Objective: To develop an HPLC method for determining feruloyltyramine in Pothi chinensis herba. Methods: The HPLC determination was performed on a Thermo ODS-2 Hypersil column(250 mm × 4. 6 mm, 5 μm) with isocratic elution of metha-nol-0. 4% phosphoric (35:65) as the mobile phase. The flow rate was 1. 0 ml·min-1 . The column temperature was at 25℃, and the detection wavelength was set at 318 nm. Results: Feruloyltyramine showed good linearity,and the recovery was 99. 40% with RSD of 1. 44% (n =9). Conclusion: The method is quick, simple and reproducible, which can be used to control the quality of Pothi chinensis herba.

TMTP1, a 5-amino acid peptide NVVRQ, obtained by using the flagella peptide library screening in our previous studies, can be used for the labeling of malignant in situ and metastatic lesions, and even micro-metastases. In this study, TMTP1 was assessed for its ability to specifically target the malignant hematopoietic cells and metastatic lesions of hematological malignancies. FITC-TMTP1 was chemically synthesized. Immunofluorescence assay and competitive test were carried out to determine the specific binding capacity of TMTPl to hematological malignant cell lines, including HL60, k562, SHI-1, Jurkat, Raji, El-4 and umbilical cord blood mononuclear cells. Mononuclear cells were isolated from the bone marrow of healthy subjects and patients with chronic myeloid leukemia. Then the cells were co-clutured with TMTP1 or scrambled peptides and the binding and affinity of TMTP1 peptide to the primary cells of hematological malignancies were flow cytometrically analyzed. The binding specificity of TMTP1 to target hematological malignancies was measured in vivo by intravenous injection of FITC-conjugated TMTP1 into El-4 lymphoma-bearing mice. The results showed that TMTP1 specifically bound to the cells of a series of hematological malignancies, including HL60, k562, Jurkat, Raji, El-4 and chronic myeloid leukemia primary cells but not to bone marrow mononuclear cells from healthy subjects. By contrast, TMTP1 could bind to the metastatic foci of lymphoma originating from the EL-4 cell line while the scrambled peptide failed to do so. Moreover, the occult metastases could be identified, with high specificity, by detecting FITC-TMTP1. We are led to conclude that TMTP1, as a novel tumor-homing peptide, can serve as a marker for primary malignant and metastatic lesions for the early diagnosis of hematological malignances and a carrier of anticancer drugs for cancer treatment.

TMTP1,a 5-amino acid peptide NVVRQ,obtained by using the flagella peptide library screening in our previous studies,can be used for the labeling of malignant in situ and metastatic lesions,and even micro-metastases.In this study,TMTP1 was assessed for its ability to specifically target the malignant hematopoietic cells and metastatic lesions of hematological malignancies.FITC-TMTP 1 was chemically synthesized.Immunofluorescence assay and competitive test were carried out to determine the specific binding capacity of TMTPI to hematological malignant cell lines,including HL60,k562,SHI-1,Jurkat,Raji,El-4 and umbilical cord blood mononuclear cells.Mononuclear cells were isolated from the bone marrow of healthy subjects and patients with chronic myeloid leukemia.Then the cells were co-clutured with TMTP1 or scrambled peptides and the binding and affinity of TMTP1 peptide to the primary cells of hematological malignancies were flow cytometrically analyzed.The binding specificity of TMTP 1 to target hematological malignancies was measured in vivo by intravenous injection of FITC-conjugated TMTP1 into El-4 lymphoma-bearing mice.The results showed that TMTP1 specifically bound to the cells of a series of hematological malignancies,including HL60,k562,Jurkat,Raji,El-4 and chronic myeloid leukemia primary cells but not to bone marrow mononuclear cells from healthy subjects.By contrast,TMTP1 could bind to the metastatic foci of lymphoma originating from the EL-4 cell line while the scrambled peptide failed to do so.Moreover,the occult metastases could be identified,with high specificity,by detecting FITC-TMTP1.We are led to conclude that TMTP1,as a novel tumor-homing peptide,can serve as a marker for primary malignant and metastatic lesions for the early diagnosis of hematological malignances and a carrier of anticancer drugs for cancer treatment.

Objective To investigate the efficacy and white matter integrity of low frequency repetitive transcranial magnetic stimulation (rTMS) and the modified electroconvulsive therapy (MECT) in patients with schizophrenia. Methods From May 2015 to October 2016,120 cases with schizophrenia were randomly enrolled into the MECT group and of the rTMS group. Patients in the MECT group were treated with the modified electric convulsive therapy for 8 times ,while patients in the rTMS group were treated with the repetitive transcranial magnetic stimulation for 12 times. PANSS were used to evalue the clinical effects. Repeatable battery for the assess-ment of neuropsychological status was used to assess the cognitive function. Treatment emergent side-effect scale was used to assess the adverse effects. Brain fractional anisotropy was used to assess white matter integrity. Results After treatment,the PANSS scores were significantly lowered,however,the RBANS scores were signifi-cantly higher in the MECT group and rTMS group than those before treatment ,with significant differences (P <0.05). No significant differences for the PANSS scores and the RBANS scores were observed between the two groups before and after treatment. There was no significant difference for the TESS scores between the two groups before treatment(P > 0.05). After treatment,the TESS scores in the MECT group were significantly higher than those in the rTMS group(P < 0.05). After treatment,the FA values of left anterior cingulate gyrus,left posterior cingulate gyrus ,left prefrontal cortex and genu of corpus callosum for both MECT group and rTMS group were significantly increased (P < 0.05 ,respectively). Compared with the MECT group ,the FA value significantly increased in the rTMS group after treatment (P < 0.05). Conclusions Both MECT and rTMS have significant clinical efficacies and can improve the cognitive function of schizophrenics. rTMS is more safe than MECT ,with a stronger effect on preventing the integrity of white matter than MECT.

