Explores the mental, physical, cellular and biochemical aspects of environmental illnesses such as obesity, diabetes, chronic fatigue syndrome, PTSD, fibromyalgia, chemical sensitivities, neurological disorders and numerous others. We advocate for better access to medical care, healthier lifestyles, resource conservation and the use of assistance animals for the disabled to promote a better quality of life.
Sunday, October 31, 2010
Nrf2 Regulates Longevity and Aging~!
CiteULike: Nrf2, a Guardian of Healthspan and Gatekeeper of Species Longevity.: "this signaling pathway plays a critical role in the determination of species longevity and that this pathway may indeed be the master regulator of the aging process."
Biologists Discover A Protein Link To Wound Healing
Biologists Discover A Protein Link To Wound Healing: "Diabetes and eczema may appear to be two completely unrelated diseases. But UC San Diego biologists have uncovered what appears to be a crucial biochemical link between the two."
Friday, October 29, 2010
Neuronal inactivation of PPAR{gamma} Coactivator 1... [J Biol Chem. 2010] - PubMed result
Neuronal inactivation of PPAR{gamma} Coactivator 1... [J Biol Chem. 2010] - PubMed result: "Neuronal inactivation of PPAR{gamma} Coactivator 1{alpha}(PGC-1{alpha}) protects mice from diet-induced obesity and leads to degenerative lesions."
Aryl Hydrocarbon Receptor Nuclear Translocator (ARNT) in Hepatocytes is Required for Aryl Hydrocarbon Receptor-Mediated Adaptive and Toxic Responses in Liver
CiteULike: Aryl Hydrocarbon Receptor Nuclear Translocator (ARNT) in Hepatocytes is Required for Aryl Hydrocarbon Receptor-Mediated Adaptive and Toxic Responses in Liver: "AHR-ARNT dimers within the hepatocyte direct the toxic and adaptive and developmental functions associated with the AHR and that developmental vascular events arise due to signaling in a distinct cell type expressing this dimeric pair"
Toluene and Other Solvents Potentiate Auditory Injury from Noise~!
CiteULike: Neuronal circuits involved in the middle-ear acoustic reflex: "depressing action of toluene on the central auditory nuclei driving the middle-ear acoustic reflex might explain the synergistic effects of a co-exposure to noise and aromatic solvents."
Red wine polyphenols prevent endothelial dysfunction induced by endothelin-1 in rat aorta: role of NADPH oxidase
Comment: I may forgetting something -- but this might be a possible benefit of polyphenols from red wine in combatting some of the effects of cigarette smoke and combustable pollutants?
Red wine polyphenols prevent endothelial dysfunction induced by endothelin-1 in rat aorta: role of NADPH oxidase
Red wine polyphenols prevent endothelial dysfunction induced by endothelin-1 in rat aorta: role of NADPH oxidase
Glucosamine Causes The Death Of Pancreatic Cells
"High doses or prolonged use of glucosamine causes the death of pancreatic cells and could increase the risk of developing diabetes,"
Read more: Glucosamine Causes The Death Of Pancreatic Cells:
Read more: Glucosamine Causes The Death Of Pancreatic Cells:
Flaxseed Oil May Protect Against Lead Toxicity~!
"flaxseed oil is a natural product can be protect against lead acetate-mediated hepatic cytotoxicity
Read abstract: CiteULike: The Redox Status in Rats Treated with Flaxseed Oil and Lead-Induced Hepatotoxicity.:."
Read abstract: CiteULike: The Redox Status in Rats Treated with Flaxseed Oil and Lead-Induced Hepatotoxicity.:."
Chronic anabolic androgenic steroid exposure alters corticotropin releasing factor expression and anxiety-like behaviors in the female mouse
Chronic anabolic androgenic steroid exposure alters corticotropin releasing factor expression and anxiety-like behaviors in the female mouse: "Chronic anabolic androgenic steroid exposure alters corticotropin releasing factor expression and anxiety-like behaviors in the female mouse"
Aflatoxin B1 and ethanol co-exposure induces hepatic oxidative damage in mice — Toxicol Ind Health
: "Co-exposure of animals to ethanol and AFB1 showed additive effects on the activities of GST and CAT as well as on the GSH level. Histopathological study revealed that these compounds interact together to exacerbate their individual effects on the liver"
Read more: Aflatoxin B1 and ethanol co-exposure induces hepatic oxidative damage in mice — Toxicol Ind Health
Read more: Aflatoxin B1 and ethanol co-exposure induces hepatic oxidative damage in mice — Toxicol Ind Health
Thursday, October 28, 2010
Regulation of neuronal oxidative and nitrosative stress by endogenous protective pathways and by disease processes.
CiteULike: Regulation of neuronal oxidative and nitrosative stress by endogenous protective pathways and by disease processes.: "the emerging importance of master regulators of antioxidant defences such as Nrf2 and PGC-1α is revealing ways by which intrinsic defences may be manipulated to combat oxidative/nitrosative stress."
CiteULike: Nrf2 and selenoproteins are essential for maintaining oxidative homeostasis in erythrocytes and protecting against hemolytic anemia.
CiteULike: Nrf2 and selenoproteins are essential for maintaining oxidative homeostasis in erythrocytes and protecting against hemolytic anemia.: "selenoprotein activity and the Nrf2 gene battery are particularly important for oxidative homeostasis in erythrocytes and for the prevention of hemolytic anemia"
Wednesday, October 27, 2010
Sulfur dioxide upregulates the aortic nitric oxide... [Eur J Pharmacol. 2010] - PubMed result
Sulfur dioxide upregulates the aortic nitric oxide... [Eur J Pharmacol. 2010] - PubMed result: "Sulfur dioxide upregulates the aortic nitric oxide pathway in rats."
