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Synergistic Effects of Injectable Platelet-Rich Fibrin and Bioactive Peptides on Dermal Fibroblast Viability and Extracellular Matrix Gene Expression: An In Vitro Study.
Molecules
Ana Giulia Lenci Paccola, Thomas Marcelino Couto Dos Santos, Maria Clara Minelo +6 more
Facial aging is a multifactorial process involving changes in bone, fat compartments, ligaments, muscles, and skin. Collagen biostimulators, including synthetic agents and autologous platelet concentrates, have gained attention for facial rejuvenation. Injectable platelet-rich fibrin (i-PRF), a second-generation autologous concentrate, has shown promising regenerative properties due to its natural composition and growth factors. Cosmetic peptides, such as palmitoyl pentapeptide-4 (Matrixyl) and Tetrapeptide-21 (GEKG), are also studied for their ability to stimulate collagen synthesis and remodel the extracellular matrix. This in vitro study examined the potential synergistic effects of i-PRF combined with Matrixyl or GEKG on human dermal fibroblast viability, proliferation, and ECM-related gene expression. Fibroblasts were cultured under six conditions: control, i-PRF alone, Matrixyl alone, GEKG alone, i-PRF + Matrixyl, and i-PRF + GEKG. Viability and proliferation were assessed via MTT, crystal violet, and RealTime-Glo™ assays. Gene expression of COL1A1, FN1, and HAS1 was measured using RT-qPCR. The combinations, especially i-PRF + GEKG, led to increased cell viability and upregulated ECM-related genes at 72 h. These effects were stronger than the individual treatments, suggesting synergistic effects, especially with GEKG. These findings highlight the clinical potential of combining autologous platelet concentrates with bioactive peptides for dermal regeneration. Further preclinical and clinical studies are warranted.
Cardiac pathology in a patient with a novel pathogenic variant c.703del (p.Ile235SerfsTer4) of the TAFAZZIN gene.
Cardiovasc Pathol
Marisa Prasanpanich, Majid Husain, Nancy J Halnon +4 more
Barth syndrome is a mitochondrial disease caused by loss-of-function mutations in the TAFAZZIN gene located on chromosome Xq28 encoding a transacylase essential for cardiolipin remodeling. Most patients develop dilated cardiomyopathy and progressive heart failure within the first year of life with some requiring cardiac transplantation.
Real-world drug safety study of somatostatin analogs based on the food and drug administration adverse event reporting system database.
Eur J Pharmacol
Wangyu Ye, Zhen Liu
Somatostatin analogs (SSAs), synthetic peptides mimicking endogenous somatostatin, are widely used to treat neuroendocrine tumors and acromegaly. However, their use is often accompanied by adverse events (AEs) that may compromise patient safety. This study systematically evaluated AE signals associated with SSAs using the FDA Adverse Event Reporting System (FAERS) database to inform clinical practice.
Adrenomedullin production by adult cardiac fibroblasts via NF-κB/STAT6 signaling enhances post-infarction lymphangiogenesis and cardiac repair.
Sci Rep
Yuimi Matsuoka, Yuuki Shimizu, Haihang Luo +5 more
Myocardial infarction (MI) remains the leading cause of death worldwide. We previously found that a specific population of human fetal cardiac fibroblasts (fCFs), which express vascular cell adhesion molecule 1 (VCAM1), have cardioprotective effects after MI, inducing reparative cardiac lymphangiogenesis. This study investigated whether adult cardiac fibroblasts (aCFs), which are more feasible for autologous transplantation, differ in surface marker expression and lymphangiogenic potential compared to fCFs. Furthermore, we examined whether aCFs could be exogenously manipulated to acquire fCF-like lymphangiogenic potential and serve as a cell therapy for MI and MI-associated heart failure. In vivo MI models (rat and mouse) and in vitro coculture assays with lymphatic endothelial cells were conducted. We found that TNF-α and IL-4 stimulation induced aCFs to express VCAM1 via NF-κB and STAT6 signaling, yielding a subpopulation termed adult VCAM1+ cardiac fibroblasts (aVCFs). These aVCFs, distinct from myofibroblasts, expressed CD90 and improved cardiac function post-MI. Adrenomedullin (ADM) was identified as a key paracrine effector, and its knockdown attenuated the pro-lymphangiogenic and cardioprotective effects of aVCFs. Our findings demonstrate that aVCFs promote cardiac lymphangiogenesis and protect cardiac function following MI, highlighting their potential as an autologous cell therapy.
