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It starts with the riff, as it almost always does. A slash from the fourth to the root, and then, an octave down, from the root up to the fourth. A second guitar, the drums, and a bass all heave in. Theres an unexpected Eb chord. An acoustic guitar wakes up in the other channel. After thirty seconds the singer leans in over the next-door fence and starts gossiping. Its one of the most exciting half a minutes in rock n roll, conjured up by way of some particularly dark arts, a spell cast to make human beings move. You may have seen it performed in stadia by aged men, peddling welcome nostalgia and peddling it well, you may have heard it a thousand times through speakers great and small, but it retains its lustre, as if it were wrought this very morning, and not some fifty years ago.

Brown Sugar adds irrefutable evidence to the case for The Rolling Stones as the greatest rock n roll band of all time. And I do mean all time, for it seems more and more unlikely with each passing year that well ever see anyone even close to their like again. You could just as easily point at anything The Stones recorded from Jumping Jack Flash up to Exile On Main St - and I would add 73s Goats Head Soup to that pile, although many would argue that point. It is the greatest artistic purple patch in history; it might just be the greatest thing in history, full stop. Yes, there are a lot of nice paintings hanging up out there, Shakespeare had some good lines, theres no denying it, democracy sounds good on paper, and modern medicine is a thing of wonder, but do any of them rock like The Stones?

Released as a single on April 16, 1971 and the opening song on the bands ninth studio album, Sticky Fingers, out a week later on the 23rd, Brown Sugars verses clang from C to F while Charlie Watts beats the living shite out of the floor tom behind them, then the band crash into G for that chorus that everyone knows even if they dont know it. Theres a barrelhouse/whorehouse/outhouse piano tinkling in the background, courtesy of Ian Stewart, happy to sit in because there's no minor chords, and a saxophone parps down near the basement during the second verse. Keith Richards once told someone that the secret to a good single is to introduce something new every thirty seconds. Set your watches.

The sax break sounds like Bobby Keys has just stepped out of a particularly boisterous knocking shop to honk about whats going on inside. In response, Jagger starts swinging his maracas. Yeah, Yeah, YEAH! WHOO! Not for the first or last time, Keith doffs his cap to his forefather Chuck with the round out riff and, when the whole thing clatters to a halt, he offers a satisfied Yeah! because he knows, that yet again theyve captured lightning in a bottle. Let me quote my wise Auntie Zena, who described it to me recently as powerful magic. She knows what shes talking about.

The lyrics reference slavery and more acceptably cunnilingus, and there may be some heroine in there too. While there has been outcry, the surprising thing is there hasnt been more of it. Jagger has always claimed he wrote it in a hurry, but this was an educated man in his mid-twenties. He knew what he was doing. He was the king of the world, the most famous certainly the most notorious rock n roller of them all. My guess is he was playing up to that. We should be glad, I suppose, that he at least saw fit to change the original title, Black Pussy. As one might expect, he has tempered those lyrics during subsequent live performances and has said, several times, that theres no way hed write or indeed get away with writing anything like that since. No one would.

Lets put it another way. In 1971 The Rolling Stones were the most famous rock n roll band in the world. Ten years before that, rock n roll was nearly dead, the originators were all in various states of distraction, and brylcreamed dreamboat crooners ruled the day. Ten years after this we would be into the eighties and heading towards the homogenisation of rock n roll in the wake of Live Aid, as noble a venture as it was. Therefore, The Rolling Stones taking a song that gleefully waved two fingers at every taboo it could think of all the way to the top of the American charts must represent some sort of pinnacle of rock n roll as a truly subversive, truly counter cultural force. By all means, be offended by it but at least acknowledge that they were refusing to play it safe. It didnt last. Only a few years later Jagger himself would be declaring that Its Only Rock N Roll. Mind you, none of that would matter in the slightest if the thing didnt rock like a bastard. Its a vital, life-affirming noise, because rock n roll at its best isnt only rock n roll. Its so much more than that.

If you were at home in front of your record player in April 1971 and you flipped the seven inch over, Bitch' was very nearly as good again. The story is told, by engineer Andy Johns, that Keith was late to the recording session and the others were playing around with a riff that was going nowhere fast. Richards arrives, sits on the floor to eat a bowl of cereal, calls for a guitar, kicks the song up several gears and that was that. Its been pointed out many times that The Stones follow Keith's guitar rather than Charlie's drums, unlike every other band. You can hear what that means in Bitch. It's driven by that guitar riff, doubled by Jim Prices trumpet and Bobby Keys saxophone, but when Richards veers into his solo, he pulls the beat out of shape, turns it around, and Watts falls in behind him. Many, many bands have tried to cover The Rolling Stones. Perhaps you were in one of them? Precisely none ever got it right, because they didnt have Keith Richards and Charlie Watts. Maybe they had a drummer as good as Charlie, although I doubt it. Maybe they had a guitar player with a sense of rhythm as unique as Keiths, although this seems unlikely. Only one band ever had both.

The album comes draped in what is probably The Stones most iconic record sleeve. While it was conceived by arch-chancer Andy Warhol, the donkey work was carried out by designer Craig Braun. Braun had helped realise the cover of The Velvet Undergrounds debut, the one with the banana. The crotch shot with something seemingly stuffed in the pocket was rumoured to be Jagger himself but Braun says it was Factory hanger-on Corey Grant Tippin, although he did hear this from someone else. The initial zipper idea was Warhols, but it was up to Braun to make it work. It was he who argued with sceptical zip manufacturers that a Stones album would be a good thing to be involved with. Braun also encouraged the Warhol signature stamp in order that potential customers might see it as a piece of art - that can be seen, when you pull down the zip and open the belt, on the y-fronts underneath a photo of Interview magazine editor, Glenn OBrien, apparently.

It is, if you will excuse the pun, a very attractive package, but there was a problem, the zip was damaging the records the album itself and anything stacked beside it. They initially circumvented this by pulling the zipper down of course so the dent was in the centre of the record, where the track listing is, but it couldnt last. The zip was replaced with a photo on later issues although it was back in place for the 2015 deluxe buy-it-again campaign.

Another first was the presence of the famous Stones tongue logo, designed by John Pasche, who gave up all claims to it for the princely sum of 26,000 in 1984. While its always associated with Jaggers ample gob, the design is actually based on the Hindu goddess, Kali ("She who is death'). According to Braun, he and illustrator Walter Velez fleshed out Pasches initial design to what we first saw on the sleeve, and then everywhere else as it became one of the most recognisable trademarks in the world.

Not exactly famed for their sense of fun, The Franco regime in Spain werent having a cover like that in their shops so a bizarre alternative was offered for the Spanish market, with fingers emerging from a treacle tin. They also demanded the expulsion of the distinctly druggy Sister Morphine. It was replaced by Chuck Berrys Let It Rock, recorded live at Leeds University on March 13, 1971. It is, alongside Little Queenie on Get Yer Ya-Yas Out! and Bye Bye Johnny on The Rolling Stones E.P. from 1964, one their best Berry covers, and there have been a few. If youve any sense, youll shell out for the super deluxe version of Sticky Fingers if you can still get it which will make you the proud owner of the entire Leeds gig and the envy of all your friends.

One final cover-related titbit: there was a Russian release with a prominent hammer and sickle design on the belt buckle. The person wearing the jeans is now either female or a male whos suffered a very unfortunate accident. Make of that what thou wilt.

After Sugar comes Sway, and its around about this point that you realise Sticky Fingers is an album of the two Micks. Mick Taylor joined the Rolling Stones in 1969 having graduated, as others did, from John Mayalls Bluesbreakers. He was brought in as a replacement for the laid off Brian Jones and his first performance with the band was in front of some 250,000 people in Hyde Park shortly after Jones death. You can hear him on a track or two on their 1969 album Let It Bleed, you can hear him on the Honky Tonk Woman single from the same year, and you can certainly hear him on the previously mentioned Get Yer Ya-Yas Out! live record but Sticky Fingers was his first full-length Stones studio outing and its one that could not have been the same without him. It is his virtuosic playing that lifts Sway two solos, one with slide, one without, the jaw-dropping improvised second half of Cant You Hear Me Knocking and the closing Moonlight Mile. He didnt receive a single song writing credit where does arranging end and song writing begin? and nor wold he on later songs like Time Waits For No One. This shafting would be no small factor in his decision to leave in late 74. The Stones were sometimes great after he left, but they would never be as great again.

