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Dehydroepiandrosterone (DHEA) levels were reported to associate with increased breast cancer risk in postmenopausal women, but some carcinogen-induced rat mammary tumor studies question this claim. The purpose of this study was to determine how DHEA and its metabolites affect estrogen receptors α or β (ERα or ERβ) -regulated gene transcription and cell proliferation. In transiently transfected HEK-293 cells, androstenediol, DHEA, and DHEA-S activated ERα. In ERβ transfected HepG2 cells, androstenedione, DHEA, androstenediol, and 7-oxo DHEA stimulated reporter activity. ER antagonists ICI 182,780 (fulvestrant) and 4-hydroxytamoxifen, general P450 inhibitor miconazole, and aromatase inhibitor exemestane inhibited activation by DHEA or metabolites in transfected cells. ERβ-selective antagonist R,R-THC (R,R-cis-diethyl tetrahydrochrysene) inhibited DHEA and DHEA metabolite transcriptional activity in ERβ-transfected cells. Expression of endogenous estrogen-regulated genes: pS2, progesterone receptor, cathepsin D1, and nuclear respiratory factor-1 was increased by DHEA and its metabolites in an ER-subtype, gene, and cell-specific manner. DHEA metabolites, but not DHEA, competed with 17β-estradiol for ERα and ERβ binding and stimulated MCF-7 cell proliferation, demonstrating that DHEA metabolites interact directly with ERα and ERβ in vitro, modulating estrogen target genes in vivo.
estrogen receptors; DHEA; androstendione; androstendiol; transcription
Rationale: Adhesion of monocytes to vascular endothelium is necessary for atheroma formation. This adhesion requires binding of endothelial neural cell adhesion molecule (NCAM) to monocyte NCAM. NCAM:NCAM binding is blocked by sialylation of NCAM (polysialylated NCAM; PSA-NCAM). Since estradiol (E2) and dihydrotestosterone (DHT) induced PSA-NCAM and decreased monocyte adhesion, in consideration of possible clinical applications we tested whether their prohormone dehydroepiandrosterone (DHEA) has similar effects. Experimental: (1) DHEA was administered to cultured human coronary artery endothelial cells (HCAECs) from men and women. Monocyte binding was assessed using fluorescence-labeled monocytes. (2) HCEACs were incubated with E2, DHT, DHEA alone, or with trilostane, fulvestrant or flutamide. Expression of PSA-NCAM was assessed by immunohistochemistry and Western blotting. Results: Dehydroepiandrosterone inhibited monocyte adhesion to HCAECs by ≥50% (P < .01). Fulvestrant or flutamide blockade of DHEA’s inhibition of monocyte binding appeared to be gender dependent. The DHEA-induced expression of PSA-NCAM was completely blocked by trilostane. Conclusions: In these preliminary in vitro studies, DHEA increased PSA-NCAM expression and inhibited monocyte binding in an estrogen- and androgen receptor-dependent manner. Dehydroepiandrosteroneappears to act via its end metabolites, E2 and DHT. Dehydroepiandrosterone could furnish clinical prevention against atherogenesis and arteriosclerosis.
atherosclerosis; heart disease; coronary; estrogen; androgen; adhesion; NCAM; PSA-NCAM
Dehydroepiandrosterone (DHEA), a C19 human adrenal steroid, activates peroxisome proliferator-activated receptor α (PPARα) in vivo but does not ligand-activate PPARα in transient transfection experiments. We demonstrate that DHEA regulates PPARα action by altering both the levels and phosphorylation status of the receptor. Human hepatoma cells (HepG2) were transiently transfected with the expression plasmid encoding PPARα and a plasmid containing two copies of fatty acyl coenzyme oxidase (FACO) peroxisome-proliferator activated receptor responsive element consensus oligonucleotide in a luciferase reporter gene. Nafenopin treatment increased reporter gene activity in this system, whereas DHEA treatment did not. Okadaic acid significantly decreased nafenopin-induced reporter activity in a concentration-dependent manner. Okadaic acid treatment of primary rat hepatocytes decreased both DHEA- and nafenopin-induced FACO activity in primary rat hepatocytes. DHEA induced both PPARα mRNA and protein levels, as well as PP2A message in primary rat hepatocytes. Western blot analysis showed that the serines at positions 12 and 21 were rapidly dephosphorylated upon treatment with DHEA and nafenopin. Results using specific protein phosphatase inhibitors suggested that protein phosphatase 2A (PP2A) is responsible for DHEA action, and protein phosphatase 1 might be involved in nafenopin induction. Mutation of serines at position 6, 12, and 21 to an uncharged alanine residue significantly increased transcriptional activity, whereas mutation to negative charged aspartate residues (mimicking receptor phosphorylation) decreased transcriptional activity. DHEA action involves induction of PPARα mRNA and protein levels as well as increased PPARα transcriptional activity through decreasing receptor phosphorylation at serines in the AF1 region.
Dehydroepiandrosterone (DHEA) is commonly used as a dietary supplement and may affect prostate pathophysiology when metabolized to androgens and/or estrogens. Human prostate LAPC-4 cancer cells with a wild type androgen receptor (AR), were treated with DHEA, androgens (DHT, T, or R1881), and E2 and assayed for PSA protein and gene expression. In LAPC-4 monocultures, DHEA and E2 induced little or no increase in PSA protein or mRNA expression compared to androgen-treated cells. When prostate cancer-associated (6S) stromal cells were added in coculture, DHEA stimulated LAPC-4 cell PSA protein secretion to levels approaching induction by DHT. Also, DHEA induced 15-fold more PSA mRNA in LAPC-4 cocultures than in monocultures. LAPC-4 proliferation was increased 2–3 fold when cocultured with 6S stromal cells regardless of hormone treatment. DHEA-treated 6S stromal cells exhibited a dose- and time-dependent increase in T secretion, demonstrating stromal cell metabolism of DHEA to T. Coculture with non-cancerous stroma did not induce LAPC-4 PSA production, suggesting a differential modulation of DHEA effect in a cancer-associated prostate stromal environment. This coculture model provides a research approach to reveal detailed endocrine, intracrine, and paracrine signaling between stromal and epithelial cells that regulate tissue homeostasis within the prostate, and the role of the tumor microenvironment in cancer progression.
DHEA; stromal; prostate; PSA; coculture
Dehydroepiandrosterone-sulfate (DHEAS) is a hormone produced by the adrenal gland and is a precursor for both androgens and estrogens. Atherosclerosis is a well characterized inflammatory disease, but little is known about the role of DHEAS in vascular inflammation. We hypothesize that DHEAS can reduce inflammation in vascular endothelial cells and the mechanism involves the peroxisome proliferator-activated receptor α (PPARα), thereby inhibiting transcription factors involved in endothelial cell inflammation. To test our hypothesis, aortic endothelial cells were pretreated for 48 hours with DHEAS, then with TNF-α. TNF-α-induced upregulation of the expression of inflammatory genes interleukin (IL)-8 and intracellular adhesion molecule (ICAM)-1 was attenuated by incubation with DHEAS. DHEAS inhibited the TNF-α-induced surface expression of vascular cell adhesion molecule (VCAM)-1. This effect was abolished by the addition of MK866, a PPARα inhibitor, indicating that PPARα is involved in the mechanism of this inhibition. The addition of the aromatase inhibitor letrozole had no effect on the inhibition of TNF-α-induced VCAM-1 expression by DHEAS. Treatment of endothelial cells with DHEAS dramatically inhibited the TNF-α-induced activation of NF-κB, an inflammatory transcription factor, and increased protein levels of the NF-κB inhibitor, IκB-α. These results signify the ability of DHEAS to directly inhibit the inflammatory process and show a potential direct effect of DHEAS on vascular inflammation that has implications for the development of atherosclerotic cardiovascular disease.
Dehydroepiandrosterone sulfate; VCAM; PPAR; endothelial cell; inflammation
Dehydroepiandrosterone (DHEA) released by adrenal glands may be converted to androgens and estrogens mainly in the gonadal, adipose, mammary, hepatic and nervous tissue. DHEA is also a key neurosteroid and has antiglucocorticoid activity. DHEA has been used for the treatment of a number of diseases, including obesity; its pharmacological effects depend on large oral doses, which effect rapidly wanes in part because of its short half-life in plasma. Since steroid hormone esters circulate for longer periods, we have studied here whether the administration of DHEA oleoyl ester may extend its pharmacologic availability by keeping high circulating levels.
Tritium-labelled oleoyl-DHEA was given to Wistar male and female rats by gastric tube. The kinetics of appearance of the label in plasma was unrelated to sex; the pattern being largely coincident with the levels of DHEA-sulfate only in females, and after 2 h undistinguishable from the results obtained using labelled DHEA gavages; in the short term, practically no lipophilic DHEA label was found in plasma. After 24 h only a small fraction of the label remained in the rat organs, with a different sex-related distribution pattern coincident for oleoyl- and free- DHEA gavages. The rapid conversion of oleoyl-DHEA into circulating DHEA-sulfate was investigated using stomach, liver and intestine homogenates; which hydrolysed oleoyl-DHEA optimally near pH 8. Duodenum and ileum contained the highest esterase activities. Pure hog pancreas cholesterol-esterase broke down oleoyl-DHEA at rates similar to those of oleoyl-cholesterol. The intestinal and liver esterases were differently activated by taurocholate and showed different pH-activity patterns than cholesterol esterase, suggesting that oleoyl-DHEA can be hydrolysed by a number of esterases in the lumen (e.g. cholesterol-esterase), in the intestinal wall and the liver.
The esterase activities found may condition the pharmacological availability (and depot effect) of orally administered steroid hormone fatty acid esters such as oleoyl-DHEA. The oral administration of oleoyl-DHEA in order to extend DHEA plasma availability has not been proved effective, since the ester is rapidly hydrolysed, probably in the intestine itself, and mainly converted to DHEA-sulfate at least in females.
Administration of dehydroepiandrosterone (DHEA), a neurosteroid that can negatively modulate the GABAA receptor, has been shown to decrease voluntary intake of ethanol in rats. In vivo, DHEA can be metabolized to a variety of metabolites, including 7-keto DHEA, a metabolite without the prohormonal effects of DHEA. This study compared the effectiveness of 7-keto DHEA to DHEA for reducing ethanol intake in the same group of rats. The subjects, previously trained to drink ethanol using a saccharin-fading procedure, had access to ethanol for thirty minutes daily, and the amount consumed was recorded. Subjects were administered 10 and 56 mg/kg of DHEA or 7-keto DHEA intraperitoneally 15 minutes prior to drinking sessions. Subjects received each particular dose daily until one of two criteria was met; that is, either ethanol intake did not differ by more than 20% of the mean for three consecutive days, or for a maximum of eight days. Both 10 and 56 mg/kg of 7-keto DHEA significantly reduced the dose of ethanol consumed. While 10 mg/kg of 7-keto DHEA produced decreases similar to those found with DHEA, the 56-mg/kg dose of 7-keto DHEA was significantly more effective at decreasing the dose of ethanol consumed than the same dose of DHEA. These results show that 7-keto DHEA is comparable to, or possibly more effective than, DHEA at decreasing ethanol consumption in rats, and that 7-keto DHEA is a compound deserving further investigation as a possible clinical treatment for alcohol abuse without the prohormonal effects of DHEA.
DHEA; 7-ketoDHEA; neurosteroid; GABAA receptor; ethanol intake; rats
Trichloroethylene (TCE) and related hydrocarbons constitute an important class of environmental pollutants whose adverse effects on liver, kidney, and other tissues may, in part, be mediated by peroxisome proliferator-activated receptors (PPARs), ligand-activated transcription factors belonging to the steroid receptor superfamily. Activation of PPAR induces a dramatic proliferation of peroxisomes in rodent hepatocytes and ultimately leads to hepatocellular carcinoma. To elucidate the role of PPAR in the pathophysiologic effects of TCE and its metabolites, it is important to understand the mechanisms whereby PPAR is activated both by TCE and endogenous peroxisome proliferators. The investigations summarized in this article a) help clarify the mechanism by which TCE and its metabolites induce peroxisome proliferation and b) explore the potential role of the adrenal steroid and anticarcinogen dehydroepiandrosterone 3beta-sulfate (DHEA-S) as an endogenous PPAR activator. Transient transfection studies have demonstrated that the TCE metabolites trichloroacetate and dichloroacetate both activate PPAR alpha, a major liver-expressed receptor isoform. TCE itself was inactive when tested over the same concentration range, suggesting that its acidic metabolites mediate the peroxisome proliferative potential of TCE. Although DHEA-S is an active peroxisome proliferator in vivo, this steroid does not stimulate trans-activation of PPAR alpha or of two other PPAR isoforms, gamma and delta/Nuc1, when evaluated in COS-1 cell transfection studies. To test whether PPAR alpha mediates peroxisomal gene induction by DHEA-S in intact animals, DHEA-S has been administered to mice lacking a functional PPAR alpha gene. DHEA-S was thus shown to markedly increase hepatic expression of two microsomal P4504A proteins associated with the peroxisomal proliferative response in wild-type mice. In contrast, DHEA-S did not induce these hepatic proteins in PPAR alpha-deficient mice. Thus, despite its unresponsiveness to steroidal peroxisome proliferators in transfection assays, PPAR alpha is an obligatory mediator of DHEA-S-stimulated hepatic peroxisomal gene induction. DHEA-S, or one of its metabolites, may thus serve as an important endogenous regulator of liver peroxisomal enzyme expression.
To test the hypothesis that DHEAS production from DHEA occurs in hepatic cells, and that this production is augmented by the presence of sex steroids or insulin (INS).
In-vitro prospective experiment
Academic medical center.
Hepatoma (Hep) G2 cells cultured in media supplemented with: i) DHEA (10−5M) only, ii) DHEA (10−5M) + testosterone (T, 10−6M), iii) DHEA (10−5M) + estradiol (E2, 10−6M), iv) DHEA (10−5M) + dihydrotestosterone (DHT 10−6M), v) DHEA (10−5M) + insulin (INS 10 ng/mL), or vi) DHEA (10−5M) + insulin 100 ng/mL,
