Biology and Life Sciences

Abstract:

The bacterial proteome is a highly dynamic landscape rather than a static reflection of the genome. Recent research revealed that proteome complexity extends far beyond canonical gene annotation, with N-terminal (Nt-)proteoforms emerging as an important underexplored additional regulatory layer. These molecular variants originate from a single genetic locus through alternative translation initiation at internal or external in-frame start sites, thereby generating N-terminal heterogeneity that can influence protein stability, subcellular localization, interaction networks, and the stoichiometric assembly of multiprotein complexes. While recent advances in riboproteogenomics, N-terminomics, and computational annotation strategies have enabled proteoform mapping at single-amino acid resolution, rapid high-throughput discovery currently outpaces downstream functional characterization. This review discusses the technological advances driving Nt-proteoform discovery, including emerging ribosome profiling and proteogenomic approaches, and further evaluates strategies for the functional characterization of Nt-proteoform. Particular emphasis is placed on the transition from conventional plasmid-based heterologous expression systems toward precise genome-engineering approaches that enable selective manipulation of alternative translation initiation events within their native genomic context. Such targeted strategies are essential to bridge the gap between Nt-proteoform identification and functional understanding, ultimately uncovering how individual bacterial genomic loci can encode proteoforms with distinct and potentially polarized roles in bacterial physiology and pathogenesis.

Abstract: In breast cancer, current knowledge of the associations between clinicopathologic characteristics, genetic changes, and subtype-specific patterns remain unclear. This research investigated how pathological and clinical variables affect the actionability of NGS-based tumor molecular data. Materials and methods: 227 breast cancer patients referred to Genekor’s laboratory for tumor molecular profile analysis were included in the study. Pathology records, available in all cases, were used to assess critical clinicopathological features including HER2, ER, PR, Ki67, grade, metastatic site, and age. A 1021 gene NGS-based multigene panel was utilized to assess tumors’ biology alongside tumor mutational burden (TMB) and microsatellite instability (MSI) Results: Comprehensive genomic profiling revealed that 95.6% of the patients harbored at least one oncogenic or likely oncogenic alteration, highlighting the high diagnostic yield of NGS-based testing. Distinct subtype-specific patterns were observed: HR+/HER2-tumors were enriched for PIK3CA and ESR1 gene alterations, while Triple Negative Breast Cancer (TNBC) was dominated by TP53 alterations. Clinically actionable alterations were most common in HR+/HER2-tumors (~60% on-label), whereas TNBC more often harbored off-label or trial-associated targets. The inclusion of tumor-agnostic biomarkers (TMB/MSI) increased on-label actionability up to 64.5% in ER−/PR+ tumors. primarily driven by TMB-high cases. Median TMB values were low, and age was the only independent predictor. Furthermore, the presence of actionable alterations was significantly higher in metastatic tumors, and TP53 alterations were associated with aggressive tumor characteristics.Conclusions: Comprehensive NGS-based genomic profiling identifies clinically actionable alterations in over half of breast cancer patients, with substantial variability across molecular subtypes. The HR+/HER2-subtype demonstrates the highest prevalence of on-label actionable biomarkers. These findings support the routine implementation of comprehensive genomic profiling, especially in metastatic HER2-negative breast cancer, to guide precision oncology strategies and enable enrollment in biomarker-driven clinical trials.

Abstract: Background: Despite circulation of evolutionarily related cold-causing coronaviruses (CCCs) in the pre-COVID era, most individuals lacked pre-existing serum IgG and/or class-switched memory B cell (B_mem) reactivity for the SARS-CoV-2 Spike (S) glycoprotein expressed by the ancestral Wuhan-Hu-1 (WH1) strain. Subsequent priming of the immune system through natural infection or prophylactic COVID-19 mRNA vaccination successfully generated robust B_mem responses against the WH1-S antigen, along with eliciting cross-reactivity for the future Omicron (BA.1) variant responsible for breakthrough infections (BTIs). However, to what extent immunological imprinting of B_mem towards the WH1-S antigen detrimentally constrains elicitation of variant-specific antibody responses following subsequent booster vaccinations or BTIs—a phenomena referred to as “original antigenic sin”—remains an unresolved and open question. Methods: Using ImmunoSpot^® we evaluated peripheral blood mononuclear cells (PBMCs) from defined human cohorts for IgG⁺ ASC reactivity against Spike proteins representing CCCs and SARS-CoV-2. Additionally, we developed a novel dual-label inverted FluoroSpot assay to distinguish between strain-specific and cross-reactive IgG⁺ ASCs recognizing epitopes in the receptor binding domain (RBD) of SARS-CoV-2 Omicron variants. Results: Our data demonstrate a lack of appreciable back-boosting of IgG⁺ B_mem recognizing structurally conserved epitopes shared between CCCs and SARS-CoV-2. Moreover, we found evidence for immunological imprinting and preferential expansion of B_mem recognizing cross-reactive epitopes in the RBD following BTI. Nevertheless, Omicron strain-specific B_mem were detected in PBMC donors collected in 2025. Conclusions: Our novel inverted dual-label FluoroSpot methodology provides a highly flexible, easily implementable technique for distinguishing between strain-specific and cross-reactive B cell responses in translational vaccine research.

