Objective To explore the correlation between the carotid atherosclerosis unstable plaque lipoprotein(a) [ Lp(a)]levels with acute cerebral infarction patients.Methods 120 patients with acute cerebral infarction were selected as the research group,and at the same period,120 health cases were selected as the control group.The level of Lp(a) of the two groups was tested,and neck vascular color dopplar ultrasound examination was conducted.Results The incidence of atherosclerotic plaque in carotid artery and unstable plaques was 70.8％,51.7％,respectively,and significantly higher than that of the control group(25.8％,6- 7％ ) ( x2 =5.12,6.43,all P ＜0.05 ).The Lp(a) level of the research group[ (273.6 ± 221.7 )ag/L] was significantly higher than that of the control group[ ( 81.6 ± 64.9) mg/L ] ( t =6.53,P ＜ 0.05 ).Conclusion High level of LP(a) is the independent risk factor of cerebral infarction.The instability of carotid atherosclerotic plaques is the important cause of cerebral infarction.

Objective: To establish a microwave digestion-inductively coupled plasma mass spectrometry assay for simultaneous determination of multiple elements in placenta. Methods: Fresh placental tissues were dried at 60 ℃ for 15 h and ground into power. Then, 0.3 g homogenized samples were digested in a microwave digestion system. The interference from mass spectrometry was removed using the kinetic energy discrimination model in the inductively coupled plasma mass spectrometry, and the baseline interference was removed by online internal standards. The contents of 17 elements were determined in placental specimens using the established microwave digestion -inductively coupled plasma mass spectrometry assay, including V, Ni, Co, Fe, Cr, Cu, Zn, Mn, As, Sn, Sb, Ba, Se, Cd, Pb, Hg and Tl. Results: Good linearity was shown for V, Ni, Co, Cr, As, Se, Cd, Pb and Tl at 1 to 50 µg/L, Fe at 100 to 5 000 µg/L, Zn, Cu, Mn and Ba at 10 to 500 µg/L, Sn and Sb at 0.1 to 5 µg/L, and Hg at 0.2 to 2 µg/L, with all correlation coefficients of 0.999 8 and higher. The detection limits of these 17 elements ranged from 0.5 to 100 μg/kg, with relative standard deviations of 2.1% to 6.5%, and recovery rates of 83.3% to 110.0%. The determination results of 17 elements were all within the normal reference range defined in the certified reference materials of chicken (GBW10018). Conclusions The microwave digestion-inductively coupled plasma mass spectrometry established based on optimized pretreatments and mass spectrometry detection conditions, is feasible for simultaneous determination of multiple elements in placenta.

Grey matter (GM) alterations may contribute to cognitive decline in individuals with white matter hyperintensities (WMH) but no consensus has yet emerged. Here, we investigated cortical thickness and grey matter volume in 23 WMH patients with mild cognitive impairment (WMH-MCI), 43 WMH patients without cognitive impairment, and 55 healthy controls. Both WMH groups showed GM atrophy in the bilateral thalamus, fronto-insular cortices, and several parietal-temporal regions, and the WMH-MCI group showed more extensive and severe GM atrophy. The GM atrophy in the thalamus and fronto-insular cortices was associated with cognitive decline in the WMH-MCI patients and may mediate the relationship between WMH and cognition in WMH patients. Furthermore, the main results were well replicated in an independent dataset from the Alzheimer's Disease Neuroimaging Initiative database and in other control analyses. These comprehensive results provide robust evidence of specific GM alterations underlying WMH and subsequent cognitive impairment.

Glycolytic metabolism enzymes have been implicated in the immunometabolism field through changes in metabolic status. PGK1 is a catalytic enzyme in the glycolytic pathway. Here, we set up a high-throughput screen platform to identify PGK1 inhibitors. DC-PGKI is an ATP-competitive inhibitor of PGK1 with an affinity of K _d = 99.08 nmol/L. DC-PGKI stabilizes PGK1 in vitro and in vivo, and suppresses both glycolytic activity and the kinase function of PGK1. In addition, DC-PGKI unveils that PGK1 regulates production of IL-1β and IL-6 in LPS-stimulated macrophages. Mechanistically, inhibition of PGK1 with DC-PGKI results in NRF2 (nuclear factor-erythroid factor 2-related factor 2, NFE2L2) accumulation, then NRF2 translocates to the nucleus and binds to the proximity region of Il-1β and Il-6 genes, and inhibits LPS-induced expression of these genes. DC-PGKI ameliorates colitis in the dextran sulfate sodium (DSS)-induced colitis mouse model. These data support PGK1 as a regulator of macrophages and suggest potential utility of PGK1 inhibitors in the treatment of inflammatory bowel disease.