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PubMed2004

Power and politics in international funding for reproductive health: the US Global Gag Rule.

Since 2001, the US government has used its power as a leading donor to family planning programmes to pursue policies in conflict with global agreements on reproductive rights. Prominent among these policies is the Mexico City Policy (or Global Gag Rule), which restricts non-governmental organisations (NGOs) in developing countries that receive USAID family planning funding from engaging in most abortion-related activities, even with their own funds. This paper reviews the history and political origins of the Gag Rule under several Republican party presidents. The Gag Rule has not achieved an overall reduction in abortions; rather, where it has disrupted family planning services, the policy is more likely to have increased the number of abortions. This paper concludes that the Gag Rule is a radical intrusion on the rights and autonomy of recipients of US funding. Regardless of whether or not it is rescinded in the future, the underlying issues in the politics of US reproductive health assistance are likely to persist. NGOs that wish to free themselves from the constraints it imposes must find the means to end their dependence on USAID funding, including turning to other donors. NGOs should also take the lead in opposing policies such as the Gag Rule that violate global agreements.

Ambulatory Care Facilities↗
PubMed2003

TorsinA protein and neuropathology in early onset generalized dystonia with GAG deletion.

Familial, early onset, generalized torsion dystonia is the most common and severe primary dystonia. Most cases are caused by a 3-bp deletion (GAG) in the coding region of the TOR1A (DYT1) gene, which is widely expressed in human brain and encodes the protein torsinA. This study compares neuropathology and torsinA expression in the normal human brain with that in dystonia cases with and without the GAG deletion. TorsinA-like protein was expressed in neuronal cytoplasm throughout the human brain, including cerebellum, substantia nigra, hippocampus, and neostriatum, with higher levels in specific neurons. This immunostaining pattern was not discernibly different in dystonia and normal brains in midbrain and neostriatal regions. However, nigral dopaminergic neurons appeared to be larger in both GAG-deletion and non-GAG-deletion dystonia brains compared to normal, and may be more closely spaced in GAG-deletion brains. Beyond these apparent changes in neuronal size and spacing in dystonia brains, there was no indication of neuron loss, inflammation, DNA strand breaks, or altered distribution of torsin-like immunoreactivity, supporting a functional rather than degenerative etiology of early onset torsion dystonia.

Adolescent↗
PubMed1999

Glycoaminoglycan (GAG) deficiency in protective barrier as an underlying, primary cause of ulcerative colitis, Crohn's disease interstitial cystitis and possibly Reiter's syndrome.

Ulcerative colitis, Crohn's disease and interstitial cystitis share many common features, the most important of which is a defect in the glycoaminoglycan (GAG) defensive barrier. This defect allows penetration of toxins causing localized inflammatory response, followed by fibrosis and distant pathological changes, together with a myriad of biochemical and immunological changes. The latter has caused confusion as to etiology of the aforementioned disorders. This hypothesis is somewhat supported by the fact that agents such as glucosamine and pentosan polysulphate (Elmiron) that replace the GAG layer, improve the conditions. The potential for extrapolation of this hypothesis to atherosclerosis and arthropathies exists. There is a great danger in modern medical research that if one misses the wood for the trees, one becomes hopelessly lost in the minutiae of research. At present, it is embarrassing that ulcerative colitis (UC), Crohn's (CR) and interstitial cystitis (IC) are the cause of a great deal of morbidity and occasionally mortality, yet after intensive research, the etiology and effective treatment eludes us. The research in the past has focused extensively on inflammatory response in the mucosal lining, and biochemical, infective and immunological changes in the serum. This has led to a vast array of research pathways that seem at the present time to be totally lost and, might I say, aimless in direction, as a cause for these conditions, that remain amongst the most imperically treated in modern medicine. Another possible syndrome in this class would be Reiter's, which has many features in common with the above. The basic tenet of a GAG deficiency hypothesis is that, as shown in Figure 1A, an intact GAG layer provides, firstly, a mechanical and electrostatic defence against penetration of infective agents, toxins, antigenic protein moieties, etc. and, secondly, the prevention of extravasation of body fluid components. A degraded GAG layer is the start of the disease cascade of the above group of illnesses.

