The gammac cytokines play an important role in proliferation and survival of T cells. Blocking the gammac signals can cause the activated donor-reactive T cells losing the ability to proliferate, and getting into apoptosis pathway, which contributes to induction of the peripheral tolerance. In this study, we induced the transplant tolerance through blocking the gammac in combination with donor-specific transfusion (DST) in the cardiac transplantation. Following DST, on the day 2, 4 and 6, C57BL/6 recipients received anti-gammac monoclonal antibodies (mAbs) injection, and those in control group were not given anti-gammac mAbs. On the day 7, Balb/c cardiac allografts were transplanted. All recipients in experimental group accepted cardiac allografts over 30 days, and two of them accepted allografts without rejection until sacrifice on the 120 day. Animals only receiving DST rejected grafts within 5 days, and the mice receiving cardiac transplantation alone rejected grafts within 9 days. Our study showed that blockade of gammac signaling combined with DST significantly prolonged allograft survival, which was probably associated with inhibition of antigen-specific T-cell proliferation and induction of apoptosis.

Objective To investigate the effects of Lp(a)on proliferation GMCs of rat model induced by lipopolysaccharide and explore the possible mechanism of Lp(a)in the proliferation of rat GMCs.Methods To observe the effects of Lp(a)on proliferation of GMCs,different dosage of Lp(a)were used,The research were divided into three groups:Control group,LPS group,Lp(a)group.After culture(at the end of 12h,24h,48h,60h and 72h),the cultured GMCs and suspension were collected to observe the rate of GMCs proliferation by MTT,the positive rate of proliferation cell nuclear antigen(PCNA)by immunohistochemisty,and the level of intercellular adhesion molecule-1(ICAM-1)by ELISA respectively.Results Compared with control and LPS group,MTT,positive rate of PCNA and ICAM-1 of GMCs were increased more significantly in Lp(a)group.MTT ,the positive rate of PCNA and ICAM-1 of GMCs were increased as Lp(a)dosage increased,a maximal effect was seen when Lp(a)was 2.5 μg/L or 5.0μg/L.When the dosage continue increased,MTT,the positive rate of PCNA and ICAM-1 activity of GMCs began to decrease in Lp(a)group.ICAM-1 showed positive correlation with MTT and the positive rate of PCNA.Conclusion Lp(a)can significantly affect the rate of GMCs proliferation,and this affection is in a dosage-and timedependent manner.Low dosage stimulates GMCs proliferation, and high dosage inhibits GMCs proliferation.ICAM-1 shows positive correlation with MTT and the positive rate of PCNA.The effect of Lp(a)on GMCs may be through ICAM-1.

To compare the concepts of pharmaceutical care and health management , analyze their internal connections both in present background and implementation process .Further development and practice of pharmaceutical care under the new health manage -ment model were discussed .

The γc cytokines play an important role in proliferation and survival of T cells. Blocking the γc signals can cause the activated donor-reactive T cells losing the ability to proliferate, and getting into apoptosis pathway, which contributes to induction of the peripheral tolerance. In this study, we induced the transplant tolerance through blocking the γc in combination with donor-specific trans-fusion (DST) in the cardiac transplantation. Following DST, on the day 2, 4 and 6, C57BL/6 recipients received anti-γc monoclonal antibodies (mAbs) injection, and those in control group were not given anti-γc mAbs. On the day 7, Balb/c cardiac allografts were transplanted. All recipients in experimental group accepted cardiac allografis over 30 days, and two of them accepted allografis without rejection until sacrifice on the 120 day. Animals only receiving DST rejected gratis within 5 days, and the mice receiving cardiac transplantation alone rejected gratis within 9 days. Our study showed that blockade of γc signaling combined with DST significantly prolonged allografi survival, which was probably associated with inhibition of antigen-specific T-cell proliferation and induction of apoptosis.