Alcohol under a microscope by Bevshots
Tracks
Science, Art and Food
Artist Caren Alpert takes these photographs of food under an electron microscope showing us what is there up close that we rarely get to see: hidden landscapes, patterns and textures.
- terra cibus no.12: cake sprinkles
- terra cibus no.39: red cabbage
- terra cibus no.6: red licorice
- terra cibus no.32: shrimp tail
- terra cibus no.2: chocolate cake 2
Shaking Death
In the 1950s and 60s, a fatal epidemic called kuru swept through the South Fore tribe of Papua New Guinea, killing over 1,000 people. Kuru means “shaking death” which is consistent to the first symptoms of the victims: tremors, headaches and loss of motor skills, since the disease affected the cerebellum, which is responsible for co-ordinarting movement. Soon the victims weren’t able to stand or eat, they sometimes lost speech and developed open sores, and then finally died six to twelve months later. It was discovered that the epidemic was linked to the tribe’s ritual of mortuary cannibalism—consuming the brains of the recently deceased. Kuru began to disappear when cannibalism was outlawed, and yet a few cases still occurred up into the 2000s, suggesting that the disease has an incubation period of up to 50 years. Kuru belongs to a class of neurodegenerative diseases that also includes what is commonly known as “Mad Cow Disease,” and is caused by abnormally folded proteins called prions. These proteins are present in all cells in their normal form, but the abnormal ones are infectious agents, able to ‘flip’ other proteins into the abnormal prion shape that then flip others, and on and on like dominoes. They gradually cause nerve cells to degenerate and die—and since nerve cells cannot be replaced, the brain tissue takes on a sponge-like appearance as it slowly dies. So, Kuru was originally caused by the victims consuming infected brain material, which then infected their own brain tissue and turned it to spongy mush.
Guys’ Y chromosomes are functional, evolutionary marvels
Once thought to be a piece of junk, new research shows that little variation in the male Y chromosome over time proves that it serves a useful function.
Neurons
(Source: Gizmodo)
Scientists have successfully removed the extra copy of chromosome 21 in cell cultures derived from a person with Down syndrome.
The cells of people with the condition contain three copies of chromosome 21 rather than the usual pair.
A triplicate of any chromosome is a serious genetic abnormality called a trisomy. Trisomies account for almost one-quarter of pregnancy loss from spontaneous miscarriages, according to the research team.
The mature retina contains five classes of neurons: photoreceptors (purple), horizontal cells (yellow), bipolar neurons (green), amacrine cells (pink and blue), and ganglion cells (pink and blue). In this cross section of an adult mouse retina, only a subset of bipolar cells, “the ON bipolar cells” are visible by their expression of GFP (green). The pink and blue speckled striations at the bottom of the image mark the fiber layer, which contains the ganglion cell axons that will form the optic nerve.
By Rachel Wong, University of Washington
The 6 phases of the cell cycle (from top left) are shown for 2 cells in the embryo of the marine worm Cerebratulus marginatus. Each image is a projection of a 40-80 0.3-μm confocal section: interphase, microtubules are long and diffuse; prophase, chromosomes condense and small asters appear; prometaphase, the nuclear envelope breaks down but the spindle is not yet built; metaphase, chromosomes aligned at the spindle equator; anaphase, sister chromatids separate along the spindle as astral microtubules grow; telophase, cleavage furrow constricts around astral microtubules and the central spindle as 2 nuclei reassemble.
By George von Dassow, University of Oregon
Things I’m learning at med school: Malaria
Basic facts:
Protozoan disease of the genus Plasmodium.
Transmitted only by female Anopheles mosquitos.
4 main species: P. falciparum, P. vivax. P. ovale and P. malariae (P. knowlesi may also infect humans but rarely does so, more commonly affecting monkeys).
When inside RBCs the parasite consumes intracellular proteins (particularly haemoglobin). As haem is potentially toxic, plasmodium detoxifies it to a biologically inert form (haemozoin), which can be seen as a coloured pigment.
