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.

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.

[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.