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Corrigendum to 'Tβ4-exosome-loaded hemostatic and antibacterial hydrogel to improve vascular regeneration and modulate macrophage polarization for diabetic wound treatment' [Mater. Today Bio,Volume 31, 2025, 101585].
Mater Today Bio
Hua Yu, Bin Wang, Zihao Li +16 more
[This corrects the article DOI: 10.1016/j.mtbio.2025.101585.].
Comparative Diagnostic Performance of Copeptin After Hypertonic Saline Infusion Versus Water Deprivation Test in Pediatric Patients with Polyuria-Polydipsia Syndrome.
Int J Mol Sci
Diana-Andreea Ciortea, Carmen Loredana Petrea Cliveți, Iolanda Cristina Vivisenco +4 more
Differentiating central diabetes insipidus (CDI), nephrogenic diabetes insipidus (NDI), and primary polydipsia (PP) in pediatric patients with polyuria-polydipsia syndrome (PPS) remains a clinical challenge. The water deprivation test (WDT) is the traditional gold standard; however, it is time-consuming, burdensome, and prone to equivocal results. Stimulated copeptin, a surrogate marker of vasopressin, has emerged as a promising diagnostic alternative. We conducted a prospective, observational, cross-sectional study involving 27 pediatric patients (ages 2-17) presenting with PPS. Each patient underwent a WDT with desmopressin and hypertonic saline infusion (3% NaCl) for stimulated copeptin testing. Diagnostic accuracy was assessed using clinical diagnoses as a reference. The WDT showed high accuracy with an area under the curve (AUC) of 0.97, and there was an increased optimal threshold of ≥14% urine osmolality after desmopressin acetate (1-deamino-8-D-arginine vasopressin, DDAVP) administration (sensitivity 88.9%, specificity 100%). Stimulated copeptin at a threshold of <6.5 pmol/L demonstrated 100% sensitivity and specificity (AUC = 1.00) for CDI versus PP. Basal copeptin ≥21.4 pmol/L accurately identified all NDI cases. The agreement between the WDT and copeptin was low (κ = 0.06, McNemar p = 0.021), suggesting that copeptin has greater specificity, particularly for borderline or partial CDI. These results support the use of stimulated copeptin as a first-line diagnostic tool in pediatric PPS, offering improved objectivity, tolerability, and diagnostic clarity compared with the WDT. Basal copeptin also demonstrated excellent performance in rapid noninvasive NDI identification.
Pathophysiology of COVID-19: A Post Hoc Analysis of the ICAT-COVID Clinical Trial of the Bradykinin Antagonist Icatibant.
Pathogens
Pierre Malchair, Jordi Giol, Javier Jacob +3 more
We used the data from a successful therapeutic assay that used icatibant in patients with hypoxemic COVID-19 pneumonia (the ICAT·COVID trial) to explore pathophysiological mechanisms. We performed concurrent-type, criterion-related validity analyses to assess the discriminative ability of a panel of nine potential serum markers (interleukin 6, ferritin, lactate dehydrogenase, C reactive protein, fibrin fragment D (D-dimer), complement 1 esterase inhibitor (antigenic and functional), complement 4 factor, and lymphocyte count) to predict the clinical milestones. Consistent with previous research, we evidenced a significant relationship between interleukin 6, lactate dehydrogenase and the lymphocyte count, and the clinical events. Furthermore, exposure to icatibant, a bradykinin B2 receptor antagonist (which improved pneumonia and mortality in the aforementioned randomised trial), attenuated this relationship, although this effect faded over time. The results reinforce the key role that the angiotensin-converting enzyme 2 has on COVID-19 pathophysiology as a point of convergence between the renin-angiotensin and kallikrein-kinin systems. This was shown clinically by the successful blocking of inflammatory pathways by icatibant at the bradykinin effector loop level early during the acute hyperinflammatory stage of the disease.
Efruxifermin in Compensated Liver Cirrhosis Caused by MASH.
N Engl J Med
Mazen Noureddin, Mary E Rinella, Naga P Chalasani +16 more
In phase 2 trials involving patients with stage 2 or 3 fibrosis caused by metabolic dysfunction-associated steatohepatitis (MASH), efruxifermin, a bivalent fibroblast growth factor 21 (FGF21) analogue, reduced fibrosis and resolved MASH. Data are needed on the efficacy and safety of efruxifermin in patients with compensated cirrhosis (stage 4 fibrosis) caused by MASH.
