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Biomedical subjects

Z Y Liu

Publications and source records attributed to Z Y Liu.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Multiprocessor study and design for digital color ultrasonic medical imaging system].

In this paper, the design of a multi-processor for digital color ultrasonic medical imaging system is discussed. It is a shared memory multiprocessor of MIMD architecture. The whole system is devided into several parts according to the complexity of the signal-processing, and each part is allocated a certain duties. Besides, the solving method of multiprocessor's bus conflicting is discussed and an architecture block diagram is given in the paper.

Equipment Design↗
PubMed1999

A minimal cytoplasmic subdomain of the erythropoietin receptor mediates erythroid and megakaryocytic cell development.

Signals provided by the erythropoietin (Epo) receptor are essential for the development of red blood cells, and at least 15 distinct signaling factors are now known to assemble within activated Epo receptor complexes. Despite this intriguing complexity, recent investigations in cell lines and retrovirally transduced murine fetal liver cells suggest that most of these factors and signals may be functionally nonessential. To test this hypothesis in erythroid progenitor cells derived from adult tissues, a truncated Epo receptor chimera (EE372) was expressed in transgenic mice using a GATA-1 gene-derived vector, and its capacity to support colony-forming unit-erythroid proliferation and development was analyzed. Expression at physiological levels was confirmed in erythroid progenitor cells expanded ex vivo, and this EE372 chimera was observed to support mitogenesis and red blood cell development at wild-type efficiencies both independently and in synergy with c-Kit. In addition, the activity of this minimal chimera in supporting megakaryocyte development was tested and, remarkably, was observed to approximate that of the endogenous receptor for thrombopoietin. Thus, the box 1 and 2 cytoplasmic subdomains of the Epo receptor, together with a tyrosine 343 site (each retained within EE372), appear to provide all of the signals necessary for the development of committed progenitor cells within both the erythroid and megakaryocytic lineages.

Animals↗
PubMed1999

Vascular cell adhesion molecule-1 expression in the renal interstitium of diabetic KKAy mice.

To investigate the mechanism of interstitial inflammation in diabetic nephropathy, we used spontaneously diabetic KKAy mice. Twelve KKAy mice were divided into two groups; six mice were fed standard mouse chow ad libitum and six mice were placed on a diet (i.e. they received the same amount of chow as six control C57BL mice). Diabetic KKAy mice developed hypercholesterolemia and albuminuria. Animals were killed at 16 weeks of age and renal tissues were immunostained for vascular cell adhesion molecule-1 (VCAM-1). In diabetic KKAy mice, the renal interstitium was infiltrated by monocytes, lymphocytes, plasma cells, and other cells. The walls of venules near the infiltrating cells were more intensely stained for VCAM-1 when compared with other sites. In contrast, the VCAM-1 staining of arterioles and peritubular capillaries was not significantly increased. There was weak VCAM-1 staining of the infiltrating cells, including lymphocytes, monocytes, and other cells. Electron microscopy demonstrated immunolabeling for VCAM-1 on the cell surface and in the cytoplasm of both infiltrating cells and vascular endothelial cells. In KKAy mice placed on a diet, there was less staining for VCAM-1 and cellular infiltration was also decreased. Thus, increased expression of VCAM-1 by the endothelial cells of venules and VCAM-1 expression by infiltrating cells were demonstrated in the interstitium of kidneys from diabetic mice. These results suggest that increased expression of VCAM-1 by endothelial cells and infiltrating cells contributes to interstitial inflammation in diabetic nephropathy.

Albuminuria↗
PubMed1999

Structural studies of initial lymphatics adjacent to gastric and colonic malignant neoplasms.

Invasion and metastases are the main causes of death from cancer, and prognosis is best correlated with invasion of malignant cells into initial lymphatics and dissemination to regional lymph nodes. Using both light and transmission electron microscopy, we examined human gastric and colonic cancers and their relation to initial lymphatics. Invasion of malignant tumor cells into the initial lymphatics was characterized by interdigitating and overlapping endothelium giving way to open junctions as lymphatic endothelial cells were apparently dissolved and destroyed. Cytoplasmic vesicles, mitochondria, and rough endoplasmic reticulum were qualitatively increased as demonstrated by image analysis.

