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S Silva

Publications and source records attributed to S Silva.

At least 73 records · Page 4Linked to original sources
PubMed1993

MHC class I expression on prelymphomatous and lymphomatous B-cells is not inhibited by an E mu-myc transgene.

Increased expression of oncogenes from the myc family has been associated with down-regulation of major histocompatibility complex (MHC) class I molecules. In certain models this has been suggested to contribute to tumour progression. Transgenic mice bearing the cellular myc oncogene coupled to the lymphoid-specific immunoglobulin heavy chain enhancer (E mu) develop clonal B lymphoid malignancies early in life. We have asked if expression of such a constitutively activated E mu-myc transgene in BALB/c mice affects MHC class I expression. H-2Kd and Dd expression on prelymphomatous and lymphomatous B-cells as well as newly established pre-B or B lymphoma cell lines derived from E mu-myc transgenic BALB/c mice were analysed. The results reveal no down-regulated or otherwise altered expression of H-2Kd or Dd on any of the cell populations examined. The results are discussed in relation to the myc associated down-regulation of MHC class I molecules observed in other experimental models.

Animals↗
PubMed1993

Inositol 1,4,5-trisphosphate mass changes from fertilization through first cleavage in Xenopus laevis.

After fertilization in Xenopus laevis, inositol 1,4,5-trisphosphate (IP3) mass increased from 53 to 261 fmol/cell and returned to near basal by 10 min after insemination. IP3 was also elevated over control egg levels during first mitosis and first cleavage. Because IP3 levels and the fertilization calcium wave decline at about the same time and because calcium ionophore or pricking the egg increased IP3, the fertilization calcium wave may be due to calcium-induced IP3 production. In addition, the onset of sperm motility was associated with an increase, whereas the acrosomal reaction was accompanied by a decrease in IP3 mass. Combining our published data with this report, the first chronology of the levels of IP3 from the induction of meiosis (maturation) through fertilization and cleavage in one cellular system is summarized. These data suggest an in vivo dose response for IP3 and calcium release. A small (17 fmol/cell) IP3 change during the induction of meiosis may not be associated with a calcium change. Larger IP3 changes at cleavage (40 fmol/cell) and mitosis (125 fmol/cell) are associated with localized small calcium increases, whereas the largest IP3 change (208 fmol/cell) is associated with the large calcium increase at fertilization.

Acrosome↗
PubMed1993

[The assessment of the histomorphological characteristics of the arteria gastroepiploica dextra and its potential as an artery for myocardial revascularization].

OBJECTIVE: Comparative analysis of the histomorphological characteristics of left (LIMA) and right (RIMA) internal mammary arteries, right gastroepiploic (RGEA) and anterior descending artery (ADA) with evaluation of the respective prevalence of atherosclerotic changes. SETTINGS: Laboratory of Anatomo-Pathology of a Central Hospital with necropsy material obtained from consecutive individuals, deceased of a non-cardiac cause and older than 60 years. MATERIAL AND METHODS: In 31 cadaver fragments of the RIMA, LIMA, GEA and ADA, were obtain, subsequently fixed and stained in order to become evident the structure of the medial layer, and the presence of possible atherosclerotic changes (intimal Hyperplasia, cholesterol clefts, foam-cells, inflammatory cells infiltrate, rupture of the internal elastic lamina, medial fibroses and calcifications). RESULTS: 1--The RGEA has the structure of a muscular artery as the ADA, opposed to the LIMA and RIMA that are elastic arteries. 2--The atherosclerotic changes were predominantly found in the ADA with no significative differences in there prevalence in the RIMA, LIMA or RGEA. CONCLUSIONS: The RGEA despite having histological characteristics diverse than the LIMA and RIMA, has a similar prevalence of atherosclerotic changes and intimal hyperplasia; those allow us to predict a behaviour and a long-term patency comparable, when used as bypass graft for myocardial revascularization.

Abdomen↗
PubMed1992

An exceptional mouse plasmacytoma with a new kappa/N-myc [T(6; 12) (C1; B)] translocation expresses N-myc but not c-myc.

