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Part of a pulmonary blood vessel exhibiting occlusion and recanalization. The nuclei in the fibrous bands that are bridging the lumendo not appear to be those of malignant cells.
"How fair do you want the elections to be Sir" The question came from senior civil servant G. Muenuddin then working as Chief Election Commissioner. It was posed to the all powerful President of Pakistan Field Marshal Mohammad Ayub Khan, N.Pk., H.J., in 1964. Ayub had not yet fallen out with the powers that be nor was there any major or visible internal dissent. Nor yet had be suffered from pulmonary embolism till then. What he therefore said was the law. "As fair as practicable" came the cryptic reply. The Field Marshal had a formidable opponent. It was no less a person than the Founder of Pakistan's sister Ms. Fatima Jinnah. The orders had been issued nevertheless. Mueenuddin was a senior member of the Indian Civil Service whose name appeared third in the gradation list of ICS turned CSP officers, appearing immediately after Justice A. R. Cornelius and Justice S. A. Rehman. Ayub Khan ruled Pakistan exclusively through his civil servants. His reliance on them was indeed so great that Yahya Khan erroneously believing that the civil service was responsible for Ayub's downfall, tried to cow them down and fell on his face. Anyway to cut a long story short, the elections could and would only be that much fair as was consistent with Ayub Khan winning them. He won - although Ms. Jinnah swept Karachi, Dacca and Chittagong!
But let us go a little back in time before this uncanny conversation. It is 1947 and the Indian sub-continent is about to be divided. A fierce argument is in process between two men. One is not only the Viceroy and Governor General of India but also the cousin of the British monarch, Lord Mountbatten. The other is a polished and brilliant lawyer in the old Anglo-Saxon tradition who liked to be called plain Mr. Jinnah. Mountbatten was trying to force and intimidating Jinnah to accept him as first Governor General of Pakistan just the way Nehru had accepted him in India. Jinnah wanted to be Governor General himself and had an intense dislike and distrust of Mountbatten who mentioned, "But Mr. Jinnah, all the powers will be with the Prime Minister". Mr. Jinnah firmly replied, "In Pakistan I will be Governor General and the Prime Minister will do what I tell him to do." The argument was over. Some opine that this decision led to the inclusion of Gurdaspur in India giving it a clear route to Jammu and Kashmir, as Mountbatten tampered with the Radcliffe Award.
But let us move on. Pakistan came into being - Jinnah was revered and the governance of Pakistan proceeded as planned by him without even an inkling of dissent from any corner. The Secretary General Cabinet Chaudhry Muhammad Ali of the Indian Audits and Accounts Service was also made head of the Planning Committee (not to be confused with the Planning Commission) to determine what decisions could be made by the Prime Minister and his cabinet and which needed to be made by the Governor General. Things proceeded seemingly well but something was amiss. Jinnah remarked to Sindh Premier M. A. Khuhro, "The Prime Minister is average and most of his cabinet is below average." It was true that there was a huge gap in the stature of the Quaid-i-Azam and the men who constituted the new Government in Pakistan. Yet the absolute parting of the ways came with the inauguration of the State Bank of Pakistan on July 1, 1948. After that no one saw Mr. Jinnah until the Secretary General Cabinet called a physician weeks later to tell him to proceed to Ziarat. When asked who the patient was, the reply was significant, "the Quaid-i-Azam". The rest of the story is rather murky and need not be repeated here. Mr. Jinnah returned to Karachi but only to die within 3-4 hours, two of which were spent in an ambulance devoid of fuel. The Prime Minister arrived at Government House Karachi weeping bitterly only after Mr. Jinnah's soul had left his body.
As the Government of Pakistan gradually came out of mourning, the pious and ineffective Khwaja Nazimuddin was installed as the Governor General and the Prime Minister soon emerged as one of the most powerful in the history of Pakistan. As with Mr. Jinnah, there was virtually no dissent against Prime Minister Liaquat Ali Khan - at least - not then - except from one source. That was Ms. Fatima Jinnah, the sister of the Founder of Pakistan who lived on to tell her tales. In 1949 two pages of her book My Brother, specifically directed against the Prime Minister and Secretary General Cabinet, were censored out. Much later they were published in Q. U. Shahab's memoirs Shahabnaama by the time Liaquat Ali Khan had been assassinated, half a dozen more prime ministers changed through palace intrigues and two martial laws had been imposed. Naturally by that time Ms. Jinnah's assertions could neither harm nor benefit anyone of the worldly wise people running Pakistan and Shahab could publish the two pages. Ms. Jinnah had died by then of - mysterious causes, to say the least.
Then came the early nineties. Lady Sughra Ghulam Hussain Hidayatullah asserted that Ms. Jinnah had actually been assassinated. The news got a one column heading in the Dawn. Lady Hidayatullah couldn't have chosen a worse timing for her disclosures.
Pakistan was then caught up in an unfortunate controversy at that time. It had been pointed out in the Supreme Court that while after the death of Gen Ziaul Haq, the court was just about to announce its judgment reverting Muhammad Khan Junejo as Prime Minister and indeed even his security escort had arrived, a courier came in the way of all that. The courier was a Law Minister and future Senate Chairman, the message was from the most powerful man of Pakistan (not to be confused with President Ishaq Khan) to the Chief Justice to let the will of the people prevail. It was one of those things that should not have happened but had happened yet could not be admitted by anyone under any pretext and hence tempers were running loose. During the process, the Chief Justice remarked that even God could not stop him from reaching the truth, immediately provoking a blasphemy charge against him. It was in these conditions that the good Lady Hidayatullah said what she said.
After around a decade came Ms. Jinnah's centenary in 2003 happened with one of her bodyguards in the Muslim League Zafrullah Khan Jamali in the saddle as Prime Minister. Ms. Jinnah had even condoled the death of the then prime minister's uncle Mir Jaffer Khan Jamali exactly three months before her own death. However, there were the same rituals with wreaths of flowers oh her grave and all the politically correct statements delivered.
As the centenary fervour seemed to die down, I sent a widely distributed email maintaining that, “It is high time that the nation attains a level of maturity whereby it can come to terms with certain realities and attempt to address certain unanswered questions relating to her (Miss Jinnah’s) life... The lady was ostracized, persecuted and marginalized to a point that people had even forgotten about her existence when she decided to take on Field Marshal Ayub Khan in the 1964 presidential elections. The manner in which the elections were conducted and their unfortunate aftermath are known to all”. I went on to ask, “What is the real truth? Will the teeming millions of Pakistan ever be considered worthy enough of being taken into confidence about these pranks played by a few chosen ones? And those naïve people amongst us who think that our press is free should reconsider their opinion. The real truth is simply not for consumption of the ordinary mortals in Pakistan”.
