Biological Link Research Articles

Topological-Similarity Based Canonical Representations for Biological Link Prediction

Topological-Similarity Based Canonical Representations for Biological Link Prediction

Chuaria and Tawuia fossils from ∼1.0 Ga rocks in North China: Implications for a polyphyletic origin of Chuaria and a potential biological link between these two widespread Proterozoic taxa

The Proterozoic witnessed the emergence and rise of early eukaryotes and Proterozoic carbonaceous compression macrofossils provide a valuable window for our understanding of this ecological expansion. Among them, the discoidal Chuaria and tomaculate Tawuia, which often co-occur in the same bedding layer, are perhaps the most common fossil forms in Proterozoic successions with extremely long temporal and broad geographical distributions. However, their phylogenetic interpretations and the relationship between them have been debated for decades, due to their simple morphologies lacking phylogenetically diagnostic features. In this study, we used an integrated application of reflected and transmitted light microscopy, scanning electron microscopy, biometric analysis, and Raman spectroscopy to characterize well-preserved carbonaceous compression macrofossils of Chuaria and Tawuia from the Tonian Liulaobei Formation in Huainan region, northern Anhui province, North China. The fossils are abundantly preserved in a ca. 1–2 cm thick homogeneous mudstone layer and can be considered to be closer to an ecological community than fossils from multiple different layers or localities. The comprehensive analysis shows that even Chuaria vesicles from the same layer may have a polyphyletic origin and three groups of Chuaria vesicles have been identified. Among them, small Chuaria vesicles with minimum diameter < 1.2 mm can be either related to the sphaeromorphic acritarch Leiosphaeridia or interpreted as multicellular aggregates. In contrast, large Chuaria vesicles with minimum diameter ≥ 1.2 mm are more comparable to the type material of Chuaria circularis from the Chuar Group and more closely related, either phylogenetically or ontogenetically, to Tawuia vesicles. This study takes a step on the path to solving the mystery of the most common and widely distributed Proterozoic macrofossil assemblage (i.e., Chuaria-Tawuia assemblage), and urges thorough and systematic evaluations to be taken on the possibility that Chuaria vesicles from the same Chuaria-Tawuia assemblages or sole Chuaria assemblages in other localities might also be polyphyletic.

Dynamic implications of the biological link between bovine milk and meat production for operationalizing the planetary health diet.

The EAT-Lancet planetary health diet (PHD) provides guidelines on a global scale and calls for red meat consumption to be halved. Operational PHD guidelines at country level have yet to be determined. Here we argue that the biological link between milk and bovine-meat production must be considered when operationalizing the globally calculated PHD to national contexts. Using a stylized computer simulation model rooted in a food system approach, we explore the impact of dietary scenarios on milk and bovine-meat production and show that ignoring this biological link can lead to substantial imbalances between national dietary guidelines and production outcomes and potentially lead to food waste. Furthermore, we assess current national dietary guidelines in Europe and find that most disregard this biological link and are incompatible with the PHD, with implications for policymakers and consumers to consider when adapting the PHD in national contexts.

Integrative Analysis of PAIP2B to Identify a Novel Biomarker for Pancreatic Ductal Adenocarcinoma.

The aim of the study was to evaluate the potential diagnostic and prognostic value of gene, Poly A-Binding Protein Interacting Protein 2B ( PAIP2B ) in pancreatic cancer. We used the gene expression data and clinical information of pancreatic adenocarcinoma patients from The Cancer Genome Atlas database and Gene Expression Omnibus database to analyze the expression of PAIP2B in pancreatic cancer samples, and validated the expression of PAIP2B in tumor tissue, using bioinformatics technology to explore the prognostic value of PAIP2B and its possible biological function. A significantly lower level of PAIP2B was observed in pancreatic cancer patients than in controls, and validated by immunohistochemistry. PAIP2B reduced the proliferation and invasion of cancer cells and had a significantly high expression in early stage. Patients with lower levels of PAIP2B had a significantly shorter median survival time than those with higher levels. DNA demethylation played an important role in PAIP2B expression. In addition, PAIP2B expression was significantly associated with the tumor-infiltrating immune cells, especially T cells CD8, T cells CD4 memory resting, macrophages M0, and dendritic cells resting. Our study also found that PAIP2B regulated miRNA function leading to disease progression in pancreatic cancer patients. Our study explored the potential value of PAIP2B as a biological link between prognosis and pancreatic cancer, and provided reference for the follow-up study on the role of PAIP2B in pancreatic cancer.

