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Abdominal aortic aneurysm(AAA) is a chronic dilated artery disease induced by atherosclerosis,infection,trauma and other related causes.The available studies about AAA mainly focus on the inflammatory response,senility,and microenvironmental changes,while the research on the metabolic changes such as glucose metabolism and lipid metabolism remains to be conducted.As a critical regulatory factor in endocrine,glucose,and lipid metabolisms,leptin is associated with a variety of signaling pathways such as adenosine monophosphate-activated protein kinase,Janus kinase/signal transducer and activator of transcription,and cytokine-cytokine receptor,as demonstrated by the KEGG pathway enrichment analysis.Moreover,these signaling pathways are generally involved in regulating the occurrence of AAA.In addition,leptin affects the occurrence of a variety of diseases such as obesity,diabetes,and hyperlipidemia,which contribute to the formation of AAA.Diabetes might be a protective factor for the formation of AAA,while the relationship of hyperlipidemia and obesity with the formation of AAA remains unclear.Therefore,leptin might play an essential role in the formation of AAA.Further studies about the effect of leptin on AAA may provide the potential research direction and facilitate the discovery of therapeutic targets.

Background Subarachnoid hemorrhage (SAH) is a cerebral hemorrhage disease that severely damages the brain and causes cognitive impairment (CI). Therefore, accurate and appropriate treatment strategies are urgently needed. The application of nimodipine can not only improve blood circulation in patients with SAH but also repair ischemic neuron injury. Purpose To investigate the effects of nimodipine and lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1)/miR-27a/microtubule-associated protein tau (MAPT) axis on CI after SAH. Methods One hundred and twenty healthy male rats were selected and equally divided into control group, sham operation group, model group, PBS group, nimodipine group (drug group), NC siRNA group, NC mimics group, NEAT1 siRNA, miR-27a mimics, MAPT siRNA, drug + NEAT1-ad, and drug + NC-ad groups by random number table. Rats in the model group were constructed by double-hemorrhage model, and expression vectors were injected into the tail to regulate the expression of lncRNA NEAT1, miR-27a and MAPT. In addition, Western blot was employed to detect brain tissue protein, flow cytometry was applied to measure brain tissue apoptosis, and MTT was utilized to determine cell activity, so as to evaluate brain damage and cognitive function in each group. Results Nimodipine, down-regulated lncRNA NEAT1, up-regulated miR-27a and down-regulated MAPT all improved brain damage and CI, inhibited brain tissue cell apoptosis, and enhanced brain cell activity. The common binding sites of lncRNA NEAT1 and MAPT were found on the miR-27a sequence fragment, and miR-27a could be paired with the former two. Nimodipine was found to cause the down-regulation of lncRNA NEAT1 and MAPT, as well as the up-regulation of miR-27a. Conclusion Nimodipine can improve CI after SAH in rats through the lncRNA NEAT1/miR-27a/MAPT axis.

Glioblastoma (GBM) is one of the most common aggressive cancers of the central nervous system in adults with a high mortality rate. Bortezomib is a boronic acid–based potent proteasome inhibitor that has been actively studied for its anti‐tumour effects through inhibition of the proteasome. The proteasome is a key component of the ubiquitin‐proteasome pathway that is critical for protein homeostasis, regulation of cellular growth, and apoptosis. Overexpression of polo‐like kinase 4 (PLK4) is commonly reported in tumour cells and increases their invasive and metastatic abilities. In this study, we established a cell model of PLK4 knockdown and overexpression in LN‐18, A172 and LN‐229 cells and found that knockdown of PLK4 expression enhanced the anti‐tumour effect of bortezomib. We further found that this effect may be mediated by the PTEN/PI3K/AKT/mTOR signalling pathway and that the apoptotic and oxidative stress processes were activated, while the expression of matrix metalloproteinases (MMPs) was down‐regulated. Similar phenomenon was observed using in vitro experiments. Thus, we speculate that PLK4 inhibition may be a new therapeutic strategy for GBM.

