-----=
Original Message-----

From: Ruben Safir <ruben-at-mrbrklyn.com>

To: Carolinedliny <carolinedliny-at-aol.com>

Cc: ruben-at-mrbrklyn.com <ruben-at-mrbrklyn.com>

Sent: Fri, May 1, 2020 2:24 am

Subject: Re: good thing they are rushing (the vaccines)



On Fri, May 01, 2020 at 03:42:06AM +0000, Carolinedliny wrote:

> they are using prophylatic heparin drips, wouldn't criteria for stepto=
kinase exclude its use once a pt is started on Heparin drip? 





Heparin doesn't break clots.  That is why we call things like TPa clot=


busters.  They actually block fibrinogin to break down the cloats... I=


think.  I know I am correct about the clot reabsortion, but I forget t=
he

exact mechanism and I am too lazy to look it up.



Mechanism of heparin action.

Jackson CM.

Abstract



Heparin catalysis of clotting proteinase inactivation occurs most

efficiently through the reaction of the proteinase with the

antithrombin-heparin complex. The efficiency of a heparin molecule in

this reaction depends on the presence of a specific pentasaccharide

sequence in it, and its molecular weight. The mechanism by which such

high affinity heparin acts when antithrombin III is the inhibitor is

promotion of the formation of an intermediate

proteinase-heparin-antithrombin complex. Heparin promotion of thrombin

inactivation by heparin cofactor II may occur by a similar mechanism.

The requirement for a specific oligosaccharide sequence within the

heparin molecule does not, however, exist for heparin cofactor II.

Binding of heparin to both thrombin and antithrombin III interferes with>
thrombin inactivation. This binding is very dependent on the ionic

strength of the reaction mixture and may explain some of the discordant

results and interpretations from early studies on the mechanism of

heparin action. Low ionic strength in in vitro reactions also results in>
cleavage of antithrombin III by thrombin in the presence of heparin and

effectively converts antithrombin III from an inhibitor to a substrate.



And TPa



The biology of tPA in the fibrinolytic system



Blood clots are formed from the aggregation of activated platelets onto

fibrin meshes. The breakdown of the fibrin meshes is achieved by

plasmin, a broad spectrum protease found in the blood as an inactive

zymogen, plasminogen. Plasmin cleaves fibrin thus breaking down the

meshwork of the clot, and it is extremely short lived; it is quickly

inactivated by =CE=B12-antiplasmin, an abundant inhibitor that restricts th=
e

action of plasmin to the vicinity of the clot (reviewed in [2] and [3]).>
Successful fibrinolysis is achieved by adequate generation of plasmin

from plasminogen by one of two Plasminogen Activators (PAs), the

tissue-type Plasminogen Activator (tPA) and the urokinase-type

Plasminogen Activator (uPA). The two are thought to have redundant

functions in the fibrinolytic system, since genetic deletion of either

one is not accompanied by major fibrinolytic defects, and only tPA/uPA

doubly deficient mice display phenotypes similar to plasminogen

deficient ones [4, 5]. As opposed to uPA, the activity of tPA is itself

regulated by binding to fibrin, which increases its catalytic efficiency>
[6, 7]. Thus, the formation of the clot initiates, with the generation

of fibrin, the fibrinolytic/ clot dissolving cascade. The catalytic

activity of tPA in the bloodstream is terminated with the binding of (a)>
protein inhibitor(s), primarily the Plasminogen Activator Inhibitor 1

(PAI 1) [8]. The inactive PAI 1-bound tPA is cleared from the

circulation by the liver via a scavenger receptor, the LDL Receptor

Related Protein 1 (LRP1) [9]. LRP1 also binds catalytically active tPA,

but with lower affinity [10]. A neuronal-specific inhibitor of tPA,

neuroserpin, is the primary modifier of tPA activity in the nervous

system [11, 12]. Inhibited tPA-neuroserpin complexes are internalized by>
LRP1, similarly to tPA-PAI 1 complexes [13]. The half-life of tPA in the>
bloodstream is rather short, 5-10 minutes in humans, as a result of

PAI-1-mediated inhibition and LRP1-mediated liver uptake [14].

Carbohydrate side chains added to the backbone of tPA protein also play

important roles in the clearance of tPA from the bloodstream and forms

of tPA with longer half lives have been generated by mutating the

glycosylation sites of tPA (reviewed in [15]).



tPA is a secreted serine protease consisting of a single polypeptide

chain with 3 or 4 glycosylation sites and numerous disulfide bonds in

its secondary structure [16, 17]. The action of plasmin cleaves tPA into>
an N-terminal light chain and a C-terminal heavy chain still held

together by disulfide bonds [18]. Two-chain tPA has higher catalytic

efficiency compared to the single chain form and is essentially

constitutively fully active, contrary to the single chain form which

only becomes fully active upon binding to fibrin [19]. The catalytic

domain of tPA lies towards its C-terminal end and comprises the light

chain of the protease [20, 21]. The protein also contains the following

domains: an N-terminal fibronectin type III finger domain, an epidermal

growth factor-like domain and two kringle domains [16, 22]. Plasminogen

binds to the second tPA kringle domain and fibrin binds to the finger

domain and the second kringle domain. Finally, inhibition by PAI 1 is

achieved by covalent binding of PAI 1 to the catalytic domain and the

formation of a complex [21]. The presence of the additional domains

beyond the catalytic one not only allows for regulation of the catalytic>
function, but also suggests hitherto unknown interactions and

potentially functions. Indeed, both fibronectin finger and growth factor>
domains are known modalities involved in protein-protein interactions.

Go to:

tPA as a thrombolytic in stroke



The use of tPA in ischemic stroke has been the subject of numerous

recent reviews, so that only key concepts are being mentioned here and

the interested reader is referred to such reviews for more information

[23, 24, 25, 26, 27, 28].



Recombinant human tPA produced in mammalian cell lines was introduced as>
a thrombolytic agent in selected cases of stroke following the results

of the National Institute of Neurological Diseases and Stroke (NINDS)

study in 1995 [29]. This study consisted of two independently powered

trials that both showed clinical benefit from the use of tPA. A European>
study conducted around the same time also showed clinical improvement,

albeit more modest, and the use of tPA was not recommended, for fear

that eligible patients could not be easily identified [30]. A second

European and Australian study showed no benefit from tPA [31], a fact

which delayed the use of the protease in Europe until 2002 when a

license was granted, provided that an observational safety study was

conducted to assess the safety profile of tPA in routine clinical

practice. The results of this study were recently published and

confirmed the positive effect of tPA [32], thus further relieving

reservations concerning its use as a thrombolytic in stroke. However,

tPA is still used only in a small number of ischemic stroke cases (3-8%,>
[33]), but this percentage greatly increases in specialized stroke

centers [28].



The rationale behind the use of tPA in ischemic stroke is that by

breaking down the clot, recanalization of the occluded blood vessel

occurs. The restoration of blood vessel patency is meaningful, however,

only if the brain tissue of the ischemic area is still viable.

Unfortunately, brain tissue is metabolically very active and thus very

sensitive to ischemia. The core of the area serviced by the occluded

vessel becomes necrotic very quickly, whereas the periphery, which

receives some perfusion by adjacent non-ischemic regions, is still

salvageable within a reasonable time frame of a few hours, and is

referred to as the penumbra. Thrombolysis by tPA resulting in successful>
recanalization potentially saves this ischemic but still viable

penumbra, but it has to be administered quickly. The positive effect of

tPA was clearly demonstrated in the two trials of the NINDS study [29],

in which the cut-off time from symptoms onset to initiation of

thrombolysis was set at three hours. The effect was more moderate in the>
ECASS study (30), where treatment was initiated within 6h from stroke

onset, but clearer in the subgroup of ECASS patients treated within the

first three hours [34]. Along the same lines tPA showed moderate benefit>
upon administration between 3 and 5 hours from stroke onset [35]. To

date the initial recommendation remains that tPA should be administered

within three hours from stroke onset [29, 36, 32]. This is a narrow time>
window since the patient needs to be transferred to the health care

unit, and at minimum a CT scan has to be performed, primarily to exclude>
the possibility of hemorrhage and to assess the size of the infarction.

Since potentially positive effects have also been reported with

administration of tPA between 3 and 5 hours from stroke onset [35, 36],

clinical trials are under way to further extend the time window for tPA

thrombolysis [37, 38].



Time is not the only parameter to be taken into account in the decision

to initiate tPA thrombolysis; novel imaging technologies may aid in the

identification of thrombolysis candidates at late time points.

Diffusion-weighted and perfusion-weighted MRIs are being employed to

identify patients with large diffusion-perfusion mismatches [39, 40],

i.e. patients with significant brain areas that still receive some

oxygen and nutrients from adjacent non-ischemic areas by diffusion,

although they do not receive any blood flow directly. These patients are>
predicted to benefit the most from recanalization which would restore

blood flow to viable, salvageable tissue even after a relatively long

time from stroke onset [40]. Perfusion CTs (PCT) and CT angiography

source image (CTA-SI) analysis are CT modalities that could substitute

for MRIs in cases where an MRI is contraindicated or not available [41].>
However, it should be noted that the usefulness of imaging techniques in>
detecting thrombolysis candidates at late time points after stroke onset>
has not yet been unequivocally proven. The results of the DEFUSE study

[40, 42] are expected to shed light on this issue.



