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Adam Epstein Talks Editing for SNL and "The Cutting Edge" Workshop
SNL editor Adam Epstein opens up on the incredibly fast workflow of editing for a weekly sketch comedy show. Adam Epstein is a freelance editor. For the last five years, he's worked with the Saturday Night Live film unit, editing parody pieces of all kinds. He's just begun a nationwide workshop tour with "The Cutting Read MoreRead More


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Sure, Justin Bieber may be a capital-D Douche Bag, but apparently, the dude is a beast on skates.
Naturally, Bieber's naked selfie on Shots has gotten more attention today, but a seriously impressive goal that he scored during a rec league hockey game is also fully deserving of your attention:
"My dangles were unreal did u see that shot...#dontf--kwiththecanadian" Bieber wrote on Instagram beneath a clip of him juking defenders out of there skates.
Obviously, homey does a lot of bragging, but in this case, it's warranted. If this whole "being the world's biggest pop star" thing doesn't work out, he may have a future in the NHL.
The Biebs has been showing off his athletic skills all over social media recently. Earlier this week, Bieber sparred with Floyd Mayweather (shirtless, of course), and he lived to tell the tale, which is an impressive feat in its own right.

subset: commoncrawl


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Related Photo Galleries
The first step to welding in your new piece is to place tack welds in key locations to simply hold the part in place. All seams are butted together, and all welds are a series of tack welds. There is no stitch welding! The goal is to achieve good weld penetration, but to use minimal heat to prevent any distortion of the area involved. The process is simple. Start by placing a tack weld about an inch apart, all along the seam. Cool the area with compressed air, and move back and forth across the part as you go. Then go around the part again, putting another tack weld in between the ones you just did. Do this a third time and you should be left with approximately quarter-inch spaces between all your welds. Resist the temptation to run short bead welds to fill in the remaining gaps. Instead, do a series of three quick tack welds, essentially tack welding the tack welds together. This might sound like it could take a lot of time, but it really progresses faster than you think, and you really save time by reducing your finish bodywork to an absolute minimum. When you have finished, use a 3M reinforced grinding wheel to grind the weld nearly flush with the sheetmetal. Watch that you don't grind any of the body panels as they will get thin quickly. When you are finished, look the seam over closely to see if there are any small gaps or pinholes that might need a quick tack to fill in. A quick pass with an 80-grit grinder is a good idea to smooth everything out.


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James H. Faghmous, Ph.D.
I'm James, it's nice to meet you!
I am a computer scientist that works at the intersection of machine learning, data mining, and spatio-temporal data analytics, or broadly speaking, spatio-temporal data mining. I am passionate about creating actionable knowledge from data, especially in socially relevant domains such as climate, cognitive neuroscience, and ecology. In 2014, my Ph.D. thesis on spatio-temporal data mining received the University of Minnesota's Best Ph.D. Dissertation Award in Physical Sciences and Engineering. For the past three years I have been part of a growing interdisciplinary community working on novel algorithms to analyze large climate datasets -- known as
Climate Informatics
or (a subset of) Computational Sustainability (think bioinformatics back in the early 1990s). My current work is funded through a $10M/5 year grant from the US National Science Foundation's Expeditions in Computing Program. The Expeditions program is the single largest investment by the NSF in basic computer science research.
What's Spatio-Temporal Data Mining
Spatio-temporal data mining (STDM) refers to a set of techniques that pay special attention to the data's spatial and temporal characteristics to build more accurate, scalable, and interpretable models relative to non-space-time aware models.
Why STDM?
STDM methods are emerging as alternatives to traditional learning algorithms that are not well-suited for spatio-temporal data. For example, some of the most elegant statistical learning algorithms impose strong independence assumptions on the data, which cannot be guaranteed in autocorrelated data where values in proximity (in space and time) tend to be related.
Value of STDM
By intelligently mining the data's spatio-temporal context we can improve upon existing methods in several ways:
: Currently, it is almost impossible to take an off-the-shelf statistical learning package and use it to analyze spatio-temporal data. This is because non-space-time aware learning methods generalize poorly to unseen spatio-temporal data. However, if we are able to transform the data (
feature engineering) based on their spatio-temporal context we may obtain more generalizable models.
Analyzing the spatio-temporal context of the data can provide an objective way to reduce the computational complexity of learning algorithms by reducing the search space or sparcifying the data.
Learning methods are constantly balancing flexibility with interpretability. The more flexible a model is, the more "accurate" but simultaneously the less interpretable. In many interdisciplinary fields, scientists place higher value on interpretability than on accuracy (
black-box models have low adoption despite their accuracy). Creating models that are interpretable in space and time creates a seamless and more intuitive experience with how people think about spcae-time phenomena.
Peer-Reviewed Publications
Conference Proceedings
Faghmous, J.H
., H. Nguyen, M. Le, and V. Kumar. Spatio-temporal Consistency for Autonomous Dynamic Object Identification in Continuous Spatio-Temporal Fields. Twenty-Eighth Conference on Artificial Intelligence (AAAI) 2014.
Faghmous, J.H
., M. Le, M. Uluyol, and V. Kumar. Parameter-Free Spatio-Temporal Data Mining to Catalogue Global Ocean Dynamics. Thirteenth IEEE International Conference on Data Mining (ICDM) 2013.
Faghmous, J.H.
, M. Uluyol, M. Le, L. Styles, V. Mithal, S. Boriah, and V. Kumar. Multiple Hypothesis Object Tracking for Unsupervised Self-Learning: An Ocean Eddy Tracking Application. Twenty-Seventh Conference on Artificial Intelligence (AAAI) 2013.
Faghmous, J.H.
, L. Styles, F. Vikebø, S. Boriah, S. Liess, M. d.S. Mesquita, and V. Kumar. EddyScan: A Physically Consistent Eddy Monitoring Application. Conference on Intelligent Data Understanding (CIDU) 2012. Best Student Paper Award
Faghmous, J.H.
, Y. Chamber, F. Vikebø, S. Boriah, S. Liess, M. d.S. Mesquita, and V. Kumar. A Novel Spatio- Temporal Method for Ocean Eddy Monitoring. Twenty-Sixth Conference on Artificial Intelligence (AAAI) 2012.
Faghmous, J.H.
, A. Banerjee, A.R. Ganguly, S. Shekhar,, M. Steinbach, N. Samatova, and V. Kumar. Data Science for a Changing Climate: From Analytics to Insights. IEEE Computer, 2014
Faghmous, J.H.
and V. Kumar A Big Data Guide to Understanding Climate Change: The Case for Theory-Guided Data Science. Big Data, 2014 Ganguly, A.R., Kodra, E. A., Banerjee, A., Boriah, S., Chatterjee S., Chatterjee, S., Choudhary, A., Das, D.,
Faghmous, J.H
., et al. Toward enhanced understanding and prediction of climate extremes using physics-guided data mining techniques. Nonlinear Processes in Geophysics 2014.
Book Chapters
Faghmous, J.H.
and V. Kumar. Spatio-Temporal Data Mining for Climate Data: Advances, Challenges, and Opportunities. In W. Chu, Ed., Data Mining and Knowledge Discovery for Big Data: Methodologies, Challenges, and Opportunities. Springer, 2013. Karpante A.,
Faghmous J.H.
, Kawale J., et al. Earth Science Applications of Sensor Data. In C. Aggarwal, Ed., Managing and Mining Sensor Data. Springer, 2012.
Invited Talks
The Impact of Expert Heuristics on The Significance of Unlabelled Spatio-Temporal Patterns. Workshop on Spatial Statistics for Environmental and Energy Challenges, King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia, March 2014 Spatio-Temporal Data Mining Methods to Identify Mesoscale Ocean Eddies from Satellite Altimeter Data. Workshop on Clouds, Convection and Data. NYU Abu Dhabi, Abu Dhabi UAE, March 2014 Parameter-Free Spatio-Temporal Data Mining to Catalogue Global Ocean Dynamics. Institute for Mathematics and Its Applications (IMA) Special Workshop on Predictability in Earth System Processes. The University of Minnesota, Minneapolis, MN November 2013 The Impact of Spatio-Temporal Variations in Sea Surface Temperatures on Atlantic Tropical Cyclone Frequency. Expeditions in Computing Annual Workshop. Northwestern University, Evanston, IL, August 2013 Climate Change and Variability: A Spatio-Temporal Data Mining Perspective. Department of Computer Science Colloquium, The University of California at Santa Barbara, CA, June 2013 ENSO's Spatial Warming Patterns and their Impact on North Atlantic Tropical Cyclone Activity. Department of Earth System Science Seminar, The University of California at Irvine, CA, June 2013 Data-Driven Methods to Leverage Satellite Altimeter Observations. California Institute of Technology, Pasadena, CA, June 2013 Scalable Spatio-Temporal Data Mining Algorithms for Global Ocean Eddy Monitoring. IEEE SuperComputing'12 Climate Knowledge Discovery Worksop, Salt Lake City, UT, November 2012 Leveraging Statistical Machine Learning to Complement Physics-Based Hurricane Models. National Center for Atmospheric Research (NCAR), Boulder, CO, April 2012 Climate Science's Big Data Challenge and How Artificial Intelligence Can Help. The Interdisciplinary Climate Seminar. The City College of New York, New York, NY March 2012 Tropical Cyclogenesis: A Machine Learning Approach. NorWRF2011, Bergen, Norway, September 2011
2013: NSF EAGER: Building and Analyzing Dynamic Functional Brain Networks. Co-PI. $116,000/1 year 2011: NSF Nordic Research Opportunity Grant. PI. $25,000/4 months 2010: NSF Expeditions in Computing - Understanding Climate Change: A Data-Driven Appraoch. Graduate Student. $10M/5 years 2007: NSF Graduate Research Fellowship. PI $150,000/3 years 2006: NIH-Neuro-Physical-Computational Graduate Fellowship. PI $100,000/2 years
The OpenEddy Project
Figure: Eddies meandering from the Gulf Stream. Figure from: http://earth.nullschool.net/
This project focuses on identifying descrete objects in continuous spatio-temporal fields. We use satellite altimeter data to monitor ocean eddy activity on a global scale. For more information please visit the OpenEddy site.