Arthritis, Reactive↗
PubMed1997

Which glycosaminoglycans are suitable for antithrombogenic or athrombogenic coatings of biomaterials? Part I: Basic concepts of immobilized GAGs on partially cationized cellulose membrane.

Six different GAGs of different natural origin such as unfractionated heparin (HE), chondroitin sulfate (CS), dermatan sulfate (DS), keratan sulfate (KS), endothelial cell surface heparan sulfate (ESHS), and hyaluronan (HA) have been ionically immobilized onto partially cationized cellulose membranes with a substitution degree of 0.06. The GAGs have been characterized in terms of total sulfate content and relative molecular weight. The amount of immobilized GAGs was 10(3) times higher than the theoretical amount for monomolecular side-to-side coordination on polymer surfaces. In a standardized perfusion system with shear rates of 1050 sec-1, 37 degrees C, and 5 minutes with citrated blood, the level of platelet adhesion was 100% for partially cationized membrane, 90% for HA, 75% for each HE, CS, DS, KS, 5% for unmodified cellulose membrane, and 5% for confluent bovine aorta endothelial cells, referred to subendothelial matrix as standard for 100% platelet adhesion. ESHS-coated membranes were completely inert to platelets. The amount of ionically released GAGs during perfusion was also estimated. The partial cationic membrane is a suitable polymer surface in combination with the perfusion system to estimate the hemocompatibility of ionically immobilized water-soluble polyanions in terms of platelet adhesion at defined shear rates. The results of platelet adhesion are discussed in terms of structure and analytical parameter of the immobilized GAGs.

Animals↗
PubMed1999

The influence of the tonsillar gag on efficacy of seal, anatomic position, airway patency, and airway protection with the flexible laryngeal mask airway: a randomized, cross-over study of fresh adult cadavers.

UNLABELLED: We conducted a randomized, controlled, cross-over cadaver study to test the hypothesis that the efficacy of seal for ventilation and airway protection, anatomic position, and airway patency with the flexible laryngeal mask airway (FLMA) are altered by the application of a Boyle Davis (B-D) gag. We also determined the airway sealing pressure (ASP) at which the FLMA prevents aspiration when large volumes of fluid are placed above the cuff. We studied 20 adult cadavers (6-24 h postmortem). Efficacy of seal for ventilation and airway protection, anatomic position, and airway patency were determined with and without a B-D gag (two blade sizes: 8 and 10 cm) for the size 3, 4, and 5 FLMA in random order. Efficacy of seal for ventilation was determined by measuring the ASP at an intracuff pressure of 60 cm H2O. Efficacy of seal for airway protection was determined by flooding the mouth with 55-135 mL of water, reducing intracuff pressure until aspiration was detected fiberoptically and measuring ASP at this intracuff pressure. Anatomic position and airway patency were determined with a fiberoptic scope at an intracuff pressure of 60 cm H2O. In addition, in vivo compliance and ASP for the FLMA were measured in 10 cadavers and 10 paralyzed, anesthetized patients. Efficacy of seal for ventilation and airway protection, anatomic position, and airway patency did not change with the application of a gag for any mask size. The mean (range) ASP at which aspiration occurred when large volumes of fluid were placed above the cuff was 11 (7-15) cm H2O. The ASP for ventilation was always higher than the ASP for airway protection (P<0.0001). The FLMA had similar in vivo compliance and ASP in cadavers and anesthetized patients. We conclude that efficacy of seal for ventilation and airway protection, anatomic position and airway patency for the FLMA are unaffected by the application of a B-D gag in adults. ASP should be >15 cm H2O if there is a maximal risk of aspiration from above the cuff. IMPLICATIONS: The flexible laryngeal mask airway forms an effective seal for ventilation and protection of the airway that is unaffected by the application of a mouth gag that provides surgical access to the oropharynx. The efficacy of the seal should be >15 cm H2O if there is a maximal risk of aspiration from above the cuff.

