#CpG islands

[biology-geology-beaches-india]

The Science Notebooks of S. Sunkavally. Page 254.

[covid-safer-hotties]

Epigenetic patterns, accelerated biological aging, and enhanced epigenetic drift detected 6 months following COVID-19 infection: insights from a genome-wide DNA methylation study - Published Aug 20, 2024

Abstract Background The epigenetic status of patients 6-month post-COVID-19 infection remains largely unexplored. The existence of long-COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), suggests potential long-term changes. Long-COVID includes symptoms like fatigue, neurological issues, and organ-related problems, regardless of initial infection severity. The mechanisms behind long-COVID are unclear, but virus-induced epigenetic changes could play a role.

Methods and results Our study explores the lasting epigenetic impacts of SARS-CoV-2 infection. We analyzed genome-wide DNA methylation patterns in an Italian cohort of 96 patients 6 months after COVID-19 exposure, comparing them to 191 healthy controls. We identified 42 CpG sites with significant methylation differences (FDR < 0.05), primarily within CpG islands and gene promoters. Dysregulated genes highlighted potential links to glutamate/glutamine metabolism, which may be relevant to PASC symptoms. Key genes with potential significance to COVID-19 infection and long-term effects include GLUD1, ATP1A3, and ARRB2. Furthermore, Horvath's epigenetic clock showed a slight but significant age acceleration in post-COVID-19 patients. We also observed a substantial increase in stochastic epigenetic mutations (SEMs) in the post-COVID-19 group, implying potential epigenetic drift. SEM analysis identified 790 affected genes, indicating dysregulation in pathways related to insulin resistance, VEGF signaling, apoptosis, hypoxia response, T-cell activation, and endothelin signaling.

Conclusions Our study provides valuable insights into the epigenetic consequences of COVID-19. Results suggest possible associations with accelerated aging, epigenetic drift, and the disruption of critical biological pathways linked to insulin resistance, immune response, and vascular health. Understanding these epigenetic changes could be crucial for elucidating the complex mechanisms behind long-COVID and developing targeted therapeutic interventions.

[angsuga]

CPGS jams in BINI-themed balik eskwela

To celebrate the start of the academic year, the College of Public Governance and Safety (CPGS) – Student Council (SC) welcomed the students in the “B.I.N.I.: Balik Iskwela, Normalista I-usa” gathering on August 14, 2024 at the Tandang Sora Hall. Centered on the theme: “A Blossoming Journey of Innovative Ideas to Bind Individuals in a Tropical Island,” students attended the three-part event…

[the-firebird69]

Strutting in STYLE 💃🏻

Once again he's kidnapping them and people have figured out where it is quite easily and they cpg shooting the s*** out of them and they see garth and others are going to join in shooting the idiots. And half of them died permanently and then the some of them about 25% died of next few days and then the rest of them will be dying in the watchmen and the first batch to kick it off and it's happening shortly and the guy is nuts and he's going to attract all the clients to attack him and it's higher up so I'll die well good portion of them from this whatever the hell it is he's doing

Thor Freya

Olympus

This guy's a waste of time he's baiting his own people. Chrissy gets away and the guy just keeps doing it over and over and his people keep getting killed off he's a loser and eventually the whole sequence begins and all the way to New Zealand where they have lost the war and you can tell they lost the island and two pseudo empire and the mutants are allowed to be there but the others show up and start screwing around with them

Zues

Sounds good happens and they don't appreciate it and they attack and really this slaughter tons of these imbeciles as dwarves and elves it's just the same people the trumpsters and they get killed pretty good tons of them and the dragon devours them with flames and tons of them die okay this is really their whole enclave is burned to his ashes you just don't leave them alone ever and they don't know better

Hera

Olympus

[jhavelikes]

Nearly all human genetic disorders result from a limited repertoire of mutations in an associated gene or its regulatory elements. We recently described an individual with an inherited form of anemia (alpha-thalassemia) who has a deletion that results in a truncated, widely expressed gene (LUC7L) becoming juxtaposed to a structurally normal alpha-globin gene (HBA2). Although it retains all of its local and remote cis-regulatory elements, expression of HBA2 is silenced and its CpG island becomes completely methylated early during development. Here we show that in the affected individual, in a transgenic model and in differentiating embryonic stem cells, transcription of antisense RNA mediates silencing and methylation of the associated CpG island. These findings identify a new mechanism underlying human genetic disease.

