Objective: Despite the increasingly widespread adoption of unilateral biportal endoscopic (UBE) decompressive laminectomy for lumbar spinal stenosis, the learning curve for surgeons new to endoscopic techniques remains a significant barrier. This study aimed to quantify this learning curve and identify strategies to expedite proficiency, focusing on reducing operative times and complications. Methods: The cumulative summation test was used to evaluate the learning curves for both the operative time and the degree of intraoperative dural tear occurrence. Moreover, clinical outcomes and postoperative complications were compared between the cranial and caudal approaches, depending on the direction of ligamentum flavum removal. Results: In total, 54 patients were included, with 22 in the cranial group and 32 in the caudal group. The operative time was notably shorter in the caudal group (cranial group, 110.86±32.63 minutes; caudal group, 79.56±24.21 minutes; p<0.01), and the complication rate was considerably lower (cranial group, 40%; caudal group, 15%; p=0.04). Twenty-six patients and 29 patients were needed to overcome the learning curves for operative time and intraoperative dural tear occurrence, respectively. Conclusion Although UBE surgery has a short learning curve, a considerable number of cases (26 and 29, respectively) were needed to achieve competency in terms of operative time and intraoperative dural tear occurrence. We highlight the caudal-to-cranial direction of ligamentum flavum dissection and removal as a way to decrease the number of dural tears and shorten the operative time.

BACKGROUND/OBJECTIVES: Accurate estimation of nutrient intake from food consumption requires reliable food composition data. However, since nutrient content changes during cooking, the application of raw ingredient composition may lead to overestimation, particularly for energy and fat in meat dishes. In this study, the suitability of applying cooked food codes for meat dishes to improve the validity of recipe-based nutrient content estimation was evaluated.MATERIALS/METHODS: Pork (thin-sliced and thick-cut belly and shoulder butt) and beef (tenderloin, loin, rib meat, and brisket point) were examined for cooking yield after grilling and their nutrient contents were estimated. Each cut was portioned to 100 g of raw meat and cooked in triplicate. Nutrient content was calculated using both raw and cooked meat codes from the Korean Standard Food Composition Table, and differences in energy, fat, and protein content were compared. RESULTS: When grilled under standardized conditions, the average cooking yield was approximately 65% for pork and 80% for beef (P < 0.0001). Thin slices of pork belly had a lower yield (62.6%) than thicker cuts (68.0%), while beef brisket point had the lowest yield among beef cuts (63.6%). Applying cooked meat codes and measured cooking yields resulted in overall decreases in energy (−10% to −50%) and fat (−20% to −60%) content, with slight increase in protein (up to +34%, P < 0.0001). For beef tenderloin, additional comparisons using matched raw and grilled data from the United States Department of Agriculture SR Legacy Database showed smaller percent differences in energy, fat, and protein than those obtained from the Korean database. CONCLUSION Incorporating measured cooking yields and corresponding cooked meat codes into recipe-based databases can improve the accuracy of nutrient intake estimation. The development of nutrient databases that reflect differences in cooking conditions—including temperature, duration, and doneness—should be prioritized to enhance the validity of national dietary surveys.

Background: General anesthesia is inevitable for pediatric patients undergoing surgery, though volatile anesthetic agents may cause neuroinflammation and neurodevelopmental impairment; however, the underlying pathophysiology remains unclear. We aimed to investigate the neuroinflammation mechanism in developing rat brains associated with sevoflurane exposure time, by identifying the specific damage-associated molecular patterns (DAMPs) pathway and evaluating the effects of non-steroidal anti-inflammatory drugs (NSAIDs) in alleviating neuroinflammation. Methods: A three-step experiment was conducted to investigate neuroinflammation induced by sevoflurane. First, the exposure time required for sevoflurane to cause neuroinflammation was determined. Next, the specific pathways of DAMPs involved in neuroinflammation by sevoflurane were identified. Finally, the effects of NSAIDs on sevoflurane-induced neuroinflammation were investigated. The expression of various molecules in the rat brain were assessed using immunohistochemistry, immunofluorescence, quantitative real-time polymerase chain reaction, western blot analysis, and enzyme-linked immunosorbent assay. Results: In total, 112 rats (aged 7 days) were used, of which six rats expired during the experiment (mortality rate, 5.3%). Expression of CD68, HMGB-1, galectin-3, TLR4, TLR9, and phosphorylated NF-κB was significantly increased upon 6 h of sevoflurane exposure. Conversely, transcriptional levels of TNF-α and IL-6 significantly increased and IFN-γ significantly decreased after 6 h of sevoflurane exposure. Co-administration of NSAIDs with sevoflurane anesthesia significantly attenuated TNF-α and IL-6 levels and restored IFN-γ levels. Conclusions In conclusion, 6 h of sevoflurane exposure induces neuroinflammation through the DAMPs pathway, HMGB-1, and galectin-3. Co-administration of ibuprofen reduced sevoflurane-induced neuroinflammation.

