Objective To compare the clinical outcomes of subxiphoid robot-assisted thoracoscopic surgery (SRATS) and intercostal robot-assisted thoracoscopic surgery (IRATS) in the treatment of anterior mediastinal tumors. Methods A retrospective analysis was conducted on patients with anterior mediastinal tumors who underwent robot-assisted surgery in the Department of Thoracic Surgery, Gansu Provincial Hospital, from May 2020 to July 2022. According to the surgical approach, patients were divided into an SRATS group and an IRATS group. Perioperative data were compared between the two groups. Results A total of 87 patients were included. There were 41 patients in the SRATS group [23 males, 18 females; mean age, (44.51±11.28) years] and 46 patients in the IRATS group [21 males, 25 females; mean age, (46.67±8.76) years]. Compared with the IRATS group, the SRATS group had significantly less intraoperative blood loss [(24.41±6.67) mL vs. (37.93±9.23) mL, P<0.001], shorter postoperative drainage duration [(1.73±0.59) days vs. (2.54±0.50) days, P<0.001], lower postoperative drainage volume [(94.46±34.08) mLvs. (116.72±24.90) mL, P=0.001], lower visual analogue scale (VAS) pain scores on postoperative day 1 [(3.66±0.76) points vs. (4.15±0.84) points, P=0.005] and day 3 [(2.41±0.59) points vs. (2.89±0.82) points, P=0.003], shorter postoperative hospital stay [(4.12±0.81) days vs. (4.98±1.02) days, P<0.001], and lower hospitalization costs [(4.51±0.65) ten thousand yuan vs. (4.86±0.68) ten thousand yuan, P=0.020]. There were no statistical differences between the two groups in operative time or incidence of postoperative complications (P>0.05). Conclusion Both SRATS and IRATS are safe and effective for the treatment of anterior mediastinal tumors. However, SRATS is less invasive and more conducive to enhanced postoperative recovery.

Osteoarthritis (OA), a highly prevalent degenerative joint disease worldwide, is defined by articular cartilage degradation, abnormal bone remodeling, and persistent chronic inflammation. It severely compromises patients’ quality of life, and currently, there is no radical cure. Abnormal mechanical stress is widely regarded as a core driver of OA pathogenesis, and the exploration of mechanical signal perception and transduction mechanisms has become crucial for deciphering OA’s pathophysiological processes. Piezo1, a key mechanosensitive cation channel belonging to the Piezo protein family, has recently gained significant attention due to its pivotal role in mediating cellular responses to mechanical stimuli in joint tissues. This review systematically examines Piezo1’s expression patterns, regulatory mechanisms, and pathological functions in OA, with a particular focus on its dual roles in modulating chondrocyte homeostasis and bone metabolism disorders, while also delving into the underlying molecular signaling pathways and potential therapeutic implications. Piezo1, consisting of approximately 2 500 amino acids and forming a unique trimeric propeller-like structure, is widely expressed in chondrocytes, osteocytes, mesenchymal stem cells, and synovial cells. It exhibits permeability to cations such as Ca²⁺, K⁺, and Na⁺, and directly responds to membrane tension changes induced by mechanical stimuli like fluid shear stress and mechanical overload. In OA patients and animal models, Piezo1 expression is significantly upregulated, especially in cartilage regions subjected to abnormal mechanical stress (e.g., human temporomandibular joint cartilage). This overexpression is closely associated with aggravated cartilage degeneration, increased chondrocyte apoptosis, accelerated cellular senescence, and intensified inflammatory responses. Mechanical overload and pro-inflammatory cytokines (e.g., IL-1β) are key inducers of Piezo1 upregulation: IL-1β activates the PI3K/AKT/mTOR signaling pathway to enhance Piezo1 expression, forming a pathogenic positive feedback loop that inhibits chondrocyte autophagy, promotes apoptosis, and further accelerates joint degeneration. Mechanistically, Piezo1 mediates OA progression through multiple interconnected pathways. When activated by mechanical stress, Piezo1 triggers excessive Ca²⁺ influx, leading to endoplasmic reticulum stress (ERS) and mitochondrial dysfunction, which directly induce chondrocyte apoptosis. This process involves the activation of downstream signaling cascades such as cGAS-STING and YAP-MMP13/ADAMTS5. YAP, a transcriptional regulator, upregulates the expression of matrix metalloproteinase 13 (MMP13) and aggrecanase (ADAMTS5), thereby accelerating cartilage matrix degradation. Additionally, Piezo1-driven Ca²⁺ overload promotes the accumulation of reactive oxygen species (ROS) and upregulates senescence markers (p16 and p21), accelerating chondrocyte senescence via the p38MAPK and NF-κB pathways. Senescent chondrocytes secrete senescence-associated secretory phenotype (SASP) factors (e.g., IL-6, IL-1β), further amplifying joint inflammation. In terms of bone metabolism, Piezo1 maintains joint homeostasis by promoting the differentiation of fibrocartilage stem cells into chondrocytes and balancing bone formation and resorption through regulating the FoxC1/YAP axis and RANKL/OPG ratio. Therapeutically, targeting Piezo1 shows promising potential. Preclinical studies have demonstrated that Piezo1 inhibitors (e.g., GsMTx4) can reduce joint damage and alleviate pain in OA mice. Simultaneously, siRNA-mediated co-silencing of Piezo1 and TRPV4 (another mechanosensitive channel) decreases intracellular Ca²⁺ concentration, inhibits chondrocyte apoptosis, and promotes cartilage repair. Conditional knockout of Piezo1 using Gdf5-Cre transgenic mice alleviates cartilage degeneration in post-traumatic OA models by downregulating MMP13 and ADAMTS5 expression. Despite existing challenges, such as off-target effects of inhibitors, inefficient local drug delivery, and interindividual genetic variability, strategies like developing selective Piezo1 antagonists, optimizing targeted nanocarriers, and combining Piezo1-targeted therapy with physical therapy provide viable avenues for clinical translation. The authors propose that Piezo1 serves as a critical therapeutic target for OA, and future research should focus on deciphering its context-dependent regulatory networks, developing tissue-specific intervention strategies, and validating their efficacy and safety in clinical trials to address the unmet medical needs of OA patients.

