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A Survey Of The Religious Landscape In America 2017
The landscape of the Christian religion in America in 2017 -- the good, the bad and the ugly....Keep Reading
Join us for the Divine Service on Sundays at 10:30 am
The landscape of the Christian religion in America in 2017 -- the good, the bad and the ugly....Keep Reading
What about the Blessed Virgin Mary? Why ask? For two reasons. Firstly, because there is a breed of activist Roman Catholic (RC) that delights in imposing its Marian faith on others; and scorning all who don't agree with a triumphalism that is unbecoming. Secondly,because Lutherans need to re-think the importance of the Blessed Virgin. Indeed, all generations must call h...Keep Reading
On Trinity Sunday many Lutheran churches confess their faith in the language of the Athanasian Creed as it is found on page 53 of TLH. The Athanasian Creed was named after St. Athanasius one of the church's most important teachers; and defenders of the Trinitarian faith. The Athanasian Creed is an official confession of the Lutheran Church. This Creed was established over...Keep Reading
Fellow Worshipers of the Father in Spirit and Truth, (John 4:24) May the Spirit of Truth, poured out on Pentecost, be your Counselor, Helper and Comforter in the face of all sin and sorrow. By his coming he has renewed the face of the earth, beginning in his chosen and promised Land, the church. Herein is found the remission of sins, life and eternal salvation. Beginning...Keep Reading


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With the chances of an immediate milk price recovery appearing slim, dairy farmers are looking for ways to ride out the storm.
Experts from Andersons, Germinal and Ecosyl, speaking at a press briefing last week, said one of the best options to consider was 'making the most of grass silage'.
Richard King, a partner in the Andersons Centre, said the current climate for dairy farmers was obviously 'tough'.
"But it is worth remembering not that long ago many dairy businesses were making good money from milk and they will do again. Things will turn around," he said.
However, he conceded it was difficult to know when this up-turn would happen and as a result dairy farmers should be looking at their management options.
Using Andersons' 'Friesian Farm' model to compare systems, Mr King said focusing on quality silage would allow significant cost reductions while maintaining relatively high yields, due to greater milk production from forage.
Figures from this theoretical farm suggested a forage-based system could lead to a 0.5ppl return for the 2015/16 year. This compared to 2.6ppl for a concentrate-based system and 0.2ppl for a grass-based system.
"Grazed grass systems have the potential for the best returns, but these systems are not going to suit everyone in terms of milk contracts, farm size and layout, soil type and climate," he said.
He also said it was often difficult to 'claw back' the extra cost associated with a higher output herd when operating under a concentrate-based system.
"The forage-based system is a mid-way point; it brings in some benefits of grazed grass but without the need to change the fundamentals of the systems in terms of breed of cows and farm layout, but it also retains a relatively high-output system."
Ben Wixey, of Germinal Seeds, said with silage-making just around the corner, dairy producers should think about a number of improvements they can make to this year's crop, without the need for major investment.
"Simply cutting at the optimum stage of growth can mean the difference of several D-value points, raising the ME of the silage and boosting milk production potential," said Mr Wixey.
"All a grass-seed plant wants to do is go to ear, so it is about cutting at the right time to get that balance between yield and quality."
He said when deciding if a field was ready for cutting, it was useful to look at the heading dates published in the grass recommended lists and also get a rough gauge of how many seed heads are coming through.
"If you were to pick 100 tillers from a grass crop and about 10 per cent of these had a seed head coming out then it is at the right stage to cut," he added.
"As a general rule try to cut silage in the afternoon as this is when the grass contains the most sugars."
When leys were made up of a mixture of grass varieties with different heading dates, he said it was important to choose varieties with a tight range of heading dates, to improve silage quality overall.
He added it was important to make sure the right material was in the grass leys in the first place.
"Reseeding rates on British farms is 2-3 per cent, which means many grass leys are down for a ridiculously long time. That figure should be nearer 15 per cent for dairy farms, to ensure grass is rejuvenated every five to six years.
"When making the investment in reseeding be sure to maximise the value by selecting the best available varieties from the independent recommended list."
Phil Jones, of Ecosyl, said: "The silage itself is never going to be better than what you put in."
But, he also added it was important to understand the biology of what was happening in the clamp.
"In a good fermentation there is a rapid domination by good bacteria to lower the pH, whereas in poorer silage, good and bad bacteria naturally present on grass compete, so fermentation is left to chance.
"Good bacteria convert the sugar in grass to lactic acid which produce the fastest pH fall and with no loss of dry matter, whereas in other types of fermentation other less effective products are also produced as well as carbon dioxide, which is effectively lost dry matter.
"In trials, adding a specially-selected strain of lactic acid bacteria with a silage additive not only produced a much quicker drop in pH in the important period of the first 24 hours after ensiling, but also improved the digestibility and gave an extra 1.2 litres of milk per day per cow."
|Yield from forage (litres)
|Milk sales
|Total output
|Variable costs
|Rent, finance and drawings
|Total costs of production
|Margin from production
|Business surplus
|Farm profit
|- £18,330

