greenmedinfo--2020-09-08--131 Ways For An Infant to Die

131 Ways For An Infant to Die

There are 130 official ways for an infant to die ( as categorized in the ICD ) , and one unofficial way for an infant to die : following an adverse reaction to one or more vaccines .
There are 130 official ways for an infant to die .
These official categories of death , sanctioned by the Centers for Disease Control and Prevention ( CDC ) and the World Health Organization ( WHO ) , are published in the International Classification of Diseases ( ICD ) .1-3 When a baby dies , coroners must choose from among these 130 @ @ @ @ @ @ @ listed in the ICD include nearly every imaginable — and tragic — possibility .
However , there is NO category for infant deaths caused by vaccines.4 This is odd because the federal government is aware that vaccines permanently disable and kill some babies — the very reason Congress established a `` death and disability '' tax on childhood vaccines more than 25 years ago when the National Childhood Vaccine Injury Act of 1986 ( Public Law 99-660 ) created the National Vaccine Injury Compensation Program ( VICP ) .
Many parents do n't @ @ @ @ @ @ @ their babies , the cost is taxed and the money goes into a special fund to compensate them if and when those vaccines seriously injure or kill their babies .
As of June 2014 , $ 2.7 billion was granted for thousands of injuries and deaths caused by vaccines .
Numerous cases are still pending .
Awards were issued for permanent injuries such as learning disabilities , seizure disorders , mental retardation , paralysis , and numerous deaths , including many that were initially misclassified as sudden infant death syndrome ( SIDS ) @ @ @ @ @ @ @ by the federal government but there is NO official classification for vaccine-related deaths in the ICD , two important questions must be asked : • Are some deaths that are listed within the 130 infant mortality death categories really deaths that are associated with vaccination ?
• Are some vaccine-related deaths hidden within the death tables ?
Prior to the introduction of organized vaccination programs , `` crib death '' was so rare that it was not mentioned in infant mortality statistics .
In the United States , national immunization campaigns were initiated @ @ @ @ @ @ @ were introduced and promoted .
For the first time in history , most U.S. infants were required to receive several doses of DPT ( diphtheria , pertussis , tetanus ) , polio , and measles vaccines.6 By 1969 , an alarming epidemic of sudden unexplained infant deaths impelled researchers to create a new medical term — sudden infant death syndrome ( SIDS ) .7 By 1972 , SIDS had become the leading cause of post-neonatal mortality ( deaths of infants from 28 days to one year old ) in the United States.8 In @ @ @ @ @ @ @ Statistics , operated by the CDC , created a new cause-of-death category to document deaths due to SIDS.9,10 SIDS is defined as the sudden and unexpected death of an infant which remains unexplained after a thorough investigation , including performance of an autopsy and review of the clinical history.11 Although there are no specific symptoms associated with SIDS , an autopsy often reveals congestion and edema of the lungs and inflammatory changes in the respiratory system.9,12 In 1984 , Congress held a hearing on vaccine safety .
The suspected link between vaccines and @ @ @ @ @ @ @ following excerpt is from a statement made by a distraught grandmother testifying before the Congressional Committee on Labor and Human Resources : My name is Donna Gary .
I am a constituent of Senator Kennedy 's from Massachusetts .
Our family should have celebrated our very first granddaughter 's first birthday last month .
Instead , we will commemorate the anniversary of her death at the end of this month .
Our granddaughter , Lee Ann , was just 8 weeks old when her mother took her to the doctor for her routine @ @ @ @ @ @ @ , her first DPT inoculation and oral polio vaccine .
In all her entire 8 weeks of life this lovable , extremely alert baby had never produced such a blood-curdling scream as she did at the moment the shot was given .
Neither had her mother ever before seen her back arch as it did while she screamed .
She was inconsolable .
Even her daddy could not understand Lee Ann 's uncharacteristic screaming and crying .
Four hours later , Lee Ann was dead .
`` Crib death , '' the doctor @ @ @ @ @ @ @ Could it be connected to the shot ? ''
her parents implored .
`` But she just had her first DPT shot this afternoon .
Could there possibly be any connection to it ? ''
`` No , no connection at all , '' the emergency room doctor said definitely .
My husband and I hurried to the hospital the following morning after Lee Ann 's death to talk with the pathologist before the autopsy .
We wanted to make sure he was alerted to her DPT inoculation such a short time before @ @ @ @ @ @ @ was something else he could look for to make the connection .
He was unavailable to talk with us .
We waited two-and-a-half hours .
Finally , we got to talk to another doctor after the autopsy had been completed .
He said it was SIDS .
In the months before Lee Ann was born , I regularly checked with a friend as to the state of her grandchild 's condition .
He is nearly a year-and-a-half older than Lee Ann .
On his first DPT shot he passed out cold for 15 @ @ @ @ @ @ @ office .
`` Normal reaction for some children , '' the pediatrician reassured .
The parents were scared , but they knew what a fine doctor they had .
They trusted his judgment .
When it was time for the second shot , they asked `` Are you sure it 's alright ?
Is it really necessary ? ''
Their pediatrician again reassured them .
He told them how awful it was to experience , as he had , one of his infant patient 's bout with whooping cough .
That baby had @ @ @ @ @ @ @ DPT shot that day .
He became brain-damaged .
This past week I had an opportunity to read through printed copies of the hearings of this committee .
I am dismayed to learn that this same talk has been going on for years , and nothing has seemed to progress to incorporate what seems so obvious and necessary to keep from destroying any more babies , and to compensate financially those who have already been damaged for life .
How accurate are our statistics on adverse reactions to vaccines when parents have been @ @ @ @ @ @ @ `` No connection to the shot , no connection at all. ''
?
What about the mother I have recently talked with who has a 4-year-old brain-damaged son ?
On all three of his DPT shots he had a convulsion in the presence of the pediatrician .
`` No connection , '' the pediatrician assured .
I talked with a father in a town adjoining ours whose son died at the age of 9 weeks , several months before our own granddaughter 's death .
It was the day after his DPT inoculation @ @ @ @ @ @ @ on the death certificate .
Are the statistics that the medical world loves to quote to say , `` There is no connection , '' really accurate , or are they based on poor diagnoses , poor record keeping ?
What is being done to provide a safer vaccine ?
Who is overseeing ?
Will it be the same scientists and doctors who have been overseeing in the past ?
How much longer does the public have to wait ?
How are physicians and clinics going to be held accountable to see that @ @ @ @ @ @ @ ?
And how are those children who should not receive the vaccine to be identified before they are damaged — or dead ?
Today is the National Day of Prayer .
My prayer is that this committee be instrumental in doing what needs to be done — and soon .
May there not be yet another year pass by with more children afflicted , and some dead , because those who can do so refuse to make the right connection.13 Throughout the 1980s , sudden infant deaths continued to skyrocket .
Parental concerns @ @ @ @ @ @ @ and SIDS reached a fever pitch .
Many parents were afraid to vaccinate their babies .
Authorities sought to reassure parents that vaccines are safe and claimed that sudden unexplained infant deaths following vaccines were merely coincidental .
In 1992 , the American Academy of Pediatrics ( AAP ) came up with a plan to reduce the unacceptable SIDS rate while reassuring concerned moms and dads that sudden unexplained infant deaths were not related to vaccines .
The AAP initiated a national `` Back to Sleep '' campaign , telling parents to place @ @ @ @ @ @ @ , during sleep .
From 1992 through 2001 , the post-neonatal SIDS rate dropped by an average annual rate of 8.6 % .
It seemed as though the `` Back to Sleep '' campaign was successful and that the real cause of SIDS was due not to vaccinations but from babies sleeping on their bellies .
However , a closer inspection of the ICD — the 130 official ways for an infant to die — revealed a loophole .
Medical certifiers , such as coroners , could choose from among several categories of @ @ @ @ @ @ @ They did n't have to list the death as SIDS .
Although the post-neonatal SIDS rate dropped by an average annual rate of 8.6 % from 1992 through 2001 following the AAP 's seemingly successful `` Back to Sleep '' campaign , the post-neonatal mortality rate from `` suffocation in bed '' ( ICD-9 code E913.0 ) increased during this same period at an average annual rate of 11.2 % .
Sudden , unexplained infant deaths that were classified as SIDS prior to the `` Back to Sleep '' campaign , were now @ @ @ @ @ @ @ in bed !
The post-neonatal mortality rate from `` suffocation other '' ( ICD-9 code E913.1-E913.9 ) , from `` unknown and unspecified causes '' ( ICD-9 code 799.9 ) , and from `` intent unknown '' ( ICD-9 code E980-E989 ) , all increased during this period as well.10 In Australia , a similar subterfuge seemed to occur .
Researchers observed that when the SIDS rate decreased , deaths attributed to asphyxia increased.14-16 From 1999 through 2001 , the number of U.S. deaths that were attributed to `` suffocation in bed '' @ @ @ @ @ @ @ .
Although the post-neonatal SIDS rate continued to decline , there was no significant change in the total post-neonatal mortality rate .
In a recent paper ( Malloy and MacDorman ) published in Pediatrics , SIDS researchers made the following observation : Reclassification of SIDS Deaths to `` Suffocation in Bed '' and `` Unknown Causes '' Figure 1 .
The postneonatal SIDS rate appears to have declined from 61.6 deaths ( per 100,000 live births ) in 1999 to 50.9 in 2001 .
However , during this period there was a significant @ @ @ @ @ @ @ suffocation in bed '' and due to `` unknown causes . ''
When these sudden unexpected causes of infant deaths are combined with SIDS deaths , the total SIDS rate remains relatively stable , resulting in a non-significant decline .
Although some studies were unable to find positive correlations between SIDS and vaccines,17-19 there is other evidence that a subset of infants may be more susceptible to SIDS shortly after being vaccinated .
For example , as early as 1933 the Journal of the American Medical Association ( JAMA ) published a paper @ @ @ @ @ @ @ two infants soon after pertussis vaccination .
The first child developed cyanosis and convulsions 30 minutes after vaccination and died suddenly a few minutes later .
The second child developed cyanosis 2 hours after vaccination and then died suddenly.20 In 1946 , Werne and Garrow published a paper in JAMA documenting the sudden deaths of identical twins 24 hours after pertussis vaccination .
The babies had symptoms of shock throughout the night prior to their fatal reactions.21 In the 1960s and 1970s Aborigine infants began to mysteriously die at astonishing rates .
In @ @ @ @ @ @ @ every 2 babies succumbed to an unexplained death — a fatality rate of 50 percent !
Kalokerinos solved the riddle when he realized that the deaths were occurring shortly after the babies were vaccinated .
Health officials had recently initiated a mass vaccination campaign to `` protect '' Aborigine babies ; their deaths corresponded with the vaccination program .
Kalokerinos realized that these babies were severely malnourished , including a vitamin C deficiency .
Their undeveloped immune systems could n't handle the additional stress of vaccination .
Kalokerinos was able to save other @ @ @ @ @ @ @ small quantities of vitamin C ( 100mg per month of age ) prior to their vaccines.22 In Japan , from 1970 through 1974 , there were 37 documented sudden infant deaths following pertussis vaccinations , inciting parents and doctors to reject the shot .
In 1975 , Japanese authorities reacted to these events by raising the age of vaccination from three months to two years .
As a result , the number of vaccine injury compensation claims that were paid out for sudden deaths following vaccination dropped from 37 cases during a 5-year @ @ @ @ @ @ @ next 6-and-a-half years ( from 1975 through August of 1981 ) .
The sudden death rate following vaccination dropped from 1.47 to 0.15 deaths per million doses — a 90 % improvement.23,24 In addition , from the early 1970s ( a period when 3-month-old infants were vaccinated ) to the mid-1980s ( ten years after the age of vaccination was raised to 2 years ) the Japanese infant mortality rate ( infant deaths per 1,000 live births ) dramatically declined from 12.4 to 5.0 — a 60 percent drop !
25 According to @ @ @ @ @ @ @ al ) that investigated the Japanese data and published their summary in Pediatrics : Cherry et al also made the following observation : There is other more recent evidence that delaying vaccinations until a later age could save babies from severe vaccine-related adverse reactions , including sudden deaths .
For example , Human and Experimental Toxicology published a study by Goldman and Miller that investigated more than 38,000 infant reports filed with the Vaccine Adverse Event Reporting System ( VAERS ) .
( This federally mandated vaccine safety surveillance program collects information about @ @ @ @ @ @ @ Cases that listed either `` hospitalization '' or `` death '' were evaluated relative to all infant reports , including those that were non-serious .
The hospitalization rate for infants that were vaccinated shortly after birth was an astonishing 20.1 % but decreased in a statistically significant linear fashion to 10.7 % for infants that were vaccinated just prior to their first birthday .
