Drugged Fish Act Different

An anti-anxiety medication that has found its way from water treatment plants into ponds and streams of Europe may alter the behavior of perch even at low concentrations, according to a study published today (February 14) in Science. Fish exposed to the drug, called oxazepam, tended to eat more quickly and were more active and less social than they had been prior to drug exposure and compared with their unexposed peers.
“It’s definitely an interesting study,” said David Skelly, an ecologist at Yale University who was not involved in the research. “It’s joining a group of exposure studies that are showing very clearly that the individual chemicals that are showing up as environmental contaminants are ecologically relevant.”
Previously researchers have raised concerns about all manner of pharmaceuticals in the water, from estrogens suggested to cause reproductive abnormalities in frogs to psychoactive drugs linked to autism in fish. Oxazepam is a type of benzodiazepine, drugs that work by binding to GABA receptors and are used to treat anxiety. Since many animals have these receptors, it stands to reason that benzodiazepines might influence animal behavior, Brodin said, but they “weren’t being studied [in animals] in environmentally relevant quantities.”
Testing effluent from a sewage treatment plant in Sweden and downstream water from the River Fyris, environmental scientist Tomas Brodin of Umeå University and colleagues found 0.58 micrograms of oxazepam per liter in the river and 0.73 micrograms per liter in the treated wastewater—concentrations consistent with previously reported levels of benzodiazepine drugs in other parts of the world.
The researchers then took European perch raised in clean water and put them in water with either a low dose of 1.8 micrograms of oxazepam per liter, or a high dose of 910 micrograms per liter. By the end of the 7-day treatment, the fish on the lower drug dose had accumulated levels of oxazepam in their tissues similar to those found in wild perch in the River Fyris.
Following exposure to the medicated water at either the high or low dose, fish spent more time swimming around their tanks. When the scientists put zooplankton in water, the exposed fish found and ate them more rapidly than the control fish, but showed low interest in other fish. The researchers also found that fish treated with the high dose of the drug scored higher on tests of boldness, or their willingness to explore novel situations.
Bodin suggested that the behavioral changes could have ecological consequences. For instance, hungry, drug-dosed fish might deplete algae-eating plankton, which could in turn cause algal blooms. On the other hand, an asocial, highly active fish might be at increased risk of being eaten.
But Skelly cautioned against going too far predicting ecological effects. “Just because you saw these changes, you can’t say very much about how it’s going to pan out in the field,” he says. In the wild, the very presence of predators might change the fish’s behavior, he noted. Oxazepam might also interact with a cocktail of other drugs that had made it into the water.
Still, Brodin said, the results are an indication of the effects benzodiazepines and many other psychoactive drugs could be having on a whole range of animals. “It’s very probable that these behavioral changes are going on in aquatic species around the world as we speak,” he said.

INSECT SOAK UP THE SUN

Aphids are one of the most unique organisms in the animal kingdom. In addition to being among the most destructive pets, some aphid species are the only animals known to produce carotenoids–light absorbing pigments that form part of the photosynthetic machinery of plants, algae, and certain fungi.
Now, an international group of researchers led by entomologist Alain Robichon from the Sophia Institute in France, have proposed that carotenoid-producing aphids can actually use the pigment in a photosynthetic-like process to produce ATP–the cellular energy molecule.

But whether the insects can use the power of light to ultimately synthesize glucose and other compounds is far from clear, Yale University geneticist Nancy Moran, who was not involved in the study, told Nature. “Energy production seems to be the least of an aphid’s problems–their diet is loaded with excessive sugar, most of which they cannot use,” she said. However, the authors counter that aphids may use the process as an energy back-up during times of stress, Nature reported.

THE HUMAN SPINE

UNDERGROND HELL IN RUSSIA

place or symbolical? Bible talks about hell several times. But I would like to share you this true to life experience of scientist named Dr. Azzacove from Russia who doesnt believe in God, in bible and hell. This news appeared in the well respected Finland newspaper, Ammenusastia.

Heres what happened, a group of geological scientist was drilling a 14.4 kilometers hole deep in Siberia, … then after using their super sensitive microphones to test the underground for sound intervals, they shocked on what they heard. First they heard a high pitched sound, they thought the sound was from their digging devices. After some adjustments: They heard a terrifying screams…, not just screams of a single human, but screams of millions human voice, a screams of pain.

Dr. Azzavoc the project manager of the scientist says. Aside from the screams they heard they were also surprised on a very high temperature around 1,100 degrees celsius. They are afraid to continue the project, and about half of the scientist quit because of fear.
Dr. Azzavoc is a communist, doesnt believe on God, and bible.. But after this event. He believes now that Hell really exist!. If you want to download the hell screaming sounds in mp3 format… click here. You may put that mp3 file in your cellphones, ipods so you can share this to other.

