Woodstock CT Café

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December 7th, 2014

New Cell Towers to be Placed at the Fairgrounds

Formerly a Student: I just skimmed the proposal. The “new cell towers being placed” in the title of this article is misleading. To summarize, they’ll be replacing a few wood utility poles in the fairgrounds with steel ones “of equal height,” and adding a battery box and extra antenna (which itself looks like a box) to the poles. The existing antennas will be moved to the top of the poles. No extra access roads, no wetland disturbance, no ground disturbance except for the actual digging of the pole, little aesthetic change, especially from a distance (169).

Sounds good to me on the surface from how they’re presenting the info. But what makes me leery is that they propose that the new antennas will initially be 700 MHz (at 500 mW power). So do they plan on adding more antennas at different frequencies? Adding more poles in the future?

However, the other frequencies only go up — to 2100 MHz. Higher frequencies are lower range, so higher power, so they’re starting off with the best range. For comparison, the Wifi in your house is 2400 or, lately, 5000 MHz frequency but only 70 mW power. Lower MHz travel farther but have more interference (think AM vs. FM radio). Speaking of radio, think of how strong those signals are, compared to the cell towers, which are everywhere and thus have lower range.

Not sure how the numbers play in to health issues, but they say these things are mainly intended for the fairgrounds, and those are usually vacant. It doesn’t seem like the signal will be excessively strong outside the grounds (have a look at the coverage maps).

But again, all this is coming from the big business trying to weasel its way in, so take it with a grain of salt.

PETITION NO. 1119 - Cellco Partnership d/b/a Verizon Wireless petition for a declaratory ruling that no Certificate of Environmental Compatibility and Public Need is required for the proposed construction, maintenance, and operation of three pole-mounted small cell telecommunications facilities on the Woodstock Fairgrounds property located at 281 Route 169, Woodstock, Connecticut.   Field Review.

November 29th, 2014

Woodstock Academy Football 1 and 32 – September 2012 to November 2014 – Subtle Signs of Improvement

Woodstock football is 1-32 since two years and 3 months ago with this week’s loss of 8-41 to 9-1 Windham.

“Several years ago the Academy chose to invest in football with a new stadium and other unneeded athletic fields rather than invest in enhanced academic programs that would help students to develop professional careers.”

The average game score this year is 9 for WA vs 39 for the opponents compared to 7 for WA vs 42 for the opponents last year, and 5 for WA vs 43 for the opponents.

This year the Woodstock Academy football team ranks 156 out of 161 CT high school varsity football teams. The results for this season are:

Windham (9-1) – 41 Woodstock (1-10) – 8

Plainfield (9-1) – 47 Woodstock (1-9) – 7

Woodstock Academy  -   8  to Norwich Free Academy – 44

Woodstock Academy  – 3 to Waterford  – 35

Vinal RVT/East Hampton/Goodwin RVT -  16 to Woodstock Academy  -  13

Griswold   – 34 to Woodstock Academy  – 0

New London – 51 to Woodstock Academy  -  6

Woodstock Academy  – 0 to Montville  – 40

St. Bernard-Norwich RVT – 14 to Woodstock Academy  -  35

Woodstock Academy  – 7 to Bacon Academy -  52

Stonington – 48 to Woodstock Academy  – 7

“Headmaster Foye said that a successful football program would produce college scholarships for Woodstock Academy senior football players” Cafe, July 28, 2008. HERE

“The misguided priorities of the Academy leadership and its ‘track record’ does not bode well for the long term viability of its students’ futures.” Cafe, May 26th, 2008. HERE

By the way, I enjoy football and faithfully support losing programs like the ones at Norwalk High (late 50s to 1960; see the heroic story of Jerry Fishman), Bethany College (1961-1966), the University of Pittsburgh (1966-1972, 16-56)  just before Dan Marino and Tony Dorsett, and currently UConn at 2-7.  I sat virtually alone in driving rain in 1968 watching the lowly Pitt team come back from a 34-0 halftime deficit to beat West Virginia 35-34, the best game I ever saw.

