Biomedical subjects

Jia Li

Publications and source records attributed to Jia Li.

At least 19 recordsLinked to original sources

PubMed2026

Age as a core disease modifier: Distinct clinical, molecular and prognostic landscapes of essential thrombocythaemia in adolescents and young adults.

Essential thrombocythaemia (ET) in adolescents and young adults (AYA, 15-39 years) is a distinct entity with an incompletely defined prognosis. In this multicentre retrospective study, 1728 ET patients from 29 centres across China were stratified into AYA (n = 328) and non-AYA (≥40 years, n = 1400) cohorts. We compared their clinical profiles, genomic landscapes, long-term outcomes and risk factors for progression to post-ET myelofibrosis (MF). AYA patients had fewer cardiovascular risks and lower thrombosis rates, but higher rates of extreme thrombocytosis. Molecularly, AYA patients were enriched for calreticulin (CALR) mutations, whereas Janus kinase 2 (JAK2) predominated in older patients. The burden of non-driver mutations (tet methylcytosine dioxygenase 2 [TET2], DNA methyltransferase 3A [DNMT3A], ASXL transcriptional regulator 1 [ASXL1], SH2‑B adaptor protein 3 [SH2B3]) was lower in AYA patients. Consequently, AYA patients achieved superior long-term outcomes across all key survival endpoints, including overall, myelofibrosis-free and leukaemia-free survival. Analysis of post-ET MF progression risks identified age-specific patterns: CALR mutations are enriched in younger patients and show an age-specific association with MF progression. AYA-ET constitutes a unique clinicomolecular subtype with a favourable prognosis, supporting age-stratified management. The enrichment of CALR mutations and their specific link to MF progression in young patients underscore the urgent need for targeted therapies against CALR-mutant clones.

adolescents and young adults (AYA)↗

PubMed2026

Natural variation in SL6 determines fatty acid components and seed longevity in rice.

Seed longevity (SL) is vital for ensuring food security worldwide. However, the genetic basis of SL has been scarcely documented. Here, we report the cloning of a major SL locus, qSL6, encoding a fatty acyl-ACP thioesterase type B. SL6 is functionally conserved in regulating palmitic acid synthesis in seeds, conferring higher oxidation durability and SL in various species. Through the VP1-SL6 module, a seed desiccation-derived ABA signal is transmitted via VP1, which directly activates SL6 transcription to alter the fatty acid composition and elevate SL in seeds. The ancestral elite allele SL6HHZ harbors a virus-derived CT-rich motif cis-element in the 5'UTR, which serves as a universal, bidirectional mRNA stabilizer, contributing to the divergence between indica and japonica in terms of SL. Moreover, manipulating SL6 expression via marker-assisted selection or transgenic approaches notably improved SL in rice cultivars and F1 hybrids without affecting major agronomic traits. Our findings provided a promising genetic locus for improving SL in rice.

Oryza↗

PubMed2026

Identification of the BrSK gene family in flowering Chinese cabbage and functional characterization of BrSK2 subfamily involvement in heat stress.

Glycogen synthase kinase 3 (GSK3) kinases are evolutionarily conserved regulators of plant development and stress signaling, yet their contributions to thermotolerance in cool-adapted Brassica crops remain poorly understood. Here, we identified 16 BrSK genes in the Caixin (Brassica rapa ssp. chinensis var. parachinensis) genome, all harboring intact catalytic motifs indicative of functional kinase activity. Spatiotemporal expression profiling revealed preferential accumulation of BrSK transcripts in stem apices and floral organs during reproductive transition, while promoter analysis identified abundant heat- and abiotic stress-responsive cis-elements. Under heat stress, BrSK21, BrSK22, and BrSK23 displayed striking genotype-specific expression dynamics. BrSK21/22/23 transcripts were stably suppressed in the heat-tolerant cultivar '49-19' but transiently declined before rapidly rebounding in the heat-sensitive 'Liuye 50', mirroring RNA-seq profiles. Protein-protein interaction assays (Y2H, BiFC, and LCI) demonstrated specific associations between BrSK kinases and BrHSFA1. Functional validation via VIGS revealed that silencing of BrSK21 significantly enhanced thermotolerance, with triple silencing of BrSK21/22/23 conferring additive protection, indicating functional redundancy within the BrSK2 subfamily. Collectively, these findings establish the BrSK2 subfamily as negative regulators of heat tolerance in Caixin, likely via modulation of BrHSFA1 expression. This work identifies high-priority targets for molecular breeding of climate-resilient Brassica vegetables.

