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The paper industry faces two critical challenges: the scarcity of raw materials and the environmental impact of chemical waste pollution. Addressing the first challenge involves harnessing alternative, sustainable raw materials, while the second challenge can be mitigated through the adoption of bio-bleaching processes, which significantly reduce chemical consumption while enhancing paper brightness and quality. This study proposes a solution to both challenges by using non-woody Calotropis procera (Ankara) and a xylanase-producing microbial consortium for sustainable handmade paper production, a combination not extensively explored in prior research. To evaluate this approach, the process was divided into three stages. In stage I, Ankara fibre was pulped through open hot digestion. In stage II, the pulp was subjected to bio-bleaching in two experimental setups: Set I (without sucrose) and Set II (with sucrose) for 5 days. In stage III, chemical bleaching was used to improve the final brightness of the treated pulps. A novel comparison was made between the bio-bleaching efficiency of an individual isolate g5 (BI) and a bacterial consortium (BC). This research highlighted that bio-bleaching with the consortium effectively removed lignin (140±60 mg/l) and colour (1830±50 PCU), especially in the presence of sucrose, compared to using a single xylanase isolate. Pulp residue/filtrate collected at each stage was estimated based on parameters such as colour and lignin content. After stage III (chemical bleaching), the release of colour and lignin in pulp filtrate was higher in BI compared to BC, indicating the consortium's effectiveness during bio-bleaching, which leaves fewer degradable lignin structures for the chemical bleaching stage. Papers crafted from consortium-treated pulp also exhibited higher brightness than those treated with the isolate. This study reveals the synergistic effect of microbial consortia, leading to more efficient lignin degradation and enhanced bio-bleaching capabilities, supporting the development of greener industrial processes. Ultimately, this study demonstrates a unique and eco-friendly approach to papermaking, combining C. procera and enzymatic bio-bleaching to reduce dependency on hazardous chemicals and support sustainable industry practices.

The dialogue between population genetics and evolutionary biology, which historically followed separate paths, has now developed into a complex and interdisciplinary field of study [...]

The first section of this paper sets the record straight regarding many of Debouwere's (2024, "Review of Education," 12, e3445) specific criticisms. The second section discusses the magnitude of the SES-achievement relationship, specifically Debouwere's (2024) contention that the correlation is strong around 0.5 or 0.6 compared to observed correlations mostly between 0.2 and 0.3. The third section deals with five issues that Debouwere (2024) raises in his paper: (1) the stability of SES vis-à-vis cognitive ability; (2) the accuracy of children's reports of parents' socioeconomic characteristics; (3) whether teachers discriminate by students' SES; (4) the importance of cognitive ability for educational differentiation (i.e., tracking and streaming); and (5) SES effects on student achievement, controlling for prior achievement. The fourth section discusses the role of genetics in student achievement. Meta-analyses and other studies indicate that about 50%-70% of the variance in student achievement is attributable to genetics (i.e., the heritability). The high heritability of student achievement accounts for its high stability, its strong correlations with cognitive ability and the weak effects of SES, net of prior achievement or cognitive ability.

Science should provide students an accurate and contemporary education on genetic influence, particularly how it impacts trait variability and developmental norms. Stories involving familial, racial, and sexual differences routinely appear in the popular media and sales of over-the-counter genetic tests are mounting. Unfortunately, research suggests genetic curricula in secondary education and university courses have little impact on genetic literacy; instead they appear to amplify genetic essentialism. This position paper reports on genetic essentialism, the impact of three components of science education (teachers, students, curriculum), and critiques existing genetic lessons in two prevalent scientific disciplines, biology and psychology. Two entrenched 19th century genetic paradigms (e.g., Mendelian inheritance and behavioral genetics) are specifically examined. The paper closes with specific recommendations for improving students' genetic literacy including important contemporary genetic science (e.g., epigenetics) and instructional approaches (e.g., learning progression, refutational teaching).

