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Background/Objectives: Miller–Fisher syndrome (MFS) is a rare Guillain–Barré variant defined by ophthalmoplegia, ataxia, and areflexia. Pediatric MFS is uncommon, and infectious triggers remain underrecognized. Human herpesvirus 6 (HHV-6) is neurotropic but rarely linked to immune-mediated neuropathies. In this paper, we describe a child with MFS associated with HHV-6 detected in cerebrospinal fluid (CSF) and review reported pediatric infections related to MFS. Methods: A 5-year-old girl presented with acute ophthalmoplegia, ataxia, and diminished reflexes. Neuroimaging, ophthalmologic tests, CSF analyses, and serologic andpolymerase chain reaction (PCR) assays were performed, including multiplex reverse transcription–PCR of cerebrospinal fluid using the BioFire® Meningitis/Encephalitis panel. A literature search was performed on Pubmed to identify pediatric (0–18 years) MFS cases with infectious triggers. Two reviewers independently screened and summarized the literature, and a PRISMA-style flow diagram was used to transparently report the study selection process. Results: HHV-6 DNA was detected via CSF PCR twice, while tests for other pathogens were negative. Anti-GQ1b and related antibodies were negative or borderline. The patient received intravenous immunoglobulin and corticosteroids, with full recovery after one month. Among 20 published pediatric cases (1997–2021), Campylobacter jejuni was most frequent, followed by Mycoplasma pneumoniae and influenza viruses. Anti-GQ1b IgM positivity and favorable outcomes were commonly reported, including cases managed conservatively. Conclusions: This case raises the hypothesis that HHV-6 may represent a potential post-infectious association in pediatric MFS. The review findings indicate that pediatric MFS generally follows infection, responds well to immunotherapy, and has an excellent prognosis. Viral testing may be considered in selected, hypothesis-generating contexts in atypical or seronegative pediatric MFS presentations.

In February 2024, the South Korean government announced a substantial increase in medical school admissions, leading to the sudden departure of most junior doctors. This unprecedented workforce shortage significantly impacted emergency departments. Pediatric care, known to require specialized readiness, may have been disproportionately affected. We conducted a retrospective study at an emergency institution with a specialized pediatric emergency center. The study period was divided into pre-policy (March 2023-January 2024) and post-policy (March 2024-January 2025) periods. All emergency visits were analyzed, and interhospital transfers were compared between periods. Interrupted time series (ITS) analysis, multivariable logistic regression and inverse probability of treatment weighting were performed to evaluate associations between the policy-driven workforce shortage and transfer occurrence. Subgroup analyses of transferred pediatric patients examined total length of stay, transfer reasons, and accompaniment by medical staff. Among 97,916 ED visits (46,165 pediatric; 51,751 adult), there were 48 and 89 pediatric transfers in the pre- and post-policy periods, respectively, and 130 and 83 adult transfers in the same periods. Notably, pediatric transfers nearly doubled (an 85% increase) despite an approximately 42% decline in pediatric ED visit volume (29,211-16,954 visits). ITS analysis showed a continuing upward trend in pediatric transfers, although this trend did not reach statistical significance. In multivariable regression, only pediatric transfers were significantly associated with the post-policy period (OR 2.49, 95% CI 1.74-3.61). Transfer reasons shifted toward the unavailability of specialized care and physician accompaniment during transfers increased significantly. This study evaluated and identified the potential association between pediatric transfers and the government policy announcement, as well as the subsequent workforce departure, using statistical analyses and adjustment methods. Compared to adults, departure of the workforce following the policy announcement was more potentially associated with rises in pediatric transfers. Also, periodic changes in characteristics of pediatric interhospital transfers were observed. These findings reflect the vulnerability and complexity of pediatric emergency care and emphasize the necessity of ensuring medical readiness and specialized workforce capacity during times of healthcare disruption.

