Extracellular vesicle‑packaged microRNAs (miRNAs) are a class of circulating miRNAs located in the plasma that are packaged into extracellular vesicles. The present study examined the expression profiles of extracellular vesicles and tissue miRNAs with the aim of investigating the miRNA signatures in early‑stage breast cancer. The present study identified and compared the extracellular vesicle‑packaged miRNA expression signature and tissue miRNA expression signature from healthy individuals (n=10) and patients with early‑stage breast cancer (n=12). A total of five miRNAs, including miRNA‑375, miRNA‑24‑2‑5p, miRNA‑548b‑5p, miRNA‑655‑3P and miRNA‑376b‑5p, were synchronized in extracellular vesicles and tissues of the breast cancer group when compared with the healthy group. The highest area under the curve (AUC) for a single miRNA was achieved with miRNA‑548b‑5p [AUC=0.785; 95% confidence interval (CI)=0.585‑0.984; P=0.022]. The highest overall AUC was achieved by the combination of miRNA‑375, miRNA‑655‑3p, miRNA‑548b‑5p and miRNA‑24‑2‑5p (AUC=0.808; 95% CI=0.629‑0.986; P=0.013). The Kaplan‑Meier curves and log test analysis results of these five miRNAs, especially those for miRNA‑548b‑5p, were partly consistent with the hypothesis. Two miRNAs (miRNA‑548b‑5p and miRNA‑376b‑5p) were positively associated with patient survival, while two miRNAs (miRNA‑375 and miRNA‑24‑2‑5p) were negatively associated with patient survival. The present study provided a set of plasma extracellular vesicle‑packaged miRNA‑based biomarkers for the diagnosis of early‑stage breast cancer.

Proper spindle formation and accurate chromosome segregation are essential for ensuring mitotic fidelity. Phosphatase and tensin homolog (PTEN) is a multifunctional protein, which is able to maintain the stability of the genome and chromosomes. The present study described an essential role of PTEN in regulating chromosome segregation to prevent gross genomic instability via regulation of mitotic arrest deficient 2 (MAD2). PTEN knockdown induced cell cycle arrest and abnormal chromosome segregation, which manifested as the formation of anaphase bridges, lagging chromosomes and premature chromatid separation. In addition, MAD2 was identified as a potential target of PTEN. Furthermore, the present study revealed that PTEN knockdown resulted in MAD2 degradation via the ubiquitin‑proteasomal pathway, while restoration of MAD2 expression partially ameliorated the mitotic defects induced by PTEN loss. The results from the present study proposed a novel mechanism by which PTEN maintains chromosome stability.

The aim of the present study was to investigate the protective effects of thymosin β4 (Tβ4) on neuronal apoptosis in rat middle cerebral artery occlusion ischemia/reperfusion (MCAO I/R) injury, and determine the mechanisms involved in this process. Forty‑eight adult male Sprague‑Dawley rats were randomly divided into three groups (n=16 per group): A sham control group, an ischemia/reperfusion group (I/R group), and a Tβ4 group. The focal cerebral I/R model was established by blocking the right MCA for 2 h, followed by reperfusion for 24 h. The Zea‑Longa method was used to assess neurological deficits. Cerebral infarct volume was assessed using 2,3,5‑triphenyltetrazolium chloride staining, and pathological changes were observed via hematoxylin and eosin staining. The terminal dexynucleotidyl transferase (TdT)‑mediated dUTP nick end labeling (TUNEL) assay was used to detect apoptosis. The expression of glucose‑regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), and caspase‑12 (CASP12) protein was assessed using immunohistochemistry and western blotting 24 h after reperfusion. Infarct volume and neuronal damage in the I/R and Tβ4 groups were significantly greater than those observed in the sham group. The Zea‑Longa score, neuronal apoptosis, and expression of GRP78, CHOP, and CASP12 in the I/R and Tβ4 groups were significantly higher than those reported in the sham group. However, the Longa score and neuronal apoptosis were lower in the Tβ4 group compared to the I/R group. The expression of GRP78 was significantly increased, whereas that of CHOP and CASP12 was significantly decreased in the Tβ4 group compared to the I/R group. The present data revealed that Tβ4 can inhibit neuronal apoptosis by upregulating GRP78 and downregulating CHOP and CASP12, thereby reducing cerebral I/R injury.

