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interesting facts about ramanujan

Interesting facts about Ramanujan

Srinivasa Ramanujan ©WikiMedia
Srinivasa Ramanujan was an Indian great Mathematician who lived during the British Rule in India. Though he had almost no formal training in pure mathematics, he made substantial contributions to mathematical analysis, number theory, infinite series, and continued fractions, including solutions to mathematical problems considered to be unsolvable. Ramanujan initially developed his own mathematical research in isolation: “He tried to interest the leading professional mathematicians in his work, but failed for the most part. What he had to show them was too novel, too unfamiliar, and additionally presented in unusual ways; they could not be bothered”.

Early life

Ramanujan (literally, “younger brother of Rama”, a Hindu deity was born on 22 December 1887 into a Tamil Brahmin Iyengar family in Erode, Madras Presidency (now Tamil Nadu), at the residence of his maternal grandparents. His father, K. Srinivasa Iyengar, originally from Thanjavur district, worked as a clerk in a sari shop. His mother, Komalatammal, was a housewife and also sang at a local temple. They lived in a small traditional home on Sarangapani Sannidhi Street in the town of Kumbakonam. The family home is now a museum. When Ramanujan was a year and a half old, his mother gave birth to a son, Sadagopan, who died less than three months later. In December 1889, Ramanujan contracted smallpox, though he recovered, unlike 4,000 others who would die in a bad year in the Thanjavur district around this time. He moved with his mother to her parents’ house in Kanchipuram, near Madras (now Chennai). His mother gave birth to two more children, in 1891 and 1894, both failing to reach their first birthdays.

On 1 October 1892, Ramanujan was enrolled at the local school. After his maternal grandfather lost his job as a court official in Kanchipuram, Ramanujan and his mother moved back to Kumbakonam and he was enrolled in the Kangayan Primary School. When his paternal grandfather died, he was sent back to his maternal grandparents, then living in Madras. He did not like school in Madras, and tried to avoid attending. His family enlisted a local constable to make sure the boy attended school. Within six months, Ramanujan was back in Kumbakonam.

Since Ramanujan’s father was at work most of the day, his mother took care of the boy as a child. He had a close relationship with her. From her, he learned about tradition and puranas. He learned to sing religious songs, to attend pujas at the temple, and to maintain particular eating habits—all of which are part of Brahmin culture. At the Kangayan Primary School, Ramanujan performed well. Just before turning 10, in November 1897, he passed his primary examinations in English, Tamil, geography and arithmetic with the best scores in the district. That year, Ramanujan entered Town Higher Secondary School, where he encountered formal mathematics for the first time.

By age 11, he had exhausted the mathematical knowledge of two college students who were lodgers at his home. He was later lent a book by S. L. Loney on advanced trigonometry. He mastered this by the age of 13 while discovering sophisticated theorems on his own. By 14, he was receiving merit certificates and academic awards that continued throughout his school career, and he assisted the school in the logistics of assigning its 1200 students (each with differing needs) to its approximately 35 teachers. He completed mathematical exams in half the allotted time, and showed a familiarity with geometry and infinite series. Ramanujan was shown how to solve cubic equations in 1902; he developed his own method to solve the quartic. The following year, Ramanujan tried to solve the quintic, not knowing that it could not be solved by radicals.

In 1903, when he was 16, Ramanujan obtained from a friend a library copy of A Synopsis of Elementary Results in Pure and Applied Mathematics, G. S. Carr’s collection of 5,000 theorems. Ramanujan reportedly studied the contents of the book in detail. The book is generally acknowledged as a key element in awakening his genius. The next year, Ramanujan independently developed and investigated the Bernoulli numbers and calculated the Euler–Mascheroni constant up to 15 decimal places. His peers at the time commented that they “rarely understood him” and “stood in respectful awe” of him.

When he graduated from Town Higher Secondary School in 1904, Ramanujan was awarded the K. Ranganatha Rao prize for mathematics by the school’s headmaster, Krishnaswami Iyer. Iyer introduced Ramanujan as an outstanding student who deserved scores higher than the maximum. He received a scholarship to study at Government Arts College, Kumbakonam, but was so intent on mathematics that he could not focus on any other subjects and failed most of them, losing his scholarship in the process. In August 1905, Ramanujan ran away from home, heading towards Visakhapatnam, and stayed in Rajahmundry for about a month. He later enrolled at Pachaiyappa’s College in Madras. There he passed in mathematics, choosing only to attempt questions that appealed to him and leaving the rest unanswered, but performed poorly in other subjects, such as English, physiology and Sanskrit. Ramanujan failed his Fellow of Arts exam in December 1906 and again a year later. Without a FA degree, he left college and continued to pursue independent research in mathematics, living in extreme poverty and often on the brink of starvation.

It was in 1910, after a meeting between the 23-year-old Ramanujan and the founder of the Indian Mathematical Society, V. Ramaswamy Aiyer, also known as Professor Ramaswami, that Ramanujan started to get recognition within the mathematics circles of Madras, subsequently leading to his inclusion as a researcher at the University of Madras.

Life in England

Ramanujan departed from Madras aboard the S.S. Nevasa on 17 March 1914. When he disembarked in London on 14 April, Neville was waiting for him with a car. Four days later, Neville took him to his house on Chesterton Road in Cambridge. Ramanujan immediately began his work with Littlewood and Hardy. After six weeks, Ramanujan moved out of Neville’s house and took up residence on Whewell’s Court, a five-minute walk from Hardy’s room. Hardy and Littlewood began to look at Ramanujan’s notebooks. Hardy had already received 120 theorems from Ramanujan in the first two letters, but there were many more results and theorems in the notebooks. Hardy saw that some were wrong, others had already been discovered, and the rest were new breakthroughs. Ramanujan left a deep impression on Hardy and Littlewood. Littlewood commented, “I can believe that he’s at least a Jacobi”, while Hardy said he “can compare him only with Euler or Jacobi.”