Spatio-Temporal Hurricane Predictions
Figure: Hurricane tracks viewed from the South Pole. Figure from IDV Solutions
This project seeks to analyze the large-scale spatio-tempoal patterns in climate data (e.g. sea surfrace temperature, surface pressure, etc.) to better predict global hurricane activity on interannual timescales.
Functional Brain Networks
Figure: A probabilistic functional brain network. Figure from Cambridge University.
This project seeks to develop novel functional brain networks where regions that serve the same purpose are grouped together. These netwroks are commonly constructed based on spatial proximity and we are attempting to group regions based on how similar their spatio-temporal activation patterns are based on fMRI data.
2014 University of Minnesota Best Ph.D. Dissertation Award in Physical Sciences and Engineering MN Cup Business Plan Competition, 2nd Place ($5000 cash prize), 2013 Mary A. McEvoy Award for Public Engagement and Leadership, University of MN, 2012 President's Student Leadership and Service Award, University of MN, 2012 Doctoral Dissertation Fellowship, University of MN, 2012 Best Student Paper Award, The NASA-IEEE Conference on Intelligent Data Understanding, 2012 National Science Foundation Graduate Research Fellowship, 2008-2011 NIH-Neuro-Physical-Computational Graduate Fellowship, 2006-2008 Grove School of Engineering Outstanding Leadership Award, City College of New York, 2006 Rhodes Scholarship nominee, City College of New York, 2006 2004 CUNYAC Scholar-Athlete Team (Men's Basketball), City University of New York, 2004
Doctor of Philosophy, Computer Science
The Univeristy of Minnesota - Twin Cities
Minneapolis, MN
Advisor: Vipin Kumar, Ph.D.
Masters of Science, Computer Science
The University of Minnesota - Twin Cities
Minneapolis, MN
Bachelors of Science, Computer Science
The City College of New York
New York, NY
Advisor: George Wolberg, Ph.D.
Advice for graduate students
How to win an NSF Graduate Research Fellowship How to pick a Ph.D. program Edsger Dijkstra's "The Three Golden Rules for Successful Scientific Research"
Musings about entrepreneurship & data science
The Single Most Important Startup Lesson: How to Perform Inception on Your Customers Digitize or Sink — The Future of Higher Education Stop Lying That You Have a Tech Startup New to Machine Learning? Avoid These Three Mistakes Read More.
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I always find it funny when I see someone who obsesses over their smartphone or tablet. Sure, they're great and all, but don't you find that some people are addicted to the Internet? To be fair, though, it is a completely reasonable addiction to have if you've also got yourself a subscription to DDF Network Mobile. I know I wouldn't be able to tear myself away from my mobile device in that situation!
If the name DDFNetworkMobile sounds familiar, then it's possible you've heard of its desktop counterpart DDF Network. Both of them provide the same content, which includes all the movies and galleries found on a variety of sites that focus on the same thing: babes with really big boobs. For the most part, we're specifically talking about European hotties with huge juggs, but you also get some famous American pornstars every now and then.
Their content is placed in order of date and most consist of both a movie and a photo set. You can go page by page, but there's also a very helpful pagination drop-down that lets you jump to any page you want. You can also choose the month you want to peruse and these go as far back as January 2001.
The good news is that you have a ton of material. There are about 12,000 photo sets and around 11,800 movies. Many of the flicks are marked with a Full HD option and each scene contains both downloadable and streaming options. Obviously not all mobile devices will be able to take advantage of both. However, the streams all look amazing, so if your device can't download, at least you aren't missing out on quality.
The network is growing at a very fast pace, with new content getting added anywhere from three times to five times on an almost daily basis. Coming from several sites, some scenes will show the model just stripping and posing, but others offer blowjobs and hardcore sex and plenty give you masturbation and lesbians. The pages aren't all auto-formatted for smaller screens like an iPod Touch, but just double-tap it or do a quick 2-finger pinch and it will all line up perfectly.
These busty beauties are simply gorgeous. The thumbnails for each episode are a good size and you can see hotties sucking on the nipples of other babes on DDF Busty Mobile, girls showing off their sexy legs and feet on Hot Legs And Feet Mobile and there's a good amount of cock sucking on Only Blowjob Mobile. If you like hairy pussies, go for the content on Hairy Twatter Mobile and House Of Taboo Mobile will satisfy those looking for some edgier fetish porn.
Also, as a nice bonus you get access to the desktop version of this site for free, so when you are in front of your computer you can enjoy all this great porn on a site formatted for the larger screen. Plus, with so much high-quality content and with so many updates every day, you're not exactly going to be needing a lot of extras anyway. It goes without saying that you get your money's worth when you sign up to DDF Network Mobile.
|By: Adam Strong
|Number of Reviews: 483
|Average Score: 62.2
$33.99/30 days (Reg. $
$114.99/365 days (Reg. $
|$0.00/2 days, rebills at $44.95
|Cross Sales: 1 pre-checked
|Pic sets: 12000+
|Pics per set: 120
|Zip sets: No
|Pic Res: N/A
|High Res: No
|Number of movies: 11800+
|HD Porn: No
|Streaming: Yes
|Average Length: 20 mins
|Full length videos: Yes
|Download Limits: No
|Video Formats:
MP4 (streaming)
|Preview DDFNetworkMobile.com members area
|Independent Biller(s):
|CCBill, VXS Billing
|Customer Service:
Pros & Cons
-amazing-looking movies
-multiple updates almost every day
-lots of content
-can't save favorites
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-expensive trial rebill
08/03/2013- Stays at 84. -Will
03/04/2013- From 82 to 84: More content and Usability score adjustments. -A.K.
- Initial review: 7/2/2012
|Content Quality
|Content Amount
|Unique Content
|Video Downloads
|Video Streaming
|Other Score
|User Score: N/A
|0 votes
|0 comments
|User Top Rated Sites


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Village Hill, Anne T. Dunphy: What's in a name?
The controversy in Williamsburg about possibly renaming the renovated Anne T. Dunphy School (full disclosure: I was a teacher's aide in the Burgy schools in the early 1980s) raises a number of questions particular to Williamsburg. The interface between the families who have been there for generations and those who are more recent arrivals has always been a bit rough. Friction is inevitable. I'm inclined to think history should be honored.
But these matters also arise here in the city. As Village Hill development continues at a rapid pace on what was not so long ago known as Hospital Hill, those of us who have lived here for even a few decades wonder why the State Hospital that once dominated that landscape and employed so many city residents (not to mention buried so many patients in the so-called "Dog Walk" area) should be so thoroughly forgotten, expunged from all mention. Only the PVTA bus and one bike path sign still bear the name Hospital Hill. Old-timers may still call the sledding hill Hospital Hill, but otherwise, memories are short.
There's supposed to be a memorial —the old fountain—someday, with new houses set to start their inexorable march over the top of the hill where once the Old Main building stood. Without some reminder, few will remember the hospital, its workers and its patients.
Or the former depths of its woodlands. I heard a thrush singing the other day. Thrushes like deep woods. We'll lose them if we destroy too much of their habitat.
Sweet summer
The linden trees are dropping their scapes, soon to release the subtle perfume of their flowers. It's also the season of roses and mock orange. While it stayed cool, the iris and peonies lasted longer.
Hoop heaven
It was the day of the final NBA championship game, and on the basketball court at Veterans Field a small towheaded boy was tossing a basketball underhand, Rick Barry foul shot style,* up and over and through the hoop, again and again, never missing all the time I watched.
*I would not have known that Rick Barry was known for that, but my husband knew.
