Publications by authors named "Hui-Hua Li"

Infiltration of immune cells into the heart plays a crucial role in the transition from adaptive hypertrophy to heart failure (HF) following chronic pressure overload. However, the key factors in myeloid cells that regulate this process are still not well defined. Here, we studied the functional role of S100A8/A9 in myeloid cells during this transition.

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Lipid peroxidation and ferroptosis are critically for the development of cardiac ischaemia-reperfusion (I/R) injury. The proteasome complex is crucial for regulating inflammation and cardiac I/R injury. Proteasome-activating peptide 1 (PAP1) is an activator of the proteasome β5i subunit, but its role in cardiac I/R injury remains unknown.

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Background: Myocardial ischemia/reperfusion (I/R) injury is a leading cause of myocardial dysfunction and is associated with inflammation, apoptosis, and fibrosis. The integrin subunit ITGAM (also known as CD11b) mainly mediates leukocyte infiltration in the inflammatory process. However, the importance of CD11b in the development of myocardial I/R injury is unclear.

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Postpartum depression is a common type of psychiatric disorder during the postpartum period. It significantly affects the mental and physical health of new mothers and has long-term negative effects on the growth and development of infants and toddlers. Consequently, there is increasing research both domestically and internationally on the treatment of postpartum depression, though the means of treatment are limited.

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Sepsis-induced cardiomyopathy (SIC) represents a severe and often fatal complication of sepsis, characterized by significant mortality. Despite extensive research, the underlying mechanisms remain incompletely understood. Recent studies have highlighted PANoptosis, an emerging form of programmed cell death, as a critical factor in inflammatory diseases.

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The mitochondrial dynamic imbalance is an important cause of myocardial ischaemia/reperfusion (I/R) injury and dysfunction. Psmb8, as one of the immunoproteasome catalytic subunits, is a key regulator of protein homoeostasis, inflammation and some cardiac diseases. Here, we found that the expression level and activity of Psmb8 were significantly reduced in the heart of I/R mice and in subjects with myocardial infarction (MI).

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BACKGROUND: The objective of this study is to investigate the clinical effectiveness of the combination of multimodal exercise (MME) with supportive music and imagery in the management of poststroke mood disorders (PSMD). METHODS: A total of 200 PSMD patients treated in the neurology department of a tertiary hospital in Jiangsu Province were enrolled. They were assigned to either a control group or the observation group using a random number table at a 1:1 ratio, with 100 patients in each group.

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Background: Alzheimer's disease (AD) can be optimally managed from a healthcare point of view if detected at a prodromal stage. Amnestic mild cognitive impairment (MCI) is known as prodromal AD, has attracted extensive attention and research.

Objective: To identify the differences in cognitive function and structural magnetic resonance imaging (MRI) features between men and women with MCI on the basis of A/T/N classification system ("A" means amyloid-β biomarker, "T" means tau biomarker, and "N" means neurodegeneration biomarker as determined by clinical imaging (e.

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Cardiac ischaemia/reperfusion (I/R) impairs mitochondrial function, resulting in excessive oxidative stress and cardiomyocyte ferroptosis and death. Nuclear factor E2-related factor 2 (Nrf2) is a key regulator of redox homeostasis and has cardioprotective effects against various stresses. Here, we tested whether CBR-470-1, a noncovalent Nrf2 activator, can protect against cardiomyocyte death caused by I/R stress.

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Angiotensin-converting enzyme 2 (ACE2), a crucial element of the renin-angiotensin system (RAS), metabolizes angiotensin II into Ang (1-7), which then combines with the Mas receptor (MasR) to fulfill its protective role in various diseases. Nevertheless, the involvement of ACE2 in sepsis-induced cardiomyopathy (SIC) is still unexplored. In this study, our results revealed that CLP surgery dramatically impaired cardiac function accompanied with disruption of the balance between ACE2-Ang (1-7) and ACE-Ang II axis in septic heart tissues.

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Background: Sepsis is a life-threatening condition that is characterized by multiorgan dysfunction and caused by dysregulated cytokine networks, which are closely associated with sepsis progression and outcomes. However, currently available treatment strategies that target cytokines have failed. Thus, this study aimed to investigate the interplay between genetically predicted circulating concentrations of cytokines and the outcomes of sepsis and to identify potential targets for sepsis treatment.

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Objectives: to assess the survival rates of removable partial dentures (RPDs) and identify factors impacting their longevity.

Methods: electronic health records were retrieved of patients aged ≥18 who received RPDs between 2010 - 2021 with a follow-up of ≥ three months. Data extracted included demographics, medical history, dental charting, periodontal screening and recording scores, prostheses details and related interventions, including new dentures/denture remakes, and maintenance.

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PANoptosis is a newly discovered type of cell death characterized by pyroptosis, apoptosis and/or necroptosis and has been implicated in the inflammatory response. Piezo1 is a mechanosensitive ion channel that plays important roles in physiological development and various diseases. However, whether cardiomyocytes undergo PANoptosis during myocardial ischaemia/reperfusion (I/R) injury and the role of Piezo1 in this process remain largely unexplored.

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The ubiquitinproteasome system (UPS) is the main mechanism responsible for the intracellular degradation of misfolded or damaged proteins. Under inflammatory conditions, the immunoproteasome, an isoform of the proteasome, can be induced, enhancing the antigen-presenting function of the UPS. Furthermore, the immunoproteasome also serves nonimmune functions, such as maintaining protein homeostasis and regulating signalling pathways, and is involved in the pathophysiological processes of various cardiovascular diseases (CVDs).

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Neuroinflammation and oxidative stress contribute to the progression of sepsis-associated encephalopathy (SAE). Angiotensin-converting enzyme 2 (ACE2) is considered to be a neuroprotective factor due to its anti-inflammatory and antioxidant properties. However, the role of ACE2 on myeloid cells in regulating SAE and the underlying mechanism warrants further exploration.

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Perioperative neurocognitive disorders (PND) are a cognitive impairment that occurs after anesthesia, especially in elderly patients and significantly affects their quality of life. The hippocampus, as a critical region for cognitive function and an important location in PND research, has recently attracted increasing attention. However, in the hippocampus the impact of anesthesia and its underlying mechanisms remain unclear.

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Persistent pressure overload commonly leads to pathological cardiac hypertrophy and remodeling, ultimately leading to heart failure (HF). Cardiac remodeling is associated with the involvement of immune cells and the inflammatory response in pathogenesis. The macrophage-1 antigen (Mac-1) is specifically expressed on leukocytes and regulates their migration and polarization.

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Article Synopsis
  • Sepsis can cause acute liver injury (ALI) in ICU patients, and the role of the enzyme ACE2 in this condition is not well understood.
  • A study found that ACE2 levels drop significantly in a mouse model of sepsis, and using ACE2-transgenic mice improved liver function and reduced cell death and inflammation compared to ACE2-knockout mice.
  • The research suggests that ACE2 protects against sepsis-induced ALI through a specific receptor pathway, indicating that enhancing ACE2 activity could be a potential treatment strategy for this condition.
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