A rare case of penetrating thoracic aortic injury.

INTRODUCTION AND IMPORTANCE: Thoracic aortic injuries could be lethal events. Penetrating injuries to aortic are highly fatal, but these cases are rare in hospital. CASE PRESENTATION: A 54-year-old man presented with cough for half a month and cough up blood for half a day before he went into our hospital. No obvious positive sign was detected in physical examination. CLINICAL FINDINGS AND INVESTIGATIONS: Chest computed tomography (CT) showed positive foreign body in the mediastinum, which penetrated the left main bronchus from front to back and penetrated the thoracic aorta backwards. INTERVENTIONS AND OUTCOME: An endovascular stent graft was implanted to ensure that the penetrating aortic injury remains stable; then bronchoscopic evaluation was performed to remove the foreign body. The patient recovered uneventfully. No discomfort has been complained of during regular follow-up. RELEVANCE AND IMPACT: Endovascular stent repair is an effective lifesaving method for patients with penetrating aortic injury and with surgical contraindications.

Upregulation of lncRNA NONRATG019935.2 suppresses the p53-mediated apoptosis of renal tubular epithelial cells in septic acute kidney injury.

Although increasing evidence has confirmed that the apoptosis of renal tubular epithelial cells (RTECs) is a crucial contributor to the onset and development of septic acute kidney injury (AKI), the pathological mechanism by which RTEC apoptosis is upregulated during septic AKI is not entirely clear. In this study, a rat model of septic AKI was induced by a cecal ligation puncture procedure or lipopolysaccharide (LPS) injection. Four differentially expressed long noncoding RNAs (DE-Lncs) in the rat model of septic AKI were determined using RNA-sequencing and verified by qRT-PCR. Among the four DE-Lncs, the expression level of lncRNA NONRATG019935.2 (9935) exhibited the most significant reduction in both septic AKI rats and LPS-treated NRK-52E cells (a rat RTEC line). The overexpression of 9935 suppressed cell apoptosis and p53 protein level in LPS-treated NRK-52E cells, and retarded septic AKI development in the rat model of septic AKI. Mechanistically, 9935 decreased the human antigen R (HuR)-mediated Tp53 mRNA stability by limiting the combination of HuR and the 3'UTR region of Tp53 mRNA in RTECs. The overexpression of HuR abrogated the inhibitory effect of pcDNA-9935 on the LPS-induced apoptosis of NRK-52E and rat primary RTECs. In conclusion, 9935 exerts its role in septic AKI by suppressing the p53-mediated apoptosis of RTECs, and this essential role of 9935 relies on its destructive effect on HuR-mediated Tp53 mRNA stability.

Whether statin use improves the survival of patients with glioblastoma?: A meta-analysis.

BACKGROUND: Glioblastomas are malignant brain tumors associated with high mortality and poor prognosis. Evidence from preclinical studies suggests that statins have an antitumor role, but their effects on the survival of patients with glioblastoma remain controversial. This meta-analysis attempts to assess the association between statins and glioblastoma. METHODS: We searched 4 databases (PubMed, Web of Science, Embase, and Cochrane Library) for articles that evaluate the effect of statins on the survival of patients with glioblastoma. Two reviewers were asked to assess the quality of the studies and extract the data regarding progression-free survival (PFS) and overall survival (OS). RESULT: A total of 5 studies met the inclusion criteria with 430 statin users and 2089 nonstatin users. All 5 studies were retrospectively analyzed. The pooled hazard ratio (HR) and 95% confidence intervals (CIs) were calculated. There was no benefit of statins found pertaining to the survival of glioblastoma patients in both PFS (HR, 0.97; CI, 0.84-1.13) and OS (HR, 0.98; CI, 0.87-1.11). In a subgroup defined by the patterns of statin use, it was determined that usage before glioblastoma diagnosis favored the OS of patients (HR, 0.85). The result, however, failed to demonstrate a statistically significant difference. CONCLUSION: Use of statins was not associated with prolonged survival of patients with glioblastoma. Further well-designed randomized controlled trials are needed to confirm.

