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drdejahang2020
5 лет назад
science

The next pandemic will come — here's how to prepare for it

The next pandemic will come — here's how to prepare for it

MAIN FOLDER ➜⇢ ➽ https://www.edocr.com/user/drdejahang02
KEY ➜⇢ MSC➤PHD RESEARCH, (MPhilPhD)➽=ALL Articles for Political Science, Mathematics and Productivity the Student Room BSc, MSc & PhD Project Mangers etc.
PPTs in SLIDESHARE International Studies Research Degrees (MPhilPhD) PPT .. http://www.slideshare.net/DrFereidounDejahang/present..
The next pandemic will come — here's how to prepare for it
Will the next pandemic resemble the Spanish flu of 1918, SARS outbreak of 2003 or COVID-19?
➜⇢ ➽ Why are young, healthy people dying from COVID-19? Genes may reveal the answer.
➜⇢ ➽ By developing a Process Model and deriving relevant mathematical formulas,…… Proactive, Protective Measures (PPD) against new type of coronavirus can be achieved. Once we understand why Some people become infected but don't develop any symptoms and don't feel unwell…. but others get seriously sick…
➜⇢ ➽Once we have scientific data for the next outbreak… only people with certain Genes will be isolated and protected and others can go to work and no more pandemic shut down…but next outbreak we must be fast first -Sample Size: How Many Survey Participants Do I Need?
So, we need a DNA bank and some people will refuse to give their DNA. We take DNA Worldwide: DNA Testing or the next flu of 1918, SARS outbreak of 2003 or COVID-19 will kill much more and….. will collapse, more people will be below poverty line…

➜⇢ ➽Collect genetic data from COVID-19 patients, known as the COVID-19 Host Genetics Initiative
➜⇢ ➽Several biobanks from all countries
➜⇢ ➽Collect DNA samples from willing patients who are currently hospitalized with COVID-19 infections
➜⇢ ➽Collected individual-case data for patients who died from COVID-19
➜⇢ ➽Develop a Model to evaluate the likelihood of who and what age is in danger
➜⇢ ➽Find Variables
➜⇢ ➽Find Determinates
➜⇢ ➽Identify and investigate the most significant factors
➜⇢ ➽Data from all cases feed on to spreadsheet
➜⇢ ➽The relationship between age group, genetic data from COVID-19 patients…….
Tests of significance, correlation vs chi-squared
You may ask- 2 ordinal variables along a Likert scale. You may decide to use the Spearman Rho for correlation statistic. You may ask-how to test significance.
Chi-squared, but there is also a significance test for the actual Spearman Rho statistic.
Chi-squared should tell whether there is a significant relationship at all, whereas the Spearman Rho p-value will tell me if the correlation coefficient is significant.

➜⇢ ➽High significant factors affecting the patient must be ranked.
Linear Regression Analysis
Regression analysis is a statistical technique that attempts to explore and model the relationship between two or more variables. For example, an analyst may want to know if there is a relationship between road accidents and the age of the driver.
Linear regression t-test
t Tests. The tests are used to conduct hypothesis tests on the regression coefficients obtained in simple linear regression. A statistic based on the distribution is used to test the two-sided hypothesis that the true slope, , equals some constant value, .

Find possible liner relationship between factor grouping and DNA etc.
Finally Governments don’t lock in all, don’t vaccines all against another more deadly like COVID-19 only people with DNA…
Please read:
https://www.thelancet.com/journals/laninf/article/PII..

