Make these changes to your diet to say goodbye to acne – Health shots

Acne is a persistent skin inflammation problem which most commonly affects the face, sometimes the shoulders, back, neck, chest, or upper arms too and results in patches and pimples. Although it can happen at any age, it frequently happens during puberty when the sebaceous glands are active. Although it is not harmful, it may leave skin scars. Acne can be caused due to multiple reasons such asexcessive production of oil (sebum), blocked hair follicles from oil and skin cells infection caused by bacteria. According to various studies, eating certain foods may exasperate acne. What are these worst foods for acne?

Following a particular dietary limitation can work in favour of those battling acne. Simrun Chopra, a well-known nutritionist and deep health coach, shared some dietary suggestions that can help you fight acne problems.

Check out her Instagram post!

A diet that excludes eating anything with gluten is known as a gluten-free diet. A gluten-free diet can help you prevent acne if your skin is gluten-sensitive. Barley, rye, triticale and wheat contain gluten and so you have to avoid eating these grains. Some natural gluten-free items include vegetables and fruit, natural and unprocessed forms of beans, seeds, legumes and nuts, eggs and non-processed meats, seafood, and poultry. You can even ask your dietician to make a gluten-free diet routine for you.

Artificial hormones are given to dairy cows, which affects how much milk they produce. According to researchers, consuming milk products may cause those hormones to disturb your hormone balance. This might result in acne.As per another hypothesis, acne will always be made worse by the growth hormones included in milk. Thus, having dairy product can worsen the situation if you have acne.

Large fatty acid intakes, like those found in an average Indian diet, are connected to higher rates of inflammation and acne. This may be due to the high levels of oils in the diet which are high in omega-6 fatty acids. This overabundance of fatty acids causes the body to become inflammatory, which may make acne worse.

Watch your acne for a week, and see if you find a difference after avoiding these foods. If you do, then you need to do an elimination protocol to see which of the three was the culprit and what do you need to remove and what to add back. For most people, these three in moderation usually works, Chopra says.

Chopra recommends a teaspoon of a good seed mix which can give you a dose of vitamins and good fats.

Omega-3 fatty acids are a nutrient that can aid with acne treatment and are found in foods like fish oil, wild salmon, nuts, and seeds. A great source of omega-3 fatty acids is fish oil. Fatty acids can help with general skin health as well as specific skin issues like eczema and acne.

Water aids in the removal of toxins and bacteria from the skin when treating bacterial acne, hence lowering the risk of pore clogging. It also helps in maintaining good skin by keeping it moisturized and promotes collagen formation and skin cell renewal.

Yellow and orange fruits and vegetables can be good for acne because of their antioxidant and anti-inflammatory properties. It is advised to have more yellow and orange fruits and vegetables such as carrots, apricots, and sweet potatoes etc.

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Make these changes to your diet to say goodbye to acne - Health shots

Doping Not Dead in American Competitive Cycling, but Another Athlete’s Career Is – GearJunkie

Home Biking Doping Not Dead in American Competitive Cycling, but Another Athletes Career Is

Wednesday, the U.S. Anti-Doping Agency (USADA) banned Jackson Huntley Nash for life based on seven separate rule violations.

Jackson Huntley Nash was once a Cat 1 (highest category) contender on United States cycling circuits. Now hell never ride professionally againafter a USADA decision.

On August 10, the substance governing body posted the results of an investigation that showed Nash violated multiple anti-doping rules, for which he would receive a lifetime ban.

The USADA said it investigated the Marietta, Ga., cyclist after it received information from a whistleblower in December 2021.

Testimony and evidence ultimately showed Nash committed seven infractions. Investigators found he used the banned substances testosterone, clenbuterol, oxandrolone, and anastrozole himself. The USADA also found he trafficked clenbuterol and oxandrolone, and that Nash administrated or attempted to administrate other athletes use of human growth hormone.

Finally, officials found he attempted to tamper with the investigation.

Nash has not raced professionally since August 2021. His results that year had proven unimpressive and ultimately marked the end of a career that was still competitive as of 2019. His lifetime ban is retroactive to June 30 this year.

CyclingNews reported hed also been in a problematic relationship with fellow pro cyclist Olivia Ray, which escalated to a family violence hearing in the Superior Court of Gwinnett County, Ga. The New Zealand cyclist could also be implicated in the findings against Nash.

Ray currently awaits the outcome of the USADAs investigation against her, which could yield up to a 4-year ban, Cycling New Zealand told CyclingNews. Her Human Powered Health team released her in March following alleged code of conduct violations.

This is yet another case that demonstrates the power of investigations in the shared fight to protect sport and athletes rights, USADA CEO Travis T. Tygart said in a statement. As always, we will thoroughly investigate and act on evidence of doping violations and greatly appreciate the assistance of those who come forward on behalf of clean sport.

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Doping Not Dead in American Competitive Cycling, but Another Athlete's Career Is - GearJunkie

Here’s why Brighton is favored to win the 2022 KLAA West football championship – Daily Press & Argus

Livingston County QB1 candidates talk about upcoming football season

Livingston County quarterbacks talk about their position battles and outlook for the 2022 football season.

Bill Khan, Livingston Daily

NORTHVILLE Of the motivational tactics at Brightons disposal in 2022, playing the disrespect card isnt among them.

The Bulldogs missed the state football playoffs last fall, but they have the attention of Kensington Lakes Activities Association coaches heading into this season.

Brighton has been chosen by league coaches as the preseason favorite to win the West Division after tying for fourth place last year with a young roster.

No team in the KLAA has more experience, as the Bulldogs return nine starters on offense and eight on defense.

The coaches dont know anything, Brighton coach Brian Lemons said with a laugh Friday during the leagues annual media day. I just picked the coach I like the most; thats the one I picked to win. No, just kidding.

Lemons doesnt mind having a large target on his teams back. It beats the alternative of having low expectations.

They deserve that type of respect, for sure, he said. But the preseason poll is meaningless if they dont go out and put the time and the work in.

Brighton last won the KLAA West in 2018 with a 7-0 record. The 2019 team that reached the state Division 1 championship game was second to Plymouth in the division before going on its run to Ford Field. The Bulldogs were second in 2019 and 2020 before tying Novi for fourth last year in a division won by Hartland and Howell.

It might put a little pressure on us, Brighton senior linebacker Griffin Bell said. Our team knows how good we can be. Weve been saying this all year that it doesnt matter if you think youre gonna be good; if you dont do anything, it doesnt matter. We just come out there to work every day. We know what weve got to do to get the job done.

After Brighton, the predicted order of finish in the KLAA West is Howell, Canton, Hartland, Novi, Northville, Plymouth and Salem.

Novi is the second-most experienced team in the West with seven returning starters on offense and seven on defense.

Brian in Week 3 or 4 made this youth movement where you went and looked and almost everybody starting for him is an underclassman, Novi coach Jim Sparks said. I think hes got five former head coaches on his coaching staff. Not just retreads, were talking Hall of Fame-caliber coaches like Mark Thomas, Denny Hopkins. These are like the best of the best. I dont know if hes got NIL over there for coaches in Brighton or what. I know what Ill do when I retire.

Following is a rundown of the KLAA West teams:

This team could be as loaded as the 2019 state runner-up squad, with returning talent at nearly every position.

Colin McKernan led Livingston County with 1,506 passing yards last year, but is being pushed for the job by 2021 back-up Grant Hetherton. Whoever is quarterback will have three solid targets in Jack Gregorich, Mason Millhouse and Ashton Tomassi. Leading rusher Carson Shrader returns.

The linebacking group of Bell, Hunter Harding and Luke Frisinger could be elite.

Our group of seniors, as a whole, shares such a brotherhood that its changing the way weve been able to operation in the offseason, Lemons said. Theyve taken responsibility. Theyve taken everything straight to the front of the room.

Canton hasnt had a losing season since 1999, so the expectation is that the Chiefs will find a way to contend, despite returning only two starters.

Josiah West and Caleb Williams, who each play running back and receiver, are the only Chiefs who played regularly last year.

