Modern - Blog Science Connections

More documents

Recommendations

Info

Fig. 4. Smears of bone marrow cells obtained from fractions of different density of a gradient containing Percoll. A Cells before centrifugation, B Cells from fraction I; C Cells from fraction 11; D Cells from fraction 111 (see methods).Smears were stained with an eosine-methylene blue stain (Diff-Quik, Harleco, Herstal, Belgium). Bar: 10 Ilm mature eosinophilic granulocytes (Fig. 4). As shown by the results in Table 2, the dense fractions II and III contained few or no target cells of AMV and AEV. In contrast, fraction II and to a lesser extent fraction III still contained MC29 target cells. Within the normal range of standard deviation, the dose-response curve obtained was in all cases linear. This indicates that the differences in the density distribution of the various types of target cells seen were not (or not only) caused by inhibitory cells. D. Discussion Our results show that in general target cells for aB three DLV types are most abundant in those fractions which consist mainly of blast-like, immature bone marrow cells. They are similar to each other with respect to both size and density. In comparison to erythrocytes, granulocytes, and CFU-C cells they are relatively large. They are also much light er than erythrocytes and granulocytes. Together with results described elsewhere (Graf et al. 1976a,b; Gazzolo et al. 1979; Graf et al. 1981) these results suggest that DLV target cells are rather immature but already committed to the erythroid or myeloid lineages. They are also in accord with the notion supported by earlier work (Graf et al. 1978, 1981) that DLVs upon transformation block the differentiation of their target cells. Our finding that a fraction of the MC29 target cells differs from those of AEV and AMV with respect to density is in accord with results described elsewhere which show that about half of the MC29 target cells in bone marrow are phagocytic and adherent, suggesting that these MC29 target cells are more mature than those of AMV, which do not express such functional markers (Graf et al. 1981). Our data conceming the relationship between normal macrophage/ granulocyte colony forming cells (CFU -C) and the target cells of MC29 and AMV are still very incomplete but suggest that they are not identical. This is also 421
Expt. No. Infecting virus Proportion of target cells' Fraction I Fraction II Fraction III Table 2. Distribution of target cells for DLVs in fractions of bone marrow cells of different density AEV MC29 AMV AEV MC29 AMV 17 ± 3.5 6 ± 3470 ± 832 2600 ± 1167 ± 290 356 ± 12.8± 3.9 4.3 ± 1058 ± 316 1321 ± 370 ± 26 150 ± 5 1 915 353± 47 32 52± 8 1.5 Np! 22 NT 14 NT 3 C MC29 7100 ± 415 950 ±350 355±106 AMV 5000 ±1300 42 ± 10 5 • Number of transformed colonies per 10 6 infected cells (average values ± standard deviation from 4 to 6 assay dishes seeded with twofold dilutions of cells). Average density of fraction I: 1.05 g/cm 3 ; fraction II: 1.09 g/cm 3 ; fraction III: 1.13 g/cm 3 . b Cells tested were from bone marrow of 2-week-old chicks C Cells tested were from the nonadherent fraction of chick bone marrow cultures maintained in grawth medium for 7 days d NT=Not tested in agreement with conc1usions reached by Gazzolo et al. (1979). In contrast to these authors, however, we were unable to observe a rapidly sedimenting subpopulation of AMV target cells in our unit gravity sedimentation studies. This could be due to technical differences in both the unit gravity sedimentation and target cell assay techniques employed by the two laboratories. An important question concerning the target cell specificity of DLVs is whether or not these viruses specifically infect and replicate in