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J Spira

Publications and source records attributed to J Spira.

At least 19 recordsLinked to original sources
PubMed1988

The evaluation of 4-hydroxy-3-methoxyphenylglycol sulfate as a possible marker of central norepinephrine turnover. Studies in healthy volunteers and depressed patients.

Much evidence indicates that urinary 4-hydroxy-3-methoxyphenylethyleneglycol (MHPG) is an insensitive measure of central norepinephrine metabolism. This conclusion, however, seems to apply mainly to total urinary MHPG, since previous findings point to the possibility that the major proportion of urinary MHPG sulfate originates in the CNS, while most urinary MHPG glucuronide originates in peripheral organs. To examine this hypothesis, experiments were performed by which we altered MHPG turnover in man at two different stages: firstly, strong physical exercise (ergometer) increased the urinary excretion rate of MHPG glucuronide and not that of MHPG-sulfate; secondly, ethanol (l g/kg), which is known to block the metabolism of MHPG to vanilmandelic acid in the liver, increases the urinary excretion rate of the glucuronide and not that of sulfate. Both experiments indicate that alteration of peripheral norepinephrine turnover changes the urinary excretion of MHPG glucuronide only and not that of sulfate, thus providing strong, albeit indirect, evidence for a primarily central origin of MHPG sulfate. Preliminary experiments in 32 depressed patients showed little difference in both MHPG fractions compared with healthy controls, apart from a slightly reduced excretion rate of glucuronide. These findings fail to provide any evidence of central, and only small changes in peripheral norepinephrine metabolism in depression.

Adult↗
PubMed1985

Mapping of the c-myc, pvt-1 and immunoglobulin kappa genes in relation to the mouse plasmacytoma-associated variant (6;15) translocation breakpoint.

A variant mouse plasmacytoma (MPC)-associated translocation chromosome has arisen by pericentric inversion and exchange of the distal segments of a Robertsonian 6;15 fusion chromosome in the CAK TEPC 1198 mouse plasmacytoma, as described earlier. In situ hybridization was performed on the normal and the inverted Rb chromosomes, using myc and kappa probes. On the normal Rb chromosome, myc was in the 15 D2/3 region, whereas kappa hybridized in the 6 C2 area, as expected. On the inverted Rb chromosome, myc remains on the centrometric side of the translocation breakpoint on the chromosome 15-derived portion, whereas kappa has moved to the chromosome 6-derived segment that joined the same breakpoint on the telomeric side. Taken together with our recent demonstration that the murine c-myc locus is oriented 'head up' on chromosome 15, and with the results of Cory and co-workers concerning the relationship between the kappa gene and the associated pvt-1 region in the CAK TEPC 1198 tumor, the following conclusions can be drawn: (i) in the variant translocation of the CAK TEPC 1198 MPC, the breakage occurs 3' of the c-myc gene, as in the human Burkitt lymphoma-associated variant translocations; (ii) the pvt-1 gene on chromosome 15 is distal to the myc gene; (iii) the kappa light chain locus is oriented 'head up' on mouse chromosome 6 and faces pvt-1 and, beyond it, c-myc, in a head-to-tail configuration.

Animals↗
PubMed1985

A new approach to gene mapping by in situ hybridization on isolated chromosomes.

A new technique was developed for in situ hybridization on isolated murine chromosomes. The safety and relative rapidity of the method is due to the ready availability of large numbers of isolated "target" chromosomes with well preserved morphology. Its applicability was demonstrated by mapping c-myc to band 15D of Robertsonian (6;15) fusion chromosomes. This localization coincides with the cytogenetic mapping of the translocation breakpoints in mouse plasmacytomas that carry the typical rcpt (12;15) translocation.

Animals↗
PubMed1979

Non-random duplication of chromosome 15 in murine T-cell leukemias induced in mice heterozygous for translocation T(14:15)6.

Trisomy of chromosome 15 is a highly regular feature of murine T-cell leukemogenesis. We have studied the chromosomal constitution of 7,12-dimethylbenza(a)anthracene (DMBA)-induced T-cell leukemias in C57BL X CBAT6T6 F1 mice. The CBAT6T6-derived chromosome T(14:15)6 was regularly duplicated whereas the C57BL-derived normal chromosome 15 was only present in one copy. It was concluded that the gene(s) that tend to duplicate in parallel with the neoplastic transformation of the prothymocyte to an overt leukemic cell have a greater chance of duplicating and/or may have a stronger promoting effect on leukemogenesis if stronger promoting effect on leukemogenesis if located on the CBA-derived, structurally rearranged T(14:15)6 than the corresponding genes located on the C57BL-derived normal chromosome 15.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Nonrandom chromosome changes involving the Ig gene-carrying chromosomes 12 and 6 in pristane-induced mouse plasmacytomas.

The karyotypes of pristane-induced mouse plasmacytomas were studied by G banding. Only primary tumors or early passage generations were analyzed. In contrast to murine T cell leukemias that showed a regular trisomy of chromosome 15, all plasmacytomas showed a consistent translocation of the distal part of chromosome 15 to either chromosome 6 [rcpT(6;15)] or 12 [T(12;15)]. The specific breakpoints were at 6C, 15D3/E ro D2/3 and 12F2. Early passage generations often showed a mixed population with two different translocations, suggesting polyclonal origin. Considered together with the known karyotypic features of murine and human lymphomas, these findings support the theory that the nonrandom chromosomal changes in lymphoproliferative malignancies are associated with the type of the target cell, rather than with the etiological agent. Moreover, the involvement of the chromosomes known to carry the heavy chain (12) and the light chain (6) determinants, respectively, raises the question of whether the translocations may be related to the DNA level rearrangements known to occur during the differentiation of normal plasma cells.

