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I wasn't too upset since I was never really fond of the pictures. The set of two frames were generic prints that someone bought for us from Bed Bath and Beyond before we got married. They had Bible verses on them so I guess that's why the person thought they'd be appropriate. They were just a nice, but kind of impersonal, temporary fix for a couple that had next to nothing when we got married. I guess having next to nothing is true for most young newlyweds. Honestly, I kind of miss having next to nothing. It kept things simple.
Okay, the frames... I found them at Target. I was so pleased when I pulled them out of their packaging and found that they came with a template for hanging. So convenient! I wish all my black frames from the photo gallery wall had that. It would've been so much faster.
I was also impressed that the frames came with photo gallery examples.
I noticed that they included the option that I chose for my gallery wall.
"Order out of the chaos." I like it. Sounds a lot like my life sometimes:)


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Ustand Khan’s intense baritone made him much popular, even to those who did not listen to classical music. Be it his ‘Piya Basanti’ or his ‘Albela Sajan Ayo re’ from the movie ‘Hum Dil De Chuke Sanam’, his voice never failed to pierce the hearts of listeners with ease.
A Padma Bhushan awardee in 2010, the maestro popularized his favourite musical instrument, the ‘Sarangi’ all over the world, carving a niche for himself since the age of eleven.
He collaborated with legends such as Ravi Shankar on George Harrison’s 1974 ‘Dark Horse World Tour’ to make the kind of music, which was classical and popular at the same time.
Sultan has won numerous musical awards. He has won the Sangeet Natya Academy Award twice, as well as the Gold Medalist Award of Maharashtra and the American Academy of Artists Award in 1998.
His funeral will take place in Jodhpur tomorrow. Not just the world of classical music, Ustad Khan also ruled the world of Hindi pop music.

domain: artistic


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9661 FANCY SCARVES LENGTHS, 5 VICTORIANA BAGS PATTERN
Price / kg:
New In Package, Uncut, Factory Folded
crisp uncut pattern bit of a sticker rub on pattern jacket.... mccall's 9661..
Glamour Becomes You
Create beautiful scarves in wonderfully luxurious fabrics.
Add fringes and trims.
Dress up any look.
Long and luxe, these scarves are 60 and 84 inches long.
Make a matching drawstring purse with the unique double drawstring construction... FIVE BAGS, FOUR SCARVES... bag A lame, metallic fabrics;; bag B to D.. embroidered silk.. bag C novelty knits.. bag E reembroidered jacquard, etc... all gorgeous.. scarf G of velvet burnout. and scarf H of silk, etc. uncut original folds pattern.
Simply pull the small loop to open...the longer cord to close.

domain: design


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Anyway, to the first of the week's comics!
My Little Pony Micro-Series #6 - Applejack
Bobby Curnow, Brenda Hickey, Heather Breckel and Neil Uyetake
Ponies! Ponies! Ponies!
Yay! Ponies! ^_^
Right, now I've got that out of the way onto the review. Alongside IDW's normal Friendship is Magic title, featuring longer stories set over 2-4 issues, there's the Micro-Series comics, single stand-alone issues concentrating on one character, or in the case of the Cutey-mark Crusaders issue a group of characters, and whilst the longer stories are nice not having to wait a month to finish a story does have its advantages too.
So, to this issue. It's Hearth's Warming Eve, a major holiday that is definitely not Christmas, and Applejack is freaking out about how much work there is to do, so business as usual then. Well, until someone or something starts replacing a whole bunch of the Apple family's crop with squashes. Something obviously needs to be done and Applejack being Applejack we get this panel:
And Applejack being Applejack it works out exactly as well as you'd expect.
Will she ever learn? Probably not.
Of course things go much better when she lets the rest of the family help.
It's a fun, well written issue with a decent little twist and well worth grabbing if you happy to be a bit of a pony fan.
Sonic The Comic Online #262
Pete Murphy, Stephen Davis, Michael Stephenson, Seumidh MacDonald, Chris Gould, Matthew Bramble and Matt Dittmer
Stephen 'Spydaman' Davis
Stephen 'Spydaman' DavisSo I did say I was going to be doing webcomics and this one is on the web, but it is released in issue form and comes out every couple of months and is a continuation of a print comic that bit the dust back in 2002, so I think it's okay. Sonic the Comic, for those that don't know, was the UK's officially licensed Sonic the Hedgehog comic (with other Sega characters in some of the back-up stories) published by Fleetway Editions / Egmont Magazines. The title launched in 1993 and was one of the publisher's best sellers, but was killed off by publisher stupidity after they implemented their five year reprint cycle, the idea being that five years was the average reader turnover and so most of the readers wouldn't have ever read the reprints. This policy was stupid for multiple reasons. With a set coninuity and plenty of callbacks to earlier issues running reprints alongside new stories didn't really make a whole lot of sense and from issue 185 to issue 223 the comic just ran reprints with no new content at all.
Then it got canned because nobody wants to keep buying the same stories over and over again.
Jump forward to May 2003 and issue 224. Except issue 224 wasn't published by Fleetway/Egmont, wasn't available in newsagents, wasn't officially licensed and most importantly wasn't a whole bunch of reruns. A fan run affair, though wih the support of some of the original comic's staff Sonic the Comic online carries on where issue 184 left off with a whole bunch of new stories.
Issue 262's a good one with three stories, a seven page lead story and two five page back-ups. It doesn't update all that often, but most of the stories are worth a read or three and with 43 standard issues and 11 specials to read there's plenty to keep you busy.
L.Y.K. and Bear #1
Here's a cute one.
I stumbled across this one on Kickstarter. It looked cute, sounded fun and any support of a dollar or more got you a digital copy of the first issue. A cute all ages comic about a kitten for a dollar? How could I pass that up?