Abstract: Hantavirus pulmonary syndrome (HPS) is a severe disease first recognised in the United States in 1993, with a case fatality rate approaching 35–50%. Since the identification of Sin Nombre virus during the Four Corners outbreak, understanding the transmission dynamics and geographic distribution of hantaviruses has become critical for public health planning and prevention. This review synthesises evidence from ecological niche modelling, epidemiological surveillance, and environmental analyses to explain patterns of hantavirus occurrence in North America. The findings indicate that HPS risk is associated with dry climates, rural and peri-urban landscapes, rodent host ecology, and increased social vulnerability, with cases primarily concentrated in the western United States. We examine how environmental conditions, rodent ecology, human–rodent interactions, and socioeconomic factors interact to influence disease risk. This synthesis provides recommendations for reducing exposure in high-risk populations and regions.

Abstract: Cytokine storm syndromes arise from a systemic collapse of immune homeostasis due to dynamic imbalance between danger load (L) and immune buffer capacity (B). Existing linear “danger signal → inflammation” models cannot explain why high antigen loads sometimes produce only mild inflammation, why hyperinflammation and immunosuppression often co‑exist, or why similar danger signals lead to divergent clinical outcomes. Here we propose a systems immunology framework: L represents the total pro‑inflammatory pressure, while B is a network of promoting and suppressive forces analogous to acid–base or coagulation buffers. We introduce a dynamic S‑index (S_actual ≈ Treg/Teff functional ratio) as an “immunological pH” for the adaptive arm. Four equilibrium states are defined – high‑buffer, low‑buffer, promoting‑dominant, and suppressive‑dominant – each with distinct storm pathways (direct vs. indirect). Three dominant dynamic states are described: innate‑driven collapse (immune‑deficiency‑associated and massive necrosis types), adaptive dynamic mismatch (a four‑stage progression), and mixed oscillatory states. Differences between PAMP and DAMP are clarified, and diverse storm phenotypes are mapped onto a unified state space. The framework explains inter‑individual heterogeneity and temporal evolution, and it provides a rationale for individualized therapy. Several experimentally testable predictions are proposed. All quantitative descriptions are purely theoretical and await experimental validation.

Abstract: Salinity poses a major threat to sustainable agriculture and coastal ecosystems resulting in a substantial loss of plant productivity and biodiversity. Although some coastal grass species exhibit natural adaptation to saline conditions, the physiological mechanisms underlying salt tolerance remain incompletely understood, particularly regarding the role of plant-associated microbial symbionts. In a previous study, a commercial cultivar of red fescue (Festuca rubra ssp. rubra cv. Rafael) was evaluated as salt sensitive grown hydroponically, whereas wild populations of F. rubra commonly occur in coastal salt marshes (possibly ssp. litoralis). We hypothesized that this difference in salt tolerance is partly associated with fungal plant-microbe interactions. To test this, we investigated whether inoculation with a root-colonizing fungal isolate (identified as Fusarium sp. 1), isolated from F. rubra growing on a salt marsh along the Dutch Wadden Sea coast, could improve the salinity tolerance of a commercial cultivar. The results showed that inoculation with Fusarium sp. 1 alleviated the salt-induced growth inhibition. At 100 mM NaCl, the shoot and root biomass of inoculated plants were partially restored compared with non inoculated controls, accompanied by a significant increase in the shoot-to-root ratio. To elucidate the physiological basis of this response, we applied the microelectrode ion flux estimation (MIFE) technique to quantify Na⁺ -induced K⁺ efflux in roots. Inoculated plants exhibited improved K⁺ homeostasis, characterized by a reduced instantaneous Na⁺-induced K⁺ efflux and a faster recovery of root fluxes. Moreover, inoculated plants grown at 50 and 100 mM NaCl showed an increases in root K⁺ influx of 333 and 397%, respectively, compared with non-inoculated controls. Our results indicated that inoculation with a root-colonizing fungal isolate can improve salinity tolerance of F. rubra, likely through enhanced root K⁺ retention. These findings suggest that commercial F. rubra cultivars remain responsive to microbial associations and highlight the potential of exploring plant- microbe interactions from natural environments to improve salinity resilience in grasses and potentially other crops.

