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3. S100B and APP Promote a Gliocentric Shift and Impaired Neurogenesis in Down Syndrome Neural Progenitors

Author

Lu, Jie, Esposito, Giuseppe, Scuderi, Caterina, Steardo, Luca, Delli-Bovi, Laurent C, Hecht, Jonathan L, Dickinson, Bryan C, Chang, Christopher J, Mori, Takashi, and Sheen, Volney

Subjects
Biochemistry and Cell Biology, Biological Sciences, Aging, Neurosciences, Neurodegenerative, Acquired Cognitive Impairment, Stem Cell Research - Induced Pluripotent Stem Cell, Stem Cell Research - Induced Pluripotent Stem Cell - Human, Down Syndrome, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Regenerative Medicine, Stem Cell Research, Stem Cell Research - Nonembryonic - Human, Alzheimer's Disease, Genetics, Pediatric, Brain Disorders, Dementia, Stem Cell Research - Nonembryonic - Non-Human, Intellectual and Developmental Disabilities (IDD), 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Neurological, Amyloid beta-Protein Precursor, Animals, Apoptosis, Blotting, Western, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Humans, In Situ Nick-End Labeling, In Vitro Techniques, Membrane Potential, Mitochondrial, Mice, Mice, Transgenic, Nerve Growth Factors, Neurogenesis, Neurons, Oxidative Stress, S100 Calcium Binding Protein beta Subunit, S100 Proteins, Stem Cells, General Science & Technology
Abstract

Down syndrome (DS) is a developmental disorder associated with mental retardation (MR) and early onset Alzheimer's disease (AD). These CNS phenotypes are attributed to ongoing neuronal degeneration due to constitutive overexpression of chromosome 21 (HSA21) genes. We have previously shown that HSA21 associated S100B contributes to oxidative stress and apoptosis in DS human neural progenitors (HNPs). Here we show that DS HNPs isolated from fetal frontal cortex demonstrate not only disturbances in redox states within the mitochondria and increased levels of progenitor cell death but also transition to more gliocentric progenitor phenotypes with a consequent reduction in neuronogenesis. HSA21 associated S100B and amyloid precursor protein (APP) levels are simultaneously increased within DS HNPs, their secretions are synergistically enhanced in a paracrine fashion, and overexpressions of these proteins disrupt mitochondrial membrane potentials and redox states. HNPs show greater susceptibility to these proteins as compared to neurons, leading to cell death. Ongoing inflammation through APP and S100B overexpression further promotes a gliocentric HNPs phenotype. Thus, the loss in neuronal numbers seen in DS is not merely due to increased HNPs cell death and neurodegeneration, but also a fundamental gliocentric shift in the progenitor pool that impairs neuronal production.

Published
2011

5. Activity on DNA of the rips from phytolaccaceae

Author

P. Delli Bovi, I. di Resta, Luciano Gaudio, A. Di Maro, Salvatore Cozzolino, G. Siniscalco Gigliano, Serena Aceto, Delli Bovi, P., di Resta, I., Di Maro, A., Aceto, S., Cozzolino, S., Siniscalco Gigliano, G., Gaudio, L., Di Resta, I., Aceto, Serena, SINISCALCO GIGLIANO, Gesualdo, Gaudio, Luciano, DELLI BOVI, P., DI RESTA, I., and DI MARO, A.

Subjects
chemistry.chemical_compound, Biochemistry, biology, chemistry, Plant Science, biology.organism_classification, Phytolaccaceae, Ecology, Evolution, Behavior and Systematic, Ecology, Evolution, Behavior and Systematics, DNA
Published
1996

6. Mitogenic and dedifferentiating effect of the K-fgf/hst oncogene on rat thyroid PC clone 3 epithelial cells

Author

C, Battaglia, M T, Berlingieri, M L, Martelli, F, Trapasso, P, Delli Bovi, and A, Fusco

Subjects
Mitosis, Thyrotropin, Cell Differentiation, Epithelial Cells, Oncogenes, Transfection, Thyroglobulin, Epithelium, Cell Line, Clone Cells, Rats, Phenotype, Culture Media, Conditioned, Animals, Fibroblast Growth Factor 1, Fibroblast Growth Factor 2, Cell Division
Abstract

Transfection of rat thyroid differentiated epithelial cells, PC clone 3, with the K-fgf/hst oncogene results in alleviation of thyrotropin dependency for growth and suppression of the differentiated phenotype without the acquisition of the fully transformed phenotype. An autocrine mechanism is responsible for these effects, since the proliferation of PC clone 3 cells, induced by K-FGF-conditioned medium, is blocked by anti-K-FGF-specific antibodies. Moreover, addition of K-FGF-conditioned medium inhibits the thyroid differentiated functions. Also, such other members of the fibroblast growth factor family as basic and acidic fibroblast growth factor are able to induce thyroid cell growth and to block expression of the differentiated functions.

Published
1993

7. Isolation of a human placenta cDNA coding for a protein related to the vascular permeability factor

Author

Giuseppe Viglietto, Domenico Maglione, V Guerriero, M G Persico, P Delli-Bovi, Maglione, D, Guerriero, V, Viglietto, Giovanni, DELLI BOVI, Pasquale, and Persico, M. G.

Subjects
Signal peptide, Vascular Endothelial Growth Factor A, Immunoprecipitation, Macromolecular Substances, medicine.medical_treatment, Placenta, Molecular Sequence Data, Endothelial Growth Factors, Biology, Pregnancy Proteins, Transfection, Cell Line, chemistry.chemical_compound, Pregnancy, Complementary DNA, Sequence Homology, Nucleic Acid, medicine, Animals, Humans, Amino Acid Sequence, Choriocarcinoma, Cloning, Molecular, Gene Library, Placenta Growth Factor, Lymphokines, Multidisciplinary, Base Sequence, cDNA library, Vascular Endothelial Growth Factors, Growth factor, Tunicamycin, DNA, Molecular biology, Recombinant Proteins, Molecular Weight, Vascular endothelial growth factor A, medicine.anatomical_structure, chemistry, Oligodeoxyribonucleotides, Uterine Neoplasms, Female, Endothelium, Vascular, Oligonucleotide Probes, Cell Division, Research Article
Abstract

A human cDNA coding for a protein related to the vascular permeability factor (VPF) was isolated from a term placenta cDNA library; we therefore named its product placenta growth factor (PlGF). PlGF is a 149-amino-acid-long protein and is highly homologous (53% identity) to the platelet-derived growth factor-like region of human VPF. Computer analyses reveal a putative signal peptide and two probable N-glycosylation sites in the PlGF protein, one of which is also conserved in human VPF. By using N-glycosidase F, tunicamycin, and specific antibodies produced in both chicken and rabbit, we demonstrate that PlGF, derived from transfected COS-1 cells, is actually N-glycosylated and secreted into the medium. In addition, PlGF, like VPF, proves to be a dimeric protein. Finally, a conditioned medium from COS-1 cells containing PlGF is capable of stimulating specifically the growth of CPA, a line of endothelial cells, in vitro.

