And the 35-year-old actress did not disappoint as she put on a jaw-dropping display after a photoshoot in Los Angeles on Friday afternoon.
Fox showcased her ample cleavage and taut tummy in a daring mesh top with a V-neckline and rhinestone detailing.
The Transformers actress wore her brunette strands in a sleek middle part and styled in voluminous curls.
As for her makeup, Fox amplified her famous cateyes with a bit of black liner and an array of warm toned shadows.
Chic: The Jennifer's Body star, protecting her modesty, layered up her look with a chic black blazer
The couple, who met on the set of their thriller film Midnight In The Switchgrass in early 2020, confirmed their relationship in May.
MGK, 31, recently paid homage to their 'one year anniversary' by sharing with his millions of social media followers of Megan: 'she said 'i love you' one year ago today.'
During an interview on Lala Kent's podcast, Megan famously said she 'knew right away that he was what I call a twin flame.'
In an Open Pose, Irina Baeva Dazzles With Her Beauty and Cleavage – SparkChronicles
Once again, the beautiful Russian actress, Irina Baeva attracted the attention of thousands of users after posting an attractive photograph on her profile, in which she took the opportunity to show off her beauty while showing off her shapely figure and charms with a sweeping open look that stole the breath of many.
In recent weeks, the protagonist of "Vino el amor" has been on the lips of all the media in Mexico, since rumors of a possible pregnancy began to emerge after she was caught in a shopping center measuring garments in large sizes with the youngest daughter of Gabriel Soto.
Fortunately, the celebrity couple did not remain silent and as soon as they arrived at the Mexico City airport, they clarified this gossip with some reporters who were waiting outside the facilities, where they flatly denied the news of Baeva’s alleged pregnancy.
And with her most recent update through her personal account on the camera’s social network, the 28-year-old beautiful girl proved to her more than three million fans that this rumor was unfounded by flaunting her toned anatomy as she comfortably enjoyed her afternoon from the couch with a book between her spread legs.
As you can see in the image, the beautiful actress of “Italian girl is getting married” wore a striking outfit in earth colors, which consisted of a sweater with an animal print that she wore open, in addition to modeling a short top with a straight neckline. and matching pants to the waist that revealed her charms and steel abdomen.
In less than 20 hours, the publication has managed to add more than 30 thousand reactions of likes in the shape of a red heart from its devoted fans, in which they also filled the comment box with beautiful words of affection and support for it.
X Factor beauty Cher Lloyd flaunts cleavage in plunging dress for red-hot display - Daily Star
The singer, best known for taking part in the X Factor more than a decade ago, posed up a storm in a plunging red dress which her cleavage exploded out of.
The bombshell looked sensational as she allowed her long brunette locks to cascade down onto her shoulders and wore bright red lipstick to match her frock.
She finished her jaw-dropping look with a dusting of make up and large eyelashes, which accentuated her pretty features.
Cher was aged 16 and a schoolgirl from Malvern, Worcestershire, when she auditioned for the X Factor.
She first impressed judge Cheryl with her impressive rendition of Soulja Boy's Turn My Swag On - and eventually came fourth in the competition.
After the series she was signed by Syco Music and has had a successful music her debut single, Swagger Jagger , released in July 2011, shot to number on in the UK chart.
She has enjoyed mainstream success in the US with the solo version of her single Want U Back, which reached the top 20 on the charts .
She said: "I got married when I was 20, you know when you grow up and dream of that fairy tale, of course, we've had our ups and downs, but honestly it is like a fairy tale with me and him.
A Place in the Sun's Danni Menzies flashes cleavage in string bikini on sunny getaway - Daily Star
A Place in the Sun presenter Danni Menzies has been sunning it up in Greek islands to film the new series.
As she returned from her trip today she sent her Instagram fans wild by sharing a snap of her posing on a boat in a leapordprint bikini as she announced she was returning home from her trip.
The tiny garment drew attention to her impressive cleavage, as the sea and cliffs formed a spectacular backdrop behind her.
The bombshell, whose hair was slicked back, oozed sex appeal as she grinned cheekily and stared seductively at the camera
The presenter showed her gratitude for being able to travel at a time when coronavirus restrictions mean options for holidaying abroad are limited for many Brits.
She wrote in the caption: "Homeward bound! What an absolute treat it was to film in the gorgeous Greek islands with such great people. So lucky at this time, I know!!! @aplaceinthesunofficial has been more popular than ever over the last year so hopefully enduring my sunny social posts will be worth it when you see the new series!"