Transcription of antisense RNA leading to gene silencing and methylation as a novel cause of human genetic disease - PubMed

[peertechz]

Unbalanced intake of methyl donor supplements, may lead to DNA methylation and cause breast cancer in offspring

Statistical data in Iran reflects a worrying trend for an increased incidence of breast cancer. recent national data on average annual crude incidence for primary breast cancer indicated 22.6 (95%CI 22.1-23.1) per 100,000. It seems that genome encoding with no changes in the sequence of DNA contributes to Lamarck’s theory as a probable causative factor for the deterioration of this disorder by supplementation. Unconscious methylation of DNA by environmental factors make genetic modifications through epigenetic process in nucleotides that create new make up for DNA and DNMTs, expedite one of the most prevalent health disorders. Uterus environment, youth up to a retired and postmenopausal age are periods for changes in genome assembly that include tiny alterations in CpG islands. A review article had been performed by the electronic search for the manuscripts that had been published among current databases and declared facts about the produced results and the main proves had ascertained from the present articles. They were included by the Med Line and PubMed database and Iran’s vital statistics. As a result consumption of selected nutrients has the ability for methylation by group donors and causes an actual transfer of a methyl to the C5 carbon of cytosine for making 5-methylcytosine. Characteristic of a living organism referred to the Genetic and Epigenetic information and unbalanced intake of selected nutrients with dual function like folic acid persuades the creation of a genetic foundation for breast cancer in offspring.

https://www.peertechzpublications.com/articles/FST-6-118.php

[rnewspost]

New gene implicated in cancer, cellular stress response

Tissue-restricted expression of mammalian HAPSTR2. a Transcript abundance of HAPSTR1 and HAPSTR2 in the indicated human tissues; GTEx RNA-seq data. TPM, transcripts per million. Same heatmap scale across other subpanels. b Gene expression, chromatin accessibility, transcription start sites, and CpG islands at human HAPSTR1 and HAPSTR2 gene loci; GTEx, ENCODE, and FANTOM5 data. Note that some…

[thechameleonlover]

Maybe I misunderstood the post. But to the anon, unless the letters A, T, G, and C resemble below, it doesn't make sense to my monkey brain

"Generally A and T are used way more than C and G so we tend not to get results that have a lot of C and G." What results?????? If you're looking at coding regions, there's about a 50% split between at and gc???? (Maybe more or less depending on organism). Like you have to ignore any concept of epigenetics, transcription, or translation to come to this conclusion (cpg islands, crispr cas9, it being overall more stable, PCR, heck even g quads).

Still so weirded out by that post. If they want a cute connection to other organisms just look at sequence similarities (heck go to uniprot and align any two organism sequences you want!). Like one Google search tells you that similar genome sequences include (these are all rounded estimates): 99% chimp/bonobo, 90%, 85-90% mouse, 80% cow, 60% banana, 60% drosophila. You don't have to make up a weird attempt at linguistic correlation that ultimately ignores languages outside of English

Accept the fact you are banana and drosophila adjacent, splicing machinery, evolution, and gene size prevented you from being so ❤ (this is a joke btw)

[modern-oedipus]

Me, a molecular biology major: Listen, I don’t care what you mean by CpG islands. I don’t care if I know the actual meaning of CpG islands, because whenever I see it on a text I imagine a nice island with beach clubs and palm trees on which “CpG” is written in big fluorescent letters.

[owlservice]

If I was DNA, first of all, I'd be highly methylated and hugging them histones so I couldn't be transcribed. Secondly I would contain non Watson-Crick base pairing. Thirdly I would be GC rich, in fact I would be nearly all GC. I would be like a crocodile. Once you annealed to me, you couldn't get away. Fourthly despite being methylated I would never let my cytosines be deaminated into thymine because I think that's not right. In other words I would be fully CpG island.

[mcatmemoranda]

I have a pt who had a colonoscopy for hematochezia. They biopsied two rectal polyps with pathology showing a traditional serrated adenoma and a villous adenoma with high grade dysplasia. I remember that these are the bad ones to have. I think she'll need to be re-screened in 3 years. This is from UpToDate:

A polyp of the colon refers to a protuberance into the lumen above the surrounding colonic mucosa. Polyps are usually asymptomatic but may ulcerate and bleed, cause tenesmus if in the rectum, and, when very large, produce intestinal obstruction. Colonic polyps may be neoplastic (eg, adenomas) or non-neoplastic (eg, inflammatory polyps). 