Effects of Kisspeptin on rabbit ovulation: a comprehensive study of ovulatory, endocrine and histological response.
Theriogenology
Silvia Gimeno-Martos, Alicia Gómez-León, Bosa Luigia +4 more
Mammalian reproductive function is regulated by hypothalamic neurons that secrete Kisspeptin (Kp), a neuropeptide that stimulates gonadotropin-releasing hormone (GnRH) secretion, triggering pituitary gonadotrophins (LH and FSH) and gonadal steroids. This study evaluated the effect of Kisspeptin-10 (Kp10) on ovulation induction in rabbits, comparing its efficacy with that of the GnRH analogue gonadorelin. Multiparous New Zealand White × California does were assigned to three groups: control group (0.5 % saline solution, i.v.), GnRH group (20 μg gonadorelin, i.m.), and Kp10 group (250 μg Kp10, i.v.). Kp10 induced ovulation in 87.5 % of does, matching the response observed in the GnRH group, with a comparable number of corpora lutea (CL) per ovulated doe (12.9 ± 1.4 vs 14.6 ± 1.4 CL/doe, respectively). On day 7, plasma progesterone (P4) was significantly higher in ovulated GnRH-treated does than in Kp10-treated ones (25.12 ± 4.17 vs 9.47 ± 4.17 ng/mL; p < 0.0211), while non-ovulated controls exhibited minimal P4 concentrations (0.86 ± 0.12 ng/mL). Plasma estradiol (E2) levels showed no significant differences across days or groups, with mean values of 32.74 ± 4.33 pg/mL on day 0 and 37.27 ± 5.49 pg/mL on day 7, respectively. Histological analysis confirmed that Kp10 promoted preovulatory follicle development and CL formation, mirroring GnRH effects. Additionally, Kp10 enhanced angiogenesis, indicated by increased vascular endothelial growth factor (VEGF) expression in more developed follicles and CL. These results suggest that Kp10 could be an alternative to GnRH for ovulation induction in rabbits, although further studies are needed to explore optimal analogues, doses, and administration routes.
Growth Hormone-Releasing Peptide 2 May Be Associated With Decreased M1 Macrophage Production and Increased Histologic and Biomechanical Tendon-Bone Healing Properties in a Rat Rotator Cuff Tear Model.
Arthroscopy
Yinghao Li, Lei Yao, Chunsen Zhang +5 more
To explore the potential of growth hormone-releasing peptide 2 (GHRP-2) for tendon-bone healing in a rat rotator cuff tear (RCT) model.
In silico evaluation of pramlintide dosing algorithms in artificial pancreas systems.
Comput Biol Med
Borja Pons Torres, Iván Sala-Mira, Clara Furió-Novejarque +4 more
Pramlintide's capability to delay gastric emptying has motivated its use in artificial pancreas systems, accompanying insulin as a control action. Due to the scarcity of pramlintide simulation models in the literature, in silico testing of insulin-plus-pramlintide strategies is not widely used. This work incorporates a recent pramlintide pharmacokinetics/pharmacodynamics model into the T1DM UVA/Padova simulator to adjust and validate four insulin-plus-pramlintide control algorithms. The proposals are based on an existing insulin controller and administer pramlintide either as independent boluses or as a ratio of the insulin infusion. The results of the insulin-pramlintide algorithms are compared against their insulin-alone counterparts, showing an improvement in the time in range between 3.00% and 10.53%, consistent with results reported in clinical trials in the literature. Future work will focus on individualizing the pramlintide model to the patients' characteristics and evaluating the implemented strategies under more challenging scenarios.
New players in the leptin orchestra: PNOC/NPY neurons tune appetite and obesity.
Neuron
Olivier Lavoie, Natalie J Michael, Alexandre Caron
Leptin regulates energy balance through the brain, yet its key neuronal targets remain unclear. Solheim et al.1 identify hypothalamic GABAergic PNOC/NPY neurons as mediators of leptin's anorectic effects, advancing our understanding of neurocircuits linking adiposity signals to feeding control.
The Synergistic and Attenuated Mechanism of Action of the Xihuang Pill in Dual Immunotherapy After Stenting for Advanced Cholangiocarcinoma: A Controlled Clinical Trial.
