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The plastic deformation behavior and mechanisms of Co-Cr-Ni-Mo alloy were investigated. The wires were subjected to different reductions using a multi-pass drawing approach and the resulting microstructures were characterized by EBSD and TEM. It was found that the alloy cold-drawn from surface to center exhibited non-uniform radial strain, with decreasing strain from surface to center. As the strain increased, the transverse texture of the alloy evolved from the initial bimodal texture consisting of strong {100}<110> and weak {110}<001> components to bimodal texture with {110}<233> and {112}<111> components, with significant twinning and mirror orientation between twin and matrix. The longitudinal texture evolution of the alloy mainly occurred on the α-fiber line, and ultimately did not form a significant texture due to grain elongation and crystal rotation. The plastic deformation mechanism of the Co-Cr-Ni-Mo alloy was dominated by dislocation slip at lower strain levels, which gradually transitioned to a combination of dislocation slip and twinning at higher strain levels. The deformation twins were typically distributed in high-density dislocation regions, and the twin boundaries transformed into high-angle sub-grain boundaries, hindering the extension of dislocation slip and deformation twin. With the increase in strain, work hardening results in a significant increase in strength and microhardness. [ABSTRACT FROM AUTHOR]

Background: The most common site of metastasis in colorectal cancer (CRC) is the liver and liver metastases occur in more than 50% of patients during diagnosis or treatment. The occurrence of metastasis depends on a series of events known as the invasive-metastasis cascade. Currently, the underlying genes and pathways regulating metastasis initiation in the liver microenvironment are unknown. Methods: We performed systematic CRISPR/Cas9 screening using an in vivo mouse model of CRC liver metastasis to identify key regulators of CRC metastasis. We present the full results of this screen,which included a list of genes that promote or repress CRC liver colonization. By silencing these genes individually, we found that chondroitin sulfate synthase 1 (CHSY1) may be involved in CRC metastasis. We verified the function of CHSY1 and its involvement in liver metastasis of CRC through in vivo and in vitro experiments. Result: The results of TCGA and CRISPR/Cas9 showed that CHSY1 was overexpressed in CRC primary and liver metastasis tissues and indicated a worse clinical prognosis. In vitro and in vivo experiments confirmed that CHSY1 facilitated the liver metastasis of CRC and CHSY1 induced CD8+ T cell exhaustion and upregulated PD-L1 expression. The metabolomic analysis indicated that CHSY1 promoted CD8+ T cell exhaustion by activating the succinate metabolism pathway leading to liver metastasis of CRC. Artemisinin as a CHSY1 inhibitor reduced liver metastasis and enhanced the effect of anti-PD1 in CRC. PLGA-loaded Artemisinin and ICG probe reduced liver metastasis and increased the efficiency of anti-PD1 treatment in CRC. Conclusion: CHSY1 could promote CD8+ T cell exhaustion through activation of the succinate metabolic and PI3K/AKT/HIF1A pathway, leading to CRC liver metastasis. The combination of CHSY1 knockdown and anti-PD1 contributes to synergistic resistance to CRC liver metastasis. Artemisinin significantly inhibits CHSY1 activity and in combination with anti-PD1 could synergistically treat CRC liver metastases. This study provides new targets and specific strategies for the treatment of CRC liver metastases, bringing new hope and benefits to patients. [ABSTRACT FROM AUTHOR]