This study also revealed a statistically significant lower mortality rate for infants that were vaccinated between 6 months and 1 year of age when compared to infants vaccinated between @ @ @ @ @ @ @ 1982 , William Torch , MD , director of Child Neurology , Department of Pediatrics , University of Nevada School of Medicine , presented a study at the 34th Annual Meeting of the American Academy of Pediatrics showing that two-thirds of babies who had died from SIDS had been vaccinated against DPT prior to death .
Of these , 6.5 % died within 12 hours of vaccination ; 13 % within 24 hours ; 26 % within 3 days ; and 37 % , 61 % , and 70 % within 1 , @ @ @ @ @ @ @ .
( Figure 2 ) Figure 2 .
In a study of 103 children who died of SIDS , more than two-thirds had been vaccinated with pertussis prior to death .
Of these , 6.5 percent died within 12 hours of vaccination ; 13 percent within 24 hours ; 26 percent within three days ; and 37 , 61 , and 70 percent within one , two , and three weeks , respectively .
Torch also found that unvaccinated babies who died from SIDS did so most often in the fall or winter @ @ @ @ @ @ @ 2 and 4 months — the same ages when initial doses of DPT were given to infants .
He concluded that : In 1983 , Pediatric Infectious Diseases published a study by Baraff et al that analyzed 17 infants that had been vaccinated within 28 days prior to their sudden deaths , which were classified as SIDS .
They calculated the expected frequency of SIDS deaths per day and compared that with the actual number of sudden deaths in each of the 28 days after vaccination .
A statistically significant number of excess @ @ @ @ @ @ @ vaccination ( 6.75 sudden deaths were expected and 17 actually occurred ) — a 250 % increase .
The greatest number of excess deaths happened within 24 hours after vaccination ( 0.96 sudden deaths were expected and 6 actually occurred ) — a 625 % increase over statistical expectations.28 In 1987 , the American Journal of Public Health published a paper by Walker et al , once again confirming an apparent link between vaccination and sudden deaths .
Babies died at a rate more than seven times greater than normal within 3 days @ @ @ @ @ @ @ , Scheibner and Karlsson presented strong evidence of an association between DPT injections and cot death ( SIDS ) at the Second National Immunisation Conference in Canberra , Australia .
They were able to develop a sophisticated microprocessor that was placed under infants ' mattresses to precisely measure their breathing patterns before and after vaccination .
The microprocessor generated computer printouts in integrals of a weighted apnea ( cessation of breathing ) hypopnea ( abnormally shallow breathing ) density ( WAHD ) .
The data clearly revealed that pertussis vaccination caused an inordinate @ @ @ @ @ @ @ ceased or stopped completely.30-32 ( Figure 3 ) The Pertussis Vaccine and Stress-Induced Breathing Patterns : A Link to SIDS Figure 3 .
This chart represents a 17-day record of one child 's breathing patterns before and after receiving the pertussis vaccine .
Values above 1000 indicate acute stress-induced breathing .
The author of this study concluded that `` vaccination is the single most prevalent and most preventablecause of infant deaths . ''
These episodes continued for months following DPT vaccinations .
The lead author of the paper concluded that `` vaccination is @ @ @ @ @ @ @ cause of infant deaths .
`` 31 In 2006 , Ottaviani et al published a paper in Virchows Archiv ( European Journal of Pathology ) documenting the case of a 3-month-old infant who died suddenly and unexpectedly shortly after being given six vaccines in a single injection .
After dissecting the brainstem and examining the cardiac conduction system , authors of the study made the following observation : `` This case offers a unique insight into the possible role of hexavalent vaccine in triggering a lethal outcome in a vulnerable baby . ''
@ @ @ @ @ @ @ of sudden unexpected death occurring ... in infancy , especially soon after a vaccination , should always undergo a full necropsy study , '' otherwise a true association between vaccination and death may escape detection.33 That same year , another team of scientists ( Zinka et al ) published a paper in Vaccine documenting six cases of SIDS that occurred within 48 hours following the administration of a hexavalent vaccine .
At postmortal examination , these cases showed `` unusual findings in the brain '' that appeared compatible with an association between hexavalent @ @ @ @ @ @ @ 2011 , Statistics in Medicine published a paper by Kuhnert et al that examined an association between multi-dose vaccinations and death .
Authors of the paper demonstrated a 16-fold increase in sudden unexpected death after the fourth dose of a pentavalent shot ( five different vaccines in one injection ) or hexavalent shot ( six different vaccines in one injection ) .35 Today , unsuspecting parents continue to experience the heartbreak of losing healthy children after vaccinations .
Here is another unnecessary death labeled as SIDS , as reported by a distraught mother @ @ @ @ @ @ @ the Death Tables '' SIDS , '' `` suffocation in bed , '' and death due to `` unknown and unspecified causes , '' are just three of the 130 official cause-of-death categories that might be concealing fatalities that were really caused by vaccination .
Several other ICD categories are possible candidates for incorrect infant death classifications : unspecified viral diseases , diseases of the blood , diseases of the nervous system , unspecified diseases of the respiratory system , and shaken baby syndrome .
All of these official categories may be repositories @ @ @ @ @ @ @ fatalities .
For example , a vaccine against rotavirus-induced diarrhea ( Rotarix ) was licensed by the Food and Drug Administration ( FDA ) in 2008 .
However , in a clinical study that evaluated the safety of this vaccine , vaccinated babies died at a significantly higher rate than non-vaccinated babies — mainly due to a statistical increase in pneumonia fatalities.37 ( One biologically plausible explanation is that natural rotavirus infection might have a protective effect against respiratory infection . )
38 Although these deaths appear to be vaccine related , coroners @ @ @ @ @ @ @ pneumonia .
Some infant fatalities that occur shortly after vaccinations are incorrectly classified as shaken baby syndrome .
Retinal and subdural bleeding can result from an adult that shook the baby or from vaccine damage .
Expert testimony by medical practitioners has exonerated innocent parents of all charges against them.39 This is just another example of how the true cause of death can be reclassified or hidden within the death tables .
The practice of reclassifying ICD data greatly concerns the CDC `` because inaccurate or inconsistent cause-of-death determination and reporting hamper the @ @ @ @ @ @ @ risk factors , and design and evaluate programs to prevent these deaths .
`` 40 Thus , medical certification practices need to be monitored to determine how often vaccine-related infant deaths are being reclassified as ordinary mortality in the ICD .
More importantly , parents need to be warned that vaccine safety is grossly overestimated when vaccine-related deaths are not being accurately documented .
There are 130 official ways for an infant to die ( as categorized in the ICD ) , and one unofficial way for an infant to die : following @ @ @ @ @ @ @ vaccines .
When vaccine-related deaths are hidden within the death tables , parents are denied the ability to ascertain honest vaccine risk-to-benefit ratios , and true informed consent to vaccinations is not possible .
When families are urged to vaccinate their children without access to accurate data on vaccine-related deaths , their human rights have been violated .
Medical health authorities , pediatricians , and the vaccine industry then become criminal accomplices to each infant death caused by vaccines — even when vaccines are not officially acknowledged as the cause of death .
@ @ @ @ @ @ @ providing families with true informed consent , and preserving human rights must be the top priorities .
2. WHO .
International Statistical Classification of Diseases and Related Health Problems , 10th Revision .
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4 .
ICD-6 , issued in 1948 , and ICD-7 , issued @ @ @ @ @ @ @ and vaccination '' as a separate cause of death category with subcategories ( codes Y40-Y49 ) for death due to `` vaccination against smallpox '' ( code Y40 ) , `` inoculation against whooping cough '' ( code Y42 ) , `` inoculation against other infectious disease '' ( code Y49 ) , etc .
The ICD-8 , issued in 1965 , deleted the subcategories for death due to inoculation against individual diseases while maintaining `` Prophylactic inoculation and vaccination '' ( code Y42 ) as a separate cause of death category .
@ @ @ @ @ @ @ , authorities removed all cause of death classifications associated with vaccination .
5 .
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( Data as of June 2 , 2014 ) .
6 .
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Pediatr Pathol 1991 ; 11 : 677–84 .
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Changing trends in the diagnosis of sudden infant death .
Am J Forensic Med Pathol 2000 ; 21 : 311–314 .
15 .
Overpeck MD , Brenner RA , Cosgrove C , Trumble AC , Kochanek K , and MacDorman M. National under ascertainment of sudden unexpected infant deaths associated with deaths of unknown cause .
@ @ @ @ @ @ @ 16 .
Byard RW and Beal SM .
Has changing diagnostic preference been responsible for the recent fall in incidence of sudden infant death syndrome in South Australia ?
J Pediatr Child Health 1995 ; 31 : 197–199 .
17 .
Vennemann MM , Butterfass-Bahloul T , Jorch G , Brinkmann B , Findeisen M , Sauerland C , et al .
Sudden infant death syndrome : no increased risk after immunisation .
Vaccine 2007 ; 25 : 336–340 .
18 .
Stratton K , Almario DA , Wizemann TM , and McCormick @ @ @ @ @ @ @ and sudden unexpected death in infancy .
Washington DC , USA : National Academies Press , 2003 .
19 .
Essery SD , Raza MW , Zorgani A , MacKenzie DA , et al .
The protective effect of immunisation against diphtheria , pertussis and tetanus ( DPT ) in relation to sudden infant death syndrome .
FEMS Immunology and Microbiology 1999 August 1 ; 25 ( 1-2 ) : 183-92 .
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Werne J and Garrow I. Fetal anaphylactic shock : occurrence in identical twins following second injection of diphtheria toxoid @ @ @ @ @ @ @ 131 : 730-35 .
22 .
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26 .
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@ @ @ @ @ @ @ : A potential cause of the sudden infant death syndrome ( SIDS ) .
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There are 130 official ways for an infant to die (as categorized in the ICD), and one unofficial way for an infant to die: following an adverse reaction to one or more vaccines
There are 130 official ways for an infant to die. These official categories of death, sanctioned by the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO), are published in the International Classification of Diseases (ICD).1-3 When a baby dies, coroners must choose from among these 130 categories.
The official causes of death listed in the ICD include nearly every imaginable -- and tragic -- possibility. However, there is NO category for infant deaths caused by vaccines.4 This is odd because the federal government is aware that vaccines permanently disable and kill some babies -- the very reason Congress established a "death and disability" tax on childhood vaccines more than 25 years ago when the National Childhood Vaccine Injury Act of 1986 (Public Law 99-660) created the National Vaccine Injury Compensation Program (VICP).
Many parents don't realize that when they purchase vaccines for their babies, the cost is taxed and the money goes into a special fund to compensate them if and when those vaccines seriously injure or kill their babies. As of June 2014, $2.7 billion was granted for thousands of injuries and deaths caused by vaccines. Numerous cases are still pending. Awards were issued for permanent injuries such as learning disabilities, seizure disorders, mental retardation, paralysis, and numerous deaths, including many that were initially misclassified as sudden infant death syndrome (SIDS).5
Since vaccine-related deaths are officially recognized by the federal government but there is NO official classification for vaccine-related deaths in the ICD, two important questions must be asked:
Are some deaths that are listed within the 130 infant mortality death categories really deaths that are associated with vaccination? Are some vaccine-related deaths hidden within the death tables?
Sudden Infant Death Syndrome (SIDS)
Prior to the introduction of organized vaccination programs, "crib death" was so rare that it was not mentioned in infant mortality statistics. In the United States, national immunization campaigns were initiated in the 1960s when several new vaccines were introduced and promoted. For the first time in history, most U.S. infants were required to receive several doses of DPT (diphtheria, pertussis, tetanus), polio, and measles vaccines.6 By 1969, an alarming epidemic of sudden unexplained infant deaths impelled researchers to create a new medical term -- sudden infant death syndrome (SIDS).7 By 1972, SIDS had become the leading cause of post-neonatal mortality (deaths of infants from 28 days to one year old) in the United States.8 In 1973, the National Center for Health Statistics, operated by the CDC, created a new cause-of-death category to document deaths due to SIDS.9,10
SIDS is defined as the sudden and unexpected death of an infant which remains unexplained after a thorough investigation, including performance of an autopsy and review of the clinical history.11 Although there are no specific symptoms associated with SIDS, an autopsy often reveals congestion and edema of the lungs and inflammatory changes in the respiratory system.9,12
In 1984, Congress held a hearing on vaccine safety. The suspected link between vaccines and sudden infant deaths was addressed. The following excerpt is from a statement made by a distraught grandmother testifying before the Congressional Committee on Labor and Human Resources:
