Search

Objective: Protecting healthcare workers is an essential component of a successful response to the COVID-19 pandemic. The resource intensive nature of infectious disease protection, budgetary constraints, and global shortages of personal protective equipment (PPE) make this a daunting task. Practical, easily implemented strategies for healthcare workers (HCW) protection are needed., Methods: We cross-reference the "Systems, Space, Staff, and Stuff" paradigm from disaster management and the "Hierarchy of Controls" approach to infection prevention from the Center for Disease Control and Prevention (CDC) to generate a narrative overview of worker protection strategies relevant to COVID-19., Results: Alternative types of PPE, management of hazards, and reorganizing how people work can optimize HCWs protection., Conclusions: A comprehensive PPE strategy can utilize the "systems, space, staff, stuff" paradigm of disaster management to identify new or underutilized solutions to HCWs protection.

Neural stem/progenitor cells (NSPCs) transplantation provides an alternative approach for various central nervous system (CNS) diseases treatment, while the difficulties in NSPC acquisition and expansion limit their further application. Unveiling the mechanism of NSPC stemness regulation may contribute to its further application. Nestin, generally recognized as a marker of NSPCs, plays a crucial role in the CNS development and NSPC stemness maintenance. Here, we report that Nestin loss triggers mitochondrial network remodeling and enhances oxidative phosphorylation (OXPHOS) in NSPCs treated with Nestin RNA interference (RNAi). Mitochondrial morphology is dynamically controlled by the balance between fission and fusion mediators; one of these mediators, the pro-fission factor, dynamin-related protein 1 (Drp1), shows decreased activation in Nestin-knockdown cells. Upstream, Drp1 phosphorylation is under control of the cytosolic cyclin-dependent kinase 5 (Cdk5). Inhibition of Cdk5 using RNAi or a chemical inhibitor (roscovitine) induces mitochondrial elongation and promotes mitochondrial respiration, indicating that Cdk5-dependent Drp1 phosphorylation participates in mitochondrial metabolism and NSPC stemness regulation. Strikingly, Nestin knockdown results in Cdk5 redistribution, with less remaining in the cytosol, leading to mitochondrial remodeling. We identify Nestin1-640 sequesters Cdk5 in the cytosol and phosphorylates Drp1 subsequently. Together, our results show that a Nestin-Cdk5-Drp1 axis negatively regulates mitochondrial OXPHOS, which is indispensable for the maintenance of NSPC stemness. Stem Cells 2018;36:589-601., (© AlphaMed Press 2018.)

The value of diatom test for the diagnosis of drowning remains controversial. The conventional forensic diatom test with low sensitivity is not a useful tool to provide accurate information about diatom in the tissues and organs. To improve the sensitivity of the diatom test, we developed a novel method called the Microwave Digestion-Vacuum Filtration-Automated Scanning Electron Microscopy (MD-VF-Auto SEM) method which resulted in a high recovery of diatoms. In this article, we analyzed 128 water-related death cases. Our results showed that the MD-VF-Auto SEM method could achieve a much higher positive rate (0.97) in drowning cases. Large amounts of diatoms are retained, even concentrated, in the lung tissues during the intense breathing movement in drowning process. This might be useful for the diagnosis of drowning. Our research indicates that the MD-VF-Auto SEM method would be a valuable methodology in the study of diatom test for the forensic community., (© 2017 American Academy of Forensic Sciences.)

Background: Once hypertension is established, increased mechanical stretch stress becomes a leading cause of vascular remodeling. Clinical antihypertension guidelines demonstrate that antihypertension drugs prevent vascular remodeling in hypertensive patients mainly by lowering blood pressure, suggesting an indirect way of reducing the effects of stretch stress (hypertension). Whether these drugs can directly block the effects of the stretch stress on vascular remodeling has not been reported to date. This study was designed to answer this question and explore the underlying mechanisms., Methods: Cultured quiescent vascular smooth muscle cells (VSMCs) were stimulated by stretch stress after pretreatment with nifedipine and hydrochlorothiazide. The phosphorylation levels of extracellular signal-regulated kinases (ERKs), c‑Jun NH 2 -terminal protein kinases (JNKs), and p38 mitogen-activated protein kinase (MAPK) in VSMCs were detected via Western blotting. The treated cells were stained using triple-labeled immunofluorescence with Ki67 antibody and a TUNEL kit in the presence of DAPI for the detection of proliferative, apoptotic, and resting cells., Results: Compared with the negative control, both nifedipine and hydrochlorothiazide had no influence on the phosphorylation of MAPKs and on the proliferation and apoptosis of VSMCs in resting state. Stretch stress could significantly induce increased phosphorylation of MAPKs as well as proliferation and apoptosis of VSMCs. Nifedipine inhibited the effects of stretch stress in a dose-dependent manner. Contrary to the effects of nifedipine, hydrochlorothiazide synergistically amplified the effects induced by stretch stress., Conclusion: Nifedipine and hydrochlorothiazide have opposing functions in the increased phosphorylation of MAPK and in the proliferation and apoptosis of VSMCs induced by stretch stress. The former plays a role as an inhibitor, while the latter functions as a promoter.

