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Biomedical subjects

S Han

Publications and source records attributed to S Han.

At least 217 records · Page 12Linked to original sources

Ultrasound velocity and broadband attenuation as predictors of load-bearing capacities of human calcanei.

The main purpose of this study was to determine whether calcaneal ultrasound parameters, measured in the mediolateral direction, reflect load-bearing capacities of human calcanei. Broadband ultrasound attenuation (BUA) and ultrasound velocity (UV) were measured in 20 cadaveric calcanei with a mean age of 74.1 (SD 8.8). Normalized BUA (nBUA) was determined by dividing BUA by the calcaneal thickness obtained using a pulse-echo technique. The bone mineral density (BMD) of each calcaneus was measured by quantitative computed tomography. The calcanei were embedded in PMMA to simulate the midstance physiologic orientation during compressive testing in the load-bearing direction. The failure load, stiffness, and energy absorption were determined for each calcaneus. It was shown that BMD was well correlated with all ultrasound parameters (P < 0.0001). BMD, BUA, nBUA, and UV were all significantly associated with calcaneal failure load, stiffness, and energy absorption capacity (P < 0.05). nBUA was found to be the strongest predictor of all compressive properties. BUA and BMD demonstrated similar predictability of stiffness and energy absorption capacity, however, BUA showed a more significant relationship to the failure load of the calcaneus than did BMD. UV was found to be inferior to BMD, as well as BUA or nBUA, in assessing failure load, stiffness, and energy absorption capacity. It was also shown that nBUA was superior to BUA in the assessment of load-bearing capacity, but not in the prediction of BMD. Multivariate regression analysis showed that the combination of BUA or nBUA with UV did not improve the predictability of failure load, stiffness, and energy absorption capacity over that of BUA or nBUA alone (P > 0.5).

Absorptiometry, Photon↗

Primary cultured chondrocytes of different origins respond differently to bFGF and TGF-beta.

Responses of rib and ear chondrocytes to basic fibroblast growth factor (bFGF) and transforming growth factor-beta (TGF-beta) were investigated using high density primary culture isolated from the same rabbit. Degrees of tritiated thymidine, leucine, and proline incorporation were used as indicators of DNA, protein and collagen syntheses, respectively. 10 ng/ml bFGF increased thymidine, proline, and leucine incorporation into rib, but not ear, chondrocytes. 1 ng/ml TGF-beta enhanced thymidine incorporation into both chondrocytes but did not affect proline or leucine incorporation into the ear cells. When both growth factors were added simultaneously, both cells showed rises in syntheses of DNA, protein and collagen. Incorporation of [35S]sulfate, used as indicator of proteoglycan synthesis, was elevated by TGF-beta but was reduced by bFGF especially in the rib cells. This inhibitory effect of bFGF was not reversed by cotreatment with TGF-beta in both cell types. Thus, the origin and cellular differentiation states of chondrocytes seem to cause different responses to these growth factors.

Animals↗

Elevated neuropeptide Y gene expression and release during hypoglycemic stress.

Our previous studies show that neuropeptide Y (NPY) is involved in mediating sympathetic nerve stimulation-induced vasoconstriction. Insulin hypoglycemia is known to produce increased sympathetic output and elevated arterial pressure. The present study examined the role of NPY in the hypertensive response to insulin by examining the effects of insulin on NPY gene expression, tissue content and release. Subcutaneous injection of insulin produced an immediate increase in plasma NPY immunoreactivity (NPYir) and delayed increases in adrenal and neuronal NPY mRNA and adrenal NPYir in rats. These results suggest that NPY may play a role in insulin-induced hypertension.

Adrenal Medulla↗

The ability of quantitative ultrasound to predict the mechanical properties of trabecular bone under different strain rates.

