15th September 2014

Photo reblogged from In The Wards with 608 notes

medicalschool:

Gross pathology of rheumatic heart disease: aortic stenosis. Aorta has been removed to show thickened, fused aortic valve leaflets and opened coronary arteries from above.

medicalschool:

Gross pathology of rheumatic heart disease: aortic stenosis. Aorta has been removed to show thickened, fused aortic valve leaflets and opened coronary arteries from above.

Source: medicalschool

14th September 2014

Photoset reblogged from Magical 4 Lyfe with 7,745 notes

sixpenceee:

The barreleye fish is also known as the spook fish. It has a completely transparent head. Its eyes are located inside the head and can rotate within the socket so the fish can look in multiple directions. (Source) (Video) (Nocturnal Creatures) 

Source: sixpenceee

14th September 2014

Photoset reblogged from Medical Examinations with 2,755 notes

theolduvaigorge:

Alexander Tsiaras’ Anatomical Photography

You’ve seen his art before on tumblr, in google search gif sets (where I found some of these images) and facebook, but you likely don’t know the author of the art because people fail to give artists credit. Tsiaras’ work pops up on my dash constantly and has never been sourced as far as I’ve seen it. So here you go, tumblr. Meet the artist. Learn more in the links provided below.

"Alexander Tsiaras, Founder, Editor-in-Chief and CEO of TheVisualMD, has been called a "Digital Age Leonardo da Vinci". He is a technology innovator, whose roots are based in his art and science photojournalism background. Tsiaras has developed cutting edge scientific imaging software that enables him to scan and record the human body at every stage; from a single cell at the moment of conception, through the biological development of man and woman and he tells compelling stories of wellness and prevention with them. His images simply and compellingly explain health and illness in terms that anyone can understand. Most importantly, they give you a visual map to plan your own optimal Health!"

See also:

(Source: Alexander Tsiaras)

Source: theolduvaigorge

14th September 2014

Photo reblogged from mistress of surgery with 1,055 notes

mynotes4usmle:

ANTIBIOTICS CHEAT SHEET :)
Also, REMEMBER!!!!
* Sulfonamides compete for albumin with:
Bilirrubin: given in 2°,3°T, high risk or indirect hyperBb and kernicterus in premies
Warfarin: increases toxicity: bleeding
* Beta-lactamase (penicinillase) Suceptible:
Natural Penicillins (G, V, F, K)
Aminopenicillins (Amoxicillin, Ampicillin)
Antipseudomonal Penicillins (Ticarcillin, Piperacillin)
* Beta-lactamase (penicinillase) Resistant:
Oxacillin, Nafcillin, Dicloxacillin
3°G, 4°G Cephalosporins
Carbapenems 
Monobactams
Beta-lactamase inhibitors
* Penicillins enhanced with:
Clavulanic acid & Sulbactam (both are suicide inhibitors, they inhibit beta-lactamase)
Aminoglycosides (against enterococcus and psedomonas)
* Aminoglycosides enhanced with Aztreonam
* Penicillins: renal clearance EXCEPT Oxacillin & Nafcillin (bile)
* Cephalosporines: renal clearance EXCEPT Cefoperazone & Cefrtriaxone (bile)
* Both inhibited by Probenecid during tubular secretion.
* 2°G Cephalosporines: none cross BBB except Cefuroxime
* 3°G Cephalosporines: all cross BBB except Cefoperazone bc is highly highly lipid soluble, so is protein bound in plasma, therefore it doesn’t cross BBB.
* Cephalosporines are ”LAME" bc they  do not cover this organisms 
L  isteria monocytogenes
A  typicals (Mycoplasma, Chlamydia)
M RSA (except Ceftaroline, 5°G)
E  nterococci

