So, you've lost 100 pounds. Now what?
Lenore Katz shed 137 pounds, gradually dropping from 272 pounds to 135 pounds, over several years. The 60-year-old grandmother from of Brooklyn, N.Y, has kept the weight off for five years, but she still has moments of panic about falling back into old habits of overeating.
"I don't trust myself to [eat] a little bit without going overboard," she says.
From NBC's "The Biggest Loser" to TODAY's "Joy Fit Club" and Jenny Craig commercials, there's no shortage of promotions for people who have transformed themselves by losing 100-plus pounds through diet and exercise programs. "I am a whole new woman," Ali Vincent, who lost 112 pounds and this week became first female winner of the hit show "Loser," told TODAY.
But what happens after the fat pants are gone?
For all the celebration over people who lose massive amounts of weight, diets usually fail in the long run, studies show. A recent weight-loss maintenance study from Duke University found that after losing an average of 18.7 pounds over six months of diet and exercise, most dieters regained an average of nine pounds over the next 2 ½ years. Up to two-thirds of dieters gain back most of the weight they lost, according to an analysis of 31 diet studies released by researchers at the University of California, Los Angeles last year.
What dieters often don't realize is, while they can relax a little about how much they eat, they have to remain vigilant. The worst mistake dieters who have lost a lot of weight make is to think that they're "done," and that they no longer have to choose their food wisely and responsibly.
In my practice, I have consulted with hundreds of men and women lost weight on various diets and then gained it back. It seemed like these dieters were willing to put up with almost any restriction, as long as they knew that, at some point, the punishing diet plan would be over. But to maintain your weight loss, you always have to pay attention to what you eat. Yes, always, no matter what you weigh.
Whether you've lost 10 pounds or 100 pounds, there's a greater chance of keeping it off if you incorporate better habits into your lifestyle, instead of radically changing it as many diet plans promote.
Allow yourself a weight-gain range of 3-5 pounds without panicking. When you're at the lower end of your range, give yourself a little freedom to enjoy some of your favorite foods. If your weight goes up another pound or two, then you'll need to pull in the reins again to keep yourself within your desired range.
Find a consistent tool to help you stay in touch with your body weight. You can weigh yourself on a scale daily or one or two days a week. I prefer weighing Fridays and Mondays — a way to control weekend splurges when overeating is most common. Or you can use an article of clothing, such as a pair of your favorite skinny pants, that will become your frame of reference. Try them on the last day of each month. Clothing doesn't lie (and don't try to blame the dry cleaner for shrinkage!).
Get rid of "fat" clothes that are too big on you and no longer fit. Why would you ever want to fit into that size again? Dress the body you have.


This camp is all about using the tools of yoga to teach our kids the foundation of a healthy, happy lifestyle! Each session will include either yoga, aerial, barre and other fun exercises that is appropriate for all levels and presented in a fun, supportive, non-competitive way. A variety of crafts will be incorporated and will help guide our kids to unplug, focus and be in the present moment in creative, fun ways!


text:
Paratylotropidia morsei är en insektsart som beskrevs av Rehn, J.A.G. och J.W.H. Rehn 1943. Paratylotropidia morsei ingår i släktet Paratylotropidia och familjen gräshoppor. Inga underarter finns listade i Catalogue of Life.

Källor

Gräshoppor
morsei

redpajama_set_name: RedPajamaWikipedia


Travel southeast on Mitchell Way which will become Airport Way. Travel 0.4 miles and turn left onto Airport Drive. Travel 0.6 miles and continue straight onto West Bakerview Road. Travel 0.3 miles and turn right onto Northwest Ave. The hotel will be on the right at the intersection of West Bakerview Road and Northwest Drive. We also offer a complimentary hotel shuttle available anytime for pick-up.
Travel west on Grant McConachie Way East. Travel 1.7 miles and make a slight right turn onto BC-99 South/Seattle/City Centre/Richmond. Merge onto Sea Island Way. Travel 1.0 miles and merge onto BC-99 South via the ramp to Victoria/Seattle. Travel 24.2 miles to the Canada/US border. After crossing the border, you will be on Interstate 5 South. Travel 18.7 miles to exit 258 for Bakerview Road/Bellingham International Airport. Turn left onto Airport Road which will become West Bakerview Road. The hotel will be on the right at the intersection of West Bakerview Road and Northwest Drive.
Travel south on Departures Drive. Travel 0.4 miles and continue onto Airport Expressway. Travel 1.3 miles. Keep right at the fork in the road and follow signs for WA-518 East/Interstate 5/Interstate 405. Merge onto WA-518 East. Travel 1.5 miles and take the exit on the left for Interstate 5 North toward Seattle. Merge onto Interstate 5 North. Travel 102 miles to exit 257 for Northwest Avenue. Merge onto Northwest Avenue and at the traffic circle continue straight to stay on Northwest Avenue. Proceed to the traffic light at West Bakerview Road and the hotel will be on the right.


text:
Political analyst: Political forces are deliberately blocking the selection of the prime minister an
by rocky on Wed 22 Jan 2020, 2:31 am
[size=35][size=35]Political analyst: Political forces are deliberately blocking the selection of the prime minister and betting on time[/size]
[size=18]A Kurdish political analyst confirmed today, Wednesday, that the political forces concerned with the selection of the next prime minister deliberately obstruct this matter in a wager on the time factor, noting that the same forces that agreed with Adel Abdul Mahdi previously returned in the same manner to search for a person who does not open the files on Most people in the political process.
Ali al-Faili said in an interview with Alsumaria News, "The political forces concerned with choosing the next prime minister intentionally obstruct this matter in betting on them over the time factor, so that they do not respond to the demands of the demonstrators in presenting a personality to which the demands of the masses and their confidence apply," noting that "the big parties and to Soon, she was fighting to name the largest bloc that had failed since the government was founded, while deliberately leaving chaos. "
Al-Faili added, "The political forces that previously agreed with Adel Abdul-Mahdi did not agree with him for the darkness of his eyes. Rather, they wanted to bring a person without political cover and a party that supports him so that they can blackmail him and obtain what they want while he is in many cases. When he clashed with their interests, they lifted the cover on him." , Pointing out that "the same forces today returned in the same manner to bring in a personality that does not open the files that exist on most people of the political process, which are either corruption files or their hands are stained with the blood of the Iraqis."
Al-Faili stressed, "The President of the Republic has strived to reach a compromise and choose a personality that suits the aspirations of the masses and satisfies the political forces, but the political forces rejected all the solutions and proposals presented by him, as I tried to blackmail him by raising incorrect and non-existent files such as corruption and intelligence after his rejection of the candidates who They wanted to recycle them again. "
He stressed that "the President of the Republic resists all pressure and seeks to present a figure that is acceptable to put an end to the crisis. As for the candidacy of a personality from the parties and the street rejects it, this means returning to the first square and increasing congestion and complexity without meeting the demands of the masses."
4 parliamentary Prime airways electronic customs 7 2 opening 6 discusses 8 3 government companies Deputy reveals Iraqi FakeNews employees boeing Parliament 1 5 12 dinar

redpajama_set_name: RedPajamaCommonCrawl


text:
S.C.: Father Who Removed Children From Mother Need Only Raise Reasonable Doubt for Good Faith Defense
By a MetNews Staff Writer
A parent who allegedly deprived the other parent of the custody of their children was not required to prove a defense of good faith by a preponderance of the evidence, but only to raise a reasonable doubt, the state Supreme Court unanimously ruled yesterday.
Affirming the Third District Court of Appeal's judgment, the justices said Yolo Superior Court Judge Michael W. Sweet erroneously applied a preponderance standard to William Neidinger, who claimed he took his children from his wife based on his belief that doing so was necessary for their physical and emotional well being.
In 2002, Neidinger was charged with two counts of maliciously depriving his wife of the custody of their two children in violation of Penal Code Sec. 278.5.
Neidinger and his wife, who wed in 1998 and had a tumultuous relationship involving numerous physical altercations, legally separated and were granted joint legal custody of their son and daughter.
The wife, who had moved with their children to West Sacramento and obtained a restraining order against Neidinger, was awarded primary physical custody. Neidinger was given weekend visitation rights.
At trial, he testified that as he visited his children frequently, he saw them regress into a lethargic and detached state and became concerned about their well-being. Though he made over 20 complaints to child protective services, he said, he did not receive a satisfactory response.
Having moved to Nevada, Neidinger sought to initiate new proceedings in that state and filed an application in a Nevada court for a domestic violence protection order.
On March 9, following an alleged incident several days earlier that threatened the children's well-being, Neidinger picked them up from West Sacramento for his regular visitation with the intent to remove them from their mother's care.
After allegedly attempting unsuccessfully to inform the West Sacramento police of his plans to remove the children, Neidinger told their mother through third parties that he would not return the children since he had moved to Nevada, which would be a better place for them.
He said he was fed up with the California court system and would not return the youngsters, an investigating officer testified.
Neidinger was ultimately arrested and charged under Sec. 278.5, which provides for the punishment of a person who "takes, entices away, keeps, withholds, or conceals a child and maliciously deprives a lawful custodian of a right to custody, or a person of a right to visitation."
At trial, he raised the Sec. 278.7(a) defense that he removed the children "with good faith and reasonable belief that the child, if left with the other person, will suffer immediate bodily injury or emotional harm." Sweet instructed jurors that Neidinger had the burden of proving by a preponderance of the evidence the facts needed to establish this defense.
The jury found him guilty on both counts and Sweet placed him on four years' probation.
On appeal, Neidinger argued Sweet's jury instruction as to the good faith defense was erroneous.
The Court of Appeal held the instruction was proper but that Sweet prejudicially erred in failing to clarify the relationship between the good faith defense and the element of malice "so that it was clear to the jury that, to the extent the evidence regarding the good faith defense also showed that defendant acted without malice, he need raise only a reasonable doubt as to that element of the offense."
While agreeing the trial judge committed prejudicial error, Justice Ming W. Chin, writing for the Supreme Court, said the error was in the instruction itself.
"[A] defendant need only raise a reasonable doubt whether the facts underlying the section 278.7(a) defense exist," he wrote.
While Neidinger clearly had the burden of presenting such facts—because they were "peculiarly within defendant's knowledge, and it would be relatively difficult or inconvenience for the prosecution to prove their nonexistence"—the burden of proof was not maximal, Chin said.
"[T]he more serious error that we have found—placing an erroneously high burden on defendant to prove the section 278.7(a) defense—was prejudicial," the justice concluded.
The case is People v. Neidinger, 06 S.O.S. 5589.


