#podocyte
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aroace-cat-lady · 1 year ago
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Bitches dont cry until God Is Really Real starts playing
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bpod-bpod · 5 months ago
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Stretcher Bearer
A protein called zyxin is important for the function of kidneys – it translates the mechanical forces experienced by podocytes [specialised cells of the kidney ], for example stretched by hypertension, acting to stabilise them
Read the published research article here
Image from work by Felix Kliewe and colleagues
Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany
Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)
Published in Communications Biology, April 2024
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regexkind · 11 months ago
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I think it's totalitarian that cells in my body can't change jobs. ACAB but what if the cop is a macrophage. Too late to change its fucking career and become a piss-filtering podocyte in the kidneys innit
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colinwilson11 · 2 months ago
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Rare Kidney Disease: An In-Depth Look
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There are over a hundred rare diseases that can impact the functioning of the kidneys. Some of the less common renal diseases include Alport syndrome, Medullary cystic kidney disease (MCKD), Autosomal dominant polycystic kidney disease (ADPKD), and Nephronophthisis.
Alport syndrome is a genetic disorder characterized by kidney failure and hearing loss. It is caused by mutations in genes coding for type IV collagen, which is an important component of the glomerular basement membrane in the kidneys. Over time, the glomeruli are damaged, resulting in proteinuria and declining kidney function. Approximately 1 in 5000 individuals are affected by Alport syndrome worldwide.
Medullary cystic Rare Kidney Disease involves the development of cysts in the medulla of the kidneys, which are the inner regions. Two main types are MCKD type 1 and type 2. They are inherited in an autosomal recessive pattern. Cysts accumulate over time, leading to kidney enlargement and eventual failure. MCKD has a prevalence rate of about 1 in 50,000.
Autosomal dominant polycystic kidney disease is one of the most common life-threatening genetic disorders. It is caused by mutations in the PKD1 and PKD2 genes and is inherited in an autosomal dominant pattern. Multiple cysts form in both kidneys, enlarging them considerably. Symptoms include high blood pressure, kidney pain, urinary tract infections, blood in urine and late-stage renal failure. ADPKD has an incidence of about 1 in 1000-4000.
Nephronophthisis is a tubulointerstitial kidney disease leading to end-stage renal failure during childhood or teenage years in most cases. It is inherited as an autosomal recessive or autosomal dominant trait. Tiny cysts form along the renal tubules as the disease progresses. Overall prevalence is estimated to be between 1 in 50,000 to 1 in 100,000.
Diagnosis And Management Challenges
Given the rarity of these disorders, diagnosing them accurately can prove difficult. Initial tests ordered by doctors usually include urine examination, ultrasound of kidneys, serum creatinine levels and creatinine clearance tests. However, definitive diagnosis requires specialist kidney biopsy in many cases to check for characteristic pathology changes under microscopy. Genetic testing is also important to confirm the specific type and mutation involved.
Lack of awareness about Rare Kidney Disease poses challenges in management. Patients often face delays before reaching specialist nephrologists. Limited published research means treatment protocols are still evolving for some conditions. Managing complications like hypertension, pain, infections etc. requires multidisciplinary teams. Coordinating long-term care and follow-up can be an issue as patients transition between pediatric and adult medical services.
Access To Novel Therapies
As understanding of disease pathways improves, new treatments are being developed for Rare Kidney Disease. For instance, antiviral drugs that block JC polyomavirus replication show promise against Nephropathia epidemica (a zoonotic infection causing tubulointerstitial nephritis). CRISPR gene editing is being explored as a curative approach for hereditary conditions. Drugs inhibiting ACE2/angiotensin pathways help slow ADPKD progression. Research is ongoing into stem cell therapy using patient-derived podocytes for Alport syndrome. Management of symptoms also incorporates dietary changes, lifestyle modifications and palliative care approaches. Government approvals have enabled access to orphan drugs for rare disorders in many countries.
The rare diseases impacting the kidneys remain an important public health problem due to their chronic nature and lack of standardized care protocols. Improving awareness, expediting diagnosis, streamlining multi-specialty management, facilitating clinical trials and making innovative therapies more affordable are some priorities. Coordinated global research programs are necessary to find new treatments and eventually cures for these challenging conditions afflicting patients worldwide.
