Someone who needs to find a dentist may find a whole list of them to choose from, whether or not they have good references from their previous dentist or their doctor. An interested client may search online to find good dentists in their area by using their home city or town's name, or even their ZIP code to find something local. A query such as "good dentists in Boston MA" or "family dentists in San Diego CA" are a fine option, and such searches may yield a whole list of local dental offices the client may consider. Some offices may already have a full patient list or may be deemed too far away to conveniently visit, but the rest can be vetted in person. A client who's looking for a family dentist or a pediatric dentist should also bring along any children they have as well.
At a dentist's office, the client may consult the staff there, mainly the dentists and their assistants, to evaluate their credentials, experience, and patient reviews. While there, the clients may also check to see which healthcare insurance policies are accepted, and the child may also provide their input. Not that kids will ask dentists for their credentials, but rather, kids may make it clear if they are comfortable in a dentist's office and around the staff. If the family dental office or pediatrician makes them uncomfortable or frightened, that office may not be a good option after all, and the parents may try out other offices from the list.
Some dental patients explore the option of mobile dentistry, which is just what it sounds like. For some patients' convenience, some dentists will have their practice in an RV, which may visit patients at their worksite or college campus. Such a mobile dental office only offers simple and basic dental care, but for certain patients, that is sufficient. Some patients may have very busy schedules or lack transportation to regular dental offices, so they make use of mobile dentists for basic dental care. An interested patient may look up such mobile dentists online and make an appointment.
Some dentists specialize in adult patients and others are more flexible, but all of them can take good care of a patient's teeth, even if surgery is required. In some cases, only a routine checkup or cleaning is needed, but other patients need more. A patient with an emerging wisdom tooth may have that tooth numbed and removed at the dentist's office, before that tooth can crowd and deform existing adult teeth in the mouth. Infected teeth may undergo a root canal, when infected fleshy pulp inside the tooth is removed to contain an infection. And if a tooth is in danger of falling out of rotted or diseased gums, the patient may have that tooth safely numbed and extracted. The tooth is coming out either way, but of course it's better to have the tooth removed on a professional's terms.
Conversely, dental implants are often put in, and a dental bridge is a realistic false tooth that will fit into a tooth gap to fill it in. Elderly patients in particular may get dentures, which replace whole rows of teeth or all of them in the mouth. Dentures can also be put into the mouth and taken out at will.


Wahooo! We praise you in taking the first steps towards learning to swim to survive.
Remember, prior to enrolment your child will be assessed in a 10 minute booked session to ensure they begin swimming at the correct level according to their ability.
No obligation swimming assessment where we will show you around the facility and assess your child and provide you with possible class options.


text:
In the birthplace of Christianity, Christians and other minorities are being persecuted, driven and wiped out, and their places of worship are being destroyed.
AboutTema Shaul2020-10-11T07:24:50+00:00
In the Middle East, the birthplace of Christianity, Christians and other minorities are being violently persecuted, driven out and wiped out. Even their places of worship are being destroyed.
Faithkeepers gives face and voice to the humanitarian crisis and genocide affecting millions in the Middle East as a result of religious and ethnic persecution.
The film is a testament to the stories of the persecuted and an inspiring portrait of the human spirit. Using personal testimonies and original animation, the film exposes daily life for those facing violence and expulsion.
Faithkeepers – the movie and the movement – will awaken, enlighten and inspire all people of faith to stand up and take action.
Faithkeepers Endorsements >
Roma DowneyExecutive Producer
A celebrated, Emmy® nominated actress and producer Roma Downey is best known for her nine seasons as the tender-hearted angel on the hit CBS television show "Touched by an Angel" for which Ms. Downey earned multiple Emmy® and Golden Globe® best actress nominations.
Full Bio >
Micah SmithDirector
Micah Smith is an award winning narrative and documentary filmmaker. His films have screened in over 40 festivals on five continents. Smith graduated from the Kanbar Institute of Film and Television at New York University's Tisch School of Arts.
Zach SichermanResearch Director/Associate Producer
Zach has assisted in the production of dozens of films and educational courses. He studied Middle Eastern History, Arabic and Political Science in Bar-Ilan University and has worked in several political think tanks, such as the Jerusalem Center for Public Affairs and the Foreign Policy Research Institution in Philadelphia.
Paula KweskinProducer
Paula Kweskin is a U.S.-trained lawyer with a focus on human rights and international humanitarian law. She recently produced the award-winning film Honor Diaries, which explores the mistreatment of women in Muslim-majority societies. She graduated with a J.D. and a B.A. from the University of North Carolina at Chapel Hill. Her articles have been featured in The Wall Street Journal, CNN and the Daily Beast.
Raphael ShoreExecutive Producer
Raphael Shore is the founder and CEO of the Clarion Project, producing its groundbreaking documentary films seen by more than 65 million people in 150 countries. His films include the critically acclaimed Obsession: Radical Islam's War against the West, The Third Jihad: Radical Islam's Vision for America, Iranium, and Honor Diaries. CNN, the New York Times, and other leading media organizations have interviewed him and featured his films.
Mitchell R. JulisExecutive Producer
Mitch Julis is Co-Founder, Co-Chairman, and Co-CEO of Canyon Partners, LLC. Prior to forming Canyon, he directed a group of professionals at Drexel Burnham Lambert. He is a graduate of the Woodrow Wilson School at Princeton University, Harvard Law School, and Harvard Business School, and helped establish the Harvard Law School Program on Jewish and Israeli Law.
Raphael Shore
Chris Dewey
Mitch Julis
Co-Producers
Robert J. Shillman
Robin Coon
Associate Producers
Martin Craig
Irma Fralic
Helene Galen
Hadara Ishak
Ryan Mauro
Adam Milstein
Robert Nicholson
Ilan Sharon
Zach Sicherman
Bob Zeidman
Producer's Circle
Doctor Bob and the Shillman Foundation
Bonnie Dawson
Rony & Toby Hersh
Dr. Kenneth Stein
Bob & Carrie Zeidman
Noel & Robin Coon
Drew & Beth Fromkin
J. Philip & Malki Rosen
Director's Circle
Paul Bernstein
Alex Blagojevic
Katherine & Craig
Judi & Sam Friedland
Bryna and Joshua Landes
Michael & Margaret Valentine
Janice & Steve Hefter
Bob & Ellis Naegele
Cinematographer's Circle
Harry Ploss
Samuel Freshman

redpajama_set_name: RedPajamaCommonCrawl


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We are excited to realizing a life long dream of being a small business owner. Today is officially 1 month since the shop has opened. Old Town Temecula is full of Holiday activities and fun. Last night Santa arrived in his sleigh with horses. It is truly a beautiful place with lots of retail shops that carry unique items only found in Old Town. We are blessed to be here in the heart of it all. This is a labor of love for all things fashion and shopping. The business is off to a great start in fact better than we originally projected. It will take a while to see any profit from our efforts because of the level of investment it takes to do a start up, but we are prepared to make it work. It is so nice to be among many other shop owners that have several years of retail experience that offer us helpful tips. God has blessed us in this project and we are so grateful for all the support of all our friends and colleagues. Please make it up to Old Town today you will not be sorry. This is small business Saturday and a good day to support local merchants. Small business is the backbone of America and part of the American dream. We are ready with lots of new inventory added yesterday to our collection. We have gift certificates available for the fashionista in your life that loves to shop.


With its prime downtown location close to Place Wilson, Place du Capitole and Place Saint Georges, the 4-star Mercure Toulouse Centre Saint Georges hotel is the perfect place to stay in the Pink city. Looking for a relaxing stay? Whether you want shopping , culture or tourism, the hotel is the ideal base for exploring Toulouse. Traveling for work? Take advantage of the attractions in the downtown area and benefit from many transport connections for your meetings: metro, tram and airport shuttle.
Choose from our Standard or Privilege Rooms. And for a long stay, the hotel invites you to discover its apartments, some with balconies overlooking the city.
Le Mahogany Club bar is open every day from 5pm. Enjoy a moment of relaxation with friends and a house cocktail made by our head bartender. Guests can also take advantage of our outdoor terrace space.


text:
Q: how to use aes mode to encrypt string in swift? I've searched for a lot of articles online and only find
[iOS 3DES with ECB return half correct data
] on Stackoverflow, however when I copy the code in this article, the complier returns a different encrypted result with that I got from the online encrypt tools.
Can anyone help me here?
Thanks
plus, I can't really read obj-c. Just turned to swift from javascript and PHP.
===========Edit===========
Now, I changed my method to AES using swift 1.2. Code is listed as follows(iv and key are kept static for test):
    let key:String = "12345678901234567890123456789012"
    let iv:String =  "12345678901234567890123456789012"

    let keyData: NSData! = (key as NSString).dataUsingEncoding(NSUTF8StringEncoding) as NSData!
    let keyBytes         = UnsafePointer<UInt8>(keyData.bytes)
    let keyLength        = size_t(kCCKeySizeAES256)

    let plainData: NSData! = (plainText as NSString).dataUsingEncoding(NSUTF8StringEncoding) as NSData!
    let dataLength    = size_t(plainData.length)
    let dataBytes     = UnsafePointer<UInt8>(plainData.bytes)

    var bufferData    = NSMutableData(length: Int(dataLength) + kCCBlockSizeAES128)!
    var bufferPointer = UnsafeMutablePointer<UInt8>(bufferData.mutableBytes)
    let bufferLength  = size_t(bufferData.length)

    let operation: CCOperation = UInt32(kCCEncrypt)
    let algoritm:  CCAlgorithm = UInt32(kCCAlgorithmAES128)
    let options:   CCOptions = UInt32(kCCOptionPKCS7Padding)

    let ivData: NSData! = (iv as NSString).dataUsingEncoding(NSUTF8StringEncoding) as NSData!
    let ivPointer = UnsafePointer<UInt8>(ivData.bytes)

    var numBytesEncrypted: size_t = 0

    var cryptStatus = CCCrypt(operation, algoritm, options, keyBytes, keyLength, ivPointer, dataBytes, dataLength, bufferPointer, bufferLength, &numBytesEncrypted)

And here's my PHP code:
    function addPkcs7Padding($string) {
        $cipher = MCRYPT_RIJNDAEL_256;
        $mode = MCRYPT_MODE_CBC;
        $blocksize = mcrypt_get_iv_size($cipher, $mode);
        $len = strlen($string);
        $pad = $blocksize - ($len % $blocksize);
        $string .= str_repeat(chr($pad), $pad);
        return $string;
    }

    function aes256cbcEncrypt($str, $iv, $key ) {
        return base64_encode(mcrypt_encrypt(MCRYPT_RIJNDAEL_256, $key, addPkcs7Padding($str) , MCRYPT_MODE_CBC, $iv));
    }

A: *

*You are not setting the length of the encrypted data to the value returned by reference: numBytesEncrypted. In this case: bufferData.length = numBytesEncrypted.