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Year of publication
Document Type
- Article (40)
- Doctoral Thesis (14)
- Conference Proceeding (1)
- Gentherapie (2)
- gene therapy (2)
- CIK cells (1)
- Fusionsinhibitor (1)
- Glykoprotein GP 41 (1)
- HIV infection (1)
- HIV-Infektion (1)
- M87o (1)
- Georg-Speyer-Haus (55)
- Medizin (23)
- Biochemie und Chemie (7)
- Biowissenschaften (7)
- Pharmazie (1)
- Ökosystem statt Nutzwald (2011)
- Wichtiger Teilerfolg in der Gentherapie : Interview mit Dr. Marion Gabriele Ott und Dr. Manuel Grez (2006)
- Die Septische Granulomatose (CGD) ist eine seltene Erkrankung, die auf einem genetischen Defekt bestimmter weißer Blutzellen beruht, die darauf spezialisiert sind, in den Körper eingedrungene Pilze und Bakterien aufzuspüren und zu vernichten. Frankfurter Ärzten und Wissenschaftlern um Prof. Dr. Dieter Hoelzer vom Klinikum der Johann Wolfgang Goethe-Universität und Dr. Manuel Grez vom Chemotherapeutischen Forschungsinstitut Georg-Speyer-Haus gelang es, eine intakte Kopie des defekten Gens in Blutstammzellen von zwei erwachsenen CGD-Patienten einzuschleusen und so die Funktion der Fresszellen teilweise wieder herzustellen. Eine vollständige Heilung gelang jedoch nicht – ein Patient verstarb zwei Jahre nach der zunächst erfolgreichen Behandlung an seiner Grunderkrankung. Im Gespräch mit Dr. Anne Hardy berichten Dr. Marion Gabriele Ott (Arbeitsgruppe Hoelzer) und Dr. Manuel Grez (Georg-Speyer-Haus) über die Höhen und Tiefen ihrer gentherapeutischen Forschung.
- Vaccination Directed against the Human Endogenous Retrovirus-K Envelope Protein Inhibits Tumor Growth in a Murine Model System (2013)
- Human endogenous retrovirus (HERV) genomes are chromosomally integrated in all cells of an individual. They are normally transcriptionally silenced and transmitted only vertically. Enhanced expression of HERV-K accompanied by the emergence of anti-HERV-K-directed immune responses has been observed in tumor patients and HIV-infected individuals. As HERV-K is usually not expressed and immunological tolerance development is unlikely, it is an appropriate target for the development of immunotherapies. We generated a recombinant vaccinia virus (MVA-HKenv) expressing the HERV-K envelope glycoprotein (ENV), based on the modified vaccinia virus Ankara (MVA), and established an animal model to test its vaccination efficacy. Murine renal carcinoma cells (Renca) were genetically altered to express E. coli beta-galactosidase (RLZ cells) or the HERV-K ENV gene (RLZ-HKenv cells). Intravenous injection of RLZ-HKenv cells into syngenic BALB/c mice led to the formation of pulmonary metastases, which were detectable by X-gal staining. A single vaccination of tumor-bearing mice with MVA-HKenv drastically reduced the number of pulmonary RLZ-HKenv tumor nodules compared to vaccination with wild-type MVA. Prophylactic vaccination of mice with MVA-HKenv precluded the formation of RLZ-HKenv tumor nodules, whereas wild-type MVA-vaccinated animals succumbed to metastasis. Protection from tumor formation correlated with enhanced HERV-K ENV-specific killing activity of splenocytes. These data demonstrate for the first time that HERV-K ENV is a useful target for vaccine development and might offer new treatment opportunities for diverse types of cancer.
- The viral vector vaccine VSV-GP boosts immune response upon repeated applications (2012)
- Poster presentation AIDS Vaccine 2012 Boston, MA, USA. 9-12 September 2012 Background: Vesicular stomatitis virus (VSV) is a potent candidate vaccine vector for various viral diseases (e.g. HIV, HCV, RSV). The biggest limitation of VSV, however, is its neurotoxicity, which limits application in humans. The second drawback is that VSV induces neutralizing antibodies rapidly and is thus ineffective as a vaccine vector upon repeated applications. Our group has recently shown that VSV pseudotyped with the glycoprotein (GP) of the lymphocytic choriomeningitis virus (LCMV), VSV-GP, is not neurotoxic. The aim of this project was to evaluate the potential of VSV-GP as a vaccine vector. Methods: For this purpose, we used Ovalbumin (OVA) as a model antigen and analyzed immunogenicity of GP-pseudotyped and wildtype VSV containing OVA (VSV-GP-OVA and VSV-OVA) in vitro and in vivo in mouse models. Results: We showed that both vectors infected murine bone marrow-derived dendritic cells (bmDCs) in vitro. These bmDCs were able to activate OVA specific CD8+ and CD4+ T cells. Immunization experiments in mice revealed that both VSV-OVA and VSV-GP-OVA induced functional OVA-specific cytotoxic T cells (CTLs) after a single immunization. In addition, with both viruses, mice generated antibodies against OVA. However, boosting with the same virus was only possible for the GP-pseudotyped virus but not for wild type VSV. The efficacy of repeated immunization with VSV-OVA was most likely limited by high levels of neutralizing antibodies, which we detected after the first immunization. In contrast, no neutralizing antibodies against VSV-GP were induced even after boosting. Conclusion: Taken together, we showed that the non-neurotoxic VSV-GP is able to induce specific T cell and B cell responses against the model antigen OVA to the same level as the wild type VSV vector. However, in contrast to wild type VSV, VSV-GP-OVA boosted the immune response upon repeated applications. Thus, VSV-GP is a promising novel vaccine vector.
- The T-cell oncogene Tal2 Is a Target of PU.1 and upregulated during osteoclastogenesis (2013)
- Transcription factors play a crucial role in regulating differentiation processes during human life and are important in disease. The basic helix-loop-helix transcription factors Tal1 and Lyl1 play a major role in the regulation of gene expression in the hematopoietic system and are involved in human leukemia. Tal2, which belongs to the same family of transcription factors as Tal1 and Lyl1, is also involved in human leukaemia. However, little is known regarding the expression and regulation of Tal2 in hematopoietic cells. Here we show that Tal2 is expressed in hematopoietic cells of the myeloid lineage. Interestingly, we found that usage of the Tal2 promoter is different in human and mouse cells. Two promoters, hP1 and hP2 drive Tal2 expression in human erythroleukemia K562 cells, however in mouse RAW cells only the mP1 promoter is used. Furthermore, we found that Tal2 expression is upregulated during oesteoclastogenesis. We show that Tal2 is a direct target gene of the myeloid transcription factor PU.1, which is a key transcription factor for osteoclast gene expression. Strikingly, PU.1 binding to the P1 promoter is conserved between mouse and human, but PU.1 binding to P2 was only detected in human K562 cells. Additionally, we provide evidence that Tal2 influences the expression of the osteoclastic differentiation gene TRACP. These findings provide novel insight into the expression control of Tal2 in hematopoietic cells and reveal a function of Tal2 as a regulator of gene expression during osteoclast differentiation.
- Target-specific glioma therapy in an immunocompetent mouse model : meeting abstract (2006)
- Objective: Establishment of an immunocompetent mouse model representing the typical progressive stages observed in malignant human gliomas for the in vivo evaluation of novel target-specific regimens. Methods: Isolated clones from tumours that arose spontaneously in GFAP-v-src transgenic mice were used to develop a transplantable brain tumour model in syngeneic B6C3F1 mice. STAT3 protein was knocked down by infection of tumour cells with replication-defective lentivirus encoding STAT3-siRNA. Apoptosis is designed to be induced by soluble recombinant TRAIL + chemical Bcl-2/Bcl-xL inhibitors. Results: Striatal implantation of 105 mouse tumour cells resulted in the robust development of microscopically (2 – 3 mm) infiltrating malignant gliomas. Immunohistochemically, the gliomas displayed the astroglial marker GFAP and the oncogenic form of STAT3 (Tyr-705-phosphorylated) which is found in many malignancies including gliomas. Phosphorylated STAT3 was particularly prominent in the nucleus but was also found at the plasma membrane of peripherally infiltrating glioma cells. To evaluate the role of STAT3 in tumour progression, we stably expressed siRNA against STAT3 in several murine glioma cell lines. The effect of STAT3 depletion on proliferation, invasion and survival will be first assessed in vitro and subsequently after transplantation in vivo. Upstream and downstream components of the STAT3 signalling pathway as well as possible non-specific side effects of STAT3-siRNA expression after lentiviral infection will be examined, too. Conclusions: Its high rate of engraftment, its similarity to the malignant glioma of origin, and its rapid locally invasive growth should make this murine model useful in testing novel therapies for malignant gliomas.
- Survival of the fittest: positive selection of CD4+ T cells expressing a membrane-bound fusion inhibitor following HIV-1 infection (2010)
- Although a variety of genetic strategies have been developed to inhibit HIV replication, few direct comparisons of the efficacy of these inhibitors have been carried out. Moreover, most studies have not examined whether genetic inhibitors are able to induce a survival advantage that results in an expansion of genetically-modified cells following HIV infection. We evaluated the efficacy of three leading genetic strategies to inhibit HIV replication: 1) an HIV-1 tat/rev-specific small hairpin (sh) RNA; 2) an RNA antisense gene specific for the HIV-1 envelope; and 3) a viral entry inhibitor, maC46. In stably transduced cell lines selected such that >95% of cells expressed the genetic inhibitor, the RNA antisense envelope and viral entry inhibitor maC46 provided the strongest inhibition of HIV-1 replication. However, when mixed populations of transduced and untransduced cells were challenged with HIV-1, the maC46 fusion inhibitor resulted in highly efficient positive selection of transduced cells, an effect that was evident even in mixed populations containing as few as 1% maC46-expressing cells. The selective advantage of the maC46 fusion inhibitor was also observed in HIV-1-infected cultures of primary T lymphocytes as well as in HIV-1-infected humanized mice. These results demonstrate robust inhibition of HIV replication with the fusion inhibitor maC46 and the antisense Env inhibitor, and importantly, a survival advantage of cells expressing the maC46 fusion inhibitor both in vitro and in vivo. Evaluation of the ability of genetic inhibitors of HIV-1 replication to confer a survival advantage on genetically-modified cells provides unique information not provided by standard techniques that may be important in the in vivo efficacy of these genes.