Abstract: Blood is often used either as a source of individual biomarkers or as input for scalar immune-age and biological-age models. This study tests a different question: whether blood-derived longitudinal measurements can be represented as a structured homeostatic state space. A rebuilt blood HRSM framework was applied to a primary repeated-measures IMM-AGE cellular object and to supporting transcriptomic blood branches. The state vector was defined by reserve-like support, trajectory recoverability, coherence or volatility control, and retained persistence. In the primary IMM-AGE object, published immune age aligned strongly with higher retained persistence, lower reserve-like support, and lower coherence, while recoverability was weak. The strongest single cellular driver was naive CD8⁺ T-cell decline, consistent with established immune-ageing biology. Longitudinal tests showed that temporal memory was strongest in the persistence axis, with reserve-like support moving in the opposite direction. A subject-level persistence index indicated stronger preservation of the 2008 blood-state configuration in younger baseline subjects. Joint HRSM entropy declined across time, suggesting compression of the accessible multivariate blood-state distribution. Sensitivity checks preserved the central ageing polarity after removal of PD1 from the persistence map, use of a reduced core map, and removal of broad lymphocyte-bulk support terms. Supporting GSE213313 analyses provided a completed transcriptomic blood branch with negative controls, comparators, and cross-dataset validation against GSE324831. Cross-dataset portability was strongest for support, recoverability, and coherence families, whereas persistence was not portable as a fixed molecular family and was better interpreted as a context-sensitive behaviour. The results support blood HRSM as a systemic gateway representation of immune ageing, not as a replacement for existing immune-age clocks and not as a universal molecular-memory claim.

Abstract: Neuroinflammation is considered as one of the core pathogenic factors of neurodegeneration in Alzheimer disease (AD) and related dementias (RD). It is also associated with other two hallmarks of AD dementia, i.e., amyloid beta (Ab) and neurofibrillary tangles (NFT), and increasingly considered as the third hallmark of AD. Abnormality in microglial pathway plays a crucial role in the neuroinflammation of AD and RD. Microglia dysfunction is linked to many neuroinflammatory signaling pathways towards the progress of developing neurodegeneration resulting to cognitive deficits or dementia. Currently, several therapeutic approaches aim to target inflammatory regulators for AD treatment, and microglia is considered as one of the vital targets. In this article we intend to highlight and discuss various microglia mediated signaling pathways that link to chronic neuroinflammation and cognitive dysfunction/dementia in AD and other diseases. This could help us to understand the degree of microglial association with the disease pathophysiology through analyzing various studies in last few decades including the latest reports. We also aim to highlight the pathways that are more and less conclusively established and determine possible pathways which may help in further exploration and narrowing down or expanding the area of studies that requires further research. AD and RD are one of the most leading causes of death in the world and there is no appropriate drug available for cure or prevention of the disease. Further research is an absolute requirement for better understanding the mechanisms underlying the disease pathophysiology and better planning of basic/therapeutic research and clinical trials. We also provide up-to-date clinical trials that used inflammatory targeting drugs and discuss the failures and promising drug targets.