My name is Donna Gary. I am a constituent of Senator Kennedy's from Massachusetts. Our family should have celebrated our very first granddaughter's first birthday last month. Instead, we will commemorate the anniversary of her death at the end of this month. Our granddaughter, Lee Ann, was just 8 weeks old when her mother took her to the doctor for her routine checkup. That included, of course, her first DPT inoculation and oral polio vaccine. In all her entire 8 weeks of life this lovable, extremely alert baby had never produced such a blood-curdling scream as she did at the moment the shot was given. Neither had her mother ever before seen her back arch as it did while she screamed. She was inconsolable. Even her daddy could not understand Lee Ann's uncharacteristic screaming and crying. Four hours later, Lee Ann was dead. "Crib death," the doctor said -- "SIDS." "Could it be connected to the shot?" her parents implored. "No." "But she just had her first DPT shot this afternoon. Could there possibly be any connection to it?" "No, no connection at all," the emergency room doctor said definitely. My husband and I hurried to the hospital the following morning after Lee Ann's death to talk with the pathologist before the autopsy. We wanted to make sure he was alerted to her DPT inoculation such a short time before her death -- just in case there was something else he could look for to make the connection. He was unavailable to talk with us. We waited two-and-a-half hours. Finally, we got to talk to another doctor after the autopsy had been completed. He said it was SIDS. In the months before Lee Ann was born, I regularly checked with a friend as to the state of her grandchild's condition. He is nearly a year-and-a-half older than Lee Ann. On his first DPT shot he passed out cold for 15 minutes, right in the pediatrician's office. "Normal reaction for some children," the pediatrician reassured. The parents were scared, but they knew what a fine doctor they had. They trusted his judgment. When it was time for the second shot, they asked "Are you sure it's alright? Is it really necessary?" Their pediatrician again reassured them. He told them how awful it was to experience, as he had, one of his infant patient's bout with whooping cough. That baby had died. They gave him his second DPT shot that day. He became brain-damaged. This past week I had an opportunity to read through printed copies of the hearings of this committee. I am dismayed to learn that this same talk has been going on for years, and nothing has seemed to progress to incorporate what seems so obvious and necessary to keep from destroying any more babies, and to compensate financially those who have already been damaged for life. How accurate are our statistics on adverse reactions to vaccines when parents have been told, are still being told, "No connection to the shot, no connection at all."? What about the mother I have recently talked with who has a 4-year-old brain-damaged son? On all three of his DPT shots he had a convulsion in the presence of the pediatrician. "No connection," the pediatrician assured. I talked with a father in a town adjoining ours whose son died at the age of 9 weeks, several months before our own granddaughter's death. It was the day after his DPT inoculation. "SIDS" is the statement on the death certificate. Are the statistics that the medical world loves to quote to say, "There is no connection," really accurate, or are they based on poor diagnoses, poor record keeping? What is being done to provide a safer vaccine? Who is overseeing? Will it be the same scientists and doctors who have been overseeing in the past? How much longer does the public have to wait? How are physicians and clinics going to be held accountable to see that parents are informed of the possible reactions? And how are those children who should not receive the vaccine to be identified before they are damaged -- or dead? Today is the National Day of Prayer. My prayer is that this committee be instrumental in doing what needs to be done -- and soon. May there not be yet another year pass by with more children afflicted, and some dead, because those who can do so refuse to make the right connection.13
Throughout the 1980s, sudden infant deaths continued to skyrocket. Parental concerns about an apparent link between childhood vaccines and SIDS reached a fever pitch. Many parents were afraid to vaccinate their babies. Authorities sought to reassure parents that vaccines are safe and claimed that sudden unexplained infant deaths following vaccines were merely coincidental.
Back to Sleep
In 1992, the American Academy of Pediatrics (AAP) came up with a plan to reduce the unacceptable SIDS rate while reassuring concerned moms and dads that sudden unexplained infant deaths were not related to vaccines. The AAP initiated a national "Back to Sleep" campaign, telling parents to place their infants supine, rather than prone, during sleep. From 1992 through 2001, the post-neonatal SIDS rate dropped by an average annual rate of 8.6%. It seemed as though the "Back to Sleep" campaign was successful and that the real cause of SIDS was due not to vaccinations but from babies sleeping on their bellies.
However, a closer inspection of the ICD -- the 130 official ways for an infant to die -- revealed a loophole. Medical certifiers, such as coroners, could choose from among several categories of death when a baby suddenly expired. They didn't have to list the death as SIDS. Although the post-neonatal SIDS rate dropped by an average annual rate of 8.6% from 1992 through 2001 following the AAP's seemingly successful "Back to Sleep" campaign, the post-neonatal mortality rate from "suffocation in bed" (ICD-9 code E913.0) increased during this same period at an average annual rate of 11.2%. Sudden, unexplained infant deaths that were classified as SIDS prior to the "Back to Sleep" campaign, were now being classified as deaths due to suffocation in bed!
The post-neonatal mortality rate from "suffocation other" (ICD-9 code E913.1-E913.9), from "unknown and unspecified causes" (ICD-9 code 799.9), and from "intent unknown" (ICD-9 code E980-E989), all increased during this period as well.10 In Australia, a similar subterfuge seemed to occur. Researchers observed that when the SIDS rate decreased, deaths attributed to asphyxia increased.14-16
From 1999 through 2001, the number of U.S. deaths that were attributed to "suffocation in bed" and "unknown causes" increased significantly. Although the post-neonatal SIDS rate continued to decline, there was no significant change in the total post-neonatal mortality rate. In a recent paper (Malloy and MacDorman) published in Pediatrics, SIDS researchers made the following observation:
If death-certifier preference has shifted such that previously classified SIDS deaths are now classified as "suffocation," the inclusion of these suffocation deaths and unknown or unspecified deaths with SIDS deaths then accounts for about 90 percent of the decline in the SIDS rate observed between 1999 and 2001 and results in a non-significant decline in SIDS.10 (Figure 1)
Reclassification of SIDS Deaths to "Suffocation in Bed" and "Unknown Causes"
Figure 1. The postneonatal SIDS rate appears to have declined from 61.6 deaths (per 100,000 live births) in 1999 to 50.9 in 2001. However, during this period there was a significant increase in post-neonatal deaths attributed to "suffocation in bed" and due to "unknown causes." When these sudden unexpected causes of infant deaths are combined with SIDS deaths, the total SIDS rate remains relatively stable, resulting in a non-significant decline.
Other Evidence Linking SIDS to Vaccines
Although some studies were unable to find positive correlations between SIDS and vaccines,17-19 there is other evidence that a subset of infants may be more susceptible to SIDS shortly after being vaccinated. For example, as early as 1933 the Journal of the American Medical Association (JAMA) published a paper by Madsen documenting the sudden deaths of two infants soon after pertussis vaccination. The first child developed cyanosis and convulsions 30 minutes after vaccination and died suddenly a few minutes later. The second child developed cyanosis 2 hours after vaccination and then died suddenly.20
In 1946, Werne and Garrow published a paper in JAMA documenting the sudden deaths of identical twins 24 hours after pertussis vaccination. The babies had symptoms of shock throughout the night prior to their fatal reactions.21
In the 1960s and 1970s Aborigine infants began to mysteriously die at astonishing rates. In some regions of Australia, 1 of every 2 babies succumbed to an unexplained death -- a fatality rate of 50 percent! Kalokerinos solved the riddle when he realized that the deaths were occurring shortly after the babies were vaccinated. Health officials had recently initiated a mass vaccination campaign to "protect" Aborigine babies; their deaths corresponded with the vaccination program. Kalokerinos realized that these babies were severely malnourished, including a vitamin C deficiency. Their undeveloped immune systems couldn't handle the additional stress of vaccination. Kalokerinos was able to save other babies from the same fate by administering small quantities of vitamin C (100mg per month of age) prior to their vaccines.22
In Japan, from 1970 through 1974, there were 37 documented sudden infant deaths following pertussis vaccinations, inciting parents and doctors to reject the shot. In 1975, Japanese authorities reacted to these events by raising the age of vaccination from three months to two years. As a result, the number of vaccine injury compensation claims that were paid out for sudden deaths following vaccination dropped from 37 cases during a 5-year period to just 3 cases during the next 6-and-a-half years (from 1975 through August of 1981). The sudden death rate following vaccination dropped from 1.47 to 0.15 deaths per million doses -- a 90% improvement.23,24 In addition, from the early 1970s (a period when 3-month-old infants were vaccinated) to the mid-1980s (ten years after the age of vaccination was raised to 2 years) the Japanese infant mortality rate (infant deaths per 1,000 live births) dramatically declined from 12.4 to 5.0 -- a 60 percent drop!25
According to a special task force (Cherry et al) that investigated the Japanese data and published their summary in Pediatrics:
The category of "sudden death" is instructive in that the entity disappeared following both whole-cell and acellular vaccines when immunization was delayed until a child was 24 months of age.24
Cherry et al also made the following observation:
It is clear that delaying the initial vaccination until a child is 24 months, regardless of the type of vaccine, reduces most of the temporally associated severe adverse reactions.24
There is other more recent evidence that delaying vaccinations until a later age could save babies from severe vaccine-related adverse reactions, including sudden deaths. For example, Human and Experimental Toxicology published a study by Goldman and Miller that investigated more than 38,000 infant reports filed with the Vaccine Adverse Event Reporting System (VAERS). (This federally mandated vaccine safety surveillance program collects information about possible adverse reactions from vaccines.) Cases that listed either "hospitalization" or "death" were evaluated relative to all infant reports, including those that were non-serious. The hospitalization rate for infants that were vaccinated shortly after birth was an astonishing 20.1% but decreased in a statistically significant linear fashion to 10.7% for infants that were vaccinated just prior to their first birthday. This study also revealed a statistically significant lower mortality rate for infants that were vaccinated between 6 months and 1 year of age when compared to infants vaccinated between birth and 6 months of age.26
In 1982, William Torch, MD, director of Child Neurology, Department of Pediatrics, University of Nevada School of Medicine, presented a study at the 34th Annual Meeting of the American Academy of Pediatrics showing that two-thirds of babies who had died from SIDS had been vaccinated against DPT prior to death. Of these, 6.5% died within 12 hours of vaccination; 13% within 24 hours; 26% within 3 days; and 37%, 61%, and 70% within 1, 2, and 3 weeks, respectively. (Figure 2)
The Pertussis Vaccine and Sudden Infant Death Syndrome
Figure 2. In a study of 103 children who died of SIDS, more than two-thirds had been vaccinated with pertussis prior to death. Of these, 6.5 percent died within 12 hours of vaccination; 13 percent within 24 hours; 26 percent within three days; and 37, 61, and 70 percent within one, two, and three weeks, respectively.
Torch also found that unvaccinated babies who died from SIDS did so most often in the fall or winter while vaccinated babies died most often at 2 and 4 months -- the same ages when initial doses of DPT were given to infants. He concluded that:
DPT may be a generally unrecognized major cause of sudden infant and early childhood death, and that the risks of immunization may outweigh its potential benefits. A need for re-evaluation and possible modification of current vaccination procedures is indicated by this study.27
In 1983, Pediatric Infectious Diseases published a study by Baraff et al that analyzed 17 infants that had been vaccinated within 28 days prior to their sudden deaths, which were classified as SIDS. They calculated the expected frequency of SIDS deaths per day and compared that with the actual number of sudden deaths in each of the 28 days after vaccination. A statistically significant number of excess deaths happened in the first week following vaccination (6.75 sudden deaths were expected and 17 actually occurred) -- a 250% increase. The greatest number of excess deaths happened within 24 hours after vaccination (0.96 sudden deaths were expected and 6 actually occurred) -- a 625% increase over statistical expectations.28
In 1987, the American Journal of Public Health published a paper by Walker et al, once again confirming an apparent link between vaccination and sudden deaths. Babies died at a rate more than seven times greater than normal within 3 days after getting a DPT vaccination.29