subset: commoncrawl


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Lyotard's Différend / Death of the Subject
With whose tongue do I speak? This is the tongue that hails the world into being—constructs street from air, right from wrong, being from non-being. Foucault saw power in language—an organisation of knowledge confined by the current paradigm of possibility (Foucault, 2002). Every episteme reorders the world, reconstructs knowable from unknowable. Again, I ask, with whose tongue do I speak?
Marxist accounts of language place its development on our practical activity (Harman, 2007, p. 116). The need to communicate amongst ourselves leads to the development of language, and subsequently, concepts unique to those experiences. As labour diversifies, so too does language. Ethnicity, gender, sexual-orientation, ability, a breadth of contingent identities develop further discourses. Language unfurls beyond its material roots as words, images and gestures take up new meanings through both cultural practices and media texts (S. Hall, 1997). This endless process of différance perpetually resignifies our understanding of the world.
In The Differend, Lyotard explores the breakdown of language. Moments when communication falters, and one is thrown into the state of victim, incapable of articulating oneself. The différend arises when two (or more) parties cannot be reconciled—their arguments so different, that the very words and concepts they negotiate in cannot be comprehended through a single overarching discourse (Lyotard, 1988, xi-xvi; Mishra, 1995, p. 88). To attempt such a thing does epistemic violence—erases the possibility of articulation for one, or both parties involved (Lyotard, 1988, p. 7; Pollack, 2012, p. 5; Spivak, 1994, pp. 76, 81-82, 91).
A victim does not merely lose their voice. Their knowledge becomes unknowable. Discursive imposition severs legitimation at four possible sites: i) the site of the referent; i.e. noumenal reality, ii) the site of the signifier, where symbolic construction occurs, iii) the site of the speaker, who must phase the signifier, and vi) the site of the listener, who must comprehend the phrase (Lyotard, 1988, p. 28). If at any site epistemic violence is done, the victim can voice no damage. This is the state of being wronged (Lyotard, 1988, p. 9).
In losing one's voice, one loses the ability to hail the world. One loses their subject position. What the victim once believed was of their own making is revealed to be nothing but a discursive node, hailed into being through the Other (Lyotard, 1988, p. 23). The différend robs the victim of what was never truly theirs, but what is necessary to be. It commits violence for the sake of settlement—so that a judgement can be made between parties, even if that judgement, circumscribed by its own discursive bounds, cannot be fair (Lyotard, 1988, xi-xvi). The victim, then, shares a similar fate to the victima—the sacrificial animal that is robbed of its life for the sake of a higher power (Van Dijk, 2009, pp. 1-2).
The Colonial Différend / Discipline and Metanarratives
Universal judgement presupposes that a single narrative can twine together all beings who seek justice. That this narrative will not tear, hitch or break when these beings subsequently reject it. In defining the différend, Lyotard critiques the failure of the metanarrative. It is revealed as modernist naivety—or, perhaps more bluntly, colonial ideology. Utopia can be had, but only through the assimilation of all subject positions into one.
No subject position is free from ideology, and no ideology is free from power (Nicholls, 2014). An ideology is inescapably normative for its formation involves the interpretation of the world, and this construction legitimates certain knowledges over others (Diprose, 1989, pp. 28-30). Where discourse provides language (what can be spoken), ideology provides judgement (how it is to be spoken). The metanarrative's rational is the unification of humankind—its reality is the erasure of plurality, and the victimisation of all who reject the global hegemony. It is under the metanarrative that the différend becomes most pervasive.
Western imperialism involved the dual subjugation of bodies and souls. Societies and their people were objectified, dehumanised and destroyed through slavery, genocide, torture, theft, biological racism and cultural erasure. For the imperialist, equality was the burden of lifting all non-Europeans to the state of European (see Kipling, The White Man's Burden). Liberalism and empiricism were reified through racist discourses that made all narratives outside of such frameworks unknowable and undesirable. The white bourgeois man became the metanarrative heart of the world.
The empiricist dream of objectivity demands the abandonment of flesh—the renunciation of subject position so one may gaze from the transcendent void and see the world-in-itself (Haraway, 1991, pp. 188-196). This position cannot exist, for one is irrevocably embedded in language. One creates the knowledge they claim to only see. Bias is nothing more than a glimpsing of the subject position—its removal the reordering of discourse, to make what was clear, invisible once more. The empiricist who professes to have escaped bias, is simply all the more blind to it (Althusser, 1970).
Liberalism, with its normative bent to define human nature, does nothing but prescribe it. By claiming the individual self-determining, it ignores the effects of institutional structures and one's own manifold identities (Baker, 2010; Crenshaw, 1991). By claiming the individual rational, it denies alternative modes of thought and expression. Liberalism makes abstract and isolated that which is our only source of connection to the world—our subjectivity.
The metanarrative is insidious for it wends its way into all aspects of existence until it seems natural, normal and necessary (Nicholls, 2014). Epistemic violence operates not simply through forceful obliteration, but psychological terror and coercion (R.E. Hall, 2010). Though the colonised would initially oppose colonial ideology, resistance always carried the risk of ridicule, exclusion or death. To defy the European norm was to prove one was not equal to Europeans, and therefore, not human. To accept it was to be abandon one's culture, but be elevated in status. In the hopes of a better life the colonised would assimilate and let their culture die.
Here we see a variant of the différend that Lyotard does not touch on. The différend that arises through the conscious choice of silence. Why? Because to voice the damage dealt would incur a pain too great to bear, so the victim chooses a lesser pain—a self-inflicted pain—the quiet death of what was.
The Spectacular Différend / Simulacra and Representation
In time, the empires broke, leaving a damaged world in their wake. Some sought to undo the wrongs that had been committed, but their reliance of metanarratives left victims further from articulation.
The discourse of human rights attempted to reify itself as the ethical paradigm of the world, and the benevolent westerner, the saviour of the oppressed. Its self-evident and inalienable rights, were, ironically, in need of being taught to the supposedly less enlightened. Colonialism could continue, as usual, but through economic, political, and cultural means rather than overt military force (which was renamed global peacekeeping).
Early postcolonial scholars attempted to create a counterhegemonic discourse by reinterpreting history from the standpoint of the subaltern (i.e. victim). Despite their radical intentions, these efforts fell in line with other western metanarratives (Spivak, 1994, p. 93). The assumption of cultural solidarity among subalterns simplified the diversities that existed within populations. Additionally, by standing in for the subaltern, these scholars did not erase subalternity—they reproduced it (Spivak, 1994, p. 102).
Both discourses hail an absent victim—one who is reduced to abstraction, cultural unit, moral dilemma. The différend also disappears, for the representative, in being able to define the damage committed, escapes it. How then, can they be said to understand the victim?
It is the same story: the representative masquerades as the bearer of truth, transparent voice of the Other, but the process of representation necessarily entails the reconstruction of knowledge, the assimilation of the Other (Spivak, 1994, pp. 87-89). Epistemic violence cannot be avoided. This is the problem all metanarratives share. Their claims of totality negate any alternative discourses that may arise. In speaking for the victim, the representative robs them of a presence already invisible. In the victim's place a simulacrum is hailed into being—a signification devoid of referent (Baudrillard, 1994). The original that never was slips from existence.
I fear I am failing to communicate the significance of this—falling into a différend of my own. What has happened is the compounding of the différend. The first struck the victim before representation. Their knowledge was rendered unspeakable, inaudible or incomprehensible through the erasure or lack of a legitimate discourse (Lyotard, 1988, xi-xvi). The second struck after representation. The benevolent representative, in standing for the victim, completely replaced them (Spivak, 1994, p. 102). The victim was subordinated beneath an artifice—a false image, incapable of relaying the specificities of their experience.
Lyotard's différend victimises through the external enforcement of an inappropriate discourse. The colonial différend victimises through the self-imposition of a new discourse (out of shame or mortal necessity). This third différend, which I name the spectacular différend (see Debord, The Society of the Spectacle), combines elements of both. It victimises through the external enforcement of a discourse, that in naming itself representative, appears to be self-determined by the victim. The victim, in being presented as empowered, is doubly subordinated.
The Eternal Différend / A Discourse of One's Own
We must wrest the victim back from the void of abstraction. Rediscover the subject position they had never left, but simply vanished from. There is a knowledge eager to be constructed into reality that has the potential to alter more than victim, perpetrator or judge. What is at stake here is the entire symbolic order. What is necessary for the victim to speak and be heard is the complete overthrow of the metanarrative episteme.
The existence of the différend testifies to the metanarrative's symbolic frailty. It is the revelation of a nebulous imaginary struggling to materialised into symbolic form. The victim reaches out but is contained by the limits of present discourse, incapable of both communicating from and communicating with. The first step requires the victim's articulation, the second, the listener's comprehension. The metanarrative silences victims through disengagement at either step. Both human rights and early postcolonial scholars fell into this trap. Neither, however, did so intentionally, for, as Spivak puts it eloquently, "Who the hell wants to […] protect subalternity?" (de Kock, 1992, p. 46).
One does not speak for the victim, nor to the victim—one speaks with the victim (de Kock, 1992, p. 46). One hails them into discursive existence and through the dialectics of speech, makes lucid the unspeakable. No, it is not easy. We have been thrown into a senseless world, severed from the Other by the bounds of subjectivity, and left to the desolation of our own loneliness (Camus, 1955). This is the human condition none can escape. The world flows without beginning or end. We can never throw existence out of us, nor enter the subjectivity of the Other (Sartre, 2010). All knowledge is situated, and all understanding arises through interpretation (Haraway, 1991, pp. 197-201; Diprose, 1989, pp. 28-30). Perhaps, however, one may find solidarity in the shared incomprehensibility of the Other (Four Leaf Studios, 2012).
I must clarify a few things. I do not seek to reify the différend into a new metanarrative. A solidarity of incomprehensibility is not a state but a process, through which recognition of the incomprehensible expands the discursive field. If anything, what I propose is an anti-metanarrative. The metanarrative attempted to unite all under a single discourse. The anti-metanarrative seeks the opposite—to revel in the unique experiences of each. Knowledge is thrown from its objective throne and celebrated as it passes from one subjectivity to another, birthing new, monstrous amalgamations. Resemblance need not be kept for the original was never accessible to begin with. The différend is resignified as a site of discursive potential, where the incomprehensibility of the Other can be comprehended anew.
Through language, we are constructed into social beings. The différend turns one into victim through the denial of sense, credibility or sanity. I have explored two variants of the différend, tracing both origins and consequences. Though well-intentioned, both colonial and postcolonial metanarratives displaced the victim's own discourse. The solution then, is a dialogue with the victim—a splitting of the metanarrative through the explosive unfurling of manifold knowledges. There is no end to this process, for the différend is only deferred, never destroyed. However, so too is knowledge.
Althusser, L. (1970). Ideology and Ideological State Apparatuses. In: Lenin and Philosophy and Other Essays. Translated by B. Brewster. Online Publication. [22-09-2016]: https://www.marxists.org/reference/archive/althusser/1970/ideology.htm
Baker, J. (2010). Claiming Volition and Evading Victimhood: Post-feminist Obligations for Young Women. Feminism and Psychology, 20, pp. 186-204.
Baudrillard, J. (1994). Simulacra and Simulation. Translated by S. Glaser. Ann Arbor: University of Michigan Press.
Camus, A. (1955). The Myth of Sisyphus. Translated by J. O'Brien. London: Hamish Hamilton.
Crenshaw, K. (1991). Mapping the Margins – Intersectionality, Identity Politics, and Violence Against Women of Color. Stanford Law Review, 43, pp. 1241-1299.
Diprose, R. (1989). Nietzsche, Ethics and Sexual Difference. Radical Philosophy, 52, pp. 27-33.
van Djik, J. (2009). Free the Victim. A Critique of the Western Conception of Victimhood. International Review of Victimology, 16, pp. 1-33.
Four Leaf Studios. (2012). Rin's Path. In: Katawa Shoujo. Visual Novel, PC. Online Publication.
Foucault, M. (2002). The Order of Things: An Archaeology of the Human Sciences. London, New York: Routledge.
Hall, R.E. (2010). Colonization as the Origin of Western Discrimination. In: An Historical Analysis of Skin Color Discrimination in America: Victimism Among Victim Group Populations. Online Publication: Springer, pp. 11-22.
Hall, S. (1997). Representation, Meaning and Language. In: Representation: Cultural Representations and Signifying Practices. London: SAGE/Open University, pp. 15-29.
Haraway, D. J. (1991). Situated Knowledges: The Science Question in Feminism and the Privilege of Partial Perspective. In: Simians, Cyborgs, and Women: The Reinvention of Nature. London: Free Association Books, pp. 183‐201.
Harman, C. (2007). Gramsci, the Prison Notebooks and Philosophy. International Socialism, 2(114), pp. 105-119.
de Kock, L. (1992). New Nation Writers Conference in South Africa. Ariel: A Review of International English Literature, 23(3), pp. 29-47.
Lyotard, J.F. (1988). Preface & The Differend. In: The Differend: Phrases in Dispute. Translated by G.V.D. Abbeele. Manchester: Manchester University Press, pp. xi-xvi, 1-31.
Mishra, V. (1995). Postcolonial Differend: Diasporic Narratives of Salman Rushdie. In: H. Bloom, ed., Salman Rushdie. Philadelphia: Chelsea House Publishers, pp. 63-91.
Nicholls, B. (2014). Ideology. In: Media Texthack Group, eds., Media Studies 101 – A Creative Commons Textbook. Online Publication. [2014]: https://mediatexthack.wordpress.com/
Pollack, S. (2012). An Imprisoning Gaze. Practices of Gendered, Racialized and Epistemic Violence. International Review of Victimology, 19, pp. 1-12.
Sartre, J.P. (2010). Nausea. Translated by R. Baldick. London: Penguin Classics.
Spivak, G.C. (1994). Can the Subaltern Speak? In: P. Williams & L. Chrisman, eds., Colonial Discourse and Post-Colonial Theory: A Reader. New York: Harvester/Wheatsheaf, pp. 66-111.


