A tribute to Mirza Ghalib, the legendary poet

coastaldigest.com web desk 
December 27, 2017

Poet and philosopher Mirza Ghalib, who contributed greatly towards Urdu and Persian literature, was paid tributes by the Google with its doodle on his 220th birth anniversary on December 27, 2017. The Google Doodle fittingly shows Ghalib with his pen and paper, knitting his imagination, with a backdrop of buildings of Mughal architecture.

In its blog post, Google said, “His (Ghalib) verse is characterised by a lingering sadness borne of a tumultuous and often tragic life — from being orphaned at an early age, to losing all of his seven children in their infancy, to the political upheaval that surrounded the fall of Mughal rule in India. He struggled financially, never holding a regular paying job but instead depending on patronage from royalty and more affluent friends.”

“But despite these hardships, Ghalib navigated his circumstances with wit, intellect, and an all-encompassing love for life. His contributions to Urdu poetry and prose were not fully appreciated in his lifetime, but his legacy has come to be widely celebrated, most particularly for his mastery of the Urdu ghazal (amatory poem),” the post added.

Born on December 27, 1797 in Agra, when Mughal Empire was counting its last days, Mirza Ghalib began his literary works at the age of 11. Although his first language was Urdu, Turkish and Persian were spoken at home too. After getting married by the age of 13, he settled in Delhi. 

In one of his letters, Ghalib describes his marriage as the second imprisonment after the initial confinement that was life itself. The idea that life is one continuous painful struggle which can end only when life itself ends, is a recurring theme in his poetry.

His poem and Ghazals have been translated and recited in multiple languages across the globe. In 1850, he was honoured with the title of Dabir-ul-Mulk by Mughal emperor Bahadur Shah Zafar II. During the last years of the Mughal Empire, Mirza Ghalib was not only an important member of the Mughal court, but also the poet tutor to the emperor's eldest son, Prince Fakhr-ud Din Mirza. The emperor also appointed him as the royal historian of the Mughal court.

Following the decline of the Mughal Empire, Mirza Ghalib struggled to make a living. Much of his fame came to him posthumously and in his lifetime, despite his best attempts, he couldn't get the British to restore his full pension.

Mirza Ghalib died in Delhi on 15 February 1869 and the house where he lived, in Old Delhi, has been turned into "Ghalib Memorial". Known as "Ghalib ki Haveli", it permanently houses Ghalib's exhibitions.

Imprints on heart and mind

One of the recurring themes in Mirza Ghalib's poems is the idea that life is a continuous painful struggle which ends only with life itself. His poems perfectly capture the pathos of love and continue to be relevant even after all these years.  Here are some of the famous sher by the legendary poet that manage to pierce the heart:

aah ko chaahiye ik umr asar hone tak
kaun jeeta hai teri zulf ke sar hone tak

(Translation: A lifetime passes before a sigh shows its effect, who would wait so long to see you fixing the tangles in your hair)

un ke dekhe se jo aa jaati hai munh par raunaq
vo samajhte hain ki beemar ka haal achha hai

(Translation: My face lights up when I see her and she feels that the sick me is now okay)

hazaron khwahishen aisi ki har khwahish pe dam nikle,
bahut nikle mire armaan lekin phir bhi kam nikle

(Translation: I have a thousand desires, all desires worth dying for,
Though many of my desires were fulfilled, many remained unfulfilled)

hum ko maalum hai jannat ki haqiqat lekin
dil ke khush rakhne ko 'ghalib' ye khayal achha hai

(Translation: We know what's the truth, but to please yourself, this thought is good)

hum toh fanaah ho gaye uskii aankhen dekh kar, Ghalib,
na jaanein woh aaina kaise dekhte hongey

(Translation: I just lost my mind after seeing her eyes, Ghalib,
I wonder how she sees herself in the mirror)

ye na thi hamari qismat ki visal-e-yaar hota
agar aur jeete rahte yahi intezar hota

(Translation: That my love be consummated, fate did not ordain
Living longer had I waited, would have been in vain)

Kaid-e-hayat O band-e-gham asalm men donon ek hain
Mauth se pahle aadmi gham se najat paye kyon?