Ramanujan spent nearly five years in Cambridge collaborating with Hardy and Littlewood, and published part of his findings there. Hardy and Ramanujan had highly contrasting personalities. Their collaboration was a clash of different cultures, beliefs, and working styles. In the previous few decades, the foundations of mathematics had come into question and the need for mathematically rigorous proofs recognized. Hardy was an atheist and an apostle of proof and mathematical rigour, whereas Ramanujan was a deeply religious man who relied very strongly on his intuition and insights. While in England, Hardy tried his best to fill the gaps in Ramanujan’s education and to mentor him in the need for formal proofs to support his results, without hindering his inspiration—a conflict that neither found easy.

Ramanujan was awarded a Bachelor of Science degree by research (this degree was later renamed PhD) in March 1916 for his work on highly composite numbers, the first part of which was published as a paper in the Proceedings of the London Mathematical Society. The paper was more than 50 pages and proved various properties of such numbers. Hardy remarked that it was one of the most unusual papers seen in mathematical research at that time and that Ramanujan showed extraordinary ingenuity in handling it.[citation needed] On 6 December 1917, he was elected to the London Mathematical Society. In 1918 he was elected a Fellow of the Royal Society, the second Indian admitted to the Royal Society, following Ardaseer Cursetjee in 1841. At age 31 Ramanujan was one of the youngest Fellows in the history of the Royal Society. He was elected “for his investigation in Elliptic functions and the Theory of Numbers.” On 13 October 1918, he was the first Indian to be elected a Fellow of Trinity College, Cambridge.

Illness and death of Ramanujan

hroughout his life, Ramanujan was plagued by health problems. His health worsened in England; possibly he was also less resilient due to the difficulty of keeping to the strict dietary requirements of his religion in England and wartime rationing during 1914–1918. He was diagnosed with tuberculosis and a severe vitamin deficiency at the time, and was confined to a sanatorium. In 1919 he returned to Kumbakonam, Madras Presidency, and soon thereafter, in 1920, died at the age of 32. After his death, his brother Tirunarayanan chronicled Ramanujan’s remaining handwritten notes consisting of formulae on singular moduli, hypergeometric series and continued fractions and compiled them.

Ramanujan’s widow, Smt. Janaki Ammal, moved to Bombay; in 1931 she returned to Madras and settled in Triplicane, where she supported herself on a pension from Madras University and income from tailoring. In 1950, she adopted a son, W. Narayanan, who eventually became an officer of the State Bank of India and raised a family. In her later years, she was granted a lifetime pension from Ramanujan’s former employer, the Madras Port Trust, and was also granted pensions from, among others, the Indian National Science Academy and the state governments of Tamil Nadu, Andhra Pradesh and West Bengal. She continued to cherish Ramanujan’s memory, and was active in efforts towards increasing his public recognition; prominent mathematicians, including George Andrews, Bruce C. Berndt and Béla Bollobás made it a point to visit her while in India. She died at her Triplicane residence in 1994.

A 1994 analysis of Ramanujan’s medical records and symptoms by Dr. D. A. B. Young concluded that his medical symptoms—including his past relapses, fevers, and hepatic conditions—were much closer to those resulting from hepatic amoebiasis, an illness then widespread in Madras, rather than tuberculosis. He had two episodes of dysentery before he left India. When not properly treated, dysentery can lie dormant for years and lead to hepatic amoebiasis, whose diagnosis was not then well established. At the time, if properly diagnosed, amoebiasis was a treatable and often curable disease; for instance, British soldiers who had contracted the disease during the First World War were being successfully cured of amoebiasis around the time Ramanujan left England.

//source : Wikipedia

Chemistry Science

What is Ionic Bonding?

Ionic bonding is a type of chemical bonding that involves the electrostatic attraction between oppositely charged ions, and is the primary interaction occurring in ionic compounds. It is one of the main bonds along with Covalent bond and Metallic bonding. Ions are atoms that have gained one or more electrons (known as anions, which are negatively charged) and atoms that have lost one or more electrons (known as cations, which are positively charged). This transfer of electrons is known as electrovalence in contrast to covalence. In the simplest case, the cation is a metal atom and the anion is a nonmetal atom, but these ions can be of a more complex nature, e.g. molecular ions like NH+
4 or SO2−
4. In simpler words, an ionic bond is the transfer of electrons from a metal to a non-metal in order to obtain a full valence shell for both atoms.

Over View of Ionic Bond

Atoms that have an almost full or almost empty valence shell tend to be very reactive. Atoms that are strongly electronegative (as is the case with halogens) often have only one or two empty orbitals in their valence shell, and frequently bond with other molecules or gain electrons to form anions. Atoms that are weakly electronegative (such as alkali metals) have relatively few valence electrons, which can easily be shared with atoms that are strongly electronegative. As a result, weakly electronegative atoms tend to distort their electron cloud and form cations.

