[Surgical management for the perforation of digestive tract with intraabdominal infection].

Perforation of digestive tract with intra-abdominal infection is one of the common causes of emergency surgery. After the resection with intestine, primary anastomosis or stoma remains a subject of debate. With the continuous improvement of surgical technology and the need to improve patients' quality of life, primary anastomosis is supposed to be the most ideal surgery. However, the rate of stoma is still high due to concerns about postoperative anastomotic leakage. This paper summarizes the surgical treatment of intra-abdominal infection caused by gastrointestinal perforation in recent years, and discuss the best operation plan according to the perforation location and etiology. We also discuss a variety of treatment methods for the prevention of anastomotic leakage (perioperative management, gastrointestinal anastomosis, enteric lavage decompression and other techniques) to improve the primary anastomosis, improve the quality of life of patients and reduce the medical burden.

[Restratifying the prognosis of acute myeloid leukemia patients with CEBPA double mutations based on CSF3R mutations and measurable residual disease].

Objective: This investigation aims to assess the impact of CSF3R mutations and the presence of measurable residual disease (MRD) on the prognosis of patients with CEBPA double mutations who have acute myeloid leukemia (AML) . Methods: The prognostic significance of these two factors was examined in the present study, which included 66 patients with complete genetic mutations and sequential MRD information. Results: Following the second course of chemotherapy, the MRD status and CSF3R mutations of these patients were linked to their long-term prognosis. CSF3R mutated patients showed inferior relapse-free survival (RFS) (5-year RFS: 15.2% vs 38.7% , P=0.006) and overall survival (OS) (5-year OS: 18.2% vs 60.6% , P=0.038) compared with those with wild-type CSF3R. After the second course of chemotherapy, patients with negative MRD had an RFS of 64 months and an OS of not reaching, which was significantly longer than that of patients with positive MRD (15 and 48 months, and the P value were 0.004 and 0.050, respectively) . CSF3R mutations (HR=0.317, 95% CI 0.129-0.779, P=0.012) , WT1 mutations (HR=0.304, 95% CI 0.115-0.804, P=0.016) , and NRAS mutations (HR=0.153, 95% CI 0.061-0.385, P<0.001) were all independently associated with a poor prognosis for RFS, and CSF3R mutations and positive MRD tended to be independently associated with a poor prognosis for OS, according to the results of a Cox proportional-hazards model analysis (P values were 0.071 and 0.088, respectively) . The patients were divided into three groups based on their CSF3R mutation status and MRD status following treatment: wide-type CSF3R and negative MRD, mutated CSF3R or positive MRD, and mutated CSF3R and positive MRD, which showed significantly different RFS (P<0.001) and OS (P=0.006) . Conclusion: Both CSF3R mutations and positive MRD were associated with poor outcome in AML patients with CEBPA double mutations. An integrity model based on these two factors may be beneficial for accurately evaluating the prognosis of these patients.

[Application of Neuroform EZ stent in the treatment of severe intracranial arterial stenosis with complex symptomatic].

OBJECTIVE: To assess the safety and efficacy of Neuroform EZ stent used in treatment of symptomatic complex severe intracranial atherosclerotic stenosis (ICAS). METHODS: Clinical data of 18 patients with symptomatic complex severe ICAS undergoing Neuroform EZ stent angioplasty from January 2016 to December 2017 were retrospectively analyzed. All the lesions of the patients in this group were considered as complex ICAS, i.e. with severe tortuous access, long (>10 mm) or occlusive or bifurcation lesions, with concurrent aneurysms near the stenotic lesion. The primary outcome was defined as any stroke (including ischemic or hemorrhagic) or deaths from any cause after stenting procedure within 30 days. The secondary outcome was defined as successful revascularization and occurrence of >50% in-stent restenosis during the follow-up period. RESULTS: All the 18 patients achieved technical success (100%) and mean stenosis rate was reduced from 85%±7% to 18%±6%. Of the 18 patients included, the 30-day stroke or death was 5.6% (1/18), which presented as basal ganglia region infarction in a patient with tandem lesions on the left vertebral artery. There was no hemorrhagic and death complications that occurred in the patients of this group. One concurrent aneurysm was embolized with micro coil (stent assisted) by stages after 1 month. In this group 12 patients were followed up with digital subtraction angiography (DSA) after hospital discharge. The follow-up period ranged from 8 months to 26 months [mean: (16±8) months]．During the follow-up period 2 patients in the 12 patients (2/12, 16.7%) developed in-stent restenosis (ISR) confirmed by DSA, and one of them was symptomatic restenosis and restored unobstructed blood flow after balloon angioplasty. CONCLUSION: Neuroform EZ stent for the treatment of highly screened symptomatic complex severe ICAS is safe and effective. It has its advantages over traditional stent.

