Fans of "Twilight" will no doubt rejoice to see Kristen Stewart covering the February issue of the Vogue, sporting a series of Proenza Schouler spring outfits.
The cult-favorite actress scowls her way through a series of photographs, including some winning outtakes posted on Vogue.com. Stewart's affections for Proenza Schouler carried over into the majority of the outfits she's wearing -- from a tweed bustier frock to a burnt-orange dress. She even poses with the two tuxedo-clad designers in one shot.
In a rather charming twist, Stewart also offers up her own tortilla soup recipe in the magazine, for any Twi-hard looking to eat like Bella Swan. As Stewart herself tells Vogue: "Masses of girls identified with Bella in a really profound way, for want of a better word."


Recently, The Savings Bank Life Insurance Company (SBLI), which provides life insurance products to individuals and families throughout the U.S., was looking to satisfy the needs of today's life insurance applicants by providing faster turnaround times, while reducing underwriting costs. To achieve these goals, they turned to advanced analytics and predictive modeling solution, LexisNexis® Risk Classifier, to accelerate life underwriting and remove the need for invasive tests.
Improvement in policy pricing and the placement of applicants into appropriate risk classes.


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The effect of information literacy on the utilization of electronic information resources in selected academic and research institutions in Uganda
Alison Annet Kinengyere
Uganda has gone a step forward in ensuring that information resources available for researchers and students are maximally utilized. Academic and research libraries are…
Uganda has gone a step forward in ensuring that information resources available for researchers and students are maximally utilized. Academic and research libraries are participating in supporting and achieving the missions of their respective institutions by teaching the competency of information literacy (IL). This paper seeks to examine the effect IL has had on the usage of electronic information resources in academic and research institutions in Uganda. It aims to focus on the innovations that Makerere University Library (the biggest and oldest academic library in Uganda) has undertaken to ensure that library users (the Makerere University community and other collaborating universities and research institutions in Uganda) are trained on how to access a variety of available information resources, evaluate the information and apply it to address their needs.
Data were collected for the study using interviews to both library staff and users of the selected institutions: two library staff in charge of e‐resources and ten students/researchers were interviewed from each institution. However, user statistics for the years 2004‐2005, as well as the IL training sessions conducted, were the main sources of information. The study focused on academic and research institutions – Makerere University, Uganda, Martyrs University, Nkozi and National Agricultural Advisory Services (NAADS). The researcher is physically involved in the IL program in Makerere University. The usage statistics were compiled and interpreted.
The paper finds that availability of information does not necessarily mean actual use. The study shows that some of the available resources have not been utilized at all. This means that users are not aware of the availability of such resources, they do not know how to access them, or they do not know what the resources offer. All this calls for continued information literacy programs. IL is very vital in influencing utilization of e‐resources. Information professionals are needed to pass on IL skills to library users, while library users should endeavor to find out what information is available online for their consumption. Their attitudes and perceptions also influence the level of utilization.
The paper shows the extent of information literacy and its influence on electronic resources in Uganda. It points out the challenges for the future and provides a number of recommendations for the way forward, which will be helpful both to the relevant communities in Uganda and to other academics in similar circumstances.
The Electronic Library, vol. 25 no. 3
Electronic media
Academic libraries
All dates (1)

redpajama_set_name: RedPajamaCommonCrawl


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Washington State Supreme Court
State Supreme Court OKs Cooke Aquaculture steelhead farming
The Washington state Supreme Court has unanimously upheld permits that will allow Cooke Aquaculture Pacific to farm steelhead trout in net pens in Washington waters. The decision clears the permit hurdle for the international aquaculture giant to change its operations from farming Atlantic salmon to steelhead.
Washington florist who refused same-sex wedding job settles with couple
A Richland florist who was in an eight-year legal battle that reached the U.S. Supreme Court will retire after settling with the same-sex couple whose wedding job she refused.
Washington Supreme Court to decide police privacy case related to Jan. 6 riot
Martha Bellisle
The Washington Supreme Court heard oral arguments Tuesday in a case that will decide whether the identities of Seattle police officers who attended events in the nation's capital on the day of the insurrection are protected under the state's public records law.
Ruling helps protect homeless people from having vehicles towed
Washington's Supreme Court issued a key decision Thursday that helps protect people living in their vehicles from having them towed, in a case that drew…
State Supreme Court to hear public records case related to Seattle police at Capitol riot
Updated at 3:15 p.m. with comment from officers' attorney.The Washington Supreme Court has agreed to hear a case involving six Seattle police officers who…
State Supreme Court reinstates King County police inquest system
The Washington Supreme Court has reinstated sweeping changes made to the King County inquest procedures in 2018, providing an expanded avenue for the…
Supreme Court turns away Washington florist who refused same-sex wedding job
The Supreme Court on Friday declined to take up the case of a Richland florist who refused to provide services for a same-sex wedding, leaving in place a…
WA lawmakers debate whether to make drug possession a crime again
Lilly Ana Fowler
Lawmakers and attorneys are still grappling with the so-called Blake decision, a Washington state Supreme Court ruling that struck down the law…
State Supreme Court says recall against Seattle councilwoman can proceed
The Washington state Supreme Court ruled Thursday that a recall effort against Seattle City Councilwoman Kshama Sawant can go forward.In September, a King…
State Supreme Court strikes down felony drug possession law
In a decision with implications for tens of thousands of cases dating back decades, the Washington Supreme Court on Thursday struck down the state's…


So how did it go? How did we do? We have been studying what love is during this holiday season. Love is being defined and described for us by God through the pen of the apostle John. Love is an unwavering, enduring commitment from a willing heart to give oneself without consideration of the extent of the cost. God has demonstrated this love for us through Jesus coming to this earth and giving himself for us. The radical display of amazing love from God is supposed to move us to love one another. In fact, loving others is our purpose. "If God so loved us, we also ought to love one another." So how did we do? Over the last two weeks how have we been doing?


Anderson, W. Attersley, E.M. Bailey, W.G.
Parr, R.P. Baynes, E. Bell, J.T.
Bennett, R. Benson, E.G. Blockley, F.
Bond, J. Booth, W. Branch, B.W.
Britton, W.A. Britton, E.W. Buckley, J.
Burgess, H.V. Burr, C.S. Burton, W.
Butler, W. Braund, W. Campbell, S.F.
Cooper, J.A. Carpenter, J. Chapman, C.
Cheesewright, J.P. Clark, E.G. Clements, J.C.
Coulter, W.H. Coyston, R.H. Craig, J.
Craig, G. Crowle, D.W. Cunningham, F.
Dart, C. Davies, C.S. Driukle, E.
Drinkle, G. Dionne, A. Dionne, G.
Dacking, W.J. French, W.E. Farrow, B.
Farrow, W.J. Fisher, W. Foster, W.H.
Fudge, W.J. Garbutt, S.E. Garrow, W.J.
Gibble, G. Gibbs, R. Gibson, J.
Gould, E.M. Dickie, G. Graham, P.
Gower, V.E. Grant, J.W. Griffiths, J.H.
Gyatt, O.J. Herrington, K. Hall, A.M.
Harding, C. Haynes, H.J. Hazard, A.J.
Hester, W. Hogarth, A.E. Horen, S.
Homes, J. Horsley, J. Hart, C.
Hort, C. Howard, A.G. Hull, W.H.
Hunking, H.H.H. Jeffries, A.E. Keyes, R.
Law, A.H. Livesey, G. Lowe, W.H.
Lucas, A.S. Luxon, C.N. Moore, H.
Meath, J. Morris, W.A. McCrimmon, N.
McCulloch, G. McGrail, F.J. MacInally, C.
McJarrow, R. Hull, W.H. McRae, J.
McMullen, J.W. Newman, T.E. Olson, W.
Owen, J. Parks, K.A. Patterson, A.
Pellolio, H. Percy, T.J. Phillips, A.E.
Phillips, P.J. Pogson, V.O. Purvis, J.
Powell, A.H. Parker, E. Reece, T.
Sayers, J. Schooling, J. Scott, T.
Slade, P. Smith, E.J. Smith, P.J.
Smith , R. Soloman, J.A. Stainton, E.S.
Stone, H. Taylor, C.H. Taylor, C.W.
Thomas, A. Travail, E. Trick, T.J.
Tratt, A.J. Tutton, A.N. Wright, E.
Waite, C. Walker, W.H. Walker, F.G.
Wallig, J.A. Wallis, A.E. Walmsley, J.H.
Waring, E. Ward, R. West, H.C.
White, C.L. White, J.R. White, J.R.
Willitts, A.W. Wilson, R.H. Wood, L.


