Objective To investigate the anticancer effects and molecular mechanism of betulinic acid (BA)on Raji cells in vitro.Methods The effects of BA on the growth of Raji cells were studied by MTT assay.Apoptosis was assessed by Annexin-V/PI double-labeled cytometry.The influence on cell cycle was studied by flow cytometer.The cyclin D3 mRNA expression was checked by Western blotting and RT-PCR techniques.Results BA showed obvious inhibition on proliferation,as well as induction potency of apoptosis on Raji cells in vitro in a time-and dose-dependent manner by Annexin-V/PI double-labeled method.With the IC_(50)value for 24 h being(39.44?0.65)?g/mL,Raji cells treated with BA showed ac- cumulation in G_0/G_1 phase and reduction in the percentage of cells in S phase.The cyclin D3 mRNA ex- pression and protein were sharply decreased in Raji cells treated with BA.Conclusion BA could inhibit the proliferation of Raji cells by regulating the cell cycle that arrests cells at G_0/G_1 phase and induces apop- tosis of Raji cells.The antitumor effects of BA may be related to down-regulation of the expression of cy- clin D3.

The anti-cancer effects of betulinic acid (BA) on Jurkat cells and its in vitro mechanism were examined by using MTT assay. Apoptosis was detected by using Hoechst33258 staining and annexin-V/PI double-labeled cytometry. The effects of betulinic acid on the cell cycle of Jurkat cells were studied by propidium iodide method. RT-PCR and Western blotting were used to analyze the changes of cyclin D3, bcl-xl mRNA and protein levels in Jurkat cells after treatment with betulinic acid. Our results showed the proliferation of Jurkat cells was decreased in betulinic acid-treated group with a 24-h IC50 value being 70.00 mumol/L. Betulinic acid induced apoptosis of Jurkat cells in a time- and dose-dependent manner. The number of Jurkat cells treated with betulinic acid showed an increase in G(0)/G(1) phase and decrease in S phase. After treatment with 0, 20, 60, 100 mumol/L betulinic acid for 24 h, the number of Jurkat cells was increased from (31.00+/-1.25)% to (58.84+/-0.32)% in G(0)/G(1) phase, whereas it was decreased from (61.45+/-1.04)% to (35.82+/-1.95)% in S phase. PBMCs were less sensitive to the cytotoxicity of betulinic acid than Jurkat cells. The expressions of cyclin D3, bcl-xl mRNA and protein were decreased sharply in Jurkat cells treated with betulinic acid. It is concluded that betulinic acid is able to inhibit the proliferation of Jurkat cells by regulating the cell cycle, arrest cells at G(0)/G(1) phase and induce the cell apoptosis. The anti-tumor effects of betulinic acid are related to the down-regulated expression of cyclin D3 and bcl-xl.
Antineoplastic Agents, Phytogenic/*pharmacology ; Apoptosis/*drug effects ; Cell Proliferation/*drug effects ; Cyclin D3/metabolism ; Down-Regulation/drug effects ; Jurkat Cells ; Triterpenes/*pharmacology ; bcl-X Protein/metabolism

Objective To determine the incidence and risk factors of postoperative residual curarization (PORC) in patients with breast cancer after total intravenous anesthesia (TIVA) with vecuronium. Methods Two hundred and fiftyseven female patients with breast cancer undergoing breast-cancer surgery were enrolled into the present study. Anesthesia was induced with target-controlled infusion of propofol (Cp 3-4µg/ml) and remifentanil (2-3 ng/ml). A bolus of vecuronium 0.1mg/ kg was administered intravenously over 5-10s as soon as the patient lost consciousness, and laryngeal mask was placed 3min later. Mechanical ventilation and TIVA were performed for maintaining anesthesia and keeping bispectral index (BIS) between 40 to 60 during the operation. According to the duration of operation, 0.02mg/kg of vecuronium was administrated intermittently. Extubation of the laryngeal tube was performed according to clinical criteria. Train-of-four ratios (TOFr) were immediately measured with Veryark-TOF (Guangzhou Weilifangzhou Technology Ltd, China) in the recovery room. The patients were divided into two groups (Group N and Group R) according to the value of TOFr at the time of extubation. N denoted the non-residual neuromuscular blockade group (TOF=0.7), and R denoted the residual neuromuscular blockade group (TOF<0.7). Results The incidence of PORC was 60.3% among 257 patients. There was no significant difference of BMI and duration of anesthesia between groups (P>0.05). In group R, age and hemoglobin level were lower (P<0.05), but the incident of anemia was same between groups (32.4% vs. 40.6%, P>0.05). More patients in Group R received neoadjuvant chemotherapy and multiple boluses of vecuronium administration, and the duration between last dose of vecuronium to extubation was also prolonged compared with Group N (P<0.05). Multivariate logistic regression analysis identified that age, neoadjuvant chemotherapy and multiple boluses of vecuronium administration were not associated with increased risk of PORC. Duration from last dose of vecuronium to extubation was associated with increased risk of PORC (OR=0.970, 95%CI 0.956-0.984, P<0.001). Conclusions PORC is commonly used in patients with breast cancer. Duration from last dose of vecuronium to extubation is associated with increased risk of PORC.