text:
require 'RitoPlz/API/base'
require 'RitoPlz/API/request'

module RitoPlz
  module API
    class FeaturedGames < Base
      def initialize(region)
        @region = region
      end

      def all
        request = Request.new(@region, api_path)
        request.get
      end

      protected

      def api_path
        "/observer-mode/rest/featured"
      end
    end
  end
end

redpajama_set_name: RedPajamaGithub


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Great little cufflinks for the 'Boss' - approximate 1.5 cm square.


text:
Instant Access to Bingo from Anywhere
October 6, 2022 by Radoslawa Borkowska
Bingo is a gambling game, first played in Italy way back in the 1500s, which in the past century became a particular favourite in the UK and the USA. Online Bingo started around 1996, and since then expanded international Internet access and smart phones have turned the game into an industry worth billions of dollars a year.
These days, avid Bingo fans can play anywhere, anytime on their mobile phones, with hundreds of variations on draw pool sizes, winning Bingo patterns, and the total number of spaces per card available. Some online and mobile operators use JavaScript or Adobe Flash software to allow players to play Bingo directly on their sites, while others provide free programs and apps for download. Whether they are on a laptop or desktop, or playing from a https://canadiangambling.net/mobile/ device like a tablet or smart phone, Bingo fans will be able to find a version of the game that suits them, and play it whenever they feel like it.
Basics of Bingo
For those not familiar with the game: Bingo is a lottery game played with random numbers, which players have to match against numbers pre-printed on their Bingo cards. In a game with 75 numbers in the draw pool, the classic cards present a grid of 5 X 5 numbers, arranged under the letters B, I, N, G and O. Players bet by buying one or more cards, and win by completing a predetermined pattern of matching numbers on one card. A single game may feature different winning patterns for different prizes, allowing for multiple winners during a game. The pattern can be a simple line (in certain special-occasion draws, even a single number), or one of several more complicated patterns; often, patterns will relate to a theme.
Traditionally, a player completing a winning pattern in a land-based game has to shout "Bingo!" to collect the win; if they miss a number and only realise they have a complete pattern after someone else has called "Bingo," they lose out. Some games have multiple stages: for example, awarding a prize when a player completes one line, another prize level for two complete lines, and the jackpot prize for a full card (known as a "full house"). In traditional land-based Bingo, players bought paper cards and the random numbers were decided by balls drawn from a spinning barrel. Online and mobile Bingo sites use random number generators both to create the players' electronic cards on screen, and to generate the winning numbers.
Perks of Online Bingo
The online versions of the game offer a number of advantages over land-based Bingo that many players find attractive. Apart from the universal easier access, the auto-daub feature marks a player's numbers on their cards and registers winning patterns automatically, which not only makes it easier to keep track of multiple cards, but also rules out the chance of a player accidentally missing a Bingo, or calling a false Bingo on an incomplete pattern.
Unlike land-based games, bingo encourages players to chat to each other during the game via direct message boards, enhancing the social atmosphere of players "ganging up" on the house. Bingo networks, which allow the players on several smaller sites combined access to the same jackpots, allow these sites to offer bigger wins than they would from their own restricted pool of players. Some sites also restrict the number of cards a player can buy per game, which keeps everyone playing for similar stakes and stops smaller players being overwhelmed by high rollers buying multiple cards.
Categories CasinoTags land-based Bingo, mobile Bingo sites Post navigation
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ARTBA.org
July 25, 2018: Update on the Florida Department of Transportation's (FDOT) Bridge Program1 x $0.00
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The biology of aging is challenging to study, particularly in humans. As a result, model organisms are used to approximate the physiological context of aging in humans. However, the best model organisms remain expensive and time-consuming to use. More importantly, they may not reflect directly on the process of aging in people. Human cell culture provides an alternative, but many functional signs of aging occur at the level of tissues rather than cells and are therefore not readily apparent in traditional cell culture models. Organoids have the potential to effectively balance between the strengths and weaknesses of traditional models of aging. They have sufficient complexity to capture relevant signs of aging at the molecular, cellular, and tissue levels, while presenting an experimentally tractable alternative to animal studies. Organoid systems have been developed to model many human tissues and diseases. Here we provide a perspective on the potential for organoids to serve as models for aging and describe how current organoid techniques could be applied to aging research.
Aging is widely held to be the consequence of the accumulation of cellular damage over time (López-Otín et al., 2013). In humans, aging is marked by declining tissue function and increased susceptibility to diseases such as cancer, diabetes, cardiovascular disease, dementia, arthritis, sarcopenia, and renal dysfunction. Aging-associated diseases and phenotypes frequently manifest on the tissue level yet have their roots in molecular and cellular damage (López-Otín et al., 2013).
Most aging research is motivated by the need to understand the process of aging in humans. However, studying aging requires observing and perturbing molecules, cells, tissues, and systems in organisms over time—requirements that are not feasible in humans. Instead, aging is studied in model systems, each of which balances a desire for biological relevance on one hand and practicality on the other. Thus, most models of aging suffer from key limitations depending on where on this spectrum they lie. Organoid culture, especially human organoid culture, has the potential to address many of the limitations of traditional aging models. By providing organotypic structure in an in vitro model, organoids enable the study of aging in tissues in a higher-throughput, experimentally accessible manner. These potential advantages may be particularly useful for studying emergent signs of aging at the tissue level, clearing the way for future human therapies.
The trade-off between relevance to humans and ease of experimentation is a limitation in any model, particularly when seeking to develop interventions to limit the effects of human aging. Organoids provide a powerful and physiologically relevant means to perform in vitro experiments on tissue and on human tissue in particular.
Nonhuman organisms and traditional cell culture have been invaluable tools for the study of fundamental aging processes, including the Nobel Prize-winning mechanisms of telomere regulation and DNA repair (Sancar and Rupp, 1983; Greider and Blackburn, 1987; Lindahl, 1993). However, model organisms may age in ways not applicable to humans. For example, Caenorhabditis elegans has a dauer stage, a stress- and aging-resistant larval form. Induction of dauer-like states may alter lifespan with questionable correlation to human aging (McElwee et al., 2006). In mice, the most common mammalian model organism, important features that affect aging, such as immune response, DNA repair, telomerase regulation, and telomere length, differ significantly between mice and humans (Rangarajan and Weinberg, 2003; Seok et al., 2013). Even naked mole rats and blind mole rats, two rodents both renowned for their sevenfold-longer lives than laboratory mice, owe their longevity to differing molecular mechanisms (Azpurua and Seluanov, 2013). Thus, different species, even within the same order, have developed distinct mechanisms for controlling lifespan and health span in relatively brief evolutionary time. These differences have practical implications. Some of the most prominent diseases of human aging, such as epithelial cancers, cardiovascular disease, osteoporosis, and Alzheimer's disease, are rare or nonexistent in aged mice, who instead predominantly suffer from mesenchymal cancers (Rangarajan and Weinberg, 2003; Vanhooren and Libert, 2013). Consequently, interventions that reduce susceptibility to human age-related diseases may not affect mouse lifespan, and vice versa.
Ultimately, studies in humans are necessary to validate therapies for human aging, but ethical, logistical, and financial challenges render routine human aging studies infeasible. A widely practiced alternative is cell culture, but the correlations to human aging may be weak because of the lack of physiological context. Many signs of aging, namely those that manifest at the tissue and organ level, may be best represented by a more complex system. These signs of aging include a breakdown in tissue homeostasis, stem cell dysfunction, and susceptibility to tissue-specific diseases and cancer (López-Otín et al., 2013).
Although more technically challenging than traditional cell culture, organoids provide increased relevance to human health via a microenvironment supportive of tissue-specific function and physiological cell–cell and cell–matrix interactions. These factors contribute to increased viability of difficult-to-culture cells, including primary cells and prostate tumors (Gao et al., 2014). Moreover, 3D culture improves cell type–specific function and gene expression in cells such as chondrocytes, hepatocytes, and mammary and kidney epithelial cells (Ben-Ze'ev et al., 1988; Astashkina et al., 2012; Caron et al., 2012; Simian and Bissell, 2017). As a result, organoids may be useful for modeling age-related declines in tissue-specific function, such as chondrocyte matrix deposition (Barbero et al., 2004). Furthermore, age-related pathologies intrinsically linked to the ECM, such as osteoarthritis, are well-suited to study in a 3D system (Lozito et al., 2013). Organoids may be the most practical way to perform aging experiments at this level of complexity, particularly on human tissues.
Organoids provide a practical alternative to whole-organism studies in mammals. Patient-derived organoids have been scaled to high-throughput screens against cystic fibrosis and cancer, which would be cost-prohibitive in mice or humans (Dekkers et al., 2016; Pauli et al., 2017; Schütte et al., 2017). Demonstrating the scalability and high-throughput potential of organoids, Pauli et al. (2017) developed patient-derived tumor organoids for screening a library of >100 drugs at different concentrations and combinations, and Danahay et al. (2015) screened nearly 5,000 proteins for their effects on basal cell fate in human lung organoids.
Improved throughput is made possible not only by larger sample sizes but also simpler assays. Some molecular signs of aging, such as protein aggregation, oxidation, and glycation, can be assayed by nondestructive, high-throughput microscopy (Meerwaldt et al., 2004; Chaudhuri et al., 2006; Jung et al., 2010). Organoids are far more amenable to live-cell imaging than whole organisms, such as mice, and can complement mouse studies with imaging and perturbations that would be otherwise impractical. High-resolution live imaging of development, stem cell dynamics, and cancer invasion has been demonstrated in several organoid systems (Sato et al., 2011; Nguyen-Ngoc et al., 2015).
Finally, manipulating microenvironmental cues and specific cell populations is more straightforward in organoids than model organisms. Organoids are typically embedded in a matrix of the investigators' choice, allowing for increased control over its source, composition, and mechanical properties. Cells acquired from tissue can be sorted, modified to delete or express specific genes, and expanded before assembly into organoids, allowing investigators to build organoids using defined building blocks from the bottom up. These organoids enable otherwise infeasible studies, such as tissues bearing gene knockouts that would be embryonically lethal. Additionally, this strategy allows the construction of organoids composed of specific proportions of cell subpopulations. For example, Sato et al. (2011) assembled intestinal organoids from stem cells with or without Paneth cells to identify Paneth cells as essential components of the intestinal stem cell (ISC) niche, a result previously obscured by incomplete lineage ablation. Moreover, viral vectors or transfection allows genetic manipulation of organoids with far less time and expense than developing a transgenic mouse (Koo et al., 2011). As a result, organoid approaches greatly enhance our capacity to study specific cell populations, phenotypes, and mutations within the context of a tissue. Organoid models of aging are in their earliest stages, but promising work, discussed in this perspective, has demonstrated their potential applicability to aging research.
