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Cornea delayed

Friedbender, M.H. and Dvorak, H.F. (1977). Morphology of delayed type hypersensitivity reactions in the guinea pig cornea. J. Immunol. 118, 1558-1566. [Pg.140]

Symptoms of exposure Strong lachrymator and nasal irritant. Eye contact may damage cornea. Skin contact may cause delayed pulmonary edema (Patnaik, 1992). An irritation concentration of 1.25 mg/m in air was reported by Ruth (1986). Inhalation of acrolein at a concentration of 153 ppm for 10 min resulted in death (quoted, Verschueren, 1983). [Pg.75]

Exposure for a short period of time to mist or diffused spray may cause stinging of the eyes and lacrimation. Splashes of the liquid in the eyes may cause severe damage including ulceration of the cornea there may be a delayed appearance of damage to the eyes, and corneal ulceration has, on rare occasions, appeared even a week or more after exposure. ... [Pg.392]

A solution of rhodium trichloride in the eye of a rabbit gave a delayed injurious reaction 0.1 mg of solution adjusted to pH 7.2 with ammonium hydroxide was placed for 10 minutes in a rabbit eye after the corneal epithelium had been removed an orange coloration of the cornea occurred that faded to faint yellow within 8 weeks. During the first 2-3 weeks, the cornea was slightly hazy in the third week, white opacities gradually developed and, finally, there was extensive opacification and vascularization. [Pg.619]

The epithelium, the most superficial cellular layer of the cornea of the eye, is chemically less resistant than the keratinized epidermis of the skin. However, during ocular accidents, we know that it takes a few seconds for the first lesions to appear. This delay is bound to multiple factors, winking reflex, protective and diluting effect of the lachrymal liquid, effect of sweeping of the palpebral movements. After a short period, a kinetic of diffusion will set up in a variable way according to the nature of the corrosive. [Pg.42]

Solids have a delay effect because they need to dissolve in the lacrymal fluid before reacting with the cornea. A solid form will aggravate the contact not only by its remanence at depth but also by the difficulty of extraction. [Pg.114]

Javadi, M., Yazdani, S., Kanavi, M., Mohammadpour, M., Baradaran-Rafiee, A., Jafarinasab, M., Einollahi, B., Karimian, F., Zare, M., Naderi, M., Rabei, H. (2007). Long-term outcomes of penetrating keratoplasty in chronic and delayed mustard gas keratitis. Cornea 26 1074-8. [Pg.592]

The ocular side effects of corticosteroids are many and are related to the route of administration. The most common concerns are increased intraocular pressure (lOP) and cataracts, but delayed epithelial woimd healing and increased risk of infection due to immime modulation and decreased tear lysozyme levels are issues for the cornea. Changes to other ocular tissues have been noted (subconjunctival hemorrhages, blue sclera, eyelid hyperemia and edema, retinal emboUc events, central serous choroidopathy) and neurologic compUcations reported (diplopia, nerve palsies, intracranial hypertension) (see Appendix 35-1). [Pg.705]

In tests performed on rabbits. Lewisite caused almost immediate edema of the lids, conjunctiva, and cornea as well as, early and severe involvement of the iris and ciliary body followed by gradual depigmentation and shrinkage of the iris stroma (Mann et al., 1946). Miosis appeared early. In this same study, miosis was not noted after mustard exposure. No long-term effects of Lewisite were noted, such as the delayed keratitis seen after mustard. [Pg.308]

One of the most distressing effects of exposure to sulphur mustard, which appears after a considerable delay, is late onset blindness associated with keratitis of the cornea. This was reported in cases of World War I mustard exposure during the 1920s and 1930s the exact explanation for this effect seems unclear. Damage to the nerve endings of the cornea reflected in comeal anaesthesia seems to play a part. [Pg.392]

Cnmene hydroperoxide is a mild to moderate skin irritant on rabbits. Snbcntaneons application exhibited a strong delayed reaction with symptoms of erythema and edema (Floyd and Stockinger 1958). Strong soln-tions can irritate the eyes severely, affecting the cornea and iris. [Pg.729]

Individuals who sustain acute ocular injury due to high-dose mustard exposure may experience difficulties even after the initial effects of the injury have subsided.109 112 Recurrent or persistent corneal ulceration can occur after latent periods of 10 to 25 years. This delayed keratopathy111113 may be accompanied by chronic conjunctivitis and corneal clouding. Anecdotal accounts suggest that low-dose exposure also causes increased sensitivity to later exposures to mustard,114 although the existence of increased sensitivity is difficult to substantiate with available scientific evidence.6 About 10% of those with eye injury in World War I had severely affected eyes, with both the cornea and the conjunctiva be-... [Pg.238]

Contact of the skin with Lewisite or Mustard-Lewisite vapors or liquid will result in local pain, swelling, and rash, followed by blistering that might be delayed for hours. If Lewisite or Mustard-Lewisite vapors or liquid contact your eyes, you will suffer immediate pain and rapid svvelling. as well as seriou.s damage to the cornea and other parts of the eye. [Pg.149]

The role of the CO/HO axis in the control of cell proliferation and differentiation is still very poorly explored. Likewise, wound healing and tissue regeneration are two scientific niches where CO must be studied with much attention. There are few data about the role of CO on cellular proliferation/differentiation and most of the published data concern HO activity. HO-1 and HO-2 are involved in cornea wound healing HO-1 induction accelerates wound healing after epithelial injury [96] and deletion of HO-2 impairs re-epitheliaUzation delaying the repair response [97]. In the hepatic model, mice treated with CO presented higher levels of hepatocytic proliferation and enhanced expression of hepatocyte growth factor (HGF) after hepatectomy [98]. [Pg.204]


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