Search PubMed⌕ Search

Biomedical subjects

D Sun

Publications and source records attributed to D Sun.

At least 415 records · Page 23Linked to original sources

[Postoperative radiation of retinoblastoma--report on 22 patients].

From July 1958 to December 1979, 22 patients with retinoblastoma were treated postoperatively by radiotherapy. All were proved by pathology. There were 12 stage I, 1 stage II, 8 stage III and 1 stage IV lesions. Radiation dose was more than 15 Gy and most of the patients received 40-50 Gy in 4-5 weeks. The overall cancer free 5 year survival rate was 55% (12/22). The 5 year survival rate of stage I patients was 75% (9/12), and that of stage III patients was 38% (3/8). None of the stage II and IV patients survived. Dose of 40-50 Gy/4-5 wk is considered to be optimal for control of the tumor. Dose higher than 60 Gy/6 wk could lead to retarded growth in the orbital and temporal bony structures if the patient survives for ten years or more.

Child↗

Synthesis and cell surface display of class II determinants by long-term propagated rat T line cells.

We have investigated the capacity of the encephalitogenic BS rat T cell line bs 83 and its variant clone bs 83.III.C6 to synthesize and express RT1.B-specific class II molecule subsets defined by monoclonal antibodies (mAb) MRC-OX6 and MRC-OX3. Earlier studies had indicated that mAb MRC-OX6 recognizes three distinct molecular species: an immature oligomeric polypeptide chain complex comprised of the polymorphic subunits alpha, beta and the invariant proteins of the gamma group; a biosynthetic intermediate composed of post-translationally modified alpha, beta and gamma chain (denoted p35) and a fully glycosylated alpha, beta two-chain complex derived from the plasma membrane. MRC-OX3 was shown to recognize a serologically distinct alpha, beta two-chain complex that coexists with the MRC-OX6-specific heterodimer at the cell surface. Here we show that premutant bs 83 cells were unable to synthesize class II molecules of either set. In contrast endogeneous synthesis by mutant cells of MRC-OX6-specific molecules was demonstrated. Unlike control spleen cells variant cells failed to synthesize the mature MRC-OX3-reactive class II subset. Instead a three-polypeptide chain complex comprised of the terminally glycosylated subunits alpha, beta and invariant chain p35 was present at the cell surface. This complex appears to represent the preserved biosynthetic intermediate that failed to release invariant chain p35 upon its transit into the plasma membrane. These latter observations support our notion of gamma chain-induced epitope diversification during post-translational maturation of RT1.B-specific class II molecules.

Animals↗

Identification of two ancillary subunits of Escherichia coli type 1 fimbriae by using antibodies against synthetic oligopeptides of fim gene products.

We have chemically synthesized oligopeptides corresponding to the NH2-terminal stretch of two gene products, designated FimG and FimH, of the fim gene cluster of Escherichia coli. These synthetic peptides, designated S-T1FimG(1-16) and S-T1FimH(1-25)C, evoked antibodies in rabbits that reacted with 14- and 29-kilodalton subunits, respectively, of dissociated fimbriae encoded by the recombinant plasmid pSH2 carrying the genetic information for the synthesis and expression of functional type 1 fimbriae. Neither of these fimbrial proteins was detected in dissociated fimbrial preparations from nonadhesive E. coli cells carrying the mutant plasmid pUT2002, containing a restriction site-specific deletion of fimG and fimH. Anti-S-T1FimH(1-25)C inhibited the adherence of type 1 fimbriated E. coli to epithelial cells. Immunoelectron microscopy revealed that anti-S-T1FimH(1-25)C, but not anti-S-T1FimG(1-16), bound to intact type 1 fimbriae of E. coli at the fimbrial tips and at long intervals along the fimbrial filaments. Anti-S-T1FimG(1-16) appeared to be directed at epitopes not accessible on the intact fimbriae and consequently failed to bind to intact fimbriae or to block fimbrial attachment. Our results suggest that the fimG and fimH gene products are components of type 1 fimbriae and that FimH may be the tip adhesin mediating the binding of type 1 fimbriated E. coli to D-mannose residues on mucosal surfaces.