A Comparison of Subperiosteal or Subgaleal Drainage with Subdural Drainage on the Outcomes of Chronic Subdural Hematoma: A Meta-Analysis.

OBJECTIVE: The aim of the present study was to compare the outcomes of patients with chronic subdural hematoma after undergoing burr hole craniotomy with subperiosteal or subgaleal drainage (SPGD) with those of patients who have undergone burr hole craniotomy with subdural drainage. METHODS: We searched 4 databases (PubMed, Web of Science, Embase, and Cochrane Library) for relevant reports from January 1995 to September 2019. Two reviewers recorded the major outcomes data as follows: recurrence, mortality, postoperative seizures, postoperative bleeding events, surgical infection, pneumocephalus, modified Rankin scale scores, and Glasgow outcome scale scores. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. RESULTS: A total of 3149 patients from 10 studies were included in our analysis. Compared with the SSD group, the SPGD group had a lower recurrence rate (OR, 0.72; 95% CI, 0.57-0.91) and a smaller risk of postoperative bleeding (OR, 0.41; 95% CI, 0.22-0.78). Also, no significant differences were found in the incidence of mortality (OR, 0.79; 95% CI, 0.54-1.18), postoperative seizures (OR, 0.74; 95% CI, 0.39-1.40), surgical infection (OR, 0.98; 95% CI, 0.55-1.76), pneumocephalus (OR, 0.58; 95% CI, 0.28-1.20), modified Rankin scale score 0-3 (OR, 1.04 at discharge; OR, 1.33 at 6 months), and Glasgow outcome scale score 4-5 (OR, 1.48; 95% CI, 0.82-2.67). CONCLUSIONS: Burr hole craniotomy with SPGD can be recommended as an effective and safe surgical therapy for patients with chronic subdural hematoma owing to its lower recurrence rate and reduced incidence of postoperative brain injuries, in addition to no increase in the rate of some postoperative complications. However, more studies are necessary for further confirmation.

Mechanism of long non-coding RNA MALAT1 in lipopolysaccharide-induced acute kidney injury is mediated by the miR-146a/NF-κB signaling pathway.

The present study aimed to examine the expression and function of the metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/microRNA (miR)-146a/nuclear factor (NF)-κB axis in lipopolysaccharide (LPS)-induced acute kidney injury (AKI). The mRNA levels of MALAT1 and miR-146a in AKI tissues and cells were detected using reverse transcription-quantitative polymerase chain reaction analysis. The NF-κB pathway proteins and cell viability were assessed using western blot analysis and the MTT method, respectively. The secretion of inflammatory factors was determined using the ELISA method. The present study also examined effects of the abnormal expression of MALAT1 and miR-146a on cytokines and the NF-κB pathway. A potential binding region between MALAT1 and miR-146a was confirmed via RNA immunoprecipitation. The results revealed that the upregulation of MALAT1 reduced the expression of miR­146a, and there was a negative linear correlation between MALAT1 and miR-146a in a RNA-induced silencing complex­dependent manner. The expression levels of miR-146a were lower in the kidney injury specimens and NRK-52E cells, compared with those in the controls. MALAT1 knockdown and the overexpression of miR-146a reduced the production of phosphorylated inhibitor of NF-κB and np65 protein. miR­146a was found to be transcriptionally induced by NF-κB, and miR-146a repressed the pro-inflammatory NF-κB pathway and downstream transcription factors. Taken together, these data indicated that the MALAT1/miR­146a/NF-κB pathway exerted key functions in LPS-induced AKI, and provided novel insights into the mechanisms of this therapeutic candidate for the treatment of the disease.

A retrospective study of pyogenic liver abscess focusing on Klebsiella pneumoniae as a primary pathogen in China from 1994 to 2015.

