For clouds with relatively high base (1 km) the anomalies of the highest magnitude are found for λ = 469, spring albedo pattern, ϑ = 53° and τ = 30: Δpps = − 0.05 for the domain and Δpps = − 0.065 for the broad domain, which is 13% and 19% of the atmospheric transmittance

of irradiance. The simulations show a considerable increase in the anomaly magnitude for low-base clouds, to − 0.065 (− 0.08 for the broad domain) for τ = 12 and h = 200 m. This is mainly because the cloud base and cloud top are below some mountain peaks, which diminishes the effective cloud optical thickness in the non-uniform case. The anomaly magnitudes are sufficiently high to be important for the radiative balance of the area buy VE-821 and for estimating cloud radiative forcing. In the case of the pp-approximation, surface shortwave cloud forcing is typically

underestimated. Channel 2 (λ = 858 nm) of the MODIS radiometer is used for cloud optical thickness retrievals over the ocean. If we assume that the cloud microphysics is known (water cloud, droplet effective radius re = 10 μm) and τ is retrieved solely from channel 858 nm, the simulated error resulting from the application of the oceanic algorithm to the cloud optical thickness retrieval is < 1 (low-level clouds, cloud BGB324 cell line base height 1 km, ϑ = 53°) for the mouth of the fjord and the central part of the fjord. However, near the shoreline (within 2 km of it) and over the inner fjord, the enhancement in the normalized nadir radiance can exceed 0.12 for τ = 5 and 0.05 for τ = 20. This leads to the overestimation of the cloud optical thickness retrieval by > 3 for τ = 5 and by > 5 for τ = 20. The error may be bigger for other than nadir observation angles but such cases were not simulated in this work. The authors express their gratitude to the Alfred Wegener Institute for providing radiosounding data from Ny-Ålesund. The PI for the radiosoundings in Ny-Ålesund is Marion Maturilli. “
“Phytoplankton cells in the sea and other water basins contain numerous sets

Dimethyl sulfoxide of pigments, which we generally divide into photosynthetic pigments (PSP) (the main abbreviations and symbols used in the text are listed in the Annex, see page 563) and photoprotecting pigments (PPP) (Goodwin, 1952, Goodwin, 1965 and Majchrowski, 2001). When solar radiation reaches these cells it is spectrally selectively absorbed by the various pigments, which initially leads to the energetic excitation of the molecules. The excitation energy of the molecules of the pigments protecting the cells from excess light (PPP) is usually dissipated radiationlessly in that it is converted into heat that is then conducted to the cell’s surroundings. On the other hand, the excitation energy of PSP is conveyed to chlorophyll a molecules, which use this energy to produce organic matter by photosynthesis. This energy is only partially consumed during photosynthesis, that is, for the assimilation of carbon.

Thus, a better understanding of negative regulatory mechanisms of JAK/STAT pathway during inflammatory response may lead to important information on periodontal disease pathogenesis and also provide a therapeutic Pictilisib perspective based on the modulation of pro-inflammatory gene expression. This study evaluated the kinetics of SOCS1 and SOCS3 expression in ligature-induced model of periodontal disease in rats. We also evaluated the

mRNA expression of TNF-α, IL-6 and IL-10 that are direct targets of SOCS proteins and the mRNA expression of RANKL, OPG and that were shown to be relevant for pathogenesis of periodontal disease and may be indirect targets of SOCS proteins. Male adult Wistar (Norvegicus albinus) rats (N = 36) were obtained from the Neratinib Multidisciplinary Center for Biological Investigation (CEMIB-UNICAMP). The animals, weighing approximately 250 g each, were maintained with food and water ad libitum. The experimental protocol was approved by the Ethical Committee on Animal Experimentation (protocol number 23/2007) of the School of Dentistry at Araraquara –