Several years ago the Academy chose to invest in football with a new stadium and other unneeded athletic fields rather than invest in enhanced academic programs that would help students to develop professional careers. This was due to the low-level visionary thinking of Headmaster Foye and the Academy Board of Trustees.

November 26th, 2014

The Latest Developments with Ebola

From John

Yesterday I was interviewed by the Des Moines Register about Merck’s acquisition of NewLink’s Ebola vaccine. This graph shows that there is something different about this Ebola outbreak compared to previous outbreaks. A little bit of immunity caused by the vaccine should have a big impact on the spread of the disease. These numbers provided by the CDC are actual confirmed cases and deaths caused by Ebola. They under report the actual cases and deaths.

November 11th, 2014

In Preparation for the Unusual Cold Spell Coming Our Way – Dealing with Global Warming So We Can Have a Better Ice Age

From John

From National Geographic News: “An instrument near the summit of Mauna Loa in Hawaii has recorded a long-awaited climate milestone: the amount of carbon dioxide in the atmosphere there has exceeded 400 parts per million (ppm) for the first time in 55 years of measurement—and probably more than 3 million years of Earth history.”

The graphics below suggest that we are about 10,000 years into a warm spell on planet Earth. Prior to the last ice age we had about 17,000 years of relative warmth before things started to go down hill. If 17,000 years is about right for our current warm spell, then we have only 7,000 years left in our Garden of Eden. But we are clearly polluting our environment. The big difference now is that in the warm spell that took place between 132,000 and 115,000 years ago there was only a million or so homo sapiens around and no polluting industry. Now we have almost 8 billion modern humans and an industrial society.

It’s clear that whomever coined the term “Global Warming” coined a misnomer because it looks as though our atmosphere was warmer 130,000 years ago. The popular phrase should be “Global Polluting” shouldn’t it? Then the nay-sayers might accept the problem and take some responsibility for it. Otherwise human beings may not be around to have the next ice age.

I’ve added some benchmarks to the graph below which shows the patterns of warming and cooling of the Earth for the last 400,000+ years. The warming and cooling of the Earth is caused by a very subtle movements closer and farther from the Sun in our eliptical orbit. This is not man-made. The last ice age took longer than the three previous ice ages shown in the graph which is based on chemical analysis of core samples from the Vostok ice sheet in Antarctica.  Two benchmarks are the demise of H. erectus and Neanderthals based upon the fossel record. These two species of Homos died off near the ends of two ice ages. Imagine what it would be like for us if the biosphere was 13 degrees colder on average than it is today. Back then their only refuge was a chilly cave or to head south. No wonder humans got their start in Africa.

Our current understanding of human history only came about since 1970 when nucleic acid hybridization became a tool for understanding the divergence of genes among all lifeforms. The rate of hybridization of two strands of DNA is a function of complimentarity of the Watson-Crick double helix.

From the last full cycle it appears that warm spells last about 18,000 years whereas the last ice age lasted about 97,000 years. It looks like archaic Homo sapiens survived two ice ages whereas Neanderthals only survived one. But our human male Y chromosome was passed on from H. erectus while the earliest date of discovery of mitochodrial DNA was during the time that archaic H. sapiens roamed sub-Saharan Africa. The mitochondrial DNA genome is inherited from mothers, not fathers; likewise in plants, chloroplasts are not carried in pollen when the female part of the plant is fertilized.

This is all very mind-boggling to consider. Will scientists have the answers for how to deal with the next ice age? Yup! Will politicians cooperate? We’ll just have to wait and see. ;-)

Graph of CO2 (Green graph), temperature (Blue graph), and dust concentration (Red graph) measured from the Vostok, Antarctica ice core. The shifts between hot and cold periods is thought to be controlled by the the Milankovich cycles:
1. The earth’s orbit changes from being nearly circular to slightly elliptical (eccentricity). This cycle is affected by other planets in the solar system and has a period of around 100,000 years.
2. The angle of tilt of the earth’s axis changes from 22.1° to 24.5° (obliquity). This cycle has a period of 41,000 years.
3. The direction of the tilt of the axis changes (precession) on a cycle of 26,000 years.

CO2 followed temperature change “with a lag of some hundreds of years” amplifies temperature change. Among other factors, CO2 is more soluble in colder than in warmer water. Higher dust levels are believed to be caused by cold, dry periods.