The genome can be damaged through several mechanisms, leading to the acquisition of genetic and epigenetic changes with age. DNA damage activates repair pathways but can also trigger mutations, apoptosis, or senescence. These outcomes can lead to aberrant behavior and deleterious effects on neighboring cells, such as inflammatory senescence-associated signaling (Parrinello et al., 2005). Epigenetically, aging cells acquire regional hyper- and hypomethylation, as well as increased variance in epigenetic marks (Jones et al., 2015). These cell-intrinsic aspects of aging are preserved in primary cells and tissue-derived organoids (Blokzijl et al., 2016).
Glycation, oxidation, and misfolding are foremost among molecular damage to proteins during aging. In particular, ECM proteins such as collagen, elastin, and crystallin are susceptible to nonenzymatic glycation, leading to stiffening of the ECM (Singh et al., 2001). Age-associated glycation, as well as altered structure, composition, and cross-linking of the ECM, has been associated with functional declines in a variety of tissues (Phillip et al., 2015). As matrix is a major component of organoid culture, organoids are a natural model for the effects of aged ECM on tissue function.
Organoid assays can enable researchers to experimentally link aging-associated changes in ECM structure to functional consequences. ECM substrates and gels for cell culture have been isolated from human and animal tissue (Voytik-Harbin et al., 2007; Zhang et al., 2009; O'Brien et al., 2010). Decreased cell proliferation and stem cell function have been observed on matrices derived from older donors, including Bruch's membrane and cardiac and skeletal muscle ECM (Gullapalli et al., 2005; Williams et al., 2014; Stearns-Reider et al., 2017). More complex phenotypes can also be linked to ECM source by using organoid models. The Schedin group (Lyons et al., 2011) has shown that ECM from rats in different reproductive states can instruct morphogenesis and invasion of human mammary and breast cancer organoids. In addition, several groups have experimentally modified the ECM via advanced glycation end product–mediated cross-linking to mimic ECM aging, demonstrating aging phenotypes such as skin and cartilage stiffening and increased invasiveness (Verzijl et al., 2002; Pageon and Asselineau, 2005; Rodriguez-Teja et al., 2015).
Chemical damage can also lead to degradation and aggregation of proteins and other biomolecules, such as lipids. Protein damage accumulates in the form of carbonylation, fragmentation, and cross-linking, whereas lipid peroxidation compromises membranes and leads to the accumulation of oxidized fatty acids. Oxidation products not only have reduced function but are also prone to cross-linking. Together with misfolding, age-associated protein oxidation results in proteolysis-resistant aggregates both intra- and extracellularly. This feature is highly conserved across species; one of the most universal signs of aging is the accumulation of intracellular lipofuscin lipid-protein aggregates (Jung et al., 2010). Although their causal role in pathogenesis is disputed, protein and lipid-protein aggregates are prominently associated with central nervous system dysfunction, such as the infamous tangles, amyloids, and Lewy bodies in neurodegenerative disease, and the retinal drusen in age-related macular degeneration (Crabb et al., 2002; Caughey and Lansbury, 2003). These late-stage manifestations of neurodegenerative pathology may be more apparent in 3D culture than in traditional cell culture, where secreted proteins diffuse freely into culture media rather than accumulate near cells. In a human stem cell–derived model of familial Alzheimer's disease, 3D culture was found to not only improve neuronal maturation but also promote tauopathy though the accumulation of β-amyloid aggregates in the ECM, observations that did not occur in 2D culture or mice (Choi et al., 2014). Similarly, scaffold-free 3D neural organoids, but not 2D culture, were shown to accumulate amyloid aggregates and model tauopathy. Significantly, these signs of human neurodegeneration were spontaneous in patient-derived organoids but are often only observed in mice after the expression of multiple human transgenes (Raja et al., 2016).
At the tissue level, accumulated molecular damage can manifest in a variety of ways. These include changes in tissue function, susceptibility to cancer and other diseases, changes in stem cell function, and alterations in the immune system (Aw et al., 2007; López-Otín et al., 2013; Blau et al., 2015). Encouragingly, a variety of organoid models have already been explored to study aspects of each of these age-related phenomena.
One feature of aging is a progressive decline in physiological function. Various signs of aging, such as lower glomerular filtration rate, reduced cardiac output, and increased susceptibility to disease, can often be tied to tissue-specific changes that may be more apparent in 3D tissues than 2D culture. For example, a semi-enclosed cardiac organoid chamber allows for the measurement of pressure and ejection fraction (Lee et al., 2008). Barrier function can be measured across a kidney- or neural-endothelial interface (Vernetti et al., 2017), which could be used to model aging-associated declines in glomerular filtration rate and blood-brain barrier function (Tan et al., 2010; Elahy et al., 2015). Additionally, gastrointestinal organoids have been used extensively to study host-microbe interactions (Bartfeld et al., 2015; Engevik et al., 2015). They would be well-suited to studying the aging microbiome and age-related susceptibility to disease caused by ordinarily asymptomatic microbes, such as Clostridium difficile (Htwe et al., 2007; Heintz and Mair, 2014). Age-associated changes in circadian rhythm may also be modeled in organoids, considering that intestinal explants and stem cell–derived organoids, but not 2D culture, have been demonstrated to spontaneously produce robust, synchronized circadian oscillations (Myers and Badia, 1995; Moore et al., 2014). In general, organotypic cultures can represent more complex and accurate phenotypes than 2D culture and are thus ideal for modeling their decline in aging.
Organoids are widespread models for cancer progression that have been used to study tumor-initiating mutations and processes, such as cancer cell dissemination (Li et al., 2014; Nguyen-Ngoc et al., 2015). A natural extension of this work would be to use organoids from donors of different ages to understand how normal, aged tissue responds to in vitro oncogenic transformation. For example, transformed human mammary epithelial cells develop phenotypes dependent on donor age. Aged cells more frequently adopted a luminal-like phenotype and expressed estrogen receptor α in organoid culture, suggesting that age is a determinant of cancer subtype (Lee et al., 2015). In addition, organoid culture permits study of the tumor microenvironment, including neighboring cells and the ECM. Age-related changes to the microenvironment may play a role in altered susceptibility to cancer. Experimental glycation of the ECM increased invasiveness and decreased epithelial differentiation in nonmalignant prostate acini (Rodriguez-Teja et al., 2015). Similarly, the accumulation of senescent cells with age may exert tumor-promoting effects on neighboring cells. By coculturing fibroblasts with nonmalignant mammary organoids, Parrinello et al. (2005) demonstrated that senescent fibroblasts secreted factors that increased invasion and proliferation, and decreased epithelial differentiation.
Organoids are excellent models for stem cell maintenance and tissue repair, because organoids can recreate in vitro the minimal unit of a stem cell niche: cells and ECM in an organotypic structure (Murrow et al., 2017). Stem cell exhaustion, or reduced proliferation and biased differentiation of stem cells, contributes to aging in several tissues, and stem cell function is a common readout in aging studies (Brack et al., 2007; Pang et al., 2011; Garbe et al., 2012). For example, mouse intestinal organoids have been used to study the proliferation and differentiation of ISCs in the context of aging research. In one study of ISC function, which declines with age, Nalapareddy et al. (2017) used organoids from aged mice to determine that the aged ISC niche was deficient in Wnt signaling. Exogenous Wnt3a supplementation in organoid culture was sufficient to restore organoid formation and lobe growth of aged ISCs. Other investigators have used organoid-formation assays to study caloric restriction, an intervention shown to have anti-aging effects in several model organisms, including nonhuman primates (Mattison et al., 2017). By combining the Paneth cells and ISCs of ad libitum-fed and calorie-restricted mice, Yilmaz et al. (2012) demonstrated that Paneth cells from calorie-restricted mice were responsible for increasing ISC organoid formation and size. The capacity to separate and perturb the contributions of individual niche components, such as growth factors and accessory cells, during aging and anti-aging interventions in a rapid, systematic manner is an important advantage that organoids provide over model organisms.
Aging of the immune system is characterized by changing proportions of immune cells, declining innate immune function, and increased chronic inflammation (Aw et al., 2007). To study how these factors intersect with age-associated diseases such as cancer and osteoarthritis, aging researchers can take advantage of existing methods for studying the effects of immune cell co-culture and pro-inflammatory stimuli in organoids. For example, co-culture of primary mouse mammary epithelial organoids and immune cells demonstrated how immune cells regulate branching morphogenesis (Plaks et al., 2015). Systemic inflammation has also been studied in organoids by adding inflammatory cytokines or antiinflammatory drugs to the culture medium. Anti-inflammatory treatment of intestinal organoids suppressed the senescence-associated inflammatory response and reduced inflammation-mediated tumorigenesis (Pribluda et al., 2013). Sun et al. (2011) used both cytokines and macrophage-conditioned media to simulate immune involvement in a 3D human chondrocyte model of osteoarthritis. In response to inflammation, the cartilage scaffolds demonstrated phenotypic features of early osteoarthritis, such as increased and atypical matrix synthesis and degradation. These examples highlight systems that integrate organoids with immune cells and inflammatory cytokines.
Organoids can be derived from several sources, most notably primary cells and tissue or pluripotent stem cells (PSCs). Cell lines are less suitable sources for most applications of organoids to aging research, because of immortalization, evasion of cellular senescence, or tumor origins. In contrast, tissues from donors of different ages are a more suitable model of the phenotypes of aging. These samples are becoming more readily available to the basic science research community. A handful of untransformed primary human cell types and tissues, such as keratinocytes, stromal and dermal fibroblasts, and mammary epithelial cells, are available from cell banks. Skin, blood, marrow, fat, breast, and muscle are relatively abundant tissues that can be acquired from healthy donors undergoing elective surgery. In addition, primary human material can be obtained from pathologically normal tumor-peripheral tissue, surgical discards, tissues ineligible for transplant, and trimmings from transplanted tissues (Barkauskas et al., 2017).
Fresh, primary tissue explants or fragments can be cultured with minimal processing, often retaining multiple cell types and the surrounding donor-derived ECM and stroma (Fig. 1 A; Tanos et al., 2013; Nguyen-Ngoc et al., 2015; Li et al., 2016). Some, such as arteries, skin, and central nervous system, are typically cultured as thin slices; alternatively, organoids may be derived from fragments of digested minced tissue. Both strategies maintain original tissue structure, minimize disruption to cell state, and may include ECM and accessory cells. The maintenance of intact paracrine signaling networks contributes to the overall function of tissue fragment-derived organoids. For example, the stromal compartment in intestinal organoids can maintain the stem cell niche without exogenous growth factors (Ootani et al., 2009). Similarly, human mammary organoids retaining stromal and ECM elements maintain hormone responsiveness and proliferate without exogenous growth factors (Tanos et al., 2013). These organoids represent the most physiologically relevant in vitro models and can be particularly valuable for studying complex, intercellular signaling networks in aging tissue. However, sample size and tissue types are limited, and it can be difficult to specifically perturb one component or cell type in the system.
