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SYMPOSIUM - UVEITIS UPDATE
Differential diagnosis of retinal vasculitis
Ahmed M Abu El-Asrar1, Carl P Herbort2, Khalid F Tabbara3
1 Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia
2 Inflammatory and Retinal Eye Diseases, Center for Ophthalmic Specialized Care and University of Lausanne, Lausanne, Switzerland
3 The Eye Center and The Eye Foundation for Research in Ophthalmology, Riyadh, Saudi Arabia
Date of Web Publication 19-Dec-2009
Ahmed M Abu El-Asrar
Department of OphthalmologyKing Abdulaziz University Hospital Airport Road, P.O. Box 245, Riyadh 11411
Retinal vaculitis is a sight-threatening inflammatory eye condition that involves the retinal vessels. Detection of retinal vasculitis is made clinically, and confirmed with the help of fundus fluorescein angiography. Active vascular disease is characterized by exudates around retinal vessels resulting in white sheathing or cuffing of the affected vessels. In this review, a practical approach to the diagnosis of retinal vasculitis is discussed based on ophthalmoscopic and fundus fluorescein angiographic findings.
Keywords: Fluorescein Angiography, Retina, Vasculitis
Abu El-Asrar AM, Herbort CP, Tabbara KF. Differential diagnosis of retinal vasculitis. Middle East Afr J Ophthalmol 2009;16:202-18
Abu El-Asrar AM, Herbort CP, Tabbara KF. Differential diagnosis of retinal vasculitis. Middle East Afr J Ophthalmol [serial online] 2009 [cited 2020 Jan 21];16:202-18. Available from: http://www.meajo.org/text.asp?2009/16/4/202/58423
Retinal vasculitis is a sight-threatening inflammatory eye condition that involves the retinal vessels. It may occur as an isolated idiopathic condition, as a complication of infective or neoplastic disorders, or in association with systemic inflammatory disease [1] [Table 1].
Detection of retinal vasculitis is made clinically, and confirmed with the help of fundus fluorescein angiography. Active vascular disease is characterized by exudates around retinal vessels resulting in white sheathing or cuffing of the affected vessels, which may be segmental (skip lesions) or confluent [Figure 1].
Although retinal arterioles or branch retinal arteries may be involved in secondary systemic vasculitides such as systemic lupus erythematosus (SLE), as well as primary systemic vasculitides such as Wegener's granulomatosus, polyarteritis nodosa, Churg-Strauss syndrome or cryoglobulinemia, [2] this usually leads to occlusion by microthrombosis, and intraocular inflammation is often not a feature of these diseases. [3],[4] Therefore, this type of occlusive vasculopathy should be recognized and distinguished from other conditions characterized by active vascular sheathing or cuffing with perivascular inflammatory infiltrate.
Retinal vasculitis results in leakage leading to retinal swelling, exudation, and macular edema. Cystoid macular edema is a significant contributing factor for poor vision in retinal vasculitis. Cystoid macular edema, when adequately treated with immunosuppressive therapy, is associated with a good prognosis. [5] Occlusive retinal vasculitis affecting the retinal arterioles may cause cotton-wool spots representing microinfarcts of the retina. Central retinal artery and branch retinal artery occlusions are also reported in patients with retinal vasculitis. [6],[7],[8],[9],[10],[11],[12] Occlusive periphlebitis can cause retinal edema, intraretinal hemorrhages, and hemorrhagic infarction of the retina. Poor visual outcome in some patients with retinal vasculitis, despite adequate therapy, may be explained by the presence of macular ischemia. [5],[13] Late changes secondary to vascular occlusion and remodeling include telangiectasis, microaneurysms, and ischemia-induced neovascularization, with sequelae such as recurrent vitreous hemorrhage, traction retinal detachment, rubeosis iridis, and neovascular glaucoma that can lead to functional loss of the eye. [6],[14],[15],[16],[17],[18],[19],[20] Inflammatory branch retinal vein occlusions are strongly associated with Behçet's disease and might contribute to visual loss. [21],[22],[23]
Fundus Fluorescein Angiography
Characteristic features seen with fluorescein angiography in active vasculitis include leakage of dye due to breakdown of the inner blood-retinal barrier, and staining of the blood vessel wall with fluorescein. Such leakage may be focal as seen in sarcoidosis or multiple sclerosis [Figure 2] or more diffuse, as seen in Behçet's disease and retinal vasculitis associated with tuberculoprotein hypersensitivity (Eales' disease) [Figure 3] and [Figure 4]. Diffuse capillary leakage is also a common finding in many conditions such as Behçet's disease and birdshot chorioretinopathy [Figure 3]. Fluorescein angiography is a more sensitive technique and will frequently show that the vasculitis is more extensive than the clinical examination suggests [Figure 4]. Fluorescein angiography is very useful to delineate areas of capillary nonperfusion, and neovascularization secondary to retinal ischemia [Figure 5]. It is also very valuable to diagnose the presence of inflammatory branch retinal vein occlusion [Figure 6].
The ability to identify retinal vasculitis as ischemic by fluorescein angiography has important implications for management and is discussed later. Other angiographic findings include cystoid macular edema [Figure 7] and optic disc leakage [Figure 8]. Leakage of dye from the optic nerve head arises from dilated capillaries, which may be due to either to primary infiltration as in sarcoidosis [24] or secondary vascular changes induced by intraocular inflammation.
In this review, we discuss a practical approach to the diagnosis of retinal vasculitis based on ophthalmoscopic and fluorescein angiographic findings [Table 2].
Identification of retinal vessels involved
Retinal vasculitis affecting predominantly the veins (phlebitis) has been described in association with Behçet's disease, tuberculosis, sarcoidosis, multiple sclerosis, pars planitis, retinal vasculitis associated with tuberculoprotein hypersensitivity (Eales' disease), human immunodeficiency virus infection (HIV) [Figure 1],[Figure 2],[Figure 4],[Figure 6]. Retinal arteritis is more commonly seen in acute retinal necrosis [Figure 9], idiopathic retinal vasculitis, aneurysms, and neuroretinitis (IRVAN) [Figure 10] and systemic vasculitides such as SLE, polyarteritis nodosa, and Wegener's granulomatosis, Churg-Strauss syndrome and cryoglobulinemia. [1]
Cotton-wool spots
Cotton-wool spots representing microinfarcts of the retina due to precapillary retinal arteriolar occlusion are most often found in association with systemic vasculitides such as SLE, plyarteritis nodosa, Wegener's granulomatosis, Churg-Strauss syndrome, and cryoglobulinemia [Figure 11].
Retinal vascular lesions are the most common ophthalmic manifestations of SLE and are due to arterial occlusion. Retinopathy generally consists of cotton-wool spots with or without retinal hemorrhages and may occur in the absence of hypertension [Figure 11]. By contrast, a less common but more severe retinal vascular occlusive disease characterized by diffuse arteriolar occlusion with extensive capillary non-perfusion has been described. [18] A more focal vascular disease, including retinal artery or vein occlusion may occur. Patients with SLE and raised antiphospholipid antibodies have a higher risk of developing occlusive retinal vascular disease. [25] In addition, a patient with severe SLE-associated frosted branch periphlebitis and exudative maculopathy was reported. [26] Exacerbations of disease activity might manifest only in the retina as a retinal vascular occlusion [7] [Figure 12]. Retinal vascular involvement in polyarteritis nodosa is primarily arterial and gives rise to retinal vasculitis, cotton-wool spots, edema, hemorrhage, and central retinal artery occlusion. The disease may also involve choroidal vessels. [9],[12],[27],[28] Curi et al. [29] reported aggressive retinal vasculitis involving both arteries and veins in a patient with polyarteritis nodosa.
Susac syndrome is a rare disease of unknown pathogenesis. It is also caused by microangiopathy affecting the arterioles of the brain, retina, and cochlea, giving the classic triad of encephalopathy, branch retinal arterial occlusions, and sensorineural hearing loss. The underlying process is believed to be a small vessel vasculitis causing microinfarcts of the retina, brain, and cochlea. Susac syndrome usually occurs in young women but can affect men. In those cases in which a brain biopsy was performed, histopathologic examination results showed microinfarcts, perivascular inflammatory infiltrates of small vessels consistent with an active small vessel angiitis. Magnetic resonance imaging of the brain often shows lesions suggestive of multiple sclerosis. Fluorescein angiography shows focal nonperfusion of retinal arterioles and arteriolar wall hyperfluorescence. [30],[31],[32],[33]
Intraretinal infiltrates
Intraretinal infiltrates are characteristic of infectious processes, but in the absence of these, they are pathognomonic of Behçet's disease [Figure 3],[Figure 7] and [Figure 8]. These transient white patches of retinitis, often with small adjacent hemorrhages, are almost always seen in patients with active posterior Behçet's uveitis. Typically, they are silent on fundus fluorescein angiography.
Necrotizing retinitis
Retinal vasculitis may be associated with necrotizing retinitis due to ocular toxoplasmosis, acute retinal necrosis, cytomegalovirus (CMV) retinitis, and rarely human T cell lymphoma virus type 1 (HTLV-1) associated uveitis. The hallmark of ocular toxoplasmosis is focal necrotizing retinitis, ultimately resulting in characteristic atrophic scars. Reactivation is frequently situated adjacent to an old atrophic scar with hyper pigmentation along the borders, indicating an old infection (satellite formation). Anterior uveitis, which may be granulomatous, and a secondary rise in intraocular pressure may also be noted. There may be an associated retinal vasculitis, which may be either near to or distant from the focus of active retinochoroiditis [Figure 13]. The arteries are often affected. Kyrieleis arterialitas refers to accumulation of periarterial exudates, which can occur either in the vicinity of the acute retinitis or elsewhere in the retina. [34] In rare cases, the vasculitis may be occlusive, resulting in retinal infarction and consequent visual field defects. A case of frosted branch angiitis secondary to toxoplasmic retinochoroiditis was reported. [35] In addition, Diaz-Valle et al., [36] reported a case of acute frosted branch angiitis without necrotizing chorioretinitis associated with acquired toxoplasmosis. The patient developed late peripheral retinochoroidal scar. Holland et al. [37] reported the development of intraocular inflammatory reactions including vitritis, iridocyclitis, and retinal vasculitis without necrotizing retinal lesions in individuals with acquired systemic toxoplasmosis. Foci of retinitis or inactive retinochoroidal scars were seen in the same eyes during follow-up examinations suggesting that the initial inflammation may be caused by the presence of parasite in retinal tissue. These data strongly suggest that acquired systemic toxoplasmosis infection should be considered in the differential diagnosis of patients with retinal vasculitis, especially in the presence of constitutional symptoms suggesting systemic toxoplasmosis. More severe or atypical ocular presentations occur in immunocompromised patients.
Acute retinal necrosis is caused by viruses of the herpes group, mainly varicella zoster, herpes simplex types 1 and 2, and rarely, cytomegalovirus. [38] The prominent features of acute retinal necrosis include peripheral necrotizing retinitis, retinal arteritis, and a prominent inflammatory reaction in the vitreous and anterior chamber [Figure 9]. Optic neuritis occurs in many affected eyes, and complicated rhegmatogenous retinal detachments are often encountered as a late sequela of the condition. [39] The disease can progress rapidly with vision loss due to macular involvement, retinal detachment, or optic neuropathy. Vasculitis is predominantly affecting peripheral arteries with closure probably at the origin of the peripheral necrosis and is suspected to be due to antigen-antibody complexes [Figure 9].
In majority of the cases, cytomegalovirus (CMV) retinitis is a manifestation of acquired immunodeficiency syndrome (AIDS), with CMV retinitis being the most common ocular infection in these patients. The classic description of CMV retinitis is one of scattered yellow-white areas of necrotizing retinitis with variable degrees of hemorrhage and mild vitreous inflammation ("cottage cheese with catsup" or "pizza pie" retinopathy). The pathway of expanding lesions can be predicted by the appearance of venous sheathing or white dots distal to the leading edge. CMV retinitis is often accompanied by varying amounts of retinal vasculitis consisting primarily of perivenous sheathing. [40],[41] Frosted branch angiitis was described in patients with AIDS associated with small patches of CMV retinitis. [42],[43] Perivasculitis of the peripheral vessels involving veins more often than arteries was described in patients with AIDS. CMV retinitis was not seen in these patients. The vasculitis was thought to be a noninfectious retinopathy associated with AIDS. [44],[45] Fine et al., [46] reported a case of HIV-infected child with frosted branch angiitis without CMV retinitis that was refractory to specific anti-cytomegalovirus therapy. The angiitis only improved after subsequent treatment with systemic corticosteroids suggesting that the frosted branch angiitis in this patient was not attributed to CMV.
HTLV-1 infection is endemic in Japan, the Caribbean islands, and parts of Central Africa and South America. The major target cell of HTLV-1 is the CD4[1] t -cell. HTLV-1 infection is the established cause of adult t-cell leukemia/lymphoma (ATL), an aggressive malignancy of CD4[1] lymphocytes; HTLV-1 associated myelopathy (HAM)/tropical spastic paraparesis (TSP), a demyelinating inflammatory disease of the spinal cord; and HTLV-1 uveitis (HU), defined as uveitis of undetermined etiology in an HTLV-1 carrier. Clinically, HU has been described as an acute granulomatous or nongranulomatous uveal reactions that were accompanied by vitritris and retinal vasculitis. The ocular disease was considered benign, resolving over weeks in response to corticosteroid treatment, with low incidence of complications and good visual prognosis. Gray-white, granular deposits scattered on the retinal vessels in the posterior pole were noted. Similar materials were also found to deposit on the vitreoretinal interface of the foveolar areas. In addition, retinal vasculitis with sheathing of retinal veins in the periphery was described in patients with HTLV-1-associated myelopathy. [47],[48],[49] Nakao and Ohba [50] reported three HTLV-1-positive Japanese teenagers presenting with extensive retinal periphlebitis resembling frosted branch angiitis. The retinal vascular disease responded poorly to systemic corticosteroids, had a smoldering course, and eventually resulted in diffuse chorioretinal degeneration. Levy-Clarke et al., [51] reported a patient with ATL presenting as a bilateral retinal vasculitis associated with necrotizing retinitis.
Aneurysmal dilatations of the retinal and optic nerve head arterioles
IRVAN is a rare clinical entity characterized by bilateral retinal arteritis, numerous aneurysmal dilatations of the retinal and optic nerve head arterioles, peripheral retinal vascular occlusion, neuroretinitis, and uveitis [Figure 10]. This syndrome typically affects young healthy individuals, has a female predominance, and is not associated with any systemic abnormalities. Visual loss is due to exudative maculopathy, and neovascular sequelae of retinal ischemia. [52],[53],[54] Recently, we reported a patient who presented with features typical of IRVAN in whom medical evaluation disclosed allergic fungal sinusitis. [55] Several reports described resolution of aneurysmal dilatations of the retinal arterioles in patients with IRVAN treated with systemic steroids and peripheral retinal photocoagulation [Figure 10]. [55],[56],[57],[58] Recently, Samuel et al. [54] recommended early panretinal laser photocoagulation when angiographic evidence of widespread retinal nonperfusion is present, and before (or shortly after) the development of neovascularization. Arterial macroaneurysms, occurring in elderly female patients with sarcoidosis associated with peripheral multifocal chorioretinitis have been described. These patients had severe cardiovascular disease. [59],[60],[61]
Frosted branch angiitis