When students think of evolution, they might imagine T. rex, or perhaps an abiotic scene of sizzling electrical storms and harsh reducing atmospheres, an Earth that looks like a lunar landscape. Natural selection automatically elicits responses that include "survival of the fittest," and "descent with modification," and with these historical biological catch phrases, one conjures up images of large animals battling it out on the Mesozoic plane. Rarely do teachers or students apply these same ideas to cancer and the evolution of somatic cells, which have accrued mutations and epigenetic imprinting and relentlessly survive and proliferate. Our questions in this paper include the following: Can cancer become an important teaching model for students to explore fundamental hypotheses about evolutionary process? Can the multi-step somatic cancer model encourage visualizations that enable students to revisit and reenter previous primary concepts in general biology such as the cell, mitosis, chromosomes, genetic diversity, ecological diversity, immune function, and of course evolution, continually integrating their biology knowledge into process and pattern knowledge? Can the somatic cancer model expose similar patterns and protagonists, linking Darwinian observations of the natural world to our body? And, can the cancer clone model excite critical thinking and student hypotheses about what cancer is as a biological process? Does this visually simple model assist students in recognizing patterns, connecting their biological curriculum dots into a more coherent learning experience? These biological dynamics and intercepting aptitudes of cells are amplified through the cancer model and can help shape the way biology students begin to appreciate the interrelatedness of all biological systems while they continue to explore pivotal points of biological fuzziness, such as the microbiome, limitations of models, and the complex coordination of genomic networks required for the function of even a single cell and the realization of phenotypes. In this paper we use clonal evolution of cancer as a model experience for students to recreate how a single, non-germline cell appears to shadow the classic pattern of natural selection in body cells that have gone awry. With authentic STEAM activities students can easily crossover and revisit previous biological topics and the ubiquitous nature of natural selection as seen in the example of somatic cells that result in a metastasizing tumor, giving students insight into natural selection's accommodating and tractable patterns throughout the planet.

Background: The most impactful research on pediatric type 1 diabetes (T1D) remains unknown. Objective: We aimed to evaluate the characteristics and impact of the 100 most-cited articles on pediatric T1D. Materials and Methods: Using a predefined bibliometric strategy, the Scopus database was searched for high-cited papers (HCPs) published from 2001 to 2020. Articles were evaluated for data on the publication year, countries, authors, journals, topics, and types. Social network analysis was performed to visualize the interaction among countries, organizations, and authors using VOSviewer software. Results: The top 100 HCPs received 390 to 4634 citations, averaging 773.5 citations per paper (CPP). The funded HCPs (n = 50) had a higher impact (CPP 791.5). The majority of HCPs (n = 83) were collaborative. Classifying by research type, 65 studies were clinical (n = 65), risk factors (n = 27), epidemiology (n = 26), pathophysiology (n = 16), treatment outcome (n = 13), genetics (n = 12), complications (n = 3), quality of life (n = 2), and prognosis (n = 1). The number of authors involved was 1,101, affiliated with 545 organizations in 27 countries; the USA (n = 64) and the UK (n = 24) were the most productive countries, whereas Australia and the UK were the most impactful. D.M. Nathan and J.M. Lawrence were the most prolific authors, while P. Raskin and J.M. Lachin were the most impactful. Conclusions: High-income countries such as the USA, UK, and Australia contribute significantly to high-impact pediatric T1D research. Funding and collaboration improve the impact of citations in publications. Less researched areas such as treatment outcomes, genetics, complications, quality of life, and prognosis should be the focus of future research on pediatric T1D. [ABSTRACT FROM AUTHOR]

This study examines the challenges of humanism and education in the 21st century as addressed by the German philosopher Peter Sloterdijk in his Elmau Speech (1999). In this lecture, titled "Rules for the Human Zoo", Sloterdijk argues that the traditional notion of humanism, specifically "humanism as a literary society," has reached its conclusion, necessitating the development of a new humanism appropriate for the contemporary era. However, the new concept of humanism emerging from what Sloterdijk terms the "anthropotechnic turn" appears to align with the discourses surrounding human enhancement that have emerged in the 21st century, thereby influencing the realm of education. The first half of this article reports on the significant concerns and criticisms expressed by the media at that time regarding this new humanism, which seems to be associated with eugenicist ideas. Taking a step further, this study critically examines the nature of the challenges around education implied by Sloterdijk, specifically the conflict between "friend of humans and friend of Übermensch", and explores the potential roles and responsibilities of education in the latter part of the paper.

