text:
For any interested readers, Tobe Witmer, pastor of Lighthouse Baptist Church in Newark, DE has briefly responded to my essay on his Bread of Life Sermon. I encourage everyone to read my essay and his response, which can be found in the comments underneath.
First and foremost, I would like to thank Pastor Witmer for considering my commentary on his sermon. As I have said elsewhere on this blog, achieving Christian unity will only occur if Christians talk to one another with respect, openness, love, and a Christ-like, zealous desire for the perfect unity that Jesus once prayed for (John 17) and St. Paul commanded. We can not ignore differences, because to do so is to ignore the author of division, Satan himself. We can not pretend differences do not exist, because to do so is to ignore a reality that is contrary to the Gospel. And we can not accept differences ("I believe what I believe, you believe what you believe."), because such a philosophy is directly contrary to the mind of God (see John 17).
But we can pray for unity, we can join our hearts with Christ's, and we can be obedient to Christ and submit our wills to him, so that if he is calling us to change our beliefs, we will exhibit the humble "obedience of faith" (see Romans 1) and follow Him where He calls us. Thy will, Lord, not mine be done!
And we can talk! How rarely Christians who disagree about fundamental doctrines actually sit down and consider what each other really believes!
When I read Pastor's response, a paragraph from a G.K. Chesterton's essay "Where All Roads Lead" came to mind. The paragraph can be read here, and it begins with the words "Now, I have noted first this common consciousness..."
The basic idea on which Chesterton so eloquently remarks is that "new" ideas grow old quickly, but the truth stays ever-young. Pastor Witmer's response speaks of an idea (a particular flavor of Christianity) that is 500 years old. I am trying to share a Christianity with Pastor Witmer that is 2,000 years young. One beautiful thing about Catholicism is that it grows fresher and more vibrant with every stale complaint made against it. And how many times have we Catholics heard the same criticism summed up with the words "faith alone?" Yet, does Pastor Witmer's response really answer or engage the teachings of that ancient church that I shared in my essay? Pastor Witmer cited the context of his message as a reason he did not address all the verses of John 6 pertinent to his topic, but are we to believe that he would have interpreted "the Bread of Life" spoken of in John 6 any differently had he dwelt longer past v. 51?
In the near future, I will revisit my essay and Pastor Witmer's response and try to draw out what seem to be the areas of explicit agreement, the areas of hidden agreement (areas that Pastor Witmer thinks contradict the principle of salvation by grace alone), and areas of real disagreement. I believe I will be able to show that there are some very real agreements between Baptists and Catholics that seem, through the lens of what Baptists are usually taught about Catholicism, to be areas of profound disagreement.
The question for our hearts always remains: are we ready to rejoice in these unities and dissolve the false divisions that we have allowed Satan to sow in Christ's mystical body?
Are we ready to open our minds and hearts to really understand what each other believe, or will we remain content to live with the straw men of our long-standing prejudices?
Again, I thank Pastor Witmer for showing a willingness to respond and begin a conversation, and I invite Pastor Witmer to respond to some of the very real arguments I made in my own essay for the Real Presence of Jesus Christ - Body, Blood, Soul, and Divinity - in the most Holy Eucharist. I especially invite Pastor Witmer to address my remarks regarding the dichotomies on which his interpretation of John 6 seems to rest.
May the Holy Spirit blow anew on Christians and bring about perfect unity, true doctrine, and a vibrant faith!


text:
The Green Bay Packers and Brett Favre are not on the greatest terms right now, but this means it gives the Green Bay Packers a chance to do the right thing. Brett Favre never wanted to go anywhere as he has always wanted to retire as a Packer. Aaron Rodgers said it best when it is time to heal and move on and do the right thing. Brett Favre gave many years to the Green Bay organization, team, and the fans. Will the Packers do the right thing and retire his No.4 before he gets inducted into Canton, Ohio?
Sometimes in football these divorces are messing ones and right now that is what this one happens to be. Brett Favre and the Packers need to work this out. Favre will always be remember as one of the greatest quarterbacks ever and should have his number retired. Even though the Packers and him are not on the best of terms we all know when Canton calls he will go in as a Green Bay Packer. Like Aaron Rodgers said it is time to heal and move on. Favre's No.4 should be retired and as soon as possible.