Pyogenic liver abscess (PLA) is a common intra-abdominal infection in adults. In this study, we aim to explore demographic and clinical characteristics of PLA focusing on Klebsiella pneumoniae (K. pneumoniae) induced PLA (KP-PLA) in mainland China. A retrospective review of medical records from all patients with KP-PLA admitted to a tertiary teaching hospital over a 21-year period (1994-2015) was performed. Among 296 PLA cases with confirmed culture-positive data, K. pneumoniae was revealed as the predominant pathogen (n = 189, 63.9%), followed by Escherichia coli (n = 39, 13.2%). Strikingly, KP-PLA patients had a higher incidence of metabolic disorders, such as diabetes mellitus (49.7% vs. 36.4%, P = 0.027; odds ratio (OR): 1.725; 95% confidence interval (CI): 1.061-2.805), hypertension (38.1% vs. 19.6%, P = 0.001; OR: 2.520; 95% CI: 1.439-4.413), and fatty liver (32.3% vs. 14.0%, P = 0.001; OR: 2.923; 95% CI: 1.564-5.462) than those with non-K. pneumoniae induced PLA (non-KP-PLA). Moreover, patients with KP-PLA had higher susceptibility to septic metastatic infection at distant sites compared to those with non-KP-PLA (10.6% vs. 3.7%, p = 0.038). Our results indicate that K. pneumoniae is the predominant pathogen of PLA in mainland China. KP-PLA is frequently diagnosed in patients with metabolic diseases and has a higher risk for septic metastatic infection.

Neuroendocrine dysfunction and insomniain in mild traumatic brain injury patients.

Mild traumatic brain injury (mTBI) has been a growing public health concern in the worldwide. To investigate the subjective and objective characteristics of insomnia following mTBI and the association between insomnia and hypothalamic-pituitary-adrenal (HPA) function of mTBI patients, 59 patients with mTBI (mTBI group) were compared with 50 healthy participants (control group) in the present study. The subjective and objective measures of insomnia were respectively obtained from Pittsburgh Sleep Quality (PSQI) and polysomnography (PSG). HPA function was measured with low-dose short synacthen test (LDSST). According to the comparative and correlation analysis of the two groups, for PSQI, the scores of sleep syndrome, sleep latency, sleep efficiency, overall sleep quality and daytime dysfunction of mTBI patients were all higher, however only sleep efficiency and daytime dysfunction of mTBI patients were related with peak cortisol on lDSST; while for PSG, sleep efficiency (SE) was lower and wake after sleep onset (WASO) was longer in mTBI patients, moreover SE and WASO of mTBI patients were correlated with peak cortisol on LDSTT; for HPA function indexes, only peak cortisol on LDSST was lower in mTBI patients. These findings suggested that mTBI patients experienced more serious subjective insomnia symptoms than objective measurement, which were associated with HPA dysfunction. This study may contribute to identifying better treatment for mTBI patients with insomnia.

DNMT1 mediates chemosensitivity by reducing methylation of miRNA-20a promoter in glioma cells.

Although methyltransferase has been recognized as a major element that governs the epigenetic regulation of the genome during temozolomide (TMZ) chemotherapy in glioblastoma multiforme (GBM) patients, its regulatory effect on glioblastoma chemoresistance has not been well defined. This study investigated whether DNA methyltransferase (DNMT) expression was associated with TMZ sensitivity in glioma cells and elucidated the underlying mechanism. DNMT expression was analyzed by western blotting. miR-20a promoter methylation was evaluated by methylation-specific PCR. Cell viability and apoptosis were assessed using the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and TdT-mediated dUTP-biotin nick end labeling assays, respectively. The results showed that compared with parental U251 cells, DNMT1 expression was downregulated, miR-20a promoter methylation was attenuated and miR-20a levels were elevated in TMZ-resistant U251 cells. Methyltransferase inhibition by 5-aza-2'-deoxycytidine treatment reduced TMZ sensitivity in U251 cells. In U251/TM cells, DNMT1 expression was negatively correlated with miR-20a expression and positively correlated with TMZ sensitivity and leucine-rich repeats and immunoglobulin-like domains 1 expression; these effects were reversed by changes in miR-20a expression. DNMT1 overexpression induced an increase in U251/TM cell apoptosis that was inhibited by the miR-20a mimic, whereas DNMT1 silencing attenuated U251/TM cell apoptosis in a manner that was abrogated by miR-20a inhibitor treatment. Tumor growth of the U251/TM xenograft was inhibited by pcDNA-DNMT1 pretreatment and boosted by DNMT1-small hairpin RNA pretreatment. In summary, DNMT1 mediated chemosensitivity by reducing methylation of the microRNA-20a promoter in glioma cells.

miR-20a mediates temozolomide-resistance in glioblastoma cells via negatively regulating LRIG1 expression.