Of course I paid more than a dollar, but you know, it was still a very good offer and that's what matters. Did I mention how cute this comic is? Little Yellow Kitten (that's what L.Y.K. stands for you know) is adorable. An absolute troublemaker, but adorable all the same. Bear is also pretty damn cute and the two of them are based on Sumser's cat and childhood teddy bear (who he still has of course) and knowing that somehow just makes the whole thing even more adorable.
The art style is simple, bright and cheerful and the story has a sort of freewheeling anything goes quality to it. Little Yellow Kitty is hungry. You'd think this would be a simple thing to fix, but no, the fridge is empty and the person who should be able to do something about that is missing and maybe, just maybe something got broken and now L.Y.K. and Bear have got themselves in a spot of bother.
I have one issue with this issue, well two I suppose.
One: There are a couple of Twitter messages shown on one page. One of them contains the hashtag #FML and the use of that acronym that I know ain't all that all ages. Yes, it's just an acronym and no, it doesn't use any actual bad words, but I still wouldn't want to be the one answering the question when a kid asks what it means.
Two: You can't seem to buy it yet if you haven't backed the Kickstarter.
So yeah, generally a great, fun and cute little comic that I would recommend, but that you can't seem to buy right now.
Count Duckula #2
Mario Capaldi, Etta Saunders, Andrew Brenner, John Burns, Nancy Hazel, Vin James, Alan Case, Cal Hamilton and Nick Abadzis
Ah, Duckula. You've gotta love old Cosgrove Hall cartoons.
There are three different Duckula / Count Duckula titles that I know of. One published by Marvel, one published by London Editions and this one by Celebrity. I've never read the Marvel one, but between this one from 1989 and the London Editions one from 1990 onwards, this one doesn't fare all that well.
It's not the art that's a problem. The art's spot on. It's not the writing either. The writing's great. There's a single story comic, a one page gag strip and a two page prose story (which would have fitted easily onto one page if they didn't use such a huge typeface).
No, the problem with this comic is that it seems to be put together all wrong and the first problem is that cover. See, that's actually an illustration of that two page story, but there's a bit of a problem with it. Here's a description of the visitor in the story:
"Before him, on the threshold, drenched with rain and lit by flashes of lightning, stands a gruesome figure. It is eight feet tall. and spectre-thin, wrapped in black robes. The face is harrowing and fierce, half-moon glasses perched on a hooked beak. The grey hair is drawn up in a bun."
That's a pretty fair description of the character on the cover I'd say, except for one little problem. Black robes and grey hair? Hmm... Nope, I definitely see green robes and light brown hair. There is clearly some kind of communication problem here. Was the writer working from an inks only version of the cover image or did the artist draw it based on the writer's description and then hand it off to the colourist without any direction and where is the editor in all this?
Then there's the speech bubbles. Somehow they've managed to include pretty much every mistake you can get.
You get panels where the speech bubbles have no outlines:
Panels where the speech bubbles have a dividing line cutting their tails off:
Panels where the borders cut off part of the speech bubbles:
Speech bubbles that don't know where their owners are:
(There are only three characters in this entire scene.)
And speech bubbles that were clearly meant to be at the edge of a panel, but have been moved into the middle for some reason:
The writing and art are both spot on for a Duckula comic. This should be a great comic, but it's a mess. I blame the editor.
The Beezer Book 1975 and The Topper Book 1976
Before that though there was The Beezer and there was The Topper, two completely seperate comic that were eventually forced together becaue neither of them were selling quite as well as they used to. Back in the '70s though? Back in the '70s they were doing just fine.
I picked up these annuals for 50p each along with a few old Dandy annuals, Beano annuals and even an old Denis the Menace book. Bargain.
Being the older one, and because the comic I used to read as a kid was called Beezer and Topper, I'll start with the Beezer. It's an interesting read, a mix of stuff I remember, stuff I've never seen before and stuff that I sort of remember, but not quite that way.
One thing that hasn't changed all that much is The Numskulls, a strip about little people that live inside someone's head and basically run the whole show.
One that should have survived, but didn't is Black Bun.
An adorable little bunny rabbit beating up a farmer. Who wouldn't want to read that? I think we should all campaign for DC Thomson to bring back this lovable little lagomorph or at the very least get them to put out a best of volume, because the world needs more comics about rabbits.
On the flipside there are some things that are probably best left in the past, whether it be this thing...
...or the comic's dubious representations of native Americans, and no, I don't mean the cover. I mean this:
Ah, the 1970s!
Now for The Topper!
Yes. Yes, you are Foxy, twice, and you manage to do it without any hugely offensive stereotypes. Well done.
The big survivor from this book is this young lady.
Beryl the Peril (unsurprisingly created by David Law, the same guy who came up with Dennis the Menace) managed to stay in print from 1953 to 2007 when she was finally dropped from the Dandy. It'd be fun to see her brought back alonside Dennis. They're very, very similar characters. I'd like to see them try and outdo each other.
Hoozee the Wotsit, the Dr Seuss-ish thing who doesn't even know what he's supposed to be himself didn't fare so well though.
Is it just me or does this character from The Fabulous Whizzers from Ozz look a bit like Fidal Castro did back in the '70s?
He's a rebel leader trying to blow up a railway bridge belonging to a British run mine, which currently has children crossing it. Later in the story he gets punched out by a remote control flying car. Subtle it ain't.
Well, that's all for now. Next week expect more My Little Pony, some Adventure Time and the better Duckula comic, plus whatever else I feel like reading. In the meantime I'll be organising the campaign to bring back Black Bun.

