Chromium (Cr) is a toxic heavy metal present in industrial effluent which could cause degenerative diseases on ingestion. Therefore, elimination of Cr from contaminated water becomes essential to preserve and sustain the quality of life. In this study, superparamagnetic iron oxide nanoparticles (SPIONs) were impregnated on activated carbon and checked for enhanced removal of Cr(VI). Thus, granular activated carbon (N-GAC) of mesh size was impregnated with SPIONs to produce SPIONs impregnated activated carbon (Sp-GAC) and characterized using UV-VIS spectrophotometer, FT-IR, SEM-EDX, XRD, and VSM. Sp-GAC was found to be possessing superparamagnetic behavior, and it was used in batch adsorption study where the adsorption parameters like pH, concentration of adsorbent, and adsorbent-adsorbate were optimized. It was found that Cr(VI) adsorption was predominant at acidic pH (pH 3) for both cases; moreover, N-GAC showed better adsorption comparatively. Both the N-GAC and Sp-GAC adsorption were found to be obeying to Langmuir.

Cancer is an impending bottleneck in the advanced scientific workflow to achieve diagnostic, prognostic, and therapeutic success. Most cancers are refractory to conventional diagnostic and chemotherapeutics due to their limited targetability, specificity, solubility, and side effects. The inherent ability of each cancer to evolve through various genetic and epigenetic transformations and metabolic reprogramming underlies therapeutic limitations. Though tumor microenvironments (TMEs) are quite well understood in some cancers, each microenvironment differs from the other in internal perturbations and metabolic skew thereby impeding the development of appropriate diagnostics, drugs, vaccines, and therapies. Cancer associated bioenergetics modulations regulate TME, angiogenesis, immune evasion, generation of resistant niches and tumor progression, and a thorough understanding is crucial to the development of metabolic therapies. However, this remains a missing element in cancer theranostics, necessitating the development of modalities that can be adapted for targetability, diagnostics and therapeutics. In this challenging scenario, nanomaterials are modular platforms for understanding TME and achieving successful theranostics. Several nanoscale particles have been successfully researched in animal models, quite a few have reached clinical trials, and some have achieved clinical success. Nanoparticles exhibit an intrinsic capability to interact with diverse biomolecules and modulate their functions. Furthermore, nanoparticles can be functionalized with receptors, modulators, and drugs to facilitate specific targeting with reduced toxicity. This review discusses the current understanding of different theranostic nanosystems, their synthesis, functionalization, and targetability for therapeutic modulation of bioenergetics, and metabolic reprogramming of the cancer microenvironment. We highlight the potential of nanosystems for enhanced chemotherapeutic success emphasizing the questions that remain unanswered.

MicroRNAs (miRNAs) are involved in the modulation of pathogenic genes by binding to their mRNA sequences’ 3′ untranslated regions (3′UTR). Interleukin-6 (IL-6) is known to promote cancer progression and treatment resistance. In this study, we aimed to explore the therapeutic effects of gold nanoparticles (GNP) against IL-6 overexpression and the modulation of miRNA-26a-5p in breast cancer (BC) cells. GNP were synthesized using the trisodium citrate method and characterized through UV-Vis spectroscopy, dynamic light scattering (DLS), and transmission electron microscopy (TEM). To predict the binding of miR-26a-5p in the IL-6 mRNA’s 3′UTR, we utilized bioinformatics algorithms. Luciferase reporter clone assays and anti-miRNA-26a-5p transfection were employed to validate the binding of miR26a-5p in the IL-6 mRNA’s 3′UTR. The activity of RelA and NF-κBp50 was assessed and confirmed using Bay 11-7082. The synthesized GNP were spherical with a mean size of 28.3 nm, exhibiting high stability, and were suitable for BC cell treatment. We found that miR-26a-5p directly regulated IL-6 overexpression in MCF-7 cells activated with PMA. Treatment of MCF-7 cells with GNP resulted in the inhibition of IL-6 overexpression and secretion through the increase of miR26a-5p. Furthermore, GNP deactivated NF-κBp65/NF-κBp50 transcription activity. The newly engineered GNP demonstrated safety and showed promise as a therapeutic approach for reducing IL-6 overexpression. The GNP suppressed IL-6 overexpression and secretion by deactivating NF-κBp65/NF-κBp50 transcription activity and upregulating miR-26a-5p expression in activated BC cells. These findings suggest that GNP have potential as a therapeutic intervention for BC by targeting IL-6 expression and associated pathways.

