Publications by authors named "Maha M Abo Gazia"

Despite the advances in the development of therapeutic wearable wound-healing patches, lack self-healing properties and strong adhesion to diabetic skin, hindering their effectiveness. We propose a unique, wearable patch made from a 3D organo-hydrogel nanocomposite containing polydopamine, titanium dioxide nanoparticles, and silver quantum dots (PDA-TiO@Ag). The designed patch exhibits ultra-stretchable, exceptional-self-healing, self-adhesive, ensuring conformal contact with the skin even during movement.

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Background: Diabetic wound represents a serious issue with a substantial impact and an exceptionally complex pathology affecting patients' mental health and quality of life. So, we have developed a novel 3D organo-hydrogel nanocomposite of polydopamine/TiO2 nanoparticles and cu (PDA-TiO2@Cu) and examined its efficacy in diabetic wound healing.

Methods: Forty-five adult male albino rats were divided into normal control rats (non-diabetic rats with non-treated skin wounds), diabetic control rats (diabetic rats with non-treated skin wounds), and organo-hydrogel-treated rats (diabetic wounds treated with topically applied organo- hydrogel once daily).

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Article Synopsis
  • Vitamin B17, or amygdalin, found in plants like apricot kernels, is being studied for its potential in cancer therapy, particularly for liver protection against Ehrlich ascites carcinoma (EAC) in mice.
  • The study involved 100 female mice divided into groups to assess the effects of VB17 in pre-treatment and co-treatment scenarios, measuring various liver health indicators.
  • Results indicated that VB17 reduced liver damage indicators like DNA damage and certain liver enzymes, while improving liver tissue health, suggesting that VB17 could help protect the liver from EAC-induced toxicity.
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This study was conducted to evaluate the effect of chitosan nanoparticles (CNPs) isolated from Artemia salina against hepatocellular carcinoma (HCC) both in vitro (HepG2) and in vivo (diethylnitrosamine-induced HCC in rats) and to investigate the involved underlying mechanisms. Administration of CNPs decreased HCC progression as evidenced by (1) induced HepG2 cell death as detected by MTT assay; (2) induced necrosis as indicated by acridine orange/propidium iodide (AO/PI) red staining, annexin V/7-AAD positive staining (detected by flow cytometry), and upregulated expression of necrosis markers (PARP1 and its downstream target, RIP1 genes), but no effect on apoptosis as revealed by insignificant changes in caspase 3 activity and mRNA levels of Bax and AIF; (3) increased intracellular ROS and decreased mitochondrial membrane potential in HepG2; (4) decreased liver relative weight, serum levels of liver enzymes (ALT, AST, and ALP), total bilirubin, and cancer markers (AFP and GGT), number and area of GST-P positive tumor nodules; and (5) reduced oxidative stress (decrease in MDA levels) and increased activities of SOD, CAT, and GPx enzymes in rat liver. The preventive (pre-treatment) effect of CNPs was better than the therapeutic (post-treatment) effect.

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