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Background: Positron emission tomography (PET) images molecular biomarkers — glucose metabolism, amyloid, tau, and dopaminergic function — that change before neurological disease is clinically obvious, but reading these scans is quantitative, operator-dependent, and reserved for specialists. Artificial intelligence (AI) is proposed to enhance how PET biomarkers are interpreted, and the question this review examines is not whether AI can reach high accuracy but whether that accuracy is the kind that would actually improve early diagnosis in real practice. Methods: This narrative review compared five roles AI plays across the PET-interpretation pipeline — image enhancement and low-dose reconstruction, cross-modal image synthesis, kinetic and parametric modeling, diagnostic classification and biomarker prediction, and interpretability or differential diagnosis — across five practicality dimensions: clinical task, data and modality requirements, reported performance, validation rigor, and clinical translatability. Results: Reported accuracy is consistently high, with pooled areas under the curve between about 0.84 and 0.97 across recent meta-analyses, but it is highest for the tasks with the cleanest reference standard, such as separating Parkinson's disease from controls on dopaminergic PET, and lower and more variable for the clinically valuable early tasks, such as forecasting conversion from mild cognitive impairment. The evidence base is dominated by small, single-center, retrospective cohorts validated internally against expert reads rather than against pathology or longitudinal outcome, and interpretability remains limited. Conclusion: No current AI-PET approach is simultaneously accurate, externally validated, interpretable, and demonstrated for early or preclinical disease. Dopaminergic classification in parkinsonism is closest to clinical readiness; generative and multimodal-prediction methods are promising but immature. The unmet need is externally validated, prospective, multi-site evidence targeting early disease.

NSRI-J-2026-0217 · Full text forthcoming

Controlled release systems aim to deliver a therapeutic agent at the right place, time and dose, yet many hydrogel carriers rely on non-specific mechanisms such as passive diffusion or bulk degradation. DNA hydrogels offer an alternative. Because their crosslinks are built from nucleic acids, the conditions under which the network holds together or falls apart can be programmed through base sequence. This literature review examines how stimuli-responsive DNA hydrogels are designed and how they release cargo. It describes the two main architectures, pure DNA networks and DNA-crosslinked polymer networks, and then reviews four families of triggers: molecular recognition (aptamers and strand displacement), chemical cues (pH and metal ions), physical cues (light and temperature) and enzymes. Representative studies show that these gels can respond selectively to a single small molecule, react rapidly to changes in pH, and be operated remotely with light. However, most evidence comes from in vitro experiments, model cargos such as gold nanoparticles, and a small number of animal studies. Nuclease degradation, slow trigger diffusion, leakage, limited mechanical strength and the cost of DNA synthesis remain barriers to clinical translation. The review closes by identifying priorities for future work: standardised release testing under physiological conditions, multi-input logic gating, and long-term in vivo safety data.

NSRI-J-2026-0212 · Full text forthcoming

Background: The gut microbiome generates a chemically diverse pool of small molecules, yet microbial production does not by itself establish exposure of neural tissue. The blood–brain barrier (BBB) is simultaneously a physical barrier, a selective transport interface, an endothelial metabolic compartment, and an inflammatory sensor. This makes the BBB a plausible control point between circulating microbiome-derived metabolites and their effects on the central nervous system (CNS). Objective: This review asks how BBB metabolic transporters regulate entry of microbiome-derived metabolites during neuroinflammation and how inflammatory remodeling of transporter abundance, localization, function, endothelial metabolism, efflux, and junctional integrity may change CNS exposure. Evidence/Synthesis approach: A narrative mechanistic synthesis was developed from peer-reviewed BBB, transporter, microbiome, metabolomics, inflammatory, and neurological disease literature, prioritizing mechanistic primary studies and authoritative reviews. Human, animal, cellular, iPSC-derived, and microfluidic evidence were considered separately rather than treated as interchangeable. Central findings: Convincing transporter-mediated BBB entry is well established for endogenous metabolite classes such as monocarboxylates and large neutral amino acids, but direct evidence that individual microbiome-derived metabolites use specific BBB transporters is uneven. Indole-3-propionate, short-chain fatty acids, bile-acid derivatives, trimethylamine-related metabolites, and phenolic products have substantial biological evidence, but their CNS effects frequently involve barrier signaling, immune modulation, endothelial sensing, or model-specific exposure rather than demonstrated transporter-dependent passage. Mechanistic interpretation: Inflammation can remodel the BBB at several layers simultaneously. Cytokines and endotoxin can change selected transporter expression, efflux activity, junctional organization, and endothelial signaling. Hypoxia, oxidative stress, and altered cellular energetics may further change transport capacity without requiring a proportional change in protein abundance. Consequently, plasma metabolite concentration should not be equated with brain exposure. Conclusions: The field would benefit from a transport-centered framework that separates transporter-dependent entry, paracellular movement, passive diffusion, endothelial metabolism, luminal receptor signaling, and perip