Its getting them the confidence and belief they can do this, Canton coach Andrew LaFata said. Just because you didnt start last year doesnt mean youre not better than that player was at Week 1 last year. You just werent in there.

The Eagles return the county leaders in rushing (Joey Mattord, 1,109 yards), tackles (Chase Kern, 128) and interceptions (Sam Clay, nine).

Clay may also double as the teams starting quarterback, as he did late last season. The skill guys should get protection behind veteran blockers Vincent Cox, Cooper Pyle and Jaxson Wilson.

Footballs a great game, Hartland coach Brian Savage said. It teaches a lot of life lessons. We at Hartland are always trying to do that. We use football as an extension of our classroom, of life.

"Obviously, weve got teams in here who have been to the ultimate life experience as far as football goes. Weve got some of us in the middle and weve got some of us on the other end now. Competing against these coaches and programs in this league is pretty impressive. Its got to be one of the top leagues in the state.

The Highlanders have a three-man battle going to replace two-year starter Nolan Petru at quarterback. Cole Quattlander will be the primary running back after getting some starts when Western Michigan recruit August Johanningsmeier was injured.

Guard Nolan Nelson leads a strong offensive line that will be called upon to run-block more often than not. The defense returns the top two tacklers from last year in linebacker Carter Kraft and safety John Lovich.

The goal for Howell this year is just to continue to improve, push for more, Howell coach Brian Lewis said. Thats a big thing for everybody in here, continue to push. … Were just trying to raise the bar in Howell.

Northville coach Matt Ladach had the quote of the day from the podium Friday.

I look around the room, he said. We dont have three cats who look like this over here from Belleville. We dont have farmers that are sprinkling the corn field with human growth hormone like theyve got over in Howell and Hartland. But what weve got is a bunch of ordinary dudes.

Luca Prior got some starts at quarterback last season.

He played quite a bit last year, so having him back is a big deal, Ladach said. Good experience and he throws the ball really well.

The Wildcats have the most experienced quarterback in the division in third-year starter Luke Aurilia, who threw for 1,080 yards and 12 touchdowns and ran for 451 and five scores last year.

The Wildcats return their three leading rushers in Aurilia, Cole Shires (433 yards, nine touchdowns) and Martez Langford (266 yards, three touchdowns).

The expectations are to compete and win every week, Sparks said. We just talked about it as a team; before a dream can come true, you have to have a dream. One thing I worked on pretty hard coming into Novi is we need to raise our expectations, so we can strive and that should spur on success.

Plymouth has gone 2-14 the last two seasons after winning the KLAA West in 2019, averaging only six points per game last year.

The Wildcats return four starters on offense and five on defense. With a small senior class, they could be building toward bigger things next season.

We grinded and the kids worked tirelessly and we really used that time to get better, Plymouth coach Greg Souldourian said. I think that played a huge role. If you look at our weight room numbers, were similar to the numbers as 2019. Numbers dont lie; they were 9-2. Well see what happens, but theyve put in the work.

Salem has a 4-30 record the last four seasons after qualifying for the state playoffs for only the third time in 2017. Its been a revolving door since then, with Brendan Murphy taking over as the Rocks third head coach in the last four years.

Quarterback Robert Ahlgren is one of five returning starters on offense to go with five on defense.

Its been a good install, so were not starting holy crap brand new right from day one. But it still is a learning curve, because its brand new from what theyve been doing the last couple years.

Contact Bill Khan at wkhan@gannett.com.Follow him on Twitter@BillKhan.

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Here's why Brighton is favored to win the 2022 KLAA West football championship - Daily Press & Argus

Human Growth Hormone (hGH) – Cleveland Clinic

What is human growth hormone (hGH)?

Human growth hormone, also known as hGH and somatotropin, is a natural hormone your pituitary gland makes and releases that acts on many parts of the body to promote growth in children. Once the growth plates in your bones (epiphyses) have fused, hGH no longer increases height, but your body still needs hGH. After youve finished growing, hGH helps to maintain normal body structure and metabolism, including helping to keep your blood sugar (glucose) levels within a healthy range.

Hormones are chemicals that coordinate different functions in your body by carrying messages through your blood to your organs, muscles and other tissues. These signals tell your body what to do and when to do it. Your body makes over 50 hormones, and many of them interact with each other, creating a complex web of processes.

Your pituitary gland is a small, pea-sized endocrine gland located at the base of your brain below your hypothalamus. Its made of two lobes: the anterior (front) lobe and posterior (back) lobe. Your anterior lobe makes hGH.

Your pituitary gland is connected to your hypothalamus through a stalk of blood vessels and nerves. This is called the pituitary stalk. Your hypothalamus is the part of your brain that controls functions like blood pressure, heart rate, body temperature and digestion. Through the stalk, your hypothalamus communicates with your pituitary gland and tells it to release certain hormones. In this case, your hypothalamus releases growth hormone-releasing hormone (GHRH), which stimulates your pituitary gland to release hGH, and somatostatin, which prevents (inhibits) that release.

Healthcare providers use a synthetic form of hGH (sometimes called recombinant hGH) to treat certain health conditions, including growth hormone deficiency. You should never take synthetic hGH without a prescription from your provider.

Your pituitary gland normally releases hGH in short bursts (pulses) throughout the day. The release of hGH is mainly controlled by two hormones your hypothalamus releases: growth hormone-releasing hormone (GHRH), which stimulates hGH release, and somatostatin, which prevents (inhibits) hGH release.

Several other endocrine hormones also regulate hGH, including insulin-like growth factor 1 (IGF-1). IGF-1 is a major suppressor of GH production, whereas thyroxine, glucocorticoids and ghrelin stimulate hGH release.

IGF-1 thats released by your liver is one of the best-characterized effects of hGH activity. IGF-1 plays a critical role in preventing (inhibiting) the release of the hGH through a negative feedback loop by stimulating somatostatin and inhibiting GHRH release. However, hGH and IGF-1 secretion are regulated by each other, where hGH triggers IGF-1 release and the IGF-1 inhibits hGH release in a feedback loop. In healthy people, hGH release is inhibited by hyperglycemia (high blood sugar) and stimulated by sleep, stress, exercise, hypoglycemia (low blood sugar) and amino acids.

Human growth hormone has two main functions: stimulating growth (mainly in children) and impacting metabolism (how your body turns the food you eat into energy).

Human growth hormone triggers growth in nearly every tissue and organ in your body. However, its most well-known for its growth-promoting effect on cartilage and bone, especially in the adolescent years during puberty. Cells in cartilage called chondrocytes and cells in bones called osteoblasts receive signals from hGH to increase replication and thus allow for growth in size.

Once the growth plates in a childs bones have fused, hGH no longer increases height. Instead, hGH helps to maintain normal body structure throughout the rest of your life.

Metabolism consists of the chemical reactions in your body that change the food you eat into energy. All of the cells in your body need energy to function properly. Several different complex processes are involved in metabolism.

hGH impacts metabolism primarily by increasing the production of insulin-like growth factor-1 (IGF-1) and its effect on cells in your body. IGF-1 is a hormone similar in structure to insulin that manages the effects of hGH in your body. Insulin is an essential hormone your pancreas makes that helps regulate your blood sugar (glucose) levels by decreasing them. Like insulin, IGF-1 has glucose-lowering effects.

Your body normally carefully regulates your blood glucose levels. Blood glucose, or sugar, is the main sugar found in your blood. You get glucose from carbohydrates in the food you eat. This sugar is an important source of energy and provides nutrients to your body's organs, muscles and nervous system.

Insulin is the main hormone your pancreas makes to lower blood glucose levels when they get too high, and glucagon is the main hormone your pancreas makes to raise glucose levels when they get too low. Other hormones can counteract the effects of insulin, such as epinephrine (adrenaline) and cortisol.

While hGH normally increases blood glucose levels when they get too low, if you have excess amounts of hGH in your body, it can counteract the effects of insulin, causing elevated blood glucose levels.

Human growth hormone increases vertical growth in children. However, once your growth plates have fused, hGH cannot make you taller. Instead, after youve reached your final height, hGH helps maintain your bodys structure and has other important effects on your metabolism.

