The "Cancer Toxin" pathogenesis theory is an innovate theoretical system for cancer pathogenesis of Chinese Medicine, which was built on the basis of "Cancer Toxin" concept initially raised by Professor ZHOU Zhong-ying. The mechanism of the transformation from inflammation to carcinoma has become one of hot-points in the field of cancer research at home and abroad in recent years. We focused on discussing the relevance of the "Cancer Toxin" pathogenesis theory with the transformation mechanism from inflammation to cancer, provided evidence for using "Cancer Toxin" pathogenesis theory in intervening transformation from inflammation to cancer, hoping to guide for Chinese medical prevention and treatment of tumor.
Biomedical Research ; Carcinoma ; physiopathology ; Humans ; Inflammation ; physiopathology ; Medicine, Chinese Traditional ; Neoplasms ; physiopathology

Objective To explore the relationship between serum placental growth factor (PLGF) and carotid atherosclerosis (CAS) in patients with type 2 diabetes mellitus (T2DM ). Methods Serum PLGF were determined by ELISA in 53 patients with T2DM ,who were divided into T2DM without carotid plague (T2DM group ,n= 27) and T2DM with carotid plague (T2DM + CAS group ,n= 26). Fasting plasma glucose (FPG) ,glycosylated hemoglobin A1c (HbA1c) and some other metabolic variables were also measured. The results were compared to those of 27 healthy controls (NC group). Results Serum PLGF levels were significantly higher in T2DM group and T2DM + CAS group than in NC group (P<0.01). T2DM+CAS group showed significantly higher serum levels of PLGF compared to that of T 2DM group(P<0.01).Correlation analysis showed that serum PLGF was positively correlated with TC ,LDL‐C , hsC‐RP and IL‐6 in T2DM patients (P<0.01). Similarly ,multiple regression analysis showed that LDL‐C and IL‐6 were the independent factors of serum PLGF level (P<0.05). Furthermore ,Serum PLGF was positively associated with carotid plague. Conclusion PLGF is positively related with chronic inflammation factors in T2DM patients. Serum PLGF may play an important role in the occurrence and development of carotid atherosclerosis and other macroangiopathy in T 2DM.

Objective To investigate the protective effects of 1-hydroxy-2, 3, 5-trimethoxyxanthone (QGS) on acute lung injury of mice induced by ip lipopolysaccharide (LPS). Methods Mice were pretreated with QGS for 7 d. Murine models of acute lung injury were duplicated by injection of LPS 20 mg/kg intraperitoneally. In 12 h, the lung weight index was observed and the NO level in the bronchoalveolar lavage fluid (BALF) was measured with kits. The lung was also assessd for the expression of I-?B, inducible nitric oxide synthase (iNOS), and cyclooxygenase-Ⅱ (COX-2) using Western blotting analysis. Lung pathological changes were also observed by HE in each group. Results The lung weight index of injury lung in mice induced by LPS was decreased in 500 mg/kg QGS group (P

It has been well known that apoptosis induction and cell cycle arrest are typical biological effects observed in cancer cells after proteasome inhibition. TH2 is a new natural xanthone analogue isolated from the resin of Garcinia hurburyi tree. Here, the cell growth inhibition of TH2 on human hepatocellular carcinoma cell line (Bel-7402) was evaluated in vitro using SRB assay. The treatment of 10 ?mol/L TH2 reduced the surviving fraction from 86% (12 h) to 17.2% (48 h). To assess whether TH2 induce apoptosis, the appearance of sub-G1 peak, a specific fraction for apoptosis was detected by flow cytometry analysis. Progressive increase in the percentage of apoptotic population was observed in a dose-and time-dependent manner. Furthermore, a cleavage of poly (ADP-ribose) polymerase (PARP), a marker of early apoptosis, was observed clearly when the cells exposed to 10 ?mol/L of TH2 for 24 h by immunoblotting analysis. In vitro activities of 20 S proteasome purified from human erythrocytes on fluorogenic peptide substrates revealed that TH2 inhibited the trypsin-like, chymotrypsin-like and peptidylglutamyl peptide hydrolyzing activities in dose-dependent manner. Moreover, the turnover of tumor suppressor p53, a sign of deregulation of cell cycle progression and apoptosis induction by classical proteasome inhibitors, was disrupted in Bel-7402 cells. All these data indicate that TH2 had inhibitory effect on the proliferation of Bel-7402 cells and induction of apoptosis, which might be related to its inhibition of proteasome.