domain: entertainment


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- Open Access
Immunodetection of occult eosinophils in lung tissue biopsies may help predict survival in acute lung injury
Respiratory Research volume 12, Article number: 116 (2011)
Acute lung injury (ALI) is a serious respiratory disorder for which therapy is primarily supportive once infection is excluded. Surgical lung biopsy may rule out other diagnoses, but has not been generally useful for therapy decisions or prognosis in this setting. Importantly, tissue and peripheral blood eosinophilia, the hallmarks of steroid-responsive acute eosinophilic pneumonia, are not commonly linked with ALI. We hypothesized that occult eosinophilic pneumonia may explain better outcomes for some patients with ALI.
Immunohistochemistry using a novel monoclonal antibody recognizing eosinophil peroxidase (EPX-mAb) was used to assess intrapulmonary eosinophil accumulation/degranulation. Lung biopsies from ALI patients (n = 20) were identified following review of a pathology database; 45% of which (i.e., 9/20) displayed classical diffuse alveolar damage (ALI-DAD). Controls were obtained from uninvolved tissue in patients undergoing lobectomy for lung cancer (n = 10). Serial biopsy sections were stained with hematoxylin and eosin (H&E) and subjected to EPX-mAbimmunohistochemistry.
EPX-mAbimmunohistochemistry provided a >40-fold increased sensitivity to detect eosinophils in the lung relative to H&Estained sections. This increased sensitivity led to the identification of higher numbers of eosinophils in ALI patients compared with controls; differences using H&Estaining alone were not significant. Clinical assessments showed that lung infiltrating eosinophil numbers were higher in ALI patients that survived hospitalization compared with non-survivors. A similar conclusion was reached quantifying eosinophil degranulation in each biopsy.
The enhanced sensitivity of EPX-mAbimmunohistochemistry uniquely identified eosinophil accumulation/degranulation in patients with ALI relative to controls. More importantly, this method was a prognostic indicator of patient survival. These observations suggest that EPX-mAbimmunohistochemistry may represent a diagnostic biomarker identifying a subset of ALI patients with improved clinical outcomes.
ALI encompasses a spectrum of pulmonary disorders that is often accompanied by life-threatening hypoxemic respiratory failure and diffuse bilateral pulmonary infiltrates. Moreover, the origins of ALI are often complex (e.g., pneumonia, sepsis, or left atrial hypertension) and not easily attributed to a defined cause [1–6]. In its most dramatic clinical form, acute respiratory distress syndrome (ARDS), precipitous impairment of gas exchange is associated with a high mortality rate (38.5%), especially among elderly patients . Therapy for most patients with idiopathic ALI is limited to supportive care and infection prevention [6, 8–10]. Select studies have suggested a benefit of corticosteroid therapy in a subset of patients with ALI/ARDS (e.g., [11–14]). However, large prospective studies have not supported a consensus opinion for the routine use of corticosteroids [15–18].
The pathogenesis of ALI remains unclear, largely a consequence of the heterogeneity of patients coming into the ICU and the broad clinical features characteristic of ALI [1, 19]. The cellular mechanisms contributing to lung tissue injury in ALI are for the most part unknown, although the potential involvement of neutrophils in the development of ALI remains the focus of many studies (see for example [21, 22]). In particular, neutrophil-derived products (e.g., extracellular matrix degrading proteinases and reactive oxygen species), inflammatory fibrotic cytokines, and growth factors [23–26] have been postulated as causative agents underlying the onset and progression of disease .
For most patients with ALI, eosinophils have not been reported as a prominent histological feature, despite their potential tissue damaging capability [5, 28] and their presence in a number of other well defined pulmonary diseases such as asthma  and acute eosinophilic pneumonia . However, among this larger literature there are some studies that have implicated this granulocyte as either a potentially important contributor to disease or, at the least, a diagnostic biomarker of events occurring in ALI patients [21, 27, 31]. Interestingly, these studies suggested a "predictive" and "discriminative" value of eosinophil activity assessments in designing an effective therapy for patients exhibiting clinical features of ALI. Unfortunately, the lack of an observable eosinophil infiltrate at the histological level remains a significant confounding issue, especially for those patients who may have been treated (even briefly) with systemic corticosteroids. In turn, the typical absence of visible eosinophils in most cases of ALI that come to biopsy has limited the further development of hypotheses and experimental studies investigating a role(s) of eosinophils in ALI.
In this study we demonstrate that standard histological evaluation of lung biopsies significantly underestimates eosinophil accumulation when compared to assessments using a novel eosinophil peroxidase (EPX)-specific monoclonal antibody (EPX-mAb) visualized by immunohistochemistry. We employed this unique increase in sensitivity to detect eosinophils and evidence of tissue degranulation in a group of ALI patients. A retrospective assessment of ALI patients who had a lung biopsy taken during the course of their acute care was conducted, comparing the results of these assessments with lung tissue from control subjects. These blinded assessments revealed that the added sensitivity of EPX-mAbimmunohistochemistry detected a significant increase in eosinophil accumulation/degranulation in ALI vs. control subjects. More importantly, EPX-mAbimmunohistochemistry identified a subset of ALI patients who survived hospitalization, suggesting its use as a prognostic indicator may represent a previously underappreciated diagnostic strategy in the management of pulmonary patients.
The patient studies presented in this manuscript were performed in accordance with NIH guidelines and Mayo Foundation institutional policies (Institutional Review Board, 08-001908 Immunohistochemical Study of Eosinophil Degradation in Archived Lung Biopsies), and in compliance with HIPPA guidelines for patient privacy.
An overview of the demographic data and pathological/clinical assessments of our ALI study subjects is presented in Tables 1 and 2. These pulmonary patients were initially identified by study personnel from a search of the Mayo Clinic Arizona Pathology Database with the search key words: lung, biopsy, acute lung injury (ALI), diffuse alveolar damage (DAD), organizing pneumonia, and ARDS. Study personnel subsequently reviewed the available pathology reports and clinical medical records to identify the subset of patients who had received a diagnosis of ALI. Thus, to be included in this study a given patient had to have a diagnosis of ALI and have undergone a biopsy during their course of treatment. It is noteworthy, that this process was not discriminatory and all patients with available biopsy material that had received an ALI diagnosis as part of their standard-of-care were included in this study. The ALI patients included in this study met AECC established clinical criteria  for an acute lung injury diagnosis and also displayed characteristic pathological changes linked with this disease. Specifically, assessments of all study patients upon admission with acute respiratory distress revealed the presence of diffuse radiographic abnormalities and hypoxia characterized by an A-a gradient (PaO2/FiO2) less than 300 [4, 32]. Indeed, the PaO2/FiO2 ratio in a subset of these cases (11 of 20 total cases) was below 150 and thus would meet clinical criteria for ARDS [4, 32]. In addition, the twenty ALI patients in this study included thirteen patients (independent of PaO2/FiO2 levels) that required mechanical ventilation during their hospitalization. Review of patient medical records also revealed the absence of typical risk factors associated with ALI, including myocardial infarction, pulmonary embolism, infection/sepsis (e.g., pneumonia), and acute drug reaction. The pathology evaluations of all study-subjects confirmed the clinical indications of ALI. That is, each patient included in our study displayed three specific histopathologies in the available biopsies : (i)The presence of fibrin in the alveoli; (ii)The demonstration of an organizing pneumonia (i.e., a prominent airway cellular infiltrate); and (iii)Evidence of reactive airway epithelial Type II cell hyperplasia. Among these twenty ALI patients, 45% (i.e., 9/20) displayed classical diffuse alveolar damage (ALI-DAD). Seven of the study group did not survive hospitalization, and of these non-surviving patients >71% (5/7) received an ALI-DAD diagnosis. A variety of co-morbid medical disorders were evident in our ALI patients, including several patients with connective tissue disorders. However, examination of the medical records and care-giver notes failed to identify elements of commonality regarding disease onset or progression. Nonetheless, the unresolved character of disease progression in these subjects was such that nineteen of the twenty patients received corticosteroid therapy during their course of treatment.