Inflammatory polyps are non-neoplastic intraluminal projections of mucosa consisting of stromal and epithelial components and inflammatory cells. Inflammatory polyps do not undergo neoplastic transformation and do not require excision unless they cause symptoms. 

Hamartomatous polyps are made up of tissue elements that are normally found at that site but are growing in a disorganized mass. Juvenile polyps and Peutz-Jeghers polyps are hamartomatous polyps. In contrast to patients with sporadic juvenile polyps, patients with juvenile polyposis coli and Peutz-Jeghers syndrome (PJS) are at increased risk for colorectal cancer.

Sessile serrated lesions are a heterogenous group of polyps with variable malignant potential. They include hyperplastic polyps, traditional serrated adenomas, and sessile serrated polyps (SSLs; synonymous with sessile serrated adenomas [SSA]).

Hyperplastic polyps are the most prevalent non-neoplastic polyps in the colon. Distal small hyperplastic polyps rarely, if ever, develop into colorectal cancers. SSLs, particularly those with foci of classic histologic dysplasia, are considered the likely precursor lesions to sporadic high microsatellite instability (MSI-H) colon cancer through a molecular pathway characterized by a high frequency of methylation of some CpG islands (CpG island hypermethylation phenotype-positive).

Adenomatous polyps are neoplastic polyps. Clinically, adenomas are generally asymptomatic and are most often detected by colon cancer screening tests. Villous histology, increasing polyp size, and high-grade dysplasia are risk factors for focal cancer within an individual adenoma. 

If a polyp is detected, we recommend colonoscopy to establish the histology, remove the polyp, and search for synchronous lesions (Grade 1A). Recommendations for subsequent treatment and surveillance depend on the number and pathologic features of the polyp(s)

[sporesgalaxy]

in the wild euphoria of understanding my homework and getting a bunch of questions right in a row i had the unironic thought “I love gene methylation :) CpG islands my beloved” and then i had to stop for a minute to cope with that

[perfectlytinyworkspace]

positional cloning: step-by-step isolation of a disease gene in the genome

step 1. linkage mapping

relative locations of DNAPMs, genes and disease loci from phenotypes and genotypes, in cM units

use DNA samples from 50+ multigenerational families – known as a mapping panel for any one area of the genome – to test for inheritance patterns of DNAPMs and disease/gene inheritance

determine RFs between relevant and analyzed DNAPMs and diseases/genes → one cM ≈ 1 kb in human genome

find DNAPMs to test with via NCBI human genome databaseafter testing for linkage between candidate region/interval and one DNAPM in a mapping panel, test with more nearby known DNAPMs in either direction 

if RF decreases with new DNAPM analysis, this DNAPM is closer to candidate region and the direction along the genome is correct

step 1A. pre-physical mapping work to do: 

once chosen DNAPMs are very tightly linked to candidate region, mapping panel may not be big enough to determine linkage closer than 1-2cM (~1000kb in humans)

thus, move to a physical map of the candidate region

step 2. physical mapping

physical locations of DNAPMs, genes and disease loci from literal overlapping fragments of DNA inside clones, in kb units

goals: order fragments in created gDNA library and determine which chromosome a fragment of interest is located along

construct gDNA library via RE partial digest, insert into large BAC or YAC vector, transform to competent clonal cells and amplify 

fluorescent in-situ hybridization (FISH) – use to narrow gDNA library clones down to particular chromosomes of interest for smaller fragmentation and detailed probing analyses

isolate portion of DNA fragment in above clone gDNA and label w/ fluorescence for probing → hybridize to denatured mitotic chromosomes from organism DNA sample 

chromosomes that show fluorescent hybridization contain the fragment sequence 

can detect whether fragment is unique to 1 chromosome or repetitive across genome, but resolution is subpar

use FISH information to identify clonal inserts’ chromosomal location and categorize gDNA library by chromosome

focus on single-chromosome collection of YACs within gDNA library allows for probing with smaller, more distinct DNA fragments with ease of detection

put YAC inserts in order along a single chromosome by cutting with many different REs and detecting similar cut patterns via Southern Blot, using small DNA fragments as probes

find STS sequences – small, unique segments along a chromosome, but non-polymorphic so not a DNAPM – and use them as probes

