A clinical trial has begun on a tuberculosis vaccine, a holy grail in the field that researchers have been seeking for decades.
From the Max Planck Society:

Since Monday of this week, the new vaccine "VPM1002" has entered the clinical phase I trial in Neuss, Germany, where it is being tested for safety on voluntary subjects. VPM1002 is based on a vaccine that has been in use since 1921, and has been genetically engineered to prevent infection with tuberculosis bacteria much more effectively than its predecessor.
The scientific basis for this was laid down by the team working with Stefan H.E. Kaufmann, Director at the Max Planck Institute for Infection Biology. "The BCG tuberculosis vaccine, which was developed by French researchers, is the most frequently administered live vaccine in the world," says Kaufmann. However, BCG (short for the bacterium Bacillus Calmette-Guérind) is now frequently ineffective. The immunologist continues: "BCG has become a blunt weapon. We wanted to use genetic engineering to sharpen it so that, rather than hiding from the human immune system, it would stimulate it as much as possible."
To do this, the researchers inserted a gene into the vaccine bacteria. Leander Grode, who at the time was a member of Stefan H.E. Kaufmann’s staff and is today heads a project at Vakzine Projekt Management GmbH (VPM), describes the process: "The vaccine bacteria are taken up by the scavenger cells of the human immune system and end up in their digestion chambers. The genetically engineered modification allows them to escape from the chambers and arm the immune system against the tuberculosis pathogens."
The scientific studies were initially undertaken at the Max Planck Institute for Infection Biology. In 2004, the vaccine was licensed to the Hanover-based VPN, which expedited the clinical study. Thus far, the new vaccine has proven to be extremely effective and safe in animal models. "We now need to prove that it has the same positive effect on humans, so that it qualifies for a license," explains VPM CEO Bernd Eisele. Kaufmann urges patience: "Even if the new vaccine proves to be well-tolerated, it will still have to undergo more testing to establish its efficacy. That will take at least ten years."

Press release: Clinical trial for new tuberculosis vaccine
Article in The Journal of Clinical Investigation…
Image: Macrophage engulfing improved BCG-vaccine organisms. Engulfment causes apoptosis in macrophages. The vaccine antigens are made more easily accessible to the immune system and thus stimulate stronger protection against tuberculosis. Max Planck Institut for Infection Biology/Volker Brinkmann

Leonid Yaroslavsky of Tel Aviv University believes that with a bit of help from sensor technology, humans may one day be able to sense their environment with their skin, similarly to how reptiles are able to do it now.
From a press release by the American Friends of Tel Aviv University:

“Some people have claimed that they possess the ability to see with their skin,” says Prof. Yaroslavsky. Though biologists usually dismiss the possibility, there is probably a reasonable scientific explanation for “skin vision.” Once understood, he believes, skin vision could lead to new therapies for helping the blind regain sight and even read.
Skin vision is not uncommon in nature. Plants orient themselves to light, and some animals — such as pit vipers, who use infrared vision, and reptiles, who possess skin sensors — can “see” without the use of eyes. Skin vision in humans is likely a natural atavistic ability involving light-sensitive cells in our skin connected to neuro-machinery in the body and in the brain, explains Prof. Yaroslavsky.

Here’s a PDF of a chapter in Advances in Information Optics and Photonics by Dr Yaroslavsky describing his work.
Press release: Seeing through the skin

Maria M. Mota and colleagues from the Howard Hughes Medical Institute have discovered that the same liver receptor that allows entry of cholesterol into hepatocytes is used by malaria parasite to sneak into the organ cells.

