Initial endothelial injury and cytomegalovirus infection accelerate the development of allograft arteriosclerosis.
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Animals↗
Biomedical subjects
F Li
Publications and source records attributed to F Li.
Pathogenicity: animal models.
Animal models offer the opportunity to study the interaction of the virus and the host and to unravel the mechanism in processes such as persistence of the virus and virus-induced pathology. Primary infection results in a generalized infection as shown by the presence of virus in many organs. During viraemia the virus is present in mononuclear cells by which it is transported through the body. In neonates and in immuno-suppressed animals the infection results in multiorgan failure, leading to death. Recent data have shown that infection of endothelial cells in the microvasculature and mononuclear cells seems to be important in the pathogenesis of cytomegalovirus (CMV)-induced disease. After primary infection the virus persists in the body. Although the exact localization of the latent virus is unknown it is clear that during latency viral DNA is present in many organs. By immune suppression the virus can reactivate from its latent state. In addition to the direct complications attributable to the virus itself, CMV has modulating effects on the immune response. Although in some instances the infection leads to immune suppression, the virus infection can also accelerate inflammatory and immune responses. Studies in mice have shown that CMV infection can exacerbate graft-versus-host reactions, and experiments in rats using allogeneic transplants indicate that CMV infection results in enhanced chronic rejection in which acceleration of the immune response is involved. Although the exact mechanism is not clear, recent data indicate that cytokines, such as tumor necrosis factor alpha are involved in these processes.
Acute Disease↗
[Construction and radioimmunodetection of nude mouse xenograft of human choriocarcinoma].
Fresh tissue of human choriocarcinoma was injected subcutaneously into the BALB/C nude mouse. The xenografts had grown up with 16-68 passages. The hCG level of the ascites or intratumoral blood was 400-20,000 mIU/ml. Radioimmunodetection was performed using 131I labelled murine anti-hCG McAb. The labelled antibody could be specifically accumulated in the tumor sites and the tumor imaging was acquired. The ideal imaging time was 72-96 hours after the injection of antibody.
Animals↗
[Effect of tetrandrine on pulmonary hypertension induced by monocrotaline in rats].
The effects of Tetrandrine (Tet) on intraacinous pulmonary arteries (IAPA) and bemodynamics were studied by means of a rat pulmonary hypertension model induced by monocrotaline. The results showed that Tet could reduce the contractive pressure of pulmonary artery, right ventricle and right atrium of heart by 28.0%, 28.3%, and 31.5% respectively. It could also decrease the vascular degeneration of endoepithelial cells of IAPA, the endoepithelial subcavity, the collagens of medial membrane and the numbers of smooth muscles of IAPA.
Alkaloids↗
Expression of stromelysin-1 and TIMP-1 in the involuting mammary gland and in early invasive tumors of the mouse.
The mammary gland, during post-lactational involution, is subjected to extensive tissue reconstruction. This process is governed by the concerted expression of extracellular-matrix-degrading enzymes and their inhibitors. During carcinogenesis, the invasive growth of tumor cells is characterized by the penetration of the basement membrane and stromal invasion. We compared the expression of the tissue-remodeling enzymes stromelysin-1, a matrix metalloproteinase, and its inhibitor, tissue inhibitor of metalloproteinase-1 (TIMP-1), during mammary gland involution and carcinogenesis in mouse. In involuting mammary glands, stromelysin-1 was expressed in myoepithelial cells, whereas TIMP-1 was confined to the stromal tissue. To analyze the involvement of these tissue-remodeling genes in tumor development, we examined mammary tumors of transgenic mice expressing either the activated Ha-ras or c-myc oncogene under the control of a milk-protein gene promoter. In the undifferentiated and metastasizing Ha-ras-induced tumors, stromelysin-1 expression was comparable to that seen in involution, whereas TIMP-1 expression was greatly elevated. During Ha-ras-induced carcinogenesis, stromelysin-1 expression was first detected in the myo-epithelial cells surrounding preneoplastic lesions. In contrast, in the well-differentiated and non-metastatic mammary tumors induced by c-myc, no expression of either gene was observed. Thus, expression of stromelysin-1 and TIMP-1 is confined to the aggressively growing tumors and is induced in the earliest stages of carcinogenesis.
Animals↗
Abnormal class I assembly and peptide presentation in the nonobese diabetic mouse.