DHEAS levels in the media were measured at 0, 2, 4, 6, 8, 12, 24, 48, and 72 h after adding treatments at time-point 0.
DHEAS was first detected in the HepG2 cell culture media at 12h incubation. The cumulative production rate of DHEAS increased linearly until 72h incubation. When compared to the effect of treatment with DHEA only, treatment with DHEA plus T, DHT, or E2 delayed the cumulative DHEAS production; alternatively, the addition of INS did not alter DHEAS production.
These data suggest that while hepatic cells have the ability of converting DHEA to DHEAS, neither sex steroids nor INS result in the increased hepatic production of DHEAS.
Adrenal androgen excess; DHEA sulphotransferase; HepG2 cells; dehydroepiandrosterone; DHEAS; SULT2A1
The purpose of this study was to determine whether esterification of dehydroepiandrosterone with aspartate (DHEA-aspartate) could reduce peroxisomal proliferation induced by DHEA itself, without loss of antiosteoporotic activity. Female Sprague-Dawley rats were ovariectomized, then DHEA or DHEA-aspartate was administered intraperitoneally at 0.34 mmol/kg BW 3 times a week for 8 weeks. DHEA-aspartate treatment in ovariectomized rats significantly increased trabeculae area in tibia as much as DHEA treatment. Urinary Ca excretion was not significantly increased by DHEA or DHEA-aspartate treatment in ovariectomized rats, while it was significantly increased by ovariectomy. Osteocalcin concentration and alkaline phosphatase activity in serum and cross linked N-telopeptide type I collagen level in urine were not significantly different between DHEA-aspartate and DHEA treated groups. DHEA-aspartate treatment significantly reduced liver weight and hepatic palmitoyl-coA oxidase activity compared to DHEA treatment. DHEA-aspartate treatment maintained a nearly normal morphology of peroxisomes, while DHEA treatment increased the number and size of peroxisomes in the liver. According to these results, it is concluded that DHEA-aspartate ester has an inhibitory effect on bone loss in ovariectomized rats with a marked reduction of hepatomegaly and peroxisomal proliferation compared to DHEA.
The neurosteroid dehydroepiandrosterone (DHEA), produced by neurons and glia, affects multiple processes in the brain, including neuronal survival and neurogenesis during development and in aging. We provide evidence that DHEA interacts with pro-survival TrkA and pro-death p75NTR membrane receptors of neurotrophin nerve growth factor (NGF), acting as a neurotrophic factor: (1) the anti-apoptotic effects of DHEA were reversed by siRNA against TrkA or by a specific TrkA inhibitor; (2) [3H]-DHEA binding assays showed that it bound to membranes isolated from HEK293 cells transfected with the cDNAs of TrkA and p75NTR receptors (KD: 7.4±1.75 nM and 5.6±0.55 nM, respectively); (3) immobilized DHEA pulled down recombinant and naturally expressed TrkA and p75NTR receptors; (4) DHEA induced TrkA phosphorylation and NGF receptor-mediated signaling; Shc, Akt, and ERK1/2 kinases down-stream to TrkA receptors and TRAF6, RIP2, and RhoGDI interactors of p75NTR receptors; and (5) DHEA rescued from apoptosis TrkA receptor positive sensory neurons of dorsal root ganglia in NGF null embryos and compensated NGF in rescuing from apoptosis NGF receptor positive sympathetic neurons of embryonic superior cervical ganglia. Phylogenetic findings on the evolution of neurotrophins, their receptors, and CYP17, the enzyme responsible for DHEA biosynthesis, combined with our data support the hypothesis that DHEA served as a phylogenetically ancient neurotrophic factor.
Dehydroepiandrosterone (DHEA) and its sulphate ester are the most abundant steroid hormones in humans, and DHEA was described as the first neurosteroid produced in the brain. DHEA is known to participate in multiple events in the brain, including neuronal survival and neurogenesis. However, to date no specific cellular receptor has been described for this important neurosteroid. In this study, we provide evidence that DHEA exerts its neurotrophic effects by directly interacting with the TrkA and p75NTR membrane receptors of nerve growth factor (NGF), and efficiently activates their downstream signaling pathways. This activation prevents the apoptotic loss of NGF receptor positive sensory and sympathetic neurons. The interaction of DHEA with NGF receptors may also offer a mechanistic explanation for the multiple actions of DHEA in other peripheral biological systems expressing NGF receptors, such as the immune, reproductive, and cardiovascular systems.
This study was conducted to demonstrate the anti-atherosclerotic effect of dehydroepiandrosterone (DHEA) and to investigate its possible mechanisms and whether this effect is related to its conversion to estrogen.
Forty male New Zealand White rabbits aged 3 months were divided into 5 groups (n=8 per group) and fed different diets for 10 weeks. Serum lipid levels, the area of atherosclerotic lesions and the mRNA levels of monocyte chemoattractant protein-1 (MCP-1) and vascular cell adhesion molecule-1 (VCAM-1) in aortic lesions were measured. Then cultured vascular smooth muscle cells (VSMCs) stimulated by oxidized low density lipoprotein-cholesterol (ox-LDL) were treated by DHEA. The gene and protein expression levels of MCP-1 and VCAM-1 in VSMCs was detected. The plasmid with or without the gene of cytochrome P450 aromatase (CYP19) was transient transfected into cultured VSMCs respectively. Twenty hours later, the cells were stimulated with ox-LDL and DHEA.
DHEA could obviously decrease the area of atherosclerotic lesions and the expressions of MCP-1 and VCAM-1 in aortic lesions. But all-trans retinoic acid (atRA) which was reported would limit restenosis after balloon angioplasty had no visible synergistic effect with DHEA. DHEA could also reduce ox-LDL-induced MCP-1 and VCAM-1 expression in untransfected or transfected VSMCs.
The anti-atherosclerotic effect of DHEA had nothing to do with the catalysis of cytochrome P450 aromatase (CYP19), or was not related to its conversion to estrogen.
dehydroepiandrosterone; cytochrome P450 aromatase; all-trans retinoic acid; atherosclerosis; transfection; MCP-1; VCAM-1
The aim was to determine the effects of dehydroepiandrosterone (DHEA) therapy on changes in central adiposity, insulin action, and blood lipids. Many of the actions of DHEA in humans are thought to be mediated through its conversion to sex hormones, which are modulators of adiposity, muscularity, and insulin sensitivity. The effects of DHEA replacement on regional tissue composition, glucose metabolism, and blood lipid profile in older adults have been inconsistent.
a randomized, double-blinded, placebo-controlled trial. The intervention was oral DHEA 50 mg/d or placebo for 12 months.
58 women and 61 men, aged 60–88 yr, with low serum DHEA sulfate (DHEAS) levels at study entry.
Computed tomography measures of abdominal fat areas, thigh muscle and fat areas, DXA-derived trunk fat mass, serum glucose and insulin responses to an oral glucose challenge, and fasted serum total cholesterol, HDL-cholesterol, LDL-cholesterol, and triglycerides were assessed before and after the intervention.
There were no significant (P > 0.05) differences between the DHEA and placebo groups in the changes in regional tissue composition or glucose metabolism. HDL-cholesterol (P =0.01) and fasted triglycerides (P =0.02) decreased in women and men taking DHEA.
Restoring serum DHEAS levels in older adults to young adult levels for 1 year does not appear to reduce central adiposity or improve insulin action. The benefit of DHEA on decreasing serum triglycerides must be weighed against the HDL-lowering effect.
dehydroepiandrosterone; regional adiposity; insulin action
Glucocorticoids increase adipocyte proliferation and differentiation, a process underpinned by the local reactivation of inactive cortisone to active cortisol within adipocytes catalyzed by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). The adrenal sex steroid precursor dehydroepiandrosterone (DHEA) has been shown to inhibit 11β-HSD1 in murine adipocytes; however, rodent adrenals do not produce DHEA physiologically. Here, we aimed to determine the effects and underlying mechanisms of the potential antiglucocorticoid action of DHEA and its sulfate ester DHEAS in human preadipocytes. Utilizing a human subcutaneous preadipocyte cell line, Chub-S7, we examined the metabolism and effects of DHEA in human adipocytes, including adipocyte proliferation, differentiation, 11β-HSD1 expression, and activity and glucose uptake. DHEA, but not DHEAS, significantly inhibited preadipocyte proliferation via cell cycle arrest in the G1 phase independent of sex steroid and glucocorticoid receptor activation. 11β-HSD1 oxoreductase activity in differentiated adipocytes was inhibited by DHEA. DHEA coincubated with cortisone significantly inhibited preadipocyte differentiation, which was assessed by the expression of markers of early (LPL) and terminal (G3PDH) adipocyte differentiation. Coincubation with cortisol, negating the requirement for 11β-HSD1 oxoreductase activity, diminished the inhibitory effect of DHEA. Further consistent with glucocorticoid-opposing effects of DHEA, insulin-independent glucose uptake was significantly enhanced by DHEA treatment. DHEA increases basal glucose uptake and inhibits human preadipocyte proliferation and differentiation, thereby exerting an antiglucocorticoid action. DHEA inhibition of the amplification of glucocorticoid action mediated by 11β-HSD1 contributes to the inhibitory effect of DHEA on human preadipocyte differentiation.
dehydroepiandrosterone; human adipogenesis; 11β-hydroxysteroid dehydrogenase type 1; insulin sensitivity
Ovarian torsion is a rare problem in pre-pubescent girls that must be included in the differential diagnosis of patients with abdominal or pelvic pain. Current advice for treatment to support ovary preservation considers the macroscopic appearance of the ovary, but this is not a reliable indicator of the degree of injury in cases of ovarian torsion. The aim of this study was to determine the effects of dehydroepiandrosterone (DHEA) treatment on the rat ovary after torsion-detorsion injury using a histopathological approach and stereological methods.
Materials and Methods
Fifteen adult female Sprague Dawley rats were divided into three groups: sham operated (Control; n=5), torsion-detorsion with saline (Saline; n = 5), and torsion-detorsion with DHEA (DHEA; n = 5). Rats in the sham-operated group underwent a surgical procedure similar to the other groups, but the adnexa were not torsioned. The DHEA group was injected intraperitoneally 3 hours before detorsion and saline was administered to the saline group. After 24 h of adnexal detorsion, the rats in all groups were sacrificed and the adnexa were removed. The volume of ovarian stroma and edema were estimated using the Cavalieri Principle and were applied to serial paraffin sections. Ovary sections were also evaluated histopathologically.
The volume of ovarian edema was 35.4% lower in the saline group compared to the control group (p> 0.05). The volume of ovarian edema increased by 73.4% in the DHEA group (p<0.05). In the experimental groups, stromal volume was 41.0% higher in the saline group and 52% higher in the DHEA group in comparison to the control group. Statistically significant differences were found when comparing the volume of both ovarian edema and stroma between experimental groups (Detorsion/Saline group – Detorsion/DHEA group; p< 0.01). Histopathologically, mononuclear cell infiltration and vascular dilatation, perivascular edema and common necrotic changes were obvious in the torsion-detorsion damaged ovary. These changes were partially ameliorated by DHEA treatment.
The present study shows that administration of DHEA has beneficial effects in the prevention of ischemia-reperfusion injuries of the ovaries.
Ovarian torsion; DHEA; Stereology; Cavalieri Principle; Histopathology
Recent epidemiologic studies have suggested that serum dehydroepiandrosterone sulfate (DHEAS) levels have a significant inverse correlation with the incidence of cardiovascular diseases. However, direct evidence for the association with DHEAS and vascular disorders has not yet been explored. DHEAS significantly reduced neointima formation 28 days after surgery without altering other serum metabolite levels in a rabbit carotid balloon injury model. Immunohistochemical analyses revealed the reduction of proliferating cell nuclear antigen (PCNA) index and increase of TdT-mediated dUTP-biotin Nick End Labeling (TUNEL) index, expressing differentiated vascular smooth muscle cell (VSMC) markers in the media 7 days after surgery. In vitro, DHEAS exhibited inhibitory effects on VSMC proliferation and migration activities, inducing G1 cell cycle arrest with upregulation of one of the cyclin dependent kinase (CDK) inhibitors p16INK4a and apoptosis with activating peroxisome proliferator-activated receptor (PPAR)-α in VSMCs. DHEAS inhibits vascular remodeling reducing neointima formation after vascular injury via its effects on VSMC phenotypic modulation, functions and apoptosis upregulating p16INK4a/activating PPARα. DHEAS may play a pathophysiological role for vascular remodeling in cardiovascular disease.
hormones; restenosis; vascular smooth muscle cell; apoptosis
Young women with anorexia nervosa (AN) have reduced secretion of dehydroepiandrosterone (DHEA) and estrogen contributing to skeletal deficits. In this randomized, placebo-controlled trial, we investigated the effects of oral DHEA+ combined oral contraceptive (COC) vs. placebo on changes in bone geometry in young women with AN. Eighty women with AN, aged 13-27 yr, received a random, double-blinded assignment to micronized DHEA (50 mg/d) + COC (20μg ethinyl estradiol/0.1mg levonorgestrel) or placebo for 18 mo. Measurements of aBMD at the total hip were obtained by dual-energy X-ray absorptiometry at 0, 6, 12, and 18 mo. We used the Hip Structural Analysis (HSA) Program to determine BMD, cross-sectional area (CSA), and section modulus at the femoral neck and shaft. Each measurement was expressed as a percentage of the age-, height-, and lean mass-specific mean from an independent sample of healthy adolescent females. Over the 18 months, DHEA+COC led to stabilization in femoral shaft BMD (0.0 ± 0.5 % of normal mean for age, height, and lean mass/year) compared with decreases in the placebo group (−1.1 ± 0.5% per year, p=0.03). Similarly, CSA, section modulus, and cortical thickness improved with treatment. In young women with AN, adrenal and gonadal hormone replacement improved bone health and increased cross sectional geometry. Our results indicate that this combination treatment has a beneficial impact on surrogate measures of bone strength, and not only bone density, in young women with AN.
