Iliya Mangarov

Premature infants are an especially vulnerable group that often needs extended intensive care. Prematurity naturally hampers the development of the immune system, significantly increasing the risk of infections. In the Neonatal Intensive Care Unit (NICU), antibiotic treatment is often a crucial, life-saving measure. For parents, the birth of a very preterm infant (before 32 weeks of gestation) turns what should be a happy event into a period filled with deep uncertainty and distress. Maintaining hope amid these difficulties relies heavily on maintaining regular communication with and trusting the medical team. Clinical realities in the NICU include a high risk of infection that requires multiple medications, including antibiotics. There is an inverse relationship between gestational age and pharmaceutical exposure. Parents worry about the amount of medication their child receives and the potential long-term effects on development. Over the past thirty years, initiatives such as antimicrobial stewardship programs have worked to reduce antibiotic use and treatment duration in the NICU, emphasizing proper care for premature infants worldwide. This article examines the ethical landscape from the perspectives of three primary stakeholders: parents, healthcare providers, and regulatory bodies. The key ethical question is whether these groups achieve meaningful cooperation or if institutional and professional priorities overshadow clinical practice. In the NICU, decision-making responsibility mainly lies with the medical team, as parents often have limited influence over treatment decisions, and regulatory oversight usually occurs indirectly. This concentration of authority underscores the complex and critical nature of neonatal intensive care.

Alpha-lipoic acid (ALA, also known as thioctic acid) was discovered nearly 90 years ago and began to be used in clinical practice in the late 1950s. Numerous nonclinical and clinical studies have investigated ALA for treating diabetic peripheral neuropathy (DPN) and various other diseases. The rising global prevalence of DPN necessitates timely treatment; however, there is currently no effective cure. Current guideline-recommended therapies for DPN provide symptom relief rather than modifying the disease. Among the pathogenesis-oriented therapies, ALA holds a unique position as a universal antioxidant, essential for every cell in the body. This review highlights the ongoing issues and challenges in using ALA to treat DPN. While confronting a complex disease with poorly understood pathophysiology, we also have an endogenous substance with pleiotropic effects on all cells in the human body. It becomes clear that this is a highly multifactorial process that will likely never be precisely defined. This does not diminish the significance of ALA in treating DPN but underscores the need for a deeper understanding of when to start therapy, dosage, duration, and monitoring. In this comprehensive review, we evaluate the achievements of the past 70 years and highlight gaps in ALA’s role in treating DPN.

The present study investigated the chemical content, analgesic, and anti-inflammatory properties of Filipendula ulmaria (L.) Maxim. (meadowsweet) aerial part extract. F. ulmaria is native to Bulgaria. Based on its phytochemicals, meadowsweet has a vast range of pharmacological activities, like antipyretic, analgesic, anti-inflammatory, antirheumatic, immunostimulating, anti-microbial, anti-allergic, and gastroprotective activity. In our experiment, F. ulmaria aerial part extract was practically non-toxic (oral LD50 > 2000 mg/kg). The performed experiments revealed that diclofenac possesses better anti-inflammatory and antinociceptive activity than F. ulmaria extracts (100 and 200 mg/kg). The results revealed a dose-dependent moderate inhibition of the inflammation and pain induced by 3 days of oral pretreatment with methanolic extract of F. ulmaria extracts. No additive effect of FUA extracts on the effects of diclofenac was noted. F. ulmaria extracts did not induce any alterations in blood biochemical analysis.

Targeting the inflammation-related molecules with nonsteroidal anti-inflammatory drugs (NSAIDs) represents a promising approach for cancer prevention/therapy. We evaluated the in vitro anticancer effects of meloxicam, lornoxicam, ketoprofen, and dexketoprofen on the proliferation, migration, and apoptosis of human cervical, colorectal, and mammary carcinoma cells. The antiproliferative activity and cytotoxicity of tested NSAIDs on HeLa, HT-29, and MCF-7 cell lines were assessed by the MTT test. The apoptosis-inducing potential was analyzed by fluorescent staining with acridine orange/ethidium bromide and DAPI. Migration activity was assessed by a wound-healing scratch assay. The tested NSAIDs reduced the viability of the used tumor cell lines. The cytomorphological analysis revealed reduced cell density and mitotic activity and the presence of cells with morphological features of early and late apoptosis. Significant inhibition of the migration capacity was established as well. In conclusion, NSAIDs could be candidates for the development of new pharmacological strategies for the treatment and prevention of cancer.

In this pilot study, we set a goal of developing collagen-induced arthritis (CIA) in normal mice of both sexes, and compared the susceptibility, prevalence and the degree of inflammation. To assess the grade of inflammation, CIA was evaluated by a visual scale, plethysmometer score and locomotor activity. Seventeen male mice (85%) and only two female mice (10%) developed symptoms of arthritis. None of the female mice that developed arthritis were rated ‘4’ on the visual scale, while 5 male mice (29.42%) were rated with ‘4’. Only animals with a degree of inflammation of ‘4’ and ‘3’ had a significant initial decrease in spontaneous locomotor activity compared to the unaffected animals. The results from this study showed that the susceptibility to development of arthritis was significantly higher in male mice compared to females.