Antineoplastic Agents, Phytogenic ; therapeutic use ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; Neoplasms ; drug therapy ; Patents as Topic ; Phytotherapy ; methods

Antineoplastic Agents, Phytogenic ; therapeutic use ; Drugs, Chinese Herbal ; isolation & purification ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; Neoplasms ; drug therapy ; Patents as Topic ; Phytotherapy ; methods ; Plants, Medicinal ; chemistry

Drugs, Chinese Herbal ; chemistry ; therapeutic use ; Female ; Humans ; Lung Neoplasms ; drug therapy ; pathology ; radiotherapy ; Male ; Middle Aged ; Phytotherapy ; Radiation Injuries ; prevention & control ; Spinal Neoplasms ; drug therapy ; secondary ; Treatment Outcome

Graphite ; Humans ; Spectrophotometry, Atomic ; methods ; Thallium ; urine

Humans ; Lymphoma, Large-Cell, Anaplastic ; diagnosis ; enzymology ; therapy ; Receptor Protein-Tyrosine Kinases

Adult ; Humans ; Male ; Middle Aged ; Phosphines ; poisoning ; Young Adult

Objective To investigate the effects of pulmonary arterial endothelium cells(PAEC) injuryed by tumor necrosis factor ? (TNF-?) on the proliferation of pulmonary arterial smooth muscle cells (PASMC) and the influence of heat stress response (HSR) on it .Methods Normal PAEC or PAEC endured with HSR were incubated with TNF-? at the concentrations of 500, 1000 and 2000u/ml in 1 hour, then cultured in DMEM without serum in 24 hours, the upper liquid was collected to prepare the endothelial cell-conditioned medium liquid (EC-CMⅠ or EC-CMⅡ ), in which PASMC were incubated in 24 hours as group Ⅰ or group Ⅱ respectively. The normal endothelial cell-conditioned medium liquid was also prepared to incubate PASMC in 24 hours as group Ⅲ.The PASMC were incubated without the endothelial cell-conditioned medium liquid as group Ⅳ.Flow cytometry was applied to determining the intracellular DNA content of the incubated PASMC. The fractions of different cytocycle phases were calculated according to the areas under the curves of DNA content.Results Compared with those of group Ⅳ, the percentage of PASMC in G0-G1 phases increased markedly ,and in S and G2-M phases decreased significantly in group Ⅲ (P

0 05) The duration of T 1 recoving to 90% of baseline was 34 57min,and the recovery index was 24 29 min No any histamine related side effects were observed in all patients Conclusions Intravenous infusion of rapacuronium can produce safe and effective neuromuscular blockasde during desflurane, sevoflurane, isoflurane, or propofol anesthesia After the rapacuronium infusion of 45 60 min, the recovery from the neuromuscular blockasde is prolonged

Objective To investigate the signal mechanism of protein kinase C alpha(PKC-α)participated in enhanced expression of type Ⅰ inositol 1,4,5-trisphophate receptors (IP3 RI) induced by tumor necrosis factor alpha(TNFα),in order to delineate the mechanisms of decreased glomerular filtration rate (GFR) in hepatorenal syndrome caused by TNFα.Methods The glomerular mesangial cells (GMCs)line from rats was chosen as experimental material.GMCs were divided into control (D),TNFα-2 h,TNFα-4 h,TNFα-8 h,and TNFα-24 h groups.Moreover,another two groups were sanflngol-8h (S),TNFα + Sanfingol-8h(TS)groups.The effect of TNFα on the expression of IP3RI was detected by immunocytochemical staining,Western blotting,teal time-polymerase chain reaction (PCR) assays.Results Immunocytochemical staining demonstrated that IP3 RI was mainly distributed in cytoplasm of GMCs.Enhanced positive staining was determined in all TNFα-treated groups,especially in TNFα-8 h group.Western blotting demonstrated that the expression of IP3RI protein was significantly higher in TNFα-4 h,TNFα-8h and TNFα-24 h groups than control group(4 h:1.82 ± 0.63 ; 8 h:2.95 ± 0.66 ; 24 h:2.48 ± 0.72 ; D:1 ±0.02 ; F =9.24,P ＜ 0.05).The expression of IP3 RI protein was the highest in TNFα-8 h and TNFα-24 h groups(P ＜0.05).No difference was found among S,TS,and control groups(S:1.39 ±0.65; TS:1.35± 0.37 ; P ＞ 0.05).Real time-PCR found the expression of IP3 RImRNA was significantly higher in all TNFα-treated groups than control group(2 h:3.35 ± 1.97; 4 h:3.16 ± 1.35; 8 h:3.70 ± 1.76; 24 h:4.49±1.70; D:1 ±0.01; F =6.167,P ＜0.05).No difference was found among all TNFα-treated groups(P ＞0.05).No difference was found among S,TS,and control groups(S:1.53 ±0.79; TS:1.32 ± 0.38 ; P ＞ 0.05).Conclusions IP3 RI was mainly distributed in cytoplasm of GMCs.TNFa could enhance the expression of IP3 RI protein and IP3 RI mRNA,which could be blocked by sanfingol,a PKCα inhibitor.It might be an important signal in the mechanisms of GFR decrease caused by TNFα in hepatorenal syndrome.

Objective To investigate the effect of tumor necrosis factor-α (TNF-α) on intracellular calcium concentration ([Ca2 +] i) and the contraction of glomerular mesangial cells (GMCs),and prove that hypercontractility of GMCs induced by TNF-α in hepatorenal syndrome(HRS) was connected with inositol 1,4,5-trisphophate receptors (IP3Rs).Methods GMCs were divided into TNF-α-treated 0 h,4h,and 24 h groups.Another 3 groups were blocked by 2-APB.The effect of TNF-α on [Ca2 +] i was identified and observed whether it could be blocked by 2-APB.Contraction of GMCs was determined by accessing the surface area of cells before and after contraction.Results TNF-α significantly increased ET-induced calcium release,in that we found higher [Ca2 +] i after stimulated by ET in TNF-α-treated 4 h group and 24 h group[4 h:(648.08 ±267.11) nmol/L; 24 h:(879.30 ±-260.29) nmol/L; 0 h:(619.93 ±258.94)nmol/L,F =5.486,4 h vs 0 h:P ＜ 0.05 ; 24 h vs 0 h:P ＜ 0.05 ;24 h vs 4 h:P ＞ 0.05].This phenomenon can be totally blocked by 2-APB in all groups.The change in planar surface area in response to ET was slightly in control cells but significantly enhanced in TNF-α-treated cells [4 h:(2198 ± 340)μm2; 24h:(2260±553)μm2; 0 h:(2436±474)μm2,F =4.001,4 h vs0 h:P ＜0.05; 24 h vs0 h:P ＜0.05;24 h vs 4 h:P ＞ 0.05].Conclusion TNF-α can enhance ET-induced sarcoplasmic reticulum Ca2 + release and increase the contractile responses of GMCs to ET,which is associated with IP3Rs.TNF-α is responsible for hyperconstractility of glomeruli in HRS.