The ability of quantitative ultrasound to predict the mechanical properties of trabecular bone under different strain rates was investigated. Ultrasound velocity (UV) and broadband attenuation (BUA) were measured for 60 specimens of human trabecular bone. Samples were divided into two equal groups and loaded in compression at the strain rates of 0.0004 and 0.08 s-1. The ultimate strength, elastic modulus, and energy absorption capacity were determined for each specimen. Specimens tested at 0.08 s-1 had a mean value of strength 63% higher than the specimens tested at 0.0004 s-1. The elastic modulus and energy absorption capacity were 82% and 42% higher, respectively, for the higher strain rate. UV and BUA were significantly associated with most mechanical properties at both strain rates. All mechanical properties were also correlated strongly with a linear combination of UV and BUA for both the low and high loading rates. The use of ultrasound parameters may provide good clinical means for assessing the resistance of trabecular bone to both low and high energy trauma.

Aged↗

Mammalian DNA repair methyltransferases shield O4MeT from nucleotide excision repair.

O6-Methylguanine (O6MeG) and O4-methylthymine (O4MeT) are potentially mutagenic DNA lesions that cause G:C-->A:T and A:T-->G:C transition mutations by mispairing during DNA replication, and the repair of O6MeG and O4MeT by DNA repair methyltransferases (MTases) is therefore expected to prevent methylation-induced transitions. The efficiency of O6MeG and O4MeT repair by different MTases can vary by several hundred-fold and the aim of this study was to establish the biological consequences of such differences in the efficiency of repair. The ability of three microbial and two mammalian MTases to prevent methylation-induced G:C-->A:T and A:T-->G:C transitions is taken as a measure of their ability to repair O6MeG and O4MeT in vivo respectively. All five MTases give complete protection against G:C-->A:T transitions. However, while the microbial MTases give complete protection against A:T-->G:C transitions, the mammalian MTases actually sensitize cells to A:T-->G:C transitions. We hypothesize that the mammalian MTases bind O4MeT lesions in vivo but that, because they are extremely slow at subsequent methyl transfer, binding shields O4MeT from repair by the nucleotide excision repair pathway. Results are presented to support this hypothesis.

Animals↗

Immunosenescence and germinal center reaction.

Dysfunction of the immune system in aged individuals includes at least two important factors: accumulation of immunocytes with reduced function and accumulation of lymphocyte clones with self-reactive potential. Coincidently, there is a profound reduction of the germinal center reaction in the aged. While this reduction is likely the result of age-associated impairment in lymphocyte function (e.g. diminished response to costimulus, altered lymphokine production etc.), the reduction of germinal centers may itself make an important contribution to further immunological dysfunction.

Aging↗

Lead exposure at an early age substantially increases lead retention in the rat.

It has been hypothesized that the high rate of bone remodeling during childhood and the consequent high calcium and lead turnover result in a substantial reduction in bone lead stores so that much of the lead incorporated in bone during childhood does not persist into adulthood. We studied the effect of age at lead exposure on blood and organ concentrations of lead, calcium, and zinc 1-5 months after termination of lead ingestion. Blood and organ lead concentrations and contents 4 weeks after lead exposure ceased were significantly higher in the rats exposed beginning at 5 weeks of age than in those exposed beginning at 10 or 15 weeks old. Bone lead declined as the time since exposure increased. Despite this trend, the rats exposed when youngest had bone lead concentrations at 20 weeks after the termination of lead exposure that were higher than those of the other rats only 4 weeks after cessation of lead ingestion. Multiple regression analysis demonstrated that age at lead exposure remained a significant predictor of blood and organ lead concentrations and contents even after the inclusion of total lead consumed, body weight, and age at organ harvesting in the regression analysis. There were only small differences in organ calcium and zinc concentrations among treatment groups except for kidney calcium. The results do not support the hypothesis of rapid depletion of bone lead stores in young animals, but rather suggest that younger age at lead exposure is associated with greater lead retention and toxicity even in the absence of continued lead exposure.

Age Factors↗

[Inhibition of respiratory syncytial virus (RSV) by moroxydine, allicin, alpha-interferon and their joint application].

