Study of the association between hemorrhage and the position of hemorrhagic stigmata in patients with esophageal varices.

The aim of the present study was to investigate the predilection position of hemorrhagic stigmata (HS) in patients with esophageal variceal hemorrhage and provide guidance on endoscopic therapy for esophageal varices. The clinical characteristics, particularly the endoscopic manifestations of HS, in the patients who presented with gastroesophageal variceal hemorrhage and cirrhosis between January 2003 and December 2013 at our hospital were summarized and patients were grouped according to the distance of the lesion site to incisors at 35-40 and ~30 cm. The association between the location of HS and active hemorrhage was assessed. The location of hemorrhage and HS at 35-40 cm from the incisors was more common in esophageal varices patients, followed by the location at ~30 cm from the incisors (P<0.0001). The incidence of HS in esophageal varices patients in the 35-40 cm group was significantly higher than that in the ~30 cm group except for HS at 9:00 position (P<0.0001). The highest incidence of HS in the ~30 cm group was at the 3:00 position, followed by the 12:00, 6:00 and 9:00 position. Among them, there were significant differences between the 3:00 and 6:00 position, the 3:00 and 9:00 position, and the 9:00 and 12:00 position (P<0.05). The order in the 35-40 cm group was similar to that in the ~30 cm group and the incidence of HS at the 9:00 position was lowest (P<0.05). A certain association between the point of location of HS and hemorrhage was identified. HS located at 35-40 cm from the lesion site to incisors was identified to be most likely to bleed, followed by that located at ~30 cm. In addition, the incidence of HS at 9:00 position was found to be lower than that in the other positions. Therefore, HS located at ~30 cm and 35-40 cm from the lesion site to incisors should be paid attention to and the 3:00, 12:00 and 6:00 rather than the 9:00 position should be prioritized during endoscopic treatment, particularly in emergency situations.

HIF-1α -1790G>A polymorphism significantly increases the risk of digestive tract cancer: a meta-analysis.

AIM: To investigate the association between hypoxia-inducible factor-1α (HIF-1α) polymorphisms (-1772C>T and -1790G>A) and the risk of digestive tract cancer. METHODS: A total of 13 eligible studies were retrieved from PubMed, EMBASE, and the China National Knowledge Infrastructure database. The odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the strength of the associations. RESULTS: By pooling the eligible studies, we found that the HIF-1α -1772C>T polymorphism was not associated with the risk of developing digestive tract cancer (dominant comparison, OR: 1.156; 95%CI: 0.839-1.593; P heterogeneity = 0.007), and no significant association was found in the Asian population or the Caucasian population. However, for the -1790G>A polymorphism, carriers of the variant -1790A allele had a significantly increased risk of digestive tract cancer compared with those with the wildtype -1790G allele (dominant comparison, OR: 3.252; 95%CI: 1.661-6.368; P heterogeneity < 0.001). Additionally, this increased risk of digestive cancer was only detected in Asians; there was no significant association in Caucasians. CONCLUSION: This meta-analysis demonstrates that the HIF-1α -1790G>A polymorphism is associated with a significantly increased risk of digestive tract cancer, while the -1772C>T polymorphism is not.

Comparative proteomic analysis of differentially expressed proteins between K562 and K562/ADM cells.

BACKGROUND: Multidrug resistance to chemotherapeutic agents is an important clinical problem during the treatment of leukemia. The resistance process is multifactorial. To realize the total factors involved in multidrug resistance, we analyzed the differentially expressed proteins of K562 and K562/ADM cells and we investigated one of the up-regulated proteins (CRKL) using siRNA to determine its role in K562/ADM cells. METHODS: Altered protein expressions between K562/S (K562 ADM-sensitive cell line) and K562/ADM (K562 multidrug resistant cell line induced by adriamycin) were identified by 2D-DIGE coupled with mass spectrometry. Meanwhile, we confirmed the differential expression of CRKL and Stathmin in both K562 and K562/ADM cells by Western blot analysis. Furthermore, we used RNA interference to silence the CRKL gene expression. RESULTS: Among the 9 differentially expressed proteins, 3 were up-regulated in K562/ADM cells, while 6 were down-regulated in the K562/ADM cells compared with its parent cell line. The expression of CRKL was up-regulated significantly in K562/ADM cells, and it can be decreased by recombinant lentivirus. Moreover, the multidrug resistance of K562/ADM cells was efficiently reversed by silence of CRKL gene expression. CONCLUSIONS: The data provided the differentially expressed proteins in K562 and its resistant cell line and highlights the power of 2D-DIGE for the discovery of resistance markers in cancer. We found CRKL may be a new protein involved in the multidrug resistance of leukaemia cells.

[Reversal of multidrug resistance in leukemic cell line K562/AO2 by chlordelazine in vitro].

OBJECTIVE: Some recent studies revealed that phenthiazine might be able to reverse tumor cell drug-resistance. Chlorderazin belongs to the phenthiazine compounds. The study aimed to investigate the reversing effect and mechanism of chlorderazin on multidrug resistance of leukemic cell line K562/AO2. METHODS: (1) The cytotoxicities of chlorderazin were assayed with the tetrazolium dye, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. (2) The reverse effect of chlorderazin on K562/AO2 cells was analyzed with MTT method. The multidrug resistance reversal index (RI) was equal to the ratio of control group IC(50)/test group half inhibition concentration IC(50). (3) The intracellular daunorubicin (DNR) concentrations were measured by the flow cytometry. (4) Mdr1 mRNA expression was detected by reverse transcription-polymerase chain reaction (RT-PCR). The ratio of mdr-1/beta-actin density was calculated. RESULTS: (1) Chlorderazin 3 micro g/ml showed little toxicity to K562/AO2 cells and the suppression rate was less than 5%, so the concentration of 3 micro g/ml chlorderazin was selected as the experiment concentration. (2) The cytotoxicities of DNR to K562/AO2 were enhanced by 3 micro g/ml of chlorderazin (P < 0.05) and RI was 1.901. (3) Chlorderazin of 3 micro g/ml could increase the intracellular DNR accumulation significantly (P < 0.05), and the fluorescence staining by the flow cytometry was higher (250.95 +/- 18.96) than the control group (112.75 +/- 15.78) and shift right in K562/AO2 cells treated with chlorderazin, and the difference was significant (P < 0.05). (4) Chlorderazin has no significant influence to the expression level of mdr-1 mRNA. Both test group and control group showed a clear mdr-1 mRNA band located at the position of 157 kb. The ratios of mdr-1/beta-actin density were 0.414 +/- 0.012 in the test group and 0.447 +/- 0.027 in the control group, respectively, and the difference was not significant (P > 0.05). CONCLUSION: Chlorderazin could reverse the multidrug resistance by increasing the intracellular DNR accumulation in K562/AO2 cells. The effects had no correlation to the mdr-1 gene. Further study is needed.