Increased DNA methylation of Igf2 in the male hippocampus regulates age-related deficits in synaptic plasticity and memory.
Brain Res Bull
Shannon Kincaid, Courtney P Stickling, Kayla Farrell +9 more
The aging process is characterized by a general decline in cognitive abilities, which affects nearly 33 % of U.S. adults over the age of 70 and is a risk factor for the development of dementia and Alzheimer's disease. Numerous studies have reported increased neuroinflammation and impaired synaptic plasticity and memory with age in the hippocampus, a major brain region involved in the formation and storage of most memories. However, much remains unknown about the mechanisms that contribute to age-related deficits in synaptic plasticity and memory. The Insulin-like growth factor 2 (Igf2) is a genomic imprinted gene that is expressed from a single allele in all species. Though IGF2 has been shown to be important in development, synaptic plasticity, and memory formation in the hippocampus and administration of IGF2 can improve memory late in life, whether changes in regulation of this gene contribute to age-related memory decline have yet to be explored. Here, we show that aged (24 months) male rats have increased CpG-site specific promoter methylation and reduced expression of Igf2 in the hippocampus relative to young adult (3 months) and middle-aged (12 months) rats. Importantly, CRISPR-dCas9 mediated increase of DNA 5-hydroxymethylation, an active transcriptional mark, of the Igf2 promoter in the hippocampus improved memory and long-term potentiation in aged, but not middle-aged, rats. These data indicate that increased DNA methylation of Igf2 in the hippocampus contributes to age-related deficits in synaptic plasticity and memory.
Exercise-Induced Muscle-Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging.
Pharmaceuticals (Basel)
Amelia Tero-Vescan, Hans Degens, Antonios Matsakas +3 more
Regular physical activity induces a dynamic crosstalk between skeletal muscle and adipose tissue, modulating the key molecular pathways that underlie metabolic flexibility, mitochondrial function, and inflammation. This review highlights the role of myokines and adipokines-particularly IL-6, irisin, leptin, and adiponectin-in orchestrating muscle-adipose tissue communication during exercise. Exercise stimulates AMPK, PGC-1α, and SIRT1 signaling, promoting mitochondrial biogenesis, fatty acid oxidation, and autophagy, while also regulating muscle hypertrophy through the PI3K/Akt/mTOR and Wnt/β-catenin pathways. Simultaneously, adipose-derived factors like leptin and adiponectin modulate skeletal muscle metabolism via JAK/STAT3 and AdipoR1-mediated AMPK activation. Additionally, emerging exercise mimetics such as the mitochondrial-derived peptide MOTS-c and myostatin inhibitors are highlighted for their roles in increasing muscle mass, the browning of white adipose tissue, and improving systemic metabolic function. The review also addresses the role of anti-inflammatory compounds, including omega-3 polyunsaturated fatty acids and low-dose aspirin, in mitigating NF-κB and IL-6 signaling to protect mitochondrial health. The resulting metabolic flexibility, defined as the ability to efficiently switch between lipid and glucose oxidation, is enhanced through repeated exercise, counteracting age- and disease-related mitochondrial and functional decline. Together, these adaptations demonstrate the importance of inter-tissue signaling in maintaining energy homeostasis and preventing sarcopenia, obesity, and insulin resistance. Finally, here we propose a stratified treatment algorithm based on common age-related comorbidities, offering a framework for precision-based interventions that may offer a promising strategy to preserve metabolic plasticity and delay the age-associated decline in cardiometabolic health.