* Disulfiram-like effect: Cefotetan & Cefoperazone (mnemonic)
* Cefoperanzone: all the exceptions!!!
All 3°G cephalosporins cross the BBB except Cefoperazone.
All cephalosporins are renal cleared, except Cefoperazone.
Disulfiram-like effect
* Against Pseudomonas:
3°G Cef taz idime (taz taz taz taz)
4°G Cefepime, Cefpirome (not available in the USA)
Antipseudomonal penicillins
Aminoglycosides (synergy with beta-lactams)
Aztreonam (pseudomonal sepsis)
* Covers MRSA: Ceftaroline (rhymes w/ Caroline, Caroline the 5°G Ceph), Vancomycin, Daptomycin, Linezolid, Tigecycline.
* Covers VRSA: Linezolid, Dalfopristin/Quinupristin
* Aminoglycosides: decrease release of ACh in synapse and act as a Neuromuscular blocker, this is why it enhances effects of muscle relaxants.
* DEMECLOCYCLINE: tetracycline that’s not used as an AB, it is used as tx of SIADH to cause Nephrogenic Diabetes Insipidus (inhibits the V2 receptor in collecting ducts)
* Phototoxicity: Q ue S T  ion?
Q uinolones
Sulfonamides
T etracyclines

* p450 inhibitors: Cloramphenicol, Macrolides (except Azithromycin), Sulfonamides
* Macrolides SE: Motilin stimulation, QT prolongation, reversible deafness, eosinophilia, cholestatic hepatitis
* Bactericidal: beta-lactams (penicillins, cephalosporins, monobactams, carbapenems), aminoglycosides, fluorquinolones, metronidazole.
* Baceriostatic: tetracyclins, streptogramins, chloramphenicol, lincosamides, oxazolidonones, macrolides, sulfonamides, DHFR inhibitors.
* Pseudomembranous colitis: Ampicillin, Amoxicillin, Clindamycin, Lincomycin.
* QT prolongation: macrolides, sometimes fluoroquinolones

mynotes4usmle:

ANTIBIOTICS CHEAT SHEET :)

Also, REMEMBER!!!!

* Sulfonamides compete for albumin with:

  • Bilirrubin: given in 2°,3°T, high risk or indirect hyperBb and kernicterus in premies
  • Warfarin: increases toxicity: bleeding

Beta-lactamase (penicinillase) Suceptible:

  • Natural Penicillins (G, V, F, K)
  • Aminopenicillins (Amoxicillin, Ampicillin)
  • Antipseudomonal Penicillins (Ticarcillin, Piperacillin)

Beta-lactamase (penicinillase) Resistant:

  • Oxacillin, Nafcillin, Dicloxacillin
  • 3°G, 4°G Cephalosporins
  • Carbapenems 
  • Monobactams
  • Beta-lactamase inhibitors

* Penicillins enhanced with:

  • Clavulanic acid & Sulbactam (both are suicide inhibitors, they inhibit beta-lactamase)
  • Aminoglycosides (against enterococcus and psedomonas)

Aminoglycosides enhanced with Aztreonam

* Penicillins: renal clearance EXCEPT Oxacillin & Nafcillin (bile)

* Cephalosporines: renal clearance EXCEPT Cefoperazone & Cefrtriaxone (bile)

* Both inhibited by Probenecid during tubular secretion.

* 2°G Cephalosporines: none cross BBB except Cefuroxime

* 3°G Cephalosporines: all cross BBB except Cefoperazone bc is highly highly lipid soluble, so is protein bound in plasma, therefore it doesn’t cross BBB.

* Cephalosporines are ”LAME" bc they  do not cover this organisms 

  • L  isteria monocytogenes
  • A  typicals (Mycoplasma, Chlamydia)
  • RSA (except Ceftaroline, 5°G)
  •  nterococci

image

* Disulfiram-like effect: Cefotetan Cefoperazone (mnemonic)

* Cefoperanzone: all the exceptions!!!

  • All 3°G cephalosporins cross the BBB except Cefoperazone.
  • All cephalosporins are renal cleared, except Cefoperazone.
  • Disulfiram-like effect

* Against Pseudomonas:

  • 3°G Cef taz idime (taz taz taz taz)
  • 4°G Cefepime, Cefpirome (not available in the USA)
  • Antipseudomonal penicillins
  • Aminoglycosides (synergy with beta-lactams)
  • Aztreonam (pseudomonal sepsis)

* Covers MRSA: Ceftaroline (rhymes w/ Caroline, Caroline the 5°G Ceph), Vancomycin, Daptomycin, Linezolid, Tigecycline.

Covers VRSA: Linezolid, Dalfopristin/Quinupristin

* Aminoglycosides: decrease release of ACh in synapse and act as a Neuromuscular blocker, this is why it enhances effects of muscle relaxants.

* DEMECLOCYCLINE: tetracycline that’s not used as an AB, it is used as tx of SIADH to cause Nephrogenic Diabetes Insipidus (inhibits the V2 receptor in collecting ducts)

* Phototoxicity: Q ue S T  ion?

