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Abstract Enhancing the device electroluminescence quantum efficiency (EQE EL ) is a critical factor in mitigating non-radiative voltage losses (V NR ) and further improving the performance of organic solar cells (OSCs). While the common understanding attributes EQE EL in OSCs to the dynamics of charge transfer (CT) states, persistent efforts to manipulate these decay dynamics have yielded limited results, with the EQE EL of high-efficiency OSCs typically remaining below 10−2%. This value is considerably lower than that observed in high efficiency inorganic photovoltaic devices. Here, we report that EQE EL is also influenced by the dissociation rate constant of singlet states (k DS ). Importantly, in contrast to the traditional belief that advocates maximizing k DS for superior photovoltaic quantum efficiency (EQE PV ), a controlled reduction in k DS is shown to enhance EQE EL without compromising EQE PV . Consequently, a promising experimental approach to address the V NR challenge is proposed, resulting in a significant improvement in the performance of OSCs.

Fusion energy investigation has stepped to a new stage adopting deuterium and tritium as fuels from the previous stage concentrating hydrogen plasma physics. Special radiation safety issues would be introduced during this stage. In addition to industrial and military uses, tungsten is also regarded as the most promising plasma facing material for fusion reactors. During the operation of fusion reactors, tungsten-based plasma facing materials can be activated via neutron nuclear reaction. Meanwhile, activated tungsten dust can be produced when high-energy plasma interacts with the tungsten-based plasma facing materials, namely plasma wall interaction. Activated tungsten dust would be an emerging environmental pollutant with radiation toxicity containing various radionuclides in addition to the chemical toxicity of tungsten itself. Nonetheless, the historical underestimation of its environmental availability has led to limited research on tungsten compared to other environmental contaminants. This paper presents the first systematic review on the safety issue of emerging activated tungsten dust, encompassing source terms, environmental behaviors, and health effects. The key contents are as follows: 1) to detail the source terms of activated tungsten dust from aspects of tungsten basic properties, generation mechanism, physical morphology and chemical component, radioactivity, as well as potential release pathways, 2) to illustrate the environmental behaviors from aspects of atmospheric dispersion and deposition, transformation and migration in soil, as well as plant absorption and distribution, 3) to identify the toxicity and health effects from aspects of toxicity to plants, distribution in human body, as well as health effects by radiation and chemical toxicity, 4) based on the research progress, research and development issues needed are also pointed out to better knowledge of safety issue of activated tungsten dust, which would be beneficial to the area of fusion energy and ecological impact caused by the routine tungsten related industrial and military applications.

Abstract Background Although the accumulation of whole-genome sequencing (WGS) data has accelerated the identification of mutations underlying complex traits, its impact on the accuracy of genomic predictions is limited. Reliable genotyping data and pre-selected beneficial loci can be used to improve prediction accuracy. Previously, we reported a low-coverage sequencing genotyping method that yielded 11.3 million highly accurate single-nucleotide polymorphisms (SNPs) in pigs. Here, we introduce a method termed selective linkage disequilibrium pruning (SLDP), which refines the set of SNPs that show a large gain during prediction of complex traits using whole-genome SNP data. Results We used the SLDP method to identify and select markers among millions of SNPs based on genome-wide association study (GWAS) prior information. We evaluated the performance of SLDP with respect to three real traits and six simulated traits with varying genetic architectures using two representative models (genomic best linear unbiased prediction and BayesR) on samples from 3579 Duroc boars. SLDP was determined by testing 180 combinations of two core parameters (GWAS P-value thresholds and linkage disequilibrium r2). The parameters for each trait were optimized in the training population by five fold cross-validation and then tested in the validation population. Similar to previous GWAS prior-based methods, the performance of SLDP was mainly affected by the genetic architecture of the traits analyzed. Specifically, SLDP performed better for traits controlled by major quantitative trait loci (QTL) or a small number of quantitative trait nucleotides (QTN). Compared with two commercial SNP chips, genotyping-by-sequencing data, and an unselected whole-genome SNP panel, the SLDP strategy led to significant improvements in prediction accuracy, which ranged from 0.84 to 3.22% for real traits controlled by major or moderate QTL and from 1.23 to 11.47% for simulated traits controlled by a small number of QTN. Conclusions The SLDP marker selection method can be incorporated into mainstream prediction models to yield accuracy improvements for traits with a relatively simple genetic architecture, however, it has no significant advantage for traits not controlled by major QTL. The main factors that affect its performance are the genetic architecture of traits and the reliability of GWAS prior information. Our findings can facilitate the application of WGS-based genomic selection.