Control lung samples consisted of uninvolved areas of lung tissue recovered from patients undergoing resection for a diagnosis of lung cancer (Table 1). None of the control subjects were receiving systemic corticosteroids, although four control subjects were receiving inhaled corticosteroids.
Recovery and processing of bronchial tissue biopsies
The twenty lung specimens obtained from patients with ALI included sixteen surgical lung biopsies and four transbronchial lung biopsies considered adequate for histologic review (i.e., containing alveolated lung parenchyma). All control biopsies were taken from uninvolved areas of surgically resected lung tissue removed for treatment of lung cancer. Lung tissue biopsies were fixed in 4% buffered formalin, embedded in paraffin, and serial 4 μm thick sections were cut.
Histopathological and immunohistochemical staining of lung tissue sections
H&E staining was performed using an automated stain processing unit in the Mayo Clinic Arizona clinical histology unit. Immunohistochemistry was performed using a EPX-mAbas previously described . Evaluations of the slides were performed with either an Olympus BX50 or a Zeiss Axiophot compound microscope.
Histopathological evaluation of patients and the quantification of EPX-mAbimmunohistochemistry
Serial sections from each biopsy were coded by clinical histopathology laboratory personnel and in each case the middle (slide 2) of the three serial sections was stained with Hematoxylin - Eosin (H&E). Slide 1 of the series was subjected to immunohistochemical staining with EPX-mAband slide 3 served as an isotype immunoglobulin negative control for the immunohistochemistry.
The eosinophil infiltration of lung tissue using H&E staining was performed in an investigator-blinded fashion independently by an experienced pulmonary pathologist with a specialty in lung diseases (KL) and a pathology resident (PG). The slides were evaluated by each individual as a numerical average calculated from 10 randomly selected hpf (high powered fields; 40x objective/10x ocular lens, 0.29 mm2 field of view); that is, a total area of ~3 mm2 per biopsy-investigator. The reported values are the mean ± SEM of all investigator-derived counts.
Quantification of eosinophil tissue infiltration within each biopsy using EPX-mAbimmunohistochemistry was independently performed in an intra/inter-blinded fashion that included investigators from pathology (KL, EJ, and PG - EPX-mAbbased eosinophil counts in lung tissue); KL and EJ - EPX-mAbassessments of eosinophil degranulation), a hospital/clinic-based pulmonary fellow (KP - EPX-mAbbased eosinophil counts in lung tissue), and a PhD graduate research fellow (LW - EPX-mAbbased eosinophil counts and degranulation in lung tissue). All evaluations were done at a magnification of 400x. The number of positively stained eosinophils was determined in the alveolar lung parenchyma as a numerical average calculated from 10 randomly selected hpf; that is, a total area of ~3 mm2 per biopsy-investigator. The reported values are the mean ± SEM of investigator-derived counts.
The level and extent of eosinophil degranulation observed within each patient biopsy was also determined by scanning 10 randomly selected hpf (40x objective/10x ocular lens, 0.29 mm2 field of view); that is, a total area of ~3 mm2 per biopsy-investigator. Each field examined was graded using a scale that permitted stratifying the available patients based on a relatively low resolution grading scale that was easily reproduced by multiple evaluators of varying levels of experience and expertise: Level 0 = No identifiable eosinophils and/or degranulation ; Level 1a = The field shows evidence of eosinophil degranulation (i.e., extracellular release of EPX) that represents ≤10% of the field's total area and has <3 independent areas within the field displaying degranulation; Level 1b = The field shows similar evidence of eosinophil degranulation as Level 1a but instead displays ≥3 independent areas within the field with evidence of degranulation; Level 2a = The field shows evidence of eosinophil degranulation that includes extracellular release of EPX, enucleated eosinophils (i.e., cytoplasmic fragments), and/or the presence of free eosinophil granules. The extent of degranulation represents 10 - 50% of the field's total area; Level 2b = The field shows similar evidence of eosinophil degranulation as Level 2a but instead has a level of degranulation representing >50% of the field's total area. Eosinophil degranulation was quantified for each of 10 randomly selected hpf of a given biopsy (i.e., patient) by initially applying an increasing numerical value to the level of degranulation evident in the field (Level 0 = 0, Level 1a = 1, Level 1b = 2, Level 2a = 3, and Level 2b = 4). The extent of eosinophil degranulation in the biopsy was then determined as the average of the numerical values assigned to each of the 10 hpf examined. This grading of eosinophil degranulation was performed independently by three outcome-blinded evaluators (an experienced pulmonary pathologist (KL), a pathology resident-fellow (EM), and a Ph.D. graduate student (LW)), all of whom were also unaware of the scores reported by the other evaluators. Degranulation scores are reported as the mean numerical value derived from all three evaluators ± SEM.
Data are expressed as the mean ± SEM. Statistical analysis for comparisons between groups was performed using either a Student's T test or a Wilcoxon Two-Sample Test for non-parametric data for comparisons between data sets that were not uniformly distributed. Differences between mean values were considered significant when p < 0.01. Intraclass correlation coefficients (ICC) were also determined between investigators reading slides as a measure of inter-rater agreement .
EPX-mAb immunohistochemistry provides an enhanced level of sensitivity for the detection of eosinophils infiltrating lung biopsies
Serial biopsy sections from either control or ALI subjects were stained for evaluations of eosinophil tissue infiltration. Representative photomicrographs of H&Estained slides as well as lung sections subjected to EPX-mAbimmunohistochemistry are shown in Figure 1. The quantitative evaluations of eosinophil density using both staining methods are presented as individual patient assessments in the histograms of Figure 2. As expected, the evaluation of the H&Estained patient biopsies revealed little evidence of eosinophil infiltration in both control and ALI subjects (0.02 infiltrating eosinophils/hpf and 0.04 infiltrating eosinophils/hpf, respectively). However, evaluation by the same pathology investigators of the serial slides subjected to EPX-mAbimmunohistochemistry demonstrated an enhanced sensitivity to detect eosinophils in these lung tissue sections. Specifically, evaluations of the lungs of control subjects using EPX-mAbimmunohistochemistry revealed a >40-fold increase in the ability to detect tissue infiltrating eosinophils relative to H&Estaining (0.81 eosinophils/hpf vs. 0.02 eosinophils/hpf, p < 0.01).
Eosinophil infiltration of the pulmonary parenchyma is higher in ALI patients compared to control subjects and is a diagnostic indicator of patient survival