Colonic Neoplasms↗
PubMed1998

The alpha-chemokine receptor CXCR4 is expressed on the megakaryocytic lineage from progenitor to platelets and modulates migration and adhesion.

CXCR4 is the receptor for the alpha-chemokine stromal cell-derived factor 1 (SDF-1) and has been shown to be expressed on a diversity of leukocytes. In this report, the expression of the CXCR4 receptor in cells of megakaryocytic lineage and the role of SDF-1 in megakaryocytopoiesis were investigated. Using flow cytometry in combination with reverse transcriptase-polymerase chain reaction (RT-PCR), we observed that bone marrow CD34(+), CD61(+) cells, blood platelets, and megakaryocytic leukemia cell lines all expressed the CXCR4 receptor. To examine the expression of the CXCR4 receptor on megakaryocyte progenitors (colony-forming units-megakaryocyte [CFU-Meg]), CXCR4-positive and -negative CD34(+) populations were separated from bone marrow and cultured in a plasma clot culture system. A subpopulation of the CFU-Meg was found in the CXCR4-positive fraction. The functional significance of CXCR4 expression on cells of the megakaryocytic lineage was examined by studying the effects of SDF-1alpha on migration and proliferation of megakaryocyte progenitor cells in vitro. We found that SDF-1alpha potently induced megakaryocyte progenitor migration and significantly enhanced adhesion of mature marrow megakaryocytes to endothelium. No marked effects of SDF-1alpha alone or in combination with thrombopoietin and stem cell factor/kit ligand on megakaryocyte production in vitro were noted. These results demonstrate for the first time that the CXCR4 alpha-chemokine receptor is expressed on cells of the megakaryocytic lineage from progenitors to platelets and that its ligand SDF-1alpha may modulate several aspects of megakaryocytopoiesis.

Antigens, CD34↗
PubMed1998

Human immunodeficiency virus tat modulates the Flk-1/KDR receptor, mitogen-activated protein kinases, and components of focal adhesion in Kaposi's sarcoma cells.

Kaposi's sarcoma (KS) spindle cell growth and spread have been reported to be modulated by various cytokines as well as the human immunodeficiency virus (HIV) gene product Tat. Recently, HIV-1 Tat has been shown to act like a cytokine and bind to the Flk-1/KDR receptor for the vascular endothelial growth factor A (VEGF-A), which is expressed by KS cells. We have characterized signal transduction pathways stimulated by HIV-1 Tat upon its binding to surface receptors on KS cells. We observed that stimulation in KS 38 spindle cells resulted in tyrosine phosphorylation and activation of the Flk-1/KDR receptor. We also report that HIV-1 Tat treatment enhanced the phosphorylation and association of proteins found in focal adhesions, such as the related adhesion focal tyrosine kinase RAFTK, paxillin, and p130(cas). Further characterization revealed the activation of mitogen-activated protein kinase, c-Jun amino-terminal kinase (JNK), and Src kinase. HIV-1 Tat contains a basic domain which can interact with growth factor tyrosine kinase receptors and a classical RGD sequence which may bind to and activate the surface integrin receptors for fibronectin and vitronectin. We observed that stimulation of KS cells with basic as well as RGD sequence-containing Tat peptides resulted in enhanced phosphorylation of RAFTK and activation of MAP kinase. These studies reveal that Tat stimulation activates a number of signal transduction pathways that are associated with cell growth and migration.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed1997

Signal transduction in human hematopoietic cells by vascular endothelial growth factor related protein, a novel ligand for the FLT4 receptor.