Objective To investigate the differences of gut microbiota between patients with abdominal aortic aneurysm and atherosclerosis.Methods From December 2018 to June 2019,20 fresh stool samples were collected respectively from the patients with abdominal aortic aneurysm and atherosclerosis treated at the Department of Vascular Surgery,Peking Union Medical College Hospital.The 16S rDNA high-throughput sequencing was employed to compare the composition,abundance,and α and β diversities of gut microbiota between the two disease groups,and further determine the significantly differential genera.Results The two groups had great similarities in the composition of gut microbiota.There was no statistical difference in α diversity.Although β diversity did not have statistically significant difference,certain microbial taxa showed differences between the two groups.The LEfSe demonstrated that the abdominal aortic aneurysm group had higher relative abundance of

Background/aims To investigate the postconditioning protective effect of penehyclidine hydrochloride (PHC) against anoxia/reoxygenation (A/R) injury in H9c2 cells along with the involved mechanism and timing effect. Methods We divided H9c2 cells into 7 groups: control group, A/R group and PHC+A/R groups at 0 min, 5 mins, 10 mins, 20 mins, 30 mins, respectively (treated with 0.1 μm/L PHC at 0 min, 5 mins, 10 mins, 20 mins, 30 mins after the reoxygenation procedure began). Cell apoptosis, oxidative stress, intracellular Ca2+ concentration, mitochondrial membrane potential and mitochondrial permeability transition pore (MPTP) opening were explored. Bcl-2, Bax, Cyt C, caspase-3 and caspase-9 levels were measured. Results A/R significantly increased both cell injury and cell apoptosis. PHC showed postconditioning protective effect by attenuating superoxide production, decreasing Ca2+ overload, restraining MPTP activities, restoring mitochondrial membrane potential, regulating cell apoptosis proteins and modulation of mitochondrial pathway. Earlier administration of PHC offered greater postconditioning protective effect. Conclusion H9c2 cells were protected by PHC from A/R injury regardless of timing of PHC administration (0 min, 5 mins, 10 mins, 20 mins, 30 mins). However, earlier administration of PHC resulted in better PHC postconditioning protection.

Objective To explore the outcomes in patients who receive the endovascular abdominal aortic aneurysm repair(EVAR)and have concomitant intra-abdominal malignancy.Methods Between January 2014 and December 2019,all the patients who underwent surgery for malignancy and/or EVAR were retrospectively reviewed.Results Twenty-eight abdominal aortic aneurysm(AAA)patients with concomitant intra-abdominal malignancy were included.The patients were treated by two-stage operation and the priority was given for EVAR in 21 patients.There was no perioperative death or major complications.In the follow-up,one patient developed graft thrombosis and one had type Ⅱ endoleak.There was no AAA-associated death.Conclusions It is preferred that EVAR should come first followed by operation for malignancy.Details of treatment strategy still need further investigation.

Background Subarachnoid hemorrhage (SAH) is a cerebral hemorrhage disease that severely damages the brain and causes cognitive impairment (CI). Therefore, accurate and appropriate treatment strategies are urgently needed. The application of nimodipine can not only improve blood circulation in patients with SAH but also repair ischemic neuron injury. Purpose To investigate the effects of nimodipine and lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1)/miR-27a/microtubule-associated protein tau (MAPT) axis on CI after SAH. Methods One hundred and twenty healthy male rats were selected and equally divided into control group, sham operation group, model group, PBS group, nimodipine group (drug group), NC siRNA group, NC mimics group, NEAT1 siRNA, miR-27a mimics, MAPT siRNA, drug + NEAT1-ad, and drug + NC-ad groups by random number table. Rats in the model group were constructed by double-hemorrhage model, and expression vectors were injected into the tail to regulate the expression of lncRNA NEAT1, miR-27a and MAPT. In addition, Western blot was employed to detect brain tissue protein, flow cytometry was applied to measure brain tissue apoptosis, and MTT was utilized to determine cell activity, so as to evaluate brain damage and cognitive function in each group. Results Nimodipine, down-regulated lncRNA NEAT1, up-regulated miR-27a and down-regulated MAPT all improved brain damage and CI, inhibited brain tissue cell apoptosis, and enhanced brain cell activity. The common binding sites of lncRNA NEAT1 and MAPT were found on the miR-27a sequence fragment, and miR-27a could be paired with the former two. Nimodipine was found to cause the down-regulation of lncRNA NEAT1 and MAPT, as well as the up-regulation of miR-27a. Conclusion Nimodipine can improve CI after SAH in rats through the lncRNA NEAT1/miR-27a/MAPT axis.