UNESP and performed in accordance with the guidelines from the Brazilian College for Animal Experimentation (COBEA). General anesthesia was induced with intramuscular injections of ketamine and xylazine chloridrate at 0.08 mL/100 g body weight and 0.04 mL/100 g body weight, respectively. The animals were divided into two experimental groups: A – sham-operated group (n = 9) – animals were anaesthetised but no ligatures were placed on the lower molars B – experimental group (n = 27) – a cotton thread ligature was placed around the cervical area of the lower first molars bilaterally to induce experimental periodontal disease. After 7, 15, and 30 days of the ligature placement (baseline), 3 animals from the control group and 9 animals from the experimental group were sacrificed per period by anesthetic overdose. The mandibular jaws were hemisected, and half of the block samples including molars with their surrounding tissues were submitted to routine

histological processing to be used in the stereometric CYTH4 evaluation. The other half of the blocks had the gingival tissue around the first molars carefully dissected for extraction of total RNA and protein for RT-qPCR and western blot analysis. After dissection of the gingival tissues, the samples were immersed in 3% hydrogen peroxide for 24 h to remove remaining soft tissues. Subsequently, these samples were stored in 70% ethanol and used for the macroscopic assessment of bone resorption. The area of bone resorption in the lingual surface of the first molars was measured macroscopically. Briefly, the pieces were removed from alcohol, dried, immersed for 5 min in a solution containing 0.7 g/L of methylene blue and washed with tap water to remove the excess dye.

The relative content of short chain fatty acids (SCFA; C4:0 and C6:0) was lower in organic milk (5.6% instead of 6.4%) than in conventional milk. The medium chain fatty acid (MCFA; C8:0–C15:0) percentage was slightly lower in organic milk (difference of 0.6%). These

data are in agreement with those reported by Collomb et al. (2008) who also did not find significant difference according to the long chain length (LCFA; C16:–C18:3) in organic and conventional milks. The proportion of saturated fatty acids (SFA) was slightly higher in conventional milk (+2%). Conversely, for Collomb et al. (2008) and Ellis et al. (2006), organic and conventional milks did not significantly Selleck DZNeP differ with respect to SFA. MUFA proportion was always lower in conventional fermented milks

(−2%). Nevertheless, these results conflict with those obtained by Ellis et al. (2006), who found higher amounts of MUFA in conventional milks. More specifically, trans-C18:1 relative content was 1.6 times higher in organic products ( Fig. 1A), in agreement with data reported by ( Bergamo et al., 2003). After all, the percentage of PUFA fraction was 1.3 times higher in organic products, than in conventional milks, as previously reported by Ellis et al. (2006). Among these PUFA, the linoleic acid (LA – C18:2) was higher in organic milk, with 1.9 ± 0.02% instead of 1.6 ± 0.01% for conventional products. The initial relative contents of CLA (1.0 ± 0.01%) and ALA (0.5 ± 0.00%) were 1.4- and 1.6-times higher in organic milk ( Fig. 1B and C). Even if Ellis et al. (2006) did not confirm that as acetylcholine selleck kinase inhibitor a general rule, similar findings were reported by Bergamo et al. (2003) and Collomb et al. (2008). Finally, the main difference observed in fatty acid composition of conventional and organic

milks was related to the higher unsaturated fatty acid content in organic milk. This could be ascribed to the feeding regimen of the cows, as demonstrated by Bergamo et al., 2003 and Butler et al., 2011 and Collomb et al. (2008). The acidification profiles of yogurt made with S. thermophilus TA040 and L. delbrueckii subsp. bulgaricus LB340, and probiotic fermented milk containing the same yogurt culture plus B. animalis subsp. lactis HN019, in organic and conventional UHT milks, are shown on Fig. 2. A similar acidification profile was observed for yogurt culture in both milks (Fig. 2A). Even if the initial pH differed slightly (pH 6.54 ± 0.01 conventional milk, instead of pH 6.65 ± 0.01 in organic milk), the higher rate of acidification in organic milk (15.3 × 10−3 upH/min) than in conventional milk (11.7 × 10−3 upH/min) (Fig. 2B) allowed the final pH to be reached at the same time (tpH4.5 = 6.2 ± 0.3 h in both fermented milks). From Fig. 2B, two maximum acidification rates were observed whatever the kind of milk. This was explained by Pernoud, Fremaux, Sepulchre, Corrieu, and Monnet (2004), who demonstrated that S.