subset: commoncrawl


text:
The endoglycosidase heparanase specifically cleaves the heparan sulfate (HS) side chains on proteoglycans, an activity that has been implicated strongly in tumor metastasis and angiogenesis. Heparanase-2 (Hpa2) is a close homolog of heparanase that lacks intrinsic HS-degrading activity but retains the capacity to bind HS with high affinity. In head and neck cancer patients, Hpa2 expression was markedly elevated, correlating with prolonged time to disease recurrence and inversely correlating with tumor cell dissemination to regional lymph nodes, suggesting that Hpa2 functions as a tumor suppressor. The molecular mechanism associated with favorable prognosis following Hpa2 induction is unclear. Here we provide evidence that Hpa2 overexpression in head and neck cancer cells markedly reduces tumor growth. Restrained tumor growth was associated with a prominent decrease in tumor vascularity (blood and lymph vessels), likely due to reduced Id1 expression, a transcription factor highly implicated in VEGF-A and VEGF-C gene regulation. We also noted that tumors produced by Hpa2-overexpressing cells are abundantly decorated with stromal cells and collagen deposition, correlating with a marked increase in lysyl oxidase expression. Notably, heparanase enzymatic activity was unimpaired in cells overexpressing Hpa2, suggesting that reduced tumor growth is not caused by heparanase regulation. Moreover, growth of tumor xenografts by Hpa2-overexpressing cells was unaffected by administration of a mAb that targets the heparin-binding domain of Hpa2, implying that Hpa2 function does not rely on heparanase or heparan sulfate. Cancer Res; 76(9); 2791–801. ©2016 AACR.
Heparanase is an endoglycosidase that specifically cleaves heparan sulfate (HS) side chains, a class of glycosaminoglycans abundantly present in the extracellular matrix (ECM) and on the cell surface. Heparanase activity is strongly implicated in tumor angiogenesis and metastasis attributed to remodeling of the subepithelial and subendothelial basement membranes (1, 2). Augmented level of heparanase was documented in an increasing number of human carcinomas and hematologic malignancies (3, 4). In many cases, heparanase induction correlates with increased tumor metastasis, vascular density, and shorter survival postoperation, thus providing a strong clinical support for the protumorigenic function of the enzyme (4–6). These studies depict compelling evidence for the clinical relevance of heparanase, making it an attractive target for the development of anticancer drugs (5, 7, 8). Cloning of a single human heparanase cDNA sequence was independently reported by several groups (9–12) implying that one active heparanase enzyme exists in mammals. Further analysis of human genomic DNA led researchers to conclude that the heparanase gene is unique, and that the existence of related proteins is unlikely. On the basis of amino acid sequence, McKenzie and colleagues nonetheless reported the cloning of heparanase homolog termed heparanase 2 (Hpa2; ref. 13). Unlike heparanase, Hpa2 lacks intrinsic HS-degrading activity, the hallmark of heparanase, but retains the capacity to bind heparin/HS (14). In fact, Hpa2 exhibits even higher affinity toward heparin/HS than heparanase, suggesting that Hpa2 may inhibit heparanase activity by competition for the HS substrate (14). Clinically, Hpa2 expression was markedly elevated in head and neck carcinoma patients, correlating with prolonged time to disease recurrence (follow-up to failure) and inversely correlating with tumor cell dissemination to regional lymph nodes, suggesting that Hpa2 functions as a tumor suppressor (14). The molecular mechanism associated with favorable prognosis following Hpa2 overexpression is unclear. Here, we provide evidence that Hpa2 overexpression in head and neck cancer cells markedly reduces tumor growth. Restrained tumor growth was associated with a prominent reduction in tumor vascularity (blood and lymph vessels) likely due to reduced Id1 expression, a transcription factor highly implicated in VEGF-A and VEGF-C gene regulation (15). Notably, heparanase enzymatic activity was not impaired in cells overexpressing Hpa2, suggesting that reduced tumor growth is not due to heparanase regulation. Moreover, growth of tumor xenografts produced by Hpa2-overexpressing cells was not affected by a mAb that targets a heparin-binding domain of Hpa2, implying that Hpa2 functions in heparanase-, and HS-independent manner.
Materials and Methods
Cells and cell culture, immunoblotting, and heparanase activity assay
Cal27 tongue carcinoma and FaDu pharyngeal carcinoma cells have been described previously (16–18). Cells were grown in DMEM (Biological Industries) supplemented with 10% FBS and antibiotics. Cells were passed in culture no more than 2 months after being thawed from authentic stocks. Cells were infected with control empty vector (Vo) or Hpa2 gene construct, selected with puromycin (2 μg/mL; Invitrogen), expended and pooled. Cell clones were isolated by limiting dilution and clones exhibiting higher Hpa2 expression versus the pool of cells were evaluated by immunoblotting, carried out essentially as described (14). Preparation of dishes coated with sulfate-labeled ECM and determination of heparanase enzymatic activity (i.e., release of sulfate-labeled HS degradation fragments) were carried out essentially as described previously (14).
Antibodies and reagents
Anti-Hpa2 polyclonal (Ab 58) and monoclonal (20c5, 1c7) antibodies have been described previously (14). Immunohistochemical grade anti-LOX and anti-LOXL2 polyclonal antibodies have been described elsewhere (19, 20). Antibodies directed against Ki67, LYVE-1, LOX, cytokeratin 13, cytokeratin 15, β3-tubulin, cleaved caspase-3, hypoxia-inducible factor-1α (HIF1α), and carbonic anhydrase IX were purchased from Abcam; Rat anti-mouse CD31 was from Dianova; anti-VEGF-A and anti-VEGF-C antibodies were from Santa Cruz Biotechnology. Anti-actin and anti-smooth muscle actin mAbs, Masson/Trichrome staining kit and β-3-aminopropionitrile fumarate (BAPN) were purchased from Sigma. Human Id1 gene construct was purchased from Addgene.
Real-time PCR
Real-time PCR analyses were performed using ABI PRISM 7000 Sequence Detection System employing SYBR Green PCR Master Mix (Applied Biosystems). The following primers were used:
Actin F: 5′-CGCCCCAGGCACCAGGGC, R: 5′-GCTGGGGTGTTGAAGGT;
Id1 F: 5′-CTGCTCTACGACATGAACGG, R 5′-GAAGGTCCCTGATGTAGTCGAT.
Tumorigenicity and IHC
Cells were detached with trypsin/EDTA, washed with PBS, and brought to a concentration of 5 × 107 cells/mL. Cell suspension (5 × 106/0.1 mL) was inoculated subcutaneously at the right flank of 6-week-old NOD/SCID mice. Xenografts size was determined by externally measuring tumors in two dimensions using a caliper. At the end of the experiment, mice were sacrificed; tumor xenografts were removed, weighed, and fixed in formalin. Paraffin-embedded 5-μm sections were subjected to immunostaining with the indicated antibody using the EnVision Kit according to the manufacturer's (Dako) instructions, as described previously (14). Immunocytochemistry was carried out essentially as described (21). Lymph and blood vessels density was quantified by the Image Pro software or were counted under light microscope at high (×40) magnification.
Statistical analysis
Data are presented as means ± SE. Statistical significance was analyzed by two-tailed Student t test. Values of P < 0.05 were considered significant. Data sets passed D'Agostino–Pearson normality (GraphPad Prism 5 utility software). All experiments were repeated at least three times with similar results.
Hpa2 overexpression attenuates tumor growth
To reveal the function of Hpa2 in head and neck cancer, FaDu pharyngeal carcinoma cells were infected with control (Vo) or Hpa2 gene constructs and expression was confirmed by immunoblotting (Supplementary Fig. S1A; Pool) and immunofluorescent staining (Supplementary Fig. S1B). Tumor xenografts produced by FaDu cells overexpressing Hpa2 were markedly smaller by volume and weight compared with control tumors (Fig. 1A; P = 0.001). Histologic examination showed that xenografts produced by control cells were highly necrotic (Fig. 1B, left). In contrast, xenografts produced by cells overexpressing Hpa2 were by far less necrotic and were decorated with large cysts (Fig. 1B, right). Similar robust cysts formation was evident in Cal27 cells overexpressing Hpa2 (Fig. 1B, bottom). In head and neck cancer patients, high levels of Hpa2 expression were associated with reduced lymph nodes metastasis and prolonged survival rates (14). We therefore examined the occurrence of lymph vessels in tumor xenografts produced by control and Hpa2 overexpressing cells. We observed a significant 2- to 3-fold decrease in lymphangiogenesis following Hpa2 overexpression (Fig. 1C and D; P = 0.002), associated with a comparable decrease in the expression of VEGF-C (Fig. 1D, bottom), a predominant factor for the proliferation of lymphatic endothelial cells (22, 23).
Tumor growth and vascularity are markedly reduced by Hpa2-overexpressing cell clones
To further delineate the impact of Hpa2 on tumor growth, we selected cell clones that exhibit high levels of Hpa2 expression. Three such cell clones were isolated from Hpa2-infected cells (clones #6, 60, 64; Supplementary Fig. S1A) and their tumorigenic capacity was compared with that of three randomly selected control cell clones (clones #3, 5, 8). Tumor xenografts produced by Hpa2-overexpressing clones were strikingly, 10-fold smaller compared with xenografts produced by control cell clones, decrease that is statistically highly significant (Fig. 2A and Supplementary Fig. S1C). Proliferating, Ki67-positive cells were detected in the entire non-necrotic tumor mass produced by control clones (Fig. 2B, left). Endothelial cells and tumor cells residing in lymphatics were also stained positive for Ki67 in control tumors (Supplementary Fig. S2A). In contrast, Ki67 reactivity was restricted to the tumor periphery in tumors produced by Hpa2 clones (Fig. 2B, right) and was decreased significantly even in these areas (Fig. 2B, bottom). In addition, tumors produced by Hpa2 clones exhibited higher levels of apoptotic cell death evident by caspase-3 staining (Supplementary Fig. S2B), altogether attenuating tumor growth. Histologically, tumors produced by control cell clones exhibited massive areas of necrosis versus large cysts that decorated the tumors produced by Hpa2 clones (Fig. 2C), in agreement with the histologic phenotype of tumors produced by cell pools (Fig. 1B). Careful pathologic examination revealed that tumors produced by Hpa2 clones exhibit higher degree of differentiation (Fig. 2C, right), and this was confirmed by a marked increase in cytokeratin 13 and cytokeratin 15 immunostaining (Fig. 2D) and immunoblotting (Supplementary Fig. S2C). Furthermore, a noticeable decrease in lymph vessels (positive for LYVE-1) density was quantified in tumor xenografts produced by Hpa2 clones compared with controls (Fig. 3A, second and fifth left panels), associating with a 3-fold decrease in VEGF-C expression levels (Fig. 3B). This agrees with decreased lymphangiogenesis and VEGF-C expression observed in the cell pools (Fig. 1C and D). Notably, while tumor cells were readily detected within lymph vessels of control tumors (Fig. 3A, second left panels), Hpa2 overexpression resulted not only in fewer lymph vessels but also reduced tumor load in lymphatics (Fig. 3A, second right panels). While this observation is in accordance with our previous experimental (Fig. 1C and D) and clinical results (14), it cannot explain the robust attenuation of tumor growth. We therefore examined also the density of blood vessels in tumors produced by control and Hpa2-overexpressing cells. We found that blood vessel density was prominently reduced in tumors produced by Hpa2-overexpressing cells compared with control tumors (Fig. 3A, third and fifth right panels), associating with a comparable decrease in VEGF-A expression (Fig. 3C and Supplementary Fig. S1D). Consequently, tumors produced by Hpa2 clones exhibited augmented tumor hypoxia evident by increased HIF1α (Fig. 3A, fourth panels) and carbonic anhydrase IX (CAIX; Supplementary Fig. S2D) staining intensity.
Hpa2 enhances collagen deposition and LOX induction
Histologic examination revealed that tumors produced by Hpa2 cells are decorated extensively with host, stromal cells (Supplementary Fig. S3A). Masson/Trichrome staining showed a marked increase in collagen staining following Hpa2 overexpression (Fig. 4A, top, blue). A similar increase in collagen staining was observed in tumors produced by Cal27 cells overexpressing Hpa2 (Supplementary Fig. S3B, second panels). We therefore examined the expression of lysyl oxidase (LOX), an enzyme that is strongly implicated in collagen deposition and tissue fibrosis (24, 25). We found a prominent increase in LOX immunostaining in cancer cells that surround the stromal elements within tumors produced by Hpa2 clones compared with control (Fig. 4A, second panel and Supplementary Fig. S4A, top). LOX upregulation by Hpa2 was further ascertained by real-time PCR (Fig. 4B). In contrast, the expression of LOX-like 2 (LOXL2) was decreased in Hpa2 clones (Fig. 4C). Notably, however, LOXL2 was predominantly localized to the nuclei of cancer (Fig. 4A, bottom right panels) and stromal cells (Supplementary Fig. S3C, arrows). Similar phenotypes were observed in tumors produced by Cal27 cells overexpressing Hpa2 (Supplementary Fig. S3B, bottom).
Hpa2 mode of action