Danni recently opened up on Instagram about developing 'really bad pigmentation her forehead called Melasma'.
She added: "Also thanks for all the feedback on things to try to help with the pigmentation and the lovely responses on keeping it natural. Going to do my best to keep it up."
Danni's post sent her Instagram fans into a frenzy, with many rushing to the comment section to shower her with compliments.
What Is ... Research and Why Is It Risky? | Mind Matters
To understand why some in the U.S. government and the NIH want to downplay funding of gain-of-function research, we need to understand what exactly it is.
All viruses mutate, some faster than others. Influenza is one of the fastest mutating viruses, followed by HIV. SARS-CoV-2 mutates slower than both viruses, which is why many scientists believe vaccine booster shots will likely be every few years, rather than annually, like the flu.
Studying mutations and predicting variants is not particularly controversial. But scientists don't just want to predict known viruses for vaccines and therapeutics. They also want to predict new viruses, especially those that may cause a pandemic. Past pandemics have happened when a virus jumps from animal to human. The Ebola outbreak in West Africa several years ago was traced to a boy who was bit by a fruit bat. New influenza viruses can come from birds (avian flu) or pigs (swine flu), so this is a legitimate concern. SARS-CoV (2002) originated in bats, then jumped to civet cats, and then humans. MERS-CoV (2012) spread to humans from camels. Scientists were concerned that a pandemic may be caused by another coronavirus like MERS or SARS.
Gain-of-function studies take known viruses and investigate which mutations cause them to become transmissible to humans. This is done either by transmitting the virus from one cell to another and across different species, as what happened in the wild with the original SARS-CoV virus, or by making genetic changes to a virus genome and then exposing it to either a human cell or "humanized mice" (i.e., mice with the ACE2 gene) to see if it enters human cells. These genetic changes to a virus either combine the genes of one known virus with another through recombinant methods, or the genetic change is inserted directly into the genome of a virus using gene editing tools like CRISPR.
So, what kinds of changes would someone want to make? Consider MERS-CoV. It has something called a "polybasic furin cleavage site" in the portion of its genome that codes for the spike protein—that would be the spike protein that gives coronaviruses their namesake. The furin cleavage site has been shown to make coronaviruses more transmissible to human cells, especially human lung cells. MERS-CoV naturally developed this type of furin cleavage site. What gain-of-function studies can do is use one of the methods above to cause a different coronavirus to gain something like the type of furin cleavage site found in MERS-CoV. This would theoretically make the modified coronavirus more susceptible to infecting human lung cells.
Here's what Peter Daszak had to say in a 2019 interview about these studies. This was prior to the pandemic:
Spike protein drives a lot of what happen with coronavirus, in zoonotic risk. So you can get the sequence, you can build the protein, and we work a lot with Ralph Baric at UNC to do this. Insert into the backbone of another virus and do some work in the lab. So you can get more predictive when you find a sequence. You’ve got this diversity. Now the logical progression for vaccine is, if you are going to develop a vaccine for SARS, people are going to use pandemic SARS, but let’s insert some of these other things and get a better vaccine.
Some scientists, including those quoted in Nicholas Wade's article, think SARS-CoV-2 could be a result of gain-of-function studies rather than naturally occurring because SARS-CoV-2 has a furin cleavage site, one of the "things" Peter Daszak was talking about:
“When I first saw the furin cleavage site in the viral sequence, with its arginine codons, I said to my wife it was the smoking gun for the origin of viruses,” said David Baltimore, an eminent virologist and former president of CalTech. “These features make a powerful challenge to the idea of a natural origin for SARS2,” he said.
What makes the Delta covid-19 variant more contagious?
After the virus binds to ACE2, the next step is to fuse with the cell. This process starts with the enzyme in the host cell cutting the spikes at two different locations. This process is called lysis. This kick activated the fusion machine. If binding is like a key to a lock, splitting is like a key turning a bolt. Vineet Menachery, a virologist at the University of Texas Division of Medicine, said: “If you don’t cut in two places, the virus cannot enter the cell.”
One of the mutations present in Delta actually occurs in one of these cleavage sites, and A new study that has not been peer-reviewed This indicates that the mutation does enhance cleavage. Menahari, who was not involved in the study, said that he has replicated these results in his laboratory. “So the virus is more likely to be activated,” he said.
It is not clear whether this will improve transmission capacity, but it can. Menachery said that when scientists delete these cleavage sites, the spread and pathogenicity of the virus decreases. Therefore, it makes sense that changes that promote division will increase transmission.