And lo and behold - a couple of days later celebrated lawyer Sharifuddin Pirzada came up with the revelation that Ms. Jinnah had actually been murdered. This was President Ayub Khan's Attorney General talking and he immediately came within the mischief of 5-6 articles of the Pakistan Penal Code for not disclosing something which was in his knowledge relating to a heinous crime. And so the matter was again hushed up.
Let us again go back in time. Mr. (later Justice) Javed Iqbal narrates in his memoirs that he was told during the late fifties or early sixties that he would make a good Law Minister of West Pakistan and advised by a friend to meet the Central Law Minister. The gentleman in question, Mr. Khursheed expresses surprise and remarks, "but you are a decent person" adding hastily "we are looking for a rogue!". The powers that be's eyes fell on Ghulam Nabi Memon who was appointed to that position. Any matter relating to Ms. Jinnah death ends up with mention of Ghulam Nabi Memon, Hon'ble Law Minister of West Pakistan and the not so honourable Commissioner of Karachi Syed Darbar Ali Shah, who was later dismissed by Yahya Khan.
Going through her apolitical activities, I find that she was chief patron of the National TB Association as it was then called for decades and took an active part in TB prevention and control. She donated 100,000 rupees in 1962 to the Sindh Madressah Board allowing it to prosper as per her brother's desire. She went about performing inaugural ceremonies of colleges and universities, with a keen focus on women's issue. The 1964 elections (actually January 1, 1965) demonstrated that had she come in power, she could have served as an indispensable bridge between East and West Pakistan and perhaps reversed the tide set in motion to the contrary almost immediately after the creation of Pakistan.
Ms. Jinnah was found dead in her bed on July 9, 1967 indicating that close to 52 years have gone by. Will someone ever tell what happened after she slept the earlier night? It is clear that those governing Pakistan had seen one Jinnah and dreaded the prospect of another ruling Pakistan. Ayub Khan would not even allow her brother's tomb to be completed and it remained a dome of mud for over 2 decades. Then as Khaled Ahmed noted in 2003 the lady "revealed too much too soon in our history". Writing in the Daily Times in 2003 , Sir Cam questioned: And who strangled Miss Jinnah? Even if not physically throttled, she was strangled by the ‘system’. Like millions of ordinary people every day.
So be it - this country didn't deserve the Jinnahs, it deserved charlatans or worse! May her soul rest in eternal peace.
Copyright: Dr Ghulam Nabi kazi
Microscopic photo. IHC stain. Original objective magnification 40x. Jian-Hua Qiao, MD, FCAP, Los Angeles, CA, USA.
Leonard Nimoy, best known for playing the character Spock in the Star Trek television shows and films, died at 83.
www.nytimes.com/2015/02/27/arts/television/leonard-nimoy-...
Leonard Nimoy, the sonorous, gaunt-faced actor who won a worshipful global following as Mr. Spock, the resolutely logical human-alien first officer of the Starship Enterprise in the television and movie juggernaut “Star Trek,” died on Friday morning at his home in the Bel Air section of Los Angeles. He was 83.
His wife, Susan Bay Nimoy, confirmed his death, saying the cause was end-stage chronic obstructive pulmonary disease.
Mr. Nimoy announced that he had the disease last year, attributing it to years of smoking, a habit he had given up three decades earlier. He had been hospitalized earlier in the week.
For Leonard Nimoy, Spock’s Hold Made Reaching Escape Velocity FutileFEB. 27, 2015
Leonard Nimoy at his 2010 one-person photography exhibition at the Massachusetts Museum of Contemporary Art in North Adams, Mass.
His artistic pursuits — poetry, photography and music in addition to acting — ranged far beyond the United Federation of Planets, but it was as Mr. Spock that Mr. Nimoy became a folk hero, bringing to life one of the most indelible characters of the last half century: a cerebral, unflappable, pointy-eared Vulcan with a signature salute and blessing: “Live long and prosper” (from the Vulcan “Dif-tor heh smusma”).
As part of the Yiddish Book Center Wexler Oral History Project, Leonard Nimoy explains the origin of the Vulcan hand signal used by Spock, his character in the “Star Trek” series.
Video by Yiddish Book Center on Publish Date February 27, 2015. Photo by Yiddish Book Center’s Wexler Oral History Project.
Mr. Nimoy, who was teaching Method acting at his own studio when he was cast in the original “Star Trek” television series in the mid-1960s, relished playing outsiders, and he developed what he later admitted was a mystical identification with Spock, the lone alien on the starship’s bridge.
Yet he also acknowledged ambivalence about being tethered to the character, expressing it most plainly in the titles of two autobiographies: “I Am Not Spock,” published in 1977, and “I Am Spock,” published in 1995.
In the first, he wrote, “In Spock, I finally found the best of both worlds: to be widely accepted in public approval and yet be able to continue to play the insulated alien through the Vulcan character.”
“Star Trek,” which had its premiere on NBC on Sept. 8, 1966, made Mr. Nimoy a star. Gene Roddenberry, the creator of the franchise, called him “the conscience of ‘Star Trek’ ” — an often earnest, sometimes campy show that employed the distant future (as well as some primitive special effects by today’s standards) to take on social issues of the 1960s.
His stardom would endure. Though the series was canceled after three seasons because of low ratings, a cultlike following — the conference-holding, costume-wearing Trekkies, or Trekkers (the designation Mr. Nimoy preferred) — coalesced soon after “Star Trek” went into syndication.
The fans’ devotion only deepened when “Star Trek” was spun off into an animated show, various new series and an uneven parade of movies starring much of the original television cast, including — besides Mr. Nimoy — William Shatner (as Capt. James T. Kirk), DeForest Kelley (Dr. McCoy), George Takei (the helmsman, Sulu), James Doohan (the chief engineer, Scott), Nichelle Nichols (the chief communications officer, Uhura) and Walter Koenig (the navigator, Chekov).
When the director J. J. Abrams revived the “Star Trek” film franchise in 2009, with an all-new cast — including Zachary Quinto as Spock — he included a cameo part for Mr. Nimoy, as an older version of the same character. Mr. Nimoy also appeared in the 2013 follow-up, “Star Trek Into Darkness.”
His zeal to entertain and enlighten reached beyond “Star Trek” and crossed genres. He had a starring role in the dramatic television series “Mission: Impossible” and frequently performed onstage, notably as Tevye in “Fiddler on the Roof.” His poetry was voluminous, and he published books of his photography.
He also directed movies, including two from the “Star Trek” franchise, and television shows. And he made records, singing pop songs as well as original songs about “Star Trek,” and gave spoken-word performances — to the delight of his fans and the bewilderment of critics.
Thank you, Leonard Nimoy, and to all the crew of Star Trek who helped me grow up in the 1970s, giving me a vision of lives organized around the thirst for knowledge.
But all that was subsidiary to Mr. Spock, the most complex member of the Enterprise crew, who was both one of the gang and a creature apart engaged at times in a lonely struggle with his warring racial halves.