Investigating active compounds from Chinese herbal medicine that can rescue myocardial cells is a good approach to preserve cardiac function. Several herbal formulae that containing Semen Ziziphi Spinosae (SZS), also called Suanzaoren in Chinese, are clinically effective in the treatment of patients with acute myocardial infarction (AMI). The present study aimed to investigate the cardioprotective effects of spinosin and 6'''‑feruloylspinosin, two flavonoid glycosides from SZS, in a rat model of myocardial ischemia and reperfusion. The left anterior descending artery (LAD) was occluded to induce myocardial ischemia. Spinosin or 6'''‑feruloylspinosin (5 mg/kg) was intraperitoneally injected into rats 30 min before LAD ligation. The protein levels of myocardial enzymes in the serum, the extent of tissue injury and the rate of apoptosis were examined after AMI in rats with or without pretreatment with spinosin or 6'''‑feruloylspinosin. Western blotting was performed to investigate the potential mechanisms underlying the function of these two flavonoid glycosides. The present results suggested that pretreatment with spinosin or 6'''‑feruloylspinosin significantly attenuated myocardial tissue injury, and reduced myocardial enzyme release and cell apoptosis in AMI rats. In addition, spinosin treatment increased light chain 3B‑II and 6'''‑feruloylspinosin, and reduced p62, indicating that autophagy was promoted after drug treatments. Treatments of spinosin and 6'''‑feruloylspinosin led to the reduction of glycogen synthase kinase‑3β (GSK3β) phosphorylation at Tyr216, and the increase of peroxisome proliferator‑activated receptor γ coactivator (PGC)‑1α and its downstream signaling proteins, including nuclear factor (erythroid‑derived 2)‑like 2 (Nrf2) and hemeoxygenase1 (HO‑1). The present data suggested that SZS flavonoids could protect myocardial cells against acute heart ischemia‑reperfusion, probably via the inhibition of GSK3β, which increased autophagy and the activity of the PGC‑1α/Nrf2/HO‑1 pathway.

Berberine (BBR) is the main component of Coptidis rhizoma, the dried rhizome of Coptis chinensis and is a potential plant alkaloid used for the treatment of cancer due to its high antitumor activity. The present study examined the therapeutic potential and molecular mechanism of action of BBR against HCC, using systematic pharmacology combined with a molecular docking approach and experimental validation in vitro. Through systematic pharmacological analysis, it was found that BBR serves a significant role in inhibiting HCC by affecting multiple pathways, especially the PI3K/AKT signaling pathway. Furthermore, the docking approach indicated that the binding of BBR to AKT could lead to the suppression of AKT activity. The present study examined the inhibitory effect of BBR on the PI3K/AKT pathway in HCC and identified that BBR downregulated the expressions of phosphorylated AKT and PI3K in MHCC97‑H and HepG2 cells, inhibiting their growth, cell migration and invasion in a dose‑dependent manner. In addition, inhibition of the AKT pathway by BBR also contributed to cell apoptosis in MHCC97‑H and HepG2 cells. Taken together, the results of the present study suggested that BBR may be a promising antitumor drug for HCC that acts by inhibiting the PI3K/AKT pathway.

Ras‑associated protein 1A (Rap1A) is a member of the Ras subfamily of small GTP‑binding proteins and is found to promote metastasis in several types of cancer. However, the functional role and molecular mechanism of action in Rap1A in esophageal squamous cell carcinoma (ESCC) is not fully understood. In the present study, Rap1A was found to be upregulated in ESCC tissues and its expression was correlated with cancer stage. Functional studies revealed that Rap1A could promote ESCC metastasis by stimulating cell migration and invasion in vivo and in vitro. Further study indicated that the transcriptional factor SP1 increased Rap1A expression via promoter binding and transcription activation. Furthermore, Rap1A promoted epithelial‑to‑mesenchymal transition, possibly through the AKT signaling pathway. Hence, the findings of the present study indicated that Rap1A may be a potential prognostic marker or therapeutic target for ESCC.