Abstract: Free software is only one of a number of free projects that have arisen in the past. These projects tend to follow the creation of new technologies. Whether they persist after the commercialization of the technology depends both on the nature of the technology and the people and organization behind that project. Previous free hardware design projects include the homebrew computer designs of the 70s and the university-based IC design systems of the 80s. The new free hardware designs have been made possible by the introduction of ever larger integrated circuits and programmable logic devices, which have also made it possible to create a market in IC designs independent from manufacture. To survive past the consolidation of this market, free hardware design has to overcome a number of practical challenges, including defining its links with manufacture, finding a viable licensing system, and clarifying its relationship with free software.


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Dear Reader #71
Post author By Goylake Publishing
3 Comments on Dear Reader #71
I made great progress this week with the writing of Branches, book two in The Olive Tree, my Spanish Civil War saga, and the editing of Operation Broadsword is nearly complete. My thoughts are turning to Operation Treasure, book four in my Eve's War Heroines of SOE Series, and Stormy Weather, Sam Smith Mystery Series book eighteen, a novel about climate change.
Met some friends on the Bwlch this morning.
My latest translation, available soon, Invasion in Afrikaans. Also, delighted that Nelmari has agreed to translate Blackmail, book three in my Ann's War series.
'Potato' Jones, captain of the cargo steamer Marie Llewellyn. During the Spanish Civil War, 'Potato' Jones ferried 800 refugees to safety. In total Welsh sea captains ferried 25,000 refugees to safety.
He also delivered fuel, food, medicines, guns and ammunition to the anti-fascists in Spain, breaking the blockade at Bilbao.
Cardiff International Brigade veteran Tom Williams: "The fight for democracy in Europe is carried on by the British ships carrying predominantly Welsh crews, and we are known on the continent as the 'Welsh Navy'."
Eve is back at #1 🙂
Merthyr Mawr this week
It's a simple job, they said. We want you to wander down to Maddox Street and Conduit Street in Mayfair and attach the main telephone cable to a new support wire…
I'm reading George Orwell at the moment, his experiences in the Spanish Civil War. Very lyrical and insightful.
Meanwhile, no irony here…
With Joana and Sandra, started work on two new translations today, Mind Games, Sam Smith Mystery Series book eleven, into Portuguese and Operation Locksmith, Eve's War Heroines of SOE book two, into German. Great respect for translators and the talent they bring to these projects.
Hands up if you've said or heard these words 🙂
Responding to QI, the other followers said 'I'd won Tweet of the Day' and 'I'd won the Internet' with this comment 😂
Incidentally, I received well over 1,000 likes, which is easily a record for me.
I've completed Operation Broadsword, book three in my Eve's War Heroines of SOE Series, and now I'm looking forward to January 2021 and Operation Treasure, book four in the series, which is now available for pre-order.
https://www.amazon.com/dp/B08L9G7V4Z/
As ever, thank you for your interest and support.
Hannah xxx
Tags Books in Afrikaans, Books in German, Climate Change, French Resistance, George Orwell, Humour, Photography, QI, Second World War, Spanish Civil War, Special Operations Executive, Twitter, Victorians
← Dear Reader #70 → Dear Reader #72
3 replies on "Dear Reader #71"
BooksBy JJ.Hughessays:
So thrilled to read about your ongoing success every week, Hannah. You are an inspiration to many of us who aspire.
grantleishmansays:
OMG – I think my Mum said just about every one of those things at some time or another. Isn't it amazing how these sayings even span cultures. Awesome blog, as always, Hannah.
Reblogged this on Grant Leishman – Author.


The long, hot days of summer are the perfect excuse to dive into some wholesome and healthy salad recipes. My go-to salad throughout the summer is this wonderful salad that's as easy to make as it is delicious to eat. Okay, I'll admit it, this is probably my favorite salad … I make it all year long.
This is an easy salad to plan for, especially if you make the farmers markets a part of your weekly routine. Depending on the season, you can find most of the items available at any time. And with just a couple of items from your pantry, you'll be eating (and enjoying) in no time.
Cut kale into bite sized pieces, removing leaves from the stems. Cut yellow pepper into bit sized pieces. Cut cherry tomatoes in half.
Place kale into large bowl. Remove avocado from skin and gently massage into kale pieces. Avocado should easily blend into kale leaves.
Divide kale onto two plates. Equally distribute tomatoes and peppers onto plates. Crumble tempeh bacon into small pieces, and equally divide.
For the honey dressing: combine honey, coconut vinegar and dijon mustard in small bowl until well blended. Salt and pepper according to taste.
Spoon dressing over both salad plates.
i'm a vegetarian, but i woudln't really say it's healthier.when you eat meat, you are for sure getting your daily amount of protein.when your a vegetarian, its a lot harder to. the first month i was a vegetarian, i ended up in the hospital because i was so weak from lack of protein. it all depends on how committed you are going to be about this lifestyle, and if you make sure you get the needed protein. all in all, neither is really healthier than the other.but think of this: if you eat meat, your body is a graveyard of dead animals, all in which died just so you could devour them for your own health reasons. when in reality, you could get the same healthfulness of protein from other things that were never living.


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Q: Scrollbars behaving badly in auto-sizing boxes on IE7, FF and Chrome If anyone has a better idea for a title, I'm all ears.
Here's a JSFiddle that demonstrates the problem: http://jsfiddle.net/VXsAg/
In a nutshell, I have an element with fixed height and stretch-to-contents width. If the contents are higher than the fixed height, there should be a vertical scrollbar. There should also be ONLY vertical scrollbar, because horizontally it can stretch as much as is needed anyway. Unfortunately I cannot get it to work in a cross-browser compatible way. Here's what I get (the top box is for reference, the bottom box demonstrates the problem):
In IE8, IE9 and Opera 11.60 it appears like this (very good):

In IE7, Chrome 17 and Firefoxes 3 & 10 it appears like this (disaster):

I can see why it happens (width is calculated before scrollbars are taken into account), but how can I work around it?

A: Apparently nobody knows. Well, I solved it via javascript. Basically I did the autosizing part myself. I calculated the size of the contents; calculated the size of the scrollbar; and set the width explicitly.