To reveal the mechanism underlying the potent suppression of tumor growth by Hpa2, we first evaluated heparanase activity in control and Hpa2-overexpressing cells, because heparanase exhibits protumorigenic properties in many types of cancers including head and neck (26), and Hpa2 can inhibit heparanase enzymatic activity (14). Notably, heparanase activity appeared unchanged in control versus Hpa2-overexpressing cells (Fig. 5A), suggesting that the decrease in tumor growth by Hpa2 is not due to heparanase inhibition. Despite its lack of HS-degrading activity, Hpa2 exhibits high affinity toward heparin/HS (14). We therefore sought to examine whether binding and clustering of HS proteoglycans (HSPG) by Hpa2 on the cell surface is responsible for tumor suppression. To this end, we screened a panel of anti-Hpa2 mAbs for inhibition of cellular binding of Hpa2 shown previously to be mediated by cell membrane HSPG such as syndecans (14). We found that mAb 1c7 efficiently inhibits cellular binding of Hpa2 in a dose-dependent manner (Fig. 5B), suggesting that this mAb targets a functional HS-binding domain of Hpa2. Importantly, tumor growth was not altered by administration of mAb 1c7 to mice inoculated with Hpa2 clones (Fig. 5C and Supplementary Fig. S5A). Interestingly, the formation of cysts within tumors appeared to be increased in mice treated with mAb 1c7 (Fig. 5C and Supplementary Fig. S5A). Immunoblotting revealed reduced levels of VEGF-A in Hpa2-overexpressing clones (Fig. 5D, top and Supplementary Fig. S1D), in agreement with real-time PCR (Fig. 3C), but VEGF-A levels were not affected by treatment with mAb 1c7 (Fig. 5D, top, +). Taken together, it appears that inhibition of tumor growth and vascularity by Hpa2 does not involve regulation of heparanase activity or the activation of cell membrane HSPG. Furthermore, treatment with BAPN, which inhibits the enzymatic activity of all LOXs (27) reduced tumor fibrosis (i.e., collagen content) but had no effect on tumor size (Fig. 5E and Supplementary Fig. S5B), implying that reduced tumor growth by cells overexpressing Hpa2 is not due to the elevation of LOX activity. We therefore considered the reduced tumor vascularity as the main cause for tumor growth inhibition by Hpa2. Interestingly, we found that expression of Id1, a transcription factor implicated in the induction of VEGF-A and VEGF-C gene transcription (15, 28), is reduced in Hpa2-overexpressing cells (Fig. 6A). Overexpression of Id1 in Hpa2 clones (Fig. 6B) resulted in a 2.5- to 3-fold increase in tumor growth (Fig. 6C) and a comparable increase in tumor vascularity (Fig. 6D and Supplementary Fig. S5C), implying that downregulation of Id1 mediates, at least in part, the tumor suppressor function of Hpa2.
Compelling preclinical and clinical evidence tie heparanase with cancer initiation and progression (8, 29–31), making it a promising drug target (5, 7). In striking contrast, the biologic significance of its close homolog Hpa2 in tumorigenesis is largely obscure. We have reported previously that Hpa2 levels are increased in head and neck carcinoma compared with adjacent normal tissue, and that patients with high levels of Hpa2 are endowed with reduced lymph node metastasis and prolonged survival rates (14). Similarly, increased Hpa2 expression was associated with prolonged survival of gastric cancer patients (32) but the mechanism underlying this favorable effect has not been resolved yet. Here, we provide evidence that high levels of Hpa2 are associated with reduced lymph vessel density. This was noted in pool of FaDu cells infected with Hpa2 gene construct (Fig. 1C and D) and was most evident in three different cell clones selected for higher levels of Hpa2 expression (Fig. 3A). Importantly, these clones express Hpa2 levels comparable with patients exhibiting high levels of Hpa2, (Supplementary Fig. S4B; ref. 14) and are thus considered relevant to the disease. Lymph angiogenesis is significant clinically for many types of cancers but most appealing in head and neck cancer because lymph node metastasis is the most important clinical parameter for this malignancy (33). We found reduced lymph vessel density in Hpa2 tumors combining with a comparable decrease in VEGF-C expression (Fig. 3B), a most potent prolymphatic mediator secreted by tumor cells (34). While decreased VEGF-C expression and lymph angiogenesis by Hpa2 nicely agrees with the clinical results (14, 32), it cannot explain the prominent decrease in tumor growth following Hpa2 overexpression (Fig. 2A and Supplementary Fig. S1C). Notably, we found that not only VEGF-C but also VEGF-A expression is reduced by Hpa2 (Figs. 3C and 5D and Supplementary Fig. S1D), associating with reduced blood vessel density (Fig. 3A) that likely attenuates tumor growth. This agrees with increased levels of hypoxia in tumors produced by Hpa2 clones, evident by higher levels of HIF1α and carbonic anhydrase IX (Fig. 3A and Supplementary Fig. S2D), well-recognized markers of hypoxic conditions. Tumors produced by Hpa2-overexpressing clones appeared significantly less necrotic despite being poorly vascularized. This is due to a marked decrease in tumor cell proliferation (Fig. 2B) and increased apoptosis (Supplementary Fig. S2B), thus balancing tumor mass and blood vessel density closer to the ratio occurring in normal tissues.
The mechanism responsible for VEGF-A and VEGF-C downregulation is not entirely clear but likely involves Id1. This transcription factor is implicated in the induction of VEGF-A and VEGF-C gene expression (35, 36) and is decreased following Hpa2 overexpression (Fig. 6A). Notably, transfection of Hpa2 clones with Id1 gene construct, resulting in 2-fold increase in its mRNA levels (not shown), restored tumor vascularity and growth (Fig. 6C and D and Supplementary Fig. S5C), thus supporting the notion that reduced Id1 levels underlie tumor inhibition by Hpa2 and suggesting that modest changes in the expression levels of this transcription factor are highly effective in modulating tumor progression. This appears relevant clinically, because Id1 expression has been shown to be elevated in a variety of primary human tumors including head and neck cancer, correlating with increased tumor aggressiveness (37). It should be noted that Id1 is thought to function as a cellular proto-oncogene (37) and regulates the transcription of several other genes implicated in tumor growth such as metalloproteinases and integrins (35). Decreased Id1 gene expression by Hpa2 may therefore affect tumor growth also by means other than reduced vascularity. Interestingly, we found that the expression of cytokeratin 13 and 15 was reduced markedly in tumors produced by Hpa2 clones overexpressing Id1 (Supplementary Fig. S6), whereas LOX expression was unchanged (Supplementary Fig. S7, bottom). Accordingly, collagen deposition, evident by Masson/Trichrome staining, was not affected by Id1 overexpression (Supplementary Fig. S7, third panel), but appeared disrupted in the large necrotic areas that accompanied accelerated tumor growth (Supplementary Fig. S7, top and second panel), suggesting that collagen deposition preceded tumor necrosis. These results may imply that cytokeratins are also regulated, directly or indirectly, by Id1. An inverse correlation between Id1 levels and cytokeratin expression was also reported in ovarian carcinoma cells (38).
Overexpression of Hpa2 affect the resulting tumors in several aspects other than reduced tumor vascularity. Despite the reduced vascularity, tumor xenografts produced by Hpa2-overexpressing cells were by far less necrotic but rather contained large cysts structures. These structures, observed in FaDu and Cal27 cell models (Figs. 1B and 2C), were negative for endothelial cell marker (CD31, Supplementary Fig. S4A, right bottom panel), thus nullifying their being abnormal vessels. Cysts are most often nonmalignant structures but can appear in primary tumors and metastases (39). The molecular mechanism responsible for cyst formation by Hpa2 is obscure but may be related to increased cellular differentiation. Histologic examination revealed that tumor xenografts produced by Hpa2-overexpressing cells and clones exhibit higher degree of differentiation (Fig. 2C) and this was evidently confirmed by a marked increase in cytokeratins levels (Fig. 2D and Supplementary Fig. S2C). Cytokeratin 15 staining was most intense in cells lining, or in close proximity with the cyst structure (Fig. 2D, bottom), but the cause and relationship between increased cell differentiation and cyst formation is yet to be resolved. Alternatively, increased formation of cyst structures in Hpa2 tumors may possibly reflect adaptation to reduced lymph vessels density and the formation of edema.
We have also noted that tumors produced by Hpa2 clones had far more nerve bundles than control tumors (β3-tubulin; Supplementary Fig. S4A, second panels). While the contribution of neurogenesis to tumorigenesis is questionable (40), a possible role for Hpa2 in neurogenesis appears relevant to urofacial syndrome (UFS). This congenital disorder features somatic motor neuropathy, obvious in the face but occasionally more widespread, and an autonomic neuropathy causing bladder dysfunction leading to renal failure (41). Notably, biallelic mutation in the HPSE2 gene is held responsible for some cases of UFS in families from different ethnic groups (42–44), resulting in frameshift or nonsense, postulated functionally null, Hpa2 variants (45). Moreover, mice carrying mutant Hpa2 exhibit bladder dysfunction (44, 46), associating with increased bladder fibrosis (46). The relevance of our findings with Hpa2-overexpressing head and neck carcinoma cells (i.e., increased cell differentiation, neurogenesis, LOX expression) to UFS and the lethality phenotype of Hpa2-mutant mice (46) are yet to be resolved.
Augmented collagen deposition was observed in tumor xenografts produced by Hpa2 clones (Fig. 4), correlating with a marked increase in LOX expression (Fig. 4). This enzyme catalyzes the cross-linking of collagen and/or elastin in the ECM, and is highly implicated in ECM remodeling and tissue fibrosis (24, 25). In tumorigenesis, LOX was first proposed to act as a tumor suppressor, inhibiting the transformation effect of HRAS. Subsequent studies revealed nonetheless that LOX plays a far more complex role in cancer. For example, the LOX propeptide (LOX-PP) domain has been shown to bear tumor-suppressor activity, whereas the active enzyme is thought to promote metastasis (27, 47). Tumor suppressor properties have also been attributed to the LOX-like 2 enzyme, LOXL2. For example, a significant decrease in LOXL2 expression was observed in prostate and non–small lung cancers compared with matched normal tissue (27) and low LOXL2 levels were associated with a more advanced pathologic tumor–node–metastasis stage and poorly differentiated lung adenocarcinomas (48). Not only the expression levels but also the cellular localization of LOXL2 appears important clinically. LOXL2 was noted to reside in the nucleus of normal esophagus, and esophageal cancer patients having nuclear LOXL2 survive longer than patients with cytoplasmic LOXL2 (49). We found that LOXL2 localizes to the nucleus of Hpa2-overexpressing cancer cells (Fig. 4) and cells that comprise the tumor microenvironment (Supplementary Fig. S3C). This agrees with the notion that nuclear localization of LOXL2 attenuates tumor growth by transcriptional regulation of tumor (50) and stromal cells that may affect tumor growth (51). Interestingly, administration of the LOX inhibitor BAPN to the drinking water of mice inoculated with Hpa2 clones did not reverse the strong attenuation of tumor growth by Hpa2 (Fig. 5E and Supplementary Fig. S5B). This may imply that LOX functions extracellularly in a manner that does not involve enzymatic activity (52), or that nuclear LOXL2 is responsible for tumor attenuation. It should be noted that in contrast with the above examples, other studies find that LOX and LOXL2 promote tumor growth and metastasis, making these enzymes a target for the development of anticancer therapeutics (24, 27). Clearly, more work is required to delineate the mode by which Hpa2 regulates LOX and LOXL2 expression and cellular localization, the clinical significance of LOX/LOXL2 expression and localization in head and neck cancer, and the implication of a Hpa2–TGFβ–LOX axis (20, 53) on tumor growth, metastasis, and fibrosis. It should be noted that while hypoxic conditions have been reported to induce LOX expression (54), increased LOX transcription was noted in Hpa2 cells grown in vitro under normoxic conditions (Fig. 4B), suggesting that Hpa2 regulates LOX gene expression directly.
The mode by which Hpa2 exerts its tumor suppressor properties is not entirely clear. An instrumental tool for deciphering this question was the finding that mAb 1c7 inhibits cellular binding of Hpa2 (Fig. 5B). Like heparanase, Hpa2 is subjected to rapid and efficient cellular binding (14). This process is due primarily to the interaction of heparanase/Hpa2 with HSPG on the cell surface because addition of heparin to cell cultures competes with cell membrane HS, resulting in accumulation of heparanase/Hpa2 in the cell culture medium (14). Unlike heparanase (18), the heparin-binding domains of Hpa2 have not been characterized yet. However, the ability of mAb 1c7 but no other anti-Hpa2 mAbs, to efficiently block cellular binding of Hpa2 (Fig. 5B) strongly implies that this mAb targets a functional domain required for the interaction of Hpa2 with HS. The consequence of the high-affinity interaction of Hpa2 with cell membrane HS has not been sufficiently resolved but likely affects cellular behavior (i.e., cell adhesion; ref. 55). Notably, tumor growth inhibition by Hpa2 does not appear to involve HS because treatment with mAb Ic7 did not affect tumor size (Fig. 5C and Supplementary Fig. S5A). Moreover, heparanase activity appeared practically identical in control and Hpa2-overexpressing cells (Fig. 5A). These results may suggest that Hpa2 exerts its tumor suppressor properties in a HS- and heparanase activity-independent manner, possibly involving as yet unrecognized Hpa2-binding protein.
Taken together, our results support the notion that Hpa2 functions as a tumor suppressor in head and neck cancer. Moreover, we provide mechanistic insights to this function of Hpa2 and describe for the first time that Hpa2 modulates gene transcription and thereby affects tumor vascularity, growth and fibrosis in apparently heparanase activity-, and HS-independent manners, thus expanding Hpa2 repertoire and mode of action.
Note Added in Proofs
The current paper is supported by the following paper, published online on March 9, 2016: Gross-Cohen et al., Heparanase 2 expression inversely correlates with bladder carcinoma grade and stage. Oncotarget, PMID: 26968815.
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Authors' Contributions
Conception and design: N. Ilan, I. Vlodavsky
Development of methodology: M. Gross-Cohen, G. Neufeld, G. Arvatz, N. Ilan, I. Vlodavsky
Acquisition of data (provided animals, acquired and managed patients, provided facilities, etc.): M. Gross-Cohen, S. Feld, I. Doweck, U. Barash, N. Ilan, I. Vlodavsky
Analysis and interpretation of data (e.g., statistical analysis, biostatistics, computational analysis): M. Gross-Cohen, I. Doweck, P. Hasson, U. Barash, I. Naroditsky, N. Ilan, I. Vlodavsky
Writing, review, and/or revision of the manuscript: M. Gross-Cohen, I. Doweck, P. Hasson, N. Ilan, I. Vlodavsky
Administrative, technical, or material support (i.e., reporting or organizing data, constructing databases): P. Hasson
Grant Support
This study was supported by research grants awarded to I. Vlodavsky by the Israel Science Foundation (grant no. 601/14); NCI, NIH (grant no. CA106456); the United States-Israel Binational Science Foundation (BSF); the Israel Cancer Research Fund (ICRF); and the Rappaport Family Institute Fund.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Note: Supplementary data for this article are available at Cancer Research Online (http://cancerres.aacrjournals.org/).
- Received July 19, 2015.
- Revision received January 24, 2016.
- Accepted February 26, 2016.
- ©2016 American Association for Cancer Research.


