bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accumulation of lipid peroxide in the content of comedones may be involved in the progression of comedogenesis and inflammatory changes in comedones
Authors: Tochio Takumi , Tanaka Hiroshi , Nakata Satoru , Ikeno Hiroshi 
Published: June 2009

SummaryBackground  Previous studies reported that lipid peroxide (LPO) caused by oxidation of sebum is associated with the progression of acne vulgaris, and that therapy with antioxidative ingredients is efficacious for treatment. In this study, we hypothesized that lipid accumulation in comedones induces progression of comedogenesis and inflammatory changes in comedones, and investigated the possible role of accumulated LPO in comedogenesis and its inflammatory changes.Methods  We first sampled comedones and the stratum corneum from patients with acne vulgaris. The quantities of LPO, interleukin‐1‐alpha (IL‐1α), and NF‐kappa‐B (NF‐κB) in comedones and in the stratum corneum from each patient were measured for comparison. Next, comedones were sampled again from the same patients and classified into five groups: microcomedo (MC), noninflammatory open comedo (NIOC), noninflammatory closed comedo (NICC), inflammatory open comedo (IOC), and inflammatory closed comedo (ICC). We measured quantities of LPO in each group.Results  The quantities of LPO, IL‐1α, and NF‐κB were significantly higher in the content of comedones than those in the stratum corneum. The quantities of LPO in the content of IOC and ICC were significantly higher than those of MC, NIOC, and NICC; however, there were no significant differences in quantities of LPO between the content of MC, NIOC, and NICC.Conclusions  We conclude that the accumulation of a certain amount of LPO in the content of comedones may play an important role in the progression of comedogenesis and the excessive accumulation of LPO may be involved in inflammatory changes in comedones.
Effects of a Brazilian herbal compound as a cosmetic eyecare for periorbital hyperchromia (“dark circles”)
Authors: Eberlin Samara , Del Carmen Velazquez Pereda Maria , De Campos Dieamant Gustavo , Nogueira Cecília , Werka Rejane Maria , De Souza Queiroz Mary Luci 
Published: June 2009

SummaryBackground Evidence suggests that periorbital hyperchromia (dark circles) occurs mainly as a consequence of postinflammatory hemodynamic congestion producing a typical bruising aspect on the lower eyelids.Aims To evaluate the clinical effects ofPfaffia paniculata/Ptychopetalum olacoidesB./Lilium candidumL.‐associated compound (PPLAC) on periorbital hyperchromia and to studyin vitroits underlying anti‐inflammatory and antioxidant mechanisms.Methods Twenty‐one volunteers presenting with periorbital hyperchromia received a serum sample containing 5.0% PPLAC, which was applied topically in the periorbital area twice a day for 28 days. Skin color was measured using variations in the individual typological angle (ΔITA0) and skin luminance (ΔL*) calculated in the area around the eyes and in the adjacent area. Colorimetric readings were taken at the onset and end of the 28‐day treatment. Volunteers were also asked to fill out a questionnaire concerning the improvement in “dark circles.” The anti‐inflammatory and antioxidant effects of PPLAC were measured by quantification of prostaglandin E2, leukotriene B4, histamine, and superoxide dismutase levels using anin vitromodel of human skin culture.Results Topical application of PPLAC led to a significant improvement in skin luminance and tone in the periorbital area, which was demonstrated by increased values of ITA0andL* in about 90% of volunteers. In addition, subjects reported reduced intensity and improved appearance of “dark circles.” A dose‐dependent decreased production of inflammatory mediators, concomitant to increased antioxidant enzyme levels, was observed in ourin vitrostudies, under basal and lipopolysaccharide‐stimulated conditions.Conclusions Although the precise mechanisms related to PPLAC remain to be clarified, our results indicate that the reduction in the inflammatory process as well as the antioxidant protection against deleterious elements may be considered as an integral approach to preserve the integrity of vascular endothelium, preventing the hemodynamic congestion that culminates in the formation of “dark circles” around the eyes.
Androgenetic alopecia in males: a histopathological and ultrastructural study
Authors: El‐Domyati Moetaz , Attia Sameh , Saleh Fatma , Abdel‐Wahab Hossam 
Published: June 2009