Pneumococcal conjugate vaccine-induced regulatory ... [Thorax. 2010] - PubMed result
I told you I was not crazy when my respiratory symptoms disappeared within hours of get this vaccine.!
Pneumococcal conjugate vaccine-induced regulatory ... [Thorax. 2010] - PubMed result: "Pneumococcal conjugate vaccine-induced regulatory T cells suppress the development of allergic airways disease."
Pneumococcal conjugate vaccine-induced regulatory ... [Thorax. 2010] - PubMed result: "Pneumococcal conjugate vaccine-induced regulatory T cells suppress the development of allergic airways disease."
T Regulatory Cells in Cord Blood-FOXP3 Demethylati... [PLoS One. 2010] - PubMed result
T Regulatory Cells in Cord Blood-FOXP3 Demethylati... [PLoS One. 2010] - PubMed result: "T Regulatory Cells in Cord Blood-FOXP3 Demethylation as Reliable Quantitative Marker."
Severe Sepsis In Seniors Likely To Have Long-term Cognitive And Physical Functioning Impact
"Patients over 65 years of age who have severe sepsis have a significantly high risk of long-term cognitive and physical functioning problems, say researchers from University of Michigan Medical School, Ann Arbor"
Read more: Severe Sepsis In Seniors Likely To Have Long-term Cognitive And Physical Functioning Impact:
Read more: Severe Sepsis In Seniors Likely To Have Long-term Cognitive And Physical Functioning Impact:
Monday, October 25, 2010
The nrf2 system as a potential target for the development of indirect antioxidants.
"critical role of Nrf2 has been demonstrated by various animal studies showing that mice with a targeted disruption of the nrf2 gene are prone to develop lesions in response to environmental toxicants/carcinogens, drugs, and inflammatory insults"
Read more: CiteULike: The nrf2 system as a potential target for the development of indirect antioxidants.:
The cap'n'collar transcription factor Nrf2 mediates both intrinsic resistance to environmental stressors and an adaptive response elicited by chemopreventive agents that determines susceptibility to electrophilic xenobiotics.
"Transcription factor Nrf2 regulates genes encoding drug-metabolising enzymes and drug transporters, as well as enzymes involved in the glutathione, thioredoxin and peroxiredoxin antioxidant pathways......."
Center to study effects of plastics chemicals on children's health
"A new research center based at the University of Illinois will investigate whether regular exposure to bisphenol A (BPA) and phthalates – chemicals widely used in plastics and other consumer products – can alter infant and adolescent development, cognition or behavior."
REad more: Center to study effects of plastics chemicals on children's health:
REad more: Center to study effects of plastics chemicals on children's health:
Friday, October 22, 2010
Thursday, October 21, 2010
First Multiple Sclerosis pill approved in US will change treatment paradigm - Boston Health News | Examiner.com
First Multiple Sclerosis pill approved in US will change treatment paradigm - Boston Health News Examiner.com: "Multiple sclerosis (MS) is an autoimmune disease in which the patients immune system attacks the myelin sheaths covering the neuronal axons in the central nervous system."
Cytoprotective role of Nrf2/Keap1 system in methylmercury toxicity
"primary mouse hepatocytes extracted from Nrf2-deficient mouse was susceptible, and hepatocyte-specific conditional Keap1-deficient mouse was resistant to MeHg-induced cytotoxicity"
Read more: CiteULike: Cytoprotective role of Nrf2/Keap1 system in methylmercury toxicity:
Read more: CiteULike: Cytoprotective role of Nrf2/Keap1 system in methylmercury toxicity:
Tuesday, October 19, 2010
Functional Genomics of Serotonin Receptor 2A (HTR2... [Neuromolecular Med. 2010] - PubMed result
Functional Genomics of Serotonin Receptor 2A (HTR2... [Neuromolecular Med. 2010] - PubMed result: "Functional Genomics of Serotonin Receptor 2A (HTR2A): Interaction of Polymorphism, Methylation, Expression and Disease Association."
CiteULike: The role of Nrf2 signaling in the regulation of antioxidants and detoxifying enzymes after traumatic brain injury in rats and mice.
iteULike: The role of Nrf2 signaling in the regulation of antioxidants and detoxifying enzymes after traumatic brain injury in rats and mice.: "Nrf2 plays a pivotal role in cell defenses against the oxidative stress of TBI. In addition, pharmacological activation of the Nrf2 signaling pathway by small molecule inducers such as SFN attenuated oxidative stress and neuronal damage following TBI."
Discovery Park - Bindley Bioscience Center - News
This sounds interesting, I wonder if any of my "close resources" have any information about this study and Dr.
Robinson from Purdue. He sounds like a wonderful man that like his reputation is climbing to real high places!
Discovery Park - Bindley Bioscience Center - News
Robinson from Purdue. He sounds like a wonderful man that like his reputation is climbing to real high places!
Discovery Park - Bindley Bioscience Center - News
Monday, October 18, 2010
Sunday, October 17, 2010
Air pollution and circulating biomarkers of oxidative stress
"Chemical components of air pollutant exposures that induce oxidative stress and subsequent inflammation may be partly responsible for associations of cardiovascular morbidity and mortality with airborne particulate matter and combustion-related pollutant gasses"
Read more: CiteULike: Air pollution and circulating biomarkers of oxidative stress:
Read more: CiteULike: Air pollution and circulating biomarkers of oxidative stress:
Saturday, October 16, 2010
Dimethyl sulfoxide elevates hydrogen peroxide-mediated cell death in Saccharomyces cerevisiae by inhibiting the antioxidant function of methionine sulfoxide reductase A.
"the DMSO's selective inhibition of the antioxidant function of MsrA in S. cerevisiae, resulting in an increase in oxidative stress-induced cytotoxicity."
