p90 ribosomal S6 kinase (p90RSK), one of the downstream effectors in ERK1/2 pathways, shows high expression in human breast cancer tissues. However, its role in breast cancer development and drug resistance is not fully understood. Here, we demonstrate that Cis-DDP treatment failed to increase cytotoxicity in MDA-MB-231 cells compared to MCF-7 cells and p90RSK activation was involved in Cis-DDP-resistance to MDA-MB-231 cells. In the study, we found that inhibition of p90RSK expression or activation using a small interfering RNA (siRNA) or dominant-negative kinase mutant (DN-p90RSK) plasmid overexpression increased Cis-DDP-induced cytotoxicity of MDA-MB-231 cells, respectively. Mechanistically, we found that Cis-DDP resistance was associated with up-regulation of epithelial growth factor (EGF) expression and EGF treatment induced cancer survival signaling pathway including activation of ERK1/2, p90RSK, and Akt. We also examined the expression of epithelial-mesenchymal transition (EMT)-associated proteins using a reverse transition-quantitative PCR analysis. Cis-DDP treatment induced EMT by increasing the expression levels of N-cadherin, Snail, and Twist, while decreasing the expression levels of E-cadherin. Furthermore, we examined the epithelial marker, Zonula occludens-1 (ZO-1) using immunofluorescence analysis and found that Cis-DDP-inhibited ZO-1 expression was recovered by p90RSK deactivated condition. Therefore, we conclude that Cis-DDP resistance is involved in EMT via regulating the EGF-mediated p90RSK signaling pathway in MDA-MB-231 cells.
Breast Neoplasms ; Cadherins ; Cisplatin ; Drug Resistance ; Epidermal Growth Factor ; Epithelial-Mesenchymal Transition ; Fluorescent Antibody Technique ; Humans ; MCF-7 Cells ; Phosphotransferases ; Plasmids ; Polymerase Chain Reaction ; Ribosomal Protein S6 Kinases, 90-kDa ; RNA, Small Interfering ; Snails ; Triple Negative Breast Neoplasms ; Up-Regulation

Objectives: . A primary reason for the low adoption of hearing aids (HAs) among the large population with sensorineural hearing loss is the perception that these devices may negatively impact remaining hearing ability. Research addressing this issue has yielded conflicting results. This study examined the long-term effects of HAs on standard audiometric changes in individuals with sensorineural hearing loss. Methods: . We retrospectively analyzed patients who acquired unilateral HAs between 2015 and 2017 and demonstrated consistent use over a 5-year period. We examined demographics, medical comorbidities, audiometric data, and questionnaire results from the Hearing Handicap Inventory for the Elderly and the International Outcome Inventory for Hearing Aids. Additionally, we reviewed each patient’s history of noise exposure and prior HA use. Results: . The study included 55 patients who used unilateral HAs, with a mean follow-up period of 5.32 years. Among them, 31 patients (56.4%) used the HA on the right side. Audiometric data from the aided side showed no significant difference from the unaided side in either the pre-fit pure-tone average of air conduction (AC) or word recognition score (WRS) (PConclusion . No significant factors were identified as contributing to hearing deterioration after prolonged HA use. Overall, the use of HAs did not adversely impact residual hearing.

Minor ginsenosides Rh1 and Rg2 were isolated from Korean red ginseng and reported to have various biological effects on anti-inflammatory and anti-stress activities. However, the effects of Rh1 and Rg2 on antioxidant activity and their regulatory effects on the antioxidant enzymes have not been studied. Since oxidative stress is one of the major toxic inflammatory responses stimulated by lipopolysaccharides (LPS), the present study investigated the role of minor ginsenosides Rh1 and Rg2 on antioxidant effects in LPS-treated RAW 264.7 cells. In this study, we found that treatment with ginsenosides Rh1 and Rg2 strongly inhibited LPS-stimulated intracellular ROS production in cells. Luciferase assay showed that treatment with LPS reduced antioxidant response element (ARE) encoding the pARE-luc promoter activity, while ginsenosides inhibited the pARE-luc promoter activity. Moreover, ginsenosides Rh1 and Rg2 exhibited anti-oxidative activity in LPS-induced cells by upregulating antioxidant enzymes including superoxide dismutase, catalase, and glutathione peroxidase. Our results suggest that minor ginsenosides Rh1 and Rg2 may be potential bio-active compounds for antioxidative effects by inhibiting the generation of ROS in RAW 264.7 cells.
Antioxidant Response Elements ; Antioxidants ; Catalase ; Ginsenosides* ; Glutathione Peroxidase ; Lipopolysaccharides ; Luciferases ; Oxidative Stress* ; Panax ; RAW 264.7 Cells* ; Reactive Oxygen Species ; Superoxide Dismutase

The development of breast implant technology continues to evolve over time, but changes in breast shape after implantation have not been fully elucidated. Thus, we performed computerized finite element analysis in order to better understand the trajectory of changes and stress variation after breast implantation. The finite element analysis of changes in breast shape involved two components: a static analysis of the position where the implant is inserted, and a dynamic analysis of the downward pressure applied in the direction of gravity during physical activity. Through this finite element analysis, in terms of extrinsic changes, it was found that the dimensions of the breast implant and the position of the top-point did not directly correspond to the trajectory of changes in the breast after implantation. In addition, in terms of internal changes, static and dynamic analysis showed that implants with a lower top-point led to an increased amount of stress applied to the lower thorax. The maximum stress values were 1.6 to 2 times larger in the dynamic analysis than in the static analysis. This finding has important implications for plastic surgeons who are concerned with long-term changes or side effects, such as bottoming-out, after anatomic implant placement.
Breast Implantation ; Breast Implants ; Breast ; Computer Simulation ; Female ; Finite Element Analysis ; Gravitation ; Mammaplasty ; Motor Activity ; Plastics ; Surgeons ; Thorax

In this article, it has been stated that this study was supported by SMtech Development Program (#2018-0006-01) and Research Fund of Chungnam National University (#2017-1794-01). This information has now been corrected as follows: This research was supported by Research Fund of Chungnam National University (#2017-1794-01).

