This is called the spillover effect. Not only does an obese person have more fat, but they’re constantly spilling that fat into their bloodstream. So that could be the link between obesity and diabetes. Fat is spilling out from our fat cells and gets lodged in our muscle cells, leading to the insulin resistance that promotes the onset of type 2 diabetes.
Tuesday, 22 November 2016
This is called the spillover effect. Not only does an obese person have more fat, but they’re constantly spilling that fat into their bloodstream. So that could be the link between obesity and diabetes. Fat is spilling out from our fat cells and gets lodged in our muscle cells, leading to the insulin resistance that promotes the onset of type 2 diabetes.
Courage is the discovery that you may not win, and trying when you know you can lose. ~ Tom Krause
Courage is the discovery that you may not win, and trying when you know you can lose. ~ Tom Krause 
FEB NEUT PX SCORES
TIME FROM LAST CHEMORX <7 DAYS= 2 POINTS ELSE 1 POINT
CRP > 60 =2 POINTS ELSE 1 POINT
FOCUS PRESENT WHICH IS NON URTI= 2 POINTS ELSE 1 POINT
ANC < 0.1 =2 POINTS ELSE 1 POINT
<7- LOW RISK
>7-HI RISK
CRP > 60 =2 POINTS ELSE 1 POINT
FOCUS PRESENT WHICH IS NON URTI= 2 POINTS ELSE 1 POINT
ANC < 0.1 =2 POINTS ELSE 1 POINT
<7- LOW RISK
>7-HI RISK
there are more than 17 000 universities in the world,
there are more than 17 000 universities in the world,
Tuesday, 15 November 2016
IF 16/8
What’s Acceptable to Drink During Fasts?
During a fast you can’t eat, but you should definitely drink. Water is the drink of choice, but coffee and tea are also great options. During longer fasts it can be wise to add a little salt too, or drink bouillon.
Anything you drink should ideally be zero calories. But it may be acceptable to cheat by adding a small amount of milk in your coffee or tea – if you absolutely need it to enjoy your drink.
LOSS
Losses you may suffer include… • Time • Freedom • Love • Peace of mind • Energy • Friendship • Money • Happiness
Even the wisest mind has something yet to learn. ~ George Santayana
Even the wisest mind has something yet to learn. ~ George Santayana 
IF 812
Coffee = awesome
During the fasts feel free to drink ANY noncaloric beverage you want, including but not limited to: water, coffee (with or without noncaloric sweetener such as stevia), tea (hot or iced, sweetened with stevia if desired), diet soda with no calories (I recommend Zevia brand sweetened with stevia), or any other beverage with no calories. However I would NOT recommend any calories AT ALL, as it takes frightfully few calories to spike insulin and sabotage your fast. Fat is the macronutrient that spikes insulin the very least, which is why so many people are using Bulletproof coffee or some other method of adding fat (butter, coconut oil, etc) to coffee in the morning.
8 TO 12 IF
When you first start out with intermittent fasting, you can have quite a bit of hunger and low energy and other symptoms. In this case I recommend starting out with “baby steps”, by just pushing breakfast out an hour or two at first, then slowly increasing the fasting interval. As time goes by and you become more “fat adapted”, it is easier and easier to fast. This is identical to exercise in those who are sedentary: it is painful and extremely difficult at first, and then once you are adapted it gets easy and even enjoyable.
Wednesday, 26 October 2016
BMBI IS LEAVING US
How to Care for a Dying Guinea Pig
Unfortunately, many small pets (especially rodents) do not live long, so we must be prepared to eventually say goodbye. Guinea pigs generally live for 5 to 8 years, assuming they do not experience any serious injuries or diseases sooner than this.[1] If your guinea pig is nearing the end of his life, there are some things you can do to help make his last moments as comfortable as possible.
Don't limit your challenges; challenge your limits. - Anon
Don't limit your challenges; challenge your limits. - Anon
Maternal SSRI use during late pregnancy was associated with an increase in infant respiratory and CNS-related disorders, hypoglycemia, and feeding difficulties
Maternal SSRI use during late pregnancy was associated with an increase in infant respiratory and CNS-related disorders, hypoglycemia, and feeding difficulties
CORPORATE WLTH
The Fortune 500 2016 - Top 10
- Walmart - annual revenue: $482bn. The US retail giant owns Asda in the UK. ...
- State Grid - $330bn. ...
- China National Petroleum - $299bn. ...
- Sinopec Group - $294bn. ...
- Royal Dutch Shell - $272bn. ...
- Exxon Mobil - $246bn. ...
- Volkswagen - $237bn. ...
- Toyota - $237bn.
