Roundtable Discussion; The Future of Mineral Sands. Watch the video here.
And remember that the stability of this stock is rather artificial due to the workings of Lago Kapital; for which they have been hired for. Everyone can see on daily basis how active they are. It is (rather) general knowledge that big time investors dislike volatility and for Faron this could be of above average importance due to the fact that they are currently closing in the turning point for the company (from money eating developer to money printing seller). The big boys can see the year 2018, so they still feel the (ever diminishing) after shakes. To discount this is to be delusional. It will rise when the key players holding the strings (quite in the open in Faron's case) are ready. There wont be any mistakes this time.
FOMO seems very strong in the current market. When there is a stagnated paper (stagnated in monthly sense) in one's portfolio, there seems to be an increased anxiety to rid oneself out of these, and hop on one of the 'other' gravy trains as fast as possible; because you might be missing out on those hefty rises we see almost every day. The patience of the investors was destroyed in the cataclysmic BEAR of March and rocket powered BULL of April. Now people run around like headless chickens.
And the stream of shares to Helsinki continues. To me it seems most of these stay in the hands of regular Finnish (or Finland based) investors. I'm getting the feeling that Nasdaq wants to rise but the constant stream of 'cheap' stock keeps the volatility down. Lago doing what they are paid to do, I quess.
What zumzum said; still, the closing time dump with lowering prices was what caught my eyes, and came out as slightly peculiar behaviour. Could not wait until tomorrow? Why?
Lago capital undercutting themselves in the sell front in Nasdaq near the closing mark. To what end?
The us governmental body is heavily invested in Gilead's remdesivir, and the pharma is in dire need of a new blockbuster drug to put its revenues back on the rise. There's a strong political backing on this project; to make it succeed no matter what.
I also want to point out that remdesivir while shown to be effective against the virus and its reproduction, does not reduce mortality in patients. This is because of the developed ARDS, against which the drug does nothing. How to alleviate this shortcoming?
I know man.. that's the reality, the true actual issue. But everyone aren't so focused on reality, especially if there's politics involved. Then it's about feelings, imagery, hyperboles, stories, narrative etc. which are all rather cloak and dagger and only tangentially rooted in reality.
Look, this is only my hypothesis about what is going on behind the stage. I know all too well how devastating ARDS can be, my mothers brother died of it (technically my uncle but I wasn't born yet then), and afterwards I've heard enough stories from her work as a hospital nurse. I'm not even arguing here, or disagreeing, I'm just being my sceptical self in the face of big people and their agendas.
Tbh, I've been on the verge of saying that at the moment, TK might be the only thing that actually works reliably against this disease. Everything else seem so.. muddled because of this race for the cure/vaccine. It's almost feels (for me - this is just my opinion) like TK isn't even in the race, but sitting at the stand eating popcorn. Waiting for the games to end, so that they could get to real work. Zen, let's agree to agree, so that this spam ends.
Zen, I know that very well, and they now that too BUT it is the virus that is causing that. The people in the spotlight, in the lack of a better word, want to cure COVID-19 and not ARDS, even though in this case those two are pretty much the same, of course (in the bad cases).
My hypothesis about solidarity trial combining TK with lopinavir/ritonavir: They must have a very strong hunch that TK is actually effective towards ARDS. However, TK is not actually antiviral drug and it's 'merely' activating one's own immune system. The big pharmas and entities like WHO don't want passive eradication of the disease, they want active purge that will look very nice on the headlines. That's why they are combining ARDS cure with an antiviral drug, so they can say they cured the COVID-19. If our own immune system slowly gets rid of the viruses after we survive the worst of the disease.. well it's not quite as conspicuous is it?
No problem.
Blast from the past. Interesting about this failure of the trial III is that it lead to the parallel listing in Nasdaq Helsinki and me finding about the Company and allowing me to become investor. Everything connects.
Arsenal, it means that some interferons may enhance the current coronavirus' ability to attack cells. However, the sum of scientific knowledge on the issue is inconclusive at best, contradictive at worst. Interferon beta 1a (Traumakine), however, is not represented in these studies to a great amount. One might think this had enhanced its chances to get into these trials (as the scientific data goes back many years - this is not new info) over the other interferons.
