Application Effect and Accuracy Analysis of Electrochemiluminescence Immunoassay and Enzyme-Linked Immunosorbent Assay in the Serological Test of Hepatitis B Virus.

Objective: To explore the validity and accuracy of electrochemiluminescence immunoassay (ECLIA) and enzyme-linked immunosorbent assay (ELISA) in the serological detection of the hepatitis B virus. Methods: From 6 February 2019 to 1 March 2020, 96 patients diagnosed with hepatitis B virus infection in our hospital were recruited and assigned at a ratio of 1 : 1 to experimental groups A (GA) and B (GB), with 48 cases in each group, and the five major serological indicators of hepatitis B were tested and analyzed using ECLIA and ELISA. In addition, 50 suspected patients were selected for two tests, respectively, to compare the accuracy of the two test methods. Results: ECLIA was associated with significantly higher expression levels and higher detection rates of HBeAg, HBeAb, HBsAg, and HBsAb versus ELISA (P < 0.05), and the difference in the expression and detection rates of HBcAb levels between the two groups did not come up to the statistical standard (P > 0.05). ECLIA yielded significantly higher sensitivity and specificity than ELISA (P < 0.05), while the two methods showed comparable detection accuracy (P > 0.05). Conclusion: Despite the inconsistent results of the latest studies on the serological detection of hepatitis B by the two techniques, ECLIA is consistently superior to ELISA and provides better diagnostic benefits and merits promotion.

Analysis of Risk Factors for Poor Short-Term Outcomes in Acute Cardioembolic Stroke Patients without Reperfusion Therapy.

PURPOSE: Few clinical indicators of a poor outcome have been defined in acute cardioembolic stroke (CES) patients. We would like to explore practical clinical factors that can predict poor outcomes of CES in the early stage. PATIENTS AND METHODS: In this single-center, retrospective, observational study, 251 consecutive patients with acute CES who did not undergo reperfusion therapy were evaluated. On the basis of the modified Rankin Scale (mRS) score at 3 months, patients were divided into the good functional outcome group (mRS ≤ 2) and the poor functional outcome group (mRS ≥ 3). Risk factors were analyzed and the independent indicators for a poor outcome were identified using a binary logistic regression model. RESULTS: One hundred (39.8%) patients had a poor outcome. Patients in the poor outcome group were significantly older (P = 0.002) and had significantly higher baseline National Institutes of Health Stroke Scale (NIHSS) score compared with those with a good outcome (P < 0.001). After adjusting for potential confounders, the baseline NIHSS score (P < 0.001), moderate to severe leukoaraiosis (P = 0.011), non-symptomatic intracranial hemorrhage (P = 0.019), stroke-associated pneumonia (P = 0.001), and fasting glucose (P = 0.040) were independent risk factors for a poor outcome. CONCLUSION: The short-term outcome in acute CES patients without reperfusion therapy can be predicted by using five practical clinical factors. These indicators should attract more attention.

Efficacy and safety of vortioxetine for the treatment of major depressive disorder: a randomised double-blind placebo-controlled study.

Objective: This study aimed to evaluate the efficacy and adverse events of vortioxetine for Chinese patients with major depressive disorder (MDD) over 10 weeks.Methods: A total of 120 patients with MDD were randomly assigned to two groups that received vortioxetine 20 mg or placebo for 10 weeks. The outcomes were the change from baseline in the Montgomery-Åsberg Depression Rating Scale (MADRS), Hamilton Anxiety Rating Scale (HAM-A), Clinical Global Impressions-Improvement (CGI-I) scale, Sheehan Disability Scale (SDS) at Week 10, and the presence of adverse events.Results: A total of 113 patients completed the study. Vortioxetine showed greater efficacy than the placebo in improving MADRS, HAM-A, CGI-I, and SDS scores at Week 10. However, no significant differences were found between the groups for any treatment-emergent adverse events. No suicide related to vortioxetine treatment was recorded.Conclusions: In summary, the results of this study showed that 10 weeks of vortioxetine treatment was efficacious and well-tolerated in patients with MDD.

SCY1-like 1 binding protein 1 (SCYL1-bp1) interacts with p53-induced RING H2 protein (Pirh2) after traumatic brain injury in rats.

