Some 1300 years ago in Karnataka there lived a genius who wrote "Gaṇitasārasan̄graha" (which is earliest text devoted entirely to mathematics)

The man who's work later borrowed by Arabs & Europeans

Thread on "Mahāvīracharya" astounding but forgotten legacy

Mahāvirachārya was patronised by rashtrakuta king amoghavarasha

His book"Gaṇita-sāra-saṅgraha"is earliest text devoted entirely to Mathematics

He has described the currently used method of calculating(LCM)of given numbers.The same method was used in Europe later in1500CE
Mahavira wrote "Gaṇita-sāra-saṅgraha" (GSS) in 8th century CE which contains some 1100 slokās & contains elementary topics in arithmetic , algebra , geometry , measurements , logic , number theory , dynamical systems etc

A sheer mathematical genius
He was devout jain
His magnum opus "Ganit sara sangraha " start with a sloka bowing to the glory of the jinas

"संख्याज्ञानप्रदिपेन जैनेंद्रन महत्वेशा,
प्रकाशितम जगतसर्व येन तम प्रणमाम्यहम"

He also praised his predecessor aryabhata , brahmagupta & other greats in his works
The importance & popularity of "Gaṇita-sāra-saṅgraha"was so huge that it enjoyed statues of most important textbook of mathematics in South Indian for over 3 centuries

A large no of manuscript copies of
"Gaṇita-sāra-saṅgraha"whr discovered in Kerala shows it's popularity
Mahāvira was the world's first mathematician to give the general formula for n C r in combinations .

Further he was one of the first mathematician to have given an approximate expression for the circumference of an ellipse(aayata vritta)
Mahāvira also made an important remark in connection with "root of negative number" .

He clearly mentioned in his work that a "negative number cannot have a square root" . This is the first remark on clear recognition of the imaginary quantities in mathematics .
He was the first one to write arithmetic in present day form , he described in details the current method of finding lowest common multiple. therefore, it was an invention not by John napier but by our very own scholar mahaviracharya in its actual form.
Mahaviracharya work was an important link in the continuous chain of Indian mathematics ,it acquired pride place particularly in South India

His work was recognised by great chalukyan ruler Raja Raja narendra who got it translated in telugu by mathematician pavuluri mallana
The credit tht Mahavira rightly deserves for discovery of various methods in the field of mathematics hs gone almost unnoticed by historians

Mahavira by his sheer achievements in several branches of mathematics has a distinct position in the history of indian & world mathematics

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2) The leading hypothesis is that the new variant evolved within just one person, chronically infected with the virus for so long it was able to evolve into a new, more infectious form.

same thing happened in Boston in another immunocompromised person that was sick for 155 days.

3) What happened in Boston with one 45 year old man who was highly infectious for 155 days straight before he died... is exactly what scientists think happened in Kent, England that gave rise to #B117.


4) Doctors were shocked to find virus has evolved many different forms inside of this one immunocompromised man. 20 new mutations in one virus, akin to the #B117. This is possibly how #B1351 in South Africa 🇿🇦 and #P1 in Brazil 🇧🇷 also evolved.


5) “On its own, the appearance of a new variant in genomic databases doesn’t tell us much. “That’s just one genome amongst thousands every week. It wouldn’t necessarily stick out,” says Oliver Pybus, a professor of evolution and infectious disease at Oxford.
Hard agree. And if this is useful, let me share something that often gets omitted (not by @kakape).

Variants always emerge, & are not good or bad, but expected. The challenge is figuring out which variants are bad, and that can't be done with sequence alone.


You can't just look at a sequence and say, "Aha! A mutation in spike. This must be more transmissible or can evade antibody neutralization." Sure, we can use computational models to try and predict the functional consequence of a given mutation, but models are often wrong.

The virus acquires mutations randomly every time it replicates. Many mutations don't change the virus at all. Others may change it in a way that have no consequences for human transmission or disease. But you can't tell just looking at sequence alone.

In order to determine the functional impact of a mutation, you need to actually do experiments. You can look at some effects in cell culture, but to address questions relating to transmission or disease, you have to use animal models.

The reason people were concerned initially about B.1.1.7 is because of epidemiological evidence showing that it rapidly became dominant in one area. More rapidly that could be explained unless it had some kind of advantage that allowed it to outcompete other circulating variants.

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