Biomedical subjects
Publications and source records attributed to X Cao.
From 1987 through 1990 we used the compound flap formed by the lateral leg flap, the fibula, and its surrounding soft tissues, pedicled on the distal peroneal vessels, to reconstruct heel and calcaneus defect in two patients. Both were successful and functionally good.
Intracellular pH (pHi) is an important regulator of vascular smooth muscle cell (VSMC) tone, contractility, and intracellular Ca2+ concentration. Among the multiple transport processes that regulate VSMC pHi, Na(+)-independent Cl-/HCO3- exchange is the major process that acidifies VSMCs in response to an alkaline load. Here, we characterize, in native and cultured VSMCs, the expression of the AE family of band 3-related anion exchangers, the best studied of these Cl-/HCO3- exchangers. A 4.2-kb AE2 mRNA was present in aorta and in all cultured VSMCs tested. Cultured VSMCs and aorta both expressed a approximately 165-kDa AE2 polypeptide, but a approximately 115-kDa polypeptide was the major AE2-related protein in aorta. AE3 mRNA levels in VSMCs and in arterial tissue were significantly lower than those for AE2, but AE3 or related polypeptides were readily detected by immunoblot and immunolocalization experiments. The approximately 125-kDa AE3 polypeptide was present in an immortalized aortic VSMC line, but the predominant AE3 epitope in aorta and most cultured cells was associated with a polypeptide of M(r) approximately 80 kDa. These data demonstrate the expression in native arteries and in VSMCs of products of the AE2 and AE3 genes, which may contribute to Na(+)-independent Cl-/HCO3- exchange activity in these tissues and cells.
Considerable controversy surrounds the role of protein kinase C (PKC) in ischemic preconditioning (PC). Previous studies have used pharmacological agents and/or measured total myocardial PKC activity; however, no information is available regarding the effects of PC on individual isoforms in vivo. We performed a comprehensive evaluation (using Western immunoblotting) of the expression and subcellular distribution of all 11 currently known PKC isoforms in the heart of conscious rabbits subjected to four different ischemic PC protocols known to induce early and/or late PC (one, three, or six cycles of 4-minute coronary occlusion [4'O]/4-minute reperfusion [4'R]; four cycles of 5-minute occlusion [5'O]/10-minute reperfusion [10'R]). Ten PKC isoforms (alpha, beta1/beta2, gamma, delta, epsilon, zeta, eta, iota, lambda, and mu) were found to be expressed in the rabbit heart. Quantitative immunoblotting demonstrated that as a subgroup, conventional PKCs (cPKCs) are more abundant than novel PKCs (nPKCs) (1445 versus 313 pg PKC/microg tissue protein, respectively) and that PKC alpha is the predominant isoform among the cPKCs (alpha, beta1, beta2, and gamma), representing 51% of this subgroup, and PKC epsilon is the most abundant among the nPKCs (delta, epsilon, zeta, and eta), accounting for 62% of this subgroup. None of the ischemic PC protocols examined caused appreciable changes in total PKC activity, in the subcellular distribution of total PKC activity, or in the subcellular distribution of PKC isoforms alpha, beta1/beta2, gamma, delta, zeta, iota, lambda, and mu. In contrast, all PC protocols caused significant translocation of PKC epsilon and PKC eta isoforms from the cytosolic to the particulate fraction. The particulate fraction of PKC epsilon increased in a dose-dependent fashion with the number of occlusion/reperfusion cycles performed, from 35+/-2% in the control group to 43+/-2% after one 4'O/5-minute reperfusion (5'R) cycle (P<.05), 52+/-2% after three cycles (P<.05 versus one cycle), and 66+/-3% after six cycles (P<.05 versus three cycles). The particulate fraction of PKC epsilon also increased, after four 5'O/10'R cycles, to 50+/-3% (P<.05 versus control). In contrast to PKC epsilon, the translocation of PKC eta was independent of the number of occlusion/reperfusion cycles performed. The particulate fraction of PKC eta increased from 67+/-3% in the control group to 84+/-2% after one 4'O/5'R cycle (P<.05), 84+/-2% after three 4'O/4'R cycles (P<.05), 86+/-3% after six 4'O/4'R cycles (P<.05), and 83+/-2% after four 5'O/10'R cycles (P<.05). When expressed as a percentage of control values, the increases in the particulate fraction of isoform epsilon were greater than those of isoform eta. The effects of 4'O without reperfusion were similar to those of one cycle of 4'O/5'R, indicating that 5'R did not attenuate isoform translocation. This is the first study to demonstrate PKC translocation after ischemic PC in vivo. The results indicate that in the conscious rabbit, ischemic PC causes selective translocation of the epsilon and eta isoforms without demonstrable changes in total myocardial PKC activity, implying that measurements of total PKC activity are not sufficiently sensitive to detect the involvement of PKC in PC. The results are consistent with the concept that the epsilon and eta isozymes play an important role in the genesis of ischemic PC in the conscious rabbit.