In one of his most memorable “Star Trek” performances, Mr. Nimoy tried to follow in the tradition of two actors he admired, Charles Laughton and Boris Karloff, who each played a monstrous character — Quasimodo and the Frankenstein monster — who is transformed by love.
In Episode 24, which was first shown on March 2, 1967, Mr. Spock is indeed transformed. Under the influence of aphrodisiacal spores he discovers on the planet Omicron Ceti III, he lets free his human side and announces his love for Leila Kalomi (Jill Ireland), a woman he had once known on Earth. In this episode, Mr. Nimoy brought to Spock’s metamorphosis not only warmth, compassion and playfulness, but also a rarefied concept of alienation.
“I am what I am, Leila,” Mr. Spock declares after the spores’ effect has worn off and his emotions are again in check. “And if there are self-made purgatories, then we all have to live in them. Mine can be no worse than someone else’s.”
Born in Boston on March 26, 1931, Leonard Simon Nimoy was the second son of Max and Dora Nimoy, Ukrainian immigrants and Orthodox Jews. His father worked as a barber.
From the age of 8, Leonard acted in local productions, winning parts at a community college, where he performed through his high school years. In 1949, after taking a summer course at Boston College, he traveled to Hollywood, though it wasn’t until 1951 that he landed small parts in two movies, “Queen for a Day” and “Rhubarb.”
He continued to be cast in little-known movies, although he did presciently play an alien invader in a cult serial called “Zombies of the Stratosphere,” and in 1961 he had a minor role on an episode of “The Twilight Zone.” His first starring movie role came in 1952 with “Kid Monk Baroni,” in which he played a disfigured Italian street-gang leader who becomes a boxer.
Mr. Nimoy served in the Army for two years, rising to sergeant and spending 18 months at Fort McPherson in Georgia, where he presided over shows for the Army’s Special Services branch. He also directed and starred as Stanley in the Atlanta Theater Guild’s production of “A Streetcar Named Desire” before receiving his final discharge in November 1955.
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He then returned to California, where he worked as a soda jerk, movie usher and cabdriver while studying acting at the Pasadena Playhouse. He achieved wide visibility in the late 1950s and early 1960s on television shows like “Wagon Train,” “Rawhide” and “Perry Mason.” Then came “Star Trek.”
Mr. Nimoy returned to college in his 40s and earned a master’s degree in Spanish from Antioch University Austin, an affiliate of Antioch College in Ohio, in 1978. Antioch University later awarded Mr. Nimoy an honorary doctorate.
Mr. Nimoy directed two of the Star Trek movies, “Star Trek III: The Search for Spock” (1984) and “Star Trek IV: The Voyage Home” (1986), which he helped write. In 1991, the same year that he resurrected Mr. Spock on two episodes of “Star Trek: The Next Generation,” Mr. Nimoy was also the executive producer and a writer of the movie “Star Trek VI: The Undiscovered Country.”
He then directed the hugely successful comedy “Three Men and a Baby” (1987), a far cry from his science-fiction work, and appeared in made-for-television movies. He received an Emmy nomination for the 1982 movie “A Woman Called Golda,” in which he portrayed the husband of Golda Meir, the prime minister of Israel, who was played by Ingrid Bergman. It was the fourth Emmy nomination of his career — the other three were for his “Star Trek” work — although he never won.
Mr. Nimoy’s marriage to the actress Sandi Zober ended in divorce. Besides his wife, he is survived by his children, Adam and Julie Nimoy; a stepson, Aaron Bay Schuck; and six grandchildren; one great-grandchild, and an older brother, Melvin.
Though his speaking voice was among his chief assets as an actor, the critical consensus was that his music was mortifying. Mr. Nimoy, however, was undaunted, and his fans seemed to enjoy the camp of his covers of songs like “If I Had a Hammer.” (His first album was called “Leonard Nimoy Presents Mr. Spock’s Music From Outer Space.”)
From 1977 to 1982, Mr. Nimoy hosted the syndicated series “In Search Of...,” which explored mysteries like the Loch Ness Monster and UFOs. He also narrated “Ancient Mysteries” on the History Channel from 1995 to 2003 and appeared in commercials, including two with Mr. Shatner for Priceline.com. He provided the voice for animated characters in “Transformers: The Movie,” in 1986, and “The Pagemaster,” in 1994.
In 2001 he voiced the king of Atlantis in the Disney animated movie “Atlantis: The Lost Empire,” and in 2005 he furnished voice-overs for the computer game Civilization IV. More recently, he had a recurring role on the science-fiction series “Fringe” and was heard, as the voice of Spock, in an episode of the hit sitcom “The Big Bang Theory.”
Mr. Nimoy was an active supporter of the arts as well. The Thalia, a venerable movie theater on the Upper West Side of Manhattan, now a multi-use hall that is part of Symphony Space, was renamed the Leonard Nimoy Thalia in 2002.
He also found his voice as a writer. Besides his autobiographies, he published “A Lifetime of Love: Poems on the Passages of Life” in 2002. Typical of Mr. Nimoy’s simple free verse are these lines: “In my heart/Is the seed of the tree/Which will be me.”
In later years, he rediscovered his Jewish heritage, and in 1991 he produced and starred in “Never Forget,” a television movie based on the story of a Holocaust survivor who sued a neo-Nazi organization of Holocaust deniers.
In 2002, having illustrated his books of poetry with his photographs, Mr. Nimoy published “Shekhina,” a book devoted to photography with a Jewish theme, that of the feminine aspect of God. His black-and-white photographs of nude and seminude women struck some Orthodox Jewish leaders as heretical, but Mr. Nimoy asserted that his work was consistent with the teaching of the kabbalah.
His religious upbringing also influenced the characterization of Spock. The character’s split-fingered salute, he often explained, had been his idea: He based it on the kohanic blessing, a manual approximation of the Hebrew letter shin, which is the first letter in Shaddai, one of the Hebrew names for God.
“To this day, I sense Vulcan speech patterns, Vulcan social attitudes and even Vulcan patterns of logic and emotional suppression in my behavior,” Mr. Nimoy wrote years after the original series ended.
But that wasn’t such a bad thing, he discovered. “Given the choice,” he wrote, “if I had to be someone else, I would be Spock.”
Correction: February 27, 2015
An earlier version of this obituary, using information from Antioch College, misstated the name of an institution that award Mr. Nimoy an honorary doctorate. It was Antioch University, not Antioch College.
12:00 pm - 12:50 pm
Doerr-Hosier Center, McNulty Room
James Crapo, Grace Anne Dorney Koppel, Ted Koppel
Property of the Aspen Institute / Photo Credit: Dan Bayer
Part of a pulmonary blood vessel exhibiting occlusion and recanalization. The nuclei in the fibrous bands that are bridging the lumen do not appear to be those of malignant cells.
The thing my mom has been dealing with this past week... is a pulmonary embolism.