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Wednesday, 11 December, 2019
Grounded Theory
The Grounded Theory Institute (Popularity: )
Dedicated to the methodology of Dr.Barney G. Glaser, Ph.D. Includes list of publications, seminars, forum, and list of officers. Includes basic webpage translator.
The Memo Pages of Grounded Theory Methodology (Popularity: )
A general method of comparative analysis to discover theory.
© 2015 Directory of Science. All Rights Reserved


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RED With Bellows Lenses
Published : 18th September 2009
Has anyone used swing and tilt bellows lenses on the RED? I want to especially make sure that they won't hit the OLPF if pushed into the lens mount all the way.
Graham Futerfas
Director of Photography
Los Angeles, CA
Graham Futerfas wrote :
>>Has anyone used swing and tilt bellows lenses on the RED? I want to especially make sure that they >>won't hit the OLPF if pushed into the lens mount all the way.
Worked like a charm, I did a test a couple of weeks ago with an Arri T/S set on one of Pace's Reds (#34) without incident. I was not working at infinity but it appeared that there was more than enough clearance for even the short focal lengths.
Gary Adcock
HD & Film Consultation
Chicago, USA
Our Arri Shift & Tilt system has been successfully used on RED cameras numerous times to great effect with no issues. ?Don't know about the Clairmont system but I doubt there would be a problem.
If these systems work fine and can never hit a spinning mirror, then they'll certainly never hit an OLPF.
Mitch Gross
Applications Specialist
Abel Cine Tech
If you are talking about the Century Precision Optics Swing Shift Bellows, it mounts with a PL mount that conforms to the 45 degree Arri safety zone (to not damage the reflex mirror). The OPLF filter is much further inside the camera mount. The PL flange to cone is 15.65mm and the flange to OPLF in the RED ONE is approximately 40 mm-big difference.
You are safe.
Peter Repich
2320 Shasta Way, Unit A
Simi Valley, CA, 93065
Office 805 577 8227
Cell 805 297 5974
Fax 805 577 7859
CML has just published the "Little RED Book"
This book is an edited collection of conversation's during 2009 about ways to use the RED one and how to get around any problems you may encounter.
Impress others with your knowledge!
Be the envy of your friends!
Buy it today!
Available as an A5 book or a PDF if you just can't wait!


