8-Oxoguanine DNA Glycosylase1 conceals oxidized guanine in nucleoprotein-associated RNA of respiratory syncytial virus.

Respiratory syncytial virus (RSV), along with other prominent respiratory RNA viruses such as influenza and SARS-CoV-2, significantly contributes to the global incidence of respiratory tract infections. These pathogens induce the production of reactive oxygen species (ROS), which play a crucial role in the onset and progression of respiratory diseases. However, the mechanisms by which viral RNA manages ROS-induced base oxidation remain poorly understood. Here, we reveal that 8-oxo-7,8-dihydroguanine (8-oxoGua) is not merely an incidental byproduct of ROS activity but serves as a strategic adaptation of RSV RNA to maintain genetic fidelity by hijacking the 8-oxoguanine DNA glycosylase 1 (OGG1). Through RNA immunoprecipitation and next-generation sequencing, we discovered that OGG1 binding sites are predominantly found in the RSV antigenome, especially within guanine-rich sequences. Further investigation revealed that viral ribonucleoprotein complexes specifically exploit OGG1. Importantly, inhibiting OGG1's ability to recognize 8-oxoGua significantly decreases RSV progeny production. Our results underscore the viral replication machinery's adaptation to oxidative challenges, suggesting that inhibiting OGG1's reading function could be a novel strategy for antiviral intervention.

CXCL3/TGF-ß-mediated crosstalk between CAFs and tumor cells augments RCC progression and sunitinib resistance.

Cancer-associated fibroblasts (CAFs) play a significant role in tumor development and treatment failure, yet the precise mechanisms underlying their contribution to renal cell carcinoma (RCC) remains underexplored. This study explored the interaction between CAFs and tumor cells, and related mechanisms. CAFs isolated from tumor tissues promoted the tumor progression and drugs resistance both in vivo and in vitro. Mechanistically, chemokine (C-X-C motif) ligand (CXCL) 3 secreted from CAFs mediated its effects. CXCL3 activated its receptor CXCR2 to active the downstream ERK1/2 signaling pathway, subsequently promoting epithelial-mesenchymal transition and cell stemness. Blocking the crosstalk between CAFs and tumor cells by CXCR2 inhibitor SB225002 attenuated the functions of CAFs. Furthermore, Renca cells facilitated the transformation of normal interstitial fibroblasts (NFs) into CAFs and the expression of CXCL3 through TGF-ß-Smad2/3 signaling pathway. In turn, transformed NFs promoted the tumor progression and drug resistance of RCC. These findings may constitute potential therapeutic strategies for RCC treatment.

Identification of novel molecules and pathways associated with fascin actin­bundling protein 1 in laryngeal squamous cell carcinoma through comprehensive transcriptome analysis.

Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumor with a poor prognosis. Fascin actin­bundling protein 1 (FSCN1) has been reported to play a crucial role in the development and progression of LSCC; however, the underlying molecular mechanisms remain unknown. Herein, a whole transcriptome microarray analysis was performed to screen for differentially expressed genes (DEGs) in cells in which FSCN1 was knocked down. A total of 462 up and 601 downregulated mRNA transcripts were identified. Functional annotation analysis revealed that these DEGs were involved in multiple biological functions, such as transcriptional regulation, response to radiation, focal adhesion, extracellular matrix­receptor interaction, steroid biosynthesis and others. Through co­expression and protein­protein interaction analysis, FSCN1 was linked to novel functions, including defense response to virus and steroid biosynthesis. Furthermore, crosstalk analysis with FSCN1­interacting proteins revealed seven DEGs, identified as FSCN1­interacting partners, in LSCC cells, three of which were selected for further validation. Co­immunoprecipitation validation confirmed that FSCN1 interacted with prostaglandin reductase 1 and 24­dehydrocholesterol reductase (DHCR24). Of note, DHCR24 is a key enzyme involved in cholesterol biosynthesis, and its overexpression promotes the proliferation and migration of LSCC cells. These findings suggest that DHCR24 is a novel molecule associated with FSCN1 in LSCC, and that the FSCN1­DHCR24 interaction may promote LSCC progression by regulating cholesterol metabolism­related signaling pathways.

