Biomedical subjects

Y Ding

Publications and source records attributed to Y Ding.

At least 253 records · Page 14Linked to original sources

PubMed1996

Retrovirus-mediated transfer of viral IL-10 gene prolongs murine cardiac allograft survival.

A murine heterotopic, nonvascularized cardiac allograft model was used to examine the effects of the immunosuppressive cytokine, viral IL-10 (vIL-10), delivered by gene transfer on graft rejection. Retroviral-mediated gene transfer and expression of vIL-10 significantly prolonged allograft survival, without conventional systemic immunosuppression, from 12.1 +/- 0.8 days to 39.4 +/- 2.5 days (p < 0.0001). The effect was specific, dose dependent, and restricted to the site of transplantation. PCR analysis demonstrated specific expression of the transferred gene within the allograft. Analysis of the cellular infiltrate in the allografts showed a reduction in T cells and alloantigen-specific cytotoxic T cells and IL-2 producing helper T cells. Thus, the transient local expression of a gene encoding an immunosuppressive protein within a graft can generate local immunosuppression, making gene therapy a viable approach for facilitating transplantation.

Animals↗

PubMed1996

Stereocontrolled synthesis of sulfur-linked analogues of the branched tetrasaccharide repeating-unit of the immunostimulant polysaccharide schizophyllan and of its beta-(1-->3)-branched, beta-(1-->6)-linked isomer.

The branched, sulfur-linked tetrasaccharide S-(beta-D-glucopyranosyl)-(1-->3)-S-[(6-S-beta-D-glucopyranosyl)-3,6-dit hio- beta-D-glucopyranosyl]-(1-->3)-S-3-thio-D-glucopyranose (9) has been conveniently prepared by SN2 displacement of the triflate group in 1,2:5,6-di-O-isopropylidene-3-O-trifluoromethylsulfonyl-alpha-D-++ +allofuranose with the sodium salt of 2,4-di-O-acetyl-3,6-di-S-(2,3,4,6-tetra-O-acetyl-beta-D-glucopyranosyl)- 1,3,6- trithio-beta-D-glucopyranose (5). Conversely, reaction of the sodium salt of 5 with 1,2,3,4-tetra-O-acetyl-6-deoxy-6-iodo-beta-D-glucopyranose afforded the positional isomer S-(beta-D-glucopyranosyl)-(1-->6)-S-[(3-S-beta-D-glucopyranosyl)-3,6-dit hio- beta-D-glucopyranosyl]-(1-->6)-S-6-thio-D-glucopyranose (12).

Adjuvants, Immunologic↗

PubMed1996

Anti-CD2 monoclonal antibody-induced receptor changes. II. Interaction of CD2 and CD3.

Anti-CD3 monoclonal antibodies (mAbs) and anti-CD2 mAbs each prolong allograft survival and cause transient downmodulation of homologous receptor expression. Anti-CD2 mAbs also act synergistically with anti-CD3 mAbs to prolong allograft survival and induce tolerance. The effect of combined anti-CD2 and anti-CD3 mAb treatment on receptor expression was further analyzed with an in vitro model. The anti-CD2 mAb 12-15 caused CD2 expression on purified splenic T cells to decrease from 72.6% [mean channel fluorescence (MCF) 0.68] to 41.5% (0.45) total positive cells while CD3 expression remained unchanged [69.1% (3.47) to 76.4% (4.04)]. The anti-CD3 mAb 2C11 caused CD2 expression to increase from 72.6% (0.68) to 93.0% (1.74) while CD3 expression decreased from 69.1% (3.47) to 62.6% (2.15). The combination of anti-CD2 plus anti-CD3 preserved CD2 expression (72.6 to 71.1%) while still decreasing CD3 expression [69.1% (3.47) to 69.9% (2.37)]. Modulation of CD2 and CD3 expression was similar on mixed splenic T lymphocytes and isolated CD4 and CD8 subsets. Modulation did not change with the addition of the cytokines IL-1, IL-2, IL-4, IL-6, IL-10, TNF alpha, or TGF beta. Kinetic studies showed that modulation of CD2 was rapid, persistent, and of the same magnitude from Day 1 to Day 7 of culture while CD3 downmodulation was transient. The results of transcriptional analysis and receptor distribution suggested that downmodulation was due to receptor internalization while upmodulation was due to increased transcription. Analysis of expression of other adhesion molecules demonstrated that CD11a, CD18, CD44, CD45, CD48, CD54, and CD62L were significantly increased by either anti-CD2 or anti-CD3 mAbs while the combination was not synergistic. However, anti-CD3 significantly decreased VLA-4 alpha (CD49d) expression and anti-CD2 enhanced this decrease. Conversely anti-CD3 significantly increased IL-2R (CD25) expression and anti-CD2 profoundly inhibited the increase. These results show that anti-CD2 and anti-CD3 mAbs significantly modulate CD2 and CD3 expression on T cells and modulation is accompanied by changes in the array of other T cell surface receptors. Changes in cell surface receptor display may provide an additional explanation for the synergistic effect of anti-CD2 plus anti-CD3 in prolonging allograft survival.