Read more: CiteULike: Dimethyl sulfoxide elevates hydrogen peroxide-mediated cell death in Saccharomyces cerevisiae by inhibiting the antioxidant function of methionine sulfoxide reductase A.:
Read more: CiteULike: Dimethyl sulfoxide elevates hydrogen peroxide-mediated cell death in Saccharomyces cerevisiae by inhibiting the antioxidant function of methionine sulfoxide reductase A.:
Friday, October 15, 2010
Alterations in Hepatic mRNA Expression of Phase-II... [Toxicol Sci. 2010] - PubMed result
Alterations in Hepatic mRNA Expression of Phase-II... [Toxicol Sci. 2010] - PubMed result: "HNF4a deficiency markedly alters hepatic mRNA expression of a large number of phase-II enzymes and transporters, probably due to the loss of HNF4a, which is a transactivator and a determinant of gender-specific expression, and/or adaptive activation of signaling pathways important in hepatic regulation of these phase-II enzymes and transporters"
Thursday, October 14, 2010
Dietary inorganic nitrate reverses features of metabolic syndrome in endothelial nitric oxide synthase-deficient mice — PNAS
Dietary inorganic nitrate reverses features of metabolic syndrome in endothelial nitric oxide synthase-deficient mice — PNAS: "Dietary inorganic nitrate reverses features of metabolic syndrome in endothelial nitric oxide synthase-deficient mice"
Ursolic Acid Attenuates D-Galactose-Induced Inflammatory Response in Mouse Prefrontal Cortex through Inhibiting AGEs/RAGE/NF-κB Pathway Activation — Cereb Cortex
Ursolic Acid Attenuates D-Galactose-Induced Inflammatory Response in Mouse Prefrontal Cortex through Inhibiting AGEs/RAGE/NF-κB Pathway Activation — Cereb Cortex: "UA significantly reduced the number of activated microglia cells and astrocytes, decreased the expression of CD11b and glial fibrillary acidic protein, downregulated the expression of iNOS and COX-2, and decreased interleukin (IL)-1β, IL-6, and tumor necrosis factor-α levels in the prefrontal cortex of D-gal–treated mice."
CCL2 modulates cytokine production in cultured mouse astrocytes
CCL2 modulates cytokine production in cultured mouse astrocytes: "The chemokine CCL2 (also known as monocyte chemoattractant protein-1, or MCP-1) is upregulated in patients and rodent models of traumatic brain injury (TBI), contributing to post-traumatic neuroinflammation and degeneration by directing the infiltration of blood-derived macrophages into the injured brain."
Wednesday, October 13, 2010
Making A Case for Tregs and LPS in Multiple Chemical Sensitivity~!
If there is injury and disruption of activities of olfactory neurons that has a connection to memory- can alteration of these proteins be a factor in MCS because of alteration of signals that exist between them?
Different studies have shown some interesting things about the sense of olfaction. It would be interesting to understand better how long-term toxic exposures alter the general patterns of operation of receptors in neurons and what circumstances make one more vulnerable. Zhang expressed that gap junctons modulate activity and sensitivity of olfactory neurons that have been shown to have receptors for one odorant whereas, cortical neurons get imputs from a number of different ones. (Buck) Kay writes that when the nose is first exposed to odor the molecules are absorbed into the olfactory receptor cells that line the mucous membranes at the back of the nostrils. There are some 350 varieties of these receptor cells, each specialized to detect certain odor molecules which convert this information into nerve impulses and then transmit them to the brain’s two olfactory bulbs (one for each nostril), which sit just behind the nose. The olfactory bulbs then translates the impulses into information the brain can understand and are sent on to the olfactory cortex where the "odor information" is processed.
Several recent studies show disruptions in the sense of smell are indicative of the early signs of diseases including Alzheimer's disease, autism, Parkinson's disease and schizophrenia. Dr. Wilson, an expert in the neurobiology of olfaction explains that olfaction is a unique "sense" because it has direct links to the amygdala that is important for regulating emotion and physiology and to the prefrontal cortex that is involved with cognition and planning. He also points out that this connection is also the short path that links olfaction with memory. (Kay) As noted, olfactory disfunction is a "early-warning" sign of schizophrenia and Turetsky's data indicates structural and functional abnormalities run from the cortex to the olfactory system. "These reflect, in part, a genetically mediated neurodevelopmental etiology. Gross structural and functional anomalies are mirrored by cellular and molecular abnormalities that suggest decreased or faulty innervation and/or dysregulation of intracellular signaling. A unifying mechanistic hypothesis may be the epigenetic regulation of gene expression." This is also in line with some of the most current hypotheses of neuroinflammation and epigenetic influences in autism.
Many patients that have chemical sensitivity describe that the worst of the symptoms began occurring after a bout of infection. Multiple chemical sensitivity is a condition where symptoms such as nausea, respiratory problems, mood changes, cognitive problems and numerous other repored symptoms occur at a very low exposure of an "odor" stimulus. In the past, we have suggestedTreg impairment may be important for the development of many responses in MCS which may be long lasting or transient depending on factors including other secondary exposures that influence or prevent their activity. In addition, Treg disfunction has been implicated in a number of co-morbid health conditions such as inflammatory bowel disease and the sensitivities in autism. Interestingly, many common current treatments for MCS were used for treatments for autism before they were used for MCS. Recent reports have also suggested that suppression of regulatory T cells from air pollution may be an important factor in the development and augmentation of respiratory disease like asthma. (Berkley) Air pollutants and particulate matter contain a variety of contaminants including LPS endotoxin from bacteria, hydrocarbons and metals. A recent study demonstrates that LPS a common contaminant of most environments can alter the expression of Cx43 and caveolin-3. The former Cx43 is a connexin protein that has been found to be important for the integrity of gap junctions shown to dictate olfactory sensitivity. Interestingly, regulatory T cells also play a role in the communication activities of gap junctions. Taking these recent studies into consideration the newest research on regulatory T cells in promotion of the adaptive response and maintaining tolerance support, one could propose that altered communication may play a role in chemical sensitivity and odor and olfactory function and prvode parallel support to the recent research of how Tregs disfunction may influence respiratory problems from air pollution. In addition, because their is a relationship gap functions to activity of NO/cGMP and its downstream targets and related biological roles in relation to memory -- this could explain some of the cognitive problems associated with MCS. Generally, suppression of Tregs and their role in gap function has implications for both animals and humans. In animals impairment of the olfactory system may negatively influence instinctual patterns of navigation and other behaviors.