In the same way that Exile On Main St. would belong to Keith Richards, Sticky Fingers belongs to the other Mick, Big Mick, Mr Jagger. While Brown Sugar might be three and three quarters of Keiths finest minutes, the song, including the riff, was written by Mick, and Sway, Dead Flowers and Moonlight Mile all sprung from the same pen. He has never received enough credit for his prowess as a singer, for of all the voices that were first heard in the sixties, his was the one that most successfully incorporated the various strands of American music and came up with something of his own. He never sang better than he did during these sessions either. Too often he would slip into self-parody in the years that followed but here, howling out Brown Sugar and Bitch, straining in the chorus of Cant You Hear Me Knocking and delivering real soul in Sway, Wild Horses and Moonlight Mile, he is at his most focused. The Disciples of Keef, who are legion, always claim that Richards is the soul of the Stones, the keeper of the flame, while Jagger is their salesman, and I was guilty of this too, as a younger, dumber man. Every clich has a grain of truth in it, but there are two of them in this partnership and, while there's been some admirable solo work, theirs is a shared immortality.

Wild Horses, like Brown Sugar and the albums sole cover version, Mississippi Fred McDowells You Gotta Move, was recorded when the band stopped off in Muscle Shoals, Alabama during their 1969 US tour, the one that ended in disaster and death at Altamont. Theres a story that these recording sessions, captured forever in their great Gimme Shelter tour movie, took place on the quiet because they didnt have the proper work permits, but the legend, like all good ones, may have been embellished since. What is certainly true is that in those rooms that had played host to Boz Scaggs and Cher before them, they captured something unique. They re-recorded Brown Sugar later on, with Eric Clapton on slide guitar, but there was just something about those Muscle Shoals recordings, and its a shame they never went back. Though some graft took place at Olympic Studios, most of the remaining work on this album utilised the soon to be famous Rolling Stones Mobile Recording Unit in the comfort of Mick's country pile, called, appropriately enough, 'Stargroves'.

Wild Horses might just be The Stones greatest ballad, and its a true Jagger/Richards collaboration, with the melody and title coming from Keith, and Jagger filling in the blanks. Its also one of their most covered songs and this was how it was heard first. Because of their on-going legal tussles with former manager, Allen Klein, the man who also famously got his hands on The Beatles, these songs were held back. Kleins company, ABKCO, still co-owns the rights to them, which is why you see them pop up on ABKCO compilations along with all the Stones 60s material. When he asked, Jagger gave his blessing to Gram Parsons to record a version with his band The Flying Burrito Brothers for their second album Burrito Deluxe, which would come out a year before the Stones' definitive reading. Featuring a high and lonesome Parsons vocal and a beautiful bit of piano playing from Leon Russell, it is, alongside Linda Ronstadts run at Tumbling Dice, one of the very best Stones covers.

Parsons, who became Keiths new best friend, was certainly an influence on The Stones, teaching Richards the difference between the Nashville and Bakersfield sounds, but author Stanley Booth, whose The True Adventures Of The Rolling Stones is probably the best book about them, was a good friend of Parsons and he dismisses any notion that Gram might have helped with the writing. You can hear that country influence though, most especially in the way that Taylors acoustic guitar employs what is known as Nashville tuning, where the bottom four strings are strung an octave up. Jagger has always claimed a love of country music but never thought it suited his voice. He saw himself as a blues singer, and reckoned Keith's croak had more country in it. Wild Horses combines both of them for its glorious chorus. They lost something when they started employing outsiders to handle the backing vocals.

While were talking about country music, Dead Flowers goes the other way altogether. Jagger plays it completely over the top, although not as much as he would on Faraway Eyes. Despite that, it still became a country classic, that even Townes Van Zandt couldnt wring the joy out of, although his version that you can hear during The Big Lebowski has a good go. Taylor could of course play near perfect country licks because he was just that good.

I Got The Blues might be the greatest song Otis Redding and Steve Cropper never wrote. Richards always claimed that Otis recording Satisfaction was akin to getting a nod from a god and The Stones return the favour here, not covering 'I've Been Loving You Too Long' exactly, but coming pretty close. Richards guitar is pure Cropper and Jagger, again, sings his arse off, playing it completely straight. Sticky Fingers is the album where they expanded their sound by letting others play along and Billy Prestons Hammond solo injects just the right amount of melancholy, while Jim Price and Bobby Keys do their best Memphis Horns impression, adding as much to this song as they do to Bitch. There's brass on Honky Tonk Woman but it's buried in the mix. This album is where Price and Keys earned their place, and theyd be all over the next one too. They, as much as anyone, helped to transform the band into the augmented rock and soul review we know today.

Sister Morphine originally surfaced as the B-side to Marianne Faithfulls Something Better in 1969, with her name down as co-writer. This mysteriously disappeared when The Stones released their version and Faithfull had to go to court to set things straight. The presence of Ry Cooder on slide guitar, who can also be heard on Love In Vain on Let It Bleed suggests this must have been recorded around the same time. I could at this point go into the whole story about Keith Richards stealing the open G guitar tuning the guitar is tuned to the chord of G allowing the player to add two fingers to go to C and Richards built his legend on these changes from Cooder, but Cooder, as great as he is, has never written anything nearly as good as Tumbling Dice so the argument seems a bit pointless to me. Anyway, Sister Morphine, a harrowing minor chord ballad with its references to various pills and powders, was the one that ran afoul of Franco, and you can perhaps hear why.

That leaves us with Moonlight Mile and Cant You Hear Me Knocking. The former is all Micks. Theres nothing else like it in their catalogue, a road song lifted higher by a beautiful string arrangement from Paul Buckmaster and one of Jaggers greatest vocal performances. Thats Jim Price moonlighting, if you will, on the piano for the songs moving denouement, he was a handy man to have around.

If you doubted me earlier when I claimed the combination of Richards and Watts as the defining factor that sets The Stones apart and above all other bands, then you only need to hear the opening bars of 'Can't You Hear Me Knocking' to know I was on the money. It would convert the staunchest of tone deaf anti-rockers to the cause. Jagger yelps his approval in the background as a riff as lean as a rake that's been wandering in the desert for forty days leers out of the speakers and makes straight for your girlfriend. Yes, the song goes off into a marvellous Santana-like jam featuring the talents of Keys and Taylor, but it is the push and pull between Keef and Charlie, with Jagger dancing across the top, that marks this out as one of their finest recordings. Put it on, turn it up and try not to get down, I dare you. The Greatest Rock N Roll Band Of All Time.

What did I leave out? We must, as we always must, take out collective hats off to the memory of Jimmy Miller, the producer who was there all the way through The Stones imperial period, before he succumbed to the devil's temptations. It was he who brought the magic out of them. We should also nod at the great Bill Wyman. Listen to his playing on Brown Sugar or behind the extended solos in Cant You Hear Me Knocking; he might have made the odd error in judgement when it came to matters matrimonial but he never put a foot wrong with a bass guitar around his neck.

Sticky Fingers was the bands first album on their own Rolling Stones Record label and it presented the band for a new decade, at the top of the heap, nigh-on untouchable. It set in place the blueprint they're still working off. They continue to dine out, at restaurants that the rest of us wouldn't even be allowed to walk past, on the work they did here, and please god they'll be coming back to an enormodome near you sometime soon to play most of it before they finally hang up their hats. Yes, I prefer what they did next, because Exile On Main St is the greatest record ever made and I'll be back next year to tell you all about it, but Sticky Fingers is right up there beside it. One more time. Yeah, Yeah YEAH! WHOO!

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If you want more Sticky Fingers - and why wouldn't you - then let me recommend the great Will Russell's poetic analysis. I apologise to him for tramping over ground he's already covered so well, but sure I couldn't help myself, and I know he knows what I mean. I would also like to thank Dr David Fanning for allowing me to forge several of these notions in the crucible of spoof on his radio show.

Continue reading here:
That Demon Life: The Rolling Stones And Sticky Fingers - hotpress.com

Although at the beginning it may have seemed easily passable, COVID-19 has significantly impacted our daily lives, and almost every industry has been affected since when it hit the whole world.

Drastic changes have taken place within the education sector due to the virus, causing, among others, many implications in the teaching process, Erudera.com reports.

As there are a bunch of things that remain unknown about COVID-19, including its source, experts at many universities and colleges across the world have gathered to find more about the virus, which has already taken millions of lives.

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There are numerous studies carried out by several internationally well-known universities, several vaccines have been developed, and many countries of the world have already started mass vaccination campaigns.

A total of 217,432 publications and 1,068,470 citations have already been published, and Erudera.com has prepared a list with universities that carried out research about COVID-19.

Harvard University tops the list of universities researching COVID-19 until March 2021, as during this period of time, it has been working on thousands of studies.

In an effort to discover more about the invisible virus, the university has carried out a total of 2,216 scientific pieces of research. In addition, a group of Harvard University researchers has found that an increase of 1ug/m3 in average PM2.5 exposure caused the immortality rate of COVID-19 to rise by 11 percent.