Efficacy and safety of incretin co-agonists: Transformative advances in cardiometabolic healthcare.
World J Cardiol
Sowrabha Bhat, Cornelius J Fernandez, Vijaya Lakshmi +1 more
The ground-breaking development of the incretin agonists by manipulation of the incretin system, including the gut hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), as well as the pancreatic hormone glucagon, has led to the emergence of promising pharmacotherapy for metabolic health. The GLP-1 receptor agonists (GLP-1RAs), namely liraglutide, dulaglutide, albiglutide, exenatide, and semaglutide, have been found to have beneficial effects on glycated hemoglobin, weight, lipid profile, and liver fat and thereby improving cardiometabolic health. Other drugs of the same group in development include Orforglipron, which has a high weight loss efficacy (-15% weight reduction). Long-acting GLP-1RAs in trials are Ecnoglutide, Efpeglenatide, TG103, and Visepegenatide. Many of these have cardiovascular benefits in terms of reduction in MACE (Non-fatal MI, Non-fatal stroke, and mortality). Tirzepatide is a dual GIP/GLP-1RA, the first drug of the group to be approved for diabetes and obesity with remarkably lower gastrointestinal side effects compared to GLP-1 monoagonists. The dual GLP-1/glucagon co-agonists cause tremendous weight loss due to the synergistic action. Most drugs in this class are long-acting and developed for once-weekly administration. The revolutionary triple agonists at the GLP-1, GIP, and Glucagon receptors have demonstrated the highest achievable weight loss with pharmacotherapy. Retatrutide and Efocipegtrutide belong to this novel group of drugs. The newer drugs in the broad category of incretin co-agonists include the GLP-1/amylin receptor agonist like CagriSema and Amycretin, oral GLP-1 agonists other than semaglutide, and the peptide YY/GLP-1 receptor dual agonists. The profound biochemical and weight loss outcomes associated with incretin co-/poly-agonists are expected to translate into outstanding cardiometabolic benefits, the theme of this evidence review.
The Renin-Angiotensin-Aldosterone System (RAAS): Beyond Cardiovascular Regulation.
Vet Sci
Agnese Valentini, Romy M Heilmann, Anna Kühne +3 more
The renin-angiotensin-aldosterone system (RAAS) plays a pivotal role in regulating cardiovascular function, fluid balance, and blood pressure. Recent research has revealed the RAAS's influence extends beyond cardiovascular physiology, encompassing key roles in inflammation, fibrosis, immune regulation, cancer progression, and organ-specific disease mechanisms. This review provides a comprehensive overview of classical and alternative RAAS pathways, focusing on the dual roles of angiotensin II (Ang II) and angiotensin-(1-7) (Ang 1-7), mediated through AT1R, AT2R, MasR, and MrgD receptors. We discuss molecular signaling cascades, including mitochondrial, nuclear, and caveolae-mediated mechanisms, and explore the impact of RAAS modulation on hepatic fibrosis, vascular remodeling, and autoimmune inflammation. Genetic models and emerging pharmacologic strategies illustrate tissue-specific RAAS actions, emphasizing the therapeutic potential of enhancing the ACE2/Ang 1-7/Mas axis while inhibiting the deleterious ACE/Ang II/AT1R signaling. Furthermore, we highlight implications for veterinary medicine, particularly in canine chronic inflammatory enteropathies, where RAAS dysfunction may contribute to treatment resistance. Understanding RAAS complexity and inter-receptor crosstalk is essential for developing new therapeutic strategies targeting cardiovascular, hepatic, and inflammatory diseases in both human and veterinary contexts.
Idiopathic Arginine Vasopressin Deficiency With an Incidental Non-functional Pituitary Microadenoma in an Elderly Diabetic Woman.