The study on the effect of hyperglycemia on offspring fatty tissue metabolism during pregnancy.

OBJECTIVE: In this study, we adopted maternal diabetes model on rats, which induced by streptozotocin to explore the metabolism changes of rat adipose tissue during the neonatal period. MATERIALS AND METHODS: The female rats were induced as diabetes models by streptozotocin (STZ), and mated with the normal male rats when they entered into adulthood. The chosen male offspring rats were executed at week 12 and the epididymis and subcutaneous fat pad were obtained. Then the adipose cells were extracted and the foundation level and absorbing of insulin induced 2-deoxyglucose (2DG) were assessed. RESULTS: Compared with normal control group, the body weight, fat pad weight of the epididymis and diameter of lipid cells for maternal diabetes offspring rats all increased. Lipid cells of epididymis and the intake of glucose induced by insulin increased. At the same time, glucose was oxidized to CO2 and increased lipid. However, there was no change in the capacity of in vitro lipid decomposition. Also, GLUT4, insulin receptor (IRß), acetyl coenzyme A (ACC), etc. increased in fat pad of maternal offspring of diabetes. CONCLUSIONS: Maternal diabetes had effect on fat metabolism of offspring; lipid storage capacity increased but the ability of lipid decomposition had no change.

[Expression of Ether à go-go 1 and its molecular mechanism of regulating the malignant phenotype of osteosarcoma].

Objective: To explore the expression of ether à go-go 1 (Eag1) in human osteosarcoma and its molecular mechanisms of regulating the malignant phenotype of osteosarcoma. Methods: The expression levels of Eag1 in osteosarcoma cell lines and human osteosarcoma tissues were detected by reverse transcription polymerase chain reaction (RT-PCR), western blot analysis and immunohistochemistry. The small interfering RNA (siRNA) was used to inhibit the expression of Eag1. The abilities of proliferation and invasion in osteosarcoma cells transfected with Eag1 siRNA were determined by CCK-8, colony formation assay, transwell assay and wound healing assay. The osteosarcoma xenograft model of nude mouse was established and tumor growth curve was drawn. Western blot analysis was performed to detect the expression of vascular endothelial growth factor (VEGF) and signal transducer and activator of transcription 3 (STAT3) in osteosarcoma cells transfected with Eag1 siRNAs. Results: Eag1 was overexpressed in the osteosarcoma cells and tissues. Compared with the scrambled siRNA group, the cell survival rates of Eag1 siRNA1 and Eag1 siRNA2 groups of the two cell lines were significantly lower. [MG-63 cells: scrambled siRNA group (100.0±4.65)%, Eag1 siRNA1 group (63.57±3.89)%, and Eag1 siRNA2 group (54.13±3.70)%; Saos-2 cells: scrambled siRNA group (100.00±5.46)%, Eag1 siRNA1 group (56.70±5.34)%, and Eag1 siRNA2 group (40.27±5.28)% (P<0.001 for all)]. Similar results were obtained from colony formation assay. The colony formation rates of MG-63 cells: the scrambled siRNA group was (92.00±3.46)%, Eag1 siRNA1 group (60.00±3.06)%, and Eag1 siRNA2 group (53.67±2.40)%; the colony formation rates of Saos-2 cells: the scrambled siRNA group was (92.00±5.57)%, Eag1 siRNA1 group (52.33±5.13)%, and Eag1 siRNA2 group (41.67±2.73)%. Compared with the scrambled siRNA group, P<0.001 for all. The tumor volumes of osteosarcoma xenograft in the Eag1 siRNA1 and Eag1 siRNA2 groups were significantly smaller than that in the scrambled siRNA group after 10 days treatment (P<0.01 for all). The invasion assay data showed that MG-63 and Saos-2 cells transfected with Eag1 siRNAs exhibited the ability of cell invasion, when compared with the cells transfected with scrambled siRNA. (Invasive cell number of MG-63 cells: the scrambled siRNA group was 134.00±3.61, Eag1 siRNA1 group 105.20±2.52, and Eag1 siRNA2 group 91.00±3.01; Invasive cell number of Saos-2 cells: the scrambled siRNA group was 132.30±3.23, Eag1 siRNA1 group 114.30±3.48, and Eag1 siRNA2 group 82.67±6.33. Compared with the scrambled siRNA group, P<0.01 for all. The migration rates were (62.48±1.83)%, (35.98±1.23)% and (32.30±1.20)% in the three groups of MG-63 cells, and (70.15±1.42)%, (41.38±1.34)% and (32.40±1.92)% in the three groups of Saos-2 cells, respectively. Compared with the scrambled siRNA group, P<0.001 for all. Notably, the expression levels of VEGF decreased evidently after Eag1 siRNAs transfection, paralleled with reduction in the expression levels of STAT3. Conclusions: Eag1 may promote osteosarcoma cell proliferation and invasion by targeting STAT3-VEGF pathway and may be a potential therapeutic target for osteosarcoma.

