Life-threatening complications of ascariasis in trauma patients: a review of the literature.

BACKGROUND: Ascariasis is one of the most common human parasitic infections worldwide. In some rare cases, ascariasis may cause serious consequences even sudden death. This study was undertaken to review the life-threatening complications of ascariasis in trauma patients reported in the literature. DATA SOURCES: Relevant articles about ascariasis and trauma were searched from Pubmed, Google scholar, Scirus, and Wanfang databases. RESULTS: Twenty-four patients with ascariasis were collected from 21 articles searched. Most of these patients were from tropical and subtropical countries. Of the 24 patients, 12 were children. Their major complications occurred in the airway passage and digestive tract. There were 3 fatal cases in these patients. Twelve of the 24 patients described in 10 articles were reported in the last 10 years. CONCLUSIONS: Early diagnosis and prompt intervention are essential to minimize the high morbidity and mortality of these serious complications in trauma patients. Physicians should be aware of the possibility of Ascaris infection in a trauma patient from endemic area of ascariasis. History of Ascaris infection and routine examination of feces for Ascaris eggs may be helpful to make a correct diagnosis.

SLP-2 overexpression is associated with tumour distant metastasis and poor prognosis in pulmonary squamous cell carcinoma.

OBJECTIVE: To investigate the role of stomatin-like protein 2 (SLP-2), a novel cancer-related gene, in pulmonary squamous cell carcinoma (PSCC) and its implications. METHODS: Immunohistochemical detection of SLP-2 was performed on 96 cases of PSCC with a tissue microarray. RESULTS: SLP-2 was overexpressed in lung cancer compared with normal lung tissue (p <0.001). High-level SLP-2 expression was significantly correlated with distant metastasis (p = 0.025), decreased overall survival (p = 0.018) and disease-free survival (p = 0.017). SLP-2 overexpression was an independent prognostic factor in multivariate analysis using the Cox regression model (p <0.05). CONCLUSION: SLP-2 overexpression is associated with tumour distant metastasis and poor prognosis in PSCC. SLP-2 could be regarded as a new significant prognostic biomarker for patients with PSCC.

Toluidine blue-mediated photoinactivation of periodontal pathogens from supragingival plaques.

This study aimed to assess the effect of toluidine blue (TB)-mediated photodynamic inactivation of periodontal pathogens (PP) from periodontopathic patients. Photodynamic therapy (PDT) was carried out using TB and 635 nm laser light irradiation. The bactericidal effect was evaluated, and important PDT parameters including light intensity, energy dose, and TB concentration were determined. Our findings suggest that TB-mediated lethal photosensitization of PP in vivo is possible. However, to obtain ideal bactericidal effect, higher doses of light and photosensitizer should be required in treatment in vivo than their planktonic counterparts. The best therapeutic effect was observed in treatment by 1 mg/ml TB combined with 12 J/cm(2) at 159 mW/cm(2) light irradiation. Moreover, because of the considerable interindividual differences of bacterial populations, TB-mediated PDT might not be equally effective among periodontopathic patients, and further studies on improvement of this therapeutic modality is needed.

Significance of COX-2 expression in human esophageal squamous cell carcinoma.

Cyclooxygenase-2 (COX-2) is well established to play an important role in the tumorigenesis of a variety of human cancers; however, the function of COX-2 in the development of esophageal squamous cell carcinoma (ESCC) remains less clear. Here, we determined, first, the pattern of COX-2 expression in normal esophageal mucosa, dysplasia, carcinoma in situ (CIS) and invasive SCC. Immunohistochemical analysis showed that, while COX-2 was weakly expressed, if at all, in normal squamous epithelium, strong COX-2 expression was detected as early as the stage of dysplasia and frequently in 20 of 26 (77%) CIS and 86 of 111 (77%) invasive SCC. Upregulation of COX-2 in ESCC was found to be significantly associated with tumor progression (R = 0.493, P < 0.01). Further, treatment of human ESCC cell lines (KYSE450 and KYSE510) with NS-398, a COX-2 specific chemical inhibitor, suppressed the production of prostaglandin E2 (PGE2) and induced cell growth inhibition, cell cycle arrest at the G1-S checkpoint, and the expression of cyclin-dependent kinase inhibitors p21waf1/cip1 and p27kip1. Finally, knockdown expression of COX-2 in KYSE450 cells by a specific COX-2 siRNA dramatically inhibited PGE2 production, cell growth and, more importantly, colony formation and tumorigenesis in nude mice. Together, this study suggested that COX-2 may be involved in an early stage of squamous cell carcinogenesis of the esophagus and has a non-redundant role in the regulation of cellular proliferation and tumorigenesis of esophageal epithelial cells.

