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Purpose It is controversial for the optimal time of breast cancer surgery after COVID-19 infection. Purpose was to assess the risk of postoperative complication in breast cancer patients with COVID-19 infection, in order to select optimal surgery timing after COVID-19 infection. Methods Breast cancer patients infected with COVID-19 and performed surgery between December 20th, 2022 to March 20th, 2023 were included in this prospective study ( n  = 577). Patients performed surgery between May 1, 2019 to October 1, 2019 were listed as control group ( n  = 329). They had not been infected with COVID-19 before surgery. Patients were grouped by time of surgery relative to COVID-19 infection. Database was evaluated using logistic regression. Results Patients infected with COVID-19 had a higher incidence of complications after surgery compared to that not-COVID-19 infection (6.59% vs. 3.04%). Multivariable logistic analysis demonstrated that timing of surgery was associated with complications (OR = 4.253; 95% CI: 0.855–21.153, P =  0.044). Patients performed surgery within 2 weeks after COVID-19 infection had the highest rates of complication (17.65%) when compared with other groups, while the incidence was decreased into 5.51% when surgery 2 weeks or more after COVID-19 infection. With a median follow-up was 10 months, all patients with complications were recovered without serious complications or death, which had no adverse effect on subsequent anti-tumor therapy. Conclusions It needs to be cautious when breast cancer surgery was performed within 2 weeks after COVID-19 infection. Although the incidence of complications in patients undergoing surgery 2 weeks after COVID-19 infection is still slightly high, surgery might be recommended considering urgency of treatment, good prognosis of complications and the lack of influence on subsequent adjuvant therapy.

Background Angiogenesis is a hallmark of cancer and plays a critical role in lung cancer progression, which involves interactions between cancer cells, endothelial cells and the surrounding microenvironment. However, the gene expression profiles and the changes in the biological phenotype of vascular endothelial cells after interactions with lung cancer cells remain unclear. Methods An indirect transwell co-culture system was used to survey the interaction between human umbilical vein endothelial cells (HUVECs) and human lung adenocarcinoma CL1-5 cells, as well as to investigate the morphological and molecular changes of HUVECs. The differentially expressed genes (DEGs) in HUVECs after co-culture with cancer cells were identified by microarray. Moreover, a publicly available microarray dataset of 293 non-small-cell lung cancer (NSCLC) patients was employed to evaluate the prognostic power of the gene signatures derived from HUVECs. Results The interaction between HUVECs and lung cancer cells changes the morphology of HUVECs, causing them to have a mesenchymal-like morphology and alter their cytoskeleton organization. Furthermore, after co-culture with lung cancer cells, HUVECs showed increased cell motility and microvessel tube formation ability and a decreased apoptotic percentage. Transcriptomic profiling of HUVECs revealed that many survival-, apoptosis- and angiogenesis-related genes were differentially expressed after interactions with lung cancer cells. Further investigations showed that the PI3K/Akt signalling pathway and COX-2 are involved in endothelial tube formation under the stimulation of lung cancer cells. Moreover, Rac-1 activation might promote endothelial cell motility through the increased formation of lamellipodia and filopodia. The inhibitors of PI3K and COX-2 could reverse the increased tube formation and induce the apoptosis of HUVECs. In addition, the gene signatures derived from the DEGs in HUVECs could predict overall survival and disease-free survival in NSCLC patients and serve as an independent prognostic factor. Conclusions In this study, we found that cancer cells can promote endothelial cell tube formation and survival, at least in part, through the PI3K/Akt signalling pathway and thus change the microenvironment to benefit tumour growth. The gene signatures from HUVECs are associated with the clinical outcome of NSCLC patients.

