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PubMedDate not supplied

[Osteopathies associated with sickle cell disease (author's transl)].

1. In all patients of African descent, and above all in all children of three months and older, the attention of the radiologist should be directed to the possibility of sickle cell anaemia in the presence of bone lesions with the following characteristics:--either diffuse pseudo-tumoural, signifying erythroblastosis secondary to anaemia;--or pseudo-osteitic, signifying thrombosis secondary to sickling. 2. These appearances from part of a rich and misleading pathological spectrum, in particular in rheumatology and pulmonary medicine, and even surgery. 3. The presumptive radiological diagnosis may be complemented by electrophoresis of haemoglobin which, alone, makes confirmation of the diagnosis possible.

Adolescent↗
PubMedDate not supplied

Sarcoma and thyroid disorders: a common etiology?

We have recently observed that many of our sarcoma patients presented also with thyroid disorders. Literature data are almost unavailable on this topic. The relationship between the sarcoma and thyroid disorders is examined. Retrospective analysis of files of patients with sarcoma and clinically overt thyroid disorders was carried out. Of the 375 patients with soft tissue sarcomas (STS) and 235 with bone sarcoma (BS) including small blue round cell tumors (SBRC), 28 patients (4.6%) had an associated significant thyroid disorder. The types of sarcoma were mainly liposarcoma followed by malignant fibrous histiocytoma, leiomyosarcoma and bone sarcoma. The primary sites were mainly limb and trunk. The interval between the diagnosis of the thyroid disorder and the sarcoma varied between -14 years (thyroid first) and +16.5 years (thyroid later) with a median of -0.2 years. Thyroid disorders included goiter, thyroiditis and carcinoma. There are both basic-science and clinical evidence to a possible common pathway that leads to the association between overt thyroid disorders and sarcomas of bone or soft tissues. Oncogene erbA activity is related to thyroid receptors to T3 and to development of sarcoma. Cross talk of the sarcoma oncogene and the erbA might contribute to the development of sarcoma. The thyroid hormone receptor and the highly related viral oncoprotein v-erbA are found exclusively in the nucleus as stable constituents of chromatin. It has been shown that v-erbA can block the spontaneous differentiation in erythroid cells transformed by various retroviral oncogenes. V-erbA can alter the spectrum of neoplasia induced by the v-src oncogene, which causes predominantly sarcomas and erythroblastosis in chicks. The erbA can cooperate with other oncogenes such as v-erbB or with v-fms, v-ras, and c-kit. Cooperation with v-myc may play a role in the development of rhabdomyosarcoma especially in thyroid hormone deficiency state. The possible clinical implications are the need to screen patients with sarcoma to thyroid disorders, and patients with thyroid disorders for malignant diseases.

Adult↗
PubMed1975

The relation between the proliferative activity and the differentiation pattern of bone marrow cells from Rauscher leukemia virus infected BALB/c mice.

The proliferative activity of bone marrow from Rauscher Leukemia Virus infected mice was studied during the course of the disease. Spleen colony assay and thin-layer agar technique, both presumably reflecting the number of pluripotent hemopoietic stem cells, showed a 2.6 times increase in colony forming units (CFU-S resp. CFU-A) at 12 days after infection. The Bradley method of culturing colonies in agar, which is stated to reflect the number of myeloid precursor cells, resulted in a slower rise in colony forming units (CFU-C) with a maximum of 2.3 times increase at 19 days after infection. These results were compared to the differentiation patterns of the bone marrow at similar intervals after infection. The course of the CFU-C curve parallelled the rise in the number of the myeloblasts in the bone marrow. The pattern of CFU-A and CFU-S curves preceded the rise in number of CFU-C by 7 days. It was found, that RLV infection apart from causing an erythroblastosis in the spleen and a severe anemia is followed by a disappearance of neutrophil granulocytes from the bone marrow. The latter phenomenon is probably the primary cause of the increase of hemopoietic stem cells.

Animals↗
PubMed1976

[Advantages and disadvantages of deliveries after induction of labour by convenience (author's transl)].

