A QoS-aware routing mechanism for multi-channel multi-interface ad-hoc networks

To accommodate real-time multimedia application while satisfying application QoS requirements in a wireless ad-hoc network, we need QoS control mechanisms. In this paper, we propose a new routing mechanism to support real-time multimedia communication by efficiently utilize the limited wireless network capacity. Our mechanism considers a wireless ad-hoc network composed of nodes equipped with multiple network interfaces to each of which a different wireless channel can be assigned. By embedding information about channel usage in control messages of OLSRv2, each node obtains a view of topology and bandwidth information of the whole network. Based on the obtained information, a source node determines a logical path with the maximum available bandwidth to satisfy application QoS requirements. Through simulation experiments, we confirmed that our proposal effectively routed multimedia packets over a logical path avoiding congested links. As a result, the load on a network is well distributed and the network can accommodate more sessions than QOLSR. We also conducted practical experiments using wireless ad-hoc relay nodes with four network interfaces and verified the practicality of our proposal.     

Synthesis and property study on Eu(III) complexes of modified poly(N-isopropylacrylamide)

Poly(N-isopropylacrylamide) with aromatic end groups (Ar-PNIPAM) were synthesized by atom transfer radical polymerization of N-isopropylacrylamide in isopropanol using phenyl 2-chloropropionate, (4′-phenyl)phenyl 2-chloropropionate, and (2′,6′-diphenyl)phenyl 2-chloropropionate as initiators and CuCl/tris(2-dimethylaminoethyl)amine (Me₆TREN) as a catalytic system. The resulting polymers had narrow polydispersity index of 1.10–1.14 and molecular weights of 3700–4600 g mol⁻¹. Then, novel functional complexes of Ar-PNIPAM, Europium(III) (Eu(III)), and α-Thenoyltrifluoroacetone (TTA) (Ar-PNIPAM/Eu(III)/TTA) with thermosensitive and fluorescent properties were synthesized and characterized by Fourier transform infrared spectra and fluorescence spectroscopy. Metal Eu(III) was not only bonded to oxygen and nitrogen atoms of polymer chain in PNIPAM, but also bonded to TTA. The maximum emission intensity of the complexes at 613 nm was enhanced about 22, 27, 33 times compared with that of the corresponding Eu(III). The lower critical solution temperatures (LCSTs) of Ar-PNIPAM/Eu(III)/TTA were slightly greater compared with that of PNIPAM. Eu(III) complexes had excellent fluorescence performance, the fluorescence spectrum presented characteristic emission of Eu(III) at 613 nm.     

A xanthine oxidase inhibitor 1'-acetoxychavicol acetate inhibits azoxymethane-induced colonic aberrant crypt foci in rats

The modifying effect of dietary administration of a xanthine oxidase inhibitor 1'-acetoxychavicol acetate (ACA) present in an edible plant Languas galanga in Thailand on the development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) was investigated in rats. Male F344 rats were given s.c. injections of AOM (15 mg/kg body wt) once a week for 3 weeks to induce colonic ACF. They were fed the diets containing 100 or 200 ppm ACA for 5 weeks, starting 1 week before the first dosing of AOM. At the termination of the study (week 5), AOM induced 118 +/- 28 ACF/colon. Dietary administration of ACA caused significant reduction in the frequency of ACF (41% inhibition by 100 ppm ACA feeding and 37% inhibition by 200 ppm ACA feeding, P<0.01). Such inhibition might be associated with suppression of the proliferation biomarkers' expression such as ornithine decarboxylase activity in the colonic mucosa, number of silver-stained nucleolar organizer regions' protein in the colonic mucosal cell nuclei and blood polyamine content. These results indicate that ACA could inhibit the development of AOM-induced ACF through its suppression of cell proliferation in the colonic mucosa and ACA might be a possible chemopreventive agent against colon tumourigenesis.     

Pathologic features of spinal disorders in patients treated with long-term hemodialysis