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The role of prostaglandin E2 (PGE2) in the modulation of cell growth is well established in colorectal cancer. The aim of this study was to elucidate the significance of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) down-regulation on the prognosis of hepatocellular carcinoma (HCC) patients.
The expression of 15-PGDH in HCC cell lines and resected HCC tissues was investigated, and the correlation between 15-PGDH expression and HCC cell-line proliferation and patient survival was explored.
The interleukin-1-β-induced suppression of 15-PGDH did not change the proliferation of PLC and Huh-7 cells in the MTS [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. The induction of 15-PGDH by transfection in HepG2 cells without baseline 15-PGDH expression was suppressed at day 2 of proliferation compared with empty-vector transfection, but there was no difference at day 3. Among the 153 patients who received curative HCC resection between 2003 and 2004 at our institution, 15-PGDH expression was observed in resected HCC tissues in 56 (36.6%), but the 5-year survival rate did not differ from that of the remaining 97 non-15-PGDH-expressing patients (57.1% vs 59.8%; P=0.93). Among 50 patients who exhibited baseline 15-PGDH expression in adjacent nontumor liver tissues, 28 (56%) exhibited a reduction in 15-PGDH expression score in HCC tissues, and there was a trend toward fewer long-term survivors compared with the remaining 22 with the same or increment in their 15-PGDH expression score in HCC tissues.
Hepatocellular carcinoma (HCC) is one of the leading causes of malignant cancer death and has an increasing incidence in worldwide.1 The prognosis of HCC is generally poor due to lack of promising molecular therapeutic targets. Recent positive randomized controlled trial of the multi-kinase inhibitor sorafenib proved beneficial therapeutic effect of molecular therapy in patients with advanced hepatocellular carcinoma2 and this result proposes necessity of studies in other molecular pathway of HCC development.
HCC is usually developed in the presence of continuous inflammation and hepatocyte regeneration during chronic hepatitis and cirrhosis. Prostaglandins, most notably prostaglandin E2 (PGE2) are products of the arachidonic acid pathway and key mediators of inflammation. Cyclooxygenase-2 (COX-2), a rate limiting enzyme in the pathway of PG synthesis has been suggested to be associated with carcinogenesis especially in colorectal cancer.3 Different authors have been reported that the increased PG production would contribute to carcinogenesis in many other cancers, including HCC.4 The expression pattern of COX-2 protein in HCC was found to be correlated with the differentiation grade which implies an important role of abnormal COX-2 expression in carcinogenesis of HCC.5 Furthermore, the COX-2 expression in well-differentiated HCC is significantly higher than that in liver cirrhosis, chronic viral hepatits and normal liver tissue.6
COX-2 is induced by a variety of stimuli such as growth factors, proinflmmatory stimuli, hormones and other cellular stresses7 and is involved in the regulation of cell growth,8 angiogenesis,9 and blastocyst implantation.10 Nonsteroidal anti-inflammatory drugs (NSAIDs) targets COX-2 which is the key step of conversion of arachidonic acid to prostaglandin then inhibits the growth of cell lines through preventing cell proliferation and potentiating apoptosis.11,12
PGE2 synthase (PGES) is the second key enzyme of synthesis of PGE2 interacting with COX-2. Three types of PGES are found: one cytosolic (cPGES) and two membrane-associated PGES, mPGES (micorosomal PGES)-1 and -2. Of three types of PGES, mPGES-1 is often found in the epithelial cells and catalyzes the synthesis of PGE2 upregulated during inflammatory condition.13 To maintain steady-state level of PGE2, synthetic pathway involving PGES and catabolic pathway including 15-hydroxyprostaglandin dehydrogenase (PGDH) needs to be balanced. PGE2 is responsible for cell proliferation, migration, angiogenesis and tumor metastasis and 15-PGDH reduces these functions as metabolizing PGE2 by oxidizing the 15(S)-hydroxyl group into a keto group producing 15-keto PGE2.14,15 With this role of 15-PGDH, many researchers reported that downregulation of 15-PGDH is related to carcinogenesis of various cancers.16,17,18,19 In recent study with human hepatoma cells, 15-PGDH is shown to be downregulated with a high COX-2 and mPGES-1 expression and suggested a relevant tumor suppressing role in HCC of 15-PGDH.20
Thus, the aim of this study was to evaluate the potential role of 15-PGDH in growth of hepatoma cell lines which expressed 15-PGDH initially or transfected with 15-PGDH vector. We compared the growth rate with naïve cells for estimating the anti-cancer effect of 15-PGDH. Furthermore we identified the level of 15-PGDH expression in human HCC tissue along with nontumor tissue and evaluated the role of 15-PGDH as a predictive factor for prognosis of HCC patients.
HCC cell lines and immunoblotting
Three human HCC cell lines (PLC, HepG2, Huh-7) were purchased from the Korean Cell Line Bank (Seoul, Korea) and they were cultured in 90% Dulbecco's Modified Eagle's Medium (DMEM) supplemented with 10% fetal bovine serum, 100 units/mL penicillin and 100 mg/L streptomycin (GIBCO) in a humidified atmosphere containing 5% CO2 at 37℃.
For immunoblotting, cells were lysed in radioimmune precipitation (RIPA) buffer (Upstate, NY, USA) supplemented with protease inhibitor. The cell lysates were electrophoresed on 10% polyacrylamide gel, transferred onto polyvinylidene difluoride membrane (Bio-Rad Laboratories, CA, USA) and blotted with appropriate primary and secondary antibodies. The signal was detected using ECL reagent kit (Biosciences, Buckinghamshire, UK) and exposed to an X-ray film. The primary antibodies used were rabbit anti-PGDH (1:5,000 dilution; Novus Biologicals, CO, USA), goat anti-COX-2 (1:500 dilution; Santa Cruz, CA, USA), and mouse anti-β-actin (1:10,000 dilution; Sigma, St. Louis, MO, USA). Goat anti-rabbit IgG antibody conjugated with horseradish peroxidase was used as the secondary antibody (Santa Cruz, CA, USA).
15-PGDH transfection
15-PGDH expression vectors were the kind gift of Prof. Seung-Jae Myung. Wild-type (WT) 15-PGDH cDNA was amplified from normal colon cDNA using the PCR primers 5'-CAGCAGTGGCTGCACCATG-3' and 5'-ATTTGTGCTTATTTTCAGCTATGGC-3', and cloned into a pcDNA3.1 expression vector (Invitrogen, Carlsbad, CA, USA) to yield pcDNA3.1-WT-15-PGDH.
HepG2 cells were transfected with pcDNA3.1-empty vector (control), or an expression vector encoding WT 15-PGDH (pcDNA3.1-WT-PGDH), for 24 hr, using Lipofectamine 2,000 (Invitrogen) according to the manufacturer's protocol. The medium was next changed to medium without fetal bovine serum, and growth continued for 12 hr. The cells were next collected for cell proliferation assay and immunoblotting for 15-PGDH in subsequent days.
Cell proliferation assay
To explore the influence of 15-PGDH on cell proliferation, proliferation assay was performed in PLC and Huh-7 cells with/without interleukin-1 beta (IL-1β) treatment and in HepG2 cells with 15-PGDH transfection. Cell proliferation was measured using the CellTiter 96 Aqueous One Solution cell proliferation assay (Promega, Madison, WI), on the basis of the cellular conversion of the colorimetric reagent MTS [3,4-(5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt] into soluble formazan by dehydrogenase enzymes found only in metabolically active, proliferating cells. Following each treatment, 20 µL of dye solution was added into each well in 96-well plate and incubated for 3 hours. Subsequently, absorbance at 490 nm was measured with an ELISA reader (Magellan, TECAN, Austria).
Tissue microarray (TMA) construction of human HCC tissues
From January 2003 to December 2004, a total of 267 patients underwent curative hepatic resection because of HCC at Asan Medical Center (Seoul, Korea) and we established tissue microarray (TMA) slides using formalin-fixed paraffin-embedded tissues from these 267 surgically resected HCC and neighboring non-neoplastic liver tissue samples. Duplicates of two cores from the tumor tissue and one core from the non-neoplastic liver tissue, measuring 1.5 mm in diameter, were arrayed from the corresponding paraffin blocks into a recipient block using an arraying machine (TMArrayer; Pathology Devices, Westminster, MD, USA). Among these patients, we excluded 99 patients who underwent other treatment for HCC before hepatic resection, 12 who were diagnosed with double primary cancer and 3 with incomplete data, leaving 153 patients in the final clinical correlation analysis. We reviewed the clinical data for the remaining 153 patients, and analyzed the association between clinical parameters and 15-PGDH expressions. The study protocol (protocol #: 2011-0387) was reviewed and approved by the institutional review board of Asan Medical Center and the need for informed consent from the patients was waived by the institutional review board.
Immunohistochemistry in TMA of human tissues
Immunohistochemistry (IHC) to detect 15-PGDH expression in HCC and neighboring nontumor tissues was performed in TMA using a monoclonal anti-PGDH antibody. IHC results were evaluated by a single pathologist (Dr. Hyo Jeong Kang). We graded expression score from 0 to 3 points for 15-PGDH expression in HCC and neighboring nontumor tissues according to the distribution range (grade 0: negative, 1: <33%, 2: 34-66%, 3: >66%).
We classified all the 153 HCC patients into 2 groups according to 15-PGDH expression in HCC tissues. HCC PGDH (-) group includes patients without any 15-PGDH expression of HCC and HCC PGDH (+) group includes patients with grade 1-3 expression. In addition, especially in patients who showed 15-PGDH expression grade 1-3 in nontumorous tissues, we also sub-grouped the patients according to the suppression of PGDH in HCC tissues or not. We compared clinical parameters and overall survivals of patients according to the 15-PGDH expression in HCC tissues to elucidate the prognostic significance of 15-PGDH expression in HCC.
Statistical analysis
Descriptive statistics were expressed as median (range) or number (%). Continuous variables were compared using Student's t test and categorical variables using chi-square or Fisher's exact test. Survival curves were estimated according to the Kaplan-Meier method and statistically compared with the log-rank test. Patients lost to follow-up were censored at the date of the last observation. To establish the factors affecting patient survival, uni and multivariate analysis was performed using the Cox regression model. P values <0.05 were taken to indicate statistically significant differences. Statistical analysis was performed using SAS version 9.1 (SAS Institute, Cary, NC, USA).
15-PGDH expression and its association with proliferation of HCC cell lines
To investigate whether 15-PGDH was expressed in HCC cell lines, we performed immunoblotting of 15-PGDH in the cell lysates of PLC, HepG2 and Huh-7 cells. Both PLC and Huh-7 cells showed 15-PGDH expression, but HepG2 did not (Fig. 1A).
In both PLC and Huh-7 cells, we performed proliferation assay with or without suppression of 15-PGDH by IL-1β treatment. We confirmed treatment of IL-1β 10 ng/mL 24 hours suppressed 15-PGDH expression in Huh-7 cells, but this suppression was not observed in PLC cells (Fig. 1B). In MTS assay, addition of IL-1β 10 ng/mL in culture media did not change proliferation rate of Huh-7 cells compared with control media (Fig. 2B).
In HepG2 cells, which did not show baseline expression of 15-PGDH, we induced 15-PGDH expression by transfection with vector encoding WT 15-PGDH. Transfection was confirmed by GFP staining (Fig. 3A) and immunoblotting for 15-PGDH (Fig. 3B). 15-PGDH expression was strongest at day 0 of transfection and then diminished slowly as time goes by (Fig. 3B). Proliferation assay showed 15-PGDH expression induction in HepG2 cells suppressed cell growth at day 2, but this growth difference disappeared at day 3 of MTS assay (Fig. 4).
15-PGDH expression in HCC and neighboring nontumor tissues in patients who underwent curative resection
IHC for 15-PGDH was performed in TMA of 153 HCC patients who received curative resection in the period of 2003 to 2004 in our institution. Among total of 153 patients, Table 1 shows frequency of 15-PGDH expression score 0-3 in HCC and neighboring nontumor tissues respectively. According to 15-PGDH expression in HCC tissues, 56 (36.6%) patient showed 15-PGDH expression and was classified as HCC PGDH (+) group, and remaining 97 (63.4%) was HCC PGDH (-) group (Table 1). In neighboring nontumor tissues, 50 (32.7%) patient showed 15-PGDH expression and 96 (62.7%) did not show baseline 15-PGDH expression. Among 50 patients who showed baseline 15-PGDH expression in nontumor adjacent liver tissues, 28 (56%) showed decrease of 15-PGDH expression score in HCC tissues (NT (+) HCC (-) group) and the remaining 22 (44%) showed 15-PGDH expression score in HCC tissues not less than nontumor tissues (NT (+)HCC (+) group) (Table 2).
Clinical parameters and overall survivals of patients who was classified according to the 15-PGDH expression in HCC tissues
We reviewed the clinical data for the patients, and analyzed the association of clinical parameters and overall survival with 15-PGDH expression in HCC tissues. According to 15-PGDH expression in HCC tissues, 56 (36.6%) patient were classified as HCC PGDH (+) group, and remaining 97 (63.4%) as HCC PGDH (-) group. Baseline characteristics such as age, sex, liver disease etiology, Child-Pugh class and HCC stage and morphology were not different between HCC PGDH (+) and HCC PGDH (-) group. Number of the patients with serum alpha-fetoprotein (AFP) >400 ng/mL was significantly more in HCC PGDH (+) group than HCC PGDH (-) group (Table 3). The overall survival of 153 patients was not different according to the 15-PGDH expression in HCC tissues and 5-year survival rate (5-YSR) was 57.1% in HCC PGDH (+) group and 59.8% in HCC PGDH (-) group (P=0.93) (Fig. 5). To investigate whether 15-PGDH expression in HCC or adjacent tissues affects overall survival of HCC patients, we performed univariate and multivariate analysis with several clinicopathological factors. In multivariate analysis, age, sex, Child-Pugh class and AJCC tumor stage were significant prognostic factors, but expression of 15-PGDH in HCC tissues did not significantly affect patients overall survival (Table 4).
HCC patients with 15-PGDH downregulation in HCC tissues showed the trend of smaller number of long term survivor
Among 50 patients who showed baseline 15-PGDH expression in nontumor adjacent liver tissues, 22 (44%) showed same or increment of 15-PGDH expression score in HCC tissues (NT (+) HCC (+) group) and the remaining 28 (56%) showed decrease of 15-PGDH expression score in HCC tissues compared with nontumor tissues (NT (+) HCC (-) group) (Table 2). All the baseline characteristics such as age, sex, liver disease etiology, Child-Pugh class serum AFP level and HCC stage and morphology were not different between NT(+) HCC (+) and NT (+) HCC (-) group (Table 5). The overall survival of 50 patients was not different according to the change of 15-PGDH expression score in HCC tissues, and 5-YSR was 54.5% in NT (+) HCC (+) group and 46.4% in NT (+) HCC (-) group (P=0.47) (Fig. 6). However, 8-YSR was 50.0 vs. 26.8% in NT (+) HCC (+) and NT (+) HCC (-) group respectively, so the patients with decrease of 15-PGDH expression in HCC tissues showed the trend of smaller number of long term survivor compared with the patients maintaining 15-PGDH expression (Fig. 6). In univariate and multivariate analysis of 50 patients, age, AJCC tumor stage and major vascular invasion were significant prognostic factors, and change of 15-PGDH in HCC tissues was not significant prognostic factor in HCC patients who showed baseline 15-PGDH expression (Table 6).
We aimed to investigate the role of 15-PGDH downregulation in HCC cell lines and patients tissues in our study. During our study, other investigators recently published in vitro evidence that 15-PGDH is downregulated in human hepatoma cells and suggested to have a relevant tumor suppressing role in HCC.20 In our HCC cell line experiments, 15-PGDH suppression with IL-1β did not change cell proliferation in PLC and Huh-7 cells, and 15-PGDH expression induction by transfection in HepG2 cells suppressed cell growth at day 2 but this inhibitory effect disappeared at day 3 of MTS assay. Actually our cell proliferation assay data after 15-PGDH induction were similar with stomach cancer cell line (SNU-719) experiment, that cell growth at day 2 after transfection was suppressed in both HepG2 and SNU-719 cells.21 This could be partially explained by the transient expression of 15-PGDH after transfection and immunoblotting of 15-PGDH after transfection also demonstrated decrease of 15-PGDH at day 3 after transfection than day 0 (12 hours) (Fig. 3B). 15-PGDH expression induction in stomach and HCC cell lines was reported to induce apoptosis in relevant cell lines, but we could not check apoptosis in our study.20,21
The characteristics of our study is that this is the first report which showed expression of 15-PGDH in the HCC tissues from the patients and investigated the correlation of 15-PGDH expression and clinical parameter and prognosis of the patients. In multivariate analysis, 15-PGDH expression did not have prognostic significance in HCC patients as a whole. However, in HCC patients with baseline 15-PGDH expression in nontumor tissue, decrease of 15-PGDH expression in HCC tissues had a trend of smaller number of long term survivors. This finding suggests 15-PGDH downregulation probably could facilitate de novo intrahepatic recurrence of HCC and affect the prognosis of HCC patients with baseline 15-PGDH expression. Considering one third of HCC patients still showed 15-PGDH expression in HCC tissues, PGE2 pathway will not be critical in the carcinogenesis of HCC. However if we confine the one third of HCC patients who showed baseline 15-PGDH in adjacent liver tissue, more than half of the patients (56%) showed decrease of 15-PGDH expression in HCC than nontumor tissue. These patients could have tendency of late recurrence of HCC and poor long term prognosis than the patients maintaining 15-PGDH expression. So, restoring 15-PGDH expression or COX-2 inhibitor treatment in this selected HCC patients could have adjuvant therapeutic impact reducing late recurrence after surgical resection. To elucidate this hypothesis, there have to be more studies with larger number of patients.
HCC is a heterogeneous tumor and well known to have several genomic alterations and aberrant activation of several signaling cascades such as epidermal growth factor receptor (EGFR), Ras/Raf/MEK/ERK, phosphoinositol 3-kinase/Akt/mammalian target of rapamycin (mTOR), Wnt/β-catenin, and hepatocyte growth factor/c-Met pathways.1 Because of this complexity of genomic aberrations in HCC, inhibition of single pathway could have limited efficacy in the treatment and there has been efforts to find out adequate combination therapy to block critical pathways in HCC without any success except multikinase inhibitor, sorafenib until now. Furthermore, there have been rigorous efforts to find out predictive biomarkers in HCC for enrichment of the patients in specific targeted therapy. In colon and lung cancer, there have been reports linking EGFR signaling and 15-PGDH expression. In these reports, EGFR inhibition exerts their anti-proliferative effect through increased expression of 15-PGDH and reduction of PGE2.22,23 This cross link between EGFR signaling and 15-PGDH was not proved in HCC cell lines or tissues, but this could suggest another potential combination strategy or explanation for escape mechanism to EGFR inhibition in HCC treatment.
After the role of PGE2 and COX-2 was reported in carcinogenesis of colon cancer, chemoprevention strategy by COX-2 inhibitor was tested in colon cancer.3,24 However fatal cardiovascular adverse event have prevented wide spread usage of COX-2 inhibitor as a cancer prevention.24,25 Considering adverse event of COX-2 inhibitors, 15-PGDH induction to inactivate PGs could be pursued based on the emerging evidences that carcinogenesis in various cancers are related to reduced level of 15-PGDH,16,17,18,19 but still there remains major obstacle in clinical usage, because of the lack of adequate method to transfer 15-PGDH expression ability to human tissues. There has to be more studies and probably innovative technical advances in gene therapy.
Small number of the patients is the major limitation of this study. Especially the number of patients with baseline 15-PGDH expression in adjacent tissues was only 50, and this might make our results much less robust and statistically not significant in overall survival analysis. Furthermore, simultaneous measurement of COX-2 with 15-PGDH and direct measurement of PGE2 would be much more helpful in the interpretation of our results and we could have checked the efficacy of COX-2 inhibitor with/without 15-PGDH expression in proliferation of HCC cell lines. Meticulous another in vitro study and prospective study with more patients would be helpful in further elucidating the role of 15-PGDH down-regulation in the subgroup of HCC patients with baseline 15-PGDH expression.
In conclusion, our study did not prove significant tumor suppressive effect of 15-PGDH in HCC cell lines and expression/absence of 15-PGDH in HCC tissues did not show prognostic significance in terms of overall survival. However, one third of whole HCC patients showed baseline 15-PGDH expression in adjacent liver tissue and more than half of the patients showed decrease of 15-PGDH expression in HCC tissues. These patients with the decreased 15-PGDH expression in HCC showed tendency of poor long term prognosis than the patients maintaining 15-PGDH expression. So, restoring 15-PGDH expression or COX-2 inhibitor treatment in this selected HCC patients could have adjuvant therapeutic impact after surgical resection. To elucidate this hypothesis, further studies with larger number of patients are warranted.
The authors wish to thank Dr. Seung-Jae Myung at University of Ulsan College of Medicine, Asan Medical Center, South Korea for the generous gift of plasmid expressing HBx protein.
This study was supported in part by a research grant (protocol No. 2011-0387) from the Clinical Research Center of Asan Medical Center, Seoul, South Korea, which was provided by Ildong Pharmaceutical Co. Ltd.
15-hydroxyprostaglandin dehydrogenase
the American Joint Committee on Cancer
confidence interval
hepatitis B virus
hepatocellular carcinoma
hepatitis C virus
hazard ratio
interleukin-1 beta
prostaglandin E2
tissue microarray
year survival rate
1. Llovet JM, Bruix J. Molecular targeted therapies in hepatocellular carcinoma. Hepatology 2008;48:1312-1327. 18821591.
2. Llovet JM, Ricci S, Mazzaferro V, Hilgard P, Gane E, Blanc JF, et al. Sorafenib in advanced hepatocellular carcinoma. N Engl J Med 2008;359:378-390. 18650514.
3. Gupta RA, Dubois RN. Colorectal cancer prevention and treatment by inhibition of cyclooxygenase-2. Nat Rev Cancer 2001;1:11-21. 11900248.
4. Dixon DA. Regulation of COX-2 expression in human cancers. Prog Exp Tumor Res 2003;37:52-71. 12795048.
5. Koga H, Sakisaka S, Ohishi M, Kawaguchi T, Taniguchi E, Sasatomi K, et al. Expression of cyclooxygenase-2 in human hepatocellular carcinoma: relevance to tumor dedifferentiation. Hepatology 1999;29:688-696. 10051469.
6. Shiota G, Okubo M, Noumi T, Noguchi N, Oyama K, Takano Y, et al. Cyclooxygenase-2 expression in hepatocellular carcinoma. Hepatogastroenterology 1999;46:407-412. 10228831.
7. Simmons DL, Botting RM, Hla T. Cyclooxygenase isozymes: the biology of prostaglandin synthesis and inhibition. Pharmacol Rev 2004;56:387-437. 15317910.
8. Vane JR, Bakhle YS, Botting RM. Cyclooxygenases 1 and 2. Annu Rev Pharmacol Toxicol 1998;38:97-120. 9597150.
9. Tsujii M, Kawano S, Tsuji S, Sawaoka H, Hori M, DuBois RN. Cyclooxygenase regulates angiogenesis induced by colon cancer cells. Cell 1998;93:705-716. 9630216.
10. Charpigny G, Reinaud P, Tamby JP, Creminon C, Guillomot M. Cyclooxygenase-2 unlike cyclooxygenase-1 is highly expressed in ovine embryos during the implantation period. Biol Reprod 1997;57:1032-1040. 9369167.
11. Casado M, Callejas NA, Rodrigo J, Zhao X, Dey SK, Bosca L, et al. Contribution of cyclooxygenase 2 to liver regeneration after partial hepatectomy. FASEB J 2001;15:2016-2018. 11511527.
12. Abiru S, Nakao K, Ichikawa T, Migita K, Shigeno M, Sakamoto M, et al. Aspirin and NS-398 inhibit hepatocyte growth factor-induced invasiveness of human hepatoma cells. Hepatology 2002;35:1117-1124. 11981761.
13. Diaz-Munoz MD, Osma-Garcia IC, Fresno M, Iniguez MA. Involvement of PGE2 and the cAMP signalling pathway in the up-regulation of COX-2 and mPGES-1 expression in LPS-activated macrophages. Biochem J 2012;443:451-461. 22268508.
14. Na HK, Park JM, Lee HG, Lee HN, Myung SJ, Surh YJ. 15-Hydroxyprostaglandin dehydrogenase as a novel molecular target for cancer chemoprevention and therapy. Biochem Pharmacol 2011;82:1352-1360. 21856294.
15. Tai HH, Chi X, Tong M. Regulation of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) by non-steroidal anti-inflammatory drugs (NSAIDs). Prostaglandins Other Lipid Mediat 2011;96:37-40. 21763448.
16. Backlund MG, Mann JR, Holla VR, Buchanan FG, Tai HH, Musiek ES, et al. 15-Hydroxyprostaglandin dehydrogenase is down-regulated in colorectal cancer. J Biol Chem 2005;280:3217-3223. 15542609.
17. Tai HH, Tong M, Ding Y. 15-hydroxyprostaglandin dehydrogenase (15-PGDH) and lung cancer. Prostaglandins Other Lipid Mediat 2007;83:203-208. 17481556.
18. Pham H, Chen M, Li A, King J, Angst E, Dawson DW, et al. Loss of 15-hydroxyprostaglandin dehydrogenase increases prostaglandin E2 in pancreatic tumors. Pancreas 2010;39:332-339. 19820419.
19. Thiel A, Ganesan A, Mrena J, Junnila S, Nykanen A, Hemmes A, et al. 15-hydroxyprostaglandin dehydrogenase is down-regulated in gastric cancer. Clin Cancer Res 2009;15:4572-4580. 19584167.
20. Castro-Sanchez L, Agra N, Llorente Izquierdo C, Motino O, Casado M, Bosca L, et al. Regulation of 15-hydroxyprostaglandin dehydrogenase expression in hepatocellular carcinoma. Int J Biochem Cell Biol 2013;45:2501-2511. 23954207.
21. Song HJ, Myung SJ, Kim IW, Jeong JY, Park YS, Lee SM, et al. 15-hydroxyprostaglandin dehydrogenase is downregulated and exhibits tumor suppressor activity in gastric cancer. Cancer Invest 2011;29:257-265. 21469975.
22. Mann JR, Backlund MG, Buchanan FG, Daikoku T, Holla VR, Rosenberg DW, et al. Repression of prostaglandin dehydrogenase by epidermal growth factor and snail increases prostaglandin E2 and promotes cancer progression. Cancer Res 2006;66:6649-6656. 16818638.
23. Yang L, Amann JM, Kikuchi T, Porta R, Guix M, Gonzalez A, et al. Inhibition of epidermal growth factor receptor signaling elevates 15-hydroxyprostaglandin dehydrogenase in non-small-cell lung cancer. Cancer Res 2007;67:5587-5593. 17575121.
24. Bresalier RS, Sandler RS, Quan H, Bolognese JA, Oxenius B, Horgan K, et al. Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial. N Engl J Med 2005;352:1092-1102. 15713943.
Table 1.
Table 2.
Table 3.
15-PGDH, 15-hydroxyprostaglandin dehydrogenase; HCC, hepatocellular carcinoma; HBV, hepatitis B virus; HCV, hepatitis C virus; AFP, alpha-fetoprotein; AJCC, the American Joint Committee on Cancer.
Table 4.
Table 5.
15-PGDH, 15-hydroxyprostaglandin dehydrogenase; HCC, hepatocellular carcinoma; HBV, hepatitis B virus; HCV, hepatitis C virus; AFP, alpha-fetoprotein; AJCC, the American Joint Committee on Cancer.
* HCC patients who showed same or increased 15-PGDH expression score in HCC tissues compared with nontumor tissues.
Table 6.


