Saturday, November 23, 2019

Anything can be called ART "Shibari bondage"

Anything( Any Stupid SHIT) can be called ART

Shibari Bondage

It evolved into an erotic activity and art form called “kinbaku” during the Edo Period, infusing the centuries-old discipline method with BDSM (the infamous photographer Nobuyoshi Araki is known for his extensive documentation of this style of rope bondage). More recently, kinbaku has moved internationally, and was coined “shibari” in the 1990s as it moved into the West. “Shibari” translates to “decoratively tie.” Drawing from Japanese tying methods, shibari artists use rope to design stunning geometric patterns that bind and accentuate the curves of each body. Whereas hojojutsu was a form of torture, kinbaku and shibari are about consensual art-making and experimentation; working together, the rigger and model engage in a simulation of extreme power dynamics to produce images and bodily experiences brimming with vulnerability, euphoria, tension, and sensuality.

https://scene360.com/art/97256/rope-bondage-photography/ 

Where are the Feminists?
Why no one complains about the debasing of female form ? 

https://scene360.com/art/87404/controversial-photographers/ 


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"Medical Prostitution"

"Medical Prostitution"

The Daily Dish from Atlantic











In 2015, one-third of America was on opioids (largely in the form of painkillers). The country is addicted.
Reuters Business Insights calls this: "the corporate creation of disease."
We not only sold our soul but allowed the devil to eat it too!

HAS MEDICINE SOLD ITS SOUL?

BY PROF ALASTAIR CAMPBELL, CENTRE FOR BIOMEDICAL ETHICS

In Doctored: The Disillusionment of an American Physician, Dr Sandeep Jauhar writes:

“Most of us went into their medicine to help people, not to follow corporate directives or to maximise income. We want to practice medicine the right way, but too many forces today are propelling us away from the bench or the bedside.”

Jauhar’s sense of betrayal and personal failure is common among many doctors today. They embarked on the practice of medicine full of high ideals, choosing it as a career, not just for prestige and a good income, but because they wanted
to help people in their time of need, to make a difference in patients’ lives, as they battle with illness or disability. But the disillusionment comes early on, as shown by many studies of medical students – as the joke puts it, they progress, not from preclinical to clinical phases of study, but from pre-cynical to cynical! Their youthful idealism fades as they encounter the realities of medical practice today and work with some senior doctors who seem to be interested only in money and personal fame, not in the health of their patients.

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excessive vomiting (hypereremesis) associated with chronic cannabis use

he young woman was hunched over a large pink basin when Dr. Amy
Hsia, a resident in her first year of training, entered the patient's cu-
bicle in the Emergency Department. The girl looked up at the doctor. Tears
streamed down her face. "l don't know if I can take this any longer," twenty-
two-year-old Maria Rogers sobbed. Since arriving at the emergency room
early that morning, she'd already been given two medicines to stop the vom-
iting that had brought her there—medicines that clearly had not worked.
"l feel like I've spent most of the last nine months in a hospital or a doc-
tor's office," Maria told the doctor quietly. And now, here she was again,
back in the hospital. She'd been perfectly healthy until just after last Christ-
mas. She'd come home from college to see her family and hang out with her
friends, and as she prepared to head back to school this strange queasiness
had come over her. She couldn't eat. Any odor—especially food—made her
feel as if she might vomit. But she didn't. Not at first.
The next day, on the drive back up to school, she'd suddenly broken
into a cold sweat and had to pull over to vomit. And once she got started,
it seemed like she would never stop. "l don't know how I made it to school
because it seems like I had to get out of the car to throw up every few min-
utes.
Back at school she spent the first few days of the semester in bed. Once
she was back in class her friends joked that she was just trying to get rid of

the extra pounds from the holidays. But she felt fine and she wasn't going
to worry about it.
Until it happened again. And again. And again.
The attacks were always the same. She'd get that queasy feeling for a
few hours, and then the vomiting would start and wouldn't let up for days.
There was never any fever or diarrhea; no cramps or even any real pain.
She tried everything she could find in the drugstore: Tums, Pepcid, PeptoBismol, Prilosec, Maalox. Nothing helped. Knowing that another attack
could start at any moment, without warning, gnawed insistently in the back
of her mind.
She went to the infirmary with each attack. The doctor there would get a

She went to the infirmary with each attack. The doctor there would get a
pregnancy test and when it was negative, as it always was, he'd give her some
intravenous fluids, a few doses of Compazine (a medicine to control nau-
sea), and, after a day or two, send her back to the dorm. Halfway through
the semester she withdrew from school and came home.
Maria went to see her regular doctor. He was stumped. So he sent her
to a gastroenterologist, who ordered an upper endoscopy, a colonoscopy,
a barium swallow, a CT scan of her abdomen, and another of her brain.
She'd had her blood tested for liver disease, kidney disease, and a handful of
strange inherited diseases she'd never heard of. Nothing was abnormal.
Another specialist thought these might be abdominal migraines. Migraine
 headaches are caused by abnormal blood flow to the brain. Less commonly,
the same kind of abnormal blood flow to the gut can cause nausea
and vomiting—a gastrointestinal equivalent of a migraine headache. That
doctor gave Maria a medicine to prevent these abdominal "headaches" and
another one to take if an attack came anyway. When those didn't help, he
tried another regimen. When that one failed, she didn't go back.
The weird thing was, she told Hsia, the only time she felt even close to
normal during these attacks was when she was standing in a hot shower.
Couldn't be a cold shower; even a warm shower didn't quite do it. But if she
could stand under a stream of water that was as hot as she could tolerate,

The weird thing was, she told Hsia, the only time she felt even close to
normal during these attacks was when she was standing in a hot shower.
Couldn't be a cold shower; even a warm shower didn't quite do it. But if she
could stand under a stream of water that was as hot as she could tolerate,
the vomiting would stop and the nausea would slowly recede. A couple of
times she had come to the hospital only because shed run out of hot water
at home.