The need for strict criteria and time-consuming diagnostic procedures

prior to the administration of tPA results from the adverse side-effects>
of tPA, most notably that of intracerebral hemorrhagic conversion [43],

even though such conversion occurs only in 6-7% of patients. This is

considered a result of systemic plasminemia/fibrinolytic activation,

i.e. the tipping of the coagulation/fibrinolysis balance towards the

latter side in the systemic circulation which is thought to disrupt

microscopic plugs that physiologically prevent hemorrhages at

transiently injured spots on vessel walls [43, 44]. Although this lytic

state can manifest itself as hemorrhage in different organs,

intracranial hemorrhage is the most dramatic manifestation and can

complicate thrombolysis taking place in the body, such as during

myocardial infarction where brain vasculature is otherwise healthy,

although not necessarily. However, it is much more common in ischemic

stroke, because brain vasculature and the Blood Brain Barrier (BBB) are

already compromised from the ischemia. In general, the greater the

severity of the ischemia and the longer the time from stroke onset, the

higher the likelihood of hemorrhage ensuing when recanalization of the

occluded vessel occurs in the course of thrombolysis [30]. Moreover, tPA>
may also directly damage the cerebrovascular endothelium and disrupt the>
BBB, as suggested by animal studies discussed below although evidence

from human trials is lacking.



One important issue in the use of tPA in stroke thrombolysis is whether

efficient and permanent recanalization of the occluded vessel occurs.

This may be the case with as little as 10% to 25% of cases [45], as tPA

only works on the surface of the clot. Therefore larger size clots would>
take a long time to break down. Moreover, tPA is rapidly removed from

the systemic circulation and its thrombolytic effect is quickly lost

after termination of its IV infusion. This short half-life results in

inability to act on subsequent and continued vessel occlusions that

occur both in bigger and smaller blood vessels. Attempts at increasing

the dose are hampered by increased incidence of hemorrhagic

complications and a potential solution would be to alter the tPA

protein, so that favorable properties (such as fibrin specificity) are

maintained or enhanced and undesirable ones (such as short half life)

are modified or abolished. Mutant forms of tPA exhibiting longer half

lives and increased fibrin specificity have been generated and their

specific mutations and properties have recently been reviewed elsewhere

[15]. Although these tPA mutants have been evaluated as thrombolytics

for myocardial infarctions, their use for ischemic stroke is still under>
investigation [46, 47, 48, 49]. Another solution would be to locally

deliver tPA via an arterial catheter in the vicinity of the clot (an

approach that seems to extend the therapeutic window) rather than

intravenously, so that higher local concentrations and hence higher

fibrinolytic efficiency are achieved. Unfortunately, it appears that

systemic plasminemia and the risk of intracranial hemorrhage are not

avoided this way [50]. This method of intra-arterial tPA administration

has been used in combination with the intravenous infusion and is

referred to as bridging therapy [45, 51]. Its disadvantages are that it

can only be used in large artery occlusions, and that it is more

interventional, thus requiring more specialized personnel and equipment

for its successful implementation. The appearance of specialized stroke

units circumvents this problem, although the cost remains considerable.



"_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3824365/





>

> -----Original Message-----

> From: Ruben Safir <"mailto:ruben-at-mrbrklyn.com">ruben-at-mrbrklyn.com>

> To: Carolinedliny <=3D"mailto:carolinedliny-at-aol.com">carolinedliny-at-aol.com>; =3D"mailto:docs-at-mrbrklyn.com" href=3D"mailto:docs-at-mrbrklyn.com">docs-at-mrbrkl=
yn.com; Hangout <lto:hangout-at-nylxs.com">hangout-at-nylxs.com>

> Sent: Wed, Apr 29, 2020 10:58 am

> Subject: Re: good thing they are rushing (the vaccines)

>

> On 4/29/20 9:59 AM, Carolinedliny wrote:

> > I don't know that everything here is accurate, I talk to my colle=
agues

> > in the ICU and they tell me they are putting pts on heparin drips=
, they

> > are using 100% oxygen, and/or high flow o2  in an attempt to=
prevent

> > hypoxia/desat without using mechanical ventilation

> >

>

> I'm not certain that these two things are inconsistant.  First of=
all,

> Heparin is not a Thrombolytic, so it is nto going to break clots down,=


> but prevents growth of new clots.  That would be consitant with w=
hat

> Keren is saying.  However, real clot busters, for pulmonary embol=
ism,

> streptokinase and friends, are they being used at all.  The granu=
larity

> is being SEEN on the xrays.

>

> Regardless, why are shut down?  My college at St Barnabas has bee=
n

> begrudging this from the beginning, rightfully so, and he is at ground=


> zero of this virus in the Bronx.

>

>

> >

> > -----Original Message-----

> > From: Ruben Safir <ef=3D"mailto:ruben-at-mrbrklyn.com">ruben-at-mrbrklyn.com>

> > To: Karen Perilman <ef=3D"mailto:kerens3ts-at-aol.com">kerens3ts-at-aol.com>; Hangout <mailto=3D"mailto:hangout-at-nylxs.com" href=3D"mailto:hangout-at-nylxs.com">hango=
ut-at-nylxs.com>; Liz

> > Moore <lto:lizmoorerph-at-gmail.com">lizmoorerph-at-gmail.com>

> > Sent: Wed, Apr 29, 2020 2:53 am

> > Subject: Re: good thing they are rushing (the vaccines)

> >

> >

> > One more thing... the women who some might think uses capital let=
ters is

> > a Nurse Anesthesiaologist who spent good part of her life working=
with

> > Doctors without Boarders...  threating patients and populati=
ons in Africa.

> >

> > Karen, meet, Rick.  Rick, meet Karen.

> >

> > ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~=
~

> > Side note to Liz -

> > I've been told today that Pharmacists aren't experts on vaccinati=
ons so

> > our opinion doesn't hold much weight....

> >

> > Just for reference, I point out the paper that Liz and I wrong on=


> > htt=
p://www.brooklyn-living.com/

> >

> > to continue on this thread...

> >

> > On to Karen...

> >

> > On 4/28/20 8:09 PM, Karen Perilman wrote:

> >> =C3=83=C2=AF=C3=82=C2=BB=C3=82=C2=BF

> >> =C3=83=C2=AF=C3=82=C2=BB=C3=82=C2=BFRuben,

> >> It=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s bee=
n a long time since we spoke,

> >

> > That is your fault!  I periodically send you email :)

> >

> >> And I must tell you, this message you sent came as a surprise=
,

> >

> > Call me when you have time 718-715-1771

> >

> >>

> >> First of all, the patients that were first largely infected i=
n Europe,

> > Italy and Spain were knee jerk treated with intubation and ventil=
ation.

> >> I say knee jerk, because never before had they seen so many p=
eople

> > with the same symptoms in mass like this.

> >>

> >> Never mind the Chinese allowed 5 million INFECTED people to l=
eave

> > China up to Jan 20th and go to work in Italy and Spain, the fashi=
on center.

> >> How do i know, because my daughter is the head senior designe=
r for

> > women in Spain for the company Zara.  They have so many Chin=
ese working

> > there, and their industry is in the HUB of China.

> >>

> >> And in October 18-19th the International militaries all met i=
n Wuhan

> > for the WUhan games for 100 COUNTRIES.  ANd when the games w=
ere over,

> > all those 100 countries became infected..... 

> >>

> >> Now, go back to where we were....

> >> All these people presenting with Shortness of breath we MISDI=
AGNOSED

> > FROM THE GET GO.

> >> WHy do I say this, because maybe you forgot I am an anestheti=
st.

> >

> >

> > I haven't forgotten anything.  Are you in New York now?

> >

> >> The presentation of SOB was way off the standards of evaluati=
on for SOB.

> >> The Corona is a virus that spread thru droplets as does EVERY=
OTHER VIRUS.

> >> But we never reacted like this before.

> >

> > I say this until I am blue in the face.  We have NEVER react=
ed like this

> > to even Small Pox!!

> >

> >

> >> Here is why we shouldn=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=
=E2=80=9E=C2=A2t have.

> >> I spoke with the head oncologist at a NY Cancer hospital....<=
br>
> >> I also spoke with the head neurologist at Northwell Hospitals=
and all

> > of us said the same thing.

> >>

> >

> > We've been working with St Barbaus and they just said the same th=
ing in

> > the NY Post today,,

> >

> >> The SOB from Corona patients was unlike a person with pneumon=
ia or ARDS.

> >> Patients were talking and even on the phones, and showing low=
Puse OX

> > readings.

> >> In Italy they didn=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=
=80=9E=C2=A2t have the time to asses as they were

> > barraged with patients,

> >> They ran out of ventilators when that was ACTUALLY what was k=
illing

> > people.

> >> Sick lungs under PEEP and ventilation only causes more proble=
ms and

> > patients vaso constrict and organs shut down,  and FAST, esp=
ecially in

> > the elderly.

> >

> > This I didn't know and I don't understand.  The ICU is packe=
d in the

> > Bronx with people on vents undergoing ID evaluation.  In the=
end, there

> > is not much I can do for them other than take the states and trac=
k

> > infection.  Infection contol on the floors is the biggest pr=
oblem we have.

> >

> >>

> >> But in the US, NO ONE took the time to look at the reason peo=
ple were

> > SOB and they ASSUMED it was a viral infection, Corona.....

> >>

> >> BIG MISTAKE!

> >> Now, looking back, we know now, that after autopsies, the pat=
ients

> > lungs and bodies were filled with CLOTS!!! 

> >

> > Bilateral Granularity on the Xrays.  We don't even need test=
ing for

> > this.  It is a presumptive diagnosis already.

> >

> > The patients were actually acting like someone with pulmonary emb=
olism.

> > The clots killed people with heart attacks and Strokes!!!!

> >>

> >> So where did this information take the doctors who were in th=
e know.