Antibodies, Bacterial↗

Immune reactivity in the nervous system: modulation of T-lymphocyte activation by glial cells.

The vertebrate central nervous system (CNS) has been traditionally thought to be inaccessible for the passenger lymphocytes of the immune system. This does not seem to be the case: activated T-lymphocytes can readily cross the endothelial blood-brain barrier (BBB) and some glial cells, notably the astrocytes, seem to be programmed to act as most efficient and complex partners for antigen-specific T-lymphocytes. We used myelin basic protein (MBP) specific permanent rat T-lymphocyte lines as probes to assess the immune status of the CNS. These cells, upon activation in vitro, are able to transfer lethal, experimentally induced autoimmune-encephalomyelitis (EAE) to normal syngeneic recipients. Activated T-lymphocytes, but not resting ones, can break through the BBB irrespective of their antigen specificity. Immune surveillance of the CNS thus seems to be executed by activated T-lymphocytes. Having crossed the BBB, the activated T-cells interact with local glial cells by releasing factors, including interferon-gamma, which induced astrocytes to synthesize and express, on their membranes, class II major histocompatibility antigens (Ia determinants), which are critically required for immunogenic presentation of antigens to T-cells. Indeed, Ia-induced astrocytes of the CNS (and the Schwann cells of peripheral nerves) are efficient antigen presenter cells, which are able strongly to up-regulate antigen-reactive T-lymphocytes. In addition, it has recently been shown that at least some astrocytes are able to down-regulate immune cells. Some, but not all, astrocytes are capable of suppressing activation of T-cells. This suppression can be modulated by interferon-gamma, and is sensitive to irradiation. The question of whether suppression is mediated by direct cell-to-cell contact or via soluble mediators (e.g. apolipoprotein E) is under investigation. Astrocytes have been found to be most subtle regulators of immuno-competent T-cells. Most probably they are centrally involved in physiological immune reactivity of the CNS, and it will be tempting to learn how far glial cells are involved in transmitting regulatory signals between the immune and nervous systems.

Animals↗

Inhibition of replication of the etiologic agent of acquired immune deficiency syndrome (human T-lymphotropic retrovirus/lymphadenopathy-associated virus) by avarol and avarone.

Avarol and avarone are two antimitotic and antimutagenic agents that preferentially inhibit proliferation of T-cell leukemia lines in vitro. This report shows that these compounds have a dose-dependent inhibitory effect on the replication of the etiologic agent of acquired immune deficiency syndrome (AIDS), human T-lymphotropic retrovirus (HTLV-III)/lymphadenopathy-associated virus, in human H9 cells in vitro. Both compounds show a significant cytoprotective effect on HTLV-IIIB-infected H9 cells at concentrations as low as 0.1 microgram/ml (0.3 microM). Both avarone and avarol block in a dose-dependent manner the expression of the p24 and p17 gag proteins of HTLV-III in H9 cells after virus infection and block viral replication, as judged by approximately 80% inhibition of reverse transcriptase activity. These results strongly suggest that these compounds may prove to be useful in the treatment of patients with AIDS and AIDS-related complex.

Acquired Immunodeficiency Syndrome↗

Clonal analysis of the population of chondrocytes from the Swarm rat chondrosarcoma in agarose culture.

Chondrocytes from the Swarm chondrosarcoma, a transplantable rat tumor, have been difficult to maintain in tissue culture for extended periods due to a time-dependent alteration of the culture to a more fibroblastic phenotype. This feature precluded the use of these cultures to examine chronic conditions that may affect cell metabolism, and the homogeneity or heterogeneity of the tumor cells within the culture population could not be examined. Use of suspension culture in agarose stabilized the chondrocyte phenotype, permitting long-term culture. Clones of tumor chondrocytes were established in agarose and were examined over 2-3 weeks for evidence that the cells were accumulating a proteoglycan-rich extracellular matrix, as determined by positive staining by Alcian blue, and were undergoing cell division. Nearly 90% of the cloned cells exhibited a prominent extracellular matrix by day 7 of culture and greater than 99% did so by day 14. Cell division did not occur to any great extent until days 6-7 of culture. After this lag, the cells appeared to undergo logarithmic growth, with a cell generation time of about 12 days. By 20 days of culture, between 80 and 90% of the initial clones contained multiple cells, indicating that nearly all the cells were in, or had entered, the cell cycle. These results suggest that the chondrocytes from the rat chondrosarcoma form a homogeneous cell population with respect to their ability to synthesize an extra-cellular matrix and divide.