Recently, a friend suggested that maybe this was a food allerw, so she
gave up just about everything but ginger ale and saltines. And that seemed
to work—for a while. But two days ago she'd woken up with that same bil-
ious feeling. She'd been vomiting nonstop since yesterday.
Maria Rogers was a small woman, a little overweight with a mass of long
brown hair now pinned back in a barrette. Her olive skin was clear though
pale. Her eyes were puffy from crying and fatigue. She looked sick, and was
clearly distressed, Hsia thought, but not chronically ill.
How often did she get these bouts of nausea? she asked the girl. Maybe
once a month, she told her. Are they linked to your periods? Hsia offered
hopefully. The girl grimaced and shook her head. Are they more common
just after you eat? Or when you're hungry? Or tired? Or stressed? NO, no,
no, and no. She had no other medical problems, took no medicines. She was
a social smoker—a pack of cigarettes might last a week, sometimes more.
She drank—mostly beer, mostly on the weekends when she went out with

Recently, a friend suggested that maybe this was a food allergy, so she
gave up just about everything but ginger ale and saltines. And that seemed
to work—for a while. But two days ago she'd woken up with that same bilious
 feeling. She'd been vomiting nonstop since yesterday.
Maria Rogers was a small woman, a little overweight with a mass of long
brown hair now pinned back in a barrette. Her olive skin was clear though
pale. Her eyes were puffy from crying and fatigue. She looked sick, and was
clearly distressed, Hsia thought, but not chronically ill.
How often did she get these bouts of nausea? she asked the girl. Maybe
once a month, she told her. Are they linked to your periods? Hsia offered
hopefully. The girl grimaced and shook her head. Are they more common
just after you eat? Or when you're hungry? Or tired? Or stressed? NO, no,
no, and no. She had no other medical problems, took no medicines. She was
a social smoker—a pack of cigarettes might last a week, sometimes more.
She drank—mostly beer, mostly on the weekends when she went out with

More Than Just the facts
Dr. Hsia was a resident in Yale's Primary Care Internal Medicine residency
training program, where I now teach. She told me about Maria Rogers be-
cause she knew I collected interesting cases and sometimes wrote about

Ste hit the  enter Key and a second later the screen 'led
her to a disease Hsia had never heard Of  cannabinoid hyperemesis—
persistent and excessive vomiting (hypereremesis) associated with chronic cannabis use.

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My Indian Kirana store ( Grocery store,department store,Supermarket) had the best consumer experience.

My Indian Kirana store ( Grocery store,department store,Supermarket) had the best consumer experience 40 years ago.
All I had to do was call the shop and give the owner the list of things I want,by reading the list I made.Sometimes he would suggest  some useful additions.
 Few hours later I would get all of it delivered  in  reusable cloth bags in which there were Packets made of recycled Newspaper.

Tell me  which Amazon or Alibaba has made it that convenient.
All they have done is  fool the consumers kill the Mom and Pop store and the variety and choice in Life.

Then there are these so called Pundits  who write  literally shitty stories  in Big magazines


Amazon Go Means Goodbye Status Quo Jul 6, 2018 the article praised "Amazon Go" in Superlative  positive terms
Chris Walton Contributor 
 
less than onemonth later the same guy wrote 
 
Aug 3, 2018 

Amazon Go Has Been Flawed From The Get-Go - Forbes

  
Retail
I write serious and sometimes comic musings on retail's evolution
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Wednesday, November 20, 2019

A Vanishing Art Physical examination in Medical Diagnosis

A Vanishing Art
Here's a Story I read nor long ago in the New England Journal of Medicine:
A man in his fifties comes to an emergency room with excruciating chest
pain. A medical student is told to check the blood pressure in both arms.
He checks the closer arm and calls Out the blood pressure. He moves to the
other side of the patient bur is unable to find a blood pressure. Worried that
this is due to his inexperience rather than a true physical finding, he says
nothing. No one noticæs. Overnight the patient is rushed to the operating
room for repair of a tear in the aorta, the vessel that carries blood out of the
heart to the rest of the body. He dies on the operating table.

A difference in blood pressure between arms or the loss of blood pressure
in one arm is strong evidence of this kind of tear, known as a dissecting
aortic aneurysm. The student's failure to speak up about his inability to read
the blood pressure on one side of the patient's body prevented the discovery
of this evidence.
Here's another story—this one from a colleague of mine:
A middle-aged woman comes to the hospital With a fever and difficulty
breathing. Shed been treated for pneumonia a week earlier. In the hospi
tal she's started on powerful intravenous antibiotics. The following day she

