucose induces toll-like receptor expression in human monocytes. Diabetes, 57(11):3090-3098.
http://www.citeulike.org/user/HEIRS/article/3207456
Himes, R. W. and Smith, C. W. (2009). Tlr2 is critical for diet-induced metabolic syndrome in a murine model. The FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
http://www.citeulike.org/user/HEIRS/article/6002948
Schachtele, S., Hu, S., Little, M., and Lokensgard, J. (2010). Herpes simplex virus induces neural oxidative damage via microglial cell toll-like receptor-2. Journal of Neuroinflammation, 7(1):35+.
http://www.citeulike.org/user/HEIRS/article/7366356
Lee, J. Y., Zhao, L., Youn, H. S., Weatherill, A. R., Tapping, R., Feng, L., Lee, W. H., Fitzgerald, K. A., and Hwang, D. H. (2004). Saturated fatty acid activates but polyunsaturated fatty acid inhibits toll-like receptor 2 dimerized with toll-like receptor 6 or 1. The Journal of biological chemistry, 279(17):16971-16979.
http://www.citeulike.org/user/HEIRS/article/3328606

EGCG, L-ascorbic acid, alpha-tocopherol, and dihydrolipoic acid on the formation of deoxyguanosine adducts derived from lipid peroxidation.

These results highlight the complexity of antioxidant mechanisms and also reveal that EGCG and DHLA are effective at suppressing lipid peroxidation-induced Acr-dG and 8-oxodG formation as well as blocking the reaction of dG with Acr

CiteULike: Effects of epigallocatechin gallate, L-ascorbic acid, alpha-tocopherol, and dihydrolipoic acid on the formation of deoxyguanosine adducts derived from lipid peroxidation.: "Nath, R. G., Wu, M. Y., Emami, A., and Chung, F.-L. L. (2010). Effects of epigallocatechin gallate, l-ascorbic acid, alpha-tocopherol, and dihydrolipoic acid on the formation of deoxyguanosine adducts derived from lipid peroxidation. Nutrition and cancer, 62(5):622-629."

Manipulating microbes in the gut may remedy disease and enhance health

"We are what we eat, but who are 'we'? New, high-powered genomic analytical techniques have established that as many as 1,000 different single-celled species coexist in relative harmony in every healthy human gut."

Read more...Manipulating microbes in the gut may remedy disease and enhance health:

Surprising find may yield new avenue of treatment for painful herniated discs

"An immune cell known to cause chronic inflammation in autoimmune disorders has been identified as a possible culprit in low back pain associated with herniated discs, according to doctors at Duke University Medical Center."

Read more...Surprising find may yield new avenue of treatment for painful herniated discs:

Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2

Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2

Endotoxemia Causes A Decrease in eNOS-Dependant Vasodilation in Microvasculature~!

"experimental endotoxemia in humans causes a specific decrease in endothelial NO-dependent vasodilation in the microcirculation which cannot be explained by a change of ADMA levels. Microvascular NO deficiency might be responsible for the heterogeneity of tissue perfusion observed in sepsis and could be a therapeutic target" Link: ACUTE ENDOTOXEMIA INHIBITS MICROVASCULAR NITRIC OX... [Shock. 2010] - PubMed result:

Why We Dream: Real Reasons Revealed

Why We Dream: Real Reasons Revealed

Paraquat-induced Oxidative Stress Impairs Glucose Uptake in Adipocytes.

"paraquat-induced oxidative stress decreased glucose transporter 4 (GLUT4) translocation to the cell surface, resulting in repression of insulin-dependent 2-deoxyglucose uptake."

Link: CiteULike: Paraquat-induced Oxidative Stress Represses Phosphatidylinositol 3-Kinase Activities Leading to Impaired Glucose Uptake in 3T3-L1 Adipocytes:

Related: HEIRS Library Tags: GLUT4

Sewage Raises West Nile Virus Risk

"Sewage that overflows into urban creeks and streams during periods of heavy rain can promote the spread of West Nile Virus, an Emory study finds."

Sewage Raises West Nile Virus Risk:

GSK-3 Knock-down Allows for Endotoxin Tolerance in Astrocytes~!

"GSK3 inhibitors or knocking down GSK3 levels promoted LPS-tolerance and astrocytes expressing constitutively active GSK3 did not develop LPS-tolerance. These findings identify the critical role of GSK3 in counteracting IL-6 inflammatory tolerance in cells of the CNS, supporting the therapeutic potential of GSK3 inhibitors to reduce neuroinflammation by promoting tolerance"

Link: CiteULike: Glycogen synthase kinase-3 regulates inflammatory tolerance in astrocytes.:

Regulatory T Cell (Tregs) Production Dependant on Methylation Modifications~!

Background: New report support that the balance of Tregs need to be maintained for suppression of immune functions that lead to autoimmune-type reactions including those that may be seen in diabetes, colitis and lupus. In previous blogs, I suggest that loss of Tregs may influence the development of chemical sensitivity through the loss of Treg suppression and "loss of tolerance" and has been suggested by other authors. In the past, I have also reviewed several research studies that identify how recent findings of aberrant methylation influence environmental disease including autism, endometriosis and PTSD.

Interesting the following study by Floess shows that epigenetic modifications must occur with immune cells for cells to develop into "suppressor-type" lineages of Tregs. Therefore, alterations in methylation may negatively influence the development of Treg cells and could cause or augment environmental disease. This also provides a mechanism for what appears an inheritability of environmental disease.