Brugada syndrome (BrS) is an arrhythmogenic disorder which was first described in 1992. This disease is a channelopathy characterized by ST-segment elevations in the right precordial leads and is susceptible to sudden death. BrS is a fatal disease with gender and age preferences. It occurs mainly in young male subjects with a structurally normal heart and silently progresses to sudden death with no significant symptoms. The prevalence of BrS has been reported in the ranges of 5-20 per 10 000 people. The disease is more prevalent in Asia. Nowadays, numerous variations in 23 genes have been linked to BrS since the first gene SCN5A has been associated with BrS in 1998. Not only can clinical specialists apply these discoveries in risk assessment, diagnosis and personal medicine, but also forensic pathologists can make full use of these variations to conduct death cause identification. However, despite the progress in genetics, these associated genes can only account for approximately 35% of the BrS cases while the etiology of the remaining BrS cases is still unexplained. In this review, we discussed the prevalence, the genes associated with BrS and the application of molecular autopsy in forensic pathology. We also summarized the present obstacles, and provided a new insight into the genetic basis of BrS.

Studies regarding sport-related sudden cardiac death (SCD) mainly focus on competitive athletes; similar data are rare in the general population, especially in China. We conducted a retrospective study (from September 1998 to August 2013) to investigate the aetiological distribution and epidemiological features of sport-related SCD in Southern China. Selections of cases are based on details, and two subgroups were established: one was the sport-related SCD group, and the other was the disease-free accident victims group which was matched with the sport-related SCD group in gender, age and year of death. Among the 3770 sudden-death cases, 1656 cases were SCD cases. A total of 65 cases (57 males) out of 1 656 SCD cases were sport-related. The age range of the 65 sport-related SCD cases was from 12 to 68 years old with a mean (35.92 ± 14.23) years old. Only two of these cases were competitive athletes. The most common circumstances of the 65 sport-related SCD cases were heavy physical labour (46.15%) and running (30.77%). The three leading forensic diagnoses were the coronary atherosclerotic disease (CAD, 28 cases), cardiomyopathy (CM, 14 cases) and sudden unexplained death (7 cases). CM was the most common forensic diagnosis in those ≤35 years old, while CAD was the most common one in those >35 years old. Left anterior descending in which atherosclerotic plaques was most commonly found was the principal artery branch associated with sport-related SCD. There was a statistically significant difference in the weight of hearts between the 65 sport-related SCD cases and 65 diseases-free accidental cases. This study highlights the need to attract public attention to sport-related SCD and to issue a prevention strategy to the public, and to make the SCD-related genetic sequencing a routine tool in both forensic pathological examination and clinic screening., (© 2020 The Author(s). Published by Taylor & Francis Group on behalf of the Academy of Forensic Science.)

A series of clinical trials have confirmed the correlation between vascular calcification (VC) and cardiovascular events and mortality. However, current treatments have little effects on the regression of VC. Potent and illustrative mechanisms have been proven to exist in both bone metabolism and VC, indicating that these two processes share similarities in onset and progression. Multiple osteoblast-like cells and signaling pathways are involved in the process of VC. In this review, we summarized the roles of different osteoblast-like cells and we emphasized on how they communicated and interacted with each other using different signaling pathways. Further studies are needed to uncover the underlying mechanisms and to provide novel therapies for VC.

The interactions of sodium balance and response of renin-angiotensin-aldosterone system are important for maintaining the hemodynamic stability in physiological conditions. However, the influence of short-term sodium intake intervention in the response of renin-angiotensin system (RAS) on hypertensive patients is still unclear. Thus, we conducted a clinical trial to investigate the effects of short-term sodium intake intervention on the response of RAS in hypertensive patients.One hundred twenty-five primary Chinese hypertensive patients were divided into high, moderate, and low sodium groups by 24-hour urinary sodium excretion (UNa). All the patients received a 10-day dietary sodium intake intervention with standardized sodium (173.91mmol/day) and potassium (61.53mmol/day). Blood pressure, urinary sodium, urinary potassium, plasma sodium, potassium, creatinine, the levels of plasma renin activity, plasma angiotensin II concentrations (AT-II), and plasma aldosterone concentrations were detected before and after the intervention.Before the intervention, no differences were found in blood pressure and RAS among 3 groups. After standardized dietary sodium intake intervention, both UNa excretion and systolic pressure decreased in high-sodium group, while they increased in moderate and low-sodium groups. Intriguingly, there were no changes in the levels of plasma renin activity, AT-II, and plasma aldosterone concentrations among 3 groups during the intervention.The present study demonstrated that the influenced sodium excretion and blood pressure by short-term sodium intake intervention were independent of RAS quick response in Chinese hypertensive patients.