Cureus
Mokkarala Satya Vamsi Krishna, Daruvuri Vishnu Sai Prasanna Babu, Mohini Singh +1 more
We present a case of idiopathic arginine vasopressin deficiency (AVP-D) in an elderly woman with type 2 diabetes, who presented with polyuria, polydipsia, and nocturia. Laboratory findings confirmed a euglycemic state, hyperosmolar serum, and hypoosmotic urine. Magnetic resonance imaging of the pituitary revealed the absence of the posterior bright spot and an incidental small, non-functional pituitary microadenoma, without any compressive effects on the pituitary stalk. The diagnosis of AVP-D was confirmed through a water deprivation test and a positive response to desmopressin. Common secondary causes, including inflammatory, granulomatous, and structural pathologies, were excluded. The patient responded well to oral desmopressin therapy, resulting in normalization of serum sodium and urine osmolality. This case underscores the challenges in diagnosing the cause of polyuria in a diabetic patient and the challenges in determining the etiology of AVP-D.
Oxytocin enhances oligodendrocyte development and improves social deficits in autistic rats.
Front Neurosci
Min Wen, Shuang Zheng, Hongbo Luo +2 more
Autism spectrum disorder (ASD) is a neurodevelopmental condition with complex etiological factors, including genetic predisposition and environmental influences. In particular, exposure to environmental stressors in utero has increasingly been implicated in disrupting fetal neurodevelopment and potentially contributing to the pathogenesis of ASD in offspring. The aim of this study was to investigate the therapeutic potential of oxytocin and to elucidate its underlying molecular mechanisms in a valproic acid (VPA) exposure-induced rat model of ASD.
Oxytocin modulation of resting-state functional connectivity network topology in individuals with higher autistic traits.
Psychoradiology
Abraham Tonny Hagan, Lei Xu, Juan Kou +7 more
Altered connectivity patterns in socio-emotional brain networks are characteristic of individuals with autism spectrum disorder. Despite recent research on intranasal oxytocin's modulation effects of network topology in autism, its specific effects on the functional connectivity network topology remain underexplored.
Primary Hepatic Neuroendocrine Tumor Treated With Lattice and External Beam Radiation: A Case Report.
Cureus
Yeidaliz Barreto Cruz, Gordon L Grado
Neuroendocrine tumors (NETs) originate from neuroendocrine cells, which receive neural input and play a key role in transmitting signals by secreting bioactive substances such as monoamines (e.g., serotonin), peptides (e.g., somatostatin), and hormones (e.g., insulin) that regulate a wide range of physiological functions. While NETs in the liver are typically metastatic, often originating from other sites in the gastrointestinal (GI) tract, they can, in rare cases, manifest as primary tumors in the liver. These are referred to as primary hepatic neuroendocrine tumors (PHNT). We present the case of a 62-year-old male patient diagnosed with PHNT confirmed through imaging and immunohistochemistry analysis. Given the rarity of this diagnosis, there are no established treatment guidelines for PHNT. In this case, lattice radiotherapy (LRT) via TomoTherapy (TomoTherapy, Inc. in Madison, WI) was selected as the first-line treatment approach for the tumor.
Physiopathology of the Brain Renin-Angiotensin System.