text:
Sunday, June 21, 2009
Quick Monogram initial note cards
I had to make some quick monogram notecard sets last week for gifts and I found myself turning to a favorite sketch of mine. You can really create a ton of notecards super fast using this basic design and whatever designer paper c/s you have on hand in a smaller print.
Using any decorative paper, cut your strip 1 inch wide x 5 1/2 inches long
Cut an accent c/s 1 1/4 inches wide x 5 1/2 inches long.
Stamp your initial of choice in same color ink as the accent c/s on 1 1/4 white circle. (I usually stamp the letter first on a sheet of white c/s and then punch it out so I can manuever the punch around to make sure the letter is centered and straight!) Mat the letter with another accent color piece of c/s that has been punched to 1 3/8. Then attach it to a scalloped circle in the same color as the ink and viola!
The Stamp set I used is by Stampin' Up! and it's one of their alphabets called Lovely Letters...I LOVE IT!
Labels: Monogram Initial Cards
No comments:
Subscribe to: Post Comments (Atom)


text:
Weekly discussion of financial markets, economics, politics, and the media. A member of Wall Street's Digital Underground since 1995
Saturday, March 30, 2013
Argentine defiance in appeal of $1.4 billion debt ruling aims at unlikely Supreme Court win
By Michael Warren, The Associated Press | The Canadian Press
BUENOS AIRES, Argentina - With just hours to go before Argentina has to show its last cards in a billion-dollar debt showdown in the U.S. courts, President Cristina Fernandez seems to be keeping up her "we're going for more" motto. Her government is reportedly preparing a response that analysts say could lead the country into another catastrophic default.
Argentina has until midnight Friday to propose how it would satisfy a $1.4 billion judgment won by plaintiffs who have insisted for a decade on getting full payment in cash, plus interest and penalties, on sovereign debt that the country hasn't paid since its world-record default in 2002.
Government officials weren't talking in public about the plan this week, but they have repeatedly said that the plaintiffs it considers "vulture funds" should get no better than what 92 per cent of other investors in Argentina accepted in 2005 and 2010 in exchange for their defaulted bonds: a package of new bonds that were initially worth less than 30 cents on the dollar.
The exact details likely won't be known until just before the deadline, but the broader aspects have been widely reported in Argentina's media: Rather than the quick cash payout ordered by the courts, it will offer new bonds that won't come fully due for up to 25 years. And rather than pay in full, the government will insist on paying no more than 30 per cent to start with.
No comments:
Subscribe to: Post Comments (Atom)


text:
Malaysia's Soon Huat Goh and Shevon Jemie Lai have a mouth-watering clash against home favourites Chris and Gabby Adcock next week, and prepared in the perfect manner with a title at the YONEX German Open.
The Malaysian duo are unseeded for the 2018 YONEX All England in Birmingham and have been drawn to play the Adcocks in the first round of the mixed doubles.
They were however seeded in Mulheim and lived up to that billing by defeating Danish duo Niclas Nohr and Sara Thygesen 21-14 22-20, surviving a late rally from the Danes.
"We knew we had the chance after reaching the final as we have beaten the Danish pair before," said a delighted Lai.
"We were eager to win and fortunately, past experiences taught us to pull ourselves together.
"We calmed down and we went on to win the match and Malaysia's first mixed doubles title in the German Open."
The Malaysian pairing will now confidently head to the YONEX All England, starting on Wednesday, as will plenty more international stars who tasted success at the YONEX German Open.
Three titles went to Japanese players in Mulheim on Sunday, with third seeds Yuki Fukushima and Sayaka Hirota beating Huang Dongping and Yu Zheng 18-21 21-14 21-6 in the women's doubles.
Fukushima and Hirota are seeded fourth for the YONEX All England and face French duo Delphine Delrue and Lea Palermo on Wednesday.
Japan also prevailed in the men's doubles - Takuto Inoue and Yuki Kaneko beat Indonesia's Fajar Alfian and Muhammad Rian Ardianto and have been drawn against seventh seeds Chen Hung Ling and Wang Chi-Lin in Birmingham.
Japan's Akane Yamaguchi is one of the favourites for the title in Birmingham and the 20-year-old came out on top against another contender – Chen Yufei – by a score of 21-19 6-21 21-12.
The situation was the same in the men's singles in Germany, with two favourites for the title at the YONEX All England, Chou Tien Chen and Ng Ka Long Angus playing out a dramatic final.
Chinese Taipei's Chou eventually came out on top 21-19 18-21 21-18, but was made to work for it by Ng in a final lasting 84 minutes.


text:
See Glen Cove NY courts and search free public court records. Courts are legal institutions which resolve disputes between parties and rule on legal cases related to civil, criminal, and administrative matters.
Glen Cove City Court 13 Glen Street Glen Cove NY 11542 516-403-2441
Sea Cliff Village Hall 300 Sea Cliff Avenue Sea Cliff NY 11579 2.3 miles from Glen Cove 516-671-0080
Lattingtown Village Court Lattingtown Rd Locust Valley NY 11560 2.9 miles from Glen Cove 516-676-6920
Matinecock Village Court 335 Duck Pond Road Locust Valley NY 11560 3.1 miles from Glen Cove 516-922-8198
Old Brookville Village Court 201 McCouns Lane Glen Head NY 11545 4.2 miles from Glen Cove 516-671-4725
Sands Point Village Court 26 Tibbits Lane Port Washington NY 11050 4.3 miles from Glen Cove 516-883-3044
Port Washington North Village Court 71 Old Shore Road Port Washington NY 11050 4.3 miles from Glen Cove 516-883-5900
Baxter Estate Village Court 2 Harbor Road Port Washington NY 11050 4.4 miles from Glen Cove 516-767-0096
Manorhaven Village Court 33 Manorhaven Boulevard Port Washington NY 11050 4.4 miles from Glen Cove 516-883-7000
Bayville Village Court 34 School Street Bayville NY 11709 4.4 miles from Glen Cove 516-628-1439
Mill Neck Village Court Frost Mill Rd Mill Neck NY 11765 4.5 miles from Glen Cove 516-922-6722
Upper Brookville Village Court 1395 Planting Fields Road Oyster Bay NY 11771 4.8 miles from Glen Cove 516-624-7715
Roslyn Harbor Village Court 500 Motts Cove Road South Roslyn NY 11576 4.8 miles from Glen Cove 516-621-7261
Flower Hill Village Court 1 Bonnie Heights Road Manhasset NY 11030 5.4 miles from Glen Cove 516-627-8877
Brookville Village Court 2 Brookville Road Glen Head NY 11545 5.4 miles from Glen Cove 516-922-8198
Roslyn Village Court 1200 Old Northern Boulevard Roslyn NY 11576 5.7 miles from Glen Cove 516-621-1961
Plandome Manor Village Court 65 South Drive Plandome NY 11030 6.0 miles from Glen Cove 516-627-3701
Plandome Village Court 65 South Drive Plandome NY 11030 6.0 miles from Glen Cove 516-627-1748
Oyster Bay Cove Village Court 25B Route 25A Oyster Bay NY 11771 6.0 miles from Glen Cove 516-922-1016
East Hills Village Court 209 Harbor Hill Road Roslyn NY 11576 6.2 miles from Glen Cove 516-621-6117
A court is a judicial body charged with resolving violations of a legal right. Judicial courts are created by the government and enforce the law by hearing civil and criminal matters.
Court records are available to the public. Court documents contain valuable information on a range of legal issues, including felony and misdemeanor cases, traffic accident reports, tax court records, and more. Many court records are available online.


text:
Let us start this tale at the very beginning. This is a tale of the girl from Slummies who meets the Shane Warne lookalike. As my bio reads, I am a small town girl. Born and breed in Slummies but lucky enough to have grown up in Cape-Town over the last 5 years.
I loved my childhood in Slummies. I have the best memories of getting up to all kinds things there, with the same bunch of friends I still have today. Everyone knows everyone and life seems to progress and you just keep following the next steps that everyone else seems to be doing, or as society deems right. Boyfriend, date for ages, get engaged, get married, buy a house, have babies. I too followed this system, albeit perhaps not in the right order.
Picture the scene: by 23 I was married to the long term boyfriend who ticked all the boxes, purchased the "dream home", was decorating up a storm, had a baby and had a great job. Seems like the perfect life. Which is was, for awhile. And then this happened….
One of my best mates from school was getting married, in November, in Cape-Town. Due the husband being a teacher the timing was not ideal with year end exams happening and next thing I knew I was road tripping to the wedding with another best mate and her husband. The plan was to leave on Thursday evening, stop over for the night in PE to break the trip.
Being the groupie that I am, I had a mate in PE who was down playing cricket for Boland. We headed out for a couple of drinks and later met up with the rest of team. It was an event filled evening with some Barney's locals wanting to throw the cricketers off the balcony. Drinks done, I head off to the wedding the next day and life carries on.
Fast forward to the end of December. I am not going to go into all the details but I had a light bulb moment, took a look at my life and just could not see myself being in that relationship forever. My folks had recently divorced and I think somewhere in the back of my mind I just did not want to be with a person I was not totally head over heels in love with. The person, the husband, had done absolutely nothing wrong, I can't even begin to find fault with him. It was a typical case of, the old favourite break up term: It's not you, it's ME.
So we separate. I move into my own place. I party like a Rock Star, as much as you can in Slummies. I soon started getting bored with the whole Numbers and Buccaneers routine.
Then in October I get a phone call.


text:
- This event has passed.
Paper Marbling
December 9, 2017 @ 1:00 pm - 3:00 pm$15.00
Event Navigation
Deadline to sign up is by Thurs. December 7 by 5pm
Learn about the mesmerizing process of paper marbling and walk away with decorative paper full of fun and colorful patterns!
Cost: Students: $15, Faculty/Alumni: $20, Community Member: $25


text:
North Korea Shifts Stance on U.S. Talks
Associated Press Writer
After months of insisting on direct talks with Washington, North Korea signaled on Saturday that it would be willing to accept U.S. demands for multilateral discussions over the communist country's alleged nuclear weapons program.
The shift is likely to ease tension on the Korean Peninsula, where recent South Korea-U.S. war-games and Washington's decision to send additional long-range bombers to the region has stoked fears in the North of an imminent U.S. invasion.
"If the U.S. is ready to make a bold switchover in its Korea policy for a settlement of the nuclear issue, the DPRK will not stick to any particular dialogue format," the North's KCNA news agency quoted a North Korean Foreign Ministry spokesman as saying. He did not say what was meant by a "bold switchover."
DPRK stands for Democratic People's Republic of Korea, the North's official name.
The United States expressed interest in the comment from North Korea, which could become a first step toward talks on ending the nuclear standoff.
"We have noted that statement with interest and we expect to follow up through the appropriate diplomatic channels," State Department spokesman Philip Reeker said Saturday.
A senior South Korean Foreign Ministry official described the North's statement as a "step forward."
The softer tone came as the war winds down in Iraq and the United States is expected to turn its attention to North Korea.
President Bush has dubbed North Korea as part of an "axis of evil" with Iraq and Iran. He has said he seeks to deal with North Korea diplomatically but has not ruled out military action.
The crisis erupted in October when U.S. officials said North Korea admitted it had a clandestine nuclear program in violation of a 1994 agreement with the United States.
The United States and its allies stopped oil shipments to the North, which retaliated by moving to restart a nuclear plant and withdrawing from the Nuclear Nonproliferation Treaty.
U.S. officials say North Korea poses a global danger and that the standoff should be solved with the participation of Russia, China, Japan and South Korea.
But until now, Pyongyang has rejected multilateral talks, insisting on one-on-one meetings to negotiate a nonaggression treaty.
"The solution to the issue depends on what is the real intention of the U.S.," said the North Korean spokesman, who was not identified by name.
"It is possible to solve the issue if the U.S. sincerely approaches the dialogue," the spokesman added. "What matters is the U.S."
However just a day before, North Korea said it would never give up its nuclear programs and compared U.N. inspections to "taking off our pants" and giving Washington an excuse to invade.
On Wednesday, the U.N. Security Council said it was concerned about the nuclear dispute. The council could eventually impose sanctions against the North if a diplomatic solution is not found.
The United States favors economic sanctions but Russia is opposed. However on Friday, Russian Deputy Foreign Minister Alexander Losyukov was quoted as saying that Moscow might reconsider if Pyongyang starts to consider producing or using nuclear weapons, Interfax reported.
The Interfax news agency also quoted Losyukov as saying the government has ordered officials to work out "preventive measures" to defend national interests and the population in the country's Far East should the Korean crisis spin out of control.
"We are disappointed and surprised by the position of some participants in the conflict, who do not seem to want to seriously address the problem through negotiations," Interfax quoted Losyukov as saying.
Earlier Saturday, South Korean President Roh Moo-hyun urged North Korea to hold talks.
"When the North comes out as a responsible member of the international community, we and the international community will not hold back on all necessary assistance," Roh's office quoted the president as saying.
South Korea, which is a close ally of the United States, hopes to persuade isolated North Korea to scrap its nuclear programs in return for aid and better ties with the outside world.
Roh, who took office in February, said he would discuss the issue with Bush when he visits Washington next month for their first summit. He said he also plans to meet with the leaders of China, Russia and Japan soon.
On Saturday, a North Korean youth group vowed loyalty to the regime ahead of the nation's biggest holiday, the April 15 birthday of late President Kim Il Sung. He died in 1994 and Kim Jong Il succeeded his father in communism's first hereditary succession.
"Once Kim Jong Il gives us an order, we, 5 million young people will become human bombs and wipe out the U.S. imperialists on this land," North Korea's KCNA news agency quoted unidentified members of the Young Vanguard as saying.


