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  • 1
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Eye -- Physiology. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (408 pages)
    Edition: 1st ed.
    ISBN: 9780080476094
    Series Statement: Issn Series ; v.Volume 10
    DDC: 612.842
    Language: English
    Note: Cover Page -- The Biology of the Eye -- Contents -- List of Contributors -- Preface -- Chapter 1: Why the Eye Is Round -- I. Introduction -- II. Why Are Things Round? -- A. Inanimate Objects -- B. Animate Objects -- III. Why Are Eyes Round? -- A. Optical Properties -- B. Eye Movement -- C. Hollow -- D. Phylogeny and/or Ontogeny -- E. Conclusions -- IV. Pressure -- A. Surface Tension -- B. Pressure in the Eye -- V. Aqueous Flow -- A. Balance of Inflow and Outflow -- B. Inflow -- C. Outflow -- VI. The Ciliary Body -- A. Structure -- B. Numbers in Science -- C. Reynolds Number -- D. Peclet Number -- E. Concentration Number -- F. Fluid Transport -- G. Ion Transport -- H. Active or Passive -- VII. Large Scale Aqueous Motions -- VIII. Control of Intraocular Pressure -- IX. Summary -- Acknowledgments -- References -- Chapter 2: Tears and Their Secretion -- I. Functions of the Tear Film -- II. Organization of the Tear Film -- III. Orbital Glands and Ocular Surface Epithelia that Secrete Tears -- IV. Secretion of the Lipid Layer of the Tear Film -- A. Meibomian Glands -- B. Functional Anatomy -- C. Regulation of Secretion -- D. Secretory Product -- E. Function of Lipid Layer -- V. Secretion of the Aqueous Layer of the Tear Film -- A. Main Lacrimal Gland -- B. Accessory Lacrimal Glands -- C. Corneal Epithelium -- D. Conjunctival Epithelium -- E. Function of the Aqueous Layer of the Tear Film -- VI. Secretion of the Tear Film Mucous Layer -- A. Goblet Cells -- B. Corneal and Conjunctival Stratified Squamous Cells -- C. Function of the Tear Film Mucous Layer -- VII. Role of Tear Secretion in Maintaining the Ocular Surface -- Acknowledgments -- References -- Further Reading -- Chapter 3: The Cornea -- Introduction -- I. Gross Anatomy -- II. Embryology -- III. Structure and Composition of Epithelium -- A. The Tear Film -- B. Light and Dark Cells. , C. Langerhans Cells -- D. Innervation -- E. Limbal Structure -- IV. Structure and Composition of Stroma -- V. Aspects of Physiology -- A. Function of the Epithelium as a Barrier -- VI. Epithelial Permeability and Electrophysiology -- VII. Nutrition and Metabolic Supply -- VIII. Metabolic Pathways in the Cornea -- IX. Renewal of Epithelium and Stroma -- A. Image Transmission Through the Cornea -- X. The Optical Quality of the Surface -- XI. Transparency of Corneal Tissue -- XII. Stromal Transparency -- A. Mechanical Stability of the Cornea -- XIII. Corneal Shape and Tissue Mechanics -- XIV. Stromal Swelling -- XV. Final Remarks -- References -- Further Reading -- Chapter 4: The Corneal Endothelium -- I. Introduction -- II. The Endothelium -- Corneal Transparency -- III. Cell Number Progression -- IV. Shape, Function, and Transparency of Endothelial Cells -- V. Electrolyte Transport by the Endothelium -- VI. Electrical Phenomena in and Around the Endothelium -- VII. Water Pathways -- VIII. The Mechanism Underlying Fluid Transport: Local Osmosis vs. Electroosmosis -- IX. Conclusions -- References -- Further Reading -- Chapter 5: Ciliary Body and Ciliary Epithelium -- I. Structure of the Ciliary body -- II. Blood Capillaries in the Ciliary Processes -- III. Barrier Function of the Ciliary Epithelium -- IV. Tight Junctions Between Nonpigmented Ciliary Epithelium Cells -- V. Polarized Distribution of Ion Transporters -- VI. Nonpigmented Ciliary Epithelium -- VII. Cooperation Between Pigmented and Nonpigmented Cell Layers -- VIII. Bilayer Model of Ion Transport -- IX. Divided Chamber Studies -- X. Hydrostatic Pressure and Oncotic Pressure -- XI. Volume Regulation and Water Movement -- XII. Controlling the Rate of Aqueous Humor Formation -- Acknowledgments -- References -- Further Reading -- Chapter 6: The Lens -- I. Introduction. , II. The Cellular Architecture of the Lens Epithelium -- A. Polarity: The Developmental Viewpoint -- B. The Paracellular and Transcellular Pathways -- C. The Cellular Architecture of the