It's a … ! Pregnant Lesley Anne Murphy and Alex Kavanagh Reveal Baby's Sex

Spilling the beans! Lesley Anne Murphy and her fiancé, Alex Kavanagh, announced the sex of their unborn baby with an adorable reveal.

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The Bachelor alum, 33, shared the news in an Instagram video posted on Friday, October 16. In the clip, the DRONEGEAR founder came home to find Murphy surrounded by pink balloons and popping a pink bottle. The pair showed off balloons that read “Oh baby” and “Baby girl” while the Temptations’ song “My Girl” plays in the background.

“Excited to announce … We’re having a BABY GIRL!!!!” the season 17 contestant captioned the post. “This is how I surprised Alex that the future is female🎉🎉🎉 #itsagirl #babygirl #girldad #thefutureisfemale.”

Excited to announce… We’re having a BABY GIRL!!!!💝This is how I surprised Alex that the future is female🎉🎉🎉 #itsagirl #babygirl #girldad #thefutureisfemale

A post shared byLesley • The Road Les Traveled (@lesleyannemurphy) on

The couple announced in September that they are expecting their first child. Murphy shared an Instagram video of herself jumping down to dance with Kavanagh before he cradled and kissed her growing bump. The sweet clip was set to The Ronettes’ “Be My Baby.”

“Started from the kitchen now we’re here,” Murphy captioned the post. “Baby Kavanagh taking flight in 2021! Finally someone to occupy the middle seat 🙂 @drone.pilot and I couldn’t be more excited to grow our little family!!! #family #love #travel #adventure #coronababy #thelastdance #kitchendance #encore.”

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The Arkansas native detailed how she discovered her pregnancy in a blog post on October 6. Murphy wrote that she found out she was expecting when she missed a period and took a pregnancy test.

“I walked into the living room and blurted out, ‘Ummmm … we’re pregnant!’” she wrote. “As I was brushing my teeth, I could hear him taking really deep breaths from our bedroom. As I walked back in, he immediately ran out and vomited in the toilet. Talk about a physiological response to pregnancy news! And I thought I was supposed to be the sick one! We laugh about it all the time. He’s very excited to become a dad regardless of the response.”

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The twosome announced their engagement in February after one year of dating. However, their wedding plans have been delayed due to the coronavirus pandemic.

“Wedding planning turned into prenatal care,” Murphy wrote in her October 6 blog post. “Scheduled flights transformed into scheduled house tours. When life gives you 2020 lemons, make lemonade because it’s yummy, refreshing and well, nonalcoholic.”

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New connections reveal how cancer evades the immune system

If cancer is a series of puzzles, a new study pieces together how several of those puzzles connect to form a bigger picture.

One major piece is the immune system and the question of why certain immune cells stop doing their job. Another piece involves how histones are altered within immune cells. A third piece is how a cell’s metabolism processes amino acids.

“Nobody knew if those questions were all connected. We were able to place several of these puzzles together and see how it works,” says Weiping Zou, M.D., Ph.D., Charles B. de Nancrede and a Professor of Surgery, Pathology, Immunology and Biology at the University of Michigan and director of the Center of Excellence for Immunology and Immunotherapy at the U-M Rogel Cancer Center.

Zou is senior author on a paper published in Nature that includes multiple labs from the Rogel Cancer Center and collaborators from Poland.

The study found a connection between these three separate puzzles that suggests targeting the amino acid methionine transporter in tumor cells could make immunotherapy effective against more cancers.

It starts with T cells, the soldiers of the immune system. Cancer can turn these cells abnormal, preventing T cells from mounting an attack against it. The question is: what causes this?

Researchers looked at the tumor microenvironment, specifically how tumors metabolize amino acids. They found an amino acid called methionine had the most impact on T cell survival and function. T cells with low levels of methionine became abnormal. Low methionine in the T cells also altered histone patterns that caused T cells to be impaired.

Introducing tumor cells to the picture creates a fight between the tumor cells and the T cells for methionine. Over and over, the tumor cells win, taking the methionine from the T cells and rendering them ineffective.

Previous research has considered a systemic approach to starve tumor cells of methionine, with the idea that the tumor cells are addicted to it. But, Zou says, this study shows why that approach may be a double-edged sword.

“You have competition between tumor cells and T cells for methionine. The T cells also need it. If you starve the tumor cells of methionine, the T cells don’t get it either. You want to selectively delete the methionine for the tumor cells and not for the T cells,” Zou says.

In fact, the study found that supplementing methionine actually restored T cell function. High enough levels of methionine meant there was enough for both tumor cells and T cells.

One key is that tumor cells have more of the transporters that deliver methionine. The researchers found that impairing those transporters resulted in healthier T cells as the T cells could compete for methionine.

Zou was awarded a $3.2 million grant from the National Cancer Institute to advance this work.

“There are still a lot of mechanistic details we have not worked out, particularly the detailed metabolic pathways of methionine metabolism. We also need to understand how metabolism pathways may be different from tumor cells and T cells. We hope to find a target that is relatively specific to tumor cells so that we do not harm the T cells but impact the tumor,” Zou says. This work will be the focus of the new grant.

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Scientists reveal relationship between Dek and Intron retention during muscle stem cells quiescence

Muscle stem cells, the reserve stem cell in the skeletal muscles, are responsible for muscle repair after damage. They are the ‘regenerative medicine’ to cure muscle diseases and muscle damage. In a healthy uninjured condition, muscle stem cells are in quiescence, a dormant state, to preserve them. Whenever there is muscle damage, they will wake up instantly and contribute themselves to building new muscles.

If this dormant state is loosely controlled, muscle stem cells will be wasted when there is no need for repair. If this dormant state is kept too tight, the muscle stem cells will not wake up when they are needed to contribute to muscle repair.

How muscle stem cells control this balance of quiescence remains a topic of heightened interest. Recently, a team of scientists at the Hong Kong University of Science and Technology revealed that intron detention (IR) is a key to the mechanism—when stem cells enter quiescence exit, Dek releases conserved introns, which allow the cell to be activated.

“Using skeletal muscle stem cells, also called satellite cells (SCs), we demonstrated prevalent intron retention (IR) in the transcriptome of quiescent SCs (QSCs),” said Prof. Tom Cheung, lead researcher of the team and SH Ho Associate Professor of Life Science at HKUST. “Intron-retained transcripts found in QSCs are essential for fundamental functions including RNA splicing, protein translation, cell-cycle entry, and lineage specification. Our analysis reveals that phosphorylated Dek protein modulates IR during SC quiescence exit.”

While Dek protein is not present in QSCs, Dek overexpression in vivo results in a global decrease of IR, quiescence dysregulation, premature differentiation of QSCs, and undermined muscle regeneration. The researchers also found in their IR analysis on hundreds of public RNA-seq data that IR is conserved among quiescent adult stem cells, which suggests that IR functions as a conserved post-transcriptional regulation mechanism that plays an important role during stem cell quiescence exit.

Their findings were published online in the journal Developmental Cell on June 4, 2020.

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