Evaluation of serial lung sections following EPX-mAbimmunohistochemistry demonstrated that the density of pulmonary eosinophils in the collective group of ALI patients is significantly higher relative to control subjects (3.6-fold, 2.88 eosinophils/hpf vs. 0.81 eosinophils/hpf (p < 0.01), respectively). More importantly, further evaluations of the ALI patients (Figure 2, shaded histograms) surprisingly showed that EPX-mAbdetection of infiltrating lung eosinophils divided these patients into subjects which survived vs. those that did not survive hospitalization (8.4 ±2.9 eosinophils/hpf vs. 1.9 ± 0.6 eosinophils/hpf, p < 0.01).
ALI patients surviving hospitalization display significant levels of eosinophil degranulation (i.e., extracellular matrix deposition of EPX) compared with non-surviving patients
Assessments of lung sections following EPX-mAbimmunohistochemistry revealed that ALI patients displayed significant and varying levels of degranulation that were quantifiable. This degranulation was often observed in these patients in the absence of identifiable intact eosinophils. The photomicrographs of Figure 3 are representative of the stratified levels of increasing degranulation observed in ALI patients from no evidence of degranulation (Level 0) in a given high powered field to >50% of the field evidencing eosinophil degranulation (Level 2b). Similar to the higher levels of eosinophil infiltration observed in the collective group of ALI patients, the collective group also evidenced a >2-fold increase in the level of eosinophil degranulation compared to control subjects (2.20 ± 0.15/hpf vs. 1.02 ± 0.38/hpf, respectively). More importantly, quantitative assessments of degranulation (i.e., mean numerical score ±SEM) based on EPX-mAbimmunohistochemistry (Table 3 and Figure 4) revealed that ALI patients surviving their hospitalization also displayed significantly higher levels of degranulation compared to non-surviving patients (2.62 ± 0.18/hpf vs. 1.58 ± 0.10/hpf, respectively).
Independent of any conclusions regarding our evaluation of ALI vs. control subjects, two technical observations regarding our assessments of the lung biopsies using EPX-mAbimmunohistochemistry relative to H&Estaining are noteworthy: (i) EPX-mAbimmunohistochemistry is an easily performed assessment that provided a >40-fold enhancement to detect tissue infiltrating eosinophils. This increased sensitivity not only allowed for the greater detection of tissue infiltrating eosinophils but also corresponding increases in the speed, accuracy, and reproducibility of this determination. (ii) EPX-mAbimmunohistochemistry provided a rapid and definitively quantitative assessment of eosinophil degranulation within the lung parenchyma, observable even in the absence of intact infiltrating eosinophils.
Unfortunately, studies of ALI patients are often incomplete and subject to ambiguities resulting from the broad and complex character of symptoms and contributing etiologies [2, 37]. Compounding these issues are the limited sample materials that are available for analysis (e.g., lung tissue or BAL fluid), including the timing of when the samples were recovered during the course of a given patient's care. In this respect, the study presented here is subject to these very same limitations. That is, our study is of a small heterogeneous cohort of patients (n = 20) whose disease origins and severity vary considerably. Moreover, we did not have control over the general demographics of these ALI patients nor could we dictate why, when, or where within the lung the biopsies for study were taken relative to the course of disease and/or patient treatment. The ALI subjects of this study were also not selected on the basis of a defined and standardized medical history or a regimented treatment plan. Finally, the control subjects available to us were limited and did not include healthy volunteer biopsies or ALI patients prior to any medical interventions.
Given the limitations of the ALI study group and our control subjects noted above, we were surprised at the ability of EPX-mAbimmunohistochemistry to distinguish ALI patients from control subjects. Specifically, eosinophils are not considered a reliable histopathological marker of ALI (reviewed in [5, 28]). Yet in a completely patient-blinded fashion that was reproducible among 3-4 independent evaluators who had no knowledge of one another's assessments, our numerical results were able to identify a group of ALI patients relative to control subjects on the a basis of both increased numbers of tissue infiltrating eosinophils and increased levels of eosinophil degranulation. Furthermore, these evaluations allowed us in a completely clinical outcome-blinded fashion to stratify the ALI patients into those surviving their hospitalization relative to the non-surviving patients. It is clear that the design and power of this study precludes us from overly provocative conclusions regarding the role of eosinophils, including their link with specific symptoms or their part in pathways that exacerbate or attenuate disease pathologies. Nonetheless, this study does suggest that EPX-mAbimmunohistochemistry may represent a previously unrecognized diagnostic tool providing prognostic information for the management of ALI patients. In addition, given the paucity of available therapeutic options and discriminatory testing modalities, [1, 6, 8, 10, 19] assays detecting the release of eosinophil products (e.g., ELISA based assessment of degranulation from biological fluids such as breath condensate, intratracheal tube secretions, and/or BAL fluid) may also represent rapid and minimally invasive biomarkers of disease to assess this difficult patient population . Indeed, this initial report provides the rationale for future studies of increased design and complexity to expand this link between ALI patients and their survival based on evidence of pulmonary eosinophils and tissue degranulation.
The studies presented in this report have identified both significant technical insights and revelations regarding eosinophils in lung biopsy samples from control and ALI patients. These observations will likely have a direct impact on the assessment of eosinophils and their role(s) in lung diseases and, more important, may lead to previously overlooked or untried diagnostic and therapeutic strategies with which to treat these problematic patients.
• Immunohistochemical detection of EPX in lung tissue biopsies provides even a board certified pathologist (with a specialty in pulmonary diseases) a >40-fold increase in sensitivity to detect tissue infiltrating eosinophils in lung tissue sections
• EPX-mAbbased immunohistochemistry allows for the unique assessment of eosinophil activation (i.e., degranulation events) within the lung even in the absence of a demonstrable eosinophil infiltrate
• The increased sensitivities afforded by EPX-mAbdemonstrate that increases in lung infiltrating eosinophils and evidence of eosinophil degranulation are surprisingly characteristic features of biopsies from ALI patients relative to control subjects
• Assessments of lung biopsies from ALI patients following EPX-mAbimmunohistochemical staining may provide a potential basis to identify a subset of the ~40% of ALI patients who will not survive their hospitalization.
Ashbaugh DG, Bigelow DB, Petty TL, Levine BE: Acute respiratory distress in adults. Lancet. 1967, 2: 319-323.
Wheeler AP, Bernard GR: Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet. 2007, 369: 1553-1564. 10.1016/S0140-6736(07)60604-7.
Rubenfeld GD, Herridge MS: Epidemiology and outcomes of acute lung injury. Chest. 2007, 131: 554-562. 10.1378/chest.06-1976.
Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, Lamy M, Legall JR, Morris A, Spragg R: The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. 1994, 149: 818-824.
Avecillas JF, Freire AX, Arroliga AC: Clinical epidemiology of acute lung injury and acute respiratory distress syndrome: incidence, diagnosis, and outcomes. Clin Chest Med. 2006, 27: 549-557. 10.1016/j.ccm.2006.06.001. abstract vii
Levitt JE, Matthay MA: The utility of clinical predictors of acute lung injury: towards prevention and earlier recognition. Expert Rev Respir Med. 2010, 4: 785-797. 10.1586/ers.10.78.
