PubMed Health⌕ Search

Biomedical subjects

G Marquis

Publications and source records attributed to G Marquis.

At least 19 recordsLinked to original sources
PubMed2005

Crustal rheology of the Himalaya and Southern Tibet inferred from magnetotelluric data.

The Cenozoic collision between the Indian and Asian continents formed the Tibetan plateau, beginning about 70 million years ago. Since this time, at least 1,400 km of convergence has been accommodated by a combination of underthrusting of Indian and Asian lithosphere, crustal shortening, horizontal extrusion and lithospheric delamination. Rocks exposed in the Himalaya show evidence of crustal melting and are thought to have been exhumed by rapid erosion and climatically forced crustal flow. Magnetotelluric data can be used to image subsurface electrical resistivity, a parameter sensitive to the presence of interconnected fluids in the host rock matrix, even at low volume fractions. Here we present magnetotelluric data from the Tibetan-Himalayan orogen from 77 degrees E to 92 degrees E, which show that low resistivity, interpreted as a partially molten layer, is present along at least 1,000 km of the southern margin of the Tibetan plateau. The inferred low viscosity of this layer is consistent with the development of climatically forced crustal flow in Southern Tibet.

Journal Article↗
PubMed1994

Abnormal delayed hypersensitivity response to antigens of Candida albicans in alloxan-diabetic mice.

Three antigens of Candida albicans were comparatively evaluated to their ability to elicit delayed hypersensitivity (DH) responses in the mouse footpad test, using alloxan-diabetic and normal mice which were primed with heat-killed C. albicans in complete Freund adjuvant. These antigens were: (1) a preparation of sonically disrupted heat-killed cells; (2) a preparation of soluble cytoplasmic material remaining in the supernatant of a broken-cell suspension centrifuged at 100,000 g; (3) a preparation obtained by extraction of pulverized defatted cells with dilute phenol and sodium bicarbonate in water. After separation by polyacrylamide gel electrophoresis, the major components of soluble cytoplasmic material and dilute phenol extract were identified as a 43-kD protein, and glycoproteins of 21, 27 and 38 kD, respectively. Fifty-eight CD-1 outbred mice, which had received a single intravenous injection of alloxan followed by a 28-day rest period, were randomized with normal littermates to distinct experimental groups. Seven days after sensitization, mice were injected with one of the antigens in the right rear footpad and saline in the left rear footpad and the net specific increase in footpad thickness determined 24 and 48 h later. All three antigens elicited significant responses in sensitized normal mice. The responses of sensitized diabetic mice were clearly inferior to those of sensitized normal mice when heat-killed cells and soluble cytoplasmic material were used. Dilute phenol extract elicited equivalent responses at 24 and 48 h in both primed diabetic and normal mice.

Animals↗
PubMed1993

Muramidase-mediated damage to Candida yeast cells. Histochemical and immunochemical characterization of accumulating wall-like material.

Hen egg-white lysozyme is known to be fungicidal to blastoconidia of Candida albicans under defined in vitro conditions. This lethal action leads to changes in the layering of cell wall and to plasmolysis, caused by unremitting accumulation of wall-like material between the yeast cell wall and cytoplasmic membrane. Here, several methods were applied on ultrathin sections to define the nature of wall-like material: histochemical staining with periodic acid-thiocarbohydrazide-silver proteinate, periodic acid-alkaline bismuth, and phosphotungstic acid at low pH; the localization of the carbohydrate residues with lectin-gold complex; immunocytochemical staining with monospecific antibodies, factor 1 and 6, which recognized major cell wall antigens. The wall-like material was almost uniformly highlighted with periodic acid-thiocarbohydrazide-silver proteinate, factor 1 antibody, concanavalin A-gold and wheat germ agglutinin-ovomucoid-gold, indicating the presence of mannoproteins and chitin. The serotype A-specific epitope recognized by factor 6 antibody was not detected in the wall-like material, although it was demonstrated in the outer cell wall layers after 2 h of exposure to lysozyme.

Antibodies, Monoclonal↗
PubMed1991

Histochemical and immunochemical study of the fate of Candida albicans inside human neutrophil phagolysosomes.