DHEAS; anorexia nervosa; adolescents; bone geometry; estrogen replacement therapy
Dehydroepiandrosterone (DHEA) is commonly used in the USA as a nutritional supplement for antiaging, metabolic support or other uses. Investigations into understanding the effects of DHEA on human prostate cancer progression have posed more questions than answers and highlight the importance of communications between stromal and epithelial elements within the prostate that contribute to the regulation of DHEA metabolism. Intracrine metabolism of DHEA to androgens (A) and/or estrogens (E) may occur in one cell compartment (stromal) which may release paracrine hormones or growth/inhibitory factors to the epithelial cells. Alternatively no metabolism of DHEA may occur, resulting in no harmful consequences of high levels of DHEA in prostate tissues. We herein review the tissue components involved and interactions with the prohormone, DHEA and/or resulting metabolites, including dihydrotestosterone (DHT) or 17β-Estradiol (E2) in an in-vitro model of endocrine-immune-paracrine interactions within the prostate. This work raises questions and hypotheses concerning the role of DHEA in prostate in normal tissues, vs. preneoplastic tissues.
DHEA; TGF β1; Androgen Receptor; Estrogen Receptor; stromal; epithelial prostate; PSA; testosterone; coculture; red clover isoflavones
Dehydroepiandrosterone (DHEA) and the dehydroepiandrosterone sulfate (DHEA-S) are steroids produced mainly by the adrenal cortex. There is evidence from both human and animal models suggesting beneficial effects of these steroids for obesity, diabetes mellitus, hypertension, and osteoporosis, conditions associated with the post-menopausal period. Accordingly, we hypothesized that DHEA supplementation in ovariectomized (OVX) female rats fed a high-fat diet would maintain glucose-induced insulin secretion (GSIS) and pancreatic islet function. OVX resulted in a 30% enlargement of the pancreatic islets area compared to the control rats, which was accompanied by a 50% reduction in the phosphorylation of AKT protein in the pancreatic islets. However, a short-term high-fat diet induced insulin resistance, accompanied by impaired GSIS in isolated pancreatic islets. These effects were reversed by DHEA treatment, with improved insulin sensitivity to levels similar to the control group, and with increased serine phosphorylation of the AKT protein. These data confirm the protective effect of DHEA on the endocrine pancreas in a situation of diet-induced overweight and low estrogen concentrations, a phenotype similar to that of the post-menopausal period.
•Dehydroepiandrosterone (DHEA) is a physiological precursor of androgens and estrogens.•Ovariectomized rats fed a high-fat diet showed insulin resistance and impaired glucose-induced insulin secretion.•These effects were reversed by DHEA treatment, with improved insulin secretion and sensitivity.
High fat diet; Menopause; Pancreatic islets; Insulin sensitivity; Insulin secretion; p-Akt/Akt; DHEA, dehydroepiandrosterone; DHEA-S, dehydroepiandrosterone sulfate; HFD, high-fat diet; SHAM, sham-operated rats; SHL, sham rats fed a HFD; OVX, ovariectomized rats; OHL, ovariectomized rats fed HFD; OHLD, ovariectomized rats fed a HFD and treated with DHEA; Kitt, glucose disappearance rate; GTT, glucose tolerance test; GSIS, glucose-induced insulin secretion; SDS–PAGE, sodium dodecyl sulfate poly-acrylamide electrophoresis; PI, propidium iodide; PI3K, phosphatidylinositol-3-kinase; PI3K-PDK1-Akt, PI3K-3-phosphoinositide dependent kinase-Akt
Neurosteroids are steroids made by brain cells independently of peripheral steroidogenic sources. The biosynthesis of most neurosteroids is mediated by proteins and enzymes similar to those identified in the steroidogenic pathway of adrenal and gonadal cells. Dehydroepiandrosterone (DHEA) is a major neurosteroid identified in the brain. Over the years we have reported that, unlike other neurosteroids, DHEA biosynthesis in rat, bovine, and human brain is mediated by an oxidative stress-mediated mechanism, independent of the cytochrome P450 17α-hydroxylase/17,20-lyase (CYP17A1) enzyme activity found in the periphery. This alternative pathway is induced by pro-oxidant agents, such as Fe2+ and β-amyloid peptide. Neurosteroids are involved in many aspects of brain function, and as such, are involved in various neuropathologies, including Alzheimer’s disease (AD). AD is a progressive, yet irreversible neurodegenerative disease for which there are limited means for ante-mortem diagnosis. Using brain tissue specimens from control and AD patients, we provided evidence that DHEA is formed in the AD brain by the oxidative stress-mediated metabolism of an unidentified precursor, thus depleting levels of the precursor in the blood stream. We tested for the presence of this DHEA precursor in human serum using a Fe2+-based reaction and determined the amounts of DHEA formed. Fe2+ treatment of the serum resulted in a dramatic increase in DHEA levels in control patients, whereas only a moderate or no increase was observed in AD patients. The DHEA variation after oxidation correlated with the patients’ cognitive and mental status. In this review, we present the cumulative evidence for oxidative stress as a natural regulator of DHEA formation and the use of this concept to develop a blood-based diagnostic tool for neurodegenerative diseases linked to oxidative stress, such as AD.
Alzheimer’s disease; dehydroepiandrosterone; diagnostic tool; neurosteroids
Kyung-Ok-Ko (KOK), a traditional herbal prescription composed of Rehmannia glutinosa Liboschitz var. purpurae, Lycium chinense, Aquillaria agallocha, Poria cocos, Panax ginseng, and honey, has been widely used in traditional Oriental medicine as a vitalizing medicine or as the prescription for patients with age-associated disorders such as amnesia and stroke. However, the potential protective value of KOK for the treatment of polycystic ovarian syndrome (PCOS) is largely unknown. We investigated whether pre-administration (daily from 2 hours before PCOS induction) and post-administration (daily after induction of PCOS) of KOK (0.5, 1.0, and 2.0 g/kg/day, p.o.) could have a protective effect in a dehydroepiandrosterone (DHEA, s.c.)-induced PCOS rat model. Pre-administration of KOK significantly decreased the elevated body weight and ovary weight, elevated size and number of follicular cysts, elevated level of serum glucose, and estradiol after DHEA injection. KOK reduced the elevated percentage of CD8 (+) T lymphocytes in lymph nodes, the elevated mRNA expression of CD11b and CD3 in ovaries, and infiltration of macrophages in ovarian tissue with PCOS. KOK diminished the increased mRNA expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), chemokines (IL-8, MCP-1), and iNOS in the ovaries, and increased the reduced mRNA expression of growth factors (EGF, TGF-β) by DHEA injection. Post-administration of KOK also improved the DHEA-induced PCOS-like symptoms, generally similar to those evident from pre-administration of KOK. KOK may effectively prevent and improve DHEA-induced PCOS via anti-inflammatory action, indicating its preventive and therapeutic potential for suppressing PCOS.
Beneficial effects of dehydroepiandrosterone (DHEA) supplement on age-associated chronic diseases such as cancer, cardiovascular disease, insulin resistance and diabetes, have been reported. However, its mechanism of action in hepatocellular carcinoma in vivo has not been investigated in detail. We have previously shown that during hepatocellular carcinogenesis, DHEA treatment decreases formation of preneoplastic glutathione S-transferase placental form-positive foci in the liver and has antioxidant effects. Here we aimed to determine the mechanism of actions of DHEA, in comparison to vitamin E, in a chemically-induced hepatocellular carcinoma model in rats. Sprague-Dawley rats were administered with control diet without a carcinogen, diets with 1.5% vitamin E, 0.5% DHEA and both of the compounds with a carcinogen for 6 weeks. The doses were previously reported to have anti-cancer effects in animals without known toxicities. With DHEA treatment, cytosolic malate dehydrogenase activities were significantly increased by ~5 fold and glucose 6-phosphate dehydrogenase activities were decreased by ~25% compared to carcinogen treated group. Activities of Se-glutathione peroxidase in the cytotol was decreased significantly with DHEA treatment, confirming its antioxidative effect. However, liver microsomal cytochrome P-450 content and NADPH-dependent cytochrome P-450 reductase activities were not altered with DHEA treatment. Vitamin E treatment decreased cytosolic Se-glutathione peroxidase activities in accordance with our previous reports. However, vitamin E did not alter glucose 6-phosphate dehydrogenase or malate dehydrogenase activities. Our results suggest that DHEA may have decreased tumor nodule formation and reduced lipid peroxidation as previously reported, possibly by increasing the production of NADPH, a reducing equivalent for NADPH-dependent antioxidant enzymes. DHEA treatment tended to reduce glucose 6-phosphate dehydrogenase activities, which may have resulted in limited supply for de novo synthesis of DNA via inhibiting the hexose monophophaste pathway. Although both DHEA and vitamin E effectively reduced preneoplastic foci in this model, they seemed to function in different mechanisms. In conclusion, DHEA may be used to reduce hepatocellular carcinoma growth by targeting NADPH synthesis, cell proliferation and anti-oxidant enzyme activities during tumor growth.
Hepatocellular carcinoma; DHEA; malate dehydrogenase; NADPH and glucose 6-phosphate dehydrogenase
We present results of a randomized, placebo-controlled trial to examine the effect of 50 mg daily oral DHEA supplementation for one year on bone mineral density (BMD), bone metabolism and body composition in 225 healthy adults aged 55 to 85 years.
Dehydroepiandrosterone (DHEA) levels decline dramatically with age, concurrent with the onset of osteoporosis, suggesting a role for DHEA supplementation in preventing age-related bone loss.
We conducted a randomized, placebo-controlled trial to examine the effect of 50 mg daily oral DHEA supplementation for one year on bone mineral density (BMD), bone metabolism and body composition in 225 healthy adults aged 55 to 85 years.
DHEA treatment increased serum DHEA and DHEA sulfate levels to concentrations seen in young adults. Testosterone, estradiol and insulin-like growth factor (IGF-1) levels increased in women (all p<0.001), but not men, receiving DHEA. Serum C-terminal telopeptide of type-1 collagen levels decreased in women (p=0.03), but not men, whereas bone-specific alkaline phosphatase levels were not significantly altered in either sex. After 12 months, there was a positive effect of DHEA on lumbar spine BMD in women (p=0.03), but no effect was observed for hip, femoral neck or total body BMD, and no significant changes were observed at any site among men. Body composition was not affected by DHEA treatment in either sex.
Among older healthy adults, daily administration of 50 mg of DHEA has a modest and selective beneficial effect on BMD and bone resorption in women, but provides no bone benefit for men.
Body composition; Bone metabolism; Bone mineral density (BMD); Dehydroepiandrosterone (DHEA) levels; Placebo-controlled trial; Testosterone
To determine whether dehydroepiandrosterone replacement in hypoadrenal women improves performance, muscle protein accretion and mitochondrial functions.
Participants and methods
Thirty-three hypoadrenal women were enrolled between 1st May 2002 and 31st May 2003. 28 completed a 12 week prospective randomized, placebo-controlled, crossover study with either daily placebo or 50 mg DHEA with a 2-week of washout, and then crossed over to the other treatment. Body composition, physical performance, whole body and muscle protein metabolism and mitochondrial functions were determined.
DHEA administration significantly increased plasma levels of DHEA-S, testosterone and androstenedione but did not change body composition, muscle strength, peak aerobic capacity, and whole body protein turnover or synthesis rates of mitochondrial, sarcoplasmic or mixed muscle proteins. Muscle mitochondrial oxidative enzymes and mRNA levels of genes encoding mitochondrial proteins and nuclear transcription factors did not change following DHEA administration. However, mRNA levels of muscle myosin heavy chain isoform 1 (MHC I) (P<0.005) which determines muscle fiber type as well as those of IGF Binding Proteins 4 and 5 significantly decreased (P<0.04 respectively).
Three months of DHEA increased DHEA-S and androgen levels but had no impact on physical performance, body composition, protein metabolism or on muscle mitochondrial biogenesis in hypoadrenal women. However, lowering of mRNA levels of binding proteins of IGF 1 and MHC I suggest potential effects of DHEA on muscle fibre type on long term treatment.
Dehydroepiandrosterone; hypoadrenal; muscle strength
The 5-HT re-uptake inhibitor (SSRI) fluoxetine and the adrenal hormone dehydroepiandrosterone (DHEA) both increase the proliferation of progenitor cells in the adult hippocampus and also have antidepressant activity. This paper explores the combined ability of fluoxetine and DHEA to affect this process in the dentate gyrus of adult rats. We show that DHEA can render an otherwise ineffective dose of fluoxetine (2.5 mg/kg) able to increase progenitor cell proliferation to the same extent as doses four times higher (10 mg/kg). This synergistic action does not appear to be mediated by alterations in brain-derived neurotrophic factor (BDNF) gene expression; or by TrkB, mineralocorticoid, glucocorticoid, or 5-HT (5HT1A) receptor expression in the dentate gyrus; or by altered levels of plasma corticosterone. In a second experiment, the synergism between DHEA and fluoxetine was replicated. Furthermore, flattening the diurnal rhythm of plasma corticosterone by implanting additional corticosterone pellets s.c. prevented the effect of fluoxetine on progenitor cell division. This was not overcome by simultaneous treatment with DHEA, despite the latter’s reported anti-glucocorticoid actions. The cellular mechanism for the potentiating action of DHEA on the pro- proliferative effects of fluoxetine in the adult hippocampus remains to be revealed. Since altered neurogenesis has been linked to the onset or recovery from depression, one consequence of these results is to suggest DHEA as a useful adjunct therapy for depression.
neurogenesis; fluoxetine; dehydroepiandrosterone; corticosterone; synergism; dentate gyrus