Frosted branch angiitis (first described in 1976 by Ito et al.), [62] occurs in young, healthy individuals who typically have acute bilateral (but sometimes unilateral) visual loss, associated with anterior and posterior segment inflammation. The retinal findings include swelling of the retina and severe sheathing of the retinal venules, creating the appearance of frosted tree branches. Additional findings include intraretinal hemorrhages, hard exudates, and serous exudative detachments of the macula and periphery [Figure 14]. Fluorescein angiography demonstrates leakage of dye from the vessels, but no evidence of decreased blood flow or occlusion. The disease usually responds rapidly to systemic corticosteroids with rapid resolution of the vascular sheathing. The visual prognosis is usually good and there is no recurrence in most patients. The term "acute frosted retinal periphlebitis" was suggested to describe the condition by Kleiner et al. [63] Kleiner [64] classified the patients with the appearance of frosted branch angiitis into three subgroups-First are patients with lymphoma or leukemia [64] whose disease is due to infiltration with malignant cells (frosted branch-like appearance) [Figure 15] Second is the group of patients who have associated viral infections or autoimmune disease. Frosted branch angiitis was reported in patients with systemic lupus erythematosus, [26] Crohn's disease, [65] toxoplasmic retinochoroiditis, [35],[36] human T cell lymphoma virus type 1 infection, [50] AIDS associated with small patches of retinitis, [42],[43] HIV without CMV retinitis, [46] herpes simplex virus infection, [66] and Epstein-Barr virus infection. [67] In these patients, frosted branch angiitis is a clinical sign, possibly of immune complex deposition (secondary frosted branch angiitis). Finally, there is the group of otherwise healthy young patients described initially (acute idiopathic angiitis). It is likely that the frosted branch angiitis that developed in these patients represents an immune reaction to a number of different stimuli. [68] A case of frosted branch angiitis complicated by bilateral retinal and optic nerve head neovascularization secondary to severe peripheral retinal ischemia was reported. [69] In addition, we reported the unusual association between severe retinal periphlebitis resembling frosted branch angiitis and nonperfused central retinal vein occlusion. [20]
Retinal ischemia
Patients with ischemic retinal vasculitis represent a major management problem. It is important to identify the presence of retinal ischemia in patients with retinal vasculitis because panretinal laser photocoagulation should be considered when angiographic evidence of widespread retinal nonperfusion is present, and before (or shortly after) the development of neovascularization.
Ischemic retinal vasculitis is frequently seen secondary to tuberculosis and retinal vasculitis associated with tuberculoprotein hypersensitivity (Eales' disease) which is typically an obliterative periphlebitis affecting the retina in multiple quadrants, starting at or anterior to the equator and progressing posteriorly. Occasionally, it can begin close to the optic nerve head, mimicking a vein occlusion. Ophthalmoscopic findings vary and depend on the stage of the disease. Initially, it presents as active retinal periphlebitis with thick exudates around the retinal veins associated with retinal hemorrhages, and hemorrhagic infarctions of the retina [Figure 1],[Figure 4],[Figure 16],[Figure 17],[Figure 18]. Healed periphlebitis results in sclerosed white venules, and abnormal vascular anastomosis [Figure 19]. The periphlebitis may cause nonperfusion of a substantial portion of the retina that may lead to proliferative vascular retinopathy with sequelae such as recurrent vitreous hemorrhage, traction retinal detachment, rubeosis iridis, and neovascular glaucoma [1],[49],[70],[71],[72],[73] [Figure 5],[Figure 17],[Figure 18],[Figure 19],[Figure 20],[Figure 21],[Figure 22]. The management of tuberculous retinal vasculitis or retinal vasculitis associated with tuberculoprotein hypersensitivity (Eales' disease) requires the use of systemic steroids and appropriate antituberculous therapy. New vessel formation associated with retinal vasculitis and capillary closure responds to panretinal photocoagulation [Figure 21]. Early vitrectomy and adequate endolaser photocoagulation should be considered in eyes with non-resolving vitreous hemorrhage associated with active fibrovascular proliferation [14] [Figure 22].
Ischemic retinal vasculitis may also be secondary to Behçet's disease and multiple sclerosis. The diagnosis is made using criteria proposed by the International Study Group for Behçet's disease in 1990. [74] The criteria require recurrent oral ulceration as an essential symptom plus any two or more symptoms of genital ulceration, eye lesions, skin lesions and a positive pathergy test to make a diagnosis of Behçet's disease. Inflammatory eye disease generally appears later than the oral ulceration and develops in about 70% of patients in Japan. The ocular manifestations of Behçet's disease typically include recurrent attacks of anterior uveitis, with or without hypopyon, cellular infiltration and opacification of the vitreous, retinal vasculitis [Figure 6] and [Figure 23], retinal infiltrates [Figure 3],[Figure 7] and [Figure 8] and hemorrhages, cystoid macular edema [Figure 8] and disc hyperemia. Retinal vasculitis and recurrent vasoocclusive episodes are the major causes of visual morbidity. In addition, inflammatory retinal vein occlusions are strongly associated with Behçet's disease [21],[22],[23],[75]] [Figure 6] and [Figure 23]. Fluorescein angiography may show diffuse retinal vascular leakage, late staining of the vasculature, leakage from the disc, macular edema, areas of capillary dropout, and neovascularization [Figure 3],[Figure 6],[Figure 7],[Figure 8] and [Figure 23].
Various ocular inflammatory changes have been described in patients with multiple sclerosis and may be the presenting sign of the disease. They include nongranulomatous and granulomatous iridocyclitis, intermediate uveitis, retinitis, periphlebitis [Figure 2] and optic neuritis. [15],[16],[17],[76],[77],[78],[79],[80],[81],[82],[83] Retinal periphlebitis has been described as a common manifestation of multiple sclerosis. It has been observed with an average frequency of 11.5% in more than 3000 published cases of MS examined for sheathing. [79] In an autopsy series of 93 eyes from patients with definite multiple sclerosis, segmental lympho-plasmacytic perivenous infiltrates were found in seven eyes and focal lymphocytic or granulomatous retinitis was present in five eyes. [76] The foci of granulomatous retinal inflammatory cells were noted in the inner retina and overlying vitreous and corresponded to white plaques visible on the inner retinal surface on gross examination. [76] Round dot-like opacities, the diameter of a medium-sized vein, visible in the vitreous immediately overlying the retina were originally described by Rucker. [81] These have come to be known as "Rucker bodies." It has been demonstrated that demyelinative plaques in the brain typically encircle a venule and that in an active lesion perivenular infiltrates are present. [82] These changes appear similar to the periphlebitis occurring in the retina. The periphlebitis can progress to occlusive peripheral vasculitis, which results in peripheral retinal neovascularization and tractional or rhegmatogenous retinal detachments or both. Peripheral scatter photocoagulation and vitrectomy may be required to stabilize the proliferative retinopathy. [15],[16],[17],[83]
Retinal periphlebitis associated with sarcoidosis is usually nonocclusive, sometimes subclinical and only visible on fluorescein angiography, associated with typical segmental cuffing or more extensive sheathing and perivenous exudates, which are usually indicated as "candle wax drippings" [Figure 24]. Multiple small round chorioretinal lesions are frequently seen in peripheral fundus. Peripheral multifocal chorioretinitis and choroidal granuloma were described. Optic disc swelling may be caused by uveitis, raised intracranial pressure, or optic nerve infiltration. Arterial macroaneurysms, occurring in elderly female patients with peripheral multifocal chorioretinitis have been described, and were associated with severe cardiovascular disease. [84],[85] Development of capillary nonperfusion, and subsequent neovascularization as well as branch and central retinal vein occlusions have been described. [86],[87],[88],[89]
Other Causes of Occlusive Retinal Vasculitis
Idiopathic recurrent branch retinal arterial occlusion is a clinical syndrome characterized by recurrent multiple branch retinal arterial occlusions of unknown cause in one or both eyes of healthy middle-aged patients. Ophthalmoscopic and fluorescein angiographic findings suggested focal arteritis and arteriolitis as the cause of the obstructions. Eyes that have large areas of retinal ischemia may subsequently develop preretinal neovascularization. The prognosis for maintaining good visual acuity is good. Detailed investigation of these patients has failed to reveal a systemic etiology. Vestibuloauditory and/or transient sensorimotor symptoms were detected in 50% of patients. It is postulated that many of the patients have mild or partial manifestations of the microangiopathic syndrome of encephalopathy, hearing loss, and retinal arteriolar occlusions. [11] Occlusive retinal vasculitis, and subsequent retinal neovascularization [6] and neovascular glaucoma [19] were also reported in patients with Crohn's disease. Occlusive retinal vasculitis has also been reported in patients infected with Rift Valley fever virus [90],[91] [Figure 25] and West Nile virus. [92],[93],[94]
The search for a cause in patients with retinal vasculitis often involves a multidisciplinary approach and laboratory investigation [2],[95] [Table 3]. Discrimination between infectious or noninfectious etiology of retinal vasculitis is important because treatment is different. Immunosuppressive therapy may be essential in certain disorders but it might be deleterious in infectious entities. Once an infectious cause is believed to be unlikely, an associated systemic disease should be considered and an appropriate investigation instituted. In cases of diagnostic doubt, malignancy must be ruled out and should certainly be considered if, after an initial improvement with therapy, the patient's disease rapidly becomes refractory to treatment. The ophthalmologist, therefore, has a major role in clarifying the nosologic and diagnostic debate in patients with retinal vasculitis.
The laboratory work-up of a patient with retinal vasculitis should be based on a differential diagnosis derived from a detailed history, review of systems, and physical examination. If the patient's medical history, review of systems, or ocular examination suggests an underlying systemic disease, then the diagnostic work-up should be tailored for that disease. The absence of any diagnostic clues from history makes idiopathic retinal vasculitis most likely. If, however, the patient has no signs or symptoms suggestive of an associated disease then the work-up of the patient is limited to a fluorescein angiogram, complete blood count, erythrocyte sedimentation rate, VDRL, FTA-ABS, blood chemistry, urinalysis, tuberculin skin testing, HIV serology, and chest radiograph. Numerous studies have shown that little additional information is gained by "blind" investigation of the patient and that pursuing this is neither time nor cost effective.
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51. Levy-Clarke GA, Buggage RR, Shen D, Vaughen LO, Chan CC, Davis JL. Human t-cell lymphotropic virus-type 1 associated t-cell leukemia/lymphoma masquerading as necrotizing retinal vasculitis. Ophthalmology 2002;109:1717-22.
52. Kincaid J, Schatz H. Bilateral retinal arteritis with multiple aneurysmal dilatations. Retina 1983;3:171-8.
53. Chang TS, Aylward W, Davis JL, Mieler WF, Oliver GL, Maberley AL, et al. Idiopathic retinal vasculitis, aneurysms, and neuro-retinitis. Ophthalmology 1995;102:1089-97.
54. Samuel MA, Equi RA, Chang TS, Mieler W, Jampol LM, Hay D, et al. Idiopathic retinitis, vasculitis, aneurysms, and neuroretinitis (IRVAN): New observations and a proposed staging system. Ophthalmology 2007;114:1526-9.
55. Abu El-Asrar AM, Jestaneiah S, Al-Serhani AM. Regression of aneurysmal dilatations in a case of idiopathic retinal vasculitis, aneurysms and neuroretinitis (IRVAN) associated with allergic fungal sinusitis. Eye 2004;18:197-9.
56. Owens SL, Gregor ZJ. Vanishing retinal arterial aneurysms: A case report. Br J Ophthalmol 1992;76:637-8.
57. Sashihara H, Hayashi H, Oshima K. Regression of retinal arterial aneurysms in a case of idiopathic retinal vasculitis, aneurysms, and neuroretinitis (IRVAN). Retina 1999;19:250-1.
58. Tomita M, Matsubara T, Yamada H, Takahashi K, Nishimura T, Sho K, et al. Long term follow up in a case of successfully treated idiopathic retinal vasculitis, aneurysms, and neuroretinitis (IRVAN). Br J Ophthalmol 2004;88:302-3.
59. Rothova A, Lardenoye C. Arterial macroaneurysms in peripheral multifocal chorioretinitis associated with sarcoidosis. Ophthalmology 1998;105:1393-7.
60. Verougstraete C, Snyers B, Leys A, Caspers-Velu LE. Multiple arterial ectasias in patients with sarcoidosis and uveitis. Am J Ophthalmol 2001;131:223-31.
61. Yamanaka E, Ohguro N, Kubota A, Yamamoto S, Nakagawa Y, Tano Y. Features of retinal arterial macroaneurysms in patients with uveitis. Br J Ophthalmol 2004;88:884-6.
62. Ito Y, Nakano M, Kyu N, Takeuchi M. Frosted branch angiitis in a child. Jpn J Clin Ophthalmol 1976;30:797-803.
63. Kleiner RC, Kaplan HJ, Shakin JL, Yannuzzi LA, Crosswell HH Jr, McLean WC Jr. Acute frosted retinal periphlebitis. Am J Ophthalmol 1988;106:27-34.
64. Kleiner RC. Frosted branch angiitis: Clinical syndrome or clinical sign? Retina 1997;17:370-1.
65. Sykes SO, Horton JC. Steroid-responsive retinal vasculitis with a frosted branch appearance in Crohn's disease. Retina 1997;17:451-4.
66. Markomichelakis NN, Barampouti F, Zafirakis P, Chalkiadakis I, Kouris T, Ekonomopoulos N. Retinal vasculitis with a frosted branch angiitis-like response due to herpes simplex virus type 2. Retina 1999;19:455-7.
67. Farrardo J, Fonollosa A, Segura A, Garcia-Arumi J. Frosted branch angiitis associated with Epstein-Barr virus sytemic infection. Ocul Immunol Inflamm 2008;16:41-3.
68. Sugin SL, Henderly DE, Friedman SM, Jampol LM, Doyle JW. Unilateral frosted branch angiitis. Am J Ophthalmol 1991;111:682-5.
69. Borkowski LM, Jampol LM. Frosted branch angiitis complicated by retinal neovascularization. Retina 1999;19:454-5.
70. Helm CJ, Holland GN. Ocular tuberculosis. Surv Ophthalmol 1993;38:229-56.
71. Rosen PH, Spalton DJ, Graham EM. Intraocular tuberculosis. Eye 1990;4:486-92.
72. Gupta A, Gupta V, Arora S, Dogra MR, Bambery P. PCR-positive tubercular retinal vasculitis: Clinical characteristics and management. Retina 2001;21:435-44.
73. Biswas J, Sharma T, Gopal L, Madhavan HN, Sulochana KN, Ramakrishnan S. Eales' disease: An update. Surv Ophthalmol 2002;47:197-214.
74. International Study Group for Behηet's Disease. Criteria for diagnosis of Behηet's disease. Lancet 1990;335:1078-80.
75. Verity DH, Wallace GR, Vaughan RW, Stanford MR. Behηet's disease: From Hippocrates to the third millennium. Br J Ophthalmol 2003;87:1175-83.
76. Arnold AC, Usaf M, Pepose JS, Foos RY. Retinal periphlebitis and retinitis in multiple sclerosis: I: Pathologic characteristics. Ophthalmology 1984;91:255-62.
77. Lim JI, Tessler HH, Goodwin JA. Anterior granulomatous uveitis in patients with multiple sclerosis. Ophthalmology 1991;98:142-5.
78. Graham EM, Francis DA, Sanders MD, Rudge P. Ocular inflammatory changes in established multiple sclerosis. J Neurol Neurosurg Psychiatry 1989;52:1360-3.
79. Engell T, Andersen PK. The frequency of periphlebitis retinae in multiple sclerosis. Acta Neurol Scand 1982;65:601-8.
80. Birch MK, Barbosa S, Blumhardt LD, O'Brien C, Harding SP. Retinal venous sheathing and the blood-retinal barrier in multiple sclerosis. Arch Ophthalmol 1996;114:34-9.
81. Rucker CW. Sheathing of the retinal veins in multiple sclerosis: Review of pertinent literature. Mayo Clin Proc 1972;47:335-40.
82. Prineas JW, Wright RG. Macrophages, lymphocytes, and plasma cells in the perivascular compartment in chronic multiple sclerosis. Lab Invest 1978;38:409-21.
83. Towler HM, Lightman S. Symptomatic intraocular inflammation in multiple sclerosis. Clin Exp Ophthalmol 2000;28:97-102.
84. Rothova A. Ocular involvement in sarcoidosis. Br J Ophthalmol 2000;84:110-6.
85. Nicholas J. Sarcoidosis. Curr Opin Ophthalmol 2002;13:393-6.
86. DeRosa AJ, Margo CE, Orlick ME. Hemorrhagic retinopathy as the presenting manifestation of sarcoidosis. Retina 1995;15:422-7.
87. Ohara K, Okubo A, Saski H. Branch retinal vein occlusion in a child with ocular sarcoidosis. Am J Ophthalmol 1995;119:806-7.
88. Kimmel AS, McCarthy MJ, Blodi CF, Folk JC. Branch retinal vein occlusion in sarcoidosis. Am J Ophthalmol 1989;107:561-2.
89. Duker JS, Brown GC, McNamara JA. Proliferative sarcoid retinopathy. Ophthalmology 1988;95:1680-6.
90. Siam AL, Meegan JM, Gharbawi KF. Rift Valley fever ocular manifestations: Observations during the 1977 epidemic in Egypt. Br J Ophthalmol 1980;64:366-74.
91. Al-Hazmi A, Al-Rajhi AA, Abboud EB, Ayoola EA, Al-Hazmi M, Saadi R, et al. Ocular complications of Rift Valley fever outbreak in Saudi Arabia. Ophthalmology 2005;112:313-8.
92. Kaiser PK, Lee MS, Martin DA. Occlusive vasculitis in a patient with concomitant West Nile virus infection. Am J Ophthalmol 2003;136:928-30.
93. Chan CK, Limstrom SA, Tarasewicz DG, Lin SG. Ocular features of West Nile virus infection in North America: A study of 14 eyes. Ophthalmology 2006;113:1539-46.
94. Teitelbaum BA, Newman TL, Tresley DJ. Occlusive retinal vasculitis in a patient with West Nile virus. Clin Exp Optom 2007;90:463-7.
95. Herbort CP, Cimino L, Abu El-Asrar AM. Ocular vasculitis: A multidisciplinary approach. Curr Opin Rheumatol 2005;17: 25-33.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18], [Figure 19], [Figure 20], [Figure 21], [Figure 22], [Figure 23], [Figure 24], [Figure 25]
[Table 1], [Table 2], [Table 3]
Abu El-Asrar AM
Herbort CP
Tabbara KF
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Online since 10th March, 2009