AIMS: Resistance to temozolomide (TMZ) is a major obstacle in the treatment of glioblastoma multiforme (GBM). MiRNAs is considered as an important modulator of drug resistance in many cancers. Here, we aimed to elucidate the relationship between miR-20a, its predicted target genes leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) and TMZ resistance in GBM. MAIN METHODS: Real-time PCR or western blot was used to measure the levels of miR-20a and LRIG1. The cell viability was obtained to investigate the sensitivity of U251 cells and TMZ-resistant U251 (U251/TMZ) cells to TMZ. MiR-20a inhibitor or miR-20a mimic was used to down-regulate or up-regulate miR-20a expression. The interaction between miR-20a and its predicted target gene LRIG1 was confirmed by 3'-UTR dual-luciferase reporter assay. pcDNA-LRIG1 was used to overexpress LRIG1 [corrected]. A xenograft tumor model was used to investigate the in vivo antitumor activity. KEY FINDINGS: MiR-20a was highly expressed and LRIG1 lowly expressed in U251/TMZ cells. Knockdown of miR-20a by treatment with miR-20a inhibitor restored sensitivity of U251/TM cells to TMZ in vivo and in vitro, whereas overexpression of miR-20a by treatment with miR-20a mimic resulted in increased TMZ resistance. The levels of LRIG1 were inversely related to miR-20a levels. And the luciferase reporter assays showed that miR-20a directly targeted the 3'UTR of LRIG1. In addition, functional knock-down of LRIG1 by gene specific siRNA reversed the effect of miR-20a inhibitor. SIGNIFICANCE: MiR-20a mediated TMZ-resistance in glioblastoma cells through negatively regulating LRIG1 expression, which suggesting that miR-20a and LRIG1 would be potential therapeutic targets for glioma therapy.

Trends in computed tomography utilization and association with hospital outcomes in a Chinese emergency department.

BACKGROUND: Excessive use of computed tomography (CT) in emergency departments (EDs) has become a concern due to its expense and the potential risks associated with radiation exposure. Although studies have shown a steady increase in the number of CT scans requested by ED physicians in developed countries like the United States and Australia, few empirical data are available regarding China. METHODS AND FINDINGS: We retrospectively analyzed a database of ED visits to a tertiary Chinese hospital to examine trends in CT utilization and their association with ED outcomes between 2005 and 2008. A total of 197,512 ED visits were included in this study. CT utilization increased from 9.8% in 2005 to 13.9% in 2008 (P<.001 for trend). The ED length of stay for visits with CT utilization was 0.6 hour longer than those in which CT was not obtained. CT utilization increased the ED cost by an average $48.2. After adjustment for patients' demographics, arrival hours and clinical condition, CT utilization during ED visits was significantly associated with high ED cost (Odds Ratio [OR]: 21.70; 95% confidence interval [CI], 17.00-27.71), long ED length of stay (OR: 1.22; 95%CI, 1.12-1.34), and more likely to receive emergency operations (OR: 2.31; 95%CI, 1.94-2.76). However, there was no significant correlation between CT use and the possibility to be admitted to inpatient wards (OR: 0.82; 95%CI, 0.65-1.04). With respect to the time-related trends, CT utilization during ED visits in all study years was significantly associated with high ED cost and more likely to receive emergency operations. CONCLUSION: CT utilization was associated with higher ED cost, longer ED length of stay and more likely to receive emergency operations, but did not correlate with a significant change in the admission rate.

Anaphylactic shock due to kiwifruit.