Purpose This prospective study aimed to investigate estrogen-induced carcinogenesis by assessing the background levels of abasic sites (apurinic/apyrimidinic sites, AP sites) in Taiwanese breast cancer patients following 5 years of postoperative treatment without recurrence (5-year survivors) (n = 70). The study also sought to compare the extent of these DNA lesions with those found in healthy controls and in breast cancer patients prior to treatment. Methods Abasic sites were measured using an aldehyde reactive probe and quantified as the total number of abasic sites per total nucleotides. Characterization of the abasic sites in subjects recruited for this study was conducted using the abasic site cleavage assay using putrescine or T7 exonuclease (T7 Exo) and/or exonuclease III (Exo III). Results The number of abasic sites detected in 5 year survivors (26.7 ± 10.2 per 106 total nucleotides, n = 70) was significantly reduced by 46.9% compared to those in breast cancer patients before treatment (50.3 ± 59.2 per 106 total nucleotides, P < 0.001), and was similar to the levels observed in healthy controls (23.3 ± 13.5 per 106 total nucleotides, P > 0.05). Further investigation into the specific types of abasic sites indicated that the number of abasic sites excisable by putrescine in controls, breast cancer patients, and 5-year survivors were 63.3%, 78.6%, and 67.7%, respectively. These findings suggest the involvement of oxidative stress rather than depurination/depyrimidination of DNA adducts in the formation of abasic sites. Further analyses were performed using exonuclease cleavage assay to characterize the specific types of abasic sites including 5′-cleaved, 3′-cleaved, intact, and residual abasic sites. Results demonstrated that the proportion of residual abasic sites detected in controls, breast cancer patients, and 5-year survivors were estimated to be 32.7%, 48.8%, and 34.0%, respectively. Conclusion Overall, these findings suggest clear evidence of treatment-related effects on the reduction of levels of abasic sites as well as on the profile of abasic sites in 5 year survivors. Plain language summary Purpose This study aimed to analyze the impact of estrogen on cancer development by measuring the baseline levels of abasic sites—specific types of DNA damage—in Taiwanese breast cancer patients who have survived for five years post-treatment without recurrence. The study compared these levels with those in healthy individuals and breast cancer patients prior to treatment. Methods The study measured abasic sites using an aldehyde reactive probe, assessing them per total nucleotides. The nature of these sites was further analyzed using assays that detect specific cleavages by putrescine, T7 exonuclease, or exonuclease III. Results The findings showed a significant reduction (approximately 47%) in abasic sites in patients five years post-treatment compared to those observed before treatment. The levels in long-term survivors were similar to those in healthy controls. Most of the abasic sites in the study were linked to oxidative stress rather than the breakdown of DNA itself. Additional detailed analysis of these sites was performed, identifying different types of abasic damages. Conclusion The study provides strong evidence that treatment significantly reduces the levels of abasic sites and alters their composition, which may be an important factor in the lack of recurrence in these patients.

During the last decade, abundant ichthyopterygian material has been found from the Triassic of South China as well as the Upper Jurassic and Lower Cretaceous of Europe and South America, significantly expanding our knowledge of ichthyopterygian diversity through the Mesozoic. Previous phylogenetic hypotheses of the group no longer account for these extensive additions, necessitating a new phylogenetic framework for the entire Ichthyopterygia to enable evolutionary studies of the group. We present here a comprehensive phylogenetic hypothesis for Ichthyopterygia based on cladistic analysis of 163 characters coded for 59 ingroup and five outgroup taxa. The monophyly of Ichthyopterygia is strongly supported by a Bremer index value of 7. Five major groups of Ichthyopterygia during the Triassic, viz., Grippioidea, Cymbospondylidae, Mixosauridae, Shastasauridae, and Toretocnemidae, are well supported by Bremer index values between 3 and 5. Major clades that evolved in the Triassic, including Merriamosauria, Euichthyosauria, and Parvipelvia, are also robustly supported, whereas most post-Triassic clades are very weakly supported with a Bremer index value of 1, with a few exceptions, such as Thunnosauria and Ophthalmosauridae. The traditional Shastasauridae is expanded to comprise six genera but excludes Callawayia, which is more closely related to Parvipelvia than to Shastasauridae. ‘C.’ wolonggangensis is a shastasaurid but does not form a monophyletic clade with Callawayia neoscapularis or Guizhouichthyosaurus tangae as previously asserted. The new phylogenetic hypothesis is generally consistent with the stratigraphic occurrences of each taxon especially for the Triassic taxa.