Spinal biomechanics, especially the range of spine motion,has close connection with spinal surgery. The change of the range of motion (ROM) is an important indicator of diseases and injuries of spine, and the essential evaluating standards of effect of surgeries and therapies to spine. The analysis of ROM can be dated to the time of the invention of X-ray and even that before it. With the development of science and technology as well as the optimization of various types of calculation methods, diverse measuring methods have emerged, from imaging methods to non-imaging methods, from two-dimensional to three-dimensional, from measuring directly on the X-ray films to calculating automatically by computer. Analysis of ROM has made great progress, but there are some older methods cannot meet the needs of the times and disappear, some classical methods such as X-ray still have vitality. Combining different methods, three dimensions and more vivo spine research are the trend of analysis of ROM. And more and more researchers began to focus on vivo spine research. In this paper, the advantages and disadvantages of the methods utilized recently are presented through viewing recent literatures, providing reference and help for the movement analysis of spine.
Animals ; Humans ; Imaging, Three-Dimensional ; instrumentation ; methods ; trends ; Radiography ; Spine ; diagnostic imaging

Adenocarcinoma, Clear Cell ; pathology ; Angiomyolipoma ; pathology ; Female ; Follow-Up Studies ; Humans ; Kidney Neoplasms ; pathology ; Male ; Middle Aged ; Neoplasms, Multiple Primary ; pathology

Recently, the immunotherapy has been highlighted among cancer treatments. Cancer-testis antigen (CTA) has been studied in a variety of solid tumors because of its specific expression in tumors, and testis, ovary and placenta tissues, but not in other normal tissues. In order to provide a new approach for multiple myeloma (MM) immunotherapy, we examined the CTA expression in MM cell lines, and primary myeloma cells in patients with MM. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect the mRNA expression of MAGE-C1/CT7, SSX1, SSX2 and SSX4 in MM cell lines of RPMI-8226 and U266, and bone marrow (BM) cells of 25 MM patients and 18 healthy volunteers. The results showed that the 4 CTAs were expressed in RPMI-8226 and U266 cell lines. The positive expression rate of MAGE-C1/CT7, SSX1, SSX2 and SSX4 in the BM cells of 25 MM patients was 28% (7/25), 80% (20/25), 40% (10/25) and 68% (17/25), respectively. In contrast, the expression of any member of the CTAs was not detected in BM cells of 18 healthy volunteers. The expression of two or more CTAs was detected in 80% (20/25) MM patients, and that of at least one CTA in 88% (22/25). The mRNA expression levels of SSX1 and SSX4 were significantly higher in patients with MM at stage III than in those at stage I and II (P<0.05). No statistically significant differences were observed in the mRNA expression levels of MAGE-C1/CT7 and SSX2 in further stratified analyses by age, gender, MM types and percentage of MM cells in BM (P>0.05). In conclusion, our present study showed that MAGE-C1/CT7, SSX1, SSX2 and SSX4 were co-expressed in MM cell lines and the primary myeloma cells in MM patients, but not expressed in BM cells of healthy subjects. The mRNA levels of SSX1 and SSX4 are associated with MM clinical stage. This work may provide a new insight into MM immunotherapy in the future.

