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Background: Mammary carcinoma, a pervasive and potentially lethal affliction, is conjectured to be profoundly influenced by physical exercise, both in prophylaxis and therapeutic contexts. This study endeavors to explore the repercussions of exercise training on the progression of mammary carcinoma, particularly the mechanisms by which the amalgamation of an exercise regimen and doxorubicin induces tumor cell apoptosis. Methods: Female BALB/c mice were categorized into four distinct groups: A sedentary group (SED), an exercise group (Ex), a doxorubicin group (Dox, 5 mg/kg), and a combined treatment group (Dox + Ex). The exercise training lasted for 21 days and included aerobic rotarod exercise and resistance training. The impact of exercise training on tumor growth, immune cell proportions, inflammatory factor levels, and cell apoptosis pathway was assessed. Results: Exercise training significantly curtailed tumor growth in a mouse model of breast cancer. Both the Ex and Dox groups exhibited significant reductions in tumor volume and weight (p < 0.01) in comparison to the SED group, while the Dox + Ex group had a significantly lower tumor volume and weight than the Dox group (p < 0.01). Exercise training also significantly increased the proportion of NK and T cells in various parts of the body and tumor tissue, while decreasing tumor blood vessels density. Exercise training also increased IL‐6 and IL‐15 levels in the blood and altered the expression of apoptosis‐related proteins in tumor tissue, with the combined treatment group showing even more significant changes. Conclusions: Physical training improves the effectiveness of doxorubicin in treating breast cancer by activating cytotoxic immune cells, releasing tumor suppressor factors, and initiating mt‐apoptosis, all while mitigating the adverse effects of chemotherapy. [ABSTRACT FROM AUTHOR]

IGF2BP2 is a new identified N6‐methyladenosine (m6A) reader and associated with poor prognosis in many tumors. However, its role and related mechanism in breast cancer, especially in triple‐negative breast cancer (TNBC), remains unclear. In this study, it is found that IGF2BP2 is highly expressed in TNBC due to the lower methylation level in its promoter region. Functional and mechanical studies displayed that IGF2BP2 could promote TNBC proliferation and the G1/S phase transition of the cell cycle via directly regulating CDK6 in an m6A‐dependent manner. Surprising, the regulation of protein levels of CDK6 by IGF2BP2 is related to the changes in translation rate during translation initiation, rather than mRNA stability. Moreover, EIF4A1 is found to be recruited by IGF2BP2 to promote the translation output of CDK6, providing new evidence for a regulatory role of IGF2BP2 between m6A methylation and translation. Downregulation of IGF2BP2 in TNBC cell could enhance the sensitivity to abemaciclib, a CDK4/6 inhibitor. To sum up, our study revealed IGF2BP2 could facilitate the translation output of CDK6 via recruiting EIF4A1 and also provided a potential therapeutic target for the diagnosis and treatment of TNBC, as well as a new strategy for broadening the drug indications for CDK4/6 inhibitors. [ABSTRACT FROM AUTHOR]

In this work, we investigated the potential for phosphorescent emitters to achieve the BT.2020 color standard in displays, where the CIE coordinates for red and green are (0.709, 0.292) and (0.170, 0.797), respectively. Optical simulations were performed for both green and red top emission organic light emitting devices (OLEDs). For the green emitter, it is possible to reach (0.170, 0.785) using a spectrum with a peak wavelength (λmax) at 526 nm and a full width at half maximum (FWHM) less than 30 nm. For the red emitter, in order to achieve (0.708, 0.292) while maintaining a high current efficiency (CE), it is important to decrease the FWHM instead of red‐shifting the spectrum. Following the guidance of these simulation results, we designed and synthesized novel deep green (DGD) and deep red phosphorescent (DRD‐II) emitters. The photoluminescent (PL) spectrum of DGD shows an FWHM of 30 nm and a λmax of 523 nm. A top‐emission green OLED built using DGD reached a CE of 171 cd/A at an operating voltage of 3.3 V and a lifetime of 95% of initial brightness (LT95) > 1300 h at 10 mA/cm2 with a CIE (x, y) = (0.170, 0.777). This is, to our knowledge, the best device performance ever reported for a green phosphorescent OLED at this CIE y. The PL spectrum of DRD‐II has a λmax of 630 nm with an FWHM of 30 nm. A top‐emission red OLED built with DRD‐II achieved a CE of 59 cd/A, an operating voltage of 3.2 V and an LT95 over 20,000 h at a drive current of 10 mA/cm2 with a CIE (x, y) = (0.708, 0.292). We also studied the angular dependence of the above devices and found they were comparable to devices with commercial emitters for the Digital Cinema Initiative P3 (DCI‐P3) standard that had a wider FWHM. Combining these green and red emitters with a commercial blue OLED at (0.131, 0.046), we are able to cover 97% of the BT.2020 color gamut. The results using DGD and DRD‐II suggest that they have great potential to satisfy BT.2020 in an organic phosphorescent system. [ABSTRACT FROM AUTHOR]