The emerging field of genomic medicine offers an opportunity for biology and anatomy teachers to bring the topics of DNA, genetics, molecular processes, and evolution together into one experience. Through the genomic medicine paradigm, students see the unbroken connection between small biological topics such as mutations and their potential connection to disease phenotypes. In this paper, we present as a main example cystic fibrosis, which is an often-studied genetic disease in general biology class, for examination through the genomic medicine lens. Concepts such as genes, the plasma membrane, variation, mutations, the nucleus, and chromosomes can be used in a narrative and visual approach to genetics through the genomic medicine standpoint to engage and connect students with next-generation genomics and with the fundamental unit of life -- the cell. It is through the genomic medicine lens that the cell's context and relationship to the evolving world takes place.

Abstract Background Broussonetia papyrifera is an economically significant tree with high utilization value, yet its cultivation is often constrained by soil contamination with heavy metals (HMs). Effective scientific cultivation management, which enhances the yield and quality of B. papyrifera, necessitates an understanding of its regulatory mechanisms in response to HM stress. Results Twelve Metallothionein (MT) genes were identified in B. papyrifera. Their open reading frames ranged from 186 to 372 bp, encoding proteins of 61 to 123 amino acids with molecular weights between 15,473.77 and 29,546.96 Da, and theoretical isoelectric points from 5.24 to 5.32. Phylogenetic analysis classified these BpMTs into three subclasses: MT1, MT2, and MT3, with MT2 containing seven members and MT3 only one. The expression of most BpMT genes was inducible by Cd, Mn, Cu, Zn, and abscisic acid (ABA) treatments, particularly BpMT2e, BpMT2d, BpMT2c, and BpMT1c, which showed significant responses and warrant further study. Yeast cells expressing these BpMT genes exhibited enhanced tolerance to Cd, Mn, Cu, and Zn stresses compared to control cells. Yeasts harboring BpMT1c, BpMT2e, and BpMT2d demonstrated higher accumulation of Cd, Cu, Mn, and Zn, suggesting a chelation and binding capacity of BpMTs towards HMs. Site-directed mutagenesis of cysteine (Cys) residues indicated that mutations in the C domain of type 1 BpMT led to increased sensitivity to HMs and reduced HM accumulation in yeast cells; While in type 2 BpMTs, the contribution of N and C domain to HMs’ chelation possibly corelated to the quantity of Cys residues. Conclusion The BpMT genes are crucial in responding to diverse HM stresses and are involved in ABA signaling. The Cys-rich domains of BpMTs are pivotal for HM tolerance and chelation. This study offers new insights into the structure-function relationships and metal-binding capabilities of type-1 and − 2 plant MTs, enhancing our understanding of their roles in plant adaptation to HM stresses.

The article offers information on the retraction of papers from a genetics journal due to concerns about informed consent for study participants, particularly from ethnic minorities in China.

Teaching chemistry and biology students about biologics design remains challenging despite its increasing importance in pharmaceutical development. Monoclonal antibodies, commonly called mAbs, are the most popular biologics. They have been developed into drugs to treat various diseases in the past decades. Multiple challenges exist for designing proper formulations to stabilize mAbs, such as preventing aggregation and mitigating viscosity. Molecular modeling and simulations can improve pharmaceutical products by examining the interactions between mAbs and other compounds, such as excipients. To introduce students to biopharmaceuticals, eight students at the Stevens Institute of Technology participated in a semester-long course to learn the challenges of pharmaceutical development and different computational skills to study biologics design. The students started with a limited background in this field. Throughout one semester, they were introduced to various literature and software tools for modeling antibodies and studying their interactions with excipients. This paper aims to develop a course structure to be replicated at other universities and institutions to teach biopharmaceutical development to students.

Quantitative methods have a long historical entanglement with oppressive ideologies, including eugenics, white supremacism, and anti-LGBTQ+ ideology. Increasingly, scholars have made attempts at rectifying quantitative methods by bringing them into conversation with critical theoretical frameworks. One such example is QuantCrit, which attempts to engage quantitative methods through Critical Race Theory. The present paper attempts to extend that vital work by engaging queer theory in quantitative methods. Several key ideas are proposed for quantitative methodologists and educational researchers to think with queer theory in quantitative research. Each idea is explored with an eye toward queer theoretical frameworks while continuously engaging QuantCrit. Finally, implications for producers and users of research are offered.

