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Burden of illness and unmet needs in patients with erythropoietic protoporphyria and X-linked protoporphyria: A large US nationwide claims analysis.
J Manag Care Spec Pharm
Maral DerSarkissian, Chelsea Norregaard, Hela Romdhani +5 more
Erythropoietic protoporphyria (EPP) and X-linked protoporphyria (XLP) are rare genetic disorders caused by the accumulation of the toxic metabolite protoporphyrin IX, which results in painful phototoxicity upon sunlight exposure. Despite their significant impact on quality of life and potential for serious complications, treatment options for EPP/XLP are limited and real-world burden of illness and unmet needs have been understudied in this population.
Octreotide ameliorates Bisphenol A-induced testicular toxicity via autophagy-inflammation pathway modulation.
Hum Exp Toxicol
Basma B Morad, Ola M Salem, Rasha Osama El-Esawy +1 more
IntroductionTesticular toxicity commonly manifests as impaired spermatogenesis and testicular atrophy. Bisphenol A (BPA), a commonly used organic plasticizer, negatively affects sperm parameters, hormonal levels, and fertility. Octreotide (OCT), a somatostatin analog, was originally used to treat acromegaly, carcinoid tumors, vasoactive intestinal peptide-secreting, and growth hormone-secreting tumors. OCT has demonstrated potential therapeutic properties beyond its traditional use in endocrine disorders. We hypothesized that OCT would attenuate BPA-induced testicular damage through its anti-inflammatory, anti-oxidant, and anti-autophagic properties. This study aimed to assess the mechanisms of BPA-induced testicular toxicity and evaluate the ameliorative effects of OCT.MethodsForty adult male Sprague Dawley (SD) rats were randomly assigned to four equal groups: group1: saline control, group2: dimethyl sulfoxide (DMSO) vehicle, group3: BPA-treated, and group4: BPA + OCT-treated. Treatments were administered for 4 weeks. Sperm count, testicular weight, serum testosterone, lactate dehydrogenase (LDH), alkaline phosphatase (ALP), total antioxidant capacity (TAC), testicular levels of malondialdehyde (MDA), tumor necrosis factor-alpha (TNFα), Beclin-1 (BECN-1), Microtubule-associated proteins 1A/1B light chain 3A (MAP1LC3A/LC3), mammalian target of rapamycin (M-TOR), histopathological examination, apoptotic index, and Johnson's score were assessed.ResultsBPA administration significantly impaired spermatogenesis, reduced serum testosterone and TAC, and increased MDA, TNFα, and autophagy-related markers, along with histopathological damage of testis. Co-treatment with OCT mitigated these effects by improving sperm parameters, hormone levels, oxidative stress markers, inflammatory cytokines, and testicular histology.DiscussionThe findings suggest that OCT exerts a protective effect against BPA-induced testicular toxicity, through its anti-inflammatory, antioxidant, and autophagy-modulating properties. OCT may offer therapeutic potential in mitigating BPA-induced testicular toxicity.
Prevalence, associated factors, and prognostic value of P wave abnormality in patients with coronary artery disease.
Int J Cardiol Cardiovasc Risk Prev
Kazutoshi Hirose, Hiroyuki Kiriyama, Shun Minatsuki +13 more
P-wave terminal force in V1 (PTFV1) on electrocardiography is an easily available and cost-effective surrogate marker reflecting myocardial electrical and structural remodeling. An abnormal PTFV1 was recently suggested to be a reliable predictor of adverse cardiovascular events, whereas its performance in the setting of coronary artery disease (CAD) remains unknown.