their target cells only. Recent studies performed on this question showed that this is c1early not the case. AEV is capable of infecting normal bone marrow macrophages without inducing any detectable transformation, while it replicates in them to almost the same titer as found in target cells. Similarly, MC29 and AMV are capable of replicating in ts34 AEVtransformed nonproducer erythroblasts without affecting their capacity to differentiate after shift to the nonpermissive temperature (Graf et äl. 1980). On the basis of these observations and our earlier work (for review, see Beug and Graf 1978) we have proposed that the observed restriction of DLV-transforming capacity to specific cell types in the bone marrow may operate at the posttranslational level (Beug and Graf 1978; Graf et al. 1978; Graf et al. 1979). In addition, we have proposed that cellular proteins homologous to the transforming proteins of DLVs (which should exist because the respective normal cellular genes and their mRNAs have been demonstrated in normal chicken cells by RousseI et al. 1979) are specifically expressed in the target cells only. To test this hypothesis, it will be necessary to characterize purified target cell populations. The techniques described in this paper could be useful as a first step in such a purification. References Beug H, v. Kirchbach A, Döderlein G, Conscience JF, Graf T (1979) Chicken hematopoietic cells transformed by seven strains of defective avian leukemia viruses display three distinct phenotypes of differentiation. Cell 18: 375-390 - Bister K, Duesberg PH (1980) Classification and structure of avian acute leukemia viruses. Cold Spring Harbor Symp Quant BioI44:801-822 - Gazzolo L, Moscovici C, Moscovici MG, Samarut J (1979) Response of hemopoietic cells to avian acute leukemia viruses: effects on the differentiation of the target cells. Cell 16:627-638 - Graf T, Beug H (1978) Avian leukemia viruses: interaction with their target cells in vivo and in vitro. Biochim Biophys Acta 516:269-299 - Graf T, Royer-Pokora B, Beug H (1976a) In vitra transformation of specific target cells by avian leukemia viruses. In: Baltimore D, Huang A, Fox F (eds) ICN-VCLA Symposia on molecular and cellular biology, Vol V. Academic Press, New York, pp 321-338 - GrafT, Royer-Pokora B, Beug H (1976b) Target cells fortransformation with avian leukosis viruses. In: Neth R, Gallo 422
Page 1 and 2:
Haematology and Blood Transfusion 2
Page 3 and 4:
Dr. Rolf Neth, Universitäts-Kinder
Page 5 and 6:
Participants of the Meeting Aaronso
Page 7 and 8:
Kurth, R, Friedrich-Miescher-Labora
Page 9 and 10:
Wilsede Scholarship Holders (Grante
Page 11 and 12:
Preface Gut ist eine Lehrart, wo ma
Page 13 and 14:
Personal and scientific discussion
Page 15 and 16:
Acknowledgement We should like to t
Page 17 and 18:
Wilsede, June 21 1978 Memorial Trib
Page 19 and 20:
limiting benign lymphoproliferative
Page 21 and 22:
this most unlikely, however (for re
Page 23 and 24:
longer subject to the same control
Page 25 and 26:
Bregula U, Wiener F, Harris H (1971
Page 27 and 28:
fresh lymph node biopsies from ten
Page 29 and 30:
Fig. 3. Binucleate mitosis in an ob
Page 31 and 32:
y Fig. 4. Schematic diagram of post
Page 33 and 34:
than that among patients with Stage
Page 35 and 36:
Tests of binding affinity, agglutin
Page 37 and 38:
N Engl J Med 297: 963-968 - Green I
Page 39 and 40:
Clinical Aspects
Page 41 and 42:
"ring chromosome". "Mar" is marker,
Page 43 and 44:
191 chromosomally abnormal patients
Page 45 and 46:
tumors of both African and non-Afri
Page 47 and 48:
Haematology and Blood Transfusion V
Page 49 and 50:
Retrospective group 26/93 evolved l
Page 51 and 52:
Page 53 and 54:
Treatment
Page 55 and 56:
advantage in terms of duration of f