text:
Philippians 3:10 Amplified Bible (AMP)
10 And this, so that I may know Him [experientially, becoming more thoroughly acquainted with Him, understanding the remarkable wonders of His Person more completely] and [in that same way experience] the power of His resurrection [which overflows and is active in believers], and [that I may share] the fellowship of His sufferings, by being continually conformed [inwardly into His likeness even] to His death [dying as He did];
Amplified Bible (AMP)
Copyright © 2015 by The Lockman Foundation, La Habra, CA 90631. All rights reserved.
Philippians 3:10-11 The Message (MSG)
10-11 I gave up all that inferior stuff so I could know Christ personally, experience his resurrection power, be a partner in his suffering, and go all the way with him to death itself. If there was any way to get in on the resurrection from the dead, I wanted to do it.
The Message (MSG)
Copyright © 1993, 1994, 1995, 1996, 2000, 2001, 2002 by Eugene H. Peterson
Philippians 3:10 New Living Translation (NLT)
10 I want to know Christ and experience the mighty power that raised him from the dead. I want to suffer with him, sharing in his death,
New Living Translation (NLT)
Holy Bible, New Living Translation, copyright © 1996, 2004, 2015 by Tyndale House Foundation. Used by permission of Tyndale House Publishers, Inc., Carol Stream, Illinois 60188. All rights reserved.


text:
> Election Commission must be autonomous
Election Commission (EC) chairman Tan Sri Abdul Rashid Abdul Rahman said the country's election system need to be reviewed to give it autonomous power and total control over the election process, the media included.
Speaking on his last day in office after 25 years service, the retiring EC chairman said a review was necessary to stop others from making accusations against the commission.
"EC has to defend itself against accusations that it is toothless. How can we act when the rules do not allow us? The rules are there but our action cannot satisfy everyone," he told reporters at the ground breaking ceremony for the site of the new EC headquarters in Presint 2 here.
The new EC building costing RM70-80 million in the shape of a ballot box is scheduled for completion in two years.
Abdul Rashid, 66, will be replaced by Home Ministry secretary-general Tan Sri Abdul Aziz Mohd Yusof effective tomorrow.
His service was extended by another year after Dewan Rakyat passed the Constitution (Amendment) Bill 2007 to extend the retirement age for EC members from 65 to 66 years.
Abdul Rashid who had handled seven general elections said EC should be in control during the campaign period telling people what to do and what not to do, and not other authorities.
"EC should be in the position to control the total network of media during elections. It should be able to tell the media their limit and role they can play during elections."
He proposed that a body be created to review the needs of EC and the country's elections laws, although it may take two, three or ten years.
However, it was up to the government whether to accept the concept or not.
"If the government accepts the concept, then it must make appointments but if it wants to wait, then I cannot comment.
"I don't know whether the situation warrants it or not. I am just speaking as a former chairman based on his experience."
Abdul Rashid said he had forwarded the proposal to Prime Minister Datuk Seri Abdullah Ahmad Badawi and offered himself to be the adviser should the body be created.
He said other countries had similar setups during elections where the EC had full control over the election process, not ministries or departments.
"It existed in other developing countries. I feel we have to follow their foot steps as it is the strengthening of democratic practices."
Abdul Rashid also said he was considering taking legal action against several opposition party members for making personal attacks against him.
He declined to reveal their names but said he had adequate information and proof for his lawyer to act.
"I did not want to sue these people earlier because I did not want to drag the EC into it. Now that I have retired and a free person, I am considering a suit against those who had said so many untruthful and bad things against me," he said - Bernama.


text:
It looks like you're using an Ad Blocker.
Please white-list or disable AboveTopSecret.com in your ad-blocking tool.
Thank you.
Some features of ATS will be disabled while you continue to use an ad-blocker.
originally posted by: NewzNose
a reply to: Krazysh0t
Proof, please.
originally posted by: WhiteHat
a reply to: Krazysh0t
You know, most muslims refuse to be treated by the female nurses or doctors. Ok, is their right.
I refuse to be treated as a second hand citizen. Is my right.
And yes it bothers me to see women abused because is right by their religion. It should bother you too.
And I said "to see", not to read. I'm talking about real life, not internet reports.
originally posted by: Krazysh0t
a reply to: WhiteHat
Erm... There are hundreds of millions of Muslims that have figured out how to live in civilized countries. Your post reeks of xenophobia and is contradictory. You just got done saying you don't fear them then proceed to say that you don't want to associate with them because you are a woman and scared of them because of your preconceived notions about how they treat other women.
originally posted by: Krazysh0t
a reply to: DBCooper71
First off, does she live in Sweden? I'm guessing no. Second, Muslim men aren't the only men who rape women... If we are going to get all scared about Muslim men due to misconceived notions brought on by media spin, then she might as well fear ALL men. Let's just go the full monty then. Because that's basically the rhetoric you are using here. "Rape exists so I should fear all men because they might rape me".
How many Muslims have you met that have actually done that to you then?
originally posted by: Krazysh0t
a reply to: WhiteHat
Well do you go into ANY ghettos and make waves? I mean you are singling out muslims here, but it's not like other ghettos are known for their welcoming attitudes or anything.
a reply to: Krazysh0t
Well then the confusion was about your fear of ghettos instead of Muslims.


text:
Orlando Pirates appear to have pulled out of the race to sign Thamsanqa Mkhize following the arrival of new coach Muhsin Ertugral.
Mkhize had been training with the Bucs squad and was believed to have passed a medical with the side following his Maritzburg United exit. Now, however, a source has revealed he no longer fits in with the club's plans.
'It's true that the deal of Mkhize to Pirates will no longer happen,' the source told KickOff.
'The coach Muhsin Ertugral felt he is not someone he is currently looking for. The player trained once with the team and he did pass the medical but he will no longer be signing with the club.'
The player's agent Sizwe Ntshangase was reluctant to discuss what went wrong with the deal but did reveal discussions with the club were still ongoing.
'We will speak to Pirates on Monday to hear the way forward,' Ntshangase said. 'But we are open with other teams who are interested in the player and life goes on.'
Ntshangase made 17 appearances in the Premiership last term, scoring once.


text:
The Makers
Yes, there's definitely a particular poetic cliche in this unsympathetic day and age: the defense of poetry. It's still relevant! It's still important! We're not just a bunch of obscure academics stultifying in our tenure writing poems that only our colleagues read! Poetry can change the world! It's slightly lame, I admit; Homer didn't need to spend time justifying his existence. (Did he? Actually, I guess he did, against people like Plato.)
But what can I say? I love poetry and I'm totally sympathetic to it.
Who can remember back to the first poets,
The greatest ones, greater even than Orpheus?
No one has remembered that far back
Or now considers, among the artifacts,
And bones and cantilevered inference
The past is made of, those first and greatest poets,
So lofty and disdainful of renown
They left us not a name to know them by.
They were the ones that in whatever tongue
Worded the world, that were the first to say
Star, water, stone, that said the visible
And made it bring invisibles to view
In wind and time and change, and in the mind
Itself that minded the hitherto idiot world
And spoke the speechless world and sang the towers
Of the city into the astonished sky.
They were the first great listeners, attuned
To interval, relationship, and scale,
The first to say above, beneath, beyond,
Conjurors with love, death, sleep, with bread and wine,
Who having uttered vanished from the world
Leaving no memory but the marvelous
Magical elements, the breathing shapes
And stops of breath we build our Babels of.
-Howard Nemerov


