Polarization improvement of CsPbClBr2 quantum dot film by laser direct writing technology.

Inorganic halogen perovskite quantum dots not only have high fluorescence quantum efficiency, but also can emit polarized light in solution or thin film. These excellent performances make perovskite quantum dots promising to be used in next-generation displays. In this study, we develop laser direct writing technology to improve the emitted light polarization of CsPbClBr2 quantum dot film. Without using an additional polarizer, we prove that the polarization degree is maximumly increased by about 56%, and the reasons are analyzed from three perspectives: laser scanning space, laser power, and film thickness. In addition, the lifetime of the fluorescence is also greatly improved after laser treatment. The results we obtain provide the possibility for production of a new generation of displays.

Controlling the nanoscale friction by layered ionic liquid films.

The nanofriction coefficient of ionic liquids (ILs), 1-butyl-3-methylimidazolium tetrafluoroborate ([BMIM][BF4]) and 1-butyl-3-methylimidazolium hexafluorophosphate ([BMIM][PF6]), on the surfaces of mica and graphite was investigated using atomic force microscopy (AFM). A pronounced layered spatial distribution was found in the IL film formed on the solid substrates and can be divided into 3 well distinguishable regions exhibiting different physical properties with increasing distance from the substrate. We found that the friction coefficient (µ) increases monotonically as the layering thickness decreases, no matter what the thickness of the bulk IL is. This suggests that the layering assembled IL at solid surfaces is more important than the bulk phase in determining the magnitude of the nanoscale friction. The increase in the friction coefficient as the layering thickness decreases is most likely attributed to the assembled ordered IL layers closer to the substrate surfaces having a greater activation barrier for unlocking the surfaces to allow shear.

The effect of nanoscale friction of mesoporous carbon supported ionic liquids on the mass transfer of CO2 adsorption.

Supported ionic liquids (ILs) are attractive alternatives for CO2 capture and the thickness of supported IL films plays a critical role in the CO2 mass transfer rate. However, the dependence of CO2 uptake on the IL film thickness differs as the system varies. In this work, atomic force microscopy (AFM) is employed to probe the 'nanofriction coefficient' to characterize the mobility of ILs at the solid interface, in which, the smaller the nanofriction coefficient, the faster are the ionic mobility and CO2 mass transfer. A monotonic and almost linear relationship for supported IL films is obtained between the resistance of CO2 mass transfer (1/k) and the nanofriction coefficient (µ), avoiding the controversy over the effect of supported IL film thickness on CO2 adsorption. The enhanced mass transfer of CO2 adsorption at IL-solid interfaces is observed at smaller resistance 1/k and friction coefficient µ. The low-friction driven local mobility (diffusion) of ILs at solid interfaces is enhanced, promoting the exchange mixing of the ILs adsorbing CO2 with the 'blank-clean' ions of the ILs, and thus accelerating the CO2 mass transfer. The proposed correlation links the nanoscale friction with the mass transfer of CO2 adsorption, providing a fresh view on the design of ultra-low frictional supported ILs for enhanced CO2 capture and separation processes.

On the ionic liquid films 'pinned' by core-shell structured Fe3O4@carbon nanoparticles and their tribological properties.

A strongly 'pinned' ionic liquid (IL, [BMIM][PF6]) film on a silicon (Si) surface via carbon capsuled Fe3O4 core-shell (Fe3O4@C) nanoparticles is achieved, revealing excellent friction-reducing ability at a high load. The adhesion force is measured to be ∼198 nN at the Fe3O4@C-Si interface by the Fe3O4@C colloidal AFM tip, which is stronger than that at both Fe3O4@C-Fe3O4@C (∼60 nN) and IL-Si (∼10 nN) interfaces, indicating a strong 'normal pin-force' towards the Si substrate. The resulting strengthened force enables the formation of lateral IL networks via the dipole-dipole attractions among Fe3O4 cores. The observed blue shift of the characteristic band related to the IL anion in the ATR-FTIR spectra confirmed the enhanced interaction. The N-Si, P-O chemical bonds formed as a result of the IL interactions with the Si substrate confirmed by XPS spectroscopy suggested that the IL lay on the Si plane. This orientation is favorable for Fe3O4@C nanoparticles to exert 'normal pin-force' and press the IL film strongly onto surfaces. The IL ions/clusters are thus anchored by these Fe3O4@C 'pins' onto the substrate to form a dense film, resulting in a smaller interaction size parameter, which is responsible for the reduced friction coefficient µ.

