As we are heading towards the high season of flu I though it would be interesting to remember how the vaccines against influenza virus (the causative agent of flu) are actually made.
Human microbiome is definitely one of the trending topics in biological science right now (admittedly, I also have been caught up in this trend and blogged about microbiome before). Each week new research announces it discovered a new role of the microbiome (last week there was a nice paper studying a link between alcohol dependency and gut microbiome) and many researcher now consider the microbiome to be another organ in our body, the functions of which we are only beginning to understand. And here is another great story about the gut microbiome but this time, maybe somewhat unexpectedly, it involves the jet lag. Continue reading
Recently I was river tracing here in Taiwan. It’s basically hiking but in the water, you just jump into some kind of a stream and go upstream, it is very fun, especially when rocks are slippery because then you always feel like a very bad ballerina. After several hours spent in the water, our fingers became very wrinkly, you know, as they always do after a long bath, a swim or any prolonged water activity. And during the lunch brake people started discussing why does that happen, why do fingers get wrinkly in the water? Most of us started to mumble something about osmosis, i.e. water entering or leaving the skin. Yes, it’s very smart of us to say ‘osmosis’ and pretend that we know something about it but really this was just another case of what episode #293 of This American Life called ‘Modern Jackass’: situations in which people act as if they are knowledgeable about something but they actually have no clue. As Nancy Updike put it, “The thing about Modern Jackass is, it’s usually not something about which you know nothing. It’s something about which you know a little bit, enough to sort of get yourself into trouble.” And to be honest osmosis doesn’t really make sense if you think about it, I mean shouldn’t then all of our body turn wrinkly in water not just the fingers, and at least I haven’t notice any particular differences about wrinkling in fresh and salt water, but clearly the osmotic pressure in the two must be quite different (it’s easy for me to speak post factum).
For many people microbes are associated with infections, diseases and in general mainly negative things but some microbes actually do more good than bad for us. We often take for granted that without microbes we would not have many things that we eat and use everyday and, as a matter of fact, humans would not even survive without these little creatures :)
I’m no expert on dinosaurs whatsoever, however, as many science geeks I find them extremely fascinating.
Hope this will spark your interest as well.
Even though we have started to appreciate the importance of human microbiome relatively recently, it is no longer a question’ if the microbiome is important?’ but rather ‘how the microbiome affects us?’. I define human microbiome as the total diversity of microbes in and on human body, however, this definition is definitely simplified version and for those interested in the subtleties of its use can go and read some of the debate in here.
Some people report that in fear-related situations time seems to slowdown. That is to say, for example, during a car crash the event takes much longer from the point of a person experiencing the crash than the observer. But how and why the brain creates this slow motion experience is not completely understood. Recently, on the World Science Festival panel called ‘The Deceptive Watchman: Mind, Brain, and Time’ David Eagleman mentioned his study on the subject, which both intrigued and amused me, so let me tell you why.
In his study Eagleman asked if in a fear situation time slows down because of increased temporal resolution of an experienced event (as when in slow-motion videos a better movement discrimination is seen because of increased number of frames in it). In other words, are people in life-threatening situations somehow able to increase their visual recording of an event, which leads to a more detailed recall and consequent slow motion-like experience?
Here comes the amusing part. To answer the question one obviously needs to place a person in a fear-inducing environment and what is better a way of doing it than a 31m freefall. The participants in this study were dropped from a huge tower in an amusement park and asked to preform a task while free falling (apparently no incentives where given, so I have a suspicion that the study is biased towards fear-junkies ☺ ).
I suppose many of us would like to have a pair of extra hands, you know, just to hold that cup of coffee in one hand, a book in another and maybe an iPhone in the third. Although, then we might also require an extra pair of eyes too… But it’s not all that easy, apart from the fact that clearly under the specific circumstances of human evolution two hands proved to be an optimal option, too many hands can pose a problem: when it comes to managing them all at the same time they might end up just tangling all over the place!
But there are animals that do have quite a few hands and not just any hands but hands full of suckers that will stick and hold on to anything in their path. Yes, I am talking about cephalopods, which include octopuses, squids, cuttlefishes and others. So how and do these animals manage to distinguish between their own hands and other objects and prevent the suckers from catching the limbs of their own?
Well, this is the question that a recent paper called “Self-Recognition Mechanism between Skin and Suckers Prevents Octopus Arms from Interfering with Each Other” has attempted to answer.