text:
Congolanthus
The genus Congolanthus is in the family Gentianaceae in the major group Angiosperms (Flowering plants).
Statistics are at the end of the page.
Species in Congolanthus
Date supplied
Infra. rec.
Congolanthus longidens (N.E.Br.) A.Raynal	 Accepted WCSP (in review) 2012-03-23
The Plant List includes 3 scientific plant names of species rank for the genus Congolanthus. Of these 1 are accepted species names.
The status of the 3 species names for the genus Congolanthus recorded in The Plant List , are as follows:
◕ Accepted 1 33.3%
◕ Synonym 2 66.7%
◕ Unplaced 0 0%
◕ Unassessed 0 0%
The status of the 3 names (including infraspecific names) for the genus Congolanthus recorded in The Plant List , are as follows:
The confidence with which the status of the 3 species names recorded in The Plant List for the genus Congolanthus, are assigned as follows:
Confidence level
Unplaced
Unassessed
High confidence 0 0 0 0 0 0%
Medium confidence 1 2 0 0 3 100%
Low confidence 0 0 0 0 0 0%
The source of the species name records found in The Plant List for the genus Congolanthus is as follows:
Source of record
Misapplied
Tropicos 0 1 0 0 0 1 33.3%
WCSP (in review) 1 1 0 0 0 2 66.7%