Related: Dysfunction of Methylation and Nrf2 in Environmental Illness - Is This A Better Explanation than NO/ONOO- ?
****Read more research blogs: Kimberly Kramer
Kay, Sharon. Memory and the Senses. New York University Physician. Spring 2010. Retrieved on October 1, 2010. webdoc.nyumc.org/nyumc/files/.../u3/NYUPhysSpring2010.pdf
The Logic of Smell. MedGadget, Internet Journal of Emerging Medical Technologies. Retrieved on October 14, 2010. http://medgadget.com/archives/2005/05/
BMC Neuroscience, Vol. 11, No. 1. (2010), 108. http://www.citeulike.org/user/HEIRS/article/7724812?show_msg=already_posted
Yang, Sarah. Air pollution alters immune function, worsens asthma symptoms. UCBerkelyNews.com. Retrieved on 10/13/2010. http://www.berkeley.edu/news/media/releases/2010/10/05_asthma.shtml
Ring, S., Karakhanova, S., Johnson, T., Enk, A. H., and Mahnke, K. (2010). Gap junctions between regulatory t cells and dendritic cells prevent sensitization of cd8(+) t cells. The Journal of allergy and clinical immunology, 125(1). http://www.citeulike.org/user/HEIRS/article/8006437
Bopp, T., Radsak, M., Schmitt, E., and Schild, H. (2010). New strategies for the manipulation of adaptive immune responses. Cancer Immunology, Immunotherapy, 59(9):1443-1448. http://www.citeulike.org/user/HEIRS/article/6973883
Yao, J., Hiramatsu, N., Zhu, Y., Morioka, T., Takeda, M., Oite, T., and Kitamura, M. (2005). Nitric oxide-mediated regulation of connexin43 expression and gap junctional intercellular communication in mesangial cells. Journal of the American Society of Nephrology : JASN, 16(1):58-67. http://www.citeulike.org/user/HEIRS/article/8006401
González-Flores, O., Beyer, C., Lima-Hernández, F. J. J., Gómora-Arrati, P., Gómez-Camarillo, M. A., Hoffman, K., and Etgen, A. M. (2007). Facilitation of estrous behavior by vaginal cervical stimulation in female rats involves alpha1-adrenergic receptor activation of the nitric oxide pathway. Behavioural brain research, 176(2):237-243. http://www.citeulike.org/user/HEIRS/article/8006383
Lowe, G., Buerk, D. G., Ma, J., and Gelperin, A. (2008). Tonic and stimulus-evoked nitric oxide production in the mouse olfactory bulb. Neuroscience, 153(3):842-850. http://www.citeulike.org/user/HEIRS/article/8006357
Liao, C.-K. K., Wang, S.-M. M., Chen, Y.-L. L., Wang, H.-S. S., and Wu, J.-C. C. (2010). Lipopolysaccharide-induced inhibition of connexin43 gap junction communication in astrocytes is mediated by downregulation of caveolin-3. The international journal of biochemistry & cell biology, 42(5):762-770. http://www.citeulike.org/user/HEIRS/article/6580463
Kawasaki, A., Hayashi, T., Nakachi, K., Trosko, J. E., Sugihara, K., Kotake, Y., and Ohta, S. (2009). Modulation of connexin 43 in rotenone-induced model of parkinson's disease. Neuroscience, 160(1):61-68. http://www.citeulike.org/user/HEIRS/article/7971659
Zhang, C. (2010). Gap junctions in olfactory neurons modulate olfactory sensitivity. BMC neuroscience, 11(1):108+. http://www.citeulike.org/user/HEIRS/article/7724812
Li, D.-q., Li, X.-j., Duan, J.-f., and Cai, W. (2010). Wuling capsule promotes hippocampal neurogenesis by improving expression of connexin 43 in rats exposed to chronic unpredictable mild stress. Journal of Chinese Integrative Medicine, 8(7). http://www.citeulike.org/user/HEIRS/article/7971605
Different studies have shown some interesting things about the sense of olfaction. It would be interesting to understand better how long-term toxic exposures alter the general patterns of operation of receptors in neurons and what circumstances make one more vulnerable. Zhang expressed that gap junctons modulate activity and sensitivity of olfactory neurons that have been shown to have receptors for one odorant whereas, cortical neurons get imputs from a number of different ones. (Buck) Kay writes that when the nose is first exposed to odor the molecules are absorbed into the olfactory receptor cells that line the mucous membranes at the back of the nostrils. There are some 350 varieties of these receptor cells, each specialized to detect certain odor molecules which convert this information into nerve impulses and then transmit them to the brain’s two olfactory bulbs (one for each nostril), which sit just behind the nose. The olfactory bulbs then translates the impulses into information the brain can understand and are sent on to the olfactory cortex where the "odor information" is processed.
Several recent studies show disruptions in the sense of smell are indicative of the early signs of diseases including Alzheimer's disease, autism, Parkinson's disease and schizophrenia. Dr. Wilson, an expert in the neurobiology of olfaction explains that olfaction is a unique "sense" because it has direct links to the amygdala that is important for regulating emotion and physiology and to the prefrontal cortex that is involved with cognition and planning. He also points out that this connection is also the short path that links olfaction with memory. (Kay) As noted, olfactory disfunction is a "early-warning" sign of schizophrenia and Turetsky's data indicates structural and functional abnormalities run from the cortex to the olfactory system. "These reflect, in part, a genetically mediated neurodevelopmental etiology. Gross structural and functional anomalies are mirrored by cellular and molecular abnormalities that suggest decreased or faulty innervation and/or dysregulation of intracellular signaling. A unifying mechanistic hypothesis may be the epigenetic regulation of gene expression." This is also in line with some of the most current hypotheses of neuroinflammation and epigenetic influences in autism.