Your pituitary gland releases hGH in pulses. The size and duration of the pulses vary with time of day and your age and sex. Because of this, random hGH measurements are rarely useful to healthcare providers in confirming or ruling out a diagnosis. Instead, hGH measurement tests are most useful when measured as part of a stimulation or suppression test.

In general, the normal range for hGh levels include:

Normal value ranges may vary from lab to lab. Be sure to reference your labs normal range on your lab report when analyzing your results. If you have any questions about your results, talk to your healthcare provider.

Having lower-than-normal levels of hGH is called growth hormone deficiency. Its usually due to an issue with or damage to your pituitary gland that results in hypopituitarism when one, several or all of the hormones your pituitary gland makes are deficient. Human growth hormone could be one of the affected hormones.

Growth hormone deficiency affects adults and children differently.

When adults have a lack of hGH, it causes the following issues:

In adults, hypopituitarism that results in hGH deficiency may develop due to a benign pituitary adenoma (a noncancerous tumor) or damage to your pituitary gland or hypothalamus.

A lack of hGH in children results in poor growth. The main sign of hGH deficiency in children is slow height growth each year after a child's third birthday. This means they grow less than about 1.4 inches in height a year. A child with hGH deficiency may also have:

In children, hypopituitarism that results in hGH deficiency may be present from birth where the cause can be unknown (idiopathic), genetic or due to injury to their pituitary gland (during fetal development or at birth).

Children can also develop hypopituitarism due to damage to their pituitary gland or hypothalamus later in life.

The main condition associated with higher-than-normal hGH levels is a condition called acromegaly, though it affects adults and children differently. Its a rare condition.

Adults with acromegaly usually have enlarged or swollen hands and feet and altered facial features.

Adults with acromegaly can also have thickened bones and enlarged organs and are more likely to have conditions such as high blood pressure (hypertension), Type 2 diabetes and heart disease. Over 99% of acromegaly cases are due to pituitary adenomas, noncancerous (benign) tumors on your pituitary gland. These tumors can produce excess amounts of hGH. Acromegaly is more common after middle-age when growth is complete. Because of this, adults with acromegaly dont get any taller. Instead, their bones can become thicker.

Very rarely, children can experience elevated growth hormone levels before they reach their final height, which can lead to excessive growth of long bones and very tall height. This condition is called pediatric acromegaly, but its sometimes called gigantism. If left untreated, children with acromegaly usually grow to be seven feet tall or taller. Children with acromegaly may also have general weakness, delayed puberty and headaches.

Pituitary adenomas are usually the cause of pediatric acromegaly.

Your healthcare provider can order a series of blood tests to check your hGH levels if youre experiencing symptoms related to hGH issues.

Your pituitary gland normally releases hGH into your bloodstream in pulses throughout the day and night, with peaks that occur mostly during the night. Because of this, a single blood test to measure hGH measurement is difficult to interpret and is not usually medically useful.

Providers most often use procedures called growth hormone stimulation and suppression tests to diagnose conditions caused by hGH deficiency or excess.

They may also order a blood test that measures the amount of insulin-like growth factor 1 (IGF-1) in your blood.

The U.S. Food and Drug Administration (FDA) has approved the synthetic form of hGH for treatment for certain conditions. The synthetic form of hGH is available only by prescription and is injected.

In children, healthcare providers prescribe hGH to treat:

In adults, providers prescribe hGH to treat:

Its important to only take synthetic hGH if your provider has prescribed it for you.

The use of synthetic hGH for medical treatment can cause certain side effects including:

Researchers dont have enough information about the long-term effects of hGH treatment.

If you or your child are experiencing symptoms related to hGH deficiency or excess, contact your healthcare provider.

If youre receiving treatment for abnormal hGH levels, its important to see your provider regularly to make sure your treatment is working.

A note from Cleveland Clinic

Human growth hormone (hGH) is a powerful hormone thats necessary for several important bodily processes. Sometimes, your pituitary gland can make too much or too little of it. If you or your child are experiencing symptoms related to hGH deficiency or excess, its important to talk to your healthcare provider. Theyre there to help.

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Human Growth Hormone (hGH) - Cleveland Clinic

The Rush: Aaron Judges 45th HR puts him on pace to join ranks of all-time greats – Yahoo Sports

Aaron Judge hit his 45th home run of the season, but will the Yankee slugger finish the season in the pantheon of all-time great dinger kings? Reds first baseman Joey Votto penned some emotional thoughts about playing in the Field of Dreams game against the Cubs in Iowa on Thursday. Plus, the Field of Dreams game got The Rush thinking about other possible baseball movie-themed games can you say, Sandlot?!?!

- Here is a Judge, who absolutely annihilates that ball. My goodness, he's done it again. Aaron Judge with his 45th home run of the season. It is August 10th.

JARED QUAY: Aaron Judge hit his 45th home run of the season last night.

- Go Yankees.

JARED QUAY: Actually, the Yankees end up losing the game to the Mariners, 4 to 3. But who cares, because Judge is smashing records. Through 112 games this season, Judge has 99 RBIs, and his 45 dingers looks mighty impressive in comparison to Yankees legend, Roger Maris, who had 41 home runs through 112 games in his record-breaking 1961 season.

All Rise is currently on pace to hit 65 home runs this season. When you look at the all-time single season home run leaders, that number will put Judge in the long ball pantheon with the steroid era dudes.

- What, too soon?

JARED QUAY: And ahead of presumably non-HGH dabbling greats, Maris and Ruth. Speaking of old timey baseball, the Field of Dreams game is going down in Iowa tonight, where the Cubs and Reds will play near the location of the classic 1989 movie.

- Build it, he will come.

JARED QUAY: Cincinnati star Joey Votto tweeted about what the film means to him. We won't show you the entire thread because it contains spoilers to a movie that you've had 33 years to watch. But, I'm courteous like that. Anyway, the Reds first baseman has the feels ahead of the game, saying, quote, "Getting the opportunity to play a game at the mythical field that sowed the seed of hope for a Major League Baseball career is a significant moment for me."

Story continues

- That's deep.

JARED QUAY: Why didn't anybody tell me Joey Votto was a goddamn poet? My eyes is almost moist, man, reading that. Anyways, I think the Field of Dreams game is cool and all, but what I need to see is the MLB set up a Sandlot game.

- Sandlot, shortcut you guys, let's go.

JARED QUAY: Instead of entering through the cornfield, you get a mastiff to chase the starters down the street and into the dugout.

- Go! Sandlot, Sandlot, Sandlot.

JARED QUAY: I feel like the Angels got to be a part of this Sandlot game, just so we could see Shohei Ohtani miked up and doing this bit from the movie.

- I'm the Great Bambino.

JARED QUAY: Ohtani has a legit claim to that comparison after becoming the first major leaguer to record 10 pitching wins and 10 home runs in a single season since Babe Ruth did it in 1918. Negro league players Bullet Rogen and Ed Rau also joined the 10 in 10 club in 1922, in 1927, respectively. And we at The Rush won't let you forget it.

Now for the Sandlot game. James Earl Jones needs to be calling the play-by-play, of course. And I know it's from a different movie, but Tom Hanks has to be there managing the team and yelling at the players from the dugout. There's no crying. There is no crying in baseball. Tom Hanks said it, which means it has to be true.

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The Rush: Aaron Judges 45th HR puts him on pace to join ranks of all-time greats - Yahoo Sports

Control of non-REM sleep by ventrolateral medulla glutamatergic neurons projecting to the preoptic area – Nature.com

Animals

All procedures were carried out in accordance with the US National Institute of Health (NIH) guidelines for the care and use of laboratory animals, and approved by the Animal Care and Use Committees of Columbia University. Both male and female adult mice (820 weeks old) were used for all experiments. The following mouse lines were used in the current study: C57BL/6J (JAX 000664), VGlut2-IRES-Cre (JAX 028863), Gad2-IRES-Cre (JAX 0101802), Ai9 (JAX 007909). Mice were housed in 12-hour light-dark cycles (lights on at 07:00 a.m. and off at 07:00p.m., temperatures of 6575F with 4060% humidity) with free access to food and water.

