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Purpose: To observe the crystalline lens rise (CLR) in horizontal and vertical orientations using anterior segment optical coherence tomography (AS-OCT). Methods: Non-invasive swept-source AS-OCT was used to measure the lens thickness, CLR, and angle-to-angle distance (ATA) in both the horizontal and vertical orientations. Anterior chamber depth (ACD) and horizontal white-to-white corneal diameter were obtained using the Pentacam HR (Oculus Optikgeräte GmbH). Axial length was obtained using the IOLMaster 700 (Carl Zeiss Meditec AG). The paired t test was used to analyze the difference in CLR between the two orientations. Pearson correlation analysis was performed to investigate the correlations between CLR and other ocular variables. Results: This prospective observational study comprised 99 eyes (99 patients) that underwent Visian Implantable Collamer Lens (STAAR Surgical) implantation for myopic correction. The mean CLR was 64.29 ± 168.04 and 208.09 ± 173.12 µm in the horizontal and vertical orientations, respectively. The vertical CLR (VCLR) was significantly greater than the horizontal CLR (HCLR) ( P < .05). Both the HCLR and VCLR were positively correlated with lens thickness and negatively correlated with ACD (all P < .05). The difference in CLR (VCLR-HCLR) was positively correlated with the axial length and the difference in ATA between the two orientations ( P < .05). Conclusions: VCLR was greater than HCLR in most patients with myopia, especially in the longer eyes. This nonuniform distribution in CLR implied different placements of the iridocorneal angles in the horizontal and vertical orientations and should be considered for the selection of ICL size and placement position. [ J Refract Surg . 2023;39(5):354–359.]

Background: To find ideal treatment regimens in unresectable hepatocellular carcinoma (u-HCC) are clinically important. This study evaluated the efficacy of five first-line regimens in u-HCC patients at 6-, 12-, 18-, 24-, and 30-month overall survival (OS) to provide reference for rational clinical treatment. Methods: We performed a systematic search using five databases. Screening and including qualified randomized controlled trials (RCT) regarding to the first-line regimens for unresectable HCC. Odds ratios (OR) were generated for dichotomous variants by network meta-analysis. The primary endpoint was OS, and the secondary endpoint was progression-free survival (PFS). The software implemented was STATA 17.0 MP. Results: Eventually, a total of six RCTs with five first-line regimens were included. HAIC-FO (OR=9.78, 95%CI: 4.21 to 22.69) was significantly superior to sorafenib on OS at 18th month. Concurrently, HAIC-FO (SUCRA=100%) had the highest ranking compared with the rest regimens. Atezolizumab plus bevacizumab (OR=5.13, 95%CI: 2.28 to 11.54) showed significantly better efficacy compared with sorafenib on PFS at 12th month. Synchronously, atezolizumab plus bevacizumab (SUCRA=87.3%) had the highest ranking. Conclusion: For patients with u-HCC, The optimal regimen we recommend is treating with HAIC-FO until 18th month, followed by sequential therapy with donafenib. Furthermore, we need more head-to-head trials to confirm these findings.

Reactive oxygen species (ROS) plays an essential role in the development of cancer. Here, we chose ROS-related miRNAs for consensus clustering analysis and ROS score construction. We find that ROS is extremely associated with prognosis, tumor immune microenvironment (TIME), gene mutations, N6-methyladenosine (m6A) methylation, and chemotherapy sensitivity in hepatocellular carcinoma (HCC). Mechanistically, ROS may affect the prognosis of HCC patients in numerous ways. Moreover, miR-210-3p and miR-106a-5p significantly increased the ROS level and stagnated cell cycle at G2/M in HCC; the results were more obvious in cells after ionizing radiation (IR). Finally, the two miRNAs suppressed cell proliferation, migration, and invasion and promoted apoptosis in huh7 and smmc7721 cells. It indicated that ROS might affect the prognosis of HCC patients through immune response and increase the sensitivity of HCC patients to radiotherapy and chemotherapy.