(Translation: The prison of life and the bondage of grief are one and the same/ Before the onset of death, why should man expect to be free of grief?)

Comments

Sameer
 - 
Tuesday, 16 Jan 2018

Good article. Translation of poem is poor.

Muhammed Ali Uchil
 - 
Wednesday, 27 Dec 2017

Super article, a fiiting tribute to this great poet

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Agencies
March 8,2020

Panic gripped big tech firms like Facebook and Twitter which decided to close their offices from Seattle to London as more employees tested positive for the new coronavirus.

Facebook shut its three London offices till Monday after an employee was diagnosed with COVID-19.

The social networking giant told nearly 3,000 employees in London to work from home after an employee, who is based in Singapore but visited the London offices between February 24-26, was diagnosed with the new coronavirus, Sky News reported on Friday.

"An employee based in our Singapore office who has been diagnosed with COVID-19 visited our London offices on February 24-26.

"We are therefore closing our London offices until Monday for deep cleaning and employees are working from home until then," the company said in a statement.

There have been 163 cases of coronavirus so far in the UK.

Earlier, Facebook recommended all its Bay Area employees in the US to work from home. The latest precautions come after San Francisco announced its first two coronavirus cases on Thursday.

Facebook has also shut its Seattle office until Monday after one of its contractors was confirmed to be infected with the virus. The infected contractor last visited the Facebook office on February 21. King County health officials said all Facebook sites should work from home until March 31.

Twitter shut its Seattle office for a 'deep clean' after an employee developed COVID-19 like symptoms though final result was still awaited.

"A Seattle-based employee has been advised by doctor about likely COVID-19, though still awaiting the final testing," Twitter said in a tweet on Friday.

"While the employee has not been at a Twitter office for several weeks and hasn't been in contact w/others, we're closing our Seattle office to deep clean," the company added.

According to The Seattle Times, at least 14 people have died due to COVID-19 in Washington State till date.

Amazon, Microsoft, Google and Facebook have advised their employees in Washington State to work from home.

Apple has reportedly suggested its employees at California campuses to work from home as an "extra precaution" while new coronavirus cases spread on the west coast in the US, especially Seattle area.

Apple's flagship developers' conference WWDC 2020 in June is also at the risk of getting cancelled as the Santa Clara public health department has warned against large public gatherings. The event draws nearly 5,000 developers from across the world.

The US death toll from the new coronavirus has climbed to 14, according to Johns Hopkins' tracker, with 329 cases reported across the country.

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August 9,2020

When researcher Monica Gandhi began digging deeper into outbreaks of the novel coronavirus, she was struck by the extraordinarily high number of infected people who had no symptoms.

A Boston homeless shelter had 147 infected residents, but 88% had no symptoms even though they shared their living space. A Tyson Foods poultry plant in Springdale, Ark., had 481 infections, and 95% were asymptomatic.

Prisons in Arkansas, North Carolina, Ohio and Virginia counted 3,277 infected people, but 96% were asymptomatic.

During its seven-month global rampage, the coronavirus has claimed more than 700,000 lives. But Gandhi began to think the bigger mystery might be why it has left so many more practically unscathed.

What was it about these asymptomatic people, who lived or worked so closely to others who fell severely ill, she wondered, that protected them? Did the "dose" of their viral exposure make a difference? Was it genetics? Or might some people already have partial resistance to the virus, contrary to our initial understanding?

Efforts to understand the diversity in the illness are finally beginning to yield results, raising hope that the knowledge will help accelerate development of vaccines and therapies - or possibly even create new pathways toward herd immunity in which enough of the population develops a mild version of the virus that they block further spread and the pandemic ends.

"A high rate of asymptomatic infection is a good thing," said Gandhi, an infectious-disease specialist at the University of California at San Francisco. "It's a good thing for the individual and a good thing for society."

The coronavirus has left numerous clues - the uneven transmission in different parts of the world, the mostly mild impact on children. Perhaps most tantalizing is the unusually large proportion of infected people with mild symptoms or none at all. The Centers for Disease Control and Prevention last month estimated that rate at about 40%.

