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The effect of chronic stress on sensitivity to dexamethasone treatment of HPA axis gene expression in C57Bl/6 mice.
Behav Brain Res
Rasha Salman, Polina Ritter, Yuliya Ryabushkina +2 more
Chronic social stress is a major risk for psychopathologies such as depression, often leading to altered hypothalamic-pituitary-adrenal (HPA) axis function and glucocorticoid resistance. This study examines how chronic social defeat stress (CSDS) affects sensitivity to dexamethasone by analyzing HPA axis genes expression in C57Bl/6 mice. Adult male mice were subjected to 30 days of stress, followed by dexamethasone or saline administration. Genes expression was analyzed in the hypothalamus, prefrontal cortex (PFC; Nr3c1 only), and adrenal glands at multiple time points post-treatment. CSDS induced marked dysregulation of HPA axis-related genes, including a decrease in hypothalamic Crh and Crhbp, and adrenal Mc2r, Nr3c1, alongside an upregulation of steroidogenic enzymes Cyp11a1 and Cyp11b1, which may account for the elevated corticosterone levels observed under chronic stress conditions. CSDS alters the genes expression response to dexamethasone, indicating a delayed recovery of glucocorticoid receptor signaling in the brain and adrenal glands. Our findings reveal significant stress-induced alterations in the expression of key HPA axis genes, suggesting impaired glucocorticoid receptor signaling and potential glucocorticoid resistance in stressed mice.
Exploring the Prospective Insights Into the Prognostics of N-terminal Pro-B-Type Natriuretic Peptide in Predicting Heart Failure Readmissions in a Tertiary Healthcare Setting.
Cureus
Ghulam Muhammad Shoaib, Uday Shree Akkala Shetty, Muhammad Zaman Baloch +1 more
Heart failure (HF) is a significant cause of morbidity and hospital readmission despite improvements in treatment. N-terminal pro-B-type natriuretic peptide (NT-proBNP) is a sensitive biomarker of ventricular wall stress and could be able to give prognostic insight into the post-discharge outcome. The aim of the study was to evaluate the prognostics of NT-proBNP in predicting heart failure readmissions in a tertiary healthcare setting.
A Case of Atrial Septal Defect Unveiled by the Treatment for Pulmonary Arterial Hypertension.
Clin Case Rep
Takaaki Fujii, Sayuri Yamabe, Yoshiro Tsuruta +10 more
We present a case of a 51-year-old woman with atrial septal defect (ASD) masked by pulmonary arterial hypertension (PAH). Three months after PAH treatment with a combination of endothelin receptor antagonist and phosphodiesterase five inhibitor, the transthoracic echocardiography revealed left-to-right shunting through a secundum ASD. The pulmonary vascular resistance decreased from 7.4 to 2.6 Wood units. Subsequent transcatheter closure of ASD using Occlutech Figulla Flex II device was successfully performed as a treat-and-repair strategy. Five months later, hemodynamics had normalized. Due to reduced shunt flow caused by PAH, ASD may not be detectable before treatment, so care must be taken not to overlook PAH associated with intracardiac defects.
Challenge of Corneal Ulcer Healing: A Novel Conceptual Framework, the "Triad" of Corneal Ulcer Healing/Corneal Neovascularization/Intraocular Pressure, and Avascular Tendon Healing, for Evaluation of Corneal Ulcer Therapy, Therapy of Neovascularization, Glaucoma Therapy, and Pentadecapeptide BPC 157 Efficacy.
