Wireless Multi Hop Access Networks and Protocols

As more and more applications and services in our society now depend on the Internet, it is important that dynamically deployed wireless multi hop networks are able to gain access to the Internet and other infrastructure networks and services. This thesis proposes and evaluates solutions for providing multi hop Internet Access. It investigates how ad hoc networks can be combined with wireless and mesh networks in order to create wireless multi hop access networks. When several access points to the Internet are available, and the mobile node roams to a new access point, the node has to make a decision when and how to change its point of attachment. The thesis describes how to consider the rapid fluctuations of the wireless medium, how to handle the fact that other nodes on the path to the access point are also mobile which results in frequent link and route breaks, and the impact the change of attachment has on already existing connections. Medium access and routing protocols have been developed that consider both the long term and the short term variations of a mobile wireless network. The long term variations consider the fact that as nodes are mobile, links will frequently break and new links appear and thus the network topology map is constantly redrawn. The short term variations consider the rapid fluctuations of the wireless channel caused by mobility and multi path propagation deviations. In order to achieve diversity forwarding, protocols are presented which consider the network topology and the state of the wireless channel when decisions about forwarding need to be made. The medium access protocols are able to perform multi dimensional fast link adaptation on a per packet level with forwarding considerations. This i ncludes power, rate, code and channel adaptation. This will enable the type of performance improvements that are of significant importance for the success of multi hop wireless networks

The Bronchoalveolar Lavage Proteome- Phenotypic associations to smoking and divergence towards development of COPD

Proteomic analysis of bronchoalveolar lavage (BAL) fluid from smokers at risk of developing chronic obstructive pulmonary disease (COPD) and never smokers is described. COPD is currently the world's fourth leading cause of death and its prevalence is increasing. The leading cause of COPD is smoking and an estimated 600 million people in the world suffer from COPD which makes it the world's most common chronic disease. The aim of this thesis was to explore and characterize the BAL proteome of never smokers and smokers. The hypotheses were that the BAL proteome reflect smoking habits in subjects, and that smokers susceptible to COPD development have a specific proteome. In order to relate the measurement of protein expression with clinical phenotypes we have developed and utilized an interdisciplinary toolbox that includes protein separation (two-dimensional gel electrophoresis and liquid chromatography), mass spectrometry identification and statistical methods for multivariate analysis. The study material used in this thesis consisted of age matched men all born in 1933, living in one city differing by lifelong smoking history. These were compared by clinical function measurements and histological assessment at the same relative time points. A follow up study after 6-7 years identified a group of subjects who had progressed to COPD GOLD stage 2. Those with COPD shared a distinct protein expression profile in the baseline BAL sample which could be identified using multivariate analysis. This pattern was not observed in BAL samples of asymptomatic smokers free of COPD at the 6-7 year follow-up. The results suggest that specific patterns of protein expression occur in the airways of smokers susceptible to COPD disease progression, before the disease is clinically measurable

Micro mobility and internet access performance for TCP connections in Ad Hoc networks

In ad hoc mobile networks nodes typically communicate over wireless channels and are capable of movement. These are networks that support multihop communication and can be formed on a temporary basis. This paper evaluates a solution that allows mobile nodes to access the wired Internet and roam from base station to base station. The solution is based on the extension of Mobile IP capabilities to the ad hoc network while a micro-mobility protocol is adapted to support local migration. We evaluate the performance of this solution with regard to reliable transport layer connections. It is shown that a high throughput is possible to achieve for high mobility speeds. It is also observed that, as the number of hops between a mobile node and the base station increases, the throughput is decreased because of the characteristics of the wireless environment and the medium access layer protocol

Proteomic Analysis of Whole Human Saliva Detects Enhanced Expression of Interleukin-1 Receptor Antagonist, Thioredoxin and Lipocalin-1 in Cigarette Smokers Compared to Non-Smokers

A gel-based proteomics approach was used to screen for proteins of differential abundance between the saliva of smokers and those who had never smoked. Subjecting precipitated proteins from whole human saliva of healthy non-smokers to two-dimensional electrophoresis (2-DE) generated typical profiles comprising more than 50 proteins. While 35 of the proteins were previously established by other researchers, an additional 22 proteins were detected in the 2-DE saliva protein profiles generated in the present study. When the 2-DE profiles were compared to those obtained from subjects considered to be heavy cigarette smokers, three saliva proteins, including interleukin-1 receptor antagonist, thioredoxin and lipocalin-1, showed significant enhanced expression. The distribution patterns of lipocalin-1 isoforms were also different between cigarette smokers and non-smokers. The three saliva proteins have good potential to be used as biomarkers for the adverse effects of smoking and the risk for inflammatory and chronic diseases that are associated with it