0–9 years 0 13 0·00% (0·00–0·00)
10–19 years 1 50 0·0408% (0·0243–0·0832)
20–29 years 49 437 1·04% (0·622–2·13)
30–39 years 124 733 3·43% (2·04–7·00)
40–49 years 154 743 4·25% (2·53–8·68)
50–59 years 222 790 8·16% (4·86–16·7)
60–69 years 201 560 11·8% (7·01–24·0)
70–79 years 133 263 16·6% (9·87–33·8)
≥80 years 51 76 18·4% (11·0–37·6)
Summary
Background
In the face of rapidly changing data, a range of case fatality ratio estimates for coronavirus disease 2019 (COVID-19) have been produced that differ substantially in magnitude. We aimed to provide robust estimates, accounting for censoring and ascertainment biases.
Methods
We collected individual-case data for patients who died from COVID-19 in Hubei, mainland China (reported by national and provincial health commissions to Feb 8, 2020), and for cases outside of mainland China (from government or ministry of health websites and media reports for 37 countries, as well as Hong Kong and Macau, until Feb 25, 2020). These individual-case data were used to estimate the time between onset of symptoms and outcome (death or discharge from hospital). We next obtained age-stratified estimates of the case fatality ratio by relating the aggregate distribution of cases to the observed cumulative deaths in China, assuming a constant attack rate by age and adjusting for demography and age-based and location-based under-ascertainment. We also estimated the case fatality ratio from individual line-list data on 1334 cases identified outside of mainland China. Using data on the prevalence of PCR-confirmed cases in international residents repatriated from China, we obtained age-stratified estimates of the infection fatality ratio. Furthermore, data on age-stratified severity in a subset of 3665 cases from China were used to estimate the proportion of infected individuals who are likely to require hospitalisation.
Findings
Using data on 24 deaths that occurred in mainland China and 165 recoveries outside of China, we estimated the mean duration from onset of symptoms to death to be 17·8 days (95% credible interval [CrI] 16·9–19·2) and to hospital discharge to be 24·7 days (22·9–28·1). In all laboratory confirmed and clinically diagnosed cases from mainland China (n=70 117), we estimated a crude case fatality ratio (adjusted for censoring) of 3·67% (95% CrI 3·56–3·80). However, after further adjusting for demography and under-ascertainment, we obtained a best estimate of the case fatality ratio in China of 1·38% (1·23–1·53), with substantially higher ratios in older age groups (0·32% [0·27–0·38] in those aged <60 years vs 6·4% [5·7–7·2] in those aged ≥60 years), up to 13·4% (11·2–15·9) in those aged 80 years or older. Estimates of case fatality ratio from international cases stratified by age were consistent with those from China (parametric estimate 1·4% [0·4–3·5] in those aged <60 years [n=360] and 4·5% [1·8–11·1] in those aged ≥60 years [n=151]). Our estimated overall infection fatality ratio for China was 0·66% (0·39–1·33), with an increasing profile with age. Similarly, estimates of the proportion of infected individuals likely to be hospitalised increased with age up to a maximum of 18·4% (11·0–7·6) in those aged 80 years or older.
Interpretation
These early estimates give an indication of the fatality ratio across the spectrum of COVID-19 disease and show a strong age gradient in risk of death.
Funding
UK Medical Research Council. https://www.thelancet.com/journals/laninf/article/PII..

Why are young, healthy people dying from COVID-19? Genes may reveal the answer.
By Nicoletta Lanese - Staff Writer
Some people may be susceptible to severe infection due to differences in their genetic code.
CORONAVIRUS BASICS
—What are coronavirus symptoms?
—How deadly is the new coronavirus?
—Is there a cure for COVID-19?
—How does coronavirus compare with seasonal flu?
—How does the coronavirus spread?
—Can people spread the coronavirus after they recover?
Young, healthy people are dying of COVID-19 infections, even if most serious cases occur in the elderly and those with preexisting conditions. Now, scientists are looking to see if genes may explain why some people fall seriously ill while others show only mild symptoms, Science magazine reported.
Several ongoing projects aim to analyze and compare the DNA of those with severe COVID-19 infection to those with mild or asymptomatic cases. Differences may lie in genes that instruct human cells to build a receptor called ACE2, which the novel coronavirus relies on to enter cells, Science reported. Alternatively, it may be that genes that support the body's immune response to the virus differ between individuals, or that those with particular blood types carry protective genetic traits that shield them from illness, as suggested by a preliminary study from China.
For now, we don't know which genes might render people susceptible to serious COVID-19 infection, but given the pace of the pandemic, researchers could identify likely candidates within a few months, Andrea Ganna, a geneticist at the University of Helsinki’s Institute for Molecular Medicine Finland (FIMM), told Science.
PLAY SOUND
Related: 10 deadly diseases that hopped across species
Ganna and FIMM Director Mark Daly are heading an international effort to collect genetic data from COVID-19 patients, known as the COVID-19 Host Genetics Initiative. Several biobanks, including FinnGen in Finland and the 50,000-participant biobank at the Icahn School of Medicine at Mount Sinai in New York, have "expressed interest" in contributing data to the study, according to Science. Some groups working with the initiative plan to collect DNA samples from willing patients who are currently hospitalized with COVID-19 infections. Alessandra Renieri, a geneticist at the University of Siena in Italy, expects 11 Italian hospitals to participate in such a study with her own research group.
"It is my opinion that [host] genetic differences are a key factor … for susceptibility to severe acute pneumonia," Renieri told Science. Jean-Laurent Casanova, a pediatrics researcher at the Rockefeller University, is organizing a similar effort within a global network of pediatricians. Their aim is to study "previously healthy" patients under age 50 who have developed severe COVID-19 infections, as their vulnerability to the virus likely lies in their genes, Casanova told Science.
As part of their own initiatives, the UK Biobank will also begin curating data from COVID-19 patients, and the Iceland-based company deCODE Genetics will partner with the country's government to do the same. In the U.S., the Personal Genome Project at Harvard University is recruiting volunteers to share their genetic data, tissue samples, health data and COVID-19 status, Science reported.
In the coming weeks and months, these and other projects may reveal why COVID-19 only triggers a transient cough in some people, while endangering the lives of many others.
• Going viral: 6 new findings about viruses
• The 12 deadliest viruses on Earth
• Top 10 mysterious diseases
Originally published on Live Science. https://www.livescience.com/genes-for-covid19-coronav..