Global research trends in palliative care for breast cancer from 2012 to 2022: A scientometric analysis.

Purpose: We used bibliometric methods to evaluate the global scientific output of palliative care breast cancer research and to explore the current status and further research directions in the field over the past decade. Methods: All relevant publications from the year 2012 to 2022 were retrieved from Web of Science. We applied VOSviewer and Bibliometrix R v4.2.1 to obtain information on subject domains, annual publication output and citations, countries and authors with the highest productivity, influential journals and articles, and popular keywords. Results: In total, 1529 publications were included in the final analysis. Health services and supportive care, pain and symptom management were the focus of the research in the field. From the year 2017 to 2021, the annual publication output was abundant and peaked in 2018. The systematic review by Fitzmaurice et al. in 2017 was the most-cited publication. The United States was the leading country with the maximum number of publications, citations, and link strengths with other countries. The most contributing institution was University of Toronto. E. Bruera was the most prolific author, ranking first among the authors in both the H and M index. The journal with the most publications was Palliative & Supportive Care. Keywords analysis indicated that exploring the significant degree of palliative care to reduce anxiety and depression in breast cancer patients may be a good research direction. In addition, how to assess the optimal timing of palliative care interventions and further exploring the specific contradiction between insufficient medical resources and palliative care are also possible research directions. Conclusion: Palliative care plays an important role in the treatment of breast cancer. With the help of a scientometric analysis in this field, researchers can clarify the current research status and hotspots worth fully exploring.

Negatively regulating mechanism of Sirpalpha1 in hepatocellular carcinoma: an experimental study.

BACKGROUND: Signal regulatory protein (Sirp) is a recently isolated, cloned and identified inhibitor receptor distributed in the membrane of hematopoietic and nonhematopoietic cells. Sirp alpha1 (Sirpalpha1) is a member of Sirp families. Sirpalpha1 can bind SHP-2 in the form of tyrosine phosphorylation by SH2 effect and negatively regulate growth factor, oncogene, or insulin-induced responses as its substrate. This study aimed to preliminarily clarify the negatively regulating proliferation mechanism of Sirpalpha1 in liver cancer. METHODS: pLXSN, Sirpalpha1 and Sirpalpha1P4Y2 plasmids were respectively transfected into Sk-Hep1 liver cancer cell line, and various stable Sk-Hep1 cell lines were obtained with screening agent of G418 (1200 microg/ml). The expressing levels of cyclin D1, CDK4, Fas, beta-catenin and gankyrin in various cell lines were determined with Western blotting. Cell cycles were determined at 0, 12 and 24 hours with flow cytometry after various synchronous cell lines were cultured without serum for 72. Cell apoptosis induced with agent of TNF-alpha (50 ng/ml) was determined with flow cytometry at 0, 0.5, 1, 3, 6 and 12 hours. RESULTS: Sirpalpha1 could significantly decrease the expression of cyclin D1, beta-catenin and gankyrin, but it couldn't affect the expression level of CDK4 and Fas. When synchronous cells were cultured for 12 hours, S phase Sk-Hep1 cell transfected with Sirpalpha1 plasmid was the lowest [(31.92+/-0.22)% vs. other cell lines, P<0.05], and the cell line was highly sensitive to TNF-alpha agent for 1 hour. (59.31+/-0.59)% of apoptotic cells occurred (vs. the other time points, P<0.05). CONCLUSIONS: Sirpalpha1 might block the cell cycle of liver cancer, inhibit cell proliferation, promote cell apoptosis by decreasing the expression of cyclin D1, beta-catenin and gankyrin. It is one of the important mechanisms inhibiting the occurrence and development of hepatocellular carcinoma.

Gradual upregulation of OCI-5 expression during occurrence and progression of rat hepatocellular carcinoma.