AAV1-EF1-double floxed-hChR2(H134R)-EYFP-WPRE-HGHpA, AAV1-Ef1-DIO-EYFP, AAV1-Syn-FLEX-GCaMP6s, AAV1-Syn-FLEX-GCaMP6f, AAV8-hSyn-DIO-hM3D(Gq)-mCherry, AAV9-hSyn-DIO-hM4D(Gi)-mCherry, AAVrg-hSyn-Cre-WPRE-hGH, AAV9-CamKIIa-ChR2-eYFP, AAV1-CAG-FLEX-tdTomato, AAV1-mDlx-NLS-mRuby2 were obtained from Addgene. AAV1-EF1a-FLEX-TVA-mCherry from UNC vector core, AAV1-FLEX-2A-G(N2C)-mKate and RABV-G -GFP-EnvA, a gift from Charles Zuker.

Mice were anaesthetized with a mixture of ketamine and Xylazine (100 and 10mgkg1, intraperitoneally), then placed on a stereotaxic frame with a closed-loop heating system to maintain body temperature. After asepsis, the skin was incised to expose the skull and a small craniotomy (~0.5mm in diameter) was made on the skull above the regions of interest. A solution containing 50200nl viral construct was loaded into a pulled glass capillary and injected into the target region using a Nanoinjector (WPI). Optical fibers (0.2mm diameter, 0.39 NA, Thorlabs) were implanted into the target region with the tip 0.4mm above the virus injection site for optogenetic manipulation. For EEG and EMG recordings, a reference screw was inserted into the skull on top of the cerebellum. EEG recordings were made from two screws on top of the cortex 1mm from midline, 1.5mm anterior to the bregma and 1.5mm posterior to the bregma, respectively. Two EMG electrodes were bilaterally inserted into the neck musculature. EEG screws and EMG electrodes were connected to a PCB board which was soldered with a 5-position pin connector. All the implants were secured onto the skull with dental cement (Lang Dental Manufacturing). After surgery, the animals were returned to home-cage to recover for at least two weeks before any experiment.

For retrograde tracing, 150200nl AAVrg-hSyn.Cre.WPRE.hGH was unilaterally or bilaterally injected into the ventrolateral preoptic area (VLPO, Bregma 0.1mm, lateral 0.9mm, ventral 5.4mm) of Ai9 mice. For rabies tracing, 200nl mix of AAV-FLEX-G(N2C)-mKate and AAV-FLEX-TVA-mCherry (1:1) was unilaterally injected into the VLPO of Gad2-Cre mice. Two weeks after AAV injection, 200nl RABV-G-GFP-EnvA was unilaterally injected into the same VLPO. For anterograde tracing, 50nl AAV1-CAG-FLEX-tdTomato was unilaterally injected into the ventrolateral medulla (VLM, Bregma 6.9mm, lateral 1.1mm, ventral 5.6mm) of Vglut2-Cre mice. The ventral coordinates listed above are relative to the pial surface.

For chemogenetic inhibition, 200nl AAV9-hSyn-DIO-hM4D(Gi)-mCherry was bilaterally injected in VLM, 200nl AAVrg-hSyn.Cre.WPRE.hGH was bilaterally injected into the VLPO of C57BL/6J mice. For chemogenetic activation, 200nl AAV8-hSyn-DIO-hM3D(Gq)-mCherry was unilaterally injected into the VLM, 200nl AAVrg-hSyn.Cre.WPRE.hGH was bilaterally injected into the VLPO of C57BL/6J mice.

For optogenetic activation experiments, 200nl AAV1-EF1-double floxed-hChR2(H134R)-EYFP-WPRE-HGHpA was unilaterally injected into the VLM, an optical fiber implanted 0.4mm on top of the viral injection site in Vglut2-cre mice. For terminal stimulation, 200nl AAV1-EF1-double floxed-hChR2(H134R)-EYFP-WPRE-HGHpA was unilaterally injected into the VLM of Vglut2-Cre mice, and an optical fiber was implanted in the POA. In in vivo pharmacological inhibition experiments, Vglut2-Cre mice were unilaterally injected with AAV1-DIO-ChR2-EYFP and implanted with anoptical fiber in the VLM, then implanted with a double guide cannula (26 gauge, P1 Technologies) bilaterally above the POA. A metal head-post was attached during surgery for head fixation during the intracranial infusion.

For slice recording, 250nl AAV1-mDlx-mRuby2 was unilaterally injected in the VLPO, 250nl AAV1-DIO-ChR2-eYFP was contralaterally injected in the VLM of Vglut2-Cre mice.

For fiber photometry in GAD2-Cre mice, 200nl AAV9-CaMKIIa-ChR2-eYFP was unilaterally injected in the VLM, 200nl AAV1-FLEX-GCaMP6s was contralaterally injected in the VLPO. An optical fiber was implanted 0.2mm above the VLPO injection site.

For microendoscopic calcium imaging, 200nl AAV1-FLEX-GCaMP6f was unilaterally injected in the VLM of Vglut2-Cre mice. A GRIN lens (0.5 or 0.6mm diameter, Inscopix) was implanted 0.2mm above the injection site. After >3 weeks, the cover was removed to expose the GRIN lens and a miniaturized, single-photon, fluorescence microscope (Inscopix) was lowered over the implanted GRIN lens until the GCaMP6f fluorescence was visible under illumination with the microscopes LED. The microscopes baseplate was then secured to the skull with dental cement darkened with carbon powder for subsequent attachment of the microscope to the head. After recovery from surgery, we did not observe any gross behavioral abnormality, and these mice exhibited normal sleepwake cycles.

Mouse sleep behavior was monitored using EEG and EMG recording along with an infrared video camera at 30 frames per second. Recordings were performed for 2448h (light on at 7:00a.m. and off at 7:00p.m.) in a behavioral chamber inside a sound-attenuating cubicle (Med Associated Inc.). Animals were habituated in the chamber for at least 4h before recording. EEG and EMG signals were recorded, bandpass filtered at 0.5500Hz, and digitized at 1017Hz with 32-channel amplifiers (TDT, PZ5 and RZ5D or Neuralynx Digital Lynx 4S). Spectral analysis was carried out using fast Fourier transform (FFT) over a 5s sliding window, sequentially shifted by 2s increments (bins). Brain states were semi-automatically classified into wake, NREM sleep, and REM sleep states using a custom-written Matlab (version 2021, MathWorks) program43 (wake: desynchronized EEG and high EMG activity; NREM: synchronized EEG with high-amplitude, delta frequency (0.54Hz) activity and low EMG activity; REM: high power at theta frequencies (69Hz) and low EMG activity). Semi-auto classification was validated manually by trained experimenters. Relative delta power was calculated by dividing the delta power in the 2-s bins by the total EEG power averaged across the recording session.

Fiber photometry recordings were performed essentially as previously described44. In brief, Ca2+-dependent GCaMP fluorescence were excited by sinusoidal modulated LED light (465nm, 220Hz; 405nm, 350Hz, Doric lenses) and detected by a femtowatt silicon photoreceiver (New Port, 2151). Photometric signals and EEG/EMG signals were simultaneously acquired by a real-time processor (RZ5D, TDT) and synchronized with behavioral video recording. A motorized commutator (ACO32, TDT) was used to route electric wires and optical fiber. The collected data were analyzed by custom MATLAB scripts. They were first extracted and subject to a low-pass filter at 2Hz. A least-squares linear fit was then applied to produce a fitted 405nm signal. The DF/F was calculated as: (F-F0)/F0, where F0 was the fitted 405nm signals. Data were smoothed using a moving average method and downsampled to 5Hz. In Supplementary Fig.6, photometric data were further normalized across animals using Z-score calculation.