Plasmodium alters the RBC membrane, making it irregular in shape, more antigenic and less deformable.
Mechanism:
Mosquito inoculates plasmodial sporozoites from its salivary glands during a blood meal and motile forms of the parasite are carried rapidly in the bloodstream to the liver where they invade hepatic cells and begin a period of asexual reproduction. An amplification process produces 10,000 – 30,000 daughter merozoites.
Infected liver cells swell and burst, discharging motile merozoites into the bloodstream. RBCs are then invaded and the merozoite takes a ring form known as a trophozoite. The trophozoite multiplies, consumes haemoglobin and fills the RBC; the RBC is now known as a schizont (shown in the image above). When the RBCs rupture, daughter merozoites are released, capable of invading more RBCs and repeating the cycle.
Some parasites may develop into longer-lived gametocytes that can transmit malaria. These may be ingested by another mosquito, which forms a zygote in the insect. It matures and migrates to the salivary glands where it can be transmitted to another human host.
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In P. vivax and P. ovale, a proportion of the intrahepatic forms remain dormant from 3 weeks – 1 year (or more) before reproduction begins (hypnozoites). These are the cause of relapses that characterise infection with these two species.
In P. falciparum, protuberances appear on the surface of RBCs; a specific type of adhesion protein that mediates attachment to receptors on venular and capillary endothelium (cytoadherence). This can lead to blockage and sequestration of RBCs in vital organs. May also adhere to other infected RBCs (agglutination) or non-infected RBCs (rosetting = decreased deformability). Sequestration allows parasites to develop out of reach of splenic processing and filtration, therefore only younger ring forms of asexual parasites are seen circulating in peripheral blood in P. falciparum, so peripheral parasitsaemia is an underestimated value.
Host response:
Splenic filtration is accelerated (becomes enlarged in later stages).
When schizont ruptures interleukin-1 is released, which causes a fever.
Temperatures exceeding 40◦C damage mature parasites, which synchronise the malarial cycle and if left untreated will present as a tertian fever (except in P. malariae which is quartan).
First symptoms: Fever, malaise, headache, fatigue, abdominal discomfort, muscle aches, nausea, vomiting, orthostatic hypertension. May have: mild anaemia, palpable spleen, slightly enlarged liver, mild jaundice.
Severe P. falciparum: Cerebral malaria due to sequestration and agglutination. May cause coma. ~20% adult mortality.
Acidosis due to accumulation of organic acids (e.g. lactic acid released from RBCs).
Hypoglycaemia as the liver is not maintaining adequate glucose levels due to failure of hepatic gluconeogenesis. There is also increased glucose consumption by host and parasite.
Other symptoms include anaemia, renal failure, pulmonary oedema, hypotension/shock, haemorrhaging, haemoglobinuria and jaundice.
Diagnosis:
Relies on asexual parasite forms in peripheral blood smears (thick and thin; x1000 oil immersion).
Parasitsaemia expressed as number of parasitised erythocytes per 1000 RBCs.
Antibody stick or card tests can also be used using finger prick blood samples.
Antimalarial Drugs:
Quinidine – Trophozoite stage. Kills gametocytes of P. v, P. o and P. m.
Chloroquine – As above but earlier in the asexual cycle.
Others include amodiaquine, mefloquine, tetra/doxycycline, halofantrine.
Prophylaxis – malarone, chloroquine, doxycycline (these will reduce the incidence of P. f infection but cannot treat it once infected).
Fixed Neuron
A multi-wavelength, three dimensional, wide-field immunofluorescence image of a fixed neuron. The projection was generated using an extended depth of field algorithm. Cell body labeled for tubulin is shown in blue, F-actin in green, and presynaptic protein in Red. Specimen courtesy of Natalie Dowell-Mesfin BMS-PhD student.