Cynthia Chen

American, 1,633 Chinese, and 1,247 Japanese eleventh‐grade students, 5 indices of maladjustment included measures of stress, depressed mood, academic anxiety, aggression, and somatic complaints. Asian students reported higher levels of parental expectation and lower levels of parental satisfaction concerning academic achievement than their American peers. Nevertheless, Japanese students reported less stress, depressed mood, aggression, academic anxiety, and fewer somatic complaints than did American students. Chinese students reported less stress, academic anxiety, and aggressive feelings than their American counterparts, but did report higher frequencies of depressed mood and somatic complaints. High academic achievement as assessed by a test of mathematics was generally not associated with psychological maladjustment. The only exception was in the United States, where high achievers indicated more frequent feelings of stress than did low achievers. Copyright © 1994, Wiley Blackwell. All rights reserved.

Increased airway smooth muscle contractility and the development of airway hyperresponsiveness are cardinal features of asthma, but the signaling pathways that promote these changes are poorly understood. Tyrosine phosphorylation is tightly regulated by the opposing actions of protein tyrosine kinases and phosphatases, but little is known about whether tyrosine phosphatases influence AHR. Here, we demonstrate that genetic inactivation of receptor-like protein tyrosine phosphatase J, which encodes CD148, protected mice from the development of increased AHR in two different asthma models. Surprisingly, CD148 deficiency minimally affected the inflammatory response to allergen, but significantly altered baseline pulmonary resistance. Mice specifically lacking CD148 in smooth muscle had decreased AHR, and the frequency of calcium oscillations in CD148-deficient ASM was substantially attenuated, suggesting that signaling pathway alterations may underlie ASM contractility. Biochemical analysis of CD148-deficient ASM revealed hyper-phosphorylation of the C-terminal inhibitory tyrosine of SRC family kinases, implicating CD148 as a critical positive regulator of SFK signaling in ASM. The effect of CD148 deficiency on ASM contractility could be mimicked by treatment of both mouse trachea and human bronchi with specific SFK inhibitors. Our studies identify CD148 and the SFKs it regulates in ASM as potential targets for the treatment of AHR.