Objective To study the surgical managements for obstructive coleratal carcinoma(OCRC).(Methods) Clinical data of 126 patients with OCRC who underwent surgical treatment between January 1995 and December 2004 were reviewed.Results Thirty-five patients received one-stage right hemicolectomy,ten patients received one-stage resection of transverse colon.forty-eight patients received one-stage left(hemicolectomy),eighteen patients received one-stage resection of left colon or proximal rectum with colostomy followed by two-staged anastomosis.For 15 patients with unresectable lesions,colostomy of transverse colon or sigmoid colon was performed.Seventeen patients(13.5%) experienced postoperative complications.The (operative) mortality was 4.8%(6/126).The 1-year,3-year and 5-year overall survival rate was(95.1)%,52.7% and 38.1%,respectively.Conclusions Proper perioperative period managements and(selection) of surgical techniques are important for better results and lower complications in the treatment OCRC.

ObjectiveTo investigate the effect of Smad7 antisense oligodeoxynucleotide (ASODN) on proliferation in human pancreatic cancer cell line SW1990,with a focus on the expression of matrix metalloproteinase-2(MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2).To explore the underlying mechanism of the role of Smad7 in the pathogenesis and development of pancreatic cancer.MethodsSmad7 ASODN was transfected into SW1990 cells through lipofectamine.Nosense oligodeoxynucleotide (NSODN),ASODN and lipofectamine was used as control. The transfection efficiency was assessed by fluorescence microscopy and flow cytometry.The expressions of Smad7,MMP-2 and TIMP-2 in transfected cells were detectedby RT-PCR and Western blot.Cell viability was assessed by dimethyl thiazoldiphenyltetrazoliumbromide (MTT) method. Results Smad7 was expressed in SW1990 cells.The transfection efficiency of SW1990 was 81.2％.The expressions of Smad7 mRNA were 0.34 ± 0.06,0.95 ±0.07,1.03 ± 0.11 in transfected group,ASODN and lipofectamine group; and the expressions of MMP-2 mRNAwere 0.54 ± 0.08,1.15 ± 0.13,1.27 ± 0.16 ; and the expressions of TIMP - 2 mRNA were 0.26 ±0.07,0.72 ± 0.13,0.78 ± 0.17,the mRNA expressions were significantly reduced in Smad7 ASODN transfected group,compared with other two groups (P ＜0.01 ).The expressions of Smad7 protein were 0.14 ± 0.03,0.29 ± 0.05,0.28 ± 0.07 in transfected group,ASODN and lipofectamine group; the expressions of MMP-2 protein were 0.17 ±0.02,0.29 ±0.05,0.31 ±0.04,and the expressions of TIMP-2 protein were 0.20 ± 0.03,0.41 ± 0.11,0.43 ± 0.09,the protein expressions were significantly reduced in Smad7 ASODN transfected group,compared with other two groups (P ＜0.01 ).The A490 values of proliferation were 0.83 ± 0.03,1.02 ±0.02,0.99 ±0.02 in transfected group,ASODN and lipofectamine group,the proliferation were significantly reduced in Smad7 ASODN transfected group,compared with other two groups (P ＜0.01 ).ConclusionsSmad7 ASODN could effectively inhibit the expressions of Smad7,therefore decrease the expressions of MMP-2,TIMP-2 and reduce the proliferation.

In our previous studies, DAZAP2 gene expression was down-regulated in untreated patients of multiple myeloma (MM). For better studying the structure and function of DAZAP2, a full-length cDNA was isolated from mononuclear cells of a normal human bone marrow, sequenced and deposited to Genbank (AY430097). This sequence has an identical ORF (open reading frame) as the NM_014764 from human testis and the D31767 from human cell line KG-1. Phylogenetic analysis and structure prediction reveal that DAZAP2 homologues are highly conserved throughout evolution and share a polyproline region and several potential SH2/SH3 binding sites. DAZAP2 occurs as a single-copy gene with a four-exon organization. We further noticed that the functional DAZAP2 gene is located on Chromosome 12 and its pseudogene gene is on Chromosome 2 with electronic location of human chromosome in Genbank, though no genetic abnormalities of MM have been reported on Chromosome 12. The ORF of human DAZAP2 encodes a 17-kDa protein, which is highly similar to mouse Prtb. The DAZAP2 protein is mainly localized in cytoplasm with a discrete pattern of punctuated distribution. DAZAP2 may associate with carcinogenesis of MM and participate in yet-to-be identified signaling pathways to regulate proliferation and differentiation of plasma cells.
Amino Acid Sequence ; Base Sequence ; Chromosomes, Human, Pair 12 ; genetics ; Chromosomes, Human, Pair 2 ; genetics ; Cytoplasm ; metabolism ; DNA Primers ; DNA, Complementary ; genetics ; Down-Regulation ; Gene Components ; Humans ; Likelihood Functions ; Models, Genetic ; Molecular Sequence Data ; Multiple Myeloma ; genetics ; metabolism ; Phylogeny ; Pseudogenes ; genetics ; RNA-Binding Proteins ; genetics ; metabolism ; Sequence Alignment ; Sequence Analysis, DNA

