Bacon-wrapped Bake Purple Potatoes

So the other day I decided to make myself brunch, for which I wanted to make something to go with poached eggs.  Now, poached eggs boiled in vinegar water four minutes each are a a little runny with the yokes only semi-congealed on the edges, so they need something starchy to sop up the yoke.  Hashbrowns could work, but I had some purple potatoes that tend to bleed their pigment, so instead I thought I'd bake them.  Then my next brainwave was to wrap them in bacon and chiles, and damn they were tasty. 

Ingredients

• Two small purple potatoes, half lengthwise
• Four strips bacon
• (optonal) Pickled green Thai chiles
• Salt and pepper, to taste
• Olive oil

Slice the potatoes in half, then salt and pepper them.  The potatoes were small, not fingerlings but not nearly full-sized baking potatoes.  Wrap the bacon around loosely so that the top is well covered.  Insert the chiles, and drizzle olive oil on top as 'starter fat' to prevent the bacon from burning.  Bake at 350 °F for about 45 minutes, until the potato is cooked through. The bottom of the potatoes should come out nice and golden, and the bacon will shrink wrap around the potatoes.  Next time I might microwave the potatoes a bit first to decrease the cooking time and to cook the bacon a little less. 

 

The finished product.

Avalanche Safety Training, Level 1

So least you readers think I am just being lazy in not posting, here is some photos from an avalanche safety course I took last weekend.  We were at Bow Summit for the practical (skiing) portion of the training, here's some pictures sans people.

 Sunset the night before.

 The skin track up.

The snowpack is about 70 cm of wind-loaded slab on top of 80 cm of very weak sugary surface hoar. The interface is obvious in the picture. In other words very dangerous for slab avalanches.  The snowpack was surprisingly strong given how bad it looked (still very dicey over 30°), probably because the top slab was still fairly plastic.  We didn't hear any whumpfting (audible evidence of snow settling when skied over). 

The view across the valley as the clouds broke up.  Ski touring is totally unlike lift-served skiing in tone.

Physical activity should be fun play-time.  I don't really get the emphasis on weight lifting in the paleo community, as it seems very boring to me.

M1 and M2 macrophages and the Herpes-virus family

Ah, the immune system.  It is what makes trillion-cell organisms possible.  Immune system cells actively patrol the body and attack bacteria, fugii, and parasites.  In the process, they often causing collateral damage to self-tissue.  The innate immune system compared to the adapted immune system is evolutionarily older and more prone to carpet bombing tactics to defeat pests. As such, when it doesn't operate properly, a broad list of symptoms can present.  The innate immune system actually has two roles: both fighting off foreign cells but also repairing damaged tissue.  When the innate immune system is always fighting and never repairing it leads to the state of chronic inflammation at the heart of many of the diseases that plague modern civilization, like diabetes, stroke, and heart disease.

What then determines which role an innate immune system cell body operates in at any given time and place in the body?  Let's look at monocytes/macrophages.

Monocytes are undifferentiated (i.e. unspecialized) immune system cells of the innate immune system that circulate in the bloodstream.  In response to chemical signals from the tissues adjacent to their blood vessels, they enter into the tissue to either fight infection or repair tissue damage.  When monocytes enter tissue, their gene expression causes them to become more specialized and they are then called macrophages (they can also become other immune system cells).  There are two basic phenotypes for macrophages, which are essentially the ying and yang of the macrophage community.

• M1 macrophages are pro-inflammatory and fight infection.  They are the classical state for macrophages that you would find described in a textbook.  Primarily, they detect and fight foreign organisms (viruses, bacteria, and parasites).  They are characterized by the production of pro-inflammatory cytokines, chemicals which alert the other cell types of your immune system to react and destroy the invader (as well as adjacent 'self' cells). 
• M2 macrophages are anti-inflammatory and repair tissue damage.  For example, when you exercise and your muscle tissue is damaged, it is M2 macrophages that infiltrate your muscle organs and affect the repairs [Tidball, 2010] after the initial M1 surge.  The characteristic cytokine of M2 macrophages is interleukin-10 (IL-10), which encourages other macrophages to enter the tissue and differentiate into M2 phenotype but also discourage the attention of cyto-toxic 'killer' cells from the lymphocyte family of the immune system.