Cervical squamous cell carcinoma (CSCC) is one of the leading causes of cancer death in women worldwide. Patients with advanced cervical carcinoma always have a poor prognosis once resistant to cisplatin due to the lack of effective treatment. It is urgent to investigate the molecular mechanisms of cisplatin resistance. Circular RNAs (circRNAs) are known to exert their regulatory functions in a series of malignancies. However, their effects on CSCC remain to be elucidated. Here, we found that cytoplasmic circARHGAP5, derived from second and third exons of the ARHGAP5 gene, was downregulated in cisplatin‐resistant tissues compared with normal cervix tissues and untreated cervical cancer tissues. In addition, experiments from overexpression/knockdown cell lines revealed that circARHGAP5 could inhibit cisplatin‐mediated cell apoptosis in CSCC cells both in vitro and in vivo. Mechanistically, circARHGAP5 interacted with AU‐rich element RNA‐binding protein (AUF1) directly. Overexpression of AUF1 could also inhibit cell apoptosis mediated by cisplatin. Furthermore, we detected the potential targets of AUF1 related to the apoptotic pathway and found that bcl‐2‐like protein 11 (BIM) was not only negatively regulated by AUF1 but positively regulated by circARHGAP5, which indicated that BIM mRNA might be degraded by AUF1 and thereby inhibited tumor cell apoptosis. Collectively, our data indicated that circARHGAP5 directly bound to AUF1 and prevented AUF1 from interacting with BIM mRNA, thereby playing a pivotal role in cisplatin resistance in CSCC. Our study provides insights into overcoming cancer resistance to cisplatin treatment. [ABSTRACT FROM AUTHOR]

Background. Approximately 10% of cancer patients worldwide have colorectal cancer (CRC), a prevalent gastrointestinal malignancy with substantial mortality and morbidity. The purpose of this work was to investigate the APOC1 gene's expression patterns in the CRC tumor microenvironment and, using the findings from bioinformatics, to assess the biological function of APOC1 in the development of CRC. Methods. The TCGA portal was employed in this investigation to find APOC1 expression in CRC. Its correlation with other genes and clinicopathological data was examined using the UALCAN database. To validate APOC1's cellular location, the Human Protein was employed. In order to forecast the relationship between APOC1 expression and prognosis in CRC patients, the Kaplan–Meier plotter database was used. TISIDB was also employed to evaluate the connection between immune responses and APOC1 expression in CRC. The interactions of APOC1 with other proteins were predicted using STRING. In order to understand the factors that contribute to liver metastasis from CRC, single-cell RNA sequencing (scRNA-seq) was done on one patient who had the disease. This procedure included sampling preoperative blood and the main colorectal cancer tissues, surrounding colorectal cancer normal tissues, liver metastatic cancer tissues, and normal liver tissues. Finally, an in vitro knockdown method was used to assess how APOC1 expression in tumor-associated macrophages (TAMs) affected CRC cancer cell growth and migration. Results. When compared to paracancerous tissues, APOC1 expression was considerably higher in CRC tissues. The clinicopathological stage and the prognosis of CRC patients had a positive correlation with APOC1 upregulation and a negative correlation, respectively. APOC1 proteins are mostly found in cell cytosols where they may interact with APOE, RAB42, and TREM2. APOC1 was also discovered to have a substantial relationship with immunoinhibitors (CD274, IDO1, and IL10) and immunostimulators (PVR, CD86, and ICOS). According to the results of scRNA-seq, we found that TAMs of CRC tissues had considerably more APOC1 than other cell groups. The proliferation and migration of CRC cells were impeded in vitro by APOC1 knockdown in TAMs. Conclusion. Based on scRNA-seq research, the current study shows that APOC1 was overexpressed in TAMs from CRC tissues. By inhibiting APOC1 in TAMs, CRC progression was reduced in vitro, offering a new tactic and giving CRC patients fresh hope. [ABSTRACT FROM AUTHOR]