Thyrotropin-releasing hormone protects hippocampal neurons against glutamate toxicity via phosphatidylinositol 3-kinase/AKT pathway and new protein synthesis.
bioRxiv
Yina Dong, Deborah J Watson
Thyrotropin-releasing hormone is best known as a neuropeptide that stimulates the release of thyroid-stimulating hormone and prolactin in hypothalamic-pituitary-thyroid (HPT) axis. Independent from its activity in the HPT axis, TRH also exerts strong neuroprotective activity against neurodegenerative diseases such as Alzheimer's disease, epilepsy and traumatic brain injury. Although multiple factors have been linked to its neuroprotective action, the cellular mechanism of TRH neuroprotection is still not clear. Here we show that TRH protects hippocampal neurons against glutamate toxicity via phosphatidylinositol 3-kinase (PI3K)/AKT pathway and new protein synthesis. Both adeno-associated virus (AAV) mediated TRH transduction and TRH peptide given exogenously over 24 hours period of time inhibit glutamate-induced lactate dehydrogenase (LDH) release. This effect is not mediated by the decreased intracellular calcium response as TRH treatment (24 hours) has no effect on glutamate-induced increase in intracellular calcium nor the calpain activity. While TRH treatment (10 minutes) significantly inhibits glutamate-induced increase in intracellular calcium, no protective effect is observed when TRH is applied 30 minutes before or after glutamate stimulation. Instead, PI3K inhibitor LY294002 but not mitogen-activated protein kinase (MAPK)/Extracellular signal-regulated kinase (ERK)1/2 inhibitor U0126 completely inhibits the protective effect of TRH. LY294002 also blocks TRH induced AKT activation. In addition, protein synthesis inhibitor cycloheximide inhibits the protective effect of TRH. Taken together, these results suggest PI3K/AKT signaling pathway and new protein synthesis are involved in the protective effect of TRH against glutamate toxicity, thereby providing mechanistic support for its action in neurodegenerative diseases.
An overview of oxytocin integrative mechanisms in autism spectrum disorder.
Discov Ment Health
Nand Lal, Bin Song, Chi Zhang +8 more
Autism Spectrum Disorder (ASD) is a multifaceted neurodevelopmental condition characterized by impairments in social interaction, communication, and repetitive behaviors. Its etiology involves a complex interplay of genetic, environmental, and neurobiological factors. The oxytocin (OT) system, central to social behavior and emotional regulation, has emerged as a key area of interest in ASD research. This review synthesizes current evidence, highlighting that dysregulation of OT and its receptor (OTR) signaling, often characterized by lower baseline OT levels and altered OTR expression due to genetic and epigenetic factors, contributes to the social and behavioral deficits observed in ASD. While aberrant OT/OTR signaling presents a potential target for therapeutic intervention, the narrative has evolved beyond simple peptide replacement. Critical analysis reveals that intranasal OT administration, as a standalone treatment, yields inconsistent results due to its non-specific delivery and inability to address core circuit-level dysfunctions established during neurodevelopment. Promising future avenues include the development of selective OTR agonists, epigenetic modulation to correct OTR expression, and the use of OT as a targeted adjunct to enhance behavioral therapy efficacy. This paper provides a comprehensive and critical overview of the integrative mechanisms linking OT/OTR signaling to ASD, evaluates the therapeutic potential of correcting this pathway, and emphasizes the necessity for personalized, biomarker-driven approaches to improve social cognition and neural connectivity in individuals with ASD.
Intestinal fructose metabolism triggers a glucagon-like peptide-1-β-cell axis to prevent post-fructose hyperglycaemia.