Page 57 and 58:
leukaemia. An analysis of 168 patie
Page 59 and 60:
11. Treatment Program Chemotherapy
Page 61 and 62:
efractory congestive heart failure
Page 63 and 64:
period (Sequence II) was gene rally
Page 65 and 66:
children with a multiple drug proto
Page 67 and 68:
DAYS 1 5 10 15 20 25 30 35 , I I I
Page 69 and 70:
Biologically Drug Outcome fit" sens
Page 71 and 72:
may counterbalance the potential be
Page 73 and 74:
Ht (0--0) 50 40 30 20 10 0 Platelet
Page 75 and 76:
10 7 ,-----------------------------
Page 77 and 78:
11. Haematological and Biochemical
Page 79 and 80:
0\ 0\ INTERFERON ... 10 3 rl E "'
Page 81 and 82:
Page 83 and 84:
("pre-B" phenotype) has been descri
Page 85 and 86:
human bone marrow cells exhibit the
Page 87 and 88:
10 9.,0 MBKCC .. .,4 B prot:oool 1'
Page 89 and 90:
demann W, Büehner T, Arlin Z, Gee
Page 91 and 92:
-...l 00 a-tLDRENS CAt«:ER S TU>Y
Page 93 and 94:
prognostic characteristics under in
Page 95 and 96:
significantly higher in HR} (14.5%,
Page 97 and 98:
normal or elevated immunoglobulin l
Page 99 and 100:
References Andreeff M, Darzynkiewic
Page 101 and 102:
R GROUP 1 ( 1970 - 1971 ) 17 PTS. R
Page 103 and 104:
Table 3. Influence of initial featu
Page 105 and 106:
LIJ (f) a.. < -1 LIJ Q: u. 0 >- I-
Page 107 and 108:
Page 109 and 110:
me nt indicated that additional the
Page 111 and 112:
42:2123-2134 - Chessells JM, Cornbl
Page 113 and 114:
Baum et al. 1979). This study was b
Page 115 and 116:
1. 0 '--'1--" 0.9 e: o .- VI VI E C
Page 117 and 118:
e: o e: 1. 0 ,.--...-- 1'"'\ ......
Page 119 and 120:
In conclusion, we can state that th
Page 121 and 122:
Haematology and Blood Transfnsion V
Page 123 and 124:
INDUCTION VCR + PRED + ASNASE (wk 3
Page 125 and 126:
SCHED.INT 1 MTX • ! Adria MTX •
Page 127 and 128:
~ looh---------ooooc>----o---c>----
Page 129 and 130:
Consoll- Irra .tlon t) .tlon Indu
Page 131 and 132:
Highrisk Standard risk Table 1. Cli
Page 133 and 134:
Cumulo/ive comp/el9 remission 1.0 .
Page 135 and 136:
10° 8 = 6 ö 4 Non T Cell .~ :ö
Page 137 and 138:
Page 139 and 140:
% SURVIVAL 100 ~ ~II 0 80 60 40 - -
Page 141 and 142:
a) Percentage of donor cell mitoses
Page 143 and 144:
Table 5. Results of bone marrow tra
Page 145 and 146:
...... w N Table 7. Clinical result
Page 147 and 148:
agent had to be added and that in t
Page 149 and 150:
Page 151 and 152:
C. Chronic Myelogenous Leukemia The
Page 153 and 154:
Patients with a suitable donor rece
Page 155 and 156:
No. Recurrent Leukaemia Other death
Page 157 and 158:
followed by dialysis against isoton
Page 159 and 160:
Page 161 and 162:
HS, HL- Heme >_ 40 0 HS I ;:. =====
Page 163 and 164:
Page 165 and 166:
knowing at present. These genes may
Page 167 and 168:
esistance to antifolates. In Vitro
Page 169 and 170:
a DNA probe specific for the gene t
Page 171 and 172:
translocation between chromosomes 9
Page 173 and 174:
Table 1. Subdivision of 1827 Myelo-
Page 175 and 176:
NORMAL CELL ®
Page 177 and 178:
some change of the primary type, in
Page 179 and 180:
Page 181 and 182:
F. Transformation of Mouse Bone Mar
Page 183 and 184:
Page 185 and 186:
were carried out with 3H-MTX in the
Page 187 and 188:
Page 189 and 190:
the lysozyme cDNA prepared from ovi
Page 191 and 192:
Page 193 and 194:
et al. 1976). The BJAB cellline in
Page 195 and 196:
dalton bands corresponding to light
Page 197 and 198:
1979). The EBV-carrying cell lines
Page 199 and 200:
producer lines (DAUDI and P3HR-1),
Page 201 and 202:
G, Giovanella B, Westman A, Stehlin
Page 203 and 204:
Page 205 and 206:
Dc;bt CT + i J.I9 Raji; 1. i .. 100
Page 207 and 208:
c. Discussion During infectious mon
Page 209 and 210:
Page 211 and 212:
C. Nonepisomal Viral DNA We have us
Page 213 and 214:
A 260 3.0 A B 1670 70 N2 2.0 c: E .