The development of 601 deliveries after induction of labour by convenience, 92 births after induced labour following pregnancies at risk and 1829 births after spontaneous onset of labour were examined and compared. The data were recorded retrospectively and submitted to an electronic data processing. Patients with whom the labour was induced had the shortest birth times, the difference amounted on average to 2 hours. In the comparison collective with spontaneous setting in of labour a hypotonic uterus motility was found to be the most frequent pathological labour activity. Pathological pattern of heart frequency, especially late decelerations were most frequently registered with fetuses of the risk group. The frequency of the operative deliveries amounted to 13% in the case of the collective of the induced labour, 35,9% in the case of patients in the risk group, and 10% in the case of the comparison collective. Threatening fetal asphyxia and protracted extrusion period were in the case of primiparas after induced labour equally often the indication for a vaginal-operative delivery, whereas with the comparison collective, in the risk group and also with multiparas after induced labour, the threatening fetal asphyxia was primarily for the carrying out of a forceps delivery or a vacuum extraction. Concerning the birth weight and size the new-borns of the collectives examined showed no significant differences. The best Apgar-score was achieved by the new-born induced labour babies. Only 0,5% of these babies showed pronounced signs of placental dysfunction, in the risk group 9,6%, and in the comparison collective 1,6% of the babies were born with a pronounced Clifford-syndrome. Induced labour babies did not need any pediatric treatment. There were no perinatal deaths. In the case of comparison collective, long term pediatric treatment was necessary for 8 babies, 1 baby died subpartual, another one in the pediatric clinic, that means a perinatal mortality of 0,1%. In the risk group 3 babies needed pediatric treatment, 1 baby died of the consequences of a serious erythroblastosis, the perinatal mortality amounted to 1,1%. In a critical evaluation of the without exception favourable obstetrical results after induced labour, the technical, personal and organisational efforts should not be overlooked. This stands in the way of a widespread use of the process in the near future. The results hitherto permit the temporary inference that 1) psychologically positive prerequisites for the birth are created if the pregnant woman knows a firm date for the delivery, 2) the whole partus can be continuously supervised and the maternal and infantile emergencies prevented in good time and 3) through the calculability of risks during pregnancy and birth, perinatal mortality and morbidity can be reduced considerably.

Apgar Score↗
PubMedDate not supplied

[Myeloid leukemia with myelofibrosis (author's transl)].

Myelofibrosis is observed in 1/5 of the cases of C.M.L. It consists of reticulin fibers with few collagen and no osteosclerosis. It involves signs which usually indicate the extension of the myelosis to other organs and other types of cells: hepatosplenomegaly, erythroblastosis, thrombocytemia. Its prognosis is always bad. In one third of the cases, myelofibrosis develops early, and in two third it is late. Chimiotherapy is not responsible for it. These forms of C.M.L. with myelofibrosis appear as a special type of myeloproliferative disorder apart from the true C.M.L. and the true osteomyelofibrosis.

Alkaline Phosphatase↗
PubMed1992

Amniotic fluid hormone profiles during normal and abnormal pregnancy.

Amniotic fluid (AF) and maternal serum (MS) chorionic gonadotropin (HCG), placental lactogen (HPL), pregnancy-specific beta 1-glycoprotein (SP1), total estrogens (ET), alpha-fetoprotein (AFP) and prolactin (PRL) were measured by enzyme-immunoassays, in 50 normal (A) and in 37 abnormal (B) pregnancies, from 16th to 40th weeks. A: the proteins HCG, AFP and PRL showed a similar decreasing trend after the 20th week, while HPL and SP1 rose progressively throughout the 2nd trimester, thereafter remaining constant. On the contrary ET showed an increasing pattern until term. Chorionic gonadotropin HPL and SP1 in MS were higher than in AF, while AF values of AFP and PRL were higher than in MS, but the ratio MS/AF of all hormone values increased significantly from the 2nd to the 3rd trimester (p < 0.005-p < 0.000001). Estrogens had about the same concentration in AF and MS during the 2nd trimester, but at term of pregnancy, their AF values were double those of MS. B: in polyhydramnios, elevated AF placental hormones were found, while PRL was very low. In erythroblastosis and diabetes, AFP was very low, but placental hormones, PRL and ET were both high and low. In toxemia, SP1, hCG and PRL were elevated, while HPL and ET were very low. In anencephaly and hydrocephaly with spina bifida, AFP was markedly elevated and ET were very low, but in simple hydrocephalus, very low AFP was found. In chromosomal anomalies very high placental hormones and very low AFP and ET were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗
PubMed1992

The nuclear oncogenes v-erbA and v-ets cooperate in the induction of avian erythroleukemia.

