#sarcolemma | Explore Tumblr Posts and Blogs

domesticsupplies · 1 year

Text

Explode Through Your Bodybuilding Plateaus with Anabolic Priming

You've probably heard bodybuilders say that you need to train your legs in order to develop your arms. This advice is not only true, but it can also be used to help you break through plateaus in training and gain muscle if you are a slow-gainer. The article describes how you can use anabolically-priming exercise to increase your workout gains.

Responses to Exercise and Adaptation

Bodybuilders, and other serious exercisers have probably experienced training plateaus. The more you work out the harder it becomes to gain muscle mass and strength. Why? Simply put, it is because the window for adaptation that was once large when starting a new workout regimen has shrunk by several times.

The weights and intensity of exercise that were used in the past to increase muscle mass and strength have no effect anymore. The human body restricts adaptation under natural conditions (non-steroids/drugs enhanced). This is to maintain balance and survival. steroids for sale fast shipping

The "natural regulation process" frustrates bodybuilders, and many turn to steroids as a way to solve the problem.

Exercise and anabolic hormone responses

We discussed in an article published on our site the interactions between bodybuilding exercises and hormonal reactions. We explained that anabolic steroids are not just responsible for "building" up and enlarging different types of tissues such as bone and muscle, but they also increase strength directly which leads to further increases in muscle size. We mentioned in the same article that exercise can manipulate anabolic hormonal response.

The NSCA – the leading authority in strength and conditioning – says that manipulating any one of these factors or a combination can boost testosterone naturally:

Use large muscles groups in your exercises

Use heavy resistance in your exercises (85-95% of 1RM).

Exercise volume: Moderate-high (multiple sets/exercises).

* Rest periods that are short between exercise (How can this kind of training create an environment more conducive to muscle growth?

Some of the mechanisms that may be responsible for the increase in anabolic states include:

* Since control of anabolic hormone release is directly dependent on the hypothalamic-pituitary axis (the link between the hypothalamus and pituitary gland), it is possible that intense physical exercise/stress itself may stimulate increased concentrations either directly or indirectly

The concentration of hormones may be increased without an actual increase due to fluid shifting from the blood cells into the tissues during intensive exercise.

The "pump" of the muscle caused by the pooling blood in its veins may lead to higher hormone levels in muscles that are being exercised, as it reduces the clearance and degrading in liver. The retention of blood within the muscles may also increase exposure time and likelihood that the hormone will bind with the receptors in the muscle tissue.

The sarcolemmas of the muscles involved are made mechanically sensitive (stretched), by force-generation stress, and more permeable for anabolic and growth hormones.

#steroids for sale fast shipping

0 notes

runandhideguys · 2 years

Text

sometimes etymology is great and sometimes you get words like sarcolemma

#biology makes me feel things #and none of them are good

0 notes

griddle-chump · 2 years

Text

Have you ever wondered how Gideon’s biceps got so swole? Have you ever wanted to flex on a necro, but the skeletal meat clinging to your humerus looks like a flesh adepts half-assed science project? Are you a Ninth House Cavalier seeking to get uncomfortably buff and help your necro achieve Lyctor status? Well, if you’re a meatbag like Gideon, look no further—for this guide to getting galactic swole is sure to increase your swordsmanship, your swoonmanship, and result in absolutely upsetting biceps. If you’re a skeleton, I’m sorry; this guide to getting swole probably won’t work for you as your sarcolemma has long since decayed.

Massive, bulging, sack-of-lemons biceps are, in fact, the key to wielding a broadsword, helping your necro earn Lyctorship, and swooning even the most waifish and ill-fated of necromancers. One cannot simply expect to defeat epic bone constructs with stringy fascicles. Despite the fact that a certain bird-boned Ninth House necro (with all of her, like, three muscles) seems to believe that one can get by simply with bone magic in this myriadic year, the ten-thousandth year of our Lord—The King Undying!, it’s clear that magic alone is not enough to save the Nine Houses of Dominicus.