redpajama_set_name: RedPajamaCommonCrawl


The new Pebble ID card printer from the French manufacturer, Evolis, is available with print drivers for Mac OS X. Traditionally, ID card printing has been a PC affair with Macintosh computers–for the most part–left on the sidelines. This has always seemed a bit ironic as many of the card designers and service bureaus have, and continue to, rely on Macs for the creation of the graphics and images used in the imaging process. The Pebble is compact, prints up to 140 full-color cards per hour, and comes in three "Mac-like" colors.
Angers, France, July 2004 – On the occasion of the next Apple Expo exhibition, Evolis Card Printer presents the New Pebble, the only color plastic card printer of its generation equipped with a printing driver compatible with Mac OS X.
Thanks to the Evolis New Pebble color printer, printing on plastic cards (credit card format) is very easy, cost-effective and gives high quality results.
The New Pebble personalizes all types of cards and badges: business cards, student cards, loyalty cards, company badges, access control badges, leisure cards, and so much more. It is especially intended to be used by associations, Press, private professionals, clubs, advertising agencies, printing houses, event organisers, educational institutions.
Thanks to its color sublimation and monochrome thermal transfer technologies, the New Pebble prints your high resolution photos, images, logos, texts and barcodes. With a 140 cards/hour print speed in full color and up to 1000 cards/hour in monochrome, the New Pebble has one of the most excellent throughputs on the market.
Deliverd as standard with its driver for Mac OS X and compatible with any software on the market, the New Pebble is extremely easy-to-use and does not require any particular computer knowledge.
Design, compact and easy-to-use, the New Pebble is just as easily integrated on a reception desk as on your office desk! It is available in 3 colors: Ruby, Glacier, or Lagoon.
Evolis Card Printer is today the only manufacturer of plastic card printers that are compatible with Mac OS X thanks to a complete printing driver, and who also offers a complete 2 year warranty, print head included.
Evolis Card Printer, a leading plastic card printer manufacturer, supplies a complete range of cost-effective and innovative solutions. Hi-Tech, design and easy-to-use, the Evolis printers personalize your cards with high resolution texts, pictures, logos, barcodes and electronically encoded information in colour or monochrome. Situated in Angers, France, Evolis is represented in 80 countries with more than 16 000 printers delivered worldwide so far.


PhpTabs provides some useful methods to calculate durations.
The following code prints duration for the first measure of the first track.
PhpTabs (>=0.6.0) provides a shortcut method to easily get this value.
The getTime() method is provided by the \PhpTabs\Music\Voice model.
The following code prints duration for the first beat of the first measure of the first track.


Coiling Core Traveling Lunges train you to move like an athlete, with effortless power. It's all about how you use your lats to coil your core, and break the rules of conventional lunges to move with the grace and power of a big cat. In this version of the exercise, we're training one side at a time, using an elastic band for resistance.
Align your head over one foot and contract that same side lat to side-bend and counter-rotate your core. The combination of these movements is called coiling.
Keep your lat contracted for the remainder of the exercise, with the intention to bring your shoulder down and back, and same side hip up and forward.
The side that you have coiled will be your front foot. With your weight on the ball of that foot, match the angle of your spine with an aggressive forward angle of your shin, and send the other foot behind you so that you are in a partial lunge.
Don't worry about keeping your knee behind your toes, because the coiling action of your core and matching spine and shin angles puts no stress (or sensation of work) in your quads or knees.
Press up out of the lunge to a tall standing position on your other leg. Then lunge forward to any depth you want, keeping your lat contracted and core coiled with maximum intent.
The glutes and upper hamstrings power these lunges with ease, and the overall movement feels effortless when you align your head over your foot and engage your lat.
Perform 8-10 lunges across the room on one side, then switch your coiling side and lunging leg to come back for another 8-10 lunges. You can repeat as many times as you like, or make these lunges as dynamic as you want. Try powering up fast from the lunge position, and adding a skipping step with your lunging foot before you get to tall standing on your other leg.