Aged↗
PubMed2003

Evidence for Gag p24-specific CD4 T cells with reduced susceptibility to R5 HIV-1 infection in a UK cohort of HIV-exposed-seronegative subjects.

AIM: To characterize HIV-1 Gag p24-specific CD4 cell responses in HIV-exposed-seronegative (ES) individuals. METHODOLOGY: Twelve ES individuals, of diverse ethnicity and wild type for the CCR5 Delta-32 mutation, were identified. Controls were HIV-negative blood donors. Gag p24-specific and total Vbeta+ CD4 cells that expressed MIP-1beta, IFN-gamma and IL-2 were enumerated by intracytoplasmic cytokine staining. beta-Chemokine expression was correlated with susceptibility to R5 HIV-1 infection, as measured by polymerase chain reaction for integrated HIV-1 and by p24 enzyme-linked immunosorbent assay. RESULTS: Similar numbers of mitogen-stimulated and Vbeta+ MIP-1beta+, IFN-gamma+ and IL-2+ T cells were found in ES and HIV-negative control subjects. However, all ES subjects tested had an HIV Gag p24-specific MIP-1beta+, IFN-gamma+ and IL-2+ CD4 T-cell response that was rare in controls. p24-Specific cells of all ES but no control subjects could be expanded by in-vitro Ag/IL-2 stimulation, and when re-stimulated with an overlapping peptide series showed evidence of a broad CD4 cell memory response directed against multiple regions of Gag p24. Mitogen-stimulated ES CD4 cells were as susceptible to HIV infection as those from control subjects, but p24-specific IFN-gamma+ CD4 cells of six out of seven ES subjects tested were less susceptible to R5 HIV-1 infection than the counterpart fraction depleted of p24-specific IFN-gamma+ cells. The addition of blocking anti-beta-chemokine antibodies did not promote R5 HIV-1 infection of p24-specific IFN-gamma+ cells. CONCLUSION: Specific CD4 cell immunity, characterized by a broadly directed memory Gag-p24 CD4 cell response and reduced susceptibility of specific CD4 cells to R5 HIV-1 infection, is a likely correlate of non-transmission.

Adult↗
PubMed1997

Differential regulation of the antibody responses to Gag and Env proteins of human immunodeficiency virus type 1.

We have studied the antibody responses to Env and Gag antigens of human immunodeficiency virus type 1 (HIV-1) in several cohorts of HIV-1-infected individuals: long-term nonprogressors, progressors to disease, acute seroconvertors, and recipients of HIV-1 protease inhibitors. We conclude that the antibody responses to Env and Gag antigens are differentially regulated and that changes in the plasma viral load in the measurable range (500 to 10(8) RNA copies per ml) do not directly affect the antibody responses to these HIV-1 proteins. We provide quantitative estimates of HIV-1-specific immunoglobulin G concentrations in plasma, which can be in excess of 1 mg/ml for both anti-gp120 and anti-p24 once the immune response to HIV-1 has stabilized after seroconversion. We discuss the apparent paradox that the absence of anti-Gag antibodies (which have, at best, limited antiviral activity) is indicative of disease progression, while the retention of anti-Env antibodies (which do have antiviral activity) is of limited (or no) prognostic value. We show that the disappearance of anti-Gag antibodies during disease progression is highly unlikely to be due to immune complexing; instead, we believe that it reflects the loss of T-cell help that is more necessary for the anti-Gag than the anti-Env response.

AIDS Vaccines↗
PubMed1987

Liposomes as carrier of methyl-GAG. Increased antitumor activity and reduced hypoglycemia in mice.