text:
Artwork Description / Detail
Exhibited: McGregor Wright Art Gallery, Wellington, February 1904, No.18
Collection: Mrs R D Todd
Private Collection, Auckland
Ascent. Frances Hodgkins, Commemorative Issue (Caxton Press with QE II Arts Council, Christchurch 1969) p. 14
Roger Collins and Iain Buchanan, Frances Hodgkins on Display 1890 – 1950 (Hocken Library 2000) p. 35
E.H McCormick, Portrait of Frances Hodgkins (Auckland University Press 1981) p. 51
I Buchanan, E Eastmond and M Dunn, Frances Hodgkins: Paintings and Drawings (Auckland University
Press 2001) p. 18
E.H. McCormick, Portrait of Frances Hodgkins (Auckland 1981) p. 47
Frances Hodgkins 1869 – 1947, Queen Elizabeth Arts Council of New Zealand (Auckland 1969) No. 6
E.H. McCormick, Works of Frances Hodgkins in New Zealand (Auckland 1954) plate 15
E. H. McCormick, The Path to Impressionism (Art New Zealand #16, Auckland 1980) p. 31
To Dorothy Richmond, 3 December 1902; from F. H., Hotel Bristol, Tangier.
Salaams from Morocco! We've arrived…………. Heavens! how beautiful it is! Why aren't you here you foolish and misguided woman… I am never going back to New Zealand – I am going to turn Moslem
– I am going to wear a haik – I am going to lie on a divan for the rest of my days with a handmaiden called Fatima to wait on me….1
In late 1902 Frances Hodgkins travelled to Morocco, accompanied by her friend Mrs Ashington, whom she had met at a summer sketching school in Caudebec. The trip can be seen as a continuation of her search for exotic subject matter, and in the old Moorish walled town of Tangier she was able to respond to the effects of sunlight, captured en plein air. In choosing to go to North Africa Hodgkins was following a path well-worn by English and French artists – including Delacroix, in 1832 – drawn by a romantic hankering for the exotic and the vogue for Orientalism.
In a letter to Dorothy Richmond, Hodgkins described the arrival at the port of Tangier:
Directly the boat stopped – some way from the landing pier – a thousand or so Moors hurled themselves on deck & began fighting violently over our baggage – some of them such magnificent looking men, bronze giants, others wizened up, wicked looking little brigands and a few coal black Nubians with plunging eyes.2
In addition to the architecture and the market places of the city, Hodgkins was attracted by the dark skin and flowing garments of the local people. She told Dorothy Richmond of one of her models, a 'ducky little Arab girl who we captured & painted in an aloe grove', and who agreed to return the next day.3
The sitter for the 1903 watercolour Study of a Sudanese has been identified as Absolom, Mrs Ashington's Arab guide. Hodgkins informed Richmond that 'Absolom the trustworthy' was their main source of Tangier gossip; 'he knows everything, and what he doesn't know he guesses at.'4 His knowledge of Tangier proved invaluable, while he also dispersed crowds of curious onlookers when Hodgkins and her companion painted in the market place, and shielded them from the Moroccan sun with an umbrella.5 In her portrait, strong sunlight falls directly on the faithful Absolom, whose eyes are downcast. Bold strokes of fluid colour flesh out the background, while the details of his garments are merely hinted at under the glare of the sun, all serving to draw attention to the face and the sitter's dark brown skin.
On the boat to Tangier, Hodgkins encountered wealthy friends from Dunedin, David and Marie Theomin. Patrons of the arts and admirers of Hodgkins' work, they commissioned a watercolour, Orange Sellers, Tangier (collection of Theomin Gallery, Olveston, Dunedin).6 In this market place scene the intensity of the sunlight has reduced a foreground display of fruit and vegetables to mere blobs of colour, in contrast to the shimmering whiteness which distinguish other areas of the composition. Here Hodgkins sought a general effect, the unique atmosphere of a street market, whereas Study of a Sudanese captured the character of an individual.
Written by Richard Wolfe
Research by Jonathan Gooderham
- Linda Gill (editor), Letters of Frances Hodgkins, Auckland University Press, 1993, p. 149
- ibid. p. 150
- ibid. p. 151
- ibid. p. 154
- Joanne Drayton, Frances Hodgkins: A Private Viewing, Godwit, Random House, Auckland, 2005, pp. 79, 84.
- Iain Buchanan, Elizabeth Eastmond and Michael Dunn, Frances Hodgkins: Paintings and Drawings, Auckland University Press, 2001, pp. 92-3.


text:
RECOMMENDED: If you have Windows errors then we strongly recommend that you download and run this (Windows) Repair Tool.
No more missed important software updates! UpdateStar 11 lets you stay up to date and secure with the software on your computer.
Error 1330.A when installing POS. I received an error 1330.A. After the uninstall process is complete, rename the QuickBooks Point of Sale 7.0 folder.
If you are facing trouble with QuickBooks Point of Sale Error 1330 then just give a ring on +1-800-274-4168 to resolve the issue with guidance of QB experts
TCP/UDP Port Number List – WhatIsMyIPAddress.com – List of well known, registered, and dynamic/private ports.
$415,000 MLS # 4500867 3 BR, 2 BA, 2 car garage 3.9 Acres on Fish Lake $89,900 MLS # 4508258 2 BR, 1 BA, Seasonal Cabin Treed lot on Eleven Lake RUSH CITY, MORA, CAMBRIDGE realhomepro.com 117 S S. Union • M.
PlaceYourAD PlaceYourAD – 2017年8月21日. ※If printing error after placement of ad, you may notify us within 3 days to make. Basic computer skill, Word, Excel, POS system, ect. Must have a food. 832- 247-1330. *堂吃外賣店售. *QuickBooks做帳. 電: 肯維培訓.
Resolve QuickBooks POS error code 1330, dial the toll free QuickBooks POS support 1855-924-9508 and get help from experts to resolve error.
Florida State has everything, providing a premier place, quality personnel, championship sports, along with world-renowned instructional applications. Florida.
A file that is required cannot be installed. error 1330. A file that is. QuickBooks Point of Sale Multi-Store 12.0 ADD A STORE
Can you help with this error: "Error 1330 A file that is required cannot. Reboot the system and proceed with a clean install of the QuickBooks Point of Sale.
Fix Quickbooks Error online by Certified Intuit professional of Quickbooks247 support , Get the details of Quickbooks error code to get resolve call Customer Care.
Volcanoes and volcanology | Geology – Kilauea; Mount Etna; Mount Yasur; Mount Nyiragongo and Nyamuragira; Piton de la Fournaise; Erta Ale
File Locking Error May 18, 2016. As the error says, you have a problem with the vg_ice1/lv_home filesystem. Type the root password to get into a prompt and run fsck. IBM WebSphere Application Server Update Installer fails. – Review the error symptoms If the Update Installer reports errors updating "java.exe" or "WASServiceMsg.dll", then proceed to the error symptom
Xp Send Error Report Windows Error Reporting – technet.microsoft.com – In Windows XP with SP1, error reporting is enabled by. How Windows Error Reporting. The opportunity to send an error report is. The Department of Energy Computer Incident Advisory Capability (CIAC) has advised against using the error reporting technology included in Office XP, Internet Explorer. Microsoft's default selection is
Express Helpline- Get answer of your question fast from real experts.
West Texas A&M University (also known as WTAMU, WT, and formerly West Texas State), part of the Texas A&M University System, is a public university located.
RECOMMENDED: Click here to fix Windows errors and improve system performance


text:
Peter and I went out for a quick run of shows this past weekend. Sometimes shows are really dumb, and you wonder why you drove six hours in a crowded vehicle taking naps with guitar cases as pillows and eating cashews and gross cheeseburgers (without the meat, of course) all afternoon. A lot of touring is like that, and it's why I honestly prefer to tour in the United Kingdom -- shorter drives, audiences that treat musicians like royalty, and funny accents. But this weekend was one of those tours where the shows were fun, the audiences were attentive, merchandise was sold, and friends were made.
FWT joined us in the trusty Volvo, and he was a lifesaver. I'd forgotten how nice it is to have a tour manager available to sell merch (or pack up your keyboard so you can go hock CDs). He also drove most of the way, so Peter was able to read. I can't read in the car without vomiting, so I rocked out to some This American Life podcasts, you know, like a real rock star.
Some highlights:
- The Atlanta Dogwood Festival had a big cooler full of Cokes (which includes Coke, Diet Coke, Sprite, etc, of course) and import beer backstage for the artists. Plus, they arranged for near-perfect weather, 72 and sunny.
- I was the sunscreen nazi among us, but I forgot to wear a hat. Or, rather, I forgot to put sunscreen on my scalp. Ouch.
- The house concert hosts in Birmingham were amazing, and they even indulged us in a grand tour of their gorgeous home ... allowing us to oooh and ahhh over their mind-blowing kitchen and mosaic tiles.
- Played a show in Atlanta with Jeremy Aggers, a folksy rootsy songwriter, whose music I really dug.
- Ate far too much and remembered why my road dresses are elastic. Brunch in Atlanta is yummmmmmmmmmmmmmmmmmmmmmmmy.
- Peter and I didn't have Jesus Christ Superstar on our iPods for the drive, so we performed as much of it as we could remember a cappella during the last bit of I-65. I'm not sure FWT appreciated that, but he didn't complain. Peter does a hell of a Judas, so casting directors, if you're looking to stage the show locally, I'm your Mary and Peter's your Judas.
- Sold some CDs, allowing us to break even and consider touring in American again. Folks, if you do nothing else at a show, please consider buying merchandise. You have NO idea how much it helps out an artist.
Monday, April 19, 2010
Notes from the Road.
Subscribe to: Post Comments (Atom)
I think I might be breaking up with yoga. We have had a long separation now. Yoga had been really good for me -- it got me in shape, and it ...
My sweet little privileged boys playing in the show! Every woman I know is on fire lately. Whether that means finally seeking out therap...
Gooooood Monday morning, y'all! I'm writing from the Norton Cancer Institute where, for the first time in months, I'm able to ac...


text:
Thursday, August 26, 2010
And may the odds be EVER in your favor...
Have you ever read a book, that from the moment you read the first chapter has so captured your attention that you can't put it down? That expression is so cliched, "can't put it down" but it was true for me and Mockingjay. This book is one that I would call life altering. It is ultimately, despite they YA classification, a novel on war. It is of course the third in the Hunger Games series and should leave anyone reading it asking...Real or not Real? Honestly, I am still trying to process and it is hard. Today has been a LONG day, and this book made me cry a lot. I promise pictures tomorrow!
2 comments:
Uh oh...I should expect crying? I'm not too far in yet.ReplyDelete
One of the books I read that arguably qualified for "can't put it down" (it was a few years ago, but I do remember really liking it) ended up sucking at the end. I heard one guy actually threw the book across the room because the ending was so horrible. Alas, what little it takes to ruin an otherwise good book.
A friend told me I wasn't allowed to rewrite the ending to it...
Subscribe to: Post Comments (Atom)


text:
Food Prices
Tree Hugger compares organic verses regular.
Now that home foreclosures and job losses are piling up, and people are tightening their belts across country, it's easy to imagine hordes of shoppers running from organics to supposedly cheaper "regular" food. (You've gotta love a world where the food that's been sprayed with toxic chemicals is normal and the other stuff gets its own tiny section of the supermarket.)