She finally heard back from her doctor this morning after calling him again (she called Thursday and Friday and didn't get a call back). He arranged for a CT scan immediately when he heard she took a shower and got so winded this morning that it took her an hour and a half to recover. The CT scan took 10 minutes to do and 10 minutes to read and then the doctor there wanted her to be transported via ambulance to emergency but my dad insisted he'd drive her instead. They were waiting for her with wheelchairs everywhere.
Once she was admitted to emergency (also immediately) she had 4 doctors (including one of the best pulmonary specialists, her doctor, her heart doctor) consulting on whether or not she should be given TPA (which is a serious clot busting medication and introduces very high risks of internal bleeding) or something not as severe. They eventually decided on the TPA because she has two clots that are large and almost fully blocking both main arteries to her lungs which has put a big strain on her heart. She has to be monitored closely for internal bleeding and right now she has some pretty bad bruising and swelling at the sites of her IVs (which can't be removed for the next 6 hours due to the drug).
She's now in cardiac ICU (with post-operative heart patients). After that she'll be moved to a heart monitoring room for the next 5-7 days as they lessen the clotting medications in severity, take CT scans of her lungs and her legs (where most clots develop) to make sure she's out of danger. Then her doctor will try and figure out what brought all this on so they can prevent it in the future.
Yes, she could have died from this.
She's the best looking and healthiest looking patient in the cardiac ICU.
Microscopic photo showing irregular interstitial nests of spindle cells with rounded to oval shaped nuclei and moderate amounts of eosinophilic cytoplasm. The spindle cells exhibit features of meningothelial cells with scattered intranuclear inclusions. H&E stain. Original magnification 20X. Jian-Hua Qiao, MD, FCAP, Los Angeles, CA, USA
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COVID-19 treatments have evolved a lot. Here's what's available now
Since March 2020, the medical world has made some pretty amazing advances in treatments for COVID-19. The right one for you will usually depend on the severity of your symptoms and how long it's been since you tested positive. But the dynamics of the pandemic also matter — especially the emergence of new coronavirus variants.
"We are in such a better position now than we were at the beginning of the pandemic, both because we have better prevention — primarily vaccines and boosters — but also because we have better treatments," Dr. Megan Ranney, emergency medicine physician and associate dean for strategy and innovation at the Brown School of Public Health, told TODAY.
The main options we have right now fall into two camps: antiviral medications and antibody treatments, Dr. Taison Bell, assistant professor of medicine in the divisions of infectious diseases and international health and pulmonary and critical care medicine at the University of Virginia, told TODAY. Antivirals help keep the virus from replicating inside your body while antibody therapies supplement your immune system's natural defenses against the virus.
For many people, especially those who are fully vaccinated, a bout of COVID-19 does not require extensive treatment or a trip to the hospital. But if you have risk factors for severe symptoms, you're likely eligible to receive some of these treatments that can help prevent you from needing to be hospitalized — including some options you can take at home.
Home COVID-19 treatments and remedies
At-home antiviral medications
There are two options for antiviral pills you can take at home: There's a combination of nirmatrelvir and ritonavir (Paxlovid) there's molnupiravir (Lagevrio), both of which received authorization from the Food and Drug Administration in December 2021. To be eligible for a prescription for these medications, you need to have a positive COVID-19 test and at least one risk factor for severe COVID-19.
Compared to IV medications, the pills are generally "less complicated from an administrative standpoint," Bell said.
The catch is that they need to be taken within three to five days of being diagnosed with COVID-19, Ranney said.
That's why quick access to COVID-19 testing and a provider who can prescribe the medication within the proper timeframe are so essential. The government's Test to Treat program was designed to help address this issue. Check the website to find locations near you where you can get both a COVID-19 test and, if the test is positive, a prescription for Paxlovid.
The other issue with these medications, though, is potential drug interactions. "There are some big categories of people that can't take Paxlovid," Ranney explained. That's because "there are some medications that can go into either dangerously high levels or dangerously low levels because of the way Paxlovid works."
That can be especially dangerous for solid organ transplant patients, Dr. Robin Avery, an infectious diseases physician at the Johns Hopkins School of Medicine, told TODAY. The ritonavir part of Paxlovid can elevate the level of drugs like tacrolimus — a "mainstay of immunosuppression" — in the body, she said, to the point where patients can experience tremors, kidney failure and even strokes.
On the other hand, people who are pregnant or breastfeeding should not take molnupiravir, Ranney added. So, if possible, they should take Paxlovid instead.
Bell recommended that patients and their providers who are concerned about potential interactions check the University of Liverpool's COVID-19 drug interactions checker. Avery also recommended perusing the interaction information in the National Institutes of Health COVID-19 treatment guidelines and those from the Infectious Diseases Society of America.
What is the Paxlovid "rebound"?
There have been reports of people taking Paxlovid, feeling better and testing negative for a few days before symptoms return and sometimes testing positive again, usually two to eight days after initial recovery. This phenomenon, nicknamed a Paxlovid rebound, seems to be "uncommon, but ... I wouldn't call it rare," Bell said.
The Centers for Disease Control and Prevention recently warned that Paxlovid rebound is a possibility.
"First of all, it does look like this subvariant does tend to cause some rebound in and of itself," Bell explained. So, as the CDC noted, some people who have COVID-19 caused by the omicron subvariants circulating now may experience a rebound of their symptoms with or without taking Paxlovid.
Another theory, Bell explained, is that a relatively short course of treatment with Paxlovid isn't enough for your body to successfully mount its own defenses. "What you're doing is buying time with this; you're keeping the virus at bay (while your body builds up its immune response)," he said. But, for some people, one course of Paxlovid might not give their body enough time to do that.
The CDC recommends that people experiencing Paxlovid rebound start their isolation over, as it's unclear how likely they are to spread the virus.
Other home remedies for COVID-19
If you have a relatively mild bout of COVID-19, there are things you can do at home to feel better, depending on your symptoms.
■ Use over-the-counter medications like acetaminophen and ibuprofen to reduce body aches and fevers, according to the CDC.
■ Stay hydrated and be sure to get plenty of rest, the Mayo Clinic advised.
■ For a cough or sore throat, try soothing remedies you might use for a seasonal cold or flu, like cough drops or tea with honey.
■ Recognize when you need medical attention. If you're having trouble breathing, notice a persistent pressure in your throat or chest, are finding it hard to stay awake at all or show any of the CDC's other major warning signs, get help immediately.
Other treatments you can take as an outpatient
Monoclonal antibodies
“The first-line treatment for someone who gets diagnosed with COVID and has a relatively high risk is to prescribe them (Paxlovid) pills,” Ranney said. But if someone can't get the pills, or they’re outside of the window where the pills might be effective, "the next treatment is monoclonal antibodies, which are an infusion." You receive it in a designated medical facility and can leave afterward.