*MCRYPT_RIJNDAEL_256 specifies a block size of 256 bits, AES only uses a block size of 128, change that in mcrypt to MCRYPT_RIJNDAEL_128. Note: the block size is not the same thing as the key size.

*The iv size is the block size (128-bits/16-bytes).

*Show example input and output data for more help.
For a Swift example this SO answer:

redpajama_set_name: RedPajamaStackExchange


Beverly Henry Ph.D., R.D., L.D.N.
Henry BW, Rooney DM, Eller S, McCarthy DM, Seivert NP, Nannicelli AP, and Vozenilek JA. What patients observe about teamwork in the emergency department: development of the PIVOT questionnaire. J Participatory Medicine. 2013 Jan 30; 5:e4.
Henry BW, Smith TJ, Ahmad S. Psychometric Assessment of the Behavior and Attitudes Questionnaire for Healthy Habits: Measuring Parents' Views on Food and Physical Activity. Public Health Nutrition. In Press.
Derscheid LE, Kim S, Zittel LL, Umoren J, Henry BW. Teachers' self-efficacy and knowledge of healthy nutrition and physical activity practices for preschoolers: Instrument development and validation. Journal of Research in Childhood Education. In Press.
Henry BW, Malu KM. Chapter 4. Coaching, Mentoring and Supervision for Workplace Learning. In: Extraordinary Learning in the Workplace. Janet P. Hafler (ed). New York, NY: Springer Publishing; 2011:63-85.
Henry BW, Duellman MC, Smith TJ. Nutrition-based standardized patient sessions increase counseling awareness and confidence among dietetic interns. Topics in Clinical Nutrition. 2009:24(1):25-34.


Ever hear if it is too good to be true, then it probably it probably is? Well that seems to be the case for the not so latest news for stem cell research.
Just weeks ago, the science world was buzzing when Japanese scientists announced that it had discovered a novel way to produce stem cells that was free of controversy, cheaper than traditional methods and simple.
By using acid to 'shock' adult skin cells, the group claimed that they had reverted the adult cells back to stem cells. Well, after several other groups tried [and failed] to reproduce results, the team has pulled its paper. They are not so quick to claim that they falsified data however, in a statement they suggested they wanted to determine where the error came from, if in fact, an error has been made.
It is unfortunate since this would have undoubtedly lead to several advances that stem cell research desperately needs to be viable in the near future for commercial use.
For those interested in science but are not quite sure what a stem cell actually is or what it does, let's go over the basics.
Stem cells are cells that can turn into any other cell in the body, not too long ago they were merely theoretical, but thanks to medical advances we now know that they are very much real and offer a way to turn back the aging process, grow new body parts that would not be rejected by the recipient, and give a whole new alternative way to treat diseases.
Stem cells [as of now] come from two different ways, the destruction of fertilized embryos, or using different scientific methods to take adult stem cells and change them back into stem cells.
Obviously the destruction of embryos route has provided a lot of controversy, especially for religious people, since they typically believe that life starts at conception. This route has been the most successful unfortunately and there have been laws limiting government funding for research with stem cells made from embryos until the Obama administration removed the restriction.
The adult stem cell route seems like it would be the better choice since it is controversy free, even if it cost more. This route has it's own set of drawbacks unfortunately, they have had several issues with the stem cells turning cancerous. Which is what you want, when you are doing testing that is, but when you can't figure out a way to reliably prevent them from turning cancerous when treating patients, then you have a problem.
It's hard to say where research will go for stem cells right now, the huge controversy about embryonic stem cells has all but stripped funding for the projects.The new technology that had offered so much hope and promise has taken two steps forward and one step back.
In all fairness I should disclose that I am fully for embryonic stem cell research and the countless number of lives this [somewhat] new technology could save. Not to mention the quality of life of the millions of people that this could help improve and treatments that we could not even think of for diseases and ageing.
That being said, I still hold out some hope for a future where stem cells can be made controversy free and be applied in the commercial setting. Who knows, it could save your life one day.
This entry was posted on March 11, 2014 by FullMetal. It was filed under Biology, Health and Medicine and was tagged with blog, health, medicine, political issues, religion, science, stem cells.


I have some very old code that has worked for years (originally written for Sybase ASA 7) but has stopped working since I upgraded from ASA 17 (build 1358) to ASA 17 (build 2053).
We use ADO 2.5 and the Sybase ASA 17 ODBC driver and this is VB6.
'We set the stored procedure we are going to use cmdStoredProc.CommandText = "sp_insert_table_A"
It does not return a parameter list and any attempt to assign to a parameter fails as it says the parameter cannot be found.
I tried upgrading to ADO 2.7 as per the documentation, but this failed too.
Can I assume you haven't tried with the the original version 17 ODBC driver and the newer database and server software to see if is just a driver version difference of a server side phenomena?
1- In DBISQL.exe:  DESCRIBE PROCEDURE sp_insert_table_A;  //connected with same login as app.
I am working through those suggestions, I am not sure I can use the other version of the driver as I am not the main software using that driver and the main product will need to patch it.
I also tested it using SAOLEDB rather than the ODBC OLE driver and it works. Unfortunately I think this is Sybase version specific and so if they changed to Sybase 18 it would cause another change.
The fact that SAOLEDB works is indeed good news. But that would indicate there could be an issue with MSDASQL either not recognizing the newer driver or a change in the ODBC driver itself.
I could well imagine the Microsoft OLE DB Provider for ODBC failing this way if it believes there is no support for stored procedures. The could be a problem in SQLGetInfo( ) or an edge-case insideof the generic provide suppport or a new API issue I don't recognize.
For these kinds of issues one would normally need 2 ODBC traces. One with the ODBC driver that works. One with the one that does not work. BUT it sounds like you have a way to mock this up. It may be best to work directly with SAP Product Support if possible.
I can provide the 2 traces tomorrow. We would hope to not make changes to the application if possible, but it has been running for 15years so it was bound to happen at some point. What is the best way to contact support, I am new to the website.
There is a regression in one of the schema queries that the 17.0.4 ODBC driver issues. "PROCEDURE_OWNER" is a column name used when running in ODBC 2.0 mode. This column name conflicts with the PROCEDURE_OWNER special value that was introduced in 17.0.0. The quoting of the column name was inadvertently removed in 17.0.4 (17.0 build 2000).
A fix will be forthcoming.
A work-around is to revert to the older 17.0.0 ODBC driver.
The correction will appear in 17.0 build 2088 (and later).
When will 17.0.4.2088 or higher be available to download as an EBF? We need this fix ASAP.
There is not a currently scheduled date for an SP containing this fix. You should consider the workaround in the interim.
Please would you confirm that to revert to the older 7.0.0.1358 driver, it is simply a case of swapping out the dbodbc17.dll file with the older build, there is nothing else required and/or no possible side effects from using mismatched builds. Many thanks.
Back from vacation... Yes, replacing the driver DLL(s) for 64-bit (bin64) and/or 32-bit (bin32) will do it.
Are you able to offer any assurance that mixing an older ODBC driver build (1359) with the newer Bin32 folder build (2053) will not have any repercussions or other unforeseen side effects for anything else? Running mismatched builds seems like a recipe for unforeseen consequences to me and this combination will clearly not have been tested in any way whatsoever.
Cf. that FAQ: What product name am I supposed to use in the Deployment Wizard?.
Considering that folks have used ODBC drivers from different major releases against database servers from other releases with success, I don't think you are taking a big risk in using an ODBC driver that is a few builds earlier than the one containing the problem. When you use an ODBC driver from an earlier major release (say 16.0) against a server from a newer release (like 17.0), you do risk not be able to access some of the latest software features but since you are staying within version 17 releases, I can't think of any issue you might run into.
Thanks. That is probably as good assurance as is possible and, in combination with a being able to run both on versions on the same machine, is the best we have for now. Looking forward to the release of the proper fix in the next EBF, so we can remove this workaround.
For reference, this bug is now fixed in the recently released version 7.0.4.2100.
Cf. the CR #799815 in the according readme.


Written by Kobi Yamada and illustrated by Mae Besom, this third hardcover book in the series questions what we do with a chance. What can they become? Will a chance lead to a new friendship, an opportunity or a challenge? Discover a bit about actions, bravery, misses and amazing results!


