there's just science fucking everywhere

neurosciencestuff: Cold plasma successful against brain cancer...

Fri, 24 May 2013 18:17:46 -0400

Cold plasma successful against brain cancer cells

For the first time, physicists from the Max Planck Institute for Extraterrestrial Physics (MPE), biologists and physicians demonstrated the synergistic effect of cold atmospheric plasma - a partly ionized gas - and chemo therapy on aggressive brain tumour cells. Laboratory tests showed that the proliferation of glioblastoma cells – the most common and aggressive brain tumour in adults – is arrested and that even resistant cell populations become sensitive to treatment with chemo therapy if pre-treated with cold atmospheric plasma. This could be the first step on the way to a new combination therapy, providing new hope for fighting this lethal cancer.

If someone is diagnosed with the type of brain tumour called glioblastoma, the prospects are dire: median survival is just a bit over one year, and less than 16% of the patients survive more than three years. It is still unknown how this cancer is triggered – only a few rare genetic factors have been identified so far – and treatment remains largely palliative, i.e. trying to alleviate the symptoms and prolonging the life of the patient. The standard therapy proceeds in three steps: Guided by an MRT scan, the tumour is removed surgically, followed by radiation and chemo therapy. But even if the treatment is successful initially, there is a high likelihood of relapse.

A recently developed new kind of treatment could offer some hope. Cold atmospheric plasma, or CAP for short, has already proven to successfully inactivate bacteria, fungi, viruses and spores, while healthy tissue remains largely unaffected. Healthcare applications such as the sterilization of surgical instruments, skin and wound disinfection paved its way into medical care. Recently also CAP sources were developed which show anti-cancer properties.

“For many patients the regular treatment is just not effective, because the brain tumours contain sub-populations for which chemo therapy does not work,” says Julia Zimmermann, who manages the Plasma Healthcare group at MPE. “So we were particularly interested to see if the CAP would be effective against these resistant tumour cells – and indeed it worked!”

For the study, the researchers used Glioblastoma cells and grew them in cell culture dishes, where they could be subjected to various combinations of treatments. For both normal and resistant tumour cell lines, the growth of the cells was more inhibited after the plasma treatment compared to the chemo therapy alone. The largest effect could be obtained for a short application time of 120 seconds; such an additional step could be easily incorporated into the clinical treatment if an appropriate plasma device can be developed.

The researchers also found that CAP stops the cell cycle and that the individual cells lose their ability to clone themselves. A combined therapy of both - CAP treatment and chemo therapy – showed the most promising results, where the amount of chemotherapeutic needed to achieve the same result as with chemo therapy alone is strongly reduced. So far, no resistance towards CAP treatment was observed. The study also showed that even those cell lines that originally were resistant against the chemo therapy drug became sensitive again after the pre-application of CAP.

“In particular, also resistant cell populations could be treated effectively with CAP, which means that there is now hope to find a therapy for the patients with a poor prognosis, i.e. those with resistant cells in the tumour,” explains Julia Köritzer, lead author of the study. Such a treatment option for resistant cells is urgently needed, because about 40% of the patients do not profit from chemo therapy. She adds: “It is a first step, now we have to further investigate the effects gained in the cell culture and integrate them for the application.”

Though, even if there is still a long way ahead before CAP can actually be used in the hospital, it offers a promising new possibility. Eventually it could be applied after surgery to treat the tissue around the extracted tumour, where some cancerous cells might have been left behind, preventing the cancer from reappearing. Devices similar to an endoscope are currently under development.

carry-on-my-wayward-butt: taengthehero: Bunny to Llama in...

Fri, 24 May 2013 14:02:59 -0400

carry-on-my-wayward-butt:

taengthehero:

Bunny to Llama in 0.8

a-tolkien-for-your-thoughts: thefingerfuckingfemalefury: ayello...

Fri, 24 May 2013 12:40:40 -0400

a-tolkien-for-your-thoughts:

thefingerfuckingfemalefury:

ayellowbirds:

ocelots are so fucking adorable.

LOOK AT ITS CUTE LITTLE FACE :D

OH GOD IT HAS DEMON EYES I BET THIS IS CROWLEY’S FAVOURITE ANIMAL OTHER THAN HELL HOUNDS AND HUMANS

Period: You want cookies

Thu, 23 May 2013 23:41:58 -0400

Period: You want cookies
Period: You want to fuck
Period: You want to fuck while eating cookies.
Period: Let's be sad about trivial things, shall we?
Period: Kill them.
Period: Kill them too.
Period: Kill them and eat their cookies.
Period: Shhhh it's okay you'll feel better soon.
Period: HAHAHAHAHA NO YOU WON'T FUCK YOU.

post-mitotic: human cortical neural stem cells labeled with...