8-Oxoguanine DNA glycosylase 1 selectively modulates ROS-responsive NF-κB targets through recruitment of MSK1 and phosphorylation of RelA/p65 at Ser276.

Nuclear factor kappa B (NF-κB) activity is regulated by various posttranslational modifications, of which Ser276 phosphorylation of RelA/p65 is particularly impacted by reactive oxygen species (ROS). This modification is responsible for selective upregulation of a subset of NF-κB targets; however, the precise mechanism remains elusive. ROS have the ability to modify cellular molecules including DNA. One of the most common oxidation products is 8-oxo-7,8-dihydroguanine (8-oxoGua), which is repaired by the 8-oxoguanine DNA glycosylase1 (OGG1)-initiated base excision repair pathway. Recently, a new function of OGG1 has been uncovered. OGG1 binds to 8-oxoGua, facilitating the occupancy of NF-κB at promoters and enhancing transcription of pro-inflammatory cytokines and chemokines. In the present study, we demonstrated that an interaction between DNA-bound OGG1 and mitogen-and stress-activated kinase 1 is crucial for RelA/p65 Ser276 phosphorylation. ROS scavenging or OGG1 depletion/inhibition hindered the interaction between mitogen-and stress-activated kinase 1 and RelA/p65, thereby decreasing the level of phospho-Ser276 and leading to significantly lowered expression of ROS-responsive cytokine/chemokine genes, but not that of Nfkbis. Blockade of OGG1 binding to DNA also prevented promoter recruitment of RelA/p65, Pol II, and p-RNAP II in a gene-specific manner. Collectively, the data presented offer new insights into how ROS signaling dictates NF-κB phosphorylation codes and how the promoter-situated substrate-bound OGG1 is exploited by aerobic mammalian cells for timely transcriptional activation of ROS-responsive genes.

Mechanisms of sunitinib resistance in renal cell carcinoma and associated opportunities for therapeutics.

Sunitinib is the first-line drug for renal cell carcinoma (RCC) treatment. However, patients who received sunitinib treatment will ultimately develop drug resistance after 6-15 months, creating a huge obstacle to the current treatment of renal cell carcinoma. Therefore, it is urgent to clarify the mechanisms of sunitinib resistance and develop new strategies to overcome it. In this review, the mechanisms of sunitinib resistance in renal cell carcinoma have been summarized based on five topics: activation of bypass or alternative pathway, inadequate drug accumulation, tumour microenvironment, metabolic reprogramming and epigenetic regulation. Furthermore, present and potential biomarkers, as well as potential treatment strategies for overcoming sunitinib resistance in renal cell carcinoma, are also covered.

MicroRNA-488: A miRNA with diverse roles and clinical applications in cancer and other human diseases.

MicroRNAs (miRNAs) are a class of small non-coding RNAs that post-transcriptionally regulate the expression of approximately 50 % of all protein-coding genes. They have been demonstrated to act as key regulators in various pathophysiological processes and play significant roles in a wide range of human diseases, particularly cancer. Current research highlights the aberrant expression of microRNA-488 (miR-488) in multiple human diseases and its critical involvement in disease initiation and progression. Moreover, the expression level of miR-488 has been linked to clinicopathological features and patient prognosis across different diseases. However, a comprehensive systematic review of miR-488 is lacking. Therefore, our study aims to consolidate the current knowledge surrounding miR-488, with a primary focus on its emerging biological functions, regulatory mechanisms, and potential clinical applications in human diseases. Through this review, we aim to establish a comprehensive understanding of the diverse roles of miR-488 in the development of various diseases.

Immune-related adverse events associated with nab-paclitaxel/paclitaxel combined with immune checkpoint inhibitors: a systematic review and network meta-analysis.