Apple - $234bn
10. BP - $226bn
Tuesday, 25 October 2016
Most people sleep about seven or eight hours a night. That leaves 16 or 17 hours awake each day. Or about 1,000 minutes. Let’s think about those 1,000 minutes as 100 10-minute blocks. That’s what you wake up with every day.
Most people sleep about seven or eight hours a night. That leaves 16 or 17 hours awake each day. Or about 1,000 minutes. Let’s think about those 1,000 minutes as 100 10-minute blocks. That’s what you wake up with every day.
AF ELEPHANTS Current populations stand at just 350,000 elephants – a loss of 30% of the continental herd in just the last 7 years. And at current rates of poaching they could all be gone within 20 years.
Current populations stand at just 350,000 elephants – a loss of 30% of the continental herd in just the last 7 years. And at current rates of poaching they could all be gonewithin 20 years.
BTO-SCULPTS OR BREAKS
I’m grateful for past betrayals, heartaches, and challenges… I thought they were breaking me; but they were sculpting me.” ~Steve Maraboli
OLS 1 SCNRIO
CALLED TO CS
39/40 B WT 3.5 KG H/O DFM
CLEAR AM FLUID, 2 CORDS AROUND NECK
DTC TBHR GONB OA 5IB SATECG REASSHRCM
CNM HP2POAM RPT5IB REASSHRCM
CM HR<60 VENT30S REASSHR
HR<60 STARTCC CPR3/1 REASSHR
HR<60 UVC ABGS
0 SEC-LIMP CYANOTIC APNEIC
DTC TBHR GONB OA 5IB SATECG REASSHRCM
1 MIN -HR50 LIMP APNEIC
CNM HP2POAM RPT5IB REASSHRCM
1MIN 30 S- HR45 LIMP APNEIC
CM HR<60 VENT30S REASSHR
2 MIN-HR45
HR<60 STARTCC CPR3/1 REASSHR
2 MIN 30 S-HR40 LIMP APNEIC
HR<60 UVC ABGS CPR3/1 CONTINUES
3 MIN -RPT ADR 4 MINLY CPR3/1 CONTD
suzuki When a feeling reaches its highest pitch, we remain silent, even 17 syllables may be too many.”
When a feeling reaches its highest pitch, we remain silent, even 17 syllables may be too many.”
Sunday, 25 September 2016
APLS TRACHY
Many children with an established tracheostomy will improve when the blocked tube is removed, allowing them to breathe through the stoma prior to replacing the blocked tube with a new one. However, there are risks in removing the tube from a newly created tracheostomy as, until the stoma track is established, attempted replacement of a tracheostomy tube may be difficult and a blind-ending false track could be created.
Parents who routinely care for their child's tracheostomy at home may be more familiar with tube suction and tube changing for their child than hospital staff in medical areas where this is rarely performed.
If you are unable to pass the suction catheter through the tracheostomy tube, then the tube must be changed immediately with the same size tube. If this fails to relieve the obstruction, or you cannot insert it:
If you are unable to pass the suction catheter through the tracheostomy tube, then the tube must be changed immediately with the same size tube. If this fails to relieve the obstruction, or you cannot insert it:
- •Try a half size smaller tube.
- •If it is not possible to insert this, thread a lubricated suction catheter through the size smaller tracheostomy tube. Insert the suction catheter into the stoma and then attempt to guide the new tracheostomy tube along the catheter and into the stoma.
- •If this is unsuccessful then remove the tracheostomy tube.
APLS ETT To estimate endotracheal tube size for emergency intubation use the following formula:
To estimate endotracheal tube size for emergency intubation use the following formula:
EVO THEORY OF DTH -BIOLF ONLY CARES ABT SAR
Suzanne Sadedin,
Updated Aug 3, 2015 · Featured in Forbes · Upvoted by Ben Waggoner, PhD in Integrative Biology, university professor, evolutionary biologist and Adriana Heguy, molecular biologist, genomics researcher
Excellent question. And before I explain the real answer, which is rather mind-bending, here are some previous arguments and why they are wrong.
Myth 1: We die to make room for younger generations.
Genes are selfish, and each individual body is a vehicle for a collection of genes. These genes are selected to favor the survival of copies of themselves. Since parents and offspring use the same resources, the death of a parent creates room ecologically for just one offspring. Each gene in the parent has a 50% chance of appearing in this offspring. But it has a 100% chance of appearing in the parent, because it's already there. It's never, then, in the evolutionary interests of a parent to die so an offspring can replace it.
Myth 2: We die because our cells/DNA get damaged with age.
This like saying bad drivers die because of blood loss. It's a proximate mechanism of death, not the evolutionary cause of mortality.
