CREB1/CRTC2 regulated tubular epithelial-derived exosomal miR-93-3p promotes kidney injury induced by calcium oxalate via activating M1 polarization and macrophage extracellular trap formation.

Background: Calcium oxalate (CaOx) crystals are known to cause renal injury and trigger inflammatory responses. However, the role of exosome-mediated epithelial-macrophage communication in CaOx-induced kidney injury remains unclear.

Methods: To identify key molecules, miRNA sequencing was conducted on exosomes derived from CaOx-treated (CaOx-exo) and control (Ctrl-exo) epithelial cells, identifying miR-93-3p as significantly upregulated.

GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses.

A common urological disorder, calcium oxalate (CaOx) stones are the most common form of kidney stones. Deposition of CaOx crystals leads to tubular damage, interstitial fibrosis, and chronic kidney disease. Understanding the intrinsic mechanisms of kidney stone formation is essential for the prevention of kidney stones and the development of new therapeutic agents.

Lgals3 Promotes Calcium Oxalate Crystal Formation and Kidney Injury Through Histone Lactylation-Mediated FGFR4 Activation.

The incidence of kidney stones is increasing worldwide. However, the underlying mechanism of the process of kidney stone formation and the kidney damage caused are not well understood. Here, it is observed that Lgals3, a β-galactoside-binding protein, is significantly increased in tissues with calcium oxalate (CaOx) stones, and in both in vivo and in vitro models.

UHRF1 promotes calcium oxalate-induced renal fibrosis by renal lipid deposition via bridging AMPK dephosphorylation.

Background: Nephrolithiasis, a common urinary system disorder, exhibits high morbidity and recurrence rates, correlating with renal dysfunction and the increased risk of chronic kidney disease. Nonetheless, the precise role of disrupted cellular metabolism in renal injury induced by calcium oxalate (CaOx) crystal deposition is unclear. The purpose of this study is to investigate the involvement of the ubiquitin-like protein containing PHD and RING finger structural domain 1 (UHRF1) in CaOx-induced renal fibrosis and its impacts on cellular lipid metabolism.

SGLT-2 inhibitors and high-dose acarbose as potential high-risk combinations for ketosis and ketoacidosis in Asian patients with T2DM: A case series.

Key Clinical Message: High-dose acarbose may increase the risk of diabetic ketosis/diabetic ketoacidosis in Asian patients on sodium-glucose cotransporter-2 inhibitors. Healthcare providers and patients should be cautious to avoid this combination.

Abstract: Low-calorie diets should be avoided in patients receiving sodium-glucose cotransporter-2 (SGLT-2) inhibitors to decrease the risk of diabetic ketoacidosis (DKA).

The identification of key molecules and pathways in the crosstalk of calcium oxalate-treated TCMK-1 cells and macrophage via exosomes.

The interplay between crystals and epithelial cells forms the cornerstone of kidney stone development, communication between epithelial cells and macrophages emerging as a pivotal role in this process. We conducted next-generation sequencing on the secreted exosomes of TCMK-1 cells treated with calcium oxalate monohydrate (OX_EXO) or controls (NC_EXO), and on the macrophage cell line RAW264.7 stimulated with OX_EXO or NC_EXO, followed by validation of differentially expressed target proteins and miRNAs through Western blot and PCR.

9-Nitro-20(S)-carbonate-camptothecin (NCP4), a novel prodrug of 9-nitrocamptothecin (9-NC), exhibits potent chemotherapeutic efficacy and improved safety against hepatocarcinoma.

9-nitrocamptothecin (9-NC), an active derivative of camptothecin (CPT), demonstrated antitumor effect on experimental tumors in mice by topoisomerase I (Topo I) inhibition. However, under human physiological conditions, the rapid opening of lactone ring of 9-NC resulting in the formation of inactive and high toxic carboxylate limited its clinical efficacy. Therefore, strategies aimed to maintain the active closed-lactone form of 9-NC in the plasma were developed, such as prodrugs.

The Impact of Coexistent Hashimoto's Thyroiditis on Central Compartment Lymph Node Metastasis in Papillary Thyroid Carcinoma.

Background: Hashimoto's thyroiditis (HT) is the most prevalent inflammatory disorder of the thyroid gland. Current studies have reported the coexistence rate between HT and papillary thyroid carcinoma (PTC) is quite high. The objective of this study was to evaluate the impact of HT on the predictive factors of central compartment lymph node metastasis (CLNM) in PTC.

Sinomenine hydrochloride inhibits the progression of plasma cell mastitis by regulating IL-6/JAK2/STAT3 pathway.

Plasma cell mastitis (PCM) is a special form of mastitis characterized by periductal inflammation and large-scale plasma cell infiltration. At present, the recurrence rate of PCM after excision is quite high, making PCM a major problem for mammary surgeons. However, no effective drug exists for the treatment of PCM.

Dihydrotestosterone regulates oxidative stress and immunosuppressive cytokines in a female BALB/c mouse model of Graves' disease.

Graves' disease (GD) is an autoimmune disease that affects more women than men. In our previous study, a potent bioactive androgen, 5α-dihydrotestosterone (DHT) showed a protective effect against GD in female BALB/c mice. Evidence indicates that abnormal oxidative stress and immunosuppressive cytokines (TGF-β, IL-35) play critical roles in the pathogenesis and development of GD.

Gender-Specific Risk of Central Compartment Lymph Node Metastasis in Papillary Thyroid Carcinoma.

Our aim was to evaluate the impact of gender on the predictive factors of central compartment lymph node metastasis (CLNM) in papillary thyroid carcinoma (PTC). A retrospective study of 590 patients treated for PTC was performed. Univariate and multivariate analyses showed that gender (female; = 0.