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Background The COVID-19 outbreak has exerted an enormous impact on various industries worldwide. During this pandemic, clinical teaching hospitals have faced unprecedented challenges regarding the management of postgraduate medical students since postgraduate students in clinical medicine have both student and resident identity characteristics. The purpose of this study was to explore the management effectiveness of Peking University Third Hospital (PUTH) based on PDCA (plan-do-check-act) cycle management and to further develop the medical student management system during the pandemic. Methods The methods of document review, questionnaire surveys and interviews were used to continuously improve the management measures for postgraduate medical students during the COVID-19 pandemic by using the PDCA cycle. Results Investigations were conducted on the management system, back-to-school arrangements, laboratory management, COVID-19 prevention and control training, online teaching, mentoring, dissertation progress, and emotional state of postgraduate medical students during the COVID-19 pandemic. We found that strengthening public health management knowledge training, increasing infectious-disease-related knowledge training, innovating online teaching methods, improving PDCA management model maps, and formulating improvement programmes are conducive to improving the quality of such management. Conclusion Given the difficulties involved in the management of postgraduate medical students during the COVID-19 pandemic, managers need to comprehensively consider and conduct overall planning and use the PDCA management model to improve the management of postgraduate medical students during this period.

Here, we investigated the role of tanshinone IIA (TSO IIA) in astrocytic swelling caused by ischemia and reperfusion-like injury in an in vitro model and the molecular mechanisms underlying this effect. Primary brain astrocytes were cultured in conditions of glucose and oxygen deprivation and reoxygenation (OGD/R). We investigated the effects of TSO IIA treatment on cell swelling and injury, and the expression levels of AQP4 protein in the plasma membrane. We then studied the involvement of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis in TSO IIA-mediated protection. Treatment with TSO IIA alleviated OGD/R-induced astrocytic swelling and the over-clustering of AQP4 protein in the plasma membrane. In addition, TSO-IIA significantly reduced over-expression of HMGB1, the high levels of NF-κB protein in the nucleus, and of IL-6 protein in cytoplasm and extracellular media induced by OGD/R. Combination of TSO IIA and recombinant HMGB1 reversed these effects. Inhibition of RAGE, the receptor of HMGB1, induced similar results to those of TSO IIA. In addition, exogenous IL-6 reversed TSO IIA-mediated effect on AQP4 over-clustering and cell swelling.TSO IIA significantly reduced astrocyte swelling after OGD/R injury in vitro, via blocking activation of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis and thereby decreasing the expression of AQP4 in plasma membrane.

Although erythropoietin (EPO) has been proven to significantly promote the proliferation of cancer cells, the mechanism for promoting glioma proliferation is poorly understood. Here, we examined the functional role of the AKT/GSK-3β/β-catenin signaling pathway in the EPO-mediated proliferation of glioma. The distribution of EPO and Ki-67 among clinical samples with different WHO grades was plotted by Immunological Histological Chemistry analysis. U87 and U251 glioma cell lines were treated with short hairpin RNA targeting (shEPO), recombinant human erythropoietin (rhEPO) and/or AKT-specific inhibitor (MK-2206). The changes in phosphorylated AKT, nuclear β-catenin, cyclin D1 and p27kip1 expression were detected. Cell cycle distributions and glioma proliferation in vitro and in vivo were analyzed. The expression level of EPO was significantly elevated with the increase of WHO grade and Ki67 in clinical glioma specimens. In vitro, knockdown of endogenous EPO in U87 and U251 cells effectively block the phosphorylation of AKT and GSK-3β and the expression of nuclear β-catenin. shEPO treatment also significantly decreased the expression of cyclin D1 and increased the expression of p27kip1. The cell cycle transition then slowed down and the proliferation of glioma cells or mouse xenograft tumors both decreased. Treatment of cells or tumors with extra rhEPO reversed the above biological effects mediated by shEPO. rhEPO-induced activation of the AKT/GSK-3β/β-catenin pathway and proliferation were abolished by MK-2206. Our study identified the AKT/GSK-3β/β-catenin axis as a critical mediator of EPO-induced glioma proliferation and further provided a clinically significant dimension to the biology of EPO.

