Catalpol regulates apoptosis and proliferation of endothelial cell via activating HIF-1α/VEGF signaling pathway.

Burn injuries, especially severe ones, causes microcirculation disorders in local wounds and distant tissues, leading to ischemia and hypoxia of body tissues and organs. The key to prevent and treat complications and improve prognosis after burns is to improve the state of ischemia and hypoxia of tissue and restore the blood supply of organs. Catalpol is an iridoid glycoside compound isolated from Rehmannia radix, which has been widely reported to have various of functions, including antioxidative stress, anti-inflammation, anti-apoptosis, and neuroprotection.

Promotion Effect of Catalpol on Angiogenesis and Potential Mechanisms: A Research Based on Network Pharmacology.

Catalpol, a natural iridoid glycoside, has potential therapeutic benefits, including anti-inflammatory and neuroprotective effects. Investigating catalpol's role in angiogenesis is critical for understanding its potential therapeutic applications, particularly in diseases where modulating angiogenesis is beneficial. This study investigates catalpol's influence on angiogenesis and its mechanisms, combining network pharmacology and in vitro experiments.

Mitochondrial Dysfunction in Cardiac Arrhythmias.

Electrophysiological and structural disruptions in cardiac arrhythmias are closely related to mitochondrial dysfunction. Mitochondria are an organelle generating ATP, thereby satisfying the energy demand of the incessant electrical activity in the heart. In arrhythmias, the homeostatic supply-demand relationship is impaired, which is often accompanied by progressive mitochondrial dysfunction leading to reduced ATP production and elevated reactive oxidative species generation.

Low-level tragus stimulation improves autoantibody-induced hyperadrenergic postural tachycardia syndrome in rabbits.

Background: Recent studies have demonstrated that antiadrenergic autoantibodies are involved in the pathophysiology of postural orthostatic tachycardia syndrome (POTS).

Objective: The purpose of this study was to test the hypothesis that transcutaneous low-level tragus stimulation (LLTS) ameliorates autoantibody-induced autonomic dysfunction and inflammation in a rabbit model of autoimmune POTS.

Methods: Six New Zealand white rabbits were co-immunized with peptides from the α1-adrenergic and β1-adrenergic receptors to produce sympathomimetic antibodies.

The role of age-associated autonomic dysfunction in inflammation and endothelial dysfunction.

Aging of the cardiovascular regulatory function manifests as an imbalance between the sympathetic and parasympathetic (vagal) components of the autonomic nervous system (ANS). The most characteristic change is sympathetic overdrive, which is manifested by an increase in the muscle sympathetic nerve activity (MSNA) burst frequency with age. Age-related changes that occur in vagal nerve activity is less clear.

Transcutaneous vagus nerve stimulation attenuates autoantibody-mediated cardiovagal dysfunction and inflammation in a rabbit model of postural tachycardia syndrome.

Purpose: Previous studies demonstrated M2 muscarinic acetylcholine receptor-activating autoantibodies (M2R-AAb) were present in some patients with postural tachycardia syndrome (POTS). This study examines how these autoantibodies might contribute to the pathophysiology of POTS, and whether low-level tragus stimulation (LLTS) can ameliorate autoantibody-mediated autonomic dysregulation in the rabbit.

Methods: Five New Zealand white rabbits were immunized with a M2R second extracellular loop peptide to produce cholinomimetic M2R-AAb.

GnRH receptor-activating autoantibodies in polycystic ovary syndrome: identification of functional epitopes and development of epitope mimetic inhibitors.

Purpose: We have recently demonstrated that gonadotrophin-releasing hormone receptor-activating autoantibodies (GnRHR-AAb) are associated with polycystic ovary syndrome (PCOS). The aim of this study was to map the antigenic epitopes of GnRHR-AAb from PCOS patients, and develop retro-inverso peptide inhibitors that specifically target GnRHR-AAb.

Methods: Serum samples from ten GnRHR-AAb-positive PCOS patients and ten GnRHR-AAb-negative healthy controls were tested.

Comparison of Total Laminectomy and Pedicle Screw Internal Fixation with Ultrasonic- and Microscopic-Assisted Laminectomy Replantation for Tumors of the Lumbar Spinal Canal: A Retrospective Study of 60 Cases from a Single Center.

BACKGROUND Total laminectomy with pedicle screw internal fixation is the most common surgical procedure for patients with primary tumors arising in the spinal canal, but the procedure has several limitations. This study aimed to compare total laminectomy and pedicle screw internal fixation with ultrasound- and microscope-assisted laminectomy replantation surgery in patients with tumors of the lumbar spinal canal. MATERIAL AND METHODS A retrospective study was conducted.

Activation of vagovagal reflex prevents hepatic ischaemia-reperfusion-induced lung injury via anti-inflammatory and antioxidant effects.

