Contamination-seeking drones - IBM Patent 9447448.

Stay back and let the drones do the dirty work. Patent 9447448 makes cognitive drones able to inspect and decontaminate places so humans don’t have to. The drones’ on-board AI system can collect and analyze samples, so it can identify and clean up any bacteria or outbreak. Meanwhile you get to hang back, safely out of harm’s way.

This is just one of the record-breaking 8,000+ patents IBM received this year. Explore the latest IBM patents. →



I’ve finally finished my biological patches set! After many months of designing, editing, and trial and error, I’m proud to post up photos of the final products!

They are woven with bright, beautiful colors that will endure many washes and adventures to come. They’re only $8 in my store:

Here are the first five patches in my biological patch set. Once all ten are made, the rainbow of studies will be complete! Each one is illustrated, digitized, and embroidered by me. Stay tuned for more! Next up is herpetology ;)

Finish Your Antibiotics

I’m sorry, this isn’t Jojo at all but I think I’ve had it for today. As a pharmacy tech, I’m tired of hearing “Well, I started to feel better so I didn’t finish them.” I always knew this but now as a Molecular and Cellular Biology major, I not only know why but how. If you’re willing to heed my advice from the title, good; be on your way. If you need to know more, keep reading.

It’s widely known–to some extent–that not completing a regiment of antibiotics can result in resistant bacteria, or even super bacteria.

But in an infection, you already have resistant bacteria lurking. Not taking antibiotics doesn’t literally create resistant bacteria. So how, then, do the antibiotics take care of the resistant ones?

A lot of antibiotics aren’t bacterialcidal: They don’t actually kill them. Many inhibit growth by some mechanism depending if the bacteria is gram negative or gram positive. For example, penicillin inhibits growth by disrupting the formation of a peptidoglycan layer on gram positive bacteria. Others target the LPS layer on gram negative ones. This keeps the non resistant bacteria at bay. So what kills the resistant ones? Your immune system. Antibiotics buy time and energy for your immune system to recognize and destroy the resistant strains. Your immune system is intelligent in that sense and can form antibodies for new illnesses. It’s important to give your immune system this time because bacteria grow, mutate, and transfer genetic material at astonishing rates. If you wanted to look at a microcosm of the mechanics that go into evolution, you’ve got it with bacteria. 

There are three methods aside from binary fission in which they transfer genes (I won’t get into the minutia of the form of informational material): Transformation, transduction and conjugation.

In transformation, a bacteria can pickup lost genes from a ruptured and dead cell.

Transduction is a way to transfer information via a viral vector.

In conjugation, genes are transferred through something called a pilus: It’s a bridge between two cells that pipes a copy of the information from one cell to another receptive cell and is the only method that doesn’t involve killing either cells. Resistant bacteria like to give around that resistance information like they’re burning a CD for their friends.

So please finish your antibiotics if you’ve been given them. It doesn’t matter if you’ve started to feel better or even great. Finish them.

(Hey science people, If I’ve missed anything or even got something wrong, help me out. There’s obviously lengthy stuff I’ve left out but I think I got the basics).


Actual water in Searles Lake, California - in the valley to the west of Death Valley. The salty landscape is stained pink by the limited types of extreme bacteria that can live in these salty waters. 

This one’s about bugs

Guys, I love ID. I really hope I get to do an ID rotation on Medicine. If you remember, I once posted the mnemonic I swear by for viruses. Well here is the bacteria counterpart. Also your micro mantra should be: sketchy is life. Love Andrew like I do (this part’s not the mantra, I just love Andrew).

Let me know if you have any questions or need clarification. This is a perfect example of a “not aesthetically pleasing tumblr study post” because sometimes your handwriting sucks and you aint got that kinda time in my life for pretty arrows and banners and I just wanna finish this shit so I can leave the library when will Step 1 even be over why is this my liiiiiife

Antimicrobial Agents - Inhibition of DNA and Protein Synthesis

Bacterial chromosome replication

DNA replication

Bacterial Topoisomerases 

  • maintain DNA in appropriate state of supercoiling 
  • cut and reseal DNA
  • DNA gyrase (topoisomerase II) introduces negative supercoils 
  • Topoisomerase IV decatenates circular chromosomes 
  • these are the targets of the quinolone antibacterial agents 


  • bind to bacterial DNA gyrase and topoisomerase IV after DNA strand breakage 
  • prevent resealing of DNA 
  • disrupt DNA replication and repair 
  • bactericidal (kill bacteria)

Fluoroquinolone is particularly useful against

  • Gram +ves: Staphylococcus aureus, streptococci 
  • Gram -ves: Enterobacteriacea; Pseudomonas aeruginosa 
  • Anaerobes: e.g. Bacteroides fragilis 
  • many applications e.g. UTIs, prostatitis, gastroenteritis, STIs 

Adverse effects

  • Relatively well tolerated
  • GI upset in ~ 5% of patients 
  • allergic reactions (rash, photosensitivity) in 1 - 2% of patients 

Inhibition of Bacterial Protein Synthesis 


  • in 1952: Erythromycin was isolated as the first macrolide (Streptomyces erythreus) 
  • Newer macrolides: clarithromycin, azithromycin 
  • Structurally they consist of a lactone ring (14- to 16-membered) + two attached deoxy sugars 

Mode of action 

  • bind reversibly to bacterial 50S ribosomal subunit 
  • causes growing peptide chain to dissociate from ribosome → inhibiting protein synthesis 
  • bacteriostatic (stops reproduction)

