Boric Acid can be used added to petroleum or vegetable oil to create a lubricant which can be applied to ceramic or metal surfaces. Boric acid is also used in the manufacturing process of textile fiberglass which are used to reinforce plastics. With its conjugate base, boric acid is commonly used as a primary or adjunct pH buffer systems in swimming pools.
This product is available in various packaging options. Please ask about custom packaging.
Please contact us to receive a quote, or call us at 715-726-3114. SDS available upon request.


Where is located the m3u8 file used for live HTTP Streaming ?
But I can't find the playlist.m3u8 physical file.
The reason I want to find it is that I want to setup multiple bit-rate streams.
As long as the SMIL file describes all the streams then it will produce the correct intermediate playlist. The playlist.m3u8 is never saved to disk. It is availe up HTTP request from the player.
You won't find them. They are well hidden. What you can do is replicate them.
Hi, I have the same problem and I didn't find the solution on the related link, Adaptive Bitrate over HLS standard include a custom index playlist and if we use "smil" method we won't be applying HLS.
which points to different playlist files with different bit rates.


text:
The Ukraine national futsal team represents Ukraine in international futsal competitions such as the FIFA Futsal World Cup and the European Championships and is controlled by the Football Federation of Ukraine.

History
In the 2008 FIFA Futsal World Cup qualification stage Ukraine finished top of Group 10 ahead of Israel, Moldova and Bulgaria. In the knockout stage of the qualification process, they advanced after beating Hungary 6:5 on aggregate (3:1 home, 3:4 away). The last stage of the 2008 FIFA Futsal World Cup took place from 30 September 2008 till 19 October 2008 in Rio, Brazil and was the largest ever edition of the tournament at the time containing 20 teams. Ukraine has history in the tournament, having a fourth-place finish in 1996 and a top eight finish in 2004, 2008 and 2012.

Tournament records

FIFA Futsal World Cup

UEFA European Futsal Championship

Grand Prix de Futsal

Players

Current squad
The following players were called up to the squad for the UEFA Futsal Euro 2022.
Head coach: Oleksandr Kosenko

Recent call-ups
The following players have been called up for the team within the last 12 months.

Head coaches
 Gennadiy Lisenchuk – from 1994 till 2012
 Yevgen Ryvkin – from 9 January 2013

Results and fixtures

2021

2020

2014

References

External links
 Futsal Association of Ukraine (ukr)

Ukraine
national
1994 establishments in Ukraine
Futsal clubs established in 1994

redpajama_set_name: RedPajamaWikipedia


text:
Did You Know…John Adams & William Daniels!
July 1, 2018 Linda Reimer
Here is our Did You Know…posting for July and it features two likely July characters, President John Adams and his shadow, actor William Daniels!
I'm sure everyone knows John Adams was the second president of the United States. He followed George Washington who, unquestionably, was a hard act to follow. And there are volumes of tomes and tomes (another great word!) you can read on John Adams – but many of them are a bit weighty and more accessible to history fans and scholars than to regular readers.
So this Did You Know…posting is going to focus on some accessible and fun materials you can check out to learn more about John Adams and his family without having to wade through thousand page books on the subject!
And if you're scratching your head and wondering…
"What on earth does an actor named William Daniels have to do with John Adams?"
Wonder no more!
William Daniels is an American actor who has portrayed John Adams numerous times on the stage and screen and this posting will offers some fun suggestions about those performances – namely where you can find them on DVD (Hint – your local public library!)
And without further ado, here we go!
Firstly regarding John Adams…
Did you know that the HBO mini-series John Adams is based upon the bestselling, and easy to read, biography, of John Adams written by David McCullough?
The Book John Adams written by David McCullough:
The HBO Mini-Series John Adams based upon the McCullough book:
David McCullough wrote the book John Adams which was published in 2001, and in 2008 HBO released a mini-series based upon the book – starring Paul Giamatti as John Adams and Laura Linney as Abigail Adams.
The mini-series opens just before the Boston Massacre and ends with John Adams's death in 1826; and in-between those two events Adams defended the British soldiers who shot into the crowd during the Boston Massacre (and got them off!), he attended the Continental Congresses, signed the Declaration of Independence, was the first U.S. Ambassador to Great Britain after the Revolutionary War (bet that was fun!), was George Washington's vice president for two terms, president for a term and then an intellectual gardener who wrote Thomas Jefferson dozens of letters from his home in Quincy, Massachusetts – and more! He was a rather busy individual during his life time!
And now, linking the historical figure John Adams to the career of the actor William Daniels…
Did you know that William Daniels portrayed John Adams in the musical play 1776 both on stage and screen?
He did!
The play 1776 was written by Sherman Edwards and Peter Stone. William Daniels starred in the Tony Award Winning play while it was on Broadway and then reprised his role for the 1972 film version.
The 1776 story opens in Philadelphia in May of 1776 where the second continental congress is meeting. John Adams (William Daniels) is the first character introduced and he demands of Ben Franklin, when does he think the congress is ever going to get around to declaring independence anyway!
Adams goes on to say he can't make a proposal for colonial independence to the congress because he is "obnoxious and disliked." And Franklin notes, that some new delegates have just arrived and perhaps they should have a talk with them on the subject of declaring independence. And lo and behold, one of the delegates just happens to be Thomas Jefferson of Virginia! Shortly thereafter another Virginia delegate, Richard Henry Lee, rides home to get approval from the colonial Virginia Assembly to put forth a motion for independence to the Congress. Lee returns, puts the proposal in front of Congress, Adams seconds it and the musical debate begins!
Some of the other actors/actresses in the film include: Howard DaSilva as Ben Franklin, Blythe Danner as Abigail Adams, Ken Howard (White Shadow) as Thomas Jefferson, John Cullum (Northern Exposure) as John Dickinson and David Ford (Dark Shadows) as John Hancock
Songs include: Piddle, Twiddle & Resolve, The Lees of Old Virginia, The Egg, He Plays the Violin, Cool Considerate Men and Is There Anybody There?
If you haven't seen the film – it is great fun and a perfect DVD for July viewing!
And did you further know…
That in addition to appearing in the both the Broadway and film versions of 1776, that William Daniels went on to portray John Quincy Adams, son of John & Abigail Adams in the PBS mini-series The Adams Chronicles?
The Adams Chronicles video mini series was played on PBS in the 1970s and can now be checked out of the library:
As can the Jack Shepherd book of the same name on which the miniseries is based:
The story of the Adams Family is fascinating and fun! And the Emmy Award Winning miniseries, was indeed based upon the book The Adams Chronicles: Four Generations of Greatness written by Jack Shepherd and published in 1976. The story opens in the last 1750s and follows as a young John Adams as he finishes law school, starts a law practice and begins to court the love of his life Abigail Smith. The story takes viewers through the lives of family members during the colonial era, focusing first on John Adams – his time in the Continental Congress, through his diplomatic missions in Europe to his time as vice-president, then president and then the main focus switches to the covering the life of John Quincy Adams (William Daniels). And John Quincy Adams had quite a life! He was, among other things, Thomas Jefferson's private secretary, a U.S. diplomat, Secretary of State, President of the United States (and a skinny dipping president at that!) and, the only president to-date, to go back into government after he left office. John Quincy Adams, who initially retired after he was defeated for a second presidential term in 1828, was elected to Congress in 1830. John Quincy was a an erudite individual, a passionate speaker, and, decidedly against slavery. And his great debating skills earned him a nickname bestowed upon him by his fellow congressmen – "Old Man Eloquent." J. Q. Adams suffered a stroke while in the House of Representatives in 1848 and died hours later. He is also the earliest president we have a photo of – his photo was taken in 1843, the year Adams turned 76.
After John Quincy's death the mini-series goes on to follow John Quincy's son Charles Francis Adams during his time in Massachusetts state government, his time as a U.S. Congressman and as U.S. Ambassador to the United Kingdom during the American Civil War. The fourth generation followed in the series consists of the six children of Charles Francis and his wife Abigail Brown Brooks –the children included Civil War soldiers John Quincy Adams II and Charles Francis Adams Jr. and the historian Brooks Adams and you get the idea – it is the story not just of individuals but of a family too.
And on a final did you know note…
Going full-circle and back to John Adams…
You probably already know the third most famous thing about John Adams, after the fact that he was President of the United States and signed the Declaration of Independence – is that he died on the same day as his friend, the third President of the United States – Thomas Jefferson and on the fiftieth anniversary of the singing of the Declaration of Independence – July 4, 1826.
But did you know that after both men left the presidency and went into retirement the former friends, turned political rivals, became friends again and wrote dozens of letters to each other in their retirements?
They did!
After a bitter falling out in the 1790s they actually never spoke to each other again!
However, in 1812 a mutual friend, and fellow signer of the Declaration of Independence, Dr. Benjamin Rush, urged Adams to write to Jefferson – and he did!
Thus friends once more, the two men wrote dozens of letters to each other in the last 14 years of their lives. Both men were exceptionally well read and – and there is, as David McCullough observed "great charm in the letters." It is apparent in reading the letters that the men both knew they were writing, not just to each other – but to posterity.
As an example consider this Adams – Jefferson Letter:
"1812, January 21: Jefferson to Adams_____________ A letter from you calls up recollections very dear to my mind. It carries me back to the times when, beset with difficulties and dangers, we were fellow laborers in the same cause, struggling for what is most valuable to man, his right of self-government. Laboring always at the same oar, with some wave ever ahead threatening to overwhelm us and yet passing harmless under our bark, we knew not how, we rode through the storm with heart and hand, and made a happy port."
The Adams Jefferson Letters are compiled in a book – should you wish to request it!
And on a final William Daniels note – you may recognize the actor from some of the many other roles he has had during the years. He is an excellent actor and whichever character his is portraying – his is worth watching! Along with his wife he was regular on St. Elsewhere portraying the grouchy Dr. Mark Craig, he portrayed Benjamin Braddock, the husband of Dennis Hoffman's Mrs. Robinson in the Graduate, appeared as Howard in the Jack Finney and Audrey Hepburn movie Two for the Road and was the voice of KITT the car in the David Hasselhoff Knight Rider series. And the library has all the aforementioned videos (I love that word too — "aforementioned" – a great word!)
And here are few related neat and fun video clips to watch!
From The HBO Series John Adams – Scenes showing the Adams Jefferson correspondence
David McCullough on the Adams Jefferson Letters
Have a great month and a Happy Fourth of July!
About the Adams-Jefferson Letters:
Full Title: The Adams-Jefferson letters; the complete correspondence between Thomas Jefferson and Abigail and John Adams – Adams, John Quincy, 1767-1848.
The collection, which you can check out of the library as a print book or eBook contains 380 letters
Their complete correspondence, which contains 380 letters written between 1777 and 1826, is known as the Adams-Jefferson Letters. The collection also includes a number of letters written before their post-Revolutionary War political falling out. However, the best of the letters, in the opinion of this humble history fan, are the ones they wrote between 1812 and 1826.
From The Correspondence of John Adams & Thomas Jefferson on Life, Religion, and the Young Republic
Click to access adamsjeffersoncor.pdf
John Adams. Thomas Jefferson Foundation. Online. Accessed June 29, 2018.
https://www.monticello.org/site/jefferson/john-adams
The John Adams LIbrary at the Boston Public Library. John Adams Historical Society. Online. Accessed June 29, 2018.
http://www.john-adams-heritage.com/john-adams-library/
Plain Speaking Review (2001, May 27). The New York Times. Accessed June 29, 2018.
https://archive.nytimes.com/www.nytimes.com/books/01/05/27/reviews/010527.27maiert.html?mcubz=2
Tagged Corning NY, John Adams, public library, Southeast Steuben County Library, William Daniels
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Welcome to the home of Flame-Waves, part 4 by Sri Chinmoy.
Question: How would you define ultimate Truth?
Question: How can I acquire lasting inner joy?
Question: I have had the experience that, when we try to help others, sometimes a kind of barrier builds up in ourselves and also in those we try to help. Could you speak about this.
Question: How can we remain unaffected by other people's undivine consciousness without cutting ourselves off from them?
Question: If our fulfilment lies in our utter consecration to the life divine, could you say something about consecration.
Question: Is there any way that we can meditate specifically to help the United Nations?
Question: How do you eradicate negativities and imperfections in the soul?
Question: About two weeks ago, a Hatha Yoga Master came to the United Nations and said that first you must conquer and overcome the body and only then can the Supreme be manifested. What are your feelings about this?
Question: Last week you mentioned something about wrestlers and people who are engaged in physical activities, saying that competition on the physical level is not what we are after. Do you feel that people who are professional wrestlers and boxers do not have a place in society?
Question: What role does the vital being play in our spiritual progress?
Question: How can we more fully surrender to the Supreme?
Question: When we meditate, to what extent do we represent and are we responsible for humanity and the world?
Question: I have just started coming to your meetings and I would like to know how to meditate. I really don't know exactly what you mean by meditating.
Question: Could you speak about the need for individuals to defend themselves?
Question: How can we remember to forgive the world for its defects and to forgive ourselves for our own defects?
Question: How can we avoid falling asleep during meditation?
Question: When I feel that my spiritual progress is not fast enough and that my meditation is not deep enough, sometimes I feel the Supreme is not happy with me. Then feelings of depression and frustration enter. How can I deal with this?
Question: Is there something that we can consciously do or practise to cultivate humility?
Question: How can I have deeper meditation?
This is the 221st book that Sri Chinmoy has written since he came to the West, in 1964.