ObjectiveTo explore the effect and mechanism of tumor necrosis factor alpha （TNF-α）-regulated circular RNA Williams Beuren syndrome chromosomal region 22 （circWBSCR22） on the malignant behaviors of cervical cancer cells. MethodsHuman cervical cancer HeLa cells were treated with TNF-α. Reverse transcription quantitative polymerase chain reaction （RT-qPCR） was used to detect the expression level of circWBSCR22. Nuclear-cytoplasmic RNA separation experiments were conducted to determine the localization of circWBSCR22 in cells. Cell migration， invasion， viability， and proliferation were assessed through Transwell assay， tetrazolium salt （MTT） assay， and colony formation assay， respectively. Dual-luciferase reporter gene assays were performed to verify the targeting relationship between microRNA-512-5p （miR-512-5p） and circWBSCR22 or family with sequence similarity 60A （FAM60A）. RT-qPCR was used to detect the RNA levels of miR-512-5p and FAM60A. Western blot was used to detect the protein level of FAM60A. ResultsCompared with the Control group， the expression level of circWBSCR22 in HeLa cells treated with TNF-α increased （P<0.05）. About 66% of circWBSCR22 was found in the cytoplasm. Compared with the control group， the migration （P<0.01） and invasion （P<0.01） of HeLa cells transfected with circWBSCR22 were enhanced， but the cell activity and cell proliferation were not significantly affected （P>0.05）. The double luciferase reporter gene assay showed that the relative luciferase activity of the co transfected circWBSCR22-WT and miR-512-5p groups was lower than that of the co transfected circWBSCR22-WT and miR-NC groups （P<0.01）. Compared with the control group， the expression level of miR-512-5p in HeLa cells transfected with circWBSCR22 decreased （P<0.01）. Compared with the control group， the migration （P<0.01） and invasion （P<0.05） ability of HeLa cells transfected with miR-512-5p decreased. Double luciferase reporter gene assay showed that compared with the co transfected FAM60A 3´-UTR-WT and miR-NC groups， the fluorescence activity of the co transfected FAM60A 3´-UTR-WT and miR-512-5p groups decreased （P<0.01）.Compared with the control group， the expression levels of FAM60A mRNA （P<0.05） and protein （P<0.01） in HeLa cells transfected with miR-512-5p decreased. Compared with the control group， the migration （P<0.01） and invasion （P<0.01） of cervical cancer HeLa cells transfected with FAM60A were enhanced. Compared with the control group， the expression levels of FAM60A mRNA （P<0.01） and protein （P<0.05） in the cells transfected with circWBSCR22 increased. The results of rescue experiment showed that compared with the pcDNA+miR-NC group， the expression levels of FAM60A RNA （P<0.01） and protein （P<0.001） in the pcDNA+miR-512-5p group decreased， and the ability of migration （P<0.01） and invasion （P<0.05） decreased； Compared with pcDNA+miR-512-5p group， the expression levels of FAM60A RNA （P<0.01） and protein （P<0.001） in circWBSCR22+miR-512-5p group increased， and the ability of migration （P<0.01） and invasion （P<0.05） was enhanced. ConclusionTNF-α promotes the migration and invasion of cervical cancer cells through the circWBSCR22/miR-512-5p/FAM60A regulatory axis.

