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Biomedical subjects

J X Lin

Publications and source records attributed to J X Lin.

At least 19 recordsLinked to original sources
PubMed1992

Effect of the vertical force component of Class II elastics on the anterior intrusive force of maxillary archwire.

Class II elastics are usually employed in the treatment of excessive overbite and overjet with the Begg technique. The effect of Class II elastics on bite opening and the extent of such an effect is uncertain. This article, based on measurements of 30 cases, illustrates that the effect of the vertical component of force from Class II elastics in reducing the intrusive force generated by the anchor bands in the upper archwire is less than previously believed. The position of the circles in the archwire for intermaxillary elastics has the greatest influence on the anterior intrusive force of the upper archwire. The direction of the Class II elastics and the length of the dental arch (a negative correlation) came second, while the force actually exerted by the elastics had the smallest influence. It is, therefore, suggested that the position of the intermaxillary elastic circles should be located according to the differing clinical objectives.

Dental Stress Analysis↗
PubMed1992

[Study of dento-maxillo-facial growth and development on anterior deep bite with linguoversion of upper incisors during permanent dentition].

By means of computer-X-ray cephalometric system to study the dento-maxillo-facial growth and development was performed in 65 patients of anterior deep bite with lingoversion of upper incisors. The patients were divided into two groups: (1) 35 cases aged 12-16 years and (2) 30 cases aged 17-26 years. The same number of the subjects with normal occlusion were used as control group. The findings were as follows: 1. Besides the dento-maxillo-facial growth and development was abnormal vertically, the posterior anterior discrepancy of the growth trend is also one of the main problems in this kind of malocclusion. 2. The growth of the alveolar bone was inhibited anteriorly by the upper incisors; 3. The deformed mandible has the growth trend to rotate forward and upward in Counterclock wise direction so that it is wise to treat of early.

Adolescent↗
PubMed1991

[Factor analysis of anterior deep bite malocclusions and its significance].

A series of 38 measurements was derived from lateral cephalometric radiographs of a large sample of 195 subjects including 130 patients with deep bite malocclusion and 65 control subjects with normal occlusion. These measurements were subjected to a factor analysis which resulted in a series of 8 factors extracted which accounted for 83.3% of the total variance. These factors in rank order of their percentage sample variability were as follows. Factor 1: vertical height; Factor 2: protrusion-retrusion of anterior teeth; Factor 3: protrusion of mid-face; Factor 4: horizontal position of posterior border of the jaws;Factor 5: protrusion of the chin; Factor 6: protrusion of lip; Factor 7: divergence of the face;Factor 8: inclination of upper Lip. The factor scores were further used in a multiple regression analysis in order to predict other cases. The data-reduction method involving a factor analysis would seem to have great significance of clinical application.

Adolescent↗
PubMed1990

Interleukin-6 induction by tumor necrosis factor and interleukin-1 in human fibroblasts involves activation of a nuclear factor binding to a kappa B-like sequence.

Using variable-length deletion constructs of the 5'-flanking region of the human interleukin-6 (IL-6) gene linked to the chloramphenicol acetyltransferase gene, we showed that the region from positions -109 to -50 mediated the bulk of the response to tumor necrosis factor (TNF) or interleukin-1 (IL-1), while it was less responsive to forskolin. DNA mobility shift assays and DNase I footprinting analysis identified a nuclear protein from TNF- or IL-1-treated fibroblasts that bound to a region comprising a kappa B-like element located between positions -72 and -63 on the IL-6 gene. On the basis of these and other experiments, we conclude that TNF and IL-1 apparently activate IL-6 gene expression by closely related mechanisms involving activation of a NF-kappa B-like factor, whereas the pathway of IL-6 induction by forskolin is, in part, different.

Base Sequence↗
PubMed1990

[The importance of variability in morphologic feature of upper central incisors in linguoversion anterior deep over bite].

190 subjects with linguoversioffl anterior deep over bite, labioversional anterior deep over bite, normal occlusion and anterior cross-bite were chosen for cephalometric analysis. The findings are that most of the upper central incisors in linguoversional anterior deep over bite exist crown-root angulation in a labiolingual direction. This may be one of the causing factors to induce and promote the anterior deep over bite. So that the crown-axis and root-axis of the upper central incisors should be traced separately in cephalometric analysis of linguoversional anterior deep over bite.

Adolescent↗
PubMed1988

Synthesis of interleukin 6 (interferon-beta 2/B cell stimulatory factor 2) in human fibroblasts is triggered by an increase in intracellular cyclic AMP.

