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Rural vitalization is a major strategy for reform and development of agriculture and rural areas in China, the key task of which is improving rural living environment. Imperfect rural solid waste (RSW) collection and transportation system exacerbates the pollution of RSW to rural living environment, while it has not been established and improved in the cold region of Northern China due to climate and economy. Through the analysis of the current situation of RSW source separation, collection, transportation and disposal in China, an RSW collection and transportation system suitable for the northern cold region was developed. Considering the low winter temperature in the northern cold region, different requirements for RSW collection, transportation and terminal disposal, scattered source points and single terminal disposal nodes in rural areas, the study focused on determining the number and location of transfer stations, established a model for transfer stations selection and RSW collection and transportation routes optimization for RSW collection and transportation system, and proposed the elite retention particle swarm optimization--genetic algorithm (ERPSO--GA). The rural area of Baiquan County was taken as a representative case, the collection and transportation scheme of which was given, and the feasibility of the scheme was clarified by simulation experiment. [ABSTRACT FROM AUTHOR]

A case of urachal signet ring cell carcinoma with transitional cell carcinoma of bladder in a 61-year-old man was reported, with a history of a palpable suprapubic mass for 1 year, an episode of gross painless hematuria for 7 days. Imaging revealed a large mass situated on the left wall of the bladder. Cystoscopic examination revealed a thickened wall and transurethral biopsy showed transitional cell carcinoma of bladder. He underwent partial cystectomy, including all urachal remnants and partial peritoneum. After resection, signet ring cell carcinoma of urachus was histological confirmed. The patient died of distant metastasis 5 months after operation. [ABSTRACT FROM AUTHOR]

Accumulating evidence has already indicated that traditional Chinese medicine (TCM) possesses tremendous potential for treating neurodegenerative diseases. Astragalus, also named Huangqi, is a famous traditional medical herb that can be applied to treat cerebral ischemia and prevent neuronal degeneration. Nevertheless, the underlying mechanisms remain largely unexplored. In the present study, Astragalus-containing serum (ASMES) was prepared and added into the culture medium of PC12 cells to explore its neuroprotective effect on 6-hydroxydopamine (6-OHDA)-caused neuronal toxicity. Our data showed that ASMES significantly ameliorated the cellular viability of cultured PC12 cells against the neurotoxicity induced by 6-OHDA (P < 0.05). Moreover, ASMES significantly decreased the cell apoptosis triggered by 6-OHDA (P < 0.01). Furthermore, 2',7'-dichlorofluorescin diacetate assay was performed to detect the changes in oxidative stress, and we showed that 6-OHDA elevated the production of reactive oxygen species (ROS), whereas ASMES significantly reversed these changes (P < 0.01). Besides, mitochondrial membrane potential (MMP) assay showed that ASMES could restore 6-OHDA-damaged MMP in cultured PC12 cells (P < 0.05). In conclusion, Astragalus could protect PC12 cells from 6-OHDA-caused neuronal toxicity, and possibly, the ROS-mediated apoptotic pathway participated in this process. Collectively, our findings provided valuable insights into the potential in treatment of neurodegenerative diseases., Competing Interests: None

Objective: To investigate the expressions of protein kinase C (PKC) isoforms in X-ray-exposed HepG2 cells and identify the PKC isoforms that induce radioresistance in HepG2 cells., Methods: Cultured HepG2 cells were divided into control group and 6 Gy radiation group for corresponding treatments. The fluorescence intensity (FI) and the percentage of positive cells were determined using flow cytometry., Results: The FI of PKCalpha and PKCdelta were 2.28 and 5.05 in the radiation group, respectively, significantly higher than those in the control group (P<0.05). The percentages of PKCalpha- and PKCdelta -positive cells were significantly higher in the radiation group than in the control group (P<0.05). The FI and the percentages of PKC zeta, gamma, epsilon, zeta positive cells were rather low and showed no significant differences between the two groups (P>0.05); PKCbeta expression was not detected in the two groups of cells. The apoptosis rates of the control and radiation groups were 1.73% and 20.90%, respectively., Conclusion: PKCalpha and PKCdelta may be involved in protecting HepG2 cells from radiation-induced apoptosis.