Abstract: Sphingolipid metabolism has emerged as a regulatory interface between lipid homeostasis, organelle stress, and genome maintenance. Although sphingolipids are essential structural components of cellular membranes, specific metabolites also function as bioactive mediators that shape cellular responses to genotoxic stress. In this review, we examine how canonical and atypical sphingolipid pathways influence the DNA damage response through three mechanistic axes. First, ceramide-centered stress signaling links radiation, chemotherapy, and inflammatory injury to kinase and phosphatase pathways, mitochondrial apoptosis, and checkpoint-associated cell-fate decisions. Second, nuclear sphingolipid metabolism, particularly sphingosine kinase 2-dependent production of sphingosine-1-phosphate, regulates chromatin-associated transcriptional programs through modulation of histone deacetylase activity. Third, persistent sphingolipid imbalance promotes metabolic stress by disrupting lysosomal turnover, mitochondrial function, endoplasmic reticulum homeostasis, and redox balance, thereby increasing endogenous oxidative DNA damage. We also discuss atypical sphingolipids, including 1-deoxysphingolipids generated through altered serine palmitoyltransferase substrate utilization, as emerging mediators of mitochondrial dysfunction and genome instability. Finally, we consider the relevance of these mechanisms to cancer, lysosomal storage disorders, and neurodegenerative diseases, where sphingolipid dysregulation may influence therapeutic responses and disease progression. Together, these findings position sphingolipid metabolism as an integrated regulatory network connecting cellular stress signaling, chromatin regulation, organelle dysfunction, and genome stability.

Abstract:

Sustainable agriculture has become a major priority in modern agricultural research and practice due to increasing concerns regarding climate change, soil degradation, biodiversity loss, and long-term food security. In this context, soil-conserving cultivation systems, such as no-till and reduced tillage technologies, are increasingly promoted because they improve soil structure, enhance water retention and organic matter accumulation, reduce erosion, and contribute to more environmentally sustainable crop production systems. This study evaluated the effects of selected sustainable agricultural technologies, including no-till, minimum tillage, and mulch-till soil tillage systems, on the nutritional composition of grains of spring barley (Hordeum vulgare L.), winter wheat (Triticum aestivum L.), and corn (Zea mays L.). The contents of starch, total dietary fibre, beta-glucans, proteins, and lipids were analysed in mature grains during two years of cultivation. The type of cereal was the dominant factor determining grain composition. Corn showed the highest starch (77.20%) and lipid (3.66%) contents, wheat accumulated the highest protein concentration (12.02%), and barley was characterized by the highest total dietary fibre (13.36%) and beta-glucans (3.75%) contents. Significant negative correlations were detected between starch and dietary fibre (r = −0.823) and between starch and beta-glucans (r = −0.827), indicating metabolic trade-offs between storage and structural compounds. Harvest year significantly influenced proteins, total dietary fibre, and lipids, whereas soil tillage exerted a weaker and metabolite-specific effect. No-till tillage technology generally promoted higher total dietary fibre, beta-glucans, and lipid contents. Principal component analysis confirmed cereal species as the major source of variability, followed by harvest year, while soil tillage showed comparatively limited effects. The results demonstrate that cereal grain nutritional quality is governed primarily by genotype, with environmental and agronomic factors acting as secondary modifiers.

Abstract: Autophagy is a carefully regulated catabolic process that utilizes assemblies of specific sets of macromolecules operating at multiple stages of the pathway. Discoveries in recent years show that autophagy markedly relies on liquid-liquid phase separation (LLPS). Here, we present parameters that indicate plasticity of autophagy proteins and their probability to undergo LLPS in macroautophagy and microautophagy. We show that microautophagy is an extremely LLPS-friendly pathway. Several mechanisms involving proteins in the autophagy machinery that drive LLPS on various types of membranes to regulate this process or that undergo LLPS as autophagic cargo are described in detail. We also summarize the factors that modulate the LLPS potential of autophagy proteins. A high probability of autophagy-related proteins to undergo spontaneous LLPS shown here can direct future research on the role of protein droplets in autophagy.

Abstract: Since the gene was first articulated as a unit of inheritance and causation, evolutionary biology has operated under a productive but unresolved tension between experimental practice and explanatory language. Perturbation experiments, association studies, and plasticity assays are routinely interpreted as if they should converge on a single notion of genetic causation, yet they rarely do. This mismatch has been sensed repeatedly—from early organicist critiques, through the work of Gould and Alberch, to contemporary contributions from systems biology and evolutionary developmental biology—but has resisted unification. Here, we argue that the persistence of this tension reflects not missing data or incomplete theory, but a fundamental mismatch between explanatory frameworks. Specifically, different experimental approaches interrogate biological systems at different organizational levels and therefore probe distinct causal regimes. By integrating insights from gene regulatory network structure, developmental buffering, canalization, and polygenic adaptation, we show that genetic necessity is a sparse, level relative property associated with structural dependence, whereas evolutionary change proceeds through widespread, small, contributory effects that are tolerated by developmental systems. Genome wide association studies succeed precisely because they map this domain of available variation, while knockouts reveal where systems are fragile rather than where evolution most readily acts. Developmental plasticity further bridges these regimes by exposing shifts in network sensitivity under environmental change. Reframing causation as contribution based and level relative resolves longstanding conflicts between genetics, development, and evolution, and provides a coherent framework for interpreting experimental results without privileging any single methodology. This perspective aligns causal language with biological organization and offers a unified account of how development structures evolutionary possibility.