To further define the ultrastructural events associated with the killing of Candida albicans by human neutrophils, four methods were used: (1) the periodate-thiocarbohydrazide-silver proteinate (PA-TCH-SP) staining of vicinal-glycol-containing complex carbohydrates; (2) the localization of thermostable immunodeterminants of the yeast cell wall, mannans or mannoproteins, using monospecific antibodies and a protein A-gold complex (monAb-gold); (3) the localization of mannose residues with concanavalin A labeled with gold particles (Con A-gold); (4) the localization of chitin oligomers using wheat germ agglutinin and ovomucoid labeled with gold particles (WGA-gold). The mannan-rich cell wall layers were progressively lost as shown by altered PA-TCH-SP reactivity and a diffuse pattern of staining with Con A-gold and monAb-gold. The de novo appearance of conspicuous amounts of glycogen-like particles near the plasmalemma and in the cell wall was interpreted as evidence of a reparative process of the yeast cell wall. Chitin was seemingly unaltered and readily demonstrated by the WGA-gold in the wall remnants of ghost cells.

Candida albicans↗
PubMed1991

Cell walls of normal and lysozyme-damaged blastoconidia of Candida albicans: localization of surface factor 4 antigen and vicinal-glycol staining.

The fungicidal effect of lysozyme on Candida albicans involves ultrastructural modifications previously described (G. Marquis, S. Montplaisir, S. Garzon, H. Strykowski, and P. Auger, Lab. Invest. 46:627-636, 1982). To further define the action of lysozyme on the yeast cell wall, we used the following: (i) the periodic acid-thiocarbohydrazide-silver proteinate (PA-TCH-SP) method to highlight vicinal-glycol-reactive sites of complex carbohydrates; (ii) a monospecific antiserum and a protein A-gold complex to study the expression of surface factor 4, a major Candida antigen; and (iii) the periodic acid-silver methenamine method to stain cell wall glycoproteins. All Candida cells were found to express surface factor 4 antigen. In normal blastoconidia, surface factor 4 was located in a glycoprotein-rich cell wall layer, underneath radially oriented bundles of filaments which form the outermost wall layer. In lysozyme-treated blastoconidia, this glycoprotein-rich layer was lost and the regular brushlike organization of the outer fibrillogranular layer was disrupted. PA-TCH-SP staining and localization of surface factor 4 antigen demonstrated an altered arrangement of bundles of filaments in the outer wall layers of blastoconidia which were morphologically intact but had abnormal cell wall appearance. Next, there was a reduction in thickness of the outer layer and the expression of surface factor 4 antigen was limited to the cytoplasmic membrane area. Later on, the cell wall was almost uniformly highlighted by PA-TCH-SP staining. These data evinced a highly plastic architecture of the cell wall in C. albicans.

Antigens, Fungal↗
PubMed1991

Detection of Giardia lamblia antigen in children living in a Peruvian periurban shantytown (Pueblo Joven).

Stool microscopy and an enzyme-linked immunosorbent assay (ELISA) for Giardia lamblia antigen detection were compared for detecting G. lamblia in 30 Peruvian infants. Of 1,131 fecal specimens, G. lamblia was detected by ELISA alone in 44, by microscopy alone in 17, and by both methods in 91. In another group of 17 children negative for G. lamblia by stool microscopy, 6 had G. lamblia detected by ELISA or duodenal aspiration: 2 only by ELISA, 1 only by duodenal aspirate examination, and 3 by both examinations. The ELISA is useful for the detection of G. lamblia in fecal specimens but compared to stool microscopy does not significantly increase the detection of cases.

Animals↗
PubMed1988

Genetics of resistance to infection with Candida albicans in mice.