Injections of parathyroid hormone (PTH) have been reported to stimulate skeletal accretion through increased bone formation in several species, and osteoblast proliferation is a critical component of bone formation. However, the biological mechanisms of PTH-stimulated bone cell proliferation are largely unknown. In this study, we demonstrated that PTH stimulates proliferation of the osteoblast precursor cell line, TE-85, in association with increasing cdc2 protein levels and its kinase activity. cdc2 antisense oligonucleotides blocked PTH-induced DNA synthesis and cell cycle progression. Analysis of the time course of PTH-stimulated cdc2 message levels demonstrated that cdc2 mRNA levels were increased 1.5- to 4-fold between 3-18 h following release from cell synchronization. Transfections of TE-85 cells with a series of cdc2 promoter-luciferase deletion constructs revealed PTH stimulation of the cdc2 promoter. Promoter constructs containing a mutation in the E2F binding site were not stimulated by PTH. Gel mobility shift assays demonstrated increased free E2F levels in TE-85 nuclear extracts in response to PTH. Furthermore, the ratios of hyperphosphorylated to hypophosphorylated forms of Rb protein were increased by PTH treatment. These results demonstrate that PTH-stimulated cdc2 expression was associated with TE-85 cell proliferation and that the mechanism of stimulating cdc2 gene expression involved increasing the levels of free E2F.
OBJECTIVE: To understand radiation-induced cell kinetic changes of human nasopharyngeal carcinoma CNE cells and clarify cell biology basis of repopulation. METHODS: Either exponential growing stage or plateau stage human nasopharyngeal carcinoma CNE cells were measured by BrdUrd/DNA bivariate flow cytometry for phase fraction, BrdUrd labeling index, S phase duration, potential doubling time (Tpot), etc. Correlation analysis of Tpot with other kinetic parameters was made. RESULTS: (1) For exponentially growing CNE cells, shortening of Tpot after irradiation was closely correlated with increased BrdUrd labeled S phase fraction (P < 0.05), whereas no correlation was found between Tpot and other kinetic parameters measured; (2) for plateau stage CNE cells, shortening of Tpot with various radiation doses was closely correlated with decreased G0/G1 phase fraction (P < 0.05) and increased G2M phase fraction (P = 0.002), whereas no correlation was found between Tpot and other parameters measured. CONCLUSION: In a range of 0-8 Gy of irradiation, an increased accelerated repopulation rate was resulted from increasing radiation dose. Recruitment of G0 cells into cell cycle might play a major role in radiation-induced accelerated repopulation for plateau stage CNE cells, while it was contributed by an increased DNA synthesis manifested by an increased BrdUrd labeled S phase fraction for exponential growing CNE cells.
OBJECTIVE: To investigate the effect of Ad-IL-2 and Ad-IL-3 on immunological recovery. METHODS: The Ad-IL-2 and/or Ad-IL-3 were i.p. injected into C57BL/6 mice having received high dose cyclophosphamide (200 mg/kg) 24 hours before. The number and cytotoxicity, Ia antigen expression of peritoneal macrophages, the proliferation and NK cell activity of splenic cells were observed. RESULTS: After i.p. injection with Ad-IL-3, the number, cytotoxicity and Ia antigen expression of peritoneal macrophagee were increased. After i.p. injection with Ad-IL-2, the proliferation and NK cell activity of splenic cells were significantly augmented. As i.p. injection with Ad-IL-2 and Ad-IL-3 simultaneously, both the peritoneal macrophages and splenic cells were activated. CONCLUSION: Intraperitoneal injection of Ad-IL-2 and Ad-IL-3 can promote immune recovery after high dose chemotherapy.