"gap junctional communication in the olfactory epithelium modulates olfactory activity at the peripheral level and alters glomerular activation patterns (odor maps) in the olfactory bulb. Topological changes in odor maps due to gap junctional modulation could affect perception of odor quality or quantity." (Zhang)To what extent do disruptions of Tregs contribute to disease development?
Many patients that have chemical sensitivity describe that the worst of the symptoms began occurring after a bout of infection. Multiple chemical sensitivity is a condition where symptoms such as nausea, respiratory problems, mood changes, cognitive problems and numerous other repored symptoms occur at a very low exposure of an "odor" stimulus. In the past, we have suggestedTreg impairment may be important for the development of many responses in MCS which may be long lasting or transient depending on factors including other secondary exposures that influence or prevent their activity. In addition, Treg disfunction has been implicated in a number of co-morbid health conditions such as inflammatory bowel disease and the sensitivities in autism. Interestingly, many common current treatments for MCS were used for treatments for autism before they were used for MCS. Recent reports have also suggested that suppression of regulatory T cells from air pollution may be an important factor in the development and augmentation of respiratory disease like asthma. (Berkley) Air pollutants and particulate matter contain a variety of contaminants including LPS endotoxin from bacteria, hydrocarbons and metals. A recent study demonstrates that LPS a common contaminant of most environments can alter the expression of Cx43 and caveolin-3. The former Cx43 is a connexin protein that has been found to be important for the integrity of gap junctions shown to dictate olfactory sensitivity. Interestingly, regulatory T cells also play a role in the communication activities of gap junctions. Taking these recent studies into consideration the newest research on regulatory T cells in promotion of the adaptive response and maintaining tolerance support, one could propose that altered communication may play a role in chemical sensitivity and odor and olfactory function and prvode parallel support to the recent research of how Tregs disfunction may influence respiratory problems from air pollution. In addition, because their is a relationship gap functions to activity of NO/cGMP and its downstream targets and related biological roles in relation to memory -- this could explain some of the cognitive problems associated with MCS. Generally, suppression of Tregs and their role in gap function has implications for both animals and humans. In animals impairment of the olfactory system may negatively influence instinctual patterns of navigation and other behaviors.
Related: Dysfunction of Methylation and Nrf2 in Environmental Illness - Is This A Better Explanation than NO/ONOO- ?
****Read more research blogs: Kimberly Kramer
Kay, Sharon. Memory and the Senses. New York University Physician. Spring 2010. Retrieved on October 1, 2010. webdoc.nyumc.org/nyumc/files/.../u3/NYUPhysSpring2010.pdf
The Logic of Smell. MedGadget, Internet Journal of Emerging Medical Technologies. Retrieved on October 14, 2010. http://medgadget.com/archives/2005/05/
BMC Neuroscience, Vol. 11, No. 1. (2010), 108. http://www.citeulike.org/user/HEIRS/article/7724812?show_msg=already_posted
Yang, Sarah. Air pollution alters immune function, worsens asthma symptoms. UCBerkelyNews.com. Retrieved on 10/13/2010. http://www.berkeley.edu/news/media/releases/2010/10/05_asthma.shtml
Ring, S., Karakhanova, S., Johnson, T., Enk, A. H., and Mahnke, K. (2010). Gap junctions between regulatory t cells and dendritic cells prevent sensitization of cd8(+) t cells. The Journal of allergy and clinical immunology, 125(1). http://www.citeulike.org/user/HEIRS/article/8006437
Bopp, T., Radsak, M., Schmitt, E., and Schild, H. (2010). New strategies for the manipulation of adaptive immune responses. Cancer Immunology, Immunotherapy, 59(9):1443-1448. http://www.citeulike.org/user/HEIRS/article/6973883
Yao, J., Hiramatsu, N., Zhu, Y., Morioka, T., Takeda, M., Oite, T., and Kitamura, M. (2005). Nitric oxide-mediated regulation of connexin43 expression and gap junctional intercellular communication in mesangial cells. Journal of the American Society of Nephrology : JASN, 16(1):58-67. http://www.citeulike.org/user/HEIRS/article/8006401
González-Flores, O., Beyer, C., Lima-Hernández, F. J. J., Gómora-Arrati, P., Gómez-Camarillo, M. A., Hoffman, K., and Etgen, A. M. (2007). Facilitation of estrous behavior by vaginal cervical stimulation in female rats involves alpha1-adrenergic receptor activation of the nitric oxide pathway. Behavioural brain research, 176(2):237-243. http://www.citeulike.org/user/HEIRS/article/8006383
Lowe, G., Buerk, D. G., Ma, J., and Gelperin, A. (2008). Tonic and stimulus-evoked nitric oxide production in the mouse olfactory bulb. Neuroscience, 153(3):842-850. http://www.citeulike.org/user/HEIRS/article/8006357
Liao, C.-K. K., Wang, S.-M. M., Chen, Y.-L. L., Wang, H.-S. S., and Wu, J.-C. C. (2010). Lipopolysaccharide-induced inhibition of connexin43 gap junction communication in astrocytes is mediated by downregulation of caveolin-3. The international journal of biochemistry & cell biology, 42(5):762-770. http://www.citeulike.org/user/HEIRS/article/6580463
Kawasaki, A., Hayashi, T., Nakachi, K., Trosko, J. E., Sugihara, K., Kotake, Y., and Ohta, S. (2009). Modulation of connexin 43 in rotenone-induced model of parkinson's disease. Neuroscience, 160(1):61-68. http://www.citeulike.org/user/HEIRS/article/7971659
Zhang, C. (2010). Gap junctions in olfactory neurons modulate olfactory sensitivity. BMC neuroscience, 11(1):108+. http://www.citeulike.org/user/HEIRS/article/7724812
Li, D.-q., Li, X.-j., Duan, J.-f., and Cai, W. (2010). Wuling capsule promotes hippocampal neurogenesis by improving expression of connexin 43 in rats exposed to chronic unpredictable mild stress. Journal of Chinese Integrative Medicine, 8(7). http://www.citeulike.org/user/HEIRS/article/7971605
Tuesday, October 12, 2010
LPS stimulates nitric oxide synthase-2 expression in murine skeletal muscle and C(2)C(12) myoblasts via Toll-like receptor-4 and c-Jun NH(2)-terminal kinase pathways.