Formation of Ionic Bond

Ionic bonding can result from a redox reaction when atoms of an element (usually metal), whose ionization energy is low, give some of their electrons to achieve a stable electron configuration. In doing so, cations are formed. An atom of another element (usually nonmetal) with greater electron affinity accepts the electron(s) to attain a stable electron configuration, and after accepting electron(s) an atom becomes an anion. Typically, the stable electron configuration is one of the noble gases for elements in the s-block and the p-block, and particular stable electron configurations for d-block and f-block elements. The electrostatic attraction between the anions and cations leads to the formation of a solid with a crystallographic lattice in which the ions are stacked in an alternating fashion. In such a lattice, it is usually not possible to distinguish discrete molecular units, so that the compounds formed are not molecular in nature. However, the ions themselves can be complex and form molecular ions like the acetate anion or the ammonium cation.

For example, common table salt is sodium chloride. When sodium (Na) and chlorine (Cl) are combined, the sodium atoms each lose an electron, forming cations (Na+), and the chlorine atoms each gain an electron to form anions (Cl−). These ions are then attracted to each other in a 1:1 ratio to form sodium chloride (NaCl).

Na + Cl → Na+ + Cl− → NaCl
However, to maintain charge neutrality, strict ratios between anions and cations are observed so that ionic compounds, in general, obey the rules of stoichiometry despite not being molecular compounds. For compounds that are transitional to the alloys and possess mixed ionic and metallic bonding, this may not be the case anymore. Many sulfides, e.g., do form non-stoichiometric compounds.

Many ionic compounds are referred to as salts as they can also be formed by the neutralization reaction of an Arrhenius base like NaOH with an Arrhenius acid like HCl

NaOH + HCl → NaCl + H2O
The salt NaCl is then said to consist of the acid rest Cl− and the base rest Na+.
The removal of electrons from the cation is endothermic, raising the system’s overall energy. There may also be energy changes associated with breaking of existing bonds or the addition of more than one electron to form anions. However, the action of the anion’s accepting the cation’s valence electrons and the subsequent attraction of the ions to each other releases (lattice) energy and, thus, lowers the overall energy of the system.

Ionic bonding will occur only if the overall energy change for the reaction is favorable. In general, the reaction is exothermic, but, e.g., the formation of mercuric oxide (HgO) is endothermic. The charge of the resulting ions is a major factor in the strength of ionic bonding, e.g. a salt C+A− is held together by electrostatic forces roughly four times weaker than C2+A2− according to Coulombs law, where C and A represent a generic cation and anion respectively. The sizes of the ions and the particular packing of the lattice are ignored in this rather simplistic argument.

Structures of Ionic Bond


Representation of ionic bonding between lithium and fluorine to form lithium fluoride. Lithium has a low ionization energy and readily gives up its lone valence electron to a fluorine atom, which has a positive electron affinity and accepts the electron that was donated by the lithium atom. The end-result is that lithium is isoelectronic with helium and fluorine is isoelectronic with neon. Electrostatic interaction occurs between the two resulting ions, but typically aggregation is not limited to two of them. Instead, aggregation into a whole lattice held together by ionic bonding is the result.

Ionic compounds in the solid state form lattice structures. The two principal factors in determining the form of the lattice are the relative charges of the ions and their relative sizes. Some structures are adopted by a number of compounds; for example, the structure of the rock salt sodium chloride is also adopted by many alkali halides, and binary oxides such as magnesium oxide. Pauling’s rules provide guidelines for predicting and rationalizing the crystal structures of ionic crystals.

Strength of Ionic Bond

For a solid crystalline ionic compound the enthalpy change in forming the solid from gaseous ions is termed the lattice energy. The experimental value for the lattice energy can be determined using the Born–Haber cycle. It can also be calculated (predicted) using the Born–Landé equation as the sum of the electrostatic potential energy, calculated by summing interactions between cations and anions, and a short-range repulsive potential energy term. The electrostatic potential can be expressed in terms of the interionic separation and a constant (Madelung constant) that takes account of the geometry of the crystal. The further away from the nucleus the weaker the shield. The Born-Landé equation gives a reasonable fit to the lattice energy of, e.g., sodium chloride, where the calculated (predicted) value is −756 kJ/mol, which compares to −787 kJ/mol using the Born–Haber cycle.[2][3] In aqueous solution the binding strength can be desribed by the Bjerrum or Fuoss equation as function of the ion charges, rather independent of the nature of the ions such as polaribility or size [4] The strenght of salt bridges is most often evaluated by measurements of equilibria between molecules containing cationic and anionioc sites, most often in solution. [5] Equilibrium constants in water indicate additive free energy contributions for each salt bridge. Another method for the identification of hydrogen bonds also in complicated molecules is crystallography, sometimes also NMR-spectroscopy.


How Works Samsung Galaxy S10’s New Fingerprint Sensor

Samsung revealed the latest generation of its Galaxy S smartphones today, a lineup of four devices packed with multiple cameras, big displays, and in one model, up to a terabyte of built-in storage. But the most interesting trick up Samsung’s metal and glass sleeve is an ultrasonic fingerprint sensor that’s built right into the display of three of these new phones. (Speaking of interesting tricks, Samsung also showed off its forthcoming Galaxy Fold phone, which, as its name implies, will have a folding screen. It will cost nearly $2,000 and be available in April.)



Any smartphone must give its users a way to unlock it, whether that’s through typing a passcode, a biometric system, or both. Current-generation iPhones have front-facing Face ID sensors, while older ones have a fingerprint reader built into the home button. Cameras and buttons, however, take up precious space, or require a notch in the display. One alternative is to put biometric sensors on the back, which is where last year’s Samsung phones, for example, had their fingerprint sensors. This year, that’s changed.

All of Samsung’s Galaxy S10 models (with the exception of the budget-minded S10 Essential) will have a fingerprint sensor hiding under their displays.