text:
Skiing : Phil Mahre Can Reach Summit This Weekend
By Bob Lochner
Phil Mahre, currently sandwiched between two Swedes near the top of the U.S. Pro Tour standings, will attempt to ski into the lead this weekend during the WinterFest races at Snow Summit.
The former World Cup and Olympic champion has 415 points so far in his comeback at the age of 31, placing him second to Jorgen Sundqvist, who has 465. Mahre, with $41,650, has earned $650 more than Sundqvist, but both have made less than Niklas Lindqvist, third in the standings with 375 points but first in line at the ATM window with $47,730.
Action at the Big Bear Lake resort gets under way today with qualifying for Sunday's slalom. The giant slalom is set for Saturday. Racing starts at 11 a.m. each day on Widowmaker Run, and there will also be a pro-celebrity event at 2 p.m. Saturday.
After 12 stops on the 16-meet pro circuit, Mahre has six slalom victories to his credit in the dual, head-to-head elimination format. Each first place is worth 35 points on a scale that drops to five points just for reaching the round of 32.
Phil's twin brother, Steve, who hadn't won a race since the opening slalom in November at Park City, Utah, is out for the rest of the season. He injured a knee last weekend at Winter Park, Colo., and underwent surgery Wednesday at Dr. Richard Steadman's clinic in South Lake Tahoe.
Spring conditions prevail at ski areas throughout California, where depths range from two to six feet in the sunny Southland, and up to 10 feet in the Sierra.
Mammoth Mountain reported eight inches of new powder and a 6 1/2-foot base Thursday, but relatively warm temperatures in midweek meant rain and wet snow farther north, around Tahoe.
Skiing seems assured about everywhere at least through Easter.
Other activities in the next few days include:
--U.S. Ski Assn.'s Freestyle Mogul Finals Saturday and Sunday on Showtime Run at Bear Mountain.
--North Lake Tahoe-Truckee Winter Carnival through Sunday at Northstar and Squaw Valley.
--Corporate Ski Challenge, with 124 teams, Monday through March 18 at Alpine Meadows.
--Top Gun on Gunbarrel mogul competition, for $10,000 in prizes, next Wednesday and Thursday at Heavenly Valley.
--National Masters' Championships, for skiers 30 and over, Sunday through next Friday at Mt. Bachelor, Ore.
And, oh yes, full-time residents of snow country will compete in their favorite ski-season pastimes during the Tahoe Local Man Winter Triathlon today at Homewood, near Tahoe City. The three sports: Installing tire chains, splitting firewood and shoveling snow.
Skiing Notes
World Cup racing, which began last November in Europe, is screeching to a halt this week at Shiga Kogen, Japan, where the schedule calls for a men's slalom today, a women's slalom Saturday and parallel races for both men and women Sunday. Alberto Tomba of Italy still has a chance to make up for a disappointing season by pulling out the slalom title today. He is third in the standings with 100 points, behind three-time overall champion Marc Girardelli of Luxembourg, who has 106, and Armin Bittner of West Germany, who has 102. Vreni Schneider of Switzerland, who has already won the women's overall cup, will be trying for a record-breaking 14th victory in one season Saturday. . . . The Alps, mostly bare throughout early winter, are becoming more skiable. Some sample snow depths passed along by Powder Ski Adventures in Mission Viejo this week include: Austria--St. Anton 12 to 100 inches, Kitzbuhel 4-46; France--Avoriaz 53-63, Chamonix 19-85, La Plagne 53-87, Val d'Isere 39-63, Val Thorens 53-79; Italy--Cortina d'Ampezzo 28-67, Val Gardena 16-55; Switzerland--Davos 18-69, Saas Fe 12-59, Verbier 12-94. . . . Tennis star Chris Evert and her husband, former U.S. downhiller Andy Mill, will be Bob Beattie's guests on "Ski World" Sunday at 2:30 p.m. on ESPN. . . . Friedl Pfeifer, 77, who "discovered" Aspen, Colo., and first developed it for skiing in the mid-1940s, was the honored guest at Ski magazine's annual Legends of Skiing banquet last Saturday night at Beaver Creek, Colo.


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Meet ServiceNow Finland Country Manager Nina Koivikko
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At ServiceNow, we make the world work better for our customers, partners, and employees. Carrying that out involves hiring the right talent. That's why we're thrilled to welcome Nina Koivikko as country manager for ServiceNow Finland.
We caught up with Nina to discuss her journey, goals, and aspirations.
I've been working in the information and communications technology industry for 26 years now—across several companies in Belgium and Finland. Before ServiceNow, I joined Microsoft to lead a newly established solution sales team in Finland, which was hugely exciting.
My role was to create value for Finnish customers on their digital transformation journeys. I'm proud to say we delivered—improving Finnish organisations' employee and customer experiences, increasing their operational efficiency, and creating new business opportunities while growing our sales and doubling the size of our team.
I've had the opportunity to work in many different parts of businesses: sales, supply chain, product management and development, customer service, and more. This gave me a wider perspective on how to help enterprise customers and public organisations with any need they may have.
Also, living in different countries, such as the U.S., France, Belgium, and Mozambique, has taught me the importance of diversity and inclusion. I'm a big believer in inclusivity.
What attracted you to ServiceNow?
I've always been a big fan of ServiceNow. At a previous job, my team was one of the first in Finland to adopt ServiceNow solutions, so I was familiar with the platform and how innovative it is, as well as how ServiceNow treats its customers. When I was approached about this role, the decision to take it was an easy one.
I see so much potential for growth in the region. Finnish customers are facing many challenges. There's a huge need for resilience and agility, which is exactly what we can help with.
Put simply, our customers need us. I'm honoured to take on this role and drive growth wherever I can—for our customers, for our partners and, naturally, for our team in Finland.
How has your experience been so far?
I'm still at the beginning of my ServiceNow journey, but I can say with absolute confidence that the onboarding process has been exceptional. The technology was streamlined, the process was logical and efficient, and it's been really easy to understand exactly what I need to do and what my team needs from me.
It was great to see our own HR solutions in action too. I love that we use our own technology to improve our internal processes. I know exactly how we can help a customer streamline their onboarding process because I've experienced it firsthand.
Beyond the processes, the team has been great too. Everybody is professional, warm, and welcoming. ServiceNow clearly values its people. That's reflected in the attitudes and values of those who work here.
How does ServiceNow serves its people?
I love how much ServiceNow respects different types of talent. There are many challenges facing the tech industry—from the digital skills gap to a lack of diversity to bias against women. ServiceNow is actively playing a role in addressing these issues.
From what I've seen, the company sets high expectations for how everyone is treated and has zero tolerance for bias. You're judged on your value, not your gender or cultural background.
It's encouraging to see that ServiceNow is helping to bridge the digital divide. Finland is considered quite tech savvy, but we're still seeing customers struggle with this. Companies like ours can help. Also, I'd like to see more diverse talent introduced to the industry. Programmes such as RiseUp with ServiceNow can help achieve this.
What are the main challenges in Finland?
In Finland, we're facing many of the same challenges as the rest of Europe: rising inflation, geopolitical turbulence, and global supply chain issues. We all need to be more efficient wherever we can. Digital transformation has never been so important for our customers.
We're in a great position to help companies of all sizes across the region. I'm extremely excited to listen to our customers and learn exactly what they need from us—whether it's scaling, growing, or learning more about automation and what it can do.
Right now, Finland's public sector is experiencing a period of major change, with new social and healthcare districts having recently been introduced. It's a challenging time for the sector, but it's also a great opportunity to ramp up digital transformation. Organisations need to introduce more value and efficiency to their processes because there's no other choice. This is where we can help.
What are your plans for the region?
As a team, we have big plans. We're in a unique position to help our customers, specifically with some of the challenges I mentioned above. Whether it's the public sector or commercial business, we can bring efficiency and agility on a wide scale.
But first, I will simply listen—to both our customers and my team. I'm working with an immensely talented group of people, so I'm excited to hear their ideas and figure out how we can work together to help organisations in the region.
I also want to make sure our customers know the full breadth of our services. I plan to have a lot of conversations to help ensure they're taking advantage of all our amazing solutions.
It's these kinds of small but important steps that will lay the groundwork for an amazing year—and lots of bigger steps to come.
Find out more about how ServiceNow can help your organisation.
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It seems like during the summer months any one who grows vegetables (or knows someone who does) is overloaded with zucchini and summer squash. I happen to have parents who are very keen gardeners and have planted a few too many zucchini and pattypan squash plants. We were all quite tired of just having them fried with garlic as a side dish so I thought it would be the perfect opportunity to make zucchini bread!
This was a first time thing for me. I thought that the idea of zucchini in a quick bread sounded kinda gross. But then I started reading a few recipes and realised that it was a bit like a carrot cake, and seeming as carrot is a vegetable and carrot cake is freaking delish then why wouldn't zucchini bread work?
I also added streusel because…well streusel is tasteh and belongs on this cake, so don't leave it out!
Put all the ingredients for the streusel in a medium bowl.
Combine the oil, sugar, eggs and vanilla in a large bowl and mix until fully combined.
Grate the zucchini and then place in a strainer over the sink and push down on it to remove the excess water. Measure the zucchini and then add to the oil mixture and mix in.
Fold in the flour, baking powder, salt, cinnamon, ginger, nutmeg and cardamom, mix until there are a few streaks of flour left.
Stir in the walnuts and currants until everything is well combined. Pour the runny mixture into your greased, floured loaf pan.
Place in the oven for 6 minutes while you make the streusel.
Using the tips of your fingers rub the butter into the dry ingredients until there are no visible lumps of butter and a mixture is produced which resembles damp sand and clumps together when you press it.
If not making streusel, the cake can be topped with a cream cheese frosting or a simple lemon glacé icing.
I am SO excited to make this bread. I love zucchini anything, especially zucchini bread! Thank you for posting. I just started blogging over at http://thenewlywedscookbook.com/ feel free to check it out! Thanks!


