Journal of Yeungnam medical science最新文献

Ungual scabies is a rare manifestation of Sarcoptes scabiei infestation in nail units and may mimic other nail diseases, resulting in diagnostic delay. Herein, we report the case of a 58-year-old woman with metastatic breast cancer who received abemaciclib and presented with recalcitrant paronychia and verruca-like periungual hyperkeratosis, sparing the finger web area without pruritus. Skin biopsy confirmed multiple mites in the stratum corneum, resulting in the diagnosis of crusted scabies with nail involvement. Topical permethrin 5% cream and oral ivermectin were then administered. The prolonged unrecognized disease in our patient led to repeated visits to long-term care facilities and tertiary hospitals, thereby increasing the risk of nosocomial transmission. This case emphasizes that clinicians, including non-dermatologists, should consider scabies in patients with chronic periungual lesions, particularly in patients who are immunocompromised such as those using abemaciclib, to prevent hospital outbreaks and excessive healthcare costs.

Pulmonary rehabilitation (PR) is a highly effective evidence-based treatment with multidisciplinary and comprehensive individualized interventions that reduce morbidity by improving functional capacity and managing respiratory symptoms. It can contribute to overall wellness, reduce symptoms related to respiratory conditions, and facilitate routine work and social activities. Hence, it is a vital component of integrated care for patients with chronic respiratory diseases. In India, PR faces several challenges arising from patients, society, and hospitals. Recent evidence suggests that PR has significant benefits in chronic respiratory diseases, including reduced morbidity and mortality, improved quality of life, and cost savings. Nevertheless, it has been significantly underutilized and has not received the necessary attention in India. The lack of proper utilization of PR can be attributed to several factors, including a lack of awareness and understanding among healthcare professionals regarding its advantages, insufficient referrals to PR programs, scarcity of specialized professionals trained in PR, and a general lack of awareness among patients about its benefits. This article aims to outline the obstacles to PR, identify the factors that influence its successful implementation, and propose possible solutions to overcome these barriers.

Background: Subarachnoid hemorrhage (SAH) is a devastating neurological condition with high morbidity and mortality rates. Although nimodipine is widely used in the management of SAH, the potential benefits of magnesium as adjunct therapy remain unclear. This meta-analysis aimed to evaluate the efficacy and safety of combining magnesium with nimodipine for the management of SAH.

Methods: A comprehensive literature search was conducted using PubMed, ScienceDirect, Google Scholar, and the Cochrane Library. Randomized controlled trials and prospective cohort studies comparing magnesium plus nimodipine versus nimodipine alone in patients with SAH were included. Key outcomes included cerebral vasospasm (CV), delayed cerebral ischemia (DCI), functional outcomes, mortality, and adverse events.

Results: Twelve studies involving 2,338 patients were included. The combination of magnesium and nimodipine significantly reduced the incidence of CV (odds ratio [OR], 0.53; 95% confidence interval [CI], 0.29-0.95; p=0.03) and DCI (OR, 0.52; 95% CI, 0.31-0.87; p=0.01) compared to nimodipine alone. However, no significant differences were found in functional outcomes (modified Rankin Scale: OR, 0.97; p=0.75; Glasgow Outcome Scale: OR, 0.81; p=0.24), mortality (OR, 0.97; p=0.83), or secondary cerebral infarction (OR, 0.38; p=0.12). The incidence of adverse events was higher in the combination group; however, this difference was not statistically significant (OR, 3.14; p=0.33).

Conclusion: Adding magnesium to nimodipine therapy in patients with SAH may help reduce CV and DCI incidence but does not significantly improve functional outcomes or mortality. Further large-scale studies are needed to optimize the dosing regimens and confirm these findings.

Hepatocellular carcinoma (HCC) accounts for 85% to 90% of primary liver cancers and generally has a poor prognosis. The hierarchical model, which posits that HCC originates from liver cancer stem cells (CSCs), is now widely accepted, as it is for other cancer types. As CSCs typically reside in the G0 phase of the cell cycle, they are resistant to conventional chemotherapy. Therefore, to effectively treat HCC, developing therapeutic strategies that target liver CSCs is essential. Clinically, HCCs exhibit a broad spectrum of pathological and clinical characteristics, ranging from well-differentiated to poorly differentiated forms, and from slow-growing tumors to aggressive ones with significant metastatic potential. Some patients with HCC also show features of cholangiocarcinoma. This HCC heterogeneity may arise from the diverse cellular origins of liver CSCs. This review explores the normal physiology of liver regeneration and provides a comprehensive overview of hepatocarcinogenesis, including cancer initiation, isolation of liver CSCs, molecular signaling pathways, and microRNAs. Additionally, the cellular origins of liver CSCs are reviewed, emphasizing hematopoietic and mesenchymal stem cells, along with the well-known hepatocytes and hepatic progenitor cells.

