Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001486 (Adenovirus)
 3,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vascular endothelial growth factor (VEGF) induces increased vessel permeability and formation of abnormal vessels. To investigate cerebral blood flow (CBF) during local overexpression of VEGF recombinant adenoviruses carrying the human VEGF165 complementary DNA (2.3 to 23. 108 pfu/mL) were injected stereotactically into the caudate nucleus of anesthetized rats. Saline and adenoviruses carrying the beta-galactosidase gene served as controls. Eleven days later (1) size and density of vessels were assessed in hematoxylin-eosin-stained sections, (2) vascular permeability was measured by intravenous Evans blue injections, and (3) local CBF (lCBF) was quantified using the iodo-[14C]antipyrine technique. Dose-dependent increases were found in (1) vessel density and size (only vessels >43 microm could be quantified morphologically), (2) Evans blue extravasation and brain edema formation, and (3) lCBF (up to eightfold). At medium doses, hyperemic areas and smaller areas of decreased lCBF were found. In low flow areas, vascular cross-sectional areas were increased 223-fold and vessel density up to 10-fold. In high flow areas, these parameters were increased 32-fold and up to 15-fold, respectively. Adenovirus mediated VEGF overexpression results in (1) increased vessel size and density, (2) areas of increased and of decreased flow, and (3) more and smaller vessels in high flow than in low flow areas. These results indicate a diverging flow pattern of newly formed vessels.
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PMID:Heterologous expression of human VEGF165 in rat brain: dose-dependent, heterogeneous effects on CBF in relation to vascular density and cross-sectional area. 1267 19

Recent studies indicate that inflammatory reaction occurs around hematoma after intracerebral hemorrhage (ICH). In this study the authors examine the hypothesis that overexpression of IL-1ra in the brain attenuate brain edema formation after ICH. Adenoviruses expressing IL-1ra (Ad.RSVIL-1ra) or LacZ (Ad.RSVLacZ) or saline were injected into the lateral ventricle. On the fifth day after virus injection, 100 microl of autologous blood or 5 U thrombin was infused into the right basal ganglia. Rats with ICH were killed 24 or 72 hours later for measurement of brain water content. Thrombin-treated rats were killed 24 hours later for edema measurements and an assessment of polymorphonuclear leukocyte (PMNL) infiltration by myeloperoxidase (MPO) assay. Compared with control groups, Ad.RSVIL-1ra treated rats had less brain edema formation in the ipsilateral basal ganglia 3 days after ICH (81.5 +/- 0.3% compared with 83.4 +/- 0.4% and 83.3 +/- 0.5% in control animals). Ad.RSVIL-1ra treated rats had also less brain edema following thrombin injection. The reduction of brain edema induced by thrombin was involved in the reduction of PMNL infiltration in basal ganglia, as assessed by MPO assay. Adenovirus-mediated overexpression of IL-1ra attenuated brain edema formation following ICH, perhaps by reduction of thrombin-induced brain inflammation.
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PMID:Overexpression of interleukin-1 receptor antagonist reduces brain edema induced by intracerebral hemorrhage and thrombin. 1475 87