J Physiol
Naoya Murao, Yusuke Seino, Risa Morikawa +10 more
Fructose ingestion increases circulating glucagon-like peptide-1 (GLP-1) and insulin, yet the specific contributions of these hormonal responses to glycaemic control remain incompletely defined. We hypothesised that fructose metabolism in intestinal L-cells triggers GLP-1 secretion, which then potentiates insulin secretion and counteracts fructose-induced hyperglycaemia. To test this hypothesis, we systematically characterised metabolic responses across multiple mouse strains after 24 h ad libitum fructose ingestion. In both lean (NSY.B6-a/a) and obese diabetic (NSY.B6-Ay/a) mice, fructose elevated plasma insulin, GLP-1 and glucose-dependent insulinotropic polypeptide (GIP). The insulin response was preserved in GIP receptor-deficient mice (Gipr-/-) but was abolished in proglucagon-deficient mice (Gcg-/-) by pharmacological GLP-1 receptor antagonism, indicating a requirement for GLP-1, but not GIP. Across strains, fructose-induced insulin response correlated with attenuation of post-fructose glycaemia, consistent with insulin being essential for suppressing fructose-induced hyperglycaemia. To explore the mechanism underlying fructose-induced GLP-1 secretion, we combined ATP-sensitive potassium channel-deficient mice (Kcnj11-/-), the GLUTag L-cell line, and metabolic tracing of 13C-labelled fructose in freshly isolated intestinal crypts. These complementary approaches support a model in which fructolysis increases the ATP/ADP ratio in L-cells, closes KATP channels and stimulates GLP-1 secretion. In obese diabetic mice, increased fructolytic flux and a higher ATP/ADP ratio were associated with elevated GLP-1 levels, further corroborating this model. Collectively, our findings indicate that intestinal fructose metabolism drives GLP-1 secretion required to potentiate insulin secretion, thereby establishing a gut-pancreas axis that counter-regulates fructose-induced hyperglycaemia. KEY POINTS: Fructose ingestion acutely increases plasma insulin levels, but the underlying mechanisms and physiological significance remain elusive. Our study demonstrates that short-term (24 h) fructose ingestion in mice elevates both insulin and glucagon-like peptide 1 (GLP-1) levels in the blood, with the plasma insulin response being GLP-1-dependent. We found that fructose metabolism in intestinal L-cells triggered GLP-1 secretion by increasing the ATP/ADP ratio and closing ATP-sensitive K+ (KATP) channels. This intestinal fructose metabolism-GLP-1-β-cell axis plays a crucial role in preventing fructose-induced hyperglycaemia, an effect that is compromised in obese diabetic mice. These insights highlight the previously unclear metabolic responses following short-term fructose ingestion and their importance in glucose homeostasis.
Chronic stress and the IL-10-mediated immunoregulatory loop in the pathogenesis of periodontitis.
Clin Sci (Lond)
Maksym Skrypnyk, Axel Spahr, Shlomo Berkovsky +9 more
Periodontitis is a chronic inflammatory condition that gradually destroys the tissues supporting the teeth, including the gingiva, periodontal ligament, and alveolar bone. Emerging evidence suggests that psychological stress plays a significant role in the initiation and progression of periodontal disease, primarily through its impact on immune regulation. Stressors activate the hypothalamic-pituitary-adrenal (HPA) axis, leading to the release of corticotropin-releasing hormone (CRH) from the hypothalamus and, in turn, adrenocorticotropic hormone (ACTH) from the pituitary gland. Activation of the HPA axis and the sympathetic-adrenal-medullary (SAM) system during stress triggers the systemic release of cortisol, epinephrine, norepinephrine, and cytokines. The HPA, SAM, and cytokines interact in both direct and indirect ways. Not only does stress induce interleukin-10 (IL-10), but IL-10 also helps regulate the stress response and cortisol levels. IL-10 can stimulate the release of CRH and ACTH, while concurrently inhibiting cortisol secretion from the adrenal glands. IL-10 has drawn increasing attention within the oral cavity owing to its dual role in modulating immune responses and maintaining periodontal tissue homeostasis. This review outlines the current understanding of stress-related neuroendocrine pathways and their relevance to periodontal health. It explores the involvement of HPA axis effectors-cortisol and IL-10-in modulating the inflammatory milieu associated with periodontitis. This includes recent insights into IL-10-expressing regulatory B cells and the potential role of IL-10 in mitigating alveolar bone loss. By integrating recent advances in neuroendocrinology, immunology, and oral biology, this review clarifies how systemic stress responses contribute to local inflammatory changes in the periodontium. Understanding the mechanisms linking psychological stress, cortisol dynamics, and IL-10-mediated regulation may offer new opportunities for early diagnosis and intervention in stress-exacerbated periodontitis.