Pharmaceuticals (Basel)
Sanja Masnec, Antonio Kokot, Tamara Kralj +16 more
To better address the challenge of corneal ulcer healing, with already available standard agents, and those recently introduced, such as stable gastric pentadecapeptide BPC 157, we introduced a novel conceptual framework-the "triad" of corneal ulcer healing↔corneal neovascularization↔intraocular pressure-and extended it to avascular tissues such as tendon. Within this framework, cytoprotection serves as the unifying principle, underscoring that therapeutic effects are not isolated but interconnected. Preclinical studies with BPC 157 therapy, as a cytoprotection agent, illustrate this integration. BPC 157 rapidly normalizes elevated intraocular pressure in glaucomatous rats, preserves retinal integrity, restores pupil function, maintains corneal transparency during ulcer or abrasion healing, and counteracts both corneal neovascularization and dry eye. In parallel, its consistent efficacy in tendon injury models highlights a cytoprotective specificity across avascular tissues. The cornea's "angiogenic privilege," preserved during healing and tendon recovery together, provides strong proof of concept. Furthermore, mapping standard therapeutic agents used for corneal ulcers, neovascularization, or glaucoma onto this triad, and linking them with tendon healing, reveals both shared pathways and inconsistencies across existing drug classes. Analyzed were the ascorbate, fibronectin, hyaluronic acid, metalloproteinase inhibitors, EGF, FGF, NGF, insulin, and IGF-1 (corneal ulcer healing), the antiangiogenic agents (endostatin, PAI-1, PEDF, angiostatin, TSP-1, TSP-2, IFN-α), corticosteroids, NSAIDs, cyclosporine A, anti-VEGF drops (treatment of corneal neovascularization), and alpha 2-agonists, beta-blockers, carboanhydrase inhibitors, muscarinic agonists, Rho-kinase inhibitors, and prostaglandin analogs (glaucoma). Taken together, these findings advance cytoprotection as a unifying therapeutic paradigm, with BPC 157 emerging as its first exemplar, and encourage further translational research toward clinical application.
Recombinant human thymosin beta 4 improves ischemic cardiac dysfunction in mice and patients with acute ST-segment elevation myocardial infarction after reperfusion.
Cardiovasc Res
Yuze Zhang, Qiuting Dong, Xiaohui Bian +22 more
Despite advancements in primary percutaneous coronary intervention (PCI), cardiac dysfunction remains a challenge in patients with ST-segment elevation myocardial infarction (STEMI). Although thymosin beta 4 has shown cardioprotective effects in preclinical MI models, its impact on chronic cardiac functional recovery post ischemia/reperfusion (I/R), especially in STEMI, warrants further investigation. This study aims to explore the therapeutic potential of recombinant human thymosin beta 4 (rhTB4) in both murine models subjected to I/R and in subjects with STEMI post-PCI.
Thymosin β4 stabilizes hypoxia induced brain microvascular endothelial cell dysfunction through S1PR1 dependent mechanisms.
Sci Rep
William G Stewart, Christina D Hejl, Rakeshwar S Guleria +1 more
Acute ischemic injury causes impairment of blood brain barrier (BBB) permeability and is considered as secondary insult in the brain after traumatic brain injury (TBI). The mechanisms underlying these events are incomprehensible and therefore therapeutic opportunities are limited. Although drugs have been showing some promise in TBI outcome, the restoration of BBB damage remain elusive. Thymosin β4 (Tβ4) is a secreted 43 amino acid peptide showed beneficial outcome in cerebral ischemia or TBI, however, it's role in hypoxia-induced BBB damage remains elusive. We hypothesize that Tβ4 protect hypoxia-induced BBB disruption via Sphingosine 1-phosphate receptor 1 (S1PR1) modulation. In the current study, we investigated the beneficial effects of Tβ4 in hypoxia induced gene expression of several tight junction proteins, S1PR1, endothelial cell permeability and tight junction dynamics in human brain microvascular endothelial cells (hBMVECs), one of the important cell types in the BBB integrity. The data suggests that pretreatment with Tβ4 reversed the hypoxia-induced damage of BBB components in hBMVECs. Furthermore, results identify S1PR1, a possible target for Tβ4. Inhibition of S1PR1 showed that Tβ4 failed to offer protection. Together, data provided evidence that S1PR1 is pivotal and Tβ4 can serve as a protective agent in BBB integrity and may offer a promising therapeutic target. In conclusion, we propose that depletion of S1PR1signaling is vital in hypoxia-induced BBB pathophysiology and Tβ4 may be tested as a potential treatment modality and warrant further investigation.
Food-specific IgG-based elimination diet decreased IL-6, TNF-α, and CGRP and improved symptoms in adults with migraine.
Front Nutr
Zhiming Zhao, Meimei Yang, Fujun Wan +4 more
Food-specific IgG antibodies have been proposed to be biomarkers to identify food that triggers an inflammation response. We aimed to evaluate the effect of a food-specific IgG-based elimination diet by assessing the changes in the symptoms of migraine and its comorbidities, inflammatory cytokines, neuropeptides, and neurotransmitters, and their correlation.
Effect of carperitide on clinical outcomes among patients with acute heart failure: a meta-analysis of randomized and propensity‑matched studies.
BMC Cardiovasc Disord
Tsuyoshi Shiga, Atsushi Suzuki, Sachie Inoue +1 more
Carperitide, which is an α-human A-type natriuretic peptide, is used intravenously for the treatment of acute heart failure (AHF) primarily in Japan. However, its clinical effectiveness has not been established. The aim of this meta-analysis was to assess the effect of carperitide on the clinical outcomes of patients with AHF.