Life (Basel)
Cristina Cueto-Ureña, María Jesús Ramírez-Expósito, María Pilar Carrera-González +1 more
The renin-angiotensin system (RAS) has evolved from being considered solely a peripheral endocrine system for cardiovascular control to being recognized as a complex molecular network with important functions in the central nervous system (CNS) and peripheral nervous system (PNS). Here we examine the organization, mechanisms of action, and clinical implications of cerebral RAS in physiological conditions and in various neurological pathologies. The cerebral RAS operates autonomously, synthesizing its main components locally due to restrictions imposed by the blood-brain barrier. The key elements of the system are (pro)renin; (pro)renin receptor (PRR); angiotensinogen; angiotensin-converting enzyme types 1 and 2 (ACE1 and ACE2); angiotensin I (AngI), angiotensin II (AngII), angiotensin III (AngIII), angiotensin IV (AngIV), angiotensin A (AngA), and angiotensin 1-7 (Ang(1-7)) peptides; RAS-regulating aminopeptidases; and AT1 (AT1R), AT2 (AT2R), AT4 (AT4R/IRAP), and Mas (MasR) receptors. More recently, alamandine and its MrgD receptor have been included. They are distributed in specific brain regions such as the hypothalamus, hippocampus, cerebral cortex, and brainstem. The system is organized into two opposing axes: the classical axis (renin/ACE1/AngII/AT1R) with vasoconstrictive, proinflammatory, and prooxidative effects, and the alternative axes AngII/AT2R, AngIV/AT4R/IRAP, ACE2/Ang(1-7)/MasR and alamandine/MrgD receptor, with vasodilatory, anti-inflammatory, and neuroprotective properties. This functional duality allows us to understand its role in neurological physiopathology. RAS dysregulation is implicated in multiple neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and neuropsychiatric disorders such as depression and anxiety. In brain aging, an imbalance toward hyperactivation of the renin/ACE1/AngII/AT1R axis is observed, contributing to cognitive impairment and neuroinflammation. Epidemiological studies and clinical trials have shown that pharmacological modulation of the RAS using ACE inhibitors (ACEIs) and AT1R antagonists (ARA-II) not only controls blood pressure but also offers neuroprotective benefits, reducing the incidence of cognitive decline and dementia. These effects are attributed to direct mechanisms on the CNS, including reduction of oxidative stress, decreased neuroinflammation, and improved cerebral blood flow.
A Rare Case of Neuroendocrine Tumor Presenting as Isolated Scalp Swelling With Paroxysmal Symptoms.
Cureus
Vivek Kumar Dubey, Kush Pathak, Kavita Sijwali
We report a 36-year-old male with a nine-year history of recurrent left frontal scalp swelling following minor trauma, associated with local warmth, sweating, and a syncopal episode during fine-needle aspiration cytology (FNAC). Histopathology confirmed grade 2 neuroendocrine tumor (NET) with a Ki-67 index of 8-10%. 68Ga-DOTANOC positron emission tomography and computed tomography (PET-CT) showed no evidence of residual, recurrent, or primary somatostatin receptor-expressing disease, confirming this as a rare case of isolated scalp NET without an identifiable primary source. This is, to our knowledge, the first reported case of its kind. The patient's syncope post-FNAC highlights the risk of carcinoid-like crisis from lesion manipulation. This case underscores the importance of a high index of suspicion, thorough immunohistochemical workup, and consideration of peri-procedural octreotide prophylaxis.
Bromelain Improves Hypothalamic Control of Energy Homeostasis in High-Fat Diet-Induced Obese Rats.
Curr Issues Mol Biol
Raviye Ozen Koca, Mustafa Berk Basaran, Hatice Solak +1 more
Obesity remains a major global health challenge with limited therapeutic options. Bromelain, a proteolytic enzyme complex derived from pineapple, has been recognized for its natural anti-inflammatory, anti-edematous, and appetite-suppressing properties. This study aimed to investigate the effects of bromelain on hypothalamic neuropeptides and metabolic markers in a high-fat diet (HFD)-induced obesity model in rats. Thirty-six male Wistar albino rats were randomly divided into four groups: standard diet (SD), standard diet with bromelain (SDBro), high-fat diet (HFD), and high-fat diet with bromelain (HFDBro). Obesity was induced by a 3-month HFD regimen, followed by bromelain supplementation (200 mg/kg/day, orally) for one month. Hypothalamic tissues were analyzed via ELISA for neuropeptide Y (NPY), pro-opiomelanocortin (POMC), glucose transporter 2 (GLUT2), fibroblast growth factor 2 (FGF2), and insulin-like growth factor 1 receptor (IGF1R). While NPY levels showed no significant changes, POMC increased in the HFD and was normalized with bromelain. GLUT2 was downregulated in the HFD and significantly restored by bromelain. FGF2 levels remained unchanged. IGF1R was upregulated in the HFD but reduced by bromelain, with an unexpected increase in SDBro. Overall, bromelain partially reversed HFD-induced disruptions in hypothalamic energy-regulating pathways, particularly affecting GLUT2 and POMC. These findings highlight bromelain's potential role in central metabolic regulation under dietary stress.