Types of organoids. (A) Tissue fragments and explants are generated from native tissue with little disruption to cell and ECM organization and no intermediate period in 2D culture. This limits total sample size and manipulability but is unmatched in mimicking the original tissue. (B) Reconstituted organoids are assembled in vitro from cultured or sorted cells. This permits cell expansion and modular assembly of components. However, some subpopulations or phenotypes, such as senescent and hormone-responsive cells, may be lost during culture. (C) Stem cell–derived organoids are differentiated from multipotent adult tissue stem cells or PSCs under the appropriate differentiation and maintenance conditions. PSCs specifically can generate rare tissue and cell types, but have limited maturity and lose the hallmarks of aging.
In contrast, primary human cells can be dissociated, optionally expanded in culture, and then reconstituted into organoids. These reconstituted organoids allow for expanded cell numbers and considerably more control over constituent cells and ECM, including the opportunity to perturb specific components (Fig. 1 B). Although tissue composition and cell state change rapidly on 2D culture, suitable conditions for preserving lineage-specific markers during expansion have been identified in a variety of tissues, including keratinocytes, fibroblasts, and mammary and lung epithelial cells (Wilson et al., 1992; Stampfer et al., 2013; Barkauskas et al., 2017). Lung epithelial cells can be expanded in culture and give rise to branched bronchial or alveolar organoids (Barkauskas et al., 2017). Human mammary epithelial cells are a notable aging resource established from surgical discards of donors of different ages and disease status, including healthy women and cancer patients (Stampfer et al., 2013). Nonimmortal mammary epithelial cells can be expanded in vitro for several passages, retain transcriptional signatures of their source tissue, and recapitulate the bilayered structure of the mammary gland in reconstituted organoids (Garbe et al., 2012; Cerchiari et al., 2015). One caveat is that expansion in culture selects for proliferative cells, potentially excluding cells with short telomeres, terminally differentiated nonproliferating cells, and cells undergoing senescence. Furthermore, 2D culture also causes loss of cell type–specific transcriptional profiles; some of this dedifferentiation can be reversed or ameliorated on transitioning to organotypic culture (Caron et al., 2012).
Primary tissue is also a source of multipotent adult tissue stem cells that can generate organoids in the presence of specific growth factors; stem cell–derived organoids are also generated from PSCs (Fig. 1 C). Organoids from multiple epithelial tissues, including stomach, small intestine, colon, liver, pancreas, breast, and prostate, have been expanded from single primary stem or progenitor cells (Table 1). However, an issue with this method is that their maintenance requires the inclusion of stem cell niche–maintaining soluble factors, which may obscure phenotypes of aging that originate in growth factor signaling (Broutier et al., 2016; Nalapareddy et al., 2017). In contrast, PSCs, including induced PSCs (iPSCs) and embryonic stem cells allow for a greater range of key human tissue types than can be practicably supplied by surgical discards, notably brain and cardiac muscle. These organoids frequently contain multiple cell types and self-organizing tissue structures that recapitulate embryonic development. For example, human iPSC-derived brain organoids have been used to model early stage and developmental disorders (Qian et al., 2016) and could become excellent models for neurodegenerative diseases such as Alzheimer's disease. Raja et al. (2016) demonstrated that iPSC organoids derived from patients with familial Alzheimer's disease develop robust pathology, including amyloid aggregation, hyperphosphorylated tau protein, and endosome abnormalities. Caution must be exercised when applying stem cell studies to aging research. Although familial disease–linked mutations are widely studied, genetic disease may differ mechanistically from sporadic, age-related disease. Furthermore, PSCs begin in a fetal-like state and require additional maturation. Many hallmarks of aging, aside from somatic mutations, are reverted on iPSC reprogramming, including DNA damage foci, epigenetic marks, oxidative damage, senescence markers, and telomere length (Horvath, 2013; Cornacchia and Studer, 2017).
Advances in organotypic culture techniques ultimately seek to obtain relevant phenotypes in vitro. Remarkable progress has been made in developing organoid techniques and culture systems, but several limitations remain to be addressed or validated. Furthermore, there are many opportunities to improve on the reproducibility and complexity of organoids, particularly by the inclusion of tissue engineering and microfluidics. These areas of current research are summarized in Table 2.
Although pluripotent stem cells are a significant source for organoids, one concern is the immaturity of cells and tissues derived from these cells, because PSCs begin in a fetal-like state. Functional and developmental maturation of stem cells is an active area of research and has been pursued by techniques such as long-term culture, altered concentrations of growth factors and inhibitors, direct differentiation, and mechanical or electrical stimulation (Chambers et al., 2012; Nicholas et al., 2013; Mertens et al., 2015; Ruan et al., 2016; Takasato et al., 2016; Tzatzalos et al., 2016). In vivo maturation, typically by implantation into a mouse, has also been demonstrated to increase organoid maturity and can be used to generate adult-like human tissue and organoids (Huch et al., 2013; Watson et al., 2014; Takebe et al., 2015).
Similarly, accelerated aging in vitro will be necessary for PSC-derived organoids and useful for studying the functional consequences of age-associated damage. Accelerated aging experiments typically involve cells derived from progeric individuals (Liu et al., 2011; Miller et al., 2013) or expose cells to aging-associated stress, such as reactive oxygen species, inflammation, or radiation, which appear to phenocopy aspects of aging (Nasto et al., 2013; Cornacchia and Studer, 2017). With regard to aging experiments, organoid culture, as opposed to cell culture, has the advantage of increased stability. This stability has allowed culture periods as long as 60 wk (Hibiya et al., 2017), which can be used to study chronological aging in vitro. For example, 120 d of culture of reconstituted human epidermis led to increased cellular senescence and morphological changes resembling those of chronological skin aging in vivo (Dos Santos et al., 2015). Furthermore, genomic stability has been reported to be higher in organoids than in traditional cell culture, as demonstrated by the use of organoid culture to clonally expand stem cells before mutational analysis (Behjati et al., 2014; Huch et al., 2015; Blokzijl et al., 2016). Notably, organoid clonal expansion was also used to quantify the accumulation of mutations in adult ISCs with age (Blokzijl et al., 2016).
Primary cell and organoid culture remains highly sensitive to culture conditions. Support of the ISC niche, for example, was a revolutionary advance, permitting long-term expansion of intestinal organoids that once could be cultured for only a couple of weeks (Ootani et al., 2009). Other tissues, such as artery or ovary, can still only be cultured for only short times. Additionally, aging studies may be particularly sensitive to culture conditions. Numerous culture parameters that can phenocopy aspects of aging, such as replicative aging, oxygen tension, and free glucose, must be carefully controlled for. Finally, long-term culture and studying tissue homeostasis require the maintenance of growth-arrested organoids resembling the resting state of adult tissues. Identifying microenvironmental conditions to transition organoid tissues from a proliferative to a more mature, growth-arrested state would represent an important contribution to aging research.
As in vitro models increasingly seek to recapitulate complex tissue- and organ-level phenotypes, transport of oxygen and nutrients by diffusion becomes limiting. Air–liquid interfaces have been used to culture larger explants, but in general, vasculature will be necessary for the survival of most organoids over a couple hundred micrometers wide (Auger et al., 2013), as well as useful for the study of aging-relevant phenotypes, such as metastasis and deterioration of the blood-brain barrier and glomerulus (Tan et al., 2010; Elahy et al., 2015). Furthermore, vascularization has the potential to network organoids into systemic, multiorgan contexts that allow the exchange of hormones, cytokines, and metabolites, which have been implicated in aging in mice (Villeda et al., 2014). Incorporation into a systemic environment presents an opportunity to complement the strengths of organoid and in vivo platforms: organoids generated and manipulated in vitro can be implanted into mice, where they mature and integrate into the host vasculature (Watson et al., 2014; Takebe et al., 2015). Such systems could be powerful tools to study the effects of an aged systemic environment on human tissues.
Similarly, microfluidics could increase the complexity of in vitro organoid systems while improving throughput and reproducibility. Multiorgan systems have been developed for the study of organ interactions via an in vivo-like sequential, organ-to-organ transfer of media, with a particular interest in drug interactions (Vernetti et al., 2017). These devices could provide insight into how aging tissues affect other parts of the body. Additionally, microfluidic devices permit lumen access and control over millimeter-scale morphology. Although complex tissue structures, such as intestinal crypts and kidney nephrons, are readily generated by organoid self-organization (Morizane et al., 2015), the process can be highly heterogeneous, making assay readout complex or impossible. For example, reproducible kidney organoids with a channel-accessible central duct would enable key functional assays, namely permeability and urea concentration. Methods for micron-scale organization of cells within a tissue or microfluidic chamber (Nelson et al., 2008; Todhunter et al., 2015; Kolesky et al., 2016) could be used to create reproducible, high-throughput organoid assays for aging and other diseases.
Organoids are a powerful emerging tool for the study of human health and disease. Aging research has long needed a model with the practical advantages of simpler organisms and traditional cell culture, as well as the complexity required to model the tissue-level phenotypes that accompany aging. As researchers develop organotypic cultures of increasing complexity, it is becoming clear that organoids will enable the study of tissue-level, and even systems-level, phenotypes of aging. Human organoids have the potential to model the human body with unmatched fidelity. With time, new models will be developed and validated, significantly accelerating human aging research and the search for therapies that will improve human health and lifespan.
We thank Drs. Hao Li and Saul Villeda for their constructive feedback and discussion.
J.L. Hu is supported by the National Science Foundation Graduate Research Fellowship Program. M.A. LaBarge and M.E. Todhunter are supported by the Era of Hope Scholar Award from the Congressionally Directed Medical Research Programs Breast Cancer Research Program (BC141351), the National Institute on Aging (R01AG040081), and the City of Hope Center for Cancer and Aging. Z.J. Gartner is a Chan Zuckerberg Biohub investigator and is supported by an Era of Hope Scholar Award (BC123047), the Center for Cellular Construction (NSF DBI-1548297), and the National Institutes of Health (DP2HD080351).
M. van den Born, et al.
. 1995. Increased production of tumor necrosis factor and interleukin-6 by arterial wall of aged rats. Am. J. Physiol. 268:H2288–H2293.
J. de Ligt, et al.
. 1998. A completely biological tissue-engineered human blood vessel. FASEB J. 12:47–56 https://doi.org/0892-6638/97/0012-0047.
. 2001. Experimental prostate epithelial morphogenesis in response to stroma and three-dimensional matrigel culture. Cell Growth Differ. 12:631–640.
. 2011. An organotypic 3D assay for primary human mammary epithelial cells that recapitulates branching morphogenesis. In 3D Cell Culture: Methods and Protocols. Z. Koledova, editor. Humana Press, New York. 125–137.
. 1993. Hormone regulation of human prostate in organ culture. Cancer Res. 53:5199–5207.
. 1992. Epithelial-specific gene expression during differentiation of stratified primary human keratinocyte cultures. Cell Growth Differ. 3:471–483.
© 2018 Hu et al. http://www.rupress.org/terms/https://creativecommons.org/licenses/by-nc-sa/4.0/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).