Lung cancer is the leading cause of cancer‐related death worldwide. Thus, developing novel therapeutic agents has become critical for lung cancer treatment. In this study, compound AS7128 was selected from a 2‐million entry chemical library screening and identified as a candidate drug against non‐small cell lung cancer in vitro and in vivo. Further investigation indicated that AS7128 could induce cell apoptosis and cell cycle arrest, especially in the mitosis stage. In addition, we also found that iASPP, an oncogenic protein that functionally inhibits p53, might be associated with AS7128 through mass identification. Further exploration indicated that AS7128 treatment could restore the transactivation ability of p53 and, thus, increase the expressions of its downstream target genes, which are related to cell cycle arrest and apoptosis. This occurs through disruption of the interactions between p53 and iASPP in cells. Taken together, AS7128 could bind to iASPP, disrupt the interaction between iASPP and p53, and result in cell cycle arrest and apoptosis. These findings may provide new insight for using iASPP as a therapeutic target for non‐small cell lung cancer treatment. From a 2‐million entry chemical library screening, we identified compound AS7128 as a candidate drug that against non‐small cell lung cancer. AS7128 could bind to iASPP, enhance the transactivation ability of p53 through decreasing the interaction between iASPP and p53, drive the gene expression of p53 downstream genes, and induce cell cycle M phase arrest and apoptosis.

Nilotinib has been approved for the treatment of Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase (Ph+ CML-CP). However, the real-world evidence of nilotinib in newly diagnosed untreated Ph+ CML-CP is limited in Taiwan. The NOVEL-1st study was a non-interventional, multi-center study collecting long-term safety and effectiveness data in patients with newly diagnosed and untreated Ph+ CML-CP receiving nilotinib. We enrolled 129 patients from 11 hospitals. Overall, 1,466 adverse events (AEs) were reported; among these, 151 were serious and 524 were nilotinib-related. Common hematological AEs were thrombocytopenia (31.0%), anemia (20.9%), and leukopenia (14.0%); common nilotinib-related AEs were thrombocytopenia (29.5%), anemia (14.7%), and leukopenia (12.4%). Early molecular response, defined as BCR-ABL ≤ 10% at Month 3, was seen in 87.6% of patients. By 36 months, the cumulative rates of complete hematologic response, complete cytogenetic response, major molecular response, molecular response 4.0-log reduction, and molecular response 4.5-log reduction were 98.5, 92.5, 85.8, 65.0, and 45.0%, respectively. Nilotinib is effective and well-tolerated in patients with newly diagnosed Ph+ CML-CP in the real-world setting. Long-term holistic care and a highly tolerable AE profile may contribute to good treatment outcomes in Ph+ CML-CP under first-line treatment with nilotinib.

The expressions of different vascular endothelial growth factor (VEGF) isoforms are associated with the degree of tumor invasiveness and the patient's prognosis in human cancers. We hypothesized that different VEGF isoforms can exert different effects on the functional and structural characteristics of tumor angiogenesis. We used dynamic contrast-enhanced MRI (DCE-MRI) and steady-state contrast-enhanced MRI (SSCE-MRI) to evaluate in vivo vascular functions (e.g., perfusion and permeability) and structural characteristics (e.g., vascular size and vessel density) of the tumor angiogenesis induced by different VEGF isoforms (VEGF121, VEGF165, and VEGF189) in a murine xenograft model of human lung cancer. Tumors overexpressing VEGF189 were larger than those overexpressing the other two VEGF isoforms. The K(trans) map obtained from DCE-MRI revealed that the perfusion and permeability functions of tumor microvessels was highest in both the rim and core regions of VEGF189-overexpressing tumors (p<0.001 for both tumor rim and core). The relative vessel density and relative vessel size indexes derived from SSCE-MRI revealed that VEGF189-overexpressing tumors had the smallest (p<0.05) and the most-dense (p<0.01) microvessels, which penetrated deeply from the tumor rim into the core, followed by the VEGF165-overepxressing tumor, whose microvessels were located mainly in the tumor rim. The lowest-density microvessels were found in the VEGF121-overexpressing tumor; these microvessels had a relatively large lumen and were found mainly in the tumor rim. We conclude that among the three VEGF isoforms evaluated, VEGF189 induces the most densely sprouting and smallest tumor microvessels with the highest in vivo perfusion and permeability functions. These characteristics of tumor microvessels may contribute to the reported adverse effects of VEGF189 overexpression on tumor progression, metastasis, and patient survival in several human cancers, including non-small cell lung cancer, and suggest that applying aggressive therapy may be necessary in human cancers in which VEGF189 is overexpressed.