Plant Proteins↗

PubMed2026

COMMD9-regulated endothelial cell abnormality-induced hypercoagulability is associated with Budd-Chiari syndrome.

BACKGROUND: Budd-Chiari syndrome (BCS) presents diagnostic and treatment challenges owing to its insidious onset. Genetic variants associated with BCS vary geographically; in Asian populations, the condition is primarily caused by membranous obstruction composed of endothelial cells (ECs). A better understanding of the genetic pathogenesis of membranous BCS may offer new insights into disease mechanisms. METHODS: This study employed whole-exome sequencing to identify candidate genes responsible for EC abnormalities in 485 patients with membranous BCS and 329 patients with vascular malformations (VaMs). Functional investigations were conducted to validate the selected genes in vitro and in vivo. RESULTS: Whole-exome data revealed that the frequency of variants in the vascular function-related KLHDC2 exceeded that of JAK2 in BCS. Knockdown of KLHDC2 promoted adhesion and suppressed proliferation of ECs. In addition, 92 genes enriched for rare variants overlapped between BCS and VaMs. Systems biology analysis revealed two gene clusters, including COMMD9, enriched in proteins intolerant to loss-of-function mutations. Furthermore, suppression of COMMD9 impaired EC migration and tube formation, inhibited subintestinal angiogenic sprouting in zebrafish, and elevated EC adhesion. Transcriptomic analysis linked COMMD9 to EC abnormalities via the PI3K-Akt pathway. Commd9 knockdown promoted venous hypercoagulability in vivo following drug or ligation-induced stenosis. CONCLUSIONS: These findings indicate that multiple rare genetic variants, particularly in COMMD9, are involved in the development of membranous BCS by regulating hypercoagulability induced by EC abnormalities. These findings may help guide future clinical research towards improved understanding and treatment of BCS.

Budd–Chiari syndrome↗

PubMed2024

The ARK2N-CK2 complex initiates transcription-coupled repair through enhancing the interaction of CSB with lesion-stalled RNAPII.

Transcription is extremely important for cellular processes but can be hindered by RNA polymerase II (RNAPII) pausing and stalling. Cockayne syndrome protein B (CSB) promotes the progression of paused RNAPII or initiates transcription-coupled nucleotide excision repair (TC-NER) to remove stalled RNAPII. However, the specific mechanism by which CSB initiates TC-NER upon damage remains unclear. In this study, we identified the indispensable role of the ARK2N-CK2 complex in the CSB-mediated initiation of TC-NER. The ARK2N-CK2 complex is recruited to damage sites through CSB and then phosphorylates CSB. Phosphorylation of CSB enhances its binding to stalled RNAPII, prolonging the association of CSB with chromatin and promoting CSA-mediated ubiquitination of stalled RNAPII. Consistent with this finding, Ark2n-/- mice exhibit a phenotype resembling Cockayne syndrome. These findings shed light on the pivotal role of the ARK2N-CK2 complex in governing the fate of RNAPII through CSB, bridging a critical gap necessary for initiating TC-NER.

DNA Repair Enzymes↗

PubMed2024

Identification of cuproptosis-realated key genes and pathways in Parkinson's disease via bioinformatics analysis.

