Programmed cell death (PCD) refers to a form of cell death governed by genetic regulation, and consists of several distinct pathways, including apoptosis, autophagy, cuproptosis, ferroptosis, necroptosis, paraptosis and pyroptosis. These pathways are crucial for maintaining intracellular stability and homeostasis, which are involved in the pathogenesis of various diseases. This review innovatively proposes an integrated framework classified by death patterns, and systematically expounds the strategic significance of targeting PCD in cancer treatment. Based on this framework, we conduct an in-depth analysis of how to design corresponding therapeutic strategies for different death patterns, with a particular emphasis on the complex cross-talk and synergistic effects among different PCD pathways. Moreover, we demonstrate that this interaction is the cornerstone for designing the next generation of combination treatment regimens. The aim is to lay a foundation and point out the future direction for the development of more effective and targeted cancer treatment strategies based on the regulation of PCD networks.

BACKGROUND:Disulfidptosis has been recently identified as a mode of programmed cell death, which is becoming a promising target for tumor treatment. However, its biological mechanism in low-grade glioma (LGG) has not yet been thoroughly investigated. Due to the molecular heterogeneity of LGG, it is essential to develop an accurate classification system to predict prognosis and therapeutic response of LGG patients based on distinct molecular characteristics. METHODS AND RESULTS:A prognostic gene signature was constructed based on differentially expressed genes between disulfidptosis-related genes-specified subtypes, which was verified to have superior prognostic performance. According to it, high-risk patients with poor prognosis were more enriched with immune cells, including CD4 + , CD8 + , and regulatory T cells. Through drug sensitivity analysis, several drugs exhibited significant correlation with risk score, and molecular docking illustrated that both dactolisib and linsitinib were capable of binding tightly with most signature genes, making them potential candidates for targeted therapeutic approaches of LGG. Additionally, this model was also found to be significantly associated with tumor mutation burden, stemness index, treatment response, and microbiota features. CONCLUSION:Thus, this model can stratify LGG patients with distinct gene expression features, immune landscape, genomic instability, and microbiota features. By stratifying patients with risk score, this risk model may improve the accuracy of prognostic prediction for LGG patients, which might provide new insights into the molecular targeted therapy for individual treatment in a risk score-specific manner.

Guangxi indigenous chickens represent valuable genetic resources characterized by diverse phenotypic features, disease resistance, and superior meat quality, making them ideal breeding materials for modern breeding systems. Elucidating the genetic basis underlying these traits in Guangxi indigenous chickens is crucial for further advancements in breeding programs. In the current study, using whole-genome sequencing, we performed comprehensive genomic analyses to characterize the genetic diversity, population structure, demographic history and selection signatures for seven Guangxi indigenous chicken breeds and two commercial breeds. The results of genetic diversity indices and effective population size demonstrated Guangxi indigenous chicken breeds maintain significantly higher genetic diversity and have undergone less intensive artificial selection than commercial breeds. Population genetic analyses revealed obvious geographic stratification, dividing Guangxi chicken breeds into southern and northern clusters. Southern populations showed closer genetic affinity to red junglefowl (Gallus gallus spadiceus) than northern populations, suggesting differential selection patterns. Genome-wide selection scans identified strong signals between southern and northern populations, uncovering genes associated with pigmentation (BCO2, SOX10, GRM5, MC1R, MITF, EDN3), body size (IGF1, POU1F1, CDH12) and egg production (AKT3, WDR25). Additionally, comparative genomic analysis with commercial breeds identified divergent selection at loci governing genes related to growth, reproduction, disease resistance and environmental adaptability, such as IGF1, LRP1B, GLI3, CDH7, KIF18A, ROBO2, EVA1A, IKZF1, GRID2, and EPHA7. These selection patterns likely reflect the unique genomic features of Guangxi indigenous chickens, shaped by ecological adaptations, traditional husbandry practices, and consumer preferences. Our findings offer new perspectives on the genetic architecture of Guangxi indigenous chickens, facilitating their conservation and utilization in modern breeding programs.