The differentiation of macrophages, from M1 to M2, is not all that distinct and is generally though to represent the two extremes of a continuum.   My reading suggests macrophage populations can make the transition from one phenotype to the other, without die-offs.  This is probably a bad thing for chronic modern diseases, in that many of the diseases that are as a result of macrophage dysfunction occur when apoptosis (programmed cell death) is impeded.

One of the beneficial effects of eating a diet low in inflammatory factors (e.g. fructose, wheat, smoking) is that the overall levels of pro-inflammatory hormones, such as cortisol or interferon, are low so the transition from high M1 expression to high M2 expression can occur more rapidly. I strongly suspect this is why most people who transition to the paleo-diet are much better able to put on muscle mass. As the Tidball article indicates, chronic exercise is another no-no because it doesn't give enough time for the M2 macrophages to enter and affect repairs, so the muscle is always in an inflamed state.  

This doesn't, in general, appear to actually reduce the ability of the body to fight infectious disease, however.  This is probably because even though the overall inflammatory condition (as determined by circulating cortisol globally or cytokines locally) is low, it can easily spike when a foreign body attacks. On the other hand, actual conditions where adrenal functions are suppressed (i.e. Addison's disease), the immune system is hamstrung by the homonal milieu it finds itself in and the immune system doesn't function properly to defend against infection.  One hypothetical cause may be that the ratio of M2 to M1 is tilted in favour of M2 in adrenal insufficiency. 

One pathogen that is known to mess with the M1/M2 expression in macrophages is human cytomegalovirus (HCMV). HCMV basically takes M2 macrophages or undifferentiated monocytes and reprograms them to be more like M1 macrophages in some ways (Chan et al., 2009 and Chan et al., 2008).  Importantly, they do not become like M1 macrophages in that they continue to release interleukin-10, which discourages the adapted immune system from deploying 'killer' lymphocytes (natural-killer cells and T-cells) but encourages more M2 macrophages (red shirts, basically) and at the same time they up-regulate the production of protein filaments that make macrophages motile, so that they can better travel about and infect other organs. So let's all remember, whenever you have massive infiltrate of an organ by macrophages, you can probably bet there's too much IL-10 being produced.

To me the various  pathogens that excel at molecular mimicry to hide from the immune system seem to be playing quite the bogey-man role in a whole host of chronic diseases. These are principally the Herpes virus family (which also includes cytomegalovirus and the Epstein-Barr virus which has been linked to chronic fatigue syndrome) and the bacteria C. Pneumoniae, which has been linked to atherosclerosis and a whole host of other chronic diseases. Paul Jaminet over at Perfect Heath Diet has also been covering C. Pneumoniae in the brain,

It also seems a lot of disease symptoms occur when macrophages manifest some combination of the M1 and M2 state.  Consider that glucose in the blood is regulated by the liver predominately, so insulin resistance (aka metabolic syndrome) reflects failure of the liver to be able to do it's job.  Largely, this is blamed on 'inflammation' in the liver, e.g. alcholic and non-alcoholic fatty liver disease, but what does that mean exactly?

A review (Olefsky and Glass, 2010) states that macrophages in tissue that produce excessive quantities of tumour necrosis factor-α (TNF-α) and interleukin-16 (IL-16) (both pro-inflammatory cytokines), to the point that they are detectable in the blood. I like the following quotation from the review, as it really lays out the problem:

The discovery that adipose tissue from obese mice and humans is infiltrated with increased numbers of macrophages provided a major mechanistic advance into understanding how obesity propagates inflammation (4, 5). Adipose tissue contains bone marrow–derived macrophages, and the content of these macrophages tracks with the degree of obesity (4, 5, 31, 32). In some reports, greater than 40% of the total adipose tissue cell content from obese rodents and humans can be composed of macrophages, compared with ~10% in lean counterparts (32).