Delta’s ability to evade the body’s immune response may also help promote transmission. Immune evasion means that more cells are infected and produce more virus, which may make people with the virus more likely to infect other people.
In any case, in the United States and the United Kingdom, only about 42% of the population has been vaccinated. Part of the reason for the surge in the virus in India is the rapid spread of Delta, and only 3.3% of the population has been fully vaccinated.
At the press conference, Fauci urged those who had not been vaccinated to get the first shot, and reminded some vaccinated people not to skip the second shot. The Biden administration hopes that at least 70% of the population will be partially vaccinated by July 4. In the UK, Delta quickly replaced Alpha as the main strain, and cases are now on the rise. “We can’t let this happen in the United States,” Fauci said.
Princess Diana: Designer Shares Story Behind Her Dress for First Royal Appearance
Shortly after announcing they were headed down the aisle — the royal family announced the engagement in February 1981 — Diana made her first official appearance with Charles as her fiancé. Only 19 years old at the time, Diana went with Charles to a London charity gala concert.
RELATED: Kate Middleton Combines 'Magic' and 'Ordinary' in a 'Better Way Than Princess Diana Did', a Royal Biographer Says
During a June 2021 interview with TODAY , designer David Emanuel recounted the story behind Diana's black strapless gown.
"She said, 'I’m going somewhere very, very posh,'" Emanuel recalled. "Wouldn’t give any other detail, happened to have a black silk taffeta bodice in the studio. I said to put that on. And, of course, with pale skin, blue eyes and blonde hair it looked ravishing."
Emanuel and his former partner, Elizabeth Emanuel, would later go on to design Diana's iconic wedding dress. But at the time Diana was just another of their clients who needed something to wear to a special occasion.
Emanuel continued, saying he told Diana she couldn't show up in "just a strapless dress." So he and his team made her a black wrap, which Diana wore to the event. He also recalled how they had no idea the dress had been for the woman who would be marrying Charles until they saw Diana on TV.
"That evening, when we switched on the news, this limousine pulls out, out got Prince Charles and there was this girl, and I said, 'That's the girl! That’s her! That’s the one we've just done the frock for!'" Emanuel said.
Diana didn't have a good time at her first big royal event. "It was a horrendous occasion," she later told biographer Andrew Morton. "I didn't know whether to go out of the door first. I didn't know whether your handbag should be in your left hand, not your right. I was terrified, really – at the time everything was all over the place."
During the event Diana confided in Hollywood actor-turned-royalty Grace, Princess of Monaco, who was also on the guest list.
Polarized endosome dynamics engage cytoplasmic Par-3 that recruits dynein during asymmetric cell
In the developing embryos, the cortical polarity regulator Par-3 is critical for establishing Notch signaling asymmetry between daughter cells during asymmetric cell division (ACD). How cortically localized Par-3 establishes asymmetric Notch activity in the nucleus is not understood. Here, using in vivo time-lapse imaging of mitotic radial glia progenitors in the developing zebrafish forebrain, we uncover that during horizontal ACD along the anteroposterior embryonic axis, endosomes containing the Notch ligand DeltaD (Dld) move toward the cleavage plane and preferentially segregate into the posterior (subsequently basal) Notch hi daughter. This asymmetric segregation requires the activity of Par-3 and dynein motor complex. Using label retention expansion microscopy, we further detect Par-3 in the cytosol colocalizing the dynein light intermediate chain 1 (Dlic1) onto Dld endosomes. Par-3, Dlic1, and Dld are associated in protein complexes in vivo. Our data reveal an unanticipated mechanism by which cytoplasmic Par-3 directly polarizes Notch signaling components during ACD.
As shown previously, in the developing zebrafish forebrain, most of the RGPs undergo ACD to generate an apical differentiating daughter with low Notch activity and a basal self-renewing daughter with high Notch activity ( 20 ). To understand how such Notch signaling asymmetry arises, we visualized internalized Notch ligand Dld using an antibody uptake assay ( 34 ) and in vivo time-lapse imaging. Intriguingly, only punctate cytoplasmic labeling was observed ( Fig. 1A ); no Dld was accumulated on the plasma membrane of mitotic RGPs. In the mib mutant, which disrupts a conserved ubiquitin E3 ligase essential for Notch ligand endocytosis ( 35 ), the punctate cytoplasmic labeling of Dld was, however, lost; fluorescence was instead largely concentrated on the plasma membrane (fig. S1A). These data indicate that the punctately labeled structures are internalized Dld in endosomes (in short, Dld endosomes). They also suggest that, in mitotic RGPs, Dld undergoes active endocytosis to be predominantly distributed in endocytic vesicles. We also evaluated whether this labeling method affected embryonic development or RGP cell division modes. The developing forebrain RGPs at this developmental stage predominantly undergo horizontal division (with the division axis parallel to the ventricular surface). No substantial differences in embryonic morphology and RGP division modes were observed between control and Dld antibody-injected embryos (fig. S1, B to D).
