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Comment |
Itchy-dry eye associated with polycystic ovary syndrome. Bonini S et al. (2007) The authors aimed to define the ocular symptomatology of women with polycystic ovaries and hyperandrogenism. Prospective, observational case series. Of the 62 consecutive patients with an ultrasonographic diagnosis of polycystic ovary (PCO), 16 were identified as having clinical and biochemical signs of hyperandrogenism. All women with a history of ocular symptoms (20/62 total patients [32.3%], 15/16 polycystic ovary syndrome (PCOS) patients [93.7%], and 5/46 PCO patients [10.8%]) underwent a complete eye examination with conjunctival impression cytologic sampling. Clinical measurements of tear function (tear film break-up time [BUT], Schirmer I test) were completed along with analysis of conjunctival goblet cell number, conjunctival immunostaining, and reverse-transcriptase polymerase chain reaction for the mucins MUC1 and MUC5AC. Clinical, histologic, and biochemical data of patients with PCOS were compared statistically with that of patients with PCO and with eight age- and gender-matched healthy controls. Eight of the most severely affected patients received systemic antiandrogen therapy and underwent further ocular evaluation four months after systemic therapy. Women with PCOS had greater conjunctival hyperemia (P < .001), dryness (P < .001), itching (P < .001), mucous discharge (P < .001), and contact lens intolerance (P < .001) than patients with PCO. Patients with PCOS had a significant reduction of the tear film BUT accompanied by a significant increase in goblet cell number and conjunctival MUC5AC messenger ribonucleic acid expression compared with both PCO patients and healthy subjects. Evaluation of the ocular surface should be considered in patients with PCO or PCOS. Women with PCOS were more likely to have itchy-dry eyes, decreased tear film BUT, and increased goblet cell density.//////////////////
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Mutations |
1 mutations
Species: mouse
Mutation name: None
type: null mutation
fertility: fertile
Comment: Muc5ac: a critical component mediating the rejection of enteric nematodes. Hasnain SZ et al. De novo expression of Muc5ac, a mucin not normally expressed in the intestinal tract, is induced in the cecum of mice resistant to Trichuris muris infection. In this study, we investigated the role of Muc5ac, which is detected shortly before worm expulsion and is associated with the production of interleukin-13 (IL-13), in resistance to this nematode. Muc5ac-deficient mice were incapable of expelling T. muris from the intestine and harbored long-term chronic infections, despite developing strong T(H)2 responses. Muc5ac-deficient mice had elevated levels of IL-13 and, surprisingly, an increase in the T(H)1 cytokine IFN-?. Because T(H)1 inflammation is thought to favor chronic nematode infection, IFN-? was neutralized in vivo, resulting in an even stronger T(H)2-type immune response. Nevertheless, despite a more robust T(H)2 effector response, the Muc5ac-deficient mice remained highly susceptible to chronic T. muris infection. Importantly, human MUC5AC had a direct detrimental effect on nematode vitality. Moreover, the absence of Muc5ac caused a significant delay in the expulsion of two other gut-dwelling nematodes (Trichinella spiralis and Nippostrongylus brasiliensis). Thus, for the first time, we identify a single mucin, Muc5ac, as a direct and critical mediator of resistance during intestinal nematode infection.
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