Lens -- D. The Cortex -- E. The Nucleus -- III. The Molecular Machinery -- A. Channels -- B. Aquaporins -- C. Connexins -- D. Potassium Conductance -- E. Sodium and Chloride Conductance -- F. Transporters -- G. The Na,K-ATPase Antiporter -- IV. The Circulating Fluxes Model -- Acknowledgments -- References -- Chapter 7: The Vitreous -- I. Introduction -- II. Gross Anatomy -- A. Ultrastructure and Biochemistry -- B. Biophysical Aspects -- C. Development -- III. Aging of the Vitreous -- References -- Further Reading -- Chapter 8: The Retina -- I. Overview of the Functional Architecture of the Retina -- II. Photoreceptor Cells -- A. Distribution of Photoreceptors -- B. Photoreceptor Electrophysiology -- C. Photopigments -- D. Activation of the Phototransduction Cascade -- E. Inactivation -- F. Photoreceptor Adaptation -- G. Regeneration of the Visual Pigments -- H. The Visual Cycle and Retinal Disease -- III. The Outer Plexiform Layer -- IV. Horizontal Cells -- V. Bipolar Cells -- A. Rod Bipolar Cells -- B. Cone Bipolar Cells -- VI. Amacrine Cells -- A. The AII Amacrine Cell -- B. The Starburst Amacrine Cells -- C. Dopaminergic Amacrine Cells -- D. DAPI-3 Amacrine Cells -- E. Nitrergic Amacrine Cells -- VII. Interplexiform Cells -- VIII. Inner Plexiform Layer -- IX. Ganglion Cells -- A. Midget Ganglion Cells -- B. Parasol Ganglion Cells -- C. Light-Sensitive Ganglion Cells -- X. Nerve Fiber Layer -- XI. Centrifugal Fibers -- XII. Neurotransmitters in the Retina -- XIII. Glial Cells -- XIV. The Retinal Extracellular Space -- XV. Retinal Circulation and Metabolism -- XVI. Development -- References -- Chapter 9: The Retinal Pigment Epithelium -- I. RPE Function. , II. Photoreceptor Outer Segment Turnover -- III. Retinoid Metabolism and the Visual Cycle -- IV. Production of Cytokines -- V. Transport -- VI. The RPE in Wound Healing and Proliferative Vitreoretinal Disease -- VII. Development -- References -- Further Reading -- Chapter 10: The Choroid and Optic Nerve Head -- I. Definition -- II. Anatomy -- III. The Choroidal Circulation -- IV. The Circulation of the Optic Disc -- V. Innervation of the Choroid -- VI. Physiology -- VII. Choroidal Blood Flow Measurements -- VIII. Development -- References -- Chapter 11: Innate and Adaptive Immunity of the Eye -- I. Introduction -- II. Innate and Adaptive Immunity -- III. The Innate Immune System and the Eye -- IV. Lactoferrin, Lysozyme, and Defensins -- V. Complement -- VI. Neutrophils, Macrophages, and NK Cells -- VII. The Adaptive Immune System -- VIII. The Spleen is Required for the Induction of ACAID -- IX. The Cellular Basis for Generation of ACAID -- X. The Molecular Basis for Induction of ACAID -- XI. Thrombospondin (TSP) and the Generation of ACAID -- XII. Peptide Hormones in AqH Exerting Immune Regulatory Activities -- XIII. Immune Regulatory Activities of Epithelial Cells Lining the Interior of the Eye -- XIV. Conclusions -- References -- Further Reading -- Chapter 12: Drug Delivery to the Eye -- I. Introduction -- II. Structure and Function of the Eye -- A. Structures of Cornea and Retina -- III. Ocular Fluid Dynamics -- A. Aqueous Humor Dynamics -- B. Fluid Flow in Vitreous Body -- IV. Factors Affecting Drug Delivery to Eye -- V. Current Modes of Administration -- A. Topical -- B. Systemic Administration -- C. Intravitreal Drug Delivery -- D. Intravitreal Implants -- E. Scleral Drug Delivery -- F. Subconjunctival -- VI. Carrier-Mediated Drug Delivery -- A. Drug Efflux Pumps in Ocular Tissues -- B. Strategy for Site-Specific Drug Delivery. , C. Prodrugs Targeted toward Transporters -- D. Transporters/Receptors in Ocular Tissues -- VII. Strategies to Improve Ocular Bioavailability By Transporter-Mediated Drug Delivery -- A. Anterior Segment -- B. Posterior Segment -- VIII. Conclusions -- Acknowledgments -- References -- Further Reading -- Chapter 13: The Sclera -- I. Anatomy -- II. Structure and Ultrastructure -- III. Biochemistry -- IV. Scleral Biomechanics -- V. Permeability of the Sclera -- VI. The Trabecular Meshwork and the Lamina Cribrosa -- VII. Embryology and Development -- VIII. Aging of the Sclera -- IX. The Role of Sclera in Disorders of the Eye -- X. Pharmaceutical Modulation of the Sclera -- References -- Index.