We next performed automated tracking analysis of 19 RGPs, which were captured throughout their entire mitotic cell cycle (from prophase to telophase) and, moreover, with consistent tracking of Dld endosomes in all frames. Tracking of more than 300 Dld endosomes from all 19 cells throughout the RGP mitotic cycle (45 time points) allowed us to visualize the progressive enrichment of endosomes toward the posterior daughter [ Fig. 1E (E1) and movie S2]. Such enrichment could be due to directional endosome movement toward the posterior, their selective degradation at the anterior, or both. The presence of supernumerary-labeled Dld endosomes made it challenging to unambiguously discern individual endosome's trajectories. Intriguingly, because of the mosaic nature of our Dld-labeling method, some RGPs contained only a single labeled Dld endosome. This enabled us to clearly track the movement of individual endosomes. We observed that the Dld endosome first moved toward the cleavage plane, followed by a directed maneuver toward the posterior side [ Fig. 1E (E2 and E3) and movies S3 to S6]. Together, these data uncover polarized dynamics of Dld endosomes during horizontal RGP division and show that Dld endosomes are asymmetrically segregated into the posterior daughter in most of the RGP divisions.
( A ) Schematic depicting the asymmetry of Dld endosomes (Dld hi ) and Notch activity (N hi ) in daughter cells. ( B ) Topology and statistics of relative daughter cell position along A-P (anteroposterior) and Ap-Ba (apicobasal) axes after horizontal division. MIP of 5-μm z-stacks (1-μm z-step) is shown. ( C ) Time-lapse images showing that Dld endosomes and Mib are segregated into different daughter cells following RGP division ( n = 25). MIP of 5-μm z-stacks (1-μm z-step) is shown. The time interval between z-stacks is 20 s, and the total acquisition time is 30 min. ( D ) The top left graph plots individual RGP's asymmetry indices for Mib-GFP ( x axis) and internalized Dld ( y axis). The top right graph shows the distribution of asymmetry indices for Mib-GFP and Dld endosomes; the dotted lines indicate the threshold of |0.2| for calling asymmetry. *** P < 0.0001, t = 6.549, df = 48, n = 25; unpaired two tailed t test. Mean with SEM is shown. The bottom pie chart shows the percentage of RGPs with indicated distribution patterns. n = 25 RGPs, from eight embryos of five repeat experiments. ( E ) Time-lapse images of a clonally labeled RGP (green) showing preferential segregation of internalized Dld to her4.1-dRFP hi daughter. MIP of 8-μm z-stacks (1-μm z-step) is shown. The time interval between z-stacks is 6 min, and the total acquisition time is ~10 hours. ( F ) Plot for quantifying her4.1 -dRFP and internalized Dld in daughter RGPs 1 hour after anaphase. n = 8 RGPs, from eight embryos of six repeat experiments.
Because of the lack of an anti-Notch antibody that works in zebrafish, we took three different approaches to address this question. First, most RGPs that we imaged in the developing zebrafish neurogenic forebrain undergo horizontal divisions along the A-P axis (fig. S1, C and D). Shortly after division, daughter cells begin interkinetic nuclear migration and adopt differential position along the apicobasal (Ap-Ba) axis. The basal daughter is previously shown to be Notch hi ( Fig. 2B , left) ( 20 ). We therefore determined the relationship between the A-P daughter position immediately following RGP mitosis and the Ap-Ba daughter position shortly thereafter. Among 42 pairs of daughter cells with observable differences in their position along the Ap-Ba axis, most (67%) had more Dld in the posterior daughter that initiated an earlier basal migration ( Fig. 2B , right). These results suggest that Dld endosomes are preferentially segregated to the posterior daughter, which later becomes the basal Notch hi daughter.
