A comparative study of late-imperial and early-republican private property rights institutions, as measured by their effects on Shanghai's early financial markets

This research presents an analysis of Shanghai's two separate, parallel but simultaneously coexisting institutional environments, one operating under control of the Chinese central government, and the other under an extraterritorial system defined by foreign (mainly British, American, and French) political and legal conceptualisations. This institutionally dichotomic condition characterised Shanghai for over one hundred years, from the mid-nineteenth to midtwentieth centuries, throughout the course of amid tumultuous political upheaval shaping the domestic political landscape. The nature of these parallel institutional environments in large part reflected the period's political events; the era's political turmoil, via their impact on the nature of institutional protections on private property, contract, and investor rights, concomitantly helped determine Shanghai's economic development, including the development of the city's financial markets. While China's broader domestic institutional framework over this period has received considerable attention in the literature, there exists debate regarding the nature of the strength and efficacy of the domestic institutional environment, particularly in regard to issues pertaining to state capacity and protection of private property rights. This debate is reflective of similar debate within Chinese economic history, one that has portrayed China's late-imperial and republican economic growth as signified mostly by failure, yet with recent revisionist work providing intriguing empirical evidence suggesting considerably stronger economic growth to have occurred throughout the period. In a parallel manifestation, a robust revisionist literature has presented an effective challenge to the standard conventional literature has tended to view the domestic institutional environment over the period as inherently weak and ineffective. In this research project, we utilise Shanghai's unique dualistic institutional setting over this period to help address this debate in the literature. Specifically, we identify how differences between these two institutional frameworks impacted economic actors' behaviour, with a particular emphasis on the revealed preferences displayed by investors acting within Shanghai's early financial markets. To undertake our analysis, we construct an original dataset based on archival records of bond and equity prices that traded on Shanghai's early stock exchanges. The market pricing and trading activity associated with similarly constructed financial instruments, differing primarily in terms of the issuer –whether a domestic or extraterritorial entity– reflect the differing perceptions that contemporaneous investors ascribed to the broader institutional environments. This economic and financial historical research project therefore utilises analysis of contemporaneous investor perceptions to examine not only Shanghai's early financial markets, but also to draw broader conclusions regarding Shanghai's dual institutional environment from a comparative perspective, as well as providing a new viewpoint on a long-standing debate in the literature regarding the efficacy and strength of China's domestic institutional foundations over the late-imperial and early republican time period

Tinnitus and Self-Perceived Hearing Handicap in Firefighters: a Cross-Sectional Study

Firefighters are susceptible to auditory dysfunction due to long-term exposure to noise from sirens, air horns, equipment, and tools used in forcible entry, ventilation, and extrication. In addition, they are exposed to ototoxic chemicals, particularly, during overhaul operations. Studies indicate that 40% of firefighters have hearing loss in the noise-sensitive frequencies of 4 and 6 kHz. Noise-induced hearing loss (NIHL) is often accompanied by tinnitus, which is characterized by ringing noise in the ears. The presence of phantom sounds can adversely affect the performance of firefighters. However, there has been limited research conducted on the prevalence of tinnitus in firefighters. We enrolled firefighters from Michigan, with at least 5 years of continuous service. The hearing handicap inventory for adults (HHIA) was used to determine the difficulty in hearing perceived by the firefighters and the tinnitus functional index (TFI) was used to determine the severity of tinnitus. Self-perceived hearing handicap was reported by 36% of the participants, while tinnitus was reported by 48% of the participants. The TFI survey indicated that 31% perceived tinnitus as a problem. More importantly, self-perceived hearing handicap was significantly associated with the incidence of tinnitus in firefighters, suggesting a potential link between occupational exposure to ototraumatic agents and tinnitus in firefighters

Molecular regulation of auditory hair cell death and approaches to protect sensory receptor cells and/or stimulate repair following acoustic trauma

International audienceLoss of auditory sensory hair cells (HCs) is the most common cause of hearing loss. This review addresses the signaling pathways that are involved in the programmed and necrotic cell death of auditory HCs that occur in response to ototoxic and traumatic stressor events. The roles of inflammatory processes, oxidative stress, mitochondrial damage, cell death receptors, members of the mitogen-activated protein kinase (MAPK) signal pathway and pro- and anti-cell death members of the Bcl-2 family are explored. The molecular interaction of these signal pathways that initiates the loss of auditory HCs following acoustic trauma is covered and possible therapeutic interventions that may protect these sensory HCs from loss via apoptotic or non-apoptotic cell death are explored

Putative LMO4 signaling in cisplatin-induced ototoxicity.