Seasonal Variation in TP53 R249S-Mutated Serum DNA with Aflatoxin Exposure and Hepatitis B Virus Infection

Background: Chronic hepatitis B virus (HBV) infection and dietary aflatoxin B1 (AFB1) exposure are etiological factors for hepatocellular carcinoma (HCC) in countries with hot, humid climates. HCC often harbors a TP53 (tumor protein p53) mutation at codon 249 (R249S). In chronic carriers, 1762T/1764A mutations in the HBV X gene are associated with increased HCC risk. Both mutations have been detected in circulating cell-free DNA (CFDNA) from asymptomatic HBV carriers

Susceptibility to COPD:Differential Proteomic Profiling after Acute Smoking

Cigarette smoking is the main risk factor for COPD (Chronic Obstructive Pulmonary Disease), yet only a subset of smokers develops COPD. Family members of patients with severe early-onset COPD have an increased risk to develop COPD and are therefore defined as "susceptible individuals". Here we perform unbiased analyses of proteomic profiles to assess how "susceptible individuals" differ from age-matched "non-susceptible individuals" in response to cigarette smoking. Epithelial lining fluid (ELF) was collected at baseline and 24 hours after smoking 3 cigarettes in young individuals susceptible or non-susceptible to develop COPD and older subjects with established COPD. Controls at baseline were older healthy smoking and non-smoking individuals. Five samples per group were pooled and analysed by stable isotope labelling (iTRAQ) in duplicate. Six proteins were selected and validated by ELISA or immunohistochemistry. After smoking, 23 proteins increased or decreased in young susceptible individuals, 7 in young non-susceptible individuals, and 13 in COPD in the first experiment; 23 proteins increased or decreased in young susceptible individuals, 32 in young non-susceptible individuals, and 11 in COPD in the second experiment. SerpinB3 and Uteroglobin decreased after acute smoke exposure in young non-susceptible individuals exclusively, whereas Peroxiredoxin I, S100A9, S100A8, ALDH3A1 (Aldehyde dehydrogenase 3A1) decreased both in young susceptible and non-susceptible individuals, changes being significantly different between groups for Uteroglobin with iTRAQ and for Serpin B3 with iTRAQ and ELISA measures. Peroxiredoxin I, SerpinB3 and ALDH3A1 increased in COPD patients after smoking. We conclude that smoking induces a differential protein response in ELF of susceptible and non-susceptible young individuals, which differs from patients with established COPD. This is the first study applying unbiased proteomic profiling to unravel the underlying mechanisms that induce COPD. Our data suggest that SerpinB3 and Uteroglobin could be interesting proteins in understanding the processes leading to COPD

Aflatoxin-Induced TP53 R249S Mutation in HepatoCellular Carcinoma in Thailand: Association with Tumors Developing in the Absence of Liver Cirrhosis

Primary Liver Cancer (PLC) is the leading cause of death by cancer among males in Thailand and the 3rd among females. Most cases are hepatocellular carcinoma (HCC) but cholangiocarcinomas represent between 4 and 80% of liver cancers depending upon geographic area. Most HCC are associated with chronic infection by Hepatitis B Virus while a G→T mutation at codon 249 of the TP53 gene, R249S, specific for exposure to aflatoxin, is detected in tumors for up to 30% of cases. We have used Short Oligonucleotide Mass Analysis (SOMA) to quantify free circulating R249S-mutated DNA in plasma using blood specimens collected in a hospital case:control study. Plasma R249S-mutated DNA was detectable at low concentrations (≥67 copies/mL) in 53 to 64% of patients with primary liver cancer or chronic liver disease and in 19% of controls. 44% of patients with HCC and no evidence of cirrhosis had plasma concentrations of R249S-mutated DNA ≥150 copies/mL, compared to 21% in patients with both HCC and cirrhosis, 22% in patients with cholangiocarcinoma, 12% in patients with non-cancer chronic liver disease and 3% of subjects in the reference group. Thus, plasma concentrations of R249S-mutated DNA ≥150 copies/mL tended to be more common in patients with HCC developing without pre-existing cirrhosis (p = 0.027). Overall, these results support the preferential occurrence of R249S-mutated DNA in HCC developing in the absence of cirrhosis in a context of HBV chronic infection