Those clues have sent scientists off in different directions: Some are looking into the role of the receptor cells, which the virus uses to infiltrate the body, to better understand the role that age and genetics might play. Others are delving into masks and whether they may filter just enough of the virus so those wearing them had mild cases or no symptoms at all.

The theory that has generated the most excitement in recent weeks is that some people walking among us might already have partial immunity.

When SARS-CoV-2, the technical name of the coronavirus that causes the disease covid-19, was first identified on Dec. 31, 2019, public health officials deemed it a "novel" virus because it was the first time it had been seen in humans who presumably had no immunity from it whatsoever. There's now some very early, tentative evidence suggesting that assumption might have been wrong.

One mind-blowing hypothesis - bolstered by a flurry of recent studies - is that a segment of the world's population may have partial protection thanks to "memory" T cells, the part of our immune system trained to recognize specific invaders. 

This could originate from cross-protection derived from standard childhood vaccinations. Or, as a paper published Tuesday in Science suggested, it could trace back to previous encounters with other coronaviruses, such as those that cause the common cold.

"This might potentially explain why some people seem to fend off the virus and may be less susceptible to becoming severely ill," National Institutes of Health Director Francis Collins remarked in a blog post this past week.

On a population level, such findings, if validated, could be far-reaching.

Hans-Gustaf Ljunggren, a researcher at Sweden's Karolinska Institute, and others have suggested that public immunity to the coronavirus could be significantly higher than what has been suggested by studies. In communities in Barcelona, Boston, Wuhan and other major cities, the proportion of people estimated to have antibodies and therefore presumably be immune has mostly been in the single digits. But if others had partial protection from T cells, that would raise a community's immunity level much higher.

This, Ljunggren said, would be "very good news from a public health perspective."

Some experts have gone so far as to speculate about whether some surprising recent trends in the epidemiology of the coronavirus - the drop in infection rates in Sweden where there have been no widespread lockdowns or mask requirements, or the high rates of infection in Mumbai's poor areas but little serious disease - might be due to preexisting immunity.

Others say it's far too early to draw such conclusions. Anthony Fauci, the United States' top infectious-disease expert, said in an interview that while these ideas are being intensely studied, such theories are premature. He said at least some partial preexisting immunity in some individuals seems a possibility.

And he said the amount of virus someone is exposed to - called the inoculum - "is almost certainly an important and likely factor" based on what we know about other viruses.

But Fauci cautioned that there are multiple likely reasons - including youth and general health - that determine whether a particular individual shrugs off the disease or dies of it. That reinforces the need, in his view, for continued vigilance in social distancing, masking and other precautions.

"There are so many other unknown factors that maybe determine why someone gets an asymptomatic infection," Fauci said. "It's a very difficult problem to pinpoint one thing."

- - -

News headlines have touted the idea based on blood tests that 20% of some New York communities might be immune, 7.3% in Stockholm, 7.1% in Barcelona. Those numbers come from looking at antibodies in people's blood that typically develop after they are exposed to a virus. But scientists believe another part of our immune system - T cells, a type of white blood cell that orchestrates the entire immune system - could be even more important in fighting against the coronavirus.

Recent studies have suggested that antibodies from the coronavirus seem to stick around for two to three months in some people. While work on T cells and the coronavirus is only getting started - testing T cells is much more laborious than antibody testing - previous research has shown that, in general, T cells tend to last years longer.

One of the first peer-reviewed studies on the coronavirus and T cells was published in mid-May in the journal Cell by Alessandro Sette, Shane Crotty and others at the La Jolla Institute for Immunology near San Diego.

The group was researching blood from people who were recovering from coronavirus infections and wanted to compare that to samples from uninfected controls who were donors to a blood bank from 2015 to 2018. The researchers were floored to find that in 40% to 60% of the old samples, the T cells seemed to recognize SARS-CoV-2.

"The virus didn't even exist back then, so to have this immune response was remarkable," Sette said.

