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Human umbilical cord matrix Wharton's jelly mesenchymal stem cells (WJ-MSCs) are commonly utilized in regenerative medicine due to their therapeutic benefits. However, the microenvironmental stress present in patients with hyperglycemia can significantly reduce mesenchymal stem cell (MSC) viability under high-glucose conditions in the body, ultimately reducing their therapeutic effectiveness. Enhancing the survival rate of MSCs following cell transplantation remains a crucial challenge. This study investigates whether Quantum Hyperlight (QHL) can counteract the detrimental effects of high glucose (HG), thereby improving MSC survival, proliferation, and mitochondrial function. We aimed to evaluate the effect of QHL on cellular viability, proliferation, and mitochondrial activity in WJ-MSCs exposed to HG. MSCs were cultured in a medium containing normal glucose (NG) (1 g/L) and HG (4.5 g/L). MSCs in the HG medium were exposed to QHL for 90 s or 180 s with an energy density of 2.4 Joules/cm 2 /minute and an average power density of 40 mW/cm 2 . Then, proliferating cell nuclear antigen (PCNA), MTT assays, and Mitotracker Green staining were performed to evaluate cell viability and proliferation. The viability of MSCs was significantly increased in the QHL-treated groups (84% in QHL-90 s and 86% in QHL-180 s) compared to the untreated HG group (65%, p < 0.001). PCNA expression in QHL-90 s and QHL-180 s groups showed significant increases (p < 0.001) compared to the untreated HG group. MitoTracker staining intensity was significantly higher in the QHL-treated groups compared to the untreated HG group (p < 0.001). The HG environment reduced viability, proliferation, and mitochondrial staining. In the context of the NG environment, MSCs exhibited notable differences. However, the viability, proliferation, and mitochondrial staining rates of MSCs were significantly higher in the HG conditions when treated with QHL compared to the group that did not receive QHL. This study introduces QHL as a novel approach to enhance the therapeutic potential of WJ-MSCs under HG conditions, demonstrating its ability to improve cellular viability, proliferation, and mitochondrial activity. This study highlights its potential as a pretreatment to improve clinical outcomes in regenerative medicine., Competing Interests: Declarations. Ethics statement: This study was approved by the Institutional Ethics Committee under approval number [2023/4434, ID:15078]. Although commercially available WJ-MSCs were used (ATCC, PCS-500–010, Manassas, USA), ethical approval was obtained to ensure compliance with institutional and regulatory guidelines for stem cell research. Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

One of the formidable challenges that may emerge in patients with breast cancer is drug resistance which is highly correlated with failure in cancer therapy and, as a result, poorer prognosis. Thus, developing novel approaches to overcome this undesirable event has always been a hot topic in the field of cancer. Photobiomodulation (PBM), also known as low-level laser therapy, is one such approach that has recently been introduced as a promising modality in clinical settings with interesting anti-tumor properties. Moreover, PBM has been considered a possible candidate to be employed in conjunction with conventional modalities such as chemotherapy. The present study investigated the potential effects of PBM at two wavelengths of 630 nm and 980 nm on chemoresistance in breast cancer MDA-MB-231 cells, which previously acquired resistance to doxorubicin (DOX) through 12 passages. Findings proposed that PBM, in conjunction with DOX, led to a reduction in the viability of resistant MDA-MB 231 cells as was evidenced by decreased IC 50 values of DOX across different groups. Furthermore, gene expression studies demonstrated that PBM inhibited the overexpression of some of the important resistance-related genes, including SOX9, MDR1, NRF2, TGF-β, and ABCC1. Although both wavelengths had considerable efficiency, at 630 nm, PBM performed better in overcoming DOX resistance. Overall, the present study suggests that PBM might play a promising role against breast cancer via reducing chemoresistance which, indeed, necessitates further research to better understand its mechanisms and clinical potential for translation., Competing Interests: Declarations. Ethics statement: Approval of the research protocol by an Institutional Reviewer Board: The research and ethics committee of the Shahid Beheshti University of Medical Sciences, Laser Application in Medical Sciences Research Center has approved this study. Competing interests: The authors declare no competing interests., (© 2025. The Author(s), under exclusive licence to Springer-Verlag London Ltd., part of Springer Nature.)