Cerebrospinal fluid (CSF) leak is possible and can be a cause of recurrent bacterial meningitis. Petrous apex meningocele (PAM) is mostly asymptomatic and is often found during incidental imaging tests. We experienced a case of CSF rhinorrhea with recurrent meningitis in bilateral PAM after adenoidectomy. This report highlights the diagnostic process of CSF leak, identification of leakage site, and surgical approach to petrous apex lesions.

The authors performed rigid reconstruction using the sandwich technique for full-thickness chest wall defects by using two layers of acellular dermal matrix and bone cement. We assessed six patients who underwent chest wall reconstruction. Reconstruction was performed by sandwiching bone cement between two layers of acellular dermal matrix. In all patients, there was no defect of the overlying soft tissue, and primary closure was performed for external wounds. The average follow-up period was 4 years (range, 2–8 years). No major complications were noted. The sandwich technique can serve as an efficient and safe option for chest wall reconstruction.

Chronic invasive aspergillosis is a life-threatening disease, especially in immunocompromised patients. The diagnosis and treatment of tracheal aspergillosis (TA) are challenging because of its rarity and nonspecific clinical presentations. The treatment standard of TA has been medical treatment like other forms of invasive aspergillosis, but patients with medically resistant TA require surgical intervention. We demonstrated a successful surgical outcome of chronic invasive TA in a 16-year-old patient with immunocompromised status related to acute myelocytic leukemia.

Macrophages play a central role in cardiovascular diseases, like atherosclerosis, by accumulating in vessel walls and inducing sustained local inflammation marked by the release of chemokines, cytokines, and matrix-degrading enzymes. Recent studies indicate that 6'-sialyllactose (6'-SL) may mitigate inflammation by modulating the immune system. Here, we examined the impact of 6'-SL on lipopolysaccharide (LPS)-induced acute inflammation using RAW 264.7 cells and a mouse model.In vivo, ICR mice received pretreatment with 100 mg/kg 6'-SL for 2 h, followed by intraperitoneal LPS injection (10 mg/kg) for 6 h. In vitro, RAW 264.7 cells were preincubated with 6'-SL before LPS stimulation. Mechanistic insights were gained though Western blotting, qRT-PCR, and immunofluorescence analysis, while reactive oxygen species (ROS) production was assessed via DHE assay. 6'-SL effectively attenuated LPS-induced p38 MAPK and Akt phosphorylation, as well as p65 nuclear translocation. Additionally, 6'-SL inhibited LPS-induced expression of tissue damage marker MMP9, IL-1β, and MCP-1 by modulating NF-κB activation. It also reduced ROS levels, mediated by p38 MAPK and Akt pathways. Moreover, 6'-SL restored LPS-suppressed Nrf2 and HO-1 akin to specific inhibitors SB203580 and LY294002. Consistent with in vitro results, 6'-SL decreased oxidative stress, MMP9, and MCP-1 expression in mouse endothelium following LPS-induced macrophage activation. In summary, our findings suggest that 6'-SL holds promise in mitigating atherosclerosis by dampening LPS-induced acute macrophage inflammation.

Macrophages play a central role in cardiovascular diseases, like atherosclerosis, by accumulating in vessel walls and inducing sustained local inflammation marked by the release of chemokines, cytokines, and matrix-degrading enzymes. Recent studies indicate that 6'-sialyllactose (6'-SL) may mitigate inflammation by modulating the immune system. Here, we examined the impact of 6'-SL on lipopolysaccharide (LPS)-induced acute inflammation using RAW 264.7 cells and a mouse model.In vivo, ICR mice received pretreatment with 100 mg/kg 6'-SL for 2 h, followed by intraperitoneal LPS injection (10 mg/kg) for 6 h. In vitro, RAW 264.7 cells were preincubated with 6'-SL before LPS stimulation. Mechanistic insights were gained though Western blotting, qRT-PCR, and immunofluorescence analysis, while reactive oxygen species (ROS) production was assessed via DHE assay. 6'-SL effectively attenuated LPS-induced p38 MAPK and Akt phosphorylation, as well as p65 nuclear translocation. Additionally, 6'-SL inhibited LPS-induced expression of tissue damage marker MMP9, IL-1β, and MCP-1 by modulating NF-κB activation. It also reduced ROS levels, mediated by p38 MAPK and Akt pathways. Moreover, 6'-SL restored LPS-suppressed Nrf2 and HO-1 akin to specific inhibitors SB203580 and LY294002. Consistent with in vitro results, 6'-SL decreased oxidative stress, MMP9, and MCP-1 expression in mouse endothelium following LPS-induced macrophage activation. In summary, our findings suggest that 6'-SL holds promise in mitigating atherosclerosis by dampening LPS-induced acute macrophage inflammation.