text:
Q: My app does not recognize JSX when I run babel I am following instructions from a React course when setting up Babel with Webpack and now I get this error:
ERROR in ./src/app.js
Module build failed: SyntaxError: C:/Users/38164/Desktop/react-course-projects/indecision-app/src/app.js: Unexpected token (4:17)
image of the error

Here are the files from the setup:
app.js

import React from 'react';
import ReactDOM from 'react-dom';

const template =
testing
;
ReactDOM.render(template, document.getElementById('app'));

webpack.config.js

const path = require("path");

module.exports = {
  entry: "./src/app.js",
  output: {
    path: path.join(__dirname, "public"),
    filename: "bundle.js",
  },
  module: {
    rules: [{
        loader: "babel-loader",
        test: /\.js$/,
        exclude: /node_modules/
      }
    ]
  }
};

package.json

{
  "name": "indecision-app",
  "version": "1.0.0",
  "main": "index.js",
  "license": "MIT",
  "scripts": {
    "serve": "live-server public/",
    "build": "webpack --watch",
    "build-babel": "babel src/app.js --out-file=public/scripts/app.js --presets=env,react --watch"
  },
  "dependencies": {
    "@babel/core": "^7.20.12",
    "@babel/preset-env": "^7.20.2",
    "@babel/preset-react": "^7.18.6",
    "babel-cli": "6.24.1",
    "babel-loader": "7.1.1",
    "live-server": "^1.2.2",
    "react": "16.0.0",
    "react-dom": "16.0.0",
    "validator": "8.0.0",
    "webpack": "3.1.0"
  }
}

.babelrs

{
    "presets": [
      "@babel/preset-env",
      "@babel/preset-react"
    ]
  }

Does anyone have any suggestions?
There is probably something minor, but I can't figure it out, as this is new for me.

redpajama_set_name: RedPajamaStackExchange


Day 9 - Teletubbies Live @ New Theatre, Oxford.
'Ere, today we are giving you another chance to bag a family ticket to Teletubbies Live at New Theatre, Oxford. Just don't ask how we got it.
It's the prize everyone is talking about, a ticket to the Teletubbies' first ever theatre show.
This is a chance for your kids to join Tinky Winky, Dipsy, Laa-Laa and Po in a show full of love, laughter and tubby toast.
Teletubbies Live will capture your children's imaginations and will encourage them to explore the world around them. On top of that, it gives the parents a chance to join in with all the songs. What a treat.
One family ticket to Teletubbies LIVE on Wednesday 29th August at 10am.
Fancy baggin the ticket? Enter below, be quick, these need to be gone by 5pm!


In the 3rd BW Hotelier Smart Hotels Conclave and Expo at The Park New Delhi, Bobby Mukherji spoke upon the 'Architect's View: Old Structures, New Technologies, a Seamless Refurbishment Experience'.
"Getting the right consultant on board is important to create the right technology in hotels," said Bobby Mukherji from Bobby Mukherji and Associates at the third BW Hotelier Smart Hotels Conclave and Expo at The Park New Delhi.
Mukherji gave his presentation on the 'Architect's View: Old Structures, New Technologies, a Seamless Refurbishment Experience'. His experience with William Leeds Architects in New York gave him the first taste of success. With the philosophy of 'Say nothing let your work speak instead', Mukherji has served different genre of clienteles including from retailers to airlines to hotels to corporate houses to private residents.
From getting the quality of the air to be purified to enhance the bathing experience, Mukherji believe that in infrastructure, getting the basics in its place should be at utmost importance. "Hence, the importance of technology plays a vital role even before the aesthetics," he said.
Mukherji also shared a fact that the smaller and standalone hotels do not pay better care to these aspects as compared to the bigger brands. "In my experience I have noticed bigger brands getting more sensitive towards getting the basics right," he stated.
According to Mukherji, using the new age materials in refurbishments have helped in creating better return on investment to the hotel owners.
During his presentation, Mukherji spoke about the renovation of Le Meridian, New Delhi. "Le Meridian is amongst the first hotel that installed LED lightings and flat screens which were appreciated by the clientele," he said.


text:
Jashodaben offers prayers in Gangavati temple, Karnataka
news Sunday, June 08, 2014 - 05:30
The News Minute | May 22, 2014 | 7.51 pm IST Prime Minister-elect Narendra Modi's wife Jashodaben visited temples in Karnataka on Wednesday to offer special prayers that are said to be part of a pilgrimage. According to a Times of India report (Jashodaben offers puja at Gangavati temple), she visited the Anjanadri Hill temple and offered prayers along with another woman. She had arrived in Hospet by a special train from Gujarat. She was reportedly accompanied by a number of people. The Vishwa Hindu Parishad's Hospet unit leader Kantilal was present at the temple when Jashoda visited. The local police however, did not have any information about Jashodaben's visit, TOI reported. The report also said that she left for Gujarat via Bangalore after the pooja was completed.