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is the most prevalent cause of chronic hepatic disease and results in non-alcoholic steatohepatitis (NASH), which progresses to fibrosis and cirrhosis. Although the Leptin deficient rodent models are widely used in study of metabolic syndrome and obesity, they fail to develop liver injuries as in patients. Methods Due to the high similarity with humans, we generated Leptin-deficient (Leptin −/− ) pigs to investigate the mechanisms and clinical trials of obesity and NAFLD caused by Leptin. Results The Leptin −/− pigs showed increased body fat and significant insulin resistance at the age of 12 months. Moreover, Leptin −/− pig developed fatty liver, non-alcoholic steatohepatitis and hepatic fibrosis with age. Absence of Leptin in pig reduced the phosphorylation of JAK2-STAT3 and AMPK. The inactivation of JAK2-STAT3 and AMPK enhanced fatty acid β-oxidation and leaded to mitochondrial autophagy respectively, and both contributed to increased oxidative stress in liver cells. In contrast with Leptin −/− pig, although Leptin deletion in rat liver inhibited JAK2-STAT3 phosphorylation, the activation of AMPK pathway might prevent liver injury. Therefore, β-oxidation, mitochondrial autophagy and hepatic fibrosis did not occurred in Leptin −/− rat livers. Conclusions The Leptin-deficient pigs presents an ideal model to illustrate the full spectrum of human NAFLD. The activity of AMPK signaling pathway suggests a potential target to develop new strategy for the diagnosis and treatment of NAFLD.

Abstract Background Chickens provide globally important livestock products. Understanding the genetic and molecular mechanisms underpinning chicken economic traits is crucial for improving their selective breeding. Influenced by a combination of genetic and environmental factors, metabolites are the ultimate expression of physiological processes and can provide key insights into livestock economic traits. However, the serum metabolite profile and genetic architecture of the metabolome in chickens have not been well studied. Results Here, comprehensive metabolome detection was performed using non-targeted LC–MS/MS on serum from a chicken advanced intercross line (AIL). In total, 7,191 metabolites were used to construct a chicken serum metabolomics dataset and to comprehensively characterize the serum metabolism of the chicken AIL population. Regulatory loci affecting metabolites were identified in a metabolome genome-wide association study (mGWAS). There were 10,061 significant SNPs associated with 253 metabolites that were widely distributed across the entire chicken genome. Many functional genes affect metabolite synthesis, metabolism, and regulation. We highlight the key roles of TDH and AASS in amino acids, and ABCB1 and CD36 in lipids. Conclusions We constructed a chicken serum metabolite dataset containing 7,191 metabolites to provide a reference for future chicken metabolome characterization work. Meanwhile, we used mGWAS to analyze the genetic basis of chicken metabolic traits and metabolites and to improve chicken breeding.

Abstract Background Autosomal dominant polycystic kidney disease (ADPKD) is a prevalent genetic disorder, mainly characterized by the development of renal cysts, as well as various extrarenal manifestations. Previous studies have shown that ADPKD is related to bronchiectasis, while its pathogenic mechanism is unclear. In previous studies, we have generated the PKD1 +/− pigs to simulate the progression of cyst formation and physiological alterations similar to those seen in ADPKD patients. Methods Phenotypic changes to airway epithelial cell and mesenchymal cell in PKD1 +/− pigs were assessed by histological analysis. The molecular mechanisms driving these processes were investigated by using PKD1 +/− pig lungs, human mesenchymal cells, and generating PKD1 deficient human epithelial cells. Results We identified bronchiectasis in PKD1 +/− pigs, which is consistent with the clinical symptoms in ADPKD patients. The deficiency of PKD1 suppressed E-cadherin expression in the airway epithelial barrier, which aggravated invasion and leaded to a perpetuated inflammatory response. During this process, extracellular matrix (ECM) components were altered, which contributed to airway smooth muscle cell phenotype switch from a contractile phenotype to a proliferative phenotype. The effects on smooth muscle cells resulted in airway remodeling and establishment of bronchiectasis. Conclusion To our knowledge, the PKD1 +/− pig provides the first model recapitulating the pathogenesis of bronchiectasis in ADPKD. The role of PKD1 in airway epithelial suggests a potential target for development of new strategies for the diagnosis and treatment of bronchiectasis.

