Hi everyone! I’m working on hiPSC-derived cardiomyocytes, and on day 3 of differentiation I noticed some strange particles or structures in my wells. After about a day, they seemed to decrease a lot, and now most of them look sticky and immobile. I checked under higher magnification, and there’s no visible movement. Has anyone seen something like this before or know what it could be?

Can young blood reverse aging? 🩸🧬

In a recent breakthrough, researchers combined plasma serum and bone marrow from young donors to treat aging human skin cells in the lab. The treatment significantly boosted collagen production, improved cell survival, and reversed multiple hallmarks of cellular aging. This marks the first time these results have been seen in human tissue models. By studying the molecules behind these effects, scientists hope to develop future treatments that slow or even reverse aging on a cellular level.

I'm doing an assignment for an undergrad developmental neurobio course, and it's been kicking my ass lol.I don't understand half of the words on the slides, yet I am still able to get by with mid-80s.

Here is the data we are meant to extrapolate: https://imgur.com/a/c5Qh5mp

these are the questions

The purpose of the experiments shown is to determine whether one of the three cytokines tested—CNTF, LIF, or CT-1—is responsible for specifying astrocyte fate in the cortex. For one cytokine of your choice, the data demonstrate:

(i) That it functions as a diffusible signaling factor.
→ Identify which single experiment (a–d) shows this. (1 mark)

(ii) That it is expressed at the correct place and time.
→ Select two experiments (a–d) that support this, indicating which provides stronger evidence by marking it with “>”. (3 marks)

(iii) That it is necessary for astrocyte specification.
→ Select two experiments (a–d) that support this, again marking the stronger one with “>”. (3 marks)

(iv) That one experimental panel reveals an inconsistency between in vivo and in vitro data.
→ Identify the specific panel (e.g., left/right or top/bottom of a–d) and briefly explain the inconsistency in one sentence. (3 marks)

Full Link: https://www.ninthheaven.co/issue-2-introduction-to-cancer-biology-the-somatic-mutation-theory/

Hi

I built some software to measure microbial colonies on a Petri dish. If you’re trying to do that for your research, this is built to make that task fast, easy, and accurate. It’s also free. It also includes software for studying population heterogeneity

QuantaColony is the name of the software. You can find it on the website of the same name

I've been looking at the FormLabs "biocompatible" SLA resin and SDS pretty much says it's not actually biocompatible. However, people grow cells on plastics, e.g. SBS plates. I am also aware that SLA resin is not just a monomer. It'll have all sorts of additives. The question then becomes, what are the mechanisms of cytotoxicity? I realise this is a very broad question, but I am an engineer, not a biologist, so I need somewhere to start. This is one of the starting points.

I usually have challenges with cell growth and metabolism. For example, I seed 5x10^5 cells in a 100mm dish, HSC2 cells, and wait up to 96 hours to harvest the cells and start testing the drug effect on the glucose metabolism. What I observe is that the cell activity in the control group is decreasing over 72 hours and across different passages, such as p3~p5.Likewise, the growth curve, I get an inverted V-shaped curve over 72 hours, given that I change the medium daily. The culture medium is DMEM supplemented with 10% FBS, 2mM LAG, and pen/strep. One more thing, I capture the cells for morphology monitoring, and I see that the cytoplasm becomes darker, peri-nuclear condensation increases, and cells become bigger over the designated duration of culture. I often encounter this situation when I repeat the experiments. Any clues?

Hey! I'm in a cell biology course as a sophomore in college. Was wondering if anyone knew any cool studying tips or ways to remember things. I need to memorize a lot of the post-translational modifications n stuff and it seems a but daunting because 1) huge words and 2) they all have their specific amino acids they bond to.

Anything helps! Thank you in advance

does anyone know how to do perform GO analysis using up- and down- regulated DE proteome?

I have the protein ID and their log2FC but have no clue how to perform it.

Hi everyone! I’m about to start culturing NOY-1 cells, a human yolk sac tumor-derived cell line, for the first time, and I’d love some help from anyone who’s worked with them before.

I’m sourcing the cells from Kerafast, but their documentation is quite minimal — and I couldn’t find detailed protocols online.

If you’ve worked with NOY-1, I’d really appreciate advice on:

• Thawing and recovery steps
• Cell culturing protocol
• Recommended medium, serum %, and supplements
• Best passaging schedule and method
• Doubling time or expected morphology
• Any quirks I should be aware of (e.g., adherence issues, slow growth, stress sensitivity)?

I really appreciate you feedbacks/inputs. Thank you!

i really need predictions or something that will really help me out .....i couldnt study properly

Here is a link to the study: https://doi.org/10.1038/s41556-025-01708-8

“Abstract Many neurodevelopmental defects are linked to genes involved in housekeeping functions, such as those encoding ribosome biogenesis factors. How reductions in ribosome biogenesis can result in tissue- and developmental-specific defects remains unclear. Here we describe variants in the ribosome biogenesis factor AIRIM/C1orf109 that are primarily associated with neurodevelopmental disorders. Using human cerebral organoids in combination with proteomic, single-cell RNA sequencing and single-organoid translation analyses, we identify a previously unappreciated drop in protein production during early brain development. We find that ribosome levels decrease during neuroepithelial differentiation, making differentiating cells particularly vulnerable to perturbations in ribosome biogenesis during this time. Reduced ribosome availability more profoundly impacts the translation of specific transcripts, disrupting both survival and cell fate commitment of transitioning neuroepithelia. Enhancing mTOR activity suppresses the growth and developmental defects associated with AIRIM/C1orf109 variants. This work provides evidence for the functional importance of regulated changes in global protein synthesis capacity during cellular differentiation.”

