Electrical injury may cause various cardiac complications, including electrocardiographic (ECG) changes that mimic acute myocardial infarction. We present a 38-year-old man who developed cardiopulmonary arrest after exposure to a 25,000-volt electrical current. The admission ECG showed inferolateral ST-segment elevation, raising suspicion for acute myocardial infarction. Cardiac biomarkers were markedly elevated, and transthoracic echocardiography demonstrated a left ventricular ejection fraction (LVEF) of 35% with inferoposterolateral wall hypokinesia accompanied by moderate mitral regurgitation. Emergency coronary angiography demonstrated no significant obstructive coronary artery disease. The post-coronary angiography ECG showed greater than 50% resolution of the ST-segment elevation. A 24-hour follow-up ECG demonstrated near-complete resolution of the ST-segment abnormalities, while repeat echocardiography showed complete recovery of left ventricular systolic function, resolution of the previously detected regional wall motion abnormalities, and regression of mitral regurgitation to a trivial degree. Although ventricular function normalized within 24 hours, the patient subsequently developed dialysis-requiring acute kidney injury, neurological deterioration, suspected pneumonia, and refractory septic shock and died on hospital day 10. This case highlights that high-voltage electrical injury may present with ST-segment elevation despite the absence of obstructive coronary artery disease, accompanied by reversible myocardial dysfunction, emphasizing the importance of considering ST-segment elevation myocardial infarction (STEMI) mimics in the differential diagnosis.

Fulminant myocarditis (FM) can rapidly progress to cardiogenic shock and cardiac arrest; however, the optimal timing of mechanical circulatory support (MCS) initiation remains uncertain, particularly regarding patients with rapidly progressive disease at risk of sudden haemodynamic deterioration.

Patients with bladder underactivity experience difficulty in sensing bladder fullness and emptying the bladder efficiently, leading to chronic urinary retention. An implantable bidirectional device that combines capturing bladder smooth muscle activities with stimulation could enable closed-loop assistance and offer benefits compared to the common timed intermittent catheterization. Most existing bidirectional systems lean on passive metal electrodes as the interface, which provide no intrinsic signal amplification for low-amplitude bladder electromyography sensing and offer limited charge-injection capacity for effective and safe stimulation. Organic electrochemical transistors (OECTs) offer an attractive alternative with high sensitivity for biopotential measurements and effective stimulation capability due to their high-capacitance polymer channels. In this study, we used a custom-made portable system for a flexible ultrathin OECT array to shape a bidirectional recording and stimulation interface for bladder smooth muscle. We validate the system's recording and stimulation performance under ex vivo conditions by using an organ bath setup equipped with a commercial force transducer as a mechanical reference. The array recordings showed stable baselines during inactive periods and clear and repeatable low-frequency output changes that matched force changes during spontaneous muscle contractions. The system also delivered programmed pulse trains that consistently triggered measurable contractions in the muscle, proving its reliable stimulation capability. These findings establish a practical foundation for OECT-enabled closed-loop bladder monitoring and stimulation and support the broader use of active organic bioelectronics as bidirectional interfaces for soft and dynamic organs.

Diabetic bladder dysfunction (DBD) is a prevalent complication of diabetes mellitus (DM), characterized by heterogeneous urological impairments including altered bladder sensation, decreased compliance, and voiding difficulties. Emerging evidence highlights mitochondrial structural and functional aberrations as pivotal drivers of DBD pathogenesis. Chronic hyperglycemia induces excessive mitochondrial reactive oxygen species (ROS) generation, cristae disruption, impaired fission-fusion dynamics, defective mitochondrial quality control, and calcium dysregulation, collectively impairing bladder smooth muscle cell (BSMCs) bioenergetics and promoting apoptosis, inflammation, and fibrotic remodeling. These processes culminate in progressive bladder dysfunction, transitioning from compensatory hyperactivity to decompensated underactivity. Mitochondria-targeted therapeutic architectures fall into two complementary categories: repurposed guideline-based pharmacological agents and conceptual prospective interventions, the latter encompassing molecular reprogramming, cell-based therapies, and cell-free regenerative platforms. This review synthesizes current mechanistic insights into mitochondrial involvement in DBD and explores potential therapeutic landscapes, emphasizing the need for integrated, mechanism-driven interventions to advance clinical management of this condition.

Background/Objectives: Subacromial impingement syndrome (SIS) may be associated with altered kinetic-chain mechanics above and below the shoulder. The posterior oblique sling integrates the gluteus maximus and latissimus dorsi through established fascial and neuromuscular connections, yet empirical evidence examining its relevance in SIS remains limited. Therefore, this cross-sectional observational study aimed to investigate the surface electromyographic (sEMG) activity of the latissimus dorsi (LD) and contralateral gluteus maximus (GM) and evaluate their associations with pain, disability, and shoulder range of motion (ROM) in young adults with SIS. Methods: Sixty sedentary young adults with SIS and matched controls were assessed using the Numeric Pain Rating Scale, Arabic QuickDASH, twin-axis electrogoniometer, and sEMG of the gluteus maximus and latissimus dorsi. Results: The SIS group had significantly lower GM activity (23.96 ± 3.54% MVIC for SIS and 34.49 ± 4.16% MVIC for controls) and significantly higher LD activity (118.63 ± 24.87% MVIC for SIS and 75.52 ± 25.93% MVIC for controls) (p = 0.001). In addition to these differences, the SIS group exhibited significantly less ROM in all directions (flexion, extension, abduction, and rotation) and greater disability and pain intensity (both p = 0.001) than controls. Correlations between sEMG activity and clinical outcome measures in the SIS group were weak and not statistically significant. Discriminant logistic regression indicated that both GM and LD sEMG were significant discriminative variables of group membership, with GM underactivity showing the greater discriminative value. Conclusions: These results indicate an altered neuromuscular activation pattern observed in participants with SIS, characterized by decreased GM and increased LD sEMG activity. They may justify further investigation of kinetic-chain-informed rehabilitation, with attention to both hip/lumbopelvic function and shoulder-based treatment.