<p>Cisplatin induces cochlear oxidative stress by activating NOX3, which eventually could facilitate the nitration of cochlear LMO4. We reported a cisplatin-induced decrease in the expression of LMO4 in the cochlea (J Biol Chem 2012, 287: 18674–18686). LMO4 has been reported to act as a scaffold by associating with IL-6 receptor glycoprotein 130 and enable the activation of JAK1, TYK2, and STAT3 (J Biol Chem 280: 12747–12757). Since activated STAT3 facilitates the up-regulation of anti-apoptotic genes, the cisplatin-induced decrease in LMO4 levels, probably due to proteolytic degradation of nitrated LMO4, appears to eventually compromise the STAT3-mediated anti-apoptotic machinery, resulting in ototoxicity. Moreover, LMO4 binds with BRCA1 and ESR1 and negatively regulates their activation (Cancer Res 65: 10594–10601). Since BRCA1 directly binds with STAT1, which has been reported to facilitate cisplatin ototoxicity, and ESR1 binds with STAT3 and inhibits its activity, the cisplatin-induced up-regulation of ESR1 and down-regulation of STAT3 in the cochlea suggests that the LMO4 signaling in cisplatin ototoxicity probably involves STAT3-mediated apoptotic pathway to induce cochlear apoptosis.</p

Modulation of Lmo4 binding partners or targets and their attenuation in the cochlea.

<p>The graph represents the relative expression levels of 10 genes, after cisplatin or Trolox co-treatment, compared to control animals. Cisplatin treatment altered the cochlear expression levels of 4 genes, which are related to Lmo4 signaling (^#p<0.05; ^##p<0.01). The cisplatin-induced modulation of 5 genes were attenuated by Trolox co-treatment (*p<0.05; **p<0.01). Actin and Rplp1 were used as housekeeping genes. Results are expressed as mean ± SE, n = 3.</p

Nitrative Stress and Auditory Dysfunction

Nitrative stress is increasingly recognized as a critical mediator of apoptotic cell death in many pathological conditions. The accumulation of nitric oxide along with superoxide radicals leads to the generation of peroxynitrite that can eventually result in the nitration of susceptible proteins. Nitrotyrosine is widely used as a biomarker of nitrative stress and indicates oxidative damage to proteins. Ototoxic insults, such as exposure to noise and ototoxic drugs, enhance the generation of 3-nitrotyrosine in different cell types in the cochlea. Nitrated proteins can disrupt critical signaling pathways and eventually lead to apoptosis and loss of sensory receptor cells in the cochlea. Accumulating evidence shows that selective targeting of nitrative stress attenuates cellular damage. Anti-nitrative compounds, such as peroxynitrite decomposition catalysts and inducible nitric oxide synthase inhibitors, prevent nitrative stress-mediated auditory damage. However, the role of nitrative stress in acquired hearing loss and its potential significance as a promising interventional target is yet to be fully characterized. This review provides an overview of nitrative stress mechanisms, the induction of nitrative stress in the auditory tissue after ototoxic insults, and the therapeutic value of targeting nitrative stress for mitigating auditory dysfunction.</jats:p

Distribution of Lmo4 in the cochlea.

<p>Immunolocalization with anti-Lmo4 detected the expression of Lmo4 proteins in the spiral ganglion, stria vascularis, and organ of Corti of rat cochlea. In the merged panels (bottom row), red indicates immunoreactivity to Lmo4, green indicates actin staining (phalloidin), and blue indicates nuclear staining (DAPI). A section obtained from the basal turn of the organ of Corti is illustrated. The images are representative samples from 2 animals.</p

Cisplatin-induced decrease in cochlear protein levels of Stat3.

<p>Immunoblots show cisplatin-induced decrease in cochlear Stat3 levels (***p<0.001) and reversal with Trolox co-treatment (**p<0.01). Stat3 expression was normalized with that of actin, and results are expressed as mean ± SE, n = 3.</p