text:
Mediators of Impaired Adipogenesis in Obesity-Associated Insulin Resistance and T2DM
By Haya Al-Sulaiti, Alexander S. Dömling and Mohamed A. Elrayess
Submitted: May 13th 2019Reviewed: July 22nd 2019Published: August 28th 2019
Home > Books > Adipose Tissue - An Update
Obesity has become a global health issue due to its high prevalence and associated comorbidities including insulin resistance (IR) and type 2 diabetes mellitus (T2DM). Obesity is associated with the expansion of adipose tissues through hypertrophy of mature adipocytes and differentiation of local preadipocytes in a process known as adipogenesis to store excess triacylglycerols (TAGs). Impairment of adipogenesis leads to ectopic fat deposition in skeletal muscles, liver, and kidneys, triggering IR in these tissues and increased risk of T2DM. Many factors contribute to impaired adipogenesis including obesity-associated mild chronic inflammation, oxidative stress, and fatty acid signaling. This review summarizes recent literature covering mediators of impaired adipogenesis and underlying molecular pathways.
adipogenesis
Haya Al-Sulaiti
Department of Drug Design, University of Groningen, Netherlands
Alexander S. Dömling
Mohamed A. Elrayess*
Biomedical Research Center (BRC), Qatar University, Qatar
*Address all correspondence to: maelrayess@hotmail.com
Adipose TissueAn UpdateEdited by Leszek Szablewski
Adipose Tissue - An Update
Edited by Leszek Szablewski
1. Obesity-associated metabolic disease
Rapidly changing lifestyle, accompanied by consumption of excess energy in the form of a calorie-rich high-fat diet, lower voluntary activity, and increased exposure to environmental pollutants, have led to an exponential rise in noncommunicable metabolic diseases [1]. A key component of chronic metabolic diseases is obesity that has become a global health problem associated with a range of comorbidities including insulin resistance and type 2 T2DM [2], coronary artery disease (CAD) [3], nonalcoholic fatty liver [4], cancers [5], and elevated risk of premature death [6, 7].
Adipose tissue is an endocrine organ that responds to obesity by secreting elevated quantities of free fatty acids, adipokines, and proinflammatory cytokines, triggering IR and risk of T2DM [8]. Obesity is also characterized by increased adiposity mediated by enlarged size of mature adipocytes (hypertrophy) and elevated number of newly recruited adipocytes (hyperplasia) [9, 10, 11, 12]. Adipose tissue dysfunction is characterized by adipocyte hypertrophy, mild chronic inflammation, and oxidative stress, causing reduced ability to generate new adipocytes from the undifferentiated precursors (preadipocytes). The impaired adipogenesis increases risk of IR and T2DM by triggering ectopic fat deposition in nonadipose tissues and proinflammatory environment characterized by impaired secretion of various adipose-derived adipokines [13].
Obesity also represents an imbalance between the primary site of storing energy (the white fat) and the site that is specialized in energy expenditure (the brown fat) [14]. White adipocytes store fat in the form of triacylglycerols as a single fat lipid droplet that gets readily hydrolyzed by lipases when energy is needed. The resulting fatty acids are mobilized to other tissues to undergo fatty acid oxidation as a source of energy [15]. The imbalance between lipolysis and lipogenesis plays a crucial role in progression of metabolic disease including T2DM and nonalcoholic fatty liver disease [16]. The brown fat, on the other hand, uses the energy derived from fatty acid oxidation for heat generation [17].
Adipocyte hypertrophy is associated with increased uptake of excess TAGs, which triggers fat accumulation within the larger subcutaneous adipose tissue (SAT) [18, 19, 20]. SAT therefore plays a buffering role as it prohibits progression of obesity-associated pathologies [21]. However, the buffering capacity becomes limited as impairment of SAT expansion causes IR [22, 23, 24] as the excess fat are deposited in the visceral adipose tissue (VAT) as well as ectopically in the skeletal muscle, liver, kidney, and heart tissues [25]. This is augmented by the infiltration of macrophages and activation of the innate immune cells [26], which triggers hyperinsulinemia that inhibits lipolysis and activates lipoprotein lipase (LPL). This causes further hyperinsulinemia, hypertriglyceridemia, increased IR in these tissues [27], and risk of T2DM [28].
Although obesity is generally associated with these comorbidities, some obese individuals seem to be protected as they maintain insulin sensitivity (IS) and show lower hypertension and proatherogenic and inflammatory profiles than their equally obese pathogenic counterparts [29, 30, 31, 32]. Investigating the underlying causes for this protective phenotype could potentially help obesity-associated pathogenicity. Although still unknown, various potential mechanisms were proposed to contribute to metabolically healthy obese (MHO) phenotype. These include lower visceral and ectopic fat deposition than subcutaneous fat accumulation due to efficient SAT adipogenesis, reduced inflammatory component in the adipose tissue, healthy levels of secreted adipokines, and more active lifestyle [33]. A genetic component was also suggested to interact with various environmental factors, although not yet determined [34]. Interestingly, lean diabetics also exhibit larger adipocytes than healthy individuals, perhaps due to impaired differentiation of preadipocytes but not a result of different frequencies of stromal vascular cells, lipolysis, or levels of inflammatory mediators [35]. Current therapeutic strategies focus on treating obesity-associated diseases instead of preventing the underlying mechanisms. Therefore, understanding the molecular mediators underlying the protective phenotype in MHO individuals could provide critical information to help individuals suffering from pathological obesity (PO). In this review, we aimed to understand the role of adipogenesis in obesity-associated IR and T2DM by screening 2317 articles investigating adipogenesis and mediators of impaired adipogenesis in PubMed with the aid of Rayyne, a systematic review web application [36].
2. The role of adipogenesis in obesity-associated IR and T2DM
The adipose tissue is a dynamic part of the endocrine system that plays a crucial role in maintaining energy balance and nutritional homeostasis [37]. Mature adipocytes constitute the most abundant distinctive cell type in the adipose tissue, occupying 90% of its volume [38]. Other components include leukocytes, macrophages, fibroblasts, endothelial cells, and preadipocytes, which constitute the stromal vascular cells (4–6 million cells per gram of adipose tissue, half of which are immune cells) [39].
Obesity-induced adipocyte hypertrophy is associated with impaired recruitment and differentiation of preadipocytes. Despite their abundance, preadipocytes fail to undergo terminal differentiation into mature adipocytes via the activation of the canonical Wnt signaling [40]. Preadipocytes are produced by mesenchymal stem cells (MSCs) under the influence of different signaling molecules. The mature adipocytes secrete BMP4 that triggers preadipocyte differentiation by inducing the separation of Wnt1 inducible-signaling pathway protein 2 (WISP2) and zinc finger protein 423 (ZNF423), allowing ZNF423 to translocate into the nucleus and activate peroxisome proliferator-activated receptors (PPARγ) and downstream cascade including CCAAT/enhancer-binding proteins β (C/EBPβ), δ, and α [41, 42] ( Figure 1 ).
Schematic representation of the role of Wnt signaling in adipogenesis.
BMP4 also plays an anti-inflammatory role by reducing tumor necrosis factor-α (TNF-α)-mediated proinflammatory cytokine induction in human adipocytes. Therefore, BMP4 plays a protective role against IR and T2DM [43]. Subsequently, PPARγ and C/EBPα activate preadipocyte differentiation and the expression of mature makers such as adiponectin, fatty acid-binding protein 4 (FABP4), glucose transporter type 4 (GLUT4), and LPL. The activation of PPARγ, therefore, maintains IS and exhibits an anti-inflammatory function, whereas IR causes impaired adipogenesis and increased risk of T2DM [44, 45].
Insulin and downstream Akt signaling also play important roles as modulators of adipose tissue growth and adipogenesis as insulin activates glucose and free fatty acid uptake, inhibits lipolysis, and de novo fatty acid synthesis in adipocytes, and induces adipogenesis [46]. The transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) has been shown to induce energy expenditure and reduce adipose tissue growth, leading to prevention of dietary obesity and lowering adipogenesis, inflammation, and IR [47]. The inhibition of inhibitor of nuclear factor kappa-B kinase subunit β (IKKβ) in mice lowers high-fat diet-induced adipogenesis and inflammation and protects from diet-induced obesity and IR [48]. MicroRNAs (miRNAs) have been also shown to play an important role in adipogenesis, IR, and inflammation as previously reviewed [49].Tonicity-responsive enhancer-binding protein (TonEBP), a key transcription factor involved in cellular adaptation to hypertonic stress, has been suggested to influence macrophage activity, adipogenesis, and IS by inhibiting the epigenetic transition of PPARγ2 [50]. Protectin DX (PDX), a ω-3 fatty acid-derived proresolution mediator, was reported to reduce inflammation and IR via an AMPK-dependent pathway and suppress adipogenesis and lipid accumulation during 3T3-L1 differentiation [51].
We have recently shown that higher adipogenic capacity of preadipocytes isolated from SAT and VAT from MHO individuals than PO counterparts may be one of the underlying mechanisms for MHO protection due to a greater ability to store TAGs in the SAT depot. This process was shown to be influenced by inflammatory mediators, oxidative stress, and fatty acid signaling [45, 52, 53, 54, 55].
3. Mediators of impaired adipogenesis in IR and T2DM
3.1 Inflammatory mediators
3.1.1 Impaired adipogenesis in response to proinflammatory signals
Obesity-associated comorbidities are mediated by chronic mild inflammation ( Figure 2 ). Lipid-laden adipocytes produce increased levels of cytokines such as Interleukin 6 (IL-6), IL-β, TNF-α, monocyte chemoattractant protein-1 (MCP-1), and IL-8 [10, 56, 57] which can inhibit preadipocyte differentiation [21, 45]. The impaired adipogenesis is associated with stress of the endoplasmic reticulum (ER) and elevated expression of unfolded protein response (UPR), both can exacerbate the proinflammatory phenotype of preadipocytes and adipocytes [58]. The effect of proinflammatory phenotype varies among various fat depots. VAT is a more inflammatory tissue than SAT as it secretes higher levels of proinflammatory cytokines. Macrophage infiltration into adipose tissue is regulated through serum resistin and leptin in obese individuals with early metabolic dysfunction [59]. The presence of macrophages in VAT contributes significantly to this phonotype. The presence of macrophages in human SAT, on the other hand, is causally related to impaired preadipocyte differentiation, which in turn is associated with systemic IR [60, 61]. Adipocyte differentiation, therefore, was shown to be significantly lower in VAT than SAT. Macrophage depletion can reduce inflammatory cytokines and trigger adiponectin secretion from both SAT and VAT adipocytes, leading to the induction of preadipocyte differentiation in SAT, but not VAT. Additionally, a negative correlation between SAT adipogenesis, but not VAT, and systemic IR was observed [62]. Chronic systemic inflammation is also associated with elevated lipolysis in white adipose tissue and lipogenesis in nonadipose tissues, causing ectopic fat deposition in nonadipose tissues and imbalance in free fatty acid homeostasis and increased risk of IR [63].
Mediators of impaired adipogenesis in IR and T2DM. Most proinflammatory cytokines as well as some anti-inflammatory mediators can impair adipogenesis (1). Similarly, various mediators of oxidative stress can impact adipogenesis both positively and negatively depending on their structure (2). Fatty acid signaling plays a key role in adipogenesis but at various degrees depending on the composition of the fatty acids (3). Finally, various environmental factors can impact adipogenesis mostly negatively (4).
