Glutamine levels were positively associated with a greater risk of stroke (OR = 1.599, p = 0.022). After treatment with glutamine, HBMECs exhibited enhanced proliferation, migration, and EndMT, all reversed by ITGB4 knockdown. In ITGB4-transfected HBMECs, the MAPK–ERK–TGF–β/BMP pathway was activated, with Smad4 knockdown reversing the EndMT. Furthermore, atorvastatin suppressed the EndMT by inhibiting Smad1/5 phosphorylation and promoting Smad4 ubiquitination in ITGB4-transfected HBMECs. Finally, ITGB4 upregulation was confirmed in the superficial temporal arteries of patients with MMD.

The diagnosis of Alzheimer's disease (AD) typically relies on costly and invasive cerebrospinal fluid (CSF) markers, causing discomfort to patients. Sun et al. propose a cost-effective method for early detection that utilizes a random forest approach to accurately estimate the Aβ1-42/Aβ-40 content. The method is based on noninvasive techniques including EEG and MRI and was tested on a sample of 82 subjects, providing valuable diagnostic information.

Scientific hypothesis: After radiation exposure, lung cancer cells undergo DNA damage, triggering RBM17 to sense signals. MSI2, assisted by RBM17, translocates into the nucleus, where it interacts with ATR and CHK1, activating downstream pathways. This activation enhances the DNA damage repair. Upon repair completion, MSI2 and RBM17 dissociate from ATR and exit the nucleus, returning to the initial state.

A set of normal values of three-dimensional right ventricular volume and function was first established in a large Chinese population, which was significantly smaller than those recommended by the international guidelines.

Amplification of 10q24.32 in CRC resulted in upregulation of NFKB2 protein levels, which directly interacts with STAT2, leading to STAT2 protein stabilization and phosphorylation, and consequently, further upregulating PD-L1. Rg5, a small-molecule inhibitor of NFKB2, could break the NFKB2-STAT2 interaction, with significant reduced PD-L1 expression and alleviated CD8⁺ T-cell exhaustion, leading to an enhanced sensitivity to PD-1 blockade-based immunotherapy.

Senescent cells exert a double-edged sword effect on tumor progression. Amplification beneficial effects while inhibition related protumorigenic pathways of senescence will help improve antitumor efficacy.

1. SBRT applying during systemic therapy is safe and effective in the management of mRCC.
2. SBRT applied disease setting and timing may be critical for clinical outcomes and needed further research.

We found that Mangxiao (MX) was a unique mineral medicine that was effective in prevention and cure colorectal cancer. It was first time to find that MX could reshape the Lactobacillus–bile acid–FXR axis, thereby inhibiting the occurrence and development of CRC. The bacterial-targeted approach to control CRC provided a basis for the development of unique anticolorectal cancer drugs.

Manageable safety and clinical benefit of inetetamab plus pyrotinib were shown in advanced HER2-mutant NSCLC. Responses were observed in patients with various HER2 aberrations including HER2 exon 20 insertion mutations, missense mutations, and HER2 amplification.

A chimeric adenovirus-vectored vaccine named Ad5-Beta/Delta was developed by introducing the RBD derived from the Delta variant (containing L452R and T478K) into the full-length spike protein of Beta variant. Immunization with Ad5-Beta/Delta induces broad-spectrum neutralizing activities against BA.5-included SARS-CoV-2 subvariants. Combination of intramuscular and intranasal delivery of Ad5-Beta/Delta induces superior systemic and mucosal immune responses. In addition, Ad5-Beta/Delta as a booster shot is able to elicit stronger protective immunity in heterologous vaccination after two injections of mRNA- and subunit protein-based vaccines.