The nuclear oncogenes v-erbA and v-ets are known to cooperate with other viral oncogenes in the induction of avian erythroleukemia. Thus, in the case of avian erythroblastosis virus (AEV), v-erbA enhances the effect of the tyrosine kinase-encoding v-erbB oncogene by blocking the terminal differentiation of erythroid cells. In the case of E26 virus a fusion of the product from v-ets to that of the nuclear oncogene v-myb is a prerequisite for leukemogenicity. Here we show that an artificial virus carrying both v-erbA and v-ets induces a rapid, acute erythroleukemia phenotypically similar to that induced by AEV. In contrast, virus constructs containing either v-erbA or v-ets alone are non-leukemogenic, although they are capable of transforming erythroid cells in vitro. Analysis of in vitro-transformed cells showed that v-erbA induces a block of differentiation without abrogating dependence on anemic serum, while v-ets predominantly causes anemic serum independence. As expected, cells transformed by both oncogenes exhibit an increased proliferative potential, are blocked in differentiation and are anemic serum independent. These data demonstrate that two separately expressed nuclear oncoproteins can complement each other in vitro and in vivo. They also show that the v-Ets protein on its own can contribute to leukemogenesis.

Animals↗
PubMed1992

V-erbA and c-erbA proteins enhance transcriptional activation by c-jun.

The ability of different transcription factors to interact with one another is an important means by which the eucaryotic cell can integrate separate growth and differentiation signals into a coherent response. We report here an analysis of the interactions of transcription factors that are also the products of oncogenes: the erbA, jun and fos proteins. We demonstrate that the c-jun polypeptide can functionally interact with the c-erbA protein (thyroid hormone receptor) to yield an enhanced activity greater than that of either factor individually. Although the avian erythroblastosis v-erbA allele is generally thought to act as a transcriptional repressor in vertebrate cells, we also report the existence of promoter contexts where v-erbA, as well as c-erbA, can serve as 'co-activators' of c-jun function. V-erbA appears to augment retinoic acid receptor function in the same context. Our results suggest that v-erbA may have unanticipated positive effect on transcription in the neoplastic cell in addition to the repressor functions previously characterized.

Base Sequence↗
PubMed1992

Functional interaction between the two zinc finger domains of the v-erb A oncoprotein.

The v-erb A oncogene of avian erythroblastosis virus is a mutated and virally transduced copy of a host cell gene encoding a thyroid hormone receptor. The protein expressed by the v-erb A oncogene binds to DNA and acts as a dominant negative inhibitor of both the thyroid hormone receptor and the closely related retinoic acid receptor. The v-erb A protein has sustained two amino acid alterations within its DNA-binding domain relative to that of c-erb A, one of which, at serine 61, is known to be important for v-erb A function in the neoplastic cell. We report here that the second alteration, at threonine 78, also plays an important, although more indirect, role: alteration of the sequence at threonine 78 such that it resembles that of c-erb A can act as an intragenic suppressor and can partially restore function to a v-erb A protein rendered defective due to a mutation at position 61. Threonine 78 lies within the D-box of the v-erb A protein, a region thought to mediate receptor-receptor dimerizations, and is not in physical proximity to the serine at position 61. It therefore appears that an indirect interaction occurs between these two sites and that this interaction is crucial for v-erb A function.

Amino Acid Sequence↗
PubMed1992

The leukaemia oncogene v-erbA: a dominant negative version of ligand dependent transcription factors that regulates red cell differentiation?

The v-erbA oncogene of avian erythroblastosis virus alters the growth properties and arrests differentiation of chick erythroid progenitor cells. The v-erbA protein is a mutated, ligand independent version of the c-erbA/T3R alpha chick receptor for T3, a ligand dependent transcriptional regulator. In reconstituted systems using idealized hormone responsive elements, over-expressed v-erbA acts as a dominant repressor of transcription mediated by liganded c-erbA/T3R alpha. This property seems to account for at least part of the phenotype of AEV transformed erythroid cells and for the transcriptional repression of some erythrocyte specific genes. However, v-erbA is likely to interfere with regulatory circuits other than those directly regulated by T3 receptors. Aspects of this hypothesis are discussed in the context of available evidence for the role of T3 and other hormones in erythroid progenitor cells proliferation/differentiation.

Animals↗
PubMedDate not supplied

Thrombocytopenia in a retrovirally-induced murine erythroleukemia.