SummaryBackground  Androgenetic alopecia is a common cosmetic hair disorder, resulting from interplay of genetic, endocrine, and aging factors leading to a patterned follicular miniaturization. Microinflammation seems to be a potential active player in this process.Aims  To study the histopathological and ultrastructural changes occurring in male androgenetic alopecia (AGA).Patients/methods  Fifty‐five subjects were included in this study (40 with AGA and 15 as normal age‐matched controls). Skin biopsies from frontal bald area and occipital hairy area were subjected to histopathological examination, immunohistochemical staining for collagen I and ultrastructural study.Results  The frontal bald area of patients showed highly significant increase in telogen hairs and decrease in anagen/telogen ratio and terminal/vellus hair ratio (P < 0.001). Perifollicular inflammation was almost a constant feature in early cases and showed a significant inverse correlation with perifollicular fibrosis (P = 0.048), which was more marked with thickening of the follicular sheath in advanced cases.Conclusion  Follicular microinflammation plays an integral role in the pathogenesis of AGA in early cases. Over time, thickening of perifollicular sheath takes place due to increased deposition of collagen, resulting in marked perifollicular fibrosis, and sometimes ends by complete destruction of the affected follicles in advanced cases.
Effects of lipid nanocarriers on the performance of topical vehicles in vivo
Authors: Moddaresi Mojgan , Tamburic Slobodanka , Williams Stefanie , Jones Stuart A , Zhao Yanjun , Brown Marc B 
Published: June 2009

SummaryBackground/aims  Nanocarrier systems have been extensively studied for their suitability in personal care formulations. Theoretically, they could enhance skin delivery of active compounds, thereby improving in vivo efficacy of the products. As such the aim of this study was to evaluate the effect of a lipid nanocarrier (LNC) system loaded with tocopheryl acetate (TA) on the hydration, biomechanical properties, and antioxidant capacity of human skin, when used in two different vehicles, and compare it with a non‐LNC formulation.Methods  TA‐loaded lipid nanocarriers (TA‐LNCs) were produced by the phase inversion method, using physiological lipids and purified by ultra‐centrifugation. They were incorporated into a hydrophilic gel and foam, and their performance compared with a saturated TA solution in silicon oil. Skin hydration and biomechanical properties were measured by means of a corneometer and a cutometer, respectively, while a high‐resolution spectrophotometer was used to assess skin redness after stimulation by methyl nicotinate in a micro‐inflammatory test. Both short‐term (3 h) and long‐term trials (4 weeks) were performed.Results  The results confirmed that the LNCs enhanced skin hydration in both studies, while skin viscoelastic parameters remained practically unchanged during the 4‐week study. The antioxidant assessment failed to show significant difference between the test sites.Conclusions  TA‐loaded LNCs exhibited the ability to enhance skin hydration, while their effect on skin biomechanical properties and on antioxidant efficacy could not be statistically proved.
Micro‐island damage with a nonablative 1540‐nm Er:Glass fractional laser device in human skin
Authors: Farkas Jordan P , Richardson James A , Hoopman John , Brown Spencer A , Kenkel Jeffrey M 
Published: June 2009