Interactions of TLRs with inflammation and tumor. TLRs are expressed on a variety of cells, including tumor cells and immune cells. TLRs signaling is involved in the carcinogenesis of the tumor microenvironment. TLRs expressed on immune cells and tumor cells are subjected to activation by pathogen-associated molecular patterns,damage-associated molecular patterns from microorganisms, viruses, parasites, injured and necrotic cancer cells. The release of cytokines and chemokines by these activated cells is an important part of the tumor microenvironment. Moreover, cytokine-activated infiltrating immune cells can subsequently induce additional cytokines that impair the function of antigen-presenting cells, leading to tumor immune tolerance.

This review presents the crucial involvement of RNA epigenetic modifications (m⁶A, m¹A, m⁵C, Ψ, m⁷G, and A-to-I editing) in pulmonary diseases, spanning chronic conditions to lung cancer. Focusing on their impact on disease regulation as promising biomarkers and therapeutic targets. Additionally, essential databases and tools are summarized, fostering insights for clinical research of pulmonary disease to improve diagnosis and treatment. m⁶A, N⁶-methylation of adenosine; m¹A, N¹-methylation of adenosine; m⁵C, 5-methylcytosine; Ψ, pseudouridine; m⁷G, 7-methylguanosine; A-to-I, adenosine to inosine; COPD, chronic obstructive pulmonary disease; IPF, interstitial lung disease, idiopathic pulmonary fibrosis; ARDS, acute respiratory distress syndrome; PTB, pulmonary tuberculosis; RMBase, RNA Modification Base Database; NGS, next-generation sequencing; LC–MS, liquid chromatography mass spectrometer; TLC, thin layer chromatography; RIP, RNA immunoprecipitation.

A schematic overview of IDO1-induced tryptophan deficiency results in GLUT1-dependent upregulation of glycolysis in pancreatic cancer.

Overview of the mechanisms of m⁶A, m¹A, m⁶Am, m⁷G, Ψ, and m⁵C regulation. RNA methylation is a dynamically reversible process that is modulated by methyltransferases (writers), demethylases (erasers), and recognition factors (readers). Under the regulation of these regulatory factors, RNA undergoes various RNA methylation modifications.

Abnormally high expression of PA28γ in oral lichen planus could promote the maturation of dendritic cells and promote the differentiation of T-cells via the CCL5-CD44 pathway.

Zhang et al. successfully regenerated iNK cells from human iPSCs with rDNA locus gene editing. IL24 enhances the antitumor activity and proliferation of armored CAR-iNK cells, which may be involved in cellular-positive upregulation and adhesion pathways.

We innovatively fused an antihuman serum albumin nanobody to a single-domain antibody–drug conjugates targeting oncofetal antigen 5T4, conferring serum albumin binding, exhibiting a 10-fold extended half-life and enhanced tumor accumulation and retention in mice. Consequently, it demonstrated significantly improved antitumor efficacy in tumor xenografts despite less frequent dosing with mitigated hepatotoxicity.

Bortezomib and IL-33 synergistically resulted in excessive accumulation of cellular reactive oxygen species (ROS) and depletion of glutathione (GSH), which in turn damaged DNA and ultimately triggered cell death. In addition, ROS overproduction hindered the nuclear translocation of NF-κB-p65, thereby decreasing the transcription levels of target stemness-related genes (SOX2, MYC, and OCT3/4). ROS elimination by N-acetylcysteine intervention can reverse the inhibition of nuclear factor kappa-B (NF-κB) activity and its transcriptional targets.

This study aimed to evaluate the relationships between essential metal levels and aortic arch calcification (AoAC) risk in a mid-aged and older population of Shenzhen, China. The results showed that plasma levels of five essential metals were associated with AoAC and showed combined effect. Blood glucose played a significant role in mediating Mn exposure-associated AoAC risks.

EHF plays a crucial role in promoting cholangiocarcinoma (CCA) by activating GLI1 transcription. Additionally, EHF proficiently recruits and activates tumor-associated macrophages via the CCL2/CCR2 axis, leading to tumor microenvironment remodeling. Furthermore, the strategic combination of GANT58 (a GLI1 inhibitor) and INCB3344 (a CCR2 inhibitor) significantly reduces EHF-driven CCA occurrence.