Simple Summary: Breast cancer is one of the most common malignant tumors in women. Its incidence rate accounts for 7–10% of all kinds of malignant tumors in the whole body, second only to uterine cancer in women, and has become the main cancer threatening women's health. Fortunately, it has been proved that combination therapy of immunotherapy with radiotherapy, targeted technology, and even nanotechnology is active and effective in treating breast cancer, which provides a broader way of studying the treatment of breast cancer. Therefore, the purpose of our review is to study the value of immunotherapy in breast cancer treatment. Moreover, because the treatment of triple-negative breast cancer (TNBC) is difficult, we will discuss this in more detail in this article. Breast cancer (BC) is a representative malignant tumor that affects women across the world, and it is the main cause of cancer-related deaths in women. Although a large number of treatment methods have been developed for BC in recent years, the results are sometimes unsatisfying. In recent years, treatments of BC have been expanded with immunotherapy. In our article, we list some tumor markers related to immunotherapy for BC. Moreover, we introduce the existing relatively mature immunotherapy and the markers' pathogenesis are involved. The combination of immunotherapy and other therapies for BC are introduced in detail, including the combination of immunotherapy and chemotherapy, the combined use of immunosuppressants and chemotherapy drugs, immunotherapy and molecular targeted therapy. We summarize the clinical effects of these methods. In addition, this paper also makes a preliminary exploration of the combination of immunotherapy, radiotherapy, and nanotechnology for BC. [ABSTRACT FROM AUTHOR]

Simple Summary: Triple-negative breast cancer (TNBC) is a type of breast cancer characterized by a lack of hormone receptors expression and HER2 gene amplification, which presents with a high probability of metastasis. Bone marrow mesenchymal stem cell-derived exosomes have an influence in the development of various tumors. This study set out to analyze the interaction of the ALKBH5/UBE2C/p53 axis and the molecular mechanism mediated by BMSC-Exos in the stemness property of TNBC cells based on the data of The Cancer Genome Atlas and Gene Expression Omnibus as well as in vivo animal experiments. which renders varieties of potential molecular targets in cancer therapy of TNBC. Background: Abnormal N6-methyladenosine (m6A) modification caused by m6A regulators is a common characteristic in various tumors. However, little is known about the role of m6A regulator AlkB homolog 5 (ALKBH5) in triple-negative breast cancer (TNBC). In this study, we analyzed the influence of ALKBH5 on the stemness of TNBC and the molecular mechanism using bioinformatics analysis and in vivo animal experiments. Methods: RNA expression data and single-cell RNA sequencing (scRNA-seq) data were downloaded from the TCGA and GEO databases. Following intersection analysis, key genes involved in the TNBC cell stemness were determined, which was followed by functional enrichment analysis, PPI and survival analysis. Exosomes were extracted from bone marrow mesenchymal stem cells (BMSC-Exos) where ALKBH5 inhibition assay was conducted to verify their function in the biological characteristics of TNBC cells. Results: Bioinformatics analysis revealed 45 key genes of ALKBH5 regulating TNBC cell stemness. In addition, UBE2C was predicted as a key downstream gene and p53 was predicted as a downstream signaling of ALKBH5. In vivo data confirmed that ALKBH5 upregulated UBE2C expression by regulating the m6A modification of UBE2C and reduced p53 expression, thus promoting the stemness, growth and metastasis of TNBC cells. BMSC-Exos suppressed the tumor stemness, growth and metastasis of TNBC cells and ALKBH5 shRNA-loaded BMSC-Exos showed a more significant suppressive role. Conclusion: Taken together, our findings indicated that ALKBH5 shRNA-loaded BMSC-Exos reduced TNBC cell stemness, growth and metastasis and define a promising strategy to treat TNBC. [ABSTRACT FROM AUTHOR]

Whether the ore-forming fluids and materials of Zhaishang Carlin/Carlin-like type gold deposit were derived from concealed Mesozoic intermediate–acidic intrusive rocks through deep faults is controversial. In this study, eight CSAMT profiles were used to investigate the electrical resistivity structure of this deposit using high-resolution 2-D inversion. A ∼1 km wide high-resistivity (>3000 Ωm) body was observed at the base of the resistivity model (∼600 m). Two slightly NE-dipping high-conductivity channels were also observed along two sides of the high-resistivity body that connected to the gold-bearing quartz veins at the surface. The data suggest that the high-resistivity body is a Mesozoic granite and the two high-conductivity channels are fault zone conductors, which may be the wings of an NE-trending anticline that formed under regional compressive stress during the Caledonian orogeny. Their reactivation during the Indosinian and Yanshanian periods likely formed conduits for rising deeply-sourced ore-forming fluids (likely magmatic water). These conduits also promoted ground and meteoric water infiltration and mixing with the rising fluids. Accordingly, at least some of the ore-forming fluids and materials in the Zhaishang deposit were derived from Mesozoic granites through concealed faults, which can provide new geophysical constraints for discussions of the deposit's metallogenic mechanism. [ABSTRACT FROM AUTHOR]