Rubenfeld GD, Caldwell E, Peabody E, Weaver J, Martin DP, Neff M, Stern EJ, Hudson LD: Incidence and outcomes of acute lung injury. N Engl J Med. 2005, 353: 1685-1693. 10.1056/NEJMoa050333.
Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000, 342: 1301-1308.
Levitt JE, Bedi H, Calfee CS, Gould MK, Matthay MA: Identification of early acute lung injury at initial evaluation in an acute care setting prior to the onset of respiratory failure. Chest. 2009, 135: 936-943. 10.1378/chest.08-2346.
Matthay MA, Zimmerman GA: Acute lung injury and the acute respiratory distress syndrome: four decades of inquiry into pathogenesis and rational management. Am J Respir Cell Mol Biol. 2005, 33: 319-327. 10.1165/rcmb.F305.
Agarwal R, Nath A, Aggarwal AN, Gupta D: Do glucocorticoids decrease mortality in acute respiratory distress syndrome? A meta-analysis. Respirology. 2007, 12: 585-590. 10.1111/j.1440-1843.2007.01060.x.
Tang J, Zhou R, Luger D, Zhu W, Silver PB, Grajewski RS, Su SB, Chan CC, Adorini L, Caspi RR: Calcitriol suppresses antiretinal autoimmunity through inhibitory effects on the Th17 effector response. J Immunol. 2009, 182: 4624-4632. 10.4049/jimmunol.0801543.
Adhikari N, Burns KE, Meade MO: Pharmacologic treatments for acute respiratory distress syndrome and acute lung injury: systematic review and meta-analysis. Treat Respir Med. 2004, 3: 307-328. 10.2165/00151829-200403050-00005.
Lin Q, Wang GF, Tang XY, Zou SL: Effects of dexamethasone on acute lung injury in rats induced by lipopolysacharide. Beijing Da Xue Xue Bao. 2006, 38: 393-396.
Meduri GU, Headley AS, Golden E, Carson SJ, Umberger RA, Kelso T, Tolley EA: Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: a randomized controlled trial. JAMA. 1998, 280: 159-165. 10.1001/jama.280.2.159.
Steinberg KP, Hudson LD, Goodman RB, Hough CL, Lanken PN, Hyzy R, Thompson BT, Ancukiewicz M: Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome. N Engl J Med. 2006, 354: 1671-1684.
Meduri GU, Golden E, Freire AX, Taylor E, Zaman M, Carson SJ, Gibson M, Umberger R: Methylprednisolone infusion in early severe ARDS: results of a randomized controlled trial. Chest. 2007, 131: 954-963. 10.1378/chest.06-2100.
Bernard GR, Luce JM, Sprung CL, Rinaldo JE, Tate RM, Sibbald WJ, Kariman K, Higgins S, Bradley R, Metz CA, et al: High-dose corticosteroids in patients with the adult respiratory distress syndrome. N Engl J Med. 1987, 317: 1565-1570. 10.1056/NEJM198712173172504.
Bernard GR: Acute respiratory distress syndrome: a historical perspective. Am J Respir Crit Care Med. 2005, 172: 798-806. 10.1164/rccm.200504-663OE.
Suratt BT, Parsons PE: Mechanisms of acute lung injury/acute respiratory distress syndrome. Clin Chest Med. 2006, 27: 579-589. 10.1016/j.ccm.2006.06.005. abstract viii
Hallgren R, Borg T, Venge P, Modig J: Signs of neutrophil and eosinophil activation in adult respiratory distress syndrome. Crit Care Med. 1984, 12: 14-18. 10.1097/00003246-198401000-00004.
Ware LB, Matthay MA: The acute respiratory distress syndrome. N Engl J Med. 2000, 342: 1334-1349. 10.1056/NEJM200005043421806.
Wittkowski H, Sturrock A, van Zoelen MA, Viemann D, van der Poll T, Hoidal JR, Roth J, Foell D: Neutrophil-derived S100A12 in acute lung injury and respiratory distress syndrome. Crit Care Med. 2007, 35: 1369-1375. 10.1097/01.CCM.0000262386.32287.29.
Swanson K, Dwyre DM, Krochmal J, Raife TJ: Transfusion-related acute lung injury (TRALI): current clinical and pathophysiologic considerations. Lung. 2006, 184: 177-185. 10.1007/s00408-005-2578-8.
Jernigan TW, Croce MA, Fabian TC: Apoptosis and necrosis in the development of acute lung injury after hemorrhagic shock. Am Surg. 2004, 70: 1094-1098.
Lange M, Hamahata A, Traber DL, Esechie A, Jonkam C, Bansal K, Nakano Y, Traber LD, Enkhbaatar P: A murine model of sepsis following smoke inhalation injury. Biochem Biophys Res Commun. 2010, 391: 1555-1560. 10.1016/j.bbrc.2009.12.124.
Hallgren R, Samuelsson T, Venge P, Modig J: Eosinophil activation in the lung is related to lung damage in adult respiratory distress syndrome. Am Rev Respir Dis. 1987, 135: 639-642.
Beasley MB: The pathologist's approach to acute lung injury. Arch Pathol Lab Med. 2010, 134: 719-727.
Bousquet J, Chanez P, Lacoste JY, Barneon G, Ghavanian N, Enander I, Venge P, Ahlstedt S, Simony-Lafontaine J, Godard P, et al: Eosinophilic inflammation in asthma [see comments]. N Engl J Med. 1990, 323: 1033-1039. 10.1056/NEJM199010113231505.
Allen JN, Davis WB: Eosinophilic lung diseases. [Review]. Am J Respir Crit Care Med. 1994, 150: 1423-1438.
Modig J, Samuelsson T, Hallgren R: The predictive and discriminative value of biologically active products of eosinophils, neutrophils and complement in bronchoalveolar lavage and blood in patients with adult respiratory distress syndrome. Resuscitation. 1986, 14: 121-134. 10.1016/0300-9572(86)90116-4.
Doyle RL, Szaflarski N, Modin GW, Wiener-Kronish JP, Matthay MA: Identification of patients with acute lung injury. Predictors of mortality. Am J Respir Crit Care Med. 1995, 152: 1818-1824.
Katzenstein A-LA, Askin FB, Livolsi VA: Acute Lung Injury Patterns: Diffuse Alveolar Damage and Bronchiolitis Obliterans- Organizing Pneumonia. Katzenstein and Askin's surgical pathology of non-neoplastic lung disease. 1997, Philadelphia: W.B. Saunders, x: 477-3
Protheroe CA, Woodruff SA, DePetris G, Mukkada V, Ochkur SI, Janarthanan S, Lewis JC, Pasha S, Lunsford T, Harris L, et al: A novel histological scoring system to evaluate mucosal biopsies from patients with eosinophilic esophagitis. Clinical Gastroenterology and Hepatology. 2009, 7: 749-755. 10.1016/j.cgh.2009.03.022.
Identifiable eosinophil infiltration and/or degranulation is defined as >1 intact eosinophil in at least a single 40x high powered field and/or ?10% of any single 40x high powered field displaying evidence of extracellular deposition of EPX without the presence of infiltrating eosinophils:
Shrout PE, Fleiss JL: Intraclass correlations: uses in assessing rater reliability. Psychol Bull. 1979, 86: 420-428.
Grigoryev DN, Finigan JH, Hassoun P, Garcia JG: Science review: searching for gene candidates in acute lung injury. Crit Care. 2004, 8: 440-447. 10.1186/cc2901.
Levitt JE, Gould MK, Ware LB, Matthay MA: The pathogenetic and prognostic value of biologic markers in acute lung injury. J Intensive Care Med. 2009, 24: 151-167. 10.1177/0885066609332603.
The authors wish to thank the members of Lee Laboratories as well as pulmonary colleagues Drs. David Jacoby and Charlie Irvin for insightful discussions and critical comments during the preparation of this review. We also wish to acknowledge the invaluable assistance of the Mayo Clinic Arizona Statistical support group (Amylou Dueck, PhD and Joseph Hentz), our staff medical graphic artist (Marv Ruona), and the excellent administrative support provided to Lee Laboratories by Linda Mardel and Shirley ("Charlie") Kern. The Mayo Foundation and grants from the NIH (HL058723, HL065228, RR0109709) were the sole sources of funding used in the performance of studies as well as data analysis. These funding sources provided salary support for individual investigators contributing to this report and funding for the supplies and reagents needed to complete the describe studies.
Copyright Statement: Copyright transfer is subject to applicable Mayo terms located on the following page: http://www.mayo.edu/copyright/.
The authors declare that they have no competing interests.
The corresponding author (JJL) had full access to all of the data reported in this study and had final responsibility for the decision to submit this report for publication. KP, LW, KL, JJL, designed research study; LW KP, CAP, EJ, PG, KL, and JJL performed research; CAP and NAL contributed new reagents/analytical tools; LW, CAP, RM, KL, and JJL analyzed data; and LW, KL, NAL, and JJL wrote the paper. All authors read and approved the final manuscript.
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Cite this article
Willetts, L., Parker, K., Wesselius, L.J. et al. Immunodetection of occult eosinophils in lung tissue biopsies may help predict survival in acute lung injury. Respir Res 12, 116 (2011). https://doi.org/10.1186/1465-9921-12-116
- Acute Lung Injury
- Acute Respiratory Distress Syndrome
- Eosinophil Peroxidase

