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- 1From: Journal of Neuroinflammation. (Vol. 9) Peer-ReviewedThe complement system, a major component of the innate immune system, is becoming increasingly recognised as a key participant in physiology and disease. The awareness that immunological mediators support various aspects...
- 2From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedCorrection to Rao J S, Kim H W, Kellom M, Greenstein D, Chen M, Kraft A D, Harry G J, Rapoport S I, Basselin M. Increased neuroinflammatory and arachidonic acid cascade markers, and reduced synaptic proteins, in brain...
- 3From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedCorrection to Dirscherl K, Karlstetter M, Ebert S, Kraus D, Hlawatsch J, Walczak Y, Moehle C, Fuchshofer R, Langmann T. Luteolin triggers global changes in the microglial transcriptome leading to a unique...
- 4From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground Aside from the skeletal health affection, vitamin D deficiency has been implicated as a potential environmental factor triggering for some autoimmune disorders. Vitamin D might play a role in the...
- 5From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground Neuroprotective and neurotrophic properties of leukemia inhibitory factor (LIF) have been widely reported. In the central nervous system (CNS), astrocytes are the major source for LIF, expression of which...
- 6From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground Activated microglial cells are an important pathological component in brains of patients with neurodegenerative diseases. The purpose of this study was to investigate the effect of He-Ne (632.8 nm, 64.6...
- 7From: Journal of Neuroinflammation. (Vol. 9) Peer-ReviewedBackground There is ample evidence that psychological stress adversely affects many diseases. Recent evidence has shown that intense stressors can increase inflammation within the brain, a known mediator of many...
- 8From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground Systemic infection leads to generation of inflammatory mediators that result in metabolic and behavioural changes. Repeated or chronic systemic inflammation leads to a state of innate immune tolerance: a...
- 9From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground Transforming growth factor-[beta]1 (TGF-[beta]1) is an important regulator of cell migration and plays a role in the scarring response in injured brain. It is also reported that 5-lipoxygenase (5-LOX) and...
- 10From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground In addition to cytotoxic mechanisms directly impacting neurons, [beta]-amyloid (A[beta])-induced glial activation also promotes release of proinflammatory molecules that may self-perpetuate reactive...
- 11From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackgrounds Increasing evidence shows that the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) possesses potent anti-inflammatory and immunomodulatory properties. It is tempting to evaluate the...
- 12From: Journal of Neuroinflammation. (Vol. 9) Peer-ReviewedBackground CD4.sup.+ .sup.CD25.sup.+ .sup.forkhead box P3 (FoxP3).sup.+ .sup.regulatory T cells (T reg cells) are known to suppress adaptive immune responses, key control tolerance and autoimmunity. Methods We...
- 13From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground More than 50% of patients undergoing lifelong suppressive antiviral treatment for HIV-1 infection develop minor HIV-1-associated neurocognitive disorders. Neurological complications during HIV-1 infection...
- 14From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground Tumor necrosis factor-[alpha] (TNF-[alpha]) is one of the most typical pro-inflammatory cytokines with both beneficial and destructive properties for the central nervous system. Increasing evidences have...
- 15From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground Perivascular macrophages and microglia are critical to CNS function. Drugs of abuse increase extracellular dopamine in the CNS, exposing these cells to elevated levels of dopamine. In rodent macrophages...
- 16From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground In sepsis syndromes the severity of the inflammation triggers microvascular dysfunction and early organ failure. We studied the effects of anti-inflammatory vagus nerve stimulation on the cerebral...
- 17From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedBackground Microglial activation plays a key role in the neuroinflammation associated with virtually all CNS disorders, although their role in normal CNS physiology is becoming increasingly appreciated....
- 18From: Journal of Neuroinflammation. (Vol. 9, Issue 1) Peer-ReviewedNeuroinflammation is a common pathological event observed in many different brain diseases, frequently associated with blood brain barrier (BBB) dysfunction and followed by cerebral edema. Neuroinflammation is...
- 19From: Journal of Neuroinflammation. (Vol. 9) Peer-ReviewedBackground Recent in vivo and in vitro studies in non-neuronal and neuronal tissues have shown that different pathways of macrophage activation result in cells with different properties. Interleukin (IL)-6 triggers...
- 20From: Journal of Neuroinflammation. (Vol. 9) Peer-ReviewedBackground Microglia are one of the main cell types to be productively infected by HIV-1 in the central nervous system (CNS). Leukotriene B.sub.4 (LTB.sub.4 ) and cysteinyl-leukotrienes such as LTC.sub.4 are some of...