Traumatic brain injury (TBI) triggers a complex series of neurochemical and signaling changes that lead to neuronal dysfunction and overreactive astrocytes. In the current study, we showed that interactions between SCYL1-bp1 and Pirh2 are involved in central nervous system (CNS) injury and repair. Western blot and immunohistochemical analysis of an acute traumatic brain injury model in adult rats revealed significantly increased levels of SCYL1-bp1 and Pirh2 in the ipsilateral brain cortex, compared to contralateral cerebral cortex. Immunofluorescence double-labeling analyses further revealed that SCYL1-bp1 is mainly co-expressed with NeuN. Terminal deoxynucleotidyl transferase-mediated biotinylated-dUTP nick-end labeling staining data supported the involvement of SCYL1-bp1 and Pirh2 in neuronal apoptosis after brain injury. We additionally examined the expression profiles of active caspase-3, which were altered in correlation with the levels of SCYL1-bp1 and Pirh2. Notably, both SCYL1-bp1 and Pirh2 were colocalized with active caspase-3, and all three proteins participated in neuronal apoptosis. Immunoprecipitation experiments further revealed interactions of these proteins with each other in the pathophysiology process. To our knowledge, this is the first study to report interactions between SCYL1-bp1 and Pirh2 in traumatic brain. Our data collectively indicate that SCYL1-bp1 and Pirh2 play important roles in CNS pathophysiology after TBI.

Upregulation of CRM1 relates to neuronal apoptosis after traumatic brain injury in adult rats.

Traumatic brain injury (TBI) initiates a complex series of neurochemical and signaling changes that leads to neuronal dysfunction and over-reactive astrocytes. There is increasing evidence that CRM1 mediated P27(Kip1), which is a potent inhibitor of G1 cyclin-dependent kinases complexes, nuclear export-dependent or -independent Jab1/CSN5, and cytoplasmic degradation in cells. Up to now, the function of CRM1 in central nervous system (CNS) is still with limited acquaintance. In our study, to investigate whether CRM1 is involved in CNS lesion, we performed a TBI model in adult rats. Western blot and RT-PCR analysis revealed that the level of protein and mRNA of CRM1 increased in ipsilateral brain cortex in comparison to the contralateral. Immunohistochemistry and immunofluorescence double labeling indicated that CRM1 was shutting into nucleus around the wound, and increased CRM1 co-localized with P27(Kip1). Terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) staining suggested that CRM1 was involved in neuronal apoptosis after brain injury. We also investigated co-localization of CRM1 and active-caspase-3 in the ipsilateral brain cortex. In addition, the expression patterns of Bax and active-caspase-3 were parallel with that of CRM1. Based on our data, we suggested that CRM1 might play an important role in neuronal apoptosis following TBI, and might provide a basis for the further study on its role in regulating the expression of P27(Kip1) and cell cycle re-entry in TBI.

Up-regulation of Che-1 relates to neuronal apoptosis after traumatic brain injury in adult rats.

Che-1, a recently identified apoptosis related protein, affects the fate of various cell types when under stress. One attractive biological function of Che-1 is promoting the transcription of p53 after DNA damage; besides, it can also regulate cell cycle via interacting with retinoblastoma protein. Although previous evidence has showed its anti-apoptotic role in cancer cells, some studies point out that Che-1 might play an opposite role in central nervous system (CNS). However, the function of Che-1 in CNS is still with limited acquaintance. To investigate whether Che-1 is involved in CNS lesion, we performed a traumatic brain injury model in adult rats. Up-regulation of Che-1 was observed in the peritrauma brain cortex by performing western blotting and immunohistochemistry. Terminal deoxynucleotidyl transferase deoxy-UTP nick-end labeling and 4',6-diamidino-2-phenylindole staining suggested that Che-1 was involved in neuronal apoptosis after brain injury. We also investigated co-localization of Che-1 and active-caspase-3 in the ipsilateral brain cortex. In addition, the expression patterns of p53, Bax and PCNA were parallel with that of Che-1. Besides this, neurotrophin receptor-interacting MAGE homolog was found to be associated with Che-1 after brain trauma. Based on our data, we suggested that Che-1 might play an important role in neuronal apoptosis following TBI; and might provide a basis for the further study on its role in regulating the expression of p53 and cell cycle re-entry in traumatic brain injury.