Objective: The combination of nanoparticle albumin-bound paclitaxel (nab-PTX)/paclitaxel (PTX) with immune checkpoint inhibitors (ICIs) has demonstrated significant efficacy in cancer patients. However, the safety of these combination regimens remains conflicting in former researches. Therefore, in order to address this issue, we performed a systematic review and network meta-analysis (NMA) to evaluate and compare the safety profile. Methods: We performed a systematic review by searching randomized controlled trials (RCTs) from PubMed, EMBASE, Cochrane Library, ClinicalTrials.gov, and Web of Science up to August 15, 2022. The primary outcomes were all-grade (grade 1-5) and high-grade (grade 3-5) immune-related adverse events (irAEs). Secondary outcomes were all-grade (grade 1-5) and high-grade (grade 3-5) irAEs of subgroups of ICIs. Results: There were 22 RCTs included in the NMA, involving a total of 15 963 patients diagnosed with any type of cancer. ICIs+nab-PTX was associated with a noticeably decreased risk of grade 3-5 pneumonitis (odds ratio [OR]=0.28, 95% credible interval [CrI]: 0.09,0.90) compared to ICI monotherapy; ICIs+PTX showed a lower risk of grade 1-5 hyperthyroidism (OR=0.46, 95% CrI: 0.22-0.96) and grade 1-5 hypothyroidism (OR=0.49, 95% CrI: 0.26-0.93) than ICIs. Compared with PD-1, PD-1+PTX was associated with a statistically significantly lower risk of grade 1-5 pneumonitis (OR=0.32, 95% CrI: 0.11-0.92). PD-L1 resulted in a noticeably lower risk of grade 1-5 hypothyroidism (OR=0.34, 95% CrI: 0.12-1.00) than PD-L1+PTX. Nearly all treatment regimens containing ICIs demonstrated significantly higher risks of irAEs compared to the standard chemotherapy groups. Conclusion: Nab-PTX/PTX+ICIs demonstrated an approach leading to decreased risk of irAEs compared with ICI monotherapy. This finding supports that ICIs+nab-PTX/PTX may be a safer treatment strategy. Moreover, we also found that the combination regimens containing ICIs had a higher risk of irAEs than standard chemotherapy. Additionally, ICIs+nab-PTX demonstrated a decreased risk of irAEs compared to ICIs+PTX. PD-1 inhibitors were associated with a higher risk of irAEs than PD-L1 inhibitors.

Emerging roles and potential clinical applications of translatable circular RNAs in cancer and other human diseases.

Circular RNAs (circRNAs) are a special class of single-stranded RNA molecules with covalently closed loops widely expressed in eukaryotic organisms. CircRNAs have long been considered to play important roles in various physiological and pathological processes as non-coding RNAs. However, circRNAs have recently garnered considerable attention due to their ability to be translated into peptides/proteins via internal ribosome entry site- or N6-methyladenosine-mediated pathways or rolling translation mechanisms. Furthermore, dysregulation of translatable circRNAs and their encoded proteins has been associated with developing and progressing diseases such as cancer. This review aims to summarize the driving mechanisms of circRNA translation and the available strategies in circRNA translation research. The main focus is on the emerging biological functions of translatable circRNAs, their regulatory mechanisms, and potential clinical applications in human diseases to provide new perspectives on disease diagnosis, prognosis, and targeted therapy.

Lower blood lipid level from the administration of plant tannins via altering the gut microbiota diversity and structure.

