The NAME should encourage authors of accepted abstracts to submit video summaries of their work. This will advertise forensic pathology research to a wider audience.

To evaluate the relationship of occupational noise, bilateral hearing loss with blood pressure and hypertension among a Chinese population.

We included 15 422 individuals from a cross-sectional survey of the key occupational diseases in 2017 in Wuhan, Hubei Province, China. Occupational noise exposure was evaluated through workplace noise level and/or the job titles. Hearing loss was defined as a pure-tone average of 25 dB or higher at speech frequency (0.5, 1, 2 kHz) or high frequency (3, 4, 6 kHz) in both ears. Hypertension was defined as blood pressure at least 140/90 mmHg or self-reported current use of antihypertensive medication.

Compared with participants without occupational noise exposure, the prevalence of hypertension was significantly higher for noise exposure duration of 5 to less than 10 years [odds ratio (OR) = 1.13, 95% confidence interval (CI) = 1.04-1.27] and at least 10 years (OR = 1.17, 95% CI = 1.09-1.30). In the sex-specific analysis, the association was significantly pronounced in male (OR = 1.18, 95% CI = 1.06-1.32 for duration of 5 to <10 years; OR = 1.25, 95% CI = 1.12-1.38 for duration ≥10 years), but not in female (OR = 1.01, 95% CI = 0.80-1.11 for duration of 5 to <10 years; OR = 1.06, 95% CI = 0.90-1.20 for duration ≥10 years). In the subsample analyses, bilateral hearing loss was associated with a higher prevalence of hypertension, no matter for speech frequency hearing loss (OR = 1.12, 95% CI = 1.02-1.30 for mild; OR = 1.35, 95% CI = 1.20-1.50 for severe) or for high-frequency hearing loss (OR = 1.24, 95% CI = 1.03-1.50 for mild; OR = 2.40, 95% CI = 1.80-3.17 for severe). The sex-subgroup analysis of hearing loss with hypertension was similar as occupational noise and hypertension.

Our study has suggested occupational noise exposure is a potential risk factor for hypertension.

Our study has suggested occupational noise exposure is a potential risk factor for hypertension.

Hyperglycemia and diabetes mellitus associate with arterial stiffness. This observational study aimed to investigate such links in two related generations from a population-based study.

Data from 2640 participants in the ongoing Malmö Offspring Study, Sweden, was used. The participants were direct descendants, that is, parents (median age 52.5 years) and children (26.9 years). In linear regressions, arterial stiffness measured through carotid–femoral pulse wave velocity was associated with markers of glucose metabolism (fasting glucose, glycated hemoglobin, skin autoflourescence of Advanced Glycation End products), adjusted for age, sex, smoking, BMI, lipids, SBP and antihypertensive medication. Analysis was first performed in all participants and then separately in each generation. T-tests with diabetes mellitus as the grouping variable were performed for all participants and per generation.

In all participants, pulse wave velocity was significantly associated with glucose (β = 0.007, P = 0.018) and hglycemia on vascular aging. However, carotid–femoral pulse wave velocity differed significantly between participants with or without diabetes mellitus in both generations, suggesting that diabetes might negatively affect arterial stiffness also at a younger age.Heart failure is a major source of morbidity and mortality, driven, in part, by maladaptive sympathetic hyperactivity in response to poor cardiac output. Current therapies target β-adrenergic and angiotensin II G protein-coupled receptors to reduce adverse cardiac remodeling and improve clinical outcomes; however, there is a pressing need for new therapeutic approaches to preserve cardiac function. β-arrestin is a multifunctional protein which has come under analysis in recent years as a key player in G protein-coupled receptor signal transduction and a potential therapeutic target in heart failure. β-arrestin attenuates β-adrenergic and angiotensin II receptor signaling to limit the deleterious response to excessive sympathetic stimulation while simultaneously transactivating cardioprotective signaling cascades that preserve cardiac structure and function in response to injury. β-arrestin signaling may provide unique advantages compared to classic heart failure treatment approaches, but a number of challenges currently limit clinical applications. In this review, we discuss the role and functions of β-arrestin and the current attempts to develop G protein-coupled receptor agonists biased towards β-arrestin activation. Furthermore, we examine the functional diversity of cardiac β-arrestin isotypes to explore key considerations in the promise of β-arrestin as a pharmacotherapeutic target in heart failure.Hypertensive crises, although somewhat rare in hypertensive patients, might become an increasingly relevant issue in the future as the number of adults living with hypertension in the United States (U.S.) increases. Many of the current U.S. clinical guidelines for the treatment and management of a variety of medical conditions do not factor hypertensive crises into their recommendations or only consider them in a limited fashion in the context of other medical conditions. This review article summarizes the definitions of hypertensive crises/urgent hypertension/emergent hypertension, the epidemiological profile and outcomes of patients, current U.S. clinical guidelines’ recommendations for the general treatment of hypertensive crises, and current U.S. clinical guidelines’ recommendations for the treatment of acute kidney injuries, acute ischemic stroke, aortic dissection, and acute heart failure in relation to hypertensive crises. All physicians who manage hypertensive patients, but particularly physicians who work in intensive care units, emergency departments and in U.S. EGFR inhibitor hospitals, should review hypertensive crises guidelines and relevant treatments, and understand current recommendations.