Up-regulation of fibronectin in oesophageal squamous cell carcinoma is associated with activation of the Erk pathway.

Fibronectin (FN) was found to be up-regulated in human oesophageal squamous cell carcinoma (ESCC) by cDNA microarray analysis in our laboratory. In order to elucidate the chronology of FN expression at various stages of oesophageal carcinogenesis, RT-PCR, immunohistochemistry and Western blot analysis were carried out on ESCC tissue samples with different pathological characteristics. FN was mainly localized in the interstitial tissues, and its up-regulation in ESCC was significantly associated with the depth of invasion by carcinoma (R = 0.803, p < 0.01). To investigate its relationship with the Erk pathway further, pRaf-1 and pErk-1/2 expression were also analysed in ESCC. Activation of Erk1/2 and Raf was identified in 63.3% and 60.3% of the tumour specimens, respectively, whereas normal mucosal epithelial tissues were negative. Moreover, a close association was observed between pErk-1/2 expression and the differentiation grade (R = -0.421, p = 0.002): pErk-1/2 signal was greater in poorly differentiated tissues than in well and moderately differentiated tissues. Co-expression of FN and pErk-1/2 was found at the invasive front of tumour nests by double immunofluorescence staining and there was a statistical correlation between the expression of FN and pErk-1/2 (p < 0.05). In the cell line EC9706, plasma FN was able to phosphorylate Raf and further activate Erk, but it did not alter MMP-2 protein expression or activity, indicating that MMP-2 may not be the downstream target gene of the Erk pathway. All the above data suggest that the up-regulation of FN contributes to the later stage of oesophageal carcinogenesis, and that activation of the Erk pathway may be involved in the roles of FN in ESCC.

Differential expression of S100 gene family in human esophageal squamous cell carcinoma.

PURPOSE: To study the differential expression of the S100 gene family at the RNA level in human esophageal squamous cell carcinoma (ESCC), and to find the relationship of the S100 gene family with ESCC. METHODS: Firstly, the specific primers were designed for the different S100 genes with Software Primer 3, which required that both primer sequences of each S100 gene were from two different exons respectively. Then, the differential expression of 16 S100 genes was examined by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) in 62 cases of ESCC versus the corresponding normal esophageal mucosa. All RT-PCR products were analyzed by 1.5% agarose gel. With Fluor-S MultiImager and Multi-Analyst software, the electrophoresis images were evaluated with statistics analysis using SAS 8.1 software. RESULTS: Eleven out of 16 S100 genes were significantly downregulated ( p<0.05) in ESCC versus the normal counterparts such as S100A1, S100A2, S100A4, S100A8, S100A9, S100A10, S100A11, S100A12, S100A14, S100B, and S100P genes. Only the S100A7 gene in the S100 family was markedly upregulated ( p<0.05). Moreover, the S100B gene was significantly correlated with histological differentiation of ESCC ( p=0.0247), and the deregulation of some S100 genes was closely correlated ( p<0.05), such as S100A10/S100A11, S100A2/S100A8, S100A2/S100A14, S100A8/S100A14, and S100A2/S100P etc. CONCLUSIONS: The S100 gene family is closely associated with ESCC.

Loss of myeloid-related proteins 8 and myeloid-related proteins 14 expression in human esophageal squamous cell carcinoma correlates with poor differentiation.

