cell nuclei

yoongi scenario | d is for dalliance

dalliance  /‘dalɪəns/  noun.  a brief involvement with someone; amorous play

genre: angst, fluff
word count: 1k
warnings: hints at sex
a stand-alone in the ‘synonymous with love’ series // d is for…

“We were dazzling – resplendent in the night’s sky. We lit up the city with our passion; every street was kindling for our fire. But the problem with stars is that they die in the end. And we were no exception.”

Those words, though repeated a thousand times, still taste dulcet on your tongue. They are delicate things, but they make you feel at ease – repeating the mantra till it throbs through you. This way you won’t forget what you are. It reminds you of the fleeting seconds you spent with him - Min Yoongi, your star boy, a sky away from you - it reminds you of the dalliance you had, great and glorious, it will repeat, it has to.

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The “rope like growth” you see from the epicenter of inoculation is a very good sign. It’s known as rhizomorphic growth and happens when two monokaryotic mycelia cells meet, join nuclei, and become dikaryotic mycelia. What all that means is they “Fuck”. Only Dikaryotic cells are capable of producing fruiting bodies (mushrooms).

P.S. I’m sure I butchered some spelling

- Peace and Love, Hozzy2Dope

Lynn Margulis (1938-2011) was an evolutionary theorist and science author, the first modern proponent of the significance of symbiosis in evolution. Her research fundamentally transformed and established the understanding of the evolution of cells with nuclei. Her work was seen as controversial and was widely rejected for years, until genetic evidence proved it definitively.

Her 1966 paper, “On the Origin of Mitosing Cells”, was rejected for publication by 15 scientific journals initially, but today it is considered a landmark in endosymbiotic theory. She also proposed the Gaia theory, which sees Earth as a self-regulating system.

anonymous asked:

you keep harping on this selfie thing lol we get it 😬

Norepinephrine (NE), also called noradrenaline (NA) or noradrenalin, is an organic chemical in the catecholamine family that functions in the brain and body as a hormone and neurotransmitter. The name “noradrenaline,” derived from Latin roots meaning “at/alongside the kidneys,” is more commonly used in the United Kingdom; in the United States, “norepinephrine,” derived from Greek roots having that same meaning, is usually preferred. "Norepinephrine" is also the international nonproprietary name given to the drug. Regardless of which name is used for the substance itself, parts of the body that produce or are affected by it are referred to as noradrenergic.

In the brain, norepinephrine is produced in closely packed brain cell neurons or nuclei that are small yet exert powerful effects on other brain areas. The most important of these nuclei is the locus coeruleus, located in the pons. Outside the brain, norepinephrine is used as a neurotransmitter by sympathetic ganglia located near the spinal cord or in the abdomen, and it is also released directly into the bloodstream by the adrenal glands. Regardless of how and where it is released, norepinephrine acts on target cells by binding to and activating noradrenergic receptors located on the cell surface.

The general function of norepinephrine is to mobilize the brain and body for action. Norepinephrine release is lowest during sleep, rises during wakefulness, and reaches much higher levels during situations of stress or danger, in the so-called fight-or-flight response. In the brain, norepinephrine increases arousal and alertness, promotes vigilance, enhances formation and retrieval of memory, and focuses attention; it also increases restlessness and anxiety. In the rest of the body, norepinephrine increases heart rate and blood pressure, triggers the release of glucose from energy stores, increases blood flow to skeletal muscle, reduces blood flow to the gastrointestinal system, and inhibits voiding of the bladder and gastrointestinal motility.

A variety of medically important drugs work by altering the actions of norepinephrine systems. Norepinephrine itself is widely used as an injectable drug for the treatment of critically low blood pressure. Beta blockers, which counter some of the effects of norepinephrine, are frequently used to treat glaucoma, migraine, and a range of cardiovascular problems. Alpha blockers, which counter a different set of norepinephrine effects, are used to treat several cardiovascular and psychiatric conditions. Alpha-2 agonists often have a sedating effect, and are commonly used as anesthesia-enhancers in surgery, as well as in treatment of drug or alcohol dependence. Many important psychiatric drugs exert strong effects on norepinephrine systems in the brain, resulting in side-effects that may be helpful or harmful.