Esophageal cancer is one of the malignant tumors with high incidence and mortality rates worldwide. Its occurrence and development involve abnormal regulation of multiple signaling pathways. In recent years, the role of Hippo signaling and PEST-containing nuclear protein (PCNP) in esophageal cancer has gradually received attention. As a key regulator of organ size and tissue homeostasis, the Hippo pathway exerts its biological effects primarily through its core effector Yes-associated protein (YAP)/TAZ; accumulating evidence confirms that aberrant activation of YAP is closely linked to esophageal cancer occurrence, progression, lymph node metastasis, and chemoresistance, making it a critical oncogenic driver. PCNP, a highly conserved nuclear protein, together with its E3 enzyme NIRF, is involved in modulating cell cycle progression, DNA damage repair, and apoptotic signaling under physiological conditions. However, its overexpression in esophageal cancer tissues has been associated with accelerated tumor growth and unfavorable patient outcomes, potentially through interactions with downstream oncogenic mediators such as NRF2. This review summarizes the research progress on the Hippo pathway and PCNP, and proposes a possible mechanistic interplay between them in esophageal cancer based on their functions, focusing on exploring their mechanisms of action, regulatory relationships, and potential therapeutic targets in the occurrence and development of esophageal cancer, in order to provide ideas for diagnosis, prognosis, and targeted therapy of esophageal cancer.

Egg production performance a critical economic trait in the poultry industry. The regulatory mechanisms underlying egg production performance mediated by non-coding RNAs remain to be characterized. To systematically investigate ovarian lncRNAs, circRNAs, and miRNAs associated with laying efficiency, we conducted comparative transcriptomic analyses using RNA sequencing (RNA-seq) of ovarian tissues from phenotypically divergent groups - high egg production (HEP) and low egg production (LEP) hens. In our study, we identified 675 lncRNAs, 140 circRNAs, and 10 miRNAs that were significantly differentially expressed (DE) between HEP and LEP. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that target genes of DE lncRNAs, DE miRNAs, and the source genes of DE circRNAs are involved in the MAPK signaling pathway, endocytosis, notch signaling pathway, among others. Furthermore, we identified five miRNA-mRNA interactions related to egg production including gga-miR-449c-3p, and five genes (GLI2, TAC1, EML6, THOC3, MMP9). These findings establish the first comprehensive ncRNA interactome driving ovarian efficiency, offering both biomarkers for breeding selection and mechanistic targets for reproductive enhancement.

BackgroundOral squamous cell carcinoma (OSCC) represents a highly malignant form of cancer characterized by molecular heterogeneity and unsatisfactory treatment outcomes, with approximately 50% of patients experiencing local recurrence and distant metastasis following therapy. Given that metastasis is the most critical determinant of OSCC prognosis, enhancing the precision of clinical interventions and identifying therapeutic targets are of paramount importance. In view of this, this study is the first to develop a machine-learning-based prognostic model integrating epithelial-mesenchymal transition (EMT), anoikis, and basement membrane remodeling genes.MethodsWe systematically evaluated 78 algorithm and parameter combinations to identify a robust prognostic model, stratifying patients into High- and Low-risk groups. Kaplan-Meier survival curves and receiver operating characteristic (ROC) analyses were employed to evaluate the predictive performance of this model. Functional enrichment of differentially expressed genes (DEGs) between risk groups revealed key OSCC progression mechanisms. We further analyzed tumor mutation burden, immune microenvironment features, and identified candidate drugs through sensitivity prediction and molecular docking.ResultsThe identified 13-gene prognostic model effectively stratified patients into high- and low-risk groups, demonstrating strong predictive power for overall survival: the high-risk group exhibited worse prognosis. Mutation landscape demonstrated significant genetic variability within these model genes, which provided insights into the association between elevated tumor mutational burden and adverse prognostic outcomes. Immune landscape revealed a distinct tumor microenvironment: high-risk group exhibited altered immune cell infiltration, along with increased tumor purity, reduced ESTIMATE score and poorer anticipated response to immunotherapy. Finally, seven promising therapeutic candidates were identified through integrated computational drug screening.ConclusionWe developed and validated a 13-gene prognostic model that integrates metastasis-related processes, improves survival prediction, and identifies therapeutic opportunities in OSCC.

The zinc finger protein 521 (ZNF521) gene is located on human chromosome 18, specifically in the 18q11.2 region. As a zinc finger DNA-binding protein, ZNF521/Zfp521 acts as a transcription cofactor involved in the regulation of cell differentiation across various cell types, including hematopoietic, neural, and mesenchyme stem cells, B progenitor cells, preadipocytes, and osteoblasts. Its interactions with key proteins such as RUNX2, EBF1, SIAH2, or BMP2 further modulate these processes. In this review, we briefly summarize the current understanding of ZNF521/Zfp521, encompassing its structural, functional, post-translational modification, and cellular signaling pathways, especially its roles in cell differentiation and related diseases. In addition, we explore the process and effects of the interaction between Zfp521 and other proteins and discuss the molecular mechanisms of its roles in adipogenic, osteogenic, chondrogenic, and neural differentiation.