Complex morphology in donor/acceptor organic heterostructures hampers the understanding of device performance. Here, the origin of the high voltage loss in organic solar cells is ascribed to the too small spacing between the donor/acceptor molecules in the active layer, and the voltage loss can be reduced by increasing the donor/acceptor spacing.

Abstract Transmembrane protein (TMEM) is a family of protein that spans cytoplasmic membranes and allows cell–cell and cell–environment communication. Dysregulation of TMEMs has been observed in multiple cancers. However, little is known about TMEM116 in cancer development. In this study, we demonstrate that TMEM116 is highly expressed in non-small-cell lung cancer (NSCLC) tissues and cell lines. Inactivation of TMEM116 reduced cell proliferation, migration and invasiveness of human cancer cells and suppressed A549 induced tumor metastasis in mouse lungs. In addition, TMEM116 deficiency inhibited PDK1-AKT-FOXO3A signaling pathway, resulting in accumulation of TAp63, while activation of PDK1 largely reversed the TMEM116 deficiency induced defects in cancer cell motility, migration and invasive. Together, these results demonstrate that TMEM116 is a critical integrator of oncogenic signaling in cancer metastasis.

Purpose: By incorporating the cost of multiple tumor-marker tests, this work aims to comprehensively evaluate the financial burden of patients and the accuracy of machine learning models in diagnosing malignant pleural effusion (MPE) using tumor-marker combinations. Methods: Carcinoembryonic antigen (CEA), carbohydrate antigen (CA)19-9, CA125, and CA15-3 were collected from pleural effusion (PE) and peripheral blood (PB) of 319 patients with pleural effusion. A stacked ensemble (stacking) model based on five machine learning models was utilized to evaluate the diagnostic accuracy of tumor markers. We evaluated the discriminatory accuracy of various tumor-marker combinations using the area under the curve (AUC), sensitivity, and specificity. To evaluate the cost-effectiveness of different tumor-marker combinations, a comprehensive score (C-score) with a tuning parameter w was proposed. Results: In most scenarios, the stacking model outperformed the five individual machine learning models in terms of AUC. Among the eight tumor markers, the CEA in PE (PE.CEA) showed the best AUC of 0.902. Among all tumor-marker combinations, the PE.CA19-9 + PE.CA15-3 + PE.CEA + PB.CEA combination (C9 combination) achieved the highest AUC of 0.946. When w puts more weight on the cost, the highest C-score was achieved with the single PE.CEA marker. As w puts over 0.8 weight on AUC, the C-score favored diagnostic models with more expensive tumor-marker combinations. Specifically, when w was set to 0.99, the C9 combination achieved the best C-score. Conclusion: The stacking diagnostic model using PE.CEA is a relatively accurate and affordable choice in diagnosing MPE for patients without medical insurance or in a low economic level. The stacking model using the combination PE.CA19-9 + PE.CA15-3 + PE.CEA + PB.CEA is the most accurate diagnostic model and the best choice for patients without an economic burden. From a cost-effectiveness perspective, the stacking diagnostic model with PE.CA19-9 + PE.CA15-3 + PE.CEA combination is particularly recommended, as it gains the best trade-off between the low cost and high effectiveness.