Efficacy of radiation therapy is compromised by hematopoietic and immune impairments, with elusive underlying causes. This study aimed to elucidate Usp11's role in radiation-induced injuries and uncover related mechanisms. Utilized ARS mouse model to observe survival rates of Usp11 -/- (KO) mice post-TBI (Total Body Irradiation). Assessed lymphocyte and MZ B (Marginal Zone B) cell rates using histological analysis, single-cell sequencing, immunofluorescence (IF), immunohistochemistry (IHC), and flow cytometry (FCM). Conducted Co-IP and ubiquitination experiments for mechanism elucidation. Quantified IgM and IgG using ELISA and FC. Explored public databases for potential correlation molecules. Our findings indicated that Usp11 -/- mice exhibited improved survival rates following TBI, with the spleen playing a pivotal role. HE staining revealed a wider marginal zone in the spleen of Usp11 +/+ mice post-irradiation. Single-cell sequencing, IF, IHC, and FCM analyses revealed a higher survival rate of MZ B cells in Usp11 -/- mice after irradiation. Furthermore, treatment with the Usp11 inhibitor, mitoxantrone, successfully targeted and inhibited Usp11, thereby alleviating the reduction in MZ B cells in the spleen following total body irradiation. Mechanistically, Usp11 sustained the survival of MZ B cells by regulating the ubiquitination of Notch's ligands, DLL1 and JAG2, thereby promoting immune cell remodeling in the spleen. In conclusion, Usp11 played a crucial role in modulating immune system damage induced by ionizing radiation, primarily through ubiquitination of Notch ligands. This study provides insights into radiation-induced immune injuries and suggests Usp11 as a potential therapeutic target., Competing Interests: Competing interests: The authors declare no competing interests. Ethics approval: All animal studies were approved by the Ethics Committee of School of Soochow University., (© 2025. The Author(s).)

The escalating utilization of wireless electronic devices, notably cellular phones, has led to a substantial augmentation in the levels of electromagnetic field radiation (EMF-r) within the environment. Consequently, an imperative arises to investigate the impact of these radiations on biological systems, specifically on plants. In this study, we examined the genotoxic and cytotoxic effects of 2100 MHz and 2300 MHz EMF-r on the Trigonella foenum-graecum L. test system, evaluating parameters such as percentage germination, growth characteristics, biochemical activities, cell viability and chromosomal aberrations. The roots and shoots of T. foenum-graecum L. were exposed to 2100 MHz and 2300 MHz EMF-r for varied exposure durations (0.5 h, 1 h, 2 h, 4 h and 8 h/day) (at a power density of 10.0 dBm). Substantial reductions in root and shoot lengths were observed after a exposure period of 4 h and 8 h at a frequency of 2100 MHz and 2300 MHz. Genotoxic studies revealed both physiological and clastogenic effects of EMF-r, as evidenced by an increase in chromosomal aberrations (CAs). Biochemical analyses demonstrated elevated malondialdehyde levels and activities of various antioxidative enzymes following 2 h and 4 h per day exposure to 2100 MHz and 2300 MHz EMF-r. Chromosomal aberrations increased by 2.88%-14.86% and 2.84%-18.49% (0.5 h-8 h per day) exposure to 2100 MHz and 2300 MHz, respectively when compared to that of the control group. Exposure to electromagnetic fields (EMF-r) at both 2100 MHz and 2300 MHz resulted in reduced cell viability. This study examines the impact of electromagnetic fields (EMF-r) at 2100 MHz and 2300 MHz on plant root meristems. The results reveal more pronounced genotoxic effects at 2100 MHz, highlighting the frequency-dependent nature of EMF-r impacts. By providing insights into these frequency-specific effects, this research addresses a critical gap in understanding how EMF-r influences plant cellular health and offers guidance for mitigating potential environmental risks from mobile communication technologies., Competing Interests: Declaration of competing interest The authors declare that they have no known financial or personal competing interests., (Copyright © 2024. Published by Elsevier Masson SAS.)