Legal risks and liability issues in medical practice serve as a primary catalyst for the current collapse of essential healthcare services in Korea. Currently, medical disputes in Korea are disproportionately focused on criminal prosecutions and high-damages civil litigation. This punitive approach fosters a culture of concealment, encourages defensive medicine, and accelerates the exodus of medical professionals from essential fields. Ultimately, this cycle deprives the system of opportunities for improvement and poses a significant threat to patient safety. In contrast, many advanced nations have adopted principles of “Just Culture” and “Safe Space,” prioritizing non-punitive reporting and systemic root-cause analysis over individual retribution. To address these issues, this paper proposes four key strategies: First, the establishment of an independent “Patient Safety Investigation Agency” to objectively investigate incidents and identify systemic flaws. Second, a transition from criminal punishment to licensing board-led management, focusing on re-education and counseling to maintain quality of care. Third, the enactment of “Apology Laws” to ensure that expressions of regret or apologies cannot be used as legal evidence of liability, thereby fostering trust and psychological recovery. Finally, the creation of a “Patient Safety Fund” to provide prompt and sufficient public compensation to victims regardless of proven negligence. In conclusion, it is imperative to shift the paradigm by defining medical accidents as “system failures” rather than individual faults. Strengthening the social safety net will encourage medical professionals to return to essential care and build a sustainable healthcare environment centered on patient safety.

The South Korean healthcare system has achieved rapid quantitative growth; however, it continues to face critical challenges in ensuring the fundamental right to health of its citizens. From the perspective of healthcare consumers and civil society, this article identifies structural problems such as imbalances in medical accessibility, instability in essential and emergency care, and the limited participation of consumers in healthcare policy-making. Although the constitution stipulates the state’s responsibility to protect public health, current healthcare policies often prioritize administrative efficiency and provider-centered interests over patient experiences and health outcomes. In particular, this article argues that these challenges are closely related to the inadequate functioning of an accountable healthcare management framework. Structural failures in essential care, workforce shortages, and regional disparities are insufficiently monitored and addressed at the system level, resulting in responsibilities being blurred or shifted to individual healthcare providers. Consequently, the risks and burdens arising from systemic weaknesses are ultimately borne by citizens. To address these issues, this article emphasizes two major shifts. First, meaningful consumer participation must be institutionalized within healthcare governance to strengthen accountability, transparency, and responsiveness. Second, family medicine and primary care should be reinforced as the cornerstone of a sustainable, community-based healthcare system that ensures continuity of care, prevention, and chronic disease management. Re-establishing the healthcare system based on the right to health is not merely a technical adjustment, but a structural transformation toward a responsible and accountable system in which the state clearly assumes responsibility for monitoring, learning, and corrective action.

The South Korean resident training system is currently at a critical turning point, facing structural crises characterized by excessive labor-intensive environments and deteriorating quality of education. Since the medical standoff in 2024, the limitations of relying on junior doctors’ labor for hospital operations have become increasingly apparent. This review examines the current status and problems of the resident training system, including long working hours exceeding Organisation for Economic Co-operation and Development (OECD) standards, lack of systematic competency-based education, and worsening regional and essential medical imbalances. By analyzing international cases from the United States, United Kingdom, Japan, and Australia, this article proposes four core strategies for reform: (1) establishing a sustainable working and educational environment through the expansion of hospitalist systems and legalizing physician assistant roles; (2) innovating the curriculum and evaluation systems based on entrustable professional activities and milestones; (3) implementing a network-based training model to bridge the gap between metropolitan and regional healthcare; and (4) securing stable financial support and strengthening governance through the establishment of an independent evaluation body (e.g., K-ACGME). Ultimately, reforming the training system is essential not only for the rights and professional growth of residents but also for ensuring patient safety and the long-term sustainability of the national healthcare system.

South Korea’s current healthcare system stands at a critical crossroads that will determine whether it can progress in a better direction over the next decade. Behind the relatively stable level of population health that has been maintained until now, it has become clear that the deterioration of patient experiences, the risk of collapse in critical emergency medical services, the burnout of healthcare providers, and the crisis in the sustainability of healthcare finances have all accumulated simultaneously. This crisis can no longer be overcome by partial fixes or short-term measures alone. The answer to what needs to change first must begin with a reaffirmation of what the healthcare system should aim for. Ultimately, what needs to be changed now is not an individual policy, but the criteria and priorities through which we view healthcare. The focus must shift from what to provide more of, to questioning what holds greater social value. If such a shift does not begin now, in ten years we won’t face a better healthcare system, but care enmeshed in a deeper crisis. Now is precisely the time to fundamentally define the direction of the healthcare system.