Objective To establish a mouse embryonic stem cell test (mEST) model and human embryonic stem cell test (hEST) model, to evaluate the embryotoxicity of di(2-ethylhexyl) phthalate (DEHP). Methods We developed mEST and hEST models according to the European Centre for the Validation of Alternative Methods (ECVAM). We used penicillin G (PN-G) as the standard negative reference and 5-fluorouracil (5-FU) as the standard positive reference, respectively, to verify validity of the models. Based on model validity, mouse embryonic stem cells D3 (mESC-D3), mouse Balb/c-3T3 (3T3), and human embryonic stem cells H9 (hESC-H9) were administered different concentrations of DEHP (15.6, 31.2, 62.5, 125.0, 250.0, 500.0, and 1 000.0 μg/ml) for 7 days. A cell counting Kit-8 was used to detect the 50%inhibitory proliferation concentration (IC50) of mESC-D3 cells, 3T3 cells, and hESC-H9 with DEHP. mESC-D3 and hESC-H9 were treated with DEHP (15.6, 31.2, 62.5, 125.0, 250.0μg/ml, and 500.0μg/ml) for 10 days based on the cytotoxicity results. At day 10, the expression of cardiomyocyte differentiation gene alpha-myosin heavy chain (α-MHC) was detected by real-time PCR and the 50% inhibition of cardiomyocycte differentiation (ID50) determined. Based on the values of IC50 and ID50, functionsⅠ,ⅡandⅡcould be calculated by three linear discriminant functions in the EST model and the embryotoxicity of DEHP described by comparing the three functions. Results Nontrophoblast lineage both ES cells were cultured under optimal conditions and highly expressed hESC markers OCT4 , SSEA4, and TRA-1-60. The embryoid bodies formed were uniform in size and shape, and these results were highly repeatable. The PN-G and 5-FU results coincided with the prediction by ECVAM. Validation of our EST models was satisfactory. Results of the three endpoints of DEHP in mEST were 197.3 μg/ml (IC50 3T3), 210.0 μg/ml (IC50 D3) and 246.8μg/ml (ID50 D3). DEHP was evaluated to be a nonembryotoxic compound based on values of functionⅠ(7.78), functionⅡ(7.58) and functionⅢ(-7.79). The three endpoints of DEHP in hEST were 195.4μg/ml (IC50 3T3), 184.8 μg/ml (IC50 D3), and 84.3 μg/ml (ID50). By comparing the values of function Ⅰ (3.21), function Ⅱ (5.77), and function Ⅲ (-6.46), DEHP was evaluated to be weakly embryotoxic. Conclusion DEHP was determined to be a nonembryotoxic compound by mEST and weakly embryotoxic by hEST. Therefore, hEST is a more sensible model for the evaluation of DEHP embryotoxicity.

Objective To establish a mouse embryonic stem cell test (mEST) model and human embryonic stem cell test (hEST) model, to evaluate the embryotoxicity of di(2-ethylhexyl) phthalate (DEHP). Methods We developed mEST and hEST models according to the European Centre for the Validation of Alternative Methods (ECVAM). We used penicillin G (PN-G) as the standard negative reference and 5-fluorouracil (5-FU) as the standard positive reference, respectively, to verify validity of the models. Based on model validity, mouse embryonic stem cells D3 (mESC-D3), mouse Balb/c-3T3 (3T3), and human embryonic stem cells H9 (hESC-H9) were administered different concentrations of DEHP (15.6, 31.2, 62.5, 125.0, 250.0, 500.0, and 1 000.0 μg/ml) for 7 days. A cell counting Kit-8 was used to detect the 50%inhibitory proliferation concentration (IC50) of mESC-D3 cells, 3T3 cells, and hESC-H9 with DEHP. mESC-D3 and hESC-H9 were treated with DEHP (15.6, 31.2, 62.5, 125.0, 250.0μg/ml, and 500.0μg/ml) for 10 days based on the cytotoxicity results. At day 10, the expression of cardiomyocyte differentiation gene alpha-myosin heavy chain (α-MHC) was detected by real-time PCR and the 50% inhibition of cardiomyocycte differentiation (ID50) determined. Based on the values of IC50 and ID50, functionsⅠ,ⅡandⅡcould be calculated by three linear discriminant functions in the EST model and the embryotoxicity of DEHP described by comparing the three functions. Results Nontrophoblast lineage both ES cells were cultured under optimal conditions and highly expressed hESC markers OCT4 , SSEA4, and TRA-1-60. The embryoid bodies formed were uniform in size and shape, and these results were highly repeatable. The PN-G and 5-FU results coincided with the prediction by ECVAM. Validation of our EST models was satisfactory. Results of the three endpoints of DEHP in mEST were 197.3 μg/ml (IC50 3T3), 210.0 μg/ml (IC50 D3) and 246.8μg/ml (ID50 D3). DEHP was evaluated to be a nonembryotoxic compound based on values of functionⅠ(7.78), functionⅡ(7.58) and functionⅢ(-7.79). The three endpoints of DEHP in hEST were 195.4μg/ml (IC50 3T3), 184.8 μg/ml (IC50 D3), and 84.3 μg/ml (ID50). By comparing the values of function Ⅰ (3.21), function Ⅱ (5.77), and function Ⅲ (-6.46), DEHP was evaluated to be weakly embryotoxic. Conclusion DEHP was determined to be a nonembryotoxic compound by mEST and weakly embryotoxic by hEST. Therefore, hEST is a more sensible model for the evaluation of DEHP embryotoxicity.