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Biomedical subjects

E el-Hifnawi

Publications and source records attributed to E el-Hifnawi.

At least 19 recordsLinked to original sources
PubMed1996

[Cyclophotocoagulation with the diode laser in contact procedure with a new focussing tip].

UNLABELLED: During contact cyclophotocoagulation (CPC) energy is transmitted through the conjunctiva and the sclera by direct contact of a plain fibre tip. Alteration and scarring of the conjunctiva and the outer parts of the sclera cannot always be avoided. We used a new fibre tip which defocuses the laser light on the conjunctiva and sclera and focuses the laser light on the ciliar body. The coupling and focusing medium between fibre and sclera is a small glass ball (3 mm diameter). METHODS: Up to now we have treated 52 human eyes of 35 patients affected by refractory glaucoma using a diode laser (Zeiss Visulas II) coupled with a 200-microns fibre and a 3-mm focusing ball tip. In all cases 20-40 spots were applied 1.5 mm posterior of the limbus, power varied between 1.5 and 2.2 W and exposure time was 1.5 s. RESULTS: In all cases the conjunctiva and the sclera was unaltered. The mean follow-up time was 224 days. The mean IOP values +/- SD before treatment and 6 days, 4 weeks and 1 year after treatment were 40.9 +/- 7.1, 19.3 +/- 7.9, 22.4 +/- 14.8 and 17.2 +/- 11.3 mmHg. No positive, linear correlation was found between number of spots and IOP drop after 6 days. There was considerable individual variance. The main complications were anterior fibrinous uveitis (10%), slight vitreous haemorrhage (2/52) and transitory hypotony (2/52). In one enucleated eye structural alterations to the pigmented and non-pigmented epithelial cells of the ciliary body were found histologically. CONCLUSIONS: Contact diode CPC can significantly reduce IOP, and the conjunctiva and sclera can be left totally unaltered by the focusing ball tip used in this study.

Aged↗
PubMed1995

Effects of enhanced extracellular ammonia concentration on cultured mammalian retinal glial (Müller) cells.

Müller (glial) cells of the neonatal rabbit retina were cultured as confluent monolayers and exposed to enhanced concentrations of ammonia (0.25, 0.5, 1, 3, 7, and 10 mM) in medium for various periods (30 min to 10 d). This caused, in a time- and dose-dependent manner, similar changes in the Müller cells as had previously been described in cultured astrocytes. The most conspicuous events were 1) an increasing size of cell nuclei, 2) an accumulation of phagocytotic vacuoles, and 3) a rearrangement of intermediate filaments. 4) A considerable number of cells died when higher ammonia concentrations were applied for more than 1 h. Simultaneous application of dibutyryl-cyclic adenosine monophosphate (dBcAMP) prevented almost completely both the increase in cell nucleus size and the changes of intermediate filaments, but only partly the early cell death of a subpopulation of cells, and the accumulation of phagocytotic vacuoles. Further changes evoked by enhanced ammonia concentration were 5) an accumulation of lipofuscin-like material ("fatty degeneration") revealed by lipophilic stain, 6) reduced immunoreactivity for cathepsin D, and increased immunoreactivity for 7) glial fibrillary acidic protein, 8) glutamine synthetase, and 9) bcl-2 protooncogene protein. These findings are discussed in respect to the possible underlying pathophysiological mechanisms.

Ammonia↗
PubMed1995

Hepatic retinopathy: morphological features of retinal glial (Müller) cells accompanying hepatic failure.