Liposarcoma (LPS) is the most prevalent soft-tissue sarcoma and the second most common malignant mesenchymal sarcoma. Molecular markers have proven instrumental in guiding the diagnosis, prognosis, and treatment strategies for LPS patients. Identifying potential therapeutic targets is essential for developing effective intervention strategies for LPS. LMNB2, an apoptosis-related gene, exhibits associations with various tumors. Therefore, exploring the feasibility of LMNB2 as a prognostic biomarker for LPS is crucial. After screening for differentially expressed genes (DEGs), which were analyzed by GEO2R, 14 apoptosis-related genes were obtained by overlapping DEGs from the GSE21122 and GSE159659 datasets. SPSS software was used for univariate analysis. Receiver operating characteristic curves were constructed by GraphPad software to compare the expression of LMNB2 between LPS and normal tissues. Kaplan–Meier curves were generated to verify the correlation between LMNB2 expression and survival time. GeneMANIA and STRING were used to construct LMNB2-related gene-gene and protein–protein interaction networks. Hiplot software facilitated function and pathway enrichment analysis to determine the potential mechanism of LMNB2-mediated LPS progression. CIBERSORT was used to evaluate the correlation between LMNB2 expression and immune cell infiltration. The expression level of LMNB2 was significantly higher in LPS, and the high expression of LMNB2 was significantly related to poor prognosis in LPS patients. Further analysis indicated that LMNB2 was mainly involved in “senescence” and “apoptosis,” further confirming its role in regulating the occurrence and development of LPS by modulating the cell cycle progression and apoptosis. This study demonstrates that the elevated expression of LMNB2 is significantly associated with poor prognostic outcomes in LPS, suggesting that LMNB2 holds high potential as a new biomarker for LPS. This study is designed to elucidate the potential mechanism of LMNB2-mediated LPS progression, with the prospect of improving therapeutic development by identifying LMNB2 as a promising prognostic biomarker for LPS.

As BAG family members, Bcl-2 associated athanogene family protein 1 (BAG1) and 2 (BAG2) are implicated in multiple cellular processes, including apoptosis, autophagy, protein folding and homeostasis. Although structurally similar, they considerably differ in many ways. Unlike BAG2, BAG1 has four isoforms (BAG1L, BAG1M, BAG1S and BAG1 p29) displaying different expression features and functional patterns. BAG1 and BAG2 play different cellular functions by interacting with different molecules to participate in the regulation of various diseases, including cancer/tumor and neurodegenerative diseases. Commonly, BAG1 acts as a protective factor to predict a good prognosis of patients with some types of cancer or a risk factor in some other cancers, while BAG2 is regarded as a risk factor to promote cancer/tumor progression. In neurodegenerative diseases, BAG2 commonly acts as a neuroprotective factor. In this review, we summarized the differences in molacular structure and biological function between BAG1 and BAG2, as well as the influences of them on pathogenesis of diseases, and explore the prospects for their clinical therapy application by specifying the activators and inhibitors of BAG1 and BAG2, which might provide a better understanding of the underlying pathogenesis and developing the targeted therapy strategies for diseases.

Liposarcoma (LPS) is the second most common kind of soft tissue sarcoma, and a heterogeneous malignant tumor derived from adipose tissue. Up to now, the prognostic value of BAG1 or BAG2 in LPS has not been defined yet. Expression profiling data of LPS patients were collected from TCGA and GEO database. Survival curves were plotted to verify the outcome differences of patients based on BAG1 or BAG2 expression. Univariate and multivariate Cox regression models were used to analyze the prognostic ability of BAG1 or BAG2. Chaperone’s regulators BAG1 and BAG2 were identified as prognostic biomarkers for LPS patients, which exhibited distinct expression patterns and survival outcome prediction performances. Patients with high BAG2 expression and/or low BAG1 expression had worse prognosis. Enrichment analysis showed that BAG1 was involved in negative regulation of TGF-β signaling. Low expression of BAG1 was associated with high abundance of regulatory T cells (Tregs). The 2-gene signature model further confirmed the improved risk assessment performance of BAG1 and BAG2: high risk patients displayed poor prognosis. BAG1 and BAG2 are supposed to be potential prognostic biomarkers for LPS and have impacts on liposarcomagenesis and immune infiltration in distinctive manners, which may function as potential therapy targets (BAG1 agonists/BAG2 inhibitors) for LPS.