INTRODUCTION: Parkinson's disease (PD) is the second most common worldwide age-related neurodegenerative disorder without effective treatments. Cuproptosis is a newly proposed conception of cell death extensively studied in oncological diseases. Currently, whether cuproptosis contributes to PD remains largely unclear. METHODS: The dataset GSE22491 was studied as the training dataset, and GSE100054 was the validation dataset. According to the expression levels of cuproptosis-related genes (CRGs) and differentially expressed genes (DEGs) between PD patients and normal samples, we obtained the differentially expressed CRGs. The protein-protein interaction (PPI) network was achieved through the Search Tool for the Retrieval of Interacting Genes. Meanwhile, the disease-associated module genes were screened from the weighted gene co-expression network analysis (WGCNA). Afterward, the intersection genes of WGCNA and PPI were obtained and enriched using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Subsequently, the key genes were identified from the datasets. The receiver operating characteristic curves were plotted and a PPI network was constructed, and the PD-related miRNAs and key genes-related miRNAs were intersected and enriched. Finally, the 2 hub genes were verified via qRT-PCR in the cell model of the PD and the control group. RESULTS: 525 DEGs in the dataset GSE22491 were identified, including 128 upregulated genes and 397 downregulated genes. Based on the PPI network, 41 genes were obtained. Additionally, the dataset was integrated into 34 modules by WGCNA. 36 intersection genes found from WGCNA and PPI were significantly abundant in 7 pathways. The expression levels of the genes were validated, and 2 key genes were obtained, namely peptidase inhibitor 3 (PI3) and neuroserpin family I member 1 (SERPINI1). PD-related miRNAs and key genes-related miRNAs were intersected into 29 miRNAs including hsa-miR-30c-2-3p. At last, the qRT-PCR results of 2 hub genes showed that the expressions of mRNA were up-regulated in PD. CONCLUSION: Taken together, this study demonstrates the coordination of cuproptosis in PD. The key genes and miRNAs offer novel perspectives in the pathogenesis and molecular targeting treatment for PD.

Humans↗

PubMed2006

Application of surface molecular imprinting adsorbent in expanded bed for the adsorption of Ni(2+) and adsorption model.

A new surface molecular imprinting adsorbent (SMIA) was used in an expanded bed. The expansion ratio and adsorption performance were studied at different volumetric rates, inlet concentrations, and pH values. A model based on the Adams-Bohart adsorption model of breakthrough curves was established. The predicted curves had good agreement with the experimental curves. The breakthrough time (T(1/2)) decreased with increasing inlet concentration when the outlet concentration was half the initial concentration (C/C(0)=0.5). The inlet concentration had little effect on the adsorption rate constant (k(1)) value when the initial concentration (C(0)) was above 150 mg/L. However, T(1/2) values increased with increasing initial pH of the inlet solution, and the k(1) value decreased due to the competition between H(+) and Ni(2+).

Adsorption↗

PubMed2006

Vascular development is disrupted by endothelial cell-specific expression of the anti-apoptotic protein Bcl-2.

Endothelial cell (EC) apoptosis has been detected in remodelling blood vessels in vivo, and inhibition of EC apoptosis appears to alter vascular morphogenesis in vitro, suggesting that EC apoptosis may play a role in blood vessel remodelling. However, apoptotic EC are difficult to quantify in vivo, and studies of the incidence of EC apoptosis and the sites at which it occurs in vivo have produced contradictory results. Therefore, the specific biological roles played by EC apoptosis remain unclear. Here, we have used a transgenic approach to determine the biological function of EC apoptosis in vivo. Anti-apoptotic Bcl-2 transgenes were expressed in mice under control of the EC-specific tie2 promoter. These transgenic mice died during the second half of gestation. While the development and remodelling of large vessels including aortic arch arteries and great veins proceeded normally, abnormally dense and disorganised networks of small vessels were present in the skin and internal organs. In addition, vessel organisation and lumen formation were disrupted in the placental labyrinth. This study provides direct experimental evidence that endothelial cell apoptosis plays an essential role during embryogenesis. Our results suggest that EC apoptosis plays an important role in determining the structure of the microcirculation but may be dispensable for large vessel development.

Animals↗

PubMed2006

Matrine induced gastric cancer MKN45 cells apoptosis via increasing pro-apoptotic molecules of Bcl-2 family.

Matrine, one of the main active components from the dry roots of Sophora flavescence, was known to induce apoptosis in a variety of tumor cells in vitro. However, the molecular mechanism of cell apoptosis induced by Matrine remains elusive. Here, we investigated the apoptosis in Matrine-treated human gastric cancer MKN45 cells. The results showed that Matrine could inhibit cell proliferation and induce apoptosis in a dose-dependent manner. Further immunoblots revealed that in Matrine-treated cells, caspase-3, -7 were activated and the pro-apoptotic molecules Bok, Bak, Bax, Puma, and Bim were also up-regulated. Our results suggested that Matrine induced gastric cancer MKN45 cells apoptosis via increasing pro-apoptotic molecules of Bcl-2 family.

Alkaloids↗

PubMed2006

4-NQO induces apoptosis via p53-dependent mitochondrial signaling pathway.