text:
Rangers, Astros lead effort for Uvalde Boys & Girls Club
MLB Winter Meetings Auction to raise funds to establish Boy and Girls Club in Uvalde
SAN DIEGO – The Rangers and Astros are spearheading this year's Winter Meetings auction. The proceeds will establish a Boys & Girls Club in Uvalde, Texas, where a mass shooter killed nine children and two teachers in a mass shooting in May.
Rangers executive VP of communications John Blake and Astros senior VP Anita Sehgal represented their respective clubs for the announcement Monday at the Manchester Grand Hyatt.
"What's great about opening a Boys and Girls Club in Uvalde is it's something that will stand the test of time," Sehgal said. "If every year we can think about this auction as building a legacy project for a community that needs it or a cause that is important, then we really as a collective Major League Baseball family, including our media partners and our community partners, are making a real difference."
The online charity auction is live through Thursday at 7 p.m. CST.
Fred McGriff reaches Hall; Clemens, Bonds don't
Tata Martino owns Mexico's utter failure
Jose Abreu is 'pumped' to join the Astros
The Astros and the Rangers have supported the Uvalde community since the tragedy at Robb Elementary. In August the Astros played host to 10-year-old Mayah Zamora, a survivor of the mass shooting.
More commitment to Uvalde
Zamora spent 66 days in the hospital recovering from the wounds she suffered. She lived a few blocks away from where the 18-year-old shooter Salvador Ramos lived. Zamora didn't want to return to her home.
The Carlos Correa Family Foundation committed to leading the effort to buy Zamora's family a new home. Gallery Furniture owner Jim "Mattress Mack" McIngvale committed to furnishing the home.
The Astros have held multiple events for the Uvalde community since the tragedy. Astros Owner Jim Crane held a brunch in Uvalde for the victims' families in July. On that trip, 60 Astros employees, volunteers helped put together a PLAY BALL activation for the community.
Then in August Lance McCullers, Jose Altuve, Alex Bregman and Dusty Baker addressed a large contingent who packed 10 buses for a trip from Uvalde to an Astros game.
Ranger continue to help
Soon after the shooting, the Rangers Baseball Foundation, Rangers fans, and the Rangers ownership group donated more than $100,000 to a fund established to support the families of the victims. Another $25,000 was donated from a Mystery Ball Fundraiser the Rangers held during a home game.
The charity items have been donated by the MLB teams, the Baseball Hall of Fame and Museum, the commissioner's office, MLB Network and minor league clubs. Hall of Famer and Rangers icon Ivan "Pudge" Rodriguez has donated an 18-hole round with two friends for the auction.
The auction includes special meet-and-greet sessions. Three-time MVP Mike Trout, Cardinals manager Oliver Marmol, Dodgers manager Dave Roberts, Seattle manager Scott Servais and Mets manager Buck Showalter, All-Star Andrés Giménez, Steven Kwan, Alek Thomas, Daulton Varsho and Christian Walker have volunteered for the meet-and-greet sessions.
The full list of auction items can be found on the league's website.
"While we're going to repair Little League fields, and we're going to help rebuild youth baseball there, this Club will provide a safe haven for families that desperately need it," Sehgal said. "Just the ability to create experiences and raise money, to leave that legacy for that community will make such a huge difference for them."


text:
Igor Vladimirovič Akinfejev (rus. Игорь Владимирович Акинфеев) (Vidnoje, 8. travnja 1986.) je ruski nogometaš koji trenutačno igra za ruski nogometni klub CSKA Moskva i rusku nogometnu reprezentaciju. Profesionalnu karijeru je započeo u 2003. godini u CSKA Moskvi, gdje još i dan danas igra. Za Konje je odigrao preko 500 službenih utakmica. Osvojio je pet puta rusku Premijer ligu, pet ruska Kupa i Kup UEFA u 2005. godini.

Reprezentacija
Za rusku nogometnu reprezentaciju je debitirao u 2004. godini i skupio je preko 80 nastupa za Rusiju. U travnju 2004. godine je odigrao prvu utakmici za domovinu protiv Norveške. Predstavljao je Rusiju na tri Europska prvenstva u 2004., 2008. i 2012., a na Svjetsko prvenstvo je branio u 2014. godini. U kvalifikacijskoj utakmici Crne Gore protiv Rusije dodijeljena je pobjeda od 3:0 za Ruse u ožujku 2015. nakon što je susret prekinut u 67. minuti zbog nasilja domaćih navijača i tučnjave igrača. Rezultat utakmice bio je 0:0, s tim da su Rusi promašili jedanaesterac nekoliko trenutaka prije prekida. Također, to je bio drugi prekid susreta, jer je u prvoj minuti Akinfejev pogođen bakljom, zbog čega je susret bio prekinut 33 minute. Ruski nogometni izbornik objavio je u svibnju 2016. popis za nastup na Europskom prvenstvu u Francuskoj, među kojim je i Akinfejev.

Izvori

Vanjske poveznice
Profil na Transfermarktu
Profil na Soccerwayu

Ruski nogometni vratari
Nogometaši CSKA Moskve
Aktivni nogometaši

redpajama_set_name: RedPajamaWikipedia


text:
Q: Disabling Internet Explorer thru Powershell Trying to disable Internet Explorer but is receiving a prompt whether to complete the operation now? [Y/N]?
Tried this command:
Disable-WindowsOptionalFeature -FeatureName Internet-Explorer-Optional-amd64 -Online -Confirm:$false
Tried this command:
Disable-WindowsOptionalFeature -FeatureName Internet-Explorer-Optional-amd64 -Online -Confirm:$false
But received an error message:

A: I agree with the suggestion given by Santiago.
The correct command to disable the Internet Explorer using the Powershell is as below.
Disable-WindowsOptionalFeature -online -FeatureName internet-explorer-optional-amd64

When you run the command, it will ask you whether you would like to restart the machine or later. You could enter the desired choice.

Note: Make sure you are running the Powershell as Administrator.

redpajama_set_name: RedPajamaStackExchange


Infamously dedicated to establishing improv as a unique art form in its own right, Del Close was an influential teacher, an impassioned, complicated guru and a true comedy maestro who pushed all artistic boundaries and trained many of the most celebrated performers of the late 20th century.
Close was born in Manhattan, Kansas, in 1934, the second cousin of Dwight D. Eisenhower. After already spending time at The Compass in St. Louis and his own stand-up act, Close joined The Second City cast in 1961, working with the company as an actor, writer and director. He was in and out of the company for years, as well as directing the 12th revue, 20,000 Frozen Grenadiers or There's Been a Terrible Accident at the Factory.
Many up-and-coming Second City performers studied with Close, and The Upright Citizens Brigade first met and formed their ensembles in his classes.
Close passed away in 1999 at the age of 64 after holding a "living wake" in the hospital the night before he died. According to Charna Halpern, his last words were, "I'm tired of being the funniest person in the room." He famously bequeathed his skull to the Goodman Theatre, to play "Yorick," the cranium in Hamlet's graveyard scene.


text:
@interface UINavigationItem (Accessor)

@property(nonatomic,assign) UINavigationBar *navigationBar;
@property(nonatomic,readonly) UIColor *tintColor;

@end

@implementation UINavigationItem (Accessor)

NSAPropertyGetter(navigationBar, @"_navigationBar");
NSAPropertyAssignSetter(setNavigationBar, @"_navigationBar");

- (UIColor *)tintColor {
    return self.navigationBar.tintColor;
}

@end

@interface UINavigationBar (Private)

- (void)pushNavigationItem:(UINavigationItem *)item;
- (id)currentBackButton; // return UINavigationItemButtonView

@end

@implementation UINavigationBar (Patch)

- (instancetype)init { return [super init]; }
- (instancetype)__init { assert(NO); return nil; }
- (instancetype)__initWithCoder:(NSCoder *)aDecoder { assert(NO); return nil; }
- (instancetype)__initWithFrame:(CGRect)frame { assert(NO); return nil; }
- (void)__setBarStyle:(UIBarStyle)barStyle { assert(NO); }
- (void)__pushNavigationItem:(UINavigationItem *)item { assert(NO); }
- (UIColor *)__tintColor { assert(NO); return nil; }
- (void)__setTintColor:(UIColor *)tintColor { assert(NO); }

- (void)_navigationBarInit {
    [self setBarStyle:self.barStyle];

    if ([self respondsToSelector:@selector(setShadowImage:)]) {
        [self setShadowImage:[[[UIImage alloc] init] autorelease]];
    }

    UIGraphicsBeginImageContext(CGSizeMake(1.0, 3.0));
    CGContextRef context = UIGraphicsGetCurrentContext();
    [(UIColor *)[UIColor colorWith8bitWhite:178 alpha:255] set];
    CGContextFillRect(context, CGRectMake(.0, 2.0, 1.0, 1.0));
    UIImage *backgroundImage = UIGraphicsGetImageFromCurrentImageContext();
    UIGraphicsEndImageContext();

    [self setBackgroundImage:backgroundImage forBarMetrics:UIBarMetricsDefault];
    [self setBackgroundImage:backgroundImage forBarMetrics:UIBarMetricsLandscapePhone];
}

- (void)_tintColorUpdated {
    [super _tintColorUpdated];
    for (UINavigationItem *item in self.items) {
        [item _tintColorUpdated];
    }
}

@end

@implementation UI7NavigationBar

+ (void)initialize {
    if (self == [UI7NavigationBar class]) {
        Class target = [UINavigationBar class];

        [target copyToSelector:@selector(__init) fromSelector:@selector(init)];
        [target copyToSelector:@selector(__initWithCoder:) fromSelector:@selector(initWithCoder:)];
        [target copyToSelector:@selector(__initWithFrame:) fromSelector:@selector(initWithFrame:)];
        [target copyToSelector:@selector(__setBarStyle:) fromSelector:@selector(setBarStyle:)];
        [target copyToSelector:@selector(__pushNavigationItem:) fromSelector:@selector(pushNavigationItem:)];
        [target copyToSelector:@selector(__tintColor) fromSelector:@selector(tintColor)];
        [target copyToSelector:@selector(__setTintColor:) fromSelector:@selector(setTintColor:)];
    }
}