Twist1 is required for embryonic development and expresses after birth in mesenchymal stem cells derived from mesoderm, where it governs mesenchymal cell development. As a well-known regulator of epithelial-mesenchymal transition or embryonic organogenesis, Twist1 is important in a variety of developmental systems, including mesoderm formation, neurogenesis, myogenesis, cranial neural crest cell migration, and differentiation. In this review, we first highlight the physiological significance of Twist1 in cell differentiation, including osteogenic, chondrogenic, and myogenic differentiation, and then detail its probable molecular processes and signaling pathways. On this premise, we summarize the significance of Twist1 in distinct developmental disorders and diseases to provide a reference for studies on cell differentiation/development-related diseases.

The overdevelopment of adipose tissues, accompanied by excess lipid accumulation and energy storage, leads to adipose deposition and obesity. With the increasing incidence of obesity in recent years, obesity is becoming a major risk factor for human health, causing various relevant diseases (including hypertension, diabetes, osteoarthritis and cancers). Therefore, it is of significance to antagonize obesity to reduce the risk of obesity-related diseases. Excess lipid accumulation in adipose tissues is mediated by adipocyte hypertrophy (expansion of pre-existing adipocytes) or hyperplasia (increase of newly-formed adipocytes). It is necessary to prevent excessive accumulation of adipose tissues by controlling adipose development. Adipogenesis is exquisitely regulated by many factors in vivo and in vitro, including hormones, cytokines, gender and dietary components. The present review has concluded a comprehensive understanding of adipose development including its origin, classification, distribution, function, differentiation and molecular mechanisms underlying adipogenesis, which may provide potential therapeutic strategies for harnessing obesity without impairing adipose tissue function.

Current research has found that adipose tissue is not only involved in energy metabolism, but also a highly active endocrine organ that secretes various adipokines, including adiponectin, leptin, resistin and apelin, which are involved in the regulation of physiology and pathology of tissues and organs throughout the body. With the yearly increasing incidence, obesity has become a risk factor for a variety of pathological changes, including inflammation and metabolic syndrome in various system (endocrine, circulatory, locomotor and central nervous system). Thus these symptoms lead to multi-organ dysfunctions, including the heart, liver, kidneys, brain and joints. An in-depth summary of the roles of adipokines in the regulation of other tissues and organs can help to provide more effective therapeutic strategies for obesity-related diseases and explore potential therapeutic targets. Therefore, this review has retrospected the endocrine function of adipose tissue under obesity and the role of dysregulated adipokine secretion in related diseases and the underlying mechanisms, in order to provide a theoretical basis for targeting adipokine-mediated systemic dysregulation.

Background: As a common soft tissue sarcoma, liposarcoma (LPS) is a heterogeneous malignant tumor derived from adipose tissue. Due to the high risk of metastasis and recurrence, the prognosis of LPS remains unfavorable. To improve clinical treatment, a robust risk prediction model is essential to evaluate the prognosis of LPS patients. Methods: By comprehensive analysis of data derived from GEO datasets, differentially expressed genes (DEGs) were obtained. Univariate and Lasso Cox regressions were subsequently employed to reveal distant recurrence-free survival (DRFS)-associated DEGs and develop a prognostic gene signature, which was assessed by Kaplan–Meier survival and ROC curve. GSEA and immune infiltration analyses were conducted to illuminate molecular mechanisms and immune correlations of this model in LPS progression. Furthermore, a correlation analysis was involved to decipher the therapeutic significance of this model for LPS. Results: A six-gene signature was developed to predict DRFS of LPS patients and showed higher precision performance in more aggressive LPS subtypes. Then, a nomogram was further established for clinical application based on this risk model. Via GSEA, the high-risk group was significantly enriched in cell cycle-related pathways. In the LPS microenvironment, neutrophils, memory B cells and resting mast cells exhibited significant differences in cell abundance between high-risk and low-risk patients. Moreover, this model was significantly correlated with therapeutic targets. Conclusion: A prognostic six-gene signature was developed and significantly associated with cell cycle pathways and therapeutic target genes, which could provide new insights into risk assessment of LPS progression and therapeutic strategies for LPS patients to improve their prognosis.

