Cleaning with Soap Nuts

Couple weeks ago, Tumblr introduced me to a natural, cheap, almost odorless, hypoallergenic, and sustainable cleaning agent called soapnuts (or soapberries)! The dried husk/shell of this fruit contains resin that is high in saponins, a naturally occurring chemical compound that reduces the surface tension of water so that it can penetrate and dislodge the solid/other liquid more effectively. Extraction of the active ingredient only requires that soap nuts be agitated in warm water; a lot of lathery foam will form. I’ve tested soap nuts as a

  • laundry detergent
  • body and hair cleanser
  • fruit/veggie and dishwashing cleanser
  • insecticide for my indoor plants

So far so good, although not fond of using it as a body cleanser; it’s too awkward to apply IMO. There are plenty of other uses, but I think this would be a particularly excellent ecofriendly way to bring along a camping trip to clean your wares.

To my gardeners: Trust me, I checked every pod. No leftover seeds, otherwise I would definitely plant a soap nut tree!

As fragile as a soap bubble seems, these films have remarkable powers of self-healing. The animation above shows a falling water droplet passing through a soap film without bursting it. An important factor here is that the water droplet is wet–passing a dry object through a soap film is a quick way to burst it, as those who have played with bubbles know. The droplet’s inertia deforms the soap film, creating a cavity. If the drop’s momentum were smaller, the film could actually bounce the droplet back like a trampoline, but here the droplet wins out. The film breaks enough to let the drop through, but its cavity quickly pinches off and the film heals thanks to the stabilizing effect of its soapy surfactants. (Image credit: H. Kim, source)

Clean-up of accidents like the 2010 Deepwater Horizon oil spill can be complicated by what goes on beneath the ocean surface. Variations in temperature and salinity in seawater create stratification, stacked layers of water with differing densities. When less dense layers are on top, the fluid is said to be stably stratified. Since oil is less dense than water, one might assume that buoyancy should make an oil plume should rise straight to the ocean surface. But the presence of additives or surfactants in the oil mixture plume can prevent that. With surfactants present, an oil mixture tends to emulsify, breaking into tiny droplets like a well-mixed salad dressing. Even if the density of the emulsion is smaller than the surrounding fluids, such a plume can get trapped at a density boundary, as seen in the photo above. Researchers report a critical escape height, which depending on the plume’s characteristics and stratification boundary, determines whether a plume escapes or becomes trapped.  (Image credit: R. Camassa et al.)

Innate Immunity - intro
  • First line of defence + first to act
  • A primitive response (exists in animals and some plants)
  • Non-specialised and without ‘memory’

Consists of:

  • Physical barriers (eg skin and mucosa//tight junctions, airflow)
  • Chemical barriers (eg enzymes, lung surfactant, antimicrobals)
  • Soluble mediators of inflammation (eg cytokines)
  • Microbal defence (eg commensal competition, secreted antimicrobals)
  • Cells (eg phagocytes)
  • Receptors to recognise presence of pathogen/injury - results in inflammation

Soluble Mediators

Complement Proteins

  • liver-derived 
  • circulate in serum in inactive form
  • activated by pathogens during innate response
  • functions include lysis, chemotaxis and opsonisation

Auxiliary Cells

Mediate inflammation as part of the immune response. The main auxiliary cells involved in the immune response are Basophils, Mast cells and Platelets.


  • Leukocyte containing granules 
  • on degranulation release histamineplatelet activating factor
  • causing increased vascular permeability and smooth muscle contraction
  • also synthesise and secrete other mediators that control the development of immune system reactions

Mast Cells

  • Also contain granules 
  • However they are not circulating cells - found close to blood vessels in all types of tissue especially mucosal and epithelial tissues.
  • rapidly release inflammatory histamine but this is IgE dependant so not innate


  • normally function in blood clotting
  • also release inflammatory mediators

Cytokines and chemokines

Produced by many cells but especially mØ (macrophages), initiate inflammatory response and act on blood vessels 

  • interferons - antiviral protection
  • chemokines - recruit cells
  • interleukines - fever inducing, IL-6 induces acute phase proteins 
  • IL-1 - encourages leukocytes to migrate to infected/damaged tissue
  • as does tumour necrosis factor (TNFa)

