Biomedical subjects

Yufeng Lu

Publications and source records attributed to Yufeng Lu.

3 recordsLinked to original sources

PubMed2006

A successive parameter estimation algorithm for chirplet signal decomposition.

In ultrasonic imaging systems, the patterns of detected echoes correspond to the shape, size, and orientation of the reflectors and the physical properties of the propagation path. However, these echoes often are overlapped due to closely spaced reflectors and/or microstructure scattering. The decomposition of these echoes is a major and challenging problem. Therefore, signal modeling and parameter estimation of the nonstationary ultrasonic echoes is critical for image analysis, target detection, and object recognition. In this paper, a successive parameter estimation algorithm based on the chirplet transform is presented. The chirplet transform is used not only as a means for time-frequency representation, but also to estimate the echo parameters, including the amplitude, time-of-arrival, center frequency, bandwidth, phase, and chirp rate. Furthermore, noise performance analysis using the Cramer Rao lower bounds demonstrates that the parameter estimator based on the chirplet transform is a minimum variance and unbiased estimator for signal-to-noise ratio (SNR) as low as 2.5 dB. To demonstrate the superior time-frequency and parameter estimation performance of the chirplet decomposition, ultrasonic flaw echoes embedded in grain scattering, and multiple interfering chirplets emitted by a large, brown bat have been analyzed. It has been shown that the chirplet signal decomposition algorithm performs robustly, yields accurate echo estimation, and results in SNR enhancements. Numerical and analytical results show that the algorithm is efficient and successful in high-fidelity signal representation.

Algorithms↗

PubMed2004

The interferon consensus sequence-binding protein activates transcription of the gene encoding neurofibromin 1.

Deficiency of the interferon consensus sequence-binding protein (ICSBP) is associated with increased myeloid cell proliferation in response to hematopoietic cytokines. However, previously identified ICSBP target genes do not indicate a mechanism for this "cytokine hypersensitivity." In these studies, we identify the gene encoding neurofibromin 1 (Nf1) as an ICSBP target gene, by chromatin immunoprecipitation. Additionally, we find decreased Nf1 expression in bone marrow-derived myeloid cells from ICSBP-/- mice. Since Nf1 deficiency is also associated with cytokine hypersensitivity, our results suggested that NF1 is a functionally significant ICSBP target gene. Consistent with this, we find that the hypersensitivity of ICSBP-/- myeloid cells to granulocyte monocyte colony-stimulating factor (GM-CSF) is reversed by expression of the Nf1 GAP-related domain. We also find that treatment of ICSBP-deficient myeloid cells with monocyte colony-stimulating factor (M-CSF) results in sustained Ras activation, ERK phosphorylation, and proliferation associated with impaired Nf1 expression. These M-CSF effects are reversed by ICSBP expression in ICSBP-/- cells. Consistent with this, we find that ICSBP activates the NF1 promoter in myeloid cell line transfectants and identify an ICSBP-binding NF1 cis element. Therefore, the absence of ICSBP leads to Nf1 deficiency, impairing down-regulation of Ras activation by GM-CSF or M-CSF. These results suggest that one mechanism of increased myeloid proliferation, in ICSBP-deficient cells, is decreased NF1 gene transcription. This novel ICSBP function provides insight into regulation of myelopoiesis under normal conditions and in myeloproliferative disorders.

Animals↗

PubMed2004

The use of differential display to isolate viral genomic sequence for rapid development of PCR-based detection methods. A test case using Taura syndrome virus.

The purpose of this study was to explore the efficacy of using differential display (DD) to isolate viral genomic sequence using tissues from infected organisms so that a PCR procedure to detect the pathogen may be developed rapidly. The model virus used was the Taura syndrome virus (TSV), a ssRNA virus that cause high rates of mortality at shrimp farms. Two random primers in combination with four anchored primers were used to isolate five cDNAs, ranging in size from 241 to 822 bp, that were differentially expressed in TSV-infected shrimp (Litopenaeus vannamei). PCR experiments revealed that four of the five encoded shrimp genes while the fifth was likely to be a TSV gene. Evidence that the putative TSV sequence is part of the TSV genome was obtained by the 97% sequence identity it shared with the published TSV genome. PCR primers were designed successfully using the differential display sequence to develop a RT-PCR-based method to detect TSV. Because differential display does not require physical isolation of the virus and only a small amount of infected sample is needed, the technique may be useful as a method to isolate nucleic acid sequences from emerging pathogens so that PCR primers for their detection may be developed rapidly.

Animals↗