Serum proteins differentially expressed in early- and late-onset preeclampsia assessed using iTRAQ proteomics and bioinformatics analyses.

BACKGROUND: Preeclampsia remains a serious disorder that puts at risk the lives of perinatal mothers and infants worldwide. This study assessed potential pathogenic mechanisms underlying preeclampsia by investigating differentially expressed proteins (DEPs) in the serum of patients with early-onset preeclampsia (EOPE) and late-onset preeclampsia (LOPE) compared with healthy pregnant women. METHODS: Blood samples were collected from four women with EOPE, four women with LOPE, and eight women with normal pregnancies, with four women providing control samples for each preeclampsia group. Serum proteins were identified by isobaric tags for relative and absolute quantitation combined with liquid chromatography-tandem mass spectrometry. Serum proteins with differences in their levels compared with control groups of at least 1.2 fold-changes and that were also statistically significantly different between the groups at P < 0.05 were further analyzed. Bioinformatics analyses, including gene ontology and Kyoto Encyclopedia of Genes and Genomes signaling pathway analyses, were used to determine the key proteins and signaling pathways associated with the development of PE and to determine those DEPs that differed between women with EOPE and those with LOPE. Key protein identified by mass spectrometry was verified by enzyme linked immunosorbent assay (ELISA). RESULTS: Compared with serum samples from healthy pregnant women, those from women with EOPE displayed 70 proteins that were differentially expressed with significance. Among them, 51 proteins were significantly upregulated and 19 proteins were significantly downregulated. In serum samples from women with LOPE, 24 DEPs were identified , with 10 proteins significantly upregulated and 14 proteins significantly downregulated compared with healthy pregnant women. Bioinformatics analyses indicated that DEPs in both the EOPE and LOPE groups were associated with abnormalities in the activation of the coagulation cascade and complement system as well as with lipid metabolism. In addition, 19 DEPs in the EOPE group were closely related to placental development or invasion of tumor cells. Downregulationof pregnancy-specific beta-1-glycoprotein 9 (PSG9) in the LOPE group was confirmed by ELISA. CONCLUSION: The pathogenesis of EOPE and LOPE appeared to be associated with coagulation cascade activation, lipid metabolism, and complement activation. However, the pathogenesis of EOPE also involved processes associated with greater placental injury. This study provided several new proteins in the serum which may be valuable for clinical diagnosis of EOPE and LOPE, and offered potential mechanisms underpinning the development of these disorders.

Maternal air pollution exposure and congenital heart defects in offspring: A systematic review and meta-analysis.

BACKGROUND: Congenital heart defects (CHDs) has a multifactorial causation with a strong genetic component and many environmental triggers. Emerging body of empirical studies suggest that air pollution is an important contributor to the development of CHDs, however, there still remains some controversy over the current evidence, and to the authors' knowledge, no studies have reviewed the most recent evidence. OBJECTIVES: We performed a systematic review and meta-analysis of epidemiological literature to investigate the relationship between maternal air pollution exposure and CHDs risk in offspring. The presence of heterogeneity and publication bias across available studies were also examined. METHODS: An extensive literature search of epidemiological studies pertaining to air pollution and CHDs, published in English language, until August 1, 2019 was conducted. Summary risk estimates of pollution-outcome combinations were calculated for i) risk per specific increment of concentration and ii) risk at high versus low exposure level in each study using fixed-effect model or random-effects model. RESULTS: A total of 26 studies were finally included. In the meta-analyses, high versus low carbon monoxide (CO) exposure was associated with an increased risk of tetralogy of Fallot [odds ratio (OR) = 1.21, 95% confidence interval (CI): 1.04-1.41], yet particulate matter ≤ 5 µm (PM2.5) exposure was marginally associated with it. Increased risk of atrial septal defects (ASDs) was found for each 10 µg/m3 and 10 ppb increment in particulate matter ≤ 10 µm (PM10) and ozone (O3) exposure, respectively (OR = 1.04, 95% CI: 1.00-1.09; OR = 1.09, 95% CI: 1.02-1.17). Categorical nitrogen dioxide (NO2) exposure was associated with an increased risk of coarctation of the aorta (OR for high versus low = 1.14, 95% CI: 1.02-1.26). Analyses for other combinations yielded none statistically significant associations. Sensitive analyses showed similar findings. CONCLUSIONS: The summary effect estimates from this study suggest statistically significant associations between increased risk of specific CHDs subtypes and PM2.5, PM10, NO2, CO, and O3 exposures. Further studies, especially conducted in developing countries, with improvements in exposure assessing, outcome harmonizing, and mechanistic understanding are needed to elaborate the suggestive associations.