BACKGROUND: OCI-5, the rat homologene of human glypican 3 (GPC3), is confirmed upregulated in hepatocellular carcinoma (HCC). The present study was undertaken to detect gene expression change of OCI-5 during occurrence and progression of rat HCC. METHODS: Male Sprague-Dawley rats were given diethylnitrosamine (DENA) to induce HCC. Three DENA-induced rats and one control rat were sacrificed every week for 18 weeks during the development of HCC. Tissues specimens were snap-frozen in liquid nitrogen and total RNA was isolated. Sk-Hep1 cells were treated with DENA at different concentrations. The gene expression levels of OCI-5 and GPC3 were detected with the RT-PCR method. RESULTS: OCI-5 was not expressed in normal rat liver tissues. When HCC occurred and aggravated, OCI-5 expression was gradually elevated to a very high level. GPC3 was not expressed in the DENA-treated Sk-Hep1 cells. CONCLUSIONS: OCI-5 was not expressed in normal rat liver tissues but in rat HCC tissues. High-expression of OCI-5 in DENA-induced rat HCC model was the gene expression change of HCC not the DENA-induced gene expression. The expression level of OCI-5 was not only elevated in rat HCC but also gradually along the occurrence and progression of HCC, indicating that GPC3 might serve as a sensitive marker of early stage HCC.

Structural basis of interaction between protein tyrosine phosphatase PCP-2 and beta-catenin.

PCP-2 is a member of receptor-like protein tyrosine phosphatase of the MAM domain family. To investigate which part of PCP-2 was involved in its interaction with beta-catenin, we constructed various deletion mutants of PCP-2. These PCP-2 mutants and wild-type PCP-2 were co-transfected into BHK-21 cells with beta-catenin individually. An in vivo binding assay revealed that the expression of wild-type PCP-2, PCP-2 deltaC1C2 (deleted PCP-2 without both PTP domains) and PCP-2 deltaC2 (deleted PCP-2 without the second PTP domain) could be immunoprecipitated by anti-catenin antibody in every co-transfection, but PCP-2 EXT (deleted PCP-2 without the juxtamembrane region and both PTP domains) was missing, which implied that PCP-2 and beta-catenin could associate directly and the juxtamembrane region in PCP-2 was sufficient for the process.

Expression of cytochrome P4502E1 gene in hepatocellular carcinoma.

AIM: To investigate cytochrome P4502E1 (CYP2E1) gene expression in occurrence and progression of hepatocellular carcinoma (HCC). METHODS: The human liver arrayed library was spotted onto the nylon membranes to make cDNA array. Hybridization of cDNA array was performed with labeled probes synthesized from RNA isolated from HCC and adjacent liver tissues. Sprague-Dawley rats were administrated diethylnitrosamine (DENA) to induce HCC. CYP2E1 expression was detected by the method of RT-PCR and Northern blot analysis. RESULTS: CYP2E1 was found by cDNA array hybridization to express differently between HCC and liver tissues. CYP2E1 only expressed in liver, but did not express in HCC tissues and expressed lowly in cirrhotic tissues. In the progression of cirrhosis and HCC, the expression level of CYP2E1 was gradually decreased and hardly detected until the late stage of HCC. CONCLUSION: Using arrayed library to make cDNA arrays is an effective method to find differential expression genes. CYP2E1 is a unique gene expressing in liver but did not express in HCC. CYP2E1 expression descended along with the initiation and progression of HCC, which is noteworthy further investigations in its significance in the development of HCC.

Gene and protein expressions of p28GANK in rat with liver regeneration.