The aim of this study was to investigate the effects of thyroid hormones tri-iodothyronine (T3), thyroxine (T4), and parathyroid hormone (PTH) from the parathyroid glands, known to regulate the developing limb and growth plate, on articular cartilage tissue regeneration using a scaffold-free in vitro model.
In Phase 1, T3, T4, or PTH was applied during weeks 1 or 3 of a 4-week neocartilage culture. Phase 2 employed T3 during week 1, followed by PTH during week 2, 3, or weeks 2 to 4, to further enhance tissue properties. Resultant neotissues were evaluated biochemically, mechanically, and histologically.
In Phase 1, T3 and T4 treatment during week 1 resulted in significantly enhanced collagen production; 1.4- and 1.3-times untreated neocartilage. Compressive and tensile properties were also significantly increased, as compared to untreated and PTH groups. PTH treatment did not result in notable tissue changes. As T3 induces hypertrophy, in Phase 2, PTH (known to suppress hypertrophy) was applied sequentially after T3. Excitingly, sequential treatment with T3 and PTH reduced expression of hypertrophic marker collagen X, while yielding neocartilage with significantly enhanced functional properties. Specifically, in comparison to no hormone application, these hormones increased compressive and tensile moduli 4.0-fold and 3.1-fold, respectively.
This study demonstrated that T3, together with PTH, when applied in a scaffold-free model of cartilage formation, significantly enhanced functional properties. The novel use of these thyroid hormones generates mechanically robust neocartilage via the use of a scaffold-free tissue engineering model.
Surgical treatment options for patients with articular cartilage damage range from pain-alleviating microfracture techniques to end-stage total knee arthroplasty, with increasing numbers of developing therapies focused on avoiding joint replacement . Nonsurgical options typically involve injection of pain-relieving, anti-inflammatory treatments that reduce inflammation in the joint space, or chondroprotective agents that serve to enhance lubrication and prevent further matrix degradation [2,3]. In general, therapies are limited to mediating the osteoarthritic environment and do not serve to facilitate active cartilage repair. Cartilage tissue engineering has emerged as a potential method to treat focal cartilage defects, thereby delaying the need for total joint arthroplasty.
A scaffold-free tissue engineering approach, based on a self-assembling process, recapitulates cartilage development [4,5] and is amenable to the application of chemical and mechanical stimuli to drive cartilage matrix synthesis and maturation [6,7]. Application of exogenous agents can produce neocartilage with mechanical properties approaching those of native cartilage tissue; for example, stimulated self-assembled neocartilage can possess a compressive stiffness over 200 kPa , in range of native articular cartilage values . More recently, cartilage developmental biology has driven the identification of new stimuli suitable for use in the self-assembling process, toward better enhancing the mechanical and biochemical properties of engineered neocartilage.
During skeletal development, the thyroid hormones tri-iodothyronine (T3), thyroxine (T4), and parathyroid hormone (PTH) from the parathyroid glands function in a highly coordinated fashion to regulate the phenotype of growth plate chondrocytes, as well as the progression of cartilage growth during endochondral ossification [9-11]. PTH in the epiphyseal growth plate is responsible for maintaining the proliferative pool of chondrocytes, while T3 promotes the transition from proliferative to hypertrophic chondrocytes. T4 is converted to T3 by removal of an iodine moiety by membrane-bound de-iodinase cell receptors . In growth plate chondrocytes, PTH signaling targets upregulation of Sox9, a major regulatory gene of articular cartilage . On the other hand, T3 signals through the canonical Wnt pathway, targeting the upregulation of Runx2 . While the roles of PTH, T3, and T4 are well established in skeletal development - specifically, in the growth plate - the effects of these thyroid hormones on chondrocytes of articular cartilage, and, in turn, on their ability to repair or regenerate articular cartilage, is not well understood.
Recently, the intra-articular injection of PTH in osteoarthritic animal models has been explored as a potential therapeutic to promote cartilage matrix production [15-17]. These studies found that PTH (1-34) (that is, PTH fragment 1-34), particularly when administered intermittently, could reduce collagen type X deposition, while recovering glycosaminoglycan (GAG) and collagen type II levels, as evaluated via tissue staining. In addition, PTH (1-34) was shown to improve the gross morphological surface topography and histological appearance of repair cartilage . By demonstrating reduction in hypertrophic markers and promoting an articular cartilage phenotype, these studies highlight the ability of articular chondrocytes to respond to PTH and suggest its use in repairing or regenerating articular cartilage. Conclusions from these studies, however, are primarily derived from gross morphological and histological evaluation. Therefore, while the potential for thyroid hormones to facilitate cartilage repair is apparent, studies that quantify the tissue-level changes beyond qualitative methods by evaluating the matrix components (that is, collagen and GAG) and functional mechanical properties of repair cartilage are needed.
Limited studies use T3 and T4 to specifically improve the functional properties of neocartilage engineered from articular chondrocytes, as existing studies largely focus on understanding hormone effects at the cellular level. For instance, T3, when applied to alginate-embedded chondrocytes, enhanced the hydroxyproline content per cell . In the presence of bone morphogenetic protein 2 (BMP-2) and insulin, T3 significantly increased collagen type II mRNA and reduced BMP-2/insulin-induced collagen type X expression . These studies demonstrate the beneficial effects of T3 in eliciting increased collagen production in articular chondrocytes in three-dimensional culture. However, the effect of T3 and T4 hormones on increasing the functional properties of engineered neocartilage is understudied.
Recent advances have employed PTH as a potential therapeutic for articular cartilage repair or regeneration and have described the interactions of PTH and T3 in the development of the growth plate; however, the use of these hormones in cartilage tissue engineering is limited by our understanding of their effects specifically on articular chondrocytes. The objective of this study was, thus, to evaluate thyroid hormones PTH, T3, and T4 in neocartilage engineering to ascertain their effects on generating mechanically functional tissues. In Phase 1, each hormone was applied at an early (week 1) or late (week 3) point of neocartilage formation with a total culture time of 4 weeks. T3 use during week 1 most significantly enhanced neocartilage biochemical and mechanical properties and was carried forward to Phase 2. Phase 2 of this study applied PTH sequentially after T3 to modulate the hypertrophic response elicited by T3. This study was motivated by the hypothesis that application of thyroid hormones to articular chondrocytes in an in vitro model of scaffold-free cartilage regeneration would induce matrix maturation and enhance matrix properties; in particular, sequential application of T3 and PTH was hypothesized to enhance neocartilage properties without hypertrophic marker expression.
Eight juvenile bovine joints were purchased from an abattoir for research purposes; no permission was needed to use the joints (Research 87, Boston, MA, USA). Within 48 hrs, articular chondrocytes were harvested from the distal femurs. Tissue was digested in 0.2% collagenase type II (Worthington Biochemical Corp., Lakewood, NJ, USA) for 18 hrs. Cells were washed in Dulbecco's modified Eagle's medium (DMEM) containing 1% penicillin-streptomycin-fungizone (PSF; Lonza BioWhittaker, Walkersville, MD, USA) before freezing in 20% fetal bovine serum and 10% dimethyl sulfoxide medium. Cells were stored at −80°C until use. Cells used in Phases 1 and 2 of this study were not sourced from the same eight bovine joints, contributing to biological variability in the results; however, results of this study are within range of prior work employing the self-assembling process.
To generate scaffold-free constructs, 5.32 M cells in Phase 1 and 4.57 M cells in Phase 2 were seeded into 5 mm-diameter nonadherent agarose (2% wt/vol phosphate-buffered saline (PBS)) wells, as previously described . Agarose wells (1 mL) were presaturated with chondrogenic medium, and constructs were supplied with an additional 0.5 mL chondrogenic medium daily. Chondrogenic medium consists of: DMEM with GlutaMAX (Gibco, Grand Island, NY, USA); 0.1 mM nonessential amino acids (Gibco); 1% insulin, human transferrin, and selenous acid (ITS+; BD Biosciences, San Jose, CA, USA); 1% PSF (Lonza BioWhittaker); 100 nM dexamethasone (Sigma-Aldrich, St. Louis, MO, USA); 50 μg/mL ascorbate-2-phosphate (Sigma-Aldrich); 100 μg/mL sodium pyruvate (Sigma-Aldrich) and 40 μg/mL L-proline (Sigma-Aldrich). When constructs grew to the edge of the agarose well, they were transferred to 48-well plates containing 1 mL chondrogenic medium to allow for continued growth until 28 days of culture. The full volume of medium was exchanged daily.
Phase 1 of this study applied 100 ng/mL PTH 1-34 (Sigma-Aldrich, P3671), T3 (Sigma-Aldrich, T6397), or T4 (Sigma-Aldrich, T2376) during week 1 (that is, daily for days 1 to 7) or week 3 (that is, daily for days 15 to 21) of a 4-week culture period. A concentration of 100 ng/mL was chosen to maximize the potential of a cellular response [11,22,23]. Phase 2 evaluated the use of 25 ng/mL PTH during week 2 (that is, daily for days 8 to 14), week 3 (that is, daily for days 15 to 21), or weeks 2 to 4 (that is, daily for days 8 to 28) sequentially after 0 or 100 ng/mL T3 application during week 1. A dosing study using PTH (0, 5, 10, 25, 50, and 100 ng/mL) revealed no differences in any measured parameters, with the exception of 25 ng/mL PTH being the highest concentration to result in the highest cellular content (Additional file 1). A concentration of 25 ng/mL PTH was thus selected for use in Phase 2. All controls received no hormone treatment.
After 4 weeks of culture, samples were imaged to obtain dimensions for construct diameter and thickness using ImageJ software (National Institutes of Health, Bethesda, MD, USA). Wet weights (mg) were recorded before samples were portioned for mechanical, biochemical, and histological analyses.
A 3 mm-diameter biopsy punch was used to obtain a compressive sample from the construct (Additional file 2), which was then subjected to creep indentation testing. A 0.8 mm-diameter flat, porous indenter tip was applied to samples using a 0.7 g or 2 g mass to achieve strains under 12%. The sample's measured aggregate modulus (HA), permeability (k), and Poisson's ratio (ν) were obtained using a semi-analytical, semi-numeric, linear biphasic model . Also using a 3 mm-diameter biopsy punch, dog bone-shaped specimens with a 1.45 mm gauge length were portioned from constructs (Additional file 2). Dog bone-shaped specimens used in this study adhered to ASTM standard testing guidelines  to ensure failure at the mid-point of the sample. After gluing dog bones to paper tabs outside of the gauge length, tabs were gripped in a uniaxial materials testing system (TestResources Inc., Shakopee, MN, USA). Samples were pulled at 1% of the gauge length per second until failure. Sample cross-sectional area was measured in ImageJ and used to generate a stress-strain curve. A least-squares fit of the linear region of the curve yielded the tensile stiffness (Young's modulus, EY) and the maximum stress reached yielded the ultimate tensile strength (UTS).
Samples portioned for biochemical analysis were weighed wet before freezing and lyophilizing. Samples were weighed dry before digestion in 125 μg/mL papain (Sigma-Aldrich) for 18 hrs at 65°C. A PicoGreen assay (Invitrogen, Carlsbad, CA, USA) was used to assess total DNA content in constructs and converted to total cell number assuming 7.7 pg DNA/cell. Total GAG content was determined using a Blyscan Glycosaminoglycan Assay (Biocolor, Carrickfergus, UK). Total collagen content was evaluated via a modified chloramine-T hydroxyproline assay . A standard curve reflecting collagen amount was generated using a Sircol collagen standard (Biocolor). Both GAG and collagen contents were normalized to construct wet weight and dry weight.
Samples portioned for histological analysis were cryoembedded, sectioned at 14 μm, and fixed in 10% formalin. To visualize collagen and GAG distribution, samples were stained with picrosirius red and Safranin-O/Fast Green, respectively. Alizarin Red staining was used to assess mineralization. For Phase 2, Safranin-O/Fast Green images were used to quantify cell diameter using ImageJ software; specifically, 6 cells from each of 8 images were assessed for a total of 48 measurements per group. While tissue volumetric changes may occur during embedding, all samples were handled identically. As a result, calculated cell diameters apply only for cryoembedded, formalin-fixed samples. Immunohistochemistry was performed for collagen type II and X. Briefly, slides were fixed in acetone for 20 min at 4°C. Endogenous peroxidases were quenched with 3% hydrogen peroxide in methanol before blocking with 1% bovine serum albumin. The primary antibody (rabbit anti-collagen type II (Fitzgerald Industries International, Acton, MA, USA) and mouse anti-collagen type X (Abcam, Cambridge, UK)) was applied for 1 hr, followed by horseradish peroxidase-conjugated secondary antibody for 30 min (Vector Laboratories, Burlingame, CA, USA). Visualization of antibody localization was performed using 3,3′-diaminobenzidine (DAB) reagent (Vector Laboratories).
One-way and two-way analysis of variance (ANOVA) designs were employed in Phase 1 and 2, respectively, followed by Tukey's post hoc test (P <0.05). JMP 9.0.1 (SAS Institute Inc., Cary, NC, USA) was used to perform statistical analyses. An n = 4-6 was used for Phase 1, and n = 6-8 was used for Phase 2. Groups not connected by the same symbol are statistically significant, and data are represented as mean ± standard deviation.
Neocartilage gross morphology is shown in Figures 1A and 2A. All constructs appeared hyaline-like; T3-treated constructs in Phase 2 exhibit curvature. The gross morphological properties and cellular content are shown in Table 1. Notably, in Phase 1, T3 and T4 application at week 1 significantly reduced neocartilage wet weight, water content, diameter, and thickness, as compared to untreated constructs. PTH treatment at week 1 or 3 did not result in significant changes. In Phase 2, T3 again yielded neocartilage with significantly reduced gross morphological parameters. Phase 1 and 2 control morphologies differ as a result of a reduced seeding density (5.32 M cells in Phase 1 and 4.57 M cells in Phase 2) and biological variability in the cell source.
Phase 1 construct morphology and histological analysis. All constructs appeared smooth and hyaline-like. T3 and T4 treatments yielded smaller, thinner constructs, as compared to PTH and untreated controls (A). Collagen and GAG staining was uniform in all constructs (B). GAG, glycosaminoglycan; PTH, parathyroid hormone; T3, tri-iodothyronine; T4, thyroxine.
Phase 2 construct morphology, histological analysis, and cell diameter quantification. Phase 2 constructs exhibited no abnormalities and were hyaline-like in appearance. Notably, T3 treatment produced neocartilage with pronounced curvature, suggestive of tissue prestress (A). Picrosirius red and Safranin-O dyes demonstrated robust deposition of collagen and GAG, respectively, in all constructs (B). T3-treated groups possessed more GAG staining than non-T3 treated groups. T3 elicited an increase in cell diameter (C), as measured for cryoembedded, formalin-fixed samples. Groups not connected by the same letter are statistically significant. Data are represented as mean ± standard deviation. GAG, glycosaminoglycan; T3, tri-iodothyronine.
Phase 1 and 2 construct morphology and cellular content. Phase 2 used a lower seeding density (for example, 4.57 versus 5.32 million cells in Phase 1) and resulted in smaller constructs. Letters represent the statistical results of a one-way and two-way ANOVA for Phase 1 and 2, respectively. Groups not connected by the same letter are statistically significant. Data are represented as mean ± standard deviation.