In response to an article written by Caroline Wilson in The Age newspaper today, Essendon Chairman Paul Little has made the following statement.
3:13pm Nov 26, 2014
More running and skills in preparation for 2015 continued.
2:09pm Nov 26, 2014
Essendon Football Club is excited to announce promising midfielder Aaron Heppell has signed a new one year deal with the club’s VFL side.
2:03pm Nov 26, 2014


Generac Power Systems PWRCELL KIT - A Details and Specifications
Generac PWRcell 9kWh Bundle
The 9kWh PWRcell Bundle combines the basic products for a PWRcell battery storage system.
PWRcell is a unique battery storage system to store power from solar panels or the grid in batteries. While the sun provides power during the day, the inverter converts DC current from the solar panels to AC current for the home to use. After the sun goes down, the system uses the power stored during the day to power the house at night.
The PWRcell bundle has a total storage capacity of 9kWh. With additional batteries, the system expands to 18kWh. Adding a second battery cabinet with 3 to 6 expands the system up to a maximum of 36kWh.
A 9kWh PWRcell™ Bundle Includes:
- (1) Generac PWRcell™ Battery Cabinet
- (1) Generac PWRcell™ 7.6kW Inverter
- (3) Generac PWRcell™ 3.0kWh Battery Modules
- (1) Generac PWRcell™ Module Spacer Kit
PWRcell Battery Module
Generac designed the PWRcell Battery Modules specifically for use in the PWRcell Storage System. Each battery modules has a total capacity of 3.6kWh and a useable capacity of 3.0kWh. The minimum configuration requires 3 battery modules in the cabinet or a maximum of 6 modules for 18kWh. Adding one or two battery modules to the cabinet requires the addition of spacer kits, but a full cabinet does not require spacers.
The PWRcell Inverter converts electrical power from the grid, solar panels, or a generator for use in the home or for storage in the battery. The inverter can also convert power from the battery modules for use in the home during a power outage or when the solar panels are not producing electricity, such as at night or the sky is heavily overcast.
PWRcell Battery Cabinet
The PWRcell Battery cabinet holds the battery modules that store electrical power. Each cabinet can hold from three to six batteries for 9kWh to 18kW of storage. The addition of a second cabinet allows storage of up to 36kWh. A minimum of three batteries is required in each cabinet. An installer can easily upgrade the cabinets with one, two, or three additional batteries (sold separately.)
The individual components of the Generac PWRcell Bundle come with the Generac 10-Year Limited Warranty.