Background: Isoquercitrin (IQ), a flavonoid with anticancer, antioxidant, anti-inflammatory, and antiallergic properties, exhibits dual effects on B16F10 melanoma cells by suppressing cell viability and inducing hyperpigmentation. This study investigated the molecular mechanisms underlying IQ-induced melanogenesis in vitro and in vivo, highlighting the potential of IQ in the treatment of vitiligo.

Methods: B16F10 melanoma cells and zebrafish were treated with various IQ concentrations and melanogenesis was evaluated using western blotting, a tyrosinase activity assay, and microscopic observation. In addition, signaling pathway modulators and IQ were used to confirm the signaling pathways involved in IQ-induced melanogenesis.

Results: IQ treatment of B16F10 melanoma cells enhanced tyrosinase activity and upregulated melanogenesis-associated proteins, including microphthalmia-associated transcription factor and tyrosinase, via the p38 and protein kinase A (PKA)/cyclic AMP response element-binding protein (CREB) signaling pathways. Cotreatment with pathway-specific inhibitors (SB203580 for p38 and H89 for PKA/CREB) attenuated melanogenesis, whereas forskolin (a PKA/CREB activator) enhanced melanogenesis, confirming the involvement of these signaling pathways. In zebrafish, IQ treatment significantly increased melanophore production in the dorsal region following hypopigmentation induction with 1-phenyl-2-thiourea (PTU). Similar to that in B16F10 melanoma cells, SB203580 and H89 suppressed IQ-induced pigmentation, whereas forskolin enhanced it.

Conclusion: These findings demonstrate that IQ promotes melanogenesis in vitro and in vivo through activation of the p38 and PKA/CREB signaling pathways, supporting its potential as a therapeutic agent for vitiligo.

Background: Hepatic ischemia-reperfusion injury (IRI) is a complex process involving multiple mediators that initiate inflammatory responses, ultimately leading to cell necrosis and apoptosis. During hepatic IRI, various inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), and reactive oxygen species (ROS) exacerbate liver injury. Infliximab is an antibody that neutralizes TNF-α, and suppression of TNF-α activity with infliximab treatment can protect the liver from IRI. Splenectomy also alleviates hepatic IRI by decreasing neutrophil infiltration, reducing the release of ROS into the hepatic sinusoids, and suppressing TNF-α release. This study aimed to evaluate the effects of infliximab on hepatic IRI based on inflammatory responses, oxidative stress, and apoptosis, and to compare these effects with those of splenectomy.

Methods: Twenty-four rats were randomly assigned to the following four groups: (1) sham, (2) hepatic ischemia reperfusion (IR), (3) hepatic IR with 10 mg/kg infliximab, and (4) hepatic IR with splenectomy. Each group consisted of six rats. Hepatic ischemia was induced for 30 minutes, followed by 2 hours of reperfusion injury. Infliximab was administered intraperitoneally 1 hour before surgery and splenectomy was performed immediately before hepatic ischemia.

Results: Infliximab and splenectomy downregulated the levels of liver enzymes (aspartate aminotransferase [p<0.001 for all] and alanine aminotransferase [p<0.001 for all]), a prooxidant (malondialdehyde [p=0.006 for infliximab; p<0.001 for splenectomy]), inflammatory cytokines (TNF-α and nuclear factor kappa B [p<0.001 for all]), and an apoptotic mediator (caspase-3 [p=0.005 for infliximab; p=0.004 for splenectomy]) compared with those with hepatic IR alone.

Conclusion: Infliximab treatment and splenectomy mitigated hepatic IRI. These protective effects are likely mediated via anti-inflammatory, antioxidative, and antiapoptotic pathways within the pathophysiology of hepatic IRI.