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- All Subjects: Regulation
Since it was officially established, China’s stock market has witnessed rapid cultural, social, economic, and legal transformations during the last two decades. But the development of China’s stock market brought with it the frequent occurrence of securities crimes and other types of white-collar crimes that harmed vast numbers of public retail stockholders.
This study reviews sociolegal theories, especially law and finance theories, to shed light on the construction of regulatory mechanisms for the Chinese stock market. The critical point for stock market regulation is to curb securities irregularities and protect investors. This study applies white-collar criminological theories, especially crime-as-choice theories, to link the theoretical analyses of the causes of securities crimes to the laws, policies and practices governing the Chinese stock market. Historical, documentary and policy analyses, case analyses, and analysis of interviews, and observations of weibos and blogs are employed in this study. The data sources consist of: (1) historical information on the development of China’s stock market and its regulation, both in terms of legislation and practice; (2) interviews with 40 retail stockholders, each of whom has more than ten years of experiences in stock trading, in two Chinese cities, Shenzhen and Haikou; and (3) online statements and comments of 30 well known Chinese economists, law scholars, financial commentators, lawyers, and securities experts in Sina weibos (microblogs) and blogs.
Based on the analyses, this study suggests revising relevant laws and establishing supporting mechanisms to reduce securities irregularities and crimes in China’s stock market and strength the protection of stock investors. My study also draws attention to the growth of rights consciousness of public retail stockholders, which has potential to propel political and legal reform for the development of the Chinese stock market.
Premature babies are at risk of death from immature lung development. For this reason, pregnant mothers at risk for preterm delivery are administered dexamethasone (DEX), a synthetic glucocorticoid that promotes fetal lung development. However, exposure to DEX in utero is associated with low birth weight and cardiovascular development pathologies. Moreover, our lab found that DEX administration in-utero leads to a sex-specific increase in stress-induced tachycardia in female, but not male offspring. This project seeks to expand on this preliminary finding of the heart by examining local effectors of activity from the sympathetic system (tyrosine hydroxylase and catechol-o-methyltransferase). Tyrosine hydroxylase was measured as it catalyzes the rate limiting step of norepinephrine synthesis while catechol-O- methyltransferase was studied as it catalyzes the degradation of norepinephrine. Acetylcholinesterase was used to measure parasympathetic activity as it catalyzes the degradation of the primary neurotransmitter of the parasympathetic nervous system, acetylcholine. Analyses of sympathetic as well as parasympathetic activity were done to determine influences of in-utero DEX exposure on autonomic regulation in adulthood. Pregnant rats were administered DEX (0.4 mg/kg, i.p.) or vehicle (20% w/v 2-hydroxypropyl ß- cyclodextran) at gestation days 18-21, with euthanasia of offspring occurring at around the time the offspring reached 13-15 weeks of age. Left ventricles and right atria were pulverized, processed and subjected to western blot analysis to determine expression of proteins of interest. Males exposed to DEX in-utero saw a decrease in tyrosine hydroxylase expression in left ventricle and right atrium when compared to vehicle control, a difference not seen with females. In addition, catechol-o-methyltransferase expression was increased in right atria from male, but not female rats. Acetylcholinesterase expression was reduced in the right atria of female, but not male rats. The present findings suggest reduced norepinephrine signaling in the heart of male, but not female DEX-exposed offspring. Given that we have previously found that female, but not male rats exhibit exaggerated stress-induced tachycardia, our current findings suggest that males possess a sex-specific compensatory mechanism allowing the heart to resist increased sympathetic signaling from the brain, one that females do not possess. The underlying mechanics of this proposed mechanism are unclear, and further investigation is needed in this subject to determine the significance of the findings from our study.