"Frost, R. A., Nystrom, G. J., and Lang, C. H. (2004). Lipopolysaccharide stimulates nitric oxide synthase-2 expression in murine skeletal muscle and c(2)c(12) myoblasts via toll-like receptor-4 and c-jun nh(2)-terminal kinase pathways. American journal of physiology. Cell physiology, 287(6)."
CiteULike: Lipopolysaccharide stimulates nitric oxide synthase-2 expression in murine skeletal muscle and C(2)C(12) myoblasts via Toll-like receptor-4 and c-Jun NH(2)-terminal kinase pathways.:
CiteULike: Lipopolysaccharide stimulates nitric oxide synthase-2 expression in murine skeletal muscle and C(2)C(12) myoblasts via Toll-like receptor-4 and c-Jun NH(2)-terminal kinase pathways.:
NO synthase II in mouse skeletal muscle is associated with caveolin 3.
NO synthase II in mouse skeletal muscle is associated with caveolin 3.: "The association of NOS II with caveolin 3 might have implications for the regulation of contraction of, and/or glucose uptake by, slow-twitch muscle fibres."
A Correlation Found Between Childhood Adversity And Exaggerated Inflammatory Response To Stress Among Seemingly Healthy People
"Seemingly healthy adults, if they were abused or neglected during childhood, may suffer physiological consequences decades later. In research published online by the journal Neuropsychopharmacology"
Read more: A Correlation Found Between Childhood Adversity And Exaggerated Inflammatory Response To Stress Among Seemingly Healthy People:
Read more: A Correlation Found Between Childhood Adversity And Exaggerated Inflammatory Response To Stress Among Seemingly Healthy People:
Infant Jaundice Linked To Higher Risk Of Autism And Psychological Development Disorders In General
"A baby with neonatal jaundice, meaning jaundice within a few days or weeks of being born, has a higher risk of being diagnosed with autism or some other psychological development disorder later on in life compared to infants who did not have neonatal jaundice,"
Read more: Infant Jaundice Linked To Higher Risk Of Autism And Psychological Development Disorders In General:
Read more: Infant Jaundice Linked To Higher Risk Of Autism And Psychological Development Disorders In General:
Monday, October 11, 2010
Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity
"The aim of this study was to investigate the possibility that a decreased mitochondrial ATP synthesis causes muscular and mental fatigue and plays a role in the pathophysiology of the chronic fatigue syndrome (CFS/ME)."
Read more: Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity:
Read more: Patients with chronic fatigue syndrome performed worse than controls in a controlled repeated exercise study despite a normal oxidative phosphorylation capacity:
Saturday, October 9, 2010
Nrf2, HSP90 and CFS - More Evidence of Increased Risk w Certain Ancestries~!
Backgound: In recent weeks we have discussed many health problems that may occur with impaired Nrf2 functioning. Past studies have also suggested that SNPs in Nrf2 which may be population specific and may increase oxidative stress in those individuals. One such SNP has been shown to be present in the Native American population and another study has suggested that while the data is limited there seems to be a significantly higher risk of chronic fatigue syndrome in Native Americans and African-Americans. It has also be suggested that HSP90 activity may be used as a marker for CFS in a past study.
Thambirajah, A. A., Sleigh, K., Stiver, H. G., and Chow, A. W. (2008). Differential heat shock protein responses to strenuous standardized exercise in chronic fatigue syndrome patients and matched healthy controls. Clinical and investigative medicine. Médecine clinique et experimentale, 31(6). http://www.citeulike.org/user/HEIRS/article/3725342
Niture, S. K. and Jaiswal, A. K. (2010). Hsp90 interaction with inrf2 (keap1) mediates stress-induced nrf2 activation. The Journal of biological chemistry. http://www.citeulike.org/user/HEIRS/article/7968348
Dinos, S., Khoshaba, B., Ashby, D., White, P. D. D., Nazroo, J., Wessely, S., and Bhui, K. S. S. (2009). A systematic review of chronic fatigue, its syndromes and ethnicity: prevalence, severity, co-morbidity and coping. International journal of epidemiology. http://www.citeulike.org/group/6033/article/4289419
Niture from the University of Maryland demonstrates that HSP90 is involved in the activity of the Nrf2. He writes that Keap1 is an adaptor for Nrf2 and that HSP90 is a stabilizer for Keap1 under stress. He reports that HSP90 interacts with this adaptor to activate Nrf2. This suggests that Nrf2 activity may be closely associated with the development of CFS and leads one to assume that mechanisms that improve the activity of Nrf2 may be beneficial for therapeutics for CFS which may have a higher incidence rate for individuals with specific ancestries.Read more: HSP90
Thambirajah, A. A., Sleigh, K., Stiver, H. G., and Chow, A. W. (2008). Differential heat shock protein responses to strenuous standardized exercise in chronic fatigue syndrome patients and matched healthy controls. Clinical and investigative medicine. Médecine clinique et experimentale, 31(6). http://www.citeulike.org/user/HEIRS/article/3725342
Niture, S. K. and Jaiswal, A. K. (2010). Hsp90 interaction with inrf2 (keap1) mediates stress-induced nrf2 activation. The Journal of biological chemistry. http://www.citeulike.org/user/HEIRS/article/7968348
Dinos, S., Khoshaba, B., Ashby, D., White, P. D. D., Nazroo, J., Wessely, S., and Bhui, K. S. S. (2009). A systematic review of chronic fatigue, its syndromes and ethnicity: prevalence, severity, co-morbidity and coping. International journal of epidemiology. http://www.citeulike.org/group/6033/article/4289419
Friday, October 8, 2010
Household poisoning cases from mercury brought fro... [Eur J Pediatr. 2010] - PubMed result
Household poisoning cases from mercury brought fro... [Eur J Pediatr. 2010] - PubMed result: "Household poisoning cases from mercury brought from school."
