The study of metals and alloys containing helium has garnered significant attention within the nuclear energy community. However, there is limited research on the mechanical behavior of bulk alloys implanted with helium. This study investigates the mechanical properties of several Al-Boron alloys implanted with helium using controlled manipulation of helium doses via boron content under a consistent neutron dose. Results show that HemVn may contribute to strength by approximately 8.4-15 MPa and 16.8-23 MPa for helium doses 3.08 × 1019/cm3 and 6.84 × 1019/cm3, respectively, while lattice damages due to neutron-aluminum reaction contribute to strength by 24∼27 MPa. Subsequent annealing leads to the formation of helium bubbles, resulting in a slightly higher strengthening effect compared to HemVn. Additionally, the work hardening behavior of the alloys can be explained by the Voce model, drawing inspiration from the resemblance between helium bubbles and nanoprecipitates in 7xxx alloys. These findings provide insights to the nuclear energy community.

The effects of irradiation on meat constituents including water, proteins, and lipids are multifaceted. Irradiation leads to the decomposition of water molecules, resulting in the formation of free radicals that can have both positive and negative effects on meat quality and storage. Although irradiation reduces the number of microorganisms and extends the shelf life of meat by damaging microbial DNA and cell membranes, it can also accelerate the oxidation of lipids and proteins, particularly sulfur-containing amino acids and unsaturated fatty acids. With regard to proteins, irradiation affects both myofibrillar and sarcoplasmic proteins. Myofibrillar proteins, such as actin and myosin, can undergo depolymerization and fragmentation, thereby altering protein solubility and structure. Sarcoplasmic proteins, including myoglobin, undergo structural changes that can alter meat color. Collagen, which is crucial for meat toughness, can undergo an increase in solubility owing to irradiation-induced degradation. The lipid content and composition are also influenced by irradiation, with unsaturated fatty acids being particularly vulnerable to oxidation. This process can lead to changes in the lipid quality and the production of off-odors. However, the effects of irradiation on lipid oxidation may vary depending on factors such as irradiation dose and packaging method. In summary, while irradiation can have beneficial effects, such as microbial reduction and shelf-life extension, it can also lead to changes in meat properties that need to be carefully managed to maintain quality and consumer acceptability.

UNASSIGNED: Previous studies suggested pre-operative platelet-to-lymphocyte ratio (PLR) and neutrophil-to-lymphocyte ratio (NLR) to be predictive factors in patients with glioblastoma multiforme (GBM). This study investigated the prognostic role of PLR and NLR prior to or at the beginning of radiotherapy.
UNASSIGNED: In 80 patients with GBM receiving conventionally fractionated radiotherapy plus concurrent temozolomide following resection or biopsy, 12 factors including PLR and NLR were retrospectively evaluated regarding progression-free survival (PFS) and overall survival (OS).
UNASSIGNED: On multivariable analyses, PLR ≤150, Karnofsky performance score (KPS) 90-100, and O6-methylguanine-DNA methyltransferase promoter methylation were significantly associated with improved PFS. Single lesion, KPS 90-100, and adjuvant chemotherapy were significantly associated with OS; PLR ≤150 showed a trend. NLR ≤3 showed a trend for associations with PFS and OS on univariable analyses.
UNASSIGNED: PLR prior to or at the beginning of radiotherapy was associated with treatment outcomes in patients irradiated for GBM and should be considered in future clinical trials.

Irradiation (IR)-induced xerostomia is the most common side effect of radiation therapy in patients with head and neck cancer (HNC). Xerostomia diagnosis is mainly based on the patient\'s medical history and symptoms. Currently, no direct biomarkers are available for the early prediction of IR-induced xerostomia. Here, we identified PIEZO1 as a novel predictive tissue biomarker for xerostomia. Our data demonstrate that PIEZO1 is significantly upregulated at the gene and protein levels during IR-induced salivary gland (SG) hypofunction. Notably, PIEZO1 upregulation coincided with that of inflammatory (F4/80) and fibrotic markers (fibronectin and collagen fibers accumulation). These findings suggest that PIEZO1 upregulation in SG tissue may serve as a novel predictive marker for IR-induced xerostomia.