Presentation of self-antigens by major histocompatibility complex (MHC) class I molecules requires the function of the MHC class II-linked genes Tap-1 and Tap-2. Evidence suggests that interruption of self-peptide presentation results in reduced cell surface expression of MHC class I molecules and the interruption correlates with progression to diabetic autoimmunity in nonobese diabetic (NOD) mice and humans. NOD mice possess a rare Tap-1 allele (Tap-1b); this is associated with reduced Tap-1 mRNA abundance in lymphocytes from diabetes-prone females and decreased conformationally correct class I molecules on the cell surface. In this study, we demonstrate that, similar to lymphoma cell lines with mutations in Tap-1 or Tap-2, the reduced expression of class I molecules on the surface of lymphocytes from diabetes-prone female NOD mice was normalized by incubation at low temperatures or by exposure to class I allele-specific peptides. As would be expected for cells that express surface class I molecules not associated with peptide, female NOD lymphocytes were resistant to lysis by class I-restricted, peptide-specific cytotoxic T lymphocytes. Furthermore, the rate of class I exit from the endoplasmic reticulum of lymphocytes from female NOD mice was delayed as demonstrated by delayed glycosylation. Male NOD mice, which are not prone to diabetes, lacked these functional defects in class I assembly and had near-normal levels of Tap-1 mRNA and exhibited normal density of class I epitopes that were peptide filled. These results are consistent with the possibility that the rare Tap-1b allele is associated with a quantitative defect in Tap-1 expression that influences disease course.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Determination of the enantiomers of bunolol in human urine by high-performance liquid chromatography on a chiral AGP stationary phase and identification of their metabolites by gas chromatography-mass spectrometry.
A high-performance liquid chromatographic method using a chiral AGP column was developed to screen and determine the enantiomers of bunolol in human urine. The recovery of (+)- and (-)-bunolol from urine was 91.79-95.23% at different concentrations. The coefficients of variation (C.V.) were less than 2.1 and 2.3% for intra- and inter-assays, respectively. Urinary metabolites were detected using GC-MS after derivatization with N-methyl(trimethylsilyl)trifluroacetamide. The influences of pH and modifier on a chiral AGP column were studied.
Adult↗
CD34+ peripheral blood progenitors as a target for genetic correction of the two flavocytochrome b558 defective forms of chronic granulomatous disease.
Chronic granulomatous disease (CGD) can result from any of four single gene defects involving components of the superoxide (O2-.)-generating phagocyte NADPH oxidase (phox). The phox transmembrane flavocytochrome b558 is composed of two peptides, gp91phox and p22phox. Mutations of gp91phox cause X-linked CGD, whereas mutations of p22phox cause one of the three autosomal recessive forms of CGD. We used the Maloney leukemia virus-based MFG retrovirus vector to produce replication defective retroviruses encoding gp91phox or p22phox. To maximize viral titer MFG retroviruses do not contain internal promoter or resistance elements. Epstein-Barr virus transformed B-lymphocyte cell lines (EBV-B) derived from normal individuals contain phox components and produce O2-., whereas those derived from CGD patients show the CGD defect. Transduction of gp91phox or p22phox-deficient CGD EBV-B lines resulted in correction of O2-. production from a barely detectable baseline to an average 7.2% and 13.8% of normal control, respectively, without any selective regimen to enrich for transduced cells. CD34+ hematopoietic progenitor cells, the therapeutic target for gene therapy of CGD, were isolated from peripheral blood of CGD patients, transduced with MFG-phox retroviruses, and differentiated in culture to mature phagocytes. Transduction of progenitors corrected the gp91phox (seven patients) and p22phox (two patients) CGD phagocyte oxidase defect to 2.5% and 4.9% of normal O2-. production, respectively, representing an 87-fold and 161-fold increase. These studies show correction of flavocytochrome b558-deficient CGD in primary hematopoietic progenitors, providing a basis for development of gene therapy for the X-linked gp91phox and autosomal p22phox-deficient forms of CGD.
Antigens, CD↗
Rapid method for screening and cloning cDNAs generated in differential mRNA display: application of northern blot for affinity capturing of cDNAs.
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Base Sequence↗
Infrequent mutation of the WT1 gene in 77 Wilms' Tumors.
Homozygous deletions in Wilms' tumor DNA have been a key step in the identification and isolation of the WT1 gene. Several additional loci are also postulated to contribute to Wilms' tumor formation. To assess the frequency of WT1 alterations we have analyzed the WT1 locus in a panel of 77 Wilms' tumors. Eight tumors showed evidence for large deletions of several hundred or thousand kilobasepairs of DNA, some of which were also cytogenetically detected. Additional intragenic mutations were detected using more sensitive SSCP analyses to scan all 10 WT1 exons. Most of these result in premature stop codons or missense mutations that inactivate the remaining WT1 allele. The overall frequency of WT1 alterations detected with these methods is less than 15%. While some mutations may not be detectable with the methods employed, our results suggest that direct alterations of the WT1 gene are present in only a small fraction of Wilms' tumors. Thus, mutations at other Wilms' tumor loci or disturbance of interactions between these genes likely play an important role in Wilms' tumor development.