redpajama_set_name: RedPajamaStackExchange


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Subcongenic Analysis of the Idd13 Locus in NOD/Lt Mice: Evidence for Several Susceptibility Genes Including a Possible Diabetogenic Role for β2-Microglobulin
David V. Serreze, Margot Bridgett, Harold D. Chapman, Emmie Chen, Scott D. Richard and Edward H. Leiter
J Immunol February 1, 1998, 160 (3) 1472-1478;
David V. Serreze
Margot Bridgett
Harold D. Chapman
Emmie Chen
Scott D. Richard
Edward H. Leiter
Although they share ∼88% of their genome with NOD mice including the H2g7 haplotype, NOR mice remain free of T cell-mediated autoimmune diabetes (IDDM), due to non-MHC genes of C57BLKS/J (BKS) origin. NOR IDDM resistance was previously found to be largely controlled by the Idd13 locus within an ∼24 cM segment on Chromosome 2 encompassing BKS-derived alleles for H3a, B2m, Il1, and Pcna. NOD stocks carrying subcongenic intervals of NOR Chromosome 2 were utilized to more finely map and determine possible functions of Idd13. NOR- derived H3a-Il1 (∼6.0 cM) and Il1-Pcna (∼1.2 cM) intervals both contribute components of IDDM resistance. Hence, the Idd13 locus is more complex than originally thought, since it consists of at least two genes. B2m variants within the H3a-Il1 interval may represent one of these. Monoclonal Ab binding demonstrated that dimerizing with the β2ma (NOD type) vs β2mb isoform (NOR type) alters the structural conformation, but not total expression levels of H2g7 class I molecules (e.g. Kd, Db). β2m-induced alterations in H2g7 class I conformation may partially explain findings from bone marrow chimera analyses that Idd13 modulates IDDM development at the level of non-hematopoietically derived cell types controlling selection of diabetogenic T cells and/or pancreatic β cells targeted by these effectors. Since trans-interactions between relatively common and functionally normal allelic variants may contribute to IDDM in NOD mice, the search for Idd genes in humans should not be limited to functionally defective variants.
Tcell-mediated autoimmune insulin-dependent diabetes mellitus (IDDM) in NOD mice is controlled by multiple susceptibility (Idd) genes both within and outside of the MHC (1, 2). Some Idd susceptibility genes, such as the H2-Abg7 MHC class II variant, may represent functionally aberrant alleles. The relatively rare H2-Ag7 MHC class II gene product is characterized by a β-chain that contains a histidine and serine residue at positions 56 and 57 in place of the more commonly observed proline and aspartic acid residues (3), and has been demonstrated to be a major contributor to the immunoregulatory defects underlying development of T cells autoreactive against insulin-producing pancreatic β cells (4, 5, 6, 7). The diabetogenicity of H2-Ag7 is further enhanced by the absence of H2-E MHC class II molecules on NOD Ag-presenting cells (APC) due to a deletion in the H2-Ea gene. This latter mutation is present in a number of other H2-E-negative inbred strains, but is not inherently diabetogenic in the absence of H2-Ag7 MHC class II molecules. Thus, not all Idd susceptibility genes necessarily represent deleterious mutations unique to the NOD mouse, but rather may be common allelic variants that have coalesced in an unfavorable array with the diabetogenic H2-Abg7 allele (8).
That common allelic variants can acquire a diabetogenic function is best illustrated by the fact that while the Kd and/or Db class I gene products encoded by the H2g7 MHC haplotype of NOD mice are also expressed by many strains without obvious autoimmune proclivity, they play an essential role in the development of IDDM. This was demonstrated by the finding that NOD mice made deficient in MHC class I expression by congenic transfer of a functionally inactivated β2-microglobulin (B2m) allele (designated NOD.B2mnull mice) remain completely free of IDDM (9, 10, 11, 12). We subsequently found this is due to the fact that the earliest initiative phases of autoimmune β cell destruction in NOD mice are mediated by CD8+ T cells that recognize Ags presented by the common Kd and/or Db class I gene products of the H2g7 MHC haplotype (13). IDDM is also inhibited in a stock of NOD mice congenic for the MHC haplotype of the CTS strain (H2ct) that shares the class II, but not the class I alleles, of the H2g7 haplotype (14). Thus, it appears that rather than developing at a high frequency in the presence of any MHC class I molecules, autoimmune IDDM in NOD mice is most readily promoted by expression of the particular class I alleles that constitute the H2g7 haplotype. Similarly, recent evidence indicates that some relatively common MHC class I variants, such as HLA-A2, may also contribute to enhanced IDDM susceptibility in humans (15, 16). The mechanism by which relatively common MHC class I gene products can acquire diabetogenic activity in both humans and NOD mice remains unknown. However, it seems likely that they do so through interactions with non-MHC associated Idd susceptibility alleles, many of which may also represent physiologically normal variants found in humans and mouse strains characterized by IDDM resistance.
Insights to diabetogenic interactions between MHC and non-MHC genes have been provided by analysis of IDDM-resistant NOR mice. The NOR/Lt strain is a recombinant congenic stock that derives ∼88% of its genome from NOD including the H2g7 MHC haplotype, but contains genetic material of C57BLKS/J (BKS) origin on regions of chromosomes (Chr.) 1, 2, 4, 5, 7, 11, 12, and 18 (17, 18). The BKS strain itself represents a recombinant congenic strain, carrying defined genomic contributions primarily from a C57BL/6 (B6) donor, but also from a "DBA/2-like" donor (19). Constitutive levels of MHC class I expression in NOD and NOR mice are equivalent to that of the BKS control strain (20). However, the ability of macrophages from NOD and NOR mice to futher up-regulate expression of H2g7 MHC class I molecules in response to stimulation with IFN-γ is differentially controlled by genes within chromosomal regions distinguishing these two strains. IFN-γ fails to up-regulate H2g7 MHC class I expression in macrophages from NOD mice, but does so normally in NOR macrophages (20). The failure of NOD macrophages to up-regulate MHC class I expression in response to IFN-γ could diminish the capacity of these APC to activate tolerogenic mechanisms that normally delete or inactivate diabetogenic CD8+ T cells. Autoreactive CD8+ T cells that are generated as a result of such tolerogenic defects in NOD mice could then be efficiently targeted to the pancreatic β cells, since these cells regulate H2g7 MHC class I expression in a normal fashion.
(NODxNOR)F2 segregation analysis demonstrated that the major genetic component contributing to IDDM resistance in NOR is the Idd13 locus on Chromosome 2 in linkage with BKS-derived genes for β2m, both isoforms of IL-1 (Il1a and Il1b), and proliferating cell nuclear Ag (Pcna)(18). Existence of the Idd13 locus was confirmed by the induction of IDDM resistance in a stock of NOD mice congenic for an ∼24 cM segment of NOR Chromosome 2 that contains these linkage markers flanked by the H3a minor histocompatability and adenosine deaminase (Ada) genes (18, 21). However, it is unknown which gene(s) within this segment of Chromosome 2 contributes to IDDM susceptibility in NOD and resistance in NOR mice, and if this effect is mediated through a modulation of H2g7 MHC class I expression or function. The present study was conducted to gain insight to these questions through an analysis of IDDM development and H2g7 MHC class I expression and function in NOD stocks carrying variable truncations of the originally defined congenic segment of NOR Chromosome 2 found to confer Idd13-mediated resistance.
NOD/Lt and NOR/Lt mice (both H2g7 = Kd, Ag7, Enull, Db) have been maintained at The Jackson Laboratory by brother-sister mating. Currently, IDDM develops in 90% of female and 63% of male NOD/Lt mice by one year of age, whereas both sexes of NOR/Lt mice are IDDM resistant. A stock of NOD mice carrying a previously defined congenic segment of NOR Chromosome 2 conferring Idd13-mediated IDDM resistance was initially utilized at the N12 backcross generation (18, 21). To further refine the localization of genes contributing to IDDM resistance within the NOR-derived Idd13 locus, the Chromosome 2 congenic segment present in this N12 stock was variably truncated by further backcrossing to the NOD parental strain. Backcross mice were screened for further recombination events on Chromosome 2 using the genotyping methodologies described below. At the 20th backcross (N21) generation, the indicated NOR-derived Chromosome 2 congenic segments were fixed to homozygosity on the NOD background by brother-sister matings. C57BLKS/J (H2d) mice were supplied by the Animal Resources Unit of The Jackson Laboratory. All mice were maintained under specific pathogen-free (SPF) conditions and allowed free access to autoclaved chow diet (diet 96WA, Emory Morse, Guilford, CT.) and acidified drinking water.
Assessment of diabetes and insulitis development
Mice from each of the indicated strains were simultaneously monitored at weekly intervals for the development of glycosuria with Ames Diastix (kindly supplied by Miles Diagnostics, Elkhart, IN). Glycosuric values of ≥3 were considered diagnostic of diabetes onset. Development of stable glycosuria was confirmed by weekly urinalysis for 2 weeks after the initial diagnosis. A subset of non-diabetic mice were necropsied for pancreatic histology at 1 year of age. Pancreata were stained with aldehyde fuchsin to detected granulated β cells and then counterstained with hematoxylin and eosin.
Genotyping methodologies
DNA samples used for genotypic analyzes were extracted from tail clips. Most polymorphic markers were typed either by PCR or Southern blotting as previously described (18, 22). Allelic variations at the H3a minor histocompatibility gene were typed as previously described (21) by assessing the sensitivity of splenic leukocytes from the various congenic stocks to lysis by cloned lines of gene product-specific cytotoxic T-lymphocytes (CTL).
Effect of B2m polymorphisms on the conformation of MHC class I molecules expressed by splenic leukocytes
Splenic leukocytes from the indicated strains were prepared as previously described (23), and resuspended at 2 × 107/ml in FACS buffer (PBS containing 0.1% sodium azide with 2% FBS). Aliquots of 1 × 106 cells (50 μl) were incubated for 30 min at 4°C with FITC-conjugated mAbs specific for the allelically variable regions of the H2Kd (SF1–1.1) or H2Db (28–14–4) MHC class I molecules, or an epitope within the MHC class I constant region that undergoes dimerization with β2m (M1/42) and is shared by all alleles. The cells were washed in FACS buffer after staining. Data for the extent of MHC class I Ab binding are presented as mean channel of log fluorescence (MFI) ± SEM, as determined by FACScan (Becton Dickinson, San Jose, CA.) using the Cell Quest 3.0 data reduction program.
Regulation of MHC class I expression by IFN-γ in peritoneal macrophage cultures
Thioglycollate-elicted peritoneal macrophages were isolated from the indicated male mice using our previously described protocols (20). Macrophages were suspended at 2.0 × 106/ml in the previously described culture medium (23) in the presence and absence of 50 U/ml rat recombinant IFN-γ (kindly supplied by P. van de Meide, Rijswijk, Netherlands) and then incubated for 6 days at 37°C. At this time macrophages were harvested by washing with calcium- and magnesium-free HBSS and subsequent treatment with enzyme-free cell dissociation buffer (Life Technologies, Gaithersburg, MD). To assess IFN-γ-regulated levels of cell surface MHC class I expression, the macrophages were stained with the FITC-conjugated mAb 31–3–4S that recognizes the Kd MHC class I molecule shared by all of the strains used for these experiments. Levels of total Kd MHC class I expression in IFN-γ-treated and untreated macrophages are presented as MFI as determined by FACScan analysis.
