Biomedical subjects
C Henry
Publications and source records attributed to C Henry.
Transformation of quail embryo fibroblasts by a retrovirus carrying a normal human c-myc gene.
We have constructed avian retroviruses expressing the human c-myc oncogene. These viruses morphologically transformed primary quail embryo fibroblasts upon transfection and infection. Transformed cells produced viruses harboring a spliced c-myc gene and contained high levels of p64-67c-myc protein. One of these infectious viruses, vSX-AHM, was molecularly cloned and the nucleotide sequence of the spliced c-myc insert determined. No mutation was found within the c-myc coding sequence of this transforming clone when compared to the normal genomic progenitor. Thus, we concluded that no mutation within the human c-myc gene is required to induce primary avian embryo fibroblast transformation.
Converting Sendai virus into a specific fusogen whose cell target can be selected.
Covalent intermolecular hybrids of Fab anti-hemagglutinin-neuraminidase (HN) monoclonal antibody and avidin were prepared and characterized. These conjugates were used to block and redirect the fusion activity of Sendai virus (SV). After incubation of SV with Fab anti-HN: avidin conjugate on ice for 1-2 h, the SV fused only those P815 or BW5147 cells which were labeled with biotin-modified anti-cell surface immunoglobulin. The levels of cell-cell fusion obtained were at least as high as those achieved with unmodified SV and unlabeled P815 or BW5147 cells. These results demonstrate that it is possible to block the normal agglutinating activity of the HN molecules of SV and to introduce a new cell recognition feature without negating the fusogenic potential of the virus. Such an approach may be useful in harnessing the fusion activity of SV to a targeted delivery system for microinjection of macromolecules into selected cell populations.
Characterization of a MH2 mutant lacking the v-myc oncogene.
We have previously reported that a virus, MH2-PA200, lacking the ability to transform quail embryo cells, could be isolated from wild type (wt) MH2 stocks passaged on chicken neuroretina cells. We report here the molecular cloning and extensive characterization of this MH2-PA200 provirus. Molecularly cloned MH2-PA200 DNA was found to stimulate the growth of neuroretina cells by transfection assays and our results indicate that this recombinant virus was derived from the RAV-1 helper virus, in which v-mil and a small part of v-myc of MH2 were acquired at the expense of helper (delta gag-pol-delta env) sequences. In order to assess the precise boundary between the myc and env genes we determined the nucleotide sequence of the junction fragment and showed that 11 of 13 nucleotides of the env gene were identical to the myc sequence at the recombination point. The nucleotide sequence of the myc-env junction fragment of another similar and independently generated MH2 mutant showed similarly 9 nucleotides of homology between the env and myc sequences at the recombination point that took place at another site, suggesting that a homologous recombination occurred between MH2 and RAV-1 viruses to generate MH2-PA200 and similar mutants.
Characterization of a myc-containing retrovirus generated by propagation of an MH2 viral subgenomic RNA.
We have previously isolated, from wild-type MH2 virus that contains the two oncogenes mil and myc, mutants defective in one or the other oncogene product. We report here the molecular cloning and extensive characterization of MH2 CL25 provirus lacking the v-mil oncogene. Our results indicate that this virus corresponds to the propagation of the 2.8-kilobase subgenomic RNA of MH21.
[Chronic perineo-buttock ulcerations and suppurations preceding Crohn's disease by 30 years].
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The four C-terminal amino acids of the v-erbA polypeptide are encoded by an intronic sequence of the v-erbB oncogene.
The genome of avian erythroblastosis virus (AEV), a defective acute leukemia retrovirus, carries two distinct cell-derived oncogenes in the structure 5' delta gag-erbA-erbB-delta env3'. The nucleotide sequence of the v-erbA gene was recently reported. In order to determine the boundary between the two adjacent oncogenes, the sequence of the v-erbA/v-erbB junction of AEV was compared to that of a recombinant lambda phage containing a chicken cellular sequence representing the 5' part of c-erbB. The four C-terminal amino acids of v-erbA are in fact encoded by a c-erbB intron-derived sequence thus demonstrating that the virus acquired a truncated c-erbA gene. Furthermore the 7 to 10 amino acid residues upstream from the 4 C-terminal amino acids mentioned above appeared to be derived from env-related sequences. The splice acceptor site at the beginning of the only open reading frame for v-erbB is also present and functional in c-erbB when expressed to generate a truncated EGF (epidermal growth factor) receptor. Thus AEV joins a truncated erbA gene to a truncated erbB gene through env-derived sequences and intronic sequences from c-erbB.