Background We evaluated the possible relationships between serum total homocysteine and folate and Vitamin B12 in patients with intracranial aneurysm. Methods We enrolled consecutive patients with intracranial aneurysm from the Han population who were admitted to the hospital, as well as control subjects who received medical examination on an outpatient basis. The serum total homocysteine, folate, and Vitamin B12 levels were measured in patients with intracranial aneurysm and the control group, and the associations between those factors were analyzed using multivariate logistic analysis. Results A total of 140 patients with intracranial aneurysm and 140 control subjects were enrolled from July 2014 to December 2015. The mean serum total homocysteine level in the patient group (19.98 ± 10.84 µmol/L) was significantly higher than that in the control group (15.13 ± 5.55 µmol/L, P Conclusions The present study provides evidence regarding the association between serum total homocysteine and folate and Vitamin B12 in patients with intracranial aneurysm. Hyperhomocysteinemia is an independent risk factor for intracranial aneurysm, and folate and Vitamin B12 are protective against intracranial aneurysm due to their roles in regulating the metabolism of homocysteine.

Glioma is the most common form of malignant brain cancer with high mortality rate in human. Therefore, finding effective therapeutic strategy and revealing the underlying molecular mechanism is necessary. Plant-extracted flavonoid glycosides have been suggested to be bioactive compounds with pleiotropic functions, such as anti-cancer, anti-inflammatory, antioxidant and effects. Our study was attempted to explore the anti-cancer role of linarin (acacetin-7-O-β-d-rutinoside) in glioma in vitro and in vivo. Nuclear factor kappa-B (NF-κB) activity is a common phenomenon in various cancers, resulting in abnormal cell proliferation, malignant transformation, or resistance to cell death. P53, an essential tumor suppressor, plays an important role in preventing tumor progression. Our data indicated that linarin suppressed glioma cell proliferation and migration by inducing apoptosis, which was through reducing cell cycle-related signals, including Survivin, p-Rb, and Cyclin D1, while promoting p21, Bax, Caspase-3 and poly (ADP-ribose) polymerase (PARP) activation. Also, we found that linarin-reduced cellular proliferation of glioma was dependent on p53 up-regulation and Nuclear factor kappa-B (NF-κB)/p65-down-regulation, thereby inhibiting glioma cell growth. We further conformed the inhibitory effect of linarin in vivo using xenograft tumor model. Linarin significantly triggered apoptosis as well as the tumor growth in animals, accompanied with p53 increase and p65 decrease. Our data illustrated that linarin could be used as a promising candidate against glioma progression.

Objective To explore the clinical effect of posterior reduction and screw⁃rod (plate) internal fixation technique for the treatment of atlantoaxial dislocation in complex craniovertebral junction region malformation. Methods Clinical data of 18 patients suffered from atlantoaxial dislocation with complex craniovertebral junction region malformation were analysed retrospectively, including 15 cases of congenital atlantoaxial dislocation, 1 case with aggravated symptoms of cervico ⁃ occipital unstability after anterior odontoid process grinding, 2 cases with trauma ⁃ induced dislocation. All patients underwent posterior decompressive reduction and screw ⁃ rod internal fixation. During surgical procedure, senory evoked potential (SEP) and electromyography (EMG) monitorings were used. Japanese Orthopaedic Association (JOA) score and imaging were used to evaluate the surgical effect. Results Postoperative imaging examination showed that fixed system and atlantoaxial reduction were good in 16 cases and bad in 1 cases. The bony fusion was good in 16 cases and bad in 1 case. The patients' clinical symptoms were improved to different degree, but one patient suddenly occurred respiratory arrest and died. Patients were followed up for 3 to 28 months (mean 6.62 months). After operation the average JOA score was 11.62 ± 3.23, while before operation it was 7.51 ± 3.82. The difference was significant (t = ⁃ 5.476, P = 0.004). Conclusion Posterior decompressed reduction and screw ⁃ rod (plate) internal fixation for atlantoaxial dislocation with complex craniovertebral junction region malformation is save and effective. It will be widely used in the future. DOI：10.3969/j.issn.1672⁃6731.2012.04.010