MNEMONIC: Diseases showing anticipation associated with Triplet Repeat Expansion

Anticipation: pattern of inheritance, symptoms of a genetic disorder become apparent at an earlier age as it is passed on to the next generation, an increase of severity of symptoms is also noted

Huntington Disease (HD)

  • Mnemonic: “HD es una CAGada” in Spanish, cagada means something bad, shitty, to be more precise. This is to remember the CAG trinucleotid repeat.
  • Autosomal Dominant, chromosome 4: “Huntin’ 4 food”
  • Chorea: purposeless movement of limbs, due to a loss of GABAergic neurons of neostriatum (caudate nucleus and putamen) of indirect pathway.
  • Personality changes, dementia, tendency for suicide

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Fragile X Syndrome

  • CGG trinucleotid repeat
  • X dominant, FMR 1
  • Mental retardation, large ears and jaw. post-pubertal macro-orchidism (males), attention deficit disorder (females)

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Friedreich Ataxia

  • GAA trinucleotid repeat
  • Autosomal recessive, Frataxin gene, chromosome 9
  • Neuronal degeneration: dorsal root ganglia, Clarke column (spinocerebellar tract), posterior column of spinal cord, dentate nucleus, Purkinje cells, Betz neurons, CN nuclei of VII, X, XII
  • Progressive gait & limb ataxia, arreflexia, hypertrophic cardiomyopathy, axonal sensory neuropathy, kyphoscoliosis, dysarthria, hand clumsiness, loss of sense of position, impaired vibratory sensation.

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MyoTonic DysTrophy

  • CTG trinucleotid repeat
  • Autosomal Dominant, MD1: chromosome 3; MD2: chromosome 19
  • Muscle loss, cardiac arrythmia, testicular atrophy, frontal baldness, cataracts.

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This is a patch of nanoscopic needles that was built to inject DNA and other nucleic acids directly into individual cells. 

The technique, developed by scientists at Imperial College London and Houston Methodist Research Institute, constructs tiny porous groups of needles out of biodegradable silicon. Each needle is 1,000 times thinner than a human hair. The team showed that their innovation could be used to deliver therapeutic nucleic acids inside human and animal cells. 

[The image (above) shows human cells (green) on the nanoneedles (orange). The nanoneedles have injected DNA into the cells’ nuclei (Blue). The image was taken by the researchers using optical microscopy. Image courtesy Chiappini et al./ICL.]

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Confocal images of growth factor–induced microvessel sprouts in collagen and fibrin. BS1 lectin-FITC (green) stains endothelial sprouts (white arrows); α-SMA-Cy3 (red) indicates supporting cells. DAPI-stained nuclei (blue). (a) VEGF-treated ring embedded in collagen. (b) bFGF-treated ring in fibrin. (c,d) PBS-treated control aortic rings in collagen and fibrin, respectively. All animals were wild-type C57BL/6 mice aged 8–12 weeks. Scale bar, 200 μm. Panel d of this figure was originally published under the Creative Commons Attribution License in ref. 12.

Marianne Baker et al. (2012) Use of the mouse aortic ring assay to study angiogenesis. Nature Protocols 7, 89–104 

Crepidula fornicata veliger larvae

Confocal image (extended focus Z stack) of a Crepidula fornicata (slipper limpet) veliger larva. Stained with phalloidin (F-actin; purple), DAPI (cell nuclei, blue), anti-serotonin (yellow), and anti-acetylated tubulin (red). The shell (green) image was created from the DIC picture collected during the confocal scan. The C-shaped line of nuclei are cells at the edge of the velum; the acetylated tubulin (red) staining reveals the ciliated surface of the velum. The F-actin staining (purple) highlights the main larval retractor muscle. Serotonin (yellow) reveals the serotonergic neuron cell bodies and axons. Joyce Pieretti (University of Chicago), Manuela Truebano (Plymouth University), Saori Tani (Kobe University) and Daniela Di Bella (Fundacion Instituto Leloir)

Courtesy of Marine Biological Laboratory, Woods Hole, and Development


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NIH3T3 cells were pre-loaded with a green fluorescent cell tracker dye prior to co-culture and prior to imaging, all cell nuclei were labelled with the DNA specific Hoechst 33342. This approach allowed to positively identify individual cells as either NIH3T3 or MDCK. Imaging reveals that even in the presence of a co-culture, the majority of cells continued to display a clear preference for growing on the ridges or in the grooves. Phase contrast and fluorescence imaging reveals that after 48 h of co-culture on 100µm wide grooves, NIH3T3 cells display a clear preference to migrate and grow on the ridge surfaces.

Leclerc et al., Biomaterials 2013

Scientists Keep a Molecule from Moving Inside Nerve Cells to Prevent Cell Death

Amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease) is a progressive disorder that devastates motor nerve cells. People diagnosed with ALS slowly lose the ability to control muscle movement, and are ultimately unable to speak, eat, move, or breathe. The cellular mechanisms behind ALS are also found in certain types of dementia.

A groundbreaking scientific study published in Nature Medicine has found one way an RNA binding protein may contribute to ALS disease progression. Cells make RNA to carry instructions for making proteins from DNA to protein-constructing machinery.

