Background: Thrombospondins (THBSs) are glycoproteins expressed in the extracellular matrix (ECM) and have critical roles in tumor development and metastasis. However, the diverse expression patterns and prognostic roles of distinct THBS genes in gastric cancer have not been fully elucidated. In the current study, we aimed to investigate the expression patterns of THBSs in gastric cancer (GC) and determine whether they are prognostic markers for this malignancy.Methods: mRNA expression status and genetic mutations of THBS family members were performed by using ONCOMINE, UCSC Xena browser, GEPIA, and cBioPortal databases. Prognostic values and function enrichment analysis of the members were assessed via Kaplan-Meier plotter and Metascape.Results: we found that the mRNA expression of THBS1, THBS2, THBS4, and COMP were higher in patients with GC tissues than those in normal gastric mucosa and there was no difference in the mRNA expression of THBS3 between GC and normal tissue. Survival analysis revealed that mRNA levels of THBSs were strongly related to worse OS in GC patients (P<0.05). Overexpression of THBSs indicated poor OS in stage III/IV GC and high expression of THBS1, THBS3, THBS4, and COMP were related to worse OS in stage II GC.Conclusions: Bioinformatics analysis revealed a better understanding the value of THBS family members in GC and suggest that THBSs might serve as potential prognostic biomarkers for GC.

The differential expression of the desired gene product in the target tissue is central for gene therapy. One approach is to use a tissue-specific promoter to drive therapeutic gene expression. UroplakinII (UPII) is a urothelium-specific membrane protein. To investigate the feasibility of targeting gene therapy for bladder cancer, a DNA fragment of 2542-bp upstream of the UPII gene was amplified by PCR and linked to a promoterless firefly luciferase reporter gene. The transient transfection showed that the DNA fragment resulted in preferential expression in bladder carcinoma cells, with negligible expression in nonurothelium cells. Furthermore, the DNA segment located between À2545 and À1608 decided the tissue-specificity of the UPII promoter, the segment located between À328 and À4 being the core promoter of UPII. We generated two recombinant adenoviruses under the control of the UPII promoter: Ad-hUPII-GFP, carrying green fluorescence protein (GFP), and Ad-hUPII-TNF, carrying the tumor necrosis factor alpha (TNFa). ELISA revealed that the secretion of TNFa by Ad-hUPII-TNF-infected bladder cancer cells was significantly higher than Ad-hUPII-TNF-infected nonurothelium cells. The conditioned medium from Ad-hUPII-TNF-infected bladder cancer cells apparently inhibited the proliferation of L929 cells, a TNFa-sensitive cell line, comparing to Ad-hUPII-TNF-infected nonurothelium cells. Intravesical inoculation with Ad-hUPII-TNF inhibited tumor growth in the orthotopic human bladder cancer model. The sustained high level of TNFa in urine was identified with ELISA. Taken together, these data suggest that most of the cis elements that confer the bladder-specificity and differentiationdependent expression of the human UPII gene reside in the 2542-bp sequence, and TNFa driven by the human UPII (hUPII) promoter is effective in the specific inhibition of bladder cancer growth both in vivo and in vitro. These results may yield a new therapeutic approach for bladder cancer and provide information on the molecular regulation of urothelial growth, differentiation, and disease.

Abstract. Non-standardized or conservative procedures are employed when parotid tumors involving the facial nerve or parotid carcinoma are misdiagnosed as benign parotid tumors prior to or during surgery. Remedial measures are usually required when the pathological diagnosis of a malignant parotid tumor is confirmed following surgery. The aim of the present study was to systematically evaluate reoperation subsequent to treatment with non-standardized procedures for malignant parotid tumors, and to explore the preoperative diagnoses, the primary procedure selection and the necessity of reoperation following non-standardized procedures in malignant parotid tumors. A total of 30 patients who met the inclusion criteria, were diagnosed with a malignant parotid tumor and underwent reoperation following the use of a non-standardized procedure were included in the present study. Surgical conditions and clinical data were analyzed. Among the patients with a malignant parotid tumor who underwent reoperation subsequent to a non-standardized procedure, the incidence of residual tumor, as confirmed by pathological examination, was 63.3% (19/30). The intact facial nerve preservation rate was 83.3% (25/30), the facial nerve branch resection rate was 6.7% (2/30), the facial partial nerve resection rate was 6.7% (2/30) and the facial nerve resection rate was 3.3% (1/30). In total, 3 patients underwent facial nerve reconstruction, 3 patients underwent a local flap repair of skin defects in the parotid region and 3 patients underwent pectoralis major muscle flap repair. The current findings indicate that the qualitative diagnosis of malignant parotid tumors prior to surgery is difficult, there is a high incidence of residual tumor following non-standardized procedures, and that reoperation in a timely manner is required in such cases.

Four species of Mastrus Förster, 1869 are reported from China. Two, Mastrus nigrus Sheng & Zeng, sp. n. reared from Arge pullata (Zaddach) and Mastrus rugotergalis Sheng & Zeng, sp. n. reared from Diprion jingyuanensis Xiao & Zhang, are new to science. One, Mastrus deminuens (Hartig, 1838), is a parasitoid of Pachynematus itoi Okutani. A key to species of Mastrus Förster known in China is provided.

Differential expression of the desired gene product in the target tissue is central to the concept of gene therapy. One approach is to use a tissue-specific promoter to drive therapeutic genes. To investigate the feasibility of tissue-specific gene therapy for bladder cancer using the mouse uroplakin II (UPII) promoter and its transcriptional control, the efficacy of this promoter as well as fragments in regulating gene expression were qualitatively and quantitatively analyzed in bladder and non-bladder tissue cell lines using DNA transfection. Our results demonstrate that the mouse UPII promoter actively drives gene expression in BIU-87, a bladder cancer cell line. Little promoter activity was detected in the non-bladder tissue cell lines. Furthermore, deleting the 5¢ end 1.5 kb of the UPII promoter by PCR, the activity was significantly decreased but was bladder-specific. However, deleting the 3¢ end 143-bp of the UPII promoter, the activity was hardly detected in any tissue cell lines. The activity of the 3¢ end 143-bp of the UPII promoter was detected in both bladder cancer and stomach cancer cell lines. These data demonstrate that the mouse UPII promoter has a high activity in human bladder cells and a low basal activity in human non-bladder cells. This suggests that targeting the gene expression of the mouse UPII promoter could be used to treat human bladder cancer. The enhancer was contained in the region of the 1.5 kb of the 5¢ end of the mouse UPII promoter. The core promoter was located in the region of the 143 bp of the 3¢ end.