Our somatic cells (the cells that are part of our body) do indeed suffer occasional mutations as they divide. These mutations can kill or damage cells, which is annoying but not generally a big problem as we can make more. However, the worst mutations do something much more dangerous: they help cells to survive and proliferate. That's how you get cancer. Because this risk accumulates over time, cells are normally allowed only a limited number of divisions before they undergo cellular senescence, that is, they die. But the genes that cause cellular senescence can also stop working. So that's one of the ways in which we get old: our somatic cell lineages get older, damaged and mutated, and some become cancerous.
However, the cell/DNA damage idea assumes that this isn't something evolution can counteract. And that's clearly false. Lifespan and cancer rates differ between species, and not in the ways you would expect if they were determined by cell/DNA damage. For instance, once you take into account body size and phylogeny, DNA repair doesn't correlate with lifespan. Lifespan does, however, correlate with ecology: mammal species who typically lead risky lives die younger (even if you protect them from those risks). At one extreme, in the harsh Australian bush we find the male agile antechinus, who dies of stress at the end of a single breeding season. At the other extreme, the naked mole rat can live for three decades in its peaceful underground colonies.
This gets even more puzzling when you start to look at genomics. We have a whole suite of genes devoted to keeping our genome pristine. My favorite is a clever gene called P53 that acts as a "gatekeeper" for cell division. If the cell has too many mutations, P53 will halt division and activate repair mechanisms. If that doesn't fix things, it will make the cell commit suicide. Mutations that break P53 are involved in about half of all human cancers. Now, here's the rub: there's a whole family of genes related to P53 in other mammals, and some work better than others. Naked mole rats, as it happens, have two particularly awesome versions that completely protect them against cancer.
We also know that it's perfectly feasible for genetic modification to immortalize cell lineages, and that going through a haploid stage is not essential for maintaining cell viability. How do we know this? From the strange case of the 11,000 year old dog. The dog as an individual is long dead, but her cells survive today as an infectious cancer on other dogs' genitalia. There's also a quaking aspen in Utah whose roots are at least 80,000 years old.
The same applies to permanent organ damage. Some organs heal and regenerate, some don't. Some species can regenerate organs that others can't. A salamander can grow a whole new leg. There's even a jellyfish that can reverse its development when it's damaged. All in all, natural selection is clearly capable of creating creatures who can fix cellular and DNA damage and repair damaged organs.
So: evolution can fix these problems for us, and it doesn't. What the heck, evolution, aren't we friends?
Well, no, actually, evolution is not our friend. If anything, it's our genes' friend. And there's a very good reason our genes don't actually care about us.
Mutations are a problem evolution can fix. But death isn't. Accidents happen. Diseases happen. Sabre-toothed cats happen (well, not any more, but you get the point). No matter how hard our genes try to help us survive, sometimes they're going to fail. These failures are often, as far as your genes are concerned, random. And that means our genes can't afford to get too invested in the survival of any individual. In the long term, the only way a gene can survive is to spread -- to copy itself through a population.
So from a gene's-eye view, every investment in your survival is a potential trade-off with the creation and survival of your potential descendants. And, rather obviously, the more likely you are to die randomly, the less it makes sense for your genes to invest in the survival side of the equation.
Every day of your life, the Universe in effect rolls a pair of many-sided dice. Snake eyes, you're dead. Every day the probability that the Universe has at some point in the past killed you increases. And at some time after your birth, on average, you're dead.
Look at this from your genes' perspective. Your genes don't know about you specifically, their behavior is selected based on statistics. They don't want to invest in somebody who is, on average, dead. Younger people are, on average, more likely to be alive. So if your genes have to choose between investing in (on average) the survival and/or reproduction of young you versus old you, they'll pick young you.
And quite often they do have to choose. Early in development, for instance, you really need genes that allow lots of cellular proliferation. Your body can't grow without it. But too much cellular proliferation when you're fully-grown is a big problem. So it's a delicate balance, and what's good for you when you're a kid can be bad for you when you're grown up. There are other genes that manage these risks by switching genes on and off throughout your life, but that makes the network even more complex and failure-prone. You end up with an intricate genomic dance going on throughout your whole life. So it's hardly surprising that some genes end up helping you now and harming you later.
One example may be Huntington's Disease, a horrible dominant genetic disorder that slowly destroys your brain and kills you. The disease usually starts to affect people in middle age. However, young people with the Huntington's gene have more children on average. It's thought that the Huntington's gene strengthens the immune system by increasing activity of P53, making them healthier and more fertile. Other possible examples include atherosclerosis, sarcopenia, prostate hypertrophy, osteoporosis, carcinoma and Alzheimer's disease.