Just behind Harvard stands the Huazhong University of Science and Technology, with a total of 1,240 study publications related to COVID-19. The university is located in Wuhan, China, which is reported to be the center of the outbreak of the deadly virus. Regarding the origins of the virus, many scientists have been working with the Chinese city of Wuhan during the past year.

One of the best universities in the world, the University of Oxford has worked in 1,131 publications about COVID-19. Oxford Universitys oncologists, along with their colleagues from the University of Leeds, the University of Birmingham, have launched the worlds first cancer Coronavirus registry.

Furthermore, scientists from the University of Oxford have also created rapid testing technology, developed especially for COVID-19. The University of Oxford has also collaborated with the British-Swedish company AstraZeneca to develop and test the ChAdOx1 nCoV-19 or AZD1222 COVID-19 vaccine.

Fourth on our list is the Boston Childrens Hospital with 1127 COVID-19 publications. Located in Boston, Boston Childrens Hospital is focused on improving and advancing the well-being of children worldwide.

Most recently, 1,695 patients younger than 21 years with COVID-19 were studied by researchers at Boston Childrens Hospital placed at 61 hospitals, and the study found out that 36 percent of them had MIS-C, from March 15 to December 15, 2020., whereas 22 percent of patients at 52 hospitals needed neurologic involvement.

The private research university in Baltimore, Maryland, Johns Hopkins University, has worked in 1,029 COVID-19 types of research, including: An interactive web-based dashboard to track COVID-19 in real-time The Incubation Period of Coronavirus Disease 2019 (COVID-19) From Publicly Reported Confirmed Cases: Estimation and Application, and more.

Amongst others, researchers at Johns Hopkins have collaborated with the University of Pennsylvania for a new study which has used computer modeling, suggesting that eviction bans authorized during pandemic have reduced the infection, protecting this way the entire community from spreading infection.

The fifth on the list is the University of Toronto, which has so far worked on 975 studies in total. Earlier, it was reported that two researchers from the University of Toronto would receive federal funding to help the country advance its capacity to deal with health emergencies such as COVID-19 through the Emerging Infectious Diseases Modelling Initiative.

University College London has carried out a total of 970 COVID-19 publications. The latter has also joined a national move coordinated by the University of Cambridge to analyze the genetic code of COVID-19, which has gathered the UKs National Health Service (NHS), Public Health Agencies, the Wellcome Sanger Institute, universities across the country, and provided them with a tool to fight the virus.

Stanford University has completed 884 publications related to COVID-19. Back in October, Stanford Medicine scientists notified about the Community Alliance to Test Coronavirus at Home (CATCH), which they said would help in researching where and how the virus is spreading in order to assist in particular those communities which do not have access to the traditional testing.

The university has carried 853 various publications about COVID-19. Universitys researchers have collaborated with researchers from other universities, most recently with Johns Hopkins University researchers.

Yale University has already published 832 research papers regarding the disease. Moreover, a large study carried out by Yale University on the safety of child care during COVID-19 found out that there is no association between childcare and Coronavirus spread.

Originally posted here:
World's Top Universities & Institutions Which Conducted Most COVID-19 Research So Far - Collegenews.org

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The greatest risk inequitably enforced in this country is the most essential: general well-being. It is allowable, under our present systems, for trans people, for women, for Black women in particular, for poor people, for fat people, for the mentally ill, for the chronically ill and disabled, all to have worse health outcomesthese things are accepted and narrated to us by powerful institutions as an unfortunate but inescapable fact of medicine. And in doing so, they reiterate that these people are of lesser value, and are in fact inconvenient. These people are a burden, and so they should be grateful for what they get.

There was a hope among some at the very early start of the pandemic that, as horrific as it was going to be, it might force people with privilege to see how inextricably all of our lives are intertwined, how the health of one person isnt just their health but yours, too. We had to learn to wear masks not to protect ourselves but to protect others. Those with money suffered inconvenience at the very least from the fact that the people who serve and enable their lifestyles had no access to health care, to childcare, to workplace protections, to a real, functioning social safety netto any of the things that would allow them to stay home when sick, instead of risking a widespread infection to pack boxes for Amazon.

It would be impossible, as well as wholly undesirable, to avoid risk entirely in medical enterprise. Medicine is science, and science is experimentation, and experimentation can only happen if we take risks. And theres just no such thing as a risk-free existence. Aversion to risk in some contexts contributed to the inequities were dealing with today: In the 1970s, the FDA decided women of childbearing age shouldnt participate in clinical trials, out of concern not for the participants themselves but for possible future fetuses. As a result, it became the norm for new medicine to be developed exclusively on men; eight of the 10 prescription drugs withdrawn from the market between 1997 and 2000 posed greater health risks for women than for men.

The problem arises when a constitutionally unequal system assumes that the calculus by which we accept risk is neutral, rather than critically analyzing not just how research and regulatory decisions are made but how services are both distributed and received. A medical establishment predicated on the acceptance of profit-driven health care will inevitably favor the wealthy and the powerful, at the expense of everyone else.

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Blood Clots, Birth Control, and the Johnson & Johnson Vaccine: What We Mean by Medical Risk - The New Republic

Introduction

SARS-CoV-2 is the virus responsible for the COVID-19 pandemic and its damaging effects on both health and economics worldwide. Transmission and pathology of the virus appears to be mediated through the respiratory system via interaction of the viral spike protein with the ACE-2 receptor13 differentially presented on various cells within the respiratory system.4,5 Expression of ACE-2 has been reported on lung alveolar epithelial cells, enterocytes of the small intestine, circulatory endothelial cells, arterial smooth muscle cells,6 adipose tissue, bone marrow, duodenum, endometrium, heart, kidney, testis, and thyroid7 suggesting a potential direct effect of COVID-19 on those tissues. Additionally, infection with COVID-19 has been associated with significant liver injuries and altered liver function tests.8

Alterations in liver function have been attributed to secondary effects of cytokine cascade, hypoxia, underlying liver disease,911 or infection of ACE-2 positive cholangiocytes.12 There have also been reports of coronavirus particles in hepatocytes without a defined mechanism for infection.13

In a recent report studying the receptome of spike binding, ACE-2 was confirmed as the primary receptor for the spike protein via the binding domain (RBD) on the spike 1 portion of the molecule and the N-terminal-domain as the sites critical for virushost interaction.14 Additionally, the report described binding of the spike protein with ectopically expressed ASGR1 and KREMEN1 in transfected non-liver cells. The results strongly suggested the existence of additional entry points into cells for the SARS-CoV-2 virus via the spike protein. Differences in primary infection sites and clinical manifestations of SARS-CoV and SARS-CoV-2, both utilizing ACE-2 as the primary site of cellular infection, suggested that other cellular receptors may be involved in SARS-CoV-2 host interactions.14

E12 TERT-immortalized multi-lineage progenitor cells (MLPC) derived from human umbilical cord blood have been differentiated into immortalized AT2-like cells (AT2) (manuscript submitted) and fused directly with primary human hepatocytes to create immortalized hepatocyte-like cells (HLC).15 The resultant E12 AT2-like cells expressed the characteristics of small airway epithelial cells associated with alveolar type 2 cells and not alveolar type 1 cells. The E12/PHH fusion cells (HLC) expressed the characteristics of fully mature and highly differentiated hepatocytes.15

This report studied the interactions of the SARS-CoV-2 spike protein with potential receptors on human cord blood-derived MLPC differentiated AT2, HLC and primary human hepatocytes (PHH) by confocal analysis. The characteristics of spike protein binding were examined using biotinylated spike proteins and blockade of binding by un-labeled spike proteins, spike protein-directed neutralizing antibodies and an antibody directed against the hepatocyte surface membrane asialoglycoprotein receptor 1 (ASGr1). The results suggested that binding and inhibition analyses can be used to assess the potential mechanisms of viral host cell interactions with a myriad of different target cells in the body, but also to assess therapeutics designed to inhibit that binding.

Immortalized AT2 and HLC could provide accurate and reproducible tools to study the differential virushost interactions between these targets of COVID-19 infection and aid in the development of therapeutics designed to inhibit binding and infection by the SARS-CoV-2 virus. In addition, the potential binding of spike protein to the ASGr1 on hepatocytes suggested a mechanism of viral entry via the clathrin-coated pit receptor-mediated pathway and direct injury to the liver.16,17

MLPC are multi-potent non-hematopoietic stem cells isolated from human umbilical cord blood.15 Umbilical cord blood was collected as part of an FDA submission to market PrepaCyte-CB, a product to de-bulk cord blood for cryo-banking and transplantation. IRB approval of the studies was conducted by the University of Minnesota, the Saint Louis Cord Blood Bank and by Quorum Review Protocol #800, March 3, 2005. The cord blood samples were collected by the American Red Cross Cord Blood Program (Saint Paul, Minnesota) and Ridgeview Medical Center (Waconia, MN). Donations were collected with donor consent for research use only.