Published
1991

8. Autocrine growth stimulation by secreted Kaposi fibroblast growth factor but not by endogenous basic fibroblast growth factor

Author

A, Wellstein, R, Lupu, G, Zugmaier, S L, Flamm, A L, Cheville, P, Delli Bovi, C, Basilico, M E, Lippman, and F G, Kern

Subjects
Heparin, Recombinant Fusion Proteins, Fibroblast Growth Factor 4, Down-Regulation, Mice, Nude, Receptors, Cell Surface, Suramin, Adenocarcinoma, Receptors, Fibroblast Growth Factor, Adrenal Cortex Neoplasms, Neoplasm Proteins, Fibroblast Growth Factors, Mice, Phenotype, Proto-Oncogene Proteins, Tumor Cells, Cultured, Animals, Humans, Fibroblast Growth Factor 2, Neoplasm Transplantation, Tumor Stem Cell Assay
Abstract

We studied the different potentials of a secreted and a nonsecreted member of the fibroblast growth factor (FGF) family to induce autocrine growth stimulation in human adrenal cortex carcinoma cells (SW-13). These epithelial cells express basic FGF (bFGF) cell surface receptors, and picomolar concentrations of bFGF suffice to induce anchorage-independent growth. The requirement for exogenously added bFGF contrasts with the intracellular storage of biologically active bFGF in SW-13 cells greater than 10,000-fold in excess of the concentration needed to stimulate anchorage independent growth. To study whether the expression of a secreted FGF would alter the growth phenotype of these cells, we transfected them with an expression vector coding for the Kaposi-fgf (K-fgf) oncogene. In contrast to controls, K-fgf-transfected cells secrete significant amounts of biologically active K-fgf protein into the growth media, show up to 50-fold increased colony formation in soft agar, and grow into rapidly progressing, highly vascularized tumors in athymic nude mice. A reversible inhibition of the autocrine growth stimulation in vitro is brought about by the polyanionic compound suramin. We conclude that FGF has to be released from SW-13 cells to function fully as a growth stimulator in vitro and in vivo.

Published
1990

9. Significant fetal-maternal hemorrhage after termination of pregnancy: Implications for....

Author

Bianchi, Diana W., Farina, Antonio, Weber, William, Delli-Bovi, Laurent C., DeRiso, Matthew, Williams, John M., and Klinger, Katherine W.

Subjects
HEMORRHAGE, ABORTION complications
Abstract

Investigates the occurrence of fetal-maternal hemorrhage following pregnancy termination. Relationship between fetal cell microchimerism and autoimmune disease; Association between detected fetal nucleated cell equivalents and gestational weeks.

Published
2001
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10. Polyomavirus growth and persistence in Friend erythroleukemic cells

Author

V De Simone, P Amati, R Giordano, P Delli Bovi, DELLI BOVI, Pasquale, DE SIMONE, Vincenzo, Giordano, R, Amati, P., DELLI BOVI, P., and Giordano, R.

Subjects
Genes, Viral, Immunology, Cell, Mutant, Clone (cell biology), Biology, Microbiology, Genome, Cell Line, Persistence (computer science), Mice, Nucleic acid thermodynamics, Virology, medicine, Animals, Cells, Cultured, Leukemia, Experimental, Blot hybridization, Nucleic Acid Hybridization, DNA Restriction Enzymes, Molecular biology, Clone Cells, Kinetics, medicine.anatomical_structure, Cell culture, Insect Science, Polyomavirus, Research Article
Abstract

Infection of Friend erythroleukemic (FL) cells by polyomavirus (Py) invariably results in the selection of persistently infected FL-Py cell lines and clones. Anti-Py serum treatment of FL-Py lines and clones leads to the loss of Py genome and consequent cell cure. Conversely, cure has not been obtained in FL-PytsA cell lines (isolated after infection by a Py thermosensitive early mutant) and their derivative clones cultivated for a long time at nonpermissive temperature (39 degrees C), where viral large-T protein is inactive. Rescue of viral particles has always been obtained after shifting cells to 32 degrees C. Integrated viral genomes were detected by blot hybridization in an FL-PytsA clone at 39 degrees C. Long-term observation of FL-Py cell lines and their derivative clones reveals a reciprocal selection mechanism (coevolution) between the viral and the cellular populations, resulting in either a completely virus-free Py-resistant FL cell line (cure) or in a continuously Py-shedding line bearing Py genome variants. Structural analysis of these viral populations has been carried out, and some viral variants have been isolated and characterized. On the basis of the results obtained, the possible mechanisms of Py persistence in FL cells will be discussed.

Published
1984
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11. The transformer gene in Ceratitis capitata provides a genetic basis for selecting and remembering the sexual fate.

Author

Attilio, Pane, Marco, Salvemini, Pasquale, Delli Bovi, Catello, Polito, and Giuseppe, Saccone

Abstract

The medfly Ceratitis capitata contains a gene (Cctra) with structural and functional homology to the Drosophila melanogaster sex-determining gene transformer (tra). Similar to tra in Drosophila, Cctra is regulated by alternative splicing such that only females can encode a full-length protein. In contrast to Drosophila, however, where tra is a subordinate target of Sex-lethal (Sxl), Cctra seems to initiate an autoregulatory mechanism in XX embryos that provides continuous tra female-specific function and act as a cellular memory maintaining the female pathway. Indeed, a transient interference with Cctra expression in XX embryos by RNAi treatment can cause complete sexual transformation of both germline and soma in adult flies, resulting in a fertile male XX phenotype. The male pathway seems to result when Cctra autoregulation is prevented and instead splice variants with truncated open reading frames are produced. We propose that this repression is achieved by the Y-linked male-determining factor (M).

Published
2002

12. Fetal nucleated erythrocyte recovery: Fluorescence activated cell sorting-based positive selection using anti-gamma globin versus magnetic activated cell sorting using anti-CD45 depletion and anti-gamma globin positive selection

Author

Wang, Ji Yi, Zhen, Dong Kai, Falco, Vincent M., Farina, Antonio, Zheng, Yuen Ling, Delli-Bovi, L.C., and Bianchi, Diana W.

Abstract

Fluorescence activated cell sorting (FACS)-based anti-gamma (γ) positive selection and magnetic activated cell sorting (MACS)-based anti-CD45 depletion followed by anti-γ positive staining have been two of the most frequently used methods to isolate fetal cells from maternal blood. To date, there has been no direct comparison of fetal cell recovery by these two methods. This study was designed to address this issue. Fluorescence in situ hybridization (FISH) was performed on nucleated anti-γ positive cells using X and Y probes. Twenty-four maternal blood samples were obtained immediately after elective termination of pregnancy to ensure a detectable number of fetal cells. The yield and purity of fetal nucleated erythrocytes (FNRBCs) was statistically higher in FACS sorted samples (P < 0.01). The specificity of staining for FNRBCs was statistically higher in MACS sorted samples (P < 0.01). The data from this study demonstrate that both techniques have benefits and limitations. FACS has the advantage of having higher yield, higher purity, higher FISH efficiency and ease in microscope analysis, and MACS has the advantage of having higher specificity and less cell loss during FISH. Cytometry 39:224–230, 2000 © 2000 Wiley-Liss, Inc.

Published
2000
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13. Selection of mouse neuroblastoma cell‐specific polyoma virus mutants with stage differentiative advantages of replication.

Author

Maione, R., Passananti, C., De Simone, V., Delli‐Bovi, P., Augusti‐Tocco, G., and Amati, P.