The SR-BI receptor is normally an entry point for HDL cholesterol and other lipids from the bloodstream into liver cells, which break them down. But new experiments show that the malaria parasite may also be using this doorway. When scientists disabled the SR-BI receptor, they saw a dramatic reduction in the number of infections from two species of malaria in mouse and human cells. The experiments are presented in the September 2008 issue of Cell Host & Microbe.
Previous research had linked the lipoprotein clearance rate by the liver to increased malaria infection, so Mota thought the parasite might enter liver cells by hijacking the liver’s own cellular machinery. The group focused its attention on the part of liver cells that filter fatty molecules like cholesterol and other lipids out of the bloodstream.
Mota’s team used RNA interference (RNAi) to examine the receptors that filter lipoproteins. The RNAi technique permitted the researchers to create cell lines with specific genes inactivated. They then tested each cell line to see how it responded to the malaria parasite. “We looked through 53 lipoprotein receptors and found one that really stood out from the rest,” Mota says. That receptor was SR-BI (class B, type I scavenger receptors). Removing SR-BI cut down infections in these cells more than any other receptor they tested.
To confirm their suspicions about SR-BI’s key role in malaria, the team conducted a series of experiments that examined mouse cells, human cells, and living mice. First, they induced mouse cells to produce much more of the protein than usual. When they exposed those cells to the parasite that causes malaria in mice, they found the cells were infected more readily than cells with a normal amount of the receptor. The team then tested the receptor’s role in a line of human cells with a human-specific malaria parasite, and got similar results.
Cells in living animals often respond differently than cultured cells, so Mota’s team explored SR-BI’s role in live mice. First they suppressed the gene for SR-BI in these mice, and later injected them with a malaria-causing parasite. Forty hours after exposure, the researchers examined whether the parasite infected the animals’ liver cells. They found that the mice with reduced SR-BI had liver infection levels 50-70 percent lower than the normal mice.

Press release: Cholesterol and Malaria May Use Same Doorway to Liver Cells

In the upcoming issue of BioMed Central’s open access journal Critical Care, investigators from University of Cambridge and University Paris-Sud will report that the thickness of the optic nerve sheath is a good marker for raised intracranial pressure (ICP), when imaged by a T2-weighted MRI.
From a press statement by BioMed Central:

The dural sheath surrounding the optic nerve communicates with the subarachnoid space and distends when ICP is elevated. Thomas Geeraerts, from Addenbrooke’s Hospital, Cambridge, led a team who investigated whether MRI can be used to precisely measure the diameter of the optic nerve and its sheath. He said, “Raised ICP is frequent in conditions such as stroke, liver failure and meningitis. It is associated with increased mortality and poor neurological outcomes. As a result, the early detection and treatment of raised ICP is critical, but often challenging. Our MRI-based technique provides a useful, non-invasive solution”.
The early detection of raised ICP can be very difficult when invasive devices are not available. As the authors report, “Clinical signs of raised ICP such as headache, vomiting and drowsiness are not specific and are often difficult to interpret. In sedated patients, clinical signs frequently appear well after the internal damage has been done. Optic nerve sheath distension could be an early, reactive and sensitive sign of raised ICP”.
The authors carried out a retrospective blinded analysis of brain MR images in a prospective cohort of 38 patients requiring ICP monitoring after traumatic brain injury and 36 healthy controls. Geeraerts said, “We found that ONSD measurement was able to provide a quantitative estimate of the likelihood of significant cranial hypertension”.

Press release: New marker for raised intracranial pressure…
Paper: Use of T2-weighted magnetic resonance imaging of the optic nerve sheath to detect raised intracranial pressure (.pdf)
Image credit: Wellcome images: Magnetic resonance image (MRI), T2 weighted axial scan of 5-year-old male with an acquired squint caused by brain stem glioma….

In an experiment that will surely bring tears to animal rights activists’ eyes, Ingemar Jönsson, of Kristianstad University in Sweden, sent up a few water bears (along with other even less lucky creatures) into space to see how they’d hold up to the vacuum, cold, and radiation. The water bears, technically called tardigrades, are actually tiny living creatures that can withstand some of the harshest environments on Earth, and so presented themselves as the most likely creatures to survive in open space.
From Nature News:

For ten days, the tardigrades were exposed to the radiation, vacuum and low temperature of space. R. coronifer did not fare terribly well — none survived when exposed to the full spectrum of ultraviolet radiation, which can be extremely damaging to DNA. But three specimens of M. tardigradum did.
And when some wavelengths of ultraviolet light were filtered out (those shorter than 280 nanometres or longer than 400 nanometres), eggs laid by space-faring Milnesium tardigradum hatched just as well as controls that had not been exposed to space vacuum or ultraviolet radiation. The results are published this week by Current Biology.

More from Nature News…
Abstract in Current Biology…
Image: Water bear (tardigrade), Hypsibius dujardini, scanning electron micrograph by Bob Goldstein.