That nearly half of fat tissue mass is actually not fat cells, but immune system cells is kind of amazing to me. A very similar thing happens in liver disease. Now, reference #32 is a mouse study (Weisberg et al., 2006) but it in turn cites two other mice studies that are more pertinent (Weisberg et al., 2003 and Xu et al., 2003).  Both articles show that gene expression for various proteins that attract immune system cells are strongly up-regulated in the adipose tissue of fat mice.  The question is why?  Is it diet?  I suspect partially, but the revelations regarding what cytomegalovirus can do to macrophages makes me suspect latent pathogens are attracting macrophages as lambs to the slaughter. Are lab mice susceptible to chronic infections given their conditions and short lifespan?  Are these latent viruses transmitted from mother to infant?

The prevalence of immune system bodies in the adipose tissue of the obese mice illustrates an example of the, "diseases of civilization," being largely driven by dysfunction of the innate immune system, probably egged on by latent viral and bacterial infections and an unnatural diet.  The pieces of the puzzle are mostly there now and evidence will continue to accumulate until we have a better view of the whole picture.  Stop the sources of inflammation (i.e. immune system activation), give the immune system the substrates it needs to fight effectively, and the other symptoms will go away.

Inov-8 F-lite 230 Review

Unfortunately I broke my fibula in March (gymnastics) and did a lot of damage to the various talo-fibula ligaments in the process.  Those ligaments are still healing, and one part of my rehab is to do a lot of pseudo-barefoot work, mostly by wearing my Chaco sandles and Vibram KSOs during day-to-day activities.  At the very least, I am trying to restore proper biomechanics to my feet, if I have to go through all this discomfort!

However as winter approached I was feeling a little trepidation, since Vibrams are totally unsuited to -20 °C weather conditions with wind and snow.  The obvious pick, for me, was to look for some minimalist running flats and stuff some warm socks into them. I'm generally not willing to buy footwear without putting it on first (with the exception of thermo-molded footwear like ski boots), so I headed down to my local eclectic running store, FastTrax, and went through their stock of running flats.  Eventually the salesman let me try on the garish blue shoes on the top shelf, the Inov-8 F-lite 230s, which I immediately liked.   They are so named for their weight, the shoes as a pair weighs in at 230 grams, or about half a pound. From what I can tell, I'm pretty damn lucky to be able to try these on in a store in Canada as they seem to be hard to find outside of the UK.

'Garish' describes the vivid blue colour quite well

The F-lite 230s is marketed as a 'mountain running flat.'  I consider them an ultra-light approach shoe. The lugs on the sole are made of sticky climbing shoe rubber, and they are quite pliable.  The heel-lift is probably 3 mm, which makes them pretty much the flattest true shoe I've ever owned.  I found them to be immediately comfortable out of the box.  The heel box is especially effective in trapping my heel and because the sole is so flexible, there's no noticeable sliding of the heel when walking or running.  These shoes are very flexible: it's easy to twist them through 180° or touch the toe to the heel.

The upper is composed of mesh, but the laces are then vertically reinforced by a pliable plastic that helps distribute the forces better so the upper doesn't collapse onto your foot.  I think this is a good design decision for light-weight uppers as compared to just a velcro strap. 

The most 'non-barefoot style' features of these shoes is: 1.) their general squishiness, and 2.) the pointed, low-volume toe-box. 

I find the pointed toe-box a little strange.  I probably sized these shoes half-a-size too large as a result; according to the Inov sizing chart I should be wearing size UK6.5 but I actually have size UK7.5s.  Realistically, I should probably size for UK7.0.  The pointed toe-box does seem to expand out without really putting pressure on my toes, so that's something to consider.  I also remember my Vibrams were tight in the right big toe (my right foot is longer than the left) as well and they stretched out.

The shoes also have quite a thick (3 mm) and squishy insole.  They can be removed of course, but for now I'm using them. In general if I take the insoles out and just walk around the shoes do not feel nearly as squishy anymore.  If I did try to size down into a UK6.5 shoe, I would probably take the insoles out in the store.  The finishing of the midsole isn't free of stiching so these shoes probably can't be worn sans insole and sans socks.