Interleukin 6 (IL-6; also referred to as interferon-beta 2, 26-kDa protein, and B cell stimulatory factor 2) is a cytokine whose actions include a stimulation of immunoglobulin synthesis, enhancement of B cell growth, and modulation of acute phase protein synthesis by hepatocytes. Synthesis of IL-6 is stimulated by interleukin 1 (IL-1), tumor necrosis factor (TNF), or platelet-derived growth factor. We examined the role of the cyclic AMP (cAMP)-dependent signal transduction pathway in IL-6 gene expression. Several activators of adenylate cyclase, including prostaglandin E1, forskolin, and cholera toxin, as well as the phosphodiesterase inhibitor isobutylmethylxanthine and the cAMP analog dibutyryl cAMP, shared the ability to cause a dramatic and sustained increase in IL-6 mRNA levels in human FS-4 fibroblasts. Actinomycin D treatment abolished this enhancement. Treatments that increased intracellular cAMP also stimulated the secretion of the IL-6 protein in a biologically active form. Increased intracellular cAMP appears to enhance IL-6 gene expression by a protein kinase C-independent mechanism because down-regulation of protein kinase C by a chronic exposure of cells to a high dose of 12-O-tetradecanoylphorbol 13-acetate did not abolish the enhancement of IL-6 expression by treatments that increase cAMP. IL-1 and TNF too increased IL-6 mRNA levels by a protein kinase C-independent mechanism. Our results suggest a role for the cAMP-dependent pathway(s) in IL-6 gene activation by TNF and IL-1.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Enhancement of cAMP levels and of protein kinase activity by tumor necrosis factor and interleukin 1 in human fibroblasts: role in the induction of interleukin 6.

Although tumor necrosis factor (TNF) and interleukin 1 (IL-1) affect many cell functions, the molecular mechanisms of TNF and IL-1 action are not understood. Our present study shows that exposure of human FS-4 fibroblasts to TNF or IL-1 caused a rapid accumulation of intracellular cAMP and an increase in protein kinase activity. Intracellular cAMP levels peaked 3-5 min after the addition of TNF or IL-1 and returned to basal level by 15 min. Increased phosphorylation of histone HII-B protein was demonstrated with extracts prepared from TNF- or IL-1-treated cells, suggesting an increase in cAMP-dependent protein kinase activity. No evidence was obtained for protein kinase C activation in TNF-treated FS-4 cells. TNF, IL-1, and forskolin all stimulated interleukin 6 (IL-6) mRNA levels in FS-4 cells. The protein kinase inhibitor H-8, inhibiting preferentially cAMP-dependent kinase activity, reduced forskolin-stimulated IL-6 mRNA induction more strongly than TNF- or IL-1-driven IL-6 mRNA induction. These results suggest that activation of cAMP-dependent protein kinase by TNF and IL-1 is important in some actions of these cytokines. In addition, our data on IL-6 induction by TNF and IL-1 suggest that other, yet unidentified, signal transduction mechanisms contribute to TNF and IL-1 actions on gene expression in human fibroblasts.

Cells, Cultured↗
PubMed1988

Interleukin-1 can inhibit interferon-beta synthesis and its antiviral action: comparison with tumor necrosis factor.

Earlier studies showed that both tumor necrosis factor (TNF) and interleukin-1 (IL1) can inhibit virus replication in cultured cells. However, in human FS-4 fibroblasts, in which recombinant human TNF protected cells from encephalomyocarditis (EMC) virus infection, recombinant human IL1 alpha and IL1 beta failed to induce antiviral protection. Moreover, both forms of IL1 inhibited the development of the TNF-induced antiviral state. To elucidate the mechanism of this inhibition, we examined the effect of IL1 on the synthesis of interferon-beta (IFN-beta), stimulated with polyinosinate.polycytidylate [poly(I).poly(C)]. When added 2 h or more before poly(I).poly(C), both forms of IL1 had a strong inhibitory effect on IFN-beta synthesis, as determined by antiviral assay of the IFN-beta protein or by quantitation of IFN-beta mRNA levels in Northern blot analysis. However, when IL1 was added simultaneously with poly(I).poly(C), or 2 h after poly(I).poly(C), IFN-beta synthesis was increased. The inhibitory action of IL1 on poly(I).poly(C)-induced IFN-beta synthesis was abolished in the presence of cycloheximide, suggesting that it is mediated indirectly by an IL1-induced product in the FS-4 cells. In addition to its ability to inhibit IFN-beta synthesis, IL1 also caused a partial reversal of the antiviral action of IFN-beta. In contrast to IL1, TNF did not inhibit IFN-beta synthesis, nor did it interfere with the antiviral action of IFN-beta. Simultaneous addition of TNF and poly(I).poly(C) to FS-4 cells enhanced IFN-beta synthesis. Under proper conditions TNF and IFN-beta showed an additive antiviral effect.