First and foremost—hit those biceps brachii from all the angles and with all the modalities. Curls for the girls, as they say. The absolute best, 100% most appropriate and totally excellent place to do bicep curls is in the squat rack. Grab that 45lb iron bar, slap some plates on the ends, and stand there, feet firmly planted, gazing into the mirror, and squeeze that skeletal meat for at least 10 solid reaps. Ignore all looks you may get from the limp-fibred mayonnaise-uncle lookalikes that may be glaring at you. Who gives a galactic fuck if they want to squat in the squat rack? You’re busy getting swole AF in the upper extremities. Leg day does not exist in the House of the Ninth, and if it did, we would still do bicep curls in the squat rack because apparently bird-like qualities are a Ninth House standard, so our goal is to look like a chicken-legged Hercules.

If the squat rack is unavailable for bicep curls, grab a set of the heaviest dumbbells you can reap and stand right in front of the dumbbell rack. Why? Because like I said, leg day does not exist in the House of the Ninth, and walking the dumbbells a decent and respectable distance away from the rack constitutes a leg workout, and we simply cannot spare any adenosine diphosphate on anything other than our biceps. Keep those elbows tucked, core tight, forearms at a 45-degree angle to your body, gaze into the mirror, and squeeze the living fuck out of those dumbbells—hold at the top!—and slowly lower the weights back down. Reap the benefits.

No dumbbells? No problem! Grab an EZ curl bar, find the most obnoxious spot to stand, and reap the fuck out of that iron. Disregard any negativity thrown your way for being “inappropriate”- you do you!

If you’re to be any respectable cavalier of the Ninth, being decently okay with a rapier is a must. The quick and sharp movements of the rapier require an enormous amount of anterior deltoid endurance, so grab the heaviest plate you can heave, and reap that sucker—reap it hard. Again, keep that core tight! You can’t fight bone constructs if you’ve thrown your back out trying to impress the ladies.

For your finisher, your smoked-meat special of blood-pumping vessels, chin-ups are an absolute must. The supinated grip of this ultimate compound movement targets not only our biceps brachii, but also our latissimus dorsi, teres major, posterior deltoid, and our deep internal core stabilizers. In short, all of the muscles required to slash a broad sword through the sinew of the beefiest bone construct.

Be sure to flex as much as possible during this workout to help with the muscle growth. Everyone knows a good dirty mirror gym flex pic helps with the gains. Chances are, other people will be using the dirty gym mirror to workout, but you, my swole cavalier-in-training, should just keep flexing away. Aww yeah.

As for how much weight should one use if they’re trying to get galatic-swole? How the fuck should I know? Gravity works a little differently in outer space, so reap as much as you possibly can. In order for muscle to grow, you need to create a lot of micro tears in the muscle fiber. This is achieved through performing moderate reaps (or reps as those not under the rule of our Lord Necro Prime—The Kindly Prince of Death!—like to call them) at 70-80% of your maximum capacity, and is called hypertrophy. Working in this reap range yields the most muscle growth, but be sure to replenish that muscle glycogen store with a good meal (or dessert, as our “worryingly fly” favorite cav prefers) within 30 minutes of finishing your workout!

So, unless you want to end up like Harrowhark Nonegesimus with her bird-boned brittleness and complete inability to lift anything heavier than her own skull, get yourself to the gym and start reaping!

So here it is, cavaliers, a totally meat-headed workout to get your upper extremities swole as fuck. Complete the workout in a circuit, adding sets, reaps, or weight to increase that volume, maximize hypertrophy, and save Dominicus.

