Delayed lactogenesis II: a comparison of four cases

Lactogenesis II is the onset of copious milk production (i.e., the milk "coming in"), which usually occurs between 30 to 40 hours postpartum. When lactogenesis II fails to occur or is delayed, it may be due to a number of underlying hormonal or non-hormonal conditions. Of the various hormonal etiologies, many can be identified with the aid of a few standard blood tests. Gestational ovarian theca lutein cysts may cause delayed lactogenesis II and are fairly easily detected by ordering testosterone levels. Although this condition can delay lactogenesis II for as long as 31 days, with proper management women affected by these cysts have established breastfeeding. Three of the four women reviewed in this article were eventually able to produce 100% of their infants' caloric requirements.     

Effects of Lutein on the Growth and Migration of Bovine Lens Epithelial Cells In Vitro

The effects of lutein on the growth and migration of bovine lens epithelial cells （BLECs） in vitro were observed in an attempt to find a drug that can prevent after-cataract. BLECs were cultured in vitro and different concentrations of lutein were added to the BLECs cultures of the second and third generations. The effects of lutein on the proliferation of BLECs in vitro were examined by the MTT method, and the migration of BLECs was evaluated by a scratch wound assay. The results showed that： （1） Lutein at concentrations of 1 to 16 μmol/L could inhibit the proliferation of BLECs in a dose-and time-dependent manner （P〈0.01）; （2） The migration of BLECs was evaluated by wound healing rate. As compared with the control group, the wound healing rate in the experimental groups was decreased from 0.672±0.164 to -0.234±0.144 and -0.597±0.063 （P〈0.01） at 1 and 2 μmol/L lutein, respectively. It was concluded that lutein at concentration of 〉1 μmol/L inhibited the proliferation and migration of BLECs in vitro, Lutein may become an effective drug to prevent after-cataract.     

叶黄素对视网膜光损伤的保护作用

叶黄素为类胡萝卜素之一,在人体内不能转化为维生素A。人体自身不能合成叶黄素,需要从食物中摄取。叶黄素和玉米黄质共同构成视网膜黄斑色素,是黄斑区唯一存在的两种类胡萝卜色素,能降低视网膜光损伤的程度。叶黄素对视网膜的保护机制主要为:(1)蓝光过滤器的作用,叶黄素对光损伤作用最大的蓝光具有很强的吸收作用;(2)抗氧化作用;叶黄素可以灭活单线态氧和捕获活性氧自由基。     

Nutritional manipulation of primate retinas. IV. Effects of n--3 fatty acids, lutein, and zeaxanthin on S-cones and rods in the foveal region

Lutein and zeaxanthin are xanthophylls selectively accumulated by primate retinas that may protect the macula from age-related macular degeneration. In this project, we manipulated n-3 fatty acids, lutein and/or zeaxanthin levels in the diet and studied their possible outcome on S-cone and rod cell density in the foveal region. Rhesus monkeys (7-16 year, n=17) were fed from birth xanthophyll-free semipurified diets with either adequate or low n-3 fatty acids. Five monkeys were supplemented with lutein and six with zeaxanthin for 6-24 months, while six remained xanthophyll-free until sacrifice. Retinas were embedded in methacrylate and serial 2 microm sections were cut along the vertical meridian. Rod nuclei, and immuno-labelled outer segments of S-cones and rods, were reconstructed and counted in an 8 microm strip. The density profiles were compared with data from control monkeys (n=7) fed a standard laboratory diet. S-cone density profiles were symmetrical along the vertical meridian and the densities decreased rapidly with retinal eccentricity. Rod densities were higher in the superior region than the inferior region in most of the control and experimental animals. Unlike the significant effects observed for retinal pigment epithelial cells of these same monkeys (Leung, I.Y-F., Sandstrom, M.M., Zucker, C.L., Neuringer, M., Snodderly, D.M., 2004. Nutritional manipulation of primate retinas. II. Effects of age, n-3 fatty acids, lutein, and zeaxanthin on retinal pigment epithelium. Invest. Ophthalmol. Vis. Sci. 45, 3244-3256), neither xanthophyll supplementation nor low dietary n-3 fatty acids produced consistent effects on S-cone or rod density profiles of the experimental animals. However, monkeys low in n-3 fatty acids had increased variability of S-cone density in the fovea and low density of foveal rod outer segments. The high variability suggests that the photoreceptors of some animals were resistant to the nutritional manipulations, while others may have been affected. Thus, the photoreceptors appear less sensitive than the retinal pigment epithelium to these nutritional manipulations. However, it is possible that more consistent effects would emerge at a later age or after exposure to stressors such as high light levels.     

