Multiple myeloma (MM) is a kind of malignant hyperplastic diseases, which is origined from B cell line and can produce monoclonal immunoglobulin. Although myeloma remains incurable, recent advances in its treatment, including the use of bortezomib, thalidomide, stem cell transplantation, targeted therapy, polypeptide vaccine are promising.

Identifying protein fold is an important issue in protein structure research. Based on the classification of SCOP1.65,17 Globin-like proteins from four homology families (

HLA-G belongs to non-classical HLA-class Ⅰ genes.It is expressed in the fetal-maternal interface on the extravillous cytotrophoblast and in such immune privilege tissues as the cornea and pancreas.However, under pathological conditions, such as tumor, inflammatory diseases and post transplantation, HLA-G is expressed abnormally.HLA-G can interact with its acceptors or immune cells and suppress the function of immune cells, which facilitates the escape of the surveillance of the human immune system and the consequent damage.In clinical studies,HLA-G is related to some clinical parameters.This review will focus on the expression, function and regulatory mechanisms of HLA-G in cancer immunology.

Objective To analyze the changes and clinical significance of C-reactive protein (CRP)、hemoglobin (Hb) and erythrocyte sedimentation rate (ESR) in different disease stage of multiple myeloma according the international staging system. Method Thirty untreated MM patients with complete clinical records were included in the stndy. The multiple myeloma patients were classified into three groups according to international staging system (ISS).Thirty megaloblastic anemia patients of similar age 、sex、hemoglobin level as the observation group.Resulets The levels of CRP (24.17±9.87 mg/L)、Hb (71.72±13.27 g/L) and ESR (105.94±27.73 mm/h) of stage Ⅲ patients were statistically different with stage Ⅰ ( CRP 8.54±1.97 mg/L; Hb 91.00±9.92g/L; ESR 73.57±20.53mm/h)、Ⅱ patients ( CRP 14.89±5.51 mg/L; Hb 91.29±8.32g/L; ESR 67.00± 15.56 mm/h) separately (P＜0.05).The levels of CRP (19.40±10.17 mg/L) and ESR (91.90±29.70 mm/h) in the MM patients were significantly higher than that in the observation group Ⅰ ( CRP 7.52±1.57mg/L; ESR 20.20±8.04mm/h) (P＜0.05 respectively).CRP and ESR level in MM patients positively correlated with myeloma cell proportion and β2-microglobulin level (P＜0.05), while Hb level negatively correlated with myeloma cell proportion and β2-microglobulin level (P＜0.05),Conclusion The levels of C-reactive protein、hemoglobin and erythrocyte sedimentation rate are closely associated with the development of multiple myeloma. C-reactive protein and hemoglobin are relatively sensitive response to disease than erythrocyte sedimentation rate. There is a clear clinical implication in detecting the patient' s condition for progress and the prognosis.