Twenty-four Tan sheep were randomly assigned into 4 groups to study the capability of tannin supplementation (0.5% in dietary DM) to lower blood lipid levels mediated through the gut microbiota. The control (NC) group was offered a basic diet, while the 3 treatment groups were the TA group, which received supplementary tannic acid (TA); GSPE group, which received supplementary procyanidins (GSPE); and the TA + GSPE group, which received supplementary TA and GSPE, besides being supplied with the basic diet for 8 weeks feeding. At the end of the experiment, the serum glucose, insulin, lipids, and cytokines were measured, and the short-chain fatty acids (SCFAs) in the colon were tested by GC/MS. Moreover, the jejunal and colonic microbiota were detected by 16S rRNA sequencing. Significant reductions in serum triacylglycerol, cholesterol, and high density lipoprotein were found in all treatments. The total SCFAs decreased, while the iso-acids were significantly increased in the TA and TA + GSPE groups. The sheep showed noticeably lower MCP-1 and higher COX-2 levels in the GSPE group than that in the NC group. IL-6 was increased in the sheep fed with TA. The tannins still caused a noticeable shift in the colonic microbiota, with significant increases in the abundances of Adlercreutzia and Oscillospira. Ultimately, it was found that the diet with low levels of tannin could reduce blood triacylglycerol and cholesterol in sheep significantly by affecting the composition of the gut microbiota.

CXCL16 Promotes Ly6Chigh Monocyte Infiltration and Impairs Heart Function after Acute Myocardial Infarction.

High CXCL16 levels during acute cardiovascular events increase long-term mortality. However, the mechanistic role of CXCL16 in myocardial infarction (MI) is unknown. Here we investigated the role of CXCL16 in mice with MI injury. CXCL16 deficiency increased the survival of mice after MI injury, and inactivation of CXCL16 resulted in improved cardiac function and decreased infarct size. Hearts from CXCL16 inactive mice exhibited decreased infiltration of Ly6Chigh monocytes. In addition, CXCL16 promoted the macrophage expression of CCL4 and CCL5. Both CCL4 and CCL5 stimulated Ly6Chigh monocyte migration, and CXCL16 inactive mice had a reduced expression of CCL4 and CCL5 in the heart after MI. Mechanistically, CXCL16 promoted CCL4 and CCL5 expression by activating the NF-κB and p38 MAPK signaling pathways. Anti-CXCL16 neutralizing Ab administration inhibited Ly6Chigh monocyte infiltration and improved cardiac function after MI. Additionally, anti-CCL4 and anti-CCL5 neutralizing Ab administration inhibited Ly6Chigh monocyte infiltration and improved cardiac function after MI. Thus, CXCL16 aggravated cardiac injury in MI mice by facilitating Ly6Chigh monocyte infiltration.

Ni-doped MoS2 embedded in natural wood containing porous cellulose for piezo-catalytic degradation of tetracycline.

Wood is a natural material with low cost and easy recovery, which porous, layered, excellent structure and mechanical properties make it possible to apply in wastewater treatment. We have successfully grown MoS2 on natural wood containing porous cellulose and introduced the high conductivity circuit path provided by Ni nanoparticles to construct a new piezoelectric three-dimensional wood block for the efficient degradation of tetracycline. Ni/MoS2/Wood exhibited excellent piezo-catalytic degradation performance, and the degradation rate of tetracycline reached 95.96 % (k = 0.0411 min-1) under ultrasonic vibration. After 5 cycles, the degradation rate still reached 90.20 %. In addition, Ni/MoS2/Wood was used as the reactor filler to degrade tetracycline through piezoelectric response triggered by hydrodynamic force, and the degradation rate reached 90.27 % after 60 min. Further, the mechanism and the possible degradation pathways of tetracycline degradation were proposed. This low-cost, recyclable and stable three-dimensional wood block piezoelectric material provides a new idea for the practical application of wastewater treatment.

DNA repair byproduct 8-oxoguanine base promotes myoblast differentiation.