YACs with same cut patterns or same STS’s at insert ends most likely have overlapping partial digest inserts and their inserts are next to one another along the chromosome

set of clones containing overlapping inserts is known as a contig

expand contigs by probing for overlap-indicative STS’s at the ends of the existing collective contig segment in other chromosomal YACs

quick note on YACs - these are linear rather than circular, and cut into two segments that are ligated onto either end of the DNA fragment » each segment “arm” has a distinct selection factor sequence to ensure both arms are ligated to fragment

step 2A. pre-sequence mapping work to do:

sequencing an entire 1500kb to 2000 kb contig into a sequence map is too much work! 

so find smaller regions that encode for genes in particular to sequence, using the following DNA characteristics that are unique to expressed genes in particular

CpG islands and exon/intron boundaries

open reading frames (ORF)

homology to other organism genes

expressed sequence tags (ESTs) from mRNA / cDNA 

step 2B. determination of isolated gene as the disease-manifesting gene

once contig’s genes are located and sequenced, determine whether each gene is likely to be the disease-manifesting gene in particular by checking for 

1. disease-tissue specific expression via Northern Blot

same general process as Southern Blotting, but for mRNA expression 

no RE cutting (REs only have double-strand recognition capabilities)

hybridize mRNA from different tissues with gene sequence from contig

can run Northern before and after treatment with some treatment (i.e., activating steroids) to assess expression levels in disease tissue

2. disease-manifesting function via assessment of corresponding protein’s role in physiological processes | i.e., whether the protein encoded by the gene plays a role in the WT function of the disease pathway

3. mutations in the gene and corresponding protein malfunction in disease-affected individuals

» assessing altered gene expression in different affected individuals and directly sequencing diseased individuals’ DNA are both still too time-consuming

» optimal rate, ease, and price: use single-strand conformation polymorphism (SSCP) method to determine whether all diseased individuals have a mutation in the hypothesized disease gene

SSCP – amplify single DNA strands from diseased and WT individuals via PCR and run gel electrophoresis 

single strands fold into complex shapes, and even 1 base difference creates a different shape that can be distinguished between mutant and WT

compare diseased and WT SSCP bands to assess for conformation change

step 3. final sequence mapping

once all above determinations have been made that a gene is incredibly likely to be the disease-causing gene, only THEN does one DNA sequence

string literal representations of DNAPMs, genes and disease loci in fundamental base pair sequences, in bp units

Human Genome Project - create ordered contigs and sequence contig segments → generate information about contig order AND fundamental gDNA GTAC sequences

Celera - shot-gun sequence entire genome and use overlapping fragmentation to determine order of sequences → generate information about gDNA GTAC sequences only, trouble with repetitive sequences along hgDNA

all sequence data in NCBI database, use to create probes or derive information about experimentally isolated sequences of interest

[hurtworld]

mesaj attım ama cevap vermedin dostum. PCR ve qPCR teknikleriyle alakalı kaynak olarak yardımcı olabilir misin?

mendeley kullanıyor musun bilmiyorum ama ben APA şeklinde buraya atayım kaynakları sen seç beğen al dostum.

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[thewookieruns]

Yeehawgust Day 24 & 25 Combined: Wild ‘n Out/New Sheriff in Town

Dusk found Captain Erich Richardson, John Hancock, and RJ MacCready on a balcony overlooking Goodneighbor. Each was wrapped up in their own thoughts while nursing their various indulgences; a Nuka-Cola for Erich, cigarettes for MacCready, and various chems for Hancock. The noises of the town filtered up through the air to the trio. It was one of the few nights where everything seemed like it was before the War.

MacCready piped up after a while. “Hey guys… do you think that the Commonwealth is any safer now that the boogeyman is gone?”

Hancock was the first to respond. “Of course, my friend. There’s a new sheriff in town in our Vaultie friend here. Things aren’t as crazy wild as they used to be.”

“Yeah, I guess… but I mean… who is actually in charge here? The Minutemen? The tin cans?” MacCready asked, taking a long drag on his cigarette. “Everything is still dangerous.”

Hancock turned to Erich. “You’re being pretty quiet there, Vaultie. Got something to say?”

Erich took a swig of his Nuka-Cola, leaning forward. “Maybe it’s time.” he answered nonchalantly.

Hancock and MacCready shared a glance. “What do you mean?” MacCready put forth.

“I mean… maybe it’s time to get an actual new sheriff here in the Commonwealth.” Erich replied. “Maybe we need to start thinking about actually establishing the CPG.”