> >> In NY and the UK, they started realizing that the patients wh=
o were on

> > blood thinners and anti inflammatories had NO clots and they were=
mildly

> > sick and got better.

> >

> >> Those patients, in particular were Cancer patients who as you=
know are

> > compromised immunologically.

> >>

> >

> > I have data clearly showing me that pts on Chemo and with advance=
d

> > cancer don't survive this.  They won't even ventolate those =
patients at

> > this point.  So please explain this further.

> >

> > BTW - the virus attacks clotting factors, and causes prolong PT t=
imes,

> > but frankly, that is common with cytosine storms, so I am not con=
vinced

> > of that data.

> >

> >> They tested the patients clotting times and saw the proof in =
the blood.

> >> Waiting for a vaccine to kill a virus that will be obsolete i=
n a year

> > is ridiculous when we know how to treat the patients NOW.

> >>

> >> If someone presents to the ER with SOB, they should have been=
assessed

> > to rule out for  clots.

> >>

> >> A retro study, and a study that moves forward should be done =
immediately,

> >> BUT because the cure for the clots is CHEAP, no one is going =
to

> > recommend ASPIRIN or Azithromycin because they won=C3=83=C2=A2=C3=
=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2t be able to

> > make MONEY.

> >>

> >

> > This has been a recurring problem.  It is almost like they a=
re purposely

> > misusing Hydroxychloroquin, which can only work in the early phas=
e of

> > the disease, in order to make way for other thearpies, and those<=
br>
> > therapies, Remdesivir, Kaletra, Nitazoxanide, Tocilizumab, etc.&n=
bsp; All of

> > them cost over $2K per treatment.  My friend Maya, who is a =
PharmD, she

> > was big on this point. They are not acting in a way that is consi=
stant

> > with a disease that shuts down civilization.  They are telli=
ng us we are

> > in moral danger and the numbers don't bare it out and they aren't=
acting

> > like it is that serious.

> >

> >> The mayor NY and the governor are 100% assholes.

> >> We have NEVER quarantined in the history of illness HEALTHY P=
EOPLE!!

> >> Sick people yes, and they should be isolated at home.

> >

> > It is unbelievable.  Never in my lifetime could I have ever =
imagined this.

> >

> >

> >> If you go to any NY hospital now in the city,  if you sh=
ow ANY signs

> > of SOB you are intubated and you DIE!!!!  They do not resusc=
itate anyone

> > suspected of corona!!

> >> That=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s i=
nsane..... If the reason people are dying are the

> > clots, they NO ONE should be intubated and they should emergently=
be

> > give blood thinners.

> >>

> >> The elderly are being treated like disposable spoilers of thi=
s virus. 

> > They die alone and it=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=
=80=9E=C2=A2s criminal.

> >>

> >

> > How do you then prevent an anurism..

> >

> >

> >> I will not fall for the BS of waiting for a vaccine, because =
patients

> > being treated right now with the new paradigm are surviving and g=
etting

> > better quicker.

> >>

> >> No patient population compares to the cancer patients who wer=
e found

> > to be Safe from the extreme sickness of Corona because so many of=
their

> > patients were on blood thinners. 

> >> The evidence is there.

> >> Even the Young patients that died, died from Strokes.!!!

> >> No one is talking about the patients that contracted corona w=
ho were

> > described as =C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=85=E2=80=9Cheal=
thy=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=82=EF=BF=BD who SMOKE; it is a joke=
.  Smokers are

> > NOT healthy, not if they smoke anything,  pot, vaping or cig=
arettes.

> >> I see people on the streets with masks and gloves SMOKING and=


> > it=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s a joke.=


> >> THey are blowing Corona and adding to the contaminating of al=
l of us.

> >> I see people wearing masks and gloves throwing them in the st=
reets,

> > not using them properly, and I tell them, will all this costuming=
, they

> > would never be allowed in the ICU to work because they have no id=
ea how

> > to used sterile masks and gloves.

> >>

> >> If you want to be mad, get mad with the medical system in NY =
fueled by

> > political idiots that want to see the economy fail, so they can b=
lame

> > politics.

> >> Even Fauci, that =C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=85=E2=
=80=9CStatistician=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=82=EF=BF=BD is out o=
f the loop.  He

> > hasn=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2t pract=
iced medicine in 20 yrs!!  And he is nothing but an

> > accountant for the numbers that other people give him.

> >>

> >> THis is BS,  I don=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=
=A2=E2=80=9E=C2=A2t give a shit about politics...

> >> I do care that we are being used for this political experimen=
t.

> >

> >

> > 100%

> >

> >

> >> The economy should have NEVER been shut down.

> >

> >

> > A strong economy is our leading weapon to fight the disease.

> >

> >

> >> It=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s lau=
ghable that all the markets and stores that are open

> > are crowded and no one has stopped shopping.

> >>

> >> Maybe they should try putting the voter machines in Target or=
Walmart.....

> >> Then we could vote out these morons that crashed our economy =
when the

> > answer--===============1452556427==
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I'm too lazy to look it up too, but if pt comes in with or develops acute i=
schemic stroke and we fill out a criteria for TPA, I'm almost certain if pt=
was started already started on heparin it would then exclude TPA=C2=A0 fro=
m being ordered because of hemorrhage risk=C2=A0


-----Original Message-----
From: Ruben Safir
To: Carolinedliny
Cc: ruben-at-mrbrklyn.com
Sent: Fri, May 1, 2020 2:24 am
Subject: Re: good thing they are rushing (the vaccines)

On Fri, May 01, 2020 at 03:42:06AM +0000, Carolinedliny wrote:
> they are using prophylatic heparin drips, wouldn't criteria for steptokin=
ase exclude its use once a pt is started on Heparin drip?=C2=A0


Heparin doesn't break clots.=C2=A0 That is why we call things like TPa clot
busters.=C2=A0 They actually block fibrinogin to break down the cloats... I
think.=C2=A0 I know I am correct about the clot reabsortion, but I forget t=
he=20
exact mechanism and I am too lazy to look it up.

Mechanism of heparin action.
Jackson CM.
Abstract

Heparin catalysis of clotting proteinase inactivation occurs most
efficiently through the reaction of the proteinase with the
antithrombin-heparin complex. The efficiency of a heparin molecule in
this reaction depends on the presence of a specific pentasaccharide
sequence in it, and its molecular weight. The mechanism by which such
high affinity heparin acts when antithrombin III is the inhibitor is
promotion of the formation of an intermediate
proteinase-heparin-antithrombin complex. Heparin promotion of thrombin
inactivation by heparin cofactor II may occur by a similar mechanism.
The requirement for a specific oligosaccharide sequence within the
heparin molecule does not, however, exist for heparin cofactor II.
Binding of heparin to both thrombin and antithrombin III interferes with
thrombin inactivation. This binding is very dependent on the ionic
strength of the reaction mixture and may explain some of the discordant
results and interpretations from early studies on the mechanism of
heparin action. Low ionic strength in in vitro reactions also results in
cleavage of antithrombin III by thrombin in the presence of heparin and
effectively converts antithrombin III from an inhibitor to a substrate.

And TPa

The biology of tPA in the fibrinolytic system

Blood clots are formed from the aggregation of activated platelets onto
fibrin meshes. The breakdown of the fibrin meshes is achieved by
plasmin, a broad spectrum protease found in the blood as an inactive
zymogen, plasminogen. Plasmin cleaves fibrin thus breaking down the
meshwork of the clot, and it is extremely short lived; it is quickly
inactivated by =CE=B12-antiplasmin, an abundant inhibitor that restricts th=
e
action of plasmin to the vicinity of the clot (reviewed in [2] and [3]).
Successful fibrinolysis is achieved by adequate generation of plasmin
from plasminogen by one of two Plasminogen Activators (PAs), the
tissue-type Plasminogen Activator (tPA) and the urokinase-type
Plasminogen Activator (uPA). The two are thought to have redundant
functions in the fibrinolytic system, since genetic deletion of either
one is not accompanied by major fibrinolytic defects, and only tPA/uPA
doubly deficient mice display phenotypes similar to plasminogen
deficient ones [4, 5]. As opposed to uPA, the activity of tPA is itself
regulated by binding to fibrin, which increases its catalytic efficiency
[6, 7]. Thus, the formation of the clot initiates, with the generation
of fibrin, the fibrinolytic/ clot dissolving cascade. The catalytic
activity of tPA in the bloodstream is terminated with the binding of (a)
protein inhibitor(s), primarily the Plasminogen Activator Inhibitor 1
(PAI 1) [8]. The inactive PAI 1-bound tPA is cleared from the
circulation by the liver via a scavenger receptor, the LDL Receptor
Related Protein 1 (LRP1) [9]. LRP1 also binds catalytically active tPA,
but with lower affinity [10]. A neuronal-specific inhibitor of tPA,
neuroserpin, is the primary modifier of tPA activity in the nervous
system [11, 12]. Inhibited tPA-neuroserpin complexes are internalized by
LRP1, similarly to tPA-PAI 1 complexes [13]. The half-life of tPA in the
bloodstream is rather short, 5-10 minutes in humans, as a result of
PAI-1-mediated inhibition and LRP1-mediated liver uptake [14].
Carbohydrate side chains added to the backbone of tPA protein also play
important roles in the clearance of tPA from the bloodstream and forms
of tPA with longer half lives have been generated by mutating the
glycosylation sites of tPA (reviewed in [15]).

tPA is a secreted serine protease consisting of a single polypeptide
chain with 3 or 4 glycosylation sites and numerous disulfide bonds in
its secondary structure [16, 17]. The action of plasmin cleaves tPA into
an N-terminal light chain and a C-terminal heavy chain still held
together by disulfide bonds [18]. Two-chain tPA has higher catalytic
efficiency compared to the single chain form and is essentially
constitutively fully active, contrary to the single chain form which
only becomes fully active upon binding to fibrin [19]. The catalytic
domain of tPA lies towards its C-terminal end and comprises the light
chain of the protease [20, 21]. The protein also contains the following
domains: an N-terminal fibronectin type III finger domain, an epidermal
growth factor-like domain and two kringle domains [16, 22]. Plasminogen
binds to the second tPA kringle domain and fibrin binds to the finger
domain and the second kringle domain. Finally, inhibition by PAI 1 is
achieved by covalent binding of PAI 1 to the catalytic domain and the
formation of a complex [21]. The presence of the additional domains
beyond the catalytic one not only allows for regulation of the catalytic
function, but also suggests hitherto unknown interactions and
potentially functions. Indeed, both fibronectin finger and growth factor
domains are known modalities involved in protein-protein interactions.
Go to:
tPA as a thrombolytic in stroke

The use of tPA in ischemic stroke has been the subject of numerous
recent reviews, so that only key concepts are being mentioned here and
the interested reader is referred to such reviews for more information
[23, 24, 25, 26, 27, 28].