STUDY DESIGN: Pathologic features of hemodialysis-associated spinal disorders were evaluated using preoperative radiographic images and histologic findings of the spinal lesions resected during surgery. OBJECTIVES: To investigate the pathology of hemodialysis-related spinal disorders and to determine the role of amyloidosis in the establishment of severe destruction of the spine. SUMMARY OF BACKGROUND DATA: The pathologic events leading to hemodialysis-associated spinal disorders are poorly understood. The distribution of amyloid deposits in the spine also has not been clarified. METHODS: Twenty patients with hemodialysis-associated spinal disorders were investigated regarding pathologic features of neural compression and spinal destruction. Preoperative radiographic images such as plain radiography, tomography, computed tomography, magnetic resonance imaging, and scintigraphy were assessed for the existence of an intracanal mass, hypertrophy of the ligamentum flavum, and destructive changes of the spinal components. Histologic examination also was conducted by light microscopy and scanning electron microscopy to determine the distribution pattern of amyloid deposits in the spinal components. RESULTS: Six patients with no destructive changes in the spine showed spinal canal stenosis. In the cervical spine, a main factor associated with spinal canal stenosis was the presence of intracanal amyloid deposits in three patients. In the lumbar spine, a main factor associated with spinal canal stenosis was hypertrophied ligamentum flavum in three patients. Destructive changes of the facet joints, intervertebral disc, and vertebral body were seen in the other 14 patients. Amyloid deposits were densely distributed at the enthesis of capsular fibers to the bone and in anular tears in the intervertebral discs. Vertebral end plates were destroyed by penetration of amyloid granulation into the vertebral body. Osteoclast activity in the destroyed vertebral bodies was enhanced, with no evidence of new bone formation. CONCLUSIONS: Amyloid deposits played an important role in the progression of spinal destruction and severe instability.     

Transforming growth factor-beta inhibits interferon-gamma secretion by lymphokine-activated killer cells stimulated with tumor cells

The effect of transforming growth factor-beta (TGF-beta) secreted by glioblastoma (T98G) cells on the secretion of interferon-gamma (IFN-gamma) by lymphokine-activated killer (LAK) cells stimulated with tumor cells was investigated in cocultures of LAK and Daudi cells supplemented with T98G culture supernatant, T98G culture supernatant preincubated with anti-TGF-beta 1 and anti-TGF-beta 2 neutralizing antibodies, anti-TGF-beta 1 and anti-TGF-beta 2 antibodies, or natural human TGF-beta 1 or recombinant human TGF-beta 2. LAK cells were incubated with anti-TGF-beta 1 and anti-TGF-beta 2 antibodies, and with T98G cells of which the supernatant contained both active and latent forms of TGF-beta 1 and TGF-beta 2, with or without neutralizing antibodies. Addition of the supernatant from T98G cells to LAK/Daudi culture caused inhibition of IFN-gamma secretion by LAK cells. The inhibition was abolished by pretreatment of the supernatants with anti-TGF-beta antibodies. Addition of TGF-beta 1 and TGF-beta 2 to the LAK/Daudi culture inhibited IFN-gamma secretion by LAK cells in a dose-dependent manner. Addition of anti-TGF-beta antibodies to the LAK culture resulted in increased IFN-gamma secretion. T98G cells failed to stimulate LAK cells to secrete more IFN-gamma. Addition of anti-TGF-beta antibodies to the LAK-T98G culture resulted in increased IFN-gamma secretion by LAK cells. These results suggest that most malignant glioma cells which secrete high levels of TGF-beta can inhibit IFN-gamma secretion by LAK cells even after tumor cell stimulation.     

L-type calcium channels in the axon terminal of mouse bipolar cells

Two types of calcium current (I(Ca)) have been identified in the bipolar cell of the mouse retina: a transient (T-) type current and a long lasting (L-) type current. It has been suggested that the former is present in the soma and the latter in the axon terminal. To establish the cellular localization of the two types of I(Ca), bipolar cells of the mouse retina was studied electrophysiologically in a slice preparation, and immunocytochemically by staining specific calcium channels in isolated cells. The dihydropyridine-sensitive L-type I(Ca) was recorded in the axon terminal, and the T-type current was recorded in the somatic region. Strong immunoreactivity to a polyclonal antibody against the L-type calcium channel was found in the axon terminal. These observations suggest that the L-type I(Ca) is generated at the axon terminal and contributes to the transmission of sustained depolarization.     

Involvement of Ras in Bruton's tyrosine kinase-mediated JNK activation

Defects in Bruton's tyrosine kinase (Btk) result in B cell immunodeficiencies in humans and mice. Recent studies showed that Btk is required for maximal activation of JNK, a family of stress-activated protein kinases, induced by several extracellular stimuli including interleukin (IL)-3. On the other hand, IL-3-induced JNK activation is dependent on Ras. In the present study we have investigated whether Ras is involved in Btk-mediated JNK activation in BaF3 mouse pro-B cells. Overexpression of wild-type Btk protein in these cells enhanced JNK activation upon IL-3 stimulation, whereas expression of kinase-dead Btk partially suppressed JNK activation. Induced expression of the dominant negative Ras(N17) in the cells overexpressing wild-type Btk suppressed JNK activation. Importantly, overexpression of Btk enhanced the level of the GTP-bound, active form of Ras in response to IL-3 stimulation. Btk overexpression also increased the Shc-Grb2 association induced by IL-3 stimulation. Expression of either N17Ras or V12Ras did not impose any effects on Btk kinase activity. These data collectively indicate that Ras plays a role of an intermediary signaling protein in Btk-mediated JNK activation induced by the IL-3 signaling pathway.