BACKGROUND: Neuroglioma is easy to recur, the focus of infection in which is rich in new vessels. Different expression of vascular endothelial growth factor (VEGF) may be related with the pathologic changes and recurrence of tumor.OBJECTIVE: To analyze the characteristics of VEGF expression in recurrent brain glioma.DESIGN: Control test.SETTLNG: Department of Neurosurgery, West China Hospital of Sichuan University.PARTICIPANTS: Forty-four (22 pairs) samples of neurogliocytoma before and after the recurrence with complete clinical data were collected from143 paraffin embedded samples, which were obtained from the operation between June 1996 and June 2001 in West China Hospital and pathologically proved to be brain gliomas. Samples were collected separately from the first operation and first recurrence, in which 8 cases belonged to grade Ⅰ of Kernohan scale, 10 were grade Ⅱ , 14 were grade Ⅲ and 12 were grade Ⅳ. The enrolled samples were divided into two groups: primary group and recurrent group with 22 cases in each group.METHODS: The immunohistochemiscal method was adopted. First antibody was goat-anti-human VEGF (mono-antibody), and second antibody was rabbit-anti-goat with the working concentration of 1:50. The phosphate buffered solution (PBS) was taken as negative control for staining instead of first antibody. The protein expression of VEGF in brain gliomas of 44 cases before and after the recurrence were detected and the cross-check analysis was conducted by combing with pathologic grades. ① The buff grains in intracytoplasm were positive signals. ②MPLAS-500 media mix chromatic pathologic imaging and literal analytical system were used to detect the PU (positive unit) value and number of tumor cells.③95% were the critical value of PU value, and the positive cell rates were calculated respectively. ④Routine hematoxylin-eosin stain was used for pathologic grades (Kernohan). MAIN OUTCOME MEASURES: ① PU value and the intensity of VEGF expression in brain glioma samples before and after the recurrence. ②The pathologic grades of brain gliomas before and after the recurrence. RESULTS: ①The expression of VEGF in primary and recurrent groups of brain glioma: the primary group was 21.927 3±6.607 and the recurrent group was 33.054 5±6.684. ② Pathologic grades: In 8 cases of primary grade Ⅰ gliomas, there were 2 cases of grade Ⅱ in recurrence, 5 cases of grade Ⅲ in recurrence, 1 case of grade Ⅳ in recurrence. In 6 cases of primary grade Ⅱ gliomas, there were 2 cases of grade Ⅱ in recurrence, 1case of grade Ⅲ in recurrence, 3 cases of grade Ⅳ in recurrence. In 6eases of primary grade Ⅲ .gliomas, 2 cases of grade Ⅲ in recurrence, 4cases of grade Ⅳ in recurrence. In 2 cases of primary grade Ⅳ gliomas,there were 2 cases of grade Ⅳ in recurrence. ③ Differences in PU value of VEGF protein expressions and pathologic grades of brain glioma samples before and after recurrence in self-compared detection were remarkable (P＜0.05).CONCLUSION: The expression of VEGF in recurrent glioma is higher than primary glioma, and there is a worsening tendency in recurrent tumor and the high-expression of VEGF in glioma plays an important role in the recurrence.

BACKGROUND:Pneumonectomy, extracorporeal circulation, lung transplantation and pulmonary embolism can cause ischemia/reperfusion injury of lung tissue. Lung ischemia/reperfusion injury is an important factor of lung function disorders after lung transplantation. OBJECTIVE:To analyze the effect of ischemic postconditioning on rat models of lung ischemia/reperfusion injury. METHODS:Twenty-four male SD rats were randomly divided into sham, ischemia/reperfusion and ischemic postconditioning groups (n = 8 rats/group) to establish the lung ischemia/reperfusion injury model. The rats in the sham group were only subjected to separation of the hilum of left lung and pulmonary arteries and veins, without blocking. The rats in the ischemia/reperfusion group were subjected to another 2 hours of reperfusion after 1 hour of lung ischemia. The rats in the ischemic postconditioning group were first subjected to 30 seconds of lung ischemia and 30 seconds of reperfusion for three times, and then to 2 hours of reperfusion. After the experiment, the specimens of lung tissue were obtained to detect the wet/dry weight ratio of lung tissue, activities of superoxide dismutase, malondialdehyde and myeloperoxidase, the contentsof inflammatory cytokines tumor necrosis factor α, interleukin-1β and interleukin-6, and the histopathological changes of lung tissue were observed. RESULTS AND CONCLUSION:Compared with the sham group, the wet/dry weight ratio of lung tissue, activities of myeloperoxidase and myeloperoxidase, the levels of tumor necrosis factor α, interleukin-1β and interleukin-6 were significantly increased (P < 0.05) in the ischemia/reperfusion and ischemic postconditioning groups, however, the increase levels of these indices were not significant in the ischemic postconditioning group, and the contents and activities in the ischemic postconditioning group were al significantly decreased (P < 0.05) compared with those in the ischemia/reperfusion group. In the ischemia/reperfusion and ischemic postconditioning groups, the activity of superoxide dismutase was obviously lower than that in the sham group, however, the activity of superoxide dismutase in the ischemic postconditioning group was obviously higher than that in the ischemia/reperfusion group. Pathological examination showed that thickened alveolar wal, edema and a large amont of inflammatory cel infiltrations were observed in the lung tissue of rats in the ischemia/reperfusion group. The degrees of alveolar wal thickening and edema in the lung tissue of rats in the ischemic postconditioning group were mild compared with the ischemia/reperfusion group, and in addition, some inflammatory cels were infiltrated. The histopathological scores of lung tissue in the ischemic postconditioning group were lower than those in the ischemia/reperfusion group. These results suggest that ischemic postconditioning plays its protective role on rat models of ischemia/reperfusion injury by inhibiting inflammatory cel accumulation, oxygen free radical production and pro-inflammatory cytokine release after ischemia/reperfusion injury.

