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Biomedical subjects

Q Bi

Publications and source records attributed to Q Bi.

8 recordsLinked to original sources
PubMed2001

Construction, expression, and characterization of recombinant hirudin in Escherichia coli.

The mutant gene of HV2-K47 was obtained by polymerase chain reaction-directed mutagenesis and expressed in Escherichia coli. Many elements that could affect its expression level were compared. The product was purified to homogeneity via three chromatographic steps--ion exchange, gel filtration, and reverse phase chromatography--on the AKTA Explorer System. The anti-thrombin activity of HV2-K47 is much higher than that of recombinant HV2. Some properties and expression conditions were investigated systematically, which would be useful for further studies of hirudin and other small proteins.

Cloning, Molecular↗
PubMed2000

Re-design of Smith predictor systems for performance enhancement

In this paper, a new design for Smith Predictor systems is presented. It employs a deliberately mismatched model to enhance performance over a perfectly matched system while using a simple primary controller. The design methodology is formulated in the frequency domain as an optimization problem and it turns out that an approximate solution can be obtained using the linear least squares method. To improve the performance further, a modified Smith Predictor system structure is also proposed, and it reduces the system into one involving second-order dynamics for the primary controller design. Illustrative simulation of several typical processes are included.

Journal Article↗
PubMed2000

[Changes of leukocyte rheologic characteristics and cell adhesion molecules in patients with multiple organ failure after severe trauma].

OBJECTIVE: To explore the changes of leukocyte rheologic characteristics and of cell adhesion molecule in patients with multiple organ failure (MOF) after severe trauma. METHODS: By using the erythrocyte deformability apparatus, platelet and thrombus adhesion dual-purpose apparatus and enzyme-linked immunosorbent assay (ELISA), We measured the leukocyte deformability (LD), leukocyte adhesion function (LAF), leukocyte CD18 expression, soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule (sVCAM-1) concentration in 36 MOF patients, 31 trauma patients, and 35 to be controls. RESULTS: The leukocyte filtration index (LFI), leukocyte adhesion rate (LAR), leukocyte CD18 expression, and sICAM-1 and sVCAM-1 concentration were significantly higher in MOF patients than in controls and trauma patients (F = 68.45 - 116.20, q = 12.161 - 21.374, P < 0.00), and the changes of these indicators in MOF deaths were more obvious than those in MOF survivors (t = 6.920 - 11. 665, P < 0.00). The LFI and LAR in MOF patients were positively related to leukocyte CD18 expression, sICAM-1, and sVCAM-1 concentration (r = 0.691 - 0.844, P < 0.001); LFI was positively related to LAR (r = 0.711, P < 0.001). CONCLUSION: The abnormalities of leukocyte rheologic characteristics and CAMs might be closely related to the occurrence of MOF and the severity of pathologic changes.

Adult↗
PubMed1999

Presenilin mutations associated with Alzheimer disease cause defective intracellular trafficking of beta-catenin, a component of the presenilin protein complex.

The presenilin proteins are components of high-molecular-weight protein complexes in the endoplasmic reticulum and Golgi apparatus that also contain beta-catenin. We report here that presenilin mutations associated with familial Alzheimer disease (but not the non-pathogenic Glu318Gly polymorphism) alter the intracellular trafficking of beta-catenin after activation of the Wnt/beta-catenin signal transduction pathway. As with their effect on betaAPP processing, the effect of PS1 mutations on trafficking of beta-catenin arises from a dominant 'gain of aberrant function' activity. These results indicate that mistrafficking of selected presenilin ligands is a candidate mechanism for the genesis of Alzheimer disease associated with presenilin mutations, and that dysfunction in the presenilin-beta-catenin protein complexes is central to this process.

Alzheimer Disease↗
PubMed1999

[Cerebrovascular diseases complications after cardiac surgery].

OBJECTIVE: To assess morbidity, mortality, sorts, risk factors, prevention and treatment of patients with cerebrovascular disease complication (CVDC) undergoing cardiopulmanary bypass (CPB). METHODS: We retrospectively reviewed 10,173 cases of CPB surgery, analysed risk factors of CVDC after CPB surgery in comparison with controls. RESULTS: After CPB surgery, the general morbidity of neurological complications (NC) was 1.44% (146/10,173), of which CVDC accounted for 59.58% (87/146). In the CVDC group, cerebral embolism accounted for 39.09%, cerebral infarction 28.74%, cerebral haemorrhage 11.49%, prosthetic valve endocarditis (PVE) with CVD 10.34%, and others 10.35%. Death occurred in 44 patients of the NC group, in which CVDC went to 47.72% (21/44). Aortic clump time and CPB time were greatly longer in the CVDC group than controls (P < 0.01). CONCLUSIONS: The main postoperative neurological complications after CPB surgery are CVDC, most of which are ischemic cerebrovascular disease. Postoperative CVDC correlates with longer aortic clump time and CPB time during the operation.

Adolescent↗
PubMed1998

[Immunohistochemical study on ANP in the atria of electrocution].

By the immunohistochemical staining for ANP with LSAB method and the analysis of areas and grays of ANP with computer image analysis, it was found that the ANP granulus in right atria of electrocution were obviously depleted, compared with that in the control groups. The results showed that depletion of ANP granules in right atria could be used as a reference for the forensic diagnosis of electrocution and might benefit for the clinical therapy to the patients suffering from electric injuries.

Adolescent↗
PubMed1989

A closed-form solution for removing the dead time effects from the poststimulus time histograms.

Discharge patterns from cochlear nerve fibers contain important information about acoustic stimuli and encoding schemes of the peripheral auditory system. Yet these patterns are distorted due to refractory or dead time effects. By modeling discharges from peripheral auditory nerves as a self-exciting Poisson process, the effects of dead time on a poststimulus time histogram can be determined, assuming the recovery time does not depend on acoustic stimuli. If the recovery function is known, a closed-form formula is available to remove the dead time distortions from the poststimulus time histogram.

Action Potentials↗