Metabolic-Associated Steatotic Liver Disease and FGF21 Dysregulation in Seipin-Deficient and BSCL2-Associated Celia's Encephalopathy Murine Models.
Int J Mol Sci
Silvia Cobelo-Gómez, Lía García-Formoso, Antía Fernández-Pombo +7 more
Seipin, a protein encoded by the BSCL2 gene, plays a crucial role in lipid metabolism, and some pathogenic biallelic variants cause lipodystrophy and associated metabolic disorders. This study investigates liver pathology and dysregulation of the FGF21 signalling pathway in two mouse models: Bscl2-/- (knock-out) and Bscl2Celia/Celia (knock-in). We evaluated liver histopathology using H&E and Oil red O staining, assessed hepatic triglyceride levels via enzymatic assays, and analyzed gene expression of key FGF21-related components (Fgf21, Ppargc1a, Fgfr1, and Klb) using quantitative real-time PCR. The liver histology was scored using the NAFLD activity score (NAS) system. Both models exhibited hepatic steatosis and inflammatory features. The Bscl2-/- mice showed more pronounced liver damage, including ballooning degeneration and fibrosis. Gene expression analysis revealed a significant increase in Fgf21 in both models, suggesting an adaptive response to liver injury. Notably, Fgfr1 and Ppargc1a expression was moderately elevated in severe neurologically affected mice showing less hepatic involvement, suggesting a potential adaptive or protective association of these genes with reduced steatosis. Seipin deficiency leads to metabolic-associated steatotic liver disease and dysregulated FGF21 signalling. These findings provide insight into the pathophysiological mechanisms of lipodystrophy and liver disease and suggest that the FGF21 pathway could be a therapeutic target for treating seipin-related metabolic disorders.
Apelin-13 Attenuates Blood-Brain Barrier Dysfunction Following Intracerebral Hemorrhage via Targeting the Keap1/Nrf2 Signaling.
CNS Neurosci Ther
Pingping Guo, Rabeea Siddique, Juanfeng Qian +3 more
Blood-brain barrier (BBB) dysfunction serves as a critical driver of the secondary brain injury following intracerebral hemorrhage (ICH). Previous research has indicated that Apelin-13 demonstrates the potential to alleviate BBB dysfunction in various cerebrovascular disorders. However, the precise mechanisms through which Apelin-13 preserves BBB integrity remain elusive. This study investigated whether Apelin-13 exerted neuroprotective effects by targeting the Keap1/Nrf2 signaling.
The Neuropsychological Dimensions to Pathogenesis of Chronic Spontaneous Urticaria Beyond Autoallergy - A Brief Narrative Review.
Indian Dermatol Online J
M Sendhil Kumaran, Sahibpreet Kaur, Davinder Parsad +1 more
Chronic spontaneous urticaria (CSU) is a burdensome dermatological condition with a complex, multifactorial pathogenesis involving intricate immune, neurological, and psychological interactions. While traditional models primarily emphasize auto-allergic mechanisms, evidence highlights the critical role of neuroimmune interaction in the chronicity and exacerbation of disease. This review examines the neuroimmune contributions to CSU pathogenesis, focusing on mast cell (MC)-sensory neuron interactions, autonomic nervous system dysregulation, neuroinflammatory pathways, and psychological comorbidities that perpetuate disease activity. A comprehensive narrative review of the literature was undertaken, evaluating mechanisms such as MC activation through immunoglobulin-E (IgE)-independent pathways, neuropeptide-mediated inflammation, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and psychiatric associations with CSU. Findings indicate that beyond the classical IgE-mediated MC degranulation, neurogenic inflammation via Mas-Related G-Protein Coupled Receptor X2 (MRGPRX2) receptors-triggered by neuropeptides such as substance P and vasoactive intestinal peptide-plays a pivotal role. Chronic psychological stress activates the HPA axis, contributing to MC hyperactivity and reinforcing the pruritus-stress cycle. Furthermore, a high prevalence of psychiatric comorbidities, including anxiety and depression, contributes to central sensitization and worsens disease severity. The interplay of T cells, basophils, eosinophils, and endothelial cells further amplifies the neuroimmune-inflammatory network. These insights suggest that optimal CSU management requires an integrated approach encompassing dermatological, immunological, and psychological interventions. Emerging therapies targeting neuroimmune pathways, such as MRGPRX2 antagonists, beta-adrenergic blockers, and cognitive-behavioral strategies, show promise. Future research should prioritize the development of personalized neuroimmune-directed therapies to enhance disease control in CSU.