This paper reported the inhibition of respiratory syncytial virus by Moroxydine (ABOB), Allicin, alpha-interferon and their joint application. The results indicated that each of the three drugs inhibited RSV in HeLa cells, and the effective dosage of ABOB was 100 mg/L, alpha-interferon 1.5 x 10(4) U/L and Allicin one eight hundred thousandth of the pure material. The combinations of 3 drugs showed synergism without antagonism, this not only decreased the dosage, toxicity but also enhanced the inhibition effects on respiratory syncytial virus obviously.

Biguanides↗

The construction and expression of deletion mutant of human pro-urokinase cDNA.

The human pro-urokinase mutant deleting 150-156 amino acids was constructed by overlap-extension PCR and other molecular cloning techniques. The mutant was expressed transiently in COS-7 cells and constitutively in CHO cells; the expression level is 450-500 IU/10(6) cells/24 h. SDS-PAGE and Western blotting analysis showed that the molecular weight of the expression product is 54 kDa, which is similar to that of the mature pro-UK and recombinant pro-UK (rPro-UK) expressed by full-length cDNA. Most of the products exist in the form of single chain; the percentage of single chain is much higher than that of rPro-UK. In addition, the mutant product is more resistant to proteinases and its affinity to fibrin is also improved slightly.

Animals↗

Neoteny in lymphocytes: Rag1 and Rag2 expression in germinal center B cells.

The products of the Rag1 and Rag2 genes drive genomic V(D)J rearrangements that assemble functional immunoglobulin and T cell antigen receptor genes. Expression of the Rag genes has been thought to be limited to developmentally immature lymphocyte populations that in normal adult animals are primarily restricted to the bone marrow and thymus. Abundant RAG1 and RAG2 protein and messenger RNA was detected in the activated B cells that populate murine splenic and Peyer's patch germinal centers. Germinal center B cells thus share fundamental characteristics of immature lymphocytes, raising the possibility that antigen-dependent secondary V(D)J rearrangements modify the peripheral antibody repertoire.

Animals↗

Alternative pathways for the selection of antigen-specific peripheral T cells.

In the thymus, maturing lymphocytes receive activation signals mediated by the T-cell antigen receptor (TCR) that either promote clonal survival (positive selection) or induce apoptosis (negative selection). This balance between life and death is mirrored by the sensitivity of cortical thymocytes to apoptotic death induced by antibodies against the CD3 component of the TCR signal-transduction complex, bacterial superantigens that bind to the TCR beta-chain, and corticosteroids. In contrast, mature peripheral T cells are positively activated by anti-CD3 antibody or superantigens and are resistant to steroid-induced death. Here we show that in splenic germinal centres, T cells regain thymocyte-like sensitivity to TCR- and steroid-induced apoptosis and undergo antigen-driven positive and negative selection. T-cell responses elsewhere in the spleen are unaccompanied by programmed cell death. Our observations define a new differentiation pathway for peripheral T cells and suggest that germinal centres induce a lymphocyte phenotype necessary for the maintenance of self-tolerance.

Animals↗

T helper cells in murine germinal centers are antigen-specific emigrants that downregulate Thy-1.

After immunization, activated splenic T cells proliferate in periarteriolar lymphoid sheaths (PALS) and subsequently migrate to the lymphoid follicle where they enter nascent germinal centers. Analysis of TCR V(D)J gene rearrangements indicates extensive emigration, frequently involving more than a single white pulp region. These migrants constitute a unique set of T helper cells that express antigen-specific alpha beta TCR, CD3, and CD4, but little or no Thy-1, a differentiation antigen present on the great majority of peripheral murine T lymphocytes. The origin of CD4+ Thy-1 follicular T cells appears to be the Thy+ population in the PALS, as both sets commonly share identical V(D)J rearrangements.

Animals↗

Regulation of the B cell response to T-dependent antigens by classical pathway complement.