Immunotherapy treatments, particularly immune checkpoint blockade, can result in benefits in clinical settings. But many pre-clinical and clinical studies have shown that resistance to anti-PD1 therapy frequently occurs, leading to tumor recurrence and treatment failure, including in patients with hepatocellular carcinoma (HCC). In this study, 10 patients with HCC were remedied with anti-PD1, and pre-treatment biopsy samples were sequenced for 289 nanostring panel RNA to compare responsive and non-responsive tumors to identify possible pretreatment biomarkers or targets of anti-PD1 therapeutic responses. Fortunately, the expression of β-Glucuronidase (GUSB) in the non-responding tumors was found to be remarkably higher than that in responding tumors. Results of the cell counting kit 8 (CCK8), 5-ethynyl-2'-deoxyuridine (EdU), transwell, wound healing test, and flow cytometry showed that GUSB facilitated proliferation, invasion, as well as migration of human HCC cells and downregulated PD-L1 expression by promoting miR-513a-5p. Additionally, as a GUSB inhibitor, amoxapine can reduce the progression of human HCC cells, and was an effective treatment for HCC and improved the sensitivity of anti-PD1 therapy. In summary, this study reveals that increased GUSB downregulates PD-L1 expression by promoting miR-513a-5p, leading to primary resistance to anti-PD1 treatment in HCC, and amoxapine enhances the sensitivity of anti-PD1 therapy by inhibiting GUSB, providing a new strategy and method for improving the efficacy of anti-PD1 therapy and bringing new prospects for therapy of HCC. [ABSTRACT FROM AUTHOR]

Background. Breast cancer (BC) is the most commonly diagnosed cancer in women worldwide. The challenge in managing this heterogeneous malignancy is that BC is highly aggressive and is always associated with chemical resistance, radiation resistance, hormone therapy resistance, and targeted therapy resistance. Therefore, there is an urgent need to find effective drugs to treat BC. Methods. Based on the Selleck drug library approved by FDA, we screened 800 drugs for anti-BC cells and found that tegaserod maleate (TM), a 5-hydroxytryptamine 4-receptor (HTR4) partial agonist had the best anti-BC effect, which was further verified. The effects of different concentrations of TM on cell proliferation, invasion, and migration were evaluated in vitro using CCK8, plate cloning, transwell, and scratch assays. The UALCAN database, Kaplan–Meier Plotter database, Human Protein Atlas, and GEPIA2 were used to explore the correlation between HTR4 expression and BC patients' clinicopathological data as well as immune response. In vivo experiments demonstrated the effect of the TM and immunotherapy drug (anti-PD1/anti-TIGIT) combination on BC tumor growth in mice. Results. TM significantly inhibited the proliferation, invasion, and migration of BC cells, and the higher the concentration, the better the inhibition effect. HTR4 was significantly downregulated in BC tissues compared to paracancerous tissues. The downregulation of HTR4 was correlated with clinicopathological data and positively correlated with BC prognosis. Interestingly, the GEPIA2 database suggested that there was a strong positive correlation between the expression of HTR4 and effector T cells, effector memory T cells, and exhausted T cells. In vitro experiments showed that TM, anti-PD1, and anti-TIGIT could all inhibit the growth and weight of BC tumors as compared with the control group. However, when anti-PD1 or anti-TIGIT was used simultaneously with TM, the inhibition of tumors significantly exceeded that in the control group. Moreover, the combination of anti-TIGIT and TM has the best inhibitory effect. Conclusion. TM inhibited the progression of breast cancer, and its combination with anti-TIGIT could effectively inhibit tumor growth and improve the sensitivity of immunotherapy in breast cancer. [ABSTRACT FROM AUTHOR]

