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ObjectiveThis study investigated the diagnostic performance of thrombin–antithrombin complex (TAT), plasmin–α2 plasmin inhibitor complex (PIC), tissue plasminogen activator–plasminogen activator inhibitor complex (t-PAIC), and thrombomodulin (TM) in predicting the progression of massive cerebral infarction to the malignant cerebral artery infarction.MethodA total of 71 patients with massive cerebral infarction confirmed by imaging examination were divided into malignant cerebral artery infarction group (MCAI) and non-malignant cerebral artery infarction group (NMCAI) based on whether they progressed to MCAI after admission. TAT, PIC, t-PAIC, and TM were measured immediately after admission. The predictive performance was analyzed by the receiver characteristic operating curve (ROC).ResultThe median plasma concentrations of TM, PIC, TAT, and t-PAIC in the MCAI patients at admission were 10.65 IU/mL, 1.17 μg/mL, 12.25 ng/mL, and 13.85 ng/mL, respectively, which were higher than those in the NMCAI patients (9.00 IU/mL, 1.07 μg/mL, 4.60 ng/mL, and 8.70 ng/mL), and the difference was statistically significant (p = 0.045, p = 0.035, p = 0.004, and p = 0.003). Elevated plasma t-PAIC concentration was shown to be an independent risk factor for progression of massive cerebral infarction to MCAI (OR = 1.131) by multivariate logistic regression analysis. ROC curve analysis showed that t-PAIC was the best predictor of MCAI (AUC = 74.7%), with a sensitivity of 75.0% and specificity of 75.9% when t-PAIC concentration was ≥12.4 ng/mL; TAT had the highest specificity in predicting MCAI, with a specificity of 90.7% when the TAT concentration was ≥13.5 ng/mL.ConclusionThe detection of PIC, TAT, t-PAIC, and TM is a comprehensive assessment of vascular endothelial damage and activation of the coagulation and fibrinolytic systems and has predictive value for poor prognosis in patients with MCAI. The widespread use of these tests will likely greatly improve the early diagnosis rate of MCAI.

AimTo explore the feasibility of Omaha system theory in the care of children with dilated cardiomyopathy (DCM), which may provide a practical basis for the continuous nursing of DCM children.MethodsA total of 1,392 records describing symptoms, signs, and nursing interventions were extracted from the medical records of 76 children suffered from DCM. Content analysis method was used to find out existent nursing problems, make precise nursing plans, and take corresponding nursing measurements according to the medical records of DCM children. Cross-mapping method was utilized to compare the conceptual consistency of the medical records and Omaha system (problem classification and intervention subsystems).ResultsOf the total 1,392 records, 1,094 (78.59%) were complete consistency, while 245 (17.60%) were partial consistency, and 53 (3.81%) were inconsistency with the Omaha system concepts. The concept matching degree of medical records and Omaha system was approximately 96.19%.ConclusionsThe Omaha system may be an effective nursing language for Chinese DCM children, which may be useful to guide nurses in the care of DCM. Further well-design studies need to fully evaluate the feasibility and effectiveness of the Omaha system in nursing children with DCM.

ObjectiveThis study investigated the diagnostic performance of the thrombin-antithrombin complex (TAT), plasmin-α2 plasmin inhibitor complex (PIC), tissue plasminogen activator-plasminogen activator inhibitor complex (t-PAIC), and thrombomodulin (TM) in the early identification of massive cerebral infarction.MethodA total of 423 patients with cerebral infarction confirmed by imaging examination were divided into the massive cerebral infarction (MCI) group and the non-massive cerebral infarction (NMCI) group. TAT, PIC, t-PAIC, and TM were measured immediately after admission. The diagnostic performance was analyzed by the receiver characteristic operating curve (ROC).ResultThe median plasma concentrations of TAT, PIC, and t-PAIC in patients with MCI at early onset were 5.10 ng/ml, 1.11 μg/ml, and 8.80 ng/ml, respectively, which were higher than those in patients with NMCI (2.20 ng/ml, 0.59 μg/ml, and 7.35 ng/ml), and the difference was statistically significant (P < 0.001). TAT was shown to be an independent risk factor for the development of massive cerebral infarction by a multivariate logistic regression analysis (OR = 1.138). A ROC curve analysis showed that PIC had the best performance in identifying MCI at an early stage (AUC = 82.8%), with a sensitivity of 80.7% and a specificity of 76.2% when the PIC concentration was ≥0.8 μg/ml; TAT had the highest specificity in identifying MCI, with a specificity of 80.6% when the TAT concentration was ≥3.97 ng/ml.ConclusionThe detection of PIC, TAT, t-PAIC, and TM is a comprehensive assessment of vascular endothelial damage and activation of the coagulation and fibrinolytic systems and has diagnostic value for early identification of patients with MCI, which, together with its ease of detection, can be used as a plasma marker for early identification of large vessel occlusion.

The number of patients in a hospital is a direct indicator of patients' choice of hospital, which is a complex process affected by many factors. Based on the national medical system and patients' preference for high-grade hospitals in China, this study establishes a three-dimensional differential equation model for calculating the time variation of the number of visits to three grades of hospitals. We performed a qualitative analysis of the system. We carried out a subsequent numerical simulation to analyze the impact on the system when the rate of leapfrog treatment and the maximum capacity of doctors and treatments changed. The results show that the sustainability of China's three levels of hospitals mainly depends on the level of hospital development. The strength of comprehensive health improvement at specific levels is the key to increasing the service efficiency of medical resources.