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  • 2
    ISSN: 1545-9985
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Artemisinins are the most important class of antimalarial drugs. They specifically inhibit PfATP6, a SERCA-type ATPase of Plasmodium falciparum. Here we show that a single amino acid in transmembrane segment 3 of SERCAs can determine susceptibility to artemisinin. An L263E replacement of a malarial ...
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 504 (1987), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] A major problem associated with studies of ascorbic acid uptake in vitro is the instability of the molecule, which is rapidly oxidized to dehydroascorbic acid and further oxidation products17. We maintained preparations of ascorbic acid at room temperature for several hours in the presence of ...
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 82 (1988), S. 107-111 
    ISSN: 1573-4919
    Keywords: water ; glucose ; channel ; pore ; osmotic permeability ; cell membrane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The possibility that the glucose transporter may serve as water channel is explored with the help of theoretical and experimental arguments. A model for a pore is drawn based on a hypothetical water channel structure, subject to the constraints that: molecules will bind to the channel wall in successive rings, forming a hollow sleeve; an integer number of molecules will exist in each ring; the pore radius will not be large enough to allow water molecules along its center, but will be large enough to allow glucose molecules across. The only configurations that meet these conditions exhibit either 5 or 6 water molecules abreast in each ring, with pore radii of 4.1 and 4.5 Å, respectively. The kinetic characteristics of such pores are estimated and found to conform to available evidence.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 140 (1994), S. 147-162 
    ISSN: 1573-4919
    Keywords: membrane protein structure ; transporters ; channels ; porins ; beta barrels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Given the sequence of transporters or channels of unknown secondary structure, it is usual to predict their putative transmembrane regions as α-helical. However, recent evidence for a facilitative glucose transporter (GLUT1_ appears inconsistent with such predictions, which has led us to propose an alternative folding model for GLUTs based on the 16-stranded antiparallel β-barrel of porins. Here we apply the same predictive algorithms we used for GLUTs to several other membrane proteins. For some of them, a high-resolution structure has been derived (β-barrels: Rhodobacter capsulatus andEscherichia coli porins; multihelical: colicin A, bacteriorhodopsin, and reaction center L chain); we use them to test the prediction procedures. The other proteins we analyze (GLUT1, CHIP28, acetylcholine receptor alpha subunit, lac permease, Na+-glucose cotransporter, shaker K+ channel, sarcoplasmic reticulum Ca2+-ATPase) are representative of classes of similar membrane proteins. As with GLUTs, we find that the predicted transmembrane segments of these proteins are consistently shorter than expected for transmembrane spanning α-helices, but are of the correct length and number for the proteins to fold instead as porin-like β-barrels.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 73 (1983), S. 95-102 
    ISSN: 1432-1424
    Keywords: dilution potential ; biionic potential ; permeability ratios ; constant field equation ; electrogenic transport ; rabbit corneal endothelium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary We have measured the dilution and biionic potentials across the isolated rabbit corneal endothelium in order to learn about the ionic selectivity of its intercellular junctions. Single-salt dilution potentials have been measured as a function of [NaCl] or [NaHCO3] gradients across the tissue. Biionic potentials were similarly measured by replacing Na+ with K+ on either side of the tissue. The potentials thus measured were fit to the constant field equation and to an approximation of it to obtain the ionic permeabilities for K+, HCO 3 − and Cl− relative to Na+. The permeability sequence obtained wasP K〉P Na〉P HCO3≅P Cl. Potentials were also measured after imposing an osmotic gradient across the preparation using sucrose. The results obtained with all these methods are consistent and suggest that this tissue is slightly more permeant to cations than anions, but that the selectivity of the intercellular junction is relatively low. From these experiments, a 30mm gradient of salt across the endothelial layer would be needed in order to explain the observed spontaneous potential difference (about 1 mV, aqueous negative) across that layer if the potential was due to the selectivity of the intercellular junctions. Such a value for the gradient is much larger than theoretical estimates of it; therefore, we favor electrogenic transport of HCO 3 − as a better explanation for the origin of the spontaneous potential difference.