Cervical cancer (CC) remains one of the leading causes of mortality of female cancers worldwide, with more than 90% being cervical squamous cell carcinoma (CSCC). ΔNp63α is the predominant isoform expressed in cervical epithelial tissues and exerts its antitumor function in CSCC. In this study, we have identified 39 long noncoding RNAs as ΔNp63α targets in CSCC through RNA sequencing and chromatin immunoprecipitation sequencing, in which we further confirmed and focused on the two tumor‐related long noncoding RNAs, PART1 (lncPART1) and MIR17HG (lncMIR17HG). Experiments from stable overexpression/knockdown cell lines revealed that lncPART1 and lncMIR17HG regulated cell proliferation, migration, and invasion. In vivo experiments further showed that lncPART1 suppresses tumor growth in CSCC‐derived tumors. Examinations of clinical tissues indicated that the expression of lncPART1 was positively correlated with ΔNp63α expression, while lncMIR17HG was negatively correlated with ΔNp63α expression, suggesting that ΔNp63α plays a central role via regulating its direct targets in the progression of CSCC. These findings provide novel insights in targeted therapy of cervical cancers. [ABSTRACT FROM AUTHOR]

Zinc (Zn) has an existence within large quantities in the human brain, while accumulating within synaptic vesicle. There is growing evidence that Zn metabolic equilibrium breaking participates into different diseases (e.g., vascular dementia, carcinoma, Alzheimer's disease). Carnosine refers to an endogenic dipeptide abundant in skeletal muscle and brains and exerts a variety of positive influences (e.g., carcinoma resistance, crosslinking resistance, metal chelation and oxidation limitation). A complex of Zn and carnosine, called Zinc- L -carnosine (ZnC), has been extensively employed within Zn supplement therapeutic method and the treating approach for ulcers. ZnC has been shown to play a variety of roles in the body, including inhibiting intracellular reactive oxygen species(ROS) and free radical levels, inhibiting inflammation, supplementing zinc enzymes and promoting wound healing and mucosal cell repair. The present study conducting a reviewing process for the advances of ZnC in tumor adjuvant therapy. [ABSTRACT FROM AUTHOR]

Breast cancer is the most common malignant tumor in women and the leading cause of cancer death in women. About 30% of breast cancer patients have metastasis every year, which greatly increases the mortality rate of breast cancer. The main target organs for metastasis are bone, brain, liver and lung. The breast cancer liver metastasis (BCLM) mechanism is not fully clarified. This is a complex process involving multiple factors, which is not only related to the microenvironment of the primary tumor and liver, but also regulated by a variety of signaling pathways. Clarifying these mechanisms is of great help to guide clinical treatment. With the in-depth study of BCLM, a variety of new treatment schemes such as targeted therapy and endocrine therapy provide new ideas for the cure of BCLM. In this review, we will summarize the molecular mechanism and treatment of BCLM. [ABSTRACT FROM AUTHOR]