Ultraviolet-B (UVB) radiation is a major physical factor that induces structural changes in human skin. The aim of this study was to determine whether the novel silent information regulator 1 (sirtuin 1 SIRT1) protein activator, penilumamide, exerted any protective effects against UVB-induced skin damage using human HaCaT keratinocytes as a model. Enzymatic assays were performed to determine the SIRT1-activating ability of penilumamide, which was compared with that of resveratrol, a potent natural product SIRT1 activator with antioxidant and anti-inflammatory properties. Penilumamide markedly activated SIRT1 enzyme activity compared to resveratrol. To further investigate the protective effect of penilumamide against UVB-induced cytotoxicity, HaCaT cells were pretreated with penilumamide (10 μM) for 24 hr followed by irradiation with UVB (40 mJ/cm 2 ). UVB (40 mJ/cm 2 ) irradiation significantly reduced cell viability in a time-dependent manner, whereas pretreatment with penilumamide blocked this effect. Further, penilumamide decreased the levels of intracellular reactive oxygen species (ROS) generated by UVB irradiation in HaCaT cells. Pretreatment with penilumamide also prevented UVB irradiation-induced changes in mitochondrial membrane potential (Δ Ψ m ). In addition, pretreatment with penilumamide significantly reduced the expression levels of pro-inflammatory cytokines, interleukin (IL)-6, IL-8, and IL-10 and phosphorylation of nuclear factor-kB (NF-kB). These results indicate that penilumamide protects HaCaT cells from UVB-induced inflammation. Taken together data demonstrate that penilumamide exerted protective effects against UVB-induced ROS generation in HaCaT cells. Therefore, penilumamide may be considered to be used as a new SIRT1 activator to protect human keratinocyte against UVB-induced damage.

Objective . Applying carbon ion beams, which have high linear energy transfer and low scatter within the human body, to Spatially Fractionated Radiation Therapy (SFRT) could benefit the treatment of deep-seated or radioresistant tumors. This study aims to simulate the dose distributions of spatially fractionated beams (SFB) to accurately determine the delivered dose and model the cell survival rate following SFB irradiation. Approach . Dose distributions of carbon ion beams are calculated using the Triple Gaussian Model. The sensitive volume of the detector used in measurements was also considered. If the measurements and simulations show good agreement, the dose distribution and absolute dose delivered by SFB can be accurately estimated. Three types of dose distributions were delivered to human salivary gland cells (HSGc-C5): uniform dose distribution (UDD), and one-dimensional (1D) grid-like dose distributions (GDD) with 6 mm and 8 mm spacing. These provided high (Peak-to-Valley Dose Ratio, PVDR = 4.0) and low (PVDR = 1.64) dose differences between peak and valley doses, respectively. Linear-Quadratic (LQ) model parameters for HSGc-C5 were derived from the UDD and cell survival fractions (SF) were simulated for 1D GDD using these values. Main results . Good agreement was observed between measurements and simulations when accounting for detector volume. However, the TPS results overestimated dose in steep gradient region, likely due to the 2.0 mm calculation resolution. LQ parameters for HSGc-C5 were α = 0.34 and β = 0.057. The 1D GDD with 6 mm spacing showed good agreement between simulations and experiments, but the 8.0 mm spacing resulted in lower experimental cell survival. Significance . We successfully simulated the GDD and conducted SF simulations. The results suggest potential cell-killing effects due to high-dose differences in SFB., (© 2025 IOP Publishing Ltd. All rights, including for text and data mining, AI training, and similar technologies, are reserved.)

Photothermal therapy, in which a laser is an effective tool, is a promising method for cancer treatment. Laser parameters, including power, irradiation time, type of laser radiation (continuous or chopped), and the concentration of the photothermal agent, can affect the efficiency of this method. Therefore, this study investigated and compared the effects of different laser parameters on the efficiency of photothermal treatment for cervical cancer, which is the fourth most prevalent cancer in women. In addition, we investigated the properties of graphene oxide (GO) synthesized as a photothermal agent under laser radiation, and its effectiveness in achieving the desired therapeutic temperature. This study examined and compared the effects of temperature, nanoparticle concentration, irradiation time, and laser power to understand their impact on heat transfer. The toxicity of graphene oxide at different concentrations in HeLa cancer cells was also evaluated. These results demonstrated low toxicity, particularly after 24 h, with approximately 10% toxicity. The study explored mortality under laser irradiation at various powers and time intervals using continuous and chopped beam irradiation. In addition, a model for temperature prediction using a regression tree was presented. Finally, the combined photothermal effects of graphene oxide and laser irradiation were investigated. The MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) test results reveal significant effects, with a mortality rate of 90% in continuous radiation with a concentration of 0.3 mg/ml and 75% in chopped beam irradiation with concentrations of 0.3 and 0.4 mg/ml. A regression tree model was developed to predict temperature changes based on the GO concentration, laser power, and irradiation time, providing valuable insights for optimizing photothermal therapy parameters. Statistical analysis showed that the combined effect of graphene oxide with continuous laser irradiation was more effective than chopped-beam laser irradiation. However, the chopped-beam irradiation method is expected to cause less damage to surrounding tissues. These findings indicate that photothermal therapy with graphene oxide, chopped, and continuous laser irradiation can potently treat HeLa cancer cells and pave the way for further exploration of targeted cancer treatments., Competing Interests: Declarations. Competing interests: The authors declare no competing interests., (© 2025. The Author(s), under exclusive licence to Springer-Verlag London Ltd., part of Springer Nature.)