In this paper I suggest a pragmatic model for the notion of 'information' used in molecular biology in the description of protein synthesis. Discarding any ontological commitments of the term 'information', I propose a view of information based on an analogy with communication. This view could at least supplement the existing information-metaphor that should be updated for two reasons: (i) the concept of information it presupposes, and (ii) the origin of the metaphor itself. Besides, the metaphorical nature of the notion of 'information' is still often overlooked, which leads to a false sense of understanding of the underlying genetic phenomena it should describe. The advantages of a model based on communication, as it is seen by the field of pragmatics, is twofold: (i) it provides a rather simple analogy between human communication and basic genetic processes, and (ii) it supplies the tools for the understanding of the non-literal use of the term 'information'.

Causal mediation analysis is a popular approach for investigating whether the effect of an exposure on an outcome is through a mediator to better understand the underlying causal mechanism. In recent literature, mediation analysis with multiple mediators has been proposed for continuous and dichotomous outcomes. In contrast, methods for mediation analysis for an ordinal outcome are still underdeveloped. In this paper, we first review mediation analysis methods with a continuous mediator for an ordinal outcome and then develop mediation analysis with a binary mediator for an ordinal outcome. We further consider multiple mediators for an ordinal outcome in the counterfactual framework and provide identification assumptions for identifying the mediation effects. Under the identification assumptions, we propose a regression-based method to estimate the mediation effects through multiple mediators while allowing the presence of exposure-mediator interactions. The closed-form expressions of mediation effects are also obtained for three scenarios: multiple continuous mediators, multiple binary mediators, and multiple mixed mediators. We conduct simulation studies to assess the finite sample performance of our new methods and present the biases, standard errors, and confidence intervals to demonstrate that our proposed estimators perform well in a wide range of practical settings. Finally, we apply our proposed methods to assess the mediation effects of candidate DNA methylation CpG sites in the causal pathway from socioeconomic index to body mass index.

Simple Summary: Much research has been conducted on the causes of childhood cancer, but many areas of uncertainty remain. We conducted a detailed search of recent studies investigating the causes of childhood cancer. Our findings, based on publications from 2014 to 2021, are summarized by topic in three separate papers: factors acting during childhood (Paper 1), factors relating to the parents and pregnancy (Paper 2), and factors relating to the environment (Paper 3). In this first paper, we summarize convincing evidence from studies that show increased childhood cancer risk associated with genetic cancer predisposition, birth defects, prior cancer, medical ionizing radiation, organ transplantation and exposure to cancer-causing viruses, and a reduced risk associated with some childhood vaccinations. Other factors discussed in this paper include the impact of the child's diet, allergies, medications, and body mass index. This review of factors associated with childhood cancer may help evidence-based efforts to reduce cancer in our pediatric populations. Purpose: To review the childhood risk factors for pediatric cancer (diagnosis before age 20). Methods: We conducted literature searches using Ovid Medline and Scopus to find primary research studies, review articles, and meta-analyses published from 2014 to 3 March 2021. Results: Strong evidence indicates that an array of genetic and epigenetic phenomena, structural birth defects, and chromosomal anomalies are associated with an increased risk of various childhood cancers. Increased risk is also associated with prior cancer, likely due to previous treatment agents and therapeutic ionizing radiation. Convincing evidence supports associations between several pediatric cancers and ionizing radiation, immunosuppression, and carcinogenic virus infection both in healthy children and in association with immune suppression following organ transplantation. Breastfeeding and a childhood diet rich in fruits and vegetables appears to reduce the risk of pediatric leukemia but the evidence is less strong. Childhood vaccination against carcinogenic viruses is associated with a lower risk of several cancers; there is less strong evidence that other childhood vaccinations more broadly may also lower risk. Ultraviolet (UV) radiation is associated with increased melanoma risk, although most melanomas following childhood UV exposure occur later, in adulthood. Evidence is weak or conflicting for the role of body mass index, other childhood infections, allergies, and certain treatments, including immunomodulator medications and human growth therapy. [ABSTRACT FROM AUTHOR]

