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Objective@#To assess the value of immunoglobulin heavy/light chain (HLC) immunoassay on therapeutic response in patients with multiple myeloma(MM).@*Methods@#A total of 45 newly diagnosed MM patients were retrospectively enrolled in Peking Union Medical College Hospital from 2013 to 2016, whose 115 serum samples were consecutively collected. HLC was tested to evaluate response and compare with other methods for M protein detection.@*Results@#①There were 30 males and 15 females in total of whom the monoclonal immunoglobulin was IgG in 27 (IgGκ∶IgGλ 12∶15) and IgA (IgAκ∶IgAλ 9∶9) in 18. The arerage age of the studied population was 59 (range 43-80) . ② In 34 patients with serum sample at diagnosis, 32 (94.1%) had abnormal HLC ratio (rHLC) while 2 patients with IgG had normal rHLC. The percentages of abnormal rHLC was 81.8% (18/22) at partial response、50.0%(9/18) at very good complete response and 16.0%(4/25) at complete response. ③In 25 patients reaching CR, there were 13 with IgG and 12 with IgA. 4 patients equally split of IgG and IgA had abnormal rHLC at complete response. ④By monitoring the rHLC of some patients consecutively, we found that the remission of rHLC was to some extent behind the remission of SPE and IEF, or even rFLC.@*Conclusion@#Immunoglobulin HLC detection is one feasible method for minimal residual disease detection.
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Objective To investigate the effects of TLR7 on imiquimod induced apoptosis of THP-1 derived macrophages.Methods Three cell lines ( THP-1 derived macrophages, MDCK cell line and HUVEC cell line) with different capabilities of expressing TLR7 were selected.The survival rates of cells af-ter the treatment with different concentrations of imiquimod were detected by MTT assay.The levels of IL-6 in the supernatants of TLR7 inhibitor chloroquine or TLR7-siRNA treated cells were detected by enzyme-linked immunosorbent assay.The apoptosis of cells was detected by flow cytometry after inhibiting the ex-pression of TLR7.Results Imiquimod induced the apoptosis of THP-1 derived macrophages, MDCK cell lines and HUVEC cell lines.The levels of IL-6 were significantly decreased as the expression of TLR7 was inhibited by treating THP-1 derived macrophages with chloroquine or TLR7-siRNA.Treating THP-1 derived macrophages with chloroquine or TLR7-siRNA did not affect the cell apoptosis induced by imiquimod.Con-clusion Imiquimod could induce the apoptosis of THP-1 derived macrophages through TLR7 independent pathway.
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Objective To study the effects of Toll-like receptor 4(TLR4) on oxidized low density lipoprotein ( ox-LDL) induced macrophage apoptosis and its possible mechanism .Methods THP-1 derived macrophages were divided into four groups including untreated control group , ox-LDL treated group , ox-LDL+LPS treated group and tunicamycin treated group .MTT assay and flow cytometry analysis were performed to measure cell vitality and cell apoptosis , respectively .Oil red O staining was used to observe the phagocytosis of lipids by macrophages .The persistent and intense endoplasmic reticulum ( ER) stress markers were de-tected by analyzing the expression of glucose-regulated protein 78 ( GRP78 ) and CCAAT/enhancer-binding protein homologous protein ( CHOP) at mRNA and protein levels by q-RT-PCR and Western blot .Small in-terfering RNA ( siRNA) was used to silence the expression of TLR 4 to further elucidate its possible mecha-nism.Results Flow cytomotry and MTT assay showed that the number of apoptotic cells in ox-LDL+LPS treated group were increased more significantly than that in ox-LDL treated group (P<0.01), and cell apop-tosis in both two groups were greater than that in control group (P<0.01).Compared with control group, the expression of GRP78 and CHOP at mRNA and protein levels were up-regulated in ox-LDL+LPS treated group and ox-LDL treated group (P<0.01), and the expression of GRP78 and CHOP in ox-LDL+LPS treated group was significantly higher than that in ox-LDL treated group (P<0.01).Silenced expression of TLR4 al-leviated the endoplasmic reticulum stress (P<0.05).Conclusion Increased expression of CHOP contribu-ted to cell apoptosis .TLR4 might promote ox-LDL induced macrophage apoptosis through accelerating endo-plasmic reticulum stress .
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Objective To research the influenza virus infection on rat vascular smooth cells number,proliferation,apoptosis,the amount of IL-6,sFas,platelet-derived growth factor(PDGF) and the mechanism of atherosclerosis.Methods Flow cytometry,enzyme-linked immunosorbent assay and cell count experiments were used to detect these indicators at 0 h,6 h,12 h,24 h,48 h.Results After influenza virus infected at 0 h,proliferation,apoptosis condition were 10.39％,0.44％,respectively; at 6 h,proliferation,apoptosis respectively increased to 12.68％,0.73％ ; proliferation reached the peak at 12 h (18.01％),instead apoptosis decreased to 0.14％ ; at 24 h,proliferation decreased to 12.89％ and apoptosis markedly increased to 1.09％ ; at 48 h,proliferation further reduced to 7.07％ and apoptosis reached the peak(4.61％).The number of cells and the cytokine secretion were statistically significant to control group (P＜0.05).Conclusion Influenza virus infection might lead to change of cell proliferation and apoptosis and involve the atherosclerosis form and development,and cytokines played an important role in them.