The culprit protein, TDP-43, normally binds to small pieces of newly read RNA and helps shuttle the fragments around inside nerve cell nuclei. The study describes for the first time the molecular consequences of misplaced TDP-43 inside nerve cells, and demonstrates that correcting its location can restore nerve cell function. Misplacement of TDP-43 in nerve cells is a hallmark of ALS and other neurological disorders including frontotemporal dementia (FTD), Alzheimer’s, Parkinson’s, and Huntington’s diseases. Studies that characterize common mechanisms behind these diseases could have widespread implications and may also accelerate development of broad-based therapies.

To find the misplaced TDP-43, the researchers viewed nerve cells donated by people who died from ALS or FTD under high powered microscopes. They discovered TDP-43 accumulates in nerve cell mitochondria, critical structures responsible for generating the enormous amount of energy nerve cells require. By physically isolating the affected mitochondria the researchers were able to pinpoint TDP-43’s exact location inside the subcellular structures. They were also able to characterize variations of the protein most likely to get misplaced.

This important work was led by Xinglong Wang, PhD, from the department of pathology at Case Western Reserve University School of Medicine and a team of scientists from his laboratory.

“By multiple approaches, we have identified the mitochondrial inner membrane facing matrix as the major site for mitochondrial TDP-43,” explained Wang. “Mitochondria might be major accumulation sites of TDP-43 in dying neurons in various major neurodegenerative diseases.”

The researchers discovered that once inside the mitochondria, TDP-43 resumes its RNA binding role and attaches itself to mitochondrial genetic material. This disrupts the mitochondria’s ability to generate energy for the cell. Wang’s team was able to precisely identify the RNA in mitochondria that was bound by TDP-43 and observe the resultant disassembly of mitochondrial protein complexes. This finding provides much needed clarity on the consequences of TDP-43 misplacement inside nerve cells and opens the door for deeper studies involving a range of neurological disorders. Although the study focused on ALS and FTD, according to Wang “mislocalization of TDP-43 represents a key pathological feature correlating strongly with symptoms in more than half of Alzheimer’s disease patients.”

Mutations in the gene encoding TDP-43 have long been linked to neurodegenerative diseases like ALS and FTD. Wang’s team found that disease-associated mutations in TDP-43 enhance its misplacement inside nerve cells. The researchers also identified sections of TDP-43 that are recognized by mitochondria and serve as signals to let it inside. These sections could serve as therapeutic targets, as the study found blocking them prevents TDP-43 from localizing inside mitochondria. Importantly, Wang’s team was able to keep TDP-43 out of nerve cell mitochondria in mice using small proteins which “almost completely” prevented nerve cell toxicity and disease progression.

“We, for the first time, provide the novel concept that the inhibition of TDP-43 mitochondrial localization is sufficient to prevent TDP-43-linked neurodegeneration,” said Wang. “Targeting mitochondrial TDP-43 could be a novel therapeutic approach for ALS, FTD and other TDP-43-linked neurodegenerative diseases.”

Wang has begun to develop small proteins that prevent TDP-43 from reaching mitochondria in human nerve cells, and has a patent pending for the therapeutic molecule used in the study.

There is no treatment currently available for ALS or FTD. The average life expectancy for people newly diagnosed with ALS is just three years, according to The ALS Association.

A Brief Explanation on Muscle Growth:

A really good explanation of muscle growth with just the right amount of science for everyone/science folk haha.

Courtesy of  Menno Henselmans.

1) When you put tension on a muscle, its fibers deform and trigger chemical activity (mechanotransduction)

2) The muscle fibres release growth factors like insulin-like growth factor-1 (IGF-1) and myokines like IL-6 (interleukin-6) to signal the need for repair (myogenic signalling)

3) The MTOR master enzyme integrates all the signals for muscle growth, such as amino acid availability and the presence of growth factors. It then translates this information for your genes (translation initiation)

4) Your genes are located within muscle cell nuclei that function as command centres in their region of a muscle fiber. They contain the blueprint to create new proteins.

5) Nearby sattelite cells are activated and fuse to the muscle fibers to enlarge them (myonuclear addition) and aid in the creation of new proteins

Txch This Week: Hello, Wooly Mammoth and Goodbye, Antarctic Ice

This week on Txchnologist, we plumbed the fundamental laws of nature with upgrades to two major physics experiments, saw robots imitating snakes and found out we might soon be able to order our own Tron suits. Now we’re bringing you the highlights and some of the news we’ve been following this week in the world of science, technology and innovation.

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Birds are weird. 

Birds, why are you so weird? 

Their blood doesn’t even look the same. Their red cells have nuclei and the white cells look weird. 

They bruise green. 

They don’t make liquid pus, only cheesy pus. 