AIM:To investigate the effects of MG132,one of the proteasomal peptide aldehydes inhibitors,on lipopolysaccharide(LPS)-induced nuclear transcription factor-kappa B(NF-?B) activation,the production of nitric oxide(NO) and tumor necrosis factor-alpha(TNF-?),as well as the expression of inducible nitric oxide synthase(iNOS) in murine macrophage line RAW264.7.METHODS:Reporter gene assay was used to examine the activity of NF-?B by pNiFty-SEAP/HEK293 cells,which were transfected with the pNiFty reporter plasmid into human embryo kidney cells(HEK293).Fluorescence substrate DAF-2DA was used to testify NO level in Raw264.7 cell line induced by LPS.Furthermore,the secretion of TNF-? was examined by ELISA.Western blotting was used to reveal the expression of iNOS and I?B-?.RESULTS:MG132 significantly decreased the secretion of TNF-? induced by LPS,with the inhibitory rates of 36.7% and 60.4% to 5 ?mol/L and 10 ?mol/L MG132,respectively.The pro-inflammatory mediator NO production was decreased in a dose-dependent manner with the inhibitory rates increasing from 29.5%(2 ?mol/L) to 55.9%(10 ?mol/L).Pretreatment with MG132 reduced the expression of iNOS,but restored the I?B restrain caused by LPS treatment.Observed by a reporter gene assay,TNF-?-induced NF-?B activity was decreased gradually by addition of increasing concentration of MG132(2.5-10 ?mol/L).CONCLUSION:Our results suggest an anti-inflammation effect of MG132 by the suppression of LPS-induced the production of pro-inflammatory mediators including NO and TNF-?,and the expression of iNOS,which probably mediates the blockage of I?B degradation and NF-?B activation.

Piroxicam has polymorphism. Different crystalline forms can exhibit different physicochemical properties and biological activities. Analysis of the intermolecular interactions is essential to reveal the formation mechanism and differences of polymorphs. In this paper, Hirshfeld surface analysis and semi-empirical methods were used to calculate and analyze the intermolecular interactions in seven polymorphic forms of piroxicam. The results show that the Hirshfeld surface analysis method can clearly and intuitively reveal the intermolecular interactions, among which H…H, O…H/H…O and N…H/H…N interactions account for 95% of the total energy. There are differences in the proportion and distribution of the forces of different crystal forms. The energy calculation shows that the lattice energy of the hydrate is significantly lower than that of the anhydrous forms, and in the specific energy distribution, the contribution of the dispersion force is the most prominent. Further interaction energy analysis was found that within the distance of 3.8 Å from the center of the piroxicam molecule, different crystalline forms of piroxicam molecule have different interaction energies with surrounding molecules.

Abscess ; therapy ; Adult ; Aged ; Catheterization ; methods ; Drainage ; methods ; Female ; Humans ; Male ; Middle Aged ; Tomography, X-Ray Computed