The creation of bone flaps which can be later repositioned and fixed in situ for repairing the bone defects during the endoscopic endonasal approaches (EEAs)—similar to transcranial craniotomies—is still a challenge. We present an in situ bone flap (ISBF) closure for the repair of bone defects after endoscopic endonasal transplanum-transtuberculum approaches (EETAs). A retrospective analysis of consecutive patients who underwent the EETAs between January 2016 and February 2019 was performed. According to whether or not to use ISBF for skull base reconstruction, these patients were divided into the ISBF group or the non-ISBF group. Of 47 patients in the ISBF group, only one patient (2.1%) developed postoperative cerebrospinal fluid (CSF) leakage, yielding a significantly lower leakage rate in the ISBF group than in the non-ISBF group (6 of 38, 15.8%, P = 0.042). Besides, when only comparing cases of hydrocephalus in the two groups, the CSF leakage rate in the ISBF group was 8.3% (1/12), which was still significantly lower than that in the non-ISBF group (62.5%, 6/8) (P = 0.018). Postoperative CSF leakages in both groups were successfully treated with lumbar drainage alone, and no cases of injury to the internal carotid arteries or optic nerves occurred in either group. An ISBF closure similar to transcranial craniotomies with repositioning bone flap in situ—is feasible, safe, and reliable. The ISBF closure combining with a pedicled nasoseptal flap (PNSF) provides the cranial base surgeon with an additional repair method that has demonstrated effectiveness at facilitating a more stable and durable reconstruction and reducing CSF leaks.

Background: Tanshione IIA (TSO IIA) has emerged as a powerful anti-inflammatory compound with multiple therapeutic properties. Here, we investigated the role of TSO IIA in astrocytic swelling caused by ischemia and reperfusion-like injury in an in vitro model and the molecular mechanisms underlying this effect. Methods: Primary brain astrocytes were cultured in vitro in conditions of glucose and oxygen deprivation and reoxygenation (OGD/R). We investigated the effects of TSO IIA treatment on cell swelling and injury, and the expression levels of AQP4 protein in the plasma membrane. We then studied the involvement of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis in TSO IIA-mediated protection. Results: Treatment with TSO IIA alleviated OGD/R-induced astrocytic swelling, changes in cell morphology and ultrastructure, the release of LDH, and the over-clustering of AQP4 protein in the plasma membrane. In addition, TSO-IIA significantly reduced over-expression of HMGB1 protein in the cytoplasm and surrounding medium, the high levels of NF-κB protein in the nucleus, and of IL-6 protein in cytoplasm and extracellular media induced by OGD/R. Combination of TSO IIA and recombinant HMGB1 (rHMGB1) reversed these effects. Inhibition of RAGE, the receptor of HMGB1, via administration of FPS-ZM1 (a RAGE antagonist) induced similar results to those of TSO IIA. In addition, exogenous IL-6 reversed TSO IIA-mediated effect on AQP4 protein clustering in the plasma membrane, cell swelling and LDH activity.Conclusions: TSO IIA significantly reduced astrocyte swelling after OGD/R injury in vitro, via blocking activation of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis and thereby decreasing the expression of AQP4 in plasma membrane.

Background: Tanshione IIA (TSO IIA) has emerged as a powerful anti-inflammatory compound with multiple therapeutic properties. Here, we investigated the role of TSO IIA in astrocytic swelling caused by ischemia and reperfusion-like injury in an in vitro model and the molecular mechanisms underlying this effect. Methods: Primary brain astrocytes were cultured in vitro in conditions of glucose and oxygen deprivation and reoxygenation (OGD/R). We investigated the effects of TSO IIA treatment on cell swelling and injury, and the expression levels of AQP4 protein in the plasma membrane. We then studied the involvement of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis in TSO IIA-mediated protection. Results: Treatment with TSO IIA alleviated OGD/R-induced astrocytic swelling, changes in cell morphology and ultrastructure, the release of LDH, and the over-clustering of AQP4 protein in the plasma membrane. In addition, TSO-IIA significantly reduced over-expression of HMGB1 protein in the cytoplasm and surrounding medium, the high levels of NF-κB protein in the nucleus, and of IL-6 protein in cytoplasm and extracellular media induced by OGD/R. Combination of TSO IIA and recombinant HMGB1 (rHMGB1) reversed these effects. Inhibition of RAGE, the receptor of HMGB1, via administration of FPS-ZM1 (a RAGE antagonist) induced similar results to those of TSO IIA. The combination of HMGB1 and FPS-ZM1 did not alter the effects mediated by FPS-ZM1 alone. In addition, exogenous IL-6 reversed TSO IIA-mediated effect on AQP4 protein clustering in the plasma membrane, cell swelling and LDH activity.Conclusions: TSO IIA significantly reduced astrocyte swelling after OGD/R injury in vitro, via blocking activation of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis and thereby decreasing the expression of AQP4 in plasma membrane.

