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cloned the receptor and used this to genetically engineer human blood stem cells.

mature T cells that can attack HIV in tissues where the virus resides and replicates.

CD4 cells are white blood cells that are an important component of the immune system, helping to fight off infections.

CD4 "helper" T cells

HIV in the blood decreased.

increased

engineering stem cells to form immune cells that target HIV is effective in suppressing the virus in living tissues in an animal model

Expanding on previous research providing proof-of-principle that human stem cells can be genetically engineered into HIV-fighting cells

The engineered stem cells developed into a large population of mature, multi-functional HIV-specific CD8 cells that could specifically target cells containing HIV proteins. The researchers also discovered that HIV-specific T cell receptors have to be matched to an individual in much the same way an organ is matched to a transplant patient.

In this current study, the researchers similarly engineered human blood stem cells and found that they can form mature T cells that can attack HIV in tissues where the virus resides and replicates. They did so by using a surrogate model, the humanized mouse, in which HIV infection closely resembles the disease and its progression in humans.

increased, while levels of HIV in the blood decreased. CD4 cells are white blood cells that are an important component of the immune system, helping to fight off infections. These results indicated that the engineered cells were capable of developing and migrating to the organs to fight infection there.

The molecule turned on genes that make cartilage components called aggrecan and type II collagen. Tests of mice with cartilage damage similar to osteoarthritis showed that kartogenin injections lowered levels of a protein called cartilage oligomeric matrix protein. People with osteoarthritis have an excess of the protein, which is considered a marker of disease severity.

kartogenin inhibits a protein called filamin A in the mesenchymal stem cells

Genes consist of several modules, separated by non-coding DNA regions (introns).

Since the introns obstruct protein synthesis, they need to be removed from the mRNA, a procedure described as splicing.

t is thought that the introns even help the splicing enzymes by folding themselves into stable RNA structures, thus directing the enzymes to the right locations.

It was found that the transfer takes place without the involvement of RNA and that the DNA apparently jumps directly from the cell's chloroplasts into its nucleus.

67 percent more neurons in their prefrontal cortex (PFC) than typical children

executive functions"—high-level thinking, such as planning ahead, inhibiting impulses and directing attention.

In brain tissue from both autistic children and autistic adults, genes coding for proteins that identify and repair mistakes in DNA were expressed at unusually low levels. Additionally, all autistic brains demonstrated unusual activity levels for genes that determine when neurons grow and die and how newborn neurons migrate during early development

Some genes involved in immune responses, cell-to-cell communication and tissue repair, however, were expressed at unusual levels in adult autistic brains, but not in autistic children's brains

Errors accumulate.

autistic child develops in the womb, something—an inherited mutation or an environmental factor like a virus, toxin or hormone—muffles the expression of genes coding for proteins that usually fix mistakes in sequences of DNA

The genetic systems controlling the growth of new neurons go haywire, and brain cells divide much more frequently than usual, accounting for the excess neurons found in the PFC of autistic children.

autistic brain grow physically larger and form more connections than in a typical child's brain.

immune system reacts against the brain's overzealous growth,

Not all researchers, however, accept

If scientists definitively link autism to a characteristic sequence of changes in gene expression and unusual neural growth, then it becomes possible to target and reverse any one of the thousands of steps in that sequence.

It’s assumed the protein complex is analyzing, but the mechanism of analysis is unknown. It’s also unknown if the UvrAB complex (or similar complex) actually does the repair, or if it signals for some other protein complex(es) to make the repair.

They fail to make the switch from embryonic to adult

The mutation has its greatest effect when gibberellin is not present during the first 24 hours of growth

The study defined a new role for a protein called polynucleotide phosphorylase (PNPASE) in regulating the import of RNA into mitochondria. Reducing the expression--or output--of PNPASE decreased RNA import, which impaired the processing of mitochondrial genome-encoded RNAs. Reduced RNA processing inhibited the translation of proteins required to maintain the mitochondrial electron transport chain that consumes oxygen during cell respiration to produce energy. With reduced PNPASE, unprocessed mitochondrial-encoded RNAs accumulated, protein translation was inhibited, and energy production was compromised, leading to stalled cell growth.

Geng Wang developed a strategy to target and import specific RNA molecules encoded in the nucleus into the mitochondria and, once there, to express proteins needed to repair mitochondrial gene mutations.

First, the researchers had to find a way to stabilize the reparative RNA so that it was moved out of the nucleus and then localized to the mitochondrial outer membrane. This was accomplished by modifying an export sequence to direct the RNA to the mitochondrion. Once the RNA was in the area of the transport machinery on the mitochondrial surface, then a second transport sequence was required to direct the RNA into the targeted organelle. With these two modifications, a wide range of RNAs were targeted to and imported into the mitochondria, where they worked to repair defects in mitochondrial respiration and energy production in two different cell line models of human mitochondrial disease.

subsequently began producing the enzyme

proved so much they no longer met the criteria for legal blindness

injected the functional genes into the previously untreated eye

improved as soon as two weeks after the operation: They could navigate an obstacle course, even in dim light, avoiding objects that had tripped them up before, as well as recognize people's faces and read large signs

brains were much more responsive to optical input as well.

second round of gene therapy further strengthened the brain's response to the initially treated eye as well as the newly treated one

that neuroplasticity plays a role

visual cortex responding to the newly flowing channel of information from the second eye bolster activity in areas of the visual cortex responding to the initially treated eye.

‘Just one damaged cell can divide and multiply uncontrollably and quite quickly develop into a large tumour. This is what causes lung cancer,

around from person to person, this raises the risk of transmitting diseases such as tuberculosi

As the mouthpiece is passe

nd hepatitis.