Tumor invasion and metastasis are regarded as main reasons for the failure of therpy and the reason of patients death.The mechnism of tumor metastasis is still uncertain.The pre-metastatic niche hypothesis provides us with new ideas to discover the mechnism.Numerous materials are involved in the formation of the pre-metastatic niche according to this hypothesis,including bone marrow-derived cells,microvesicles,exosomes,CD44,and so on.A further research on this hypothesis helps to deeply understand the nature of metastasis and leads clinical doctors to explore novel targets for clinical diagnoses and therapies.

BACKGROUNDPaclitaxel plus cisplatin is an effective regimen in the treatment of non-small cell lung cancer (NSCLC), but it has severe adverse toxicities. The aim of this clinical trial is to evaluate the effect and safety of paclitaxel plus oxaliplatin compared with paclitaxel plus cisplatin in the treatment of advanced NSCLC.

METHODSFrom January, 2002 to October, 2004, 83 initially treated patients with advanced NSCLC were randomized into two groups: the trial group was treated with paclitaxel 175mg/m², and oxaliplatin 130mg/m² on day 1;and the control group was treated with paclitaxel 175mg/m² and cisplatin 80mg/m² on day 1. Both of them were repeated every 21 days and 2-6 cycles were given to patients. The evaluation of efficacy and safety was performed after chemotherapy regularly.

RESULTSAll patients were evaluable and received 2 cycles chemotherapy at least. The response rate of the trial group and control group was 34.1% (14/41) and 33.3% (14/42) respectively, median time to progression of them was 6.0 months and 5.5 months, median survival time was 10.7 months and 10.5 months, 1-year survival was 39.0% (16/41) and 40.5% (17/42) respectively. The following adverse effects of the two groups were different: the incidence rate of III+IV leukopenia was 4.9% and 28.6% in the trial group and the control group respectively, III+IV thrombocytopemia was 0 and 14.3%, III+IV nausea and vomiting was 7.3% and 26.2%. The difference of the incidence rate of III+IV nerve abnormality (9.8% and 9.5%), imparied renal function (0 and 7.1%), myalgia and anthralgia (0 and 2.4%) was insignificant.

CONCLUSIONSThe regimen of paclitaxel plus oxaliplatin have the similar efficacy and less adverse toxicities as compared to Paclitaxel plus Cisplatin in treatment of advanced NSCLC.

Objective:To explore the clinical features and pathogenic causes of a Chinese Han family with Wagner syndrome, and to analyze the relationship between VCAN gene mutation and patient phenotype. Methods:The method of family pedigree investigation was adopted.A Chinese Han family with Wagner syndrome in 3 generations including 13 family members was collected in Xiamen Eye Center of Xiamen University in January 2020, and 5 patients from 3 generations were diagnosed.All members underwent a comprehensive medical history collection and routine ophthalmological examinations, including visual acuity, intraocular pressure, slit lamp microscopy, and ophthalmoscopy to analyze the condition of anterior segment and fundus.Anterior segment photography, fundus photography, optical coherence tomography and ultrasound biological microscopy were carried out in the proband and some patients to analyze the condition of anterior segment, fundus and anterior chamber angle.The peripheral venous blood of all family members was collected for genomic DNA extraction, and pathogenic gene variation analysis for verification was through high-throughput target region capture sequencing and Sanger sequencing.Variants were scored using the American College of Medical Genetics and Genomics (ACMG) guidelines, and the structure and function of variants were predicted through PredictProtein.This study adhered to the Declaration of Helsinki.The study protocol was approved by the Ethics Committee of Xiamen Eye Center of Xiamen University (No.MR-35-22-002800).Written informed consent was obtained from each subject.Results:The Chinese pedigree with Wagner syndrome was in accordance with autosomal dominant inheritance pattern, and all patients had no history of systemic disease or other abnormal manifestations.The common ophthalmic features of the patients were abnormal suspensory ligament, premature cataract, vitreous cavity, vitreous condensation, veil-like proliferative membrane in the vitreous cavity, retinal choroid atrophy and thinning, tractional retinal detachment, and retinal pigmentation.The proband had binocular cataract surgery, and binocular intraocular lens dislocation occurred after the operation.Genetic analysis revealed that a heterozygous splice site variation c.9265+ 1G>A in the VCAN gene in this family was co-segregated with the disease phenotype and graded as a likely pathogenic variant by the ACMG guidelines.This variant base pair substitution could cause the formation of a protein product with 1 754 amino acids shorter, resulting in insufficient haploid dosage and severe reduction of glycosaminoglycan attachment sites, making the versican protein dysfunctional. Conclusions:It is the first time to report a Chinese family with Wagner syndrome in China, and it is confirmed that the family has a heterozygous variation in the VCAN gene c.9265+ 1G>A by molecular genetic analysis.