Objective To explore the causes of ruptured anterior communicating artery aneurysms presenting with paraplegia, and summarize the key points of diagnosis and treatment methods. Methods A total of 260 patients with ruptured anterior communicating artery aneurysms were received medical treatment in the Department of Neurosurgery, Shanxi Provincial People's Hospital from Jan. 2012 to Mar. 2015. Of which 6 patients were clinically presented with paraplegia, their clinical data including CT/MR/DSA were retrospectively analyzed, and based on the analysis, aneurysm embolization and anti-vasospasm treatment were performed. Results Besides headache and discomfort in the neck, 5 of the 6 patients were with double lower limbs paraplegia, and the another one presented quadriplegia. By symptomatic treatment of aneurysm embolization and anti vasospasm, the myodynamia of the paraplegic limbs recovered from 0-Ⅰto Ⅳ-Ⅴgrade, and 2 of the 6 patients spent a shorter recovery time (about 2 weeks), the other 4 recovered in 3 months. The limbs myodynamia of the 6 patients recovered completely in half-and one year follow up. Conclusions The mechanism of ruptured anterior communicating artery aneurysms presenting with paraplegia may be the insufficient blood supply to the primary motor area and supplementary motor area (SMA) of brain cortex caused by aneurysms rupture. Aneurysm embolization should be performed in clinical treatment, supplemented with anti vasospasm and symptomatic treatment of improving neurological function. DOI: 10.11855/j.issn.0577-7402.2016.09.14

To investigate the expression of serum lost goodwill target (LGT) proteome, and to analyze its clinical significance in evaluating prognosis of patient with critical illness on the basis of acute physiology and chronic health evaluation II (APACHEII) score.The serum samples were collected from 96 patients with critical illness and 30 healthy volunteers as healthy control. The expression of serum LGT proteome was detected by surface enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF-MS) protein chip technology. The abundance value of LGT proteome in patients at admission was measured, and at the same time APACHE II score was estimated, in order to analyze its clinical significance in patients with critical illness.The amount of LGT proteome in APACHEII≥15 group [n =35, (9.26 ± 7.51)%] was significantly higher than that of APACHEII and it;15 group [n=61, (4.19 ± 4.07)%], and the LGT proteome amount in both groups was significantly higher than that of the healthy control group [(1.52 ± 0.47)%, both P0.01]. Spearman correlation analysis showed that there was significant positive correlation between the abundance of LGT proteome and the APACHE II score (r =0.317 ,P =0.002). The abundance of LGT proteome in death group[n =23, (10.14 ± 9.23)%] was significantly higher than that in survival group [ n =73, (5.8 3 ± 3.57)%, P0.01]. The fatality rate of the LGT proteome group with average abundance exceeding 5% [68.0% (17/25)] was significantly higher than that of the LGT proteome group with average abundance lower than 5% [8.5% (6/71), P0.01]. According to the LGT proteome abundance to evaluate the prognosis of the patients,the positive predict rate was 68.0 %,the negative predict rate was 91.5 %, the false positive rate was 32.0%, the false negative rate was 8.5%.The LGT proteome was intimately correlated with the severity degree of disease condition and prognosis in patients with critical illness. The determination of LGT proteome combined with APACHE IIscore evaluation can probably be an important indicator in evaluating the prognosis of patient with critical illness. Further research on LGT proteome is warranted to facilitate the prognostication and clinical decision making.