Briefly, isolated leukocytes were incubated overnight in MSCGM (PT-4105, Lonza, Walkerville, MD) after which non-adherent cells were removed. Cells were cultured in MSCGM until 8090% of cells had a fibroblastic morphology. These cells were transfected with the gene for TERT, as previously described15 and were cloned by limited dilution. The E12 clone was selected for both immortality and differentiating potential. The E12 MLPC, expanded and cryopreserved for over 14 years, were used as undifferentiated control cells and as the source of cells for the development of the AT2-like cells and the fusion partner in the development of MLPC/hepatocyte hybrid cells.15 For confocal analysis, E12 cells (106/mL in MSCGM, 200 L per well) were plated in non-coated 16 well chamber slides (Nalge, Nunc International, Rochester, NY) and allowed to attach overnight before use in the analysis.

AT2-like cells were developed from the differentiation of E12 MLPC. Briefly, E12 cells (3 x 105 cells/mL) in MSCGM were added to non-coated tissue culture vessels and allowed to attach overnight. Medium was then exchanged with SAGM (SAGM, Lonza, Walkerville, MD, cat # 3118) and allowed to culture for 814 days with 3 medium changes per week. Upon achieving 70% confluence, cells were harvested by treatment with Tryp-LE (12605028, Life Technologies, Grand Island, NY) allowed to dissociate from the culture vessel and used for confocal analysis, as a positive control for binding spike proteins and ACE-2 expression. Cells (106/mL in SAGM, 200 L per well) were plated in non-coated 16 well chamber slides and allowed to adhere overnight prior to confocal analysis.

Hepatocyte-like fusion cells were created by the fusion of E12 MLPC with primary human hepatocytes, as previously described.15 Equal numbers of E12 MLPC and primary hepatocytes were fused using 50% polyethylene glycol in RMPI + 0.01% EDTA. Resultant cells were plated into collagen-coated 75 cm2 tissue culture flasks and were cultured for 7 days in RPMI + 20% FBS. After 7 days, non-fused PHH were no longer viable and did not contribute to the HLC cell lines. HLC were examined for hepatocyte-specific markers including albumin and urea production. HLC were demonstrated to express markers and production consistent with fully mature and well-differentiated hepatocytes. HLC (106/mL in hepatocyte expansion medium, 200 L per well) were plated in collagen-coated 16 well chamber slides and were allowed to adhere overnight prior to confocal analysis. Hepatocyte expansion medium consisted of Williams Medium E supplemented with 2% fatty acid-free BSA (Sigma, A7030), 1% ITS solution (Lonza, 17838Z), 5mM hydrocortisone 21-hemisuccinate (Sigma, H2270) and glutamax (35050, Gibco) supplemented with FGF basic (20 ng/mL) (233-FB), FGF-4 (20 ng/mL) (7460-F4), HFG (40 ng/mL) (294-HG), SCF (40 ng/mL) (255-SC), Oncostatin M (20 ng/mL) (295-OM), BMP-4 (20 ng/mL) (314-BP), EGF (40 ng/mL) (236-EG) and IL-1 (20 ng/mL)(201-LB) all from R&D Systems (Minneapolis, MN).

Cryo-preserved primary human hepatocytes and media were obtained from Zenotech (Kansas City, KS). Cells were thawed with OptiThaw medium and enumerated with OptiCount medium in a standard hemacytometer. Hepatocytes were diluted to a final concentration of 106 cells/mL of OptiPlate medium and were plated in collagen-coated 16 well chamber slides at 200 L per well. After 4 hours of plating, the medium was changed to OptiCulture medium to allow overnight attachment and spread of cells prior to confocal analysis.

Cells were prepared for staining with antibodies and binding of spike proteins by fixing the cells in 1% formaldehyde for 1 hour. Cells were then washed x 2 with PermaCyte permeabilization medium (WBP-1000, CMDG, St. Paul, MN). All staining took place in the presence of PermaCyte. Cells were incubated with an unlabeled primary antibody (100 ng) for 30 minutes at room temperature. ACE-2 (labeled with alexa 594, FAB9332T), albumin (MAB1456) and asialoglycoprotein receptor 1 (MAB4394) antibodies were obtained from R&D Systems (Minneapolis, MN). Unbound antibody was removed by washing with PermaCyte and the cells were counterstained with a secondary antibody specific for mouse (A-11005) antibody labelled with Alexa 594 dye (Life Technologies, (Eugene, OR)). Marker expression was confirmed by positive staining when compared to cells stained with antibody isotype controls (QTC1000, CMDG, St. Paul, MN). The nuclei of the cells were visualized by staining with DAPI.

The binding of SARS-CoV-2 spike and spike 1 proteins was analyzed by confocal microscopy using biotinylated spike proteins. Cells were prepared as described above. Cells were labelled with 250 ng of either biotinylated spike (RBD) (SPD-C8E9, ACROBiosystems, Newark, DE) or biotinylated spike 1 protein (SIN-C82E8, ACROBiosystems) for 30 minutes. Unbound spike proteins were removed by washing cells twice with PermaCyte medium. Bound spike proteins were visualized by secondary staining with streptavidin-alexa 594 (S11227 Life Technologies). Cells were counterstained with DAPI to visualize the nuclei.

Specificity of biotinylated spike proteins binding to the cells was confirmed by blockade of binding by a 5 molar excess of unlabeled spike protein. Cells were prepared as per the confocal analysis of antibody binding. Cells were incubated with 1.25 g of unlabeled spike protein (ACROBiosystems, SPD-S52H6) or spike 1 protein (ACROBiosystems, S1N-C52H3) for 1 hour. Without washing the unbound unlabeled spike protein, biotinylated spike and spike 1 proteins were added to the cells and incubated for 30 minutes. Cells were washed twice with PermaCyte medium to remove any unbound proteins. Bound biotinylated spike proteins were observed by secondary labeling with streptavidin-alexa 594. Cells were counterstained with DAPI to visualize the nucleus.

The effects of antibodies on the binding of the spike proteins to the cells were examined using two commercially available neutralizing antibodies obtained from ACROBiosystems (SAD-S35) and Novatein Biosystems (PR-nCOV-mABS1, Boston, MA) and the ASGr1-specific antibody (R&D Systems). One g of either neutralizing antibody was preincubated with the spike protein for one hour prior to the addition of the mixture to the cells prepared as described for binding of the spike proteins. The ASGr1 antibody (300 ng) was preincubated with cells prior to the addition of the spike protein. Visualization of the binding of biotinylated spike protein was accomplished by secondary staining with streptavidin-alexa 594. The nuclei of the cells were visualized with DAPI.

Cells were analyzed on the Olympus Fluoview 1000 confocal microscope. The confocal images in Figures 14 are representative of at least 3 studies done on different days.

Figure 1 Biotinylated spike and spike 1 protein binding to E12 differentiated AT2-like cells and inhibition by unlabeled spike protein and neutralizing antibodies. Bound biotinylated spike proteins were visualized by sequential labeling with streptavidin-alexa 594. Cells positive for binding are shown by red fluorescence. Blue nuclei were visualized by counterstaining with DAPI. (A) Binding of biotinylated spike protein (containing RBD). (B) Inhibition of biotinylated spike protein binding by co-incubation with a 5 molar excess of unlabeled spike protein (RBD). (C) Binding of spike 1 protein. (D) Inhibition of biotinylated spike protein binding by preincubation with a neutralizing antibody from ACROBiosystems. (E) Lack of binding inhibition by neutralizing antibody from Novatein Bio. (F) Inhibition of biotinylated spike 1 binding by unlabeled spike (RBD) protein.

Abbreviation: RBD, receptor-binding domain.

Figure 2 Expression of ACE-2, ASGr1 and serum albumin. Undifferentiated E12 MLPC data are shown in (AD). E12 HLC fusion cell results are presented in (EH). Primary human hepatocytes (PHH) are shown in (IL). Cells were incubated with unlabeled primary antibody and sequentially stained with secondary antibody labeled with alexa-594. Positive binding is shown by red fluorescence. Blue nuclei were visualized by DAPI counterstaining. Figures (A, E and I) were stained with isotype control antibodies. Figures (B, F and J) were stained with antibody specific for ACE-2. Figures (C, G and K) were stained with antibody specific for the asialoglycoprotein receptor 1 (ASGr1). Figures (D, H and L) were stained with antibody specific for serum albumin.

