Biomedical subjects
Publications and source records attributed to X Fei.
Due to the regularity of activity of the heart and similarity among each period of ECG signal, there is high correlation between DCT coefficients of every two frames of ECG data. Using this characteristic, we present a compression method for ECG data in this paper, by which we can get a higher compression ratio(CR) than the compression method just via DCT does.
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The lats gene has been identified as a tumour suppressor in Drosophila melanogaster using mosaic screens. Mosaic flies carrying somatic cells that are mutant for lats develop large tumours in many organs. The human LATS1 homologue rescues embryonic lethality and inhibits tumour growth in lats mutant flies, demonstrating the functional conservation of this gene. Biochemical and genetic analyses have revealed that LATS1 functions as a negative regulator of CDC2 (ref. 3). These data suggest that mammalian LATS1 may have a role in tumorigenesis. To elucidate the function of mammalian LATS1, we have generated Lats1-/- mice. Lats1-/- animals exhibit a lack of mammary gland development, infertility and growth retardation. Accompanying these defects are hyperplastic changes in the pituitary and decreased serum hormone levels. The reproductive hormone defects of Lats1-/- mice are reminiscent of isolated LH-hypogonadotropic hypogonadism and corpus luteum insufficiency in humans. Furthermore, Lats1-/- mice develop soft-tissue sarcomas and ovarian stromal cell tumours and are highly sensitive to carcinogenic treatments. Our data demonstrate a role for Lats1 in mammalian tumorigenesis and specific endocrine dysfunction.
The aim of this study was to observe the morphological changes of muscle in the process of rigor mortis. The quadriceps of 40 rats at various postmortem intervals were observed under the scanning electron microscope (SEM) and the light microscope by phosphotungstic acid-haematoxylin (PTAH) stain. The results showed that the striations of muscle were blurred within 4 h, but they became apparent from 6 h to 24 h after death. The authors suggest that this phenomenon be associated with the increased resistance of muscle against the postmortal changes. The observations by scanning electron microscopy and light microscopy have revealed that the muscles do contract in the process of rigor mortis because the distance between two Z lines shortens and the 1 band narrows, compared with those in anaesthetised animals. The basic biochemical process for the formation of rigor mortis is the same as that of muscle contraction except that the former happens postmortem and the latter antemortem.
Our study indicates that when small pieces of lung or muscles of chest wall are cultured, erythrocytes and leukocytes (PMNs) leave the tissues first, followed by vascular endothelial cells (ECs). Fibroblasts and other mixed cells grow after 72 hr culture. The ECs can then be isolated avoiding mechanical and chemical injuries. The lung tissue is obtained from the peripheral surface and muscles from the chest. It is then cut into pieces and cultured with DMEM containing 20% fetal bovine serum. After 60 hr culture, the tissues are discarded. The flask contains only ECs and blood cells. Blood cells can be cleared out after the cells are subcultured once or twice. The primary cells and the subcultured cells cultured on gelatinized culture dish give the capillary-like structure. Cells cultured on untreated dishes have regular cobblestone morphology and junctional contacts. The isolated cells were not mesothelial cells because the cells did not react to antibody against cytokeratin 18, while mesothelial cells reacted strongly to the antibody. The cells can be isolated from the lung tissue without pleura. The primary microvascular ECs are also cultured on microcarriers (cytodex 3). Because both mechanical and proteolytic injuries are avoided, the cells may be more similar to cells in the in vivo state. There are no significant differences in PMN-endothelium adherence and monolayer responses to second messengers, platelet activating factor, and phospholipase A2 when pulmonary and muscular microvascular endothelial cells are compared.
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A study on the suppressive effect of interferon on the formation of filtering surgical scar was carried out. Trabeculectomy was performed on 6 rabbit eyes. 100,000 Units of interferon were subconjunctivally injected at the filtering bleb during the operation and on the 3rd and 7th post-operative day. The filtering blebs, filtering function and the scanning electron microscopic examinations of the surgical areas of the walls of the globes were observed. The results show that interferon can reduce the scar, improve filtering function and can be tried clinically.