All optogenetic stimulation were conducted unilaterally. Mice were habituated in the behavioral chamber for at least 4hours before the experiment. Light pulses (20Hz, 10ms) with different durations (30s, 1min, 2min) from a 473nm laser diode (Shanghai laser & Optics Century Co., Ltd) were controlled by a microcontroller board (Arduino Mega 2560, Arduino). Laser power is set to 46mW for somatic stimulation in the VLM and 1015mW for terminal stimulation in the VLPO. We used two methods to trigger laser stimulation: (1) wake-trigger stimulation: An IR-camera (30 fps) was placed on the ceiling to videotape animal behavior. A custom Matlab program45 was used to real-time process video frames to detect animals location by subtracting each frame from the pre-acquired background image (without the mouse). Laser stimulation was automatically triggered when animal movement continued for a period (5min). A minimal interval of 30min was set between trials. In no-light control experiments, the same trigger method was applied except the laser power was off. (2) fixed interval stimulation: inter-stimulation interval for optogenetic stimulation is fixed to 45min. To compare optogenetic-induced and natural NREM sleep (Fig.7e), we used the first NREM sleep episode (if existed) following laser stimulation in 15-min time windows (5min before laser, 10min after laser) as optogenetic-induced sleep, used all NREM sleep episodes from 15-min time windows between laser stimulation (at least 15min away from previous or next stimulation) in the same recording sessions as natural sleep, and calculated bout durations and relative delta power of NREM sleep episodes.

Imaging sessions took place during the light cycle in a behavioral chamber placed within a sound-attenuated cubicle (Med. Associates). Calcium activity was acquired using the nVista 3.0 hardware and IDPS software (Inscopix) with 475nm LED illumination (10Hz, 0.41.2mW/mm2). EEG and EMG were acquired using Neuralynx Digital Lynx 4S controlled by a custom-built MATLAB program via Neuralynx API. A TTL signal delivered from the Inscopix system to the Neuralynx system throughout the recording session was used to synchronize the timing between the imaging and EEG/EMG recordings. Each recording session lasted 60120min, and for each mouse the data from a single recording session was included. Imaging data were processed in IDPS (Inscopix, version 1.6.0.3225) and MATLAB46. First, the acquired images were spatially down-sampled by a factor of 4. To correct for lateral motion of the brain relative to the GRIN lens, we used the motion correction function in IDPS, as in previous studies47,48. Regions of interest (ROIs) were then manually identified. The pixel intensities within each ROI were averaged to create a fluorescence time series. For individual neurons, the DF/F was calculated as the difference between the calcium activity at each bin and the averaged calcium activity of the whole recording time, divided by the average. To quantify the calcium activity, we used the OASIS fast deconvolution algorithm49. The identified events were reviewed along with calcium imaging video by an experimenter and motion-induced artifacts were excluded for further analysis. To compare the activity in different brains states, we used the integrated area under curve (AUC) of detected events and normalized it to the durations (in minute) of each state, which yields relative activity per minute. The N-W or R-W selectivity index was calculated as:

$${{{{{rm{Index}}}}}}=({{{{{{rm{AUC}}}}}}}_{{{{{{rm{a}}}}}}}-{{{{{{rm{AUC}}}}}}}_{{{{{{rm{b}}}}}}})/({{{{{{rm{AUC}}}}}}}_{{{{{{rm{a}}}}}}}+{{{{{{rm{AUC}}}}}}}_{{{{{{rm{b}}}}}}})$$

where AUCa and AUCb refer to AUC activity in brain state a (e.g., NERM sleep) and b (e.g., wake) respectively. Index ranges from 1 to 1, with 0 indicating no selectivity between two states.

For the analysis of calcium activity during the transitions (Fig.2d), we calculated AUC activity in the NREM active cells before and after wake-to-NREM or NREM-to-wake transitions. A 30-s window in each brain state (e.g. 30-s wake, 30-s NREM for W-N transitions) was used for quantification. Transitions with less than 30s-episodes in either state were excluded for analysis.

After habituation for 12h in the testing chamber, C57BL/6J mice expressing hM4Di or hM3Dq in the VLM were injected with saline (day 1) and CNO (day 2, 1mg/kg body weight) intraperitoneally (i.p.) at the same time of the days. Injections were performed in light cycles (10:00a.m.) for chemogenetic inhibition and in dark cycles (9:3010:00 PM) for chemogenetic activation. In control experiments, wild type mice without viral injection were treated with CNO and saline either in light cycles or dark cycles. Sleep recording started at least 1h before saline injection and lasted 24h after CNO injection. EEG and EMG in the time window (012h after CNO or saline injection) were used for data analysis.

On the day of the experiment, mice were habituated and tested with photostimulation in a behavioral chamber for overnight (pre-test). Following the pre-test, the selective AMPA receptor antagonist NBQX (5mg/ml in 0.9% NaCl, 0.25l, Tocris Bioscience) was bilaterally infused into the POA using two 1l microsyringes (Hamilton) and two internal cannulas (P1 Technologies) inserted into the double guide cannula that implanted above the POA. The infusion rate was approximately 0.04l/min controlled by a syringe pump (Harvard Apparatus). As a control, saline (0.9% NaCl) was similarly applied. After the intracranial infusion, mice were moved back to the chamber for further optogenetic experiments. The first laser stimulation started 30min after drug infusion. A total of 68 trials in the first 4h was used for data analysis.

To identify neurons projecting to the POA, we unilaterally injected ~200nl AAVrg-hSyn.Cre.WPRE.hGH in the VLPO of Ai9 reporter mice. Six weeks after viral injection, mice were perfused with phospho-buffered saline (PBS) containing 10 U/ml heparin, followed by 4% paraformaldehyde. Brains were then harvested and post-fixed in 4% paraformaldehyde for 3h at room temperature. The whole brains were cleared by the CUBIC method as previously described39,50. Briefly, mouse brains were washed 3 times in PBS before immersion in CUBIC reagent-1 (diluted 1:2 in water) overnight, incubated in reagent-1 for 710 days. Then, brains were washed with PBS, degassed in PBS overnight, and immersed in reagent-2 (diluted 1:2 in PBS) for 624h before incubated in reagent-2 containing TO-PRO-3 (1:5000, Thermo Fisher Scientific) for additional 710 days. Reagent 1 contained 25wt% urea (Sigma- Aldrich), 25wt% N,N,N,N-tetrakis (2-hydroxypropyl) ethylenediamine (Sigma- Aldrich) and 15wt% Triton X-100 (Nacalai Tesque). Reagent 2 contained 50wt% sucrose (Sigma-Aldrich), 25wt% urea, 10wt% triethanolamine (Sigma-Aldrich) and 0.1% (v/v) Triton X-100. All clearing procedures were performed at room temperature with gentle shake to prevent sample deformation caused by temperature fluctuation and fluorescence loss. Reagent 1 and Reagent 2 were refreshed every 3 days. Samples were imaged in an oil mix (mineral oil and silicone oil 1:1) horizontally from ventral to dorsal by Light-sheet fluorescence microscopy (UltraMicroscope, LaVision BioTec) as previously described39. The images were acquired with a z-step size of 5 m. Exposure time was 50ms per channel per z step. Data was processed in ImageJ (version 1.52i). The gamma value of the images was set to 0.5 for display purposes. The whole-brain data was registered to a reference atlas (Allen Brain Institute, 25-m resolution volumetric data with annotation map, http://www.brain-map.org) using elastix (version 5.0)51,52. The voxel size of both sample data and reference template were scaled to 6.5 m. The 3D reconstruction, cell tracing, and structure labeling were performed in Imaris (version 9.6, Bitplane).

In sleep deprivation experiments, mice were allocated into three groups: (1) control, (2) sleep deprivation (SD), (3) recovery sleep (RS) after deprivation. Each group was placed in a behavioral chamber, which was further contained in a sound-attenuating cubicle (Med Associates Inc). Mice were habituated for 48h before Fos induction. For sleep deprivation, a stepper motor controlled by an Arduino board was used to move a rod to sweep the floor from one side to the other at a speed of 2cm/s. As a motor control, Mice in the first group were subject to sweeping movement for 2h before perfusion. SD mice were subject to 30-s sweeping movement followed by a 90-s interval for 6h, and then sacrificed for perfusion. RS mice were perfused 2h after 6-h SD. All sleep manipulation was carried out in the light cycle, and animals were sacrificed between 4:00p.m. and 6:00p.m. Mouse brains were sectioned coronally at 100 m and processed for immunostaining as previously described53. Tissue sections were incubated with guinea pig c-Fos antibody (1:1000, Synaptic Systems, cat#226308) for 24h at 4C. Fluorescently tagged secondary antibodies (Alexa-488 donkey anti-guinea pig, 1:500, Jackson ImmunoResearch, cat#706-545-148) were used to visualize Fos expression. All sections were imaged using a Zeiss 810 confocal microscope. Cell counting (brain sections from AP-6.5mm to AP-7.2mm) was performed manually in ImageJ.

