Multiple myeloma (MM) is a malignant hematologic disorder.The early diagnosis,accurate staging and timely therapeutic evaluation have great impact on the treatment planning,disease monitoring and prognosis.Although X-ray examination is the standard staging modality for MM,18F-FDG PET/CT has been proved additionally valuable for diagnosis,outcome prediction of MM.This article is to update the clinical role of 18F-FDG PET in the evaluation of MM.The application of other PET radiopharmaceuticals including 11 C-MET,11 C-acetate,11 C-choline and 18 F-FLT are also reviewed.

Objective To investigate the expression of nuclear factor-kappa Bp65 (NF-κBp65)and Toll-like receptor 4(TLR4)protein in the brain tissues of 7-day-old Sprague-Dawley(SD) rats with cerebral hypoxia-ischemia encephalopathy (HIE) and to explore the role of TLR4 and NF-κBp65 in the pathogenesis of neonatal rats with hypoxic-ischemic brain damage.Methods Seven-day SD rats were randomly divided into the experimental group and the control group.Brain pathological changes were observed in light microscopy at 6 h、12 h、24 h、72 h、7 d after HIE.The expression of TLR4 and NF-κBp65 in brain tissues were analyzed by immunohistochemistry method.Results NF-κBp65 and TLR4 were expressed in the neuron and microglia of control group and experimental group.The expression were most significant at cerebral cortex and hippocamp.However,the expression of NF-κBp65and TLR4 began to increase at HIE 6h:NF-κBp65 (0.219 3 ± 0.024 7,0.215 7 ±0.030 4)and TLR4(0.327 1 ±0.033 3,0.303 9 ±0.037 9),and achieved the hightest at HIE 24h:NF-κBp65 (0.3564±0.0235,0.3365 ±0.023 2)and TLR4(0.434 2 ±0.0428,0.4193 ±0.041 3),then decreased at HIE 72 h:NF-κBp65 (0.289 2 ± 0.032 0,0.260 9 ± 0.021 2) and TLR4 (0.300 5 ± 0.020 9,0.282 0 ± 0.022 6),and HIE 7 d:NF-κBp65(0.247 9 ±0.0340,0.242 1 ±0.025 4) and TLR4(0.274 4 ±0.0288,0.257 1 ±0.027 5).Conclusion There is a positive correlation between NF-κBp65 and TLR4 in rats with HIE.It suggested that they may have the same pathophysiology development in HIE.

Objective:To explore the mechanism underlying microRNA (miR) -125a-mediated inhibition of proliferation of keratinocytes.Methods:After 24-hour pretreatment with interleukin (IL) -23, human HaCaT keratinocytes were divided into miR-125a group and miR-NC group transfected with a miR-125a overexpression plasmid and a control plasmid, respectively. Cell counting kit-8 (CCK8) assay was performed to evaluate the proliferative ability of HaCaT cells in the two groups at 0, 24, 48 and 72 hours after transfection, real-time fluorescence-based quantitative PCR to determine the mRNA expression of miR-125a and IL-23 receptors (IL-23R) in the two groups 24 hours after transfection, and Western blot analysis to determine the protein expression of IL-23R, Janus kinase 2 (JAK2) , protein kinase B (AKT) and phosphorylated AKT (p-AKT) in the two groups 48 hours after transfection. Dual-luciferase reporter assay was performed to verify the targeting relationship between miR-125a and IL-23R. Comparison of means between two groups was carried out by using t test, and changes in the proliferative ability of HaCaT cells over time were evaluated by using repeated measures analysis of variance. Results:After plasmid transfection, the relative expression of miR-125a was significantly higher in the miR-125a group (6.377 ± 0.745) than in the miR-NC group (0.700 ± 0.222; t=7.305, P=0.002) . At 0, 24 and 48 hours after transfection, there was no significant difference in cellular proliferative ability between the miR-125a group and the miR-NC group ( t=0.663, 0.623 and 1.930, respectively, all P > 0.05) ; at 72 hours after transfection, the cellular proliferative ability was significantly lower in the miR-125a group than in the miR-NC group ( t=4.407, P < 0.05) . The IL-23R mRNA expression was significantly lower in the miR-125a group than in the miR-NC group ( t=3.082, P < 0.05) . Compared with the miR-NC group, the miR-125a group showed significantly decreased protein expression of IL-23R, JAK2 and p-AKT ( t=11.715, 6.996, 12.424, P < 0.001,=0.002, < 0.001, respectively) . Dual-luciferase reporter assay showed targeted binding of miR-125a to IL-23R. Conclusion:MiR-125a may inhibit the proliferation of keratinocytes by negatively regulating the IL-23R/JAK2/AKT signaling pathway.

Objective:To investigate the correlation between microRNA-125a (miR-125a) expression and inflammatory cytokine levels in skin lesions of patients with psoriasis vulgaris, and to evaluate the effect of miR-125a on the proliferation of a human immortalized keratinocyte cell line HaCaT.Methods:Totally, lesional and adjacent non-lesional skin tissues were collected from 40 patients with psoriasis vulgaris in the Seventh People′s Hospital of Shenyang from 2017 to 2018, and real-time fluorescence-based quantitative reverse transcription PCR was performed to determine the expression of miR-125a in the skin tissues, as well as the mRNA expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-17 in the lesional skin tissues. HaCaT cells were divided into 4 groups to be transfected with a miR-125a overexpression plasmid (miR-125a overexpression group), an overexpression control plasmid (overexpression control group), a miR-125a interference plasmid (miR-125a interference group) and an interference control plasmid (interference control group), respectively. Cell counting kit-8 (CCK8) assay was performed to assess the proliferative ability of HaCaT cells in the groups at 0, 24, 48, 72 hours after transfection, and double-antibody sandwich enzyme-linked immunosorbent assay (ELISA) to detect the levels of TNF-α, IL-1β, IL-6 and IL-17 in the culture supernatant of HaCaT cells. Spearman rank correlation test was used for correlation analysis, and t test for the comparison of means between two groups. Results:The relative expression of miR-125a was significantly lower in the lesional skin tissues (expressed as 2 -ΔΔCt, 0.389 ± 0.354) than in the non-lesional skin tissues (1.106 ± 0.396, t = 7.717, P < 0.001) in patients with psoriasis vulgaris. The expression of miR-125a was negatively correlated with the mRNA expression of TNF-α, IL-1β and IL-17 in psoriatic lesions ( r = -0.447, -0.424, -0.436, all P < 0.01). Immediately and 24 hours after transfection with the plasmids, there was no significant difference in the cell proliferative ability between the miR-125a overexpression group and overexpression control group ( t = 0.282, 1.445, respectively, both P > 0.05), or between the miR-125a interference group and interference control group ( t = 0.120, 1.543, respectively, both P > 0.05). Forty-eight and 72 hours after the transfection, the cell proliferative ability was significantly lower in the miR-125a overexpression group than in the overexpression control group ( t = 3.222, 4.563, respectively, both P < 0.05), but significantly higher in the miR-125a interference group than in the interference control group ( t = 3.036, 3.269, respectively, both P < 0.05). In addition, the miR-125a overexpression group showed significantly decreased levels of TNF-α and IL-1β compared with the overexpression control group ( t = 4.318, 3.813, respectively, both P < 0.05) . Conclusions:MiR-125a is lowly expressed in skin lesions of patients with psoriasis vulgaris. MiR-125a can inhibit the proliferation of keratinocytes, and may play a protective role in the occurrence and development of psoriasis.

China/epidemiology* ; Humans ; Pemphigoid, Bullous/epidemiology* ; Retrospective Studies