Mitochondria are key regulators of hematopoietic stem cell (HSC) homeostasis. Our research identifies the transcription factor Nynrin as a crucial regulator of HSC maintenance by modulating mitochondrial function. Nynrin is highly expressed in HSCs under both steady-state and stress conditions. The knockout Nynrin diminishes HSC frequency, dormancy, and self-renewal, with increased mitochondrial dysfunction indicated by abnormal mPTP opening, mitochondrial swelling, and elevated ROS levels. These changes reduce HSC radiation tolerance and promote necrosis-like phenotypes. By contrast, Nynrin overexpression in HSCs diminishes irradiation (IR)-induced lethality. The deletion of Nynrin activates Ppif, leading to overexpression of cyclophilin D (CypD) and further mitochondrial dysfunction. Strategies such as Ppif haploinsufficiency or pharmacological inhibition of CypD significantly mitigate these effects, restoring HSC function in Nynrin-deficient mice. This study identifies Nynrin as a critical regulator of mitochondrial function in HSCs, highlighting potential therapeutic targets for preserving stem cell viability during cancer treatment.

BACKGROUND: In reconstructive surgery, local flaps might develop tissue necrosis or partial flap loss especially after previous irradiation, which may be necessary in many tumor entities. The application of stem cells seems promising to improve flap perfusion and might be a possible solution to optimize flap survival.
METHODS: Twenty rats received harvesting of bilateral random pattern fasciocutaneous flaps. The right flaps received 20 Gy ionizing radiation 4 weeks prior to the surgery, while the left flaps served as the non-irradiated control. After flap harvest, four different stem cell mixtures (5 × 106 ASC, ASC-HUVEC, MSC, MSC-HUVEC) were applied under both right and left flaps using 1 mL fibrin glue as the delivery vehicle. Flap size and its necrotic area were examined clinically. Two weeks after the surgery, HE staining and immunohistochemical staining for CD68 and ERG, as well as PCR analysis (Interleukin 6, HIF-1α and VEGF), were performed.
RESULTS: Application of ASCs, ASCs-HUVECs and MSCs resulted in a lower number of CD68-stained cells compared to the no cell group. The expression of Hif1α was higher in the ASC group compared to those in the MSC and previously treated no cell groups. Treatment with MSCs and MSCs-HUVECs prevented shrinking of the flaps in this series.
CONCLUSIONS: Application of ASCs, MSCs and ASCs-HUVECs was shown to have an antiinflammatory effect. Treatment with MSCs and MSCs-HUVECs can prevent early shrinking of the flaps.

A study of rats liver DNA damages under the influence of X-ray radiation at a dose of 6.5 Gy(LD60) was carried out. The radioprotective properties of newly synthesized Cu(II) L-Schiff Histidinate complexes were also studied. The survival of rats was determined over a 30-day period after exposure to X-rays without pretreatment and also after preadministration of Cu(II) L-Histidinate-Schiff base complexes. The structural defects of rat\'s liver DNA were detected at 3, 7, 14, and 30 days post-irradiation extracted. The results obtained revealed that irradiation with a 6.5Gy dose in the control group degraded the characteristics of rat liver DNA in comparison to healthy DNA. On all investigated experimental days, a decrease in the melting temperature (Tm), a widening of the melting interval (ΔT), and a decrease in hypochromicity (Δh) were observed in the DNA samples of irradiated animals compared to the norm. The rat\'s pretreatment by Cu(II) L-Histidinate complexes 1 or 24 hours prior to irradiation improved DNA characteristics. Electrophoretic studies of DNA were in good agreement with the melting data. Based on the study results, it can be concluded that Cu(II) L-Histidinate complexes exhibit radioprotective properties under the studied conditions and can protect DNA from damage.