Among immunocompromised patients, this type of therapy "has made the most difference in early treatment," Avery said. It's kept people from developing severe symptoms and needing to come to the hospital, she added.
But the effectiveness of monoclonal antibody treatments depends on the coronavirus variants that are circulating at any given time. Experts now understand that these antibody therapies, like the antibodies your body makes naturally in response to an infection, work by binding to a small part of the coronavirus' spike protein. If the spike protein is different from variant to variant, these treatments may not work as well.
That's why some treatments, like bamlanivimab, that were used early on are now no longer effective. Instead, the NIH recommended using sotrovimab during the winter omicron wave and now recommends using bebtelovimab against BA.2.
IV antiviral treatments
Remdesivir (Veklury), is an antiviral treatment that you can receive at certain medical centers and health care locations.
It's given through an IV and requires three consecutive days of treatment, the NIH explained. So although there's evidence remdesivir can be effective at keeping people out of the hospital, "it's logistically tricky," Avery said. "A lot of centers don't necessarily have an area where they can do these outpatient fusions three days in a row."
One major benefit of remdesivir? Its helpfulness isn't likely to be affected by changes in dominant variants. "It works on the level of the RNA polymerase, not the spike protein," Avery explained. "So mutations in the spike protein wouldn't be expected to affect its efficacy."
Treatments you might receive in the hospital
Patients in the hospital will also receive a standard set of supportive treatments, like those that help fight and prevent blood clots, Ranney said. But there aren't many options to treat COVID-19 specifically.
“If you’re sick enough to get hospitalized, we have many fewer choices,” Ranney said. “By that point, COVID has already started to cause damage to a large extent.” Here's what you might get:
Dexamethasone
Alongside remdesivir, patients who are hospitalized and require oxygen may receive the corticosteroid dexamethasone. Medications like this can be used to halt the "upswing of the inflammatory phase, which causes the respiratory failure so forth in inpatients," Avery said.
Bell reiterated that this is not something that people should take outside of a doctor's supervision. "There's a risk-benefit to steroids because in addition to calming down inflammation, which could be a benefit, it also suppresses your immune system," he explained. "So you're always walking that line."
If dexamethasone isn't available, the NIH recommended looking into other corticosteroids, such as prednisone.
Baricitinib and tocilizumab
These are both drugs that are normally used to treat rheumatoid arthritis. For hospitalized COVID-19 patients, either one may be given along with dexamethasone or another corticosteroid, the NIH said.
Convalescent plasma
Plasma from donors who've recovered from COVID-19 can be given to hospitalized patients to help them heal. In the early days of the pandemic, it seemed like convalescent plasma could be helpful. But today, the NIH recommends against using any plasma collected before the emergence of omicron and recommends only using it in people who are immunocompromised.
But this is one therapy option where "the pendulum may swing back," Avery said, pointing to the work of her colleague Dr. Arturo Casadevall. In a recent study published in the New England Journal of Medicine, a team of researchers including Casadevall found there could be benefits to using convalescent plasma among unvaccinated people within nine days of symptom onset.
"We've actually used a lot of convalescent plasma throughout the pandemic in our immunocompromised patients because we feel that they often don't mount enough antibody response (to the vaccine or infection)," she explained.
What experts want you to know:
As much progress as we've made in developing COVID-19 treatments, there is still work to do — especially when it comes to making those options actually accessible.
“We have a situation now where these (treatments) are widely available physically,” Bell said. “But, functionally, there are still barriers to getting them.” Not everyone has a primary care provider who can easily prescribe them Paxlovid, for instance.
Ranney agreed: "Unfortunately, there are groups across the country that continue to be unaware of the ability to get these treatments or simply don't have access to them," she said, noting recent research showing that Black, Asian and Hispanic people were less likely than white people to be prescribed monoclonal antibody treatment.
Also, it pays to know what risk factors you have for severe COVID-19 and, maybe, to have a conversation about that with your doctor before you get infected, Avery said. Those risk factors can include having a high BMI, being over 60 years old, being a former smoker, and having diabetes or heart disease.
"If people have one or more of these risk factors, they should consult with their providers and actually make a plan in advance," Avery said. "At the very least, that person and their provider should have a discussion" about whether they're eligible for therapies like Paxlovid and whether there are potential drug interactions to be aware of.
And the experts also underscored that treatment is not a replacement for prevention measures. "The therapeutics are always the second line," Bell said. Getting vaccinated, getting boosted and wearing a high-quality mask are still the best way to prevent getting COVID-19.
Go to Page with image in the Internet Archive
Title: Scritti di Carlo Forlanini : scelti e pubblicati a cura della "Fondazione Carlo Forlanini"
Creator: Forlanini, Carlo, 1847-1918. n 84805739
Publisher: Bologna : L. Cappelli
Sponsor: Wellcome Library
Contributor: Wellcome Library
Date: 1928
Language: ita
Includes bibliographic references
If you have questions concerning reproductions, please contact the Contributing Library.
Note: The colors, contrast and appearance of these illustrations are unlikely to be true to life. They are derived from scanned images that have been enhanced for machine interpretation and have been altered from their originals.
Read/Download from the Internet Archive
This represents a late effect of organization of a thrombus/thromboembolus which is no longer present.
Incidentally diagnosed pulmonary hypertension at the age of 9. The presence of this lesion in a lung biopsy practically means that the disease is in a progressed stage.
Microscopic photo showing a pulmonary caseating granulomas. H&E stain. objective magnification of 20X. The insert is positive AFB stain (objective magnification of 100X under oil). Jian-Hua Qiao, MD, FCAP, Los Angeles, CA, USA.
Pulmonary blastoma is a biphasic malignant neoplasm occurring in adults that contains an epithelial component (usually fetal adenocarcinoma) and a sarcomatous component that may be undifferentiated or that may have foci of osteosarcoma, chondrosarcoma or rhandomyosarcoma. This image contains fetal type adenocarcinoma and undifferentiated sarcoma.
Microscopic photo. H & E stain. Original objective magnification 10x. Jian-Hua Qiao, MD, FCAP, Los Angeles, CA, USA.
Cardio Pulmonary exercise test (CPET) performed on young Indonesian patient on a treadmill with Quark CPET (www.cosmed.com/quarkcpet) metabolic cart and heart rate monitor (source @donnyakusuma)
IPF = idiopathic pulmonary fibrosis. The quote is from the cover of the Radio Times - from a lovely BBC journalist who has another sort of terminal illness. An excellent thing to remember every morning as I come into the kitchen.
Pleuroparenchymal fibroelastosis (PPFE) was first designated as a rare type of idiopathic interstitial pneumonia by WHO in 2013. Prior cases of “pulmonary upper lobe fibrosis (PULF)” and cases of “idiopathic upper lobe fibrosis” appear to be identical to FFPE.