BackgroundEpidemiological investigations have established unhealthy lifestyles, such as excessive leisurely sedentary behavior (especially TV/television watching) and breakfast skipping, increase the risk of type 2 diabetes (T2D), but the causal relationship is unclear. We aimed to understand how single nucleotide variants contribute to the co-occurrence of unhealthy lifestyles and T2D, thereby providing meaningful insights into disease mechanisms.MethodsCombining summary statistics from genome-wide association studies (GWAS) on TV watching (N = 422218), breakfast skipping (N = 193860) and T2D (N = 159208) in European pedigrees, we conducted comprehensive pairwise genetic analysis, including high-definition likelihood (HDL-method), cross-phenotype association studies (CPASSOC), GWAS-eQTL colocalization analysis and transcriptome-wide association studies (TWAS), to understand the genetic overlap between them. We also performed bidirectional two-sample Mendelian randomization (MR) analysis for causal inference using genetic instrumental variables, and two-step MR mediation analysis was used to assess any effects explained by body mass index, lipid traits and glycemic traits.ResultsHDL-method showed that T2D shared a strong genetic correlation with TV watching (rg = 0.26; P = 1.63×10-29) and skipping breakfast (rg = 0.15; P =2.02×10-6). CPASSOC identifies eight independent SNPs shared between T2D and TV watching, including one novel shared locus. TWAS and CPASSOC showed that shared genes were enriched in lung, esophageal, adipose, and thyroid tissues and highlighted potential shared regulatory pathways for lipoprotein metabolism, pancreatic β-cell function, cellular senescence and multi-mediator factors. MR showed TV watching had a causal effect on T2D (βIVW = 0.629, PIVW = 1.80×10-10), but no significant results were observed between breakfast skipping and T2D. Mediation analysis provided evidence that body mass index, fasting glucose, hemoglobin A1c and high-density lipoprotein are potential factors that mediate the causal relationship between TV and T2D.ConclusionsOur findings provide strong evidence of shared genetics and causation between TV watching and T2D and facilitate our identification of common genetic architectures shared between them.

Hydroxyapatite (HAP) was a highly efficient decontamination material for its strong adsorption capacity used in the immobilization of heavy metals, while the particle-size effect was insufficiently investigated during the sorption process. In the present study, the mechanisms of nickel (Ni(II)) adsorption on HAPs with two different particle sizes were investigated by combing batch experiments, desorption, and XRD analysis. The results showed that the adsorption capacity of 20 nm HAP (nano-HAP) was much higher than that of 12 μm HAP (micro-HAP). It was noticed that the results of the present study also clarified the distinct mechanisms in each adsorption process. As for micro-HAP, Ni2+ adsorbed through slow diffusion and replacement with Ca2+ and then incorporated in the lattice at pH between 6.5 and 9.0, which was confirmed by the results of kinetics, thermodynamics, and desorption. And a more compact crystalline structure and irreversible desorption behavior of micro-HAP after Ni(II) adsorption was confirmed by results of XRD and desorption isotherms, respectively. At pH>9.0, lattice incorporation and precipitation controlled together. However, for nano-HAP, the sharp increase of Ni(II) adsorption and ionic strength dependent at pH 6.5 to 9.0 revealed that the dominant mechanisms were ionic exchange and inner-sphere complexation. XRD results showed that characteristic peaks of cassidyite appeared in Ni(II)-loading nano-HAP. At pH>9.0, a precipitate of Ni(II) was the dominant mechanism. The experimental finds demonstrated that nanoscale HAP was a more fast, efficient, and desorbable adsorbent than micro-HAP for Ni(II) removal. These findings would be favorable for investigating the removal mechanisms of heavy metals on the HAP materials and designing the synthesis methods.

The contractile activity, high oxygen consumption and metabolic rate of skeletal muscle cause it to continuously produce moderate levels of oxidant species, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS). Under normal physiological conditions, there is a dynamic balance between the production and elimination of ROS/RNS. However, when the oxidation products exceed the antioxidant defense capacity, the body enters a state of oxidative stress. Myogenesis is an important process to maintain muscle homeostasis and the physiological function of skeletal muscle. Accumulating evidence suggests that oxidative stress plays a key role in myogenesis and skeletal muscle physiology and pathology. In this review, we summarize the sources of reactive oxygen species in skeletal muscle and the causes of oxidative stress and analyze the key role of oxidative stress in myogenesis. Then, we discuss the relationship between oxidative stress and muscle homeostasis and physiopathology. This work systematically summarizes the role of oxidative stress in myogenesis and muscle diseases and provides targets for subsequent antioxidant therapy and repair of inflammatory damage in noninflammatory muscle diseases.

