Clinical Features of Aortic Dissection in the Emergency Department: A Single-center Experience from South China.

OBJECTIVES: Our goal in this study was to determine 1) whether there are any differences in clinical characteristics between Chinese and Western patients with aortic dissection (AD), and 2) the mortality rate of AD patients in the emergency department (ED) and identify the risk predictors for death. METHODS: We retrospectively analyzed patients who were diagnosed with AD and admitted to our ED between September 1, 2017-August 31, 2020. Data on age, gender, clinical manifestation, medical history, routine blood tests, liver and kidney function, coagulation, myocardial enzymology, and mortality were collected. RESULTS: We enrolled 535 AD patients (422 men and 113 women) with a mean age of 54.7±14.1 years. Type A AD constituted 40% of the total number of AD cases, while type B AD constituted 60%. The proportion of those who were females, 10-92 years, with type A AD, and hypertension in the Chinese population was lower than that in the Western population (P <0.05 for all). Type A AD patients had a higher proportion of acute AD clinical manifestations than did patients with type B AD (P = 0.0084, P <0.05). The mortality rate of type A AD patients (10.75%) was higher than that of type B AD patients (1.87%) (P <0.0001) in the ED. Higher values of white blood cells, neutrophils, high-density lipoprotein, activated partial thromboplastin time, and D-dimer level with worsened hepatic and renal function were found in the deceased group, and multivariate logistic regression revealed that blood urea nitrogen (BUN) levels (P = 0.0031, P <0.05) were significantly associated with death. CONCLUSION: In South China, patients with AD had a mean age of 54.7 years, with 78.88% prevalence in males and 66.92% hypertension rate. Type A AD accounted for 40% of all AD cases, and 10.70% of patients with type A AD died in the ED. Elevated BUN levels may be a risk predictor for death in patients with type A AD.

Therapeutical plasma exchange for thrombotic thrombocytopenic purpura in the emergency department: A single center experience.

INTRODUCTION: Thrombotic thrombocytopenic purpura (TTP) is a rare, life-threatening and easily misdiagnosed thrombotic microangiopathy disease. Few studies have reported the use of therapeutic plasma exchange (TPE) for TTP in emergency departments in China. The present study was a retrospective analysis of patients with TTP who were treated with TPE in our emergency intensive care unit (EICU). METHODS: This study retrospectively analyzed patients with TTP who received TPE management from July 1, 2014 to February 1, 2020. The following clinical data of these patients were collected: laboratory results, first symptoms, ADAMTS13 levels, glucocorticoid levels, TPE times and outcomes. RESULTS: The study included 19 patients (9 male and 10 female) with 20 clinical episodes, and 1 female patient had two episodes. TPE was used in 17 patients, and TPE was performed once every 2-3 days in patients. The volume for each TPE treatment was 2000 ml. In total, 4 male patients died, and 15 patients survived. One female experienced a relapse. No significant differences in age, RBC, HGB, PLT, ALT, AST, BUN, Cr, LDH, or bilirubin were noted between the survival and death groups. The mortality rate of male patients was significantly higher than that of female patients(p = 0.0325, p < 0.05), and the mean age of deceased patients was 64.25 ± 4.78 years, which was older than the mean age of survivors (47.38 ± 4.30). However, no significant difference was noted (p = 0.0787). CONCLUSION: TPE had satisfactory results for TTP patients although it was not performed every day. Older male TTP patients exhibited a relatively increased risk of death.

Hydrogen-rich saline protects rat from oxygen glucose deprivation and reperusion-induced apoptosis through VDAC1 via Bcl-2.

BACKGROUND: Hydrogen is received as an inert gas that thought to be non-functional in vivo previously. Recently, emerging evidences showed that in ischemia/reperfusion (IR) condition, hydrogen reduced cellular reactive oxygen species (ROS) production and ameliorated cell apoptosis. However, the underlying mechanism of hydrogen on IR-induced apoptosis remains elusive. Here we tried to unravel the mode of action of hydrogen with rat adrenal medulla cell line PC-12 in vitro. METHODS: The mitochondrial functions before and after oxygen glucose deprivation and reperfusion (OGD/RP) were determined with corresponding dyes. The expression of Bcl-2, Bax, VDAC1, cytochrome c and caspase 9 was detected using qRT-PCR and Western Blotting method. Then Bcl-2 inhibitor, AB-199, was applied to investigate the role of Bcl-2 in OGD/RP-induced cell apoptosis. Finally, we manipulated the expression of VDAC1 with plasmids transfection to understand the effects of VDAC1 on Bcl-2-mediated anti-apoptosis in OGD/RP. RESULTS: In this study, we demonstrated that hydrogen-rich saline (HRS) reduced OGD/RP-mediated neuronal loss by stimulating the expression of Bcl-2, which suppressed the activity of VDAC1. Consequently, HRS maintained the mitochondrial functions, restrained the release of cytochrome c and caspase 9 activation, resulting in ameliorated cell viability. CONCLUSIONS: HRS ameliorated OGD/RP-induced PC-12 cell apoptosis and provided a novel treatment option for ischemia.

