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Powerful DebuggingPowerful DebuggingIntegrated debugging is a core part of every Visual Studio product. You can step through your code and look at the values stored in variables, set watches on variables to see when values change, examine the execution path of your code, and just about anything else you need to check out under the hood.
Examine the LocalServer32 key under the CLSID for the application that you want to automate. Make sure that the LocalServer32 key points to the correct location for the application. Make sure that the path name is in a short path (DOS 8.3) format. You do not have to register a server by using a short path name. However, long path names that include embedded spaces may cause problems on some systems.To examine the path key that is stored for the server, start the Windows Registry Editor, as follows:
Note Short path names may seem correct when they are not correct. For example, both Office and Microsoft Internet Explorer (if they are installed in their default locations) have a short path that is similar to C:\PROGRA~1\MICROS~X\ (whereX is a number). This name may not initially appear to be a short path name.To determine whether the path is correct, follow these steps:
Verify that the application runs correctly.If the application runs after you click OK, the server is registered correctly. If the application does not run after you click OK, replace the value of the LocalServer32 key with the correct path. Use a short path name if you can.
Quick query re: Horizon 7 and published applications. From testing, it seems that if you try and open a file located on a UNC path (i.e.a network redirected folder), and select Open With to launch a published application, the Horizon View client opens the application, but unsuccessfully tries to pass the file through as a \\tsclient hosted file. This of course fails, but suggests that in order to open any UNC hosted files, the user must do this within the published application, rather than leveraging a simple double click. Are you aware of this limitation? Mapping the UNC path as a fixed drive letter is a workaround but surely this is more of a known and widespread issue?
Once FileMaker Key removes password protection from a FileMaker file, it displays the account names and the path to the unprotected copy of the database. Open the unprotected copy in FileMaker and type an account name displayed by FileMaker Key. Leave the password field empty and open the document.
Pathologic myopia represents a subgroup of myopia and affects up to 3%of the world population. Vision lossrelated to pathologic myopia is of great clinical significance as it can beprogressive, irreversible and affects individuals during their most productiveyears. High myopia is defined asrefractive error of at least -6.00D or an axial length of 26.5mmor more. The definition of pathologic myopia in early studies has been inconsistent and mostly revolved around a combination of refractive error and axial length, which may simply reflect a high degree of myopia. Additionally, there was no clear evidence for the cutoff values chosen. In recent years, the definition of pathologic myopia has shifted to "the presence of myopic maculopathy equal to or more severe than diffuse chorioretinal atrophy." Myopic maculopathy includes diffuse chorioretinal atrophy, patchy chorioretinal atrophy, lacquer cracks, myopic choroidal neovascularization (myopic CNV), and CNV-related macular atrophy.
Theoverall global prevalence is estimated to be 0.2-3.8% with regional variability, but varying definitions of pathologic myopia used in early epidemiological studies may limit the comparability of findings. The prevalence ofpathologic myopia-related visual impairment has been reported as 0.1%-0.5% inEuropean studies and 0.2% to 1.4% in Asian studies.
The main factors proposed for driving the development of pathologic myopia are elongation of the axial length and posterior staphyloma. Biomechanical forces related to axial elongation of the eye result in stretching of the ocular layers and progressive thinning of the retina, choroid and sclera.
Both environmental and genetic factors play a role in the development of myopia, which is further discussed in the corresponding article. Currently, the roles of known myopia-associated genetic variants have not been well established in the development of pathologic myopia. Primary risk factors for pathologic myopia include older age, greater axial length, and higher myopic spherical equivalent. Additional possiblerisk factors such as female gender, larger optic disc area and family historyof myopia have been suggested. The role of education level in the development of pathologic myopia is currently unclear.
Assessment of visual acuity, intraocular pressure, pupillaryreaction and dilated fundus exam are essential. A thorough macular examination and peripheral depressed examination are key to detecting complications related to pathologic myopia. In particular, lacquer cracks, myopic schisis, or choroidal neovascularization in the macular area and holes or tears in the periphery of the retina. Assessment of visual fields and Amsler grid testing may be beneficial.