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The effect of pentoxifylline (Pen) on platelet activating factor (PAF)-induced pulmonary injury was studied in isolated guinea pig lungs perfused with cell-free Tris buffered Ringer solution. PAF (1.0 nmol.L-1) increased lung weight and pulmonary filtration coefficient (Kf), which indicated the formation of high permeable pulmonary edema. Pen (0.5 and 1.0 mmol.L-1) markedly attenuated the PAF-induced increment of lung weight and vascular permeability, but not the increment of pulmonary capillary pressure and venous resistance. There was no correlation between the severity of lung edema and the number of leukocytes in the perfusates. These results suggest that Pen has direct anti-permeability effect on pulmonary microvessels.
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The neuronal cell surface is believed to carry a mitogenic signal for peripheral glial cells. We have purified a mitogen from fetal bovine brain membranes that, in common with the PNS neuronal mitogen, stimulates the proliferation of Schwann cells in vitro and binds heparin. The purified mitogen has an apparent molecular weight of 50,000 daltons as estimated by elution of activity from non-reducing polyacrylamide gels. Since the developing central nervous system is a rich source of mitogen, we tested whether the protein is mitogenic for one or more cell types isolated from the developing brain. Purified mitogen was added to enriched cultures of astrocytes or developing oligodendrocytes, or to microglial cells. The analyses demonstrated that the protein is mitogenic for developing oligodendrocytes but not astrocytes or microglial cells. These results suggest that during development a membrane-associated mitogen present in the brain might regulate the proliferation of developing oligodendrocytes, and consequently, the population size of oligodendrocytes in the brain.
One of the major problems in extensive burns is the relative lack of available donor sites for skin grafting. Keratinocyte cell culture in the laboratory was carried out successfully in Singapore General Hospital and shows promise as an alternative source for skin replacement. Our experience further proved that a fibroblast base is necessary for keratinocyte cell culture. It is observed that heterogenous cell source can grow concurrently and become confluent. The colony forming efficiency from trypsinized skin is about 1-4% in primary cultures and 35-40% in secondary cultures. The time taken to reach confluency are 20-21 days and 10-12 days respectively. The thickness of cultured skin is estimated as 0.5 mm (5-6 layers) under light microscope. The size of the harvested cultured skin is approximately one third of the cultured area due to contraction. The expansion ratio before shrinkage is estimated to be approximately 6000-fold based on our data.
Intravenous injection of E. coli endotoxin 30 mg/kg to rats resulted in a systemic hypotension and rapid decrease in mesenteric arteriolar blood flow velocity (MABFV). The mesenteric arterioles constricted within 3 min followed by a short period of vasodilation after endotoxin administration. Pretreatment with the platelet-activating factor receptor antagonist SRI 63-441 attenuated the endotoxin-induced systemic hypotension and the decrease in MABFV, and abolished the mesenteric vasodilation effect of endotoxin infusion. The results suggest that PAF may be a mediator of endotoxic shock.
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Lung injury induced by phospholipase A2 (PLA2, 0.046 IU/ml perfusate) was studied in a continuous weighing system of isolated perfused guinea pig lungs. The results revealed that lung weight increased progressively during the 30-min perfusion of PLA2. No change of pulmonary arterial pressure was observed in the same period. Albumin permeability-surface area product, lung index, lung water content, exudate from pleura, and angiotensin-converting-enzyme activity increased significantly at the end of 30 min PLA2 perfusion. p-Bromophenacyl bromide, a PLA2 inhibitor, may block the above changes nearly completely. The effects of inhibitors of cyclooxygenase (indomethacin, IM), lipoxygenase (diethylcarbamaxine, DE), and platelet-activating factor (SRI 63-441) on PLA2-induced lung injury were also studied. We found: (1) PLA2 may induce high permeability lung edema. The role of endothelial injury in the permeability change remains to be further investigated. (2) DE ameliorated lung injury significantly within 10 min of PLA2 treatment but showed no effect after 15 min. IM ameliorated lung injury during the whole experimental period. SRI 63-441 had no effect. It is suggested that PLA2 may damage lung by inducing products of cyclooxygenase and lipoxygenase besides its direct effect.
The actions of platelet-activating factor (PAF) on rat mesenteric microcirculation were studied by laser Doppler microscopy in vivo. PAF 0.2 -0.6 micrograms/kg iv produced a dose-related decrease in the blood flow velocity and an increase in the diameters of the mesenteric arterioles and venules. These responses were completely reversed by pretreatment with PAF receptor antagonist SRI 63441. The results suggest that PAF may be a mediator of microcirculatory disturbances in the disease conditions associated with excessive PAF release.