As life goes on, your genes effectively stop caring what happens to you. After a certain point, it's so unlikely that you're still alive that your genes can safely assume you'll already be dead. So your genomic programming can contain all sorts of wacky stuff that only kicks in after this point, just because there's no noticeable selection against it.
The really fascinating part (by which I mean the really depressing part) is how this effect reinforces itself. The more likely it is that you're dead, the less your genes care about you. The less your genes care about you, the more likely it is that you're dead. And this has been going on throughout our evolutionary history, so we've accumulated all sorts of weird malfunctions that kick in late in our lives. The human genome is riddled with them, and most of the genes involved are also part of normal development and reproduction. These malfunctions cluster around a certain age: the age when evolution stops caring about us because, statistically speaking, we're already dead.
So mortality is an evolutionary prophecy that fulfills itself in a multitude of ways. And that's why there's no single key to eternal life. Poor old Gilgamesh.
Myth 1: We die to make room for younger generations.
Genes are selfish, and each individual body is a vehicle for a collection of genes. These genes are selected to favor the survival of copies of themselves. Since parents and offspring use the same resources, the death of a parent creates room ecologically for just one offspring. Each gene in the parent has a 50% chance of appearing in this offspring. But it has a 100% chance of appearing in the parent, because it's already there. It's never, then, in the evolutionary interests of a parent to die so an offspring can replace it.
Myth 2: We die because our cells/DNA get damaged with age.
This like saying bad drivers die because of blood loss. It's a proximate mechanism of death, not the evolutionary cause of mortality.
Our somatic cells (the cells that are part of our body) do indeed suffer occasional mutations as they divide. These mutations can kill or damage cells, which is annoying but not generally a big problem as we can make more. However, the worst mutations do something much more dangerous: they help cells to survive and proliferate. That's how you get cancer. Because this risk accumulates over time, cells are normally allowed only a limited number of divisions before they undergo cellular senescence, that is, they die. But the genes that cause cellular senescence can also stop working. So that's one of the ways in which we get old: our somatic cell lineages get older, damaged and mutated, and some become cancerous.
However, the cell/DNA damage idea assumes that this isn't something evolution can counteract. And that's clearly false. Lifespan and cancer rates differ between species, and not in the ways you would expect if they were determined by cell/DNA damage. For instance, once you take into account body size and phylogeny, DNA repair doesn't correlate with lifespan. Lifespan does, however, correlate with ecology: mammal species who typically lead risky lives die younger (even if you protect them from those risks). At one extreme, in the harsh Australian bush we find the male agile antechinus, who dies of stress at the end of a single breeding season. At the other extreme, the naked mole rat can live for three decades in its peaceful underground colonies.
This gets even more puzzling when you start to look at genomics. We have a whole suite of genes devoted to keeping our genome pristine. My favorite is a clever gene called P53 that acts as a "gatekeeper" for cell division. If the cell has too many mutations, P53 will halt division and activate repair mechanisms. If that doesn't fix things, it will make the cell commit suicide. Mutations that break P53 are involved in about half of all human cancers. Now, here's the rub: there's a whole family of genes related to P53 in other mammals, and some work better than others. Naked mole rats, as it happens, have two particularly awesome versions that completely protect them against cancer.
We also know that it's perfectly feasible for genetic modification to immortalize cell lineages, and that going through a haploid stage is not essential for maintaining cell viability. How do we know this? From the strange case of the 11,000 year old dog. The dog as an individual is long dead, but her cells survive today as an infectious cancer on other dogs' genitalia. There's also a quaking aspen in Utah whose roots are at least 80,000 years old.
The same applies to permanent organ damage. Some organs heal and regenerate, some don't. Some species can regenerate organs that others can't. A salamander can grow a whole new leg. There's even a jellyfish that can reverse its development when it's damaged. All in all, natural selection is clearly capable of creating creatures who can fix cellular and DNA damage and repair damaged organs.
So: evolution can fix these problems for us, and it doesn't. What the heck, evolution, aren't we friends?
Well, no, actually, evolution is not our friend. If anything, it's our genes' friend. And there's a very good reason our genes don't actually care about us.
Mutations are a problem evolution can fix. But death isn't. Accidents happen. Diseases happen. Sabre-toothed cats happen (well, not any more, but you get the point). No matter how hard our genes try to help us survive, sometimes they're going to fail. These failures are often, as far as your genes are concerned, random. And that means our genes can't afford to get too invested in the survival of any individual. In the long term, the only way a gene can survive is to spread -- to copy itself through a population.