complains of in her back and weakness in her legs. She has a history of
chronic back pain and her doctors give her painkillers. They do not examine
her. When her fever spikes and her white blood cell count soars, the team
gets a CT scan Of the chest, looking for something in her lungs that would
account for a worsening infection. What they find instead is an abscess on
her spinal cord. She is rushed to surgery.
Had the team examined her, they would have found a loss of sensation
and reflexes, which would have alerted them to the presence Of the spinal
cord lesion.
This Story was recently presented at Grand Rounds, a high-profile weekly
lecture for physicians, at Yale:
A man has a heart attack and is rushed to the hospital, where the blocked
coronary artery is reopened. In the ICU, his blood pressure begins to drop;
he complains of feeling cold and nauseated. The doctors Order intravenous
fluids to bring up his dangerously low blood pressure. They do not examine
him. When, after several hours, his blood pressure continues to drop, the
him. When, after several hours, his blood pressure continues to drop, the
cardiologist is called and she rushes back. When she examines him she sees
that his heart is beating rapidly but is barely audible. The veins in his neck
are distended and throbbing. She immediately recognizes these as signs that
the man has bled into the sac around his heart—a condition known as tamponade. It is a well-known complication Of (he procedure shed done just
hours before. She rushes him back to the OR and begins draining the blood,
which by now completely fills the sac, preventing the heart from beating.
Despite her efforts, the man dies on the table. Had the doctors in the
examined the patient, rather than paying attention only to the monitors
tracking his vital signs, they would have been able to diagnose this potentially reversible complication.
This is another kind Of Story doctors tell one another in hospital hallways
and stairwells—cautionary tales from the pages of our best journals, cases
presented at the weekly Grand Rounds Or Morbidity and Mortality Conferences, where medical errors are traditionally discussed. These are the
tragic stories Of patients Who worsen and sometimes die because clues that
could have and should have been picked up With a simple physical examination were overlooked or ignored. We repeat them to one another as lessons learned—a prayer and talisman. We tell them with sympathy because
we fear that any one of us might have been that doctor, that resident, that
medical student.
These anecdotes reveal a truth already accepted by most doctors: the
physical exam—once our most reliable tool in understanding and diagnosing a sick patient—is dead.
wasn't a sudden or unanticipated death. The death of the physical
exam has been regularly and carefully discussed and documented in hospital hallways and auditoriums and in the pages Of medical journals for over
twenty years. Editorials and essays have posed
once unthinkable questions
like: "Physical diagnosis in the 1990s: Art or artifact?" or "Has medicine
Outgrown physical diagnosis?" and "Must doctors examine patients?" And
finally in 2006, the flat announcement Of the long-anticipated death was
valued part Of being a doctor.

finally in 2006, the flat announcement Of the long-anticipated death was
carried in the pages Of the New Journal of Medicine. In "The De-
mise of the Physical Exam," Sandeep Jauhar tells the story of that inexperienced medical
 student couldn't find a blood pressure on a man With chest pain and an aortic dissection Who dies as a result. It is the tasty opening anecdote in an Obituary—not for the patient but for this once
valued part Of being a doctor.
The physical exam was once the centerpiece of diagnosis. The patient's
story and a careful examination would usually suggest a diagnosis, and then
tests, when available, could be used to confirm the finding. These days,
when confronted with a sick patient, doctors often skip the exam altogether,
instead shunting the patient directly to diagnostic imaging or the lab, where
doctors can cast a wide net in search of something they might have found
more quickly had they but looked. Sometimes a cursory physical examination-
 is attempted but With expectations as physicians, instead, eagerly
await results Of a test they hope Will tell them the diagnosis.
Many doctors and researchers are troubled by this   shift. They complain

about the overuse of expensive high-tech tests and decry' the decline of the
skills needed to conduct an effective physical exam. Yet despite this uneasi-
ness, doctors and even patients increasingly prefer What they perceive to be
the certainty Of high-technology testing to a low-tech, hands-on examina-
tion by a physician.
Measuring the loss of Skills
In the early 1 Salvatore Mangione, a physician and researcher at Thomas
Jefferson University Medical Center in Philadelphia, began studying how
well doctors were able to recognize and interpret common findings on one
fundamental component of the physical exam, the examination of the heart.
He rested 250 medical students, residents, and postgraduate fellows specializing in cardiology from nine different training programs. The investigation
Was straightforward enough: students and doctors Were given an hour to
listen to twelve important and Common heart sounds and answer questions
about what they heard.


The results were stunning and controversial. A majority Of the medical
students could identify only two out of the twelve sounds correctly. The
other ten were recognized by only a handful of the students. Surprisingly,
the residents did no better. Despite their additional years of experience
and training, they were able to correctly identify only the same two examples. Perhaps most disturbing Of all, most Of the doctors holding a post residency fellowship in cardiology were unable to identify six out of the twelve sounds.
In a similar test on lung sounds, Mangione again found that students and
residents failed to identify many Of the most common and most important
sounds of the body. If letter grades were being handed out, all but a handful
Of these participants would have gotten a big fat F.
In the years since Mangione first published his studies, editorials and lec-
curers have bemoaned this loss of skills and warned that if action isn't taken
to remedy the problem, we'll end up with teachers who know no more than their students
Sort of Blind leading the blind.
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Aatish Taseer's OCI revocation. rahul gandhi's British citizenship.

Shikha Dalmia writes in  "The week"  about  the  outrage  of  Aatish Taseer's OCI revocation.