Regulatory T cells suppress antigen-driven CD4 T c... [J Leukoc Biol. 2010] - PubMed result
Regulatory T cells suppress antigen-driven CD4 T c... [J Leukoc Biol. 2010] - PubMed result: "these findings demonstrate that Tregs can actively control the in vivo expansion and reactivity of antigen-stimulated, naïve CD4 T cells following severe injury."
Regulatory T cells as a potent target for controll... [Biochem Biophys Res Commun. 2010] - PubMed result
Regulatory T cells as a potent target for controll... [Biochem Biophys Res Commun. 2010] - PubMed result: "role of Tregs in the pathogenesis and treatment of bone loss in metabolic bone diseases."
Thursday, October 7, 2010
Constituents from Cistus salvifolius (Cistaceae) A... [Planta Med. 2010] - PubMed result
Constituents from Cistus salvifolius (Cistaceae) A... [Planta Med. 2010] - PubMed result: "PPAR γ represents a candidate molecule for the mediation of improvement of glucose metabolism by botanical/nutritional products."
IDENTIFICATION OF THE ARYL HYDROCARBON RECEPTOR TA... [J Biol Chem. 2010] - PubMed result
IDENTIFICATION OF THE ARYL HYDROCARBON RECEPTOR TA... [J Biol Chem. 2010] - PubMed result: "The vitamin B3 constituent, nicotinamide (NAM), prevented TCDD suppression of glucose output, NAD(+), and gluconeogenic genes and stabilized PGC1α. The corrective effects of NAM could be attributed to increased NAD(+) levels and suppression of AHR target gene induction."
Wednesday, October 6, 2010
Tuesday, October 5, 2010
Cellular Immune Processes in IBD Activated By Smoke, Burning and More!
"Modulation of AhR signaling pathway via the diet, cessation of smoking, or administration of AhR antagonists could be viable strategies for the treatment of IBD."
Arsenescu, R., Arsenescu, V., Zhong, J., Nasser, M., Melinte, R., Dingle, C. W., Swanson, H., and de Villiers, W. J. (2010). Role of the xenobiotic receptor in inflammatory bowel disease. Inflammatory bowel diseases.
http://www.citeulike.org/user/HEIRS/article/7950224
Arsenescu, R., Arsenescu, V., Zhong, J., Nasser, M., Melinte, R., Dingle, C. W., Swanson, H., and de Villiers, W. J. (2010). Role of the xenobiotic receptor in inflammatory bowel disease. Inflammatory bowel diseases.
http://www.citeulike.org/user/HEIRS/article/7950224
Transient Repeated Dose of Broccoli Compound Has Prolonged Protection Against Cell Damage!
CiteULike: Repeated Transient Sulforaphane Stimulation in Astrocytes Leads to Prolonged Nrf2-mediated Gene Expression and Protection from Superoxide-induced Damage.: "Bergström, P., Andersson, H. C., Gao, Y., Karlsson, J.-O. O., Nodin, C., Anderson, M. F., Nilsson, M., and Hammarsten, O. (2010). Repeated transient sulforaphane stimulation in astrocytes leads to prolonged nrf2-mediated gene expression and protection from superoxide-induced damage. Neuropharmacology."
Monday, October 4, 2010
Using small molecule GSK3β inhibitors to treat inf... [Curr Med Chem. 2010] - PubMed result
Using small molecule GSK3β inhibitors to treat inf... [Curr Med Chem. 2010] - PubMed result: "Using small molecule GSK3β inhibitors to treat inflammation"
Stress Hormone Causes Epigenetic Changes
Stress Hormone Causes Epigenetic Changes: "During stressful situations, we produce steroid hormones called glucocorticoids that affect many systems throughout the body. These effects are mediated by the hypothalamic-pituitary-adrenal (HPA) axis, a network involving the hypothalamus and pituitary gland in the brain and the adrenal glands near the kidneys."
Prenatal Polycyclic Aromatic Hydrocarbon Exposure Leads to Behavioral Deficits and Downregulation of Receptor Tyrosine Kinase, MET — Toxicol Sci
"common pollutants, such as the polycyclic aromatic hydrocarbon benzo(a)pyrene, can have a direct, negative impact on the regulated developmental expression of an autism risk gene with associated negative behavioral learning and memory outcomes."
Read more: Prenatal Polycyclic Aromatic Hydrocarbon Exposure Leads to Behavioral Deficits and Downregulation of Receptor Tyrosine Kinase, MET — Toxicol Sci:
Read more: Prenatal Polycyclic Aromatic Hydrocarbon Exposure Leads to Behavioral Deficits and Downregulation of Receptor Tyrosine Kinase, MET — Toxicol Sci:
Modulation of aryl hydrocarbon receptor-regulated gene expression by arsenite, cadmium, and chromium.