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VERY FINE/NEAR MINT(W) Scott Snyder (A) Jock (CA) Blank CoverLeft rattled by the events of DARK NIGHTS: METAL, Bruce Wayne must come face to face with the nightmares spawned from the Dark Multiverse. But even though evil devoured evil in the collapse of Challengers Mountain, the Dark Knight still has his doubts. He discovers that the Batman Who Laughs not only survived the fight with The Joker at the end of METAL, but now he is enacting a sinister plan across the Multiverse-something both terrifying and oddly familiar. But when Bruce Wayne realizes the only way to stop this madman is to kill him, he must consider violating the very rule Batman won't break…the same rule that created this insatiable villain-the Batman Who Laughs!Date Available: 12/12/2018
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T hree-6-5 days ago, this was just another wordpress.com weblog
H ere its umbilical chord was cut, it became The Shooting Star.
E nchanted by its first post, first reader & first comment, this blog
S ang its way into the blogosphere, with cliched themes & bizarre.
H ome to 105 posts & graced by 16,000 readers, now is a moment
O f reflection & joy, and gratitude & celebration.
O nce upon a time, a blog was merely meant
T o be a goofy forum; today it redefines communication
I n a world where time & ideas are hard to find.
N ow I deviate from this happy, proud occasion,
G lad indeed that The Shooting Star has defined
S omething in my life that was once mere anticipation.
T hrough this journey, my blog has become a part of me
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R eally, all I want to say is, dear blog, Happy Birthday!
On The Shooting Star's first birthday, I must thank all my fellow bloggers for keeping me company through this incredible journey! A special thanks to Amit, Premanjali, Varun, Radhika, Aadil, Akanksha, Pranav, Jayesh & Mahak.
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"in this busy play-novel of downed vodka and photographic 'shots', I found that the drama has the consistency of one of Luzhin's caramel wafers"
There is a lot of exposure in this production. There is no curtain for a start, no flats, no scene painting, nothing obviously comfortable on stage but utility furniture. Across the back, exposed, is a dressing room, liquor bottles and music kit, for the (a)ttiring house of the Shakespearian theatre equips this new adaptation of Dostoyevsky's unsettling Crime and Punishment. The company gathers, warming up, as the audience sits down and a full-on Psalm 130, De Profundis, 'Out of the depths … hear [our] prayer', shifts seeming rehearsal to actual performance. What you are about to see could be barefaced and brazen.
In fact the way to enjoy this co-production with Glasgow's Citizens and Liverpool's Playhouse is to look at it as an amateur photographer and to accept that fiddling with your dramatic settings will affect what you see. Some scenes will be sharp, others appreciably less so; some clearly sequenced, others vaguely. The programme casts this as 'fluidity of the staging, with its seamless transitions'.
Depth of field, then, is key. Rodion Raskolnikov, the ur-student transgressor, is more in focus than out of it, which is to actor Adam Best's credit as the character is in the fever grip of irresolution to the point of passing out on his sofa or remaining mute and motionless while a policeman snuggles onto him and licks his shaven head. Raskolnikov's idea of responding to the love-of-his-life, Sonya, is to bow down before her unhappiness. He is fixated on the genius of Napoleon but has the strategic nouse of a double axe-murderer. Best is lucid and good at the verbal and facial tics that impede Raskolnikov's nihilistic raptures.
Adjust for comic relief and enter George Costigan first as Marmeladov, drunk, and then as Porfiry Petrovich, detective and examining magistrate. Now we're learning about portrait photography: the two subjects are nicely observed, properly defined, and hold your attention. However, the entertaining, disconcerting, scenes might as well be framed: Meet a Drunk, Cross-examination, Youdunnit – as they illustrate what happens when police procedural meets comic accent and turn. Costigan's Petrovich proves a wry nemesis.
Cate Hamer's two principal roles as Pulkeria, Raskolnikov's mother, and as Katerina, Marmeladov's wife, are demanding and prominent but they cannot provide humour. Hamer has to do destitution, torn affections, and mental breakdown in vignettes of scenes where there are no decorative borders. The effect is monochrome.
There is a lot of creative energy and skill expended in this production. Supporting parts are bright and live in the moment, notably Obioma Ugoala as the unselfish Razumikhin. Writer, Chris Hannan, knows his Dostoyevsky and pares the novel down with evident respect and sensitivity. Thematically it is pretty intact, not least its all-Russian face-off between social cataclysm and (Christian) redemption, between the polemic of 'new ideas, new economics', and Sonya's New Testament. Raskolnikov is criminally self-absorbed and the play's script interrogates him. Stage microphones amplify his breathing; other characters 'resting' back-of-stage also judge him. Domininc Hill's direction is clever – a door on wheels makes for fast entrances and exits, digitised blood slashes red and the soundscape is close to a Threekopek Opera – but finally, inevitably maybe, in this busy play-novel of downed vodka and photographic 'shots', I found that the drama has the consistency of one of Luzhin's caramel wafers.
Reviewer: Alan Brown (Seen 30 October)


