Shoolini University

Lead halide perovskite solar cells (LHPSCs) have achieved outstanding power conversion efficiencies, yet their long-term operational stability remains the primary barrier to commercialisation. Device degradation arises from both intrinsic factors like ion migration, light-induced phase segregation, and crystallographic instabilities, and extrinsic stressors such as moisture, oxygen, thermal stress, ultraviolet radiation, and electrical bias. These mechanisms collectively accelerate perovskite decomposition, interfacial deterioration, and electrode corrosion, ultimately reducing device efficiency and operational lifespan. To systematically address these challenges, this review critically examines engineering strategies across multiple structural and functional levels. Bulk compositional modification and defect passivation improve intrinsic material stability and suppress ion migration. Surface and interface passivation enhances energy-level alignment while reducing non-radiative recombination losses. Charge transport layer optimisation ensures effective carrier extraction and improved thermal resilience, while electrode engineering mitigates metal diffusion and chemically induced deterioration. Finally, we outline future directions centred on stability-by-design principles, integrating advanced materials and interface engineering, robust encapsulation, operando characterisation, and artificial intelligence and machine learning-driven optimisation to overcome key degradation pathways and enable long-lasting, high-performance LHPSCs.

Climate change is accelerated by increasing levels of greenhouse gases (GHGs) as a result of human activity, particularly the release of carbon dioxide (CO2). Soil carbon (C) sequestration, or the transfer of atmospheric CO2 to soil organic matter (SOM) with long-term stabilization within the soil, is an important process of C removal from the atmosphere. For the accounting of soil C and offset markets in most countries including Australia, the standard soil sampling depth is 0–30 cm, although deeper sampling is recommended for more accurate C stock assessments and to capture long-term sequestration potential. While 30 cm soil depth accounts for most short-term management impacts on C storage, a significant portion of soil C is stored below this depth (i.e., deep soil C), and sampling at greater depths can provide a more complete account of total C stocks and potential sequestration benefits. This paper aims to provide a comprehensive review, including a bibliometric analysis and a critical discussion of the link between deep soil C storage and sequestration potential in relation to climate change mitigation and soil health. Deep soil layers contain over 850 Pg C worldwide, which is approximately 50

Lung cancer, a global concern with high mortality rates, has multiple causative factors, including exposure to air pollution. This risk extends to microplastics, now recognized as constituents of particulate matter, a well-known carcinogen for lung cancer. Numerous studies have consistently shown the prevalence of microplastics originating from various sources, accumulating in the lungs upon inhalation. However, their direct influence on lung carcinogenesis remains less explored, highlighting the urgent need for high-priority research. This comprehensive review aims to analyze the effects of microplastics on lung carcinogenesis, drawing insights from a wide range of research studies. It addresses the sources and transport of microplastics infiltrating humans from indoor environments, leading to inflammation, oxidative stress, DNA damage, genomic instability, and immune modulation—factors closely associated with lung cancer development. The review also emphasizes pertinent in vitro and in vivo studies on microplastic exposure and their potential implications for lung cancer. Furthermore, it delves into the least explored and complex interplay between microplastics and particulate matter in the context of lung cancer, based on global cohort studies and meta-analyses. This review provides critical insights into microplastic and particulate matter exposure, emphasizing the need for extensive, long-term investigations across diverse human populations and regions to inform public health policies. Such research endeavors are essential for developing effective intervention strategies to mitigate the risks associated with these environmental contaminants.

The pathological condition known as ischemia reperfusion injury (IRI) is characterized by an initial restriction in the amount of blood supply followed by reperfusion which paradoxically aggravates irreversible neuronal damage and cell death. In Central Nervous System, IRI disrupts cytoskeletal integrity, causes dysruption in intracellular calcium homeostasis, and worsens mitochondrial function. Accruing evidence identifies endoplasmic reticulum (ER) stress and dysregulation of the unfolded protein response (UPR) as key contributors to ischemia-induced neurodegeneration. While transient ER stress activates adaptive signaling that supports cell survival, sustained or severe ER stress shifts UPR signaling toward pro-apoptotic pathways involving CHOP induction, calcium overload, mitochondrial dysfunction, and caspase activation. This review critically examines recent advances linking ER stress to neuronal injury following cerebral ischemia and reperfusion, with a particular emphasis on ER-mitochondrial crosstalk and apoptotic signaling. Importantly, we summarize and evaluate emerging therapeutic strategies targeting ER stress pathways including chemical chaperones, UPR modulators, calcium homeostasis regulators, and metabolic interventions—and discuss their neuroprotective potential and translational limitations. By integrating mechanistic insights with therapeutic perspectives, this review highlights ER stress as a promising but complex target for neuroprotection after ischemic injury.

Aflatoxin contamination in stored grains due to its severe health effects, economic losses, and persistence under post-harvest conditions remains a critical global food safety challenge. Aflatoxin B1 (AFB1), classified as a Group 1 carcinogen, poses significant mutagenic, hepatotoxic, and immunosuppressive risks. Conventional detection techniques including HPLC, LC-MS, and ELISA offer high sensitivity but are limited by complex instrumentation, lack of field applicability and high cost. Recent advancements in nanotechnology for rapid detection and effective mitigation of aflatoxins provide transformative solutions. The present review comprehensively discusses nanoparticle-based biosensors including metallic nanoparticles, carbon and graphene quantum dots, up-conversion nanoparticles, and surface-enhanced Raman spectroscopy (SERS) techniques for ultra-sensitive and onsite detection of AFB1. Detection limits ranging from pg/mL to ng/mL levels demonstrate the excellent analytical performance of nanotechnology-driven systems. Furthermore, nanocomposites, nano-encapsulated antifungal agents, green-synthesized nanoparticles, and nanoparticle-mediated RNA interference approaches for their role in suppressing fungal growth and inhibiting aflatoxin biosynthesis are emphasized. Mechanistic insights reveal that nanoparticles induce reactive oxygen species generation, gene downregulation in aflatoxin biosynthetic pathways, and structural toxin degradation. Additionally, nanocomposite-based grain storage materials improve barrier properties, reducing moisture and fungal proliferation. Despite promising advancements, concerns regarding nanoparticle toxicity, environmental accumulation, regulatory compliance, and large-scale implementation remain critical challenges. Overall, nanotechnology offers a multifunctional, sensitive, and sustainable strategy for strengthening aflatoxin detection, detoxification, and post-harvest management systems, thereby enhancing global grain safety and food security.