So from a gene's-eye view, every investment in your survival is a potential trade-off with the creation and survival of your potential descendants. And, rather obviously, the more likely you are to die randomly, the less it makes sense for your genes to invest in the survival side of the equation.
Every day of your life, the Universe in effect rolls a pair of many-sided dice. Snake eyes, you're dead. Every day the probability that the Universe has at some point in the past killed you increases. And at some time after your birth, on average, you're dead.
Look at this from your genes' perspective. Your genes don't know about you specifically, their behavior is selected based on statistics. They don't want to invest in somebody who is, on average, dead. Younger people are, on average, more likely to be alive. So if your genes have to choose between investing in (on average) the survival and/or reproduction of young you versus old you, they'll pick young you.
And quite often they do have to choose. Early in development, for instance, you really need genes that allow lots of cellular proliferation. Your body can't grow without it. But too much cellular proliferation when you're fully-grown is a big problem. So it's a delicate balance, and what's good for you when you're a kid can be bad for you when you're grown up. There are other genes that manage these risks by switching genes on and off throughout your life, but that makes the network even more complex and failure-prone. You end up with an intricate genomic dance going on throughout your whole life. So it's hardly surprising that some genes end up helping you now and harming you later.
One example may be Huntington's Disease, a horrible dominant genetic disorder that slowly destroys your brain and kills you. The disease usually starts to affect people in middle age. However, young people with the Huntington's gene have more children on average. It's thought that the Huntington's gene strengthens the immune system by increasing activity of P53, making them healthier and more fertile. Other possible examples include atherosclerosis, sarcopenia, prostate hypertrophy, osteoporosis, carcinoma and Alzheimer's disease.
As life goes on, your genes effectively stop caring what happens to you. After a certain point, it's so unlikely that you're still alive that your genes can safely assume you'll already be dead. So your genomic programming can contain all sorts of wacky stuff that only kicks in after this point, just because there's no noticeable selection against it.
The really fascinating part (by which I mean the really depressing part) is how this effect reinforces itself. The more likely it is that you're dead, the less your genes care about you. The less your genes care about you, the more likely it is that you're dead. And this has been going on throughout our evolutionary history, so we've accumulated all sorts of weird malfunctions that kick in late in our lives. The human genome is riddled with them, and most of the genes involved are also part of normal development and reproduction. These malfunctions cluster around a certain age: the age when evolution stops caring about us because, statistically speaking, we're already dead.
So mortality is an evolutionary prophecy that fulfills itself in a multitude of ways. And that's why there's no single key to eternal life. Poor old Gilgamesh.
MILLIGAN Money couldn't buy friends, but you got a better class of enemy.
Money couldn't buy friends, but you got a better class of enemy.
The illiterate of 21st century will not be those who cannot read and write ,but those who cannot learn, unlearn and relearn - Alvin Toffler
The illiterate of 21st century will not be those who cannot read and write ,but those who cannot learn, unlearn and relearn - Alvin Toffler
Mindful dishwashing can decrease stress and calm the mind, a new study finds.
Mindful dishwashing can decrease stress and calm the mind, a new study finds.
Human history has been shaped by three major revolutions: the Cognitive Revolution (70,000 years ago), the Agricultural Revolution (10,000 years ago), and the Scientific Revolution (500 years ago).
Human history has been shaped by three major revolutions: the Cognitive Revolution (70,000 years ago), the Agricultural Revolution (10,000 years ago), and the Scientific Revolution (500 years ago).
CAS REVOLN
CAS REVOLN
KOL DR PRACTICE we tend to forget the many who fail, remember the few who succeed
we tend to forget the many who fail, remember the few who succeed
INET COGNITIVE OFFLOADING
The more times people look up facts online, the less they prefer to rely on their own memories for even the simplest questions.
Psychologists have called this ‘cognitive offloading’.
CAMUS You will never be happy if you continue to search for what happiness consists of. You will never live if you are looking for the meaning of life.”
You will never be happy if you continue to search for what happiness consists of. You will never live if you are looking for the meaning of life.”