Collagen supplementation and regenerative health: advances in biomarker detection and smart material integration.
Front Nutr
Tatjana Ivaskiene, Jonas Viskelis, Paulina Streimikyte +3 more
Collagen, the most abundant structural protein in the human body, plays a key role in skin integrity, tissue repair, and extracellular matrix organization. With increasing consumer and clinical interest, collagen supplementation has expanded rapidly, yet scientific evidence supporting its efficacy in anti-aging and regenerative applications remains inconsistent. This review critically evaluates current evidence on oral collagen supplementation, integrating insights from over 60 clinical studies assessing its effects on skin aging, musculoskeletal health, and hair disorders. Emerging data suggest that hydrolyzed collagen peptides may improve skin elasticity, joint function, and recovery after exercise, particularly when co-supplemented with vitamin C, silica, or resveratrol. Beyond supplementation, recent advances in biosensing and material science have enabled novel approaches to collagen detection and targeted delivery. Electrochemical, optical, and molecularly imprinted polymer (MIP)-based biosensors facilitate real-time monitoring of collagen biomarkers such as CTX-I, MMPs, and hydroxyproline, supporting precision assessment of collagen metabolism. In parallel, collagen-based hydrogels, nanoparticles, and electroresponsive scaffolds have shown promise as biocompatible carriers for controlled drug release and regenerative therapy. Collectively, these developments outline a translational framework connecting collagen supplementation, detection, and delivery. Continued integration of biosensing and smart material technologies may enhance clinical monitoring and therapeutic efficacy, advancing collagen-based interventions toward precision dermatology and regenerative medicine.
Involvement of substance P/NK1 receptor system in central sensitization in chronic pain.
Neurosci Lett
Juan Chen, Yimin Lai, Wei Li
Chronic pain has become a serious health issue, affecting more than 30% of people worldwide. One of the main mechanisms of chronic pain is central sensitization. It is well known that substance P (SP) and its receptor, Neurokinin 1 receptor (NK1R), play an important role in transmission of nociceptive signals. However, whether SP/NK1R system is involved in central sensitization in chronic pain remains controversial. In the present study, we adopted spared nerve injury (SNI) mouse model to induce neuropathic pain and assessed the role of SP/NK1R system in the development of hyperalgesia and central sensitization. We observed that hyperalgesia occurred in non-injured body part of SNI mice in tail withdrawal test. We also demonstrated hyperexcitability of S1 apical dendrites in SNI mice. Notably, the hyperalgesia behavior and hyperactivity of S1 apical dendrites were alleviated by NK1R antagonist L-703606. These results indicate that SP/NK1R system is involved in central sensitization in chronic pain.
Uridine-Cytidine Kinase 2 (UCK2)/Uridine-Cytidine Kinase Like 1 (UCKL1) complex exacerbates the differentiation of myocardial fibroblasts via TRIM21/Smurf2/Smad3 pathway after myocardial infarction.
Mol Biomed
Xiao Zhou, Yu Zhang, Hao Wang +5 more
Cardiac fibrosis following myocardial infarction (MI) is a pivotal driver of ventricular dysfunction and heart failure, yet the molecular checkpoints orchestrating the persistent activation of cardiac fibroblasts remain incompletely defined. Here, we uncover a non-canonical, metabolism-independent function of Uridine-Cytidine Kinase 2 (UCK2) and Uridine-Cytidine Kinase Like-1 (UCKL1) as synergistic regulators of pathological remodeling. We demonstrate that both proteins are robustly upregulated in the border zone of ischemic murine hearts and transforming growth factor-β (TGF-β)-activated human cardiac fibroblasts (HCFs). Mechanistically, UCK2 and UCKL1 physically assemble into an obligate functional complex that acts as a molecular scaffold rather than a metabolic enzyme. This complex recruits the E3 ubiquitin ligase Tripartite Motif Containing 21 (TRIM21) to orchestrate the specific ubiquitination and degradation of the negative regulator SMAD Specific E3 Ubiquitin Protein Ligase 2 (Smurf2), thereby sustaining SMAD Family Member 3 (Smad3) phosphorylation and amplifying fibrogenic TGF-β signaling. Disruption of this axis via combined genetic silencing exerts a synergistic protective effect by abrogating myofibroblast differentiation and extracellular matrix production. Furthermore, therapeutic intervention using adeno-associated virus (AAV)-mediated knockdown of UCK2/UCKL1 significantly attenuates adverse ventricular remodeling, limits scar expansion, and preserves cardiac function in a murine MI model. Collectively, these findings identify the UCK2/UCKL1-TRIM21-Smurf2-Smad3 axis as a novel, druggable signalosome linking kinase "moonlighting" functions to transcriptional reprogramming, offering a transformative therapeutic strategy to arrest the progression of post-ischemic heart failure.