Fuchs spots (also referred to as Forster-Fuchs spots) is an area of RPE hyperplasia suspected to be the response of the RPE to previous regressed CNV. Myopic CNV is the most common cause of vision loss in high myopia and has been reported in 5% to 10% of cases of pathologic myopia.
Staphyloma development, characterized by outpouching of scleral tissue typically involving the optic disc or macula, is a common occurrence, estimated in 35% of eyes with high myopia. This can be difficult to appreciate with bio-microscopy but is evident on Optical Coherence Tomography (OCT) or B scan ophthalmologic ultrasound. Staphylomata are commonly associated with lacquer cracks, RPE attenuation, epiretinal membrane and macular or foveal schisis.
Given the lack of a centralized definition and terminology for pathologic myopia, an international group of experts in high myopia developed a simplified, systematic classification based on a meta-analysis of pathologic myopia (META-PM). Myopic maculopathy was classified into five different categories based on atrophic change.
Recently, it has been noted that many patients with macular changes from pathologic myopia are not sufficiently represented by an atrophy-centered classification system. A newly proposed ATN classification system for myopic maculopathy includes atrophic (A), tractional (T) and neovascular (N) components.
Fluorescein Angiography is useful for evaluating myopic patients for development of CNV. Early images may show transmission defects in patches or areas of RPE atrophy in the macula and/or around the optic disc. Angiography can identify lacquer cracks in early and transit phases by linear distribution of transmission defect. In pathologic myopia, the development of CNV tends to be smaller and less exudative compared to CNV seen in AMD. Myopic CNV may appear as a focus of hyperfluourescence with a rim of hypoflourescence corresponding to hyperpigmentation at the border of the lesion. Any associated hemorrhage will result in blocked fluorescence. Leakage is seen in late images with or without blurring of the pigmented rim. The leakage present with myopic CNV is more subtle than with CNV related to AMD, and it is common that the CNV leakage may be partially or completely obscured by overlying subretinal hemorrhage.
Indocyanine green angiography (ICG) may be more sensitive for detecting CNV as the vascular leakage in pathologic myopia is typically less prominentthan for AMD-related pathology and can be more easily missed on fluorescein angiography. Despitesubtler findings on imaging studies with myopic CNV compared to those with AMD-related CNV, patients often note that these smaller lesions alter the visual perception significantly.
Recently, swept source and ultra-widefield (UWF) OCT have been implemented to evaluate various tissues affected by pathologic myopia. Swept-source OCT uses a wavelength-sweeping laser as the light source and has less sensitivity roll-off with tissue depth than conventional spectral-domain OCT. Using a longer central wavelength, penetration into deeper tissues and enhanced evaluation of the choroid and sclera are potentially possible. UWF-OCT is similar to swept source OCT but uses multiple scan lines to generate scan maps, which has been utilized to visualize posterior staphylomas, myopic macular retinoschisis, and dome-shaped macula. The data provided by these newer imaging techniques may help in understanding the pathophysiology of pathologic myopia as well as new therapeutic approaches.
There is no topical, local or systemic pharmacotherapy or surgery that is known to alter effectively the increase in axial length and thinning that occurs in the sclera, choroid, and retina of eyes with pathologic myopia. Animal and in-vitro studies have shown some promise in scleral collagen crosslinking to arrest the progression of pathologic myopia but further research is needed to elucidate these effects. There are, however, treatments available for CNV, a major complication of pathologic myopia.
The first widely adopted therapy for CNV in pathologic myopia wasphotothermal laser ablation of the new vessels. This treatment was complicated by a high rate of recurrence and thetendency of the photocoagulation scars to expand over time, increasing the risk of central vision loss as the border of the laser scar encroached or expanded into the fovea. 2b1af7f3a8