Understanding biological mechanisms is fundamental for improving animal production and health to meet the growing demand for high-quality protein. As an emerging biotechnology, single-cell transcriptomics has been gradually applied in diverse aspects of animal research, offering an effective method to study the gene expression of high-throughput single cells of different tissues/organs in animals. In an unprecedented manner, researchers have identified cell types/subtypes and their marker genes, inferred cellular fate trajectories, and revealed cell‒cell interactions in animals using single-cell transcriptomics. In this paper, we introduce the development of single-cell technology and review the processes, advancements, and applications of single-cell transcriptomics in animal research. We summarize recent efforts using single-cell transcriptomics to obtain a more profound understanding of animal nutrition and health, reproductive performance, genetics, and disease models in different livestock species. Moreover, the practical experience accumulated based on a large number of cases is highlighted to provide a reference for determining key factors (e.g., sample size, cell clustering, and cell type annotation) in single-cell transcriptomics analysis. We also discuss the limitations and outlook of single-cell transcriptomics in the current stage. This paper describes the comprehensive progress of single-cell transcriptomics in animal research, offering novel insights and sustainable advancements in agricultural productivity and animal health. [ABSTRACT FROM AUTHOR]

Simple Summary: Myeloid-derived suppressor cells (MDSCs) are immature cells that expand in the circulation of patients with cancer, sepsis or chronic inflammation, modulate the immune response against cancer (favoring tumor onset and progression) and promote neoangiogenesis. These premises suggest that MDSCs could be involved in the pathogenesis of primary myelofibrosis (PMF) (a myeloproliferative neoplasm characterized by chronic inflammation and extensive neoangiogenesis in bone marrow and spleen). In this paper, we found that (1) MDSCs are increased both in the circulation and in the spleen of PMF patients and strongly correlate with disease progression; and (2) reduced CXCR4 expression on MDSCs along with increased plasmatic SDF-1α can be involved in their mobilization. These findings suggest that circulating MDSCs can be considered a parameter of disease severity and set MDSCs as potential new targets for cancer therapy. Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by a chronic inflammatory state that plays a relevant role in the disease pathogenesis (as proven by high levels of inflammatory cytokines with prognostic significance and by a persistent oxidative stress) and by extensive neoangiogenesis in bone marrow (BM) and spleen. Myeloid-derived suppressor cells (MDSCs) are immature cells that expand in patients with cancer, sepsis or chronic inflammation, favoring tumor onset and progression mainly through the decrease in immune surveillance and the promotion of neoangiogenesis. In this paper, we evaluated the presence of circulating MDSCs in PMF patients, the plasmatic factors involved in their mobilization/expansion and the correlations with laboratory, genetic and clinical parameters. The data indicated that MDSCs could have a relevant role in PMF as a new pathogenic mechanism contributing to explaining the phenotypic diversity observed during the clinical course of the disease, or a potential new target for personalized treatment. [ABSTRACT FROM AUTHOR]

Major depressive disorder (MDD) is a severe psychiatric illness known to be highly complex due to its difficulty in identifying genetic factors and its polygenic nature. While genetic studies and research into epigenetic changes have advanced our understanding of MDD, the precise role of genetics in MDD's manifestation remains elusive. This paper reviews the current state of research on MDD genetics, encompassing findings on MDD's biological blueprint and investigations into epigenetic modifications associated with MDD development. Furthermore, this paper explores the interplay between depression and the immune system and the impact of inflammation on the disorder. Neuroimaging studies have also impacted comprehension of MDD, revealing alterations in brain size and chemistry. These insights shed light on the biological underpinnings of MDD and hold promise for developing more effective treatments and therapies for patients. [ABSTRACT FROM AUTHOR]

