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Manipulated Slow Release of Florfenicol Hydrogels for Effective Treatment of Anti-Intestinal Bacterial Infections.
Int J Nanomedicine
January 2025
Department of Clinical Pathology, Faculty of Veterinary Medicine, Benha University, Moshtohor, Toukh, 13736, Egypt.
Objective: The difficulty of establishing slow release at intestinal infection sites, weak antibacterial effects, as well as the limited broad use of florfenicol oral formulations are the main targets of the current study. Novel hydrogels derived from sodium alginate were developed using a complexation form for florfenicol delivery to achieve slow release at the site of intestinal infection and enhance its antibacterial activity against .
Methods: The optimal formulation, physicochemical properties, stability, pH-responsive performance, antibacterial activity, and in vitro biosafety of the florfenicol hydrogels have been studied systematically.
Oral iron sulfide prevents acute alcohol intoxication by initiating the endogenous multienzymatic antioxidant defense system.
Sci Adv
January 2025
State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin 300353, People's Republic of China.
Acute alcohol intoxication could cause multiorgan damage, including nervous, digestive, and cardiovascular systems, and in particular, irreversible damage to the brain and liver. Emerging studies have revealed that the endogenous multienzymatic antioxidant defense system (MEAODS) plays a central role in preventing oxidative stress and other toxicological compounds produced by alcohol. However, few available drugs could quickly regulate MEAODS.
View Article and Find Full Text PDFThe MIR181A2HG/miR-5680/VCAN-CD44 Axis Regulates Gastric Cancer Lymph Node Metastasis by Promoting M2 Macrophage Polarization.
Cancer Med
January 2025
Department of Gastrointestinal Surgery, Affiliated Hospital and Medical School of Nantong University, Nantong, China.
Background: Lymphatic metastasis in gastric cancer (GC) profoundly influences its prognosis, but the precise mechanism remains elusive. In this study, we identified the long noncoding RNA MIR181A2HG as being upregulated in GC and associated with LNs metastasis and prognosis.
Methods: The expression of MIR181A2HG in GC was identified through bioinformatics screening analysis and qRT-PCR validation.
Therapeutic regimens against infection without proton pump inhibitors in patients with corpus atrophic gastritis: a real-life single-centre longitudinal observational study.
Therap Adv Gastroenterol
January 2025
Digestive Disease Unit, Department of Medical-Surgical Sciences and Translational Medicine, Sant'Andrea Teaching Hospital, Sapienza University of Rome, via di Grottarossa 1035, Rome 00189, Italy.
Background: Efficacy of eradication regimens in (Hp) infection is commonly reported with proton pump inhibitors (PPIs). In patients with corpus atrophic gastritis, characterized by impaired acid secretion, PPI treatment is questionable.
Objectives: The current study aimed to assess in clinical practice the tolerability and eradication rate of modified eradication regimens without PPI as first-line treatment in patients with histologically Hp-positive corpus atrophic gastritis.
Long-term blood glucose control via glucose-activated transcriptional regulation of insulin analogue in type 1 diabetes mice.
Diabetes Obes Metab
January 2025
National Engineering Research Center for Biomaterials, College of Biomedical Engineering, Sichuan University, Chengdu, Sichuan, People's Republic of China.
Aim: To achieve glucose-activated transcriptional regulation of insulin analogue in skeletal muscle of T1D mice, thereby controlling blood glucose levels and preventing or mitigating diabetes-related complications.
Materials And Methods: We developed the GANIT (Glucose-Activated NFAT-regulated INSA-F Transcription) system, an innovative platform building upon the previously established intramuscular plasmid DNA (pDNA) delivery and expression system. In the GANIT system, skeletal muscle cells are genetically engineered to endogenously produce the insulin analogue INSA-F (Insulin Aspart with Furin cleavage sites).
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