TRNA modifications: insights into their role in human cancers.

Transfer RNA (tRNA) plays a central role in translation by functioning as a biological link between messenger RNA (mRNA) and proteins. One prominent feature of the tRNA molecule is its heavily modified status, which greatly affects its biogenesis and function. Modifications within the anticodon loop are crucial for translation efficiency and accuracy, whereas other modifications in the body region affect tRNA structure and stability. Recent research has revealed that these diverse modifications are critical regulators of gene expression. They are involved in many important physiological and pathological processes, including cancers. In this review we focus on six different tRNA modifications to delineate their functions and mechanisms in tumorigenesis and tumor progression, providing insights into their clinical potential as biomarkers and therapeutic targets.

Socioeconomic and Inflammatory Correlates of Plasma Cortisol Among Individuals with Sickle Cell Disease

Introduction: Cortisol plays a critical role in the biological link between stress and health outcomes. It is frequently investigated in the association between socioeconomic stress and morbidity, and the hypothesized biological mechanism by which socioeconomic stress and cortisol impact health is through chronically elevated systemic inflammation. This research is relevant to individuals with sickle cell disease (SCD) for several reasons. First, up to 40% of children and adolescents with SCD are impacted by neighborhood poverty. Furthermore, individuals with SCD are faced with significant disease-related morbidities, such as chronic and acute pain, renal injury, and cerebrovascular disease that are further complicated by elevated inflammatory markers. Finally, cortisol is heavily understudied in this population, with no research investigating socioeconomic or inflammatory correlates. The purpose of this study was to investigate plasma cortisol and its association with neighborhood-level socioeconomic factors (income and poverty) and immunomodulatory cytokines (IL-6, IL-10), among individuals with SCD. Method: Plasma from individuals with SCD within Children's Hospital of Philadelphia (CHOP) and University of Pennsylvania School of Medicine (Penn Medicine) BioBanks were identified. A cortisol radioimmunoassay was used to determine plasma cortisol levels. The Olink immune response panel was used to measure plasma levels of 92 proteins involved in inflammatory pathways. Home address collected from electronic health records was used to determine neighborhood census tract geoid, which was then used to collect data on median neighborhood income and percentage of families living in poverty from the 2020 American Census Survey. Bivariate and multivariate analyses were conducted across 4 subgroups in the total sample: pediatric patients, adult patients, SCA (HbSS/HbSß 0), and other SCD genotypes (HbSC/HbSß +). Control samples (healthy and sickle cell trait; n = 22) without neighborhood information were also available for comparison. Results: Fifty-four independent outpatient samples were identified after excluding duplicates and siblings. Twenty-seven samples were from children and adolescents receiving pediatric care at CHOP (Range age = .8 to 21; Mage= 13.6, SD = 5.3; 51.9% female, 74.1% SCA) and 27 samples were from adults receiving care at Penn Medicine (Range age = 19 to 56; Mage= 35.8, SD = 10.1; 51.9% female, 51.9% SCA). There were no significant differences in cortisol levels across each subgroup ( Mpeds= 16.6, SDpeds = 6.2; Madult= 13.4, SDadult = 6.9; MSCA= 15.1, SDSCA = 7.1; MSCD= 14.9, SDSCD = 6.3). Neighborhood income and poverty did not differ across pediatric and adult patients, and income did not differ across SCD types. However, neighborhood poverty was lower among patients with SCA ( M = 13.9; SD = 11.9) relative to other SCD genotypes ( M = 21.7; SD = 13.5; p = .041). Bivariate Spearman analyses found that neighborhood variables were not correlated with cortisol or cytokines in the total sample or subgroups. Yet, multivariate analyses controlling for sex and time of blood draw showed a positive main effect for patient age ( p = .019) and a significant age by poverty interaction ( p = .041) predicting cortisol among pediatric patients. Cortisol levels were higher with age, yet the association among poverty and cortisol was strongest in younger patients. Analyses also showed a sex*poverty interaction among pediatric patients that approached significance ( p = .081), such that poverty only predicted cortisol in male patients. There were no significant differences for immunomodulatory cytokines across each SCD subgroups; however, IL-6 and IL-10 were elevated in patients with SCA relative to healthy controls ( p IL6 = .021; p IL10 = .003). Bivariate Spearman correlations showed that cortisol was positively related to IL-6 (rho [ρ]= .38, p = .027) and IL-10 (ρ= .34, p = .048) among patients with SCA. There were no additional significant bivariate or multivariate effects. Conclusion: Neighborhood factors likely have downstream effects on the biological stress response and inflammation in SCD. Further research must be conducted to elucidate concurrent and prospective associations among neighborhood socioeconomic factors, stress-related cortisol response, and inflammatory outcomes when extending this work to investigate the impact of stress on SCD morbidity and mortality.