Abstract: Alzheimer’s disease (AD) affects more women than men, and risk rises precipitously during and after the menopausal transition. Estrogen deficiency has been the most prominent hypothesis to explain this sex difference, but increasing evidence also implicates follicle-stimulating hormone (FSH) as an independent contributor to neurodegenerative risk. This narrative review integrates the literature on reproductive aging, AD pathobiology, and sex differences in AD, with an emphasis on endocrine, metabolic, and inflammatory mechanisms relevant to their relationship. PubMed and Google Scholar were searched for peer-reviewed human studies, animal models, and mechanistic investigations published through early 2026, prioritizing primary research and systematic reviews on FSH signaling, ApoE biology, and AD pathophysiology. FSH rises in a graded fashion across the menopausal transition and has been associated with multiple pathways implicated in AD, including C/EBPβ–δ-secretase signaling, mitochondrial function, neuronal glucose metabolism, and autophagic-lysosomal clearance - though the causal directionality of many of these relationships remains to be established in humans. Dysfunction in these interrelated systems has been associated with Aβ accumulation, tau pathology, and chronic neuroinflammation. FSH also appears to influence apolipoprotein biology, particularly ApoE, through actions on lipid metabolism, protein lipidation, and clearance, with downstream effects on Aβ aggregation and inflammatory signaling that differ by ApoE isoform. In addition, reproductive aging is associated with changes in vascular integrity and blood-brain barrier function that may precede classical AD pathology. This review describes the mechanistic pathways through which chronically elevated FSH may contribute to AD risk in women and discusses the potential therapeutic implications of FSH modulation, while acknowledging that much of the current mechanistic evidence derives from preclinical models and requires validation in human populations.

Abstract: This study presents the development and application of an integrated Geographic Information System (GIS)-based Marine Spatial Planning (MSP) framework for identifying suitable offshore aquaculture development zones in Cyprus. The methodology, developed within the OS AQUA project, combines environmental exclusion analysis, weather and proximity assessment, stakeholder and policy evaluation, and carrying-capacity estimation within a unified spatial decision-support framework. A sequential three-phase analytical workflow was applied to progressively refine candidate offshore areas under environmental, operational, infrastructural, regulatory, and governance considerations. The analysis identified four candidate offshore aquaculture zones in Cyprus — Xylofagou West, Larnaka (Faros area), Governor’s Beach, and Aphrodite Hills/Avdimou — demonstrating comparatively favourable conditions for offshore aquaculture development. The results highlight the importance of integrating environmental compatibility, operational feasibility, accessibility, stakeholder acceptance, and sustainability considerations within offshore aquaculture planning processes. Carrying-capacity assessment further indicated substantial offshore production potential under precautionary operational assumptions. Beyond the Cyprus case study, the proposed GIS-MSP framework offers a transferable methodological roadmap for offshore aquaculture zoning, Allocated Zones for Aquaculture (AZA) establishment, and sustainable marine spatial planning in the Mediterranean region.