The present study demonstrates that the levels of NA in sausages may be reduced by adding erythorbic acid and that the extent of the inhibition increases with increasing amount of erythorbic acid, at least up to the highest tested level of 1104 mg kg−1. The effect of concurrent presence of ascorbyl palmitate (26, 150, 450, 750 and 874 mg kg−1) however seems to have the opposite effect, i.e. to stimulate the formation of NA or to counter act the effect of erythorbic acid. Haem has been suggested to play an essential role in the endogenous formation of NA linked with high consumption Dolutegravir cell line of red and processed meat (Bingham et al., 2002, Cross et al., 2003 and Pierre et al.,

2013). Lunn et al. (2007)

also found that in an aqueous solution no nitrosation of morpholine occurred even at elevated levels of nitrite, however if haem iron was also added NMOR was produced (Lunn et al., 2007). Calcium, which can chelate the iron in haem, was by Pierre et al. (2013) found to prevent a haem induced increase in endogenous formation of nitroso compounds in humans (Pierre et al., 2013). Iron plays an essential role in lipid peroxidation processes occurring in meat and antioxidants as ascorbate/erythorbic acid inhibit these unwanted processes Bosutinib order (Igene et al., 1979 and Ladikos and Lougovois, 1990). The results of the study are presented in Fig. 5. The levels of NSAR, NDMA and NPYR were in all the tested combinations at or below the LOQ of the method. The observed effects on the levels of these three NA Pyruvate dehydrogenase are therefore associated with high uncertainty and the results for these are not included in Fig. 5. The observations are however described as indicative results in the following. No significant effects were observed by supplementing the sausage meat with haem (myoglobin) (Fig. 5A1–E1). However a slight reduction in the levels of NPIP (Fig. 5C1), NSAR and NPYR were indicated.

This reduction may be the result of increased competition for the nitrosating species because more NO was bound to the added haem. Slight indications of calcium counteracting this inhibiting effect were observed for NHPRO (Fig. 5A2), NDMA and NPYR. The levels of NHPRO and NMTCA were found to increase significantly by adding Fe (III) (Fig. 5A1 and E1). An increase was also indicated for NTCA (Fig. 5D1) and NPYR. For the remaining NA no effect was observed by adding Fe(III). Erythorbic acid was also in this setup found to reduce the NA levels (Fig. 5A1–E1) except for NDMA and NPYR. The reduction was found to be significant for NHPRO, NPRO, NPIP and NTCA. Interaction between iron and erythorbic acid was indicated for NTCA and NMTCA, though only significantly for NMTCA (Fig. 5E2). Addition of Fe(III) cancelled the otherwise inhibiting effect of erythorbic acid (Fig. 5D2 and E2).

The hexane extract was concentrated under Nutlin-3 chemical structure reduced pressure, yielding an oil (26.9 g). The oil was then purified via silica gel column chromatography (Merck 7734) and eluted with 20% acetone/hexane. It was further purified using the same method (Merck 9385), followed by octadecyl silica gel column chromatography (YMC GEL ODS-A) with a gradient of methanol in water to yield urushiols. The final concentration of extracted urushiol was 10 mg/mL. Age-matched 6-week-old male C57BL/6 mice (Dooyeol Biotech, Inc., Seoul, Korea) were used in all experiments. Only male mice were used, given the hormonal changes of female mice. The mean body weights of the mice in each group are listed in Table 1. A total of 60 male C57BL/6 mice were housed individually

in steel microisolator cages maintained at 22°C with a 12-hour/12-hour light/dark cycle. The mice were randomly assigned to six dietary groups (n = 10). Each group of mice received one of the following six diets for 10 weeks:

