Objective To investigate the effects of troglitazone on cholesterol homeostasis and secretion of 3T3-L1 cells by sirolimus and the underlying mechanisms. Methods In vitro cultured 3T3-L1 cells were divided into control group,sirolimus (100 nmol/L) group,sirolimus(100nmol/L)+ troglitazone (10 μmol/L) group and troglitazone (10 μmol/L) group.High performance liquid chromatography (HPLC) was used to measure intracellular cholesterol accumulation.ELISA was used to measure leptin excretion.Quantitative real-time PCR and Western blotting were used to examine mRNA and protein expression of PPARγ. Results Free cholesterol of sirolimus +troglitazone group was 1.19 times of sirolimus group (P＜0.05).The leptin secretion levels of control group,sirolimus group,sirolimus+troglitazone group and troglitazone group were (19.02±0.52) μg/L,(15.62±0.47) μg/L,(16.45±0.51) μg/L,(18.07±0.66) μg/L,respectively.And the leptin secretion level of sirolimus+ troglitazone group was 1.05 times of sirolimus group (P＜0.05).The PPARγmRNA expressions of sirolinus group,sirolimus + troglitazone group and troglitazone group were 0.60±0.14,1.12±0.27,1.30±:0.14 folds of control,and the PPARγ mRNA expression of sirolimus + troglitazone group was higher than that of sirolimus group (P＜0.05).PPARγ protein expression had the same tendency. Conclusion Troglitazone reduces the inhibitory effect of sirolimus on PPARγ transactivation and the inhibitory effect of sirolimus on 3T3-L1 cells differentiation and adipogenesis.

Objective To preliminarily study and establish a method for measurement of the transuranic nuclide ²⁴¹Am in fecal samples, and to provide technical support for internal radiation monitoring of staff. Methods Fecal samples were collected with a self-made stool sampler and treated with a self-made carbonization and ashing furnace. DGA resin was used to separate and purify ²⁴¹Am from fecal samples. With ²⁴³Am as the tracer, the orthogonal method was used for condition optimization. Results The optimum conditions for separation and purification were: the acidity of HNO₃ added into the column, 6 mol/L; column flow rate, 0.6 mL/min; and the volume of analytical solution,12 mL. The method based on inductively coupled plasma mass spectrometry showed a detection limit of 9.79×10⁻⁴ Bq for ²⁴¹Am in fecal samples, which was satisfactory and feasible. Conclusion This method fills the vacancy of ²⁴¹Am measurement in fecal samples to some extent, which is of practical significance for internal radiation monitoring and protection for analysts.

Objective To establish a method for measurement of ²³⁹Pu in fecal samples based on inductively coupled plasma-mass spectrometry (ICP-MS), and to provide a novel method for assessing the internal exposure of workers. Methods Fecal samples were collected from workers and labeled. The samples were pretreated with carbonization ashing and microwave digestion devices, purified on TEVA resin, and measured using ICP-MS. Results The detection limit of ²³⁹Pu in fecal samples based on ICP-MS was 1.91 × 10⁻⁴ Bq. Conclusion In the routine monitoring of class S substances characterized by a 5 μm aerodynamic diameter during 12 months, the committed effective dose corresponding to the detection limit is 0.17 mSv. This value meets the requirements of relevant national standards and ICP-MS can be used as a novel means for accurate evaluation of internal exposure for workers.

Inflammatory bowel disease (IBD) is a formidable disease due to its complex pathogenesis. Macrophages, as a major immune cell population in IBD, are crucial for gut homeostasis. However, it is still unveiled how macrophages modulate IBD. Here, we found that LIM domain only 7 (LMO7) was downregulated in pro-inflammatory macrophages, and that LMO7 directly degraded 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) through K48-mediated ubiquitination in macrophages. As an enzyme that regulates glycolysis, PFKFB3 degradation led to the glycolytic process inhibition in macrophages, which in turn inhibited macrophage activation and ultimately attenuated murine colitis. Moreover, we demonstrated that PFKFB3 was required for histone demethylase Jumonji domain-containing protein 3 (JMJD3) expression, thereby inhibiting the protein level of trimethylation of histone H3 on lysine 27 (H3K27me3). Overall, our results indicated the LMO7/PFKFB3/JMJD3 axis is essential for modulating macrophage function and IBD pathogenesis. Targeting LMO7 or macrophage metabolism could potentially be an effective strategy for treating inflammatory diseases.