AIM: To study the expression of myeloid-related proteins(MRP)8 and myeloid-related proteins(MRP)14 in human esophageal squamous cell carcinoma and to investigate if there was any correlation between MRP8 and MRP14 expression level and histopathological grade in these tumors. METHODS: In this study, 65 cases of advanced esophageal squamous cell carcinoma were assessed for MRP8 and MRP14 expression using immunohistochemistry. Statistical analysis was performed for the comparison of MRP8 and MRP14 expression in normal and tumor tissues, and their relationship with clinicopathological features. RESULTS: Reduced or absent expression of MRP8 and MRP14 was observed in esophageal squamous cell carcinoma, with a significant difference between tumor tissues and normal tissues (P<0.01 and P<0.01 for MRP8 and MRP14, respectively). Poorly differentiated tumors presented a greater decrease than well and moderately differentiated tumors, with a correlation between their protein level and histopathological grading (P<0.001 and P<0.001, respectively). However, no significant association was found between MRP8 and MRP14 expression and age or gender (P>0.05). CONCLUSION: These findings suggest that the decreased expression of MRP8 and MRP14 might play an important role in the pathogenesis of human esophageal squamous cell carcinoma, being particularly associated with poor differentiation of tumor cells.

[Expression of annexin II in human esophageal squamous cell carcinoma].

OBJECTIVE: To evaluate the expression of annexin II in human esophageal squamous cell carcinoma (ESCC) and its relation with clinicopathological data. METHODS: The expression of annexin II mRNA and protein in paired cancer tissues and their adjacent quasi-normal tissues were detected by RT-PCR, immunohistochemical method and densitometric scanning. The relation between annexin II expression and the status of tumor differentiation was analyzed. RESULTS: The expression of annexin II was significantly lower in the tumor tissue than that in its paired normal counterpart both in mRNA and protein level (P < 0.05, P < 0.01). The protein expression of annexin II was significantly lower in moderately and poorly differentiated tumors than those in well differentiated ones (P < 0.05). CONCLUSION: Down-regulation of annexin II in esophageal carcinogenesis may play an important role in squamous cell differentiation.

The deregulation of arachidonic acid metabolism-related genes in human esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is 1 of the most common cancers worldwide. In our study, cDNA microarray comprising 14,803 genes was employed to identify gene-specific expression profile in 6 paired samples of ESCC. Nine genes identified were commonly upregulated and 36 downregulated in tumors, as compared to normal esophageal squamous epithelia. Among these genes, we found that 9 of the altered expression genes were related to arachidonic acid (AA) metabolism, such as annexin-I, annexin-II, S100A8, S100A10, S100P, glutathione peroxidase-3, phosphatidylcholine transfer protein, aldo-keto reductase family 1 and cyclooxygenase-2 (COX-2). To gain insights into the regulation of the AA metabolism pathway involved in the carcinogenesis of ESCC, we investigated the expression of 8 genes related to the AA metabolism by semiquantitative reverse transcript (RT)-PCR and/or Western blot and immunohistochemistry. These genes include annexin-I, annexin-II, COX-2, cyclooxygenase-1 (COX-1) and cytosolic phospholipase A(2) (cPLA(2)), 5-lipoxygenase (5-LOX), 5-lipoxygenase activating protein (FLAP) and 12-lipoxygenase (12-LOX) (not included in the array data). The expression level of annexin-I, annexin-II was downregulated in esophageal cancer, whereas cPLA(2), FLAP, COX-2, 5-LOX and 12-LOX were upregulated. These data suggested that AA metabolism pathway and its altered expression may contribute to esophageal squamous cell carcinogenesis.

[Association of genetic polymorphisms in the DNA repair gene XPD with risk of lung and esophageal cancer in a Chinese population in Beijing].