Neuroimmune Crosstalk in Psoriasis: Mechanisms and Therapeutic Implications.
Inflammation
Hanlin Gao, Yi Fang, Yue Zhang +3 more
Psoriasis is a chronic, immune-mediated inflammatory skin disorder characterized by keratinocyte hyperproliferation, dermal vascular remodeling, and dense immune cell infiltration. While the conventional immunopathological model emphasizes the IL-23/Th17 axis and aberrant T-cell responses, growing evidence highlights the central role of neuroimmune crosstalk in the initiation, amplification, and persistence of disease. This review systematically dissects the cellular and molecular mechanisms underpinning neuroimmune interactions in psoriasis, focusing on the dynamic interplay between peripheral nerve fibers, keratinocytes, and immune cells. Key neuropeptides—such as calcitonin gene-related peptide (CGRP), substance P (SP), nerve growth factor (NGF), and vasoactive intestinal peptide (VIP)/PACAP—emerge as critical mediators that activate proinflammatory signaling cascades and perpetuate a positive feedback loop involving IL-23, IL-17, and other cytokines. Concurrently, neurotransmitters including norepinephrine (NE), acetylcholine (ACh), and dopamine (DA) modulate dendritic cell activation, Th17 polarization, and epidermal inflammation via adrenergic, cholinergic, and dopaminergic pathways. Importantly, both central and peripheral nervous systems are implicated in neuroinflammatory sensitization, with IL-17 A, IL-1β, and TNF-α disrupting neuronal homeostasis and contributing to pruritus, pain, and stress-induced relapse. We further summarize emerging therapeutic strategies targeting the neuroimmune axis—such as TRPV1 antagonists, botulinum neurotoxins, NK1R inhibitors, and vagus nerve stimulation—which offer promising avenues for personalized and mechanism-based interventions. By reframing psoriasis as a neuroimmune disorder, this review provides new conceptual insights into disease heterogeneity and points toward innovative treatment paradigms.
Exogenous hydrogen sulfide inhibits the progression of vascular dysfunction and hypertension mediated by the renin-angiotensin system in chronic kidney disease.
Biochem Pharmacol
Jorge A Tapia-Martínez, Diana L Silva-Velasco, Jesus H Beltran-Ornelas +3 more
Chronic kidney disease (CKD) overactivates the renin-angiotensin system (RAS), causing vascular dysfunction and hypertension. Additionally, hydrogen sulfide (H2S) is a gasotransmitter that modulates the cardiovascular system by attenuating the RAS. Therefore, this study aimed to investigate the effects of chronic administration of sodium hydrosulfide (NaHS, an exogenous H2S donor) on RAS-mediated vascular responses, oxidative stress, and progression of hypertension in rats with CKD. Thirty-two normotensive male Wistar rats were divided into four groups (n = 8): 1) sham + vehicle (1 mL/kg/d, 100 mM of phosphate buffer, PBS), 2) sham + NaHS (5.6 mg/kg/d), 3) CKD induced by 5/6 nephrectomy + vehicle, and 4) CKD + NaHS. One week after surgery, pharmacological treatments began and were administered intraperitoneally daily for six weeks. Hemodynamic variables, renal function, and H2S serum levels were assessed. Additionally, H2S formation, oxidative stress, and the expression of AT1, AT2, Mas receptors, and H2S-synthesizing enzymes, along with vascular responses to angiotensin (1-7), angiotensin II and H2S were assessed in the thoracic aorta. CKD impairs: 1) RAS-mediated vascular responses; 2) downregulates Mas receptor expression; 3) upregulates AT1 and AT2 receptor expression; 4) increases H2S-mediated vascular response, 5) decreases H2S levels, tissue production of H2S and the expression of the producing enzymes; and 6) induces oxidative stress. Interestingly, NaHS treatment prevented CKD-induced impairments. In conclusion, NaHS administration protects against RAS-mediated vascular dysfunction and progression of hypertension by preventing alterations in AT1, AT2, Mas receptors, H2S-synthesizing enzymes, and oxidative stress.