BACKGROUND: Ultraviolet-B (UVB) radiation is the leading environmental cause of skin damage and photoaging. The epidermis and dermis layers of the skin mainly absorb UVB. UVB stimulates apoptosis, cell cycle arrest, generation of reactive oxygen species, and degradation of collagen and elastin fibers.
OBJECTIVE: This study investigated the potential of human growth hormone (hGH) in protecting the skin fibroblasts and keratinocytes (HFFF-2 and HaCaT cell lines) from UVB-induced damage.
METHODS: The MTT assay was performed to evaluate UVB-induced mitochondrial damage via assessing the mitochondrial dehydrogenase activity, and flow cytometry was carried out to investigate the effects of UVB and hGH on the cell cycle and apoptosis of UVB-irradiated cells. In addition, the fold change mRNA expression levels of Type I collagen and elastin in HFFF-2 cells were evaluated using the qRT-PCR method following UVB exposure.
RESULTS: We observed that treatment of cells with hGH before UVB exposure inhibited UVB-induced loss of mitochondrial dehydrogenase activity, apoptosis, and sub-G1 population formation in both cell lines. We also found that hGH-treated HFFF-2 cells showed up-regulated mRNA expression of Type I collagen, elastin, and IGF-1 in response to UVB irradiation.
CONCLUSIONS: These findings suggest hGH as a potential anti-UVB compound that can protect skin cells from UVB-induced damage. Our findings merit further investigation and can be used to better understand the role of hGH in skin photoaging.

Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest of human malignancies and carries an exceptionally poor prognosis. It is mostly driven by multiple oncogenic alterations, with the highest mutation frequency being observed in the KRAS gene, which is a key oncogenic driver of tumorogenesis and malignant progression in PDAC. However, KRAS remained undruggable for decades until the emergence of G12C mutation specific KRAS inhibitors. Despite this development, this therapeutic approach to target KRAS directly is not routinely used for PDAC patients, with the reasons being the rare presence of G12C mutation in PDAC with only 1-2% of occurring cases, modest therapeutic efficacy, activation of compensatory pathways leading to cell resistance, and absence of effective KRASG12D or pan-KRAS inhibitors. Additionally, indirect approaches to targeting KRAS through upstream and downstream regulators or effectors were also found to be either ineffective or known to cause major toxicities. For this reason, new and more effective treatment strategies that combine different therapeutic modalities aiming at achieving synergism and minimizing intrinsic or adaptive resistance mechanisms are required. In the current work presented here, pancreatic cancer cell lines with oncogenic KRAS G12C, G12D, or wild-type KRAS were treated with specific KRAS or SOS1/2 inhibitors, and therapeutic synergisms with concomitant MEK inhibition and irradiation were systematically evaluated by means of cell viability, 2D-clonogenic, 3D-anchorage independent soft agar, and bioluminescent ATP assays. Underlying pathophysiological mechanisms were examined by using Western blot analyses, apoptosis assay, and RAS activation assay.

BACKGROUND: The combination of senescence triggers with senolytic drugs is considered a promising new approach to cancer therapy. Here, we studied the efficacy of the genotoxic agent etoposide (Eto) and irradiation in inducing senescence of Panc02 pancreatic cancer cells, and the capability of the Bcl-2 inhibitor navitoclax (ABT-263; Nav) to trigger senolysis.
METHODS: Panc02 cells were treated with Eto or irradiated with 5-20 Gy before exposure to Nav. Cell survival, proliferation, and senescence were assessed by trypan blue staining, quantification of DNA synthesis, and staining of senescence-associated β-galactosidase (SA-β-Gal)-positive cells, respectively. Levels of mRNA were determined by real-time polymerase chain reaction, and protein expression was analyzed by immunoblotting. Panc02 cells were also grown as pancreatic tumors in mice, which were subsequently treated with Eto and Nav.
RESULTS: Eto and irradiation had an antiproliferative effect on Panc02 cells that was significantly or tendentially enhanced by Nav. In vivo, Eto and Nav together, but not Eto alone, significantly reduced the proportion of proliferating cells. The expression of the senescence marker γH2AX and tumor infiltration with T-cells were not affected by the treatment. In vitro, almost all Eto-exposed cells and a significant proportion of cells irradiated with 20 Gy were SA-β-Gal-positive. Application of Nav reduced the percentage of SA-β-Gal-positive cells after irradiation but not after pretreatment with Eto. In response to triggers of senescence, cultured Panc02 cells showed increased protein levels of γH2AX and the autophagy marker LC3B-II, and higher mRNA levels of Cdkn1a, Mdm2, and PAI-1, while the effects of Nav were variable.
CONCLUSIONS: In vitro and in vivo, the combination of senescence triggers with Nav inhibited tumor cell growth more effectively than the triggers alone. Our data also provide some evidence for senolytic effects of Nav in vitro.