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.

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.

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.

This report presents a case of contralateral breast cancer in a BRCA mutation-positive patient who had previously undergone delayed free transverse rectus abdominis myocutaneous flap reconstruction for unilateral breast cancer. Having used up the available abdominal autologous tissue in the first reconstruction, a direct-to-implant procedure was employed for the reconstruction of the second, contralateral breast. Therefore, one breast was reconstructed using autologous tissue from the abdomen, while the other was asymmetrically reconstructed with an implant. If the risk of contralateral breast cancer had been anticipated initially, we might have opted for implant-based reconstruction from the start to facilitate a more symmetrical outcome in the event of subsequent contralateral reconstruction. This case underscores the importance of reviewing the risk of contralateral breast cancer in patients with unilateral breast cancer who also carry mutations in BRCA and other breast cancer susceptibility genes. Furthermore, it encourages consideration of how mutations in breast cancer susceptibility genes, including BRCA, influence the choice of plastic surgery reconstruction techniques. The findings from genetic testing for breast cancer susceptibility are now crucial to achieving aesthetic completeness in breast reconstruction.

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.

Sudden death during or after percutaneous coronary intervention (PCI) could be led to potential medicolegal disputes. This study aimed to investigate the clinical and postmortem findings in PCI-related deaths-focusing on the current statusto inform preventive strategies against these fatalities. Forty-three cases were retrieved from the National Forensic Service's postmortem records between 2015 and 2021, and the corresponding postmortem findings and clinical information were analyzed. The analyses revealed a relatively consistent annual incidence of PCI-related deaths. Immediate deaths during or shortly after PCI occurred in 17 cases (39.5%), and delayed PCI-related deaths after discharge from the hospital occurred in 26 cases (60.5%). The causes of PCI-related deaths in the postmortem cases were categorized into four groups: PCI complications (11 cases, 26%), acute myocardial infarction (23 cases, 53%), ischemic heart disease (8 cases, 19%), and others (1 case, 2%). Postmortem examinations played a critical role in determining the cause of death and obtaining medical evidence, including pathological findings of the heart as well as those of coronary artery and stent insertion. Our findings suggest that a detailed examination of the heart, coronary arteries, stent status, and atherosclerosis in PCI-related deaths could help provide more accurate information as medical evidence and prevent/resolve potential medicolegal issues. Further, this could advance our understanding of PCI-related deaths and inform future preventive strategies.

Objectives: . A crooked nose is frequently caused by nasal bony vault deviation, and proper management of the bony vault is an integral part of rhinoplasty. Conventional osteotomy to correct a deviated nose favors simultaneous medial and lateral osteotomies, which allows the free independent movement of each nasal bone. However, patient satisfaction with deviated nose surgery is sometimes low. In the present study, we introduce a one-unit osteotomy procedure that combines bilateral and root osteotomies with unilateral triangular bony wedge resection to allow symmetry of both nasal bones. Methods: . Twenty consecutive patients who presented with bony vault deviation and underwent one-unit osteotomy were enrolled in this retrospective single-center study. The Nasal Obstruction Symptom Evaluation (NOSE) questionnaire was used to evaluate each patient’s functional outcome. The angle of bony vault deviation before and after one-unit osteotomy was measured using a protractor and compared with the results of 14 patients who had undergone conventional osteotomy. The improvement in dorsal deviation was evaluated using facial photography preoperatively and 3 months postoperatively. Results: . NOSE values improved from 8.4±6.4 to 4.1±4.2 (P =0.021). The angle of bony vault deviation improved from 6.9°±2.2° to 2.1°±1.2° (P <0.001) in one-unit osteotomy and from 7.3°±4.0° to 2.7°±1.2° (P =0.001) in conventional osteotomy. The preoperative deviation angle improved by 70.3% in one-unit osteotomy compared with 56.6% in conventional osteotomy, which was a significant difference (P =0.033). The mean grade of the postoperative esthetic outcomes for the remaining deviation was 1.6±0.5, which was similar to that in the conventional osteotomy group. Conclusion . One-unit osteotomy is a relatively simple procedure that balances the width of both lateral walls by removing excessive bony fragments from the wider bony wall and providing better structural integrity. This technique improves functional outcomes and has equivalent esthetic results to those of the traditional procedure.

Objective: The prolonged coronavirus disease-2019 (COVID-19) pandemic is likely to cause psychological distress in people. This systematic review aimed to identify the effectiveness of virtual reality (VR)-based psychological intervention among individuals with psychological distress during the COVID-19 crisis. PubMed, Ovid MEDLINE, Cochrane Library, Web of Science, Embase, and PsycINFO databases were searched for articles published until July 2022. Methods: The available citations were deduplicated and screened by two authors using the title and abstract information. Eligibility criteria were constructed according to the PICOT guidelines. Empirical studies of all designs and comparator groups were included if they appraised the impact of an immersive VR intervention on any standardized measure indicative of psychological distress (stress, anxiety, depression, and post-traumatic symptoms) or improvements in quality of life in participants, including COVID-19 patients, medical staff working with COVID-19 patients, and people who had experienced strict social distancing during the COVID-19 pandemic. Results: The results were discussed using a narrative synthesis because of the heterogeneity between studies. Seven of the studies met the inclusion criteria. There were two randomized controlled trials and five uncontrolled studies on VR interventions. Conclusion All studies reported significant improvement in a wide range of psychological distress during COVID-19, ranging from stress, anxiety, depression, and post-traumatic symptoms to quality of life, supporting the efficacy of VR-based psychological intervention. Our results suggest that VR intervention has potential to ameliorate COVID-19-related psychological distress with efficacy and safety.