Inhibition of nitric oxide production. Mechanisms of vascular albumin leakage

The mechanisms by which nitric oxide modulates microvascular albumin exchange were investigated by monitoring leukocyte-endothelial cell adhesion and fluorescein isothiocyanate-albumin leakage in rat mesenteric venules exposed to NG-nitro-L-arginine methyl ester (L-NAME). L-NAME elicited an initial rapid increase followed by a slower rate of albumin accumulation in the interstitial space. The initial phase of albumin leakage preceded the L-NAME-induced leukocyte adherence and emigration, whereas the magnitude of the albumin leakage observed in the later phase of L-NAME exposure was highly correlated with the number of adherent and emigrated leukocytes in the same segment of venule. Monoclonal antibodies (MAbs) directed against adhesion molecules CD11/CD18, ICAM-1, or P-selectin, but not a nonbinding MAb, attenuated the albumin leakage induced by L-NAME. WEB2086, a platelet activating factor antagonist, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-br-cGMP) reduced the leukocyte adherence and emigration as well as the increased albumin leakage. Only 8-br-cGMP and the P-selectin MAb attenuated the platelet-leukocyte aggregation elicited by L-NAME. Phalloidin, which promotes endothelial junctional integrity, inhibited both the early and late phases of albumin leakage. Overall, these findings suggest that the increased albumin leakage observed in postcapillary venules after inhibition of nitric oxide production involves a mechanism that includes a role for cGMP, platelet activating factor, leukocyte-endothelial cell adhesion, and the endothelial cell cytoskeleton.     

Asynchronous migration for parallel genetic programming on a computer cluster with multi-core processors

An island model is a typical implementation of genetic programming on parallel computers with distributed memory. The island model has a migration facility that sends/receives some individuals in an island to/from another island to maintain diversity. The island model requires synchronization to migrate same-generation individuals between islands, and this synchronization causes an increase in computation time. This article proposes a new parallel genetic programming implementation based on the island model with asynchronous migration. Most recent computers are equipped with one or more multi-core processors, and are suitable for multi-threading. Therefore we employ a communication thread for migration between islands. The communication thread on a processor communicates with the communication thread on another processor to migrate individuals at appropriate intervals. Since the migration and other genetic operations can be independently processed on each core, and since we allow the exchange of individuals of different generations, no synchronization is needed in our implementation. In addition, a fitness calculation is also executed in parallel by the remaining cores. Experimental results show that the proposed method can reduce the computation time to about 17% in serial GP by using 40 threads.     

Scalable fair reliable multicast using active services

Scalability is of paramount importance in the design of reliable multicast transport protocols, and requires careful consideration of a number of problems such as feedback implosion, retransmission scoping, distributed loss recovery, and congestion control. In this article, we present a reliable multicast architecture that invokes active services at strategic locations inside the network to comprehensively address these challenges. Active services provide the ability to quickly and efficiently recover from loss at the point of loss. They also exploit the physical hierarchy for feedback aggregation and effective retransmission scoping with minimal router support. We present two protocols, one for packet loss recovery and another for congestion control, and describe an experimental testbed where these have been implemented. Analytical and experimental results are used to demonstrate that the active services architecture improves resource usage, reduces latency for loss recovery, and provides TCP-friendly congestion control     

Modeling TCP Reno performance: a simple model and its empiricalvalidation

The steady-state performance of a bulk transfer TCP flow (i.e., a flow with a large amount of data to send, such as FTP transfers) may be characterized by the send rate, which is the amount of data sent by the sender in unit time. In this paper we develop a simple analytic characterization of the steady-state send rate as a function of loss rate and round trip time (RTT) for a bulk transfer TCP flow. Unlike the models of Lakshman and Madhow (see IEE/ACM Trans. Networking, vol.5, p.336-50, 1997), Mahdavi and Floyd (1997), Mathis, Semke, Mahdavi and Ott (see Comput. Commun. Rev., vol.27, no.3, 1997) and by by Ott et al., our model captures not only the behavior of the fast retransmit mechanism but also the effect of the time-out mechanism. Our measurements suggest that this latter behavior is important from a modeling perspective, as almost all of our TCP traces contained more time-out events than fast retransmit events. Our measurements demonstrate that our model is able to more accurately predict TCP send rate and is accurate over a wider range of loss rates. We also present a simple extension of our model to compute the throughput of a bulk transfer TCP flow, which is defined as the amount of data received by the receiver in unit time     

Scalable reliable multicast using multiple multicast channels

We examine an approach for providing reliable, scalable multicast communication, involving the use of multiple multicast channels for reducing receiver processing costs and reducing network bandwidth consumption in a multicast session. In this approach a single multicast channel is used for the original transmission of packets. Retransmissions of packets are done on separate multicast channels, which receivers dynamically join and leave. We first show that protocols using an infinite number of multicast channels incur much less processing overhead at the receivers compared to protocols that use only a single multicast channel. This is due to the fact that receivers do not receive retransmissions of packets they have already received correctly. Next, we derive the number of unwanted redundant packets at a receiver due to using only a finite number of multicast channels, for a specific negative acknowledgment (NAK)-based protocol. We then explore the minimum number of multicast channels required to keep the cost of processing unwanted packets to a sufficiently low value. For an application consisting of a single sender transmitting reliably to many receivers we find that only a small number of multicast channels are required for a wide range of system parameters. In the case of an application where all participants simultaneously act as both senders and receivers a moderate number of multicast channels is needed. Finally, we present two mechanisms for implementing multiple multicast channels, one using multiple IP multicast groups and the other using additional router support for selective packet forwarding. We discuss the impact of both mechanisms on performance in terms of end-host and network resources     

