Deep Learning Techniques in Intelligent Fault Diagnosis and Prognosis for Industrial Systems: A Review.

Fault diagnosis and prognosis (FDP) tries to recognize and locate the faults from the captured sensory data, and also predict their failures in advance, which can greatly help to take appropriate actions for maintenance and avoid serious consequences in industrial systems. In recent years, deep learning methods are being widely introduced into FDP due to the powerful feature representation ability, and its rapid development is bringing new opportunities to the promotion of FDP. In order to facilitate the related research, we give a summary of recent advances in deep learning techniques for industrial FDP in this paper. Related concepts and formulations of FDP are firstly given. Seven commonly used deep learning architectures, especially the emerging generative adversarial network, transformer, and graph neural network, are reviewed. Finally, we give insights into the challenges in current applications of deep learning-based methods from four different aspects of imbalanced data, compound fault types, multimodal data fusion, and edge device implementation, and provide possible solutions, respectively. This paper tries to give a comprehensive guideline for further research into the problem of intelligent industrial FDP for the community.

Nimodipine Attenuates Early Brain Injury by Protecting the Glymphatic System After Subarachnoid Hemorrhage in Mice.

The glymphatic system (GS) plays an important role in subarachnoid hemorrhage (SAH). Nimodipine treatment provides SAH patients with short-term neurological benefits. However, no trials have been conducted to quantify the relationship between nimodipine and GS. We hypothesized that nimodipine could attenuate early brain injury (EBI) after SAH by affecting the function of the GS. In this study, we assessed the effects of nimodipine, a dihydropyridine calcium channel antagonist, on mice 3 days after SAH. The functions of GS were assessed by immunofluorescence and western blot. The effects of nimodipine were assessed behaviorally. Concurrently, correlation analysis was performed for the functions of GS, immunofluorescence and behavioral function. Our results indicated that nimodipine improved GS function and attenuated neurological deficits and brain edema in mice with SAH. Activation of the cAMP/PKA pathway was involved in this process. GS function was closely associated with perivascular AQP4 polarization, cortical GFAP/AQP4 expression, brain edema and neurobehavioral function. In conclusion, this study shows for the first time that nimodipine plays a neuroprotective role in the period of EBI after SAH in mice through the GS.

Anti-Inflammatory Activity of Mulberry Leaf Flavonoids In Vitro and In Vivo.

Mulberry (Morus alba L.) is a flowering tree traditionally used in Chinese herbal medicine. Mulberry leaf flavonoids (MLFs) have been reported to exert important anti-inflammatory and antioxidant properties. The purpose of this study was to select the MLF with the best anti-inflammatory and antioxidative activities from MLFs eluted by different ethanol concentrations (30%, 50%, and 75%) and explore its pharmacological properties. Three types of MLFs inhibited the production of nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and inflammatory cytokines in lipopolysaccharide (LPS)-induced RAW 264.7 cells. All MLFs boosted the antioxidative capacity by decreasing the reactive oxygen species (ROS) production and the scavenging of 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radicals and improving the metal ion chelating activity and reducing power. The results revealed that the MLFs eluted by 30% ethanol exhibited the best anti-inflammatory and antioxidative activities. A nontargeted metabolomic analysis was used to analyze 24 types of differential flavonoids between the MLFs. Quercetin, kaempferol, and their derivatives in 30%MLF were more abundant than the other two MLFs. Furthermore, we evaluated the pharmacological activities of 30%MLF in dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) mice. The 30%MLF could alleviate the clinical symptoms, reduce the secretion of inflammatory cytokines, and inhibit the activation of the inflammatory pathway in DSS-induced colitis mice. This study will provide valuable information for the development of MLFs eluted by 30% ethanol as a functional food.

Assessment of CD27 expression on T-cells as a diagnostic and therapeutic tool for patients with smear-negative pulmonary tuberculosis.