Recombinant human tPA produced in mammalian cell lines was introduced as
a thrombolytic agent in selected cases of stroke following the results
of the National Institute of Neurological Diseases and Stroke (NINDS)
study in 1995 [29]. This study consisted of two independently powered
trials that both showed clinical benefit from the use of tPA. A European
study conducted around the same time also showed clinical improvement,
albeit more modest, and the use of tPA was not recommended, for fear
that eligible patients could not be easily identified [30]. A second
European and Australian study showed no benefit from tPA [31], a fact
which delayed the use of the protease in Europe until 2002 when a
license was granted, provided that an observational safety study was
conducted to assess the safety profile of tPA in routine clinical
practice. The results of this study were recently published and
confirmed the positive effect of tPA [32], thus further relieving
reservations concerning its use as a thrombolytic in stroke. However,
tPA is still used only in a small number of ischemic stroke cases (3-8%,
[33]), but this percentage greatly increases in specialized stroke
centers [28].

The rationale behind the use of tPA in ischemic stroke is that by
breaking down the clot, recanalization of the occluded blood vessel
occurs. The restoration of blood vessel patency is meaningful, however,
only if the brain tissue of the ischemic area is still viable.
Unfortunately, brain tissue is metabolically very active and thus very
sensitive to ischemia. The core of the area serviced by the occluded
vessel becomes necrotic very quickly, whereas the periphery, which
receives some perfusion by adjacent non-ischemic regions, is still
salvageable within a reasonable time frame of a few hours, and is
referred to as the penumbra. Thrombolysis by tPA resulting in successful
recanalization potentially saves this ischemic but still viable
penumbra, but it has to be administered quickly. The positive effect of
tPA was clearly demonstrated in the two trials of the NINDS study [29],
in which the cut-off time from symptoms onset to initiation of
thrombolysis was set at three hours. The effect was more moderate in the
ECASS study (30), where treatment was initiated within 6h from stroke
onset, but clearer in the subgroup of ECASS patients treated within the
first three hours [34]. Along the same lines tPA showed moderate benefit
upon administration between 3 and 5 hours from stroke onset [35]. To
date the initial recommendation remains that tPA should be administered
within three hours from stroke onset [29, 36, 32]. This is a narrow time
window since the patient needs to be transferred to the health care
unit, and at minimum a CT scan has to be performed, primarily to exclude
the possibility of hemorrhage and to assess the size of the infarction.
Since potentially positive effects have also been reported with
administration of tPA between 3 and 5 hours from stroke onset [35, 36],
clinical trials are under way to further extend the time window for tPA
thrombolysis [37, 38].

Time is not the only parameter to be taken into account in the decision
to initiate tPA thrombolysis; novel imaging technologies may aid in the
identification of thrombolysis candidates at late time points.
Diffusion-weighted and perfusion-weighted MRIs are being employed to
identify patients with large diffusion-perfusion mismatches [39, 40],
i.e. patients with significant brain areas that still receive some
oxygen and nutrients from adjacent non-ischemic areas by diffusion,
although they do not receive any blood flow directly. These patients are
predicted to benefit the most from recanalization which would restore
blood flow to viable, salvageable tissue even after a relatively long
time from stroke onset [40]. Perfusion CTs (PCT) and CT angiography
source image (CTA-SI) analysis are CT modalities that could substitute
for MRIs in cases where an MRI is contraindicated or not available [41].
However, it should be noted that the usefulness of imaging techniques in
detecting thrombolysis candidates at late time points after stroke onset
has not yet been unequivocally proven. The results of the DEFUSE study
[40, 42] are expected to shed light on this issue.

The need for strict criteria and time-consuming diagnostic procedures
prior to the administration of tPA results from the adverse side-effects
of tPA, most notably that of intracerebral hemorrhagic conversion [43],
even though such conversion occurs only in 6-7% of patients. This is
considered a result of systemic plasminemia/fibrinolytic activation,
i.e. the tipping of the coagulation/fibrinolysis balance towards the
latter side in the systemic circulation which is thought to disrupt
microscopic plugs that physiologically prevent hemorrhages at
transiently injured spots on vessel walls [43, 44]. Although this lytic
state can manifest itself as hemorrhage in different organs,
intracranial hemorrhage is the most dramatic manifestation and can
complicate thrombolysis taking place in the body, such as during
myocardial infarction where brain vasculature is otherwise healthy,
although not necessarily. However, it is much more common in ischemic
stroke, because brain vasculature and the Blood Brain Barrier (BBB) are
already compromised from the ischemia. In general, the greater the
severity of the ischemia and the longer the time from stroke onset, the
higher the likelihood of hemorrhage ensuing when recanalization of the
occluded vessel occurs in the course of thrombolysis [30]. Moreover, tPA
may also directly damage the cerebrovascular endothelium and disrupt the
BBB, as suggested by animal studies discussed below although evidence
from human trials is lacking.

One important issue in the use of tPA in stroke thrombolysis is whether
efficient and permanent recanalization of the occluded vessel occurs.
This may be the case with as little as 10% to 25% of cases [45], as tPA
only works on the surface of the clot. Therefore larger size clots would
take a long time to break down. Moreover, tPA is rapidly removed from
the systemic circulation and its thrombolytic effect is quickly lost
after termination of its IV infusion. This short half-life results in
inability to act on subsequent and continued vessel occlusions that
occur both in bigger and smaller blood vessels. Attempts at increasing
the dose are hampered by increased incidence of hemorrhagic
complications and a potential solution would be to alter the tPA
protein, so that favorable properties (such as fibrin specificity) are
maintained or enhanced and undesirable ones (such as short half life)
are modified or abolished. Mutant forms of tPA exhibiting longer half
lives and increased fibrin specificity have been generated and their
specific mutations and properties have recently been reviewed elsewhere
[15]. Although these tPA mutants have been evaluated as thrombolytics
for myocardial infarctions, their use for ischemic stroke is still under
investigation [46, 47, 48, 49]. Another solution would be to locally
deliver tPA via an arterial catheter in the vicinity of the clot (an
approach that seems to extend the therapeutic window) rather than
intravenously, so that higher local concentrations and hence higher
fibrinolytic efficiency are achieved. Unfortunately, it appears that
systemic plasminemia and the risk of intracranial hemorrhage are not
avoided this way [50]. This method of intra-arterial tPA administration
has been used in combination with the intravenous infusion and is
referred to as bridging therapy [45, 51]. Its disadvantages are that it
can only be used in large artery occlusions, and that it is more
interventional, thus requiring more specialized personnel and equipment
for its successful implementation. The appearance of specialized stroke
units circumvents this problem, although the cost remains considerable.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3824365/