Ultra Sonic

The new fingerprint reader is “ultrasonic,” meaning that it uses sound waves to detect a three-dimensional image of your fingerprint. Those sound waves bounce off your finger and return to the phone, allowing it to see the ridges of your print as well as the depth of those valleys.



Anil Jain, a professor of computer science at Michigan State University and expert in biometrics, says that the sound waves are typically around 200 kilohertz when measuring something like a fingerprint. At higher frequencies, ultrasonic testing is used in medicine (you’ve heard of ultrasounds, no doubt), or to look for a flaw inside a metal object, like an airplane wing, Jain says.

In this case, the sensor is using sound waves to measure something it doesn’t have to penetrate deeply: your fingerprint. Samsung says that the sensor can see your print in three-dimensions. “Three-dimensional simply means that they can look at the depth of the ridges and valleys,” Jain says.

This technology is different from other kind of fingerprint sensors, which are either capacitive or optical. The older iPhones, for example, had capacitive sensors built into their home buttons. Those sensors aren’t actively emitting any kind of sound waves, but are just detecting the two-dimensional pattern of your print. A capacitive sensor, for example, is detecting the differing electrical charges caused by the height difference of the ridges and valleys as they push against the sensor, Jain says. An optical fingerprint sensor uses an image of your print.

In general, ultrasonic fingerprint sensors can have their advantages. They can sense “blood flow,” Jain says. That means that if a movie-style villain cuts off your finger and tries to use it to unlock a phone, it might not work, because your amputated digit has no more blood flowing in it. Ultrasonic sensors also do a better job of reading a fingerprint than if it is wet, dry, or dirty, than an optical or capacitive sensor, Jain says.

The only new Samsung phone not to have this sensor is the S10e, which has a capacitive fingerprint reader on the side.


Azolla :in botany

Sporophyte of Azolla:

The sporophyte is extremely small when compared with Marsilea and Sal­vinia. It is distinguishable into stem, leaves and roots. The stem is often called the rhizome. It is profusely branched and on its upper surface is covered with dense leaves. The leaves are alternate and are arranged in two rows. Each leaf has two lobes, the upper lobe being aerial and green in color.

Sporophyte -Azolla

© Picsy Photography

The lower lobe is thin and colourless, and is completely submerged in water. The dorsal lobe encloses large mugilage filled cavities. Inhabiting these mucilage cavities is found a Cyanophycean alga-Anabaena azollae.

According to Oes (1913), the relationship between alga and Azolla is symbiotic. While the alga provides nitrogen to the plant the latter gives it shelter. The same species of Anabaena occurs in Azolla all over the world. The rhizome on its lower surface produces simple roots either singly or in clusters. These roots help in stabilising the plants in water.

Anatomy of Azolla:

The rhizome, anatomically, resembles other ferns. A cross section shows an epidermis, a middle cortex and a central stele. Epidermis is single layered and it encloses a cortex which is 4-8 cells broad. There are no air cavities in the cortex as in Salvinia. The stele is surrounded by an indistinct endodermis. Internal to the endodermis is the pericycle.

The vascular elements are greatly reduced. There are a few tracheids surrounded by phloem elements. It is difficult to determine the stelar type. While Smith (1955) considers it protostelic, Eames (1936) says it is apparently siphonostelic.

T.S. of Azolla

©Picsy Photography

Anatomically, the dorsal lobe of leaf shows two epidermal layers enclosing a thin mesophyll. Stomata are found on both the epidermal layers. The upper epidermis has a number of one to two celled layers. The mesophyll is made up of loosely arranged cells.

Within the mesophyll is found a mucilage filled cavity containing Anabaena. It has been suggested that the hormogones of Anabaena enter into the cavity through a small pore and get themselves established. A cross section of the root shows a thin walled epidermis enclosing a two layered cortex. Next to the cortex is the endodermis made up of six tracheids surrounded by four phloem elements.


The main method of reproduction in Azolla seems to be vegetative fragmenta­tion. The lateral branches get separated and develop into new individuals.

Spore Production:

The spores in Azolla are produced in sporangia which in turn are enclosed in sporocarps as in Marsilea and Salvinia. The sporocarps are usually borne on the first leaf of the lateral branch. In fertile leaves, the submerged lobe is usually divided only twice, and on each a sporocarp is produced terminally. The upper lobe of the leaf forms a marginal flap covering the sporocarp.

The sporocarps are mono-sporangiate. They have either microsporangia or mega-sporangia. There is a size difference also between mega-sporocarps and micro-sporocarps. The former are small and have only one mega-sporangium, while the latter are large and have a number of microsporangia.

The wall of sporocarp is two layered. In a mega-sporocarp, the mega-sporangium arises on a small receptacle at the base. The sporangium is covered by a two layered inducium. In a microsporocarp there is a central cushion like receptacle which gives rise to a number of microsporangia.

The development of the sporangium is of the leptosporangiate type. As the sporangia begin to emerge, a ring of meristematic tissue surrounds the sporangium and forms the sporocarp wall. The wall ultimately becomes two layered thick. In some cases the filaments of Anabaena which are commonly present above the stem apex may get enclosed in the top of the sporocarp cavity.

In a megasporagium there are usually eight mega-sporocytes surrounded by a layer of tapetum. The tapetal cells break down and form a Plasmodium within which are enclosed the sporocytes.

The mega-sporocytes undergo reduction division and produce 32 spores of which all but one degenerate. The dis-organising tapetal cells by now form four massulae. Of these one contains the functional megaspore while the other three hold together the remaining 31 abortive spores.