- Role of p53 serine 46 in p53 target gene regulation (2011)
- The tumor suppressor p53 plays a crucial role in cellular growth control inducing a plethora of different response pathways. The molecular mechanisms that discriminate between the distinct p53-responses have remained largely elusive. Here, we have analyzed the p53-regulated pathways induced by Actinomycin D and Etoposide treatment resulting in more growth arrested versus apoptotic cells respectively. We found that the genome-wide p53 DNA-binding patterns are almost identical upon both treatments notwithstanding transcriptional differences that we observed in global transcriptome analysis. To assess the role of post-translational modifications in target gene choice and activation we investigated the genome-wide level of phosphorylation of Serine 46 of p53 bound to DNA (p53-pS46) and of Serine 15 (p53-pS15). Interestingly, the extent of S46 phosphorylation of p53 bound to DNA is considerably higher in cells directed towards apoptosis while the degree of phosphorylation at S15 remains highly similar. Moreover, our data suggest that following different chemotherapeutical treatments, the amount of chromatin-associated p53 phosphorylated at S46 but not at pS15 is higher on certain apoptosis related target genes. Our data provide evidence that cell fate decisions are not made primarily on the level of general p53 DNA-binding and that post-translationally modified p53 can have distinct DNA-binding characteristics.
- Retargeted natural killer cells for adoptive cancer immunotherapy (2011)
- NK cells are part of the innate immune system, and are important players in the body's first defence line against virus-infected and malignantly transformed cells. While T cells recognize neoplastic cells in an MHC-restricted fashion, NK cells do not require prior sensitization and education about the target. In leukemia and lymphoma patients undergoing allogeneic hematopoietic stem cell transplantation not only T cells but also NK cells have been found to mediate potent graft-versus-tumor effects. Hence, autologous or donor-derived NK cells hold great promise for cancer immunotherapy. Since the generation of highly purified NK cell products for clinical applications is labor-intensive and time consuming, established human NK cell lines such as NK-92 are also being considered for clinical protocols. NK-92 cells display phenotypic and functional characteristics similar to activated primary NK cells. While NK-92 cells are highly cytotoxic towards malignant cells of hematologic origin, they do not affect healthy human tissues. NK-92 cells can be expanded under GMP-compliant conditions, and can therefore be provided in sufficient numbers with defined phenotypic characteristics for clinical applications. Safety of NK-92 cells for adoptive immunotherapy was already shown in two phase I/II clinical trials. In contrast to malignant cells of hematologic origin, most solid tumor cells are not sensitive to unmodified NK-92 cells. Hence, to overcome resistance mechanisms of tumor cells and to broaden the target spectrum of NK-92 cells, gene-modified variants have been generated which express chimeric antigen receptors (CARs) that specifically target tumor surface antigens. The expression of these CARs is sufficient to redirect their cytotoxic activity towards otherwise NK cell-resistant target cells. Extending these earlier approaches, in the framework of this work optimized CAR constructs that target the pancarcinoma antigen epithelial cell adhesion molecule (EpCAM) were derived and functionally characterized. In collaboration with Heike Daldrup-Link's laboratory (University of California San Francisco, USA) non-invasive imaging modalities to analyze biodistribution and tumor homing properties of retargeted NK-92 cells were evaluated. To enhance the persistence of adoptively transferred NK-92 cells in vivo, means to overcome NK-92 cells' dependence on exogenous IL-2 for survival and cytolytic activity were investigated. EpCAM is expressed on a variety of tumors of epithelial origin including ovarian, gastric, colorectal, pancreatic, breast, lung and endometrial cancers. In epithelial cells EpCAM is mainly expressed at basolateral membranes, and EpCAM is involved in calcium-independent homotypic cell-cell adhesions. In tumor cells high and de novo EpCAM expression is not only restricted to basolateral membranes but can also be found on apical membranes. Tumor cells retain EpCAM expression throughout tumorigenesis and metastasis formation. Due to its surface expression and immunogenicity EpCAM has been exploited as target for immunotherapy. In earlier work in our group a prototypic, first generation EpCAM-specific CAR construct (31.z) harboring a murine flexible hinge region and murine CD3 ζ as signaling domain was derived and functionally characterized in NK-92 cells. To reduce the immunogenicity for their potential clinical application, this CAR construct was humanized by exchanging the hinge region and the intracellular signaling domain with corresponding sequences of human origin. In T cells incorporation of additional co-stimulatory domains derived from CD28 and 4-1BB significantly enhanced persistence and anti-tumor effects of adoptively transferred cells. Based on these findings a modified, second generation CAR construct encompassing transmembrane and intracellular regions of CD28 in addition to CD3 ζ intracellular signaling domains was derived (31.28.z). Both CAR constructs were stably expressed in NK-92 cells, and furthermore, expression of both CAR variants promoted antigen-specific lysis of antigen-expressing prostate and breast cancer cell lines. In competition experiments the cytotoxic activity of NK-92/31.z and NK-92/31.28.z cells towards antigen-expressing tumor cells was significantly reduced in the presence of parental MOC31 monoclonal antibody, indicating that binding of the EpCAM-specific CAR to its antigen on tumor cells is necessary to trigger antigen-specific cytotoxicity. At high effector to target ratios NK-92/31.28.z cells displayed slightly higher cytotoxic activity towards EpCAM-expressing target cell lines than NK-92/31.z cells, suggesting that incorporation of co-stimulatory domains had beneficial effects on the cytotoxic activity. For clinical applications the development of non-invasive imaging methods is necessary to follow the biodistribution of adoptively transferred cells and guide the identification of responders and non-responders at an early time point. In collaboration with Heike Daldrup-Link's laboratory the homing properties of EpCAM-specific NK-92 cells to prostate tumor xenografts in rodent models was analyzed (University of California San Francisco, USA). At that time NK-92 cells expressing the second generation EpCAM-specific CAR 31.28.z were not yet available, and thus homing experiments were performed with NK-92 cells expressing the first generation CAR 31.z. For magnetic resonance imaging studies parental and EpCAM-specific NK-92 cells were labeled with clinical applicable ferumoxide particles. Labeled, gene-modified NK-92 cells displayed reduced CAR expression and reduced cytotoxic activity towards EpCAM-expressing DU145 prostate cancer cells in vitro. Nevertheless, MRI revealed specific accumulation of ferumoxide labeled EpCAM-specific NK-92 cells in DU145 tumor xenografts in athymic rats. In tumor sections of treated animals the presence of EpCAM-specific NK-92 cells was verified by Prussian blue and CD57 staining of tumor sections. In another study homing of DiD-labeled EpCAM-specific NK-92 cells to DU145 tumor xenografts was shown by optical imaging. These findings imply that specific targeting of NK-92 cells is retained in vivo, and that non-invasive imaging strategies can be employed to analyze biodistribution of NK-92 cells. Enhanced persistence of adoptively transferred cytotoxic effector cells has a major impact on the effectiveness of immunotherapy. Primary cytotoxic effector cells as well as NK-92 cells require IL-2 for their proliferation and to gain full activity of their effector functions. To bypass the need of exogenously supplied cytokines, the expression of chimeric cytokine receptors (CCR) harboring IL-2R β and IL-2R γ chains instead of CD3 ζ as signaling domains might initiate cytokine-like signals upon contact with the respective antigen. These interactions might support growth and survival of NK-92 cells in the absence of exogenous IL-2. As a starting point, a codon-optimized ErbB2-specific CAR consisting of the scFv(FRP5) single chain antibody fragment, a human CD8 α hinge region and human CD3 ζ transmembrane and intracellular domains was used. Transmembrane and intracellular domains of IL-2R β and IL-2R γ chains were amplified from NK-92 cell-derived cDNA, and were used to exchange the CD3 ζ domain in the ErbB2-specific construct. In human primary tumors EpCAM and ErbB2 overexpression are frequently found, and often correlate with poor prognosis. Hence, co-expression of ErbB2-specific CCRs with an EpCAM-specific CAR may provide NK cells with antigen-specific killing via EpCAM recognition and with