Pemetrexed/carboplatin followed by pemetrexed was well tolerated and active for front-line treatment of advanced nonsquamous NSCLC. Encouraging survival outcomes were observed even in EGFR-wild type patients.

Pniifrd in Bel~iiiiii -a// right.i resened Copyighr 0 Munksgourd IY 94 4CTA NEUROLOGICA SCANDINAVICA value of cerebrospinal fluid neuron-specific enolase and S-lOOb protein in Guillain-Barre syndrome. Acta Neurol Scand 1994: 89: 27-30. 0 Munksgaard 1994.We measured the cerebrospinal fluid (CSF) concentrations of neuron-specific enolase (NSE) and S-100b protein (S-100b) using enzyme immunoassay methods, in 24 patients with Guillain-Barre syndrome and 46 controls, and examined their prognostic values. Sixteen of 24 patients showed elevated levels ( > the mean + 2SD levels of controls) of NSE, S-IOOb, or both, and in those with higher NSE or S-100b levels there was a rather longer Material and methodsGBS pafients -Twenty-four patients (1 5 men and 9 women) aged 14 to 64years old (mean? SD,

Tenascin, an extracellular matrix glycoprotein, has been reported to be expressed predominantly on glioma tissue in the CNS, both in a cell associated and an excreted form. Recently, a highly sensitive sandwich type enzyme immunoassay for quantitative determination of tenascin was developed. In the present study, the amount of tenascin in CSF was measured. They also reported that tenascin was present in the serum of patients with melanoma and that the concentration of tenascin in serum was a tumour marker for advanced melanomas because they found lower concentrations in patients with low tumour burden and in normal donors.8 Recently, we developed a sandwich type enzyme immunoassay for tenascin9 and showed, with this assay system, that not only human melanoma, but also human lung cancer and glioma cells secreted 1-14 jug/ml of tenascin in vitro (data not shown). In the present study, serum and CSF were obtained from patients with various neoplastic and non-neoplastic neurological diseases, and the amount of tenascin was quantitatively determined. It was expected that an increased level of expression of this extracellular matrix glycoprotein would be found in neoplasms compared with other diseases of the CNS, and that the level of expression would be useful in indicating the type of brain tumour.Patients and methods SANDWICH TYPE ENZYME IMMUNOASSAY Details of the methodology of the sandwich type enzyme immunoassay for tenascin has been reported elsewhere.9 Briefly, an antiserum to human tenascin was raised in rabbits. Two antihuman tenascin monoclonal antibodies, 8C9 (RCBl)'0 and 9B2, were supplied by Amano Pharmaceutical Co, Aichi, Japan and F(ab)'2 fragments of both antibodies, prepared from lgG by pepsin digestion, were used. The RCB1 fragment was immobilised non-covalently on polystyrene beads and the 9B2 fragment was coupled to ,B3D-galactosidase. Polystyrene beads with antibodies were incubated with various amounts of purified tenascin or samples of serum and CSF (10 Ml) in a final volume of 051 ml with sodium phosphate buffer for three hours. After washing twice with buffer, the beads were left standing overnight with 1 mU of ,B D-galatosidase labelled antibodies (mixed 0 5 mU of 8C9 and 9B2) in 02 ml of buffer solution at 4°C. Beads were again washed twice

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To determine whether cytokines or lipopolysaccharide (LPS) are involved in the induction of superoxide dismutase (SOD) in the nervous system, we examined the effects of these substances on the levels of SOD in cultured mouse astrocytes. Treatment of astrocytes with 102 to 104 U/ml tumor necrosis factor‐α for 3 days increased the levels of Mn SOD in a dose‐ and time‐dependent manner to as much as six times the level under nontreated conditions. Treatment with 1.0 µg/ml LPS for 3 days elicited a fourfold increase in levels of Mn SOD, and the effect of LPS was also dose dependent. Furthermore, Mn SOD in astrocytes was induced by a 3‐day exposure to interleukin‐1α at concentrations of 102 or 103 U/ml. However, these stimuli had no effect on levels of copper‐zinc SOD (Cu/Zn SOD) in astrocytes. By contrast, interferon‐γ did not change the levels of either Mn or Cu/Zn SOD in the cells. The results indicate that the selective induction of Mn SOD by cytokines and LPS, which has been observed in nonnervous tissues, may also occur in nervous tissues. The induction of Mn SOD may represent a mechanism for protection of cells from oxidative stress.