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The chicken industry, in which broiler chickens are bred, is the largest poultry industry in Taiwan. In a traditional poultry house, breeders must usually observe the health of the broilers in person on the basis of their breeding experience at regular times every day. When a breeder finds unhealthy broilers, they are removed manually from the poultry house to prevent viruses from spreading in the poultry house. Therefore, in this study, we designed and constructed a novel small removal system for dead chickens for Taiwanese poultry houses. In the mechanical design, this system mainly contains walking, removal, and storage parts. It comprises robotic arms with a fixed end and sweep-in devices for sweeping dead chickens, a conveyor belt for transporting chickens, a storage cache for storing chickens, and a tracked vehicle. The designed system has dimensions of approximately 1.038 × 0.36 × 0.5 m3, and two dead chickens can be removed in a single operation. The walking speed of the chicken removal system is 3.3 cm/s. In order to enhance the automation and artificial intelligence in the poultry industry, the identification system was used in a novel small removal system. The conditions of the chickens in a poultry house can be monitored remotely by using a camera, and dead chickens can be identified through deep learning based on the YOLO v4 algorithm. The precision of the designed system reached 95.24% in this study, and dead chickens were successfully moved to the storage cache. Finally, the designed system can reduce the contact between humans and poultry to effectively improve the overall biological safety.

Detecting dead chickens in broiler farms is critical for maintaining animal welfare and preventing disease outbreaks. This study presents an automated system that leverages CCTV footage to detect dead chickens, utilizing a two-step approach to improve detection accuracy and efficiency. First, stationary regions in the footage—likely representing dead chickens—are identified. Then, a deep learning classifier, enhanced through knowledge distillation, confirms whether the detected stationary object is indeed a chicken. EfficientNet-B0 is employed as the teacher model, while DeiT-Tiny functions as the student model, balancing high accuracy and computational efficiency. A dynamic frame selection strategy optimizes resource usage by adjusting monitoring intervals based on the chickens’ age, ensuring real-time performance in resource-constrained environments. This method addresses key challenges such as the lack of explicit annotations for dead chickens, along with common farm issues like lighting variations, occlusions, cluttered backgrounds, chicken growth, and camera distortions. The experimental results demonstrate validation accuracies of 99.3% for the teacher model and 98.7% for the student model, with significant reductions in computational demands. The system’s robustness and scalability make it suitable for large-scale farm deployment, minimizing the need for labor-intensive manual inspections. Future work will explore integrating deep learning methods that incorporate temporal attention mechanisms and automated removal processes.

Whole dead poultry birds obtained from commercial layer farms were assessed for fat in the whole carcass and then dry rendered in three different rendering regimens T₁, T₂ and T₃ (temperature = 120, 130 and 140 °C and shell pressure = 1, 2 and 3 kg/cm² respectively) and the effect on the yield and quality of the rendered chicken oil were studied. The overall fat percentage of the whole dead poultry carcass was 14.55 ± 0.17 % and the fat content of ‘greaves’ was 14.49 ± 0.38 %. In the dry batch rendering trials, the mean overall fat recovery was 24.46 ± 1.19, 26.78 ± 3.14 and 22.42 ± 2.32 % and the overall fat yield was 3.52 ± 1.72, 3.84 ± 0.44 and 3.22 ± 0.33 % of the carcass weight in T₁, T₂ and T₃ respectively. Solvent extraction of fat could recover 96.10 ± 0.14 % of fat from ‘greaves’ which was significantly higher than the mechanical centrifugation method. Among the quality characteristics of the rendered chicken oil (RCO), moisture content ranged from 0.61 % (T₂) to 1.09 % (T₁) and the mean specific gravity was 0.91 at 30 °C. The FFA values of RCO obtained from the T₃ rendering regimen were significantly (p < 0.05) higher than the FFA values of T₂ and T₁. The mean acid value, iodine number, peroxide value, saponification value and unsaponifiable matter present in RCO showed no significant difference. The fatty acid profile and calorific values were studied. The RCO was converted to biodiesel by transesterification and the physico-chemical properties of the biodiesel were studied and compared with the Indian biodiesel specification.