Cochlear implants (CIs) are recognized as a safe and effective treatment for auditory rehabilitation for people of all ages with severe to profound sensorineural hearing loss. As the indications for CIs have expanded, recent advances in technology have focused mostly on preserving residual hearing. Because trauma to the internal structure of the cochlea can affect residual hearing, development has been focused on minimally invasive surgical procedures using robot technology along with the growth of interest in the field of CI surgery over the recent years. Maintaining a slow, steady rate of electrode insertion is widely accepted as an important factor associated with reduced intraoperative inner ear trauma and improved postoperative hearing outcomes. The use of robots have resulted in maintaining a slow rate of electrode insertion and reduced the degree of innate hand tremor in the movement of electrode array. We hereby present our experience of a successful robotic CI using iotaSOFT (iotaMotion, Inc.) and also present a review of the literature.

Chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality throughout the world, is a highly complicated disease that includes chronic airway inflammation, airway remodeling, emphysema, and mucus hypersecretion.For respiratory function, an intact lung structure is required for efficient air flow through conducting airways and gas exchange in alveoli. Structural changes in small airways and inflammation are major features of COPD. At present, mechanisms involved in the genesis and development of COPD are poorly understood. Currently, there are no effective treatments for COPD. To develop better treatment strategies, it is necessary to study mechanisms of COPD using proper experimental models that can recapitulate distinctive features of human COPD. Therefore, this review will discuss representative established mouse models to investigate inflammatory processes and basic mechanisms of COPD. In addition, human COPD-mimicking human lung organoid models are introduced to help researchers overcome limits of mouse COPD models.

Chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality throughout the world, is a highly complicated disease that includes chronic airway inflammation, airway remodeling, emphysema, and mucus hypersecretion.For respiratory function, an intact lung structure is required for efficient air flow through conducting airways and gas exchange in alveoli. Structural changes in small airways and inflammation are major features of COPD. At present, mechanisms involved in the genesis and development of COPD are poorly understood. Currently, there are no effective treatments for COPD. To develop better treatment strategies, it is necessary to study mechanisms of COPD using proper experimental models that can recapitulate distinctive features of human COPD. Therefore, this review will discuss representative established mouse models to investigate inflammatory processes and basic mechanisms of COPD. In addition, human COPD-mimicking human lung organoid models are introduced to help researchers overcome limits of mouse COPD models.

Chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality throughout the world, is a highly complicated disease that includes chronic airway inflammation, airway remodeling, emphysema, and mucus hypersecretion.For respiratory function, an intact lung structure is required for efficient air flow through conducting airways and gas exchange in alveoli. Structural changes in small airways and inflammation are major features of COPD. At present, mechanisms involved in the genesis and development of COPD are poorly understood. Currently, there are no effective treatments for COPD. To develop better treatment strategies, it is necessary to study mechanisms of COPD using proper experimental models that can recapitulate distinctive features of human COPD. Therefore, this review will discuss representative established mouse models to investigate inflammatory processes and basic mechanisms of COPD. In addition, human COPD-mimicking human lung organoid models are introduced to help researchers overcome limits of mouse COPD models.

Autophagy is a process of eliminating damaged or unnecessary proteins and organelles, thereby maintaining intracellular homeostasis. Deregulation of autophagy is associated with several diseases including cancer. Contradictory dual roles of autophagy have been well established in cancer. Cytoprotective mechanism of autophagy has been extensively investigated for overcoming resistance to cancer therapies including radiotherapy, targeted therapy, immunotherapy, and chemotherapy. Selective autophagy inhibitors that directly target autophagic process have been developed for cancer treatment. Efficacies of autophagy inhibitors have been tested in various pre-clinical cancer animal models. Combination therapies of autophagy inhibitors with chemotherapeutics are being evaluated in clinal trials. In this review, we will focus on genetical and pharmacological perturbations of autophagy-related proteins in different steps of autophagic process and their therapeutic benefits. We will also summarize combination therapies of autophagy inhibitors with chemotherapies and their outcomes in pre-clinical and clinical studies. Understanding of current knowledge of development, progress, and application of cytoprotective autophagy inhibitors in combination therapies will open new possibilities for overcoming drug resistance and improving clinical outcomes.

Tumor-to-tumor metastasis (TTM) is defined as the hematogenous metastasis within a primary host tumor from a donor neoplasm. Since there is insufficient evidence regarding the pathophysiology, clinical course, and management of TTM, there are no precise guidelines for its management. A 73-yearold female patient diagnosed with breast cancer was found to have convexity meningioma. Since the size of tumor and peritumoral brain edema increased during follow-up period, the meningioma was treated with surgical resection. Postoperatively, histopathologic examination confirmed metastasis of invasive ductal carcinoma within a secretory meningioma. The final diagnosis was TTM of breast cancer in meningioma. Here, we report a rare case of intra-meningioma metastasis and a review of literature to provide a better understanding of this rare phenomenon.