At maturity the wall of the sporocarp as well as of the sporangium break open helping in the further development. The development of the microsporangium is similar to that of mega-sporangium until the sporocyte stage. In the microsporan­gium all the 32 spores are functional. These spores get enclosed by the tapetal Plasmodium. Here also the Plasmodium forms four massulae, each containing more than one microspore.

In Azolla filiculoides and A. caroliniana, many hooked processes arise from the massulae. These are called ‘Glochidia’. Soon after the maturation, the sporangial wall dehisces and massulae with microspores lie freely in the cavity of the sporocarp. Subsequently, when the sporocarp wall ruptures the massulae with the spores come out. The glochidia help in the attachment of the microspore massulae to the megaspore massulae.

Gametophyte of Azolla:

The mature sporocarps usually sink to the bottom of the pond where the release of the massulae from the sporocarp takes place.

Development of Male Gametophyte:

The microspore germinates within the massula. The spore wall breaks open and a small projection comes out. This projection is cut off by a cross wall at its base. The large cell filling the spore cavity cuts off a small lenticular basal call.

The outer cell divides into three, by cross walls. Of these, the outer and inner cells do not divide and they develop into the cap and basal cells of the antheridium. In the central two cells, a periclinal divisions take place forming a central cell and two jacket cells.

A division in one of the outer cells ultimately results in a total of five jacket cells surrounding a central cell. By further divisions the central cell produces eight spermatocytes. The spermatocytes metamorphose into spermatozoids.

Development of Female Gemetophyte:

Germination takes place in situ. The gametophyte never comes out of the confines of the spore. In the early stages of development Azolla resembles Salvinia. The first division forms a large basal cell and a terminal lenticular cell.

The lenticular cell by further divisions forms an apical cushion from which an archegonium is formed. At this stage, the spore wall breaks open and the gametophyte bulges out a little. The archegonium in its structure and development resembles that of Salvinia. The lower large cell undergoes free nuclear divisions and serves as a store house of reserve food material.

Fertilization of Azolla:

Fertilisation is effected when the sperms released from the micro-gametophyte reach the archegoniuim.


The first division of zygote is transverse. Subsequent divisions form the quadrant, from which develop the four primary organs of the plant namely, foot, root, stem, and leaf. The lower quadrant forms the root and foot while the upper quadrant forms the leaf and stem.

The foot is cylindrical. It does not have further growth. The other three organs grow by means of an apical cell. The first leaf is like a funnel and it surrounds the stem apex. The development of the root is very slow. As the embryo continues its growth the upper portions of the sporocarp and massulae are thrown off. The embryo rises to the surface of water when air chambers develop within the first leaf.

Phylogeny of Azolla:

The two genera, Salvinia and Azolla share many characters and also have many differences. The similarity in reproductive details are very striking though there is difference in the morphology of the plant body between the two genera. It is clear that Azolla has a natural affinity with Savinia, though the same cannot be said with Marsilea.

According to Eames (1964), the Salviniaceae includes Azolla also, because the similarities between the two are so close as to be placed in a single family. He also opines that the Salviniaceae represents a highly specialized offshoot arising from a primitive Leptosporangiate group.


Lyme disease A tick-borne illness & Symptoms of Disease

Medical Definition of Lyme disease

An acute inflammatory disease that is usually characterized initially by the skin lesion erythema migrans and by fatigue, fever, and chills and if left untreated may later manifest itself in cardiac and neurological disorders, joint pain, and arthritis and that is caused by a spirochete of the genus Borrelia (B. burgdorferi) transmitted by the bite of a tick especially of the genus Ixodes (I. scapularis synonym I. dammini in the eastern and midwestern United States, I. pacificus especially in some parts of the Pacific coastal states of the United States, and I. ricinus in Europe)

What are the symptoms of Lyme disease?


Early symptoms of Lyme disease involve:

  • A rash that looks like a bull’s eye ( scientific name: erythema migrans)
  • Fever
  • Chills
  • Headache
  • Fatigue
  • Muscle and joint aches
  • Swollen lymph nodes

According to the CDC, symptoms can start between 3 to 30 days after the tick bite (average is about 7 days). The rash expands gradually and can reach up to 12 inches. or in some cases even more. It can also feel warm to the touch but is rarely itchy or painful.

Later signs and symptoms:

  • Severe headaches and neck stiffness
  • Rashes on other parts of the body
  • Arthritis with severe joint pain and swelling, especially in the knees.
  • Loss of muscle tone
  • Intermittent pain in tendons, muscles, joints, and bones
  • Heart palpitations or an irregular heartbeat
  • Dizziness or shortness of breath
  • Inflammation of the brain and spinal cord
  • Shooting pains, numbness, or tingling in the hands or the feet
  • Short-term memory problems

Treatment of Lyme disease by antibiotics

Most people with Lyme disease recover completely with appropriate antibiotic treatment. For those who develop syndromes after their infection is treated, pain medication may provide symptomatic relief.


Stops the growth of or kills bacteria.
Penicillin antibiotic
Stops growth of or kills specific bacteria.
Nonsteroidal anti-Inflammatory drug
Relieves pain, decreases inflammation and reduces fever.

Most Common Diseases caused by Air Pollution
Diseases Science

10 Most Common Diseases caused by Air Pollution in 2019

Air Pollution is one of the most widespread pollution and is one of the inevitable ones. Being an ever-pervading medium and carrier, air can transfer the pollutants very fast in no time; making it almost impossible for any person breathing in the polluted air, to avoid the infection. Though the pollutant level, reaction to the pollutants and infestation of the pollutant based diseases in every person is different; the fact that air pollution can have injurious effects on the human body can just not be ignored.