Effect of endometrial injury during menstruation on clinical outcomes in frozen-thawed embryo transfer cycles: A randomized control trial.

AIM: To explore the clinical effect of endometrial injury (EI) on the third day of the menstrual cycle before frozen-thawed embryo transfer (frozen-thawed ET) on patients experienced two or more implantation failures. METHODS: A total of 200 patients who suffered at least two failed hormone-replacement therapies and frozen-thawed ET were randomly divided into two groups: EI group and control group (n = 100 in each group). Patients in the EI group received local EI with a Pipelle catheter on the third day of the menstrual cycle before frozen-thawed ET. Primary outcomes were live birth, clinical pregnancy and implantation rates. Secondary outcomes were biochemical, multiple and ectopic pregnancy rates and abortion rates. RESULTS: The rate of live birth in EI group (51.00%) was significantly higher than that of control group (36.00%) (P = 0.032). Clinical pregnancy and implantation rates in EI group were significantly higher comparing to control group (64.00% vs 48.00%, P = 0.023 and 46.74% vs 30.11%, P = 0.001). The rate of multiple pregnancy in EI group (37.50%) was significantly higher than that of control group (18.75%) (P = 0.031). No significant difference in ectopic pregnancy rate and abortion rate was observed between EI group and control group. CONCLUSION: Applying EI to patients experienced two or more implantation failures on the third day of the menstrual cycle before frozen-thawed ET can improve clinical outcomes.

Incidence and Natural Progression of Neurogenic Shock after Traumatic Spinal Cord Injury.

Neurogenic shock, a distributive type of circulatory shock after spinal cord injury (SCI), results in profound hypotension. The consequent hemodynamic instability complicates clinical management, delays surgical intervention, and impacts neurological outcome. Moreover, the reported incidence of this condition varies significantly. We establish the true incidence of neurogenic shock by comparing the most common clinical definitions used to diagnose the condition. Further, we characterize the acute progression and recovery of neurogenic shock. Daily blood pressure, heart rate, and fluid management as well as vasopressor therapy and neurologic status were collected over 30 days from 84 adults admitted to our tertiary trauma center after cervical (n = 56) and thoracic (n = 28) SCI. We found that the reported incidence of neurogenic shock varied greatly depending on which clinical definition was applied. By using a novel combination of hemodynamic and laboratory criteria to define neurogenic shock, the calculated incidence (29% cervical SCI) in our sample most appropriately reflects the true incidence, finding that hypovolemia was the primary factor responsible for the inconsistency in incidence reports between studies. In addition, we found a characteristic decline in blood pressure after the first week post-injury and that fluid management is not currently an integral aspect of clinical management (all persons were treated at a net fluid intake ≤ zero). The results demonstrate the need for accurate identification of neurogenic shock through consistent and appropriate criteria, which is not only important from a clinical point of view, but also in establishing accurate epidemiology to responsibly allocate resources to its management.

CAEP position statement on cellphone use while driving.

Distracted driving caused by cellphone use is a significant source of needless injuries. These injuries place unnecessary financial burden, emotional stress and health care resource misuse on society. This paper states the Canadian Association of Emergency Physician's (CAEP's) position on cellphone use while driving. In recent years, numerous studies were conducted on the danger of cellphone use while driving. Research has shown that cellphone use while driving negatively impacts cognitive functions, visual fields, reaction time and overall driving performances. Some studies found that cellphone use is as dangerous as driving under the influence of alcohol. Moreover, vehicle crash rates were shown to be significantly higher when drivers used cellphones. Countermeasures have been implemented in recent years. Over 50 countries worldwide have laws limiting the use of cellphones while driving. Six Canadian provinces, Newfoundland and Labrador, Nova Scotia, Quebec, Ontario, British Columbia and Saskatchewan, currently have legislation prohibiting cellphone use. Other provinces are considering implementing similar bans. As emergency physicians, we must advocate for injury prevention. Cell phone related road traumas are avoidable. CAEP supports all measures to ban cellphone use while driving.