November 4th, 2014

The Vote in Woodstock at 8:30 PM


Dan Malloy/Wyman (D) – 1254

Tom Foley/Somers (R) – 1637

Representative to Congress

Joe Courtney (D) – 1568

Lori Hopkins-Cavanagh (R) – 1230

State Senator

Tony Guglielmo (R) – 2044

Andrea Penta (WFP) – 370

State Representative

Mike Alberts (R) – 2243


Secretary of State

Denise Merrill (D) – 1193

Peter Lumaj (R) -1609


Denise Napier (D) – 1228

Tim Herbst (R) -1609


Kevin Lembo (D) – 1143

Sharon McLaughlin (R) – 1581

Attorney General

George Jepsen (D) – 1303

Kei Westby (R) – 1436

Judge of Probate

Leah Schad (D) – 1958


Registrar of Voters

Suzanne Woodward (D) -1320

Mary Place (R) – 1485

Constitutional Amendment – Easier to vote

yes – 1196

no – 1417

October 27th, 2014

Explaining the Relevance of Risk Calculation in Choosing a (Chemo)Therapy

Reading Jeff’s explanation of risk calculation below was like taking the Ice Bucket Challenge. My views on that phenomenon are published HERE. This article is very helpful in understanding the nuances and adding perspective to statistical analyses like those published on coffee drinking below. Ultimately one needs to understand the actual biochemical mechanism that explains the benefits of coffee and any other drugs used to treat disease to verify their statistical merits. Until then, I will continue to take my timed-release gram of vitamin C in the morning and pick up a large Dunkin Donuts coffee on my way to work. John Leavitt

From Jeff Gordon, M.D.

Relative Risk is not the same as an actual increase or a decrease in risk.

The Absolute Risk is the risk of developing a disease (such as cancer) over a defined period of time.

The Relative Risk is the risk difference when comparing two groups of people, for example people who smoke cigarettes and people who do not smoke cigarettes. The Hazard Ratio expresses this relative risk difference, but by a different number mechanism.

Let’s say that the risk of developing lung cancer is 80% higher in people who smoke than in people who do not smoke. This means the Relative Risk is an 80% increase. The Hazard Ratio states this as being 1.8. A Hazard Ratio of 1 means the difference between the two groups (smokers and non-smokers) is zero. Numbers higher than 1 mean increased risk. Numbers lower than 1 mean decreased risk. So, 1.8 means the smoking group has an 80% increase of getting lung cancer than does the non-smoking group.

First, this does not mean that the risk of getting lung cancer in the non-smoking group is 0. It just means the risk of getting lung cancer if you smoke is higher than if you do not smoke.

Second, the 80% risk increase may sound like a lot when looking superficially at the number “80%”. But, what is the Absolute Risk increase?

Let’s say the risk in non-smokers of getting lung cancer is 1 in 100,000. For smokers, this risk is increased by 80%, so the risk goes from 1 in 100,000 to 1.8 in 100,000. The absolute difference of 0.8 is very small. If the population were 300 million, then a 1 out of 100,000 risk increasing to a 1.8 out of 100,000 risk would translate into 3,000 cases of lung cancer increasing to 5,400 cases of lung (an increase of just 2,400 cases).

That puts things in perspective.

But, what if the Relative Risk increase is 800%? The Absolute Risk increases from 1 in 100,000 (for non-smokers) to 8 in 100,000 (for smokers). If the population were 300 million, then a 1 out of 100,000 risk increasing to a 8 out of 100,000 risk would translate into 3,000 cases of lung cancer increasing to 24,000 cases of lung (an absolute increase of 21,000 cases).

Even as the Relative Risk goes up, the Absolute Risk increase in this example is not staggeringly high because the baseline risk is not high.

But, what if the risk of getting lung cancer in a non-smoker is 1 out of 100? If the Relative Risk increase is 80% for non-smokers, then given a population of 300 million, as in the example above, then the cases of lung cancer go from 300,000 up to 540,000. This is an absolute increase of 240,000 cases. The increase in total cases goes up more due to the higher baseline Absolute Risk.