Animals↗

PubMed1996

The initial stages of development of the retinocollicular projection in the wallaby (Macropus eugenii): distribution of ganglion cells in the retina and their axons in the superior colliculus.

The time course of ingrowth of retinal projections to the superior colliculus in the marsupial mammal, the wallaby (Macropus eugenii), was determined by anterograde labelling of axons from the eye with horseradish peroxidase, from birth to 46 days, when axons cover the colliculus contralaterally and ipsilaterally. The position of retinal ganglion cells giving rise to these projections over this period was determined in fixed tissue by retrograde labelling from the colliculus with a carbocyanine dye. Axons first reach the rostrolateral contralateral colliculus 4 days after birth and extend caudally and medially, reaching the caudal pole at 18 days and the far caudomedial pole at 46 days. The first contralaterally projecting cells are in the central dorsal and temporal retina, followed by cells in the nasal and finally the ventral retina. They are distributed closer to the periphery with increasing age. The first sign of a visual streak appears by 18 days. Axons reach the ipsilateral colliculus a day later than contralateral axons and come from a similar region of the retina. The sparser ipsilateral projection reaches the caudal and medial collicular margins by 46 days but by 16-18 days, ganglion cells giving rise to this transient projection are already concentrated in the temporoventral retina. The orderly recruitment of ganglion cells from retinotopically appropriate regions of the retina as axons advance across the contralateral colliculus suggests that the projection is topographically ordered from the beginning. The ipsilateral projection is less ordered as cells are located in the temporoventral crescent at a time when their axons are still transiently covering the colliculus prior to becoming restricted to the rostral colliculus. Features of mature retinal topography such as the visual streak and the location of ipsilaterally projecting cells begin to be established very early in development, before the period of ganglion cell loss and long before eye opening at 140 days.

Age Factors↗

PubMed1996

Towards oligosaccharide libraries: a study of the random galactosylation of unprotected N-acetylglucosamine.

A single reaction of an unprotected beta-D-GlcNAc glycoside with tetra-O-acetyl-alpha-D-galactopyranosyl trichloroacetimidate in dioxane, catalyzed by BF3-etherate, was shown to yield all six possible Gal-GlcNAc disaccharides. This result is surprising not only because significant amounts of alpha-linked disaccharides were formed, despite the presence of a participating group at O-2 of the glycosyl donor, but also because glycosylation of the primary OH-6 is not the dominant reaction. These results suggest 'random-glycosylation' to be a valid strategy for the rapid production of oligosaccharide libraries.

Acetylglucosamine↗

PubMed1996

Cathepsin G in gingival tissue and crevicular fluid in adult periodontitis.

The presence, localization and activities of cathepsin G in gingival tissue specimens and crevicular fluid (GCF) from 9 adult periodontitis patients and 6 controls with clinically healthy periodontium were studied by use of avidinbiotin-peroxidase complex method, Western and dot blotting, and spectrophotometric activity assay. In contrast to healthy gingival tissue specimens, gingival tissue specimens collected from adult periodontitis patients contained inflammatory cells in lamina propria, beneath the oral sulcular epithelium, 10-50% of which were cathepsin G positive polymorphonuclear neutrophilic leukocytes (PMNs) and monocyte/macrophage-like cells. Cathepsin G activities were increased in adult periodontitis GCF when compared to periodontally healthy controls' GCF (p < 0.05). In adult periodontitis GCF, Western blotting disclosed free cathepsin G but also clear complexes of cathepsin G with its predominant endogenous inhibitor alpha 1-antichymotrypsin (alpha 1-ACT). The present results demonstrate that part of the cathepsin G, despite the presence of increased concentrations of alpha 1-ACT, was in an uncomplexed, free and functionally active form. Our results suggest that GCF cathepsin G reflects the disease process in adjacent inflamed gingiva and also increased host response to microbiota and/or dental plaque in the periodontitis lesions. Cathepsin G may contribute to periodontal tissue destruction directly and indirectly, via proteolytic activation of latent neutrophil procollagenase (promatrix metalloproteinase-8 [proMMP-8]).

Adult↗

PubMed1996

Matrix metalloproteinases and their inhibitors in gingival crevicular fluid and saliva of periodontitis patients.

