Herbal medicines are widely used worldwide and much appreciated because of their fewer side effects and the ability to fight diseases at the root cause. Active ‘phyto’ ingredients require a scientific approach and a mechanism to distribute components at the target site for better therapeutic results. Nanotechnology, on the other hand, has created new hope for cancer treatment but is still far from being proven in clinical settings. This article combines a unique approach to synthesis with the use of Pleurotus sajor-caju, followed by microwave irritation of silver and gold nanoparticles that ensures the capping of the active phyto ingredient and further enhances the effects of nanomedicine to fight colon cancer, thus opening a new era of what we call herbonanoceutics. The article also compares the characteristics and properties of silver (Au) and gold (Ag) nanoparticles synthesized by an in house developed novel microwave-assisted rapid green synthesis method. The as-prepared Ag NPs and Au NPs were compared using ultraviolet-visible spectroscopy (UV-Vis), Fourier transform infrared (FTIR) spectroscopy, X-ray diffraction (XRD), transmission electron microscopy (TEM), and energy dispersive spectroscopy (EDS). Our comparative study revealed that both assemblies display face-centred cubic structures (FCCs) and are nanocrystalline in nature. The advantage of the approach was that the sizes of gold and silver were identical in range with a similar distribution pattern. This has helped us to study the activity against colon cancer cell line (HCT-116) without incoherence since size plays a key role in the application. More specifically, morphological changes, cell viability, the production of reactive oxygen species (ROS) and the fragmentation of DNA have been further reported to assess better the results obtained with the two metals. Our results suggest that the newly adopted synthesis method may ensure the dual benefits from phyto ingredients which further enhances the effectiveness of advanced nanomedicine.

Neutrophils, a first-line defender, has a multifaceted presence in chronic inflammation, autoimmune pathology, and tumor progression. The microenvironmental cues facilitate functional plasticity and phenotypic heterogeneity to neutrophils that enable both their protective and pathogenic roles. Autoimmune diseases including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and juvenile idiopathic arthritis (JIA) display the presence of dysregulated subsets of neutrophil, such as low-density granulocytes (LDGs) that promote proinflammation and contribute to tissue damage via NETosis and type I interferon-mediated signaling. In cancer, particularly tumors, they exhibit tumor-associated neutrophils (TANs) which may polarize either towards anti-tumorigenic ‘N1’ or pro-tumorigenic ‘N2’ phenotypes based on available modulators such as TGF-β and leucine-driven epigenetic modifications. The development in neutrophil biology has introduced several novel therapeutic strategies that allow NET targeting, inhibition of chemokine receptors like CXCR2, and exploration of neutrophil-derived biomarkers for diagnosis and disease monitoring. Such findings encourage the importance of neutrophils as both effectors and therapeutic targets in inflammatory and neoplastic conditions.

Mitochondrial Ca ²⁺ levels are regulated to balance stimulating respiration against the harm of Ca ²⁺ overload. Contributing to this balance, the main channel transporting Ca ²⁺ into the matrix, the mitochondrial Ca ²⁺ uniporter, can incorporate a dominant-negative subunit (MCUB). MCUB is homologous to the pore-forming subunit MCU, but when present in the pore-lining tetramer, inhibits Ca ²⁺ transport. Here, using cell lines deleted of both MCU and MCUB, we identify three factors that contribute to MCUB-dependent inhibition. First, MCUB protein requires MCU to express. The effect is mediated via the N-terminal domain (NTD) of MCUB. Replacement of the MCUB NTD with the MCU NTD recovers autonomous expression but fails to rescue Ca ²⁺ uptake. Surprisingly, mutations to MCUB that affect interactions with accessory subunits or the conduction pore all failed to rescue Ca ²⁺ uptake, suggesting the mechanism of inhibition may involve global rearrangements. Second, using concatemeric tetramers with varying MCU:MCUB ratios, we find that MCUB incorporation does not abolish conduction, but rather inhibits Ca ²⁺ influx proportional to the amount of MCUB present in the channel. Reducing rather than abolishing Ca ²⁺ transport is consistent with MCUB retaining the highly-conserved selectivity filter DIME sequence. Finally, we apply live-cell Förster resonance energy transfer to establish that the endogenous stoichiometry is 2:2 MCU:MCUB. Taken together, our results suggest MCUB preferentially incorporates into nascent uniporters, and the amount of MCUB protein present linearly correlates with the degree of inhibition of Ca ²⁺ transport, creating a precise, tunable mechanism for cells to regulate mitochondrial Ca ²⁺ uptake.