Histological results of this study are illustrated in Figures 1B and 2B. Constructs from both phases demonstrated robust production of GAG, as indicated by Safranin-O/Fast Green staining, as well as collagen, as indicated by picrosirius red staining. Differences in staining intensity among hormone treatments were not apparent. Alizarin Red staining was negative for all groups (data not shown). In Phase 2, cell diameters, as measured from Safranin-O/Fast Green images, are shown in Figure 2C. T3 resulted in a statistically significant increase in cell diameter, as compared to non-T3 treated groups. Specifically, diameters were increased from 12.0 ± 0.9 μm to 14.8 ± 1.0 μm with T3 treatment. Sequential treatment with PTH did not have an effect on cell diameter.
Construct functional properties, as assessed by compressive and tensile evaluation, are shown in Figure 3. In Phase 1 of this study, T3 and T4 application during week 1 led to significant enhancement of compressive and tensile properties. Specifically, T3 and T4 treatment during week 1 increased the aggregate modulus, a measure of compressive stiffness, to 229 ± 68 kPa and 271 ± 66 kPa, respectively, as compared to control values of 138 ± 67 kPa. T3 treatment at week 1 also had the most significant effect on tensile properties - resulting in a Young's modulus and UTS of 1.90 ± 0.42 MPa and 0.59 ± 0.16 MPa, respectively, as compared to control values of 0.97 ± 0.32 MPa and 0.24 ± 0.05 MPa for Young's modulus and UTS, respectively.
Functional mechanical properties of Phase 1 and 2 neocartilage. In Phase 1, the compressive stiffness (aggregate modulus), tensile stiffness (Young's modulus), and ultimate tensile strength were significantly enhanced with T3 and T4 treatments during week 1. PTH treatment during either week did not have an effect on construct mechanical properties. In Phase 2, T3 elicited significant increases in compressive and tensile properties. When applied sequentially after T3 in Phase 2, PTH did not alter the T3-induced improvements in mechanical properties. Groups not connected by the same letter are statistically significant. Data are represented as mean ± standard deviation. PTH, parathyroid hormone; T3, tri-iodothyronine; T4, thyroxine.
In Phase 2 of this work, T3 treatment again contributed to significant enhancement of compressive and tensile properties. T3-treated neocartilage exhibited an aggregate modulus of 260 ± 12 kPa as compared to non-T3 treated constructs of 65 ± 3 kPa. The Young's modulus was increased from 0.51 ± 0.05 MPa for constructs receiving no T3, to 1.60 ± 0.19 MPa for constructs treated with T3. PTH treatments, applied alone or sequentially after T3 in Phase 2, did not have a statistically significant effect on any functional properties of generated neocartilage.
Neocartilage biochemical composition is shown in Figure 4 (GAG content) and Figure 5 (collagen content). T3 and T4 application during week 1 resulted in a significant decrease in GAG content, when normalized to dry weight, to 0.340 ± 0.016 and 0.377 ± 0.003 mg GAG/mg dry weight (GAG/DW), respectively, from a control value of 0.449 ± 0.040 mg/mg. When normalized to tissue wet weight (GAG/WW), however, this reduction of GAG was not statistically significant. T3 and T4 week 1 treatments led to a significantly higher level of collagen, increasing collagen per dry weight (COL/DW) of the neotissue to 0.146 ± 0.007 and 0.139 ± 0.002 mg/mg, respectively, over nontreated controls of 0.103 ± 0.003 mg/mg. These differences were maintained when collagen content was normalized to tissue wet weight (COL/WW). PTH treatment during either week did not result in a significant change in GAG or collagen content as compared to untreated constructs.
GAG composition of Phase 1 and 2 constructs. Neocartilage GAG composition was normalized to tissue dry weight (GAG/DW) and wet weight (GAG/WW). No significant change was observed with PTH treatment in Phase 1, while T3 and T4 application during week 1 resulted in significant changes in GAG/DW. In Phase 2, T3 elicited significantly more GAG/WW production. Notably, when applied sequentially, PTH did not affect the T3-induced changes in GAG/WW content. Groups not connected by the same letter are statistically significant. Data are represented as mean ± standard deviation. GAG, glycosaminoglycan; PTH, parathyroid hormone; T3, tri-iodothyronine; T4, thyroxine.
Collagen composition of Phase 1 and 2 constructs. Collagen content was normalized to tissue dry weight (COL/DW) and wet weight (COL/WW). PTH treatment in Phase 1 did not result in significant changes; however, T3 and T4 application during week 1 or 3 resulted in significant increases in collagen content. In Phase 2, T3 elicited the same effects. Sequential application of PTH did not alter the increases in collagen content induced by T3. Groups not connected by the same letter are statistically significant. Data are represented as mean ± standard deviation. PTH, parathyroid hormone; T3, tri-iodothyronine; T4, thyroxine.
T3 application in Phase 2 of this study resulted in a significant reduction of GAG content only when normalized to tissue wet weight. In line with Phase 1 of this work, T3 significantly enhanced collagen content per dry weight to 0.125 ± 0.006 mg/mg, over non-T3 treated constructs of 0.083 ± 0.004 mg/mg. Increased duration of PTH treatment led to reductions in both collagen per DW and WW, with week 3 treatment causing a statistically significant reduction in both, as compared to groups that received no PTH.
Figure 6 and Additional file 3 show the results of immunohistochemical assessment of collagen type X and II, respectively, for Phase 2 of this study. It is well known that T3 is responsible for promoting the transition of proliferative growth plate chondrocytes into hypertrophic chondrocytes; however, as the effect of T3 on articular chondrocytes is yet unclear, immunohistochemistry for hypertrophic marker collagen type X was conducted. T3 treatment resulted in deposition of collagen type X. When treated with increasing durations of PTH, however, collagen X staining was decreased. Most notably, sequential application of PTH for weeks 2 to 4 was most effective at reducing the staining. PTH treatment alone did not elicit collagen X deposition. Collagen type II was distributed in the interterritorial matrix, with no appreciable differences in collagen type II staining observed among groups.
Immunohistochemical evaluation of Phase 2 neocartilage. T3 treatment caused deposition of collagen X. However, increasing duration of sequential PTH application post-T3 treatment reduced collagen X staining. PTH, parathyroid hormone; T3, tri-iodothyronine.
This investigation examined the effects of hormones T3, T4, and PTH on functional neocartilage formation in an in vitro model. It was hypothesized that the application of these thyroid hormones to articular chondrocytes in an in vitro model of scaffold-free cartilage formation would induce matrix maturation and enhance matrix mechanical properties. In addition, it was hypothesized that scaffold-free neocartilage treated with T3 may exhibit markers of hypertrophy, but that sequential application of T3 and PTH would reduce hypertrophic marker expression. Both hypotheses were shown to be true: (1) application of T3 at week 1 elicited a dramatic 4.0- and 3.1-fold increase in neocartilage compressive and tensile stiffness, respectively (Phase 2); (2) sequential application of PTH reduced hypertrophic marker collagen X expression while maintaining the functional properties elicited by T3. In addition, T3 treatment resulted in a 2.2- and 1.5-fold increase in collagen and GAG content, respectively. The results of this study thus demonstrate that, in our in vitro model, thyroid hormones have a significant impact on neocartilage formation, with T3 eliciting the most significant increases in functional properties. To our knowledge, this study is the first to demonstrate that articular chondrocytes can indeed respond to T3, T4, and PTH, allowing them to be employed in an in vitro model of cartilage generation to produce mechanically robust neocartilage.
Hormone concentrations, gradients, and transients are tightly coordinated in vivo [27,28]. For example, the ability of hormones to affect tissues undergoing endochondral development has been studied by mapping receptor expression in tissues over time . Recent preclinical studies utilizing injectable PTH have found that intermittent, but not continuous, application of PTH resulted in enhanced cartilage regeneration , indicating the importance of timing of hormone application. In line with these results, in Phase 1 of this study, early treatment with hormones T3 and T4 at week 1 improved properties as compared to a later treatment at week 3, indicating that neocartilage is more susceptible to hormone treatment while the matrix is still in early phases of development. Earlier treatment may allow for prolonged matrix synthesis, but may also allow for hypertrophy. Phase 2 of this study similarly demonstrated the importance of hormone duration. Compared to the other PTH regimens, treatment during weeks 2 to 4 resulted in the greatest reduction of collagen type X deposition, suggesting that chondrocytes require time to respond to hormonal stimuli. Collectively, this study demonstrates that the timing and duration of hormone application must be optimized for use as an appropriate stimulus in neocartilage engineering.
Extensive exploration into the molecular mechanism of T3 and PTH signaling has been conducted on growth plate  and limb bud cells . T3 is known to elicit hypertrophy through Wnt signaling  in both growth plate cells  and mesenchymal stem cells (MSCs) [33-35]. However, the effect of these hormones - particularly of T3 - on articular chondrocytes and their subsequent matrix synthesis has not been well studied. Specifically, investigation into the de-iodinase receptor profile of osteoarthritic articular chondrocytes has shown their ability to promote the conversion of T4 to T3 . In addition, differential responses of articular chondrocytes from different zones have been demonstrated , but are limited to gene expression and focused on mineralization, and do not evaluate functional properties. T3-treatment of alginate-encapsulated articular chondrocytes similarly demonstrated changes in gene and protein content . The present experiment - using a mixed population of articular chondrocytes - showed that T4 treatment was effective in enhancing neocartilage functional properties in Phase 1. These results thus demonstrate that juvenile articular chondrocytes are able to convert T4 to T3, though T4 stimulation was not as potent as T3. Also, T3 treatment significantly benefited functional tissue properties; specifically, T3 increased neocartilage collagen content 2.2-fold with a paralleled 3.2-fold increase in tensile stiffness, as compared to non-T3 treated neocartilage. To the best of our knowledge, this study is the first to demonstrate the beneficial functional effects of stimulating articular chondrocytes with thyroid hormones T3 and PTH to generate mechanically robust neocartilage.
An important finding in this study is that the sequential application of T3 followed by PTH enhances matrix formation while mitigating T3′s hypertrophic effects. Simultaneous application of T3 and PTH does not result in reduction in collagen type X expression , whereas sequential application of T3 and PTH, in this study, demonstrated a reduction in collagen type X. Mechanistically, T3 and PTH act on distinct pathways: PTH upregulates Sox9 and downregulates Runx2; T3 has the opposite effect by upregulating Runx2 . Together, the balance of Sox9 and Runx2 regulate hypertrophic marker expression. Therefore, in this study, T3 application elicited hypertrophic marker expression, while the subsequent application of PTH was critical to downregulate hypertrophy. Prolonged duration of PTH (that is, weeks 2 to 4) further increased hypertrophic downregulation, as evident in the reduction of collagen type X in Phase 2. Excitingly, the functional properties elicited by T3 are not compromised when PTH is applied, suggesting that these increased functional properties are not dependent on the hypertrophic phenotype, but instead represent robust and persistent hyaline-like matrix maturation. The novelty of sequential hormone application in this model of in vitro cartilage generation may lead to the use of other hormones that, in combination or in sequence, can be used in cartilage tissue engineering.
Despite the encouraging findings of this work, further investigation of thyroid hormones and their use in scaffold-free cartilage engineering is warranted. This study examined neocartilage after 28 days of culture; earlier analysis may elucidate the time course of PTH-induced cellular proliferation or collagen X deposition. In this study, T3 elicited a hypertrophic cellular morphology (that is, enlarged diameter) that was not mitigated by PTH; these results may be altered with longer culture duration. The hormone concentrations and timing of application for this study were motivated by the existing literature; however, the use of a scaffold-free system may justify additional optimization of hormone dosing, timing, and duration. It is also important to note that control constructs between Phases 1 and 2 of this study exhibited differences in wet weight, diameter, and thickness, likely as a result of the reduced seeding density used in Phase 2. Use of a calcein-based live/dead stain in future studies may prove informative to assess cell viability, as the present study employed the trypan blue assay, which assesses only membrane integrity and not metabolic activity. Finally, the phenotypic stability and regenerative potential of neocartilages generated with hormonal application should be assessed via implantation in an animal model. To build upon this study, future work should explore the use of other hormones and application regimens on the ultimate success of implanted neocartilage in vivo.
To the best of our knowledge, this work is the first to investigate the use of thyroid hormones in scaffold-free cartilage tissue engineering. In particular, a series of experiments determined the efficacy of generating robust neocartilage using thyroid hormones T3 and PTH, especially when applied sequentially. These hormones had not previously been examined for their ability to enhance articular chondrocyte-based neocartilage functional properties. Excitingly, T3 was able to significantly enhance neocartilage mechanical properties, up to 4-times the compressive stiffness of untreated controls. Moreover, T3-induced hypertrophy was mediated by sequential PTH application. These findings motivate future work to enhance neocartilage mechanical properties through the application of other hormones. Neocartilage produced with sequential hormone stimulation achieved mechanical properties approaching those of native tissue and may be applicable for the clinical repair or regeneration of articular cartilage defects.
This publication was made possible by support from the National Institutes of Health (R01AR061496) and from the National Institute of General Medical Sciences (NIGMS) for JKL (T32-GM00799). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH or NIGMS.
Additional file 1: Cellular data from PTH dosing study. A PTH dosing study was conducted before running Phase 2. Concentrations ranging from 0 to 100 ng/mL PTH were applied to neocartilage during week 3 of a 4-week culture. Cellular content was the only measured parameter that demonstrated statistically significant effects. A 25 ng/mL PTH concentration was the highest concentration to achieve the greatest DNA content and was carried forward to Phase 2.
Additional file 2: Construct portioning for mechanical testing. Neocartilage constructs from Phases 1 and 2 possessed diameters ranging from 5.53 ± 0.09 mm to 6.28 ± 0.12 mm (A). From the whole construct (B), a 3 mm-diameter biopsy punch is taken using a dermal punch (C). From the remainder of the construct (D), the same dermal punch is used to form a narrow bridge of tissue (E). Final cuts (F) are made with a scalpel to yield a dog bone-shaped tensile testing specimen (G). ImageJ is used to measure the gauge length width and thickness from top-down and side views (H) of the dog bone, respectively.
Additional file 3: Collagen type II immunohistochemical evaluation of Phase 2 neocartilage. Collagen type II deposition was detected in all groups, with no apparent differences among hormone treatments.
All authors contributed to: conception of the study design, execution of the study and collection and analysis of data; and drafting, revising, and approving the manuscript. Specifically, JKL, JCH, and KAA conceived and designed the experiments. JKL and CAG executed the studies (that is, performed the cell culture), and collected and analyzed all data (that is, mechanical tests and biochemical assays). JKL, CAG, JCH, AHR, and KAA critically interpreted the data. JKL and CAG drafted the manuscript, while JCH, AHR, and KAA critically revised the manuscript. All authors read and approved the final manuscript.