domain: literature


text:
Lightning has brought the Iowa Corn Cy-Hawk game to a halt.
Twice in the first 20 minutes of game action lightning has struck within an eight-mile radius, prompting an automatic 30-minute delay. The delay clock re-starts after each lightning strike.
In the first quarter, the game was delayed officially for 49 minutes, while the current delay began at 4:45 p.m.
here’s the play in full https://t.co/biUXjAAccF— noah (@noahrohlfing) September 14, 2019
Following the first delay, Iowa State scored a touchdown on a wide receiver pass trick play, with Deshaunte Jones finding La'Michael Pettway to put the Cyclones up 7-3.
Iowa State will have the ball at its own 20 with 13:24 left in the second quarter when play resumes.

domain: game


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Written on: September 15, 2020 by SprayTM
The U.S. Environmental Protection Agency (EPA) has confirmed the acceptance of Zep Antibacterial Disinfectant & Cleaner with Lemon, Zep Spirit II Ready-To-Use Detergent Disinfectant and Zep All Purpose Bathroom Disinfectant to protect against COVID-19. It was based on testing that demonstrated the products kill the virus on hard non-porous surfaces in 60 seconds.
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Zep has worked with regulatory authorities to secure and commercialize a label against SARS-CoV-2 for these three products (listed under EPA Registration No. 1839-83), based on the primary registrant status. Additionally, 17 other Zep disinfectants are already included on the EPA’s List N and contain an emerging virus pathogen claim for use against SARS-CoV-2.
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domain: chemistry


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|Nov. 16, 2017||【Web Release】Prof Junji KIDO was selected as one of "Highly Cited Researchers for 2017" for four consecutive years.|
Prof Junji KIDO was selected as one of “Highly Cited Researchers (HCR)” for four consecutive years by Clarivate Analytics, a world information service company. This year 6 researchers from Japan are listed in Materials Science field.
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domain: news


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Is it just us, or has TV been double-dipping in the character pool a lot lately? From mystical look-alike ancestors to long-lost twins, EW ranked each twist pairing from the least to the most bananas. Just call them (drumroll, please!) “banana splits.”
Tobias Menzies, Outlander
The fantasy drama introduced Menzies — time-traveling Claire’s historian husband — in 1945…
“Black Jack” Randall
…but, as revealed in the pilot, Frank gets his looks from a sadistic ancestor Claire faces in 1743.
RATING: 1 BANANA. Frank and Black Jack’s resemblance is entirely plausible.
Patti LuPone, Penny Dreadful
LuPone’s witch — nicknamed the “Cut-Wife” — dealt with the devil in a season 2 episode…
…and lived long enough to produce a distant descendant who shares her visage — but not her coif — in season 3.
RATING: 2 BANANAS. It’s one unexpected, hair-raising return.
Seth Meyers, The Mindy Project
Meyers wooed Mindy at a bookstore and won her over with frozen yogurt in a 2012 episode…
…and reappeared this season as himself to help Morgan find his missing dog.
RATING: 3 BANANAS. Mindy never forgets a suitor. Maybe “Matt” is Meyers’ alias?
Dan Amboyer, Younger
Kelsey’s fiancé bit the dust this season after finding out Liza’s age-defying secret…
…but Thad turned out to have a secret of his own: a poncho-wearing twin brother.
RATING: 4 BANANAS. Liza never saw a second dirtbag love interest for Kelsey coming.
Yael Grobglas, Jane the Virgin
Petra has had her fair share of telenovela-worthy drama…
…and this twist — a long-lost twin — might be the toughest she’s faced.
RATING: 5 BANANAS. How did Petra, who knows everything about everyone, miss this?
A version of this story appears in issue #1414 of Entertainment Weekly, available here.


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With New Partner, Rackspace Builds Out Support for Rivals’ Clouds
San Antonio — [Updated 4/27/16, 3:32 p.m. See below.] Cloud-computing giant Rackspace has made a deal to work with a Boston company that helps large businesses transfer their IT services to cloud-based infrastructures like Amazon Web Services. It’s a move that comes as Rackspace is increasingly finding ways to make money along with the public cloud services it competes with.
Rackspace (NYSE: RAX), which builds and manages public and private cloud IT environments for some 300,000 business customers worldwide, wrote in regulatory filings as recent as March 2014 about the competition it faces from “substantial investments” being made in cloud computing by “large, diversified companies such as Amazon, Google, HP, IBM and Microsoft.”
How quickly things change—or appear to, anyway. By October 2014, the company had announced an agreement to work with customers of Google Cloud, specifically its workplace productivity suite Google Apps for Work, which was followed in 2015 by deals with Amazon Web Services (AWS) and Azure, and others this year. [Wording added to clarify that Rackspace provides support for Google’s workplace productivity suite, not to be confused with Google Compute Engine.]
Based in the San Antonio suburb of Windcrest, TX, Rackspace has done well with its traditional means of making money, reporting $2 billion in 2015 revenue. It builds cloud-based IT infrastructures—public, private, or dedicated—for customers that are hosted by its 11 data centers worldwide, and manages the cloud infrastructures with customer service that it brands as “fanatical” support. The work with companies like Google and Amazon allows Rackspace to make money on its customer support side, even if isn’t on the hosting.
Founded in 1998, Rackspace’s mission is no different now than when the company was started, says Tom Bressie, director of marketing for the Rackspace division focused on Amazon Web Services. Even though Rackspace has its own storage offerings, it wants to provide IT expertise to customers regardless of the technology infrastructure they choose, Bressie says.
“What we want to do is basically serve as an expert for the market, where if they want help in choosing an infrastructure, we can help. If they’ve already made an infrastructure decision and want services and support, we can provide that as well,” he says. “Our customers pull for a variety of different infrastructure options, and that’s why you see the variety [of services] at Rackspace.”
Rackspace’s new deal with Boston-based Cloud Technology Partners is furthering the company’s expansion into supporting customers even if they have chosen other cloud providers. Cloud Technology Partners has built its business on helping large companies migrate their IT services to the cloud environments of AWS, Azure, and Google Cloud. The company targets larger, Fortune 500-sized businesses that not only need help building the architecture for their IT system in the cloud environment, but also want assistance transferring and optimizing various applications and technology, according to Brian Ott, a vice president at Cloud Technology Partners.
“We go through a logical set of steps looking at their application portfolio, their security, their architecture, and help them build their target architecture, helping with the migration of the applications, the automation of applications that help support and sustain the cloud,” Ott says.
In the deal, both companies will work with the client throughout the process, making sure they can help the client to manage and work in the new cloud system, Ott says. How the revenues will be shared will depend on the agreement with the client, Ott says.
“Enterprises are making that transformation from that current set of technologies into the cloud because they see value in what the cloud offers for their business,” Bressie says. “Once you get them there, you’re not done. You still need experts to run things on a day by day basis, if you don’t want to be distracted from your business’s core mission.”
Rackspace’s shift to building out the business for managing sales and support for cloud services like AWS and Google has had an impact. It moderately slowed revenue growth, which was 11.5 percent in 2015, down from 16.8 percent a year earlier, the company wrote in a regulatory filing.
“These represent large and rapidly growing target markets in which Rackspace is well positioned, but as with any new businesses we project that they will take time to reach the scale required to re-accelerate our revenue growth,” the company wrote in a filing.
Along with the deal, Rackspace made an investment in Cloud Technology Partners, Ott says. He declined to specify the amount.
Cloud Technology Partners was founded in 2011 and has raised $17.4 million (before the Rackspace investment) from investors that include Pritzker Group Venture Capital, Oak Investment Partners, State Street Bank, and Greylock Partners. Started by Chris Greendale, one of the founders of Cambridge Technology Partners, Cloud Technology Partners said in 2015 that its revenues had increased 100 percent year over year.
A plethora of companies, from Accenture to IBM, offer services to help large enterprises transfer their applications, servers, and other IT tools to the cloud. Ott contends that Cloud Technology is appealing because users can choose between multiple cloud providers, rather than being confined to one vendor, and that working with Rackspace provides an “end-to-end” service, from transfer to management.
For Rackspace, which already provides similar transfer services, its new partner is attractive because Cloud Technology Partners already has the trust of large enterprises and is better able to deal with the scale and “drastically complex IT portfolios” of those larger businesses, Bressie says.
Rackspace typically acts as a reseller of services such as AWS. If a user pays Rackspace for managing AWS, it typically also pays Rackspace for the AWS consumption, which Rackspace in turn pays to Amazon, Bressie says.