Animals↗
PubMed1979

Is trisomy cause or consequence of murine T cell leukemia development? Studies on Robertsonian translocation mice.

Trypsin-Giemsa banding studies on T cell leukemias induced in Robertsonian translocation mice by dimethylbenz[a]anthracene and Moloney leukemia virus show a trisomy of chromosome 15 even in cases in which chromosome 15 has undergone centromeric fusion with chromosomes 1, 5, or 6. These results suggest that the duplication of gene(s) located on chromosome 15 is of critical importance for murine T cell leukemia development.

Animals↗
PubMed1978

Chromosome changes (trisomy 15) in murine T-cell leukemia induced by 1,12-dimethylbenz(a)anthracene (DMBA).

The banding pattern of DMBA-induced leukemias in C57BL/6 mice revealed a very constant chromosome pattern: the presence of trisomy 15 in almost all leukemic cells. This finding strongly suggests that chromosome 15 trisomy is the first detectable specific chromosome change associated with the development of DMBA-induced T-cell lymphomas. A similar association was previously shown with regard to development of radiation-leukemia-virus-induced T-cell lymphoma. It is conceivable that in tumors of diverse etiologies common cytogenetic changes may appear in the same common target-cell precursor, by a process of the "convergent microevolution" type.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Chromosome changes (trisomies #15 and 17) associated with tumor progression in leukemias induced by radiation leukemia virus.

An experimental system was developed that permitted nonrandom chromosome changes that occur in radiation leukemia virus (RadLV)-induced lymphomas to be followed during tumor progression. RadLV variant-induced preleukemia and leukemia cells originating from female inbred C57BL/6 mice were injected into male animals of the same strain. Since all donors were females and all recipients were males, the sex chromosome complements (XX and XY) were used to distinguish the preleukemia and leukemia cells from those of host origin. The G-banding analysis revealed that more than 50% of animals that were inoculated with preleukemia cells and that developed leukemia possessed tumor stem-lines of 41 chromosomes with a tristomy of chromosome #15. In animals inoculated with overt leukemia cells and in which tumor progression occurred, the G-banding an additional trisomy of chromosome #17. The cytogenic data strongly suggested that the trisomy of chromosome #15 was the first specific tumor-associated chromosome change that occurred in the process of conversion of RadLV-induced preleukemia cells to fully autonomous tumor cells.

Animals↗
PubMed1977

Chromosome banding, isoenzyme studies and determination of Epstein-Barr virus DNA content on human Burkitt lymphoma/mouse hybrids.

Four independently fused hybrid clones derived from a cross between the mouse mammary carcinoma TA3Ha and the human Burkitt lymphoma line Daudi were tested for the EBV-determined nuclear antigen (EBNA), EBV-DNA and the presence of human chromosomes, in the course of serial propagation in vitro. EBNA and EBV-DNA were lost in parallel with the loss of human chromosomes. It seems that the persistence of EB-viral genetic information does not require the presence of a specific human chromosome(s) in this particular hybrid combination.

Animals↗
PubMed1975

Biological effects evaluated as a function of patient thickness, beam quality, SSD,and treatment schedule.

Continuing efforts are being made by clinical radiotherapists to evaluate radiationcomplications to normal tissue and organs by specific time-dose parameters. Currently,the NSD concept of Ellis is receiving wide application in the literature in the reporting of radiation complications and normal tissue tolerances. To afford an easy and broad application of the NSD concept to the evaluation of physiological, functional, or structural changes, the authors have evolved mathematical expressions for the calculations of NSD as a function of patient thickness, beam energy, SSD, and treatment schedule involving coplanar field arrangements whether the fields are treated alternately or simultaneously. Several interesting aspects evolving form the concepts of treatment planning interms of the NSD or biological effects indicate that 1) for beam energies above 22 MeV, treatment is more ideally performed by treating only one field per day, since the depth of electronic equiliberium provides more effective sparing of superficial organs andtissues; 2) large-field therapy, such as the total nodal irradiation of Hodgkin'sdisease, can be more effectively treated in terms of tissue sparing by higher energy beamsthan cobalt-60 or 4-MeV for practically all patient dimensions; 3) a new concept ofintegral biological dose,the "gram-ret", is proposed, which represents the quantitation of total biological effect; 4) a series of tables with multiplication factors programmed on a digital computeris presented, which very quickly make available the NSD in any fractionated radiation treatment cycle to any plane of the body as a fuction of the beam energy, SSD, patient thickness, and continuous or split-course therapy schedule.

Dose-Response Relationship, Radiation↗
PubMed1975

Variation of percentage depth dose with beam area of 43 MV roentgen ray beam from a betatron.

The central axis percentage depth dose of a 43 MV roentgen ray beam from a betatron, is found to decrease with increasing beam area at depths more than the depth of maximum dose build-up. At depths less than the depth of maximum dose build-up, a reverse trend is seen. This type of variation of central axis percentage depth dose with beam area is found due to the presence of extraneous radiation originating in the field flattening filter (compensator) and the collimator of the betatron.

Radiotherapy Dosage↗