Among the proinflammatory cytokines, IL-6 is produced by adipocytes, activated leukocytes, and endothelial cells [64] in obesity [65, 66, 67, 68]. IL-6 shows a synergistic effect with other mediators of metabolic disease, collectively contributing to the progression of other obesity-associated comorbidities such as CAD and T2DM [64, 69]. IL-6 impairs the LPL function leading to increased levels of circulating fat [69, 70]. Moreover, obesity-associated increase in IL-6 is linked to reduced insulin-triggered glucose uptake [60, 61]. Previous reports have indicated that insulin treatment improves the glucose transport activity of adipocytes in T2DM [21] and lowers IL-6 and TNF-α levels [53]. Although the precise mechanisms of IL-6-associated IR is not well characterized, human adipocytes from IR individuals were shown to exhibit significantly higher IL-6 expression levels [45]. IL-6 impairs insulin action by inhibiting expression of insulin receptor, insulin receptor substrate-1 (IRS-1), and GLUT4 in human preadipocytes as well as 3T3-L1 adipocytes [45, 71]. Furthermore, IL-6 was shown to reduce IS through decrease in adiponectin expression and secretion [72] and via impairment of insulin signaling in hepatocytes [73].
Various other cytokines have been shown to impact adipogenesis [74]. The proinflammatory cytokines IL-1 β, TNF-α, and MCP1 can also influence the hyperplastic expansion of adipose tissue and impair adipogenesis [59]. IL-1β triggers a proinflammatory response in human adipose tissues, particularly in VAT depot. IL-1β also inhibits insulin signal transduction, leading to impaired IS in adipose tissue [75]. IL-1β and cyclooxygenase-2 (COX-2) play a detrimental role in adipose tissue dysfunction in obesity [76]. With obesity, levels of MCP-1 and TNF-α increase in VAT before macrophage infiltration, suggesting a highly proinflammatory phenotype of the visceral depot prior to infiltration of immune cells and macrophage phenotype switch [77]. Unlike IL-6, IL-1 β, and TNF-α, MCP-1 and MCP-1-induced protein (MCPIP) were shown to induce adipogenesis. Treatment of reactive oxygen species (ROS) inhibitor, apocynin, reduced the MCPIP-triggered adipogenesis [78]. Other cytokines involved in adipogenesis include interferon-γ (IFN-γ), a central mediator of macrophage function. Compared to obese wild-type control animals, obese IFN-γ knockouts exhibit better IS, smaller adipocyte size, and lower cytokine expression [79].
3.1.2 Impaired adipogenesis in response to anti-inflammatory signals
Contrary to the notion that inflammation plays a negative role in metabolism, some studies suggest that proinflammatory signals in the adipocytes are actually needed for functional adipose tissue homeostasis ( Figure 2 ). Indeed, adipose tissue inflammation was shown in various animal models of adipose tissue-specific reduction of proinflammatory potential to be required as an adaptive response, allowing proper storage of excess fat and filtering of gut-derived endotoxins [80]. Additionally, various molecules with anti-inflammatory properties were shown to influence adipogenesis and risk of IR. Myokines, for example, secreted by skeletal muscle cells during exercise such as β-aminoisobutyric acid, can impair adipogenesis via activating AMPK signaling pathway and reducing levels of proinflammatory cytokines such as TNF-α [81]. Another example is the ubiquitin-editing enzyme A20 that impairs IL-6 secretion from adipocytes, leading to modulation of differentiation of MSCs [82]. The overexpression of A20 was also shown to reduce lipogenesis and adipogenesis via lowering levels of sterol regulatory element binding protein-1c (SREBP-1c) and aP2, causing lower fat accumulation in differentiated 3T3-L1 cells [83]. A third example is the nonerythropoietic EPO-derived peptide that plays an anti-inflammatory and anti-adipogenic roles in high-fat die mice with IR [84]. On the other hand, other anti-inflammatory molecules could rescue impaired adipogenesis. Glucose-dependent insulinotropic polypeptide (GIP), for example, is a potent activator of adipogenesis through modulation of inflammation in adipose tissue [85]. Additionally, the expression of neuronatin (Nnat), a proteolipid involved in neuronal development, in response to inflammation and dietary excess, has been suggested to play an important role in adipogenesis through lowering oxidative stress and inflammation [86].
3.2 Oxidative stress
Obesity leads to the accumulation of ROS, the hallmark of oxidative stress, in the adipose tissue causing impaired adipogenesis and increased risk of IR and T2DM. The balance between ROS generation and activation of endogenous antioxidants is crucial for cells undergoing adipogenesis [87] ( Figure 2 ). The oxidative damage and changes in the expression of antioxidant enzymes with age are similar between SAT and VAT. However, preadipocytes from SAT are significantly more resistant than VAT-derived cells to cell death caused by oxidative stress [88]. Interestingly, within SAT and VAT depots, preadipocytes from insulin-sensitive obese subjects were more prone to oxidative damage than preadipocytes from equally obese insulin-resistant individuals [52, 53]. The depletion of ROS from adipose tissue in mice models of oxidative stress was associated with increased adipose tissue mass, lower ectopic fat deposition, and enhanced IS. Similarly, ROS accumulation limited the expansion of adipose tissue, leading to elevated ectopic fat accumulation and increased risk of IR [89]. Elevated ROS within the adipose tissue triggers lipid peroxidation [45] and accumulation of reactive aldehydes including the bioactive lipid peroxidation product 4-hydroxynonenal (4-HNE) [90]. Elevated 4-HNE causes damage of cell structure and function through the formation of the stable adducts 4-hydroxyalkenals with proteins, phospholipids, and DNA [91, 92]. Increased 4-HNE levels have been associated with impaired adipogenesis and IR [53, 93, 94, 95, 96]. Another marker of oxidative damage is 8-hydroxy-2-deoxyguanosine (8-OHdG) which was recently shown to exert anti-inflammatory effects, by reducing TNF-α-induced IR in vitro. It was also shown to reduce adipose tissue mass in vivo through activation of adipose triglyceride lipase and lowering the expression of fatty acid synthase [97]. Levels of cholesterol oxidation-derived oxysterols increase in adipose tissues of T2DM patients and act as inhibitors of adipogenesis through activation of Wnt pathway [98]. Heme oxygenase (HO), a major cytoprotective enzyme, functions upstream of Wnt signaling and lowers lipogenesis and adipogenesis, decreasing lipid accumulation and levels of proinflammatory cytokines [99].
Conversely, ROS was also shown to enhance adipogenesis by lowering sirtuin 1 (Sirt1) expression [100, 101]. Heme-induced oxidative stress was shown to inhibit Sirt1, leading to increased adipogenesis [102]. The expression of deleted in bladder cancer protein 1 (DBC1), another inhibitor of the Sirt1, is reduced with obesity, leading to lower adipogenesis and VAT dysfunction [103]. Sirt3 plays a crucial role in mitochondrial function. Silencing of Sirt3 can cause adipocyte dysfunction which impairs adipogenesis and causes IR [104]. Nonselenocysteine-containing phospholipid hydroperoxide glutathione peroxidase (NPGPx) is a sensor of oxidative stress. Lack of NPGPx causes elevation in ROS and promotion of adipogenesis through ROS-dependent dimerization of protein kinase A regulatory subunits and activation of C/EBPβ [105]. Additional evidence suggesting ROS involvement in promotion of adipogenesis comes from antioxidant supplementation experiments where lower levels of ROS resulting from antioxidants contribute to adipose tissue dysfunction and IR [106]. Indeed, antioxidant supplementation exhibited a negative impact when used before induction of oxidative stress as a result of lowering physiological ROS levels because ROS plays a role as second messengers in adipogenesis, lipid metabolism, and insulin signaling [107]. For example, the supplementation with N-acetylcysteine, a known antioxidant and precursor of glutathione, was shown to reduce fat deposition during adipogenic differentiation of mouse fibroblasts [108]. Activation of beta-3 adrenergic receptor (β3-AR) enhances ROS accumulation in cultured adipocytes. Antioxidants enhance β3-AR-triggered mitochondrial ROS production, suggesting that chronic supplementation of antioxidants could indeed generate an elevation in oxidative stress associated with mitochondrial dysfunction in adipocyte [109]. On the other hand, glutathione depletion was shown to inhibit adipogenesis as the result of lowering cell proliferation during the initial mitotic clonal expansion of the adipocyte differentiation process [110].
3.3 Fatty acid signaling
The main role of adipocytes is TAG storage. Although TAGs do not function as signaling molecules per se, the lipid intermediates generated during lipogenesis and lipolysis influence intracellular insulin signaling and participate in progression of IR. These include free fatty acids, diacylglycerols (DAGs), and ceramides [111].
Lipolysis-driven efflux of fatty acids triggers TAG synthesis and causes stress of the ER and activation of June kinase pathway in the adipose tissues [112, 113]. This leads to an elevation in the levels of both DAGs and ceramides and progression of IR in adipocytes [114]. Ceramides were shown to influence lipid-mediated IR in muscles. Delta 4-desaturase, sphingolipid 1 (DEGS1) is a desaturase that mediates ceramide biosynthetic pathway. Ablation of DEGS1 in preadipocytes prevented adipogenesis and decreased lipid accumulation [115]. There are essential enzymes responsible for TAG hydrolysis including hormone-sensitive lipase (HSL), adipose triglyceride lipase (ATGL), and monoglyceride lipase (MGL) [116]. ATGL regulates lipolysis by transcription factor specificity protein 1 (Sp1). Insulin-mediated transcription of Sp1 is critical for this regulation. In mature adipocytes, PPARγ reverses transcriptional repression by Sp1 at the ATGL promoter, leading to stimulation of ATGL mRNA expression. During obesity and IR, the transcription of ATGL becomes downregulated. The extent of the downregulation depends on interactions between Sp1 and PPARγ [117].
A number of factors influence the function of fatty acids in regulating adipogenesis. The number of carbons and the position and number of double bounds are crucial determinants of properties of the fatty acids. Changes in fatty acids including elongation, desaturation, β-oxidation, peroxidation, and incorporation into phospo- and complex lipids can play an essential role in their metabolic function. Fatty acids and their metabolites can control protein expression involved in lipid and energy metabolism by influencing gene transcription, mRNA processing, and posttranslational modifications [118, 119, 120, 121]. Most fatty acids activate all three members of the PPAR family [122, 123, 124, 125]. Polyunsaturated fatty acids (PUFAs), except for erucic acid, are more potent stimulators of PPARγ than monounsaturated fatty acids (MUFAs) and saturated fatty acids [122, 123, 124, 125, 126] ( Figure 2 ). The optimal binding affinity is reached with 16–20 carbon-containing compounds. DHA too was shown to stimulate PPARs [124]. Various studies have reported the beneficial effects of PUFAs on lipid-related human disorders [127, 128, 129, 130, 131], which largely depend on the structure of the fatty acids and their metabolic properties. PUFAs can inhibit lipogenic gene transcription by downregulating the expression SREBPs [132, 133, 134, 135] and act as antagonists of liver X receptors (LXR) [136, 137] and as agonists for PPARs [122, 123, 124, 138, 139]. PUFAs, but not saturated or MUFAs, inhibit lipogenic genes by downregulating SREBP-1c. PPAR alpha plays an important role in metabolic adaptation to fasting by enhancing mitochondrial and peroxisomal fatty acid oxidation and ketogenesis [140]. Dietary PUFAs were also shown to stimulate expression of PPARα target genes, induce β-oxidation, and lower plasma TAGs [141, 142, 143, 144, 145, 146, 147, 148, 149]. Fatty acids can also play a role as modulators of kinase signaling pathways [150, 151, 152, 153, 154, 155].