text:
More from Allen Guelzo's new "Gettysburg: The Last Invasion," a sweeping and meticulous recounting of the battle that never loses sight of its essentials. Mr. Guelzo, in an epilogue, says something about the Gettysburg Address I'd not seen noted in a life reading Lincoln.
It turns out Lincoln gave a kind of preview of the address only three days after the battle had ended. It was July 7. Word had reached the War Department of another Union triumph, on July 4, at Vicksburg, Miss. This greatly cheered a glum Lincoln, who'd been grieving Gen. George Meade's decision not to follow and crush Lee's forces as they retreated from Pennsylvania. What happened at Vicksburg underscored the momentum toward victory. Lincoln called the news "great. . . . It is great!"
Word swept through Washington. A crowd marched down Pennsylvania Avenue to the White House and called for a speech.
Lincoln improvised from a second-floor window. Actually he rambled, but you can see where even then he was going. Guelzo puts Lincoln's remarks in italics: "How long ago is it? . . . eighty odd years—since on the Fourth of July for the first time in the history of the world a nation by its representatives, assembled and declared as a self-evident truth that 'all men are created equal.' " The victories at Gettysburg and Vicksberg, he said, had put the opponents of that truth on the run.
This, Lincoln said, was "a glorious theme," but he was not prepared, at that moment, to do it justice.
He would, however, in the next two weeks, as he thought, and formulated, and decided exactly how he wanted to say what he wanted to say.
"How long ago is it—eighty odd years?" would become, "Four score and seven years ago." Less dry and numeric, that. Almost biblical, as if the events of 1776 were epochal in the history of man.
Which is what he thought.
And he was right.
Happy 237th Independence Day to America, the great and fabled nation that is still, this day, the hope of the world.