..continues
I could not find any relevant information regarding IFN-beta upregulating ACE2 by searching the databases by Rusikova et al. Interestingly there are studies that IFNalpha/gamma inhibited the SARS-COV (the old coronavirus - which also uses ACE2 for attachment) replication by reducing ACE2 expression, completely contradicting information here. There is information available in scientific studies that could support almost any scientific view (or opinion). One that is mostly missing (in a negative sense) is INFbeta (1a), which, surprise surprise, has been chosen as a treatment candidate in at least two big COVID-19 trials (I think you know what they are by now). These Harvard findings mean nothing to Traumakine, in my (professional) opinion.
ACE2 expression is the thing to look at here, as it is the protein which is used by SARS-CoV-2 to attach to cells and infect them.
"To further extend and substantiate these findings, as above, we stimulated primary mouse tracheal basal cells, the commonly-used human bronchial cell line BEAS-2B, and upper airway basal cells from two human donors (Figure 5A-D). We confirmed appropriate induction of an IFN response in each cell type by performing differential expression testing between untreated cells and IFN-treated cells for each condition (Table S7). Within each cell type, stimulation with IFNalpha2, IFNbeta, or IFNgamma resulted in dose-dependent upregulation of canonical ISGs, including STAT1/Stat1, BST2/Bst2, XAF1/Xaf1, IFI35/Ifi35, MX1/Mx1, and GBP2/Gbp2. Notably, Ace2 expression was not robustly induced in basal cells derived from healthy mouse trachea under any interferon stimulation condition. The magnitude of ACE2 upregulation was diminished in BEAS2B cells relative to our original findings in primary human upper airway epithelial cells, but reached statistical significance compared to the untreated condition following IFNgamma exposure."
"Our study finds that Type I IFNs, and to a lesser extent Type II IFNs, upregulate ACE2. This is based on several lines of evidence: 1) we identify a human goblet secretory cell subset in upper airway nasal epithelium enriched for ACE2 expression to have the highest IFNalpha-induced gene signature; 2) we find that IFNalpha, and to a lesser extent IFNbeta or IFNgamma, induced ACE2 expression in a published data set of air-liquid interface cultures derived from human nasal epithelial cells (Giovannini-Chami et al., 2012; Ordovas-Montanes et al., 2018); 3) we extend our search through the Interferome database (Rusinova et al., 2013) and find that, in epithelial barrier tissues, Type I IFNs upregulate ACE2 in multiple studies, especially in primary bronchial cells and keratinocytes (Rusinova et al., 2013); 4) we find two STAT1 binding sites in the promoter of ACE2; 5) in our unpublished atlas of SHIV-infected macaques, known to have elevated levels of chronic IFN signaling, we find ACE2 upregulation in absorptive enterocytes; 6) we directly provide evidence for IFNalpha, and to some extent IFNgamma, inducing ACE2 expression in primary human upper airway basal cells; and, 7) influenza infection in humans, a known inducer of the IFN pathway, leads to increased ACE2 expression in goblet secretory cells of the nasal epithelium (Cao et al., 2020)." continues..
I'm looking at the article right now; will be back in a minute. Meanwhile, Pot, I wouldn't go too deeply into the etymology of traumakine as "trauma" just means "injury", so that part is essentially meaningless. Traumakine works by inhibiting the leaking of fluids through epithelial cell protective layers which line most "border" areas in the body. This unrestricted fluid flow may accumulate, for example, in lung alveoli or other parts in various organs, causing them to lose functionality (in a VERY critical way - by that I mean that death will follow).
For now there seem to be an eerie lack of mentions for interferon beta's, let alone 1a. Remember that "interferons" is a decently large group of proteins (about 20 of them) and all of them have their function. Traumakine is just one of them. In my opinion is VERY dangerous and borderline political to say that "interferons" cause this and that. There is definitely a conglomerate of political agendas packed within the parties that have affiliated themselves with or financed this piece of research.
Not bigger than the timeframe we'll be getting results from the Remap and Solidarity trials. I'd say that's definitely "in the short term".
I would not be surprised, if everything worked with Traumakine. The trail's end is just around the corner and the view will be definitely interesting.
I guess they continue doing what they're doing, as long as the commissions are running. The sp seems to be mostly irrelevant to them, especially Lago. AIM must be getting pretty damn dry soon, or am I crazy?
Finnish /= Swedish, I was so confused for a second.