Get more insights on this topic:  https://www.trendingwebwire.com/rare-kidney-disease-understanding-the-uncommon-causes-of-kidney-failure/
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fruit-worm-papers · 7 months ago
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Podocyte exopher-formation as a novel pathomechanism in membranous nephropathy
http://dlvr.it/T5Ckpc
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ribosome-papers · 11 months ago
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The loss of profilin1 is catastrophic to podocytes
Pubmed: http://dlvr.it/T0BYS0
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pompompompeii · 11 months ago
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what if we were podocytes wrapped around the same glomerular capillary and we intertwined our limbs between one another’s
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willowcatkinblossom · 1 year ago
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3 good things
1. ahh finally figured out the subepithelial thing, can't believe it's the podocytes
2. finished writing up a note
3. sweet potatoes 🍠
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medicowesome · 1 year ago
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humancelltournament · 1 year ago
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Podocytes please : )
They're in!
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popgenpapers · 1 year ago
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Enhancing gene transfer to renal tubules and podocytes by context-dependent selection of AAV capsids
http://dlvr.it/SsvfkT
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doomergirlai · 1 year ago
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Tissue ( 06 07 2023 )
The story starts from cleavage division in zygote ( cleavage because its one of a kind division where cell doesn't grow in size but divide continuously ; this is due to tough zona pellucida and other tough coverings to protect zygote )
As zygote undergo cleavage and movement from fallopian tube to uterus , it forms a muticelled morula , then blastula. Morula is a cell aggregate while blastula has an outer cell layer and condensed inner cell mass with blastocoel. Blastula is called blastocyst in ncert , blastomeres are the cells of blastocyst.The tough covering has dissolved around this time and Blastula gets implanted in endometrium. It transform to gastrula ( called that mainly because of appearance of gastrocoel- alimentary canal precursor ). Gastrula also has a transverse cell mass embryonic disc above the longitudinal hollow gastrocoel . Embryonic disc form ectoderm , and cells added by it below give mesoderm. Gastrocoel give endoderm ( three germ layers ).
simple tissue - same appearance cells , compound epithelium - different appearance cells ; but all tissue have cells of similar origin and coordinates to perform a common function.
Epithelium is contributed by all the three germ layers , muscle is formed by just mesoderm ( ectodermal muscles - iris muscles , one more muscle in eye , and hair follicle muscle) , nervous tissue is formed by ectoderm and connective tissue is formed by mesoderm.
Epithelium provides covering , connective tissue supports , muscular tissue moves , neural tissue transmission of nerve impulse.
Epithelium - protection/secretion/absorption/diffusion.
Epithelium -a. has a non cellular basement membrane ( dead ) , except transistional epithelium in bladder. b. has a free surface facing either body fluid or outside environment. c. has secretion/absorption functions if single layer , protection more prevalent in multi-layered , d. non vascular , no blood supply . e. Highly dividing , f. Has no to little ( junctions - tight/gap/adhering ) intercellular space and matrix. Tight junction allow no leakage or transfer across cells , adhering keeps neighbour cells together and gap is "connections in adhering junctions"??? , that allows rapid transfer of small ions , molecules and sometimes big molecules.
Simple epithelium - morpho/anatomy* simple cuboidal : cubical cells , centrally located round nucleus. Simple squamous : squashed cuboidal , flat cells ( front view : tessellated , upper view : pavement , irregular tiles )with transverse flat oval nucleus close to basement membrane . Simple columnar: longitudinally squashed cuboidal , nucleus oval longitudinally and towards base .