PURPOSE: We determined the efficacy of pars plana vitrectomy in a series of patients with complicated Eales disease. METHODS: Clinical records were reviewed on 47 consecutive patients (49 eyes) who underwent vitrectomy for persistent vitreous hemorrhage (PVH) and/or traction retinal detachment (TRD) with neovascular membranes (NVM). All cases were divided into 4 subgroups of eyes with PVH (without obvious NVM, n = 9), NVD (NVM from the optic disc, n = 10), NVP (peripheral NVM, n = 11), or ENV (extensive NVM and logn-standing TRD, n = 17). RESULTS: The study included 8 women and 39 men with a mean age of 27.3 years (range, 16 to 50 years). The visual acuity was light perception in 15 eyes, hand motions in 18 eyes, counting fingers in 6 eyes and 0.02 to 0.1 in 10 eyes before vitrectomy. Visual acuity improved postoperatively in all eyes with PVH, NVD of NVP with a mean visual acuity of 0.32 (range, 0.05 to 1.0, n = 28) except 3 eyes unchanged. There was no significant difference (P > 0.05) in the patient age, preoperative visual acuity, or visual improvement after vitrectomy among these 3 subgroups. In the eyes with ENV, however, postoperative visual improvement was obtained but limited in 9 eyes (range, 0.02 to 0.15). Visual acuity was unchanged in 9 eyes. There was a significant difference (P < 0.01) in postoperative visual acuity between the eyes with ENV and the eyes with PVH, NVD or NVP. CONCLUSIONS: Vitrectomy with removal of persistent vitreous hemorrhage and focal neovascular membranes and endolaser photocoagulation may lead to improved visual acuity in the majority of eyes with Eales disease. However, extensive fibrovascular membranes and long-standing retinal detachment result in poor visual outcome. Earlier surgery can be considered to prevent visual loss in the patients.
OBJECTIVE: To investigate the antitumor mechanism of interleukin-2 (IL-2) and interleukin-6 (IL-6) gene therapy. METHODS: IL-2 DNA liposome and IL-6 DNA liposome were i. p injected into EL-4 lymphoma-bearing mice. The function of macrophages from the mice was assayed. RESULTS: The cytotoxicity, the MHC Ia expression and IL-1 and TNF secretion of the macrophage were all augmented after i.p injection of IL-2 or IL-6 DNA liposomes, and more efficient activation was observed in the mice treated with IL-2 DNA liposome. IL-2 combined with IL-6 gene therapy showed the maximal activation of macrophages from the lymphoma-bearing mice. CONCLUSION: IL-2 and IL-6 gene therapy can relieve the suppression of macrophages of the lymphoma-bearing mice, and activate the antitumor immune responses efficiently.
OBJECTIVE: To investigate the anti-leukemia activity of IL-2 and IL-3 genes co-transfected leukemia vaccine. METHODS: The vaccine was prepared with FBL-3 erythroleukemia cells which were in vitro transfected with IL-2 and/or IL-3 genes by recombinant adenovirus and then inactivated by 60Co irradiation. The vaccine was injected peritoneally into FBL-3 leukemia mice, and the tumor growth, survival time of the mice, cytotoxicities of the peritoneal macrophages, splenic NK cells and CTL cells were observed. RESULTS: A fter treatment with the vaccine, the leukemic cell tumor in the mice showed significant growth inhibition and the survival time of the mice were prolonged when treated with IL-2 transfected vaccine, the cytotoxicities of splenic NK and CTL were increased significantly, while in the case of IL-3 transfected vaccine, the number and cytotoxicity of peritoneal macrophages were increased. The antileukemia effect was augmented when treated with IL-2 and IL-3 genes co-transfected vaccine. The antileukemia activity of the vaccine was also augmented by low dose cyclophosphamide administration. CONCLUSION: Leukemia vaccine gained more antitumor effect via induction of antitumor immunity.
