1: Can J Ophthalmol. 2008 Jun 25;43(3):8 [Epub ahead of print] 

Unexpected control of a patient\'s refractory epilepsy when treating glaucoma
with acetazolamide.

Lyall DA.

PMID: 18443620 [PubMed - as supplied by publisher]

2: Can J Ophthalmol. 2008 Jun 25;43(3):7-8 [Epub ahead of print] 

Ultrasound biomicroscopy for membranous congenital cataract.

Sugimoto M, Kuze M, Uji Y.

PMID: 18443619 [PubMed - as supplied by publisher]

3: Can J Ophthalmol. 2008 Jun 25;43(3):6-7 [Epub ahead of print] 

Idiopathic central retinal artery occlusion in a 6-year-old.

Heckler LV, Lederer DE, Alwadani F, Koenekoop RK.

PMID: 18443618 [PubMed - as supplied by publisher]

4: Can J Ophthalmol. 2008 Jun 25;43(3):4-5 [Epub ahead of print] 

Pars plana vitrectomy and internal limiting membrane peeling in an eye with
foveal lipid deposition after focal laser surgery for diabetic macular edema.

Etter J, Fekrat S.

PMID: 18443617 [PubMed - as supplied by publisher]

5: Can J Ophthalmol. 2008 Jun 25;43(3):3 [Epub ahead of print] 

Retained perfluoron postvitreoretinal surgery causing secondary open-angle
glaucoma.

Toffoli D, Arbour JD, Harasymowycz P.

PMID: 18443616 [PubMed - as supplied by publisher]

6: Can J Ophthalmol. 2008 Jun 25;43(3):3-4 [Epub ahead of print] 

Central retinal vein occlusion in an AIDS patient with presumed Pneumocystis
carinii pneumonia.

Yeh S, Lam HY, Albini TA, Holz ER.

PMID: 18443615 [PubMed - as supplied by publisher]

7: Can J Ophthalmol. 2008 Jun 25;43(3):2 [Epub ahead of print] 

Closed-angle glaucoma after topiramate therapy for migraine in a patient with
undiagnosed pseudotumor cerebri.

Giuliari GP, Banda RM, Vann VR, Gonzalez VH, McMillin RB.

PMID: 18443614 [PubMed - as supplied by publisher]

8: Can J Ophthalmol. 2008 Jun 25;43(3):1-4 [Epub ahead of print] 

Nitric oxide and cyclic guanosine monophosphate signaling in the eye.

Murad F.

This brief review describes the components and pathways utilized in nitric oxide
(NO) and cyclic guanosine monophosphate (cGMP) signaling. Since the discovery of
the effects of NO and cGMP on smooth muscle relaxation about 30 years ago, the
field has expanded in many directions such that many, but not all, biochemical
and biological effects seem to be regulated by these unique signaling molecules.
While many of the effects of NO are due to activation of soluble guanylyl
cyclase (sGC) that can be considered the receptor for NO, cGMP, in turn, can
activate a cGMP-dependent protein kinase (PKG) to phosphorylate an array of
proteins. Some of the effects of cGMP can be independent of PKG and are due to
effects on ion channels or cyclic nucleotide phosphodiesterases. Also, some of
the effects of NO can be independent of sGC activation. The isoenzymes and
macromolecules that participate in these signaling pathways can serve as
molecular targets to identify compounds that increase or decrease their
activation and thus serve as chemical leads for discovering novel drugs for a
variety of diseases. Some examples are given. However, with about 90,000
publications in the field since our first reports in 1977, this brief review can
only give the readers a sample of the excitement and opportunities we have found
in this cell signaling system.

PMID: 18443613 [PubMed - as supplied by publisher]

9: Can J Ophthalmol. 2008 Jun 25;43(3):1-7 [Epub ahead of print] 

Ocular blood flow in diabetes and age-related macular degeneration.

Pemp B, Schmetterer L.

ABSTRACT * RESUMEThe 2 leading causes of blindness in adults in the
industrialized nations, diabetic retinopathy and age-related macular
degeneration, have been investigated thoroughly with respect to their
pathogenesis. In recent years, it has been discovered that dysfunctional ocular
microcirculation appears to play a part in the development of both diseases. In
diabetic retinopathy, it has been shown that the disease is associated with
early retinal vascular dysregulation. In the later states of the disease,
retinal tissue hypoxia is a major trigger of sight-threatening
neovascularization. In age-related macular degeneration, there is increasing
evidence that reduced blood flow in the choroid is associated with the
development and progression of the disease. Knowledge of the pathophysiological
vascular states underlying these diseases is essential for the assessment and
development of future therapies.

PMID: 18443612 [PubMed - as supplied by publisher]

10: Can J Ophthalmol. 2008 Jun 25;43(3):1-5 [Epub ahead of print] 

Vascular anatomy of the optic nerve head.

Mackenzie PJ, Cioffi GA.

ABSTRACT * RESUMEAlthough intraocular pressure remains the main modifiable risk
factor for open-angle glaucoma, other factors such as vascular perfusion likely
play a significant role. It is not clear how mechanical deformation, axonal
damage, glial responses, and ischemia interact to lead to the tissue remodeling
seen clinically as glaucomatous cupping. To understand the potential role of
vascular risk factors in glaucoma, it is important to understand the vascular
anatomy of the optic nerve head (ONH). The focus of this review is to provide a
description of the vascular anatomy of the ONH and to desccribe recent work in
the central nervous system that suggests that astrocytes play a key role in
vascular regulation. Finally, the evidence for vascular regulation in the ONH
and retina is reviewed.

