The heterogeneity of target recognition by lymphokine-activated killer precursor cells.

Lymphokine-activated killer (LAK) cells were generated from peripheral blood lymphocytes (PBL) that were depleted of mature cytotoxic natural killer (NK) cells. PBL NK activity was abolished by pretreatment of effector cells with the toxic lysosomotropic agent L-leucine methyl ester (LME) or by depletion of effector cells by K562 monolayer absorption (MA). Both treatments markedly reduced the proportion of cells expressing NK-associated markers such as CD 16 (Leu 11b, B73.1), Leu 7, and NKH-1 (Leu 19), whereas these treatments had minimal effects on cells expressing T cell markers (CD 3, CD 4, and CD 8). LME and MA also drastically decreased the proportion of K562 target-binding lymphocytes. LAK activity against NK-sensitive and NK-resistant targets can be generated from the NK cell-depleted PBL by incubation with interleukin-2. Peak LAK activity generated from MA-treated PBL was later than the peak of LAK activity generated from either untreated or LME-treated PBL. Although MA of PBL on NK-resistant S4 sarcoma targets had little effect on NK activity, LAK activity against both K562 and S4 targets was reduced. These results suggest that there are at least three LAK precursor subpopulations in PBL: mature NK cells that can bind and kill K562 targets (LME-sensitive and MA-sensitive); "pre-NK" cells that can bind but cannot kill (LME-resistant and MA-sensitive); and non-NK cells that cannot bind and cannot kill K562 targets (MA-resistant)

Reappraisal of early CT signs to predict the arterial occlusion site in acute embolic stroke

Patients: 105 consecutive patients with acute embolic stroke affecting the anterior circulation. Methods: Four early signs were evaluated on cranial CT within six hours of stroke onset: loss of the insular ribbon (LIR); attenuation of the lentiform nucleus (ALN); hemispherical sulcus effacement (HSE); and the hyperdense middle cerebral artery sign (HMCAS). The arterial occlusion site was definitively identified on cerebral angiography within two hours of the CT examination. Results: LIR was present in 55% of patients with internal carotid artery occlusion. ALN was present in 65% of patients with occlusion of the sphenoidal portion (M1) of the middle cerebral artery. HSE was present in 47% of patients with middle cerebral artery branch occlusion. LIR was related independently to internal carotid artery occlusion (odds ratio (OR) 2.8 (95% confidence interval, 1.2 to 6.8)), ALN to M1 occlusion (OR 2.9 (1.2 to 7.4)), and isolated HSE without ALN or LIR to branch occlusion (OR 12.8 (3.2 to 51.5)). The combined presence of the three signs was indicative of internal carotid artery occlusion (p < 0.05), and the presence of ALN and LIR without HSE was indicative of M1 occlusion (p < 0.05) by univariate analysis. HMCAS bore no relation to either arterial occlusion site. Conclusions: LIR, ALS, HSE, and combinations of these were useful predictors of the arterial occlusion site

The heterogeneity of target recognition by lymphokine-activated killer precursor cells.

Lymphokine-activated killer (LAK) cells were generated from peripheral blood lymphocytes (PBL) that were depleted of mature cytotoxic natural killer (NK) cells. PBL NK activity was abolished by pretreatment of effector cells with the toxic lysosomotropic agent L-leucine methyl ester (LME) or by depletion of effector cells by K562 monolayer absorption (MA). Both treatments markedly reduced the proportion of cells expressing NK-associated markers such as CD 16 (Leu 11b, B73.1), Leu 7, and NKH-1 (Leu 19), whereas these treatments had minimal effects on cells expressing T cell markers (CD 3, CD 4, and CD 8). LME and MA also drastically decreased the proportion of K562 target-binding lymphocytes. LAK activity against NK-sensitive and NK-resistant targets can be generated from the NK cell-depleted PBL by incubation with interleukin-2. Peak LAK activity generated from MA-treated PBL was later than the peak of LAK activity generated from either untreated or LME-treated PBL. Although MA of PBL on NK-resistant S4 sarcoma targets had little effect on NK activity, LAK activity against both K562 and S4 targets was reduced. These results suggest that there are at least three LAK precursor subpopulations in PBL: mature NK cells that can bind and kill K562 targets (LME-sensitive and MA-sensitive); "pre-NK" cells that can bind but cannot kill (LME-resistant and MA-sensitive); and non-NK cells that cannot bind and cannot kill K562 targets (MA-resistant)

Ten year recurrence after first ever stroke in a Japanese community: the Hisayama study

Background: Very few population based cohort studies have focused on the long term recurrence of stroke. Objective: To examine 10 year cumulative recurrence rates for stroke in a Japanese cohort according to pathological type and clinical subtype of brain infarction. Methods: During a 32 year follow up of 1621 subjects ⩾40 years of age, 410 developed first ever stroke. These were followed up prospectively for 10 years after stroke onset. Results: During follow up, 108 (26%) experienced recurrent stroke. The cumulative recurrence rates were 35.3% at five years and 51.3% at 10 years. The 10 year recurrence rates of subarachnoid haemorrhage (SAH), brain haemorrhage, and brain infarction were 70.0%, 55.6%, and 49.7%, respectively; the difference between SAH and brain infarction was significant (p = 0.004). Most recurrent episodes after SAH or brain haemorrhage happened within a year after the index stroke, whereas recurrence of brain infarction increased consistently throughout the observation period. Cardioembolic stroke had a higher recurrence rate (75.2%) than lacunar infarction (46.8%) (p = 0.049). The 10 year risk of stroke recurrence increased with age after lacunar or atherothrombotic brain infarction, but not after the other types or subtypes. After atherothrombotic brain infarction, cardioembolic stroke, or SAH, the type and subtype of most recurrent strokes were the same as for the index stroke, but recurrence after lacunar infarction or brain haemorrhage showed divergent patterns. Conclusions: Japanese people have higher recurrence rates of stroke than other populations. Recurrence rate after a first brain infarct increases consistently through the next 10 years