He's such a long standing modder, I'm sure he'll be back.FLOZi wrote:G_Z hasn't visited in over 10 days, so we can probably assume he's disappeared back into the ether.
I don't think you can do UV-mapping in Rhino3D. Nor meddle with, uh, normals and welding and smooth or hard edges and those kind of things I don't have experience with. I'd recommend using Wings3D. Wings3D is simple enough to become quickly productive, yet Wings3D is powerful enough to cover all your Spring modelling and unwrapping needs. It just has all that is needed, and none of that is un-needed , which is a plus, that way you don't get lost in a maze of menu. You'll need a tutorial open for your first models, because modelling in Wings3D is done in a different way than in Rhino3D, but after maybe 2 models you'll manage alone. If you've never done it you'll need to read a tutorial on UV-mapping in Wings3D, but Wings3D unwrapper is so nice to use you could almost do without help.GrOuNd_ZeRo wrote:What are the standards today? especially for UV mapped models? what software is the standard? Rhino3D still good?
Some people model with Blender. Blender is much more powerful than Wings3D. However, half of Blender possibilities are irrelevant for modelling Spring units. And Blender has an horrible interface, while it's said to be efficient once your learn it, learning it is a real obstacle.
Of course, there's plenty of other quality modelling software out there, and I bet many can do UV-mapping, but then not only you'd have to buy it, but you'll also be on your own to learn to use it, while there's lots of Spring-specific Wings3D help and tutorial around, since that's what the majority of Spring modders use.
Oh and AFAIK you still need UpSpring to convert models to s3o, though there's an ongoing coding effort to remove that.
Otherwise, you need a image editor than handles alpha channel. Gimp would do it, but if you have photoshop, that's better. Personnaly I use an old Paint Shop Pro to draw images, and Gimp only to assemble the 4 channels and save (as the non-sensical interface of Gimp is highly irritating, items are never in the menu they ought to be).
And a text editor. I'd recommend Notepad++. While it doesn't seem much at first, using Notepad++ instead of Microsft Notepad or Wordpad to type your FBI and TDF and LUA really does make a difference on the long run.
For writing unit animation scripts, you can still use Scriptor. People will tell you to drop Scriptor and to write animation script in Lua instead. Sure, that's a possibility, but if you have 8 years of experience with Scriptor, do you really want to have to re-learn how to write an animation?
Wings3D, Blender, Gimp and Notepad++ are free.
UpSpring and Scriptor are getting lost in the depth of Spring forums & wiki dead links.
There is a Subforum: Modelling & Texturing Tutorials & Resources, Spring's wiki, and lastly, don't forget googling for tutorials.


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Manx teams took part in inaugural competition in Guernsey
The Isle of Man's men's and ladies' darts teams have been praised for their displays at a inaugural competition held in Guernsey at the weekend.
Twenty players represented the Island at the first ever Island Internationals which was held at the St Pierre Park Hotel in the crown dependency from 27-29 January.
For the ladies team, despite a tough start with a 5-2 defeat to Guernsey and 6-1 loss to Ireland, the Manxies rallied back to take a 5-2 victory over Jersey.
They then went on to overcome Jersey again by a scoreline of 4-0 in the third and fourth place play-off.
Meanwhile, the men's team started with a narrow 6-7 loss to Guernsey, before a 12-1 defeat to Ireland and 4-9 loss to Jersey.
But the men's squad - which saw several players making their international debuts with a number of senior figures unavailable - then put in a valiant display in the third and fourth place play-off with Guernsey despite eventually losing out 4-7.
The Isle of Man Darts Organisation says it's 'very proud' of all those who competed for the Island, saying they represented the Manx flag 'fantastically' across the weekend.


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23 May 2008
John Nost Sartorius (1759-1828)
signed and dated 'J.N. Sartorius p.t 1809' (lower right)
oil on canvas
19 x 26 5/8 in. (49 x 67.5 cm.)
with Arthur Ackermann & Sons Ltd, London.
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Pop art was not an all-American phenomenon — the UK, in fact, was where it started. Illustrated with works from our Modern British Art sales in June
Artists, patrons and critics have argued for centuries over the right way to frame a painting. Ultimately, it’s a matter of personal taste, says Andrew Graham-Dixon
What a newcomer need to know about the highly collectable, grain-based liquor served at all Chinese state banquets
The designer and decorator shows us around his Santa Monica HQ, and enthuses over the forthcoming Rooms as Portraits auctions in London and New York


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|Carambola Botanical Gardens is a popular destination just a few miles outside of West End and one of the tours of choice for the flocks of cruise ship visitors to the island. I met Vanessa, one of the tour guides who works at the park one day back in December when I was travelling by collectiva into Coxen's Hole to try to Christmas shop for John. I was full of questions about the flora along the bus route because I'm try to learn to identify all the plants and trees, a daunting task because there are countless species in the rain forest and the jungles.
Vanessa remembered me when John and I showed up at the park one day this week. We browsed through the huge garden and hiked the jungle and mountain trails, amazed how cool it was in the shade despite the heat of the day. The view from the top of Anthony's Cay below was spectacular.
Back at the boat the Captain built a frame for the 75 watt solar panel and a small 10 watt panel that he picked up for next to nothing. The 75 watt panel gives us 4.7 amps of power. Our fridge used 3.2 amps, leaving only 1.5. The small 10 watt panel gives us an additional .5 watts or approx 30% more power over and above the fridge. It wasn't easy lifting it up on to the top of the flybridge and I was shocked when John, with his fear of heights told me he planned to climb on to a two by four wedged behind the spotlight so that I could hand the unit up to him. Then I ran up into the flybridge and guided it as he passed it up. This new location will give us several additional hours of sunlight on the panels vs the temporary location on the deck which was in shade by about 2:30-3 pm when the sun is shining on the back of the boat. Except for rare occasions when a storm comes, the predominant winds blow from the east and since we are on an anchor we also face east, with the back deck facing west, perfect for watching the sun set in the evening.

domain: travel