Aim: To investigate the significance and function of IFN-gamma on the changes of peripheral blood platelet count during tumor-rejection induced by a low dose of melphalan in C57BL/6 mice., Methods: Mouse tumor rejection model induced by a single dose of melphalan was used in this experiment. Different gene-type tumor-bearing mice (IFN-gamma(+/-) and IFN-gamma(-/-)), which had the same genetic background of C57BL/6, were treated intraperitoneally with melphalan (7.5 mg/kg). Tumor size was observed and recorded every one to three days in these different gene-type mice subsequently. Blood samples were obtained from orbital venous sinus on different days before and after melphalan treatment, and then complete blood counts were performed. The function of IFN-gamma on the efficacy of chemotherapy and the changes of blood platelet count in IFN-gamma(+/-) and IFN-gamma(-/-) mice after melphalan treatment was analyzed., Results: There was no significant difference in tumor sizes and blood platelet count between IFN-gamma(-/-) and IFN-gamma(+/-) mice (P>0.05). On the first day after melphalan (7.5 mg/kg) treatment, there were no significant changes in tumor sizes between mice in these two groups (P>0.05). Tumors shrank a little in IFN-gamma(-/-) mice and then grew gradually. Tumors relapsed in 2 w after melphalan injection in all IFN-gamma(-/-) mice, while tumor volumes decreased progressively and tumor cured at last in IFN-gamma(+/-) mice. The number of blood PLT in IFN-gamma(+/-) mice increased to (1935+/-378) x 10(9)/L 6 h after melphalan treatment, significantly higher than before (P<0.01); While in IFN-gamma(-/-) mice it was (1183+/-186) x 10(9)/L 6 h after melphalan treatment, no obvious increase than before. There was significant difference in blood PLT 6 h after melphalan treatment between IFN-gamma(+/-) and IFN-gamma(-/-) mice (P<0.01). Later, the numbers of blood PLT in IFN-gamma(+/-) mice decreased gradually and it dropped to normal (1158+/-270) x 10(9)/L on 11th day after melphalan treatment (P>0.05); While it sustained in normal range in IFN-gamma(-/-) mice. There was no significant difference in blood platelet count between IFN-gamma(-/-) and IFN-gamma(+/-) mice., Conclusion: Peripheral blood platelet count increased on the first day after melphalan treatment and tumors cured in IFN-gamma(+/-) mice; While tumors relapsed and there is no increase in blood platelet count on the first day after melphalan treatment in IFN-gamma(-/-) mice. These data indicated that the increase of blood PLT count was related to the function of IFN-gamma in tumor-bearing mice in vivo during tumor rejection induced by a low dose of melphalan.

Aim: To investigate the relationship between changes of peripheral blood counts and tumor rejection induced by a low dose of melphalan in C57BL/6 mice., Methods: Mouse lymphoma EL4 cells were inoculated subcutaneously into wild type C57BL/6 mice. Twelve days later, 7.5 mg/kg melphalan were administered intraperitoneally and the same volume of Normal Saline as control. Tumor sizes were observed and recorded subsequently. Blood samples were obtained from orbital venous sinus on different days before and after melphalan treatment, and then complete blood counts were performed and the relationship between the alterations of blood counts and tumor shrinkage after melphalan treatment was analyzed., Results: Tumor sizes decreased and tumors disappeared after 7.5 mg/kg melphalan treatment; while tumors grow continuously in control mice. The number of WBC was increased a little (10.6 + or - 2.3) x 10(9)/L 6 h after melphalan treatment, but there was no significant difference with mice before melphalan injection (9.8 + or - 0.32) x 10(9)/L (P>0.05); The number of WBC decreased significantly at 4(th) day after melphalan treatment (P<0.01); Later it increased a little, but at 28(th); day after melphalan it still obviously lower than that of the normal (P<0.01). Hemoglobin (Hb) concentration decreased from (132 + or - 7) g/L before melphalan treatment to (110 + or - 14) g/L at 6 h after melphalan treatment (P<0.05). Later, the amount of Hb was decreasing and at 7th day it got to its lowest point (96 + or - 5) g/L. It increased gradually back to normal in 2 weeks after melphalan treatment. The platelet count increased to (1502 + or - 142) x 10(9)/L 6 h after melphalan treatment, significantly higher that that (914 + or - 322) x 10(9)/L before melphalan injection (P<0.01). It maintained at a high level for one week and it recovered back to normal level at 28(th) day after melphalan treatment., Conclusion: Tumor shrinkage after melphalan treatment was not related to the decreased number of WBC or RBC, but correlated with the increased number of platelet in 10 days after melphalan treatment.

