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At least 109 records · Page 6Linked to original sources
PubMed2002

[Psychic aspects of the overactive gag reflex (gagging) in connection with a clinical case].

The overactive gag reflex is one of the etiologic categories of psychosomatic symptoms, which most often arise from environmental stressors. If organic disturbances, anatomic anomalies, or biomechanical inadequacies of existing prostheses are not key causes, the services of trained specialists are needed to help with behavioural management of the problem. Hypnosis can provide the clinician with a set of techniques, which may be used to augment or facilitate a particular course of treatment. In the case report, the patient's history and her overactive gag reflex suggested to use hypnosis therapy. The responsibility of a dentist can be found in his possible recognition of eventually necessary psychotherapy when consulting a patient.

Aged↗
PubMed2006

Impact of Gag sequence variability on level, phenotype, and function of anti-HIV Gag-specific CD8(+) cytotoxic T lymphocytes in untreated chronically HIV-infected patients.

The role of cytotoxic T lymphocyte responses in controlling viral replication during chronic HIV infection remains controversial. Viral escape mutations driven by immune pressure have been postulated to be an important mechanism contributing to the evasion of CD8(+) T cell responses. To explore this issue in more detail, HIV-1 p17 sequence variability was examined in chronically HIV-infected patients, in parallel with the level, phenotype, and function of HIV-SL9-specific CD8(+) T cell. Thirty-one HLA-A*0201(+) (A2(+)) and 10 HLAA* 02() (A2()) patients were included. The phenotype of SL9-specific CD8(+) T cell and their ability to produce IFN-gamma were analyzed by multiparameter flow cytometry. The HIV Gag p17 was sequenced and the mean variability score for each residue within SL9 and the two epitope flanking regions were calculated using Shannon entropy. The mean variability of SL9 and the proportion of patients with amino acid changes within SL9 were similar in A2(+) and A2() patients. Patients without Tet(+) cells had a significantly higher prevalence of aminoacid changes in SL9 than patients with Tet(+) cells. Interestingly, in patients with Tet(+) cells, the Y79F mutation within SL9 tended to be associated with lower levels of Tet(+) cells. We did not find any association between amino acid changes within SL9 and the differentiation stage of Tet(+) cells, or with IFN-gamma production. A similar analysis within the epitope flanking sequences did not reveal differences in the variability of these regions. These results suggest that viral mutations driven by immune selection pressure may play an important role in evading the immunological response in chronically HIV-infected individuals.

CD8-Positive T-Lymphocytes↗
PubMed2006

Mutant murine leukemia virus Gag proteins lacking proline at the N-terminus of the capsid domain block infectivity in virions containing wild-type Gag.

We have investigated the properties of murine leukemia virus Gag mutants in which the p12-CA cleavage site is altered. In one mutant, the cleavage is blocked; in the other, the conserved proline at the N-terminus of CA has been replaced with glycine. No infectivity was detected in either mutant. Mutant particles cannot synthesize full-length DNA upon infecting permissive cells. Particles composed of a mixture of wild-type and mutant proteins have severely impaired infectivity. These mixed particles are defective in their ability to synthesize DNA upon infection, but this defect is less severe than the loss of infectivity. Thus, proteins lacking the correct N-terminus of CA inhibit DNA synthesis and also interfere with formation or integration of a full-length, normal provirus. The results imply that CA proteins function as part of a large, highly organized structure in reverse transcription and apparently at a later step as well.

Animals↗
PubMedDate not supplied

Serine- and threonine-specific protein kinase activities of purified gag-mil and gag-raf proteins.

Retroviruses carry cell-derived oncogenes (v-onc) that have the potential to transform cells in culture and induce tumours in vivo. One of the few carcinoma-inducing viruses is the acutely transforming retrovirus MH2, which carries the putative oncogene v-mil and the known oncogene v-myc. Recently, a high degree of homology was discovered between v-mil and v-raf, the transforming gene of the murine retrovirus 3611 murine sarcoma virus (MSV), whereas homology to v-src is low. Both viruses express their oncogenes as the gag-fusion polyproteins p100gag-mil and p75gag-raf (of respective relative molecular mass (Mr) 100,000 and 75,000), while the myc oncogene of MH2 is expressed by means of a subgenomic messenger RNA. We have recently demonstrated that p100gag-mil is not a nuclear protein. Here we report that purified p100gag-mil and p75gag-raf exhibit protein kinase activities in vitro which, in contrast to the src-related p130gag-fps of Fujinami sarcoma virus (FSV) and all other characterized oncogene-encoded protein kinases, phosphorylate serine and threonine but not tyrosine. Both types of protein kinases phosphorylate lipids in vitro.