Arachidonic acid (AA), a polyunsaturated omega-6 fatty acid, is the major PUFA that has been implicated in the regulation of adipogenesis. Short exposure of 3T3-L1 mouse preadipocytes to AA triggers adipocyte differentiation, associated with increase in (FABP4/aP2). Calcium, protein kinase C, and ERK play critical role in this pathway through which AA induces the expression of adipocyte protein 2 (aP2) [156]. AA binds to PPAR-γ2 to stimulate GLUT4 expression in HepG2 cell line, exhibiting an alternative insulin-independent activation of GLUT4 [157]. AA cascade is then controlled by cyclooxygenases enzymes, lipoxygenases, and P450 epoxygenases. When AA is generated from plasma membrane via phospholipases and then metabolized by prostaglandin G/H synthase, different prostaglandins are produced, causing opposing effects on adipocyte differentiation. The proadipogenic effect of AA is mediated by prostaglandin product (prostacyclin) and is thus cyclooxygenase dependent [158, 159, 160]. Among prostaglandin classes, 15-deoxy-Δ12,14-prostaglandin J2 (15-d-PGJ2) was shown to be proadipogenic [161, 162]. On the other hand, prostaglandin F2α (PGF2α) was shown to exert anti-adipogenic effects in primary preadipocytes [163, 164, 165], 1246 cells [164], and 3T3-L1 cells [166, 167, 168]. The anti-adipogenic effect of PGF2α is mediated through prostaglandin F receptor-mediated elevation in intracellular calcium and DNA synthesis [168] and activation of MAPK, causing reduction in PPARγ phosphorylation [169]. The role of prostaglandin E2 (PGE2), the third main prostaglandin, in adipogenesis is controversial as PGE2 exhibits antilipolytic effect in mature adipocytes but shows no effect on preadipocytes [170]. However, it was recently demonstrated that PGE2 inhibited adipogenesis of 3T3-L1 cells [171, 172]. Epoxyeicosatrienoic acids (EETs), AA metabolites, and AA-derived cytochrome P450 (CYP) epoxygenase metabolites exert anti-inflammatory effects in the vasculature. The expression of CYP2J, a member of P450 subfamily with a role in the bioactivation of AA in extrahepatic tissues, inhibits NF-κB and MAPK signaling pathways and activates of PPARγ, thus reducing IR and diabetic phenotype [173]. n-3 PUFAs, on the other hand, reduce adipose growth and play a role in adipogenesis in various rodent studies [174, 175, 176, 177, 178, 179, 180, 181, 182, 183].
Medium-chain fatty acids (MCFAs) (C8–C10) bind the PPARγ ligand binding domain in vitro, causing full inhibition of phosphorylation of PPARγ by cyclin-dependent kinase 5 (cdk5) and reversal of IR in adipose tissue. MCFAs that bind PPARγ also inhibit thiazolidinedione-dependent adipogenesis in vitro [184]. On the other hand, MUFAs were shown to induce adipogenesis and enhance TAG accumulation in 3T3-L1 mouse preadipocytes. Levels of TAGs were greater in cells treated with c-22:1 than c18:1 and c-20:1. Among the c-22:1 fatty acids, c9–22:1 treatment showed higher fat accumulation, associated with increased expression of adipogenic and lipogenic transcription factors, such as PPARγ and C/EBPα and SREBP-1. However, c-20:1 FAs exhibited less effect than c-18:1 and c-22:1 [185]. Alpha-lipoic acid (ALA) activates insulin signaling pathway and exerts insulin-like properties in adipose and muscle cells. However, 3T3-L1 preadipocytes treated with LA exhibit lower insulin-induced differentiation by modulating activity and/or expression of various anti-adipogenic transcription factors mainly through activating the MAPK pathways that negatively regulate PPARγ and C/EBPα [141]. 10-oxo-12(Z)-octadecenoic acid, a linoleic acid metabolite, triggered adipocyte differentiation through PPARγ activation and elevated adiponectin secretion and insulin-triggered glucose uptake [142]. Dietary n-3 fatty acids showed more effective activation of PPARα in the liver of rodents [143, 144, 145] than n-6 fatty acids [146]. Figure 3 summarizes the effect of various fatty acid species on the proadipogenic capacity of 3T3L-1 cells in the presence or absence of insulin (Madsen et al.) [147].
Adipogenic capacity of various fatty acids in 3T3L-1 cells in the absence or presence of 1 μg/ml insulin in differentiation medium (MDI) containing 0.5 mM isobutyl-1-methylxanthine and 1 μM dexamethasone in DMEM and 10% FBS. 100 μM palmitic acid (palm), oleic acid (ole), erucic acid, linoleic acid (LA), arachidonic acid (AA), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), or 1 μM rosiglitazone (rosi) dissolved in DMSO were added when differentiation was induced at day 0 and were present throughout the differentiation period (adapted from Madsen et al.) [147].
Lipidomics studies were performed to investigate differences between SAT and VAT depots. These studies have shown evidence of depot-specific enrichment of certain species of TAGs, glycerophospholipids, and sphingolipids and specific correlations between certain lipid species and body mass index, inflammation, and IS [148, 149]. We have recently shown in human SAT and omental (OM) adipose tissue biopsies from 64 obese individuals a number of TAGs that changed with increased risk IR and T2DM including C46:4, C48:5, C48:4, C38:1, C50:3, C40:2, C56:3, C56:4, C56:7, and C58:7. Enrichment analysis showed C12:0 fatty acid to be associated with TAGs that are least abundant in T2DM. Our data also indicated that C18:3 was present in both depleted and enriched TAGs in T2DM [55]. Secretion of interleukin IL-6 was found to be significantly lower after treatment with C18:2, C22:6, and C16:0 through blocking NF-κB and activating PPARγ [186]. Our data also showed positive correlations between C56:4 and C57:4, both containing C18:2 and C16:0, with SC adipogenic capacity. OM adipogenic capacity was associated with C49:1, C38:0, and C56:2, containing C16:0, C18:1, and C14:0 [55]. Table 1 summarizes a list of TAGs associated with SAT and OM adipogenic capacity. These fatty acids were reported to stimulate adipogenesis in rodents [187, 188, 189, 190, 191] and potentially in human preadipocytes.
Metabolic trait
Fatty acid composition
Fatty acid identities
SC adipogenic 0.9 0.16 C58:10 926.8 C18:2, C18:2, C22:6 Linoleic acid, linoleic acid, docosahexaenoic acid
0.16 C56:4 910.8 C18:1, C18:2, C20:1 Oleic acid, linoleic acid, gadoleic acid
0.14 C57:4 924.7 C22:0, C19:4, C16:0 Behenic acid, C19:4, palmitic acid
0.09 C40:1 692.7 C18:1, C16:0, C6:0 Oleic acid, palmitic acid, caproic acid
0.08 C60:1 970.8 C24:0, C24:0, C18:1 Lignoceric acid, oleic acid
0.22 C38:1 664.7 C18:1, C16:0, C4:0 Oleic acid, palmitic acid, butyric acid
OM adipogenic 1 0.18 C48:1 804.8 C18:0, C16:1, C14:0 Stearic acid, palmitoleic acid, myristic acid
0.14 C49:1 818.7 C18:1, C17:0, C14:0 Oleic acid, heptadecanoic acid, myristic acid
0.11 C56:1 916.8 C18:0, C18:0, C20:1 Stearic acid, stearic acid, gadoleic
0.09 C54:0 890.8 C18:0, C18:0, C18:0 Stearic acid, stearic acid
0.06 C38:0 666.7 C10:0, C14:0, C14:0 Capric acid, myristic acid
0.05 C56:2 914.8 C18:1, C18:1, C20:0 Oleic acid, oleic acid, arachidic acid
0.04 C51:1 846.7 C18:1, C15:0, C18:0 Oleic acid, pentadecanoic acid, stearic acid
List of TAGs associated with IR, SC, and OM adipogenic capacity.
4. Environmental factors
Various types of environmental factors were shown to influence adipogenesis. These include environmental pollutants. Among the environmental pollutants, polybrominated diphenyl ethers (PBDEs) represent a widely used type of flame retardants in commercial products and a main source of environmental contaminants. PBDEs accumulate in adipose tissue, potentially changing its endocrine function causing elevation in the risk of IR. We have previously shown that specific congeners of PBDEs (28, 47, 99, and 153) were predominant in VAT from obese individuals and that PBDEs 99, 28, and 47 were elevated in obese IR compared to obese IS. Treatment of human VAT-derived preadipocytes from obese IS individuals with PBDE28 inhibited insulin signaling and reduced adipogenesis [54]. In addition to PBDEs, evidence linking accumulation of other persistent organic pollutants (POPs) and risk of IR and T2DM was previously described [54, 192]. Additionally, the association between inorganic arsenic exposure and the risk of T2DM and obesity was previously reported [193]. Arsenic-induced T2DM is suggested to be mediated by inflammation, oxidative stress, and apoptosis, playing a significant role in the pathogenesis of obesity. Arsenic inhibits adipogenesis and enhances lipolysis, leading to obesity. Other reports have suggested that arsenic may induce lipodystrophy [193]. Another evidence suggests that uremic toxin-treated 3T3-L1 cells and MSC-derived adipocytes exhibit impaired adipogenesis and apoptosis through activation of the Na/K-ATPase/ROS amplification cycle [194]. Other types of environmental pollutants include organotins, widely used antifouling biocides for ships and fishing nets, play a role as endocrine disruptors as they bind to PPARγ/RXRα, induce adipogenesis, and repress inflammatory genes in different mammalian cells [195].
The pathology of obesity-associated IR and T2DM involves ectopic fat deposition in response to elevated energy intake and poor fat storage. The latter is due to impaired adipogenesis as newly recruited preadipocytes become unable to differentiate into fully functional adipocytes. This review presents several factors that influence adipogenesis in pathological obesity including inflammatory mediators, oxidative stress, fatty acid signaling, and other environmental factors. Most proinflammatory cytokines such as IL-6, IL-1β, TNF-α, IL-8, and IFNγ as well as some anti-inflammatory mediators including β-aminoisobutyric acid, A20 enzyme, and EPO have been shown to impair adipogenesis, leading to adipocyte hypertrophy, ectopic fat accumulation, and increased risk of IR and T2DM. However, basal level of adipose tissue inflammation has been shown to be required for normal adipogenesis and functional adipose tissue homeostasis. Similarly, various mediators of oxidative stress were shown to impact adipogenesis positively such as lipid peroxidation product 4-HNE and negatively such as the marker of oxidative damage 8-OHdG. Targeting lipid peroxidation products was shown to reverse impairment of adipogenesis and sustain IS. However, complete depletion of oxidative stress could also lead to impairment of adipogenesis as basal oxidative stress was shown to be required for normal adipogenesis. Fatty acid signaling also plays a very important role in adipogenesis as various fatty acid species such as PUFAs, MUFAs, and MCFAs were shown to regulate preadipocyte differentiation at various degrees depending on their composition. Finally, various environmental factors were suggested to impact adipogenesis, mainly through triggering inflammation and oxidative stress, leading to impairment of adipogenesis and increased risk of IR.
All authors participated in reviewing the literature and preparing and approving the manuscript. MAE is responsible for the integrity of the work as a whole.
COX-2 cyclooxygenase-2
15-d-PGJ2 15-deoxy-Δ12,14-prostaglandin J2
4-HNE 4-hydroxynonenal
8-OHdG 8-hydroxy-2-deoxyguanosine
AA arachidonic acid
ATGL adipose triglyceride lipase
BMP4 bone morphogenetic protein 4
C/EBP CCAAT/enhancer-binding protein
CAD Coronary artery disease
cdk5 cyclin-dependent kinase 5
DAGs diacylglycerols
DBC1 deleted in bladder cancer protein 1
DHA docosahexaenoic acid
DMEM dexamethasone
DMSO dimethyl sulfoxide
EETs epoxyeicosatrienoic acids
EPA eicosapentaenoic acid
EPO nonerythropoietic derived peptide
ER endoplasmic reticulum
FABP4 fatty acid-binding protein 4
GIP glucose-dependent insulinotropic polypeptide
HSL hormone-sensitive lipase
IFN-γ interferon-γ
IKKβ inhibitor of nuclear factor kappa-B kinase subunit β
IL-6 interleukin 6
IR insulin resistance
IS insulin sensitive
LA linoleic acid
LPL lipoprotein lipase
LXR liver X receptors
MCFAs medium chain fatty acids
MCP-1 monocyte chemoattractant protein-1
MCPIP Mcp-1-induced protein
MDI insulin in differentiation medium
MGL monoglyceride lipase
MHO metabolically healthy obese
miRNAs microRNAs
MUFAs monounsaturated fatty acids
NF-kappa-B nuclear factor kappa-light-chain enhancer of activated B cells
Nnat neurontin
NPGPx nonselenocysteine-containing phospholipid hydroperoxide glutathione peroxidase
Ole oleic acid
OM omental adipose tissue
Palm palmitic acid
PBDEs diphenyl ethers
PDX protectin DX
PGE2 prostaglandin E2
PGF2α prostaglandin F2α
PO pathological obesity
POPs organic pollutants
PPAR peroxisome proliferator-activated receptors
PUFAs polyunsaturated fatty acids
ROS reactive oxygen species
Rosi rosiglitazone
SAT subcutaneous adipose tissue
Sirt1 sirtuin 1
Sp1 transcription factor specificity protein 1
SREBP-1c sterol regulatory element binding protein 1C
T2DM type 2 diabetes
TAGs triacylglycerols
TNF-α tumor necrosis factor-α
TonEBP tonicity-responsive enhancer-binding protein
UPR unfolded protein response
VAT visceral adipose tissue
WISP2 inducible-signaling pathway protein 2
ZNF423 zinc finger protein 423
β3-AR beta-3 adrenergic receptor
MSCs mesenchymal stem cells
Ap2 adipocyte protein 2
CYP cytochrome P450
ALA alpha-lipoic acid
1.Obesity-associated metabolic disease
2.The role of adipogenesis in obesity-associated IR and T2DM
3.Mediators of impaired adipogenesis in IR and T2DM
4.Environmental factors
Haya Al-Sulaiti, Alexander S. Dömling and Mohamed A. Elrayess (August 28th 2019). Mediators of Impaired Adipogenesis in Obesity-Associated Insulin Resistance and T2DM, Adipose Tissue - An Update, Leszek Szablewski, IntechOpen, DOI: 10.5772/intechopen.88746. Available from:
Introductory Chapter: Adipose Tissue
By Leszek Szablewski
Adipose TissueEdited by Leszek Szablewski
Introductory Chapter: Types of Adipose Tissue