>=20
> -----Original Message-----
> From: Ruben Safir
> To: Carolinedliny ; docs-at-mrbrklyn.com; Hangout ngout-at-nylxs.com>
> Sent: Wed, Apr 29, 2020 10:58 am
> Subject: Re: good thing they are rushing (the vaccines)
>=20
> On 4/29/20 9:59 AM, Carolinedliny wrote:
> > I don't know that everything here is accurate, I talk to my colleagues
> > in the ICU and they tell me they are putting pts on heparin drips, they
> > are using 100% oxygen, and/or high flow o2=C2=A0 in an attempt to preve=
nt
> > hypoxia/desat without using mechanical ventilation
> >=20
>=20
> I'm not certain that these two things are inconsistant.=C2=A0 First of al=
l,
> Heparin is not a Thrombolytic, so it is nto going to break clots down,
> but prevents growth of new clots.=C2=A0 That would be consitant with what
> Keren is saying.=C2=A0 However, real clot busters, for pulmonary embolism=
,
> streptokinase and friends, are they being used at all.=C2=A0 The granular=
ity
> is being SEEN on the xrays.
>=20
> Regardless, why are shut down?=C2=A0 My college at St Barnabas has been
> begrudging this from the beginning, rightfully so, and he is at ground
> zero of this virus in the Bronx.
>=20
>=20
> >=20
> > -----Original Message-----
> > From: Ruben Safir
> > To: Karen Perilman ; Hangout ; Li=
z
> > Moore
> > Sent: Wed, Apr 29, 2020 2:53 am
> > Subject: Re: good thing they are rushing (the vaccines)
> >=20
> >=20
> > One more thing... the women who some might think uses capital letters i=
s
> > a Nurse Anesthesiaologist who spent good part of her life working with
> > Doctors without Boarders...=C2=A0 threating patients and populations in=
Africa.
> >=20
> > Karen, meet, Rick.=C2=A0 Rick, meet Karen.
> >=20
> > ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
> > Side note to Liz -
> > I've been told today that Pharmacists aren't experts on vaccinations so
> > our opinion doesn't hold much weight....
> >=20
> > Just for reference, I point out the paper that Liz and I wrong on
> > http://www.brooklyn-living.com/
> >=20
> > to continue on this thread...
> >=20
> > On to Karen...
> >=20
> > On 4/28/20 8:09 PM, Karen Perilman wrote:
> >> =C3=83=C2=AF=C3=82=C2=BB=C3=82=C2=BF
> >> =C3=83=C2=AF=C3=82=C2=BB=C3=82=C2=BFRuben,
> >> It=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s been a long =
time since we spoke,
> >=20
> > That is your fault!=C2=A0 I periodically send you email :)
> >=20
> >> And I must tell you, this message you sent came as a surprise,
> >=20
> > Call me when you have time 718-715-1771
> >=20
> >>
> >> First of all, the patients that were first largely infected in Europe,
> > Italy and Spain were knee jerk treated with intubation and ventilation.
> >> I say knee jerk, because never before had they seen so many people
> > with the same symptoms in mass like this.
> >>
> >> Never mind the Chinese allowed 5 million INFECTED people to leave
> > China up to Jan 20th and go to work in Italy and Spain, the fashion cen=
ter.
> >> How do i know, because my daughter is the head senior designer for
> > women in Spain for the company Zara.=C2=A0 They have so many Chinese wo=
rking
> > there, and their industry is in the HUB of China.
> >>
> >> And in October 18-19th the International militaries all met in Wuhan
> > for the WUhan games for 100 COUNTRIES.=C2=A0 ANd when the games were ov=
er,
> > all those 100 countries became infected.....=C2=A0
> >>
> >> Now, go back to where we were....
> >> All these people presenting with Shortness of breath we MISDIAGNOSED
> > FROM THE GET GO.
> >> WHy do I say this, because maybe you forgot I am an anesthetist.
> >=20
> >=20
> > I haven't forgotten anything.=C2=A0 Are you in New York now?
> >=20
> >> The presentation of SOB was way off the standards of evaluation for SO=
B.
> >> The Corona is a virus that spread thru droplets as does EVERY OTHER VI=
RUS.
> >> But we never reacted like this before.
> >=20
> > I say this until I am blue in the face.=C2=A0 We have NEVER reacted lik=
e this
> > to even Small Pox!!
> >=20
> >=20
> >> Here is why we shouldn=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=
=C2=A2t have.
> >> I spoke with the head oncologist at a NY Cancer hospital....
> >> I also spoke with the head neurologist at Northwell Hospitals and all
> > of us said the same thing.
> >>
> >=20
> > We've been working with St Barbaus and they just said the same thing in
> > the NY Post today,,
> >=20
> >> The SOB from Corona patients was unlike a person with pneumonia or ARD=
S.
> >> Patients were talking and even on the phones, and showing low Puse OX
> > readings.
> >> In Italy they didn=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=
=A2t have the time to asses as they were
> > barraged with patients,
> >> They ran out of ventilators when that was ACTUALLY what was killing
> > people.
> >> Sick lungs under PEEP and ventilation only causes more problems and
> > patients vaso constrict and organs shut down,=C2=A0 and FAST, especiall=
y in
> > the elderly.
> >=20
> > This I didn't know and I don't understand.=C2=A0 The ICU is packed in t=
he
> > Bronx with people on vents undergoing ID evaluation.=C2=A0 In the end, =
there
> > is not much I can do for them other than take the states and track
> > infection.=C2=A0 Infection contol on the floors is the biggest problem =
we have.
> >=20
> >>
> >> But in the US, NO ONE took the time to look at the reason people were
> > SOB and they ASSUMED it was a viral infection, Corona.....
> >>
> >> BIG MISTAKE!
> >> Now, looking back, we know now, that after autopsies, the patients
> > lungs and bodies were filled with CLOTS!!!=C2=A0
> >=20
> > Bilateral Granularity on the Xrays.=C2=A0 We don't even need testing fo=
r
> > this.=C2=A0 It is a presumptive diagnosis already.
> >=20
> > The patients were actually acting like someone with pulmonary embolism.
> > The clots killed people with heart attacks and Strokes!!!!
> >>
> >> So where did this information take the doctors who were in the know.
> >> In NY and the UK, they started realizing that the patients who were on
> > blood thinners and anti inflammatories had NO clots and they were mildl=
y
> > sick and got better.
> >=20
> >> Those patients, in particular were Cancer patients who as you know are
> > compromised immunologically.
> >>
> >=20
> > I have data clearly showing me that pts on Chemo and with advanced
> > cancer don't survive this.=C2=A0 They won't even ventolate those patien=
ts at
> > this point.=C2=A0 So please explain this further.
> >=20
> > BTW - the virus attacks clotting factors, and causes prolong PT times,
> > but frankly, that is common with cytosine storms, so I am not convinced
> > of that data.
> >=20
> >> They tested the patients clotting times and saw the proof in the blood=
.
> >> Waiting for a vaccine to kill a virus that will be obsolete in a year
> > is ridiculous when we know how to treat the patients NOW.
> >>
> >> If someone presents to the ER with SOB, they should have been assessed
> > to rule out for=C2=A0 clots.
> >>
> >> A retro study, and a study that moves forward should be done immediate=
ly,
> >> BUT because the cure for the clots is CHEAP, no one is going to
> > recommend ASPIRIN or Azithromycin because they won=C3=83=C2=A2=C3=A2=E2=
=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2t be able to
> > make MONEY.
> >>
> >=20
> > This has been a recurring problem.=C2=A0 It is almost like they are pur=
posely
> > misusing Hydroxychloroquin, which can only work in the early phase of
> > the disease, in order to make way for other thearpies, and those
> > therapies, Remdesivir, Kaletra, Nitazoxanide, Tocilizumab, etc.=C2=A0 A=
ll of
> > them cost over $2K per treatment.=C2=A0 My friend Maya, who is a PharmD=
, she
> > was big on this point. They are not acting in a way that is consistant
> > with a disease that shuts down civilization.=C2=A0 They are telling us =
we are
> > in moral danger and the numbers don't bare it out and they aren't actin=
g
> > like it is that serious.
> >=20
> >> The mayor NY and the governor are 100% assholes.
> >> We have NEVER quarantined in the history of illness HEALTHY PEOPLE!!
> >> Sick people yes, and they should be isolated at home.
> >=20
> > It is unbelievable.=C2=A0 Never in my lifetime could I have ever imagin=
ed this.
> >=20
> >=20
> >> If you go to any NY hospital now in the city,=C2=A0 if you show ANY si=
gns
> > of SOB you are intubated and you DIE!!!!=C2=A0 They do not resuscitate =
anyone
> > suspected of corona!!
> >> That=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s insane....=
. If the reason people are dying are the
> > clots, they NO ONE should be intubated and they should emergently be
> > give blood thinners.
> >>
> >> The elderly are being treated like disposable spoilers of this virus.=
=C2=A0
> > They die alone and it=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=
=C2=A2s criminal.
> >>
> >=20
> > How do you then prevent an anurism..
> >=20
> >=20
> >> I will not fall for the BS of waiting for a vaccine, because patients
> > being treated right now with the new paradigm are surviving and getting
> > better quicker.
> >>
> >> No patient population compares to the cancer patients who were found
> > to be Safe from the extreme sickness of Corona because so many of their
> > patients were on blood thinners.=C2=A0
> >> The evidence is there.
> >> Even the Young patients that died, died from Strokes.!!!
> >> No one is talking about the patients that contracted corona who were
> > described as =C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=85=E2=80=9Chealthy=C3=
=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=82=EF=BF=BD who SMOKE; it is a joke.=C2=
=A0 Smokers are
> > NOT healthy, not if they smoke anything,=C2=A0 pot, vaping or cigarette=
s.
> >> I see people on the streets with masks and gloves SMOKING and
> > it=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s a joke.
> >> THey are blowing Corona and adding to the contaminating of all of us.
> >> I see people wearing masks and gloves throwing them in the streets,
> > not using them properly, and I tell them, will all this costuming, they
> > would never be allowed in the ICU to work because they have no idea how
> > to used sterile masks and gloves.
> >>
> >> If you want to be mad, get mad with the medical system in NY fueled by
> > political idiots that want to see the economy fail, so they can blame
> > politics.
> >> Even Fauci, that =C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=85=E2=80=9CStati=
stician=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=82=EF=BF=BD is out of the loop.=
=C2=A0 He
> > hasn=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2t practiced m=
edicine in 20 yrs!!=C2=A0 And he is nothing but an
> > accountant for the numbers that other people give him.
> >>
> >> THis is BS,=C2=A0 I don=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=
=9E=C2=A2t give a shit about politics...
> >> I do care that we are being used for this political experiment.
> >=20
> >=20
> > 100%
> >=20
> >=20
> >> The economy should have NEVER been shut down.
> >=20
> >=20
> > A strong economy is our leading weapon to fight the disease.
> >=20
> >=20
> >> It=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s laughable th=
at all the markets and stores that are open
> > are crowded and no one has stopped shopping.
> >>
> >> Maybe they should try putting the voter machines in Target or Walmart.=
....
> >> Then we could vote out these morons that crashed our economy when the
> > answer to save people was right under our noses.
> >>
> >>
> >>
> >>
> >> Sent from my iPad
> >>
> >>> On Apr 28, 2020, at 5:46 PM, Ruben Safir > > > wrote:
> >>>
> >>> =C3=83=C2=AF=C3=82=C2=BB=C3=82=C2=BF
> >>> We wouldn't want to distribute anything until we are absolutely sure =
it
> >>> is safe, because WTF!!=C2=A0 11K are already dead in NYC alone and 23=
million
> >>> are on indefinite lockdown!
> >>>
> >>> Take your time boys.=C2=A0 Make sure you get it right..
> >>>
> >>>
> >>> ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~=
~
> >>> Wall Street Journal today:
> >>>
> >>> Pfizer could start distributing a possible vaccine on an emergency ba=
sis
> >>> in the fall if all testing proves successful.
> >>> Photo: Sipa USA via AP
> >>> By Jared S. Hopkins
> >>> April 28, 2020 1:14 pm ET
> >>>
> >>> Pfizer Inc. PFE -1.10% said Tuesday it could have a coronavirus vacci=
ne
> >>> ready for use on an emergency basis in the fall if it proves to work
> >>> safely in testing.
> >>>
> >>> Testing of the vaccine, which has already started in Germany, could
> >>> start in the U.S. as early as next week if health regulators sign off=
,
> >>> Pfizer Chief Executive Albert Bourla said in an interview. Results fr=
om
> >>> the study could come as early as next month, Mr. Bourla said.
> >>>
> >>> Pfizer would need to do more testing to make sure the vaccine works
> >>> safely. If all testing proves successful, Pfizer could start
> >>> distributing the vaccine on an emergency basis in the fall and receiv=
e
> >>> approval for widespread distribution by year=C3=83=C2=A2=C3=A2=E2=80=
=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s end, Mr. Bourla
> > said.
> >>>
> >>> =C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=85=E2=80=9CThis is a crisis righ=
t now, and a solution is desperately
> > needed by
> >>> all,=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=82=EF=BF=BD Mr. Bourla said.
> >>> --
> >>> So many immigrant groups have swept through our town
> >>> that Brooklyn, like Atlantis, reaches mythological
> >>> proportions in the mind of the world - RI Safir 1998
> >>> http://www.mrbrklyn.com
> >>> DRM is THEFT - We are the STAKEHOLDERS - RI Safir 2002
> >>>
> >>> http://www.nylxs.com - Leadership Development
> > in Free Software
> >>> http://www.brooklyn-living.com
> >>>
> >>> Being so tracked is for FARM ANIMALS and extermination camps,
> >>> but incompatible with living as a free human being. -RI Safir 2013
> >=20
> >=20
> > --=20
> > So many immigrant groups have swept through our town
> > that Brooklyn, like Atlantis, reaches mythological
> > proportions in the mind of the world - RI Safir 1998
> > http://www.mrbrklyn.com
> > DRM is THEFT - We are the STAKEHOLDERS - RI Safir 2002
> >=20
> > http://www.nylxs.com - Leadership Development in
> > Free Software
> > http://www.brooklyn-living.com
> >=20
> > Being so tracked is for FARM ANIMALS and extermination camps,
> > but incompatible with living as a free human being. -RI Safir 2013
>=20
>=20
> --=20
> So many immigrant groups have swept through our town
> that Brooklyn, like Atlantis, reaches mythological
> proportions in the mind of the world - RI Safir 1998
> http://www.mrbrklyn.com
> DRM is THEFT - We are the STAKEHOLDERS - RI Safir 2002
>=20
> http://www.nylxs.com - Leadership Development in Free Software
> http://www.brooklyn-living.com
>=20
> Being so tracked is for FARM ANIMALS and extermination camps,
> but incompatible with living as a free human being. -RI Safir 2013