Floess, S., Freyer, J., Siewert, C., Baron, U., Olek, S., Polansky, J., Schlawe, K., Chang, H.-D., Bopp, T., Schmitt, E., Klein-Hessling, S., Serfling, E., Hamann, A., and Huehn, J. (2007). Epigenetic control of the foxp3 locus in regulatory t cells. PLoS Biol, 5(2):e38+.
http://www.citeulike.org/user/HEIRS/article/1080288

Proteins Play Role In Massive Neuron Death

Proteins Play Role In Massive Neuron Death: "A team of researchers, led by scientists at the University of California, San Diego, have identified a key player in the dramatic loss of neurons in mice and fly models, a discovery that could help illuminate the role of mitochondrial dysfunction in human neurodegenerative disorders, such as Parkinson's disease."

The imbalance between regulatory and IL-17-secreting CD4+ T cells in lupus patients

"The present study indicates that active SLE appears to exist as an imbalance between Treg and Th17 cells. Correction of this Treg/Th17 imbalance may have therapeutic impact for patients with SLE."

Link: CiteULike: The imbalance between regulatory and IL-17-secreting CD4+ T cells in lupus patients:

Targeting flight-or-fight hormone response to combat hea... ( We've all experienced the strong hea...)

"We've all experienced the strong heartbeat that accompanies emotions such as fear and rage. But can the body's natural response to these emotions be used to combat heart failure? Results of a study published online today in the journal Circulation Research present a strong case"

Targeting flight-or-fight hormone response to combat hea... ( We've all experienced the strong hea...):

Preparation of Selenium/Zinc-Enriched Probiotics and Their Effect on Blood Selenium and Zinc Concentrations, Antioxidant Capacities, and Intestinal Microflora in Canine.

The supplemental group showed increased antioxidants in the blood, an increase in lactobacillus and bifidobacterium in feces and a decrease in malondialdehyde and lower levels of pathogenic bacteria in the feces.

CiteULike: Preparation of Selenium/Zinc-Enriched Probiotics and Their Effect on Blood Selenium and Zinc Concentrations, Antioxidant Capacities, and Intestinal Microflora in Canine.: "Ren, Z., Zhao, Z., Wang, Y., and Huang, K. (2010). Preparation of selenium/zinc-enriched probiotics and their effect on blood selenium and zinc concentrations, antioxidant capacities, and intestinal microflora in canine. Biological trace element research."

Consult with a veterinarian before giving your pet any supplement or changing diets.

Pine bark extract may ease hayfever symptoms: Study

Pine bark extract may ease hayfever symptoms: Study

Ingredient in red wine may prevent some blinding diseases

Ingredient in red wine may prevent some blinding diseases: "Ingredient in red wine may prevent some blinding diseases"

Methylation by Folate May Be Lead to Therapeutics for Spinal Injuries~!

"The vitamin folate appears to promote healing in damaged rat spinal cord
tissue by triggering a change in DNA, according to a laboratory study funded by
the National Institutes of Health."

Researchers Discover How Folate Promotes Healing In Spinal Cord Injuries:

Ammonia metabolism, the brain and fatigue; revisit... [Prog Neurobiol. 2010] - PubMed result

Could conditions like this contribute to health problem like CFS?

"Plasma concentrations of ammonia during exercise often achieve or exceed those measured in liver disease patients, resulting in increased cerebral uptake. In this article we propose that exercise-induced hyperammonemia may lead to concomitant disturbances in brain function, potentially through similar mechanisms underpinning pathology, which may impact on performance as fatigue or reduced function, especially during extreme exercise."

Ammonia metabolism, the brain and fatigue; revisit... [Prog Neurobiol. 2010] - PubMed result:

CRH and Tregs in Autoimmunity: Possible Connections to Chemical Sensitivity~!

Background: In earlier posts we described how commensal bacteria in the gut regulates the induction of T regulatory cells called Tregs that are important for immune functions. The loss of which may include autoimmune-type expressions and may be influential in MCS by loss of tolerance. In addition, we have also discussed how cortico-releasing hormone (CRH or CRF) has many effects and tissue targets, can be influenced by odors, may influence addictive-type behaviors and abherrant signaling may lead to altered signaling that can lead to mood disorders and have other negative influences on behaviors. The activation of CRH is part of the stress response and therefore, become an important part of the response to environmental cues. This same response activates the inflammatory cascade and therefore, the existence of one may coincide with the activation of the other. In addition, inflammatory cascades include activation of immune cells including mast cells.

Christy and Brown explain that Tregs are important in autoimmune disease and have the potential upon induction to prevent and reverse these conditions including diabetes and multiple sclerosis. Both of which are now considered to have an environmental connection. In addition the author notes that lupus, another condition with possible environmental triggers, and other autoimmune conditions are not just a loss of Tregs but a condition where other immune cells called Ag-effector cells become resistent to Treg suppression. At this point, one would suggest that other physiological pathways may be involved and this potentiates the non-adaptive conditions that lead to MCS. In other blogs, we have discussed a number of these conditions including nutrition and expression of cytokines, as well as, the expression of Nrf2.