More than 80 years ago, Alzheimer described changes in the brains of patients who had suffered hepatic failure. Astrocytes are primarily affected; their nuclei become swollen, their intermediate filament protein composition is altered and their cytoplasm becomes vacuolated. Cells with these features are called Alzheimer type II astrocytes and these changes have been attributed to the toxic effects of elevated ammonia levels. The present study investigates whether the dominant glia of another part of the central nervous system, the Müller cells of the retina, undergo similar changes. Retinae of patients who had died with symptoms of hepatic failure were processed for histology, histochemistry, and immunocytochemistry. Cell nuclei were measured from brain astrocytes (insula cortex), Müller cells, and retinal bipolar neurons. Hepatic failure resulted in the enlargement of nuclei in astrocytes and Müller cells, and the enhanced expression in Müller cells of glial fibrillary acidic protein, cathepsin D, and the beta-subunit of prolyl 4-hydroxylase (glial-p55). In some retinae, signs of gliosis were also observed. We conclude that increased levels of serum ammonia resulting from hepatic insufficiency cause changes in Müller cells that are similar to those seen in brain astrocytes. We term this condition hepatic retinopathy.

Adult↗
PubMed1995

Alterations of Müller (glial) cells in dystrophic retinae of RCS rats.

We have carried out a light microscopical study of Müller cells in the retinae of rats with inherited retinal dystrophy (Royal College of Surgeons rats). Isolated retinae of both control and Royal College of Surgeons rats were exposed to a Procion Yellow solution which is taken up selectively into Müller cells. The shape of the cells was then studied by confocal microscopy. Enzymatically isolated Müller cells were studied immunocytochemically with antibodies against glial fibrillary acidic protein, cathepsin D, beta-amyloid precursor protein, bcl-2 protooncogene product, and glutamine synthetase. Müller cells from RCS retinae were shorter than those from control retinae, and showed a coarse hypertrophy of their distal (sclerad) processes. In Müller cells isolated from the retinae of Royal College of Surgeon's rats, the expression of glial fibrillary acidic protein, cathepsin D, beta-amyloid precursor protein and bcl-2 protooncogene product was increased, and the expression of glutamine synthetase was reduced. Obviously, loss of neighbouring neurons leads to major alterations of both the shape and metabolism of Müller cells. The expression of enzymes that serve functional glio-neuronal interactions, such as glutamine synthetase, seems to be down-regulated, whereas proteins involved in cell reconstruction (cathepsin D), cell repair (possibly beta-amyloid precursor protein), and protection against apoptotic cell death (bcl-2 protooncogene product), are up-regulated, together with the 'pathological marker' glial fibrillary acidic protein.

Amyloid beta-Protein Precursor↗
PubMed1995

Localization of cathepsin D in rat ocular tissues. An immunohistochemical study.

Numerous studies have demonstrated that cathepsin D as a major lysosomal acid protease plays an important role in the degradation of protein in several tissues. An important function of the retinal pigment epithelium is to interact with the photoreceptor cells in the renewal process. During the renewal process, the RPE cell phagocytosis discarded photoreceptor discs which are then degraded in the RPE phagolysosomes. It is believed that cathepsin D plays a main role in the degradation of rod outer segments and rhodopsin into glycopeptides. The cellular localization of cathepsin D immunoreactivity was examined at the light microscopic level in the ocular tissues of non-affected RCS-rdy+ rats strain by use of the alkaline phosphatase-antialkaline phosphatase (APAAP) technique. The presence of cathepsin D immunoreactivity was found in the cell cytoplasm of the following ocular tissues: retinal pigment epithelium; Müller cells; ganglion cells; pigmented and non-pigmented ciliary body; iris tissue; epithelium and endothelium of the cornea; endothelium of various vessels, including the tunica vasculosa lentis. High activity of cathepsin D was found in the RPE cells, as well as in the cytoplasm of Müller cells, especially expressed in their foot plates lying close to the inner limiting membrane.

Aging↗
PubMed1995

Evidence of a direct role for growth hormone (GH) in mammary gland proliferation and lactation.

