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Titolo:
CEREBRAL GLUCOSE-TRANSPORTER EXPRESSION IN HIV-INFECTION
Autore:
KOVITZ CA; MORGELLO S;
Indirizzi:
MT SINAI MED CTR,DEPT PATHOL,DIV NEUROPATHOL,BOX 1134,1 GUSTAVE L LEVY PL NEW YORK NY 10029 MT SINAI MED CTR,DEPT PATHOL,DIV NEUROPATHOL NEW YORK NY 10029 MT SINAI MED CTR,DEPT PATHOL,FISHBERG CTR NEUROBIOL NEW YORK NY 10029
Titolo Testata:
Acta Neuropathologica
fascicolo: 2, volume: 94, anno: 1997,
pagine: 140 - 145
SICI:
0001-6322(1997)94:2<140:CGEIH>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-BRAIN-BARRIER; AIDS DEMENTIA COMPLEX; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; GENE-EXPRESSION; ALZHEIMERS-DISEASE; GLUT1; LOCALIZATION; ZIDOVUDINE; IMMUNOCYTOCHEMISTRY; ENDOTHELIA;
Keywords:
GLUCOSE TRANSPORTER; GLUT1; GLUT3; HIV;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
C.A. Kovitz e S. Morgello, "CEREBRAL GLUCOSE-TRANSPORTER EXPRESSION IN HIV-INFECTION", Acta Neuropathologica, 94(2), 1997, pp. 140-145

Abstract

Abnormalities in cerebral glucose metabolism have been demonstrated in patients with AIDS dementia complex (ADC), with increased consumption in early disease and decreased utilization in late stages. The basisof these changes is unknown. Accordingly, a pilot study was undertaken to determine whether levels of cerebral glucose transporters GLUT1 and GLUT3 were altered by HIV disease. Frontal gray and white matter membrane preparations from patients with HIV encephalitis (HIVE), MTV infection without parenchymal neuropathology,;Gild non-infected controlswere utilized in quantitative immunoblots to measure GLUT1 and GLUT3. Results were expressed as a ratio of glucose transporter to structural protein actin. Within-group patient variability was great, precluding statistically significant differences between groups for any one brain region. However, when data for gray and white matter was pooled, results obtained statistical significance, with levels of GLUT1 increasing in HIV infection without neuropathology, and declining with HIVE. Increased GLUT1 in HIV infection without parenchymal neuropathology maybe important in the biology of increased glucose consumption described with early ADC. With progression to HIVE, reduced levels of glucose transporters may contribute to late stage hypometabolism.

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Documento generato il 31/03/20 alle ore 21:32:56