Production of bone marrow chimeras
Females from the indicated strains were lethally irradiated (1200R from a 137Cs source) at 4 wk of age, and then reconstituted as previously described (24) with 5 × 106 bone marrow cells isolated from the indicated 8-wk-old female donors. Bone marrow chimeras were then monitored through a 21-wk postreconstitution for the development of IDDM as described above. Upon the onset of IDDM or at 21 wk of postreconstitution, chimerization was assessed by genotyping splenic DNA for donor or recipient type B2m polymorphisms by Southern blot analysis of a BglI restriction fragment length variant (B2ma = 801 bp fragment; B2mb = 575 and 226 bp fragments). A B2m-specific probe was generated by PCR amplification of C57BL/10J genomic DNA with the primer set 5′-CACGCCACCCACCGGAGAATG-3′ and 5′-GATGCTGATCACATGTCTCG-3′.
IDDM development in NOD mice congenic for various intervals of NOR Chromosome 2-carrying Idd13 resistance alleles
As shown in Table I⇓, three congenic intervals derived from NOR Chromosome 2 were fixed to homozygosity on the NOD inbred background at the 20th backcross generation. The first of these congenic stocks carries the largest segment of NOR Chromosome 2 spanning a ∼31.5 cM interval encompassing the linkage markers D2Mit490 through D2Mit144 (designated NOD.D2Mit490-Mit144NOR). This large congenic segment contains all markers previously found to be linked to Idd13-mediated IDDM resistance in NOR mice (18). This segment of NOR-derived Chromosome 2 is originally derived from the B6 strain contribution to the BKS genome (18) such that the H3aa and B2mb alleles, as well as the microsatellite-based markers are the same as found in the B6 genome. The present analysis extends the proximal boundary of this NOR-derived Chromosome 2 congenic segment by ∼4 cM to the D2Mit490 rather than the H3a marker, and the distal boundary by ∼3 cM to D2Mit144 rather than Ada. Smaller intervals derived from this large segment of NOR Chromosome 2 through selection of recombinants have been fixed to homozygosity in two other NOD congenic stocks. One of these carries an ∼6.0 cM congenic interval of NOR Chromosome 2 spanning the linkage markers H3a through Il1a (designated NOD.H3a-Il1NOR). The other carries an ∼1.2 cM segment of NOR Chromosome 2 spanning the interval delineated by Il1a and Pcna (designated NOD.Il1-PcnaNOR).
Table I.
Comparative lengths of NOR-derived Chromosome 2 congenic segments crossed to the NOD genetic background
As shown in Figure 1⇓, by 30 wk of age the female incidence of IDDM in the NOD.D2Mit490-Mit144NOR congenic stock (16%) was significantly less than in standard NOD mice (100%). By 52 wk, IDDM incidence in these congenic females had increased to only 26% (5 of 19), and no diabetes was observed in a group of 18 NOD.D2Mit490-Mit144NOR congenic males (compared with 50% incidence in a group of 18 standard NOD/Lt males). Histologic analysis of insulitis in pancreata from of three of these non-diabetic congenic mice of each sex necropsied at a year of age showed widespread perivascular/periductular leukocytic infiltrates. When associated with islets, these were primarily peri-insular, with granulated β cell mass largely preserved in >80% of the islets. This histopathology was similar to that observed in year-old NOR/Lt mice of both sexes. This confirmed the results originally observed at an earlier backcross generation (18) that Idd13-mediated IDDM resistance in NOR mice did not prevent the pancreatic T-lymphoaccumulation characteristic of NOD mice, but rather retarded activation of autoimmune effector functions. In this regard, the pancreatic histopathology in non-diabetic NOD.D2Mit490-Mit144NOR congenic mice was very reminiscent of that observed in a NOD stock made IDDM resistant through the elimination of B-lymphocyte development by congenic transfer of a null mutation in the Igμ heavy chain locus (25).
IDDM susceptibility or resistance is controlled by multiple genes within the originally defined Idd13 locus on Chromosome 2. IDDM development was assessed in stocks of female NOD mice in which various congenic intervals derived from NOR Chromosome 2 were fixed to homozygosity at the 20th backcross generation. Symbols: NOD (▪, n = 18), NOD.D2Mit490-Mit144NOR (□, n = 19), NOD.H3a-Il1NOR (•, n = 17), NOD.Il1-PcnaNOR (○, n = 21). * IDDM incidence significantly less (p < 0.0001, Kaplan Meier life table analysis) than in standard NOD mice. †IDDM incidence significantly greater (p < 0.003, Kaplan Meier life table analysis) than in the congenic NOD.D2Mit490-Mit144NOR stock.
Evidence that the Idd13 locus is genetically more complex than initially reported was provided by the finding that the strong IDDM resistance conferred by an ∼31.5 cM region of NOR Chromosome 2 spanning D2Mit490 through D2Mit144 was partially attenuated upon differential truncation of this interval in two subcongenic stocks of NOD mice (Fig. 1⇑). By 30 wk of age, the female incidence of IDDM in both the NOD.H3a-Il1NOR (56%) and NOD.Il1-PcnaNOR (62%) congenic stocks was significantly lower than in standard NOD mice, but significantly higher than in the NOD.D2Mit490-Mit144NOR congenic stock. Similarly, the male incidence of IDDM in these two subcongenic stocks was significantly less than that observed in standard NOD mice. By a year of age, the cumulative incidence of IDDM in the NOD.H3a-Il1NOR stock reached 62% (10 of 16) in females and 25% (4 of 16) in males. In the NOD.Il1-PcnaNOR stock, IDDM developed in 75% (9 of 12) of females and 12% (2 of 17) of males by 46 wk of age. Thus, the H3a-Il1 and/or Il1-Pcna intervals on Chromosome 2 carry at least one, but not the complete set of polymorphic genes contributing to Idd13 locus-mediated IDDM susceptibility in NOD and resistance in NOR mice.
Contributions of the Idd13 locus to differential regulation of H2g7MHC class I expression in IFN-γ-stimulated macrophages from NOD and NOR mice
While no defects in constitutive expression were observed, our previous studies demonstrated that IFN-γ stimulation fails to further up-regulate H2g7 MHC class I levels in NOD macrophages (20). Such a defect could conceivably reduce the ability of these APC in NOD mice to activate tolerogenic mechanisms that normally delete or inactivate diabetogenic CD8+ T cells. We hypothesized that this possible APC tolerogenic defect might be controlled by a gene(s) within the Idd13 locus since H2g7 MHC class I expression is up-regulated normally in IFN-γ-stimulated macrophages from IDDM-resistant NOR mice. To test this hypothesis, we compared the pattern of IFN-γ-regulated MHC class I expression in macrophages from the NOD.D2Mit490-Mit144NOR congenic stock at the N12 backcross generation to similarly treated macrophages from NOD, NOR, and BKS control mice. The BKS strain that has provided the genetic source of IDDM resistance to the NOR strain is characterized by the standard H2d haplotype, and thus expresses a Kd MHC class I gene product also encoded within H2g7. As expected, FACS analysis utilizing the Kd specific mAb 31–3–4S confirmed that expression of this MHC class I molecule was up-regulated normally in IFN-γ-treated macrophages from both NOR and BKS control mice (Fig. 2⇓). However, as previously observed, IFN-γ stimulation failed to up-regulate Kd expression in NOD macrophages. Stimulation with IFN-γ also failed to up-regulate Kd expression in macrophages from the NOD.D2Mit490-Mit144NOR congenic stock. While not excluding the possibility that aberrant regulation of MHC class I expression in IFN-γ-stimulated macrophages contributes to autoimmune IDDM susceptibility in NOD mice, these results conclusively demonstrate that this defect is not controlled by the Idd13 locus on Chromosome 2.
The Idd13 locus does not contribute to the failure of IFN-γ-stimulated NOD macrophages to up-regulate MHC class I expression. Peritoneal macrophages from NOD.D2Mit490-Mit144NOR congenic males at the N12 backcross generation or NOD, NOR, and BKS control males were cultured for 6 days in the presence or absence of 50 U/ml IFN-γ. Data represent mean fluorescence intensity (MFI) for binding of the FITC-conjugated mAb 31–3–4S that recognizes the Kd MHC class I molecule shared by all of these strains. White bars represent Ab staining of macrophages cultured in medium only, and black bars represent Ab staining of macrophages cultured with IFN-γ. Similar results were obtained in a second experiment.
Effect of dimerization with different isoforms of β2m on the expression levels and structural conformation of H2g7MHC class I molecules
We have previously found that the relatively common MHC class I gene products of the H2g7 haplotype (e.g., Kd and/or Db) mediate T cell responses essential to the initiation of autoimmune IDDM in NOD mice (11, 13). It is likely that these same H2g7 MHC class I molecules do not mediate diabetogenic T cell responses in NOR mice, due to functions exerted by resistance variants of non-MHC Idd genes. It has been reported that interacting with different isoforms of β2m may lead to alterations in the structural conformation of MHC class I molecules (26, 27, 28), which can skew the array of Ags they bind and present to CD8+ T cells (29). The B2m gene maps within the H3a-Il1 interval on Chromosome2, which we have shown to contain at least one component of Idd13. Thus, the β2m isoforms distinguishing NOD (β2ma) from the B6-derived allele present in NOR mice (β2mb) may respectively provide one component of Idd13-mediated IDDM susceptibility or resistance through an ability to differentially alter the structural conformation, and hence the function of H2g7 MHC class I molecules shared by these two strains.
To test this possibility, splenic leukocytes from NOD mice plus the NOD.H3a-Il1NOR, and NOD.Il1-PcnaNOR congenic stocks were stained with FITC-conjugated mAbs specific for allelically variable regions of the Kd (SF1–1.1) and Db (28–14–8) H2g7 MHC class I gene products, or an epitope within the MHC class I constant region shared by all allelic variants that undergoes dimerization with β2m (M1/42). As shown in Table II⇓, the Kd and Db allele-specific Abs bound equivalently to splenocytes from NOD mice and both NOD stocks congenic for intervals of NOR Chromosome 2 carrying partial sets of Idd13 resistance alleles. However, the level of M1/42 binding to the constant region of these MHC class I molecules was significantly different on β2mb positive splenocytes from the NOD.H3a-Il1NOR congenic stock than on β2ma positive splenocytes from NOD mice or the NOD.Il1-PcnaNOR congenic stock. Thus, while the total expression levels of H2g7 MHC class I molecules are equivalent on splenocytes from NOD mice and both NOD stocks congenic for intervals of NOR Chromosome 2 carrying partial sets of Idd13 resistance alleles (based on Kd and Db allele-specific staining), the structural conformation of these molecules (assessed by M1/42 staining) appears to differ depending on the isoform of β2m with which they have dimerized.
Table II.
H2g7 MHC class I molecules differ conformationally when associated withβ2ma (NOD type) andβ2mb (NOR type)
Contributions of the Idd13 locus to the selection and targeting of diabetogenic T cells