Carly Rosalie Vandergriendt left her hometown in Southern Ontario for Montreal in her early twenties, after stints in New Zealand, India, and Mexico. She has worked as a tree planter, community organizer, support worker, and server, and currently works as a freelance writer and English/ESL teacher. Carly holds a BSc in Psychology from the University of Guelph and an MFA in Creative Writing from the University of British Columbia.
Her writing has appeared in Journey Prize Stories 30, Maisonneuve, THIS Magazine, The Malahat Review, The Fiddlehead, PRISM international, Prairie Fire, Room, Riddle Fence, Plenitude, Matrix, and elsewhere. She won first place in the Humber Literary Review's Emerging Writers Fiction Contest in 2018 and was shortlisted for the Carter V. Cooper Short Fiction Prize in 2017. She is currently at work on her first novel.


The colorful and luxurious Bagh Phulkari features beautiful hand-done silk embroidery on top of a cotton fabric. Phulkari means "flower work" and is very descriptive of this vibrant, delicate pillow. Phulkari fabrics are often used in ceremonies concerning birth and marriage.
Pillow has a hidden zipper, linen back, and comes with a down blend filler.


This hole is a 90-degree dogleg left. Both sides of the first leg of the dogleg are hugged by dense trees, which makes "cutting the corner" a risky proposition. The best tee shot is one that starts straight with a slight draw that turns the corner. This will leave you with roughly 200 yards to the center of the green. A straight tee shot will need to travel at least 200 yards in order to clear the corner, while anything over 240 yards will likely run through the fairway and end up in the rough. Of course, the further to the right your tee shot lands, the further from the green you will be. The approach shot, which is hit to a green you can't see, can range from 150 yards for those who cut the corner to 250 yards for those who slice their tee shots to the right. A long approach shot also brings the water into play. Typically, the best approach shot is a low shot that lands just over the hill that hides the green, which often helps the ball roll up onto the green. The green slopes from back to front and from right to left. Be sure to ring the bell once you've cleared the 150-yard marker.


