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BIG UPDATE!

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:

https://www.etsy.com/shop/Monsternium



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).

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.

β-lactams 

  • 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. 

Glycopeptides 

Polypeptide agents - basic structural elements amino acids 

Vancomycin

  • 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 
theguardian.com
Organisms created with synthetic DNA pave way for entirely new life forms
E coli microbes have been modified to carry an expanded genetic code which researchers say will ultimately allow them to be programmed
By Ian Sample

Scientists in the US modified common E coli microbes to carry a beefed-up payload of genetic material which, they say, will ultimately allow them to program how the organisms operate and behave.

The work is aimed at making bugs that churn out new kinds of proteins which can be harvested and turned into drugs to treat a range of diseases. But the same technology could also lead to new kinds of materials, the researchers say.

In a report published on Monday, the scientists describe the modified microbes as a starting point for efforts to “create organisms with wholly unnatural attributes and traits not found elsewhere in nature.” The cells constitute a “stable form of semi-synthetic life” and “lay the foundation for achieving the central goal of synthetic biology: the creation of new life forms and functions,” they add.

The race to map the human body — one cell at a time

The first time molecular biologist Greg Hannon flew through a tumour, he was astonished — and inspired. Using a virtual-reality model, Hannon and his colleagues at the University of Cambridge, UK, flew in and out of blood vessels, took stock of infiltrating immune cells and hatched an idea for an unprecedented tumour atlas.

“Holy crap!” he recalls thinking. “This is going to be just amazing.”

On 10 February, the London-based charity Cancer Research UK announced that Hannon’s team of molecular biologists, astronomers and game designers would receive up to £20 million (US$25 million) over the next five years to develop its interactive virtual-reality map of breast cancers. The tumour that Hannon flew through was a mock-up, but the real models will include data on the expression of thousands of genes and dozens of proteins in each cell of a tumour. The hope is that this spatial and functional detail could reveal more about the factors that influence a tumour’s response to treatment.

The project is just one of a string that aims to build a new generation of cell atlases: maps of organs or tumours that describe location and make-up of each cell in painstaking detail.

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Proteus OX19 and the Polish Schindler,

Proteus OX19 is a strain of the bacterium Proteus vulgaris, a simple gram negative bacteria that is commonly found in dirt and water.  It is a fairly unremarkable bacteria, some exposed to it might suffer urinary tract infections or infections of wounds.  However, most infected with the bacteria will suffer few symptoms as the body’s immune system eradicates the invading microbe.  It does have one interesting reaction, however.  People exposed to Proteus OX19 often test false positive for typhus, a disease which is much deadlier and can cause terrible outbreaks and epidemics.

When Germany invaded Poland on Sept. 1st, 1939, Dr. Eugeniusz Lazowski served as an army doctor with the Polish Army.  After the occupation of Poland by Germany, Dr. Lazowski returned home to Rozwadow to continue his private medical practice.  However, he heard news of mass deportations of Poles and Jews by the Nazi’s.  Hundreds of thousands of Jews were being rounded up and deported to concentration camps.  Hundreds of thousands of Poles were also being deported to Germany as forced labor.  It was only a matter of time before the Germans demanded the deportation of Poles from Rozwadow, and Lazowski was determined that the Nazi’s would go empty handed.

Lazowski solution was ingenious and audacious; to keep the Germans away from Rozwadow by simulating a fake typhus epidemic. At the time, Germany was terrified of the prospect of a typhus outbreak spreading across the Fatherland, and strict protocols were in place to isolate and quarantine infected areas.  Inspired by the Proteus microbe, Lazowski informed German medical officials that Rozwadow was being ravaged by a terrible typhus epidemic.  With the help of his friend, Dr Stanisław Matulewicz, Dr. Lazowski injected the people of Rozwadow with proteus OX19, as well as the residents of several nearby Jewish ghettos, so that they would all test false positive for typhus.  He then sent blood samples to German medical officials.  As predicted, the samples all tested false positive for typhus.

In response, the Germans sent three medical inspectors to assess the seriousness of the epidemic.  The three inspectors were greeted cordially and plied with food and generous amounts of vodka.  They were then given a short tour of the town.  Due to fears of contracting the disease, the Germans only made a cursory examination of the town.  Then they were led to a fake medical ward filled with severely ill patients.  Dr. Lazowski claimed they were suffering from typhus, and again due to the German’s fear of contracting the disease, they made no medical assessments.  Instead they took Dr. Lazowski at his word and sped out of Razwadow, declaring the town and surrounding area to be in a state of quarantine.  Little did they know, the so called “patients” the German’s were led to were people with flu and pneumonia, told to act as sick as possible.

Due to the quarantine, the Germans never deported anyone from Razwadow or the ghettos.  As a result, he is credited with saving 8,000 Jews from certain death, and thousands of other Poles from deportation.  Throughout the rest of the war he lent his medical services to the Polish resistance, and worked to smuggle Jews to safety from the Nazi’s.  After the war he moved to the United States and worked as a pediatrician.  He died in 2006 at the age of 96.

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 

Quinolones

  • 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 

Macrolides 

  • 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 

Aminoglycosides

  • 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