Single nucleotide polymorphisms on SHIP2 is associated with Type 2 diabetes mellitus in Chinese Han population.

OBJECTIVE: Type 2 diabetes mellitus (T2DM) is a chronic disease characterized by insulin resistance in the target tissue of insulin with insufficient insulin secretion in pancreatic ß-cells. Src homology 2-containing 5'-inositol phosphatase 2 (SHIP2) is a lipid phosphatase that hydrolyzes PI3-kinase product PI(3,4,5)P3 to PI(3,4)P2, which contributes to the negative regulation of insulin signaling both in vitro and in vivo. Some polymorphisms of SHIP2 have been reported to be associated with the metabolic syndrome including T2DM and hypertension in British, French and Japanese T2DM population. PATIENTS AND METHODS: In our present study, we investigated the relation between single nucleotide polymorphisms (SNPs) on SHIP2 gene and the pathogenesis of T2DM in Chinese Han population. RESULTS AND CONCLUSIONS: Our results indicated that the genotype and allele frequency of SHIP2 (+1893CC/AA) locus in T2DM patients showed significantly different from between the healthy control population. In addition, the G allele of SHIP2 (+2945A/G) seemed to increase the susceptibility to hypertension for T2DM patients.

Aberrant RSPO3-LGR4 signaling in Keap1-deficient lung adenocarcinomas promotes tumor aggressiveness.

The four R-spondins (RSPO1-4) and their three related receptors LGR4, 5 and 6 (LGR4-6) have emerged as a major ligand-receptor system with critical roles in development and stem cell survival through modulation of Wnt signaling. Recurrent, gain-of-expression gene fusions of RSPO2 (to EIF3E) and RSPO3 (to PTPRK) occur in a subset of human colorectal cancer. However, the exact roles and mechanisms of the RSPO-LGR system in oncogenesis remain largely unknown. We found that RSPO3 is aberrantly expressed at high levels in approximately half of Keap1-mutated lung adenocarcinomas (ADs). This high RSPO3 expression is driven by a combination of demethylation of its own promoter region and deficiency in Keap1 instead of gene fusion as in colon cancer. Patients with RSPO3-high tumors (~9%, 36/412) displayed much poorer survival than the rest of the cohort (median survival of 28 vs 163 months, log-rank test P<0.0001). Knockdown (KD) of RSPO3, LGR4 or their signaling mediator IQGAP1 in lung cancer cell lines with Keap1 deficiency and high RSPO3-LGR4 expression led to reduction in cell proliferation and migration in vitro, and KD of LGR4 or IQGAP1 resulted in decrease in tumor growth and metastasis in vivo. These findings suggest that aberrant RSPO3-LGR4 signaling potentially acts as a driving mechanism in the aggressiveness of Keap1-deficient lung ADs.

A high sensitivity gas sensor for formaldehyde based on CdO and In(2)O(3) doped nanocrystalline SnO(2).