"The official line is that Taseer, who was born in England to an Indian mother and a Pakistani father, committed fraud by failing to reveal his father's heritage on his OCI application.  
This accusation is beyond absurd given that Taseer comes from an extremely prominent family whose history has been public knowledge for decades"

So now legal documents on which these members of the so called  "prominent families" lie, need to be  over looked  just because of public knowledge"
What about  Rahul Gandhi's affidavit and  British Citizenship . Did any  Media outlet do some investigation to  put this to rest ?
 Isn't Gabdhi's family also a "prominent" one ?
By the  same logic  Rahul Gandhi should get  Italian citizenship .



Rahul Gandhi got his  Amethi nomination accepted on a technicality
the  issue  of his  affidavit  and alleged British citizenship claim are still not conclusively proved  wrong.

When he was Born to Sonia Gandhi She was holding  an Italian passport. Does it make him an Italian Citizen ?

From Wikipedia
Former senior Congress leader and former President of India Pranab Mukherjee said that she surrendered her Italian passport to the Italian Embassy on 27 April 1983
And she was granted  Indian citizenship By registration 3 days  after wards on April 39 1983

 From FrontLine


A citizenship question

The Supreme Court dismisses two election petitions which base themselves on a challenge of the Indian citizenship status of Sonia Gandhi, citing deficiency in pleadings.
V.VENKATESAN
in New Delhi
EVER since Congress(I) president Sonia Gandhi signalled some years ago her intention to enter electoral politics, her political adversaries have raised constitutional and legal questions with regard to her very right to claim Indian citizenship, and her eligibility to become a Member of Parliament or be chosen for political office. Sonia Gandhi was first elected to the Lok Sabha from two seats - Amethi in Uttar Pradesh and Bellary in Karnataka - in the 13th Lok Sabha elections held in 1999. She relinquished the Bellary seat.
AJIT KUMAR/AP
Congress(I) president and Leader of the Opposition Sonia Gandhi.
Three election petitions were filed in the Allahabad High Court challenging her election on the grounds that she, being an Italian citizen, did not satisfy the prerequisites for registration as a citizen of India. Of the three petitions, two were filed by candidates who had lost in Amethi in 1999: Hari Shanker Jain and Hari Krishna Lal. The third petition was filed by Prem Lal Patel, a voter in Amethi. The Lucknow Bench of the Allahabad High Court which heard the petitions, had held that none of the three petitions disclosed any cause of action or triable issue and as such none was maintainable under Section 86 of the Representation of the People Act, 1951, dealing with the trial of election petitions.
Jain had also challenged the legality of Section 5(1)(c) of the Citizenship Act, 1955, under which Sonia Gandhi acquired her Indian citizenship through registration. Under this provision, persons who are, or have been married to, citizens of India and are ordinarily resident in India and have been so resident for a period of 12 months immediately before making an application for registration, would be eligible to apply for Indian citizenship by means of registration. (This provision was amended in 1986 whereby the requirement regarding the length of residence was made five years.) Based on her application under this Section, she was issued a certificate of citizenship by the Government of India on April 30, 1983.
The Allahabad High Court dismissed the petitions on May 20, 2000 on the plea that a challenge relating to citizenship or the constitutionality of the Citizenship Act itself could not be adjudicated upon by the High Court in the course of considering an election petition. The High Court also held that the citizenship certificate granted to Sonia Gandhi was final and binding, and unless it was cancelled by the Central government the issue could not be questioned as part of an election petition.
Jain and Lal appealed against the High Court verdict in the Supreme Court. The Supreme Court Bench consisting of Chief Justice A.S. Anand, Justices R.C. Lahoti and Doraiswamy Raju, in its order of September 12, rejected the High Court judgment that an election petition could not challenge a citizenship certificate or the constitutionality of the Citizenship Act. However, the Bench dismissed the appeals because the petitions made only bald and vague averments about Sonia Gandhi's eligibility for Indian citizenship, and therefore, did not satisfy the requirements of pleading material facts under Section 83(1)(a) of RPA, 1951.
Article 84 of the Constitution says that a person shall not be qualified to be chosen to fill a seat in Parliament unless he or she is a citizen of India. Article 102 provides that a person shall be disqualified from being chosen as, and for being, a member of either House if he or she is not a citizen of India or has voluntarily acquired the citizenship of a foreign state, or is under any acknowledgement of allegiance or adherence to a foreign state. That a returned candidate was 'not qualified' or 'was disqualified' to be chosen on the date of his election, is specifically a ground for declaring his/her election void under Section 100(1)(a) of RPA, 1951. Section 16 of RPA, 1950 provides that a person shall be disqualified for registration in an electoral roll if he or she is not a citizen of India.
Therefore, the objections against Sonia Gandhi's citizenship have to be objectively examined. The petitions challenging Sonia Gandhi's election from Amethi had averred that she could not have renounced the Italian citizenship and become a citizen of India when she applied for and was issued a certificate of citizenship under Section 5(1)(c) of the Citizenship Act. However, the petitioners did not give indications of any such clause in the Italian law on which they had based their averments.
Gourab K. Banerji, counsel for Sonia Gandhi, told Frontline that a new Italian Citizenship Act which came into force on August 15, 1992, allows for, in principle, multiple citizenship. This was previously possible only in specific cases. Thus, before August 15, 1992, when an Italian citizen acquired another citizenship he/she automatically lost the Italian citizenship. Indeed, according to the new Citizenship Act, a person can lose Italian citizenship only by formally renouncing it, on condition that one has another citizenship. To renounce citizenship, one must sign a formal statement at the Consulate. According to the 'Information on Citizenship', released by the Consulate General of Italy, an Italian citizen who acquired the citizenship of another country before August 15, 1992 has, in all likelihood, lost Italian citizenship and, unless he/she applies for re-acquisition, is to be considered by Italy as a foreigner.
Sonia Gandhi applied for Indian citizenship by registration, under Section 5(1)(c) of the Citizenship Act, on April 7, 1983 by virtue of her marriage to Rajiv Gandhi in 1968. She voluntarily renounced her Italian citizenship by surrendering her Italian passport to the Italian Embassy in New Delhi on April 27, 1983. This, says Janata Party president, Dr. Subramanian Swamy (who has also been raising questions with regard to Sonia Gandhi's citizenship), had been confirmed by the then Italian Ambassador to India on April 29. The Ambassador had apparently stated that Sonia Gandhi had returned her Italian passport by claiming that she had renounced her Italian citizenship. Even if Subramanian Swamy's argument - that surrendering the passport would not legally amount to renunciation of citizenship - is conceded, Sonia Gandhi would have lost her Italian citizenship on April 30, 1983 when she acquired Indian citizenship by registration. (This writer had stated erroneously in Frontline, June 18, 1999 on page 30, that she became an Indian citizen by naturalisation on April 13, 1983.) Item 10 of Form II (before it was revised in 2000), which is used as an application for registration as a citizen of India under Section 5(1)(c) of the Citizenship Act, only required an undertaking from the applicant that she would renounce the citizenship of her country in the event of her application being sanctioned, while Item 9 of the form gave the applicant an option to state whether she had renounced or lost the citizenship of the other country. Indeed, the form as it stands today, after revision in 2000, seems more liberal, as it retains only Item 10 (now renumbered 11).
More important, it was not necessary - as her critics would seem to imply - that Sonia Gandhi should have resided in India for a continuous period of 12 months before registration as a citizen of India in 1983. The Explanation to Rule 4 of Citizenship Rules, 1956, which deals with the form of application for registration under Section 5(1)(c) makes the point that in computing the period of 12 months (now five years), broken periods of residence may be taken into account.
The petitions have also alleged that Sonia Gandhi's name was wrongly entered in the voters' list - an argument that could not be sustained in the face of the citizenship certificate secured by her in 1983. It is true that her name figured in the electoral roll of the New Delhi Lok Sabha constituency in 1980, and that it was deleted only after an expose by the media. However, in the absence of any proof that she had exercised her franchise before acquiring her citizenship, the inclusion of her name in the voters' list in 1980 could be explained away as an inadvertent entry made by some overzealous enumerators then working under the Election Commission.
A major part of the election petitions against Sonia Gandhi contended that in the constitutional scheme of citizenship a distinction has been drawn between 'citizen of India' and being an 'Indian citizen', restricting electoral rights only to the former, in whom the citizenship vests by right, that is, by birth or by descent. Thus while Articles 5 to 10 use the expression 'Citizen of India', Article 11 which empowers Parliament to make laws with respect to the acquisition and termination of citizenship and all other matters relating to citizenship speaks of 'citizenship' and not of 'citizenship of India', the petitioners argued. They, therefore, suggested that the Citizenship Act, 1955 wrongfully confers the privileges of citizens of India on Indian citizens.
The Bench appreciated the forensic ability of the petitioners in making such a plea, but refused to entertain or adjudicate it for two reasons. First, the petitioners had not stated all material facts to enable the court to examine such a plea with far-reaching implications. Secondly, the challenge so sought to be laid to the constitutional validity of the provisions of the Citizenship Act is very wide and cannot be adjudicated upon without impleading the Central government as a party to the proceedings. In other words, the issue cannot be conveniently tried in an election petition on the basis of vague and indefinite pleas. A serious legal challenge to Sonia Gandhi's citizenship, it appears, is yet to emerge.