Cold atmospheric plasma (CAP) treatment induces cancer cell death through the generation of reactive oxygen and nitrogen species (RONS). However, the efficacy of RONS delivery into cells remains limited by membrane permeability. Here, we investigated whether combining CAP with pulsed electric fields (PEFs) could enhance cancer cell death through increased intracellular RONS uptake. HeLa cells were treated with argon atmospheric pressure plasma jet (Ar-APPJ), PEF, or their combination. The combined treatment showed significantly enhanced cell death compared to single treatments. While PEF treatment alone induced membrane permeabilization, the combination with Ar-APPJ resulted in more pronounced and sustained membrane disruption, as evidenced by increased calcein leakage. This enhanced effect was attributed to Ar-APPJ-induced lipid peroxidation interfering with membrane resealing after PEF-induced electroporation. We also demonstrated that PEF-induced membrane electroporation facilitates the intracellular uptake of CAP-generated RONS. These findings provide mechanistic insights into the synergistic effects of combined CAP and PEF treatments, suggesting enhanced cell death via multiple pathways.

Background: Electromagnetic radiation (EMR) from wireless technology and mobile phones, operates at various frequencies. The present study analyses the major impact of short-term exposure to 2.4 GHz frequency EMR, using the two model systems chick embryos and SH-SY5Y cell lines. We hypothesized that exposure to this frequency would induce oxidative stress and apoptosis in neurons., Methods and Results: Chick embryos were exposed continuously to 2.4 GHz EMR for 4 h each day over a 5-day period, and comparisons were made with a control group. At the end of the exposure, brain tissues were dissected for histopathological analysis, antioxidant assays, and reactive oxygen species (ROS) detection. Additionally, SH-SY5Y cells were exposed to 2.4 GHz EMR to assess cell viability, DNA damage, and apoptosis. Our results showed that exposure to 2.4 GHz EMR induces oxidative stress in both chick embryos and the SH-SY5Y cells, though no significant tissue-level impact was observed. In SH-SY5Y cells, ROS production increased after 4 h of exposure, accompanied by moderate DNA damage and early markers of apoptosis, such as upregulation of the Bax gene. Furthermore, we observed that antioxidants, such as NAC and Mito-TEMPO, helped mitigate the cytotoxic effects of EMR in both the study models., Conclusion: In conclusion, short-term exposure (4 h) to 2.4 GHz EMR induced moderate cellular and molecular changes, primarily oxidative stress. The oxidative stress was reduced by antioxidants, which suggests potential benefits in preventing EMR-induced cytotoxicity. Extended exposure to EMR beyond 4 h may pose adverse health risks to humans, endorsing further investigation., Competing Interests: Declarations. Ethical approval: Ethical approval is not applicable to this study (Short-term exposure of 2.4 GHz electromagnetic radiation on cellular ROS generation and apoptosis in SH-SY5Y cell line and impact on developing brain tissue). Competing interests: The authors declare no competing interests., (© 2025. The Author(s), under exclusive licence to Springer Nature B.V.)

Objective . Mathematical modeling can offer valuable insights into the behavior of biological systems upon treatment. Different mathematical models (empirical, semi-empirical, and mechanistic) have been designed to predict the efficacy of either hyperthermia (HT), radiotherapy (RT), or their combination. However, mathematical approaches capable of modeling cell survival from shared general principles for both mono-treatments alone and their co-application are rare. Moreover, some cell cultures show dose-dependent saturation in response to HT or RT, manifesting in survival curve flattenings. An advanced survival model must, therefore, appropriately reflect such behavior. Approach . We propose a mathematical approach to model the effect of both treatments based on the general principle of sublethal damage (SLD) accumulation for the induction of cell death and irreversible proliferation arrest. Our approach extends Jung's model on heat-induced cellular inactivation by incorporating dose-dependent recovery rates that delineate changes in SLD restoration. Main results . The resulting unified model (Umodel) accurately describes HT and RT survival outcomes, applies to simultaneous thermoradiotherapy modeling, and is particularly suited to reproduce survival curve flattening phenomena. We demonstrate the Umodel's robust performance (R2 0.95) based on numerous clonogenic cell survival data sets from the literature and our experimental studies. Significance . The proposed Umodel allows using a single unified mathematical function based on generalized principles of accumulation of SLD with implemented radiosensitization, regardless of the type of energy deposited and the mechanism of action. It can reproduce various patterns of clonogenic survival curves, including any flattening, thus encompassing the variability of cell reactions to therapy, thereby potentially better reflecting overall tumor responses. Our approach opens a range of options for further model developments and strategic therapy outcome predictions of sequential treatments applied in different orders and varying recovery intervals between them., (Creative Commons Attribution license.)