Christy and Brown also present another important factor that very well may influence the development of MCS by contributing to loss of tolerance and that is the production of CRH from mast cells. These cells are often produced from inflammatory reactions such as those conditions that produced and reported from environmental toxin exposure. The authors discuss how the role of CRH produced from these inflammatory cells in basically an uptapped area of immune science. On the other hand, Soderholm does note that mast cells and CRH are implicated in disruptions of barrier function in irritable bowel syndrome and to a degree, it it now understood they are produced in inflamed tissue and increase inflammation. This protein has been implicated in reactions in rheumatoid arthritis and other inflammatory conditions during stress. For this reason, one can suggest that inflammatory conditions and production of mast cells which can produce this protein may contribute to the response and long-term activation can have important effects on downstream targets and participate in autoimmune-type response such as those observed in chemical sensitivities.

Past HEIRS Blogs: Related Tags: CRF , CRH , Nrf2


Christy, A. L. and Brown, M. A. (2007). The multitasking mast cell: Positive and negative roles in the progression of autoimmunity. J Immunol, 179(5):2673-2679.
http://www.citeulike.org/user/HEIRS/article/7357936
McKay, D. M. (2005). Good bug, bad bug: in the case of enteric inflammatory disease does the epithelium decide? Memórias do Instituto Oswaldo Cruz, 100(s1):205-210.

http://www.citeulike.org/user/HEIRS/article/7357955
Teitelbaum, A. A., Gareau, M. G., Jury, J., Yang, P. C., and Perdue, M. H. (2008). Chronic peripheral administration of corticotropin-releasing factor causes colonic barrier dysfunction similar to psychological stress. Am J Physiol Gastrointest Liver Physiol, 295(3):G452-459. http://www.citeulike.org/user/HEIRS/article/7357961

Commensal Bacteria Induce Tolerance via Tregs and Anti-Inflammatory Cytokine in Gut~!

Background: It has been suggested that multiple chemical sensitivity may be a consequence of loss of tolerance and (Tregs) by the immune system. In addition, this condition may also influence other environmental illnesses as well. One would assume any environmental condition that disturbs the natural environment of the intestinal tract could lead to the potential for chemical sensitivity if this is true. Considering this to be true, anything that improves healthy gut flora and reduces inflammation may be of benefit to those who suffer from this condition.

"Bacteroides fragilis, directs the development of Foxp3(+) regulatory T cells (Tregs) with a unique 'inducible' genetic signature. Monocolonization of germ-free animals with B. fragilis increases the suppressive capacity of Tregs and induces anti-inflammatory cytokine production exclusively from Foxp3(+) T cells in the gut. We show that the immunomodulatory molecule, polysaccharide A (PSA), of B. fragilis mediates the conversion of CD4(+) T cells into Foxp3(+) Treg cells that produce IL-10 during commensal colonization. Functional Foxp3(+) Treg cells are also produced by PSA during intestinal inflammation, and Toll-like receptor 2 signaling is required for both Treg induction and IL-10 expression"

Inducible Foxp3+ regulatory T-cell development by ... [Proc Natl Acad Sci U S A. 2010] - PubMed result:

View Similar Posts: Tregs

The role of T cell PPARgamma in mice with experime... [BMC Gastroenterol. 2010] - PubMed result

"The deficiency of PPAR gamma in T cells accelerated the onset of disease and body weight loss. Examination of colon histopathology revealed significantly greater epithelial erosion, leukocyte infiltration, and mucosal thickening in the CD4cre mice on day 7. CD4cre mice had more CD8+ T cells than WT mice and fewer CD4+FoxP3+ regulatory T cells (Treg) and IL10+CD4+ T cells in blood and MLN, respectively."

The role of T cell PPARgamma in mice with experime... [BMC Gastroenterol. 2010] - PubMed result:

Homocysteine Enhances Transmigration of Rat Monocytes Through a Brain Capillary Endothelial Cell Monolayer via ICAM-1.

Homocysteine Enhances Transmigration of Rat Monocytes Through a Brain Capillary Endothelial Cell Monolayer via ICAM-1.

Oxidative and nitrosative stress contribute to lupus disease activity

University of Texas Medical Branch researchers have uncovered an association between free radical-mediated reactions and the severity and progression of system lupus erythematosus (SLE). Higher levels of oxidative and nitrosative stress markers were found in SLE patients with greater disease activity suggesting a causal relationship. Full findings of the study are available in the July issue of Arthritis & Rheumatism, a journal published by Wiley-Blackwell on behalf of the American College of Rheumatology.

Oxidative and nitrosative stress contribute to lupus disease activity:

Not enough folate may quicken hearing loss: Study

"Low blood levels of folate are associated with a 35 per cent increased risk of hearing loss, says a new study from Australia that strengthens the link between B vitamins and hearing."

Not enough folate may quicken hearing loss: Study:

Oxidative stress and inflammation modulate peroxisome proliferator-activated receptors with regional discrepancy in diabetic heart.

"Diabetes can modulate PPARs through increased inflammatory cytokines and oxidative stress, which are attenuated by ascorbate treatment."

CiteULike: Oxidative stress and inflammation modulate peroxisome proliferator-activated receptors with regional discrepancy in diabetic heart.:

Heavy Metals Elevates Antioxidant Capacity to Combat Oxidative Stress in Mine Workers~!

"Taken together, the results indicate that exposure to combination of Pb and Zn in mine elevates total antioxidant capacity of body in a reflex to overcome to oxidative stress. Especially, in the present case, it seems that toxic effect of Pb has been greater than positive effects of Zn, but the combination exposure has resulted in not such a critical toxicity situation."

