Billmeik wrote:What the hell is an auto antibody?
An autoantibody is an antibody (a type of protein) manufactured by the immune system that is directed against one or more of the individual's own proteins. It is derived from the Greek "auto" which means "self", "anti" which means "against" and "body". Many autoimmune diseases, notably lupus erythematosus, are caused by such autoantibodies.
Trace Elements in Human Health and Disease: An Update
The many functions of zinc in inflammatory conditions of the gastrointestinal tract
gastric diseases; inflammatory bowel disease; intestinal permeability; inflammation; zinc
A variety of inflammatory gastrointestinal diseases are associated with altered zinc metabolism or deficiency. Acute and chronic diarrheal disorders may cause deficiency because of increased losses, altered immunity or decreased absorption. When the small intestinal barrier is altered by inflammation, zinc supplementation may be beneficial not only in correcting the deficiency but also because it improves the small bowel mucosal capacity of absorbing water and electrolytes. Zinc is known to have antioxidant properties being a membrane stabilizer, scavenging reactive oxygen metabolites and regulating cytokine synthesis through the activation of transcription factors and this has relevant potential in inflammatory bowel diseases. Moreover, the element stimulates tissue healing and repair in experimental ulcers directly through promoting cell proliferation, protein synthesis and growth factors production and scavenging free radicals. Interest is growing in supplementary therapies with elements and vitamins but current research suggests great caution and to balance the benefits and dangers of uncontrolled administration, since zinc can also stimulate an increased acute phase response and this can exacerbate chronic relapsing diseases. Zinc plays an important role in inflammation. The metal has catalytic, co-catalytic and structural functions in many zinc-dependent enzymes of the body through the regulation of gene expression. Moreover, the involvement of zinc finger proteins in the genetic expression of growth factors has been established. Zinc stabilizes cellular membranes especially interacting at the SH levels and preventing depolarization of phospholipids. The effects on cellular immunity and especially on the activity of serum thymulin and natural killer cells, T-lymphocyte proliferation and interleukin-2 production are also well-known. A growing body of evidence suggests a role for zinc in antioxidant defence systems. The metal has only one stable oxidation state (divalent) and is not affected by free radicals or oxidative stress. It may act as a scavenger of radical products through the synthesis of enzymes such as superoxide dismutase (SOD) and metallothionein (MT) or it may affect cytokine-activated transcription factors. J. Trace Elem. Exp. Med. 13:33-39, 2000. © 2000 Wiley-Liss, Inc.
Kir4.1 Potassium Channel Subunit Is Crucial for Oligodendrocyte Development and In Vivo Myelination
To understand the cellular and in vivo functions of specific K+ channels in glia, we have studied mice with a null mutation in the weakly inwardly rectifying K+ channel subunit Kir4.1. Kir4.1−/− mice display marked motor impairment, and the cellular basis is hypomyelination in the spinal cord, accompanied by severe spongiform vacuolation, axonal swellings, and degeneration. Immunostaining in the spinal cord of wild-type mice up to postnatal day 18 reveals that Kir4.1 is expressed in myelin-synthesizing oligodendrocytes, but probably not in neurons or glial fibrillary acidic protein-positive (GFAP-positive) astrocytes. Cultured oligodendrocytes from developing spinal cord of Kir4.1−/− mice lack most of the wild-type K+ conductance, have depolarized membrane potentials, and display immature morphology. By contrast, cultured neurons from spinal cord of Kir4.1−/− mice have normal physiological characteristics. We conclude that Kir4.1 forms the major K+ conductance of oligodendrocytes and is therefore crucial for myelination.The Kir4.1 knock-out mouse is one of the few CNS dysmyelinating or demyelinating phenotypes that does not involve a gene directly involved in the structure, synthesis, degradation, or immune response to myelin. Therefore, this mouse shows how an ion channel mutation could contribute to the polygenic demyelinating diseases.
Is the Kir4.1 mRNA itself regulated by hypoxia? Cultured astrocytes were placed in an
environmental chamber for 4 or 16 h in 5% CO 2 /95% N 2 . Under the microscope, the 4-h hypoxic
cultures appeared normal, whereas after 16 h there was obvious cell death
Hydrocephalus is characterized by impaired cerebrospinal fluid (CSF) flow with enlargement of the ventricular cavities of the brain and progressive damage to surrounding tissue. Bulk water movement is altered in these brains. We hypothesized that increased expression of aquaporins, which are water-permeable channel proteins, would occur in these brains to facilitate water shifts. We used quantitative (real-time) RT-PCR, Western blotting and immunohistochemistry to evaluate the brain expression of aquaporins (AQP) 1, 4, and 9 mRNA and protein in Sprague–Dawley rats rendered hydrocephalic by injection of kaolin into cistern magna. AQP4 mRNA was significantly up-regulated in parietal cerebrum and hippocampus 4 weeks and 9 months after induction of hydrocephalus (P < 0.05). Although Western blot analysis showed no significant change, there was more intense perivascular AQP4 immunoreactivity in cerebrum of hydrocephalic brains at 3–4 weeks after induction. We did not detect mRNA or protein changes in AQP1 (located in choroid plexus) or AQP9 (located in select neuron populations). Kir4.1, a potassium channel protein linked to water flux, exhibited enhanced immunoreactivity in the cerebral cortex of hydrocephalic rats; the perineuronal distribution was entirely different from that of AQP4. These results suggest that brain AQP4 up-regulation might be a compensatory response to maintain water homeostasis in hydrocephalus.
In normal brain tissue, AQP4 and Kir4.1 were detected around the microvessels. In pathological brain tissue, AQP4 was upregulated in astrocytes in oedematous regions and Kir4.1 was upregulated in astrocytes in damaged brain.
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