Abstract

Two mouse neuroblastoma cell lines were analyzed for their permissivity for polyoma virus growth. One (N18) is fully permissive for polyoma replication, the other (41A3) shows limited permissivity and the viral genome persists, without noticeable cell death. Virus persistence does not seem to alter the cells' ability to differentiate in vitro and leads to selection of viral mutants altered in the untranscribed regulatory region of the genome. The mutant types obtained appear to be related to the degree of host cell differentiation. Nucleotide sequence analysis of the restriction fragment covering the regulatory region shows that duplications are present in all mutants, while deletions in the non‐duplicated segment are only present in mutants selected from less differentiated cells. These alterations involve both domains of the regulatory region that are considered to be essential for DNA replication and for enhancer activity. Mixed infections with polyoma wild type show that the selected mutants have cis‐advantage in replication in neuroblastoma cells and not in 3T6 cells. Mutants carrying the deletion in the non‐duplicated segment of the enhancer show a selective advantage in replication over the undeleted one in mixed infection. This advantage is much stronger in neuroblastoma cells in suspension (less‐differentiated stage) than in monolayer cells (more‐differentiated stage). An interpretation of the overall structure of the regulatory enhancer region, based on the observed differences between the mutants selected at different stages of differentiation in neuroblastoma and previously described mutants selected in undifferentiated cells, is discussed.

Published
1985
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14. Processing, secretion, and biological properties of a novel growth factor of the fibroblast growth factor family with oncogenic potential

Author

Delli-Bovi, P, Curatola, A M, Newman, K M, Sato, Y, Moscatelli, D, Hewick, R M, Rifkin, D B, and Basilico, C

Abstract

We recently reported that the protein encoded in a novel human oncogene isolated from Kaposi sarcoma DNA was a growth factor with significant homology to basic and acidic fibroblast growth factors (FGFs). To study the properties of this growth factor (referred to as K-FGF) and the mechanism by which the K-fgf oncogene transforms cells, we have studied the production and processing of K-FGF in COS-1 cells transfected with a plasmid encoding the K-fgf cDNA. The results show that, unlike basic and acidic FGFs, the K-FGF protein is cleaved after a signal peptide, glycosylated, and efficiently secreted as a mature protein of 176 or 175 amino acids. Inhibition of glycosylation impaired secretion, and the stability of the secreted K-FGF was greatly enhanced by the presence of heparin in the cultured medium. We have used the conditioned medium from transfected COS-1 cells to test K-FGF biological activity. Similar to basic FGF, the K-FGF protein was mitogenic for fibroblasts and endothelial cells and induced the growth of NIH 3T3 mouse cells in serum-free medium. Accordingly, K-fgf-transformed NIH 3T3 cells grew in serum-free medium, consistent with an autocrine mechanism of growth. We have also expressed the protein encoded in the K-fgf protooncogene in COS-1 cells, and it was indistinguishable in its molecular weight, glycosylation, secretion, and biological activity from K-FGF. Taken together, these results suggest that the mechanism of activation of this oncogene is due to overexpression rather than to mutations in the coding sequences.

Published
1988
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15. Poly‐FISH: a technique of repeated hybridizations that improves cytogenetic analysis of fetal cells in maternal blood

Author

Zhen, D. K., Wang, J. Y., Falco, V. M., Weber, W., Delli‐Bovi, L., and Bianchi, D. W.

Abstract

Prenatal diagnosis of fetal chromosomal abnormalities using interphase fetal nucleated erythrocytes (FNRBCs) separated from maternal peripheral blood can be technically challenging due to the limited number of FNRBCs available for analysis, the limited number of probes that can be used simultaneously, and low FISH efficiency on the formaldehyde‐fixed and immunohistochemically stained interphase FNRBCs. We developed a technique of sequential FISH analysis that involves removal of the previous hybridized probe under denaturing conditions, and rehybridization with different probes to improve FISH efficiency. This technique facilitates the analysis of multiple chromosome‐specific probes on the same nuclei. Results from our experiments show that FISH can be performed at least nine times on the same interphase nucleus and at least three different probes can be used simultaneously. Thus, theoretically, at least 24 different chromosomes can be analysed on a single interphase fetal cell isolated from maternal blood. We have termed this technique ‘Poly‐FISH’, and have successfully diagnosed trisomy 21, triploidy, and other chromosome abnormalities in FNRBCs using this technique. Copyright © 1998 John Wiley & Sons, Ltd.

Published
1998
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16. Isolation of a human placenta cDNA coding for a protein related to the vascular permeability factor.

Author

Maglione, D, Guerriero, V, Viglietto, G, Delli-Bovi, P, and Persico, M G

Abstract

A human cDNA coding for a protein related to the vascular permeability factor (VPF) was isolated from a term placenta cDNA library; we therefore named its product placenta growth factor (PlGF). PlGF is a 149-amino-acid-long protein and is highly homologous (53% identity) to the platelet-derived growth factor-like region of human VPF. Computer analyses reveal a putative signal peptide and two probable N-glycosylation sites in the PlGF protein, one of which is also conserved in human VPF. By using N-glycosidase F, tunicamycin, and specific antibodies produced in both chicken and rabbit, we demonstrate that PlGF, derived from transfected COS-1 cells, is actually N-glycosylated and secreted into the medium. In addition, PlGF, like VPF, proves to be a dimeric protein. Finally, a conditioned medium from COS-1 cells containing PlGF is capable of stimulating specifically the growth of CPA, a line of endothelial cells, in vitro.

Published
1991
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17. Isolation of a rearranged human transforming gene following transfection of Kaposi sarcoma DNA.

Author

Delli Bovi, P and Basilico, C

Abstract

By transfecting high molecular weight DNA from a Kaposi sarcoma lesion into murine NIH 3T3 cells, we have identified and molecularly cloned a set of human DNA sequences capable of inducing focus formation, growth in agar, and tumorigenicity in these cells. The human DNA sequences present in primary, secondary, and tertiary NIH 3T3 transformants encompass about 32 kilobases (kb) and contain four rearrangements with respect to normal human DNA and a portion of the c-fms protooncogene (FMS in human gene nomenclature). However, the minimal transforming region (6.6 kb) identified in our cloned DNA borders on the c-fms DNA region but does not contain c-fms coding sequences. The fms sequences are also not represented in the two transcripts (approximately equal to 1.2 and 3.5 kb) detected in NIH 3T3 transformants; however, they might provide elements regulating expression. Hybridization to several known oncogene probes and preliminary sequencing data indicate that we have identified a previously unrecognized "activated" oncogene. Since the rearrangements present in our cloned DNA sequences are not detectable in the original Kaposi tumor DNA used for transfection, it is possible that this oncogene was generated during gene transfer.

Published
1987
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18. Polyomavirus growth and persistence in Friend erythroleukemic cells

Author

Delli Bovi, P, De Simone, V, Giordano, R, and Amati, P

Abstract

Infection of Friend erythroleukemic (FL) cells by polyomavirus (Py) invariably results in the selection of persistently infected FL-Py cell lines and clones. Anti-Py serum treatment of FL-Py lines and clones leads to the loss of Py genome and consequent cell cure. Conversely, cure has not been obtained in FL-PytsA cell lines (isolated after infection by a Py thermosensitive early mutant) and their derivative clones cultivated for a long time at nonpermissive temperature (39 degrees C), where viral large-T protein is inactive. Rescue of viral particles has always been obtained after shifting cells to 32 degrees C. Integrated viral genomes were detected by blot hybridization in an FL-PytsA clone at 39 degrees C. Long-term observation of FL-Py cell lines and their derivative clones reveals a reciprocal selection mechanism (coevolution) between the viral and the cellular populations, resulting in either a completely virus-free Py-resistant FL cell line (cure) or in a continuously Py-shedding line bearing Py genome variants. Structural analysis of these viral populations has been carried out, and some viral variants have been isolated and characterized. On the basis of the results obtained, the possible mechanisms of Py persistence in FL cells will be discussed.