To determine differences in susceptibility, 234 naive mice including xid and beige mutants were infected intravenously with Candida albicans and monitored with survival analysis and quantitative culture of the kidneys. By using survival time as the criterion, animals of seven inbred strains were separated into three groups. C3H/HeJ and Dw/+ were most susceptible; C57BR/cdJ, BRVR and CBA/N (xid) were intermediate in susceptibility; C57BL/KsJ and C57BL/6J were least susceptible. Mean survival times (MST) were markedly influenced by the number of Candida cells injected while the ranking of mouse strains by survival alone was unchanged. There was a dissimilar behaviour of the strains to produce organ weight changes in response to infection when compared with uninfected mice which were matched for age and genetic lineage. Black mice had lower colony forming units (CFU) per mg of tissue at the time of death than animals of other genetic lineage. Nevertheless, the finding that MST and CFU studies were loosely correlated in a few strains of mice indicated that the proliferation of the fungus in the kidneys was not always the major cause of death. The beige mutation was found to determine an increased susceptibility to systemic Candida infection. The differences in survival for beige and nonbeige mice were influenced by the genetic lineage of the host, being much greater in the C57BL/6 strain (36.7 days) than in the C3H/He strain (5 days). C57BL/6 beige-J had significantly higher CFU per organ and per unit of weight than C57BL/6 +/+ mice. These data evinced an important contribution of host genetic factors to resistance to systemic candidiasis. It is suggested that innate resistance genes regulate the differentiation in the bone marrow and the function of cells of granulocyte-macrophage lineage.

Animals↗
PubMed1985

[Actinobacillus actinomycetemcomitans infectious endocarditis. Apropos of 2 cases and review of the literature].

This work reports two cases of endocarditis caused by Actinobacillus actinomycetemcomitans. As noted in the medical literature, the mean clinical features are a subacute infection without know source of bacteremia, in a male patient aged 40 years or older and who is suffering from a heart disease. In our two presentations, the good response to single antibiotic treatment, although the optimal therapeutic approach is not yet defined, and the lack of embolism phenomena are of special interest. Spectrum of bacteria which can be responsible of infective endocarditis is widening rapidly; this study is an example of this trend.

Actinobacillus Infections↗
PubMed1985

Genetic resistance to murine cryptococcosis: increased susceptibility in the CBA/N XID mutant strain of mice.

In a survey of 301 normocomplementemic inbred mice (belonging to nine different strains: BALB/cN nu/nu and nu/+, CBA/N, C57BL/KsJ, C57BR/cdJ, CBA/CaJ, BRVR, DW/+, and C57BL/6J) for natural resistance to Cryptococcus neoformans, cumulative survival values were found to range from 12 to 22 days. When the average organ weights of infected animals were compared with reference values obtained in uninfected mice of the same age and genetic lineage, the following changes were documented. In the CBA/N strain, the mean spleen and brain weights increased 313 and 13.5%, respectively, whereas the mean liver weight remained unchanged. In the CBA/Ca strain, cerebral cryptococcosis was the dominant clinical feature, and a 54% increase in mean brain weight was recorded at the time of death. The averaged liver weight was drastically lower, whereas spleen weight values evinced a biphasic pattern of transient splenomegaly followed by involution. At the median time of death, CBA/N mice had significantly more cryptococci in the liver and spleen than corresponding CBA/Ca mice. In the (CBA/N X CBA/Ca)F1 mice, susceptibility to C. neoformans segregated according to the sex-linked inheritance of the X-linked immunodeficiency (xid) gene. It is concluded that (i) susceptibility to cryptococcosis is under multigenic control, (ii) the xid locus on the X chromosome influences susceptibility to cryptococcosis, and (iii) xid mice behave differently than CBA/Ca mice in their organ response during the course of the infection.

Animals↗
PubMed1985

Genetic resistance to murine cryptococcosis: the beige mutation (Chédiak-Higashi syndrome) in mice.

The influence of the bgJ and bg2J mutations on the susceptibility of mice to experimental cryptococcosis was studied in inbred mice of the C57BL/6J and C3H/HeJ strains. Although infected animals with the bg/bg genotype had a significantly shorter lifespan than bg/+ or +/+ animals, C3H/He beige-2J mice were less susceptible than C57BL/6 beige-J mice when compared with nonbeige mice of similar background. On days 18 and 19 after infection, quantitation of cryptococci in the brain, liver, and spleen revealed that the overall burden of organisms in infected C57BL/6 beige-J mice was in excess of one log unit above that found in the brain, liver, and spleen of infected C57BL/6 +/+ mice. At that time, C57BL/6 beige-J mice showed a 53% increase in mean brain weight, a 67.8% decrease in mean liver weight, and a 58.6% decrease in mean spleen weight, when compared with uninfected animals of the same age and genetical lineage. The corresponding figures for C57BL/6 +/+ mice were a 32% increase in mean brain weight, a 41.4% decrease in mean liver weight, and a 23.4% decrease in mean spleen weight. From these data, it is concluded that the beige mutation in mice is associated with increased susceptibility to cryptococcosis, the accrued susceptibility of the beige mutant is related to more rapid changes in the weight profile of the target organs as well as to a higher rate of growth or decreased clearance of Cryptococcus neoformans or both, and other autosomal genes are likely to be involved in the genetic control of susceptibility to murine cryptococcosis.