text:
No. 4 Auburn softball caps undefeated weekend with power-hitting victory over LIU-Brooklyn
An early start time Sunday didn't seem to impact the Auburn softball team, which finished its undefeated run in the USF Spring Classic with a 9-4 victory over LIU-Brooklyn.
The No. 4 Tigers (27-3) extended their winning streak to six games in a nonconference matchup that started at 8 a.m. CT. But Auburn's offense was wide awake, engineering a seven-run third inning behind triples and home runs from its top four hitters — Carlee Wallace, Kasey Cooper, Haley Fagan and Kendall Veach.
Makayla Martin (12-3) opened and closed the contest with four scoreless innings separated in the middle by relief appearances from Ashlee Swindle and Jenna Abbott. Martin allowed only one base runner, continuing the great form from fellow starting pitcher Kaylee Carlson, who had a perfect game Saturday.
WEEKEND REWIND: Game 1 and Game 2 | Game 3 and Carlson's perfect Game 4
Player of the game
SS Haley Fagan: 1 for 3 with 1 HR and 3 RBI
Auburn senior shortstop Haley Fagan didn't have the best of starts to the weekend after being named SEC player of the week for her work against LSU.
Fagan found herself in a mini-slump heading into Sunday's game, but she changed all of that with one swing of the bat in the third inning.
Fagan crushed a tying two-run homer in the third that bounced off the scoreboard in Clearwater. She excelled in the final game of the weekend in her home state, adding a sacrifice fly in the bottom of the sixth to give Martin some more insurance.
Turning point
Auburn's offense came alive in the third after a LIU-Brooklyn home run.
After two perfect innings to start the game from Martin, Auburn's coaching staff made the decision to give freshman Ashlee Swindle some work with a 1-0 lead. She allowed a three-run homer in the top of the third that put the Blackbirds ahead, but the Tigers didn't let her stay down for long.
Cooper led off with a triple, and Fagan drilled her home run on the next at-bat. After a Courtney Shea single, Veach mashed a no-doubt two-run homer to put the Tigers back on top. The bottom of the order engineered some more base runners, and Wallace brought two home on a triple that she quickly scored on thanks to a throwing error.
In total, Auburn had 7 runs on 6 hits — including two home runs and two triples — in the bottom of the third inning. It was the best offensive outburst of the weekend for the heavy-hitting Tigers.
Statistically speaking
Auburn keeps its groove going with runners on base on Sunday.
During the first three games of the weekend, Auburn had underwhelming performances with runners on base — including a 2 for 18 game against Illinois on Saturday. But the Tigers got things rolling again against Ohio State, and that carried over against LIU-Brooklyn.
Auburn batted an impressive .545 with runners on and .500 with runners in scoring position against the Blackbirds. The Tigers also went 6 for 12 with two outs, which kept things going in its monster third inning.
After a slower offensive start in the tournament, Auburn needed a pair of games like it had against Ohio State and LIU-Brooklyn, especially with a trip to No. 2 Florida on the docket for next weekend.
What's next for Auburn softball
Auburn travels back to Florida next weekend — this time to face the No. 2 Gators.
The Tigers return to the Sunshine State next weekend to take on No. 2 Florida, which is receiving first-place votes in the NFCA Coaches Poll. The Gators (25-1) have won 17 straight games heading into Sunday, when they'll look to wrap up a sweep of SEC opponent South Carolina.
The series will run from Saturday to Monday instead of the usual weekend order. The Saturday and Sunday games will be televised on ESPN2, with the Monday finale going on the SEC Network.
Auburn split its four games against Florida last season, losing two of three in an opening regular season series before knocking off the then-No. 1 Gators in the SEC Tournament semifinals.


text:
New York based Turkish designer Sıla Karakaya, graduated from New York University, TISCH School of the Arts, with a MFA degree in Production Design and Scenic Design.
Nowadays, she designs theatrical, cinematographic and architectural sets, and brings film and theater characters to life. Most recently, Sıla Karakaya worked on the set of Spike Lee's last movie, "Red Hook Summer." Her next project will involve set designing and production for an Emma Thompson's movie to be shot in London.
In a recent interview, Sila Karakaya said,"My design background from MFA, Lighting Design from Parsons School of Design and BFA, Interior Architecture from Bilkent University—make for a very comprehensive set of skills," and, she adds, "I feel very lucky to have taken lessons from legendary filmmakers like Woody Allen and Martin Scorsese during my education at NYU."
Perhaps just as obvious as her skill and preparation, is her passion for her work.
Here are my longer articles on Hurriyet USA and Hurriyet Turkey daily newspapers in Turkish.


text:
How to Prepare for and Survive a Nuclear Fallout
After hearing multiple people comment that they did nothing because they thought they were going to die, Luke Evslin and Tanya Gamby compiled information from various reputable sources on ways that families can protect themselves. […read more]
7 Ways Technology Can Bring Your Family Closer
Most parents can agree that it's a good idea to set aside technology-free family time. At the same time, it's also helpful to remember all the ways technology can bring families closer. Young people, in […read more]
Why is Physical Exercise Important for the Elderly
Physical activity is vital at any age, but as you grow older, changes set in that make exercise even more crucial. Conditions that typically develop with aging can be delayed when you stay active. Physical […read more]
Quality Care and Respite for Loved Ones
Mrs. Dolores "Dolly" Alpeche, born and raised on Kaua'i, at the age of 88, finds herself enjoying life, meeting new friends, and staying active. In her younger days, Dolly was primarily a housewife and as […read more]
Puberty: A Parents Survival Guide
Ahhh… puberty. The inevitable time in our lives where our emotions are like roller coasters, our body is sprouting hair in all kinds of places, and the confusing time where one minute we demand independence whereas […read more]


text:
I'm back. I was on blog hiatus, enjoying my final week with my family before heading back to the office this week.
This is our third installment in a series on the kingdom of God. If you missed the first two, you might not get all I'm saying in this one… so, if you like, simply scroll down a little and get caught up.
Definition: the Kingdom of God is any time and any place in which the rule and reign of God is expressed.
That definition becomes inadequate as soon as you point out that the rule and reign of God is universal and eternal, and it is always expressed even when we fail to acknowledge it. And since the writers of Scripture do not make the equation that the (kingdom of God) = (everything, all the time), let's make an addition.
Definition: The k.o.g. is any time and any place in which the rule and reign of God is expressed AND respected/enjoyed/responded to.
End it however you like; it entails a manifestation of the reign of God that summons forth a positive response from those who encounter it. In part one, I identified 8 manifestations of the k.0.g. In part 2, I introduced #8: the Kingdom of God Within. Today, I'd like to say a little more about #8, the Kingdom Within.
Or, as I have called it in my churches, the Royal Palace of the Soul.
I've heard all kinds of so-called Christian reactions to the culture around us. I've heard that we should be separate and different. I've heard that we should be integrated and involved. I've been told that society is going downhill so fast that we shouldn't have kids. And as a dad with two little kids, I am concerned about the environment my children will grow up in.
But as a Christian, I have something I'm even more concerned about, and you should be too: not the environment my kids grow up in, but the environment that grows up in my kids.
God is not only concerned with your environment, he is at least equally concerned with your invironment.
That is why Jesus emphasizes the Kingdom within; an emphasis that is strangely overlooked in most Bible teaching today. I'm not sure why, but I have a hunch: pastors and teachers are overly concerned with works and behavior, and pressure their churches into activity. All branches and no roots. Or, to stick w/the analogy, all superstructure and no substructure.
1. The Bible compares your inner life to a construction project: ""Therefore whoever hears these sayings of Mine, and does them, I will liken him to a wise man who built his house on the rock:" Matthew 7:24, NKJV. "Through wisdom a house is built, And by understanding it is established; By knowledge the rooms are filled With all precious and pleasant riches." Proverbs 24:3, 4, NKJV. The word EDIFICATION refers to the building up of this inner structure. The task of the church is to convict sinners and EDIFY saints.
2. The purpose of the structure is to provide a suitable dwelling place for the Spirit of Christ. ""I have been crucified with Christ; it is no longer I who live, but Christ lives in me; and the life which I now live in the flesh I live by faith in the Son of God, who loved me and gave Himself for me." Galatians 2:20, NKJV. And since it is God/Christ/Spirit living in us, that makes the dwelling a palace, does it not? That's where I get the term: Royal Palace of the Soul (RPS).
I equate the RPS with the kingdom of God within. Why? Because what else would God be constructing in our souls but an increasing respect for his rule and reign? The RPS is a metaphor for an growing awareness of and responsiveness to the sovereign rule of God in our lives and our world. When that awareness/responsiveness become second nature, you're will on your way to an intact Royal Palace of the Soul.
3. The degree to which God's reign is manifest in you depends on the degree to which you build your very own Royal Palace in your soul. Consider the RPS a dwelling place for God in your soul. One of the word-pictures the Bible uses to teach this concept is the word edification. The Greek word (oiko-domeo) means "to build a house." In the Bible, to edify doesn't simply mean to encourage. It means to create structures in your soul that are capable of enjoying, manifesting, savoring, and responding to the presence of God himself. So all I can say is that if you really want to bring God in your your home, your classroom, your neighborhood, your marriage, your kids, your church, your job… then get building! You have a house to build IN YOU FIRST. "that Christ may dwell in your hearts through faith; that you, being rooted and grounded in love, may be able to comprehend with all the saints what is the width and length and depth and height– to know the love of Christ which passes knowledge; that you may be filled with all the fullness of God." Ephesians 3:17-19, NKJV. God gave church leaders for "for the equipping of the saints for the work of ministry, for the edifying of the body of Christ," Ephesians 4:12, NKJV. "…But we do all things, beloved, for your edification." 2 Corinthians 12:19, NKJV. Is not edification the principal duty of church leadership as regards believers?
4. The RPS is not only for God, it is for you too. It is God's plan that you carry within you a Royal Palace: an environment INSIDE of you that can be a shelter from the storms of life; a place of rest and peace and luxury no matter what is happening outside of you. In 1913, Charles Miles wrote a hymn that became a classic
I come to the garden alone
While the dew is still on the roses.
And the voice I hear, falling on my ear;
The Son of God discloses.
And He walks with me,
And He talks with me,
And He tells me I am His own,
And the joy we share as we tarry there;
None other has ever known.
What is he talking about? He's talking about the RPS, though he's not calling it that. It's a place where no matter how crazy life becomes, you can quietly, restfully, lavishly meet with God. And it's in you. It's like a Garden, it's like Paradise. And it's for you if you want it. "Peace I leave with you, My peace I give to you; not as the world gives do I give to you. Let not your heart be troubled, neither let it be afraid." John 14:27, NKJV. You can have chaos outside you and peace inside you, in your heart. How? By building the RPS, the kingdom of God within you.
5. The Royal Palace is a supernatural building project. The builder is supernatural, and the building materials are supernatural too. The builder is the Holy Spirit and the material is the Word of God. Each brick is a verse, a promise, a principle, a doctrine, a rebuke… a truth from the Word of God. Does not the Spirit use the Word as his weapon/tool (Eph 6:17)? God is building a PALACE in you; consider it a BEACHHEAD for the kingdom of God in your daily life. As it grows, it changes your words, thoughts, and actions. It is the palace your heart was always intended to be–a place of communion with God, and shelter from the storms of life. God himself builds this as you continue to take in the Word of God.
"But Jesus answered him, saying, "It is written, 'Man shall not [really] live by bread alone, but by every word of God.'"" Luke 4:4, NKJV.
"But He said, "More than that, blessed are those who hear the word of God and keep it!"" Luke 11:28, NKJV. [Keep translates the Gk word phulasso, which means to build a garrison in your soul; another function of the RPS: warfare!]
1Th 2:13 "For this reason we also thank God without ceasing, because when you received the word of God which you heard from us, you welcomed it not as the word of men, but as it is in truth, the word of God, which also effectively works in you who believe." The phase, "effectively works" is there for all our readers who are concerned for good works. There you have it; the word of God does good works… IN YOU, before it does them AROUND YOU. The seed bears the fruit. The seed is the word of God… the construction material for the royal palace, the kingdom of God within you.
And one more principle, which to me is the big one…
6. The Royal Palace builds in you the same structures of thinking that feeling that Jesus had in his soul.
"Let this MIND be in you which was also in Christ Jesus…" (humility, grace orientation, mission) Phil 2:5.
"Arm yourself with the same mind [as Christ]" 1 Pe 4:1.
You can't live like Jesus unless you think like Jesus, and you can't think like Jesus without the Word of God. Question: in the soul of Jesus, was the kingdom of God primarily a set of ACTIVITIES, or a WAY OF THINKING? I say (b), a way of thinking.
Have no fear, those of you who think I'm advocating years of training before engaging in service. I am not. I believe we should grow in grace, grow mature, and grow spiritually ASAP… grow fast… and serve fast too. Just always leave a reasonable lag time between your being (first) and your doing (second).
The Kingdom of God within you, the royal palace of the soul. Try these verses on for size with that interpretation in mind:
- ""But seek first the kingdom of God and His righteousness, and all these things shall be added to you." Matthew 6:33, NKJV.
- "for the kingdom of God is not eating and drinking, but righteousness and peace and joy in the Holy Spirit." Romans 14:17, NKJV.
- "For the kingdom of God is not in word but in power." 1 Corinthians 4:20, NKJV.
I fear that many church leaders are not confident in the divine process of growing the kingdom within each believer. They end up pressuring outward behavior without enabling inner transformation. Isn't that exactly what the Pharisees did?
Bottom line: to build a Royal Palace is to grow up spiritually. To grow up spiritually is to exhibit & respond to the rule and reign of God. To exhibit and respond to the rule & reign of God is to live in the kingdom of God. To live in the kingdom is to love God and to love the world for whom Christ died. Isn't that our task? It all flows out of growing up.
- ""So now, brethren, I commend you to God and to the word of His grace, which is able to build you up and give you an inheritance among all those who are sanctified." Acts 20:32, NKJV.


