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Adult hippocampal neurogenesis persists throughout the human lifespan, yet declines in Alzheimer’s disease and major depression, associated in part with reduced brain-derived neurotrophic factor (BDNF) levels. For rodents, environmental enrichment, dichotomised primarily as physical activity and spatial complexity, robustly promotes adult hippocampal neurogenesis, but no framework has translated these findings to human environments. This review is the first to synthesise evidence across the full translational pathway, arguing that spatial complexity and physically active navigation in neighbourhoods and buildings constitute a humanised form of environmental enrichment. It proposes that standard indoor environments may represent a functionally impoverished condition for the human hippocampus, paralleling standard laboratory caging. An applied model is presented, mapping built environment features onto the neurobiological mechanisms regulating adult hippocampal neurogenesis, with BDNF as the central translatable biomarker linking environmental exposures to neurogenic outcomes. A methodological roadmap for future empirical validation is also outlined. This framework repositions the built environment as a modifiable determinant of adult hippocampal neurogenesis in humans, with implications for mitigating the risk of depression, cognitive impairment, and Alzheimer’s disease.

Introduction: The causative agent of toxoplasmosis is Toxoplasma gondii (T. gondii); an intracellular obligate parasite causes abortion in humans and animals. The review aims to clarify the situation of the disease in humans and animals in different parts of the country so that data will be available for any future work regarding the control of the disease. Methodology: All humans and animal research studies published in the last 18 years between 2000 and 2018 in Saudi Arabia were targeted, including prevalence or seroprevalence of T. gondii infection or antibodies. The searched strategy included human or pregnant women or children as well as animals or any particular species. Results: The result showed that approximately one-third of the population in Saudi Arabia had IgG seropositivity, and 6.4% had IgM seropositivity. Moreover, the disease was widespread in almost all the regions except AL- Jouf, where no data published. The prevalence of the chronic infection was high in sheep in Riyadh 68%, and the prevalence of acute was found in Najran 19% in sheep, goats, and camels. Conclusions: The current article showed the importance of the disease in Saudi Arabia for both humans and animals. The educational programs should be established to impart people to avoid the infection by the parasite.

The membrane-associated RING-CH-type finger ubiquitin ligase MARCHF8 is a human homolog of the viral ubiquitin ligases Kaposi’s sarcoma herpesvirus K3 and K5 that promote host immune evasion. Previous studies have shown that MARCHF8 ubiquitinates several immune receptors, such as the major histocompatibility complex II and CD86. While human papillomavirus (HPV) does not encode any ubiquitin ligase, the viral oncoproteins E6 and E7 are known to regulate host ubiquitin ligases. Here, we report that MARCHF8 expression is upregulated in HPV-positive head and neck cancer (HNC) patients but not in HPV-negative HNC patients compared to normal individuals. The MARCHF8 promoter is highly activated by HPV oncoprotein E6-induced MYC/MAX transcriptional activation. The knockdown of MARCHF8 expression in human HPV-positive HNC cells restores cell surface expression of the tumor necrosis factor receptor superfamily (TNFRSF) death receptors, FAS, TRAIL-R1, and TRAIL-R2, and enhances apoptosis. MARCHF8 protein directly interacts with and ubiquitinates the TNFRSF death receptors. Further, MARCHF8 knockout in mouse oral cancer cells expressing HPV16 E6 and E7 augments cancer cell apoptosis and suppresses tumor growth in vivo. Our findings suggest that HPV inhibits host cell apoptosis by upregulating MARCHF8 and degrading TNFRSF death receptors in HPV-positive HNC cells.