Although the pathogenesis of PPFE has not been established, several potential initiating factors for have been reported, the commonest of which are bone marrow and hematopoietic stem cell transplantation and lung transplants. A history of chemotherapy treatment, autoimmune or connective tissue disease, acute lung injury particularly with infective complications, chronic hypersensitivity pneumonitis (HP), and occupational exposure to asbestos and aluminum have also been associated with PPFE. A history of pulmonary infections is frequently encountered in individuals with PPFE.
RADIOLOGY
The characteristic radiologic findings are upper lobe pleural thickening with subpleural fibrosis and limited, if any, lower lobe involvement. Tractional distortion of the airways within areas of PPFE is common, reflecting the dense surrounding fibrosis. Lobar volume loss is common, and the radiographic changes may be progressive. Overt lung fibrosis of varying patterns can coexist with PPFE, most frequently UIP, NSIP, or HP.
Anteroposterior associated flattening of the chest (platythorax) occurs commonly as does deepening of the suprasternal notch.; both are due to lung volume decrease and weight loss. Pneumothorax and pneumomediastinum may be seen.
The commonest pattern of fibrotic ILD to coexist with PPFE is usual interstitial pneumonia (UIP), reported in one-fourth to one-half of cases (27, 31, 32). Coexistent UIP or even nonspecific interstitial pneumonia (NSIP) occurs most frequently in the lower lobes, away from the main areas of PPFE, but in common with the latter, each pattern will typically progress over time. PPFE has also been reported in patients diagnosed with chronic HP.
PATHOLOGY
A histopathological diagnosis of PPFE requires demonstration of intra-alveolar fibrosis and elastosis (IAFE), and visceral pleural fibrosis. The latter may be absent in biopsies because of its patchy distribution. IAFE comprises dense collagenous fibrosis filling alveolar spaces, with the residual alveolar walls highlighted by elastin deposition These features dominate in the upper lobes and are more readily seen on elastin van Gieson stain. Inflammation is typically mild and nonspecific. At low power, IAFE commonly appears just deep to the visceral pleura, although it may extend into the deeper parenchyma, typically around interlobular septa and bronchovascular bundles
Foci of granulomatous inflammation may be present in approximately 15% of cases, although it is unclear whether granulomas represent a coexistent condition such as HP or infection.
The differential diagnosis includes apical “cap,” radiation-induced lung injury, pulmonary paraquat toxicity, and chronic postinjury remodeling due to failure of acute respiratory distress syndrome to resolve.
The clinical course of disease may be indolent, extending over several years or decades. However, in some patients the disease exhibits relatively rapid progression with death occurring in 5 years or less. There is currently no effective treatment for PPFE.
Images contributed by Dr. Irene Sansano - @SansanoValero and, Dr Pedro Eduardo Dacosta - @EduDacostaE
Reference - Chua F, Desai SR, Nicholson AG, et al. Pleuroparenchymal Fibroelastosis. A Review of Clinical, Radiological, and Pathological Characteristics. Ann Am Thorac Soc. 2019;16(11):1351-1359. doi:10.1513/AnnalsATS.201902-181CME. Much of the above description of PPFE has been extracted from this publication.
68 yo patients having 5 days history of chest pain -chest xray showing congestion
ST elevations at inferior leads
chest pain with ST elevations at inferior leads and reciprocal changes on the anterior - lateral leads
The most frequent pulmonary lesions in scleroderma are pulmonary hypertensive arteriopathy and interstitial pneumonia most often resembling UIP. Either or both of these lesions may be present; in this case both are present. This image shows a large fibroblastic focus.
May the 4th be with you. (starwars day. May the force be with you)
Perhaps on May the 4th, it really was.
The prior wednesday i got home and felt i was breathing a little heavy (no jokes people). But as I was on crutches (i've also hurt my knee), i attributed it to me getting more daring on the crutches and just pushing myself too far. But come thursday, i was breathing a little more heavier and i thought i may be coming down with a bug.
By friday morning, i couldn't even walk 50 yards without feeling dizzy and wanting to throw up. But i decided to push on through and go to work. By 12pm i was reconsidering my decision to go to work, and asked to go home. But whilst at the bus stop, something made me decide to go to hospital. I couldn't tell you I was desperately ill, or suffering. There were no outward symptoms but i decided to go anyway
By 130pm, i was seeing a doctor who decided to send me for a CT scan. In the meantime i had got changed into some tracksuit bottoms (It was easier for the Docs to look at my knee) and i could hardly breath, even when doing something as simple as slowly swapping clothes. By 330pm I was diagnosed with large "bi lateral pulmonary embolism" (BLPE) and my condition was described as "life threatening" and critical. Things now really got interesting.
I was hooked up to 40% oxygen, blood pressure monitors and heart rate monitors, and moved to the fast track ward of the hospital, where they keep you monitored 24/7. I was also getting given injections in my tummy and given warfarin tablets. I was quickly seen by a Doctor, who immediately told me the bad news. I was to be given no privacy whilst on the ward! I couldn't leave the bay i was in! I couldn't use the bathroom! How awful is that! It was yards away! So close, and yet so far..........
But i understood why. Because the BLPE were so large and completely blocking one lung and almost entirely blocking the other one, I wasn't to move too much or do anything strenous in case the BLPE moved to my heart or my brain. Well, where my brain is. I can't say it gets much use ;)
So began 10 days in hospital. Having never spent a night in hospital before in my life, it was an interesting experience. Trying to sleep in a new place whilst trying not to disconnect the monitors is a game all in itself. But for the first night i didn't sleep at all. How do people do it? But over the next few days, the amount of monitoring dropped from hourly, to bi hourly to 4 hourly to 6 hourly so i could settle and do things. And get a couple more hours continous sleep each night. But i'll still never get comfortable peeing into a bottle with alot of people just behind a very thin curtain.