Colonic cancer has become a main reason of mortality associated with cancer; however, left and right‑sided colonic cancer have diverse outcomes in terms of epidemiological, histological, clinical parameters and prognosis. We aimed to examine the discrepancies between these two types of colon cancers to identify potential therapeutic targets. In the present study, three gene expression profiles (GSE44076, GSE31595, GSE26906) from Gene Expression Omnibus (GEO) database were downloaded and further analyzed. A PPI (protein‑protein interaction) network of the differentially‑expressed genes (DEGs) of GSE44076 between tumor and normal was established with the Search Tool for the Retrieval of Interacting Genes database. Then, the DEGs of these two colon cancers (left, right) samples were identified. Subsequently, the intersection of DEGs of left and right‑sided colon cancer samples obtained from three databases, and DEGs of tumor and normal samples were analyzed. Collagen type XI α1 chain (COL11A1), Twist family bHLH transcription factor 1 (TWIST1), insulin‑like 5 and chromogranin A were upregulated proteins, while 3β‑hydroxysteroid dehydrogenase was downregulated protein in right colon cancer than in left‑sided tumor samples. Through further experimental verification, we revealed that COL11A1 and TWIST1 were significantly upregulated at the mRNA and protein levels within right‑sided colon cancer compared with in left‑sided colon cancer samples (P<0.05), consistent with bioinformatical analysis. Furthermore, a positive correlation between COL11A1 and TWIST1 protein expression was observed (P<0.0276). Collectively, our data showed that COL11A1 and TWIST1 may be potential prognostic indicators and molecular targets for the treatment of right‑sided colon cancer.

Postoperative cognitive dysfunction (POCD) is a common and well‑known complication following surgery, particularly cardiopulmonary bypass (CPB) surgery. There are currently no suitable treatments for POCD, which is associated with increased illness and mortality rates. The present study aimed to identify a novel treatment for POCD. The protective effect of kappa opioid receptor (KOR) agonists on POCD in rats following CPB was determined and the regulatory mechanism of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway was examined. The rats were randomly divided into five groups: Sham operation (Sham group), CPB operation (CPB group), KOR agonist + CPB (K group), KOR agonist + norbinaltorphimine (nor‑BNI) + CPB (NK group), and KOR agonist + JAK2‑STAT3 specific pathway inhibitor + CPB (AG group). A water maze test and neurological function scores were used to evaluate POCD. Hematoxylin and eosin staining was used to observe hippocampal neurons. ELISA was used to detect the levels of inflammatory factors, oxidative stress factors and brain injury markers. Immunofluorescence was used to visualize the neurons. TUNEL staining and western blotting were used to detect neuronal apoptosis, and western blotting was also used to detect JAK2/STAT3 pathway‑related proteins. The KOR agonists significantly improved POCD. S‑100β and NSE detection revealed that KOR agonists alleviated brain damage in CPB rats, and this result was reversed by KOR antagonists. The KOR agonists led to a significantly reduced inflammatory response and oxidative stress, as determined by ELISA detection, and attenuated hippocampal neuronal apoptosis, as revealed by TUNEL staining and western blotting, compared with the results in the CPB group. Finally, the KOR agonists inhibited the expression levels of phosphorylated (p‑)JAK2 and p‑STAT3, rather than total JAK2 and STAT3, compared with levels in the CPB group. Taken together, KOR agonists improved POCD in rats with CPB by inhibiting the JAK2/STAT3 signaling pathway.

The present study aimed to investigate the anti‑ferroptosis effects of the HMGB1 inhibitor glycyrrhizin (GLY). The present study used a cell and animal model of acute liver failure (ALF), induced using tumor necrosis factor‑α, lipopolysaccharide and D‑galactosamine, to investigate the effects of GLY. The expression of glutathione peroxidase 4 (GPX4) and high mobility group protein B1 (HMGB1), heme oxygenase‑1 (HO‑1) and nuclear factor erythroid 2‑related factor 2 (Nrf2) were detected were detected by western blotting in L02 hepatocytes and mouse liver. The expression of GPX4 and HMGB1 in L02 hepatocytes and mouse liver was detected by immunofluorescence. The pathological changes to liver tissues were determined by hematoxylin and eosin staining. The levels of lactate dehydrogenase (LDH), Fe2+, reactive oxygen species (ROS) and glutathione (GSH) were tested using kits. Compared with the normal group, the degree of liver damage and liver function in the model animal group was severe. The protein levels of HMGB1 in L02 cells and liver tissues were significantly increased. The expression of NRF2, HO‑1 and GPX4 was significantly decreased. The levels of LDH, Fe2+, malondialdehyde (MDA) and ROS were increased, whereas the level of GSH was decreased. Treatment with GLY reduced the degree of liver damage, the expression of HMGB1 was decreased, and the levels of Nrf2, HO‑1 and GPX4 were increased. The levels of LDH, Fe2+, MDA, ROS were decreased, while the level of GSH was increased by GLY treatment. The results of the present study indicated that HMGB1 is involved in the process of ferroptosis. The HMGB1 inhibitor GLY significantly reduced the degree of ferroptosis during ALF by inhibiting oxidative stress.