Dendrimers are highly branched macromolecules. The structural chemistry of dendrimers could be shaped by their topological invariants to target the particular design with appropriate properties to bring the drugs to mark a carrier vehicle. This study is about some new topological indices of dendrimer generations. Here, we calculate K Banhatti indices for five generations of dendrimers. Precisely speaking, we computed the 1st K Banhatti redefined Zagreb index, 2nd K Banhatti redefined Zagreb indices, and 3rd K Banhatti redefined Zagreb index for the dendrimers D i p for i = 1,2,3,4,5 .

Background PLK3, a gene played an important role in cell cycle progression and stress response, was identified in different carcinomas. However, the PLK3 expression, molecular characteristics, and prognostic value in glioma still remained unknown. Methods Total 2265 glioma samples from the CGGA RNA-seq, TCGA RNA-seq, CGGA microarray, GSE16011, as well as their clinical information and genomic profiles were selected in our research. Survival analysis based on Kaplan–Meier and Cox proportional hazard model methods was performed to evaluate the prognostic value. Results Expression of PLK3 was compared in different WHO grade, isocitrate dehydrogenase (IDH) status, and molecular subtype of gliomas. We found that increased level of PLK3 was associated with malignancy and invasiveness of glioma, and high expression of PLK3 may represent malignant entities with amplification of driver oncogenes and deletion of suppressor genes. Moreover, PLK3 played a crucial role in inflammatory and immune response, and was involved in suppressive T cell anti-tumor functions. Furthermore, PLK3 was synergistic with other checkpoint members in glioma. Finally, high expression of PLK3 was associated with malignant process and reduced survival in patients with glioma. Conclusion PLK3 may serve as an indicator of poor prognosis in glioma and a potential target for immunotherapy of glioma. These results demonstrated that PLK3 may serve as a biomarker and a potential target of glioma.

Yu-Xin Wang,1,* Feng-Lian Li,1,* Li-Xin Du,1 Jun-Fang Liu,2 Li-Gang Huo,1 Shu-Qing Li,3 Bin Tian1 1Department of Clinical Laboratory, Hengshui Fifth People’s Hospital, Hengshui City, 053000, People’s Republic of China; 2Department of Pathology, Hengshui Fifth People’s Hospital, Hengshui City, 053000, People’s Republic of China; 3Department of cardiothoracic surgery, Hengshui Fifth People’s Hospital, Hengshui City, 053000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Feng-Lian LiDepartment of Clinical Laboratory, Hengshui Fifth People’s Hospital, No. 1638 Shengli West Road, Hengshui City, Hebei Province, 053000, People’s Republic of ChinaTel +86 318-2316645Email fenglianlidr@163.comObjective: The aim of this study was to quantify the expression of melanoma-antigen family A proteins (MAGE-A) and New York esophageal squamous cell carcinoma-1 (NY-ESO-1) in breast cancer and establish the prognosis of breast cancer patients with MAGE-A and NY-ESO-1 co-expression.Methods: A total of 122 patients with breast cancer were recruited for this study. Their clinicopathological data were collected retrospectively, and the MAGE-A and NY-ESO-1 expressions in paraffin-embedded specimens from the 122 patients were evaluated using immunohistochemical analysis. In addition, the survival states of the patients were recorded.Results: Fifty-four patients (44.26%) were MAGE-A positive and 46 (37.70%) were NY-ESO-1 positive. Interestingly, 22 of the 46 NY-ESO-1-positive cases co-expressed MAGE-A. The expression of MAGE-A was positively associated with estrogen-receptor status (χ2 = 4.026, p = 0.045) and human epidermal growth factor receptor 2 status (χ2 = 5.482, p = 0.019), while the expression of NY-ESO-1 was positively associated with p53 expression (χ2 = 4.541, p = 0.033). Of the 122 patients, the lowest survival rate was observed in patients with NY-ESO-1 (+)/MAGE-A (+), with a 5-year survival rate of 59.09% and a median survival of 97 months.Conclusion: The results showed that MAGE-A and NY-ESO-1 were frequently expressed in breast cancer patients. The co-expression of MAGE-A and NY-ESO-1 occurred in about 18% of these patients, and it may indicate a poor prognosis.Keywords: breast cancer, cancer/testis antigens, MAGE-A, NY-ESO-1, co-expression