Introduction: Pancreatic cancer (PC) is one of the most aggressive and lethal malignancies, calling for enhanced research. Pancreatic ductal adenocarcinoma (PDAC) represents 70-80% of all cases and is known for its resistance to conventional therapies. Carbon-ion radiotherapy (CIRT) has emerged as a promising approach due to its ability to deliver highly localized doses and unique radiobiological properties compared to X-rays. In vitro radiobiology has relied on two-dimensional (2D) cell culture models so far; however, these are not sufficient to replicate the complexity of the in vivo tumor architecture. Three-dimensional (3D) models become a paradigm shift, surpassing the constraints of traditional models by accurately re-creating morphological, histological, and genetic characteristics as well as the interaction of tumour cells with the microenvironment. Materials and Methods: This study investigates the survival of pancreatic cancer cells in both 2D and spheroids, a 3D model, following photon, proton, and carbon-ion irradiation by means of clonogenic, MTT, spheroid growth, and vitality assays. Results: Our results demonstrate that carbon ions are more efficient in reducing cancer cell survival compared to photons and protons. In 2D cultures, carbon-ion irradiation reduced cell survival to approximately 15%, compared to 45% with photons and 30% with protons. In the 3D culture model, spheroid growth was similarly inhibited by carbon-ion irradiation; however, the overall survival rates were higher across all irradiation modalities compared to the 2D cultures. Carbon ions consistently showed the highest efficacy in reducing cell viability in both models. Conclusions: Our research highlights the pivotal role of 3D models in unraveling the complexities of pancreatic cancer radiobiology, offering new avenues for designing more effective and precise treatment protocols.

To enhance the treatment of tumors that are resistant to radio- and chemotherapy while minimizing the side effects of radiochemotherapy, researchers are continuously seeking new active compounds for use in combination with radiotherapy. Therefore, the aim of our study was to examine the cytotoxic and radiosensitizing effects of an extract from St. John's Wort ( Hypericum perforatum) , referred to as HP01, on human epithelial tumor cells in vitro. The growth of MCF-7 (breast carcinoma) and HT-29 (colon carcinoma) cells was examined under the influence of HP01. In combination with radiation, the effects of HP01 on cytotoxicity and long-term survival were assessed using a colony formation assay. The number of DNA double-strand breaks was analyzed using the γH2AX assay, while cell cycle distribution was examined via flow cytometry. A growth-inhibiting and cytotoxic effect was observed for both tumor cell lines starting at a concentration of 10 µg/mL HP01. Treatment with HP01 resulted in an inhibition of clonogenic survival of tumor cells after ionizing radiation (6 Gy). The number of DNA double-strand breaks (DSBs) in tumor cells increased with HP01 treatment, but the repair of radiation-induced DNA DSBs was not affected. Cell cycle analysis revealed that HP01, in addition to radiation, enhanced G2/M arrest in MCF-7 and HT-29 cells. Overall, HP01 not only showed a growth-inhibiting effect but also demonstrated a radiosensitizing effect on human tumor cells for the first time. We conclude that the HP01-induced G2/M accumulation of cells may be the main rationale for the drug-induced radiosensitivity. It is therefore a promising candidate for combined therapy in tumor diseases and warrants further investigation.