Intracranial aneurysm (IA) is a cerebrovascular disease with a high mortality rate. The pathogenesis of IA remains unclear and the treatment limited. The purpose of the present study was to identify the key genes expressed in IAs and provide the basis for further research and treatment. The raw dataset GSE75436 was downloaded from Gene Expression Omnibus, including 15 IA samples and 15 matched superficial temporal artery (STA) samples. Then, differentially expressed genes (DEGs) were identified using the limma package in R software. Hierarchical clustering analysis was performed on the DEGs using the gplot2 package in R. Database for Annotation, Visualization, and Integrated Discovery (DAVID) online tools were used to perform gene ontology (GO) functional enrichment analysis. DAVID and gene set enrichment analysis were separately used to perform the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. The intersections of the two results were selected as common KEGG pathways. Protein‑protein interaction (PPI) analysis among the DEGs involved in the common KEGG pathways was performed using Search Tool for the Retrieval of Interacting Genes online tools, and visualized with Cytoscape software. A total of 782 DEGs were identified, comprising 392 upregulated and 390 downregulated DEGs. Hierarchical clustering demonstrated that the DEGs could precisely distinguish the IAs from the STAs. The GO enrichment analysis demonstrated that the upregulated DEGs were mainly involved in the inflammatory response and the management of extracellular matrix, and the downregulated DEGs were mainly involved in the process of vascular smooth muscle contraction. The KEGG pathway enrichment analysis demonstrated that the common pathways were 'leishmaniasis', 'Toll‑like receptor signaling pathway' and 'vascular smooth muscle contraction'. In the PPI network, tumor necrosis factor (TNF), interleukin 8 and Toll‑like receptor 4 had the highest degrees; they were associated with the inflammatory response. The Toll‑like receptor signaling pathway and TNF gene may serve as targets for future research and treatment.

The aim of this study was to evaluate the QT dispersion and echocardiographic parameters in patients before and after transcatheter aortic valve implantation (TAVI).

Rationale: Pulmonary hypertension (PH) is a life-threatening cardiopulmonary disorder in which inflammation and immunity have emerged as critical early pathogenic elements. Although proinflammatory processes in PH and pulmonary arterial hypertension (PAH) are the focus of extensive investigation, the initiating mechanisms remain elusive.Objectives: We tested whether activation of the complement cascade is critical in regulating proinflammatory and pro-proliferative processes in the initiation of experimental hypoxic PH and can serve as a prognostic biomarker of outcome in human PAH.Methods: We used immunostaining of lung tissues from experimental PH models and patients with PAH, analyses of genetic murine models lacking specific complement components or circulating immunoglobulins, cultured human pulmonary adventitial fibroblasts, and network medicine analysis of a biomarker risk panel from plasma of patients with PAH.Measurements and Main Results: Pulmonary perivascular-specific activation of the complement cascade was identified as a consistent critical determinant of PH and PAH in experimental animal models and humans. In experimental hypoxic PH, proinflammatory and pro-proliferative responses were dependent on complement (alternative pathway and component 5), and immunoglobulins, particularly IgG, were critical for activation of the complement cascade. We identified Csf2/GM-CSF as a primary complement-dependent inflammatory mediator. Furthermore, using network medicine analysis of a biomarker risk panel from plasma of patients with PAH, we demonstrated that complement signaling can serve as a prognostic factor for clinical outcome in PAH.Conclusions: This study establishes immunoglobulin-driven dysregulated complement activation as a critical pathobiological mechanism regulating proinflammatory and pro-proliferative processes in the initiation of experimental hypoxic PH and demonstrates complement signaling as a critical determinant of clinical outcome in PAH.