I won't describe all the people who were patients, or all the staff, but there were some who make you think. The guy who kept waking up and not knowing where he was. He was so polite, but yet so lost. The nurses would get him to change into his bedclothes, and he would sneakily get changed again, hide in the bathroom or make his break for freedom down the hall. This happened for a few hours, until finally in the early hours of the morning, he accepted defeat and lay in bed. But when i woke up, he was gone and a new patient was in his place. Again, an elderly guy, but with a beard and intelligent eyes. Wild hair too. I liked him. He wasn't worried where he was, and looked like he knew his situation. He was content and seemed to know he was getting out soon enough. I hope he did
There was another guy and i don't know how i felt about him. Again, very polite, but i'm not so sure if it was because it was his nature, or because of his situation. He'd speak very deliberately and slowly, and end every sentence with the title of the person he was speaking to. So it'd be "yes nurse" or "yes doctor" but every sylable was very clearly pronounced. He was in for breathing problems too, but of a different sort. He told the staff he smoked 20 roll ups a day, and couldn't stop. I'm glad i don't smoke, and whilst writing this it made me ponder. Whilst in the hospital, my sympathy for him diminished. He was there because he made a choice and his choice put him where he is. If he wanted life to get better, he had an option. But thinking about it now, maybe those 20 were his small enjoyment for each day. I overheard him tell the staff he could take 3 steps and then had to stop to catch his breath. 3 steps. 1 2 3. then stop. He lived alone and couldn't get very far. Is that his life? Or is that him existing, taking the slow road to an inevitable end. I thought myself lucky, that presumably i will make a good recovery and will soon be able to walk 3 miles before even having to think about my breathing. I still don't know if i feel sorry for him, but i hope things get better for him soon
There was also another guy. I left before i saw too much of him, but i think he had heart problems, and you could see him pondering things out. I think he genuinely reconsidered his life. He had the wide eyes of someone who had just experienced something he hadn't expected, something he didn't want, and the frown of a man who knew he had to change the things from his past. A silence overcame him when he was alone. I hope he did ok. He had a lot of different people visit him. He was well liked
I did discover during my time, that according to some visitors to the wards, that nurses, doctors and all people with medical training know nothing about making people better, and relatives know everything. This made me sad. The people who looked after me on this ward (and in all the other wards) did a fantastic job, despite very impatient patients, and very ungrateful relatives. Not all visitors were like this, but too many were
After this, i was moved to my own room on a different ward. A huge stroke of good fortune :) Going from a monitored ward to a room, with my OWN SHOWER!!! Hell yeah!! By this time, i had a beard, so that was the first thing to go and i could lie in peace, without various visitors going through the ward and casting curious looks at me. I still had nurses making regular visits to check my 02 level and my blood pressure, but it was good. A professor came to see me each day and discuss what was going on with me, and why, and i spent 10 days in that room. A physio also came to see me to help with my knee and my breathing, so i could get up and going. Things were looking up
Things are still looking up. I am getting better. I can breathe more easily every day, get further and do it faster, and take less time to recover. But i'm still miles away from where i should be. Where i will be. The future is different for me now. I'll be on warfarin for life now, so my blood isn't as sticky as yours, so i'll have to be careful in some ways, but i have a lot to look forward too.
So do you
I dont know if I should have written the above, or if i have conveyed anything useful or inspiring. But this is the first time i've actually written about my time in hospital. I'm still recovering at home. there is lots more to say, but this will do for now. if i only ever say one more thing, it'd be thanks to the hospital for all the care and time they gave me.
Coarse granular cytoplasmic staining. This antibody is highly sensitive and specific for pulmonary adenocarcinoma.
Microscopic photo. H & E and GMS fungal stains. 40X objective magnification. Jian-Hua Qiao, MD, FCAP, Los Angeles, CA, USA.
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Fibrous obliteration of lumen of small pulmonary vein. Elastic tissue stain. Pulmonary veno-occlusive disease.
Image contributed by Dr. Yale Rosen - @yro854
The most frequent pulmonary lesions in scleroderma are pulmonary hypertensive arteriopathy and interstitial pneumonia most often resembling UIP. Either or both of these lesions may be present; in this case both are present. This image shows interstitial pneumonia with extensive inflammation and some fibrosis. A large fibroblastic focus is seen in the left half of the image.
Although necrotizing granulomas are the characteristic lesion of tuberculosis, non-necrotizing granulomas occur as well and may be the only type of granuloma seen in small biopsy specimens.
The most frequent pulmonary lesions in scleroderma are pulmonary hypertensive arteriopathy and interstitial pneumonia most often resembling UIP. Either or both of these lesions may be present; in this case both are present. This image shows interstitial pneumonia with extensive inflammation, fibrosis and honeycomb changes. The pulmonary arterioles and arteries show marked medial muscle hyperplasia and intimal fibrosis with significant lumenal narrowing. A large fibroblastic focus is seen in the center of the upper half of the image..
Microscopic photo showing dendeiform type of diffuse pulmonary ossifications. Fatty marrow tissue is noted. H & E stain. 4X. Jian-Hua Qiao, MD, FCAP, Los Angeles, CA, USA.
Pulmonary giant cell carcinoma represents a rare variety of non-small cell lung carcinoma that is characterized by the presence of numerous tumor giant cells and an influx of inflammatory cells that are mostly polymorphonuclear leukocytes admixed with macrophages. The dense oval aggregates of polymorphonuclear leukocytes seen in this image are probably located in the cytoplasm of tumor giant cells (emperiopolesis) that have been sectioned in a plane that does not include their nuclei
The outside of file HOSP/STAN/07/01/02/2697, a patient at Stannington Sanatorium being treated for primary Pulmonary Tuberculosis after the introduction of antibiotics at the sanatorium. Read more about this file on the album description.
Date: 1952 -1954.
This image is part of our Stannington Sanatorium Flickr collection of albums of patient files, as part of our Stannington Sanatorium project. They are from our archive collections at Northumberland Archives. Feel free to share them within the spirit of the Commons. If you have any enquiries or would like copies please contact collections@woodhorn.org.uk for more information.
“PERINATAL PHARMACOLOGY: INDIVIDUALIZED NEONATAL THERAPY”
Systems Medicine series
Hygeia Press
1st edition: October 2012
The origin of this book lies on the awareness that we have to do more for identifying unmet needs and improving a tailor-made treatment for each newborn.
After a large introduction on developmental pharmacology, this book analyses in detail new advances on antibiotics (aminoglycosides), antifungals, antivirals (CMV, RSV, HIV), analgosedatives, steroids, caffeine, and cardiovascular drugs. An updated pharmacologic treatment of respiratory diseases (respiratory distress syndrome, meconium aspiration syndrome, chronic lung disease, persistent pulmonary hypertension) is presented, as well as for persistent patent ductus arteriosus and retinopathy of prematurity. Finally, neuroprotection is considered, with special emphasis on antioxidants and melatonin.
A special part is devoted to drug-induced renal toxicity and liver toxicity and completes the volume, also quoting the so-called ‘-omics’ sciences such as genomics and metabolomics.
The topics are covered by international experts in the field and the subtle red line that links all the chapters together is the perspective of individualized treatments to reach our ultimate goal: the right therapy for each newborn without any side effects.