Aim To investigate the effects of Curcumin on Heme oxygenase isozymes in SH-SY5Y cells and explore a new mechanism of Curcumin in neuroprotection. Methods The human SH-SY5Y cells were cultured in vitro and treated with Curcumin at 0,1.25,5.0,20 ?mol?L-1 for 24 h,or with Curcumin at 5.0 ?mol?L-1 for 0,12,24,and 48 h. The active oxygen was detected by fluorescent probe DCFH-DA and fluorospectro-photometer. RT-PCR was used to detect the expression of HO-1 and HO-2 mRNA. Western blot was performed to detect the levels of HO-1 and HO-2 protein.Results The results showed that Curcumin could inhibit the levels of active oxygen(P

Aim To investigate the effect of Curcumin on the expression of HO-1 and Nrf-2,and explore the machanism of neuroprotection of Curcumin. Methods SH-SY5Y cells were treated with Curcumin at 0,1. 25, 5. 0,20. 0 ?mol?L -1,or with Curcumin at 5. 0?mol? L -1 for 12,24,48 h for the time course assay. RT-PCR and Western blot assays were carried out to detect mRNA and protein expression of Nrf-2 and HO-1. Nrf-2 siRNA was used to dectect the expression of HO-1 with the absence of Nrf-2. Results RT-PCR and Westernblot results indicated that the mRNA and protein expression of HO-1 and Nrf-2 all increased in a dose-and time-dependent manner after Curcumin treatment in the SH-SY5Y cells ( P

Aim: To study the effect of Eudragit S-100, a pH-responsive polymer, on protein refolding level, using recombinant human keratinocyte growth factor-2 (rhKGF-2) as a model protein. Methods: The refolding of rh-KGF-2 was performed by directly diluting denatured rhKGF-2 into a refolding buffer containing different concentrations of Eudragit. The ability of Eudragit S-100 to enhance protein refolding level was investigated using MTT assay, reverse phase HPLC, fluorescence emission spectroscopy and circular dichroism spectroscopy. Results: The addition of Eudragit S-100 in the refolding buffer significantly increased the rhKGF-2 refolding yield to 71%, when dilution refolding was conducted at 0. 5 mg/mL rhKGF-2. The outcome from the refolding study showed possibility of a special interaction between rhKGF-2 and Eudragit, suggesting that the refolding-enhancing ability of Eudragit S-100 was due to this interaction between Eudragit S-100 and rhKGF-2. Mean while, the result showed that the concentration of urea was also an important factor for the optimization of the refolding in the presence of Eudragit. Conclusion: Eudragit S-100 can significantly increase the refolding level of rhKGF-2.

Microbiome dysbiosis is strongly associated with alcoholic liver disease(ALD).Recent studies on comprehensive analyses of microbiome compositional and functional changes have begun to uncover the mechanistic relation between microbiome and the pathogenesis of ALD.Importantly,targeting the microbiome has become a potential strategy for the prevention and treatment of ALD.In this review,we summarize the clinical evidence of microbiome dysbiosis in ALD patients,and experimental advances in microbiome and metabolomic functional changes in animals with different species and genetic back-grounds in ALD.We also summarize the studies in humanized intestinal microbiome and fecal micro-biota transplantation in mice.We introduce new developments in the studies on the role of the circulating bacterial microbiome,oral bacterial microbiome and fungal microbiome in the development of ALD.We highlight the potential mechanisms by which microbiome dysbiosis contributes to ALD,including short chain fatty acid changes,bile acid metabolism,intestinal barrier function,release of bacterial and fungal products,and inflammation.In addition,we summarize the recent developments targeting the microbiome in prevention and treatment of ALD,including dietary nutrient interference,herbal medicine,antibiotics,anti-fungal agents,probiotics,engineered bacterial therapy,fecal trans-plantation and oral hygiene.Although recent preclinical studies have advanced our understanding of the microbiome and ALD,clinical studies,especially prospective studies with large samples,are needed to better understand the cause-effect of microbiome dysbiosis in ALD.Identifying new precision-based strategies targeting the microbiome are expected to be developed as more effective therapies in ALD.