Thyroid cancer is one of the most prevalent cancers in the world, accounting for the increased sensitivity of diagnostic assessments, the environment, and extensive imaging. While open thyroidectomy still forms the base surgical treatment of differentiated thyroid carcinoma (DTC), its visible scarring and postoperative morbidity have mandatorily propelled a longitudinal shift to minimally invasive techniques. Robotic thyroidectomy using the bilateral axillo-breast approach (BABA) is an emerging transformative technique that combines robotic precision and visualization with oncologic efficacy and superior cosmetic outcomes to enhance recovery. Molecular diagnostics such as next-generation sequencing (NGS) and microRNA classifiers have transformed preoperative planning. These tools aid in accurate risk stratification, enabling clinicians to determine the course of surgery and avoid overtreatment. Artificial intelligence (AI) enhances precision medicine by improving nodule classification, predicting surgical risks, providing intraoperative navigation guidance, and supporting postoperative histopathological evaluations. Despite these innovations, cost, accessibility, and ethical governance issues highlight persistent challenges. This review consolidates the current state of robotic-assisted surgery for thyroid cancer with molecular profiling and AI. It proposes future aims and strides toward precision surgery that is accessible worldwide.

Objective: This study investigated the value of multiparametric MRI (mpMRI) in predicting Gleason score (GS) upgrading and downgrading in radical prostatectomy (RP) compared with presurgical biopsy. Materials and Methods: Clinical and mpMRI data were retrospectively collected from 219 patients with prostate disease between January 2015 and December 2021. All patients underwent systematic prostate biopsy followed by RP. MpMRI included conventional diffusion-weighted and dynamic contrast-enhanced imaging. Multivariable logistic regression analysis was performed to analyze the factors associated with GS upgrading and downgrading after RP. Receiver operating characteristic curve analysis was used to estimate the area under the curve (AUC) to indicate the performance of the multivariable logistic regression models in predicting GS upgrade and downgrade after RP. Results: The GS after RP was upgraded, downgraded, and unchanged in 92, 43, and 84 patients, respectively. The AUCs of the clinical (percentage of positive biopsy cores [PBCs], time from biopsy to RP) and mpMRI models (prostate cancer [PCa] location, Prostate Imaging Reporting and Data System [PI-RADS] v2.1 score) for predicting GS upgrading after RP were 0.714 and 0.749, respectively. The AUC of the combined diagnostic model (age, percentage of PBCs, tPSA, PCa location, and PIRADS v2.1 score) was 0.816, which was larger than that of the clinical factors alone (P < 0.001). The AUCs of the clinical (age, percentage of PBCs, ratio of free/total PSA [F/T]) and mpMRI models (PCa diameter, PCa location, and PI-RADS v2.1 score) for predicting GS downgrading after RP were 0.749 and 0.835, respectively. The AUC of the combined diagnostic model (age, percentage of PBCs, F/T, PCa diameter, PCa location, and PI-RADS v2.1 score) was 0.883, which was larger than that of the clinical factors alone (P < 0.001). Conclusion Combining clinical factors and mpMRI findings can predict GS upgrade and downgrade after RP more accurately than using clinical factors alone.

Objective: This study investigated the value of multiparametric MRI (mpMRI) in predicting Gleason score (GS) upgrading and downgrading in radical prostatectomy (RP) compared with presurgical biopsy. Materials and Methods: Clinical and mpMRI data were retrospectively collected from 219 patients with prostate disease between January 2015 and December 2021. All patients underwent systematic prostate biopsy followed by RP. MpMRI included conventional diffusion-weighted and dynamic contrast-enhanced imaging. Multivariable logistic regression analysis was performed to analyze the factors associated with GS upgrading and downgrading after RP. Receiver operating characteristic curve analysis was used to estimate the area under the curve (AUC) to indicate the performance of the multivariable logistic regression models in predicting GS upgrade and downgrade after RP. Results: The GS after RP was upgraded, downgraded, and unchanged in 92, 43, and 84 patients, respectively. The AUCs of the clinical (percentage of positive biopsy cores [PBCs], time from biopsy to RP) and mpMRI models (prostate cancer [PCa] location, Prostate Imaging Reporting and Data System [PI-RADS] v2.1 score) for predicting GS upgrading after RP were 0.714 and 0.749, respectively. The AUC of the combined diagnostic model (age, percentage of PBCs, tPSA, PCa location, and PIRADS v2.1 score) was 0.816, which was larger than that of the clinical factors alone (P < 0.001). The AUCs of the clinical (age, percentage of PBCs, ratio of free/total PSA [F/T]) and mpMRI models (PCa diameter, PCa location, and PI-RADS v2.1 score) for predicting GS downgrading after RP were 0.749 and 0.835, respectively. The AUC of the combined diagnostic model (age, percentage of PBCs, F/T, PCa diameter, PCa location, and PI-RADS v2.1 score) was 0.883, which was larger than that of the clinical factors alone (P < 0.001). Conclusion Combining clinical factors and mpMRI findings can predict GS upgrade and downgrade after RP more accurately than using clinical factors alone.