Background: Cerebral spinal fluid (CSF) leak remains an important issue in endoscopic endonasal surgery. A standard protocol of skull base closure has not been established yet, and application of rigid buttress has not been given sufficient attention. To emphasize the functions of support and fixation from rigid buttress in reconstruction, we introduce a technique of cruciate embedding fascia-bone flap (CEFB) using autologous bone graft to buttress fascia lata attaching to partially sutured skull base dural defect, and evaluate its efficacy in a consecutive case series of grade II-III CSF leak in EES.METHODS: Data of consecutive patients with grade II-III CSF leak during EES were collected between May 2015 and May 2020. Skull base reconstructions were performed either with the CEFB, conventional PNSF, or combination of 2 methods. Related clinical data were compared and analyzed respectively.RESULTS: There are 110, 65, and 23 patients included in CEFB, PNSF, and combination group respectively. CEFB demonstrated statistically similar effects on postoperative CSF leak (2.7%) and intracranial infection (4.5%) compared to PNSF (3.1%, 3.1%), but with less morbidity of epistaxis (CEFB: 0%, PNSF: 6.2%) and nasal discomforts (CEFB: 0%, PNSF: 7.7%). The bed stay time (CEFB: 5.74d, PNSF: 8.83d) and hospitalization time (CEFB: 10.49d, PNSF: 13.58d) were shortened in CEFB group. Combination of CEFB and PNSF achieved 0 postoperative CSF leak in 23 highly susceptible patients with grade III leak and multiple high risk factors.CONCLUSION: The CEFB technique is reliable and feasible to prevent postoperative CSF leak in EES. It can be used safely without PNSF in suitable cases, or applied in association with PNSF with high compatibility and security when necessary.Trial Registration：Current Controlled Trials ChiCTR2100044764 (Chinese Clinical Trial Registry), as well as the date of registration 27th March, 2020. Retrospectively registered.

Backgrounds Pilocytic astrocytomas (PAs) are World Health Organization (WHO) grade I tumors, which are relatively common, and are benign lesions in children. PAs could originate from the cerebellum, optic pathways, and third ventricular/hypothalamic region. Traditional various transcranial routes are used for hypothalamic PAs (HPAs). However, there are few studies on hypothalamic PAs treated through the endoscopic endonasal approach (EEA). This study reports the preliminary experience of the investigators and results with HPAs via expanded EEAs. Methods All patients with HPAs, undergone EEA in our hospital from 2017 to 2019, were retrospectively reviewed. The demographic data, clinical symptoms, complications, skull base reconstruction, prognosis, and endocrinological data were all recorded and analyzed in detail. Results Finally, five female patients were enrolled. The average age of patients was 28.6 ± 14.0. All patients had complaints about their menstrual disorder. One patient had severe bilateral visual impairment. Furthermore, only one patient suffered from severe headache due to acute hydrocephalus, although there were four patients with headache or dizziness. Four cases achieved gross-total resection, and one patient achieved subtotal resection. Furthermore, there was visual improvement in one patient (case 5), and postoperative worsening of vision in one patient (case 4). However, only one patient had postoperative intracranial infection. None of the patients experienced a postoperative CSF leak, and in situ bone flap (ISBF) techniques were used for two cases for skull base repair. In particular, ISBF combined with free middle turbinate mucosal flap was used for case 5. After three years of follow-up, three patients are still alive, two patients had no neurological or visual symptoms, or tumor recurrence, and one patient had severe hypothalamic dysfunction. Unfortunately, one patient died of severe postoperative hypothalamus reaction, which presented with coma, high fever, diabetes insipidus, hypernatremia and intracranial infection. The other patient died of recurrent severe pancreatitis at one year after the operation. Conclusion Although the data is still very limited and preliminary, EEA provides a direct approach to HPAs with acceptable prognosis in terms of tumor resection, endocrinological and visual outcomes. ISBF technique is safe and reliable for skull base reconstruction.