(1) standard chow diet (normal feed); (2) alcohol diet (a Lieber–DeCarli liquid diet with 10% alcohol); (3) control diet (a Lieber–DeCarli liquid diet with http://www.selleckchem.com/GSK-3.html 10% alcohol and normal feed); (4) KRG diet (200 mg/kg/day of KRG with normal feed for 4 weeks after a Lieber–DeCarli liquid diet with 10% alcohol for 6 weeks); (5) urushiol diet (0.128 mg/mL/day of urushiol with normal feed for 4 weeks after a Lieber–DeCarli liquid diet with 10% alcohol for 6 weeks); and (6) probiotics diet (1 mg/mL/day Epothilone B (EPO906, Patupilone) of L. rhamnosus R0011 and L. acidophilus R0052 with normal feed for 4 weeks after a Lieber–DeCarli liquid diet with 10% alcohol for 6 weeks; Fig. 1). The liquid diets were based on the Lieber–DeCarli ethanol formulation and purchased from Dooyeol Biotech, Inc. Protein, fat, and carbohydrates constitute, respectively, 18.9%,

16.5%, and 64.5% of the calories of the Lieber–DeCarli liquid diet. Lacidofil, KRG, and urushiol suspended in distilled water were orally administered using a gastric tube five times a week, for 4 weeks. At the end of the treatment period, the animals were sacrificed via isoflurane inhalation. A midline abdominal incision was performed, and blood was collected through the orbital canal. Whole-blood (600 μL) samples were centrifuged at 1,500 × g for 15 minutes to collect the serum. The liver was rapidly excised and stored at −80°C. The animals received humane care, and all procedures were conducted in accordance with the National Institutes of Health Guidelines for the Care and Use of Laboratory Animals. The Institutional Animal Care and Use Committee of the Hallym University College of Medicine, Gangwon Do, Korea approved this study. Levels of aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transferase were analyzed with a biochemical blood analyzer (KoneLab 20, Thermo Fisher Scientific, Waltham, Finland). After rinsing the tissue samples with a cell wash buffer once, they were cut into 3 mm × 3 mm pieces and transferred to a 2 mL tissue grinder.

This shows higher sensitivity to relational than non-relational information, consistent with hierarchical incrementality. Fast encoding of an “easy” agent before 400 ms was then followed by a shift of attention to the patient around 400 ms. In Selleck HA 1077 other words, speakers did not continue fixating the subject character after 400 ms as predicted by the strong version of linear incrementality (Gleitman et al., 2007), but systematically shifted their gaze back to the patient. This type of character-by-character encoding is consistent with a weaker version of linear incrementality, where speakers do attempt to encode information about both

characters early in the formulation process but, crucially, they encode this information sequentially. Thus the rise and fall of fixations to the agent after 400 ms was also predicted by Agent codability: fixations to agents were generally delayed after 400 ms if agents attracted more attention before 400 ms, and vice versa. Specifically, formulation in events with “harder” agents showed that there is a benefit to distributing attention more evenly between the two characters before 400 ms: formulation after 400 ms continued with rapid,

preferential encoding of the agent. Importantly, shifts of gaze to the agent after 400 ms and away from the agent after 1000 ms Crizotinib ic50 were also influenced by Event codability: as predicted by hierarchical incrementality, speakers began fixating the patient earlier in higher-codability

events than lower-codability events. As expected, the lexical primes produced analogous effects to Agent codability: within 400 ms of picture onset, speakers directed more fixations to the agent after agent primes than after patient primes and neutral primes. This shows ID-8 that the agent primes selectively influenced encoding of the agent character and that they increased the likelihood of speakers prioritizing encoding of this character (non-relational information) shortly after picture onset. A shift of gaze away from the agent was then observed after 400 ms, confirming the tendency to encode sentences character by character after priming non-relational information. Finally, after 1000 ms speakers looked at the agent for less time after agent and patient primes than neutral primes, and thus shifted their gaze to the patient earlier when either character had been primed than when the primes mentioned an unrelated character. Taken together, the results show a direct link between the ease of encoding non-relational and relational information and the timecourse of formulation, both during the early deployment of attention to the subject character and then the deployment of attention to the object character around speech onset.