Amino Acid Sequence↗
Carboxyterminal propeptide of type I procollagen in osteomalacia.
Carboxyterminal propeptide of type I procollagen (PICP) was measured in sera from 25 patients with osteomalacia due to privational vitamin D deficiency. The mean value of serum PICP was significantly raised in patients with osteomalacia compared with 40 normal subjects (mean +/- SD, 161 +/- 82 ng/ml and 113 +/- 31 ng/ml, respectively; P = 0.01). The raised serum PICP reflected the accelerated bone turnover in this condition as did the elevated serum total alkaline phosphatase (ALP), but the variation in values of serum PICP noted in individual patients may reflect the different stages of osteomalacia. The normalization of serum PICP and ALP, indicating a healing process of the bone disorder, needed longer time of vitamin D and calcium therapy. In contrast, adjusted serum calcium and inorganic phosphate (IP) responded and normalized rapidly. Serum PICP and total ALP appeared to behave differently in the disease and in its response to vitamin D therapy suggesting that these two markers may represent different functions of osteoblasts in osteomalacia.
Adult↗
DNA inoculation as a novel vaccination method against human retroviruses with rheumatic disease associations.
There are a number of rheumatologic manifestations of human retroviral infections associated with human immunodeficiency virus type I (HIV-I) and the human T-cell leukemia virus type I (HTLV-I) including arthritis, Sjøgren's syndrome-like symptoms as well as other varied autoimmune phenomena. Infection with HTLV-1 may be directly involved in the etiology and/or pathogenesis of an arthritic condition similar to rheumatoid arthritis. We have been characterizing a new vaccination strategy against human retroviral infections, designated DNA inoculation. This procedure involves the intramuscular injection of DNA plasmids which express specific human retroviral antigens. This technique results in the development of humoral and cellular immune responses against these proteins. Specifically, this method has been successfully used to develop immune responses against HIV-I and HTLV-I. The availability of rat and rabbit infection models for HTLV-I, coupled with the successful development of immune responses in these animals after DNA inoculation with an HTLV-I envelope expressing plasmid, will allow the efficacy of this vaccination technique to be evaluated with protection against in vivo viral challenge as an endpoint.
Animals↗
Effects of pre-conditioning and microbial composition on the sensing efficacy of a BOD biosensor.
Sensitivity and the linear range of BOD measurement of a microbial BOD sensor using a mixed cell population of Bacillus subtilis and Bacillus licheniformis 7B depend significantly on the proportion of the two microorganisms and on the cell population immobilized on the biofilm. Optimum characteristics were obtained with equal proportion of the two microorganisms and an immobilized cell population of not less than 10(8) in the biofilm. Pre-conditioning of newly installed biofilm was best carried out in high BOD solutions and the time required to fully activate the microbial system decreased with increasing cell population. Fully activated biofilm remained stable and gave reproducible results for over 200 measurements covering a time period of more than 2 months. The technique of cell immobilization used in the present study provided a close control of the population and composition of the two microorganisms in the biofilm. Consistent and reproducible quality biofilms can therefore be produced for the preparation of the microbial BOD sensor.
Bacillus↗
Persistent and transient antibody responses to hepatitis E virus detected by western immunoblot using open reading frame 2 and 3 and glutathione S-transferase fusion proteins.
Recombinant proteins containing amino acid sequences from open reading frame (ORF) 2 and ORF3 of a Chinese strain of hepatitis E virus (HEV) were constructed as fusions with glutathione S-transferase (GST). Stable fusion proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the proteins were transferred to nitrocellulose membranes, and the immobilized proteins were probed with sera from hepatitis E patients from various regions or from rhesus monkeys (Macaca mulatta) experimentally infected with the Chinese strain of HEV. Immunoglobulin G-class antibodies were detected with chemiluminescence and anti-human immunoglobulin G conjugated to horseradish peroxidase. Anti-ORF3 antibodies were detected in most patients and monkeys within 17 days of exposure, but this humoral response declined with time and was usually undetectable by approximately 100 days. Anti-ORF2.1 antibody was usually detected as early as anti-ORF3 but persisted in all animals and many patients, whereas reactivity to the larger GST-ORF2.2 fusion protein was more transient, even though all sequences present in GST-ORF2.1 are present in GST-ORF2.2. Rechallenge of these monkeys with HEV suggested that immunity to reinfection was incomplete, as levels of anti-ORF2.1 (but not anti-ORF2.2) were boosted after each rechallenge. The results demonstrate that the carboxy-terminal region of HEV ORF2 contains epitopes which are recognized by convalescent-phase antibody and are likely to be associated with limited immunity to infection, but these epitopes may be masked when larger portions of ORF2 are expressed as recombinant proteins.