A variant strain of Rauscher leukemia virus (RLV-A) obtained from a transplantable murine monomyelocytic leukemia causes a disease characterized by frank anemia, wasting, hepatosplenomegaly and erythroblastosis. The involvement of platelets in this disease are reported here. The RLV-A induced a severe thrombocytopenia (25 percent of control level) at the terminal stage of disease. This thrombocytopenia was not associated with disseminated intravascular coagulopathy since the prothrombin times were always within normal limits. The partial thromboplastin time was elevated in the terminal stages of disease and was found to be associated with factor deficiencies, possibly owing to the presence of anti-factor antibodies, in the intrinsic coagulation pathway, especially factor VIII. Further, splenectomy did not abolish the thrombocytopenia, since splenectomized, virally infected animals also developed severe thrombocytopenia (29 percent of control levels). The ensuing splenomegaly during progression of disease was not the cause of the thrombocytopenia. A physiological response to the severe thrombocytopenia was the production of larger size platelets. At terminal stages of the disease, platelet volume increased to 4.2 mu 3 (normal is 3.0 mu 3). An increase in platelet volume was also observed in splenectomized, virally infected animals. Electron microscopy indicated that these circulating platelets contained c-type viral particles. Viral infection was associated with decreased life span of circulating platelets, as measured by 75Se-methionine at mid and terminal stages of the disease. Our results suggest that direct viral infection of platelets and/or megakaryocytes with subsequent cell lysis is a possible cause of the observed thrombocytopenia observed in RLVA-induced disease and may also occur in other retrovirally-induced diseases.

Animals↗
PubMed1979

[Neonatal thrombocyte values in children with Down's syndrome and other autosome trisomies].

Platelet counts were determined in 70 neonates with trisomy-21, 10 neonates with trisomy-18 and 6 neonates with trisomy-13 during the first days of life. 60% of all infants with trisomy-aberrations were found to have thrombocytopenia. Platelet counts in Down's syndrome averaged 104600 (SD 53000; median 90500; 10- and 90-percentile at 45000 and 175000) per microliter. A correlation with other hematological features of trisomy-21 was examined. There was no significant correlation between platelet counts and hemoglobin concentration. Similarly the difference in platelet counts between trisomy-neonates with and without polycythemia was statistically not significant. In contrast, 27 normal neonates with polycythemia showed significantly higher platelet counts (mean = 13400) than their trisomy-counterparts (mean = 98900; P = 0.01). In addition, there was no correlation, in trisomy infants, between either erythroblastosis or low birth weight and platelet count. These findings point to defective hematopoiesis as a primary cause of thrombocytopenia in trisomy-infants.

Birth Weight↗
PubMed1991

[Blood picture findings in children with Parvovirus B19 infections (fifth disease/erythema infectiosum)].

The human parvovirus B19 provokes erythema infectiosum ("e.i."); moreover there is a wide range of diseases due to parvovirus B19 without exanthema/rash. The erythropoietic blast cells of the bone marrow seems to be the main target cells for this virus. Therefore in cases of prenatal infection the consequences are extremely similar to fetal erythroblastosis ("non-immunological" fetal hydrops). In postnatal life the parvovirus B19 infection causes hyporegenerative phases of the erythropoiesis with anaemia after 3-4 weeks. We studied the white blood cell count (WBC), erythrocytes and thrombocytes in children suffering from (serologically well documented) parvovirus B19 infection with exanthem/"e.i." (group 1; n = 23), without exanthem (group 2; n = 46) and with unknown febrile exanthematous rashes (group 3; n = 76). We did not find any characteristic data in the WBC for a diagnosis of parvovirus B19 infection. However we have for the first time documented a significant thrombocytopenia in "e.i." (group 1) not found in group 2. The thrombocytopenia appears earlier than the anaemia, because the lifespan of thrombocytes is considerably shorter than that of erythrocytes. These data suggest that parvovirus B19 attacks not only "erythropoietic" blast cells but also immature bone marrow cells, which are later responsible for the thrombocytopoiesis.

Adolescent↗
PubMed1991

A subpopulation of the v-erb A oncogene protein, a derivative of a thyroid hormone receptor, associates with heat shock protein 90.

The v-erb A oncogene of avian erythroblastosis virus is derived from a host gene for a thyroid hormone receptor and is able to block differentiation of erythroid cells and modify the growth properties of fibroblasts. Unlike its host cell progenitor, the v-erb A protein is found in both cytoplasmic and nuclear fractions of the cell. I report here that the cytoplasmic form of the v-erb A protein is associated in a higher molecular weight complex with heat shock protein 90, the same polypeptide found in association with the unliganded steroid receptors and with the soluble forms of the src oncogene.

Animals↗
PubMed1991

Thyroid hormone receptor/and v-erbA. A single amino acid difference in the C-terminal region influences dominant negative activity and receptor dimer formation.