The last drawback of these shoes is that the lugs, being composed of climbing rubber, aren't super durable.  Inov does have very similar shoes with harder wearing rubber compounds, but I didn't have any choice of models in the store.   

It's sort of difficult for me to properly review these things given how I can't really run properly yet, but I have been running in them three times now.  Twice was just running to school (about 2 km), which is on pavement.  I do not heel strike in these shoes on pavement, even with my limited range of motion in my right ankle.  The third time was a trail run at the bottom of the scramble shown in the above picture, and they performed spectacularly well in the soft trail.  Foot sensitivity is not as apparent as in the Vibrams, in that small pebbles are unnoticeable but the larger rocks and branches are still felt through the flexible sole just fine, and the lugs make them  grip far better in soft ground. 

Up on 'Vision Quest' in the David Thompson range.

I have to say, Inov has a very extensive stable of minimalist running shoes designed for natural activities.  I find their product line personally pretty compelling (in that I sort of want to buy one of each).  If you like hiking and other non-road running activities, go take a look at what they offer on their website.  I hope that my local shop brings in some more models, and hopefully I can try a smaller size come summer-time.

Photovoltaics: Multiple Electrons from one Photon

 A month ago a report appeared in Science magazine on a new prototype solar cell that could produce more than one electron, a packet of electrical energy, from one photon, a packet of light energy.  This trick isn't new, I discussed a bunch of such concepts years ago in a post on quantum photovoltaics. What's new is that Samber et al. report in "Multiple Exciton Collection in a Sensitized Photovoltaic System," have achieved high efficiency in this process.

The typical goal for these sort of 'quantum' solar projects is to better match the wavelengths of light the photovoltaic system can absorb to that of the spectrum of light that is produced by the sun (and filtered by the atmosphere). The theoretical limit for Silicon alone in a photovoltaic system is 33.7 %, which is known as the Shockley-Quiesser limit. Of course, most commercial PV systems are only around 12 % efficient or less, so there is still considerable room for growth.  An example of such a spectrum-matched system is Spectrolab's space photovoltaics, which are actually stacks of multiple photovoltaic systems all operating at different wavelengths, and achieve roughly 30 % efficiency in a commercial product. 

 Figure 1: The air-mass 1.5 standard spectra (indigo line), which is an estimate for the spectra that arrives at the Earth's surface after passing through the atmosphere.  The red line is the band-gap for Silicon; for longer wavelengths (red-er) Si cannot absorb the photon.  For shorter (blue-er) wavelengths the extra energy is lost.

If you could get one electron out from a infrared photon and two from a blue photon, then the energy gained is fairly significant.  This result has been reported on before, but in this paper, for the first time, the overall system produced more electrons out than photons in, as observed to just isolated nanoparticles.  In photovoltaic parlance, the number of electrons produced per photon is known as the quantum yield, but this doesn't describe how many electrons actually escape and result in electrical current.  That quantity has the wordy name, absorbed photon-to-current efficiency.

Figure 2:  Absorbed photon-to-current efficiency (APCE) as a function of wavelength for the described cells.  The x-axis  is in electron volts, to convert to wavelength, divide 1240 nm by the photon energy [Fig 4. from Sambur et al., 2010].

Overall,this would be a really interesting paper except for one obvious drawback: the active layer of quantum dots is really really thin.  There's only a single layer of quantum dots and given an average diameter of 10 nm, that's not very think for visibile light.  Compare that to a standard Silicon cell being hundreds of microns, or a thin-film cell at 10 μm which is still a thousand times thicker. In fact it's so thin that they absorb only 1-2 % of the incoming light. 

Since the problem with quantum dot strategies is always getting the electrons out, and not absorbing the light, I'm not sure that this work will have a great impact when scaled up.  At the very least, however, it does show that it's possible to build a quantum dot solar cell that works as advertised, producing more than one electron per photon, and doing that quite well.

Schizophrenia and Vitamin D

 A recent short article published in the Archives of General Psychiatry by McGrath et al. (2010) highlights that abnormal vitamin D status in newborn babies is a predictive factor for developing schizophrenia later in life.  The study was conducted on 424 patients and 424 controls, all born in Denmark since 1981.  Presumably the population the data set was constructed from was very large if they were able to find 424 babies who later developed schziophrenia. 