This post shall be focusing on 10 such diseases caused by the air pollution and what pollutants cause them.

#1 — Asthma:

This is one of the most common diseases that can affect the humans breathing in the polluted air. This is a chronic disease in which inflammation is caused in the air passages of the human body and the person finds it difficult to breathe. Heavy breathing while doing normal routine activities and strenuous ones are some of the basic symptoms of the disease.

Asthma is caused by the particulate matter, oxides of sulfur and nitrogen and ground-level ozone. Tobacco smoke can also be a cause of the same and the parents, friends, family members and other people in close contact with the patient should refrain from smoking in his or her presence.

One of the things that the asthma patients can do is use the Fresh Air Bottles in order to give a blast of pure and fresh air to their lungs and respiratory system. However, the consultation with a physician first is advised.

#2 — Lung Cancer:

Owing to the presence of various carcinogens in the air, the lungs can get infested with them which in turn can lead to lung or pulmonary cancer. The disease involves uncontrolled growth of the cells in one or both of the lungs causing a reduction in the oxygen-carrying capacity and malfunctioning in the complete working of the respiratory system.

Though the lung cancer cures depend on the type of cancer and the level of infection in the lungs, the Fresh Air Cans may be a possible solution to reduce the effect of such carcinogens in the polluted air.

#3 — COPD (Chronic Obstructive Pulmonary Disease)

COPD is caused by the air pollution in which the air passages and air sacs or the alveoli change their shape and become distended. Thus, the patient finds it difficult to breathe even while sitting or doing nothing. Emphysema and Chronic Bronchitis are two types of COPD which are common and can lead to cancer and premature deaths as well.

The most affected people are the people working in the mines, quarries and docks etc that are in constant contact with the dust, fine dust, and diesel fumes etc.

Using air purifiers and Fresh Air Cans may be prevention but complete cure requires intensive doctoral involvement and medicines.

#4 — Leukemia:

It is a disease (the type of cancer) caused by exposure to the benzene vapors and is fatal as well. The WBCs or the White Blood Cells get increased in the amount owing to persistent infection caused by the infection and the respiratory tract is infected heavily.

#5 — Pneumonia:

Polluted air also carries bacteria that get inhaled into the respiratory tract which in turn causes pneumonia. The disease might get worse with continued breathing of the polluted air and the disease might get worse with some other disease caused by the pollution.

Using air filters wherever possible and Fresh Air Bottles might be a probable prevention of the disease and might prove beneficial for the patients as well. But immediate doctor assistance is important and advised in all cases.

#6 — Birth defects and immune system defects:

There are a number of defects that can occur in the newborn as well as unborn babies owing to exposure to the polluted air and breathing of polluted air by the pregnant mother respectively. The babies born in the areas with air pollution will have lower immunity against the infections, cough, and cold and might also exhibit some inborn allergies as well.

The pregnant ladies can consult with the doctors and use the air filters as well as the Fresh Air Cans which are immunity boosters and nullify the effect of the pollutants on the respiratory system.

#7 — Autism:

Recent studies have revealed that air pollution can also cause Autism — a disease in which the patient has a tendency to live alone.

#8 — Weakening of Lung Function:

If the level of the air pollution is not high, there might be a general or gradual weakening of the lung function in the people breathing in the polluted air. This can be exhibited in a number of forms such as allergies, panting while doing heavy or normal daily routine activities and very low immunity to a cough and cold etc.

Auzair Fresh Air Bottles may help in counter-effecting all such infections and thus help the body to regain its strength.

#9 — Cardiovascular Diseases:

Owing to the presence of a number of poisonous substances in the polluted air, poisonous gases, and particulate matter, the people living in the polluted environment exhibit a lot of cardiovascular diseases of various kinds. The extent of exposure to the pollutants can determine the degree of the disease and infection.

#10 — Premature Deaths:

It has been found that pollutants in the air can lead to premature deaths owing to different reasons such as asphyxiation and extreme reactions caused by the body to the pollutant matter. Every year a huge number of premature deaths are registered all across the world owing to the pollution.

Though the ever pervading air pollution is really difficult to be handled and fought with, the Fresh Air Bottles can be a big help. These bottles are filled with pure air, every single breath of which sends a boost of freshness and life down to the cellular level.

Charles Darwin

Charles Darwin : Writer of The Descent of Man


Charles Darwin, in full Charles Robert Darwin, (born February 12, 1809, Shrewsbury, Shropshire, England—died April 19, 1882, Downe, Kent), English naturalist whose scientific theory of evolution by natural selection became the foundation of modern evolutionary studies. An affable country gentleman, Darwin at first shocked religious Victorian society by suggesting that animals and humans shared a common ancestry. However, his nonreligious biology appealed to the rising class of professional scientists, and by the time of his death evolutionary imagery had spread through all of science, literature, and politics. Darwin, himself an agnostic, was accorded the ultimate British accolade of burial in Westminster Abbey, London.

Darwin formulated his bold theory in private in 1837–39, after returning from a voyage around the world aboard HMS Beagle, but it was not until two decades later that he finally gave it full public expression in On the Origin of Species (1859), a book that has deeply influenced modern Western society and thought.