Page 215 and 216:
vivo. Nature 260:302-306 - Kirk JTO
Page 217 and 218:
Fig. 1. a Polyacrylamide gelelectro
Page 219 and 220:
Page 221 and 222:
1979). The lymphocyte subpopulation
Page 223 and 224:
lysin 0 antigens are found, and mix
Page 225 and 226:
Pope JH (1978) Long-term T cell-med
Page 227 and 228:
Haematology and Blood Transfnsion V
Page 229 and 230:
Charaeteristie Morphologie maturati
Page 231 and 232:
after TPA-induction (Table 3). The
Page 233 and 234:
PA (1978) Reactivity of a rabbit an
Page 235 and 236:
Blood Monocyte. B lood Monocytes 1-
Page 237 and 238:
Page 239 and 240:
and nonhistone proteins can serve a
Page 241 and 242:
Page 243 and 244:
The findings of the evaluation of s
Page 245 and 246:
Fig. 3. Tumor grawth of L 428 cells
Page 247 and 248:
Cell biological and Immunological A
Page 249 and 250:
consideration. Sanel (1973) obtaine
Page 251 and 252:
endotoxin serum, were used. A parti
Page 253 and 254:
monocytic leukemia cell line in cul
Page 255 and 256:
B. Isolation, Characterization and
Page 257 and 258:
Page 259 and 260:
don al hemopathies generally displa
Page 261 and 262:
nitors. Blood Cells 6:595-607 - Min
Page 263 and 264:
\I) ....I ....I IU Jl 200 r 100 90
Page 265 and 266:
their haemopoietic cells' ability t
Page 267 and 268:
normal normal ALL ALL ALL persons p
Page 269 and 270:
64.5 { V)
Page 271 and 272:
References Biermann E, Neth R, Gros
Page 273 and 274:
ehambers, the growth pattern observ
Page 275 and 276:
References Anderssen LC, 10kinen M,
Page 277 and 278:
REH CELL UNE TO CALLb~Ö ~q~ V.M. c
Page 279 and 280:
Page 281 and 282:
the macrophage series in which the
Page 283 and 284:
Page 285 and 286:
Table 1. Production of factor depen
Page 287 and 288:
Page 289 and 290:
Table 1. Characteristics of the adh
Page 291 and 292:
Fig. 3. A human marrow culture at 6
Page 293 and 294:
300 250 • HYPERPROLIFERATIVE PATT
Page 295 and 296:
Fig. 9. Nonadherent population from
Page 297 and 298:
The cobblestone areas were often no
Page 299 and 300:
L (1976) Induction of colony format
Page 301 and 302:
B. Materials and Methods J. Tissue
Page 303 and 304:
Fig. 2. Ultrastructural appearance
Page 305 and 306:
Page 307 and 308:
Page 309 and 310:
Table 1. Monoclonal antibody reacti
Page 311 and 312:
al. 1979; Janossy et al. 1979) is e
Page 313 and 314:
to which this is an exact replica o
Page 315 and 316:
inger JL (1976) Distribution of la-
Page 317 and 318:
I region antigens were found to be
Page 319 and 320:
have been reported to be present on
Page 321 and 322:
V. FunctionalAssays Assays for PHA
Page 323 and 324:
Functional studies of UCHT1 separat
Page 325 and 326:
Page 327 and 328:
40 ,...... (5 L.. C o u 30 .9 ~ .~
Page 329 and 330:
with immunohistochemieal methods (L
Page 331 and 332:
Page 333 and 334:
