The paper quantizes symptom data through binary coding,divides 8 syndromes summed up by experts into excess and de-ficiency syndromes,values and quantizes them,and establishes the model for classification of excess and deficiency syndromes of colorec-tal cancer based on BP neural network and decision tree.The result shows that BP neural network classification model is more applicablefor the handling of the nonlinear mapping relation compared with decision tree classification model.

Objective To investigate the effects of fluid shear stress on interleukin-8(IL-8)mRNA expression in human endothelial cell line-EA.Hy926 cells.Methods Weibel-Palade body and factor Ⅷ related antigen were detected to identify cultured EA.Hy926 cells.Quantitative reversal transcription-polymerase chain reaction was also used to assay IL-8 mRNA expression.Results It was found that the growth feature of EA.Hy926 cells in vitro culture was similar with that of human umbilical vein endothelial cells(HUVECs).Meanwhile,it also had the typical features of endothelial cells,i.e.Weibel-Palade body in plasma and express factor Ⅷ related antigen.IL-8 mRNA expression of endothelial cells exposed to low shear stress(0.420 Pa)increased at 1 h and reached its peak value at 2 h,then gradually decreased at 3 h and kept the descending trend throughout the remained time course of the study,as compared with that in cells not treated with shear stress.Also after exposed to shear stress of different levels(0.182,0.420,1.000,1.640 Pa)for 2 h,in which IL-8 mRNA expression of EA.Hy926 cells decreased with the increase of the intensity of the shear stress.Conclusion The results suggest that fluid stress can induce the expression of IL-8 mRNA in EA.Hy926 cells.EA.Hy926 cells might be used as a cell source in the field of biorheological research of endothelial cells.

Objective To investigate ABCA3 gene polymorphism and its relationship with neonatal respiratory distress syndrome (NRDS) in the Guangxi Zhuang Autonomous Region of China by genotyping and haplotype analysis.Methods Using a tagging single nucleotide polymorphism (tSNP) strategy and TaqMan (r) real-time PCR,we genotyped 4 tSNPs (rs4787273,rs 1 50929,rs 11867129,and rs 17135889) and one additional coding SNP(rs13332514) of the ABCA3 gene in preterm infants with NRDS(NRDS group,n =45) and without NRDS (non-NRDS group,n =45) and subsequently predicted the haplotypes.The minor allele frequency and the haplotype 'distribution were compared between the two groups.Results The minor allele A(0.14 vs.0.05,P =0.046) and genotype AG (0.289 vs.0.111,P =0.035) frequency of SNP rs17135889 in NRDS group were significantly higher than those in non-NRDS group.Totally 6 haplotypes occurred at a frequency ≥0.01,among which,the haplotype TGGAG,depended on rs17135889,was significantly higher in NRDS group than that in non-NRDS group (0.061 vs.0.000,P =0.014).Conclusion The results suggested that SNP rs17135889 of ABCA3 gene might be related to NRDS in preterm population of the Guangxi Zhuang Autonomous Region.Allele A contributes to NRDS susceptibility in preterm infants.

Objective To study the distribution of surfactant protein A2 (SP-A2) haplotype and its association with preterm respiratory distress syndrome (RDS) susceptibility in a local Chinese cohort.Methods Using population base and case-control study cohorts,genotyping for four single nucleotide polymorphism (SNP) was performed,rs1059046,rs17886395,rs1965707,rs1965708,in 80 term infants,50 preterm infants with RDS (RDS group) and 50 preterm infants without RDS(control group) by using TaqMan (R) real-time polymerase chain reaction.Infants in RDS group and control group were matched according to gender and gestational age.Frequency of each haplotype was compared between preterm infants with RDS and without RDS,term infants and preterm infants without RDS.Results Most common haplotypes in term infants were 1A0,1A5,1A1.In each preterm infants groups with RDS and without RDS,1A0,1 A5,1 A1 were also the most common haplotypes.Among these three common haplotypes,frequency of 1A0 was lower in preterm infants,including RDS group and control group,than that in term infants.No significant difference was found between preterm groups with RDS and without RDS (P ＞ 0.05),neither in preterm infants with gestational age ≥32 or ＜ 32 weeks.Haplotype 1A0 frequency(0.542) in term infants was significantly higher than that in preterm infants ＜ 32 weeks without RDS (0.329) (x2 =6.06,P =0.01).Conclusions SP-A2 haplotype distribution in a local Chinese population shows ethnic characteristics to some extent.Only SP-A2 does not contribute to the susceptibility for preterm RDS.