A panel of monoclonal antibodies to the growth hormone (GH) receptor/binding protein was used to demonstrate the existence and detail the expression of GH receptors in ductal and alveolar epithelial cells from rat and rabbit mammary glands by immunohistochemistry. Intense immunoreactivity was present in membrane, cytoplasm and some nuclei of epithelial cells during proliferation and lactation. Receptor expression decreased during weaning and was absent or weak in regressive mammary glands. Immunoreactivity was weak in ductal epithelial cells from virgin adult animals. Pronounced expression of GH receptor/binding protein was observed with two monoclonal antibodies and lesser reactivity was seen with others, paralleling their affinities for the receptor. The cytoplasmic presence of this putatively plasma membrane located GH receptor is accounted for by the existence of a soluble form on the GH receptor, namely the growth hormone binding protein derived from the membrane receptor by cleavage. Primary localization of the receptor in proliferating and lactating epithelial cells suggests that the rat and rabbit mammary gland is a GH target tissue. This finding is in contradiction to both classical GH action and the somatomedin hypothesis and challenges the widely held view that GH has no direct influence on mammary growth and function.

Animals↗
PubMed1995

[Case study of a solitary vitreous body cyst].

Vitreous cysts are rare and their origin unclear. We present a case of a 47-year-old woman who, after undergoing retinal detachment surgery on several occasions, developed disturbing vitreous opacities with which she presented for possible vitrectomy. Besides the typical postoperative vitreous condensations and opacifications, a solitary spherical cystic structure was present in the anterior vitreous cavity. The cystic structure was attached at its posterior aspect onto a vitreous membrane and was otherwise floating within a vitreous body lacuna. The vitreous opacities and the cyst were removed by performing a pars plana vitrectomy. The patient's visual acuity improved from 0.5 to 0.7. We presume that the cyst was acquired in association with the retinal detachment or the operations.

Cysts↗
PubMed1994

Localization of lysosomal enzymes in the retina and retinal pigment epithelium of RCS rats.

Using ultrahistochemical and immunohistochemical techniques, localization of acid phosphatase and cathepsin D was demonstrated in the retina and pigment epithelium of 1 to 42 day old RCS rats and its nonaffected congenic rat strain. Both enzymes are present in the pigment epithelium of the normal and dystrophic rat eye. As early as the age of 1 week, it was found that the lysosomes in the dystrophic rat retina are less stable in releasing acid phosphatase than those of control animals. Infiltration of cathepsin D into the subretinal space could first be detected with certainty in 2-week-old animals. The fragility of the lysosomal membrane and, therefore, the release of both enzymes became more pronounced as the animals aged. The findings of this study indicate that the instability of the lysosomal membrane in the RCS rat pigment epithelium may initiate degeneration of photoreceptors and pigment epithelium. The demonstration of cathepsin D activity has proved very helpful in revealing the physiological or pathophysiological condition of retinal pigment epithelium.

Acid Phosphatase↗
PubMed1994

Ultrastructure and regression of the tunica vasculosa lentis in newborn Wistar rats.

In this study, regression of the hyaloid vessels has been followed in the tunica vasculosa lentis (TVL) of the Wistar rat using light, transmission and scanning electron microscopy. The investigation extended from the 1st to the 32nd postnatal day. On day one, the posterior tunica vasculosa lentis is made up of radiating capillaries connected by side-arm branches, the vascular walls of which possess a continuous endothelium, a basement membrane and an incomplete pericyte covering. Endothelial cell specialization is apparent in the form of extreme thinning and fenestration in capillary regions lying opposite the lenticular capsule. The earliest detectable regressive changes become apparent on approximately day 3 and initially involve the short connecting capillaries surrounding the posterior pole of the lens and proceed from there. Regression takes place in the presence of rarefaction of vessel wall cells and the accumulation of endothelial cells in the adjacent capillaries. This leads to the formation of acellular channels which are made up of only basement membrane tubes. After the complete disappearance of these transitional acellular channels, the capillary meshwork coarsens. Remnants of these capillaries are detectable until the 30th postnatal day.

Aging↗
PubMed1994

Immunohistochemical localization of growth hormone receptor binding protein in the mammalian cerebellum.