text:
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"It's a Unique Dynamic:" The Odenigbo Siblings and Their Little-Brother-Big-Brother Relationship
Photo Credit: Brace Hemmelgarn (USA Today Sports)
By Sam Ekstrom - July 26, 2019
EAGAN — You might not know these brothers are related at first glance; one a fluid pass-rusher, the other a burly defensive tackle.
But it's easy to hear the Odenigbo voice come through after a few minutes of conversation — animated, fast-talking and genuine.
Ifeadi and Tito Odenigbo are teammates once again.
"It's kind of unique," said Tito, an undrafted rookie. "I haven't really been seeing him every day on a consistent level since high school. The last time I played football with him was my sophomore year of high school, so my family's really excited, my friends and community are all really excited. It's fun, but at the same time it's still a business."
The two defensive linemates, both with 53-man roster aspirations, played together eight years ago at Centerville High School in their native Ohio when Ifeadi was a Big-Ten-bound pass rusher and Tito was a Big-Ten-bound run-stuffer.
Since then, Ifeadi went to Northwestern while Tito grew up a bit more and landed with Illinois, setting up an Odenigbo vs Odenigbo matchup in 2015 and 2016. That's when both their paths got more complicated.
After a 23.5-sack career in college, Ifeadi got drafted in the seventh round by the Vikings and became a practice squad stalwart. He was eventually waived in 2018 and spent stints with the Cleveland Browns and Arizona Cardinals before returning to Minnesota's practice squad later that year.
Tito played four years at Illinois, his favorite childhood team, but with hopes of catching pro scouts' eyes in his final season, he became a graduate transfer and landed with the Miami Hurricanes.
"Miami put me in the position to be in the NFL because I don't think I'd have the same opportunity if I was at Illinois," said Tito. "But the University of Illinois, all my friends and my classes just taught me how to become a man. Just two phases of a different culture."
Illinois State Redbirds quarterback Jake Kolbe (16) is sacked by Northwestern Wildcats defensive lineman Ifeadi Odenigbo (7). Mandatory Credit: David Banks-USA TODAY Sports
And now that they are reunited — 60 pounds heavier than they were in high school — they've been making up for lost time.
The brothers lived together in the Twin Cities when Tito was brought in as undrafted free agent in early May. After mandatory mini-camp they went to Kentucky, just south of their parents' Ohio home to train at Ignition Athletics, putting in three-to-four-hour sessions working on mobility, explosion, conditioning and lifting. Upon their return to Eagan, they'll share a defensive line room led by position coach Andre Patterson, who was instrumental in bringing Tito Odenibo to town.
"I told [Patterson], 'Look out for him,'" Ifeadi relayed to his coach before the draft. "Throughout the whole free agency process our coach was like, 'I think your brother has a lot of potential. You've grown a lot over the past three years, I think I can do the same with your brother if he buys in and works hard.'"
'Older brother jerk'
The big-bro-little-bro dynamic is alive and well with the Odenigbos.
Ifeadi and Tito, along with their brother Sonto, grew up with their Nigerian-born parents competing in sports and, as Tito described, "butting heads."
"I hated him, he was really annoying," Tito said of his boyhood relationship with Ifeadi, "but I always respected him. He always did the right things, was extremely hard-working, so he's kind of a good role model to look after his work ethic. The older we get the more I respect him."
But Tito didn't end his compliment without a final jab.
"He's just annoying as a person — older brother jerk."
Ifeadi smirks about the dynamic between he and his brother. He confesses to being hard on Tito, but says it's because of his high expectations. After giving Patterson the recommendation to scout his younger brother, Ifeadi wants to see Tito make a name for himself in the NFL, even if it's not with the Vikings.
Photo Credit: Rich Barnes (USA Today Sports)
"I guess the way I approach things I can be a little mean, I guess, or a little hard at times," Ifeadi said. "I'm trying to tell him, do this, do that, do that. He's a typical younger brother so I'm going to do me. And I'm trying to help him with that, tell him that this is not college. Here with everything you've got to be precise. If you can get technique down, whatever happens here, you'll be fine because that technique will travel."
Shooting for the 53
Ifeadi Odenigbo made a name for himself in the preseason of 2018 when he got two sacks as a fill-in defensive end against Jacksonville, making his eventual release more difficult that September. After his travels to Cleveland and Arizona, Minnesota brought him back to the practice squad midway through the 2018 season and eventually converted him to full-time defensive end.
The older brother believes he'll be used as a pass-rushing 3-technique, as well, similar to Brian Robison's role in 2017. With defensive end Tashawn Bower out indefinitely with a torn Achilles, Ifeadi sees an opening.
"I think the coaches have come to agreement that I'm a lot better at D-end than D-tackle," Ifeadi said.
Listed at 315 pounds, Tito Odenigbo has the body of a nose tackle. He said he played football in high school at about the same weight as his older brother despite being two grades younger.
"Recently I found out what food was," Tito joked.
While Ifeadi was a tweener for the first couple years of his career, Tito has a clear role. He doesn't play as splashy a position as Ifeadi, posting only one sack is his college career at Illinois and Miami. He'll need to perfect his technique as an inside gap-filler in order to contend at a position where the Vikings may have openings too.
"I think the coaches have come to agreement that I'm a lot better at D-end than D-tackle."
"Just getting my footwork on par to how we're going to run the defense," Tito Odenigbo said. "It's different than college, but not too difficult. … Adapting to new things is probably the biggest thing I've got to be working on right now."
Not only will the younger Odenigbo get instruction from his big brother, but he'll hear it from established veterans too. Head coach Mike Zimmer says he appreciates the way the veterans pass on their knowledge at the defensive line position.
"The veteran guys we have, Everson and [Linval Joseph] and those guys, they do a good job coaching them and keeping them in line," Zimmer said. "A lot of these guys come in here and they think they know everything. We're trying to do it a certain way."
There are plenty of pairs of brothers that play in the NFL but few that play on the same team. Ifeadi and Tito Odenigbo hope to join the ranks of Ryan and Matt Kalil (Panthers) Shaquem and Shaquill Griffin (Seahawks) and Devin and Jason McCourty (Patriots) — brothers that got to wear the same logo on their jersey.
"He has to do his thing," said Tito, "I have to do my thing, and hope for the best."
Sam Ekstrom
Sam Ekstrom is a Zone Coverage staff writer and podcaster in his sixth year covering the Minnesota Vikings and Minnesota Golden Gophers men's basketball team. After moving to the Twin Cities in 2014, Sam started working as a radio engineer, producer and host for "Sports Radio 105 The Ticket," where Zone Coverage was first formed. He grew up in Vermillion, S.D. rooting for the USD Coyotes (not SDSU) and graduated from Dordt (not "dork") University in Sioux Center, Iowa.
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The Minnesota Vikings' new offensive coordinator, John DeFilippo, will be critical in defining the future of the franchise even if he only stays with the team for […]
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text:
Q: construir una baraja de cartas usando un ciclo For Tengo un string String str_one = "\uD83C\uDCA2" que me pinta una carta de poker pero quisiera saber si es posible generar todas las cartas con un ciclo for.
He intentado reemplazar los 2 últimos caracteres, pero no he podido.
Tampoco teniendo algo como String str_two = "uD83CuDCA2" y luego usar el str_two.replaceAll("u", "\u")
Necesito saber si hay otra forma de generar las cartas aprovechando el patrón que tienen en su representación Unicode.
No tiene que ser con strings, puede ser con Character o con una representación hexadecimal, sólo quiero saber si es posible generar las 52 cartas aprovechando el patrón que tienen.
Actualización:
He usado el string "symbol" como está a continuación para la creación de una carta y los métodos set y get para "symbol" y "value", pero más adelante necesitaré el entero "codepoint", cómo me regreso del string "symbol" al entero "codepoint" ?
for (int c2 = 1, value=1; c2 <= 0xE; c2++, value++) {
    for (int c1 = 0xA; c1 <= 0xD; c1++) {
        if (c2!=0xC) {
            str = String.format("1F0%X%X", c1, c2);
            codePoint = Integer.parseInt(str, 16);
            symbol = String.format("%c", codePoint);

            cards.add(new Card (symbol, value));
        } else {
            value = 11;
        }
    }
    System.out.println();
}