Objective: To investigate the effects and clinical value of percutaneous nephrostomy (PCN) in the management of postrenal acute renal failure (PARF)., Methods: The clinical data of 40 cases of PARF for the treatment of PCN and 20 cases with open surgery were retrospectively analyzed., Results: The success rate of PCN was 100%, renal function of all patients was restored to normal range after 2-7 days of PCN, in whom 30 patients recovered. In 10 patients nephrostomy was prolonged, among them 2 patients had recurrent abdominal tumors, and 8 patients had cervical cancer in late phase. There was no death, and no complications except hematuria. In the open surgery group, renal function of 19 cases recovered to normal range after 2-7 days of drainage. Lung infection occurred in 3 patients after operation, and they recovered with antibiotic therapy. One patient died of multiple organ dysfunction failure (MOF)., Conclusion: For PARF, PCN is preferable because of minimal trauma, less blood loss, as well as rapid recovery and better effect on recovery of renal function.

Aim: To establish a mouse model for BTT739 tumor-bearing mice cured by a low dose of cyclophosphamide (CTX). And then to observe the dynamic changes and significance of peripheral blood counts especially blood platelet count during tumor shrinkage induced by a low dose of CTX in T739 mice., Methods: Mouse bladder carcinoma tissues were inoculated subcutaneously into T739 mice. Seven days later, different doses of CTX or the same volume of NS were administered intraperitoneally to treat these tumor-bearing T739 mice. Tumor sizes were observed and recorded subsequently to find out the minimal dose of CTX that could cure most of these tumor-bearing mice. Then another 12 tumor-bearing mice were randomly divided into 15 mg/kg CTX treatment group and control group. Blood samples were obtained from orbital venous sinus on different times after CTX treatment. Complete blood counts were performed and the relationship between peripheral blood platelet counts and tumor shrinkage was analyzed., Results: Within 2 weeks after CTX treatment, the speed of tumor shrinkage had a positive relationship with the dose of CTX used; but the survival rate of the tumor-bearing mice had a negative relationship with the dose of CTX used in 2 months after CTX treatment. 15 mg/kg CTX could cure most of the tumor bearing mice, while it had no remarkably inhibitive effects on peripheral blood cells. The perpherial platelet count increased to (1483.4+/-184.4)x10(9)/L in mice 6 h after CTX treatment. There was significant difference compared with that in mice of control group (1086.6+/-81.0)x10(9)/L (P<0.01). During the 2nd to 14th day after CTX treatment, there was no obvious difference in the platelet count between treatment group and control group (P>0.05)., Conclusion: CTX 15 mg/kg could cure most of bladder tumor-bearing T739 mice. The transient increase of the peripheral platelet count in 6 h after CTX treatment may relate to the antitumor effects of CTX.

Aim: To investigate the relationship between the alterations of complete blood counts and tumor shrinkage during tumor rejection induced by a high dose of 5-FU in C57BL/6 mice., Methods: Wild type C57BL/6 tumor-bearing mice were treated with different doses of 5-FU intraperitoneally. 75 mg/kg 5-FU was the minimal effective dose of 5-FU that could cure the tumor-bearing mice. Then another 6 tumor-bearing mice were treated intraperitoneally with 5-FU (75 mg/kg). Blood samples were obtained from orbital venous sinus on different days before and after 5-FU treatment, and then complete blood counts were performed and the relationship between the alterations of blood counts and tumor shrinkage after 5-FU treatment was analyzed., Results: Tumor sizes decreased steadily and tumors disappeared within the first week after 5-FU treatment; and at the same time 75 mg/kg 5-FU also had side effects on peripherial blood cells. The number of WBC significantly decreased from the first day after 5-FU treatment (P<0.001). But during the 7 th to 15 th day the number of WBC rebounced back to normal level (P>0.05). Later it decreased again and it couldn't recover back to normal level at the 28th day after 5-FU treatment (P<0.01). The concentration of Hb decreased at the first day and lasted for 2 weeks (P<0.01). It increased gradually back to normal in 2 weeks after 5-FU treatment. The inhibitory effect of 5-FU on platelets count was not obvious. The platelet count increased significantly at the first and at the 11th day after 5-FU treatment respectively (P<0.01)., Conclusion: Tumor shrinkage after 5-FU treatment is not related to the decreased number of WBC or RBC, but correlated with the increased number of platelet at the first day after 5-FU treatment.