  • uinolones
  • Sulfonamides
  • T etracyclines

image

* p450 inhibitors: Cloramphenicol, Macrolides (except Azithromycin), Sulfonamides

* Macrolides SE: Motilin stimulation, QT prolongation, reversible deafness, eosinophilia, cholestatic hepatitis

Bactericidal: beta-lactams (penicillins, cephalosporins, monobactams, carbapenems), aminoglycosides, fluorquinolones, metronidazole.

* Baceriostatic: tetracyclins, streptogramins, chloramphenicol, lincosamides, oxazolidonones, macrolides, sulfonamides, DHFR inhibitors.

Pseudomembranous colitis: Ampicillin, Amoxicillin, Clindamycin, Lincomycin.

QT prolongation: macrolides, sometimes fluoroquinolones

Source: mynotes4usmle

7th September 2014

Photoset reblogged from Hikikomori-Style with 52,632 notes

tommytv:

nychealth:

Let’s stop HIV in New York City

  • If you are HIV-negative, PEP and PrEP can help you stay that way.
  • If you are HIV-positive, PEP and PrEP can help protect your partners.

 

Daily PrEP

PrEP is a daily pill that can help keep you HIV-negative as long as you take it every day.

  • Ask your doctor if PrEP (Pre-exposure Prophylaxis) may be right for you.
  • Condoms give you additional protection against HIV, other sexually transmitted infections, and unintended pregnancy.

 

Emergency PEP

If you are HIV-negative and think you were exposed to HIV, immediately go to a clinic or emergency room and ask for PEP (Post-exposure  Prophylaxis).

  • PEP can stop HIV if started within 36 hours of exposure.
  • You continue taking PEP for 28 days.

Many insurance plans including Medicaid cover PEP and PrEP. Assistance may be available if you are uninsured. Visit NYC Health’s website to find out where to get PrEP or PEP in New York City.

This is such a giant step that barely any people know about it seems, so amazing to see progress in the treatment of HIV

Source: nychealth

2nd September 2014

Photo reblogged from science in a can with 797 notes

sciencesoup:

What’s up with all those giant volcanoes on Mars?
Mount Everest is an enormous and awe-inspiring sight, towering 9 kilometres above the Earth’s surface. But if you were to stick it on Mars right next to Olympus Mons, the largest volcano in the solar system, it would look foolishly small—Olympus Mons triples the height of Everest and spans the state of Arizona.
Mars is sprinkled with huge volcanoes, hundreds of kilometres in diameter and dozens of kilometres tall. The largest volcano on Earth, on the other hand, is Mauna Loa in Hawaii, which rises only 4 km above sea level.
So why is Mars blessed with these monsters of the solar system? Why doesn’t Earth have any massive lava-spewing structures?
Geology, my friends.
Earth’s crust is split up into plates that move and collide. Usually, volcanoes are formed at the boundaries where two plates meet, and one subducts below the other and melts in the heat below the surface. This melt rises as magma and causes volcanism.
But in some places on Earth, there are “hot spots” in the middle of plates, where magma rises up from the core-mantle mantle in plumes. When this magma is spewed up onto the surface, it cools and solidifies into rock, and over the years, the rock builds up and up. When plumes open out in the middle of the ocean, the magma builds islands.

Plumes are fixed, always pushing magma up to one spot, but the Earth’s plates don’t stop for anything. While the magma rises, the plates move over the hotspot—at a rate of only a few centimetres a year, but still, they move and take the newly-made volcanoes with them. So, gradually, the plates and volcanoes move on, while the plume remains in the same spot, building a whole new volcano on the next bit of the plate. As the plate moves on and on, the plume builds up a whole chain of islands, called island arcs. This is how the Hawaiian Islands were formed.

The island-volcanoes never get too big, because the plates keep moving onwards. On Mars, however, the volcanoes are enormous because the magma appears to keep rising, cooling and solidifying in the same place, taking its sweet time to build up colossal mounds of volcanic rock kilometres high.
So far, we’ve seen no volcanic arcs like we do on Earth, and this is generally taken as evidence that Mars has no tectonic plates.

sciencesoup:

What’s up with all those giant volcanoes on Mars?