can be dissected by cloning. Utiliz
Page 335 and 336:
Table 1. Origin and marker profile
Page 337 and 338:
Page 339 and 340:
complete identity of gp 100 from no
Page 341 and 342:
Table 1. Reaction of single anti se
Page 343 and 344:
Page 345 and 346:
media. Following 24-h incubation, c
Page 347 and 348:
nonleukemic eells (Greaves 1979). L
Page 349 and 350:
Page 351 and 352:
Fig. 2. Cytocentrifuged smears of b
Page 353 and 354:
Modification of amino-groups of hum
Page 355 and 356:
disturb this balance in the directi
Page 357 and 358:
The majority of human blood lymphoc
Page 359 and 360:
of the EBV infected B cells. Howeve
Page 361 and 362:
and immunoglobulins. J Immunol 120:
Page 363 and 364:
" K 10 • j ~ ALL RNlL AL wtfh les
Page 365 and 366:
tion akuter Leukämiezellen in "spo
Page 367 and 368:
D. Results and Discussion J. Acute
Page 369 and 370:
selectively responsive to different
Page 371 and 372:
Page 373 and 374:
l1J ~ 100 ~ Q. ::) l1J Z 0 ~ z >- .
Page 375 and 376:
Table 2. Growth inhibition of S49 e
Page 377 and 378:
Reverse Infectious ASC/2X1Q6 transc
Page 379 and 380: Haematology and Blood Transfusion V
Page 381 and 382: munized animals to 1316 tumor cells
Page 383 and 384: Haematology and Blood Transfnsion V
Page 385 and 386: Fig. 3. Expression of retroviral gp
Page 387 and 388: pg70. J Exp Med 143: 151-166 - McGr
Page 389 and 390: Table 1. Expression of tumor antige
Page 391 and 392: Virological and Molecularbiological
Page 393 and 394: Table 1. Oncogenic properties of re
Page 395 and 396: also Fig. 1). It followed that the
Page 397 and 398: whether this sequence is related to
Page 399 and 400: zed in infected cells argue that th
Page 401 and 402: a specific viral transforming prote
Page 403 and 404: detect viral RNA as the only charac
Page 405 and 406: Eisen H (1980) Myeloproliferate vir
Page 407 and 408: p,60- -34K - 1 2 3 4 Fig. 1. In vit
Page 409 and 410: .. p - • a'T ... I .t'l Fig. 4. D
Page 413 and 414: Fig. 2. Photomicrographs of NY68 in
Page 415 and 416: DEAE (o(lJmn 'liI GI -2 2 o e s 1
Page 417 and 418: vity was deterrnined. For endogenou
Page 419 and 420: pr 180 - - - P 12/15 - A B c D E F
Page 421 and 422: 85,- 66- -27 - -66 40- 27- -1'9 19-
Page 425 and 426: = 0.5 o E Q. o ILI 0.4 (J) « ILI .
Page 427 and 428: Table 1. Oncogenic potential of avi
Page 429: 100 III GI c: o "8 80 > w
Page 433 and 434: Haematology and Blood 'fransfusion
Page 435 and 436: sequences, provided its gag portion
Page 437 and 438: 77:3009-3013 - Hu SSF, Moscoviei C,
Page 439 and 440: RI 2.2 md and Hind III 2.6 md leuke
Page 443 and 444: RELATIONSHIP OF ENDOGENOUS AND EXOG
Page 445 and 446: E ........ E Cl. U E :::l .... Q) (
Page 447 and 448: References Astrin S (1978) Endogeno
Page 449 and 450: the same animal were examined (e.g.
