Biomedical subjects

Bo Yan

Publications and source records attributed to Bo Yan.

23 records · Page 2Linked to original sources

PubMed2003

[Studies on direct and indirect economic burden of disease and related factor in countryside of Qingdao city in 2001].

OBJECTIVE: To study the condition of economic burden of disease in the countryside and to explore the related factors. METHODS: Human capital method and two-step method were used in the calculation of economic burden of disease. RESULTS: The total economic burden of disease among 3359 persons was 3072 225 Yuan. Noncommunicable conditions were accounted for 62.95%, while communicable disease, maternal and perinatal conditions accounted for 24.25%, and injury accounted for 9.83% respectively. The direct economic burden of disease was 1,559,619 Yuan and the indirect economic burden of disease was 1,472,606 Yuan. The economic burden of disease for each person was 914 Yuan. The equal burden of disease among patients with disability and without disability were 3070 Yuan and 680 Yuan respectively (P < 0.001). There was significant difference among different age groups. The influencing factors were found to include having noncommunicable disease, age, disability and the condition of marriage. CONCLUSION: Corresponding policy to cope with conditions of different age groups needs to be developed to reduce the economic burden of disease in the countryside.

Absenteeism↗

PubMed2003

[Hearing impairment in senile dementia of Alzheimer's type].

OBJECTIVE: To evaluate the pure tone hearing threshold and word recognition score of senile dementia of the Alzheimer's disease (AD) patients, and to analyze the relationship between hearing loss and the cognition impairment. METHODS: Pure tone audiometry, word recognition score (WRS), acoustic immittance and auditory brainstem response (ABR) are used to evaluate the auditory function of 43 patients with AD and 50 subjects of the control group. The confounding factors are controlled. RESULTS: The average age of 43 dementia patients was 72.7 +/- 6.4, and 69.7% was female. Bilateral hearing thresholds are similar in all subjects. All indices but Mini-mental scale of equastionnaire (MMSE) of patients and control group were not statistically different. There was no significant difference in pure tone audiometry (PTA), PTA2 (dB HL, mean +/- s) and WRS (%, mean +/- s) between the two groups (P > 0.05), therefore the hearing threshold of AD group (PTA = 26.3 +/- 8.5, PTA2 = 29.1 +/- 8.7, WRS = 85.5 +/- 15.5) is lower than that of control group (PTA = 23.2 +/- 10.6, PTA2 = 26.2 +/- 11.8, WRS = 87.6 +/- 16.8). No significant difference was found between the two groups in audiometry reliability, acoustic immittance and ABR (P < 0.05). CONCLUSION: No significant difference was found between the peripheral hearing dysfunction of AD patients and that normal elderly people, i.e., PTA, PTA2 and WRS were not related to MMSE.

Aged↗

PubMed2002

The human acid alpha-glucosidase gene is a novel target of the Notch-1/Hes-1 signaling pathway.

Acid alpha-glucosidase (GAA) is a lysosomal enzyme that degrades glycogen. A deficiency of GAA is responsible for a recessively inherited myopathy and cardiomyopathy, glycogenosis type II. Previously, we identified an intronic repressor element in the GAA gene and demonstrated that Hes-1, a basic helix-loop-helix factor, binds to a C class E box within the element and functions as a transcriptional repressor in HepG2 cells. Hes-1 is a well studied downstream target gene in the Notch signaling pathway. In this study, over-expression and depletion of Notch-1 intracellular domain (NICD) strategies were used to investigate whether expression of the GAA gene is under the control of Notch-1/Hes-1 signaling. In co-transfection experiments, Hes-1, up-regulated by over-expressed NICD, enhanced the repressive effect of the DNA element with wild type Hes-1 binding sites but not with mutant Hes-1 binding sites. Conversely, depletion of Notch-1 with phosphorothioated antisense oligonucleotides, corresponding to the fourth ankyrin repeat within NICD, led to reduced Hes-1. Constitutively over-expressed Hes-1 and Notch-1 repressed GAA gene expression. Therefore, our data establish that the human GAA gene, encoding a lysosomal enzyme, is a downstream target of the Notch-1/Hes-1 signaling pathway.

Base Sequence↗

PubMed2002

Hes-1, a known transcriptional repressor, acts as a transcriptional activator for the human acid alpha-glucosidase gene in human fibroblast cells.

Hes-1, the mammalian homologue 1 of Drosophila hairy and Enhancer of split proteins, belongs to a family of basic helix-loop-helix proteins that are essential to neurogenesis, myogenesis, hematopoiesis, and sex determination. Hes-1 is a transcriptional repressor for a number of known genes including the human acid alpha-glucosidase (GAA) gene as we have previously shown in Hep G2 cells. The human GAA gene encodes the enzyme for glycogen breakdown in lysosomes, deficiency of which results in Glycogen Storage Disease type II (Pompe syndrome). Using constructs containing the DNA element that demonstrates repressive activity in Hep G2 cells and conditions in which the same transcription factors, Hes-1 and YY1, bind, we have shown that this element functions as an enhancer in human fibroblasts. Site-directed mutagenesis and overexpression of Hes-1 showed that Hes-1 functions as a transcriptional activator. The dual function of Hes-1 we have found is likely to contribute to the subtle tissue-specific control of this housekeeping gene.

Adult↗

PubMed2002

Fluctuations and randomness of movement of the bead powered by a single kinesin molecule in a force-clamped motility assay: Monte Carlo simulations.

The motility assay of K. Visscher, M. J. Schnitzer, and S. M. Block (Nature, 400:184-189, 1999) in which the movement of a bead powered by a single kinesin motor can be measured is a very useful tool in characterizing the force-dependent steps of the mechanochemical cycle of kinesin motors, because in this assay the external force applied to the bead can be controlled (clamped) arbitrarily. However, because the bead is elastically attached to the motor and the response of the clamp is not fast enough to compensate the Brownian motion of the bead, interpretation or analysis of the data obtained from the assay is not trivial. In a recent paper (Y. Chen and B. Yan, Biophys. Chem. 91:79-91, 2001), we showed how to evaluate the mean velocity of the bead and the motor in the motility assay for a given mechanochemical cycle. In this paper we extend the study to the evaluation of the fluctuation or the randomness of the velocity using a Monte Carlo simulation method. Similar to the mean, we found that the randomness of the velocity of the motor is also influenced by the parameters that affect the dynamic behavior of the bead, such as the viscosity of the medium, the size of the bead, the stiffness of the elastic element connecting the bead and the motor, etc. The method presented in this paper should be useful in modeling the kinetic mechanism of any processive motor (such as conventional kinesin and myosin V) based on measured force-clamp motility data.

Binding Sites↗