1. Barbell Biceps curls (3 sets, 10 reaps)

2. Dumbbell/EZ Curls (3 sets, 10 reaps)

3. Front Detoid Raises (3 sets, 10 reaps)

4. Chin ups (3 sets, As Many As Possible)

#legit would die for Gideon

0 notes

dritalotto · 2 years

Text

Muscle spindle

Perimysium is a slightly thicker layer of connective tissue consisting mainly of type I and III collagen and surrounds a group of fibers. It is made up of a delicate layer of reticular fibers and permits only small-diameter nerve fibers and capillaries, thus acting as a site of metabolic exchange. Endomysium surrounds individual muscle fibers. There are three types of connective tissue sheaths named for their location. Skeletal muscle tissue is made up of a collection of muscle fibers wrapped in connective tissue sheaths. They have a small amount of cytoplasm and because of their locations can sometimes be mistaken for skeletal muscle cell nuclei. Satellite cells are precursors to skeletal muscle cells and are responsible for the ability of muscle tissue to regenerate. They are accompanied by satellite cells between the external lamina and sarcolemma. Nuclei of skeletal muscle tissue are oval-shaped and located at the periphery of the cell. Because the cells are fused and multinucleated, they form a structural syncytium. This fusion results in a characteristic multinucleated structure. Skeletal muscle tissue develops through the fusion of individual myoblasts, or early muscle cells. Under a microscope, sarcomeres give skeletal muscle a striated appearance. The actin and myosin filaments making up the myofibrils are organized into sarcomeres. Myofibrils are rod shaped subunits of muscle cells. In contrast, muscle fibers making up the stapedius, a small muscle of the inner ear, are only a few millimeters in length. In the anterior thigh, a muscle fiber may be a meter long. The length of a skeletal muscle fiber varies by location. Individually, skeletal muscles cells are referred to as muscle fibers. A muscle fiber may also be referred to as a myofiber. The plasma membrane is called the sarcolemma and the endoplasmic reticulum is called the sarcoplasmic reticulum. The cytoplasm of a muscle cells is referred to as sarcoplasm. Muscle tissue terms often begin with myo-, mys-, or sarco. Special terms are used to describe structures associated with skeletal muscle tissue. Muscular dystrophy, actin aggregate myopathy, myotubular myopathies Place on the sarcolemma where motor fiber synapses with muscle in order to deliver contraction command Neurotransmitter is acetylcholine Perimysium - around multiple muscle fibers -> arranges them in fascicles Type IIb - get energy from anaerobic glicolysis, appear pink, fast-twitch and prone to fatigue Type IIa - get energy from oxidative glicolysis have high amount of glycogen, birhgter than type I, they are fast-twitch and resistant to fatigue Type I - use aerobic metabolysm to function they appear red because of the high amount of myoglobin they are slow-twitch and resestant to fatigue Sarcomere - functional unit (made of actin and myosin)Īccessory proteins - titin, tropomodulin, alpha-actinin, desmin, nebulin, dystrophin, myomesin Sarcomplasmic reticulum - modified endoplasmic reticulum T-tubules - invaginations of sarcolemma that transfer action potentials to the inside of the muscle cell Terminal cisterna - extension of sarcolemma that stores calcium Key facts about the skeletal muscle Function This article will discuss the histology of the skeletal muscle. Extensible tissue can be stretched and elastic tissue is able to return to its original shape following distortion. Skeletal muscle tissue is also extensible and elastic. Contractile tissue is able to generate tension of force. Excitable tissue responds to stimuli through electrical signals. It attaches to bones and the orbits through tendons. Skeletal muscle is an excitable, contractile tissue responsible for maintaining posture and moving the orbits, together with the appendicular and axial skeletons. Striated skeletal muscle, Textus muscularis striatus skeletalis

#Muscle spindle

0 notes

drawittoknowitmedical · 5 years

Link

Did you know you can find some of our tutorials on YouTube?

#cardiac muscle contraction #physiology tutorials #youtube #mcat #usmle #meded #medical school #drawmedicine #draw to learn #cardiac muscle #heart muscle #myofibrils #myofilaments #sarcolemma

7 notes · View notes

emmanuelm23 · 2 years

Text

SKELETAL MUSCLES

Skeletal muscles (commonly referred to as muscles) are organs of the vertebrate muscular system that are mostly attached by tendons to bones of the skeleton.The muscle cells of skeletal muscles are much longer than in the other types of muscle tissue, and are often known as muscle fibers.The muscle tissue of a skeletal muscle is striated – having a striped appearance due to the arrangement of the sarcomeres.

Skeletal muscle exhibits a distinctive banding pattern when viewed under the microscope due to the arrangement of two contractile proteins myosin, and actin – that are two of the myofilaments in the myofibrils. The myosin forms the thick filaments, and actin forms the thin filaments, and are arranged in repeating units called sarcomeres. The interaction of both proteins results in muscle contraction.

The sarcomere is attached to other organelles such as the mitochondria by intermediate filaments in the cytoskeleton. The costamere attaches the sarcomere to the sarcolemma.

Every single organelle and macromolecule of a muscle fiber is arranged to ensure that it meets desired functions. The cell membrane is called the sarcolemma with the cytoplasm known as the sarcoplasm. In the sarcoplasm are the myofibrils. The myofibrils are long protein bundles about one micrometer in diameter. Pressed against the inside of the sarcolemma are the unusual flattened myonuclei. Between the myofibrils are the mitochondria.