Long term dietary supplementation with zeaxanthin reduces photoreceptor death in light-damaged Japanese quail

The purpose of these studies was to evaluate the effects of light damage on Japanese quail whose retinal carotenoids had been experimentally manipulated through altered diets. The birds were raised 6 months on a commercial turkey diet (T), on a custom carotenoid-deficient diet (C-) containing 90% less carotenoid than the T diet, or on Z+ diet [the C- diet supplemented with natural zeaxanthin (35mgkg(-1) food)]. Equal numbers of males and females on each diet were exposed to nine intervals (1hr on, 2hr off) of 3200lux cool white light, then placed in the dark for 14hr before tissue collection. One retina was immediately frozen for HPLC analysis; the other eye was immediately fixed and processed for microscopy. There were no significant differences in the retinal carotenoid concentrations in hatch-mates that were and were not exposed to light. Supplementation resulted in three- to four-fold increases in retinal zeaxanthin and no change in retinal lutein or alpha-tocopherol, but the C- diet did not reduce the retinal carotenoid concentration in C- birds below that in T birds. The light-exposed retinas had significant numbers of apoptotic photoreceptors and photoreceptor ghosts. The number of ghosts was negatively correlated with the number of dying photoreceptors (P<0.05), and with retinal concentrations of zeaxanthin, alpha-tocopherol or gamma-tocopherol (P<0.04, 0.02, 0.04, respectively), but not with lutein. The number of dying photoreceptors was positively correlated with alpha-tocopherol and the sum alpha-tocopherol plus zeaxanthin (P<0.1; P0.04). Photoreceptor death was semi-quantitatively scored, assuming that ghosts were formed by removal of apoptotic photoreceptors with nuclear condensation. Stepwise regression produced a good model (r(2)=0.67;P <0.0001) for predicting death scores from retinal concentrations of zeaxanthin (Standard Coefficient=-0.76) and lutein (Standard Coefficients=+0.43). Absence of lutein in gender-specific analyses suggests lutein served as surrogate marker for gender. Combined analysis of the C- and T birds also demonstrated that dying photoreceptors were negatively correlated with retinal zeaxanthin. These data confirm our previous report that retinal carotenoids prevent photoreceptor cell death, and provide the first direct evidence that retinal zeaxanthin protects photoreceptors from light-induced death.     

Macular pigment and lutein supplementation in choroideremia

Choroideremia is an incurable X-linked retinal degeneration caused by mutations in the gene encoding Rab escort protein-1. A group of clinically defined and genotyped patients were studied to determine: (1) the degree of rod and cone dysfunction and structural abnormality in the central retina and the level of macular pigment; and (2) the response of macular pigment and foveal vision to a 6 month trial of supplementation with oral lutein (at 20 mg per day). Rod and cone-mediated function was measured with dark-adapted static perimetry; in vivo retinal structure was determined with optical coherence tomography; and macular pigment optical density was measured with heterochromatic flicker photometry. In this cohort of patients (ages 15-65 years), both rod- and cone-mediated central function declined with age as did central retinal thickness. Macular pigment levels did not differ between patients and male control subjects. Supplementation of oral lutein in a subset of patients led to an increase in serum lutein and macular pigment levels; absolute foveal sensitivity did not change. It is concluded that macular pigment density can be augmented by oral intake of lutein in patients with choroideremia. There was no short-term change in the central vision of the patients on the supplement, but long-term influences of lutein supplementation on disease natural history warrant further study.     

叶黄素对二甲基甲酰胺所致小鼠急性肝损伤的保护作用

目的:用生化及病理学方法研究叶黄素对二甲基甲酰胺(DMF)所致小鼠急性肝损伤的保护作用。方法:将48只小鼠随机分为4组,分别为对照组、DMF模型组、20mg/kg及40mg/kg叶黄素处理组。小鼠连续灌胃叶黄素5天,对照组和DMF模型组给予等体积玉米油。灌胃叶黄素3天后,除对照组腹腔注射生理盐水,其余三组均一次性腹腔注射1.5g/kg DMF。DMF染毒48h后,所有动物内眦取血,处死后剖取肝脏,检测其AST、ALT等指标。结果:DMF模型组小鼠血清ALT和AST活性显著升高,肝脏组织匀浆中MDA含量明显增加,SOD活性升高。叶黄素可降低血清AST及ALT活性及肝组织SOD活性、MDA水平,改善肝脏损伤小鼠病理组织学变化。结论:叶黄素通过抗氧化作用对DMF所致肝脏毒性具有一定保护作用。     