We have recently identified a novel ligand of the vascular endothelial growth factor (VEGF) family termed VEGF-related protein (VRP), which specifically binds to the FLT4 receptor. To characterize the signaling events after VRP engagement of its cognate receptor in hematopoietic cells, a population of human erythroleukemia (HEL) cells, termed HEL-JW, expressing high levels of FLT4 receptor was isolated. Stimulation of HEL-JW cells with VRP alone and in combination with the c-kit ligand/stem cell factor increased cell growth. VRP induced tyrosine phosphorylation of various proteins, including the FLT4 receptor. Further characterization of these tyrosine phosphorylated molecules revealed that Shc, Grb2, and SOS form a complex with the activated FLT4 receptor. HEL-JW cells also expressed RAFTK, a recently identified member of the focal adhesion kinase family. RAFTK was phosphorylated and activated upon VRP treatment, and there was an enhanced association of this kinase with the adaptor protein Grb2. Furthermore, the c-Jun NH2-terminal kinase (JNK), involved in growth activation and shown to mediate RAFTK signaling in other cell types, was activated by VRP stimulation. We also observed that VRP treatment of HEL-JW cells resulted in the phosphorylation of the cytoskeletal protein paxillin. This treatment resulted in an increased association of paxillin with RAFTK, which was mediated by the C-terminal region of RAFTK. These studies indicate that VRP stimulation induced the formation of a signaling complex at its activated receptor as well as activation of RAFTK. VRP-mediated activation of RAFTK may facilitate signal transduction to the cytoskeleton and downstream to the JNK pathway in FLT4-expressing blood cells.

Carrier Proteins↗
PubMed1997

Characterization of signal transduction pathways in human bone marrow endothelial cells.

Human bone marrow endothelial cells immortalized with the T antigen of SV40 (TrHBMEC) have previously been characterized by us with regard to their properties that are similar to primary marrow endothelial cells and their utility as a model system. We now report that TrHBMEC express a recently discovered signal transduction molecule termed RAFTK (related adhesion focal tyrosine kinase), also called Pyk2 or CAK-beta. RAFTK, the second member of the focal adhesion kinase (FAK) family, is known to be activated in response to calcium flux in neuronal cells and integrin stimulation in megakaryocytes and B cells. We have studied the effects of cytokines on RAFTK activation in TrHBMEC. Treatment of TrHBMEC with the vascular endothelial growth factor (VEGF), as well as the VEGF-related protein (VRP), the recently identified ligand for the FLT-4 receptor, resulted in enhanced tyrosine phosphorylation of RAFTK. Similar changes in RAFTK phosphorylation were observed upon stimulation of TrHBMEC with basic fibroblast growth factor (bFGF) or oncostatin M (OSM). Stimulation of these cells with growth factors also resulted in an increase in RAFTK activity and the c-Jun NH2-terminal kinase (JNK). RAFTK coimmunoprecipitated with the cytoskeletal protein paxillin through its C-terminal proline-rich domain in TrHBMEC. These results suggest that, in marrow endothelium, activation of RAFTK by VEGF, VRP, OSM, and bFGF represents a new element in the signal transduction pathways used by these growth factors and likely acts to coordinate signaling from their surface receptors to the cytoskeleton, thereby modulating cell growth and function.

Bone Marrow↗
PubMed1997

Cytokine signaling through the novel tyrosine kinase RAFTK in Kaposi's sarcoma cells.

A number of cytokines, including basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), oncostatin M (OSM), IL-6, and tumor necrosis factor alpha (TNF-alpha), have been postulated to have a role in the pathogenesis of Kaposi's sarcoma (KS). The proliferative effects of bFGF and OSM may be via their reported activation of the c-Jun NH2-terminal kinase (JNK) signaling pathway in KS cells. We now report that KS cells express a recently identified focal adhesion kinase termed RAFTK which appears in other cell systems to coordinate surface signals between cytokine and integrin receptors and the cytoskeleton as well as act downstream to modulate JNK activation. We also report that the tyrosine kinase receptor FLT-4, present on normal lymphatic endothelium, is robustly expressed in KS cells. Treatment of KS cells with VEGF-related protein (VRP), the ligand for the FLT-4 receptor, as well as with the cytokines bFGF, OSM, IL-6, VEGF, or TNF-alpha resulted in phosphorylation and activation of RAFTK. Following its activation, there was an enhanced association of RAFTK with the cytoskeletal protein paxillin. This association was mediated by the hydrophobic COOH-terminal domain of the kinase. Furthermore, JNK activity was increased in KS cells after VEGF or VRP stimulation. We postulate that in these tumor cells RAFTK may be activated by a diverse group of stimulatory cytokines and facilitate signal transduction to the cytoskeleton and downstream to the growth promoting JNK pathway.

Animals↗
PubMed1997

The China Productivity Project: results and conclusions.

