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Amyloid beta-protein (Abeta) is present in soluble form in the plasma and cerebrospinal fluid (CSF) of normal people and patients with Alzheimer's disease (AD). However, in AD patients, Abeta gets fibrillized as the main constituent of amyloid plaques in the brain. Soluble synthetic Abeta also forms amyloid-like fibrils when it is allowed to age. The(More)
Microviscosity of the biological membranes is determined by measuring the fluorescence polarization of diphenylhexatriene (DPH). DPH, a hydrophobic probe, has negligible fluorescence in the solution. When DPH is incorporated into the membrane, it is localized in the membrane hydrophobic core and fluoresces strongly. We report here that DPH also fluoresces(More)
Current Food and Drug Administration-approved cancer nanotherapeutics, which passively accumulate around leaky regions of the tumor vasculature because of an enhanced permeation and retention (EPR) effect, have provided only modest survival benefits. This suboptimal outcome is likely due to physiological barriers that hinder delivery of the nanotherapeutics(More)
The blood vessels of cancerous tumours are leaky and poorly organized. This can increase the interstitial fluid pressure inside tumours and reduce blood supply to them, which impairs drug delivery. Anti-angiogenic therapies--which 'normalize' the abnormal blood vessels in tumours by making them less leaky--have been shown to improve the delivery and(More)
Amyloid beta-protein (Abeta), in its soluble form, is known to bind several circulatory proteins such as apolipoprotein (apo) E, apo J and transthyretin. However, the binding of Abeta to intracellular proteins has not been studied. We have developed an overlay assay to study Abeta binding to intracellular brain proteins. The supernatants from both rat and(More)
We examined the effect of cerebrospinal fluid (CSF) from 23 Alzheimer's disease (AD) patients and 22 age-matched non-demented controls with apolipoprotein E4/4, 3/3, or 3/2 phenotypes on in vitro aggregation of amyloid beta-protein (A beta) 1-40 by Thioflavin T fluorescence spectroscopy. CSF from both AD and control groups inhibited A beta aggregation, as(More)
Cancer and stromal cells actively exert physical forces (solid stress) to compress tumour blood vessels, thus reducing vascular perfusion. Tumour interstitial matrix also contributes to solid stress, with hyaluronan implicated as the primary matrix molecule responsible for vessel compression because of its swelling behaviour. Here we show, unexpectedly,(More)
High particle uniformity, high photoluminescence quantum yields, narrow and symmetric emission spectral lineshapes and minimal single-dot emission intermittency (known as blinking) have been recognized as universal requirements for the successful use of colloidal quantum dots in nearly all optical applications. However, synthesizing samples that(More)
Previously, it has been found that phenobarbital inhibited protein kinase C (PKC) and the enzymes of the metabolism of polyphosphoinositide, especially phosphatidylinositol 4-phosphate (PIP) kinase (PIP-kinase). As a continuation of these studies, a number of barbiturates (barbituric acid, barbital, butabarbital, pentobarbital, amobarbital, phenobarbital,(More)
Fibrillar amyloid beta-protein (Abeta) is the major protein of amyloid plaques in the brains of patients with Alzheimer's disease (AD). The mechanism by which normally produced soluble Abeta gets fibrillized in AD is not clear. We studied the effect of neutral, zwitterionic, and anionic lipids on the fibrillization of Abeta 1-40. We report here that acidic(More)