antigen-dependent growth via binding to ErbB2. However, attempts to activate CCRs in NK-92 cells via co-incubation with antigen-expressing cells or cross-linking of the CCRs with recombinant antigen did not result in cytokine-independent but antigen-dependent growth. Likewise, no triggering of signal transducer and activator of transcription 5 (STAT5) was observed, which is a hallmark of IL-2 mediated signal transduction. The interactions between CCRs and their antigen might not be strong enough to trigger cytokine-like signals supporting the growth of cells in the absence of exogenous cytokines, and furthermore, might not lead to a significant up-regulation of STAT5-mediated signal transduction. An alternative approach to circumvent the need of exogenous cytokines is ectopic expression of homeostatic cytokines IL-2 and IL-15 in lymphocytes. In T cells expression of these cytokines is sufficient to render cells independent from exogenously supplied cytokines. In this work a lentiviral expression vector encoding IL-15 (SIEW-IL15) was generated, and used for transduction of NK-92 cells. This resulted in ectopic expression of IL-15 and cellular proliferation in the absence of exogenously supplied cytokines. Even after prolonged culture without exogenous IL-2, NK-92/IL15 cells retained their cytotoxic activity towards NK-sensitive target cells. Although expression of IL-15 in HC11 and COS-7 cells using the same vector led to secretion of bioactive IL-15 into culture supernatants, neither secreted nor surface-bound IL-15 was detected in NK-92/IL15 cells, implying that IL-15 promotes survival of gene-modified cells in a strictly autocrine fashion. In addition, NK-92 cells that were freshly transduced with SIEW-IL15 could be efficiently enriched by cytokine withdrawal. NK-92/IL15 cells that were co-transduced with an EpCAM-specific CAR retained their ability to grow in the absence of exogenously supplied cytokines and their antigen-specific cytotoxic activity. Based on these results, a bicistronic vector construct was generated allowing the simultaneous expression of a CAR construct and IL-15 as selection marker. EpCAM-specific CAR constructs (31.28.z and 31.TM) were inserted into the bicistronic expression cassette. NK-92 cells were transduced with these bicistronic expression constructs and selected by cytokine withdrawal. After 14 to 21 days of culture in the absence of IL-2 transduced cells grew out from which CAR-expressing NK-92 cells with high and homogenous surface expression were further enriched by FACS sorting. NK-92/31.28.z.IL15 cells displayed high cytotoxic activity towards EpCAM-expressing breast cancer cell lines, while EpCAM-negative melanoma cells were not lysed. The results of this work demonstrate that the expression of first (31.z) and second (31.28.z) generation CARs in NK-92 cells is sufficient to induce antigen-specific cytotoxicity. Furthermore, a specific accumulation of NK-92/31.z cells but not unmodified NK-92 cells was detected in EpCAM-expressing prostate carcinoma xenografts in athymic rats, indicating that specific targeting of these cells is retained in vivo. Ectopic expression of IL-15 renders the cells independent from exogenous cytokines, while they retain their cytotoxic activity even after prolonged culture without IL-2. Furthermore, ectopic expression of IL-15 in NK-92 cells can be used for selective enrichment of gene-modified cells by cytokine withdrawal. Subsequently, bicistronic expression constructs that allow simultaneous expression of a CAR construct and IL-15 as selection marker were generated. Expression of these bicistronic expression vectors in NK-92 cells is feasible, and might facilitate enrichment of gene-modified cells for clinical applications.
- Resistenz polyklonaler, reifer T-Zellen gegenüber der Transformation durch retrovirale Transduktion (2008)
- Nach den ersten Erfolgen der Gentherapie bei angeborenen Immundefekten wurden einige Fälle von Leukämie nach gammaretroviralem Gentransfer in Blutstammzellen bei Patienten mit "severe combined immunodeficiency" (SCID-X1) veröffentlicht. Diese entfachten eine Diskussion über das Risiko der Insertionsmutagenese bei der Verwendung gammaretroviraler Vektoren. Durch eine insertionsbedingte Transaktivierung potentieller Onkogene und damit verbundenen malignen Veränderungen können gammaretroviral transduzierte Blutstammzellen Leukämien hervorrufen. Aber nicht nur Blutstammzellen werden als Zielzellen in der Gentherapie genutzt. In der Gruppe von Laer wurde in den letzten Jahren eine neue Gentherapie der HIV-1 Infektion entwickelt. Hierbei werden dem Patienten genetisch geschützte, autologe T-Lymphozyten infundiert. Die Gefahr einer Leukämie durch Insertionsmutagenese sollte im Zuge dieser Studie für reife T-Lymphozyten evaluiert werden. In einer vergleichenden Analyse wurde untersucht, ob der gammaretrovirale Gentransfer in reife T-Lymphozyten die gleiche Genotoxizität birgt wie in hämatopoetische Stammzellen. Hierzu wurden reife T-Lymphozyten und hämatopoetische Progenitoren von C57BL/6(Ly5.1)-Mäusen mit multiplen Kopien gammaretroviraler Vektoren transduziert, die für die potenten T-Zell Onkogene LMO2, TCL1, dTrkA oder das Kontrollgen GFP kodierten. Es wurden sehr hohe Transduktionseffizienzen mit bis zu 70% für reife T-Lymphozyten und bis zu 98% für hämatopoetische Progenitoren erzielt, um möglichst leukämiefördernde Bedingungen zu schaffen. Nach Transplantation in kongene Rag-1 defiziente Empfängertiere (Ly5.2) entwickelten Onkogen-modifizierte Stammzellen nach einer charakteristischen Latenzperiode Leukämien/Lymphome. Am häufigsten wurden unreife, CD8+CD4+ doppelpositive T-Vorläufer Leukämien/Lymphome beobachtet. In einigen Rezipienten führte außerdem eine Überexpression von TCL1 in hämatopoetischen Stammzellen zu der Entwicklung von reifzelligen T-Zell Leukämien/Lymphomen und B-Zell Leukämien/Lymphomen. Die Integrationsanalyse ergab oligo- bis monoklonale Tumore, wobei keine offensichtlich tumorfördernden, die gammaretroviralen Insertionen flankierenden Gene identifiziert werden konnten. Bemerkenswerterweise entwickelte keines der T-Zell transplantierten Empfängertiere ein/e Lymphom/Leukämie, obwohl auch diese Zellen mit den gleichen Vektoren modifiziert wurden und über einen sehr langen Zeitraum persistierten. Um die Kontrollmechanismen dieser Resistenz näher zu untersuchen, wurde eine für den TCR monoklonale, adulte T-Zell Population mit dTrkA transduziert. Nach einer kurzen Latenzperiode entwickelten sich reifzellige T-Zell Leukämien/Lymphome. Anscheinend existiert eine Verbindung zwischen der relativen Transformationsresistenz reifer T-Lymphozyten und dem Konkurrenzverhalten verschiedener T-Zell Klone um stimulatorische MHC-TCR Nischen. Weiterhin wurde in vitro durch gammaretroviralen Transfer von LMO2 ein immortalisierter T-Zell Klon generiert. Dieser zeigte zwar nach einer langen Beobachtungszeit einen CD8-CD4-doppelnegativen Phänotyp, aber auch einen rekombinierten TCR. In vitro überwuchs er eine unmanipulierte Kompetitorpopulation, konnte jedoch nach Transplantation kein/e T-Zell Lymphom/Leukämie induzieren. Die LM-PCR Analyse des Klons lieferte eine sehr interessante Integration zwischen den Genen für die alpha-Ketten des IL-2 und des IL-15 Rezeptors, welche dadurch konstitutiv exprimiert wurden. Dies könnte das erste Beispiel für eine insertionsbedingte Immortalisierung eines adulten T-Zell Klons sein. In der vorliegenden Arbeit konnte zum ersten Mal eindeutig gezeigt werden, dass polyklonale, reife T-Zell Populationen in vivo eine hohe Transformationsresistenz aufweisen. Durch bestimmte Bedingungen können jedoch durchaus maligne Veränderung adulter, reifer T-Lymphozyten induziert werden. Für die Sicherheitsabschätzung gammaretroviraler Gentherapie-Studien mit reifen T-Lymphozyten sind die vorgestellten Ergebnisse von großer Bedeutung und könnten darüber hinaus Aufschluss über die populationsdynamischen Kontrollmechanismen reifer T-Zell Leukämien/Lymphome geben.


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- OS: Mac ×
Games Software
- Real Time Strategy
- First Person Shooters
- Turn Based Strategy
- Role-Playing
- Simulation
- Multi-User Dungeons (MUD)
- Puzzle Games
- Board Games
- Side-Scrolling/Arcade Games
- Card Games
- Console-based Games
- Flight simulator
- Hobbies
- Multiplayer
- Game development framework
- Sports
- Real Time Tactical
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FemTechNet Hopes to Revolutionize SA's Higher Education Possibilities
Published: September 18, 2013
Each Tuesday at Geekdom, starting September 24, any and all are welcome to gather with Boyer and Varela, watch a video of well-known feminist thinkers and academics discussing the topic of the week, and then stay for a loosely structured dialogue, aided by local advisors, about the video. The video topic schedule appears here, and includes "Sexualities," "Difference," "Archive" and so on. While there's plenty of extracurricular resources available on FTN's website, Boyer and Varela say it's not necessary to have a computer or internet access at all to stay engaged in the digital technology dialogue.