Abstract The sorption mechanism of nickel (Ni) at the illite/water interface was investigated using batch, sorption modelling, extended X-ray absorption fine structure (EXAFS), and extraction approaches. The results showed that Ni(II) sorption on illite was strongly dependent on pH, contact time, temperature, and initial Ni(II) concentration. At a low initial Ni(II) concentration, the ion exchange species of ≡X2Ni° and the inner-sphere complexes including ≡SsONi+, ≡SwONi+ and ≡SwONiOH° species are observed on the sorption edges of Ni(II) on illite. As the initial Ni(II) concentration increased to 1.7 × 10−3 mol/L, precipitates including surface-induced precipitation of s-Ni(OH)2 and amorphous Ni(OH)2 became more significant, especially under neutral to alkaline conditions. EXAFS analysis confirmed that Ni-Al layered double hydroxide (LDH) can gradually form with an increase in the contact time. At pH 7.0, α-Ni(OH)2 was produced in the initial stage and then transformed to the more stable form of Ni-Al LDH with increasing contact time because of the increased Al3+ dissolution. With an increase in temperatures, α-Ni(OH)2 phase on illite transformed to Ni-Al LDH phase, indicating a lower thermodynamic stability compared to Ni-Al LDH phase. These results are important to understand the geochemical behaviors to effectively remediate soil contaminated with Ni(II).

Abstract Introduction Ginseng polysaccharide (GPS, same as Panax polysaccharide) is a kind of polysaccharide extracted from ginseng. It has been reported that GPS has the ability to activate innate immunity, regulates blood sugar balance, and improves antioxidant capacity, but the effect on feeding behavior and its mechanism remains unclear. Method To investigate the possible effect of GPS on feeding behavior of animals, mice were supplied with GPS in water, and food intake, hedonic feeding behavior, anxiety‐like behavior, expression of appetite‐regulation peptides in the central nervous system and glucose‐related hormone levels in the serum of mice were measured. Results Ginseng polysaccharide significantly increased the average daily food intake in mice and promoted hedonic eating behavior. Meanwhile, the levels of serum glucose and glucagon were significantly reduced by GPS, and GPS promoted hypothalamic neuropeptide Y expression, inhibited proopiomelanocortin (POMC) expression, and reduced dopamine D1 receptor (DRD1) levels in the midbrain. We also found that the anxiety level of mice was significantly lower after GPS intake. In conclusion, oral supplementation with GPS promoted food intake in mice, most likely through the regulation of circulating glucose levels.

A 4 MV flash x-ray radiographic machine based on induction voltage adders has been developed. The configuration and design of this machine are reviewed. A three-dimensional, fully electromagnetic model and a circuit simulation model are established to compare with the experiments. The simulation results are in overall agreement with the electrical measurements. The pulsed power performances and output fluctuations of this machine over successive shot sequences are demonstrated. Among the 54 shots, the average peak output voltage is 4.4±0.3 MV (1-σ) and the average diode current is 81.6±4.5 kA (1-σ). Four typical malfunction modes are identified shot by shot including the diode-impedance collapse, insulator flashover, core saturation, and drive mistiming. Some remarkable features from each fault mode are recognized. The first-to-last time spreads of the four drive pluses, t_{spread}, are chosen to quantify the drive synchronization and the influences of the t_{spread} on the peak voltages and diode currents are summarized from the almost 100 shots since the machine was commissioned. It is found that, in order to achieve a voltage of up to 4 MV, t_{spread} should not exceed 25 ns, which is approximately twice the time for electromagnetic wave propagation from the first cavity to the last cavity in vacuum. In addition, the rise time and FWHM duration of output voltages varying with t_{spread} are given. The results indicate that the rise time changes little at the beginning but increases exponentially once the t_{spread} exceeds 30 ns. The FWHM duration nearly increases linearly with t_{spread}.

The interactions between contaminations of U(VI) and silicon oxide nanoparticles (SONPs), both of which have been widely used in modern industry and induced serious environmental challenge due to their high mobility, bioavailability, and toxicity, were studied under different environmental conditions such as pH, temperature, and natural organic matters (NOMs) by using both batch and spectroscopic approaches. The results showed that the accumulation process, i.e., sorption, of U(VI) on SONPs was strongly dependent on pH and ionic strength, demonstrating that possible outer- and/or inner-sphere complexes were controlling the sorption process of U(VI) on SONPs in the observed pH range. Humic acid (HA), one dominated component of NOMs, bounded SONPs can enhance U(VI) sorption below pH~4.5, whereas restrain at high pH range. The reversible sorption of U(VI) on SONPs possibly indicated that the outer-sphere complexes were prevalent at pH 5. However, an irreversible interaction of U(VI) was observed in the presence of HA (Fig 1). It was mainly due to the ternary SONPs-HA-U(VI) complexes (Type A Complexes). After SONPs adsorbed U(VI), the particle size in suspension was apparently increased from ~240 nm to ~350 nm. These results showed that toxicity of both SONPs and U(VI) will decrease to some extent after the interaction in the environment. These findings are key for providing useful information on the possible mutual interactions among different contaminants in the environment.