Research teams from five other locations reported similar findings. In a study from the Netherlands, T cells reacted to the virus in 20% of the samples. In Germany, 34%. In Singapore, 50%.

The different teams hypothesized this could be due to previous exposure to similar pathogens. Perhaps fortuitously, SARS-CoV-2 is part of a large family of viruses. Two of them - SARS and MERS - are deadly and led to relatively brief and contained outbreaks. Four other coronavirus variants, which cause the common cold, circulate widely each year but typically result in only mild symptoms. Sette calls them the "less-evil cousins of SARS-CoV-2."

This week, Sette and others from the team reported new research in Science providing evidence the T cell responses may derive in part from memory of "common cold" coronaviruses.

"The immune system is basically a memory machine," he said. "It remembers and fights back stronger."

The researchers noted in their paper that the strongest reaction they saw was against the spike proteins that the virus uses to gain access to cells - suggesting that fewer viral copies get past these defenses.

"The current model assumes you are either protected or you are not - that it's a yes or no thing," Sette added. "But if some people have some level of preexisting immunity, that may suggest it's not a switch but more continuous."

- - -

More than 2,300 miles away, at the Mayo Clinic in Cleveland, Andrew Badley was zeroing in the possible protective effects of vaccines.

Teaming up with data experts from Nference, a company that manages their clinical data, he and other scientists looked at records from 137,037 patients treated at the health system to look for relationships between vaccinations and coronavirus infection.

They knew that the vaccine for smallpox, for example, had been shown to protect against measles and whooping cough. Today, a number of existing vaccines are being studied to see whether any might offer cross-protection against SARS-CoV-2.

When SARS-CoV-2, the technical name of the coronavirus that causes the disease covid-19, was first identified on Dec. 31, 2019

The results were intriguing: Seven types of vaccines given one, two or five years in the past were associated with having a lower rate of infection with the new coronavirus. Two vaccines in particular seemed to show stronger links: People who got a pneumonia vaccine in the recent past appeared to have a 28% reduction in coronavirus risk. Those who got polio vaccines had a 43% reduction in risk.

Venky Soundararajan, chief scientific officer of Nference, remembers when he first saw how large the reduction appeared to be, he immediately picked up his phone and called Badley: "I said, 'Is this even possible?'"

The team looked at dozens of other possible explanations for the difference. It adjusted for geographic incidence of the coronavirus, demographics, comorbidities, even whether people had had mammograms or colonoscopies, under the assumption that people who got preventive care might be more apt to social distance. But the risk reduction still remained large.

"This surprised us completely," Soundararajan recalled. "Going in we didn't expect anything or maybe one or two vaccines showing modest levels of protection."

The study is only observational and cannot show a causal link by design, but Mayo researchers are looking at a way to quantify the activity of these vaccines on the coronavirus to serve as a benchmark to the new vaccines being created by companies such as Moderna. If existing vaccines appear as protective as new ones under development, he said, they could change the world's whole vaccine strategy.

- - -

Meanwhile, at NIH headquarters in Bethesda, Md., Alkis Togias has been laser-focused on one group of the mildly affected: children. He wondered whether it might have something to do with the receptor known as ACE2, through which the virus hitchhikes into the body.

In healthy people, the ACE2 receptors perform the important function of keeping blood pressure stable. The novel coronavirus latches itself to ACE2, where it replicates. Pharmaceutical companies are trying to figure out how to minimize the receptors or to trick the virus into attaching itself to a drug so it does not replicate and travel throughout the body.

Was it possible, Togias asked, that children naturally expressed the receptor in a way that makes them less vulnerable to infection?

He said recent papers have produced counterintuitive findings about one subgroup of children - those with a lot of allergies and asthma. The ACE2 receptors in those children were diminished, and when they were exposed to an allergen such as cat hair, the receptors were further reduced. Those findings, combined with data from hospitals showing that asthma did not seem to be a risk factor for the respiratory virus, as expected, have intrigued researchers.

"We are thinking allergic reactions may protect you by down-regulating the receptor," he said. "It's only a theory of course."