The gas-sensing characteristics of In(2)O(3) and CdO doped nanocrystalline SnO(2) compounds for formaldehyde were investigated in this study. The phases of the resulting materials and the morphologies of the sensing layers were characterized by x-ray diffraction (XRD) and scanning electron microscopy (SEM), respectively. Indirect-heating sensors using SnO(2)-In(2)O(3)-CdO compounds as sensitive materials were fabricated on an alumina tube with Au electrodes and platinum wires. All measurements were performed at several operating temperatures from 100 to 180 °C. Good gas-sensing responses to formaldehyde have been found for all the prepared samples. It is shown that the sensors exhibited high sensitivity at low operating temperature (133 °C), making them promising candidates for practical detectors for formaldehyde.

Absence of association between two insertion/deletion coding genetic polymorphisms of TIM-1 gene and asthma in Chinese Han population.

TIM-1, a member of T-cell immunoglobulin domain and mucin domain (TIM) gene family, was implicated as an asthma susceptibility gene in previous studies. TIM-1 was expressed on CD4(+) T cells after activation and its expression was sustained preferentially in T-helper type 2 (T(H)2) but not in T(H)1 cells, therefore TIM-1 became a good candidate gene for atopic diseases. Recent studies indicated that two insertion/deletion (ins/del) coding genetic polymorphisms in exon 4 of TIM-1 were associated with asthma susceptibility in some but not in all populations. In order to investigate the relationship between TIM-1 genetic polymorphisms and asthma in Chinese Han population, we performed a case-control study for two insertion/deletion polymorphisms in TIM-1 exon 4 (5383_5397ins/del and 5509_5511delCAA) and a single nucleotide polymorphism (SNP) in intron 8 (IVS 8+9 G/A) between a healthy control group of 309 people and an asthma patient group of 352 people recruited from Chinese Han population. The polymorphisms were genotyped and the allele and genotype frequencies were analysed, but none of the three polymorphisms showed association with asthma susceptibility in single-locus association analyses. Linkage disequilibrium (LD) analyses demonstrated that the two insertion/deletion polymorphisms were in strong LD but the haplotypes constructed from these two polymorphisms showed no significant association with asthma. In conclusion, our findings suggest that 5383_5397ins/del, 5509_5511delCAA and SNP IVS 8+9 G/A polymorphisms are not associated with asthma susceptibility in Chinese Han population.

Lack of association between ADAM33 gene and asthma in a Chinese population.

Asthma is a complex polygenic disease with gene-environment interactions being important. It has been previously suggested that ADAM33, which is a member of a gene family that encodes membrane-anchored proteins with a disintegrin and a metalloprotease domain, is primarily expressed in lung fibroblasts and bronchial smooth muscle cells and has been associated with airway remodelling and bronchial hyperresponsiveness. A significant association has previously been demonstrated between single nucleotide polymorphisms (SNPs) and haplotypes of the ADAM33 and asthma in ethnically diverse populations. To assess whether SNPs or haplotypes of ADAM33 are related to asthma in a Chinese Han population, we genotyped three SNPs of ADAM33 (7575G/A in intron 6, 11188A/T in intron 19, and 12433T/C in exon 20) in a case-control study involving 296 patients with asthma and 270 healthy controls. No significant association was detected between these three SNPs and asthma susceptibility in the Chinese population.

[Linkage analysis and mutation detection of GRIA3 in Smith--Fineman--Myers syndrome].

To determine the role of GRIA3 in the etiology of Smith--Fineman--Myers syndrome (SFMS), polymorphic short tandem repeats within GRIA3 gene were genotyped by PCR and denaturing polyacrylamide gel electrophoresis to test linkage between GRIA3 and the gene responsible for SFMS. The open reading frame of GRIA3 was detected for mutation by PCR amplification and direct sequencing in affected and normal males from SFMS family. One of the two short tandem repeats was informative in SFMS family. Tight linkage between SFMS locus and GRIA3 gene was established by STR3 within GRIA3 gene. No disease--causing mutation was found within the open reading frame of GRIA3 gene. The disease in SFMS family from Shandong (China) is not caused by the mutation within open reading frame of GRIA3 gene.