Wanting positive experience is a negative experience; accepting negative experience is a positive experience
Wanting positive experience is a negative experience; accepting negative experience is a positive experience
APLS Intubation should take no longer than approximately 30 seconds, or, as a very rough guide, for how long the operator can hold their breath easily
Intubation should take no longer than approximately 30 seconds, or, as a very rough guide, for how long the operator can hold their breath easily
Children born in the later preterm period have been shown to exhibit lower school readiness, spatial abilities, verbal reasoning, educational achievement, and poorer school performance in the early school years than their peers born after 37 weeks
Children born in the later preterm period have been shown to exhibit lower school readiness, spatial abilities, verbal reasoning, educational achievement, and poorer school performance in the early school years than their peers born after 37 weeks
APLS If evidence of massive haemothorax: •insert chest drain •commence blood volume replacement, simultaneously if possible
If evidence of massive haemothorax:
- •insert chest drain
- •commence blood volume replacement, simultaneously if possible
APLS If evidence of tension pneumothorax: •perform immediate needle decompression •follow with chest drain
If evidence of tension pneumothorax:
- •perform immediate needle decompression
- •follow with chest drain
APLS If chest injury: •consider tension pneumothorax and haemothorax, flail segment and open pneumothorax TOFH
T-TENSION PNTHX
O-OPEN PNTHX
F-FLAIL CHEST
H-HMTHX
O-OPEN PNTHX
F-FLAIL CHEST
H-HMTHX
APLS If dealing with a trauma case: •control of major haemorrhage occurs simultaneously •consider cervical spine
If dealing with a trauma case:
- •control of major haemorrhage occurs simultaneously
- •consider cervical spine
The art of being happy lies in the power of extracting happiness from common things. ~ Henry Ward Beecher
The art of being happy lies in the power of extracting happiness from common things. ~ Henry Ward Beecher 
APLS Resuscitation efforts are unlikely to be successful and cessation can be considered if there is no return of spontaneous circulation at any time with up to 20 minutes of cumulative life support and in the absence of recurring or refractory VF/pVT
Resuscitation efforts are unlikely to be successful and cessation can be considered if there is no return of spontaneous circulation at any time with up to 20 minutes of cumulative life support and in the absence of recurring or refractory VF/pVT
EXCEPT POISONING AND HYPOTHERMIA
EXCEPT POISONING AND HYPOTHERMIA
APLS Saturations should then be maintained between 94% and 98%
Saturations should then be maintained between 94% and 98%
CREATE A THOUGHT- ANGER ANGER ANGER ANGER ANGER, DROWSY DROWSY DROWSY ......
DITRACTED DISTRACTED DISTRACTED......
APLS CAPNOGRAPHY Adrenaline will decrease and bicarbonate increase the measured CO2. Levels of less than 2 kPa (15 mmHg) should prompt attention to chest compression adequacy.
Adrenaline will decrease and bicarbonate increase the measured CO2. Levels of less than 2 kPa (15 mmHg) should prompt attention to chest compression adequacy.
MURDOCH "Between saying and doing, many a pair of shoes is worn out."
"Between saying and doing, many a pair of shoes is worn out."
PETER"It's better to have loved and lost than to have to do forty pounds of laundry a week."
"It's better to have loved and lost than to have to do forty pounds of laundry a week."
Saturday, 24 September 2016
CHAPLIN Life is a tragedy when seen in close-up, but a comedy in long-shot."
Life is a tragedy when seen in close-up, but a comedy in long-shot."
Every one is my teacher, every event a gift, we are all peers; One
Every one is my teacher, every event a gift, we are all peers; One
MID AGE TIME FLIES
Our brain encodes new experiences, but not familiar ones, into memory, and our retrospective judgment of time is based on how many new memories we create over a certain period. In other words, the more new memories we build on a weekend getaway, the longer that trip will seem in hindsight.
high-fat and high-sugar diet causes problems with memory inhibition in the hippocampus.
high-fat and high-sugar diet causes problems with memory inhibition in the hippocampus.
APLS Amiodarone is the treatment of choice in shock-resistant VF and pVT.
Amiodarone is the treatment of choice in shock-resistant VF and pVT.
hypothermia
Unlike cooling, rewarming should be gradual and take place over 8-24 hours. If the patient is stable, simply reset the Arctic Sun at 37C with a rewarming rate of0.1C/hr. If the patient develops hemodynamic instability, dysrhythmia, or severe bleeding while being cooled, start rewarming to 37C immediately at a rate of 0.3C/hr
WRIGHT "Curiosity killed the cat, but for a while I was a suspect."
"Curiosity killed the cat, but for a while I was a suspect."
ADMED Low ALT levels are associated with increased long-term mortality among middle-aged patients with stable coronary heart disease
Low ALT levels are associated with increased long-term mortality among middle-aged patients with stable coronary heart disease
MCD he rash is initially erythematous, maculopapular and appears first on the wrist and ankles, then becomes palpable petechiae, mimicking Rocky Mountain spotted fever. The rash quickly spreads to the rest of the body coalescing into palpable purpura.
he rash is initially erythematous, maculopapular and appears first on the wrist and ankles, then becomes palpable petechiae, mimicking Rocky Mountain spotted fever. The rash quickly spreads to the rest of the body coalescing into palpable purpura.
