The trend toward miniaturization and multi-functionalization of implantable medical devices is shifting the paradigm of medicine from treatment to prevention and precision management; however, it faces a bottleneck due to the energy density limits of batteries. Existing power transfer technologies based on electromagnetic induction or radio frequency cause rapid efficiency degradation and electromagnetic interference issues in micro-scale devices. This paper reviews laser-based optical wireless power transfer technology as an innovative alternative to these issues, with particular emphasis on its potential medical applications. We provide an in-depth analysis of strategies to maximize penetration depth using near-infrared windows and light propagation characteristics within biological tissue, optimization of conversion efficiency through bandgap engineering of silicon (Si) and gallium arsenide (GaAs) based photovoltaic cells, and the latest wavefront shaping and optical phased array technologies to overcome dynamic scattering. Furthermore, by chronologically organizing research trends over the past 20 years, we discuss the paradigm shift from passive devices to active intelligent systems and present the technical and regulatory challenges for clinical adoption based on international safety standards (IEC 60825-1, ISO 14708-1), ultimately providing a technical roadmap for the energy autonomy of next-generation bio-electronic medicine.

Background: Elevated active glucocorticoids (GCs) are implicated in skin barrier dysfunction, notably in aging and diabetes. The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts inactive GCs to active forms, potentially exacerbating this dysfunction. Objective: We aimed to investigate the impact of a novel 11β-HSD1 inhibitor on skin inflammation using both in vitro and in vivo models. Methods: To elucidate the efficacy of a new 11β-HSD1 inhibitor in mitigating skin inflammation induced by various triggers, including dexamethasone treatment, ultraviolet B irradiation, and high glucose levels, in cultured human keratinocytes and the db/db mice as a type 2 diabetes murine model. In cultured keratinocytes, we assessed the effects of the 11β-HSD1 inhibitor on cortisol levels, 11β-HSD1 expression, and cytokine production under conditions simulating inflammation. In db/db mice, we evaluated the inhibitor’s impact on skin barrier function, hemoglobin A1c (HbA1c) levels, corticosterone levels, 11β-HSD1 expression, and cytokine profiles following a 2-week treatment regimen. Results: Our results demonstrated that both the novel 11β-HSD1 inhibitor and a known inhibitor reduced cortisol levels, 11β-HSD1 expression, and inflammatory cytokine production in cultured keratinocytes. In db/db mice, treatment with either inhibitor improved skin barrier function, lowered serum HbA1c levels, and decreased corticosterone, 11β-HSD1, and inflammatory cytokine expression. Conclusion A new 11β-HSD1 inhibitor, “11b-0048,” showed a significant inhibitory effect on the expression of 11β-HSD1 in keratinocytes activated by various conditions and diabetic skin.

Background: Warm ischemia is a major contributor to ischemic cholangiopathy and non-anastomotic biliary strictures (NAS) after liver transplantation, particularly in donation-after-circulatory-death grafts. However, the isolated impact of warm ischemia on peribiliary fibrosis is difficult to delineate because clinical settings involve overlapping effects of cold ischemia, reperfusion injury, and alloimmunity. This study aimed to establish a non-transplant rat model that isolates warm ischemic biliary injury and to compare the antifibrotic effects of rapamycin and tacrolimus. Methods: Warm ischemia was induced in Sprague–Dawley rats by ligating both ends of the peribiliary vascular plexus and the hepatic artery, followed by 30 minutes of portal vein clamping. Rats were randomly assigned to control, tacrolimus (1 mg/kg/day), or rapamycin (1 mg/kg/day) groups (n=15 per group). Serum alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transferase, and total bilirubin were measured serially. Hematoxylin and eosin (H&E) and Sirius red staining were performed at 1, 3, and 6 weeks. Peribiliary fibrosis was quantified using digital image analysis of collagen area fraction. Results: Warm ischemia induced acute hepatobiliary injury with transient enzyme elevations, but no significant intergroup differences were observed. Histologically, biliary epithelial proliferation and collagen deposition increased progressively and became prominent at 6 weeks. At this time point, fibrosis ratios differed significantly (overall p=0.002): controls showed the highest fibrosis (4.8%), followed by tacrolimus (2.4%) and rapamycin (1.7%). Both immunosuppressants significantly reduced fibrosis compared with controls (p<0.05), whereas the difference between tacrolimus and rapamycin was not significant. Conclusion This warm ischemia model demonstrates that isolated ischemic injury alone can induce progressive peribiliary fibrosis. Rapamycin and tacrolimus attenuated fibrosis, with rapamycin producing the lowest collagen deposition. These findings provide mechanistic insight into ischemic cholangiopathy after liver transplantation—particularly in donation after circulatory death grafts—and underscore the need for further studies using models that incorporate cold ischemia, reperfusion, and alloimmune factors.