Alcian Blue↗

Calmodulin: localization in plant tissues.

Calmodulin was purified from bovine brain by preparative SDS-polyacrylamide gel electrophoresis. The denatured, purified calmodulin was used to immunize rabbits to produce antiserum. This antiserum was used to study the distribution of calmodulin in plant tissues by indirect immunohistochemistry. The root tips from corn seeds, oat seeds, peanuts, spaghetti squash seeds, and the terminal buds of spinach were investigated. A method for plant tissue sectioning and inhibition of endogenous peroxide activity was developed. In the corn root section, reaction product from anti-calmodulin was found mainly in the root cap cells. Lesser but significant amounts of calmodulin were localized in metaxylem elements, in some stele cells surrounding metaxylem elements, in apical initials, and in the cortical cells. Similar findings were also observed in other root tips from oat seeds, peanuts, and spaghetti squash seeds. In the terminal buds of the spinach, calmodulin-stained cells were highly concentrated in the apical meristem and leaf primordium. These findings suggest that the high concentration of calmodulin in the root cap may be important in relation to gravitropism and growth development.

Calmodulin↗

Suppressor mutations for crs mutants of Bacillus subtilis.

Mutants of Bacillus subtilis which carried suppressor mutations for catabolite-resistance gene crsA47 were isolated from methylmethanesulfonate-treated cultures of GLU-47 (crsA47). The suppressor mutation, sca19, suppressed resistance of crsA47 mutant to glucose and other inhibitors of sporulation. Moreover, the suppressor mutation could restore the rate of growth and the level of IMP dehydrogenase and alkaline phosphatase of crsA47 mutant to the wild-type level. The scal19 mutation was also able to suppress catabolite resistance of other crs mutants. The map position of the sca19 mutation indicated that this mutation was an intergenic suppressor for the crs mutants. It was also found that an erythromycin-resistance mutation, eryl, could suppress the catabolite resistance of some of the crs mutants. Our results were discussed in relation to the importance of a proper state of metabolic activities and membrane functions during the initiation of sporulation.

Alkaline Phosphatase↗

Killer-cell lines derived from mouse thymus, resembling large granular lymphocytes and expressing natural killer-like cytotoxicity.

Murine thymus cells were maintained in vitro with supernatant-factors derived from Concanavalin-A-stimulated spleen cells. After an initial phase of vigorous proliferation, large granular cells (GC), which were not observed in fresh thymus cell preparations, appeared in these cultures. GC, derived from C3Hf/Tif-, BALB/c-, and C57BL/10-thymus cultures, could be slowly expanded and have been maintained as increasingly homogeneous (oligoclonal) lines for up to six months. During this time, other types of thymus cells died or were diluted out. Thymic GC differ functionally and histochemically from macrophages and mast cells. They do not phagocytize zymosan particles, bind opsonized SRBC, express nonspecific esterases or contain detectable amounts of histamine. GC share many features with natural killer (NK) cells and large granular lymphocytes (LGL). One morphologically representative line (C3Hf/Tif) had the following surface phenotype: Thy-1+, Lyt-1-, Lyt-2-, H-2K+, I-A-, asialo Gm1+. GC bind peanut agglutinin (PNA) on their surface and contain azurophilic granules. These cytoplasmic granules are considerably larger than those in LGL. Cells of a GC line derived from mouse strain C3Hf/Tif (H-2k) lysed the NK-sensitive YAC-1 (H-2a) and EL-4 (H-2b), but not the NK-insensitive P815 cells.

Animals↗

Functionally different subpopulations of mouse macrophages recognized by monoclonal antibodies.