Matrix metalloproteinases (MMPs) and serine proteinases seem to be related to tissue destruction in periodontitis. The presence of MMPs in gingival crevicular fluid (GCF) and saliva, however, has not been studied comprehensively with the enzyme-linked immunosorbent assay (ELISA)-technique. We therefore examined the levels of MMP-1, -3, -8 and -9, and their endogenous inhibitor, tissue inhibitor of matrix metalloproteinases (TIMP-1), in GCF and saliva of patients with adult periodontitis (AP) and localized juvenile periodontitis (LJP). Elevated levels of MMP-1 were detected in LJP GCF compared to AP and control GCF. Elevated levels of TIMP-1 were also detected in LJP GCF in comparison to AP and control GCF. Higher MMP-8 levels were detected in AP GCF compared to LJP and control GCF. The relative low levels of MMP-3 were present in all studied GCF samples. Elevated levels of MMP-8 were further detected in saliva of AP compared to LJP and the controls. Both MMP-1 and TIMP-1 were detected in all studied saliva samples, but not significant differences were detected between the studied groups. Our ELISA-results confirm that (i) PMN MMP-8 and MMP-9 are the main collagenase and gelatinase in AP GCF, whereas GCF collagenase in LJP seems to be of the MMP-1-type; (ii) only low levels of TIMP-1, endogenous MMP-inhibitor, are present in AP GCF, which emphasises the importance of doxycycline as a possible adjunctive drug in the treatment of AP patients; (iii) tests based on specific antibodies against PMN MMPs, especially MMP-8, might serve as a reliable method of measuring and monitoring enzyme levels in GCF from different periodontitis patients.

Adolescent↗

PubMed1996

Membrane components of Treponema denticola trigger proteinase release from human polymorphonuclear leukocytes.

Tissue destruction during periodontitis is believed to be primarily brought about by leukocyte proteinases. We postulate that oral spirochetes cause discharge of polymorphonuclear leukocyte (PMN) lysosomal enzymes. Effects of Treponema denticola 53-kDa outer membrane protein, lipopolysaccharide (LPS), and peptidoglycan on degranulation of matrix metalloproteinases (MMP)-8 (collagenase) and -9 (gelatinase), cathepsin G, and elastase by human peripheral blood PMNs were studied by specific enzyme assays and Western blot analysis. T. denticola 53-kDa kDa outer membrane protein was found to be a particularly efficient inducer of MMP-8 release. The induction was comparable with that of phorbol myristate acetate, a known inducer of PMN specific granule discharge. All of the treponemal substances, most notably the 53-kDa protein and LPS, induced release of MMP-9, a component of C-type granules. Both collagenase and gelatinase released from PMNs were mostly in active forms. Release of cathepsin G and elastase was also observed with the 53-kDa protein treatment. The other T. denticola substances did not induce release of these serine proteinases. Lactate dehydrogenase was not released from PMNs by the treatments, indicating that the degranulation was specific and not caused by toxic effects of the substances. This was confirmed by transmission electron microscopy of PMNs treated with the 53-kDa protein that showed rapid vacuole formation and cell shape changes but no disintegration of the cells. Thus, T. denticola may participate in the PMN-dependent extracellular matrix degradation during the course of periodontal inflammation by triggering the secretion and activation of matrix metalloproteinases.

Acute-Phase Proteins↗

PubMed1996

Antithrombin III inhibits mesangial cell proliferation.

Thrombin stimulates and heparin and heparan sulfate inhibit mesangial cell proliferation. In addition, heparin has been shown to inhibit thrombin-stimulated smooth muscle cell proliferation. The anticoagulant action of heparin is mediated by antithrombin III. This study investigated whether heparin's antiproliferative action is also mediated by antithrombin III. To this end, the effect of antithrombin III on thrombin-stimulated mesangial cell growth was examined. As expected, thrombin stimulated DNA synthesis and cell growth in cultured human mesangial cells. The effect of thrombin on DNA synthesis and mesangial cell proliferation was inhibited by standard heparin and antithrombin III, separately or together. The magnitude of the inhibitory action of antithrombin III was equal to that of equimolar concentrations of heparin and that observed with the combination of the two. Experiments carried out in serum (hence antithrombin III)-free medium revealed that heparin's inhibitory effects are independent of antithrombin III. It was concluded that antithrombin III, an endogenous inhibitor of thrombin's coagulant activity, is an equally effective inhibitor of thrombin's mitogenic action.

Anticoagulants↗

PubMed1996

Characterization of matrix metalloproteinase (MMP-8 and -9) activities in the saliva and in gingival crevicular fluid of children with Down's syndrome.