Purpose: Weight reduction (WR) can reduce liver volume, affecting the graft-to-recipient weight ratio (GRWR). This study aimed to evaluate the decrease in liver volume after WR and analyze risk factors affecting liver volume reduction in potential liver donors with steatosis. Methods: We retrospectively reviewed data of 147 potential liver donors with steatosis who participated in a WR program prior to liver transplantation between January 2016 and December 2021. Total liver volume (TLV) was measured using CT and MRI. Risk factors for large liver volume reduction (≥10%) were analyzed using multivariate logistic regression. Results: Ninety-seven donors (66.0%) underwent donor hepatectomy after WR. Liver volumes showed a statistically significant decrease (from 1,399.6 ± 315.4 mL to 1,283.6 ± 271.2 mL, P < 0.05). Thirty-eight donors (42.7%) showed large liver volume reduction. There was a more significant reduction in weight, AST, and ALT in the large liver volume reduction group than in the small liver volume reduction group (all P < 0.05). WR percentage and ALT abnormalities were independent risk factors for large liver volume reduction (odds ratio, 1.184 [95% confidence interval, 1.054–1.329] and odds ratio, 5.502 [95% confidence interval, 1.660–18.229], respectively; all P < 0.05). Conclusion Potential liver donors with 7% or more WR or ALT abnormality require liver volume/GRWR remeasurement after WR to ensure adequate graft size and prevent small-for-size syndrome.

Purpose: We investigated the antiadhesive effects of lidocaine, methylene blue, and atorvastatin, with a focus on preventing remote adhesions in a rat model of postoperative adhesions. Methods: Models were assigned to either the control group (saline infusion only) or treatment groups (group L, lidocaine;group M, methylene blue; or group S, atorvastatin). Adhesions were induced by intestinal or abdominal wall injuries. The rats were sacrificed 2 weeks after surgery. Results: The number of remote adhesions was markedly lower in groups L, M, and S than in the control group. The macroscopic adhesion score was substantially lower in groups L, M, and S than in the control group. Acute and chronic inflammation, as well as fibrosis scores, were also markedly lower in groups L, M, and S than in the control group. IL-1βlevels were considerably reduced in groups L, M, and S at 2 hours after surgery and remained substantially lower in group S at 48 hours. IL-6 levels were markedly reduced in groups M and S at 2 hours and in all treatment groups at 48 hours than in the control group. Conclusion Intraperitoneal administration of lidocaine, methylene blue, and atorvastatin effectively reduced remote adhesion formation, macroscopic and microscopic adhesion scores, and inflammatory cytokine levels in a rat adhesion model.

Purpose: Right lobe living donor liver transplantation (LDLT) with dual portal veins (PVs) remains technically challenging.This study aimed to identify independent risk factors for PV complications. Methods: We retrospectively analyzed 111 recipients of dual PV LDLT between 2011 and 2020. Recipient characteristics, anatomical geometry, and surgical factors were evaluated. Outcomes were overall PV complications and major PV complications (Clavien-Dindo grade ≥III). Logistic regression was performed. Results: PV complications developed in 41 patients (36.9%), including 16 major events (14.4%). Univariate analysis revealed associations with right posterior PV (RPPV) diameter, axial angle, and coronal angle. On multivariate analysis, larger RPPV diameter (odds ratio [OR], 1.79; P = 0.041) and wider axial angle (OR, 1.08; P = 0.015) were independent predictors of major PV complications. Reconstruction method was not significant. Patients with overall major Clavien-Dindo grade ≥IIIcomplications had inferior 100-month survival (80% vs. 100%; P = 0.014, log-rank test). Conclusion In dual PV LDLT, anatomical geometry—specifically RPPV diameter and axial angle—independently predicts major PV complications, whereas surgical technique does not. Preoperative 3-dimensional imaging and anatomical risk stratification should inform donor selection and surgical planning.