Figure 3 Undifferentiated E12 MLPC confocal microscopy is shown in (AD). E12 HLC fusion cell data are presented in (E-H). Primary human hepatocytes (PHH) are shown in (IL). Positive binding is indicated by red fluorescence. Blue nuclei were visualized with DAPI counterstaining. Figures (A, E and I) were labeled with Sav-594. Figures (B, F and J) were labeled with biotinylated spike protein followed by sequential staining with streptavidin-alexa 594. Figures (C, G and K) were labeled with biotinylated spike 1 protein followed by sequential staining with streptavidin-alexa 594. Figures (D, H and L) biotinylated spike protein binding was blocked by a 5 molar excess of unlabeled spike protein (RBD) followed by sequential staining with streptavidin-alexa 594.

Figure 4 Inhibition of biotinylated spike binding by neutralizing antibodies to spike 1, spike and ASGr1. E12 HLC fusion cell data are shown in (AD). Primary human hepatocytes (PHH) are shown in (EH). Positive binding of biotinylated spike proteins is shown by red fluorescence. Blue nuclei are visualized by counterstaining with DAPI. Figures (A and E) confocals show the inability of a 5 molar excess of unlabeled spike 1 protein to block the binding of biotinylated spike protein. Figures (B and F) show inhibition of binding of biotinylated spike protein by neutralizing antibody from ACROBiosystems. Figures (C and G) show binding inhibition of biotinylated spike protein by neutralizing antibody from Novatein Bio. Figures (D and H) demonstrate inhibition of any detectable binding of biotinylated spike protein by antibody specific for the hepatocyte membrane ASGr1.

In a parallel study that surveyed the differentiation of E12 MLPC to AT2-like cells, it was demonstrated that AT2-like cells were positive for markers associated with AT2 cells (surfactant protein C, ACE2, TM4SF1, HT2-280), negative for markers associated with AT1 cells (AGER, caveolin 1 and aquaporin) and positive for markers not unique to AT2 cells but known to be expressed on AT2 cells (CK19, CD26 and EpCAM). These results were identical to primary small airway epithelial cells. Both cell types were also shown to bind spike and spike 1 proteins. Biotinylated spike proteins could be blocked by unlabeled spike protein (RBD). Pre-incubation with neutralizing antibodies prevented the binding of biotinylated spike protein by the ACROBiosystems neutralizing antibody, but not the Novatein antibody. Expressions of ACE-2, spike protein binding and inhibition were repeated for this study to confirm the involvement of the ACE-2 receptor (Figure 1).

The expressions of ACE-2, ASGr1 and albumin in control E12 MLPC, HLC and PHH were studied by antibody staining. E12 MLPC were shown to be negative for ACE-2, ASGr1 and albumin expression. In contrast, ASGr1 and albumin were shown to be strongly expressed by both HLC and PHH. ACE-2 was not detectible in either cell type (Figure 2).

The ability of E12 MLPC, HLC and PHH to bind spike and spike 1 proteins was studied using biotinylated spike proteins. E12 MLPC were unable to bind either spike or spike 1 proteins. HLC and PHH were able to bind spike protein but not spike 1 protein. The binding of biotinylated spike protein could be blocked by pre-incubation with unlabeled spike protein (Figure 3). The binding of biotinylated spike protein could not be blocked by spike 1, but could be blocked by ACROBiosystems and Novatein neutralizing antibodies and also an antibody directed against the ASGr1 (Figure 4).

It is critical to elucidate the mechanisms of virus/host interactions of the SARS-CoV-2 for the development of therapeutics designed to inhibit the binding and internalization of the virus to a myriad of cell types. The overarching strategy for the development of vaccines or therapeutics has involved the interaction between the S1 portion of the viral spike protein and the ACE-2 cellular receptor found in the respiratory tract and in various other tissues.47 Differences in transmission, pathology and organ involvement between SARS-CoV and SARS-CoV-2 (both dependent upon ACE-2 binding) suggested that additional receptors may contribute to the attachment and internalization of the SARS-CoV-2 virus14 in both the respiratory lungs and other organ systems.

The potential infection of tissues that are ACE-2 negative has spurred the search for additional receptor interactions of the spike protein. Some of these potential spike protein receptor targets include neuropilin-1,18 ASGR1 and KREMEN1.14 The observation of SARS-CoV-2 particles in hepatocytes8 and the robust expression of ASGr1 receptors and neuropilin-1 on hepatocytes suggested that altered liver function associated with COVID-19 infection may be directly caused by infection with the virus and mediated by binding to one or both receptors.

We investigated the potential virus: receptor interactions via the spike protein using fluorescent confocal microscopy and biotinylated spike (RBD) and spike 1 proteins. In a parallel study, E12 MLPC were differentiated to AT2-like cells (manuscript submitted). These cells expressed markers associated with AT2 cells (surfactant protein C, ACE2, TM4SF1, HT2-280), negative for markers associated with AT1 cells (AGER, caveolin 1 and aquaporin) and positive for markers not unique to AT2 cells but known to be expressed on AT2 cells (CK19, CD26 and EpCAM). These results were identical to primary small airway epithelial cells. The binding of biotinylated spike proteins and specific blocking by unlabeled protein and neutralizing antibodies confirmed that the primary interaction of spike protein with AT2-like cells and primary small airway epithelial cells was via the S1 portion of the protein with the ACE-2 receptor. We repeated those studies in support of our findings with the HLC and PHH. The differential inhibition of spike protein binding with two different antibodies suggested that viral neutralization could result from mechanisms other than direct inhibition of S1 (RBD) binding to ACE-2.

The characteristics of SARS-CoV-2 interactions with hepatocytes were studied by observing the binding of biotinylated spike (RBD) and spike 1 proteins to HLC and PHH using the undifferentiated E12 as a known negative control. It was observed that HLC and PHH were both negative for ACE-2, precluding that as a potential site of viral binding. This was confirmed by the inability of the cells to bind S1 protein. The binding of biotinylated spike protein and blockade by unlabeled spike protein on HLC and PHH suggested that the binding was specific, and via a mechanism distinct from ACE-2. The complete inhibition of spike binding by an antibody directed against the ASGr1 is strongly suggestive that ASGr1 is a binding site for the spike protein on hepatocytes. Interestingly, blockade of spike binding by both neutralizing antibodies on HLC and PHH was distinct from AT2 cells where inhibition occurred solely with the antibody that was directed against the RBD. This is suggestive of neutralizing activity that can occur outside the RBD.

Utilization of multiple cell types to study the interactions of spike protein binding will help identify additional receptor pathways for infection with COVID-19. They could also provide a powerful tool to aid in the development of therapeutics against multiple sites on the spike protein or receptors of the host cells. With the existent emergence of new variants and mutations of the SARS-CoV-2 exhibiting enhanced transmissibility, it is especially important to expand our repertoire of cellular models to investigate the effects of the mutations on the binding characteristics of the virus to host cells. The availability of immortalized cells with the stable characteristics of human alveolar type 2 cells and mature well-differentiated hepatocytes could provide an accurate and reproducible tool to effectively study the various virushost interactions via spike proteins by providing potential viral receptors that are segregated according to cell type. We believe that AT2 and HLC provide such a tool.

Dr Daniel P Collins reports personal fees from BioE, LLC, during the conduct of the study. In addition, Dr Daniel P Collins has a patent Composition for an in vitro culture medium to maintain and expand stem cell-derived hepatocyte-like cells pending, as well as,a patent Methods to develop immortalized hybrid hepatocyte-like cells, also pending. The authors report no other conflicts of interest in this work.

