This review explores strategies to enhance meat quality in poultry, focusing on both management and genetic methods. Poultry meat quality is influenced by many factors, including rearing conditions, nutrition, animal welfare, and post-slaughter processing. Key management factors such as stocking density, ventilation, temperature, and humidity are emphasized for their significant impact on bird welfare and the resulting meat texture, color, and microbial stability. Welfare-enhancing practices like gentle handling, environmental enrichment, and thermal comfort are highlighted for their direct effects on stress levels and meat properties such as water-holding capacity and pH. Innovations in slaughtering and chilling techniques, including electrical and gas stunning and rapid chilling, are shown to preserve meat quality and prevent common defects like pale, soft, and exudative (PSE) or dark, firm, and dry (DFD) meat. The review also underscores the importance of hygiene protocols, hazard analysis and critical control points (HACCP) systems, and traceability technologies to ensure food safety and foster consumer trust. On the genetic front, it discusses conventional selection, marker-assisted selection (MAS), and genomic selection (GS) as tools for breeding birds with better meat quality traits, including tenderness, intramuscular fat, and resistance to conditions like woody breast. Functional genomics and gene editing are identified as the leading edge of future advances. Ultimately, the review advocates for an integrated approach that balances productivity, quality, animal welfare, and sustainability. As consumer expectations increase, the poultry industry must adopt precise, science-based strategies across the entire production process to reliably deliver high-quality meat products.

This study examined the tracheal and cecal microbiome composition across three broiler chicken genotypes including a heritage New Hampshire × Columbian cross (NHC) and modern Ross × Ross 308 (R308) and Ross YP × Ross 708 (R708) broilers, using full-length 16S rRNA sequencing. Birds were reared in floor pens, and at 56 d of age, cecal and tracheal samples were collected from 8 birds per genotype and subjected to DNA extraction followed by PCR amplification of full-length 16S rRNA. Obtained amplified PCR product was sequenced using MinION. A total of 1.8 million reads for tracheal samples and 1.2 million reads for ceca samples were obtained from 24 birds. Despite similar alpha diversity matrixes (Shannon, Simpson, Pielou's evenness, and Chao1) across genotypes in both tracheal and cecal samples, beta diversity analysis revealed significant differences in community composition. Tracheal and cecal microbiota varied significantly among genotypes, particularly NHC with the R308 and R708 groups. At the phylum level, Bacillota (Firmicutes) dominated both tracheal and cecal samples across genotypes. In the trachea, NHC and R708 birds exhibited high relative abundance of Enterococcus cecorum, while Jeotgalicoccus meleagridis dominated R308. Differential abundance analysis showed higher abundance of potentially beneficial bacteria such as Limosilactobacillus pontis and Aerococcus viridans in R308 and R708, while NHC birds had higher levels of species like Merdibacter massiliensis and Agathobaculum butyriciproducens. Cecal microbiome analysis revealed genotype-specific enrichment of species, with NHC birds showing higher abundance of potential pathogens like Shigella boydii and Escherichia fergusonii compared to R708. In contrast, R308 birds harboured more potentially beneficial taxa, including Lactobacillus acidophilus and Limosilactobacillus vaginalis, compared to R708. Pairwise comparisons further highlighted Intestinibacter bartlettii and other potentially beneficial microbes being significantly enriched in R308 over R708. Overall, while microbial richness remained consistent, significant genotype-associated differences in bacterial community structure and genotype-specific microbial abundance were observed, emphasizing the influence of host genetics on microbiota composition and potential implications for poultry health and performance.

The study evaluated the efficacy of four different fat sources in broiler feed on Salmonella presence in litter, spleen, liver, ceca, and carcasses. In this study, 1152, day-old chicks were allocated into four different treatments randomized among 48 pens. Fat source-based treatments included Soy Oil (T1), Poultry Fat (T2), Soap Stock (T3), and Palm Oil (T4). All birds were orally challenged on day 7 with 10^8 CFU of S. Enteritidis and S. Typhimurium cocktail. On days 14, 21, 28, 35, and 42, litter was sampled from each pen using boot swabs and spleen, liver, and cecal contents were sampled from one bird from each pen for Salmonella recovery. On day 43, 16 post-pick carcass rinsates per treatment were collected for Salmonella recovery. Data was analyzed using PROC GLM of SAS and Chi-square test in R. On day 14, Salmonella was detected from 16 %, 25 %, 41 %, and 33 % of spleen and 83 %, 66 %, 50 %, and 75 % of liver samples from T1, T2, T3, and T4, respectively (P > 0.05). Salmonella prevalence decreased in liver to 0 % at day 42 in all treatments except for 1 liver from T1. At day 14, cecal contents were 92 %, 83 %, 92 %, and 92 % Salmonella positive for T1, T2, T3, and T4 with an average of 3.5 to 4.6 log₁₀CFU/g. However, by day 42, Salmonella was not detected by direct plating in cecal contents and prevalence decreased to 25 %, 45 %, 42 %, and 25 % from T1, T2, T3, and T4, respectively. Post-pick carcass rinses were 100 %, 100 %, 100 %, and 81 % positive from T1, T2, T3, and T4, respectively. No significant differences in Salmonella counts or prevalence were observed among different dietary fat source treatment groups. These results indicate that the clearance pattern of Salmonella from internal organs over time was not influenced by fat sources. Although internal Salmonella contamination appeared to have mostly cleared by day 42, the continued presence and survival of Salmonella in the litter may have resulted in post-pick carcass contamination.