Animals↗
PubMed2005

Induction of Gag-specific T-cell responses by therapeutic immunization with a Gag-expressing Sendai virus vector in macaques chronically infected with simian-human immunodeficiency virus.

Recent prophylactic vaccine trials inducing virus-specific CD8+ T-cell responses have shown control of primary infections of a pathogenic simian-human immunodeficiency virus (SHIV) in macaques. In the chronic phase, therapeutic immunization replenishing virus-specific CD8+ T-cells is likely to contribute to sustained control of virus replication. In this study, we have administered a recombinant Sendai virus (SeV) vector into five rhesus macaques that had received prophylactic vaccinations and had controlled SHIV replication for more than 1 year after challenge. Our results indicate that virus-specific CD8+ T-cell responses can be expanded and broadened by therapeutic immunization with SeV vectors in the chronic phase after prophylactic vaccine-based control of primary immunodeficiency virus infections.

Animals↗
PubMed1986

Glutamine starvation of murine leukaemia virus-infected cells inhibits the readthrough of the gag-pol genes and proteolytic processing of the gag polyprotein.

The production of Moloney murine leukaemia virus from chronically infected cells was inhibited after starvation of glutamine. While the rate of synthesis of the precursor of the core proteins, Pr65gag, was not affected in the starved cells, its proteolytic processing was blocked. Pulse-chase experiments indicated that glutamine was required during the synthesis of Pr65gag to facilitate its subsequent processing. In addition, the synthesis of Pr200gag-pol, the precursor of the protease, reverse transcriptase and endonuclease, was inhibited in the glutamine-starved cells. Starvation for other essential amino acids such as tyrosine and isoleucine affected neither the synthesis nor the processing of the virus proteins. These results suggest that the readthrough mechanism which enables synthesis of the Pr200gag-pol polyprotein is modulated in the chronically infected cells by glutamine levels. Since the viral protease is part of the pol gene, its synthesis may be inhibited in the glutamine-starved cells and Pr65gag is therefore not processed.

Animals↗
PubMed1999

Heparin-induced thrombocytopenic potential of GAG and non-GAG-based antithrombotic agents.

We have undertaken these studies of the heparin-like, or glycosaminoglycan, and nonglycosaminoglycan-based antithrombotics in an effort to add to the understanding of the pathophysiologic mechanism of heparin-induced thrombocytopenia by investigations of how glycosaminoglycan-related agents interact with the heparin-induced thrombocytopenia antibodies. The low molecular weight heparins, originally thought to be useful alternatives to heparin because of their smaller size, show platelet activation and aggregation responses in platelet heparin-induced thrombocytopenia serum systems (P-selectin expression, microparticle formation, serotonin release, platelet aggregation). Although the molecular mass and sulfation of the heparinoid Lomoparan is similar to that of heparin and low molecular weight heparins, its chemical structure is different and probably is not recognized by the heparin-induced thrombocytopenia antibodies. The heparin-related pentasaccharide did not show a positive reaction in any system of platelet activation/aggregation. These studies have shown that the antibodies produced in patients with heparin-induced thrombocytopenia are reactive to highly sulfated glycosaminoglycans and nonglycosaminoglycan agents and less dependent on the molecular mass of these agents; whether the agent is a heparin or nonheparin compound was not critical. A combination of a moderate sulfation but low molecular mass in a heparin-like molecule was sufficient to prevent interaction with the heparin-induced thrombocytopenia antibodies. However, a chemical structure that is different from heparin (e.g., a heparinoid or a thrombin inhibitor) will also be nonreactive to platelet activation by heparin-induced thrombocytopenia antibodies.

Antibodies↗