A: De acuerdo con Wikipedia, los códigos Unicode (en hexadecimal) para las cartas de poker tienen el siguiente patrón: comienzan con 1F0, luego una letra, de la A a la D; después un número o letra, del 1 al 9 o de la A a la E.
❐ Código:
En Java es posible representar un número en hexadecimal de manera literal. Sólo hay que añadir el prefijo 0x al número deseado. Y esto se puede aprovechar para crear dos ciclo for anidados, uno para el primer carácter y el otro para el segundo carácter. Es decir:
for (int c1 = 0xA; c1 <= 0xD; c1++) {
    for (int c2 = 1; c2 < 0xE; c2++) {
        String str = String.format("1F0%X%X", c1, c2);
        int codePoint = Integer.parseInt(str, 16);
        System.out.printf("%c U+%s %s%n", codePoint, str, Character.getName(codePoint));
    }
}

c1 va de 0xA a 0xD y c2 va de 0x1 a 0xE, tal como se requiere.
❐ Salida:
 U+1F0A1 PLAYING CARD ACE OF SPADES
 U+1F0A2 PLAYING CARD TWO OF SPADES
 U+1F0A3 PLAYING CARD THREE OF SPADES
 U+1F0A4 PLAYING CARD FOUR OF SPADES
 U+1F0A5 PLAYING CARD FIVE OF SPADES
 U+1F0A6 PLAYING CARD SIX OF SPADES
 U+1F0A7 PLAYING CARD SEVEN OF SPADES
 U+1F0A8 PLAYING CARD EIGHT OF SPADES
 U+1F0A9 PLAYING CARD NINE OF SPADES
 U+1F0AA PLAYING CARD TEN OF SPADES
 U+1F0AB PLAYING CARD JACK OF SPADES
 U+1F0AC PLAYING CARD KNIGHT OF SPADES
 U+1F0AD PLAYING CARD QUEEN OF SPADES
 U+1F0B1 PLAYING CARD ACE OF HEARTS
 U+1F0B2 PLAYING CARD TWO OF HEARTS
 U+1F0B3 PLAYING CARD THREE OF HEARTS
 U+1F0B4 PLAYING CARD FOUR OF HEARTS
 U+1F0B5 PLAYING CARD FIVE OF HEARTS
 U+1F0B6 PLAYING CARD SIX OF HEARTS
 U+1F0B7 PLAYING CARD SEVEN OF HEARTS
 U+1F0B8 PLAYING CARD EIGHT OF HEARTS
 U+1F0B9 PLAYING CARD NINE OF HEARTS
 U+1F0BA PLAYING CARD TEN OF HEARTS
 U+1F0BB PLAYING CARD JACK OF HEARTS
 U+1F0BC PLAYING CARD KNIGHT OF HEARTS
 U+1F0BD PLAYING CARD QUEEN OF HEARTS
 U+1F0C1 PLAYING CARD ACE OF DIAMONDS
 U+1F0C2 PLAYING CARD TWO OF DIAMONDS
 U+1F0C3 PLAYING CARD THREE OF DIAMONDS
 U+1F0C4 PLAYING CARD FOUR OF DIAMONDS
 U+1F0C5 PLAYING CARD FIVE OF DIAMONDS
 U+1F0C6 PLAYING CARD SIX OF DIAMONDS
 U+1F0C7 PLAYING CARD SEVEN OF DIAMONDS
 U+1F0C8 PLAYING CARD EIGHT OF DIAMONDS
 U+1F0C9 PLAYING CARD NINE OF DIAMONDS
 U+1F0CA PLAYING CARD TEN OF DIAMONDS
 U+1F0CB PLAYING CARD JACK OF DIAMONDS
 U+1F0CC PLAYING CARD KNIGHT OF DIAMONDS
 U+1F0CD PLAYING CARD QUEEN OF DIAMONDS
 U+1F0D1 PLAYING CARD ACE OF CLUBS
 U+1F0D2 PLAYING CARD TWO OF CLUBS
 U+1F0D3 PLAYING CARD THREE OF CLUBS
 U+1F0D4 PLAYING CARD FOUR OF CLUBS
 U+1F0D5 PLAYING CARD FIVE OF CLUBS
 U+1F0D6 PLAYING CARD SIX OF CLUBS
 U+1F0D7 PLAYING CARD SEVEN OF CLUBS
 U+1F0D8 PLAYING CARD EIGHT OF CLUBS
 U+1F0D9 PLAYING CARD NINE OF CLUBS
 U+1F0DA PLAYING CARD TEN OF CLUBS
 U+1F0DB PLAYING CARD JACK OF CLUBS
 U+1F0DC PLAYING CARD KNIGHT OF CLUBS
 U+1F0DD PLAYING CARD QUEEN OF CLUBS

──────────────
NOTA: Dependiendo del navegador (y a veces también del sistema operativo), los caracteres anteriores podrán ser renderizados correctamente:

 UPDATE
El código se modifica, de acuerdo con los comentarios del OP, como sigue:
for (int c1 = 0xA; c1 <= 0xD; c1++) {
    for (int c2 = 1; c2 < 0xE; c2++) {
        if (c2 != 0xC) {
            String str = String.format("1F0%X%X", c1, c2);
            int codePoint = Integer.parseInt(str, 16);
            System.out.println(Character.toChars(codePoint));
        }
    }
}


Vodafone UK has informed Reuters that they have been the victim of an hack which allowed the cyber criminals to view nearly 2000 customer accounts.
He also stated that the cybercriminals were able to gain access as they had acquired credentials from an unknown external source.
Vodafone UK also stated that the company is contacting the customers which are involved and that other customers do not need to be concerned. The spokesperson also stated that the chance is there that the obtained information might be used by cybercriminals in future attacks.


Day 1 Nairobi/Amboseli. Morning drive to Amboseli National Park, lunch, afternoon game drive, dinner and overnight at Ol Tukai lodge FB.
Day 4 Treelodge/Samburu. Morning drive across the Equator to the edge of the Northern Frontier. Lunch, afternoon game drive, dinner and overnight at a Samburu lodge FB.
Day 6 Samburu/Nakuru. Morning drive via Nyahururu Falls down to the floor of the Rift Valley to Lake Nakuru National Park. Lunch, afternoon game drive, dinner and overnight at Lion Hill Sarova lodge FB.
Day 7 Nakuru/Maasai Mara. Morning drive across the Rift Valley down to the Maasai Mara Game Reserve. Lunch, afternoon game drive, dinner and overnight at Lion Hill Sarova lodge FB.
Day 8 Maasai Mara. Experience the magical Maasai Mara; with morning and afternoon game drives, lunch, dinner and overnight at Mara Simba lodge FB.
Day 9 Maasai Mara/Nairobi. Early morning game drive followed by breakfast. Return to Nairobi in time for lunch on own.


PAC-MAN… What have you DONE!
The wonderful people behind the world of Pakkuman!, know to many of you as PAC-MAN. Have decided that now would be an awesome time to push a new property from the same intellectual root form. So they are crowdsourcing some of the design. a little A&R work in the form of a survey on their Facebook page.
I Don't even know where to begin, First off… Where is Clyde? That sucker owes me money, preferably in quarter form. Secondly why do the ghosts all have radically different designs? They should be the same or at least look like they were done by the same artist. The old show was fine, and frankly i love some of the other people's response to this. Specifically I love the response from Gabe of Penny-Aracde, he actually has the individual panels available for download on the site as well. Awesome graphics!
Why do we need to go down this road again. Why are the designs all horrible And while i'm still complaining, why the hell does Pac-Man have cat ears? The Official Mascot has freaking cat ear eyebrows?
Hey Silly Mascot get off my lawn!


xfsaild stands for XFS Active Item List Daemon.
As with ext3 and ext4, XFS is a journaling file system. Its journal log is temporarily stored in log buffer of main memory and finally written to disk.
The state of the log that exists in the log buffer of the main memory and has not yet been written to the disk is called " Active " and it is stored in the list " Active Item List " on the memory.
The process responsible for managing this "Active Item List" is xfsaild.
The following logs are frequently seen with xfsaild related errors.
INFO: task xfsaild / dm - 0: 415 blocked for more than 120 seconds.
This is a log reporting that xfsaild was unable to access disk for 120 seconds or more due to disk loading and other reasons.The impact is mixed, but there are cases where it develops into Call Trace.
For Call Trace, please refer to the following.
If the disk load is too high or the disk failure occurs, in some cases the result of "ps" command is as follows.
D State is one of the process status of general Linux and means "TASK_UNINTERRUPTIBLE".
Process or thread is in sleep mode and is not responding to asynchronous signal process.In other words, kill -9 can not stop the process.


-There are cases when your skin pigmentation will be altered in the process of healing and you are likely to end up with uneven skin tone. You will also experience marks and dark spots due to breaking up of blood veins caused by acne lesions. Different patches of brown, purple and even red on the skin are likely to appear.


text:
Q: slide show with bootstrap I try to make a slide show with bootstrap, so that you slide through the images. But the images are not showing. Only the next and previous buttons are showing. I am using asp.net mvc5
this is the jquery:
$(document).ready(function () {
            $myModal = $('#myModal');

            $('.row img.img-responsive').on('click', function () { // <-- notice the selector change
                var $this = $(this),
                    src = $this.attr('src'),
                    html = '';

                //Start
                var index = $(this).parent('.row img.img-responsive').index();
                var html = '';
                html += html;
                html += '
';
                html += 'next »';
                html += '« prev';
                html += '
';
                //End

                updateModalBody($myModal, html);
                $myModal.modal();
            });

            $myModal.on('hidden.bs.modal', function () {

                updateModalBody($myModal, '');
            });

            function updateModalBody($modal, html) {
                $modal.find('.modal-body').html(html);
                $modal.modal('hide');
            }

        })

        $(document).on('click', 'a.controls', function () {
            //this is where we add our logic
            var index = $(this).attr('href');
            var src = $('ul.row li:nth-child(' + index + ') img').attr('src');

            $('.modal-body img').attr('src', src);

            var newPrevIndex = parseInt(index) - 1;
            var newNextIndex = parseInt(newPrevIndex) + 2;

            if ($(this).hasClass('previous')) {
                $(this).attr('href', newPrevIndex);
                $('a.next').attr('href', newNextIndex);
            } else {
                $(this).attr('href', newNextIndex);
                $('a.previous').attr('href', newPrevIndex);
            }

            var total = $('ul.row li').length + 1;
            //hide next button
            if (total === newNextIndex) {
                $('a.next').hide();
            } else {
                $('a.next').show()
            }
            //hide previous button
            if (newPrevIndex === 0) {
                $('a.previous').hide();
            } else {
                $('a.previous').show()
            }

            return false;
        });

and this the css/html:

        @foreach (var item in Model.LolaBikePhotos)
        {

            @model  ContosoUniversity.Models.UserProfile
            @*
*@

                @**@

                    <button type="button" class="close" data-dismiss="modal" aria-label="Close">×</button>

        }

Thank you
I have to edit this:
html += html;

But I dont know how to change that.
This is how you will see it:

A: To make this simple
If you look at the HTML from
http://getbootstrap.com/javascript/#carousel
Copy the first one and add some Razor, this should generate a Carousel for you.
@model List<YOUR_MODEL_NAME>
    @{var j = 0;}

     @for (var i = 0; i < Model.Count(); i++)
     {

      }

 @foreach (var item in Model)
  {

  @(j = 1)
  }

Previous

Next

EDIT
Following is an Example of a Thumbnails, when the thumbnails are clicked it will open a modal-dialog with a carousel in it.
I have created a JSFiddle of your scenario:
http://jsfiddle.net/u7hxy3zc/1/
You should use the following code as an example and use in your View, Renaming all models and parameters.
Note: The following code has not been compiled May have syntax errors
// DISPLAY THUMBNAILS

@for(int i =0; i < Model.Count(); i++)
  {

  }

.......... REMOVE HTML TO MAKE EXAMPLE CLEAR
... MODAL DIALOG START.................