Mouse plasmacytomas (MPC) carry one of three reciprocal translocations that juxtapose c-myc to one of the three immunoglobulin (Ig) loci. Here we describe an exceptional MPC, induced by pristane oil and Abelson (A-MuLV) virus. It does not carry any of the three c-myc/Ig translocations, but contains a previously unknown reciprocal T(6;12) translocation affecting the bands known to carry the IgK (6C/1) and N-myc (12B) loci, respectively. Northern blot analysis showed high N-myc but no c-myc expression. This is consistent with the constitutive activation of N-myc by a juxtaposition of the IgK and N-myc loci. Reciprocal translocation in B-cell derived tumors are believed to involve the Ig loci by the action of some enzyme that participates in the physiological rearrangement of the Ig loci. Only transcriptionally active chromatin regions are accessible to such recombinases (Alt et al. 1987). N-myc is not expressed in B-cells, but it is transcriptionally active during the early pro- and pre-B cell stage, whereafter it and the surrounding chromatin region becomes inactive (Smith et al. 1992). It is therefore most likely that the N-myc/Kappa translocation has arisen at an early stage of B-cell differentiation. This would imply that the myc/Ig translocations do not block B-cell differentiation. They also reaffirm the functional equivalence of N- and c-myc in relation to B-cell carcinogenesis, as shown by our previous work on tumor induction in N-myc transgenic mice (Wang et al. 1992).

Animals↗
PubMed1992

Insulin and progesterone increase 32PO4-labeling of phospholipids and inositol 1,4,5-trisphosphate mass in Xenopus oocytes.

After a 4-6 h induction period, insulin or progesterone induces Xenopus oocytes to enter prophase of meiosis. During the period of induction, both insulin and progesterone induced an increase in 32PO4 labeling of phosphatidylcholine and phosphatidylinositol. Through a mass assay, we found that insulin and progesterone increase inositol 1,4,5-trisphosphate (IP3) at about 15-30 s, 15 min and at about 2-3 h (0.5 GVBD50) after hormone addition. Since IP3 increases were small (from a basal of 66 to 104 nM), the results agree with prior conclusions that progesterone does not induce a large, cytosolic calcium elevation. Insulin is probably acting through the insulin-like growth factor-1 receptor as insulin concentrations greater than about 50 nM are required to increase IP3.

Animals↗
PubMed1992

How reliable is bio-electrical impedance analysis for individual patients?

We performed bio-electrical impedance analysis (BIA) on 38 healthy adults with an initial body mass index (+/- s.d.) of 30 kg/m2 (+/- 5) before and after a low calorie diet. Five weeks later a mean weight loss of 4.2 +/- 2.3 kg was observed. According to BIA, fat-free mass (FFM) decreased in 28 subjects and increased in ten. In four cases the reduction was greater than the weight loss. At the end of the ten week diet regimen all 27 subjects followed up demonstrated a further weight reduction. According to BIA, FFM decreased in 22 subjects, increased in four and did not change in one case. In one case the reduction was greater than the weight loss. Although mean FFM values assessed by skinfolds and BIA were not significantly different before and after the weight loss period, no correlations were found among the individual changes in FFM evaluated by the two methods. Our results suggest that single frequency (50 KHz) impedance must be used with care in clinical conditions.

Adult↗
PubMed1991

Differential susceptibility of BALB/c and DBA/2 cells to plasmacytoma induction in reciprocal chimeras.

Reciprocal chimeras were generated between BALB/c and DBA/2 mice by inoculating newborn recipients of either strain with bone-marrow (BM) cells of the other through the periorbital vein. DBA/2 mice inoculated with the BALB/c with proven chimerism will be referred to as C----D, the reciprocal as D----C. The BALB/c cells carried a Robertsonian 6;15 (Rb6;15) chromosome marker to facilitate identification. The chimeric mice contained between 5% and 70% of donor cells when examined at 4 to 5 weeks of age. Six of 10 C----D developed plasmacytomas (MPC) after 3 x 0.5 ml monthly pristane treatment (incidence 60%) and 8 of 25 (incidence 32%) after 2 to 3 x 0.5 ml pristane followed by Abelson virus (A-MuLV) infection. Seven of 15 D----C developed MPC after pristane treatment (incidence 47%) and 4 of 17 after pristane + A-MuLV (incidence 24%). All tumors that have arisen in both reciprocal chimeras originated from BALB/c cells independently of the degree of chimerism. All tumors contained an Ig/myc translocation. Among the C----D chimeras, 5 carried t(12;15) and I t(6;15) in the pristane-treated group, while 4 carried t(12;15), I t(6;15) and 3 t(15;16) in the pristane + A-MuLV. Among the D----C chimeras 6 carried t(12;15) and I t(6;15) in the pristane-treated group, while 3 t(12;15) and I t(6;15) in the pristane + A-MuLV. No tumors developed in 18 pristane- and 22 pristane + A-MuLV-treated DBA/2 mice nor in 15 pristane- and 17 pristane + A-MuLV-treated (BALB/c x DBA/2)F1 mice. The data indicate that BALB/c and DBA/2 cells differ in their propensity to transform into plasmacytoma in identical host environments after both pristane and pristane + A-MuLV treatment. They also show that the oil granuloma can support MPC development in either type of chimeric host.