Abstract: The Life-Ratios Hypothesis (LRH) is proposed as a quantitative framework for DNA-based habitability in polar-hydride solvents. The central idea is that DNA’s biological function is temperature-range constrained not by absolute molecular energies but by dimensionless ratios of those energies to the thermal scale kBT. LRH is a calibrate-then-predict approach with no free adjustable parameters. The framework is calibrated on terrestrial liquid H2O via the hydrogen-bond dissociation ratio over the observed temperature limits of terrestrial life. The calibrated ratio values are Rdiss(ℓ)≡DHB(ℓ)/kBT∈[6.0,10.4], and Rdiss(ℓ)(H2O)≈8.4 at Tbio=310K. The framework yields three falsifiable results. First, a bond-replacement self-cancellation theorem: when a Watson–Crick base pair opens in a polar-hydride solvent, the enthalpic hydrogen-bond residual cancels topologically whenever the solvent’s N or O atom matches a base nitrogen or oxygen atom. The theorem is near-exact in water, exact in ammonia (every Watson–Crick bond contains nitrogen), and preserved at every H2O–NH3 composition. Second, the cross-solvent invariance of Rdiss(ℓ) is postulated, and, when applied to D2O, the framework predicts a +7.25K shift in biological temperature, matching the observed +7.2K shift in the temperature of maximum density. Third, when applied to liquid NH3, the framework predicts a cold solvent-network window of 198–270K, optimum 226K, accessible at 0.07–3.73atm, where warm or hot ammonia-based DNA life is excluded as a negative prediction. Combined, these results give a continuous corridor of predicted optimum biological temperatures across H2O–NH3 mixtures, from 226K in pure ammonia to 310K in pure water, over wide pressure ranges in which the corresponding solvent mixtures remain liquid. This corridor defines where DNA-based or DNA-like life should be sought if such biochemistry is possible; it does not imply that such life exists.

Abstract: Metallo-β-lactamase (MBL)-producing multidrug-resistant (MDR) bacteria have emerged as one of the most critical threats to global public health. These zinc-dependent enzymes, particularly NDM, VIM, and IMP, hydrolyze carbapenems, the last-resort antibiotics for treating severe Gram-negative infections. Unlike serine-β-lactamases, MBLs evade all clinically approved β-lactamase inhibitors, leaving a profound therapeutic vacuum. This review synthesizes evidence from 204 peer-reviewed articles (1970–2026) to examine the molecular diversity, global burden, diagnostic approaches, risk factors, and future directions for MBL-producing pathogens, including Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Acinetobacter baumannii. MBL genes are predominantly disseminated via mobile genetic elements (plasmids and integrons) and high-risk clones, facilitating rapid cross-border spread. Geographic disparities are striking: Asia accounts for 80% of MBL-producing Acinetobacter reports, while the Eastern Mediterranean and Africa show the highest prevalence of carbapenem-resistant A. baumannii (42.1% and 36.1%, respectively). In contrast, Europe and the Americas report prevalence below 1%, though absolute case numbers remain substantial due to robust surveillance. Phenotypic detection methods (combined disc test, E-test, and modified Hodge test) are practical in resource-limited settings but suffer from poor specificity and subjective interpretation. Genotypic methods (PCR, whole-genome sequencing, and MALDI-TOF MS) offer definitive gene identification but require specialized infrastructure and expertise. Critical risk factors for MBL acquisition include prior carbapenem exposure, prolonged ICU stays, invasive devices, immunosuppression, and healthcare-associated transmission. The absence of Food and Drug Administration (FDA)-approved MBL inhibitors forces reliance on antibiotics that have limited efficacy, high toxicity, and emerging resistance. Addressing this crisis demands a coordinated, multi-pronged strategy: strengthening global genomic surveillance; deploying rapid molecular diagnostics at the point of care; accelerating the development of novel MBL inhibitors; enforcing antimicrobial stewardship to curb carbapenem overuse; and implementing rigorous infection prevention and control measures.

Abstract: Microorganisms naturally produce many pharmaceutically and industrially relevant secondary metabolites. For this process they usually use biosynthetic units. For example, microbes from the genus Streptomyces possess great ability to produce a variety of natural products in such manner, which is possible due to complicated crosstalk between primary and secondary metabolism. These microbial cell factories produce more than 2/3 of antibiotics used in medicine, and a large variety of other bioactive compounds. Although bacterial producer hosts, including Bacillus spp. and Streptomyces spp., have been studied for decades, the engineering of these bacteria remains challenging, and the genetic potential has not been fully utilized. This is due to limited genetic toolbox, restriction activity and occurrence of silent biosynthetic gene clusters. Recent advancements in genetic manipulation of microorganisms allowed to improve the turnaround time of strain engineering, but still has strain-specific limitations. However, a new perspective offered by synthetic biology to exploit the potential of existing and novel pathways in primary and secondary metabolism allows combining of different biosynthetic steps originating from diverse bacteria using a limited toolbox. Synthetic biology has emerged as a robust strategy to understand, investigate, design, and engineer the biosynthetic capability of bacterial antibiotics machinery, including such in Streptomyces. Innovative synthetic biology and metabolic engineering tools have rapidly accelerated the discovery of new natural products as well as engineering of Streptomyces, e.g. enzymatic modules for secondary metabolite production can be combined in synthetic cells to produce new derivatives of natural products. Furthermore, with the recent advances in molecular biology and genome editing, Synthetic biology has focused at generation of controlled phenotypes from a given input and at other sophisticated approaches. In this review, developments of novel approaches of Synthetic biology for microbial engineering with focus on antibiotics producers like Streptomyces spp. are discussed.