SummaryBackground and objectives  Fractional photothermolysis produces micro‐islands of thermal injury to the skin while preserving areas among treated tissue sites in order to promote wound healing. Histological changes associated with single and multiple passes of the 1540‐nm Er:Glass fractional laser were examined using in vivo human skin.Methods and materials  Panni of five abdominoplasty patients were treated intraoperatively with a Fractional Lux1540 erbium glass laser system at various laser parameters, with single and multiple passes. Biopsies were removed and examined using standard histological stains.Results  Deep coagulated columns of collagen separated by regions of unaffected tissue were observed at variable fluence parameters. A direct correlation between the depth of penetration of the coagulated microcolumns and increasing energies was observed. Micro‐islands of coagulation were ∼250 μm in diameter and separated by ∼800 μm of unaffected tissue. With multiple passes, significantly more disruption of the dermal–epidermal junction (DEJ) occurred at higher fluences. In contrast to the controlled fractional columns observed with single‐pass treatments, nonuniform coagulated columns were distributed randomly throughout the tissue when instituting multiple passes over the same treatment region.Conclusion  Micro‐islands of thermal damage were observed at variable energy parameters. Pathological changes within the skin were clearly dependent on amount of energy and number of passes of the laser treatment. Significantly more superficial damage, accompanied by disruption of the DEJ was observed with multiple passes when compared with single pass at similar fluences. However, with multiple passes, depth of thermal injury did not increase with increasing energies but did disrupt the micro‐island array observed with single‐pass fractional treatments.
Amyloid β‐peptide 31–35‐induced neuronal apoptosis is mediated by caspase‐dependent pathways via cAMP‐dependent protein kinase A activation
Authors: Zhao Li , Qian Zhong‐Ming , Zhang Ce , Wing Ho Yung , Du Fang , Ya Ke 
Published: June 2009

SummaryThis study aims to investigate the roles of the protein kinase A (PKA)‐ and caspase‐dependent pathways in amyloid β‐peptide 31–35 (Aβ[31–35])‐induced apoptosis, and the mechanisms of neuroprotection by group III metabotropic glutamate receptor (mGluR) activation against apoptosis induced by Aβ[31–35] in cortical neurons. We demonstrated that Aβ[31–35] induces neuronal apoptosis as well as a significant increase in caspase‐3, ‐8 and ‐9. Activation of group III mGluRs byl‐serine‐O‐phosphate and (R,S)‐4‐phosphonophenylglycine (two group III mGluR agonists), which attenuate the effects of Aβ[31–35], provides neuroprotection to the cortical neurons subjected to Aβ[31–35]. We also showed that Rp‐cAMP, an inhibitor of cAMP‐dependent PKA, has the ability to protect neurons from Aβ[31–35]‐induced apoptosis and to reverse almost completely the effects of Aβ[31–35] on the activities of caspase‐3. Further, we found that Sp‐cAMP, an activator of cAMP‐dependent PKA, can significantly abolish thel‐serine‐O‐phosphate‐ and (R,S)‐4‐phosphonophenylglycine‐induced neuroprotection against apoptosis, and decrease caspase‐3, ‐8 and ‐9 in the Aβ[31–35]‐treated neurons. Our findings suggest that neuronal apoptosis induced by Aβ[31–35] is mediated by the PKA‐dependent pathway as well as the caspase‐dependent intrinsic and extrinsic apoptotic pathways. Activation of group III mGluRs protects neurons from Aβ[31–35]‐induced apoptosis by blocking the caspase‐dependent pathways. Inhibition of the PKA‐dependent pathway might also protect neurons from Aβ[31–35]‐induced apoptosis by blocking the caspase‐dependent pathways. Taken together, our observations suggest that Aβ[31–35] might have the ability to activate PKA, which in turn activates the caspase‐dependent intrinsic and extrinsic apoptotic pathways, inducing apoptosis in the cortical neurons.
Black tea polyphenols mimic insulin/insulin‐like growth factor‐1 signalling to the longevity factor FOXO1a
Authors: Cameron Amy R. , Anton Siobhan , Melville Laura , Houston Nicola P. , Dayal Saurabh , McDougall Gordon J. , Stewart Derek , Rena Graham 
Published: June 2009