BACKGROUND: There is a global focus on illness diagnosis in smear-negative and latent tuberculosis infectious populations (SN-TB and LTBI). CD27 has been suggested to play a direct role in active TB. Little is known about smear-negative individuals. Here, we tried to investigate whether it has a role in smear-negative populations. The expression of CD27 and MTB-specific CD27 in CD4+ T cells ("CD27-CD4+" and "CD27-IFN-γ+CD4+") was evaluated in MTB-unexposed controls (HC), TB contacts (TB-C) and SN-TB individuals by flow cytometry. The sensitivity, specificity and AUC (area under curve) of "CD27-IFN-γ+CD4+" cells to distinguish SN-TBs from HCs and TB-Cs were determined by receiver operating characteristic (ROC) curve analysis. The clinical index was selected from the clinical laboratory and evaluated for correlation with "CD27-IFN-γ+CD4+" cells by Spearman statistical analysis. RESULTS: We observed that the percentages of "CD27-IFN-γ+CD4+" cells were significantly increased in the SN-TB group compared with the HC and TB-C groups (AUC was 0.88, sensitivity was 82.14%, specificity was 80.00%, and P < 0.0001). The percentage of "CD27-IFN-γ+CD4+" cells was negatively correlated with WBC (white blood cell count) (r = - 0.3019, P = 0.0182) and positively correlated with IgE (immunoglobulin E) (r = 0.2805, P = 0.0362). Furthermore, "CD27-IFN-γ+CD4+" cells were significantly decreased, especially in the > 50 years group, after clinical treatment. CONCLUSION: The present results demonstrated that the percentage of "CD27-IFN-γ+CD4+" cells might be a conceivable molecular indicator in the diagnosis of SN-TB and was influenced by its outcome of therapy.

Comparative Proteomic Analysis of Tolerant and Sensitive Varieties Reveals That Phenylpropanoid Biosynthesis Contributes to Salt Tolerance in Mulberry.

Mulberry, an important woody tree, has strong tolerance to environmental stresses, including salinity, drought, and heavy metal stress. However, the current research on mulberry resistance focuses mainly on the selection of resistant resources and the determination of physiological indicators. In order to clarify the molecular mechanism of salt tolerance in mulberry, the physiological changes and proteomic profiles were comprehensively analyzed in salt-tolerant (Jisang3) and salt-sensitive (Guisangyou12) mulberry varieties. After salt treatment, the malondialdehyde (MDA) content and proline content were significantly increased compared to control, and the MDA and proline content in G12 was significantly lower than in Jisang3 under salt stress. The calcium content was significantly reduced in the salt-sensitive mulberry varieties Guisangyou12 (G12), while sodium content was significantly increased in both mulberry varieties. Although the Jisang3 is salt-tolerant, salt stress caused more reductions of photosynthetic rate in Jisang3 than Guisangyou12. Using tandem mass tags (TMT)-based proteomics, the changes of mulberry proteome levels were analyzed in salt-tolerant and salt-sensitive mulberry varieties under salt stress. Combined with GO and KEGG databases, the differentially expressed proteins were significantly enriched in the GO terms of amino acid transport and metabolism and posttranslational modification, protein turnover up-classified in Guisangyou12 while down-classified in Jisang3. Through the comparison of proteomic level, we identified the phenylpropanoid biosynthesis may play an important role in salt tolerance of mulberry. We clarified the molecular mechanism of mulberry salt tolerance, which is of great significance for the selection of excellent candidate genes for saline-alkali soil management and mulberry stress resistance genetic engineering.

Abnormally expressed long noncoding RNA B3GALT5-AS1 may serve as a biomarker for the diagnostic and prognostic of gastric cancer.

Early diagnosis of gastric cancer (GC) is an effective method to improve prognosis. Increasing number of long noncoding RNAs (lncRNAs) have been reported as biomarkers for several cancers. We aim to detect the level of lncRNA B3GALT5-AS1 and its association with clinical parameters and to further explore its application value in GC. We measured serum B3GALT5-AS1 expression in 107 patients with GC, 40 polyp patients, and 87 normal controls to explore the significance of serum B3GALT5-AS1 in GC using the quantitative real-time polymerase chain reaction method. The result demonstrated that B3GALT5-AS1 level was markedly richer in GC patients than that in normal people (P < .001). B3GALT5-AS1 may be served as a diagnostic marker for distinguishing GC patients from healthy people, and the proportion under the receiver operating characteristics curve is 0.816 (95% confidence interval, 0.758-0.874; P = .03). Further exploration validated that high serum B3GALT5-AS1 level was related to TNM stage (P = .024), and lymph node metastasis (P = .023). Our study suggested that serum B3GALT5-AS1 may be employed as an ideal biomarker for early screening of GC.