Mount Everest is an enormous and awe-inspiring sight, towering 9 kilometres above the Earth’s surface. But if you were to stick it on Mars right next to Olympus Mons, the largest volcano in the solar system, it would look foolishly small—Olympus Mons triples the height of Everest and spans the state of Arizona.

Mars is sprinkled with huge volcanoes, hundreds of kilometres in diameter and dozens of kilometres tall. The largest volcano on Earth, on the other hand, is Mauna Loa in Hawaii, which rises only 4 km above sea level.

So why is Mars blessed with these monsters of the solar system? Why doesn’t Earth have any massive lava-spewing structures?

Geology, my friends.

Earth’s crust is split up into plates that move and collide. Usually, volcanoes are formed at the boundaries where two plates meet, and one subducts below the other and melts in the heat below the surface. This melt rises as magma and causes volcanism.

But in some places on Earth, there are “hot spots” in the middle of plates, where magma rises up from the core-mantle mantle in plumes. When this magma is spewed up onto the surface, it cools and solidifies into rock, and over the years, the rock builds up and up. When plumes open out in the middle of the ocean, the magma builds islands.

image

Plumes are fixed, always pushing magma up to one spot, but the Earth’s plates don’t stop for anything. While the magma rises, the plates move over the hotspot—at a rate of only a few centimetres a year, but still, they move and take the newly-made volcanoes with them. So, gradually, the plates and volcanoes move on, while the plume remains in the same spot, building a whole new volcano on the next bit of the plate. As the plate moves on and on, the plume builds up a whole chain of islands, called island arcs. This is how the Hawaiian Islands were formed.

image

The island-volcanoes never get too big, because the plates keep moving onwards. On Mars, however, the volcanoes are enormous because the magma appears to keep rising, cooling and solidifying in the same place, taking its sweet time to build up colossal mounds of volcanic rock kilometres high.

So far, we’ve seen no volcanic arcs like we do on Earth, and this is generally taken as evidence that Mars has no tectonic plates.

31st August 2014

Photo reblogged from this future M.D. with 187 notes

neurosciencestuff:

Scientists Link Alcohol-Dependence Gene to Neurotransmitter
Scientists at The Scripps Research Institute (TSRI) have solved the mystery of why a specific signaling pathway can be associated with alcohol dependence. 
This signaling pathway is regulated by a gene, called neurofibromatosis type 1 (Nf1), which TSRI scientists found is linked with excessive drinking in mice. The new research shows Nf1 regulates gamma-aminobutyric acid (GABA), a neurotransmitter that lowers anxiety and increases feelings of relaxation.
“This novel and seminal study provides insights into the cellular mechanisms of alcohol dependence,” said TSRI Associate Professor Marisa Roberto, a co-author of the paper. “Importantly, the study also offers a correlation between rodent and human data.”
In addition to showing that Nf1 is key to the regulation of the GABA, the research, which was published recently in the journal Biological Psychiatry, shows that variations in the human version of the Nf1 gene are linked to alcohol-dependence risk and severity in patients.
Pietro Paolo Sanna, associate professor at TSRI and the study’s corresponding author, was optimistic about the long-term clinical implications of the work. “A better understanding of the molecular processes involved in the transition to alcohol dependence will foster novel strategies for prevention and therapy,” he said.
A Genetic Culprit
Researchers have long sought a gene or genes that might be responsible for risk and severity of alcohol dependence. “Despite a significant genetic contribution to alcohol dependence, few risk genes have been identified to date, and their mechanisms of action are generally poorly understood,” said TSRI Staff Scientist Vez Repunte-Canonigo, co-first author of the paper with TSRI Research Associate Melissa Herman.
This research showed that Nf1 is one of those rare risk genes, but the TSRI researchers weren’t sure exactly how Nf1 affected the brain. The TSRI research team suspected that Nf1 might be relevant to alcohol-related GABA activity in an area of the brain called the central amygdala, which is important in decision-making and stress- and addiction-related processes.
“As GABA release in the central amygdala has been shown to be critical in the transition from recreational drinking to alcohol dependence, we thought that Nf1 regulation of GABA release might be relevant to alcohol consumption,” said Herman.
The team tested several behavioral models, including a model in which mice escalate alcohol drinking after repeated withdrawal periods, to study the effects of partially deleting Nf1. In this experiment, which simulated the transition to excessive drinking that is associated with alcohol dependence in humans, they found that mice with functional Nf1 genes steadily increased their ethanol intake starting after just one episode of withdrawal. Conversely, mice with a partially deleted Nf1 gene showed no increase in alcohol consumption.
Investigating further, the researchers found that in mice with partially deleted Nf1 genes, alcohol consumption did not further increase GABA release in the central amygdala. In contrast, in mice with functional Nf1 genes, alcohol consumption resulted in an increase in central amygdala GABA.
In the second part of the study, a collaboration with a distinguished group of geneticists at various U.S. institutions, the team analyzed data on human variations of the Nf1 gene from about 9,000 people. The results showed an association between the gene and alcohol-dependence risk and severity.
The team sees the new findings as “pieces to the puzzle.” Sanna believes future research should focus on exactly how Nf1 regulates the GABA system and how gene expression may be altered during early development.