Animals↗
PubMed1983

[Endocarditis caused by Candida parapsilosis (para-krusei)].

This paper describes a case of Candida Parapsilosis endocarditis in a patient with a mitral valve prosthesis implanted two years previously. This history started with a cerebrovascular accident associated with pyrexia. A complex medico-surgical therapeutic approach controlled the infection. This consisted of systemic and local (immersion of the prosthesis) antifungal therapy, bathing the left heart chambers in 5 p. 100 iodine solution and two valve replacements at 8 months intervals. The second surgery was not related to recurrence of the candida infection but to a perivalvular leak attributed to the insertion of the prosthesis into tissues inflamed by recent infection. Despite the improvement in the prognosis of fungal infection due to an early surgical approach, it is still essential to try and prevent the disease, the mortality rate still being over 80 p. 100. It is essential to be very careful when using intravenous catheters and aerosols; the indications of antibiotherapy must also be respected.

Candidiasis↗
PubMed1982

Fungitoxicity of muramidase. Ultrastructural damage to Candida albicans.

The antifungal activity of hen egg-white lysozyme was investigated in vitro using a hypotonic medium designed to support an anabolic cellular state with minimal growth stimulation. The pathogenic yeast Candida albicans was found to be sensitive to microgram amounts of hen egg-white lysozyme. This susceptibility was evidenced by sluggish growth and a dose-dependent killing process. Transmitted and scanning electron microscopic observations on lysozyme-treated C. albicans yeast cells revealed the following ultrastructural modifications: (1) plasmolysis, vacuolar expansion and wrinkled surface configuration; (2) unremitting accumulation of wall-like material that bulged into the periplasmic space; (3) qualitative changes in the organization of the wall. Ongoing structural modifications within the wall were highlighted with the cationic heavy metal dye ruthenium red. A disruption in the permeability of the cytoplasmic membrane was evidenced by modification 1 and by differential staining characteristics in light microscopy. The superimposed osmotic imbalance was identified as the cause of cell death. It is proposed that lysozyme acts on C. albicans by two distinct complementary mechanisms: enzymatic hydrolysis of N-glycosidic bonds that link polysaccharides and structural proteins of the wall; injury to the cytoplasmic membrane as a result of a cationic protein kind of interaction.

Candida albicans↗
PubMed1981

Infective endocarditis update experience from a heart hospital.

In a retrospective study of 50 patients with infective endocarditis (IE), we found an overall mortality of 44%: among the 26 patients with natural valves (NV) the mortality was 19%; among the 24 with prosthetic valves (PV) it was 71%. Congenital heart disease was recognized in 17 of our cases, with a significant clustering in the NV group (50% vs 17%, p = 0.029); the most frequently encountered malformation was the bicuspid aortic valve. The incidence of rheumatic heart disease was 46% in the NV group and 83% in the PV group (p = 0.015). Manifestations of IE were protean and multisystemic. We calculated an average of 4.6 symptoms and 4.7 signs for each patient. Although sepsis was abated with appropriate antibiotics, death often ensued from multiple complications: congestive heart failure, arrhythmia, stroke, embolic myocardial infarction, valvular destruction or dehiscence, coagulopathy. New features of natural valve infective endocarditis are a rising incidence in the elderly and a survival rate seemingly at its peak. Features of prosthetic valve infective endocarditis include overwhelmingly frequent embolization to the central nervous system (p = 0.004), spleen (p = 0.009) and kidney (p = 0.010). Advances in therapy for this disease may come from early surgery in late prosthetic valve endocarditis and from future prospective studies to define how the host response influences the outcome.

Adult↗