Glypican-3 (GPC3), a membrane-bound heparan sulfate proteoglycan, has long been found to be dysregulated in human lung adenocarcinomas (LUADs). Nevertheless, the function, mutational profile, epigenetic regulation, co-expression profile, and clinicopathological significance of the GPC3 gene in LUAD progression are not well understood. In this study, we analyzed cancer microarray datasets from publicly available databases using bioinformatics tools to elucidate the above parameters. We observed significant downregulation of GPC3 in LUAD tissues compared to their normal counterparts, and this downregulation was associated with shorter overall survival (OS) and relapse-free survival (RFS). Nevertheless, no significant differences in the methylation pattern of GPC3 were observed between LUAD and normal tissues, although lower promoter methylation was observed in male patients. GPC3 expression was also found to correlate significantly with infiltration of B cells, CD8+, CD4+, macrophages, neutrophils, and dendritic cells in LUAD. In addition, a total of 11 missense mutations were identified in LUAD patients, and ~1.4% to 2.2% of LUAD patients had copy number amplifications in GPC3. Seventeen genes, mainly involved in dopamine receptor-mediated signaling pathways, were frequently co-expressed with GPC3. We also found 11 TFs and 7 miRNAs interacting with GPC3 and contributing to disease progression. Finally, we identified 3 potential inhibitors of GPC3 in human LUAD, namely heparitin, gemcitabine and arbutin. In conclusion, GPC3 may play an important role in the development of LUAD and could serve as a promising biomarker in LUAD.

COVID-19 has raised significant concern regarding its neurological impact, particularly during the early pandemic waves when severe systemic inflammation and neuroimmune dysregulation were more common. Although SARS-CoV-2 has been extensively studied, the precise mechanisms underlying its neurological effects remain incompletely understood, and much of the available evidence is derived from early variants with higher pathogenicity. Current research indicates that neuroinflammatory processes—driven primarily by systemic cytokine elevation, microglial activation, and blood–brain barrier dysfunction—contribute to a wide range of neurological symptoms. Severe complications such as encephalopathy, stroke, and cognitive impairment were predominantly reported in critically ill patients infected with the Wuhan, Alpha, or Delta variants, while such manifestations are considerably less frequent in the Omicron era. Most proposed mechanisms, including ACE2-mediated viral entry into the central nervous system, are supported mainly by experimental or preclinical studies rather than definitive human evidence. Biomarkers such as IL-6 and TNF-α, along with neuroimaging modalities including MRI and PET, offer useful but indirect indicators of neuroinflammation. Therapeutic approaches continue to focus on controlling systemic inflammation through immunomodulatory agents, complemented by targeted non-pharmacological strategies—such as physical rehabilitation, cognitive support, and psychological interventions—for the minority of patients with persistent neurological deficits. Overall, current evidence supports a variant-dependent neuroinflammatory profile and underscores the need for longitudinal, mechanism-focused studies to better characterize long-term neurological outcomes and refine therapeutic strategies.

This study investigated the longitudinal dynamics of the cecal microbiome in male and female broiler chickens from hatch (d 0) to market age (d 42) using full-length 16S rRNA gene sequencing via Oxford Nanopore Technology. Microbial composition, diversity, and differential abundance were assessed across four time points (d 0, 14, 28, and 42). Alpha diversity analyses showed no significant differences between male and female within the same age group. The longitudinal comparisons revealed significantly lower diversity on d 0 compared to later timepoints in both male and female. Beta diversity analyses using Bray-Curtis and Jaccard metrics demonstrated distinct microbial community clustering at d 0 and a major compositional shift by d 14. PERMANOVA confirmed age as a significant factor influencing microbial composition. However, both sex and age influenced the dominant bacterial species. On d 0, Enterococcus faecalis was the most abundant in both males (58.57%) and females (61.35%). Whereas on d 42, Romboutsia ilealis (14.12%) became the predominant species in female and Negativibacillus massiliensis (9.7%) in males. In addition to the variation in the dominant species, differential abundance analysis revealed that bacterial species such as Clostridium celatum, C. disporicum, C. jeddahitimonense, and C. saudiense, had significantly higher abundance at d 0 compared to later time points in both males and females. Whereas bacterial species such as Bittarella massiliensis, Turicibacter bilis,and Turicibacter sanguinis had significantly higher abundance at d 28 and 42. Furthermore, core microbiome analysis showed microbial richness plateaued at approximately 330-350 species from d 14 onward. Our results indicate that early microbial communities are more sex-specific and they gradually converge over time probably due to extrinsic environmental factors.