AIM: To observe the gene and protein expression changes of p28GANK in regenerating liver tissues, and to reveal the biological function of p28GANK on the regulation of liver regeneration. METHODS: One hundred and thirty two adult male Sprague-Dawley rats were selected, weighing 200-250 g, and divided randomly into sham operation (SO) group and partial hepatectomy (PH) group. Each group had eleven time points: 0, 2, 6, 12, 24, 30, 48, 72, 120, 168 and 240 h, six rats were in each time point. The rats were undergone 70% PH under methoxyflurane anesthesia by resection of the anterior and left lateral lobes of the liver. SO was conducted by laparotomy plus slight mobilization of the liver without resection. Liver specimens were collected at the indicated time points after PH or SO. The expression level of p28GANK mRNA was determined by Northern blot as well as at protein level via immunohistochemical staining. The expressions of p28GANK mRNA in these tissues were analyzed by imaging analysis system of FLA-2000 FUJIFILM and one way analysis of variance. The protein expressions of p28GANK in these tissues were analyzed with Fromowitz' method and Rank sum test. RESULTS: The expression of p28GANK mRNA in the regenerating liver tissues possessed two transcripts, which were 1.5 kb and 1.0 kb. There was a significantly different expression patterns of p28GANK mRNA between SO and PH groups (P<0.01). The expression of p28GANK mRNA increased 2 h after PH, the peak time was 72 h (SO group: 163.83+/-1.4720; PH group: 510.5+/-17.0499, P<0.01). There was a significant difference in the 1.5 kb transcript, which decreased gradually after 72 hours. The protein expression of p28GANK was mainly in the cytoplasm of regenerating hepatocytes, and increased near the central region 24 h after PH, and became strongly positive at 48 h (+++, vs the other time points P<0.05), but decreased 72 h after PH. CONCLUSION: The expression of p28GANK mRNA increases in the early stage of rat liver regeneration, the protein expression of p28GANK is mainly in the cytoplasm of regenerating liver cells. It suggests that the gene of p28GANK may be an important regulatory and controlled factor involved in hepatocyte proliferation during liver regeneration.

[PTEN expression and its significance in human primary hepatocellular carcinoma].

OBJECTIVES: To explore the significance of PTEN (phosphatase and tensin homolog deleted on chromosome 10) in the development of human primary hepatocellular carcinoma (HCC). METHODS: PTEN protein expression in cancerous liver tissues and paired para-carcinoma liver tissues from 60 HCC patients was detected by immunohistochemistry and PTEN mRNA expression was analyzed by northern blot. The significance of PTEN in the development of HCC was analyzed by investigating the relationship between the expression levels of PTEN protein and mRNA, and the clinicopathological parameters of HCC patients. RESULTS: PTEN protein was immunohistochemically stained in the cytoplasmic region of para-carcinoma liver tissues in all the 60 patients, while only 48.3% (29/60) of the patients were positive for PTEN protein in cancerous liver tissues. The positive rate of PTEN protein in HCC tissues were relative to the histological gading and the presence of tumor thrombus. In grade I - II, III, and IV, the positive rates were 84.0%, 23.8%, and 21.4% respectively, and in the group with tumor thrombus was 26.7%, while in the group without tumor thrombus was 55.6%. Northern blot showed that there existed four PTEN mRNA transcripts with the length of 5.5kb, 4.4kb, 2.4kb, and 1.8kb respectively. The level of PTEN mRNA expression in HCC tissues was much lower than that in the paired para-carcinoma liver tissues. The low expression level of the 5.5kb and 4.4kb transcripts was significantly associated with serum AFP value, presence of tumor thrombus, state of satellite lesion and histological grading. The low expression level of the 2.4kb transcript in HCC was significantly associated with the presence of tumor thrombus and satellite lesions in HCC patients. However, no evident relationship between the lowered expression level of the 1.8kb transcript and the clinicopathological parameters of HCC was observed in these 60 patients. CONCLUSIONS: Down-regulation of PTEN expression may play an important role in the development of HCC and the expression level of PTEN may be a potential adjuvant parameter in forecasting the progress and prognosis of HCC.

Upregulation of Glypican-3 expression in hepatocellular carcinoma but downregulation in cholangiocarcinoma indicates its differential diagnosis value in primary liver cancers.