BACKGROUND We previously reported that astragaloside IV (As-IV) can alleviate myocardial damage induced by lipopolysaccharide (LPS). However, the anti-inflammatory effects of As-IV following LPS stimulation in mice and H9C2 cardiomyocytes remain unclear. The present study was designed to explore the mechanism of action of As-IV. MATERIAL AND METHODS In vivo, C57BL/6J mice were randomly divided into 5 groups: the control group, the LPS group (10 mg/kg), and 3 LPS groups receiving different doses of As-IV (20, 40, and 80 mg/kg). The protective effect of As-IV on LPS-stimulated H9C2 cardiomyocytes was evaluated in vitro. Cardiac function was detected by echocardiography, and H&E staining was used to evaluate morphologic changes. Cardiomyocyte viability was detected by MTT assay. ELISA was used to detect free fatty acid (FFA), interleukin-6 (IL-6), interleukin-1ß (IL-1ß), and tumor necrosis factor alpha (TNF-alpha) levels in mouse serum and in cell supernatant. Adenosine triphosphate (ATP) and adenosine monophosphate (AMP) contents in myocardial tissues and cells were detected by high-performance liquid chromatography. ATP5D and TLR4/NF-kappaB/PPARalpha signaling pathway proteins (TLR4, NF-kappaB, p65, and PPARalpha) were detected by Western blotting. RESULTS As-IV significantly improved cardiac function, myocardial cell viability, and pathological changes and reduced FFA, IL-1ß, IL-6, and TNF-alpha levels. The ATP/AMP ratio in the cardiac tissues of mice and in H9C2 cardiomyocytes was increased compared to that in the LPS group. In addition, As-IV enhanced ATP synthase and PPARalpha protein expression. In H9C2 cardiomyocytes, the p65-specific inhibitor BAY11-7082 exerted similar effects as As-IV. CONCLUSIONS As-IV alleviates LPS-induced myocardial damage by modulating TLR4/NF-kappaB/PPARalpha signaling-mediated energy biosynthesis.

HIV-1 replicates via a low-fidelity polymerase with a high mutation rate; strong conservation of individual nucleotides is highly indicative of the presence of critical structural or functional properties. Identifying such conservation can reveal novel insights into viral behaviour. We analysed 3651 publicly available sequences for the presence of nucleic acid conservation beyond that required by amino acid constraints, using a novel scale-free method that identifies regions of outlying score together with a codon scoring algorithm. Sequences with outlying score were further analysed using an algorithm for producing local RNA folds whilst accounting for alignment properties. 11 different conserved regions were identified, some corresponding to well-known cis-acting functions of the HIV-1 genome but also others whose conservation has not previously been noted. We identify rational causes for many of these, including cis functions, possible additional reading frame usage, a plausible mechanism by which the central polypurine tract primes second-strand DNA synthesis and a conformational stabilising function of a region at the 5' end of env.

The origins of new genes are among the most fundamental questions in evolutionary biology. Our understanding of the ways that new genetic material appears and how that genetic material shapes population variation remains incomplete. De novo genes and duplicate genes are a key source of new genetic material on which selection acts. To better understand the origins of these new gene sequences, we explored the ways that structural variation might alter expression patterns and form novel transcripts. We provide evidence that chromosomal rearrangements are a source of novel genetic variation that facilitates the formation of de novo exons in Drosophila. We identify 51 cases of de novo exon formation created by chromosomal rearrangements in 14 strains of D. yakuba. These new genes inherit transcription start signals and open reading frames when the 5' end of existing genes are combined with previously untranscribed regions. Such new genes would appear with novel peptide sequences, without the necessity for secondary transitions from non-coding RNA to protein. This mechanism of new peptide formations contrasts with canonical theory of de novo gene progression requiring non-coding intermediaries that must acquire new mutations prior to loss via pseudogenization. Hence, these mutations offer a means to de novo gene creation and protein sequence formation in a single mutational step, answering a long standing open question concerning new gene formation. We further identify gene expression changes to 134 existing genes, indicating that these mutations can alter gene regulation. Population variability for chromosomal rearrangements is considerable, with 2368 rearrangements observed across 14 inbred lines. More rearrangements were identified on the X chromosome than any of the autosomes, suggesting the X is more susceptible to chromosome alterations. Together, these results suggest that chromosomal rearrangements are a source of variation in populations that is likely to be important to explain genetic and therefore phenotypic diversity.

Human papillomavirus (HPV) related tumours account for a significant proportion of head and neck squamous cell carcinomas (HNSCCs) in developed countries. They respond better to chemo- and radio-therapy, and have a better stage specific prognosis. To establish their prevalence in China, we assessed a series of histology confirmed HNSCCs collected in Zhejiang and Guangdong provinces by PCR for HPV DNA and by immunohistochemistry for p16 protein status. Among 303 HNSCCs, HPV DNA was detected in 26.4%, with HPV16 DNA in 71% of these. Of HNSCC located in the oropharynx, 38.55% (32/83) were HPV+ve. In this series, p16 status was a relatively poor predictor of HPV status as detected by PCR. The stage specific survival time of HPV+ HNSCCs was significantly longer than for HPV- HNSCC. HPV status should be assessed for oropharyngeal cancers in China to assist with appropriate management, and prophylaxis against HPV infection should be considered to reduce the incidence of this disease.