A panel of monoclonal antibodies to the growth hormone (GH) receptor/binding protein was used to demonstrate the existence and detail the expression of GH receptors in the cerebellum of 2, 10, 28 days old postnatal and adult rats and 10, 20 days old and adult rabbits by immunohistochemistry to define potential targets for endogenous GH action in the cerebellum. Receptors were localized in membrane and cytoplasmic components of neurons and glial cells and expression decreased with age. Intense immunoreactivity was observed in the cytoplasm and dendrites of Purkinje cells and in cells of the cerebellar nuclei. Glial cells also showed receptor expression. Strong immunoreactivity was observed with two monoclonal antibodies and lesser reactivity was seen with others, paralleling their affinities for the receptor. The cytoplasmic presence of this putatively plasma membrane located GH receptor is accounted for by the high receptor content of endoplasmic reticulum and the existence of a soluble form of the GH receptor, namely the GH binding protein (BP) derived from the membrane receptor by cleavage, and receptor localization reported here correlate well with the distribution of insulin-like growth factor 1 (IGF-1) mRNA and immunoreactivity in cerebellar Purkinje cells and glial cells. Primary localization of the receptor in the cerebellum is in direct contradiction to both classical GH action and the somatomedin hypothesis and supports and extends the theory of genetically regulated macroneuronal maturation.

Animals↗
PubMed1994

[Experimental studies on the effect of the Er:glass and Cr:Tm:Ho:YAG laser in thermokeratoplasty].

So far the dose-effect ratio of the Holmium laser (wavelength 2.12 microns) and the erbium laser (1.54 microns) for laser thermokeratoplasty (LTK) are not defined in detail. Our study was designed not only to compare the erbium contact and the holmium non-contact applications but also to throw light on the influence of different geometrical application patterns, pulse energies, pulses per coagulation site and repetition rates under experimental conditions. Enucleated sheep and pig eyes were used 2-6 h post mortem, pressurized to 25 mmHg and moisturized with saline solution. Before and after LTK, pachymetry and keratometry were performed. Some specimens were prepared for light and scanning microscopy. The coagulation threshold for the erbium laser in a contact mode with a 200-microns fibre was 25 J/cm2 (ca. 8 mJ/pulse) and for the holmium laser 8 J/cm2 (ca. 2.5 mJ/pulse). The erbium laser was used in a single shot per spot mode, the holmium laser in repeated pulse per spot mode. With the single shot per spot mode, we were able to induce a promising hyperopic shift of up to -3.47 +/- 0.61 D, while myopic changes could only be induced up to +1.89 +/- 0.74 D. Higher changes of up to +8.27 +/- 1.3 D could be achieved by means of repeated pulses per spot (20 pulses, 45 mJ, 10 Hz). Our experiments showed an obvious increase of dioptric changes when using a higher repetition rate while pulse energy and number were kept constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Lectin histochemical studies of retinal pigment epithelium in retinal detachment].

The retinal pigment epithelium (RPE) exhibits a broad spectrum of morphological changes under pathological conditions. Since RPE cells cannot be immunocytochemically characterized with certainty, lectin histochemical investigations were performed to study the lectin binding pattern of different morphological RPE variants in human globes. Normal RPE with attached retinas was compared to reactive changes in RPE following retinal detachment. Lectin binding sites were visualized by a modified PAP technique performed on paraffin-embedded tissue sections. Eight lectins of different sugar affinity (Con A, WGA, PNA, RCA 1, SBA, UEA 1, DBA, LPA) were tested for binding sites on the RPE. Both normal and reactively changed RPE possess receptors for Con A, WGA, PNA, and RCA 1. Modifications in the lectin binding pattern occurred simultaneously with the morphological changes within the RPE cells. RPE cells which form a monolayer on Bruch's membrane mainly have lectin binding sites in their apical portions. Proliferating and migrating RPE cells, especially RPE macrophages, which have withdrawn from the basal cell layer were found to contain lectin binding sites dispersed over the entire cytoplasm. RPE macrophages exhibited additional binding sites for the lectin SBA. These results indicate that RPE cell variants can be designated by means of their specific combination of lectin binding sites for Con A WGA, PNA, and RCA 1 not found on other cell types in the retina.

Humans↗
PubMed1990

[Lectin histochemical studies of retinal pigment epithelium following photocoagulation].