The P300 component of evoked potential can reflect cognitive state in dementia patients. The purpose of this study was to investigate the value of P300 as an indicator of cognition in Binswanger's disease (BD) and to explore the possible causes of dementia in BD patients. P300 was measured at Cz site in 21 patients with BD and 21 controls matched with age, sex, handedness, and education. This measurement included P300 latency and amplitude. All patients were also given WAIS-RC test and scanned with computerized tomography (CT), and were treated with hyperbaric oxygenation (HBO). The relationships among P300, CT and WAIS-RC score were studied. BD patients had significantly prolonged P300 latency and a tendency of low amplitude P300, but the amplitude difference was not significant compared with controls. P300 latency was found to be negatively correlated with WARS-RC scale, and positively correlated with the change of white matter low attenuation (WMLA). WMLA was also correlated with WAIS-RC score. Treatment with HBO reduced P300 latency and had effect on the cognitive part of P300 but had no effect on CT changes. The significant association between neurophysiological and neuropsychological measurement suggests that P300 measurement reflects a disrupted aspect of cognitive function in BD patients, and it may be a useful means to assess the degree of subcortical cognitive deterioration and the effect of therapy. White matter lesion in BD is concerned to the occurrence of dementia by disturbing axonal conduction.
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OBJECTIVE: To investigate the induction of antitumor immune response and therapeutic effects of the vaccination with the fused cells between tumor cells and GM-CSF gene -modified dendritic cells. METHODS: The dendritic cells were isolated from the spleens of C57BL/6 mice, infected with GM-CSF adenovirus, and then fused with B16 murine melanoma cells. The positive fused cells were enriched by magnetic cell sorting with anti-Ia antibody and adherent culture. The protective and therapeutic effects of the vaccination with the fused cells were investigated. RESULTS: Vaccination with the inactivated fused cells induced more potent CTL activity against parental B16.F10 cells, and led to the resistance against the rechallenge of alive parental B16.F10 cells. After treatment with the inactivatedly fused cells, the survival time of the tumor-bearing was mice greatly extended and the metastatic tumor nodules on the pulmonary surfaces reduced. CONCLUSIONS: Vaccination with the fused cells between tumor cells and dendritic cells could elicit potent antitumor responses, and combined with GM-CSF gene transfection, more potent results can be achieved.
In this paper, we propose an iterative algorthm called FAHE., which is based on the relativity between the current local histogram and the one before the sliding window moving. Comparing with the basic AHE, the computing time of FAHE is decreased from 5 hours to 4 minutes on a 486dx/33 compatible computer, when using a 65 x 65 sliding window for a 512 x 512 with 8 bits gray-level range.
OBJECTIVE: To investigate the generation of dendritic cells and the change of antigen-presenting function during the differentiation of FBL-3 erythroleukemia cells induced by GM-CSF. METHODS: The effects of GM-CSF on the phenotype, ultrastructure and antigen-presenting function of FBL-3 erythroleukemia cells were observed by FACS, electromicroscopy and 51Cr-release assay. RESULTS: After treatment with 100 ng/ml GM-CSF for 3 days, the expressions of 33 D1 and NLDC 145 which are the specific markers on dendritic cells were increased significantly; MHC-II B7-1, B7-2, ICAM-1, VCAM-1 and CD40 were also upregulated. The membrane of FBL-3 cells was changed into villous surface with dendritic projections. There were plenty of mitochondria in cytoplasm, the nucleus became lobulated. The GM-CSF-treated FBL-3 cells could apparently stimulate the proliferation of allogeneic T lymphocytes, induce the production of IL-2 and improve the specific cytotoxic activity of CTL on FBL-3 cells. CONCLUSION: Erythroleukemia cells were induced to differentiate into the dendritic cells by GM-CSF and obtained the antigen-presenting function.