We developed a novel, deep red phosphorescent emitter (DRD‐II), with a photoluminescence (PL) spectrum as narrow as 30 nm at full‐width‐half‐maximum (FWHM). A top‐emission red organic light emitting device (OLED) built with DRD‐II achieved a current efficiency (CE) of 59 cd/A, operating voltage of 3.2 V and lifetime to 95% of initial brightness (LT95) over 20,000 h at a drive current of 10 mA/cm2 with CIE (x, y) = (0.707, 0.293). We also developed a green phosphorescent organic emitter (GD) whose PL spectrum shows FWHM of 30 nm and peak wavelength (λmax) of 523 nm. A top‐emission green OLED was built with this GD and reached CE of 171 cd/A, voltage of 3.3 V and LT95 > 1,300 h at 10 mA/cm2 with CIE (x, y) = (0.169, 0.777). This is, to our knowledge, the best efficiency and lifetime combination ever reported for a green OLED at this CIE y. Combining these red and green emitters with a commercial blue OLED at CIE (0.131, 0.046), we are able to cover 97% of the BT.2020 color gamut. Through optical simulation, we also provide guidance to further improve red and green emitters. It is found that a red emitter with smaller FWHM not only maintains saturated color at a shorter peak wavelength but also gains luminance efficiency owing to the elimination of longer wavelengths. On the other hand, the simulation demonstrates that it is indeed challenging for phosphorescent green emitters to satisfy BT.2020. Nevertheless, it is possible to reach CIE y = 0.785 with a narrow line shape and minimal shoulder peak. [ABSTRACT FROM AUTHOR]

Raman spectroscopy (RS) has been used in clinical diagnostics, tissue engineering, and toxicology experiments owing to its label‐free, low‐destructive, high sensitivity, and strong specificity. Nonetheless, their application has been limited because of the integrated analysis of biological experimental methods and RS. In this study, it was challenged that applied RS in combination with biological experiments to distinguish colorectal cancer (CC) cells from which treated with artesunate (ART), which has obvious antitumor effects. Heavy water (D2O) was used to detect changes in colorectal cancer cell metabolism. The Raman spectral intensity of the C–D band at 2100–2300 cm−1 was significantly weakened in CC (SW480, SW620, and HCT116) treated with ART. According to the CCK‐8, wound healing, and Transwell assays, the activity of SW480 and SW620 cells was significantly inhibited by ART. Through literature tracking and transcriptome sequencing, multiple signal pathways of SW480 and SW620 cells have changed significantly after treatment with ART, such as "apoptotic signaling pathway," "cell cycle phase transition," "mitochondrial part," and "mRNA metabolic process." The Raman peak area significantly decreased at 490 cm−1, 746 cm−1, 1126 cm−1, 1311 cm−1, 1337 cm−1, and 1582 cm−1 in SW480 and SW620 cells treated with ART. It showed that these Raman bands are associated with ART‐induced apoptosis‐related signaling pathways. In addition, we found that application of the RS in cell type identification will be prosperous. By integrating RS with biological mechanisms, its application in the biomedical field is increasing, and its significance in biological sample detection has become more prominent. [ABSTRACT FROM AUTHOR]

The neurotoxicity of local anesthetics (LAs) has attracted more and more attention, However, they lack preventive and therapeutic measures. Many studies have shown that apoptosis plays an important role in the process of LA‐induced neurotoxicity. As an important signaling molecule to activate apoptosis, p53 has been proved to be involved in the neurotoxicity induced by LAs, but the mechanism is unclear. In this study, we explored the effect of pifithrin‐α (PFT‐α), a p53 inhibitor, on apoptosis by ropivacaine (Rop) in vivo and in vitro. Cell viability and apoptosis detected by CCK‐8 and a JC‐1 apoptosis detection kit, the changes of spinal cord structure observed after hematoxylin and eosin staining, apoptosis of the spinal cord measured by terminal deoxynucleotidyl transferase dUTP nick end labeling staining, behavioral assessment of the nerve Injury evaluated by the detection of sciatic nerve conduction velocity (SNCV) andmechanical withdrawal threshold (MWT), the expression of p53 and many apoptosis‐related genes included Bax, Bcl‐2, and caspase‐3 detected by quantitative real‐time polymerase chain reaction, Western blot analysis, immunofluorescence, and immunohistochemistry. Results showed that PC12 cell viability decreased because of Rop, but the pretreatment of PFT‐α could protect it. And PFT‐α reduced the injuries in the spinal cord by Rop included vacuoles or edema. The results of immunofluorescence and immunohistochemistry testing showed that PFT‐α inhibited the p53 protein upregulated by Rop. Apoptosis rate and many proapoptotic genes include p53, Bax, caspase‐3 messenger RNA, and proteins were increased by Rop, but PFT‐α could decrease it. In conclusion, PFT‐α inhibited cell apoptosis and spinal cord injuries induced by Rop. [ABSTRACT FROM AUTHOR]