Studying can be stressful for students and a challenge for their parents. Here are some useful tips to help improve your child's study skills.
Time management – Finding the time to study can be difficult with school activities, friends and family events. However, the best way to get your studying in during the week is to create a schedule that works. The timetable should also include time to rest and socialize which creates a balanced lifestyle.
Essay planning – Students can be overwhelmed to produce a clear concise essay, that will get them the grades they want. To create a well thought out essay, planning is crucial to saving time as well as to produce a well-balanced assignment.
Memory tricks – Mnemonic is a tool that is very useful even today. The technique involves many creative tricks that help your right brain retain information. These techniques will also help children who are imaginative, as creative methods will always be easier to remember. These techniques are especially useful to remember names, facts, figures, dates, and sequences that need to be learned by heart.
Mind mapping –This form of study will see children literally drawing their thoughts visually. This technique is great for revision, as it will give your brain shortcuts that will help students remember quickly.
Note taking – students should learn to take down notes from a lecture and not all the content spoken by the lecturer. This method will see students jotting down keywords that they can later reference and expand on.


text:
Route nationale 3b (N3b) – to utwardzona droga krajowa o długości 106 km, biegnąca na terenie Madagaskaru. Zaczyna się w pobliżu miasta Sambava, po czym biegnie na południowy zachód. Magistrala kończy się w mieście Andapa.

Linki zewnętrzne

Przypisy

Drogi na Madagaskarze
Sava


The strategic leveraging of multiple financial flows is an important piece of the puzzle when it comes to implementing the Agenda 2030 and its Sustainable Development Goals (SDGs). The funding model, largely dominated by hard earmarking — funds channelled through projects — cannot fully deliver the SDGs. The short-term and sectoral nature of earmarked project funding weakens opportunity for building long-term, sustained and strategic partnerships that can drive transformative change. Flexible investment, when available in the right balance, quality and scale, can help reduce transaction costs, reduce fragmentation, create synergies and coherence. This article highlights some results from a successful flexible multi-partner mechanism (FMM) towards achieving transformative change.
The Flexible Multi-partner Mechanisms (FMM) was established in 2010 as a multi-partner pooled instrument for managing less-earmarked funds support to the Food and Agricultural Organization's (FAO) Strategic Framework. The fund totalled $75 million (2010-2017), of which $47 million covered 2014-17. The governments of Sweden (2010-21), the Netherlands (2010-2017) and the Kingdom of Belgium (2013-2020) are the main contributors. Others include the Flemish government (Flanders Cooperation Agency) (2011-13), Switzerland (2017-18) and Italy (2019). More countries are negotiating their commitments in the new phase (2018-21).
Over the years, the FMM has supported 32 projects in 70 countries and five regions, and has benefitted hundreds of thousands of people around the world. With these funds, the FAO has successfully leveraged its capacity, at the global, regional and country levels to achieve concrete results and transformative change. Below are some examples from seven of FMM projects.
As part of the effort to achieve zero hunger, FMM funded the 'Voices of the Hungry' (VoH) project, which FAO developed a global food security and nutrition (FSN) indicator for member countries. VoH measured food insecurity worldwide, using an experience-based food insecurity scale module called the Food Insecurity Experience Scale (FIES). Twenty-two countries incorporated FIES into their national household surveys. FIES has been endorsed as the official indicator to monitor SGD2 — Target 2.1. FIES data from 58 countries contributed to FAO's State of Food Insecurity in the World (SOFI) Report 2017.
Another good example is the project on 'Voluntary Guidelines on the Responsible Governance of Tenure of Land, Fisheries and Forests' (VGGT), in the Context of National Food Security. The VGGT strengthened capacities of civil society organizations (CSO) and grassroots organizations to participate in policy dialogues on the governance of tenure in their countries. It provides countries with a framework for best practices in tenure-related policies, laws, regulations and strategies. This helped advance the mainstreaming of food security and nutrition (FNS) in sectoral policies and investment programmes, and the development of cross-sectoral FNS policy frameworks.
A global initiative on Sustainable Food and Agriculture (SFA) was launched in 2014 to address sustainable development in agriculture, forestry and fisheries. The SFA facilitates the adoption of integrated and multisector approaches at the ecosystem level. Its implementation was piloted in Bangladesh, Morocco and Rwanda. A new SFA Guideline was published in 2018 that outlined 20 interconnected actions to guide decision-makers, each describing approaches, practices, policies and tools that interlink the SDGs, integrate sustainable development, and partnership among key actors.
As part of the initiatives to combat climate change, three related FMM projects were funded on Climate Smart Agriculture (CSA). A National Adaptation Plans project implemented in Malawi and Uganda provided crucial support to ensure that agriculture is part of the processes on adaptation to climate change at national level. It analysed the effects of climate change on food systems in Malawi and Zambia through a multi-disciplinary team to inform policy makers, and key policy messages emerged. The results provided basis for evidence-based decisions on the adoption of practices, investment plans and the formulation of policies that will contribute to the adaptation to climatic change. A CSA Source Book is also an important flagship product.
As part of a Blue Growth initiative project, bamboo crab-fattening cage innovation was introduced to a group in Dabaso, Kenya. This group produced more than 600 crabs (averaging 400 grams each), which were sold for a total of $1,000 in four months. In the coastal communities of Kwale County in Kenya, the capacity of 140 community members was strengthened to produce and process the seaweed, including post-harvest and market linkages. These smallholder seaweed entrepreneurs sold 41 tonnes of seaweed, fetching them $ 13, 000, which has helped them diversify incomes.
The Forest and Farm Facility (FFF) project strengthened Producer organizations (POs), improved dialogue between them and governments, and facilitated dialogue and networking among rural households. By the end of 2017, the FFF had strengthened 947 POs at the regional, national and local levels, representing more than 30 million producers, resulting in changes in policies, rules or regulations in favour of their interests. It helped poor rural people enhance their business skills, build their own enterprises, increase access to markets, services, knowledge and technologies and improve access to, control over and sustainable management of natural resources.
The Dimitra project improved rural people's livelihoods, gender equality, and reduce rural poverty. The Dimitra Clubs' approach is a signature approach that unites women, men and young people in collective action to create better lives. By end of 2017, about 1,600 Dimitra Clubs were established in Africa. It contributed to strengthening rural organisations and institutions in Burundi, Democratic Republic of Congo, Ghana, Niger, Mali and Senegal where more than 50,000 rural women and men are better organised and empowered.
The FMM provides a very good example of a well-designed, flexible, pooled less-earmarked fund that are more effective and cost efficient. It provides catalytic funds for strategically important and critical areas. The results above are just examples showing that flexible funding can deliver real value and concrete results. FMM has enabled FAO to test and support the scaling up of proven initiatives that are innovative, and to leverage bigger and more impactful initiatives. By creating synergies, FMM helps reduce risks and provides better incentives for collaboration across sectors in relevant contexts. It also provides greater coherence and opportunity to leverage other sources of funding to achieve catalytic, synergistic and transformative impacts. Due to its flexibility, FMM offers added advantage of its agility in responding to emerging challenges and opportunities with timely interventions. Moving forward, the success of flexible funds depends on the ability to effectively leverage wide range of partnerships with other actors, including their technical capacity and financial resources to achieve catalytic outcomes.
The author wishes to thank all the resource partners of FMM—Sweden, Netherlands, Belgium, Flanders and Switzerland, as well as the co-funders of all the individual projects supported by FMM.