Objective To identify the characteristics of hippocampal 3-dimensional MRI in patients diagnosed as having subtypes of amnestic mild cognitive impairment(aMCI)using hippocampal surfacebased analytic technique.Methods Fifry aMCI patients and 16 healthy controls who were equivalent in age and education(NC)were recruited.Every subiect carried out a 3-dimensional MRI scan.After the imaging data were acquired.the borders of the hippocampus were manually traced in coronal vlew using the software of InsightSNAP1.4.1. Hippocampal volume was computed automatically and statistically analysed.Hippocampal 3-dimension MRI were transformed into 3-dimension parametric surface mesh models of 400×200 prids.Hippocampal radial distance measures which was the distance from the surface point to the central axis were statistically compared between two groups.The radial atrophy significance maps were acquired and adjusted for multiple comparisons.Hippocampal morphological difference maps of aMCI in contrast with NC were acquired.Results The average normalized volume of left hippocampus were(3247.5±600.2)mm3 in aMCI patients and(3467.9±451.3)mm3 in NC subjects.The average normalized volume of right hippocampus were(3416.8±699.1)mm3 in aMCI patients and(3469.1±358.9)mm3 in NC subjects.Comparison of hippocampal volume did not differ significantly between aMCI patients and NC subjects(t=1.161,P=0.255;U=0.178,P=0.859).By using hippocampal surface-based morphologic analytic technique,3-dimension hippocampal morphological difference maps between two groups were acquired,showing significant atrophy on the lateral and inferior hippocampal surface which corresponded to CA1 and subiculum hippocampal subfields bilaterally in aMCI patients compared with NC subjects. Conclusions aMCI patients do not have significant volume loss in the hippocampus. Through hippocampal surface-based morphologic analyses, partial regional atrophy of hippocampus at some degree is found, mainly localizing in the lateral and inferior hippocampal regions which correspond to CA1 and subiculum hippocampal subfields bilaterally in aMCI compared with NC. These results may reflect the early image marker in aMCI.

Four salts of ticagrelor, ticagrelor-3,5-dinitrobenzoic acid, ticagrelor-pyrazinamide, ticagrelor-D-proline and ticagrelor-L-proline were prepared by solvent suspension and liquid-assisted grinding to improve the solubility of ticagrelor. The compounds were characterized by powder X-ray diffraction, Fourier transform infrared spectroscopy, differential scanning calorimetry, nuclear magnetic resonance spectroscopy, elemental analysis, and the intermolecular salt-bonding forces were analyzed. The equilibrium solubility of salts and pure drug in hydrochloride buffer pH 1.2 and phosphate buffer pH 6.8 were measured by high-performance liquid chromatography. Ticagrelor was salted with 3,5-dinitrobenzoic acid, pyrazinamide, D-proline, L-proline all in a stoichiometric ratio of 1∶1; with the exception of ticagrelor-D-proline, the solubility of the other three salts provided significantly improved solubility in hydrochloride buffer pH 1.2, and the equilibrium solubility of ticagrelor-3,5-dinitrobenzoic acid was increased by approximately 1.7 folds as compared to pure drug. Salt-forming technology is convenient and can improve the solubility of ticagrelor.

OBJECTIVETo summarize current understanding of the roles of anti-inflammatory and proinflammatory mechanisms in the development of atherosclerosis and acute coronary syndrome and to postulate the novel concept of inflammation stress as the most important factor triggering acute coronary syndrome. Moreover, markers of inflammation stress and ways to block involved pathways are elucidated.

DATA SOURCESA literature search (MEDLINE 1997 to 2002) was performed using the key words "inflammation and cardiovascular disease". Relevant book chapters were also reviewed.

STUDY SELECTIONWell-controlled, prospective landmark studies and review articles on inflammation and acute coronary syndrome were selected.

DATA EXTRACTIONData and conclusions from the selected articles providing solid evidence to elucidate the mechanisms of inflammation and acute coronary syndrome were extracted and interpreted in the light of our own clinical and basic research.

DATA SYNTHESISInflammation is closely linked to atherosclerosis and acute coronary syndrome. Chronic and long-lasting inflammation stress, present both systemically or in the vascular walls, can trigger acute coronary syndrome.

CONCLUSIONSInflammation stress plays an important role in the process of acute coronary syndrome. Drugs which can modulate the balance of pro- and anti-inflammatory processes and attenuate inflammation stress, such as angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers, statins, and cytokine antagonists may play active roles in the prevention and treatment of acute coronary syndrome when used in addition to conventional therapies (glycoprotein IIb/IIIa receptor antagonists, mechanical intervention strategies, etc).

Angina Pectoris ; etiology ; Arteriosclerosis ; etiology ; Biomarkers ; blood ; Blood Vessels ; physiopathology ; Humans ; Inflammation ; complications ; drug therapy ; physiopathology ; Myocardial Infarction ; etiology ; Stress, Physiological ; complications ; Syndrome