Togias, who is in charge of airway biology for the National Institute of Allergy and Infectious Diseases, is looking at how those receptors seem to be expressed differently as people age, as part of a study of 2,000 U.S. families. By comparing those differences and immune responses within families, they hope to be able to better understand the receptors' role.

Separately, a number of genetic studies show variations in genes associated with ACE2 with people from certain geographic areas, such as Italy and parts of Asia, having distinct mutations. No one knows what significance, if any, these differences have on infection, but it's an active area of discussion in the scientific community.

- - -

Before the pandemic, Gandhi, the University of California researcher, specialized in HIV. But like other infectious-disease experts these days, she has spent many of her waking hours thinking about the coronavirus. And in scrutinizing the data on outbreaks one day, she noticed what might be a pattern: People were wearing masks in the settings with the highest percentage of asymptomatic cases.

The numbers on two cruise ships were especially striking. In the Diamond Princess, where masks weren't used and the virus was likely to have roamed free, 47% of those tested were asymptomatic. But in the Antarctic-bound Argentine cruise ship, where an outbreak hit in mid-March and surgical masks were given to all passengers and N95 masks to the crew, 81% were asymptomatic.

Similarly high rates of asymptomatic infection were documented at a pediatric dialysis unit in Indiana, a seafood plant in Oregon and a hair salon in Missouri, all of which used masks. Gandhi was also intrigued by countries such as Singapore, Vietnam and the Czech Republic that had population-level masking.

"They got cases," she noted, "but fewer deaths."

The scientific literature on viral dose goes back to around 1938 when scientists began to find evidence that being exposed to one copy of a virus is more easily overcome than being exposed to a billion copies. Researchers refer to the infectious dose as ID50 - or the dose at which 50% of the population would become infected.

While scientists do not know what that level might be for the coronavirus (it would be unethical to expose humans in this way), previous work on other nonlethal viruses showed that people tend to get less sick with lower doses and more sick with higher doses. A study published in late May involving hamsters, masks and SARS-CoV-2 found that those given coverings had milder cases than those who did not get them.

In an article published this month in the Journal of General Internal Medicine, Gandhi noted that in some outbreaks early in the pandemic in which most people did not wear masks, 15% of the infected were asymptomatic. But later on, when people began wearing masks, the rate of asymptomatic people was 40% to 45%.

She said the evidence points to masks not just protecting others - as U.S. health officials emphasize - but protecting the wearer as well. Gandhi makes the controversial argument that while people mostly have talked about asymptomatic infections as terrifying due to how people can spread the virus unwittingly, it could end up being a good thing.

"It is an intriguing hypothesis that asymptomatic infection triggering immunity may lead us to get more population-level immunity," Gandhi said. "That itself will limit spread."

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Agencies
August 8,2020

Kozhikode, Aug 8: The death toll in Kozhikode air crash is likely to rise as the condition of 22 injured passengers is said to be extremely critical. A total of 149 injured passengers have been admitted to hospitals in Malappuram and Kozhikode districts. 22 others have been discharged after first aid, says K Gopalakrishnan, Malappuram Collector

Deceased passengers:
Mohammed Riyas VP, 24 years - Palakkad, 
Saheer Sayed, 38 years -Malappuram, 
Lailabi KV, 51 years -Malappuram, 
Rajeevan Cherikka Parambil, 61 years - Kozhikode, 
Manal Ahamed, 25 years - Kozhikode, 
Sharafudheen, 35 years - Kozhikode, 
Janaky Kunnoth, 55 years - Kozhikode, 
Azam Muhammed Chembayi ,1 year - Kozhikode, 
Santha Marakkat, 59 years - Malappuram, 
Sudheer Vaariyath, 45 years -Malappuram, 
Sheza Fathima, 2 years -Malappuram, 
Remya Muraleedharan, 32 years - Kozhikode
Aysha Dua, 2 years – Palakkad 
Shivathmika, 5 Years- Kozhikode
Zhenobia, 40 years – Kozhikode
Sahira Banu, 29 years - Kozhikode

Deceased crew:
Deepak Sathe (Pilot)
Akhilesh Kumar (Copilot)

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