Hydroxypyridinone-Coumarin Inhibits the Proliferation of MHCC97 and HepG2 Human Hepatocellular Carcinoma Cells and Down-Regulates the Phosphoinositide-3 Kinase Pathway.

BACKGROUND Worldwide, hepatocellular carcinoma (HCC) is one of the most commonly diagnosed malignant diseases and is the third leading cause of cancer-related death. This study aimed to investigate the effect of hydroxypyridinone-coumarin (HPC) on MHCC97 and HepG2 human HCC cells and the mechanisms involved. MATERIAL AND METHODS MHCC97 and HepG2 human HCC cells were cultured in vitro. An MTT cytotoxicity assay was used to assess cell viability and proliferation, with and without treatment with HPC. Cell autophagosomes were labeled with GFP-LC3 using confocal fluorescence microscopy. Western blot was used to measure protein expression. RESULTS HPC significantly reduced the cell proliferation rate in a concentration-dependent manner, with 2 µM of HPC resulting in a reduced proliferation rate of MHCC97 cells (by 36%) and HepG2 cells (by 29%) (P<0.02). HPC significantly reduced autophagy in MHCC97 and HepG2 cells. Western blot showed that treatment with HPC significant upregulated Atg5, beclin-1, LC3-phosphatidylethanolamine conjugate (LC3-II), and Atg-3, reduced p62 and Akt protein expression, and induced phosphorylation of ERK1/2. GFP-LC3B labeling in MHCC97 and HepG2 cells was increased following HPC treatment. CONCLUSIONS HPC induced autophagy and inhibited the proliferation of MHCC97 and HepG2 HCC cells in vitro and involved activation of ERK1/2 and down-regulation of the Akt pathway.

MYBL2 is a Potential Prognostic Marker that Promotes Cell Proliferation in Gallbladder Cancer.

BACKGROUND: Gallbladder cancer (GBC) is an aggressive and highly lethal biliary tract malignancy, with extremely poor prognosis. In the present study, we analyzed the potential involvement of MYBL2, a member of the Myb transcription factor family, in the carcinogenesis of human GBC. METHODS: MYBL2 expression levels were measured in GBC and cholecystitis tissue specimens using quantitative real-time PCR (qRT-PCR) and immunohistochemical (IHC) assays. The effects of MYBL2 on cell proliferation and DNA synthesis were evaluated using Cell Counting Kit-8 assay (CCK-8), colony formation, and 5-ethynyl-2'-deoxyuridine (EdU) retention assay, flow cytometry analysis, western blot, and a xenograft model of GBC cells in nude mice. RESULTS: MYBL2 expression was increased in GBC tissues and associated with histological differentiation, tumour invasion, clinical stage and unfavourable overall survival in GBC patients. The downregulation of MYBL2 expression resulted in the inhibition of GBC cell proliferation, and DNA replication in vitro, and the growth of xenografted tumours in nude mice. Conversely, MYBL2 overexpression resulted in the opposite effects. CONCLUSIONS: MYBL2 overexpression promotes GBC cell proliferation through the regulation of the cell cycle at the S and G2/M phase transitions. Thus, MYBL2 could serve as a potential prognostic and therapeutic biomarker in GBC patients.

Upregulated TRIM32 correlates with enhanced cell proliferation and poor prognosis in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a major type of primary liver cancer and the sixth most prevalent human malignancies worldwide. However, the molecular mechanisms underlying hepatocarcinogenesis remain unclear. For HCC patients, there is not only a lack of effective therapeutic targets but also a lack of predictive or prognostic biomarkers. In this article, we reported that TRIM32 was obviously upregulated in HCC tumor tissues and HCC cell lines. Its expression patterns were positively correlated with histological grade, tumor sizes, and HBsAg of HCC patients. TRIM32 expression was a significant predictor for the overall survival time of HCC patients. Moreover, the overexpression of TRIM32 in cells accelerated the G1-S phase transition, promoted cell proliferation rates, and induced the resistance of HCC patients to oxaliplatin. All these findings suggest that TRIM32 might play important roles in the hepatocarcinogenesis. TRIM32 could be a novel direction to explore the mechanism underlying HCC pathogenesis.

