Search PubMed⌕ Search

Biomedical subjects

M M Rodrigues

Publications and source records attributed to M M Rodrigues.

At least 91 records · Page 5Linked to original sources
PubMed1986

Polymerization of intact beta 2-microglobulin in tissue causes amyloidosis in patients on chronic hemodialysis.

Systemic amyloidosis with a predilection for bone and synovium may complicate the course of patients on long-term hemodialysis. This form of amyloidosis can be typed as distinct from other amyloid diseases by using small tissue samples obtained by bone biopsy and at postmortem. Immunoblot analysis of two-dimensional gels of partially solubilized amyloid fibrils established that tissue deposits are composed of monomers, dimers, and higher polymers of beta 2-microglobulin (beta 2m) and that amyloid P component was also present. Anti-beta 2m antiserum recognized fibrils, as shown by immunoelectron microscopy. Purified monomer isolated from dissociated fibrils yielded peptides corresponding to the entire known sequence of beta 2m. Virtually all serum beta 2m, as well as that present in tissue fluid bathing amyloid fibrils, was monomeric. Hemodialysis-related amyloidosis is an example of a deposition disease occurring in hemodialysis patients. We have shown conclusively that, in this amyloid disease, polymerization of an intact normal serum protein to a fibrillar configuration may occur without proteolysis. We propose the designation A beta 2m for this form of amyloid fibril subunit protein.

Amino Acid Sequence↗
PubMed1986

Characterization of cellular immune response to chemically defined glycoconjugates from Leishmania mexicana subsp. amazonensis.

Two defined glycoconjugates (GP-10/20 and FR II Phe) purified from Leishmania mexicana subsp. amazonensis were analyzed with respect to their ability to induce cellular responses in immunized and infected mice. Each glycoconjugate was recognized by specific immune cells, as assessed by the proliferative response of lymph node cells of immunized mice. The response to GP-10/20 depended on helper T cells and antigen-presenting cells and was restricted by a major histocompatibility complex class II gene product. A specific anti-GP-10/20 T-cell line was established, and it was able to transfer a delayed-type hypersensitivity (DTH) response to normal mice. Both antigens were also recognized during an ongoing disease, as assessed by DTH response of infected mice. By this response, it was possible to distinguish susceptible from resistant strains of mice. In the course of the disease in resistant mice a correlation between the size of the primary lesion and the DTH response to GP-10/20 was observed. The presence of the glycoproteins on both promastigote and amastigote forms of the parasite, the antigenic similarities between both fractions, and the distribution of the GP-10/20 antigen in other trypanosomatids were studied. The results showed that both antigens were present on promastigotes and amastigotes. GP-10/20 shared no epitopes with FR II Phe, was included as part of the crude preparation leishmanin, and had some cross-reactive determinants with Leishmania donovani and Crithidia deanei.

Animals↗
PubMed1986

Immunohistochemical characterization of extracellular matrix in the developing human cornea.

Collagen, fibronectin and laminin are important components of the extracellular matrix of the human cornea. We used the immunofluorescence technique with polyclonal antibodies directed against these proteins and to bullous pemphigoid antigen (BPA), in order to study their distribution in human corneas from 8 weeks of gestation to term and in adult corneas. Immunoreactivity was observed with antibodies to type I collagen in the limbus and the corneal stroma at 8 weeks of gestation. At 11 weeks of gestation it was found in epithelial basement membrane (EBM) and Descemet's membrane (DM) and continued thus throughout fetal and adult life. Type II collagen was not detected in fetal or adult cornea. Type III collagen was detected during 8-20th weeks of gestation in the EBM, DM and stroma. After 27th weeks of gestation, type III collagen could no longer be detected in the central cornea. Type IV collagen was detected in the EBM as early as 8 weeks of gestation and remained positive throughout fetal and adult life. Descemet's membrane was negative for type IV collagen at 8 weeks of gestation and became positive thereafter. Immunostaining for fibronectin in DM was negative at 8 weeks of gestation, followed by patchy staining of corneal stroma and EBM up to the age of 37 weeks of gestation. Staining in the EBM was negative or variable up to 70 years of age, and then became positive again in a 77 year old individual. Staining for LN was positive in the EBM after 8 weeks of gestation. Staining was negative in DM at that age, but became positive after 9 weeks of gestation. Staining for BPA was negative at 8-9 weeks of gestation, then gradually became positive.

Antibodies↗
PubMed1986

Clinical, electron microscopic, and monoclonal antibody studies of intraocular epithelial downgrowth.