BACKGROUND/AIM: Expression alteration of Glypican-3 (GPC3) is associated with several malignancies and has been identified as an overexpressed gene in hepatocellular carcinoma (HCC). In this study GPC3 expression in intrahepatic chanlangiocarcinoma (ICC), gallbladder cancer and HCC was quantitatively detected. METHODS: Real-time quantitative reverse transcription polymerase chain reaction was used to detect the expression level of GPC3. RESULTS: GPC3 expression was elevated more than two-fold in HCC compared with adjacent tissue in 90 of 100 HCC cases. The average expression level of GPC3 was significantly higher in HCC than that in adjacent liver tissues (P<0.0001). Only in four of 21 ICC cases GPC3 expression was upregulated more than two-fold in tumor tissues. GPC3 expression was downregulated in gallbladder cancer in 12 of 13 cases and the average expression level was significantly lower than that in normal gallbladder tissues (P<0.05). CONCLUSION: The different expression patterns of GPC3 in HCC and ICC suggested that it might play a different role in theses tumors and could serve as a biomarker for differential diagnosis of HCC and ICC.

Increased level of polymerase III transcribed Alu RNA in hepatocellular carcinoma tissue.

There have been extensive observations that RNA containing repetitive elements accumulates in transformed cells and tumor tissues. In the present study, we first obtained result consistent with previous observations by in situ hybridization. Then we used primer extension analysis to determine the level of polymerase III directed Alu RNA and found an increased expression of Alu RNA in hepatocellular carcinoma.

Effects of SIRPalpha1 on liver regeneration after partial hepatectomy in rat.

BACKGROUND: SIRPalpha1 is well known as a negative regulator for cell proliferation through the regulation of the activity of receptor tyrosine kinase with ITAM motif. No investigation to data was undertaken on SIRPalpha1 involving liver regeneration. MATERIALS AND METHODS: Adult male Sprague-Dawley rats underwent approximately 70% partial hepatectomy (PH) or sham operation (SO). Liver specimens were collected at 2, 6, 12, 24, 30, 48, 72, 120, 168, and 240 h after PH or SO. SIRPalpha1 expression was determined in mRNA level by Northern blotting as well as in protein levels via immunohistochemical staining. RESULTS: SO treatment did not induce remarkable changes in SIRPalpha1 expression; however, the level of a 3.9-kb transcript for SIRPalpha1 was significantly up-regulated after PH (versus SO, P < 0.05). SIRPalpha1 mRNA expression in the regenerating liver displayed a biphasic response with its first large peak at as early as 12h followed by a second phase of up-regulation from 48 to 120 h post-PH. SIRPalpha1 mRNA expression returned to its physiological level 168 h later. As seen from immunohistochemistry experiments, SIRPalpha1 protein mainly located in membrane was expressed uniquely in regenerating hepatocytes. Similarly, PH-induced overexpression for SIRPalpha1 protein occurred between 12 and 168 h with a peak level at 24h after surgery. CONCLUSION: SIRPalpha1, a principle negative regulator for cell proliferation, may also play a role in the termination of hepatic proliferation during liver regeneration induced by physiological stress or pathological states, such as PH, drugs, toxins, etc.

Negative regulation of hepatocellular carcinoma cell growth by signal regulatory protein alpha1.

Signal regulatory protein (SIRP) alpha1 is a member of the SIRP family that undergoes tyrosine phosphorylation and binds SHP-2 tyrosine phosphatase in response to various mitogens. The expression levels of SIRPalpha1 were decreased in HCC tissues, compared with the matched normal tissues. Exogenous expression of wild type SIRPalpha1, but not of a mutant SIRPalpha1 lacking the tyrosine phosphorylation sites, in SIRPalpha1-negative Huh7 human HCC cells resulted in suppression of tumor cell growth both in vitro and in vivo. Treatment of Huh7 transfectants with EGF or HGF induced tyrosine phosphorylation of SIRPalpha1 and its association with SHP-2, which were accompanied by reduced ERK1 activation. Expression of SIRPalpha1 significantly suppressed activation of NF-kappaB and also sensitized Huh7 cells to TNFalpha or cisplatin-induced cell death. In addition, SIRPalpha1-transfected Huh7 cells displayed reduced cell migration and cell spreading in a fashion that was dependent on SIRPalpha1/SHP-2 complex formation. In conclusion, a negative regulatory effect of SIRPalpha1 on hepatocarcinogenesis is exerted, at least in part, through inhibition of ERK and NF-kappaB pathways.