NSRI-J-2026-0208 · Full text forthcoming

BACKGROUND. Macrophages couple pathogen and damage sensing to rapid changes in transcription, energy metabolism, mitochondrial function, and organelle quality control. Inflammasomes, especially NLRP3, provide a major route by which cellular stress is converted into caspase-1 activation, maturation of IL-1β and IL-18, gasdermin D pore formation, and, in many contexts, pyroptotic cell death. Yet inflammasome activity is not intrinsically synonymous with chronic inflammation: a response can be transient and protective or recurrent and tissue damaging. OBJECTIVE. This review asks: “How does cellular metabolic state determine whether macrophage inflammasome activation becomes transient host defense or persistent sterile inflammation?” The organizing hypothesis is that metabolic state changes the cellular context in which inflammasome priming, activation, execution, and recovery occur, but that the direction and magnitude of these effects are strongly context dependent. EVIDENCE SYNTHESIS. Evidence is examined across glycolysis, oxidative phosphorylation, TCA-cycle remodeling, succinate, fumarate, citrate, itaconate and lactate, mitochondrial reactive oxygen species and mitochondrial DNA, lysosomal integrity, lipid handling, autophagy and mitophagy, and the AMPK-mTOR-HIF-1α signaling axis. Primary macrophage, human, animal, mechanistic biochemical, genetic and pharmacological studies are compared with correlative omics and review literature. Particular emphasis is placed on separating metabolic changes that precede inflammasome signaling from those generated by inflammasome activation itself. CENTRAL ARGUMENT. Metabolic state appears capable of altering inflammasome threshold and downstream outcome, but no single metabolic pathway functions as a universal switch. Instead, a recurring theme is the coupling among energetic state, ion gradients, mitochondrial and lysosomal integrity, redox control, lipid burden, and the capacity to restore homeostasis. In this framework, persistence may arise when inflammatory signaling and cellular stress reinforce one another after the initiating danger signal has diminished. CONCLUSIONS. The literature supports metabolism as an important regulator and consequence of inflammasome activity, while providing weaker evidence for a single deterministic metabolic signature of persistence. A testable synthesis is therefore proposed: pathological persistence may depend disproportionately on failure of metabolic recovery rather than simpl

NSRI-J-2026-0207 · Full text forthcoming

Background: Sleep disruption encompasses more than short sleep. Fragmentation, insomnia symptoms, irregularity, circadian misalignment, shift work, altered sleep timing, and sleep-disordered breathing can perturb metabolic, autonomic, endocrine, immune, and vascular physiology. Cardiometabolic disease is likewise socially patterned, raising the possibility that social inequality changes not only the probability of sleep disruption but also its biological consequences. Problem/gap: Sleep epidemiology and health-disparities research often address these domains separately, making it difficult to distinguish confounding, mediation, and effect modification. Objective: This review develops an integrative mechanistic framework for understanding how unequal social conditions may modify the sleep–cardiometabolic relationship through behavioral and biological pathways. Evidence synthesis: Experimental sleep-restriction studies provide causal evidence that insufficient or disrupted sleep can impair insulin sensitivity, alter autonomic regulation, affect appetite-related processes, and perturb vascular or inflammatory physiology. Prospective and observational studies associate several adverse sleep phenotypes with hypertension, type 2 diabetes, obesity, cardiovascular disease, and mortality, although effect estimates vary by sleep phenotype and population. Social and environmental exposures—including work schedules, neighborhood conditions, financial strain, food insecurity, housing instability, discrimination, caregiving demands, and unequal healthcare access—can shape sleep opportunity, sleep continuity, circadian alignment, and access to treatment. The strongest conceptual interpretation is therefore interactive: social disadvantage may increase exposure to sleep disruption, constrain compensatory behaviors, and heighten physiological stress reactivity, while cardiometabolic disease can in turn worsen sleep. Conclusion: Social inequality should be treated as a potential effect modifier and upstream determinant rather than merely a covariate. A socially informed model of sleep-related cardiometabolic risk links structural conditions to sleep phenotype, behavioral response, neuroendocrine and autonomic activation, inflammation, metabolic dysfunction, and vascular injury, while allowing for resilience and recovery. More informative causal studies will require repeated multidimensional sleep measurement, explicit social-context characterization, longitudinal biomarker

NSRI-J-2026-0206 · Full text forthcoming

Aging is accompanied by a persistent, low-grade inflammatory state commonly termed inflammaging. Although initially conceptualized as a consequence of cumulative immune stimulation and declining stress resilience, inflammaging is increasingly understood as an emergent phenotype produced by interacting changes in immune regulation, mitochondrial homeostasis, autophagy and mitophagy, cellular senescence, intercellular signaling, and tissue repair.