Aim: To investigate the immunological mechanism of anti-tumor effect of 5-FU by establishing lymphoma EL4 tumor-bearing mouse models in wild type C57BL/6 mice and nude C57BL/6 mice, respectively., Methods: The mouse lymphoma EL4 cells were inoculated subcutaneously into wild type C57BL/6 mice (immune-competent mice). Twelve days later, 5-FU of different doses was administered intraperitoneally to treat these wild type C57BL/6 tumor-bearing mice. The size of tumors in the wild type C57BL/6 mice was observed and recorded to explore the minimal dose of 5-FU that could cure the tumor-bearing mice. Then the same amount of EL4 tumor cells was inoculated subcutaneously into wild type C57BL/6 mice and nude C57BL/6 mice (T cell-deficient mice) simultaneously, which had the same genetic background of C57BL/6. Twelve days later, 5-FU of the minimal dose was given intraperitoneally to treat both the wild type and nude C57BL/6 tumor-bearing mice. The size of tumors in the two different types of mice was observed and recorded., Results: A single dose of 5-FU (75 mg/kg) cured both the EL4 tumor-bearing wild type C57BL/6 mice and the EL4 tumor-bearing nude C57BL/6 mice in the first week. Two weeks after 5-FU treatment, all of the nude mice died of tumor relapse while most of the wild type C57BL/6 mice were fully recovered., Conclusion: A single dose of 5-FU has marked anti-tumor effects on lymphoma EL4 tumor-bearing C57BL/6 mice with or without T lymphocytes. The relapse of tumors after 5-FU treatment might be related to the function of T lymphocytes.

Objective: To study the relationship of the sensitivity of tumor cells to chemotherapeutic agent between in vivo and in vitro., Methods: Mouse lymphoma cells of the line E14 were cultured and melphalan resistant EL4 cell line (EL4/melphalan) was established by culturing EL4 cells with continuous low-concentration and intermittent gradually-increasing-concentration of melphalan in vitro. MTT assay was used to evaluate the drug sensitivity and the resistance index of the EL4/melphalan cells to melphalan was calculated. EL4/melphalan and EL4 cells of the concentration of 5 x 10(8)/L were inoculated separately into 20 C57BL/6 mice subcutaneously. 12 days later, the EL4 and EL4/melphalan tumor-bearing mice were randomly divided into 2 groups respectively, 5 mice in each group. Treatment groups were given 7.5 mg/kg melphalan intraperitoneally, and control groups were given the same volume of normal saline. The tumor size was observed every other day., Results: Compared with the EL4 cells, the EL4/melphalan cells had no obvious changes morphologically. They could grow in RPMI 1640 medium containing 5 mg/ml melphalan. The resistance index was 2.87 against melphalan. After the treatment of melphalan of the dose 7.5 mg/kg, the tumor sizes of the treatment groups and control groups inoculated with both EL4 cells and the EL4/melphalan cells gradually decreased at the similar speed, and about one week later all tumors disappeared. However, the tumors of the control groups grew progressively and all the mice died at last., Conclusion: The chemotherapeutic effects of tumors in vivo have nothing to do with the effects of the chemotherapeutic agents on tumor cells in vitro. The tumor cells resistant to melphalan in vitro remain sensitive to the drug in vivo.

Aim: To investigate the relationship between TNFalpha and tumor rejection induced by a single dose of melphalan in C57BL/6 mice., Methods: Different gene type mice (TNFR1(+/+), TNFR1(+/-) and TNFR1(-/-)) with the same genetic background of C57BL/6 were used in this experiment. Murine lymphoma EL4 cells were inoculated subcutaneously into the different gene type mice simultaneously. Twelve days later, 7.5 mg/kg melphalan was used intraperitoneally to treat the tumor-bearing mice with TNFR1(+/+), TNFR1(+/-) and TNFR1(-/-). The tumors in the different gene type mice were observed and recorded every one to three day., Results: After the treatment of 7.5 mg/kg melphalan during the first week, the tumors in the different gene type mice shrank at a similar rate. In the following 2 months, the tumors in the TNFR1(+/+) and TNFR1(+/-) C57BL/6 mice gradually shrank and were cured but most tumors in the TNFR1(-/-) C57BL/6 mice relapsed after melphalan treatment., Conclusion: TNFalpha plays an important role in melphalan-induced tumor rejection. The anti-tumor effect of melphalan has no relationship with the expression of tumor necrosis factor 1 in tumor-bearing mice. TNFR1 is required to prevent or avoid the relapse of tumors in mice instead of tumor cells.