Obesity: Clinical Impact, Pathophysiology, Complications, and Modern Innovations in Therapeutic Strategies.
Medicines (Basel)
Mohammad Iftekhar Ullah, Sadeka Tamanna
Obesity is a growing global health concern with widespread impacts on physical, psychological, and social well-being. Clinically, it is a major driver of type 2 diabetes (T2D), cardiovascular disease (CVD), non-alcoholic fatty liver disease (NAFLD), and cancer, reducing life expectancy by 5-20 years and imposing a staggering economic burden of USD 2 trillion annually (2.8% of global GDP). Despite its significant health and socioeconomic impact, earlier obesity medications, such as fenfluramine, sibutramine, and orlistat, fell short of expectations due to limited effectiveness, serious side effects including valvular heart disease and gastrointestinal issues, and high rates of treatment discontinuation. The advent of glucagon-like peptide-1 (GLP-1) receptor agonists (e.g., semaglutide, tirzepatide) has revolutionized obesity management. These agents demonstrate unprecedented efficacy, achieving 15-25% mean weight loss in clinical trials, alongside reducing major adverse cardiovascular events by 20% and T2D incidence by 72%. Emerging therapies, including oral GLP-1 agonists and triple-receptor agonists (e.g., retatrutide), promise enhanced tolerability and muscle preservation, potentially bridging the efficacy gap with bariatric surgery. However, challenges persist. High costs, supply shortages, and unequal access pose significant barriers to the widespread implementation of obesity treatment, particularly in low-resource settings. Gastrointestinal side effects and long-term safety concerns require close monitoring, while weight regain after medication discontinuation emphasizes the need for ongoing adherence and lifestyle support. This review highlights the transformative potential of incretin-based therapies while advocating for policy reforms to address cost barriers, equitable access, and preventive strategies. Future research must prioritize long-term cardiovascular outcome trials and mitigate emerging risks, such as sarcopenia and joint degeneration. A multidisciplinary approach combining pharmacotherapy, behavioral interventions, and systemic policy changes is critical to curbing the obesity epidemic and its downstream consequences.
Hypocretin: a promising target for the regulation of homeostasis.
Front Neurosci
Yutong Wang, Su Fu, Jian Mao +2 more
Hypocretin, also known as orexin, is a hypothalamic neuropeptide that regulates essential physiological processes including arousal, energy metabolism, feeding behavior, and emotional states. Through widespread projections and two G-protein-coupled receptors-HCRT-1R and HCRT-2R-the hypocretin system exerts diverse modulatory effects across the central nervous system. The role of hypocretin in maintaining wakefulness is well established, particularly in narcolepsy type 1 (NT1), where loss of hypocretin neurons leads to excessive daytime sleepiness and cataplexy. However, the mechanisms by which hypocretin stabilizes transitions between sleep stages remain incompletely understood. Additionally, while hypocretin integrates metabolic signals such as glucose, leptin, and ghrelin to promote feeding and energy expenditure, NT1 patients paradoxically experience weight gain despite reduced caloric intake-highlighting unresolved questions about hypocretin's role in energy homeostasis. In the affective domain, preclinical studies suggest hypocretin enhances stress resilience and modulates anxiety- and depression-related behaviors. Yet, human data remain inconsistent, in part due to methodological variability and the limited availability of cerebrospinal fluid sampling to accurately assess central hypocretin function. Therapeutically, the hypocretin system is a promising target across several domains. Dual hypocretin receptor antagonists (DORAs), such as suvorexant and daridorexant, are clinically approved for insomnia. Selective HCRT-2R agonists-including TAK-861 and ALKS-2680-are in clinical trials for NT1 and show encouraging results. Additionally, HCRT-2R antagonists like seltorexant are being explored for major depressive disorder. This review will highlight the anatomical distribution, receptor mechanisms, and physiological functions of the hypocretin system. It will also focus to discuss its role in narcolepsy, metabolic regulation, and mood disorders, while addressing key challenges and open questions that must be resolved to fully harness hypocretin's therapeutic potential.