The key finding is that the risk of schziophrenia has a U-shaped curve with neonatal serum concentration, which is illustrated in figure 2 of the article.The findings were statistically significant with a maximum relative risk of 2.1 for having very low vitamin D status compared to the optimum level.

One figure that's sadly lacking from the publication is a histogram of the entire population for vitamin D serum concentration.  Since Figure 2 is only given in percentiles, we cannot evaluate what the actual optimal vitamin D concentration is, nor what is too high.  I think this is a major oversight in this article. 

The potential links between the general family of autism, schizophrenia, and bipolar disorder and vitamin D deficiency have been hypothesized before, such as in this article from the Vitamin D council.  Obviously, with a relative risk of 2.0 vitamin D isn't the whole story here, but it likely plays a role in the regulation of brain development.  The question is how?  Is it a precursor hormone to a development hormone?  McGrath referenced an earilier article (on which he was also an author), Eyles et al. (2005) which suggests that vitamin D plays a direct role as a paracrine hormone in the mammalian brain.

Gone Paddling

So I'm off to Portland, Oregon for a staid conference and a little fun (hopefully) on some of the copious Oregon rivers.  Of course on the drive down I'm stopping off in Fernie, BC so I'll have some fun for sure.

I realize the old blog hasn't been getting a lot of attention in the past few months.  Basically, I'm busy enjoying my summer and working hard on my Ph.D. program so I really haven't had a lot of spare time on my hands.
I'll be back, it's just that blogging in a purely altruistic activity for me, so something it gets pushed way back on the priority list. If you haven't already done so I would respectfully suggest you use some sort of subscription service, such as Google Reader, to watch my blog.

Meanwhile, some pictures of what I been doing this summer for your enjoyment:

Surfing the Brierlies hole on the North Saskatchewan, near Rocky Mountain House.


A straight-forward little drop on the Castle river, pretty much the only shots I have of me running rapids.


Edging through the rolling waves.


The Mistaya river at low water, at the junction of Jasper and Banff National Park.


The Portage rapid on the Kicking Horse near Golden.  The scale is a little deceptive here, those waves are about as tall as a person.


The float before the fun part of the Sunwapta river in Jasper National Park.


I seem to see an absurd number of double rainbows on my travels.


 Watching for swimming beginners on the Whirlpool river in Jasper National Park.

Sadly, as things get more difficult in whitewater, the tendency to take pictures drops off, so not too many really fun pictures here.  Maybe I should get a helmet camera...

Blog Format Change

I changed the format of the blog last weekend to allow me to incorporate some widgets more easily.  I still have to do a lot of boring HTML work here.

I am having some trouble figuring out how to get the post body and sidebars to fill the screen instead of just the middle third.  My old template was so much different in terms of HTML coding.  If anyone has a clue how to do this easily within the template XML, please let me know.

Vitamin D Reduces Premature Births

So on the new front for Vitamin D supplementation it appears that maintaining high levels of vitamin D greatly reduces the risk for premature births (hat-tip to Sharon Kirkey of the Ottawa Citizen).  Supplementing with 4000 IU of vitamin D per day compared to 400 IU per day reduces the risk of a premature birth by half.  This may have to do with the role of vitamin D in the innate immune system.  Previous research published in the New England Journal of Medicine found that around 25-40 % of pre-term events may have been caused by vaginal infections (Goldenburg et al., 2000). 

This research isn't published in a peer-reviewed journal yet but rather was presented at the Pediatric Academic Societies meeting in Vancouver, May 1-4.  I did, however, manage to track down the abstracts for the conference:

[1665.6] Vitamin D Supplementation during Pregnancy Part 2 NICHD/CTSA Randomized Clinical Trial (RCT): Outcomes

Carol L. Wagner, Donna Johnson, Thomas C. Hulsey, Myla Ebeling, Judy Shary, Pamela G. Smith, Betty Bivens, Bruce W. Hollis. Pediatrics/Obstetrics, Medical University of SC, Charleston, SC.