SummaryIn vertebrates and invertebrates, relationships between diet and health are controlled by a conserved signalling pathway responsive to insulin‐like ligands. In invertebrate models for example, forkhead transcription factor family O (FOXO) transcription factors in this pathway regulate the rate of aging in response to dietary cues, and in vertebrates, obesity and age‐induced deficits in the same pathway are thought to contribute to dysregulation of hepatic gluconeogenesis through genes such as phosphoenolpyruvate carboxykinase (PEPCK). Recently, we have begun to screen for dietary constituents capable of regulating this pathway in our cell culture model. Here, we identify three black tea theaflavins, theaflavin 3‐O‐gallate, theaflavin 3′‐O‐gallate, theaflavin 3,3′di‐O‐gallate and thearubigins as novel mimics of insulin/IGF‐1 action on mammalian FOXO1a, PEPCK and moreover we provide evidence that the effects on this pathway of the green tea constituent (‐)‐epigallocatechin gallate depend on its ability to be converted into these larger structures. With the exception of water, tea is the most popular drink globally, but despite this, little is known about the biological availability of black tea polyphenols in vivo or the molecular target(s) mediating the effects presented here. Further investigation in these two areas might provide insight into how age‐related metabolic disease may be deferred.
Delayed kinetics of DNA double‐strand break processing in normal and pathological aging
Authors: Sedelnikova Olga A. , Horikawa Izumi , Redon Christophe , Nakamura Asako , Zimonjic Drazen B. , Popescu Nicholas C. , Bonner William M. 
Published: June 2009

SummaryAccumulation of DNA damage may play an essential role in both cellular senescence and organismal aging. The ability of cells to sense and repair DNA damage declines with age. However, the underlying molecular mechanism for this age‐dependent decline is still elusive. To understand quantitative and qualitative changes in the DNA damage response during human aging, DNA damage‐induced foci of phosphorylated histone H2AX (γ‐H2AX), which occurs specifically at sites of DNA double‐strand breaks (DSBs) and eroded telomeres, were examined in human young and senescing fibroblasts, and in lymphocytes of peripheral blood. Here, we show that the incidence of endogenous γ‐H2AX foci increases with age. Fibroblasts taken from patients with Werner syndrome, a disorder associated with premature aging, genomic instability and increased incidence of cancer, exhibited considerably higher incidence of γ‐H2AX foci than those taken from normal donors of comparable age. Further increases in γ‐H2AX focal incidence occurred in culture as both normal and Werner syndrome fibroblasts progressed toward senescence. The rates of recruitment of DSB repair proteins to γ‐H2AX foci correlated inversely with age for both normal and Werner syndrome donors, perhaps due in part to the slower growth of γ‐H2AX foci in older donors. Because genomic stability may depend on the efficient processing of DSBs, and hence the rapid formation of γ‐H2AX foci and the rapid accumulation of DSB repair proteins on these foci at sites of nascent DSBs, our findings suggest that decreasing efficiency in these processes may contribute to genome instability associated with normal and pathological aging.
Oestradiol or genistein rescues neurons from amyloid beta‐induced cell death by inhibiting activation of p38
Authors: Vallés Soraya L. , Borrás Consuelo , Gambini Juan , Furriol Jessica , Ortega Angel , Sastre Juan , Pallardó Federico V. , Viña Jose 
Published: June 2009

SummaryOestrogenic compounds have been postulated as neuroprotective agents. This prompted us to investigate their mechanism action in neurons in primary culture. Cells were pretreated with physiological concentrations of 17‐β estradiol (0.2 nm) or with nutritionally relevant concentrations of genistein (0.5 µm), and 48 h later treated with 5 µm of amyloid beta (Aβ) for 24 h. We found that Aβ increased oxidative stress, measured as peroxide levels or oxidized glutathione/reduced glutathione ratio, which in turn, caused phosphorylation of p38 MAP kinase. Amyloid beta subsequently induced neuronal death. Inhibiting the MAP kinase pathway prevented cell death, confirming the role of p38 in the toxic effect of Aβ. All these effects were prevented when cells were pretreated for 48 h with oestradiol or genistein. Therefore, oestrogenic compounds rescue neurons from Aβ‐induced cell death by preventing oxidative stress, which in turn inhibits the activation of p38, protecting neurons from cell death. Because hormone replacement therapy with oestradiol could cause serious setbacks, the potential therapeutic effect of phyto‐oestrogens for the prevention of Aβ‐associated neurodegenerative disorders should be more carefully studied in clinical research.
Dynamic regulation of PGC‐1α localization and turnover implicates mitochondrial adaptation in calorie restriction and the stress response
Authors: Anderson Rozalyn M. , Barger Jamie L. , Edwards Michael G. , Braun Kristina H. , O’Connor Clare E. , Prolla Tomas A. , Weindruch Richard 
Published: June 2009