Thyroid hormone receptors are cellular homologues (c-erbAs) of the v-erbA oncoprotein of the avian erythroblastosis virus. Exclusive of the viral gag region, v-erbA differs from the chick c-erbA-alpha receptor by two amino acid changes N-terminal of the DNA binding domain, two amino acid changes in the DNA binding domain, nine amino acid changes in the C-terminal region corresponding to the ligand binding domain of c-erbA, and a nine-amino acid deletion near the C terminus. v-erbA does not bind thyroid hormone and when expressed in cells inhibits the activity of wild-type thyroid hormone receptors. We reported previously that mutants of chick c-erbA/thyroid hormone receptor which lack the DNA binding domain (DBD-) inhibit transcriptional activition by wild-type thyroid hormone and retinoic acid receptors (Forman, B. M., Yang, C.-R., Au, M., Casanova, J., Ghysdael, J., and Samuels, H. H. (1989) Mol. Endocrinol. 3, 1610-1626). This dominant negative activity mapped to a series of hydrophobic heptad motifs which are conserved in the C terminus of these receptors and have been suggested to play a role in receptor dimerization. In this study we show that unlike DBD- c-erbA, DBD- v-erbA does not block receptor activity, suggesting that v-erbA acts by competing for DNA response elements rather than by formation of nonfunctional v-erbA/c-erbA heterodimers. This difference in activity was localized to a single Pro to Ser change in v-erbA just N-terminal of the last heptad motif. Introduction of this Pro to Ser change into DBD- c-erbA resulted in a protein which was inactive both functionally and in blocking receptor dimer formation in vitro.

Alpharetrovirus↗
PubMed1991

Cell transformation by the epidermal growth factor receptor and v-erbB.

It has become increasingly apparent that growth factor receptors can function as oncogenic proteins and play causal roles in cell transformation. A prime example is the epidermal growth factor receptor (EGFR), which belongs to the ligand-activated tyrosine kinase receptor family and is overexpressed in certain human tumors. The transforming gene of avian erythroblastosis virus, v-erbB, encodes a truncated form of the EGFR whose kinase domain is constitutively activated by deletion of the ligand binding domain. Recent comparative studies of the v-erbB gene in different viral isolates have revealed that subtle sequence changes (point mutations, small deletions) can alter both the pathogenic spectrum of the virus and the range of cell types susceptible to transformation in vitro. Therefore, the possibility exists that similar, as-yet-unidentified, mutations may exist in the EGFR gene; if so, the EGFR may be an oncogenic factor in tumors other than those with which it has been associated to date.

Animals↗
PubMed2006

Trend of blood groups and Rh factor in the twin cities of Rawalpindi and Islamabad.

OBJECTIVE: To determine the prevalence of different blood groups and Rh factors in a random population sample from urban and rural areas of Rawalpindi and Islamabad region of Pakistan. METHODS: Blood group and Rh factor determination was carried out by the antigen-antibody agglutination test from October 2003 to October 2004, and encompassed 2518 subjects. RESULTS: The percentages of various groups among male and female subjects, respectively, were recorded as 27.01% and 24.02% (for blood group A), 33.75% and 32.87% (for blood group B), 8.93% and 11.20% (for blood group AB) and 30.31% and 31.91% (for blood group O). The Rh positive and negative distribution in the studied population was 92.45% and 7.55% respectively. CONCLUSION: The determination of the frequency of blood groups in the region would not only help in blood transfusion services, but also eliminate the risk of erythroblastosis foetalis in the neonates.

ABO Blood-Group System↗
PubMed1992

Transformation of murine pre-B-lymphocytes by v-erb-B: progression to growth factor independence and tumorigenicity.

v-erb-B is the principal transforming gene of avian erythroblastosis virus, a replication defective retrovirus that transforms erythroid and fibroblast cells in vitro and causes erythroleukemia and fibrosarcoma in vivo. We have used a recombinant murine retrovirus, based on the truncated genome of Moloney murine leukemia virus and containing a chimeric gag-v-erb-B gene, to determine the murine hematopoietic cells transformed by v-erb-B. Infection of day 16.5 murine embryonal cells in liquid culture with this virus resulted in the outgrowth of foci of loosely to non-adherent hematopoietic cells which grew in close association with an adherent monolayer. After several weeks in culture a clonal population of transformed pre-B-lymphocytes emerged from this transformation initiated, though still growth factor dependent, population. These transformed cells were growth factor independent, and were tumorigenic in syngeneic mice. The results indicate that although v-erb-B can initiate transformation of murine hematopoietic cells, additional events are required for establishment of the fully transformed growth factor independent, tumorigenic phenotype. This v-erb-B induced progression from growth factor dependence to independence provides an in vitro model system for analysing events involved in the initiation and maintenance of leukemia.

Animals↗