Thymosin β4 released by mast cells under stress conditions impairs intestinal epithelial barrier via IL22RA1/JAK1/STAT3 signaling in irritable bowel syndrome.
World J Gastroenterol
Yue-Shan Sun, Xiao-Qin Bai, Kai-Di Sun +6 more
Mast cells (MCs) under stress conditions contribute to the development of irritable bowel syndrome (IBS), yet their precise mechanisms in IBS remain unclear.
Central administration of docosahexaenoic acid, eicosapentaenoic acid, or linoleic acid activates hypothalamic fatty acid sensing and is involved in reproductive regulation in spotted scat (Scatophagus argus).
Fish Physiol Biochem
Siqin Wang, Jie Luo, Xinghua Lin +6 more
The binding of fatty acid (FA) to fatty acid translocase (FAT/CD36) and subsequent regulation of lipid metabolism transcription factors, such as peroxisome proliferator-activated receptors α (PPARα) and sterol regulatory element-binding protein-1c (SREBP-1c), is an important hypothalamic fatty acid-sensing mechanism in vertebrates. The hypothalamus exhibits responsiveness to specific fatty acids and is involved in reproductive regulation. However, the link between FA sensing and reproductive regulation in the hypothalamus remains poorly understood teleosts. Therefore, the expression of genes involved in the FA-sensing mechanism-such as fat/cd36, pparα, and srebp1c, as well as gonadotropin-releasing hormone (GnRH: cgnrh, sgnrh, sbgnrh) in the hypothalamus-was investigated after intracranial administration and hypothalamic incubation of polyunsaturated fatty acids (PUFAs), including docosahexaenoic acid (DHA), eicosapentanoic acid (EPA), and linoleic acid (LA) for 4 h in the spotted scat (Scatophagus argus). Compared to the control, intracranial administration and hypothalamic incubation of DHA and LA, as well as hypothalamic incubation of EPA, increased the levels of fat/cd36, pparα, and srebp1c. However, the expression of fat/cd36 and pparα was significantly decreased, and the level of srebp1c showed a downward trend only in the EPA group when co-incubated with the FAT/CD36 inhibitor Sulfo-N-succinimidyl oleate sodium (SSO), compared to incubation with EPA alone. After the application of PPARα antagonist GW6471, the expression of pparα in the hypothalamus decreased significantly in the DHA, EPA, and LA treatment groups, compared to incubation with DHA, EPA, and LA alone. Levels of fsh and lh in the pituitary gland were changed significantly after the intracranial administration of DHA, EPA, and LA. Compared to the control, the levels of cgnrh, sgnrh, and sbgnrh increased in the hypothalamus after both hypothalamic incubation and intracranial administration of EPA and LA. Levels of cgnrh increased in the hypothalamus after incubation, but not after intracranial administration of DHA. However, compared to the control, levels of sgnrh and sbgnrh increased after hypothalamic incubation with DHA and EPA. Only sgnrh levels decreased after incubation with LA in the presence of SSO compared to the FA treatment group alone. In the presence of GW6471, only sgnrh levels decreased after incubation with LA in the presence of SSO compared to the FA treatment group alone; the levels of cgnrh, sgnrh, and sbgnrh after LA incubation, the levels of sbgnrh after EPA incubation, and the levels of sbgnrh after DHA incubation were all significantly decreased compared to the control. These results showed that DHA, EPA, and LA could activate fat/cd36 and pparα, which are involved in reproductive regulation in the hypothalamus of the spotted scat. These results provide evidence that hypothalamic FA sensing is involved in regulating reproduction in teleosts.
Glucagon, the Alpha Cell, and Potential Targets for Diabetes Treatment.