Aim: To investigate the relationship between IFN-gamma and anti-tumor effects of melphalan in vivo., Methods: Different gene-type mice (IFN-gamma(+/+), IFN-gamma(+/-) and IFN-gamma(-/-)), which had the same genetic background of C57BL/6, were used in this experiment. Murine lymphoma EL4 cells were inoculated subcutaneously into different gene-type mice simultaneously. Twelve days later, 7.5 mg/kg melphalan was used intraperitoneally to treat all these IFN-gamma(+/+), IFN-gamma(+/-) and IFN-gamma(-/-) tumor-bearing mice. Tumor size was observed and recorded every one to three days in these different gene-type mice subsequently., Results: After melphalan (7.5 mg/kg) treatment, tumor size decreased at a similar rate in IFN-gamma(-/-), IFN-gamma(+/-) and IFN-gamma(+/+) mice within the first 3 d. Tumors shrank further or completely disappeared in most of IFN-gamma(+/-) and IFN-gamma(+/+) mice, whereas tumors grew gradually in all IFN-gamma(-/-) mice., Conclusion: 7.5 mg/kg melphalan has obvious anti-tumor effects on tumor-bearing IFN-gamma(+/+) and IFN-gamma(+/-) mice, but little effects on IFN-gamma(-/-) mice. These data suggest that IFN-gamma is required for the anti-tumor effects of melphalan on tumor-bearing mice in vivo.

Aim: To establish mouse lymphoma EL4 tumor-bearing mouse models in wild type C57BL/6 mice and nude C57BL/6 mice respectively, and to further investigate the immunological mechanisms of anti-tumor effect of melphalan., Methods: Mouse lymphoma EL4 cells were inoculated subcutaneously into wild type C57BL/6 mice (immune-competent mice). Twelve days later, melphalan of different doses were administered intraperitoneally to treat these wild type C57BL/6 tuomr-bearing mice. Tumor sizes were observed and recorded subsequently to find out the minimal dose of melphalan that could cure the tuomr-bearing mice. Then the same amount of EL4 tumor cells were inoculated subcutaneously into wild type C57BL/6 mice and nude C57BL/6 mice (T cell-deficient mice) simultaneously, which had the same genetic background of C57BL/6. Twelve days later, melphalan of the minimal dose was given intraperitoneally to treat both the wild type and nude C57BL/6 tuomr-bearing mice. Tumor sizes were observed and recorded in these two different types of mice subsequently., Results: A single dose of melphalan (7.5 mg/kg) could cure EL4 tumor-bearing wild type C57BL/6 mice, but could not induce tumor regression in EL4 tumor-bearing nude C57BL/6 mice., Conclusion: A single dose of melphalan has obvious anti-tumor effect on mouse lymphoma EL4 tumor-bearing wild type C57BL/6mice, which requires the involvement of T lymphocytes in the host probably related to their killing functions.

Objective: To investigate protein kinase C (PKC) expression and its association with multidrug resistance (MDR) in KBV200 cells., Methods: KBV200 cells were preincubated with PKC activator phorbol-12-myristate-13-acetate (PMA, 200 nmol/L) and PKC activity was assayed by measurement of peptide substrate (32)P incorporation from [gamma-(32)P]ATP, with the cells without PMA preincubation serving as the control. Western blotting was performed for assessing the expression of PKC isoform, and the cell inhibition rate was evaluated by MTT assay., Results: PMA preincubation of the cells significantly enhanced the activity of the total PKC and the membrane fraction, but lowered the PKC activity of the cytosol fraction, as compared with the cells without PMA treatment (P<0.01). PKC-alpha expression was upregulated in the membrane fraction and down-regulated in the cytosol fraction in KBV200 cells after PMA preincubation. PKCbeta expression was slightly elevated in the cytosol fraction but exhibited no obvious changes in the membrane fraction after PMA pretreatment of the cells. The values of IC(50) of vincristine and adriamycin in PMA-treated cells were increased to 2275.5 nmol/L and 233.25 nmol/L, respectively (P<0.01)., Conclusion: PMA can increase the multidrug resistance of KBV200 cells, which suggests the possible involvement of PKC in the mechanism of multidrug resistance of tumor cells.