CiteULike: Study on clinical and biochemical toxicity biomarkers in a zinc-lead mine workers:

Abusive mothering aggravates the impact of stress hormones

In a new Biological Psychiatry article, Dr. Regina Sullivan and colleagues have dissected the behavior of mother rats and their infant pups, modeling nurturing by stroking and abuse with electric shock. In this animal model of infant abuse, they took into consideration the unique infant neurobehavioral learning attachment system that ensures infant rats' attachment to their caregiver regardless of the quality of care received.

Abusive mothering aggravates the impact of stress hormones

Eye damage reversed with stem cells: study

Eye damage reversed with stem cells: study

Study of the nitric oxide system in the rat cerebellum during aging

CiteULike: Study of the nitric oxide system in the rat cerebellum during aging: "Blanco, S., Molina, F. J., Castro, L., Del Moral, M. L., Hernandez, R., Jimenez, A., Rus, A., Martinez-Lara, E., Siles, E., and Peinado, M. A. (2010). Study of the nitric oxide system in the rat cerebellum during aging. BMC Neuroscience, 11(78):1-33."

BPA: Exampls of Epigenomic Disruption in Early Development

dietary BPA exposure was shown to hypomethylate both the A(vy) and the Cabp(IAP) metastable epialleles. This hypomethylating effect was counteracted with dietary supplementation of methyl donors or genistein. These results are consistent with reports of BPA and other EDCs causing epigenetic effects. Epigenotoxicity could lead to numerous developmental, metabolic, and behavioral disorders in exposed populations. The heritable nature of epigenetic changes also increases the risk for transgenerational inheritance of phenotypes. Thus, epigenotoxicity must be considered when assessing these compounds for safety.

CiteULike: Epigenomic disruption: The effects of early developmental exposures.: "Bernal, A. J. and Jirtle, R. L. (2010). Epigenomic disruption: The effects of early developmental exposures. Birth defects research. Part A, Clinical and molecular teratology."

Cigarette smoke extract induces HO-1 expression in mouse cerebral vascular endothelial cells via NADPH oxidase pathway.

CiteULike: Cigarette smoke extract induces HO-1 expression in mouse cerebral vascular endothelial cells: Involvement of c-Src/NADPH oxidase/PDGFR/JAK2/STAT3 pathway.: "CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was regulated by c-Src or c-Src activated- NADPH oxidase/ROS."

Tumor Necrosis Factor-Induced Neutrophil Adhesion Occurs Through SphK-1 Activation of Integrin

"TNFalpha activated endothelial cells being sphingosine kinase-1, alpha5beta1, and angiopoietin-2 dependent. Moreover, this work supports the notion that sphingosine kinase-1 may be the single target required for an effective broad spectrum approach to combat inflammation and immune disorders."

Tumor Necrosis Factor-Induced Neutrophil Adhesion ... [Am J Pathol. 2010] - PubMed result:

SphK1 regulates proinflammatory responses associated with endotoxin and polymicrobial sepsis.

"critical role for SphK1 in endotoxin signaling and sepsis-induced inflammatory responses and suggest that inhibition of SphK1 is a potential therapy for septic shock."

CiteULike: SphK1 regulates proinflammatory responses associated with endotoxin and polymicrobial sepsis.:

Mouse Study Sheds Light on Diabetes-Heart Disease Link

"high blood sugar elevates reactive molecules that contain the oxygen atom (called reactive oxygen species) in autonomic neurons. This chemical change inactivates the neurotransmitter receptors at these synapses, they noted." Mouse Study Sheds Light on Diabetes-Heart Disease Link:

Compound Found in Red Wine Neutralizes Toxicity of Proteins Related to Alzheimer's

"An organic compound found in red wine – resveratrol – has the ability to neutralize the toxic effects of proteins linked to Alzheimer’s disease, according to research led by Rensselaer Professor Peter M. Tessier. The findings, published in the May 28 edition of the Journal of Biological Chemistry, are a step toward understanding the large-scale death of brain cells seen in certain neurodegenerative diseases."

Compound Found in Red Wine Neutralizes Toxicity of Proteins Related to Alzheimer's:

Researchers explain why red wine and green tea stop prostate cancer growth

"prostate cancer cell lines and mouse models to demonstrate that treatment with these dietary agents results in inhibition of the sphingosine kinase-1/sphingosine 1-phosphate (SphK1/S1P) pathway."
Researchers explain why red wine and green tea stop prostate cancer growth

Subnormal vitamin B12 concentrations and anaemia in older people: a systematic review.

Subnormal vitamin B12 concentrations and anaemia in older people: a systematic review.

NIH-Supported Study Finds Novel Pathway May Open Doors for New Blood Pressure Treatments, June 21, 2010 News Release - National Institutes of Health (NIH)

"Researchers have found that increasing certain proteins in the blood vessels of mice, relaxed the vessels, lowering the animal’s blood pressure. The study provides new avenues for research that may lead to new treatments for hypertension."

NIH-Supported Study Finds Novel Pathway May Open Doors for New Blood Pressure Treatments, June 21, 2010 News Release - National Institutes of Health (NIH):

Trans Cis - conjugated linoleic acid inhibits skeletal muscle differentiation and GLUT4 expression independently from NF-kappaB activation

t10, c12-CLA inhibits myogenic differentiation and GLUT4 expression, independently from NF-kB activation.