The studies described above demonstrated that dimerization with different isoforms of β2m may alter the structural conformation of H2g7 MHC class I molecules. Such B2m-controlled alterations in the structural conformation of H2g7 MHC class I molecules expressed on cell types regulating the original selection of diabetogenic T cells (thymic epithelium and hematopoietically derived APC) and/or on the pancreatic β cells targeted by these autoreactive effectors may represent one mechanism by which the Idd13 locus contributes to IDDM susceptibility or resistance. This possibility was tested by assessing IDDM development in a series of bone marrow chimeras in which Idd13 susceptibility or resistance variants could be differentially expressed in cell types controlling T cell selection and in pancreatic β cells. As expected, IDDM developed in 75% of NOD females over a 21-wk period following reconstitution with syngeneic NOD marrow (Table III⇓). However, reconstitution with NOD bone marrow elicited a significantly lower incidence of IDDM (15.4%) in NOR females. Conversely, reconstitution with NOR marrow elicited a significantly higher incidence of IDDM in NOD (55.5%) than in syngeneic NOR female recipients (0%). Thus, some portion of the Idd susceptibility or resistance variants distinguishing NOD from NOR mice control functions in non-hematopoietically derived cell types that regulate the development and/or functional activation of the diabetogenic T cells that normally differentiate from NOD bone marrow. Providing support that Idd13 variants are at least partial contributors to this process was the finding that reconstitution with NOD bone marrow resulted in a significantly lower incidence of IDDM in NOD.D2Mit490-Mit144NOR (37.5%) than in syngeneic NOD female recipients (75%). Furthermore, IDDM developed in 77.8% of standard NOD females reconstituted with NOD.D2Mit490-Mit144NOR marrow. This was significantly greater than the IDDM incidence in NOD.D2Mit490-Mit144NOR recipients of syngeneic marrow (26.7%), but did not differ from that of NOD recipients reconstituted with syngeneic marrow.
Table III.
Idd13 is expressed in non-hematopoietically derived cell types and affects the selection and/or functional activation of β cell autoreactive T cellsa
We have previously demonstrated that the major genetic component contributing to T cell-mediated autoimmune IDDM susceptibility in NOD mice vs resistance in the H2g7 identical NOR strain is the Idd13 locus on Chromosome 2 (18). The present study demonstrates that multiple polymorphic genes within the originally defined Idd13 locus contribute to IDDM susceptibility or resistance. Our data demonstrates that the Idd13 locus does not contribute to autoimmune IDDM by controlling the previously described phenotype of defective vs normal trans-regulation of IFN-γ-stimulated H2g7 MHC class I expression in hematopoietically derived macrophages from NOD and NOR mice (20). Indeed, the present studies indicate that at least some portion of the multiple genes contributing to Idd13-mediated IDDM susceptibility or resistance exert their effects in non-hematopoietically derived cell types. These could include thymic epithelial cells contributing to the original selection of the T cell repertoire, and/or the pancreatic β cells targeted by autoreactive T cells in IDDM. Along these lines it should be noted that Idd13 represents the first locus we have found that does not exert a pathogenic or protective effect at the level of hematopoietically derived cell types (30).
The H3a-Il1 and Il1-Pcna intervals on Chromosome 2 carry at least one, but not the complete set, of polymorphic genes contributing to Idd13-mediated IDDM susceptibility in NOD and resistance in NOR mice. Since the H3a-Il1 and Il1-Pcna intervals overlap, it is possible that they share a gene contributing to IDDM susceptibility or resistance. One seemingly good candidate would be the structural genes for both isoforms of IL-1 that are contained within both of these intervals. Their candidacy is based on the findings that NOD macrophages are poor producers of IL-1 (23, 31), and that IDDM is inhibited in NOD mice treated with IL-1 in vivo (31). However, arguing against the candidacy of NOD-derived Il1 alleles as contributors to IDDM is that despite the presence of BKS-derived Il1 variants, macrophages from NOR mice are also defective in IL-1 production (17). The unlikely contribution of Il1 variants to IDDM susceptibility or resistance supports the possibility that H3a-Il1 and Il1-Pcna intervals carry separate components of Idd13. However, regardless of whether the H3a-Il1 and Il1-Pcna intervals are characterized by shared or different Idd genes, it remains possible that additional polymorphic genes outside of these regions, but within the larger segment flanked by D2Mit490 and D2Mit144, also contribute to Idd13-mediated IDDM susceptibility or resistance. Subcongenic analysis of the Idd10 region on Chromosome 3 (32) and the Idd2 region on Chromosome 9 (this laboratory, unpublished) are similarly providing evidence that Idd loci initially inferred to be composed of single genes in fact represent contributions from multiple genes.
Within the H3a-Il1 interval, allelic variants of B2m represent an excellent candidate for representing one component of Idd13-mediated IDDM susceptibility in NOD and resistance in NOR mice. The β2ma (NOD type) and β2mb (NOR type) isoforms exert trans-acting effects that alter the structural conformation, but not the total expression levels, of H2g7 MHC class I molecules shared by NOD and NOR mice. Such alterations in the structural conformation of H2g7 MHC class I molecules elicited by dimerization with different isoforms of β2m may skew their ability to bind and present certain Ags, and hence contribute to IDDM susceptibility or resistance by effecting the selection and/or targeting of β cell autoreactive CD8+ T cells. Support for this possibility is provided by previous reports that dimerization with different β2m isoforms can alter the structural conformation of MHC class I molecules (26, 27, 28), which may in turn skew the array of antigenic peptides they bind and present to CD8+ T cells (29). Our bone marrow chimera studies indicate that any such effects are manifest at the level of non-hematopoietically derived thymic epithelial cells contributing to the original selection of the T cell repertoire, or at the level of pancreatic β cells targeted by autoreactive T cells in IDDM. Supporting this hypothesis is that in retrospect, all nominally resistant mouse stocks that developed IDDM following reconstitution with NOD marrow have been at least heterozygous for the B2ma allele (24, 33, 34, 35, 36, 37). Further evidence that heterozygous expression of the B2ma allele may be sufficient to support IDDM development is provided by our previous finding that the NOR-derived Idd13 locus (containing B2mb) can only inhibit disease when in the homozygous state (18). It should also be noted that neither the B2ma or B2mb variant can be considered to represent a deleterious mutant allele since the gene products encoded by both function normally in terms of mediating the transport to and stable expression of MHC class I molecules on cell surfaces. Thus, if future studies ultimately demonstrate that B2m variants represent actual Idd susceptibility and resistance alleles, it would strongly support the previously proposed hypothesis (8) that autoimmune IDDM is not produced by rare mutations, but rather a set of common genetic variants that have coalesced in a dysfunctional array.
The present findings in no way support previous assertions by a single laboratory (38, 39, 40) that NOD splenic leukocytes are characterized by aberrantly low constitutive levels of MHC class I molecules as a consequence of defects in expression of the intra-MHC Tap1 gene. None of the findings from this aforementioned laboratory have been replicated by other investigators (10, 11, 20, 41, 42, 43, 44, 45). The erroneous conclusion that constitutive MHC class I expression was decreased can be explained by the fact that T lymphocyte numbers, which normally express lower levels of class I than other other leukocyte populations, are proportionally increased in NOD lymphoid organs relative to that observed in diabetes-resistant strains (42, 44). A polymorphism in an intron of the NOD Tap1 gene was shown by others not to affect loading of Ag to MHC class I molecules or their presentation to CTLs (21, 46). The conclusion that mice lacking a functional B2m gene developed spontaneous autoimmune diabetes (38) has also not been replicated (9, 10, 11, 12). As emphasized above, NOD and NOR mice are H2g7-identical, and thus share the same Tap genes. Neither strain is β2m deficient; the allelic polymorphism distinguishing NOD from NOR entails a single amino acid difference at position 85 (47). Dimerization with these subtly different isoforms of β2m may affect the structural conformation of the H2g7 MHC class molecules, but not their overall (normal) level of expression.
In conclusion, our studies have demonstrated that multiple polymorphic genes within the originally defined Idd13 locus on Chromosome 2 contribute to IDDM susceptibility in NOD mice and resistance in the H2g7 identical NOR strain. It is possible that normal allelic variants of B2m represent one component of Idd13 through an ability to differentially alter the structural conformation of the relatively common H2g7 MHC class I molecules and hence promote or inhibit their ability to select and/or target diabetogenic T cells. If correct, this would indicate that some of the processes that underlie the development of autoimmune IDDM in NOD mice are controlled by trans-interactions between relatively common and functionally normal allelic variants. That trans-interactions between relatively common and functionally normal allelic variants may contribute to autoimmune IDDM in NOD mice indicates that the search for Idd genes in humans should not be limited to functionally defective variants.
↵1 This work was supported by National Institutes of Health Grants DK46266, DK51090, and AI41469 (D.V.S.), DK36175 and DK27722 (E.H.L.), as well as by grants from the Juvenile Diabetes Foundation International, and Cancer Center Support (CORE) CA34196.
↵2 Address correspondence and reprint requests to Dr. David V. Serreze, The Jackson Laboratory, Bar Harbor, Maine 04609.
Accepted October 9, 1997.
Copyright © 1998 by The American Association of Immunologists
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David V. Serreze, Margot Bridgett, Harold D. Chapman, Emmie Chen, Scott D. Richard, Edward H. Leiter
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Ever wonder what the most popular meat is in the world? Yeah, I know, that's a random thought. And, there's debate on that and different opinions, so research on and dig deeper if you want to know. Here in the United States my white meat of choice is chicken. And, my red meat of choice is beef. Some think that goat meat is the most popular meat in the world. But, the Huffington Post is challenging that belief. I really haven't eaten a lot of goat meat in my life, but I admit, I do have some goat meat stew chunks in my freezer. They came from a local rancher here in Colorado, and I can't wait to use it!
Regardless of the debate or thoughts, for me, as I said, I'm a chicken lover. And, I'm always looking for ways to prepare chicken in new simple creative tasty ways that highlights this bird's wonderful flavors. One thing I do when purchasing chicken is look for organic chicken. I love all cuts of chicken. Bone in. Filets. Skin on. Skinless. Legs. Thighs. Wings. Even the carcasses that provide me with an amazing chicken stock!
Now this cast iron skillet chicken caprese is an example of a dish that is bursting with flavor. Shining with beauty. And, exploding with great versatility! It's kind of like chicken parmesan but without all the breading. So, you're saving some major calories and carbs. Like a lot of stews, soups and sauces, this chicken caprese is even tastier and more delicious the next day, so if there's any leftover then you know what lunch is gonna be!
Rinse and pat dry with paper towels the chicken breasts. Coat both sides with cooking spray then sprinkle both sides with salt and pepper.
Put the onion soup/dip mix and water in a large measuring cup. Whisk together well.
Place a large cast iron skillet (10"+) on a medium high blaze. Let it get hot. Coat well with cooking spray. Put the chicken in and let it pan sear about 3-4 minutes on each side. Use tongs to remove the chicken to a plate.
Add the chicken back to the skillet. Put the tomatoes on top of the chicken. Let the mixture cook (starting to simmer boil), stirring occasionally, for about 20 to 25 minutes.
Cover with a lid. Reduce heat to simmer. When ready to serve add the basil on top the tomatoes. Serve with pasta, mashed potatoes, rice or your favorite side!