Endocrinology
Savita Dhanvantari, E Danielle Dean
Glucagon is a 29-amino acid hormone synthesized and secreted by the pancreatic alpha cell in the islets of Langerhans. It is the primary glucose counter-regulatory hormone, secreted by the alpha cell to maintain euglycemia by stimulating hepatic gluconeogenesis and glycogenolysis. In addition to glucose, the alpha cell senses and responds to a number of inputs, such as paracrine factors, neurotransmitters, and other nutrients, including amino acids, to regulate the secretion of glucagon. Disruption of this fine regulation results in excessive glucagon secretion (hyperglucagonemia) and contributes to the pathogenesis of diabetes. In this mini-review, we summarize the current understanding of glucagon biosynthesis and intracellular trafficking, and we discuss emerging concepts in amino acid sensing and signaling that underpin the biology of the alpha cell and that may provide clues to the control of the hyperglucagonemia of diabetes.
Real-world disease burden and health care resource utilization for patients with Barth syndrome.
J Med Econ
Lindsay Marjoram, Yonglin Huang, Mary Kay Koenig +2 more
Barth syndrome (BTHS) is an ultra-rare, X-linked genetic disorder for which there is limited economic data. Because compiling such data that target rare indications is difficult, we assessed real-world data to increase understanding of the cost of BTHS based on disease burden and health care resource utilization (HCRU).
Can diets alleviate constipation and promote bowel movement? Exploring the underlying mechanisms of effects.
Food Res Int
Xi Gui, Lan Wu, Kaijun Huang +7 more
Constipation is a common gastrointestinal disorder with a significant impact on quality of life. Diets play an important role as a modifiable lifestyle factor that can affect the onset and progression of constipation. This review examines the effects and mechanisms of multiple dietary patterns, including a high-fat diet, Mediterranean diet, fiber-rich diet, and plant-based diet, on constipation, microecological agents (probiotics, prebiotics, and synbiotics), and bioactive compounds (polysaccharides and polyphenols). In summary, the Mediterranean and plant-based diets can reduce the risk of constipation with favorable changes in gut microbiota, increase contents of short-chain fatty acids (SCFAs), and reduce the inflammatory markers. A fiber-rich diet increases stool bulk, retains water due to its high water-binding capacity, and serves as a substrate for gut microbiota. Additionally, microbiota can ferment fiber-rich diet to produce gases and SCFAs, which create an osmotic load and accelerate intestinal transit. Conversely, a high-fat diet correlates with an increased incidence of constipation with unfavorable changes in gut microbiota and reduces 5-hydroxytryptamine (5-HT) availability and mucin secretion. Meanwhile, probiotics, prebiotics, and synbiotics relieve constipation by restoring the imbalance of gut microbiota and increasing the contents of SCFAs and neurotransmitters. Also, polyphenols alleviate constipation by enhancing intestinal barrier, balancing neurotransmitters, and suppressing gut inflammation. Polysaccharides upregulate the expression of gastrointestinal transport proteins and genes (such as transient receptor potential vanilloid 1 [TRPV1], aquaporin 3 [AQP3], vasoactive intestinal peptide receptor 1 [VIPR1]) to maintain intestinal peristalsis. Furthermore, given the inter-individual in metabolic responses to dietary intake, we propose a framework for developing personalized diets for individuals with constipation, tailored to their specific compositions of gut microbiota.
The Role of Growth Hormone-Releasing Hormone and the Hypothalamic-Pituitary-Somatotropic Axis in Aging: Potential Therapeutic Applications and Risks.
Horm Metab Res
Ioannis Oikonomakos, Richard Siow, Stefan R Bornstein +1 more
Aging is marked by a gradual decline in multiple physiological functions, increasing the risk of age-related disorders. Multiple factors have been identified as contributors to aging, many of which are regulated by the hypothalamus. Growth hormone-releasing hormone (GHRH) produced in the hypothalamus is a key regulator of growth hormone (GH) secretion. With aging, both GHRH and GH levels decline, leading to muscle loss, increased fat accumulation, metabolic dysregulation, and cognitive impairments. GH replacement therapy has been explored as a potential intervention to counteract these effects; however, its long-term use is associated with significant risks, including metabolic disturbances, cardiovascular complications, and potential cancer promotion. In contrast, studies suggest that GHRH-based therapies can improve body composition, muscle strength, cognitive function, and cardiovascular health while avoiding the risks linked to direct GH administration. Additionally, preclinical findings indicate that GHRH agonists may offer cardioprotective and immunomodulatory benefits. In this review, we summarize current knowledge on the roles of GHRH and GH in aging, highlight the limitations of GH-based therapies, and discuss the potential of GHRH-based approaches in mitigating age-related decline and improving health span.
