Homocysteine (Hcy) is an important intermediate product in methionine metabolism which plays a key role in the methylation of DNA, RNA and proteins. High level of Hcy can induce endothelial cell damage, promote the release of inflammatory factors, stimulate oxidative stress and inhibit the fibrinolytic system. Numerous studies have confirmed the close relationship between hyperhomocysteinemia (HHcy) and the occurrence/development of various diseases such as cardiovascular diseases, neurological disorders, thrombotic diseases, and tumors. With the rising incidence of thyroid diseases, the relationship between Hcy and thyroid diseases has attracted widespread attention. It has been found that HHcy may be directly or indirectly associated with the development of hypothyroidism, but the findings with hyperthyroidism, chronic lymphocytic thyroiditis and reduced thyroid hormone sensitivity are controversial. This article reviews the research progress of Hcy and thyroid diseases, with a view to providing new ideas for the prevention and clinical treatment of diseases.

Enterococci are a common cause of infective endocarditis (IE). This study aimed to assess the diagnostic performance of the 2015 and 2023 Duke versions of the European Society of Cardiology (ESC) Duke criteria, as well as the 2023 Duke International Society of Cardiovascular Infectious Diseases (ISCVID) clinical criteria, for identifying IE among patients with enterococcal bacteremia.

We included adult retrospective patients with enterococcal bacteremia from 3 independent cohorts across 2 Swiss university hospitals between 2015 and 2024. An interdisciplinary Endocarditis Team classified each case as either IE or not IE. Each episode was then classified as definite, possible, or rejected IE according to the 2015 Duke-ESC, 2023 Duke-ESC, and 2023 Duke-ISCVID clinical criteria. Patients with IE (reference standard) classified as definite IE by the Duke criteria were considered true positives, while those without IE classified as rejected IE were considered true negatives.

Among 827 episodes with enterococcal bacteremia, IE was diagnosed in 173 (21%) episodes. The sensitivity of the 2015 Duke-ESC, 2023 Duke-ISCVID, and 2023 Duke-ESC clinical criteria for diagnosing IE was 67% (95% CI, 59%-74%), 79% (95% CI, 72%-85%), and 74% (95% CI, 67%-80%), respectively. Specificity was 86% (95% CI, 83%-89%) for the 2015 Duke-ESC criteria, 55% (95% CI, 51%-59%) for the 2023 Duke-ISCVID criteria, and 69% (95% CI, 65%-72%) for the 2023 Duke-ESC criteria.

Among the evaluated Duke criteria versions, the 2023 Duke-ISCVID criteria demonstrated the highest sensitivity for diagnosing IE in patients with enterococcal bacteremia. However, this was at the expense of specificity.

G protein-coupled receptors (GPCRs) are the largest family of membrane proteins in eukaryotes, with nearly 800 genes coding for these proteins. They are involved in many physiological processes, such as light perception, taste and smell, neurotransmitter, metabolism, endocrine and exocrine, cell growth and migration. Importantly, GPCRs and their ligands are the targets of approximately one third of all marketed drugs. GPCRs are traditionally known for their role in transmitting signals from the extracellular environment to the cell's interior via the plasma membrane. However, emerging evidence suggests that GPCRs are also localized on mitochondria, where they play critical roles in modulating mitochondrial functions. These mitochondrial GPCRs (mGPCRs) can influence processes such as mitochondrial respiration, apoptosis, and reactive oxygen species (ROS) production. By interacting with mitochondrial signaling pathways, mGPCRs contribute to the regulation of energy metabolism and cell survival. Their presence on mitochondria adds a new layer of complexity to the understanding of cellular signaling, highlighting the organelle's role as not just an energy powerhouse but also a crucial hub for signal transduction. This expanding understanding of mGPCR function on mitochondria opens new avenues for research, particularly in the context of diseases where mitochondrial dysfunction plays a key role. Abnormalities in the phase conductance pathway of GPCRs located on mitochondria are closely associated with the development of systemic diseases such as cardiovascular disease, diabetes, obesity and Alzheimer's disease. In this review, we examined the various types of GPCRs identified on mitochondrial membranes and analyzed the complex relationships between mGPCRs and the pathogenesis of various diseases. We aim to provide a clearer understanding of the emerging significance of mGPCRs in health and disease, and to underscore their potential as therapeutic targets in the treatment of these conditions.

Ischemic Stroke (IS) is a severe neurological disease with high mortality rates worldwide, involving a complex cascade reaction in which the ubiquitination process of nuclear factor kappa B (NF-[Formula: see text]B) pathway has been proposed as a therapeutic target for IS on account of the fact that NF-[Formula: see text]B can be suppressed by the Ubiquitin-Proteasome System (UPS). This review systematically discusses the epidemiology of IS, the NF-[Formula: see text]B signaling pathway, and the anti-inflammatory and anti-apoptotic effects that TCM monomers and formulations exert by regulating the ubiquitination process of the NF-[Formula: see text]B signaling pathway. We initially offer an overview of the incidence and treatment of IS, following which the canonical pathway and non-canonical pathway of NF-[Formula: see text]B are introduced. Next, the ubiquitination mechanisms of NF-[Formula: see text]B when using traditional Chinese medicine (TCM) to treat IS were highlighted. We also discussed the involvement of MyD88, an upstream protein, in the herb-based treatment of IS. Finally, we proposed future research directions for screening advantageous herbal components. Given previous research, we anticipate that TCM drugs will present promising candidates for IS treatment in clinical medicine.