However, because the course was directly inspired by the perceived lack of women in technology, each participant is encouraged to engage in creative, digitally-based projects before the course ends in December. One of the projects involves "Wiki-storming," in which participants directly address the lack of women and feminist theory in technology by creating or augmenting Wikipedia pages to reflect the participation and influence of various women in relevant fields. Other projects may include short video production, feminist mapping and substantive blog commenting. Many nodals will offer object-making as the final project, which, with its emphasis on DIY and/or craft methods and intention that the end product is then given as a gift to someone else, seems a little Portlandia at first blush. However, the process purports to help students think outside of capitalistic norms, create community and connect their learning to a tangible object, or "artifact" as the FTNers are fond of saying. In keeping with the FTN ethos, nodals like Boyer and Varela's Taller may employ all, none or some of these project ideas. The San Antonio facilitators hope their participants end the course leaving behind "a beautiful digital object" that will be of use to future FTNers' study.
Coincidentally, Varela, who has taught as an adjunct at UTSA, had recently been approached by the University to teach a MOOC about film. She turned down the opportunity, citing her preference to teach face-to-face with students. "[MOOCs] can't be intimate in that way," said Varela, noting that her classes we based primarily on two-way dialogues about the films. "[The students] needed these discussions to happen," she said "and the projects that come out of that."
Varela is far from the only educator skeptical of the MOOC, despite the millions of students and growing list of big league universities signing on to the relatively new end-run around pricey college courses. In a 2011 article published in the International Review of Research in Open and Distance Learning, Rita Kop noted that the MOOC structure of online video lectures followed by quizzes and tests (oftentimes multiple choice) did not include much in the way of community building, resource sharing or even an alternative to professor office hours for students struggling with material. Similar assessments have been made in The New York Times, C-Net and the Associated Press. In a November 2, 2012 article titled "The Year of the MOOC", Times education reporter Laura Pappano wrote "How do you make the massive feel intimate? That's what everyone is trying to figure out."
> Email Callie Enlow with additional reporting by Maribel Hermosillo
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The permeable courtyard surface, paved in crushed granite and a locally sourced specialty slate mix, allows rainwater to seep to the home's subsurface drainage system. Design from the 2012 HGTV Green Home.
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First Hurricane Irene flooding the Northeast, then wild fires consuming the Southwest, and now THIS.
Washington has zeroes in with laser-like focus on the most pressing issue of our day–the unacceptable level of unemployment. No, wait! Just kidding. It's cutting the size of government, which of course, matters more than anything else to the millions of Americans who can't find work, who have lost or are in are in danger of losing their homes, who can't afford health insurance, who are increasingly desperate as this recession lingers on and on. As the day this country must raise debt ceiling or default on its obligations approaches, the president and the leaders of both parties are working day and night to hammer out an agreement cutting the deficit mostly by shredding the safety net; the only question is by how much and whether the rich will be asked to shoulder any of the burden, or whether it will fall entirely on the neediest and most vulnerable among us. Whatever happened to jobs being the most important thing on the agenda? Come back later. Preferably after the next election. Can't you see we're busy?
The economy continues to lurch along, gaining a little bit of steam, then falling back again. Unemployment stays stubbornly around 9%, homes are still being foreclosed at a ferocious rate, and the housing industry remains in a deep funk, Meanwhile, official Washington is consumed with the debate over the debt ceiling. Will someone please explain to me how cutting long-term spending (something I agree we need to do sometime soon) is going to jump-start the economy so that it can create the jobs needed to pull us out of this trough? Several of the conservative friends I've asked this question insist that solving the deficit now will give businesses the market certainty they need to start hiring again. Even if they're right, his seems like awfully week tea, given the depth of the problem. These are the same folks who recite the mantra that cutting taxes always produces economic growth and reduce the deficit (See effect of Bush tax cuts). They are, of course, also the people who claim that the stimulus did nothing at all (See auto sales, GM. See also, state budget cuts after the stimulus money was exhausted). If anyone can tell me when an austerity budget ever pulled us out of a recession, I'd be willing to listen. I can't think of one. I do know that the rush to cut the deficit during the Great Depression helped lengthen it by a decade.
What annoys me the most in all of this is that Democrats lack the courage to lay out an ambitious plan for jobs and economic growth based on the principles that they know work. Instead, they negotiate with deficit hawks and tax-cut absolutists whose ideas have been repudiated again and again by history, but who cling to the same tired theories no matter the evidence. As a result, Congress and the president play Russian roulette with the debt ceiling at a time when we should be focused on creating jobs, and the Great Recession lingers on and on.
The post-2010 Obama style is emerging. Out is the optimistic liberal standard bearer. In is the Clintonian triangler. Let the Republicans frame the agenda, stay above the fray, expend as little political capital as possible, then step in as the mediator to forge a last-minute consensus. Hey, it worked brilliantly for Clinton, and it might just get Obama reelected.
Clinton had the benefit of a booming economy and didn't have to give up much. As we saw from the last two of Obama's "successes," the price was giving up on extending the Bush tax cuts for the wealthy, and this time around, surrendering a significant portion of environmental protection, family planning, renewable energy funding, community health care, and other essential services.
Now Obama wants to enter discussions about the long-term deficit. House budget committee chairman Paul Ryan has already put his much-ballyhooed plan forward, and it's a disaster. It cuts trillions from the Medicare and Medicaid budgets while staying "revenue neutral." Translation, big cuts for those who rely on those programs for their health care in the coming decades, the promises made to retirees and the poor broken in the name of fiscal responsibility, and more tax cuts for the wealthiest Americans. If Obama plays the game of meeting this plan halfway, of surrendering a little less than Ryan envisions in order to get a deal, we will all be the losers. The safety net will be irretrievably shredded, and the ruinous trend toward even greater income inequality will be accelerated even further, with the wealthy taking even more, the middle class losing more ground, and the poor totally forgotten.
Does Obama have any plan for resetting the agenda more in line with the progressive core values he articulated in his campaign for the presidency, or will his recent pragmatism, at a cost too high to contemplate, win out in the end? I'm afraid to look.
We may yet get a budget deal without a government shutdown, but it won't be any credit to the Tea Party absolutists who see ANY compromise as a betrayal of their core principles. It will be because feckless Democrats caved on theirs. The last I heard, the Dems were so desperate for a deal they were considering selling out the EPA. They've already given way too much on so-called discretionary spending. The cuts will be painful to the poor, to schools, to women, to the unemployed, but not, of course, to the wealthy or to big corporations, who will not be asked to sacrifice in any way. Right now, a handful of Tea Party freshmen appear to be driving the entire GOP agenda, which must be driving Speaker Boehner nuts. He's been around long enough to understand that compromise is how things get done, and that the Tea Party radicals will destroy his party's advantage in short order if they insist on getting their way at all costs. I only hope the Democrats don't bail him out by caving even more.
I'm betting nobody yells "You Lie!" at the president tomorrow night. Civility is the word of the day, at least for a little while. Obama, bowing to the new reality of a divided Congress and a weakened Democratic Party, will present a centrist address, and both parties will make a show of togetherness for the cameras. That will all change tomorrow, but for one evening, it will be a pleasant time out from the toxic climate of the last two years.
I probably shouldn't draw cartoons I dream up in the middle of the night. I tried for days to come up with a New Year cartoon, without success. Last night at 3 am, this came to me. I'm not entirely sure it works, but deadlines do have a way of making cartoon ideas look better the closer they get. I just like the image of the GOP elephant wielding the scythe as Father Time departs the scene.
The emboldened Republicans come into 2011 with an agenda to undo most of Obama's accomplishments. Right behind Obamacare on the hit list is the Dadd-Frank financial reform package. It's not nearly as strong or comprehensive as I'd have liked, but it's more than the GOP and its Wall Street puppetmasters want. In the fantasy world of the Republican party, government is the only reason anything ever goes wrong, and the private sector, if the busybodies in Washington would just leave it the heck alone, will solve all problems. So the economic meltdown had nothing whatever to do with greed on Wall Street or banks creating trillions of dollars in complex derivatives backed by pixie dust, and we don't need anyone looking over their shoulders to make sure they don't do it again.
Now that they've preserved the tax cuts for the rich, the rest of us will need to pay for it somehow, which means "fixing" Social Security–a euphemism for cutting benefits. The next time you hear the term "redistribution of wealth," think about the social safety net being plundered for the benefit of the wealthiest citizens.
We now have two commissions recommending ways to trim the deficit. The one the president appointed made its preferred approach known last week, and now an independent commission has come up with an even stronger approach. Given the current state of affairs in washington, both approaches are dead on arrival. The GOP will have nothing whatever to do with anything that even remotely appears to be a tax increase. Democrats are incensed at the idea of laying a finger on entitlements. The Tea Partiers, even farther removed from reality than the mainstream of either party, have a laser focus on earmarks, which make up less than one-half of one percent of the budget. Those of us not inside the beltway appear to understand that we will need both to reduce spending and to increase taxes, and that there will be some pain for everyone if we are to get serious about getting the deficit under control. So, of course, we keep electing people who will do neither. The turkey is safe for another year.