While the muscle fiber does not have smooth endoplasmic cisternae, it contains sarcoplasmic reticulum. The sarcoplasmic reticulum surrounds the myofibrils and holds a reserve of the calcium ions needed to cause a muscle contraction. Periodically, it has dilated end sacs known as terminal cisternae. These cross the muscle fiber from one side to the other. In between two terminal cisternae is a tubular infolding called a transverse tubule (T tubule). T tubules are the pathways for action potentials to signal the sarcoplasmic reticulum to release calcium, causing a muscle contraction. Together, two terminal cisternae and a transverse tubule form a triad.

Exercise is often recommended as a means of improving motor skills, fitness, muscle and bone strength, and joint function. Exercise has several effects upon muscles, connective tissue, bone, and the nerves that stimulate the muscles. One such effect is muscle hypertrophy, an increase in size of muscle due to an increase in the number of muscle fibers or cross-sectional area of myofibrils. Muscle changes depend on the type of exercise used.

Generally, there are two types of exercise regimes, aerobic and anaerobic. Aerobic exercise (e.g. marathons) involves activities of low intensity but long duration, during which the muscles used are below their maximal contraction strength. Aerobic activities rely on aerobic respiration (i.e. citric acid cycle and electron transport chain) for metabolic energy by consuming fat, protein, carbohydrates, and oxygen. Muscles involved in aerobic exercises contain a higher percentage of Type I (or slow-twitch) muscle fibers, which primarily contain mitochondrial and oxidation enzymes associated with aerobic respiration. On the contrary, anaerobic exercise is associated with exercise or short duration but high intensity (e.g. sprinting and weight lifting). The anaerobic activities predominately use Type II, fast-twitch, muscle fibers.Type II muscle fibers rely on glucogenesis for energy during anaerobic exercise.During anaerobic exercise, type II fibers consume little oxygen, protein and fat, produces large amounts of lactic acid and are fatigable. Many exercises are partially aerobic and anaerobic; for example, soccer and rock climbing.

The presence of lactic acid has an inhibitory effect on ATP generation within the muscle. It can even stop ATP production if the intracellular concentration becomes too high. However, endurance training mitigates the buildup of lactic acid through increased capillarization and myoglobin.This increases the ability to remove waste products, like lactic acid, out of the muscles in order to not impair muscle function. Once moved out of muscles, lactic acid can be used by other muscles or body tissues as a source of energy, or transported to the liver where it is converted back to pyruvate. In addition to increasing the level of lactic acid, strenuous exercise results in the loss of potassium ions in muscle. This may facilitate the recovery of muscle function by protecting against fatigue.

Delayed onset muscle soreness is pain or discomfort that may be felt one to three days after exercising and generally subsides two to three days later. Once thought to be caused by lactic acid build-up, a more recent theory is that it is caused by tiny tears in the muscle fibers caused by eccentric contraction, or unaccustomed training levels. Since lactic acid disperses fairly rapidly, it could not explain pain experienced days after exercise

3 notes · View notes

wearethekat · 3 years

Link

Have you ever wondered how Gideon’s biceps got so swole? Have you ever wanted to flex on a necro, but the skeletal meat clinging to your humerus looks like a flesh adept’s half-assed science project? Are you a Ninth House Cavalier seeking to get uncomfortably buff and help your necro achieve Lyctor status? Well, if you’re a meatbag like Gideon, look no further—for this guide to getting galactic swole is sure to increase your swordsmanship, your swoonmanship, and result in absolutely upsetting biceps. If you’re a skeleton, I’m sorry; this guide to getting swole probably won’t work for you as your sarcolemma has long since decayed.

presented without comment.

#tor.com staff are treasures #gideon the ninth #gideon's guide to getting galactic swole: an epic tale of skele-flex trashbaggery #tamsyn muir

25 notes · View notes

mcatmemoranda · 4 years

Text

Going through questions:

The genetic code is degenerate because more than one codon can code for 1 amino acid. Every tRNA goes with a specific amino acid; due to the degeneracy of the genetic code, the tRNA will respond to whichever codons go with its specific amino acid. The wobble hypothesis is that the third nucleotide doesn't have to do traditional base pairing.