OBJECTIVE: To investigate the effects of blocking the activation of ERK pathway on the expression of matrix metalloproteinase-9 (MMP-9) and the formation of cerebral edema in SD rats after brain injury. METHODS: Ninety SD rats were randomly divided into 3 equal groups, including a sham-operated group, modified Feeney's traumatic brain injury model group, and ERK inhibition group where the ERK inhibitor SCH772984 (500 μg/kg) was injected via the femoral vein 15 min before brain trauma. At 2 h and 2 days after brain trauma, the permeability of blood-brain barrier was assessed by Evans blue method, the water content of the brain tissue was determined, and the phosphorylation level of ERK and the expression level of MMP-9 mRNA and protein were measured by RT-PCR and Western blotting. RESULTS: Compared with the sham-operated group, the rats with brain trauma exhibited significantly increased level of ERK phosphorylation at 2 h and significantly increased expression of MMP-9 mRNA and protein 2 days after the injury (P < 0.01). Treatment with the ERK inhibitor significantly decreased the phosphorylation level of ERK after the injury (P < 0.01), suppressed over-expression of MMP-9 mRNA and protein 2 days after the injury (P < 0.01). The permeability of blood-brain barrier increased significantly 2 h after brain trauma (P < 0.05) and increased further at 2 days (P < 0.01); the water content of the brain did not change significantly at 2 h (P > 0.05) but increased significantly 2 d after the injury (P < 0.01). Treatment with the ERK inhibitor significantly lowered the permeability of blood-brain barrier and brain water content after brain trauma (P < 0.01). CONCLUSION: Blocking the activation of ERK pathway significantly reduced the over-expression of MMP-9 and alleviates the damage of blood-brain barrier and traumatic brain edema, suggesting that ERK signaling pathway plays an important role in traumatic brain edema by regulating the expression of MMP-9.

Background: As a major antioxidant in serum, uric acid (UA) was once considered only as the leading cause of gout; however, recent studies have validated its neuroprotective role in ischemic stroke. Because the potential protective effects of UA in traumatic brain injury (TBI) remain largely unknown, this study investigated the role of UA in TBI in both clinical patients and experimental animals. Methods: In TBI patients, serum UA concentrations were measured within 3 days after injury. Clinical outcomes at discharge were classified according to the Glasgow Outcome Scale: good outcome (4-5) and poor outcome (1-3). Risk factors for good outcome were identified via backward logistic regression analysis. For the animal study, a controlled cortical impact (CCI) injury model was established in mice. These mice were given UA at different doses intraperitoneally, and subsequent UA concentrations in mouse serum and brain tissue were determined. Neurological function, oxidative stress, inflammatory response, neuronal maintenance, cerebral blood flow, and lesion size were also assessed. Results: The serum UA level was significantly lower in TBI patients who had a good outcome (P0.05). Conclusions: UA acted to attenuate neuronal loss, cerebral perfusion impairment and neurological deficits in TBI mice through suppression of neuronal and vascular oxidative stress. Following TBI, active antioxidant defense in the brain may result in consumption of UA in the serum, and thus, a decreased serum UA level could be predictive of good clinical recovery.

The high viscosity of crude oil, high permeability and strong edge water in some heavy oil reservoirs usually result in the failure of traditional water shutoff agents. In this paper, a novel water shutoff agent, the smectite-superfine cement dispersion, was produced based on traditional cement plugging agent. The high temperature stability test, simulated formation injection test and plugging strength test were conducted to evaluate the water shutoff performance. The results showed that the smectite-superfine cement dispersion exhibited perfect water shutoff performance and could fit into reservoirs with different permeability values by adjusting the cement content. The SEM analyses indicated that the hydration productions of superfine cement and smectite grew in a crisscross way and formed a stable microstructure, which ensures the composite with high strength.

Glioma stem cells (GSCs) have been considered to be responsible for treatment failure due to their self-renewal and limitless proliferative property. Recently, the Na+/K+-ATPase a1 (ATP1A1) subunit was described as a novel therapeutic target for gliomas. Interestingly, our previous proteomics study revealed that ATP1A1 is remarkably overexpressed in GSCs. In the current study, we investigated the role of ATP1A1 in regulating growth, survival, and tumorigenicity of primary human GSCs and the underlying molecular mechanism. We tested RNA and protein expression of ATP1A1 in glioma tissues and GSCs. In addition, we knocked down ATP1A1 in GSCs and assessed the effects thereof on growth, survival, and apoptosis. The role of ATP1A1 in signaling pathways was investigated in vitro. We found that the ATP1A1 expression level was associated with the grade of glioma. Knockdown of ATP1A1 in GSCs in vitro inhibited cell proliferation and survival, increased apoptosis, and halted cell-cycle progression at the G1 phase. Cell proliferation and survival were resumed upon rescue of ATP1A1 expression in ATP1A1-knockdown GSCs. The ERK1/2 and AKT pathways were inhibited through suppression of Src phosphorylation by ATP1A1 knockdown. Collectively, our findings suggest that ATP1A1 overexpression promotes GSC growth and proliferation by affecting Src phosphorylation to activate the ERK1/2 and AKT signaling pathways.

