Chih-Cheng Wu

Background/Objectives: Cardiac surgery involves unique complexities that differ from those of general ICU populations. Traditional scoring systems often underperform due to the significant class imbalance between survival and mortality. This study utilized the MIMIC-IV database, integrating machine learning (ML) and feature engineering to develop an in-hospital mortality prediction model specifically for open-heart surgery patients. Methods: We included 6941 cases (mortality: 76, 1.095%). Sixty-eight variables from the first ICU day were extracted. Following data preprocessing and imputation, four ML models—logistic regression, random forest (RF), XGBoost, and multilayer perceptron (MLP)—were constructed using stratified 10-fold cross-validation. SMOTE was applied to address class imbalance. A streamlined 17-variable model was developed and compared against the Sequential Organ Failure Assessment (SOFA) and the Oxford Acute Severity of Illness Score (OASIS). Results: Among the 68-variable models, RF achieved the highest area under the receiver operating characteristic curve (AUROC) of 0.915 (95% CI, 0.855–0.966). For the 17-variable models, MLP performed best (AUROC: 0.920; 95% CI, 0.865–0.964), significantly outperforming SOFA (0.688) and OASIS (0.690). Regarding the area under the precision-recall curve (AUCPR), the 17-variable MLP also yielded the highest score (0.203; 95% CI, 0.060–0.389) compared with SOFA (0.161) and OASIS (0.046). SHapley Additive exPlanations (SHAP) analysis identified bicarbonate levels, mechanical ventilation, and mean pulmonary arterial pressure as the top predictors, consistent with clinical expectations. Conclusions: The streamlined MLP model significantly outperforms traditional scoring systems and may serve as a useful tool for early postoperative risk stratification after open-heart surgery.

Background: The emergency room is a fast-paced, high-pressure environment that de-mands efficient, streamlined medical procedures. Preoperative femoral nerve blocks re-main underutilized and less discussed compared to traditional intravenous opioid ad-ministration. This study evaluates the analgesic efficacy of femoral nerve blocks and in-vestigates whether they can reduce opioid use, thereby decreasing the workload for emer-gency healthcare professionals. Methods: Patients with femoral fractures presenting to the emergency room were enrolled. A single emergency physician administered femoral nerve blocks in the treatment group (Group 1). The primary outcome was the improvement in pain scores measured by the numerical rating scale (NRS), while the secondary outcome was the frequency of intravenous opioid administration. These outcomes were compared with a standard care group receiving only intravenous opioids (Group 2). Results: Group 1 exhibited a greater reduction in NRS pain scores, with an average decrease of 4.96 com-pared to 3.99 in Group 2. Although the difference in opioid administration frequency ap-proached significance (1.35 in Group 1 vs. 1.64 in Group 2, p = 0.063), the trend favors re-duced opioid use in Group 1. Additionally, the mean time to an extra opioid administra-tion after the nerve block was 6.49 hours. Conclusions: Femoral nerve blocks provide su-perior analgesia for femoral fractures and may lower the reliance on intravenous opioids, potentially reducing the burden on emergency staff. Further research is warranted to con-firm these findings and assess the impact on opioid administration frequency.

Background and Objectives: Adequate pain management during early rehabilitation is mandatory for improving the outcomes of patients undergoing total knee arthroplasty (TKA). Conventional pain management, mainly comprising opioids and epidural analgesia, may result in certain adverse effects such as dizziness, nausea, and motor blockade. We proposed a multimodal analgesic (MA) strategy involving the use of peripheral nerve block (NB), periarticular injection (PAI), and intravenous patient-controlled analgesia (IVPCA). This study compared the clinical efficacy and adverse effects of the proposed MA strategy and patient-controlled epidural analgesia (PCEA). Materials and Methods: We enrolled 118 patients who underwent TKA under spinal anesthesia. The patients followed either the MA protocol or received PCEA after surgery. The analgesic effect was examined using a numerical rating scale (NRS). The adverse effects experienced by the patients were recorded. Results: A lower proportion of patients in the MA group experienced motor blockade (6.45% vs. 22.98%) compared to those in the PCEA group on the first postoperative day. Furthermore, a lower proportion of patients in the MA group experienced numbness (18.52% vs. 43.33%) than those in the PCEA group on the first postoperative day. Conclusions: The MA strategy can be recommended for reducing the occurrence of motor blockade and numbness in patients following TKA. Therefore, the MA strategy ensures early rehabilitation while maintaining adequate pain relief.

Vagus nerve stimulation through the action of acetylcholine can modulate inflammatory responses and metabolism. α7 Nicotinic Acetylcholine Receptor (α7nAChR) is a key component in the biological functions of acetylcholine. To further explore the health benefits of vagus nerve stimulation, this study aimed to investigate whether α7nAChR agonists offer beneficial effects against poststroke inflammatory and metabolic changes and to identify the underlying mechanisms in a rat model of stroke established by permanent cerebral ischemia. We found evidence showing that pretreatment with α7nAChR agonist, GTS-21, improved poststroke brain infarction size, impaired motor coordination, brain apoptotic caspase 3 activation, dysregulated glucose metabolism, and glutathione reduction. In ischemic cortical tissues and gastrocnemius muscles with GTS-21 pretreatment, macrophages/microglia M1 polarization-associated Tumor Necrosis Factor-α (TNF-α) mRNA, Cluster of Differentiation 68 (CD68) protein, and Inducible Nitric Oxide Synthase (iNOS) protein expression were reduced, while expression of anti-inflammatory cytokine IL-4 mRNA, and levels of M2 polarization-associated CD163 mRNA and protein were increased. In the gastrocnemius muscles, stroke rats showed a reduction in both glutathione content and Akt Serine 473 phosphorylation, as well as an elevation in Insulin Receptor Substrate-1 Serine 307 phosphorylation and Dynamin-Related Protein 1 Serine 616 phosphorylation. GTS-21 reversed poststroke changes in the gastrocnemius muscles. Overall, our findings, provide further evidence supporting the neuroprotective benefits of α7nAChR agonists, and indicate that they may potentially exert anti-inflammatory and metabolic effects peripherally in the skeletal muscle in an acute ischemic stroke animal model.

Metformin may offer benefits to certain cancer populations experiencing metabolic abnormalities. To extend the anticancer studies of metformin, a tumor model was established through the implantation of murine Lewis Lung Carcinoma (LLC) cells to Normal Diet (ND)-fed and High-Fat Diet (HFD)-fed C57BL/6 mice. The HFD-fed mice displayed metabolic and pro-inflammatory alterations together with accompanying aggressive tumor growth. Metformin mitigated tumor growth in HFD-fed mice, paralleled by reductions in circulating glucose, insulin, soluble P-selectin, TGF-β1 and High Mobility Group Box-1 (HMGB1), as well as tumor expression of cell proliferation, aerobic glycolysis, glutaminolysis, platelets and neutrophils molecules. The suppressive effects of metformin on cell proliferation, migration and oncogenic signaling molecules were confirmed in cell study. Moreover, tumor-bearing HFD-fed mice had higher contents of circulating and tumor immunopositivity of Neutrophil Extracellular Traps (NETs)-associated molecules, with a suppressive effect from metformin. Data taken from neutrophil studies confirmed the inhibitory effect that metformin has on NET formation induced by HMGB1. Furthermore, HMGB1 was identified as a promoting molecule to boost the transition process towards NETs. The current study shows that metabolic, pro-inflammatory and NET alterations appear to play roles in the obesity-driven aggressiveness of cancer, while also representing candidate targets for anticancer potential of metformin.