Interleukin-6 upregulates extracellular matrix gene expression and transforming growth factor β1 activity of tendon progenitor cells

BackgroundProlonged inflammation during tendon healing and poor intrinsic healing capacity of tendon are causal factors associated with tendon structural and functional degeneration. Tendon cells, consisting of mature tenocytes and tendon progenitor cells (TPC) function to maintain tendon structure via extracellular matrix (ECM) synthesis. Tendon cells can succumb to tissue cytokine/chemokine alterations during healing and consequently contribute to tendon degeneration. Interleukin-(IL-)1β, IL-6 and TNFα are key cytokines upregulated in injured tendons; the specific effects of IL-6 on flexor tendon-derived TPC have not been discerned.MethodsPassage 3 equine superficial digital flexor tendon (SDFT)-derived TPC were isolated from 6 horses. IL-6 impact on the viability (MMT assay with 0, 1, 5 and 10 ng/mL concentrations), migration (scratch motility assay at 0, 10ng/mL concentration) of TPC in monolayer culture were assessed. IL-6 effect on tendon ECM and chondrogenic gene expression (qRT-PCR), TGFβ1 gene expression and activity (ELISA), and MMP-1, -3 and − 13 gene expression of TPC was evaluated.ResultsIL-6 decreased TPC viability and migration. IL-6 treatment at 10 ng/mL significantly up-regulated TGFβ1 gene expression (6.3-fold; p = 0.01) in TPC, and significantly increased the TGFβ1 concentration in cell culture supernates. IL-6 (at 10 ng/mL) significantly up-regulated both tendon ECM (COL1A1:5.3-fold, COL3A1:5.4-fold, COMP 5.5-fold) and chondrogenic (COL2A1:3.9-fold, ACAN:6.2-fold, SOX9:4.8-fold) mRNA expression in TPC. Addition of SB431542, a TGFβ1 receptor inhibitor, to TPC in the presence of IL-6, attenuated the up-regulated tendon ECM and chondrogenic genes.ConclusionIL-6 alters TPC phenotype during in vitro monolayer culture. Pro- and anti-inflammatory roles of IL-6 have been implicated on tendon healing. Our findings demonstrate that IL-6 induces TGFβ1 activity in TPC and affects the basal TPC phenotype (as evidenced via increased tendon ECM and chondrogenic gene expressions). Further investigation of this biological link may serve as a foundation for therapeutic strategies that modulate IL-6 to enhance tendon healing.

Exploring Shared Biomarkers of Myocardial Infarction and Alzheimer's Disease via Single-Cell/Nucleus Sequencing and Bioinformatics Analysis.

Patients are at increased risk of dementia, including Alzheimer's disease (AD), after myocardial infarction (MI), but the biological link between MI and AD is unclear. To understand the association between the pathogenesis of MI and AD and identify common biomarkers of both diseases. Using public databases, we identified common biomarkers of MI and AD. Least absolute shrinkage and selection operator (LASSO) regression and protein-protein interaction (PPI) network were performed to further screen hub biomarkers. Functional enrichment analyses were performed on the hub biomarkers. Single-cell/nucleus analysis was utilized to further analyze the hub biomarkers at the cellular level in carotid atherosclerosis and AD datasets. Motif enrichment analysis was used to screen key transcription factors. 26 common differentially expressed genes were screened between MI and AD. Function enrichment analyses showed that these differentially expressed genes were mainly associated with inflammatory pathways. A key gene, Regulator of G-protein Signaling 1 (RGS1), was obtained by LASSO regression and PPI network. RGS1 was confirmed to mainly express in macrophages and microglia according to single-cell/nucleus analysis. The difference in expression of RGS1 in macrophages and microglia between disease groups and controls was statistically significant (p < 0.0001). The expression of RGS1 in the disease groups was upregulated with the differentiation of macrophages and microglia. RelA was a key transcription factor regulating RGS1. Macrophages and microglia are involved in the inflammatory response of MI and AD. RGS1 may be a key biomarker in this process.