叶黄素对顺铂所致大鼠急性肝损伤的防治作用

目的:观察叶黄素(LU)对顺铂(CP)诱导的大鼠急性肝损伤的保护作用。方法:将30只SD大鼠随机分为5组,分别为对照组、顺铂组、不同剂量叶黄素(10mg/kg、20mg/kg和40mg/kg)+顺铂组。大鼠连续灌胃叶黄素10天,第7天灌胃后l h腹腔注射顺铂(5mg/kg)。顺铂处理后,在第5天采血,测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)。采血后处死动物,测定肝脏系数、肝匀浆丙二醛(MDA)、一氧化氮(NO)、还原型谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)活力,同时观察肝组织结构变化。结果:肝损伤模型组大鼠血清ALT、AST含量均明显高于对照组,肝组织匀浆中MDA及NO含量显著增加,而GSH含量及SOD活性显著下降。叶黄素可降低肝损伤大鼠血清ALT及AST水平,降低肝组织匀浆MDA及NO水平,提高组织GSH含量及SOD活性,并可改善顺铂损伤大鼠肝病理组织学变化,随着叶黄素剂量增加,其保护作用增强。结论:叶黄素通过抗氧化作用减轻顺铂诱导的大鼠肝损伤作用。     

Heritability of the spatial distribution and peak density of macular pigment: a classical twin study

Purpose

To elucidate the heritability of peak density and spatial width of macular pigment (MP) using a Classical Twin Study.

Methods

Fundus autofluorescence images were obtained at 488 nm from 86 subjects or 43 twin pairs (21 monozygotic (MZ) and 22 dizygotic (DZ)) (27 male, 59 female) aged from 55 to 76 years (mean 62.2±5.3 years). The relative topographic distribution of MP was measured using a grey scale of intensity (0–255 units) in a 7° eccentricity around the fovea. Relative peak MP density (rPMPD) and relative spatial distribution of MP (rSDMP) were used as the main outcome measure in the statistical analysis.

Results

A significantly higher correlation was found within MZ pairs as compared with that within DZ pairs for rPMPD, (r=0.99, 95% confidence interval (95% CI) 0.93 to 1.00) and 0.22, 95% CI −0.34 to 0.71), respectively, suggesting strong heritability of this trait. When rSDMP was compared, there was no significant difference between the correlations within MZ pairs (r=0.48, 95% CI −0.02 to 0.83) and DZ pairs (r=0.63, 95% CI 0.32 to 0.83), thus rSDMP is unlikely to have a considerable heritable component. In addition, there was no difference between any MP parameter when normal maculae were compared with early age-related macular degeneration (AMD) (rPMPD 0.36 vs 0.34, t=1.18 P=0.243, rSDMP 1.75 vs 1.75, t=0.028 P=0.977).

Conclusions

rPMPD is a strongly heritable trait whereas rSDMP has minimal genetic influence and a greater influence by environmental factors. The presence of macular changes associated with early AMD did not appear to influence any of these pigment parameters.     

Macular pigment optical density in wet age-related macular degeneration among Indians

PurposeTo estimate the value of macular pigment optical density (MPOD) in adult south Indian population with wet age-related macular degeneration (AMD).MethodsA total of 33 patients with wet AMD and 29 age-matched controls >50 years of age underwent MPOD measurement with the macular densitometer. The patients were also tested for their dietary intake of carotenoids, smoking history, and lifetime UV exposure.ResultsThe mean MPOD values in the Indian population with wet AMD was 0.23 (95% CI: 0.18-0.29) vs control was 0.43 (95% CI: 0.37-0.49), P<0.0001, at 0.5° eccentricity. Ex-smokers had a lower MPOD than non-smokers (0.16 (0.09-0.23) vs 0.28 (0.22-0.34), P=0.026) and the lowest level of carotenoids intake had 48% lower MPOD than the highest level (0.14 (0.08-0.21) vs 0.33 (0.24-0.43), P=0.012). There was no significant age-related decline or gender variation in MPOD.ConclusionThis study establishes the MPOD in adult Indian population with wet AMD, with a lack of macular pigment in association with wet AMD.