SummaryThere is increasing evidence that longevity and stress resistance are connected, but the mechanism is unclear. We report that mitochondria are regulated in response to oxidative stress and calorie restriction through a shared mechanism involving peroxisome proliferator‐activated receptor‐γ co‐activator 1α (PGC‐1α). We demonstrate that PGC‐1α subcellular distribution is regulated, and its transcriptional activity is promoted through SIRT1‐dependent nuclear accumulation. In addition, the duration of PGC‐1α activity is regulated by glycogen synthase kinase beta (GSK3β), which targets PGC‐1α for intranuclear proteasomal degradation. This mechanism of regulation permits the rapidity and persistence of PGC‐1α activation to be independently controlled. We provide evidence that this pathway of PGC‐1α regulation occurs in vivo in mice, both in the oxidative stress response and with calorie restriction. Our data show how mitochondrial function may be adapted in response to external stimuli, and support the concept that such adaptation is critically involved in cellular survival and in lifespan extension by calorie restriction.
Bringing It Home: A Study of the Incentives Surrounding the Repatriation of Foreign Earnings Under the American Jobs Creation Act of 2004
Authors: BLOUIN JENNIFER , KRULL LINDA 
Published: June 2009

ABSTRACTThe American Jobs Creation Act of 2004 (the Act) creates a temporary tax holiday that effectively reduces the U.S. tax rate on repatriations from foreign subsidiaries from 35% to 5.25%. Firms receive the reduced tax rate by electing to take an 85% dividends received deduction on repatriations in 2004 or 2005. This paper investigates the characteristics of firms that repatriate under the Act and how they use the repatriated funds. We find that firms that repatriate under the Act have lower investment opportunities and higher free cash flows than nonrepatriating firms. Further, we find that repatriating firms increase share repurchases during 2005 by approximately $60 billion more than nonrepatriating firms, an amount that cannot be explained by differences in earnings between the two groups of firms. This increase represents about 20% of the $291.6 billion repatriated by our sample firms under the Act.
Use of Compliance Rewards in Agri‐environmental Schemes
Authors: Yano Yuki , Blandford David 
Published: June 2009

AbstractEnsuring that farmers comply with the terms of agri‐environmental schemes is an important issue. This paper explores the use of a ‘compliance–reward’ approach under heterogeneous net compliance costs with respect to cost‐share working lands programmes such as the Environmental Quality Incentives Program (EQIP) in the United States. Specifically, we examine the use of a reward under asymmetric information and output price uncertainty. We examine two possible sources of financing under the assumption of budget neutrality: (i) funds obtained by reducing monitoring effort; and (ii) money saved by reducing the number of farmers enrolled. We discuss the advantages and disadvantages of each source of funding and analyse these numerically for both risk‐neutral and risk‐averse farmers. We also examine the trade‐off between increased expenditure on monitoring effort and compliance rewards when additional budgetary resources are available. We show that under certain conditions a compliance reward can increase compliance rates. For risk‐averse farmers, however, conditions that ensure a positive outcome become more restrictive.
Modelling Farmers’ Participation in an Agri‐environmental Scheme using Panel Data: An Application to the Rural Environment Protection Scheme in Ireland
Authors: Hynes Stephen , Garvey Eoghan 
Published: June 2009

AbstractPrevious studies that have attempted to model the participation decision of farmers in agri‐environmental schemes have used a static framework where it was not possible to examine changes in the participation decision of farmers over time. This is rectified in this paper by utilising an 11‐year panel that contains information on 300 farmers for each year. The structure of this dataset allows us to employ discrete time duration random effects panel data logit models to model the determinants of entering the Irish Rural Environment Protection Scheme (REPS). We introduce a dynamic element into a number of the models by using the random effects logit model estimator, with lagged dependent variables as additional explanatory variables. The results point to the fact that systems of farming that are more extensive and less environmentally degrading remain those most likely to participate in the REPS. In addition, the results highlight the fact that where no attempt is made to control for unobserved heterogeneity or path dependency the effects of the farm‐ and farmer‐specific characteristics may be overestimated.