Hepatocellular carcinoma (HCC) is one of the most common cancers and the fourth leading cause of death in men. YEATS domain containing 2 (YEATS2) gene encodes a scaffolding subunit of the ATAC complex. We found that YEATS2 was upregulated in HCC tissues and was associated with a poor prognosis. However, the role of YEATS2 in HCC remains unclear. The purpose of this study was to investigate the effect of YEATS2 on the progression of HCC and to elucidate its related mechanisms. We found that overexpression of YEATS2 promoted tumor cell proliferation, migration, and invasion through the PI3K/AKT signaling pathway and regulation of extracellular matrix. These findings help to understand the role of YEATS2 in HCC, and YEATS2 may become a new target for HCC therapy.

Aims: To verify the hypothesis that the hepatic vein ligation (HVL) alone may produce similar results to the live venous deprivation (LVD or HVL/PVL). Methods: Rats were assigned to 5 groups, the control group; R group: the right median hepatic vein (RMHV) was ligated; M group: the middle median hepatic vein (MMHV) was ligated, RM group: both the RMHV and MMHV were ligated; LVD group: both the right median portal vein (RMPV) and the RMHV were ligated. Liver hypertrophy effect and liver enzymes were determined. The methylene blue staining and retrograde pressurized perfusion assay were performed to observe the hemodynamic changes. Results: The RM and LVD groups exhibited similar significant hypertrophy in the future liver remnants when compared to the control group, and almost no additional hypertrophy effect were observed in the R and M group. A remarkable elevation in serum transaminase levels in both those groups. The methylene blue staining indicated that there are pressured-dependent collaterals between the contigeous drainage areas, the R+MMHVL procedures block the outflow of RML. Conclusion: The extended ligation of hepatic vein (R+MMHVL) obtained the similar hypertrophy effect and hepatic damage to the LVD in rat model, and the intrahepatic venovenous collaterals play key roles.

Genomic instability is a hallmark of all cancers. RMI2 is a crucial component of the BLM-TopoIIIa-RMI1-RMI2 complex that maintains genome stability. It has been shown to accelerate tumor progression in lung cancer, cervical cancer, and prostate cancer. However, its expression and function in hepatocellular carcinoma (HCC) remain poorly defined. In this study, gene expression data and corresponding clinical information of HCC were downloaded from the TCGA, ICGC, and GEO databases. The expression level and clinical significance of RMI2 in HCC were then analyzed. In addition, cellular and molecular biology experiments were conducted to explore the effects of silencing and overexpression of RMI2 on human liver cancer cells and the associated mechanisms. The results showed that RMI2 expression was elevated in HCC tissues. High expression of RMI2 was correlated with shorter survival and poor prognosis of patients. The results of CCK-8, Edu, and clonogenic assays confirmed that RMI2 overexpression promoted the proliferation of HCC cells. Flow cytometric analysis demonstrated that RMI2 overexpression enhanced G1-S phase transition and decreased apoptosis. Moreover, the protein expression of key effector molecules in the p53 signaling pathway was reduced following RMI2 overexpression. In summary, these results indicate that RMI2 promotes the growth of HCC cells and suppresses their apoptosis by inhibiting the p53 signaling pathway. This study provides new insights into the mechanisms driving HCC tumorigenesis and new therapeutic targets.

RNA-binding proteins (RBPs) can regulate multiple pathways by binding to RNAs, playing a variety of functions, such as localization, stability, and immunity. In recent years, with the development of technology, researchers have discovered that RBPs play a key role in the N6-methyladenosine (m6A) modification process. M6A methylation is the most abundant form of RNA modification in eukaryotes, which is defined as methylation on the sixth N atom of adenine in RNA. Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) is one of the components of m6A binding proteins, which plays an important role in decoding m6A marks and performing various biological functions. IGF2BP3 is abnormally expressed in many human cancers, often associated with poor prognosis. Here, we summarize the physiological role of IGF2BP3 in organisms and describe its role and mechanism in tumors. These data suggest that IGF2BP3 may be a valuable therapeutic target and prognostic marker in the future.