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My husband and I had the pleasure of working with Rob on two occasions, to buy our dream house and sell our old condo. With both processes he was patient, thorough, and so helpful. We literally didn't know that the excellent area we live in existed until Rob showed us around a relatively new location. He is an expert at assisting home buyers for new construction, a daunting process but went smoothly with Rob. We cannot thank him enough for going the extra mile to sell our old condo when we were unable to do much with a newborn at home.
We have been very pleased with his professionalism and honesty. He was always available for whatever schedule or request we had. We were from out of state, so the entire process of us looking took months. Rob would keep us updated through email, text or telephone as necessary. He would respond quickly to our questions. Once we decided on a house, he led us through the offer, purchase and closing. Along the way he recommended a mortgage broker that we were very happy with. At no point did he become impatient or pushy about our continued house hunting or indecision. We have been very pleased with his performance throughout the entire process.
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text:
package io.github.helvalius.boids.boid.rule;

import io.github.helvalius.boids.boid.IRule;
import io.github.helvalius.boids.data.Boid;
import io.github.helvalius.boids.data.Vector;
import io.github.helvalius.boids.data.VectorMath;

import java.util.List;

public class Separation implements IRule {
    private final double DISTANCE;

    public Separation(double distance) {
        this.DISTANCE = distance;
    }

    @Override
    public Vector consider(Boid b, List<Boid> flock) {
        final Vector change = Vector.zero();
        flock
            .stream()
            .filter(otherBoid -> !otherBoid.equals(b))
            .filter(otherBoid -> otherBoid.isInDistance(b,DISTANCE))
            .forEach(otherBoid -> {
                change.subtract( VectorMath.sub(otherBoid.getPosition(), b.getPosition()));
            });

        return change.div(8);
    }
}

redpajama_set_name: RedPajamaGithub


text:
News & Media Hawker tells court it may reduce jet products
Hawker tells court it may reduce jet products
June 18, 2012 By Alton K. Marsh
The Wichita Eagle has received an April court document from the bankruptcy filing of Hawker Beechcraft detailing its options for reorganizing. The company has previously indicated that an option to take bids and sell the company was just a routine formality, although the bids have been received by the bankruptcy court but are undisclosed.
All three options for a reorganized, and still independent, Hawker Beechcraft call for keeping the military aircraft (King Airs and the T-6 Texan II trainer/ground attack aircraft) and piston aircraft, along with the commercial King Air line. None of the plans as reported by the The Wichita Eagle's Molly McMillan would keep the Premiere or its upgraded cousin, the Hawker 200. The 200 was shown as a mockup last year during the National Business Aviation Association convention in Las Vegas.
One option takes Hawker Beechcraft out of the jet market altogether, while two options eliminate the Hawker 4000. The venerable $700,000 Bonanza, developed in the late 1940s, and the $1.2 million Baron both survive under all scenarios.
Topics: Aviation Industry
Delta drops degree requirement for pilot applicants
Sonex employee purchases the company


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text:
Q: Does Loop Quantum Gravity predict general relativity in semi-classical Limit? Recently i read about Loop Quantum Gravity in Wikipedia and found this below statement here.

Presently, no semiclassical limit recovering general relativity has been shown to exist.

But i also came across a paper in arxiv whose abstract claims that Einstein's equations arise as a result of Semi-Classical Limit from Covariant Loop Quantum Gravity.

In this paper we explain how 4-dimensional general relativity and in particular, the Einstein equation, emerge from the spinfoam amplitude in loop quantum gravity.

So is the Wikipedia article outdated or is the paper's idea falsified?

A: The confusion arises because there are essentially two different approaches to the LQG dynamics in the literature.
The canonical approach pioneered by Thiemann is to define the matrix elements of the Hamiltonian constraint operator acting on spin networks, and then postulate the kernel of that operator to be the physical Hilbert space of LQG. It is extremely hard to make any physical predictions with this mathematical object as it is so extremely complex. However, it is possible to prove that it is mathematically well defined.
The spinfoam approach is based on the so-called EPRL spinfoam model, which is what the paper you linked talks about. It indeed reproduces General Relativity (or rather its triangulated version – the Regge theory, which becomes General Relativity when the triangulation is refined) in the $\hbar \rightarrow 0$ limit if the boundary states are taken to be the coherent (semiclassical) Livine-Speziale states. Rovelli has a nice chapter with a detailed calculation in his textbook called "Covariant Loop Quantum Gravity".
The spinfoam formulation, unlike the canonical formulation, has not been made into a mathematically well-defined and consistent formalism so far. Due to infrared divergences, it isn't clear whether the projective limit of spinfoam amplitudes exists or not, and whether, if it does exist, it specifies a projection operator onto the physical state space of quantum gravity.
This situation is a lot like the one in perturbative QFT. The theory gives meaningful physical predictions, but so far no one has been able to prove that this theory exists mathematically.