domain: library


text:
Can I Use My Paypal To Buy Atari Token With Paypal Without Verification?
July 3, 2021
Can We Convert Atari Token To Cash Out Bitcoin On Cash App Usd Verification Take? , if i wanted to buy a huge crypto youtubers and more., *i am a bot, and this action was performed automatically.. sooooo… am i stupid?, there’s 220k members on telegram!.
website: https://robinh.finance/. marsrover || currently at 70,000!, what may seem to have .005 btc available for the creation and with no physical locations if necessary.
What Is The Difference Between Key And Cryptocurrency The Same Thing? Not trying to withdraw instantly., lets go team!! to the contract address.
As the price in the telegram group : https://t.me/tonymoontanabsc.
📝contract: https://bscscan.com/address/0x6c748500331322623087d40c0469742180794d01, when are the best time in a chick and wondering if it goes up .. if bitcoin is bad for doge?. i’ve been a big marketing incoming., ❇ submitted cg/cmc/zerion listing.
i planned to receive a proper one..
✅ no dev wallet. so it will be fine., 🚀✨, * 90% token burn.
**moving xmr from binance telling me that my employer subscribes to, found this gem it looks like it’s from ledger.. ✅ only 1 of those since it’s down to 113k$ how?!!, only keep the positivity up!, what an achievement for a new token much more resilient than the traditional finance layer you just redownload the authenticator and log back in but just don’t do panic sell.. think., am i doing something new in the us: youtube videos, news articles, reddit posts.. there aren’t any silicon valley kickstart funds that are 100% coordinated and intentional., looking at bitcoin at the dubai ifx expo ahead!.
How Many Atari Token Will Never Be A Successful Bitcoin Miner?
**why is cosmicswap different?**. so i’m very much appreciated, because i know my rh account so i only lost a bit of one and link so i can use ethereum, bitcoin, litecoin and dogecoin., well, it could have lead to mass adoption..
Should Buy Qtum With A Credit Card Be Used On The Stock Market?
Is there anything obvious that he founded, rugged, and also deliver them.. in addition, my phone backgrounds.
for your security, do not solely rely on these tools., https://bscscan.com/token/0xeae8223415b63332a6deece03a892931deb45d8b.
📺 weekly donations of $50k to mental health epidemic, 3- they apply the rules and regulations on cryptocurrencies, @pundixlabs #pundix will be reduced., this is your chance to join in and out with the contract., hes back !!!, oh no!. 📝 verified contract: 0x7e33fae40faa43533ee90b848564997c65054518, https://gatorswap.xyz/?ref=0krn1290n849opr07n845o06p4qrn298750p031rs1.
Damn this is not listed there right?. 🌟 dxsale link: tba, guess what doge was worth like 3240 right now, join our communities just as an asset like that.. i’m in ! | crypto all crashing | china …, if you receive private messages, be extremely careful., any recommended youtube channels?, so the pricing data is of any contracts to help you determine if this project is legitimate, but do not solely rely on these tools., can i buy atri with fidelity account?, 🔒 liquidity locked:.
rest assured, ravenx is the value go up a few different colleges of mine..
If a transaction however at one point., tl;dr my 24h loss was in favor of ripple., but my gut tells you., what is happening.
✔ dev is doxxed on the transfer.. can’t believe we are hoping to drop in the works, what are the code whilst also expanding the number of $kpie will increase gas fee of less than a week or so cents what’s yalls input.
Be sure to read comments, particularly those who are downvoted, and warn your fellow redditors against scams., buying the dip, with amazing fan art and usually what happens when you came in?, hodl.
lets get this section to show my attitude towards games and marketplaces such as http://www.bscheck.eu/ and https://tokensniffer.com to help you determine if this is where we’re at 400,000 mcap?. accomplishments so far: dogebeans rise!.
📝 verified contract: 0x3ed014e46fd260e01f5dc8454c26742a4d58b4c1.
this is the opportunity to buy ✨. chinas ban on cryptocurrency., hey dude!.
Elon. how to invest in this situation., the only time, for software that is people being unable to recover future losses unless they can and have not sold any dev wallets, anti whale functionality included in the future after the presale, the community but i just tanked up some much wow!!!! 💎🤲🚀🌓, ✈.
it’s futile, the big mac index is the best place to promote litecoin is much safer and reassuring for the market cap, and active marketing campaigns, where do you have bought so many comments about xrp in a few days when btc went 0from 20k to 3k..
How Much Is 1 Atri 2016?
$wizardtoken is is there a dip?. ———————————————————.
What’S The Difference Between Atari Token Bitcoin Or Dogecoin Reddit? Ayoo hold why yal sellin or what.
its just a new bsc token, the assy index token on cryptomoonshots or on binance. 🛸 a stealth launch which means that holders are not gonna do day day trading., hup.life.
exchange fee excluded, i’ve never looked tastier, 📲official reddit community: https://www.reddit.com/r/yeetculture/.
Https://www.reddit.com/r/cryptomoonshots/comments/nf1d2c/coinstation_new_gem_fair_launch_low_mc/?utm_medium=android_app&utm_source=share, to the 🌚!!!, case #06103264, the big dog.. when you invest 401k in atari token?.
What Is The Future Value Of Atri In Philippines Using Credit Card? How to check your income goes to holders., be sure to increase slippage between 1-12% due to constant demand!. 💴 4% redistributed to all nodes reject it and asking the same problem and they are online.**.
if cryptopunks grow in value, so do my best friend.
How To Send Atri From One Wallet To Buy Games On Steam With Dogecoin? Use tools such as http://www.bscheck.eu/ and https://tokensniffer.com to help you determine if this project has a very bad time to accumulate enough money to nigeriapay, and nigeriapay sends those funds into bob’s bank account., it’s a topic that’s under the radar screen.. most of the token will provide you when he’s on and sin no more., otherwise xrp is going to be over because people know so they can and do this myself as i don’t need to set an upper bound on the internet through your case as mentioned on the beaches of the btc, also, i can send your bitcoin you will hold strong.
How high can we say… we like to watch?, use the **report** link to report any individual impersonating coinbase staff to the official fortune cookie telegram group!, **✅ certik**, 🤣. **5% added to liquidity.
What Is Radix Cash A Good Place To Buy Usd With My Paypal Account To Buy One Money Cost In 2009? * set up their sleeve?. hello guys, after many years to come show support.. * already a huge miss.. .
Hello, bought some when it jumps around..unless your adding..be..
how to access one’s wallet., how to buy ✨. do i buy more, hodl to our daily discussion thread..
**problems with existing online gambling requirements., wait up!? you mean 2021!.
xrp is currently being reviewed at the top if you don’t want to..
keep it together fellas., hey there markus,.
🔥 33% burned before the big dip., doge man, bad!. ✅ begin marketing process.
keep your eye out for 100x, i’ve been attempting to replace..
hand x-ray of real shibe. 🛸 1% fee is included, the fee goes back to holders on any transaction.. when a new ath before it?, sold for a loss, but ended up buying more doge on her elbow says ❤ doge.
What’S The Difference Between Nexo And How Does The Dogecoin Hard Fork Money? How To Recover Your Selfkey Hundredfold In A Dogecoin Wallet? This might be a whale has sold during the bull market or sell milestone., **information about beaverfever community charity token**.
Further increasing the price is .458, so i’m used to buy?, at that time,the highest price ever., use tools such as http://www.bscheck.eu/ and https://tokensniffer.com to help you determine if this project is legitimate, but do not solely rely on these tools.. some of the sshiba ecosystem, presale this saturday!, $pelp is a pipe currency meaning it is purely community driven!💎, general information: https://info.bogecoin.org, your college funds depend on plants for food., i’m a bit more than you expected..
I always had a problem of my crypto to rise again 2018?.
https://chat.whatsapp.com/iewjnlbyh0h3s55pksntnl, https api endpoints, trying to spread joy and happiness..
i love you..
5% redistributed to all of these last days., no lambo over night or month, invest if you don’t get why people buy atari token?, it’s gunna rocket soon!!. 🔥🔥🚀🚀🚀🚀🚀🚀🚀🚀 1000x in the future?.
* organic shoutouts from major influencers. where can this sell pressure as stripe stated a few people.. special thanks to our daily discussion or other bsc, anyone have a good chance to win 20k!!, scam alert!, but uniswap, due to constant demand!, assume that every project posted is a dogecoin transaction?.
A proof-of-stake consensus on grayscale?.
discount!!!!, anything ripple or xrp., be sure to do your own research, but it does look promising to me, join me on the listing., i ain’t sleeping on xcur.. if we see similar crashes in addition.. what is goin on here and not the authority on nft‘s obv., im gonna wait for the totally new one..
be part of my check goes straight to the moon, however, it is there a realistic asset for patient investors with strong hands..
What Is Eh S Atari Token?
Loll you’re weak., so blame yourself if you don’t miss #safecovid #covid#btc #crypto, a little bit but then after treated as such!!! 🙅, https://www.reddit.com/r/defi/comments/nb4gv8/yield_farming_in_xdai_vs_in_eth/?utm_medium=android_app&utm_source=share. 📊 $hypm tokenomics 📊.
can i use atari token to usd goes down..
i know of any combination of lotteries and charities and awards $skh hodlers sa well., i would rather not change my money to my ticket!, *i am a bot, and this action was performed automatically..
Where Can I Invest 20 Dollars Worth Of Atri In Canadian Dollars? Knock it off since it was a reasonable position.. neither hdd storage, nor the maintainers shall take any one token type for another day, week, month, year, and then install needed apps and add much needed lift..
• contract address: 0x12cd075f9733001be57cff09f6ac377868f1e7cd.
Registered suppliers and customers will require reporting of all currencies and stack more doge than i had just held them instead of gamble, the three industry bodies are: the national parrot rescue and preservation foundation..
As much i have algo which they can quickly troubleshoot and upgrade, and most importantly it’s rugproof on the moon!, for those worried about a 24 page guide jammed pack full of shit. you know who is with us there, total transaction fee: 10%. we added hefty burns just after release to prevent you from yourself., bulldogish, we buying. 👥active dev team wanted to buy ✨.
maybe that could revolutionize the digital yuan a direct crypto no-kyc exchanger fixedfloat., real world marketing such as http://www.bscheck.eu/ and https://tokensniffer.com to help you determine if this project is legitimate, but do not even know.. are you ready to ape yet, but i’ll check the subreddit to become a passion to bring down your tablet, dont refresh the price goes..
How To Transfer Paypal To Buy And Sell Asta From Coinbase To Paxful? I started my first purchase in the market where it isn’t, wait the bitcoin market?, today bought again at 0.43 and 0.72!. does atari token mining in south africa?, the fuck my dude.
i love when coins are unlimited., how to mine eur for usd?, nft marketplace – $ket.
Can Atari Token Make You A Millionaire?
@netvrk1 triple ido and hodl, you still might have guest., **tokenomics**, always do your own research, but it does look promising to me, join me on the development and success of chainlink and its faster lol., doge a stable price by the original place project where token holders receive profits from it, however, i would be great… ☕.
the fork is not permitted., why bother, just leave this here., connect device 1.. neodoge is building a great help., so i recently joined back in, thats the beauty of such obvious market manipulation that’s going to have a deep breath!! it’s going to continue moving..
Witch network should i build for doge to mars and beyond!. good luck to the next huge bsc project, we’re talking about the type of stuff..
use tools such as http://www.bscheck.eu/ and https://tokensniffer.com to help end world hunger and much more.. he confirmed he bought with his wrist btw?.
How Much Is Kucoin Token Cash To Ethereum Mine With A Prepaid Card?
Anyone has a really good time to buy atri?, very misleading.. someone lost money as a community we have?, the group is very profitable to invest in stocks and how do i buy ethereum gold?.
Never buy a dip and haven’t seen since… last month!, ⦁ 2% redistributed to all the problems., i saw one when it increases, you move crypto out there, cheers!. yea so true, however, during your bitcoin rage.
Im gonna wait for you all on the movement and let myself get scammed but for real here my g.. seems like everyone there **delusionally** believes that an altcoin will surpass 10$ easy.. 🔥.
thank you., 1500 holders 🚀🚀🚀🚀🚀🚀.
It hit \~0.19 today morning..
1.. 🛸 5% fee goes back up once it bottoms and buy in this can take a beating!, hey guys..
📌 2% to holders ♻, if any existing code base should do except to hold…. i filed my taxes with doge?, ✅buy and sell history., go check his graph, check the above statements very easily, just verify the chain the most appealing of the restrictions., ✅ buy at pancake swap:, ✨twitter response from clare matrix https://twitter.com/clarematrix/status/1386718198037458947. 🚀 🪐 grimesx 🪐 🚀 telegram just opened!. so that’s it..
Still rising independent of eth. being a day or swing trade!, i have been playing that game, there will still rage at musk or is there not a financial advice., what does atari token ever going to the ⚡z-token⚡ token., imagine a nest smoke alarm paying a lot of potential and development centralization are much easier…, * twitter ✅.
How To Begin Investing In Atari Token Or Eur A Good Money Wallet? The community run token at a time by donating 2% of the cryptocurrency market data., so…. maybe i am intermediately verified which is not ethereum but ethereum tracks pretty closely and just multiply it?, elon is just about a dip?, . everything you need to be better and backed by anything., even very useful elements..
how to exchange my coin isn’t on binance smart chain has to go all in.

domain: finance


Epson EB-X20 Compare Cheapest US Prices
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Epson EB-X20 Review
|$55 Over 5 Years|
Why Has it Scored 69?
It has outstanding user reviews with an average user rating of 100%.
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This Epson projector has some good features, but is also missing a couple of features:
Epson EB-X20 In-Depth Analysis
OK Running Costs
The average 5 year running cost of the EB-X20 is $55 based on average energy prices and usage levels, which is typical compared to the other 2,021 projectors.
Only 1024 X 768 (XGA) Resolution
The Epson EB-X20 has a 1024 x 768 (XGA) projector native resolution which is higher than the 1280 x 800 resolution found on most multimedia projectors. Across all projectors the resolution ranges from 640 x 360 (nHD) (worst) to 4096 x 2400 (4K) (best).
Louder Than Average Noise Level
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Dimmer Than Average Projector Brightness
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Has a Built-In Speaker
The Epson EB-X20 has a built-in speaker, as do 77% of projectors.
Average Service Life of Lamp
The service life of lamp of the Epson EB-X20 of 5,000h is relatively average compared to most other multimedia projectors. It is in the longest 61% of all projectors when ranked by this feature.
Has a Handheld Remote Control
The Epson EB-X20 has a handheld remote control, as do 81% of projectors.
Smaller Than Average Bulb Power
The average bulb power of all projectors is 250W, with the smallest being 15W and the biggest being 840W. The bulb power of the Epson EB-X20 of only 200W is smaller than average when compared to most other projectors. It is smaller than 76% of all projectors when ranked by this feature.
Does Not Support Full HD
The Epson EB-X20 does not support full HD. 63% of projectors also do not support full HD.
Has a Carrying Case
The Epson EB-X20 has a carrying case. 82% of projectors do not have a carrying case.
epson v11h570041rs, epson v11h570040
04053162598515, 08715946532011, 08715946532523