Ischemic postconditioning regulates cardiomyocyte autophagic activity following ischemia/reperfusion injury.

Ischemic postconditioning (IPostC) is a promising protective mechanism for combating reperfusion injury. However, the role of autophagy in the protective effects of IPostC and the associated signaling pathways have remained to be elucidated. Male Sprague Dawley rats were subjected to 30 min ischemia and 1, 2, 3, 6, 12 and 24 h of reperfusion, with or without IPostC treatment. Autophagic flux was evaluated by detecting mRNA and protein expression levels of microtubule associated protein 1 light chain 3 and p62. Phosphorylated (p)-P70S6 kinase (P70S6K), p-adenosine monophosphate-activated kinase (AMPK) and Beclin 1 protein levels were measured by western blot analysis. Myocardial infarct size was measured using staining with Evans blue dye and myocardial apoptosis was evaluated by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling staining. Autophagic activity was observed to be inhibited within the first hour of reperfusion, increased during 2-6 h and reduced from 12-24 h following IPostC compared with reperfusion without IPostC. Inhibition of autophagy by chloroquine significantly reversed the effects of IPostC on myocardial infarct size and the levels of apoptosis. IPostC significantly increased Beclin 1 levels, inhibited AMPK activation and increased P70S6K activation within the first hour compared with reperfusion without IPostC. IPostC attenuated the upregulation of Beclin 1 levels, increased AMPK activation and reduced P70S6K activation between 2 and 12 h, and subsequently exerted the opposite effects on these molecules between 12 and 24 h. IPostC was demonstrated to regulate autophagic activity in a time­dependent manner. The Beclin 1 and AMPK-mammalian target of rapamycin signaling pathways are suggested to be involved in the regulation of IPostC in autophagy.

Decreased levels of cell-division cycle 42 (Cdc42) protein in peripheral lymphocytes from ischaemic stroke patients are associated with Golgi apparatus function.

OBJECTIVES: To investigate levels of cell-division cycle 42 (Cdc42) protein, and their relationship with Golgi apparatus function in peripheral lymphocytes, in patients following ischaemic stroke. METHODS: Patients with acute cerebral ischaemic stroke (within 24-72 h of the onset of focal neurological symptoms) and healthy control subjects were enrolled in this prospective case-control study. The cellular location of Cdc42 in peripheral lymphocytes was demonstrated using immunofluorescence. Protein levels of Cdc42 and trans-golgi network protein 2 (TGN46) in peripheral lymphocytes were determined by immunocytochemical staining and Western blotting. RESULTS: A total of 38 patients with stroke and 38 control subjects were studied. The mean ± SD percentage of Cdc42-positive lymphocytes from patients with stroke was significantly lower than that in control subjects (39.53 ± 13.55% versus 66.61 ± 23.30%, respectively). Similar findings were demonstrated for TGN46. Cdc42 levels were positively correlated with TGN46 levels (r = 0.92). CONCLUSIONS: Acute ischaemic stroke was associated with reduced levels of Cdc42 protein. These findings might lead to the development of drugs that could have therapeutic benefits in patients with acute ischaemic stroke.

Differential changes of local blood supply in rat retinae are involved in the selective loss of retinal ganglion cells following the acute high intraocular pressure.

PURPOSE: To detect changes in local blood supply to central, middle, and peripheral retina following acute high intraocular pressure and to investigate the effects of changes in local retinal blood supply on the selective loss of retinal ganglion cells. METHODS: The acute high intraocular pressure model of Sprague-Dawley rats was established by increasing the anterior chamber pressure to 110 mmHg via a normal saline perfusion system. Blood supply to the central, middle, and peripheral retina at 3, 6, and 12 h, and 1, 3, 7, and 14 d following induction of acute high intraocular pressure was detected by using gelatin-ink perfusion and fluorescent microsphere injection. Retinal ganglion cell loss following acute high intraocular pressure was detected by fluorogold retrograde labeling. Finally, the relationship between changes in local retinal blood supply and loss of retinal ganglion cells was investigated. RESULTS: The increased ratio of blood supply of peripheral retina was less than that of the central and middle retina at 3 h to 14 d following acute high intraocular pressure. The percent of retinal ganglion cell loss in the peripheral retina was clearly greater than that in the central and middle retina during the first 3 d following induction of acute high intraocular pressure (p < 0.05). Using either the gelatin-ink infusion method or the microsphere injection method (p < 0.05), a significantly negative correlation between the percent of retinal ganglion cell loss and the corresponding increased local blood supply after induction of acute high intraocular pressure (r = -0.57 or -0.72) was found. Moreover, a significant negative correlation in the peripheral retina (r = -0.80 or -0.91; p < 0.05) was observed. CONCLUSION: A disparity exists between changes in local blood supply to the central and middle retina, and the peripheral retina following induction of acute high intraocular pressure in rats. This inequality of changes in local blood supply in rat retina is related to the selective loss of retinal ganglion cells.