Int J Gen Med
Peng Wang, Yu-Huan Wang, Yun Tao +2 more
This study aims to investigate the synergistic and attenuation mechanism of Xihuang pill in the treatment of cholangiocarcinoma (CCA), thereby providing a reliable scientific basis for the selection of postoperative treatment strategies in cholangiocarcinoma patients.
Evaluating Hepatokines in the Progression of Non-alcoholic Fatty Acid Liver Disease by Decoding Liver-Derived Molecular Pathologies.
Cureus
Shehwar Ahmed, Muhammad Ahmed, Faizan Abbas +6 more
Non-alcoholic fatty liver disorder (NAFLD), also called metabolic dysfunction-associated steatotic liver disease (MASLD), is a leading cause of global liver disorders. Hepatokines are increasingly being used in the diagnosis of NAFLD. This study evaluated the association between the hepatokines and NAFLD progression and guided further therapeutic research. Data search was conducted across PubMed, Embase, Scopus, and Web of Science up to March 2025. Studies that assessed hepatokines in NAFLD were selected based on defined inclusion criteria. The Newcastle-Ottawa Scale (Version 2011), the Cochrane Risk of Bias 2 (RoB 2) tool, and the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) methodology were used to evaluate the RoB and the certainty of evidence. Pooled estimates were synthesized by using a random-effects meta-analysis model. Ten studies passed the eligibility criteria and involved a pooled sample size of 4,215 participants. Meta-analysis of six studies revealed that an increase in hepatokine levels was modestly correlated with NAFLD (odds ratio (OR) 1.11; 95% confidence interval (CI) 1.01-1.22; P = 0.037; I² = 84%). Individual biomarkers such as Fetuin-A, angiopoietin-like protein 8 (ANGPTL8), fibroblast growth factor 21 (FGF21), and retinol-binding protein 4 (RBP4) showed varying degrees of correlation. RoB was moderate across eight studies, low and high across one study each, and GRADE assessments displayed low to moderate quality of evidence. The research findings established a steady connection between NAFLD and variation in hepatokine levels. Fetuin-A and FGF21 showed promise as biomarkers against NAFLD diagnosis. However, uncertainty remained because of high variability and moderate levels of experimental bias. Further research needs to be conducted through standardized methods for assays in multicenter longitudinal studies to confirm hepatokine diagnostic and therapeutic effectiveness in treating patients with NAFLD.
Oxytocin can ameliorate social deficits and brain developmental impairments in a rat model of early life excessive screen time exposure.
Brain Res Bull
Mozhan Parsa, Monireh Mansouri, Hamidreza Pouretemad
In recent years studies have shown that early life excessive screen time exposure may significantly contribute to the emergence of social deficits and autistic-like behaviors. However, the exact underlying mechanisms and the optimal treatment strategies are not completely understood, with conflicting results of preceding findings. This study investigates the effect of oxytocin on autism-related behaviors, and associated brain structure abnormalities induced by excessive audiovisual stimulation (EAVS) as an early life excessive screen exposure model in rats. Neonatal rat pups were exposed to EAVS from postnatal day (PND) 12 to PND 35, and intranasal oxytocin (OXT) at a dose of 0.8 IU/kg was administrated from PND21 to PND35. Behavioral assessment including social interaction, repetitive behavior, locomotor activity, and anxiety-like behavior, along with three-dimensional brain structure measurements were done during adolescence (PND50-PND55). The results revealed EAVS-induced anomalies in social interaction, hyperactivity, and changes in the volume, and neuron number of brain regions including the amygdala and anterior cingulate cortex (ACC) in the EAVS group which were modulated by oxytocin. Our findings suggest that OXT may mitigate adverse effects of early life excessive exposure to digital screens, enhancing social preferences through modulating brain plasticity. The observed neuroanatomical and behavioral alterations highlight the vulnerability of the developing brain to early life excessive screen exposure and suggest a potential therapeutic path through OXT to tackle social impairments induced by EAVS.
2024 SOGC, 2024 NCCN, 2022 ESO-ESMO, and 2018 ASCO: a comparison of female cancer survivorship guidelines for the management of sexual health concerns.
Support Care Cancer
Jashmira K Bhinder, Samantha K F Kennedy, Carmen Faouk Al Aadah +1 more
Female cancer survivors often experience sexual dysfunction, which is a significant and increasingly recognized aspect of survivorship. This review compares guidelines from the American Society of Clinical Oncology (ASCO), the European School of Oncology-European Society of Medical Oncology (ESO-ESMO), the National Comprehensive Cancer Network (NCCN), and the Society of Obstetricians and Gynaecologists of Canada (SOGC) for managing sexual health symptoms.
