A total of 473 patients of diabetic nephropathy (DN) with normal serum creatinine were recruited.Blood routine,blood lipids and urine albumin/creatinine ratio (UACR) were measured.They were divided into microalbuminuria group (DN1,n =246 ) and macroalbuminuria group (DN2,n =227 ).The white blood cell (WBC) count,monocyte count and CRP significantly increased with the progression of DN in the DN2 group versus those in the DNI group [ (6.8 ± 1.7 ) × 109/L vs.(6.3 ± 1.5 ) × 109/L,(0.49±0.23) ×109/Lvs.(0.32 ±0.21) ×109/L,(4.1 ±1.1)mg/Lvs.(1.7±0.3) mg/L,all P＜ 0.05].According to multiple linear regression analysis,WBC,monocyte,low density lipoproteincholesterol and lymphocyte were found to be independent influencing factors for the elevation of UACR.

Objective To construct a new recombinant immunotoxin expression vector by using human VEGF165 and a truncated pseudomonas exotoxin A ramification (PE38) gene, and explore the expression of the VEGF165-PE38 fusion protein in HEK293 cells. Methods VEGF165 was cloned by polymerase chain reaction (PCR). PE38 gene was gained from an vector plasmid pRB391 by restriction endonuclease digestion, and then inserted to the eukaryotic expression vector pIRES2-EGFP. After the eukaryotic recombinant vector pIRES2-VEGF165-PE38-EGFP was identified by restriction endonuclease digestion and sequence analysis, the vector was transfected into HEK293 cells by liposome protocol. RT-PCR and ELISA method was used to confirm the expression of the fusion gene in the HEK293 cells. Results Restriction endonuclease digestion and sequence analysis revealed the VEGF165-PE38 fusion gene was cloned into the eukaryotic expression plasmid vector pIRES2-EGFP successfully. The pIRES2-VEGF165-PE38-EGFP fusion gene could express in the HEK293 cells. Conclusion The result provide the basis for search of the targeted cytotoxic activity to tumor vascular endothelial cells and may have some potential value in clinical application.

OBJECTIVE: To investigation the clinic long-term result and explore the prognostic factor of patients with laryngectomy. METHOD: Three hundred and fifteen patients with laryngectomy were analysed. The survival rate and the cause of death were collected from this study. RESULT: Five years later, 233 cases were still alive, 60 cases were dead, 22 cases failed to be followed-up. Overall 5-year survival rate was 73.97%, 5-year survival rate for patients of early stage was 82.69. Whereas, for patients of late stage was 62.64%. Five year survival rate for patients of supraglottic carcinoma, glottic carcinoma, subglottic carcinoma and transglottic carcinoma was respectively 73.76%, 82. 55%, 55.56%, 68.75%. Five year survival rate for patients with partial laryngectomy was 79.89%, whereas, for total laryngectomy was 1.03%. The cause of death were local recurrence and cervical glands metastasis. CONCLUSION Early diagnosis was the key points to both larynx preservation and survival rate. for improving survival rate, we should handle the indications strictly. remain sufficient security cutting edge and follow-up visit.
Carcinoma, Squamous Cell ; mortality ; surgery ; Humans ; Laryngeal Neoplasms ; mortality ; surgery ; Laryngectomy ; mortality ; Neoplasm Staging ; Survival Analysis ; Survival Rate ; Treatment Outcome

Objective: Bioinformatics methods were used to annotate the suspicious pathogenic genes of congenital microtia in detail, and construct the protein-protein interaction (PPI) networks to clarify the function and interaction of pathogenic genes, so as to predict the potential pathogenic genes. Methods: The pathogenic genes of congenital microtia were searched using the mouse genome informatics (MGI). The results were summarized into the STRING database to construct PPI networks. The Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were carried out. Results: Sixty-eight congenital microtia-related pathogenic genes such as FGF8, EYA1 and HOXA2 were searched by MGI. The PPI network contained 65 nodes and 174 edges. The average node degree was 5.35. The clustering coefficient was 0.437 and the PPI enrichment P = 0. The key node proteins were screened in PPI networks. The top ten were CTNNB1, FGF8, EGFR, BCL2, PAX6, FGF3, FGF10, WNT5A, FGFR1 and MAPK1. GO analysis and KEGG pathway analysis showed: the pathogenic genes were involved in the biological process of ear morphogenesis, ear development and embryonic organ morphogenesis. They also get involved in the molecular regulation, including sequence-specific DNA binding and regulatory region DNA binding. Expression of different genes were located in nucleus and other sub-microscopic cell components. Pathogenic genes were also involved in cancer pathway, melanoma, MAPK signaling pathways, RAS signaling pathways and other signaling pathways. Conclusions By using bioinformatics tools, we constructed the PPI networks of the congenital microtia pathogenic genes, and obtained detailed GO enrichment and KEGG pathway data. The key nodes contained the confirmed pathogenic genes of congenital microtia, which preliminarily proved the feasibility of the bioinformatics method in this study. We found some nodes were closely linked with FGF and WNT, which may be potential mutant genes of congenital microtia, although further study is needed.

Objective: To identify a pig model with bilateral external ear defects accompanied by aural atresia and investigate its application in plastic surgery. Methods: Erhualian×Shaziling F₂ pig inbreeding population was introduced, and examination of external ear morphology was conducted in all individuals. Temporal computed tomography scanning and mutational detection of HOXA1 gene were conducted in one affected and one normal individuals. Results: In Erhualian×Shaziling F₂ pig inbreeding population, there were 57 normal and 18 affected individuals among the 75 pigs. Affected subjects presented bilateral external ear defects accompanied by aural atresia; temporal computed tomography scanning showed bilateral aural atresia and dysplasiaof middle ear; and gene detection identified homozygous mutation of HOXA1 gene. Conclusions Pig model with HOXA1 gene homozygous mutation resembles human microtia at different levels. Our findings provide the theoretical basis for its application to study further pathological mechanism for human microtia.

Objective: To investigate the curative effect of auricular deformity repaired by concha cartilage. Methods: From January 2017 to June 2018, 15 cases with auricular deformities were repaired using the autologous concha cartilage which combined with the retroauricular flap or retroauricular fascia with skin grafting. 9 males and 6 females, aged 10-40 with an average age of 19; 3 cases of upper 1/3 traumatic auricle defect, 2 cases of congenital Stahl's ear, 5 cases of congenital cup-shaped ear and 5 cases of congenital cryptotia. Results: Total 15 patients were followed up for 12-18 months after the surgery. The area of concha cartilage resection was about 0.5 cm×1.0 cm. The shape and size of the repaired ears were similar to the healthy ear. The transplanted cartilages were not absorbed or deformed. The incision was healed well and retroauricular flap, retroauricular fascia, and skin grafting were preserved well without complications like hemorrhage, necrosis, and infection. Conclusions This method is harmless and simple, which has reliable and satisfactory effects on various auricular deformities.

Glioma is a common tumor in the central nervous system. Because the natural immunosuppression of tumor microenvironment is conducive to tumor growth, transformation and migration, the traditional treatment has little effect and is difficult to make a breakthrough. Glioma-associated microglia and macrophage (GAM), an important part of brain tumor microenvironment, plays a more and more key role in tumor progression and regulation of anti-tumor immune response. This article reviews the latest progress of the source, recruitment, polarization and the role in development of gliomas as well as potential therapeutic targets of gliomas.