Background: With similarities in heritability, neurobiology and symptomatology, the question has been raised whether schizophrenia and bipolar disorder are truly distinctive disorders or belong to a continuum. This narrative review summarizes common and distinctive findings from genetics, neuroimaging, cognition and clinical course that may help to solve this ethiopathogenetic puzzle. Methods: The authors conducted a literature search for papers listed in PubMed and Google Scholar, using the search terms "schizophrenia" and "bipolar disorder" combined with different terms such as "genes", "neuroimaging studies", "phenomenology differences", "cognition", "epidemiology". Articles were considered for inclusion if they were written in English or Spanish, published as full articles, if they compared subjects with schizophrenia and bipolar disorder, or subjects with either disorder with healthy controls, addressing differences between groups. Results: Several findings support the hypothesis that schizophrenia and bipolar disorder are discrete disorders, yet some overlapping of findings exists. The evidence for heritability of both SZ and BD is obvious, as well as the environmental impact on individual manifestations of both disorders. Neuroimaging studies support subtle differences between disorders, it appears to be rather a pattern of irregularities than an unequivocally unique finding distinguishing schizophrenia from bipolar disorder. The cognitive profile displays differences between disorders in certain domains, such as premorbid intellectual functioning and executive functions. Finally, the timing and trajectory of cognitive impairment in both disorders also differs. Conclusion: The question whether SZ and BD belong to a continuum or are separate disorders remains a challenge for further research. Currently, our research tools may be not precise enough to carve out distinctive, unique and undisputable differences between SZ and BD, but current evidence favors separate disorders. Given that differences are subtle, a way to overcome diagnostic uncertainties in the future could be the application of artificial intelligence based on BigData. Limitations: Despite the detailed search, this article is not a full and complete review of all available studies on the topic. The search and selection of papers was also limited to articles in English and Spanish. Selection of papers and conclusions may be biased by the personal view and clinical experience of the authors. [ABSTRACT FROM AUTHOR]

Non-shared environmental influences are non-genetic influences that are uncorrelated in family members. Monozygotic twins have the same genes and shared environment. Any differences in the behaviour of monozygotic twins can be attributed to non-shared environmental influences. Qualitative methods can help study in depth the non-shared environmental influences causing discordance among monozygotic twins. I conducted a literature review, as part of my KURF Project, evaluating how qualitative methods can be utilised to study non-shared environmental influences causing discordance among monozygotic twins. This essay summarises and reflects on the journey of taking on a research project, the challenges of working in an independent environment and the skills acquired by the end of the project. [ABSTRACT FROM AUTHOR]

Fertility treatment enables involuntary childless people to have genetically related children, something that, for many, is a valuable life project. In this paper, I respond to two sets of objections that have been raised against expanding state‐funded fertility treatment provision for existing treatments, such as in vitro fertilisation (IVF), and against funding new treatments, such as uterine transplantation (UTx). Following McTernan, I refer to the first set of objections as the 'one good among many' objection. It purports that it is unjustifiable for the state to prioritise the funding of the life project of becoming a parent through fertility treatment provision over the funding of other life projects that people might have. Following Lotz, I refer to the second set of objections as the 'norm‐legitimation' objection. It maintains that the provision of costly forms of fertility treatment, such as UTx, would legitimise problematic social norms concerning genetic relatedness, reproduction and parenting, and that states should not engage in such a legitimation. In response to these objections, I defend the view that (reproductive) preferences ought to be taken more seriously when discussing fertility treatment provision and parental projects, and that not doing so can be costly, especially for women. The approach defended in this paper seeks to avoid disregarding and policing preferences and to reconcile their fulfilment with political projects aimed at improving the material and social conditions of sub‐fertile people: people who, for social or biological reasons (or an intersection of the two), are unable to reproduce unassisted. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA), a prevalent chronic disease among the elderly, presents a complex pathogenesis and currently lacks effective treatment. Traditional observational studies are time-consuming, labor-intensive, susceptible to confounding factors, and cannot establish causal relationships. Mendelian randomization (MR) analysis, leveraging genetic variation to assess causal associations between exposures and outcomes, offers a cost-effective and efficient alternative. Over the past decade, large-scale genome-wide association studies have identified numerous genetic variants linked to OA risk factors, facilitating MR study design. In this review, we systematically identified 52 MR studies meeting specific criteria and evaluated their quality, exploring the impact of lifestyle, nutrition, comorbidities, circulating metabolites, plasma proteins, and other health factors on OA risk. We discuss the results and potential mechanisms of MR findings, addressing conflicting evidence based on existing literature and our prior research. With the ongoing expansion of genome-wide association data, we anticipate MR's role in future OA studies to broaden, particularly in drug development research using targeted MR approaches. We thus aim for this paper to offer valuable insights for researchers and clinicians in related fields. [ABSTRACT FROM AUTHOR]