Low-level laser (LLL) therapy is a well-known noninvasive treatment that stimulates fibroblasts to improve wound healing. LLL can improve fibroblast proliferation and migration without causing toxicity. The present study aimed to evaluate the effects of two laser wavelengths at different irradiation times on canine fibroblasts. Fibroblasts were isolated from canine oral mucosa. After seeding for 24 hr, the fibroblasts were irradiated using the Erchonia ® EVL dual-diode laser at wavelengths of 405 nm (5 mW) and 640 nm (7.5 mW) with irradiation times of 120, 360, and 1,800 sec. The proliferating and viability cells were evaluated 24 hr after laser irradiation. Wound closure rates were calculated at 0, 24, and 48 hr after laser irradiation. Parameters, including proliferation cell, cell viability, and cell migration, tended to be higher in the 360-sec group (405 nm) and 120-sec group (640 nm) than in other groups. Our findings suggest that LLL therapy at wavelengths of 405 and 640 nm with an irradiation time of 120-360 sec (0.26-0.51 J/cm 2 ) can stimulate the proliferation and migration of canine fibroblasts. This finding may contribute to a better understanding of the beneficial role of LLL stimulation in canine wound healing.

The vast majority of breast cancer patients require radiotherapy but some of them will develop local recurrences and potentially metastases in the future. Recent data show that exosomal cargo is essential in these processes. Thus, we investigated the influence of ionising radiation on exosome properties and their ability to modify the sensitivity and biology of non-irradiated cells. Exosomes were isolated from breast cancer cell lines (MDA-MB-231, MCF7, and SKBR3) irradiated with 2 Gy (Exo 2 Gy) or no irradiation (Exo 0 Gy). Despite some differences in their molecular profiles, they did not affect cell viability, proliferation, cell cycle phase distribution, and radioresistance; however, both populations showed the ability to modify cell migration and invasion potential, as confirmed by the downregulation of β-catenin, which is responsible for maintaining the epithelial phenotype. Interestingly, exosomes from irradiated BCa cells were more actively deposited in the endothelial cells (EA.hy926). Furthermore, exosomes tend to lower the expression of CD31, which is responsible for maintaining intact vascularity. This preliminary study demonstrates the vital role of exosomes and their altered profile due to irradiation in the pathobiology of breast cancer.

Background: Radioresistance is a major clinical challenge in cancer treatment, as it reduces the effectiveness of radiation therapy (RT). While advances in radiation delivery have enabled the clinical use of high-dose hypofractionated RT, its impact on radioresistant tumors remains unclear. This study aimed to compare the effects of single high-dose RT with conventional fractionated RT on radioresistant breast cancer cells and explore the underlying mechanisms., Methods: Radioresistant cell lines were previously established by exposing SK-BR-3 and MCF-7 cells to 48 Gy and 70 Gy of radiation, respectively, in multiple fractions. We compared the effects of 2 Gy × 5 and 7 Gy × 1 fractions on these cells using clonogenic survival assays and western blot analysis. In vivo antitumor effects were assessed in SR tumor-bearing BALB/c mice irradiated with either 2 Gy × 5 or 7 Gy × 1 fractions., Results: 7 Gy x1 was more efficient at killing radioresistant breast cancer cells than 2 Gy x5. Furthermore, the 7 Gy x1 fraction produced higher levels of reactive oxygen species (ROS) and decreased the expression of radioresistance factors such as p-STAT3, ACSL4, FOXM1, RAD51, Bcl-xL, and survivin. Consistent with the in vitro studies, the 7 Gy × 1 fraction also showed superior antitumor effects in SR tumor-bearing BALB/c mice., Conclusions: Single high-dose RT offers superior advantages over conventional fractionated RT in regard to overcoming radioresistance, supporting its potential as a promising treatment for recurrent tumors.

The widespread use of wireless communication technologies has increased human exposure to radiofrequency electromagnetic fields (RF-EMFs). Considering the brain's close proximity to mobile phones and its entirely electrical transmission network, it emerges as the organ most profoundly impacted by the RF field. This study aims to investigate the potential effects of RF radiation on cell viability, apoptosis, and gene expressions in glioblastoma cells (U118-MG) at different exposure times (1, 24, and 48 h). To achieve this, we designed and implemented an in vitro RF exposure system operating at a frequency of 2.1 GHz, specifically for cell culture studies, with an average specific absorption rate (SAR) of 1.12 ± 0.18 W/kg determined through numerical dosimetry calculations. Results reveal a significant influence of a 48 h exposure to a 2.1 GHz RF field on U118-MG cell viability, gene expression, and the induction of caspase (CASP) dependent apoptosis. Notably, increased CASP3, CASP8, and CASP9 mRNA levels were observed after 24 and 48 h of RF treatment. However, only the 48 h RF exposure resulted in apoptotic cell death and a significant elevation in the BAX/BCL-2 ratio. This observed effect may be influenced by extended exposure durations surpassing the cell's doubling time. The increased BAX/BCL-2 ratio, which acts as a key switch for apoptosis, and the heterogeneous morphology of the astrocyte-derived U118-MG cell line may also play a role in this effect., (© 2025 Bioelectromagnetics Society.)

