Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brain inflammation has been implicated in the development of brain edema and secondary brain damage in ischemia and trauma. Adhesion molecules, cytokines and leukocyte chemoattractants released/presented at the site of blood-brain barrier (BBB) play an important role in mobilizing peripheral inflammatory cells into the brain. Cerebral endothelial cells (CEC) are actively engaged in processes of microvascular stasis and leukocyte infiltration by producing a plethora of pro-inflammatory mediators. When challenged by external stimuli including cytokines and hypoxia, CEC have been shown to release/express various products of arachidonic acid cascade with both vasoactive and pro-inflammatory properties, including prostaglandins, leukotrienes, and platelet-activating factor (PAF). These metabolites induce platelet and neutrophil activation and adhesion, changes in local cerebral blood flow and blood rheology, and increases in BBB permeability. Ischemic CEC have also been shown to express and release bioactive inflammatory cytokines and chemokines, including IL-1beta, IL-8 and MCP-1. Many of these mediators and ischemia in vitro and in vivo have been shown to up-regulate the expression of both selectin and Ig-families of adhesion molecules in CEC and to facilitate leukocyte adhesion and transmigration into the brain. Collectively, these studies demonstrate a pivotal role of CEC in initiating and regulating inflammatory responses in cerebral ischemia.
 ...
PMID:Inflammatory mediators of cerebral endothelium: a role in ischemic brain inflammation. 1066 1

The patient was a 46-year-old male, who suffered from mild head trauma in January 2002, and general convulsions with unconsciousness on February 28. Slight right hemiparesis and aphasia were presented after the epilepsy attack. CT scan revealed a large lesion of mixed density occupying the left temporal space. It showed linear high density in its medial margin and had compressed the left temporal lobe strongly, causing mid-line shift. The lesion was suspected to be a calcified chronic subdural hematoma and the patient was admitted to our hospital on February 28. The symptoms had improved the next day but they began to get worse again gradually after admission. T1-weighted MR image showed high intensity areas under the subdural hematoma, which were suspected to be subcortical hemorrhage. Six days after admission, consciousness disturbance became progressive. The calcified hematoma had not enlarged but brain edema had increased. On CT, an operation was performed and the calcified old hematoma and the new subdural hematoma surrounding it were removed. The diagnosis of organized chronic subdural hematoma was made at the time of the operation. The contents of this calcified subdural hematoma was mostly old dark-gray substance, but some fresh bleeding point was seen at the inner surface of the outer membrane. At the bottom there was a hard, calcified layer which adhered tightly to the brain. Adhesion between the inner membrane of the hematoma and brain surface which related to the subcortical hemorrhage was presented. It seemed impossible to remove the inner membrane without damaging the brain so no attempt was made to do so. The aphasia and right hemiparesis improved 3 weeks after the operation and the patient was discharged on April 4. He has no neurological deficits and is under periodic observation. A calcified chronic subdural hematoma has rarely been encountered and the etiology, imaging diagnosis, and management are unclear. We presented the interesting image findings on this case and discussed the etiology of this disease.
 ...
PMID:[Calcified chronic subdural hematoma complicated with subcortical hemorrhage: case report]. 1268 80