+ (void)patch {
    Class target =  [UINavigationBar class];

    [self exportSelector:@selector(init) toClass:target];
    [self exportSelector:@selector(initWithCoder:) toClass:target];
    [self exportSelector:@selector(initWithFrame:) toClass:target];
    [self exportSelector:@selector(setBarStyle:) toClass:target];
    [self exportSelector:@selector(pushNavigationItem:) toClass:target];
    if (![UIDevice currentDevice].iOS7) {
        [self exportSelector:@selector(tintColor) toClass:target];
        [self exportSelector:@selector(setTintColor:) toClass:target];
    }
}

- (instancetype)init {
    self = [self __init];
    if (self) {
        [self _navigationBarInit];
    }
    return self;
}

- (instancetype)initWithFrame:(CGRect)frame {
    self = [self __initWithFrame:frame];
    if (self) {
        [self _navigationBarInit];
    }
    return self;
}

- (instancetype)initWithCoder:(NSCoder *)aDecoder {
    self = [self __initWithCoder:aDecoder];
    if (self) {
        [self _navigationBarInit];
    }
    return self;
}

- (void)setBarStyle:(UIBarStyle)barStyle {
    [self __setBarStyle:barStyle];

    UIColor *backgroundColor = [[UI7NavigationBar appearance] backgroundColor];
    UIColor *titleColor = nil;
    switch (barStyle) {
        case UIBarStyleDefault: {
            backgroundColor = backgroundColor ? backgroundColor : [UI7Color defaultBarColor];
            titleColor = [UIColor blackColor];
        }   break;
        case UIBarStyleBlackOpaque:
        case UIBarStyleBlackTranslucent: {
            backgroundColor = backgroundColor ? backgroundColor : [UI7Color blackBarColor];
            titleColor = [UIColor whiteColor];
        }   break;
        default:
            break;
    }

    if (titleColor) {
        NSDictionary *dict = @{
                               UITextAttributeFont: [UI7Font systemFontOfSize:17.0 attribute:UI7FontAttributeMedium],
                               UITextAttributeTextShadowColor: [UIColor clearColor],
                               UITextAttributeTextColor: titleColor,
                               UITextAttributeTextShadowOffset: [NSValue valueWithUIOffset:UIOffsetZero],
                               };
        self.titleTextAttributes = dict;
        // Trick to force rerender title
        NSString *title = [self.topItem.title retain];
        self.topItem.title = @"";
        self.topItem.title = title;
        [title release];
    }
    if (backgroundColor) {
        self.backgroundColor = backgroundColor;
    }
}

//- (void)setItems:(NSArray *)items animated:(BOOL)animated {
//    [super setItems:items animated:animated];
//}
//
- (void)pushNavigationItem:(UINavigationItem *)item {
    [self __pushNavigationItem:item];
    dlog(DEBUG_NAVIGATIONBAR, @"pushNavigationItem: %@", self.backItem.backBarButtonItem);
    if (self.backItem.backBarButtonItem == nil) {
        UIBarButtonItem *barButtonItem = [[UI7BarButtonItem alloc] initWithTitle:nil style:UIBarButtonItemStyleBordered target:nil action:nil];  // this may cause problem if some code depends on existance of this value.
        barButtonItem.appearanceSuperview = self.backItem;
        [barButtonItem _tintColorUpdated];
        self.backItem.backBarButtonItem = barButtonItem;
    }
//    item.navigationBar = self;
    [item _tintColorUpdated];
}
//
//- (id)currentBackButton {
//    id button = [super currentBackButton];
//    dlog(DEBUG_NAVIGATIONBAR, @"ccurrentBackButton: %@ %@", button, [button title]);
//    return button;
//}

- (UIColor *)tintColor {
    UIColor *color = [self __tintColor];
    if (color == nil) {
        color = [self _tintColor];
    }
    return color;
}

- (void)setTintColor:(UIColor *)tintColor {
    [self __setTintColor:tintColor];
    [self _tintColorUpdated];
}

@end

@implementation UINavigationItem (UI7NavigationItem)

- (void)_tintColorUpdated {
    UIBarButtonItem *item = nil;
    item = self.leftBarButtonItem;
    if (item) {
        item.appearanceSuperview = self;
        [item _tintColorUpdated];
    }
    item = self.rightBarButtonItem;
    if (item) {
        item.appearanceSuperview = self;
        [item _tintColorUpdated];
    }
    item = self.backBarButtonItem;
    if (item) {
        item.appearanceSuperview = self;
        [item _tintColorUpdated];
    }
}

@end

@implementation UINavigationItem (Patch)

- (instancetype)__init { assert(NO); return nil; }
- (instancetype)__initWithCoder:(NSCoder *)aDecoder { assert(NO); return nil; }
- (instancetype)__initWithTitle:(NSString *)title { assert(NO); return nil; }
- (void)__setLeftBarButtonItem:(UIBarButtonItem *)leftBarButtonItem animated:(BOOL)animated { assert(NO); }
- (void)__setRightBarButtonItem:(UIBarButtonItem *)rightBarButtonItem animated:(BOOL)animated { assert(NO); }
- (void)__setBackBarButtonItem:(UIBarButtonItem *)backBarButtonItem { assert(NO); }
- (void)__setLeftBarButtonItems:(NSArray *)items animated:(BOOL)animated { assert(NO); }
- (void)__setRightBarButtonItems:(NSArray *)items animated:(BOOL)animated { assert(NO); }

@end

@implementation UI7NavigationItem

+ (void)initialize {
    if (self == [UI7NavigationItem class]) {
        Class target = [UINavigationItem class];

        [target copyToSelector:@selector(__initWithCoder:) fromSelector:@selector(initWithCoder:)];
        [target copyToSelector:@selector(__initWithTitle:) fromSelector:@selector(initWithTitle:)];
        [target copyToSelector:@selector(__setLeftBarButtonItem:animated:) fromSelector:@selector(setLeftBarButtonItem:animated:)];
        [target copyToSelector:@selector(__setRightBarButtonItem:animated:) fromSelector:@selector(setRightBarButtonItem:animated:)];
        [target copyToSelector:@selector(__setBackBarButtonItem:) fromSelector:@selector(setBackBarButtonItem:)];
        [target copyToSelector:@selector(__setLeftBarButtonItems:animated:) fromSelector:@selector(setLeftBarButtonItems:animated:)];
        [target copyToSelector:@selector(__setRightBarButtonItems:animated:) fromSelector:@selector(setRightBarButtonItems:animated:)];
    }
}

+ (void)patch {
    Class target = [UINavigationItem class];

    [self exportSelector:@selector(initWithCoder:) toClass:target];
    [self exportSelector:@selector(initWithTitle:) toClass:target];
    [self exportSelector:@selector(setLeftBarButtonItem:animated:) toClass:target];
    [self exportSelector:@selector(setRightBarButtonItem:animated:) toClass:target];
    [self exportSelector:@selector(setBackBarButtonItem:) toClass:target];
    [self exportSelector:@selector(setLeftBarButtonItems:animated:) toClass:target];
    [self exportSelector:@selector(setRightBarButtonItems:animated:) toClass:target];
}

- (instancetype)initWithCoder:(NSCoder *)aDecoder {
    self = [self __initWithCoder:aDecoder];
    if (self != nil) {

    }
    return self;
}

- (instancetype)initWithTitle:(NSString *)title {
    self = [self __initWithTitle:title];
    if (self != nil) {

    }
    return self;
}

- (void)setLeftBarButtonItem:(UIBarButtonItem *)barButtonItem animated:(BOOL)animated {
    [self __setLeftBarButtonItem:barButtonItem animated:animated];
    barButtonItem.appearanceSuperview = self;
    [barButtonItem _tintColorUpdated];
}

- (void)setRightBarButtonItem:(UIBarButtonItem *)barButtonItem animated:(BOOL)animated {
    [self __setRightBarButtonItem:barButtonItem animated:animated];
    barButtonItem.appearanceSuperview = self;
    [barButtonItem _tintColorUpdated];
}

- (void)setBackBarButtonItem:(UIBarButtonItem *)barButtonItem {
    [self __setBackBarButtonItem:barButtonItem];
    barButtonItem.appearanceSuperview = self;
    [barButtonItem _tintColorUpdated];
}

- (void)setLeftBarButtonItems:(NSArray *)items animated:(BOOL)animated {
    [self __setLeftBarButtonItems:items animated:animated];
    for (UIBarButtonItem *barButtonItem in items) {
        barButtonItem.appearanceSuperview = self;
        [barButtonItem _tintColorUpdated];
    }
}

- (void)setRightBarButtonItems:(NSArray *)items animated:(BOOL)animated {
    [self __setRightBarButtonItems:items animated:animated];
    for (UIBarButtonItem *barButtonItem in items) {
        barButtonItem.appearanceSuperview = self;
        [barButtonItem _tintColorUpdated];
    }
}

//- (UIBarButtonItem *)backBarButtonItem {
//    UIBarButtonItem *item = [super backBarButtonItem];
//    return item;
//}
//
//- (void)setBackBarButtonItem:(UIBarButtonItem *)backBarButtonItem {
//    [super setBackBarButtonItem:backBarButtonItem];
//}

@end

redpajama_set_name: RedPajamaGithub


The MUT-15 from Millitech is a Frequency Multiplier with Input Frequency 16.67 to 25 GHz, Output Frequency 50 to 75 GHz, Input Power 16 to 23 dBm, Output Power 1 to 3 dBm, Harmonics -30 dBc. Tags: Module with Connectors, Waveguide, Waveguide Multiplier. More details for MUT-15 can be seen below.