In optogenetic stimulation experiments (Supplementary Fig.14), Vglut2-Cre mice were injected with AAV-DIO-ChR2-eYFP unilaterally in the VLM. To maximize the c-Fos signals, a 30-min laser stimulation (20Hz, 45mW) was applied. Mice were kept in the recording chamber for additional 40minutes after stimulation, then perfused for c-Fos staining as described above. The injection site and other sleep/wake related brain regions were examined for c-Fos expression.

Mice were deeply anaesthetized, and fresh frozen brains were sectioned at 20 m thickness using a cryostat. FISH was performed using RNAscope Multiplex Fluorescent Assay V2 (Advanced Cell Diagnostics). Reagents: Fos in situ hybridization probe: cat# 316921, Slc17a6 in situ hybridization probe: cat# 319171, Slc32a1 in situ hybridization probe: cat# 319191. Tyrosine hydroxylase (TH) in situ hybridization probe: cat# 317621 (Advanced Cell Diagnostics). Images were acquired using a Zeiss 810 confocal microscope. Cell counting (brain sections from AP-6.5mm to AP-7.2mm) was performed manually in ImageJ.

Viral expression and placement of optical implants were verified at the termination of the experiments using DAPI counterstaining of 100 m coronal sections (Prolong Gold Antifade Mountant with DAPI, Invitrogen). Images were acquired using a Zeiss 810 confocal microscope. Cell numbers were counted manually in ImageJ.

Four weeks after viral injection, mice were quickly decapitated under isoflurane sedation. Brains were placed in artificial cerebral spinal fluid (aCSF). Coronal slices (300m) containing the POA were cut on a vibratome (Leica VT1200) in sucrose cutting solution containing 2.5mM KCl, 10mM MgCl2, 0.5mM CaCl2, 1.25mM NaH2PO4, 26mM NaHCO3, 234mM sucrose, 11mM glucose. Slices were then transferred to aCSF containing 126mM NaCl, 26mM NaHCO3, 2.5mM KCl, 1.25mM NaH2PO4, 2mM CaCl2, 1mM MgCl2, and 10mM d-glucose bubbled with 95% O2 and 5% CO2. Slices were incubated at 341C for 30min before resting at room temperature prior to the experiment. Regular pipette intracellular solution contained 127mM potassium gluconate, 8mM NaCl, 4mM ATP-Mg, 0.6mM EGTA, 0.3mM GTP, 10 HEPES, and 8.1mM biocytin adjusted to pH 7.37.4 with KOH. Osmolarity was adjusted to 290300mOsm.

Inhibitory GABAergic cells in the POA were located using the presence of mRuby fluorescence. Cells were targeted approximately 20100m from the slice surface. Patch-clamp Scientifica MicroStar micromanipulators were controlled using LinLab2 software (Scientifica). Recordings were performed in juxtacellular or whole-cell mode with MultiClamp 700B amplifiers (Molecular Devices) in the current clamp or voltage clamp mode at 341C bath temperature. Data acquisition was performed through an Axon Digidata 1550B (Molecular Devices) connected to a PC running pClamp 11 (Molecular Devices). Recordings were sampled at 10kHz and filtered with a 2-kHz Bessel filter. Patch pipettes were pulled with a Flaming/Brown micropipette puller P-80PC (Sutter Instruments) and had an initial resistance of 38 M. Series resistance was automatically compensated at 15M. The membrane potential values given were not corrected for the liquid junction potential which was approximately 16mV. Cells were stimulated with blue LED light through a 40 water-immersion objective using pE-300ultra (CoolLED Limited) at approximately ~18.8mW. Stimulation protocols comprised of 10 sweeps of paired pulses at 2, 5, 10, 20, and 40, and 60Hz delivered with a light on time of 1ms. 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX; 10M) and DL-2-Amino-5-phosphonopentanoic acid (DL-AP5; 10M) was bath applied in some recordings.

Unitary excitatory post-synaptic potentials (EPSPs) and post-synaptic currents (EPSCs) were analyzed using custom Matlab scripts. EPSPs or EPSCs were considered if the absolute value is >2 times ofthe standard deviation of the baseline. Baseline was calculated as the mean of 10ms prior to the stimulation or pre-synaptic action potential. Amplitudes were found at the maximum or minimum point within a 1.518ms time window after the stimulation onset. Lower- or upper-bounds of detection windows were adjusted when necessary. The rise time was determined as the time interval encompassing 2080% of the amplitude. Latencies were determined by calculating the onset time of the PSP or PSC and subtracting the stimulation onset. This onset time represented the intersection of the line at baseline and the line through the 20% and 80% amplitude points.

No statistical methods were used to predetermine sample size, and investigators were not blinded to group allocation. No method of randomization was used to determine how animals were allocated to experimental groups. Mice in which post hoc histological examination showed viral targeting or fiber implantation was in the wrong location were excluded from analysis. Two-sided paired t-test, unpaired t-test, and MannWhitney U-test were used and indicated in the respective Figure legends. Values are tested against normal distributions using the KolmogorovSmirnov test with statistical significance set at p<0.05. All analyses were performed in MATLAB. Data are presented as meanSEM.

Further information on research design is available in theNature Research Reporting Summary linked to this article.

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Control of non-REM sleep by ventrolateral medulla glutamatergic neurons projecting to the preoptic area - Nature.com

Dairy and acne: Can milk be a cause of your acne problem? – Health shots

Are you someone who starts and ends your day with a huge glass of milk? While that is a very healthy choice but if you have been suffering from severe acne breakouts, you may want to reconsider your milk or overall dairy intake.

There can be countless reasons why one goes through this horrid problem of acne. Especially if you are a teenager, this phase is basically a rite of passage for you. But if there is a possibility that you are getting breakouts because of milk consumption, Health Shots is here with information that will help decode the mystery that surrounds dairy and acne.

According to popular dermatologist Dr. Jaishree Sharad, it has been proven by various studies that milk can cause you to have acne. In her recent Instagram post, she explained how this happens:

1. Sometimes cows are administered with bovine growth hormones to increase the amount of milk they produce. Now, because of this growth hormone, the milk produced by these cows is high in IGF1 (Insulin-like Growth Factor) which causes us to have acne.

2. Drinking this milk leads to an increase in insulin and an increase in IGF1 in our blood.

3. These two leads to an increase in oil production, an increase in androgen (hormones responsible for puberty) production and an increase in absorption of male hormones which causes acne.

It has been found that skimmed milkwhere all milk fat is removed from whole milkis more likely to cause breakouts. According to studies cited by the American Academy of Dermatology (AAD):

* Among more than 47,000 women in the US, those who drank at least two glasses of skim milk a day as teenagers were 44 percent more likely to have had acne.

* Among just over 6,000 girls between ages 9 and 15, those who drank the most cows milk were more likely to have acne, with no differences based on the fat content of the milk.

* Among more than 4,000 boys between ages 9 and 15, those who drank skim milk were more likely to have acne.

Dairy is a huge part of our lives and many people find it hard to even start their day without a cup of steaming hot milk based tea.

1. Opt for plant-based milk. Plant milk is a plant beverage with a color resembling that of milk. Plant milks are non-dairy beverages made from a water-based plant extract for flavoring and aroma. Plant milks are consumed as alternatives to milk, and often provide a creamy mouthfeel.

2. You may also take yogurt, buttermilk, paneer and cheese but in moderation. Even though these are by-products of milk, still studies found them not guilty of causing acne.

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Dairy and acne: Can milk be a cause of your acne problem? - Health shots

Beauty Sleep: The Toll Poor Sleep Takes on Your Appearance and Health – CNET

When you think about all the things that can affect your skin, sleep isn't usually the first thing to come to mind. You may have heard that quality sleep is essential for our overall well-being, but did you know that it's also a big factor that impacts our appearance? However, it's not always easy for us to get those recommended 7 to 9 hours of beauty sleep. According to the Centers for Disease Control and Prevention, an estimated 70 million Americans suffer from chronic sleep disorders.

