Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The genus Ocimum (family Lamiaceae) has been revered for its diverse biological activities. Various species have been used traditionally to treat CNS disorders and are proven to have neuroprotective effect that is often attributed to their significant antioxidant activity. Ocimum kilimandscharicum (Karpoora Thulasi), a prominent member of this genus is reported to have marked antioxidant activity but its neuroprotective potential has not been explored. Thus, present study was designed to evaluate the cerebroprotective effect of O. kilimandscharicum leaf extract (OKLE) in mice against ischemia reperfusion (I-R) induced brain injury. Bilateral common carotid artery occlusion (BCCAO) for 15min followed by 24h reperfusion was used to induce brain damage in Swiss Albino mice. Animals were treated with OKLE (200 and 400mg/kg, po) once daily for 7days after I-R. Morris water maze and elevated plus maze tests were used to assess long and short term memory while neurological severity score was used to determine motor coordination. Histopathological evaluation (TTC staining) along with brain biochemical parameters (TBARS, reduced GSH and SOD activity) were determined to outline neuroprotective mechanism of OKLE. I-R resulted in marked cognitive impairments, motor incoordination in mice, significant brain damage and increased oxidative stress. Treatment with OKLE produced functional recovery in mice which is manifested by improved memory and motor coordination; reduced cerebral infarct size and brain oxidative stress (TBARS levels) and elevated endogenous antioxidants (reduced GSH and SOD activity). In addition, OKLE showed DPPH radical scavenging and reducing power in-vitro. These results show that O. kilimandscharicum mitigated the neurodegenerative changed induced by I-R in mice probably due to its antioxidant activity.
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PMID:Amelioration of ischemia-reperfusion induced functional and biochemical deficit in mice by Ocimum kilimandscharicum leaf extract. 2791 25

Periventricular leukomalacia (PVL), a brain injury affecting premature infants is commonly associated with cerebral palsy. PVL results from hypoxia-ischemia (HI) with or without infection and is characterized by white matter necrotic lesions, hypomyelination, microglial activation, astrogliosis, and neuronal death. It is important to study a PVL mouse model that mimics human PVL in symptomatology, anatomic and molecular basis. In our neonate mice model, bilateral carotid arteries were temporary ligated at P5 followed by hypoxic exposure (FiO2 of 8% for 20 min.). At P5 in mice, the white matter is more vulnerable to HI injury than the grey matter. In our PVL model, mice suffer from significant hind limb paresis, incoordination and feeding difficulties. Histologically they present with ventriculomegally, white matter loss, microglial activation and neuronal apoptosis. HI injury increases proinflammtory cytokines, activates NF-kB, activates microglia and causes nitrative stress. All these inflammatory mediators lead to oligodendroglial injury and white matter loss. Neurobehavioral analysis in the PVL mice model at P60 showed that the HI group had a significant decrease in hind limb strength, worsening rotarod testing and worsening performance in the open field test. This new PVL model has great advantages far beyond just mimicking human PVL in clinical features and histopathology. Long term survival, the development of cerebral palsy and the ability of using this model in transgenic animals will increase our understanding of the mechanistic pathways underlying PVL and defining specific targets for the development of suitable therapeutics.
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PMID:A model of Periventricular Leukomalacia (PVL) in neonate mice with histopathological and neurodevelopmental outcomes mimicking human PVL in neonates. 2840 31

Labyrinthitis is inflammation of the membranous and bony labyrinth of the inner ear. Typical portals of entry includehematogenous spread from the cochlear vasculature, passage of otitis media pathogens through the round window, and mostcommonly, meningogenic spread from the subarachnoid space. The sequela of chronic inner ear inflammation is labyrinthitisossificans, in which inner ear structures are replaced by fibrous and osseous tissues. Labyrinthitis in humans has been reportedconcurrently with infection due to various viruses (for example, varicella-zoster, measles, mumps) and bacteria (for example,Treponema pallidum, Streptococcus pneumoniae) and may be associated with vertebrobasilar ischemia and meningitis. Profoundsensorineural hearing loss is a common, serious complication of this disease. Here, we report a case of labyrinthitisossificans in a cynomolgus macaque (Macaca fascicularis) with a potential infectious etiology. Historically, this animal hadan indwelling femoral intravenous catheter for more than 4 y. He presented with a right-sided head tilt and incoordinationof 2 mo duration. The macaque was treated with NSAID and antibiotics, which corrected the incoordination but not the headtilt. MRI revealed right-sided labyrinthitis, and euthanasia was elected due to clinical signs that were refractory to treatment.Gross pathology was unremarkable, but histopathology revealed chronic labyrinthitis ossificans with local fibroplasia andvestibuloauditory neuritis. We describe here the clinical features, imaging, and histologic lesions of labyrinthitis in a macaque.
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PMID:Labyrinthitis Ossificans in a Cynomolgus Macaque (Macaca fascicularis). 2965 59


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