Muscle contraction increases the level of reactive oxygen species (ROS), which has been acknowledged as key signaling entities in muscle remodeling and to underlie the healthy adaptation of skeletal muscle. ROS inevitably endows damage to various cellular molecules including DNA. DNA damage ought to be repaired to ensure genome integrity; yet, how DNA repair byproducts affect muscle adaptation remains elusive. Here, we showed that exercise elicited the generation of 8-oxo-7,8-dihydroguanine (8-oxoG), that was primarily found in mitochondrial genome of myofibers. Upon exercise, TA muscle's 8-oxoG excision capacity markedly enhanced, and in the interstitial fluid of TA muscle from the post-exercise mice, the level of free 8-oxoG base was significantly increased. Addition of 8-oxoG to myoblasts triggered myogenic differentiation via activating Ras-MEK-MyoD signal axis. 8-Oxoguanine DNA glycosylase1 (OGG1) silencing from cells or Ogg1 KO from mice decreased Ras activation, ERK phosphorylation, MyoD transcriptional activation, myogenic regulatory factors gene (MRFs) expression. In reconstruction experiments, exogenously added 8-oxoG base enhanced the expression of MRFs and accelerated the recovery of the injured skeletal muscle. Collectively, these data not only suggest that DNA repair metabolite 8-oxoG function as a signal entity for muscle remodeling and contribute to exercise-induced adaptation of skeletal muscle, but also raised the potential for utilizing 8-oxoG in clinical treatment to skeletal muscle damage-related disorders.

8-Oxoguanine targeted by 8-oxoguanine DNA glycosylase 1 (OGG1) is central to fibrogenic gene activation upon lung injury.

Reactive oxygen species (ROS) are implicated in epithelial cell-state transition and deposition of extracellular matrix upon airway injury. Of the many cellular targets of ROS, oxidative DNA modification is a major driving signal. However, the role of oxidative DNA damage in modulation profibrotic processes has not been fully delineated. Herein, we report that oxidative DNA base lesions, 8-oxoG, complexed with 8-oxoguanine DNA glycosylase 1 (OGG1) functions as a pioneer factor, contributing to transcriptional reprogramming within airway epithelial cells. We show that TGFß1-induced ROS increased 8-oxoG levels in open chromatin, dynamically reconfigure the chromatin state. OGG1 complexed with 8-oxoG recruits transcription factors, including phosphorylated SMAD3, to pro-fibrotic gene promoters thereby facilitating gene activation. Moreover, 8-oxoG levels are elevated in lungs of mice subjected to TGFß1-induced injury. Pharmacologic targeting of OGG1 with the selective small molecule inhibitor of 8-oxoG binding, TH5487, abrogates fibrotic gene expression and remodeling in this model. Collectively, our study implicates that 8-oxoG substrate-specific binding by OGG1 is a central modulator of transcriptional regulation in response to tissue repair.

A Single-dose, Two-Period Crossover Bioequivalence Study Comparing Two Liraglutide Formulations in Healthy Chinese Subjects.

Liraglutide, a glucagon-like peptide 1 receptor agonist, is indicated as an adjunct to diet and exercise to improve glycemic control in patients with type 2 diabetes. The original liraglutide products are costly, which limits patient access to this therapeutic treatment. Herein, a biosimilar was developed that is highly similar to the reference drug in molecular structure and bioactivity, and is expected to have similar pharmacokinetic (PK) and safety profiles in clinical studies. This study aimed to primarily evaluate the bioequivalence of 2 liraglutide formulations and secondarily assess their safety in healthy Chinese subjects following a single-dose subcutaneous injection. Thirty-two healthy volunteers were recruited in this randomized, open-label, single-dose, 2-period crossover bioequivalence study (ChiCTR2100043348). The geometric mean ratios (GMRs) of the test drug to the reference drug (T/R) and corresponding 90% confidence intervals (CIs) for maximum concentration (Cmax ) and the area under the concentration-time curve from time 0 to the time of the last quantifiable concentration (AUC0-t ) were estimated using a mixed-effects model, and bioequivalence was determined to have been achieved if the 2-sided 90%CI fell within the predefined range of 80%-125%. PK parameters were comparable between T and R, with GMRs of T/R for Cmax and AUC0-t being 105.7% and 107.7%, respectively, the 90%CI of which met the acceptance criteria for bioequivalence. We also observed a similar and favorable safety profile in the T and R arms, with adverse events being predominantly mild in severity and of gastrointestinal origin. Our findings indicate that the test drug is safe and well tolerated, bioequivalent to the reference drug, and warrants further testing in a phase III clinical trial.