These findings support prior concerns and special consideration by physicians in those at risk for metabolic dysregulation and diabetes.
Wipedia

CiteULike: <I>Trans</I>-10, <I>cis</I>-12 conjugated linoleic acid inhibits skeletal muscle differentiation and GLUT4 expression independently from NF-kappaB activation: "Hommelberg, P. P. H., Plat, J., Remels, A. H. V., van Essen, A. L. M., Kelders, M. C. J. M., Mensink, R. P., Schols, A. M. W. J., and Langen, R. C. J. (2010). trans-10, cis-12 conjugated linoleic acid inhibits skeletal muscle differentiation and glut4 expression independently from nf-kappab activation. Molecular Nutrition & Food Research, 9999(9999):NA+."

Ascorbic Acid May Prevent Lead-Induced Hypertension via Nitric Oxide!

"ascorbic acid as an antioxidant prevents the lead induced hypertension. This effect may be mediated by inhibition of NOc oxidation and thereby increasing availability of NO."

Effect of ascorbic acid supplementation on nitric oxide metabolites and systolic blood pressure in rats exposed to lead Mohammad A, Ali N, Reza B, Ali K - Indian J Pharmacol:

AMP-activated protein kinase mediates activity-dep... [Neuroscience. 2010] - PubMed result

"Administration of resveratrol in vivo significantly activates AMPK activity and attenuates the effects of MD on mitochondria by significant increase in PGC-1alpha and NRF-1 levels, mitochondria amount, and coupled respiration. These results strongly indicate that AMPK is an essential upstream mediator that couples neuronal activity to mitochondrial energy metabolism by regulation of PGC-1alpha-NRF-1 pathway in neurons"

AMP-activated protein kinase mediates activity-dep... [Neuroscience. 2010] - PubMed result:

HEIRS Blogs Tags: resveratrol

Metformin: an anti-diabetic drug that is also anti-aging? « Ouroboros

"Energy sensor AMPK and AMPK-activating kinase LKB1, which are activated in mammals by metformin treatment, are essential for health benefits in C. elegans, suggesting that metformin engages a metabolic loop conserved across phyla. We also show that the conserved oxidative stress-responsive transcription factor SKN-1/Nrf2 is essential for metformin healthspan benefits in C. elegans, a mechanistic requirement not previously described in mammals. skn-1, which functions in nematode sensory neurons to promote DR longevity benefits and in intestines for oxidative stress resistance lifespan benefits, must be expressed in both neurons and intestines for metformin-promoted healthspan extension, supporting that metformin improves healthy middle-life aging by activating both DR and antioxidant defense longevity pathways"

Metformin: an anti-diabetic drug that is also anti-aging? « Ouroboros:

Metformin: an anti-diabetic drug that is also anti-aging? « Ouroboros

"Energy sensor AMPK and AMPK-activating kinase LKB1, which are activated in mammals by metformin treatment, are essential for health benefits in C. elegans, suggesting that metformin engages a metabolic loop conserved across phyla. We also show that the conserved oxidative stress-responsive transcription factor SKN-1/Nrf2 is essential for metformin healthspan benefits in C. elegans, a mechanistic requirement not previously described in mammals. skn-1, which functions in nematode sensory neurons to promote DR longevity benefits and in intestines for oxidative stress resistance lifespan benefits, must be expressed in both neurons and intestines for metformin-promoted healthspan extension, supporting that metformin improves healthy middle-life aging by activating both DR and antioxidant defense longevity pathways"

Metformin: an anti-diabetic drug that is also anti-aging? « Ouroboros:

Living fast and dangerously: Hormones influence the 'pace of life' of songbirds

Living fast and dangerously: Hormones influence the 'pace of life' of songbirds

HO-1, Nrf2 in Induction of NRF-1 and Mitochondrial Biogenesis!

"endogenous carbon monoxide (CO) generated by HO-1 overexpression stimulates superoxide dismutase-2 upregulation and mitochondrial H2O2 production, which activates Akt/PKB. Akt deactivates glycogen synthase kinase-3β, which permits Nrf2 nuclear translocation and occupancy of 4 antioxidant response elements (AREs) in the NRF-1 promoter. The ensuing accumulation of nuclear NRF-1 protein leads to gene activation for mitochondrial biogenesis,"

Heme Oxygenase-1 Regulates Cardiac Mitochondrial Biogenesis via Nrf2-Mediated Transcriptional Control of Nuclear Respiratory Factor-1 -- Piantadosi et al. 103 (11): 1232 -- Circulation Research:

Role of CO in cardiac mitochondrial biogenesis

"Mitochondrial biogenesis is activated by gene and protein expression of the nuclear respiratory factor 1 (NRF1) and NRF2, of peroxisome proliferator-activated receptor gamma co-activator-1, and of mitochondrial transcription factor A (TFAM), which augmented the copy number of mitochondrial DNA (mtDNA). This is independent of nitric oxide synthase (NOS), as demonstrated by the identical responses in wild-type and endothelial NOS (eNOS)-deficient mice, and by the inhibition of inducible NOS (iNOS)."

A new activating role for CO in cardiac mitochondrial biogenesis -- Suliman et al. 120 (2): 299 -- Journal of Cell Science:

Resveratrol Protects Against Dopamine Neurotoxicity by Inhibiting NADPH Oxidase!