So, what does poor sleep do to your appearance and health? Here's what we know.

Read more: Fall Asleep Faster by Doing This Thing Right Before Bed

You might have heard the term "beauty sleep" before. Turns out, it's real and may be the closest thing to the fountain of youth you can get. When you sleep, your body enters recovery mode and each stage of sleep is crucial to skin recovery.

During varying stages of sleep, the body produces multiple hormones including human growth hormone, melatonin and cortisol. These hormones play critical roles in recovery including repairing skin from daily damage, keeping our skin looking youthful and protecting your skin from free radicals that can cause damage to cells.

When sleeping, every hour counts. If you're having trouble getting the recommended hours of sleep, check out our guide on how to get better sleep.

A 2017 study found that lack of sleep has the potential to negatively affect your facial appearance and may decrease others' willingness to socialize with the sleep-deprived person. Here's how not getting enough shut-eye affects your appearance.

Skin: Let's start with the basics. Lack of sleep affects your appearance by making you look tired. You know, bags under the eyes and all that jazz. Not only does poor sleep affect your skin but also its normal functions -- like collagen production. Excess cortisol due to the stress of sleep deprivation is a common cause of acne.

Hair: Lack of sleep also impacts your hair growth since collagen production is affected when we don't get enough sleep, making your hair more prone to thinning or hair loss. Sleep deprivation can also cause stress on the body and increase cortisol, which can lead to hair loss.

Eyes: Just one night of poor sleep is enough to cause dark circles under your eyes. Lack of sleep can cause the blood vessels around your eyes to dilate and create dark circles or puffiness. Depending on your natural skin tone, these dark circles may be visible as shades of blue, purple, black or brown.

Read more: How to Fall Asleep in 10 Minutes or Less

Sleep deprivation goes beyond affecting the way you look. Lack of sleep can also affect the way your body and mind work.

Prolonged deprivation can make you feel sluggish and fatigued, which means less energy to get you through the day. Other studies have linked lack of sleep to an increased risk of heart disease, stroke, diabetes and high cholesterol due to the higher levels of cortisol.

Studies show that sleep deprivation can affect memory function and emotional stability, as well as impair decision-making skills. Poor sleep can hurt your performance at work, lead to mood swings and enhance emotions like anger and sadness.

Data from a 2021 study found that people ages 50 through 60 who got 6 hours or less of sleep were at greater risk of developing dementia. Those who got less sleep than the recommended seven hours, were 30% more likely to be diagnosed with dementia later in life than those who got the recommended hours of sleep.

In addition to how you look, how you sleep can also impact your weight. Sleep deprivation has been linked to weight gain and a higher risk of obesity in men and women. Similarly, people with severe sleep apnea tend to experience increased weight gain.

One study that followed 68,000 middle-aged American women for 16 years found that women who slept five hours or less a night where 15% more likely to become obese over the course of the study than those who slept seven hours.

Ready to catch up on some beauty rest? Follow these tips for sleeping for better skin:

How to build a good routine? Here are four steps to try:

1. Go to bed at approximately the same time each night.2. Wake up at approximately the same time every morning.3. Limit your naps to 30 minutes or less.4. Maintain a regular sleep schedule on weekends.

Read more: How to Create the Ideal Environment for Better Sleep

The information contained in this article is for educational and informational purposes only and is not intended as health or medical advice. Always consult a physician or other qualified health provider regarding any questions you may have about a medical condition or health objectives.

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Beauty Sleep: The Toll Poor Sleep Takes on Your Appearance and Health - CNET

Q&A: A year in the life of the mouse lemur – Stanford University

By Kanika Khanna|Part of our Next-Generation Neuroscience series

Wu Tsai Neurosciences Institute Interdisciplinary Scholar Shixuan Liu studies seasonal rhythms in the diminutive mouse lemur in the Stanford laboratories of Mark Krasnow and James Ferrell.Photo credit: Steve Fisch

Animals in the wild may not have an annual planner to keep track of the year, but they nonetheless manage to keep to a strict calendar for example knowing just what time of the year to breed and when to hibernate. Research into the circadian clocks that regulate our 24-hour cycles led to a recent Nobel Prize, but very little is known about how animals maintain much longer-term seasonal rhythms.

Shixuan Liu aims to tackle this thorny question using her deep expertise in quantitative biology. The Wu Tsai Neurosciences Institute Interdisciplinary Postdoctoral Scholar has previously used systems biology approaches to study molecular oscillations in cells and quantitative imaging to explore the dynamics of cell division that operate on a timescale of hours. But now she is taking a leap across biological and temporal scales applying her quantitative know-how to understand year-long oscillatory patterns across an entire organism.

Mouse lemurs are primates that are about twice the size of a mouse and live exclusively on Madagascar.Photo credit: Robert Siegel

To study these long-term oscillations, Liu turned to the mouse lemur, a diminutive primate native to Madagascar that exhibits robust seasonal rhythms breeding during the summer and hibernating during the winter. There is a great deal of excitement about establishing the mouse lemur as a model organism in neuroscience and primate biology as it is genetically more closely related to humans than mice, reproduces fast and is easy to breed in the lab.

Working in the labs of James Ferrell in the Department of Chemical and Systems Biology and Mark Krasnow in the Department of Biochemistry, Liu is currently leading a massive global effort to build a molecular cell atlas of the mouse lemur. With a team of collaborators around the world, she is looking at gene activity simultaneously in hundreds of cells types in different tissues all across the animal during different seasons.

Using this atlas, Liu hopes to uncover the intrinsic master calendar that controls seasonal rhythms in the mouse lemur. By understanding the biology behind seasonal rhythms, we may gain insights into important medical mysteries, such as why some psychological disorders and metabolic syndromes display seasonal variations and why globally more people die in winter than any other time of year.

We spoke with Liu about her work in establishing the mouse lemur as a model system to study seasonal rhythms, how hormone regulation may play an important role in this process and how the scientific community at large can benefit from open-access resources her work has created.

Liu has helped lead an international effort to create a molecular cell atlas for the mouse lemur, a public resource which she hopes will advance ability of researchers around the world to use this valuable model organism to better understand the evolution and function of the primate brain.Photo Credit: Steve Fisch

I have always been interested in quantitative biology. My PhD work focused on understanding molecular pathways that control cell cycle dynamics using quantitative microscopy. For my postdoctoral research, I wanted to apply this systems biology approach to understand molecular interactions at an organismal level. So at the end of my PhD, I talked with James Ferrell (Jim), a systems biologist at Stanford who studies the cell cycle oscillator and builds theoretical models of oscillator mechanisms in various biological systems.

Jim was interested in the idea of long-term biological oscillators. He had been talking with Mark Krasnow, who has been doing really exciting work to establish an animal called the mouse lemur as a new primate model organism. This also happens to be an appealing model for studying seasonal rhythms that are widespread in wild animals, yet we do not have a good understanding of how they work. One of the problems is that domesticated animals like laboratory mice have lost seasonal rhythms and hence, are not ideal candidates for the study of seasonal rhythms.

Mouse lemurs are among the smallest primate in size, only about 11 inches long and weighing ~60 grams. They share many logistical advantages of working with mice in the laboratory such as rapid reproduction. At the same time, they are more closely related to humans than mice on the evolutionary tree. As a part of a large international consortium, Marks lab is doing groundbreaking work to establish useful resources to study this emerging model organism. I was very excited to explore new frontiers in a cutting-edge research area and joined the two labs for my postdoc.

Mouse lemurs exhibit striking seasonal changes in body mass and reproduction. During the summer, they have higher metabolic rates and are relatively lean. Summer is also their breeding season. During the winter, however, the animals transition into hibernation or torpor to conserve energy as resources become scarce. Their metabolic rates decrease and they accumulate fat in different body parts, especially the tail.