CiteULike: Modulation of aryl hydrocarbon receptor-regulated gene expression by arsenite, cadmium, and chromium.: "These results show that the ability of metals to alter the capacity of AhR ligands to induce the bioactivating phase I and the detoxifying phase II enzymes will influence the carcinogenicity and mutagenicity of the AhR ligands."
Sunday, October 3, 2010
Neuroinflammation and Microglia: Considerations and approaches for neurotoxicity assessment
"Recent work, however, has clearly demonstrated that the cellular activities are, for the most part, beneficial. It is when the strict regulatory control normally imposed on them is altered that these cells may begin to show detrimental effects. One could speculate that such functions could be related to senescence and the inability to perform normal activities or the production of pro-inflammatory cytokines exceeding the down-regulatory capacity of the system with either an acute or chronic induction"
Harry, G. J. J. and Kraft, A. D. (2008). Neuroinflammation and microglia: considerations and approaches for neurotoxicity assessment. Expert opinion on drug metabolism & toxicology, 4(10):1265-1277. http://www.citeulike.org/user/HEIRS/article/7943439
Harry, G. J. J. and Kraft, A. D. (2008). Neuroinflammation and microglia: considerations and approaches for neurotoxicity assessment. Expert opinion on drug metabolism & toxicology, 4(10):1265-1277. http://www.citeulike.org/user/HEIRS/article/7943439
Saturday, October 2, 2010
Neurodegeneration in an animal model of Parkinson's disease is exacerbated by a high-fat diet
"diet high in fat and the resulting insulin resistance may lower the threshold for developing PD, at least following DA-specific toxin exposure."
Read more:Neurodegeneration in an animal model of Parkinson's disease is exacerbated by a high-fat diet:
Read more:Neurodegeneration in an animal model of Parkinson's disease is exacerbated by a high-fat diet:
Molecular On-Off Switches For Cancer And Autoimmunity Defined By Scientists
"new report published in the October 2010 print issue of The FASEB Journal offers a ray of hope in the search for new cancer drugs. By examining the seemingly conflicting roles of how oncogenes and tumor suppressor genes handle cellular stress,"
Read more: Molecular On-Off Switches For Cancer And Autoimmunity Defined By Scientists:
Read more: Molecular On-Off Switches For Cancer And Autoimmunity Defined By Scientists:
Friday, October 1, 2010
Beyond Pesticides Daily News Blog » Blog Archive » Study Links Low Dose POPs Exposure to Type 2 Diabetes
Beyond Pesticides Daily News Blog » Blog Archive » Study Links Low Dose POPs Exposure to Type 2 Diabetes: "study published in the September 2010 issue of the journal Environmental Health Perspectives links low dose exposure to some persistent organic pollutants (POPs) to type 2 diabetes. The authors report that some POPs, including highly chlorinated PCBs, PBB153 and the organochlorine insecticides trans-nonachlor, oxychlordane and mirex, were associated with type 2 diabetes over an 18-year period, especially in obsese people."
Insulin Resistance Linked to Reduced Mitochondrial Function - In fasting subjects, elevated free fatty acids and intramuscular fat accumulation could be cause - ModernMedicine
Insulin Resistance Linked to Reduced Mitochondrial Function - In fasting subjects, elevated free fatty acids and intramuscular fat accumulation could be cause - ModernMedicine: "Insulin resistance appears to have a negative effect on mitochondrial function that isn't due to hyperglycemia, as seen in research on fasting individuals published in the September issue of Diabetes."
Characterization of Developmental neurotoxicity of As, Cd and Pb mixture: Synergistic Action of Metal Mixture in Glial and Neuronal Functions — Toxicol Sci
: "together, these observations are the first to show that mixture of As, Cd and Pb has the capacity to induce synergistic toxicity in astrocytes that may compromise the BBB, and may cause behaviroal dysfunction in developing rats."
Read more: Characterization of Developmental neurotoxicity of As, Cd and Pb mixture: Synergistic Action of Metal Mixture in Glial and Neuronal Functions — Toxicol Sci
Read more: Characterization of Developmental neurotoxicity of As, Cd and Pb mixture: Synergistic Action of Metal Mixture in Glial and Neuronal Functions — Toxicol Sci
Mitochondrial decay is involved in BaP-induced cer... [Free Radic Biol Med. 2010] - PubMed result
Mitochondrial decay is involved in BaP-induced cer... [Free Radic Biol Med. 2010] - PubMed result: "Mitochondrial decay is involved in BaP-induced cervical damage."
Iron species mediated dopamine oxidation, proteasome inhibition and dopaminergic cell demise, implications to iron related dopaminergic neuron degeneration.
"Zhou, Z. D. D., Lan, Y. H. H., Tan, E. K. K., and Lim, T. M. M. (2010). Iron species mediated dopamine oxidation, proteasome inhibition and dopaminergic cell demise, implications to iron related dopaminergic neuron degeneration. Free radical biology & medicine."
CiteULike: Iron species mediated dopamine oxidation, proteasome inhibition and dopaminergic cell demise, implications to iron related dopaminergic neuron degeneration.:
CiteULike: Iron species mediated dopamine oxidation, proteasome inhibition and dopaminergic cell demise, implications to iron related dopaminergic neuron degeneration.:
Astrocyte Glutamine Synthetase: Importance in Hyperammonemic Syndromes and Potential Target for Therapy
"Ammonia is normally detoxified in the liver and extrahepatic tissues by conversion to urea and glutamine, respectively. In the brain, glutamine synthesis is largely confined to astrocytes, and it is generally accepted that in hyperammonemia excess glutamine compromises astrocyte morphology and function."
Read more: Astrocyte Glutamine Synthetase: Importance in Hyperammonemic Syndromes and Potential Target for Therapy:
Read more: Astrocyte Glutamine Synthetase: Importance in Hyperammonemic Syndromes and Potential Target for Therapy:
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