Previous studies have shown increased susceptibility to periodontal diseases in children with Down's syndrome (DS). The mechanisms involved in the periodontal inflammatory processes in DS are not fully understood. The present study characterized the periodontal status of 9 non-institutionalized DS children 9 to 17 years old (mean 13.6 years) relative to their age-matched systemically and periodontally healthy controls. The periodontal status was assessed by visible plaque index (VPI), gingival bleeding index (GBI), and probing depth. We also assessed, by sodium dodecyl sulphate polyacrylamide gel electrophoresis/laser densitometry and by zymography, the collagenase and gelatinase activities in the gingival crevicular fluid (GCF) and saliva samples collected from DS patients and from the controls. Eight of the nine DS children showed a periodontium comparable to that seen in healthy controls; beginning alveolar bone loss was radiographically seen in the DS patient with deep periodontal pockets. The endogenously active collagenase and total collagenase activities were slightly higher in GCF of DS children compared to healthy controls. Western blot demonstrated that GCF collagenase of DS patients was human neutrophil collagenase (MMP-8 or collagenase-2), which occurred in 75 kDa proMMP-8 and in DS patients, but not in controls, also in 65 kDa active MMP-8 form and occasionally lower 40-50 kDa MMP-8 species. Zymographic analysis revealed the presence of 120 kDa (MMP-9 complexed with neutrophil gelatinase associated lipocalin or NGAL), 92 kDa (MMP-9) and 72 kDa (MMP-2) gelatinases in DS and control GCF. Especially in DS GCF MMP-9 occurred in part in 82-85 kDa activated form. Salivary collagenase in DS was high when compared to controls but of the same MMP-8 type as in control saliva. Our findings suggest that in vivo activated MMP-8 in GCF derived from triggered PMNs and/or cytokine-induced periodontal fibroblasts may reflect periodontal tissue and alveolar bone destruction seen in the early stages of gingivitis/periodontitis associated with Down's syndrome.

Adolescent↗

PubMed1996

Extreme obesity may be linked to markers flanking the human OB gene.

Mice with mutations of the ob gene are extremely obese, and the human homologue (OB) has been cloned and physically mapped. The protein product of the ob gene (leptin) reduces body fat in mice when given exogenously, and leptin has been proposed to provide a lipostatic signal that regulates adiposity. Variation in the OB gene may be one genetically determined cause of obesity in human populations. To test this hypothesis, we genotyped siblings from 78 families at markers flanking the human OB gene. Pairs of siblings with extreme obesity (BMI > or = 40; n = 59) shared haplotypes identical-by-descent for the region containing the OB gene at greater than chance levels (corrected P = 0.04). Furthermore, one haplotype containing the OB gene was transmitted by heterozygous parents to extremely obese (BMI > or = 40) offspring more frequently than expected by chance, indicting significant allelic disequilibrium (corrected P = 0.027). One explanation for these linkage findings is that some individuals with extreme obesity have an allelic variant of the OB gene, although other nearby genes could contribute to obesity in these families.

Adipose Tissue↗

PubMed1996

[The effect of air purification on 10,000 degree clean room in supply rooms].

This article introduced that purifying equipments were installed in the major operating departments of supply rooms in hospital, and that experimental tests were done on the packing department. In statil state, the air humidity and the number of bacteria in the room after purification was obviously lower than that before purification (P < 0.01). In trending conditions, the main technical index on 10,000 degree clean rooms were examined, all of the results were up to the national standards.

Air Microbiology↗

PubMed1996

[The postnatal changes of follicle-stimulating hormone receptor mRNA level in rat testis].

It was found in this study that the follicle-stimulating hormone receptor (FSHR) mRNA levels varied between days 2 and 60. The FSHR mRNA rised slightly in the neonatal rat testis and then declined. In the prepuberty the content of FSHR mRNA remained at a Constant level. During the puberty the FSHR mRNA increased to its highest level on days 25 and finally it rised again after days 40.

Animals↗

PubMed1996

[Surgical treatment of hypertensive cerebral and cerebellar haemorrhage and its influence factors].

Two hundred and ten patients with hypertensive cerebral and cerebellar haemorrhage were surgically treated with four patterns. The preoperative status graded as I-V stages was improved among 151 cases, and 59 cases (28.0%) died. The authors concluded that individualized selection of available surgical pattern combined with CT findigs according to neurologic grading will lower the operative mortality. Factors affecting the prognosis, such as location of haemorrhage, the volume of hematoma, haemorrhage rupture into the ventricles, and the timing of surgery were analysed. Postoperative rebleeding, intracranial pneumatosis, multiple organ failure and curative means are discussed.