The aim of this study was to fabricate an ideal nature-based tissue engineered blood vessel (TEBV) scaffold. It should have several special characteristics such as little immunogenicity and good biocompatibility, and it should be similar in mechanical property to fresh tissue. New-got canine aortas were dipped in ion-free water for 12 h under 4 degrees C to make the cells disrupted, then fixed in a kind of polyepoxy compounds solution (EX-810) for 72 h, and finally treated with sonication to remove the cell debris. Histological slices of the TEBV scaffold were stained with H&E. The results showed that our method could effectively remove the cells in fresh tissues because there was no visible nuclear stain. A series of biomechanical analyses revealed that these TEBV scaffold had nearly the same mechanical properties as fresh tissues. Also, these TEBV scaffolds showed good cell-compatibility, and their surfaces were suitable for endothelial cells and smooth muscle cells to grow on.
Animals ; Aorta ; cytology ; Biocompatible Materials ; Blood Vessel Prosthesis ; Cell Separation ; Dogs ; Endothelium, Vascular ; cytology ; Epoxy Resins ; chemistry ; Tissue Engineering ; methods ; Tissue Scaffolds

It was reported that pancreatic arteries constricted during the early phase of bile salt-induced acute pancreatitis (AP), leading to pancreatic microcirculatory disturbance. We conducted this experiment to verify whether the above-mentioned finding was true. AP was induced with intraductal injection of taurodeoxyholate. Small pancreatic artery pressure in dogs was recorded. Functional capillaries were counted and calibrated by multiplying wet weight of pancreas. Pancreatic perfusion was measured with Laser Doppler flowmeter. Pancreatic arterioles of rats dilated during the initial 20 min of AP, and pancreatic arterial pressure declined during the early phase of AP in dogs (from 104.5 +/- 4.8 mmHg to 54.6 +/- 5.6 mmHg). The hematocrit of blood from inferior vena cava was significantly lower than that of portal vein at 5 min after pancreatitis induction. The "true" pancreatic functional capillary density increased. The early pancreatic microcirculatory disturbance coincided with a marked increase of portal vein pressure (PVP) as high as 9.18 +/- 0.78 mmHg. Reduction of PVP to baseline level was followed by a marked increase of pancreatic perfusion (by 1.4-fold). Arterial dilatation, but not constriction, occurred during the early phase of bile salt-induced AP. The pancreatic microcirculatory disturbance was due to a marked rise in PVP that greatly reduced the pressure difference in the pancreatic blood vessels and increased plasma extravasation which led. to local hemoconcentration.
Animals ; Bile Acids and Salts ; adverse effects ; Hypertension, Portal ; complications ; Male ; Microcirculation ; drug effects ; physiology ; Pancreas ; blood supply ; Pancreatitis ; etiology ; physiopathology ; Portal Pressure ; Portal Vein ; physiopathology ; Rats ; Rats, Sprague-Dawley

Accumulating evidence has confirmed the links between transfer RNA (tRNA) modifications and tumor progression. The present study is the first to explore the role of tRNA methyltransferase 5 (TRMT5), which catalyzes the m1G37 modification of mitochondrial tRNAs in hepatocellular carcinoma (HCC) progression. Here, based on bioinformatics and clinical analyses, we identified that TRMT5 expression was upregulated in HCC, which correlated with poor prognosis. Silencing TRMT5 attenuated HCC proliferation and metastasis both in vivo and in vitro, which may be partially explained by declined extracellular acidification rate (ECAR) and oxygen consumption rate (OCR). Mechanistically, we discovered that knockdown of TRMT5 inactivated the hypoxia-inducible factor-1 (HIF-1) signaling pathway by preventing HIF-1α stability through the enhancement of cellular oxygen content. Moreover, our data indicated that inhibition of TRMT5 sensitized HCC to doxorubicin by adjusting HIF-‍1α. In conclusion, our study revealed that targeting TRMT5 could inhibit HCC progression and increase the susceptibility of tumor cells to chemotherapy drugs. Thus, TRMT5 might be a carcinogenesis candidate gene that could serve as a potential target for HCC therapy.
Humans ; Carcinoma, Hepatocellular/pathology* ; Cell Hypoxia ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism* ; Liver Neoplasms/pathology* ; Signal Transduction/genetics* ; tRNA Methyltransferases/metabolism*

SIRT6 belongs to the conserved NAD⁺-dependent deacetylase superfamily and mediates multiple biological and pathological processes. Targeting SIRT6 by allosteric modulators represents a novel direction for therapeutics, which can overcome the selectivity problem caused by the structural similarity of orthosteric sites among deacetylases. Here, developing a reversed allosteric strategy AlloReverse, we identified a cryptic allosteric site, Pocket Z, which was only induced by the bi-directional allosteric signal triggered upon orthosteric binding of NAD⁺. Based on Pocket Z, we discovered an SIRT6 allosteric inhibitor named JYQ-42. JYQ-42 selectively targets SIRT6 among other histone deacetylases and effectively inhibits SIRT6 deacetylation, with an IC₅₀ of 2.33 μmol/L. JYQ-42 significantly suppresses SIRT6-mediated cancer cell migration and pro-inflammatory cytokine production. JYQ-42, to our knowledge, is the most potent and selective allosteric SIRT6 inhibitor. This study provides a novel strategy for allosteric drug design and will help in the challenging development of therapeutic agents that can selectively bind SIRT6.