Analysis of growth hormone releasing hormone and its analogs in urine using nano liquid chromatography coupled with quadrupole/orbitrap mass spectrometry.
J Pharm Biomed Anal
Ebru Uçaktürk, Emirhan Nemutlu
Growth hormone-releasing hormone (GHRH) and its synthetic analogs are considered performance-enhancing substances and are therefore prohibited by the World Anti-Doping Agency (WADA). The analysis of GHRH and its analogs in urine presents significant analytical challenges due to their inherent in vivo instability, rapid renal clearance, and low urinary concentrations. The present study aimed to develop a robust nano-LC quadrupole/orbitrap mass spectrometry (nano-LC-Q/Orbitrap MS) method for both screening and confirmation analyses of GHRH and its synthetic analogs (sermorelin/CJC-1293, tesamorelin, and CJC-1295) and the primary metabolite of sermorelin in urine, in accordance with WADA requirements. The sample preparation workflow was systematically investigated. Existing solid-phase extraction (SPE) protocols were compared, and two additional commercially available SPE cartridges were evaluated. Within the SPE step, the influence of various washing and elution solvent strengths on peptide recovery was also systematically examined. The effectiveness of different cleanup solvents during the ultrafiltration step was further assessed. Based on these evaluations, a refined approach was developed, incorporating an initial ultrafiltration step followed by SPE. The proposed method was fully validated according to WADA guidelines, assessing key parameters such as selectivity, reliability, limits of detection (LOD), carryover, limits of identification (LOI), robustness, autosampler stability, and matrix effects. The validation results confirmed the method's suitability and robustness for anti-doping testing. Achieved LODs (≤ 0.5 ng/mL) and LOIs (0.5-0.75 ng/mL) demonstrated sufficient sensitivity for effective detection and confirmation analysis of the target peptides in urine.
Impact of glucocorticoid therapy on hypothalamic-pituitary-adrenal axis function in pediatric nephrotic syndrome: A narrative review.
World J Clin Pediatr
Subhankar Sarkar, Asiri Samantha Abeyagunawardena, Rajiv Sinha
Glucocorticoids (GCs) such as prednisolone are widely used in conditions like nephrotic syndrome, asthma, and autoimmune diseases. However, prolonged or high-dose use may suppress the hypothalamic-pituitary-adrenal (HPA) axis, leading to secondary adrenal insufficiency (AI). This condition occurs when the adrenal glands fail to produce adequate cortisol, which is essential for regulating metabolism, immune response, and stress adaptation. Corticotropin-releasing hormone (CRH) from the hypothalamus stimulates the pituitary to release adrenocorticotropic hormone (ACTH), which then triggers cortisol production in the adrenal glands. Prolonged GC use disrupts this system by inhibiting CRH and ACTH secretion, leading to adrenal atrophy and reduced cortisol production. HPA axis suppression is primarily diagnosed through dynamic tests. Early morning cortisol levels above > 18 ng/mL typically indicate normal function, while levels < 3 ng/mL suggest AI. Intermediate values require additional testing, such as the insulin tolerance test, ACTH stimulation test, and metyrapone test. Prednisolone in nephrotic syndrome suppresses the HPA axis, heightening AI risk, influenced by dose, duration, and timing of administration. Careful GC management is essential to balance disease control with risks of HPA axis suppression. Early recognition and timely intervention can prevent adrenal crises and improve outcomes in pediatric patients.
PFKFB3 Promotes Myofibroblast Differentiation and Cardiac Fibrosis Through its Intra- and Extra- Cellular Roles.