4-Nitroquinoline N-oxide (4-NQO) as an UV-mimetic agent leading to DNA damage is a potent mutagen and carcinogen, and can induce apoptosis in various types of cells. However, the mechanism of apoptosis induced by 4-NQO is still not quite clarified. In this study we found that 4-NQO could not only induce apoptosis in KB cells, but also caused considerable damage to the mitochondrial membrane. Therefore, we inferred that 4-NQO might induce apoptosis through the mitochondrial signaling pathway resulting from DNA damage. Further investigation showed that the apoptosis induced by 4-NQO was p53-dependent. Furthermore, the expression levels of bax and bcl-2, closely related to mitochondrial signaling pathway, were up- and down-regulated, respectively. Meanwhile, the activity of caspase-9 and -3, lying in downstream of mitochondrial, was also enhanced. At the same time, the expression level of p21 also was increased by 4-NQO exposure, leading to the cell cycle arrested in G(1) phase. The results indicated that 4-NQO arrested cell cycle in G(1) phase, thus allowing enough time for DNA repair; on the other hand, if the cellular DNA were not repaired, apoptosis may follow through the p53-dependent mitochondrial signaling pathway, and mechanism of apoptosis induced by 4-NQO is not exactly the same that induced by UV radiation, as the later induces apoptosis through death receptors and mitochondrial signaling pathway.

4-Nitroquinoline-1-oxide↗

PubMed2006

Conserved alpha-helix acts as autoinhibitory sequence in AMP-activated protein kinase alpha subunits.

AMP-activated protein kinase (AMPK) acts as an energy sensor, being activated by metabolic stresses and regulating cellular metabolism. AMPK is a heterotrimer consisting of a catalytic alpha subunit and two regulatory subunits, beta and gamma. It had been reported that the mammalian AMPK alpha subunit contained an autoinhibitory domain (alpha1: residues 313-392) and had little kinase activity. We have found that a conserved short segment of the alpha subunit (alpha1-(313-335)), which includes a predicted alpha-helix, is responsible for alpha subunit autoinhibition. The role of the residues in this segment for autoinhibition was further investigated by systematic site-directed mutation. Several hydrophobic and charged residues, in particular Leu-328, were found to be critical for alpha1 autoinhibition. An autoinhibitory structural model of human AMPK alpha1-(1-335) was constructed and revealed that Val-298 interacts with Leu-328 through hydrophobic bonding at a distance of about 4 A and may stabilize the autoinhibitory conformation. Further mutation analysis showed that V298G mutation significantly activated the kinase activity. Moreover, the phosphorylation level of acetyl-CoA carboxylase, the AMPK downstream substrate, was significantly increased in COS7 cells overexpressing AMPK alpha1-(1-394) with deletion of residues 313-335 (Deltaalpha394) and a V298G or L328Q mutation, and the glucose uptake was also significantly enhanced in HepG2 cells transiently transfected with Deltaalpha394, V298G, or L328Q mutants, which indicated that these AMPK alpha1 mutants are constitutively active in mammalian cells and that interaction between Leu-328 and Val-298 plays an important role in AMPK alpha autoinhibitory function.

AMP-Activated Protein Kinases↗

PubMed2006

Adverse effects of dopamine on systemic hemodynamic status and oxygen transport in neonates after the Norwood procedure.

OBJECTIVES: The purpose of this study was to evaluate the effects of dopamine on hemodynamic status and oxygen transport in neonates after the Norwood procedure. BACKGROUND: Dopamine is widely used to augment cardiac performance and increase oxygen delivery (DO2) in patients after cardiopulmonary bypass (CPB). This might be at the expense of increased myocardial and systemic oxygen consumption (VO2), thus offsetting the improved DO2. This balance is particularly fragile in critically ill neonates. METHODS: Systemic oxygen consumption was continuously measured with respiratory mass spectrometry in 13 sedated, paralyzed, and mechanically ventilated neonates for 72 h after the Norwood procedure. Arterial, superior vena caval, and pulmonary venous blood gases were measured to calculate pulmonary blood flow (Q(p)) and systemic blood flow (Q(s)), DO2, and oxygen extraction ratio (ERO2). Rate-pressure product was calculated. Dopamine at a dose of 5 microg/kg/min was routinely administered at cessation of CPB and terminated within the first 48 h. Hemodynamic and oxygen transport measures were obtained before and at 100 min after the termination of dopamine. RESULTS: Terminating dopamine was not associated with significant changes in arterial pressure, Q(p), Q(s), or DO2 but was associated with a significant decrease in heart rate (p = 0.003), rate-pressure product (p = 0.03), and VO2 (-20 +/- 11%, p < 0.0001), resulting in a significant decrease in ERO2 (p = 0.01). CONCLUSIONS: Dopamine induces a significant increase in VO2 in neonates after the Norwood procedure, and termination is associated with an improved balance of VO2-DO2. These data further emphasize the importance of understanding changes in VO2 as well as DO2 in infants after cardiac surgery.