If the Relative Risk were 800%, then the number of cases goes from 300,000 to 2,400,000 cases. The increase in total cases is much, much higher because both the baseline Absolute Risk and the Relative Risk are increased.

An example I use daily in my medical practice is explaining the potential risk reduction of dying from a cancer if someone takes a recommended treatment (such as chemo). Look at how the numbers change even if the Relative Risk reduction of dying is the same if the same chemo is used.

· Baseline risk of death is 10%. A 50% Relative Risk reduction by using chemo translates into an Absolute Risk reduction of 5%, so the risk of dying of the breast cancer drops from 10% to 5% after chemo. The risks of having a serious problem from chemo could be 2%, let’s say, so the benefit is larger than the risk of chemo, but not by much.

· Baseline risk of death is 50%. A 50% Relative Risk reduction by using chemo translates into an Absolute Risk reduction of 25%, so the risk of dying of the breast cancer drops from 50% to 25% after chemo. The risks of having a serious problem from chemo could be 2%, let’s say, so the benefit outweighs the risk of chemo.

· Baseline risk of death is 90%. A 50% Relative Risk reduction by using chemo translates into an Absolute Risk reduction of 45%, so the risk of dying of the breast cancer drops from 90% to 45% after chemo. The risks of having a serious problem from chemo could be 2%, let’s say, so the benefit much outweighs the risk of chemo. However, there is still a sizable remaining risk of dying of the cancer even after chemo given the very high baseline risk even with a sizable Relative Risk Reduction.

There are many ways to try to explain this.

Another number worthy of knowing is the Number Needed To Treat (NNT).

Let’s say that chemotherapy has a 50% Relative Risk reduction in the risk of dying of breast cancer. If the Absolute Risk of dying of breast cancer without chemo is 10%, then the Number Needed To Treat with chemo to benefit one person is 20. That means 20 people get chemo so that one person can get the actual benefit. A lot of people would be getting chemo without benefit because the baseline Absolute Risk of death from the breast cancer is low and the Absolute Risk Reduction is low.

But, if the same 50% Relative Risk reduction from chemo is applied to a baseline Absolute Risk of 90% of dying without chemo, then the NNT is 2.2, which means that 2.2 people get treatment so 1 can benefit (which is the same as 22 people getting treatment so 10 can benefit).

Of course, nowadays, we are much better with individualized benefit and risk assessments of breast cancer to minimize people getting treatment that won’t benefit them, thereby focusing on giving treatment to the people who could benefit the most from it.

So, the next time you read a news story trying to wow you with statistics about how great something is, keep these questions in mind:

What is the baseline Absolute Risk of the disease?
What is the Absolute Risk Reduction of a treatment for the disease?
What are the risks of side effects of the treatment?
How many people need to be treated for one person to get benefit?
What is the cost for treating an individual and what are the costs for treating a whole population?

October 25th, 2014

Is Coffee Good or Bad for You?

From John

These are the findings of very recent major meta-analyses of multiple clinical trials, some of which examined >100,000 to >1,000,000 subjects. The arrows point to the data of completely separated studies. I’ve included some tea drinkers and studies on caffeine drinkers, as well. The “relative risk” (risk ratio) is the key measurement. If you are in a group that has a relative risk of 0.80 then you have a 20% lower chance of developing the disease being examined. Likewise if you are in a group with a relative risk of 0.60, 0.40, 0.20, then you have a 40%, 60%, or 80% lower chance of getting the disease being examined, respectively. Over the years I have looked at past meta-analyses and they tell the same story. Rarely has a negative relationship between coffee or tea drinking been found.

Click to enlarge the actual data and its source:

October 21st, 2014

Woodstock Registered Voters Can’t Hide and the Ballot for November 4th

From John

Voter registration lists have always been available. Now CT’s registered voters can be searched by zip code and name (use the Find option when in the list of registered voters for a specific zip code). I looked at my home town of Rowayton and Woodstock. By doing this I can find out who is living in my past houses in my youth right down to their names and phone numbers. For a particular address you might see who lived there in the past also. For example, Andy Rooney’s wife Marge, who passed away a decade ago, is still listed at their former residence in Rowayton. She’s listed as inactive at that address. My sister Phoebe lived with Otis L in Rowayton for several years and voted  from there. Even though she has lived elsewhere for the last seven years, she’s still listed as active. Becki and I are listed in Woodstock. You can hyperlink to a second page which discloses your registered party affiliation and when you voted from 2000 on including referendums. See Connvoters.com for all zips in CT and see the Woodstock CT registered voters. Again, this information has always been available for the savvy.



