Objective To evaluate laparoscopy for insertion of peritoneal catheters in continuous ambulatory peritoneal dialysis (CAPD) patients. Methods Twenty patients of end-stage renal disease.During laparoscopic surgery,the peritoneal catheter was advanced into the abdomen by inducing thread.Results All procedures were completed by laparoscopy successfully. There was no intraoperative complication or surgical mortality. Conclusion Laparoscopy is feasible, safe, and effective for peritoneal catheters placement.

Objective To evaluate the feasibility of getting retroperitoneal lymph node biopsy via technique of natural orifice transluminal endoscopic surgery(NOTES)in human being with current available devices.Methods We performed trans-gastric endoscopic biopsy of retroperitoneal lymph node with the aid of laparoscopy in a 50-year-old man,who presented with abdominal pain and enlarged retroperitoneal lymph nodes and signed a written informed consent before the procedure.After routine anesthesia and abdominal skin sterilization,a pneumoperitoneum was induced with a Veress needle placed in the umbilical area,followed by the introduction of a 5-mm trocar.Gastral cavity Was sterilized with antibiotics and povidone iodine.Under laparoscopie optical control,we made a styliform incision in the anterior wall of gastric corpus with a needle knife,and enlarged the incision by a dilatation balloon and then entered the peritoneal cavity with a sterile endoscope.We got two biopsies from the enlarged lymph node with a heat forceps assisted by laparoscopy.The specimen was taken out by retrieval basket through the stomach.The gastric incision Was closed with metal clips.Results The biopsy by means of NOTES was successfully performed without intra-or postoperative complications.The diagnosis was confirmed as lymphoma pathologically.The patient received chemotherapy and was discharged on the sixth postoperative day.There was no short or long-term complication.Conclusion Transgastric access for laparoscopy-assisted biopsy of retroperitoneal lymph node is feasible and safe in human being.

Objective To evaluate the nutritional status of morbid obesity (MO) before and after laparoscopic adjustable gastric banding (LAGB), and the safety of LAGB.Methods LAGB was performed in 15 cases from Jun.2003 to Nov.2003.Patients′ nutritional parameters were determined before and 1, 3 and 6 months postoperatively.Results There was a significant reduction of weight and body mass index (BMI) ( P 0.05).Conclusion No major nutritional deficiencies were found following LAGB.It is an effective and safe procedure for the treatment of morbid obesity.

OBJECTIVETo improve the water solubility and biological activity of neoligans (magnolol and honokiol) and test the antitumor activity of the modified compounds.

METHODSThe glycosylated products of magnolol and honokiol were obtained by enzymatic synthesis using a UDP-glycosyltransferase (YjiC) from Bacillus. The products were characterized by high-performance liquid chromatography (HPLC), liquid chromatography-mass spectrometry (LC-MS), and nuclear magnetic resonance (NMR) analysis. MTT assay was used to detect the growth inhibition of 4 human cancer cell lines induced by the compounds.

RESULTSWe obtained two glucosides of neolignans (magnolol and honokiol) for the first time by enzymatic synthesis using a UDP-glycosyltransferase. Based on the spectroscopic data, the glucosides were identified as magnolol-2- O-β-D-glucopyranoside (1) and honokiol-4'-O-β-D-glucopyranoside (2). Compounds 1-4 exhibited moderate anti-proliferative activities against the 4 human cancer cell lines, with IC50 values ranging from 9.41 to 111.21 µmol/L.

CONCLUSIONThe glycoslated products show enhanced water solubility and drug sensitivity against SMMC7721 cells, suggesting their value as potential therapeutic drugs.

Antineoplastic Agents, Phytogenic ; chemistry ; Biphenyl Compounds ; chemistry ; Cell Line, Tumor ; Chromatography, High Pressure Liquid ; Glucosides ; chemistry ; Glycosylation ; Humans ; Lignans ; chemistry ; Magnetic Resonance Spectroscopy ; Mass Spectrometry

OBJECTIVETo explore the effect of the Hsp90 inhibitor anacardic acid on cell proliferation, invasion and migration of breast cancer MDA-MB-231 cells.

