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  • cerebral blood flow  (3)
  • DEATH
  • COMPLEXES
  • COMPLEX
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  • 1
    Keywords: RECEPTOR ; APOPTOSIS ; CELL ; Germany ; INHIBITION ; PATHWAY ; DEATH ; PROTEIN ; RNA ; transcription ; ACTIVATION ; COMPLEX ; COMPLEXES ; FAMILY ; nuclear bodies ; COMPONENT ; MAMMALIAN-CELLS ; MITOCHONDRIA ; TRANSLOCATION ; GLUCOCORTICOID-RECEPTOR ; FLICE ; PML ; CD95 ; RE ; FAMILIES ; INTERFERENCE ; RNA INTERFERENCE ; CASPASE-8 ; MEDIATED APOPTOSIS ; senescence ; death receptor ; SIGNALS ; FLASH ; CD95 (Fas/APO-1)
    Abstract: Caspase-8-binding protein FLICE-associated huge protein ( FLASH) has been proposed to regulate death receptor CD95-induced apoptosis through facilitating caspase-8 activation at the death-inducing signaling complex. Here, we found that FLASH interacts with the PML nuclear body component Sp100 and predominantly resides in the nucleus and nuclear bodies (NBs). In response to CD95 activation, FLASH leaves the NBs and translocates into the cytoplasm where it accumulates at mitochondria. The nucleo-cytoplasmic translocation of FLASH requires CD95-induced caspase activation and is facilitated by the Crm1-dependent nuclear export pathway. Downregulation of FLASH by RNA interference or inhibition of its nucleocytoplasmic shuttling reduced CD95-induced apoptosis. Furthermore, we show that the adenoviral anti-apoptotic Bcl-2 family member E1B19K traps FLASH and procaspase-8 in a ternary complex at mitochondria, thereby blocking CD95-induced caspase-8 activation. Knock-down of Sp100 potentiated CD95-activated apoptosis through enhancing nucleo-cytoplasmic FLASH translocation. In summary, our findings suggest that CD95 signals via a previously unrecognized nuclear pathway mediated by nucleo-cytoplasmic translocation of FLASH
    Type of Publication: Journal article published
    PubMed ID: 17245429
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  • 2
    ISSN: 0942-0940
    Keywords: Acute head injury ; barbiturate coma ; cerebral blood flow ; cerebral metabolism ; hyperventilation ; indomethacin ; intracranial pressure ; intracranial hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In five head-injured patients with cerebral contusion and oedema in whom it was not possible to control intracranial pressure (ICP) (ICP〉20 mmHg) by artificial hyperventilation (PaCO2 level 3.5–4.0 kPa) and barbiturate sedation, indomethacin was used as a vasoconstrictor drug. In all patients, indomethacin (a bolus injection of 30 mg, followed by 30 mg/h for seven hours) reduced ICP below 20 mmHg for several hours. Studies of cerebral circulation and metabolism during indomethacin treatment showed a decrease in CBF at 2h. After 7h, ICP remained below 20 mmHg in three patients, and these still had reduced CBF. In the other patients a return of ICP and CBF to pretreatment levels was observed. In all patients indomethacin treatment was followed by a fall in rectal temperature. These results suggest that indomethacin due to its cerebral vasoconstrictor and antipyretic effect should be considered as an alternative for treatment of ICP-hypertension in head-injured patients.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0942-0940
    Keywords: Adaptation ; cerebral blood flow ; hypercapnia ; hypoxia ; indomethacin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a randomized study of healthy volunteers indomethacin bolus injection followed by continuous infusion decreased CBF from normal levels ranging from 45 to 80 ml/100 g/min to levels ranging from 24 to 57 ml/100 g/min. These low levels were sustained during a six hour infusion period. Periods of hypoxia during inhalation of 17% oxygen and hypercapnia during inhalation of 2–4% CO2 normalized CBF.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0942-0940
    Keywords: Head injury ; indomethacin reactivity ; hyperventilation ; intracranial pressure ; cerebral blood flow ; cerebral ischaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The purpose of this study was to compare the effect of hyper-ventilation and indomethacin on cerebral circulation, metabolism and pressures in patients with acute severe head injury in order to see if indomethacin may act supplementary to hyperventilation. Fourteen severely head injured patients entered the study. Intracranial pressure (ICP), mean arterial blood pressure (MABP) and cerebral perfusion pressure (CPP) were monitored continuously. Within the first four days after the trauma the CO2 and indomethacin vasoreactivities were studied by measurements of cerebral blood flow (CBF) (Cerebrograph 10a, intravenous133Xe technique) and arterio-venous difference of oxygen (AVdO2). Ischaemia was evaluated from changes in CBF, saturation of oxygen in the jugular bulb (SvjO2), lactate and lactate/oxygen index (LOI). Data are presented as medians and ranges, results are significant unless otherwise indicated. Before intervention ICP was well controlled (14.8 (9–24) mmHg) and basic CBF level was 39.1 (21.6–75.0) ml/100 g/min). The arterio-venous oxygen differences were generally decreased (AVdO2 = 4.3 (1.8–8.1) ml/100 ml) indicating moderate luxury perfusion. Levels of CMRO2 were decreased (1.54 (0.7–3.2) ml/100 g/min) as well. Duringhyperventilation (ΔAPaCO2 = 0.88 (0.62–1.55) kPa) CBF decreased with 11.8 (−33.4−29.7) %/kPa and ICP decreased with 3.8 (0–10) mmHg. AVdO2 increased 34.0 (4.0–139.2) %/kPa, MABP was unchanged, CMRO2 and CPP increased (ΔCPP = 3.9 (−10−20) mmHg). AVD (lactate) and LOI were unchanged. No correlations between CBF responses to hypocapnia and outcomes were observed. An i.v. bolus dose ofindomethacin (30 mg) decreased CBF 14.7 (−16.7−57.4) % and ICP decreased 4.3 (−1−17) mmHg. AVdO2 increased 27.8 (−40.0−66.7)%, MABP (ΔMABP = 4.9 (−2−21) mmHg) and CPP (ΔCPP = 8.7 (3–29) mmHg) increased while CMRO2 was unchanged. No changes in AVd (lactate) and LOI indicating cerebral ischaemia were found. Compared to hyperventilation (changes per 1 kPa, at PaCO2 level = 4.05 kPa) the changes in MABP, CPP and CBF were significantly greater after indomethacin, while the changes in AVdO2, ICP, SvjO2, and LOI were of the same order of magnitude. Nocorrelation between relative reactivities to indomethacin and CO2, evaluated from changes in CBF and AVdO2, or between the decrease in ICP after the two procedures were found. Thus, some patients reacted to indomethacin but not to hyperventilation, and vice versa. These results suggest that indomethacin and hyperventilation might act independently, or in a complementary fashion in the treatment of patients with severe head injury.
    Type of Medium: Electronic Resource
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