Animals↗
Phase unwrapping in the three-point Dixon method for fat suppression MR imaging.
PURPOSE: TO present an algorithm for performing phase unwrapping for fat and water signal separation in the three-point Dixon (3PD) method of magnetic resonance (MR) imaging. MATERIALS AND METHODS: The algorithm is based on a two-dimensional region-growing approach, which tracks phase evolution in 3PD images and unwraps the phase when a 2 pi jump is detected. The unwrapped phase data are consecutively used to calculate fat and water signal components on a per-pixel basis. The method was tested in eight volunteers. RESULTS: The algorithm creates four output images: standard spin-echo, fat suppression, water suppression, and phase map images. This method corrects for the effects of magnetic field inhomogeneities and provides spatially uniform fat signal suppression superior to that achievable with the standard method. CONCLUSION: This method of 3PD data reconstruction appears to be promising for routine application of fat suppression MR imaging in a clinical setting.
Humans↗
A comprehensive study of pressure distribution in the ankle joint with inversion and eversion.
The understanding of load transfer characteristics is the baseline for biomechanics of the ankle joint. Changes in contact patterns of the articular cartilage from the norm may indicate pathologic conditions. Measurement of the contact in human cadaver ankles provides a direct measurement for this understanding. The force transfer characteristics of the three facets of the ankle joint were investigated. Five fresh-frozen cadaver lower extremities were tested in 12 positions under three axial loads of 490, 686, and 980 N. Fuji film served as the pressure transducer and the prints were analyzed by a computerized video digitizer. The results demonstrated that as the foot was moved into inversion or eversion with the ankle in neutral flexion or dorsiflexion, there was a decrease in total contact area and an increase in the average high pressure. In plantarflexion, the contact area was lower and the average high pressure was higher, indicating a greater force per unit area as compared with dorsiflexion and neutral flexion. In plantarflexion, however, little change was noted with inversion or eversion. In dorsiflexion, the total contact area was higher and the average high pressure slightly lower as compared with neutral flexion. With inversion, the contact area of the medial facet of the ankle increased and with eversion it increased on the lateral facet, especially in dorsiflexion. With an increase in loading, the pressure did not significantly increase but the contact area did increase. The centroid of the contact moved anteriorly to posteriorly on the talus as the joint moved from dorsiflexion to plantar-flexion.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Anti-MAG antibodies: major effects of antigen purity and antibody cross-reactivity on ELISA results and clinical correlation.
There is controversy regarding the relationship of polyneuropathy syndromes to the presence of serum antibody binding to myelin-associated glycoprotein (MAG). Using standard ELISA methodology, we identified 74 sera that appeared to have high titers of IgM binding to MAG and found that only 34% of these sera stained MAG using Western blot methodology. Follow-up studies showed that two factors greatly influence concordance between ELISA and Western blot testing for anti-MAG antibodies. Sera with high titers of binding to both MAG and histone H3 identified by ELISA rarely stain MAG on Western blot. In addition, sera analyzed by ELISA often bind to impurities in the semipure MAG that is frequently used in ELISA assays. Further purifications to separate MAG from other contaminants improved concordance between ELISA and Western blot results to 85% to 90% in a retrospective analysis, as well as in a prospective study of 49 additional sera. Patients with a polyneuropathy and serum IgM binding to MAG preparations by ELISA but not by Western blot methodology had several different clinical syndromes, including gait disorders and asymmetric motor neuropathies. Patients with IgM binding to MAG by both assay methods usually had a distal, sensory-motor, symmetric polyneuropathy with some features of demyelination on electrodiagnostic testing.
Adult↗
The mitochondrial DNA mutation at position 11778 in Chinese families with Leber's hereditary optic neuropathy.
We amplified the 340 bp of mitochondrial DNA (mtDNA) by PCR including the recognized sequence of restriction enzyme of SfaN I. After amplification and digestion of SfaN I, two bands of 190 bp and 150 bp appeared in the mtDNA of four normal individuals but only one band of 340 bp appeared in the mtDNA with the mutation of G to A at the site of the nucleotide 11778 because such mutation destroyed the recognized sequence of SfaN I. We studied the mtDNAs of the patients with Leber's hereditary optic neuropathy from 19 Chinese families and their maternal relatives as well as the normal individuals i. e. the husbands of the female members of the pedigrees. The results show that 66.7% of the patients (30/45) and 54.7% of the maternal relatives (29/53) have such a mutation, while no such a mutation exists in the four normal individuals. So, we conclude that the mutation of mitochondrial DNA at position 11,778 is also a major cause of LHON in China.
Asian People↗