Sony's Venom movie is rumored to include a cameo from Tom Holland's Spider-Man. After the Andrew Garfield-starring The Amazing Spider-Man 2 failed to launch a shared universe full of characters connected to Peter Parker, Sony made a deal with Marvel Studios to welcome Spider-Man into the Marvel Cinematic Universe. Holland first debuted as the wall-crawling superhero in 2016's Captain America: Civil War, then received his first solo outing in the MCU with last year's Spider-Man: Homecoming.
However, Sony was meanwhile planning their own superhero universe using Spider-Man characters. They announced a Venom movie starring Tom Hardy with Ruben Fleischer on board as the director, and tapped Gina Prince-Bythewood to helm Silver and Black, a film following Silver Sable and Black Cat. Still, it quickly became unclear whether Holland's Spidey would be included in these films or this universe. Marvel Studios head Kevin Feige said, in no uncertain terms, Venom wouldn't be connected to the MCU, but Sony producer Amy Pascal caused confusion in stating it would be "adjunct" to the MCU. Now, a new rumor will add further confusion and speculation to the fire.
Kristian Harloff, head of development for Collider Video, tweeted that Collider Video host Jon Schnepp dropped the scoop on Collider Movie Talk that Holland's Spider-Man will, in fact, appear in Sony's Venom movie. It must be noted that the revelation should be taken as a rumor with a grain of salt until further confirmation is provided.
UPDATE: The episode has been released and can be watched from 1:40 in the below video.
UPDATE 2: Schnepp clarified his report, stating Holland's Peter Parker will appear in Venom, but not necessarily the actor's Spider-Man.
Update 3: Here's the scene where Tom Holland's Peter Parker may appear in Venom!
If Holland's Spider-Man does appear in Venom, it will be a major connection between Sony's offshoot superhero universe and the established MCU. Fans of Marvel Studios' expansive world would no doubt welcome the connection, as it would provide viewers with a different look at the universe - and lay the groundwork for Hardy's Venom and Holland's Spider-Man to one day team up or battle each other in a more official capacity. Further, it would mean that characters used in Sony's films - Venom, Silver Sable, and Black Cat - could potentially appear in Marvel movies, though that still seems unlikely (and even more unlikely is the potential for any Marvel Studios characters beyond Spider-Man appearing in one of Sony's movies).
Still, this is just a rumor as of now. Holland has become notorious for accidentally leaking Marvel secrets so if he does have a part, it's likely we'll get a hint of it from his social media presence - that is, of course, unless Sony takes extreme measures to protect this secret. Additionally, Hardy hasn't been shy about sharing photos from the set of Venom, though they've carefully revealed very little about the project. Recently, the first official Venom image was released, featuring Hardy as Brock rather than the symbiote.
All that said, if Holland is appearing in Venom, it's likely we'll hear further rumors about it before the movie wraps production. So, fans should be on the lookout for hints from the Venom production and Holland's social media.


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We obtain personal information from you such as your name, address, account number, shopping history, e-mail address and telephone number when you give us that information when shopping or using our services. For example, we may obtain personal information about you when you register to use our website; place an order with us; participate in advertising promotions or sweepstakes.
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text:
Archives [ 2018 ]
New Partnership with the Ministry of Higher Education and Scientific Research, The Government of Arab Republic of Egypt (Cairo, Egypt)
Letter of Intent between the Ministry of Higher Education and Scientific Research, The Government of Arab Republic of Eg[...]
New Partnership with Faculty of Mathematics and Natural Sciences, Institut Teknologi Bandung (Indonesia)
Graduate School of Engineering, University of Fukui has newly established an academic exchange agreement with Faculty of[...]
Welcome to UF! 84 new international students started new life in Fukui
We welcomed 84 new international students from 17 countries/regions, and they start their study from this October. Op[...]
New Partnership with College of Engineering, National Cheng Kung University (Tainan City, Taiwan)
Graduate School of Engineering, University of Fukui has newly established an academic exchange agreement with College of[...]
UF Severe Weather Policy : Cancellation of Classes, Exams, Trainings, etc.
Expansion of Partnership with Faculty of Engineering and Architecture & Faculty of Sciences and Liberal Arts, Rajamangala University of Technology Isan (Nakhon Ratchasima, Thailand)
Faculty of Engineering and Architecture, Rajamangala University of Technology Isan (Nakhon Ratchasima, Thailand) and Gra[...]
Manuscripts of William Griffis donated from Rutgers University and recap of the UF-Rutgers Partnership
UF's partnership with Rutgers University took another step forward during a recent visit to UF by Professor Paul Schalow[...]
【学術交流協定締結】パヤップ大学(タイ)
New Partnership with Payap University (Chiang Mai, Thailand) University of Fukui has newly established an academic ex[...]
New Partnership with Rangsit University (Pathum-Thani, Thailand)
University of Fukui has newly established an academic exchange agreement with Rangsit University (Pathum-Thani, Thailand[...]
New Partnership with Texas A&M University-Kingsville (Texas, U.S.A)
University of Fukui has newly established an academic exchange agreement with Texas A&M University (Texas, U.S.A). W[...]
Opening Ceremony of "Japanese Culture Experience Program" for UCLAN students (U.K.) was held
On June 12, Opening Ceremony of "Japanese Culture Experience Program 2018" for 8 students from the University of Central[...]
New Partnership with National Chi Nan University (Nantou County, Taiwan)
University of Fukui has newly established an academic exchange agreement with National Chi Nan University (Nantou County[...]
New Partnership with Dixie State University (Utah, U.S.A.)
University of Fukui has newly established an academic exchange agreement with Dixie State University (Utah, U.S.A.). We [...]
2018 Spring Semester "International Student Orientation" and "Welcome Party" were held
2018 Spring Semester International Student Orientation was held from April 2 to April 6, 2018. This orientation is aimed[...]
米国ラトガース大学と本学が学生交換協定を締結しました
4月19、20日の両日、眞弓光文学長の一行が、米国・ニューブランズウィック市(ニュージャージー州)にあるラトガース大学を本学学長としては37年振りに訪問し、学生交換協定(an Agreement of Cooperation to Esta[...]
2019 Guidelines for application to GCS for privately financed international students
Please refer to the page for entrance examination information in 2019 academic year as below ◎Student Application Gui[...]
New Partnership with Faculty of Health, Birmingham City University (United Kingdom)
Faculty of Medical Sciences, University of Fukui has newly established the academic exchange agreement with Faculty of H[...]
New Partnership with Chiang Mai University (Chiang Mai, Thailand)
University of Fukui has newly established an academic exchange agreement with Chiang Mai University (Chiang Mai, Thailan[...]


I am a storyteller and filmmaker who specializes in creating engaging, quality media on cost effective budgets. My work has shown in festivals across the U.S. and internationally. I approach storytelling from a place of discovery...bringing distinct perspective, voice and visuals to projects that entertain and provoke discussion.
I aim to create a singular style for each project, highlighting the aesthetics and tone that make that particular story world interesting. Because I am experienced with the key creative roles in filmmaking – writing, producing, directing and editing – I bring an independent and holistic approach to filmmaking. When projects need to be scaled up, I draw from a roster of co-producers, cinematographers, production designers and other collaborators. I believe in cultivating diverse and inclusive productions with leadership that encourages everyone to contribute their best.
My unique insights and humor allow me to explore challenging subjects in a way that makes them accessible and engaging. And I'm often told I have a knack for finding the perfect music to complement the visuals.
My work speaks to clients who want to break past traditional messaging and engage with audiences in new and imaginative ways. Are you looking to create a promotional video with a progressive edge? Do you want to develop a web series to generate buzz about your product? Do you have a difficult topic that requires a new approach? I will help you create the unique videos you want on the timeline and budget you have.
I can be reached via the contact page.
" Humor is the affectionate communication of insight "
Andy delivered in spades! The camera work, directing and editing are impeccable, and the vision of each video definitely came through. I trusted him and it paid off.
Andy knows how to tell a story – all the key moments are seamlessly cut together with good transitions, pace and arc. Music tracks, titles and graphics are thought out and executed nicely.
Andy was instrumental in our success – an excellent editor with remarkable ingenuity and instinct! His charm and undeniable skills are superb. Adamantly recommended.
Surpassed all my expectations! Andy took challenging footage and made it look absolutely terrific. Working with him remotely was seamless and his turnaround time was fast.
Folsom Street Events wanted to create two original, narrative videos to promote the 2016 Folsom Street Fair and its official dance party ("Magnitude").
I brainstormed several concepts for the client based on their messaging goals. For the main Folsom Street Fair promo (shown above), they picked my "vintage sitcom" idea. And for the Magnitude dance party promo, they went with my idea about the crazy things we might think about when anticipating a big night out. The client was very excited about the finished scripts, so I began assembling my production team. Producing, casting and filming two shorts back to back is a huge challenge in and of itself. Doing so on a micro-budget in a matter of weeks requires quick thinking, creative solutions and a lot of favors. So with my producing partner, we quickly put together a game plan for budgeting, scheduling, crewing, casting, production design and filming.
Completing production and post-production on two separate shorts took everything we had: 18 hour work days, sleepless nights, tag-team collaboration, and constant revisions to our approach as we faced one hurdle after another (including last minute location changes, actors dropping out, a huge switch in the art direction, etc). But positive attitude and perseverance go a very long way. Filming was an exercise in controlled chaos, and editing was a particular challenge because we hadn't been able to get all the shots in our ambitious agenda. However, with unwavering dedication and a supportive crew, I was able to pull together two stylized and quirky ensemble pieces that fulfilled the intentions of the scripts and the client goals – all on a tight-budget.
The client absolutely loved the finished videos, each of which received well over 10,000 views on their Vimeo page within days of launch. Feedback on social media has been overwhelmingly positive, with comments such as "Tears pouring out of my eyes from laughter," "Knocked it out of the park!" and "Absolutely stunning."
" The key to wisdom is this – constant and frequent questioning "
Behind every story is another story: how it got made.
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" Film is the best option if you actually want to change the world, not just re-decorate it. "
Feedback? Looking for consultation or assistance in writing, directing, producing or post-production?
@crazyjulieta @Madonna @maluma Why were you irritated?