Top Questions About Darwin

Charles Darwin’s theory of evolution by natural selection is the foundation upon which modern evolutionary theory is built. The theory was outlined in Darwin’s seminal work On the Origin of Species, published in 1859. Although Victorian England (and the rest of the world) was slow to embrace natural selection as the mechanism that drives evolution, the concept of evolution itself gained widespread traction by the end of Darwin’s life.
Charles Darwin’s theory of evolution had three main components: that variation occurred randomly among members of a species; that an individual’s traits could be inherited by its progeny; and that the struggle for existence would allow only those with favorable traits to survive. Although many of his ideas have been borne out by modern science, Darwin didn’t get everything right: traces of Jean-Baptiste Lamarck’s outdated theory of evolution remained in Darwin’s own. He was also unable to correctly establish how traits were inherited, which wasn’t clarified until the rediscovery of Gregor Mendel’s work with peas.
Growing up, Charles Darwin was always attracted to the sciences. In 1825 his father sent him to the University of Edinburgh to study medicine. There he was exposed to many of the dissenting ideas of the time, including those of Robert Edmond Grant, a former student of the French evolutionist Jean-Baptiste Lamarck. He transferred to Christ’s College, Cambridge, in 1828, where his mentors mostly endorsed the idea of providential design. A botany professor suggested he join a voyage on the HMS Beagle—a trip that would provide him with much of his evidence for the theory of evolution by natural selection.

Darwin formulated his bold theory in private in 1837–39, after returning from a voyage around the world aboard HMS Beagle, but it was not until two decades later that he finally gave it full public expression in On the Origin of Species (1859), a book that has deeply influenced modern Western society and thought.

Charles Darwin's

HMS Beagle voyage A map of Charles Darwin’s voyage on the HMS Beagle in 1831–36

Early life and education

Darwin was the second son of society doctor Robert Waring Darwin and of Susannah Wedgwood, daughter of the Unitarian pottery industrialist Josiah Wedgwood. Darwin’s other grandfather, Erasmus Darwin, a freethinking physician and poet fashionable before the French Revolution, was author of Zoonomia; or the Laws of Organic Life (1794–96). Darwin’s mother died when he was eight, and he was cared for by his three elder sisters. The boy stood in awe of his overbearing father, whose astute medical observations taught him much about human psychology. But he hated the rote learning of Classics at the traditional Anglican Shrewsbury School, where he studied between 1818 and 1825. Science was then considered dehumanizing in English public schools, and for dabbling in chemistry Darwin was condemned by his headmaster (and nicknamed “Gas” by his schoolmates).

His father, considering the 16-year-old a wastrel interested only in game shooting, sent him to study medicine at Edinburgh University in 1825. Later in life, Darwin gave the impression that he had learned little during his two years at Edinburgh. In fact, it was a formative experience. There was no better science education in a British university. He was taught to understand the chemistry of cooling rocks on the primitive Earth and how to classify plants by the modern “natural system.” At the Edinburgh Museum he was taught to stuff birds by John Edmonstone, a freed South American slave, and to identify the rock strata and colonial flora and fauna.

More crucially, the university’s radical students exposed the teenager to the latest Continental sciences. Edinburgh attracted English Dissenters who were barred from graduating at the Anglican universities of Oxford and Cambridge, and at student societies Darwin heard freethinkers deny the Divine design of human facial anatomy and argue that animals shared all the human mental faculties. One talk, on the mind as the product of a material brain, was officially censored, for such materialism was considered subversive in the conservative decades after the French Revolution. Darwin was witnessing the social penalties of holding deviant views. As he collected sea slugs and sea pens on nearby shores, he was accompanied by Robert Edmond Grant, a radical evolutionist and disciple of the French biologist Jean-Baptiste Lamarck. An expert on sponges, Grant became Darwin’s mentor, teaching him about the growth and relationships of primitive marine invertebrates, which Grant believed held the key to unlocking the mysteries surrounding the origin of more-complex creatures. Darwin, encouraged to tackle the larger questions of life through a study of invertebrate zoology, made his own observations on the larval sea mat (Flustra) and announced his findings at the student societies.

The young Darwin learned much in Edinburgh’s rich intellectual environment, but not medicine: he loathed anatomy, and (pre-chloroform) surgery sickened him. His freethinking father, shrewdly realizing that the church was a better calling for an aimless naturalist, switched him to Christ’s College, Cambridge, in 1828. In a complete change of environment, Darwin was now educated as an Anglican gentleman. He took his horse, indulged his drinking, shooting, and beetle-collecting passions with other squires’ sons, and managed 10th place in the Bachelor of Arts degree in 1831. Here he was shown the conservative side of botany by a young professor, the Reverend John Stevens Henslow, while that doyen of Providential design in the animal world, the Reverend Adam Sedgwick, took Darwin to Wales in 1831 on a geologic field trip.

Fired by Alexander von Humboldt’s account of the South American jungles in his Personal Narrative of Travels, Darwin jumped at Henslow’s suggestion of a voyage to Tierra del Fuego, at the southern tip of South America, aboard a rebuilt brig, HMS Beagle. Darwin would not sail as a lowly surgeon-naturalist but as a self-financed gentleman companion to the 26-year-old captain, Robert Fitzroy, an aristocrat who feared the loneliness of command. Fitzroy’s was to be an imperial-evangelical voyage: he planned to survey coastal Patagonia to facilitate British trade and return three “savages” previously brought to England from Tierra del Fuego and Christianized. Darwin equipped himself with weapons, books (Fitzroy gave him the first volume of Principles of Geology, by Charles Lyell), and advice on preserving carcasses from London Zoo’s experts. The Beagle sailed from England on December 27, 1831.