With a bipolar pulse power, wear-resistant ceramic coatings with high micro-hardness were in-situ fabricated on 2A50 aluminum alloy using micro-arc oxidation method in silicate electrolyte. The effect of cathodic voltage on microstructure, phase structure, micro-hardness and wear properties was investigated by changing cathodic voltage from 0 to −200 V. The phase structure, microstructure, micro-hardness and wear resistance were determined by XRD, SEM, HVS-1000 Vicker's micro-hardness tester and tribology tester. The results show that the phase of the obtained coatings is mainly composed of γ-Al2O3. The coating consists of the inner dense layer and the outer loose layer. As the cathodic voltage increases, the quantity and size of the micro-pores in the coatings first decrease and then increase. Micro-arc oxidation can greatly strengthen 2A50 aluminum alloy, the micro-hardness increases from 75 HV0.5 to 1321 HV0.5 after a micro-arc oxidation under a cathodic voltage of −100 V. The friction coefficient of the ceramic coatings are in the range of 0.35–0.55, and the coating obtained under −100 V exhibits the best wear resistance. The wear mechanism is deduced to be the combination of abrasive and adhesive wear.

To report our experience of the management of 60 patients with craniopharyngioma with endoscopic endonasal surgery (EES) and evaluate the feasibility and safety of EES for craniopharyngiomas.The clinical data of 60 patients with craniopharyngioma who underwent EES between November 2014 and December 2017 were analyzed retrospectively. All patients had vascularized nasoseptal flaps, and the most recent 4 patients had "in situ bone flaps" for better skull base reconstruction. Visual improvements, tumor resection extents, recurrence rates, endocrine functional changes, and surgical complications were evaluated.The resection rates were as follows: gross total, 68.3% (41 patients); near total (95% of tumor removed), 15% (9 patients); subtotal (≥80% of tumor removed), 10% (6 patients); and partial (partial resection80% of tumor removed), 6.7% (4 patients). Fifty-two patients presented with visual impairment; of these, 46 (88.5%) improved or returned to normal after surgery. Regarding the 32 patients with hypopituitarism before surgery, pituitary function was unchanged in 15 (46.8%), improved or normalized in 4 (12.5%), and deteriorated in 13 (40.6%). Eleven patients (18.3%) suffered from diabetes insipidus before treatment, and 27 more patients had this condition after surgery. Twenty-two patients had hyposmia postoperatively, and 17 patients experienced significant weight gain. Four patients had recent memory loss, and 2 of them had a temporary recent mental disorder. Three (5%) patients had cerebro-spinal fluid leakage after surgery. Three patients (5%) contracted meningitis and were cured with antibiotic treatment. One patient showed recurrence by magnetic resonance imaging re-examination, at the mean follow-up time of 22 months (range, 8-45 months; standard deviation, 11 months).EES can provide surgeons with excellent exposure and can achieve a high extent of removal of most craniopharyngiomas, even those with intraventricular extensions, In our view, vascularized pedicled septal flaps and in situ bony flaps were used in skull base reconstruction.

OBJECTIVE: To determine whether erythropoietin (EPO) promotes rapid proliferation of glioma through Akt pathway. METHODS: We detected the expression of EPO in human glioma tissues using immunohistochemistry. A nude mouse model bearing human glioma U87 cell xenograft was established and given intraperitoneal injection of EPO or saline every other day, and the tumor growth was observed. In the in vitro experiment, U87 cells were treated with PBS (control), EPO, or EPO with Akt inhibitor, and the expression of p-Akt and cyclin D1 was detected using Western blotting; the cell proliferation rate was determined using cell counting kit-8 and clone formation assay, and the cell cycle changes were analyzed with flow cytometry. RESULTS: Compared with low-grade glioma tissues, high-grade glioma tissues exhibited a significantly increased EPO expression (P=0.0002). In the tumor-bearing mice, EPO treatment significantly increased the expression of EPO (P=0.0006) and p-Akt (P=0.0003) in the tumor and obviously increased the tumor volume (P < 0.0001) and weight (P=0.0003). In U87 cells cultured in vitro, EPO treatment obviously accelerated the cell proliferation (P=0.020 on day 3 and 0.028 on day 5), promoted clone formation (P=0.0010), and increased proliferation index (P=0.0028); EPO significantly enhanced the protein expression of p-Akt (P=0.0020) and cyclin D1 (P=0.0022). The application of Akt inhibitor significantly suppressed the effect of EPO in enhancing cyclin D1 and p-Akt expression (both P < 0.0001) and promoting cell proliferation. CONCLUSION: EPO can significantly accelerate the proliferation of glioma through Akt pathway.