In 1991, Scheibner and Karlsson presented strong evidence of an association between DPT injections and cot death (SIDS) at the Second National Immunisation Conference in Canberra, Australia. They were able to develop a sophisticated microprocessor that was placed under infants' mattresses to precisely measure their breathing patterns before and after vaccination. The microprocessor generated computer printouts in integrals of a weighted apnea (cessation of breathing) hypopnea (abnormally shallow breathing) density (WAHD). The data clearly revealed that pertussis vaccination caused an inordinate increase in episodes where breathing either nearly ceased or stopped completely.30-32 (Figure 3)
The Pertussis Vaccine and Stress-Induced Breathing Patterns: A Link to SIDS
Figure 3. This chart represents a 17-day record of one child's breathing patterns before and after receiving the pertussis vaccine. Values above 1000 indicate acute stress-induced breathing. The author of this study concluded that "vaccination is the single most prevalent and most preventablecause of infant deaths."
These episodes continued for months following DPT vaccinations. The lead author of the paper concluded that "vaccination is the single most prevalent and most preventable cause of infant deaths."31
In 2006, Ottaviani et al published a paper in Virchows Archiv (European Journal of Pathology) documenting the case of a 3-month-old infant who died suddenly and unexpectedly shortly after being given six vaccines in a single injection. After dissecting the brainstem and examining the cardiac conduction system, authors of the study made the following observation: "This case offers a unique insight into the possible role of hexavalent vaccine in triggering a lethal outcome in a vulnerable baby." They also noted that "any case of sudden unexpected death occurring ... in infancy, especially soon after a vaccination, should always undergo a full necropsy study," otherwise a true association between vaccination and death may escape detection.33
That same year, another team of scientists (Zinka et al) published a paper in Vaccine documenting six cases of SIDS that occurred within 48 hours following the administration of a hexavalent vaccine. At postmortal examination, these cases showed "unusual findings in the brain" that appeared compatible with an association between hexavalent vaccination and sudden infant death syndrome.34
In 2011, Statistics in Medicine published a paper by Kuhnert et al that examined an association between multi-dose vaccinations and death. Authors of the paper demonstrated a 16-fold increase in sudden unexpected death after the fourth dose of a pentavalent shot (five different vaccines in one injection) or hexavalent shot (six different vaccines in one injection).35
Today, unsuspecting parents continue to experience the heartbreak of losing healthy children after vaccinations. Here is another unnecessary death labeled as SIDS, as reported by a distraught mother:
Our beautiful 2-month-old daughter recently died. What was unusual was that earlier on the day that she died, I had taken her to the military base hospital for her two-month checkup. The doctor told me that she was just perfect. Then he said that she needed four shots. I replied, "Four!"? She assured me that it was completely normal. That evening after feeding our daughter, we laid her down to sleep. We checked on her 45 minutes later and discovered that she was dead. I told the police, coroner, and investigators that I thought it was from the shots because she was perfectly fine that day and before the shots. But after three weeks we finally got an answer from the autopsy that it was SIDS. To this day, I believe that her death was caused by the shots. No one can convince me otherwise.36
More Vaccine Fatalities - Hidden in the Death Tables
"SIDS," "suffocation in bed," and death due to "unknown and unspecified causes," are just three of the 130 official cause-of-death categories that might be concealing fatalities that were really caused by vaccination. Several other ICD categories are possible candidates for incorrect infant death classifications: unspecified viral diseases, diseases of the blood, diseases of the nervous system, unspecified diseases of the respiratory system, and shaken baby syndrome. All of these official categories may be repositories of vaccine-related infant deaths reclassified as common fatalities.
For example, a vaccine against rotavirus-induced diarrhea (Rotarix) was licensed by the Food and Drug Administration (FDA) in 2008. However, in a clinical study that evaluated the safety of this vaccine, vaccinated babies died at a significantly higher rate than non-vaccinated babies -- mainly due to a statistical increase in pneumonia fatalities.37 (One biologically plausible explanation is that natural rotavirus infection might have a protective effect against respiratory infection.)38 Although these deaths appear to be vaccine related, coroners are likely to have misclassified them as pneumonia.
Some infant fatalities that occur shortly after vaccinations are incorrectly classified as shaken baby syndrome. Retinal and subdural bleeding can result from an adult that shook the baby or from vaccine damage. Expert testimony by medical practitioners has exonerated innocent parents of all charges against them.39 This is just another example of how the true cause of death can be reclassified or hidden within the death tables.
The practice of reclassifying ICD data greatly concerns the CDC "because inaccurate or inconsistent cause-of-death determination and reporting hamper the ability to monitor national trends, ascertain risk factors, and design and evaluate programs to prevent these deaths."40 Thus, medical certification practices need to be monitored to determine how often vaccine-related infant deaths are being reclassified as ordinary mortality in the ICD. More importantly, parents need to be warned that vaccine safety is grossly overestimated when vaccine-related deaths are not being accurately documented.
Vaccine Safety, Informed Consent and Human Rights
There are 130 official ways for an infant to die (as categorized in the ICD), and one unofficial way for an infant to die: following an adverse reaction to one or more vaccines. When vaccine-related deaths are hidden within the death tables, parents are denied the ability to ascertain honest vaccine risk-to-benefit ratios, and true informed consent to vaccinations is not possible. When families are urged to vaccinate their children without access to accurate data on vaccine-related deaths, their human rights have been violated. Medical health authorities, pediatricians, and the vaccine industry then become criminal accomplices to each infant death caused by vaccines -- even when vaccines are not officially acknowledged as the cause of death. Finding ways to increase vaccine safety, providing families with true informed consent, and preserving human rights must be the top priorities.
References
1. WHO. International Classification of Diseases, 9th Revision. Geneva, Switzerland: World Health Organization, 1979.
2. WHO. International Statistical Classification of Diseases and Related Health Problems, 10th Revision. Geneva, Switzerland: World Health Organization, 1992.
3. CDC. Table 31. Number of infant deaths and infant mortality rates for 130 selected causes, by race: United States, 2006. Natl Vital Stat Rep 2009; 57: 110-112.
4. ICD-6, issued in 1948, and ICD-7, issued in 1955, included "Prophylactic inoculation and vaccination" as a separate cause of death category with subcategories (codes Y40-Y49) for death due to "vaccination against smallpox" (code Y40), "inoculation against whooping cough" (code Y42), "inoculation against other infectious disease" (code Y49), etc. The ICD-8, issued in 1965, deleted the subcategories for death due to inoculation against individual diseases while maintaining "Prophylactic inoculation and vaccination" (code Y42) as a separate cause of death category. When the ICD-9 was issued in 1979, authorities removed all cause of death classifications associated with vaccination.
5. Health Resources and Services Administration. National Vaccine Injury Compensation Program. U.S. Department of Health and Human Services. (Data as of June 2, 2014).
6. The measles vaccine was administered at 9 months of age from 1963 to 1965. ACIP. Measles prevention: recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR (December 29, 1989) / 38(S-9): 1-18.
7. Bergman AB, Beckwith JB, Ray CG, eds. Sudden Infant Death Syndrome. Proceedings of the Second International Conference on Causes of Sudden Death in Infants, Seattle and London: University of Washington Press, 1970:18.
8. Bergman AB. The "Discovery" of Sudden Infant Death Syndrome. New York, NY, USA: Praeger Publishers, 1986: 209 (Appendix III).
9. MacDorman MF and Rosenberg HM. Trends in infant mortality by cause of death and other characteristics, 1960-88 (vital and health statistics), Volume 20. Hyattsville,MD, USA: National Center for Health Statistics, U.S. Government Printing, 1993.
10. Malloy MH and MacDorman M. Changes in the classification of sudden unexpected infant deaths: United States, 1992-2001. Pediatrics 2005; 115: 1247-1253.
11. Willinger M, James LS, Catz C. Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development. Pediatr Pathol 1991; 11: 677-84.
12. Goldwater PN. Sudden infant death syndrome: a critical review of approaches to research. Arch Dis Child 2003; 88: 1095-100.
13. Vaccine Injury Compensation. Hearing Before the Committee on Labor and Human Resources; 98th Congress, 2nd Session, (May 3, 1984): 63-67.
14. Mitchell E, Krous HF, Donald T, and Byard RW. Changing trends in the diagnosis of sudden infant death. Am J Forensic Med Pathol 2000; 21: 311-314.
15. Overpeck MD, Brenner RA, Cosgrove C, Trumble AC, Kochanek K, and MacDorman M. National under ascertainment of sudden unexpected infant deaths associated with deaths of unknown cause. Pediatrics 2002; 109: 274-283.
16. Byard RW and Beal SM. Has changing diagnostic preference been responsible for the recent fall in incidence of sudden infant death syndrome in South Australia? J Pediatr Child Health 1995; 31: 197-199.
17. Vennemann MM, Butterfass-Bahloul T, Jorch G, Brinkmann B, Findeisen M, Sauerland C, et al. Sudden infant death syndrome: no increased risk after immunisation. Vaccine 2007; 25: 336-340.
18. Stratton K, Almario DA, Wizemann TM, and McCormick MC. Immunization safety review: vaccinations and sudden unexpected death in infancy. Washington DC, USA: National Academies Press, 2003.
19. Essery SD, Raza MW, Zorgani A, MacKenzie DA, et al. The protective effect of immunisation against diphtheria, pertussis and tetanus (DPT) in relation to sudden infant death syndrome. FEMS Immunology and Microbiology 1999 August 1; 25(1-2): 183-92.
20. Madsen T. Vaccination against whooping cough. JAMA 1933; 101: 187-88.
21. Werne J and Garrow I. Fetal anaphylactic shock: occurrence in identical twins following second injection of diphtheria toxoid and pertussis antigen. JAMA 1946; 131: 730-35.
22. Kalokerinos A. Every Second Child Was Doomed to Death -- Unless One Dedicated Doctor Could Open His Colleagues' Eyes and Minds. New Canaan, CT: Keats Publishing, Inc., 1974.
23. Noble GR., et al. Acellular and whole-cell pertussis vaccines in Japan: report of a visit by U.S. scientists. JAMA 1987; 257: 1351-56.
24. Cherry JD., et al. Report of the task force on pertussis and pertussis immunization. Pediatr (Jun 1988); 81(6): 933-84.
25. Congressional Budget Office. Factors contributing to the infant mortality ranking of the United States. CBO Staff Memorandum (February 1992): Table 2, International Infant Mortality Rates by Ranking.
26. Goldman GS and Miller NZ. Relative trends in hospitalizations and mortality among infants by the number of vaccine doses and age, based on the Vaccine Adverse Event Reporting System (VAERS), 1990-2010. Human and Experimental Toxicology 2012; 31(10): 1012-1021.
27. Torch WC. DPT immunization: A potential cause of the sudden infant death syndrome (SIDS). Amer Acad of Neur, 34th Annual Meet, Apr 25-May 1, 1982. Neur 32(4): pt. 2.
28. Baraff LJ, Ablon WJ, Weiss RC. Possible temporal association between diphtheria-tetanus toxoid-pertussis vaccination and sudden infant syndrome. Pediatric Infectious Disease Journal 1983; 2: 7-11.
29. Walker AM., et al. Diphtheria-tetanus-pertussis immunization and sudden infant death syndrome. Am J Public Health (August 1987); 77(8): 945-51.
30. Scheibner V. and Karlsson LG. Evidence of the association between non-specific stress syndrome, DPT injections and cot death. Proceedings of the 2nd National Immunisation Conference in Canberra (May 27-29, 1991).
31. Scheibner V. Vaccination: 100 Years of Orthodox Research Shows that Vaccines Represent a Medical Assault on the Immune System. Blackheath, NSW, Australia: Scheibner Publications, 1993: 59-70; 225-235; 262.
32. Scheibner V. Dynamics of critical days as part of the dynamics of non-specific stress syndrome discovered during monitoring with Cotwatch breathing monitor. Journal of the Australasian College of Nutritional & Environmental Medicine (December 2004); 23(3): 1-5.
33. Ottaviani G, Lavezze AM, and Matturri L. Sudden infant death syndrome (SIDS) shortly after hexavalent vaccination: another pathology in suspected SIDS? Virchows Archiv 2006; 448: 100-104.
34. Zinka B, Rauch E, Buettner A, Rueff F and Penning R. Unexplained cases of sudden infant death shortly after hexavalent vaccination. Vaccine 2006; 24(31-32): 5779-5780.
35. Kuhnert R, Hecker H, Poethko-Muller C, Schlaud M, Vennemann M, Whitaker HJ, et al. A modified self-controlled case series method to examine association between multidose vaccinations and death. Stat Med 2011; 30(6): 666-677.
36. Unsolicited correspondence received by the Thinktwice Global Vaccine Institute.
37. GlaxoSmithKline. Rotarix1 (Rotavirus Vaccine, Live, Oral) Oral Suspension. Product insert from the manufacturer (April 2008): 6.
38. FDA. Center for biologics evaluation and research, vaccines and related biological products advisory committee meeting (February 20, 2008): 127-128.
39. Buttram H and England C. Shaken Baby Syndrome or Vaccine-Induced Encephalitis: Are Parents Being Falsely Accused? Bloomington, Indiana: Author House, 2011.
40. CDC. About the sudden unexpected infant death investigation (SUIDI) reporting form. Department of Health and Human Services (accessed May 13, 2013).