OBJECTIVE: XPD polymorphisms at Asp312Asn and Lys751Gln sites have been shown to modulate DNA repair capacity. The authors therefore assessed the relationship between these XPD polymorphisms and susceptibility to lung and esophageal cancer in a Chinese population via a hospital-based, case-control study. METHODS: Genotypes were determined by PCR-restriction fragment length polymorphism approaches in 383 healthy controls, 351 patients with lung cancer, and 325 patients with esophageal squamous cell carcinoma (SCC). The adjusted odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariate logistic regression. RESULTS: Individuals carrying at least one 312Asn variant allele (Asp/Asn and Asn/Asn genotypes) were at an increased risk for lung SCC as compared with those with the Asp/Asp genotype (OR 1.80; 95% CI: 1.10-2.93; adjusted for age, sex and smoking), but this increased risk was not observed among patients with adenocarcinoma of the lung (adjusted OR: 1.07; 95% CI: 0.55-2.08). Furthermore, stratified analysis indicated a multiplicative interaction between tobacco smoking and the variant XPD 312Asn and 751Gln alleles on risk of lung SCC. The ORs of lung SCC for the variant XPD 312Asn and 751Gln alleles with smoking>or=29 pack/year were 12.44 (95% CI: 4.97-31.17) and 10.74 (95% CI: 4.51-25.57), respectively. No significant association between the Asp312Asn or Lys751Gln polymorphism and the risk of esophageal cancer was found. CONCLUSION: The above findings indicate that the Asp312Asn and Lys751Gln polymorphisms in the XPD locus are associated with the risk of lung SCC but not lung adenocarcinoma or esophageal SCC in this Chinese population.

Overexpression of ETS2 in human esophageal squamous cell carcinoma.

AIM: To study the expression pattern of ETS2 (erythroblastosis virus oncogene homolog 2) in human esophageal squamous cell carcinoma (ESCC). METHODS: Reverse transcription polymerase chain reaction (RT-PCR) and Northern blot were performed to examine the expression level of ETS2 mRNA in 37 pairs of ESCC tissue samples. Western blot and immunohistochemistry were carried out to check the expression level of ETS2 protein in 30 pairs of ESCC tissue specimens. RESULTS: RT-PCR and Northern blot analysis showed that ETS2 mRNA upregulated in 75.7 % (28/37) examined ESCC tissues relative to matched normal tissues. From those 37 cases, 14 cases were randomly selected to perform Western blot and the results revealed that ETS2 protein overexpressed in 71.4 % (10/14) checked ESCC tissues compared with the corresponding normal tissues. Moreover, the expression patterns of ETS2 protein in those 14 cases were identical to those of ETS2 mRNA displayed by RT-PCR or Northern Blot. Immunohistochemistry analysis showed that the expression level of ETS2 protein rose in 75 % (12/16) tumor epithelial cells contrasted to the normal cells. Altogether the expression level of ETS2 protein increased in 73.3 % (22/30) checked ESCC tissue samples contrary to their normal counterparts. CONCLUSION: The results suggested that ETS2 overexpressed in paired human ESCC tissue samples at both mRNA and protein levels and may be associated with the tumorigenesis of esophagus.

[Cloning of human uracil N-glycosylase and its detection in cancer tissues by quantitative RT-PCR].