The anti-cancer effects of betulinic acid (BA) on Jurkat cells and its in vitro mechanism were examined by using MTT assay. Apoptosis was detected by using Hoechst33258 staining and annexin-V/PI double-labeled cytometry. The effects of betulinic acid on the cell cycle of Jurkat cells were studied by propidium iodide method. RT-PCR and Western blotting were used to analyze the changes of cyclin D3, bcl-xl mRNA and protein levels in Jurkat cells after treatment with betulinic acid. Our results showed the proliferation of Jurkat cells was decreased in betulinic acid-treated group with a 24-h IC50 value being 70.00 μmol/L. Betulinic acid induced apoptosis of Jurkat cells in a time- and dose-dependent manner. The number of Jurkat cells treated with betulinic acid showed an increase in G0/G1 phase and decrease in S phase. After treatment with 0, 20, 60, 100 μmol/L betulinic acid for 24 h, the number of Jurkat cells was increased from (31.00±1.25)% to (58.84±0.32)% in G0/G1 phase, whereas it was decreased from (61.45±1.04)% to (35.82±1.95)% in S phase. PBMCs were less sensitive to the cytotoxicity of betulinic acid than Jurkat cells. The expressions of cyclin D3,bel-xl mRNA and protein were decreased sharply in Jurkat cells treated with betulinic acid. It is coneluded that betulinic acid is able to inhibit the proliferation of Jurkat cells by regulating the cell cycle,arrest cells at G0/G1 phase and induce the cell apoptosis. The anti-tumor effects of betulinic acid are related to the down-regulated expression of cyclin D3 and bcl-xl.

Objective To observe the Th17, IL-17 and Tr cells equilibrium state as well as their changes of HIV infected or AIDS suffered patients in one-year HAART treatment. Methods Select 33 HIV/AIDS patients received HAART treatment while 33 healthy volunteers as controls. Flow cytometry was used to analyze Th17 and Tr cells in venous blood at the time of pre-therapy, 6th, 12th month when IL-17 levels in serum are tested by ELISA. Results The ratio of Th17 cells in CD4 cells in HIV/AIDS patients and volunteers were (1.20±0.37)%, (2.50±1.03)%, (3.70±1.56)%, (4.70±1.43)%, respectively; The ratio of Tr cells were (9.16±3.33)%, (7.19±2.91)%, (5.53±1.88)%, (4.43±0.97)%, respectively; The levels of IL-17 in serum were (5.3±2.5) pg/ml, (7.7±2.4) pg/ml, (10.4±3.1) pg/ml, (17.7±6.6) pg/ml respectively. The Th17 cells' level was positively correlative with the amount of CD4 cells, negatively correlate with the count of viral load. However, the Tr cells level is positively correlative with the count of viral load, negatively relate to the quantity of CD4 cells. Conclusion HIV could make IL-17, Th17 cells and Tr cells lost their balance, but the immune equilibrium state may gradually recover after HAART treatment. Which indicates the IL-17, Th17 cells and Treg cells may play an important role in the pathogenesis of AIDS, and they are likely to be the effective indexes to observe the progress of AIDS and the treatment effect of highly active antiretroviral therapy(HAART).

Accidents, Occupational ; statistics & numerical data ; China ; epidemiology ; Humans

OBJECTIVETo investigate the anticancer effects of betulinic acid (BA) on Jurkat cells in vitro and its molecular mechanism.

METHODSThe effects of betulinic acid on the growth of Jurkat cells were studied by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5diphenyl-2H-tetrazolium (MTT) assay. Apoptosis was assessed by Hoechst33258 staining and annexin-V/PI double-labeled cytometry. The effect of betulinic acid on the cell cycle of Jurkat cells was studied by propidium iodide staining. RT-PCR and Western blot were used to analyze the changes of cyclin D3, bcl-xl mRNA and protein levels in Jurkat cells after treatment with betulinic acid.

RESULTSThe proliferation of Jurkat cells was decreased in betulinic acid-treated group at a 24 h IC50 value of 70.0 micromol/L. The effect of betulinic acid to induce apoptosis in Jurkat cells was in a time- and dose-dependent manner. Jurkat cells treated with betulinic acid showed an increase of G0/G1 phase and decrease of S phase. The Jurkat cells treated with 0, 20, 60, 100 micromol/L betulinic acid for 24 h, showed an increased G0/G1 phase from 31.0% to 58.8%, whereas decreased S phase from 61.5% to 35.8%, respectively. PBMC was less sensitive to the cytotoxic effect of betulinic acid than Jurkat cells. The expression of cyclin D3, bcl-xl mRNA and protein were decreased sharply in Jurkat cells treated with betulinic acid.

CONCLUSIONBetulinic acid can inhibit the proliferation of Jurkat cells by regulating the cell cycle that arrests cells at G0/G1 phase and induces apoptosis in Jurkat cells. The antitumor effects of betulinic acid may be related to down-regulation of the expression of cyclin D3 and bcl-xl.

Antineoplastic Agents, Phytogenic ; pharmacology ; Apoptosis ; drug effects ; Betula ; chemistry ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Cyclin D3 ; genetics ; metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Jurkat Cells ; Plant Bark ; chemistry ; Plants, Medicinal ; chemistry ; RNA, Messenger ; metabolism ; Triterpenes ; pharmacology ; bcl-X Protein ; genetics ; metabolism