METHODSThe inhibitory effect of anacardic acid on Hsp90 was assessed with in vitro ATPase inhibition assay and ATP-sepharose binding assay. MTT assay was used to detect the growth inhibition induced by anacardic acid in MDA-MB-231 cells. Transwell assays were used to evaluate MDA-MB-231 cell invasion and migration. Western blotting was performed to assess the effect of anacardic acid in triggering the degradation of MMP-9, TIMP-1, Hsp90, and Hsp70.

RESULTSAnacardic acid exhibited a modest activity of ATPase inhibition with an IC50 value of 82.5 µmol/L. Anacardic acid significantly suppressed the proliferation of MDA-MB-231 cells in a dose-dependent manner (IC50 value of 29.3 µmol/L). Treatment with 12.5, 25, and 50 µmol/L anacardic acid for 36 h caused inhibition of cell invasion by 23.6%, 56.6%, and 67.0% in MDA-MB-231 cells, respectively (P<0.05), and anacardic acid treatment for 24 h inhibited the cell migration by 30.0%, 45.5%, and 77.5%, respectively (P<0.05). Anacardic acid dose-dependently induced MMP-9 degradation, but did not obviously affect Hsp90 or Hsp70 expressions.

CONCLUSIONAnacardic acid can significantly inhibit the proliferation, invasion, and migration of MDA-MB-231 cells, the mechanism of which may involve the inhibition of Hsp90 ATPse activity and down-regulation of MMP-9 expression.

Anacardic Acids ; pharmacology ; Breast Neoplasms ; pathology ; Cell Line, Tumor ; drug effects ; Cell Movement ; Cell Proliferation ; Down-Regulation ; HSP90 Heat-Shock Proteins ; antagonists & inhibitors ; metabolism ; Humans ; Matrix Metalloproteinase 9 ; metabolism ; Tissue Inhibitor of Metalloproteinase-1 ; metabolism

Objective To explore the effect of the Hsp90 inhibitor anacardic acid on cell proliferation, invasion and migration of breast cancer MDA-MB-231 cells. Methods The inhibitory effect of anacardic acid on Hsp90 was assessed with in vitro ATPase inhibition assay and ATP-sepharose binding assay. MTT assay was used to detect the growth inhibition induced by anacardic acid in MDA-MB-231 cells. Transwell assays were used to evaluate MDA-MB-231 cell invasion and migration. Western blotting was performed to assess the effect of anacardic acid in triggering the degradation of MMP-9, TIMP-1, Hsp90, and Hsp70. Results Anacardic acid exhibited a modest activity of ATPase inhibition with an IC50 value of 82.5 μmol/L. Anacardic acid significantly suppressed the proliferation of MDA-MB-231 cells in a dose-dependent manner (IC50 value of 29.3 μmol/L). Treatment with 12.5, 25, and 50μmol/L anacardic acid for 36 h caused inhibition of cell invasion by 23.6%, 56.6%, and 67.0%in MDA-MB-231 cells, respectively (P<0.05), and anacardic acid treatment for 24 h inhibited the cell migration by 30.0%, 45.5%, and 77.5%, respectively (P<0.05). Anacardic acid dose-dependently induced MMP-9 degradation, but did not obviously affect Hsp90 or Hsp70 expressions. Conclusion Anacardic acid can significantly inhibit the proliferation, invasion, and migration of MDA-MB-231 cells, the mechanism of which may involve the inhibition of Hsp90 ATPse activity and down-regulation of MMP-9 expression.