Abelson murine leukemia virus↗
PubMed1991

v-abl does not abolish IL-6 requirement by murine plasmacytoma cells.

Activation of c-myc by juxtaposition to an immunoglobulin locus and introduction of the v-abl oncogene act synergistically in generating a mouse plasmacytoma (PC). The question arose whether the effect of v-abl could be attributed to a deregulation of interleukin-6 (IL-6) production or responsiveness, in view of the fact that IL-6 exerts potent growth-stimulatory activity on PC cells. We studied the effect of IL-6 on the in vitro growth of primary PCs induced by pristane alone (TEPCs) or by pristane + A-MuLV (ABPCs). Five of 13 TEPCs and 3 of 7 ABPCs responded to IL-6. Macrophage supernatants prepared from both TEPCs and ABPCs had similar stimulatory effects on PC cells. From 30 primary PCs (including both TEPCs and ABPCs), we established 9 in vitro lines, 2 of which expressed v-abl. All were able to grow on macrophage feeder layers. Three types of behavior could be distinguished on the basis of growth in feeder-free cultures in the presence and absence of IL-6. Group I contained 4 IL-6-dependent lines. Group II contained 2 IL-6-independent lines (one v-abl expressor) that grew faster in the presence of IL-6. Group III consisted of 3 feeder-dependent lines (one v-abl expressor) that were not significantly stimulated by IL-6. These findings indicate that v-abl expression does not influence IL-6 dependence or responsiveness by itself. The supernatant of one line in group II was able to stimulate PC cells. All 6 lines of Groups I and II carried a typical (12;15) translocation, while all 3 lines in group III had a variant (6;15) or (15;16) translocation.

Abelson murine leukemia virus↗
PubMed1991

Endogenous opiate response to pain in rheumatoid arthritis and cortical and subcortical response to pain in normal volunteers using positron emission tomography.

Identification of the main areas in the brain that respond specifically to the "suffering" components of pain has been achieved by using serial dynamic measurements of blood flow as an index of synaptic activity. Specific response to a repeated painful thermal stimulus as compared to a non-painful thermal stimulus in normal male volunteers identified the anterior cingulate cortex and the thalamus contralateral to the side of stimulation as the main sites of significant response. It was concluded that it was these areas where pain was likely to be experienced. Changes in opioid receptor binding in the brain was measured using 11C-diprenorphine and positron emission tomography in three patients with rheumatoid arthritis. In the two patients with active rheumatoid arthritis substantial changes in opioid receptor binding in the brain are described. The significance of these findings are discussed.

Arthritis, Rheumatoid↗
PubMed1991

A new variant 15; 16 translocation in mouse plasmacytoma leads to the juxtaposition of c-myc and immunoglobulin lambda.

Mouse plasmacytomas (MPCs) induced by pristane oil, or by a combination of pristane oil and Abelson virus, carry one of two chromosomal translocations. The typical 12; 15 translocation leads to the juxtaposition of c-myc and immunoglobulin heavy-chain sequences, whereas the 6; 15 translocation links the kappa light-chain locus with the pvt-1 (plasmacytoma variant translocation) locus, located at least 75kb 3' of c-myc [Cory, S., Graham, M., Webb, E., Corcoran, L. & Adams, J. (1985). EMBO J., 4, 675-681]. Unlike the human Burkitt's lymphoma-associated translocation, the lambda/myc juxtaposed variant translocation has not been found previously in MPCs. Using unconventional MPC induction systems in which the tumor precursor cell was induced to proliferate in a secondary host, we have recently identified a 15; 16 translocation in six of the derived MPCs [Wiener, F., Silva, S., Sugiyama, H., Babonits, M. & Klein, G. (1990). Genes Chromosomes Cancer, 2, 36-43]. Chromosome 16 harbors the lambda light-chain gene. To explore whether the 15; 16 translocation represents the lambda/myc juxtaposition, we have mapped the breakpoints on chromosomes 15 and 16 by pulsed-field gel electrophoresis (PFGE). The pvt-1 region was mapped to approximately 220 kb 3' of c-myc. The breakpoint on chromosome 15 in ABPC-Ch-163-10, one of the six 15; 16 translocation-carrying MPCs, was situated approximately 80 kb 3' of c-myc and 140 kb 5' of pvt-1b, the major breakpoint cluster region of the previously analysed 6; 15 variant MPCs. The breakpoint on chromosome 16 was found to cut between the V1 and C3 regions of the lambda locus. Co-migration experiments showed that the C3 and the myc gene were juxtaposed head to tail on the 15; 16 translocation chromosome. On the reciprocal product V1 was juxtaposed to pvt-1.