Effect of Enterococcus faecalis on osteoclastogenesis under cobalt-mimicked hypoxia in vitro.

OBJECTIVE: The bone destruction in persistent apical periodontitis associated with infection and a periapical hypoxic microenvironment is not well known. Thus, we aimed to investigate the effects of Enterococcus faecalis on osteoclastogenesis under cobalt-mimicked hypoxia. MATERIALS AND METHODS: Mouse bone marrow-derived macrophages (BMMs) were isolated as osteoclast precursors and stimulated by heat-killed E. faecalis in an environment of cobalt-mimicked hypoxia environment. The cell proliferation and apoptosis were detected using CCK-8 and flow cytometry, respectively. Osteoclast differentiation was determined via tartrate-resistant acid phosphatase staining (TRAP) and immunofluorescence staining. The osteoclastogenic protein and gene expressions were measured by western blotting and real-time PCR. RESULTS: Under cobalt-mimicked hypoxia, E. faecalis markedly inhibited the proliferation of the BMMs and significantly promoted the apoptosis of the BMMs. The differentiation of the BMMs into osteoclasts was enhanced in the presence of the E. faecalis under hypoxia, and the expression of Blimp, c-Fos, and NFATc1 was up-regulated, while the expression of RBP-J was inhibited. CONCLUSIONS: E. faecalis markedly promotes osteoclast differentiation under cobalt-mimicked hypoxia in vitro.

Depicting Fecal Microbiota Characteristic in Yak, Cattle, Yak-Cattle Hybrid and Tibetan Sheep in Different Eco-Regions of Qinghai-Tibetan Plateau.

The gut microbiota is closely associated with the health and production performance of livestock. Partial studies on ruminant microbiota are already in progress in the Qinghai-Tibetan Plateau Area (QTPA) in China, but large-scale and representative profiles for the QTPA are still lacking. Here, 16S rRNA sequencing was used to analyze 340 samples from yak, cattle, yak-cattle hybrids, and Tibetan sheep, which lived in a shared environment from 4 eco-regions of the QTPA during the same season, and aimed to investigate the fecal microbiota community composition, diversity, and potential function. All samples were clustered into 2 enterotypes, which were derived from the genera Ruminococcaceae UCG-005 and Acinetobacter, respectively. Environment, human activity, species, and parasitization all affected the fecal microbiota. By assessing the relationship between the fecal microbiota and the above variables, we identified a scattered pattern of fecal microbiota dissimilarity based more significantly on diet over other factors. Additionally, gastrointestinal nematode infection could reduce the capacity of the bacterial community for biosynthesis of other secondary metabolites, carbohydrate metabolism, and nucleotide metabolism. Ultimately, this study provided a fecal microbiota profile for ruminants living in 4 eco-regions of the QTPA and its potential future applications in developing animal husbandry regimes. IMPORTANCE Cattle, yak, and sheep reside as the main ruminants distributed throughout most regions of Qinghai-Tibetan Plateau Area (QTPA) in China. However, there is a lack of large-scale research in the QTPA on their fecal microbiota, which can regulate and reflect host health as an internalized "microbial organ." Our study depicted the fecal microbiota community composition and diversity of yak, cattle, yak-cattle hybrids, and Tibetan sheep from 4 eco-regions of the QTPA. Additionally, our results demonstrated here that the ruminant samples could be clustered into 2 enterotypes and that diet outweighed other factors in shaping fecal microbiota in the QTPA. This study provided a basis for understanding the microbiota characteristic of ruminants and its possible applications for livestock production in the QTPA.

Innate Immune Responses to RSV Infection Facilitated by OGG1, an Enzyme Repairing Oxidatively Modified DNA Base Lesions.