Simple epithelium - physio* . Simple squamous - diffusion . Eg - alveoli , tunica intima of artery , vein , capillary endothelium , abundant in nephrons : ¹⁰-¹²l,⁵-⁷b,²-³h cm, one million nephron per kidney , 1 lakh nephron per cm , the channi ( double walled cup ) of bowman capsule ( podocytes ) , outer wall of bowman , DHL , thin AHL , collecting duct. | Simple cuboidal : ciliated - thick AHL ( to push filtrate against gravity ) , trachea , primary bronchi [ trachea - p.bronchi - s.bronchi-t.bronchi-initial bronchiole)-(terminal bronchiole)-(respiratory bronchiole-alveolar duct-alveolar sac ] . Brush bordered ( secretion absorption) (evagination ) - PCT ( more ) , DCT ( less ). Pigmented - retina , choroid ( bluish/blackish )| Simple columnar : brush border- microvilli illeum ( no lumen needed ). Ciliated - fallopian tube - move zygote or unfertilized ovum to uterus ( affordable beacuse wide lumen )
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rnomics · 2 years ago
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Long noncoding #RNA ENST00000436340 promotes podocyte injury in diabetic kidney disease by facilitating the association of PTBP1 with RAB3B
Dysfunction of podocytes has been regarded as an important early pathologic characteristic of diabetic kidney disease (DKD), but the regulatory role of long noncoding #RNAs (l#ncRNAs) in this process remains largely unknown. Here, we performed #RNA sequencing in kidney tissues isolated from DKD patients and nondiabetic renal #cancer patients undergoing surgical resection and discovered that the novel l#ncRNA ENST00000436340 was upregulated in DKD patients and high glucose-induced podocytes, and we... https://pubmed.ncbi.nlm.nih.gov/36792603/?utm_source=dlvr.it&utm_medium=tumblr&utm_campaign=None&utm_content=1RYYbE7j9SUSBe_aHniaI_J1MQIFIBbfLuFxoWdLNMNDzVVIWF&fc=None&ff=20230218022829&v=2.17.9.post6%2086293ac
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tumimmtxpapers · 2 years ago
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Identification of ARMH4 and WIPF3 as human podocyte proteins with potential roles in immunomodulation and cytoskeletal dynamics
The podocyte is a specialized cell type critically involved in maintaining the selective filtration barrier of the kidney. Podocytes are primary or secondary targets for a multitude of kidney diseases. Despite intense investigation, the transcriptome and proteome of human podocytes remain incompletely characterized. Here, we analyzed publicly available RNA-Seq data from human kidneys (n = 85) to computationally identify potential novel podocyte markers. For confirmation, we used an online... http://dlvr.it/Sh2frh
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ikeepwatchinghelicopters · 2 years ago
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This is so great, I love it 😂
Napoleon would definitely mess with Illya in every form. The setting with Illya as an astrocyte is brilliant. Similarly, he could also be a podocyte. And Gaby could be an endothelial cell in the capillary (being hugged by Illya) or a mesangial cell close to him. I think I like her as a mesangial cell more, because being endothelium feels to passive for Gaby. And Napoleon could still be a wandering cell in the blood. He could be an erythrocyte and everytime he swings by in the kidney, he tries to pass through the fenestrations and slip by Illya's defenses. Of course Illya never lets him. I mean, then Napoleon could get peed out of the body. And then Illya would miss him. And that would mean Illya's not doing his job properly, which is unacceptable. (Also, let's ignore how short-lived red blood cells are.)
But I can also imagine the concept of Napoleon and Illya both being immobile hence being forced to be together. Even better if they have to work together closely. Like a stem cell in the crypt of the small intestine and a Paneth cell. Not sure what Gaby would be in this scenario, though 😅
Also, also them as immune cells is so amazing. I agree that Napoleon and Illya would make great antigen-presenting cells. The idea of them fighting over who's antigen is better made me laugh so hard 😂😂 I need that as a crack one-shot 😂
But also imagine the potential angst of Napoleon being a natural killer cell and Illya being some kind of cell infected by a virus. Napoleon knows he should induce apoptosis, but he cannot bring himself to kill Illya. Also, this one article (Zwirner and Zibalt, "Regulation of NK Cell Activation and Effector Functions by the IL-12 Family of Cytokines: The Case of IL-27", 2017) I found says that for NK cells establish "bidirectional cross talk (...) with other cells of myeloid origin such as dendritic cells (DC) and macrophages". I didn't read the whole article, so I have no idea how exactly it all works, but if Gaby was a cell of myeloid origin, maybe Napoleon would need her help with the infection in Illya, which would mean even more angst. (Now we're getting into more antrophomorphic, fictional territory than anything truly biological.) Perhaps Napoleon's supposed to induce apoptosis and Gaby's supposed to kick off the rest of the immune response to the pathogen. And Gaby knows that if she sends out signals to activate other cells, it will draw attention to Illya being infected, making it widely known that he should be forced to undergo apoptosis. And what if Napoleon (and Gaby?) refuse to kill Illya (despite his protests), but the infection that was inside him spreads and eventually kills the whole human? Man, how did this turn so dark?