1. Shang J, Wan Y, Luo C, et al. Cell entry mechanisms of SARS-CoV-2. Proc Natl Acad Sci USA. 2020;117(21):1172711734. doi:10.1073/pnas.2003138117

2. Lan J, Ge J, Yu J, et al. Structure of the SARS-CoV-2 spike receptor-binding domain bound to the ACE2 receptor. Nature. 2020;581(7807):215220. doi:10.1038/s41586-020-2180-5

3. Premkumar L, Segovia-Chumbez B, Jadi R, et al. The receptor-binding domain of the viral spike protein is an immunodominant and highly specific target of antibodies in SARS-CoV-2 patients. Sci Immunol. 2020;5(48):eabc8413. doi:10.1126/sciimmunol.abc8413

4. Hikmet F, Mar L, Edvinsson , et al. The protein expression profile of ACE2 in human tissues. Mol Sys Biol. 2020;16(7):e9610. doi:10.15252/msb.20209610

5. Sungnak W, Huang N, Bcavin C, et al. SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes. Nat Med. 2020;26(5):681687. doi:10.1038/s41591-020-0868-6

6. Hamming I, Timens W, Bulthuis MLC, Lely AT, Navis GJ, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS corona virus. A first step in understanding SARS pathogenesis. J Pathol. 2004;203(2):631637. doi:10.1002/path.1570

7. Wang D, Eraslan B, Weiland T, et al. A deep proteome and transcriptome abundance atlas of 29 healthy human tissues. Mol Syst Biol. 2019;15(2):e8503. doi:10.15252/msb.20188503

8. Wang Y, Liu S, Liu H, et al. SARS-CoV-2 infection of the liver directly contributes to hepatic impairment in patients with COVID-19. J Hepatol. 2020;73(4):807816. doi:10.1016/jhep.2020.05.002

9. Desai N, Neyaz A, Szabolcs A, et al. Temporal and spatial heterogeneity of host response to SARS-CoV pulmonary infection. Nat Comm. 2020;11(1):6319. doi:10.1038/s41467-020-20139-7

10. Mehta P, McAuley DF, Brown M, et al. COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet. 2020;395(10229):10331034. doi:10.1016/S0140-6736(20)30628-0

11. Chu H, Chan JF, Wang Y, et al. Comparative replication and immune activation profiles of SARS-CoV-2 and SARS-CoV in human lungs: an ex vivo study with implications for the pathogenesis of COVID-19. Clin Infect Dis. 2020;71(6):14001409. doi:10.1093/cid/ciaa410

12. Chai X, Hu L, Zhang Y, et al. Specific ACE2 expression in cholangiocytes may cause liver damage after 2019-nCoV infection. bioRxiv. 2020. doi:10.1107/2020.02.03.931/766

13. Lozano-Sepulveda SA, Galan-Huerta K, Martnez-Acua N, Arellanos-Soto D, Rivas-Estilla AM. SARS-CoV-2 another kind of liver aggressor, how does it do that? Ann Hepatol. 2020;19(6):592596. doi:10.1016/j.aohep.2020.08.062

14. Gu Y, Cao J, Zhang X, et al. Interaction network of SARS-CoV-2 with host receptome through spike protein. bioRxiv. 2020. doi:10.1101/2020.09.09.28/508

15. Collins DP, Hapke JH, Aravalli RN, Steer CJ. Development of immortalized human hepatocyte-like hybrid cells by fusion of multi-lineage progenitor cells with primary hepatocytes. PLoS One. 2020;15(6):e234002. doi:10.1371/journal.pone.0234002

16. DSouza AA, Devarajan PV. Asialoglycoprotein receptor mediated hepatocyte targeting strategies and applications. J Control Release. 2015;203:126139. doi:10.1016/j.jconrel.2015.02.022

17. Huang X, Leroux JC, Castagner B. Well-defined multivalent ligands for hepatocytes targeting via asialoglycoprotein receptor. Bioconjug Chem. 2017;28(2):283295. doi:10.1021/acs.bioconjchem.6b00651

18. Daly JL, Simonetti B, Klein K, et al. Neuropilin-1 is a host factor for SARS-CoV-2 infection. Science. 2020;370:861865. doi:10.1126/science.abd3072

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[Full text] Binding of the SARS-CoV-2 Spike Protein | HMER - Dove Medical Press

Mushrooms indicated by cancer type

Reishi mushroom, scientifically known as Ganoderma lucidum or Ganoderma sinense, has been commonly known as the mushroom of longevity or immortality. Out of all of the different types of mushrooms, reishi mushrooms seem to be the most widely used mushrooms for cancer prevention and to inhibit tumor growth. Mushrooms play a role in boosting the immune system and brain function.

Reishi has been used medicinally in East Asia since ancient times. It is a traditional medicine used throughout Asia for cancer prevention.

Reishi mushrooms were outed to prolong life, prevent aging and increase energy. In China, mushrooms are used to fortify theimmune systemofpeople with cancer who receivechemotherapyorradiation therapy.

These mushrooms are known as reishi In Japan. In China,G. lucidumis known as chizhi andG. sinenseis known as zizhi.

Different types of mushrooms that are effective against different types of cancer are listed below.

Table 1. Medicinal mushrooms indicated by cancer types

What are medicinal mushrooms?

Medicinal mushrooms are mushrooms that are used as medicines. They are mainly used in the treatment of

Reported benefits of medicinal mushrooms include

In Japan and China, mushrooms have been used safely for a long time, either alone or in combination with chemotherapy or radiotherapy. There are more than 100 types of mushrooms used to treat cancer. The most common ones include

Research has been conducted to determine the antitumor activity of mushrooms and mushroom extracts.

Some of the traditionally used mushroom species include

Why people with cancer use medicinal mushrooms

Medicinal mushrooms contain several biologically active compounds that are effective against the development of cancer cells. They contain a class of polysaccharides known as beta-glucans. Beta-glucans have shown anti-cancer activity.

Who should not take medicinal mushrooms?

Medicinal mushrooms are not approved by the U.S. Food and Drug Administration (FDA) because they come under the category of dietary supplements. Hence, take mushrooms at your risk. You shouldnt take medicinal mushrooms if

What are the risks of taking medicinal mushrooms?

Generally, mushrooms are considered safe to include in your daily diet. However, there have been reports of side effects with medicinal mushrooms. These include

A few types of mushrooms may cause hallucinations because of the content of psilocybin. It is important to differentiate psychogenic, medicinal and poisonous mushrooms before you consume them.

Medically Reviewed on 4/6/2021

References

National Cancer Institute

Memorial Sloan Kettering Cancer Center

Oncotarget

Fungal Diversity

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What Is the Best Mushroom to Fight Cancer? - MedicineNet

A trained medical doctor, Dr Gindi models her three-dimensional figures by revealing the multiple levels of infinity inherent in our existence. She is an Art Salon 2021 finalist for her recent work Transfigured Immortality. Dr Gindi is living and working in Switzerland.

1. What inspired you to work as sculptor as you were associated with the medical field?

I was educated as medical doctor. The more time I spent working as physician, the more I wanted to create art to reflect on what I was experiencing, particularly the essence of physical fragility. I learned that our preconscious and unconscious desires are buried deep below the surface. Connecting human anatomy with the anachronism of the human psyche became the lexicon of my work and the monad of me as a sculptor I am a sculptor dedicated to model the infinity of our existence.

As a sculptor, I want to break free from the constraints of the rational mind. Educated in classic sculpting two decades after my initial foray into medicine I now oscillate between references in the material world and the intended depth of universal oblivion.

2. Does your training as a medical doctor helped you as a sculptor?

My training as a medical doctor and study of human anatomy might have led to higher levels of purity in my sculptures. The inner elements that impart authenticity are almost naturally evolving into morphological structures. As a result, my works do not represent the depiction of lifeless specimens; rather I aspire to explore the essence of the way we are.

The human is always in the centre of my creative musings I revel in the physical aspect of humanity, but also in the psyche of the fleshy nature. The finer elements that impart authenticity are almost naturally accomplished and thus compelling in and of themselves. As an artist, I then apply the intertwined processes that create both human subjects and human objects.

3. Could you describe your style of work?

Sculpture is a world of three-dimensional media enabling to step into the viewers world in a very direct and physical way. When you witness sculpture, you dont just experience it from one perspective, you view it from multiple angles like a thousand compositions mould into one, you also relate to it differently. It is probably one of the oldest art forms to exist, rooting itself as a widespread practice even in the ancient Nile Valley Civilisation. In ancient times, sculptures played a significant part in documenting life.

Talking about my own style, I start to work with pieces of clay. I am going to form the first contours, put further bits of clay on, the figure grows in front of my eyes. This process is mostly intuitive. The bend of a bone, the edge of a drape, the texture of a surface.

Very much depending on the mood for the day. It rarely happens that the first touch becomes the finished sculpture. I know that I and my sculpture are going to transform during this whole process, but I just start somehow, somewhere. As paradoxical it may sound: I am not making the sculpture, the sculpture makes itself and surprises me, with blazing intensity.

4. Why do you favor bronze in your sculptures?

I currently mostly work with bronze, starting with the anatomical modelling of the subject in clay. I choose bronze for its perenniality and its vibrational traits, as well as its ability to lock and reveal placed ardour. There is something intrinsically sensual about bronze, especially the alloy.

You can touch the skin of your sculptures, it is part of you and it embodies and imbues the personality and lustre of the spectator. Bronze has an eerie element of perseverance it can last for thousands of years and ages gracefully, acquiring with time a variety of finishes due to the intensity of the patina and how it interacts with the environment. The alchemy of patination symbolizes the very transient nature of being.