neurosciencestuff:

Scientists Link Alcohol-Dependence Gene to Neurotransmitter

Scientists at The Scripps Research Institute (TSRI) have solved the mystery of why a specific signaling pathway can be associated with alcohol dependence.

This signaling pathway is regulated by a gene, called neurofibromatosis type 1 (Nf1), which TSRI scientists found is linked with excessive drinking in mice. The new research shows Nf1 regulates gamma-aminobutyric acid (GABA), a neurotransmitter that lowers anxiety and increases feelings of relaxation.

“This novel and seminal study provides insights into the cellular mechanisms of alcohol dependence,” said TSRI Associate Professor Marisa Roberto, a co-author of the paper. “Importantly, the study also offers a correlation between rodent and human data.”

In addition to showing that Nf1 is key to the regulation of the GABA, the research, which was published recently in the journal Biological Psychiatry, shows that variations in the human version of the Nf1 gene are linked to alcohol-dependence risk and severity in patients.

Pietro Paolo Sanna, associate professor at TSRI and the study’s corresponding author, was optimistic about the long-term clinical implications of the work. “A better understanding of the molecular processes involved in the transition to alcohol dependence will foster novel strategies for prevention and therapy,” he said.

A Genetic Culprit

Researchers have long sought a gene or genes that might be responsible for risk and severity of alcohol dependence. “Despite a significant genetic contribution to alcohol dependence, few risk genes have been identified to date, and their mechanisms of action are generally poorly understood,” said TSRI Staff Scientist Vez Repunte-Canonigo, co-first author of the paper with TSRI Research Associate Melissa Herman.

This research showed that Nf1 is one of those rare risk genes, but the TSRI researchers weren’t sure exactly how Nf1 affected the brain. The TSRI research team suspected that Nf1 might be relevant to alcohol-related GABA activity in an area of the brain called the central amygdala, which is important in decision-making and stress- and addiction-related processes.

“As GABA release in the central amygdala has been shown to be critical in the transition from recreational drinking to alcohol dependence, we thought that Nf1 regulation of GABA release might be relevant to alcohol consumption,” said Herman.

The team tested several behavioral models, including a model in which mice escalate alcohol drinking after repeated withdrawal periods, to study the effects of partially deleting Nf1. In this experiment, which simulated the transition to excessive drinking that is associated with alcohol dependence in humans, they found that mice with functional Nf1 genes steadily increased their ethanol intake starting after just one episode of withdrawal. Conversely, mice with a partially deleted Nf1 gene showed no increase in alcohol consumption.

Investigating further, the researchers found that in mice with partially deleted Nf1 genes, alcohol consumption did not further increase GABA release in the central amygdala. In contrast, in mice with functional Nf1 genes, alcohol consumption resulted in an increase in central amygdala GABA.

In the second part of the study, a collaboration with a distinguished group of geneticists at various U.S. institutions, the team analyzed data on human variations of the Nf1 gene from about 9,000 people. The results showed an association between the gene and alcohol-dependence risk and severity.

The team sees the new findings as “pieces to the puzzle.” Sanna believes future research should focus on exactly how Nf1 regulates the GABA system and how gene expression may be altered during early development.