Overexpression of DLX2 is associated with poor prognosis and sorafenib resistance in hepatocellular carcinoma.

The mechanism underlying poor prognosis and sorafenib resistance in patients with hepatocellular carcinoma (HCC) is unknown and, to date, no useful predictive biomarkers of sorafenib resistance have been identified. Distal-less homeobox 2 (DLX2) is a transcription factor involved in cell cycle regulation that is closely correlated with cancer prognosis. In this study, we showed that DLX2 is overexpressed in HCC tissues and cell lines and that the level of DLX2 overexpression is positively correlated with histological grade, metastasis and Ki67 expression, which are indicators of poor prognosis. We also found that DLX2 accumulates in proliferating HCC cells, where it is associated with the expression of proliferating cell nuclear antigen (PCNA), Cyclin D1 and Cyclin A. Flow cytometry and cell counting kit-8 (CCK-8) assays indicated that DLX2 depletion causes cell cycle arrest at the G1 phase and hinders cell proliferation. Moreover, the sensitivity of HCC cells to sorafenib is restored when the DLX2 gene is knocked down using a short interfering RNA. We demonstrated that DLX2 facilitates sorafenib resistance by promoting the expression of markers of epithelial-mesenchymal transition and by activating the extracellular signal-regulated protein kinase pathway. Our findings reveal that DLX2 plays a regulatory role in HCC cell proliferation and suggests that targeting DLX2 represents a novel strategy to increase sorafenib efficacy in the management of HCC. In conclusion, DLX2 is a novel marker of poor prognosis and sorafenib resistance in patients with HCC.

The suppressor of cytokine signaling SOCS1 promotes apoptosis of intestinal epithelial cells via p53 signaling in Crohn's disease.

The suppressor of cytokine signaling SOCS1 is a member of the cytokine signaling pathway inhibitor family, which is induced by the IFN-γ induced JAK signaling pathway. The expression of SOCS1 has been found to increase in Crohn's disease (CD) patients, but the role of SOCS1 in intestinal epithelium is unclear. This study was designed to investigate whether SOCS1 has a role in the death of intestinal epithelial cells and intestinal injury. The results showed that the expression of SOCS1 increased in CD patients, and the expression of SOCS1, p-p53 and PUMA increased in the mouse TNBS induced colitis model. Using IFN-γ treated HT-29 cells as an apoptotic model of intestinal epithelial cells in vitro, we confirmed that SOCS1 promoted apoptosis of intestinal epithelial cells by activating p53. In HT-29 cells which were treated with IFN-γ, the interaction between p53 and SOCS1 and phosphorylation of p53 were significantly higher than untreated cells. When knocking SOCS1 down by using SOCS1 siRNA, phosphorylation of p53 and apoptosis of intestinal epithelial cells which was induced by IFN-γ were significantly inhibited. In summary, our findings suggest that SOCS1 may promote apoptosis of intestinal epithelial cells at least partly through mediating p53 signaling.

Decreased Expression of EHD2 Promotes Tumor Metastasis and Indicates Poor Prognosis in Hepatocellular Carcinoma.