Different functions of HIPK2 and CtBP2 in traumatic brain injury.

Traumatic brain injury (TBI) initiates a complex series of neurochemical and signaling changes that lead to neuronal dysfunction and over-reactive astrocytes. In our study, homeodomain interacting protein kinase 2 (HIPK2) can interact with C-terminal binding protein 2 (CtBP2) in rat brain, which is a component of Wnt-regulated transcription. Up to now, the functions of HIPK2 and CtBP2 in CNS are still with limited acquaintance. In our study, we found that the interaction between HIPK2 and CtBP2 was involved in central nervous system (CNS) injury and repair. We performed an acute TBI model in adult rats. Western blot and immunohistochemistry analysis revealed that both HIPK2 and CtBP2 significantly increased in the peritrauma brain cortex in comparison to contralateral cerebral cortex. And immunofluorescence double-labeling revealed that HIPK2 was mainly co-expressed with NeuN but less GFAP. Meanwhile, we also examined that the expression profiles of active-caspase-3 was correlated with the expression of HIPK2 and the expression profiles of the proliferating cell nuclear antigen (PCNA) was correlated with the expression of CtBP2. HIPK2 participated in apoptosis of neurons, but CtBP2 was associated with the activation and proliferation of astrocytes. Immunoprecipitation further showed that they enhanced the interaction with each other in the pathophysiology process. In conclusion, this was the first description that HIPK2 interacted with CtBP2 in traumatic brains. Our data suggest that HIPK2 and CtBP2 might play important roles in CNS pathophysiology after TBI, and might provide a basis for the further study on their roles in regulating the prognosis after TBI.

Increased expression of actin filament-stabilizing protein tropomyosin after rat traumatic brain injury.

Tropomyosin (TM), is a coiled-coil dimmer which modulates actin filament properties, has been implicated in the control of actin filament dynamics during cell migration, morphogenesis, and cytokinesis. However, the expressions and possible functions of tropomyosin in central nervous system (CNS) lesion remain unknown. In this study, we found the expression of tropomyosin gradually increased in rat brains subjected to traumatic brain injury (TBI). Double immunofluorescence staining showed tropomyosin was expressed in neurons and reactive astrocytes following TBI but not in quiescent astrocytes in normal brains. Furthermore, we detected that proliferating cell nuclear antigen (PCNA) had the co-localization with GFAP, and tropomyosin. In conclusion, this was the first description of tropomyosin expression in rat traumatic brain. Our date suggested that tropomyosin might be involved in the astrocytes proliferation following TBI.

An upregulation of SENP3 after spinal cord injury: implications for neuronal apoptosis.

SENP3 (SUMO-specific proteases 3), a member of the small ubiquitin-like modifier specific protease family, was identified as a molecule that deconjugates SUMOylation of modified protein substrates and functions as an isopeptidase by disrupting SUMO homeostasis to facilitate cancer development and progression. However, its expression and function in nervous system injury and repair are still unclear. In this study, we employed an acute spinal cord injury (SCI) model in adult rats and investigated the dynamic changes of SENP3 expression in the spinal cord. Western blot analysis indicated a gradual increase in SENP3 expression, which peaked 3 days after SCI, and then declined over the following days. Immunohistochemistry results further confirmed that SENP3 was expressed at low levels in the gray and white matter in the non-injured condition and increased after SCI. Moreover, immunofluorescence double-labeling showed that SENP3 was co-expressed with the neuronal marker, NeuN. Furthermore, the SENP3-positive cells that were co-expressed with NeuN had also expressed active caspase-3 after injury. To investigate whether SENP3 plays a role in neuronal apoptosis, we applied H(2)O(2) to induce neuronal apoptosis in vitro. Western blot analysis showed a significant upregulation of SENP3 and active caspase-3 following H(2)O(2) stimulation. Taken together, these results suggest that SENP3 may play important roles in the pathophysiology of SCI.

The cell-specific upregulation of bone morphogenetic protein-10 (BMP-10) in a model of rat cortical brain injury.