Page 451 and 452: I) 'IQ a \0 - CL -- Fig. 2. Restrie
Page 453 and 454: ~ ..................... ~ Cell 3' 5
Page 455 and 456: a :Sa,C! + . ~ 111 i' ( " '~ .J. b
Page 457 and 458: Table 1 Sampie Tissue TS fragment"
Page 459 and 460: a b Sac I / rep ._-_.-_ K J nl rep
Page 461 and 462: Haematology and Blood 'fiansfusion
Page 463 and 464: Osteopetrosis and osteosarcomas occ
Page 465 and 466: Lymphoma cellline Table 1. T and B
Page 467 and 468: Table 2. In vivo growth and oneogen
Page 471 and 472: Table 1. Transforming aetivity of c
Page 473 and 474: Table 3. Transformation aetivity of
Page 475 and 476: - Shoemaker C, Goff S, Gilboa E, Pa
Page 477 and 478: indieate a shifting of target eell
Page 479 and 480: Table 2. Expression of Jl and Sourc
Page 481 and 482:
Page 483 and 484:
~ i ,..1---------,,':::::::::::::::
Page 485 and 486:
fragment of pBR322 DNA, a 3.0-kbp S
Page 487 and 488:
Mak TW (1979) Proc Natl Acad Sci US
Page 489 and 490:
Table 1. Transformation of 3T3 cell
Page 491 and 492:
inserts in the genome of rapidly tr
Page 493 and 494:
pulations, it seemed likely that th
Page 495 and 496:
contains antigens which react with
Page 497 and 498:
Page 499 and 500:
le of reacting in sensitive radioim
Page 501 and 502:
Page 503 and 504:
gic approach. In: Hiatt HH, Watson
Page 505 and 506:
12 Eco R [ Fig. 1. Hybridization pa
Page 507 and 508:
Page 509 and 510:
10 - '1~ )( -~ S:! E A U I o 1 2
Page 511 and 512:
Haematology and Blood 'fransfusion
Page 513 and 514:
cultures. These cells did not conta
Page 515 and 516:
indication of malignant T-cells in
Page 517 and 518:
Fig. 3. Thin-section electron micro
Page 519 and 520:
Table 3. Lack of detectable related
Page 521 and 522:
J. HTLV Was Present in the Primary
Page 523 and 524:
specific signals into nonspecific s
Page 525 and 526:
Table 2. Distribution of HTLV-relat
Page 527 and 528:
u 10 ~ 20 ~ :c 30 a 40 o Fig. 1. Ki
Page 529 and 530:
Page 531 and 532:
SSV TrS-gp labeled effectively with
Page 533 and 534:
Page 535 and 536:
60 HFF/SSV cDNA CELL RNAs: 0 HF/SSV
Page 537 and 538:
Antisera a Table 1. Immunofluoresce
Page 539 and 540:
Haematology and Blood 'ftansfusion
Page 541 and 542:
y competition RIA yielded virtually
Page 543 and 544:
SiS'V' gp70: ANTIGEN, ANTI BODY, IM
Page 545 and 546:
type-C virus p30 antigen in cells f
Page 547 and 548:
c. Results The fractionated whole-b
Page 549 and 550:
induced antibodies as well as exper
Page 551 and 552:
- Fig. la-f. Retravirus particles p
Page 553 and 554:
eplication of infecting murine leuk
Page 555 and 556:
Page 557 and 558:
immunodeficiency, multic10nal lymph
Page 559 and 560:
Bovine leukemia --, proteins of 499
Page 561 and 562:
Human T- cell - -, characterization
Page 563 and 564:
RNA -, of tumor virus 439 Rous sarc
Page 565 and 566:
Haematology andBlood Transfusion Su
show all

Modern - Blog Science Connections

Create successful ePaper yourself

Delete template?

Save as template?