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Golliwog's Cakewalk-Artistic Preparation and Performance Series - Debussy, Claude
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From Mystery to Mastery
co-author Ingrid Clarfield comes a unique approach to this Debussy favorite. Students are provided with specific instructions on how to go about learning the piece, section by section, for the optimum artistic performance.
Publisher: Alfred Publishing Company, Series: Alfred's Masterwork Library - Single Composer Literature
Publisher Item #: 00-18899
Composer: Claude Debussy, Editor: Ingrid Jacobson Clarfield
Instrument: Piano, Level: Early Advanced, Format: Collection / Songbook, Sheet Music
Ensemble: Piano Solo, Genre: Classical, 20th Century, Impressionism
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Some people think the word "mute" in the name means the dog doesn't bark. While they tend to be less vocal than many breeds, the Alaskan Malamute can vocalize, though they tend to howl more often than bark. These dogs were first domesticated by the Mahlemuts – a tribe of people who saw the benefit of using the animals for work and companionship. Often, these dogs attached to sleds were the only real mode of transportation available – meaning a well-trained group of dogs was extremely valuable in terms of sheer ability to survive.
The natural harshness of the Northern regions made it necessary for the Alaskan Malamute to be a strong dog with a heavy coat. Those features have changed little over the centuries of domestication. And in fact, it's easy to see some other tendencies of this breed that make the ancestry clear.
For example, the Alaskan Malamute does well in a "pack" situation – whether that means it prefers to be outdoors with other dogs or indoors with its people. These dogs don't typically do well when they're left to their own devices for too long. Remember that they had to be cunning to survive in the Alaskan wild. That cunning comes to their aid in finding ways to entertain themselves when their human owners fail to provide sufficient exercise and play time. They might dig their way free of a confined yard or simply tear up whatever they can reach. Either way, it's much safer to be sure that you can provide ample opportunities for the Alaskan Malamute to be with you and to vent his energy in a productive way.
Today, the Alaskan Malamute is still sometimes used as a pack or sled animal. They're also used in many types of competition, including weight pulling and racing. They've been featured by many writers and have been used in several movies – mainly depicting the trials of polar sledding.
Though they make excellent work animals, many have found themselves pampered family pets. Remember that the heavy coat makes them ideal for cooler climates, but they should be sheltered from heat.
Keep in mind that these are large dogs – weighing in at almost 100 pounds for a typical male. Add to that the fact that they tend to love to play well into adulthood and you may find that this is simply more dog that you're ready to handle. Alaskan Malamutes can be trained to be extremely well behaved, though it doesn't come naturally to them. They just like to have fun, and their sheer size sometimes makes that a problem.
If your Alaskan Malamute is going to have a fenced in yard, be sure that the fence is high and that you include some sort of underground barrier – such as burying a portion of the fence. These dogs are excellent athletes – they can jump and dig with the pros, and they're nothing if not tenacious about getting their way.
- Affectionate, Loyal, Playful
- AKC Breed Popularity: Ranks 58 of 191
- Height: 25 inches (male), 23 inches (female)
- Weight: 85 pounds (male), 75 pounds (female)
- Life Expectancy: 10-14 years
- Group: Working Group
Alaskan Malamute Club of America


