Objective To assess the status and severity of bone disease in patients with multiple myeloma (MM) by using chest computerized tomography (CT) and the relationship between clinical prognostic parameters and bone disease.Methods All 46 newly diagnosed MM in-patients received both imaging tests of chest CT and plain X ray.An experienced radiologist reviewed all the imaging data.Clinical laboratory parameters,stages of Durie-Salmon (DS) and International Staging System (ISS) were evaluated.Five cytogenetic abnormalities of bone marrow myeloma cells were tested by fluorescence in situ hybridization (FISH).Results The sensitivity of CT and X ray to determine pathological fractures was comparable,the positive rates of which were 41.3％ (19/46) and 30.4％ (14/46) respectively (P =0.29).Nevertheless,the positive rate of osteolytic lesions ascertained by CT was significantly higher than that by X ray (P ＜ 0.001),60.9％ (28/46) vs 13.0％ (6/46) with diameter 5-10 mm and 50.0％ (23/46) vs 10.9％ (5/ 46) with diameter more than 10 mm.Osteolytic lesion numbers found by CT were more than those by X ray [5(0-21) vs0(0-4) lesions with diameter5-10 mm (P＜0.001),2(0-14) vs0(0-2) lesions with diameter more than 10 mm (P ＜ 0.001),respectively].Patients with positive osteolytic lesions had higher percentage of RB1 gene deletion[46.7％ (14/30) vs 18.8％ (3/16),P ＜0.001],D13s319 deletion [43.3％ (13/30) vs 18.8％ (3/16),P ＜0.001] and high risk cytogenetic abnormalities[50.0％ (15/30) vs 25.0％ (4/16),P ＜ 0.001].Conclusions Chest CT is more sensitive than plain X ray in detecting osteolytic myeloma bone disease.Osteolysis determined by CT is relevant to clinical DS stages and risk stratification of cytogenetic abnormalities.

Objective To investigate the role and mechanism of SDF-1/CXCR4 in the development of chronic rejection (CR) in rat models.Methods CR rat models were established using Fisher 344 to Lewis rats.In the blank control group (n=10),Lewis rats getting isotransplantation were treated with Cyclosporine A.CR rat models were established in positive group (n=10) and the rats were treated with Cyclosporine A.CR rat models were also established in CXCR4 antagonism group (n=10) and the rats were treated with both Cyclosporine A and AMD3100 (1 mg/kg).The serum creatinine levels were monitored every week.Kidney grafts were harvested 12 weeks after transplantation for histological analysis.We evaluated graft injuries using chronic allograft damage index (CADI) scores.Q-PCR and Western blotting were used to measure CXCR4,TGF-β1/Smad3 signaling pathway and α-smooth muscle actin (α-SMA) expression in renal allograft tissues.Results The serum creatinine levels in blank control group and CXCR4 antagonism group were significantly lower than those in positive control group (P<0.05).The blank control group and CXCR4 antagonism group presented milder pathological manifestations of CR.The CADI score in CXCR4 antagonism group was 3.54,which was lower than that of positive control group (P<0.05).The expression of biological markers in TGF-β1/Smad3 signaling pathway and SDF-1/CXCR4 signaling pathway was significantly lower in blank control group and CXCR4 antagonism group than in positive control group (P<0.05).Conclusion SDF-1/CXCR4 signaling pathway may play a crucial role in the development of CR.The usage of SDF-1/CXCR4 antagonist can protect renal allograft by inhibiting the TGF-β1/Smad3 pathway.Therefore,antagonism of CXCR4 may provide a novel way to prevent the development of CR.

Objective To evaluate the effects of interleukin-22 (IL-22) on the expression of CC chemokine ligand 27 (CCL27) in human epidermal keratinocytes,and to explore its mechanism.Methods Immunohistochemical study was performed to determine the expression of CCL27 in skin lesions of 10 patients with psoriasis and skin tissues of 5 healthy controls.Cultured HaCaT cells were divided into 8 groups:control group treated with PBS,5 IL-22 groups treated with 12.5,25,50,100 and 200 μg/L IL-22 respectively,2 signaling pathway inhibition groups treated with 50 μrmol/L AG490 (JAK2/STAT3 signaling pathway inhibitor) or PD98059 (MAPK-ERK1/2 signaling pathway inhibitor) for 2 hours followed by the treatment with 50 μg/L IL-22 in the 5％ CO2 incubator at 37 ℃.After 24-hour cultivation,total proteins were extracted,and culture supernatants were collected,and both Western blot analysis and enzyme-linked immunosorbent assay (ELISA) were performed to determine the expression of CCL27.Results Immunohistochemical study showed that the expression of CCL27 was significantly higher in the skin lesions of the patients with psoriasis than in the skin tissues of the healthy controls.Western blot analysis revealed that the protein expression of CCL27 in the 12.5-,25-,50-,100-and 200-μg/L IL-22 groups was 0.491 ± 0.013,0.620 ± 0.019,0.623 ± 0.014,0.802 ± 0.052 and 1.138 ± 0.013 respectively,which were all higher than that in the control group (0.413 ± 0.013,all P ＜ 0.01).The expression of CCL27 was significantly lower in the IL-22 + AG490 group (0.411 ± 0.019) and IL-22 + PD98059 group (0.280 ± 0.012) than in the 50-μg/L IL-22 group (both P ＜ 0.01).ELISA also showed the same trend of changes in the level of CCL27 in the above groups as Western blot showed.Conclusion IL-22 can promote the expression of CCL27 in HaCaT cells,which may be associated with the MAPK-ERK 1/2 and JAK2/STAT3 signaling pathways.

Primary biliary cholangitis (PBC) is an autoimmune disease. Although PBC has the features of autoimmune disease, it has poor response to immunosuppressants and good response to the drugs participating in bile acid metabolism, such as ursodeoxycholic acid. Studies have shown that the bicarbonate secretion of biliary epithelial cells is impaired in PBC patients, and bile acid not blocked by HCO3- umbrella enters biliary epithelial cells and mediates their damage and apoptosis, leading to the expression of autoantibodies in apoptotic cells and immunologic injury. In order to explore the role of HCO3- umbrella secreted by biliary epithelial cells in the pathogenesis of PBC, this article briefly introduces the physiological function and production mechanism of HCO3- umbrella and the influencing factors for HCO3- secretion, and it is pointed out that reduced HCO3- secretion may be a key link in the pathogenesis of PBC and a potential therapeutic target.

Autoimmune hepatitis (AIH) is a chronic progressive inflammatory disease of the liver caused by the attack of liver cells by the autoimmune system, with the features of positive serum autoantibodies, high IgG, and/or γ-globulinemia. Current studies on pregnancy in patients with AIH mainly focus on labor complications, and there is still a lack of systematic recommendations for the evaluation, treatment, and management of diseases in the progestational stage, during pregnancy, and after delivery. Although immunity is suppressed during pregnancy, poor disease control within one year before pregnancy and spontaneous drug withdrawal during pregnancy can significantly increase adverse pregnancy outcomes. Therefore, this article describes how to implement multidisciplinary collaboration and management of the whole cycle of pregnancy, so as to improve maternal and fetal safety.