Thymosin beta 4 as an Alzheimer disease intervention target identified using human brain organoids.
Stem Cell Reports
Peng-Ming Zeng, Xin-Yao Sun, Yang Li +6 more
The developmental origin of Alzheimer disease (AD) has been proposed but is arguably debated. Here, we developed cerebral organoids from induced pluripotent stem cells (iPSCs) with mutations in amyloid precursor protein (APP) associated with familial AD (fAD) and analyzed the dynamic changes of cellular states. We found that mature neurons induced in fAD organoids markedly decreased compared to that of health control, accompanied with increased cell senescence and β-amyloid (Aβ) production. Interestingly, the expression level of the gene TMSB4X that encodes thymosin beta 4 (Tβ4) significantly decreased both in fAD organoids' neurons and AD patients' excitatory neurons. Remarkably, the neurodevelopmental deficits and Aβ formation in fAD organoids were rescued by treatment with Tβ4. The beneficial effects of Tβ4 were also revealed in 5xfAD model mice. Thus, this study has identified Tβ4 as a neuroprotective factor that may mitigate altered neurogenesis and AD pathology, highlighting a potential for disease intervention.
An injectable hydroxyapatite microsphere filler loaded with GHK-Cu tripeptide for anti-Inflammatory and antioxidant.
Colloids Surf B Biointerfaces
Die Hu, Xuexun Zhang, Shiwen Gong +7 more
With the wide application of soft tissue fillers, implant material-induced inflammatory reactions have become a key factor affecting the therapeutic efficacy. This study developed an injectable filler with enhanced anti-inflammatory and antioxidant effects by adsorbing glycyl-L-histidyl-L-lysine copper complex (GHK-Cu) onto hydroxyapatite microspheres (HAPs), marking the first combination of HAPs and GHK-Cu to address inflammation caused by soft tissue fillers. GHK-Cu was successfully loaded onto HAPs by electrostatic adsorption. HAPs were then mixed with carboxymethyl cellulose (CMC), glycerol (GLY), and water to form GHK-Cu@CMHA gel. The study focus on the effective combination of HAPs as a carrier for sustained GHK-Cu delivery and the anti-inflammatory properties of GHK-Cu. GHK-Cu@CMHA exhibits sustained release properties for 7 days, which ensures prolonged therapeutic effects, minimizes peptide waste and reduces injection frequency, with good flowability and injectability. In the model of LPS-induced inflammation model in vivo and in vitro, GHK-Cu@CMHA gel reduced levels of inflammatory factors and Reactive oxygen species (ROS) levels decreased, while superoxide dismutase (SOD) activity was enhanced. In this process, H&E staining and Masson staining revealed significant collagen deposition. These findings further confirm that GHK-Cu@CMHA is a novel injectable soft tissue filler with good anti-inflammatory and antioxidant properties, which holds well potential for inflammation inhibition.
A single blood luteinizing hormone level of triptorelin stimulation test can diagnose hypothalamic-pituitary-gonadal axis activation in girls with high body mass index.
Front Pediatr
Beilei Zeng, Yinyin Huang, Yuan Zhou +4 more
Body mass index (BMI) may influence peak luteinizing hormone (PLH) levels during gonadotropin releasing hormone (GnRH) or GnRH analogues stimulation testing. BMI effects should be considered when interpreting test results for pubertal disorders in girls with overweight/obesity, but few studies have excluded it.