Source: neurosciencestuff

31st August 2014

Photo reblogged from mistress of surgery with 195 notes

usmle-notes:

Respiratory tree anatomy and histology

usmle-notes:

Respiratory tree anatomy and histology

Source: usmle-notes

29th June 2014

Photo reblogged from BPoD with 28 notes

bpod-mrc:

28 June 2014
Take One Onion…
For patients with multiple drug prescriptions, remembering what to take and when can be tricky – giving out the right drugs daily on hospital wards is a time-consuming task. Researchers have found a new way to deliver drugs in ‘slow-release’ packages that could make this easier. They created microscopic drug delivery molecules with multiple layers, like an onion, inspired by the natural outer layers of some bacterial cells. The molecules were made simply by mixing particles called dendrimers – which have similar properties to the components of our cell membranes – with water, which made stable layers form spontaneously. Drugs could be packaged and released slowly from these molecules, layer by layer, so that they don’t have to be taken repeatedly – or different drugs could be contained in different layers so they could be released in sequence, simplifying the drug administration process.
Written by Emma Saxon
—
Image by Virgil Percec and colleagues University of Pennsylvania, USAOriginally published under a Creative Commons Licence (BY 4.0)Research published in PNAS, June 2014
—
You can also follow BPoD on Twitter and Facebook

bpod-mrc:

28 June 2014

Take One Onion…

For patients with multiple drug prescriptions, remembering what to take and when can be tricky – giving out the right drugs daily on hospital wards is a time-consuming task. Researchers have found a new way to deliver drugs in ‘slow-release’ packages that could make this easier. They created microscopic drug delivery molecules with multiple layers, like an onion, inspired by the natural outer layers of some bacterial cells. The molecules were made simply by mixing particles called dendrimers – which have similar properties to the components of our cell membranes – with water, which made stable layers form spontaneously. Drugs could be packaged and released slowly from these molecules, layer by layer, so that they don’t have to be taken repeatedly – or different drugs could be contained in different layers so they could be released in sequence, simplifying the drug administration process.

Written by Emma Saxon

Image by Virgil Percec and colleagues
University of Pennsylvania, USA
Originally published under a Creative Commons Licence (BY 4.0)
Research published in PNAS, June 2014

You can also follow BPoD on Twitter and Facebook

22nd June 2014

Photoset reblogged from Diary of a medical scientist with 2,022 notes

compoundchem:

science-junkie:

Antibiotic Resistance Is Now Rife across the Globe

Dangerous antibiotic-resistant bacteria and other pathogens have now emerged in every part of the world and threaten to roll back a century of medical advances. That’s the message from the World Health Organization in its first global report on this growing problem, which draws on drug-resistance data in 114 countries.
 
“A post antibiotic-era—in which common infections and minor injuries can kill—far from being an apocalyptic fantasy, is instead a very real possibility for the 21st century,” wrote Keiji Fukuda, WHO’s assistant director general for Health Security, in an introduction to the report. The crisis is the fruit of several decades of overreliance on the drugs and careless prescribing practices as well as routine use of the medicines in the rearing of livestock, the report noted.
 
Antibiotic resistance is putting patients in peril in both developing and developed countries, as bacteria responsible for an array of dangerous infections evolve resistance to the drugs that once vanquished them.
 
Gonorrhea, once well treated by antibiotics, is once again a major public health threat due to the emergence of new, resistant strains. Drugs that were once a last resort treatment for the sexually transmitted disease—which can lead to infertility, blindness and increased odds of HIV transmission if left untreated—are now the first-line treatment and are sometimes ineffective among patients in countries such as the U.K., Canada, Australia, France, Japan, Norway, South Africa, Slovenia and Sweden.
 
Drugs to treat Klebsiella pneumoniae—a common intestinal bacteria that can cause life-threatening infections in intensive care unit patients and newborns—no longer work in more than half of patients in some countries. And fluoroquinolones, drugs used to treat urinary tract infections, are also ineffective in more than half of sufferers in many parts of the world. Efforts to limit the spread of multidrug-resistant tuberculosis, malaria and HIV are also all under threat due to increasing bacterial resistance.
 
Although the development of resistance is to be expected over time, overuse of the drugs has accelerated the process by supplying additional selective pressure, noted the report, which was authored by an extensive team of researchers with WHO. And there are few drugs to replace the ones that are now ineffective: The last entirely new class of antibacterial drugs was discovered 27 years ago, according to the report.

Read more via scientificamerican.com

Infographic by who.int

Important stuff, and accompanied by a nicely done graphic.

Also, a graphic on the different major types of antibiotics would definitely be an interesting one - one for my to-do list!

Source: scientificamerican.com