Hsin-Hung Chen

The conceptual landscape of clinical oncology and cancer biology has undergone a profound transformation in recent decades, evolving from static anatomical staging and broad histopathological classification into a dynamic, molecularly stratified discipline

Excessive administration of epinephrine and norepinephrine in critically ill patients may trigger a catecholamine storm and contribute to acute kidney injury (AKI) through activation of β-adrenoceptor signaling. Although clinical observations link high-dose catecholamine exposure to increased AKI risk, experimental models and mechanistic studies remain limited. We established a rodent model of combined epinephrine and norepinephrine infusion to investigate the renoprotective effects of subtype-selective β-adrenoceptor blockers. Animals received the β1-selective blockers metoprolol or atenolol, or the β2-selective blocker ICI 118,551. β1-adrenoceptor blockade, particularly with metoprolol, significantly attenuated renal histopathological injury and improved biochemical markers of kidney dysfunction. These protective effects were associated with suppression of ferroptosis-related pathways in the renal cortex. Atenolol partially improved biochemical parameters but did not significantly reduce tubulointerstitial damage, whereas β2-adrenoceptor blockade conferred limited functional benefit despite modest morphological improvement. Collectively, our findings indicate that β1-adrenoceptor activation plays a critical role in catecholamine-induced AKI by promoting ferroptosis. Targeting β1-adrenoceptors, especially with metoprolol, may represent a potential therapeutic strategy for preventing renal injury during catecholamine storms.

Background: Post-stroke autonomic dysfunction is a critical determinant of long-term prognosis. Reduced baroreceptor sensitivity (BRS), a marker of this dysfunction, has been linked to adverse outcomes, but its independent predictive value for functional recovery requires clarification. Aim: To evaluate the independent prognostic value of BRS measured in the acute phase of a first-ever ischemic stroke for predicting 12-month functional outcomes. Design: A prospective, single-center, observational cohort study. Methods: We enrolled 292 patients with a first-ever acute ischemic stroke. BRS was measured within 7 days of onset, typically between days 4 and 7, using the sequence method under standardized conditions. Patients were dichotomized into low-BRS (≤11 ms/mmHg) and high-BRS groups. The primary endpoint was 12-month functional outcome, assessed by the modified Rankin scale (mRS) and Barthel index (BI). We used inverse probability of treatment weighting (IPTW) and multiple logistic regression to assess the independent association between BRS and outcomes. Results: After adjustment, low BRS remained a significant independent predictor of poor 12-month outcomes. Patients in the low-BRS group had more than double the adjusted odds of an unfavorable outcome (mRS 3–6; adjusted OR 2.06, 95% CI 1.12–3.78) and more than triple the adjusted odds of moderate-to-severe dependency (BI ≤ 90; adjusted OR 3.13, 95% CI 1.63–6.00) compared with the high-BRS group. Conclusions: Reduced BRS in the acute phase of ischemic stroke was independently associated with poor 12-month functional outcomes. If confirmed in external cohorts and implemented with standardized protocols, BRS assessment may help early risk stratification after stroke.

Hypoxia during the postnatal period represents a significant risk factor for renal injury in neonates, yet the molecular mechanisms linking oxygen deprivation to kidney damage remain unclear. In this study, we explored whether ferroptosis serves as a key mediator in hypoxia-induced acute kidney injury (AKI). Using a neonatal rat model, we demonstrated that hypoxic exposure disrupts iron homeostasis, leading to iron accumulation and excessive lipid peroxidation in renal tissues. These alterations were associated with marked tubular injury, glomerular damage, and progressive fibrotic remodeling. Importantly, reoxygenation attenuated ferroptosis-related signaling pathways and improved renal structural and functional outcomes, although incomplete recovery was observed in fibrotic changes. Our findings suggest that ferroptosis is not only involved in the initiation of hypoxia-induced renal injury but may also contribute to its progression toward chronic kidney pathology. Targeting ferroptosis and iron metabolism may therefore represent a promising strategy for preventing or treating neonatal hypoxia-related AKI.