5. What were your idea behind exploring infinity?

I have been interested in creative expressions in one form or another for as long as I can remember. While infinity caught my imagination even during my younger years, I began dwelling upon it deeply as a freshwoman in medical school.

We are all bound together by the human question of origin and destiny. Over the years, my experience in both science and life has taught me that our existence and options are infinite if we allow them to be. Submitting to fate and having a sense of resignation can often be the norm, but if we can metamorphosize these attitudes, we will be able to model the infinity of our existence.

Transfigured Immortality is a current work that explores an area that is on the periphery of infinity. It is one that most humans, since antiquity, will no doubt have pondered upon of bequeathing a legacy. It depicts a female pharaonic character in the prime of her life, leaning on her last place of rest. Anticipating her death, she is shaping the future with a sense of purpose.

This piece originated in a phase of mourning after the death of a close Egyptian relative. I wanted to explore the essence of infinity omnipresent in ancient Egyptian mythology. Death is not the end of life but rather the assumption of a different dimension. By realizing and grasping the ultimate infinity inherent with our own life we can live fearlessly and vigorously.

Readers can communicate with Dr Gindi through http://www.dr-gindi.com or Instragram @gindisculptor

Published April 7th, 2021

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Sculptor Dr Gindi: I Revel in the Physical Aspect of Humanity, but also in the Psyche of the Fleshy Nature - Influencive

Easter celebrates the Christian belief that Jesus Christ rose from the dead. In so doing, he overcame sin and death on behalf of all of us. The resurrection of Jesus was a guarantee that, for those who believed in him, they too would do the same. As St. Paul put it, He who raised Christ from the dead will give life to your mortal bodies also.

That said, the resurrected body of Jesus was a very ambiguous one. He ate fish and bread, but he could also pass through closed doors. Similarly, there has always been an uncertainty about the nature of our resurrection bodies.

By the end of the second century, Christianity had absorbed the Greek tradition of the immortality of the soul. From that time on, it viewed the human person as consisting of an immortal soul and a mortal body.

This meant that, immediately after death, the individual soul continued its existence. It also meant at the end of history, the individual body would rise from the dead and be reunited with its soul. God would then judge it as worthy of eternal happiness in heaven or eternal punishment in hell.

Christianity shared with Judaism, Zoroastrianism, and later Islam, a belief in the final resurrection of the body.

Read more: 5 things to know about the traditional Christian doctrine of hell

What will resurrected bodies be like? Saint Augustine in his work The City of God gave us some clues early in the fifth century. They will be physical bodies but animated by an immortal soul. They will appear to be about 30 years old, the age that Christ reached.

Men will arise in male bodies and women in female bodies. But there will be no sexual desire and hence no marriages in heaven. The flesh will serve the spirit and not the reverse as happens in the present life.

Critics then, like critics now, thought it a ridiculous idea and panned it mercilessly. Even though Augustine thought the critics were being frivolous, he attempted to give serious answers to their questions. Will aborted foetuses rise? What size will they be? What will the bodies of monstrous births, the disfigured, and the deformed be like? What will be the fate of those devoured by beasts, consumed by fire, drowned, or eaten by cannibals?

By the 13th century, these questions had become matters of serious philosophical discussion within Christianity and not merely responses to critics of it. Thomas Aquinas, the greatest philosopher of Roman Catholicism, for example, picked up where Augustine left off.

On the day of resurrection, he believed, bodies will have the same gender and the same organs as when they were alive. But they wont have the same uses because there will be no desire to eat, drink, or have sex.

Therefore, there will be no need for food, clothing, transportation, or medicine. There will be no need for heavenly plants nor (pet or meat lovers read no further!) animals. Those in hell would have bodies suitable to their character ugly, sluggish, black, gross, and capable of suffering.

Read more: Friday essay: what might heaven be like?

By the 17th century, the new sciences were adding fresh answers to a key problem. How would all the dispersed bits of people get back together? For example, Robert Boyle, the father of modern chemistry, worried about bodies that were eaten by animals, fish or cannibals.

At least a tiny bit of us, Boyle suggested, will be able to be retrieved from the bodies of animals, sharks, or cannibals enough for God to work with. Moreover, his own chemical experiments on the long-lasting texture of bones assured him they would still be around on resurrection day. In the end, however, he like many others, was forced to fall back on Gods miraculous powers to get all of our bits and pieces back into one piece.

Vast amounts of theological ink were spilt on the attempt to defend what, at the end of the day, was really rationally indefensible. It is no surprise that, as the feasibility of the miraculous disappeared in the 18th century, so rational defences of the resurrection of the physical body disappeared from intellectual history. They were buried in a forgotten and unmarked theological grave.

These days, at least to more liberal Christians, the resurrection of the body remains a matter of faith rather than reason. It is pretty much ignored. The afterlife in general tends to be thought of as the survival of a spirit immediately after death or even only as a brief period of time in the memories of those still alive.

But whatever Christians believe about our resurrection body, they still believe Jesus rose physically, or perhaps spiritually, from the dead. It is a life and a death that continues to influence 2.3 billion people throughout the world.

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How will our bodies be put back together? What about those eaten by cannibals? A brief history of Christian resurrection beliefs - The Conversation AU

The leading candidate for the NY mayoralty is never tired to think outside of the box but inside of reality as presented by research.

In the past, he had been very outspoken about the Nazi-roots of BDS. And many left-wing people were not happy with that.

So, I was much pained that he suddenly seemed open to BDS. But hes now said that he regrets his poor choice of words. And so do I.

Yes, singling out Israel as the only illegitimate nation state is anti-Semitic.

But Im glad hes back. This is important.

Not that we have anything to fear from the US leadership. Pelosi, Biden, and Harris are staunch believers in Jews. Yang really fits their company.

His Israel support isnt axiomatic. Obama too was very smart, knew racism all too well, was surrounded by Jews, but he emerged as an anti-Zionist.

Surprisingly and disturbingly, Yang was a no show at a mayoral candidates event organized by the Yeshiva University Political Action Club on Monday. He has mostly said the right thing about Jewish education (and its not so simple). But, at the end of the day, youve got to come talk with the folks.

We need future President Yang to fancy facts over feelings. Is he back?

MM is a prolific and creative writer and thinker, a daily blog contributor to the TOI. He is a fetal survivor of the pharmaceutical industry (https://diethylstilbestrol.co.uk/studies/des-and-psychological-health/), born in 1953 to two Dutch survivors who met in the largest concentration camp in the Netherlands, Westerbork, and holds a BA in medicine (University of Amsterdam). He taught Re-evaluation Co-counseling, became a social activist, became religious, made Aliyah, and raised three wonderful kids. He wrote an unpublished tome about Jewish Free Will. He's a strict vegan since 2008. He's an Orthodox Jew but not a rabbi. * His most influential teachers (chronologically) are: his parents, Nico (natan) van Zuiden and Betty (beisye) Nieweg, Wim Kan, Mozart, Harvey Jackins, Marshal Rosenberg, Reb Shlomo Carlebach, and, lehavdil bein chayim lechayim: Rabbi Dr. Natan Lopes Cardozo, Rav Zev Leff, and Rav Meir Lubin. * Previously, for decades, he was known to the Jerusalem Post readers as a frequent letter writer. For a couple of years, he wrote hasbara for the Dutch public. His fields of attention now are varied: Psychology (including Sexuality and Abuse), Medicine (including physical immortality), Science (statistics), Politics (Israel, the US and the Netherlands, Activism - more than leftwing or rightwing, he hopes to highlight Truth), Oppression and Liberation (intersectionally, for young people, the elderly, non-Whites, women, workers, Jews, LGBTQIA, foreigners and anyone else who's dehumanized or exploited), Integrity, Philosophy, Jews (Judaism, Zionism, Holocaust and Jewish Liberation), Ecology and Veganism. Sometimes he's misunderstood because he has such a wide vision that never fits any specialist's box. But that's exactly what many love about him. Many of his posts relate to affairs from the news or the Torah Portion of the Week or are new insights that suddenly befell him. * He hopes that his words will inspire and inform, reassure the doubters but make the self-assured doubt more. He strives to bring a fresh perspective rather than bore you with the obvious. He doesn't expect his readers to agree. Rather, original minds must be disputed. In short, his main political positions are: anti-Trumpism, for Zionism, Intersectionality, non-violence, democracy, anti the fake peace process, for original-Orthodoxy, Science, Free Will, anti blaming-the-victim and for down-to-earth optimism. Read his blog how he attempts to bridge any discrepancies. He admits sometimes exaggerating to make a point, which could have him come across as nasty, while in actuality, he's quite a lovely person to interact with. He holds - how Dutch - that a strong opinion doesn't imply intolerance of other views. * His writing has been made possible by an allowance for second-generation Holocaust survivors from the Netherlands. It has been his dream since he was 38 to try to make a difference by teaching through writing. He had three times 9-out-of-10 for Dutch at his high school finals but is spending his days communicating in English and Hebrew - how ironic. G-d must have a fine sense of humor. In case you wonder - yes, he is a bit dyslectic. November 13, 2018, he published his 500th blog post with the ToI. If you're a native English speaker and wonder why you should read from people whose English is only their second language, consider the advantage of having a peek outside of your cultural bubble. * To find his earlier blog posts on a certain subject XXX, among his over 1200 ones, go to the right-top corner of the Times of Israel page, click on the search icon and search "zuiden, XXX". His second daily active less tame blog, to which one may subscribe, one may find here: https://mmvanzuiden.wordpress.com/ or by clicking on the globe icon next to his picture on top. * To send any personal reaction to him, scroll to the top of the blog post and click Contact Me.

