The combined metformin/mirabegron treatment not only prevents the development of diet-induced obesity but also promotes weight loss in established diet-induced obesity. Furthermore, metformin/mirabegron treatment induces a greater reduction in body weight than either treatment when used alone. Mechanistically, these benefits on weight loss were mainly achieved by activating brown adipose tissue thermogenesis and promoting subcutaneous white adipose tissue browning, leading to enhanced energy expenditure.

Osthole (OS) suppressed the positive feedback circuit transglutaminase 2 (TGM2)/Myc/WTAP-facilitated NF-κB signaling to attenuate the pathological phenotype of RA-fibroblast-like synoviocytes as well as impair the proliferation and polarization of CD11b⁺ M2 macrophages in the control of RA and RA-interstitial lung disease (ILD) progression. OS might serve as an effective anti-RA and anti-RA ILD drug without toxicity, and TGM2 might be applied as a target for RA treatments.

CTX treatment leads to immunosuppression and gut microbiota dysbiosis in mice. PPD treatment can protect against CTX-induced gut microbiota dysbiosis by increasing the abundance of beneficial bacteria and inhibiting the proliferation of pathogenic bacteria. The beneficial bacteria metabolize to produce immune-enhancing metabolites and anti-inflammatory metabolites, which contribute to the immune-enhancing and anti-inflammatory functions of PPD-M in CTX-induced immunosuppressed mice, including promoting bone marrow hematopoiesis to increase the number of peripheral blood white blood cells, proliferating splenic lymphocytes, and eliminating inflammation.

This study used the participants from the Asymptomatic Polyvascular Abnormalities in Community (APAC) to develop a new sex-specific prediction equation that involves physical activity (PA equation) for cardiovascular (CVD) risk prediction. The developed sex-specific PA equations have shown good performance to predict CVD for a physical active cohort in the Kailuan population that will help to improve the prevention and treatment of CVD.

We prepared a Delta full-length spike protein sequence-based mRNA vaccine (Figure A, B) and developed a recombinant trimeric receptor-binding domain (RBD) protein vaccine (Figure C). Later, the mRNA vaccine was injected as the “priming” shot, and the RBD–HR/trimer vaccine was used as a third heterologous booster (Figure D).

In the 7,12-dimethylbenzoanthracene/tetradecylphorbol-13-acetate two-stage skin cancer induction model, interleukin weakened the expression of CD40/CCR7 and the secretion of C-X-C motif chemokine ligand 9/CXCL10 in CD103⁺DCs through single immunoglobulin interleukin-1-related receptor-activated protein kinase-Akt signal axis, which leads to the suppression the function of CD8⁺T cells and accelerating the growth of tumor.

This study suggested that RTN3 can interact with GRP78 on the endoplasmic reticulum. The increased expression of RTN3 can facilitate interactions between RTN3 and GRP78, thereby decreasing the activity of GRP78 in regulating AMPK phosphorylation, which further reduces the expression IDH2, finally resulting in mitochondrial dysfunction, increased reactive oxygen species, and NAFLD.

The pro-inflammatory cytokine IL-1β could be triggered and released from macrophages (Mφ) by lactate derived from tumor cells. Interleukin (IL)-1β, in turn, drove an immune inhibitory phenotype on tumor cells, especially on the increase in programmed death-ligand 1, by activating the nuclear factor-κB (NF-κB) signaling pathway. Thus, tumor-released lactate and Mφ-derived IL-1β mediated the crosstalk loop and caused immunosuppression. Moreover, activated NF-κB signaling promoted C-C motif chemokine ligand 2 secretion in tumor cells, leading to further monocyte recruitment and replenishment of the Mφ population, which maintained the malignant feedback loop (Figure 7).

This genome-wide association study discovered 14 and 3 independent loci that had potential associations with Tuberculosis (TB) susceptibility in the Chinese Han and Tibetan populations, respectively (p < 1 × 10^-5). Further imputation-based meta-analysis on another two East Asia cohorts verified one independent locus harbored by the human leukocyte antigen class II genes that was genome-wide significantly associated with TB (lead single nucleotide polymorphism rs111875628 with a p-value of 2.20 × 10^-9).