As global urbanisation is rising and public health challenges intensify, this systematic review is conducted at a critical time to explore and explain the associations between the parameters of green environments and nuanced adaptive neuroplasticity in the human brain to advance the development of health-focused sustainable cities and buildings in line with the concept of neurosustainability. This review includes studies involving participants of all ages and genders, with no restrictions on health conditions, exposed to green environments regardless of built environment comparisons. A systematic search of Scopus, PubMed, and Web of Science identified relevant studies published up to November 2024. The risk of bias was assessed using the PEDro scale and ROBINS-I domains, and data were analysed narratively due to heterogeneity. Twenty-three studies were included, conducted across the USA, UK, Germany, Spain, Bulgaria, the Netherlands, Japan, and South Korea. Findings reveal that green environments are associated with positive, region-specific brain changes across the lifespan, surprisingly from before birth to late adulthood. While forests showed more significant effects than blue spaces or urban green spaces, residential greenness emerged as a consistently effective exposure, especially within a 300–500 m buffer around home addresses, provided that sky visibility is present. Notably, no studies have examined green architecture or biophilic interiors, although they are more proximal, are associated with greater exposure time, have antagonistic effects, and may potentially limit sky visibility, highlighting a key gap for future research. Limitations include heterogeneity in exposure definitions, methodologies, and targeted brain regions. Still, this review offers a novel synthesis, providing insight into how greening the built environment may sustain not only the planet but also the plasticity of the brain. This review is registered with INPLASY (INPLASY2024110103) and forms part of a doctoral research project funded by the Cambridge Trust in partnership with the Jameel Education Foundation.

This paper bridges critical gaps through proposing a novel, environmentally mediated brain-derived neurotrophic factor (BDNF)-interactive model that promises to sustain adult hippocampal neurogenesis in humans. It explains how three environmental enrichment mechanisms (physical activity, cognitive stimulation, and mindfulness) can integratively regulate BDNF and other growth factors and neurotransmitters to support neurogenesis at various stages, and how those mechanisms can be promoted by the physical environment. The approach enables the isolation of specific environmental factors and their molecular effects to promote sustainable BDNF regulation by testing the environment’s ability to increase BDNF immediately or shortly before it is consumed for muscle repair or brain update. This model offers a novel, feasible method to research environment enrichment and neurogenesis dynamics in real-world human contexts at the immediate molecular level, overcoming the confounds of complex environment settings and challenges of long-term exposure and structural plasticity changes. The model promises to advance understanding of environmental influences on the hippocampus to enhance brain health and cognition. This work bridges fundamental gaps in methodology and knowledge to facilitate more research on the enrichment–neuroplasticity interplay for humans without methodological limitations.

Hardware Trojans (HTs) are hidden threats embedded in the circuitry of integrated circuits (ICs), enabling unauthorized access, data theft, operational disruptions, or even physical harm. Detecting Hardware Trojans (HTD) is paramount for ensuring IC security. This paper introduces a novel Siamese neural network (SNN) framework for non-destructive HTD. The proposed framework can detect HTs by processing power side-channel signals without the need for a golden model of the IC. To obtain the best results, different neural network models such as Convolutional Neural Network (CNN), Gated Recurrent Unit (GRU), and Long Short-Term Memory (LSTM) are integrated individually with SNN. These models are trained on the extracted features from the Trojan Power & EM Side-Channel dataset. The results show that the Siamese LSTM model achieved the highest accuracy of 86.78%, followed by the Siamese GRU model with 83.59% accuracy and the Siamese CNN model with 73.54% accuracy. The comparison shows that of the proposed Siamese LSTM is a promising new approach for HTD and outperform the state-of-the-art methods.

Chronic stress is among the most pervasive health challenges of contemporary urban life, yet its persistence is not simply a matter of external pressure. When adult hippocampal neurogenesis is impaired, the brain loses its capacity to regulate the hypothalamic–pituitary–adrenal (HPA) axis and distinguish new threats from familiar ones through dentate gyrus pattern separation, rendering stress self-perpetuating. Physical activity is widely recognised as a promoter of neurogenesis through brain-derived neurotrophic factor (BDNF), yet the built environments in which most people spend approximately 90% of their time simultaneously suppress BDNF through chronic stress and deny sufficient physical activity intensity to restore it, a condition known as type 2 allostatic overload sustained by architectural impoverishment. This paper proposes architectural enrichment as a theoretical framework designed to resolve this problem at its root through two independent but synergistic mechanisms: architecturally mediated voluntary stair use to elevate peripheral BDNF via metabolic pathways, and neurobiophilic design based on the Neurobiophilia Index to attenuate cortisol and passively support BDNF and neurogenesis. Twelve hypothesised neurobiological profiles are derived in a framework that advances the concept of hippocampal neurosustainability, proposing that buildings can be designed not merely to avoid harming the brain but to actively sustain its capacity for resilience amid the stressors of modern urban living.