The second approach to discern the relationship between Dld endosome segregation and Notch activity involved analysis of the E3 ubiquitin ligase Mib, which is asymmetrically segregated to the apical-differentiating daughter following RGP ACD in zebrafish ( 20 ). Similar observations are also reported in the chick neural progenitors ( 37 ). By simultaneously tracking Dld endosomes and Mib distribution in 25 RGPs, we found that they were largely segregated into different daughter cells ( Fig. 2C , fig. S4, and movie S7): 64% RGPs had anteriorly enriched Mib while posteriorly enriched Dld ( Fig. 2D ). Note that Mib–green fluorescent protein (GFP) showed anterior enrichment early on during the cell cycle, when Dld distribution appeared random. While this observation implied a potential asymmetric endocytosis, it does not appear to contribute to Dld asymmetry as internalized Dld appeared randomly distributed in RGPs during prometaphase. Together, this observation supports the notion that Dld endosomes preferentially segregate to the posterior-then-basal Notch hi daughter and away from the Mib-high apical daughter.
Imaging of internalized Dld in par-3 morphants uncovered that, while Dld endosomes underwent largely normal subcortical association and congregation toward the future cleavage plane, their final asymmetric segregation into the posterior daughter was significantly disrupted ( Fig. 3, B and E to G , and movie S9). This defect was rescuable by Par-3-GFP mRNA injection (fig. S6). These data, together with the observed knockdown of Par-3 protein in RGPs (fig. S8), validate the MO specificity and efficacy in our system and suggest that Par-3 is essential for polarized segregation of Notch signaling endosomes during RGP ACD.
( A to D ) Time-lapse sequence of images showing Dld endosome dynamics in mitotic RGPs from 28-hpf control MO (A) and embryos deficient for par-3 activity (B), treated with the dynein inhibitor CBD (C), deficient for dynein intermediate light chain 1 ( dlic1 ) (D). Centrosomes are labeled with GFP-centrin, and membrane is labeled with Myr-TdTomato reporter. For (A) to (D), all images shown are the MIP of five confocal z-stacks (1−μm z-step). The time interval between each volume of z-stacks is 15 s, and the total acquisition time is 25 min. ( E ) Kymograph of horizontal projection of (A) to (D) showing distribution of all tracked Dld endosomes along the anteroposterior (A-P) axis ( x ) over time ( y ). The red line delineates center point of the axis defined by two centrosomes. ( F ) Scatter plot showing asymmetry indices in telophase RGPs. Thirty-three control MO RGPs were from 25 embryos of eight repeat experiments, 22 par-3 MO RGPs were from 9 embryos of six repeat experiments, 15 CBD-treated RGPs were from 7 embryos of four repeat experiments, and 15 dlic1 MO RGPs were from 8 embryos of four repeat experiments. The unpaired two tailed t test shows significance between ctrl versus par-3 MO, **** P < 0.0001 ( t = 4.706, df = 53); ctrl MO versus CBD, * P = 0.0129 ( t = 2.589, df = 46); ctrl versus dlic1 MO ** P = 0.0007 ( t = 3.645, df = 46). Mean with SEM is shown for each group. ( G ) Bar graph showing the percentage of RGPs with different patterns of internalized Dld distribution. Disruption of either Par-3 or dynein activity results in a significant decrease of asymmetric posterior Dld segregation. **** P < 0.0001, χ 2 test (chi-square = 95.62, df = 6).
The origins of COVID needs a thorough investigation | Toronto.com
Even if the coronavirus did leak from a Wuhan lab, that wouldn't necessarily mean it was
Two weeks ago, President Joe Biden asked the US intelligence community to redouble its efforts to find out how the pandemic started: Did the coronavirus jump from animals to people, or did it leak from a Chinese lab?
The starting point nearly all scientists agree on in this debate is that two known bat coronaviruses are a 96% and 97% match for the coronavirus' genetic make-up. A recent study suggests another virus found in bats from southern China could be an even closer relative.
Those who consider the lab theory to be unlikely are quick to point out that the coronavirus's genetic code has no tell-tale hallmarks of being engineered. A March 2020 study analyzed the virus' DNA and concluded that it "is not a laboratory construct or a purposefully manipulated virus."
Quay told Insider, however, that 11 labs around the world "have purposefully put in a furin site to make a virus more infectious."
David Baltimore, a Nobel Prize-winning biologist, has called the coronavirus' furin cleavage site a "smoking gun" for the lab-leak theory. He told journalist Nicholas Wade last month that the site's presence in the coronavirus poses a "powerful challenge to the idea of a natural origin."
However, Baltimore has since walked back that comment , saying Wade took his quote out of context.
Former CDC director Robert Redfield, too, has said the virus could have gotten better at infecting people in a facility like the WIV.
Indeed, scientists sometimes introduce viruses to human cells in a lab over and over again to see if the virus will evolve to become better at infecting those cells.
That's probably what led the virus "to be pretty well adapted when first recognized," Fauci said in March.
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