The uracil in DNA comes from either the misincorporation of dUTP in place of dTTP or deamination of cytosine. In the latter case, it can result in a GC to AT transition mutation if the uracil is not removed before DNA replication. Base excision repair (BER) is a major pathway for removing DNA lesions arising from endogenous processes as well as those induced by exposure to exogenous chemicals or irradiation. BER is initiated by DNA glycosylases that excise aberrant bases from DNA by cleavage of the N-glycosidic bond linking to the base of its deoxyribose sugar. Uracil N-glycosylase (UNG) is the enzyme responsible for the first step in the BER pathway that specifically removes uracil from DNA. The UNG gene undergoes both temporal and spatial regulation mainly at the level of transcription. Normally cancer cells undergo over-proliferation and up-regulate their UNG during tumorigenesis. In this study we examine the correlation between UNG level and carcinogenesis, and explore the possibility of using UNG as a marker for cancer diagnosis. Human UNG gene was amplified from the total RNA of the human choriocarcinoma cell line, JEG-3, by RT-PCR. After purification, the 942bp full-length UNG cDNA coding sequence was digested with EcoR I and Sal I, and cloned into the digested pET-21 to construct a recombinant vector, pUNG. The UNG protein was expressed under the control of T7 promoter in E. coli BL21 (DE3) cells induced with IPTG. After ultrasonic treatment, the cell lysate and precipitate were analyzed by SDS-PAGE and a 39kD band was detected. The plasmid was serially diluted at appropriate concentrations and employed as standards in the subsequent quantification. Total RNAs were extracted from 18 pairs of clinical samples, each pair contains a sample of esophageal squamous cell carcinoma (ESCC) tissue and its surrounding normal esophageal epithelia. The copy numbers of UNG mRNA in these RNA samples were determined by real-time quantitative RT-PCR using a Lightcycler (Roche). UNG was present in 13 cases of ESCC (13/18, n = 18) but absent in all of the normal tissues. The results indicated that there was a correlation between high level of UNG expression and the carcinogenesis of ESCC.

Down-regulation of gut-enriched Kruppel-like factor expression in esophageal cancer.

AIM: Esophageal carcinoma is one of the most common malignant tumors in China. But the molecular mechanisms of esophageal carcinoma remains unclear. Gut-enriched Kruppel-like factor (GKLF) is a newly identified transcription factor which is expressed abandantly in the epithelial cells of the gastrointestinal tract and deregulation of GKLF was linked to several types of cancer. It is of interest to study the expression and role of GKLF in esophageal carcinoma. METHODS: Semi-quantitative RT-PCR was used to compare GKLF expression in esophageal squamous cell carcinoma to normal mucosa of the same patients. The serum deprivation inducibility of GKLF was observed in an esophageal squamous cancer cell line by comparison to the primary culture of human fibroblast. The effect of antisense GKLF transfection on the proliferation and adhesion of esophageal squamous cancer cell line was also observed. RESULTS: The level of GKLF transcript is lower in esophageal squamous cell carcinoma compared to paired normal-appearing mucosa in 14 of 17 of the tumors analyzed. The serum deprivation inducibility of GKLF was greatly decreased in an esophageal squamous cancer cell line compared to the primary culture of human fibroblast. Decreased expression of GKLF in the esophageal cancer cell by antisense GKLF transfection increased its proliferation rate compared with that of vector transfected cell control (P<0.05). Transfection of antisense GKLF decreased its adhesion ability (P<0.05). CONCLUSION: The findings of this study demonstrate the down-regulation of GKLF in esophageal squamous cancer, and suggest that deregulation of GKLF may play a role in initiation and/or progression as well as the metastasis of esophageal squamous cancer.

Arsenic trioxide (As(2)O(3)) induced apoptosis and its mechanisms in a human esophageal squamous carcinoma cell line.

OBJECTIVE: To study whether As(2)O(3) has an apoptotic effect on human solid tumor cells, and the possible cellular and molecular mechanisms of this treatment using human esophageal squamous carcinoma cells (EC8712) as a model. METHODS: DNA microarray, biochemical and cytological analyses were used. RESULTS: The growth and survival of EC8712 cells were markedly inhibited by As(2)O(3) treatment at a concentration of 1, 2 and 4 micromol/L. EC8712 cells were obviously arrested at G2/M phase with As(2)O(3) treatment and apoptosis induced at micromolar As(2)O(3) concentrations, as shown by morphology, histogram related nuclear DNA contents, and DNA gel electrophoresis. As(2)O(3) activated caspase-3, which might be involved in the process of As(2)O(3), induced apoptosis in EC8712 cells. CONCLUSIONS: As(2)O(3) changes the expression of many genes at transcription level. The regulation of expression of many genes might be involved in the process of As(2)O(3) inducing apoptosis. These results suggest that As(2)O(3) can be clinically useful for solid tumor treatment.