New Findings: What is the central question of this study? Does vagus nerve stimulation have protective effects against both direct liver damage and distant lung injury in a rat model of hepatic ischaemia-reperfusion? What is the main finding and its importance? Vagus nerve stimulation provides protection through anti-inflammatory and anti-oxidative stress effects, possibly achieved by the vagovagal reflex.

Abstract: Hepatic ischaemia-reperfusion (I/R) is not an isolated event; instead, it can result in remote organ dysfunction. The aim of this study was to investigate whether vagus nerve stimulation (VNS) can alleviate hepatic I/R-induced lung injury and to explore the underlying mechanism.

Increased testosterone and proinflammatory cytokines in patients with polycystic ovary syndrome correlate with elevated GnRH receptor autoantibody activity assessed by a fluorescence resonance energy transfer-based bioassay.

Purpose: The recently identified agonistic autoantibodies (AAb) to the gonadotropin-releasing hormone receptor (GnRHR) are a novel investigative and therapeutic target for polycystic ovary syndrome (PCOS). In this study, we used a new cell-based fluorescence resonance energy transfer (FRET) bioassay to analyze serum GnRHR-AAb activity and examine its relationship with testosterone and proinflammatory cytokines in patients with PCOS.

Methods: Serum samples from 33 PCOS patients, 39 non-PCOS ovulatory infertile controls and 30 normal controls were tested for GnRHR-AAb activity and proinflammatory cytokines in a FRET-based bioassay and multiplex bead-based immunoassay, respectively.

Impact of deltamethrin-resistance in Aedes albopictus on its fitness cost and vector competence.

Background: Aedes albopictus is one of the most invasive species in the world as well as the important vector for mosquito-borne diseases such as dengue fever, chikungunya fever and zika virus disease. Chemical control of mosquitoes is an effective method to control mosquito-borne diseases, however, the wide and improper application of insecticides for vector control has led to serious resistance problems. At present, there have been many reports on the resistance to pyrethroid insecticides in vector mosquitoes including deltamethrin to Aedes albopictus.

Gonadotrophin-releasing hormone receptor autoantibodies induce polycystic ovary syndrome-like features in a rat model.

New Findings: What is the central question of this study? Is there a causal relationship between gonadotrophin-releasing hormone (GnRH) receptor-activating autoantibodies and polycystic ovary syndrome (PCOS)? What is the main finding and its importance? Induction of GnRH receptor-activating autoantibodies in rats resulted in increased luteinizing hormone pulsatility and testosterone concentrations, disrupted oestrous cycles, increased atretic follicles, and activation of insulin signalling in the pituitary and ovary. These changes replicate those seen in humans with PCOS, suggesting that GnRH receptor-activating autoantibodies might be involved in the pathogenesis of PCOS.

Abstract: Gonadotrophin-releasing hormone receptor-activating autoantibodies (GnRHR-AAb) are associated with polycystic ovary syndrome (PCOS).

M muscarinic autoantibodies and thyroid hormone promote susceptibility to atrial fibrillation and sinus tachycardia in an autoimmune rabbit model.

New Findings: What is the central question of this study? Do autoantibodies to the M muscarinic receptor (M2R-AAbs) have the potential to facilitate specific sustained tachyarrhythmias in the presence of thyroxine (T ) in rabbits? What is the main finding and its importance? The M2R-AAb and T jointly destabilized the electrophysiological properties, thus promoting the occurrence of atrial and sinus tachyarrhythmias in rabbits. These findings provide a practical basis for understanding the pathophysiological role of M2R-AAb alone and with T in arrhythmia induction and might provide an innovative option for treatment of Graves' disease with rhythm disturbance.

Abstract: Activating autoantibodies toward the β -adrenergic receptors (β1/2AR-AAbs) and M muscarinic receptor (M2R-AAbs) are present in a high proportion of patients with Graves' disease.

Autoimmune activation of the GnRH receptor induces insulin resistance independent of obesity in a female rat model.

Polycystic ovary syndrome (PCOS), a metabolic and reproductive disease, is frequently associated with type 2 diabetes. We have demonstrated activating autoantibodies (AAb) directed toward the second extracellular loop (ECL2) of the gonadotropin-releasing hormone receptor (GnRHR) are present in a significant subgroup of PCOS patients. It is unclear whether GnRHR-AAb can induce peripheral tissue insulin resistance (IR) in animal models.

Role of Nicotinic Acetylcholine Receptors in Cardiovascular Physiology and Pathophysiology: Current Trends and Perspectives.

Nicotinic acetylcholine receptors (nAChRs) comprise a large family of ligand-gated ion channels that have a broad distribution in neurons and non-neuronal cells throughout the body. Native nAChRs, activated by acetylcholine (ACh) endogenously, are involved in a variety of physiological and pathophysiological processes. They regulate processes necessary for network operations through neurotransmitter release, cell excitability and neuronal integration.