After successfully changing the color and font of the headers everything was looking good.
Suddenly any new header has a yellow background. At the same time this happened, the yellow arros that scroll to the top became square and lost their style.
How can I reverse this? How did it happen?
I granted access so you cna take a look.... and have no plugins activated yet. This is anew site.
Looks like you added some css broke the styling. Can you remove any code you added ?
I made no custom CSS changes to H3 or the effected style. I cut and paste the default CSS Global code from a new install... still the problem persists. THe problem occurs on the new install too.
Here is what is really happening. Whenever a change is made to the color of this preset elements - everything goes haywire. I fixed some by re-selecting the type of button and the button selection at the bottom - after you click edit presets - you can select a different button type.
After changing colors on some elements - everything goes awry.
No changes were made on Css - the theme is glitching out.
CLosedt his ticket.. Deleted entire install and started from scratch.


Good afternoon everyone! I hope all is well! Today I have the second half of the new Leave the Sun Behind Me Collection and new Siren Series Limited Edition from Blue-Eyed Girl Lacquer. Yesterday I shared three stunning neons from the Leave the Sun Behind Me Collection and if you missed it, you need to check out soon. The new collection releases at 3:30 PM EST time today so get those fingers ready!
First up today we are taking a look at 40/41. This is a stunning neon teal with cobalt Nfu Oh style flakes. 40/41 is a one time run blend so grab a bottle while you can. In my photos I am wearing three coats of 40/41 and one coat of clear.
Next up we have It's In the Itinerary. This is a squish neon purple jelly with blue to magenta to teal to gold ultra chrome flakes. Application was super smooth and the flakes laid nicely. In my photos I am wearing two coats of It's In the Itinerary and one coat of clear.
Lastly for the Leave the Sun Behind Me Collection we have Rubby. This is an incredibly bright neon pink creme with a lovely purple shimmer. Application and formula were very easy to work with and the color built to opacity with out the need of a base color. In my photos I am wearing three coats of Rubby and one coat of clear.
Now for the new Siren Series limited. Siren's Mint Smash is a STUNNING neon mint green jelly with gold to green to blue shifting glass flecks. I can not even put this beauty into words. With only 34 bottles being made, you need to grab this guy FAST. You will regret it if you don't, it is that beautiful. In my photos I am wearing three coats of Siren's Mint Smash and one coat of clear.
So what do you guys think of the rest of the Leave the Sun Behind Me and the new Siren Series limited? I love them all and they are a great twist on your standard neon creme so you will most likely not have anything in your collection like them. The new Leave the Sun Behind Me and Siren Series LE will be released today at 3:30 PM EST so set your timers, we are close. Be sure to also give Blue-Eyed Girl Lacquer a follow on Facebook, Twitter, and Instagram for up to date info. Thank you so much for stopping by today and I will see you all again tomorrow.