 
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Monday, November 18, 2019

There is much more to nasal mucosa than smell!


I remember my father  who used to carry a Vick's inhaler and  Amrutanjan bottle with him always.
in those days  i did not  know about  vasomotor  rhinitis  and  Perennial rhinitis .

our understanding  of  mechanisms of nasal congestion  are still primitive  but  much info is  there  in basic research  which has not been translated into clinical use


. Author manuscript; available in PMC 2014 Oct 26.
Published in final edited form as:
PMCID: PMC4209299
NIHMSID: NIHMS166499
PMID: 19686200

Neuroregulation of Human Nasal Mucosa

James N. Baraniuk and Samantha J. Merck
Author information Copyright and License information Disclaimer

Abstract

Multiple subsets of nociceptive, parasympathetic, and sympathetic nerves innervate human nasal mucosa. These play carefully coordinated roles in regulating glandular, vascular, and other processes. These functions are vital for cleaning and humidifying ambient air before it is inhaled into the lungs. The recent identification of distinct classes of nociceptive nerves with unique patterns of transient receptor potential sensory receptor ion channel proteins may account for the polymodal, chemo- and mechanicosensitivity of many trigeminal neurons. Modulation of these families of proteins, excitatory and inhibitory autoreceptors, and combinations of neurotransmitters introduces a new level of complexity and subtlety to nasal innervation. These findings may provide a rational basis for responses to air-temperature changes, culinary and botanical odorants (“aromatherapy”), and inhaled irritants in conditions as diverse as allergic and nonallergic rhinitis, occupational rhinitis, hyposmia, and multiple chemical sensitivity.
Keywords: transient receptor potential, TRPV1, nociceptive axon response, nociception