greenmedinfo--2020-09-08--The Failure of GMO Cotton in India

The Failure of GMO Cotton in India

This website is for information purposes only .
By providing the information contained herein we are not diagnosing , treating @ @ @ @ @ or preventing any type of disease or medical condition .
Before beginning any type of @ @ @ @ @ treatment regimen , it is advisable to seek the advice of a licensed healthcare professional @

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.
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greenmedinfo--2020-09-08--Studies Question Transmission of 1918 Spanish Flu


greenmedinfo--2020-09-08--Oridonin can inhibit the growth of RM-1 prostate cancer cells.

OBJECTIVE : To investigate the therapeutic effect and the related mechanism of oridonin on mice with prostate cancer .
METHODS : Sixty BALB/C male nude mice were selected .
A model of RM-1 cell transplantation tumor of prostate cancer was built by the subcutaneous inoculation of RM-1 cells .
After that , those 60 experimental mice were randomly divided into groups A , B and C. Each group had 20 mice .
Mice in group A were treated with 0.2 mL of normal saline ( 0.9 % ) by intraperitonealinjection once a day ; mice in group B received intraperitoneal @ @ @ @ @ @ @ a day ; and mice in group C received intraperitoneal injection of 7.5 mg/mL of oridonin once a day .
Mice in the three groups were treated uninterruptedly for 5 weeks and were all killed .
Then , tumors were excised and weighed to calculate their growth inhibitory rate , volume increment and anti-tumor rate .
Thymus and spleen of mice in the three groups were collected to calculate the thymus and spleen index .
Immunohistochemical staining was applied to observe the expression of caspase-3 in prostate cancer tissue of mice of the @ @ @ @ @ @ @ and volume increment of tumors in groups B and C were significantly lower than those of group A ( P 0.05 ) .
Immumohistochemical staining revealed that the caspase-3 protein in prostate cancer tissue of mice of group A expressed negatively with colorless or light-colored karyon ; while the caspase-3 protein in prostate cancer tissue of mice of group B expressed positively with dark-colored karyon , centralized distribution and granular sensation ; and the caspase-3 in prostate cancer tissue of mice of group C showed strong positive expression with big and darker colored @ @ @ @ @ @ @ Oridonin can inhibit the growth of RM-1 prostate cancer cells effectively and have great therapeutic effects on RM-1 cell transplantation tumor of prostate cancer .