NSRI-J-2026-0204 · Full text forthcoming

Glucose homeostasis is traditionally described as the integrated product of insulin secretion, insulin sensitivity, hepatic glucose production, nutrient availability, and energy expenditure. Increasing evidence demonstrates that these processes are also temporally organized. The circadian timing system coordinates behavior, endocrine signaling, tissue-specific gene expression, substrate utilization, and cellular energy sensing over approximately 24-hour cycles. Disruption of this temporal organization has been associated with insulin resistance, obesity, metabolic syndrome, impaired glucose tolerance, and type 2 diabetes.

NSRI-J-2026-0203 · Full text forthcoming

Background: Dental caries is a biofilm-mediated disease in which repeated ecological perturbation at the tooth–biofilm interface can shift a resident oral community toward sustained acid production and net mineral loss. Contemporary microbiome research challenges single-pathogen explanations by showing that caries-associated states can involve community restructuring, altered metabolic activity, spatial organization, and host–microbiome interactions.

NSRI-J-2026-0202 · Full text forthcoming

Insufficient sleep is increasingly recognized as a modifiable exposure associated with altered eating behavior, impaired glucose regulation, and adverse cardiometabolic outcomes. Yet the proposition that sleep loss simply “increases hunger” is mechanistically incomplete. This narrative/mechanistic review integrates evidence from controlled human sleep-restriction experiments, randomized clinical trials, neuroimaging studies, endocrine investigations, prospective cohorts, systematic reviews, meta-analyses, and selected animal studies to explain how sleep loss can alter energy intake through interacting behavioral, circadian, neuroendocrine, neural-reward, stress, and executive-control pathways. Acute and recurring sleep restriction are distinguished from total sleep deprivation, circadian misalignment, poor sleep quality, and sleep-disordered breathing because these exposures perturb overlapping but non-identical biological systems. Experimental evidence indicates that several nights of curtailed sleep can increase subjective hunger and energy intake in some settings, while meta-analytic evidence suggests that effects on circulating leptin and ghrelin are less consistent than often assumed. In parallel, sleep restriction can modify neural responses to food cues within reward, salience, interoceptive, and control networks and can enhance the hedonic value of energy-dense foods. Endocannabinoid signaling, insulin sensitivity, HPA-axis regulation, gastrointestinal peptides, autonomic activity, and circadian timing may act as mediators or effect modifiers. Importantly, increased caloric intake may also reflect extended waking opportunity, environmental exposure to food, emotional eating, and reduced inhibitory control rather than a unitary change in physiological hunger. Experimental work supports a causal contribution of sleep restriction to short-term changes in several metabolic and eating outcomes, whereas long-term obesity pathways remain partly inferential and strongly influenced by confounding and reverse causation. Emerging intervention trials suggest that sleep extension can reduce energy intake, but evidence that sleep improvement alone produces durable weight loss remains incomplete. The field therefore requires longer, better-phenotyped, circadian-controlled studies integrating hormonal, neural, behavioral, and metabolic measures. Overall, sleep loss should be conceptualized as a systems-level perturbation that can shift the balance between homeosta

NSRI-J-2026-0201 · Full text forthcoming

Patient mortality outcomes may be impacted by differences in healthcare access and resources between rural and urban emergency departments in the United States. This systematic review of mortality rates evaluates the difference between these 2 areas. A literature search on Google Scholar and other databases yielded 33 studies. After screening, studies were excluded if they did not focus on the United States population, lacked data on mortality, or didn’t compare rural and urban areas. 10 articles went through a full review. 6 of those were removed due to non-relevant data. 4 studies met the criteria. However, there were differences in the number of patients, design, and mortality outcomes. These variations led us to compare with descriptions rather than combining the data. The four studies represented over one million patients across many emergency departments. Some of the studies found lower mortality rates in rural hospitals, while others reported higher mortality rates that were associated with rurality. These variations were also due to differences in patient numbers and clinical conditions. Overall, these findings show that mortality differences between rural and urban emergency departments are not consistent. This suggests that it depends more on the patients and clinical factors. Geographic location alone does not fully explain variations in mortality, highlighting the need for additional research.

