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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Saito M, Chihara J, Mouri T, Kurachi D, Yamamoto T, Nakajima S

Fourth Department of Internal Medicine, Kinki University School of Medicine, Osaka, Japan.

Gen Pharmacol. 1996 Apr;27(3):483-6. doi: 10.1016/0306-3623(95)02073-x.

We measured the neopterin level in the supernatant of cultured alveolar macrophages from patients with interstitial lung diseases (ILD patients) as a marker for the activation of alveolar macrophage. 2. In ILD patients, the supernatant neopterin level (40.1 +/- 7.8 pmol/ml) was significantly higher (P < 0.01) than that in control subjects (10.0 +/- 1.6 pmol/ml). 3. We also found that macrophage-colony stimulating factor (M-CSF) and interleukin-2 (IL-2) augmented neopterin production from alveolar macrophage in both ILD patients (51.6 +/- 10.4 and 60.1 +/- 10.8 pmol/ml, respectively, P < 0.01) and control subjects (28.1 +/- 6.0 and 25.7 +/- 4.9 pmol/ml, respectively). 4. These findings suggest that alveolar macrophages produce neopterin by M-CSF or IL-2.

我们检测了间质性肺疾病患者（ILD患者）培养的肺泡巨噬细胞上清液中的新蝶呤水平，作为肺泡巨噬细胞活化的标志物。2. 在ILD患者中，上清液新蝶呤水平（40.1±7.8 pmol/ml）显著高于对照组（10.0±1.6 pmol/ml，P<0.01）。3. 我们还发现，巨噬细胞集落刺激因子（M-CSF）和白细胞介素-2（IL-2）均可增加ILD患者（分别为51.6±10.4和60.1±10.8 pmol/ml，P<0.01）和对照组（分别为28.1±6.0和25.7±4.9 pmol/ml）肺泡巨噬细胞的新蝶呤产生。4. 这些发现提示肺泡巨噬细胞通过M-CSF或IL-2产生新蝶呤。

Saito M, Chihara J, Mouri T, Kurachi D, Yamamoto T, Nakajima S

Fourth Department of Internal Medicine, Kinki University School of Medicine, Osaka, Japan.

Gen Pharmacol. 1996 Apr;27(3):483-6. doi: 10.1016/0306-3623(95)02073-x.

We measured the neopterin level in the supernatant of cultured alveolar macrophages from patients with interstitial lung diseases (ILD patients) as a marker for the activation of alveolar macrophage. 2. In ILD patients, the supernatant neopterin level (40.1 +/- 7.8 pmol/ml) was significantly higher (P < 0.01) than that in control subjects (10.0 +/- 1.6 pmol/ml). 3. We also found that macrophage-colony stimulating factor (M-CSF) and interleukin-2 (IL-2) augmented neopterin production from alveolar macrophage in both ILD patients (51.6 +/- 10.4 and 60.1 +/- 10.8 pmol/ml, respectively, P < 0.01) and control subjects (28.1 +/- 6.0 and 25.7 +/- 4.9 pmol/ml, respectively). 4. These findings suggest that alveolar macrophages produce neopterin by M-CSF or IL-2.

我们检测了间质性肺疾病患者（ILD患者）培养的肺泡巨噬细胞上清液中的新蝶呤水平，作为肺泡巨噬细胞活化的标志物。2. 在ILD患者中，上清液新蝶呤水平（40.1±7.8 pmol/ml）显著高于对照组（10.0±1.6 pmol/ml，P<0.01）。3. 我们还发现，巨噬细胞集落刺激因子（M-CSF）和白细胞介素-2（IL-2）均可增加ILD患者（分别为51.6±10.4和60.1±10.8 pmol/ml，P<0.01）和对照组（分别为28.1±6.0和25.7±4.9 pmol/ml）肺泡巨噬细胞的新蝶呤产生。4. 这些发现提示肺泡巨噬细胞通过M-CSF或IL-2产生新蝶呤。