6B,C). The induction of ginsenoside-Rh2-mediated apoptosis by p38 MAPK inhibitor SB203580 suggests that p38 MAPK signaling is important in protecting cancer cell against apoptosis. However, the molecular mechanism involved in the antiapoptotic role of p38 MAPK remains unclear and needs to be studied further. Recently, several reports have also linked AMPK activity to p38 MAPK. AMPK activator AICAR increases glucose uptake by activating the p38 MAPK pathway, but

the p38 MAPK inhibitor did not affect AMPK activation by AICAR in skeletal muscle [46]. The retinoic acid-mediated activation of p38 MAPK was inhibited by check details treatment with the AMPK inhibitor, compound C [47]. However, a further study suggests that AMPK activation leads to p38 MAPK inhibition. p38 MAPK is induced by the addition of cAMP to serum-starved H4IIE cells, and it is inhibited with AICAR treatment [48]. Even though several reports show that AMPK regulates p38 MAPK activity, the underlying mechanism of this interaction is not clearly understood.

In this regard, we also examined if there is any crosstalk between AMPK and p38 MAPK (Fig. 6C), but there was no signaling crosstalk between these two kinases. Our present observations provide the rationale for a combination of AMPK and p38 MAPK inhibitors in the treatment of cancer, and future studies focusing on the molecular mechanism of AMPK and p38 MAPK in ginsenoside-Rh2-induced apoptosis would greatly extend our understanding of the chemotherapeutic potency of ginsenoside-Rh2 Fluorouracil in vivo in human cancer. All authors declare no conflicts of interest. This work was supported by a grant from the Kyung Hee University in 2010 (KHU-20100849). “
“Ginseng is a perennial plant DAPT order belonging to the genus Panax and has been reported to exhibit a wide range of pharmacological and physiological actions [1]. American ginseng (AG) is a popular dietary supplement and one of the most commonly used herbal medicines in the USA, which grows as Panax quinquefolius L. (Araliaceae) in the USA and Canada. By contrast,

Panax ginseng Meyer (Araliaceae) has been mainly cultivated in Asia (most notably in Korea and China), and has been used extensively in traditional Chinese medicine [2] and [3]. Both AG and Asian ginseng extracts have been reported to exhibit free radical scavenging activities, which, from different ginseng species and specific parts, have been thought to be related to their ginsenoside contents [4]. Ginsenosides, which are 30-carbon glycosides derived from the triterpenoid dammarane, as shown in Fig. 1, are regarded as the main active components in AG, as well as Asian ginseng. We previously identified that the structural changes in ginsenosides by heat-processing are closely associated with increased free radical-scavenging activities of AG and Asian ginseng [5] and [6]. Moreover, we have also recently reported the increased anticancer efficacy of ginsenosides derived from heat-processed Asian ginseng in human gastric cancer cells [7].