The encapsulation efficiency and the leakage on storage of various types of liposomes prepared from different lipid compositions containing the anticancer drug methyl-GAG (methylglyoxal-bis-guanylhydrazone) were investigated. Treatment with methyl-GAG in a q.d. 1-4 schedule resulted in the murine leukemias P 388 and L 1210 (i.v.) in nearly the same increase in life span as the corresponding dose in liposomes. In a q.d. 1, 3 schedule methyl-GAG containing liposomes revealed comparable effects as the 4-day treatment with the free drug. The hypoglycemic effect of 80 mg/kg methyl-GAG, q.d. 1-4, could be normalized when the drug was administered in reverse-phase evaporation vesicles. We conclude that the liposomal encapsulation of methyl-GAG leads to a depot effect with a slight relief of toxicity.

Animals↗
PubMed2006

A review of gagging problems in dentistry: aetiology and classification.

Some people have a pronounced gag reflex that can be a severe limitation to their ability to accept dental care and the clinician's ability to provide it. It can compromise all aspects of dentistry, from diagnostic procedures to active treatment and can be distressing for all concerned. Many techniques have been described that attempt to overcome the problem. Dentists will undoubtedly see patients with gagging problems and knowledge of a variety of management strategies is necessary to aid the delivery of dental care. This first paper looks at the background to gagging problems and their classification and categorization prior to clinical treatment. The second article will look at the clinical assessment of the patient presenting for dental treatment with a history of gagging problems. It will also review methods used to manage patients with gagging reflexes during dental treatment.

Journal Article↗
PubMed1985

Effects of dexamethasone, progesterone, and testosterone on IOP and GAGs in the rabbit eye.

The effects of steroids on intraocular pressure and on aqueous outflow pathway (AOP) and adjacent anterior segment tissue glycosaminoglycans (GAGs) were studied in New Zealand Red rabbits treated for 4 wk with dexamethasone, hydroxymethyl-progesterone and methyl-testosterone. Only topical administration of dexamethasone resulted in a significant increase in intraocular pressure. The eyes were labeled in vitro for 1 hr with GAG precursors, [3H]-glucosamine and [35S]-sulfate, and maintained as whole organ cultures. The GAGs were biochemically isolated, fractionated by gel filtration chromatography and subjected to selective GAG degradative procedures. The total content of hyaluronic acid and chondroitin sulfate was analyzed by high performance liquid chromatography. In dexamethasone-treated eyes, the total content of hyaluronic acid was decreased in the AOP, although the specific activity of [3H]-glucosamine did not change. The total content of chondroitin sulfate was increased in the AOP and iris-ciliary body, while the specific activity of the [35S]-label was decreased in the AOP, iris-ciliary body, and sclera. The changes in the AOP GAGs in dexamethasone-treated eyes may be important factors for the development of dexamethasone-induced ocular hypertension in the rabbit.

Animals↗
PubMed1984

Selective PF4 release in vitro induced by heparin and related glycosaminoglycans (GAGs)--correlation with beta-TG release and platelet aggregation.

We studied human platelet aggregation and beta-TG/PF4 release induced by heparin and related GAGs in vitro both in normal PRP and in PRP after aspirin. In our experimental conditions, heparin and related GAGs always caused PF4 release in vitro from normal platelets, whether or not there was measurable platelet aggregation in the aggregometer. Significant beta-TG release was induced only by the mucosal heparin preparation (which also induced platelet aggregation in some citrated PRP). Therefore, while beta-TG release in vitro seems to correlate with platelet aggregating activity of heparin, the selective PF4 release, caused by heparin and related GAGs also in conditions in which neither platelet aggregation nor beta-TG are measurable, is probably associated with the high affinity of PF4 for heparin. The degree of affinity of GAGs for PF4 (heparin greater than DeS greater than HS) seems to correlate with PF4 release. Moreover, the significant reduction in PF4 release in vitro after aspirin suggests that GAGs-induced PF4 release is related to a cyclooxygenase-dependent activation process.

Adenosine Diphosphate↗
PubMed1980

Influence of proteoglycans (PG) and glycosaminoglycans (GAG) on ADP-, collagen- and thrombin-induced platelet aggregation.