RASH PEDS PEMV
four broad categories based on visual and tactile characteristics:[2]
- Petechial/Purpuric
- Erythematous
- Maculopapular
- Vesiculobullous
PEMV
RASH PEDS
Historical and physical “red flags” in a patient with an unknown rash include:[1]
- Fever
- Toxic appearance
- Hypotension
- Mucosal lesions
- Severe pain
- Very old or young age
- Immunosuppressed
- New medication
APLS -SOL RP if at any time there are signs of life, such as regular respiratory effort, coughing, eye opening or a sudden increase in end tidal CO2, stop CPR and check the monitor:
if at any time there are signs of life, such as regular respiratory effort, coughing, eye opening or a sudden increase in end tidal CO2, RCEC-stop CPR and check the monitor:
- If still VF/pVT, continue with the sequence as above
- •If asystole, change to the asystole/PEA sequence
- •If organised electrical activity is seen, check for signs of life and a pulse; if there is ROSC, continue post resuscitation care. If there is no pulse (or a pulse below 60 beats/min with no signs of circulation) and no other signs of life continue the asystole/PEA sequence
APLS Whenever venous access is not attainable within 1 minute, intraosseous access should be used as it is rapid and effective
Whenever venous access is not attainable within 1 minute, intraosseous access should be used as it is rapid and effective
APLS Many AEDs can detect VF/pVT in children of all ages and differentiate ‘shockable’ from ‘non-shockable’ rhythms with a high degree of sensitivity and specificity.
Many AEDs can detect VF/pVT in children of all ages and differentiate ‘shockable’ from ‘non-shockable’ rhythms with a high degree of sensitivity and specificity.
APLS Recommended sizes are 4.5 cm for children UNDER 10 kg and 8–12 cm for children OVER10 kg. One pad is placed over the apex in the mid-axillary line, whilst the other is put immediately below the clavicle just to the right of the sternum.
Recommended sizes are 4.5 cm for children <10 kg and 8–12 cm for children >10 kg. One pad is placed over the apex in the mid-axillary line, whilst the other is put immediately below the clavicle just to the right of the sternum.
APLS With immediate identification of VF/pVT, asynchronous electrical defibrillation of 4 joules per kilogram (J/kg) should be carried out immediately and the protocol continued as below.
With immediate identification of VF/pVT, asynchronous electrical defibrillation of 4 joules per kilogram (J/kg) should be carried out immediately and the protocol continued as below.
PROBLEM 2: Dark energy The universe is flying apart faster and faster
PROBLEM 2: Dark energy
The universe is flying apart faster and faster
APLS Recognised causes of VF/pVT in children include underlying cardiac disease, usually congenital, hypothermia and some drug overdoses. A sudden witnessed collapse is also suggestive of a VF/pVT episode.
Recognised causes of VF/pVT in children include underlying cardiac disease, usually congenital, hypothermia and some drug overdoses. A sudden witnessed collapse is also suggestive of a VF/pVT episode.
PROBLEM 1: Dark matter Galaxies rotate too quickly for their visible matter
PROBLEM 1: Dark matter
Galaxies rotate too quickly for their visible matter
PEDS RASH A rash associated with fever or hypotension should make you worry about potentially deadly diagnoses
A rash associated with fever or hypotension should make you worry about potentially deadly diagnoses
There’s only a one in 135 chance that there’s a single pair of exact doppelgangers
There’s only a one in 135 chance that there’s a single pair of exact doppelgangers
CRT PED
Perhaps the true value in measuring CRT is that it provides a cognitive stop point in the management of a sick child – five seconds to get ourbreathing under control – before going forward. There is data to suggest that pressing for longer leads to a longer CRT (by up to 1.4 seconds) but these results were inconsistent.
emergency medicine has taken from surgery and pediatrics, critical care and obstetrics, endocrinology and psychiatry, and we have created something unique. And in doing so, we altered the world’s expectations of what medicine should be.
emergency medicine has taken from surgery and pediatrics, critical care and obstetrics, endocrinology and psychiatry, and we have created something unique. And in doing so, we altered the world’s expectations of what medicine should be.
“Emergency Medicine is the most interesting 15 minutes of every other specialty.”