The 2019 Subaru Forester is a redesigned, compact, crossover sport utility vehicle.
If Subaru were a surfer dude, it would be riding the crest of a very big wave, and its 2019 Forester likely will help keep it there.
The redesigned, compact, crossover sport utility vehicle, now in its fourth generation, arrives with more streamlined and sophisticated styling, as well as a host of new features.
Built on a new global platform that also underpins the Ascent, Impreza and Crosstrek, the Forester delivers improved access for passengers and cargo, a new engine and transmission combination with automatic idle stop-start for improved fuel economy, additional safety measures and standard all-wheel drive.
Except for the company's rear-drive BRZ sports coupe, developed with Toyota, all Subaru cars and crossover SUVs put the power to the ground with all four wheels. The Forester doesn't have the off-road credentials of muscular Jeeps and Land Rovers. But it can handle foul weather conditions and moderately challenging terrain, especially on versions with X-Mode, which includes hill descent control.
There are five trim levels, starting with the $25,270 Base, followed by the $27,070 Premium, new $29,770 Sport, $31,770 Limited and $35,270 Touring. Prices include the $975 destination charge.
All Foresters come with Subaru's EyeSight Driver Assist Technology, which includes pre-collision throttle management and braking, adaptive cruise control, and lane-keeping assist with lane departure and sway warning.
The tested Sport model came with a $2,045 option package that included blind spot detection, rear cross-traffic alert, reverse automatic braking, and a power rear tailgate with push-button closing and adjustable open height.
The package also covered Subaru's Starlink infotainment system with an eight-inch touch screen, premium Harman Kardon audio, Bluetooth connectivity, Apple Car Play and Android Auto, and SXM satellite radio. It brought the Sport's bottom-line price to $31,815.
Power surges from a newly-engineered 2.5-liter horizontally-opposed four-cylinder engine that makes 182 horsepower and 176 pound-feet of torque with city/highway/combined fuel consumption of 26/33/29 miles to the gallon.
It is mated to Subaru's Lineartronic continuously-variable automatic transmission. CVTs ordinarily multiply torque seamlessly without shift points. However, on the Forester Sport, the CVT incorporates a computer-generated seven-speed manual shift mode with paddle shifters on the steering wheel. Under hard acceleration in automatic mode, it also mimics a conventional automatic's upshifts.
The Forester is equipped with a system called SI-Drive that allows the driver to select throttle characteristics for fuel economy ("intelligent") or maximum performance ("sport"), called "sport sharp" on the Sport trim.
The horizontally-opposed engine, also called a boxer or flat engine, has cylinders that lie supine, feet to feet, on both sides of the crankshaft instead of standing upright or leaning as with an inline or V configuration. Its low profile results in a lower center of gravity, which contributes to more secure road-holding and handling.
As a vehicle that is oriented toward small families and adventuresome singles, the new Forester is designed to be both practical and comfortable. The rear doors are wider than before and swing open nearly 90 degrees for adults to easily step in. Also, the cargo area, with 33 cubic feet of space, has an opening more than 43 inches wide and 32 inches high for ease of loading large objects. Fold the rear seatbacks flat and the space expands to 71 cubic feet.
Though not a racer, the Forester Sport's suspension tuning and performance-oriented wheels and tires, aided by brake-engaged torque vectoring, enhance handling on curving roads. At highway speeds, it tracks true and is quiet except for some intrusion of engine noise under hard acceleration.
The ride is compliant on all but the roughest roads and the Sport comes with supportive front seats upholstered in sturdy and comfortable cloth.
One shortcoming: If the driver inadvertently shuts down the engine with the transmission in "drive," the Forester will roll away. If that happens on many other vehicles, the transmission automatically shifts to "park." The rollway scenario has been receiving increasing attention as a safety hazard.
Even at that, the Forester is a highly desirable vehicle and a staunch competitor in the compact crossover class. Since its introduction in 1997, it has totaled sales of 1.8 million, with many owners keeping them beyond expected trade-in times.
As a company, Subaru has been uncommonly successful, one of a few manufacturers that thrived despite the recession of a decade ago. In the last nearly seven years, it has had 81 consecutive months of year-over-year sales growth.
Model: 2019 Subaru Forester Sport four-door crossover sport utility vehicle.
Engine: 2.5-liter horizontally-opposed four-cylinder; 182 hp, 176 lb-ft torque.
Transmission: Continuously-variable automatic with seven-speed manual shift mode and all-wheel drive.
EPA passenger/cargo volume: 108/33 cubic feet.
EPA city/highway/combined fuel consumption: 26/33/29 mpg.
Base price, including destination charge: $29,770.