Neonatal AVPR1a Methylation and In-Utero Exposure to Maternal Smoking.

(1) Introduction: Epigenetic changes have been proposed as a biologic link between in-utero exposure to maternal smoking and health outcomes. Therefore, we examined if in-utero exposure to maternal smoking was associated with infant DNA methylation (DNAm) of cytosine-phosphate-guanine dinucleotides (CpG sites) in the arginine vasopressin receptor 1A AVPR1a gene. The AVPR1a gene encodes a receptor that interacts with the arginine vasopressin hormone and may influence physiological stress regulation, blood pressure, and child development. (2) Methods: Fifty-two infants were included in this cohort study. Multivariable linear models were used to examine the effect of in-utero exposure to maternal smoking on the mean DNAm of CpG sites located at AVPR1a. (3) Results: After adjusting the model for substance use, infants with in-utero exposure to maternal smoking had a reduction in DNAm at AVPR1a CpG sites by -0.02 (95% CI -0.03, -0.01) at one month of age. In conclusion, in-utero exposure to tobacco smoke can lead to differential patterns of DNAm of AVPR1a among infants. Conclusions: Future studies are needed to identify how gene expression in response to early environmental exposures contributes to health outcomes.

Acceptability, feasibility and cost of point of care testing for sexually transmitted infections among South African adolescents where syndromic management is standard of care

BackgroundYoung people (YP) in southern Africa are at substantial risk of HIV and sexually transmitted infections (STIs). Despite the epidemiological and biological link between STIs and HIV transmission and acquisition, infections such as Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG) remain widely undiagnosed. Syndromic STI management is the standard of care in low- and middle-income countries (LMICs) despite a high prevalence of asymptomatic infections. We conducted an observational study to explore the acceptability, feasibility, and cost of a STI test-and-treat service for YP in Cape Town.MethodsYP attending a mobile clinic (MC) and a youth centre clinic (YC) were offered STI screening. Urine testing for CT and NG using a 90-min molecular point-of-care (POC) test on the GeneXpert platform was conducted and treatment provided. Data were collated on demographics, sexual behaviour, presence of symptoms, uptake of same-day treatment, prevalence of CT/NG, and service acceptability.ResultsThree hundred sixty six participants were enrolled (median age 20, 83% female).57% (209/366) of participants tested positive for either CT (126/366, 34%) or NG (57/366, 16%) or co-infection (26/366, 7%).Clinical symptoms were a poor predictor of GeneXpert diagnosed CT or NG, with a sensitivity of 46.8% and 54.0% for CT and NG respectively. Although half of participants initially chose to receive same day results and treatment, only a third waited for results on the day. The majority of participants (91%) rated the service highly via a post-visit acceptability questionnaire.ConclusionCurable STIs are highly prevalent in this population. STI screening using POC testing was feasible and acceptability was high. The study provides further impetus for moving policy beyond syndromic management of STIs in South Africa.

The specific viral composition in triple-negative breast cancer tissue shapes the specific tumor microenvironment characterized on pathological images

Numerous studies have shown that different subtypes of breast cancer (BC) have significant differences in terms of the tumor microbiome, host gene expression, and histopathological image, whereas the biological links between these cancer-associated indicators are still unknown. Here, we performed a comprehensive analysis with 610 patients of the four subtypes of BC with matched tissue microbiota, host transcriptome, and histopathological image samples. Correlation analysis showed that the composition of intratumoral viruses shaped the tumor microenvironment (TME) of patients with BC, and the TME was further reflected in the histopathological images. Of the four subtypes, patients with triple-negative breast cancer (TNBC) had unique intratumoral viral community composition, non-cancer cell infiltration in the TME, and histopathological image characteristics. Furthermore, we detected multiple virus-cell-image association axes in TNBC, in which tumor-associated macrophages (TAMs) have clinical prognostic implication. This study provides a comprehensive map of the associations between the intratumoral virome, TME, and histopathological image of TNBC, as well as insights into disease prognosis that can be crucial for precise therapeutic intervention strategies.