Previous studies have suggested that bone morphogenetic protein-6 (BMP-6) has a pronounced upregulation in rat brains subjected to traumatic brain injury. Bone morphogenetic protein-10 (BMP-10) is a newly identified cardiac-specific peptide growth factor that belongs to the TGF-ß superfamily. To elucidate the dynamic expression changes and cellular localization of BMP-10 during traumatic brain injury (TBI), we performed an acute traumatic brain injury model in adult rats. Western blot analysis, immunohistochemistry and RTPCR revealed that BMP-10 expression in impaired cerebral cortex was more strongly induced not only at protein level but also at mRNA level compared to that in normal group. Double immunofluorescence labeling suggested that BMP-10 was localized mainly in the cytoplasm of neurons, microglias, and astrocytes within 3 mm from the lesion site at day 3 post-injury. And there was a specific upregulation of BMP-10 in astrocytes following brain injury. Besides, co-localization of BMP-10 and proliferating cell nuclear antigen (PCNA) was detected in Glial fibrillary acidic protein (GFAP) (+) cells. We also examined the expression profiles of PCNA and GFAP whose change was correlated with the expression profiles of BMP-10 in the incised injury model used here. Another experiment in which astrocytes were treated with BMP-10 was also performed to confirm the relationship between the upregulation of BMP-10 and proliferation of astrocytes following TBI. Taken together, this is the first description of BMP-10 expression during the central nervous system (CNS) lesion and repair. Thus, the present data suggested that BMP-10 may be implicated in CNS pathophysiology after TBI. But, further studies are needed to understand the cell signal pathway which can direct the exact role of BMP-10 following traumatic brain injury.

Cyclic AMP response element modulator-1 (CREM-1) involves in neuronal apoptosis after traumatic brain injury.

The cyclic AMP response element-binding protein (CREB) family can regulate biological functions of various types of cells by forming homo- or heterodimers to bind the target DNA sequences; it plays an essential role in individual neuronal function and entire neuronal circuits. One attractive activity of the CREB family is regulating the transcription of apoptosis-suppressor gene bcl-2. Cyclic AMP response element modulator-1 (CREM-1) is one member of the family with limited acquaintance. To investigate whether CREM-1 is involved in central nervous system injury and repair, we performed an acute traumatic brain injury (TBI) model in adult rats. Western blot analysis and immunohistochemistry showed a significant upregulation of CREM-1 in ipsilateral peritrauma cortex. Immunofluorescent labeling indicated that CREM-1 was localized mainly in the nuclei of neurons; co-localization of CREM-1 and active-caspase-3 in the ipsilateral cortex suggested that CREM-1 might participate in neuronal apoptosis. To further investigate the function of CREM-1, a neuronal cell line PC12 was employed to establish an apoptosis model. We analyzed the association of CREM-1 with p-CREB on PC12 cells by Western blot, immunofluorescent labeling, and co-immunoprecipitation. The result implied that the association of CREM-1 with p-CREB was enhanced in apoptotic cells. Additionally, knocking CREM-1 down with siRNA demonstrated the probable pro-apoptotic role played by CREM-1 in neuronal apoptosis. Together with our data, we hypothesized that CREM-1 might play an important role in regulating neuronal death after TBI by interacting with CREB.

Increased expression of BAG-1 in rat brain cortex after traumatic brain injury.

BAG-1 protein was initially identified as a Bcl-2-binding protein. It was reported to enhance Bcl-2 protection from cell death, suggesting that BAG-1 represents a new type of anti-cell death gene. Moreover, recent study has shown that BAG-1 can enhance the proliferation of neuronal precursor cells, attenuate the growth inhibition induced by siah1. However, its function and expression in the central nervous system lesion are not been understood very well. In this study, we performed a traumatic brain injury (TBI) model in adult rats and investigated the dynamic changes of BAG-1 expression in the brain cortex. Double immunofluorescence staining revealed that BAG-1 was co-expressed with NEURON and glial fibrillary acidic protein (GFAP). In addition, we detected that proliferating cell nuclear antigen had the co-localization with GFAP, and BAG-1. All our findings suggested that BAG-1 might involve in the pathophysiology of brain after TBI.