...........CAROUSEL START............

@for(var i = 0 ; i< Model.Count(); i++)
{

}

@for(var i = 0; i < Model.Count(); i++)
{

  // DISPLAY i for Testing
    @i

}

........... REMOVED REST OF CAROUSEL......(NEXT / PREV BUTTONS).........

.............CAROUSEL END...................

Then add this jQuery at the end to trigger the click event:
$('body').on('click', '*[data-action="image"]', function (e) {
    e.stopPropagation();
    var img = $(this);
    var currentId = img.data('id');
    $('#myModal').modal();
    var currentSlide = "*[data-slide-to='" + currentId + "']";
    var currentImagSlide = "*[data-image-id='" + currentId + "']";

    console.log(currentSlide);

    $("*[data-slide-to]").removeClass("active");
    $(".item").removeClass("active");

    var item = $('.carousel-indicators').find(currentSlide);
    var imgItem = $('.carousel-inner').find(currentImagSlide);
    console.log(item);
    item.addClass("active");
    imgItem.addClass("active");
});

A:

        ...

    ...

Definitely look into bootstrap carousel


Tory Burch sold an equity stake to a Mexican investment firm in a deal that values her fashion business at upwards of $500 million, sources told The Post.
That's a steep discount to the price tag demanded by the red-hot fashion designer last year, when she was telling investors the fast-growing franchise was worth as much as $1 billion, according to sources close to the situation.
Nevertheless, insiders said Burch and her ex-husband and business partner Chris Burch — who founded the business together five years ago — did well to close the deal, given the challenging retail climate. Recently, top-tier labels like Brioni and Roberto Cavalli have sought to sell minority stakes without success.
Under the agreement, Tresalia Capital of Mexico City poured in more than $100 million in exchange for between 20 percent and 25 percent of Tory Burch, sources said.
The fat price tag speaks to the continued strength of Tory Burch's business, which despite the collapse of luxury spending is still "doing close to what it was doing last year," according to one source.
While Tory Burch touted prospects for growth in Latin America under the deal, one source close to the situation said that was "baloney," and that Tresalia won simply because it was the highest bidder for the business.
"This was about taking money off the table," the source said.
Tory Burch was advised by a group led by Barclays Capital.


Yes, I know, it's been a long time so sit tight ready to get engaged with the goings on at Green Lane; perhaps a cuppa (or something stronger!) might sustain you through the marathon that is both updating and December.
What a find! Whilst browsing in the local Hospice Shop I spotted a rather brilliant geometric fabric still on its cardboard pole. £2.00! Surely not! It was – wow! I had no idea what I would make with it but at that price I had to have it. Later I turned it into a Roman Blind for Chris's Room, edging it with the remnants from two other projects both of which I had used in Chris's room; so, wonderful coordinating. Chris was pleased with the results but he had no idea what I had lined up on my 'list' of things pre-Christmas.
Later in the month, I used the cardboard tube for the base of my garland decorations – waste not want not. Then recycled once the decorations came down.
Having been inspired by the progress made as the downstairs started to look so much better and more finished, he decided to try his hand at plastering. The door that we had replaced in the kitchen had remained an eyesore for over a year but as can be seen it started to improve as Chris re-routed electric cables, put up new lights and plastered the window surrounds. I later painted it and it all looked great for Christmas. Thanks, Chris, job well done.
But this was just the start of his madly creative period – he then looked at my design ideas for my room and translated them into reality. I am REALLY thrilled with my almost finished room. It looks just as I imagined it. It is a light and calm room filled with photos and sentimental knick knacks.
Following this I took a quick look around the charity shops and found two rugs – one for Chris's room and one for mine. Job almost done. I now have another purpose built shelf under my desk area for the printer and space for a basket holding files and stationery – perfect!
Yes – I know there are two tea cosy covers but when I had made one my sensible husband suggested that there might be further demand for said item so he advised that I made another one, which I did. The cake was decorated using my Mum's original cake decorations from the 1960's. I just had to use them all.
Well, is that all you did, I hear – no, on the second weekend of December my Mother was volunteered to help the grandchildren and me wrap and label all their presents that they had bought for family and friends.They had saved their pocket money, made lists of friends and a joint list for family and we hit the shopping heights at Skippingdale Retail Park which seemed to provide nearly all their requirements. Each grandchild had their own basket and I had three envelopes filled with their saved pocket money.
Look at Madeleine's gift bags already done and arranged on the window sill – still more to go though. Daisy wrote every single one of her gift labels but we did have to stop her writing her name in full – we felt that everyone already knew that it was Daisy Sullivan giving the gift (so no need for her surname, even if it was written in her best handwriting!) Matthew quietly got on even though we did have to do a bit of top up shopping in the Barton charity shops – Aunty Lucy was the lucky recipient of one such bargainacious find!
Not bad, now what's next?
The first fortnight of December was quite full on as we celebrated Daisy's 6th birthday on December 10th and Lucy had her first birthday celebration as part of our family on December 11th.
A perfect start to a great birthday. Birthday breakfast followed by a trip to Normanby Hall as a family for tea, feeding the reindeer and a visit to see Father Christmas.
What a lovely day and we know that James organised lovely things for Lucy but perhaps not a trip to see Santa!
On Thursday 14th December Chris and I celebrated 39 years together – I know, where does the time go? Also, Northernpowergrid turned up as scheduled, to remove the redundant electricity pole outside our driveway. This was the final part of a request I made when we first moved in – so, only three years. Worth the wait though. Everyone was efficient and the pole was removed quickly – it just took another week for the hole to be filled in. Oh well!
… as if this was not enough I had also asked him to construct a Christmas tree shaped log-store from the leftover lap-edge fencing. I think he enjoys the challenge.
I think you'll agree that they really added something to our garden.
Usually being the person who arranges and organises things I was completely unprepared for what occured on my birthday – Thursday 21st December rolled around, James and Lucy had arrived on the 20th and we were all starting to get into the swing of things; David and Heather were due later on so all was going to plan. Hannah had asked if she and the children could come over for breakfast – of course, we were delighted. I was amazed and thrilled when my sister Suzanne and my niece Samantha turned up from Harrogate with bubbly, salmon, caviar, bagels and cake! What a beautiful and loving surprise. Thank you so much. We were all having such a great time that no one took any photos so you will just have to imagine how lovely it was. It doesn't hurt to say thank you again though, so a very big loving thank you.
Yes! I know! It is brilliant!
And look at how well it fits the dining space and that it will seat eight people comfortably and ten if needed. Just what I wanted – a table fit for purpose. Hairpin legs bought online and scaffolding boards from B&Q. Excellent.
The cheery Christmas vibe is definitely apparent now – decorations up in the dining room and in the front and back gardens, lights twinkling and of course the real Christmas tree (number 4).
In the front room I put up my LED tree with the jolly Santas and delicate Angels as well as the polar bear ornaments for the grandchildren.
Like us the 'children' had been busy decorating their homes, creating DIY Advent calendars, making unusual Christmas trees and making festive goodies to give as gifts or to share throughout the Yuletide. All were a great and delicious success.
The granddaughters not to be left out had decorated and labelled a dozen little cress heads. Over a period of time Chris and I had collected egg shells in preparation for Daisy to grow mustard and cress in them; about ten days before Christmas she seeded the eggshells stuffed with damp cotton wool and watered them regularly until they had all grown a fine 'mop of green hair'. Hannah suggested that they make place names out of them. Carefully the girls illustrated and coloured and labelled each 'hairy egg' – fantastic and what a great addition to the Christmas table. Well done, girls, I can't wait to see what you do for next Christmas.
I think they tailored each one to suit the recipient!
Christmas dinner which we had at Prospect House with Hannah, Matt and family was superb. The food looked beautiful and almost jewelled and it tasted divine; what a menu and what a great team of cooks working together. Who can forget the garlic /lemon prepared Turkey, the delicious stuffings, vegan offerings, pickled red cabbage, the gravies, sauces, custards and special Islay Marmalade Pudding! Phew! What a blowout!
Despite it being half way through January we want to wish you all a very wonderful 2018.
Previous PostPart II – Foreign Fields, Fencing, Fruitfulness, Fixing, Flowering – and finally the FWord!