Objective To explore the effect of the Hsp90 inhibitor anacardic acid on cell proliferation, invasion and migration of breast cancer MDA-MB-231 cells. Methods The inhibitory effect of anacardic acid on Hsp90 was assessed with in vitro ATPase inhibition assay and ATP-sepharose binding assay. MTT assay was used to detect the growth inhibition induced by anacardic acid in MDA-MB-231 cells. Transwell assays were used to evaluate MDA-MB-231 cell invasion and migration. Western blotting was performed to assess the effect of anacardic acid in triggering the degradation of MMP-9, TIMP-1, Hsp90, and Hsp70. Results Anacardic acid exhibited a modest activity of ATPase inhibition with an IC50 value of 82.5 μmol/L. Anacardic acid significantly suppressed the proliferation of MDA-MB-231 cells in a dose-dependent manner (IC50 value of 29.3 μmol/L). Treatment with 12.5, 25, and 50μmol/L anacardic acid for 36 h caused inhibition of cell invasion by 23.6%, 56.6%, and 67.0%in MDA-MB-231 cells, respectively (P<0.05), and anacardic acid treatment for 24 h inhibited the cell migration by 30.0%, 45.5%, and 77.5%, respectively (P<0.05). Anacardic acid dose-dependently induced MMP-9 degradation, but did not obviously affect Hsp90 or Hsp70 expressions. Conclusion Anacardic acid can significantly inhibit the proliferation, invasion, and migration of MDA-MB-231 cells, the mechanism of which may involve the inhibition of Hsp90 ATPse activity and down-regulation of MMP-9 expression.

OBJECTIVETo investigate the effect of 3-bromopyruvate (3-BP) in sensitizing hepatocellular carcinoma cells to cisplatin-induced apoptosis and its possible mechanism.

METHODSThe growth inhibition of HepG2 and SMMC7721 cells following exposures to different concentrations of 3-BP and cisplatin was measured by MTT assay. The apoptosis of cells treated with 100 µmol/L 3-BP with or without 8 µmol/L cisplatin was assessed using flow cytometry with PI staining, and the activity of caspase-3 and intracellular ATP level were detected using commercial detection kits; the expression of XIAP and PARP was analyzed using Western blotting.

RESULTS3-BP produced obvious inhibitory effects on HepG2 and SMMC7721 cells at the concentrations of 50-400 µmol/L with IC50 values of 238.9∓13.9 µmol/L and 278.7∓11.7 µmol/L for a 48-h treatment, respectively. Cisplatin also inhibited the growth of HepG2 and SMMC7721 cells at the concentrations of 2-32 µmol/L, with IC50 values of 16.4∓0.9 µmol/L and 20.9∓1.8 µmol/L after a 48-h treatment, respectively. Treatment with 100 µmol/L 3-BP combined with 8 µmol/L cisplatin for 48 h resulted in a growth inhibition rate of (60.6∓2.2)% in HepG2 cells and (56.8∓2.3)% in SMMC7721 cells, which were significantly higher than those in cells treated with 3-BP or cisplatin alone. The combined treatment for 48 h induced an apoptotic rate of (51.1∓4.3)% in HepG2 cells and (46.5∓3.9)% in SMMC7721 cells, which were also markedly higher than those in cells with 3-BP or cisplatin treatment alone.

CONCLUSION3-BP can sensitize HepG2 and SMMC7721 cells to cisplatin-induced apoptosis possibly by causing intracellular ATP deficiency, down-regulating XIAP, and increasing caspase-3 activity.

Adenosine Triphosphate ; metabolism ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; pathology ; Caspase 3 ; metabolism ; Cisplatin ; pharmacology ; Hep G2 Cells ; Humans ; Liver Neoplasms ; pathology ; Pyruvates ; pharmacology ; X-Linked Inhibitor of Apoptosis Protein ; metabolism