Buttock augmentation is an increasingly popular cosmetic procedure designed to enhance buttock contour, size, and shape. However, the safety profile of this procedure remains insufficiently established, and it carries risks of complications, including foreign body reactions and infections. These complications may be exacerbated by filler migration, resulting in large soft-tissue cavities that resemble pseudocysts. In this study, we describe two patients who developed severe complications following massive filler injections to the buttocks. A 56-year-old female patient presented with a 6×5 cm soft-tissue defect associated with an extensive underlying dead space, sinus tract formation, and a large pocket extending across the buttock. Additionally, a 50-year-old female patient developed diffuse cellulitis and multiple abscesses secondary to migration of an infected filler-related pseudocyst. Both patients underwent successful en bloc capsulectomy, resulting in marked clinical improvement without recurrence or postoperative complications. These cases underscore the serious complications associated with large-volume filler injections and highlight the importance of comprehensive surgical management in addressing late-stage adverse outcomes.

This study examined the inhibitory effects of pluviatolide, a lignan derived from Podophyllum hexandrum, on mast cell activation and IgE-mediated type I hypersensitivity, focusing on FcεRI-dependent and calcium-mediated pathways. Using bone marrowderived mast cells (BMMCs) and rat basophilic leukemia (RBL)-2H3 cells, we found that pluviatolide significantly decreased β-hexosaminidase release and suppressed the expression and secretion of TNF-α and IL-6 in a concentration-dependent manner, without causing cytotoxicity. While we initially hypothesized that it would selectively modulate antigen-specific FcεRI signaling, pluviatolide also inhibited degranulation induced by calcium ionophore and thapsigargin, indicating its effects extend to receptorindependent, Ca2+-dependent activation mechanisms. Immunoblot analyses revealed decreased phosphorylation of proximal kinases (Lyn, Syk), adaptor proteins (LAT, PLCγ1), MAPKs (ERK1/2, JNK, p38), and NF-κB p65. In a passive cutaneous anaphylaxis (PCA) mouse model, oral administration of pluviatolide significantly reduced Evans blue extravasation and mast cell degranulation in ear tissues. These findings demonstrate that pluviatolide suppresses both early and late-phase mast cell responses through multi-nodal inhibition of activation pathways, highlighting its potential as a therapeutic candidate for both IgE-mediated and non-IgE-mediated allergic disorders.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine that selectively targets cancer cells and induces apoptosis. However, many cancers, including bladder cancer, develop resistance to TRAIL, limiting the efficacy of TRAIL-based therapies. This study investigated whether betulinic acid (BA), a pentacyclic triterpenoid with anticancer and chemosensitizing properties, increases TRAIL-mediated apoptosis in TRAIL-resistant human bladder cancer cells. Combination treatment with BA and TRAIL significantly increased cytotoxicity and apoptosis compared to either treatment alone. This combination treatment also increased reactive oxygen species (ROS) production, increased Bax expression and Bid cleavage (tBid formation), and downregulated Bcl-2 levels. These effects were accompanied by caspase activation via extrinsic and intrinsic pathways, leading to cytochrome c release via mitochondrial membrane destabilization, thereby contributing to increased apoptosis. Furthermore, the combination treatment inhibited phosphoinositide 3-kinase (PI3K) and Akt phosphorylation; this effect was amplified by a PI3K inhibitor but abrogated by ROS inhibition. Collectively, our results suggest that BA sensitizes bladder cancer cells to TRAILinduced apoptosis via ROS-dependent activation of the apoptotic pathway and inhibition of PI3K/Akt signaling. Therefore, the BA and TRAIL combination exhibits potential to overcome TRAIL resistance in human bladder cancer.

Purpose: Radiotherapy is used to reduce the risk of breast cancer recurrence after surgery, but it is a potential cause of secondary cancer. We validated the risk of secondary cancer in primary breast cancer who received radiotherapy compared with those who did not from a matched cohort using a large-scale observational study of the Observational Health Data Sciences and Informatics (OHDSI) data network. Materials and Methods: A retrospective comparative cohort study using propensity score-matched cohorts was performed using two Observational Medical Outcome Partnership common data model databases, from tertiary general hospitals in South Korea. Among female patients who underwent surgery after the diagnosis of breast cancer, the risk of secondary primary malignant occurrence after 1:1 matching was analyzed. Results: Among 27,078 patients with breast cancer, there was no significant difference in the risk of secondary cancer following radiotherapy in 4,426 patients after 1:1 propensity-score matching. Further, there were no significant differences in the sensitivity analysis according to age, latency period, and number of radiation treatments. Conclusion There was no difference in the risk of secondary cancer in the patients diagnosed with breast cancer depending on whether or not radiotherapy was performed after surgery. In the future, it is necessary to analyze including data generated during cancer treatment.