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The ideal methodology for the quantitative measurement of regional cerebral blood flow (rCBF) in the human brain is by invasive techniques, but noninvasive brain perfusion techniques are becoming more widespread as imaging devices develop. A serious drawback in previous efforts to establish quantitative methods in the human brain, however, has been the weak correlation observed between cerebral blood flow (CBF) measurements determined noninvasively by single-photon emission computerized tomography (SPECT) or by positron emission tomography (PET) and the invasive determinations by the use of inhalation of radioactive tracers such as [14C]iodoantipyrine. In this study, an attempt was made to understand the difference between the macroscopic and microscopic regional CBF measurements made by these techniques and the variability of these measurements. An effort was made to make quantitative evaluations of the relationship between the PET and the invasive CBF determinations. Cerebral blood flow maps were created from dynamic MRI that were used to study the CBF distributions in relation to the morphological features of various brain regions. In addition, we were also able to perform in vivo quantitative measurements of rCBF in the brains of rats and mice, and also in the rabbit brain. The data obtained by these measurements have been integrated with the anatomical information obtained from MRI into quantitative maps. Microscopic regional CBF determinations in the rabbit brain showed a correlation of r > 0.9 between the 2 techniques. These results confirm the hypothesis that the SPECT and PET CBF measurements are indeed correlated with CBF measurements determined from the macroscopic arteriovenous CBF measurements made in the same animal. Furthermore, it appears that MAP measurements can be used to correct the PET or SPECT measurements to obtain a more accurate and reliable CBF measurement.
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Parkinson’s disease is a devastating neurodegenerative disorder associated with motor symptoms including resting tremor, bradykinesia, muscle rigidity, and postural instability. Parkinson’s disease can also be accompanied by non-motor symptoms including constipation, emotional instability, depression, anxiety and sleep disorder, and cognitive impairment. A recent study identified two novel proteins, JNK-interacting protein 3 (JIP3) and JNK-interacting protein 3-like 1 (JIP3L1), that are associated with Parkinson’s disease. By knocking out the two genes in the mice, the study showed that they exhibit behavioral phenotypes that closely resemble those of Parkinson’s disease. Such in vivo findings demonstrating that JIP3 and JIP3L1 are causally involved in the pathophysiology of this disease.
Compared with conventional Parkinson’s disease drug therapies, the long-term side effects of gene therapy may require new approaches to be developed, and progress in this field has made headway in several experimental studies. In this case, researchers at the University of California, San Diego School of Medicine and their collaborators from the National Institute on Aging and the National Institute of Neurological Disorders and Stroke, established a gene therapy for Parkinson’s disease that could be used to deliver a functional protein into affected brain cells.
The new study, published in the journal Genes & Development, describes a robust therapeutic platform for in vivo delivery of functional proteins to treat Parkinson’s disease. Using this system, the researchers administered a plasmid bearing a functional copy of the JIP3 gene into the mouse brain, and observed that it was able to halt the progression of Parkinson’s disease as evidenced by motor symptoms, such as tremors and movement defects.
To study whether the plasmid contained a complete, functional copy of the JIP3 gene, the researchers prepared a plasmid expressing a shortened version of JIP3 with impaired regulatory function (S3, a.k.a., dnJIP3), and delivered that to the mice brains. The dnJIP3 plasmid led to alterations in the motor system that closely mimicked the non-synonymous, functional variation found in JIP3, and dnJIP3 expression alone in the mouse brain rescued the motor function defects seen in the JIP3-deficient mice.
“The enzyme, PNK, has
What’s New in the?
What do you think of Heroku now? – ebun
======
samwilliams
It’ll take time for the developers to build something they like. They have
kind of already.
The only ‘problem’ really is that it’s not a ‘business’ as such (if we leave
out the IPO drama). An enterprise environment in terms of scaling and
convenience could never exist on the Heroku platform, at least as it stands
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We prospectively evaluated the potential role of the platelet glycoprotein IIb/IIIa complex (GPIIb/IIIa) in acute myocardial infarction by a quantitative flow cytometric analysis of platelet GPIIb/IIIa expression. We studied 104 patients with myocardial infarction and 68 with unstable angina in whom GPIIb/IIIa expression was measured 1-6 days after onset of the event. Acute myocardial infarction was confirmed by serial electrocardiographic and enzyme changes and by at least one of the following: myocardial perfusion imaging, intravenous thallium-201 single photon emission computed tomography, or coronary angiography. Unstable angina was diagnosed by recurrent symptoms and biopsy of unstable plaque. There were 72 men and 32 women (mean age, 66 +/- 14 years) in the myocardial infarction group and 22 men and 46 women (mean age, 64 +/- 12 years) in the unstable angina group. The proportion of patients with GPIIb/IIIa expression on platelets increased from 0% in patients with unstable angina to 62% in patients with myocardial infarction (p Water
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