Elevated plasma cancer antigen-125 level is associated with increased risk of new-onset atrial fibrillation after acute myocardial infarction.
Front Cardiovasc Med
Yuan Fu, Kun Zuo, Mulei Chen +2 more
New-onset atrial fibrillation (NOAF) is the most commonly encountered arrhythmia during the course of acute myocardial infarction (AMI) and is independently associated with a worse prognosis.
Interleukin-35 alleviates pulmonary arterial hypertension by suppressing the VEGFA/VEGFR2 signaling pathway.
Life Sci
Jie Feng, Kai Li, Leilei Han +2 more
Pulmonary arterial hypertension (PAH) is a serious circulatory disorder defined by elevated pulmonary arterial pressure (PAP) with normal pulmonary capillary wedge pressure (PCWP), driven by pathological remodeling of pulmonary arterioles. If left untreated, it can lead to severe health complications and death. Current treatments, such as endothelin receptor antagonists and phosphodiesterase-5 inhibitors, prostacyclin analogs, and soluble guanylate cyclase stimulators-these agents relieve symptoms, improve exercise capacity, and delay disease progression but do not target the underlying vascular pathology. Because these therapies fail to improve long-term prognosis, they impose a heavy burden on patients, families, and society. Thus, there is an urgent need to develop new therapeutic agents that can treat PAH more effectively. Interleukin-35 (IL-35), which is primarily produced by regulatory T cells, is a potent molecule exhibiting significant anti-inflammatory and immunomodulatory properties. Recent research suggests that IL-35 shows promise as a novel therapeutic agent for PAH. However, the precise mechanism by which IL-35 influences pulmonary hypertension remains to be elucidated through further experimentation. To address this, we established animal and cellular models and analyzed molecular, functional, and structural changes using western blotting, PAP measurements, flow cytometry, EdU staining, scratch assay, blood biochemistry, immunofluorescence, enzyme-linked immunosorbent assay (ELISA), hematoxylin and eosin (H&E), Immunohistochemistry (IHC) and Masson's trichrome staining. Our results suggest that IL-35 alleviates PAH-induced inflammation, apoptosis, and smooth muscle cell proliferation, reduces PAP, and restores vascular remodeling, thereby mitigating both structural and functional damage in PAH.
Use of Sotatercept to Facilitate Transition From Intravenous to Oral Prostacyclin Therapy.
Clin Respir J
Chebly Dagher, Maria Akiki, Kristen Swanson +4 more
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by increased pulmonary vascular resistance (PVR) leading to right ventricular failure and high mortality. Parenteral prostacyclin therapy remains the cornerstone for high-risk patients but is limited by complications and reduced quality of life. Sotatercept, an activin signaling inhibitor, has recently emerged as an effective adjunct therapy in PAH, improving functional and hemodynamic outcomes. This case series evaluated whether the addition of sotatercept could facilitate the transition from intravenous (IV) to oral prostacyclin in eight high-risk PAH patients who had previously failed transition attempts. All patients received background dual therapy with endothelin receptor antagonists and phosphodiesterase-5 inhibitors and were transitioned from IV to oral treprostinil following the fifth dose of sotatercept. At 24 weeks, all eight patients successfully maintained oral therapy without re-initiation of IV prostacyclin. Significant improvements were observed in 6-min walk distance, WHO functional class, right ventricular systolic pressure, and PVR. No treatment discontinuations or serious adverse events occurred. These findings suggest that adjunctive sotatercept may enable safe and effective transition from parenteral to oral prostacyclin therapy, expanding treatment flexibility and improving quality of life in high-risk PAH patients. Prospective studies are warranted to confirm long-term outcomes.
Unusual Development of Central Diabetes Insipidus after Endovascular Treatment for a Medial Tentorial Dural Arteriovenous Fistula.
J Neuroendovasc Ther
Yuta Oka, Yoshinobu Horio, Munenari Matsuishi +7 more
Medial tentorial dural arteriovenous fistulas (DAVFs) are rare lesions that may cause intracranial hemorrhage or non-hemorrhagic symptoms due to venous congestion from retrograde deep venous drainage. We report a case of a medial tentorial DAVF presenting with cognitive decline and impaired consciousness, successfully treated with transvenous embolization (TVE) and straight sinus angioplasty, and complicated postoperatively by central diabetes insipidus (CDI).