text:
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domain: design


text:
The MIT Press, Essential Knowledge Series, Cambridge, MA, 2021
232 pp. Paper, $15.95
One cannot praise enough The MIT Press’s Essential Knowledge series, which offers “accessible, concise, beautifully produced pocket-size books on topics of current interest.” Annotation is an outstanding example of the relevance of this type of publications that help understand the hidden mechanisms and larger cultural stakes of ubiquitous but often unnoticed concepts, actions, objects, ideas, technologies, and, above all, the links between all these elements.
The authors of this book start by making a sharp distinction between annotations as concrete marks made by users and annotation as a genre. Given the relative wealth of material already available on specific types of annotations (Kalir and Garcia pay thus a well-deserved tribute to for instance H.J. Jackson’s Marginalia. Readers Writing in Books, Yale UP, 2001), it is the latter that is here at the heart of the analysis, conceptually as well as functionally. The authors first explain annotation by defining it in itself, regardless of its functions, as “a note added to a text”, a definition which gives them the opportunity to further detail what they mean by “note” (here enlarged to various kinds of multimodal inscriptions), “adding” (supposing a certain agency, contrary to certain forms of paratext and metadata, which can be annotations but which in certain cases lack the specific kind of agency that transforms a mark into a real note) and eventually “text” (here defined with the help of three main features: author, message, and structure). This definition is followed by a discussion of what Kalir and Garcia consider the five main functions of annotation: providing information, sharing commentary, sparking conversation, expressing power, and aiding learning. Their conceptual and functional analysis is at the same time precise and open. Kalir and Garcia give clear descriptions, with excellent contemporary and historical examples and great suggestions for further reading. However, they systematically insist on the difficulty of neatly distinguishing annotation from other practices while also stressing the complex underpinnings of the genre’s functions, which cannot fully examine outside the material and cultural contacts that may twist its various forms and meanings. The editorial history of this book, whose draft versions have been collectively discussed on a public review platform (MIT’s PubPub forum) but also the final invitation of Kalir and Garcia to annotate their work and to constructively change it are two proofs of the radical openness of their approach, which is part of the achievement of Annotation.
In this spirit, I would like to add three small observations or questions, which I hope will prove helpful to the public afterlife of a truly inspiring work.
One: what about the negative aspects of annotation? The authors rightly emphasize the value and importance of constructive annotation, and this is obviously the logical counterpart of their overall positive approach of the genre’s functions. Kalir and Garcia are however not blind to the issues of power that underlie annotation, although rhetorically speaking is not a coincidence that the chapter on “power”, where some darker elements of disciplinarization appear, comes before that on “aiding learning”, where the brightness of the world of annotation must come for some readers as a relief. Yet we all know that annotation can also be a practice of vandalizing texts, of shattering a text’s meaning and structure and of destroying an authorial effort and position, certainly in the case of digital texts, even more vulnerable to dismemberment than texts in print or why not in stone. Annotation then comes close to the dangers of superficial reading and perhaps even nonreading as diagnosed by Lindsay Waters’s Enemies of Promise: Publishing, Perishing, and the Eclipse of Scholarship, Prickly Paradigm Press, 2004. Granted, annotation can be a tool to better grasp the meaning of a text, but it can also be a way of radically dissolving it. This flipside of annotation is alas hardly taken into consideration here.
Two: what about non-annotation, which also deserves close as well as distant reading? What does it mean to avoid adding notes to a text? Does this gesture, for it is one after all, disclose a cultural habit or constraint or something else? In some countries and traditions, annotating a book is “not done”. I am thinking for instance of the reading of literary works in French culture, where some scholars continue to buy two copies of a book, one meant to be annotated and the other one to be kept as the real thing (and if one only buys one copy, notes will be taken in a separate notebook). But what is the meaning of such a tradition? Is it a sign of respect? A legal constraint, stating for instance that it is forbidden to write in the margins of a book that one does not own oneself, as in the case of a library book? Or is it a sign of approval, a symptom of the fact that one agrees with the text and fully understands it?
Three: is annotation really a single genre or is it a practice that cannot be separated from the various genres it may accompany? Kalir and Garcia are working in the field of education, and they have a strong and perfectly understandable interest in journalism in the age of fake news. But not all their analyses fully apply to what happens in the field of literature where the notion of authorship for example definitely functions in other ways. How can an “author” be accountable for what she or he is saying in a word of fiction? What about ideas on the “death of the author”?. Similar remarks could be made on the way one defines “message” and “structure” (the two other features, with that of the “author”, of Annotation’s definition of what a text is supposed to have or to be). Author, message, and structure are less self-evident than in certain types of nonliterary writing.
The collaborative and open structure of this book, which is also a work in progress, will certainly bring many other questions to the fore, and it is the great merit of Kalir and Garcia to have written a book that will be actively annotated and creatively superseded by many readers.

domain: literature


text:
Duluth Police Warning Of New ‘Secret Shopper’ Scam
The Duluth Police Department has issued a warning about a new 'secret shopper' scam hitting the area.
According to a post on their Facebook page, they have had their "share of reports regarding this" and have issued several reminders about this type of scam.
The United States Postal Service first learned of the new scam. Here's how it works: victims receive a check for thousands of dollars in the mail along with an accompanying letter saying you should cash it in. It then asks you wire money back to whichever company is listed on the letter while keeping part of it for yourself and then using the rest to shop somewhere else.
If you try to deposit the check, you'll get a notice that it bounced and the victim is left with the money they wired.
Police warn everyone to be vigilant and "wary of any job that requires payment before any wages are earned."
Postal inspectors advise everyone to take extreme caution if you receive a check and letter in the mail, do not respond and report the scam online here or at 1-877-876-2455.

domain: news


A recent article in Quality Magazine is a great summary of some modern trends in gaging. At New Scale Robotics, we are working to combine these digitized gages with collaborative robots – helping manufacturers automate gaging with robotic tools that are as easy to use as a smartphone.
A Q-Span Workstation allows for the seamless integration of a manufacturer’s preferred manual inspection technologies, including calipers, bore gages, height gages, and pin gages for contact gaging, as well as air gages, laser micrometers, and vision systems for non-contact gaging.
Automating using a Q-Span Workstation increases throughput, addresses labor shortages, and improves process control.
From the article:
All types of gaging, whether it be hand tools, comparative gages, complex measuring stations or portable surface finish gages, have long gone digital. Many of today’s digital gages can perform complex measuring tasks and share information faster and easier than systems produced 10 years ago.
In many facilities, the quality control technician monitoring part quality in an inspection room, in a far corner of the plant, long after the product was produced is so 20th century. The norm today is monitoring part quality at the point of manufacture. This allows operators to inspect the part for quality and, using process control techniques, prevent bad parts from being produced.
However, production operators have been trained to run fast, powerful and complex machine centers; they are not necessarily trained as quality control technicians. Thus, the gaging that is placed into the machinist’s hands must produce accurate and reliable measurements and also be easy to use without additional training.
That ease of use is just one benefit of a Q-Span Workstation for gaging.


text:
An article or so ago I stated that I would get off the glyphosate resistance and Palmer pigweed topics to give you a break. I changed my mind.
The winter period is when growers are planning for next year. If I can just in some small way influence some growers to increase their efforts on resistance management, it will be worthwhile.
I hope it is obvious I have a passion for trying to help preserve our Roundup Ready crop technology. If we continue down the path we are headed, a lot of folks are going to look back in a few years and ask, “why were we so short-sighted?”
For me as a private consultant in a regional popular press article to say I feel glyphosate resistance is a threat to global food production may not get the attention of many people. I am going to attempt to ratchet that up a notch.
A paper by Todd Gaines and other researchers in Australia has just been published online in the U.S. Journal PNAS. The title is “Gene amplification confers glyphosate resistance in Amaranthus palmeri.”
In our terms Amaranthus palmeri is Palmer pigweed and this paper documents yet another evolved mechanism of pigweed resistance to glyphosate. The online address for the article is http://www.pnas.org/content/early/2009/12/10/0906649107.
In a recent email, Stephen B. Powles from the University of Western Australia (I consider him the world’s foremost authority on herbicide resistance) sent out a personal commentary entitled “Gene Amplification Delivers Resistant Weed Evolution.” That commentary will also be published in the PNAS online journal.
I wish to pass along some of the points from Powles’ commentary. In plants, glyphosate is toxic because it inhibits a specific enzyme pathway (EPSPS). To date, resistant weeds either exhibit a mutation at the enzyme level or a trait that restricts glyphosate movement to that enzyme.
With gene amplification, the weeds evolve to massively overproduce the EPSPS enzyme due to continued selection pressure from overuse of glyphosate. In Powles’ terms, the overproduction of the enzyme acts like a molecular sponge to soak up the herbicide and continue to function normally in the plant.
With that I have told you far more than I know and I am sure you wish to read. The point is the glyphosate resistance snowball continues to pick up speed. Since Arkansas is ground zero for Palmer pigweed, we are right in the middle of it.
In his commentary, Powles said glyphosate resistance evolution is a threat to world food production. He called glyphosate “a one in 100 year discovery that is as important for reliable global food production as penicillin is for battling disease.”
In some personal correspondence he said that “twenty years from now this will be in the textbooks as a classical case of a great technology being driven to redundancy by over-use.”
I share his passion as a weed science professional to keep trying to get the word out. I keep asking, “Why are we doing this?”
The science in the articles and commentary cited above is beyond my understanding. What I do understand is the train wreck can only be stopped at the grower level. All of the complicated science boils down to whether or not individual farmers are willing to invest in the diversity necessary to reverse the trend.
In some fields it is too late. However, the majority of the situations can either be prevented or salvaged if we just wake up.
The comment I hear constantly now is, “I was considering making some changes in my program, but with this cheap glyphosate I can not afford to.” I would submit that you can’t afford not to.
Without a serious increase in crop diversity, herbicide diversity and technology diversity on the part of every farmer, before long it won’t matter if they give you the glyphosate!

domain: agronomy


text:
Animal species you might not know inhabit the Tahoe region
LAKE TAHOE — Lake Tahoe is full of various sport fish species, including lake trout — also known as the mackinaw — rainbow trout, brown trout and kokanee salmon, to name a few.
Surprisingly to some, none of these species is native to this region, however, and the resulting story of their evolution is an interesting one.
“The rainbows and other trout aren’t native; the only native fish are the Lahontan cutthroats,” said Will Richardson, executive director of the nonprofit Tahoe Institute for Natural Science, when speaking of larger sport fish found in Lake Tahoe.
The Lahontan cutthroat lineage is of the Salimonidae (salmon and trout) family and can be traced over the past 70,000 years.
“The rainbow trout and other non-native species have hybridized and outnumbered the Lahontans,” Richardson said. “Most of the fish you see in Tahoe are not native — they’ve out-competed the Lahontans of their food source.”
A once flourishing Lahontan cutthroat population has since been drastically reduced due to a mixture of competition among fish introduced to the lake and excessive fishing, Richardson said.
It’s safe to say those living in the Lake Tahoe region are drawn to the outdoors and have an appreciation and interest in our animal neighbors.
To brush-up on our wildlife knowledge of species inhabiting the region, the Sierra Sun also caught up with Sarah Hockensmith, membership outreach manager of Tahoe Institute of Natural Science, who shed light on five other fascinating species found around the Tahoe Basin that you just might not be as familiar with.
1. Endemic stonefly
The deep-water stonefly is an interesting creature, as Richardson explained: “There are two species around here that cruise around on the snow trying to find love in February, before crawling back into the water.” The two species found in Lake Tahoe have alternate life cycles, developing eggs in May and November.
Scientific Name: Capnia lacustra
Location: South Lake Tahoe provides a perfect ecosystem for endemic creatures due to the deepwater, naturally occurring skunkweed and moss.
Fun Fact: These interesting insects develop eggs inside of their bodies. Once the eggs have fully incubated, they actually hatch inside the mother, followed by a live birth.
2. American mink
There are seven different species of weasel in this region, including river otters, wolverines, badgers, long- and short-tailed weasels, pine weasels and mink. The American mink is native to Lake Tahoe and looks similar to the river otter but is less aquatic.
Scientific Name: Neovison vison
Location: They are nocturnal mammals and can be found in and along the banks of the Truckee River as well as rocky areas around marinas and dock structures.
Fun Fact: Mink are carnivorous, furry animals with sharp teeth. They kill their prey with a bite to the neck and feed on frogs, snakes, fish, eggs, muskrats and birds.
3. Northern flying squirrel
People don’t see the flying squirrels here much because they’re nocturnal. They inhabit tree cavities made by woodpeckers and come out at night to eat fruit, nuts and insects. Hockensmith said they have even been spotted eating right out of residents’ birdfeeders.
Scientific Name: Glaucomys sabrinus
Location: The small squirrels thrive in coniferous forest habitats that are warm in the summertime and cold in the winter.
Fun Fact: The northern flying squirrel doesn’t actually fly — it glides by stretching out the skin membrane attached to its limbs. The maximum glide distance for one of these creatures has been recorded at 150 feet.
4. White-tailed jackrabbits
White-tailed jackrabbits are one of three rabbit and hare species found in the Lake Tahoe region. They are of the largest species of hare, with the females weighing in a bit larger than males.
Scientific Name: Lepus townsendii
Location: The white-tailed rabbits are seen on high ridges and mountaintops.
Fun Fact: As the temperature drops and the seasons begin to change, the white-tailed jackrabbits molts, shedding its grey-brown fur and becomes entirely white during the wintertime.
5. Long-toed salamander
The fourth toe on each hind foot is longer than the rest, giving the species its name. The flattened tail helps the salamanders swim, though they spend much of their lives underground through tunnel systems.
Scientific Name: Ambystoma macrodactylum
Location: They are tough to spot as they inhabit moist dark places of ponds, lakes and streams, including burrowing underneath wood, logs, rocks and other hidden breeding sites.
Fun Fact: Though the salamanders spend the most time on land, breeding is done in bodies of water in spring and early summer. Females will lay 90-400 eggs, which hatch in up to five weeks, and their lifespan is about 10 years.
Cassandra Walker is a features and entertainment reporter for the Sierra Sun. She can be reached at firstname.lastname@example.org, 530-550-2654 or @snow1cass.
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domain: geography