Animals↗
PubMed1990

Abelson murine leukemia virus transforms preneoplastic Emu-myc transgene-carrying cells of the B-lymphocyte lineage into plasmablastic tumors.

E mu-myc transgenic mice were back-crossed to BALB/c mice up to back-cross generation 3. The offspring that included transgene-carrying and -negative mice in approximately equal proportions were randomly divided into 2 groups. Thirty-four mice (group I) were treated with pristane, followed by A-MuLV, and 40 (group II) were injected with A-MuLV alone. Altogether, 16 lymphoid tumors developed in group I and 17 in group II. Nine of the tumors in group I and 4 in group II appeared as ascitic tumors. The ascites contained lymphoblasts and 10 to 45% plasmacytoid cells. These tumors were designated as plasmablastic lymphomas (PLs). All tumors except one were transgene-positive and did not carry translocations. An exceptional tumor in group I carried a variant 6;15 translocation but not the transgene. It obviously corresponds to the regular Abelson + pristane-induced plasmacytoma. Among 11 tested PLs, 10 had a single retroviral insertion site, while one tumor showed 3. Among 18 untreated transgenic descendants (group III), chosen randomly during serial back-crosses, 15 (83%) developed lymphomas, with no sign of plasmacytoid differentiation. The incidence was comparable in all 3 groups, assuming 50% of the mice in groups I and II to be transgenic. The time distribution of tumor development was also similar. Spleen cells from transgene-carrying mice with no clinical sign of lymphoma were infected in vitro with A-MuLV and transplanted i.p. into BALB/c recipients. PLs developed in 26 of 31 pristane-treated recipients, but in only one of 18 untreated recipients. One of 6 PLs tested was monoclonal, whereas the remaining 5 were oligoclonal. They all expressed v-abl. These results show that some of the preneoplastic B-cells that expressed constitutively active myc transgene turned into plasmablasts after infection with A-MuLV. Full development of their neoplastic potential was facilitated by the presence of pristane-granuloma.

Animals↗
PubMed1990

The "missing" mouse plasmacytoma (MPC) associated translocation T(15;16) occurs repeatedly in new MPC induction systems.

A reciprocal translocation between chromosomes 15 and 16 has been detected in seven murine plasmacytomas induced by a combination of pristane and Abelson virus. Six of the tumors were induced in a new, unconventional experimental system based on transfer of uninfected or Abelson virus infected bone marrow and spleen cells, respectively, into pristane treated mice. All six tumors were of donor type. The seventh tumor appeared in a conventional pristane + Abelson virus treated mouse. This tumor was unusual in carrying both the 15;16 variant translocation and the typical 12;15 translocation, in the same tumor cells. In the new 15;16 variant, the breakpoint of chromosome 15 was at the interphase of the D2/3 sub-bands, as in mouse plasmacytomas with the previously well-known typical 12;15 and variant 6;15 translocations. The breakpoint on chromosome 16 was mapped to band 16B1, corresponding to the presumed cytogenetic site of the Ig-lambda gene. In three of the seven tumors with the 15;16 translocation, the derivative chromosome 15 had undergone a duplication, a feature that has not been previously encountered in the MPC-associated 12;15 and 6;15 translocation carriers. The reciprocal derivative chromosome 16 was lost from one of the seven tumors. We postulate that the 15;16 translocation results in juxtaposition of the myc gene to lambda sequences, probably in a similar orientation as previously described for the variant 6;15 translocation.

Abelson murine leukemia virus↗
PubMed1990

A murine plasmacytoma with a variant (15;16)(D2/3;B1) translocation that involves the c-myc and lambda light chain gene-carrying chromosomes.

A murine plasmacytoma (MPC) with a reciprocal translocation between chromosomes 15 and 16 with breakpoints in 15D2/3 and 16B1 is reported. The breakpoint on chromosome 15 is identical to the breakpoint in the MPC-associated typical (12;15) and kappa variant (6;15) translocation. Therefore it probably involves the c-myc gene as well. Unlike the Burkitt lymphoma (BL) system, a lambda/myc variant translocation has not been described in the MPC system. Chromosome 16 is known to carry the lambda gene. Therefore, the 15;16 translocation probably represents the "missing" lambda/myc variant in MPC, suggesting that the lambda gene is localized at 16B1.

Animals↗