Formation of new neurons (called neurogenesis) is considerably reduced in adults compared to infants. Considering the fact that new neurons would have to compete with the old ones for the space and connections (i.e. synaptic connections that are present between neurons), it makes sense that the old connections might sometimes be replaced by the new ones during neurogenesis. Consequently, if the old connections were storing memories then their replacement would fragment or completely delete those memories. If we take a step further this would imply that, compared to adult mice, the young mice would not be very good at making long-term memories because in their brains active neurogenesis is taking place, old neurons are replaced, and new connections are made- a process which should delete all the things that were stored in the old neuronal network.
Consistent with these ideas is the observation of ‘infant amnesia’ in many animals. Namely, animal infants, including human, forget things more readily than adults (can you remember your first, second or third birthdays?). With these premises scientists decided to investigate if neurogenesis could be the cause of infant amnesia in mice and other animals.
Firstly, to prove that the adult mice have reduced neurogenesis in dentate gyrus (part of brain within hippocampus that is linked to memory formation and storage) they injected a retrovirus into dentate gyrus (the retrovirus is a type of virus that will stably integrate into cell’s DNA). The retrovirus was carrying a green fluorescent protein gene (GFP), which after integration will be expressed by the cell. If neurons are dividing then the number of neurons with GFP signal will increase because it will be passed on to new cells from their progenitors but if cells don’t divide then the signal remains stable. The scientists show that in infant mice GFP signal increases and in adults it does not.
Next the study looked at formation of dentate gyrus-dependent memory in young and old mice. Old mice and young mice were trained by placing them in a specific room and giving a series of foot shocks. 28 days later the two age groups were placed in the same room (but no shock was given) and their reaction was observed. The old mice all froze in place in that room indicating the recollection of the shock-memory, however, the younglings showed no response suggesting that they have forgotten the link between the room and the foot shock training.
Okay, so now we know that old mice have little neurogenesis and that they remember the past events better than young mice. But no link between the two events has yet been shown. So, the next step is to increase the neurogenesis in old mice and see if they start forgetting things. As it turns out, neurogenesis in old mice can be increased by as much as 50% simply by making them exercise, namely running in a scroll-wheel. So after several days of exercise , the amount of neurogenesis was measured in the old mice by the same GFP method and an increased neurogenesis was found. Now again the same foot-shock experiment was done: mice are given foot-shocks, put into space with scroll-wheel (mice like to run so they are sure to exercise on it) and placed back into the same room where the foot-shocks were given. As predicted adult mice showed reduced freezing behaviour because of increased neurogenesis, moreover, if the mice exercised before foot-shock training the old mice were still able to recall the training well, indicating that the neurogenesis after the training prevented stable memory formation. The same results were also confirmed by administering drug that induces neurogenesis (and therefore led to forgetting in old mice) and using transgenic mice in which neurogenesis can be inhibited with a drug (the inhibition led to higher rates of remembering in mice that were allowed to exercise as well as the infant mice).
Different animals are born at different stages of brain maturity depending on the length of gestation period. For example, in guinea pigs gestation takes 65 days compared to 21 days in mice, so therefore, guinea pigs should have lower neurogenesis rates as their development after birth is already quite advanced in time. And indeed, when scientists used the same foot-shock experiment to test patterns of memory recall in young and old guinea pigs they found no difference between them. Not surprisingly, injection of drug that increases neurogenesis in guinea pigs led to decreased memory formation.
In conclusion, the study has determined that neurogenesis contributes to the loss of dentate gyrus-linked memory formation. Other studies, however, have previously shown the reverse effects of neurogenesis, i.e. suggesting that it improves memory. Overall, the picture now seems to be that neurons at different neurogenesis stages might play different roles in memory formation; for example, sufficiently mature neurons could provide more space for new memories. It sort of make sense, I mean if we extrapolate it to humans (and I know that from animal models this might not always be the best thing to do), for infants long-term memories are not as important because parents will provide the missing context for them. As we mature neurogenesis decreases and memories become more stable, while a low amount of new neurons formed contribute to an increased requirements for memory storage space. And for those who might now be scared to exercise because they might start forgetting stuff, well again the neurogenesis in adults is very low and a bit of increase in it thus far seems to be only a good thing. This study, for example, shows that exercise caused increase in hippocampus volume reverses the effects of ageing-linked memory loss and even improves it!