The effect of smoking on the risk of developing inflammatory bowel diseases (IBD) may be heterogeneous across ethnicity and geography. Although trends in smoking for the general population are well described, it is unknown whether these can be extrapolated to the IBD cohort. Smoking prevalence trends specific to the global IBD cohort over time have not been previously reported. This is a systematic review of smoking prevalence specific to the IBD cohort across geography.

The Best Possible Self (BPS) exercise promotes a positive view of oneself in the best possible future, after working hard towards it. Since the first work that attempted to examine the benefits of this intervention in 2001, studies on the BPS have grown exponentially and, currently, this is one of the most widely used Positive Psychology Interventions. However, little is yet known about its overall effectiveness in increasing wellbeing outcomes. Thus, the aim of this meta-analysis is to shed light on this question. A systematic literature search was conducted, and 29 studies (in 26 articles) met the inclusion criteria of empirically testing the intervention and comparing it to a control condition. In addition, BPS was compared to gratitude interventions in some of the included studies. A total of 2,909 participants were involved in the analyses. The outcome measures were wellbeing, optimism, depressive symptoms, and positive and negative affect. Results showed that the BPS is an effective intervention to improve wellbeing (d+ = .325), optimism (d+ = .334) and positive affect (d+ = .511) comparing to controls. Small effect sizes were obtained for negative affect and depressive symptoms. Moderator analyses did not show statistically significant results for wellbeing, except for a trend towards significance in the age of the participants (years) and the magnitude of the intervention (total minutes of practice). In addition, the BPS was found to be more beneficial for positive and negative affect than gratitude interventions (d+ = .326 and d+ = .485, respectively). These results indicate that the BPS can be considered a valuable Positive Psychology Intervention to improve clients' wellbeing, and it seems that it might be more effective for older participants and with shorter practices (measured as total minutes of practice).

Perfusion-related information is reportedly embedded in the low-frequency component of a blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) signal. The blood-propagation pattern through the cerebral vascular tree is detected as an interregional lag variation of spontaneous low-frequency oscillations (sLFOs). Mapping of this lag, or phase, has been implicitly treated as a projection of the vascular tree structure onto real space. While accumulating evidence supports the biological significance of this signal component, the physiological basis of the "perfusion lag structure," a requirement for an integrative resting-state fMRI-signal model, is lacking. In this study, we conducted analyses furthering the hypothesis that the sLFO is not only largely of systemic origin, but also essentially intrinsic to blood, and hence behaves as a virtual tracer. By summing the small fluctuations of instantaneous phase differences between adjacent vascular regions, a velocity response to respiratory challenges was detected. Regarding the relationship to neurovascular coupling, the removal of the whole lag structure, which can be considered as an optimized global-signal regression, resulted in a reduction of inter-individual variance while preserving the fMRI response. Examination of the T2* and S0, or non-BOLD, components of the fMRI signal revealed that the lag structure is deoxyhemoglobin dependent, while paradoxically presenting a signal-magnitude reduction in the venous side of the cerebral vasculature. These findings provide insight into the origin of BOLD sLFOs, suggesting that they are highly intrinsic to the circulating blood.

Individuals of many species utilise social information whilst making decisions. While many studies have examined social information in making large scale decisions, there is increasing interest in the use of fine scale social cues in groups. By examining the use of these cues and how they alter behaviour, we can gain insights into the adaptive value of group behaviours. We investigated the role of social information in choosing when and where to dive in groups of socially foraging European shags. From this we aimed to determine the importance of social information in the formation of these groups. We extracted individuals' surface trajectories and dive locations from video footage of collective foraging and used computational Bayesian methods to infer how social interactions influence diving. Examination of group spatial structure shows birds form structured aggregations with higher densities of conspecifics directly in front of and behind focal individuals. Analysis of diving behaviour reveals two distinct rates of diving, with birds over twice as likely to dive if a conspecific dived within their visual field in the immediate past. These results suggest that shag group foraging behaviour allows individuals to sense and respond to their environment more effectively by making use of social cues.