A comparison of sender-initiated and receiver-initiated reliablemulticast protocols

Sender-initiated reliable multicast protocols based on the use of positive acknowledgments (ACKs) can suffer performance degradation as the number of receivers increases. This degradation is due to the fact that the sender must bear much of the complexity associated with reliable data transfer (e.g., maintaining state information and timers for each of the receivers and responding to receivers' ACKs). A potential solution to this problem is to shift the burden of providing reliable data transfer to the receivers-thus resulting in receiver-initiated multicast error control protocols based on the use of negative acknowledgments (NAKs). We determine the maximum throughputs for generic sender-initiated and receiver-initiated protocols for two classes of applications: (1) one-many applications where one participant sends data to a set of receivers and (2) many-many applications where all participants simultaneously send and receive data to/from each other. We show that a receiver-initiated error control protocol which requires receivers to transmit NAKs point-to-point to the sender provides higher throughput than a sender-initiated counterpart for both classes of applications. We further demonstrate that, in the case of a one many application, replacing point-to-point transfer of NAKs with multicasting of NAKs coupled with a random backoff procedure provides a substantial additional increase in the throughput of a receiver-initiated error control protocol over a sender-initiated protocol. We also find, however, that such a modification leads to a throughput degradation in the case of many-many applications     

Amelioration of chronic inflammation by ingestion of elemental diet in a rat model of granulomatous enteritis

The beneficial effect of elemental diet (ED) in the treatment of Crohn's disease is reported, although the exact mechanism for this remains to be elucidated. In this study the effects of ED on intestinal inflammation were investigated in a rat model of granulomatous enteritis. Intestinal inflammation was induced by a single intramural injection of peptidoglycan-polysaccharide (PG-PS) from group A streptococci into rat ileal Peyer's patches. A single injection of PG-PS in combination with fibrinogen, which retains PG-PS at the injection site, induced severe granulomatous inflammation associated with mucosal ulceration. Immunohistochemical study and immunocytochemical analysis of the cell suspension from Peyer's patches showed accumulation of macrophages and an increase in interleukin-2 receptor (IL-2R)-positive T cells after PG-PS treatment. Chemiluminescence (ChL) activity and nitrite and nitrate (NOx) levels in the mesenteric venous blood as well as Ca(2+)-independent (inducible) nitric oxide synthase (NOS) activity in Peyer's patches were increased by PG-PS treatment. In rats fed with ED, both macroscopic and histologic damage scores were significantly decreased as compared with those in rats fed with the control diet. ED inhibited the increase in the numbers of macrophages and IL-2R-positive T cells in Peyer's patches. Increased ChL activity, NOx levels, and Ca(2+)-independent NOS activity were also reduced significantly by feeding with ED. These data suggest that ED reduces progression of PG-PS-induced chronic intestinal inflammation by modulating activation of T cells, production of nitric oxide, and generation of oxygen free radicals.     

Mesomorphic phase formation of plasticized poly(l‐lactic acid)

The effects of the crystallization temperature, T_c, on the crystal structure as well as its thermal behavior of plasticized poly(l ‐lactic acid) were investigated by means of wide‐angle X‐ray diffraction (WAXD), Fourier‐transform infrared spectroscopy (FTIR), and differential scanning calorimetry (DSC). PLLA blended with succinic acid‐bis[2‐[2‐(2‐methoxyethoxy)ethoxy]ethyl] ester (SAE) showed clear difference in T_c dependence of crystalline form compared to PLLA homopolymer. PLLA with 26 wt % SAE crystallized into orthorhombic α form for T_c above 80°C, while a peculiar disordered structure (mesophase) was obtained for T_c at 40°C. A detailed FTIR analysis of the mesophase of PLLA, focusing on the intra‐ and inter‐chain interaction in the structure, indicated that mesophase had a large degree of disorder in 10/3 helical conformation as well as its packing manner of disordered 10/3 helical chain. Upon heating, mesophase showed a steep exothermic peak at 80°C in DSC thermogram, indicating the phase transformation from mesophase to a form crystal. FTIR results showed that the degree of interchain interaction of C=O in PLLA started to decrease above 60°C, followed by steep increase at 80°C due to the recrystallization into a form. Melt‐recrystallization process in mesophase‐α transformation was clarified. © 2013 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2014 , 131, 39762.     

Improvement of isoamyl acetate productivity in sake yeast by isolating mutants resistant to econazole

Sake yeast strains were improved so as to produce larger amounts of isoamyl acetate than the parental strain by isolating econazole-resistant mutants. Econazole, an imidazole antimycotic, directly interacts with unsaturated fatty acids in the yeast cell membrane, where it also inhibits the synthesis of ergosterol and decreases the ratio of unsaturated to saturated fatty acids. In contrast, alcohol acetyltransferase (AATase), which catalyzes the synthesis of isoamyl acetate, is inhibited by unsaturated fatty acids. Fifty econazole-resistant mutants were isolated from a sake yeast, Kyokai no. 701, several of which produced approximately 1.4 to 2.4 times more isoamyl acetate and an almost equal amount of isoamyl alcohol compared with the parental strain. The AATase activities of the mutants in koji extract were 1.2 to 1.4 times higher, and the unsaturated to saturated fatty acid ratios were lower, than in the parental strain.