Advanced hepatocellular carcinoma (HCC) remains difficult to treat due to high tumor burden and limited systemic options. This study evaluated the efficacy and safety of drug-eluting bead transarterial chemoembolization (DEB-TACE) combined with intra-arterial infusion of PD-L1 inhibitor TQB2450 and oral Anlotinib as first-line treatment in patients with advanced HCC. In this prospective, single-arm phase 2 trial, 31 patients with BCLC stage C HCC received DEB-TACE, transarterial infusion of TQB2450 (1200 mg every 3 weeks), and oral Anlotinib (12 mg/day, 2 weeks on/1 week off). Tumor responses were assessed using mRECIST criteria. Primary endpoint was objective response rate (ORR); secondary endpoints included progression-free survival (PFS), overall survival (OS), and safety. The ORR was 54.5%, with 3 patients (9.7%) achieving complete response. The median PFS and OS were 5.1 and 9.6 months, respectively. The most common grade ≥3 adverse events were thrombocytopenia (16.1%) and elevated bilirubin (12.9%). Most toxicities were manageable. This triple-combination therapy demonstrated potentially beneficial antitumor activity and an acceptable safety profile in patients with advanced HCC. These findings support further investigation in randomized controlled trials. Chinese Clinical Trials Database (ChiCTR2200056222).

Although therapeutically targeting a single signaling pathway that drives tumor development and/or progression has been effective for a number of cancers, in many cases this approach has not been successful. Targeting networks of signaling pathways, instead of isolated pathways, may overcome this problem, which is probably due to the extreme heterogeneity of human tumors. However, the possibility that such networks may be spatially arranged in specialized subcellular compartments is not often considered in pathway-oriented drug discovery and may influence the design of new agents. Hsp90 is a chaperone protein that controls the folding of proteins in multiple signaling networks that drive tumor development and progression. Here, we report the synthesis and properties of Gamitrinibs, a class of small molecules designed to selectively target Hsp90 in human tumor mitochondria. Gamitrinibs were shown to accumulate in the mitochondria of human tumor cell lines and to inhibit Hsp90 activity by acting as ATPase antagonists. Unlike Hsp90 antagonists not targeted to mitochondria, Gamitrinibs exhibited a \"mitochondriotoxic\" mechanism of action, causing rapid tumor cell death and inhibiting the growth of xenografted human tumor cell lines in mice. Importantly, Gamitrinibs were not toxic to normal cells or tissues and did not affect Hsp90 homeostasis in cellular compartments other than mitochondria. Therefore, combinatorial drug design, whereby inhibitors of signaling networks are targeted to specific subcellular compartments, may generate effective anticancer drugs with novel mechanisms of action.

To evaluate an EW-7197-eluting nanofiber-covered stent (NFCS) for suppressing granulation tissue formation after stent placement in a canine urethral model. All experiments were approved by the committee of animal research. A total of 12 NFCSs were placed in the proximal and distal urethras of six dogs. Dogs were divided into two groups with 3 dogs each. The control stent (CS) group received NFCSs and the drug stent (DS) group received EW-7197 (1000 μg)-eluting NFCSs. All dogs were sacrificed 8 weeks after stent placement Histologic findings of the stented urethra were compared using the Mann-Whitney U test. Stent placement was technically successful in all dogs without procedure-related complications. On urethrographic analysis, the mean luminal diameter was significantly larger in the DS group than in the CS group at 4 and 8 weeks after stent placement (all p < 0.001). On histological examination, mean thicknesses of the papillary projection, thickness of submucosal fibrosis, number of epithelial layers, and degree of collagen deposition were significantly lower in the DS group than in the CS group (all p < 0.001), whereas the mean degree of inflammatory cell infiltration was not significantly different (p > 0.05). The EW-7197-eluting NFCS is effective and safe for suppressing granulation tissue formation after stent placement in a canine urethral model.