J Cardiovasc Transl Res
Bing Han, Zhaowei Zhu, Yongxiang Wang +4 more
Cardiac fibrosis remains a major clinical challenge with limited therapeutic options, and the role of PFKFB3 in its pathogenesis remains unclear. Single-cell RNA sequencing analysis was applied and the results demonstrated that glycolysis was most prominently enhanced in activated cardiac myofibroblasts (myoCFs) in cardiomyopathy. Western blot analysis revealed that PFKFB3 expression was significantly increased in fibrotic hearts and TGF-β1-stimulated myoCFs. Genetic (Pfkfb3+/-) and pharmacological (3PO) inhibition of PFKFB3 attenuated myoCF activation, proliferation, and migration, while also reducing cardiac fibrosis in isoproterenol- and coronary ligation- induced mouse models. Mechanistically, TGF-β1 upregulated PFKFB3 in a HIF-1α-dependent manner, and extracellular PFKFB3 further promoted fibroblast activation and inflammatory responses. Clinically, elevated plasma PFKFB3 levels, as measured by ELISA, were significantly associated with fibrosis severity in patients with cardiomyopathy. These findings reveal for the first time that PFKFB3 drives cardiac fibrosis dually through intracellular glycolytic regulation and extracellular signaling, highlighting its translational potential.
Medical treatment in acromegaly: a network meta-analysis.
Eur J Endocrinol
Chrysi Kaparounaki, Mirela-Diana Ilie, Dario De Alcubierre +6 more
Acromegaly is a rare disorder caused by a growth hormone-secreting pituitary adenoma. Clinical trial evidence for its management is limited. This study compared medical treatments for acromegaly through a network meta-analysis, assessing biochemical and radiological responses.
Prevalence of heart failure stages in elderly population: from a community-dwelling elderly people survey.
BMC Geriatr
Manyun Huang, Min Wang, Xin Gong +7 more
Heart failure (HF) is a major public health concern in China, but there is a lack of epidemiological data on the prevalence of early-stage HF in the elderly.
Cerebrospinal Fluid Human Neutrophil Peptides 1-3: A Potential Prognostic Marker in Intracerebral Hemorrhage.
Genet Test Mol Biomarkers
Zhi He, Jun Xie, Fu-Ling Yan +4 more
Background: This study aims to investigate whether elevated human neutrophil peptides 1-3 (HNP 1-3) levels in cerebrospinal fluid (CSF) are associated with disease severity and clinical outcomes in patients with intracerebral hemorrhage (ICH). Materials and Methods: HNP 1-3 levels were measured in CSF samples collected within 3 days after hemorrhage onset in ICH patients and control subjects. Results: HNP 1-3 levels were significantly higher in ICH patients with moderate-severe coma and hematoma volume >30 mL group. Univariate and multivariate logistic regression analyses demonstrated that CSF HNP 1-3 levels were associated with unfavorable outcomes. Receiver operating characteristic analysis revealed that CSF HNP 1-3 concentrations >466.95 ng/mL could distinguish ICH patients at risk for an unfavorable prognosis. Conclusions: HNP 1-3 exhibit satisfactory diagnostic efficiency for predicting the prognosis of ICH patients.
High Rate Triggers Increased Atrial Release of BMP10, A Biomarker for Atrial Fibrillation and Stroke, and BMP10 Affects Ventricular Cardiomyocytes.
Circ Arrhythm Electrophysiol
Laura C Sommerfeld, Jessica Schrapers, Karl-Felix Müller +19 more
BMP10 (bone morphogenetic protein 10) is a ligand of the TGF (transforming growth factor) β superfamily secreted mainly by atrial cardiomyocytes. Elevated BMP10 blood concentrations predict atrial fibrillation (AF), AF recurrence after ablation, and AF-related cardiovascular complications like stroke. The conditions increasing BMP10 secretion and the downstream effects of BMP10 in cardiomyocytes are poorly understood. We assessed BMP10 secretion dynamics and BMP10 effects in a human 3-dimensional model of atrial and ventricular engineered heart tissue (EHT).