Androgenetic alopecia (AGA) is a prevalent hair loss disorder and influenced by genetic, hormonal, and environmental factors. Minoxidil and finasteride have been widely used for treating AGA. However, the side effects associated with these drugs often lead to poor patient compliance. In contrast, photobiomodulation (PBM), due to its safety and non-invasiveness, holds promising prospects for use. Although the promoting effects of PBM on AGA have been reported, the mechanisms by which PBM affects dermal papilla cells (DPCs) remain largely unknown. Hence, this study explored the impacts of both continuous wave (CW) and pulsed wave (PW) PBM on DPCs, and revealed the underlying actions of light parameters in PBM. Orthogonal experiments were conducted to evaluate the effects of CW PBM on DPCs at varying irradiances and doses, indicating that irradiance was the crucial parameter, as well as cell viability and proliferation were maximized at 8 mW/cm 2 and 8 J/cm 2 . For PW PBM, response surface methodology was employed to determine the influences of duty cycles, frequencies, and doses. The findings highlighted frequency as a primary factor, with the optimum cell viability observed at peak irradiance 10 mW/cm 2 , duty cycle 80 %, 500 Hz, and 8.8 J/cm 2 . Notably, PBM could enhance cell viability, proliferation, and migration in DPCs by activating the Wnt/β-Catenin signaling and suppressing Transforming Growth Factor signaling, particularly when applied in pulsed mode. Overall, this study determined the key light parameters that influence PBM effectiveness, further identified the optimal light conditions, and preliminary revealed into the mechanisms of PBM in DPCs, highlighting that PW PBM may be a competitive therapeutic option for alleviating AGA in the future., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Diffuse intrinsic pontine gliomas (DIPG) are highly aggressive and treatment-resistant childhood primary brainstem tumors with a median survival of less than one year after diagnosis. The prevailing standard of care for DIPG, radiation therapy, does not prevent fatal disease progression, with most patients succumbing to this disease 3-8 months after completion of radiation therapy. This underscores the urgent need for novel combined-modality approaches for enhancing therapy responses. This study demonstrates that the cellular redox modulating drug, copper (II)-diacetyl-bis(N4-methylthiosemicarbazone) (Cu-ATSM) dose-dependently (1-3 μM) decreased clonogenic cell survival in SU-DIPG50 and SU-DIPG36 cell lines during 6 h of exposure but had no significant effect on survival in normal human astrocytes (NHA). Additional significant (>90%) decreases in DIPG clonogenic survival were observed at 24 h of Cu-ATSM exposure. However, NHAs also began to show dose-dependent 10-70% survival decreases at this point. Notably, 3 μM Cu-ATSM for 6 h resulted in additive clonogenic cell killing of DIPG lines when combined with radiation, which was not seen in NHAs and was partially inhibited by the copper chelator, bathocuproinedisulfonic acid. Cu-ATSM toxicity in DIPG cells was also inhibited by overexpression of mitochondrial-targeted catalase. These results support the hypothesis that Cu-ATSM is selectively cytotoxic to DIPGs by a mechanism involving H2O2 generation and copper and being additively cytotoxic with ionizing radiation., (© 2025 by Radiation Research Society. All rights of reproduction in any form reserved.)

Background: The clinical advantages of light-emitting diode (LED) therapy in skin healing and its underlying mechanism remain subjects of ongoing debate., Objective: This study aims to explore the impact of LED therapy on normal skin keratinocytes (HaCaT) and in the repair of full-thickness dorsal wounds in Wistar rats., Methods: HaCaT cell viability (SRB assay) and migration (scratch assay) were assessed under LED therapy, comparing stress conditions (2.5% FBS) with sham irradiation and optimal conditions (10% FBS). In vivo, 50 rats with induced wounds were divided into Sham and LED (daily treatment) groups. Euthanasia occurred at 3, 5, 10, 14, and 21 days for clinical, morphological, oxidative stress (MDA, SOD, and GSH), and cytokine analyses (IL-1β, IL-10, TNF-α)., Results: LED therapy significantly enhanced keratinocytes viability compared to sham irradiation, with minimal impact on cell migration. Clinical benefits were prominent on day 10, influencing inflammation progression and resolution on days 3 and 10. Re-epithelization remained unaffected. Reduced MDA and increased GSH levels were observed throughout, while SOD levels varied temporally. Notably, on day 10, LED significantly decreased IL-1β, IL-10, and TNF-α., Study Limitations: Although translational, clinical trial confirmation of observed benefits is warranted., Conclusions: LED therapy expedites cutaneous healing in the experimental model, primarily modulating inflammation and enhancing antioxidant activity., Competing Interests: Conflicts of interest None declared., (Copyright © 2024 Sociedade Brasileira de Dermatologia. Published by Elsevier España, S.L.U. All rights reserved.)