OBJECTIVE: To investigate the therapeutic effect and the related mechanism of oridonin on mice with prostate cancer.
METHODS: Sixty BALB/C male nude mice were selected. A model of RM-1 cell transplantation tumor of prostate cancer was built by the subcutaneous inoculation of RM-1 cells. After that, those 60 experimental mice were randomly divided into groups A, B and C. Each group had 20 mice. Mice in group A were treated with 0.2 mL of normal saline (0.9%) by intraperitonealinjection once a day; mice in group B received intraperitoneal injection of 1.875 mg/mL of oridonin once a day; and mice in group C received intraperitoneal injection of 7.5 mg/mL of oridonin once a day. Mice in the three groups were treated uninterruptedly for 5 weeks and were all killed. Then, tumors were excised and weighed to calculate their growth inhibitory rate, volume increment and anti-tumor rate. Thymus and spleen of mice in the three groups were collected to calculate the thymus and spleen index. Immunohistochemical staining was applied to observe the expression of caspase-3 in prostate cancer tissue of mice of the three groups.
RESULTS: The qualities and volume increment of tumors in groups B and C were significantly lower than those of group A (P < 0.05); the qualities and volume increment of tumors in groups C were evidently lower than those of group B (P < 0.05); the tumor volume increment and anti-tumor rate in group C were obviously higher than those of group B (P < 0.05); the thymus and spleen indexes of groups B and C were distinctly higher than those of group A (P < 0.05); comparison of the thymus and spleen indexes between group B and group C showed no statistical differences (P > 0.05). Immumohistochemical staining revealed that the caspase-3 protein in prostate cancer tissue of mice of group A expressed negatively with colorless or light-colored karyon; while the caspase-3 protein in prostate cancer tissue of mice of group B expressed positively with dark-colored karyon,centralized distribution and granular sensation; and the caspase-3 in prostate cancer tissue of mice of group C showed strong positive expression with big and darker colored karyon and dense distribution.
CONCLUSIONS: Oridonin can inhibit the growth of RM-1 prostate cancer cells effectively and have great therapeutic effects on RM-1 cell transplantation tumor of prostate cancer.


greenmedinfo--2020-09-08--Oridonin inhibits cell proliferation and induces apoptosis in rheumatoid arthritis fibroblast-like s

Oridonin inhibits cell proliferation and induces apoptosis in rheumatoid arthritis fibroblast-like synoviocytes.

Oridonin , an active diterpenoid compound from Rabdosia rubescens , has anti-tumor effects .
Rheumatoid arthritis fibroblast-like synoviocytes ( RAFLS @ @ @ @ @ of RA , exhibits '' tumor-like '' phenotype .
Here , we investigated the effects @ @ @ @ @ and apoptosis of RAFLS .
Cell viability was measured by the 3- ( 4,5-dimethylthiazol-2-yl ) @ @ @ @ @ assay .
Apoptosis and mitochondrial membrane potential were detected by flow cytometry .
Western blot @ @ @ @ @ the phosphorylation of extra-cellular regulated kinases ( ERK1/2 ) , C-Jun N-Terminal Kinase ( JNK @ @ @ @ @ protein kinases and the expression of apoptosis-related proteins .
Oridonin inhibited cell proliferation and induced @ @ @ @ @ IL-1β ) -treated FLS .
z-VAD-fmk , a pan-caspase inhibitor , significantly ( P

Oridonin, an active diterpenoid compound from Rabdosia rubescens, has anti-tumor effects. Rheumatoid arthritis fibroblast-like synoviocytes (RAFLS), a pathological hallmark of RA, exhibits"tumor-like"phenotype. Here, we investigated the effects of oridonin on the proliferation and apoptosis of RAFLS. Cell viability was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. Apoptosis and mitochondrial membrane potential were detected by flow cytometry. Western blot analysis was performed to examine the phosphorylation of extra-cellular regulated kinases (ERK1/2), C-Jun N-Terminal Kinase (JNK), and p38 mitogen-activated protein kinases and the expression of apoptosis-related proteins. Oridonin inhibited cell proliferation and induced cell apoptosis in interleukin-1β (IL-1β)-treated FLS. z-VAD-fmk, a pan-caspase inhibitor, significantly (P < 0.05) attenuated oridonin-induced apoptosis of FLS. Oridonin suppressed IL-1β-mediated phosphorylation of ERK1/2 and JNK in a dose-dependent manner. Meanwhile, oridonin alone dose-dependently suppressed FLS proliferation, triggered cell apoptosis, and reduced mitochondrial membrane potential (ΔΨm) through activating caspase-3, caspase-9, and PARP, leading to translocation of cytochrome c into cytoplasm. z-VAD-fmk significantly (P < 0.05) inhibited oridonin-induced apoptosis. The accumulation of cellular reactive oxygen species (ROS) was about sevenfold increase in oridonin-treated cells. Pretreatment of N-acetylcysteine (NAC), an inhibitor of ROS, significantly attenuated oridonin-triggered apoptosis, indicating the involvement of ROS production in oridonin-induced mitochondrial apoptosis. Oridonin inhibits cell proliferation, induces cell apoptosis, and decreases the phosphorylation of ERK1/2 and JNK in IL-1β-exposed RAFLS. Oridonin induces mitochondrial apoptosis by enhancing the production of ROS in FLS.


greenmedinfo--2020-09-08--Oridonin suppresses proliferation of human ovarian cancer cells.

Oridonin , an ent-kaurane diterpenoid compound isolated from the traditional Chinese herb Rabdosia rubescens , has shown various pharmacological and @ @ @ @ @ , anti-bacterial , and anti-inflammatory properties .
However , the effect of oridonin on human @ @ @ @ @ not been determined .
In this study , we demonstrated that oridonin inhibited ovarian cancer @ @ @ @ @ invasion in a dose-dependent manner .
Furthermore , we showed oridonin inhibited tumor growth of @ @ @ @ @ ) in vivo .
We then assessed mechanisms and found that oridonin specifically abrogated the @ @ @ @ @ In summary , our results indicate that oridonin is a potential inhibitor of ovarian cancer @ @ @ @ @ pathway .

Oridonin, an ent-kaurane diterpenoid compound isolated from the traditional Chinese herb Rabdosia rubescens, has shown various pharmacological and physiological effects such as anti-tumor, anti-bacterial, and anti-inflammatory properties. However, the effect of oridonin on human ovarian cancer cell lines has not been determined. In this study, we demonstrated that oridonin inhibited ovarian cancer cell proliferation, migration and invasion in a dose-dependent manner. Furthermore, we showed oridonin inhibited tumor growth of ovarian cancer cells (SKOV3) in vivo. We then assessed mechanisms and found that oridonin specifically abrogated the phosphorylation/activation of mTOR signaling. In summary, our results indicate that oridonin is a potential inhibitor of ovarian cancer by blocking the mTOR signaling pathway.


greenmedinfo--2020-09-08--Oridonin effectively reverses cisplatin drug resistance in human ovarian cancer cells.

Cisplatin is a first generation platinum‑based chemotherapeutic agent , however , the extensive application of cisplatin inevitably results in drug resistance , which is a major obstacle in cancer chemotherapy .
The aim of the present study was to investigate the efficiency of reversing cisplatin‑resistance with the use of combination therapy with oridonin and cisplatin in human ovarian cancer cells , and attempt to reduce the side effects of the therapeutic agents when used alone .
The half maximal inhibitory concentration ( IC50 ) values of cisplatin were determined in cisplatin‑sensitive and cisplatin‑resistant ovarian cancer cells using an MTT assay @ @ @ @ @ @ @ , A2780/DDP , SKOV3 and SKOV3/DDP cells were significantly decreased in a time‑dependent manner .
The antitumor effect of oridonin in A2780/DDP cells was also detected by the MTT assay and the inhibitory effects of oridonin increased in a dose‑and time‑dependent manner .
A2780/DDP cells were treated with 20 µM oridonin in combination with increasing concentrations of cisplatin for 48 h , and the result demonstrated that oridonin synergistically increased the antitumor effects of cisplatin in A2780/DDP cells .
Notably , the combination treatment of oridonin and cisplatin effectively reversed cisplatin resistance and @ @ @ @ @ @ @ 50.97 µM and 135.20 to 26.12 µM and 73.00 µM in A2780/DDP and SKOV3/DDP cells at 48 h , respectively .
Furthermore , oridonin induced cell apoptosis in a dose‑dependentmanner and promoted cell‑cycle arrest at the G0/G1 phase in ovarian cancer cells .
Oridonin and cisplatin synergistically increased the cell apoptosis rate of A2780/DDP cells , which was detected by fluorescence‑activated cell sorting analysis .
Downregulated expression levels of Bcl‑2 and upregulated the expression of Bax protein were demonstrated by western blot analysis , further indicating increased apoptosis .
In addition , the @ @ @ @ @ @ @ ) ‑2 and MMP‑9 decreased in a dose‑dependent manner with oridonin treatment .
The results from the present study demonstrated that oridonin exerted a synergistic effect with cisplatin to inhibit proliferation and induce cell apoptosis in cisplatin‑resistant ovarian cancer cells .
Thus , combination therapy with oridonin and cisplatin effectively reversed cisplatin resistance in human ovarian cancer cells , which may have useful clinical applications .

Cisplatin is a first generation platinum‑based chemotherapeutic agent, however, the extensive application of cisplatin inevitably results in drug resistance, which is a major obstacle in cancer chemotherapy. The aim of the present study was to investigate the efficiency of reversing cisplatin‑resistance with the use of combination therapy with oridonin and cisplatin in human ovarian cancer cells, and attempt to reduce the side effects of the therapeutic agents when used alone. The half maximal inhibitory concentration (IC50) values of cisplatin were determined in cisplatin‑sensitive and cisplatin‑resistant ovarian cancer cells using an MTT assay. IC50 values of cisplatin in A2780, A2780/DDP, SKOV3 and SKOV3/DDP cells were significantly decreased in a time‑dependent manner. The antitumor effect of oridonin in A2780/DDP cells was also detected by the MTT assay and the inhibitory effects of oridonin increased in a dose‑and time‑dependent manner. A2780/DDP cells were treated with 20 µM oridonin in combination with increasing concentrations of cisplatin for 48 h, and the result demonstrated that oridonin synergistically increased the antitumor effects of cisplatin in A2780/DDP cells. Notably, the combination treatment of oridonin and cisplatin effectively reversed cisplatin resistance and the IC50 values were significantly decreased from 50.97 µM and 135.20 to 26.12 µM and 73.00 µM in A2780/DDP and SKOV3/DDP cells at 48 h, respectively. Furthermore, oridonin induced cell apoptosis in a dose‑dependentmanner and promoted cell‑cycle arrest at the G0/G1 phase in ovarian cancer cells. Oridonin and cisplatin synergistically increased the cell apoptosis rate of A2780/DDP cells, which was detected by fluorescence‑activated cell sorting analysis. Downregulated expression levels of Bcl‑2 and upregulated the expression of Bax protein were demonstrated by western blot analysis, further indicating increased apoptosis. In addition, the expression levels of matrix metalloproteinase (MMP)‑2 and MMP‑9 decreased in a dose‑dependent manner with oridonin treatment. The results from the present study demonstrated that oridonin exerted a synergistic effect with cisplatin to inhibit proliferation and induce cell apoptosis in cisplatin‑resistant ovarian cancer cells. Thus, combination therapy with oridonin and cisplatin effectively reversed cisplatin resistance in human ovarian cancer cells,which may have useful clinical applications.


greenmedinfo--2020-09-08--Oridonin might prevent synaptic loss and improve behavioural symptoms in Aβ1-42-induced Alzheimer's

Oridonin might prevent synaptic loss and improve behavioural symptoms in Aβ1-42-induced Alzheimer's disease mice.