PMID: 18443611 [PubMed - as supplied by publisher]

11: Can J Ophthalmol. 2008 Jun 25;43(3):1-6 [Epub ahead of print] 

What can we learn from the disc appearance about the risk factors in glaucoma?

Drance SM.

The author has been involved in 3 studies, the multicentre collaborative
normal-tension glaucoma study, a study of 4 phenotypes of glaucomatous disc
appearances and their associations, and a study reporting on biostatistical
evidence for 2 distinct chronic open-angle glaucoma populations. These studies
have some common threads whose clinical implications are discussed.

PMID: 18443610 [PubMed - as supplied by publisher]

12: Can J Ophthalmol. 2008 Jun 25;43(3):1-9 [Epub ahead of print] 

Measuring and interpreting ocular blood flow and metabolism in glaucoma.

Harris A, Kagemann L, Ehrlich R, Rospigliosi C, Moore D, Siesky B.

There is a growing body of evidence suggesting that vascular dysfunction is
related to several prominent ophthalmic diseases, including glaucoma. The vast
majority of studies providing data on ocular circulation and disease
pathophysiology use a relatively small number of complicated ocular blood flow
imaging techniques. Although these imaging technologies are not commonly used in
clinical settings, understanding the medical literature characterizing ocular
blood flow requires familiarity with their methodology and function. This review
highlights the imaging technologies most commonly used to investigate ocular
blood flow, including color Doppler imaging, confocal scanning laser
ophthalmoscopic angiography with fluorescein and indocyanine green dye, Canon
laser blood flowmetry, scanning laser Doppler flowmetry, and retinal
photographic oximetry. Each imaging technique\'s ability to define vascular
function and reveal pathology is discussed as are limitations inherent to each
technology. The ultimate goal of this review is to provide the physician with a
clinically relevant foundation for differentiating the various ocular blood flow
outcome measures often presented in the literature and determine how they are
related to ocular health and disease.

PMID: 18443609 [PubMed - as supplied by publisher]

13: Can J Ophthalmol. 2008 Jun 25;43(3):1-4 [Epub ahead of print] 

Influencing ocular blood flow in glaucoma patients: the cardiovascular system
and healthy lifestyle choices.

Tsai JC.

The cardiovascular system and lifestyle choices play important roles in
influencing ocular blood flow regulation in patients with glaucoma. This
includes the presence of vascular risk factors, abnormal autoregulatory
responses, tissue oxygenation, and mitochondrial oxidative stress. Based on this
comprehensive review, novel therapeutic approaches may be considered in selected
patients for preventing and (or) delaying the progression of glaucoma.

PMID: 18443608 [PubMed - as supplied by publisher]

14: Can J Ophthalmol. 2008 Jun 25;43(3):1-3 [Epub ahead of print] 

Femtosecond laser astigmatic keratotomy for postkeratoplasty astigmatism.

Harissi-Dagher M, Azar DT.

Case report: Two eyes of 2 patients with high astigmatism following penetrating
keratoplasty were treated with femtosecond laser-assisted paired arcuate
keratotomies in the donor cornea. Outcome measures included best-corrected
visual acuity, refraction, keratometry, and topographic findings. The
preoperative cylinder was 8.5 diopters (D) in the first case and 7.0 D in the
second case. Respectively, the postoperative cylinder improved to 4.9 D after a
follow-up of 8 months and to 4.3 D after a follow-up of 7 months. Best-corrected
visual acuity improved from 20/100 to 20/30 in the first case and from 20/200 to
20/60 in the second case. No complications were encountered; no
microperforations were observed, and neither graft rejection nor failure
occurred.Comments: The results of astigmatic keratotomy performed with
femtosecond laser were reliable and predictable. Femtosecond astigmatic
keratotomy may prove to be a safe procedure with satisfactory results.

PMID: 18443607 [PubMed - as supplied by publisher]

15: Can J Ophthalmol. 2008 Jun 25;43(3):1-3 [Epub ahead of print] 

Tubular aggregate myopathy associated with retinal degeneration.

Parulekar MV, Halliday W, Brent M, Kong K, Wong AM.

Case report: We report a case of congenital tubular aggregate myopathy
associated with retinal degeneration.Comments: Bilateral, asymmetric retinal
degeneration developed in a 37-year-old woman with a history of congenital
tubular aggregate myopathy. The major pathological feature was the presence of
tubular aggregates, believed to arise from the sarcoplasmic reticulum, which are
present in skeletal muscles only. The abnormal functioning of the smooth muscles
of the pupillary dilator, together with retinal degeneration in our patient,
suggests that tubular aggregates may represent a more generalized disequilibrium
of intracellular calcium homeostasis that may not be confined to skeletal
muscles.

PMID: 18443606 [PubMed - as supplied by publisher]

16: Can J Ophthalmol. 2008 Jun 25;43(3):1 [Epub ahead of print] 

Elevated levels of transforming growth factor beta and prostaglandin E2 in
aqueous humor from patients undergoing filtration surgery for glaucoma.

Freedman J, Goddard D.

PMID: 18443605 [PubMed - as supplied by publisher]

17: Can J Ophthalmol. 2008 Jun 25;43(3):1 [Epub ahead of print] 

Corrigendum: Ring melanoma of the ciliary body: clinical and ultrasound
biomicroscopic characteristics.

Vasquez LM, Pavlin CJ, McGowan H, Yucel Y, Simpson ER.

PMID: 18443604 [PubMed - as supplied by publisher]

18: Can J Ophthalmol. 2008 Jun 25;43(3):1 [Epub ahead of print] 

F.Y.Eye.

McIlraith I.

PMID: 18443603 [PubMed - as supplied by publisher]