Chonnam medical journal最新文献

The protective effects of vitamins E and D, stemming from their antioxidant and anti-inflammatory capabilities were investigated in the context of tamoxifen-induced liver toxicity. The study involved twenty-five female rats divided into five experimental groups: group C (olive oil: 500 µL), group T (tamoxifen: 40 mg/kg), groups TE (tamoxifen: 40 mg/kg and vitamin E: 100 IU/kg), group TD (tamoxifen: 40 mg/kg and vitamin D: 500 IU/kg) and group TED (tamoxifen: 40 mg/kg, vitamin E: 100 IU/kg and vitamin D: 500 IU/kg). Calorimetric methods were used to measure biochemical variables, hepatic level of Total antioxidant capacity (TAC), Total oxidant status (TOS), Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPx). Hepatic level of tumor necrosis factor-α (TNF-α) was assayed by ELISA. Hematoxylin-eosin staining method was also employed to assess Tamoxifen-induced liver lesions. Tamoxifen treatment resulted in a significant increase in ALP (p-value<0.01), TOS, and OSI (p-value<0.01), a marked decrease in TAC level (p-value<0.01), and an increase in TNF-α level. Simultaneous treatment with combined supplementation of vitamins E and D effectively stopped the decrease of TAC and the increase of TOS, OSI, and MDA. Although treatment with tamoxifen led to a decrease SOD, CAT, and GPX compared with group C, the difference wasn't significant. Treatment with vitamins considerably caused to increase SOD and CAT activity in comparison with groups C and T. The current study's findings demonstrated that the combined supplementation of vitamins E, and D effectively alleviated Tamoxifen-associated liver damage and oxidative stress.

Breast cancer is one of the most common causes of death all over the world. Therapeutic options applied to the patients include surgery, chemotherapy, and radiotherapy. However, far advanced disease often leads to chemoresistance and toxicity. Innovative therapies are needed to address these challenges. Melatonin has the potential to prevent and treat cancer, as it has been revealed in numerous clinical studies. Melatonin is a nontoxic agent that is mostly produced in the pineal gland, inducing various mechanisms of action such as the induction of apoptosis, antiangiogenic, antiproliferative, and metastasis-inhibitory effects. Therefore, melatonin increases therapeutic sensitivity when combined with conventional medication in breast cancer. Melatonin (3-20 mg/day) may reduce breast cancer cell growth in preclinical studies and enhance chemotherapy efficacy. Small human trials suggest potential benefits, but larger studies are needed. Higher doses (≥20 mg/day) are sometimes used alongside chemotherapy. This manuscript reviews research that has demonstrated the antitumor properties of melatonin, thereby focusing on its actions on angiogenesis, apoptosis, metastasis, and antiproliferative properties. We also discuss recent advances in the understanding of the actions of melatonin on epigenetic mechanisms (especially DNA methylation) and telomere length. The data in this review were obtained from journal articles up to May 2024. Regarding the study, Google Scholar and ScienceDirect were used as engines to search for open access. We searched the ISI, Pubmed and Scopus as valid external databases, and as internal databases, ISC and Iran medex. By finding mean keywords such as 'breast cancer', 'estrogen', 'melatonin', 'cell death', 'cell proliferation', 'telomerase' and 'DNA methylation', we reached to the formula with maximum collectivity in searching, then equivalent terms were found by Mesh database. The review also covers recent clinical investigations of melatonin in breast cancer.

This study aimed to investigate changes in candidemia incidence, species distribution, antifungal susceptibility, initial antifungal use, and mortality trends in Korea before and during the COVID-19 pandemic. A retrospective analysis was conducted on candidemia cases from two tertiary care hospitals in Korea between 2017 and 2022. Data were compared between the pre-pandemic (2017-2019) and pandemic (2020-2022) periods. Statistical methods included incidence rate ratios (IRRs) and multivariate Cox regression to assess 30-day mortality risk factors. A total of 470 candidemia cases were identified, with 48.7% occurring pre-pandemic and 51.3% during the pandemic. While the overall incidence of candidemia remained similar across the two periods (IRR 1.15; p=0.13), the incidence in intensive care units (ICUs) significantly increased during the pandemic (IRR 1.50; p<0.01). The distribution of Candida species did not differ significantly between the two periods. Fluconazole non-susceptibility in C. albicans markedly decreased (10.0% vs. 0.9%, p<0.01), whereas C. glabrata exhibited a significant rise in caspofungin non-susceptibility during the pandemic (0% vs. 22.4%, p<0.01). Echinocandin use increased (21.8% vs. 34.4%; p<0.01), while fluconazole use declined (48.0% vs. 32.8%; p<0.01). Although the 30-day mortality rate was higher during the pandemic (60.2% vs. 57.2%), the difference was not statistically significant (p=0.57). The findings highlight the need for region-specific surveillance and tailored management strategies to improve candidemia outcomes, especially during healthcare disruptions like the COVID-19 pandemic.

Mild cognitive impairment (MCI) is a condition characterized by noticeable deficits in memory retrieval or other cognitive domains than the individuals with the same age but do not significantly interfere with daily functioning. It represents an intermediate stage between normal aging and dementia, and a crucial opportunity for intervention prior to extensive cognitive decline. Transcranial direct current stimulation (tDCS), a non-invasive neuromodulation technique, has shown promise in enhancing global cognition in MCI. Current evidence suggests that tDCS provides short-term cognitive benefits, particularly in memory and attention, with moderate effects observed in processing speed. However, its impact on executive function and language remains inconsistent, highlighting variability in individual responses and study methodologies. While long-term efficacy remains uncertain due to limited longitudinal research and short follow-up periods, safety concerns, especially with self-administered tDCS such as in home-based tDCS, underscore the need for proper training and device innovation. Despite this, tDCS is a promising, portable tool for cognitive enhancement in MCI, with potential to delay progression to dementia. Addressing challenges such as optimizing stimulation protocols, accounting for individual neuroanatomical variability, and establishing long-term effectiveness will be essential for its broader clinical adoption. Future research should focus on standardizing methodologies, incorporating biomarkers to predict treatment response, and conducting large-scale, longitudinal studies to refine its therapeutic application.

Redox imbalances, which result from excessive production of reactive oxygen species (ROS) or malfunctioning of the antioxidant system, are the source of oxidative stress. ROS affects all structural and functional components of cells, either directly or indirectly. In addition to causing genetic abnormalities, excessive ROS also oxidatively modifies proteins by protein oxidation and peroxidation and alters lipid structure via advanced lipoxidation, decreasing function and promoting damage or cell death. On the other hand, low levels of ROS constitute important redox-signaling molecules in various pathways that maintain cellular homeostasis and regulate key transcription factors. As a result, ROS can affect various cellular processes, such as apoptosis, migration, differentiation, and proliferation. ROS can act as signaling molecules, controlling various normal physiological activities at the cellular level. Furthermore, there is an increasing body of evidence indicating the role of ROS in various clinical conditions. In this review, we will summarize the role of ROS in physiological and pathological processes and antioxidant action during oxidative stress.