Abstract: Using marine resources’ colouring agents as nutrients, medicaments and in luxury products colouring is rooted in human history. The handy obtainable marine biological pigments (MBPs), consider as inexpensive materials since colourants. They were a part e of blue technology for colouring purposes, as nutrient additives, cosmetic gradients, beauty products, staining addresses and fashion colour in luxury. Today, they still broaden many new applications. They can be concentrated on the bodies of marine creatures providing unique colour, properties and complement activities. They can stand alone to process unique activities. In addition, some are essential for host survival. Out of their primary hosts, they stay either unmodified or can be changed or associated with other micro and/or macromolecules in their secondary hosts (consumers). Few were extracted, purified, identified and formulated as drugs. Many share properties like being antioxidants, having the ability to protect from sunlight (as UV waves) and improving eye vision. They are involved in health protection or illness treatment, as anticancer, anti-inflammatory, anti-neuro-degradation, antiaging, anti-wrinkle, and as antimicrobial. Even they hold many undiscovered properties that make them an uncountable source for de nevo applications with innumerable chances that mastery the colourful fields. This review summarizes the importance of marine pigments and addresses important applicable properties that made them interesting in nutraceutical, medicinal, pharmaceutical, cosmeceutical and industrial applications. In addition, it is concerned with discussing some facts that have attracted the attention of humans in the past today and some expectations for the MBPs future.

Abstract: Sudden cardiac death (SCD) is a natural death of cardiac origin and accounts for millions of deaths worldwide each year, representing a major public health issue. Despite its significance, scientific investigation into SCD is often limited. Not all laboratories collect biological samples, such as blood or tissue, for genetic testing, and even when such analyses are performed, pathogenic or clinically relevant genetic variants are not always detected or fully informative. This review aims to highlight biological specimens that are frequently overlooked and underutilized in genetic analyses due to their complex nature: formalin-fixed, paraffin-embedded (FFPE) tissues. Although FFPE samples are suboptimal for traditional genetic investigations, they often represent the only available material when fresh or properly frozen tissue has not been collected. The main limitation in using FFPE tissues arises from formalin-induced modifications that can compromise DNA quality. Recent research, however, has identified novel biomarkers of interest, particularly microRNAs (miRNAs), short non-coding RNAs that remain stable in their expression even under suboptimal environmental conditions. The focus of this review is to emphasize the potential of FFPE tissues, historically used for histological studies, as valuable sources for innovative molecular analyses employing these novel biomarkers. By leveraging miRNAs and other emerging molecular targets, FFPE specimens could provide insights previously inaccessible through conventional DNA-based testing, thereby expanding the toolbox for postmortem investigations in SCD. This review underlines the importance of reconsidering archived FFPE tissues not merely as historical or morphological resources, but as promising matrices for cutting-edge molecular and forensic research.

Abstract: Linking community variation to environmental gradients is central to reservoir ecology and monitoring, yet the strength of detected associations can depend on how community change is represented. Using phytoplankton surveys from a tropical reservoir (Corumbá River, Brazil) sampled across wet and dry seasons, we compared taxonomic beta diversity with two functional representations: Reynolds functional groups and a set of widely used morphological traits combined into functional beta-diversity indices. We partitioned beta diversity into turnover and richness-difference components and quantified environment–community associations with constrained ordination. Overall, the representation chosen altered both the magnitude and the seasonal consistency of environmental associations: trait-based indices (particularly dendrogram-based metrics weighted by biovolume) tended to show stronger associations with environmental gradients related to mixing, light availability and nutrients, whereas functional groups and species-level data emphasized complementary aspects of community change. Turnover and richness-difference components did not respond uniformly across representations, highlighting that component choice can shift ecological interpretation. Rather than providing a universal ‘best’ approach, our results suggest practical trade-offs among representations when the goal is to detect and interpret environmental structuring along reservoir gradients, especially during highly dynamic conditions typical of early post-impoundment phases.