Paracrine Puns

I do understand that in juxtacrine signaling cells can use gap junctions. I also understand the notch patway.

However, I am reading Langman’s embryology and it says that in juxtacrine signaling ligands in extracellular matrix secreted by one cell can interact with receptors on their neighboring cell. It goes on to talk about the extracellular matrix and what basal lamina and integrins are. But what it says about the ligand and its receptor, that to me sounds like paracrine signaling.

Can someone explain it a little better?

It’s on page 7 in the book.

Regenerative Medicine & how transplanted stem cells work : Regenerative Medicine is dealing with repair & restoration of function of damaged tissue. Repair & regeneration of damaged tissue could happened in two ways transplanted stem cells could replace damage tissue by proliferation and self renewal , replacement of dead cells. Secondly regeneration and repair of damaged tissue happened by paracrine effects of transplanted stem cells.here we are discuss about paracrine effects of stem cells in detail. Paracrine effect of transplanted stem cells: Transplanted stem cells secreate certain types of protein molecules , cytokines,growth factors which stimulate existing cells of that particular organ in such a way that cells start proliferate & self renew & because of that final outcome is repair of damaged tissue,every dead or damaged cells secreate certain type of chemicals called as cytokines which triggered by transplanted stem cells & further in return these cells secreate proteins . with reference to many preclinical studies it was found that repair of damaged tissue was done after donor stem cell transplant but when repaired tissue were analysed the donor cells were missing,further it was investigated & surprisingly found that repair was done through paracrine effect of donor cells.in mammalian existing cells are capable for wound healing until unless certain signalling should be initiated by donor stem cells. Initially Scientists were disappointed when they observe that donor cells weren't actually contribute in regeneration of damaged tissue , transplanted unmatched donor cells could alive upto 1 or 2 weeks,in this short period paracrine effect completed & tissue regeneration happened.mesenchymal stem cells & hematopoietic stem cells are paracrine effect cells.these cells could be derived from bone marrow,fat, umbilical cord tissue and cord blood. Damaged cells secreate certain proteins & cytokines which act as mediator to initiate immune response ,in return donor stem cells secreate proteins, cytokines which stimulate patients stem cells & help in to reduce inflammation,help in vascularization,increase blood flow to heal damaged tissue & help in to prevent death of patient cells . Mesenchymal stem cells & cord blood cells shows significant effectiveness in heart muscle,skeletal muscle,nerve cell regeneration. In one preclinical studies shows donor cord blood cells improve lower limb mobility and r

DHT is a hormone that is produced and used in individual cells, or only signals cells nearby (intracrine and paracrine, respectively). Assuming DHT inhibition is helpful (ergo finasteride is efficacious), why is there no way to suppress DHT acutely in the scalp? The science of the hormone suggests that there is no need to reduce DHT systemically to reduce hair loss. DHT stays where is it synthesized, it doesn’t travel throughout the body to a significant extent.

If I’m wrong on any of this feel free to correct me

When I was in undergrad, I used to know these and they were not at all that difficult to understand but for some reason I have had a lot of trouble remembering these terms, what they mean, and examples of them. If anyone could explain these in a way that's easy to remember, maybe in a mnemonic or something, that would be great. It's so basic but for some reason my brain doesn't retain it. Thanks!

This weird interaction triangle between the hormones confuse me. Other than somatostatin being an inhibitory hormone, is there a reason that it inhibits both insulin and glucagon?

I would understand if it inhibited just insulin to increase glucose levels. Somatostatin is inhibitory of Growth Hormone, and GH is stimulated by hypoglycemia, and inhibited by hyperglycemia. So an elevated glucose levels by virtue of insulin inhibition would achieve GH inhibition.

But why inhibit glucagon?

Thanks!

I was recently reading a paper in which the authors showed that in a coculture of two different cell types (mammalian), there was a paracrine effect found in a transwell assay, but the same effect was not found when applying conditioned media from one cell type to the other. Does anyone know why this would be?

TL;DR I’m bullish based on the science alone. I summarize why and how their product works. Extended trial completion in June and results in July. Their product was already approved to treat another condition so it’s already been proven safe.

I just found out about Organicell $BPSR last week. Their stock went up like 1200% and dropped back down to 762%. This is due to a recent trial with 10 patients that showed positive results. I will focus on their earlier 3 person trial because I haven’t been able to find the papers for the latest trial.

Also, the trial a lot of people are focused on is in India but they have a US trial on the go as well:

https://www.clinicaltrialsarena.com/news/organicell-enrolment-covid-19-trial/

That trial, due to the red tape in the USA, won’t conclude until the 3rd quarter of 2021. They just concluded patient enrolment this month so the US trial is lagging a bit behind the trial in India.

I’m sceptical by nature so I wanted to know if this was just another COVID money grab or if there was actual science behind it.

Disclosure: I’m still bullish after doing the research and I bought in anyway despite missing the spike.

I had some time on the weekend to read their case report published in “Frontiers in Medicine”.

https://www.frontiersin.org/articles/10.3389/fmed.2021.583842/full

I will summarize because it’s a really long and wordy report. I will make it as simple as possible without leaving out the important stuff.

Their product Zofin has previously been tested in HIV and some other illnesses. It’s now being given to critically ill COVID patients.

It’s derived from the soluble and nanoparticle fraction (extracellular vesicles and exosomes) of human amniotic fluid. Sounds absolutely disgusting. But it works. Like Buckleys but in your veins.

All the patients they tested it on had been diagnosed with respiratory failure (ARDS).

Zofin uses cell-secreted and tissue-secreted paracrine factors instead of the actual cells. The reason for this is that with cellular therapy the cells normally don’t last and most of the benefit is derived from those excretions. They’re removing a step that fails which gives them an edge over other cellular therapies.

When COVID patients get inflammation and a cytokine storm typical treatments don’t properly reduce the inflammation or cytokine response and they also make the patient vulnerable to getting another infection because they suppress the immune system and also reduce clearance of the virus