Aim: The present study was undertaken to study the etiopathology of dead-in-shell embryos of PB-2 male x Indigenous female crossbred chicken egg. Materials and Methods: A total of 1377 eggs were incubated which was collected from a flock of crossbreed bird (PB2xIndigenous) chicken. Out of which 568 (41.25 %) egg failed to pip out, were utilized for further study. All the dead in shell embryos were examined for different anomalies and pathological condition thorough necropsy examination. For bacteriological isolation a piece of liver, lung and yolk sac contents were collected from 25 nos. of dead in shell embryos and send to the Department of Microbiology for further examination. Results: A total of 241 (42.42 %) egg were recorded as dead-in-shell embryos out of 568 eggs which were fail to pip out. The percentage of dead-in-shell was higher on 21st day (61.34%) than 18th day (38.66 %) of incubation. Out of 241 nos. of dead in shell embryos, 47 (19.50%) cases showed malpositions,19 (7.88%) malformation, 6 (2.49%) adhesion,4 (1.66%) dehydration, 67 (27.80%) pathological condition and 98 (40.66%) cases showed no definite abnormalities and 327 (57.57%) numbers of egg were found as infertile. Conclusion: The dead in shell embryo may be due to genetic factor, breed, some pathological condition, frequent power failure, lack of proper hygiene etc. Keywords: crossbred chicken egg, dead in shell embryo, etiopathology.

Retinoic acid-inducible gene I ( RIG-I ) activates mitochondrial antiviral signaling proteins, initiating the antiviral response. RIG-I and RNF135 , a ubiquitin ligase regulator, are missing in domestic chickens but conserved in mallard ducks. The chickens’ RIG-I loss was long believed to be linked to increased avian influenza susceptibility. We reinstated both genes in chickens and examined their susceptibility to infection with an H7N1 avian influenza virus. Uninfected RIG-I -expressing chickens exhibited shifts in T and B cells. At the same time, the H7N1 infection led to severe disease, persistent weight loss, and increased viral replication. The simultaneous expression of RIG-I and RNF135 potentiated the RIG- I activity and was associated with exacerbated inflammatory response and increased mortality without influencing virus replication. Additional animal infection experiments with two other avian influenza viruses validated these findings. They confirmed that the harmful effects triggered by RIG-I or RIG-I - RNF135 -expression require a minimum degree of viral virulence. Our data indicate that the loss of RIG-I in chickens has likely evolved to counteract deleterious inflammation caused by viral infection and highlight an outcome of restoring evolutionary lost genes in birds.

Efficient long-term cultivation of chicken primordial germ cells (cPGCs) is essential for various avian research and biotechnology applications. Our study aimed to address the challenge of inconsistent culture success by investigating strain-specific variations and optimizing culture conditions using two distinct media: Ovotransferrin-enriched medium (OTM) and chicken serum-supplemented medium (CSM). We demonstrated that each chicken strain has unique nutritional requirements, with Hubbard cPGCs thriving in OTM and Bovans cPGCs favoring CSM. This strain-specific variation was effective in derivation and proliferation rates and the expression of stem cell-specific markers such as POU5F3/OCT4 and NANOG. Furthermore, our study confirmed the sustained germ cell identity of long-term cultured cPGCs through the expression of DAZL, DDX4, and EMA1 germ cell markers. We also showed that cultured cPGCs retained their migratory abilities and transfectability, successfully generating G0 germline chimeras and G1 transgenic Bovans chickens. These findings highlight the importance of optimized culture conditions depending on the genotype to enhance the viability and genetic stability of cPGCs, paving the way for more effective genetic modifications and conservation strategies in avian species.