Management of ocular hypertension.
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[Contribution of the barium enema to the diagnosis of postoperative recurrence of malignant tumors of the rectum and sigmoid colon].
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[The differential diagnosis of ovarian tumors using computerized tomography].
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Sequencing the erbA gene of avian erythroblastosis virus reveals a new type of oncogene.
Avian erythroblastosis virus (AEV) contains two distinct oncogenes, erbA and erbB . The erbB oncogene, which is homologous to a portion of the epidermal growth factor receptor, is related to the src family of oncogenes and efficiently transforms erythroblasts, whereas erbA potentiates the effects of erbB by blocking the differentiation of erythroblasts at an immature stage. This "potentiator" was sequenced; the amino acid sequence deduced from it was clearly different from the sequences of other known oncogene products and was related to carbonic anhydrases. These enzymes participate in the transport of carbon dioxide by erythrocytes, the precursors of which are main targets of avian erythroblastosis virus. A src-related oncogene such as erbB in synergy with an activated specific cell-derived gene such as erbA can profoundly affect early erythroid differentiation.
[Circulatory and respiratory effects of celioscopy in the obese].
Hemodynamic and respiratory variations were measured in ten obese women scheduled for laparoscopy. Peritoneal insufflation was associated with a decreased cardiac index (from 2.80 to 2.26 1 X min-1 X m-2; p less than 0.01) and increased systemic vascular resistances (from 1,230 to 1,940 dyn X s X cm-5). Heart rate remained stable (from 85 to 86 c X min-1). Mean arterial pressure was increased (from 86 to 104 mmHg; p less than 0.01). Placing the patients in Trendelenburg's position was associated with a small increase in cardiac index (from 2.26 to 2.49 l X min-1 X m-2; p less than 0.05). Under controlled ventilation, Paco2 was slightly increased (from 26 to 30 mmHg; p less than 0.01). A decrease in venous return due to intraperitoneal vascular compression explained the decrease in cardiac output. The rise in PaCO2 could be explained by CO2 reabsorption from the peritoneal cavity, and also by a change in the ventilation/perfusion ratio due to the curarization, mechanical ventilation and increased abdominal pressure. These results did not differ from the data available in non obese patients.
Matters of conscience: the ethics of ethics.
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[Long-lasting analgesia by intrathecal diffusion of morphine from an implanted reservoir].
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The relation of idiotype expression to isotype and allotype in the anti-p-azobenzenearsonate response.
The distribution of idiotype-positive plaques in mice of various strains injected with T-independent (TI) and T-dependent conjugates of p-azobenzenearsonate (Ars) has been investigated. With maturation of the responses there is a progressive loss of dominance of the major cross-reactive idiotype (CRI) in A/J and C.AL-20 mice. The extremes are represented by the predominantly CRI+ IgM plaque response to a single injection of the TI antigen, Ars-coupled Brucella organisms (Ars-Br), and the low frequency of CRI+ plaques in the polyisotypic response elicited by Ars-KLH (keyhole limpet hemocyanin) in adjuvant. The secondary response to Ars-Br was characterized by an intermediate display of idiotype-positive plaques in IgM, the IgG subclasses and IgA. Detailed analyses of the distribution of CRI+ plaques between isotypes in 60 mice hyperimmunized with Ars-KLH revealed that the expression of idiotype in any of the IgG subclasses and IgA was constant and independent. This is interpreted to indicate random assembly of VH with C gamma and C alpha genes during the switch. BALB/c and C3H mice also express a predominant idiotype during primary and secondary responses to Ars-Br as detected by our heterologous anti-A/J CRI serum. These strains only very rarely maintain the idiotype after hyperimmunization with Ars-KLH. We conclude that hyperimmune responses which probably involve multiple modes of regulation give a poor indication of the germ-line V gene repertoire.
Gas within the wall of the stomach report of a case and review of the literature.
Gas within the stomach wall is a rare occurrence. A case of intramural gas is presented. When air or gas is seen within the gastric wall on x-ray, gastric emphysema, emphysematous gastritis, or pneumatosis intestinalis is diagnosed. These classifications have become vague and contradictory. Gas in the gastric wall can only come from the environment or have been produced within the wall. Gastric emphysema and emphysematous gastritis refer to these situations, respectively. These classifications are expanded and pneumatosis intestinalis is deleted as a clinical or pathological diagnosis.
On the precision of the plaque count.
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