A 44-year-old male patient was admitted to our emergency department (ED) with an episode of severe anaphylaxis displaying generalized urticaria and dyspnea 1 hour after consuming a kiwifruit. Initially, the patient reported discrete itching of his abdominal skin and was in moderate respiratory distress. The patient's wheal response and itch were attenuated 30 minutes after emergency treatment with intravenous antianaphylaxis drugs. However, he had symptoms of the chest distress, dizzy, and dysphoria. His vital signs exacerbated. After sufficient antianaphylaxis treatment, the patient's anaphylaxis shock symptoms had not been significantly improved. We reviewed the history. The patient had eaten a full fresh kiwifruit, so there may be some kiwifruit pulp left in the patient's stomach. After self-induced vomiting, the patient's clinical condition gradually improved without any changes in dosage of dopamine. After another 10 hours of observation and preventive therapy training, the patient was discharged. Cases of patients with anaphylactic reaction to kiwifruit and dragon fruit have not been reported yet. In the ED, it is easy to overlook the prolonged exposure to allergen in patients with oral allergy syndrome. If the patient has consumed much food or drugs to cause the allergic reaction, self-induced vomiting or gastric lavage to clean allergen may be useful.

High hospital occupancy is associated with increased risk for patients boarding in the emergency department.

BACKGROUND: Boarding admitted patients in the emergency department due to high hospital occupancy is a worldwide problem. However, whether or not emergency department-boarded patients managed by emergency department providers subjects them to increased serious complications needs further clarification. METHODS: A multivariate logistic regression analysis was used to examine the relationship of patient's age, sex, arrival hours, diagnostic category, triage category, daily emergency department visits, and daily hospital occupancy to the occurrence of serious complications within 24 hours for 20,276 emergency admissions in a 4-year period. RESULTS: A vast majority of study days (86.5%) saw very high occupancy ≥90%. Serious complications incidence was 13.62 per 1000 patient days when hospital occupancy was ≤90%, and it increased significantly to 17.10 and 22.52 per 1000 patient days for occupancy at 90%-95% and ≥95%, respectively. In the multivariate analysis, significant risk factors for serious complications included daily occupancy ≥95% (adjusted odds ratio [OR] 1.73; 95% confidence interval [CI], 1.26-2.39), triage category (adjusted OR 0.20; 95% CI, 0.17-0.24), and specific diagnoses (injury and poisoning [adjusted OR 1.62; 95% CI, 1.22-2.84], respiratory [adjusted OR 2.48; 95% CI, 1.37-4.49], and circulatory [adjusted OR 3.24; 95% CI, 1.80-5.80]). CONCLUSION: High hospital occupancy was associated with an increased incidence of serious complications within 24 hours for patients admitted but still boarded in the emergency department and managed by emergency department providers.

Changes of dipalmitoyl phosphatidyl choline after mechanical ventilation in patients with acute cerebral injury.

OBJECTIVE: To detect the levels of dipalmitoyl phosphatidyl choline (DPPC) in the sputum of the patients with acute cerebral injury without primary pulmonary injury after mechanical ventilation treatment. METHODS: DPPC levels in sputum of 35 patients with acute cerebral injury but without pulmonary injury were detected with high performance liquid chromatography at the beginning of ventilation and 16-20 days, 21-40 days, and 41-60 days after ventilation, respectively. RESULTS: There was no significant difference of the DPPC levels between 16-20 days after ventilation (3.36+/-0.49) and at the beginning of ventilation (3.37+/-0.58) (P>0.05). The mean levels of DPPC decreased significantly at 21-40 days (2.87 mg/ml+/-0.26 mg/ml, P<0.05) and 41-60 days (1.93 mg/ml+/-0.21 mg/ml, P<0.01) after ventilation compared with that at the beginning of ventilation. At the same period, the peak inspiratory pressure and the mean pressure of airway increased significantly, whereas the static compliance and the partial pressure of oxygen in artery decreased significantly. Among the 25 patients who received ventilation for more than 20 days, 8 (32%) had slightly-decreased partial pressure of oxygen in artery compared with that at the beginning of ventilation. CONCLUSIONS: Mechanical ventilation can decrease the DPPC levels, decrease the lung compliance and increase the airway pressure, even impair the oxygenation function in patients with acute cerebral injury. Abnormal DPPC is one of the major causes of ventilator-associated lung injury.