The Role of GnRH Receptor Autoantibodies in Polycystic Ovary Syndrome.

Objective: Is polycystic ovary syndrome (PCOS) associated with activating autoantibodies (AAb) to the second extracellular loop (ECL2) of gonadotropin-releasing hormone receptor (GnRHR)?

Design And Methods: We retrospectively screened sera from 40 patients with PCOS and 14 normal controls (NCs) with regular menses using enzyme-linked immunosorbent assay (ELISA) for the presence of GnRHR-ECL2-AAb. We obtained similar data from 40 non-PCOS ovulatory but infertile patients as a control group (OIC) of interest. We analyzed GnRHR-ECL2-AAb activity in purified immunoglobulin (Ig)G using a cell-based GnRHR bioassay.

Ginsenoside Rg1-induced activation of astrocytes promotes functional recovery via the PI3K/Akt signaling pathway following spinal cord injury.

Aims: To determine whether ginsenoside Rg1 is involved in scratch wound healing through altered expression of related molecules in astrocytes and improved functional recovery after spinal cord injury (SCI).

Materials And Methods: Astrocytes were isolated from rats, followed by Rg1 treatment. The wound healing test was performed to observe the scratch wound healing in different groups.

Activation of α7nAChR via vagus nerve prevents obesity-induced insulin resistance via suppressing endoplasmic reticulum stress-induced inflammation in Kupffer cells.

Obesity is a major risk factor for type 2 diabetes mellitus and insulin resistance (IR). In the state of obesity, excess fat accumulates in the liver, a key organ in systemic metabolism, altering the inflammatory and metabolic signals contributing substantially to the development of hepatic IR. Current therapies for these metabolic disorders have not been able to reverse their rapidly rising prevalence.

Vagus Nerve Stimulation Ameliorates Renal Ischemia-Reperfusion Injury through Inhibiting NF-B Activation and iNOS Protein Expression.

Objective: In renal ischemia/reperfusion injury (RIRI), nuclear factor B (NF-B (NF-B (NF.

Methods: Eighteen male Sprague-Dawley rats were randomly allocated into the sham group, the I/R group, and the VNS+I/R group, 6 rats per group. An RIRI model was induced by a right nephrectomy and blockade of the left renal pedicle vessels for 45 min.

Fast emerging insecticide resistance in Aedes albopictus in Guangzhou, China: Alarm to the dengue epidemic.

Dengue is one of the most serious mosquito-borne infectious diseases in the world. Aedes albopictus is the most invasive mosquito and one of the primary vectors of dengue. Vector control using insecticides is the only viable strategy to prevent dengue virus transmission.

Vagus Nerve Stimulation Attenuates Hepatic Ischemia/Reperfusion Injury via the Nrf2/HO-1 Pathway.

It has been demonstrated that vagus nerve stimulation (VNS) plays a protective role in ischemia/reperfusion (I/R) injury of various organs. The present study investigates the protective effect of VNS on hepatic I/R injury and the potential mechanisms. Male Sprague-Dawley rats were randomly allocated into three groups: the sham operation group (Sham; = 6, sham surgery with sham VNS); the I/R group ( = 6, hepatic I/R surgery with sham VNS); and the VNS group ( = 6, hepatic I/R surgery plus VNS).

Vagus nerve stimulation protects against acute liver injury induced by renal ischemia reperfusion via antioxidant stress and anti-inflammation.

Objective: Renal ischemia reperfusion (I/R) is not an isolated event; however, it results in remote organ dysfunction. Vagus nerve stimulation (VNS) has shown protective effects against renal I/R injury via an anti-inflammatory mechanism. This study aimed to investigate whether VNS could attenuate liver injury induced by renal I/R and identify the underlying mechanisms.

Gut microbe-derived metabolite trimethylamine N-oxide activates the cardiac autonomic nervous system and facilitates ischemia-induced ventricular arrhythmia via two different pathways.

Background: We previously demonstrated the gut microbes-derived metabolite trimethylamine N-oxide (TMAO) could activate the atrial autonomic ganglion plexus and promote atrial arrhythmia. The cardiac sympathetic nervous system (CSNS) play important roles in modulating ventricular arrhythmia (VA).

Methods: Part 1: To test whether TMAO can directly activate the CSNS, we performed local injection of TMAO into the left stellate ganglion (LSG).

Vagus Nerve Stimulation Attenuates Acute Skeletal Muscle Injury Induced by Ischemia-Reperfusion in Rats.

Vagus nerve stimulation (VNS) has been shown to attenuate ischemia-reperfusion (I/R) injury in multiple organs. The present study aimed at investigating whether VNS could exert protective effects against I/R injury in the skeletal muscle. Male Sprague-Dawley rats were randomly divided into 3 groups: the control, I/R, and I/R+VNS groups.