Hancock sat up ramrod straight. “You mean actually get the Commonwealth Provisional Government? Actually get settlements together to form one central government? I dunno… isn’t that what caused the Great War? Sounds like a bad idea to me.”

“I know, John. But it’s the best chance we have. You said that I’m the new sheriff in town… and I don’t think I’m going to be around forever. Hell, I really enjoy my “retirement” on the Island. And I know I haven’t always made the best call when it comes to trying to help people out here. With the CPG, the Brotherhood, the Minutemen, whoever, can’t have full sway over what happens out there.” Erich replied, his voice weary.

“Does it really wear you out that much, boss?” MacCready asked. Erich nodded.

“Yeah… it does, RJ. And frankly, I’m getting tired of being the middleman between everyone. I say make them talk about like people, not savages. Make them act like settlers, not raiders.” Erich responded.

“Well… I don’t think Goodneighbor would join. I’m still for the idea of the people, by the people.” Hancock piped in with a mildly snide tone.

“Even if it was better for everyone in the Commonwealth, Hancock?” MacCready asked, his tone hard. “Even if it made your job easier to do?”

“Hey, let’s knock it off, guys.” Erich cut in, ending the tension. “I’m not saying that it’s going to happen in one hue wild day. It’ll take time. But for now, let’s leave things wild ‘n out there while we get ready to change the world.”

The trio fell silent, each once again left in their own musings. “It’ll be a hell of a change, Richardson. Hell of a change.” Hancock said after a long silence.

“Let’s hope so.”

[chasedawaybytime]

Quarter II Rants (sorry)

I deserve a good long summer vacation!!

(4/8/19: Samal Island, Davao del Norte, PH)

☕ Quarter I was all about finishing tasks, senior thesis, and graduation. Those three months finally passed and I’m grateful to say I did a pretty good job keeping my shit together. This is my self-report of my second quarter of 2019 with the intention of moving on after six years of my environment molding me into an anxious stem student but who also has the intention of doing art in the future. It was hard juggling two different things, and I bet it will also get harder soon. I flunked my exam to get to my dream uni/arts course. The only doors open for me were science courses but soredemo I’m still grateful for these chances. Maybe the universe is still saying “not yet” to myself for now.

Days after I checked my exam results and the morning after graduation day, I immediately flew south to attend a youth conference with my relatives. To me, it felt like an escape from my problems back home by sheltering myself through the event. There were lots of self-reflection and I can definitely say it helped me made some decisions. Don’t get me wrong, I actually did had a fun time!! No regrets.

(4/9/19: Pithecophaga jifferyi sketches - The Philippine Eagle Center, Malagos, Davao City, PH)

☕ Witnessed Kamikazee and December Avenue music huhu 💕 Feels surreal to hear your songs from spotigy/youtube on replay to live concerts with tons of people.

(4/2919: Kamikazee - HNU Oval)

(5/1/19: December Avenue - CPG Sports Complex)

☕ Did a beach/underwater-themed wedding guestbook commission!! I had fun experimenting different textures for the cover, illustrating a photo of them together, and painting different sea creatures on the pages!!

☕ Had a 20-days summer job at the provincial capitol. They newly built the place and was assigned to a very pretty office. Also met new found friends!! 💕

☕ We did our part for World Oceans Day with a beach cleanup held by Plastic Free Bohol (a local NGO I hope to volunteer more often!!) After picking up trashes, we went ahead to find a good spot to chill/sun bask with my friends.

(6/8/19: World Oceans Day - Doljo Beach, Panglao Island & Bool, Tagbilaran City, Bohol)

Other friends also did a mini mangrove planting project in Bool’s coastal areas!! So proud of my batch mates 💕

As someone who’s taking a college course that mainly covers ocean conservation and marine life (maybe in another post hehe), figured at least participate local cleanups (as if it’s our last haha) even if commuting to the venue’s a challenge, all efforts definitely doesn’t go to waste :)

Quarter II was an experience of taking my longest break and I definitely believe that I deserved that haha! Quarter III starts this month and all college prep should start now. School starts in August so I think I still have time lounging on this cave lol

I think I made good decisions so far and had good realizations during my break. Whatever happens, happens. I did my work and arrived setbacks, but I’ll try and try again no matter how long it takes. I’m also interested in my upcoming field in uni so I’ll take it as a stepping stone to my intentions, old and new. :)

Lalaban po ako ulit.

Hopes and dreams,

- 花 🌸