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Pericytes are distinctive regulators of angiogenesis and are adumbrated to provide vessel stability and control of endothelial proliferation. The present article spotlights the persona of pericytes in physiological angiogenesis, recruitment of pericytes and different mechanisms of pericyte depletion. Developing retina appears particularly dependent on pericytes, and pericyte loss is considered as hallmark of early diabetic retinopathies. Several factors are contemplated to be engaged in pericyte conscription including angiopoietin-1 and its receptor tyrosine kinase Tie-2, vascular endothelial growth factor-A and its receptor flk-1 and the platelet-derived growth factor PDGF-B/PDGF-beta system. At present, the mechanisms by which diabetes persuade apoptosis in the retinal microvasculature remain indecisive, albeit oxidative stress, formation of advanced glycation end products , upregulation of protein kinase C, increased polyol pathway flux and focal leukostasis may be important. In this context, accelerated microvascular cell death may become a constructive surrogate end-point in pharmacological studies of experimental diabetic.

PurposeIn the present study, the visual discomfort induced by smart mobile devices was assessed in normal and healthy adults.MethodsFifty-nine volunteers (age, 38.16 ± 10.23 years; male : female = 19 : 40) were exposed to tablet computer screen stimuli (iPad Air, Apple Inc.) for 1 hour. Participants watched a movie or played a computer game on the tablet computer. Visual fatigue and discomfort were assessed using an asthenopia questionnaire, tear film break-up time, and total ocular wavefront aberration before and after viewing smart mobile devices.ResultsBased on the questionnaire, viewing smart mobile devices for 1 hour significantly increased mean total asthenopia score from 19.59 ± 8.58 to 22.68 ± 9.39 (p < 0.001). Specifically, the scores for five items (tired eyes, sore/aching eyes, irritated eyes, watery eyes, and hot/burning eye) were significantly increased by viewing smart mobile devices. Tear film break-up time significantly decreased from 5.09 ± 1.52 seconds to 4.63 ± 1.34 seconds (p = 0.003). However, total ocular wavefront aberration was unchanged.ConclusionsVisual fatigue and discomfort were significantly induced by viewing smart mobile devices, even though the devices were equipped with state-of-the-art display technology.

PurposeEsophageal candidiasis (EC) is the most frequent opportunistic fungal infection in immunocompromised host. However, we have found EC in healthy individuals through esophagogastroduodenoscopy (EGD). The aim of this study was to determine the prevalence and risk factors for EC in healthy individuals.Materials and MethodsWe retrospectively reviewed the medical records of 281 patients who had been incidentally diagnosed with EC. We also conducted age and sex matched case control study to identify the risk factor for EC.ResultsThe prevalence of EC was 0.32% (281/88125). The most common coexisting EGD finding was reflux esophagitis (49/281, 17.4%). An antifungal agent was prescribed in about half of EC, 139 cases (49.5%). Follow-up EGD was undertaken in 83 cases (29.5%) and 20 cases of candidiasis was persistently found. Case control study revealed EC were more often found in user of antibiotics (p=0.015), corticosteroids (p=0.002) and herb medication (p=0.006) as well as heavy drinking (p<0.001).ConclusionThe prevalence of EC was 0.32% (281/88125) in Korea. Use of antibiotics, corticosteroids and herb as well as heavy drinking were significant risk factors for EC in healthy individuals.

Vitamin D may play a role in glucose metabolism. A low vitamin D level has been associated with increased risk of diabetes mellitus, but the association has not been confirmed in Asians. Our objective was to examine the association of serum 25-hydroxyvitamin D [25(OH)D] levels with insulin resistance and diabetes mellitus in Korean adults based on a large population-based survey. Cross-sectional analyses were carried out on 5787 Korean adults (2453 men and 3334 women) who were 20 y or older and participated in the Fourth Korea NHANES conducted in 2008. Diabetes mellitus was defined as fasting plasma glucose ≥7 mmol/L or current use of oral hypoglycemic agents or insulin. Insulin resistance was estimated by homeostatic model assessment for insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI). Compared to individuals with a sufficient serum 25(OH)D concentration ≥75 nmol/L, the OR (95% CI) for diabetes mellitus were 1.73 (1.09-2.74), 1.30 (0.91-1.84), and 1.40 (0.99-1.98) for serum 25(OH)D concentrations <25, 25 to <50, and 50 to <75 nmol/L, respectively, after multiple adjustments (P-trend < 0.0001). Furthermore, the serum 25(OH)D level was inversely associated with HOMA-IR (β = -0.061; P = 0.001) and positively associated with QUICKI (β = 0.059; P = 0.001) in overweight or obese participants. In conclusion, a low serum vitamin D concentration is associated with a high risk of diabetes mellitus in Korean adults and the concentration is inversely associated with insulin resistance in those who are overweight or obese.

Recent episodes of severe air pollution in eastern Asia have been reported in the scientific literature and news media. Therefore, there is growing concern about the systemic effects of air pollution on human health. Along with the other well-known harmful effects of air pollution, recently, several animal models have provided strong evidence that air pollutants can induce liver toxicity and act to accelerate liver inflammation and steatosis. This review briefly describes examples where exposure to air pollutants was involved in liver toxicity, focusing on how particulate matter (PM) or carbon black (CB) may be translocated from lung to liver and what liver diseases are closely associated with these air pollutants.

Toll-like receptor 7 (TLR7) signaling predominantly regulates production of type I Interferons (IFNs), which has been suggested in clinical studies to be anti-fibrotic. However, the mechanistic role of the TLR7-type I IFN axis in liver fibrosis has not been elucidated. In the present study, liver fibrosis was induced in wild-type (WT), TLR7-deficient, and IFN-α/β receptor-1 (IFNAR1)-deficient mice and TLR7-mediated signaling was assessed in liver cells isolated from these mice. TLR7-deficient and IFNAR1-deficient mice were more susceptible to liver fibrosis than WT mice, indicating that TLR7-type I IFN signaling exerts a protective effect against liver fibrosis. Notably, the hepatic expression of IL-1ra was suppressed in TLR7- or IFNAR1-deficient mice compared with respective WT mice, and treatment with recombinant IL-1ra reduced liver fibrosis. In vivo activation of TLR7 significantly increased IFNa4 and IL-1ra expression in the liver. Interestingly, each cytokine had different cellular source showing that dendritic cells (DCs) are responsible cell type for production of type I IFN, while Kupffer cells (KCs) mainly produce IL-1ra in response to type I IFN. Furthermore, TLR7 activation by R848 injection suppressed liver fibrosis and production of pro-inflammatory cytokines, and these effects were dependent on type I IFN signaling. Consistent with in vivo data, IFNα significantly induced IL-1ra production in primary KCs. Conclusions TLR7 signaling activates DCs to produce type I IFN, which in turn induces anti-fibrogenic IL-1ra production in KCs. Thus, manipulation of the TLR7-type I IFN-IL-1ra axis may be a new therapeutic strategy for the treatment of liver fibrosis.

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