298 research outputs found

    Protecting the Aging Retina

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    Aging retina, notably the aging macula, is prone to develop degenerative diseases, such as age-related macular degeneration (AMD), the leading cause of visual loss in individuals aged 65 or above in developed countries. However, current treatments are very limited. Since degeneration, dysfunction, and death of retinal neurons are demonstrated in the pathogenesis of AMD, neuroprotective strategies could serve as a possible way to treat AMD. In this chapter, we will briefly introduce risk factors, pathophysiology, affected neurons, classification, clinical manifestation, and current treatments of AMD. Finally, neuroprotection in both AMD animal models and patients will be discussed

    Lutein and the Aging Eye

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    Lutein is a carotenoid highly concentrated in the macula of the retina. Lutein cannot be synthesized and must be supplied in the diet, for example, dark green leafy vegetable and egg yolk. Lutein is believed to absorb blue light, leading to the protection of retina from light-related damage. It can also protect the retina against oxidative stress and inflammation. In fact, dietary and supplementary lutein have been shown to be associated with possible reduced risk of age-related macular degeneration, a leading cause of elderly blindness, attributed largely to lutein’s antioxidant properties. Lutein is also beneficial as a nutritional supplement in preventing diabetic retinopathy. Moreover, lutein is very safe and widely used. In this chapter, we will discuss the basic chemistry of lutein; its uptake, transport, distribution, and functions in the normal eye. Lastly, the effects of lutein in age-related eye diseases will be summarized

    Animal Models of Diabetic Retinopathy (Part 2)

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    Diabetic retinopathy (DR) is one of the leading causes of preventable vision impairment and blindness in the working-age population worldwide. Numerous animal models have been developed for therapeutic drug screening and to further increase our understanding of the molecular and cellular pathological processes involved in DR. Following our discussion of mouse models in “Animal Models of Diabetic Retinopathy Part 1,” we describe the cellular, molecular, and morphological features of both rodent and nonrodent models of DR and their respective advantages and limitations in this chapter. To date, no animal model can holistically reproduce the pathological progression of human DR; most only display early or advanced lesions of DR. However, a thorough understanding of genotypic and phenotypic expressions of existing models will facilitate researchers’ selection of the appropriate model to simulate their desired clinical scenarios

    Cut Diagrams for High Energy Scatterings

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    A new approach is introduced to study QCD amplitudes at high energy and comparatively small momentum transfer. Novel cut diagrams, representing resummation of Feynman diagrams, are used to simplify calculation and to avoid delicate cancellations encountered in the usual approach. Explicit calculation to the 6th order is carried out to demonstrate the advantage of cut diagrams over Feynman diagrams.Comment: uu-encoded file containing a latex manuscript with 14 postscript figure

    Identification of essential histidine residues in a recombinant alpha-amylase of thermophilic and alkaliphilic Bacillus sp strain TS-23

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    To understand the structure-function relationships of a truncated Bacillus sp. strain TS-23 alpha-amylase, each of His-137, His-191, His-239, His-269, His-305, His-323, His-361, His-436, and His-475 was replaced with leucine. The molecular masses of the purified wild-type and mutant enzymes were approximately 54 kDa. The specific activity of His323Leu and His436Leu was decreased by more than 52%, while His239Leu, His305Leu, and His475Leu showed activity similar to that of the wild-type enzyme. As compared with the wild-type enzyme, His323Leu and His436Leu exhibited a 62% decrease in the value of k(cat)/K-m. Alterations in His-191, His-239, His-305, and His-475 did not cause a significant change in the K-m or k(cat) values. At 70degreesC, a decreased half-life was observed in His436Leu. These results indicate that His-137, His-269, and His-361 of Bacillus sp. strain TS-23 alpha-amylase are important for proper catalytic activity and that His-436 may contribute to the thermostability of the enzyme

    Visiting urban green space as a climate-change adaptation strategy: Exploring push factors in a push–pull framework

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    Urban green space (UGS) offers users multiple ecosystem services and amenities. This study investigated whether residents used UGS visitation in summer as a sustainable measure to tackle hot weather and associated climate-change impacts in humid-subtropical Hong Kong. Attributes of the indoor residential environment, seldom examined in park-visitation studies, were evaluated as push factors to visit UGS through a push–pull theoretical framework. A questionnaire survey of 483 respondents targeted urban park users. The results indicated that UGS visit frequency and stay duration were relatively low in hot summer. Ordinal multiple regression showed that indoor living conditions, residence location, living routine, and habit and personal health impacts were significantly correlated with UGS visits. Interdependence between push and pull factors was detected, demonstrating that intrinsic UGS environmental conditions could constrain UGS visits despite the motivations of push factors. The results indicated the need to improve the microclimate-regulating function in UGS. It could be achieved mainly by optimizing the nature-based design to promote UGS as an adaptive measure to combat the thermal stress brought by climate change. The findings yielded hints to shape visiting habits and suggestions to improve UGS management

    Genes for tesin, villin and desmin are linked on mouse Chromosome 1

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47016/1/335_2004_Article_BF00354299.pd

    Ischemic Tolerance Protects the Rat Retina from Glaucomatous Damage

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    Glaucoma is a leading cause of acquired blindness which may involve an ischemic-like insult to retinal ganglion cells and optic nerve head. We investigated the effect of a weekly application of brief ischemia pulses (ischemic conditioning) on the rat retinal damage induced by experimental glaucoma. Glaucoma was induced by weekly injections of chondroitin sulfate (CS) in the rat eye anterior chamber. Retinal ischemia was induced by increasing intraocular pressure to 120 mmHg for 5 min; this maneuver started after 6 weekly injections of vehicle or CS and was weekly repeated in one eye, while the contralateral eye was submitted to a sham procedure. Glaucoma was evaluated in terms of: i) intraocular pressure (IOP), ii) retinal function (electroretinogram (ERG)), iii) visual pathway function (visual evoked potentials, (VEPs)) iv) histology of the retina and optic nerve head. Retinal thiobarbituric acid substances levels were assessed as an index of lipid peroxidation. Ischemic conditioning significantly preserved ERG, VEPs, as well as retinal and optic nerve head structure from glaucomatous damage, without changes in IOP. Moreover, ischemia pulses abrogated the increase in lipid peroxidation induced by experimental glaucoma. These results indicate that induction of ischemic tolerance could constitute a fertile avenue for the development of new therapeutic strategies in glaucoma treatment
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