From first contact at Chesapeake Dental Arts, Dr. Esposito is committed to your individual attention and strives to provide personalized oral health care tailored for your unique dental needs and goals. The staff works hard to create the ultimate stress-free and comfortable dental experience.
"Your health and comfort are our top priorities, and we do what it takes to help every patient understand their symptoms and treatment options in a relaxed office setting. As a wife and mother myself I know what it's like to bring your child to their first appointment, or to coordianate the care of your againg parents."
It is our mission to educate and provide our patients with the best dental care in Arnold. For that reason, we've designed this website to provide you with all of the important information you need to make healthy decisions about your teeth and gums. We encourage you to browse our office page, service details and patient education library whenever you have a question about our practice or your oral health. From routine cleanings to full mouth rehabilitations, we meet the needs of the enire family in a single office. We see patients beginning at age 3.
Achieving quality dental care shouldn't be difficult, so at Chesapeake Dental Arts we make it simple to achieve your healthiest, most beautiful smile. Whether you are looking for information on implants, teeth whitening, crowns, or preventive care, you can learn more about all of your options from our services page. For your convenience, you can also request an appointment online with our Arnold dentist and download patient forms directly from our website.
Feel free to contact our Arnold office with any questions. We look forward to making each visit to our office a positive experience.
Dr. Meredith Esposito graduated from dental school in 2001 and opened Chesapeake Dental Arts in 2009.


text:
Professor Behind $12 Billion Empire Fuels China's Tech Rise
Jane Zhang
18 September 2022, 6:00 pm ·7-min read
(Bloomberg) -- Li Zexiang grew up in rural China during the Cultural Revolution, when capitalists were the enemy. Now the 61-year-old academic has quietly emerged as one of the country's most successful angel investors, backing more than 60 startups including drone giant DJI.
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Li was among the first Chinese to study in the US before returning to teach in Hong Kong's pre-eminent technology university. From there, he's groomed a generation of entrepreneurs and set up an incubation academy, funding or nurturing promising players in robotics and artificial intelligence valued at almost $12 billion.
Intentionally or not, the robotics expert is playing an increasingly pivotal role in a battle between the US and China to dominate defining technologies. As Washington prepares to broaden sweeping curbs against its rival's chip and AI sectors, Li's talent for ferreting out scientific achievements is likely to prove more crucial than ever.
"In crisis is opportunity born," he told Bloomberg News on the sidelines of a conference in Hong Kong. "Historically, Chinese companies and their technology have been second choice for even local companies. But now they have the chance to transcend that."
It's a characteristically optimistic perspective from Li, member of a select club of venerated intellectuals-turned-financiers that includes Turing Award-winner Andrew Chi-Chih Yao. Like his peers, the robotics savant Li has been at the forefront of some of the most important Chinese innovations of the past decade -- tracking the country's evolution from world's factory to hothouse for technology giants.
Li wouldn't comment at length on Washington's efforts to contain China's ascendancy -- a sensitive topic as relations between the two countries edge toward their most tense in decades.
"No matter how intense the conflict gets between the US and China, no matter how the decoupling proceeds, the fact is it's akin to losing 800 soldiers for every 1,000 killed," he said.
But it's clear the pendulum has swung in his favor, as Beijing galvanizes efforts to replace US hardware and circuitry, and cracks down on a decade of free-wheeling expansion by internet giants. Li, who operates privately and without ties to the government, nonetheless has good official contacts. He was among about 40 honorees chosen by the Shenzhen government in 2020 for their role in helping transform the once sleepy fishing village into a southern economic powerhouse.
While social media and retail internet pioneers from ByteDance Ltd. to Alibaba Group Holding Ltd. and Tencent Holdings Ltd. once hogged the limelight, an increasing amount of capital is now flowing into hard-core tech pursuits like semiconductors, robotics and AI. Xi Jinping this month renewed calls for China to step up the development of such technologies for the sake of national security.
Read more: How a 75-Year-Old Harvard Grad Propels China's AI Ambitions
That's where Li comes in.
He studied in the US in the 1970s and 1980s, joining the early waves of Chinese students along with fellow academic Yao. It was a life-changing experience for a native of the same landlocked agrarian province of Hunan that birthed Mao Zedong.
While awaiting college admission, Li worked in a school-run factory making electric insect traps. He was one of the lucky ones -- winning a seat at a local school before discovering the joys of scientific rigor abroad.
After getting a PhD in electrical engineering and computer science from the University of California at Berkeley, he became a research scientist at the Massachusetts Institute of Technology, then joined the robotics lab at New York University.
"Going to college in the US was a big turning point for me," Li said, adding he benefited from the liberal thinking prevalent at Berkeley.
In 1992, he finally headed homeward to join the Hong Kong University of Science and Technology.
It was in the Asian financial center that he developed a passion for cultivating startups. In nearly three decades spent there, he's backed scores of startups via his incubation platform, Xbotpark. Their total market value now exceeds 80 billion yuan ($11.5 billion), according to Li.
Some are leaders in their respective spheres, others attracted global financiers including Sequoia China and Hillhouse Capital. None are better known than SZ DJI Technology Co.
Li is credited with salvaging the startup when it hit its nadir, and still holds the post of chairman. Many employees, disillusioned with its prospects, had quit. Several even began copying and selling its products. Founder Wang Tao needed $100,000 to keep his year-old startup afloat -- so he turned to his college mentor Li.
The professor made his protege wait outside his classroom for two hours, but finally agreed to the capital infusion. Crucially, the MIT-trained academic brought many of his other students on board. That was in 2007. Today DJI is valued at $15 billion and commands three-quarters of the consumer drone market.
"DJI was China's version of the American dream," Li told Bloomberg News last month. "It was a student-led vision that became reality without a single bit of military or government resources -- just the markets at work."
A pattern emerged of Li pushing beyond scholarly endeavor and into real-world results, to the extent he often staked his most promising students some cash to get them started.
The founders of ePropulsion in 2012 for instance were torn between focusing on the technology over going commercial, till Li stepped in and advised them to get a more popular low-powered electric motor to market first. That saved the company, recalled co-founder and CEO Tao Shizheng.
"Talk is cheap, show me your code. Paper is cheap, show me your project," said Zhang Di, the founder of Direct Drive Tech, reciting a favorite mantra of Li's. Ironically, Zhang dropped out of Li's masters program soon after his teacher stumped up 300,000 yuan for his drive motors startup. His company is now backed also by 5Y Capital.
DJI's Wang, who also goes by Frank, is arguably the best-known of Li's disciples. After Wang's brush with piracy, the professor advised the model airplane enthusiast to focus overseas first, then expand into industrial drones. Wang's company even developed a driving system for a car with SGMW, a venture between SAIC Motor Corp., General Motors Co. and Liuzhou Wuling Motors Co., that went on sale in August.
DJI's success laid the foundation for Xbotpark, Li's current passion. The professor sold part of his stake in the drone giant to bankroll the incubation platform with two professors in 2014 in Dongguan, less than two hours from manufacturers and shipping terminals in Shenzhen, Guangzhou and Hong Kong.
It's had a few notable hits. Hai Robotics, a provider of robotics systems to Philips and SF Express, got over $100 million of financing in June at a valuation of almost $2 billion. Robo-vacuum maker Narwal was the first project incubated at Li's Xbotpark and now, valued at more than 10 billion yuan, cleans a million households worldwide. Sequoia China and Hillhouse Capital-backed EcoFlow, the battery unicorn founded by a former DJI employee that won a coveted "Little Giant" label from Beijing in 2021, is preparing a domestic IPO.
Not all of Li's bets have paid off. Of the dozens of ideas he's financed or endorsed over the years, only a handful have evolved into unicorns or global names. But more often than not, his proteges benefit from his contacts in finance and tech. "Professor Li's personal brand is very influential in the industry," Zhang said.
It helps that Li's efforts dovetail with Beijing's vision. In robotics alone, the Ministry of Industry and Information Technology is targeting average annual revenue growth of more than 20% to 2025 in a five-year plan unveiled December.
In recent years, Li opened satellite XbotPark locations across the country from Ningbo to Chongqing. He also set up an investment fund with Sequoia and Hillhouse to directly finance members, including Zhang's Direct Drive Tech, though he declined to provide specifics on its capital.
He envisions Xbotpark becoming one of several unicorn birthing grounds, just as Beijing diverts more capital toward semiconductors, AI, cleantech and cars. But it's a little like setting out to scale the world's tallest peaks, Li admits.
"These politicians, all they can see are the giant companies," he said. "What they fail to notice is the grassroots technology movement, yet the firms that spring from that represent our future hopes and dreams."
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Learn about the Cosmetology Certificate's Gainful Employment Disclosure.
Hairdressers are increasingly in demand, with the Bureau of Labor Statistics (BLS) predicting that the profession will see 12.7 percent growth by 2022. Attending cosmetology school, however, doesn't just prepare students to cut hair — hairdressers are also adept at skin treatments, styling, manicures, pedicures, and ensuring that their clients feel good about their new look.
There are many career paths for cosmetology graduates as well, with opportunities to become creative stylists for film shoots and fashion shows, salon owners, product developers, or cosmetology teachers. With a healthy client list or an entertainment position, hairdressers can earn over $50,000 a year. It's a profession that takes a certain personality type, spatial awareness, and a creative bent. For sociable, warm people who love styling hair, there is no better job out there.


The ex-CEO said "I don't know" in regard to numerous questions about the company he led.
Former Exxon CEO Rex Tillerson shocks Senate by asserting he doesn't know whether the company lobbied for or against sanctions that killed a $500 billion deal with Russia he had negotiated. Screenshot of C-SPAN.
In his hearing to be confirmed as Secretary of State, Exxon's Rex Tillerson portrayed himself as a Chief Executive Officer (and Board Chair) who had no idea what the company was doing in several areas, including that of his greatest responsibility: Russia.
Perhaps the most jaw-dropping exchange of the day occurred when Sen. Menendez (D-NJ) followed up on Tillerson's amazing claim that neither he nor Exxon ever lobbied against sanctions against Russia in response to their incursions in Ukraine. Menendez showed Tillerson the documents Exxon filed, which proved they had lobbied on sanctions.
Tillerson then professed utter ignorance of whether Exxon was lobbying for or against sanctions, saying, "I don't know" twice.
Jaw-dropping-Tillerson-lieSenate hearingwww.c-span.orgThe idea that Tillerson doesn't know how Exxon lobbied — on an issue of clear interest to the company he was leading — defies logic.
Tillerson was in charge of Exxon's holdings in Russia beginning in January 1998. Tillerson was "the long-time director of a U.S.-Russian oil firm based in the tax haven of the Bahamas," as the UK Guardian reported last month. In 2013, Putin gave then-CEO Tillerson the highest award a foreigner can receive — the Order of Friendship — for negotiating a $500 billion deal with Rosneft, Russia's state-owned (i.e. Putin-controlled) oil company.
When Tillerson hedged on Exxon's lobbying, Menendez appeared shocked. The Senator knows Exxon would never pay millions of dollars to lobby for sanctions that killed deals with Russia worth hundreds of billions of dollars.
Since Tillerson feigned ignorance regarding Exxon's position on sanctions, he also had to claim to be ignorant about USA*Engage, an organization Exxon is part of that exists to oppose sanctions. Yet, from mid-2003 to mid-2007, the co-chair of USA*Engage had been a senior Exxon employee. But Tillerson claimed to know nothing about it.
Yet when presented at his confirmation hearing with clear evidence that Exxon had lobbied on the sanctions, Tillerson had the chutzpah to assert he didn't know which side Exxon lobbied on.
This was only the most outrageous of many unbelievable assertions by Tillerson. He didn't think we knew enough about Putin's crimes to call him a "war criminal." He testified that he and Trump didn't talk about any specific Russian issues when they met. He claimed ignorance on how Exxon used a foreign joint venture to skirt the Iranian sanctions — even though Exxon had responded in detail to SEC questions on this issue after he had become CEO. And he simultaneously feigned ignorance and refused to answer the question of whether Exxon had kept funding disinformation on climate science even after the company had promised to stop.
The "best" interpretation of the hearing is that Tillerson was a terrible CEO who knew nothing about what was happening at the company he was running. But the far more likely truth is that Tillerson, like ExxonMobil (and Trump and Putin), is a master of straight-faced disinformation.
Either alternative points to the conclusion that Tillerson is unfit for this ultra-essential cabinet post, which was first held by Thomas Jefferson, and is fourth in line to be president of the United States.