NEW DISCOVERY BY SALAMI TAIWO

1) The tooth is the only part of the human body that cant repair  itself.
2) In an average adult the volume of blood is one eleventh of the body weight, or between 5 and 6 quarts.
3) The feet account for one quarter of all the human bodies bones.That is 52 bones in the feet alone.
4) The first toy balloon,made of vulcanized rubber, was thought of by someone in the J.G Ingram company in          London,England in 1847.
5) A cough releases an explosive charge of air that moves at speeds up to 60 mph.
6) Do not cut or push back your toenail cuticles,Cuticles protect you against bacterial infection.
7) Saturn rings are about 500,000 miles in circumference but only about a foot thick.

WHY WE YAWN

Yawning, which opens the sinuses located to the left and right of the nose, acts to cool the brain when it gets too hot.
Excessive yawning, argue the researchers, appears to be a symptom of conditions that increase the brain or core temperature, such as damage to the central nervous. In addition, fits of yawning often precede epileptic seizures and migraines. Therefore, the authors say, understanding the physiological purpose of the reflex could have medical relevance.
Earlier work by the authors showed that the brains of mice increased in temperature just before a yawn and decreased directly after. The authors propose that the mucus within the sinus constantly evaporates and, like a refrigerator, cools the surrounding blood vessels and cerebrospinal fluid. A yawn, they suggest, would amplify this process by stretching the jaw, which flexes the walls of the sinus bringing new air into it rapidly cooling an overheated brain.

How Blood Cells Thwart Malaria

Two hemoglobin mutations, including one that causes sickle cell anemia, may protect people from severe malaria by gumming up the cellular machinery the parasite uses to transmit deadly proteins to the cell surface. The findings, published today (November 10) in Science Express, suggest potential ways to fight the deadly disease.

“It’s a great study,” said Rick Fairhurst, who studies malaria pathogenesis and immunity at the National Institute of Allergy and Infectious Diseases, and was not involved in the study. “It really takes us a huge, giant leap forward.” By showing what mutations enable cells to avoid the deadliest consequences of malaria, the research may also point to potential treatment targets, he added.
For decades, researchers have known that people who carry a gene for sickle cell anemia are highly resistant to dying from malaria. Research has shown that it is the mutation to one of their hemoglobin genes, which codes for the oxygen-transporting protein in red blood cells, that was responsible for the fortuitous effect, and that other mutations in that same gene were also protective. But despite years of research, no one knew why.
Fairhurst and his colleagues published a paper showing that compared to normal cells, red blood cells carrying two hemoglobin mutations had lower surface concentrations of a virulent, sticky protein produced by the malaria parasite, Plasmodium falciparum. The protein, which is normally shuttled from the parasite’s protein making factory inside the cells to the cell surface, prevents the body from clearing infected blood cells. But in the blood cells with mutated hemoglobin, that didn’t seem to happen—the parasite proteins never made it to the surface of the cells.
To find out why, parasitologist Michael Lanzer of Heidelberg University in Germany and his colleagues flash froze red blood cells with and without the mutations and used electron microscopy to visualize the cells before and after infection.
They found that uninfected cells contained short pieces of actin that help keep the membrane skeleton rigid. After infection, in normal cells, long actin filaments appeared, linking a cellular component made by the parasite called the Maurer’s cleft, which looks a bit like a stack of pancakes, to the cell membrane. “We concluded that the parasite mines that actin from the membrane skeleton of the host, and uses this mined actin to generate actin filaments of its own design,” Lanzer said—namely to transmit the proteins to the outside surface of the red blood cell.
By contrast, in cells with mutated hemoglobin, the Maurer’s cleft looked more like a big blob and the disordered actin filaments did not connect the cleft to the cell membrane. Somehow, it seemed, the mutations were preventing the parasite from setting up its protein factory effectively, thereby reducing protein transport outside the cell.
The team also took a closer look at the hemoglobin, and found that  the difference between the mutated and wild-type cells was that mutated forms were more easily oxidized.  When they placed actin filaments in the presence of both the normal and mutated copies of hemoglobin, the researchers found that mutated forms of hemoglobin led to shorter actin chains than wild-type hemoglobin. Actin placed with oxidized hemoglobin similarly failed to form long chains, suggesting that oxidation was indeed responsible for the difference in the parasite’s protein machinery seen in cells with mutated and normal hemoglobin.
Taken together, the findings suggest that the hemoglobin mutations blunt the deadliness of malaria because the oxidized hemoglobin inhibits actin reorganization, thereby preventing the malaria parasite from shuttling its proteins to the surface red blood cells, Lanzer said.
Future work should confirm that the same effects are seen in cells that carry only one copy of the mutated hemoglobin, since the vast majority of people who carry these mutations and have a survival advantage against malaria are heterozygous for the mutated hemoglobin, Fairhurst said.
Understanding how the body gets around malaria’s deadliness could guide the design of drug therapies, he added, for instance by finding small molecules that inhibit the parasite’s protein trafficking machinery.
“Mother Nature had 10,000 years or so to mutate the genome in ways that would actually protect against death,” Fairhurst said. “We want to use these mutations to teach us something about how you protect children.”