Abstract High-intensity selection has dramatically increased growth rate and daily weight gain in broilers, but the accompanying problem is the excessive deposition of abdominal fat. According to our previous transcriptome analysis, insulin-like growth factor binding protein 2 (IGFBP2) and miR-1434 were identified as involved in abdominal fat. In this study, we further investigated their function in the proliferation and differentiation of chicken preadipocytes. The results indicated that overexpression of IGFBP2 promoted the proliferation and differentiation of preadipocytes, while interference of IGFBP2 inhibited cell proliferation and lipogenic differentiation. The regulatory effect of miR-1434 on the proliferation and differentiation of preadipocytes was opposite to that of IGFBP2. Dual-luciferase reporter assay proved that miR-1434 directly binds to the 3'-untranslated region (3'UTR) of IGFBP2. As expected, the miR-1434 mimics eliminated the impact of the overexpression vector of IGFBP2 on preadipocytes. In brief, we revealed that miR-1434 promoted the proliferation and differentiation of preadipocytes by blocking IGFBP2expression, thus impacting deposition in broilers. These findings may provide a novel target for improving chicken meat quality.

The avian eggshell is formed in the uterus. Changes in uterine function may have a significant effect on eggshell quality. To identify the vital genes impacting uterine functional maintenance in the chicken, uteri in three different periods (22W, 31W, 51W) were selected for RNA sequencing and bioinformatics analysis. In our study, 520, 706 and 736 differentially expressed genes (DEGs) were respectively detected in the W31 vs W22 group, W51 vs W31 group and W51 vs W22 group. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated DEGs were enriched in the extracellular matrix, extracellular region part, extracellular region, extracellular matrix structural constituent, ECM receptor interaction, collagen-containing extracellular matrix and collagen trimer in the uterus ( P < 0.05). Protein–protein interaction analysis revealed that FN1 , LOX , THBS2 , COL1A1 , COL1A2 , COL5A1 , COL5A2 , POSTN , MMP13 , VANGL2 , RAD54B , SPP1 , SDC1 , BTC , ANGPTL3 might be key candidate genes for uterine functional maintenance in chicken. This study discovered dominant genes and pathways which enhanced our knowledge of chicken uterine functional maintenance.

Fat deposition is a vital factor affecting the economics of poultry production. Numerous studies on fat deposition have been done. However, the molecular regulatory mechanism is still unclear. In the present study, the whole-transcriptome RNA sequencing in abdominal fat, back skin, and liver both high- and low-abdominal fat groups was used to uncover the competitive endogenous RNA (ceRNA) regulation network related to chicken fat deposition. The results showed that differentially expressed (DE) genes in abdominal fat, back skin, liver were 1207(784 mRNAs, 330 lncRNAs, 41 circRNAs, 52 miRNAs), 860 (607 mRNAs, 166 lncRNAs, 26 circRNAs, 61 miRNAs), and 923 (501 mRNAs, 262 lncRNAs, 15 circRNAs, 145 miRNAs), respectively. The ceRNA regulatory network analysis indicated that the fatty acid metabolic process, monocarboxylic acid metabolic process, carboxylic acid metabolic process, glycerolipid metabolism, fatty acid metabolism, and peroxisome proliferator-activated receptor (PPAR) signaling pathway took part in chicken fat deposition. Meanwhile, we scan the important genes, FADS2, HSD17B12, ELOVL5, AKR1E2, DGKQ, GPAM, PLIN2, which were regulated by gga-miR-460b-5p, gga-miR-199-5p, gga-miR-7470-3p, gga-miR-6595-5p, gga-miR-101-2-5p. While these miRNAs were competitive combined by lncRNAs including MSTRG.18043, MSTRG.7738, MSTRG.21310, MSTRG.19577, and circRNAs including novel_circ_PTPN2, novel_circ_CTNNA1, novel_circ_PTPRD. This finding provides new insights into the regulatory mechanism of mRNA, miRNA, lncRNA, and circRNA in chicken fat deposition.