Of course, many wild animals exhibit seasonal rhythms. For instance, certain Arctic species routinely change the color of their coat to snowy white in winters. This phenomenon called seasonal molting involves the shedding of an external layer of the animal like fur or feathers and provides camouflage in snow.

Humans may not show obvious seasonality, but several reports suggest certain trends. A famous example is the seasonal affective disorder (SAD) where patients face depression in winters and naturally recover in the spring. In addition, more people die during winters than summers. In the northern hemisphere, deaths are higher in December, January and February, while in the southern hemisphere, deaths are higher in corresponding winter months of June and July. In the US alone, death rates are about 10% higher in winter months.

Recently, Michael Snyders lab at the Department of Genetics identified many blood biomarkers and hormones that show seasonal trends. For example, they found that HbA1c, a common biomarker for type 2 diabetes peaks in summer and declines in winter. Similarly, molecular signatures associated with immune responses, hypertension and cardiovascular diseases also often peak seasonally. Recently, Uri Alons lab at the Weizmann Institute systematically analyzed millions of blood tests of the Israeli population from the last 15 years and observed seasonal rhythms in many hormones, like peaking of sex hormones in winter and growth hormones in spring. So, if we understand the mechanisms of seasonal rhythms in humans, we can potentially design treatment strategies for season-related illnesses or deaths.

A heat-map plot from the mouse lemur cell atlas online portal allows researchers to cross-reference gene expression data from more than 750 cell types. Image credit: Tabula Microcebus

In order to study a new model organism, it is essential to build a cellular and molecular foundation. The Molecular Cell Atlas of the mouse lemur is essentially a detailed catalog of over 750 types of cells and expression levels of proteins in different tissues in the lemur. We built this atlas using a technique called single-cell RNA-sequencing which allows us to measure expression of individual cells in different tissues of the organism.

This project depended on bringing in people from different fields including biologists, pathologists and genomicists as part of the Tabula Microcebus Consortium, which consists of ~150 scientists from over 50 labs at 15 institutions worldwide.

We have created a publicly accessible online portal hosted by The Chan-Zuckerberg Biohub where the scientific community can study cell types of the mouse lemur by tissue, organ and function. The data can be used to compare cell types to each other in different parts of the body and also for comparison across species like human and mouse where similar information is available. We believe the atlas will be useful in understanding not only seasonal rhythms in the mouse lemur but also broader questions in the field of primate biology and evolution. The pipeline can also be used to build similar atlases for emerging new model organisms.

We know about cells in the hypothalamus that coordinate the 24-hour circadian cycle, but we do not know much about cells or molecules that coordinate the 12-month annual cycle in animals. Fortunately for us, mouse lemurs are ideal animals to study seasonal rhythms. Our collaborators Fabienne Aujard, Martine Perret, Jeremy Terrien and their colleagues at the National Natural History Museum in France have established a large breeding colony of ~500 mouse lemurs and unlike standard lab animals they exhibit seasonal rhythms in the lab, including seasonal weight changes, hibernation, and breeding behaviors.

Many animals, including the mouse lemur, can sustain seasonal rhythms even when the length of the day remains constant. This suggests an internal calendar controls these rhythms, independent of environmental cues. The molecular cell atlas of the mouse lemur we created gives us detailed information about what biological markers that are produced in different types of cells across different tissues of the animal. I am now comparing samples collected during summer and winter to create a seasonal version of this atlas. This will allow us to identify factors regulating and driving seasonal rhythms by measuring changes in levels of molecules in different cells of the body in different seasons.

We think hormone regulation may be vital for seasonal rhythms due to the kind of phenotypic changes observed in different seasons. In our recent preprint, we described 12 hormones that differed in concentration during summer and winter, including testosterone, melatonin, thyroid and several gut hormones. We also found that these hormones target a broad range of cells and tissues. We know about changes in appearances in some tissues during different seasons, for example, increased fat in adipose tissues and decreased size in gonads during winter. Our data suggest that many other cell types likely experience changes in their physiology or function in response to the seasonal hormones. In the future, we may be able to tease apart these mechanisms and compare them to seasonally varying hormones in other organisms like humans to understand season-associated human diseases.

Traditionally, in order to study a biological process, we have often focused on only one or few molecules and pathways. A molecular cell atlas, on the other hand, provides insights into relationships between different cell types and organs on an organism-wide level. We are now using the atlas to study mouse lemur gene evolution, physiology, and disease with different collaborators. In collaboration with Prof. Peter Perham at the Stanford School of Medicine, we are studying expression levels of immune genes in different cell types. We also have an ongoing collaboration with Prof. Bo Wang at Stanford Bioengineering to study the evolution of gene expression patterns across human, lemur, and mouse. We hope this rich data can be further exploited by the broader research community to better understand primate biology and disease.

All our data and pipelines are publicly accessible. We believe this will be a valuable resource for establishing cell atlases in emerging model organisms. This will also serve as a new way to identify genes and their function by doing organism-wide comparisons and break away from the mold of studying select few genes in only select model organisms.

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Q&A: A year in the life of the mouse lemur - Stanford University

Sure Signs You Have Liver Disease, Say Physicians Eat This Not That – Eat This, Not That

Liverdisease can be very sneakyif people don't know the signs, it can be easy to miss until the disease is advanced. "That's the tough part of treatment," says Anurag Maheshwari, MD, a gastroenterologist with the Institute for Digestive Health and Liver Disease at Mercy Medical Center in Baltimore. "Convincing patients that they need to act now in order to avoid complications in the future can sometimes be a challenge, because they don't feel any different today." Here are five sure signs of liver disease, according to doctors. Read onand to ensure your health and the health of others, don't miss these Sure Signs You've Already Had COVID.

Carrying excess weight and having diabetes are strongly correlated with fatty liver disease, doctors say. "Two risk factors for NAFLD, obesity and diabetes, are becoming more prevalent," says Laura Dichtel, MD, MHS, of Massachusetts General Hospital and Harvard Medical School. "We currently do not have any FDA-approved treatments for NAFLD, and weight loss is the only effective treatment. Understanding how growth hormone improves liver fat and inflammation in people with NAFLD could lead to the development of novel targeted treatments."

"One of the most common and debilitating symptoms among individuals with liver disease is fatigue," says Melissa Palmer, MD. "It is universal to all varieties of liver disease from Primary Biliary Cirrhosis to Chronic Hepatitis C. In some patients, fatigue begins several years after the diagnosis of liver disease is made. In others, it was the primary reason for seeking medical attention. In such individuals multiple visits are made to a variety of physicians in search of a cause of their extreme lassitude. Some patients even seek psychiatric evaluation, as an accompanying symptom is often depression."

Jaundice is a common symptom of liver disease, and should never be ignored. "Many disorders that cause jaundice, particularly severe liver disease, cause other symptoms or serious problems," says Danielle Tholey , MD, Sidney Kimmel Medical College at Thomas Jefferson University. "In people with liver disease, these symptoms may include nausea, vomiting and abdominal pain, and small spider-like blood vessels that are visible in the skin (spider angiomas).

Abdominal pain could be because of ascites, a sign of liver damage. "Ascites is fluid buildup in the abdominal cavity caused by fluid leaks from the surface of the liver and intestine," according to Johns Hopkins Medicine. "Ascites due to liver disease usually accompanies other liver disease characteristics, such as portal hypertension. Symptoms of ascites may include a distended abdominal cavity, which causes discomfort and shortness of breath."

Unexplained weight loss could be a sign of liver disease, experts warn. "Because the liver plays a key role in the digestive system, cirrhosis and cancer in the liver can both cause you to lose your appetite and you may lose weight," according to the Cancer Council of New South Wales.

If you experience any symptoms of liver disease, seek medical attention immediatelythe earlier liver disease is diagnosed, the better your chances for treatment. "You don't want to turn yellow with jaundice or feel pain in your upper right abdomen because those are signs your liver is already very sick," says Saleh Alqahtani, MD, director of clinical liver research for Johns Hopkins Medicine. "It is far better to stop liver disease before it gets too serious."6254a4d1642c605c54bf1cab17d50f1e

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Sure Signs You Have Liver Disease, Say Physicians Eat This Not That - Eat This, Not That