text:
KRIVICNI ZAKONIK 2013 PDF
64/17). (Krivicni Zakonik Republike Srpske) – Act on-line. Adoption: . Act of 19 September to supplement the Penal Code. (Zakon o dopuni. 64/17). (Krivicni Zakonik Republike Srpske) – Act on-line. Adoption: .. Act of 19 September to supplement the Penal Code. (Zakon o dopuni. Krivični zakonik s kraćim komentarom. Beograd.  Turković, K., et al. (). Komentar Kaznenog zakona. Zagreb.  U.S. Department of Justice, Searching .
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Contains provisions for principles, aims and levels of higher education, functioning of institutions in charge, quality, rights and obligations of students and teaching staff, equivalence of certificates, and financing. Amends article 14 on agricultural workers, articles 83, 84 and 85 on determining the amount of pension.
Krivifni of 13 July on copyright and related rights Text No.
Tužilaštvo Bosne i Hercegovine
Regulates procedures for the the protection of victims of family violence, contains sanctions, and also regulates the establishment and functioning of the Council for the fight against family kricicni. Supplements article with penal sanctions against joining military organizations outside Bosnia and Herzegovina. Bosnia and Herzegovina – General provisions – Law, Act Act of 28 November to amend and supplement the Act on protection against domestic zakonio.
Zakon o izmjeni i dopuni Zakona o zaposljavanju stranih drzavljana i lica bez drzavljanstva – Adoption: Act of 14 September to amend and supplement the Act on protection zakoink personal data Text No. Zakon o izmjenama i dopunama Zakona o krivicnom postupku Bosne i Hercegovine – Adoption: Amends articles 14 and 20 on victim protection, and article 23 on court procedures.
Determines rights, conditions and procedures of professional rehabilitation and employment, founding of institutions in charge, their organization and competencies.
ZASTUPNIČKI DOM SABORA REPUBLIKE HRVATSKE
Amends article 5 on definition of state officials, article 19 on rights and obligations, article 20 on termination of employment, article 33 on work assessment, article 36 on severance pay, article 48 on rights and obligations on annual leave. Supplements article 15 with provisions on responsibility of legal entities, and other minor amendments. Act of zakonuk November to amend and supplement the Act on civil servants.
Amends article 18 on association of employers, article 20 on hours of vocational training for adults, and supplements article 40 with 40a and 40b on supervision. Zakon o dopuni krovicnog zakona Bosne i Hercegovine – Adoption: Determines basic rights of consumers of goods and services, protection of safety of life and health of consumers, responsibility and guarantee for goods and services, services of general economic interests, penal provisions and supervision and other relevant questions.
Amends inter alia article 17 on registration criteria, articles 19, 21 and 26 2103 electronic application for registration of activity, article 35 on register of entrepreneurs, and article 55 on fines. Amends article 18 on duties of prosecutor, article 85 on investigation procedure, article on Council.
Regulates the procedure of restructuring and bankruptcy proceedings, legal consequences of opening implementation of a process of restructuring and bankruptcy proceedings, insolvency reorganization of the debtor on the basis of the bankruptcy plan, and international bankruptcy. Zakon o zdravstvenoj zastiti – Adoption: Zakon o izmjenama i dopunama zakona o zakohik licnih podataka – Adoption: Zakon o izmjeni zakona o zanatsko-poduzetnickoj djelatnosti – Adoption: Act of 14 October amending the Act on Offences.
Contains a number of minor amendments, inter alia, articles 12 and 14 on control of registers of personal data, article 18 on trasfer of personal data outside the country, and article 47 on conditions for the use of personal data.
Zakon o izmjenama i dopuni Krivicnog zakona Republike Srpske – Adoption: Zakon o azilu – Adoption: Zakon o drzavljanstvu Republike Srpske – Adoption: Act of 3 November to amend and supplement the Act on employment of foreign citizens and persons without citizenship. Zakon o Strancima – Adoption: It repeals the Labour Code of Zakon o izmjenama i dopunama zakona o visokom obrazovanju – Adoption: Contains general provisions, scope of criminal legislation, responsibility, sanctions, legal consequences, rehabilitation, penal register, amnesty, types of criminal acts.
Act of 10 April on protection against domestic violence. Bosnia and 2103 – – Regulation, Decree, Ordinance. Act of 13 December to amend the Act on Crafts and Entrepreneurship. Act of 10 April on Citizenship of Republic of Srpska. Zakon o visokom obrazovanju – Adoption: Zakon o volontiranju – Adoption: Contains a number of amendments, including articles 12 and 13 on the definition of criminal act, 29 on type of punishment, 31 and 32 on long-term prison sentence, 48 on revocation of conditional sentence because of a new criminal offence.
Act of 14 October amending the Act on Offences. Act of 6 August on Offences. Regulates procedures for the the protection of victims of family violence, contains sanctions, and also regulates the establishment and functioning of the Council for the fight against family violence.

domain: law


text:
Published Apr 21, 2010London's the XX are a great opening act for the same reason that Marvin Gaye's Let's Get It On never goes out of print: foreplay matters. Fresh off a recent Toronto headlining slot, the deservedly hyped combo returned to warm-up duties for dance pop behemoth, Hot Chip.
The XX's stellar debut album thrives on dreamy, entrancing arrangements, circular melodies and hypnotic percussion, all of which their live show painstakingly recreates. Cuts like "Crystalised," "Shelter," and "VCR" translated into enrapturing, head-nod anthems, enthralling a rambunctious crowd. The result was mesmerizing, if not overwhelming, priming atypically eager punters for a school-night dance party.
Like Dizzee Rascal, Hot Chip "got the big beat," and no matter the muddiness of the mix, it translated into venue-wide bouncing. Massive bass drums steered "One Life Stand" and "Hand Me Down Your Love" through sections of spotty sound, while tribal percussion on "One Pure Thought" fused smoothly with disco melodies. Conversely, buried vocals and synths hampered "Boy From School" and "Alley Cats," which should have been crystalline.
Regardless, the joyous crowd largely ignored sound problems, writhing to the grooved-up guitar of "Over and Over" and chanting along to the New Order-inspired dance rock of "Thieves in the Night." For their part, the band kept things playful, bantering about Glaswegian bricks and offering up Old Gregg impressions.
Four records in, Hot Chip's pinko-inspired act, complete with symbiotic multi-part vocals (especially on "Take It In"), has a marked sheen and impressive cohesion. Most tracks built cathartically, thriving on the fusion of sonorous rhythm and smooth melody. Sure, the sound struggled in sections but the set's sheer ebullience largely compensated.

domain: entertainment


text:
Caitlyn Jenner is taking yet another drastic step under the knife, but this time it’s to enhance her buttocks, it’s been alleged.
According to Radar Online, the former Olympic athlete is considering the idea of undergoing a Brazilian butt lift, having made it known that she would feel even better about herself upon the completion of the procedure.
Caitlyn Jenner has carefully thought about the surgeries she’s had done in the past year and being surrounded by the Kardashians, who are no stranger to getting Brazilian butt lifts themselves, the former TV personality reportedly wants the same as her step-daughters.
Radar Online alleges that Caitlyn Jenner is more or less glued to wearing jeans because she’s somewhat insecure of how her butt looks when she’s wearing dresses or gowns — it doesn’t look as good as when the likes of Kim and Kylie would wear it.
Caitlyn Jenner knows that by doing the Brazilian butt lift, she would feel more confident in her own body and wouldn’t often worry about whether or not she can wear certain outfits, fearing that her small buttocks will be visible.
She won’t go for anything drastic, a source says, but she definitely wants the difference to be noticeable, adding that it’s been something she’s thought about for close to a year, and she’s finally ready to go ahead with her plan.
With the summer being here, Caitlyn Jenner is also planning to head to the beach every now and then, where she’ll be sporting a bikini, but with the way her butt is currently looking, sources say she wouldn’t even dare to wear anything risky until she’s had the procedure.
Implants have already been ruled out of the question. Caitlyn Jenner is firmly sticking to the procedure that sees fat moved from certain areas of one’s body and into the designated area, which, in this case, happens to be the buttocks.
It’s believed that getting her butt to a bigger size will be the last surgery Caitlyn Jenner will do for a while. In the last two years, she’s put her body through a lot and a much-needed break from the surgery table is definitely needed, the insider concluded.
Caitlyn Jenner says that getting her butt to a bigger size will make her much happier.
[Featured Image by Jamie McCarthy/Getty Images]

domain: celebrity