Thu, 23 May 2013 22:31:46 -0400

post-mitotic:

human cortical neural stem cells labeled with TUJ-1 (neuron-specific tubulin, green) and astrocytes with GFAP (red); nuclei in blue for both

credit: Kymmy Lorrain

Photo

Thu, 23 May 2013 22:00:24 -0400

immawearitasaworm-stache: giver-of-armbands: Gwen’s just...

Thu, 23 May 2013 21:37:07 -0400

immawearitasaworm-stache:

giver-of-armbands:

Gwen’s just like ‘godammit Jack’

neurosciencestuff: Taming suspect gene reverses...

Thu, 23 May 2013 17:11:33 -0400

neurosciencestuff:

Taming suspect gene reverses schizophrenia-like abnormalities in mice

Scientists have reversed behavioral and brain abnormalities in adult mice that resemble some features of schizophrenia by restoring normal expression to a suspect gene that is over-expressed in humans with the illness. Targeting expression of the gene Neuregulin1, which makes a protein important for brain development, may hold promise for treating at least some patients with the brain disorder, say researchers funded by the National Institutes of Health.

Like patients with schizophrenia, adult mice biogenetically-engineered to have higher Neuregulin 1 levels showed reduced activity of the brain messenger chemicals glutamate and GABA. The mice also showed behaviors related to aspects of the human illness. For example, they interacted less with other animals and faltered on thinking tasks.

“The deficits reversed when we normalized Neuregulin 1 expression in animals that had been symptomatic, suggesting that damage which occurred during development is recoverable in adulthood,” explained Lin Mei, M.D., Ph.D.External Web Site Policy , of the Medical College of Georgia at Georgia Regents University, a grantee of NIH’s National Institute of Mental Health (NIMH).

Mei, Dong-Min Yin, Ph.D., Yong-Jun Chen, Ph.D., and colleagues report on their findings May 22, 2013 in the journal Neuron.

“While mouse models can’t really do full justice to a complex brain disorder that impairs our most uniquely human characteristics, this study demonstrates the potential of dissecting the workings of intermediate components of disorders in animals to discover underlying mechanisms and new treatment targets,” said NIMH Director Thomas R. Insel, M.D. “Hopeful news about how an illness process that originates early in development might be reversible in adulthood illustrates the promise of such translational research.”

Schizophrenia is thought to stem from early damage to the developing fetal brain, traceable to a complex mix of genetic and environmental causes. Although genes identified to date account for only a small fraction of cases, evidence has implicated variation in the Neuregulin 1 gene. For example, postmortem studies have found that it is overexpressed in the brain’s thinking hub, or prefrontal cortex, of some people who had schizophrenia. It codes for a chemical messenger that plays a pivotal role in communication between brain cells, as well as in brain development.

Prior to the new study, it was unclear whether damage caused by abnormal prenatal Neuregulin 1 expression might be reversible in adulthood. Nor was it known whether any resulting behavioral and brain deficits must be sustained by continued errant Neuregulin 1 expression in adulthood.

To find out, the researchers engineered laboratory mice to mimic some components of the human illness by over-expressing the Neuregulin 1 gene in the forebrain, comparable to the prefrontal cortex in humans. Increasing Neuregulin 1 expression in adult animals was sufficient to produce behavioral features, such as hyperactivity, social and cognitive impairments, and to hobble neural communications via the messenger chemicals glutamate and GABA.

Unexpectedly, the abnormalities disappeared when the researchers experimentally switched off Neuregulin 1 overexpression in the adult animals. Treatment with clozapine, an antipsychotic medication, also reversed the behavioral abnormalities. The researchers traced the glutamate impairment to an errant enzyme called LIMK1, triggered by the overexpressed Neuregulin 1 — a previously unknown potential pathological mechanism in schizophrenia.

The study results suggest that even if their illness stems from disruptions early in brain development, adult patients whose schizophrenia is rooted in faulty Neuregulin 1 activity might experience a reduction in some of the symptoms following treatments that target overexpression of the protein, say the researchers.

post-mitotic: (attempted) fertilization of ovum by sperm it’s...

Thu, 23 May 2013 16:26:25 -0400

post-mitotic:

(attempted) fertilization of ovum by sperm

it’s no easy task

first of all, 99% of the sperm don’t even make it to the cervix

yup

for the lucky 1% that do (a number that amounts to approximately 300 to 500 of the original 200 to 300 million), multiple challenges await: a wall of corona radiata cells, the zona pellucida glycoprotein matrix, and finally the ovum’s plasma membrane (booby-trapped, of course)

and it’s a race

once the winner reaches that finish line, lysosomal enzymes are immediately released from cortical granules lining the ovum’s plasma membrane

these enzymes cross-link the zona pellucida glycoproteins, hardening the matrix into an impenetrable shell to ensure fertilization by only a single sperm

tough love

colored SEM

credit: Science Photo Library

eteo: skysoaring: have a photoset of snakes laughing at your...