Epithelial downgrowth developed in three patients following cataract extraction and keratoplasty. Light and electron microscopy of the downgrowth tissue disclosed stratified squamous epithelium, but could not determine whether they were derived from conjunctival or corneal epithelium. The epithelial downgrowth contained cells that were connected laterally by desmosomal junctions and displayed well-defined basement membranes. Surface epithelial cells exhibited myriad microvillous processes scant to moderate mitochondria. In one case, prominent hemidesmosomal junctions were present. Immunohistochemical staining with monoclonal antikeratin antibodies revealed immunoreactivity with AE1, AE3, and AE11 in all cases, but with a cornea-specific antibody, AE5, in only one case. We concluded that in this last case, the epithelial downgrowth appears to have originated from the corneal epithelium.

Adult↗
PubMed1986

Retinitis pigmentosa: immunohistochemical and biochemical studies of the retina.

Several immunohistochemical and biochemical characteristics of retinas from two patients with retinitis pigmentosa (RP) were examined. Histochemically, interphotoreceptor retinoid-binding protein (IRBP) was found in the interphotoreceptor space in small areas of preserved peripheral retina, although enzyme-linked immunosorbent assay suggested that little IRBP was present. Antibodies to glial fibrillary acidic protein and factor VIII-related antigen corroborated retinal gliosis and retinal vessel attenuation, respectively, in the RP cases. Fibronectin showed similar staining in normal and affected tissue.

Aged↗
PubMed1986

Alterations in stromal glycoconjugates in macular corneal dystrophy.

Nine biotinylated lectins were used as histochemical probes to localize the carbohydrates residues of glycoconjugates in normal corneas and in corneas with macular and granular dystrophy. The lectin binding patterns of normal corneas and of corneas with granular dystrophy were indistinguishable from one another, but were distinctly different from those found in corneas with macular dystrophy. Concanavalin A reacted weakly with normal corneal stromal matrix, but stained stromal matrix of corneas with macular dystrophy intensely. Furthermore, unlike the normal corneal matrix, stromal matrix of corneas with macular dystrophy reacted positively with wheat germ agglutinin (WGA), Ricinus communis agglutinin I (RCA-I), Ulex europeus I, Dolichos biflorus, Bandeiraea simplicifolia I, Bandeiraea simplicifolia II, and soybean and peanut lectins. This study demonstrates specific alterations in glycoconjugates which occur in the corneal matrix of patients with macular dystrophy, namely the presence of oligosaccharides with terminal alpha-fucose, beta-galactose, N-acetylglucosamine and N-acetylgalactosamine residues, and oligosaccharide chains with a beta-galactose-N-acetylgalactosamine sequence.

Adult↗
PubMed1986

Fuchs' corneal dystrophy. A clinicopathologic study of the variation in corneal edema.

Corneal buttons from six patients with Fuchs' dystrophy had varying degrees of clinical edema measured in most cases by preoperative optical or ultrasonic pachymetry. These were sectioned in the operating room so that histologic correlations could be made. Histologically, marked thickening of Descemet's membrane and abnormal corneal endothelium corresponded to areas of severe clinical edema and were usually located in the central and paracentral regions. Descemet's membrane displayed multiple prominent guttata of varying size and shape, either facing the anterior chamber, or buried within multilaminar Descemet's membrane. In some corneas, aggregates of 10 nm fibrils were seen at the edges of guttata, corresponding to areas that stained for oxytalan fibrils. The endothelium was attenuated underlying the guttata. Clinical edema was not present unless accompanied by marked thickening of Descemet's membrane with multiple guttata and attenuation of corneal endothelium. The peripheral cornea was relatively clear clinically and showed minimal histologic changes.

Aged↗
PubMed1985

Threshold for lens damage during Q-switched Nd:YAG laser iridectomy. A study of rhesus monkey eyes.

Clinical and pathologic examinations were performed after 18 iridectomies had been created in six eyes of three rhesus monkeys using increasing Q-switched neodymium (Nd):YAG laser energy, pulses per burst, and number of bursts. Treatment parameters bracketed the threshold for lens damage during iridectomy. Iridectomy with one or two bursts of one or two Q-switched pulses at 5 to 6.2 mJ per pulse was achieved without lens damage. Slight increase of pulse energy or an increase to three pulses per burst (without pulse energy increase) caused local damage to the underlying lens. Marked increase of any of the treatment parameters caused slightly larger iridectomies and slightly larger, localized damage of the underlying lens. Synechiae developed between the monkey posterior iris surface at the iridectomy and the damaged area in 80% of the lens lesions. In monkeys, the small pulsed laser iridectomies created with pulses of energies up to 6.5 mJ became occluded during the healing process.