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1435-702X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract • Background: Anterior chamber miotic solutions are widely used in ophthalmic surgery to induce pupillary contraction. We investigated whether the acetylcholine, carbachol, or mannitol present in perfusing solutions can affect corneal endothelial function. • Methods: Freshly dissected deepithelized rabbit corneas were mounted in a Dikstein-Maurice chamber at 36 °C. The endothelial sides were perfused with six solutions: (A) 55 mM (1%) acetylcholine Cl plus modified balanced salts; (B) control for A, with acetylcholine Cl replaced by sucrose; (C) 0.55 mM (0.01%) carbachol Cl plus balanced salts; (D) balanced salts solution (BS; control for C); (E) 3% mannitol plus modified balanced salts; and (F) modified balanced salts (control for E, with mannitol replaced by sucrose). Corneal thickness was followed for 3 h in each experiment. The effect of solution E did not differ from that of solution F. • Results: The carbachol-containing solution produced a small increase in corneal thickness compared to the control solution, while the acetylcholine-containing solution resulted in corneal thickness lower than that in control preparations. • Conclusion: From these data, acetylcholine is harmless to the endothelium, and may actually stimulate its fluid pump mechanism. Carbachol, on the other hand, appears to have a detrimental effect.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1573-6903
    Keywords: Glucose transport ; blood-brain-barrier ; GLUT-1 ; GTPS ; DeVivo Disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Impaired glucose transport across brain tissue barriers causes infantile seizures, developmental delay and acquired microcephaly. Since the first report in 1991 (De Vivo et al, NEJM, 1991) 17 patients have been identified with the glucose transporter protein syndrome (GTPS). The diagnostic feature of the syndrome is an unexplained hypoglycorrhachia in the clinical setting of an infantile epileptic encephalopathy. We review our clinical experience by highlighting one illustrative case: a 6-year old girl who presented at age 2 months with infantile seizures and hypoglycorrhachia. The CSF/blood glucose ratio was 0.33. DNA sequencing identified a missense mutation in exon 7 (C1108T). Erythrocyte GLUT1 immunoreactivity was normal. The time course of 3-0-methyl-glucose (3OMG) uptake by erythrocytes of the patient was 46% that of mother and father. The apparent Km was similar in all cases (2–4 mmol/L), but the apparent Vmax in the patient was only 28% that of the parents (500 versus 1,766 fmol/s/106RBC; p 〈 0.004). In addition, a 3-month trial of oral thioctic acid also benefited the patient and increased the Vmax to 935 fmol/s/106 RBC (p 〈 3 × 10−7). Uptake of dehydroascorbic acid by erythrocytes of the patient was impaired to the same degree as that of 3OMG (Vmax was 38% of that of the mother's), which supports previous observations of GLUT1 being multifunctional. These studies confirm the molecular basis of the GTPS and the multifunctional role of GLUT1. The need for more effective treatment is compelling.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Graefe's archive for clinical and experimental ophthalmology 231 (1993), S. 359-364 
    ISSN: 1435-702X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The pathomechanisms of hypotonia after vitrectomy remain obscure. To examine the possible escape of intraocular fluid through the ocular wall, hydraulic fluid conductivity was measured across preparations of retina, pigmented epithelium, and choroid isolated from rabbit eyes 1, 3, 5, or 7 weeks after the production of laser or cryopexy lesions. The hydraulic conductivity measured in a modified Fischbarg-Bourguet chamber, was 0 in controls. At 1 and 3 weeks after transpupillary diode laser coagulation of the equatorial retina, hydraulic conductivity was measurable. However, the conductivity of these preparations returned to 0 by 5 weeks. After transscleral cryopexy, conductivity remained elevated for 7 weeks. Break-up of residual cortical vitreous with hyaluronidase increased the conductivity of “mature” cryopexy lesions to the values obtained 1 week after injury. These results suggest that there is escape of fluid across retinochoroidal lesions; fluid conductance typically decreases over time; an intact cortical gel can hinder conductance and seal the retinochoroidal leak. Thus, the risk factors for hypotonia appear to include extensive retinochoroidal lesions and the absence of a normal cortical vitreous in aphakia and/or after aggressive vitrectomy.
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