Acute phase proteins

  • Liver derived proteins 
  • plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation
  • called the acute-phase reaction 
  • triggered by inflammatory cytokines ( IL-1, IL-6, TNFα)
  • help mediate inflammation ( fever, leukocytosis, increased cortisol, decreased thyroxine, decreased serum iron, etc)
  • activate complement opsonisation 



Cytotoxic Cells

  • Eosinophils/natural killer cells, cytotoxic T cells
  • kill target via release of toxic granules 
  • dendritic cell derived IL-12 helps activate NK cells


  • mono-nuclear = long-lived; polynuclear = short-lived
  • engulf, internalize and destroy 
  • phagosome forms around microbe
  • enzyme filled with lysosomes fuses to form phagolysosome
  • organism is digested
  • fragments are either ‘presented’ or exocytosed

phagocytosis requires recognition of microbe via receptors for

  • PAMPs (pathogen associated molecular patterns - eg flagella or capsule) - recognised by toll-like receptors 
  • activated complement
  • antibody

The innate immune response primes for the adaptive 

  • B-cells are primed by activated complement
  • Th1 cell differentiation needs pro-inflammatory cytokines

Hello my friends! I decided to put together a masterpost filled with links to information and how-to’s for us girls (and guys!) with curly hair. I didn’t see one currently out there, and I figured it would be a fantastic addition to my blog, and really helpful for anyone who is starting out on their own journey of loving and taking care of their natural hair. If there’s anything that I need to add, please let me know! 


The Science of Curly Hair
Texture Typing
Find Your Curl Type (Quiz)
Surfactants, Sulfates, and You
Which Sulfates are Safe?
All About Alcohols
The Curly Girl Method
The No Poo Method
Curly Girl Dictionary
Deva Cut Info
Ouidad Cut Info
Curly Salon Finder
Curly Hair Commandments 
Curly Cocktails: A Beginner’s Guide 
Frizz Forecast 
Second Day Hair Tips 
Big Chop Survival Guide 
Transitioning Tips


How to Plop Your Hair
How to Pineapple Your Hair
How to Do The Curly Girl Method
How to Rake and Shake
How to Use a Diffuser
How to Use a Bonnet Dryer 
How to Do Bantu Knots 
How to Get a Perfect Twist Out 
Quick Fixes for Second-Day Hair 
How to Get A Perfect Wash and Go


Clarifying Recipes
Coconut Deep Conditioning Recipe
Sweet Avocado Deep Conditioning Recipe
Honey Deep Conditioning Recipe
Hot Oil Treatment
Flax Seed Homemade Hair Gel Recipe
Leave-In Conditioner Recipe
Protein Pre-Poo Recipe


Easy Up-Do 
Quick Summer Hairstyles 
Hairstyles for Short/Medium Hair 
Cute Wedding Hairstyle 
French Braided Up-Do 
Messy Bun 
Back to School Hairstyles

August 7, 1963: Trying to Save the President's Baby

Sometimes, it’s easy to forget how far we have come in the past fifty years. On August 7, 1963, First Lady Jackie Kennedy delivered her second son, Patrick Bouvier Kennedy. The baby was five and a half weeks premature and weighed 4 pounds 10 ½ ounces. Today, a baby born at 34 weeks enjoys a 98% survival rate. However, in 1963, if the premature baby developed respiratory distress, odds were that the baby would die. There simply was no treatment at that time. Sadly, in the early morning hours of August 9, 1963, as President Kennedy stood watch, Patrick Kennedy succumbed to “hyaline membrane disease”, despite being cared for by the most knowledgable medical team in the country.

Interestingly, when Patrick Kennedy died, most doctors didn’t even really understand what caused “hyaline membrane disease”. The common theory was that a glassy membrane formed making it nearly impossible for the baby’s lungs to extract sufficient oxygen when air was inhaled. However, after decades of research, doctors finally realized that 

(h)yaline membrane disease was not caused by the presence of something in the lungs but rather by the absence of something. The lungs of babies who died of hyaline membrane disease lacked a substance called surfactant, which lines the alveoli, the small air sacs at the end of the lungs’ numerous, branching airways. The problem did not lie only with breathing in, as had long been assumed, but also with breathing out. The baby took that first breath, perhaps even a good deep breath, as any baby would. But if the newborn baby’s immature lungs lacked surfactant, the alveoli tended to collapse when the baby breathed out. 