Obesity and Cancer

It is a key priority in public health to treat illnesses due to the rising frequency of obesity-related malignancies. Around 11.9% of male and 13.1% of female cancer cases worldwide have an obesity-related malignancy as their primary cause. In addition to colorectal, postmenopausal ovarian, breast, gallbladder, thyroid, and multiple myeloma cancers, endometrial, esophageal, hepatocellular carcinoma, gastric cancer, renal and pancreatic adenocarcinomas, and thyroid cancer, the relationship between obesity and cancer is clear in many anatomical sites. This article provides a thorough overview of the most recent epidemiological data on obesity and its connection to cancer in light of this urgent issue. The contradiction of weight increase and cancer risk and death. Furthermore, examining BMI differences in obesity-related malignancies offers a comprehensive grasp of the disease's complexities. These mechanisms include adipokine pathophysiology, cellular and micro environmental changes, ectopic fat accumulation, disruptions in dietary nutrients, circadian cycles, and potential factors like alteration of the intestinal flora and mechanical influences on weight. The conclusion's discussion of potential future approaches to prevention, detection, and treatment highlights the pressing need for more study and action on this important public health problem. The main objective is to increase knowledge of the complexity of obesity-related malignancies and increase awareness of it to create efficient methods for prevention and treatment. This review offers insight into how potential processes and risk factors combine on target tissues, ultimately causing them to take on a feature of cancer by addressing these important aspects. This review focuses on the Epidemiology of obesity influencing cancer, links between obesity and cancer, the influence of cancer by weight growth, somatometry, biological links, ectopic fat deposition, insulin sensitivity, adiponectin, obesity influencing widely occurring cancers, and FTO protein.

An Early Neoplasia Index (ENI10), Based on Molecular Identity of CD10 Cells and Associated Stemness Biomarkers, is a Predictor of Patient Outcome in Many Cancers.

We identified a molecular signature called ENI10 which, owing to its biological link with stem cell properties, predicts patient outcome and drugs efficiency in breast and several other cancers. ENI10 should allow early and optimized clinical management of a broad number of cancers, regardless of the stage of tumor progression.

Advanced glycation end products initiate the mutual promoting cycle between centrosome amplification and the release of inflammatory cytokines in human vascular endothelial cells

Inflammation is implicated in the development of diabetic complications including vascular pathology. Centrosome is known to play a role in cell secretion. We have reported that diabetes can trigger centrosome amplification (CA). Thus, in the present study, we investigated the relationship between CA and the release of proinflammatory cytokines interleukin-1β, tumor necrosis factor-α and interleukin-6 in hCMEC/D3 human endothelial cells treated with advanced glycation end products (AGEs). We found that AGEs induced CA via PLK4 and increased the biosynthesis of the three cytokines via NF-κB. Importantly, treatment of the cells with AGEs also increased the release of the three cytokines. Inhibiting CA by knockdown of polo like kinase 4 (PLK4) attenuated the cytokine release but not their biosynthesis. Knockdown of the cytokines inhibited the CA, while addition of the cytokines individually to the cell culture increased the protein level of PLK4 and CA to a moderate level. Addition of the three cytokines together into the cell culture markedly enhanced the CA, to a level higher than that in the AGEs-treated group. In conclusion, our results provide the direct evidence that the cytokines can induce CA, and suggest that there is a mutual promoting cycle between CA and cytokine release in the treated samples. It is proposed that the cycle of CA-cytokine release is a candidate biological link between diabetes and its complications such as vascular pathologies.

Exhaustion and cardiovascular risk factors: the role of vagally-mediated heart rate variability

PurposeExhaustion symptoms are known to be associated with cardiovascular disease (CVD) risk; however, the underlying mechanisms remain unclear. Autonomic imbalance, as indicated by reductions in vagally-mediated heart rate variability (vmHRV), appears to be a valid candidate for such a biological link, as it has been associated with both exhaustion symptoms and CVD risk and mortality. MethodsThe present study examined a potential mediation of vmHRV on the association between exhaustion symptoms and self-reported CVD risk factors as well as the age dependency of this mediation in a large, heterogeneous sample of the Dresden Burnout Study (N = 388; 72.9% females; Mage = 42.61, SD = 11.67). ResultsResults indicate that exhaustion symptoms were indirectly associated with CVD risk factors through vmHRV even after adjusting for well-known confounders (i.e., sex, body mass index, depressive symptoms). Moreover, this pattern was significant only among middle-aged (i.e., 54.27 years) and older individuals. ConclusionsOur findings add to growing evidence that autonomic imbalance may be a key biological link between exhaustion symptoms and CVD risk in middle-aged and older individuals. Implications for public health are discussed.