--=20
So many immigrant groups have swept through our town
that Brooklyn, like Atlantis, reaches mythological
proportions in the mind of the world - RI Safir 1998
http://www.mrbrklyn.com=20

DRM is THEFT - We are the STAKEHOLDERS - RI Safir 2002
http://www.nylxs.com - Leadership Development in Free Software
http://www2.mrbrklyn.com/resources - Unpublished Archive=20
http://www.coinhangout.com - coins!
http://www.brooklyn-living.com=20

Being so tracked is for FARM ANIMALS and extermination camps,=20
but incompatible with living as a free human being. -RI Safir 2013


------=_Part_434999_98040565.1588374567840
Content-Type: text/html; charset=UTF-8
Content-Transfer-Encoding: quoted-printable

I'm too lazy to look it up too=
, but if pt comes in with or develops acute ischemic stroke and we fill out=
a criteria for TPA, I'm almost certain if pt was started already started o=
n heparin it would then exclude TPA  from being ordered because of hem=
orrhage risk 

-----=
Original Message-----

From: Ruben Safir <ruben-at-mrbrklyn.com>

To: Carolinedliny <carolinedliny-at-aol.com>

Cc: ruben-at-mrbrklyn.com <ruben-at-mrbrklyn.com>

Sent: Fri, May 1, 2020 2:24 am

Subject: Re: good thing they are rushing (the vaccines)



On Fri, May 01, 2020 at 03:42:06AM +0000, Carolinedliny wrote:

> they are using prophylatic heparin drips, wouldn't criteria for stepto=
kinase exclude its use once a pt is started on Heparin drip? 





Heparin doesn't break clots.  That is why we call things like TPa clot=


busters.  They actually block fibrinogin to break down the cloats... I=


think.  I know I am correct about the clot reabsortion, but I forget t=
he

exact mechanism and I am too lazy to look it up.



Mechanism of heparin action.

Jackson CM.

Abstract



Heparin catalysis of clotting proteinase inactivation occurs most

efficiently through the reaction of the proteinase with the

antithrombin-heparin complex. The efficiency of a heparin molecule in

this reaction depends on the presence of a specific pentasaccharide

sequence in it, and its molecular weight. The mechanism by which such

high affinity heparin acts when antithrombin III is the inhibitor is

promotion of the formation of an intermediate

proteinase-heparin-antithrombin complex. Heparin promotion of thrombin

inactivation by heparin cofactor II may occur by a similar mechanism.

The requirement for a specific oligosaccharide sequence within the

heparin molecule does not, however, exist for heparin cofactor II.

Binding of heparin to both thrombin and antithrombin III interferes with>
thrombin inactivation. This binding is very dependent on the ionic

strength of the reaction mixture and may explain some of the discordant

results and interpretations from early studies on the mechanism of

heparin action. Low ionic strength in in vitro reactions also results in>
cleavage of antithrombin III by thrombin in the presence of heparin and

effectively converts antithrombin III from an inhibitor to a substrate.



And TPa



The biology of tPA in the fibrinolytic system



Blood clots are formed from the aggregation of activated platelets onto

fibrin meshes. The breakdown of the fibrin meshes is achieved by

plasmin, a broad spectrum protease found in the blood as an inactive

zymogen, plasminogen. Plasmin cleaves fibrin thus breaking down the

meshwork of the clot, and it is extremely short lived; it is quickly

inactivated by =CE=B12-antiplasmin, an abundant inhibitor that restricts th=
e

action of plasmin to the vicinity of the clot (reviewed in [2] and [3]).>
Successful fibrinolysis is achieved by adequate generation of plasmin

from plasminogen by one of two Plasminogen Activators (PAs), the

tissue-type Plasminogen Activator (tPA) and the urokinase-type

Plasminogen Activator (uPA). The two are thought to have redundant

functions in the fibrinolytic system, since genetic deletion of either

one is not accompanied by major fibrinolytic defects, and only tPA/uPA

doubly deficient mice display phenotypes similar to plasminogen

deficient ones [4, 5]. As opposed to uPA, the activity of tPA is itself

regulated by binding to fibrin, which increases its catalytic efficiency>
[6, 7]. Thus, the formation of the clot initiates, with the generation

of fibrin, the fibrinolytic/ clot dissolving cascade. The catalytic

activity of tPA in the bloodstream is terminated with the binding of (a)>
protein inhibitor(s), primarily the Plasminogen Activator Inhibitor 1

(PAI 1) [8]. The inactive PAI 1-bound tPA is cleared from the

circulation by the liver via a scavenger receptor, the LDL Receptor

Related Protein 1 (LRP1) [9]. LRP1 also binds catalytically active tPA,

but with lower affinity [10]. A neuronal-specific inhibitor of tPA,

neuroserpin, is the primary modifier of tPA activity in the nervous

system [11, 12]. Inhibited tPA-neuroserpin complexes are internalized by>
LRP1, similarly to tPA-PAI 1 complexes [13]. The half-life of tPA in the>
bloodstream is rather short, 5-10 minutes in humans, as a result of

PAI-1-mediated inhibition and LRP1-mediated liver uptake [14].

Carbohydrate side chains added to the backbone of tPA protein also play

important roles in the clearance of tPA from the bloodstream and forms

of tPA with longer half lives have been generated by mutating the

glycosylation sites of tPA (reviewed in [15]).



tPA is a secreted serine protease consisting of a single polypeptide

chain with 3 or 4 glycosylation sites and numerous disulfide bonds in

its secondary structure [16, 17]. The action of plasmin cleaves tPA into>
an N-terminal light chain and a C-terminal heavy chain still held

together by disulfide bonds [18]. Two-chain tPA has higher catalytic

efficiency compared to the single chain form and is essentially

constitutively fully active, contrary to the single chain form which

only becomes fully active upon binding to fibrin [19]. The catalytic

domain of tPA lies towards its C-terminal end and comprises the light

chain of the protease [20, 21]. The protein also contains the following

domains: an N-terminal fibronectin type III finger domain, an epidermal

growth factor-like domain and two kringle domains [16, 22]. Plasminogen

binds to the second tPA kringle domain and fibrin binds to the finger

domain and the second kringle domain. Finally, inhibition by PAI 1 is

achieved by covalent binding of PAI 1 to the catalytic domain and the

formation of a complex [21]. The presence of the additional domains

beyond the catalytic one not only allows for regulation of the catalytic>
function, but also suggests hitherto unknown interactions and

potentially functions. Indeed, both fibronectin finger and growth factor>
domains are known modalities involved in protein-protein interactions.