Introduction

The nose is the contact zone that scrubs particulate and water-soluble volatile compounds from inhaled air so that only clean, humidified air reaches the lungs. The processes that carry out these functions are under strict physiological control that depends on local mucosal feedback systems and sensory and autonomic reflexes. The histological distributions of sensory and autonomic nerves and their neurotransmitters define the potential functions of each of these sets of nerves. Sensory neurons contain calcitonin gene related peptide (CGRP), gastrin releasing peptide (GRP), the tachykinins (neurokinins) substance P and neurokinin A (NKA), and possibly other peptides. CGRP receptors are most dense on arterial and arteriovenous vessels. This is consistent with the potent vasodilator action of this neuropeptide. Neurokinin receptors are widely expressed on many cell types, while GRP receptors are most dense on glands. Glutaminergic afferent neurons may also be present. Parasympathetic neurons may have two populations: larger diameter acetylcholine containing neurons and smaller diameter neurons that release vasoactive intestinal peptide (VIP) and nitric oxide. Sympathetic neurons also have at least two subpopulations that contain norepinephrine with or without neuropeptide Y (NPY). These are short- and long-acting vasoconstrictors, respectively. Adenosine triphosphate may also be a transmitter in nasal sympathetic neurons. The sensory neurons convey information about the conditions of inhaled air from the epithelium to the brain stem, and release neurotransmitters locally within the mucosa by the efferent axon response mechanism. This response is a rapidly induced defense mechanism for hypersecretion of mucus and protection of the nasal mucosa. Acetylcholine stimulates muscarinic M3 and possibly M1 receptors on glands to cause exocytosis. Sympathetic discharge constricts the vessels of the mucosa, squeezes the blood out of the erectile venous sinusoids, and so thins the mucosal lining. This process regulates the cross-section area for airflow, and so nasal patency.

Type C Neurons and Sensory Receptors

Nonmyelinated Type C neurons have specific multimodal chemoreceptors that activate the nasal mucosal trigeminal chemoreceptor system. Irritants, such as carbon dioxide, powdered mannitol, adenosine, hypertonic saline (HTS) solution, and other nociceptive agents, stimulate trigeminal neural responses that are distinct from olfactory sensations. Inhalation of odorless CO2 stimulates limited brain cortical regions, such as the cingulate gyrus. In contrast, hydrogen sulfide stimulates olfactory neurons that activate frontal, entorhinal, occipital, and cerebellar cortical regions. Capsaicin, the spicy essence of chili peppers, activates laryngeal and pharyngeal vagal and glossopharyngeal afferents that induce the urge to cough. Functional magnetic resonance imaging demonstrates activation of the primary and visceral insular sensory cortices, anterior midcingulate and orbitofrontal cortices responsible for planning and executive functions, and execution or repression of an active cough via the supplementary motor area and cerebellum.
HTS sprayed onto the inferior turbinate generates a rapid onset, sharp burning sensation (“first pain”) that is likely mediated by fast conducting, thinly myelinated Aδ nerve fibers. A parasthetic, tingling, “second pain” sensation follows. Both the intensity of the first pain and duration of the second pain were related to the HTS dose. HTS may have stimulated Type C neurons that have nerve endings in the epithelium but also are extensively branched around submucosal glandular acini, since substance P was released during the first 3-min period. Other colocalized neurotransmitters, such as NKA and GRP, may also have been released at the same time and sites. Tachykinin NK-1 receptor mRNA and autoradiographic GRP binding sites have been localized to glands., These neuropeptides may have stimulated the HTS dose-dependent glandular secretion that occurs during the 3- to 5-min period after HTS application. This secretion is not altered by the anticholinergic drug ipratropium bromide, indicating that central parasympathetic reflexes were not recruited. There was also no change in albumin concentration in nasal lavage fluid, indicating no alteration in baseline vascular permeability. This finding was reproduced in normal, acute allergic rhinitis, and acute and chronic rhinosinusitis subjects.
These findings suggest that HTS-induced axon responses in humans induce copious glandular exocytosis with no significant vascular component. Thus, human nasal mucosal neurogenic inflammation is a rapid-onset mucosal defense mechanism designed to stimulate secretion of submucosal gland mucins and antimicrobial proteins onto the nasal epithelial lining fluid where they will replenish gel and sol phase components to adsorb inhaled irritants and particulate material and kill or neutralize microbes and their toxins.
Histamine nasal provocation causes itch, vascular permeability, and cholinergic reflex-mediated glandular secretion. These effects are consistent with the symptoms of allergic rhinoconjunctivitis that follow mast cell histamine release. Histamine H1 receptors have been localized to a population of very narrow-diameter neurons that are localized to distinct spinal cord dorsal horn regions, ascending pathways, thalamus, and thalamocortical radiations from capsaicin-sensitive neurons. HistamineH3andH4 receptors on these and other neurons act as inhibitory autoreceptors that inhibit neuron depolarization. H2 receptors are present on epithelium and glands. Histamine-induced axon responses have not been clearly demonstrated in human airway mucosa.
“Itch” neurons may rely in part on GRP as a pruritogenic neurotransmitter. GRP receptors are restricted to lamina I of the dorsal horn of the spinal cord, which receives input from Type C neurons. Mice with point mutations in GRP receptors have reduced scratching behavior in response to pruritogenic stimuli, yet intact thermal, mechanical, neuropathic, inflammatory, and pain responses.
The population of itch-specific neurons may be small. Other H1 receptor-bearing neurons appear to express the capsaicin receptor that may mediate a burning, prickly heat sensation. The capsaicin receptor is a multimodal sensory receptor and ion channel that has been classified as the transient receptor potential vanilloid 1 (TRPV1) protein. Other distinct combinations of proteins, such as purinergic P2X receptors and acid sensing ion channel 3 (ASIC3), may also be present on subsets of TRPV1 neurons. These would respond to ATP, adenosine, H+, K+, and Ca2+ that may be released by cellular injury or ischemia, or during inflammation. The functions of these neurons may be significantly modulated by inflammatory mediators, such as leukotriene B4, nerve growth factor (NGF; TrkA receptor), brain-derived neurotrophic factor (BDNF), and neurotrophin-4 (NT-4) (TrkB receptor), and NT-3 (TrkC receptor). These can induce plasticity of neurotransmitter, sensory, and inhibitory autoreceptor expression, which alters the sensations or sensitivities of dorsal root ganglion and dorsal horn interneuron subpopulations.
Cold dry air inhalation causes a dose-dependent obstruction of nasal airflow in humans with idiopathic nonallergic rhinitis. Healthy controls do not develop obstruction. In contrast, individual mediators with G protein-coupled 7-transmembrane receptors, such as bradykinin and endothelin 1, could not discriminate between these idiopathic rhinitis and control subjects. In contrast, both bradykinin and endothelin 1 were able to stimulate nociceptive neurons and recruit parasympathetic reflexes during severe allergic rhinitis, indicating the induction of mucosal hypersensitivity., Other trigeminal irritants, such as low-dose chlorine that does not induce any sensory perception, can induce neurogenic nasal airflow obstruction without neuropeptide release. A local mucosal mechanism is hypothesized.