Published
1984
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19. Protection of mice against tumor growth by immunization with an oncogene-encoded growth factor.

Author

Talarico, D, Ittmann, M, Balsari, A, Delli-Bovi, P, Basch, R S, and Basilico, C

Abstract

The K-fgf/hst oncogene encodes a growth factor of the fibroblast growth factor (FGF) family that is secreted and transforms cells through a mechanism of autocrine cell proliferation. K-fgf-transformed cells are highly tumorigenic in immunocompetent allogeneic and syngeneic animals. BALB/c mice were immunized with a bacterial fusion protein consisting of a portion of the MS2 polymerase and of the human K-FGF precursor lacking only the first 4 amino acids or with a recombinant protein corresponding to the mature, secreted form of K-FGF (176 amino acids). They were then challenged with syngeneic K-fgf- or H-ras-transformed cells. Vaccinated animals exhibited a significant degree of protection against tumor induction, which was specific for K-fgf-transformed cells and correlated with the ability of the immunized mice to produce high titers of anti-K-FGF antibodies. Thus immunization with a single oncogene product can protect animals against tumor cells expressing this oncogene.

Published
1990
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20. Presence of chromosomal abnormalities and lack of AIDS retrovirus DNA sequences in AIDS-associated Kaposi's sarcoma

Author

P, Delli Bovi, E, Donti, D M, Knowles, A, Friedman-Kien, P A, Luciw, D, Dina, R, Dalla-Favera, and C, Basilico

Subjects
Chromosome Aberrations, Recombination, Genetic, Acquired Immunodeficiency Syndrome, Hepatitis B virus, Factor VIII, Base Sequence, DNA, Viral, Cytomegalovirus, HIV, Humans, HLA-DR Antigens, Sarcoma, Kaposi, Cells, Cultured
Abstract

The frequent occurrence of Kaposi's sarcoma (KS) in association with the acquired immune deficiency syndrome (AIDS) could be due to the fact that the etiological agent of this tumor is the same retrovirus causing AIDS, to another oncogenic virus frequently found in AIDS patients, or to the unmasking of the tumorigenic potential of KS cells by immunosuppression. We have therefore investigated the presence of DNA sequences homologous to the AIDS retrovirus, cytomegalovirus (CMV), and hepatitis B virus in 13 KS necropsies and biopsies from AIDS patients. All KS DNA samples were negative for AIDS retrovirus or hepatitis B DNA sequences. Two DNAs from necropsies contained CMV DNA, but the data suggested the presence of replicating CMV DNA due to generalized infection. We have also studied cell cultures derived from KS skin biopsies of AIDS patients. These cultures had a short lifetime in vitro and expressed some markers of endothelial cells. The cells were not tumorigenic in nude mice but contained a number of chromosomal rearrangements which were often monoclonal within the same culture. However, these abnormalities were different from culture to culture and even in cultures from the same biopsy. The presence of these chromosomal abnormalities seemed to correlate with the cell positivity for endothelial markers. Taken together these results indicate that neither the AIDS retrovirus, CMV, or hepatitis B virus is directly responsible for the altered growth of KS cells, that KS may be polyclonal even within the same lesion, and that KS cells have a tendency to karyotypic rearrangements.

Published
1986

21. Rapid rise of serum testosterone following discontinuation of long term treatment of prostate carcinoma with an LHRH-agonist

Author

P Delli Bovi, Vincent Vinciguerra, D.R. Budman, and Willi Kreis

Subjects
Male, Cancer Research, medicine.medical_specialty, Neoplasms, Hormone-Dependent, Buserelin, Internal medicine, medicine, Humans, Testosterone, Serum testosterone, LHRH Agonist, business.industry, Goserelin, Prostatic Neoplasms, Testosterone (patch), Hematology, Prostate carcinoma, Discontinuation, Substance Withdrawal Syndrome, Endocrinology, Oncology, Rapid rise, Drug Evaluation, business, medicine.drug
Published
1988

22. Isolation of a rearranged human transforming gene following transfection of Kaposi sarcoma DNA

Author

P. Delli Bovi, Claudio Basilico, DELLI BOVI, Pasquale, and Basilico, C.

Subjects
Transcription, Genetic, Biology, Transfection, DNA sequencing, Cell Line, chemistry.chemical_compound, Mice, Plasmid, Transcription (biology), Animals, Humans, Cloning, Molecular, Gene, Sarcoma, Kaposi, Genetics, Multidisciplinary, Base Sequence, Gene rearrangement, DNA, Neoplasm, Oncogenes, Molecular biology, chemistry, Genes, Transforming Growth Factors, embryonic structures, Nucleic Acid Conformation, Peptides, DNA, In vitro recombination, Research Article
Abstract

By transfecting high molecular weight DNA from a Kaposi sarcoma lesion into murine NIH 3T3 cells, we have identified and molecularly cloned a set of human DNA sequences capable of inducing focus formation, growth in agar, and tumorigenicity in these cells. The human DNA sequences present in primary, secondary, and tertiary NIH 3T3 transformants encompass about 32 kilobases (kb) and contain four rearrangements with respect to normal human DNA and a portion of the c-fms protooncogene (FMS in human gene nomenclature). However, the minimal transforming region (6.6 kb) identified in our cloned DNA borders on the c-fms DNA region but does not contain c-fms coding sequences. The fms sequences are also not represented in the two transcripts (approximately equal to 1.2 and 3.5 kb) detected in NIH 3T3 transformants; however, they might provide elements regulating expression. Hybridization to several known oncogene probes and preliminary sequencing data indicate that we have identified a previously unrecognized "activated" oncogene. Since the rearrangements present in our cloned DNA sequences are not detectable in the original Kaposi tumor DNA used for transfection, it is possible that this oncogene was generated during gene transfer.

Published
1987

23. Regulation of Gene Expression from the Polyoma Late Promoter

Author

F. G. Kern, P. Delli-Bovi, Claudio Basilico, and Sandra Pellegrini

Subjects
Regulation of gene expression, Transactivation, Lytic cycle, Transcription (biology), Early region, Transcriptional regulation, Biology, Gene, Selectable marker, Cell biology
Abstract

An experimental system has been developed in which foreign coding sequences for easily assayed genes or selectable markers are placed under the control of the polyoma late promoter. The use of this system has allowed the elucidation of the cisacting elements that control expression from this promoter and the demonstration of transactivation of this promoter by the viral early proteins. In addition to these forms of transcriptional control, the results also suggest that late transcription, both in polyoma transformed cells and early in the course of a lytic infection, may also be regulated at a posttranscriptional level.