Aged↗

PubMed1996

[The role of serum osmolality monitoring in patients with severe intracranial lesion].

We dynamically determined serum osmolality in 1379 patients with severe intracranial lesion for 2843 times between January 1992 and July 1995. Using auto-control and after abandoned osmolality related interference factors we obtained the following results. Quantitative correlation analysis on the level of serum osmolality, intracranial pressure and the dose of mannitol showed that there was a negative correlation between the level of serum osmolality and intracranial pressure, while a positive correlation existed between the intracranial pressure and the dose of mannitol. The reasonable dose of mannitol was that which elevated the level of serum osmolality some 15-20 mOsm/kgH2O than its normal upper limit. The level of serum osmolality increesed to raised up 20-30 mOsm/kgH2O after administration of a single dose of mannitol. Complication increased with the increased level of osmolality of 300 mOsm/kgH2O, a warning level. An elevation of osmolality over 320 mOsm/kgH2O was considered the critical level for developing acute renal failure. The level of over 330 mOsm/kg H2O was another warning level for inducing nonketotic hyperosmotic diabetic coma. The efficious duration of mannitol, two different ways of diminishing or withdrawing the dose of mannitol, and the more safer velocity for correcting the state of hyperosmolality were also discussed. We conclude that to monitor the dynamic change of serum osmolality from time to time is of great help in lowering the incidence and mortality of hyperosmotic complications. Serum osmolality monitoring plays an important role in making fluid balance and compromizing the contradiction between dehydration and infusion as well as prevention and therapy of hyperosmotic complications, and outcome estimation as well.

Adolescent↗

PubMed1996

[Comprehensive treatment of intracranial aneurysm complicated by postoperative vasospasm].

Forty six patients suffered from intracranial aneurysm complicated by postoperative vasospasm and delayed cerebral ischemia were monitored dynamically both by clinical observation of neurologic status and multiple items such as transcranial Doppler, serum osmolality, intracranial pressure and other somatic physiologic items related to monitoring. Patients were intensively and comprehensively treated according to individualized grading of vasospasm. Forty four patients (95.6%) were completely recovered from postoperative vasospasm and delayed cerebral ischemia, while 2 patients (4.3%) complicated by hemipalsy as a consequence of delayed cerebral ischemia. The occurrence of vasospasm and delayed cerebral ischemia, the criteria of TCD grading, the valuableness of multiple physiologic items and problems related to comprehensive treatment are discussed.

Adult↗

PubMed1995

Complexes between chaperonin GroEL and the capsid protein of bacteriophage HK97.

The 42 kDa capsid protein of bacteriophage HK97 requires the GroEL and GroES chaperonin proteins of its Escherichia coli host to facilitate correct folding, both in vivo and in vitro. In the absence of GroES and ATP, denatured gp5 forms a stable complex with the 14 subunit GroEL molecule. We characterized the electrophoretic and biochemical properties of this complex. In electrophoresis on a native (nondenaturing) gel, the band of the gp5-GroEL complex shifts to a slower migrating position relative to uncomplexed GroEL. The results show that there is only one subunit of gp5 bound to each GroEL 14-mer and that the shift in band position is due primarily to a change in the overall charge of the complex relative to uncomplexed GroEL, and not to a change in size or shape. GroEL forms similar complexes with proteolytic fragments of gp5, with a series of sequence duplication derivatives of gp5, and with other proteins. Electrophoretic examination of these complexes shows that a band shift occurs with proteins larger than 31-33 kDa but not with smaller proteins. For those proteins that cause a band shift upon complex formation, the magnitude of the shift is correlated with the predicted if the charge of the complex were simply the sum of the charge of GroEL and the charge of the substrate protein. We suggest that binding of a substrate protein to GroEL is accompanied by a net binding of solution cations to the complex, but only in the case of proteins above a minimum size of 31-33 kDa. The gp5-GroEL complex is in an association/dissociation equilibrium, with a binding constant measured in the range of 11-17 microM-1.

Adenosine Triphosphate↗

PubMed1995

Computing back-calculation estimates of AIDS epidemic.

The method of back-calculation estimates the number of HIV infections from AIDS incidence data and projects future AIDS incidence. We explore a conditional likelihood approach for computing estimates of the number of HIV infections and the parameters in the epidemic density. This method is asymptotically equivalent to the usual likelihood method. The asymptotic normal distribution of the estimates facilitates the computation of confidence intervals. We compute standard deviations for the estimates of HIV incidence and project AIDS incidence from the underlying multinomial distributions. We illustrate the methods with applications to AIDS data in the United States.

Acquired Immunodeficiency Syndrome↗