Synaptic loss induced by beta-amyloid ( Aβ ) plays a critical role in the pathophysiology of Alzheimer 's disease ( @ @ @ @ @ mechanisms underlying this process remain unknown .
In this study , we found that oridonin @ @ @ @ @ loss induced by Aβ1-42 in vivo and in vitro and attenuated the alterations in dendritic @ @ @ @ @ the hippocampus of AD mice .
In addition , Ori increased the expression of PSD-95 @ @ @ @ @ activity in the synaptosomes of AD mice .
Ori also activated the BDNF/TrkB/CREB signaling pathway @ @ @ @ @ mice .
Furthermore , in theMorris water maze test , Ori reduced latency and searching @ @ @ @ @ of platform crosses in AD mice .
These data suggest that Ori might prevent synaptic @ @ @ @ @ in Aβ1-42-induced AD mice .

Synaptic loss induced by beta-amyloid (Aβ) plays a critical role in the pathophysiology of Alzheimer's disease (AD), but the mechanisms underlying this process remain unknown. In this study, we found that oridonin (Ori) rescued synaptic loss induced by Aβ1-42 in vivo and in vitro and attenuated the alterations in dendritic structure andspine density observed in the hippocampus of AD mice. In addition, Ori increased the expression of PSD-95 and synaptophysin and promoted mitochondrial activity in the synaptosomes of AD mice. Ori also activated the BDNF/TrkB/CREB signaling pathway in the hippocampus of AD mice. Furthermore, in theMorris water maze test, Ori reduced latency and searching distance and increased the number of platform crosses in AD mice. These data suggest that Ori might prevent synaptic loss and improve behavioral symptoms in Aβ1-42-induced AD mice.


Banking on COVID-19


greenmedinfo--2020-09-08--Oridonin demonstrated its tumor suppressive effects in gastric cancer cells.

Lysine acetylation has been reported to involve in the pathogenesis of multiple diseases including cancer .
In our screening study @ @ @ @ @ lysine acetyltransferase inhibitor ( KATi ) activity , oridonin was found to possess acetyltransferase-inhibitory effects @ @ @ @ @ , GCN5 , Tip60 , and pCAF .
In gastric cancer cells , oridonin treatment @ @ @ @ @ concentration-dependent manner and down-regulated the expression of p53 downstream genes , whereas p53 inhibition by @ @ @ @ @ of oridonin .
Moreover , oridonin treatment induced cell apoptosis , increased the levels of @ @ @ @ @ and decreased the mitochondrial membrane potential in gastric cancer cells in a concentration-dependent manner .
@ @ @ @ @ proapoptosis effect of oridonin .
In conclusion , our study identified oridonin as a novel @ @ @ @ @ suppressive effects in gastric cancer cells at least partially through p53-and caspase-3-mediated mechanisms .

Lysine acetylation has been reported to involve in the pathogenesis of multiple diseases including cancer. In our screening study to identify natural compounds with lysine acetyltransferase inhibitor (KATi) activity, oridonin was found to possess acetyltransferase-inhibitory effects on multiple acetyltransferases including P300, GCN5, Tip60, and pCAF. In gastric cancer cells, oridonin treatment inhibited cell proliferation in a concentration-dependent manner and down-regulated the expression of p53 downstream genes, whereas p53 inhibition by PFT-α reversed the antiproliferative effects of oridonin. Moreover, oridonin treatment induced cell apoptosis, increased the levels of activated caspase-3 and caspase-9, and decreased the mitochondrial membrane potential in gastric cancer cells in a concentration-dependent manner. Caspase-3 inhibitionby Ac-DEVD-CHO reversed the proapoptosis effect of oridonin. In conclusion, our study identified oridonin as a novel KATi and demonstrated its tumor suppressive effects in gastric cancer cells at least partially through p53-and caspase-3-mediated mechanisms.


greenmedinfo--2020-09-09--High dose of calcifediol or 25-hydroxyvitamin D significantly reduced the need for ICU treatment of

High dose of calcifediol or 25-hydroxyvitamin D significantly reduced the need for ICU treatment of patients requiring hospitalization due to COVID-19.

OBJECTIVE : The vitamin D endocrine system may have a variety of actions on cells and tissues involved in COVID-19 progression especially by decreasing the Acute Respiratory Distress Syndrome .
Calcifediol can rapidly increase serum 25OHD concentration .
We therefore evaluated the effect of calcifediol treatment , on Intensive Care Unit Admission and Mortality rate among Spanish patients hospitalized for COVID-19 .
SETTING : university hospital setting ( Reina Sofia University Hospital , Córdoba Spain . )
PARTICIPANTS : 76 consecutive patients hospitalized with COVID-19 infection , clinical picture of acute respiratory infection , confirmed by a radiographic pattern of @ @ @ @ @ @ @ PCR with CURB65 severity scale ( recommending hospital admission in case oftotal score > 1 ) .
PROCEDURES : All hospitalized patients received as best available therapy the same standard care , ( per hospital protocol ) , of a combination of hydroxychloroquine ( 400 mg every 12 hours on the first day , and 200 mg every 12 hours for the following 5 days ) , azithromycin ( 500 mg orally for 5 days .
Eligible patients were allocated at a 2 calcifediol:1 no calcifediol ratio through electronic randomization on the day @ @ @ @ @ @ @ 0.532 mg ) , or not .
Patients in the calcifediol treatment group continued with oral calcifediol ( 0.266 mg ) on day 3 and 7 , and then weekly until discharge or ICU admission .
Outcomes of effectiveness included rate of ICU admission and deaths .
RESULTS : Of 50 patients treated with calcifediol , one required admission to the ICU ( 2 % ) , while of 26 untreated patients , 13 required admission ( 50 % ) p value XFischer test p CONCLUSION : Our pilot study demonstrated that administration @ @ @ @ @ @ @ 25-hydroxyvitamin D , a main metabolite of vitamin D endocrine system , significantly reduced the need for ICU treatment of patients requiring hospitalization due to proven COVID-19 .
Calcifediol seems to be able to reduce severity of the disease , but larger trials with groups properly matched will be required to show a definitive answer .

OBJECTIVE: The vitamin D endocrine system may have a variety of actions on cells and tissues involved in COVID-19 progression especially by decreasing the Acute Respiratory Distress Syndrome. Calcifediol can rapidly increase serum 25OHD concentration. We therefore evaluated the effect of calcifediol treatment, on Intensive Care Unit Admission and Mortality rate among Spanish patients hospitalized for COVID-19.
DESIGN: parallel pilot randomized open label, double-masked clinical trial.
SETTING: university hospital setting (Reina Sofia University Hospital, Córdoba Spain.) PARTICIPANTS: 76 consecutive patients hospitalized with COVID-19 infection, clinical picture of acute respiratory infection, confirmed by a radiographic pattern of viral pneumonia and by a positive SARS-CoV-2 PCR with CURB65 severity scale (recommending hospital admission in case oftotal score>1).
PROCEDURES: All hospitalized patients received as best available therapy the same standard care, (per hospital protocol), of a combination of hydroxychloroquine (400 mg every 12 hours on the first day, and 200 mg every 12 hours for the following 5 days), azithromycin (500 mg orally for 5 days. Eligible patients were allocated at a 2 calcifediol:1 no calcifediol ratio through electronic randomization on the day of admission to take oral calcifediol (0.532 mg), or not. Patients in the calcifediol treatment group continued with oral calcifediol (0.266 mg) on day 3 and 7, and then weekly until discharge or ICU admission. Outcomes of effectiveness included rate of ICU admission and deaths.
RESULTS: Of 50 patients treated with calcifediol, one required admission to the ICU (2%), while of 26 untreated patients, 13 required admission (50%) p value XFischer test p < 0.001. Univariate Risk Estimate Odds Ratio for ICU in patients with Calcifediol treatment versus without Calcifediol treatment: 0.02 (95%CI 0.002-0.17). Multivariate Risk Estimate Odds Ratio for ICU in patients with Calcifediol treatment vs Without Calcifediol treatment ICU (adjusting by Hypertension and T2DM): 0.03 (95%CI: 0.003-0.25). Of the patients treated with calcifediol, none died, and all were discharged, without complications. The 13 patients not treated with calcifediol, who were not admitted to the ICU, were discharged. Of the 13 patients admitted to the ICU, two died and the remaining 11 were discharged.
CONCLUSION: Our pilot study demonstrated that administration of a high dose of Calcifediol or 25-hydroxyvitamin D, a main metabolite of vitamin D endocrine system, significantly reduced the need for ICU treatment of patients requiring hospitalization due to proven COVID-19. Calcifediol seems to be able to reduce severity of the disease, but larger trials with groups properly matched will be required to show a definitive answer.


greenmedinfo--2020-09-09--Curcumin stimulates exosome/microvesicle release in an in vitro model of intracellular lipid accumul

Curcumin stimulates exosome/microvesicle release in an in vitro model of intracellular lipid accumulation by increasing ceramide synthesis.

Curcumin , a hydrophobic polyphenol found in the rhizome of Curcuma longa , has been shown to reduce intracellular lipid @ @ @ @ @ lysosomal storage diseases such as Niemann-Pick type C. Exosomes are small extracellular vesicles secreted by @ @ @ @ @ in intracellular ceramide composition .
Curcumin can induce exosome/microvesicle release in cellular models of lipid @ @ @ @ @ mechanism by which curcumin stimulates this release is unknown .
In a model of lipid @ @ @ @ @ cells , we show that curcumin stimulated ceramide synthesis by increasing the intracellular concentration of @ @ @ @ @ exosome/microvesicle secretion 10-fold , thereby reducing the concentration of lipids in the endolysosomal compartment .
@ @ @ @ @ inhibitors of serine palmitoyltransferase ( myriocin ) and ceramide synthase ( fumonisin B1 ) .
@ @ @ @ @ decrease in intracellular lipid deposition induced by curcumin is mediated by increased ceramide synthesis and @ @ @ @ @ may represent an additional health benefit of curcumin .

