Yan Xu - research works

Mendelian randomization confirmed that CKD is a significant risk factor for CAD.

We identified 12 genes shared by AMI, CKD, and PANoptosis, and determined SOCS3 and HSPA1A as key diagnostic genes.

Functional analysis showed enrichment in pathways including JAK STAT signaling and apoptosis.

Animal experiments demonstrated that knockdown of SOCS3 significantly inhibited expression of key PANoptosis molecules such as CASP1, CXCL10, and ZBP1 after MI, reduced inflammation, and improved cardiac function.

The initial volume of ropivacaine (0.2%) was 0.5 mL/kg, adjusted by 0.05 mL/kg based on the previous patient's response.

The study continued until seven inflection points were observed from failure to success.

Patient demographics, postoperative pain scores, and adverse events were monitored.

No adverse events were observed during the perioperative period.

Among the 48 enrolled patients with suspected HNL, 37 were confirmed by pathological diagnosis and the remaining 11 were diagnosed based on clinical criteria.

The median Nil level was significantly elevated in HNL patients [0.82 IU/mL, interquartile range (IQR): 0.36-1.18] compared with patients with systemic juvenile idiopathic arthritis (sJIA, median = 0.07 IU/mL, P < 0.0001), Kawasaki disease (KD, median = 0.09 IU/mL, P < 0.0001) and Bacterial Lymphadenitis (BL, median = 0.09 IU/mL, P < 0.0001).

The most experienced radiologist had the lowest missed diagnosis rate.

9.09% [95% CI: 3.80-19.84%], p = 0.019).

16.36% [95% CI: 8.38-28.82%], p < 0.001).