Jack Dawson… Penniless artist who wins a ticket onto Titanic in 1912, attends a first class dinner, develops a taste for the finer things in life, pockets the Heart of the Ocean, survives the sinking, pawns the diamond, spends the following ten years building his wealth and in 1922 moves to West Egg as Jay Gatsby… Millionaire with a shady past and fear of swimming pools.
IT ALL MAKES SENSE.
Then Inception happens
No, my friend, inception is risky business and we are already many layers deep…
(via doctor-guillen)
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.
(via thescienceblog)
Amniotic fluid embolism
It is apparently the 5th most common cause of maternal mortality in the world. And yet, it is so rare (6-14 per 100,000) that most clinicians will never come across it in their practicing career. Is it rare or just under diagnosed?
The mechanism is not understood. The cause has yet to be explained. But virtually all amniotic emobli deaths occurs at time of birth. If death does not occur immediately, then the patient will often go into DIC. Clinical signs are respiratory distress, cardiovascular collapse and hypotension (which clinically moves you away from ecclampsia or volume overload).
Anonymous Asked: Hi, I am a pre-med student who is at a community college. I am very depressed right now because my gpa is a 2.91 and I am graduating next semester (fall). I haven't taken a lot of pre-req classes. I'm taking 8 credits this summer (2 bio classes) and 14 credits in the fall (including chem 1). Is there still hope for me? I am transfering to a 4 year college spring 2014Hi, I’m glad you asked about this, rather than it just eat away at you. However, I am from England and I have no clue what gpa, pre-req classes or credits are, I’m sorry!
Maybe one of my followers could help?
I know that this blog has some impeccable advice :)
http://wayfaringmd.tumblr.com/tagged/advice_to_premeds
