Assessment and establishment of a reference interval for Roche Cobas t 711 coagulation analyzer for a hospital in China.

INTRODUCTION: Due to the use of different detection reagents and methods, coagulation analyzers can produce different results. Therefore, detection instruments, reagents and methods are important factors affecting the results of coagulation test. Therefore, this paper aims to establish reference intervals applicable to our laboratory for the Roche Cobas t 711 for routine coagulation assays.Methods:We completed a preliminary evaluation of the analytical performance of the cobas t 711 before any experiment. Healthy volunteer recruitment and ostensibly healthy patients via physical examination were performed to collect individual reference samples. Data were grouped and compared according to age, and the Z test was used to determine whether there was a statistically significant difference between the mean values after grouping. RESULTS: The self-established PT, APTT and TT reference intervals were 8.4-10.2s, 26.8-42.3s and 14.5-17.1s, respectively. The reference ranges of FIB, AT and DD for people aged 50 years or below were 1.85-3.78 (g/l), 83.9-113.2 (%) and 0-0.45 (mg/l), respectively, and those for people older than 50 years were 2.22-3.86 (g/l), 76.0-112.0 (%) and 0-0.52 (mg/l), respectively. CONCLUSION: The self-built reference intervals for the Roche t 711 were basically consistent with those in the instructions, except the APTT ranges were slightly wider. Laboratories should establish applicable reference intervals according to their own conditions to provide guidance for the diagnosis, monitoring and prognosis of clinically related diseases.

Differential expression analysis of the SRB1 gene in fluconazole-resistant and susceptible strains of Candida albicans.

To study differences in SRB1 gene expression between Candida albicans fluconazole-resistant strains and fluconazole-sensitive strains, and to identify new antifungal drug treatment targets. We studied 30 fluconazole-resistant and 47 fluconazole-sensitive C. albicans strains. The strains were routinely cultured, and total RNA was extracted, reverse transcribed into cDNA and analyzed with real-time PCR amplification with 18S rRNA used as an internal reference gene. The expression levels of the two groups were analyzed in Light Cycler system software version 3.0, and independent Student's t test was performed in SPSS 19.0 statistical software. P < 0.05 was considered to indicate a statistical difference. DNAMAN multiple sequence alignment analysis was used to randomly analyze SBR1 related sequences of four resistant strains and four sensitive strains. An evolutionary tree was constructed with the maximum likelihood method in Mega6.0 software. The mean SRB1 gene expression in the drug-resistant group was 0.75138 × 10-3, and that in the sensitive group was 1.6664 × 10-3. Independent Student's t test indicated a statistically significant difference (T = -3.972, P = 0.000, P < 0.05). DNAMAN multiple sequence alignment analysis showed that the sequence identity of the CDS in the eight strains was 75.17%, and that of sequences 1000 bp upstream of the CDS was 96.35%. Cluster analysis showed that the CDS and sequences 1000 bp upstream of the CDS showed no significant differences between groups. At the mRNA level, the SRB1 gene expression in fluconazole-resistant C. albicans was lower than that in fluconazole-sensitive strains, thus suggesting that the gene may be associated with drug resistance and that the regulatory mechanism leading to this difference is complex.

Inhibition of miR-221 alleviates LPS-induced acute lung injury via inactivation of SOCS1/NF-κB signaling pathway.

The role of inflammation response has been well documented in the development of acute lung injury (ALI). However, little is known about the functions of miRNAs in the regulation of inflammation in ALI. The aim of this study was to explore the effects of miRNAs in the regulation of inflammation in ALI and to elucidate the biomolecular mechanisms responsible for these effects. The expression profiles of miRNAs in lung tissues from lipopolysaccharide (LPS)-induced ALI mice model were analyzed using a microarray. It was observed that microRNA-221-3p (miR-221) was significantly increased in lung tissues in ALI mice. The inhibition of miR-221 attenuated lung injury including decreased lung W/D weight ratio and lung permeability and survival rates of ALI mice, as well as apoptosis, whereas its agomir-mediated upregulation exacerbated the lung injury. Concomitantly, miR-221 inhibition significantly reduced LPS-induced pulmonary inflammation, while LPS-induced pulmonary inflammation was aggravated by miR-221 upregulation. Of note, suppressor of cytokine signaling-1 (SOCS1), an effective suppressor of the NF-κB signaling pathway, was found to be a direct target of miR-221 in RAW264.7 cells. Overexpression of SOCS1 by pcDNA-SOCS1 plasmids markedly reversed the miR-221 inhibition-mediated inhibitory effects on inflammation and apoptosis in LPS-treated RAW264.7 cells. Finally, it was found that miR-221 inhibition suppressed LPS induced the activation of the NF-κB signaling pathway, as demonstrated by downregulation of phosphorylated-IκBα, p-p65 and upregulation of IκBα, whilst miR-221 overexpression had an opposite result in ALI mice. Our findings demonstrate that inhibition of miR-221 can alleviate LPS-induced inflammation via inactivation of SOCS1/NF-κB signaling pathway in ALI mice.

Polarization-interleave-multiplexed discrete multi-tone modulation with direct detection utilizing MIMO equalization.

Discrete multi-tone (DMT) modulation is an attractive modulation format for short-reach applications to achieve the best use of available channel bandwidth and signal noise ratio (SNR). In order to realize polarization-multiplexed DMT modulation with direct detection, we derive an analytical transmission model for dual polarizations with intensity modulation and direct diction (IM-DD) in this paper. Based on the model, we propose a novel polarization-interleave-multiplexed DMT modulation with direct diction (PIM-DMT-DD) transmission system, where the polarization de-multiplexing can be achieved by using a simple multiple-input-multiple-output (MIMO) equalizer and the transmission performance is optimized over two distinct received polarization states to eliminate the singularity issue of MIMO demultiplexing algorithms. The feasibility and effectiveness of the proposed PIM-DMT-DD system are investigated via theoretical analyses and simulation studies.

Polymorphism of stromal cell-derived factor-1 selectively upregulates gene expression and is associated with increased susceptibility to coronary artery disease.

Stromal cell-derived factor-1 (SDF-1) plays critical roles in vascular development and hematopoiesis. Here, we investigated the function of SDF-1 rs1801157G/A polymorphism in various immune cells and examined its association with susceptibility to coronary artery disease (CAD). Protein and mRNA levels of SDF-1 were tested in peripheral CD4+ T cell, CD8+ T cells, monocytes, and natural killer (NK) T cells from healthy donors with different genotypes of rs1801157G/A polymorphism. Prevalence of the polymorphism was compared between CAD patients and healthy controls. Data revealed that SDF-1 mRNA and protein were detectable in CD4+ T cells, CD8+ T cells, monocytes and NK T cells. Interestingly, both protein level and mRNA level of SDF-1 were significantly increased in the monocytes with rs1801157AA genotype, whereas the same phenomenon was not observed in the other three cell types. Blockage of CD14 completely inhibited the upregulation of SDF-1 in the monocytes with rs1801157AA genotype. Association analysis showed that frequencies of the rs1801157AA genotype and A allele were significantly higher in CAD cases than in controls (odds ratio [OR]=2.28, 95% confidence interval [CI], 1.50-3.29, p<0.0001, and OR=1.46, 95% CI, 1.21-3.73, p<0.0001, respectively). Also, prevalence of rs1801157AA genotype was further increased in cases with ST-elevation myocardial infarction (OR=1.65, 95% CI, 1.04-2.56, p=0.028). Our data suggest a novel pathway for regulating SDF-1 and a new risk factor for CAD.