Chronic pelvic pain and lower urinary tract dysfunction are associated with a high prevalence of depression, anxiety, trauma history, and stress-related disorders, with worsening of symptoms in these groups. This review characterizes the mechanisms behind these associations and the benefits of intervention.

Takotsubo cardiomyopathy, also known as Gebrochenes-Herz syndrome, transient apical ballooning syndrome, apical ballooning cardiomyopathy, stress-induced cardiomyopathy, or broken heart syndrome, is a rare disease triggered by stressful events, such as a high plasma concentration of catecholamines and their metabolites, which resembles acute coronary syndrome. It is characterized by transient regional systolic dysfunction of the left ventricle mimicking acute myocardial infarction. The term Takotsubo originates from the Japanese word for an "octopus trap," which resembles the shape of the ventricle during systole. A 28-year-old woman in the early postpartum period presented to the emergency department with a sudden onset retrosternal chest pain and shortness of breath. At first, electrocardiography and laboratory evaluation workups suggested acute coronary syndrome. Transthoracic echocardiography revealed hypokinesia of the basal and mid left ventricular segments with preserved apical contractility, resulting in a left ventricular ejection fraction of 35%. The patient underwent immediate coronary angiography, which showed normal coronary arteries as well as no obstructive disease. Follow-up echocardiography showed recovery of left ventricular function with an improvement of the left ventricular ejection fraction to 55%, consistent with a diagnosis of reverse Takotsubo cardiomyopathy, occurring in the postpartum period which is an important STEMI mimic. Takotsubo cardiomyopathy is an important differential diagnosis in postpartum women presenting with acute coronary syndrome-like symptoms and requires careful multimodal evaluation to distinguish it from peripartum cardiomyopathy and myocarditis. The patient stabilized following supportive management, with complete recovery of left ventricular function.

Peripheral autonomic disorders, including autonomic neuropathies, lead to autonomic failure, a condition characterized by reduced autonomic function. The clinical manifestations involve multiple organ systems: in the cardiovascular system, orthostatic hypotension, postprandial hypotension, and supine/hypertension; in the gastrointestinal tract, gastroparesis, constipation, and diarrhea; and in the lower urinary tract, an underactive bladder. Peripheral autonomic disorders predominantly affect the postganglionic autonomic nerves, resulting in characteristic clinical features. The management of autonomic symptoms relies primarily on non-pharmacological interventions, with pharmacological therapy introduced when these measures are insufficient. This article reviews the clinical features, underlying pathophysiology, and treatment of symptoms associated with peripheral autonomic disorders.

Bladder dysfunction comprises diverse lower urinary tract disorders lacking treatments that restore tissue integrity and neural control. While mesenchymal stem cells (MSCs) show promise in regenerative urology, their benefits primarily stem from paracrine mechanisms. Consequently, MSC-derived extracellular vesicles (MSC-EVs) have emerged as superior cell-free alternatives, recapitulating the parent cells' regenerative potential with enhanced biosafety, stability, and controllability.This review summarizes advances in MSC- and MSC-EV-based therapies for bladder conditions, including neurogenic, diabetic, overactive/underactive bladder, outlet obstruction, and interstitial cystitis. Mechanistically, these therapies exert multi-target effects: modulating immunity, suppressing fibrosis (via TGF-β inhibition), attenuating inflammation (via NF-κB/NLRP3), promoting angiogenesis, and enhancing neuroregeneration. MSC-EVs drive these processes by precisely transferring bioactive microRNAs and proteins.We propose a paradigm shift from conventional cell therapies to MSC-EV-centric, cell-free strategies, which overcome traditional transplantation limitations like low engraftment and immunogenicity. While early data confirm feasibility and safety, challenges in standardizing EV isolation, dosing, and long-term efficacy remain. Ultimately, this review establishes MSC-EVs as a next-generation therapeutic framework, guiding future clinical translation in regenerative urology.

The study examined sex-specific differences in the autonomic response to simulated hypokinesia. Nine healthy males (23±3 years) and nine females (26±3 years) underwent 5‑day dry immersion. Heart rate variability (HRV) analysis and factor analysis (8 indices) were used to assess autonomic regulation. Factor analysis revealed three factors explaining >80% of variance. Factor 1 (SDNN, RMSSD) was universal for both sexes, but only in males did it also include heart rate with the opposite sign. Factor 2 comprised LF in females and VLF with HF, % (opposite signs) in males. Factor 3 comprised VLF in females and LF in males. Thus, adaptation to hypokinesia involves both universal (SDNN, RMSSD) and fundamentally different sex-specific regulatory strategies: modular organization in females (independent LF and VLF) versus integrated, reciprocal organization in males (VLF and HF coupling). Analysis of the dynamics of individual HRV parameters revealed that in women, the role of vagal modulations is initially more pronounced, and their weakening passively enhances the contribution of other regulatory branches; in men, by contrast, all regulatory levels are engaged simultaneously. These results highlight the importance of considering sex as a factor determining autonomic strategy. They also provide a basis for further research under conditions of reduced mobility using larger pooled cohorts and a longer follow-up period.