The primary cause of morbidity and mortality from infection with respiratory syncytial virus (RSV) is the excessive innate immune response(s) (IIR) in which reactive oxygen species (ROS) play key role(s). However, the mechanisms for these processes are not fully understood. We hypothesized that expressions of IIR genes are controlled by the ROS-generated epigenetic-like mark 7,8-dihydro-8-oxo(d)guanine (8-oxo(d)Gua) and 8-oxoguanine DNA glycosylase1 (OGG1). Here, we report that ROS not only generates intrahelical 8-oxo(d)Gua, but also enzymatically disables OGG1 in RSV-infected human airway epithelial cells and mouse lungs. OGG1 bound to 8-oxo(d)Gua in gene regulatory sequences promotes expression of IIR genes, and consequently exacerbates lung inflammation, histological changes, and body weight loss of experimental animals. Pharmacological inhibition of OGG1 substrate binding decreased expression of RSV-induced chemokine and cytokines and significantly lessened clinical symptoms. Results of mechanistic studies show that OGG1 binding at 8-oxo(d)Gua promoter regions modulated loading of transcription factors via transient cooperative interactions in RSV-infected lungs and airway epithelial cells. Other base specific DNA repair proteins had no effects. Collectively, this study identifies unprecedented roles of ROS-generated DNA base lesion(s) and cognate repair protein as a determinant of RSV-induced exuberant inflammation. Pharmaceutical inhibition of OGG1 interaction with its DNA substrate may represent a novel strategy in prevention/intervention of respiratory viral infections.

Novel Single Nucleotide Polymorphisms and Haplotype of MYF5 Gene Are Associated with Body Measurements and Ultrasound Traits in Grassland Short-Tailed Sheep.

Myogenic factor 5 plays active roles in the regulation of myogenesis. The aim of this study is to expose the genetic variants of the MYF5 and its association with growth performance and ultrasound traits in grassland short-tailed sheep (GSTS) in China. The combination technique of sequencing and SNaPshot revealed seven SNPs in ovine MYF5 from 533 adult individuals (male 103 and female 430), four of which are novel ones located at g.6838G > A, g.6989 G > T, g.7117 C > A in the promoter region and g.9471 T > G in the second intron, respectively. Genetic diversity indexes showed the seven SNPs in low or intermediate level, but each of them conformed HWE (p > 0.05) in genotypic frequencies. Association analysis indicated that g.6838G > A, g.7117 C > A, g.8371 T > C, g.9471 T > G, and g.10044 C > T had significant effects on growth performance and ultrasound traits. The diplotypes of H1H3 and H2H3 had higher body weight and greater body size, and haplotype H3 had better performance on meat production than the others. In addition, the dual-luciferase reporter assay showed that there are two active regions in the MYF5 promoter located at −1799~−1197 bp and −514~−241 bp, respectively, but g.6838G > A and g.7117 C > A were out of the region, suggesting these two SNPs influence the phenotype by other pathway. The results suggest that the MYF5 gene might be applied as a promising candidate of functional genetic marker in GSTS breeding.

Measurement of scattered rays from different materials using an inorganic scintillator based optical fiber sensor and its application in radiotherapy.

Measurements using an Optical Fiber OFS including an inorganic scintillator placed on the surface of a phantom show that the particle energy distribution inside the phantom remains unchanged. The backscattered intensity measured using an Optical Fiber Sensor (OFS) exhibits a linear relationship with the total radiation dose delivered to the phantom, and this relationship shows that the OFS can be used for indirect dose measurement when located on the surface of the phantom i.e. that arising from the energetic backscattered electrons and photons. Such a device can therefore be used as a clinicalin-vivodosimeter, being located on the patient's body surface. In addition, the measurement results for the same OFS located inside and outside the radiation field of a compound water based phantom are analyzed. The differences in measurement of the fluorescence signal in response to various tissue materials representing bone or tumor tissue in the irradiation field are strongly related to the material's ability to block the scattered rays from the water phantom, as well as the scattered x-rays generated by the material located within the phantom.