Objective: To investigate the toxicity attenuation and efficacy potentiation effects of Sijunzi decoction (SJZD) on bladder carcinoma treated by chemotherapy in mice., Methods: T739 mice were randomly divided into 8 groups after subcutaneous inoculation of bladder carcinoma cells, the control group (A); two mitomycin C (MMC) group, treated with MMC of routine dosage (B) and low-dosage (C) respectively; three SJZD groups, treated with SJZD of high (D), medium (E) and low-dosage (F) respectively; and two combined treatment groups, treated with SJZD of high-dosage + MMC of routine dosage(G) and SJZD of high-dosage + MMC of low-dosage(H). The medication was begun at 24 hrs after inoculation. The tumor inhibitory rate, activity of peritoneal macrophages after 14 days of treatment and change of peripheral white blood cells after 7 days of treatment were determined and the survival time of mice was observed., Results: The survival time of mice in Group D was significantly higher than that in Group A (P < 0.05), while those in Group E and F showed insignificant difference as compared with those in Group A (P > 0.05). The highest tumor inhibitory rate was shown in Group B, but the survival time in that group showed no significant difference as compared to those in Group A (P > 0.05). The longest survival time (32.7 +/- 1.3 days) was shown in Group H, which was obviously different to that in other groups (P < 0.05). And the leukocyte counts and macrophage activity in Group H were better than those in Group B, C and G (P < 0.05), except that the tumor inhibitory rate was significantly lower than that in Group B, C and G (P < 0.05)., Conclusion: Combined chemotherapy of SJZD with low dosage MMC has definite effect in inhibiting tumor growth in mice with bladder carcinoma, displaying special effects of toxicity attenuation and efficacy potentiation.

Aim: To prepare and purify the antibody against ribonuclease inhibitor(RI)., Methods: RI was extracted from human placenta and purified by affinity chromatography. Rabbits anti-RI antibody was obtained after immunization and then purified through rProtein A Sepharose Fast Flow chromatography column. The characters of the antibody was identified by SDS-PAGE, ELISA and Western blot., Results: An anti-RI antibody was obtained and purified. SDS-PAGE analysis showed that the purified anti-RI antibody has high purity. The results of Western blot and ELISA indicated that anti-RI antibody had high specificity and good stability., Conclusion: The anti-RI antibody with high titer, high specificity and good stability has been acquired, which lays the foundation for further research on RI.

Objective: To investigate the association of protein kinase C (PKC) isoforms and multidrug resistance (MDR) mechanism in KBV200 cells., Methods: Western blotting was utilized to examine the expression and subcellular distribution of PKC isoforms were measured in KBV200 cells with MDR and drug-sensitive KB cells, and the fluorescence intensity of PKC isoforms was detected by flow cytometry (FCM)., Results: KBV200 cells possessed higher PKC activities, with increased percentage of membrane fraction. As compared with parental KB cells, the expression of PKCalpha was significantly increased in KBV200 cells, while PKCbeta and epsilon expressions remained unchanged, and PKCgamma and zeta failed to be detected. Fluorescence intensity of PKCalpha in KBV200 cells was increased., Conclusion: PKC might contribute to MDR phenotype in KBV200 cells, and of the isoforms so far detected, PKCalpha might play an important role in MDR phenotype.

Objective: To investigate the relationship between protein kinase C (PKC) and multidrug resistance (MDR) in cancer cell line KBV200., Methods: MTT assay was used to evaluate the IC50 of vincristine (VCR) and adriamycin (ADR) in KB cell line and its VCR-resistant derivative KBV200 cells. PKC activities in the 2 cell lines were assayed by measuring the incorporation of (32)P from [gamma-(32)P] ATP into the peptide substrates., Results: The IC50 values of VCR and ADR in KBV200 cells was 64.03 and 18.8 folds greater than those in KB cells. PKC activities of the membrane and cytosol fraction in KBV200 cells were increased compared with that in KB cells, with the total PKC activity 1.12-fold higher. Phorbol-12-myristate-13 -acetate increased PKC activity of the membrane fraction and IC50 values of KBV200 cells, while staurosporine worked to the opposite effects., Conclusion: PKC may contribute to MDR mechanism in KBV200 cells.