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This year in gaming is shaping up to be one of the most memorable ones on record—and E3 (the trade show where new games and consoles are usually announced) hasn't even happened yet. One of the most anticipated titles here at Complex HQ is coming out this November in Uncharted 3, and we're ready to get our monthly update of what's going on over at Naughty Dog, the development studio behind the game.
Thankfully, Justin Richmond, Uncharted 3's game director, was happy to oblige us. And while he didn't give away what's in store for their grand E3 rollout, we got a full rundown of where the game stands, how it's going to compete for the hearts and minds of competitive gamers on the PlayStation Network, and—speaking of which—what he thinks about Sony's disastrous month of outages and hacks. Oh, and we have a possible Uncharted 4 semi-spoiler announcement and who at Naughty Dog does the best Nathan Drake (or, rather, Nolan North) impression. Read on while the reading's still good...
Interview by Troy Mounis
We're less than six months away from the debut of Uncharted 3. How far along is the game?
Richmond: We're still in the middle of development, so I don't want to talk too much about how far along we are. We'll continue to develop, tweak, and add things up until the very last moment. That's just part of our nature. But I will say this—you haven't seen anything yet. Be prepared to be blown away at E3.
Yes, we've got a Cintamani Stone's worth of crap in our pants waiting in anticipation. So, why set this one in the desert anyway?
In every one of the Uncharted games, we focused on unique locations with amazing visuals and an intriguing historical mystery. During some of our early research, [creative director] Amy Hennig came across the legend of Ubar, or the "Atlantis of the Sands," a prosperous city that mysteriously disappeared in the Arabian Desert. We were fascinated with the true-life mystery. And like the past Uncharted games, we also wanted to take on a new technical challenge, something we hadn't done before. In the previous games it was water and the jungle, or ice and snow. So, as we started to talk about where we wanted to go for Uncharted 3, the desert just appealed to us. Not only was it a part of the world that Drake had never been, but it also presented one of the greatest technical design challenges: the way sand blows over and curls over the tops of dunes, the way it displaces and flows, almost like a liquid. Organic elements like water, fire, and sand are technically difficult to credibly render, and we wanted to push ourselves to see what we could accomplish.
What's been the biggest obstacle thus far in the game's development?
Our constant need to out-do ourselves. Each game set a high bar not only for the PlayStation, but for us as a developer. We're constantly trying to top what we've delivered before—creating amazing new experiences for players while still delivering an engrossing story that's engaging enough to bring in new players, as well as being rewarding to fans of the franchise.
Tell us some of the major new additions to the single-player experience.
In the single-player campaign, we're building out a bunch of new and improved gameplay mechanics and systems. For example, we've included a new melee fighting system that allows Drake to take on multiple enemies at one. We also have some new stealth moves that allow us to play with different contextual takedowns. This has given us the opportunity to create new scenarios and battles that were never possible before. We're also expanding our traversal gunplay to give you more ways to engage in combat. We've expanded Drake's maneuverability by introducing traversable objects that let Drake climb around free-standing environmental objects with fully realized physics—such as a swaying chandelier—especially during puzzle-based gameplay.
That sounds like you're throwing in a bunch of stuff we know fans wanted from the second game. You've mentioned in the past that Uncharted 3's multiplayer component is being built to rival some of the other popular multiplayer titles out on the market, the CoDs and Halos of the world. What do you think those games bring to the table that attracts their fans?
I think that both Halo and Call of Duty bring different things to the table. With Halo, you have one of the best examples of a tournament ready, skill-based multiplayer experience on any console. A better player will beat a less skilled player 99 percent of the time in Halo. They also have amazing user-generated content and tools with the Forge system. Call of Duty excels at making every player feel like they are advancing and moving forward with every game. WithModern Warfare, they brought the idea of progression in competitive multiplayer into the mainstream. The idea of an XP grind in a multiplayer game became hugely influential to the rest of the industry.
Are you hoping to replicate that with an Uncharted spin to it, or are you building a more novel experience? What makes it unique?
We're taking our signature Uncharted gameplay and incorporating it into multiplayer in a very unique way that we think brings something completely fresh to online gaming. With Uncharted 3, we're introducing an action-adventure multiplayer experience where we've taken the big, cinematic set-piece moments of our single player campaign and integrated them into our multiplayer mode. These events create incredibly intense moments in competitive play that are different from other online multiplayer games. The unique gameplay mechanics in Uncharted have also opened up the possibilities for multiplayer.
How are you changing things up to take on some of the big boys in multiplayer?
Since we announced Uncharted 3, we've stated that multiplayer is going to be a huge focus for us in this game, and the multiplayer you'll find in Uncharted 3 is a noticeable evolution from Uncharted 2. We're expanding on the gameplay technology, the depth, and overall experience is so many different ways. We're introducing new features like 3D stereoscopic support, single-console splitscreen sign in, and brand new competitive modes including Three Team Deathmatch (2 vs. 2 vs. 2) and Free For All. And that's just the beginning.
Customization is a major focus for us this time around and we're introducing countless ways for players to create their own unique play styles and characters. Players can now make their own hero or villain characters and choose from hundreds of customizable accessories, as well as weapon customization and modifications. Uncharted 3 is also introducing a Paid Booster slot, allowing players to spend some of their cash for a one-time booster, along with Medal Kickbacks, which allow players to activate a performance-based reward after collecting a number of medals during a match. With all these options to keep track of, we've also added player load-out slots to help them choose their weapons, mods, Boosters, and Kickbacks to create their own individualized load-out that matches their play style for each game and map.
We're also introducing a host of new social media features and functionality to multiplayer in Uncharted 3. In addition to being able to directly upload to YouTube and Facebook, we're also deeply integrating Facebook in ways that that are unique to console games so far. We've also expanded the Cinema Mode for creating and sharing videos, and we'll be launching a new feature called Uncharted TV that will showcase some of the best user-generated content and videos from You Tube, viewable directly in-game.
Obviously there is so much more to come as we continue to talk about Uncharted 3 in the coming months, but this should give you a flavor of what to expect.
Damn, Gina. That's a lot to look forward to. Is there anything that you guys actually left on the cutting room floor?
I wish I could give you some juicy tidbits, but those ideas are often the ones that integrated into our future games, and I don't want to let the cat out of the bag!
That's cool—we'll assume you just accidentally announced Uncharted 4. Quick question, since it is so timely and relevant to you, considering the larger focus on multiplayer: How much did Sony screw the proverbial pooch with all that's going on with the PlayStation Network?
As fellow gamers, we can understand how this can be frustrating. But we know that Sony is taking the situation very seriously and is committed to doing everything they can to make sure the network is a safe and secure environment. We're heads down right now developing Uncharted 3 and are looking forward to kicking off our multiplayer beta this summer.
Which is June 28, last we heard. For shits and giggles: Who at Naughty Dog does the best impersonations of Nathan Drake and Sully?
For Nathan Drake, I kinda have to give it to [lead animator] Jeremy Yates. He does some of the mocap for Drake as well, and he has the character down. As for Sully, I have to say that there isn't a person on the team who doesn't give a hearty "Goddamn it!" with that signature Sully rumble every now and then.
You heard it here first, folks. Naughty Dog: Dedicated Breakers of the Third Commandment.


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General Rules
• Members must be 21 years of age or over.
esquire SPORTS Specific Rules
Straight Line Payoffs (Football and Basketball)
Straight Wagers
This is the most common type of sports wager, based on the results of a single game. One team is favored over another by a point spread. The favorite is indicated by a minus sign (-3) and the underdog by a plus sign (+3).
Totals Wagers
The totals wager is based on the combined total number of points or goals scored by two teams in a single game. A player bets on whether the combined total number of points or goals scored by the two teams in the game will be over or under the total set by the odds maker/handicapper.
Money Line Wager
A money line wager, instead of a point spread, may be used to bet on a match-up between two teams. In effect, if a match-up is determined by a money line, like Major League Baseball, then it will cost the player more to wager on the favorite.
Parlay Wager
A parlay wager is a bet on two or more teams or selections. It is one of the more versatile forms of sports wagering. The player can combine different sports, point spreads and money lines. In a parlay wager the original stake and winnings are re-invested on the next game, and all selections must be correct, that is, one loss and the parlay loses.
Teaser Wager
A teaser wager is a wager on two or more teams or selections. The difference between the teaser wager and the parlay is that the player can adjust or tease the line in his/her own favor. For example, if the Denver Broncos are favored by seven points in one game, and the Seattle Seahawks are favored by 10 points in a second game, a teaser could very well favor the player. That is, a six point two team teaser would adjust the point spread six points in favor of the player. In effect, Denver would now be favored by one point (7-6 = 1) and Seattle would be favored by four points (10-6 = 4).
IF - Win Wager
An if - win wager is a bet that carries over to a second team if the player wins on his initial selection. For example, the player has to wager a fixed amount on one team. If that team wins, or the game is tied, then another fixed amount, up to the original amount wagered, shall be placed on a different team.
Reverse Wager
A reverse wager is the same as two if - win wagers. This means that if wager A wins, the bet goes to wager B. Likewise, if wager B wins, the bet goes to wager A. On the other hand, if wager A loses, the bet does not go to wager B. And again, if wager B loses, the bet does not go to wager A. If wager A wins, the bet goes to wager B, but if wager B loses, the bet does not go to wager A.
Total (over/under)
Wagering on the total points combined on the game: To win on the "over", the total score for each team will be added together and it must exceed 40 points. When betting the "under", the total score for each team is added together and cannot exceed 39 points to win the wager, if the total score a "push" and the money is credited to your account.
Money Line Wagering
When wagering on the money line, you must win the game on the field in order to win your bet. Wagering on SAN FRANCISCO $-290, just wagering on them to win, the point spread does not matter. You must risk $290 to win $100. Wagering on SEATTLE $+240, you stake $100 to win $240.
Parlays *
Football and Basketball
Football Teasers
Basketball Teasers
Any loss, constitutes a loss for the entire teaser wager