Macrolides’ spectrum of activity

  • good antistaphylococcal and antistreptococcal activity 
  • treatment of respiratory & soft tissue infections and sensitive intracellular pathogens • e.g. Chlamydia, Legionella 

Adverse effects

  • Generally well tolerated
  • nausea 
  • vomiting 
  • diarrhoea 
  • rash 


  • large family of antibiotics produced by various species of Streptomyces (“mycin”) and Micromonospora (“micin”) 
  • include: streptomycin, neomycin, kanamycin, gentamicins, tobramycin 
  • Structure = linked ring system composed of aminosugars and an aminosubstituted cyclic polyalcohol 

Mode of action of aminoglycosides

  • Bind irreversibly to 30S ribosomal subunit 
  • disrupt elongation of nascent peptide chain 
  • translational inaccuracy → defective proteins 
  • bactericidal 

Spectrum of activity 

  • broad spectrum; mainly aerobic G-ve bacilli (e.g. P. aeruginosa) 
  • used to treat serious nosocomial infections (hospital acquired infections)
  • First TB antibiotic
  • Used for cystic fibrosis 

Adverse effects

  • all aminoglycosides have low Therapeutic Index (only a small amount needed to become toxic)
  • renal damage, ototoxicity, loss of balance, nausea 

Colour-changing burns bandages begin clinical trials

Bandages that change colour and glow when a wound gets infected could be manufactured as early as 2017 if clinical trials go well. 

The bandages, developed at the University of Bath, are being tested with patient samples from four UK hospitals to statistically determine how effective they are. 

Sadly burns often have symptoms of infection but actual infection is much rarer. At the moment infection diagnosis takes up to two days and requires removing dressings, a painful and upsetting process for burns patients which can slow healing and cause scarring. Antibiotics are also prescribed as a precaution while the tests are conducted.

Colour-changing bandages would give an early-warning that real infection is taking hold, meaning medics could provide better and quicker treatment. 

The bandage contains gel in tiny capsules. When infection-causing bacteria are present the capsules dissolve and release the gel which then fluoresces bright yellowy-green, alerting patients and medics to the problem. 

If they do make it onto wards the bandages would not only improve treatment but save money through cutting down on the cost of tests and drug prescriptions. They would also help tackle the threat of drug-resistant bacteria because there wouldn’t be a need to prescribe as many antibiotics as a precaution. 

Images: University of Bath

Antimicrobial Agents  - Cell wall inhibitors

Based on mode of action • divided into families based on chemical structure

 Modes of action Interference with: 

  • cell wall synthesis 
  • protein synthesis 
  • nucleic acid synthesis 
  • plasma membrane integrity 
  • metabolic pathway 

Inhibitors of Bacterial Cell Wall (peptidoglycan) Synthesis 

  • The Beta-lactam Family 
  • The Glycopeptides 

Peptidoglycan is composed of N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) repeat units, and amino acids.  Each NAM is linked to peptide chain and the peptide chains are cross-linked.


  • Includes penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems.
  • class of broad-spectrum antibiotics containing a β-lactam ring
  • Bacterial transpeptidase enzymes are responsible for catalysing cross-linking of the peptide chains
  • β-lactam ring bind to these transpeptidases – this inhibits cross-linking between peptide chains and prevents synthesis of stable PG
  • Cell wall synthesis ceases and the bacterial cells eventually die due to osmotic instability or autolysis. 


Polypeptide agents - basic structural elements amino acids 


  • complexes with peptide portion of peptidoglycan’s precursor units 
  • vancomycin is a large hydrophilic molecule able to form hydrogen bonds with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides
  • preventing PG transglycosylation reaction – PG precursor subunits (NAG-NAM+peptide) cannot be inserted into peptidoglycan matrix;
  • Vancomycin also alters bacterial-cell-membrane permeability and RNA synthesis

Uses:  serious Gram positive infections e.g. MRSA wound infection

Adverse effects:

  • damage to auditory nerve 
  • hearing loss (ototoxicity) 
  • “Red man/neck” syndrome - rash on face, neck, upper torso 

Think near-boiling water is too hot to support life? Think again. The geysers and hot springs of Yellowstone National Park host an array of thermophillic, or heat-loving, microorganisms that can tolerate temperatures as high as 175 degrees Fahrenheit. These bacteria, along with other microorganisms like archaea, create the vivid color palettes of some of Yellowstone’s famed springs and geysers, like the Grand Prismatic Spring pictured here.

The blue center is the heart of the spring, where nearly boiling water makes it impossible for anything to survive, resulting in a startlingly blue hue. As the temperature dips farther out from the hot spring’s superheated center, though, more and more kinds of bacteria, fungi, and other microorganisms are able to endure. The different rings of color emanating from the steaming epicenter represent different microbial communities that call the spring home.

The most heat-tolerant cyanobacteria dominate the still-extreme temperatures in the yellow-colored ring, while the outer, orange layer hosts an array of organisms that can’t stand the heat quite as well as their neighbors. The colors of these rings also change in response to the time of year and other environmental factors. The cooler outer rings, meanwhile, form ecosystems of their own, hosting flies, mites, spiders, and other animals. Ephydrid flies feast on the bacterial communities and lay their eggs there, while predators like wolf spiders and parasites such as mites are drawn here because of the presence of the flies.

Find out about more amazing species thriving in exceptional environments in the special exhibition Life at the Limits, open now through January 2016.