Development and validation of a predictive model assessing the risk of sarcopenia in rheumatoid arthritis patients.

Background: Sarcopenia is linked to an unfavorable prognosis in individuals with rheumatoid arthritis (RA). Early identification and treatment of sarcopenia are clinically significant. This study aimed to create and validate a nomogram for predicting sarcopenia risk in RA patients, providing clinicians with a reliable tool for the early identification of high-risk patients. Methods: Patients with RA diagnosed between August 2022 and January 2024 were included and randomized into training and validation sets in a 7:3 ratio. Least Absolute Shrinkage and Selection Operator (LASSO) regression analysis and multifactorial logistic regression analysis were used to screen the risk variables for RA-associated muscle loss and to create an RA sarcopenia risk score. The predictive performance and clinical utility of the risk model were evaluated by plotting the receiver operating characteristic curve and calculating the area under the curve (AUC), along with the calibration curve and clinical decision curve (DCA). Results: A total of 480 patients with RA were included in the study (90% female, with the largest number in the 45-59 age group, about 50%). In this study, four variables (body mass index, disease duration, hemoglobin, and grip strength) were included to construct a nomogram for predicting RA sarcopenia. The training and validation set AUCs were 0.915 (95% CI: 0.8795-0.9498) and 0.907 (95% CI: 0.8552-0.9597), respectively, proving that the predictive model was well discriminated. The calibration curve showed that the predicted values of the model were basically in line with the actual values, demonstrating good calibration. The DCA indicated that almost the entire range of patients with RA can benefit from this novel prediction model, suggesting good clinical utility. Conclusion: This study developed and validated a nomogram prediction model to predict the risk of sarcopenia in RA patients. The model can assist clinicians in enhancing their ability to screen for RA sarcopenia, assess patient prognosis, make early decisions, and improve the quality of life for RA patients.

FTH promotes the proliferation and renders the HCC cells specifically resist to ferroptosis by maintaining iron homeostasis.

BACKGROUND: Ferroptosis is a newly identified type of programmed cell death, which preferentially targets iron-rich cancer cells such as hepatocellular carcinoma (HCC). Ferritin heavy chain (FTH) is a major iron storing nanocage to store redox-inactive iron, and harbors ferroxidase activity to prevent the iron-mediated production of ROS. Our previous studies have demonstrated that FTH acts as a protective role to increase the cellular resistance to ferroptosis. However, the specific role of FTH in the development of HCC and ferroptosis resistance remains unclear. METHODS: The indicated databases were used for bioinformatics analysis. The abilities of cell proliferation, migration were measured by cell proliferation assay, transwell assay and wound healing assay. The levels of reactive oxygen species (ROS), lipid peroxide, free iron, mitochondrial superoxide, mitochondrial morphology and mitochondrial membrane potential (MMP) were determined by DCF-DA, C11-BODIPY, mitoSOX, mitoTracker, JC-10 and TMRM staining, respectively. The mitochondrial oxygen consumption rate was monitored by the Seahorse XF24 Analyzer. RESULTS: The pan-cancer analysis was performed and showed that FTH expression is upregulated in multiple cancers, such as LIHC, CHOL, HNSC, compared to corresponding normal tissues. In addition, the level of serum ferritin is positively associated with the progression of hepatitis, cirrhosis liver and hepatocellular carcinoma. Further investigation shed light on the strong correlation between FTH expression and tumor grades, cancer stages and prognosis of HCC. Importantly, the proteins interaction network elucidated that FTH is involved in iron homeostasis maintenance and lysosomal-dependent degradation. Enforced expression of FTH accelerates proliferation, migration and endows HCC cells specifically resistant to ferroptosis, but does not protect against cell death caused by cytotoxic compounds like oxaliplatin, irinotecan, and adriamycin. Mechanically, FTH reconstituted cells exhibit diminished peroxides accumulation, reduce mitochondrial ROS level, attenuate the impaired mitochondrial respiratory and rescue the mitochondrial homeostasis. Notably, FTH expression boosts tumorigenic potential in vivo with increased PCNA staining and lesser lipid peroxides generation. CONCLUSION: These results provide new insights that FTH acts as an oncogene in the carcinogenesis and progression of HCC, and is hopeful to be a potential target for therapeutic intervention through ferroptosis.

[A study of refractive state in premature infants without retinopathy of prematurity during their early life].

OBJECTIVE: To understand the development of the refractive status in premature infants during their early life. METHODS: It was a cross-sectional study. Two hundred fifty-three premature infants without retinopathy of prematurity (ROP) were screened for ROP at 4-6 weeks after born. Refraction with cycloplegic retinoscopy was determined. The refractions of 38 infants were compared with those of mature infants at 40-44 weeks' correct gestational age (CGA). RESULTS: The spherical equivalent (SE) increased progressively (become more hypermetropic) along with increasing gestational age (GA), birth weight (BW) and CGA at test. BW was the main factor for SE. The incidence of myopia and astigmatism was 14.43% (73 eyes) and 10.28% (52 eyes). The former decreased and the latter did not change along with increasing CGA. The median of astigmatism was 1.00DC, while Percentile 25 (P25) and Percentile 75 (P75) were 0.50DC and 1.13DC, respectively. The degree of astigmatism increased along with increasing CGA and did not change along with GA or BW. The median of axis of astigmatism (AX) was 90 degrees, while P25 and P75 were 90 degrees and 100 degrees, respectively. The AX was not correlated with CGA, GA or BW. Five observations, including SE, incidence of myopia and astigmatism, the degree and axis of astigmatism between premature and mature infants at 40 to 44 weeks' CGA, were compared. It shows that there was no statistical difference between the two groups in all items mentioned above but SE, which indicating that there was more myopic in premature infants. CONCLUSIONS: The refraction of premature infants shifts towards hypermetropia along with development, but is still more myopic than mature infants at 40 to 44 weeks' CGA. Further studies on the underlying mechanisms of myopia and the subsequent refractive development are needed.