While the human brain has evolved extraordinary abilities to dominate nature, modern living has paradoxically trapped it in a contemporary “cage” that stifles neuroplasticity. Within this modern environment lurk unseen natural laws with power to sustain the human brain’s adaptive capacities - if consciously orchestrated into the environments we design. For too long our contemporary environments have imposed an unyielding static state, while still neglecting the brain’s constant adaptive nature as it evolves to dominate the natural world with increasing sophistication. The theory introduced in this article aims to go back in nature without having to go back in time, introducing and expounding Neurosustainability as a novel paradigm seeing beyond the contemporary confines to architect environments and brains in parallel. Its integrated neuro-evidenced framework proposes four enrichment scopes—spatial, natural, aesthetic, and social—each holding multifaceted attributes promising to sustain regions like the hippocampus, cortex and amygdala. Neurosustainability aims to liberate the quintessential essence of nature to sustain and enhance neuroplastic processes through a cycle that begins with design and extends through epigenetic changes. This paradigm shift aims to foster cognitive health and wellness by addressing issues like stress, depression, anxiety and cognitive decline common in the contemporary era thereby offering a path toward a more neurosustainable era aiming to nurture the evolution of the human brain now and beyond.

Hippocampal neurogenesis is critical for improving learning, memory, and spatial navigation. Inhabiting and navigating spatial complexity is key to stimulating adult hippocampal neurogenesis (AHN) in rodents because they share similar hippocampal neuroplasticity characteristics with humans. AHN in humans has recently been found to persist until the tenth decade of life, but it declines with aging and is influenced by environmental enrichment. This systematic review investigated the impact of spatial complexity on neurogenesis and hippocampal plasticity in rodents, and discussed the translatability of these findings to human interventions. Comprehensive searches were conducted on three databases in English: PubMed, Web of Science, and Scopus. All literature published until December 2023 was screened and assessed for eligibility. A total of 32 studies with original data were included, and the process is reported in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement and checklist. The studies evaluated various models of spatial complexity in rodents, including environmental enrichment, changes to in-cage elements, complex layouts, and navigational mazes featuring novelty and intermittent complexity. A regression equation was formulated to synthesize key factors influencing neurogenesis, such as duration, physical activity, frequency of changes, diversity of complexity, age, living space size, and temperature. Findings underscore the cognitive benefits of spatial complexity interventions and inform future translational research from rodents to humans. Home-cage enrichment and models like the Hamlet complex maze and the Marlau cage offer insight into how architectural design and urban navigational complexity can impact neurogenesis in humans. In-space changing complexity, with and without physical activity, is effective for stimulating neurogenesis. While evidence on intermittent spatial complexity in humans is limited, data from the COVID-19 pandemic lockdowns provide preliminary evidence. Existing equations relating rodent and human ages may allow for the translation of enrichment protocol durations from rodents to humans.

Herein, a novel composite of Corchorus olitorius-derived biochar and Bi 12 O 17 Cl 2 was fabricated and utilized for the degradation of tetracycline (TC) in a solar photo-oxidation reactor. The morphology, chemical composition, and interaction between the composite components were studied using various analyses. The biochar showed a TC removal of 52.7% and COD mineralization of 59.6% using 150 mg/L of the biochar at a pH of 4.7 ± 0.5, initial TC concentration of 163 mg/L, and initial COD of 1244 mg/L. The degradation efficiency of TC increased to 63% and the mineralization ratio to 64.7% using 150 mg/L of bare Bi 12 O 17 Cl 2 at a pH of 4.7 ± 0.5, initial TC concentration of 178 mg/L, and COD of 1034 mg/L. In the case of biochar/Bi 12 O 17 Cl 2 composite, the degradation efficiency of TC and COD mineralization ratio improved to 85.8% and 77.7% due to the potential of biochar to accept electrons which retarded the recombination of electrons and holes. The synthesized composite exhibited high stability over four succeeding cycles. According to the generated intermediates, TC could be degraded to caprylic acid and pentanedioic acid via the frequent attack by the reactive species. The prepared composite is a promising photocatalyst and can be applied in large-scale systems due to its high degradation and mineralization performance in a short time besides its low cost and stability.