Literature-Based Discovery to Elucidate the Biological Links between Resistant Hypertension and COVID-19.

Multiple studies have reported new or exacerbated persistent or resistant hypertension in patients previously infected with COVID-19. We used literature-based discovery to identify and prioritize multi-scalar explanatory biology that relates resistant hypertension to COVID-19. Cross-domain text mining of 33+ million PubMed articles within a comprehensive knowledge graph was performed using SemNet 2.0. Unsupervised rank aggregation determined which concepts were most relevant utilizing the normalized HeteSim score. A series of simulations identified concepts directly related to COVID-19 and resistant hypertension or connected via one of three renin-angiotensin-aldosterone system hub nodes (mineralocorticoid receptor, epithelial sodium channel, angiotensin I receptor). The top-ranking concepts relating COVID-19 to resistant hypertension included: cGMP-dependent protein kinase II, MAP3K1, haspin, ral guanine nucleotide exchange factor, N-(3-Oxododecanoyl)-L-homoserine lactone, aspartic endopeptidases, metabotropic glutamate receptors, choline-phosphate cytidylyltransferase, protein tyrosine phosphatase, tat genes, MAP3K10, uridine kinase, dicer enzyme, CMD1B, USP17L2, FLNA, exportin 5, somatotropin releasing hormone, beta-melanocyte stimulating hormone, pegylated leptin, beta-lipoprotein, corticotropin, growth hormone-releasing peptide 2, pro-opiomelanocortin, alpha-melanocyte stimulating hormone, prolactin, thyroid hormone, poly-beta-hydroxybutyrate depolymerase, CR 1392, BCR-ABL fusion gene, high density lipoprotein sphingomyelin, pregnancy-associated murine protein 1, recQ4 helicase, immunoglobulin heavy chain variable domain, aglycotransferrin, host cell factor C1, ATP6V0D1, imipramine demethylase, TRIM40, H3C2 gene, COL1A1+COL1A2 gene, QARS gene, VPS54, TPM2, MPST, EXOSC2, ribosomal protein S10, TAP-144, gonadotropins, human gonadotropin releasing hormone 1, beta-lipotropin, octreotide, salmon calcitonin, des-n-octanoyl ghrelin, liraglutide, gastrins. Concepts were mapped to six physiological themes: altered endocrine function, 23.1%; inflammation or cytokine storm, 21.3%; lipid metabolism and atherosclerosis, 17.6%; sympathetic input to blood pressure regulation, 16.7%; altered entry of COVID-19 virus, 14.8%; and unknown, 6.5%.

Intergenerational differences in healthy eating beliefs among British Pakistanis with type 2 diabetes.

There are growing concerns on how to prevent, slow down and induce remission of type 2 diabetes mellitus (T2DM). Recent evidence has found diet and lifestyle interventions can cause remission of T2DM, however, there are challenges for diverse groups such as British Pakistanis who are four times more at risk of T2DM. There is a need to understand the food behaviours of different generational groups to develop culturally appropriate strategies to support diabetes prevention programmes. This study explores beliefs about healthy eating and food practices related to T2DM among British Pakistanis to understand the challenges they face in implementing healthy diets. We carried out 26 semi-structured qualitative interviews via telephone and face-to-face. The sample included T2DM British Pakistanis living in Bradford (UK), aged between 18 and 71 with a mean age of 50 (SD = 17.04). Among the participants, 14 were women (54%) and 12 were men (46%), with interviews conducted in both English (76%) and Urdu (24%). Participants were grouped under three generation groups based on age (first generation 65+; second generation 40-64; younger generation 18-39 years). There was no biological link between the generational groups, and they were not part of the same family. Data were analysed using qualitative reflexive thematic analysis. Findings were categorised into three themes: knowledge and awareness of diabetes symptoms; social and family context of food practices and making sense of healthy eating. The family was the fundamental unit of understanding food-related health behaviours. Eating traditional food was perceived as healthy and deemed practical for first generations who were the initial members of their family to settle in the UK as well as the second generations who had parents born in Pakistan. Younger British Pakistanis were born in the UK and reported that they struggled to eat alternative foods within the home and manage their T2DM. These findings improve our understanding of how three generations of British Pakistanis with T2DM negotiate healthy diets. There is a need for culturally tailored diet modifications and interventions, where different generational needs can be specifically targeted to adopt healthier diets which should be shared and encouraged.

