Mitogen-activated protein kinase (MAP kinase) plays a central role in the signal transduction for diverse cellular responses, such as proliferation, differentiation, stress response and cell death, via activation after binding of growth factors to the respective receptors on the cell membrane. In the human placental tissues, however, little is known about the expression and activation of the classical MAP kinases, extracellular signal-regulated kinase1/2 (ERK1/2). We therefore examined the expression of ERK1/2 in the human chorionic and placental tissues between 5 and 41 weeks of gestation, using Western blotting, immunohistochemistry and in situ hybridization. To explore the activation of ERK1/2 protein, we used an antibody that reacts with both phosphorylated and non-phosphorylated ERK1/2 (total ERK1/2), as well as antibodies that react only with phosphorylated ERK1/2. The expression pattern of phosphorylated ERK1/2 in the trophoblasts was compared with that of various growth factor receptors, such as c-met, IGF-1R, flt-1, EGFR, PDGFR, Bek, and flg. Total ERK1/2 was immunolocalized in the villous cytotrophoblasts (CTs), but not in the syncytiotrophoblasts (STs), throughout pregnancy. In situ hybridization also showed the localization of ERK1 mRNA in the villous CTs. Interestingly, however, phosphorylated ERK1/2 was immunolocalized in the villous CTs only up to 12 weeks of gestation. Western blot also showed the stronger bands of phosphorylated ERK1/2 in the tissues of the first trimester. Among the growth factor receptors, c-met was strongly expressed in the villous CTs during the first trimester, and resembled the expression pattern of phosphorylated ERK1/2. These findings suggest that the MAP kinase pathway is activated in the villous CTs during the first trimester in the human placenta.

Adult↗

PubMedDate not supplied

Epidemiologic studies of lung disease due to mycobacteria other than Mycobacterium tuberculosis in Japan.

The incidence of lung disease due to mycobacteria other than Mycobacterium tuberculosis (atypical mycobacteria) in Japan was estimated to be 0.9--1.9 per 10(5) population per year in 1971--1979. Although the incidence of lung tuberculosis is steadily decreasing, the incidence of lung disease due to atypical mycobacteria has remained at almost the same level. The number of patients newly infected per year in recent years was calculated to be approximately 2,000. The ratio of the number of patients with lung disease due to atypical mycobacteria to the number of patients with lung disease due to atypical mycobacteria to the number of patients with lung disease due to all species of mycobacteria was highest in hospitals on the southwest coast of the Pacific. The atypical mycobacteria that caused disease most frequently belonged to the Mycobacterium avium-intracellulare complex. Of the 537 cases of disease due to atypical mycobacteria, 491 (89.6%) were due to these organisms; 43 (8.0%), to Mycobacterium kansasii; and 7 (1.3%), to Mycobacterium fortuitum. The disease due to M. kansasii appeared most frequently in hospitals in the Tokyo and Kanagawa prefectures. Patients with lung tuberculosis had a high risk of lung infection due to M. avium-intracellulare. The incidence of such disease in tuberculous patients was estimated to be 18.7 per 10(5) population per year, a rate that is approximately 10 times that found in the general population.

Humans↗