October 17th, 2014

The Ebolavirus Infectious Process of a Liver Cell

From John

In August of 2013, Gordian Schudt and colleagues at The University of Marburg (Germany) published a study of live-cell imaging of the Ebolavirus infectious process in human hepatocytes. I will try to summarize their observations here.

They re-assembled Ebola nucleocapids (viral particles empty of the RNA genome) in a human hepatocyte cell line and then examined the trafficking of the these viral particles from the site of cellular entry across the cell cytoplasm to an exit door where the viral particles are secreted from the cell.

This table on the left gives us a handle on the relative sizes of this virus and the cells that they infect. The Ebolavirus particle is a cylinder with a diameter of about 80 nanometers (nm) and length of about 800 nm (an unusual shape for a virus); most human/animal cells have a diameter of about 30 micrometers or 30,000 nanometers. Simple math tells us that the Ebolavirus diameter is about 1/380th the diameter of a cell.

The investigators recorded live-cell time-lapse images using a high-powered Leica microscope to follow the fate of the viral particles from entry to exit from the cell. They could track this fate because the viral particles were re-assembled with fluorescent molecular tags that allowed them to see the particles as they moved through the live cell cytoplasm. They were trying to determine how the particles were transported through the cell and secreted with the hope that if the transport process was discovered, this knowledge might suggest a target of the transport process that could be used therapeutically.

The Ebolavirus enters the cell by attaching to a cell surface receptor followed by endocytosis (engulfment by the cell plasma membrane). The negative stranded RNA genome is unwrapped and translated into seven viral proteins using the human cell’s protein synthetic machinery. The viral RNA is replicated by its own RNA polymerase. Multiple viral particles are re-assembled into infectious viruses by this process. This is where we start Gordian Shudt’s study of the transport of the re-assembled particles to a cellular site where they can be released to infect other cells.

Viruses have been known to be transported along the architectural filamentous structures of mammalian cells. There are three filamentous networks in the cytoplasm of human and other animal cells – microtubules, intermediate sized filaments, and the most abundant microfilament network. The investigators found that it was the microfilament network that trafficked the newly assembled viruses to the exit door. The photo on the left shows how the microfilament network is organized in a human cell. These fibers are composed primarily of polymerized actin  – the most abundant and most highly conserved protein of human and all other eukaryotic cells (cells with a nucleus) [Human actin was first sequenced and cloned by yours truly.]

The investigators clocked the movement of the transported viral particles at three different transport velocities of about 100, 200, or 400 nanometers per second which could be caused by three different sets of actin-based motors (the width of a actin microfilament is about 8 nanometers) which catalyze the movement of a myosin motor protein along a microfilament. At 200 nm/sec the viral particle might reach the exit door fully assembled in about 105 seconds after the basic core of the particle had been assembled in the cytoplasm. The illustration below shows what this transport process looks like at the macromolecular level – the particle with myosin legs actually walks on an actin filament to the exit door.

The strand along the bottom is the actin filament with a motor protein (myosin) transporting the particle across the cell cytoplasm – energy is produced for this transport process by removal of phosphate groups from ATP.

Where is the exit door? It’s in the filopodia which are long cellular projections at the cell surface. The viral particle is transported into filopodia on its actin filament track where it then buds from the cell through the plasma membrane of the filopodia. It’s this site of budding that gives the Ebolavirus some protection from its victim’s immune system because filopodia attach to neighboring cells permitting direct cell-to-cell transmission of the virus.

October 16th, 2014

Some Basic Facts About Ebola Pathology

From John

Ebola is potentially the most debilitating infectious disease known to mankind; it rapidly ravages many organs of the human body such that it is the most highly fatal acute disease on record.

