Tacrolimus depresses local immune cell infiltration but fails to reduce cortical contusion volume in brain-injured rats.

The immunosuppressant drug tacrolimus (FK-506) failed to show an anti-edematous effect despite suppressing pro-inflammatory cytokines in cerebrospinal fluid following focal traumatic brain injury. By questioning the role of the inflammatory response as a pharmacological target, we investigated the effects of FK-506 on immune cell infiltration in brain-injured rats. Following induction of a cortical contusion, male Sprague-Dawley rats received FK-506 or physiological saline intraperitoneally.

Intratumoral infusion of interleukin-1beta and interferon-gamma induces tumor invasion with macrophages and lymphocytes in a rat glioma model.

Malignant gliomas are hard to treat successfully. Like other treatments immune therapy fails presumably due to low concentration of immune modifiers within the tumor. However, convection-enhanced delivery (CED) may overcome this problem.

Norepinephrine infusion increases interleukin-6 in plasma and cerebrospinal fluid of brain-injured rats.

Background: Significantly increased plasma and CSF IL-6 levels reflect underlying tissue damage following clinical and experimental traumatic brain injury (TBI). Catecholamines, used under clinical conditions to maintain adequate cerebral perfusion pressure, induce a sustained IL-6 release. Thus an additional elevation in IL-6 could aggravate brain edema in the acute posttraumatic phase.

Oligodeoxynucleotides induce brain inflammation in rats when infused intracerebroventricularly.

Antisense oligodeoxynucleotides (ODNs) can inhibit gene expression in a specific manner. However, several studies described problems with cerebral ODN application. Here, we investigated the immune effects (interleukin-6 (IL-6) release, cell invasion into cerebrospinal fluid (CSF) and brain parenchyma) of 'non-sense' randomized ODNs with different counterions (NH(4)(+), Na(+)) and modifications (with or without thioat-backbone) which were administered intracerebroventricularly for 48 h using osmotic mini-pumps in a rat model.

Nordesferriferrithiocin. Comparative Coordination Chemistry of a Prospective Therapeutic Iron Chelating Agent(1).

Nordesferriferrithiocin, NDFFTH(2), is a derivative of the siderophore desferriferrithiocin, DFFTH(2), in which the methyl group is substituted by a hydrogen atom. Both compounds show high oral activity as possible drugs for the treatment of iron overload. While DFFTH(2) is significantly toxic, NDFFTH(2) exhibits a lower toxicity and offers a much better therapeutic window than other orally active iron chelators.