guided by Spirit to fulfill your purpose.
Spiritual Badasses Helping You Experience Your Greatness.
"Your path has always been there for you. You simply got lost. You didn't trust it. In your need to be assured, you became disconnected from yourself, but fortunately not forever. This path will amaze you at times and shock you at others. To be sure, it will be anything but certain. That's why it's exciting. It's the path of surprise. It's the path of constant engagement. It's the path of life. The path of freedom. The path of your purpose. The path to become who we truly are. "
The quote above comes from a business help book titled "The E-Myth". Although Guided Warriors was founded before I read the book, I was profound by these words, it's truth, and meaning. This is the path of Guided Warriors. This is who we are. Getting reconnected with Spirit to become who we Already Are. Removing the conditioned thoughts and experiencing life through Spirit, Love, and Abundance.
"My journey is to love, to motivate, to give, and to be everything but "normal"."
A devoted spiritual coach, life coach, motivational speaker, and inspirational spirit, Nathaniel journey has taken him from struggle to success, depression to lifted, and a giver to humanity.
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What is page rank checker?
The page rank checking tool works individually for every web page. It is meant for checking the relevance of a web page for the website by analyzing its linking. There is a mathematical algorithm of google for checking the backlinking work for every individual web page.
When you type or paste the URL of that page in page rank checker, it deeply analyzes to conclude some important results. The results of a page rank checking tool are based on backlinking. Not only the number of backlinks, but their quality also matters when it comes to the purpose of ranking.
More backlinks for a web page with high-quality backlinks will have more probability to reflect on the top 10 search criteria of Google search engine.
This is the list of top trending tools of page ranking that you will be able to see on the topmost search results. Take an example of these websites. Their web pages are appearing on the topmost results because of the better backlinking than others. All of them have the same functioning but the procedure may differ. Als, most of the page rank checkers come with a bundle of other tools that are necessary for SEO practices.
All strategies of digital marketing are implemented in order to improve the ranking of a web page whether they are organic or paid. The main focus of every marketer is to establish strong footprints of organic optimization because it is long lasting.
Search Engine Optimization is the traditional as well as a universally accepted method of organic digital marketing that is evolving day by day with better. An SEO executive promotes every page of the website by using backlinks. The backlinks play a significant role in promoting a specific web page that is coming at the top results of Google Search Engine.
Now, the question is, how to find which pages of website her more important than others so that you can do something to rank them. Apart from a home page, there are many other aspects of a website that require better exposure at the search engine results. Here comes the role of PageRank checker tool. This is an online tool accessible through various websites for free of cost. Scroll down to gain more information.
Why do we need page rank checker?
Every digital marketer needs a page rank checker tool because it is helpful in examining the overall performance of a website on the search engine results. The main purpose of backlinks is to improve the score of a web page. After implementing all ethical strategies of SEO, it is important to know the results of all these practices.
When the crawlers go through a web page, they identify the backlinks and their quality. On the basis of these facts, the ranking of a page is specified at the search results. Rather than going with the entire website, you need to focus on every single page according to its relevance for customers. For instance, your service page must also come at the topmost results of a search engine in order to guide the visitors directly for what they want.
When you focus on the optimization of a web page, it is important to analyze the difference after implementing every single strategy. After investing in buying good quality backlinks, it is also important to know whether they are actually working for your website or not. This tool is the answer to all these questions.
The page rank checker tool has great importance from the perspective of SEO as well as domain owner too. Even without having any in-depth knowledge regarding digital marketing strategies, one can easily check the rank of their every individual web page.
There are some rumors that this tool as no more significance for SEO right now. However, the truth is, it is still a great significance in digital marketing. Officially, Google has discontinued this toolbar in 2016 by hiding the ranks publically still, it exists and working secretly. If it is still existing, there must be some importance too.
How does the page rank checker works?
The page rank checker is a simple as well as powerful tool comprising capability of concluding many results with one click. It is very easy to use if you have opened the right URL. When you open the tool, a blank space will appear to enter the domain name.
From this long list of data, you can get information relevant to ranking purpose. The higher number of external backlinks signify better ranking status on the Google search engine.
The page rank checking tool helps in identifying the status to a web page individually that you want to target on the search engine.
The SEO experts get a detailed report of a page altogether without using different tools like Alexa ranking & DA checker separately.
It helps in identifying the results of backlinks that you associate with a particular web page.
The final report of ranking can help in planning a strategy to improve the current ranking status.
What is Page Rank according to google?
Page Rank is a number given by Google from 1 to 10 to your website or web page based on importance, quality information and authority of the page. The more the Page Rank Google prefers the page to index and rank in the top of search results, Page rank is determined by the page relevancy regarding keyword and content, the page which has higher page rank will settle at the top of search results.
To know your page rank just enter the 1 website URL or 100 URL and click submit button. The Page rank checker tool analyses your page authority information and Pagerank.
If you are an SEO executive, the page ranking tool has great significance for your practices. It gives you a real-time report of every strategy. If the backlinks are not giving expected results even after investing heavily, you can make important changes and prevent remaining monetary from exhausting unnecessarily on low quality or irrelevant backlinks.


text:
Q: How to use multiprocessing in stacking algorithm in jupyter notebook I want to use multi processing for my stacking algorithm. I have already trained five different algorithms (Random forest, KNN, SVM , MLP and Gradient Boosting CLassifer) for my classifiers in Stacking algorithm. Now i want to tune the hyperparameters of the meta classifier. I tried with Grid Search CV but i dont think it works on the meta classifier in the stacking algorithm. I have six for loops to tune six hyperparameters and its taking a lot of time when run on a single core. Any help or ideas?
n_estimators=range(50,550,50)
max_depth=[5,10,15,20,25,30,35,40,45,50,None]
criterion=['gini','entropy','log_loss']
max_features=['sqrt','log2',None]
min_split=[2,3,4]
min_leaf=[1,2,3,5,10,20,40,50]
results=[]

for i in n_estimators:
    for j in max_depth:
        for k in criterion:
            for l in max_features:
                for m in min_split:
                    for n in min_leaf:
                        model_rf=RandomForestClassifier(n_estimators=i,max_depth=j, criterion=k,
                                                        max_features=l, min_samples_split=m, min_samples_leaf=n,
                                                        random_state=0)
                        model_RF_stack = StackingClassifier(classifiers =[model_RF,model_KNN,model_SVM,model_MLP],
                                            meta_classifier = model_rf)
                        model_RF_stack.fit(x_train,y_train)
                        y_pred=model_RF_stack.predict(x_test)
                        acc=accuracy_score(y_pred,y_test)
                        x=[acc,i,j,k,l,m,n]
                        results.append(x)