Ghost authors revealed: The structure and function of human N6 -methyladenosine RNA methyltransferases.

Despite the discovery of modified nucleic acids nearly 75 years ago, their biological functions are still being elucidated. N6 -methyladenosine (m6 A) is the most abundant modification in eukaryotic messenger RNA (mRNA) and has also been detected in non-coding RNAs, including long non-coding RNA, ribosomal RNA, and small nuclear RNA. In general, m6 A marks can alter RNA secondary structure and initiate unique RNA-protein interactions that can alter splicing, mRNA turnover, and translation, just to name a few. Although m6 A marks in human RNAs have been known to exist since 1974, the structures and functions of methyltransferases responsible for writing m6 A marks have been established only recently. Thus far, there are four confirmed human methyltransferases that catalyze the transfer of a methyl group from S-adenosylmethionine (SAM) to the N6 position of adenosine, producing m6 A: methyltransferase-like protein (METTL) 3/METTL14 complex, METTL16, METTL5, and zinc-finger CCHC-domain-containing protein 4. Though the methyltransferases have unique RNA targets, all human m6 A RNA methyltransferases contain a Rossmann fold with a conserved SAM-binding pocket, suggesting that they utilize a similar catalytic mechanism for methyl transfer. For each of the human m6 A RNA methyltransferases, we present the biological functions and links to human disease, RNA targets, catalytic and kinetic mechanisms, and macromolecular structures. We also discuss m6 A marks in human viruses and parasites, assigning m6 A marks in the transcriptome to specific methyltransferases, small molecules targeting m6 A methyltransferases, and the enzymes responsible for hypermodified m6 A marks and their biological functions in humans. Understanding m6 A methyltransferases is a critical steppingstone toward establishing the m6 A epitranscriptome and more broadly the RNome. This article is categorized under: RNA Interactions with Proteins and Other Molecules > Protein-RNA Recognition RNA Interactions with Proteins and Other Molecules > RNA-Protein Complexes RNA Interactions with Proteins and Other Molecules > Protein-RNA Interactions: Functional Implications.

Artificial Intelligence and the Paths of Its Use in Agricultural Processes

A distinctive feature of the functioning of biological links as elements of biomachine systems (BMS) is shown. The basic concepts of artificial intelligence and the structure of an intelligent system, which includes three main blocks a knowledge base, a solver and an intelligent interface that allows you to communicate with a computer without special programs for data entry are presented. Classification models for managing biomachine systems in crop and livestock production and examples of the use of AI in fast-flowing technological processes in these industries are considered.

Structure of data in cell biology research

Bioinformatics is a scientific field on the border between informatics and biology where problems in the field of biology are solved using statistical methods. Another part of it are database systems which serve to store data necessary for meta-analysis. In recent years, there has been a boom mainly thanks to enabling technologies that make it possible to obtain big data about the functioning of living cells of organisms. Bioinformatics tools are necessary to process these data and form an integral part of research in modern biological and medical sciences. Scientific research focused on molecular biology, as well as medicine, is increasingly focusing on data storage. It is understood that the correct structure of the database is important for the correct interpretation of the results of their research activities. For communication between tables in the database, it is essential to set the data type, assign Primary key and Foreign key, ensure data integrity, remove data plurality and understand the research logic. Based on these needs, we created a relational database using SQL Server 2017 and Microsoft SQL Server Management Studio 2017 (SSMS). We created the source code for programming the database and filling it with data in Structured Query Language (SQL) and T-SQL on the Microsoft platform. Of the data types, we used float for numbers with a floating decimal line, integer values were assigned an integer (int), date had a date data type, and text strings had a defined nvarchar data type. Our results bring new information in the field of bioinformatics about the creation of a database structure for data storage in cell biology research. These new insights will help big data in meta-analyses of data and applying scientific results to medical and scientific practice. The database will store data obtained in real time, which will ensure relevance in pointing out biological trends, regularities, relationships and links between cellular structures. All these aspects are very important for the spatial modeling of data and the creation of models of interactions of cell structures with use for applications in medical and biological practice.