Published
1987
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24. Ultrastructural observations of polyoma infected Friend erythroleukemic cells

Author

C, Taddei, P, Delli Bovi, R, Giordano, and P, Amati

Subjects
Cell Nucleus, Cytoplasm, Mice, Microscopy, Electron, Cell Survival, Animals, Leukemia, Erythroblastic, Acute, Crystallization, Polyomavirus, Cell Line, Friend murine leukemia virus
Abstract

Friend erythroleukemic cells (FLC) infected by Polyoma (Py) virus were studied at the electron microscope both during their lytic cycle, which occurs within the first 96 hr after infection, and in the surviving stabilized cells 30 days after infection. The results showed that the Polyoma virus and Friend leukemic virus (FLV) coexist and mature together in the same cell. During the lytic cycle, the Py particles were scattered in the nucleoplasm, and sometimes they were also found aggregated into crystals. Instead crystalline aggregates of Py particles were always present in the few surviving virus-carrying cells 30 days after infection. A possible interpretation could be that the crystal aggregation serves to maintain the viruses in a latency that allows the survival of the host cells.

Published
1982

25. The FGF-related oncogene, K-FGF, maps to human chromosome region 11q13, possibly near int-2

Author

K, Huebner, A C, Ferrari, P, Delli Bovi, C M, Croce, and C, Basilico

Subjects
Fibroblast Growth Factors, Chromosomes, Human, Pair 11, Multigene Family, Proto-Oncogene Proteins, Fibroblast Growth Factor 3, Chromosome Mapping, Humans, Oncogenes, Hybrid Cells, Transfection, Sarcoma, Kaposi
Abstract

The protein encoded in a novel human oncogene isolated by transfection of Kaposi's sarcoma DNA is a growth factor with significant homology to basic and acidic FGFs. The genomic structure of this oncogene (designated K-FGF), as originally isolated, carried DNA rearrangements upstream and downstream of the coding region. The normally discontinuous sequence upstream of the K-FGF coding region derived from the 3' end of the c-fms gene and thus originated from human chromosome 5. In order to determine the normal chromosomal location of the K-FGF gene and of the DNA sequences adjacent to its 3' end, we have correlated the presence of these sequences with retention of specific human chromosome regions in rodent-human somatic cell hybrids. These experiments mapped the K-FGF gene to human chromosome region 11q13----11q23, and in situ hybridization localized it more precisely to region 11q13 near int-2, which also belongs to the FGF family. The sequence downstream of the gene in transfectants and discontinuous with K-FGF in normal human DNA derives from chromosome region 12p12----12q13, possibly near the int-1 locus.

Published
1988

26. Selection of mouse neuroblastoma cell-specific polyoma virus mutants with stage differentiative advantages of replication

Author

Paolo Amati, Rossella Maione, G Augusti-Tocco, V De Simone, Claudio Passananti, P Delli-Bovi, Maione, R., C. PASSANANTI, C., DE SIMONE, Vincenzo, DELLI BOVI, Pasquale, AUGUSTI TOCCO, G., and Amati, P.

Subjects
DNA Replication, Cellular differentiation, Mutant, Biology, Virus Replication, medicine.disease_cause, General Biochemistry, Genetics and Molecular Biology, Cell Line, Mice, Neuroblastoma, medicine, Animals, Cloning, Molecular, Enhancer, Molecular Biology, Mutation, Base Sequence, General Immunology and Microbiology, General Neuroscience, DNA replication, Nucleic Acid Hybridization, DNA Restriction Enzymes, Molecular biology, Viral replication, Cell culture, DNA, Viral, Polyomavirus, Oncovirus, Research Article
Abstract

Two mouse neuroblastoma cell lines were analyzed for their permissivity for polyoma virus growth. One (N18) is fully permissive for polyoma replication, the other (41A3) shows limited permissivity and the viral genome persists, without noticeable cell death. Virus persistence does not seem to alter the cells' ability to differentiate in vitro and leads to selection of viral mutants altered in the untranscribed regulatory region of the genome. The mutant types obtained appear to be related to the degree of host cell differentiation. Nucleotide sequence analysis of the restriction fragment covering the regulatory region shows that duplications are present in all mutants, while deletions in the non-duplicated segment are only present in mutants selected from less differentiated cells. These alterations involve both domains of the regulatory region that are considered to be essential for DNA replication and for enhancer activity. Mixed infections with polyoma wild type show that the selected mutants have cis-advantage in replication in neuroblastoma cells and not in 3T6 cells. Mutants carrying the deletion in the non-duplicated segment of the enhancer show a selective advantage in replication over the undeleted one in mixed infection. This advantage is much stronger in neuroblastoma cells in suspension (less-differentiated stage) than in monolayer cells (more-differentiated stage). An interpretation of the overall structure of the regulatory enhancer region, based on the observed differences between the mutants selected at different stages of differentiation in neuroblastoma and previously described mutants selected in undifferentiated cells, is discussed.

Published
1985

33. 908 FETAL LUNG DEVELOPMENT AFTER AMNIOCENTESIS

Author

Blackburn, Will R, Logsdon, Phylis A, and Delli-Bovi, Jan

Abstract

The effects of amniocentesis (Ax) on the growth and development of fetal rat lung were studied in littermate fetuses subjected to minimum (Ax-Min; 0.1 ml) and maximum volume (Ax-Max; 0.5 ml+) amniocentesis at 17 days gestation. Non-operated littermates served as controls. Lungs of 12-14 fetuses/group were analyzed at term (22 days) for weight, composition (DNA, glycogen, lipid, phospholipid, phosphatidyl-choline) and histology (light and EM). Only Ax-Max reduced the weight of the lung (p>.1). DNA content was not influenced by Ax. Both Ax-Max (p>.02) and Ax-Min (p>.1) reduced lung glycogen. Ax did not alter the quantity of lung lipid at birth. The phospholipid fraction/lung was reduced (p>.05) after Ax-Max but not Ax-Min. The lungs of Ax-Max fetuses showed reduced alveolar space size and type II pneumocytes with few lamellar bodies and little glycogen. Histologic changes were not observed after Ax-Min. These studies indicated that large volume Ax reduces lung size by obliterating the fetal lung space rather than inhibiting lung cell proliferation. Ax-Max also reduces the phospholipid and surfactant pool size. Ax-min results in few detectable changes in lung growth or development. These studies explain certain aspects of the pulmonary dysfunction of infants with prolonged oligohydramnios.

Published
1978
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35. Inequalities in screening policies and perioperative protection for patients with acute appendicitis during the pandemic: Subanalysis of the ACIE Appy study

