Objective To explore the content change of Alpha Fetal Protein(AFP) and Alpha Fetal Protein Variants(AFP-L3) pre-and post-liver transplantation operation for liver cancer patients.Methods AFP-L3 was de-termined by micro centrifugal column from twelve cases of successive sera(For each case,one original shale pre-oper-ation,and mole shares post-operation successively),and preserved from patients who were diagnosed as fiver cancer and completed fiver transplantation operation.simultaneously the content of AFP and AFP-L3 in the original serum were also determined.and the ratio of AFP-L3 in AFP was calculated in order to compare the content change of AFP and the ratio of AFP-L3 pre-and post-liver transplantation operation.Results Compared with twelve cases of pre-and post-operation,the AFP in only five cases turned tO negative;The AFP in other cases keeped positive though AFP-L3%tumde to negative.and the content of AFP in some specific cases still keeped in a high level.Regarding AFP-L3,besides two casses turning to negative immediately after operation,the content of AFP-L3 in other patients de-creased gradually after operation,and it approached to negative(AFP-L3%<10%).Through statistical analysis,be-tween the half lives of AFP and AFP-L3%,there waa no statistic significance.Therefore,AFP-L3% could be considered as an independent reference item.Conclusion After a radical cure of liver resection or liver transplantation operation,AFP-L3%usually turned to negative in a rather short period (about 1 to 20 days).The ratio of AFP-L3 in AFP became be-low 10%,and it indicated that the operation would be quite complete,remaining liver would have hepatitis or hepatocirrho-sis.Otherwise,the ratio was not decrease during a long period,and it indicated the operation had not eliminated focuses completdy.

Objective:To evaluate the role of spinal peroxisome proliferation-activated receptor-γ (PPAR-γ) in protectin D1 (PD1)-induced reduction of neuropathic pain (NP) in rats.Methods:Forty-eight clean-grade healthy male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 4 groups ( n=12 each) by a random number table method: sham operation group (Sham group), NP group, NP plus PD1 group (NP+ PD group), and NP plus PD1 plus GW9662 group (NP+ PD+ GW group). Neuropathic pain was induced by spared nerve injury in anesthetized rats.In NP+ PD and NP+ PD+ GW groups, PD1 900 ng (diluted to 20 μl in dimethyl sulfoxide [DMSO]) was intrathecally injected once a day for 8 consecutive days starting from 30 min before establishing the model.In NP+ PD+ GW group, the PPAR-γ antagonist GW9662 200 ng (diluted to 20 μl in DMSO) was intrathecally injected once a day for 8 consecutive days starting from 45 min before establishing the model.The equal volume of DMSO was intrathecally injected in Sham group.The mechanical paw withdrawal threshold (PWT) was measured before establishing the model and at 1, 3, 5, 7, 10 and 14 days after establishing the model.Six rats in each group were sacrificed on day 14 after establishing the model, and their lumbar enlargements were removed for determination of the expression of PPAR-γ, TNF-α and IL-6 by Weston blot.Six rats in each group were sacrificed on day 14 after establishing the model, L 4, 5 segments of the spinal cord were removed, and the co-expression of PPAR-γ with neuron-specific nucleoprotein (NeuN), glial fibrillary acidic protein (GFAP) or serum calcium binding adapter molecule 1 (Iba-1) was determined by immunofluorescence staining. Results:Compared with group Sham, PWT was significantly decreased at each time point after establishing the model, the expression of PPAR-γ was down-regulated, and the expression of TNF-α and IL-6 was up-regulated in the other three groups ( P<0.05). Compared with group NP, PWT was significantly increased at 7-14 days after establishing the model, the expression of PPAR-γ was up-regulated, and the expression of TNF-α and IL-6 was down-regulated in group NP+ PD, and no significant change was found in the parameters mentioned above in group NP+ PD+ GW ( P>0.05). Compared with group NP+ PD, PWT was significantly decreased at 7-14 days after establishing the model, the expression of PPAR-γ was down-regulated, and the expression of TNF-α and IL-6 was up-regulated in group NP+ PD+ GW ( P<0.05). The results of immunofluorescence staining of the spinal cord showed that PPAR-γ was co-expressed with NeuN and GFAP. Conclusion:The mechanism by which PD1 mitigates NP is related to promoting the activation of PPAR-γ in spinal cord neurons and astrocytes and inhibiting inflammatory responses in rats.