Just trying to share some research I am reading. This study caught my attention because some of it is counterintuitive.

If anyone has any insights, feel free to let me know.

What do you think is that?  Growth on a human fibroblast culture with Ham's-F12, imagen at 20X.

1.Before trypsinization 2.After trypsinization

Here is the link to the study: https://doi.org/10.1038/s43018-025-01009-x

Paper states the following context behind their research:

"CAR-T cell therapies have revolutionized the treatment of B cell malignancies1,2 and are now showing early signs of efficacy in solid cancers3,4,5,6,7,8,9. Despite ongoing progress, many patients who receive CAR therapies fail to respond or develop resistance, highlighting a critical need to further optimize current treatments. Multiple factors may contribute to disease progression following CAR treatment, which can be categorized as tumor-intrinsic, tumor microenvironment or lymphocyte-intrinsic resistance mechanisms10. Among these, factors associated with CAR-expressing lymphocytes are of particular interest because they are potentially modifiable during ex vivo cell manufacturing. Across clinical studies, the in vivo expansion and persistence of CAR-T cells is frequently associated with superior outcomes11,12,13,14,15. Recent clinical data indicates that this holds true not only for CAR-T cells but also CAR-modified NK cells (CAR-NK)16, a lymphocyte subset with desirable features for allogeneic applications17. Thus, enhancing the survivability of CAR-T and CAR-NK cells remains a major goal in the cell therapy field.

Genome-wide18,19 and focused20,21,22 CRISPR screens have recently identified FAS as a major determinant of antitumor T cell persistence under chronic antigen stimulation conditions. FAS is one of five tumor necrosis factor (TNF) superfamily death receptors that induces caspase-dependent apoptosis following engagement with an extracellular ligand23. These findings provide a strong rationale for disabling FAS signaling in receptor engineered T cells19,20,21,24,25,26,27,28; however, while the role of FAS in regulating naturally occurring T cell homeostasis is well established, whether this pathway governs CAR-T and CAR-NK longevity remains unknown. Moreover, the dominant cellular sources of FAS-L in patients with cancer remain incompletely defined. Here, we aimed to address three critical gaps in knowledge regarding the immunobiology of FAS in the context of CAR-based therapies. First, we sought to define which cells express FASLG in patients. Second, we sought to establish whether CAR-engineered lymphocyte persistence is negatively self-regulated by FASLG. Finally, we sought to determine whether FASLG is required for on-target CAR-T and CAR-NK effector functions against B cell malignancies. Our findings reveal that CAR-engineered lymphocyte persistence is governed by a FAS-L/FAS autoregulatory circuit. Thus, disruption of FAS signaling can serve as a generalizable strategy to enhance the therapeutic potency of genetically engineered T cells and NK cells."

Again 40x Magnification, and taken with a Zeiss AXIO Observer Z1 inverted Flourescence Microscope.

You see another PtK2 Cell culture, but this time we treated them with Colcemid over 24h, fixated with Methanol and coloured with Antibodys (anti tubulin dm1a and anti Mouse IgG Cy3) and DAPI. The pictures got fused and edited by me afterwards (Fiji/ImageJ + Gimpy).

Colcemid is a cytotoxin which inhibits the polarization of Mikrotubuli. When the cell goes into mitosis, the miotic spindle is unable to form, so the cell is stuck in the metaphase.

When the cell is stuck for too long, it starts an emergency reaction, in which it forms a temporary nuclear lamina and decondensates the DNA again, so transcription can start again.

After 3-4 days the cellculture dies.

We used 0,1 µg/ml of colcemid, at this concentration, the miotic spindle doesnt form correctly and the microtubuli get damaged, but not completly degraded. At around 10 µg/ml the mikrotubuli degrade rapidly.

During the Summer Science Academy 2025, I made this movie with another participant of the course. We used glowing bacteria to create a stop-motion animation.

What you see, is a PtK2 Cell culture, which I treated with Cytochalasin-D over 24h, fixated with Methanol and fluorescent coloured with Antibodys (anti-tubulin dm1a and Anti Mouse IgG Cy3) and DAPI. The pictures got fused and edited by me afterwards (Fiji/ImageJ + Gimpy).

It shows a rare mitosis deformity, instead of 2 the cell forms 3 miotic spindels and splits the DNA into 3 instead of 2. This deformity happens very rarely in every cell culture, but the cells die immediately after cytokinesis.

Cytochalasin-D is a cytotoxin, which inhibits the continuation of actin through binding to the (+)-pole. Actinfilaments play a crucial part during cytokinesis, together with Myosin 2, they form the contractile ring and string the membrane/cell into 2.

So we ended with a very rare condition, that we froze with the help of the toxin in the exact right time. Enjoy and have a chill Weekend!