As an RNA binding protein (RBP), DDX5 is widely involved in the regulation of various biological activities. While recent studies have confirmed that DDX5 can act as a transcriptional cofactor that is involved in the formation of gametes, few studies have investigated whether DDX5 can be used as a transcription factor to regulate the formation of primordial germ cells (PGCs). In this study, we found that DDX5 was significantly up-regulated during chicken PGC formation. Under different PGC induction models, the overexpression of DDX5 not only up-regulates PGC markers but also significantly improves the formation efficiency of primordial germ cell-like cells (PGCLC). Conversely, the inhibition of DDX5 expression can significantly inhibit both the expression of PGC markers and PGCLC formation efficiency. The effect of DDX5 on PGC formation in vivo was consistent with that seen in vitro. Interestingly, DDX5 not only participates in the formation of PGCs but also positively regulates their migration and proliferation. In the process of studying the mechanism by which DDX5 regulates PGC formation, we found that DDX5 acts as a transcription factor to bind to the promoter region of BMP4—a key gene for PGC formation—and activates the expression of BMP4. In summary, we confirm that DDX5 can act as a positive transcription factor to regulate the formation of PGCs in chickens. The obtained results not only enhance our understanding of the way in which DDX5 regulates the development of germ cells but also provide a new target for systematically optimizing the culture and induction system of PGCs in chickens in vitro.

Innate immune system is triggered by pattern recognition receptors (PRRs) recognition. Retinoic acid-inducible gene 1 (RIG-I) is a major sensor that recognizes RNA ligands. However, chickens have no homologue of RIG-I; instead, they rely on melanoma differentiation-associated protein 5 (MDA5) to recognize RNA ligands, which renders chickens susceptible to infection by influenza A viruses (IAVs). Here, we engineered the cMDA5 viral RNA sensing domain (C-terminal domain, CTD) such that it functions similarly to human RIG-I ( hRIG-I ) by mutating histidine 925 into phenylalanine, a key residue for h RIG-I RNA binding loop function, or by swapping the CTD of cMDA5 with that of hRIG-I or duck RIG-I ( dRIG-I ). The engineered cMDA5 gene was expressed in cMDA5 knockout DF-1 cells, and interferon-beta ( IFN-β ) activity and expression of interferon-related genes were measured after transfection of cells with RNA ligands of h RIG-I or human MDA5 ( h MDA5). We found that both mutant cMDA5 and engineered cMDA5 triggered significantly stronger interferon-mediated immune responses than wild-type cMDA5 . Moreover, engineered cMDA5 reduced the IAV titer by 100-fold compared with that in control cells. Collectively, engineered cMDA5/RIG-I CTD significantly enhanced interferon-mediated immune responses, making them invaluable strategies for production of IAV-resistant chickens . Key points • Mutant chicken MDA5 with critical residue of RIG-I (phenylalanine) enhanced immunity. • Engineered chicken MDA5 with CTD of RIG-I increased IFN-mediated immune responses. • Engineered chicken MDA5 reduced influenza A virus titers by up to 100-fold.

The innate immune system, which senses invading pathogens, plays a critical role as the first line of host defense. After recognition of foreign RNA ligands (e.g., RNA viruses), host cells generate an innate immune or antiviral response the interferon-mediated signaling pathway. Retinoic acid-inducible gene I (RIG-1) acts as a major sensor that recognizes a broad range of RNA ligands in mammals; however, chickens lack a RIG-1 homolog, meaning that RNA ligands should be recognized by other cellular sensors such as melanoma differentiation-associated protein 5 (MDA5) and toll-like receptors (TLRs). However, it is unclear which of these cellular sensors compensates for the loss of RIG-1 to act as the major sensor for RNA ligands. Here, we show that chicken MDA5 (cMDA5), rather than chicken TLRs (cTLRs), plays a pivotal role in the recognition of RNA ligands, including poly I:C and influenza virus. First, we used a knockdown approach to show that both cMDA5 and cTLR3 play roles in inducing interferon-mediated innate immune responses against RNA ligands in chicken DF-1 cells. Furthermore, targeted knockout of cMDA5 or cTLR3 in chicken DF-1 cells revealed that loss of cMDA5 impaired the innate immune responses against RNA ligands; however, the responses against RNA ligands were retained after loss of cTLR3. In addition, double knockout of cMDA5 and cTLR3 in chicken DF-1 cells abolished the innate immune responses against RNA ligands, suggesting that cMDA5 is the major sensor whereas cTLR3 is a secondary sensor. Taken together, these findings provide an understanding of the functional role of cMDA5 in the recognition of RNA ligands in chicken DF-1 cells and may facilitate the development of an innate immune-deficient cell line or chicken model.