Lectins are histochemical probes for specific carbohydrate residues found in cell membranes and the cytoplasm. Lectin binding sites were determined in normal and morphologically altered retinal pigment epithelium (RPE) in photocoagulation scars using a modified PAP method. Tissue sections of human bulbi obtained during enucleation for various reasons were incubated with eight lectins of different sugar affinity: ConA, WGA, PNA, RCA I, SBA, UEA I, DBA, LPA. The comparative study of normal and reactive migrating and proliferating RPE revealed lectin binding sites for Con A, WGA, PNA and RCA I. Differences in the lectin binding pattern of various morphological cell types occurred within the intracellular topographical distribution and density of lectin binding sites. SBA, UEA I, DBA and LPA are not found to react with the RPE. These results indicate that lectin histochemistry allows cytochemical identification of normal and reactive RPE, which shows positive staining with Con A, WGA, PNA and RCA I not found in other cell types of retinal origin.

Histocytochemistry↗
PubMed1989

[Canthaxanthin retinopathy and macular pucker--clinical picture and ultrastructural findings of macular pucker].

Canthaxanthine retinopathy is a crystalline retinopathy that follow oral ingestion of canthaxanthine-containing drugs. We describe the clinical course of a patient with canthaxanthine retinopathy and preexisting idiopathic macular pucker over a period of 2.5 years. Light microscopic investigation of the macular pucker revealed a fibrocellular membrane containing granular, birefringent material and vacuoles within the cells of the membrane resulting from canthaxanthine deposits in the epiretinal membrane. Long-term follow-up shows a slight, but significant, reduction of the retinal crystals.

Aged↗
PubMed1989

[Cellular lectin binding sites in the human retinal pigment epithelium and photoreceptors--method of lectin histochemistry and results with peroxidase marked lectins in paraffin sections].

Lectins are sugar-binding proteins or glycoproteins which bind to specifically complementary sugar residues found in cell membranes and the cytoplasm. Lectin-binding sites are determined by histochemical methods. Cellular lectin-binding sites change with morphological and functional alterations of the cell, and the determination of lectin receptors can be used to identify specific cell types in histological sections. Lectin-binding sites of the human retinal pigment epithelium (RPE) and photoreceptor cells under normal and pathological conditions have not been examined. Lectin-binding sites of normal retinal pigment epithelium and photo-receptor cells obtained from enucleated human bulbi were identified by a modified PAP method. Eight lectins differing in their sugar affinity (Con A, WGA, PNA, RCA I, SBA, UEA, DBA, LPA) were used to investigate a wide range of glycoconjugate specificity. Normal RPE have receptors for the lectins Con A, WGA, PNA and RCA I, mostly localized in the apical portions of the cells. Binding sites for these lectins are also found on photoreceptor cells, but with different binding characteristics. Photoreceptor cells bind additional lectins (UEA, SBA, DBA), which are not found on the RPE.

Humans↗
PubMed1988

[Secondary pigmented macular pucker].

The clinical course and histologic findings in a case of macular pucker with secondary pigmentation are described. The macular pucker occurred following argon laser coagulation of a peripheral hole and consisted of elements of the inner limiting membrane, an extracellular matrix of collagen fibrils, and retinal pigment epithelial cells with varying degrees of differentiation. No retinal glial cells were found. The pigment epithelial cells had presumably migrated through the peripheral retinal hole and settled on the retinal surface.

Female↗
PubMed1988

[Acute retinal necrosis].

The authors report on three patients with acute retinal necrosis who were treated with the virostatic agent Acyclovir and who underwent vitreoretinal surgery with silicone oil filling for total retinal detachment. In two eyes the retina was reattached, but useful vision was only preserved in one patient. Titers from blood and the vitreous, as well as microscopic findings in retinal biopsies, support the view that the necrosis is caused by a herpes simplex virus infection. After therapy with Acyclovir was instituted no further progression on the necrosis was observed. However, the development of retinal detachment could not be prevented. Early diagnosis and antiviral therapy are essential to improve the otherwise poor prognosis in this rare syndrome.

Acute Disease↗