Objective:To analyze the clinical and molecular genetic characteristics of a Chinese family with congenital cataract-microcornea syndrome.Methods:The method of pedigree investigation was adopted.A Chinese Han family with congenital cataract-microcornea syndrome was recruited in Xiamen Eye Center of Xiamen University.All the family members received detailed ophthalmologic examination including the best corrected visual acuity, intraocular pressure measurement by handheld applanation tonometry, slit lamp biomicroscopy, color fundus photography, B-scan ultrasonography, corneal diameter, anterior segment optical coherence tomography, ultrasound biomicroscopy, corneal endoscopy, and corneal topography.Genomic DNA was extracted from peripheral venous blood from some patients and unaffected family members.Targeted high-throughput DNA sequencing was performed on the proband.The sequencing chip contained 188 known pathogenic genes related to lens abnormalities.Suspected pathogenic genes were verified by Sanger sequencing in phenotypically normal family members to identify the co-segregation and the disease-causing gene.Bioinformatics analysis was performed to analyze the pathogenicity of variants by REVEL.Conserved protein domains were analyzed by InterPro.Physicochemical property of the mutant protein was analyzed by ProtParam.The deleteriousness of the protein was predicted by PolyPhen-2.Homology of the variants in pathogenic gene was analyzed by NCBI website to compare the conservation among various species.This study followed the Declaration of Helsinki.The study protocol was approved by the Ethics Committee of Xiamen Eye Center of Xiamen University (No.XMYKZX-LW-2009-003).Written informed consent was obtained from each subject prior to entering the study cohort.Results:There were 39 members of 4 generations in this family including 11 patients with an autosomal dominant inheritance pattern.Clinical features of the patients included congenital cataract and microcornea.No obvious abnormality was found in ophthalmic and general examination.A heterozygous mutation c. 61C>T in the CRYAA gene was found, resulting in the mutation of the amino acid from arginine to tryptophan (p.Arg21Trp) at position 21, consistent with co-segregation.The number of cationic cluster in the mutant protein decreased, and the hydrophilicity and stability were reduced.The variant was predicted to be deleterious and was highly conserved in multiple species. Conclusions:A novel heterozygous mutation c.61C>T p. Arg21Trp in CRYAA gene is considered as the causal gene of this family.It is the first time this variant has been reported in China.

Primitive mammalian heart transforms from a single tube to a four-chambered muscular organ during a short developmental window. We found that knocking out global microRNA by deleting Dgcr8 microprocessor in Mesp1 cardiovascular progenitor cells lead to the formation of extremely dilated and enlarged heart due to defective cardiomyocyte (CM) differentiation. Transcriptome analysis revealed unusual upregulation of vascular gene expression in Dgcr8 cKO hearts. Single cell RNA sequencing study further confirmed the increase of angiogenesis genes in single Dgcr8 cKO CM. We also performed global microRNA profiling of E9.5 heart for the first time, and identified that miR-541 was transiently highly expressed in E9.5 hearts. Interestingly, introducing miR-541 back into microRNA-free CMs partially rescued their defects, downregulated angiogenesis genes and significantly upregulated cardiac genes. Moreover, miR-541 can target Ctgf and inhibit endothelial function. Our results suggest that microRNAs are required to suppress abnormal angiogenesis gene program to maintain CM differentiation.