These data emphasize the need for structural modifications of GAG-mimetics in order to confer irreversible binding to the

viral attachment protein and thereby cause permanent inactivation of viral infectivity. Human RSV targets ciliated LY294002 concentration cells of the bronchial epithelium and type 1 pneumocytes in the alveoli (Zhang et al., 2002, Johnson et al., 2007 and Welliver et al., 2007) causing acute bronchiolitis and pneumonia in infants, the elderly, and immunocompromised individuals (for review, see Collins and Graham (2008)). Experiments in cultured cells revealed that an initial step of the RSV infectious cycle is the binding of the virus attachment protein G (Levine et al., 1987) to cell surface sulfated GAGs (Krusat and Streckert, 1997), mainly to iduronic acid-containing GAGs such as heparan sulfate or chondroitin sulfate B (Hallak et al., 2000). It is uncertain whether

RSV uses GAGs to infect humans since heparan or chondroitin sulfate chains are poorly or not at all expressed at the surface of airway epithelium (Zhang et al., 2005 and Monzon et al., 2006). However another type Epigenetics Compound high throughput screening of GAG chain, i.e., keratan sulfate, is abundantly expressed on the apical surface of ciliated cells of well differentiated cultures of bronchial epithelium (Zhang et al., 2002). This suggests that GAGs or GAG-like receptors may promote RSV infection of humans, and that compounds that mimic GAG chains may protect humans from Phenylethanolamine N-methyltransferase RSV. The anti-cancer drug candidate muparfostat (formerly known as PI-88) (Parish et al., 1999) is a mixture of highly sulfated mannose-containing di- to hexasaccharides with penta- and tetrasaccharides as predominant components. In addition to anti-cancer activities (for review, see Kudchadkar et al., 2008), it also exhibits anti-HIV (Said et al., 2010), anti-HSV (Nyberg et al., 2004), anti-dengue and -encephalitic flavivirus (Lee et al., 2006), and anti-malarial (Adams et al., 2006) activities. In an attempt to improve antiviral activity

of muparfostat we paid attention to an observation that certain polysulfonated compounds such as PRO2000, composed of chains of aromatic/lipophilic moieties instead of relatively hydrophilic sugar residues, exhibited virucidal activity (Cheshenko et al., 2004) and provided some protection of women against HIV (Cohen, 2009). It has also been reported that the peptide-based inhibitors of cell entry of HIV (Ingallinella et al., 2009) or some paramyxoviruses (Porotto et al., 2010) exhibited greatly enhanced antiviral activity when conjugated with cholesterol. In the present work we conjugated specific lipophilic groups to the reducing end of sulfated tetra- and pentasaccharides and tested whether this modification would affect anti-RSV activity. Our study demonstrated that the cholestanyl-conjugated tetrasaccharide glycosides exhibited improved anti-RSV potency including virucidal activity, a feature absent in native sulfated oligosaccharides.

, 2011). Thus, in view of the growing numbers of immunosuppressed patients, the development of alternative anti-adenovirus treatment options is required Ipatasertib chemical structure to decrease adenovirus-mediated mortality among immunocompromised patients, and also to decrease economic losses caused by milder forms of adenovirus-related disease. RNA interference (RNAi) is a post-transcriptional mechanism of gene silencing conserved among

eukaryotic cells (Carthew and Sontheimer, 2009, Ghildiyal and Zamore, 2009, Huntzinger and Izaurralde, 2011, Hutvagner and Simard, 2008 and Kawamata and Tomari, 2010). It is mediated through small double-stranded RNAs (dsRNAs), of ∼21–25 nt in length, which guide the RNA-induced silencing complex (RISC) to the respective target mRNAs (Fire et al., 1998). Depending on the degree of complementarity between the so-called antisense (or guide) strand of the dsRNA and target mRNA, RNAi can bring about the cleavage of the mRNA (in the case of full or nearly full complementarity), accelerated degradation (as a consequence of deadenylation), or translational repression. Following the discovery

that the introduction of synthetic small interfering RNAs (siRNAs) into cells can trigger RNAi (Elbashir et al., 2001), this mechanism was rapidly harnessed as a tool to silence disease-associated human, and also viral genes (Davidson and McCray, 2011). Since then, siRNA-mediated silencing of viral genes has been employed Selleckchem MEK inhibitor to inhibit the replication of a variety of DNA and RNA viruses, in vitro and also in vivo ( Arbuthnot, 2010, Haasnoot et al., 2007 and Zhou and Rossi, 2011).