PGs and GAGs have been isolated from fresh bovine aortas according to the method of Hascall and chemically characterized. These PGs and GAGs had only little effects on ADP- and collagen-induced platelet aggregation, but had very potent inhibitory action on thrombin-induced platelet aggregation and prolonged thrombin-clotting-time. Of the standard GAGs investigated hyaluronic acid, chondroitin-4-sulfate and chondroitin-6-sulfate had only little inhibitory action on thrombin-induced platelet aggregation, whereas heparin was very potent in this respect. The unsaturated disaccharides originating after degradation of GAGs with chondroitinases had no effect on platelet aggregation. No differences between PGs and GAGs in inhibiting thrombin-induced platelet aggregation could be detected.

Adenosine Diphosphate↗
PubMed1994

Pseudoknot-dependent read-through of retroviral gag termination codons: importance of sequences in the spacer and loop 2.

Retroviruses whose gag and pol genes are in the same reading frame depend upon approximately 5% read-through of the gag UAG termination codon to make the gag-pol polyprotein. For murine leukemia virus, this read-through is dependent on a pseudoknot located eight nucleotides 3' of the UAG. Other retroviruses whose gag and pol genes are in the same frame can potentially form similar pseudoknots 3' of their UAG codons. Beyond the similar secondary structures, there is strong sequence conservation in the spacer region and in loop 2 of the pseudoknots. The detrimental effects of substitutions of several of these conserved spacer and loop 2 nucleotides in the murine leukemia virus sequence show their importance for the read-through process. The importance of specific nucleotides in loop 2 of the pseudoknot contrasts with the flexibility of sequence in loop 2 of the most intensively studied frameshift-promoting pseudoknot which occurs in infectious bronchitis virus. Two nucleotides in loop 2 of the murine leukemia virus pseudoknot, which were shown to be important by mutagenic analysis, display hypersensitivity to the single-strand specific nuclease, S1. They are likely to be particularly accessible or are in an unusually reactive conformation.

Base Sequence↗
PubMed1994

Functional consequences of mutations in HIV-1 Gag p55 selected by CTL pressure.

Amino acid changes in the CA domain of the p55 Gag protein of HIV-1 have been observed during the course of an infection that appear to correlate with escape from cytotoxic T cell surveillance (Phillips et al., Nature 354, 453-459, 1991). A corollary of this observation is that all such changes should be functionally silent but, as the changes were observed in populations of virus, this has not been formally demonstrated. We have introduced the amino acid changes representative of those observed to occur in vivo into the Gag p55 gene cloned in the baculovirus expression system where the wild-type gene product produces virus-like particles (VLP). We show that none of these mutations affect particle formation as judged by VLP morphology and density despite their location within a sequence of the Gag open reading frame known to be important for assembly. These data add tacit support to the hypothesis that CTL pressure can drive virus evolution in HIV and add to the fine mapping of sequences involved in Gag subunit interactions.

Amino Acid Sequence↗
PubMed1991

cis Acting RNA sequences control the gag-pol translation readthrough in murine leukemia virus.

The pol gene of the Moloney murine leukemia virus (M-MuLV) is expressed as a Gag-Pol fusion protein through an in-frame suppression of the UAG termination codon located between the two genes. The role of nucleotide context in suppression was investigated, in a rabbit reticulocyte lysate translation system, using site-directed mutagenesis. The results indicate that the translational readthrough is mediated by at least 50 bases long RNA sequence located 3' to the gag UAG termination codon. Within this sequence a short purine-rich sequence adjacent to the amber codon, highly conserved among different retroviruses, appears essential for M-MuLV suppression. Two alternative putative stem and loop like RNA structures can be drawn at the gag-pol junction, one abutting the gag UAG codon, and the second downstream to it. None of these structures appears to be important to the suppression process.