This understanding led to the eventual development of artificial surfactants, the practice of giving steroids (which speed up the natural production of surfactant) to women at risk of premature labor, and the introduction of better ventilator/respirator technology & methods. 

When people ask me if I want to return to a simpler time such as the 1950s or early 60s, I always think (for many reasons), “Are you crazy?" I have no desire to return to a time where infants born at 34 weeks had a 3% survival rate. Today that survival figure is 98%. Think about that. It’s a truly remarkable turnaround in a relatively short number of years. On what would have been his 49th birthday, I pause to pay respects to baby Patrick whose short life undoubtedly attracted public attention to hyaline membrane disease and helped fuel further research, leading to effective treatments that save the lives of tens of thousands of newborns each year. 

Watch on

It is common in many industries to use oil as a defoamer to break up existing foams or prevent foams from forming. But with the right surfactants–additives that change the foam’s surface tension–it’s possible to make aqueous foams that are actually stabilized by the presence of oil. This video explores some of the ways that oil can interact with these kinds of foam, beginning with capillary action, which draws the oil up into the junctions between foam films. For more, see Piroird and Lorenceau. (Video credit and submission: K. Piroird)


What an eclipse would look like from the surfact of the moon

The Signs As Cell Types

Leo: Von Ebner’s gland cell in tongue (washes taste buds)

Libra: Lacrimal gland cell (tear secretion)

Cancer: Eccrine sweat gland dark cell (glycoprotein secretion)

Virgo: Apocrine sweat gland cell (odoriferous secretion, sex-hormone sensitive)

Aries: Sebaceous gland cell (lipid-rich sebum secretion)

Sagittarius: Bowman’s gland cell in nose (washes olfactory epithelium)

Aquarius: Brunner’s gland cell in duodenum (enzymes and alkaline mucus)

Gemini: Uterus endometrium cell (carbohydrate secretion)

Scorpio: Type II pneumocyte of lung (surfactant secretion)

Taurus: Paneth cell of small intestine (lysozyme secretion)

Capricorn: Gastric gland oxyntic cell (hydrochloric acid secretion)

Pisces: Eccrine sweat gland clear cell (small molecule secretion)

Science art: Driven. Evolving patterns over film on silicon wafer
Anton Darhuber, Benjamin Fischer and Sandra Troian
Microfluidic Research and Engineering Laboratory, Department of Chemical Engineering This image illustrates evolving dynamical patterns formed during the spreading of a surface-active substance (surfactant) over a thin liquid film on a silicon wafer. After spin-coating of glycerol, small droplets of oleic acid were deposited. The usually slow spreading process was highly accelerated by the surface tension imbalance that triggered a cascade of hydrodynamic instabilities. Such surface-tension driven flow phenomena are believed to be important for the self-cleaning mechanism of the lung as well as pulmonary drug delivery. source: Art of Science Competition

Differences in surface tension cause fluid motion through the Marangoni effect. Because an area with higher surface tension pulls more strongly on nearby liquid than an area of low surface tension, fluid will flow toward areas of higher surface tension. Here surfactants, shown in white, are constantly injected onto a layer of water dyed blue. You can also see the flow in motion in this video. Outside of the central source flow, the pattern features lots of 2D mushroom-like shapes reminiscent of Rayleigh-Taylor instabilities. But these shapes are driven by variations in surface tension rather than unstable density variations. For more, check out the original paper or learn about other examples of Marangoni effect. (Photo credit: M. Roché et al.)

Another cool thing I’ve learned since starting medical school: lamellar bodies. Produced by Type II pneumocytes deep in the lung, they contain the protein and phospholipid components of surfactant. Surfactant decreases surface tension in the small alveoli to keep them from collapsing. 

Also, pretty bad ass that this picture was taken by shooting electrons through/around shit that’s so tiny.