Resveratrol reduced NADPH oxidase-mediated generation of reactive oxygen species. Second, LPS-induced translocation of NADPH oxidase cytosolic subunit p47 to the cell membrane was significantly attenuated by resveratrol. Third and most importantly, resveratrol failed to exhibit neuroprotection in cultures from NADPH oxidase-deficient mice. Furthermore, this neuroprotection was also related to an attenuation of the activation of mitogen-activated protein kinases and nuclear factor-kappaB signaling pathways in microglia. These findings suggest that resveratrol exerts neuroprotection against LPS-induced dopaminergic neurodegeneration and NADPH oxidase may be a major player in resveratrol-mediated neuroprotection.

CiteULike: Resveratrol protects dopamine neurons against lipopolysaccharide-induced neurotoxicity through its anti-inflammatory actions.: "Zhang, F., Shi, J.-S. S., Zhou, H., Wilson, B. C., Hong, J.-S. S., and Gao, H.-M. M. (2010). Resveratrol protects dopamine neurons against lipopolysaccharide-induced neurotoxicity through its anti-inflammatory actions. Molecular pharmacology."

Coal workers' pneumoconiosis and progressive massive fibrosis are increasingly more prevalent among workers in small underground coal mines in the United States

Coal workers' pneumoconiosis and progressive massive fibrosis are increasingly more prevalent among workers in small underground coal mines in the United States

Smell Key to Early Parkinson's?

Smell Key to Early Parkinson's?

Light Therapy Decreases Certain Immune Complexes While Increasing Tregs in psoriasis-like condition~!

PUVA induced the Th2 pathway and IL-10-producing CD4+CD25+Foxp3+Tregs with disease-suppressive activity that was abolished by anti-CTLA4 mAb treatment. These findings were paralleled by macroscopic and microscopic clearance of the diseased murine skin. Anti-IL-17 mAb treatment also diminished the psoriatic phenotype of the mice. This indicated that both induced Tregs involving CTLA4 signaling and inhibition of the IL-23/Th17 axis are central for the therapeutic action of PUVA.

CiteULike: 8-methoxypsoralen plus ultraviolet A therapy acts via inhibition of the IL-23/Th17 axis and induction of Foxp3+ regulatory T cells involving CTLA4 signaling in a psoriasis-like skin disorder.: "Singh, T. P. P., Schön, M. P., Wallbrecht, K., Michaelis, K., Rinner, B., Mayer, G., Schmidbauer, U., Strohmaier, H., Wang, X.-J. J., and Wolf, P. (2010). 8-methoxypsoralen plus ultraviolet a therapy acts via inhibition of the il-23/th17 axis and induction of foxp3+ regulatory t cells involving ctla4 signaling in a psoriasis-like skin disorder. Journal of immunology (Baltimore, Md. : 1950), 184(12):7257-7267."

Downregulation of Th17 cells in the small intestine by disruption of gut flora in the absence of retinoic acid.

CiteULike: Downregulation of Th17 cells in the small intestine by disruption of gut flora in the absence of retinoic acid.: "Cha, H.-R. R., Chang, S.-Y. Y., Chang, J.-H. H., Kim, J.-O. O., Yang, J.-Y. Y., Kim, C.-H. H., and Kweon, M.-N. N. (2010). Downregulation of th17 cells in the small intestine by disruption of gut flora in the absence of retinoic acid. Journal of immunology (Baltimore, Md. : 1950), 184(12):6799-6806."

Resveratrol Metabolites Induces HO-1 via Nrf2 through KEAP1 Residue Modification.

It is hence likely that piceatannol modifies specific cysteine residues of Keap1, which allows Nrf2 to translocate into the nucleus and bind to ARE, leading to enhancement of the expression of HO-1. The characteristic catechol moiety of piceatannol appears to be critical for induction of Nrf2 activation and subsequent upregulation of HO-1.

CiteULike: Piceatannol induces heme oxygenase-1 expression in human mammary epithelial cells through activation of ARE-driven Nrf2 signaling.: "Lee, H.-H. H., Park, S.-A. A., Almazari, I., Kim, E.-H. H., Na, H.-K. K., and Surh, Y.-J. J. (2010). Piceatannol induces heme oxygenase-1 expression in human mammary epithelial cells through activation of are-driven nrf2 signaling. Archives of biochemistry and biophysics."

High Fat Diet Increases Oxidative Stress and Cognitive Impairment in Mice Brain Through reduced Nrf2

These data suggest that while adiposity and insulin resistance following HFD consumption are linked to increased morbidity, the relationship between these factors and brain homeostasis during aging is not a linear relationship. More specifically, these data implicate impaired Nrf2 signaling and increased cerebral oxidative stress as mechanisms underlying HFD-induced declines in cognitive performance in the aged brain.

CiteULike: High Fat Diet Increases Hippocampal Oxidative Stress and Cognitive Impairment in Aged Mice: Implications for decreased Nrf2 signaling.: "Morrison, C. D., Pistell, P. J., Ingram, D. K., Johnson, W. D., Liu, Y., Fernandez-Kim, S. O. O., White, C. L., Purpera, M. N., Uranga, R. M., Bruce-Keller, A. J., and Keller, J. N. (2010). High fat diet increases hippocampal oxidative stress and cognitive impairment in aged mice: Implications for decreased nrf2 signaling. Journal of neurochemistry."