text: This day in music history, January 27th 1973, the #1 song on the Billboard charts was Stevie Wonder with Superstition. A few months earlier he was working on his new album called Talking Book. He was certain that the song he was working on for the album, Big Brother, would be a big hit and should be the single released from the album. Motown was certain it should be Superstition. Stevie said he wrote the song for Jeff Beck. He felt it more suited Jeffs style of music. Stevie said he was certain Jeff would release Superstition before he did since he was still working on the album. However, since Stevies version of the song was already finished Motown released his version before the album in November of 1972. A few weeks later it was the #1 song in the country.


text:
Bitcoin – QuickStart to Prosper with Cryptocurrency
The best way to make money with and earn Bitcoin right now is through Cloud Mining with reputable companies like HashFlare. Sign up today and invest as little or as much as you like and reinvest your daily earnings to acquire more bitcoin or Cryptocurrency Get Started Today!
To Buy, Save, and Exchange your Bitcoin or Cryptocurrency you'll need a Coin Wallet.
The most popular and trusted online wallet is CoinBase. This is your starting point. Actually if you sign up with them, they'll even give you $10 for your first $100 you deposit. Create A Wallet
Your Coin Wallet gives you an Address, it's like an email, but it is a unique string of numbers that you use to securely send and receive digital money.
To store your money offline for safe keeping you can use a hardware wallet.
Ledger wallets are very popular especially in Europe. Amazon has a lot of great new storage products as well.


text:
13 Aug 2018 - 15 Aug 2018
23 days to go
Sands Expo & Convention Center
Las Vegas / Nevada / United States of America
Agenda Las Vegas is the most diverse and creative lifestyle fashion trade show in the world. The show is where passion becomes profit and the business of creativity is conducted in a truly authentic environment. This 3 days trade show is being organized by Agenda, LLC. The venue of this event is Sands Expo & Convention Center which is located in Las Vegas, Nevada, United States of America. The event will be held from 13 August 2018, Monday to 15 August 2018, Wednesday. Agenda Las Vegas will showcase a wide range of products and services related to apparel and fashion sectors from the leading exhibitors, for example, lifestyle, streetwear, contemporary, women's, accessories, action sports, outdoor, footwear, and both surf and skate hardgoods. Over 250 exhibitors are expected at this event to showcase their products and services. Over 10,000 visitors are expected at this trade show. Visitor profile of this event includes buyers, brands, investors, distributors, and media. The frequency of Agenda Las Vegas is biannual (twice a year).
Address : 201 Sands Avenue
City : Las Vegas, NV
Country : United States of America
Phone : +1 702-733-5556
Website : Click here for venue website
Located at The Venetian, Sands Expo & Convention Center is a large convention center with 1.8 million square feet of combined meeting and event space. Whether you have a small or large meeting, trade show, convention etc., the venue offers flexible individual meeting rooms, expansive exhibit halls, hospitality suites and executive boardrooms.
MRKET New York
New York Global Fashion Trade Show
Texworld USA
North America's largest sourcing event for apparel
Bridal Spectacular Las Vegas Wedding Show
PBA Beauty Week
Professional Beauty Association Beauty Week
ASD Las Vegas Summer
ASD MARKETWeek Summer
Agenda, LLC organizes the most diverse and creative lifestyle fashion trade shows in the world since 2003.
Address: 110 E 9th Street Suite B445
City: Los Angeles, CA
Country: United States of America
Phone: 213-223-5111
Fax: 213-443-1249
Email: info[at]agendashow.com
Website: Click here for organizer website
|Event Type
|International Trade Show
|Start Date
|13 August 2018, Monday
|End Date
|15 August 2018, Wednesday
|23 days to go
|Apparel & Clothing
|Sands Expo & Convention Center
|Las Vegas, NV
|United States of America
|Agenda, LLC
|Open to
|Trade visitors


text:
Ok, here's a chance for the Senators to show us something. Win and we're still in striking range for the division. Lose and we hand it to the Habs. I'm finally feeling human again, so I'm having a beer with my hockey (which is the normal state) and looking forward to the match.
I flip on the tube to find Mr. Magoo is doing the game. Oh boy! This guy must have pictures of someone with someone else doing somethings; possibly naughty or illegal things, otherwise, how the hell does he still have a job. Not to mention that he worked in the playoffs last year; unbelievable. I wouldn't let him work a Monopoly game. Oh well…here we go:
Period One
Please take your time getting across the crease, Herr Gerber. I'm sure there's no hurry. 1-0 Habs.
Watching Randy Robitaille trying to lay a check reminds me a bit of my 6 year old niece cozying up to my dog. It's really kinda sad. I was thinking that I would give him credit for at least trying to hit someone, but it's just so lacking in conviction that I can't muster any love.
This is shaping into a crappy night. The Habs are really taking it to the Senators; out-hitting, out-skating and dare I say, out-caring.
Wade gets an owie behind the net so there's not much help in front of Gerber for the inevitable rebound; 2-0 Habs.
Some more crappy play and more crappy crap and the freakin' crap is crappy crap crap; 3-0 Habs. There's going to have to be something extraordinary happen for me to continue this post. And I was so excited for hockey….and a beer.
Changing Horses in Mid-stream; NCAA Baskeball
Let me start out by saying that I have run an NCAA pool since I was a freshman in high school (that's 25 years). I played college basketball. (Emery in goal to start the second period) I've played basketball since I was 6. I was the kid in town who always had a ball with him; I carried it around like little girls carry around a Barbie. But, I'm losing interest in March Madness and I'm not running a pool this year. Here's a partial list of things I watched instead of NCAA basketball over the last four days: hockey, English football, golf, M*A*S*H (no, they're not making new episodes), Survivorman, March of the Penguins (not hockey related, btw), and (a very crappy movie) Sahara. That's not to say I didn't watch at all. It was on the TV as I napped a bit and I even watched the full games when the Badgers played. (It's 6-1 Habs now) But, here's the thing….for most of the game I end up yelling at the TV begging for traveling calls; it's just such a joke now. At one point in a Tennessee game, a player changed his pivot foot twice and there was no call. The college game is more and more like the pro game every day which is to say, it's sucky. I can barely muster a molecule in my body that wants to watch anything that resembles professional basketball. That's where I am.
The powers that be must think that taking 3 steps to make some bullshit playground move makes for more exciting basketball. Well, I demand a little more integrity than that. I'm sorry folks; I'm out!
It's 7-1 Habs now. I'm going to watch the third period to see if we come out and pound Max Lapierre into a bloody pulp, which would show me that we, at least, have a pulse. It's funny; the day after the last Habs game which we won 3-0, the talk shows on Team 1200 were all about how the Senators reminded the Canadiens who the big boys really are. I suspect I may be sending an email to the Morons tomorrow.
Take heart, Leafs' fans; alas this is all you have left: The Senators are not a good hockey team right now. Rush over to TSN to tell the world how bad we are. Go on…git, now; TSN is thirsting for your brilliance.
I really try hard to not get too high with a win or too low with a loss, but I just wonder when the Senators are going to start to show some urgency (if ever). This is not a team I have much faith in at this point.
I'd like to say something nice about the teasing comeback the Senators made in the third period, but nahhhh…..it had as much to do with the Habs coasting as any extra effort on the part of the Sens. And the worst part of it is, the Ottawa media and perhaps the Senators' players will "take some positives" from it. NOOOOO!!!!!!…..they need to be punished for this crapass performance. Here's a radical idea; how about a bag skate on game day? We take our lumps against the Buffaloes tomorrow and then see if the boys are made of anything other than wet sand the rest of the way. Or maybe I'm just extraordinarily cranky today. What started as an evening full of energy has ended with me feeling like a slug. Perhaps I'll chuck myself into a salt pot.
Tags: cats, dogs, drain my blood slowly from my body, pet food


text:
I think most of us can agree we love a nice tan but not the burn that usually comes with it. I am digging R+F's sunless tanner. It was easy to apply without any mess! I love how light the product is and how even my color is. My before and after results are after one application. Available Here! ☀
Summer Time: Rodan + Fields Sunless Tanner ☀


text:
Who We Are and Our Mission
In March, 2008, the leaders of over forty academic survey research organizations agreed to join together to form a new association of organizations, the Association of Academic Survey Research Organizations [AASRO]. Their vision was that AASRO would grow to be recognized as a leading voice in support and promotion of excellence in survey research conducted in academic settings. In May, 2008 AASRO became a formal organization with the mission of facilitating mutual support among member organizations in the following ways:
- Promote excellence and integrity in the conduct of survey research;
- Help academic survey centers advance the research, educational and service goals of their respective colleges and universities by providing both formal and informal education and training for effective organization and administration of academic survey research organizations;
- Ensure the ability of academic survey centers to educate the next generation of survey researchers by advancing the educational and research role of survey research organizations across diverse university structures;
- Advance society and the social and behavioral sciences by promoting the values of academic survey research: methodological innovation, scientifically-grounded data collection practices and public dissemination of important survey research results.
2019 AASRO Annual Meeting – Save the Date!
AASRO Annual meeting – February 28-March 2, 2019 University of Nebraska-Lincoln Lincoln, NE AASRO will be returning to the mid-west for the 2019 annual meeting. The meeting will be hosted by the Bureau of Sociological Research at the University of [...]
Summary of the 2018 annual meeting
A summary of the annual meeting is now available for members to review. Visits the "Reports" section of the members' area to access the summary.
Dr. Timothy P. Johnson Named 2018 John M. Kennedy Achievement Recipient
Dr. Timothy Johnson of the University of Illinois at Chicago (UIC) is being recognized for his outstanding work promoting high quality, objective research aimed at understanding and improving the world around us, and his tireless contributions to survey methods quality [...]
Andrew Hopkins and Casey Seay Named Winners of 2018 John Tarnai Memorial Scholarship
Andrew Hopkins of the University of North Florida Public Opinion Laboratory and Casey Seay of the University of Nebraska-Lincoln Bureau of Sociological Research have been awarded the 2018 John Tarnai Memorial Scholarship by the Association of Academic Survey Research Organizations [...]