Experiments were conducted to determine what factors cause variation in individual work output (economic productivity). Forty-five young male Chinese cycle haulers from Beijing were assessed for physiological work capacity, size and body composition, health, nutritional status, cold resistance, household social environment, and motivation. Experiments were conducted in the laboratory as well as under actual working conditions; ethnographic observations were made in the household and on the job during the Beijing winter of 1992. Overall work motivation correlated to actual monthly distance/load measures of productivity the most strongly (r = 0.518), followed by physiological capacity estimated by heart rate:speed ratio during field experiments (r = -0.473). Alcohol consumption (a negative factor), household health, and carbohydrate intake were all moderate predictors. Maximum oxygen uptake showed lower correlation (r = 0.261), and among anthropometric values only relatively long lower legs were predictive (r = 0.298). Since many of these variable categories were relatively independent of each other, multiple regression analysis showed that together they explained 61.6% of the work output variance. Simultaneous prediction by FASEM (LISREL) is also very strong.

Adaptation, Physiological↗
PubMed1997

Randomized, controlled trial of high-dose intravenous pyridoxine in the treatment of recurrent seizures in children.

To determine the efficacy of pyridoxine in treating seizures, 90 infants and children with recurrent convulsions primarily due to acute infectious diseases were enrolled in the present study. Forty patients were treated with high-dose pyridoxine (30 or 50 mg/kg/day) by intravenous infusion, and 50 subjects served as controls. Antiepileptic drugs and other therapies were similar in the two groups except for pyridoxine. Clinical efficacy criteria were based on the frequency of convulsions per day and on the duration of individual seizures after therapy was initiated. The results indicated that total response rates in the pyridoxine group and control group were 92.5% and 64%, respectively (chi-square = 14.68, P < .001). After initiation of therapy, seizures resolved after 2.4 +/- 1.4 days in the pyridoxine group and after 3.7 +/- 2.0 days in the control group (t = 3.67, P < .001). No adverse effects of pyridoxine were apparent during the observation period. We conclude that pyridoxine is an effective, safe, well-tolerated, and relatively inexpensive adjunct to routine antiepileptic drugs for treatment of recurrent seizures in children.

Anticonvulsants↗
PubMed1996

Hand and finger skin temperatures in convective and contact cold exposure.

The present study aimed at investigating the spatial variability of skin temperature (Tsk) measured at various points on the hand during convective and cold contact exposure. A group of 8 subjects participated in a study of convective cooling of the hand (60 min) and 20 subjects to contact cooling of the finger pad (5 min). Experiments were carried out in a small climatic chamber into which the hand was inserted. For convective cold exposure, Tsk was measured at seven points on the palmer surface of the fingers of the left hand, one on the palmar surface and one on the dorsal surface of the hand. The air temperature inside the mini-chamber was 0, 4, 10 and 16 degrees C. With the contact cold exposure, the subjects touched at constant pressures an aluminum cube cooled to temperatures of -7, 0 and 7 degrees C in the same mini-chamber. Contact Tsk was measured on the finger pad of the index finger of the left hand. The Tsk of the proximal phalanx of the index finger (on both palm and back sides), and of the middle phalanx of the little finger was also measured. The variation of Tsk between the proximal and the distal phalanx of the index finger was between 1.5 to 10 degrees C during the convective cold exposure to an air temperature of 0 degree C. Considerable gradients persisted between the hand and fingers (from 2 to 17 degrees C at 0 degree C air temperature) and between the phalanges of the finger (from 0.5 to 11.4 degrees C at 0 degree C air temperature). The onset of cold induced vasodilatation (CIVD) on different fingers varied from about 5 to 15 min and it did not always appear in every finger. For contact cold exposure, when Tsk on the contact skin cooled down to nearly 0 degree C, the temperature at the area close to the contact skin could still be 30 degrees C. Some cases of CIVD were observed in the contact skin area, but not on other measuring points of the same finger. These results indicated that local thermal stimuli were the temperature may require five or more measuring points. Our results strongly emphasised a need to consider the large spatial and individual variations in the prediction and modelling of extremity cooling.

Adult↗
PubMed1996

[Effect of dimethyl-4,4'-dimethoxy-5,6,5',6'-dimethylenedioxybiphenyl-2, 2'-dicarboxylate (DDB) on several phenotypes of Bel-7402 hepatocarcinoma cell line and its mechanism].