Reduced Cortical BDNF Expression and Aberrant Memory in Carf Knock-Out Mice

Reduced Cortical BDNF Expression and Aberrant Memory in Carf Knock-Out Mice

Early Life Activation of Toll-Like Receptor 4 Reprograms Neural Anti-Inflammatory Pathways

Early Life Activation of Toll-Like Receptor 4 Reprograms Neural Anti-Inflammatory Pathways

A Calorie-Restricted Diet Decreases Brain Iron Accumulation and Preserves Motor Performance in Old Rhesus Monkeys

A Calorie-Restricted Diet Decreases Brain Iron Accumulation and Preserves Motor Performance in Old Rhesus Monkeys

Acute Disruption of the NMDA Receptor Subunit NR1 in the Honeybee Brain Selectively Impairs Memory Formation

Acute Disruption of the NMDA Receptor Subunit NR1 in the Honeybee Brain Selectively Impairs Memory Formation

ATP-Sensitive Potassium Channel-Mediated Lactate Effect on Orexin Neurons: Implications for Brain Energetics during Arousal

ATP-Sensitive Potassium Channel-Mediated Lactate Effect on Orexin Neurons: Implications for Brain Energetics during Arousal

BDNF Controls Cannabinoid CB1 Receptor Function in the Striatum

Brain-Derived Neurotrophic Factor Controls Cannabinoid CB1 Receptor Function in the Striatum

Panel Puts $300 Million Price Tag on Agent Orange Cleanup

Panel Puts $300 Million Price Tag on Agent Orange Cleanup

Human Primordial Germ Cell Formation is Diminished by Exposure to Environmental Toxicants Acting Through the AHR Signaling Pathway

Human Primordial Germ Cell Formation is Diminished by Exposure to Environmental Toxicants Acting Through the AHR Signaling Pathway

Antidiabetogenic diet returns tolerance to commensal bacteria in subclinical colitis!

CiteULike: Inflammatory tendencies and over production of IL-17 in the colon of young NOD mice are counteracted with diet change.: "Young NOD mice show signs of subclinical colitis but the symptoms are alleviated by a diet change to an antidiabetogenic diet. Disrupted immune tolerance in the distal intestine may influence peritoneal cell pools and B-cell mediated activation of diabetogenic T cells."

Luminal leptin inhibits L-glutamine transport in rat small intestine: involvement of ASCT2 and B0AT1

Luminal leptin inhibits L-glutamine transport in rat small intestine: involvement of ASCT2 and B0AT1

Regulation of NF-{kappa}B responses by epigenetic suppression of I{kappa}B{alpha} expression in HCT116 intestinal epithelial cells

Regulation of NF-{kappa}B responses by epigenetic suppression of I{kappa}B{alpha} expression in HCT116 intestinal epithelial cells

Clinical trial shows reduced oxidative stress of preterm neonates w/ Omega 3

"Oxidative stress was significantly reduced in those neonates fed with ω-3 fatty acids, whereas no effect was observed in the neonates fed with standard lipids. Intervention had no effect on infants’ growth and clinical outcome."

European Journal of Clinical Nutrition - Abstract of article: A double-blind, randomized clinical trial of the effect of [omega]-3 fatty acids on the oxidative stress of preterm neonates fed through parenteral nutrition:




Ultra EPA - Fish Oil (90 softgels)

Supplementation with the antioxidant lycopene significantly decreases oxidative stress parameters and the bone resorption marker N-telopeptide of type I collagen in postmenopausal women

Supplementation with the antioxidant lycopene significantly decreases oxidative stress parameters and the bone resorption marker N-telopeptide of type I collagen in postmenopausal women

Compound in grape skins confers endothelial protection via activation of Nrf2

Resveratrol confers endothelial protection via activation of the antioxidant transcription factor Nrf2

Resistin decreases eNOS and May Play Major Role in Oxidative Stress and Mitochondrial Dysfuntion!

Resistin: Resistin is a protein secreted by immune and epithelial cells in some mammals including primates and dogs and secreted in adipocytes in mice and rats. Recent discoveries of its role include inflammation and energy regulation as well as, observations in playing a part in insulin resistance. (Wipedia)

Three antioxidants, seleno-L-methionine, ginsenoside Rb1, and MnTBAP (superoxide dismutase mimetic), effectively blocked resistin-induced eNOS downregulation....Thus resistin directly induces eNOS downregulation through overproduction of ROS and activation of p38 and JNK in HCAECs. Resistin-induced mitochondrial dysfunction and imbalance in cellular redox enzymes may be the underlying mechanisms of oxidative stress.

HEIRS Library Tags: Resistin

CiteULike: Resistin decreases expression of endothelial nitric oxide synthase through oxidative stress in human coronary artery endothelial cells: "Chen, C., Jiang, J., Lu, J.-M., Chai, H., Wang, X., Lin, P. H., and Yao, Q. (2010). Resistin decreases expression of endothelial nitric oxide synthase through oxidative stress in human coronary artery endothelial cells. Am J Physiol Heart Circ Physiol, 299(1):H193-201."