• Lnc-LIF-AS can promote the proliferation of cervical cancer cells. • Lnc-LIF-AS can promote the migration and invasion of cervical cancer cells. • Lnc-LIF-AS will be a new biomarker or therapeutic target for cervical cancer. This study explored the effect of LncRNA Lnc-LIF-AS on cell proliferation, migration and invasion in the human cervical cancer (HCC) cell line SiHa. SiHa cells had the lowest expression of Lnc-LIF-AS in the 4 human cervical cancer cell lines (SiHa, ME-180, C-33A and HeLa) and were transfected and divided into the SiHa/con (transfected with pMIGRI) cell group, SiHa/Lnc-LIF-AS (transfected with pMIGRI-Lnc-LIF-AS) cell group, and SiHa/Lnc-LIF-AS-DN (transfected with pMIGRI-Lnc-LIF-AS-DN, in which the sequences overlapping with LIF mRNA was deleted) cell group. Overexpression of Lnc-LIF-AS could promote the proliferation, colony formation, invasion and migration in SiHa and ME-180 cells. And the low expression of Lnc-LIF-AS suppress the proliferation, colony formation invasion and migration in HeLa cells when the Lnc-LIF-AS expression has been suppressed. In the SiHa/Lnc-LIF-AS cells group, the cell cycle was mainly halted in the S phase and overexpression of Lnc-LIF-AS had no effect on the apoptosis of SiHa cells. Overexpression of Lnc-LIF-AS could promote the secretion of LIF in SiHa cells, and the supernatant from SiHa/Lnc-LIF-AS cells could promote cell proliferation in the SiHa/con cells. The STAT3 inhibitor could inhibit cell proliferation in the SiHa/Lnc-LIF-AS cells. The expression level of Lnc-LIF-AS in cervical cancer tissues was higher than that in normal tissues and the expression level of Lnc-LIF-AS was positively correlated with the level of LIF. In the SiHa/con and SiHa/Lnc-LIF-AS-DN cell groups, there were no significant differences in cell proliferation, cell migration and cell invasion. The overexpression of Lnc-LIF-AS can promote cell proliferation, migration and invasion in cervical cancer cells, and the core function domain of this lncRNA was located in the overlapping a 3′-UTR base sequence of LIF mRNA. [ABSTRACT FROM AUTHOR]

The crystal structures and magneto-transport properties of GdIn 3− x Mn x have been investigated using X-ray diffraction and magnetic and electric measurements. GdIn 3− x Mn x crystallize in cubic structure, and their lattice parameters tend to decrease with increasing Mn content due to the size effect at In site by Mn substitution for In. Mn doped GdIn 3− x Mn x order antiferromagnetically at low temperature. However, Mn doping into GdIn 3 causes the decrease of Néel temperature due to the distortion of Gd(In,Mn) 3 tetrahedron formed by Gd at corners and (In,Mn) at face centers in unit cell. The resistivities of GdIn 3− x Mn x are going up with increasing Mn content. The electric phase transition is associated with the magnetic transition, and the magneto-transport follows electron–magnon scattering model in low temperature region and the Stoner spin fluctuation model in high temperature region, respectively. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic has affected millions of people and posed an unprecedented burden on healthcare systems and economies worldwide since the outbreak of the COVID-19. A considerable number of nations have investigated COVID-19 and proposed a series of prevention and treatment strategies thus far. The pandemic prevention strategies implemented in China have suggested that the spread of COVID-19 can be effectively reduced by restricting large-scale gathering, developing community-scale nucleic acid testing, and conducting epidemiological investigations, whereas sporadic cases have always been identified in numerous places. Currently, there is still no decisive therapy for COVID-19 or related complications. The development of COVID-19 vaccines has raised the hope for mitigating this pandemic based on the intercross immunity induced by COVID-19. Thus far, several types of COVID-19 vaccines have been developed and released to into financial markets. From the perspective of vaccine use in globe, COVID-19 vaccines are beneficial to mitigate the pandemic, whereas the relative adverse events have been reported progressively. This is a review about the development, challenges and prospects of COVID-19 vaccines, and it can provide more insights into all aspects of the vaccines. [Display omitted] ● COVID-19 and immune system. ● The Evolution of COVID-19 vaccines. ● Classification of vaccines. ● Adverse reactions of vaccines. ● Vaccination strategies. ● The VOCs of COVID-19 and the second-generation vaccines. [ABSTRACT FROM AUTHOR]