Adenoviruses contain a linear dsDNA genome, ∼36 kb long. The first gene to be expressed during the infection cycle is E1A. This gene has a central role, because it reprograms the cell in a way that promotes efficient virus replication (Berk, 2005, Pelka et al., 2008 and Zhao et al., 2003). Deletion of E1A renders adenoviruses replication deficient. E1A expression ultimately leads to the activation of other early and late promoters and triggers the onset of viral DNA replication. Viral DNA replication is dependent on three viral proteins: the viral DNA polymerase; the preterminal protein (pTP); and the DNA-binding protein (DBP) (de Jong et al., 2003). Besides creating PD184352 (CI-1040) dsDNAs for packaging into capsids (accomplished with the help of the IVa2 protein) (Zhang and Imperiale, 2003), replication of the adenoviral genome activates the expression of other viral genes, e.g., IVa2 ( Flint, 1986 and Iftode and Flint, 2004) and genes transcribed from the major late promoter (MLP) ( Shaw and Ziff, 1980). Upregulation of major late (ML) gene expression also involves the IVa2 protein ( Tribouley et al., 1994), and results in the synthesis of gene products that primarily constitute structural components of the virion or are involved in its assembly. The major component of the capsid is the hexon protein ( Russell, 2009).

Rg3 and F4 are unique to Korean Red Ginseng. These results may suggest the importance of Korean Red Ginseng for treating cartilage degradation disorders. In conclusion, some ginsenoside-enriched fractions

(n-BuOH fraction, GDF, and GDF/F4) were, for the first time, found to inhibit MMP-13 expression from chondrocytes, at least in part, via blocking the activation of p38 MAPK, JNK, and STAT-1/2. GDF/F4 also showed some protective activity against cartilage degradation in rabbit cartilage tissue culture. Our study may open a new therapeutic area for red ginseng product(s). These products may be beneficial for chondroprotection in cartilage degradation-related disorders such as osteoarthritis. All authors have no conflict of interest to declare. This study was supported by 2014 Research Grant AZD8055 order from Kangwon National University (No. 120140154) and BK21-plus project from Ministry of Education (Korea, No. F14SR08T4520). A part of this study was also supported by an MRC grant to Y.S. Kim funded by

the National Research Foundation of Korea (No. 2011-0030635). The bioassay facilities of the New Drug Development Institute (Kangwon National University, Chunchon, selleck screening library Korea) were used. “
“The α and β estrogen receptors (ERs) regulate various brain functions in an estradiol-dependent manner. Signaling pathways elicited via ER-α and ER-β activation are interrelated and feedback inhibition

occurs mainly by estradiol engagement of the ER-α receptor. Most studies involving ER-β have focused on brain functions and behavioral patterns [1] and [2]. ER-β is a member of the nuclear receptor superfamily [3]. Upon ligand binding, ER-β regulates gene expression by binding directly to regulatory regions of target genes or by interacting with other transcription factors such as nuclear factor κB, activating until protein 1, and stimulating protein 1 [4]. ER-β also controls gene expression by activating signaling pathways that stimulate kinases such as protein kinase A, protein kinase C, and mitogen-activated protein kinase [5]. Recent studies show that ER-β has neuroprotective, anti-inflammatory, antiproliferative, antioxidant, and immune-modulatory activities [2] and [6]. However, the effects of stress on ER-β expression in the brain cells remain largely unknown. ERs regulate activation of phosphatidylinositol-3 kinases (PI3Ks) by interacting with the p85 regulatory subunit of PI3K [7]. Activation of ER-α upregulates PI3K/Akt signaling, which in turn stimulates cell growth in breast cancer cells [8]. ER-β also activates signaling through PI3K/Akt and improves myocardial function in female hearts following acute ischemia [9].