Author

Pellino, G., Podda, M., Pata, F., Di Saverio, S., Ielpo, B., Caruso, R., Gravante, G., Orengia, A., Chowdary, A., Kulkarni, A., Kuvvetli, A., Navarro, A., Smith, A., Ibiricu, A. C., Nacion, A. J. D., Alsaleh, A., Alhazmi, A., Elmabri, A., Wani, A., Rencuzogullari, A., Lasarte, A. S., Rubio, A. V., Bavikatte, A., Kumar, A., Jamiri, A. -R., Padilla, A. M. A., Cacurri, A., de San Ildefonso, A., Porcu, A., Sartori, A., Rocca, A., Paz Yanez, A., Becaria, A., Solis-Pena, A., Sretenovic, A., Urbistondo, A., Bandin, A., Najar, A., De Luca, A., Boddy, A., Charalabopoulos, A., Tzivanakis, A., Amendola, A., de Velasco, A. R. -G., Yildirim, A. C., Frontali, A., Toure, A. O., Garcia-Granero, A., Martinez Roldan, A., Larrainzar, A. S., Ratnayake, A. S., Gonzalez-Ganso, A. M., Minaya-Bravo, A. M., Das, A., Bondurri, A., Costanzi, A., Lucchi, A., Mazzari, A., Musig, A., Peloso, A., Piano, A., Police, A., Mihailescu, A., Pouy, A., Romano, A., Iossa, A., Leonetti, A. C., Guariniello, A., Isaac, A., Bovi, A. P. D., Chessa, A., Tromba, A., Martinez, A. A., Brillantino, A., Caira, A., Castaldi, A., Ferronetti, A., Giuliani, A., Prestera, A., Ramos-De la Medina, A., Tarasconi, A., Tornambe, A., Picciariello, A., Ioannidis, A., Leppaniemi, A., Khan, A., Rashid, A., Perez-Sanchez, A. L. E., Mittal, A., Mitul, A. R., Mehraj, A., Laharwal, A., Dorisme, A., Marinis, A., Iqbal, A., Moncada, A., Braccio, B., Alkhafaji, B., de Andres Asenjo, B., Martin-Perez, B., De Simone, B., Perez, B. S., Creavin, B., Cali, B., Pascotto, B., Stubbs, B., Retes, B. Z., Jovanovic, B., Goh, B. K. P., Sensi, B., Biddau, C., Gazia, C., Vallicelli, C., Fagundes, C. A., Santacruz, C. C., Chirico, C., Diaz, C. J. G., Petrola, C., Rodriguez, C. S., Benitez, C. Y., Dammaro, C., Lo Faro, C., Reinke, C., Paez, C. D., Oliva, C., Paranjape, C., Thomas, C., Chia, C. F., Kong, C. K., De Lucia, C., Chao, C. O., Arcudi, C., Guerci, C., Chia, C., Parise, C., Folliero, C., Varela, C., Ferguson, D. M., Camacho, D., Popowich, D., Lima, D. S., Rega, D., Delogu, D., Zigiotto, D., Vinci, D., D'Antonio, D., Parini, D., Merlini, D. A., Zimmerman, D. D. E., Moro-Valdezate, D., Pertile, D., Giusti, D. M., Keller, D. S., Tarik, D., Kalivaci, D., Mazingi, D., Maldonado-Pintado, D. G., Sasia, D., Linardoutsos, D., Osilli, D., Murrone, D., Russello, D., Rodas, E., Roa, E. A. A., Ricciardi, E., Rosso, E., Saladino, E., Flores-Villalba, E., Ajs, E. R., Smith-Singares, E., Baili, E., Kouroumpas, E., Bourmpouteli, E., Douka, E., Martin-Perez, E., Guaitoli, E., Samadov, E., Francone, E., Vaterlini, E., Morales, E., Pena, E., Zhao, E., Del Pozo Andres, E., Benzoni, E., Erdas, E., Pinotti, E., Colas-Ruiz, E., Aytac, E., Laterza, E., Agastra, E., Foianini, E., Moscoso, E., Laviano, E., Marra, E., Cardamone, E., Licardie, E., Mpaili, E., Pinna, E., Varo, E., Navarro, F. M., Marino, F., Medas, F., Romano, F., Maraska, F., Saliu, F., Madrid, F., Rosa, F., Mastella, F., Gheza, F., Luvisetto, F., Alconchel, F., Vieira, F. M., Pareja, F., Agresta, F., Luna, F., Bonilla, F., Cordera, F., Burdio, F., Mendoza-Moreno, F., Flores, F. M., Aranda, F. P., Taylor, F., Ramos, F. L., Fernandes, F., Tropeano, F. P., Balestra, F., Bianco, F., Ceci, F., Colombo, F., Di Marzo, F., Ferrara, F., Lancellotti, F., Lazzarin, F., Litta, F., Martini, F., Pizza, F., Roscio, F., Virdis, F., Antona, F. B., Ramirez, F. C., Fernandez, F. M., Llinares, F. O., Quezada, F., Schlottmann, F., Herrera-Almario, G., Massaferro, G., Bislenghi, G., van Ramshorst, G., Gallo, G., Luglio, G., Bointas, G., Kampouroglou, G., Papadopoulos, G., Manrique, G. A., Calini, G., Nastri, G., Formisano, G., Galiffa, G., Palini, G. M., Colucci, G., Pagano, G., Vanni, G., Pattacini, G. C., De Paola, G., Lisi, G., Partida, G., Bellanova, G., De Nobili, G., Necchi, G. S., Sinibaldi, G., Tebala, G., Bagaglini, G., Izzo, G., Argenio, G., Brisinda, G., Candilio, G., Di Grezia, G., Esposito, G., Faillace, G., Frazzetta, G., La Gumina, G., Nigri, G., Romeo, G., Amatriain, G. C., Ortega, G., Martin-Martin, G., Stavrou, G. A., Gunadi, Ugon, G. A., Machain, G., Marcucci, G., Martinez-Mier, G., Machain, G. M., Nari, G., Calvo, H., Fathy, H., Hamilton, Ahmed, H., Faraj, H., Nava, H., Macias, H. O., Nikaj, H., Solano, H., Khan, H. A., Alarcon, H. S., Ebied, H., Giani, I., Ateca, I. V., Neri, I., San Roman, I. A., Fidoshev, I., Rodriguez, I. M., Negoi, I., Ortega, I., Bernescu, I., Russo, I. S., Rodriguez, I. V., Palomares, I., Baltazar, I., Torrejimeno, I. J., Jurado, I. M. C., Reccia, I., Hussain, I., Toledo, I. B., Mora-Guzman, I., al-Najami, I., Dogaru, I., Romic, I., Balciscueta, I., Kenington, J. C., Sagolsem, J., Jang, J. Y., Olivier, J., Lammel-Lindemann, J., Dziakova, J., Villavicencio, J. I. R., Salinas, J., Pejanovic, J., Parreira, J. G., Perez, J. R., Reyes, J. A. S., Luque, J. A. M., Mak, J., Rodriguez, J. S., Kok, J. H. H., Krook, J., Diaz-Elizondo, J. A., Castell, J., Garcia-Flores, J. E., Navalon, J. M. J., Rodrigues, J. M. S., Pinto, J. P., Gomez, J. T. C., Luque, J. B., del Olmo, J. C. M., Salamea, J. C., Olivier, J. F. C., Laina, J. L. B., Ordonez, J. M., Gutierrez, J., Abba, J., Sofi, J. A., Sherafgan, K., Sahnan, K., Yanaga, K., Beatson, K., Asim, L., Alvarez, L., Siragusa, L., Farber, L., Ong, L., Athanasios, L., Garcia-Bruna, L., De Martino, L., Ferrario, L., Giordano, L., Gordini, L., Pio, L., Ponchietti, L., Moletta, L., Curella, L., Poggi, L., Taglietti, L., Bonavina, L., Conti, L., Goffredi, L., Ruiz, L. A. G., Barrionuevo, L., Fregoso, L. E., Cabrera, L. F., Rodriguez, L. G., Grande, L., Osoria, L. G., Gonzalez, L. J. K., Sanchez-Guillen, L., Tallon-Aguilar, L., Tresierra, L., Giavarini, L., Hasabelnabi, M., Odovic, M., Uemura, M., Khan, M., Artiles-Armas, M., David, M., Di Martino, M., Spampinato, M. G., Ribeiro, M. A. F., Viola, M., Angrisani, M., Calussi, M., Cannistra, M., Catarci, M., Cereda, M., Conte, M., Giordano, M., Pellicciaro, M., Marino, M. V., Vaterlini, M. E., Jimenez, M. F., Lolli, M. G., Bellini, M. I., Lemma, M., Chiarello, M. M., Nicola, M., Arrigo, M., Mejia, M. C., Manrique, M. M., Rodriguez-Lopez, M., Serradilla-Martin, M., Lara, M. Z., Martinez, M., Bagnall, M., Peter, M., Lara, M. C., Gomez, M. J., Paniagua-Garcia-Senorans, M., Gonzalez, M. P., Rutegard, M., Salo, M., Franceschilli, M., Silveri, M., Veroux, M., Pezzulo, M., Nardi, M., Rottoli, M., Tolonen, M., Ciro, M. P., Zuluagua, M., Cannavo, M., Cervellera, M., Iacobone, M., Montuori, M., Dominguez, M. G., Bingol-Kologlu, M., Tahir, M., Lim, M., Wilson, M. S. J., Wilson, M., Campanelli, M., Bisaccia, M., De Rosa, M., Maruccia, M., Paterno, M., Pisano, M., Torre, M., Trevino, M., Zuolo, M., Bartolome, M. A. H., Farina, M., Pera, M., Calvo, M. P., Sotelo, M., Thway, M. M., Hassan, M., Hassan, M. S. E., Azfar, M., Bouhuwaish, M., Taha, M., Zaieem, M., Korkoman, M., Guraieb, M., Shalaby, M., Raza, M. A., Younis, M. U., Elhadi, M., Zulfiqar