Four rat anti-mouse macrophage monoclonal antibodies are described. Three of them are highly specific for macrophages, and one cross-reacts with granulocytes. All 4 antibodies do not react with membrane antigens shared by all macrophages, but with antigens present only on subpopulations of 20-50% of the cells. All antibodies are directly or indirectly cytotoxic for macrophages. The subpopulations defined by these antibodies can be correlated with certain macrophage functions. Thus, antibody M 43 eliminates macrophages that are activated by lymphokine to cytotoxicity. Antibodies M 43 and M 57 eliminate macrophages that kill antibody-coated tumor targets, and clone 102 (strictly macrophage-specific) eliminates natural killer cells. Only M 143, reacting with 10-30% of macrophages, has not yet been correlated with any function. With the use of these antibodies, cells of the macrophage lineage with specific functions can be recognized and eliminated from a given population.

Animals↗

Macrophages as cytotoxic effector cells.

Cells of the mononuclear phagocyte system can be activated by lymphokines to both increased extracellular cytotoxicity against tumor targets and intracellular cytotoxicity against micro-organisms. In addition, these effector cells can kill antibody-coated target cells in an ADCC system. These two cytotoxic mechanisms can co-operate and act synergistically. Such an synergistic action is characterized by the specificity of the antibody which coats the target cells and not by the non-specific activation induced by high dosages of lymphokine. The lymphokine MCF has partially been purified and separated from a variety of other lymphokines. This purified material, when injected into mice intraperitoneally, activates the macrophages to strong cytotoxicity. Evidence obtained by the use of different rat anti-mouse macrophage monoclonal antibodies suggests that there exist different subpopulations of macrophage and that some of these subpopulations can be correlated to defined functions.

Animals↗

Value of postoperative radiotherapy for thyroid cancer.

A series of 405 patients with thyroid cancer treated by surgery with or without postoperative radiotherapy from February 1958 through 1979 is reported. The immediate evaluation of the operation was that it was either incomplete or complete. Incomplete surgery implied that there was (1) possible residual tumor in the operative field, the result of difficult dissection of the tumor off the neighboring organs or tissues, as assessed by the surgeon; (2) multiple (more than five) lymph nodes involved; (3) positive border of the removed lesions; or (4) microscopic evidence of tumor in the operative field. Complete surgery implied through extirpation of cancer grossly and microscopically. In 297 patients who had complete surgery, 238 patients treated by surgery alone had a 5-year survival rate of 92% (218/238), while 59 patients who received postoperative radiotherapy had a 5-year survival rate of 78% (46/59). The optimum dose of postoperative radiotherapy was 50-70 Gy in 5 to 8 weeks, with the spinal dose kept under 40 Gy. Our experience shows that postoperative radiotherapy did not improve the survival of patients who had had complete surgery. Yet, in 108 patients who had incomplete surgery, surgery alone yielded a 5-year survival rate of 33% (19/57), while surgery plus radiotherapy yielded a 5-year survival of 71% (36/51). Our observation shows a remarkable benefit with postoperative radiotherapy in patients who have had incomplete surgery (P less than 0.05). According to pathologic criteria, postoperative radiotherapy was more effective in well-differentiated cancers than in poorly differentiated ones. It was equally effective in untreated as well as recurrent lesions. The prognosis for younger patients was better, but the sex of the patients did not affect prognosis.

Adolescent↗

The tumor suppressor p53 can reduce stable transfection in the presence of irradiation.

The tumor suppressor p53 is believed to play an essential role in maintaining genome stability. Although it is currently unknown how p53 is involved in this important biological safeguard, several previous publications indicate that p53 can help to maintain genome integrity through the recombination-mediated DNA repair process. The integration of linearized plasmid DNA into the host chromosome utilizes the same repair process, and the frequency can be measured by clonogenic assays in which cells that were stably transfected by plasmid integration can be scored by their colony-forming abilities. To gain insight into whether p53 has a direct role in plasmid integration into the host chromosome, we determined the frequency of stable transfection with CHO cells expressing either wild-type or mutant p53 in the presence and absence of irradiation. We found that low-dose irradiation ( approximately 50 to 100 cGy) increased stable transfection frequencies in CHO cells regardless of their p53 status. However, the increase of transfection frequency was significantly lower in CHO cells expressing wild-type p53. Our data thus suggest that wild-type p53 can suppress plasmid DNA integration into the host genome. This p53 function may play a direct and significant role in maintaining genome stability.

Animals↗