Regarding host range, Ebolaviruses cause often fatal, hemorrhagic fever in several species of simian primates. While fruit bats are considered a natural reservoir, the involvement of other species in the virus transmission cycle is unclear, especially for domesticated animals. Dogs and pigs are, so far, the only domestic animals identified as species that can be infected with Ebolavirus. In 2009 the Reston-Ebolavirus was the first Ebolavirus to infect swine followed by transmission to humans in the Philippines. A survey in Gabon found over 30% seroprevalence in dogs (production of anti-Ebola antibodies due to infection) during the Ebola outbreak in 2001-2002. Infections in dogs, as in bats, appears to be asymptomatic, while pigs experimentally infected with Ebolavirus can develop clinical disease, depending on the virus strain and possibly the age of the infected animals (Weingartl  et al, 2013; from the Canadian Science Centre for Human and Animal Health, Winnipeg, Canada)

Regarding transmission to humans, introduction from the wild into humans most likely occurs through direct contact with bats or their excretions or secretions or through contact with other end hosts such as monkeys and possibly dogs and pigs. Human-to-human transmission leads to ‘outbreaks’, which are often started by a single introduction from the wildlife or domesticated animal reservoir. Ebolavirus variants exhibit little genetic diversity, as in the current outbreak in West Africa ( Feldmann, Oct 9, 2014; from the Rocky Mountain Laboratories of the National Institute of Allergy and Infectious Diseases, NIAID). The current Ebolavirus genome has been sequence although as of yet the role of genetic variations does not explain the aggressiveness of this particular outbreak.

In spite of the fact that >5000 Africans have died from Ebola, few detailed autopsies have been reported. From the little that has been done, it appears that the pathogenesis of Ebolavirus infections is complex and involves a systemic cytokine storm during which circulating white blood phagocytic cells (macrophages, etc.) are activated resulting in release of proinflammatory cytokines, chemokines and growth factors which cause direct organ and endothelial damage and extensive (blood) coagulopathy ( Martines et al, Oct 9, 2014; from the CDC in Atlanta, GE). Elevated levels of proinflammatory cytokines by our inflammatory immune system, particularly IL-6, trigger the coagulation cascade. Vascular endothelial impairment is caused by an indirect immune-mediated mechanism, e.g. the cytokine storm. This systemic storm of immune inflammatory mediators such as nitric oxide, prostacyclin, interferons, interleukins and chemokines modifies vascular tone and causes hemorrhagic permeability, thrombosis, and inflammation. The massive release of these proinflammatory mediators and vasoactive substances promotes systemic inflammation and coagulation, but renders the adaptive immune system (antibody production) unable to effectively prevent systemic spread of the virus. In the lungs, for example, Ebola cases show congestion, focal alveolar edema, and hemorrhage. Tissue histology shows viral antigens in alveolar macrophages, endothelial cells, fibroblasts, and others interstitial cells within the lungs. In the liver, for example, hepatocyte necrosis ranges from focal to widespread and hepatocytes show characteristic intracellular oval virus inclusions. Ultrastructurally, these hepatocyte inclusions are composed of aggregates of viral particles.

A thorough description of the science of Ebola disease transmission can be found in a recent paper by Olival and Hayman, Apr 2014; from EcoHealth Alliance and Colorado State University, respectively.

October 15th, 2014

Ebola Talking Heads Are Not Addressing the Most Frightening Scenario

The problem with Ebola lies in Africa, not the USA

If the epidemic can spread to the USA why not throughout sub-Saharan Africa. Africa has a population of >1 billion. If Ebola spreads throughout Africa, then this increases the possibility that it will spread to India and southeast Asia as far east as the Philippines by migration of fruit bats, and possibly Australia. If that scenario occurs, then the likelihood of the virus reaching the USA is far greater.