Animals↗
PubMed1985

Endothelial damage thresholds for retrocorneal Q-switched neodymium:YAG laser pulses in monkeys.

Laser pulses were focused within 1 mm of the rhesus monkey corneal endothelium using the Coherent Model 9900 laser at energies of 3, 6, 9, and 12 mJ. Sixteen slightly off-axis pulses were applied with no contact lens on the eye. Corneal damage was studied clinically and by scanning electron microscopy. Q-switched pulses of 12 mJ or less are not likely to damage the cornea if focused more than 0.75 mm from the endothelium. The retrocorneal focal distance for a 50% incidence of endothelial damage for 6, 9, and 12 mJ pulses was found to be less than 0.5 mm. For 3 mJ pulses, it was less than 0.25 mm. The severe early effect of suprathreshold pulses is edema of endothelial cells in a 0.2- to 0.6-mm diameter circular zone surrounding a small central pit through Descemet's membrane. At two months, irregular enlargement of endothelial cells surrounding and partially covering the persistent pit exists at sites of severe damage. The extent of the longer-term change is proportional to the severity of the original insult, but in no case was there clinically significant, persistent damage in the healed corneas.

Animals↗
PubMed1985

Endothelial damage from retrocorneal mode-locked neodymium:YAG laser pulses in monkeys.

Laser pulses were focused 0.85 to 1.60 mm from the rhesus monkey corneal endothelium using a mode-locked laser at 3.3 and 4.5 mJ. Sixteen slightly off-axis pulses were applied with no contact lens on the eye. Corneal damage was studied clinically and by scanning electron microscopy. The retrocorneal distance for a 50% incidence of endothelial damage (LD 50 = lesion distance, 50%) for 3.3 mJ mode-locked pulses was found to be 1.60 mm. All mode-locked pulses of 4.5 mJ focused 0.85 to 1.60 mJ from the endothelium caused damage. In comparison, Q-switched pulses of 12 mJ or less are not likely to damage the cornea if focused more than 0.75 mm from the endothelium. The severe, early effect of mode-locked pulses is edema of endothelial cells in a 0.2- to 0.3-mm diameter circular zone surrounding a 0.1-mm diameter denuded zone with a small central break of Descemet's membrane. By two months, mild and moderate lesions heal with little or no distortion of the endothelial mosaic. Irregular enlargement of endothelial cells surrounding and covering the previously denuded area of severe lesions is caused by both mode-locked and Q-switched treatment. In no case was there clinically significant, persistent damage in the healed monkey corneas.

Animals↗
PubMed1985

Dominantly inherited retinitis pigmentosa. Ultrastructure and biochemical analysis.

A 66-year-old white man had dominant retinitis pigmentosa. He developed progressive restriction of his visual field, night blindness, pallor of the optic discs, pigmentary retinopathy and posterior subcapsular cataracts. Postmortem examination of the eyes included electron microscopy and biochemical analysis of cyclic nucleotides and interphotoreceptor retinoid-binding protein (IRBP). Except for the fovea and periphery, the retina showed extensive gliosis and neuronal loss with loss of photoreceptor cells. The choriocapillaris was variably occluded in the regions of absent retinal pigment epithelium (RPE). In places, the pigment epithelium invaded the retina to the level of the internal limiting membrane. Biochemical analysis revealed that the interphotoreceptor retinoid-binding protein (IRBP), an important glycoprotein of the interphotoreceptor space, was virtually absent even in retinal areas where photoreceptor cells were still present. Cyclic nucleotide determinations indicated a decrease in the cyclic GMP concentration that reflected the general loss of photoreceptor elements. On the other hand the cyclic AMP levels in all retinal areas tested were abnormally elevated, indicating the possible involvement of this nucleotide in the pathogenesis of the disease.

Aged↗
PubMed1985

Disseminated bilateral chorioretinitis due to Histoplasma capsulatum in a patient with the acquired immunodeficiency syndrome.

A 31-year-old white male homosexual was healthy until March 1984, when he developed Pneumocystis carinii pneumonia, which resolved with treatment. In April 1984 he developed fever, followed by hepatosplenomegaly, headaches, blurred vision, pancytopenia and pulmonary infiltrates. On June 11, intracytoplasmic yeast were noted within leukocytes on a peripheral blood smear, and amphotericin B was started. The patient developed progressive respiratory and renal insufficiency and died on June 13, 1984. Autopsy histopathology demonstrated disseminated histoplasmosis and Histoplasma capsulatum was cultured from numerous tissues. Ocular histopathologic examination using special fungal stains and electron microscopy revealed numerous budding yeasts characteristic of Histoplasma capsulatum in the choroid, retina and central retinal vein. Their identification as H. capsulatum was confirmed by immunofluorescent staining.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Immunohistochemistry and electron microscopy of choroidal infiltrates and Dalen-Fuchs nodules in sympathetic ophthalmia.