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Even in his death at the age of 52 in 1942, Jamnalal Bajaj lived up to the image. His entire share in the family wealth, amounting to Rs 5 lakh, went into setting up the Jamnalal Bajaj Seva Trust. Gandhi himself drafted the Memorandum and Articles of Association of the trust and its objectives as per the wishes of his fifth adopted son.
The primary objectives of the trust included assisting Sarvodya workers and Gandhian constructive programmes. In 1960, the trust set up an International Sarvodya Centre, Vishwaneedam, sprawling over 400 acres in Bangalore, for promoting and propagating the Sarvodya philosophy. The trust is also involved in rural development, agriculture, dairy development, and training local women and youth forself-employment.
The Jamnalal Bajaj Seva Trust is only one amongst several trusts and foundations run by the Bajaj group. Prominent among them are Jamnalal Bajaj Foundation, Gita Pratishthan, Gita Mandir, Shiksha Mandal, Institute of Gandhian Studies, Gandhi Gyan Mandir, etc. Elaborates Rahul Bajaj, chairman of Bajaj group of companies, ``We are only continuing the good work started by our ancestors. I personally can't take any credit for it. Of course, I have my way which is very different. I don't want to do everything and do it badly. I am bringing in more focus. Also, more efficiency.''
Elaborates Niraj Bajaj, managing director of group company, Mukand Ltd, ``We have consciously tried not to shift our focus from Gandhian work. We feel, given our history, we have a moral responsibility towards the poor.'' Most of the community work undertaken by the group is centred under him. Adds he, ``So, our philanthropic work is aimed at the poorest of the poor, who are concentrated in the rural areas.'' This isevident in the fact that most of the activities are Gandhi-centric or rural oriented.
The Jamnalal Bajaj Foundation was established in 1976 for promoting Gandhian constructive programmes and assisting people dedicated to the national cause. The foundation is widely recognised because of the four prestigious awards it has instituted to recognise outstanding contributions in the field of constructive work; application of science and technology for rural development; uplift of women and children and/or Gandhian constructive work by women workers, and promotion of Gandhian values outside India by individuals other than Indian citizens.
Similarly, the Institute of Gandhian Studies, and the Gandhi Gyan Mandir, as the names indicate, are dedicated to Gandhian Studies. The Institute of Gandhian Studies organises, sponsors and promotes short-term as well as long-term courses of study on Gandhian thought and methodology, runs extension projects and publishes the results of Gandhian Studies and Research. While asthe Gandhi Gyan Mandir is not only a research centre for Gandhian Study, but also a library of Gandhian literatureBesides, the thrust is on rural development. Most of the trusts, including Jankidevi Bajaj Gram Vikas Sansthan, Jamnalal Bajaj Foundation, Jammalal Kaniram Bajaj Trust and Jamnalal Bajaj Seva Trust, and group companies, like Bajaj Auto, Bajaj Hindusthan, Hind Lamps, have rural development on their social agenda. Some projects are executed independently, and others in partnership with CAPART, Khadi & Vllage Industries Commission, state governments and NGOs.
In addition to supporting various income generation programmes, the rural development activities centre around health, sanitation, drinking water, improved agriculture practices, sericulture, horticulture, social forestry, waste land reclamation, handicarfts, etc.
Education is another social passion with the group. Way back in 1915, the group set up Shiksha Mandal in Wardha. The Mandal runs three commerce colleges, one science college, anagricultural and rural institute, and a polytechnic. The group also made a donation to the University of Bombay for establishing the first management institute in the state, the Jamnalal Bajaj Institute of Management Studies. A recent grant to the institute has been for running a course on ethics in business. Besides, a donation of Rs 7.5 million has been given to SNDT Women's University in Mumbai for setting up an Institute of Management Studies for Women.
Not content with undertaking community projects only, the group trusts also encourage others working in these fields. For example, the Jankidevi Bajaj Purskar for Rural Entrepreneurship was instituted in 1992 to encourage and develop business entrepreneurship in rural areas and recognise the outstanding contributors. The list is endless. Little wonder, the net worth of the charitable trusts of the Bajaj group has swelled to approximately Rs 5,000 million, and their contributions total nearly Rs 70-80 million every year. Now, the emphasis is on quality.Says Niraj Bajaj, ``We are always looking at how to do whatever we are doing better and better so that more and more people benefit.'' And if the past is any indication, it looks set to better its own track record.
Copyright © 2000 Indian Express Newspapers (Bombay) Ltd.


text:
BE FOREWARNED - Discussion includes Avatar: The Last Airbender, The Promise (Part One), Nick.com's "Welcome To Republic City" and Chapters 1-4 of The Legend of Korra.
Good Morning Benders and Non-Benders alike and welcome back to the Republic City Dispatch, a radio programme covering Nickelodeon's Legend of Korra series.
This week, we'll be covering Chapter 4 of Book One: Air "The Voice In The Night," which aired Saturday April 28th. Is Republic City drawing closer to all out war? Can The Avatar master Airbending in time to unite the city her predecessor created?
Hosted by Devindra Hardawar of the /Filmcast and Da7e and Matt Patches of Operation Kino.
Did you get the idea the Satos are up to no good? (Did you pronoucne Sato correctly? Because we messed it up a few times) Is Patches crazy for doubting the Korra is the The Avatar? FUTURE AANG?
Send us questions and comments through: Tumblr, E-mail, and Twitter.
Make sure to subscribe to us on iTunes (and kick us a review if you like what you hear!)
You can also subscribe through Soundcloud and our RSS there.
Are you part of TEAM TRANSCRIPTION? Would you like to be an Transcription Bender for our international listeners? E-mail us here.
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OPENLY BASHING M. NIGHT AND HIS 'HORRIBLE' FILM! I am tickled pink, all over the Nick sponsored tumblr and everything
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Just listen… some really extreme theories though… but informative..
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Interesting recap of the episode :O
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08 Jul
Posted by Jayce Ooi as Software
Who want Windows Phone 7 Mango (7592) ROM on your HTC HD2? It is time for you to download and install it now. DFT released WP7 Mango ROM for HTC HD2 but the mango is in green colour (beta release). For your information, I did not test it out yet. Or maybe won't install and test it at all even with the Marketplace is working…
Windows Phone 7 ~ Green Mango
XDA Developer, elfinlazz created a WP7 Mango ROM with developer unlock for sideloading apps and changed device name for Marketplace. Check out more information at XDA website. Try it out and let me know the result.
Download Windows Phone 7 (WP7) Mango ROM for HTC HD2 here.
via: xda-developers
Tags: HTC HD2, Mango, Windows Phone 7, WP7, xda-developers


text:
A Newport News man was sentenced Friday in federal court to 30 years in prison for engaging in gang activity, including shooting into a Williamsburg home, according to a news release from the U.S. Attorney's Office.
Marcellus Williams, 27, pleaded guilty in April to charges of racketeering conspiracy and possessing and discharging a firearm in furtherance of a crime of violence, the release indicates. It states he was sentenced Friday by U.S. District Judge Arenda Wright Allen. Williams is also known as "Math," "P-Shooter" and "Manny."
Williams was a "First Superior" with the Black P-Stones, a violent street gang operating primarily in the Beechmont, Woodview and Courthouse Green neighborhoods in the Denbigh area of Newport News, according to the release, which cited a statement of facts from Williams plea agreement. It notes that in his role as a First Superior, "Williams directed and participated in the gang's criminal activities, including robberies, attempted murder and marijuana sales."
The release states Williams was accused in three shootings in just over a 10-month period in 2008-09.
In April 2008, Williams and other Black P-Stones members targeted a rival gang member in broad daylight on Warwick Boulevard in Newport News, the document indicates. The rival was shot twice, suffering injuries to his mouth, neck and shoulder.
Eight months later Williams and other gang members fired up to eight bullets into a rival gang member's home in Williamsburg while two people were inside, according to the release. It states the incident was retaliation against a rival who disrespected Williams's girlfriend.
The release notes that the following March, Williams and members of the Black P-Stones shot into another rival gang member's home, nearly striking one occupant. The incident was retaliation for a previous altercation, according to the document.
The Federal Bureau of Investigation's Safe Streets Peninsula Task Force led the investigation and was assisted by Newport News and James City police and the Virginia State Police.


text:
I do it from the terminal! | 27 comments | Create New Account
The following comments are owned by whoever posted them. This site is not responsible for what they say.
I do it from the terminal!
Why run an applescript when you can get your hands dirty in Terminal? :)
Here are the commands you need to know to play with this feature
defaults read com.apple.mail UserHeaders
This will return "The domain/default pair of (com.apple.mail, UserHeaders) does not exist" if you have none set)
defaults write com.apple.mail UserHeaders '{"Reply-To" = "email@example.com"; }'
defaults write com.apple.mail UserHeaders '{"Reply-To" = "email@example.com"; "Bcc" = "firstname.lastname@example.com"; }'
You can add as many headers as you like in this format. And finally,
defaults delete com.apple.mail UserHeaders
To get back to the default. Note that this doesn't give you an input box in Mail.app - Should it do?
I do it from the terminal!
The term commands are great, but in fact, what I want is the boxes in which to input email addresses manually. I'm gonna take a look at the script.