The electrochemical behavior of nickel at different pH values in industrial electrolyte was investigated by means of cyclic voltammetry, chronoamperometry and scanning electron microscopy. The results show that the cathodic reaction of nickel ions on glassy carbon electrode surface in industrial electrolyte is a quasi-reversible nucleation and growth process controlled by diffusion. The process is carried out in a three-dimensional instantaneous nucleation and growth mode, and pH values only influence the growth process. The grain size decreased, the deposition rate increased and the density of deposition layer on electrode surface increased with the increase in pH. When the electrolyte pH is 4.8, the grains are uniformly distributed on the electrode surface in a spherical shape with the size of 80 nm, which is the optimum pH value for preparing fine-grained nano-nickel.

The tumor immune microenvironment (TIME) is now considered as an important factor during gastric cancer (GC) development. This study identified a novel immune-related risk model for predicting prognosis and assessing the immune status of GC patients. Transcriptomic data were obtained from the TCGA database. The differential expressed immune-related genes (IRGs) were identified through the ImmPort portal. Enrichment analysis was performed to explore the potential molecular mechanism of these IRGs. By the Cox regression analysis, we constructed the immune prognostic model. Then, the association between the model and the immune microenvironment was estimated. The model was validated in the GSE84433 dataset. Totally, we identified 222 differentially expressed IRGs. These IRGs were closely correlated with immune response and immune signaling pathways. Through the Cox regression analysis, we developed the immune prognostic model based on the expression of seven IRGs (CXCL3, NOX4, PROC, FAM19A4, RNASE2, IGHD2-15, CGB5). Patients were stratified into two groups according to immune-related risk scores. Survival analysis indicated that the prognosis of high-risk patients was poorer than low-risk patients. Moreover, the immune-related risk score was an independent prognostic biomarker. More importantly, we found that the infiltration level of immunosuppressive cells and the expression of inhibitory immune checkpoints were higher in high-risk patients. The immune microenvironment tended to be a suppressive status in patients with high-risk scores. This study demonstrated that our model had predictive value for prognosis and the TIME in GC. It might be a robust tool to improve personalized patient management.

MAX dimerization protein 3 (MXD3), a transcriptional regulator of the MXD3 superfamily, is a part of the MYC–MAX–MXD network. However, its role in tumors has been reported in several cancers, such as B-cell acute lymphoblastic leukemia, medulloblastoma, neuroblastoma, and glioblastoma. Based on TCGA and GEO data, our first pancancer study of MXD3 confirmed the high expression of MXD3 in cancer tissues. Our results revealed that patients suffering from cancers with higher MXD3 expression had poor OS, DSS, DFI, and PFI. We further explored the methylation status of the MXD3 gene body and gene promoter in cancer. Patients with a higher MXD3 gene body have better OS, while the prognosis of patients with a high MXD3 promoter is more complex. We also verified the differential expression of three clinical phenotypes of MXD3: age, sex, and tumor stage, in a variety of tumors, suggesting a correlation between MXD3 and clinical characteristics. We explored the negative relationship between MXD3 and TMB and MSI in most types of cancer, indicating the poor prognosis of patients with high MXD3 expression. We further investigated the relationship between MXD3 and immune infiltrating cells and identified the relationship between MXD3 and immune genes, immunosuppressive genes, and antigen-presenting genes. All of the above findings established a solid relationship between MXD3 and the immune environment and immune cells. These results demonstrated that MXD3 might also be a potential immune factor. We also found a higher expression of MXD3 and promoter according to the increasing glioma WHO grade or histologic types. Glioma patients with high MXD3 or MXD3 promoter expression had poor survival. Finally, we used IHC to verify the higher expression of MXD3 in glioma samples compared to normal samples. Our study shows that MXD3, as a poor prognostic factor, plays a significant role in many cancers, especially glioma. Although more clinical evidence for MXD3 as a clinical therapeutic target and an immunotherapy site is needed, MXD3 can play an important guiding role in multiple clinical treatments, including immunotherapy and demethylation therapy.