Animals↗
PubMed1991

Confronting the hypervariability of an immunodominant epitope eliciting virus neutralizing antibodies from the envelope glycoprotein of the human immunodeficiency virus type 1 (HIV-1)--II. Synthetic peptides linked to HIV-1 carrier proteins gag and nef.

Combining of subtype specific peptides from the hypervariable loop of the envelope glycoprotein gp120 of divergent HIV-1 isolates may help in designing a broadly protective immunogen against HIV-1 infection. To enhance the immunogenicity of such a polyvalent antigen, in the absence of oil-containing adjuvants, it is necessary to link the peptides to a protein carrier. It is preferable to use as carriers those proteins from HIV-1 itself which may contribute to eliciting protective immunity. The structural and non-structural proteins, gag P18 and nef, respectively, which can be prepared in high yields by recombinant DNA techniques in Escherichia coli, were selected for this purpose. The corresponding peptide-protein conjugates, each containing 21 distinct peptides, were prepared using the cross-linking reagents N-succinimidyl-3-(2-pyridyldithio)-propionate (SPDP) or m-maleimidobenzoyl-N-hydroxysulfosuccinimide ester (sulfo-MBS). Conjugates prepared by the second method elicited approximately 10-100 times higher levels of antibodies recognizing the homologous peptides and the HIV-1 envelope glycoproteins. The sulfo-MBS conjugation procedure preserved the antigenicity of both gag P18 and nef and the respective conjugates elicited an immune response to these proteins. Despite the low immunization dose of single peptides (10 micrograms) present in the mixture of peptides collectively linked to the carriers, antibody responses to most of the individual peptides were high (dilution endpoints 1: greater than 16,000, 1: greater than 80,000 for the nef and gag P18 conjugates, respectively). Conjugates consisting of a multitude of HIV-1 envelope-derived peptides in combination with gag P18 and nef carriers are expected to elicit broadly protective immunity against distinct HIV-1 subtypes.

Animals↗
PubMed2006

Effect of promoter strength on protein expression and immunogenicity of an HSV-1 amplicon vector encoding HIV-1 Gag.

Helper-free herpes simplex virus type-1 (HSV-1) amplicon vectors elicit robust immune responses to encoded proteins, including human immunodeficiency virus type-1 (HIV-1) antigens. To improve this vaccine delivery system, seven amplicon vectors were constructed, each encoding HIV-1 Gag under the control of a different promoter. Gag expression levels were analyzed in murine and human cell lines, as well as in biopsied tissue samples from injected mice; these data were then compared with Gag-specific T cell responses in BALB/c mice. The magnitude of the amplicon-induced immune response was found to correlate strongly with the level of Gag production both in vitro and in vivo. Interestingly, the best correlation of the strength of the amplicon-induced immune response was with antigen expression in cultured DC rather than expression at the tissue site of injection or in cultured cell lines. These findings may have implications for the generation of improved HSV-1 amplicon vectors for HIV-1 vaccine delivery.

3T3 Cells↗
PubMed2005

Interaction of HIV-1 Gag with the clathrin-associated adaptor AP-2.

The envelope glycoprotein (Env) of HIV-1 interacts with the clathrin-associated adaptor complex AP-2 during the late phase of the viral replication cycle. Upon its synthesis, Env, therefore, is retrieved from the cellular surface unless internalization is inhibited by viral Gag. Here we demonstrate that not only Env, but also HIV-1 Gag, specifically binds to AP-2. Gag-AP-2 association was found to depend on tyrosine residue 132 and valine residue 135 at the matrix-capsid junction in the Gag polyprotein. Results of a morphological analysis of viral egress from cells expressing dominant-negative AP-2 suggest an involvement of AP-2 in confining HIV-1 exit to distinct microdomains. Further, particle release from AP-2-mutant cells was enhanced compared to release from wild-type cells but the infectivity of virus released from these cells was moderately reduced. Together these data attribute a role to the AP-2 complex in the regulation of HIV-1 assembly/release.

Adaptor Protein Complex 2↗