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The Myriad Expressions of Solidarity Amongst Female Prisoners in the Concentration Camps
Mehak Burza
Keywords: Cookbooks, dehumanizing, gender, kashariyot, Ravensbrück, recipe, solidarity, survival
The Holocaust, which was the organized, state sponsored execution resulting in the annihilation of six million Jews stands as the touchstone of trauma in the global history. While the Nazi Germany was impartial in its treatment and execution plan towards the victims, an event as horrific as the Holocaust elicits different responses from both the genders. My paper aims to explore the manifestations of solidarity among female prisoners as well as females employed in vocations in the concentration camps during the Holocaust. Being always in double jeopardy, firstly as Jews and secondly as women, made their survival more arduous in the dehumanizing camp conditions. The women thus resorted to various survival strategies in order to keep up the struggle for survival in the camps. My paper, which also forms a part of my ongoing research, thus intents to analyze the various ways in which the women prisoners sought solidarity and the stratagems they employed for their survival. Besides, it will also trace the role of kashariyot- the courier girls who formed a vital segment of the resistance against the Nazi-occupied Europe.
Mehak Burza is a Doctoral Research Scholar in the Department of English, Jamia Millia Islamia (New Delhi, India) and an Assistant Professor of English, University of Delhi. Her thesis title is Literary Representations of The Holocaust; An Assessment. Her primary interests include Holocaust/Genocide Studies, Jewish Studies, Gender, Identity, Trauma Studies and PTSD (Post Traumatic Stress Disorder). She presented papers at national and international conferences. Her translations have been published in Purple Ink, the online journal of Brown University, Los Angeles. On the creative front, her short story and several poems have been published.
1. Bridenthal, Renate, Atina Grossmann and Marion Kaplan, editors. When Biology Became Destiny, Women in Weimar and Nazi Germany. Monthly Review Press, 1989.
2. Goldenberg, Myrna, and Amy H. Shapiro. Different Horrors, Same Hell. Gender and The Holocaust. University of Washington Press, 2013.
3. Grunwald-Spier, Agnes. Women's Experiences In The Holocaust. In Their Own Words. Amberley, 2019.
4. Helm, Sarah. If This is a Woman: Inside Hitler's Concentration Camp for Women. iBooks, Little Brown, 2015.
5. Jacobs, Janet. Memorializing The Holocaust Gender, Genocide And Collective Memory. I.B. Tauris, 2010.
6. La Capra, Dominick. Representing the Holocaust: History, Theory, and Trauma. Cornell UP, 1994.
7. Laska, Vera. Women in Resistance and in the Holocaust: The Voices of Eyewitnesses. Praeger Publishers, 1983.
8. Levi, Primo. If This is a Man: Survival In Auschwitz. Translated by Stuart Woolf, iBooks, The Orion Press, 1959.
9. Nyiszłi, Mikłos. Auschwitz: A Doctor's Eyewitness Account. Penguin, 1946.
10. Ofer, Dalia, and Leonore Weitzman, editors. Women in the Holocaust. Leonore Weitzman. Yale University Press, 1998.
11. Ringelblum, Emmanuel. Notes from the Warsaw Ghetto: The Journal of Emmanuel Ringelblum. Edited and Translated by Jacob Sloan, Schocken Books, 1975.
12. Ringelheim, Joan. "Women and the Holocaust: A Reconsideration of Research." Communities of Women, vol. 10, no. 4, 1985, pp. 741-761.
13. Rittner, Carol, and John K. Roth. Different Voices: Women and the Holocaust. Paragon House, 1993.
14. Roden, Claudia. The Book of Jewish Food: An Odyssey from Samarkand and Vilna to the Present Day. Knopf, 1996.
15. Szpilman, Władysław. The Pianist: The Extraordinary True Story of One Man's Survival in Warsaw, 1939-1945. Picador, 1946.
16. Tillion, Germaine. Ravensbrück: An eyewitness account of a women's concentration camp. Translated by Gerald Satterwhite, Anchor Press, 1975.
17. Waxman, Zoë. Women in the Holocaust: A Feminist History. Oxford UP, 2017.
18. Wiesel, Elie. Night: A Memoir. Translated by Marion Wiesel, 2nd ed., iBooks, Hill and Wang, 2006.
Burza, M. "The Myriad Expressions of Solidarity Amongst Female Prisoners in the Concentration Camps". Contemporary Literary Review India, Vol. 7, no. 4, Nov. 2020, pp. 120-4, doi:10.201411/clri.v7i4.711.
Copyright (c) 2020 Mehak Burza
Mehak Burza, Book Review of Agnes Grunwald-Spier's Women's Experiences In The Holocaust In Their Own Words , Contemporary Literary Review India: Vol 7 No 3: CLRI August 2020
Mehak Burza, Khurshid Alam, Book Review on Khurshid Alam's Key to Happiness , Contemporary Literary Review India: Vol 7 No 4: CLRI November 2020


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Interview with Nutritionist in Training - Rachel Fletcher
Rachel has changed career from working for Derbyshire Police as a Detective Inspector to training as a Nutritionist. She is in her second year studying an AfN accredited BSc Nutrition, Diet and Lifestyle degree at Sheffield Hallam University.
She tells us why a career change appeals to her, when she made the decision, and what impact she wants to make through her future work.
Why does a total career change appeal to you?
I had been in my previous career in the police for 19 years and whilst I had achieved a lot, due to a significant change in my personal circumstances, my heart was no longer in it and I felt I needed to go in a completely different direction.
I initially took a job which was quite similar in many aspects but quickly realised it wasn't for me. Again, the pull for something very different was there but I didn't quite know what that looked like. I knew that a total career change was needed.
What was the moment that you made the decision?
I have been interested in the world of health and wellbeing for a while and increasingly felt pulled towards this as a career change. I had been following nutrition related accounts on Instagram and buying books. I'd also done a Level 2 nutrition course through work. This, along with my love of cooking led me to research careers in this field.
Via the Association for Nutrition I found a degree I was interested in at Sheffield Hallam University. I rang them to see if I would be eligible to apply, not thinking I would as I don't have a science academic background. In all honesty, I almost rang them to rule it out…! 10 minutes later they offered me a place.
My immediate gut instinct was to take the place, I felt really excited by it but the rational part of me was saying not to quit a well paid job to study for 3 years. I'm usually quite methodical and sensible making decisions but with this, I really did follow my gut. And whilst I spoke to close friends and family about it, my decision was made as soon as I had the offer. In fact, it was my Dad who said 'you've already made your decision'. It was a huge leap for me but I don't regret it at all.
How do you want to make an impact through your future work?
I've always been in a career that helped people; directly and indirectly and I still want to do this. I passionately believe in accessible evidence based nutritional advice, which is tailored to the individual. I want to cut through all the nutribollocks that you see on social media. It's not just about weight loss for me, I want to help people achieve their optimum health and feel great.
Where does your sense of adventure come from?
I did smile at this question because I'm not sure I have a great sense of adventure! However, I do like to challenge myself and learn new things. Studying for my nutrition degree is a huge adventure for me.
When do you think is the best time to make an important decision?
This is a hard one to answer as I think it can be different, sometimes you just 'know', other times circumstances can dictate. For me, I'd usually make a list of 'pros' and 'cons' because I find that helpful in taking a step back. Also, getting a clear head. This can be by going outside, taking a walk, doing something completely different, or sitting in silence for a while. I like mindfulness meditation for this. Listen to your gut. It will tell you. I had the fear when making my career change decision but it was an excited fear.
The best place to find Rachel is on Instagram where she posts tempting recipes and nutrition information along with her lovely photography. Click here for her food and nutrition account. Over on her personal account you'll discover photos of nature, retreats and more lovely food! Click here to connect.
I met Rachel during her first year at Sheffield Hallam University via their career mentoring scheme. Since then we have continued to meet up for coffees, delicious food and great conversations. She inspires me to cook and eat better, to keep learning, and to experiment with recipes.
About The Adventure Podcast
sarah@sarahventurer.com
© About The Adventure - 2022 All Rights Reserved


distance between Bahawalpur Airport, Punjab, Pakistan and Port Sudan, Red Sea, Sudan on public roads is — km or miles. The distance between the points in the coordinates — 3640 km or 2184 miles. To overcome this distance at an average vehicle speed of 80 km / h require — 45.5 h. or 2730.0 minutes.
The length of this distance is about 9.1% of the total length of the equator. Airliner Airbus A380 will fly the distance in 4.0 h., and the train 52.0 h. (No high-speed train).


CD6 (also known as Cluster of Differentiation 6) is a human protein encoded by the CD6 gene on Chromosome 11. CD6 protein is found on the outer membrane of T-lymphocytes.The encoded CD6 protein contains three scavenger receptor cysteine-rich (SRCR) domains and a binding site for an activated leukocyte cell adhesion molecule. Studies have shown CD6 regulates T-cell responses through activation-dependent recruitment of the positive regulator SLP-76. TThe gene product is important for continuation of T cell activation. This gene may be associated with susceptibility to multiple sclerosis.