Background: Curcuma longa L. (turmeric) is a widely used medicinal plant with potent antioxidant and anti-inflammatory properties. It has been traditionally employed to manage inflammatory diseases such as osteoarthritis. This study explored the therapeutic potential of turmeric fermentation liquid (TF) in reducing oxidative stress, inflammation, and cartilage degradation in a monosodium iodoacetateinduced rat model of knee osteoarthritis (KOA). Methods: Fresh turmeric was washed, sliced, and fermented using Lactobacillus strains under controlled conditions to enhance its bioavailability and produce TF. Male Wistar rats were divided into four groups: Control, MIA, MIA+glucosamine hydrochloride, and MIA+TF. TF was administered orally for four weeks, and its effects were assessed through ELISA, histological staining, and immunohistochemistry to measure oxidative stress markers, inflammatory cytokines, and cartilage integrity. Results: TF enhanced antioxidant capacity and significantly reduced lipid peroxidation. It suppressed pro-inflammatory cytokines (TNF-α, IL-1β) and increased anti-inflammatory IL-10 levels. Histological analysis revealed cartilage preservation, reduced proteoglycan loss, and decreased synovitis severity. Safranin O staining confirmed higher proteoglycan retention in TF-treated cartilage, while immunohistochemistry showed reduced IL-6 and IL-1β expression. Furthermore, TF improved synovial fluid quality and decreased chondrocyte apoptosis, resulting in better joint mobility and reduced pain behavior in KOA rats. Conclusion: Turmeric fermentation liquid exhibits potential as a natural therapy for KOA by addressing oxidative stress and inflammation. The fermentation process enhances bioavailability, providing a novel approach for preserving joint health and function. Further clinical studies are needed to confirm its efficacy and safety in humans.

Shared decision‐making (SDM) in intensive care units (ICUs) aids family decision‐making and mental health; its impact on emergency management knowledge, anxiety, and mental health is unclear. In a quasi‐experimental pre–post study at a teaching hospital in southern Taiwan, 60 family members of terminally ill ICU patients (30 SDM, 30 control) were enrolled. The SDM group received a three‐talk model intervention (choice, options, decision talk); the control group received usual care. Emergency management knowledge, anxiety, and mental health were assessed via self‐administered questionnaires before and after the intervention. Data were analyzed using Mann–Whitney U and Wilcoxon signed‐rank tests and multivariable linear regression. In the SDM group, emergency management knowledge increased from a pretest mean of 16.87 (SD 3.45) to a post‐test mean of 19.33 (SD 1.49), albeit statistically significant ( p < 0.05). Anxiety scores rose in the SDM group (post‐test mean 47.13, SD 4.77) versus a slight decrease in controls (post‐test mean 43.63, SD 6.56), with no significant intergroup difference ( p = 0.284). Mental health scores (a secondary outcome) declined in both groups, indicating persistent emotional distress. After adjusting for confounders, the SDM intervention remained a significant predictor of increased knowledge. SDM enhanced knowledge of emergency management but did not alleviate anxiety or improve mental health among ICU family members. Integrating targeted emotional support into SDM models warrants exploration.

Stroke remains a leading cause of acquired physical disability globally, with upper limb motor impairment significantly affecting independence and quality of life. Currently, objective neurophysiological biomarkers are not routinely incorporated into stroke care. This study aimed to investigate the predictive value of MEPs for upper limb outcomes in acute ischemic stroke. This prospective cohort study included 133 adults experiencing their first acute ischemic stroke. Within 10 days of onset, participants underwent Motor-evoked potential (MEP) testing via transcranial magnetic stimulation (TMS) and were categorized as MEP+ (with preserved responses) or MEP- (with absent responses). Outcome measures included the Fugl-Meyer Assessment (FMA), Barthel Index, and modified Rankin Scale (mRS), assessed at baseline and 90 days. Logistic regression models adjusted for age and baseline stroke severity were used to determine the independent predictive value of MEP status. Among 133 patients (mean age 63.6 ± 12.2 years; 57.9% male), those with preserved MEPs (57.1%) demonstrated significantly better motor and functional outcomes at 90 days. MEP+ patients had higher FMA scores (61.0 ± 9.5 vs. 33.5 ± 25.5), Barthel Index scores (80.3 ± 25.0 vs. 57.7 ± 30.0), and greater odds of achieving minimal disability (mRS ≤ 1: 52.6% vs. 17.5%; all p < 0.001). Proportional recovery was also significantly higher in the MEP+ group for both the FMA and the Barthel Index (both p < 0.001). Early MEP assessment is a valuable prognostic tool for upper-limb stroke recovery, supporting its routine incorporation into clinical practice.