Curcumin, a hydrophobic polyphenol found in the rhizome of Curcuma longa, has been shown to reduce intracellular lipid accumulation in mouse models of lysosomal storage diseases such as Niemann-Pick type C. Exosomes are small extracellular vesicles secreted by cells in response to changes in intracellular ceramide composition. Curcumin can induce exosome/microvesicle release in cellular models of lipid deposition; however, the mechanism by which curcumin stimulates this release is unknown. In a model of lipid trafficking impairment in C6 glia cells, we show that curcumin stimulated ceramide synthesis by increasing the intracellular concentration of ceramide-dihydroceramide. Ceramide overload increased exosome/microvesicle secretion 10-fold, thereby reducing the concentration of lipids in the endolysosomal compartment. These effects were blocked by inhibitors of serine palmitoyltransferase (myriocin) and ceramide synthase (fumonisin B1). It is concluded that the decrease in intracellular lipid deposition induced by curcumin is mediated by increased ceramide synthesis and exosome/microvesicle release. This action may represent an additional health benefit of curcumin.


greenmedinfo--2020-09-09--Nobiletin aymeliorates NLRP3 inflammasome-mediated inflammation through promoting autophagy via the

Nobiletin aymeliorates NLRP3 inflammasome-mediated inflammation through promoting autophagy via the AMPK pathway.

Multiple lines of evidence have shown that neuroinflammation and autophagy are highly involved in the process of depression .
Nobiletin ( NOB ) displays neuroprotective effects and anti-depressant-like effects .
Given the evidence that NOB exerts anti-inflammatory effects and regulates autophagy , we investigate the anti-neuroinflammatory properties and the effect of regulating the autophagy of NOB and subsequently uncover the potential anti-depressant mechanisms of NOB .
The behavioral changes of rats were observed after prolonged lipopolysaccharide ( LPS ) treatment and NOB administration .
Rat hippocampus and BV2 cells treated by LPS and NOB were evaluated .
The methods of @ @ @ @ @ @ @ immunostaining , and adenovirus transfection were employed to determine neuroinflammation , autophagic markers , and nucleotide-binding oligomerization domain-like receptor 3 ( NLRP3 ) activation .
Our study showed LPS enhanced the expression of pro-inflammatory cytokines and NLRP3 inflammasome activation but inhibited autophagy in both rat hippocampus and BV2 cells .
NOB significantly improved the behavioral deficits and ameliorated the neuroinflammation induced by LPS in rats .
Furthermore , NOB promoted autophagy and attenuated NLRP3 inflammasome activation induced by LPS , involving in the process the adenosine monophosphate-activated protein kinase ( AMPK ) pathway @ @ @ @ @ @ @ relied on its effects of promoting autophagy and suppressing the activation of NLRP3 , in which process of AMPK pathway may be involved .

Multiple lines of evidence have shown that neuroinflammation and autophagy are highly involved in the process of depression. Nobiletin (NOB) displays neuroprotective effects and anti-depressant-like effects. Given the evidence that NOB exerts anti-inflammatory effects and regulates autophagy, we investigate the anti-neuroinflammatory properties and the effect of regulating the autophagy of NOB and subsequently uncover the potential anti-depressant mechanisms of NOB. The behavioral changes of rats were observed after prolonged lipopolysaccharide (LPS) treatment and NOB administration. Rat hippocampus and BV2 cells treated by LPS and NOB were evaluated. The methods of real-time PCR analysis, Western blot, immunostaining, and adenovirus transfection were employed to determine neuroinflammation, autophagic markers, and nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) activation. Our study showed LPS enhanced the expression of pro-inflammatory cytokines and NLRP3 inflammasome activation but inhibited autophagy in both rat hippocampus and BV2 cells. NOB significantly improved the behavioral deficits and ameliorated the neuroinflammation induced by LPS in rats. Furthermore, NOB promoted autophagy and attenuated NLRP3 inflammasome activation induced by LPS, involving in the process the adenosine monophosphate-activated protein kinase (AMPK) pathway. Neuroprotective and anti-depressant actions of NOB relied on its effects of promoting autophagy and suppressing the activation of NLRP3, in which process of AMPK pathway may be involved.


greenmedinfo--2020-09-09--Nobiletin selectively inhibits oral cancer cell growth by promoting apoptosis and DNA damage in vitr

Nobiletin selectively inhibits oral cancer cell growth by promoting apoptosis and DNA damage in vitro.

OBJECTIVES : The aim of this study was to investigate whether nobiletin ( NOB ) can inhibit the proliferation of oral squamous cell carcinoma ( OSCC ) cells by promoting apoptosis , oxidative stress ( reactive oxygen species [ ROS ] ) , and DNA damage .
STUDY DESIGN : OSCCs were treated with different concentrations of NOB ( 25 , 50 , and 100µM ) for different amounts of time ( 0 , 24 , 48 , and 72 hours ) .
The viability of NOB was assessed by using MTT-based cell viability assays .
Flow cytometry was used @ @ @ @ @ @ @ expressions of capase-3 and poly ( adenosine diphosphate-ribose ) polymerase ( PARP ) were assessed by quantitative real-time polymerase chain reaction ( qRT-PCR ) and Western blot analyses .
The intensity of ROS fluorescence was measured by using a spectrophotometer .
The expression of γH2AX and 8-Oxo-20-deoxyguanosine ( 8-oxodG ) were assessed to determine the degree of DNA damage .
RESULTS : We observed that NOB decreased OSCC cell viability in a dose- and time-dependent manner but had little effect on primary normal human oral epithelial cells ( H0 ECs ) .
Moreover @ @ @ @ @ @ @ and treatment time , capase-3 , PARP messenger RNA ( mRNA ) , and protein levels gradually increased , as did annexin V- and 7 adducin ( ADD ) -mediated apoptosis .
In addition , NOB also increased the levels of ROS and DNA damage in a concentration- and time-dependent manner .
CONCLUSIONS : NOB can inhibit OSCC cell by promoting apoptosis , ROS production , and DNA damage .

OBJECTIVES: The aim of this study was to investigate whether nobiletin (NOB) can inhibit the proliferation of oral squamous cell carcinoma (OSCC) cells by promoting apoptosis, oxidative stress (reactive oxygen species [ROS]), and DNA damage.
STUDY DESIGN: OSCCs were treated with different concentrations of NOB (25, 50, and 100µM) for different amounts of time (0, 24, 48, and 72 hours). The viability of NOB was assessed by using MTT-based cell viability assays. Flow cytometry was used to assess cell apoptosis, and the expressions of capase-3 and poly (adenosine diphosphate-ribose) polymerase (PARP) were assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analyses. The intensity of ROS fluorescence was measured by using a spectrophotometer. The expression of γH2AX and 8-Oxo-20-deoxyguanosine (8-oxodG) were assessed to determine the degree of DNA damage.
RESULTS: We observed that NOB decreased OSCC cell viability in a dose- and time-dependent manner but had little effect on primary normal human oral epithelial cells (H0 ECs). Moreover, with the increase in NOB concentration and treatment time, capase-3, PARP messenger RNA (mRNA), and protein levels gradually increased, as did annexin V- and 7 adducin (ADD)-mediated apoptosis. In addition, NOB also increased the levels of ROS and DNA damage in a concentration- and time-dependent manner.
CONCLUSIONS: NOB can inhibit OSCC cell by promoting apoptosis, ROS production, and DNA damage.


greenmedinfo--2020-09-09--Anti-inflammatory effects of gallic acid in human gestational tissues in vitro.

Spontaneous preterm birth is the leading cause of neonatal mortality and morbidity globally .
Activation of the maternal immune system leads to a downstream cascade of proinflammatory events that culminate in the activation of spontaneous uterine contractions and the rupture of the foetal membranes .
Anti-inflammatory agents may be a novel therapeutic approach to prevent inflammation-induced myometrial contractions and premature rupture of foetal membranes .
The polyphenol gallic acid has been previously shown to exert potent anti-inflammatory effects .
Thus , this study aimed to determine the effect of gallic acid on proinflammatory and pro-labour mediators in cytokine-stimulated gestational tissues @ @ @ @ @ @ @ isolated from myometrium and foetal membranes ( decidua , and amnion mesenchymal and epithelial cells ) , gallic acid treatment suppressed inflammation-induced expression of proinflammatory cytokines and chemokines and extracellular matrix-degrading and matrix-remodelling enzymes .
Gallic acid also significantly inhibited inflammation-induced myometrial activation as evidenced by decreased expression of contraction-associated proteins , the uterotonic PGF2α and collagen cell contractility .
Using a global proteomic approach , gallic acid may differentially regulate proteins associated with collagen synthesis , cell contractility and protein synthesis in primary myometrial and decidual cells .
In summary , gallic @ @ @ @ @ @ @ labour in primary cells isolated from myometrium and foetal membranes .
These in vitro studies suggest that the polyphenol gallic acid may be able to suppress the production of proinflammatory and pro-labour mediators involved in myometrial contractions and rupture of foetal membranes .
Future preclinical studies may elucidate the efficacy of gallic acid in preventing inflammation-driven preterm birth .

Spontaneous preterm birth is the leading cause of neonatal mortality and morbidity globally. Activation of the maternal immune system leads to a downstream cascade of proinflammatory events that culminate in the activation of spontaneous uterine contractions and the rupture of the foetal membranes. Anti-inflammatory agents may be a novel therapeutic approach to prevent inflammation-induced myometrial contractions and premature rupture of foetal membranes. The polyphenol gallic acid has been previously shown to exert potent anti-inflammatory effects. Thus, this study aimed to determine the effect of gallic acid on proinflammatory and pro-labour mediators in cytokine-stimulated gestational tissues in vitro. In primary human cells isolated from myometrium and foetal membranes (decidua, and amnion mesenchymal and epithelial cells), gallic acid treatment suppressed inflammation-induced expression of proinflammatory cytokines and chemokines and extracellular matrix-degrading and matrix-remodelling enzymes. Gallic acid also significantly inhibited inflammation-induced myometrial activation as evidenced by decreased expression of contraction-associated proteins, the uterotonic PGF2α and collagen cell contractility. Using a global proteomic approach, gallic acid may differentially regulate proteins associated with collagen synthesis, cell contractility and protein synthesis in primary myometrial and decidual cells. In summary, gallic acid inhibited inflammation-induced mediators involved in active labour in primary cells isolated from myometrium and foetal membranes. These in vitro studies suggest that the polyphenol gallic acid may be able to suppress the production of proinflammatory and pro-labour mediators involved in myometrial contractions and rupture of foetal membranes. Future preclinical studies may elucidate the efficacy of gallic acid in preventing inflammation-driven preterm birth.