Azolla is the only plant with a co-evolving nitrogen-fixing (diazotrophic) cyanobacterial symbiont (cyanobiont), Nostoc azollae, resulting from whole-genome duplication (WGD) 80 million years ago in Azolla's ancestor. Additional genes from the WGD resulted in genetic, biochemical, and morphological changes in the plant that enabled the transmission of the cyanobiont to successive generations via its megaspores. The resulting permanent symbiosis and co-evolution led to the loss, downregulation, or conversion of non-essential genes to pseudogenes in the cyanobiont, changing it from a free-living organism to an obligate symbiont. The upregulation of other genes in the cyanobiont increased its atmospheric dinitrogen fixation and the provision of nitrogen-based products to the plant. As a result, Azolla can double its biomass in less than two days free-floating on fresh water and sequester large amounts of atmospheric CO2, giving it the potential to mitigate anthropogenic climate change through carbon capture and storage. Azolla's biomass can also provide local, low-cost food, biofertiliser, feed, and biofuel that are urgently needed as our population increases by a billion every twelve years. This paper integrates data from biology, genetics, geology, and palaeontology to identify the location, timing and mechanism for the acquisition of a co-evolving diazotrophic cyanobiont by Azolla's ancestor in the Late Cretaceous (Campanian) of North America. [ABSTRACT FROM AUTHOR]

Aim: The study is on the emerging role of artificial intelligence in the forensic sciences. After clarifying the basic concepts and a brief historical overview, the possibilities of using AI in various forensic fields are discussed: genetics, pattern recognition, chemistry, toxicology, anthropology, forensic medicine, and scene reconstruction. Methodology: The study synthesises several recently published international papers. Findings: The penetration of the application of artificial intelligence into some fields of science is undoubtedly an ongoing process. Most of the varied forensic fields also cannot avoid this development. Analysing large databases unmanageable with traditional methods, pattern recognition, and machine learning can all be important tools for forensic science. However, an important conclusion is that AI is a supporter of human expert work, not a substitute. Value: In the field of forensic sciences, no such detailed summary article has been published in Hungarian so far. [ABSTRACT FROM AUTHOR]

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Transcriptome-wide association studies (TWAS) goal is to better understand the etiology of diseases and develop preventative and therapeutic approaches by examining the connections between genetic variants and phenotypes while overcoming the limitations of the genome-wide association study (GWAS). It is a valuable complement to GWAS, reducing the negative effects of multiple tests and enabling a more thorough investigation of gene expression patterns in various tissues. A systematic review is presented in this paper to identify articles that utilize TWAS to understand the genetic factors behind complex diseases. A detailed selection process was carried out using standard PRISMA criteria to select relevant articles for the review. Twenty-five articles passed the inclusion criteria and were selected for additional review. The studies cover a diverse range of disorders, including Tourette's syndrome, Alzheimer's disease, rheumatoid arthritis, and major depression. Leveraging gene expression data from different tissues and populations, these investigations successfully identified novel genes and pathways associated with the studied conditions. The collective findings highlight the transformative impact of integrative genomics in advancing our understanding of complex diseases, providing insights into potential therapeutic targets, and laying the foundation for precision medicine approaches. [ABSTRACT FROM AUTHOR]

The first section of this paper sets the record straight regarding many of Debouwere's (2024, Review of Education, 12, e3445) specific criticisms. The second section discusses the magnitude of the SES‐achievement relationship, specifically Debouwere's (2024) contention that the correlation is strong around 0.5 or 0.6 compared to observed correlations mostly between 0.2 and 0.3. The third section deals with five issues that Debouwere (2024) raises in his paper: (1) the stability of SES vis‐à‐vis cognitive ability; (2) the accuracy of children's reports of parents' socioeconomic characteristics; (3) whether teachers discriminate by students' SES; (4) the importance of cognitive ability for educational differentiation (i.e., tracking and streaming); and (5) SES effects on student achievement, controlling for prior achievement. The fourth section discusses the role of genetics in student achievement. Meta‐analyses and other studies indicate that about 50%–70% of the variance in student achievement is attributable to genetics (i.e., the heritability). The high heritability of student achievement accounts for its high stability, its strong correlations with cognitive ability and the weak effects of SES, net of prior achievement or cognitive ability. [ABSTRACT FROM AUTHOR]