Apolipoprotein E (ApoE) is a multifunctional protein involved in lipid transport and lipoprotein metabolism, mediating lipid distribution/redistribution in tissues and cells. It can also regulate inflammation and immune function, maintain cytoskeleton stability, and improve neural tissue Function. Due to genetic polymorphisms of ApoE (ε2, ε3, and ε4), its three common structural isoforms (ApoE2, ApoE3, ApoE4) are also associated with the risk of many diseases, especially degenerative diseases, such as vascular degenerative diseases including atherosclerosis (AS), coronary heart disease (CHD), and neurodegenerative disease like Alzheimer's disease (AD). The frequency of the ε4 allele and APOE variants were significantly higher than that of the ε2 and ε3 alleles in the patients with CHD or AD. In recent years, ApoE has frequently appeared in tumor research and become a tumor biomarker gradually. It has been found that ApoE is highly expressed in most solid tumor tissues, such as glioblastoma, gastric cancer, pancreatic ductal cell carcinoma, etc. Studies illustrated that ApoE could regulate the polarization changes of macrophages, participate in the construction of tumor immune microenvironment, regulate tumor inflammation and immune response and play a role in tumor progression, invasion, and metastasis. Of course, many functions of ApoE and its relationship with diseases are still under research. By reviewing the structure and function of ApoE from degeneration diseases to tumor neoplasms, we hope to better understand such a biomarker and further explore the value of ApoE in later studies. • The Character and Function of ApoE. • ApoE gene polymorphism and degenerative disease. • ApoE gene polymorphism associated with CAD. • ApoE is as a "bifacial" Biomarker for malignant tumors. • 5. ApoE and potential therapies [ABSTRACT FROM AUTHOR]

Continuous Al 2 O 3 fiber reinforced TiAl composite (Al 2 O 3,f /TiAl) is expected to be promising to satisfy the tougher conditions in space industry. However, the thermostability of Al 2 O 3 fibers in TiAl alloy has not been well studied. In this work, continuous Al 2 O 3 fibers (containing 28 mol.% SiO 2) have been introduced in Ti-48Al-4Nb-2Cr alloy by powder metallurgy technology at different hot pressing temperatures. The erosion reactions of Al 2 O 3 fibers in TiAl matrix have been investigated by thermodynamic calculation. A evolution model of the interface regions has been established. It has been determined in this study that micropores can be eliminated completely at hot pressing temperature of 1050 °C while ensuring the integrity of Al 2 O 3 fibers. Thermal exposure tests revealed the erosion reaction of fibers was mainly dominated by element diffusions of Ti and Si, and the erosion product was determined to be Ti 5 Si 3. Based on the regulation of erosion reactions, a novel multilayer fiber structure with higher modulus has been achieved which could be matched with TiAl alloy and expected to improve strength/toughness of the Al 2 O 3,f /TiAl composite. This structure contains a core of original fiber and coated by three composite ceramic layers, which can be obtained at hot pressing condition of 1050 °C/50 MPa/2 h and thermal exposure of 1050 °C/60 min • Erosion reaction is mainly dominated by element diffusions of Ti and Si, and the erosion product is Ti 5 Si 3. • Al 2 O 3 fibers would be eroded into a network structure containing Al 2 O 3 and Ti 5 Si 3. • A multilayer fiber structure could be matched with TiAl matrix for strengthening and toughening Al 2 O 3 ,f/TiAl compositess. [ABSTRACT FROM AUTHOR]