“Emergency Medicine is the most interesting 15 minutes of every other specialty.”
ion at www.meditation.org.au Saturday, 16 July 2016 - What we are today comes from our thoughts of yesterday, and our present thoughts build our life of tomorrow: Our life is th e creation of our mind. – Buddha
ion at www.meditation.org.au
| |
| What we are today comes from our thoughts of yesterday, and our present thoughts build our life of tomorrow: Our life is th e creation of our mind. – Buddha |
VEGAN X REDUCED CA
Only the vegan group got a significant drop in IGF-1. These findings demonstrate that, unlike in rodents, long-term severe caloric restriction in humans does not reduce the level of this cancer-promoting hormone. It’s not how many calories we eat, but the protein intake that may be the key determinant of circulating IGF-1 levels in humans; and so, reduced protein intake may become an important component of anti-cancer and anti-aging dietary interventions.
Friday, 23 September 2016
BUDDHISM IS AN EDUCN SYSTEM
////////////////////ME ABRHMC RELIGNS ARE FAITHS
///////////////////level of carbon dioxide in the atmosphere has been rising. It has been monitored since 1956 at the Mauna Loa Observatory (MLO) in Hawaii. Mauna Loa was originally chosen as a carbon dioxide monitoring site because it is located far from any continent and offers a good average value for the air over the central Pacific.
////////////////////NO GREED HATRED DELUSION IS NIRVANA
///////////////////MIDDLE WAY = GENEROSITY COMPASSION WISDOM
///////////////////KARMA IS ACTION OF BODY SPEECH MIND
//////////////////GOOD KARMA VS BAD KARMA eg GREED HATRED DELUSION VS GENEROSITY COMPASSION WISDOM BY BODY SPEECHMIND
/////////////EINSTEIN MOST RECOGNISABLE SCIENTIST IN WORLD WHEN ASKED WHO ARE YOU? I AM A STUDENT OF PHYSICS
//////////////MONKS ARE HAPPY TO BE MONKS
///////////////
///////////////////B MONK MEAL -EAT FROM BOWL WHATEVER IS THERE -NO CRAVING
//////////////////I WANT IT I M NOT GETTING IT-TANHA-CAUSE COMING FROM WITHIN-DEALING WITH IT - B MONK TRAINING
//////////////////DTHING another “rainbow” in the process of dissolving from this world
//////////////////////////
///////////////////level of carbon dioxide in the atmosphere has been rising. It has been monitored since 1956 at the Mauna Loa Observatory (MLO) in Hawaii. Mauna Loa was originally chosen as a carbon dioxide monitoring site because it is located far from any continent and offers a good average value for the air over the central Pacific.
////////////////////NO GREED HATRED DELUSION IS NIRVANA
///////////////////MIDDLE WAY = GENEROSITY COMPASSION WISDOM
///////////////////KARMA IS ACTION OF BODY SPEECH MIND
//////////////////GOOD KARMA VS BAD KARMA eg GREED HATRED DELUSION VS GENEROSITY COMPASSION WISDOM BY BODY SPEECHMIND
/////////////EINSTEIN MOST RECOGNISABLE SCIENTIST IN WORLD WHEN ASKED WHO ARE YOU? I AM A STUDENT OF PHYSICS
//////////////MONKS ARE HAPPY TO BE MONKS
///////////////
Ah! Vanitas Vanitatum! Which of us is happy in this world?
Which of us has his desire? Or having it, is satisfied?
Which of us has his desire? Or having it, is satisfied?
—William Makepeace Thackeray, Vanity Fair
///////////According to the Second Noble Truth, desire, or craving (tanha in Pali, trishna in Sanskrit, translated as “thirst”) is the source of dukkha, dissatisfaction.
//////////A Chinese proverb describes the cycle: Man takes a drink; drink takes a drink; drink takes the man.)
///////////poet Marianne Moore as ultimate truth: “satisfaction is a lowly / thing, how pure a thing is joy.” Satisfaction was the opiate of the masses, I declared, and joy the nectar of the gods. I wanted nectar.
///////// Buddha, “one who is awake.”
/////////////ONLY THE HAPPY MIND CAN UNDERSTAND SUFFERING
///////////JUNG craving for alcohol as “a low level of the spiritual search of our being for wholeness, expressed in medieval language: the union with God.
//////////Diamond Sutra:
All composite things are like
a dream, a fantasy, a bubble
and a shadow
Like a dewdrop and a flash of
lightning—
They are thus to be regarded.
a dream, a fantasy, a bubble
and a shadow
Like a dewdrop and a flash of
lightning—
They are thus to be regarded.
///////////Buddhism teaches us that desire, for all the agony and ecstasy, is no match for the truth.
/////////////VAN GOGH
"I dream of painting and then I paint my dream."
//////////////////I WANT IT I M NOT GETTING IT-TANHA-CAUSE COMING FROM WITHIN-DEALING WITH IT - B MONK TRAINING
//////////////////DTHING another “rainbow” in the process of dissolving from this world
//////////////////////////
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