In this study, a polar extract of Aconitum lycoctonum L. was used for the synthesis of silver nanoparticles (AgNPs), followed by their characterization using different techniques and evaluation of their potential as antioxidants, amylase inhibitors, anti-inflammatory and antibacterial agents. The formation of AgNPs was detected by a color change, from transparent to dark brown, within 15 min and a surface resonance peak at 460 nm in the UV–visible spectrum. The FTIR spectra confirmed the involvement of various biomolecules in the synthesis of AgNPs. The average diameter of these spherical AgNPs was 67 nm, as shown by the scanning electron micrograph. The inhibition zones showed that the synthesized nanoparticles inhibited the growth of Gram-positive and negative bacteria. FRAP and DPPH assays were used to demonstrate the antioxidant potential of AgNPs. The highest value of FRAP (50.47% AAE/mL) was detected at a concentration of 90 ppm and a DPPH scavenging activity of 69.63% GAE was detected at a concentration of 20 µg/mL of the synthesized AgNPs. 500 µg/mL of the synthesized AgNPs were quite efficient in causing 91.78% denaturation of ovalbumin. The AgNPs mediated by A. lycoctonum also showed an inhibitory effect on α-amylase. Therefore, AgNPs synthesized from A. lycoctonum may serve as potential candidates for antibacterial, antioxidant, anti-inflammatory, and antidiabetic agents.

We report a Saudi girl who presented at birth with neonatal diabetes, duodenal atresia, and progressive cholestasis. After other gene testing was negative, the clinical diagnosis of Mitchell-Riley syndrome was ultimately considered and further genetic analysis revealed a novel missense homozygous variant in RFX6: c.983A>T (p.asp328Val). Despite intensive management, the patient died from severe Klebsiella pneumoniae sepsis at 5 months of age. This rare syndrome should be suspected in any neonate with hyperglycemia complicated by intestinal atresia and/or progressive cholestasis that could suggest biliary hypoplasia. Early recognition and diagnosis through genetic testing are essential for guiding aggressive clinical management as well as family counseling, particularly in light of the high possibility of early death in this highly complex disorder.

Despite being one of the most consumed analgesics worldwide, liver injury is an adverse effect of diclofenac (DF). In pursuit of reliable hepatoprotective natural remedies, this study aimed to investigate the potential protective effect of ferulic acid (FA) and its mechanism against DF‐induced liver injury. Various network databases and datasets were used to collect targets corresponding to FA and DF‐induced liver injury. Enrichment analyses of common targets were performed, a protein‐protein interaction (PPI) network was constructed, the hub genes were identified, and the upstream miRNA interacting with the top hub gene was later predicted. A DF‐induced liver injury rat model was established to verify FA’s protective effects, and the selected hub gene expression level with its upstream regulatory miRNA and a downstream set of targets was examined to elucidate the underlying mechanism. A total of 18 genes were identified as potential targets of FA to protect against DF‐induced liver injury. Data from the enrichment and PPI analyses and the prediction of the upstream miRNAs indicated that the most worthwhile pair to study was miR‐296‐5p/Jun. In vivo findings showed that coadministration of FA significantly reduced the DF‐induced alterations in the liver function indices, oxidative stress, and liver histology. Mechanistically, FA downregulated the expression of Jun, Bim, Bax, Casp3, IL‐1β, IL‐6, and TNF‐α, whereas it upregulated the expression of rno‐miR‐296‐5p and Bcl2. In conclusion, combining network pharmacology and an in vivo study revealed that miR‐296‐5p/Jun axis could mediate the mitigative effect of FA against DF‐induced liver injury.

We report a case of a 36-month-old Saudi girl who presented with recurrent episodes of unexplained hypoelectrolytaemia. Her cystic fibrosis CFTR (Cystic Fibrosis Transmembrane conductance Regulator) full gene sequence confirmed that she was homozygous for D579G mutation.