BACKGROUND: Metastasis remains the most common cause of lethal outcomes in hepatocellular carcinoma (HCC) after curative resection. Understanding molecular mechanisms that regulate metastasis process is crucial for improving treatment of hepatocellular carcinoma. AIMS: In this article, we examined whether Eps15 homology domain-containing 2 (EHD2) played a critical role in hepatocellular carcinoma metastasis and explored the possible mechanism. METHODS: EHD2 and E-cadherin expression levels in hepatocellular carcinoma patients were examined using Western blotting and immunohistochemistry. The cell migration and invasion were evaluated by wound-healing assay and trans-well assay. Epithelial-mesenchymal transition was analyzed by immunofluorescence, and the vital markers were detected by Western blotting. The correlation of EHD2 and E-cadherin was confirmed by co-immunoprecipitation. RESULTS: EHD2 expression, along with the epithelial marker E-cadherin, was markedly reduced in tumor tissues than in adjacent noncancerous tissues. Moreover, EHD2 was positively correlated with E-cadherin, histological grade, tumor metastasis, and microvascular invasion. Kaplan-Meier survival analysis showed that hepatocellular carcinoma patients with decreased EHD2 expression had shorter overall survival times than those with higher EHD2 expression. Knockdown of EHD2 induced an increase in cell invasion and changes characteristic of epithelial-mesenchymal transition, while overexpression of EHD2 inhibited these processes. CONCLUSIONS: Molecular data indicated that EHD2 inhibited migration and invasion of hepatocellular carcinoma probably by interacting with E-cadherin and it might be an independent, significant risk factor for survival after curative resection.

Influence of the interface in quantum corrections on the low-temperature resistance of La(2/3)Sr(1/3)MnO3 trilayer masking thin films.

We report the low-temperature resistance upturn in sandwiched structures of La2/3Sr1/3MnO3/ZrO2/La2/3Sr1/3MnO3 and La2/3Sr1/3MnO3/LaMnO3/La2/3Sr1/3MnO3, while it disappeared when the interlayer was replaced by YBa2Cu3O7. The experimental data have been analyzed qualitatively and quantitatively. The results show that the low temperature resistance upturn is mainly due to the quantum correction effects driven by the weak localization and the electron-electron interaction in such a strongly correlated system, and the contribution of each factor varies with grain boundaries. Moreover, the resistance upturns are suppressed by a local magnetic field. These findings will help to further understand the physical mechanism of low-temperature resistance upturn in colossal magnetoresistance manganites. Furthermore, it is also helpful to reveal the intrinsic transport mechanism at the interfaces of semiconductor/ferromagnetism and antiferromagnetism/ferromagnetism.

Comparison of Dexmedetomidine versus Propofol for Sedation after Uvulopalatopharyngoplasty.

BACKGROUND: Adequate sedation is important in the post-anesthesia care unit (PACU) following uvulopalatopharyngoplasty (UPPP) to ensure patient comfort and decrease the duration of mechanical ventilation (MV), PACU stay, and bleeding. This study aimed to compare dexmedetomidine and propofol as sedatives after UPPP in the PACU. MATERIAL AND METHODS: We randomized 124 mechanically ventilated adults following UPPP who were managed in the PACU of the General Hospital of the Shenyang Military Region between January 2014 and June 2014, to receive either dexmedetomidine or propofol. The patients in the propofol group received an infusion of propofol (3 mg/kg/h) titrated up to 6 mg/kg/h to attain a Ramsay sedation score ≥4. The dexmedetomidine group patients received 1.0 µg/kg of dexmedetomidine over a period of 10 minutes and then 0.5 to 1.0 µg/kg/h infusion to maintain a Ramsay sedation score ≥4. RESULTS: Bispectral index (BIS) values were significantly lower in the dexmedetomidine group than in the propofol group at Ramsay sedation scores of 4 and 5. The mean times to spontaneous breathing, waking, and extubation were shorter in the dexmedetomidine group. Tramadol requirement was significantly reduced in the dexmedetomidine group (P<0.05). Incidence of cough during the extubation process in the propofol group was higher than in the dexmedetomidine group. After extubation, Bruggemann comfort scale (BCS) and Rass agitation scores (RASS) were decreased in the dexmedetomidine-sedated patients. CONCLUSIONS: Dexmedetomidine provides safe and effective sedation for post-UPPP surgical patients and significantly reduces the use of analgesics, with minimal adverse effects.

Risk Factors and Location of Intracranial Aneurysm Rupture in a Consecutive Chinese Han Population.