Glioma is the most important tumor of the nervous system. LncRNA plays an important role in the occurrence, development, and metastasis of glioma. The immune status of glioma plays an important role in its treatment and prognosis. In lower-grade glioma (LGG), based on the results of the Weighted correlation network analysis (WCGNA) of lncRNA, we used lasso regression, random forest model, and stepwise regression to establish the lncRNA prognostic model: 0.58349*CYTOR + 0. 47804*LINC01831 + 0. 24933*HOTAIRM1 + 0. 73600*AC022034 + 0. 62351*AC104407 = lncRNA model prognosis score (LMPS). Concomitantly, we explored the correlation of LMPS with the Estimation of STromal and Immune cells in MAlignant Tumours using Expression data (ESTIMATE), Tumor IMmune Estimation Resource (TIMER) infiltrating immune cells. We also established the reciprocal network of the model and verified the significant prognostic significance of the hub genes of the network and the significant impact on immunity. Finally, by connectivity Map (cMap) analysis, we obtained the drugs about the WCGNA module where the model is. Our study highlights the close role of the lncRNA model with patient prognosis, immunity, and clinical staging, and can guide immunotherapy. The network is constructed with the model as the core. Its core genes also have a guiding role in patient prognosis, immunity, and treatment. We identified loratadine and fidaxomicin as possible drugs.

Keratin 18 (KRT18), one of the most abundant keratins in epithelial and endothelial cells, has been reported to be aberrantly expressed in many malignancies and extensively regarded as a biomarker and important regulator in multiple cancers, including gastric cancer (GC). But the molecular regulatory mechanisms of KRT18 in GC patients and cells are largely unknown. In the present study, we analyzed the expression level of KRT18 in 450 stomach adenocarcinoma tissue samples from TCGA database and found a significantly higher expression level in tumor tissues. We then explored the potential functions of KRT18 in AGS cells (human gastric adenocarcinoma cell line) by KRT18 knockdown using siRNA and whole transcriptome RNA-seq analysis. Notably, KRT18 selectively regulates expression of cell proliferation and apoptotic genes. Beyond this, KRT18 affects the alternative splicing of genes enriched in apoptosis, cell cycle, and other cancer-related pathways, which were then validated by reverse transcription–quantitative polymerase chain reaction approach. We validated KRT18-KD promoted apoptosis and inhibited proliferation in AGS cells. We then used RNA-seq data of GC samples to further demonstrate the modulation of KRT18 on alternative splicing regulation. These results together support the conclusion that KRT18 extensively modulates diverse alternative splicing events of genes enriched in proliferation and apoptosis processes. And the dysregulated splicing factors at transcriptional or posttranscriptional level by KRT18 may contribute to the alternative splicing change of many genes, which expands the functional importance of keratins in apoptotic and cell cycle pathways at the posttranscriptional level in GC.

The effects of three different substrate materials (glassy carbon, gold, and nickel electrodes) on the electrocrystallization behavior of nanocrystalline nickel in an industrial electrolyte with complex compositions were studied by cyclic voltammetry (CV), single potential step chronoamperometry. The CV results indicated that the initial deposition potentials of nickel shift to the positive direction in the order glassy carbon

Malignant tumors are always a critical threat to human health, with complex pathogenesis, numerous causative factors, and poor prognosis. The features of cancers, such as gene mutations, epigenetic alterations, and the activation and inhibition of signaling pathways in the organism, play important roles in tumorigenesis and prognosis. MicroRNA (miRNA) enables the control of various molecular mechanisms and plays a variety of roles in human cancers, such as radiation sensitivity and tumor immunity, through the regulation of target genes. MiR-149-5p participates in the process and is closely related to lipogenesis, the migration of vascular endothelial cells, and the expression of stem-cell-related proteins. In recent years, its role in cancer has dramatically increased. In this review, we summarize the regular physiological roles of miRNAs, specifically miR-149-5p, in the organism and discuss the tumor-suppressive or oncogenic roles of miR-149-5p in different human cancers with respect to signaling pathways involved in regulation. Possible clinical applications of miR-149-5p in future targeted therapies and prognosis improvement in oncology are suggested.