Most Common Infectious Diseases

Infectious diseases are disorders caused by organisms — such as bacteria, viruses, fungi or parasites. Many organisms live in and on our bodies. They’re normally harmless or even helpful, but under certain conditions, some organisms may cause disease. Some infectious diseases can be passed from person to person.

Hepatitis B

According to current statistics, hepatitis B is the most common infectious disease in the world, affecting some 2 billion people — that’s more than one-quarter of the world’s population. This disease, which is characterized by an inflammation of the liver that leads to jaundice, nausea, and fatigue, can lead to long-term complications such as cirrhosis of the liver or even liver cancer. The concern is primarily for those who carry the chronic form of the disease, which is estimated to be about 350 million people.

Perhaps one of the best known therapies here is Gilead Sciences’ (NASDAQ:GILD) Viread, which was approved in the U.S. in 2008 and blocks an enzyme that the hepatitis B virus needs to replicate in liver cells. According to Gilead’s third-quarter report, sales of the drug were up 11% through the first nine months over the previous year, and it should deliver more than $900 million in cumulative sales by the time fiscal 2013 is over. With a strong presence in AIDS therapies as well, Gilead is quickly becoming an infectious-disease juggernaut.

Another name to keep an eye on here is Dynavax Technoloogies (NASDAQ:DVAX). Although the FDA has been less than cooperative with Dynavax’s attempts to bring Heplisav to market, implying that the company may need to run an additional trial to satisfy its safety concerns, Heplisav had demonstrated impressive efficacy in clinical trials.


Malaria, a mosquito-borne disease that tends to affect children the most in tropical and subtropical climates, affects more than 500 million people annually and results in anywhere between 1 million and 3 million deaths. Behind hepatitis B, it appears to be the second most-common infectious disease, and it certainly is one of the most deadly on an annual basis.

Increasing public awareness of the dangers of mosquitoes in tropical and subtropical climates has helped somewhat, but malaria cases have unfortunately been on the rise again in recent years. The most common anti-malarial medication available is an oral therapy known as Lariam, which the U.S. Army invented in the late 1980s but was licensed to Roche (NASDAQOTH:RHHBY), which sold it through August 2009. The drug is now sold in generic versions.

While a relatively effective first-line preventative treatment and second-line therapy following contraction of the disease, Lariam also has a laundry list of side effects, including serious neurological and psychiatric side effects that, in July, prompted the FDA to beef up its stance concerning Lariam with a black-box warning.

Hepatitis C

Hepatitis C is a less common and less severe form of hepatitis, but it almost always develops into a chronic, not acute, condition, unlike hepatitis B. Although only 3 million to 4 million new cases are reported each year, some 180 million people worldwide suffer from this chronic condition, which can lead to liver cancer or cirrhosis of the liver over time.

Advancements in the U.S. for treating hepatitis C have been nothing short of breathtaking over the past three years. Three years ago, the standard of treatment involved pegylated interferon and a ribavirin over the course of 24 or 48 weeks. The net result was a response (not a cure, just a response) in around 50% of HCV-positive patients. With the approval of Gilead Sciences’ Sovaldi earlier this month, patients with genotype 1 (the most common form of the disease) can expect a sustained virologic response, or SVR (an undetectable level of disease), after 12 weeks in more than 90% of cases.

In addition, AbbVie (NYSE:ABBV) is also developing its own direct-acting antiviral combo drug, which has demonstrated a 12-week SVR of greater than 90% as well in the tough-to-treat genotype 1 patient subset. It’s extremely rare to develop a cure for such a global disease nowadays, but we could well be on our way to one when it comes to treating hepatitis C.


It’s at times like these that we curse mosquitoes, because a very specific type of mosquito (Aedes aegypti) is responsible for the transmission of dengue to approximately 50 million people each year. Dengue is most common in Africa and Asia and thankfully occurs in only mild to moderate forms, which can cause high fever, severe headaches, and joint and muscle pain, but rarely leads to the death of the infected patient.

Amazingly enough, even though this infectious disease affects some 50 million people annually, there isn’t a specific drug designed to treat dengue fever. The most commonly prescribed medication to reduce the symptoms associated with dengue fever is … Tylenol. That’s right, Johnson & Johnson’s (NYSE:JNJ) Tylenol, whose active ingredient is acetaminophen, works to reduce both fever and muscle pain in patients. In the most serious cases of dengue fever, IVs and blood transfusions may be needed.


As I mentioned previously, estimating new and ongoing cases for some of these diseases can be downright difficult, and perhaps none more so than tuberculosis. TB is caused by a bacteria found in the lungs that can cause chest pain and a bad cough, as well as lead to a number of other nasty side effects. According to WHO, it’s also the second-leading global killer behind AIDS as a single infectious agent.

The majority of TB-associated deaths (95%) occur in low- to middle-income countries where TB awareness and prevention simply aren’t where they need to be. The good news is that TB death rates on a global basis are falling; however, there were still 8.6 million new cases of TB reported last year, and roughly one-third of the world’s population carries a latent form of TB, meaning they’ve been infected but aren’t ill and can’t transmit the disease yet.

While many of today’s TB treatments have long since come off patent, the FDA did approve a new drug in late 2012 named Sirturo, made by Johnson & Johnson, to treat multidrug-resistant TB. Plainly put, not all strains of TB respond to the common forms of treatment, and MDR-TB is an especially virulent killer, so Sirturo has a genuine shot at treating what is essentially the worst of the worst when it comes to TB strains. Peak sales estimates for the drug range between $300 million and $400 million.

source :The Motley Fool