OBJECTIVE: The aim of the present study was to retrospectively analyze and investigate the clinical data of 704 cases of ruptured intracranial aneurysms (RIAs) and unruptured intracranial aneurysms (UIAs). The risk factors predicting aneurysm rupture were explored from the perspective of the clinical characteristics of intracranial aneurysm (IA). METHODS: The clinical data of 704 patients with RIAs (494 patients) and UIAs (210 patients) admitted to the Department of Neurosurgery of Tianjin Medical University General Hospital and Tianjin Fifth Central Hospital between January 2016 and May 2022 were analyzed. A detailed analysis of sex, age, history, personal history, drug intake, and site of aneurysm occurrence was performed. Age was analyzed in segments and strata, and parameters with significant differences in the preliminary analysis results were analyzed by logistic regression to predict factors associated with the risk of aneurysm rupture. RESULTS: Among 494 patients with RIA (70.2%) and 210 patients with UIA (29.8%), the logistic regression showed that IA location appeared to be the most significant factor associated with RIA (OR, 95% CI: internal carotid artery (ICA), reference; anterior communicating artery,27.864,12.548-61.878; posterior communicating artery,12.408,6.658-23.124; anterior cerebral artery,5.804,2.333-14.440; middle cerebral artery,9.284,4.599-18.744; posterior circulation arteries, 4.224,2.011-8.871). Age was not a significant factor associated with RIA in the model and Hyperlipidemia (OR: 0.365; 95% CI: 0.171-0.779), Atherosclerosis (OR: 0.277; 95% CI: 0.172-0.446) and Multiple aneurysms (OR: 0.275; 95% CI: 0.177-0.425) patients were less likely to have RIA.IA location and age were the best predictors of RIA using the model. CONCLUSIONS: The present findings indicated that hyperlipidemia and atherosclerosis have a protective effect on aneurysm rupture, and different anatomical sites of IA may be risk factors for the occurrence of IA rupture. Among the anatomical sites of IA, the anterior communicating artery and posterior communicating artery have a higher fracture risk.

Metabolomic and transcriptomic analysis of flavonoids biosynthesis mechanisms in mulberry fruit (Hongguo 2) under exogenous hormone treatments.

The mulberry fruit is prized for its superior nutrition value and abundant color due to its high flavone content. To enhance comprehension of flavone biogenesis induced by external hormones, we sprayed exogenous ethylene (ETH), indoleacetic acid (IAA) and spermine (SPM) on mulberry fruit (Hongguo 2) during its color-changed period. The levels of anthocyanin, titratable acid, soluble sugar and endogenous hormones were determined after hormone treatment, integrated transcriptome and metabolome analysis were performed for mechanism exploration. Our results indicated that exogenous ETH, SPM, and IAA play important roles in mulberry ripening, including acid reduction, sugar increase and flavonoid synthesis.

Mulberry leaves supplementation alters lipid metabolism and promotes fatty acid ß oxidation in growing mutton sheep.

Mulberry leaves (MLs) are an unconventional feed with fiber and various active ingredients, and are acknowledged as likely to regulate lipid metabolism, while the molecular mechanism remains undefined. Therefore, our objective was to define the role of MLs on the overall lipid metabolism. We conducted a feeding experiment of three groups on growing mutton sheep fed with dried mulberry leaves (DMLs), with fermented mulberry leaves (FMLs), or without MLs (as control). Analyses of transcriptome and widely target lipids demonstrated the addition of MLs triggered big perturbations in genes and metabolites related to glycerolipid, phospholipid, ether lipid, and sphingolipid metabolism. Additionally, the variations of the above lipids in the treatment of MLs possibly facilitate immunity enhancement of growing mutton sheep via the activation of complement and coagulation cascades. Furthermore, treatments with MLs could expedite proceedings of lipid degradation and fatty acid ß oxidation in mitochondria, thereby to achieve the effect of lipid reduction. Besides, added DMLs also fuel fatty acid ß-oxidation in peroxisomes and own much stronger lipolysis than added FMLs, possibly attributed to high fiber content in DMLs. These findings establish the novel lipid-lowering role and immune protection of MLs, which lays the foundation for the medicinal application of MLs.