This study is aimed at evaluating the association between Coronavirus disease 19 (COVID‐19) and the primary complete blood count (CBC) parameters in confirmed positive patients. In a retrospective cross‐sectional study, 384 files of patients with confirmed COVID‐19 diagnosis hospitalized at King Saud Medical City, Riyadh, were chosen randomly as a study group for hematological parameters, with another 384 non‐COVID‐19 files of patients without history of any disease which could influence the hematological profile were selected as a control group. The gender, age, and nationality of the control group were matched with those of the study group. Anemia and thrombocytopenia prevalence was significantly higher in COVID‐19 positive patients compared with negative. However, the positive cases were 3.4 times more likely to be anemic and approximately 5.3 times as likely to be thrombocytopenic, while the prevalence of leukopenia showed no statistical significance between the two groups. However, the Mean Cell Volume (MCV), Total White Blood Cell (WBC) count, lymphocyte count, and basophil count median values showed a nonsignificant difference between the two groups. Anemia and thrombocytopenia may be highly developed in severe positive cases, and therefore, further studies are recommended to validate these findings.

An aqueous extract of Syzygium cumini seeds was utilized to green synthesize titanium dioxide nanoparticles (TiO₂ NPs). UV-Visible, DLS, FTIR, XRD, FESEM, TEM, SAED, EDAX, and photoluminescence spectroscopy techniques were employed to characterize the prepared TiO₂ nanoparticles. The rutile crystal structure of TiO₂ NPs was revealed by XRD study. The TEM and FESEM images of the TiO₂ NPs revealed an average particle size of 50–100 nm. We employed EDAX to investigate the elemental compositions of TiO₂ NPs. The O-Ti-O stretching bands appeared in the FTIR spectrum of TiO₂ NPs at wavenumbers of 495 cm⁻¹. The absorption edge peaks of TiO₂ NPs were found in the UV-vis spectra at 397 nm. The MTT study revealed that TiO₂ NPs effectively inhibited the growth of liver cancer Hep3 and Hep-G2 cells. The results of the corresponding fluorescent staining assays showed that TiO₂ NPs significantly increased ROS generation, decreased MMP, and induced apoptosis in both liver cancer Hep3 and Hep-G2 cells. TiO₂ nanoparticles lessened SOD, CAT, and GSH levels while augmenting MDA contents in Hep3 and Hep-G2 cells. In both Hep3 and Hep-G2 cells treated with TiO₂ NPs, the Bax, CytC, p53, caspase-3, -8, and -9 expressions were remarkably augmented, while Bcl-2 expression was reduced. Overall, these findings revealed that formulated TiO₂ NPs treatment considerably inhibited growth and triggered apoptosis in Hep3 and HepG2 cells.

Objective: Triple-negative breast cancer (TNBC) is a very aggressive form of cancer that grows and spreads very fast and generally relapses. Therapeutic options of TNBC are limited and still need to be explored completely. Gold nanoparticles conjugated with citrate (citrate-AuNPs) are reported to have anticancer potential; however, their role in regulating microRNAs (miRNAs) in TNBC has never been investigated. This study investigated the potential of citrate-AuNPs against tumorigenic inflammation via modulation of miRNAs in TNBC cells.Methods: Gold nanoparticles were chemically synthesized using the trisodium-citrate method and were characterized by UV-Vis spectrophotometry and dynamic light scattering studies. Targetscan bioinformatics was used to analyze miRNA target genes. Levels of miRNA and mRNA were quantified using TaqMan assays. The pairing of miRNA in 3'untranslated region (3'UTR) of mRNA was validated by luciferase reporter clone, containing the entire 3'UTR of mRNA, and findings were further re-validated via transfection with miRNA inhibitors.Results: Newly synthesized citrate-AuNPs were highly stable, with a mean size was 28.3 nm. The data determined that hsa-miR155-5p is a direct regulator of SOCS1 (suppressor-of-cytokine-signaling) expression and citrate-AuNPs inhibits SOCS1 mRNA/protein expression via modulating hsa-miR155-5p expression. Transfection of TNBC MDA-MB-231 cells with anti-miR155-5p markedly increased SOCS1 expression (p<0.001), while citrate-AuNPs treatment significantly inhibited anti-miR155-5p transfection-induced SOCS1 expression (p<0.05). These findings were validated by IFN-γ-stimulated MDA-MB-231 cells. Moreover, the data also determined that citrate-AuNPs also inhibit IFN-γ-induced NF-κB p65/p50 activation in MDA-MB-231 cells transfected with anti-hsa-miR155-5p.Conclusion: Newly generated citrate-AuNPs were stable and non-toxic to TNBC cells. Citrate-AuNPs inhibit IFN-γ-induced SOCS1 mRNA/protein expression and deactivate NF-κB p65/50 activity via negative regulation of hsa-miR155-5p. These novel pharmacological actions of citrate-AuNPs on IFN-γ-stimulated TNBC cells provide insights that AuNPs inhibit IFN-γ induced inflammation in TNBC cells by modulating the expression of microRNAs.