Anyway, I love everything about your ideas and imagining everyone as a cell was strangely fun. Lol, I hope I didn't say anything too inaccurate 😅
A TMFU alternate universe where everyone is a cell in the human body.
Bless you, anon, it's been a while since I got a truly unhinged AU idea in my ask box.
I probably spent too long contemplating this, but that's what you get when you ask such things of a biology professor. Also, this is HARD. Possibly because I know too much about this shit so I get hung up on obscure cell types very few people will have heard of, but also thoughts like hmmm but what cell is charming and sneaky and a bit of a cheeky bastard but fiercely loyal to his friends, and the answer is none of them, lol. If you want to read my vague ramblings about which cells fit them best in canon, see below the cut.
But for an AU story, I like the idea that Illya is a fixed cell somewhere—let's say an astrocyte, maintaining the blood-brain barrier, mostly for the hell of it—and Napoleon is a wandering cell in the blood, and Napoleon swings by every so often to try to chat and sneak things past Illya's defenses just for kicks. Of course Illya is Very Dedicated to his job and nothing gets past him (except alcohol, whoops), and he refuses to be distracted by Napoleon, but he looks forward to his visits even though he won't admit it (it gets kind of boring, staying in one place all the time). Maybe Gaby is also a wandering cell and sometimes their visits to Illya's area of the brain coincide. I don't know what happens beyond that, because there isn't much more that reasonably CAN happen, but there you go.
Anyway, thank you for the challenge, anon, this was worse than the fruit AU, tbh. 😂 I always enjoy these, though, really gives the creativity muscles a workout.
Oh, you actually wanted to read more on this?? 😅 Well, here you go.
Honestly it probably makes sense to set them all as immune cells, given the protective function they serve. I wanted to make Illya a natural killer cell because they are part of defending the body and the name is badass, but NK cells kill the body's own infected cells, and that didn't sound quite right. Dendritic cells are really the information-gathering portion of the immune system, monitoring the various parts of the body and alerting various lymphocytes if a larger response is warranted. They're macrophages, too, which means they destroy the invader, then take the evidence and tell other immune cells what to look out for. Waverly feels like a regulatory or memory T-cell to me (one of the types that the dendritic cells would interact with and which would mediate an immune response), and I kind of like Gaby as a T-cell too (helper T, I think), because they just kind of hang out until they're activated by other cells, which is perfect for a sleeper agent.
All the stories possible here are tough to really flesh out. Like, maybe Napoleon and Illya are dendritic cells in different areas of the body and pick up intel on some invading pathogen, then meet in a lymph node to activate Gaby and fight (?) over who's antigen is better (??), but then that's kinda it, these things aren't very long-lived lol. I suppose we can pretend that Illya and Napoleon would work together with Gaby and Waverly to fight off the invaders, even though that's not exactly what would happen. But this is a fictional AU of anthropomorphized cells, so everything is fair game I guess.
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healthinnovations · 4 years ago
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Blocking brain signals detected in the kidney could help unlock treatments for kidney failure.
Blocking brain signals detected in the kidney could help unlock treatments for kidney failure. Thoughts health innovators?
Chronic kidney disease (CKD) is a major public health issue, affecting over 10 percent of the global population, frequently occurring as a result of other disorders such as hypertension, diabetes, obesity, or metabolic syndrome. An early sign of CKD is the increased level of liver protein albumin in the urine, also known as albuminuria. Shown to damage the glomerulus, the kidney’s filtering…
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