During follicular development, a series of key events such as follicular recruitment and selection are crucially governed by strict complex regulation. However, its molecular mechanisms remain obscure. To identify the dominant genes controlling chicken follicular development, the small white follicle (SWF), the small yellow follicle (SYF), and the large yellow follicle (LYF) in different laying stages (W22, W31, W51) were collected for RNA sequencing and bioinformatics analysis. There were 1866, 1211, and 1515 differentially expressed genes (DEGs) between SWF and SYF in W22, W31, and W51, respectively. 4021, 2295, and 2902 DEGs were respectively identified between SYF and LYF in W22, W31, and W51. 5618, 4016, and 4809 DEGs were respectively identified between SWF and LYF in W22, W31, and W51. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that extracellular matrix, extracellular region, extracellular region part, ECM-receptor interaction, collagen extracellular matrix, and collagen trimer were significantly enriched ( P < 0.05). Protein–protein interaction analysis revealed that COL4A2 , COL1A2 , COL4A1 , COL5A2 , COL12A1 , ELN , ALB , and MMP10 might be key candidate genes for follicular development in chicken. The current study identified dominant genes and pathways contributing to our understanding of chicken follicular development.

为了解广西地方鸡的肉质特征,且为进一步推动广西地方鸡品种选种选育提供基础依据,对广西南丹瑶鸡(NDY)、霞烟鸡(XY)、广西三黄鸡(SH)、龙胜凤鸡(LSF)、广西麻鸡(GXM)和东兰乌鸡(DLW)6个地方鸡品种以及艾维茵快大型商品肉鸡于上市日龄进行屠宰,采集胸肌和腿肌,利用仪器分别测定了肉色、电导率、pH、剪切力、肌内脂肪含量等共14个指标.结果显示:广西麻鸡公鸡的胸肌和腿肌Opto值(比色值)显著高于其他品种(P<0.05);东兰乌鸡腿肌肌内脂肪含量显著高于其他地方鸡品种(P<0.05),霞烟鸡胸肌肌内脂肪含量最高但仅与南丹瑶鸡、东兰乌鸡和艾维茵鸡差异显著(P<0.05);龙胜凤鸡胸肌的肌肉电导率45 min最高且除与霞烟鸡和艾维茵鸡差异不显著外(P>0.05),与其他四个地方鸡都差异显著(P<0.05),但腿肌电导率45 min最高为霞烟鸡且除与艾维茵鸡差异不显著外(P>0.05),与其他五个地方鸡品种都差异显著(P<0.05);龙胜凤鸡母鸡胸肌的肌内脂肪含量和剪切力均显著高于其他品种(P<0.05),腿肌的肌内脂肪含量也最高但仅与广西三黄鸡、广西麻鸡和南丹瑶鸡差异显著(P<0.05),腿肌剪切力最高的为广西麻鸡,且除与龙胜凤鸡差异不显著(P>0.05)外和其他品种鸡都差异显著(P<0.05);霞烟鸡胸肌和腿肌的电导率45 min都显著高于其他品种(P<0.05).由此可知,广西麻鸡和广西三黄鸡胸肌腿肌的色泽鲜亮,霞烟鸡公鸡胸肌部位风味相对较好,而腿肌部位则是东兰乌鸡风味较好,龙胜凤鸡公鸡和霞烟鸡母鸡的肌肉电导率较高,一定程度上反映出肌肉系水能力弱.

为深入了解广西地方鸡种肌肉的营养价值,本实验选取120日龄广西三黄鸡、南丹瑶鸡、广西麻鸡、广西乌鸡(东兰乌鸡)和霞烟鸡5个广西地方鸡种各20只,公、母各半,测定其胸肌和腿肌肌肉氨基酸的组成和含量.基于联合国粮农组织和世界卫生组织(FAO/WHO)标准模式谱对其营养价值进行评定.结果显示:在5个广西地方鸡种中,霞烟鸡的必需氨基酸含量、氨基酸总量和味觉氨基酸含量最高,分别为16.88、42.76、22.95 g/100g;5个地方鸡种胸肌和腿肌的必需氨基酸含量存在一定差异,且胸肌显著高于腿肌;不同品种胸肌和腿肌的必需氨基酸/氨基酸总量(EAA/TAA)、必需氨基酸/非必需氨基酸(EAA/NEAA)均符合FAO/WHO提出的理想蛋白源标准;缬氨酸是广西三黄鸡的第一限制性氨基酸,蛋氨酸+胱氨酸是其他4个品种的第一限制性氨基酸.5个地方鸡种的胸肌和腿肌具有丰富的味觉氨基酸,风味氨基酸/氨基酸总量均高于50％,且腿肌比胸肌风味更佳.