Voltage-gated Ion Channel Protein Family

TRPV1 was the first of a family of 143 human voltage-gated ion channels to be identified and its activating ligands characterized. This family includes other sensors: sodium channels responsible for cell depolarization; calcium channels that mediate complete depolarization that activates the functions of neuron, gland, muscle, and other electro-excitable cells; and potassium channels that repolarize and maintain the resting membrane potential of these cells.– The basic motif of this family of transmembrane proteins is the presence of a single extracellular loop that dips into, but does not cross, the plasma membrane. Transmembrane alpha helices bracket this intramembrane loop. These proteins polymerize into tetramers with adjacent intramembrane loops that form the pores that regulate the flow of specific ions into or out of cells. Heterotetramers may form that have modified responses compared to homotetramers.
TRPV1 is a highly promiscuous polymodal chemoreceptor. Capsaicin, temperatures above 43°C, local anesthetics, nicotine, ethanol, endocannabinoid family of arachidonic acid metabolites, and products of 12- and 15-lipoxygenases interact with distinct portions of TRPV1 to activate a rapid influx of Na+ and Ca2+. Other receptors, such as the bradykinin B2 receptor, activate intracellular phosphokinases that can phosphorylate the C-terminal region of TRPV1 to further fine-tune its responses.
TRPV1 was initially thought to be present only on nociceptive nerves, but it is also present in the substantia nigra, hippocampus, and hypothalamus. In addition,TRPV1is also present on airway, skin, gastrointestinal, bladder, and rectal epithelial cells. This means that capsaicin and its many other ligands can activate a broad array of tissues without neural involvement. Expression of TRPV1 and probably other, related sensors on epithelium greatly expands the potential for complex interactions between these cells, intermediate messenger molecules, and Type C neurons. Human 293t embryonic kidney cells transfected with TRPV1 exhibited calcium ion influx indicative of depolarization when stimulated with capsaicin and cyclohexanone. Wild-type and transfected cells did not respond to other chemically related trigeminal and olfactory agents, such as acetic acid, R-(−)-carvone, S-(+)-carvone, amyl acetate, toluene, benzaldehyde, (−)-nicotine, or R-(+)-limonene. This implies that additional, separate TRP, olfactory, or other sensory receptor proteins that mediate the trigeminal, irritant actions of these chemicals remain to be identified.

The TRP Thermometer and Aromatherapy

TRPV1 is the only capsaicin-sensitive channel. However, other culinary spices have played major roles in the discovery of TRP protein families. Many of these proteins are multimodal and respond to specific temperature and osmolality ranges. A “TRP thermometer” can be constructed to illustrate this diversity (Fig. 1). TRPV3 and TRPV4 respond to ambient temperatures. They are also mechanicosensitive and are activated by changes in cell swelling caused by hyper- and hypoosmolar conditions. Temperatures ≥42°C activate TRPV1, while TRPV2 responds to dangerously high, tissue damaging temperatures ≥52°C. TRPV2 are likely present on rapidly responding Aδ neurons. TRP melanostatin 8 (TRPM8) menthol receptors respond to temperatures between 8°C and 22°C. TRPM8 proteins also respond to lysophospholipids and may be sensors of membrane fluidity. Temperature-dependent changes in fluidity may alter the shape of TRPM8 leading to pore opening, calcium influx, and cellular depolarization that lead to differences in the frequencies of depolarization rates in order to convey different temperatures. The TRP melanostatin 4 (TRPM4) responds to mint and the odorless, topical coolant icilin found in many cutaneous ointments, but does not respond to menthol or cool temperatures. “Very cold” temperatures, mustard oil and garlic isocyanate compounds, and tetrahydrocannabinol activate theTRPA1 (ankryn) receptor and “cold pain.”