The ligands are combined with nano-zinc hydroxide carriers to guide aptamer and siUSP14 to specifically bind to the surface of DDP-resistant A549/DDP cells. After internalization of the paired aptamer and carriers, intracellular pH changes cause the active release of the siUSP14, followed by inactivation of epidermal growth factor receptor (EGFR)/PI3K/protein kinase B (AKT) signaling pathway, resulting in decreased DDP resistance in A549/DDP cells.

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive and lethal malignancy with a high rate of recurrence and a dismal 5-year survival rate. A recent shift toward a neoadjuvant approach to treating PDAC has been sparked by the numerous benefits neoadjuvant therapy (NAT) has to offer compared with upfront surgery. This review bridges the molecular understanding of PDAC with its clinical significance, development of novel therapies, and shifting directions in treatment paradigm with an emphasis on the use of NAT.

Several microbes, such as Fn, Helicobacter pylori, Fusobacterium, Staphylococcus aureus, Peptostreptococcus anaerobius, and Porphyromonas gingivalis, promote cancer progression. Other microbes, such as Lactobacillus, Bifidobacterium, Clostridium butyricum, Bacillus subtilis, Bifidobacteria, Lactobacoilli, Streptococcus thermophilus, Leptotrichia, Bacteroides thetaiotaomicron, and Faecalibacterium prausnitzii, can inhibit cancer progression. Possible therapeutic approaches for cancer include fecal microbiome transplantation (FMT), probiotics, synbiotics, antibiotics, oncolytic virus, and nanospheres.

This review highlighted the importance in elucidating the regulation of biomolecular condensates, which is urgently needed for the development of novel therapies. The characteristics, formation mechanism and functions of biomolecular condensates, and the therapeutic targets for diseases are systematically summarized in this review. The available regulatory targets and methods are also discussed in this review. Moreover, this review depicted the significance and challenges of targeting these condensates.

A schematic overview of severe acute respiratory syndrome coronavirus 2 mediated neurological damages in coronavirus disease 2019 causing cerebral ischemia.

This article presented the metabolic reprogramming of tumor cells to adapt to their microenvironment distinct from normal cells. And this study reviewed the driving factors of metabolic reprogramming, the specific metabolic pathway changes affected, and the related treatment options, in order to provide some suggestions for future tumor treatment.

In the Omicron wave, two emerging subvariants, BQ.1 and XBB, have rapidly become a global public health concern. This diagram illustrates the critical spike mutations in these subvariants, which can lead to immune escape from prior COVID-19 vaccines, boosters, and therapeutic monoclonal antibodies (mAbs). Notably, XBB.1.5, which carries a rare F486P mutation, has demonstrated significantly higher receptor-binding domain (RBD)-ACE2 binding affinity and transmissibility compared to other subvariants, making it the dominant strain in several countries.

• FMRP is regulated by Myc and is highly expressed in a variety of human and mouse tumor tissues.
• FMRP recruits Treg and M2 macrophages to form an immunosuppressive tumor microenvironment by IL3, PROS1 and exosomes.
• FMRP-KO up-regulates tumor cell secretion of CCL7, which directly activates and recruits CD8+ T cells.
• FMRP-KO recruits CCR5 and CXCR4 receptor-positive CD8 T cells indirectly by promoting M1 macrophages to secrete CCL5, CXCL9, and CXCL10.

PRMT5 promotes ovarian cancer growth and Taxol response through enhancing glycolysis pathway, which mediated by regulating the symmetric dimethylation of arginine (SDMA) modification of ENO1.

This paper reviews not only the structure, replication mechanism, and variants of severe acute respiratory syndrome (SARS)-CoV-2 but also exposes all the details of the pandemic, such as how it came out, how it spread, what precautions should be taken, and prevention strategies in every aspect. It also compares the molecular and serological assays used for SARS-CoV-2 diagnosis and lists the COVID-19 vaccines approved by the countries.