Blood Pressure↗

PubMed2006

Using unnatural protein fusions to engineer resveratrol biosynthesis in yeast and Mammalian cells.

Resveratrol is a naturally occurring defense compound produced by a limited number of plants in response to stresses. Besides cardiovascular benefits, this health-promoting compound has been reported to extend life spans in yeasts, flies, worms, and fish. To biosynthesize resveratrol de novo, tyrosine ammonia lyase (TAL), 4-coumarate CoA-ligase (4CL), and stilbene synthase (STS) were isolated from Rhodobacter sphaeroides, Arabidopsis thaliana, and Vitis vinifera, respectively. Yeast cells expressing 4CL and STS produce resveratrol when fed with 4-coumaric acid, the substrate of 4CL. When a translational fusion protein joining 4CL and STS was used, yeast cells produced 15-fold more resveratrol than the cotransformed cells, suggesting that physical localization of 4CL and STS facilitate resveratrol production. When the resveratrol pathway was introduced into human HEK293 cells, de novo biosynthesis was detected, leading to intracellular accumulation of resveratrol. We successfully engineered an entire plant natural product pathway into a mammalian host.

Acyltransferases↗

PubMed2006

Isoquinoline-1,3,4-trione and its derivatives attenuate beta-amyloid-induced apoptosis of neuronal cells.

Caspase-3 is a programmed cell death protease involved in neuronal apoptosis during physiological development and under pathological conditions. It is a promising therapeutic target for treatment of neurodegenerative diseases. We reported previously that isoquinoline-1,3,4-trione and its derivatives inhibit caspase-3. In this report, we validate isoquinoline-1,3,4-trione and its derivatives as potent, selective, irreversible, slow-binding and pan-caspase inhibitors. Furthermore, we show that these inhibitors attenuated apoptosis induced by beta-amyloid(25-35) in PC12 cells and primary neuronal cells.

Amyloid beta-Peptides↗

PubMed2006

Transgenic rice plants ectopically expressing AtBAK1 are semi-dwarfed and hypersensitive to 24-epibrassinolide.

Brassinosteroids (BRs) are endogenous plant hormones essential for plant growth and development. Brassinosteroid insensitive1 (BRI1)-assocaiated receptor kinase (BAK1) is one of the key components in the BR signal transduction pathway due to its direct association with the BR receptor, BRI1. Although BRI1 and its orthologs have been identified from both dicotyledonous and monocotyledonous plants, less is known about BAK1 and its orthologs in higher plants other than Arabidopsis. This article provides the first piece of evidence that AtBAK1 can greatly affect growth and development of rice plants when ectopically expressed, suggesting that rice may share similar BR perception mechanism via BRI1/BAK1 complex. Interestingly, transgenic rice plants displayed semi-dwarfism and shortened primary roots. Physiological analysis and cell morphology assay demonstrated that the observed phenotypes in transgenic plants were presumably caused by hypersensitivity to endogenous levels of BRs, different from BR insensitive and deficient rice mutants. Consistently, several known BR inducible genes were also upregulated in transgenic rice plants, further suggesting that BAK1 was able to affect BR signaling in rice. On the other hand, the transgenic plants generated by overproducing AtBAK1 may potentially have agricultural applications because the dwarfed phenotype is generally resistant to lodging, while the fertility remains unaffected.

Agriculture↗

PubMed2006

Berberine-stimulated glucose uptake in L6 myotubes involves both AMPK and p38 MAPK.