BACKGROUND: Vitamin D (vitD) deficiency during pregnancy is a serious public health issue, affecting mother and fetus. Establishing optimal vitD requirements of pregnant women is vital in preventing vitD deficiency and its health-associated comorbidities.
OBJECTIVE: Evaluate the effectiveness of high dose vitD supplementation in decreasing pregnancy comorbidity risks.
DESIGN/METHODS: Following their consent, pregnant women 12-16 wks' gestation were randomized into 1 of 3 tx grps stratified by race: 400, 2000 or 4000 IU vitD₃/day until delivery. Women were evaluated for safety (Abstr#750939), efficacy and effectiveness with monthly 25(OH)D; 1,25(OH)₂D; serum Ca, Cr, phos, and urinary Ca/Cr levels, all measured using standardized methodology. Comorbidities of pregnancy (preeclampsia, gest diabetes, any infection, preterm labor (PTL)/preterm birth (PTB) <37 wks GA) were recorded prospectively for each subject. Investigators and health team were blinded to tx grp.
RESULTS: Of the 494 women who enrolled in the study, 350 women continued until delivery: 98 African American (AA), 137 Hispanic (Hisp) and 115 Caucasian (Cauc) women; with 111 controls, 122 in 2000 IU and 117 in 4000 IU groups. There were no differences in baseline vitD status between dose groups. The mean 25(OH)D by dose group at delivery, as chronic level, and 1-month before delivery were significantly different between control and 2000, control and 4000, and 2000 vs. 4000 (p<0.0001). 25(OH)D had a direct influence on 1,25(OH)₂D levels throughout pregnancy (p<0.0001) with 25(OH)D of 40 ng/mL required to obtain maximum 1,25(OH)₂D production. In bivariate analyses controlling for race, PTL/PTB and infection were inversely related to 25(OH)D and were lowest in the 4000 IU grp (p<0.0001). In logistic regression, comparing 400 vs. 4000 IU and controlling for race, the risk of comorbidities were 0.50 (CI 0.27-0.95; p=0.03) among those in the 4000 IU grp. Using least sq means, when adjusting for race, 25(OH)D of women with comorbidities was 33.4 ng/mL compared to 39.0 ng/mL in those women without (p < 0.008).
CONCLUSIONS: VitD sufficiency was strongly associated with decreased risk for PTL/PTB and infection during pregnancy and comorbities of pregnancy, with the greatest effect with 4000 IU vitamin D/day regimen. Therefore, to attain a minimal 25(OH)D level of 40 ng/mL, we recommend 4000 IU/day for all pregnant women.E-PAS20101665.6

Not that infection rates were inversely related to serum vitamin D levels.

Now, there used to be concerns over whether high vitamin D levels could cause birth defects related to calcium metabolism.  The researchers found these claims to be baseless.

Vitamin D Supplementation during Pregnancy Part I NICHD/CTSA Randomized Clinical Trial (RCT): Safety Considerations

Carol L. Wagner, Donna Johnson, Thomas C. Hulsey, Myla Ebeling, Judy Shary, Pamela G. Smith, Betty Bivens, Bruce W. Hollis. Pediatrics, Medical University of SC, Charleston, SC.