The incessant arms race between viruses and hosts has led to numerous evolutionary innovations that shape life’s evolution. During this process, the interactions between viral receptors and viruses have garnered significant interest since viral receptors are cell surface proteins exploited by viruses to initiate infection. Our study sheds light on the arms race between the MDA5 receptor and 5’ppp-RNA virus in a lower vertebrate fish, Miichthys miiuy . Firstly, the frequent and independent loss events of RIG-I in vertebrates prompted us to search for alternative immune substitutes, with homology-dependent genetic compensation response (HDGCR) being the main pathway. Our further analysis suggested that MDA5 of M. miiuy and Gallus gallus , the homolog of RIG-I, can replace RIG-I in recognizing 5’ppp-RNA virus, which may lead to redundancy of RIG-I and loss from the species genome during evolution. Secondly, as an adversarial strategy, 5’ppp-RNA SCRV can utilize the m 6 A methylation mechanism to degrade MDA5 and weaken its antiviral immune ability, thus promoting its own replication and immune evasion. In summary, our study provides a snapshot into the interaction and coevolution between vertebrate and virus, offering valuable perspectives on the ecological and evolutionary factors that contribute to the diversity of the immune system. Before the immune system can eliminate a bacterium, virus or other type of pathogen, it needs to be able to recognize these foreign elements. To achieve this, cells in the immune system have proteins called pattern recognition receptors (PRRs) which can identify distinct molecular features of certain pathogens. One specific group of PRRs is a family of retinoic acid-induced RIG-I-like receptors (RLRs), which help immune cells detect different types of viruses. Members of this family recognize distinct motifs on the genetic material of viruses known as RNA. For instance, RIG-I recognizes a marker known as 5’ppp on the end of single-stranded RNA molecules, whereas MDA5 recognizes long strands of double-stranded RNA. Many vertebrates – including various mammals, birds, and fish – lost the RIG-I receptor over the course of evolution. However, Geng et al. predicted that some animals lacking the RIG-I receptor may still be able to activate an immune response against viruses that contain the 5’ppp-RNA motif. To investigate this possibility, Geng et al. studied chickens and miiuy croakers (a type of ray-finned fish) which no longer have a RIG-I receptor. They found that both animals can still sense and eliminate two 5’ppp-RNA viruses called VSV and SCRV. Further experiments revealed that these two viruses are detected by a modified MDA5 receptor that had evolved to bind to 5’-ppp and activate the antiviral response. Viruses are also continuously evolving new ways to escape the immune system. This led Geng et al. to investigate whether SCRV, which causes serious harm to marine fish, has evolved a way to evade the MDA5 protection mechanism. Using miiuy croakers as a model, they found that SCRV causes the transcripts that produce the MDA5 protein to contain more molecules of m6a. This molecular tag degrades the transcript, leading to lower levels of MDA5, reducing the antiviral response against SCRV. The findings of Geng et al. offer valuable perspectives on how the immune system adapts over the course of evolution, and highlight the diversity of antiviral responses in vertebrates. Chickens and miiuy croakers are commonly farmed animals, and further work investigating how viruses invade these species could prevent illnesses from spreading and having a negative impact on the economy.