Their voicebox isn’t in their throat, it’s down in their chest where the airway splits. 

Their lungs don’t collapse and expand. 

Their spines (aside from the neck) are almost totally fused, with only 1 or two vertebrae that aren’t. 

Birds, man. 

Match It Monday!

Plant stem, neural stem cells, or a alveoli in lungs? How did you fare?

Though not the most popular guess, this is actually a micrograph of neural stem cells specializing into mature neurons. Blue staining marks the nuclei of cells, while green and red staining mark growing axons, which can be seen growing on the periphery. This intricate pattern probably arose due to a specialized matrix on which the cells were cultured. Neural stem cells hold tremendous promise in regenerative medicine and drug discovery as they provide an essentially limitless supply of cells that can be turned into desired cell types of the nervous system.

Image by Regis Grailhe and Arnaud Ogier, Institut Pasteur, Seongnam, Korea.

anonymous asked:

How do I keep my pussy wet?

the cells in your vagina that make it wet are long and thin. they align with one another so that all their tips are facing the same direction, like stacked bottles of wine. deep inside the cells, their nuclei unspool the region of your DNA that encodes the recipe for vaginal lubricant. the nucleus exposes this region of DNA as a long noose, which is found by a transcription enzyme. this enzyme makes a copy of your DNA and other enzymes shuttle it out of small holes in the nucleus. once outside of it, one end of the transcribed recipe is fed into the open jaw of a ribosome. the ribosome snaps shut and begins to read the recipe. the strand is pulled through the the mouth of the ribosome and a mechanism in the ribosome’s body reads the series of thee genetic bases that each correspond to a command like ‘GET THIS AMINO ACID’ or ‘GET THAT AMINO ACID’ or ‘STOP READING THIS RECIPE IT IS FINISHED.’ 

at the other end of the ribosome, a protein strand is assembled from amino acids in a long chain, the sequence of which was encoded in the recipe. the protein strand is attracted to itself in several strategic places, and as it is squirted out of the ribosome, it begins to fold into a shape unique to that sequence of amino acids. 

at the same time, blood begins to engorge the walls of your vagina. so much blood flows into the vessels near the interior surface of your vagina that the vessels start to leak. serum, the watery component of your blood that is centrifuged off when you donate, starts to pour into your vagina. 

back in the lubricating cells, the proteins that your DNA caused to be manufactured are piling up. the proteins have been designed to cover themselves in water molecules and expand into enormous, criss-crossing networks of protein mesh. this loose meshwork of protein and trapped water slides over and through itself very easily and dries out much less quickly than ordinary water. this is how it lubricates. the thin cells collect the proteins in large, spherical balloons called vesicles. the vesicles migrate towards the other end of the cells and, one by one, they burst through the cell wall and spray their lubricating protein into your vagina. the proteins unfurl and trap the serum that has leaked from your vagina’s engorged blood vessels, creating the well-known lubricant. 

all this production is very hard on the thin cells, and after around four days their machinery starts to break down. they begin to produce incorrect sequences of protein, which in turn curl into the wrong shape for lubrication. the cell detects these errors and sets into motion a chain of events that eventually causes the DNA in its nucleus to unspool a noose containing the recipe for killing the cell it inhabits. the cell commits suicide and a new cell takes its place. 

to make your pussy wet you are relying on the deaths of millions of cells who gave their lives to keep it that way. who lived and died so that when the walls of your pussy become engorged, the bloodless blood that leaks from them will become slippery and stick around.

the lesson to take from your cells killing themselves so that you can remain comfortably lubricated is to (like ezra pound) MAKE IT NEW. remember also that you’re shedding blood to stay wet. 


Under the Sea, a Missing Link in the Evolution of Complex Cells

Unlike bacteria, humans have big, complex cells, packed with nuclei containing DNA and mitochondria that produce energy. All so-called eukaryotes share our cellular complexity: animals, plants, fungi, even single-celled protozoans like amoebae. Scientists estimate that the first eukaryotes evolved about 2 billion years ago, in one of the greatest transitions in the history of life. But there is little evidence of this momentous event, no missing link that helps researchers trace the evolution of life from simple microbes to eukaryotes.. On Wednesday, a team of scientists announced the discovery of just such a transitional form. At the bottom of the Arctic Ocean, they found microbes that have many — but not all — of the features previously only found in eukaryotes. These microbes may show us what the progenitors of complex cellular organisms looked like. “This is a genuine breakthrough,” said Eugene Koonin, an evolutionary biologist at the National Center for Biotechnology Information who was not involved in the research. “It’s almost too good to be true.”

(via Under the Sea, a Missing Link in the Evolution of Complex Cells - NYTimes.com)