In order to observe the collateral sprouting capacity of the nerve trunk after end-to-side anastomosis, a window was made on the epineurim of the donor nerve through which the result of the end-to-end anastomosis of nerves could be compared. Sixteen SD rats were chosen and divided into 4 groups randomly. Group 1, the peroneal nerve was severed, the epineurium of the tibial nerve was fenestrated and sutured the peroneal stump with the tibial nerve by end-to-side neurorrhaphy. Group 2, operative procedures were almost the same as that of Group 1, but no fenestration on the epineurium was done. Group 3, the distal peroneal nerve stump was sutured in paralell with the tibial nerve without fenestration on the tibial nerve and Group 4, severed the peroneal nerve and sutured the stumps by end-to-end anastomosis immediately. The peroneal function index(PFI) and acetylcholine transferase (ChAT) activity were assessed and the histological examination was performed in all rats. The results showed: between group 1 and 2, there was no difference in PFI and ChAT activity (P > 0.05). The existence of collateral sprouting in all groups was proved by histological examination. Even in Group 3, there were plenty of nerve fibers turned into tiny myelined nerve fibers through collateral sprouting. But the ChAT activity in Group 1 was only two thirds of that in Group 4. It was suggested that the epineurial sheath did not influence the collateral sprouting of the nerve.
The capacity of osteoclasts to resorb bone depends, in part, on the surface expression of the integrin alpha v beta 3. We have investigated whether the steroid hormone retinoic acid, known to stimulate bone resorption, regulates the appearance of the alpha v beta 3 complex in avian osteoclast presursors. Using surface labeling, followed by immunoprecipitation with a alpha v beta 3-specific antibody, we show that retinoic acid increases surface expression of the heterodimer in a dose- and time-dependent manner. Northern analysis reveals that the high basal steady-state levels of alpha v mRNA do not change, while those for beta 3 rise significantly from their initially low levels. Nuclear run-on studies confirm that steroid treatment stimulates transcription of the beta 3, but not the alpha v gene. Osteoclast precursors treated with retinoic acid exhibit increased multinucleation and expression of the osteoclast marker enzyme tartrate-resistant acid phosphatase. However, the fused cells do not have an increased capacity to resorb bone. In summary, multinucleated cells generated in this study do not represent fully differentiated bone-resorbing polykaryons. These results suggest that treatment of osteoclast precursors with retinoic acid is necessary, but insufficient, for expression of the mature osteoclast phenotype.
In Swiss 3T3 fibroblasts, basic fibroblast growth factor (bFGF) stimulates the unique tyrosine phosphorylation of a protein complex around 90 kDa, as ascertained by high resolution 2-D PAGE and anti-phosphotyrosine blotting. The majority of this complex consists of the protein(s) designated previously as SNT (suc1-associated neurotrophic factor target). Tyrosine phosphorylated SNT binds to both p13suc1 protein and the SH2 domain of Grb2. Binding of SNT to Grb2 is likely to be mediated through the consensus binding motif, pYXN, on SNT. The binding of SNT to p13suc1 is independent of the pYXN motif. Tyrosine phosphorylated SNT is localised in the plasma membrane where it could form a complex with Grb2 and Sos, enabling the initiation of a novel FGF-specific signalling pathway.
We have identified a novel steroid hormone response element in the avian beta3 integrin promoter. This sequence, comprising three hexameric direct repeat half-sites separated by nine and three nucleotides binds vitamin D receptor (VDR)-retinoid X receptor (RXR) and retinoic acid receptor (RAR)-RXR heterodimers. VDR-RXR binds direct repeats separated by three base pairs, and RAR-RXR recognizes half-sites separated by nine bases, whereas the central half-site interacts with both heterodimers. Retinoic acid and 1, 25-dihydroxyvitamin D3 activate both a genomic fragment including the transcriptional start site and an oligonucleotide containing the three repeats, linked to a heterologous promoter. Co-addition of the steroids produces neither synergy nor an additive effect; rather the result equals that for retinoic acid alone. Scatchard analysis demonstrates that RAR-RXR has greater affinity than VDR-RXR for the composite element. Based on these findings we propose a model in which there is specific, polarity-defined binding of VDR-RXR and RAR-RXR to three half-sites, which form two overlapping steroid response elements, with the central half-site common to both. Our results identify a novel mechanism by which one steroid hormone can modulate the activity of a second, by competing for a shared half-site in a composite response element.