Mulberry leaves (MLs) are rich in a wide variety of active ingredients and are also a kind of traditional Chinese medicine with the same origin as medicine and food. Previous studies have found that MLs may regulate lipid metabolism. But the exact mechanism remains unclear. Our study reveals that ML supplement not only alters lipid metabolism including glycerol phospholipid, ether lipid as well as sphingolipid metabolism, which may help to improve immunity but also promote fatty acid degradation as well as ß oxidation to achieve the effect of fat reduction.

Efficient molecular conformation generation with quantum-inspired algorithm.

CONTEXT: Conformation generation, also known as molecular unfolding (MU), is a crucial step in structure-based drug design, remaining a challenging combinatorial optimization problem. Quantum annealing (QA) has shown great potential for solving certain combinatorial optimization problems over traditional classical methods such as simulated annealing (SA). However, a recent study showed that a 2000-qubit QA hardware was still unable to outperform SA for the MU problem. Here, we propose the use of quantum-inspired algorithm to solve the MU problem, in order to go beyond traditional SA. We introduce a highly compact phase encoding method which can exponentially reduce the representation space, compared with the previous one-hot encoding method. For benchmarking, we tested this new approach on the public QM9 dataset generated by density functional theory (DFT). The root-mean-square deviation between the conformation determined by our approach and DFT is negligible (less than about 0.5Å), which underpins the validity of our approach. Furthermore, the median time-to-target metric can be reduced by a factor of five compared to SA. Additionally, we demonstrate a simulation experiment by MindQuantum using quantum approximate optimization algorithm (QAOA) to reach optimal results. These results indicate that quantum-inspired algorithms can be applied to solve practical problems even before quantum hardware becomes mature. METHODS: The objective function of MU is defined as the sum of all internal distances between atoms in the molecule, which is a high-order unconstrained binary optimization (HUBO) problem. The degree of freedom of variables is discretized and encoded with binary variables by the phase encoding method. We employ the quantum-inspired simulated bifurcation algorithm for optimization. The public QM9 dataset is generated by DFT. The simulation experiment of quantum computation is implemented by MindQuantum using QAOA.

Resection of the tumor in the trigone of the lateral ventricle via the contralateral posterior interhemispheric transfalcine transprecuneus approach with multi-modern neurosurgery technology: a case report.

Choroid plexus papilloma (CPP) is a rare benign intracranial tumor origin that predominantly manifests in the lateral ventricle in children, accounting for 0.3%-0.6% of all primary intracranial tumors. It is extremely rare to have the CPP in the trigone of the lateral ventricle through the contralateral posterior interhemispheric transfalcine transprecuneus approach (PITTA). Herein, we report this rare case. A 7-year-old girl presented with headache. Magnetic resonance imaging of the brain showed periatrial lesions, and histopathological examination confirmed CPP (WHO grade I). The contralateral PITTA is a safe, effective, reasonable, and appropriate for some lesions in the trigone of the lateral ventricle. It provides a wider surgical angle (especially for the lateral extension) and reduces the risk of disturbance of the optic radiation compared with the conventional approaches. The use of multiple modern neurosurgical techniques, including interventional embolization, intraoperative navigation, microscope, and electrophysiological monitoring, make the procedure much easier and more accurate, and the neuroendoscope adds to the visualization of the microscope and can reduce surgical complications.

[Corrigendum] FKBP11 protects intestinal epithelial cells against inflammation­induced apoptosis via the JNK­caspase pathway in Crohn's disease.

Subsequently to the publication of the above article, the authors realized that Fig. 4 in their paper had been assembled containing two erroneously placed gel slices; essentially, the GAPDH bands featured in Fig. 4A had also been included in Fig. 5, and the data for the FKBP11 bands in Fig. 4A had also been included to show the GRP78 bands in Fig. 4. The authors were able to revisit their original data and to correct the data that had been featured incorrectly in Fig. 4. The corrected version of Fig. 4, now showing the true data for the GRP78 protein bands in Fig. 4C and the correct GAPDH protein bands for Fig. 4A, is shown on the next page. Note that these errors did not significantly affect the results or the conclusions reported in this paper. All the authors agree to the publication of this Corrigendum, and are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to correct this error. Moreover, the authors apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 18: 4428­4438, 2018; DOI: 10.3892/mmr.2018.9485].