Cyclin-dependent kinase 5 (CDK5) and ataxia-telangiectasia mutated (ATM) are involved in normal human neurodevelopment and serves as a switch between neuronal survival and death. However, the molecular mechanisms underlying CDK5-ATM-induced neuronal injury caused by intracerebral hemorrhage (ICH) remain unclear. In this work, we used rat ICH models and thrombin-induced cell models to investigate the potential role of CDK5-ATM signals. Our findings revealed that CDK5 protein levels and kinase activities (p-histone H1 expression) were enforced in hematoma-surrounding neuron tissues following ICH. Besides, the expression of p25, p-ATM, and active caspase-3 protein was also upregulated after ICH. According to in vitro assays, the expression of CDK5, p-ATM, and active caspase-3 was all upregulated in cell viability-decreasing ICH cell models. However, blocking of either CDK5 or ATM suppressed the phosphorylation of ATM and the expression of active caspase-3, and attenuated the inhibition of neuronal survival. When p35/p25 was silenced, CDK5-ATM pathway was further inhibited, and cell viability was obviously ameliorated. In conclusion, this work suggested that ATM could be phosphorylated by CDK5 to induce the active caspase-3 and neuronal injury when intracerebral hemorrhage or ischemia occurred. Thus, the CDK5-AMT signal pathway has an important role in ICH process and may be a therapeutic target to prevent brain injury.

Microstructure and properties of DP590 steel in overaging process of continuous annealing were investigated in the laboratory. Effects of the overaging temperature (OT) in conventional process (Process A) and reheated overaging temperature (ROT) of the proposed process (Process B) on microstructure and mechanical properties were analyzed. The results showed that, in process A, with the increase of the OT from 280 °C to 400 °C, the amount of granular retained austenite increases, the tensile strength decreases, the yield strength and elongation both increase. In process B, with the increase of the ROT from 310 °C to 400 °C, the tensile strength decreases, whereas the yield strength changes little. Compared with the conventional process, the tensile strength of the experimental steel increases obviously and the ratio of yield-to-tensile strength decreases in process B. The variation of instantaneous work hardening index ( n ⁎ ) with tensile strain can be divided into three stages. The increase in the OT or ROT leads to the continuous increase of n ⁎ in the third stage.

Autophagy is a cellular catabolic mechanism in response to stress conditions and has been implicated in the progression and chemoresistance of various cancers. Human microR-137 (MIR137) is involved in neuronal maturation and neurogenesis, while little is known about its role in cancer. In this study, we showed that starvation increased the formation of autophagic marker microtubule-associated protein 1 light chain 3 (LC3) without significant change of MIR137 level in U87 cells. In addition, overexpression of MIR137 decreased LC3 expression and inhibited the degradation of the autophagy receptor sequestosome 1(SQSTM1/p62), while the MIR137 antagomirs showed the opposite effect on these autophagic markers. Moreover, MIR137 overexpression decreased, while its antagomirs increased the expression of autophagy-related 7(ATG7) mRNA and protein. MIR137-mediated inhibition of autophagy was prevented by ATG7. Finally, MIR137 promoted the sensitivity of U87 cells to adriamycin, an anticancer drug. Taken together, our study demonstrated that MIR137 attenuated starvation-induced autophagy by regulating the expression of ATG7.

In this paper, we investigate the multiple attribute decision making MADM problem with hesitant fuzzy uncertain linguistic information. Then, motivated by the ideal of traditional arithmetic and geometric operation, we have developed some aggregation operators for aggregating hesitant fuzzy uncertain linguistic information: hesitant fuzzy uncertain linguistic correlated aggregation HFULCA operator and hesitant fuzzy uncertain linguistic correlated geometric HFULCG operators. The prominent characteristic of these proposed operators are studied. Then, we have utilized these operators to develop some approaches to solve the hesitant fuzzy uncertain linguistic multiple attribute decision making problems. Finally, a practical example for evaluating the risk of the building construction project is given to verify the developed approach and to demonstrate its practicality and effectiveness.