BACKGROUND: Vitamin D (vitD) deficiency during pregnancy is a serious public health issue that affects both mother and fetus. Establishing the optimal vitD requirements of the pregnant woman is vital in preventing vitD deficiency.
OBJECTIVE: Evaluate the safety of high dose vitD supplementation during pregnancy in a RCT.
DESIGN/METHODS: Following their consent, pregnant women 12-16 wks' gestation were randomized into 1 of 3 treatment (tx) groups (grps) stratified by race: 400, 2000 or 4000 IU vitD₃/day until delivery. Women were evaluated for safety, efficacy and effectiveness with monthly 25(OH)D; 1,25(OH)₂D; serum Ca, Cr, phos, and urinary Ca/Cr levels, all measured using standardized methodology. Investigators & health team were blinded to tx grp.
RESULTS: Of the 494 women who enrolled in the study, 350 women continued until delivery: 98 African American, 137 Hispanic and 115 Caucasian women; with 111 controls, 122 in 2000 IU and 117 in 4000 IU grps. There were no differences in baseline 25(OH)D by dose grp. The mean 25(OH)D by dose grp at delivery, as chronic level, and 1-month before delivery were significantly different between control and 2000, control and 4000, and 2000 vs. 4000 (p<0.0001). 25(OH)D had a direct influence on 1,25(OH)₂D levels throughout pregnancy (p<0.0001). Throughout the study, there were no differences between grps on any safety measure: serum Ca, Cr, urinary Ca/Cr ratios (pNS between grps). Not a single adverse event was attributed to vitD supplementation by the DSMB. Neonatal 25(OH)D was significantly correlated with maternal 25(OH)D overall, 1-month prior and at delivery (r²=0.6; OR 0.50); and was significantly different by tx group: 18.2±10.1 (control), 22.8±9.8 (2000 IU) and 26.5±10.3 ng/mL (4000 IU), (p<0.0001).

An interesting pair of abstracts to be sure.  I look forward to seeing the data for myself when it's published.

Silicon Nanowire Photovoltaics

In the 14 February 2010 issues of Nature Materials, Kelzenburg et al. report on their progress in developing a photovoltaic cell composed of an array of Silicon nanowires: Enhanced absorption and carrier collection in Si wire arrays for photovoltaic applications.  Also see the supplementary information on the fabrication process.

Theoretically an array of nanowires has some advantages over flat or patterned silcon when it comes to light trapping and absorption. The disadvantages come from difficultly in getting the electron-hole pairs out of the wires, both in having sufficient conductivity of the wires and a good electrical contact to the outside world. On the negative side using patterning requires some sort of controlled deposition onto the thin-film substrate when ideally you would like to use some sort of self-assembled system that doesn't require a carefully patterned mask and has a huge through-put for manufacturing.

Figure 1 from (Kelzenburg et al. 2010): (a) SEM image of regular nanowire array embedded in PDMS and (b) schematic of system.

The arrays in question are rods 8-12 μm long that cover 5 % of the areal density of the surface. Let's compare that to a wafer-type Silicon photovoltaic cell, which might have 250 μm of high-quality Silicon in it, the Silicon nanowire PV cell is using about 0.24 % as much material. Since photovoltaic-grade Silicon is quite expensive, this is potentially a cost advantage. From a practical perspective, this concept is robust because the silicon nanowires are embedded in a polymer that protects them from damage.

The authors also added aluminium oxide (Al₂O₃) nanoparticles to the sides of their nanowires in an effort to increase scattering within the cell and hence light trapping. This had a very significant effect and they achieved a maximum of 84.6 % of light absorption compared to 87.2 % for a commercial cell. Remember this is with a tiny fraction of the amount of Silicon used in a commercial cell.

Figure 4 (from Kelzenburg et al., 2010):  Compare the solid red to solid blue lines in (a).  The nanowire arrangement is slightly inferior in the visible spectrum but is markedly superior in the near-infrared.  In (b) area under the curves indicates total light absorption and hence electron generation.

Designing the film so that the nanowires were oriented in a regular, periodic pattern gives a high packing fraction, thereby enhancing light absorption, but it also results in certain orientations being 'dead zones' where light is not well absorbed. In particular, when the rods are facing the sun dead-on, they do not absorb well. However, the regular array of wires would be well suited to situations where the photovoltaic panel was always oriented away from the sun, such as vertical mounts on a wall or horizontal mounts on a flat roof.

Lastly, it was reported at the end of the supplementary information (where better place to hide such details?) that they saw some evidence of sub-bandgap absorption.  That is, light longer than 1120 nm was being absorbed.  This isn't supposed to happen and it tends to reflect parasitic absorption that doesn't contribute to moving electrons (and in fact reduces the output current).  Thus there is some concern that the increase in infrared absorption — the main claim to fame here — was due to parasitic effects rather than something that would actually enhance the electric current being produced. They did not, however, find that all of their cells had sub-bandgap absorption so it may be largely a quality control problem.