NSRI-J-2026-0200 · Full text forthcoming

The accelerated expansion of the Universe provides a central unresolved problem in modern cosmology. The standard ΛCDM model provides an accurate phenomenological description of a broad range of observations, but the physical origin of cosmic acceleration remains unknown. Modified theories of gravity provide an alternative possibility in which late-time cosmological dynamics arise from corrections to the gravitational sector rather than from a fundamental cosmological constant. We investigate a modified-gravity framework obtained by extending the Einstein–Hilbert action with a quadratic curvature correction, R², and supplementing the gravitational sector with a canonical scalar field. We take f(R) = R + αR², where α controls the strength of the higher-curvature contribution. The field equations are derived by variation of the action with respect to the metric and scalar field and are then specialized to a spatially flat Friedmann–Lemaître–Robertson–Walker background. The resulting background equations define a numerical program for obtaining H(z). A consistent perturbation treatment is then required to predict the growth of matter fluctuations and observables such as fσ8(z) and S8. The model is designed to be confronted with publicly available cosmological observations and compared with a ΛCDM reference model using likelihood-based and Bayesian methods. This manuscript is a theoretical and methodological study: the numerical likelihood analysis has not yet been executed. Accordingly, no parameter estimates, posterior distributions, goodness-of-fit values, or observational claims are reported. These quantities are reserved for a completed analysis. Keywords: modified gravity; f(R) gravity; scalar field; dark energy; cosmology; R² gravity; Hubble parameter; σ8; structure growth; Bayesian inference.

NSRI-J-2026-0198 · Full text forthcoming

Academic pressure and examination stress are increasingly recognized as important challenges to adolescent mental health. High school students may experience pressure from examinations, academic workloads, parental expectations, peer competition, educational institutions, and concerns regarding future educational and career opportunities. These pressures may contribute to anxiety, depressive symptoms, sleep disturbance, and academic burnout, particularly when students perceive academic demands as exceeding their coping resources. This narrative literature review synthesizes evidence on the relationship between academic pressure and examination stress and mental health among high school students, with emphasis on anxiety and depression, sleep, burnout, coping, and school-based interventions. Relevant peer-reviewed literature was identified through structured bibliographic searches, prioritizing PubMed-indexed studies and systematic reviews, and was synthesized narratively because substantial heterogeneity in designs, populations, exposures, and outcomes precluded a defensible quantitative meta-analysis within the present project. A systematic review of 52 studies reported that 48 studies found a positive association between academic pressure or school-year timing and at least one adverse mental-health outcome, while 39 studies were cross-sectional, limiting causal interpretation. A school-based study of 1,426 adolescents in Belagavi, India, found that 74% reported high academic stress. Prospective research indicates greater sleep fragmentation during examination periods, while longitudinal evidence links school burnout with subsequent depressive symptoms. A systematic review of school-based interventions identified 31 eligible studies across 13 countries and found the strongest evidence for cognitive-behavioral therapy-based approaches, while also noting important methodological limitations. Overall, the literature supports a multidimensional model in which academic demands interact with family, peer, school-system, and individual factors. Prevention should combine reasonable academic challenge with supportive expectations, sleep protection, accessible school mental-health services, and evidence-based stress-management interventions. Stronger longitudinal and randomized research is needed to distinguish correlation from causation and to determine which intervention components produce durable benefits.

NSRI-J-2026-0197 · Full text forthcoming

This study investigated how chemical leachates from heat-stressed plastic containers affected water movement across synthetic cell membranes. Plastic chemical contamination was widespread in food and water supplies around the world, and understanding how these chemicals disrupted membrane barriers was crucial for evaluating biological risks. Synthetic cell pouches filled with sugar solution were submerged in clean water and water exposed to heated plastics. Mass changes were recorded hourly over four hours and analyzed using a One-Way Analysis of Variance (ANOVA). Cell pouches in clean water gained twenty-six percent of their mass after four hours. Pouches exposed to heat-stressed bottle water gained ten point five percent, while those in microwaved plastic water gained eight percent. Statistical analysis confirmed a significant reduction in water transport for exposed pouches. These findings indicate that chemicals leaching from heat-stressed plastics reduce the rate of passive osmosis across a synthetic membrane model.

NSRI-J-2026-0194 · Full text forthcoming