EDITORS
Jacob V. Aranda
Vassilios Fanos
John N. van den Anker
AUTHORS
Massimo Agosti
Karel Allegaert
Jacob V. Aranda
Salvatore Aversa
Caterina Silvia Barbàra
Ignazio Barberi
Pier Paolo Bassareo
Kay Beharry
Paolo Biban
Giuseppe Buonocore
Daniel Canal-Tristancho
Maria Grazia Capretti
Virgilio P. Carnielli
Elio Castagnola
Massimo Castagnola
Carla Cerasaro
Francesca Ciuffini
Paola E. Cogo
Mariarosa Colnaghi
Giovanni Corsello
Laura Cuzzolin
Roosmarijn De Cock
Sahera Dirajlal-Fargo
Gavino Faa
Daniela Fanni
Vassilios Fanos
Daniele Farina
Monica Fumagalli
Bruna Gabriele
Clara Gerosa
Yukio Gibo
Eloisa Gitto
Mario Giuffrè
Maria Beatriz Guedes
Hercília Guimarães
Nicoletta Iacovidou
Eveline Jacqz-Aigrain
Spyros Kloudas
Catherijne Knibbe
Amir Lahav
Marcello Lanari
Douglas R. Lazarro
Tiziana Lazzarotto
Paolo Manzoni
Lucia Marseglia
Giuseppe Mercuro
Fabio Midulla
Corrado Moretti
Fabio Mosca
Sonia Nemolato
Stefano Nobile
Eren Özek
Paola Papoff
Serafina Perrone
Valentina Polimeni
Natella Y. Rakhmanina
Gustavo Rocha
Serena Salvadei
Davide Silvagni
Henrique Soares
Paulo Soares
Paola Sogno Valin
Gemma Stazzoni
Mauro Stronati
Aggeliki Syggelou
Maria Luisa Tataranno
Gloria B. Valencia
John N. van den Anker
Bart Van Overmeire
Theodoros Xanthos
Murat Yurdakök
Emily Zimmerman
Cover pictures: a case of drug-induced liver disease (DILI). On the front cover: macrovesicular steatosis; on the back cover: microvesicular steatosis (Prof. Gavino Faa, with permission).
For more information: www.hygeiapress.com/individualizedmedicine/?p=155
Rank:Private
Service No:9414
Cause of Death Pulmonary Tuberculosis
Date of Death:22/06/1917 - Age:44
North Staffordshire Regiment
Re-enlisted - 21/09/1914
Posted - 30/09/1914 - 9th Bn
Dis-embarked 28/07/1915 - France
Hosp - 15/03/1916 - St Helens
Discharged - 15/06/1915 - Sickness
Grave Reference: 32. R.C. 15.
Awarded 14-15 Star, BWM & VM
Silver War Badge (119765)
Previous Occupation Collier
Additional Information:
Son of the late Peter and Helen Convey;
Husband of the late Margaret Convey,
of 2, Hick St., Newcastle-under-Lyme.
Miliary tuberculosis can occur when tuberculous lung lesions erode pulmonary veins or when when extrapulmonary tuberculous lesions erode systemic veins.This results in hematogenous dissemination of tubercle bacilli producing myriads of 1-2 mm. lesions throughout the body in susceptible hosts. Miliary spread limited to the lungs can occur following erosion of pulmonary arteries by tuberculous lung lesions. In this image a small focus of granulomatous inflammation is centered on an arteriole.
FNA of a slowly growing lung mass. Diagnosis: nodular pulmonary amyloidosis (NPA)
Left image - Amorphous material similar in appearance to colloid. PAP stain.
Right image – Congo Red stain polarized showing typical green birefringence of amyloid.
Nodular pulmonary amyloidosis is usually composed of AL amyloid which has been shown to have differences in AL composition and subtype ratios compared to systemic amyloidosis. In NPA, a subtype kappa derived amyloid chain exists at higher levels than the gamma-derived amyloid protein in systemic amyloidosis. Also, deposition in tissues of heavy chains of the AL protein is more common in NPA than systemic amyloidosis. Some NPA lesions consist of ATTR amyloid protein that is usually associated associated with age-related amyloidosis and tracheobronchial amyloidosis.
Reference: PMID: 36874267
Images contributed by Dr. Arash Lahouti - @ArashLahouti
Bone marrow pulmonary embolism (BMPE) is a potentially serious condition that can occur after trauma.
BMPE usually occurs after severe traumatic events, such as bone fractures or crush injuries. The trauma disrupts the integrity of the bone marrow, leading to the release of fat droplets and elements of the marrow into the bloodstream. In bone marrow embolism (BME) the pulmonary vessels are the most affected. However, some cases of BME were reported in the absence of trauma. Options include cancer in which bone marrow metastasis is a suggestive cause, liposuction, drug abuse, pulmonary hypertension, cardiac massage, and heart failure. Although usually seen in autopsy lungs in association with rib fractures associated with cardiopulmonary resuscitation, bone marrow emboli are sometimes seen in surgical lung specimens obtained following intraoperative rib fracture to permit access.
The embolus is mainly composed of bone marrow elements including marrow adipocytes. Small-sized pulmonary arteries are the most affected.
Image source - National Association of Medical Examiners (NAME) - @theNAME1966
Pulmonary giant cell carcinoma represents a rare variety of non-small cell lung carcinoma that is characterized by the presence of numerous tumor giant cells and an influx of inflammatory cells that are mostly polymorphonuclear leukocytes.Some of the tumor giant cells contain polymorphonuclear leukocytes within their cytoplasm (emperiopolesis). See note.
Correspondence accompanying the file HOSP/STAN/07/01/02/2697, a patient at Stannington Sanatorium being treated for primary Pulmonary Tuberculosis after the introduction of antibiotics at the sanatorium. Read more about this file on the album description.
Date: 1952 -1954.
This image is part of our Stannington Sanatorium Flickr collection of albums of patient files, as part of our Stannington Sanatorium project. They are from our archive collections at Northumberland Archives. Feel free to share them within the spirit of the Commons. If you have any enquiries or would like copies please contact collections@woodhorn.org.uk for more information.
Persistent interstitial pulmonary emphysema (PIPE) occurs mainly in preterm infants subjected to artificial ventilation for the respiratory distress syndrome. It caused by alveolar rupture resulting in dissection of air along bronchovascular bundles and interlobular septae; dissection of air may extend into the mediastinum and/or pericardium and may disrupt the visceral pleura resulting in pneumothorax. When present for more than a week the adjective "persistent" replaces "acute" Foreign body type giant cells overlie the loose connective tissue wall of this air cyst. The present of foreign body giant cells lining the cysts separates PIPE from acute interstitial emphysema. Thee giant cells are reacting to air. Other situations in which there are giant cells reacting to air include reactive eosinophilic pleuritis associated with pneumothorax, pneumatosis intestinalis and pneumatosis vaginalis.
Miliary tuberculosis can occur when tuberculous lung lesions erode pulmonary veins or when when extrapulmonary tuberculous lesions erode systemic veins.This results in hematogenous dissemination of tubercle bacilli producing myriads of 1-2 mm. lesions throughout the body in susceptible hosts. Miliary spread limited to the lungs can occur following erosion of pulmonary arteries by tuberculous lung lesions.
This is from a 15-year-old girl with acute myeloid leukemia. She presented with the "febrile neutropenia" syndrome. The branching fungi were easily visible with the H&E stain. The lung parenchyma was partially necrotic and the hyphae were filling thrombosed vascular lumina.