Recently, N6-methyladenosine (m6A) RNA methylation in eukaryotic mRNA has become increasingly obvious in the pathogenesis and prognosis of cancer. Moreover, tumor microenvironment is involved in the regulation of tumorigenesis. In our research, the clinical data, including 374 tumor and 50 normal patients, were obtained from The Cancer Genome Atlas (TCGA). Then 19 m6A regulators were selected from other studies. Hepatocellular carcinoma (HCC) patients were clustered in cluster1/2, according to the consensus clustering for the m6A RNA regulators. We found that m6A regulators were upregulated in cluster1. The cluster1 was associated with higher programmed death ligand 1 (PD-L1) expression level, higher immunoscore, worse prognosis, and distinct immune cell infiltration compared with cluster2. Five risk signatures were identified, including YTH N6-methyladenosine RNA-binding protein 1, YTHDF2, heterogeneous nuclear ribonucleoprotein C, WT1-associated protein, and methyltransferase-like 3, based on univariate Cox and least absolute shrinkage and selection operator regression analysis. High-risk group and low-risk group HCC patients were selected based on the risk score. Similarly, the high-risk group was extremely associated with higher PD-L1 expression level, higher grade, and worse overall survival (OS). Also, cluster1 was mainly enriched in high-risk group. Receiver operating characteristic (ROC) and a nomogram were used to predict the ability and the probability of 3- and 5-year OS of HCC patients. The time-dependent ROC curve (AUC) reached 0.77, 0.67, and 0.68 at 1, 3, and 5 years in the training dataset. Also, AUC areas of 1, 3, and 5 years were 0.7, 0.63, and 0.55 in the validation dataset. The gene set enrichment analysis showed that MTOR signaling pathway and WNT signaling pathway were correlated with cluster1 and high-risk group. Collectively, the research showed that the m6A regulators were significantly associated with tumor immune microenvironment in HCC. Risk characteristics based on m6A regulators may predict prognosis in patients with HCC and provide a new therapeutic target for improving the efficacy of immunotherapy.

Aims As vital regulators of post-transcription gene expression, microRNAs are involved in the initiation and progression of hepatocellular carcinoma (HCC), including antitumor immune responses. We aimed to identify an immune-related microRNA signature and explore the influence of this signature on the prognosis and immunity of HCC. Materials and methods Differentially expressed immune-related microRNAs were identified between high- and low-immunity groups in the TCGA-HCC dataset. Then, Cox regression models were used to construct an immune-related microRNA signature. We assessed the prognostic value and clinical relevance of this signature. Furthermore, we analyzed the effect of the immune-related microRNA signature on immune cells and immune checkpoints. Key findings We screened 41 differentially expressed immune-related microRNAs, of which 7 microRNAs were used to construct the immune signature. Survival analysis showed that high-risk patients had a shorter survival. The immune-related microRNA signature was an independent prognostic marker and was associated with the clinical stage. To understand the functional mechanism of the seven-microRNA signature, we predicted target genes of microRNAs. Enrichment analysis indicated that these target genes participated in immune responses. Moreover, we found that the microRNA signature was related to tumor-infiltrating immune cells. In high-risk patients, there was a higher expression of inhibitory immune checkpoints. On the contrary, the expression of stimulatory immune checkpoints was lower in high-risk patients. Significance We successfully identified an immune-related microRNA signature that was strongly correlated with the prognosis and immune microenvironment of HCC. The immune-related microRNAs signature might have important implications for improving the clinical outcomes of HCC patients.

To investigate the effect of tantalum on plastic deformation behavior of Co-8.8Al-9.8W-xTa (x = 0 and 2 at. %) superalloy at room temperature, compressive tests were adopted with constant strain rate. It is interesting that stacking faults occur in γ channels in initial microstructure of both alloys. Deformation substructures were selected from samples after 5% and 10% strains, and determined by transmission electron microscope to study their evolution. Dislocations preferentially nucleated in the γ channels, then bypassed or sheared into γ′ precipitates during deformation. With the shearing of LPDs, stacking faults orderly aligned in the γ/γ′ coherent microstructure and passed through γ channels and adjacent γ′ particles. Both alloys failed by brittle fracture with mixed fractures.