MOTS-c-modified functional self-assembly peptide hydrogels enhance the activity of nucleus pulposus-derived mesenchymal stem cells of intervertebral disc degeneration.
Mater Today Bio
Yuan Lin, Ruo-Yu Yang, Jie Li +10 more
Intervertebral disc degeneration (IDD) is characterized by oxidative-stress driven progressive apoptosis and senescence of nucleus pulposus mesenchymal stem cells (NP-MSCs). MOTS-c, a 16-amino acid peptide encoded by the mitochondrial 12S rRNA open reading frame, has emerged as a key regulator of cellular metabolism, oxidative stress, and senescence. This study investigated the therapeutic potential of MOTS-c in countering tert-butyl hydroperoxide (TBHP)-induced oxidative damage in NP-MSCs, and we developed a novel biomaterial strategy for IDD treatment.Key findings include.
Carpal Tunnel Syndrome Attributed to Medication Use: A Pharmacovigilance Study.
Cureus
Andrew Mihalache, Emily Volfson, Ryan Huang +2 more
Carpal tunnel syndrome (CTS) is a prevalent compression neuropathy with multiple well-documented mechanical and systemic risk factors. However, the role of pharmacological agents in the development of CTS remains underexplored. This study aims to identify drugs disproportionately associated with CTS reports using data from the Food and Drug Administration Adverse Event Reporting System (FAERS).
The Prognostic Significance of TMSB4X in Glioma Patients.
Int J Gen Med
Sijie Li, Tianyi Fan, Zengyao Hao +6 more
The goal of this study was to analyze in depth the importance of the thymosin beta 4 X-linked gene (TMSB4X) in the disease process of gliomas for the prediction of patient prognosis.
SASH1 Mutations and Hereditary Disorders of Pigmentation: Review of Literature.
Pigment Cell Melanoma Res
Anuradha Bishnoi, Aarushi Arunima, Keshavamurthy Vinay +2 more
Dyschromatosis universalis hereditaria (DUH) is a rare genodermatosis characterized by asymptomatic hyper- and hypopigmented macules appearing in infancy and persisting for life. Although mutations in ABCB6 account for many DUH cases, recently, the SAM and SH3 domain-containing 1 (SASH1) gene has emerged as a key player in DUH. Additionally, SASH1 mutations have been associated with the pure-lentiginous phenotype of familial pigmentation. In this review of literature, we found 22 different SASH1 mutations, most inherited in an autosomal dominant manner. These variants cause distinct phenotypes, including DUH, lentiginosis, and rarely, an autosomal recessive syndromic form with alopecia, palmoplantar keratoderma, and increased risk of malignancies. Functional studies have revealed that SASH1 acts as both a tumor suppressor and a pro-melanogenic factor. It modulates key pathways such as p53-POMC-α-MSH-MC1R-MITF and Gαs-SASH1-IQGAP1-E-cadherin pathways, affecting melanosome production, transport, and melanocyte migration. This unique dual role of SASH1 highlights its importance in melanocyte homeostasis and UV-induced pigmentation. Understanding the role of SASH1 in regulating pigmentation can help foster novel therapeutic approaches for these genodermatoses and related pigmentary anomalies, ultimately improving patient care and outcomes.
Ifosfamide-Induced Partial Arginine Vasopressin Resistance Responsive to Vasopressin/Desmopressin and Amiloride.
Cureus
Nicholas Ma, Haley Wilt, Patrick Donabedian +1 more
This is a case of partial arginine vasopressin resistance following the sixth cycle of doxorubicin-ifosfamide-mesna therapy for recurrent spindle cell sarcoma of the thigh. Polyuria and symptomatic hypernatremia started by the second day of the two-day chemotherapy cycle. The diagnosis was confirmed with serum and urine chemistry testing showing urine hypo-osmolality (161 mOsm/kg) with polyuria (4.8 L urine output) in 24 hours, serum hyperosmolality (355 mOsm/kg), and an elevated baseline plasma copeptin of 82 pmol/L. Treatment with intravenous vasopressin followed by amiloride and supraphysiologic doses of oral desmopressin improved symptomatic hypernatremia.
Oxytocin and autism: Insights from clinical trials and animal models.