YAG materials have a number of unique properties, the application is very extensive. In order to improving the properties of YAG porous materials, the effect of forming processing on the properties of YAG porous ceramics is investigated. Through the results and analysis, the conclusions showed that the porosity of YAG porous ceramics gradually decreased with the molding pressure increases, and the compressive strength of YAG porous ceramics shows a rising trend. The size and number of pores in the microstructure are reduced with increasing the forming pressure, there are inherently many voids in the YAG porous ceramics body at low forming pressures. The porosity of YAG porous ceramic decreases with the increase of dwell time, however, the process of extending from 5 min to 10 min is much faster than the rate of descending from 10 min to 15 min. The size and number of pores in the microstructure are reduced with extending the holding pressure time, which also makes YAG porous ceramics pose the higher mechanical strength. Through the analysis of the results, when the forming pressure is 10MPa, the porosity of YAG porous ceramics is 41.11% and the compressive strength is 5.8MPa, the porosity and compressive strength of YAG porous ceramics is better.

YAG materials has a number of unique properties, the application is very extensive. In this paper, the superfine YAG powder materials were prepared by hydrothermal precipitation method. The influence of synthesis process on the morphology of the powder was investigated. The results showed that when the molar ratio of salt to alkali that Y3+: OH- is 1:8, the more uniform morphology of the particles can be prepared, when the molar ratio of salt to alkali is increased, the morphology of the particles will not change. The reaction time is longer, the particle size will be thicker. The smaller the concentration of Y3+ ions is, the larger the particle size will be small. The experimental results show that the rod-like particles have a poly-crystal structure at the reaction temperature of 200°C, reaction time of 2 days and the molar ratio of salt to alkali of 1:8. The diameter of the rod-like particles is most of the powders have a particle size of 1000 nm and a small amount of powder has a particle size of about 5000 nm. The purity of powder is higher through the test of XRD.

A high-performance quartz sand insulation brick was prepared by using low grade quartz sand under different sintering process conditions. The optimum sintering process conditions were obtained by analyzing the relationship between microstructure and sintering process. Through the compounding, pulping, forming, drying and sintering processes, and the performance test of the porous brick, the following conclusions can be drawn, the comprehensive performance in all aspects, the porosity is similar, the preferred high compressive strength conditions, in order to get a best The bonding point, brick body sintering temperature of 1150 °C, porosity of 74.56%, compressive strength of 2.1 MPa of porous brick, and the pores are smooth, more uniform distribution. With the prolonging of the holding time, the porosity of the porous brick is reduced, and the performance is 1h, the porosity is 77.22% and the compressive strength is 2.05 MPa. When the raw material ratio is 60% quartz sand, 30wt% kaolin, calcium carbonate 9.6wt%, foaming agent 0.4wt%, water ratio 0.9 holding time at 1h sintering at 1150°C can get better porosity and compressive strength of the insulation brick. The porous material was sintered at 1150 °C, the content of foaming agent was 0.2wt%, the ratio of water to material was 0.9, and the compressive pressure and porosity were the better.