Search

Growth modes of single wall carbon nanotubes are investigated during chemical vapor deposition within an environmental transmission electron microscope and in furnace reactors at different gas pressure and flow conditions. The nanotube pivoting observed by in situ microscopy can be explained by dynamic catalyst crystallite reshaping for base growth. Microfabricated substrate barriers and gaps allow for the distinction between “crawling” and “flying” nanotubes, referring to either a continuous intimate contact with the substrate dominated by van der Waals forces or a mere substrate anchoring of nanotubes held afloat during growth. Flying nanotubes grow unobstructed and straight to millimeter lengths and are susceptible to external forces. Crawling nanotubes are strongly affected by substrate topography. We relate this to tip and base growth regimes and discuss how the growth modes can be controlled.

We present a simple method to stabilize single-wall carbon nanotube (SWNT) dispersions in N-methyl-2-pyrrolidone (NMP) by polyvinylpyrrolidone (PVP). A significant population of isolated SWNTs as well as small bundles of SWNTs in NMP is obtained by ultrasonic treatment followed by vacuum filtration through glass fiber filters. The resulting dispersions in pure NMP are monitored by photoluminescence (PL) spectroscopy over a period of 3 weeks. The PL intensities of such dispersions decrease with time, suggesting slow microscopic aggregation of nanotubes. However, addition of PVP dramatically improves the stability. In addition, PVP also spontaneously “debundles” some nanotube aggregates, increasing the isolated SWNT population without further ultrasonic treatment.

Peripheral inflammation triggers exacerbation in the central brain's ongoing damage in several neurodegenerative diseases. Systemic inflammatory stimulus induce a general response known as sickness behaviour, indicating that a peripheral stimulus can induce the synthesis of cytokines in the brain. In Parkinson's disease (PD), inflammation was mainly associated with microglia activation that can underlie the neurodegeneration of neurons in the substantia nigra (SN). Peripheral inflammation can transform the “primed” microglia into an “active” state, which can trigger stronger responses dealing with neurodegenerative processes. Numerous evidences show that systemic inflammatory processes exacerbate ongoing neurodegeneration in PD patient and animal models. Anti-inflammatory treatment in PD patients exerts a neuroprotective effect. In the present paper, we analyse the effect of peripheral infections in the etiology and progression in PD patients and animal models, suggesting that these peripheral immune challenges can exacerbate the symptoms in the disease.