Bloom syndrome is an autosomal recessive mutation in the BLM gene. It causes defect of helicase and presents with growth retardation, photosensitivity, immunodeficiency, and microcephaly.

Lyonization = X inactivation; in females, one of the X chromosomes is methylated and becomes a Barr body. This inactivated X chromosome becomes tightly would heterochromatin that isn't expressed. Heterochromatin = methylated DNA +deacetylated histones. I recall from listening to OnlineMedEd that acetylation makes DNA accessible. So deacetylation makes DNA less accessible. DNA is wrapped around histones. Methylation of DNA and deacetylation of histones makes the DNA less accessible for transcription. Euchromatin is not methylated and is easily accessible.

Precursor mRNA (pre-mRNA, aka heterogeneous nuclear RNA, hnRNA) is processed before leaving the nucleus--it gets the 5' cap and poly A tail added and introns are spliced out. Once all that happens, it's mature mRNA, which can leave the nucleus. There are also these things called P bodies that regulate mRNA in the cytoplasm. P bodies are involved in mRNA decay.

Uniparental disomy = the offspring receives 2 copies of a chromosome from 1 parent, and no copy from the other parent; leads to issues with imprinting. Uniparental disomy-> improper imprinting-> Prader-Willi and Angelman syndromes.

Down syndrome is often due to nondisjunction in meoisis, but can also be due to unbalanced Robertsonian translocations (you get too much of one copy of a gene and not enough of the other--this one I took detailed notes about from OnlineMedEd videos in my red notebook; if Robertsonian translocation causes Down syndrome, the pt will actually have a normal number of chromosomes [46], but the amount of genetic information from chromosome 21 will be more than it should be on the chromosomes the pt has, so it presents like there is an extra chromosome 21) or mosaicism (nondisjunction in mitosis causes some cells to have an extra chromosome 21, but not all cells).

Gowers’ sign is when pts with Duchenne muscular dystophy use their arms to get up; looks like they use their arms to “walk up” their own bodies. From Wikipedia:

Gowers' sign is a medical sign that indicates weakness of the proximal muscles, namely those of the lower limb. The sign describes a patient that has to use their hands and arms to "walk" up their own body from a squatting position due to lack of hip and thigh muscle strength.

Duchenne muscular dystrophy is an X-linked recessive mutation in the dystrophin gene. Frameshift and nonsense mutations cause shortened dystrophin gene. In unaffected people, dystrophin links with actin for support of glycoproteins in the plasma membrane of skeletal muscle cells. Defective dystrophin-> breakdown of sarcolemma, degeneration of muscle fibers, calf enlargement (it's really not the calf muscles that are enlarged--it's fat resulting from breakdown of the muscles), increased serum creatine.

Huntington disease is due to CAG trinucleotide repeats in the HTT gene. The more of these there are, the earlier the disease comes on and the more severe it is, which is called anticipation. Huntington's presents with chorea, depression/aggression/apathy, and dementia. Friedreich ataxia, fragile X syndrome, and myotonic dystrophy are also trinucleotide repeat diseases.

From Wikipedia:

Friedreich's ataxia (FRDA or FA) is an autosomal recessive genetic disease that causes difficulty walking, a loss of sensation in the arms and legs and impaired speech that worsens over time. Symptoms generally start between 5 and 20 years of age. Many develop hypertrophic cardiomyopathy and will require a mobility aid such as a cane, walker or wheelchair in their teens. As the disease progresses, people lose their sight and hearing. Other complications include scoliosis and diabetes mellitus.

FRDA is an autosomal recessive disorder that affects a gene (FXN) on chromosome 9 which produces an important protein called frataxin.[5]

In 96% of cases the mutant FXN gene has 90–1,300 GAA trinucleotide repeat expansions in intron 1 of both alleles.[6] This expansion causes epigenetic changes and formation of heterochromatin near the repeat.[5] The length of the shorter GAA repeat is correlated with the age of onset and disease severity.[7] The formation of heterochromatin results in reduced transcription of the gene and low levels of frataxin.[8] People with FDRA might have 5-35% of the frataxin protein compared to healthy individuals. Heterozygous carriers of the mutant FXN gene have 50% lower frataxin levels but this decrease is not enough to cause symptoms.