Transgenic chickens as bioreactors have several advantages, such as the simple establishment procedure, correct glycosylation profile of expressed proteins, etc. Lysozyme is widely used in food industry, livestock farming, and medical field as a replacement of antibiotics because of its antibacterial and complement system-modulating activity. In this study, we used RT-PCR, Western blot, and immunofluorescence to detect the expression of recombinant human lysozyme (rhLY) in the transgenic chicken. We demonstrated that the transgene of rhLY was genetically stable across different generations. We next optimized the purification procedure of rhLY from the transgenic eggs by utilizing two steps of cation-exchange chromatography and one gel-filtration chromatography. About 6 mg rhLY with the purity exceeding 90% was obtained from ten eggs, and the purification efficiency was about 75%. The purified rhLY had similar physicochemical and biological properties in molecular mass and antibacterial activity compared to the commercial human lysozyme. Additionally, both of them exhibited thermal stability at 60°C and tolerated an extensive pH range of 2 to 11. In conclusion, our study proved that the transgenic chickens we have previously generated were genetically stable and suitable for the production of active rhLY. We also provided a pipeline for purifying the recombinant proteins from transgenic eggs, which could be useful for other studies.

The expression of oviduct-specific recombinant proteins in transgenic chickens is a promising technology for the production of therapeutic biologics in eggs. In this study, we constructed a lentiviral vector encoding an expression cassette for human neutrophil defensin 4 (HNP4), a compound that displays high activity against Escherichia coli, and produced transgenic chickens that expressed the recombinant HNP4 protein in egg whites. After the antimicrobial activity of the recombinant HNP4 protein was tested at the cellular level, a 2.8-kb ovalbumin promoter was used to drive HNP4 expression specifically in oviduct tissues. From 669 injected eggs, 218 chickens were successfully hatched. Ten G0 roosters, with semens identified as positive for the transgene, were mated with wild-type hens to generate G1 chickens. From 1,274 total offspring, fifteen G1 transgenic chickens were positive for the transgene, which was confirmed by PCR and Southern blotting. The results of the Southern blotting and genome walking indicated that a single copy of the HNP4 gene was integrated into chromosomes 1, 2, 3, 4, 6 and 24 of the chickens. As expected, HNP4 expression was restricted to the oviduct tissues, and the levels of both transcriptional and translational HNP4 expression varied greatly in transgenic chickens with different transgene insertion sites. The amount of HNP4 protein expressed in the eggs of G1 and G2 heterozygous transgenic chickens ranged from 1.65 μg/ml to 10.18 μg/ml. These results indicated that the production of transgenic chickens that expressed HNP4 protein in egg whites was successful.

Chicken egg lysozyme (cLY) is an enzyme with 129 amino acid (AA) residue enzyme. This enzyme is present not only in chicken egg white but also in mucosal secretions such as saliva and tears. The antibacterial properties of egg white can be attributed to the presence of lysozyme, which is used as an anti-cancer drug and for the treatment of human immunodeficiency virus (HIV) infection. In this study, we constructed a lentiviral vector containing a synthetic cLY signal peptide and a 447 bp synthetic human lysozyme (hLY) cDNA sequence driven by an oviduct-specific ovalbumin promoter, and microinjected into the subgerminal cavity of stage X chick embryos to generate transgenic chicken. The transgene inserted in the chicken chromosomes directs the synthesis and secretion of hLY which has three times higher specific activity than cLY. Three G1 transgenic chickens were identified, the only female of which expressed recombinant human lysozyme (rhLY) at 57.66 ± 4.10 μg/ml in the egg white and the G2 transgenic hens of the G1 transgenic cock A011 expressed rhLY at 48.72 ± 1.54 μg/ml. This experiment demonstrated that transgenic hens with stable oviduct-specific expression of recombinant human lysozyme proteins can be created by microinjection of lentiviral vectors. The results of this research could be contribute to the technological development using transgenic hens as a cost-effective alternative to other mammalian systems, such as cow, sheep and goats, for the production of therapeutic proteins and other applications.