Ali, M., Quazi, N., Dudi-Venkata, N. N., Alselaim, N., Loria, N., Ramirez, N. V., Win Than, N., Smart, N., Trelles, N., Pinto, N., Allievi, N., Petrucciani, N., Antonacci, N., Cillara, N., De'Angelis, N., Gica, N., Nicolaescu, D. C., Krystek, N., Falco, N., Pecorelli, N., Tamini, N., Dallas, N. A., Machairas, N., Brito, N., Fieturi, N. A., Ortega, N., Mercado, O. A., Irkorucu, O., Alsherif, O., Valles, O., Ioannidis, O., Palmas, O. H., Palmas, O. I. H., Guadarrama, O. S., Bozbiyik, O., Omelanczuk, P., Ottolino, P., Rodrigues, P., Ruiz, P., Campenni, P., Chiarade, P., Olivares, P. P., Baroffio, P., Panaccio, P., Wintringer, P., Di Fronzo, P., Talento, P., Favoriti, P., Sendino, P., Marsanic, P., Mifsut, P., Andrade, P., Ajawin, P., Abadia-Barno, P., Castaneda, P. A. N., Arevalos, P. O. S., Bellver, P. P., Koh, P. S., Souza, P., Major, P., Bali, R. S., Khattar, R. M., Lui, R., Melo, R. B., Ebrahiminia, R., Azar, R., Murga, R. L., Pirolo, R., Brady, R., Davies, R. J., Dholakia, R., Rattan, R., Singhal, R., Lim, R., Angelico, R., Isernia, R. M., Tutino, R., Faccincani, R., Peltrini, R., Carrera-Ceron, R., Tejos, R., Kashyap, R., Fajardo, R., Lozito, R., Pareja, R. M., Garbarino, S., Morales-Conde, S., Benli, S., Mansour, S., Flores, S., Suarez, S. L., Lopez, B. S., Fuentes, S., de las Casas, S. G., Napetti, S., de Guzman, S. O., Awad, S., Lujan, S. A. W., Gentilli, S., Grimaldi, S., Pizarro, S. O., Tayar, S., Nabi, S., Chan, S. M., Junaid, S., Rojas, S., Monetti, S., Garcia, S., Salvans, S., Tenconi, S., Shaw, S., Santoni, S., Parra, S. A., Cardenas, S., Perez-Bertolez, S., Chiappetta, S., Dessureault, S., Delis, S., Bonapasta, S. A., Rausei, S., Scaringi, S., Keswani, S., Ali, S. M., Cetinkunar, S., Fung, T. L. D., Rawashdeh, T., Lopez, T. N., De Campos, T., Duque, T. C., Perra, T., Liakakos, T., Daskalakis, T., Barnes, T., Koeter, T., Zalla, T., Gonzalez, T. E., Elosua, T., Campagnaro, T., Brown, T., Luoto, T., Oumar, T. A., Giustizieri, U., Grossi, U., Bracale, U., Rivas, U., Sosa, V., Testa, V., Andriola, V., Tonini, V., Balassone, V., Celentano, V., Progno, V., Raju, V., Carroni, V., Cavallaro, V., Rao Katta, V., De Simone, V., Primo Romaguera, V., Garcia Orozco, V., Luraschi, V., Rachkov, V., Turrado-Rodriguez, V., Visag-Castillo, V., Dowling, V., Graham, V., Papagni, V., Vigorita, V., Fonseca, V. C., Carneros, V. J., Bellato, V., Goncalves, W., Powers, W. F., Grigg, W., Bechstein, W. O., Lim, Y. B., Altinel, Y., Golubovic, Z., Balciscueta, Z., Ielpo, B, Podda, M, Pellino, G, Pata, F, Caruso, R, Gravante, G, Di Saverio, S, Orengia, A, Chowdary, A, Kulkarni, A, Kuvvetli, A, Navarro, A, Smith, A, Cavero Ibiricu, A, D Nacion, A J, Alsaleh, A, Alhazmi, A, Elmabri, A, Wani, A, Rencuzogullari, A, Sarriugarte Lasarte, A, Valle Rubio, A, Bavikatte, A, Kumar, A, Jamiri, A-R, M Alvarado Padilla, A, Cacurri, A, de San Ildefonso, A, Porcu, A, Sartori, A, Rocca, A, Paz Yáñez, A, Becaria, A, Solís-Peña, A, Sretenović, A, Urbistondo, A, Bandin, A, Najar, A, De Luca, A, Boddy, A, Charalabopoulos, A, Tzivanakis, A, Amendola, A, Ramirez-Gutierrez de Velasco, A, Cihat Yildirim, A, Frontali, A, O Toure, A, García-Granero, A, Martínez Roldan, A, Sanz Larrainzar, A, Sanjiva Ratnayake, A, M Gonzalez-Ganso, A, M Minaya-Bravo, A, Das, A, Bondurri, A, Costanzi, A, Lucchi, A, Mazzari, A, Musig, A, Peloso, A, Piano, A, Police, A, Mihailescu, A, Pouy, A, Romano, A, Iossa, A, C Leonetti, A, Guariniello, A, Isaac, A, P Delli Bovi, A, Chessa, A, Tromba, A, Álvarez Martínez, A, Brillantino, A, Caira, A, Castaldi, A, Ferronetti, A, Giuliani, A, Prestera, A, Ramos-De la Medina, A, Tarasconi, A, Tornambè, A, Picciariello, A, Ioannidis, A, Leppäniemi, A, Khan, A, Rashid, A, E Pérez-Sánchez, A L, Mittal, A, Rahman Mitul, A, Mehraj, A, Laharwal, A, Dorismé, A, Marinis, A, Iqbal, A, Moncada, A, Braccio, B, Alkhafaji, B, de Andrés Asenjo, B, Martin-Perez, B, De Simone, B, Sánchez Pérez, B, Creavin, B, Calì, B, Pascotto, B, Stubbs, B, Zavala Retes, B, Jovanovic, B, P Goh, B K, Sensi, B, Biddau, C, Gazia, C, Vallicelli, C, A Fagundes, C, Cerdán Santacruz, C, Chirico, C, J Gómez Díaz, C, Petrola, C, Sánchez Rodriguez, C, Yánez Benítez, C, Dammaro, C, Lo Faro, C, Reinke, C, Dominguez Paez, C, Oliva, C, Paranjape, C, Thomas, C, Fung Chia, C, Kwan Kong, C, De Lucia, C, Ovalle Chao, C, Arcudi, C, Guerci, C, Chia, C, Parise, C, Folliero, C, Varela, C, M Ferguson, D, Camacho, D, Popowich, D, Souza Lima, D, Rega, D, Delogu, D, Zigiotto, D, Vinci, D, D'Antonio, D, Parini, D, A Merlini, D, E Zimmerman, D D, Moro-Valdezate, D, Pertile, D, M Giusti, D, S Keller, D, Tarik, D, Kalivaçi, D, Mazingi, D, G Maldonado-Pintado, D, Sasia, D, Linardoutsos, D, Osilli, D, Murrone, D, Russello, D, Rodas, E, A Acuña Roa, E, Ricciardi, E, Rosso, E, Saladino, E, Flores-Villalba, E, Ruiz Ajs, E, Smith-Singares, E, Baili, E, Kouroumpas, E, Bourmpouteli, E, Douka, E, Martin-Perez, E, Guaitoli, E, Samadov, E, Francone, E, Vaterlini, E, Morales, E, Peña, E, Zhao, E, Del Pozo Andres, E, Benzoni, E, Erdas, E, Pinotti, E, Colás-Ruiz, E, Aytac, E, Laterza, E, Agastra, E, Foianini, E, Moscoso, E, Laviano, E, Marra, E, Cardamone, E, Licardie, E, Mpaili, E, Pinna, E, Varo, E, M Navarro, F, Marino, F, Medas, F, Romano, F, Maraska, F, Saliu, F, Madrid, F, Rosa, F, Mastella, F, Gheza, F, Luvisetto, F, Alconchel, F, Monge Vieira, F, Pareja, F, Agresta, F, Luna, F, Bonilla, F, Cordera, F, Burdió, F, Mendoza-Moreno, F, Muñoz Flores, F, Pardo Aranda, F, Taylor, F, L Ramos, F, Fernandes, F, P Tropeano, F, Balestra, F, Bianco, F, Ceci, F, Colombo, F, Di Marzo, F, Ferrara, F, Lancellotti, F, Lazzarin, F, Litta, F, Martini, F, Pizza, F, Roscio, F, Virdis, F, Blanco Antona, F, Cervantes Ramírez, F, M Fernandez, F, O Llinares, F, Quezada, F, Schlottmann, F, Herrera-Almario, G, Massaferro, G, Bislenghi, G, van Ramshorst, G, Gallo, G, Luglio, G, Bointas, G, Kampouroglou, G, Papadopoulos, G, Arredondo Manrique, G, Calini, G, Nastri, G, Formisano, G, Galiffa, G, M Palini, G, Colucci, G, Pagano, G, Vanni, G, Casoni Pattacini, G, De Paola, G, Lisi, G, Partida, G, Bellanova, G, De Nobili, G, Sammy Necchi, G, Sinibaldi, G, Tebala, G, Bagaglini, G, Izzo, G, Argenio, G, Brisinda, G, Candilio, G, Di Grezia, G, Esposito, G, Faillace, G, Frazzetta, G, La Gumina, G, Nigri, G, Romeo, G, Chocarro Amatriaín, G, Ortega, G, Martin-Martin, G, A Stavrou, G, Gunadi, G, Armand Ugon, G, Machain, G, Marcucci, G, Martínez-Mier, G, M 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Subjects
medicine.medical_specialty, business.industry, COVID-19, Perioperative, Appendicitis, COVID-19 testing, humans, healthcare disparities, mass screening, perioperative care, Perioperative Care, Settore MED/18 - Chirurgia Generale, Healthcare Disparitie, COVID-19 Testing, Pandemic, Acute appendicitis, medicine, Humans, Mass Screening, Surgery, Appendiciti, Healthcare Disparities, Intensive care medicine, business, Human
Abstract