Large micropore with a pore size of 1–2 nm can allow high charge storage capability while ensure fast ions transport, which serves to improve the energy density of supercapacitors without sacrificing high power density. Herein, we report a large micropore dominant microporous carbon derived from a biomass waste, flaxseed residue from the edible oil industry, for high-performance supercapacitors. The reported material exhibits a large specific surface area of up to 3230 m2 g−1, and more than 70.1% of micropore volume is contributed by large micropores. The specific capacitance of the obtained material reaches up to 369 and 398 F g−1 in KOH and H2SO4 electrolyte, respectively. Meanwhile, the assembled supercapacitor device based on the obtained material exhibits excellent rate and cycle performance. Over 92.7% of the initial capacitance is retained even under a large current density of 20 A g−1 and the capacitance retention is more than 98.1% after 10000 times cycle in KOH electrolyte. The energy density of the assembled supercapacitor device reaches 61.2 Wh kg−1 at a power density of 468.8 W kg−1, and a high energy density of 43.5 Wh kg−1 is retained at a large power density of 13.3 kW kg−1 in ionic liquid EMIMBF4 electrolyte.

Absrtact Carbon nanotubes has attracted much attentions due to its huge application potential in various high-tech fields. Exploition of the simple and cost-efficient synthesis method for carbon nanotubes is crucial for its practical application. Herein, multi-wall carbon nanotubes (MCNTs) was successfully synthesized by one-step pyrolysis of a mixture of benzene and ferrocene in a sealed autoclave under autogenetic-pressure. A pyrolysis temperature of 800 °C, pyrolysis time for 30 min and a ferrocene/benzene molar ratio of 1:2 is found to be the optimal conditions for synthesizing the MCNTs via the mentioned autogenetic-pressure method. The synthesized MCNTs exhibits a “bamboo joint”-like multi-wall structure with about 12 layers of highly graphited tube wall and uniform external diameter of ca 20 nm. The specific capacitance of the synthesized MCNTs reaches 64 F g-1, which value is about 3.0 times higher than that of the typical commercial MCNTs. The synthesized MCNTs also exhibits very excellent superior rate and cycle performance. More than 95.5% initial specific capacitance is retained even under a large current density of 20 A g-1, and no apparent specific capacitance decrement is observed after 10,000 times charge-discharge cycles. The energy density of the synthesized MCNTs-based supercapacitor arrives 2.27 Wh kg-1 at a power density of 157 W kg-1, and 2.07 Wh kg-1 of energy density is still retained at a power density of 5.3 kW kg -1, while an energy density of 0.72 Wh kg-1 is arrived at a power density of 2.6 kW kg-1 for the typical commercial MCNTs-based supercapacitor. The superior capacitance performance of the synthesized MCNTs than that of the typical commercial MCNTs is ascribed to the higher conductivity induced by the higher graphitization degree than that of the typical commercial MCNTs, good surface wettability due to the high content of oxygen-contained functional groups on surface, and the supplementary contribution of pseudo-capacitance.

PURPOSE: To compare the corneal biomechanical properties before and after small incision lenticule extraction (SMILE) and femtosecond laser-assisted LASIK in different levels of myopia with the Ocular Response Analyzer (Reichert Ophthalmic Instruments, Depew, NY). METHODS: A total of 187 and 79 eyes that received SMILE or LASIK, respectively, between January and June 2013 at Zhongshan Ophthalmic Center were enrolled in this study. Patients were grouped according to surgery type (SMILE or LASIK) and −6.00 diopters (D) or less (⩽ −6.00 D) or myopia greater than −6.00 D (>−6.00 D). Corneal hysteresis, corneal resistance factor, and 37 waveform parameters were recorded and compared preoperatively and at 1 week and 1 and 3 months postoperatively. RESULTS: There was a significant decrease of corneal hysteresis, corneal resistance factor, p1area, and p2area, and an increase of path1 and path2 in both SMILE and LASIK. In myopia −6.00 D or less, the differences between SMILE and LASIK were not significant ( P > .05), but in myopia greater than −6.00 D, the corneal hysteresis, corneal resistance factor, p1area, and p2area decreased significantly more in LASIK than in SMILE ( P < .05). CONCLUSIONS: When comparing SMILE with LASIK, myopia was greater than −6.00 D, and the corneal hysteresis, corneal resistance factor, p1area, and p2area decrease was less after SMILE. [ J Refract Surg . 2014;30(10):702–707.]