Curr Opin Neurobiol
Chuan Xing, Xiang Yu
Autism spectrum disorder is a highly heritable and heterogeneous neurodevelopmental disorder, characterized by impaired social interactions and repetitive behaviors. Despite its complex etiology, increasing evidence has linked autism to the oxytocin system. The oxytocin peptide has long been known as the "social hormone," and has been shown to increase attention to social cues, elevate salience of socially relevant stimuli, and increase learning and reward in social situations. Reduced oxytocin levels and mutations in the oxytocin system have been reported in autism patients, while exogenously delivered oxytocin has been shown to alleviate social interaction deficits in both patients and animal models. Here, we summarize the results of recent clinical trials using oxytocin nasal spray to treat individuals with autism, as well as studies of autism animal models with oxytocin system deficits, and the rescue of their social behavior deficits by oxytocin. Finally, we discuss factors influencing clinical outcomes and reflect on future directions.
The mitochondrial-targeted peptide therapeutic elamipretide improves cardiac and skeletal muscle function during aging without detectable changes in tissue epigenetic or transcriptomic age.
bioRxiv
Wayne Mitchell, Gavin Pharaoh, Alexander Tyshkovskiy +3 more
Aging-related decreases in cardiac and skeletal muscle function are strongly associated with various comorbidities. Elamipretide (ELAM), a novel mitochondrial-targeted peptide, has demonstrated broad therapeutic efficacy in ameliorating disease conditions associated with mitochondrial dysfunction across both clinical and pre-clinical models. ELAM is proposed to restore mitochondrial bioenergetic function by stabilizing inner membrane structure and increasing oxidative phosphorylation coupling and efficiency. Although ELAM treatment effectively attenuates physiological declines in multiple tissues in rodent aging models, it remains unclear whether these functional improvements correlate with favorable changes in molecular biomarkers of aging. Herein, we investigated the impact of 8-week ELAM treatment on pre- and post- measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways. We found that health status, as measured by frailty index, cardiac strain, diastolic function, and skeletal muscle force are significantly diminished with age, with skeletal muscle force changing in a sex-dependent manner. Conversely, ELAM mitigated frailty accumulation and was able to partially reverse these declines, as evidenced by treatment-induced increases in cardiac strain and muscle fatigue resistance. Despite these improvements, we did not detect statistically significant changes in gene expression or DNA methylation profiles indicative of molecular reorganization or reduced biological age in most ELAM-treated groups. However, pathway analyses revealed that ELAM treatment showed pro-longevity shifts in gene expression such as upregulation of genes involved in fatty acid metabolism, mitochondrial translation and oxidative phosphorylation, and downregulation of inflammation. Together, these results indicate that ELAM treatment is effective at mitigating signs of sarcopenia and heart failure in an aging mouse model, but that these functional improvements occur independently of detectable changes in epigenetic and transcriptomic age. Thus, some age-related changes in function may be uncoupled from changes in molecular biological age.
ELABELA-32 Alleviates Doxorubicin-Induced Chronic Cardiotoxicity by Inhibiting the TGF-β/Smad Signaling Pathway.
Cardiovasc Toxicol
Shuang Zhou, Zhuo Meng, Lin Lu +5 more
Cardiac fibrosis, oxidative stress, and cardiomyocyte apoptosis are key contributors to the progression of doxorubicin (DOX)-induced cardiotoxicity. ELABELA (ELA) is an early endogenous ligand of apelin receptor (APJ/APLNR), which is a G protein-coupled receptor with seven transmembrane domains. Our present study aimed to investigate the protective role and underlying mechanism of ELA-32 in mitigating oxidative stress and fibrosis associated with DOX-induced cardiotoxicity. Using a mouse model of chronic DOX cardiotoxicity (5 mg/kg, i.p, once a week for four times, the total cumulative dose is 20 mg/kg), it was found that exogenous administration of ELA-32 using a microinjection pump significantly improved cardiac function, reduced oxidative stress, and myocardial fibrosis, and enhanced survival. Furthermore, pretreatment with ELA-32 peptide protected rat cardiomyocytes (H9C2 cells) from DOX-induced cytotoxicity in vitro. However, these cardioprotective effects of ELA-32 were no longer observed after activation of the Smad signaling pathway using TGF-β1. In summary, ELA-32 attenuated DOX-induced cardiac fibrosis through by modulating the TGF-β/Smad signaling pathway, thus highlighting its potential as a therapeutic agent for preventing chronic DOX-related cardiotoxicity.