BY ANDREAS KLUTH
BLOOMBERG
• JAN 24, 2020
ARTICLE HISTORY
• PRINT
• SHARE

Absolutely with pinch of salt …Just look at what is happening in New York Death censorships and…
NEW YORK – As a new coronavirus spreads within China and to other countries, I’m reminded of my time in Hong Kong during the SARS outbreak of 2003.
Back then, I spent an otherwise beautiful spring wearing masks in public but mostly working from home, as I reported on the disease and the struggle to contain it.
Every day at the same time I checked an official Hong Kong website, which I trusted completely, to see that day’s new cases. I remember my relief as the number finally trended down. When it was over, it felt as though SARS had been just a shot across the world’s bow.
For one thing is certain: The next pandemic will come, and it may resemble the Spanish flu of 1918, which infected half a billion people. The questions are when, where and how, and whether we’ll be ready collectively. I say “collectively” because a pandemic, like climate change, doesn’t respect passports or borders. We don’t quarantine, cure or save “America First,” or “China First” or anybody first; we either put humanity first or we all lose.
There are other links between climate change and pandemics (and, to be clear, the current outbreak is still far from being one). The main connection is that global warming actually creates new disease vectors. As the permafrost thaws in places like Siberia, viruses that have been frozen for millenniums, and against which animals and humans no longer have any resistance, will resurface.
And as desertification and other side effects of warming move the boundaries between habitats, species will come into contact with creatures they’ve never encountered before. That’s how viruses start their journey.
What, then, are my lessons from the SARS outbreak? First, we must plan for human nature, both in its perfidy and its heroism. I observed SARS crash into various cultures in totally different ways.
China at first suppressed information about it, fearing economic loss or political turmoil. But that allowed the virus to spread farther and faster for longer than was necessary. And once China did open up on the subject, its people no longer trusted the government’s information. Rumors circulated and often prevailed over facts, hampering the official response.
Singapore, by contrast, lived up to its reputation for iron discipline with immediate quarantines that I initially considered draconian and illiberal but came reluctantly to respect. Taiwan initially showed the darker side of individualism, as some hospital workers, to protect themselves and their families, shirked their duties. In Hong Kong (and then Taiwan and other places, too) the opposite happened, as nurses and doctors cared for the victims and valiantly fought the virus.
Nobody who’s read Albert Camus’ “The Plague” or Jose Saramago’s “Blindness” should be surprised that human beings, individually and in crowds, will respond unpredictably to such crises. Some will hoard scarce medicine or food that’s more urgently needed by others. Some will break quarantines to be with loved ones. Some will do their duty, others won’t.
The biggest lesson, which China seems to have learned, is that the government must be ruthlessly honest and transparent. The more facts, the better. Hide nothing. It was my trust in that Hong Kong website that eventually made me believe SARS was waning. Once trust between the population and the state breaks down, controlling an outbreak becomes almost impossible.
Another lesson is, thankfully, one we’ve already learned. Screening and surveillance, which should be used with caution in free societies, becomes necessary in an outbreak and is effective. Even now various airports around the world are digitally observing the body temperatures of passengers arriving from Wuhan, the center of the new outbreak.
Quarantine should be voluntary at first and actively encouraged by employers and government. Whoever can work from home, via Skype and such, should do so, without fearing recrimination. The more people can keep acting on their own volition, the more “agency” they believe they have, the calmer and more cooperative they will remain. Once an outbreak goes out of control, of course, quarantines must become mandatory.
But the most profound lesson is that we must cooperate as a species, with a geopolitical approach that seems to have gone out of fashion: multilateralism. We’ve always been locked in an arms race between the evolution of viruses, bacteria and fungi and our medicines against them. When a new virus appears, it potentially threatens all of us and should be fought by all of us together.
That means a new bug’s genome, wherever it’s first collected, should be sequenced and immediately made available, like open-source computer code, to certified researchers everywhere. (You still need the World Health Organization or some such body to accredit the scientists, lest the genome gets into the hands of terrorists). All labs and scientists should then share their insights with the entire profession.
The bad news is that we cannot be sure that humans will rise to global threats such as climate change or pandemics, because we’re so prone to put what we perceive to be our own interests, or our nations’, first, only to suffer the consequences later.
The good news — and this too is something I learned from SARS — is that every time we do join together to defeat a new threat, we’re reminded how much we have in common, and fight better the next time. https://www.japantimes.co
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