Effect of electric charging on the velocity of water flow in CNT.

The role of electrical charge in controlling the velocity of water molecules in a finite single-walled carbon nanotube (CNT) was studied in detail using molecular dynamics simulation. Different test cases were examined to determine the parameters affecting the control of water-flow velocity in CNT upon electrically charging the surface of a CNT. The results showed that charge magnitude and volume, as well as the charging scenario, are the parameters having greatest effect. The implementation of electric charge on the surface of a CNT was demonstrated to decrease the resistance of CNT to incoming water flow at the entrance, but to increase friction-type resistance to flow along the CNT. Therefore, through controlling the magnitude of electric charge, water flow through the CNT may be accelerated, or decelerated. The results show that the velocity of molecular flow in the CNT increases to a maximum value, and then decreases with electric charge regardless of its sign. In the case studied here, this maximum velocity occurs at electric charging of ±0.25e/atom. It was also shown that, to reach similar flow velocities in a CNT, it is not sufficient to merely implement equal volumes of electric charge, where the volume of electric charging is defined as charge magnitude × charging time. In fact , both magnitude of charging and volume of electric charging must be equal to each other. These findings, together with options to implement scenarios with alternative charging, provide the means to effectively adjust desired velocities in a CNT.

Pancreatic islet beta cell protective effect of oral vanadyl sulphate in streptozotocin-induced diabetic rats, an ultrastructure study.

We sought to determine the ultrastructure of pancreatic islet beta cells of streptozotocin-induced diabetic rats treated with oral vanadyl sulphate. Diabetes was induced in male Wistar rats by intravenous injection of 40 mg kg(-1) streptozotocin. The same volume of normal saline was injected in sham animals. Animals were divided into treated and control groups. Vanadyl sulphate was added to the drinking water of the treated animals at a concentration of 1 mg mL(-1) up to three months. Two months after vanadyl sulphate withdrawal animals were killed. Ultrastructure of islet beta cells were studied by transmission electron microscope. In diabetic treated rats plasma glucose and fluid intake returned to normal levels within three months while control animals remained diabetic. Well granulated cytoplasm, well developed endoplasmic reticulum, increase in the number of immature granules in the cytoplasm with no clear signs of cell injury were found in the islet beta cells of diabetic treated rats. Lymphocyte filteration, nuclear picnosis, cytoplasmic vacuolization were found frequently in the islet beta cells of untreated diabetic rats. In conclusion as was evident in thin sections of panceatic islet beta cells of treated diabetic rats in this study, vanadyl sulphate through preserving islet beta cells structure and ultrastructure contributes in reversing diabetic signs and symptoms in streptozotocin induced diabetic rats.

Tachykinin regulation of basal synovial blood flow.

1. Experiments were performed to investigate the role of endogenously released tachykinins in the regulation of blood flow to the rat knee joint. Synovial perfusion was assessed by laser Doppler perfusion imaging, which permitted spatial measurement of relative changes in perfusion from control (pre drug administration), expressed as the percentage change. Most experiments were performed on the exposed medial aspect of the knee joint capsule. 2. Neither the selective tachykinin NK1 receptor antagonist, FK888, nor the selective tachykinin NK2 receptor antagonist, SR48968, significantly influenced synovial blood flow at doses of 10(-12), 10(-10) and 10(-8) mol. However, topical co-administration of these agents produced significant dose-dependent reductions in basal synovial perfusion of 6.3 +/- 4.6 and 12.0 +/- 3.4 and 19.9 +/- 2.6%, respectively; n = 29. The non-selective tachykinin NK1/NK2 receptor antagonist, FK224, also produced significant (at 10(-10) and 10(-8) mol), but less potent, reductions in perfusion of 5.3 +/- 4.0, 8.4 +/- 2.2 and 5.9 +/- 2.8%, respectively; n = 25. 3. Topical administration of the alpha 1-, alpha 2-adrenoceptor antagonist phenoxybenzamine elicited a 31.3 +/- 6.2% increase in blood flow which was substantially reduced to 10.4 +/- 3.8% by co-administration of the FK888 and SR48968 (both at 10(-8) mol; n = 8-13), suggesting that normally there is sympathetic vasoconstrictor "tone' which is opposed by the vasodilator action of endogenous tachykinins. 4. One week after surgical interruption of the nerve supply to the knee joint, co-administration of FK888 and SR48968 (both at 10(-8) mol) now produced slight vasodilatation (6.7 +/- 4.6%; n = 9) which did not differ significantly from vehicle treatment. Depletion of tachykinins from sensory nerve fibres by systemic capsaicin administration also resulted in abolition of the vasoconstrictor effect of FK888 and SR48968 (both at 10(-8) mol), with these agents only producing a slight vasodilatation (2.5 +/- 5.3%; n = 6). 5. By use of a near infra-red laser source it was possible to image knee joint perfusion transcutaneously, the overlying skin being left intact. In this more physiological situation, close intra-arterial injection of the combination of FK888 and SR48968 (both at 10(-8) mol) again elicited vasoconstriction (48.8 +/- 16.2% reduction in blood flow; n = 4). 6. These results indicate that endogenous tachykinins may be continuously released from sensory fibers innervating the joint. Basal release of tachykinins could therefore be an important physiological influence opposing sympathetic vasoconstrictor tone.