Akers KG, Martinez-Canabal A, Restivo L, Yiu AP, De Cristofaro A, Hsiang HL, Wheeler AL, Guskjolen A, Niibori Y, Shoji H, Ohira K, Richards BA, Miyakawa T, Josselyn SA, & Frankland PW (2014). Hippocampal neurogenesis regulates forgetting during adulthood and infancy. Science (New York, N.Y.), 344 (6184), 598-602 PMID: 24812394
Viruses infect all kinds of organisms, from amoebas to humans. Naturally, we hear little about most viruses, which do not have an immediate effect on our lives. Have you ever heard about White Spot Syndrome virus, which infects shrimps and causes $1000 Million loss each year in Asian shrimp industry? Or Sputnik virus, that is a virus that hitches a ride in other viruses to infect amoebas (sputnik means “fellow traveler” in Russian, although most people will probably relate it to the satellite)? Basically, name a species and Google will find a virus for it, as long as some scientist has bothered to look in that species. And so many interesting stories about strange viruses tend to go unnoticed in the press because very few of us really are interested in them. Therefore, I was very pleased this morning to hear Bob McDonal discussing a recent study on insect iridovirus on the Quirks & Quarks podcast.
Iridoviruses are DNA viruses that can infect insects. A team from Dalhousie University in Canada has initially noticed that there’s something strange with their cricket (Gryllus texensis) colony: the females in it stopped laying eggs. After dissection of several females it was noted that the fat body, an organ that has important metabolic and immune functions in insects, had a bluish shine to it. This blue shine apparently is a common phenotype of iridovirus infection. Using electron microscopy and PCR methods they then confirmed that the infection was indeed caused by iridovirus and in particular a cricket iridovirus variant 6. Figure below shows beautiful EM from the published paper in which the icosahedral particles are the iridoviruses in the fat body. Some viral proteins were also later identified in the cricket hemolymph, an insect equivalent of blood.
Next, the team investigated the effects of infection on various physiological and behaviour aspects of the crickets. They found that infected females had significantly reduced number of eggs and fewer developing follicles in the ovaries. By contrast, males produced the same amount of sperm, however it had reduced motility. In addition, animal’s immune system was also affected. Usually, infected animals, including insects, tend to exhibit a so called ‘sickness behaviour’. One aspect of sickness behaviour includes an illness-induced anorexia, meaning, that animal eats considerably less, which possibly reduces the nutrients available for the pathogen and prevents its replication. However, the study found that infected crickets did not show this type of sickness behaviour and in addition the production of antimicrobial compounds by the fat body was also decreased. To show that this is not just some weird cricket species that doesn’t have sickness behaviour scientists infected healthy crickets with heat killed bacteria and in that case crickets indeed showed sickness behaviour. In fact, when crickets with virus in them were given heat killed bacteria they also showed no sickness behaviour, meaning that virus somehow actively prevents induction of this behaviour.
It’s quite common that in insects pathogens are sexually transmitted and indeed, the fact that the virus has an effect on cricket reproductive tissues hints to the same idea. Not surprisingly, therefore, when scientist looked if an infected cricket can transmit the virus to an uninfected animal through mating they found that that indeed was the case. The uninfected cricket had 50% chance to get an infection after mating with infected partner.
Not only that but virus also seems to change cricket’s courting behaviour. Although infected and uninfected crickets were as likely to court, the infected males began their courtship singing sooner than the noninfected counterparts, so virus-containing insects tended to mate more readily. Sexual transmission of this virus also explains why the cricket shows no sickness behaviour. From an evolutionary perspective an animal that looks sick is less likely to get a mate, so naturally virus will “want” to reduce this behaviour for it to have more chance of being passed to another animal.
Now, how did the viruses get into the cricket colony in the lab in the first place is also an interesting story. As the main researcher discuss on the podcast, she had students in her lab who worked on a different project concerning predator and pray situation. The pray in this case was cricket and the predator was a bearded lizard. As it turns out the lizard was an asymptomatic carrier of the cricket iridovirus and possibly acquired the virus through being fed infected crickets from a pet store (of course, no one knew that the crickets were infected). The lizard itself shows no symptoms of infection and likely gets rid off the virus soon after eating the crickets, but for some time, it seems, it acted as a carrier of the virus and infected the colony of crickets in the lab.
That’s how serendipity in science works!
Here are the links to the original paper and the podcast:
(the paper is called “A viral aphrodisiac in the cricket Gryllus texensis“, though I’m not quite sure if ‘aphrodisiac’ is the right word to use :). Having said that probably just the title will attract more readers)