A: About a decade ago, Ashoke Sen did some calculations that show that you can use Euclidean methods compute the logarithmic corrections to the entropy of Schwarzchild black holes in terms of low-energy, classical data.  He remarked that these entropies had also been calculated within loop quantum gravity, and that the results do not match the answer.  This strongly suggests that LQG does not give the correct semi-classical limit.


Call Sucré Sweets and Socials at 309-291-5065.
We're located at 321 S. First Avenue in Morton, Illinois. Our location sits next to Memorial Park between Main Street and First Avenue. Parking is available in our parking lot and along First Avenue.


Thursday night my collegue and good friend Matt joined us in Rio and we decided that after a few days on the beaches of Ipanema and Copacabana it was time for some sightseeing again. Pao de Acucar or Sugra Loaf is almost as famous as Christ The Redeemer statue on Corcovado and much more enjoyable if you ask me. From city center you take the cablecars up the first mountain and from here you can wander around in lush green enviroment with a stunning view of Rio and the ocean and islands surrounding Rio. We stopped for some fresh fruits and lunch and enjoyed the peece and quiet away from the never ending Rio traffic. Further we took the second cablecar up to Sugar Loaf and got some even more stunning views of Rio. Sun was shining, temperatur of about 34deg and hanging out with good friends. Cannot complain! Life is not so bad!
Her er det østlig storm på vei og meldt opptil 50cm snø.


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Most of the time, here, with these mostly quite "first drafts" I am to a chosing of a "title" first and then to a sticking with the title. Today I have no idea how to title thoughts, yet.
And, now I have figured out a way to title an untitled.
And, now I have figured out that is what I was/am to a writting to - "untitle the titled?" - "title the untitled?"
Quite an oddity and yet an "oddity - in character, for Clintons" could still be said to be such that I may have heard the best speach from the Senate floor by no other than Senator Hillary Clinton as speaches about President Washington's wisdom and prudence to leaving presidency for to mark and key our United States of America away from fiefdoms and royalty.
Entusiastic! To the point! And classic in "Clintonesque" to the opposite point in its erudition.
I wish I now knew a link for such from days so long ago that Madam Secretary Mrs. William Jefferson Clinton was still Senator Clinton and President Clinton was still of as much an expectation from her to subjugate herself and her career to himself and his, as again pressed yet now from on high in erudite as President Clinton from The White House podium. Such speach on wisdoms of Washington given maybe in memory of another may still be the best yet from the floor of our Senate yet on points not writ to clever "counter-point" oddity so "Clintonesque."
So, so, so odd! A Clinton of high oratory best of and for the opposite of their practice and hope(s).
How the "envy" had to be tempered so, how the "greed" and "power" reaching "covered up"?
President Obama cannot "pull a Clinton" - now way - no how!
President Obama shouldn't "pull a Clinton" - now way - no how!
President Clinton for "smaller government better government" still a contradictory useful "Clintonesque" oddity?
What would Perry Mason think? What would Perry Mason argue?
What would Citizen Kane think! What would Orson Welles ink/print?
What will Big Sister Hillary say? What did George Orwell think?
Take: SMALLER GOVERNMENT BETTER as CLINTON SPEAK: A lesson from the MIRACLE ON 34TH STREET: For a Clinton to say such is like a Macy's Santa saying "Go to Gimbles…" but not?
Sure Clintons played Santa Claus for eight years but really where was the "morality" and "prudence" in such? Sure Clintons said "smaller government better" but wasn't such only as long as it would be "better for them" and to "holding of power" past Washingtons' prudence and sense?
Yes "Washingtons' prudence and sense" for where would we all be without Martha Washington.
Oh, Madam Secretary Mrs. William Jefferson Clinton should be absolutely furious.
Oh, Gloria Steinem can speak for herself - have to imagine she should be as furious.
Oh, President Obama wasn't that some clever politicing so parading "Bill" Clinton now past HILLARY FOR PRESIDENT - CLINTON TWO-FER to like expectation that HILLARY JUST AS CAPABLE.
Yes "Washingtons' prudence and sense."
Oh, but the oddity of erudition to "Clintonesque"?
"Smaller government better government" like "shop at Gimbles" - but from Corporate Macy's?
If you are going to write you should be dedicated and even to attempting such as a "pursuit of happiness."
What can feminists say now, now with President Clinton called for a parading in humility before The White House Press Corp, such a slam to Hillary Rodham Clinton, Secretary of State?
What can feminists say now of "Hillary" but like 'still willing to subjugate herself and still put her husbands career and needs before her own.'?
What can feminists say now, again with "Bill" up in "Hillary's" career and "space" meant "her turn"? Why did he do it? How could he do it? Didn't he agree it was her turn?
Such another "Clintonesque" oddity, though now far less successful in the counter-point erudite to an oration less successful in alternate "or"?
A definition of "is" now less "triangulatable"?
And so to conclude: "Go big or go home" as secret to the rise and fall of Clintons for the selling to "go big" sold on emotions of electorate and global markets to political vultures hooked for such brought a big promise to a "big fall"?
And so to conclude: "Go big or go home" so Clintonesque in the "go big" and "go big the otherway simultaneously" and again and again simultaneously against modern economic science and general prudence? To where is the fall we "stayed tune" for - it should be huge?
And so to conclude: I have no idea why or how the Jets could have let Danny Woodhead go.
And so to conclude: President Obama shouldn't attempt a "Clinton" nor a "1984" for the charm initiative of Clintons was all so unrealistic "go big" - "go big…" as mentioned and with "smaller government better…" as a clever way of such career politicians as Clintons to be base in agreeing for it would conclude "them better" while their method and practice all one sided but "Clintonesque" in contradictory better not contrary administering, as the one side not one side of an issue but just "their side" in their selfish hoarding and power grabbing.
We have seen the coming of the Clintons, we have seen it as the coming of Obama.
We haven't seen their promises balanced though "balanced" and to irresponsible "popular" "go big" also to surplus such that near half of their two trillion cut in a mere few years was spending necessary and not to be undone, at least if you buy into the "morality" or "need" if any of Obama priorities.
So many classic Clinton moments effected to the opposite of presented somehow and someway, selfish even in "smaller government" a embrace practicle simply to "better if we are still in power and gain powers."
So, so, so odd, and sorry I don't have a link to the maybe best speach I have yet heard from our Senate floor on the subject here too to why Clintons should be better respecting Washingtons' prudence and sense of state, and especially after 90s when such an "example" made more appropriate for the globe, yet lacking, alas, for the Clintons and their reaching and reaching.
Maybe we haven't all been robbed of the "great fall" we expected from all the Clinton hyping and hyping, and hyping even higher.
That podium parading, a first indicator?
If Madam Secretary of State Mrs. William Jefferson Clinton even going to use "Hillary" any more? Has she finally escaped her "cover" of "feminism" now and can stop trying to hide her true self and grit to a willing and wilful subjugation to her man and for her man, first and last?
Secretary of State Hillary Rodham Clinton?


Even if World of Warcraft is back up to 10.1 million subscribers, that's far short of what its studio brother Overwatch has accomplished. The multiplayer team shooter recently crossed its 20 millionth player barrier, a feat that's made more impressive when you consider that it did so in less than five months following its May 24th release.
This means that the game's population has doubled from 10 million, a number that it reached back in June.
The ball could keep rolling with Overwatch considering that it's running a Halloween Terror event and promotion for the remainder of the month. How large will Overwatch's population grow before it hits the ceiling? Well, there is about 7.3 billion people on the planet, so there's the hard limit. Something a little short of that is our guess.


Self Description: Lovely, friendly, simple and gentle kind of woman. Full of love and care. Ready to give all my love to the right man. I am very friendly and easy to get along with. I want a family to love and share my life with. I am loyal to one man and expect the same. Most people say I am very loyal and fun to be around.
Comments: The man I'm looking for should be sincere, kind , loving , committed, truthful, respectful. Seeking a companion, a best friend. A man that I can look into his eyes and say I love you and only you with all my heart. And I would like someone to join me in love, happiness and spirit. To start a new life in a far away land, then start a conversation with me and let's see what happens. I have no trouble in traveling to your home to meet you and family.


text:
Q: How do I grab an index from an array in a HashMap? I've got a HashMap<Object, String[]> I just want to grab the 0 index position from the String[]. How do I do that?
Can I just do this? mMap.get(position)[0]?

A: Yes, you can do what you've indicated, provided position is a key in the map.

A: HashMap doesn't have a 0index and it doesn't have a String[]
You cannot do what you ask because it doesn't make sense.

Can I just do this? mMap.get(position)[0]?