Neuropeptidergic and autonomic control of the vasculature of the rat knee joint revealed by laser Doppler perfusion imaging.

An imaging technique (laser Doppler perfusion imaging, LDI), based on measurement of backscattered Doppler-broadened laser radiation, was used to provide two-dimensional images of perfusion in the exposed rat knee joint capsule. In control animals, frequency-dependent constriction of knee joint blood vessels occurred during electrical stimulation of sympathetic nerve fibres whilst dose-dependent vasodilatation of these vessels was elicited by direct application of the sensory neuropeptide substance P (SP) to the capsule. Intra-articular injection of the neurotoxic agent capsaicin did not affect vasoconstrictor responses when tested 5-7 days later, but substantially reduced dilator responses to SP. These findings indicate that capsaicin is selectively neurotoxic for sensory unmyelinated fibres but not sympathetic postganglionic fibres and is also capable of modifying receptor-mediated effects of SP. LDI is a useful method for mapping tissue perfusion, particularly in structures such as joints where the spatial distribution of blood flow is heterogeneous.

Prolonged alteration of vasoconstrictor and vasodilator responses in rat knee joints by adjuvant monoarthritis.

Both neurogenic influences and the regulatory neuropeptide substance P (SP) have been implicated in the development of joint inflammation. Using the laser Doppler perfusion imaging technique to quantify relative changes in joint blood flow, the effects of nerve stimulation and topical SP application were examined in normal and chronically inflamed rat knee joints. Synovial inflammation was induced by unilateral intra-articular injection of Freund's complete adjuvant and experiments were carried out 1 week and 3 weeks later. Normal knees showed a frequency-dependent vasoconstriction in response to saphenous nerve stimulation over the range of 5-30 Hz and a dose-dependent vasodilation in response to SP administration. These vasoactive responses were completely abolished in the chronically inflamed knee joint, the abolition persisting throughout the investigation. Since articular cartilage is critically dependent on synovial fluid formation for its nutrition, loss of neurovascular control of the synovial microcirculation could contribute to the degenerative changes that commonly accompany chronic inflammatory joint diseases.

Alteration of substance P-mediated vasodilatation and sympathetic vasoconstriction in the rat knee joint by adjuvant-induced inflammation.

The effects of nerve stimulation and topical administration of substance P (SP) on the blood flow supplying the rat knee joint were measured using laser Doppler perfusion imaging. A comparison was made between the responses found in normal knees and those observed in a group of animals with unilateral chronic inflammation induced by intra-articular injection of Freund's adjuvant, 1 week prior to experimentation. In control knees, nerve stimulation produced a frequency-dependent vasoconstriction over the range of 5-30 Hz and application of SP caused a dose-dependent vasodilatation. Chronically inflamed joints showed virtually no response to either nerve stimulation or SP application, suggesting a radical alteration in sympathetic and neuropeptidergic actions.