Despite substantial breakthroughs in the treatment of hepatocellular carcinoma (HCC) in recent years, many patients are diagnosed in the middle or late stages, denying them the option for surgical excision. Therefore, it is of great importance to find effective therapeutic targets of HCC. In this study, it is found that Gap junction protein beta-2 (GJB2) is highly enriched in malignant cells based on single-cell RNA sequencing and higher expression of GJB2 indicates a worse prognosis. The localization of GJB2 in HCC cancer cells is changed compared with normal liver tissue. In cancer cells, GJB2 tends to be located in the cytoplasm and nucleus, while in normal tissues, GJB2 is mainly located on the cell membrane. GJB2 is related to glycolysis, promoting NF-κB pathway via inducing the ubiquitination degradation of IκBa, and activating HIF-1α/GLUT-1/PD-L1 pathway. In addition, GJB2 knockdown reshapes tumor immune microenvironment and Salvianolic acid B inhibits the activity of GJB2. In conclusion, GJB2 promotes HCC progression by activating glycolysis through cytoplasmic translocation and generating a suppressive tumor microenvironment. Salvianolic acid B inhibits the expression of GJB2 and enhances the sensitivity of anti-PD1 therapy, which may provide insights into the development of novel combination therapeutic strategies for HCC., (© 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH.)

A new type of small-period long-period fiber grating (SP-LPFG) consisting of a series of annuli inscribed by a femtosecond laser in a single-mode fiber is proposed and demonstrated. The effects of the annuli radii and the number of annuli in each period on the transmission spectrum are studied. The transmission spectrum of the annular SP-LPFG exhibits both strong Bragg resonances and cladding mode resonances, which have similar temperature sensitivities of 9.26 and 9.75 pm/°C, respectively. The Bragg resonances are insensitive to the change of environment refractive index (RI), while the cladding mode resonances show a RI sensitivity of 141.89 nm/RIU. The proposed sensor offers a potential solution for biomolecular sensing applications by effectively eliminating the issue of temperature cross-sensitivity. Its compact design and ease of spectral acquisition enhance its practicality and convenience.

Hepatocellular carcinoma (HCC) is responsible for a significant number of cancer-related deaths worldwide and its incidence is increasing. Locoregional treatments, which are precision procedures guided by imaging to specifically target liver tumors, play a critical role in the management of a substantial portion of HCC cases. These therapies have become an essential element of the HCC treatment landscape, with transarterial chemoembolization (TACE) being the treatment of choice for patients with intermediate to advanced stages of the disease. Other locoregional therapies, like radiofrequency ablation, are highly effective for small, early-stage HCC. Nevertheless, the advent of targeted immunotherapy has challenged these established treatments. Tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors (ICIs) have shown remarkable efficacy in clinical settings. However, their specific uses and the development of resistance in subsequent treatments have led clinicians to reevaluate the future direction of HCC therapy. This review concentrates on the distinct features of both systemic and novel locoregional therapies. We investigate their effects on the tumor microenvironment at the molecular level and discuss how targeted immunotherapy can be effectively integrated with locoregional therapies. We also examine research findings from retrospective studies and randomized controlled trials on various combined treatment regimens, assessing their validity to determine the future evolution of locoregional therapies within the framework of personalized, comprehensive treatment., (Copyright ©2024 Chinese Journal of Cancer Research. All rights reserved.)

Creating a vivid video from the event or scenario in our imagination is a truly fascinating experience. Recent advancements in text-to-video synthesis have unveiled the potential to achieve this with prompts only. While text is convenient in conveying the overall scene context, it may be insufficient to control precisely. In this paper, we explore customized video generation by utilizing text as context description and motion structure (e.g. frame- wise depth) as concrete guidance. Our method, dubbed Make-Your-Video, involves joint-conditional video generation using a Latent Diffusion Model that is pre-trained for still image synthesis and then promoted for video generation with the introduction of temporal modules. This two-stage learning scheme not only reduces the computing resources required, but also improves the performance by transferring the rich concepts available in image datasets solely into video generation. Moreover, we use a simple yet effective causal attention mask strategy to enable longer video synthesis, which mitigates the potential quality degradation effectively. Experimental results show the superiority of our method over existing baselines, particularly in terms of temporal coherence and fidelity to users' guidance. In addition, our model enables several intriguing applications that demonstrate potential for practical usage. The code, model weights, and videos are publicly available at our project page: https://doubiiu.github.io/projects/Make-Your-Video/.