Acute appendicitis remains a common reason for hospital admission. Reports have suggested a reduction in patients attending emergency departments during the acute phase of the SARSCoV- 2 pandemic. Moreover, a global surge in conservative management of acute appendicitis has recently been registered by the Appy Study of the Association of Italian Surgeons in Europe (ACIE)1. This is a treatment option that has been known for some years, although quite seldom used before the pandemic2–4. As most countries are experiencing new waves of the pandemic, the attitude of surgeons towards SARS-CoV-2 screening policies and personal protective equipment (PPE) used during the management of patients with acute appendicitis need to be established. According to a subanalysis of the ACIE Appy Study, half of surgeons globally were testing patients for SARS-CoV-2 only when symptomatic or there was suspicion of infection; approximately 12 per cent did not test patients at all (Fig. 1 and Table S1). There were regional differences. In Europe, respondents tested all patients (50.8 per cent) or those with suspected infection (43.9 per cent), with only 5.3 per cent not being tested at all. In the USA, the majority of participants only tested patients with a suspected infection (65.6 per cent). A similar picture of testing only those with a suspected infection was also reported from Latin America (57.2 per cent), Asia/Middle East (76.8 per cent), and Africa (41.7 per cent). Even more worrisome, 58.3 per cent of respondents from Africa and 27.6 per cent from Latin America were not testing patients at all before appendicectomy. Concerning the screening modality, most respondents used PCR alone or in combination with chest imaging. Serology was rarely used overall and never in Africa (Fig. 1 and Table S2 ). It is now accepted that chest imaging is not routinely required and that PCR is an accurate screening modality. Serology might, however, be useful to shed light on the disease course and previous exposure to the virus, but respondents from some countries still have restricted access to this test. In terms of PPE during appendicectomy, most African respondents did not use different PPE compared with the prepandemic period in patients who tested negative for COVID-19. More concerning is that 58.3 per cent did not use different PPE in untested patients. This differed from other regions where the rate of those not considering a change of PPE in untested patients did not exceed 22 per cent. One in 10 respondents from Latin America also reported that they were not using different PPE compared with the prepandemic phase in patients who tested positive for COVID-19. These data, and taking into account the high prevalence of acute appendicitis, leads to the conclusion that omission of routine patient screening may have contributed to local clusters among patients and threatened the safety of healthcare workers5. In this respect, it is likely that limited access to PPE explains the attitude of surgeons towards patients with unknown SARSCoV- 2 status or those infected, raising ethical concerns about the safety of surgical staff. It is of outmost importance that, even during challenging times and stress on economic stability, industrialized countries make efforts to sustain low-income countries and those with limited resources. This would ensure equal working conditions, safer treatment for patients with acute appendicitis, and better control of the pandemic

Published
2021

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