text:
Kurt Baumeister
Writer, Author of PAX AMERICANA
PAX AMERICANA Press Release
Reviews and Praise
PAX AMERICANA Review/Author Interview at RAIN TAXI
PAX AMERICANA Selected to Best of 2017 List (PANK Magazine)
PAX AMERICANA: Coverage on National Book Critics Circle Blog by Daisy Fried
PAX AMERICANA Selected by LitReactor as One of the Best of 2017…So Far…
Pax Americana Reviewed by Critic John Domini for Vol. 1 Brooklyn
Jan Elizabeth Watson Reviews PAX AMERICANA for Electric Literature
Pax Americana Reviewed by Jennifer Spiegel for Live Oak Review
Excerpts from Pax Americana
An Excerpt from Pax Americana (Literary Orphans/The Tavern Lantern)
An Excerpt from PAX AMERICANA (The Weeklings)
An Excerpt from Pax Americana (The Nervous Breakdown)
Kurt Baumeister Interviewed by Tobias Carroll for Vol. 1 Brooklyn
Kurt Baumeister Interviewed by Matt Norman for J.M.W.W.
Largehearted Boy Book Notes – Kurt Baumeister "Pax Americana"
Kurt Baumeister: The TNB Self-Interview
Caroline Leavitt Interviews Kurt Baumeister + Bonus Excerpt
Kurt Baumeister Interviewed by Bestselling Author Christine Sneed
THE BOOK OF LOKI
THE BOOK OF LOKI, a novel excerpt (published initially by GUERNICA)
Columns and Essays
Under the Influence #14, Peace
Under the Influence #13
Under the Influence #10, Taste
Under the Influence #9, Meditations
Under the Influence #8, Perspective
Under the Influence #7, Magic
Under the Influence #6, Negative Capability
Under the Influence #5, The Literary Psyche
Under the Influence #4, Nabokov's Hyperbole
Under the Influence #3, Rediscovery
Under the Influence #2, Son of Kid of Baby
Under the Influence #1, The Origins Issue
Entropy Magazine's "Under the Influence": Call for Submissions
LOOKING BACK AT THE ABYSS: REFLECTIONS ON BINGE-WATCHING "HANNIBAL"
Deaths of Distant Friends (or, John Updike F#cking Rocks)
Found in Translation (50 Things You Don't Mean and What You Really Do)
U2: All That You Can't Leave Behind
Donald Trump's America
THE HEROES WE NEED
POLITICAL TIME MACHINE
Beware the Ides of Trump
SCREAM, DREAM, NIGHTMARE
THE BITTER AND THE SWEET: MY UPGRADE TO WINDOWS 10
THE WORST PEOPLE IN AMERICA: WAYNE LAPIERRE
SEVEN THINGS WE DON'T CARE ABOUT THIS WEEK: SEMI-CROWD-SOURCED, SUMMER BLOCKBSTER, TRIPLE CROWN, JAM-PACKED-WITH-CARING-AND-UNCARING EDITION
"MAD MEN" EULOGIES: DON DRAPER
THE SATURDAY RUMPUS ESSAY: FEMALE PRESIDENT? TV SAYS, "DEFINITELY, MAYBE."
LET'S FOLLOW THIS MICKEY MOUSE JURISPRUDENCE TO ITS LOGICAL CONCLUSION AND REPLACE THE SUPREME COURT JUSTICES WITH NINE CARTOON CHARACTERS
DAWN OF IRONY ON THE PLANET OF THE APES
RICK PERRY, BIZARRO SUPERMAN?
DEAR FRANK UNDERWOOD, OR, THERE'S A HOMICIDAL POLITICIAN LIVING IN MY BASEMENT
TRUE DETECTIVE: JOURNEY TO THE END OF THE AMERICAN NIGHT
WHY THE LEFT SHOULD STOP LISTENING TO RALPH NADER
A SIMPLE REALITY IN THE U.S. TAX CODE THAT AFFECTS US ALL
Vol. 1 Brooklyn: Charles Yu's Interior Chinatown Reviewed by Kurt Baumeister
TNB Book Review: Teddy Wayne's Apartment Reviewed by Kurt Baumeister
The Brooklyn Rail: And I Do Not Forgive You by Amber Sparks
The Brooklyn Rail: No Good Very Bad Asian by Leland Cheuk
The Brooklyn Rail: Trump Sky Alpha by Mark Doten
TNB Book Review: Gabino Iglesias's Coyote Songs, reviewd by Kurt Baumeister
The Nervous Breakdown's Review Microbrew, Volume 8
TNB Book Review: The Sarah Book, by Scott McClanahan
TNB Book Review: Joseph by Dena Rash Guzman
TNB Book Review: Robert Burke Warren's Perfectly Broken
Success and Its Trappings, a review of Matt Bell's latest
THE NOVEL LIVES: A REVIEW OF THE SILENT END BY SAMUEL SATTIN
TNB Book Review: The Game of Love and Death by Martha Brockenbrough
TNB Book Review: The Guild of St. Cooper, by Shya Scanlon
Honesty and All its Oddities: This Is Your Life, Harriet Chance! by Jonathan Evison
The Sounds of Madness: The Subprimes by Karl Taro Greenfeld
REVIEW: The Sea-God's Herb by John Domini
REVIEW: Station Eleven by Emily St. John Mandel
THE ARENA OF LOVE, a short story
SUPERMAN'S LAST FLIGHT
Fallen Flowers
3 Poems: Mecca, Tsarist Pop Star, and God and Judy Garland
if there were
Dead Heart
On July 20, 2019 July 20, 2019 By kurtbaumeisterIn Uncategorized
Wherein Gillian Cummings pens an achingly beautiful tribute to Sylvia Plath and death; Natalie Singer praises the sharp eye of Lia Purpura, a talent for observation so keen it rekindles her own; Brendan Lorber goes fragmentary and nautical in his shout-out to Rimbaud; and Caroline Leavitt tunes in to Maggie O'Farrell and the beauty beyond the darkness. Please read and enjoy…
by Caroline Leavitt
I'm under the influence of the sublime Maggie O'Farrell. I first read her After You'd Gone because the premise so excited me: a young woman deliberately steps off a curb in a teeming city and goes into coma. What? Why? As she's in coma, we learn about her life, the person she achingly loves, the secrets that rise to the surface. I was hooked.
Recently, she's taught me yet another lesson—in her latest book I Am, I Am, I Am, which is about the darkest, thorniest thing you can imagine. Her experiences nearly dying, and then her daughter's experiences—how close death is to us at all times. Yep, totally dark, but exhilarating, because I was learning that writing dark does not mean you are pulling people under. It doesn't mean that you have no hope. I haven't listened for a long time when people say, "Oh, readers want pure entertainment, they want escape, they want dragons and romance." Nothing wrong with those things, but sometimes facing the dark, looking at death, is all about the brave beauty that is life.
Caroline Leavitt is the New York Times bestselling author of Pictures of You and Is This Tomorrow, as well as Cruel Beautful World and 11 other books, or 12 if you count the one she's writing now, and yes, they are all dark and she hopes they are also brave and beautiful.
by Brendan Lorber
3 a.m. at the Nuyorican Poets Café. Open reading about to start. An impossibly old man, maybe 24 or 25, passes me the Lettres du voyant, Arthur Rimbaud's how-to of the visionary. After hours, early in life, the perfect instant to intercept their call for rational disordering of the senses. To let my keel break and sink into the sea, and so become a seer. I copy a passage ritually on the back of a poem I'm about to read into the dented mic. My bad poem is only good here in the café's predawn altered alertness, as the single misstep that begins a wild journey.
Brendan Lorber is the author of If This Is Paradise Why Are We Still Driving? and several chapbooks, most recently Unfixed Elegy and Other Poems (Butterlamb). His work appears in in the American Poetry Review, Fence, McSweeney's, and elsewhere. Since 1995, he has published and edited Lungfull! Magazine, an annual anthology of contemporary literature. He lives atop the tallest hill in Brooklyn, New York, in a little castle across the street from a five-hundred-acre necropolis.
by Natalie Singer
For years, I've kept Lia Purpura's words on my nightstand, often her essay collections On Looking and Rough Likeness. I discovered Purpura a decade ago when I moved from journalistic writing to the more personal. I was struggling to maintain my honed objectivity and close observation skills (the "eye") while burrowing into the intimate, subjective "I." I couldn't calibrate the two, until I found Purpura. If it's possible to turn a microscope, with its ocular and objective lenses, on the world, Purpura does, magnifying the miniscule and mundane (window pane, thawing snow, spires), and gathering and bending the light to focus and contextualize the image into the most affecting specimen. Whenever I forget how to look, I turn to Purpura and the world opens again.
Natalie Singer is the author of the lyric memoir California Calling: A Self-Interrogation (Hawthorne Books, 2018). She teaches creative writing and has worked as a journalist at newspapers around the West. Natalie hold an MFA in Creative Writing and Poetics from the University of Washington. Originally from Montreal, she now lives in Seattle. Her website isnataliesingerwrites.com and she forces herself to use Twitter (@Natalie_Writes).
by Gillian Cummings
I first read "Elm" as a college freshman: "I know the bottom, she says. I know it with my great tap root: / It is what you fear. / I do not fear it: I have been there." As a young woman who'd attempted suicide by overdose just two years before, I could feel Plath's sadness as if borne in my own bones. Older and closer to my own death, I can feel it. I wrote about it in The Owl Was a Baker's Daughter, as if it had already happened—because in a way it had: During my suicidal depression of recent years, I had experienced coma. I am shy, quiet. I want my death to be like a dandelion spore that just lifts and lightly floats off, unnoticed by the world and unfelt except by the stem that once held me firmly to earth. But I want my words to stay, as Plath did; love may go off "like a horse," but some stone remains, "echoing, echoing."
Gillian Cummings is the author of My Dim Aviary, winner of the 2015 Hudson Prize, as well as the chapbooksOphelia, Petals as an Offering in Darkness, and Spirits of the Humid Cloud. Her poems have appeared in Boulevard, theCincinnati Review, Colorado Review, Denver Quarterly, the Laurel Review, the Massachusetts Review, Quarterly West,Verse Daily, and others. A graduate of Stony Brook University and of Sarah Lawrence College's MFA program, she was awarded the Dorothy Sargent Rosenberg Memorial Fund Poetry Prize in 2008. Cummings lives in Westchester County, New York.
There are all sorts of mediations. Some, the traditional, religio-philosophical sort, have us concentrating on not concentrating; chanting, intoning, and/or third-eye seeing a synesthesia of peace and joy. There are musical mediations and sonic meditations, artistic meditations and mathematical meditations. Then there's the literary brand of the meditation, something that can countenance a multiplicity of subjects, a grouping of which this outro would be but one.
Above, you have mediations on beauty and darkness, life and death, observation and…Rimbaud. What unifies them isn't tone, subject matter, or even style. It's the fluidity and calmness of mind you sense reading the output.
For me, and I think for a lot of writers, being able to lose focus on the physical world, to concentrate only on what you're setting down, is one of the great joys of writing. The feeling of being immersed in (reading) a book is similar. You lose time, lose yourself. And it doesn't have to be because of story or plot. You can lose yourself in ideas or prose. That is possible, though not as easy for the average bear as certain very serious, exceedingly literary writers might wish it to be.
But what's born of the literary meditation, of immersion in subject? An understanding of the subject, obviously; but also, an understanding of self. That's the healing aspect of writing—the self-directed psychotherapy of it all. Which, I guess, breeds a different sort of stillness of mind, one born not of forgetting but of understanding.
Admittedly, the logic of these outros is getting dodgier as Under the Influence chugs forward into the double digits. I'm free-writing more than I was at the beginning of this, back in April or May or whenever. My points are getting more elliptical, at best. And I still haven't pulled my trump, much as I hate to use that word these days. I still haven't started trotting out my own influences: brazenly forcing you to listen to me talk about Martin Amis and Don DeLillo. I could do that, but I'm trying hard not to. So, send me your submissions!
Kurt Baumeister has written for Salon, Electric Literature, Guernica, The Weeklings, The Nervous Breakdown, The Rumpus, The Good Men Project, and others. Now a Contributing Editor with The Weeklings, Baumeister's Review Microbrew column is published by The Nervous Breakdown. His debut novel, a satirical thriller entitled Pax Americana, was published by Stalking Horse Press in 2017. He is currently at work on a novel, The Book of Loki, and a hybrid collection of fiction, nonfiction, and poetry entitled Superman, the Seven Gods of Death, and the Need for Clean, Romantic Poetry. Find him on Facebook, Twitter, or at www.kurtbaumeister.com.
El Kurt