Blotting, Northern↗
PubMed1987

Tumor necrosis factor and interleukin-1 cause a rapid and transient stimulation of c-fos and c-myc mRNA levels in human fibroblasts.

Tumor necrosis factor (TNF) and interleukin-1 (IL-1) were shown previously to be mitogenic for human fibroblasts. Here we show that recombinant human TNF and recombinant human IL-1 alpha increase steady state levels of c-fos and c-myc proto-oncogene mRNAs in quiescent human FS-4 fibroblasts. Proto-oncogene mRNA levels were enhanced within 20 min of TNF or IL-1 addition, peaked at 30 min, and declined to undetectable levels (c-fos) or basal levels (c-myc) by 60 or 90 min. A similar rapid increase in c-fos and c-myc mRNA was seen in quiescent FS-4 cells exposed to cycloheximide. However, in the presence of cycloheximide, both proto-oncogene mRNA levels continued to rise for at least 90 min. The transient nature of the increase in c-myc mRNA levels appears to be a response characteristic for TNF and IL-1 because in quiescent FS-4 cells exposed to 10% fetal bovine serum, steady state levels of c-myc mRNA remained elevated for at least 4 h.

Cycloheximide↗
PubMed1986

Bacterial lipopolysaccharide-induced interferon-gamma production: roles of interleukin 1 and interleukin 2.

Bacterial lipopolysaccharide (LPS) induced human peripheral blood mononuclear cells (PBMC) to produce interferon-gamma (IFN-gamma). Monocytes play a mandatory accessory role in this process, because purified T lymphocytes failed to produce IFN-gamma in response to LPS and the addition of 2% monocytes to T cell cultures resulted in an optimal LPS-induced IFN-gamma production. IFN-gamma production was abolished in the presence of monoclonal antibodies specific for HLA-DR antigen. Addition of exogenous interleukin 2 (IL 2) markedly enhanced IFN-gamma secretion by PBMC induced with LPS. The addition of anti-Tac antibody specific for IL 2 receptors abrogated IFN-gamma production, suggesting that an interaction of IL 2 with IL 2 receptors was involved. By using a specific antibody binding assay, LPS was shown to amplify IL 2 receptor expression on PBMC, whereas exogenous IL 2 showed only a negligible enhancing effect on the expression of its own receptors. Interleukin 1 (IL 1), a product of LPS-stimulated monocytes, potentiated IL 2-induced IFN-gamma production in the absence of LPS. Neither IL 1 nor IL 2 alone induced IFN-gamma production in purified T lymphocyte cultures. When added together, however, substantial levels of IFN-gamma were induced. An enhanced IL 2 receptor expression on T cells was also demonstrated as a result of the combined action of IL 1 and IL 2. These results suggest that induction of IFN-gamma by LPS is due mainly to the generation of IL 1 and an enhanced expression of IL 2 receptors.

Animals↗
PubMed1986

Efficient expression of unfused human alpha D-interferon in Escherichia coli using overlapping termination and initiation codons (TGATG) in its signal sequence.

A plasmid carrying the lambda PL promoter was constructed to express efficiently unfused human alpha D-interferon (HuIFN-alpha D) in Escherichia coli using a TGATG site in its signal sequence, which occurs also in the lambda DNA sequence. The unfused nature of HuIFN-alpha D expressed by pBV867 in E. coli (BMH 71-18) was confirmed by the following evidence: first, the purified IFN showed a single band of 19.5K in sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE); a 27K band, representing lambda N-HuIFN-alpha D fusion protein, was not detected. Second, the peak of IFN activity coincided with the 19.5K protein. Third, the peak of absorbent material for human leukocyte IFN antibody coincided with that of IFN activity. Finally, amino-terminal sequencing of purified IFN demonstrated an unfused HuIFN-alpha D. This suggests that E. coli is able to process the signal sequence of HuIFN-alpha D. Studies on the mechanism of "translational coupling" initiation of gene expression were carried out by the construction of two hybrid plasmids and titration of the IFN activities produced by them. The level of expression by the ATG-TGATG initiation mode was found to be six times higher than that of the single ATG mode.

Bacteriophage lambda↗