Magnetic shielding of grain-oriented silicon steel was investigated. Ball scribing with spacing of 2 to 16 mm was performed at peak flux densities of 8.0 mT to 1.3 T. Magnetic shielding efficiency was calculated, including absorption, reflection and inner multi-reflection shielding efficiencies. Magnetic shielding efficiency (MSE) increase ratios after different scribing spacing were compared, and thickness requirement to achieve absorption shielding of 50 dB was also calculated. The results show that magnetic shielding efficiencies of C711 and H668 silicon steels increase by 4.79 and 3.15 dB respectively after scribing of 16 mm. Before scribing, shielding efficiency of H668 steel was higher than that of C711 steel, while after scribing, both absorption and shielding efficiency gaps were largely abridged between C711 and H668 steels. Plate thickness of C711 steel could be reduced from 3.18 mm without scribing to 2.20 mm after scribing of 16 mm. There is no apparent thickness reduction at lower flux densities; while the peak flux density is above 0.3 T, the shielding effect becomes apparent, and the thickness could be reduced from 2.28 mm without scribing to 1.70 mm with scribing spacing of 16 mm. Magnetizing process and its effect on variation of magnetic shielding were also analyzed.

In order to optimize the production process, improve the production efficiency and accelerate the development and application of the domestic dual-phase steel, the effects of heat treatment process parameters on micro-structure and mechanical properties of DP440 cold rolled strip were studied by the CAS-300 simulated continuous annealing equipment. When the heating rate increased from 5 to 100 °C/s, both the tensile strength and yield strength increased because of the decreased grain size. When the intercritical annealing temperature increased from 780 to 850 °C, the martensite content decreased so that the tensile strength decreased first, then increased, and the yield strength increased. When the rapid cooling rate increased from 25 to 100 °C/s, because the martensite content increased, the tensile strength increased, while the yield strength decreased. When the overaging temperature increased from 260 to 400 °C, the tensile strength decreased, while the yield strength increased. When the overaging time increased from 240 to 480 s, the tensile strength decreased a little, while the yield strength increased a little.

Effect of ball scribing on magnetic Barkhausen noise (MBN) of conventional grain-oriented (CGO) and high-permeability grain-oriented (HGO) electrical steel was investigated. The results showed that after ball scribing, root mean square of MBN (MBNrms) of CGO electrical steel increased 9.8% with 4 mm scribing spacing at 1.2 T, and that of HGO electrical steel apparently decreased 17.3% with 16 mm scribing spacing at 1.2 T. Through the formation and development of free magnetic poles and secondary magnetic domains due to compressive stress, primary magnetic domain space of grain-oriented electrical steel becomes smaller, which reflects as a variation of MBN in the macroscopic magnetic properties. Through correlation formula derivation of MBNrms and equilibrium distance between domain walls, effect of domain refinement on grain-oriented electrical steel was also interpreted, and optimum equilibrium distance between domain walls was determined.

Information barrier technology could meet the dual requirements to protect sensitive information and have a high confidence in the verification. It is an integrated mature technology in many fields which include nuclear detection science, nuclear electronics, and data encryption processing, and so on. It uses mature hardware and software technology to form multiple layers of protection to get the purpose of the protection of sensitive information. In this paper, the information barrier functional requirements and objectives are combined, the verification information barrier program is designed, and the system authentication method is discussed.

Recent in vivo studies have shown that erythropoietin (EPO) offers strong protection against brain edema. However, the intracellular and molecular mechanisms behind this beneficial effect have not been specified. The aim of this study was to determine whether human erythropoietin (rhEPO) reduces the astrocytic swelling created by oxygen-glucose deprivation followed by reoxygenation (OGD/Reox) in vitro and whether this effect can be mediated through the modulation of aquaporin4 (AQP4) expression in the plasma membrane (PM) and phosphorylation of the mitogen-activated protein kinase pathway (MAPK) pathway. Our results showed that OGD/Reox produced increase in cell volume, morphological swelling, and mitochondrial swelling. These changes were associated with the up-regulation of AQP4 in PM and the over-activation of MAPK. Silencing AQP4 expression using small interfering ribonucleic acid for AQP4 was found to block astrocytic swelling. Inhibition of the over-activation of MAPK mitigated the PM AQP4 overabundance and cellular swelling. As expected, treatment with rhEPO significantly reduced the OGD/Reox-induced increase in cell volume, morphological swelling, and mitochondrial swelling as well as the up-regulation of AQP4 in PM. In addition, cultures treated with the neutralizing anti-EPO antibody worsened the PM AQP4 abundance and cellular swelling, abolishing the protective effects mediated by rhEPO treatment. Furthermore, the over-activation of these MAPK after OGD/Reox was attenuated by rhEPO treatment significantly. In conclusion, our data strongly suggest that rhEPO can protect astrocytes from swelling caused by ischemia and reperfusion-like injury. This neuroprotective capacity is partially mediated by diminishing the MAPK-activity-dependent overabundance of AQP4 in PM.