Laser-irradiation-assisted cell gene transfection is sterile and nontoxic, but the low transfection efficiency cannot meet the application requirements. To improve the efficiency, a temporal and spatial shaping method of a femtosecond laser is proposed. Using the time shaping method, we can segment the pulse into subpulses of varying energies and with a defined delay, thereby influencing the interaction between electrons and photons, ultimately enhancing transfection efficiency. The transfection efficiency is further improved by spatially shaping the laser pulse to extend the focusing beam's working distance and reduce the cell's sensitivity to the focal position. Through the characterization of the viability and transfection efficiency of HEK-293T cells, the method achieved efficient and active transfection, with a maximum transfection efficiency of 45.1% and a cell survival rate of 93.6%. This method provides key technical support for femtosecond laser transfection and promotes its further application in clinical practice., (© 2024 Wiley‐VCH GmbH.)

Branched-chain amino acids (BCAAs) facilitate cancer cell proliferation and survival. Stresses, including X-irradiation, increase BCAA uptake. However, the role of BCAA metabolism in cancer cell survival remains unclear. Therefore, this study aimed to elucidate the role of the BCAA catabolic pathway in cancer cell survival following X-irradiation. X-irradiation dose-dependently dephosphorylated branched-chain α-keto acid dehydrogenaseE1α (BCKDHA) suggesting the activation of the BCKDH complex, which catalyzes the rate-determining step of BCAA catabolism. We considered that activation of BCKDH promoted the BCAA catabolism, which resulted in cancer cell resistance to X-irradiation. Consistent with this notion, cells with BCKDHA knockdown exhibited increased radiosensitivity, which was associated with the increase in mitotic catastrophe and residual double-strand breaks by decreasing cellular ATP levels after X-irradiation. Our results suggest that BCKDHA dephosphorylation promotes BCAA catabolism, leading to cell survival by mitigating DNA damage after X-irradiation. Thus, BCAA catabolic pathway may be a target for radiation therapy., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Photodynamic Therapy (PDT) is a therapeutic modality that combines the application of a photoactive compound (photosensitizer, PS) with low-power light to generate reactive oxygen species in the target tissue, resulting in cytotoxic damage and cell death, while sparing adjacent tissues. The objective of this study was to evaluate the phototoxicity of a cyanine dye with two chromophores (biscyanines, BCD) in systems with varying levels of cellular organization, and we used the Photogem® (a photosensitizer approved by the Brazilian ANVISA agency for clinical use in Photodynamic Therapy) as a positive control., Materials and Methods: The cytotoxicity of the compounds was assessed in vitro in 2D monolayers, 3D spheroid cultures, and artificial skin models. Four tumoral cell lines A375 (melanoma), HCB-541 (cutaneous squamous cell carcinoma), Vu120T and Vu147T (head and neck cancer), and two normal cell lines fibroblastic HFF-1 and keratinocyte HACAT were used in this study. Cell viability, migration, production of reactive oxygen species, expression of proteins linked to DNA damage and repair, internalization, and skin permeation of PS agents., Results: Light irradiation in the presence of the PS resulted in greater cytotoxic effects for BCD as compared to Photogem®, which was accompanied by an increase in the production of reactive oxygen species including H 2 O 2 , elevated levels of cleaved PARP, and a higher rate of phosphorylated H2AX protein. BCD demonstrated enhanced internalization and bioaccumulation in the spheroids and equivalent skin models., Conclusion: BCD, as a photosensitizer, showed higher cytotoxicity, with an increased ability to generate reactive oxygen species. This led to reduced cell viability, inhibited migration, and upregulated DNA damage-related proteins. Additionally, its enhanced cellular uptake improved skin barrier permeability, making BCD a strong candidate for in vivo Photodynamic Therapy., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)