In light of the post-genomic era, epigenetics brings about an opportunity to better understand how the molecular machinery works and is led by a complex dynamic set of mechanisms, often intricate and complementary in many aspects. In particular, epigenetics links developmental biology and genetics, as well as many other areas of knowledge. The present work highlights substantial scopes and relevant discoveries related to the development of the term from its first notions. To our understanding, the concept of epigenetics needs to be revisited, as it is one of the most relevant and multifaceted terms in human knowledge. To redirect future novel experimental or theoretical efforts, it is crucial to compile all significant issues that could impact human and ecological benefit in the most precise and accurate manner. In this paper, the reader can find one of the widest compilations of the landmarks and epistemic considerations of the knowledge of epigenetics across the history of biology from the earliest epigenetic formulation to genetic determinism until the present. In the present work, we link the current body of knowledge and earlier pre-genomic concepts in order to propose a new definition of epigenetics that is faithful to its regulatory nature. [ABSTRACT FROM AUTHOR]

Simple Summary: The incidence of gastric cancer (GC) is increasing. Many people receive an advanced diagnosis of GC. Furthermore, a large number of patients are surgically inoperable and are unresponsive to preoperative chemotherapy. Patients with GC do not currently have an immunotherapy option. Our study's objective was to provide insight into extracellular vesicles (EVs) and GC. EVs in GC can be studied, as this article explains. EVs screening, which is available for all patients, is an option for combatting GC. Extracellular vesicles, or EVs, are membrane-bound nanocompartments produced by tumor cells. EVs carry proteins and nucleic acids from host cells to target cells, where they can transfer lipids, proteomes, and genetic material to change the function of target cells. EVs serve as reservoirs for mobile cellular signals. The collection of EVs using less invasive processes has piqued the interest of many researchers. Exosomes carry substances that can suppress the immune system. If the results of exosome screening are negative, immunotherapy will be beneficial for GC patients. In this study, we provide an update on EVs and GC based on ongoing review papers and clinical trials. [ABSTRACT FROM AUTHOR]

• CFTR-related disorders (RD) are a group of conditions caused by CFTR protein dysfunction, but to a level of dysfuncton not satisfying the diagnostic crtieria for cystic fibrosis (CF). • This paper discusses the individual disorders, including congenital absence of the vas deferens (CAVD), diffuse bronchiectasis, chronic or acute recurrent pancreatitis, allergic bronchopulmonary aspergillosis, chronic rhinosinusitis, primary sclerosing cholangitis and aquagenic wrinkling of the palms. • The CFTR functional and genetic evidence in support of each condition being a CFTR-RD are discussed and guidance for reaching the diagnosis is provided. • Gaps in our knowledge and future areas of research, including the role of CFTR modulators, are highlighted. This is the third paper in the series providing updated information and recommendations for people with cystic fibrosis transmembrane conductance regulator (CFTR)-related disorder (CFTR-RD). This paper covers the individual disorders, including the established conditions - congenital absence of the vas deferens (CAVD), diffuse bronchiectasis and chronic or acute recurrent pancreatitis - and also other conditions which might be considered a CFTR-RD, including allergic bronchopulmonary aspergillosis, chronic rhinosinusitis, primary sclerosing cholangitis and aquagenic wrinkling. The CFTR functional and genetic evidence in support of the condition being a CFTR-RD are discussed and guidance for reaching the diagnosis, including alternative conditions to consider and management recommendations, is provided. Gaps in our knowledge, particularly of the emerging conditions, and future areas of research, including the role of CFTR modulators, are highlighted. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD) is a complex disease that develops through a sequence of molecular events that are still poorly defined. This process is driven by a multitude of context-dependent genes that play different roles based on their environment. The complexity and multi-faceted nature of these genes make it difficult to study the genetic basis of IBD. The goal of this article is to review the key genes in the pathophysiology of IBD and highlight new technology that can be used in further research. This paper examines Nanostring RNA probe technology, which uses tissue analyzed without the use of enzymes, transcription, or amplification. Nanostring offers several panels of genes to test, including an inflammation panel of 234 genes. This article analyzes this panel and reviews the literature for each gene's effect in IBD for use as a framework to review the pathophysiology of the disease. The panel was narrowed to 26 genes with significant evidence of mechanistic potential in IBD, which were then categorized into specific areas of pathogenesis. These include gut barrier breakdown, inappropriate recognition of commensal bacteria, immune cell activation, proinflammatory cytokine release, and subsequent impairment of the anti-inflammatory response. The eventual goal of this paper is the creation of a customized panel of IBD genes that can be used to better understand the genetic mechanism of IBD and aid in the development of future therapies in IBD. [ABSTRACT FROM AUTHOR]