Curcumin Exerts Neuroprotective Effects Against Homocysteine Intracerebroventricular Injection-Induced Cognitive Impairment and Oxidative Stress in Rat Brain

Curcumin Exerts Neuroprotective Effects Against Homocysteine Intracerebroventricular Injection-Induced Cognitive Impairment and Oxidative Stress in Rat Brain

ER Stress in Adipocytes Inhibits Insulin Signaling, Represses Lipolysis, and Alters the Secretion of Adipokines Without Inhibiting Glucose Transport

ER stress in adipocytes might initially lead to changes resembling early prediabetic stages, which at least in part support the regulation of systemic energy homeostasis.

HEIRS Research Tags: ER Stress
Library: Endoplasmic reticulum stress

CiteULike: ER Stress in Adipocytes Inhibits Insulin Signaling, Represses Lipolysis, and Alters the Secretion of Adipokines Without Inhibiting Glucose Transport: "Xu, L., Spinas, G. A., and Niessen, M. (2010). Er stress in adipocytes inhibits insulin signaling, represses lipolysis, and alters the secretion of adipokines without inhibiting glucose transport. Hormone and Metabolic Research."


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Cochlospermum vitifolium induces vasorelaxant and antihypertensive effects mainly by activation of NO/cGMP signaling pathway.

CiteULike: Cochlospermum vitifolium induces vasorelaxant and antihypertensive effects mainly by activation of NO/cGMP signaling pathway.: "Sánchez-Salgado, J. C. C., Castillo-España, P., Ibarra-Barajas, M., Villalobos-Molina, R., and Estrada-Soto, S. (2010). Cochlospermum vitifolium induces vasorelaxant and antihypertensive effects mainly by activation of no/cgmp signaling pathway. Journal of ethnopharmacology."

Cochlospermum vitifolium induces vasorelaxant and antihypertensive effects mainly by activation of NO/cGMP signaling pathway.

CiteULike: Cochlospermum vitifolium induces vasorelaxant and antihypertensive effects mainly by activation of NO/cGMP signaling pathway.: "Sánchez-Salgado, J. C. C., Castillo-España, P., Ibarra-Barajas, M., Villalobos-Molina, R., and Estrada-Soto, S. (2010). Cochlospermum vitifolium induces vasorelaxant and antihypertensive effects mainly by activation of no/cgmp signaling pathway. Journal of ethnopharmacology."

Hypoglycemic, vasorelaxant and hepatoprotective effects of Cochlospermum vitifolium (Willd.) Sprengel: a potential agent for the treatment of metabolic syndrome.

CiteULike: Hypoglycemic, vasorelaxant and hepatoprotective effects of Cochlospermum vitifolium (Willd.) Sprengel: a potential agent for the treatment of metabolic syndrome.: "Sánchez-Salgado, J. C., Ortiz-Andrade, R. R., Aguirre-Crespo, F., Vergara-Galicia, J., León-Rivera, I., Montes, S., Villalobos-Molina, R., and Estrada-Soto, S. (2007). Hypoglycemic, vasorelaxant and hepatoprotective effects of cochlospermum vitifolium (willd.) sprengel: a potential agent for the treatment of metabolic syndrome. Journal of ethnopharmacology, 109(3):400-405."

Dioxin Causes Changes in Blood Vessels Through AhR in Developing Zebrafish!

Dioxins: bioaccumulatives chemical compounds formed through combustion and manufacturing. Incidents include backyard burning, applications of herbicides, wastewater treatment, coal-fires, diesel trucks, cigarette smoke, etc(Wipedia)




A recent study shows "activation of Ahr2/Arnt1 pathway by TCDD and BNF affects the shape of certain blood vessels in the brain of developing zebrafish." Past studies have demonstrated a significant impact of AhR signaling on the immune system that may also alter the Nrf2 antioxidant system. For this reason, we have suggested an important relationship of AhR and Nrf2 signaling in environmental illness and alterations of blood flow may be a factor in environmental illness symptoms. Dinatale showed AhR signaling initiates an inflammatory cascade that includes Il-6 via Il-1 and NF-kappaB and present in autoimmune and chronic proliferative diseases.




CiteULike: Malformation of certain brain blood vessels caused by TCDD activation of Ahr2/Arnt1 signaling in developing zebrafish.:



Teraoka, H., Ogawa, A., Kubota, A., Stegeman, J. J., Peterson, R. E., and Hiraga, T. (2010). Malformation of certain brain blood vessels caused by tcdd activation of ahr2/arnt1 signaling in developing zebrafish. Aquatic toxicology (Amsterdam, Netherlands).
http://www.citeulike.org/user/HEIRS/article/7149860

Dinatale, B. C., Schroeder, J. C., Francey, L. J., Kusnadi, A., and Perdew, G. H. (2010). Mechanistic insights into the events that lead to synergistic induction of il6 transcription upon activation of the ah receptor and inflammatory signaling. The Journal of biological chemistry.
http://www.citeulike.org/user/HEIRS/article/7339715

AhR and NF-E2-related factor 2 are key regulators of human MRP4 expression

Our findings indicate that AhR and Nrf2 play important roles in regulating MRP4 expression and suggest that agents that activate their activity may be of therapeutic benefit for cholestasis.

CiteULike: Aryl hydrocarbon receptor and NF-E2-related factor 2 are key regulators of human MRP4 expression: "Xu, S., Weerachayaphorn, J., Cai, S.-Y., Soroka, C. J., and Boyer, J. L. (2010). Aryl hydrocarbon receptor and nf-e2-related factor 2 are key regulators of human mrp4 expression. Am J Physiol Gastrointest Liver Physiol, 299(1):G126-135."