I do it from the terminal!
That script doesn't do it either. There's got to be a way to permanently have those fields available.
I do it from the terminal!
It's important to note that (as of Mail.app 4.2), adding a BCC UserHeader in this way overwrites any other BCCs you may have added manually to your email, and applies this to all accounts. I'm still looking for a better way to automatically BCC an email address on a per-account basis.
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Jim Watts, District Architect, Facilities Management Branch, San Diego City Schools, San Diego
At Issue:
› Bond Referendums
› Maintenance Budgets
Maintaining more than 14 million square feet of space; providing 138,000-plus students with safe, comfortable learning environments; keeping up with more than 200 school and support sites: The numbers alone sound daunting. Being the second-largest school district in California – and one of the 10 largest districts in the United States – offers its own set of challenges. But Jim Watts, district architect for San Diego City Schools' Facilities Management Branch, and the dedicated district team have found ways to maintain order and manage some of their most pressing issues.
Besides fielding the typical responsibilities of their department, the professionals involved in the Facilities Management Branch are engrossed in a capital facilities program – Proposition MM. A $1.5-billion bond measure split between work on existing facilities and new construction, this plan will help San Diego City Schools modernize 161 existing school sites and build 15 new schools. "We have sort of a unique situation in San Diego right now," explains Watts. "We've been in a growth mode since 1980. From 1980 to 2000, all we did was grow. But, we peaked in 2000, and now we're starting to decline. It's not a precipitous decline, but it is a decline. In some ways, I view [this] as an opportunity … to realign our facilities, which include 2,700 portable classrooms, and [dispose] of some of our oldest buildings so we don't have to keep maintaining them."
Obtaining adequate maintenance budgets is a critical issue that Watts deals with annually. As a response, the district is moving toward "site-based budgeting," which gives each school site more control over its operational budget for certain items. "They can decide how much custodial service they want to 'buy,' [for example]," explains Watts. "There's a certain ratio that we need to keep – or that we typically want to keep – in the classroom, [but] the sites are going to be able to determine more and more how those resources are allocated. Site-by-site, a principal and his or her governance team get to make those decisions. We're providing the level of service to meet what they want." Another way Watts is addressing maintenance budgets? "We've gone into greater detail [with] site assessments – assessing mechanical systems, lighting systems, window systems, roofing systems district-wide – so that we can put together a more comprehensive plan. The next step is convincing our board that we need the proper resources allocated."
As with any school district – and almost any organization nationwide – Watts is faced with limited resources to maintain San Diego City Schools' facilities. "We've had to make some pretty draconian cuts – for example, releasing two-thirds of our landscape workers last year. At the same time, we're still designing and [are] going to be building new schools," he says. In response to restricted resources, providing supervisors with a broader span of control has allowed the department to reduce its number of supervisory staff members. Instead of replacing a retiree, for example, resources are consolidated and existing supervisors are given the opportunity to take on additional responsibilities. Staff augmentation is another opportunity Watts and the facilities team have taken advantage of when allocating resources. In the case of the Proposition MM bond measure, Watts indicates that a combination of staff augmentation and "staffing up in-house" was the right answer.
With a school district as big as San Diego's, and considering the extra square footage that Proposition MM will add, the department has hired two full-time staff members to "get the word out" about their work. "It took us a couple of years to get this smart – but we finally realized that we needed to have a much more coordinated communications plan and communications outreach. We want to lay the groundwork for a future facilities bond, and we want that to be based on us doing a good job," says Watts.
Taking advantage of available technology is another subject Watts and his team are addressing head-on. They just finished switching out ceiling-mounted classroom television sets (which can be hazardous in a California earthquake) and installed overhead projection systems – it's safer for building occupants and addresses educators' requests for larger television screens. In addition, the team has implemented a computer-aided facilities management program district-wide. "Now we can keep track of all the square footage, with an interactive graphic interface. It's been a struggle just to get all of our sites in, and then [enter] the additional square footage that we're providing under [Proposition MM]. But now that we've got that, we're looking at how we can build on it – add more fields, track more information – to be able to better manage our facilities."
The numbers may still sound daunting – but in the face of budget constraints and tight resources, Watts and the district's facilities team are finding ways to produce results.
Leah B. Garris, Associate Editor (email@example.com)
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text:
|Table of Contents
|Vol. 28, No. 3, 2007
Issue release date: August 2007
Validity of Stroke Diagnoses in a National Register of PatientsKrarup L.-H. · Boysen G. · Janjua H. · Prescott E. · Truelsen T.
aDepartment of Neurology, Copenhagen University Hospital Bispebjerg, and bDanish Epidemiology Science Center at the Institute of Preventive Medicine of Copenhagen, Copenhagen, Denmark
Background: Many registers containing routine medical information have been developed for research and surveillance purposes. In epidemiological research assessment of endpoints is often conducted via registers. In the present study we validated stroke and transient ischemic attack (TIA) diagnoses in the Danish National Register of Patients (DNRP). Methods: Subjects from a Danish cohort study, the Copenhagen City Heart Study (n = 19,698), were crosslinked with the DNRP. The following International Classification of Disease 10th revision codes were used to identify possible strokes and TIAs: I60–I69 and G45. Two independent raters reviewed all cases. Positive predictive values of stroke, TIA and stroke subtypes were estimated by dividing the confirmed cases by the total number of cases located in the DNRP. Interrater reliability was tested using ĸ statistics. Results: Of 236 possible cerebrovascular events, 1 in 6 stroke diagnoses did not meet study criteria. The majority of events in the DNRP were registered as unspecified stroke (I64), n = 105 (44%), of which two thirds were diagnosed as ischemic stroke events by the raters. Intracerebral hemorrhage and ischemic stroke had a positive predictive value from 74 to 97%, respectively. Conclusion: Our results show that the DNRP tends to overestimate the number of cerebrovascular events, while ischemic stroke is underestimated.
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text:
Yahoo! May! Buy! Tumblr! For! One! BEELLION! Bucks!
Yahoo! has reportedly opened its chequebook, pencilled in nine zeroes with a one in front, and waved it around in the general direction of blogging site Tumblr. Adweek says Yahoo! is willing to write the billion-dollar cheque because Tumblr is so cool it will excite advertisers. The Wall Street Journal quotes Yahoo! officials …
Oh man, yahoo is just a grave yard of once-promising projects.
I bet anyone with an interest in tumblr failing are rubbing their hands in glee right now.
Has Yahoo EVER successfully integrated a purchased company's product? Flickr is about as close as it gets, and they mostly drove the userbase away once they bought it.
Given the often loud and needy tumblr userbase, I think it's time to make some popcorn. This gonna be good.
No. Just no.
Yahoo. Please. Don't. Ruin. My. Tumblr.
oh! NO!!!
they destroyed Flickr! do not let them near Tumblr .. pleaseeeeeeeee!!!
Re: oh! NO!!!
Can you actually quantify "ruined"? Flickr is largely identical to how it was prior to the deal.
Re: oh! NO!!!
Oh, NOW I see how they've ruined it. What a mess.
It's sad, really.
Can't Yahoo! just figure out how to fix what they have first?
(It should be easy, just quit doing what they did to break it in the first place.)
Instead, they're going terminal, and smashing everything around them in their death throws.
Damn you autocomplete!
That was supposed to be "throes" not "throws"!
Re: It's sad, really.
What exactly is broken?
Where does Yahoo! Get their cash supply from?
They're a dead company, yet they keep finding value to buy and ruin other companies. How do they do it? Are they actually an accountancy tax loss scheme for someone else?
Re: Where does Yahoo! Get their cash supply from?
Guess what? Yahoo! is still the 1st/2nd/3rd most visited website in the world friend...
Buy Tumblr > make Yahoo cool
Yeah. Just like dad doing Gangnam Style dance > make dad cool.
"tumblr"? What's that?
New one on me ... Is it important enough to be worth a gigabuck?
Somehow, I seriously doubt it ... Quite honestly, I've never heard of it.
Re: "tumblr"? What's that?
If only Yahoo! had a search engine, then you could use that to look up "tumblr". Oh well...
Re: "tumblr"? What's that?
I quite admire Tumblr in its dedication to return the World Wide Web to its original intended purpose, which was, of course, the acquisition, cataloguing and dissemination of lovingly curated collections of pr0n.
Or so I've heard, anyway...
Re: "tumblr"? What's that?
It's a blogging site with a very low technical barrier to entry. Consequently, it's loaded with young people, most if not all of which will react violently to being monetized. With Yahoo in charge, it could easily turn into the next geocities.
As entertaining as it might be to watch the dinosaur eat something bigger than its head, hopefully tumblr tells them to stuff it.
Re: "tumblr"? What's that?
Not particularly for the content of your post, but for surprising me enough with a "someone hasn't heard of Twitter?!" moment that I realised I'd mis-read not only the original article, but every subsequent comment until yours.
I've got it now. Tumblr, not Twitter.
Actually, that's worse. I don't use Twitter, but I do use Tumblr. Oh noes!.... etc.
where the hell does yahoo get 1 billion from
what do they even sell?
Dear Tumblr
Take the money.
Even though they will mess it up.
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