TRP thermometer and aromatherapy: the trigeminal chemosensory nervous system. Used with permission of the copyright holder.
The TRP thermometer may provide insights into the specific airway obstruction caused by cold dry air in idiopathic, nonallergic, noninfectious, noneosinophilic rhinitis. The cold temperature may directly activate TRPM8 or TRPA1 ion channels on Type C or Aδ neurons. Activation of cold receptors in the nose regulates brain stem motor afferents that modify the breath-to-breath work of breathing. Activation of TRPM8 by menthol and cold air has long been known to produce a transient sensation of airway patency and reduced inspiratory muscle effort. Dry air must become fully hydrated in the nose in order to prevent desiccation of laryngeal, tracheobronchial, and alveolar airways. The evaporation of water from the epithelial lining fluid into the inhaled air has an additional cooling effect due to the enthalpy change. Evaporation increases the tonicity of the epithelial lining fluid and so may act in the same fashion as the HTS provocation model. This further supports a potential role for osmolarity changes and cellular deformation that may induce torsion of putative mechanicosensors on sensory nerves. Osmosensors, such as TRPV3 and TRPV4, may be instrumental in transducing these events by depolarizing sensory neurons. These conjectures may prove to be premature, but investigation of these mechanisms may lead to the development of novel drugs that reduce dyspnea that is currently untreatable but very bothersome in chronic obstructive pulmonary disease, and to reduce the sensation of nasal congestion or fullness that occurs in all virtually all forms of rhinosinusitis.

Conclusions

The regulation of nasal mucosal function by distinct classes of neurons is a new and exciting development. The exchange of neurotransmitters and cellular signaling molecules may generate bilateral trophic effects that regulate epithelial cell, superficial lamina propria vascular, submucosal gland, and deep venous sinusoid activities. Axon response release of neurotransmitters in the mucosa may influence innate and acquired immune responses given the high density of neuropeptide receptors on antimicrobial protein-rich serous cells and lymphocytes, respectively. The HTS provocation model indicates that nociceptive nerve axon responses and “neurogenic inflammation” lead to glandular exocytosis with no vascular leak in human airway mucosa. This is in stark contrast to effects in rat trachea and other rodents, where vascular permeability is induced. Irritant responses may be initiated by activation of TRP, acid-sensing ion channel, purinergic, and other sensory receptors on epithelial cells as well as Type C neurons. These polymodal responses may work in concert with specific mediator receptors to transduce a wide variety of temperature, osmolality, irritant chemical exposure, and other information about the conditions of inhaled air from the nasalmucosa to the central nervous system. A better understanding of the dynamic interactions of the many potential combinations of excitatory sensory and regulatory voltage-gated ion channels, inhibitory autoreceptors, and plasticity of peptidergic and nonpeptidergic neurotransmitters expressed in distinct trigeminal neuron sub populations will provide for more sophisticated insights into the roles of nociceptive and other nerve subpopulations in regulating nasal mucosal functions.
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Sunday, November 17, 2019

Can Acalypha indica be used to attract other big cats like tigers and lions in the wild ?

Can Acalypha indica be used to attract other big cats like tigers and lions in the wild ?


Effect on domestic cats

Throughout the area where the plant grows, it is widely known for its effect on domestic cats, which react very strongly and favorably to the root of the plant. In this regard it is very similar to catnip, but the effect is much more pronounced. For this reason it is called Poonamayakki in Tamil, and Pokok Kucing Galak (Excited Cat Tree) in Malay.

Acalypha indica

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Acalypha indica
Acalypha indica.JPG
Scientific classification edit
Kingdom: Plantae
Clade: Tracheophytes
Clade: Angiosperms
Clade: Eudicots
Clade: Rosids
Order: Malpighiales
Family: Euphorbiaceae
Subtribe: Acalyphinae
Genus: Acalypha
Species:
A. indica
Binomial name
Acalypha indica
Synonyms
  • Acalypha bailloniana Müll.Arg.
  • Acalypha canescens Benth., nom. nud.
  • Acalypha bailloniana Müll.Arg.
  • Acalypha caroliniana Blanco, nom. illeg.
  • Acalypha chinensis Benth.
  • Acalypha ciliata Benth., nom. nud.
  • Acalypha cupamenii Dragend.
  • Acalypha decidua Forssk.
  • Acalypha fimbriata Baill.
  • Acalypha indica var. bailloniana (Müll.Arg.) Hutch.
  • Acalypha indica var. minima (H.Keng) S.F.Huang & T.C.Huang
  • Acalypha minima H.Keng
  • Acalypha somalensis Pax
  • Acalypha somalium Müll.Arg.
  • Acalypha spicata Forssk.
  • Cupamenis indica (L.) Raf.
  • Ricinocarpus baillonianus (Müll.Arg.) Kuntze
  • Ricinocarpus deciduus (Forssk.) Kuntze
  • Synonym Ricinocarpus indicus (L.) Kuntze[1]
Acalypha indica (English: Indian Acalypha, Indian Mercury, Indian Copperleaf, Indian Nettle, Three-seeded Mercury) is an herbaceous annual that has catkin-like inflorescences with cup-shaped involucres surrounding the minute flowers. It is mainly known for its root being attractive to domestic cats, and for its various medicinal uses. It occurs throughout the Tropics.
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