Mice deficient in complement components C3 (C3 -/-) and C4 (C4 -/-) were found to have a profound defect in their Ab response to a T-dependent Ag (bacteriophage (phi X174). Characterization of the deficient mice demonstrated a diminished level of peanut agglutinin+ germinal centers and a failure in isotype switching despite normal B cell signaling in vitro. The nature of the defect was found to lie at the B cell level, as the T cells were primed in C3- and C4-deficient mice as well as those in wild-type mice. These results, and the finding that the defect could be partly reversed by a 10-fold increase in Ag dose, support the hypothesis that covalent attachment of complement ligands, i.e., C3b and C3d to the Ag-Ab complex, increases its immunogenicity.

Animals↗

CD28 is required for germinal center formation.

Previous studies have demonstrated that the T cell costimulatory molecule, CD28, is important in the development of humoral immunity. CD28-deficient mice exhibit defects in isotype switching and are more susceptible to pathogens that depend on an effective Ab response. To determine the basis of these defects, we have examined B cell responses of CD28-deficient mice at the microenvironmental level. Early in a normal T-dependent immune response, small numbers of B cells undergo activation in the T cell-rich zone of secondary lymphoid tissues and then migrate to B cell areas. These migrant B cells found developing germinal centers by proliferative expansion, during which individual cells acquire mutations in their rearranged Ig genes. B cell mutants retaining higher affinities for Ag undergo positive selection in germinal centers, resulting in the establishment of the memory B cell compartment. In the present study, we demonstrate that although potentially Ag-reactive cells within the lymphoid follicle accumulate following antigenic challenge, these cells fail to undergo proliferative expansion to form germinal centers and do not acquire somatic mutations in CD28-deficient animals. Thus, the CD28 activation pathway is required for Ab responses to T-dependent Ags. cell compartment. In the present study, we demonstrate that although potentially Ag-reactive cells within the lymphoid follicle accumulate following antigenic challenge, these cells fail to undergo proliferative expansion to form germinal centers and do not acquire somatic mutations in CD28-deficient animals. Thus, the CD28 activation pathway is required for Ab responses to T-dependent Ags.

Animals↗

Antibody response to a T-dependent antigen requires B cell expression of complement receptors.

Several lines of evidence indicate that antibody responses to T-dependent antigens require complement receptors expressed on either B lymphocytes or follicular dendritic cells. We have used RAG-2 deficient blastocyst complementation to create mice specifically lacking B cell complement receptors. Despite normal expression of complement receptor 1 (CR1[CD35]) and CR2 (CD21) on follicular dendritic cells, these mice have a profound defect in their capacity to mount a T-dependent antibody response. This is the first direct demonstration in vivo that B cell expression of complement receptors is required for a humoral immune response. This is the first direct demonstration in vivo that B cell expression of complement receptors is required for a humoral immune response. This suggests that CD21 and/or CD35 on B lymphocytes may be required for cellular activation, adsorptive endocytosis of antigen, recruitment to germinal centers, and/or protection from apoptosis during the humoral response to T-dependent antigens.

Animals↗

Ultrasound velocity and broadband attenuation over a wide range of bone mineral density.

Ultrasound velocity (UV) and broadband ultrasound attenuation (BUA) were studied in human and bovine bone with a wide range of bone mineral density (BMD). The BMD of 98 fresh specimens was measured by quantitative computed tomography: 42 cancellous specimens from women in the age group of 64 +/- 4 years; 51 bovine cancellous and 5 bovine cortical. BMD values ranged from 90 to 400 mg/cm3 for the human cancellous bone, 310 to 870 mg/cm3 for the bovine cancellous bone, and 1750 to 1780 mg/cm3 for the bovine cortical bone. BMD showed a strong linear correlation with apparent density over the entire range of density (r = 0.979). UV of human and bovine cancellous bone was 1480-2650 m/s and 2880-3100 m/s for bovine cortical bone. BUA values were 1-61 dB/MHz/cm for the cancellous specimens and 5-12 dB/MHz/cm for cortical specimens. UV was found to be linear with BMD for all specimens; however, BUA was linear with BMD only for the specimens from elderly women. A quadratic relationship between BUA and BMD was found when the bovine samples were included.

Animals↗