Go to:

tPA as a thrombolytic in stroke



The use of tPA in ischemic stroke has been the subject of numerous

recent reviews, so that only key concepts are being mentioned here and

the interested reader is referred to such reviews for more information

[23, 24, 25, 26, 27, 28].



Recombinant human tPA produced in mammalian cell lines was introduced as>
a thrombolytic agent in selected cases of stroke following the results

of the National Institute of Neurological Diseases and Stroke (NINDS)

study in 1995 [29]. This study consisted of two independently powered

trials that both showed clinical benefit from the use of tPA. A European>
study conducted around the same time also showed clinical improvement,

albeit more modest, and the use of tPA was not recommended, for fear

that eligible patients could not be easily identified [30]. A second

European and Australian study showed no benefit from tPA [31], a fact

which delayed the use of the protease in Europe until 2002 when a

license was granted, provided that an observational safety study was

conducted to assess the safety profile of tPA in routine clinical

practice. The results of this study were recently published and

confirmed the positive effect of tPA [32], thus further relieving

reservations concerning its use as a thrombolytic in stroke. However,

tPA is still used only in a small number of ischemic stroke cases (3-8%,>
[33]), but this percentage greatly increases in specialized stroke

centers [28].



The rationale behind the use of tPA in ischemic stroke is that by

breaking down the clot, recanalization of the occluded blood vessel

occurs. The restoration of blood vessel patency is meaningful, however,

only if the brain tissue of the ischemic area is still viable.

Unfortunately, brain tissue is metabolically very active and thus very

sensitive to ischemia. The core of the area serviced by the occluded

vessel becomes necrotic very quickly, whereas the periphery, which

receives some perfusion by adjacent non-ischemic regions, is still

salvageable within a reasonable time frame of a few hours, and is

referred to as the penumbra. Thrombolysis by tPA resulting in successful>
recanalization potentially saves this ischemic but still viable

penumbra, but it has to be administered quickly. The positive effect of

tPA was clearly demonstrated in the two trials of the NINDS study [29],

in which the cut-off time from symptoms onset to initiation of

thrombolysis was set at three hours. The effect was more moderate in the>
ECASS study (30), where treatment was initiated within 6h from stroke

onset, but clearer in the subgroup of ECASS patients treated within the

first three hours [34]. Along the same lines tPA showed moderate benefit>
upon administration between 3 and 5 hours from stroke onset [35]. To

date the initial recommendation remains that tPA should be administered

within three hours from stroke onset [29, 36, 32]. This is a narrow time>
window since the patient needs to be transferred to the health care

unit, and at minimum a CT scan has to be performed, primarily to exclude>
the possibility of hemorrhage and to assess the size of the infarction.

Since potentially positive effects have also been reported with

administration of tPA between 3 and 5 hours from stroke onset [35, 36],

clinical trials are under way to further extend the time window for tPA

thrombolysis [37, 38].



Time is not the only parameter to be taken into account in the decision

to initiate tPA thrombolysis; novel imaging technologies may aid in the

identification of thrombolysis candidates at late time points.

Diffusion-weighted and perfusion-weighted MRIs are being employed to

identify patients with large diffusion-perfusion mismatches [39, 40],

i.e. patients with significant brain areas that still receive some

oxygen and nutrients from adjacent non-ischemic areas by diffusion,

although they do not receive any blood flow directly. These patients are>
predicted to benefit the most from recanalization which would restore

blood flow to viable, salvageable tissue even after a relatively long

time from stroke onset [40]. Perfusion CTs (PCT) and CT angiography

source image (CTA-SI) analysis are CT modalities that could substitute

for MRIs in cases where an MRI is contraindicated or not available [41].>
However, it should be noted that the usefulness of imaging techniques in>
detecting thrombolysis candidates at late time points after stroke onset>
has not yet been unequivocally proven. The results of the DEFUSE study

[40, 42] are expected to shed light on this issue.



The need for strict criteria and time-consuming diagnostic procedures

prior to the administration of tPA results from the adverse side-effects>
of tPA, most notably that of intracerebral hemorrhagic conversion [43],

even though such conversion occurs only in 6-7% of patients. This is

considered a result of systemic plasminemia/fibrinolytic activation,

i.e. the tipping of the coagulation/fibrinolysis balance towards the

latter side in the systemic circulation which is thought to disrupt

microscopic plugs that physiologically prevent hemorrhages at

transiently injured spots on vessel walls [43, 44]. Although this lytic

state can manifest itself as hemorrhage in different organs,

intracranial hemorrhage is the most dramatic manifestation and can

complicate thrombolysis taking place in the body, such as during

myocardial infarction where brain vasculature is otherwise healthy,

although not necessarily. However, it is much more common in ischemic

stroke, because brain vasculature and the Blood Brain Barrier (BBB) are

already compromised from the ischemia. In general, the greater the

severity of the ischemia and the longer the time from stroke onset, the

higher the likelihood of hemorrhage ensuing when recanalization of the

occluded vessel occurs in the course of thrombolysis [30]. Moreover, tPA>
may also directly damage the cerebrovascular endothelium and disrupt the>
BBB, as suggested by animal studies discussed below although evidence

from human trials is lacking.



One important issue in the use of tPA in stroke thrombolysis is whether

efficient and permanent recanalization of the occluded vessel occurs.

This may be the case with as little as 10% to 25% of cases [45], as tPA

only works on the surface of the clot. Therefore larger size clots would>
take a long time to break down. Moreover, tPA is rapidly removed from

the systemic circulation and its thrombolytic effect is quickly lost

after termination of its IV infusion. This short half-life results in

inability to act on subsequent and continued vessel occlusions that

occur both in bigger and smaller blood vessels. Attempts at increasing

the dose are hampered by increased incidence of hemorrhagic

complications and a potential solution would be to alter the tPA

protein, so that favorable properties (such as fibrin specificity) are

maintained or enhanced and undesirable ones (such as short half life)

are modified or abolished. Mutant forms of tPA exhibiting longer half

lives and increased fibrin specificity have been generated and their

specific mutations and properties have recently been reviewed elsewhere

[15]. Although these tPA mutants have been evaluated as thrombolytics

for myocardial infarctions, their use for ischemic stroke is still under>
investigation [46, 47, 48, 49]. Another solution would be to locally

deliver tPA via an arterial catheter in the vicinity of the clot (an

approach that seems to extend the therapeutic window) rather than

intravenously, so that higher local concentrations and hence higher

fibrinolytic efficiency are achieved. Unfortunately, it appears that

systemic plasminemia and the risk of intracranial hemorrhage are not

avoided this way [50]. This method of intra-arterial tPA administration

has been used in combination with the intravenous infusion and is

referred to as bridging therapy [45, 51]. Its disadvantages are that it

can only be used in large artery occlusions, and that it is more

interventional, thus requiring more specialized personnel and equipment

for its successful implementation. The appearance of specialized stroke

units circumvents this problem, although the cost remains considerable.



"_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3824365/





>

> -----Original Message-----

> From: Ruben Safir <"mailto:ruben-at-mrbrklyn.com">ruben-at-mrbrklyn.com>

> To: Carolinedliny <=3D"mailto:carolinedliny-at-aol.com">carolinedliny-at-aol.com>; =3D"mailto:docs-at-mrbrklyn.com" href=3D"mailto:docs-at-mrbrklyn.com">docs-at-mrbrkl=
yn.com; Hangout <lto:hangout-at-nylxs.com">hangout-at-nylxs.com>

> Sent: Wed, Apr 29, 2020 10:58 am

> Subject: Re: good thing they are rushing (the vaccines)

>

> On 4/29/20 9:59 AM, Carolinedliny wrote:

> > I don't know that everything here is accurate, I talk to my colle=
agues

> > in the ICU and they tell me they are putting pts on heparin drips=
, they

> > are using 100% oxygen, and/or high flow o2  in an attempt to=
prevent

> > hypoxia/desat without using mechanical ventilation

> >

>

> I'm not certain that these two things are inconsistant.  First of=
all,

> Heparin is not a Thrombolytic, so it is nto going to break clots down,=


> but prevents growth of new clots.  That would be consitant with w=
hat

> Keren is saying.  However, real clot busters, for pulmonary embol=
ism,

> streptokinase and friends, are they being used at all.  The granu=
larity

> is being SEEN on the xrays.

>

> Regardless, why are shut down?  My college at St Barnabas has bee=
n

> begrudging this from the beginning, rightfully so, and he is at ground=


> zero of this virus in the Bronx.

>

>

> >

> > -----Original Message-----

> > From: Ruben Safir <ef=3D"mailto:ruben-at-mrbrklyn.com">ruben-at-mrbrklyn.com>

> > To: Karen Perilman <ef=3D"mailto:kerens3ts-at-aol.com">kerens3ts-at-aol.com>; Hangout <mailto=3D"mailto:hangout-at-nylxs.com" href=3D"mailto:hangout-at-nylxs.com">hango=
ut-at-nylxs.com>; Liz

> > Moore <lto:lizmoorerph-at-gmail.com">lizmoorerph-at-gmail.com>

> > Sent: Wed, Apr 29, 2020 2:53 am

> > Subject: Re: good thing they are rushing (the vaccines)

> >

> >

> > One more thing... the women who some might think uses capital let=
ters is

> > a Nurse Anesthesiaologist who spent good part of her life working=
with

> > Doctors without Boarders...  threating patients and populati=
ons in Africa.