You can. Have you tried this to see if it works?  Note: it will fail if map.get() returns null

A: A map is not an array.  It's a dictionary of keys that map to items.  So there is no ordered index in the Map part, there's a lookup key.  This means that a Map has no "next" item.
In the event that you stored a String[] in the map, then you could get the first element of the String array like so:
String first = ((String[])mMap.get(lookupKey))[0];

Since you are using generics, your compiler will make the casting unnecessary, simplifying the answer to
String first = mMap.get(lookupKey)[0];

Note that this is not using the position to access the item stored in the Map, it's using the lookup key.  In addition, there is a casting of the returned Object into a String[] (because we stored a String[] in the map earlier), and then there is a dereferncing of the first ('0') element.

A: Here is a little demo program that does what you're asking.
import java.util.Map;
import java.util.HashMap;

public class FirstElementInHashMap {

    public static void main(String[] args) {
        Map<Object,String[]> mMap = new HashMap<Object,String[]>();
        mMap.put("myKeyA", new String[] { "myValue1", "myValue2", "myValue3" });
        mMap.put("myKeyB", new String[] { "myValue4", "myValue5", "myValue6" });
        mMap.put("myKeyC", new String[] { "myValue7", "myValue8", "myValue9" });

        Object position = "myKeyB";
        String[] strings = mMap.get(position);

        // make sure position exists in the Map and contains a non-empty array
        // so we don't throw an NullPointerException
        String firstStringInArray = null;
        if (strings != null && strings.length > 0) {
            firstStringInArray = strings[0];
        }
        System.out.println(firstStringInArray);
    }
}

The output of the above program is:
myValue4


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text:
Position Paper by Human Rights Organisations' on the Independence of the Palestinian Judicial System
12، Aug 2020
Palestinian human rights organisations are following, with concern, the rapidly unfolding developments in the Palestinian Judicial Authority, coinciding with additional serious challenges facing the Palestinian people. In addition to the so-called "Deal of the Century", the Israeli occupying authorities continue to advance and entrench their annexation, emboldened and supported by the United States, in flagrant violation of international human rights and humanitarian law. Such times require the urgent restoration of the Palestinian political system and the consolidation of public authorities and institutions, most notably the Judicial Authority, based on competence, impartiality, and transparency, to strengthen the separation of powers and rule of law, as a basis of good governance, and to reinforce Palestinian institutions in the face of imminent challenges.
Since 2007, the internal Palestinian political divide has increased challenges and risks to the political system. The inaction, and later dissolution, of the Palestinian Legislative Council (PLC) have further exacerbated the situation. This is evidenced in the Executive Authority exercising the law-making power, promulgating laws by decrees as "exceptional legislations", in contravention to the requirements set forth by Article 43 of the Palestinian Basic Law, which restricts it to cases of necessity that cannot be delayed, and largely without community and political participation. In the Gaza Strip, the PLC's Reform and Change Bloc continues to convene PLC sessions and pass regulations contrary to the Basic Law and PLC Standing Orders. Consequently, the abuse of powers has negatively affected public rights and freedoms, which has undermined all that remains of the political system and allowed for normalizing the state of internal political divide under various pretexts.
The Judicial Authority has not been immune to the consequences of the internal Palestinian political divide. Instead of serving as a single body that contributes to the unity of the Palestinian people, the judicial system has itself become part of the internal political divide that needs to be consolidated. Two judicial councils are now in place, one in the West Bank and another in the Gaza Strip. The same is true for the Public Prosecution, with two Attorney Generals operating there. As such, the Judicial Authority has been drawn into political division and rivalries, providing a key avenue and additional tools to further entrench the split and tighten the grip on all authorities.
For 13 years, attempts to achieve national reconciliation and end the internal Palestinian political divide have been at a standstill, allowing for an undemocratic environment to prevail across all components of the Palestinian political system. Legislative and presidential elections have not been held, which are long overdue as of 2010, eroding the legitimacy of all authorities due to the absence of democratic practices. This has led to the executive, legislative, and judicial powers to operate contrary to the Palestinian Basic Law. As a result, an entire generation has been deprived of their right to political participation and access to decision-making circles. Meanwhile, a set of interests have been allocated to certain groups, who perceive the end to the political division as a threat to their own.
The structure of the Palestinian political system viewed that the Palestinian High Court is capable of delivering the tasks and powers of a Supreme Constitutional Court (SCC). Under such capacity, the SCC has convened and rendered judgements for over 15 years, without indications of a pressing necessity requiring the issuance of a declaration to establish a Supreme Constitutional Court. The formation of the current SCC has been dominated be political considerations, whereas its decisions have provoked widespread controversy across Palestinian society, necessitating that its law and formation be reconsidered.
Overtime, in the absence of prospects for national reconciliation, the judicial system has continued to decline and exacerbate. The Executive branch's interference in the judiciary is key to the absence of judicial independence and a violation to the principle of the rule of law. For example, the appointment of Chairs of the High Judicial Council (HJC) contravenes the provisions of the Judicial Authority Law No. 1 of 2002. In addition, requesting HJC Chairs to sign a resignation letter before they are appointed seriously breaches the principles of judicial independence and impartiality. This has resulted in increased interference in judicial affairs, with ramifications on the internal state of the judiciary, and creating a split within the Judicial Authority and judges. This has adversely impacted the image and integrity of the judiciary and undermined public confidence in it, besides the negative and serious effects on rights and freedoms, as well as the individual rights of litigants.
The Executive branch's interference in the judiciary has included the establishment of the Presidential Committee for the Development of the Justice Sector, and later the dissolution of the permanent HJC. It also included the formation of a Transitional HJC, the forced transfer of several judges to retirement against their will, and the secondment of judges to non-judicial government jobs while preserving their judicial capacity and privileges, contrary to customary secondment. These measures have not achieved an independent and effective Palestinian judicial system, which would provide prompt, efficient, and impartial justice to people, based on financial, operational and administrative independence. This would restore respect for, and public confidence in, the judiciary, while allowing it to contribute to Palestinian perseverance, as a main pillar of the Palestinian political system.
The Judicial Authority Law No. 1 of 2002 has never posed a challenge to the development of the Palestinian judicial system. Instead, the interference in judicial affairs, the surpassing of the Judicial Authority Law, and the absence of a political will to prevent such interference are all key factors for the declining judicial performance and low public confidence in the judiciary. To this end, the provisions of the Judicial Authority Law should be duly respected and upheld.
An independent, impartial, and fair judicial system requires competent judges, with relevant experience, professionalism, and good conduct. It also requires effective oversight tools, grounded in law, adopting principles of equality and non-discrimination, while ensuring accountability and fair trial – based on the respect for human rights, equitable law enforcement, and combating corruption. Transparent and professional evaluation and accountability should be applied to promote equal opportunities and fair competition at both judicial and administrative levels. This will further necessitate the provision of all means to guarantee a decent living standard for judges, in a way that maintains their eminence thus the integrity of the judicial system.
Having acceded to international human rights conventions, the State of Palestine is obliged to enhance institutional performance in line with the standards of judicial independence and impartiality, particularly those provided by the Basic Principles on the Independence of the Judiciary (adopted by the UN General Assembly in 1985) and the International Covenant on Civil and Political Rights. Compliance with these norms should reinforce the international status of Palestine, and reinforce the political leadership's efforts and calls on the international community and UN Security Council to recognise Palestine as a full member state of the United Nations.
Considering the consequences of recent developments at the judiciary level and the negative impact of continued interference in judicial affairs on rights and freedoms, the undersigned human rights organisations emphasise the following demands:
Apply the Judicial Authority Law No. 1 of 2002 in good faith, instead of amending its provisions, and until such time national elections are held and an elected parliament is established.
Restore the permanent High Judicial Council expeditiously without delay, in line with the Judicial Authority Law No. 1 of 2002, while ensuring non-interference in judicial affairs.
Launch consultations by the permanent High Judicial Council with all official and non-official bodies to present its vision, reflected in a plan with a clearly defined timeframe, to promote and advance the Palestinian judiciary.
Revisit the formation and law of the Supreme Constitutional Court, ensuring its independence, impartiality, and non-politicisation.
Take serious steps to restore democratic life, foremost by putting an end to the internal Palestinian political divide and calling for legislative and presidential elections as soon as practicable. These will ensure the right of all people to participate and engage in national decision-making processes and strengthen institutional performance, rights, freedoms and the rule of law.
Palestinian Center for Human Rights
Coalition for Accountability and Integrity (AMAN)
Al-Haq
Civil Commission for the independence of the Judiciary and the Rule of Law (ISTIQLAL)
Mezan Center for Human Rights
Jerusalem Legal Aid and Human Rights Center
Palestinian Center for the Independence of the Judiciary and the Legal Profession (MUSAWA)
Hurryyat – Centre for Defense of Liberties and Civil Rights
Aldameer Association for Human Rights
Palestinian Working Women Society for Development
Ramallah Center for Human Rights Studies
Human Rights and Democracy Media Center (SHAMS)
Center for Women's Studies
Defence for Children International – Palestine Section
Palestinian Initiative for the Promotion of Global Dialogue and Democracy – MIFTAH