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Andrew Yang walks back his walking back of his tough anti-BDS stance - The Times of Israel

INDIANAPOLIS -- Two more days until the Final Four field is set.

Before we take that huge step to the ultimate stage of the season, let's look for a few minutes at the Elite Eight and evaluate how this octet of schools got here. Time for a rank and re-seed. I'm listing the teams based on a combination of tournament performance and team strength. I watched every one of these squads win in the past two days, so some in-person takeaways will be included as well.

It's an assorted group, this Elite Eight. This year marks the first time since 2011 that we won't have a regional final between a No. 1 and No. 2 seed. No. 11 UCLA's upset of No. 2 Alabama secured the 13th upset of this tournament (an upset is defined by the NCAA as a team seeded five spots or worse defeating its opponent). The 2021 Big Dance is now tied with 1985 and 2014 as the most upset-riddled brackets in history. And we've still go three rounds to go -- and three more opportunities in the next two days.

All of these teams have been impressive -- how could you not be when you make it this far? -- but here's how I would rank them heading into Monday evening.

Who they've beaten: No. 16 Norfolk State, No. 8 Oklahoma, No. 5 CreightonWhat I've seen: The best team in college basketball this season -- and in many seasons. It was a joy to watch Gonzaga peacefully pull away, like a stroll through a field, vs. Creighton Sunday afternoon at Hinkle Fieldhouse. (Zags 83, Jays 65.) The Bulldogs have won their first three games by an average of 22.3 points and are showing almost no signs of weakness. Corey Kispert was the team's leading scorer in the first round; Drew Timme has been the most valuable player, and high scorer, the past two. Tuesday night it may well be Jalen Suggs, who is maybe the most irresistible player in terms of watchability in this tournament. Three wins down, three more to go for sports immortality. No. 6 USC should provide Gonzaga's toughest test since December.

Who they've beaten: No. 16 Hartford, No. 9 Wisconsin, No. 5 VillanovaWhat I've seen: A team that's almost completely fallen back into its groove of dominance. The Bears have won their three games by an average of 16.0 points and performed as the fourth-best defensive unit in the tournament, according to BartTorvik.com's metrics. Scott Drew's Bears were down 30-23 at the half vs. Villanova at Hinkle on Saturday -- then outscored Nova 37-21 in the second half and held the Wildcats to one of their worst offensive outputs in tournament play in program history. Against Wisconsin, Baylor had just four turnovers, none of which were of the live-ball variety. Against Nova, just six turnovers. BU's 6.7 turnover average is the lowest of any team still standing. One more win gets the Bears to their first Final Four since 1950, under Bill Henderson.

Who they've beaten: No. 16 Texas Southern, No. 8 LSU, No. 4 Florida StateWhat I've seen: A skillfully coached team that was faded hard by many and predicted to fall prior to the Elite Eight (OK, and the Sweet 16) but has nonetheless averaged 81.3 points without its best player (Isaiah Livers) and separated from all of its opponents by the 10-minute mark of the second half. I almost put Michigan above Baylor, but without Livers I think the seeding needs to still be this way. The Wolverines got buckets at will Sunday at Bankers Life Fieldhouse vs. Florida State. U-M had 15 second-half layups and disassembled FSU's intimidating, long defense to cruise along again. Juwan Howard has pulled off a fabulous coaching job. No school has more NCAA Tournament wins since 2013 than Michigan's 17.

Who they've beaten: No. 11 Drake, No. 3 Kansas, No. 7 OregonWhat I've seen: An overlooked team finally getting its respect. USC has won its three games by 64 points, which is the second-largest aggregate margin of victory by any seed No. 6 or worse in history. Listen, my bracket is sort of a shambles. (Though five out of eight isn't TOO bad.) But the one non-obvious Elite Eight pick I nailed was the same one I've been telling you about in the Power Rankings and on CBS Sports HQ since January: USC is legit, a team I tabbed as a Final Four dark horse months ago. The Trojans elbowed Oregon out of the way early in the first half of Sunday's final tip and never looked back. This team is more than the Mobley Bros., but having them sure does present one mind-meld of a puzzle for opponents. Andy Enfield basically built this team with almost nothing but transfers. It's going to be an unreal story if it can pull off the upset Tuesday.

Who they've beaten: No. 15 Cleveland State, No. 10 Rutgers, No. 11 SyracuseWhat I've seen: The No. 3-ranked team at KenPom get a little bit lucky but also exert its will on teams. The victory against Cleveland State is an afterthought at this point, but how about the Rutgers escape from last weekend? Had the Scarlet Knights not forgotten how to play basketball for much of the final two minutes of that game, Houston's hanging at the crib at this point. Houston went Houston, though; it won ugly, and proudly. The win against Syracuse Saturday night was authoritative. I saw Kelvin Sampson's team decide, with emphasis, that Syracuse was just done. The 62-46 win marked SU's lowest point total in program history in the NCAAs. If Houston wins Monday, it will become the first team to make the Final Four without playing a single-digit seed.

Who they've beaten: No. 11 Michigan State, No. 6 BYU, No. 14 Abilene Christian, No. 2 AlabamaWhat I've seen: A revival of a blue blood. UCLA's 88-78 win over Alabama Sunday night at Hinkle was a game I'd rank in the top three of the tournament. The vibe of that building in a good game is tantalizing, even at 25% capacity. They have to figure out a way to play tourney games in Hinkle every four years or so moving forward. It would be a missed opportunity otherwise. The way UCLA pulled off its OT win on Bama was probably not something that can be duplicated in the next decade-plus of tournament competition. UCLA had merely 25 points in the second half ... then dropped 23 on Alabama's head in OT, doing so after the Crimson Tide's Alex Reese hit a 26-foot shot at the end of the second half to (temporarily) save the Tide's hide. UCLA lost its best player, Johnny Juzang, to a foul-out with 2:26 to go in a 60-all game. UCLA is the first team since VCU in 2011 to play in the First Four and reach the Elite Eight. UCLA's also the third No. 11 seed to beat a No. 2 in history.

Who they've beaten: No. 14 Colgate, No. 6 Texas Tech, No. 15 Oral RobertsWhat I've seen: The team that's had the shakiest way to get to this point. The Razorbacks beat TTU and Oral Roberts by two points apiece and would no longer be in the field had Max Abmas' 3-point attempt been two inches to the right. But it wasn't, and Arkansas is still dancing. The No. 3 seed in the South is set for a SWC reunion vs. Baylor. Per Torvik, Arkansas is pretty clearly playing the least efficiently of any team still left. But it won't be put last because this is obviously not the worst of the group. Eric Musselman knows his team has to have better shot selection in order to get the Hogs back to the Four for the first time since 1995. Could be a spicy one vs. Baylor Monday night.

Who they've beaten: No. 5 Tennessee, No. 4 Oklahoma State, No. 8 Loyola ChicagoWhat I've seen: One of the most unlikely regional-final runs from a power-conference team in history. Oregon State's win at Bankers Life Fieldhouse on Saturday afternoon was a dose of Loyola's own medicine. The Beavers are back in the Elite Eight for the first time in 39 years, doing so in no small part because of foul shooting. Oregon State is shooting 86.2% from the stripe (56 for 65), the highest rate in this year's Dance. With UCLA and OSU still alive, it marks the third time an NCAA Tournament has two double-digit seeds playing in the Elite Eight (1990 and 2002 the other ones). OSU's opponents are shooting 23.1% from 3-point range, which in turn has made OSU the third-stingiest defense, behind USC and Gonzaga, in the tournament.

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March Madness 2021: Re-seeding the teams in the Elite Eight of the NCAA Tournament - CBS Sports