> >

> > Karen, meet, Rick.  Rick, meet Karen.

> >

> > ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~=
~

> > Side note to Liz -

> > I've been told today that Pharmacists aren't experts on vaccinati=
ons so

> > our opinion doesn't hold much weight....

> >

> > Just for reference, I point out the paper that Liz and I wrong on=


> > htt=
p://www.brooklyn-living.com/

> >

> > to continue on this thread...

> >

> > On to Karen...

> >

> > On 4/28/20 8:09 PM, Karen Perilman wrote:

> >> =C3=83=C2=AF=C3=82=C2=BB=C3=82=C2=BF

> >> =C3=83=C2=AF=C3=82=C2=BB=C3=82=C2=BFRuben,

> >> It=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s bee=
n a long time since we spoke,

> >

> > That is your fault!  I periodically send you email :)

> >

> >> And I must tell you, this message you sent came as a surprise=
,

> >

> > Call me when you have time 718-715-1771

> >

> >>

> >> First of all, the patients that were first largely infected i=
n Europe,

> > Italy and Spain were knee jerk treated with intubation and ventil=
ation.

> >> I say knee jerk, because never before had they seen so many p=
eople

> > with the same symptoms in mass like this.

> >>

> >> Never mind the Chinese allowed 5 million INFECTED people to l=
eave

> > China up to Jan 20th and go to work in Italy and Spain, the fashi=
on center.

> >> How do i know, because my daughter is the head senior designe=
r for

> > women in Spain for the company Zara.  They have so many Chin=
ese working

> > there, and their industry is in the HUB of China.

> >>

> >> And in October 18-19th the International militaries all met i=
n Wuhan

> > for the WUhan games for 100 COUNTRIES.  ANd when the games w=
ere over,

> > all those 100 countries became infected..... 

> >>

> >> Now, go back to where we were....

> >> All these people presenting with Shortness of breath we MISDI=
AGNOSED

> > FROM THE GET GO.

> >> WHy do I say this, because maybe you forgot I am an anestheti=
st.

> >

> >

> > I haven't forgotten anything.  Are you in New York now?

> >

> >> The presentation of SOB was way off the standards of evaluati=
on for SOB.

> >> The Corona is a virus that spread thru droplets as does EVERY=
OTHER VIRUS.

> >> But we never reacted like this before.

> >

> > I say this until I am blue in the face.  We have NEVER react=
ed like this

> > to even Small Pox!!

> >

> >

> >> Here is why we shouldn=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=
=E2=80=9E=C2=A2t have.

> >> I spoke with the head oncologist at a NY Cancer hospital....<=
br>
> >> I also spoke with the head neurologist at Northwell Hospitals=
and all

> > of us said the same thing.

> >>

> >

> > We've been working with St Barbaus and they just said the same th=
ing in

> > the NY Post today,,

> >

> >> The SOB from Corona patients was unlike a person with pneumon=
ia or ARDS.

> >> Patients were talking and even on the phones, and showing low=
Puse OX

> > readings.

> >> In Italy they didn=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=
=80=9E=C2=A2t have the time to asses as they were

> > barraged with patients,

> >> They ran out of ventilators when that was ACTUALLY what was k=
illing

> > people.

> >> Sick lungs under PEEP and ventilation only causes more proble=
ms and

> > patients vaso constrict and organs shut down,  and FAST, esp=
ecially in

> > the elderly.

> >

> > This I didn't know and I don't understand.  The ICU is packe=
d in the

> > Bronx with people on vents undergoing ID evaluation.  In the=
end, there

> > is not much I can do for them other than take the states and trac=
k

> > infection.  Infection contol on the floors is the biggest pr=
oblem we have.

> >

> >>

> >> But in the US, NO ONE took the time to look at the reason peo=
ple were

> > SOB and they ASSUMED it was a viral infection, Corona.....

> >>

> >> BIG MISTAKE!

> >> Now, looking back, we know now, that after autopsies, the pat=
ients

> > lungs and bodies were filled with CLOTS!!! 

> >

> > Bilateral Granularity on the Xrays.  We don't even need test=
ing for

> > this.  It is a presumptive diagnosis already.

> >

> > The patients were actually acting like someone with pulmonary emb=
olism.

> > The clots killed people with heart attacks and Strokes!!!!

> >>

> >> So where did this information take the doctors who were in th=
e know.

> >> In NY and the UK, they started realizing that the patients wh=
o were on

> > blood thinners and anti inflammatories had NO clots and they were=
mildly

> > sick and got better.

> >

> >> Those patients, in particular were Cancer patients who as you=
know are

> > compromised immunologically.

> >>

> >

> > I have data clearly showing me that pts on Chemo and with advance=
d

> > cancer don't survive this.  They won't even ventolate those =
patients at

> > this point.  So please explain this further.

> >

> > BTW - the virus attacks clotting factors, and causes prolong PT t=
imes,

> > but frankly, that is common with cytosine storms, so I am not con=
vinced

> > of that data.

> >

> >> They tested the patients clotting times and saw the proof in =
the blood.

> >> Waiting for a vaccine to kill a virus that will be obsolete i=
n a year

> > is ridiculous when we know how to treat the patients NOW.

> >>

> >> If someone presents to the ER with SOB, they should have been=
assessed

> > to rule out for  clots.

> >>

> >> A retro study, and a study that moves forward should be done =
immediately,

> >> BUT because the cure for the clots is CHEAP, no one is going =
to

> > recommend ASPIRIN or Azithromycin because they won=C3=83=C2=A2=C3=
=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2t be able to

> > make MONEY.

> >>

> >

> > This has been a recurring problem.  It is almost like they a=
re purposely

> > misusing Hydroxychloroquin, which can only work in the early phas=
e of

> > the disease, in order to make way for other thearpies, and those<=
br>
> > therapies, Remdesivir, Kaletra, Nitazoxanide, Tocilizumab, etc.&n=
bsp; All of

> > them cost over $2K per treatment.  My friend Maya, who is a =
PharmD, she

> > was big on this point. They are not acting in a way that is consi=
stant

> > with a disease that shuts down civilization.  They are telli=
ng us we are

> > in moral danger and the numbers don't bare it out and they aren't=
acting

> > like it is that serious.

> >

> >> The mayor NY and the governor are 100% assholes.

> >> We have NEVER quarantined in the history of illness HEALTHY P=
EOPLE!!

> >> Sick people yes, and they should be isolated at home.

> >

> > It is unbelievable.  Never in my lifetime could I have ever =
imagined this.

> >

> >

> >> If you go to any NY hospital now in the city,  if you sh=
ow ANY signs

> > of SOB you are intubated and you DIE!!!!  They do not resusc=
itate anyone

> > suspected of corona!!

> >> That=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s i=
nsane..... If the reason people are dying are the

> > clots, they NO ONE should be intubated and they should emergently=
be

> > give blood thinners.

> >>

> >> The elderly are being treated like disposable spoilers of thi=
s virus. 

> > They die alone and it=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=
=80=9E=C2=A2s criminal.

> >>

> >

> > How do you then prevent an anurism..

> >

> >

> >> I will not fall for the BS of waiting for a vaccine, because =
patients

> > being treated right now with the new paradigm are surviving and g=
etting

> > better quicker.

> >>

> >> No patient population compares to the cancer patients who wer=
e found

> > to be Safe from the extreme sickness of Corona because so many of=
their

> > patients were on blood thinners. 

> >> The evidence is there.

> >> Even the Young patients that died, died from Strokes.!!!

> >> No one is talking about the patients that contracted corona w=
ho were

> > described as =C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=85=E2=80=9Cheal=
thy=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=82=EF=BF=BD who SMOKE; it is a joke=
.  Smokers are

> > NOT healthy, not if they smoke anything,  pot, vaping or cig=
arettes.

> >> I see people on the streets with masks and gloves SMOKING and=


> > it=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s a joke.=


> >> THey are blowing Corona and adding to the contaminating of al=
l of us.

> >> I see people wearing masks and gloves throwing them in the st=
reets,

> > not using them properly, and I tell them, will all this costuming=
, they

> > would never be allowed in the ICU to work because they have no id=
ea how

> > to used sterile masks and gloves.

> >>

> >> If you want to be mad, get mad with the medical system in NY =
fueled by

> > political idiots that want to see the economy fail, so they can b=
lame

> > politics.

> >> Even Fauci, that =C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=85=E2=
=80=9CStatistician=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=82=EF=BF=BD is out o=
f the loop.  He

> > hasn=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2t pract=
iced medicine in 20 yrs!!  And he is nothing but an

> > accountant for the numbers that other people give him.

> >>

> >> THis is BS,  I don=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=
=A2=E2=80=9E=C2=A2t give a shit about politics...

> >> I do care that we are being used for this political experimen=
t.

> >

> >

> > 100%

> >

> >

> >> The economy should have NEVER been shut down.

> >

> >

> > A strong economy is our leading weapon to fight the disease.

> >

> >

> >> It=C3=83=C2=A2=C3=A2=E2=80=9A=C2=AC=C3=A2=E2=80=9E=C2=A2s lau=
ghable that all the markets and stores that are open

> > are crowded and no one has stopped shopping.

> >>

> >> Maybe they should try putting the voter machines in Target or=
Walmart.....

> >> Then we could vote out these morons that crashed our economy =
when the

> > answer