No abstract

The problem of 'social withdrawal' among young adults is the focus of considerable attention in Japan today. Among the various manifestations of social withdrawal, a 'primary social withdrawal' group has been identified that cannot be diagnosed by the established classification of mental disorders. In an earlier report it was suggested that the onset mechanism for primary social withdrawal is not merely a problem of the withdrawn person themselves, but also includes problems of family relationships. The aim of the present study was to identify the characteristics and problems in family relationships associated with primary social withdrawal. For that purpose a survey was conducted using David H. Olson's Family Adaptability and Cohesion Evaluation Scale as well as a questionnaire that the present authors devised on family interactions and the personal situation of the withdrawn person. The results pointed to the following four characteristics of primary social withdrawal families: (i) there are definite rules within the family; (ii) the families share values and an unfounded pride; (iii) there is a lack of emotional exchange in the family, and it is difficult for members to sympathize with each other's negative feelings; and (iv) although concerned about each other, there is little verbal exchange. From these family characteristics, the onset mechanism for withdrawal is triggered by insignificant matters such as minor setbacks in the developmental issues of youth. Then, given the person's personality traits and aforementioned characteristics in family relationships, the person becomes mired in social withdrawal.

This is the first observation of ZEB1 expression in epithelial cells of benign disease. The preferential expression of ZEB1 in epithelial cells of endometriotic lesions suggests that these cells may have, at least in part, a higher level of mesenchymal features possibly via ZEB1-driven epithelial-mesenchymal transition than normal endometria and that ZEB1 can be a potential indicator of invasiveness or severity of endometriosis.

Objectives: Although skeletal muscle atrophy is common in critically ill patients, biomarkers associated with muscle atrophy have not been identified reliably. Titin is a spring-like protein found in muscles and has become a measurable biomarker for muscle breakdown. We hypothesized that urinary titin is useful for monitoring muscle atrophy in critically ill patients. Therefore, we investigated urinary titin level and its association with muscle atrophy in critically ill patients. Design: Two-center, prospective observational study. Setting: Mixed medical/surgical ICU in Japan. Patients: Nonsurgical adult patients who were expected to remain in ICU for greater than 5 days. Interventions: None. Measurements and Main Results: Urine samples were collected on days 1, 2, 3, 5, and 7 of ICU admission. To assess muscle atrophy, rectus femoris cross-sectional area and diaphragm thickness were measured with ultrasound on days 1, 3, 5, and 7. Secondary outcomes included its relationship with ICU-acquired weakness, ICU Mobility Scale, and ICU mortality. Fifty-six patients and 232 urinary titin measurements were included. Urinary titin (normal range: 1–3 pmol/mg creatinine) was 27.9 (16.8–59.6), 47.6 (23.5–82.4), 46.6 (24.4–97.6), 38.4 (23.6–83.0), and 49.3 (27.4–92.6) pmol/mg creatinine on days 1, 2, 3, 5, and 7, respectively. Cumulative urinary titin level was significantly associated with rectus femoris muscle atrophy on days 3–7 (p ≤ 0.03), although urinary titin level was not associated with change in diaphragm thickness (p = 0.31–0.45). Furthermore, cumulative urinary titin level was associated with occurrence of ICU-acquired weakness (p = 0.01) and ICU mortality (p = 0.02) but not with ICU Mobility Scale (p = 0.18). Conclusions: In nonsurgical critically ill patients, urinary titin level increased 10–30 times compared with the normal level. The increased urinary titin level was associated with lower limb muscle atrophy, occurrence of ICU-acquired weakness, and ICU mortality.

We herein report two cases of primary ciliary dyskinesia (PCD) with different responses to macrolides. Case 1: a 17-year-old Japanese man with Pseudomonas aeruginosa infection and combined defect of both inner and outer dynein arms in the cilia was unsuccessfully treated with long-term macrolides (clarithromycin, erythromycin, and azithromycin). Case 2: a 70-year-old Japanese man with deficiency of only the inner dynein arm was successfully treated with clarithromycin. Though the reasons for the different responses to macrolides are unclear, differences of ultrastructural abnormalities of the cilia might be one of the predictive factors in PCD just as in Pseudomonas aeruginosa infection.