BackgroundDreams can be affected by recent life events and long-term life experiences. Previous evidence has shown that childhood adverse experiences are associated with sleep quality and dream experiences.ObjectiveThe aim of this study was to explore the relationship between childhood adverse experiences and dream content in adults.Participants and SettingA total of 163 participants without current or past physical or mental disorders aged between 18 and 35 were screened in the hospital. Among them, 120 subjects who completed a dream content record at home and whose anxiety and depression levels and sleep quality were within the normal range were included in the data analysis.MethodsA cross-sectional survey was conducted from June 2017 to December 2019. Dream content for 10 consecutive days was recorded by the participants and coded by the Hall and Van de Castle coding system. Childhood adversity was assessed by the Childhood Trauma Questionnaire (CTQ). In the end, 719 dreams out of 626 nights for 120 participants (44 female) were included in the data analysis, gender differences between groups were analyzed using t-tests or U tests, and Spearman’s partial correlation and multiple linear regression were used to investigate the relationship between childhood trauma and dream content.ResultsChildhood adversity was associated with characters, friendly interactions, and objects in dream content. Regression models of childhood adversity predicting characters and objects in dream content were constructed. There were no gender differences in general demographic data, sleep quality, emotional state, childhood adversity, dream recall frequency, or dream content.ConclusionChildhood adversity is associated with adult dream content.

The oncogene c-Jun is activated by Jun N-terminal kinase (JNK). Exosomes are nanometer-sized membrane vesicles released from a variety of cell types, and are essential for cell-to-cell communication. By using specific JNK inhibitor SP600125 or CRISPR/Cas9 to delete c-Jun, we found that exosomes from SP600125-treated A549 cancer cells (Exo-SP) or from c-Jun-KO-A549 cells (Exo-c-Jun-KO) dramatically inhibited tube formation of HUVECs. And the miR-494 levels in SP600125 treated or c-Jun-KO A549 cells, Exo-SP or Exo-c-Jun-KO, and HUVECs treated with Exo-SP or Exo-c-Jun-KO were significantly decreased. Meanwhile, Exo-SP and Exo-c-Jun-KO enhanced expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN). Addition of miR-494 agomir in Exo-c-Jun-KO treated HUVECs inhibited PTEN expression and promoted tube formation, suggesting the target of miR-494 might be PTEN in HUVECs. Moreover, A549 tumor xenograft model and Matrigel plug assay demonstrated that Exo-c-Jun-KO attenuated tumor growth and angiogenesis through reducing miR-494. Taken together, inhibition of c-Jun in A549 cancer cells exhibited antiangiogenic activity in vitro and in vivo through exosome/miRNA-494-3p/PTEN signal pathway.

Lansoprazole (Lpz) is an FDA-approved proton pump inhibitor (PPI) drug for the therapy of acid-related diseases. Aiming to explore the new application of old drugs, we recently investigated the antitumor effect of Lpz. We demonstrated that the PPI Lpz played a tumor suppressive role in non-small cell lung cancer (NSCLC) A549 cells. Mechanistically, Lpz induced apoptosis and G0/G1 cell cycle arrest by inhibiting the activation of signal transducer and activator of transcription (Stat) 3 and the phosphoinositide 3-kinase (PI3K)/Akt and Raf/ERK pathways. In addition, Lpz inhibited autophagy by blocking the fusion of autophagosomes with lysosomes. Furthermore, Lpz in combination with gefitinib (Gef) showed a synergistic antitumor effect on A549 cells, with enhanced G0/G1 cell cycle arrest and apoptosis. The combination inhibited Stat3 phosphorylation, PI3K/Akt and Raf/ERK signaling, affecting cell cycle-related proteins such as p-Rb, cyclin D1 and p27, as well as apoptotic proteins such as Bax, Bcl-2, caspase-3, and poly (ADP-ribose) polymerase (PARP). In vivo, coadministration with Lpz and Gef significantly attenuated the growth of A549 nude mouse xenograft models. These findings suggest that Lpz might be applied in combination with Gef for NSCLC therapy, but further evidence is required.

Renal fibrosis is the common manifestation of the pathogenesis of end-stage renal disease that results from different types of renal insult, and is a hallmark of chronic kidney disease (CKD). The main pathologic characteristics of renal fibrosis are renal interstitial fibroblast hyperplasia and the aberrant and excessive deposition of extracellular matrix, pathologies that lead to the destruction of normal renal tubules and interstitial structures. However, the biological significance of fibrosis during the progression of CKD is not clear, and there are no approved clinical treatments for delaying or reversing renal fibrosis. Studies of the mechanism of renal fibrosis and of potential measures of prevention and treatment have focused on erythropoietin (EPO), a hormone best known as a regulator of red blood cell production. These recent studies have found that EPO may also provide efficient protection against renal fibrosis. Future therapeutic approaches using EPO offer new hope for patients with CKD. The aim of the present review is to briefly discuss the role of EPO in renal fibrosis, to identify its possible mechanisms in preventing renal fibrosis, and to provide novel ideas for the use of EPO in future treatments of renal fibrosis.