An immunohistological study using monoclonal antibodies directed at specific membrane antigens of various inflammatory cells was carried out in order to evaluate the identity and topographic localization of the immuno-competent cells in an enucleated eye from a 6-year-old black patient with a three-month history of sympathetic ophthalmia. Correlative light and transmission electron microscopic examination of serial sections was also performed. The data demonstrated that the predominant cells within the choroidal infiltrate were T-lymphocytes (Leu 1+). T-cell subset analysis disclosed that most of these cells harbored specific antigenic determinants of the helper phenotype (Leu 3a+). A smaller proportion of the T cells demonstrated the specific determinants of the suppressor subtype (Leu 2a+). The helper/suppressor ratio varied slightly and ranged in most areas of the choroid between 3:1 and 4:1. Additionally, approximately 15% of the infiltrating lymphocytes harbored the Leu 14+ determinant specific for B cells. The latter were located in the outer choroid adjacent to the sclera. Very few natural killer (NK) cells (Leu 7+) were identified throughout the choroid. The granulomatous foci in the choroid were composed mainly of epithelioid cells and histiocytes expressing the OKM1+ and M221+ antigenic determinants on their membranes and demonstrating a high cytoplasmic nonspecific esterase activity (ANAE+). Within the Dalen-Fuchs nodules, similar to the choroidal nodules, there was a predominance of histiocytes and epithelioid cells (OKM1+, M221+, ANAE+), a few T-helper cells (Leu 1+, Leu3a+) and some OKM1-, M221- cells whose origin could not be determined. These findings were corroborated by electron microscopic observations of serial sections. Careful light and electron microscopic studies disclosed breaks in Bruch's membrane underlying some of Dalen-Fuchs nodules. In our opinion, these observations may be interpreted as the demonstration that Dalen-Fuchs' nodules and the choroidal granulomatous foci could be formed by identical cells of similar function and origin.

Child↗
PubMed1985

Histopathology of neodymium: YAG laser iridectomy in humans.

Fifteen peripheral iridectomy specimens were obtained, with informed consent, from patients with primary narrow angle glaucoma, after previous neodymium:YAG (Nd:YAG) laser iridectomy. The iridectomies were performed three hours to ten weeks after laser application. Iridectomy specimens were examined by scanning and/or transmission electron microscopy. Early effects of the Nd:YAG laser on the iris were mild hemorrhage and fibrinous aggregates. There were no inflammatory cell infiltrates. At later time intervals (up to 2 months post-laser treatment) the holes showed irregular thickness of iris pigment epithelium at the margins, and tissue atrophy limited to the immediate margins of the hole. Elsewhere the iris was structurally intact. The diameter of the holes varied from 60 to 500 microns. The larger holes corresponded to cases that had received more application shots.

Aged↗
PubMed1985

Change in epithelial keratin expression during healing of rabbit corneal wounds.

Corneal epithelial wound healing following full-thickness trephination and transcorneal freeze injury was studied by electron microscopy and immunofluorescent microscopy using monoclonal antibodies AE1, AE2, and AE3 to human epithelial keratin. Wounds were evaluated at various time intervals between 4 hr and 2 mo after injury. By scanning and transmission electron microscopy, epithelial migration was evident 4 hr after injury and was characterized by thinning of the epithelium and extension of filopodial processes. AE1 monoclonal antibody, which stains specifically the superficial cells of normal corneal epithelium, reacted to cells at the leading edge of the migrating epithelium. By 24 hr, all cells migrating over the wound displayed positive fluorescence with AE1 while the epithelium over the undamaged cornea exhibited normal fluorescence limited to the superficial epithelial cells. In full-thickness corneal wounds, reepithelialization was complete by 1-2 wk; however, all epithelial cells covering the wound remained positive for the AE1 antikeratin antibody. By 2 mo, the AE1 fluorescence returned to normal. In transcorneal freeze injuries, reepithelialization was complete by 4 to 7 days after injury, with all cells overlying the wound reacting with the AE1 antibody. By 2 wk after freeze injury, all epithelial cells appeared to express a normal AE1 staining pattern. No change was noted in the fluorescent distribution of either AE2 antibody, which did not react with the corneal epithelium, or AE3, which reacts with all corneal epithelial cells. These results suggest that healing of corneal epithelial wounds involves changes in keratin expression of the corneal epithelium.

Animals↗