Objective To investigate the effect of 3-bromopyruvate (3-BP) in sensitizing hepatocellular carcinoma cells to cisplatin-induced apoptosis and its possible mechanism. Methods The growth inhibition of HepG2 and SMMC7721 cells following exposures to different concentrations of 3-BP and cisplatin was measured by MTT assay. The apoptosis of cells treated with 100μmol/L 3-BP with or without 8μmol/L cisplatin was assessed using flow cytometry with PI staining, and the activity of caspase-3 and intracellular ATP level were detected using commercial detection kits; the expression of XIAP and PARP was analyzed using Western blotting. Results 3-BP produced obvious inhibitory effects on HepG2 and SMMC7721 cells at the concentrations of 50-400 μmol/L with IC50 values of 238.9 ± 13.9 μmol/L and 278.7 ± 11.7 μmol/L for a 48-h treatment, respectively. Cisplatin also inhibited the growth of HepG2 and SMMC7721 cells at the concentrations of 2-32μmol/L, with IC50 values of 16.4±0.9μmol/L and 20.9±1.8μmol/L after a 48-h treatment, respectively. Treatment with 100μmol/L 3-BP combined with 8 μmol/L cisplatin for 48 h resulted in a growth inhibition rate of (60.6 ± 2.2)% in HepG2 cells and (56.8 ± 2.3)% in SMMC7721 cells, which were significantly higher than those in cells treated with 3-BP or cisplatin alone. The combined treatment for 48 h induced an apoptotic rate of (51.1±4.3)%in HepG2 cells and (46.5±3.9)%in SMMC7721 cells, which were also markedly higher than those in cells with 3-BP or cisplatin treatment alone. Conclusion 3-BP can sensitize HepG2 and SMMC7721 cells to cisplatin-induced apoptosis possibly by causing intracellular ATP deficiency, down-regulating XIAP, and increasing caspase-3 activity.

Objective:To synthesize new bakuchiol aminoguanidine derivatives and test their effect on viability and apoptosis of human triple-negative breast cancer(TNBC)cells.Methods:Two bakuchiol derivatives 1 and 2 were obtained by formylation and Shiff base reaction of bakuchol.The structures of derivatives 1 and 2 were identified by 1H-NMR,13C-NMR,and high-resolution electrospray ionization mass spectrometry(HR-ESI-MS)analysis.Human TNBC MDA-MB-231 cells were treated with bakuchiol and its derivatives and cell viability was measured by MTT assay.Apoptosis was detected by fluorescence microscopy and flow cytometry with Annexin V-FITC/PI staining.The expressions of apoptosis-related proteins were analyzed with Western blotting.The JC-1 and reactive oxygen species(ROS)assay kits were used to determine the effect of new bakuchiol derivatives on mitochondrial function.Results:Based on spectroscopic analysis,a new bakuchiol schiff base derivative was elucidated as 2-{(E)-5-[(S,E)-3,7-dimethyl-3-vinylocta-1,6-dien-1-yl]-2-hydroxylbenzylidene}hydrazine-1-carboximidamide(derivative 2).Bakuchiol and its derivatives 1 and 2 all showed cytotoxic activity against the MDA-MB-231 cells.Derivative 2 exhibited the most potent cytotoxic activity to MDA-MB-231 cell with IC50 of(13.11±1.09),(6.91±1.78),and(2.23±1.32)μmol/L after 24,48,and 72 h.It had low toxicity to normal mouse liver(AML-12)cells with IC50 of(31.23±1.58)μmol/L at 72 h.Fluorescence microscopy and flow cytometry demonstrated apoptosis in breast cancer cells after treating with derivative 2 in a concentration dependent manner.Western blotting showed that after derivative 2 treatment,the expression of apoptosis-related proteins cytochrome C,cleaving caspase-3 and Bax/Bcl-2 radio in MDA-MB-231 cells increased;in addition,apoptosis was associated with the decreased mitochondrial membrane potential and increased reactive oxygen species accumulation.Conclusion:The novel bakuchiol aminoguanidine derivative(derivative 2)is capable of inducing apoptosis in MDA-MB-231 cells,but has low toxicity to normal liver cells,suggesting that it may be used as a lead compound for an anti-TNBC agent.