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Why are you so white?
Posted on May 12, 2011
Part 1 of recent hospital adventures …
On a crisp Tuesday afternoon, I admitted myself to the emergency ward of the hospital down the road. My personal Wikipedia diagnosis suggested the options that were gifting me with tremendous side pain were not particularly nice ones, and, with my mother's voice ringing in my head – 'don't muck around when it's your health, Livvy' – I threw myself at the bewildered looking man propped up behind the reception desk. I was rewarded, if only because of my pallid complexion and leaking eyes, with a speedy appointment which ultimately stretched across several tests in several departments and me getting lost several times, being, as I was, quite unable to recall the German name for the emergency department.
Diagnosed with a kidney infection, I was let go a few hours later, by a brusque, no nonsense doctor – of the type who inexplicably does away with all cosmetics (understandable) except shimmery eye-shadow (not understandable) – with painkillers and antibiotics. The abnormality in my kidney picked up by the sonographie was brushed aside by No Nonsense and she pencilled me in for 8.30am on Friday for my follow up. Fine. I had a week off work anyway, to lounge around in bed like a giant slug. No skin off my nose. Sure, 8.30am was a touch early for a Friday morning appointment, but I wasn't going t argue for fear she'd laser me with her shimmery eyes. So I meekly took my medication and slipped out, hoping the woman on the front desk who looks after parking, would not recognise me from my earlier, 'I need to see a doctor' plea. Lounging in bed, slug like, over the next few days, I formulated a lovely Friday plan that would see me present my healthy self to the hospital on Friday, after which my friend and her dot of a 2 year old daughter would pick me up and we would repair to my place for coffee. A simple plan, of the type I historically enjoy spicing up with a bit of unexpected excitement.
And so I returned. In style. At 8.30 on Friday morning, I was sitting, hand outstretched, ready to part with more blood (an act I truly despise and may or may not be partially phobic of). Duly parted with, I fainted. Or, more accurately, lurched out of the room and into the nurse's station, politely asked for water, and slithered down the doorframe. I recall, as I slithered, the nurse's plaintive cry, oddly in English, 'why are you so white?'
The resulting stretcher and indeed stretchering around of my prone form, boots poking out the end, to various tests in various departments was just a touch embarrassing. I closed my eyes through most of it, to avoid the pitying gazes of passers by. I didn't want them to see through to my fraudulent soul. Clearly there were others more in need of the stretcher. Back waiting for the doctor, I passed the time by deciphering my blood and sonographie reports (Germans use their own medical names, as well as the Latin). I was vaguely – although only vaguely, to be honest – concerned to learn my gall bladder is of normal size with no discernable problems, largely because my gall bladder was removed eight years ago.
Nine hours later, many of which were spent in the comforting company of my dear friend and her daughter, I was admitted. This was unexpected. I looked at the doctor, who may or may not have been twelve (an ongoing theme at the hospital, it would unfold … or maybe I'm just getting old) and said 'here. Tonight. Here.' It was, to be frank, rather annoying. I was certain I had, with the assistance of a delicious hot chocolate, reproduced the blood taken earlier that day and was quite ready for some Criminal Minds streaming in bed with the remainder of my antibiotics course and a cup of tea. Obviously I could not explain this to Youth Face, who seemed intent on committing me to a ward, for reasons that weren't exactly clear, so I duly called my wonderful flatmate and asked her to bring over a bag of necessities. This turned out to be my laptop, QANTAS pyjama pants and corn chips. It would appear she knows me too well.


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- PD Range: 55-71
- Prescription Range: -20.00 ~ +12.00
- Available as Progressive / Bifocal : Yes
- Rim: Full Rim
- Shape: Round
- Material: TR
- Feature: Lightweight , Universal Bridge Fit
- Tags: All Kids Eyeglasses , Teen Guys Glasses , Teen Girls Glasses , Teen Glasses , College Glasses
- Frame Width: 135 mm
- Lens Width: 50 mm
- Bridge: 18 mm
- Temple Length: 142 mm
- Lens Height: 43 mm
- Frame Weight: 13 grams
These round glasses offer incredible comfort and style at an unbeatable price. Made with lightweight TR90 plastic, the medium-sized frame is flexible yet durable. It comes in two glossy options, clear with tortoiseshell temple arms and black pattern with black temple arms, as well as three matte options: slate blue with blush temple arms, taupe with brick temple arms, and cranberry with gradient pattern.


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A typical morning at Huguenot Nursery School will include:
Center time - Children choose from planned activities available in learning centers
Circle time - A group time that might include stories, songs, finger-plays, show and tell, movement, discussion or group story-writing.
Outdoor Time - More than recess, this time provides physical challenges, as well as opportunities for sand, water and dramatic play.
Clean up Time - An important time for learning responsibility and care of equipment
Snack Time - In a large or small group, snack time provides a social setting in which children can converse, learn basic manners, and practice self-help skills


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Costa Mesa, CA -- December 06, 2018 -- InvestorsHub NewsWire -- M Line Holdings, Inc. (OTC Pink: MLHC; "M Line" or the "Company"), announces that it has signed a Letter of Intent to acquire 37.7 acres of land in Golden Valley located at 3743 US Highway 93, Golden Valley, Arizona, 86413 and 0.6 acres of land in Dolan Springs, Arizona, one operating restaurant and event center in Golden Valley and two operating restaurants in Dolan Springs, Arizona. We expect to close these transactions in the next few days.
The land at Golden Valley was appraised earlier this year for $2,900,000 by Wiltchik Appraisal, Inc., Certified Appraisers, out of Irvine, California. The land at Dolan Springs is estimated to be worth approximately $500,000. The revenue of the restaurants through October exceeds $800,000 with net profit over 20% of revenue.
We are securing contracts with a major oil company to build a gas station including a truck and travel center on the Golden Valley property which is located on the new Interstate 11 freeway under construction from Las Vegas to Phoenix. This funding to invest up to a $1 million to support the construction will be finalized very soon.
Tony Anish, CEO of M Line, commented: "Although this is a slightly different business than those we have acquired to date, we are securing strong assets to strengthen our Balance Sheet and good cash flow from the restaurants and event center as well as the gas station as soon as we can get it built. In addition, some of the land can potentially be used to cultivate hemp that can be turned into THC free CBD for use by our joint venture partner who is manufacturing the "Rise" CBD line of products."
Tony Anish continued: "We have had a number of questions from our shareholders regarding transactions that we have announced but not yet closed. All these transactions are in the process of being closed and we will keep you informed regarding these and new opportunities that are currently under review. Stay tuned we have so much more to tell you."
About M Line Holdings, Inc.
M Line is a Holding Company. It controls subsidiaries involved in the Beverage Branding and Distribution industry that includes our VEA and TORQUE® branded drinks. In addition, M Line controls two subsidiaries in Florida in the Food and Beverage distribution business and M Line has now expanded into the Cannabis Industry with the acquisition of our C-Pod manufacturing business. Furthermore, M Line will continue with its business financing activities while looking for other opportunities in the Beverage, Distribution and Cannabis industries as well as other prospects that make sense to management.
Safe Harbor and Informational Statement
This press release may contain forward-looking information within the meaning of Section 21E of the Security Exchange Act of 1934, as amended (the Exchange Act), including all statements that are not statement of historical fact regarding the intent, belief or current expectations of the company, its directors or its officers with respect to, among other things: (i) the company's financing plans; (ii) trends affecting the company's financial conditions or results of operations; (iii): the company's growth strategy and operating strategy; and (iv) the declaration and payment of dividends.
The words "may", "would", "will", "expect", "estimate", "anticipate", "believe", "intend", and similar expressions and variations thereof are intend to identify forward-looking statements. Investors are cautioned that any such forward-looking statement is not a guarantee of future of future performance and involve risks and uncertainties, many of which are beyond the company's ability to control, and that actual results may differ materially from those projected in the forward-looking statements as a result of various factors including the risk disclosed in the company's statements and reports filed with the OTC Markets. The Company claims the safe harbor provided by Section 21E(c) of the Exchange Act for all forward-looking statements.
For more information contact Tony Anish EMail: email@example.com Follow us on Twitter: @mlinehcWeb site: www.mlinehc.com Caravel Web site: www.drinkvea.com / @DrinkVeaWeb site: www.drinktorque.com / @DrinkTorque
1 Year : From Dec 2018 to Dec 2019
Today : Sunday 8 December 2019


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What we do
Global Outsourced IT means placing us in the driver seat of your IT infrastructure, no matter where in the world your company and its branches are located and entrusting us to deliver an optimal service and taking care of all your IT needs and requirements at all times..
Remote IT Support
By making use of the best in RMM tools there is almost no support we cannot do remotely. We can even fix your pc
We apply monitoring triggers to your crucial systems which allows us to have the upper hand and start working on your issues before are even aware of the problem .
Project Management
Whether you are changing ISP's or have cabling done, we will take ownership of all IT related projects while working closely with your management of choice
Cloud Backup
With Barracuda backup the headache and concern surrounding backups are in the past. With Barracuda's line of Backup products, there is virtually no data left unprotected.
Collaberation services
We all know how vital teamwork is and therefor supply our clients with the best in collaboration tools so all departments and staff can work closely together, from anywhere in the world
3CX VoIP PBX
The pinnacle of VoIP systems, virtual or cloud driven. Providing you with conferencing tools as well as collaboration software which easily integrates with your email system and mobile devices
Utilizing initiative. Solving Big Problems
Are you ready to hand over the keys to your infrastructure and allow us to take you to the next level?
Why we are different
Service delivery is vital and directly affects your business, which is why we provide an international standard of service at all times with lightning fast SLA response times and expertise in our field os service offerings.
We also believe that our clients should not be overpaying for both support and hardware which is why we, in most cases do not charge any mark-up fees on items sold.
Our Patrtners
We only associate our brand with top level global peers which allows us to provide our clients with the best solutions at the lowest prices
Our Skills
A bit anxious entrusting us with your IT? See some of our highlited skills below
- Remote Support – 99%
- Office 365 – 97%
- Cloud Backup – 93%
- Web Design – 83%
Whatever hardware or software your company requires, we can deliver at the lowest available cost to you
a word From Our Clients
Below are some feedback from our clients
Cloudbound IT has been working with Cape Reed International and it's global branches for the last 3 years and has been providing an exceptional level of service. Cloudbound IT has really helped our company throughout the years in making the work environment more efficient and assisting us with our growth and IT needs. I am confident about the services of Cloudbound IT and I can surely recommend the services.Francois vd Vyver
Since we have been with Cloudbound IT, our systems have improved and stabalized dramatically.I think it is safe to say that our IT issues are of the past and would highly recomend Cloudbound IT's services to any other business out there.Schalk Jooste
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Have a few questions or perhaps ready to have us take you to the next level? Chat with us!


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I've been playing with OpenBSD -current on my MacBook Pro.
Not all of the hardware works. Most notably: the ATI Radeon Mobility X1600, wireless, Fn key and acpi/apm.
I can get X working with the VESA driver at 1024x768.
So, I cannot right-click, recording through the azalia sound driver is not working (though deanna@ is making great strides with the Mac audio capabilities), none of the Fn-Fx keys (sound, brightness, ...) are working, I cannot suspend or get any power status. But, it's a fast, fast, fast build machine. :)