DDB is a hepatoprotectant and has been widely used for the treatment of chronic viral hepatitis in China. The drug markedly improved the abnormal liver function particularly in lowering the elevated serum transaminases in patients. It is known that there is a close correlation between primary hepatocarcinoma and chronic viral hepatitis. The aim of the present study is to evaluate the effect of DDB on hepatocarcinoma cell line. The results showed that the growth and clonogenicity of Bel-7402 human hepatocarcinoma cell line cultured with DDB were markedly inhibited. The nucleoles of the cells treated with DDB disappeared or their numbers and nucleus/cytoplasm ratio decreased under electron microscopic observation. DDB at the concentration of 10(-4) mol.L-1 significantly increased the contents of cAMP and calmodulin (CaM) in Bel-7402 hepatocarcinoma cells. DDB was also found to inhibit topoisomerase II activity of Bel-7402 hepatocarcinoma cells. These results suggest that the mechanism of inhibition of DDB on several phenotypes of Bel-7402 cell line may be related to its effect on cAMP and CaM content as well as topoisomerase II activity.

Antineoplastic Agents↗
PubMed1995

Experimental tracheal allograft revascularization and transplantation.

The feasibility of tracheal allotransplantation with a fascial vascular carrier was examined in three groups with varied dose sequences of immunosuppression. A control group (group 1) received no medication. The three experimental groups were given daily cyclosporine intramuscular doses of 5 mg/kg (group 2), 5 mg/kg plus 3 mg/kg methylprednisolone (Solu-Medrol) (group 3), and 10 mg/kg (group 4) for 6 weeks or until death. Grafts were assessed by silicone dye infusion of the artery of the fascial flap to examine their microcirculation and by quantitative histologic study. Group 1 evidenced complete rejection after a heterotopic revascularization period of 14 days. The allografts of the experimental groups remained viable after 14 days of revascularization and could be transplanted orthotopically after this period. After transplantation, the viability of group 2 tracheas was unpredictable with changes ranging from mild to complete rejection. Group 3 evidenced well-preserved transplant viability with infection-induced necrosis at the anastomoses caused by the corticosteroid component. All group 4 animals survived the follow-up period with normal allograft viability. Cyclosporine in a dosage of 10 mg/kg per day can effectively suppress the immune response after transplantation of vascularized tracheal allografts. This experimental model will allow future studies to examine airway wall immunogenicity.

Acute Disease↗
PubMed1994

Tissue specific expression of human erythropoietin receptor in transgenic mice.

We have made transgenic mice using the human erythropoietin receptor (hEpoR) encoding gene contained within a 15-kb DNA fragment. The transgenic mice that incorporated the hEpoR transgene into the genome were analyzed for tissue specific expression of hEpoR mRNA using reverse transcriptase and DNA amplification. In the control animals, endogenous EpoR transcripts were identified in bone marrow and spleen; no transcripts were detected in heart, kidney, liver, or brain. In the transgenic mice, hEpoR transcripts were detected in bone marrow and spleen but not in heart, kidney, or liver, suggesting that the transgene contains sufficient genetic information to direct appropriate expression in hematopoietically active tissues. The hematological parameters of the transgenic mice were within normal limits, consistent with the relatively low level of hEpoR transcripts detected. Surprisingly, hEpoR transcripts but not mouse EpoR transcripts were detected in the brains of the transgenic mice. Brain hEpoR transcripts were observed in all transgenic mice assayed, indicating that transgene expression in the brain did not result from the effects of aberrant integration sites. Comparable expression of the transgene was also observed in the embryonic brain. Interestingly, we observed significant expression of the endogenous EpoR gene in the early embryonic brain (Day 10) of normal mice at levels comparable to that observed in the adult spleen and bone marrow. The level of endogenous EpoR expression in the brain decreased during embryonic development to nondetectable levels prior to birth preceding the decrease of endogenous EpoR expression in the fetal liver, while hEpoR expression in the brains of transgenic mice persisted throughout embryonic development into adulthood. These data suggest that the hEpoR transgene contains appropriate regulatory sequences to direct tissue specific expression in tissues associated with hematopoietic activity and in the embryonic brain, but lacks the control elements to provide levels of expression comparable to that of the endogenous gene or to selectively silence brain expression in the adult mouse.

Animals↗