October 14th, 2014

Ebola Update

From John

I constructed this graph from the announcement from the World Health Organization that is now projecting 10,000 new cases of Ebola PER WEEK by the end of December. In the last week the number have cases has risen by 1000. WHO is also projecting a 70% death rate. If the new cases rise to 10,000 per week by the end of the year, the projected number of cases in the graph will be closer to 50,000. So I asked the CDC why the difference between this outbreak and previous outbreaks. The CDC has not gotten back to me. See the article in the NYtimes

In this rapidly evolving story, the TV news media is either acting stupid and/or being manipulated. This started to get out of control when Charlie Rose asked Dr. LaPook, “What’s the worst scenario?” LaPook responded, “You journalists!” It’s kind of comical. Yesterday WHO started to answer Charlie’s question after the heads of the CDC and NIAID (NIH Inst. of Allergy and Infectious Disease) had tried to avoid hysteria by reassuring the public that things were understood and completely under control. Yesterday Chris Matthews berated Fauci (NIAID) because there was no “Ebola Czar” or Surgeon General. I read the expression on Fauci’s face to reflect the insulting behavior by Matthews. He was probably thinking ‘I am the Czar and there is no need for other Czars.’ This morning it was reported that nurses at the Dallas Hospital had contacted a national nurses union and reported that there “was no protocol” at the hospital to deal with dying Duncan. Days earlier Fauci and the head of the CDC, as well as Dallas judge, had tried to persuade the TV media that the first nurse infected by Duncan was due to a “breach of protocol” putting the onus on the nurses. But if there was no protocol, how could there be a breach of protocol? Then at 4 AM this morning a second nurse was diagnosed with Ebola because of breach of a fictitious protocol.

October 13th, 2014

African Fruit Bat – Likely Reservoir for Ebolavirus – 5-9 inch wing span

There are a gazillion of these migratory bats in sub-Saharan Africa. Transmission may result from contact with guano and eating these bats.

October 10th, 2014

Basic Information On Ebola and Ebolavirus

From John

These are the eight largest outbreaks of Ebola since the first significant outbreak in 1976 (data from the World Health organization, WHO). You don’t have to be a mathematician to see the difference in the current outbreak which is still growing. A representative of the CDC said yesterday that this epidemic reminiscent of the emergence of the HIV epidemic in 1981. That comparison while dramatic does not shed light on the lethality of Ebola. The problem with HIV is that the carriers were asymptomatic and they spread the virus without knowing it initially. HIV and Ebola work very differently.

The map below shows the locations of these eight outbreaks. Thus far Ebola infections have been confined to central Africa. The only infections outside of Africa have been carried by travelers from Africa.

October 7th, 2014

Ebola: “What’s the Worst Scenario?”

from John

This morning, October 7th, I was amused to hear Charlie Rose (CBS Morning News) ask Medical Advisor, Jon LaPook MD, “What’s the Worst Scenario?” regarding the Ebola outbreak. This question produced a rare moment in national news coverage when LaPook blurted out “You reporters!” which left a stunned expression on Charlie’s face (check tomorrow to see if LaPook or Charlie is still with CBS). Becki (my wife), immediately answered Charlie’s question with raised voice by answering factiously, “The virus will spread to wipe out the human race!” Charlie asked a question that put LaPook on the spot because if he had speculated and answered the question the way Becki did, CBS might have become the cause of worldwide mass hysteria.

If LaPook had had time to think and had read Becky Ryznar’s article (find on Google by searching Ryznar+Nerac+Ebola; must create a log in) on Ebola, he would have been able to say as Becky states, “it is plausible that a variant (virus) with an extremely high mutation rate and one that is replicating enough times throughout the population, could potentially mutate to become airborne. Can we rule out the possible Ebola viral evolutionary path to airborne transmission? The possibility of the virus mutating such that it would be highly transmissible in the air is a scary thought …” This is a plausible scenario because of the size of the outbreak in West Africa – it’s interesting that this scenario has never been raised by LaPook or any of the news media.

Let’s imagine that Ebola became airborne and spread around the world over a few months. The human race would not be wiped out because at worst only 45% of the population would die and the remaining 55% would develop immunity from the virus unless it mutated to produce a new serotype. Wandering further astray I am still immune to polio from the infection I got in 1949; my high titer of anti-polio antibodies was confirmed at the FDA in 1978 before I started growing poliovirus in the lab.

So if the worst scenario comes about, rent the movie Omega Man, starring Charlton Heston, to learn the end to this scenario.

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