Recent therapeutic strategies to suppress restenosis after biliary stent placement are insufficient. Here, we demonstrate the usefulness of a self-expandable metal stent (SEMS), a stent mesh coated with silver nanoparticles (AgNPs), for suppression of both stent-induced tissue hyperplasia and biliary sludge formation in the rabbit bile duct. The AgNP-coated SEMSs were prepared using a simple bio-inspired surface modification process. Then, the prepared SEMSs were successfully placed in 22 of 24 rabbits. Sludge formation in the AgNP-coated SEMS groups was significantly decreased compared to the control group on gross findings. Cholangiographic and histologic examinations demonstrated significantly decreased tissue hyperplasia in the AgNP-coated SEMS groups compared with the control group (p < 0.05 for all). There were no differences between the AgNP-coated SEMS groups (p > 0.05 for all). However, in the group coated with the greatest concentration of AgNPs (Group D), submucosal fibrosis was thicker than in the other AgNP-coated groups (p < 0.05 for all). The AgNP-coated metallic stent mesh significantly suppressed stent-induced tissue hyperplasia and biliary sludge formation in the rabbit bile duct. Taken together, the AgNP coating strategy developed in this study could be widely utilized in non-vascular medical devices for anti-bacterial and anti-inflammatory responses.

Bone metastasis is a prevalent complication of malignant tumors, often resulting in restricted mobility, severe pain, and diminished quality of life. This study aimed to assess the analgesic effect and safety of a co-ablation system that combines elements of hyperthermic ablation and cryoablation in patients with bone metastases. This retrospective study included patients with histologically confirmed painful bone metastases treated with the co-ablation system between January and October 2024. Pain intensity was assessed using the numerical rating scale (NRS), and functional status was evaluated using the Karnofsky Performance Status score at baseline and during a 12-week follow-up. Technical success, adverse events, analgesic use, and pain response (defined as a ≥2-point reduction in NRS) were analyzed. Nine patients were included. Technical success was achieved in all procedures, with no procedure-related adverse events observed. Median NRS scores decreased progressively from 5 (IQR 4-6) at baseline to 2 (IQR 1-3) at 12 weeks. By the fourth week, 8 (88.9%) patients achieved a clinically meaningful pain reduction. Karnofsky Performance Status scores showed gradual improvement during follow-up. No patients required escalation of analgesic therapy, and some experienced dose reductions. The co-ablation system appeared to be feasible and was associated with short-term pain reduction in patients with bone metastases, with no ablation-related adverse events observed.

We report herein on the design, synthesis and biological activity of Ru-based self-assembled supramolecular bowls as a potent anticancer therapeutic in human hepatocellular cancer. The potent complex induces production of reactive oxygen species (ROS) by higher fatty acid β-oxidation and down-regulation of glucose transporter-mediated pyruvate dehydrogenase kinase 1 via reduced hypoxia-inducible factor 1α. Also, overexpressed acetyl-CoA activates the tricarboxylic acid cycle and the electron transport system and induces hypergeneration of ROS. Finally, ROS overexpressed through this pathway leads to apoptosis. Furthermore, we demonstrate that the naphthalene derived molecular bowl activates classical apoptosis via crosstalk between the extrinsic and intrinsic signal pathway. Our work into the mechanism of Ru-based self-assembled supramolecular bowls can provide valuable insight into the potential for use as a promising anticancer agent.

Secondary lymphedema is a severe complication of cancer treatment, but there is no effective curative method yet. Lymph node dissection and radiation therapy for cancer treatment may lead to secondary lymphedema, which is a chronic disease induced by malfunction of lymphatic flow. The lymphatic channel sheet (LCS) is an artificial micro‐fluidic structure that was fabricated with polydimethylsiloxane to maintain lymphatic flow and induce lymphangiogenesis. The structure has two‐dimensional multichannels that increase the probability of lymphangiogenesis and allow for relatively easy application. We verified the efficacy of the lymphatic channel sheet through macroscopic and microscopic observation in small animal models, which underwent brachial lymph node dissection and irradiation. The lymphatic channel sheet enabled the successful transport of lymphatic fluid from the distal to the proximal area in place of the removed brachial lymph nodes. It prevented swelling and abnormal lymphatic drainage during the follow‐up period. Lymphangiogenesis was also identified inside the channel by histological analysis after 8 weeks. According to these experimental results, we attest to the roles of the lymphatic channel sheet as a lymphatic pathway and scaffold in the rat upper limb model of secondary lymphedema. The lymphatic channel sheet maintained lymphatic flow after lymph node dissection and irradiation in an environment where lymph flow is cut off. It also relieved symptoms of secondary lymphedema by providing a lymph‐friendly space and inducing lymphangiogenesis.