The condition is caused by mutations in the "FXN" gene on chromosome 9. The FXN gene makes a protein called frataxin. In FRDA, the patient produces less frataxin. Degeneration of nerve tissue in the spinal cord causes the ataxia; particularly affected are the sensory neurons essential for directing muscle movement of the arms and legs through connections with the cerebellum. The spinal cord becomes thinner, and nerve cells lose some myelin sheath.

No effective treatment exists, but there are several therapies in trials. FRDA shortens life expectancy due to heart disease, and some people can live into their sixties or older.

FRDA affects 1 in 50,000 people in the United States and is the most common inherited ataxia. Rates are highest in people of Western European descent. The condition is named after the German physician Nikolaus Friedreich, who first described it in the 1860s.

Homeobox (HOX) genes code for transcription regulators. A homeobox is highly conserved DNA of 180+ nucleotides. Mutations in homeobox genes lead to limbs in the wrong place and skeletal abnormalities. Homeobox genes make sure your leg isn't where your head should be!

From Wikipedia:

A homeobox is a DNA sequence, around 180 base pairs long, found within genes that are involved in the regulation of patterns of anatomical development (morphogenesis) in animals, fungi, plants, and numerous single cell eukaryotes.[2] Homeobox genes encode homeodomain protein products that are transcription factors sharing a characteristic protein fold structure that binds DNA to regulate expression of target genes.[3][4][2] Homeodomain proteins regulate gene expression and cell differentiation during early embryonic development, thus mutations in homeobox genes can cause developmental disorders.[5]

Homeosis is a term coined by William Bateson to describe the outright replacement of a discrete body part with another body part, e.g. antennapedia—replacement of the antenna on the head of a fruit fly with legs.[6] The "homeo-" prefix in the words "homeobox" and "homeodomain" stems from this mutational phenotype, which is frequently observed when these genes are mutated in animals. The homeobox domain was first identified in a number of Drosophila homeotic and segmentation proteins, but is now known to be well-conserved in many other animals, including vertebrates.[3][7][8]

CAAT and TATA are promoters necessary to start transcription. CAAT is 75 bases upstreat from the start codon and the TATA (Hogness) box is 25 bases upstream from the start codon. The promoters are where RNA pol II and transcription factors bind.

Heteroplasmy is mixture of two types of genetic material; it's the fact that some cells have normal mitochondria and others have mutated mitochondria because during mitosis, the mutation may distribute more to some cells than others. This affects the severity of the disease. Due to random chance, one offspring may be more severely affected than the other because that's just how the mutation distributed amongst cells during mitosis. This is what happens in syndromes such as MELAS syndrome (Mitochondrial Encephalopyopathy with Lactic Acidosis and Stroke-like episodes), which is due to mutation of mtDNA. All the offspring of an affected mother will be affected because you only get mtDNA from your mom, whose eggs have a lot of it. MELAS syndrome causes seizures, stroke-like episodes, muscle weakness, lactic acidosis.

G6PD deficiency is X-linked recessive; this means that affected males will make unaffected sons (because they can't give their sons the bad X) and carrier daughters (who don't have the disease themselves because they have one good X to counteract the bad X). Females who carry X-linked recessive chromosomes have a 50% change of having affected sons and a 50% chance of having carrier daughters.

An enhancer sequence is found in the introns, upstream, or downstream of a gene. In eukaryotes, RNA pol II makes mRNA from DNA template; enhancer sequences bind to activator proteins that help DNA to bend, which lets the activator proteins interact with the transcription factors and RNA pol II, which causes faster transcription. Silencers bind to repressor proteins and decrease rate of transcription.

Hemophilia A is X-linked recessive = factor VIII deficiency.

Nucleosomes = DNA wrapped around a core of 8 histone proteins. Histone H1 is outside of the histone core of nucleosomes and promotes compaction of heterochromatin.

Ok, I think it's prokaryotes that have DNA pol I, II, and III and eukaryotes that have RNA pol I, II, and III. Eukaryotes have 5 DNA polymerases (alpha, beta, gamma, delta, and epsilon). DNA pol I, II, and III have 3'-> 5' exonuclease (proofreading) capability; but only DNA pol I has 5'-> 3' exonuclease activity, which allows it to remove RNA primers and repair damaged DNA. I got more than one question on this. So remember that DNA pol 1 has 5’-> 3’ exonuclease activity. Eukaryotes have multiple origins of replication whereas prokaryotes have 1.

4 notes · View notes