Berberine is a plant alkaloid used in traditional Chinese medicine and has been reported to have antihyperglycemic activity in NIDDM patients. However, the molecular basis for this action is yet to be elucidated. Here we investigate the effects and signaling pathways of berberine on L6 rat skeletal muscles. Our study demonstrates that berberine stimulates glucose uptake in a time- and dose-dependent manner. Intriguingly, berberine-stimulated glucose uptake does not vary as insulin concentration increases, and could not be blocked by the PI 3-kinase inhibitor wortmannin. Berberine only weakly stimulates the phosphorylation of Akt/PKB, a key molecule in the insulin signaling pathway, but strongly promotes the phosphorylation of AMPK and p38 MAPK. The effects of berberine are not a result of pro-oxidant action, but a consequence of an increased cellular AMP:ATP ratio. Moreover, berberine-stimulated glucose uptake is inhibited by the AMPK inhibitor Compound C and the p38 MAPK inhibitor SB202190. Inhibition of AMPK reduces p38 MAPK phosphorylation, suggesting that AMPK lies upstream of p38 MAPK. These results suggest that berberine circumvents insulin signaling pathways and stimulates glucose uptake through the AMP-AMPK-p38 MAPK pathway, which may account for the antihyperglycemic effects of this drug.

AMP-Activated Protein Kinases↗

PubMed2006

Effect of iodine intake on thyroid diseases in China.

BACKGROUND: Iodine is an essential component of thyroid hormones; either low or high intake may lead to thyroid disease. We observed an increase in the prevalence of overt hypothyroidism, subclinical hypothyroidism, and autoimmune thyroiditis with increasing iodine intake in China in cohorts from three regions with different levels of iodine intake: mildly deficient (median urinary iodine excretion, 84 microg per liter), more than adequate (median, 243 microg per liter), and excessive (median, 651 microg per liter). Participants enrolled in a baseline study in 1999, and during the five-year follow-up through 2004, we examined the effect of regional differences in iodine intake on the incidence of thyroid disease. METHODS: Of the 3761 unselected subjects who were enrolled at baseline, 3018 (80.2 percent) participated in this follow-up study. Levels of thyroid hormones and thyroid autoantibodies in serum, and iodine in urine, were measured and B-mode ultrasonography of the thyroid was performed at baseline and follow-up. RESULTS: Among subjects with mildly deficient iodine intake, those with more than adequate intake, and those with excessive intake, the cumulative incidence of overt hypothyroidism was 0.2 percent, 0.5 percent, and 0.3 percent, respectively; that of subclinical hypothyroidism, 0.2 percent, 2.6 percent, and 2.9 percent, respectively; and that of autoimmune thyroiditis, 0.2 percent, 1.0 percent, and 1.3 percent, respectively. Among subjects with euthyroidism and antithyroid antibodies at baseline, the five-year incidence of elevated serum thyrotropin levels was greater among those with more than adequate or excessive iodine intake than among those with mildly deficient iodine intake. A baseline serum thyrotropin level of 1.0 to 1.9 mIU per liter was associated with the lowest subsequent incidence of abnormal thyroid function. CONCLUSIONS: More than adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis.

Adolescent↗

PubMed2006

The distribution of substance P and met-enkephalin in vocal control nuclei among oscine species and its relation to song complexity.

Substance P (SP) and methionine-enkephalin (ENK) have been reported to appear in song control nuclei of oscine species. However, it remains unknown whether or not SP and ENK location in song control nuclei is correlated with song behavior. To address this issue, the present study first measured two variables for song complexity, i.e., song repertoire sizes, and syllable repertoire sizes in 11 oscine species. Then, we examined the distribution of SP and ENK in four control nuclei, two in the motor pathway, i.e., HVC and the robust nucleus of arcopallium (RA), and the other two in the forebrain pathway, i.e., Area X and the lateral magnocellular nucleus of the anterior nidopallium (LMAN). Finally, we measured the relative amounts of immunoreactivity for SP and ENK in song control nuclei, and tested whether they were correlated with song complexity. Our results showed that: (1) SP and ENK were broadly distributed in the song control nuclei of studied species. However, SP immunohistochemistry was more robust in comparison with ENK, and SP is generally more abundant in the two song learning nuclei than those in the two song producing ones; (2) SP and ENK staining patterns in song control nuclei did not show any obvious phylogenetic relationship among studied oscine species; (3) there was a significant correlation between the relative amounts of immunoreactivity for SP and the song and syllable repertoire sizes. Our results suggest that SP or ENK might be involved in song behavior, such as birdsong learning or memory.

Animals↗