Wed, 22 May 2013 23:20:39 -0400

eteo:

skysoaring:

have a photoset of snakes laughing at your misfortune

this is fine

mazarin221b: johnnybooboo: buzzfeedceleb: Benedict...

Wed, 22 May 2013 22:53:42 -0400

mazarin221b:

johnnybooboo:

buzzfeedceleb:

Benedict Cumberbatch deleted shower scene from Star Trek Into Darkness

OMG.

confused-companion: whoever wrote this line needs to receive a...

Wed, 22 May 2013 19:42:12 -0400

confused-companion:

whoever wrote this line needs to receive a medal

neurosciencestuff: Finding a family for a pair of orphan...

Wed, 22 May 2013 19:04:07 -0400

neurosciencestuff:

Finding a family for a pair of orphan receptors in the brain

Researchers at Emory University have identified a protein that stimulates a pair of “orphan receptors” found in the brain, solving a long-standing biological puzzle and possibly leading to future treatments for neurological diseases.

The results are published in the Proceedings of the National Academy of Sciences, Early Edition.

The human genome is littered with orphans: proteins that look like they will bind and respond to a hormone or a brain chemical, based on the similarity of their sequences to other proteins. However, scientists haven’t figured out what each orphan’s partner chemical is yet.

Orphans that look like GPCRs (G protein-coupled receptors) currently number about 100. GPCRs are the targets of many drugs and are involved in vision, smell and brain cells’ responses to a host of hormones and neurotransmitters. One orphan GPCR, called GPR37, has attracted interest from researchers because it is connected with an inherited form of Parkinson’s disease. It is abundant in the dopamine-producing neurons that degenerate in Parkinson’s. But its partner chemical, or “ligand,” has not been found.

“We reasoned that GPR37 had to be doing something important, besides becoming misfolded in some forms of Parkinson’s,” says senior author Randy Hall, PhD, professor of pharmacology at Emory University School of Medicine.

Working with Hall, graduate student Rebecca Meyer devised a way to detect when cells producing GPR37 were reacting with GPR37’s ligand.

“Usually, cells remove GPCRs from their surfaces when they encounter their ligand,” Meyer says. “So we set things up so that GPR37 would be labeled red on the surface of the cell, but would appear green once internalized.”

They discovered that cells producing GPR37 – and also a close relative, GPR37L1 — respond to a protein known as prosaposin, which was discovered by John O’Brien of University of California San Diego in the 1990s.

Prosaposin is a growth factor for brain cells and protects them from stress. Scientists studying it had worked out that it stimulates cells via a GPCR – but which one was unclear until now. In animal models, prosaposin has shown potential for treating conditions such as stroke, Parkinson’s and neuropathic pain. An artificial fragment of prosaposin called prosaptide has been tested in clinical studies, but it quickly breaks down in the body.

“That’s the reason why it was so important to find the receptor,” Hall says. “Then we can actually do some pharmacology.”

Now, Hall’s laboratory is planning to look for other compounds that can activate GPR37 as well. These could be more stable in the body than the previously studied protein fragment and thus better potential drugs.

Doctors have reported a few cases of genetic deficiency in prosaposin, leading to severe neurodegeneration. Mice engineered to lack GPR37 have more subtle brain perturbations, so Hall also plans to test the hypothesis that prosaposin acts by both GPR37 and GPR37L1, by “knocking out” both in mice, potentially duplicating the same severe effects seen in the human cases of prosaposin deficiency.

agentgraham: #no one is more frustrated with the state of the...

Wed, 22 May 2013 15:59:09 -0400

agentgraham:

#no one is more frustrated with the state of the human condition than steve harvey is

Photo

Wed, 22 May 2013 13:09:40 -0400

claydols: im trying to be more positive sheds electrons and becomes highly unstable

Wed, 22 May 2013 00:32:48 -0400

claydols:

im trying to be more positive *sheds electrons and becomes highly unstable*

starrysleeper: high-blogging: while my prof was setting up...

Wed, 22 May 2013 00:29:09 -0400

starrysleeper:

high-blogging:

while my prof was setting up for his lecture…

gold

excuse me while I reblog this for the 36th time

i hope yahoo realizes they paid $1.1 billion for a site that’s basically porn. i’m not...

Wed, 22 May 2013 00:16:48 -0400

i hope yahoo realizes they paid $1.1 billion for a site that’s basically porn. i’m not totally sure how they plan on making this family-friendly.

toramorigan: daksinakke: funfrom4chan: So my cat likes...

Wed, 22 May 2013 00:10:58 -0400

toramorigan:

daksinakke:

funfrom4chan:

So my cat likes unpacking..

thats the happiest fucking cat ive ever seen

Aww yiss.

Mother.

Fucking.

Air Pacs.

Photo

Tue, 21 May 2013 22:21:38 -0400